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Flashcards in patho Deck (3078):
1

Specialized tye of "grinder" that selectively chews up denatured proteins, releasing peptides

Proteasomes(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

2

It synthesizes new proteins for the plasma membrane

Rough endoplasmic reticulum(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

3

Abundant in liver and gonads where it is used for steroid hormone and lipoprotein synthesis, and modification of hydrophobic compounds into water-soluble molecules

Smooth endoplasmic reticulum(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

4

Intracellular organelles that contain degradative enzymes that permit digestion of macromolecules

Lysosomes(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

5

Cell organelle that break down fatty acids, generating hydrogen peroxide in the process

Peroxisomes(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

6

The ability of cells to adopt a particular shape, maintain polarity, organize relationship of intracellular organelles, and move about depends on this intracellular scaffolding of proteins

Cytoskeleton(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.10

7

It shuttles internalized material to the appropriate intracellular siters or direct newly synthesized materials to the cell surface or targeted organelle.

Endosomal vesicles(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

8

Source of ATP and metabolic intermediates needed for anabolic metabolism, site of heme synthesis, and contain important sensors of cell damaga that can initiate and regulate the process of programmed cell death.

Mitochondria(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.6

9

Water and carbon dioxide diffuse across the cell lipid bilayers through what process (type of diffusion)

Passive membrane diffusion(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.9

10

The process by which large molecules are exported from cells.

Exocytosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.9

11

The movement of endocytosed vesicles between the apical and basolateral compartments of cells for transferring large amount of protein across epithelial barrier and rapid movement of large volumes of solute.

Transcytosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.9

12

Non-coated plasma membrane invagination ("little caves") associated with cAMP, GPI-linked molecules, SRC-family kinases, and folate receptor.

Caveolae(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.9

13

A fluid-phase process during which the plasma membrane invaginates and is pinched off to form a cytoplasmic vesicle.

Pinocytosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.9

14

Major uptake mechanism for macromolecules such as transferrin and LDL, which bind to receptors localized in clathrin coated pits.

Receptor-mediated endocytosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.20

15

Most abundant cytosolic protein in cells.

Actin(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 11

16

They serve as connecting cables for "molecular motor" proteins that use ATP to move vesicles, organelles, or other molecules.

Microtubules(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 11

17

Cell junction that seal adjacent cells together to create a continuous barrier that restrics paracellular movement of ions and other molecules.

Occluding junctions (tight junctions)(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 11

18

Cell junctions that mechanically attach cells and their intracellular cytoskeletons to other cells or to extracellular matrix.

Anchoring junctions (desmosomes) (tight junctions)(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 11

19

Junctions that mediate the passage of chemical or electrical signals from one cell to another.

Communicating junctions (gap junctions) (TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 12

20

Cell organelle that consists of stacked cisternae that progressively modify protein

Golgi apparatus(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 12

21

Cell-cell signaling pathway: cells in immediate vicinity are affected.

Paracrine signaling(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 16

22

Cell-cell signaling pathway: molecules secreted by a cell affect tat same cell.

Autocrine signaling(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 16

23

Cell-cell signaling pathway: activated neurons secrete neurotransmitters at specialized cell junctions onto target cells.

Synaptic signaling(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 16

24

Cell-cell signaling pathway: A mediator is released into the bloodstream and acts on target cells at a distance.

Endocrine signaling(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 16

25

Vitamin D and steroid hormones are cell-permeable ligands for this type of receptor.

Intracellular receptors(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 16

26

Its major role is to stimulate the activity of genes required for cell growth and cell division.

Growth factors(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 18

27

Growth factor: Stimulate keratinocyte migration and formation of granulation tissue

Epidermal growth factor(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 19

28

Growth factor: stimulate proliferation of hepatocytes and other epithelial cells.

Transforming growth factor-alpha(TGF-a)(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 19

29

Growth factor: enhances proliferation of hepatocytes and increases cell motility

Hepatocyte growth factor(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 19

30

Growth factor: stimulates proliferation of endothelial cells and increases vascular permeability

Vascular endothelial growth factor (VEGF)(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 19

31

Growth factor: chemotactic for neutrophils, fibroblasts, and smooth muscles, and activates proliferation of fibroblasts and endothelial cells.

Platelet-derived growth factor (PDGF) (VEGF)(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 19

32

Growth factor: chemotactic and mitogenic for fibroblasts and stimulates angiogenesis and ECM protein synthesis

Fibroblast growth factors (FGFs) (VEGF)(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 19

33

Component of ECM responsible for the ability of tissues to recoil and recover their shape after physical deformation.

Elastin(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 23

34

Component of ECM that confer resistance to compressive forces, also provide lubrication between bony surfaces.

Proteoglycan(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 23

35

The most abundant glycoprotein in basement membrane.

Laminin(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 24

36

A major component of the interstitial ECM.

Fibronectin(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 24

37

A large family of transmembrane glycoproteins that allow cells to attach to ECM constituents, linking the intracellular cytoskeleton with the outside world.

Integrins(TOPNOTCH)Robbins Basic Pathology 9th ed. p. 24

38

Sequence of events in cell cycle

G1/Presynthetic growth-S/DNA synthesis-G2/Premitotic growth- M/mitotic phase (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.25

39

Two important properties of stem cells

Self-renewal and assymetric division. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 26

40

Most undifferentiated stem cells which are totipotent, and can be induced to form specialized cells of all three germ cell layers.

Embryonic stem cells(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 27

41

Variety of stem cell with limited repertoire of differentiated cells that they can generate.

Tissue stem cells(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 27

42

Increase in size of cells resulting in increased size of organ.

Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 34

43

Increase in number of cells.

Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.35

44

Hypertrophy of hyperplasia?Uterus during pregnancy

Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 9th ed. p.34

45

Hypertrophy or hyperplasia?Wound healing

Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4

46

Hypertrophy or hyperplasia?
Female breast at puberty

Both. (TOPNOTCH) Robbins Basic Pathology 9th ed., p 36

47

Cellular adaptation of non-dividing cells such as myocardial fibers.

Hypertrophy (TOPNOTCH)

48

A 50 y/o male has untreated hypertension for several years. What cellular alteration will be most likely seen in the myocardium?

Hypertrophy (TOPNOTCH)

49

A 40 y/o male underwent partial hepatectomy. What cellular adaptation will the liver most likely undergo?

Hyperplasia(TOPNOTCH)

50

The most common stimulus for hypertrophy of muscle

Increased workload (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.34

51

A 65 y/o male presents with 3-month history of weak stream, straining, and hesitancy. There is no history of prostate cancer. Prostate was severely enlarged without nodules. PSA level is 3 mcg. What cellular adaptation does the prostate most likely undergo?

Hyperplasia(Case of BPH) (TOPNOTCH)

52

Stimulus for hyperplasia in BPH

Hormonal stimulation by androgens. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 36

53

Cellular adaptation in papilloma virus infection

Hyperplasia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 36

54

Reduction in the size of an organ or tissue due to decrease in cell size and number

Atrophy(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 35

55

A 60 y/o female has been experiencing hot flushes and irritability. Her uterine epithelium will most likely reveal what type of cellular adaptation?

Atrophy(in menopause)(TOPNOTCH)

56

Chronic production of this cytokine is thought to be responsible for appetite suppression and lipid depletion, culminating in muscle atrophy and marked muscle wasting (cachexia)

Tumor necrosis factor (TNF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 35

57

A reversible change in which one differentiated cell type is replaced by another cell type.

Metaplasia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37

58

A 49 y/o female had a chronic history of heartburn. Biopsy done showed glandular changes in the distal epithelium of the esophagus. What cellular adaptation is present?

Metaplasia. This is a case of Barret's esophagus (squamous to glandular epithelium) (TOPNOTCH)

59

The basal cell changes seen in reflux esophagitis is an example of this adaptive change

Metaplasia (TOPNOTCH)

60

Most common epithelial metaplasia

Columnar to squamous(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37

61

Type of metaplasia in trachea and bronchi in habitual cigarette smoking

Columnar to squamous(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 37

62

Its hallmarks are reduced oxidative phosphorylation with resultant depletion of energy stores in the form of ATP and cellular swelling

Reversible injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 38

63

Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.

Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7

64

Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.

Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7

65

Type of cell death which results from a pathologic cell injury.

Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9

66

Type of cell death associated with inflammation.

Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

67

It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is characterized by nuclear shrinkage and increased basophilia.

Pyknosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.42

68

It is the destructive fragmentation of the nucleus of a dying cell.

Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

69

It is the complete dissolution of the chromatin of a dying cell.

Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10

70

This is the first manifestation of almost all forms of injury to cells.

Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8

71

Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.

Hydropic change or Vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23

72

Appearance of lipid vacuoles in the cytoplasm.

Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23

73

Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.

Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

74

Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.

Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

75

Cell injury with loss of microvilli, blunting, appearance of smal amorphous densities, ER dilation and disaggregation of granular and fibrillar elements.

Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.41

76

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, 9th ed. p.43

77

Characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass.

Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology , 9th ed. p.43

78

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, 9th ed., p. 44

79

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, 9th ed., p. 44

80

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

81

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, 9th ed. p.43

82

Friable, white appearance of necoris. It appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border.

Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 9th ed. p.43

83

Obstruction of the blood supply would lead to which type of pathologic process in the brain parenchyma?

Liquefactive necrosis (TOPNOTCH)

84

The type of necrosis seen in tissue injury associated with acute pancreatitis

Enzymatic fat necrosis. (TOPNOTCH)

85

A 32 y/o male complains of chronic cough and weight loss. CXR showed an ill-defined mass along the apex of the right lobe. Sputum AFB was positive. Biopsy of the lung will most likely reveal what kind of necrosis?

Caseation necrosis (TOPNOTCH)

86

These are chemical species with a single unpaired electron in the outer orbital.

Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

87

They block free radical formation or inactivate free radicals. Examples of these are the lipid-soluble vitamins E, A, and C, and glutathione in the cytosol.

Antioxidants(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 48

88

Most common cause of cell injury in clinical medicine.

Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

89

Patient presented with heaviness in the chest, nausea, and diaphoresis. Troponin I and CKMB were noted to be elevated. What is the mechanism of the elevation of cardiac enzyme?

Leakage of intracellular proteins through the damaged cell membrane reflecting irreversible injury and cell death in the tissues. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 50

90

Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.

Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19

91

Characterized by cell shrinkage, chromatic condensation, formation of cytoplasmic blebs and apoptotic bodies, and phagocytosis by macrophages.

ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 53

92

Type of cell death in embryogenesis

ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 52

93

Type of cell death in menopause

ApoptosisTOPNOTCH) Robbins Basic Pathology, 9th ed., p. 52

94

Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.

Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18

95

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.

Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22

96

Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.

Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22

97

It involves sequestration of cellular organelles into cytoplasmic autophagic vacuoles that fuse with lysosomes and digest enclosed material.

Autophagy(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 61

98

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.

Fatty change/Steatosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

99

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.

Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24

100

Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons.

Xanthomas(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24

101

Hypertrophy or hyperplasia?Cardiomegaly due to hypertension

Hypertrophy due to increased workload(TOPNOTCH)

102

Most common exogenous pigment?

Carbon(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

103

"Wear and Tear pigment"?

Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

104

Pigment produced by tyrosinase-catalyzed oxidation of tyrosine to dihydroxyphenylalanine.

Melanin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

105

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

106

Histochemical reaction used to identify hemosiderin.

Prussian blue test(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

107

Abnormal calcium deposition occuring in the absence of calcium metabolic derangements.

Dystrophic calcification.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

108

Calcium deposition in normal tissues occuring in the presence of hypercalcemia.

Metastatic calcification (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

109

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

110

A result of a progressive decline in the proliferative capacity and lifespan of cells.

Cellular aging(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.29

111

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

112

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

113

Clear vacuoles within parenchymal cells, displacing the nucleus to the cell periphery.

Fatty change (TOPNOTCHRobbins Basic Pathology, 8th ed. p.24

114

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

115

Rounded, eosinophilic accumulation of newly synthesized immunoglobulins in the rough ER of plasma cells.

Russel bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25

116

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

117

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

118

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

119

What substance accumulates in the cytoplasm of liver cells in steatosis?

Triglyceride (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

120

Mechanism of triglyceride accumulation in malnutrition

Defective transport (TOPNOTCH)

121

A 70 y/o woman was brought to the clinic because of a 3 year history of progressive memory impairment, difficulty finding words, and irritability. What is the pathogenesis of this condition?

Abnormal folding of AB peptides causing aggregation within neurons and apoptosis (Case of Alzheimer Disease) (TOPNOTCH)

122

Pathogenesis: abnormal folding of PrPSC causing neuronal death (affected prion protein)

Creutzfeldt-Jacob disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 58

123

Pathogenesis: absence of enzymatic activity in lungs causing destruction of elastic tissue

Alpha-1-antitrypsin deficiency (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 58

124

Fundamental cause of necrotic cell death

Reduction in ATP levels(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 45

125

Other term for fatty change

Steatosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

126

Most common causes of significant fatty change in the liver

Alcohol abuse and non-alcoholic fatty liver disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 62

127

Alteration within the cells or in the extracellular space that gives a homogeneous, glassy, pink appearnce in H&E histologic section

Hyaline change(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 61

128

In this disease, glycogen can be seen in renal tubular epithelial cells, liver cells, B cells of islets of Langerhans, and heart muscle cells.

Diabetes mellitus(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 64

129

A condition when there is systemic overload of iron, hemosiderin may be deposited in many organs and tissues.

Hemosiderosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 65

130

An inherited disease characterized by extreme accumulation of iron, associated with liver, heart, and pancreatic damage, and resulting in liver fibrosis, heart failure, and diabetes mellitus.

Hemochromatosis. (TOPNOTCH)

131

A rare metabolic disease causing black pigment deposition in the skin, connective tissue, and cartilage.

Alkaptonuria(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 64

132

Foci of dystrophic calcification which appears as lamellated configurations because of their resemblance to grains of sand. Seen in some types of papillary cancer.

Psammoma bodies (TOPNOTCH)

133

Jaundice is due to accumulation of what pigment?

Bilirubin. (TOPNOTCH)

134

What type of necrosis is most characteristic of ischemia involving the heart or kidney?

Coagulative necrosis (TOPNOTCH)

135

What type of necrosis is most often caused by sudden ischemia from vascular occlusion?

Coagulative necrosis (TOPNOTCH)

136

A 56 y/o man died after 24-hour hospitalization for severe crushing chest pain. The type of necrosis of myocardium will most likely reveal:

Coagulative necrosis (TOPNOTCH)

137

The kidney in nephrocalcinosis is an example of what type of calcification? Dystrophic or metastatic?

Metastatic calcification (TOPNOTCH)

138

Dystrophic or metastatic calcification? Calcific aortic stenosis

Dystrophic calcification(TOPNOTCH)

139

Dystrophic or metastatic calcification?Left anterior descending coronary artery with atheromatous plaques

Dystrophic calcification(TOPNOTCH)

140

Dystrophic or metastatic calcification? Sarcoidosis

Metastatic calcification (TOPNOTCH)

141

Dystrophic or metastatic calcification? Paget disease

Metastatic calcification (TOPNOTCH)

142

After a tibial fracture in a 19 year old football player, the leg is immobilized to permit healing. The leg muscles decrease in size due to: (A) decrease in cell size, (B) decrease in cell number, (C) inadequate nutrition, (D) loss of hormonal stimulation

decrease in cell size (atrophy) (TOPNOTCH) Robbins Basic Pathology, 8th ed. P. 4

143

A 30 year old thalassemic male has been receiving multiple blood transfusions throughout his life. What is the expected intracellular accumulation in the parenchymal cells of his liver, heart, and endocrine organs?

Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

144

An 80 year old female is found to have calcified aortic valves. Which of the following is the likely cause? (A) renal failure with secondary hyperparathyrodism, (B) accumulation of calcium in damaged valves despite absence of calcium derangements, (C) parathyroid-related protein production from an underlying malignancy, (D) hypercalcemia from multiple myeloma

Accumulation of calcium despite absence of calcium derangements (dystrophic calcification) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp26-27.

145

In industrialized nations, what are the most common causes of fatty change in the liver?

Alcohol abuse and diabetes (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 23.

146

A 22 year old female is on the first day of her menses. Which of the following characterizes the events in her endometrial cells: (A) endometrial cells show shrinkage and nuclear condensation, (B) neutrophils accumulate around the cells, (C) severe mitochondrial swelling and plasma membrane destruction, (D) accumulation of amorphous pink material

Endometrial cells show shrinkage and nuclear accumulation (Apoptosis) (TOPNOTCH) Robbins Basic Pathology 8th ed., pp 19-20

147

It is a response of vascularized tissues to infection and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.

Inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 69

148

The first step in a typical inflammatory reaction

Recognition of offending agent (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 70

149

The main components of inflammation

Vascular reaction and cellular response. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 72

150

The sequential steps in a typical inflammatory reaction

Recognition of offending agent, recruitment of leukocytes and plasma proteins, removal of agent, regulation of response, repair.(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 70

151

Inflammation which is characterized by exudation of fluid and plasma protein and a predominantly neutrophilic leukocyte accumulation.

Acute inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71

152

Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and deposition of connective tissue.

Chronic inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71

153

Five cardinal signs of inflammation

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71

154

Initial vascular response to injury

Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33

155

Three major components of acute inflammation

Vasodilation, increased permeability, leukocyte emigration. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

156

An ultrafiltrate of blood which contains little protein, little or no cellular material and low specific gravity as a result of osmotic or hydrostatic imbalance across the vessel wall without increase in vascular permeability.

Transudate. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

157

An extravascular fluid with high protein content. Its presence implies an increased vascular permeability, triggered by tissue injury and ongoing inflammatory reaction.

Exudate(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

158

Denotes an excess fluid in the interstitial tissue or serous cavities

Edema (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

159

Effect of histamine on vascular smooth muscle

Vasodilation. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

160

The most common mechanism of increased vascular permeability.

Contraction of endothelial cells resulting in increased interendothelial spaces. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 74

161

Proliferation of lymphatic vessels and painful enlarged lymph nodes secondary to inflammation.

Reactive or inflammatory lymphadenitis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 74

162

State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Rolling

Selectins (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

163

State the molecule in the lymphocyte responsible for this stage of vascular inflammatory response:Firm adhesion

Integrins(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

164

State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Transmigration

PECAM-1/CD 31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

165

State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion

ICAM -1(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

166

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin

Sialyl-Lewis X modified glycoprotein (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

167

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin

Sialyl-Lewis X modified glycoprotein (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

168

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1

Integrins (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

169

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31

CD-31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

170

The process of leukocyte accumulation at the periphery of blood vessels

Margination(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75

171

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, 9th ed. p. 72

172

Arrange the steps in leukocyte recruitment:A. TransmigrationB. Rolling C. MarginationD. Firm adhesion

C, B, D, A (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75

173

Process of coating microorganisms with proteins that facilitate phagocytosis.

Opsonization (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75

174

A lymphocyte with ingested microorganism fused with lysosome is called _______.

Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 78

175

The process of migration of the leukocytes through the endothelium.

Transmigration or diapedesis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

176

Process of leukocyte migration toward sites of infection or injury along a chemical gradient.

Chemotaxis (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

177

The most important lysosomal enzyme involved in bacterial killing.

Elastase(TOPNOTCH)

178

A peptide leukocyte granule constituent which kills microbes by creating holes in their membranes.

Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40

179

Predominant form of leukocyte during the first 6 - 24 hours of inflammation?

Neutrophils(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

180

Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?

Monocytes(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

181

Predominant cellular infiltrate in Pseudomonas infection.

Neutrophils(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

182

Predominant cellular infiltrate in viral infections

Lymphocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

183

Predominant cellular infiltrate in allergic reactions

Eosinophils (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

184

Sequential steps in phagocytosis

Recognition and attachment of particle to be ingested, engulfment and formation of phagocytic vacuole, killing or degradation of ingested material. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.78

185

First step in phagocytosis

Recognition and attachment of particle to be ingested(TOPNOTCH) Robbins Basic Pathology, 9th ed. P.78

186

Substances responsible for leukocyte-induced tissue injury

Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)

187

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

188

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

189

Results from a defect in the protein involved in membrane docking and fusion.

Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41

190

NADPH deficiency or defect resulting in decreased oxidative burst.

Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42

191

Type of inflammatory mediators that are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus.

Cell-derived mediators.(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 82

192

Type of mediators that are produced mainly in the liver and are present in the circulation as inactive precursors that must be activated by proteolytic cleavages to acquire their biologic properties.

Plasma-derived mediators. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

193

The richest sources of histamine

Mast cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

194

Effects of histamine of arterioles and venules

Dilation of arterioles and increases permeability of venules. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

195

Arachidonic acid metabolites/derivatives

Prostaglandin, prostacyclin, thromboxane, leukotrienes, lipoxin. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

196

Arachidonic acid derivative that causes vasoconstriction and promotes platelet aggregration.

Thromboxane A2 (TXA2) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

197

Arachidonic acid metabolite implicated in increased vascular permeability and bronchospasm

LTC4, LTD4, and LTE4 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

198

Arachidonic acid metabolite that causes chemotaxis and leukocyte adhesion.

Leukotriene B4 (LTB4) and hydroxyeicosatetraenoic acid (HETE). (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

199

Cytokines that induce systemic acute-phase response associated with infection or injury, and are implicated in sepsis.

TNF, IL-1 (and IL-6) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 86

200

The cytokines that are important mediators of acute-phase reaction causing fever.

TNF, IL-1 (and IL-6) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 99

201

3 Functions of complement proteins

Inflammation, opsonization and phagocytosis, and cell lysis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

202

Morphologic hallmarks of acute inflammation

Vasodilation and accumulation of leukocytes and fluid in the extravascular tissue. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

203

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, 9th ed. p. 90

204

Fluid in a serous cavity is called ______.

Effusion (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

205

This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.

Fibrinous inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

206

Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.

Fibrinous inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

207

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, 9th ed. p. 90

208

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, 9th ed. p. 90

209

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, 9th ed. p. 91

210

Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.

Serotonin, Histamine (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

211

Complement fragments which are anaphylotoxins.

C3a, C5a (A for anaphylotoxin) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

212

Complement fragment which aids in opsonization.

C3b (b for binding)(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

213

Membrane attack complex

C5b, C6-9 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

214

Deficiency of the terminal components of complement predisposes to what infection.

Neisseria infections. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

215

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, 9th ed. p. 89

216

Platelet-activating factor (PAF) is a phospholipid-derived mediator that is now known to have multiple inflammatory effects. What are these?

Platelet aggregration, vasoconstriction (vasodilation in low concentration), bronchoconstriction, and increased venular permeability. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

217

Enzyme blocked by NSAIDS.

Cyclooxygenase 1 and 2 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 85

218

Enzyme inhibited by glucocorticoids

Phospholipase A2 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 85

219

Polypeptide products of many cell types that function as mediators of inflammation and immune response.

Cytokines (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 86

220

They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.

Chemokines (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 87

221

Major cytokines in acute inflmmation.

TNF and IL-1 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 86

222

A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.

Nitric oxide (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 80

223

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

224

Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.

Chronic Inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 93-94

225

Macrophages in the liver

Kupffer cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

226

Macrophages in the spleen and lymph nodes

Sinus histiocytes(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

227

Macrophages in the CNS

Microglial cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

228

Pathway of macrophage activation induced by microbial products such as endotoxin, cytokines, or foreign substance to produce substance for host defense and inflammatory reactions

Classical pathway. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

229

Pathway of macrophage activation induced by cytokines produced by T lymphocytes and other cells with the principal function of tissue repair.

Alternative pathway. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 95

230

Macrophages in the lungs

Alveolar Macrophages (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

231

A focus of epitheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.

Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

232

Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli

Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

233

Acid-fast bacilli in macrophages, noncaseating granulomas

Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

234

Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellular outline

Gumma (Syphilis)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

235

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

236

Noncaseating granulomas with abundant activated macrophages

Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

237

Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate

Crohn's disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

238

Cells with pink, granular cytoplasm with indistinct boundaries.

Epitheloid cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

239

40-50 um in size, consisting of a large mass of cytoplasm and many nuclei.

Giant cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

240

Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.

Caseous necrosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

241

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57

242

A form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes.

Granulomatous inflammation. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

243

Diseases with granulomatous inflammation

TB, Leprosy, syphilis, cat-scratch disease, sarcoidosis, Crohn's disease, systemic mycoses (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

244

True or false. Schistosomiasis may cause granulomatous inflammation

True. (TOPNOTCH)

245

True or false. Histoplasmosis may cause granulomatous inflammation

True. (TOPNOTCH)

246

A 5 y/o child touches a lit candle and develops a small blister on his right hand. The blister is an example of what type of inflammation?

Serous inflammation. (TOPNOTCH)

247

The hallmark of chronic inflammation

Tissue destruction (TOPNOTCH)

248

A 20 y/o male was admitted due to RLQ pain of 18 hours duration. Appendectomy and revealed an edematous and erythematous appendix. An infiltrate of what cells would be most likely seen?

Neutrophils (TOPNOTCH)

249

Heat and redness in acute inflammation is due to what pathogenetic mechanism?

Increased blood flow (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 74

250

An 18 year old college student accidentally scalds his hand while ironing, where a large unruptured blister forms. What is seen in the blister? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) large necrotic center surrounded by neutrophils (D) epithelioid macrophages and giant cells

protein poor fluid (Morphologic patterns of acute inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 43-44

251

A 64 year old stroke patient at the ICU with a chest radiograph showing a cavitary lesion in the right lower lung lobe with fluid levels. What is seen in that lobe? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) extensive necrosis and neutrophilic infiltrates (D) epithelioid macrophages and giant cells

large necrotic center surrounded by neutrophils (Morphologic patterns of acute inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 43-44

252

A rheumatologist auscultates a friction rub in a 33 year old admitted lupus patient. What is seen in her pericardial cavity? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) large necrotic center surrounded by neutrophils (D) epithelioid macrophages and giant cells

eosinophilic meshwork of amorphous coagulum (Morphologic patterns of acute inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 43-44

253

A 33 year old female who underwent partial thyroidectomy for a colloid nodule 5 years ago underwent a completion thyroidectomy for persistent enlargement. On her present thyroid specimen, the original excision site shows a sutured area. Microscopic examination of that area will show (A) epithelioid cells with occasional giant cellssurrounding a necrotic center (B) neutrophils surrounding a necrotic center (C) protein poor fluid (D) giant cells surrounding refractile bodies

giant cells surrounding refractile bodies (Granulomatous Inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 56

254

What is expected in the involved intestine of a patient with Chron disease? (A) eosinophilic network of amorphous coagulum (B) foci of neutrophils with necrotic debris (C) occasional noncaseating granulomas with dense chronic inflammatory infiltrate (D) pockets of protein poor fluid

occasional noncaseating granulomas with dense chronic inflammatory infiltrate (Granulomatous Inflammation) (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

255

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

256

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

257

Cells of these tissues are considered to be terminally differentiated and nonproliferative in postnatal life.

Permanent tissues(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62

258

Labile, stable or permanent tissues:Bone marrow

Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

259

Labile, stable or permanent tissues:Vaginal epithelium

Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

260

Labile, stable or permanent tissues:Salivary glands

Labile(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

261

Labile, stable or permanent tissues:Liver parenchyma

Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

262

Labile, stable or permanent tissues:Endothelium

Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

263

Labile, stable or permanent tissues:Smooth muscle cells

Stable(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

264

Labile, stable or permanent tissues:Neurons

Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62

265

Labile, stable or permanent tissues:Cardiac muscle

Permanent(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.62

266

Type of collagen found in basement membrane

Type IV collagen(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.67

267

This is the most abundant glycoprotein in basement membrane.

Laminin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.68

268

The pink, soft, granular tissue seen beneath the scab of a skin wound.

Granulation tissue(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70

269

Maturation and reorganization of fibrous tissue

Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.70

270

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

271

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

272

Wound strength reaches 70 - 80 % of normal in ______ months.

3 months(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77

273

Single most important cause of delay in wound healing.

Infection(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77

274

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

275

Refers to the restoration of tissue architecture and function after an injury.

Repair (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77

276

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

277

Process of replacing damaged components of a tissue, returning to a normal state.

Regeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.77

278

Migration and proliferation of fibroblasts with deposition of ECM.

Scar formation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.72

279

Maturation and reorganization of fibrous tissue

Remodeling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.73

280

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

281

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

282

In the cell cycle, this is called the presynthetic growth phase.

G1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

283

In the cell cycle, this is also called the premitotic growth phase.

G2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

284

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

285

These enzymes promote DNA replication and various aspects of mitosis. They are required for cell cycle progression. Forms complexes with cyclin.

Cyclin-dependent kinases (CDK)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.61

286

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)

287

This cytokine increases vascular permeability and is mitogenic for endothelial cells.

Vascular Endothelial Growth Factor (VEGF)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.71

288

Pattern of extracellular signaling wherein the target cell is itself.

Autocrine(TOPNOTCH)

289

Pattern of extracellular signaling wherein the target cell is adjacent to the secretory cell.

Paracrine(TOPNOTCH)

290

Pattern of extracellular signaling wherein the target cell is distant to the secretory cell.

Endocrine(TOPNOTCH)

291

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)

292

Component of ECM which confers tensile strength and recoil.

Fibrous proteins s.a. Collagen and elastin(TOPNOTCH)

293

Component of ECM that permits resilience and lubrication.

Proteoglycans, hyaluronan(TOPNOTCH)

294

Component of ECM that connect the elements to one another and to the cells.

Adhesive glycoproteins(TOPNOTCH)

295

What is the hallmark of tissue repair?

Tissue granulation. (TOPNOTCH)

296

A 28 y/o male suffered from traumatic injury of the muscles of his left lower extremity. In this type of tissue, repair is typically dominated by? Scar formation or regeneration?

Scar formation. In permanent tissues like skeletal and cardiac muscle, repair is dominated by scar formation. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 101

297

Liver, kidney and pancreas. Labile, stable or permanent tissues?

Stable. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 101

298

A patient has a large wound on his right arm as a result of a vehicular crash. Initially his wound is filled with granulation tissue composed of fibroblast and new blood vessels. What is responsible for inducing formation of new blood vessels?

Vascular Endothelial Growth Factor (VEGF)(TOPNOTCH)

299

Following hepatectomy, liver undergo repair by __________.

Regeneration. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 102

300

Steps in scar formation

Angiogenesis, Formation of granulation tissue, Remodelling. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 102

301

It is characterized by proliferation of fibroblast and new thin walled, delicate capillaries in a loose ECM often admixed with inflammatory cells.

Granulation tissue. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 103

302

Roles of macrophage in tissue repair.

Clear offending agent and dead tissue, provide growth factor, secrete cytokines for fibroblast proliferation and connective tissue synthesis.(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 104

303

Granulation tissue appear after how many days after injury?

3-5 days. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 104

304

A 50 y/o coal worker experienced gradual onset of dyspnea and non-productive cough. He was then diagnosed with pulmonary fibrosis. What is the most important cytokine that causes the development of fibrosis following chronic inflammation?

Transforming growth factor-? (TGF-?) is the most important cytokine for synthesis and deposition of connective tissue protein. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 105

305

A 52 y/o diabetic female patient developed a non-healing wound on his right foot. She is currently on an anti-hyperglycemic and an antihypertensive.What factor is the most likely implicated in the abnormal wound healing?

Presence of uncontrolled blood glucose level/Diabetes. (TOPNOTCH)

306

Cells present within 24 hours of tissue injury.

Neutrophils (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 106

307

Predominant cells on Day 3 after tissue injury

Macrophages.(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 106

308

An important feature in healing by secondary intention/secondary union.

Wound contraction involving formation of myofibroblasts at the edge of the wound. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 108

309

True or False. Wound strength returns to normal 3 months after a carefully sutured wound.

False. Only up to 70-80% of normal and usually does not improve beyond that. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 108

310

Patient X had a laceration on his right arm and underwent suture and repair. Wound healing continues, however, the site was disfiguring and developed a raised nodule after 2 months. The abnormality presented is ___.

Keloid formation (TOPNOTCH)

311

Patient receiving glucocorticoid therapy for the autoimmune disease developed an abscess. Poor wound healing may result from glucocorticoid therapy due to:

Inhibition of TGF-B and diminished fibrosis secondary to glucocorticoid therapy. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 106

312

One week after an exploratory laparatomy, a 30-year old obese female patient had "rupture of the wound". This complication in tissue repair is due to inadequate formation of granulation tissue or scar formation.

Dehiscence. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 109

313

A 5 y/o patient had second degree burn of the palms. She is more prone to what type of abnormality in tissue repair?

Contracture. (TOPNOTCH)

314

Collagen deposition in cellular repair is largely a function of what cells?

Fibroblasts (TOPNOTCH)

315

The hallmark of tissue healing is:

Granulation tissue (TOPNOTCH)

316

Vitamin C retards wound healing because

Collagen synthesis is inhibited (TOPNOTCH)

317

Phase of cutaneous wound healing: formation of granulation tissue, proliferation and migration of connective tissue cells and re-epithelialization of wound surface

Proliferation (2nd phase) (TOPNOTCH)

318

Phase of cutaneous wound healing: ECM deposition, tissue remodeling and wound contraction

Maturation (3nd phase) (TOPNOTCH)

319

Its characteristic feature is the presence of new small blood vessels and proliferation of fibroblasts

Granulation tissue (TOPNOTCH)

320

True or False. Granulation tissue is more prominent in healing by secondary union.

True (TOPNOTCH)

321

Hypertrophic scar is due to accumulation of excessive amount of___.

Collagen (TOPNOTCH)

322

In wound healing, collagen is produced by:

Myofibroblasts(TOPNOTCH)

323

A 33 year old man sustains a stab injury on his right forearm. Two days after the incident, what can be seen in his stab wound? (A) dense collagen deposition (B) pink amorphous material devoid of cellular elements (C) accumulation of fibroblasts and macrophages (D) fibroblasts and capillaries in a loose extracellular matrix

fibroblasts and capillaries in a loose extracellular matrix (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 70-71

324

What is expected in the surgical scar of a 21 year old who underwent appendectomy one month ago? (A) Absence of dermal appendages (B) fibroblasts and capillaries in a loose extracellular matrix (C) intense intlammation and large amounts of granulation tissue (D) peak neovascularization

Absence of dermal appendages (Healing by First Intention) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp74-76

325

A 19 year old black male who got his right earlobe pierced 3 months ago developed a raised scar on that area. If examined microscopically, what should be seen? (A) dense collagen deposited in bundles (B) thickened stratum corneum of the epidermis (C) large amounts of granulation tissue (D) neutrophil aggregates with necrotic centers

dense collagen deposited in bundles (TOPNOTCH) Robbins Basic Pathology 8th ed, p 77

326

What is the cell responsible for wound contraction, especially in wounds that heal by second intention?

myofibroblast (TOPNOTCH) Robbins Basic Pathology 8th ed, p 76

327

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

328

It is a severe and generalized edema with profound subcutaneous tissue swelling.

Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81

329

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

330

Edema secondary to increased vascular permeability and inflammation.

Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82

331

The serum protein most responsible for maintaining intravascular colloid osmotic pressure.

Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83

332

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

333

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

334

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

335

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

336

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

337

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

338

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

339

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

340

It is an active process resulting from augmented blood flow due to arteriolar dilation. Affected tissue is redder than normal, because of engorgement with oxygenated blood.

Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

341

It is a passive process resulting from impaired venous rturn out of a tissue.Tissue has a blue-red color due to accumulation of hemoglobin in the affected tissue.

Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84

342

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

343

Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.

Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

344

Hemosiderin- laden macrophages

Heart-failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85

345

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

346

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

347

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

348

Extravasation of blood from vessels into the extravascular space.

Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

349

Accumulation of blood within a tissue.

Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

350

1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.

Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

351

3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.

Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

352

1-2cm subcutaneous hematomas/bruises.

Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

353

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

354

Pathologic form of hemostasis.

Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

355

It occurs after an initial injury, as a result of reflex neurogenic mechanisms.

Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

356

A potent endothelium-derived vasocontrictor.

Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

357

Receptors responsible for platelet adhesion.

GpIb receptors- platelet Von Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

358

Deficiency of GpIb receptors.

Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

359

Deficiency of GpIIb-IIIa receptors.

Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88

360

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

361

Formation of a hemostatic plug due to platelet aggregation

Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

362

Hemostasis characterized by activation of thrombin through the coagulation cascade.

Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86

363

True or false:The primary aggregation of platelets is irreversible.

False.(TOPNOTCH)

364

Two substances essential for the formation of a primary hemostatic plug.

ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87

365

True or false:Activation of the coagulation cascade and subsequent thrombin formation is reversible.

False. Irreversible(TOPNOTCH)

366

Substance that activates the coagulation proteins.

Calcium(TOPNOTCH)

367

Substance that mediates further platelet aggregation and degranulation.

ADP(TOPNOTCH)

368

Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.

TXA2(TOPNOTCH)

369

Most important initiator of the coagulation cascade.

Tissue factor(TOPNOTCH)

370

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)

371

Components of Virchow's triad?

Endothelial injuryStasisHypercoagulability(TOPNOTCH)

372

It is a major contributor to the development of VENOUS thrombi.

Stasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.94

373

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

374

Alteration in blood flow that contributes to arterial and cardiac thrombosis 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

375

Any alteration of the coagulation pathway that predisposes to thrombosis.

Hypercoagulability(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.95

376

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

377

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

378

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

379

Thrombi occuring in heart chambers or aortic lumen

Mural thrombi(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

380

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

381

Thrombi on heart valves.

Vegetations(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

382

Sterile, verrucous endocartidis occuring in patients with SLE.

Libman-Sacks endocartidis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

383

Vegetations occuring in the presence of non-infected valves in hypercoagulable states.

Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.96

384

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

385

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

386

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

387

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

388

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

389

Most common site of venous thrombosis.

Superficial or deep veins of the leg(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

390

Most common sequelae of deep venous thrombosis.

Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.97

391

Tumor-associated procoagulant release largely 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

392

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

393

Fates of a thrombus (4)

PropagationResolution/DissolutionOrganization and recanalizationEmbolization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.98

394

Embolus occluding a bifurcation in the pulmonary tree.

Saddle embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

395

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

396

A venous embolus which entered the systemic circulation through an interarterial or interventricular defect.

Paradoxical embolus(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

397

Most common symptom of pulmonary embolism.

None/ Asymptomatic (60-80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

398

Right Ventricular failure secondary to pulmonary hypertension.

Cor pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

399

Emboli in the arterial circulation.

Systemic thromboembolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

400

Most common origin of systemic thrombi.

Intracardiac mural thrombi (80%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

401

Major site of arteriolar embolization.

Lower extremities (75%)Brain (10%)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

402

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

403

Symptoms of pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia characterize what syndrome?

Fat embolism syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

404

Gas bubbles within the circulation obstructing vascular flow and causes distal ischemic injury.

Air embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

405

Amount of air in the circulation which produces clinical effects of air embolism.

>100 mL(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.99

406

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

407

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

408

Gas bubbles in the lung vasculture causing edema, hemorrhages, focal atelectasis and emphysema.

Chokes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

409

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

410

Treatment of choice for decompression sickness.

Hyperbaric compression chamber(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

411

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

412

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

413

White or red infarct?Venous occlusion

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

414

White or red infarct?Lung infarction

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

415

White or red infarct?Intestinal infarct

Red infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

416

White or red infarct?Myocardial infarction

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

417

White or red infarction?Splenic infact

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

418

White or red infarction?Wedge infarct

White infarct(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

419

The dominant histologic characteristic of infarction.

Ischemic coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

420

Histologic characteristic of brain infarcts.

Liquefactive necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

421

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

422

Most common sequalae of septic infarcts.

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.101

423

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

424

Neurons undergo irreversible damage when deprived of their blood supply for _______.

3-4 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

425

Myocardial cells undergo irreversible damage after ______ minutes of ischemia.

20-30 minutes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

426

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

427

End results of shock (3)

HypotensionImpaired tissue perfusionHypoxia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

428

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

429

This type of shock results from loss blood or plasma volume.

Hypovolemic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.102

430

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

431

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

432

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

433

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

434

Septic shock caused by gram negative bacilli.

Endotoxic shock(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.103

435

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

436

Adrenal changes in shock.

Cortical cell lipid depletion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

437

Kidney changes in shock.

Acute tubular necrosis resulting in oliguria, anuria, and electrolyte disturbances.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

438

Gastrointestinal changes in shock.

Focal mucosal hemorrhage and necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

439

Lung changes in shock.

Diffuse alveolar damage if due to bacterial sepsis and trauma.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.106

440

The main mechanism of edema in inflammatory disease is:

increase vascular permeability (TOPNOTCH)

441

Sudden death in pulmonary embolism is due to:

Acute right heart failure (TOPNOTCH)

442

Accumulation of fluid within tissues

Edema (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 113

443

Accumulation of fluid within body cavities

Effusion (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 113

444

Patient presented with pain, swelling, and tenderness of left leg. What is the mechanism of edema in this condition?

Increased hydrostatic pressure. It is caused by impaired venous return as a result of DVT.(TOPNOTCH)

445

Patient presented with dyspnea, orthopnea, easy fatigability, and bipedal edema. The mechanism of edema in this condition is.

Increased hydrostatic pressure (TOPNOTCH)

446

Patient presented with periorbital edema and ankle edema. Lab result shows high lipid levels, and low serum albumin. What is the mechanism of edema in this condition?

Reduced plasma oncotic pressure secondary to protein/albumin loss (case of Nephrotic syndrome) (TOPNOTCH)

447

Mechanism of edema in severe liver disease

Reduced plasma osmotic pressure due to reduced protein synthesis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 114

448

Mechanism of edema caused by Wuchereria bancrofti

Lymphatic obstruction(in Filariasis)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 114

449

A chronic alcoholic male presented with easy fatigability and orthopnea. Chest radiograph showed bilateral pleural effusion, while abdominal ultrasound showed ascites and small liver. What is the mechanism of effusion in this condition?

Reduced plasma oncotic pressure (TOPNOTCH)

450

Patient X presented with pitting edema of the legs, jugular vein distention, and elevated transaminases. If the liver showed a nutmeg appearance, the patient most likely have:

Chronic passive congestion of the liver secondary to congestive heart failure (TOPNOTCH)

451

Patient with left-sided heart failure may develop pulmonary edema because of what mechanism?

Increased hydrostatic pressure (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th ed., p. 114

452

Assay that assesses the function of proteins in the extrinsic pathway (factors VII, X, V, II, fibrinogen)

Prothrombin time (PT) (TOPNOTCH) RobbIns Basic Pathology, 9th ed., p. 119

453

Assay that screens the function of proteins in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen)

Partial thromboplastin time (PTT) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 119

454

Most important coagulation factor, its various enzymatic activities control diverse aspects of hemostasis

Thrombin (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 119

455

Prostacyclin, nitric oxide and adenosine diphosphatase action: platelet activation or platelet inhibition?

Platelet inhibition(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 121

456

Patient presents with epistaxis and GI bleeding. Lab result showed low platelet count. The patient may have defect in _____. Primary or secondary hemostasis?

Primary hemostasis (TOPNOTCH)

457

Patient presented with knee joint and swelling after a soccer game. However, no physical evidence of injury was noted. He is most likely suffering from what defect in hemostasis?

Secondary hemostasis. Bleeding into joints following minor trauma is particularly characteristic of hemophilia. (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 122

458

Fatal and most feared complication of severe thrombocytopenia

Intracerebral hemorrhage (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 122

459

Patient was on anticoagulation therapy for the treatment of arterial thromboembolism. However, few days later she was noted to have blood in the urine and reddish spots on her legs. Platelet count was 20. What is the pathophysiologic mechanism for this condition?

Formation of antibodies against complexes of heparin and platelet factor 4 on platelet surface resulting to platelet activation, aggregration, and consumption. (HIT)(TOPNOTCH)

460

Syndrome presenting with recurrent thromboses, repeated miscarriages, cardiac valve vegetation, and thrombocytopenia.

Antiphospholipid antibody syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.124

461

Most common site of arterial thrombi

Coronary arteries (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 125

462

True or False. Saphenous vein thrombosis often cause embolization.

False. Superficial vein thrombosis rarely embolize. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126

463

Lower extremity DVT are often associated with____. Turbulent blood flow, endothial injury or hypercoagulable state?

Hypercoagulable state (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126

464

Major cause of arterial thromboses

Atherosclerosis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 126

465

Systemic activation of thrombin leading to widespread formation of thombi in microcirculation, and consumption of platelets and coagulation factors.(TOPNOTCH)

Disseminated Intravascular Coagulation/Consumptive coagulopathy(TOPNOTCH)

466

Patient X fractures his right femur after falling from a height of 10 meters. After 2 days of hospitalization, he developed sudden onset of dyspnea, tachycardia, and restlessness. Diffuse petechial rashes was noted on his trunk. What is the most likely diagnosis?

Fat emboli (TOPNOTCH)

467

A 60 y/o female, bed-ridden, was admitted to the hospital with shortness of breath and hemoptysis. Physical examination finds the patient to be afebrile, tachycardic, calf tenderness and widely split S2. What is the most likely diagnosis?

Pulmonary embolism (TOPNOTCH)

468

A 30 year old female experienced dyspnea and edema after being injected with antibiotic. She later lost consciousness and BP rapidly declined, and later went into shock. The is due to:

Anaphylactic shock (TOPNOTCH))

469

A bedridden elderly patient experienced sudden onset of dyspnea and hemoptysis. The underlying lesion that led to this complication was most likely located in which site?

Veins lof lower extremity. It is the most common site of DVT leading to pulmonary embolism. (TOPNOTCH)

470

Exudate or transudate? Inflammation

Exudate(TOPNOTCH)

471

Exudate or transudate? Nephrotic syndrome

Transudate(TOPNOTCH)

472

Exudate or transudate? Chronic liver disease

Transudate(TOPNOTCH)

473

A stillborn baby with Turner syndrome is found to have generalized edema and a large lymphangioma around her neck at autopsy. Heart and aorta findings were unremarkable. What is the mechanism for her edema? (A) Reduced oncotic pressure (B) lymphatic obstruction (C) sodium retention (D) inflammation

Lymphatic obstruction (TOPNOTCH) Robbins Basic Pathology 8th ed. pp82-83

474

Which of the following will most likely produce pulmonary edema? (A) mitral valve stenosis (B) pulmonary hypertension (C) tricuspid stenosis (D) subpulmonic valve stenosis

mitral stenosis (TOPNOTCH) Robbins Basic Pathology 8th ed. P 84

475

In which of the following cases would cerebral edema be more generalized? (A) a meningioma on the parietal cortex (B) viral encephalitis (C) occlusion of the right cerebral artery (D) frontal abscess

viral encephalitis (TOPNOTCH) Robbins Basic Pathology 8th ed. P84

476

A patient with congestive heart failure dies. At autopsy, his liver appears grossly similar to nutmeg. Which describes an expected microscopic finding? (A) lymphocytic infiltrates in the portal tracts (B) hepatocyte necrosis around central veins (C) hepatocyte necrosis around hepatic arterioles (D) vacuolated hepatocytes and giant cell formation

hepatocyte necrosis around central veins (TOPNOTCH) Robbins Basic Pathology 8th ed., p. 85.

477

A Stage IV breast cancer patient on prolonged bed rest suddenly develops difficulty of breathing and dies. At autopsy, a blood clot in the main pulmonary artery is found. Which of the following supports a thromboembolic origin, rather than a postmortem clot? (A) pale platelet and fibrin layers alternating with darker erythrocyte-rich layers (B) gelatinous consistency, with a dark dependent portion and a yellow supernatant (C) chicken fat appearance (D) lines of Kahn

pale platelet and fibrin layers alternating with darker erythrocyte-rich layers (lines of Zahn) (TOPNOTCH) Robbins Basic Pathology 8th ed, p96

478

A pregnant patient in her third trimester is hit by a car and sustains a femoral fracture. She subsequently goes into labor and delivers a preterm baby via vaginal delivery. A few minutes later, she has sudden dyspnea, cyanosis, and dies. At autopsy, there was pulmonary edema, a ventricular septal defect, and squamous cells in the microcirculation. What is the immediate cause of death? (A) amniotic fluid embolism (B) fat embolism (C) paradoxical embolism (D) air embolism

Amniotic fluid embolism(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.100

479

In pure hypovolemic shock, which of the following organs will manifest the least cellular changes? (A) brain (B) adrenals (C) kidneys (D) lungs

Lungs (TOPNOTCH) Robbins Basic Pathology 8th ed. P 105.

480

These agents cause transmissible spongiform encephalopathies.

Prions(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 321

481

Infected cells show distinct nuclear and ill-defined cytoplasmic inclusions.

CMV infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322

482

Infected cells show glassy nuclear inclusions, frequently with a surrounding halo.

Herpesvirus infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322

483

Infected hepatocytes show diffuse granular (ground-glass) cytoplasm.

Hepatitis B viral infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 322

484

Sexually transmitted protozoan that can colonize the vagina and male urethra.

Trichomonas vaginalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 325

485

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

486

Size of microorganisms for them to be inhaled directly into the alveoli.

5 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327

487

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

488

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

489

Helminth that causes iron deficiency anemia by chronic loss of blood.

Hookworms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327

490

Helminth that depletes vitamin B12 giving rise to an illness resembling pernicious anemia.

Diphyllobotrium latum(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 327

491

Placentofetal route as a mode of transmission is also referred to as ________.

Vertical transmission(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 329

492

The ability of bacteria to cause disease.

Virulence(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 331

493

Bacterial surface molecules that bind to host cells.

Adhesins(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 332

494

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

495

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

496

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

497

Examples of antigen presenting cells.

Dendritic cellsMacrophagesB-cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334

498

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

499

Collection of neutrophils which gives rise to localized liquefactive necrosis.

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 334

500

High risk agents of bioterrorism which are easily disseminated and has high potential for mortality. An example is smallpox.

Category A(TOPNOTCH)

501

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

502

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)

503

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)

504

An 8 y/o female presented with fever, sore throat, conjunctivitis, and blotchy, reddish brown rashes on the face, trunk, and extremities. In this condition, lymphoid organs have marked follicular hyperplasia, large germinal center, and randomly distributed Warthin-Finkeldey cells. The most likely cause of this disease is:

Rubeola virus. Warthin-Finkeldey cells are multinucleate giant cells with eosinophilic nuclear and cytoplasmic inclusion bodies. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 355

505

Ulcerated mucosal lesion near the opening of Stensen duct marked by necrosis, neutrophilic exudate, and neovascularization.

Koplik spots - pathognomonic of measles (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 355

506

What protects against reinfection with measles?

Antibody-mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 355

507

Most common extrasalivary gland complication of mumps infection

Aseptic meningitis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356

508

A 10 y/o male presented with fever and bilateral swelling and pain of parotid glands aggravated by intake of sour food. What is the most likely finding in the gland interstitium in this disease?

Edematous, diffusely infiltrated by macrophages, lymphocytes, and plasma cells(Mumps) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356

509

True of false. Poliovirus infects only humans.

True(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356

510

Mode of transmission of West Nile virus

Vector-borne (mosquito) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 356

511

Viruses that most frequently establish latent infections in humans

Herpesviruses (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357

512

A 10 y/o child presented with vesicular around the lips and cervical lymphadenopathy. Histopathologic finding showed cells containing large, pink to purple intranuclear inclusion that consist of viral replication proteins. The etiologic agent for this condition is:

HSV-1 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357

513

A 28 y/o female complained of itchiness and vesicular lesions on her genitalia which later progress to ulcerations. The cause of this condition is:

HSV-2 causing genital herpes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357

514

Latent infection with this virus is seen in neuron and/or satellite cells around neurons in the dorsal root ganglia.

Varicella-Zoster Virus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 357

515

A 62 y/o male presented with painful vesicular rash in a stripe-like pattern over the left side of his trunk. On microscopy, the sensory ganglia contain a dense, predominantly mononuclear infiltrate, with herpetic intranuclear inclusions within neurons. This is a case of:

Shingles/Herpes zoster (TOPNOTCH)

516

Syndrome caused by varicella zoster virus with involvement of geniculate nucleus causing facial paralysis

Ramsay Hunt Syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 359

517

A neonate was noted to have jaundice, anemia, and hepatosplenomegaly. Patient also had microcephaly, and brain showed foci of calcification. The most likely diagnosis is:

Cytomegalic inclusion disease (caused by CMV) (TOPNOTCH)

518

Morphology of cells in CMV

Prominent intranuclear basophilic inclusion set off from nuclear membrane by a clear halo (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 359

519

A 6 y/o male presented with fever, lymphadenopathy, and hepatomegaly. Lab showed abnormal liver function test and lymphocytosis. These are the most common clinical manifestion in

CMV infection in immunocompetent host. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 360

520

Virus implicated in nasopharyngeal carcinoma and some lymphomas.

Epstein-Barr Virus. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 360

521

A 16 y/o male presented with high fever for a week, sore throat, enlarged lymph node in the posterior cervical and axillary region, and splenomegaly. Peripheral smear showed large lymphocytes with abundant cytoplasm containing clear vacuolization, an oval, indented nucleus and scattered cytoplasmic azurophilic granules (10% atypical lymphocytes). The main target cells of this condition is/are:

B cells and epithelial ells of the oropharynx. (EBV infection) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 360

522

Patient with EBV infecction will have a positive or negative heterophile antibody reaction (Monospot test)

Positive heterophile antibody reaction. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 362

523

A disorder caused by mutations in the SH2D1A gene, which encodes a signaling protein that participates in T-cell and NK-cell activation and antibody production. It is characterized by an ineffective immune response to EBV.

X-linked lymphoproliferation syndrome (Duncan Disease) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 362

524

Toxin responsibe for Ritter's disease

Exfoliative A and B toxin(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 363

525

Other term for staphylococcal scalded-skin syndrome.

Ritter's disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 363

526

A 5 y/o male was admitted due to sunburn-like rash over the entire body and evolving into fragile bullae. Presence of desquamation of the epidermis occurs at the level of the granulosa layer. What is the cause of this condition?

Staphylococcus aureus (causing Staphylococcal scalded skin syndrome) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.364

527

Coagulase-negative organism causing opportunistic infections in catheterized patients,patients with prosthetic valves and drug addicts.

Staphylococcus epidermidis (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.364

528

A 30 y/o female was noted to have dyspnea and generalized erythematous rash. She developed hypotension, renal failure, coagulopathy and liver dysfunction. History revealed the use of tampons. The most likely diagnosis is:

Toxic shock syndrome caused by S. aureus (TOPNOTCH) Robbins Basic Pathogy, 9th Ed p. 363

529

A 50 y/o female presented with a 1-week history of progressive, productive cough, and 2 days of spiking fever. Chest examination was notable for decreased breath sounds on the right lower lung field. Chest radiograph demonstrated a right lower lobe infiltrate. A blood culture was subsequently positive for gram positive cocci in pairs. what is the likely organism causing this illness?

Streptococcus pneumoniae. (TOPNOTCH)

530

An 18 y/o female presented with painful swelling in her feet, knees, and wrist. The patient had been well until 10 days prior to admission when she developed a severe sore throat accompanied by fever. What is the most likely cause of his illness?

Streptococcus pyogenes/GABHS(TOPNOTCH)

531

Surface protein present in S. pyogenes responsible for antibodies and T cells cross-reacting with cardiac proteins.

M protein. (TOPNOTCH)

532

A 6 y/o male presented with tonsillopharyngitis, circumoral pallor and erythematous, sandpaper like rashes covering the trunk and extremities. What is the most likely cause of this illness?

This is a case of Scarlet fever caused by Streptococcus pyogenes (TOPNOTCH)

533

A 35 y/o female presented with rapidly spreading erythematous cutaneous swelling on the face with rashes that are sharp, welll-demarcated , serpiginous border forming a butterfly distribution on the face. On histologic exam, there is a diffuse, edematous, neutrophilic inflammation of the dermis and dermis extending to the subcutaneous tissue. This is caused by what microorganism?

S. pyogenes (case of erysipelas) (TOPNOTCH)

534

A 43 y/o male had a two-week history of fever, chills, weakness, and anorexia following a dental extraction. On physical examination, patient had high pitched murmur best heard at the apex. Echocardiogaphy done showed an irregular vegetation attached to mitral valve. The most likely cause of endocarditis in this case is:

Streptococcus viridans. (TOPNOTCH)

535

A 26 y/o previously healthy woman develops fever within 24 hours of delivery of an infant born at 32 weeks. Vaginal swab of the mother revealed Gram positive coci. Blood culture showed organism that are catalase negative, beta-hemolytic on blood agar. The most likely cause of bacteremia is:

Streptococcus agalactiae (Group B Streptococcus) (TOPNOTCH)

536

A 5 y/o old unimmunized child presented with persistent sore throat , cough and fever for 1 week. On examination, the neck was diffusely swollen with tender, bilateral cervical adenopathy. There were hemorrhagic areas on the hard palate and necrotic grayish membrane on the soft palate and tonsils. Morphologic finding of Intense neutrophilic infiltration in the tissues with marked vascular congestion, interstitial edema, and fibrin exudation were noted. This is caused by

Corynebacterium diphtheriae (TOPNOTCH)

537

True or false. Toxin produced by Corynebacterium diphtheriae are the ones responsible for the clinical manifestations of diphtheria.

True. (TOPNOTCH)

538

A 2 mo old male was admitted to the hospital with a history of fever, vomiting, and convulsions. Birth history was unremarkable. CNS finding were suggestive of meningitis. Gram staining of CSF showed mononuclear cells with moderate Gram positive bacilli with tumbling motility. The most likely etiologic agent for this condition is:

Listeria monocytogenes. (TOPNOTCH)

539

This organism causes a painless, pruritic papule developing into a vesicle, which ruptures with remaining ulcer becoming covered with a characteristic eschar.

Bacillus anthracis. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 366

540

Lesion caused by this organism are typified by necrosis and exudative inflammation rich in neutrophils and macrophages and presence of large, boxcar-shaped gram-positive extracellular bacteria in chains.

Bacillus anthracis. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 367

541

A 48 y/o male was admitted with a 4 month history of cough with purulent sputum, hremoptysis, and fever. He wa diagnosed with AIDS 2 years earlier and was on antiretivirals irregularly. On examination, HR=98bpm, RR= 26 /min. Chest auscultation revealed decreased breath sounds on the upper third of right hemithorax. CXR demonstrated consolidation in the upper lobe of the right lung. Bronchoscopy with lavage revealed presence of branching filamentous gram positive organism. The organism described is

Nocardia asteroides. (TOPNOTCH)

542

A 17 y/o college student presented with fever, chills, headache, joint pains and myalgia. On physical examination, she is tachycardic, febrile, with mild hypotension. There was noted petechial rashes on her trunk and legs. Gram stain revealed gram-negative coffee-bean shaped diplococci. The most likely cause of this condition is

Neisseria meningitidis. (TOPNOTCH)

543

A 25 y/o female complained of severe pelvic pain and fever. A greenish yellow cervical discharge was detected on physical examination. Gram negative diplococci were isolated from the endocervical swab. What is the most likely cause?

Neisseria gonorrhea (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 368

544

A 2-month old infant was admitted with fever, lymphocytosis, and bouts of violent coughing that often end in vomiting. Blood culture showed small gram-negative rods. The most likely diagnosis is:

Pertussis (TOPNOTCH)

545

Mechanism on how B. pertussis toxin impair host defenses.

Inhibits phagocytosis, inhibits neutrophils and macrophages and paralyzing cilia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 369

546

Bacteria causing laryngotracheobronchitis with features of bronchial mucosal erosion, hyperemia, and copious, mucopurulent exudate. It may present with hypercellularity and enlargement of mucosal lymph follicles and peribronchial lymph nodes along side a marked peripheral lymphocytosis (up to 90%)

Bordetella pertussis. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 369

547

A 67 y/o female was admitted with a 1 week history of cough and pleuritic chest pain. Physical examination revealed tachypnea, rhonchi in both upper lobes. The next day, patient's condition deteriorated and had severe respiratory distress. Autopsy revealed extensive bilateral bronchopneumonia and necrosis in the terminal airways in a fleur-de-lis pattern, with striking pale necrotic centers and red, hemorrhagic peripheral areas. The most likely cause of this disease is:

Pseudomonas aeruginosa (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 369

548

An opportunistic aerobic gram-negative bacillus that is frequent, deadly pathogen of people with cystic fibrosis, severe burns, or neutropenia.

Pseudomonas aeruginosa (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 369

549

A 32 y/o female on chronic immunosuppressive therapy was admitted for the management of her abdominal wound infection. On hospital day 18, patient developed erythematous papulovesicules on the left upper chest and right medial leg progressing rapidly to necrotic and hemorrhagic oval ulcers. What organism most likely cause this condition?

Pseudomonas aeruginosa (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 370

550

Organism that causes lymph node enlargement (buboes) with distinct histologic features of massive proliferation of organism, early appearance of effusions with few inflammatory cells, necrosis of tissues and blood vessels with hemorrhage and thrombosis, and neutrophilic infiltrates in necrotic areas.

Yersinia pestis (TOPNOTCH) Robbins Pathologic Basis of Disease, 9th Ed p. 370

551

A 25 y/o male initially presented with a tender erythematous papule on the penis which produce an irregular, painful, non-indurated ulcer over several days. The base of the ulcer is covered by shaggy, yellow-gray exudate. Microscopically, the ulcer contains a superficial zone of neutrophilic debris and fibrin, and an underlying zone of granulation tissue containing areas of necrosis and thrombosis. This infection is caused by:

Haemophilus ducreyi (causing Chancroid) (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 370

552

A 45 y/o sexually active male presented with a 3-month history of few painless ulcerated lesions on the penis and scrotum. The painless nodules slowly evolved to red ulcerated lesions over 1 month. Physical examination revealed multiple, raised, beefy-red nontender round ulcers on the shaft of penis and scrotum. The ulcers had clean friable granulating bases. Microscopic examination with Giemsa stain revealed numerous encapsulated coccobacilli in macrophages. The most likely diagnosis is:

Granuloma inguinale/donovanosis (Klebsiella granulomatis) (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 370

553

A 25 y/o male initially presented with a tender erythematous papule on the penis which produce an irregular, painful, non-indurated ulcer over several days. The base of the ulcer is covered by shaggy, yellow-gray exudate. Microscopically, the ulcer contains a superficial zone of neutrophilic debris and fibrin, and an underlying zone of granulation tissue containing areas of necrosis and thrombosis. This infection is caused by:

Klebsiella granulomatis (TOPNOTCH)

554

True or false. A positive tuberculin test differentiates active disease from infection.

False. A positive tuberculin test signifies T-cell mediated immunity to mycobacterial antigen. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 371

555

How many days or weeks after mycobacterium infection will it develop delayed hypersensitivity to M. tuberculosis as detected by Mantoux skin test?

2-4 weeks (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 371

556

The critical mediator that enables macrophages to contain M. tuberculosis infection by stimulating maturation of phagolysosome, stimulation of expression of inducible nitric oxide synthase and mobilization of defensins against bacteria.

IFN gamma(TOPNOTCH) Robbins Pathologic Basis of Disease, 9th Ed p. 372

557

True or False. Immunity to M. tuberculosis is primarily mediated by TH1 cells.

True. TH1 cells stimulate macrophages to kill the bacteria (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 373

558

Secondary pulmonary tuberculosis classically involves what part of the lungs?

Apex of the upper lobes of one or both lungs. (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 373

559

True or false. The absence of characteristic granulomas in tissues in HIV-positive patients precludes (rule out) the diagnosis of tuberculosis.

False. Atypical features of TB in HIV-positive patients include increase frequency of false-negative sputum smears, tuberculin tests, and absence of granuloma, particularly in the late stages of HIV.(TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 374

560

A 1 to 1.5 cm area of gray-white inflammation with consolidation in primary tuberculosis.

Ghon focus (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 374

561

Most frequent presentation of extrapulmonary tuberculosis.

Lymphadenitis (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 376

562

A 42 y/o male nonsmoker with AIDS began to experience cough, mild hemoptysis, and progressive dyspnea. CD4 cell count was 45 cell/ul. A chest radiograph revealed hilar adenopathy and perihiral infiltrates. AFB smear was negative. Bronchoscopy was done and microscopic finding showed an abundnat acid-fast bacilli within macrophages. The organism causing the illness is:

Mycobacterium avium complex (TOPNOTCH)

563

Pattern of leprosy presenting with dry, scaly skin lesions that lack sensation and often have assymetric involvement of large peripheral nerves.

Tuberculoid leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377

564

Pattern of leprosy causing symmetric skin thickening and nodules with widespread invasion of mycobacteria into Schwann cells and into endoneural and perineural macrophages damaging the peripheral nervous system.

Lepromatous leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377

565

Pattern of leprosy characterized by TH1 response associated with production of IL-2 and IFN gamma

Tuberculoid leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377

566

Pattern of leprosy associated with weak TH1 response and in some cases increase in TH2 response resulting to weak cell-mediated immunity.

Lepromatous leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377

567

A 30 y/o male presented with a flat, red, anesthetic skin lesions on his left thigh extending to his knee which had been present for 2 years. These lesions enlarged and develop irregular shapes with indurated, elevated, hyperpigmented margins and depressed pale centers. On microscopic examination, all sites of involvement have granulomatous lesions. Bacilli are almost never found. This is a case of__.

Tuberculoid leprosy/Paucibillary leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 377

568

This disease presents with macular, papular, or nodular lesion on the face, ears, wrists, elbows and knees, progressing to coalescence of nodular, anesthetic lesions. (+) leonine facies. Morphologic findings of this disease reveals skin and peripheral nerve lesions containing large aggregates of lipid laden macrophages (lepra cells) often filled with asses (globi) of acid fast bacilli.

Lepromatous/multibacillary leprosy (TOPNOTCH) Robbins Basic Pathology, 9th Ed p. 378

569

A 19 y/o male presents to the clinic because of a lesion on his penis. Genital exam showed a red, solitary, raised , indurated, non-tender lesion on the ventral side of his penis. Neurologic exam was within normal limits. What is the most likely diagnosis?

Primary syphilis(chancre)(TOPNOTCH)

570

A 34 y/o male presented with circular violaceous, papulosquamous lesions on his palms, soles, and entire body. He admitted having unprotected sex with his new partner 6 weeks before the onset of his lesions. Broad-based plaques were noted in the inner thighs and anogenital region. Silver-gray erosions were noted on the pharyngeal and genital area. What is the most likely diagnosis(and stage)?

Secondary syphilis. (TOPNOTCH)

571

Characteristic of all stages of syphilis

Proliferative endarteritis. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 379

572

Serologic test/s that are sensitive for secondary syphilis

Both non-treponemal antibody tests and antitreponemal antibody tests. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 379

573

Serologic tests that are very sensitive for tertiary and latent syphilis.

Treponemal tests (Fluorescent Treponemal antibody absorption test, T pallidum enzyme immunoassay test) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 379

574

Most frequent involvement of tertiary syphilis

Aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 380

575

A 39 y/o male presented with a white-gray and rubbery mass on the forehead that had been slowly progressive over the previous 6 years. Biopsy showed that lesion have centers of coagulated, necrotic material and margins composed of plump, palisading macrophages and fibroblasts surrounded by large number of mononuclear leukocytes. What is the lesion described?

Syphilitic gumma (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381

576

A neonate presented with snuffles, bullous eruption of the palms and soles, saddle nose deformity, and anterior bowing of the tibia. What is the most likely cause?

T. pallidum (causing congenital syphilis) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381

577

Late manifestations of congenital syphilis (triad)

Interstitial keratitis, Hutchinson teeth, and eighth-nerve deafness (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381

578

Disseminated infection from this microorganism cause secondary skin lesions, lymphadenopathy, migratory joint and muscle pain, cardiac arrythmias, and meningitis.

Borrelia burgdorferi (causing congenital syphilis) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 381

579

A 60 y/o male presented with severe pain and edema of left foot and leg, bullous vesicles, and foul-smelling wound discharge 3 days after sustaining a crushing injury. Crepitations were noted over the inflamed muscles. What is the most likely cause of this condition?

Clostridium perfringens (causing gas gangrene/clostridium myonecrosis) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 383

580

Most common sexually transmitted bacterial disease

Chalmydia trachomatis infection(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 383

581

A 28 y/o male presented with painful, swollen lymph node at the inguinal area, associated with fever, and myalgia. Two weeks prior, patient recalled had a small, painless pustule on the scrotum. The most likely diagnosis is:

Lymphogranuloma venereum (TOPNOTCH)

582

Lymph node involvement in this condition is characterized by a granulomatous inflammatory reaction associated with irregularly shaped foci of necrosis containing neutrophils (stellate abscess).

Lymphogranuloma venereum (caused by Chlamydia trachomatis)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 384

583

Presents with dysphagia and retrosternal pain; endoscopic findings of white plaques and pseudomembranes resembling oral thrush on the esophageal mucosa.

Candida esophagitis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 386

584

Associated with intense itching and thick, curd-like discharge common in women who are diabetic, pregnant, or on OCP.

Candida vaginitis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 386

585

A 70 y/o male, with prior history of TB, presents with occassional cough, hemoptysis, fever, and respiratory distress. CXR showed a mass surrounded by a crescentic rim on the right upper lobe within a cavitary lesion. Biopsy done revealed no malignant cell. This is most likely a case of:

Pulmonary aspergilloma (TOPNOTCH)

586

A 60 y/o diabetic female presented with fever and left periorbital pain and sweling. A nasal eschar involving the enitre nose with discharge from the nasal cavity. Biopsy from the eschar showed foci of nonseptate fungal hyphae and hyphal branches at right angles. The most likely cause of her condition is:

Mycormycetes (TOPNOTCH)

587

The etiology of cerebral malaria, wherein brain vessels are plugged with parasitized red vessels. Around the vessels are ring hemorrhages related to local hypoxia. (TOPNOTCH)

Plasmodium falciparum (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 392

588

What is the major cause of sudden death in Chagas disease?

Cardiac arrythmia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 395

589

The causative agent of Chagas disease

Trypanosoma cruzi (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 394

590

Nematode that causes patchy interstitial myocarditis characterized by many eosinophils and scattered giant cells.

Trichinella spiralis (TOPNOTCH) Robbins Basic Pathology, 9th ed., 397

591

Pathogenesis of hepatic fibrosis in schistomiasis

Eggs carried into the parenchyma cause severe chronic inflammation; TH2 response and activated macrophages. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 398

592

Pipe-stem fibrosis of the liver, portal enlargement without intervening regenerative nodules, and granuloma are associated with infection caused by:

Schistosoma mansoni and S. japonicum. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 398

593

A chronic carrier state of typhoid fever is most likely due to persistence of the organism in the:

Gall bladder (TOPNOTCH)

594

A 38 y/o man with AIDS present with deteriorating mental status. Lumbar tap was done. CSF was stained with india ink and mucicarmine revealed capsulated yeasts that stain bright red. What is the most likely diagnosis?

Cryptococcosis (TOPNOTCH)

595

A 53 year old woman presents with 5 days of productive cough and high grade fevers. Crackles were auscultated at the left lung. Sputum cultures grew Streptococcus pneumoniae. Her lungs will show which histologic picture? (A) suppurative inflammation with sparing of alveolar septa (B) thickened alveolar septa with mononuclear infiltrates (C) lysis of alveolar walls and coalescing abscesses (D) epithelioid macrophages and giant cells

suppurative inflammation with sparing of alveolar septa (TOPNOTCH)Robbins Basic Pathology, 8th Ed p334-335

596

A 44 year old HIV-positive man is admitted for diarrhea of one month duration. Fecalysis did not show parasitic ova or cysts. Colonoscopy showed a diffusely erythematous mucosa. Biopsy was performed which showed sheets of macrophages filled with filamentous structures that were bright pink on acid fast staining. The likely organism is (A) Cryptosporidium parvum (B) Isospora belli (C) Mycobacterium bovis (D) Mycobacterium avim-intracellulare

Mycobacterium avium-intracellulare dx Infectious mononucleosis case (TOPNOTCH) pp326-327

597

This term refers to protection against infections.

Immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108

598

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

599

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

600

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

601

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

602

Type of adaptive immunity mediated by T lymphocytes.

Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109

603

Mediated by antibodies and is effective against extracellular microbes.

Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109

604

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

605

Reaction of immune system against one's own cells.

Autoimmunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.119

606

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

607

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

608

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

609

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

610

Indicate type of hypersensitivity reaction:SLE

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

611

Indicate type of hypersensitivity reaction:Multiple sclerosis

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

612

Indicate type of hypersensitivity reaction:Transplant rejection

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

613

Indicate type of hypersensitivity reaction:Anaphylaxis

Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

614

Indicate type of hypersensitivity reaction:Goodpasture syndrome

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

615

Indicate type of hypersensitivity reaction:Serum sickness

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

616

Indicate type of hypersensitivity reaction:Arthus reaction

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

617

Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

618

Indicate type of hypersensitivity reaction:Allergies

Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

619

Indicate type of hypersensitivity reaction:Type I DM

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

620

Indicate type of hypersensitivity reaction:Tuberculosis

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

621

Indicate type of hypersensitivity reaction:Bronchial asthma

Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

622

Indicate type of hypersensitivity reaction:Acute rheumatic fever

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

623

Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

624

Indicate type of hypersensitivity reaction:Polyarteritis nodosa

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

625

Indicate type of hypersensitivity reaction:Rheumatoid arthritis

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

626

Indicate type of hypersensitivity reaction:Inflammatory bowel disease

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

627

Indicate type of hypersensitivity reaction:Tuberculin reaction

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

628

Indicate type of hypersensitivity reaction:Reactive arthritis

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

629

Indicate type of hypersensitivity reaction:Graves disease

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

630

Indicate type of hypersensitivity reaction:Acute rheumatic fever

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

631

Indicate type of hypersensitivity reaction:Myasthenia gravis

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

632

Indicate type of hypersensitivity reaction:Insulin resistant DM

Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

633

Indicate type of hypersensitivity reaction:Pernicious anemia

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

634

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

635

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

636

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

637

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

638

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

639

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

640

SOAP BRAIN MD mnemonic for SLE stands for?

SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140

641

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

642

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

643

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

644

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

645

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

646

Cytokine which plays a central role in the pathogenesis of RA.

TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146

647

A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.

Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148

648

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

649

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

650

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

651

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

652

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

653

Autosomal recessive form of SCID is due to deficiency of what enzyme?

Adenosine deaminase (ADA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154

654

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

655

HIV viral surface proteins essential for viral entry into cells.

gp41 and gp120(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.157

656

A form of pneumonia in HIV patients caused by a yeast-like fungus.

Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)

657

Main cellular target of HIV.

CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.158

658

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

659

Most common secondary infection of the CNS in patients with AIDS.

Toxoplasmosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163

660

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

661

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

662

Cells of immune system

T- and B-lymphocytes, dendritic cells, macrophages, natural killer cells, innate lymphoid cells. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 190

663

Tissues of the immune system

Bone marrow, thymus, lymph nodes, spleen, mucosal and cutaneous lymphoid tissue. (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 193

664

The most important antigen-presenting cells for initiating T-cell responses against protein antigens

Dendritic cells(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 191

665

A 48 y/o male patient underwent kidney transplant suddenly developed bloody urine few hours after the procedure. Nephrectomy was done and revealed a cyanotic, mottled, and flaccid kidney and necrotic kidney cortex. There is neutrophilic accumulation in the arterioles, glomeruli, and peritubular capillaries. Glomeruli undergo thrombotic occlusion of capillaries and fibrinoid necrosis in arterial walls. The most likely diagnosis is:

Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233

666

A 45 y/o female presented with signs of kidney failure 2 months after her renal transplant. Immunohistochemical staining reveals both CD4+ and CD8+ lymphocytes. Morphologic findings showed an extensive interstitial inflammation with infiltration of tubules and focal tubular injury. This is a case of:

Acute cellular (T-cell mediated) rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 234

667

Preformed antidonor antibodies present in the circulation of the recipient is implicated in what type of rejection pattern?

Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233

668

A 30 y/o male developed oliguria and subsequent renal failure 3 weeks after an uneventful kidney transplant. Renal findings showed inflammation of glomeruli and peritubular capillaries, deposition of complement breakdown and focal small vessel thrombosis. This is a case of:

Acute antibody-mediated rejection (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 234

669

A 24 y/o female diagnosed with renal failure underwent renal transplant. Four years later, increasing levels of creatinine was noted, and biopsy showed an interstitial fibrosis and tubular atrophy, glomerulopathy with duplication of basement membrane, and multilayering of peritubular capillary basement membranes. Interstitial mononuclear cell infiltrates, NK cells and plasma cells were also noted. This is a case of:

Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.234

670

The result of hypoplasia or lack of thymus in DiGeorge Syndrome

Variable loss of T-cell mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.241

671

The hallmark of AIDS

Profound immune deficiency, primarily cell-mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 245

672

A 32-year old female, presents to the clinic with symptoms of fatigue, joint pains, and malar rash. CBC revealed anemia and low platelet count. The most likely diagnosis is:

Systemic Lupus Erythematosus (TOPNOTCH)

673

The hallmark of SLE

Production of autoantibodies (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 218

674

The fundamental defect in SLE

Failure of mechanisms that maintain self-tolerance (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 219

675

Most common manifestation of SLE

Hematologic manifestation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 218

676

Most common hematologic finding in SLE

Anemia(TOPNOTCH)

677

Most common and most severe form of lupus nephritis

Diffuse lupus nephritis/Class IV(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 224

678

The most common causes of death in SLE

Renal failure and intercurrent infections (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 225

679

Cytokine most firmly implicated in the pathogenesis of Rheumatoid arthritis

TNF (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 1210

680

Major cytokine produced by TH1, stimulates macrophage activation and IgG antibody production. Plays a role in autoimmune and other chronic inflammatory diseases.

IFN-gamma(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198

681

The dominant immune reactions of these subset of helper cells are the stimulation of IgE production and activation of mast cells and eosinophils.

TH2(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198

682

These are the mediators of adaptive immunity and the only cells that produce specific and diverse receptors for antigens

Lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 199

683

Immunity mediated by antibodies and is effective against extracellular microbes in the circulation and mucosal lumens.

Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 9th ed p. 200

684

Type of immunity design to combat phagocytosed microbes and microbes in the cytoplasm of infected cells.

Cell-mediated immunity(TOPNOTCH)Robbins Basic Pathology, 9th ed p. 200

685

These are cells the help B cells to make antibodies, activate macrophages to destroy ingested microbes, stimulate recruitment of leukocytesand regulate all immune responses to protein antigens.

CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200

686

These are cells that express antigens in the cytoplasm that are seen as foreign, such as virus-infected and tumor cells.

CD8+ cytotoxic T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200

687

The most potent vasoactive and spasmodic agents causing increasing vascular permeability and causing bronchial smooth muscle contraction.

Leukotrienes C4 and D4(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 203

688

A lipid mediator produced by some mast cell populations, not derived from arachidonic acid, causing platelet aggregation, increased vascular permeability, and vasodilation.

Platelet-activating factor(PAF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 203

689

True or False. Atopic individuals tend to have higher serum IgE levels and more IL-4 producing Th2 cells.

True. (TOPNOTCH)

690

This disease presents with nephritis and lung hemorrhage due to complement and Fc receptor-mediated inflammation due to antibody against noncollagenous protein in basement membranes of kidney glomeruli and lung alveoli.

Goodpasture syndrome(TOPNOTCH)Robbbins Basic Pathology, 9th ed., p. 206

691

This disease causes demyelination in CNS is perivascular inflammation due to inflammation mediated by TH1 and TH17 cytokines, myelin destruction by activated macrophages.

Multiple sclerosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 209

692

Type of immunity primarily affected by AIDS

Cell-mediated immunity(TOPNOTCH)

693

Mucocutatnous ulcerations involving the mouth, esophagus, external genitalia, and perianal region in AIDS patient may be caused by

Herpes simplex virus infection(TOPNOTCH)

694

An 18 year old female presents with a day-old circular erythematous plaque with vesicles on her neck. She relates a history of wearing a new metallic pendant three days ago, and has had a similar history with other metallic jewelry. If the plaque is biopsied, which inflammatory cell is expected to predominate? (A) neutrophil (B) eosinophil (C) mast cell (D) lymphocyte

Lymphocyte (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp128-130

695

An 8 year old male with a strep throat four weeks ago develops tea-colored urine. A kidney biopsy showed hypercellular glomeruli with neutrophils. Electron microscopy showed subepithelial "humps." These findings are caused by (A) antibodies against glomerular basement membrane (B) antibodies against endothelium (C) immune complex deposition (D) T-cell mediated recruitment of neutrophils

immune complex deposition (TOPNOTCH) Robbins Basic Pathology, 8th ed. P126

696

A 5 year old female with a strep throat two weeks ago develops joint pains and fever. Auscultation revealed a friction rub. What type of hypersensitivity is responsible?

Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

697

A 33 year old female presents with morning stiffness of the PIP and MCP joints of the hands. On workup, she is positive for rheumatoid factor. Which of the following is expected in the involved joints? (A) synovial hypertrophy with dense lymphoid aggregates (B) synovial atrophy with epithelioid macrophages (C) synovial hypertrophy devoid of leukocytes (D) synovial atrophy with dense lymphoid aggregates

synovial atrophy with dense lymphoid aggregates (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp145-146

698

A 50 year old female with chronic red eye is diagnosed with keratoconjunctivitis sicca and is referred to by her ophthalmologist for bilateral infraauricular masses. Her oral mucosa has multiple fissures. Biopsy of the infraauricular masses will likely show (A) epithelial and myoepithelial cells admixed with chondroid stroma (B) lymphoplasmacytic infiltration with ductal hyperplasia (C) basaloid cells in cribriform structures (D) highly pleomorphic epithelial cells and numerous atypical mitoses

lymphoplasmacytic infiltration with ductal hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp148-149

699

Patients with diffuse scleroderma have sclerotic atrophy of the skin. Which other organ is most commonly involved? (A) kidneys (B) heart (C) lungs (D) gastrointestinal tract

gastrointestinal tract (90% of patients) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 149-150

700

A 22 year old male has unprotected sex and develops generalized lymphadenopathy five days later. The following month, he tests positive on HIV screening. Excision biopsy of one of his lymph nodes would likely show (A) marked follicular hyperplasia (B) epithelioid macrophages and giant cells (C) diffuse infiltration by atypical mononuclear cells (D) subcapsular necrosis

marked follicular hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 165

701

A 68 year old female with multiple myeloma dies of acute renal failure. At autopsy, her kidneys and liver were pale gray, with waxy cut sections, while her spleen showed tapioca-like granules. On histology, these organs show deposits that (A) have empty vacuoles that uptake Sudan black (B) are infiltrated by neutrophils and histiocytes (C) will fluoresce an apple green color when stained with Congo red (D) are bluish, with concentric lamellations

will fluoresce an apple green color when stained with Congo red (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 169-170

702

This term literally means "new growth".

Neoplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

703

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

704

Study of tumors.

Oncology(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

705

Benign or malignant?Localized

Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

706

Benign or malignant?Amenable to surgical removal

Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

707

Benign or malignant?Invades and destroys adjacent tissues.

Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

708

What are the two basic components of tumors?

Parenchyma and Stroma(TOPNOTCH)

709

Benign or malignant?Metastasis

Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

710

This component of tumors largely determines its biologic behavior.

Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

711

This component of tumors determines the name of the growth.

Parenchyma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.174

712

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

713

Benign or malignant?Fibroma

Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

714

Benign or malignant?Chondroma

Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

715

Benign or malignant?Adenoma

Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

716

Benign or malignant?Hepatoma

Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

717

Benign or malignant?Papilloma

Benign(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

718

Malignant neoplasms arising in mesenchymal tissue or its derivatives.

Sarcomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175

719

Benign tumor arising in fibrous tissue is called?

Fibroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175

720

A benign cartilagenous tumor is called?

Chondroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175

721

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

722

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

723

A mass that projects above a mucosal surface to form a macroscopically visible structure.

Polyps(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175

724

A cancer of fibrous tissue origin.

Fibrosarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175

725

Malignant neoplasms of epithelial cell origin.

Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.175

726

Carcinoma of squamous cell origin.

Squamous cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

727

Benign or malignant?Lymphoma

Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

728

Benign or malignant?Seminoma

Malignant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

729

The extent to which neoplastic cells resemble their normal forebears morphologically and functionally.

Differentiation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.176

730

This is considered a hallmark of malignancy, which literally means "to form backward".

Anaplasia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.177

731

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

732

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

733

Defined as dysplastic changes which involve the entire thickness of the epithelium.

Carcinoma -in- situ(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178

734

True or false?Dysplasia always progress to cancer.

False(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.178

735

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

736

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

737

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

738

Methods of dissemination of malignant neoplasms? (3)

SeedingLymphatic spreadHematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180

739

This is the mode of dissemination of cancers of the ovary and CNS.

Spread by seeding(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180

740

This is the mode of dissemination more typical of carcinomas.

Lymphatic spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180

741

This is the mode of dissemination more typical of sarcomas.

Hematogenous spread(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.180

742

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

743

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

744

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

745

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

746

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

747

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

748

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

749

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

750

Inherited gene : Cancer syndromeRB gene :__________

Retinoblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

751

Inherited gene : Cancer syndromep53 : ______________

Li Fraumeni Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

752

Inherited gene : Cancer syndrome__________ : Familial Adenomatous Polyposis / Colon CA

APC Gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

753

Inherited gene : Cancer syndrome_________ : Breast on Ovarian Tumors

BRCA 1 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

754

Inherited gene : Cancer syndrome_________ : Breast Cancer only

BRCA 2 gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

755

Inherited gene : Cancer syndromeRET gene : _________

Multiple Endocrine Neoplasia 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

756

Inherited gene : Cancer syndrome__________ : Colon cancer

kras gene(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.184

757

Normal cellular genes whose products promote cell proliferation.

Proto-oncogenes(TOPNOTCH)

758

Normal cellular genes whose products promote cell proliferation.

Proto-oncogenes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.188

759

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

760

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

761

These substances require metabolic conversion to be carcinogenic.

Indirect - acting carcinogens(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.209

762

These substances stimulate proliferation of the mutated cells.

Promoters(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.210

763

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

764

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

765

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

766

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

767

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

768

Which hepatitis virus leads to hepatocellular carcinoma?

HBV, HCV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213

769

This is the first bacterium to be classified as a carcinogen.

Helicobacter pylori(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.213

770

What type of cancer can be caused by H.pylori?

Gastric adenocarcinoma Gastric MALT lymphomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.214

771

These are benign epithelial neoplasms, growing on any surface that produce microscopic or macroscopic finger-like fronds.

Papillomas(TOPNOTCH)

772

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

773

Single most important defining characteristic of malignancy

Metastasis (TOPNOTCH)

774

A biopsy of the stomach reveals an area of normal appearing pancreatic tissue. This is an example of what type of lesion?

Choristoma (TOPNOTCH)

775

Bronchogenic carcinoma tends to metastasize where?

Adrenals and brain (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 274

776

The most frequent form of cancer in males

Prostate cancer (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 276

777

The most frequent form of cancer in females

Breast cancer (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 276

778

Most common cause of cancer death in both male and female

Lung cancer (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 276

779

Most important infectious agent associated with cervical carcinoma and head and neck cancers.

Human papilloma virus (TOPNOTCH)

780

Leukoplakia may give rise to what type of carcinoma?

Squamous carcinoma (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 279

781

Most common type of abnormality involving proto-oncogenes in human tumors

Point mutations of RAS family genes(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 286

782

Activation of ABL nonreceptor tyrosine kinase by chromosomal translocation and creation of BCR-ABL fusion gene is associated with what type of leukemia

CML, ALL(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 290

783

"Guardian of the genome", a tumor suppressor gene that regulates cell cycle progression, DNA repair, cellular senescence, and apoptosis, and the most frequently mutated gene in human cancers

TP53 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 293

784

"Gatekeeper of colonic neoplasia"; tumor suppressor that function by downregulating growth-promoting signaling pathways.

APC (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 296

785

Steps in invasion of cancer cells

Dissociation of cancer cells-Degradation of ECM-Attachment to novel ECM components-Migration and invasion of tumor cells. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 306

786

Autosomal dominant disorder characterized by familial carcinomas of the colon predominantly cecum and proximal colon.

Hereditary nonpolyposis colon cancer (HNPCC) syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 314

787

Syndrome causing colon cancer resulting from defects in a family of genes encoding a group of proteins that work together to carry out DNA mismatch repair.

Hereditary nonpolyposis colon cancer (HNPCC) syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 314

788

The increased incidence of skin cancer following UV light exposure associated with xeroderma pigmentosus is caused by:

Disorder of DNA repair/inability to repair pyrimidine dimers(HNPCC) syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 314

789

Pathogenesis of this tumor involves the translocation resulting to overactivity of MYC gene

Burkitt lymphoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 317

790

Philadelphia chromosome is characteristic of what type of leukemia

CML(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 317

791

An important cause of benign warts, cervical cancer, and oropharyngeal cancer

HPV (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 329

792

Implicated in gastric adenocarcinoma and MALT lymphoma

H. pylori(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 329

793

Cytokine implicated in cancer cachexia

TNF-alpha(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330

794

The most common endocrinopathy ; usually seen in small-cell lung carcinoma

Cushing syndrome(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330

795

The most common paraneoplastic syndrome related to cancer; seen in patients with squamous cell carcinoma

Hypercalcemia(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330

796

The most important humoral factor associated with paraneoplastic hypercalcemia of malignancy.

PTHRP(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 330

797

Tumor marker:Medullary carcinoma of thyroid

Calcitonin(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337

798

Tumor marker:Trophoblastic tumors

Human chorionic gonadotropin(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337

799

Tumor marker: liver cell cancer and nonseminomatous germ cell tumor

Alpha fetoprotein(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337

800

Tumor markers: prostate cancer

PSA and prostatic acid phosphatase (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.337

801

Tumor marker: pheochromocytoma

Catecholamine(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337

802

Tumor marker: ovarian cancer

CA-125(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 337

803

Cervical biopsy of a 35 y/o female with cervical erosion shows squamous epithelium that exhibit atypia, pleomorphism, disorderly spatial arrangement. This adaptive response is:

Dysplasia (TOPNOTCH)

804

RAS oncogene qualitatively changes function of proto-oncogene through which form of mutation?

Point mutations (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 286

805

Chemical carcinogen implicated in the causation of mesothelioma

Asbestos(TOPNOTCH)

806

A 56 year old woman with a breast mass has a preoperative diagnosis of invasive ductal carcinoma by core needle biopsy, with no palpable axillary lymph nodes. She undergoes surgery where her breast mass is injected with a blue dye, and the first axillary node that takes up the dye is submitted to pathology. Which method is next done on the node if the surgeon wants to know within minutes if there is metastasis? (A) fine needle aspiration (B) frozen section (C) immunohistochemistry (D) flow cytometry

frozen section (TOPNOTCH)Robbins Basic Pathology, 8th Ed, p 220

807

A 25 year old male with an intranasal mass undergoes a tissue biopsy that shows malignant round cells. The pathologist needs to know if it is an undifferentiated carcinoma or a lymphoma. What can be done to differentiate? (A) Frozen section (B) Immunohistochemistry (C) Flow cytometry (D) serologic tumor markers

Immunohistochemistry (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp220-221

808

A 12 year old female presents with pallor and gum bleeding. A complete blood count with peripheral smear shows numerous blasts. What is needed to be done on her bone marrow for a more precise diagnosis? (A) frozen section (B) papanicolau smear (C) aspiration and flow cytometry (D) serologic tumor markers

aspiration and flow cytometry (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 221

809

These disorders are derived from one's parents, transmitted through gametes through the generations, and are therefore familial.

Hereditary disorders(TOPNOTCH)

810

This term literally means "present at birth".

Congenital(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227

811

This term refers to permanent changes in the DNA.

Mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227

812

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

813

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

814

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

815

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

816

These mutations are characterized by amplification of a sequence of three nucleotides.

Trinucleotide repeat mutations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227

817

Disease characterized by CGG trinucleotide repeats.

Fragile X Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.227

818

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

819

Genetic mutation in Huntington's disease?

CAG trinucleotide repeats(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.229

820

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

821

Genetic mutation found in myotonic dystrophy?

CTG Trinucleotide repeats(TOPNOTCH)

822

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)

823

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)

824

A point mutation wherein a purine is replaced by a pyrimidine or vice versa.

Transversion(TOPNOTCH)

825

Diseases caused by single gene defects are called?

Mendelian Disorders(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228

826

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

827

The presence of many allelic forms of a single gene is called _______.

Polymorphism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228

828

This occurs when one gene influences or leads to multiple phenotypic traits.

Pleiotropy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.228

829

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

830

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

831

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

832

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

833

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

834

Integral component of elastic fibers defective in Marfan Syndrome.

Fibrillin 1(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230

835

Fibrillin 1 is encoded by what gene?

FBN1 gene (chromosome 15q21)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.230

836

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

837

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)

838

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

839

Enzyme deficient in classic PKU.

Phenylalanine hydroxylase (PAH)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.234

840

An autosomal recessive disorder of galactose metabolism characterized by jaundice, liver damage, cataracts, neural damage, vomiting and diarrhea.

Galactosemia(TOPNOTCH)

841

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

842

Enzyme deficient in galactosemia.

Galactose-1-phosphate uridyltransferase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.235

843

Lysosomal storage disease due to deficiency of glucosylceramidase.

Gaucher disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236

844

Lysosomal storage disease due to deficiency of B-Hexosaminidase A.

Tay-Sachs disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236

845

Lysosomal storage disease due to deficiency of a-Galactosidase A.

Fabry disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236

846

Lysosomal storage disease due to deficiency of Sphingomyelinase.

Niemann-Pick disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.236

847

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

848

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

849

What do you call the pathognomonic cell characterized by "wrinkled tissue paper" cytoplasmic appearance.

Gaucher cell(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.238

850

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

851

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

852

An X-linked mucopolysaccharidosis which is due to a deficiency of L-iduronate sulfatase. Symptoms are similar to Hurler syndrome, but without corneal clouding.

Hunter syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.239

853

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

854

von Gierke's disease is due to a deficiency of what enzyme?

Glucose-6-phosphatase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240

855

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

856

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

857

Enzyme deficient in McArdle syndrome.

Muscle phosphorylase(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.240

858

These disorders may result from alterations in the number or structure of chromosomes and may affect autosomes or sex chromosomes.

Cytogenetic disorders(TOPNOTCH)

859

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

860

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

861

This refers to a lack of one chromosome of the normal complement (e.g. XO).

Monosomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244

862

This refers to the presence of three copies of a particular chromosome, instead of two.

Trisomy(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244

863

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

864

This mechanism implies transfer of a part of one chromosome to another chromosome.

Translocation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243

865

This mechanism involves loss of a portion of a chromosome.

Deletion(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.243

866

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

867

Down syndrome is also called _________

Trisomy 21(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245

868

Trisomy 18 is also called ________ syndrome.

Edwards syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245

869

Trisomy 13 is also called _________ syndrome.

Patau syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.244

870

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

871

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

872

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

873

Syndrome characterized by congenital heart disease affecting outflow tracts, facial dysmorphism and developmental delay.

Velocardiofacial syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.245

874

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

875

The q from 22q11.2 refers to ________.

"Long arm" of chromosome 22.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246

876

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

877

Syndrome manifested by a eunochoid body habitus, reduced facial, body and pubic hair, gynecomastia, testicular atrophy, decreased serum testorerone and increased urinary gonadotropin levels. It is the most common cause of hypogonadism in males.

Klinefelter syndrome (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246

878

Most common chromosomal derangement in Klinefelter syndrome.

47XXY(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.246

879

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

880

Inheritance associated with mitochondrial DNA.

Maternal inheritance(TOPNOTCH)

881

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)

882

Inheritance associated with mitochondrial DNA.

Maternal inheritance(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.247

883

An epigenetic process wherein certain genes are differentially "inactivated" during paternal and maternal gametogenesis.

Genomic imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.252

884

This refers to transcriptional silencing of the maternal allele.

Maternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251

885

Refers to the transcriptional silencing of the paternal allele.

Paternal imprinting(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.251

886

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

887

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

888

These represent primary errors of morphogenesis due to an intrinsically abnormal developmental process.

Malformations(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.254

889

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

890

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

891

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

892

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

893

Elements of the TORCH complex.

TOxoplasmaTreponema pallidumRubellaCytomeglovirusHerpesvirus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.256

894

Most common cause of neonatal mortality.

Congenital anomalies(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.253

895

Second most common cause of neonatal mortality.

Prematurity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.257

896

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

897

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

898

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

899

Characteristic lesion in the retina of infants suffering from retrolental fibroplasia?

Neovascularization or retinal vessel proliferation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258

900

Main component of pulmonary surfactant.

Dipalmitoylphosphatidylcholine (DPPC) ~40%(TOPNOTCH)

901

Characteristic abnormality in bronchopulmonary dysplasia?

Alveolar hypoplasia or a decrease in the number of mature alveoli.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258

902

What is the fundamental abnormality in neonatal RDS?

Insufficient pulmonary surfactant(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.258

903

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

904

Microscopic features of NEC.

Presence of submucosal gas bubbles, transmural coagulative necrosis, ulceration and bacterial colonization.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.259

905

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

906

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

907

Results from antibody-induced hemolytic disease in the newborn 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

908

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)

909

Isolated postnuchal fluid accumulation in fetuses with hydrops.

Cystic hygroma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261

910

A lethal condition characterized by generalized edema of the fetus.

Hydrops fetalis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.261

911

Increased hematopoietic activity leading to the presence of large number of immature red cells, including reticulocytes, normoblasts and erythroblasts. Characteristic finding in fetal anemia-associated hydrops.

Erythroblastosis fetalis(TOPNOTCH)

912

Primary gene defect in cystic fibrosis.

Abnormal CFTR (CF transmembrane conductance regulator) Chromosome 7q31.2(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.262

913

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

914

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

915

How is cystic fibrosis diagnosed?

Persistently elevated sweat chloride concentration(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267

916

Most common tumors of infancy.

Hemangioma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267

917

Microscopically normal cells or tissues that are present in abnormal locations.

Heterotopia or choristoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267

918

Port wine stains are associted with these syndromes. (2)

von Hippel-Lindau Sturge-Weber syndromes(TOPNOTCH)

919

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

920

Large, flat to elevated, irregular, red-blue masses in the skin.

Port wine stains(Large hemangiomas)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.267

921

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

922

What do you call the rosettes found in neuroblastomas?

Homer-Wright pseudorosettes(TOPNOTCH)

923

Most common germ cell tumors of childhood,associated with meningocoele and spina bifida.

Sacrococcygeal teratomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.268

924

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

925

This is used in the screening of patients with neuroblastoma.

Urinary vanillylmandelic acid and homovanillic acid (VMA/HVA)(TOPNOTCH)

926

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

927

Disseminated neuroblastoma with multiple cuteaneous metastases with deep blue discoloration to the skin.

"Blueberry muffin baby"(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.270

928

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

929

Rosettes in retinoblastoma are called _______.

Flexner-Wintersteiner rosettes(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271

930

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

931

Most common primary tumor of the kidney in children.

Wilm's tumor / Nephroblastoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.271

932

Components of the WAGR syndrome.

Wilm's tumorAniridiaGenital abnormalitiesMental retardation(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272

933

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

934

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

935

Associated with inactivation of the WT1 gene of chromosome 11p13.

WAGR syndrome and Denys-Drash syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.272

936

Patient presents with mental retardation, motor incoordination, and blindness. Ophthalmologic exam showeed cherry-red spots on the macula. Brain showed neurons ballooned with cytoplasmic vacuoles. What is the enzyme deficiency?

Hexosaminidase A. (Case of Tay-Sachs Disease) (TOPNOTCH)

937

An 18 y/o male was recently diagnosed with a genetic disorder. His parents do not manifest the disease, but one of his parent carries the gene with phenotypic expression. Some of his relatives manifest the same disease but with different presentation. What type of Mendelian disorder does the patient most likely have?

Autosomal dominant disorder. With this type, some patient do not have affected parents, has variations in penetrance and expressivity, age at onset is delayed. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 140

938

True or False. Male patient with hemophilia does not transmit the disorder to his sons, but all daughters are carriers.

True. Hemophilia is an X-linked disorder. (TOPNOTCH)

939

True or False. Female hemophilia carrier will transmit the disease to half her sons and half her daughter.

False. X-linked disorders are transmitted by heterozygous females to their sons, who manifest the disease. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 142

940

True or False. Female hemophilia carrier will manifest with decrease Factor VIII.

False (TOPNOTCH)

941

True or False. In female hemophilia carrier, only one of the X chromosome shows abnormality.

True (TOPNOTCH)

942

True or False. In X-linked disorders, female carriers are usually protected because of random inactivation of one X chromosome.

True (TOPNOTCH)

943

True or False. In X-linked disorders, heterozygous female carrier will never manifest the disease.

False (TOPNOTCH)

944

A 26 y/o male was referred to a cardiologist due to presence of murmur at the aortic area. On history, patient suffered from severe myopia at the age of 6. His development was normal except that he was taller than the rest of his family members and friends. Examination of abdomen showed visible pulsation above the umbilicus. The most striking feature in this syndrome is:

Skeletal abnormalities. (case of Marfan Syndrome) (TOPNOTCH)

945

The most life-threatening feature of Marfan syndrome

Cardiovascular lesions (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 145

946

The 2 most common lesions of Marfan Syndrome

Mitral valve prolapse and dilation of ascending aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 145

947

A 4 y/o male presented with cutaneous xanthomas on the extensor surfaces of his arms, knees, and elbow since he was 1 year old. He was found to have serum cholesterol greater than 1000 mg/dl and triglyceride level of 170 mg/dl. Both parents had high cholesterol levels. What is the cause of hypercholesterolemia in this condition?

Impared transport of LDL into the cells (Case of Familial Hypercholesterolemia) (TOPNOTCH)

948

A 6 mo old infant presented with failure to thrive, vomiting, fever, and hepatosplenomegaly. Progressive deterioration of the infant led to death. Autopsy finding showed lipid laden phagocytic foam cells widely distributed in the spleen, liver, lymph nodes, GIT and lungs. Tissue cells are enlarged, with innumerable vacuoles staining for fat, and lysosome contain concentric lamellated myelin figures. The patient is deficient of what enzyme?

Sphingomyelinase (case of Niemann-Pick Disease Type A) (TOPNOTCH)

949

A 1 y/o infant succumbed to death. Autopsy finding showed shrunken gyri and widened sulci. There is vacuolation and ballooning of neurons noted. Cells are enlarged with innumerable small vacuoles of uniform size, imparting foaminess to the cytoplasm. This is a case of:

Niemann-Pick Disease (TOPNOTCH)

950

Presents with fractures, bone pain and thrombocytopenia. Morphologic findings of distended phagocytic cells and have fibrillary type of cytoplasm, intensely positive for PAS staining.

Gaucher disease (TOPNOTCH)

951

A 21 y/o female of short stature presented with primary amenorrhea, shield-shaped chest, "thick neck", and absence of secondary female characteristics. Estrogen level were decreased, while FSH and LH are increased. What is the most likely diagnosis?

Turner syndrome (TOPNOTCH)

952

The most common chromosomal disorder

Down Syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 161

953

The most common genetic cause of mental retardation.

Down Syndrome(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 161

954

Most common pathogenesis of Trisomy 21

Meiotic nondisjunction (TOPNOTCH)

955

Most common congenital heart defects in Trisomy 21

Endocardial cushion defects(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 163

956

Why are patients with DiGeorge syndrome has T-cell immunodeficiency?

Because of thymic hypoplasia (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 163

957

A 14 y/o male presented with gynecomastia and small testes. He was noted to have difficulties in school when he was 8. He was tall for his age. You would suspect:

Klinefelter syndrome (TOPNOTCH)

958

Classic karyotype patttern of Klinefelter syndrome

47,XXY(TOPNOTCH)

959

Single most important cause of primary amenorrhea

Turner syndrome (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 166

960

Most important cause of increased mortality in children with Turner syndrome.

Cardiovascular abnormalities (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 166

961

Patient presents with mental retardation, long face with large mandible, large everted ears, and large testicles. The most likely diagnosis is:

Fragile X Syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 169

962

Most distinctive feature of Fragile X syndrome

Macro-orchidism(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 169

963

The neonate was noted to have microcephaly, short palpebral fissure, maxillary hypoplasia, growth retardation, and psychomotor disturbances. The mother denies intake of drugs during pregnancy. The most likely cause

Alcohol (TOPNOTCH)

964

Deficiency in homogentisic oxidase results in this condition which manifests black discoloration of the urine

Alkaptonuria (TOPNOTCH)

965

Most common cause of respiratory distress in the newborn

Hyaline Membrane Disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 457

966

This teratogenic drug disrupts expression of homeobox proteins implicated in the patterning of lims, vertebrae, and craniofacial structures.

Valproic acid (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 456

967

Most commonly responsible for fetal growth restriction.

TORCH infections (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 457

968

Most common maternal condition associated with SGA infants

Vascular diseases (chronic hypertension, preclampsia) (TOPNOTCH) Robbins Basic Pathology, 9th ed, p. 457

969

A 28 week old male delivered via CS by a diabetiic mother presented with dyspnea and cyanosis. Fine rales are heard over both lung fields. CXR revealed uniform minute reticulogranular densities, producing a ground glass appearance. The fundamental defect in this condition is:

Pulmonary surfactant (Case of RDS) (TOPNOTCH)

970

The most common cause of mortality in children ages 1-4 years old.

Accidents (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 452

971

A 28 week old male dies 20 hours after birth. Autopsy findings showed a solid, airless, and reddish purple lungs with poorly developed alveoli. Necrotic cellular debris incorporated within eosinophilic hyaline membranes lines the respiratory bronchioles, alveolar ducts and alveoli. The most likely cause of death of the neonae is:

Respiratory distress syndrome/Hyaline membrane disease (TOPNOTCH)

972

Premature infant, bottle-fed, developed bloody stool, abdominal distention. Abdominal radiograph showed pneumotis intestinalis. Diagnosis:

Necrotizing enterocolitis(TOPNOTCH)

973

Morphology: intestinal segment is distended, friable and congested, with transmural coagulative necrosis, ulceration, bacterial colonization, and submucosal bubbles.

Necrotizing enterocolitis(TOPNOTCH)

974

Most common cause of early-onset neonatal sepsis and early-onset bacterial meningitis

Group B streptococcus(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 460

975

The most serious threat of fetal hydrops

CNS damage -kernicterus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 463

976

Most common site of neuroblastoma

Adrenal medulla (TOPNOTCH)

977

Presents with a large abdominal mass crossing the midline, hematuria, intestinal obstruction, and hypertension.

Wilm's tumor (TOPNOTCH)

978

A 22 year old male consults an ophthalmologist for sudden blindness on the right. He is found to have lens subluxation. He is unusually tall and lean, with long limbs and fingers. These findings are due to abnormalities in fibrillin 1, which is secreted by (A) megakaryocytes (B) fibroblasts (C) histiocytes (D) fibroclasts

fibroblasts (TOPNOTCH)Robbins Basic Pathology, 8th Ed, p 230

979

A lysosomal storage disease with a mutation in the gene that encodes glucosylceramidase presents with an accumulation of glucosylceramide in mononuclear phagocytic cells in the liver, spleen, and marrow. These pathognomonic cells are (A) enlarged, with a "wrinkled tissue paper" cytoplasm (B) epithelioid, with "slipper-shaped" nuclei (C) multinucleated, with 8 to 20 nuclei (D) studded with reddish brown cytoplasmic granules

enlarged, with a "wrinkled tissue paper" cytoplasm (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp237-238

980

A baby is born with epicanthic folds, flat facial profile, simian crease, and a gap between the first and second toe. Auscultation reveals a holosystolic murmur. The clinical findings are due to an extra chromosome that is most commonly caused by (A) meiotic duplication (B) meiotic nondisjunction (C) fertilization by two spermatozoa (D) translocation

meiotic nondisjunction (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 244

981

A premature female neonate admitted at the PICU develops sepsis, with blood cultures showing growth of Candida sp. She is also found to be persistently hypocalcemic. She dies on her 7th day. On autopsy, she was found to have fungal endocarditis and thymic hypoplasia. She most likely has (A) an extra chromosome 22 (B) a deletion in chromosome 22 (C) a 9:22 chromosomal translocation (D) a duplication in chromosome 22

a deletion in chromosome 22 (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 245-246

982

A stillborn fetus is found to have polydactyly, an umbilical hernia, and cleft lip and palate. Autopsy showed a ventral septal defect, renal dysplasia, and holoprosencephaly. Karyotyping will likely show (A) Monosomy X (B) Deletion in chromosome 5 (C) Trisomy 13 (D) Trisomy 18

Trisomy 13 (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 245.

983

A 19 year old female consults a gynecologist for primary amenorrhea. Apart from her short stature, there are no other unusual clinical findings. Why must Turner Syndrome be ruled out? (A) mosaicism or partial monosomy may produce a mild form of the syndrome (B) 45,X abnormalities manifest in only half of females by the age of 18 (C) when combined with Fragile X, the typical features such as neck webbing and cubitus valgus are masked (D) supplementation with folate during gestation masks the typical features of neck webbing and cubitus valgus

mosaicism or partial monosomy produces a milder form (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp247-248

984

A stillborn male fetus delivered to a 41 year old G7P7 is found to have flattened facies and clubbed feet. Autopsy showed renal agenesis and pulmonary hypoplasia. What is the main culprit of the findings in the fetus? (A) maternal age (B) multiparity (C) renal agenesis (D) pulmonary hypoplasia

renal agenesis (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 253-254

985

A G3P3 mother has premature rupture of membranes at 35 weeks age of gestation, and delivers a live baby boy with poor APGAR scores. The obstetrician delivered a placenta with dull-looking membranes, which showed chorioamnionitis on histopathology. Culture of which organism from the placental tissue suggests an transcervical origin of infection? (A) Group B Streptococcus (B) Toxoplasma (C) Plasmodium (D) Rubella

Group B Streptococcus (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 256

986

A G1P1 preeclamptic mother delivers a live baby boy at 27 weeks age of gestation. The baby develops respiratory distress a few minutes later and is admitted at the PICU. He dies the next day, and is sent for autopsy. Which of the following supports respiratory distress syndrome of the newborn? (A) thickened alveolar septa with lymphocytic infiltrates (B) alveolar spaces filled with neutrophils (C) eosinophilic material lining the alveolar walls (D) hemosiderin laden macrophages in the alveolar spaces

eosinophilic material lining the alveolar walls (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 257-258

987

A premature male neonate who was delivered at 33 weeks AOG and admitted at the PICU develops abdominal distention, bloody stools, and hypotension. An abdominal radiograph shows gas within the intestinal wall. What is the expected histologic findings of the involved intestine? (A) coagulative necrosis of the mucosa and muscularis (B) arteriovenous fistulas in the submucosa (C) melanosis of the mucosa (D) crypt abscesses and noncaseating granulomas

coagulative necrosis of the mucosa and muscularis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 259

988

What is the most common autopsy finding in sudden infant death syndrome? (A) patent ductus arteriosus (B) multiple petechiae in the thymus and pleural surfaces (C) bilateral adrenal hemorrhage (D) flattening of gyri in the cerebral cortex

multiple petechiae on the thymus and visceral surfaces (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 260

989

How does parvovirus B19 infection cause fetal hydrops? (A) it causes a chronic myocarditis leading to heart failure (B) it infects the lymphatic ducts causing peripheral fluid accumulation (C) it causes placental villi atrophy, exposing the fetal circulation to maternal antibodies (D) it infects erythroid precursors, causing anemia

it infects erythroid precursors, causing anemia (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 262

990

A 4 month old infant with abdominal enlargement presents with multiple bluish-gray subcutaneous nodules. Workup showed a 10 cm mass in the paravertebral region. Biopsy of the nodules showed small round cells with dark nuclei scanty cytoplasm, some forming rosettes arranged in a finely fibrillar matrix. Immunohistochemical studies showed the cells to be positive for neuron specific enolase and negative for leucocyte common antigen. These tumor cells are derived from (A) antigen presenting cells in the dermis (B) neural crest (C) nephrogenic rests (D) lymphoid precursors

neural crest (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 269-270

991

A 2 year old male is noticed to have a whitish pupil on photographs. Workup showed a tumor in the posterior chamber. The eye is enucleated, and the tumor shows sheets of small round cells with hyperchromatic nuclei and scant cytoplasm. Occasional clustering around central lumens are seen. On further history, a cousin also had a similar tumor and died. The patient has an increased risk of developing which tumour later in life: (A) hepatoblastoma (B) pheochromocytoma (C) osteosarcoma (D) Wilms tumour

osteosarcoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 271

992

A 4 year old female undergoes left nephrectomy for Wilms tumor. Which of the following findings in the nephrectomy specimen is associated with an increased risk of developing the same tumor in the right kidney? (A) nephrogenic rests (B) abortive tubules or glomeruli (C) extensive fibrosis (D) adipose tissue, cartilage, and osteoid

nephrogenic rests (TOPNOTCH)Robbins Basic Pathology, 8th Ed p 272

993

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

994

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

995

Carbon monoxide in the blood is called _______.

Carboxyhemoglobin(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 282

996

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

997

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

998

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

999

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

1000

Antidote for mercury poisoning.

Thimerosal(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285

1001

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

1002

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

1003

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

1004

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

1005

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

1006

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

1007

It is the most preventable cause of human death.

Smoking(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287

1008

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

1009

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

1010

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

1011

A long acting tetracycline which can cause a diffuse blue-gray pigmentation of the skin.

Minocycline(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 293

1012

Oral contraceptives have a protective effect against these cancers.

Endometrial and ovarian CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294

1013

Oral contraceptives may increase the risk of developing this type of cancer in women.

Cervical CA(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294

1014

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

1015

Toxic metabolite of paracetamol or acetaminophen causing centrilobular necrosis that may progress to liver failure.

NAPQI (N-acetyl-p-benzoquinoneimine)(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 422

1016

Toxic dose for acetaminophen.

15-25 grams/day(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294

1017

Antidote for acetaminophen poisoning.

N-acetylcysteine(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 294

1018

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

1019

Adult toxic dose of aspirin.

10-30 grams(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294

1020

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

1021

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

1022

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

1023

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

1024

Psychoactive substance found in marijuana.

Delta 9- Tetrahydrocannabinol (THC)(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297

1025

Mechanism of action of aspirin.

Irreversibly blocks the enzyme cyclooxygenase.(TOPNOTCHRobbins Basic Pathology, 8th Ed p. 297

1026

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

1027

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

1028

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

1029

A wound inflicted by a sharp instrument, wherein bridging blood vessels are severed.

Incision(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298

1030

A wound caused by a long, narrow instrument.

Puncture wound(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298

1031

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

1032

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

1033

Partial thickness burn that involves both the epidermis and superficial dermis.

Second degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298

1034

Partial thickness burn that involves the epidermis only.

First degree burn(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298

1035

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

1036

These burns are pink or mottled with blisters and are painful.

Second degree burn (partial thickness)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298

1037

Histologic change in the skin during burns.

Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 298

1038

Leading cause of death in burn patients.

Organ system failure secondary to burn sepsis.(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299

1039

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

1040

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

1041

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

1042

Two types of injuries caused by electricity.

BurnsVFib or cardiac and respiratory center failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 299

1043

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

1044

Malnutrition caused by lack of nutrients from the diet.

Primary malnutrition(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 304

1045

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

1046

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

1047

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

1048

Self-induced starvation, resulting in marked weight loss.

Anorexia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306

1049

A condition wherein a patient binges on food and then induces vomiting.

Bulimia(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 306

1050

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

1051

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

1052

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

1053

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

1054

Symptoms of cheilosis, glossitis, dermatitis, and peripheral neuropathy.

Vitamin B6 (Pyridoxine)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 314

1055

Leading causes of death in developed countries

Ischemic heart disease and cerebrovascular disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 405

1056

The most important catalyst of phase I reactions; detoxify xenobiotics

Cytochrome P-450 enxyme system (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 407

1057

A 55 y/o male presented to the ER following a house fire. He was lethargic, tachycardic, tachypneic and displayed memory disturbance. Skin was noted to be cherry red. What is the most likely cause?

Carbon monoxide poisoning (TOPNOTCH)

1058

A 5 y/o boy presented to the clinic due to hyperactivity and impulsiveness. Hearing acuity was below normal, and speech and language were slightly delayed. History reveals that the boy lives in an old house in the community. PBS showed hypochromia and microcytosis. What is the most likely diagnosis?

Lead poisoning (TOPNOTCH)

1059

Toxic effects of this heavy metal include cerebral palsy, deafness, blindness, and kidney damage. Cause of Minamata disease.

Mercury (TOPNOTCH)

1060

"King of poisons"

Arsenic (TOPNOTCH)

1061

Most toxic form of arsenic

Trivalent compounds of arsenic(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 412

1062

The most serious consequence of chronic exposure to this heavy metal is the increased risk for the development of cancers, particularly of the lungs, bladder, and skin.

Arsenic (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 412

1063

The principal toxic effects of toxicity to this heavy metal are obstructive lung disease and renal tubular damage that may progress to ESRD.

Cadmium (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 413

1064

Exposure to benzene increases risk of what hematologic condition

Leukemia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 413

1065

Exposure to vinyl chloride used in the synthesis of polyvinyl resins leads to the development of what tumor?

Angiosarcoma of the liver (TOPNOTCH) Robbins Basic Pathology, 9th ed.,p.414

1066

Main enzyme system involved in alcohol metabolism

Alcohol dehydrogenase(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 417

1067

Enlarged and fatty liver is seen in kwashiorkor or marasmus?

Kwashiorkor(TOPNOTCH)

1068

A major complication of anorexia nervosa and bulimia

Cardiac arrythmia and sudden death due to hypokalemia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 435

1069

Symptos of acute toxicity to these vitamin include headache, diziness, vomiting, stupor, and blurred vission, which may be confused with those of a brain tumor (pseudotumor cerebri)

Vitamin A(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 438

1070

Craniotabes, frontal bossing, squared appearance of the head, rachitic rosary, pigeon chest deformity, lumbr lordosis, and bowing of the legs are associated with what vitamin deficiency?

Vitamin D deficiency (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 441

1071

Toxicity of this vitamin may cause calcification of soft tissue and bone pain.

Vitamin D(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 441

1072

Rash around the eyes, mouth,and nose, anorexia, diarrhea, growth retardaation, depressed wound healing and impaired nigh vision are associated with ____ deficiency

Zinc(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 443

1073

Muscle weakness, neurologic defects and abnormal collagen cross-linking are associated with ___ deficiency.

Copper(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 443

1074

Disease characterized by bone disease in growing children and by hemorrhages and healing defects in both children and adults.

Scurvy(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 443

1075

Syndrome composed of respiratory abnromalities in very obese persons.

Hypoventilation syndrome/pickwickian syndrome (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 448

1076

Hormone synthesized by fat cells which regulates food intake an energy expenditure. Its binding to its receptors in the hypothalamus increases energy consumption by stimulating POMC/CART neurons.

Leptin(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 448

1077

Aflatoxin is implicated in what type of cancer?

Hepatocellular carcinoma(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 449

1078

True or False. High animal intake and low fiber has been imlicated in colon cancer.

True (TOPNOTCH)

1079

Lead has a more damaging effect on the brains of children than in adults because of (A) a more permeable blood-brain barrier (B) immature lenticular nuclei (C) less microglia and astrocytes(D) greater proportion of fetal hemoglobin in the blood

a more permeable blood-brain barrier (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 283

1080

Chronic exposure to arsenic is associated with the development of the following malignancies EXCEPT (A) squamous cell carcinoma of the skin (B) mucoepidermoid carcinoma of the salivary glands (C) lung carcinoma (D) basal cell carcinoma

mucoepidermoid carcinoma of the salivary glands (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 285

1081

Exposure to vinyl chloride has been found to cause (A) multiple uterine leiomyomas (B) hepatic angiosarcoma (C) squamous cell carcinoma of the skin (D) transitional carcinoma of the bladder

hepatic angiosarcoma (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 287

1082

Tobacco smoke, when combined with this, is known to have a multiplicative effect on the risk of developing laryngeal cancer (A) alcohol (B) diet rich in animal fat (C) dietary nitrates (D) oral sex

alcohol (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 289

1083

Progestin is added to estrogen in hormone replacement therapy for menopausal women to reduce the risk of (A) breast cancer (B) endometrial cancer (C) thromboembolism (D) all of the above

endometrial cancer (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 293

1084

During a routine ultrasound, a 38 year old G1P0 was found to have a solitary, 4 cm diameter, hepatic mass in the right lobe, beneath the capsule. She has a history of regular oral contraceptive use since 18 years old, and stopped 1 year ago. She has never been infected by HBV or HCV. She does not drink alcohol. If the mass is excised, it would most likely show (A) benign-looking hepatocytes in cords and sheets, absent portal tracts, and prominent blood vessels (B) proliferation of endothelial cells some containing lumens with RBCs (C) portal tracts with chronic inflammation and bile duct proliferation (D) pleomorphic cells, bizarre giant cells, atypical mitoses, and necrosis

benign-looking hepatocytes in cords and sheets, absent portal tracts, and prominent vessels (hepatic adenoma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294, p664)

1085

Liver damage in acetaminophen overdose is characterized histologically by (A) brisk neutrophilic infiltration of portal tracts (B) hepatocytes with extensively vacuolated cytoplasm (C) centrilobular necrosis (D) bile duct proliferation

centrilobular necrosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294

1086

A 65 year old man has been regularly taking aspirin and acetaminophen for 20 years. This predisposes him to developing (A) chronic interstitial nephritis (B) renal papillary necrosis (C) transitional cell carcinoma of the renal pelvis (D) all of the above

all of the above (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 294, 564

1087

An 4 year old orphan boy with a scar on his forehead was found locked in a small room under the stairs by his abusive uncle and aunt. He has been kept there and fed crackers and milk since he was 1 year old. He has a squared appearance of the head, a pigeon breast deformity, lumbar lordosis, and bowing of the legs. These physical findings are due to deficiency of (A) calcium (B) vitamin A (C) vitamin C (D) vitamin D

vitamin D (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 309-312

1088

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

1089

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

1090

These are the principal control points for regulation of physiologic resistance to blood flow.

Arterioles(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 340

1091

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

1092

Diameter of an RBC.

7-8 um(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341

1093

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

1094

These are small spherical dilatations, typically in the circle of Willis.

Developmental/berry aneurysms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 341

1095

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

1096

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

1097

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

1098

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

1099

Characterized by intimal lesions called atheromas that protrude into vascular lumina.

Atherosclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 343

1100

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

1101

Non-modifiable risk factors for atherosclerosis. (4)

Increasing ageMale genderFamily historyGenetic abnormalities(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 344

1102

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)

1103

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

1104

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

1105

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

1106

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

1107

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

1108

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

1109

Most common cause of hypertension.

Idiopathic (essential hypertension)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 355

1110

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

1111

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

1112

It is a localized abnormal dilation of a blood vessel or heart.

Aneurysm(TOPNOTCH)

1113

It is a localized abnormal dilation of a blood vessel or heart.

Aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357

1114

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

1115

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

1116

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

1117

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

1118

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

1119

Two most important causes of aortic aneurysms.

AtherosclerosisCystic medial degeneration of the arterial media(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357

1120

Infection of a major artery that causes weakness to its wall.

Mycotic aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 357

1121

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

1122

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

1123

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

1124

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

1125

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

1126

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

1127

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

1128

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

1129

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

1130

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

1131

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

1132

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

1133

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

1134

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

1135

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

1136

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

1137

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

1138

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

1139

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

1140

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

1141

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

1142

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

1143

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

1144

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

1145

Common and serious complication of of deep vein thrombosis (DVT).

Pulmonary embolism(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371

1146

The acute inflammation elicited when bacterial infections spread into and through the lymphatics.

Lymphangitis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 371

1147

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

1148

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

1149

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

1150

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

1151

A specialized arteriovenous structure involved in thermoregulation.

Glomus body(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 373

1152

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

1153

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

1154

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

1155

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

1156

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

1157

Form of hypertension characterized by systolic pressure more than 200 mmHg or diastolic pressure more than 120 mmHg, renal failure, and retinal hemorrhages and exudates.

Malignant Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 488

1158

The most important independent risk factor for atherosclerosis.

Family history(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 492.

1159

The initial event in the pathogenesis of atherosclerosis

Endothelial injury and dysfunction. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494

1160

The major lipoprotein involved in the pathogenesis of atherosclerosis.

LDL(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494

1161

2 most important causes of endothelial dysfunction

Hemodynamic disturbances and hypercholesterolemia. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 494

1162

The key processes in atherosclerosis

Intimal thickening and lipid accumulation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 496

1163

The major structural component of fibrous cap in an atheromatous plaque

Collagen(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 500

1164

Medial ischemia leading to degenerative changes of aorta, leading to scarring, loss of elastic fibers, inadequate extracellular matrix synthesis, and production of amorphous ground substance. This can be seen in Marfan syndrome and scurvy.

Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 502

1165

Most common etiology associated with ascending aortic aneurysm

Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 502

1166

A 70 y/o male, hypertensive, present with sudden severe abdominal pain. On physical examination, there is a presence of pulsatile abdominal mass. The most likely diagnosis is:

Abdominal aortic aneurysm(TOPNOTCH)

1167

The most frequent preexisting histologically detectable lesion in aortic dissection

Cystic medial degeneration(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 504

1168

Presents with sudden onset of excruciating pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward.

Aortic dissection(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 505

1169

Most common cause of death in aortic dissection.

Rupture of the dissection into the pericardial, pleural or peririthoneal cavities.(TOPNOTCH) Robbins Basica Pathology, 9th ed., p. 505

1170

A 38 y/o male presents with severe headache and diplopia associated with fever and fatigue. Area along the course of the superficial temporal artery was painful to palpation. Biopsy done revealed intimal thickening of the artery, granulomatous inflmmation of the internal elastic lamina with infiltrate of T cells and macrophages. What is the most likely diagnosis?

Giant cell arteritis (TOPNOTCH)

1171

Patient initially present with fatigue, weight loss and fever and then reduced blood pressure and weak pulses in the carotids and upper extremities, ocular disturbances and neurologic deficits. The most likely diagnosis is:

Takayasu arteritis(TOPNOTCH)

1172

Most common involved blood vessel in Takayasu arteritis.

Aortic arch (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 509

1173

This disease presents with rapidly accelerating hypertension, abdominal pain, bloody stool, myalgia and peripheral neuritis. The most likely diagnosi:

Polyarteritis nodosa(TOPNOTCH)

1174

A 4 y/o female presented with fever and maculopapular rash on her trunk and extremities. This is associated with conjunctival erythema, edema of the hands and feet, and cervical lymph node enlargement. The patient is at risk for what type of blood vessel involvement?

Coronary artery aneurysm which may lead to acute MI. (Case of Kawasaki Disease) (TOPNOTCH)

1175

Patient presents with asthma, allergic rhinitis, palpable purpura, GI bleeding, renal disease, and cardiomyopathy. Histologic findings showed vascular granulomata and hypereosinophilia. The most likely diagnosis is:

Churg-Strauss syndrome(TOPNOTCH)

1176

It presents as a clinical triad of recurrent oral apthous ulcers, genital ulcers, and uveitis.

Behcet Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 511

1177

This disease presents with persistent pneumonitis with bilateral nodular infiltrates, chronic sinusitis, mucosal ulceration of the nasopharynx, and renal disease. Histologic findings of upper respiratory tract lesion showed mucosal granuloma with geographic patterns of central necrosis and vasculitis. The most likely diagnosis:

Granulomatosis with polyangitis/Wegener granulomatosis(TOPNOTCH)

1178

A 30 y/o male, smoker, presents with severe leg pain aggravated by exercise and relieved on rest. It further progressed to extremity ulcerations. What is the most likely diagnosis?

Thromboangiitis obliterans (Buerger disease)(TOPNOTCH)

1179

Most imprortant risk factor for DVT

Prolonged immobiliztion resulting in venous stasis. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 514

1180

A 50 y/o male, diagnosed with lung cancer, presented with edema and cyanosis of the head , neck, and arms with cyanosis. This is a case of:

Superior vena cava syndrome (TOPNOTCH)

1181

The most common etiologic agent in lymphangitis.

Group A beta hemolyitc streptococcus. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 515

1182

An autosomal dominant disorder caused by mutations in genes that encode components of TGF-B signaling pathway. Presents with telengiectasia that are widely distributed over the skin and mucus membranes.

Hereditary hemorrhagic telengiectasia/Osler-Weber-Rendu disease (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 516

1183

Most common type of hemangioma

Capillary hemangioma(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 516

1184

Painful tumors arising from modified smooth muscle cells of arteriovenous structure, most commonly found in the distal portion of the digits.

Glomus tumor (Glomangioma)(TOPNOTCH)Robbins Basic Pathology, 9th Ed p. 517

1185

A 13 year old male dies of a stray bullet to the head on New Year's Eve. At autopsy, there is a flat yellowish streak seen on the intimal surface of his abdominal aorta, near the bifurcation of the renal arteries. This streak (A) causes minor disturbance in blood flow (B)is expected in his age group (C) is composed of hemosiderin-filled foam cells (D) would have certainly evolved into an atheromatous plaque if he lived to old age

expected in his age group ("fatty streak" (TOPNOTCH)Robbins Basic Pathology, 8th Ed pp 348-349)

1186

Early atherosclerotic lesions are usually focal, patchy, and eccentric because (A) there are differences in the vascular hemodynamics at various points (B) the expression of LDL receptors along the blood vessels is varied (C) concentrations of macrophage-activating cytokines are different along blood vessels (D) certain endothelial cells are more sensitive to toxins and hyperglycemia than others

there are differences in vascular hemodynamics at various points (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 349

1187

A 65 year old diabetic female with poor glycemic control and a 5 year history of intermittent chest pain develops pallor, shortness of breath and diaphoresis. She dies 16 hours later. At autopsy, the left ventricular wall is thickened, with dark mottling of the anterior portion, along with the septum and apex. Which of the following describes the likely histology of her left anterior descending artery? (A) an eccentric atheromatous plaque with a fibrous cap (B) a ruptured fibrous cap with calcifications in the lumen of the vessel (C) a ruptured fibrous cap with thrombus formation (D) complete occlusion of the original lumen by fibrous tissue, with neovascularization in the periphery

a ruptured fibrous cap with thrombus formation (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.351

1188

What is the most common cause of aneurysms?

atherosclerosis (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358

1189

What is the most common site of atherosclerotic aneurysms?

abdominal aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 358

1190

A 75 year old male with heart failure symptoms of 10 years dies. At autopsy, his aortic trunk is dilated, with fibrous scars and wrinkling of the intima. The aortic valve is also dilated, and the left ventricle is markedly enlarged. Microscopic examination of the aorta shows narrowed or obliterated vasa vasorum to be narrowed, with a dense rim of lymphocytes and plasma cells, some extending into the media. Which of the following can suggest the etiology of the patient's findings? (A) family history of diabetes (B) chronic alcohol intake (C) history of sexually transmitted infection (D) occupational exposure to benzene

history of sexually transmitted infection (tertiary/cardiovascular syphilis) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.359, 703

1191

A 30 year old female with 3 year history of fever, weight loss and fatigue presents with right eye blindness. PE showed weak pulses in the upper extremities. Which of the following suggests that she has Takayasu arteritis, rather than temporal arteritis? (A) age (B) constitutional symptoms (C) giant cells in the large blood vessels (D) giant cells in the medium blood vessels

age (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 364-365

1192

Classic polyarteritis nodosa affects small to medium sized vessels most commonly in which organ? (A) kidneys (B) heart (C) liver (D) GI tract

kidneys (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 365

1193

A 2 year old boy presents with erythema of the conjunctiva, oral mucosa, palms and soles, with focal erosions. Palpation shows enlarged cervical lymph nodes. He suddenly dies a few hours after ER admission. Autopsy showed marked mononuclear infiltration of his left anterior descending artery, with fibrinoid necrosis and lumen occlusion. What could have prevented this fatal sequela? (A) low dose corticosteroids (B) Hepatitis B vaccine (C) Beta-lactam and aminoglycoside combination (D) intravenous immunoglobulin

intravenous immunoglobulin (Kawasaki disease) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.366

1194

A 42 year old man with 2 weeks of epistaxis undergoes an intranasal biopsy, which showed chronic granulomatous inflammation with giant cells. Xray showed cavitary lung lesions. He is treated with anti-Koch's for 6 months, but the epistaxis recurred. He also developed hematuria. Which of the following can help support a diagnosis of Wegener's granulomatosis, rather than TB? (A) positive P-ANCA (B) positive C-ANCA (C) urinalysis with RBC morphology (D) biopsy of the lung lesion

positive C-ANCA (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 367-368

1195

A 27 year old Israeli expat presents with intermittent pain and pallor of the right index and middle fingers, precipitated by smoking and cold temperature. He reports symptomatic relief whenever he stops smoking. What is expected in the arteries of the involved fingers? (A) thrombus with neutrophil aggregates and necrosis (B) histiocytes and giant cells (C) ruptured fibrous cap and underlying foamy cells (D) eosinophils and lymphocytes in the media and intima

thrombus with neutrophil aggregates and necrosis (Buerger disease) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.368

1196

A 21 year old G1P0, 24 weeks AOG, has a reddish 1.0 cm diameter nodule on her left lower gum. She reports that the nodule appeared at 1 month of pregnancy. A biopsy showed shows capillaries with an acute and chronic inflammatory infiltrate and stromal edema. There is no pleomorphism, necrosis, or atypical mitosis. This nodule (A) can be found in 20% of pregnant women (B) is malignant (C) may spontaneously regress or fibrose after pregnancy (D) is metastatic from an ovarian primary

may spontaneously regress or fibrose after pregnancy (granuloma gravidarum/pregnancy tumor/pyogenic granuloma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.373

1197

A 3 year old female with a large "port wine stain" on the right side of her face has occasional seizures. Further examination showed mental developmental delay. She may also have (A) more extensive vascular malformations (B) multiple colonic polyps (C) color blindness (D) alpha thalassemia

more extensive vascular malformations (Sturge-Weber syndrome) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.374

1198

A 38 year old HIV-positive man has multiple reddish-purple plaques and nodules on his arms and legs. He has never been on antiretroviral therapy. Biopsy of one of the nodules showed sheets of plump spindle cells encompassing small vessels and slit-like spaces, with focal hemorrhage, hemosiderin deposits, lymphocytes, and macrophages. Mitotic figures are common. This neoplasm has been shown to be infected with (A) HPV 16 (B) HHV 8 (C) Hepatitic C (D) HPV 18

HHV8 (Kaposi Sarcoma) (TOPNOTCH)Robbins Basic Pathology, 8th Ed p. 375

1199

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

1200

Hemosiderin laden macrophages are also called _______

Heart failure cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

1201

This is usually the earliest and most significant compaint of patients in Left sided HF.

Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

1202

Most common cause of right sided HF.

Left sided HF(TOPNOTCH)

1203

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

1204

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

1205

Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.

Cardiac cirrhosis(TOPNOTCH)

1206

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

1207

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

1208

This is a hallmark of right sided HF.

Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382

1209

Most congenital heart disease arise from faulty embryogenesis during what AOG?

3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382

1210

An abnormal communication between chambers of the heart or blood vessels.

Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383

1211

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)

1212

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

1213

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

1214

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

1215

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

1216

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 may become dilated.

Patent ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385

1217

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

1218

Components of Tetralogy of Fallot.

Pulmonary valve stenosisOverriding of aortaRight ventricular hypertrophyVentricular septal defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386

1219

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

1220

Predominant manifestation of TGA?

Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387

1221

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

1222

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

1223

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

1224

Left-to-right or Right-to-Left shunt?Atrial septal defect

Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1225

Left-to-right or Right-to-Left shunt?TOF

Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1226

Left-to-right or Right-to-Left shunt?VSD

Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1227

Left-to-right or Right-to-Left shunt?Eisenmenger syndrome

Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1228

Left-to-right or Right-to-Left shunt?Transposition of great arteries

Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1229

A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.

Angina pectoris(TOPNOTCH)

1230

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

1231

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

1232

This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.

Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1233

This can result from a lethal arrythmia following myocardial ischemia.

Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

1234

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

1235

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

1236

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

1237

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

1238

Angina occuring at rest due to coronary artery spasm.

Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390

1239

Infarct involving >= 50% of the myocardial wall thickness.

Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391

1240

Most common blood vessel involved in myocardial infarction?

Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392

1241

Electron microscope findings 30 minutes after an ischemic event.

Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)

1242

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

1243

Coagulation necrosis ensues how many hours after MI?

4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394

1244

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

1245

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

1246

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

1247

Myocardial rupture may occur how many days after MI?

3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397

1248

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

1249

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

1250

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

1251

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

1252

In this disease the left ventricle may exceed 2.0cm in thickness and the heart may 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

1253

It is the failure of a valve to open completely, obstructing forward flow.

Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401

1254

This results from failure of a valve to close completely, thereby allowing reversed flow.

Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401

1255

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

1256

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

1257

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

1258

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

1259

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

1260

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

1261

Most common valve involved in RHD.

Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405

1262

Major components Jones Criteria for RF.

CarditisMigratory polyarthritisSubcutaneous nodulesErythema marginatumSyndenham chorea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

1263

Minor components Jones criteria for RF

FeverArthralgiaElevated acute phase reactants (e.g. CRP)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

1264

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

1265

Endocarditis of previously normal valves, the most common causative agent is S. aureus.

Acute bacterial endocarditis(TOPNOTCH)

1266

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

1267

Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.

Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

1268

Most consistent sign of infective endocarditis.

Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407

1269

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

1270

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

1271

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

1272

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

1273

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

1274

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

1275

Mechanism of heart failure in hypertrophic cardiomyopathy.

Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412

1276

A common cause of sudden death in young athlethes.

Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412

1277

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

1278

Mechanism of heart failure in restrictive cardiomyopathy.

Diastolic dysfunction or impaired compliance(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413

1279

Inflammation of the myocardium.

Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

1280

Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.