Patho Flashcards
1
Q
Increase in size of cells resulting in increased size of organ.
A
Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
2
Q
Increase in number of cells.
A
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
3
Q
Hypertrophy of hyperplasia?Uterus during pregnancy
A
Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3
4
Q
Hypertrophy or hyperplasia?Wound healing
A
Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4
5
Q
Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.
A
Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7
6
Q
Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.
A
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7
7
Q
Type of cell death which results from a pathologic cell injury.
A
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9
8
Q
Type of cell death associated with inflammation.
A
Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
9
Q
It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.
A
Pyknosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
10
Q
It is the destructive fragmentation of the nucleus of a dying cell.
A
Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
11
Q
It is the complete dissolution of the chromatin of a dying cell.
A
Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
12
Q
This is the first manifestation of almost all forms of injury to cells.
A
Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8
13
Q
Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.
A
Hydropic change or Vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
14
Q
Appearance of lipid vacuoles in the cytoplasm.
A
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
15
Q
Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.
A
Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
16
Q
Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.
A
Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
17
Q
These are chemical species with a single unpaired electron in the outer orbital.
A
Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
18
Q
Most common cause of cell injury in clinical medicine.
A
Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
19
Q
Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.
A
Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19
20
Q
Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.
A
Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18
21
Q
Pathway of apoptosis trigerred by loss of survival signals, DNA damage and accumulation of misfolded proteins. Inhibited by Anti-apoptotic members of the Bcl family.
A
Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
22
Q
Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.
A
Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22
23
Q
Refers to any abnormal accumulation of triglycerides within parenchymal cells. Most often seen in the liver but can also occur in the heart, sk m., and kidneys.
A
Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23
24
Q
Other name for macrophages in contact with lipid debris of necrotic cells or abnormal forms of lipoproteins. Filled with minute, membrane-bound vacuoles of lipid, imparting a foamy appearance to their cytoplasm.
A
Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
25
Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons.
Xanthomas(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
26
Hypertrophy or hyperplasia?Cardiomegaly due to hypertension
Hypertrophy Due to increased workload(TOPNOTCH)
27
Most common exogenous pigment?
Carbon(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
28
"Wear and Tear pigment"?
Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
29
Pigment produced by tyrosinase-catalyzed oxidation of tyrosine to dihydroxyphenylalanine.
Melanin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
30
Hemoglobin-derived granular pigment that is golden-yellow to brown in color. Accumulates in excess of iron.
Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
31
Histochemical reaction used to identify hemosiderin.
Prussian blue test(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
32
Abnormal calcium deposition occuring in the absence of calcium metabolic derangements.
Dystrophic calcification.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
33
Calcium deposition in normal tissues occuring in the presence of hypercalcemia.
Metastatic calcification (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
34
Grossly seen as fine white granules or clumps, often felt as gritty deposits. Histologically, intra/extracellular basophilic deposits.
Calcium salts(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.27
35
A result of a progressive decline in the proliferative capacity and lifespan of cells.
Cellular aging(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.29
36
Appears as round or oval masses with intensely eosinophilic cytoplasm, nuclei with various stages of chromatin condensation and aggregation, karyorrhexis.
Apoptotic cell(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20
37
Membrane bound vesicles of cytosol and organelles quickly extruded and phagocytosed without eliciting inflammatory response.
Apoptotic bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20
38
Clear vacuoles within parenchymal cells, displacing the nucleus to the cell periphery.
Fatty change (TOPNOTCHRobbins Basic Pathology, 8th ed. p.24
39
Focal, intracellular fat deposits creating alternating bands of yellowed myocardium with alternating bands of darker red-brown uninvolved heart or "tigered effect".
Fatty change of the heart(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24
40
Rounded, eosinophilic accumulation of newly synthesized immunoglobulins in the rough ER of plasma cells.
Russel bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25
41
Eosinophilic cytoplasmic inclusion in liver cells composed of aggregated intermediate filaments which resist degradation. Seen in patients woth alcoholic liver disease.
Mallory body / "alcoholic hyalin"(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25
42
Aggregated protein inclusions that contain microtubule-associated proteins and neurofilaments, reflecting disrupted neuronal cytoskeleton.
Neurofibrillary tangles in Alzheimer's disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
43
An insoluble brownish-yellow granular intracellular material that accumulates as a function of age and atrophy. Appears as perinuclear electron-dense granules on electron microscopy.
Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26
44
A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
45
Refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction.
Fat necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11
46
A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called "fibrinoid" (fibrin-like) by pathologists.
Fibrinoid necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11
47
Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue.
Liquefactive necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
48
This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.
Gangrenous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10
49
It is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.31
50
Inflammation which is characterized by plasma protein exudation and a predominantly neutrophilic leukocyte accumulation.
Acute inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
51
Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and fibrosis.
Chronic inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
52
Five cardinal signs of inflammation?
Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
53
Initial vascular response to injury?
Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33
54
An ultrafiltrate of blood which contains little protein. Results from arteriolar vasodilation and increased blood flow.
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
55
Results from increased vascular permeability, leading to leakage of protein into tissues.
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
56
Fluid accumulation in extravascular space.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
57
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Rolling
Selectins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
58
State the molecule in the lymphocyte responsible for this stage of vascular inflammatory response:Firm adhesion
Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
59
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Transmigration
PECAM-1/CD 31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
60
State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion
ICAM -1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
61
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin
Sialyl-Lewis X modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
62
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin
Sialyl-Lewis X-Modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
63
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1
Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
64
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31
CD-31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
65
The process of luekocyte accumulation at the periphery of blood vessels is called ______.
Margination(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
66
Arrange the following steps in the inflammatory response:A. Recruitment of leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. Resolution
C, A, D, B, E(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35
67
Arrage the steps in leukocyte recruitment:A. TransmigrationB. Rolling C. MarginationD. Firm adhesion
C, B, D, A(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35
68
Process of coating microorganisms with proteins that facilitate phagocytosis.
Opsonization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.38
69
A lymphocyte with ingested microorganism fused with lysosome is called _______.
Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.39
70
The most important lysosomal enzyme involved in bacterial killing.
Elastase(TOPNOTCH)
71
Process of leukocyte migration toward sites of infection or injury along a chemical gradient.
Chemotaxis(TOPNOTCH)
72
The most important lysosomal enzyme involved in bacterial killing.
Elastase(TOPNOTCH)
73
A peptide Leukocyte granule constituent which kills microbes by creating holes in their membranes.
Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40
74
Predominant form of leukocyte during the first 6 - 24 hours of inflammation?
Neutrophils(TOPNOTCH)
75
Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?
Monocytes(TOPNOTCH)
76
Substances responsible for leukocyte-induced tissue injury?
Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)
77
Defective synthesis of CD 18 B-subunit of leukocyte integrins LFA-1 and Mac-1 leading to impaired leukocyte adhesion and migration through endothelium.
Leukocyte adhesion deficiency type 1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
78
Caused by a defect in fucose metabolism resulting in absence of sialyl-lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium.
Leukocyte adhesion deficiency type 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
79
Results from a defect in the protein involved in membrane docking and fusion.
Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
80
NADPH deficiency or defect resulting in decreased oxidative burst.
Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42
81
Type of acute inflammation characterized by the outpouring of watery, relatively protein-poor fluid derived from the serum or endothelial lining of peritoneal, pleural, and pericardial cavities.
Serous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
82
Fluid in a serous cavity is called ______.
Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
83
This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
84
Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
85
This type of inflammation is manifested by the presence of large amounts of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid.
Suppurative (purulent) inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
86
Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
87
It is an excavation of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of inflammatory necrotic tissue.
Ulcer(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
88
Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.
Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
89
Complement fragments which are anaphylotoxins.
C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
90
Complement fragment which aids in opsonization.
C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
91
Membrane attack complex
C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
92
It is the cytolytic endproduct of the complement cascade, which forms a transmembrane channel causing osmotic lysis of target cells.
Membrane attack complex (C5b,C6-9)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
93
Enzyme blocked by NSAIDS.
Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
94
Enzyme inhibited by glucocorticoids
Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
95
Polypeptide products of many cell types that function as mediators of inflammation and immune response.
Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
96
They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.
Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
97
Major cytokines in acute inflmmation.
TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
98
A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.
Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49
99
This component of the coagulation cascade initiates four systems involved in the inflammatory response, namely the kinin, clotting, fibrinolytic and complement systems.
Activated Hageman Factor / Factor XIIa(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.52
100
Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.
Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53
101
Macrophages in the liver
Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
102
Macrophages in the spleen and lymph nodes
Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
103
Macrophages in the CNS
Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
104
Macrophages in the lungs
Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
105
A focus of epiheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.
Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
106
Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli
Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
107
Acid-fast bacilli in macrophages, noncaseating granulomas
Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
108
Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellulr outline
Gumma (Syphilis)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
109
Rounded or stellate granuloma containing central granular debris and recognizable neutrophils, giant cells uncommon.
Cat-scratch Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
110
Noncaseating granulomas with abundant activated macrophages
Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
111
Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate
Chron disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
112
Cells with pink, granular cytoplasm with indistinct boundaries.
Epitheloid cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
113
40-50 um in size, consisting of a large mass of cytoplasm and many nuclei.
Giant cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
114
Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.
Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
115
Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.
TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57
116
Cells of these tissues are continuously being lost and replaced by maturation from stem cells and by proliferation of mature cells. Can readily regenerate after injury as long as the pool of stem cells is preserved.
Labile tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
117
Cells of theses tissues are quiescent and have only minimal replicative activity in their normal state. Capable of proliferating in response to injury or loss of tissue mass.
Stable tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
118
Cells of these tissues are considered to be terminally differentiated and nonproliferatvie in postnatal life.
Permanent tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
119
Labile, stable or permanent tissues:Bone marrow
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
120
Labile, stable or permanent tissues:Vaginal epithelium
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
121
Labile, stable or permanent tissues:Salivary glands
Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
122
Labile, stable or permanent tissues:Liver parenchyma
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
123
Labile, stable or permanent tissues:Endothelium
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
124
Labile, stable or permanent tissues:Smooth muscle cells
Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
125
Labile, stable or permanent tissues:Neurons
Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
126
Labile, stable or permanent tissues:Cardiac muscle
Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62
127
Type of collagen found in basement membrane
Type IV collagen(TOPNOTCH)
128
Type of collagen found in basement membrane
Type IV collagen(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.67
129
This is the most abundant glycoprotein in basement membrane.
Laminin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.68
130
The pink, soft, granular tissue seen beneath the scab of a skin wound.
Granulation tissue(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70
131
Maturation and reorganization of fibrous tissue
Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70
132
Healing of a clean, uninfected surgical incision approximated by surgical sutures
Healing by first intention / Primary Union(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.74
133
Type of healing wherein tissue is allowed to heal by itself before suturing. Used in large wounds, in the presence of abscess, or ulceration.
Healing by secondary intention / secondary union(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.76
134
Wound strength reaches 70 - 80 % of normal in ______ months.
3 months(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
135
Single most important cause of delay in wound healing.
Infection(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
136
True or false: Complete restoration can occur only in tissues composed of stable and labile cells.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
137
Refers to the restoration of tissue architecture and function after an injury.
Repair (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
138
True or false:Injury to tissues composed of permanent cells does not result to scarring.
False. Injury to tissues composed of permanent cells, inevitably results to scarring.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
139
Process of replacing damaged components of a tissue, returning to a normal state.
Regeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77
140
Migration and proliferation of fibroblasts with deposition of ECM.
Scar formation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72
141
Maturation and reorganization of fibrous tissue
Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.73
142
The pink, soft, granular tissue seen beneath the scab of a skin wound.
Granulation tissue(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.73
143
Arrange the steps in cutaneous wound healing:A. Formation of granulation tissueB. ECM remodelingC. Inflammation
C, A, B(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72
144
It consists of a series of steps at which the cell checks for the accuracy of replication and mitosis and instructs itself to proceed to the next step.
Cell cycle(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
145
In the cell cycle, this is called the presynthetic growth phase.
G1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
146
In the cell cycle, this is also called the premitotic growth phase.
G2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
147
These steps in the cell cycle prevents DNA replication or mitosis of damaged cells and either transiently stop the cell cycle to allow repair, or eliminate irreversibly damaged cells by apoptosis.
Checkpoint control(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
148
These enzymes promote DNA replication and various aspects of mitosis. They are required for cell cycle progression. Forms complexes with cyclin.
Cyclin-deoendent kinases (CDK)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61
149
This cytokine is released from activated macrophages, and is mitogenic for keratinocytes and fibroblasts. It also stimulates keratinocyte migration and granulation tissue formation.
Epidermal Growth Factor (EGF)(TOPNOTCH)
150
This cytokine increases vascular permeability and is mitogenic for endothelial cells.
Vascular Endothelial Growth Factor (VEGF)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.71
151
Pattern of extracellular signaling wherein the target cell is itself.
Autocrine(TOPNOTCH)
152
Pattern of extracellular signaling wherein the target cell is adjacent to the secretory cell.
Paracrine(TOPNOTCH)
153
Pattern of extracellular signaling wherein the target cell is distant to the secretory cell.
Endocrine(TOPNOTCH)
154
Synthesized by mesenchymal cells, present in the spaces between cells in connective tissue, between epithelium and supportive vascular and smooth muscle structures.
Interstitial Matrix(TOPNOTCH)
155
Component of ECM which confers tensile strength and recoil.
Fibrous proteins s.a. Collagen and elastin(TOPNOTCH)
156
Component of ECM that permits resilience and lubrication.
Proteoglycans, hyaluronan(TOPNOTCH)
157
Component of ECM that connect the elements to one another and to the cells.
Adhesive glycoproteins(TOPNOTCH)
158
Extravasation of fluid into interstitial spaces due to increases in vascular volume or pressure, decreases in plasma protein content or alterations in endothelial function.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
159
It is a severe and generalized edema with profound subcutaneous tissue swelling.
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
160
The edema fluid occuring with volume or pressure overload or under conditions of reduced plasma protein.
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
161
Edema secondary to increased vascular permeability and inflammation.
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
162
The serum protein most responsible for maintaining intravascular colloid osmotic pressure.
Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
163
In breast cancer, infiltration and obstruction of superficial lymphatics can cause edema of the overlying skin, called _______ appearance.
Peau d' orange(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
164
Microscopically, it is reflected primarily as a clearing and separation of the extracellular matrix elements with subtle cell swelling.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
165
Diffuse edema usually more prominent in certain body areas as a result of the effects of gravity.
Dependent edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
166
True or false:Dependent edema is a prominent feature of left-sided heart failure.
False.Dependent edema is a feature of right-sided HF, while pulmonary congestion is a feature of left-sided HF.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
167
Edema due to renal dysfunction which manifests disproportionately in tissues with loose connective tissue matrix, e.g. Eyelids.
Periorbital edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
168
Finger pressure over significantly edematous subcutaneous tissue displacing the interstitial fluid, leaving a finger-shaped depression on the skin.
Pitting edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
169
Condition wherein the lungs weigh 2-3x the normal, and on sectioning reveals frothy, sometimes blood-tinged mixture of air, fluid and extravasated red cells.
Pulmonary edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
170
Condition wherein the brain is grossly swollen, with narrowed sulci and distended gyri showing signs of flattening against the underlying skull.
Brain edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
171
It is an active process resulting from augmented blood flow due to arteriolar dilation.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
172
The affected tissue is redder than normal, because of engorgement with oxygenated blood.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
173
It is a passive process resulting from impaired venous rturn out of a tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
174
Tissue has a blue-red color due to accumulation of hemoglobin in the affected tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
175
Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage.
Acute pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
176
Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.
Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
177
Hemosiderin- laden macrophages
Heart- failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
178
The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration. The periportal hepatocytes are better oxygenated.
Acute hepatic congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
179
The central regions of the hepatic lobules are grossly red-brown and slightly depressed and are accentuated against the surrounding zones of uncongested tan, sometimes fatty liver (nutmeg liver).
Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
180
Presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage and hemosirin-laden macrophages
CPC of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
181
Extravasation of blood from vessels into the extravasclar space.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
182
Accumulation of blood within a tissue.
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
183
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
184
3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.
Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
185
1-2cm subcutaneous hematomas/bruises.
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
186
It is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.
Normal hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
187
Pathologic form of hemostasis.
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
188
It occurs after an initial injury, as a result of reflex neurogenic mechanisms.
Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
189
A potent endothelium-derived vasocontrictor.
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
190
Receptors responsible for platelet adhesion.
GpIb receptors- plateletVon Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
191
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)
192
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
193
Deficiency of GpIIb-IIIa receptors.
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
194
Deficiency of Factor VIII.
Von Willebrand Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
195
It is a membrane-bound procoagulant glycoprotein synthesized by endothelium, which becomes exposed at the site of injury.
Thromboplastin/Factor III(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
196
Formation of a hemostatic plug due to platelet aggregation
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
197
Hemostasis characterized by activation of thrombin through the coagulation cascade.
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
198
True or false:The primary aggregation of platelets is irreversible.
FalseReversible(TOPNOTCH)
199
Two substances essential for the formation of a primary hemostatic plug.
ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87
200
True or false:Activation of the coagultion cascade and subsequent thrombin formation is reversible.
FalseIrreversible(TOPNOTCH)
201
Substance that activates the coagulation proteins.
Calcium(TOPNOTCH)
202
Substance that medites further platelet aggregation and degranulation.
ADP(TOPNOTCH)
203
Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.
TXA2(TOPNOTCH)
204
Most important initiator of the coagulation cascade.
Tissue factor(TOPNOTCH)
205
A protein found on endothelial cells involved in the breakdown of blood clots which catalyzes conversion of plasminogen to plasmin.
Tissue plasminogen activator (t-PA) and Urokinase(TOPNOTCH)
206
Components of Virchow's triad?
Endothelial injuryStasisHypercoagulability(TOPNOTCH)
207
It is a major contributor to the development of VENOUS thrombi.
Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
208
Type of blood flow found in normal blood vessels, wherein platelets flow centrally in the vessel lumen, separated from the endothelium by a slow moving clear zone of plasma.
Laminar flow(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
209
This contirbutes to arterial and cardic thrombisis by causing endothelial injury or dysfunction as well as formation of countercurrents and local pockets of stasis.
Turbulence(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94
210
Any alteration of the coagulation pathway that predisposes to thrombosis.
Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
211
A detached, intravascular solid, liquid or gaseous mass that is carried by the blood distal to its point of origin.
Embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95
212
Apparent laminations seen in a thrombus, representing pale platelet and fibrin layers alternating with darker erythrocyte-rich layers.
Lines of Zahn(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
213
Significance of Lines of Zahn?
Represents thrombosis in the setting of blood flow, seen in antemortem clots.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
214
Thrombi occuring in heart chambers or aortic lumen
Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
215
Gelatinous thrombi with a dark red dependent portion where red cells have settled by gravity with a yellow "chicken fat" supernatant. Usually unattached to underlying wall.
Postmortem thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
216
Thrombi on heart valves.
Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
217
Sterile, verrucous endocartidis occuring in patients with SLE.
Limban-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
218
Thrombi occuring in heart chambers or in aortic lumen.
Mural thrombi(TOPNOTCH)
219
Vegetations occuring in the presence of non - infected valves in hypercoagulable states.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96
220
Fate of a thrombus wherein the thrombus accumulates additional platelets and fibrin, eventually causing vessel obstruction.
Propagation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
221
Fate of a thrombus wherein it may dislodge or fragment and transported elsewhere in the vasculature.
Embolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
222
Fate of a thrombus as a result of of fibrinolytic activity leading to rapid shrinkage and even total lysis of recent thrombi.
Dissolution(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
223
Fate of a thrombus wherein it may induce inflammation and fibrosis and establish some degree of blood flow.
Organization and recanalization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
224
True or false:Therapeutic administration of fibrinolytic agents is generally effective only within a few hours of thrombus formation.
True(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
225
Most common site of venous thrombosis.
Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
226
Most common sequelae of deep venous thrombosis.
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97
227
Tumor-associated procoagulant release largey responsible for the increased risk of thromboembolic phenomena seen in disseminated cancers.
Migrating thrombophlebitis or Trousseau's syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
228
Hardening or thickening of the arteries as a result of the accumulation of fatty materials, macrophages, platelets and other inflammatory mediators.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
229
Fates of a thrombus (4)
PropagationResolution/DissolutionOrganization and recanalizationEmbolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98
230
Embolus occluding a bifurcation in the pulmonary tree.
Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
231
True or false:A patient who has had one pulmonary embolus has a decreased risk of developing another embolus.
False.The patient is at risk of developing more pulmonary emboli.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
232
A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.
Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
233
Most common symptom of pulmonary embolism.
None/ Asymptomatic (60-80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
234
Right Ventricular failure secondary to pulmonary hypertension.
Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
235
Emboli in the arterial circulation.
Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
236
Most common origin of systemic thrombi.
Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
237
Major site of arteriolar embolization.
Lower extremities (75%)Brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
238
Microscopic fat globules found in the circulation after fractures of long bones or after soft-tissue trauma.
Fat embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
239
Symptoms of pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia characterize what syndrome?
Fat embolism syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
240
Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.
Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
241
Amount of air in the circulation which produces clinical effects of air embolism.
>100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99
242
This occurs when individuals are exposed to sudden changes in atmospheric pressure (e.g. Deep sea divers, scuba divers).
Decompression sickness(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
243
The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and around joints causing pain.
Bends(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
244
Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.
Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
245
More chronic form of decompression sickness where persistence of gas emboli in the bones leads to multiple foci of ischemic necrosis.
Caisson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
246
Treatment of choice for decompression sickness.
Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
247
Underlying cause of amniotic fluid embolism.
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)
248
Underlying cause of amniotic fluid embolism.
Entry of amniotic fluid into the maternal circulation through a tear in the placetal membranes and rupture of uterine veins.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
249
Presence of marked pulmonary edema, diffuse alveolar damage, and presence of squamous cells in the pulmonary circulation shed from fetal skin, lanugo hair, fat and mucin.
Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
250
White or red infarct?Venous occlusion
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
251
White or red infarct?Lung infarction
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
252
White or red infarct?Intestinal infarct
Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
253
White or red infarct?Myocardial infarction
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
254
White or red infarction?Splenic infact
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
255
White or red infarction?Wedge infarct
White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100
256
The dominant histologic characteristic of infarction.
Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
257
Histologic characteristic of brain infarcts.
Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
258
This occurs when bacterial vegetations from a heart valve embolize or when microbes seed an area of necrotic tissue.
Septic infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
259
Most common sequalae of septic infarcts.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
260
Major determinants of the eventual outcome of an infarct. (4)
Nature of vascular supplyRate of development of occlusionVulnerability to hypoxiaOxygen content of blood(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101
261
Neurons undergo irreversible damage when deprived of their blood supply for _______.
3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
262
Myocardial cells undergo irreversile damage after ______ minutes of ischemia.
20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
263
It is the final common pathway for severe hemorrhage, extensive trauma, burns, large MI, pulmonary embolism and sepsis.
Shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
264
End results of shock (3)
HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
265
This type of shock results from failure of the cardic pump which maybe caused by MI, ventricular arrythmias, cardiac tamponade or outflow obstruction.
Cardiogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
266
This type of shock results from loss blood or plasma volume.
Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
267
This type of shock is caused by microbial infection, caused by gram negative and gram positive bacteria and fungi
Septic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
268
True or false:Systemic bacteremia must be present to induce septic shock.
FalseHost inflammatory response to local extravascular infections may be sufficient to induce septic shock.(TOPNOTCHRobbins Basic Pathology, 8th ed. p.102
269
Type of shock which occurs in the setting of an anesthetic accident or spinal cord injury as a result of loss of vascular tone and peripheral pooling of blood.
Neurogenic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
270
This type of shock represents systemic vasodilation and increased vascular permeability caused by IgE hypersensitivity reaction.
Anaphylactic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102
271
Septic shock caused by gram negative bacilli.
Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
272
Criteria for SIRS.
Temp 38 CelciusHR >90 bpmRR >20 or PaCO2 12,000 cells/mm3 or 10% bands(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103
273
Adrenal changes in shock.
Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
274
Kidney changes in shock.
Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
275
Gastrointestinal changes in shock.
Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
276
Lung changes in shock.
Diffuse alveolar damage if due to bacterial sepsi and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106
277
These agents cause transmissible spongiform encephalopathies.
Prions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 321
278
Infected cells show distinct nuclear and ill-defined cytoplasmic inclusions.
CMV infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
279
Infected cells show glassy nuclear inclusions, frequently with a surrounding halo.
Herpesvirus infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
280
Infected hepatocytes show diffuse granular (ground-glass) cytoplasm.
Hepatitis B viral infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322
281
Sexually transmitted protozoan that can colonize the vagina and male urethra.
Trichimonas vaginalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325
282
Protozoan acquired either by contact with oocyte-shedding kittens or by consumption of cyst-ridden undercooked meat.
Toxoplasma gondii(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325
283
Size of microorganisms for them to be inhaled directly into the alveoli.
5 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
284
These microorganisms grow in contaminated food and releases powerful enterotoxins that cause food poisoning symptoms without any bacterial multiplication in the gut.
Staphylococcal strains(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
285
Intestinal helminth that cause disease when present in large numbers or cause obstruction of the gut.
Ascaris lumbricoides(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 326
286
Helminth that causes iron deficiency anemia by chronic loss of blood.
Hookworms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
287
Helminth that depletes vitamin B12 giving rise to an illness resembling pernicious anemia.
Diphyllobotrium latum(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327
288
Placentofetal route as a mode of transmission is also referred to as ________.
Vertical transmission(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 329
289
The ability of bacteria to cause disease.
Virulence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 331
290
Bacterial surface molecules that bind to host cells.
Adhesins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332
291
Filamentous proteins on gram negative bacteria which allow exchange of genes between bacteria, and also involved in adherence.
Fimbriae/pili(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332
292
Clostridium perfringens produces this toxin that disrupts plasma membranes resulting in digestion of host tissues and collagen.
Alpha toxin (lecithinase)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
293
Bacterial toxins with the capacity to stimulate large populations of T lymphocytes, functionally resulting in a "cytokine storm".
Superantigens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
294
Examples of antigen presenting cells.
Dendritic cellsMacrophagesB-cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
295
A superantigen secreted by S. aureus which causes inflammation, fever and shock. Found in the vagina of menstruating women.
Toxic shock syndrome toxin (TSST-1)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
296
Collection of neutrophils which gives rise to localized liquefactive necrosis.
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334
297
High risk agents of bioterrorism which are easily disseminated and has high potential for mortality. An example is smallpox.
Category A(TOPNOTCH)
298
A distinctive form of mononuclear inflammation usually evoked by infectious agents that resist eradication, but are capable of stimulating strong T cell mediated immunity. Characterized by epitheloid cells which may fuse to form giant cells.
Granulomatous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 335
299
Agents that are relatively easy to disseminate and produces moderate morbidity and low mortality. An example is E.coli O157:H7 which can cause HUS.
Category B(TOPNOTCH)
300
Includes emerging pathogens that have the potential for mass dissemination with high morbidity and mortality. Examples are Nipah virus and Hanta virus.
Category C(TOPNOTCH)
301
This term refers to protection against infections.
Immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
302
It is the collection of cells and molecules that are responsible for defending against pathogenic microbes.
Immune system(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
303
Type of immunity mediated by neutrophils, macrophages and natural killer cells and includes epithelial barriers of the skin, GIT and respiratory tract.
Innate immunity (natural/native)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
304
Type of immunity mediated by lymphocytes and their products, and is normally silent and responds to the presence of microbes by becoming active, expanding and generating potent mechanisms for neutralizing and eliminating microbes.
Adaptive immunity (acquired/specific)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
305
Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
306
Type of adaptive immunity mediated by T lymphocytes.
Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
307
Mediated by antibodies and is effective against extracellular microbes.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
308
Reaction of T-lymphocytes, designed to combat cell-associated microbes (e.g. Phagocytosed microbes and microbes in the cytoplasm of infected cells).
Cell-mediated immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
309
Reaction of immune system against one's own cells.
Autoimmunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.119
310
Results from activation of TH2 CD4+ helper T cells by environmental antigens, leading to the production of IgE antibodies, which become attached to mast cells.
Type I Hypersensitivity (immediate)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
311
Caused by antibodies that bind to fixed tissue or cell surface antigens and promote phagocytosis and destruction of the coated cells or trigger pathologic inflammation in tissues.
Type II Hypersensitivity (Antibody-mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
312
Caused by antibodies binding to antigens to form complexes that circulate and may deposit in vascular beds and stimulate inflammation, secondary to complement activation.
Type III Hypersensitivity (immune complex mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
313
Cell-mediated immune responses in which T lymphocytes cause tissue injury, either by producing cytokines that induce inflammation and activate macrophages, or by directly killing cells.
Type IV Hypersensitivity (T-cell mediated/Delayed)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
314
Indicate type of hypersensitivity reaction:SLE
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
315
Indicate type of hypersensitivity reaction:Multiple sclerosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
316
Indicate type of hypersensitivity reaction:Transplant rejection
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
317
Indicate type of hypersensitivity reaction:Anaphylaxis
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
318
Indicate type of hypersensitivity reaction:Goodpasture syndrome
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
319
Indicate type of hypersensitivity reaction:Serum sickness
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
320
Indicate type of hypersensitivity reaction:Arthus reaction
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
321
Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
322
Indicate type of hypersensitivity reaction:Allergies
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
323
Indicate type of hypersensitivity reaction:Type I DM
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
324
Indicate type of hypersensitivity reaction:Tuberculosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
325
Indicate type of hypersensitivity reaction:Bronchial asthma
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
326
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
327
Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
328
Indicate type of hypersensitivity reaction:Polyarteritis nodosa
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
329
Indicate type of hypersensitivity reaction:Rheumatoid arthritis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
330
Indicate type of hypersensitivity reaction:Inflammatory bowel disease
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
331
Indicate type of hypersensitivity reaction:Tuberculin reaction
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
332
Indicate type of hypersensitivity reaction:Reactive arthritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
333
Indicate type of hypersensitivity reaction:Graves disease
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
334
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
335
Indicate type of hypersensitivity reaction:Myasthenia gravis
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
336
Indicate type of hypersensitivity reaction:Insulin resistant DM
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
337
Indicate type of hypersensitivity reaction:Pernicious anemia
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
338
A special form of graft rejection occuring in the setting where preformed antidonor antibodies are present in the circulation of the host before transplant. Occurs within minutes to a few hours after transplantation.
Hyperacute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
339
Rejection which occurs within days to weeks of transplantation in a nonimmunosuppressed host. Caused by both cellular and humoral immune mechanisms.
Acute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
340
Acute rejection most commonly seen within the first months after transplantation, typically accompanied by signs of renal failure. Extensive CD4+ and CD8+ T-cell infiltration with edema and mild interstitial hemorrhage.
Acute cellular rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
341
Acute rejection caused by antidonor antibodies. May take the form of necrotizing vasculitis with endothelial cell necrosis, neutrophilic infiltration, deposition of antibody, complement, and fibrin, and thrombosis.
Acute humoral rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
342
Rejection which present clinically months to years after transplantation with a progressive rise in serum creatinine levels. Dominated by arteriosclerosis, interstitial fibrosis and loss of renal parenchyma.
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
343
A multisystem autoimmune disease which principally affects the skin, kidneys, serosal membranes, joints and heart. Associated with autoantibodies including ANAs.
Systemic Lupus Erythematosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.139
344
SOAP BRAIN MD mnemonic for SLE stands for?
SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
345
How many symptoms must be present in a patient for her/him to be diagnosed as having SLE?
4 out of 11 symptoms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
346
Most serious and most common form of renal lesion in SLE. "Wire-loop" appearance of glomerular capillary walls.
Diffuse proliferative glomerulonephritis (Class IV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.142
347
Cardiac manifestation of SLE, which occurs as nonspecific mononuclear infiltrates and the presence of irregular 1-3mm warty deposits on either surface of the leaflets.
Libman-Sacks Endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.144
348
A systemic, chronic inflammatory disease affecting many tissues but principally attacking the joints to produce a nonsuppurative proliferative synovitis that frequently progress to destroy articular cartilage and underlying bone with resulting disabling arthritis.
Rheumatoid arthritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.145
349
Characteristic lesion in RA, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue and fibrous connective tissue.
Pannus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
350
Cytokine which plays a central role in the pathogenesis of RA.
TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
351
A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.
Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148
352
Characterized by progressive fibrosis involving the skin, GIT and other tissues. May be a result of activation of fibroblasts by cytokines produced by T cells.
Systemic sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.149
353
A vascular disorder characterized by reversible vasospasm of the arteries. Typically the hands turn white due to vasospasm, then blue due to cyanosis, then red due to reactive hyperemia.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.151
354
One of the more common forms of primary immune deficiency characterized by absent or markedly decreased numbers of B-cells in the circulation, with depressed serum levels of all classes if immunoglobulin.
X-linked agammaglobulinemia (Bruton disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.152
355
Most common of all the primary immune deficiencies characterized by recurrent sinopulmonary infections and diarrhea.
Isolated IgA deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
356
A constellation of genetically distinct syndromes with common feature of defects in both humoral and cell-mediated immune responses, making affected infants susceptible to severe recurrent infections by bacteria, viruses, fungi, protozoans, and opportunistic infections.
Severe Combined Immunodeficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
357
Autosomal recessive form of SCID is due to deficiency of what enzyme?
Adenosine deaminase (ADA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
358
An X-linked recessive disease characterized by thrombocytopenia, eczema, and marked vulnerability to recurrent infection ending in early death.
Wiskott-Aldrich Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.155
359
HIV viral surface proteins essential for viral entry into cells.
gp41 and gp120(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.157
360
A form of pneumonia in HIV patients caused by a yeast-like fungus.
Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)
361
Main cellular target of HIV.
CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.158
362
P.carinii pneumonia occurs in AIDS patients with CD4+ T cell count of ______.
Less than 200 cells/uL(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
363
Most common secondary infection of the CNS in patients with AIDS.
Toxoplasmosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
364
Most common neoplasm in AIDS patients, caused by HHV8. Characterized by cutaneous lesions with or without internal involvement.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.164
365
A disorder of protein misfolding, causing extracellular deposition of pink or red colored deposits stained with Congo red, with apple-green birefringence in polarized light.
Amyloidosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.166
366
This term literally means "new growth".
Neoplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
367
An abnormal mass of tissue the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after the cessation of stimuli which evoked the change.
Neoplasm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
368
Study of tumors.
Oncology(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
369
Benign or malignant?Localized
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
370
Benign or malignant?Amenable to surgical removal
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
371
Benign or malignant?Invades and destroys adjacent tissues.
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
372
What are the two basic components of tumors?
Parenchyma and Stroma(TOPNOTCH)
373
Benign or malignant?Metastasis
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
374
This component of tumors largely determines its biologic behavior.
Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
375
This component of tumors determines the name of the growth.
Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
376
This component of tumors is crucial to the growth of neoplasms since it carries the blood supply and provides support to the growth of cells.
Stroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
377
Benign or malignant?Fibroma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
378
Benign or malignant?Chondroma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
379
Benign or malignant?Adenoma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
380
Benign or malignant?Hepatoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
381
Benign or malignant?Papilloma
Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
382
Malignant neoplasms arising in mesenchymal tissue or its derivatives.
Sarcomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
383
Benign tumor arising in fibrous tissue is called?
Fibroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
384
A benign cartilagenous tumor is called?
Chondroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
385
This is a benign epithelial neoplasm which produces glandular patterns or neoplasms derived from glands but not necessarily exhibit glandular patterns
Adenoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
386
These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.
Papillomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174
387
A mass that projects above a mucosal surface to form a macroscopically visible structure.
Polyps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
388
A cancer of fibrous tissue origin.
Fibrosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
389
Malignant neoplasms of epithelial cell origin.
Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175
390
Carcinoma of squamous cell origin.
Squamous cell carcinoma(TOPNOTCH)
391
Carcinoma of squamous cell origin.
Squamous cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
392
Benign or malignant?Lymphoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
393
Benign or malignant?Seminoma
Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
394
The extent to which neoplastic cells resemble their normal forebears morphologically and functionally.
Differentiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176
395
This is considered a hallmark of malignancy, which literally means "to form backward".
Anaplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177
396
These cells display marked pleomorphism, nuclei are variable and bizzare in size and shape. Chromatin is course and clumped. Mitoses are often numerous and distinctly atypical.
Anaplastic cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177
397
This term is defined by disorderly but non-neoplastic proliferation of cells, described as a loss in uniformity of individual cells and in their architectural orientation.
Dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
398
Defined as dysplactic changes which involve the entire thickness of the epithelium.
Carcinoma -in - situ(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
399
True or false?Dysplasia always progress to cancer.
False(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178
400
True or false?Lack of capsule in a neoplastic growth indicates malignancy.
FalseSome benign tumors are not encapsulated.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
401
This term describes the development of secondary implants discontinuous with the primary tumor, in remote tissues.
Metastasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
402
Next to metastasis, this is the most reliable feature that distinguishes malignant from benign tumors.
Local invasiveness(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.179
403
Methods of dissemination of malignant neoplasms? (3)
SeedingLymphatic spreadHematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
404
This is the mode of dissemination of cancers of the ovary and CNS.
Spread by seeding(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
405
This is the mode of dissemination more typical of carcinomas.
Lymphatic spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
406
This is the mode of dissemination more typical of sarcomas.
Hematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
407
It is defined as the first lymph node in a regional lymphatic basin that receives lymph flow from a primary tumor.
Sentinel lymph node(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180
408
What are the most common sites of metastasis involved in hematogenous dissemination of cancer?
Liver and lungs(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.181
409
This substance is a byproduct of metal smelting, a component of alloys, electrical and semiconductor devices which could cause cancer of the lungs and skin and hemangiosarcomas.
Arsenic and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
410
This substance was formerly used for fire-resistant textiles and construction materials which could cause lung cancer and more prominently malignant mesothelioma
Asbestos(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
411
This substance is commonly used as a solvent in paint, rubber, dry cleaning, adhesives and detergents which could cause leukemias and Hodgkin lymphoma.
Benzene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
412
This substance is used as hardener for metal alloys used in aerospace applications and nuclear reactors which is commonly associated with cancer of the lung.
Beryllium and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
413
This substance is used in solders, batteries and metal alloys commonly associated with cancers of the prostate.
Cadmium and its compounds(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
414
This substance is a refrigerant and used as adhesive for plastics, which causes hepatic angiosarcoma.
Vinyl chloride(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.183
415
Inherited gene : Cancer syndromeRB gene :__________
Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
416
Inherited gene : Cancer syndromep53 : ______________
Li Fraumeni Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
417
Inherited gene : Cancer syndrome__________ : Familial Adenomatous Polyposis / Colon CA
APC Gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
418
Inherited gene : Cancer syndrome_________ : Breast on Ovarian Tumors
BRCA 1 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
419
Inherited gene : Cancer syndrome_________ : Breast Cancer only
BRCA 2 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
420
Inherited gene : Cancer syndromeRET gene : _________
Multiple Endocrine Neoplasia 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
421
Inherited gene : Cancer syndrome__________ : Colon cancer
kras gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184
422
Normal cellular genes whose products promote cell proliferation.
Proto-oncogenes(TOPNOTCH)
423
Normal cellular genes whose products promote cell proliferation.
Proto-oncogenes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.188
424
It is a naturally occurring carcinogenic agent produced by some strains of Aspergillus, a mold that grows on improperly stored grains and nuts.
Aflatoxin B(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
425
There is a strong correlation between the dietary level of Aflatoxin and what type of cancer?
Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
426
These substances require metabolic conversion to be carcinogenic.
Indirect - acting carcinogens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209
427
These substances stimulate proliferation of the mutated cells.
Promoters(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
428
How does ionizing radiation cause cancer?
Through chromosome breakage, translocations and point mutations leading to genetic damage and carcinogenesis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
429
What is the mechanism of action of UV rays in the formation of neoplastic cells?
UV rays induce formation of pyrimidine dimers within DNA leading to mutations.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210
430
This is the only retrovirus that has been demonstrated to cause cancer in humans.
Human T-cell Leukemia Virus -1 (HTLV-1)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.211
431
HPV strains which has been implicated in the genesis of cervical and anorectal cancer.
HPV 16, 18(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.212
432
EBV has been implicated in the pathogenesis of the following cancers except:A. Burkitt lymphomaB. Lymphoma in HIV patientsC. Nasopharyngeal carcinomaD. Hodgkin lymphomaE. None of the above
E. none of the above(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.212
433
Which hepatitis virus leads to hepatocellular carcinoma?
HBV, HCV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213
434
This is the first bacterium to be classified as a carcinogen.
Helicobacter pylori(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213
435
What type of cancer can be caused by H.pylori?
Gastric adenocarcinoma Gastric MALT lymphomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.214
436
These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.
Papillomas(TOPNOTCH)
437
Tumor antigens are presented on the cell surface by MHC Class I molecules to which type of T lymphocytes?
CD8+ T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.215
438
These disorders are derived from one's parents, transmitted through gametes through the generations, and are therefore familial.
Hereditary disorders(TOPNOTCH)
439
This term literally means "present at birth".
Congenital(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
440
This term refers to permanent changes in the DNA.
Mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
441
This type of mutation results from the substitution of a single nucleotide base by a different base, resulting in the replacement of one amino acid by another.
Missense mutation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
442
This type of mutation results in the replacement of one amino acid by a stop codon, resulting in chain termination.
Nonsense mutation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
443
Missense, nonsense and silent mutations are examples of ________ mutations, wherein only one base pair is replaced.
Point mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
444
This type of mutation occur when the insertion or deletion of one or two bse pairs alters the reading frame of the DNA strand.
Frameshift mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
445
These mutations are characterized by amplification of a sequence of three nucleotides.
Trinucleotide repeat mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
446
Disease characterized by CGG trinucleotide repeats.
Fragile X Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227
447
This is a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems.
Huntington's disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
448
Genetic mutation in Huntington's disease?
CAG trinucleotide repeats(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
449
This disorder is a chronic, slowly progressing inherited genetic disorder characterized by muscle wasting, cataracts, heart conduction defects, endocrine changes and myotonia.
Myotonic Dystrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
450
Genetic mutation found in myotonic dystrophy?
CTG Trinucleotide repeats(TOPNOTCH)
451
A point mutation wherein a single base pair is replaced but codes for the same amino acid, therefore has no effect on the functioning of the protein.
Silent mutation(TOPNOTCH)
452
An example of point mutation wherein a purine base is replaced by another purine base or a pyrimidine base is replaced by another pyrimidine base.
Transition(TOPNOTCH)
453
A point mutation wherein a purine is replaced by a pyrimidine or vice versa.
Transversion(TOPNOTCH)
454
Diseases caused by single gene defects are called?
Mendelian Disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
455
A condition wherein both dominant and recessive alleles of a gene pair may be fully expressed in the heterozygote.
Codominance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
456
The presence of many allelic forms of a single gene is called _______.
Polymorphism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
457
This occurs when one gene influences or leads to multiple phenotypic traits.
Pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
458
A phenomenon wherein a single phenotype or genetic disorder may be caused by mutations of several genetic loci or allele.
Genetic heterogeneity Note: compare with pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228
459
A transmission pattern of inheritance which is manifested in the heterozygous state, wherein at least one parent of an index case is usually affected, both males and females are affected and both can transmit the condition.
Autosomal dominant (AD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
460
This pattern of inheritance occur when BOTH of the alleles at a given gene locus are mutants, wherein the parents are not affected, but offspring have 1 in 4 chance (25%) of being affected.
Autosomal recessive(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
461
Pattern of inheritance wherein the disorder is transmitted by heterozygous female carriers only to 50% of the sons. An affected male does not transmit the disorder to sons but all daughters are carriers.
X-linked disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229
462
An autosomal dominant disorder of connective tissues characterized by abnormally long legs, arms and fingers, joint hyperextensibility, pectus excavatum, lens subluxation and increased risk of aortic dissection.
Marfan Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
463
Integral component of elastic fibers defective in Marfan Syndrome.
Fibrillin 1(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
464
Fibrillin 1 is encoded by what gene?
FBN1 gene (chromosome 15q21)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230
465
A collection of disorders caused by defects in collagen synthesis or structure, characterized by hyperextensible skin and joint hypermobility, rupture of internal organs and poor wound healing.
Ehlers-Danlos SyndromesThere are 6 variants to Ehlers-Danlos (nice to know)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.231
466
This autosomal recessive inborn error of metabolism is characterized by inability to convert phenylalanine to tyrosine, strong mousy or musty odor of urine and sweat, decreased pigmentation of hair and skin, eczema, seizures and mental retardation.
Phenylketonuria (PKU)(TOPNOTCH)
467
This autosomal dominant disorder is caused by a mutation in the gene that specifies the receptor for LDL, impairing the intracellular transport and catabolism of LDL.
Familial hypercholesterolemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.232
468
Enzyme deficient in classic PKU.
Phenylalanine hydroxylase (PAH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234
469
An autosomal recessive disorder of galactose metabolism characterized by jaundice, liver damage, cataracts, neural damage, vomiting and diarrhea.
Galactosemia(TOPNOTCH)
470
Deficiency of this enzyme can also cause symptoms of phenylketonuria due to decreased synthesis of a cofactor in the conversion of phenylalanine to tyrosine.
Dihydrobiopteridine reductase (DHPR)Enzyme responsible for the reduction of Dihydrobiopterin (BH2) to Tetrahydrobiopterin (BH4).(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234
471
Enzyme deficient in galactosemia.
Galactose-1-phosphate uridyltransferase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.235
472
Lysosomal storage disease due to deficiency of glucosylceramidase.
Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
473
Lysosomal storage disease due to deficiency of B-Hexosaminidase A.
Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
474
Lysosomal storage disease due to deficiency of a-Galactosidase A.
Fabry disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
475
Lysosomal storage disease due to deficiency of Sphingomyelinase.
Niemann-Pick disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
476
Lysosomal storage disease common among Ashkenazi Jews characterized by motor weakness, mental retardation, blindness, neurologic dysfunction and death.
Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236
477
Lysosomal storage disease characterized by accumulation of glucosylceramide in mononuclear phagocytic cells, which enlarge, forming "wrinkled tissue paper" cytoplasmic appearance.
Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
478
What do you call the pathognomonic cell characterized by "wrinkled tissue paper" cytoplasmic appearance.
Gaucher cell(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
479
These disorders result from the accumulation of mucopolysaccharides in many tissues including the liver, spleen, heart, blood vessels, brain, cornea and joints. Affected patients have coarse facial features.
Mucopolysaccharidoses(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238
480
Mucopolysaccharidosis characterized by corneal clouding, coronary arterial and valvular depositions, which occurs due to deficiency of a-L-iduronidase, leading to accumulation of dermatan and heparan sulfate.
Hurler syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239
481
An X-linked mucopolysaccharidosis which is due to a deficiency of L-iduronate sulfatase. Symptoms are similar to Hurler sundrome, but without corneal clouding.
Hunter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239
482
Glycogen storage disease characterized by hepatomegaly, renomegaly, hypoglycemia, hyperlipidemia and hyperuricemia, leading to gout and skin xanthomas.
von Gierke's disease (Type I)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
483
von Gierke's disease is due to a deficiency of what enzyme?
Glucose-6-phosphatase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
484
Glycogen storage disease characterized by accumulation of glycogen in skeletal muscles leading to painful cramps during strenuous exercise and myoglobinuria.
McArdle syndrome (type V)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
485
Glycogen storage disease characterized by mild hepatomegaly, cardiomegaly, muscle hypotonia, and may lead to cardiorespiratory failure.
Pompe disease (type II)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
486
Enzyme deficient in McArdle syndrome.
Muscle phosphorylase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240
487
These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.
Cytogenetic disorders(TOPNOTCH)
488
These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.
Cytogenetic disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.241
489
It is a term used to describe the presence of two or more populations of cells in the same individual.
Mosaicism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.242
490
This refers to a lack of one chromosome of the normal complement (e.g. XO).
Monosomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
491
This refers to the presence of three copies of a particular chromosome, instead of two.
Trisomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
492
This mechanism occurs due to the failure of chromosome pairs to separate properly during meiosis stage 1 or 2.
Nondisjunction(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
493
This mechanism implies transfer of a part of one chromosome to another chromosome.
Translocation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
494
This mechanism involves loss of a portion of a chromosome.
Deletion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243
495
Patients with this syndrome have severe mental retardation, flat facial profile, epicanthic folds, cardiac malformations, increased risk of leukemia, and premature development of Alzheimer's disease.
Down syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
496
Down syndrome is also called _________
Trisomy 21(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
497
Trisomy 18 is also called ________ syndrome.
Edwards syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
498
Trisomy 13 is also called _________ syndrome.
Patau syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244
499
Syndrome characterized by a prominent occiput, low set ears, micrognathia, rocker-bottom feet, renal malformation, mental retardation and heart defects.
Edwards syndrome / trisomy 18(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
500
Syndrome characterized by mental retardation, microcephaly, micropthalmia, polydactyly, cleft lip and palate, cardiac and renal defects, umbillical hernia and rocker-bottom feet.
Patau syndrome/Trisomy 13(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
501
Syndrome characterized by thymic hypoplasia with diminished T-cell immunity and parathyroid hypoplasia with hypocalcemia.
DiGeorge syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
502
Syndrome characterized by congenital heart disease affecting outflow tracts, facial dysmorphism and developmenta delay.
Velocardiofacial syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
503
Deletion of genes from this chromosome gives rise to DiGeorge and velocardiofacial syndromes.
22q11.2Remember mnemonic CATCH22(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245
504
The q from 22q11.2 refers to ________.
"Long arm" of chromosome 22.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
505
Syndrome defined as male hypogonadism that develops when there are at least two X chromosomes and one or more Y chromosomes.
Klinefelter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
506
Syndrome manifested by a eunochoid body habitus, reduced facial, body and pubic hair, gynecomastia, testicular atrophy, decreased serum testorerone and incresed urinary gonadotropin levels. It is the most common cause of hypogonadism in males.
Klinefelter syndrome (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
507
Most common chromosomal derangement in Klinefelter syndrome.
47XXY(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246
508
Syndrome which results from the partial or complete monosomy of the short arm of the X chromosome.
Turner syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247
509
Inheritance associated with mitochondrial DNA.
Maternal inheritance(TOPNOTCH)
510
Neurodegenerative disease which manifests as progressive bilateral loss of central vision that leads to blindness. This is the prototypical disorder of mutations in mitochondrial genes.
Leber hereditary optic neuropathy(TOPNOTCH)
511
Inheritance associated with mitochondrial DNA.
Maternal inheritance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247
512
An epigenetic process wherein certain genes are differentially "inactivated" during paternal and maternal gametogenesis.
Genomic imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.252
513
This refers to transcriptional silencing of the maternal allele.
Maternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
514
Refers to the transcriptional silencing of the paternal allele.
Paternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
515
Syndrome characterized by mental retardation, short stature, hypotonia, obesity, small hands and feet, and hypogonadism. Paternal imprinting.
Prader-Willi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
516
Syndrome manifested as mental retardation, ataxic gait, seizures and inappropriate laughter. Also called the "happy puppet syndrome". Maternal imprinting.
Angelman syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251
517
These represent primary errors of morphogenesis due to an intrinsically abnormal developmental process.
Malformations(TOPNOTCH)
518
These represent primary errors of morphogenesis due to an intrinsically abnormal developmental process.
Malformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
519
These result from secondary destruction of an organ or body region that was previously normal in development, due to an extrinsic disturbance in morphogenesis.
Disruptions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
520
These are due to generalized compression of the growing fetus by abnormal biomechanical forces, for example uterine constraint.
Deformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
521
This refers to multiple congenital anomalies that result from secondary effects of a single localized aberration in organogenesis. The initiating event may be a malformation, deformation or disruption.
Sequence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254
522
This refers to the presence of several defects that cannot be explained on the basis of a single localizing initiating error in morphogenesis.
Malformation syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253
523
Elements of the TORCH complex.
TOxoplasmaTreponema pallidumRubellaCytomeglovirusHerpesvirus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.256
524
Most common cause of neonatal mortality.
Congenital anomalies(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253
525
Second most common cause of neonatal mortality.
Prematurity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
526
Lungs of infants with this disease are normal size but are heavy and relatively airless. They have a mottled purple color, with poorly developed atelectatic alveoli.
Neonatal Respiratory Distress Syndrome / Hyaline Membrane Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
527
Characteristic eosinophilic membranes line the respiratory bronchioles, alveolar ducts and random alveoli, which contain necrotic epithelial cells admixed with extravasated plasma proteins.
Hyaline Membrane Disease / Neonatal RDS(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257
528
Two well known complications of high concentration ventilator administered oxygen in infants suffering from RDS.
Retrolental fibroplasia / retinopathy of prematurityBronchopulmonary dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
529
Characteristic lesion in the retina of infants suffering from retrolental fibroplasia?
Neovascularization or retinal vessel proliferation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
530
Main component of pulmonary surfactant.
Dipalmitoylphosphatidylcholine (DPPC) ~40%
531
Characteristic abnormality in bronchopulmonary dysplasia?
Alveolar hypoplasia or a decrease in the number of mature alveoli.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
532
What is the fundamental abnormality in neonatal RDS?
Insufficient pulmonary surfactant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
533
This condition occurs more commonly in very-low-birth-weight infants, as a result of intestinal ischemia, bacterial colonization of gut and formula milk feeding.
Necrotizing enterocolitis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258
534
Microscopic features of NEC.
Presence of submucosal gas bubbles, transmural coagulative necrosis, ulceration and bacterial colonization.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.259
535
Defined as the sudden death of an infant under 1 year of age which remains unexplained after a thorough investigation.
Sudden Infant Death Syndrome / SIDS(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.260
536
Multiple petechiae of the thymus, visceral and parietal pleura and epicardium, congested lungs with vascular engorgement with or without pulmonary edema.
Sudden Infant Death Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.260
537
Results from antibody-induced hemolytic disease in the nnewborn that is caused by blood group incompatibility between mother and fetus, leading to edema fluid accumulation.
Immune Hydrops(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
538
Erythroid precursors with large homogenous, intranuclear inclusions and a surrounding peripheral rim of residual chromatin can be seen in the bone marrow aspirate of an infant infected with this virus. This leads to development of non-immune hydrops.
Parvovirus B19(TOPNOTCH)
539
Isolated postnuchal fluid accumulation in fetuses with hydrops.
Cystic hygroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
540
A lethal condition characterized by generalized edema of the fetus.
Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261
541
Increased hematopoietic activity leading to the presence of large number of immature red cells, including reticulocytes, normoblasts and erythroblasts. Characteristic finding in fetal anemia-associted hydrops.
Erythroblastosis fetalis(TOPNOTCH)
542
Primary gene defect in cystic fibrosis.
Abnormal CFTR (CF transmembrane conductance regulator) Chromosome 7q31.2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262
543
Lungs with extensive mucous plugging and dilated tracheobronchial tree. Pancreatic ducts dilated and plugged with eosinophilic mucin, atrophic parenchymal glands replaced by fibrous tissue. Hepatic steatosis, Azoospermia and infertility are some of the features of this disease.
Cystic fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262
544
Patients with cystic fibrosis are prone to developing infections caused by these three organisms.
S. aureusH. InfluenzaeP. aeruginosa(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.266
545
How is cystic fibrosis diagnosed?
Persistently elevated sweat chloride concentration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
546
Most common tumors of infancy.
Hemangioma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
547
Microscopically normal cells or tissues that are present in abnormal locations.
Heterotopia or choristoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
548
Port wine stains are associted with these syndromes. (2)
von Hippel-Lindau Sturge-Weber syndromes(TOPNOTCH
549
This refers to an excessive but focal overgrowth of cells and tissues native to the organ in which it occurs.
Hamartoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
550
Large, flat to elevated, irregular, red-blue masses in the skin.
Port wine stains(Large hemangiomas)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267
551
These represent the lymphatic counterpart of hemangiomas characterized as cystic and cavernous spaces lined by endothelial cells and surrounded by lymphoid aggregates,usually containing pale fluid.
Lymphangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268
552
What do you call the rosettes found in neuroblastomas?
Homer-Wright pseudorosettes(TOPNOTCH)
553
Most common germ cell tumors of childhood,associated with meningocoele and spina bifida.
Sacrococcygeal teratomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268
554
Tumor of the adrenal medulla composed of small, primitive-appearing cells with dark nuclei, scant cytoplasm, and poorly defined cell borders growing in solid sheets within a finely fibrillar matrix. Rosettes can be found in which tumor cells are concentrically arranged about a CENTRAL SPACE FILLED with neuropil.
Neuroblastomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.269
555
This is used in the screening of patients with neuroblastoma.
Urinary vanillylmandelic acid and homovanillic acid (VMA/HVA)(TOPNOTCH)
556
Differentiated lesions containing more large cells with vesicular nuclei and abundant eoinophilic cytoplasm, in the absence of neuroblasts, usually accompanied by mature spindle shaped Schwann cells.
Ganglioneuroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270
557
Disseminated neuroblastoma with multiple cuteaneous metastases with deep blue discoloration to the skin.
"Blueberry muffin baby"(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270
558
This tumor is composed of small, round cells with large hyperchromatic nuclei and scant cytoplasm, with characteristic structures consisting of clusters of cuboidal or short columnar cells arranged around a CENTRAL LUMEN. The nuclei are displaced away from the lumen, which appears to have a limiting membrane.
Retinoblastoma(Differentiate with neuroblastoma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
559
Rosettes in retinoblastoma are called _______.
Flexner-Wintersteiner rosettes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
560
Clinicial findings include poor vision, strabismus, whitish hue to the pupils ("cat's eye reflex"), pain and tenderness to the eye.
Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
561
Most common primary tumor of the kidney in children.
Wilm's tumor / Nephroblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271
562
Components of the WAGR syndrome.
Wilm's tumorAniridiaGenital abnormalitiesMental retardation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
563
Presents grossly as a large, solitary, well-circumscribed mass. On cut-section, tumor is soft, homogenous, and tan to gray, with occasional foci of hemorrhage, cystic degeneration and necrosis.
Wilm's tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
564
Microscopically, a combination of blastemal, stromal and epithelial cell types is observed. (Triphasic combination) Blastemal components described as sheets of small blue cells with few distinctive features. Stromal cells are fibrocytic or myxoid in nature. Epithelial cells take the form of abortive tubules or glomeruli.
Wilm's tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
565
Associated with inactivation of the WT1 gene of chromosome 11p13.
WAGR syndrome and Denys-Drash syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272
566
A gas formed by sunlight-driven reactions involving nitrogen oxides. Together with oxides and fine particulate matter, it forms "smog".
Ozone(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
567
A nonirritating , colorless, tasteless, odorless gas produced bu the imperfect oxidation of carbonaceous materials. Binds to hemoglobin with high affinity causing systemic asphyxiation and CNS depression.
Carbon monoxide(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
568
Carbon monoxide in the blood is called _______.
Carboxyhemoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282
569
Acute poisoning of carbon monoxide produces this characteristic color of the skin and mucous membranes.
Cherry red color(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
570
Microcytic, hypochromic anemia, with basophilic stippling of erythrocytes, peripheral demyelinating neuropathy which manifests as footdrop and wristdrop, colic characterized by extremely severe, poorly localized abdominal pain, and chronic renal damage are the features of poisoning with this heavy metal.
Lead(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283
571
Main source of exposure to this heavy metal are contamintaed fish and dental amalgams, causing tremor, gingivitis and bizarre behavior.
Mercury(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
572
Consumption of fish contaminated with methyl mercury causing cerebral palsy, deafness, blindness, and major CNS defects in children exposed in utero.
Minamata disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
573
Antidote for mercury poisoning.
Thimerosal(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
574
Chronic exposure with this heavy metal results in hyperpigmentation and hyperkeratosis which may develop into basal or squamous cell carcinomas.
Arsenic(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
575
This heavy metal is used mainly in batteries and fertilizers, which can contaminate soil. Can cause obstructive lung disease and kidney damage.
Cadmium(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
576
Disease caused by cadmium in Japan, presenting as a combination of osteoporosis and osteomalacia, associated with renal disease.
Itai-itai disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285
577
May be released from combustion of fossil fuels, burning of coal and gas, and also present in tar and soot. Among the most potent carcinogens, implicated in lung and bladder cancer.
Polycyclic hydrocarbons(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
578
Synthetic products that resist degradation and are lipophilic, typically used as pesticides, with anti-estrogenic and anti-androgenic activity, and causes neurologic toxicity.
Organochlorines (e.g. DDT)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
579
These can cause skin disorders such as folliculitis and chloracne, consisting of acne, cyst formation, hyperpigmentation, and hyperkeratosis, around the face and behind the ears.
Dioxins and Polychlorinatedbiphenyls (PCB)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
580
It is the most preventable cause of human death.
Smoking(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287
581
Components of cigarette smoke that are potent carcinogens in animals and are most likely involved in the causation of lung carcinomas in humans.
Polycyclic hydrocarbons and nitrosamines(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 288
582
A long acting tetracycline which can cause a diffuse blue-gray pigmentation of the skin.
Minocycline(TOPNOTCH)
583
Chronic alcoholics are at an increased risk of developing this type of cancer as a result of liver injury.
Hepatocellular carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 290
584
These refer to untoward effects of drugs that are given in conventional therapeutic settings.
Adverse drug reactions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 291
585
A long acting tetracycline which can cause a diffuse blue-gray pigmentation of the skin.
Minocycline(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 293
586
Oral contraceptives have a protective effect against these cancers.
Endometrial and ovarian CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
587
Oral contraceptives may increase the risk of developing this type of cancer in women.
Cervical CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
588
Prolonged use of oral contraceptives is associated with the development of this rare benign tumor especially in older women.
Hepatic adenoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
589
Toxic metabolite of paracetamol or acetaminophen.
NAPQI (N-acetyl-p-benzoquinoneimine)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
590
Toxic dose for acetaminophen.
15-25 grams/day(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
591
Antidote for acetaminophen poisoning.
N-acetylcysteine(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 294
592
Manifested by headache, dizziness, tinnitus, difficulty of hearing, mental confusion, drowsiness, nausea, vomiting, and diarrhea, with CNS changes that can progress to convulsions and coma.
Salicylism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
593
Adult toxic dose of aspirin.
10-30 grams(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
594
Mixtures of aspirin and phenacetin, or its active metabolite acetaminophen, when taken over several years can cause tubulointerstitial nephritis and renal papillary necrosis called _______.
Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294
595
This drug of abuse can precipitate lethal arrythmias, hyperpyrexia, seizures, amd respiratory arrest during acute overdose. Causes nasal septal perforation, decrease in lung diffusing capacity in those who inhale smoke and dilated cardiomyopathy during chronic use.
Cocaine or "crack" (cocaine derivative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 295
596
Addictive opiod derived from the poppy plant which can cause euphoria, hallucinations, somnolence, sedation, and increased risk of sudden death.
Heroin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 296
597
Drug made from the leaves of Cannabis sativa plant which can cause distortion of sensory perception and impairs motor coordination.
Marijuana(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 297
598
Psychoactive substance found in marijuana.
Delta 9- Tetrahydrocannabinol (THC)(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297
599
Mechanism of action of aspirin.
Irreversibly blocks the enzyme cyclooxygenase.(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297
600
A wound produced by scraping or rubbing resulting in removal of superficial layer of the skin.
Abrasion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
601
A wound usually produced by a blunt object, characterized by damage to blood vessels and extravasation of blood into tissues.
Contusion (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
602
A tear or disruptive stretching of tissue caused by the application of force by a blunt object, causing jagged and irregular edges to the skin.
Laceration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
603
A wound inflicted by a sharp instrument, wherein bridging blood vessels are severed.
Incision(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
604
A wound caused by a long, narrow instrument.
Puncture wound(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
605
Burn classification which involves total destruction of the epidermis and dermis, with loss of thermal appendages.
Full thickness burn (3rd and 4th degree)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
606
Burn classification wherein the thermal appendages are spared but involves at least the deeper portions of the skin.
Partial thickness burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
607
Partial thickness burn that involves both the epidermis and superficial dermis.
Second degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
608
Partial thickness burn that involves the epidermis only.
First degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
609
Grossly, these burns are white or charred and anesthetic due to nerve ending destruction.
Full thickness burns(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
610
These burns are pink or mottled with blisters and are painful.
Second degree burn (partial thickness)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
611
Histologic change in the skin during burns.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298
612
Leading cause of death in burn patients.
Organ system failure secondary to burn sepsis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
613
Cramping of voluntary muscles in association with vigorous exercise as a result of electrolyte loss via sweating.
Heat cramps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
614
Most common hyperthermic syndrome. A sudden onset of prostration and collapse, resulting from failure of the cardiovascular system to compensate for hypovolemia, secondary to water depletion.
Heat exhaustion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
615
Associated with high ambient temperatures and high humidity. Thermoregulatory mechanisms fail, sweating ceases and core body temperature rises. Due to marked generalized peripheral vasodilation with peripheral pooling of blood and decreased effective circulating volume.
Heat stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
616
Two types of injuries caused by electricity.
BurnsVFib or cardiac and respiratory center failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299
617
This may injure cells directly or indirectly by generating free radicals from water or molecular oxygen, damages DNA and rapidly dividing cells. Exposure may predispose to neoplastic transformation, vascular damage, sclerosis and tissue fibrosis.
Ionizing radiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 300
618
Malnutrition caused by lack of nutrients from the diet.
Primary malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304
619
Malnutrition caused by malabsorption, impaired nutrient utilization or storage, excess losses or increased nutrient needs.
Secondary or conditioned malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304
620
Protein energy malnutrition which occurs when protein deprivation is relatively greater than reduction in total calories. Associated with generalized edema, flaky paint appearance of the skin, alternating bands of pale and dark hair, enlarged fatty liver, apathy, listlessness and loss of appetite.
Kwashiorkor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 305
621
Protein energy malnutrition caused by a decrease in both protein and calorie intake, and weight falls below 60% of normal for sex, height and age. Serum albumin is normal or slightly reduced.
Marasmus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 305
622
Self-induced starvation, resulting in marked weight loss.
Anorexia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306
623
A condition wherein a patient binges on food and then induces vomiting.
Bulimia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306
624
Deficiency of this vitamin causes night blindness, xerophthalmia, keratomalacia, Bitot spots and eventually corneal ulceration.
Vitamin A(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 307
625
Condition in children as result of vitamin D deficiency causing the following signs and symptoms: frontal bossing of the head, rachitic rosary, pigeon breast deformity, lumbar lordosis and bow legs.
Rickets (children)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 309
626
Deficieny of this vitamin causes impaired collagen formation, leading to gum bleeding, easy bruisability, and impaired wound healing.
Vitamin C (Scurvy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 312
627
Symptoms of cheilosis, stomatitis, glossitis, dermatitis and corneal vascularization results from deficiency of this vitamin.
Vitamin B2 (Riboflavin)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314
628
Symptoms of cheilosis, glossitis, dermatitis, and peripheral neuropathy.
Vitamin B6 (Pyridoxine)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314
629
In these arteries, elastic fibers alternate in layers with smooth muscle cells. Examples are the common carotid artery, iliac arteries and pulmonary arteries.
Large or elastic arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
630
In these arteries, tunica media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina. Examples are the coronaries and renal arteries.
Medium-sized or muscular arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
631
These are the principal control points for regulation of physiologic resistance to blood flow.
Arterioles(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340
632
These vessels are approximately the diameter of an RBC, have an endothelial cell lining but no media.
Capillaries(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
633
Diameter of an RBC.
7-8 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
634
These are thin-walled, endothelium lined channels that drain excess interstitial tissue fluid, returning it to blood via the thoracic duct.
Lymphatics(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
635
These are small spherical dilatations, typically in the circle of Willis.
Developmental/berry aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
636
These are abnormal, typically small, direct connections between arteries and veins that bypass the intervening capillaries.
Arteriovenous fistulas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
637
Focal, irregular thickening of the walls of medium and large muscular arteries. Segments of the vessel wall are focally thickened by combination of irregular medial and intimal hyperplasia and fibrosis, causing luminal stenosis.
Fibromuscular dysplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341
638
Literally means hardening of the arteries, term reflecting arterial wall thickening and loss of elasticity, affecting small arteries and arterioles.
Arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
639
Characterized by calcific deposits in muscular arteries, typical in persons older than 50 yrs old. The radiographically visible, palpable calcifications do not encroach on the vessel lumen, and are not clinically significant.
Mockenberg medial calcific sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
640
Characterized by intimal lesions called atheromas that protrude into vascular lumina.
Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343
641
Three principal components of an atheromatous plaque.
1. Cells (SM cells, macrophages, T cells)2. Extracellular matrix (collagen, elastic fibers, proteoglycans)3. Intracellular and extracellular lipidFibrous cap, central lipid core, neovascularization(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
642
Non-modifiable risk factors for atherosclerosis. (4)
Increasing ageMale genderFamily historyGenetic abnormalities(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344
643
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)
644
Composed of lipid-filled foam cells but are not significantly raised and thus do not cause any disturbance in blood flow. Can appear as early as 1 year, and present in virtually all children older than 10 years old.
Fatty streaks(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349
645
Arrange in descending order, based on which blood vessel is most extensively involved in development of atherosclerosis.Popliteal arteries, internal carotid arteries, circle of Willis, coronaries, abdominal aorta
Abdominal aorta > coronaries > popliteal arteries > internal carotid arteries > circle of Willis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 350
646
Fate of an atheromatous plaque wherein the luminal surface exposes the bloodstream to highly thrombogenic substances and induces thrombus formation.
Rupture, ulceration or erosion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
647
Fate of an atheromatous plaque due to rupture of the overlying fibrous cap or the thin-walled vessels in the areas of neovascularization.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
648
Fate of an atheromatous plaque causing discharge of debris into the bloodstream, producing microemboli composed of plaque contents.
Atheroembolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
649
Fate of an atherosclerotic plaque due to increased pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, leading to weakness of the vessel wall.
Aneurysm formation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 351
650
Most common cause of hypertension.
Idiopathic (essential hypertension)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 355
651
This vascular lesion consists of a homogenous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen. A major morphologic characteristic in benign nephrosclerosis.
Hyaline arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
652
Characteristic of malignant hypertension, associated with "onion-skin" concentric, laminated, thickening of the walls of arterioles with luminal narrowing. These laminations consist of smooth muscle cells and thickened duplicated basement membrane.
Hyperplastic arteriolosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 356
653
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)
654
It is a localized abnormal dilation of a blood vessel or heart.
Aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
655
Aneurysm which involves all three layers of the arterial wall, or the attenuated wall of the heart.
True aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
656
A breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space.
False aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
657
Arises when blood enters the wall of an artery, as a hematoma dissecting between its layers. Often, but not always aneurysmal in origin.
Arterial dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
658
Aneurysms which are spherical outpouchings, involving only a portion of the vessel wall, varying in size from 5-20cm in diameter and often contain thrombi.
Saccular aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
659
Aneurysms which involve diffuse, circumferential dilation of a long vascular segment, varies in diameter and length, and can involve extensive portions of the aortic arch, abdominal aorta,and iliacs.
Fusiform aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
660
Two most important causes of aortic aneurysms.
AtherosclerosisCystic medial degeneration of the arterial media(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
661
Infection of a major artery that causes weakness to its wall.
Mycotic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357
662
This disease can more commonly affects men >50 years old. Lesion usually positioned below the renal arteries and above the aortic bifurcation. Can be saccular or fusiform.
Abdominal aortic aneurysm (AAA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
663
Abdominal aortic aneurysm characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic infiltrate with manybmacrophages and often giant cells.
Inflammatory AAA(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 358
664
Atherosclerotic lesions infected by lodging of circulating microorganisms in the wall, particularly in the setting of bacteremia from a Salmonella gastroenteritis. Suppuration further destroys the media, potentiating rapid dilation and rupture.
Mycotic abdominal aortic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358
665
Small blood vessels and vasa vasorum show luminal narrowing and obliteration (obliterative endarteritis), scarring of the vessel wall and a dense surrounding rim of lymphocytes and plasma cells that may extend into the media. Characteristic of the tertiary stage of syphilis.
Syphilitic aortitis(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 359
666
Most common point of origin of an aortic dissection.
Ascending aorta, 10 cms from the aortic valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 360
667
Most frequent pre-existing histologically detectable lesion in aortic dissection, characterized by elastic tissue fragmentation and separation of the elastic and smooth muscle cell elements of the media by cystic spaces filled with amorphous proteoglycan-rich extracellular matrix.
Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
668
Classification of aortic dissection involving either them ascending aorta only or both the ascending and descending aorta.
Type A dissections (proximal) Type I DeBakey - ascending aorta only Type II DeBakey - ascending and descending aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
669
Classification of aortic dissections involving the descending aorta only, usually distal to the subclavian artery.
Type B dissection / type III DeBakey(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 361
670
Granulomatous inflammation frequently involving the temporal artery, occuring in patients >50 years old, associated with polymyalgia rheumatica.
Giant cell (Temporal) arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 363
671
Granulomatous inflammation usually occuring in patients younger than 50 years old. Classically involves the aortic arch, with intimal hyperplasia and irregular thickening of the vessel wall. Origin of great vessels are obliterated causing weakness of peripheral pulses.
Takayasu arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
672
Used to distinguish between giant cell arteritis and takayasu arteritis of the aorta.
Age of patient40 Giant cell arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
673
In this disease, affected blood vessels develop nodular intimal thickening, granulomatous inflammation within the inner media centered on the internal elastic membrane, and fragmentation of the internal elastic lamina. Typically involves temporal and ophthalmic arteries.
Giant - cell/Temporal arteritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364
674
A systemic vasculitis causing transmural necrotizing inflammation of small to medium sized vessels, with mixed infiltvrate of neutrophils, eosinophils, and mononuclear cells, frequently accompanied by fibrinoid necrosis.Typically involves renal arteries but spares pulmonary vessels.
Polyarteritis Nodosa (PAN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365
675
Arteritis associated with mucocutaneous lymph node syndrome, which usually occurs in children. Coronary arteries can be involved with aneurysm formation or thrombosis. Fibrinoid necrosis usually less prominent.
Kawasaki disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 366
676
Granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels, including cresencteric glomerulonephritis. Associated with c-ANCA.
Wegener granulomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367
677
A necrotizing vasculitis that generally affects capillaries, arterioles and venules, with few or no immune deposits. Necrotizing glomerulonephritis and pulmonary capillaritis are common. Associated with p-ANCA.
Microscopic polyangiitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
678
Eosinophil-rich and granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels. Associated with asthma and blood eosinophilia. Associated with p-ANCA.
Churg-Strauss syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
679
Characterized by sharply segmental avute and chronic vasculitis of medium sized and small arteries, predominantly of the extremities. There is acute and chronic inflammation accompanied by luminal thrombosis, containing microabscess composed of neutrophils surrounded by granulomatous inflammation. Stromg relationship with cigarette smoking.
Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 368
680
Results from an exaggerated vasoconstriction of digital arteries and arterioles, inducing paroxysmal pallor or cyanosis of the digits of the hands and feet.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
681
Reflects an exaggeration of central and local vasomotor responses to cold or emotion. Structural changes in the arterial walls are absent except late in course when intimal thickening can appear.
Primary Raynaud phenomenon (Raynaud disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 369
682
Reflects vascular insufficiency of the extremities in the context of arterial disease caused by other entities including SLE, Buerger disease, or atherosclerosis.
Secondary Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
683
Abnormally dilated, tortous veins produced by prolonged increase in intraluminal pressure and loss of vessel wall support. Veins show wall thinning at the points of maximal dilation with smooth muscle hypertrophy and intimal fibrosis. Focal thrombosis and venous valve deformities are common.
Varicose veins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
684
Most common blood vessels involved in development of varicose veins.
Superficial veins of the upper and lower leg(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
685
Three sites of varices produced in the presence of portal hypertension.
GEJ (Esophageal varices)Rectum (Hemorrhoids)Periumbillical veins (Caput medusae)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 370
686
Common and serious complication of of deep vein thrombosis (DVT).
Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
687
The acute inflammation elicited when bacterial infections spread into and through the lymphatics.
Lymphangitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371
688
These are bright red to blue lesions, that vary from a few millimeters tomseveral centimeters in diameter. Unencapsulated aggregates of closely packed, thin-walled capillaries, usually blood-filled and lined by flattened endothelium. Vessels are separated by scant connective tissue stroma.
Capillary hemangiomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 372
689
Appears as red-blue, soft, spongy masses 1-2 cm in diameter, which can affect large subcutaneous areas of the face, extremities, and othe body regions. Mass is sharply defined but not encapsulated, composed of large, cavernous, blood-filled spaces.
Cavernous hemangioma(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 372
690
This form of capillar hemangioma is a rapidly growing peduncular red nodule on the skin, gingival, or oral mucosa, bleeds easily and is often ulcerated.
Pyogenic granuloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
691
These are round, slightly elevated, red-blue firm nodules, less than 1 cm diameter that can resemble a minute focus of hemorrhage UNDER THE NAIL. Histologically, these are aggregates, nests, and masses of tumor cells intimately associated with branching vascular channels.
Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
692
A specialized arteriovenous structure involved in thermoregulation.
Glomus body(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373
693
This lesion is the ordinary "birthmark" and is the most common form of ectasia. Characteristically a flat lesion on the head or neck, ranging in color from light pink to deep purple.
Nevus flammeus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
694
This non-neoplastic vascular lesion grossly resembles a spider. There is radial, often pulsatile array of dilated subcutaneous arteries or arterioles about a central core, that blanches when pressure is applied to its center.
Spider telangiectasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
695
An opportunistic infection in immunocompromised persons that manifest as vascular proliferations involving skin, bone, brain and other organs. Characterized grossly by red papules and nodules, or rounded subcutaneous masses. Histologically, there is capillary proliferation with prominent epitheloid EC's showing nuclear atypia and mitoses. Lesions contain stromal neutrophils, nuclear dust nd purplish granular material.
Bacillary angiomatosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 374
696
Common in patients with AIDS, caused by HHV 8, causing skin lesions ranging from patches, plaques to nodules.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375
697
These are malignant endothelial neoplasms, with varying histology from plump, anaplastic but recognizable endothelial cells producing vascular channels to widely undifferentiated tumors having solid, spindle cell appearance and producing nondefinite blood vessels.
Angiosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 376
698
The morphologic and clinical effects of this condition primarily result from progressive damming of blood within the pulmonary circulation. The left ventricle is hypertrophied and dilated, with secondary left atrial dilation. The lungs are heavy and boggy, with perivascular and interstitial transudate, alveolar septal edema, and intra-aleolar edema. Hemosiderin-laden macrophages are present.
Left sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
699
Hemosiderin laden macrophages are also called _______
Heart failure cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
700
This is usually the earliest and most significant compaint of patients in Left sided HF.
Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
701
Most common cause of right sided HF.
Left sided HF(TOPNOTCH)
702
This is a particularly dramatic form of breathlessness, awakening patients from sleeo with attacks of extreme dyspnea bordering on suffocation.
Paroxysmal nocturnal dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
703
Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.
Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
704
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.
Cardiac cirrhosis(TOPNOTCH)
705
The liver is increased in size and weight, a cut section reveals congested red centers of liver lobules surrounded bybpaler, sometimes fatty peripheral regions.
Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
706
Right-sided HF produces a tense, enlarged spleen, achieving weights of 300-500 grams. Sinusoidal dilation present.
Congestive splenomegaly(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
707
This is a hallmark of right sided HF.
Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
708
Generalized, massive edema is called ______.
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
709
Most congenital heart disease arise from faulty embryogenesis during what AOG?
3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
710
An abnormal communication between chambers of the heart or blood vessels.
Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
711
These a typically smooth-walled defects near the foramen ovale, usually without associated cardiac abnormalities. Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy and dilation of the pulmonary artery.
Ostium secundum ASD(TOPNOTCH)
712
Reversal of blood flow through a prolonged (left-to-right shunt) due to pulmonary hypertension, yielding right-sided pressures that exceed those on the left side. This causes unoxygenated blood to go into circulation, causing cyanosis.
Eisenmenger syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
713
These occur at the lowest part of the atrial septum and can extend to the mitral and tricuspid valves. Abnormalities of the AV Valves are usually present, forming a cleft in the anterior leaflet of the mitral valve or septal leaflet of the tricuspid valve.
Ostium primum ASD(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384
714
Incomplete closure of the ventricular septum leading to left-to-right shunting. The right ventricle is hypertrophied and often dilated. Diameter of pulmonary artery is increased because of the increased volume by the right ventricle.
Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
715
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
716
In this condition, some of the oxygenated blood flowing from the left ventricle is shunted back to the lungs. Proximal pumonary arteries, left atrium and ventricle can become dilated.
Patent ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
717
The most common cause of cyanotic congenital heart disease. Heart is large and "boot shaped" as a result of right ventricular hypertrophy.
Tetralogy of Fallot(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
718
Components of Tetralogy of Fallot.
Pulmonary valve stenosisOverriding of aortaRight ventricular hypertrophyVentricular septal defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
719
It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa. Right ventricular hypertrophy becomes prominent, while the left ventricle becomes somewhat atrophic.
Transposition of the Great Arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
720
Predominant manifestation of TGA?
Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
721
Characterized by tubular narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus. DA is usually patent and is the main source of blood to the distal aorta. RV is hypertrophied and dilated, pulmonary trunk is also dilated.
Preductal "infantile" coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
722
Aorta is sharply constricted by a ridge of tissue at or just distal to the ligamentum arteriosum. Constricted segment is made of smooth muscle and elastic fibers that are continuous with the aortic media, and lined by thickened intima. Ductus arteriosus is closed. Proximally, the aortic arch and its vessels are dilated, LV is hypertrophic.
Postductal "adult" coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
723
There is upper extremity hypertension, due to poor perfusion of the kidneys, but weak pulses and low blood pressure in the lower extremities. Claudication and coldness of the lower extremities also present. Enlarged intercostal and internal mammary arteries due to collateral circulation, seen as rib "notching" on xray.
Postductal coarctation of the aorta (without a PDA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
724
Left-to-right or Right-to-Left shunt?Atrial septal defect
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
725
Left-to-right or Right-to-Left shunt?TOF
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
726
Left-to-right or Right-to-Left shunt?VSD
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
727
Left-to-right or Right-to-Left shunt?Eisenmenger syndrome
Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
728
Left-to-right or Right-to-Left shunt?Transposition of great arteries
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
729
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)
730
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
731
A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.
Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
732
This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.
Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
733
This can result from a lethal arrythmia following myocardial ischemia.
Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
734
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?
70-75% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
735
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest?
90%(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389
736
Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand. Pain described as crushing or squeezing substernal sensation which can radiate to left arm. Relieved by rest or vasodilators.
Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
737
Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.
Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
738
Angina occuring at rest due to coronary artery spasm.
Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
739
Infarct involving >= 50% of the myocardial wall thickness.
Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391
740
Most common blood vessel involved in myocardial infarction?
Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392
741
Electron microscope findings 30 minutes after an ischemic event.
Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)
742
An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?
12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393
743
Coagulation necrosis ensues how many hours after MI?
4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
744
Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.
Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
745
Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.
Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
746
This cardiac enzyme is detectable in the blood within 2-4 hrs of MI, peaks at 24-48 hrs and returns to normal within approximately 72 hrs.
CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
747
Myocardial rupture may occur how many days after MI?
3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
748
This occurs within 2-3 days of a transmural infarct and typically resolves within time. It is the epicardial manifestation of the underlying myocardial inflammation.
Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
749
A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.
Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
750
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.
Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
751
Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
752
In this disease the left ventricle may exceed 2.0cm in thickness and the heartvmay weigh >500 grams. Microscopically, myocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia ("box-car nuclei"), and increased interstitial fibrosis.
Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
753
It is the failure of a valve to open completely, obstructing forward flow.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
754
This results from failure of a valve to close completely, thereby allowing reversed flow.
Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
755
The hallmark of this disease is heaped-up calcified masses on the outflow side of the cusps, which protrude intonthe sinuses of Valsalva and mechanically impede valve opening. Cusps may become secondarily fibrosed and thickened.
Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
756
This is characterized by ballooning or hooding of the mitral leaflets. Affected leaflets are enlarged, redundant, thick and rubbery. The tendinous cords are elongated, thinned and occasionally ruptured. Histologically, there is thinning of the fibrosa layer of the valve, accompanied by expansion of the middle spongiosa layer with increased deposition of mucoid material.
Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
757
Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.
Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
758
Pathognomonic sign for rheumatic fever,consisting of of a cental zone of degenerating, hypereosinophilic ECM infiltrated by lymphocytes, ocassional plasma cells and plump, activated macrophages.
Aschoff bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
759
These cells have abundant cytoplasm and central nuclei with chromatin arrayed in a slender, wavy ribbon (caterpillar cells) which can be found in all three layers of the heart in rheumatic fever. A component of Aschoff bodies.
Anitschkow cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
760
Characterized by organization and subsequent scarring, as a sequelae of rheumatic fever. The mitral (or tricuspid) valve is involved, with leaflet thickening, commisural fission and shortening, thickening and fusiong of the chordae tendinae. Fibrous bridging across valvular commisures create "fishmouth" or " buttonhole" deformity.
Chronic Rheumatic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
761
Most common valve involved in RHD.
Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405
762
Major components Jones Criteria for RF.
CarditisMigratory polyarthritisSubcutaneous nodulesErythema marginatumSyndenham chorea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
763
Minor components Jones criteria for RF
FeverArthralgiaElevated acute phase reactants (e.g. CRP)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
764
How many major and/or minor manifestations are needed to diagnose RF?
Remember: 20122 major 0 minor or1 major 2 minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
765
Endocarditis of previously normal valves, the most common causative agent is S. aureus.
Acute bacterial endocarditis(TOPNOTCH)
766
Serious infection characterized by microbial invasion of heart valves or mural endocardium, often with destruction of the underlying cardiac tissues. The heart valves are friable, bulky and potentially destructive.
Infective endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
767
Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.
Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
768
Most consistent sign of infective endocarditis.
Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
769
Characterized by deposition of sterile, non-inflammatory, nondestructive and small (1mm) masses of fibrin, platelets and other blood components on cardiac valves, along the line of closure of leaflets or cusps.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
770
Sterile vegetations thatvcan develop on the valves of patients with SLE. These are small, granular, pinkish vegetations 1-4mm in diameter and can be located on the undersurface of AV valves, on the cords or endocardium.
Libman-Sacks endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
771
The lesions of this disease are distinctive, glistening white intimal plaquelike thickenings on the endocardial surfaces of the cardiac chambers and valve leaflets seen in patients with carcinoid tumors. The lesions are composed of muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix.
Carcinoid heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
772
Cardiomyopathy which is characterized by progressive cardiac dilation and contractile dysfunction. The heart is characteristically enlarged and flabby, with dilation of all chambers,the ventricular thickness may be less than, equal to or greater than normal.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
773
Alcohol intake and infection with coxsackie B virus are some of the causes of this cardiomyopathy.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
774
Characterized by myocardial hypertrophy, abnormal diastolic filling and ventricular outflow obstruction. The heart is thick-walled, heavy and hypercontracting. There is an assymetrical septal hypertrophy described as "banana-like". Histologically, there is severe myocyte hypertrophy and disarray with interstitial fibrosis.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
775
Mechanism of heart failure in hypertrophic cardiomyopathy.
Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
776
A common cause of sudden death in young athlethes.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
777
The ventricles are of approximately normal size or slightly enlarged, the cavities not dilated, and the myocardium is firm. Biatrial dilation is common. Microscopically, there is interstitial fibrosis, varying from minimal to patchy to extensive and diffuse.
Restrictive cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
778
Mechanism of heart failure in restrictive cardiomyopathy.
Diastolic dysfunction or impaired compliance(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
779
Inflammation of the myocardium.
Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
780
Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.
Lymphocytic myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
781
Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils.
Hypersensitivity myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
782
Myocarditis characterized by widespread inflammatory infoltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis.
Giant-cell myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
783
Myocarditis distinctive by virtue of parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages and occasional eosinophils.
Chagas myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
784
Viruses which account for most cases of myocarditis.
Coxsackie A and B(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
785
Type of pericarditis found in patients with uremia or viral infection. The exudate imparts an irregular apperance to the pericardial surface (bread and butter pericarditis).
Fibrinous pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
786
Bacterial pericarditis manifests with this type of exudate.
Fibrinopurulent (suppurative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
787
Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.
Constrictive pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
788
Normal amount of pericardial fluid in pericardial sac.
30 - 50 mL of thin, straw-colored fluid(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
789
Serous pericardial effusion can be caused by _________
CHF, hypoalbuminemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
790
Chylous pericardial fluid can be caused by _______
Mediastinal lymphatic obstruction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
791
Rapidly developing collections of fluid within the pericardial sac can restrict diastolic cardiac filling producing this fatal sequelae.
Cardiac tamponade(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
792
The most common tumor of the heart.
Metastatic tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
793
Most common primary tumor of the adult heart.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
794
Major clinical manifestations of this cardiac tumor are due to valvular "ball-valve" obstruction, embolization or a syndrome of constitutional symptoms.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
795
The most frequent primary tumor of the heart in infants and children. These are generally small gray-white myocardial masses composed of a mixed population of cells, the most characteristic of which are large, rounded or polygonal cells containing numerous glycogen-laden vacuoles separated by strands of cytoplasm, so-called spider cells.
Rhabdomyomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
796
Serosanguinous pericardial effusion can be caused by ________
Blunt chest trauma, malignancy, ruptured MI, aortic dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
797
Average volume per cell, expressed in femtoliters.
Mean cell volume (MCV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
798
A reduction in the oxygen-transporting capacity of blood.
Anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 422
799
The average content of hemoglobin per red cell, expressed in picograms.
Mean cell hemoglobin (MCH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
800
The average concentration of hemoglobin in a given volume of packed red cells, expressed in g/dL.
Mean cell hemoglobin concentration (MCHC)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
801
The coefficient of variation of red cell volume.
Red cell distribution width (RDW)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
802
Anemia of acute blood loss is described as ______.
Normocytic, normochromic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 423
803
Life span of a normal red cell.
120 days(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
804
Anemia characterized by an increased rate of cell destruction, a compensatory increase in erythropoeisis that results in reticulocytosis, and retention of products of cell destruction, including iron.
Hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
805
A circulating protein that binds and clears free hemoglobin.
Haptoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
806
Hemolysis that can result from mechanical trauma, or biochemical or physical agents that damage the red cell membrane.
Intravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
807
Hemolysis which takes place largely within phagocytic cells of the spleen and liver.
Extravascular hemolysis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
808
This disorder is characterized by an intrinsic defect in the red cell membrane, that renders the cells spheroidal, less defomable and vulnerable to splenic sequestration and destruction.
Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 424
809
Small, dark nuclear remnants seen within red cells in PBS of hereditary spherocytosis.
Howell-Jolly bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
810
On PBS, red cells are spherical which lack central pallor, and they show increased osmotic fragility when placed in hypotonic salt solutions.
Hereditary spherocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
811
Structural proteins that are defective in hereditary spherocytosis.
Spectrin and ankyrin(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 425
812
This results from substitution of valine for glutamic acid at the 6th position of the B-chain, producing HbS.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 426
813
Bizarre, elongated, spindled or boat-shaped cells on PBS.
Sickel cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427
814
Prominent cheekbones and changes in skull resembling a "crew-cut" skull x-ray.
Sickle cell anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 427
815
Patients with sickle cell disease are predisposed to infections caused by these type of bacteria.
Encapsulated bacteria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
816
Treatment for sickle cell disease by increasing levels of HbF.
Hydroxyurea(TOPNOTCH)
817
Treatment for sickle cell disease by increasing levels of HbF.
Hydroxyurea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
818
Feared complication of sickle cell disease which can be trigerred by pulmonary infections or fat emboli from necrotic marrow that secondarily involve the lung.
Acute chest syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
819
Major complication of sickle cell disease which occurs in the setting of acute chest syndrome, causing ischemic injury to the CNS.
CNS stroke(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
820
Represents a sudden but usually temporary cessation of erythropoeisis, usually trigerred by parvovirus B19 infections in patients with sickle cell disease.
Aplastic crises(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 428
821
In beta thalassemia, an individual who inherits one abnormal allele (out of 2) has this asymptomatic to mildly symptomatic condition.
B- Thalassemia minor/trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
822
Individuals with B-thalassemia who inherit two abnormal alleles, with severe anemia requiring regular blood tranfusions.
B- Thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
823
Red cells with a central, dark-red puddle due to collection of hemoglobin.
Target cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
824
Target cells are often seen in this condition.
B-thalassemia minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
825
In the PBS of this condition, nucleated red cells (normoblasts) are seen, which reflect underlying erythropoeisis.
B-thalassemia major(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
826
Anemia of beta thalassemia.
Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 430
827
Disease caused by deletion of 3 alpha globin genes.
Hemoglobin H disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
828
Condition caused by deletion of 1 alpha globin gene.
Silent carrier(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
829
Condition caused by deletion of 2 alpha globin genes.
Alpha thalassemia trait(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 431
830
Condition caused by deletion of all four alpha globin genes.
Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 429
831
Precipitates of denatured globin seen in RBC's.
Heinz bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
832
Heinz bodies are seen in the blood smear of this condition.
G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
833
Bite cells are seen in ________.
G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
834
A rare disorder of unknown etiology, causes hemolytic anemia which results from an acquired membrane defect secondary to a mutation that affects myeloid stem cells. Hemolysis occurs during sleep.
Paroxysmal nocturnal hemoglobinuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
835
Hemolysis caused by IgG or IgA antiodies that are active at 37 degC, which results in opsonization of red cells by the autoantibodies.
Warm antibody immunohemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
836
Anemia caused by low-affinity IgM which bind to red cell membranes only at temp <30degC, commonly experienced by distal parts of the body.
Cold antibody immunohemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
837
Anemia observed in a variety of pathologic states, in which small vessels become particularly obstructed.(e.g. DIC, malignant HTN, SLE, etc.)
Microangiopathic hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
838
Schistiocytes, burr cells, helmet cells, triangle cells are seen in this condition.
Microangiopathic hemolytic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 433
839
X-linked disorder in which red cells are unusually susceptible to damage cause by oxidants.
G6PD Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 432
840
Red blood cells in iron deficiency anemia.
Microcytic, hypochromic(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 436
841
Diagnostic criteria for iron deficiency anemia:____ Ferritin____Serum iron level____Transferrin saturation____Total Iron Binding Capacity (TIBC)
Low ferritinLow serum iron levelsLow transferrin saturationIncreased TIBC(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 435
842
Diagnostic criteria for anemia of chronic disease:____ Ferritin____Serum iron level____Transferrin saturation____Total Iron Binding Capacity (TIBC)
Increased ferritinLow serum iron levelsLow transferrin saturationDecreased TIBCNormocytic, normochromic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 435
843
Principal causes of megaloblastic anemia.
Folate deficiencyVitamin B12 deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437
844
Bone marrow is markedly hypercellular as a sult of increased number of megaloblasts, which are large cells that have delicate, finely reticulated nuclear chromatin and abundant basophilic cytoplasm.
Megaloblastic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437
845
PBS finding in neutrophils and red cells of patients with megaloblastic anemia.
Hypersegmented neutrophils, large, egg-shaped macro-ovalocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 437
846
Difference between megloblastic and pernicious anemia.
Presence of neurologic abnormalities in pernicious anemia.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438
847
Deficiency in folate causes this type of anemia.
Megaloblastic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438
848
Deficiency in Vitamin B12 causes this type of anemia.
Pernicious anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438
849
Etiology of pernicious anemia.
1.Vitamin B12 malabsorption secondary to autoantibodies against parietal cells and intrinsic factor which is needed in its absorption.2. Gastrectomy or ileal resection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 438
850
Principal neurologic lesion in pernicious anemia.
Demyelination of posterior and lateral columns of the spinal cord.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 439
851
Bone marrow is markedly hypocellular, with >90% of the intertrabecular space being occupied by fat.
Aplastic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 439
852
Tear drop cells are also called __________.
Dacrocytes(TOPNOTCH)
853
Tear drop cells are also called __________.
Dacrocytes(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 440
854
Dacrocytes are found in peripheral blood of patients with this type of anemia.
Myelophthisic anemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 440
855
Increase in blood concentration of red cells, with an increase in Hgb concentration.
Polycythemia or erythrocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441
856
Polycythemia secondary to reduced plasma volume.
Relative polycythemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441
857
Polycythemia secondary to abnormal proliferation of myeloid stem cells and low erythropoeitin levels.
Primary polycythemia (Absolute)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441
858
Polycythemia secondary to increased erythropoeitin levels due to lung disease, high-altitude living, cyanotic heart disease and EPO secreting tumors.
Secondary polycythemia (Absolute)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441
859
Total white cell count is reduced to 1000 cells/uL. Affected persons are extremely susceptible to bacterial and fungal infections.
Neutropenia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 441
860
A self-limited disease of adolescents and young adults that is causd by B lymphocytotropic EBV characterized by fever, sore throat and generalized lymphadenitis, an increase of atypical lymphocytes in blood and an antibody and T cell response to EBV.
Infectious mononucleosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 442
861
Cells with abundant cytoplasm 12-16um in diameter that contains azurophilic granules, and an oval, indented or folded nucleus.
Atypical lymphocytes (Infectious mononucleosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 442
862
Inflamed nodes are swollen, gray-red and engorged. There are large germinal centers containing numerous mitotic figures. Affected nodes are tender and fluctuant if with extensive abscess formation.
Acute nonspecific lymphadenitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444
863
This pattern is associated with infections or inflammatory processes that activate B cells which create a follicular or germinal center reaction. Lymph node architecture is preserved, lymphoid nodules vary in shape and size, mixed lymphocytic infiltrates with prominent phagocytic and mitotic activity within germinal centers.
Follicular hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444
864
Reactive pattern characterized by distention and prominence of the lymphatic sinusoids, due to marked hypertrophy of lining endothelial cells and an infiltrate of histiocytes. Encountered in lymph nodes draining cancers.
Sinus histiocytosis(TOPNOTCH)
865
Characterized by reactive changes within T-cell regions of the lymph node, usually encountered during viral infections, following certain vaccinations, and immune reactions induced by certain drugs.
Paracortical hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444
866
Formation of sarcoid-like ganulomas that undergo central necrosis associated with neutrophil accumulation. This irregular stellate necrotizing granuloma is seen in patients presenting with a raised inflammatory node, vesicle or eschar at site of injury. History of exposure to cats.
Cat scratch disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444
867
Causative agent for cat scratch disease(TOPNOTCH)
Bartonella henselae(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 444
868
Lymphoblasts with irregular nuclear contours, condensed chromatin , small nucleoli and scant agranular cytoplasm. Blasts compose >25% of marrow cellularity. Most common childhood leukemia.
Acute lymphocytic leukemia (ALL)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 447
869
Frequent small "cleaved" cells mixed with large cells, growth pattern nodular, centroblasts present. Occurs in older adults, usually involves nodes, marrow, spleen. Associated with t(14;18).
Follicular lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 451
870
Small to intermediate-sized irregular lymphocytes growing in a diffuse pattern, no centroblasts and proliferation centers. Occurs mainly in older males, GI tract commonly affected. Associated with t(11;14).
Mantle cell lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 452
871
Plasma cells in sheets, with prominent nucleoli or inclusion containing Ig. Presents as disseminated bone disease, with destructive lytic lesions.
Plasmacytoma / plasma cell myeloma(TOPNOTCH)
872
Intermediate-sized round lymphoid cells with 2-5 prominent nucleoli. Nuclear remnants phagocytosed by interspersed macrophages with abundant clear cytoplasm, "starry sky pattern"
Burkitt lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 453
873
Sheets of small, round lymphocytes and scattered ill-defined foci of larger, actively dividing cells diffusely efface involved LN. A foci of mitotically active cells called proliferation centers are pathognomonic.
Small lymphocytic leukemia (SLL) / Chronic lymphocytic leukemia (CLL)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 450
874
Fragile neoplastic lymphocytes that are frequently disrupted during smear preparation.
Smudge cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 450
875
Smudge cells are seen in this type of leukemia.
CLL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 450
876
Tumor cells have large nuclei with open chromatin and prominent nucleoli. Most important type of lymphoma in adults, accounting to ~50% of adult NHL.
Diffuse large B-cell lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 452
877
Multifocal destructive bone lesions seen as punched-out defects in bone radiographs.
Multiple myeloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 455
878
Excess lightvor heavy chains along with complete Igs synthesized by neoplastic plasma cells.
Bence-Jones proteins(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 454
879
Cells with two mirror-image nuclei or nuclear lobes, each containing a large acidophilic nucleolus surrounded by a distinctive clear zone, imparting a n owl-like appearance.
Reed-Sternberg cell(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 456
880
A distinctive groups of neoplasms that arise almost invariably in a single lymph node or chain of lymph nodes and spread characteristically in a stepwise fashion to anatomically contiguous nodes.
Hodgkin Lymphoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 456
881
Most common form of Hodgkin lymphoma, characterized by a large cell which has a single multilobate nucleus with small nucleoli and an abundant pale-staining cytoplasm called lacunar cells.
Nodular sclerosis HL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 457
882
Most common form of HL in patients greater than 50 years old, with male predominance, plentiful RS cells and heterogenous cellular infiltrates.
Mixed cellularity HL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 458
883
Cells found in adult T-cell lymphoma which appear to have multilobulated nuclei.
Cloverleaf or flower cell(TOPNOTCH)
884
Subgroup of HL characterized by a large number of small resting lymphocytes admixed with a variable number of benign histiocytes. Variant RS cells described as multilobed, puffy nucleus Which appears like a "popcorn". Excellent prognosis.
Lymphocyte-predominance HL(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 458
885
Cells with fiery red cytoplasm.
Flame cells(TOPNOTCH)
886
Cells with pink globular cytoplasmic inclusions.
Russell bodies(TOPNOTCH)
887
Cells with blue globular nuclear inclusions.
Dutcher bodies(TOPNOTCH)
888
Multiple nuclei, prominent nucleoli, and cytoplasmic droplets containing Ig.
Bizarre, multinucleated cells(TOPNOTCH)
889
Bizarre multinucleated cells, flame cells, Russel bodies and Dutcher bodies are all seen in what disease?
Multiple myeloma(TOPNOTCH)
890
Bone marrow aspirate shows hypercellular martow packed with myeloblasts and azurophilic needle-like material called Auer rods.
Acute Myelogenous Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 462
891
Leukemia of children most responsive to chemotherapy.
Acute Lymphoblastic Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 461
892
Mature B-cell tumor in the elderly, where cells have fine hair-like projections (hairy cells).
Hairy cell leukemia(TOPNOTCH)
893
Hodgkin lymphoma subgroup most commonly associated with EBV infection.
Lymphocyte depleted(TOPNOTCH)
894
Mature B-cell tumor in the elderly, where cells have fine hair-like projections (hairy cells).
Hairy cell leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 459
895
t(9;22) is also called ______.
Philadelphia chromosome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 465
896
Hodgkin lymphoma subgroup with highest count of RS cells.
Mixed cellularity type(TOPNOTCH)
897
This correlates with good prognosis in Hodgkin lymphoma.
High Lymphocyte : Reed-Sternberg cell ratio(TOPNOTCH)
898
Hodgin lymphoma subgroup not associated with EBV.
Nodular sclerosis and lymphocyte predominant(TOPNOTCH)
899
Hodgkin lymphoma subgroup with poorest prognosis.
Lymphocyte depleted HL(TOPNOTCH)
900
Tumor of the thymus associated with myastheni gravis and pure red cell aplasia.
Thymoma(TOPNOTCH)
901
Pentalaminar tubules, often with a dilated terminal end (tennis racket-like appearance).
Birbeck granules(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467
902
Proliferative disorder of the dendritic cells which has birbeck granules.
Langerhans Cell Histiocytosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467
903
Pathology behind polycythemia vera.
Mutation in tyrosine kinase JAK2, which acts in signalling pathways of the erythropoeitin receptors, rendering them hypersensitive to erythropoeitin.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 466
904
Treatment for polycythemia vera.
Phlebotomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 466
905
Collection of aggressive tumors that are comprised of immature myeloblasts which replace the marrow and suppress normal hematopoiesis.
Acute Myelogenous Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467
906
Myeloid tumor arising from a pluripotent stem cell associated with mutatios of the BCR-ABL gene. If untreated, may progress to a blast crisis.
Chronic Myelogenous Leukemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467
907
Most common myelodysplastic syndrome. A myeloid tumor in which abnormal megakaryocytes stimulate marrow fibroblasts to release collagen, replacing the marrow space, leading to pancytopenia and extramedullary hematopoeisis.
Myeloid metaplasia with Myelofibrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 467
908
Other name for acute disseminated Langerhans cell histiocytosis.
Letterer-Siwe disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 468
909
Caused by a systemic activation of coagulation pathways, leading to formation of thrombi throughout the microcirculation.
Disseminated intravascular coagulation(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 469
910
Characterized by spontaneous bleeding, prolonged bleeding time, and normal PT and PTT.
Thrombocytopenia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 471
911
Drug-induced disorder caused by IgG antibodies that bind to platelet factor IV on platelet surfaces, which activates platelets and induce their aggregation.
Heparin-Induced Thrombocytopenia (HIT)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472
912
Associated with pentad of fever, thrombocytopenia, microangipathic hemolytic anemia, transient neurologic deficits and renal failure.
Thrombotic thrombocytic purpura(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472
913
Associated with childhood onset microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. No neurologic symptoms.
Hemolytic uremic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472
914
Caused by antiplatelet antibodies directed against glycoproteins IIb-IIIa, Ib-IX.
Immune thrombocytopenic purpura(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472
915
Decreased gp Ib leads to defective platelet adhesion, associated with decreased platelet count.
Bernard-Soulier Syndrome(TOPNOTCH)
916
Caused by deficiency of ADAMTS13, a vWF metalloprotease.
Thrombotic thrombocytopenic purpura(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472
917
Caused by shiga-like toxin in EHEC (E. coli O157:H7) from improperly cooked burgers.
Hemolytic uremic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 472
918
Decreased gp IIb-IIIa leads to defective platelet aggregation, associated with normal platelet count.
Glanzmann thrombasthenia(TOPNOTCH)
919
Most common bleeding disorder.
vWF disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474
920
Most common hereditary disease associated with life threatening bleeding,
Hemophilia A(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474
921
An X-linked recessive disorder caused by reduction in factor VII activity.
Classic Hemophilia/ Hemophilia A(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474
922
An X-linked disorder caused by deficiency of Factor IX, or Christmas factor. Bleeding time is normal, PTT is prolonged.
Hemophilia B/ Christmas Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 474
923
A state associated with excessive removal of formed elements of blood, resulting in anemia, leukopenia or thrombocytopenia.
Hypersplenism(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 476
924
Loss of lung volume cause by inadequate expansion of airspaces, resulting in shunting of inadequately oxygenated blood from pulmonary arteries into veins.
Atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 480
925
Atelectasis which occurs when an obstruction prevents air from reaching distal airways.
Resorption atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 480
926
Atelectasis usually associated with accumulation of fluid, blood, or air within the pleural cavity, which mechanically collapse the adjacent lung.
Compression atelectasis (aka passive or relaxation atelectasis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 481
927
Atelectasis which occurs when either local or generalized fibrotic changes in the lung or pleura hamper expansion and increase elastic recoil during expiration.
Contraction or cicatricial atelectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 481
928
Lungs are dark red, firm, airless and heavy. There is capillary congestion, necrosis of alveolar epithelial cells, interstitial and intra-alveolar edema and hemorrhage and neutrophils in capillaries. Hyaline membrane is also characteristic, lining the alveolar ducts.
Acute Respiratory Distress Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 482
929
Diffuse pulmonary disease characterized by limitation of airflow, usually resulting from an increase in resistance caused by partial or complete obstruction atvany level.
Obstructive pulmonary disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
930
Diffuse pulmonary disease characterized by reduced expansion of lung parenchyma accompanied by decreased total lung capacity.
Restrictive lung disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
931
Lung volumes in obstructive lung disease:FEV1FVCFEV1:FVC ratio
FEV1 - decreasedFVC - normal / increasedFEV1:FVC ratio - decreased(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
932
Lung volumes in restrictive lung diseaseFEV1FVCFEV1:FVC ratio
FEV1 - normal/decreasedFVC - decreasedFEV1:FVC ratio - near normal(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 483
933
Characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls without obvious fibrosis. There is thinning oof the alveolar walls and loss of elastic tissue.
Emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485
934
Type of emphysema involving the central or proximal parts of the acini, formed by respiratory bronchioles, while distal parts are spared. Lungs deep pink and less voluminous, affecting the upper 2/3 of the lungs. Occurs in smokers.
Centriacinar (centrilobular) Emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485
935
Type of emphysema wherein the acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal alveoli. Occurs more commonly in the lower lung zones. Occurs in a-antitrypsin deficiency.
Panacinar (panlobular) emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 485
936
Type of emphysema wherein only the distal part is primarily involved. Lesion is adjacent to the pleura along the lobular connective tissue septa and at the lobe margins. More severe at the upper half of the lungs, forming bullae.
Distal acinar (paraseptal) emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 486
937
Barrel-chested, dyspneic, prolonged expiration, sits forward in a hunched-over position, adequate oxygenation of oxygen. "Pink puffers".
COPD predominantly emphysema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
938
History of recurrent infections with purulent sputum, less prominent dyspnea and respiratory drive, becomes hypoxic and are pften cyanotic and obese. "Blue bloaters".
COPD predominantly chronic bronchitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
939
Defined as persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.
Chronic bronchitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
940
Mucosal lining of the larger airways is usually hyperemic and swollen with edema fluid, often covered by a layer of mucinous or mucopurulent secretions. Trachea and bronchi have enlarged mucus-secreting glands.
Chronic bronchitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
941
Characterized by goblet cell metaplasia, mucus plugging, inflammation and fibrosis, and sometimes complete obliteration of the lumen due to fibrosis.
Chronic bronchiolitis (small airway disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
942
Most important underlying risk factor for chronic bronchitis.
Cigarette smoking(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
943
Triad of 1.intermittent and reversible airway obstruction2.chronic bronchial inflammation with eosinophils3.bronchial smooth muscle cell hypertrophy and hyperreactivity
Asthma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 489
944
Collections of crystalloids made up of eosinophil proteins.
Charcot-Leyden crystals(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492
945
Whorls of shed epithelium found in mucus plugs.
Curschmann spirals(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492
946
Curshmann spirals and Charcot-Leyden crystals are found histologically in this disease.
Asthma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 492
947
Permanent dilation of bronchi and bronchioles caused by destruction of theuscle and elastic supporting tissue, resulting from chronic necrotizing infections.
Bronchiectasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 493
948
An autosomal recessive disorder frequently associated with bronchiectasis and sterility in males.
Kartagener syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 493
949
Refers to a pulmonary disorder of unknown etiology characterized patchy interstitial fibrosis. Grossly, pleural surfaces of the lung have the appearance of cobblestones because of retraction scars along the interlobular septa.
Idiopathic Pulmonary Fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 495
950
A thrombus that lodges astride a pulmonary artery bifurcation, which causes pulmonary hypertension, which can lead to hypoxia and cor pulmonale.
Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 505
951
Most common symptom of pulmonary embolism.
None, asymptomatic 60-80% of the time.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 506
952
Mean pulmonary pressures reach one-fourth or more of systemic pressures.
Pulmonary hypertension(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 506
953
Encountered in young persons, more commonly in women, marked by fatigue, syncope, dyspnea on exertion, and sometimes chest pain. Cause of increased pulmonary pressures is unknown.
Primary pulmonary hypertension(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 506
954
Clinical features of this disease reflect the underlying disease, with accentuation of respiratory insufficiency and right-sided heart strain.
Secondary pulmonary hypertension(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 507
955
Pneumonia with a patchy distribution of inflammation involving more than one lobe.
Bronchopneumonia(TOPNOTCH)
956
Pneumonia with a patchy distribution of inflammation involving more than one lobe.
Bronchopneumonia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 509
957
Four stages of pneumococcal pneumonia.
Congestion, red hepatization, gray hepatization, resolution(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 510
958
Affected areas are red-blue, congested and subcrepitant. Inflammatory reaction is largely confined within the walls of the alveoli. Septa widened and edematous, with mononuclear infiltrates of lymphocytes, histiocytes and plasma cells. Alveolar spaces are free of cellular exudate.
Atypical pneumonia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 513
959
A localized area of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities.
Lung abscess(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 515
960
Pulmonary abscess resulting from aspiration of infective material are much more common on the left or right side?
Right side since it's shorter and more vertical.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 515
961
Form of tuberculosis that develops in a previously unexposed, unsensitized person.
Primary tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 518
962
Implantation of the inhaled M. tuberculosis bacilli in the distal airspaces of the lungs, causes the formation of this 1 - 1.5 cm area of gray-white inflammatory consolidation.
Ghon focus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 518
963
Ghon focus + nodal involvement = ________
Ghon complex(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 518
964
Radiographically detectable calcified Ghon complex.
Ranke complex(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 518
965
Pattern of disease that arises in previously sensitized host to M. tuberculosis.
Secondary or reactivation TB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 520
966
Occurs when TB bacilli drain through the lymphtics into lymphatic ducts, which eventually empty into the rightside of the heart and into pulmonary circulation. Individual lesions are small, visible foci of yellow-white consolidation scattered through the parenchyma.
Miliary TB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 520
967
The most frequent form of extrapulmonary TB.
TB Lymphadenitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 521
968
TB lymphadenitis of the cervical LN.
Scrofula(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 521
969
Round to oval small yeast forms measuring 2-5 um in diameter.
Histoplasma capsulatum(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 523
970
Thick walled non-budding spherules 20-60 um diameter, often filled with small endospores.
Coccidiodomycosis immitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 523
971
Round to oval and larger fungi, which reproduce by broad-based budding.
Blastomycosis dermatitidis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 523
972
Cells infected by this virus exhibit gigantism of the cell and nucleus. An enlarged inclusion surrounded by a clear halo "owl's eye" is seen. It is the most common opportunistic viral pathogen in AIDS.
Cytomegalovirus (CMV)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 524
973
Opportunistic infection of the lungs having a characteristic intra-alveolar foamy, pink-staining exudate "cotton candy exudate", with thickened septa and mononuclear infiltrate.
Pneumocystis carinii pneumonia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 526
974
Most frequent disease-causing fungus.
Candida albicans(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 526
975
The fungus is a 5-10 um yeast, has a thick, gelatinous capsule and reproduces by budding. Most likely acquired through bird droppings. Visualized by India ink or Giemsa stain.
Cryptococcus neoformans(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 527
976
Which type of lung cancer is treated by chemotherapy only? Why?
Small cell lung carcinomaIt is an aggressive tumor which usually have metastasized at the time of diagnosis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 529
977
Lung carcinoma best treated with surgery since they respond poorly to chemotherapy.
Non-small cell lung carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 529
978
Types of lung cancer with strongest association with tobacco exposure.
Squamous cell carcinomaSmall-cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 530
979
Lung cancer which are peripherally located, most common type of lung cancer in women and nonsmokers. Grows slowly and metastasize early. Assumes a variety of forms, incliding acinar, papillary and solid types.
Adenocarcinoma(TOPNOTCH)
980
Lung cancer which are peripherally located, most common type of lung cancer in women and nonsmokers. Grows slowly and metastasize early. Assumes a variety of forms, incliding acinar, papillary and solid types.
Adenocarcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 531
981
Lung carcinoma which typically have large, prominent nucleoli, and a moderate amount of cytoplasm, with minimal glandular or squamous differentiation.
Large-cell carcinoma(TOPNOTCH)
982
Lung carcinoma which typically have large, prominent nucleoli, and a moderate amount of cytoplasm, with minimal glandular or squamous differentiation.
Large-cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 531
983
Lung carcinoma which appear as pale gray, centrally located masses. Nests and cords of polygonal cells with scant cytoplasm, granular chromatin and inconspicuous nuclei. FNAB shows nuclear molding of adjacent cells. Associated with several paraneoplastic syndromes.
Small cell lung carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 532
984
Other name for small cell lung carcinoma.
Oat cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 532
985
Paraneoplastic syndromes associated with oat cell carcinoma.
Cushing syndromeSIADH Lambert-Eaton myasthenic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 532
986
Hypercalcemia due to excessive production of PTH related protein is usually seen in patients with this type of lung carcinoma.
Squamous cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 532
987
Form of lung cancer that is thought to arise from neuroendocrine cells, called Kulchitsky cells, that line the bronchial mucosa and resemble intestinal carcinoids. Nests of small, rounded, uniform cells with "salt and pepper" chromatin.
Bronchial carcinoids(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 534
988
Presence of fluid in the pleural space.
Pleural effusion(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 535
989
Air or other gas in the pleural sac.
Pneumothorax(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 535
990
A collection of whole blood in the pleural cavity.
Hemothorax(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 535
991
A pleural collection of a milky lymphatic fluid containing microglobules of lipid.
Chylothorax(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 535
992
A rare cancer seen in patients who work in shipyards, miners and insulators. Lesion is preceeded by extensive pleural fibrosis and plaque formation. May be epithelial, sarcomatoid or biphasic in morphology.
Malignant mesothelioma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 536
993
Rare neoplasm with strong links to EBV and high frequency among the Chinese population. Characterized by large epithelial cells having indistinct borders (syncitial growth) and prominent eosinophilic nucleoli.
Nasopharyngeal carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 537
994
Smoothe, hemispherical protrusions located on the true vocal cords, composed of fibrous tissue and covered by stratified squamous mucosa.
Vocal cord nodules(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 537
995
A benign neoplasm usually on the true vocal cords that forms a soft, raspberry-like excresence rarely more then 1 cm in diameter. Consists of multiple, slender, finger-like projections.
Laryngeal papilloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 537
996
A glomerular syndrome dominated by the acute onset of usually grossly visible hematuria, mildly moderate proteinuria, azotemia, edema and hypertension.
Acute nephritic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
997
A glomerular syndrome characterized by heavy proteinuria, hypoalbunemia, severe edema, hyperlipidemia and lipiduria.
Nephrotic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
998
Characterized by bacteriuria and pyuria, which may be asymptomatic.
Urinary tract infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
999
Most common type of collagen found in glomerular basement membrane.
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 543
1000
Most frequent cause nephrotic syndrome in children. Under light microscope, the glomerular basement membrane appears normal, but on electrin microscopy, GBM shows uniform and diffuse effacement of foot processes of the podocytes. Good response to corticosteroid therapy.
Minimal change disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
1001
A lesion characterized histologically by sclerosis affecting some but not all glomeruli and involving only segments of each affected glomerulus.
Focal segmental glomerulosclerosis (FSGS)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
1002
Slowly progressive disease characterized by the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane. Histologically, there is diffuse thickening of the BM. (+) spike and dome pattern on electron microscopy. Often resistant to steroid therapy.
Membranous glomerulonephritis (Membranous Nephropathy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 551
1003
Characterized by discrete SUBENDOTHELIAL electron-dense deposits in irregular granular pattern.
Type I MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
1004
GBM is thickened, showing a "tram-track" appearance on PAS stains. There is proliferation of mesangial and endothelial cells as well as infiltrating leukocytes.
MPGN(Membranoproliferative Glomerulonephritis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
1005
MPGN wherein the lamina densa and the SUBENDOTHELIAL space of the GBM are transformed into an irregular, ribbon-like extremely electron dense structure.
Type II MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 554
1006
Caused by glomerular deposition of immune complexes resulting in diffuse proliferation and swelling of resident glomerular cells. There is uniformly increased cellularity of glomerular tufts. Electron microscopy show subepithelial "humps" against the GBM, with granular deposits of IgG and complement.
Acute postinfectious (poststreptococcal) Glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
1007
Most common cause of recurrent microscopic or gross hematuria and is the most common glomerular disease revealed by renal biopsies.
IgA Nephropathy (Berger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
1008
Pathologic hallmark of this disease is the deposition of IgA in the mesangium.
IgA nephropathy (Berger Disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
1009
Nephritis accompanied by nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy.
Alport syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
1010
Caused by mutations in genes encoding GBM collagen, manifest as hematuria and slowly progressing proteinuria and declining renal function. GBM has "basket-weave" appearance due to splitting and lamination of the lamina densa.
Hereditay nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
1011
A clinical syndrome characterized by rapid and progressive lossof renal function with features of nephritic syndrome,often with severe oliguria. Histologic feature is the presence of crescents.
Rapidly Progressive Glomerulonephritis (Crescentic GN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
1012
CrGN characterized by linear deposits of IgG and C3 on the GBM. anti-GBM Ab also bind to pulmonary alveolar capillary basement membranes to produce pulmonary hemorrhages associated with renal failure.
Anti-Glomerular Basement Membrance Antibody (Type I) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
1013
CrGN which are immune complex-mediated disorders, as a complication of any of the IC nephritides including PSGN, IgA Nephropathy and HSP. There is segmental necrosis and characteristic granular pattern of the underlying immune complex disease.
Immune Complex-Mediated (Type II) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
1014
CrGN defined by the lack of anti-GBM Ab and immune complex deposition. Glomeruli show segmental necrosis, negative immunofluorescence.
Pauci-immune (Type III) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
1015
An important cause of end-stage renal disease presenting as chronic renal failure. Kidneys are symmetrically contracted, surfaces are red-brown and diffusely granular. Glomeruli are obliterated with marked interstitial fibrosis.
Chronic glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 559
1016
A common suppurative inflammation of the kidney and renal pelvis caused by bacterial infection, either by hematogenous spread or through ascending infection.
Pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 560
1017
Hallmark of this disease is scarring involving the pelvis or calyces, or both, leading to papillary blunting and marked calyceal deformities.
Chronic pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 562
1018
Nephritis with prominent eosinophilic and mononuclear inflitrate, with pronounced edema.
Acute Drug-Induced Interstitial Nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 563
1019
A clinicopatholigic entity characterized by damaged tubular epithelial cells and clinically by acute suppression of renal function.Most common cause of acute renal failure.
Acute tubular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
1020
Characterized by necrosis of short segments of the tubules, seen in the straight portions of the PCT and TALOH. There is a variety of tubular injuries, associated with proteinaceous casts in the distal tubules and collecting ducts.
Ischemic ATN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
1021
ATN characterized by necrosis and injury of the PCT with sparing of the tubular membranes.
Toxic ATN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
1022
Phase of ATN lasting about 36 hrs, dominated by the inciting medical, surgical or obstetric event. Slight decline in renal output and a rise in serum creatinine.
Initiation phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
1023
Phase of ATN where urine output falls markedly, between 50-400mL/day. Dominated by signs and symptoms of uremia and fluid overload.
Maintenance phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
1024
Phase of ATN characterized by a steady increase in urine volume, electrolyte imbalance and increased vulnerability to infection.
Recovery(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
1025
Chronic interstitial nephritis associated with renal papillary necrosis. The necrotic papillae appear yellowish-brown, showing coagulative necrosis associated with loss of cellular detail with preservation of tubular outlines.
Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
1026
T-cell mediated immune reaction of the kidneys to an offending agent, characterized by interstitial inflammation, with abundant eosinophils and edema.
Drug-induced interstitial nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
1027
Renal changes in benign hypertension, associated with hyaline arteriolosclerosis, appearing as homogenous, pink hyaline thickening of arterial walls. Larger blood vessels show fibroelastc hyperplasia.
Benign nephrosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
1028
Acute renal injury assiciated with malignant hypertension. The kidneys show small, pinpoint petechial hemorrhages, "flea-bitten" appearance. Concentric arrangement of cells, described as "onion-skin" lesions cause marked narrowing of arterioles and small arteries.
Malignant nephrosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 567
1029
Characterized by widespread thrombosis and presence of fibrin thrombi in glomeruli and small vessels resulting in acute renal failure. Consequence of childhood HUS and TTP.
Thrombotic microangiopathies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568
1030
One of the main causes of acute renal failure in children.
Hemolytic Uremic Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568
1031
Innocuous lesions of the kidney, 1-5cm in diameter, translucent, lined by a gray, glistening, smooth membrane, filled with clear fluid. Composed of a single layer of cuboidal or flattened cuboidal epithelium, usually confined to the cortex.
Simple renal cyst(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
1032
Autosomal dominant. Kidneys are enlarged, composed solely of cysts without intervening parenchyma. Cysts are filled with clear or turbid fluid. Cysts may arise at any level of the nephron, with variable, often atrophic lining.
Adult polycystic kidney disease (APKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
1033
What is the pathology behind APKD?
Defective gene PKD1,which codes for polycystin-1.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
1034
Function of policystin-1?
Protein that is involved in cell-cell or cell-matrix adhesion.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
1035
Autosomal recessive. There are numerous small cysts in the cortex and medulla, giving the kidney a "sponge-like" appearance. Cysts have uniform cuboidal epithelium. Associated with multiple cysts in the liver.
Childhood Polycystic Kidney Disease (CPKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 570
1036
An under-recognized vause of chronic kidney disease in children and young adults, associated with mutations in several genes that encode neohrocystins that may be involved in ciliary function. Kidneys are contracted and contain multiple cysts.
Medullary cystic disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
1037
Calculus formation at any level of the urinary collecting system.
Urolithiasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
1038
Most common composition of kidney stones. Precipitates in the presence of alkaline urine.
Calcium oxalate and/or calcium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
1039
Most important cause of kidney stone formation.
Supersaturation(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1040
Kidney stones occuring in patients with alkaline urine due to UTI, particularly Proteus vulgaris and Staphylococci.
Struvite stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1041
Component of struvite stones.
Magnesium ammonium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1042
Kidney stones seen in patients with gout and leukemias. Urine pH is decreased.
Uric acid stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1043
Kidney stones associated with a defect in the renal transportation of certain amino acids. Forms in acidic urine.
Cystine stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1044
Branching structures which create a cast of the renal pelvis and calyceal system.
Stagnorn calculi(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1045
Most common composition of staghorn calculi.
Magnesium ammonium phosphate (Struvite)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1046
Dilation of the renal pelvis and calyces, accompanied by atrophy of the renal parenchyma, caused by obstruction to urine outflow.
Hydronephrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
1047
Dilation of the ureters secondary to obstruction.
Hydroureter(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
1048
Most common malignant tumor of the kidney.
Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
1049
Tumors derived from renal tubular epithelium, located primarily at the cortex. With three common forms, clear cell, papillary renal cell and chromophobe renal carcinomas.
Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
1050
Most common form of renal cell carcinoma.
Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
1051
Renal carcinoma, usually solitary and large, spherical masses reaching up to 15cms in diameter. Cut surface show yellow orange to gray-white, with prominent areas of cystic softening and hemorrhage. Cells appear vacuolated or may be solid.
Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
1052
Renal carcinoma exhibiting varying degrees of papilla formation with fibrovascular cores. Cells have clear to pink cytoplasm.
Papillary renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
1053
Renal cell carcinoma which tends to be tan-brown, cells have clear, flocculent cytoplasm with very prominent, distinct cell membranes. Nuclei surrounded by halos of cleared cytoplasm.
Chromophobe-type renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
1054
Tumor of the urinary bladder, characterized as small, frond-like structures having delicate fibrovascular core covered by multilayered, well-differentiated transitional epithelium.
Benign papilloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575
1055
Dominant clinical presentation of bladder carcinoma.
Painless hematuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575
1056
Protozoa associated with increased risk of bladder carcinoma.
Schistosoma haematobium(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
1057
Chemotherapeutic agent associated with development of hemorrhagic cystitis and increased risk of bladder carcinoma.
Cyclophosphamide(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
1058
Electron Microscopy: Subepithelial humps
PSGN (TOPNOTCH)
1059
Light Microscopy: Hyalinized glomeruli
Chronic Glomerulonephritis (TOPNOTCH)
1060
Electron Microscopy: Subepithelial deposits
Membranous glomerulopathy (TOPNOTCH)
1061
Electron Microscopy: Loss of foot processes
Minimal Change Disease (TOPNOTCH)
1062
Electron Microscopy: Subendothelial deposits
MPGN Type 1 (TOPNOTCH)
1063
Flourescence Microscopy: Linear IgG and C3
Goodpasture's disease (TOPNOTCH)
1064
Light Microscopy: Normal, with lipid in tubules
Minimal Change Disease (TOPNOTCH)
1065
What is the most common type of Renal Cell Carcinoma (RCC)?
Clear cell RCC (TOPNOTCH)
1066
What are the 3 classic diagnostic features of RCC?
1. Costovertebral Pain (TOPNOTCH)2. Palpable Mass3. Hematuria
1067
Among the 3 classic diagnostic features of RCC, which feature is the most reliable?
Hematuria (TOPNOTCH)
1068
RCC morphology: pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a concentration of the largest cells around the blood vessels
Chromophobe RCC (TOPNOTCH)
1069
RCC morphology: rounder or polygonal shape and have abundant clear or granular cytoplasm with stains with glycogen and lipid
Clear Cell RCC (TOPNOTCH)
1070
RCC morphology: arise from DCT and are typically hemorrhagic and cystic
Papillary RCC (TOPNOTCH)
1071
RCC morphology: irregular channels lined by highly atypical epithelium with a hobnail pattern.
Collecting Duct Carcinoma (TOPNOTCH)
1072
RCC morphology: Interstitial foam cells and psamomma bodies
Papillary Carcinoma (TOPNOTCH)
1073
Urolithiasis: most common type
Calcium Oxalate stones (TOPNOTCH)
1074
Urolithiasis: staghorn calculi
Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)
1075
Urolithiasis: caused by genetic defects in the renal absorption of amino acids
Cystine stones (TOPNOTCH)
1076
Urolithiasis: associated with urea-splitting bacteria
Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)
1077
Urolithiasis: radiolucent
Uric Acid Stones (TOPNOTCH)
1078
Urolithiasis: common in patients with leukemia
Uric Acid Stones (TOPNOTCH)
1079
What is the most common cause of renal artery stenosis?
Occlussion by an atheromatous plaque at the origin of the renal artery (TOPNOTCH)
1080
What is the most common type of Fibromuscular Dysplasia; intimal, medial, or adventitial?
Medial (TOPNOTCH)
1081
Gross morphology: flea bitten appearance of the kidneys
Malignant Hypertension (TOPNOTCH)
1082
What are the two histological alterations in the blood vessels of patients with malignant hypertension?
1. Fibrinoid Necrosis of arterioles2. Onion-skinning (TOPNOTCH)
1083
What are the 3 complications of acute pyelonephritis?
1. Papillary Necrosis2. Pyonephrosis3. Perinephric Abscess (TOPNOTCH)
1084
Among the 3 complications of acute pyelonephritis, which one is mainly seen in diabetics and in those with urinary tract obstruction?
Papillary necrosis (TOPNOTCH)
1085
Morphology: acute neutrophilic exudate within tubules and the renal substance
Acute pyelonephritis (TOPNOTCH)
1086
ATN morphology: focal tubular epithelial necrosis at multiple points along the nephron, with large skip areas in between
Ischemic ATN (TOPNOTCH)
1087
ATN morphology: manifested by acute tubular injury with non specific tubular necrosis
Toxic ATN (TOPNOTCH)
1088
ATN morphology: Eosinophilic hyaline casts containing Tamm Horsfall protein
Ischemic ATN (TOPNOTCH)
1089
ATN morphology: severely injured cells that are not yet dead might contain large acidophilic inclusions
Mercuric Chloride ATN (TOPNOTCH)
1090
ATN morphology: accumulation of neutral lipids in injured cells
Carbon Tetrachloride poisoning (TOPNOTCH)
1091
ATN morphology: marked ballooning and hydrophic or vacuolar degeneration of proximal convulated tubules and often times calcium oxalate crystals are seen in the lumen
Ethylene Glycol ATN (TOPNOTCH)
1092
Morphology: patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis
Acute pyelonephritis (TOPNOTCH)
1093
Gross morphology: irregularly scarred; if bilateral, the involvement is asymmetric
Chronic pyelonephritis (TOPNOTCH)
1094
Gross morphology: kidneys are diffusely and symmetrically scarred
Chronic glomerulonephritis (TOPNOTCH)
1095
Morphology: hallmark is the coarse, discrete, corticomedullary scar overlying a dilated, blunted, or deformed calyx
Chronic pyelonephritis (TOPNOTCH)
1096
What is the main cause of renal dysfunction in Multiple Myeloma?
Bence Jones protein (TOPNOTCH)
1097
Morphology: bence jones tubular casts appear as pink to blue amorphous masses, sometimes concentrically laminated, often with fractured and angulated appearance, filling and idstending the lumens
Multiple Myeloma (TOPNOTCH)
1098
Morphology: narrowing of the lumens of arterioles and small arteries, caused by thickening and hyalinization of the walls (hyaline arteriolosclerosis)
Benign nephrosclerosis (TOPNOTCH)
1099
Morphology: classic diagnostic finding is enlarged hypercellular glomeruli
PSGN (TOPNOTCH)
1100
Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla
Renal infarcts (TOPNOTCH)
1101
What is the most common cause of clinical pyelonephritis?
Ascending infection (TOPNOTCH)
1102
What is the first step in the pathogenesis of ascending infection that leads to pyelonephritis?
Colonization of the distal urethra and introits by coliform bacteria (TOPNOTCH)
1103
Morphology: "fibrin caps" and "capsular drops"
Diabetic kidney (TOPNOTCH)
1104
Morphology: diffuse increase in mesangial matrix and characteristic PAS positive nodules
Diabetic glomerulosclerosis (TOPNOTCH)
1105
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
1106
Morphology: "tram track" "double contour" glomerular capillary walls
Membranoproliferative Glomerulonephritis (TOPNOTCH)
1107
Morphology: collapsed glomerular tufts and the crescent shaped mass of proliferating cells and leukocytes internal to Bowman capsule
Rapidly Progressive Glomerulonephritis (TOPNOTCH)
1108
Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla
Renal infarcts (TOPNOTCH)
1109
What is the most common cause of clinical pyelonephritis?
Ascending infection (TOPNOTCH)
1110
What is the first step in the pathogenesis of ascending infection that leads to pyelonephritis?
Colonization of the distal urethra and introits by coliform bacteria (TOPNOTCH)
1111
Morphology: "fibrin caps" and "capsular drops"
Diabetic kidney (TOPNOTCH)
1112
Morphology: diffuse increase in mesangial matrix and characteristic PAS positive nodules
Diabetic glomerulosclerosis (TOPNOTCH)
1113
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
1114
Morphology: "tram track" "double contour" glomerular capillary walls
Membranoproliferative Glomerulonephritis (TOPNOTCH)
1115
Morphology: collapsed glomerular tufts and the crescent shaped mass of proliferating cells and leukocytes internal to Bowman capsule
Rapidly Progressive Glomerulonephritis (TOPNOTCH)
1116
Morphology: glomeruli show thickening and sometimes splitting of capillary walls, due largely to endothelial and subendothelial swelling, and deposits of fibrin-related materials in the capillary lumens, subendothelially, and in the mesangium.
Childhood Hemolytic Uremic Syndrome(TOPNOTCH)
1117
Gross morphology: flea bitten appearance of the kidney
Malignant hypertension(TOPNOTCH)
1118
Gross morphology: fine, leathery granularity of the surface of the kidney
nephrosclerosis(TOPNOTCH)
1119
What is the emerging viral pathogen that causes pyelonephritis in kidney allografts?
Polyoma virus(TOPNOTCH)
1120
Morphology: enlarged tubular epithelial cells with nuclear inclusions
Polyoma kidney (TOPNOTCH)
1121
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
1122
Electron microscopy: irregular thickening of the BM of the glomerulus, lamination of the lamina densa, and foci of rarefaction
Alport Syndrome (TOPNOTCH)
1123
Morphology: lamina densa of the GBM is transformed into an irregular, ribbon like, extremely electron dense structure
Dense Deposti Disease or Type II MPGN (TOPNOTCH)
1124
ESRD is defined as GFR less than how many percent of normal?
5%(TOPNOTCH)
1125
Renal failure is defined as GFR less than how many percent of normal?
20%-25%(TOPNOTCH)
1126
In renal insufficiency is defined as GFR less than how many percent of normal?
20%-50%(TOPNOTCH)
1127
Diminished renal reserve is define as GFR less than how many percent of normal?
50%(TOPNOTCH)
1128
Lesion of the female vulva characterized by thinning of the epidermis and disappearance of rete pegs, hydropic degeneration of basal cells, superficial hyperkeratosis, dermal fibrosis with scant perivascular, mononuclear inflammatory cell infiltrate. Occurs most commonly in postmenopausal women.
Lichen sclerosus(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 713
1129
This disorder of the vulva is marked by epithelial thickening, expansion of the stratum granulosum, significant surface hyperkeratosis and pronounced leukocytic infiltrate. Appears clinically as an area of leukoplakia.
Lichen simplex chronicus(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 713
1130
These are flat, moist, minimally elevated lesions that occur in secondary syphilis.
Condyloma lata(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 713
1131
Lesions of the anogenital area which may be papillary and distinctly elevated or may be somewhat flat and rugose. Characteristic cellular morphology is the presence of cytoplasmic vacuolization with nuclear angular polymorphism and koilocytosis. Hallmark of HPV infection.
Condyloma acuminata(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 713
1132
Red, scaly plaque, microscopically characterized by the spread of malignant cells within the epithelium, occasionally with invasion of underlying dermis. May have underlying carcinoma of a vulvar or perineal gland.
Paget disease of the Vulva(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 715
1133
A soft polypoid mass, which is a rare form of primary vaginal cancer. Usually encountered in infants and children less than 5 y/o.
Sarcoma botryoides (embryonal rhabdomyosarcoma)(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 716
1134
Most commonly develops in the transformation zone of the cervix. Produces a "barrel cervix" if the tumor encircles the cervix and invades the underlying stroma.
Invasive carcinoma of the cervix(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 719
1135
Protruding polypoid masses which are inflammatory in origin, soft, yields to palpation, and have a smooth, glistening surface with underlying cystically dilated spaces filled with mucinous secretion.
Endocervical polyp(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 721
1136
Refers to the growth of the basal layer of the endometrium down to the myometrium. Nests of endometrial stroma, glands or both are found in the myometrium, in between muscle bundles.
Adenomyosis(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 721
1137
Characterized by the presence of endometrial glands and stroma in a location outside the endomyometrium. Undergoes cyclic bleeding. Also called "chocolate cysts".
Endometriosis(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 722
1138
These are sharply circumscribed, firm, gray-white masses of the uterus, with "whorled" cut surface.
Leiomyoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 721
1139
Solitary tumors of the uterus which arise de novo from the mesenchymal cells of the myometrium. Characterized byvtche presence of tumor necrosis, cytologic atypia and mitotic activity.
Leiomyosarcomas(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 725
1140
Type of endometrial carcinoma associated with estrogen excess and endometrial hyperplasia.
Endometroid carcinoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 727
1141
Type of endometrial carcinoma which occurs in older women and is usually associated with endometrial atrophy.
Serous carcinoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 727
1142
Small, fluid-filled cysts which originate from the unruptured graafian follicles or in follicles that have ruptured and immediately sealed.
Follicle and luteal cysts(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 728
1143
Triad of oligomenorrhea, infertility and obesity in young women secondary to excessive production of estrogens and androgens.
Polycystic ovaries(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 728
1144
Other name for polycystic ovary syndrome?
Stein-Leventhal syndrome(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 728
1145
Two most important risk factors for development of ovarian cancer.
Nulliparity and family history(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 729
1146
Mutation of this gene is associated in the development of both ovarian and breast cancers.
BRCA 1(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 729
1147
Mutation of this gene is associated with the development of breast cancer only,
BRCA 2(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 729
1148
Benign lesion of the ovary most commonly seen in women 30-40 years old. Most frequent of the ovarian tumors. Serosal covering is smooth and glistening. Characterized histologically by tall, columnar epithelium and the presence of Psammoma bodies.
Serous tumor of the ovary(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 730
1149
Large, multilocular tumors of the ovaries, without psammoma bodies. Composed of mucin-producing epithelial cells.
Mucinous Tumors (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 731
1150
Metastasis of mucinous tumor of the gastrointestinal tract to the ovaries is called?
Krukenberg tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 731
1151
A rare, solid, unilateral ovarian tumor consisting of an abundant stroma containing nests of transitional-like epithelium resembling that of the urinary tract.
Brenner Tumor (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1152
Unilateral ovarian tumor composed of sheets or cords of large cleared cells separated by scant fibrous strands. Stroma may contain lymphocytes and occasional granuloma. Usually occur on the 2nd-3rd decade of life.
Dysgerminoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1153
Unilateral ovarian tumor which occur during the 1st 3 decades of life. Characterized by small, hemorrhagic focus with syncitiothrophoblast and cytotrophoblast. Metastasize early.
Choriocarcinoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1154
Sex cord tumor seen most commonly in postmenopausal women. Lesions may be tiny or large, gray to yellow (with cystic spaces). Produce large amounts of estrogen. (+) Call-Exner bodies
Granulosa-thecal cell tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1155
Sex cord tumor characterized by solid gray fibrous cells to yellow (lipid-laden) plump thecal cells. Most hormonally inactive.
Thecoma-fibroma tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1156
Sex cord tumor seen as small, gray to yellow-brown, and solid lesions. May resemble development of testis with tubules, or cords and plump pink Sertoli cells. May be masculinizing or defeminizing.
Sertoli-Leydig cell tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1157
On transection, filled with sebaceous secretion and matted hair, bonw and cartilage, nests of bronchial or gastrointestinal epithelium, and other recognizable lines of development are also present.
Benign (Mature) Cystic Teratomas / Dermoid Cyst(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 733
1158
Microscopically, the distinguishing feature is a variety of immature or barely recognizable areas of differentiation toward cartilage, bone, muscle, nerve, and other structures. Found early in life.
Immature Malignant Teratomas (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 733
1159
Tumor of the ovary composed entirely of mature thyroid tissue. May hyperfunction and produce hyperthyroidism. Appear as small, solid, unilateral brown ovarian masses
Struma ovarii (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 733
1160
A voluminous mass of swollen, sometimes cystically dilated, chorionic villi, appearing grossly as grapelike structures.
Hydatidiform Mole (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 735
1161
This type of H. mole shows hydropic swelling of chorionic villi and virtual absence of vascularization of villi. No fetal parts seen.
Complete mole (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 736
1162
This type of H. mole shows villous edema that involves only some of the villi and the trophoblastic proliferation is focal and slight, with characteristic irregular scalloped margin. Fetal parts/embryo may be seen.
Partial mole(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 736
1163
These are complete moles that are more invasive locally but do not metastasize. Microscopically, the epithelium of the villi is marked by hyperplastic and atypical changes, with proliferation of both cuboidal and syncytial components.
Invasive Mole (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 736
1164
Appear as very hemorrhagic, necrotic masses within the uterus. The tumor is purely epithelial, composed of anaplastic cuboidal cytotrophoblast and syncytiotrophoblast, chorionic villi are not formed. High propensity for metastasis.
Choriocarcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 737
1165
A cystic dilation of an obstructed duct that arises during lactation.
Galactocele (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1166
Multifocal, bilateral blue-brown cysts ("blue dome cysts") of the breast, measuring 1-5 cm diameter, filled with serous turbid fluid. Occurs normally in the menstrual cycle.
Simple fibrocystic change of the breast(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1167
Term used to describe hyperplasia that cytologically resemble lobular carcinoma in situ, but the cells do not fill or distend more than 50% of the acini within a lobule.
Atypical lobular hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1168
The lumen of the ducts, ductules, or lobules of the breast is filled with a heterogeneous population of cells of different morphologies. Irregular slit-like fenestrations are prominent at the periphery.
Epithelial Hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1169
These lesions are characterized by proliferation of lining epithelial cells and myoepithelial cells in small ducts and ductules, yielding masses of small gland patterns within a fibrous stroma. The acini are arranged in a swirling pattern, and the outer border is usually well circumscribed.
Sclerosing Adenosis (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 741
1170
A nonbacterial chronic inflammation of the breast associated with inspissation of breast secretions in the main excretory ducts.
Mammary duct ectasia (periductal or plasma cell mastitis) (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1171
The lesion is small, often tender, rarely more than 2 cm in diameter, and sharply localized, with a central focus of necrotic fat cells surrounded by neutrophils and lipid-filled macrophages. Caused by some antecedent trauma to the breast.
Traumatic fat necrosis (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1172
The most common benign neoplasm of the female breast.
Fibroadenoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1173
A discrete, usually solitary, freely movable nodule, 1 to 10 cm in diameter, easily "shelled out" lesion of the breast. Histologically there is a loose fibroblastic stroma containing ductlike, spaces lined by a layer of epithelium that are regular and have a well-defined, intact basement membrane.
Fibroadenoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1174
Small lobulated and cystic lesion of the breast that may grow rapidly. Exhibit "leaflike" clefts and slits on gross section.
Phyllodes Tumor (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 743
1175
A neoplastic papillary growth within a duct, usually solitary and less than 1 cm in diameter, consisting of delicate, branching growths within a dilated duct or cyst.
Intraductal Papilloma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 743
1176
A type of noninvasive carcinoma of the breast that tends to fill, distort, and unfold involved lobules and thus appears to involve ductlike spaces.
Ductal Carcinoma in Situ(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 745
1177
A type of noninvasive carcinoma of the breast expands but does not alter the underlying lobular architecture. cells are monomorphic with bland, round nuclei and occur in loosely cohesive clusters in ducts and lobules. Tend to be bilateral, and increases risk for development of breast CA.
Lobar Carcinoma in Situ(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 746
1178
Caused by the extension of DCIS up to the lactiferous ducts and into the contiguous skin of the nipple.
Paget disease of the nipple (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 746
1179
This type of cancer produces a desmoplastic response, replacing normal breast fat and forms a hard, palpable mass. Advanced cancers may cause dimpling of the skin, retraction of the nipple, or fixation to the chest wall.
Invasive ductal carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1180
Breast cancer defined by the clinical presentation of an enlarged, swollen, erythematous breast, usually without a palpable mass. The blockage of numerous dermal lymphatic spaces by carcinoma results in the clinical appearance (e.g peau d' orange)
Inflammatory carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1181
Breast cancer which consists of cells morphologically identical to the cells of LCIS. Occasionally they surround cancerous or normal-appearing acini or ducts, creating a so-called "bull's-eye pattern."
Invasive lobular carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1182
A rare subtype of carcinoma consisting of sheets of large anaplastic cells with pushing, well-circumscribed borders, with a pronounced lymphoplasmacytic infiltrate.
Medullary carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1183
A rare subtype of carcinoma which appear grossly as a soft and gelatinous mass which abundant quantities of extracellular mucin that dissects into the surrounding stroma.
Colloid (mucinous) carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1184
Usually present as irregular mammographic densities. Microscopically, the carcinomas consist of well-formed tubules with low-grade nuclei. Lymph node metastases are rare, and prognosis is excellent.
Tubular carcinomas (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1185
Grossly, appears as a button-like, subareolar swelling. in bilateral breasts of males.
Gynecomastia (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 750
1186
Large, multilocular tumors of the ovaries, without psammoma bodies. Composed of mucin-producing epithelial cells.
Mucinous Tumors (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 731
1187
Metastasis of mucinous tumor of the gastrointestinal tract to the ovaries is called?
Krukenberg tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 731
1188
A rare, solid, unilateral ovarian tumor consisting of an abundant stroma containing nests of transitional-like epithelium resembling that of the urinary tract.
Brenner Tumor (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1189
Unilateral ovarian tumor composed of sheets or cords of large cleared cells separated by scant fibrous strands. Stroma may contain lymphocytes and occasional granuloma. Usually occur on the 2nd-3rd decade of life.
Dysgerminoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1190
Unilateral ovarian tumor which occur during the 1st 3 decades of life. Characterized by small, hemorrhagic focus with syncitiothrophoblast and cytotrophoblast. Metastasize early.
Choriocarcinoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1191
Sex cord tumor seen most commonly in postmenopausal women. Lesions may be tiny or large, gray to yellow (with cystic spaces). Produce large amounts of estrogen. (+) Call-Exner bodies
Granulosa-thecal cell tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1192
Sex cord tumor characterized by solid gray fibrous cells to yellow (lipid-laden) plump thecal cells. Most hormonally inactive.
Thecoma-fibroma tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1193
Sex cord tumor seen as small, gray to yellow-brown, and solid lesions. May resemble development of testis with tubules, or cords and plump pink Sertoli cells. May be masculinizing or defeminizing.
Sertoli-Leydig cell tumor(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 732
1194
On transection, filled with sebaceous secretion and matted hair, bonw and cartilage, nests of bronchial or gastrointestinal epithelium, and other recognizable lines of development are also present.
Benign (Mature) Cystic Teratomas / Dermoid Cyst(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 733
1195
Microscopically, the distinguishing feature is a variety of immature or barely recognizable areas of differentiation toward cartilage, bone, muscle, nerve, and other structures. Found early in life.
Immature Malignant Teratomas (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 733
1196
Tumor of the ovary composed entirely of mature thyroid tissue. May hyperfunction and produce hyperthyroidism. Appear as small, solid, unilateral brown ovarian masses
Struma ovarii (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 733
1197
A voluminous mass of swollen, sometimes cystically dilated, chorionic villi, appearing grossly as grapelike structures.
Hydatidiform Mole (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 735
1198
This type of H. mole shows hydropic swelling of chorionic villi and virtual absence of vascularization of villi. No fetal parts seen.
Complete mole (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 736
1199
This type of H. mole shows villous edema that involves only some of the villi and the trophoblastic proliferation is focal and slight, with characteristic irregular scalloped margin. Fetal parts/embryo may be seen.
Partial mole(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 736
1200
These are complete moles that are more invasive locally but do not metastasize. Microscopically, the epithelium of the villi is marked by hyperplastic and atypical changes, with proliferation of both cuboidal and syncytial components.
Invasive Mole (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 736
1201
Appear as very hemorrhagic, necrotic masses within the uterus. The tumor is purely epithelial, composed of anaplastic cuboidal cytotrophoblast and syncytiotrophoblast, chorionic villi are not formed. High propensity for metastasis.
Choriocarcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 737
1202
A cystic dilation of an obstructed duct that arises during lactation.
Galactocele (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1203
Multifocal, bilateral blue-brown cysts ("blue dome cysts") of the breast, measuring 1-5 cm diameter, filled with serous turbid fluid. Occurs normally in the menstrual cycle.
Simple fibrocystic change of the breast(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1204
Term used to describe hyperplasia that cytologically resemble lobular carcinoma in situ, but the cells do not fill or distend more than 50% of the acini within a lobule.
Atypical lobular hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1205
The lumen of the ducts, ductules, or lobules of the breast is filled with a heterogeneous population of cells of different morphologies. Irregular slit-like fenestrations are prominent at the periphery.
Epithelial Hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 739
1206
These lesions are characterized by proliferation of lining epithelial cells and myoepithelial cells in small ducts and ductules, yielding masses of small gland patterns within a fibrous stroma. The acini are arranged in a swirling pattern, and the outer border is usually well circumscribed.
Sclerosing Adenosis (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 741
1207
A nonbacterial chronic inflammation of the breast associated with inspissation of breast secretions in the main excretory ducts.
Mammary duct ectasia (periductal or plasma cell mastitis) (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1208
The lesion is small, often tender, rarely more than 2 cm in diameter, and sharply localized, with a central focus of necrotic fat cells surrounded by neutrophils and lipid-filled macrophages. Caused by some antecedent trauma to the breast.
Traumatic fat necrosis (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1209
The most common benign neoplasm of the female breast.
Fibroadenoma(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1210
A discrete, usually solitary, freely movable nodule, 1 to 10 cm in diameter, easily "shelled out" lesion of the breast. Histologically there is a loose fibroblastic stroma containing ductlike, spaces lined by a layer of epithelium that are regular and have a well-defined, intact basement membrane.
Fibroadenoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 742
1211
Small lobulated and cystic lesion of the breast that may grow rapidly. Exhibit "leaflike" clefts and slits on gross section.
Phyllodes Tumor (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 743
1212
A neoplastic papillary growth within a duct, usually solitary and less than 1 cm in diameter, consisting of delicate, branching growths within a dilated duct or cyst.
Intraductal Papilloma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 743
1213
A type of noninvasive carcinoma of the breast that tends to fill, distort, and unfold involved lobules and thus appears to involve ductlike spaces.
Ductal Carcinoma in Situ(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 745
1214
A type of noninvasive carcinoma of the breast expands but does not alter the underlying lobular architecture. cells are monomorphic with bland, round nuclei and occur in loosely cohesive clusters in ducts and lobules. Tend to be bilateral, and increases risk for development of breast CA.
Lobar Carcinoma in Situ(TOPNOTCH) Robbins Basic Pathology, 8th ed., p 746
1215
Caused by the extension of DCIS up to the lactiferous ducts and into the contiguous skin of the nipple.
Paget disease of the nipple (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 746
1216
This type of cancer produces a desmoplastic response, replacing normal breast fat and forms a hard, palpable mass. Advanced cancers may cause dimpling of the skin, retraction of the nipple, or fixation to the chest wall.
Invasive ductal carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1217
Breast cancer defined by the clinical presentation of an enlarged, swollen, erythematous breast, usually without a palpable mass. The blockage of numerous dermal lymphatic spaces by carcinoma results in the clinical appearance (e.g peau d' orange)
Inflammatory carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1218
Breast cancer which consists of cells morphologically identical to the cells of LCIS. Occasionally they surround cancerous or normal-appearing acini or ducts, creating a so-called "bull's-eye pattern."
Invasive lobular carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1219
A rare subtype of carcinoma consisting of sheets of large anaplastic cells with pushing, well-circumscribed borders, with a pronounced lymphoplasmacytic infiltrate.
Medullary carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1220
A rare subtype of carcinoma which appear grossly as a soft and gelatinous mass which abundant quantities of extracellular mucin that dissects into the surrounding stroma.
Colloid (mucinous) carcinoma (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1221
Usually present as irregular mammographic densities. Microscopically, the carcinomas consist of well-formed tubules with low-grade nuclei. Lymph node metastases are rare, and prognosis is excellent.
Tubular carcinomas (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 747
1222
Grossly, appears as a button-like, subareolar swelling. in bilateral breasts of males.
Gynecomastia (TOPNOTCH) Robbins Basic Pathology, 8th ed., p 750
1223
Morphology: large macrophages with granular PAS positive cytoplasm and several dense, round Michaelis Gutmann bodies.
Malacoplakia (TOPNOTCH)
1224
In gonococcal infection of the female reproductive system, inflammatory changes will appear about how many days after the inoculation of the organism?
2-7 days (TOPNOTCH)
1225
These cells are distinguised by a clear separation "halo" from the surrounding epithelial cells and a finely granular cytoplasm containing mucopolysaccharide that stains with PAS, Alcian Blue, and Mucicarmine
Paget cells (TOPNOTCH)
1226
What is the probable precursor of vaginal adenocarcinoma?
Vaginal adenosis (TOPNOTCH)
1227
What do you call the glandlike structures filled with an acidophilic material similar to immature follicles that are seen in Granulosa Theca Cell tumors?
Call Exner bodies (TOPNOTCH)
1228
Presence of these structures characterize serous tumors of the ovaries
Psammoma bodies (TOPNOTCH)
1229
These tumors are distinguished from serous and mucinous tumors of the ovaries by the presence of tubular glands that resemble the endometrium
Endometriod tumor (TOPNOTCH)
1230
Morphology: whorled pattern of smooth muscle bundles and well differentiated spindle shaped smooth muscle cells
Leiomyoma (TOPNOTCH)
1231
A key factor in the development of endometrial hyperplasia and related cancers is the inactivation of what tumor suppressor gene?
PTEN (TOPNOTCH)
1232
What is the most common location of vaginal adenocarcinoma?
Anterior wall of the upper third of Vagina (TOPNOTCH)
1233
This is a condition in which glandular columnar epithelium of mullerian type either appears beneath the squamous epithelium or replaces it
Vaginal Adenosis (TOPNOTCH)
1234
What are the 4 cardinal histologic features of Lichen Sclerosus of the Vulva or Chronic atrophic vulvitis?
Atrophy of the epidermis with disappearance, of the rete pegs, hydrophic degeneration of the basal cells, replacement of the underlying dermis by dense collagenous fibrous tissue, and monoclonal band like lymphocytic infiltrate (TOPNOTCH)
1235
Morphology: acanthosis of the vulvar squamous epithelium frequently with hyperkeratosis
Lichen SImplex Chronicles (TOPNOTCH)
1236
Morphology: presence of large tumor cells lying singly or in small lusters within the epidermis and its appendages
Extra mammary Paget Disease (TOPNOTCH)
1237
Morphology: tumor cells resemble tennis racket with small protrusions of cytoplasms from one end
Embryonal Rhabdomyosarcoma (TOPNOTCH)
1238
Clustering of tumor cells in a so called "Cambium Layer" is seen in what type of rhabdomyosarcoma?
Embryonal Rhabdomyosarcoma (TOPNOTCH)
1239
On histological examination of the cervix, epithelial spongiosis is associated with what type of infection?
T. vaginal infection (TOPNOTCH)
1240
On histological examination of the cervix, epithelial ulcers with intranuclear inclusions within the epithelial cells and lymphocytic infiltration is associated with what type of infection?
HSV (TOPNOTCH)
1241
Morphology: these are composed of dense fibrous stroma covered with endocervical columnar epithelium
Endocervical polyp (TOPNOTCH)
1242
What is considered the most important agent in cervical oncogenesis?
HPV (TOPNOTCH)
1243
Koilocytic atypia is considered what type of CIN lesion?
CIN I (TOPNOTCH)
1244
What is the most common pattern seen in invasive cervical carcinoma?
Fungating (TOPNOTCH)
1245
On histological examination of the endometrium, what is the earliest morphological evidence of ovulation?
Basal vacuolation (TOPNOTCH)
1246
Morphology: ectopic endometrial glands and stroma with numerous macrophages containing hemosiderin
Endometriosis (TOPNOTCH)
1247
Morphology: hydrophic swelling of most chorionic villi and virtual absence or inadequate development of vascularization of villi
Complete mole (TOPNOTCH)
1248
The combination of ovarian tumor, hydrothorax, and ascites is designated as
Meigs Syndrome (TOPNOTCH)
1249
What type of ovarian cancer is best considered as the counterpart of the seminoma of the testes?
Dysgerminoma (TOPNOTCH)
1250
About 1% of the dermoids undergo malignant transformation of any one of the component elements present, but most commonly, they differentiate into what type of carcinoma?
Squamous Cell Carcinoma (TOPNOTCH)
1251
Morphology: epithelial component consists of nests of transitional cells resembling the lining of the urinary bladder
Brenner Tumor (TOPNOTCH)
1252
Morphology: characterized by a lining of tall columnar epithelial cells with apical mucin and the absence of cilia, resembling cervical or intestinal epithelium
Mucinous tumors (TOPNOTCH)
1253
Morphology: lined by a rim of bright yellow luteal tissue containing luteinized granulosa cells
Luteal cyst (TOPNOTCH)
1254
Morphology: characterized chiefly by dilations of ducts, inspissation of breast secretions, and marked periductal and interstitial chronic granulomatous reaction
Mammary Duct Ectasia (TOPNOTCH)
1255
What are the 3 principal patterns of morphologic changes seen in Fibrocystic Changes of the breast?
1. Cyst formation with apocrine metaplasia2. Fibrosis3. Adenosis (TOPNOTCH)
1256
Morphology: "leaflike" architecture
Phyllodes Tumor (TOPNOTCH)
1257
Morphology: proliferation of intralobular stroma surrounding and often pushing and distorting the associated epithelium. The border is sharply delimited from the surrounding tissue
Fibroadenoma (TOPNOTCH)
1258
What is the most important prognostic factor useful as a predictive factor for the response of therapy in patients with breast cancer?
Presence of estrogen and progesterone receptors (TOPNOTCH)
1259
In breast cancer, what is the most important prognostic factor for invasive carcinoma in the absence of distant metastases?
Lymph node metastases (TOPNOTCH)
1260
Morphology: tumor cells are prsent as small clusters within large pools of mucin
Mucinous colloid carcinoma (TOPNOTCH)
1261
Morphology: characterized by solid syncytium like sheets occupying 75% of the tumor , prominent lymphoplasmacytic infiltrate and a non inflitrative border
Medullary carcinoma of the breast (TOPNOTCH)
1262
The histologic hallmark of this tumor is the pattern of single infiltrating tumor cells, often only one cell in width, or in loose clusters or sheets
Invasive lobular carcinoma (TOPNOTCH)
1263
This is a rare manifestation of breast cancer and presents as a unilateral erythematous eruption with a scale crust
Paget disease (TOPNOTCH)
1264
These are stellate lesions characterized by a central nidus of entrapped glands in a hyalinized stroma
Complex Sclerosing Lesion or Radial Scar (TOPNOTCH)
1265
Morphology: composed of multiple branching fibrovascular cores, each having a connective tissue axis lined by luminal and myoepithelial cells
Papillomas (TOPNOTCH)
1266
What is the most common clinical presentation of breast disease
Pain (TOPNOTCH)
1267
The principal mammographic signs of breast carcinoma
densities and calfications (TOPNOTCH)
1268
Morphology: the main histologic feature is keratinizing squamous epithelium extending to an abnormal depth into the orifices of the nipple ducts
Periductal mastitis (TOPNOTCH)
1269
Mammographic appearance: Large lobulated "popcorn" calcifications
Fibroadenoma (TOPNOTCH)
1270
Morphology: characterized by solid sheets of pleomorphic cells with high-grade nuclei and central necrosis detected mamographically as clusters or linear and branching microcalcifications
Comedocarcinoma (TOPNOTCH)
1271
Morphology: Terminal ducts (without lobule formation) are lined by a multilayered epithelium with small papillary tufts and surrounding periductal hyalinization and fibrosis.
Gynecomastia (TOPNOTCH)
1272
Morphology: terminal duct lobular unit is enlarged, and the acini are compressed and distorted within the lumens. Calcifications are often present within the lumens.
Sclerosing adenosis(TOPNOTCH)
1273
Morphology: central fibrovascular core extends from the wall of a duct. The papillae arborize within the lumen and are lined by myoepithelial and luminal cells
Intraductal papilloma(TOPNOTCH)
1274
Cellular proliferation resembling ductal carcinoma in situ or lobular carcinoma in situ but lacking sufficient qualitative or quantitative features for a diagnosis of carcinoma in situ
Atypical hyperplasia(TOPNOTCH)
1275
Refers to a proliferation of cells identical to those of LCIS but the cells do not fill or distend more than 50% of the acini within a lobule.
Atypical Lobular hyperplasia(TOPNOTCH)
1276
Recognized by its histologic resemblance to ductal carcinoma in situ, including a monomorphic cell population, regular cell placement, and round lumina. However, the lesions are characteristically limited in extend, and the cells are not completely monomorphic in type or they fail to completely fill ductal spaces
Atypical hyperplasia(TOPNOTCH)
1277
What are the two major risk factors for breast carcinoma?
Hormonal and Genetics/family history(TOPNOTCH)
1278
This is a subtype of DCIS which is recognized by bulbous protrusions without a fibrovascular core, often forming complex intraductal patents.
Micropapillary DCIS(TOPNOTCH)
1279
Small, painful, rounded superficial erosions of the mouth, covered with a gray-white exudate and having an erythematous rim.
Aphthous ulcers (canker sores)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 580
1280
Extremely common infection caused by herpes simplex virus type 1.
Herpetic stomatitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 580
1281
Test used to identify HSV infection.
Tzanck test(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 580
1282
Glassy, intranuclear acidophilic inclusion bodies.
Herpes simplex virus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 580
1283
Adherent white, curd-like, circumscribed plaque within the oral cavity. The pseudomembrane can be scraped off revealing an underlying granular erythematous inflammatory base.
Oral candidiasis /"thrush"(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 581
1284
An oral lesion seen in patients with HIV. White confluen patches with "hairy" or corrugated surface with marked epithelial thickening.
Hairy leukoplakia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 581
1285
Hairy leukoplakia is caused by what infectious agent?
Epstein-Barr virus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 581
1286
A whitish, well-defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis, commonly seen in the vermillion border of the lower lip, buccal mucosa, hard and soft palates.
Leukoplakia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 581
1287
Oral lesion showing a corrugated surface caused by excessive hyperkeratosis. Recurring and spreads insiduously, resulting in a warty-type lesion.
Verrucous leukoplakia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 582
1288
Red, velvety, granular, circumscribed lesions of the mouth with poorly defined, irregular boundaries. High malignant transformation rate.
Erythroplakia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 582
1289
Most frequent site of oral cavity carcinomas.
Vermillion border of the lateral margins of the lower lip(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 582
1290
Pearly white to gray, circumscribed thickenings of the oral mucosa, which grows in exophytic pattern to produce a visible and palpable nodular, eventually fungating lesions.
Oral cavity carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 583
1291
Most common lesion of the salivary glands resulting from blockage or rupture of a salivary gland duct.
Mucocele(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 583
1292
Inflammation of the salivary glands.
Sialadenitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 583
1293
Salivary and lacrimal gland inflammatory enlargement presenting as painless lesions, and dry mouth. Can be caused by sarcoidosis, leukemia, and lymphoma.
Mikulicz syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 583
1294
Incomplete relaxation of lower esophageal sphincter in response to swallowing.
Achalasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1295
Destruction of the myenteric plexus of the esophagus, duodenum, colon and ureter caused by a flagellate protozoa.
Chagas disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1296
Causative agent for Chagas disease.
Trypanosoma cruzi(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1297
Adult with progressive dysphagia to solids and eventually to all foods, caused by a narrowing of the lower esophagus, usually as a result of chronic inflammatory disease.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1298
A congenital defect which causes the esophagus to end in a blind-ended pouch.
Esophageal atresia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1299
Most common type of esophageal atresia.
Esophageal atresia with distal tracheoesophageal fistula(Type C)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1300
Thin membranes of normal esophageal tissue consisting of mucosa and submucosa that can partially obstruct the esophagus.
Esophageal web(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1301
Congenital esophageal webs commonly appear in which segment of the esophagus?
Middle and inferior third of the esophagus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 585
1302
A diverticulum of the mucosa of the pharynx just above the cricopharyngeal muscle.
Zenker's diverticulum(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 586
1303
A triangular area in the pharyngeal wall where a Zenker's diverticulum may develop.
Killian's triangle(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 586
1304
Protrusion of the stomach above the diaphragm, creating a bell-shaped dilation, bounded below by the diaphragmatic narrowing.
Sliding hernia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 586
1305
Hernia wherein a portion of the stomach, usually along the greater curvature, enters the thorax through the widened space between the muscular crura.
Paraesophgeal (rolling) hernia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 586
1306
Longitudinal tears along the gastroesophageal junction seen in chronic alcoholics after a bout of retching or vomiting.
Mallory-Weiss tears(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 586
1307
Tortuous dilated veins lying within the submucosa of the distal esophagus and proximal stomach due to increased portal pressure, usually due to cirrhosis. May cause massive hemorrhage if ruptured.
Esophageal varices(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 587
1308
Presence of eosinophils in the epithelial layer, basal zone hyperplasia and elongation of lamina propria papillae are histologic findings in this condition.
Reflux esophagitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 588
1309
Defined as the replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells. A complication of long-standing GERD.
Barrett esophagus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 591
1310
Esophageal lesion at risk of developing adenocarcinoma:Reflux esophagitis or Barrett esophagus?
Barrett esophagus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 589
1311
Squamous cell carcinoma of the esophagus commonly occur at which segment of the esophagus?
Proximal 2/3 of the esophagusAdenocarcinoma- distal 1/3(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 591
1312
Most common symptoms of esophageal cancer.
Dysphagia and odynophagia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 591
1313
Mucin-producing glandular tumors of the distal esophagus showing intestinal-type features.
Adenocarcinoma of the esophagus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 591
1314
Presence of chronic inflammatory changes in the mucosa of the stomach eventually leading to mucosal atrophy and epithelial metaplasia.
Chronic gastritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 592
1315
Most important etiologic association with chronic gastritis. A non-invasive, non-spore forming S-shaped gram negative rod.
Helicobacter pylori(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 592
1316
Gastritis resulting from production of autoantibodies to the gastric gland parietal cells, leading to gland destruction and mucosal atrophy with loss of acid and intrinsic factor.
Autoimmmune gastritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 592
1317
Refers to the replacement of gastric epithelium with columnar and goblet cells of intestinal variety.
Intestinal metaplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 592
1318
A acute mucosal inflammatory process of the stomach, marked by mucosal edema and inflammatory infiltrate of neutrophils and chronic inflammatory cells. Regenerative replication of cells in the gastric pit is prominent.
Acute gastritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 593
1319
One of the major causes of hematemesis, especially in alcoholics.
Acute gastritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 593
1320
A breach in the mucosa that extends through the muscularis mucosae into the submucosa or deeper.
Ulcers(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 593
1321
Breach in the epithelium of the gastrointestinal mucosa only.
Erosions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 593
1322
Chronic, solitary lesions that occur in any portion of the GIT exposed to the aggressive action of acidic peptic juices.
Peptic ulcers(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 594
1323
Major cause of peptic ulcer disease in patients without H. pylori disease.
NSAID use(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 595
1324
Histologic layers in a chronic, nonperforated, open ulcer.
From luminal surface:NecrosisInflammationGranulation tissueScar(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 596
1325
Chief complication of peptic ulcer.
Bleeding(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 596
1326
Increases risk of developing gastric adenocarcinoma:Acute gastritis vs. peptic ulcer disease?
Acute gastritisPUD is NOT a premalignant lesion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 596
1327
Acute gastric ulceration which occurs in the presence of extensive burns.
Curling ulcer(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 596
1328
Acute gastric ulceration which occurs in the presence of injury to the CNS.
Cushing ulcer(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 596
1329
Composed of hyperplastic gastric mucosal epithelium and an inflamed edematous stroma. A mass lesion arising from the mucosa.
Gastric polyp(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 597
1330
Most common site of gastric carcinoma within the stomach.
Pylorus and antrum (50-60%), along the lesser curvatureCardia (25%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 598
1331
What are the two most important factors in the genesis of colonic diverticula?
Focal weakness in the colonic wall and increased intraluminal pressure(TOPNOTCH)
1332
Morphologic feature of gastric carcinomas with greatest impact on prognosis.
Depth of invasion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1333
Gastric carcinoma confined to the mucosa and submucosa, regardless of the presence or absence of perigastric LN metastasis.
Early gastric carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1334
Gastric carcinoma which has extended below the submucosa into the muscular wall.
Advanced gastric carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1335
Three macroscopic growth patterns of gastric carcinoma.
Exophytic - protrusion of mass into lumenFlat or depressed - no obvious tumor mass within the mucosaExcavated - a shallow or deeply eroded crater(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1336
Rigid and thickened stomach, secondary to extensive malignant infiltration.
Linitis plastica(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1337
Histologic classification of gastric carcinoma composed of malignant cells forming neoplastic intestinal glands resembling colonic adenocarcinoma. Associated with H. pylori induced chronic gastritis.
Intestinal variant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1338
Histologic classification of gastric carcinoma composed of gastric-type mucous cells that do not form glands but permeate the mucosa and wall as "signet-ring" cells in an infiltrative growth pattern.
Diffuse variant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1339
A malignancy in the ovary that metastasized from a gastric adenocarcinoma.
Krukenberg tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 599
1340
Complete failure of development of the intestinal lumen.
Atresia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 600
1341
Narrowing of the intestinal lumen with incomplete obstruction.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 600
1342
Most common intestinal anomaly which results from the failure of involution of the omphalomesenteric duct, leaving a persistent blind-ended tubular protrusion as long as 5-6cm.
Meckel diverticulum(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 600
1343
A congenital defect of the periumbillical abdominal musculature that creates a membranous sac, into which intestines herniate.
Omphalocoele(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 600
1344
Extrusion of the intestines caused by lack of formation of a portion of the abdominal wall.
Gastroschisis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 600
1345
Condition that prevents the intestines from assuming their normal intra-abdominal positions.
Malrotation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 600
1346
Critical lesion in the development of Hirschprung disease.
Lack of ganglion cells in the muscle wall and submuco lf the affected segment.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 601
1347
Ischemic lesion of the intestines which extends only up to the muscularis mucosae.
Mucosal infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 601
1348
Ischemic lesion of the intestines involving the mucosa and submucosa, sparing the muscular wall.
Mural infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 601
1349
Ischemic lesion of the intestines involving all of the visceral layers.
Transmural infarct(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 601
1350
Most common cause of transmural infarction of the intestines.
Acute occlusion of a major mesenteri artery(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 602
1351
Development of sudden abdominal pain out of proportion to the physical signs. Sometimes accomplanied by bloody diarrhea. May progress to shock and vascular collapse within hours.
Ischemic bowel injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 602
1352
A weakness or defect in the wall of the peritoneal cavity, which permits protrusion of a pouch-like serosa lined sac of peritoneum.
Hernia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 603
1353
A blind pouch that communicates with the lumen of the gut. Histologically describes as small, flask-like or spherical outpouchings, usually 0.5 to 1 cm diameter.
Diverticula(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 602
1354
Telescoping of a proximal segment of a bowel into the immediately distal segment
Intussusception(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 604
1355
Refers to twisting of a loop of bowel or other structure about its base of attachment, constricting venous outflow and sometimes the arterial supply.
Volvulus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 604
1356
Characterized by transmural inflammation of the bowel, associated with noncaseating granulomas and fistula formation. Intestinal walls are rubbery and thick. (+) skip lesions, creeping fat mesentery
Chron's disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 613
1357
An ulceroinflammatory disease of the colon which is limited to the mucosa and submucosa. No granulomas, no skip lesions. High risk of carcinoma development.
Ulcerative colitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 614
1358
Small, nipple-like, hemispherical, smooth protrusions of the intestinal mucosa. May occur singly or multiple.contains abundant crypts luned by well-differentiated goblet or epithelial cells separated by scant lamina propria.
Hyperplastic polyps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 617
1359
Hamartomatous proliferations mainly of lamina propria, enclosing widely spaced, dilated cystic glands. Occur most frequently in children younger than 5 years old.
Juvenile polyps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 618
1360
Most common type of intestinal adenoma, which are tubular glands with slender stalks and raspberry-like heads composed pf neoplastic epithelium forming branching glands lined by tall, hyperchromatic cells.
Tubular adenomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 618
1361
Larger, more ominous intestinal epithelial polyp. Tends to occur in older persons at the rectum or rectosigmoid. Sessile, velvety and cauliflower-like mass projecting 1-3cm above the surrounding mucosa. Frondlike villiform extensions covered by dysplastic columnar epithelium.
Villous adenomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 618
1362
Composed of broad mix of tubular and villous areas, an intermediated between tubular and villous lesions.
Tubulovillous adenomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 618
1363
Uncommon autosomal dominant disorder with propensity for malignant transformation. Patients with this disease typically develop 500 to 2500 colonic adenomas that carpet the mucosal surface.
Familial adenomatous polyposis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 619
1364
Uncommon hamartomatous polyps associated with melanotic mucosal and cutaneous pigmentation. Caused by germ-line mutations in LKB1 gene.
Peutz-Jeghers syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 619
1365
Polypoid, exophytic masses that extend along the wall of capacious cecum and ascending colon. Symptoms of fatigue, weakness and iron deficiency anemia.
Right sided colorectal carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 623
1366
Annular, encircling lesions, "napkin-ring" constrictions of the bowel and narrowing of the lumen. Symptoms pf occult bleeding, changes in bowel habit or crampy left lower quadrant discomfort.
Left-sided colorectal carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 623
1367
Tumor of the small intestines, showing spindle cells with elongated nuclei with fine chromatin and eosinophilic fibrillar cytoplasm. (+) c-KIT gene mutation
Gastrointestinal stromal tumors (GIST)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 628
1368
Most common site of carcinoid tumors.
Appendix(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 627
1369
Tumors arising from endocrine cells along the GIT. Solid, yellow-tan appearance on transection. Neoplastic cells have a scant, pink granular cytoplasm and a round-to-oval stippled nucleus.
Carcinoid tumors(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 627
1370
What is the most common ectopic tissue rests seen in the esophagus?
Ectopic Gastric Mucosa seen in the upper third of the esophagus (TOPNOTCH)
1371
What is the most common location of Mallory Weiss Tears?
Esophagogastric junction or in the proximal gastric (TOPNOTCH)
1372
Definitive diagnosis of Barret Esophagus is made when what type of cells is seen in the columnar mucosa?
Intestinal Goblet Cells(TOPNOTCH)
1373
What type of esophagitis presents with punched out linear ulcers with nuclear inclusions seen in degenerating epithelial cells?
Herpesvirus esophagitis(TOPNOTCH)
1374
What type of esophagitis presents with linear ulcerations of the esophageal mucosa with histologic findings of intranuclear and cytoplasmic inclusions?
CMV esophagitis(TOPNOTCH)
1375
98% of Peptic Ulcers are located in what part of the GIT?
First portion of the anterior part of the duodenum(TOPNOTCH)
1376
What is the most common location of gastric ulcer?
Lesser curvature (TOPNOTCH)
1377
What is the most common location of gastric carcinoma is?
Pylorus and antrum > Cardia > body and fundus(TOPNOTCH)
1378
What is the morphologic feature of gastric carcinoma that has the greatest impact on the clinical outcome?
Depth of invasion(TOPNOTCH)
1379
What is the most common primary source of gastric metastasis?
Systemic lymphoma(TOPNOTCH)
1380
What is the usual organism that cause spontaneous bacterial peritonitis in patients with nephrotic syndrome?
E. coli(TOPNOTCH)
1381
In bacterial peritonitis, approximately how many hours from the time of initiation before there is loss of the gray, glistening quality of the peritoneal surface and it becomes dull and lusterless?
2-4 hours(TOPNOTCH)
1382
What is the histologic criterion for the diagnosis of acute appendicitis?
Presence of neutrophilic infiltration of the muscularis propria.(TOPNOTCH)
1383
What is the most common site of gut carcinoid tumors?
Appendix(TOPNOTCH)
1384
What is the most important prognostic indicator of colorectal carcinoma?
The extent of the tumor at the time of diagnosis or the stage(TOPNOTCH)
1385
Morphology: a type of adenoma that has frondlike villiform extensions of the mucosa, covered by dysplastic, sometimes very disorderly columnar epithelium
Villous adenomas(TOPNOTCH)
1386
These structures represent islands of inflamed regenerating mucosa surrounded by ulceration
Inflammatory or pseudopolyps(TOPNOTCH)
1387
Most adenomas are seen in what part of the GIT?
Ampulla of Vater(TOPNOTCH)
1388
Most tubular adenomas are found in what part of the GIT?
Colon(TOPNOTCH)
1389
Gross morphology: small, flask like or spherical outpouchings, usually 0.5 to 1 cm and located in the sigmoid colon
Colonic diverticula(TOPNOTCH)
1390
Morphology: thin wall composed of flattened or atrophic mucosa, compressed submucosa, and attenuated or totally absent muscularis propria.
Colonic diverticula(TOPNOTCH)
1391
What are the two most important factors in the genesis of colonic diverticula?
Focal weakness in the colonic wall and increased intraluminal pressure(TOPNOTCH)
1392
What is the most common site of angiodysplasia?
Cecum(TOPNOTCH)
1393
Morphology: these are tortuous dilations of submucosal and mucosal blood vessels
Angiodysplasia(TOPNOTCH)
1394
What area of the GIT is at greatest risk of ischemic injury?
Splenic flexure(TOPNOTCH)
1395
Morphology: diffuse active inflammation with crypt abscess and glandular architectural distortion
Ulcerative Colitis(TOPNOTCH)
1396
What is the earliest lesion seen in Crohn Disease?
Focal neutrophilic infiltration into the epithelial layer, particularly overlying mucosal lymphoid aggregates(TOPNOTCH)
1397
What is the hallmark of inflammatory bowel disease, both CD and UC?
Chronic mucosal damage(TOPNOTCH)
1398
Gross morphology: narrowing of lumen, bowel wall thickening, serosal extension of mesenteric fat, and linear ulceration of the mucosal surface
Crohn disease(TOPNOTCH)
1399
What are the two key pathogenic abnormalities seen in Idiopathic Inflammatory Bowel disease?
Strong immune response against normal flora and defects in epithelial barrier function(TOPNOTCH)
1400
Gross morphology: intestinal wall is rubbery and thick, as a consequence of edema, inflammation, fibrosis and hypertrophy of the muscularis propria
Crohn disease(TOPNOTCH)
1401
Morphology: small intestinal mucosa laden with distended macrophages in the lamina propria which are PAS positive and contains numerous bacilli and diastase resistant granules
Whipple disease(TOPNOTCH)
1402
Intestinal lipodystrophy is associated with what disease entity?
Whipple disase(TOPNOTCH)
1403
Morphology: diffuse severe atrophy and blunting of villi, with a chronic inflammatory infiltrate in the lamina propria
Celiac disease(TOPNOTCH)
1404
Morphology: focal crypt cell necrosis or apoptosis with minimal to absent inflammatory cell response in the lamina propria
Acute GVHD(TOPNOTCH)
1405
Morphology: marked blunting of the small intestinal villi with a mixed inflammatory infiltrate resembling the atrophic stage of celiac disease
Giardiasis(TOPNOTCH)
1406
Morphology: superficial erosion of the mucosa and an adherent pseudomembrane of fibrin, mucus, and inflammatory debris
Pseudomembranous colitis(TOPNOTCH)
1407
Morphology: small intestinal mucosa usually exhibits modestly shortened villi and infiltration of the lamina propria by lymphocytes
Viral gastroenteritis(TOPNOTCH)
1408
What virus affecting the GIT can produce a flat mucosa resembling celiac sprue?
Rotavirus(TOPNOTCH)
1409
Morphology: characterized by the absence of ganglion cells and ganglia in the muscle wall and submucosa of the affected segment
Congenital Aganglionic Megacolon(TOPNOTCH)
1410
Stercoral ulcers are seen in what disease entity?
Congenital aganglionic megacolon(TOPNOTCH)
1411
The majority of these tumors are positive for c-KIT (CD 117)
Gastrointestinal Stromal Tumor(TOPNOTCH)
1412
What is the most common site of gastric carcinoma?
Pylorus and anthrum 50%-60%(TOPNOTCH)
1413
What is the most favored site of gastric carcinoma?
lesser curvature of the anthropyloric region(TOPNOTCH)
1414
What is the morphologic feature of gastric carcinoma that has the greatest impact on clinical outcome?
Depth of invasion(TOPNOTCH)
1415
This is a variant of gastric carcinoma composed of neoplastic intestinal glands resembling those of colonic adnocarcinoma and the neoplastic cells contain apical mucin vacuoles and abundant mucin may be present in gland lumens
Intestinal type(TOPNOTCH)
1416
This is a variant of gastric carcinoma which is composed of gastric type mucous cells, which generally do not form glands, but rather permeate the mcosa and wall as scattered individual cells or small clusters in an infiltrative growth pattern
Diffuse type(TOPNOTCH)
1417
What is the most common type of gastric polyp?
Hyperplastic polyp(TOPNOTCH)
1418
In gastritis, histologically, what signifies an active inflammation?
Presence of neutrophils above the basement membrane.(TOPNOTCH)
1419
H. pylori infection in duodenal ulcers is present in about how many percent of patients?
Virtually ALL (70% in patients with gastric ulcer(TOPNOTCH)
1420
Marked cell enlargement with irregularly clumped cytoplasm showing large, clear spaces.
Ballooning degeneration (TOPNOTCH) Robbins Basic Pathology, 8th ed, p633
1421
Multiple tiny fat droplets that do not displace the nucleus which appear in such conditions as alcoholic liver disease, Reye syndrome, and acute fatty liver of pregnancy.
Microvesicular steatosis Robbins Basic Pathology, 8th ed, p633
1422
A single large fat droplet that displaces the nucleus seen in alcoholic liver disease or in the livers of obese or diabetic individuals.
Macrovesicular steatosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
1423
Diffuse, foamy, swollen appearance to the hepatocyte caused by retained biliary material.
Feathery degeneration(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
1424
Poorly stained mummified hepatocytes.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
1425
Isolated hepatocytes become shrunken, pyknotic, and intensely eosinophilic.
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
1426
Hepatocyte necrosis is distributed immediately around the central vein, extending into the midzonal area in the setting of ischemia and several drug and toxic reactions.
Centrilobular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
1427
A pattern of nonrhythmic, rapid extension-flexion movements of the head and extremities, best seen when the arms are held in extension with dorsiflexed wrists, seen in patients with hepatic encephalopathy.
Asterixis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p635
1428
A diffuse process characterized by bridging fibrous septa, in the form of delicate bands or broad scars around multiple adjacent lobes, and the conversion of normal liver architecture into structurally abnormal nodules, encircled by fibrotic bands. Liver architecture is disrupted.
Liver Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p635
1429
Presence of "ground-glass" hepatocytes, a finely granular, eosinophilic cytoplasm and "sanded" nuclei, shown by electron microscopy
Hepatitis B infection(TOPNOTCH)Robbins Basic Pathology, 8th ed, p645
1430
Necrotic cells appear to have "dropped out," with collapse of the sinusoidal collagen reticulin framework where the cells have disappeared; scavenger macrophage aggregates mark sites of dropout.
Hepatocyte cytolysis (in viral hepatitis)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647
1431
Hepatocytes shrink, become intensely eosinophilic, and have fragmented nuclei; effector T cells may be present in the immediate vicinity.
Hepatocyte apoptosis (in viral hepatitis)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647
1432
The hallmark of serious liver damage.
Fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647
1433
May occur as solitary or multiple lesions, ranging from millimeters to massive lesions, many centimeters in diameter. They are generally produced by gram-negative bacteria such as Escherichia coli and Klebsiella sp.
Pyogenic (bacterial) hepatic abscesses (TOPNOTCH)Robbins Basic Pathology, 8th ed, p648
1434
Liver is enlarged (4-6kg), soft, yellow and greasy.
Hepatic Steatosis (Fatty Liver)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p649
1435
Lipid accumulates to the point of creating large clear macrovesicular globules, compressing and displacing the nucleus to the periphery of the hepatocyte.
Hepatic Steatosis (Fatty Liver)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p649
1436
Eosinophilic, cytoplasmic inclusions characteristic of alcoholic hepatitis.
Mallory bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
1437
Almost always accompanied by a brisk sinusoidal and perivenular fibrosis; occasionally periportal fibrosis may predominate.
Alcoholic hepatitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
1438
Liver is yellow-tan, fatty, and enlarged, usually weighing over 2 kg. Over the span of years it is transformed into a brown, shrunken, nonfatty organ, sometimes weighing less than 1 kg.
Alcoholic Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
1439
Pattern of cirrhosis in viral hepatitis.
Macronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
1440
Pattern of cirrhosis in alcoholic hepatitis.
Micronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
1441
The liver may shrink to 500 to 700 gm and become transformed into a limp, red organ covered by a wrinkled, overly large capsule. Necrotic areas have a muddy red, mushy appearance with blotchy bile staining. Complete destruction of hepatocytes in contiguous lobules leaves only a collapsed reticulin framework and preserved portal tracts.
Massive hepatic necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p653
1442
Characterized by deposition of hemosiderin in the following organs: liver, pancreas, myocardium, pituitary, adrenal, thyroid and parathyroid glands, joints, and skin; cirrhosis; and pancreatic fibrosis
Hereditary hemochromatosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655
1443
Golden-yellow granules in the cytoplasm of periportal hepatocytes, which stain blue with the Prussian blue stain.
Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655
1444
Green to brown deposits of copper in Descemet membrane in the limbus of the cornea.
Kayser-Fleischer rings (TOPNOTCH)Robbins Basic Pathology, 8th ed, p656
1445
Excessive copper deposition in the liver causing hepatic changes ranging from mild fatty change to massive liver necrosis. In the brain, injury affects the basal ganglia, demonstrating atrophy and cavitation. Kayser-Fleischer rings are characteristic.
Wilson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655
1446
Hepatocytes with round to oval cytoplasmic globular inclusions which are strongly positive in a periodic acid-Schiff stain. By electron microscopy they lie within smooth, and sometimes rough, endoplasmic reticulum.
Alpha-1 antitrypsin Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th ed, p657
1447
A rare disease characterized by microvesicular fatty change in the liver and encephalopathy. Microscopy of hepatocellular mitochondria reveals pleomorphic enlargement and electron lucency of the matrices, with disruption of cristae and loss of dense bodies.
Reye syndrome / "mitochondrial hepatopathies" (TOPNOTCH)Robbins Basic Pathology, 8th ed, p658
1448
A chronic, progressive, and often fatal cholestatic liver disease, characterized by a nonsuppurative destruction of small and medium-sized intrahepatic bile ducts ("florid duct lesion"). On cut surface, the liver is hard, with a finely granular appearance, with extraordinary yellow-green pigmentation.
Primary biliary cirrhosis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p659
1449
A chronic cholestatic disorder, characterized by progressive fibrosis and destruction of extrahepatic and large intrahepatic bile ducts. Affected portal tracts show concentric periductal "onion-skin" fibrosis and a modest lymphocytic infiltrate. Progressive atrophy of the bile duct epithelium leads to obliteration of the lumen, leaving behind a solid, cordlike fibrous scar.
Primary sclerosing cholangitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p660
1450
Liver is slightly enlarged, tense, and cyanotic, with rounded edges. Microscopically, there is congestion of centrilobular sinusoids. With time, centrilobular hepatocytes become atrophic, resulting in markedly attenuated liver cell cords. Liver fibrosis mostly "centrilobular".
Passive congestion of the liver secondary to right-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p660
1451
Hepatocytes in the central region of the lobule undergo ischemic necrosis. The liver takes on a variegated mottled appearance, reflecting hemorrhage and necrosis in the centrilobular regions, alternating with pale midzonal areas, known traditionally as the "nutmeg" liver.
Passive congestion of the liver secondary to left-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p661
1452
A rare condition wherein there is primary dilation of sinusoids, impeding hepatic blood efflux. Associated with exposure to anabolic steroids, OCP's and danazol.
Peliosis hepatis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p661
1453
Results from the thrombosis of two or more major hepatic veins and is characterized by hepatomegaly, weight gain, ascites, and abdominal pain. The liver is swollen, is red-purple, and has a tense capsule. The affected hepatic parenchyma reveals severe centrilobular congestion and necrosis.
Budd-Chiari syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p662
1454
Caused by toxic injury to sinusoidal endothelium. Damaged endothelial cells slough off and create emboli that block blood flow. Accompanied by passage of red blood cell into the space of Disse, proliferation of stellate cells, and fibrosis of terminal branches of the hepatic vein.
Sinusoidal Obstruction Syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p662
1455
Well-demarcated but poorly encapsulated lesion, consisting of hyperplastic hepatocyte nodules with a central fibrous scar. Appears in noncirrhotic livers and may reach up to many centimeters in diameter. It occurs in response to local vascular injury.
Focal nodular hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664
1456
These appear in cirrhotic livers, are larger than surrounding cirrhotic nodules but do not display atypical features. Contains more than one portal tract, have an intact reticulin framework, and do not seem to be precursors of malignant lesions.
Macroregenerative nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664
1457
These are lesions larger than 1 mm in diameter that appear in cirrhotic livers. Considered to be precursors of hepatocelluar cancers, are often monoclonal, and may contain chromosome aberrations similar to those present in liver cancers.
Dysplastic nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664
1458
May appear grossly as (1) a unifocal, usually massive tumor, (2) a multifocal tumor made of nodules of variable size or (3) a diffusely infiltrative cancer, permeating widely and sometimes involving the entire liver, blending imperceptibly into the cirrhotic liver background.
Primary Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p665
1459
A distinctive variant of HCC, which occurs in young male and female adults (20-40 years of age) of equal incidence, no association with cirrhosis or other risk factors. usually consists of a single large, hard "scirrhous" tumor with fibrous bands coursing through it. Composed of well-differentiated polygonal cells growing in nests or cords and separated by parallel lamellae of dense collagen bundles.
Fibrolamellar carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p665
1460
Gallbladder stones that are mostly radiolucent, ovoid and firm; can occur singly but most often there are several, with faceted surfaces resulting from apposition to one another. They are pale yellow but w/ increasing proportions of CaCO3, phosphates and bilirubin, they turn gray-white to black and radiopaque.
Cholesterol stones (TOPNOTCH)Robbins Basic Pathology, 8th ed, p668
1461
May arise anywhere in the biliary tree and are trivially classified as black and as brown. Contain calcium salts of unconjugated bilirubin and lesser amounts of other calcium salts, mucin glycoproteins, and cholesterol.
Pigment stones(TOPNOTCH)Robbins Basic Pathology, 8th ed, p668
1462
A type of pigment stone found in sterile gallbladder bile, usually small and present in large quantities and crumble easily. 50% to 75% are radiopaque.
Black pigment stones (TOPNOTCH)Robbins Basic Pathology, 8th ed, p668
1463
A type of pigment stone found in infected intrahepatic or extrahepatic ducts. Tends to be single or few in number and are soft with a greasy, soaplike consistency that results from the presence of retained fatty acid salts released by the action of bacterial phospholipases on biliary lecithins. Contains calcium soaps, and are radiolucent.
Brown pigment stones(TOPNOTCH)Robbins Basic Pathology, 8th ed, p668
1464
Gallbladder is usually enlarged (twofold to threefold) and tense, and it assumes a bright red or blotchy, violaceous to green-black discoloration, imparted by subserosal hemorrhages. The gallbladder lumen is filled with a cloudy or turbid bile that may contain fibrin, blood, and frank pus.
Acute cholecystitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p669
1465
Condition wherein the exudate contained in the gallbladder is composed virtually of pure pus.
Empyema of the gallbladder(TOPNOTCH)Robbins Basic Pathology, 8th ed, p669
1466
Severe cholecystitis wherein the GB is transformed into a green-black necrotic organ.
Gangrenous cholecystitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p669
1467
The gallbladder may be contracted, of normal size, or enlarged. Presence of stones in the absence of inflammation is diagnostic.
Chronic cholecystitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p669
1468
Defined as a complete obstruction of bile flow caused by destruction or absence of all or part of the extrahepatic bile ducts.
Biliary atresia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p670
1469
Appears as a poorly defined area of diffuse thickening and induration of the gallbladder wall that may cover several square centimeters or involve the entire gallbladder, scirrhous and very firm in consistency.
Infiltrating pattern of gallbladder carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p671
1470
This pattern of GB carcinoma grows into the lumen as an irregular, cauliflower mass, but at the same time it invades the underlying wall.
Exophytic pattern of gallbladder carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p671
1471
Appear typically with an abundant fibrous stroma (desmoplasia) explaining their firm, gritty consistency Most exhibit clearly defined glandular and tubular structures lined by somewhat anaplastic cuboidal to low columnar epithelial cells. Bile pigment and hyaline inclusions are not found within the cells.
Cholangiocarcinomas (TOPNOTCH)Robbins Basic Pathology, 8th ed, p672
1472
Morphology: Characterized by fibrosing cholangitis of bile ducts, with a lymphocytic infiltrate, and progressive atrophy of the bile duct epithelium, and obliteration of the lumen
Primary Sclerosing Cholangitis(TOPNOTCH)
1473
Morphology: Concentric periductal fibrosis or Onion-Skin fibrosis with solid, cordlike fibrous scar.
Primary Sclerosing Cholangitis(TOPNOTCH)
1474
"Beading" of barium column in radiographs of the intrahepatic and extrahepatic biliary tree
Primary Sclerosing Cholangitis(TOPNOTCH)
1475
Morphology: Panlobular giant cell transformation of hepatocytes and formation of hepatocyte "rosettes"
Neonatal Cholestasis(TOPNOTCH)
1476
What is the histological hallmark of irreversible liver damage?
Deposition of fibrous tissue(TOPNOTCH)
1477
"Ground Glass Hepatocytes" are seen in what type of Viral Hepatitis?
Hepatitis B(TOPNOTCH)
1478
What type of viral hepatitis frequently show lymphoid aggregates within portal tracts?
Hepatitis C(TOPNOTCH)
1479
A characteristic feature of this type of viral hepatitis is the high mortality rate among pregnant women, approaching 20%
Hepatitis E(TOPNOTCH)
1480
A distinctive variant of hepatocellular carcinoma that occurs in young adults and has no association with HBV or cirrhosis risk factors.
Fibrolamellar Carcinoma(TOPNOTCH)
1481
What is the most common liver tumor of young childhood?
Hepatoblastoma(TOPNOTCH)
1482
What are the most common benign neoplasm in the liver?
Hemangiomas(TOPNOTCH)
1483
These benign neoplasms tend to occur in young women who have used oral contraceptives and regress on discontinuance of their use.
Liver cell Adenoma(TOPNOTCH)
1484
Rokitansky- Aschoff sinuses are structures seen in what organ?
Gallbladder(TOPNOTCH)
1485
What is the most common congenital anomaly of the gallbladder?
Presence of Phrygian Cap (folded fundus)(TOPNOTCH)
1486
What is the tetralogy of cholesterol stone formation?
1. Supersaturation of bile with cholesterol2. Gallbladder hypomotility3. Cholesterol nucleation4. Hypersecretion of GB mucus(TOPNOTCH)
1487
AKA Strawberry Gallbladder
Cholesterolosis(TOPNOTCH)
1488
Acute calculous cholecystitis is most commonly precipitated by what condition?
Obstruction of the neck or cystic duct by a Gallbladder stone(TOPNOTCH)
1489
Morphology: Prominence of Rokitansky-Aschoff sinuses
Chronic Cholecystitis(TOPNOTCH)
1490
What is the most common cause of cholangitis?
Choledocholithiasis(TOPNOTCH)
1491
True or False. Gallstones are seen in 60%-90% of Carcinoma of the Gallbladder.
True(TOPNOTCH)
1492
What is the most common growth pattern of Gallbladder carcinoma? Infiltrating or Exophytic?
Infiltrating(TOPNOTCH)
1493
These are tumors arising from the part of the common bile duct between the cystic duct junction and the confluence of the right and left hepatic ducts at the liver hilus
Klatskin tumors(TOPNOTCH)
1494
Morphology: feathery degeneration and focal detergent dissolution of hepatocytes, giving rise to bile lakes filled with cellular debris and pigment
Cholestasis(TOPNOTCH)
1495
What does unrelieved cholestasis lead to?
Portal tract fibrosis(TOPNOTCH)
1496
What is the outcome of 85% of Acute Hepatitis infection?
Chronic Hepatitis(TOPNOTCH)
1497
These inclusions are a characteristic but not specific feature of alcoholic liver disease.
Mallory bodies(TOPNOTCH)
1498
Morphology: macrovesicular steatosis, involving most regions of the hepatic lobule. The intracytoplasmic fat is seen as clear vacuoles.
Alcoholic liver disease(TOPNOTCH)
1499
What zone of the liver if particularly vulnerable of ischemic injury and number of drug and toxic reactions?
Centrilobular zone(TOPNOTCH)
1500
What zone of the liver is particularly affected in eclampsia?
Periportal zone(TOPNOTCH)
1501
At least how many percent of the liver must be damaged before hepatic failure ensues?
at least 80%(TOPNOTCH)
1502
What are the 4 major consequences of portal hypertension?
Ascites, formation of portosystemic venous shunts, congestive splenomegaly, and hepatic encephalopathy(TOPNOTCH)
1503
Ascites becomes clinically detectable at what amount?
500 ml(TOPNOTCH)
1504
Morphology: portal tract expansion with inflammatory cells and fibrous tissue and interface hepatitis with spillover of inflammation into the adjacent parenchyma. Lymphoid aggregates can also be seen.
Chronic Viral Hepatitis C(TOPNOTCH)
1505
Morphology: hepatocytes show diffuse granular cytoplasm, so called ground glass hepatocytes
Hepatitis B viral infection(TOPNOTCH)
1506
Morphology: liver biopsy shows steatosis, multifocal parenchymal inflammation, Mallory hyaline, hepatocyte death, and sinusoidal fibrosis
Steatohepatitis or Nonalcoholic Steatohepatitis(TOPNOTCH)
1507
In Hemochromatosis, what is the most common site of hemosiderin deposition?
Liver(TOPNOTCH)
1508
What are the 3 clinical features of Hemochromatosis?
Deposition of hemosiderin, cirrhosis, and pancreatic fibrosis(TOPNOTCH)
1509
Morphology: characterized by the presence of round to oval cytoplasmic globular inclusions in hepatocytes, which in routine H and E stains are acidophilic and indistinctly demarcated from the surrounding cytoplasm
A1 antitrypsin deficiency(TOPNOTCH)
1510
Morphology: Panlobular giant cell transformation of hepatocytes and formation of hepatocyte "rosettes"
Neonatal Cholestasis(TOPNOTCH)
1511
Morphology: characterized by coarse fibrous septae that subdivide the liver in a jigsaw like pattern
Secondary biliary cirrhosis(TOPNOTCH)
1512
Morphology: florid duct lesion
Primary Biliary Cirrhosis(TOPNOTCH)
1513
The combination of hypoperfusion and retrograde congestion acts synergistically to generate what type of necrosis in the liver?
Centrolobular hemorrhagic necrosis(TOPNOTCH)
1514
Morphology: periportal sinusoids contain fibrin deposits with hemorrhage into the space of Disse, leading to periportal hepatocellular coagulative necrosis
Pre-Eclampsia/Eclampsia(TOPNOTCH)
1515
Type of liver transplant rejection : severe obliterative arteritis of small and larger arterial vessels results in ischemic changes in the liver parenchyma
Chronic Rejection(TOPNOTCH)
1516
Type of liver transplant rejection: infiltration of a mixed population of inflammatory cells into portal tracts, bile ducts, and hepatocyte injury and endothelitis
Acute cellular rejections(TOPNOTCH)
1517
What do you call the small tubular channels that are sometimes burried within the gallbladder wall adjacent to the liver?
Ducts of Luschka(TOPNOTCH)
1518
What is the most common congenital anomaly seen in the Gallbladder?
A folded fundus or so called phrygian cap(TOPNOTCH)
1519
Gross morphology: the mucosal surface of the gallbladder is studded with minute yellow flecks
Strawberry Gallbladder(TOPNOTCH)
1520
What type of pigment stones are generally seen in infected intrahepatic or extra hepatic ducts?
Brown pigment stones(TOPNOTCH)
1521
Gross morphology: GB is shrunken, nodular, and chronically inflamed with foci of necrosis and hemorrhage
Xanthogranulomatous cholecystitis(TOPNOTCH)
