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2

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

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

2

It is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.

Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.31

3

Increase in number of cells.

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

3

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

Acute inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

4

Hypertrophy of hyperplasia?Uterus during pregnancy

Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3

4

Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and fibrosis.

Chronic inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

5

Hypertrophy or hyperplasia?Wound healing

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

5

Five cardinal signs of inflammation?

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

6

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

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

6

Initial vascular response to injury?

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

7

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

7

An ultrafiltrate of blood which contains little protein. Results from arteriolar vasodilation and increased blood flow.

Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

8

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

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

8

Results from increased vascular permeability, leading to leakage of protein into tissues.

Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

9

Type of cell death associated with inflammation.

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

9

Fluid accumulation in extravascular space.

Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

10

It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.

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

10

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

Selectins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

11

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

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

11

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

Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

12

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

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

12

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

PECAM-1/CD 31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

13

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

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

13

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

ICAM -1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

14

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

14

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

Sialyl-Lewis X modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

15

Appearance of lipid vacuoles in the cytoplasm.

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

15

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

Sialyl-Lewis X-Modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

16

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

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

16

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

Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

17

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

17

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

CD-31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

18

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

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

18

The process of luekocyte accumulation at the periphery of blood vessels is called ______.

Margination(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

19

Most common cause of cell injury in clinical medicine.

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

19

Arrange the following steps in the inflammatory response:A. Recruitment of leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. Resolution

C, A, D, B, E(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35

20

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

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

20

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

C, B, D, A(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35

21

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

21

Process of coating microorganisms with proteins that facilitate phagocytosis.

Opsonization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.38

22

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

22

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

Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.39

23

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

23

The most important lysosomal enzyme involved in bacterial killing.

Elastase(TOPNOTCH)

24

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

24

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

Chemotaxis(TOPNOTCH)

25

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

25

The most important lysosomal enzyme involved in bacterial killing.

Elastase(TOPNOTCH)

26

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

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

26

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

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

27

Hypertrophy or hyperplasia?Cardiomegaly due to hypertension

Hypertrophy Due to increased workload(TOPNOTCH)

27

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

Neutrophils(TOPNOTCH)

28

Most common exogenous pigment?

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

28

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

Monocytes(TOPNOTCH)

29

"Wear and Tear pigment"?

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

29

Substances responsible for leukocyte-induced tissue injury?

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

30

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

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

30

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

31

Hemoglobin-derived granular pigment that is golden-yellow to brown in color. Accumulates in excess of iron.

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

31

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

32

Histochemical reaction used to identify hemosiderin.

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

32

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

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

33

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

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

33

NADPH deficiency or defect resulting in decreased oxidative burst.

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

34

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

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

34

Type of acute inflammation characterized by the outpouring of watery, relatively protein-poor fluid derived from the serum or endothelial lining of peritoneal, pleural, and pericardial cavities.

Serous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43

35

Grossly seen as fine white granules or clumps, often felt as gritty deposits. Histologically, intra/extracellular basophilic deposits.

Calcium salts(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.27

35

Fluid in a serous cavity is called ______.

Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43

36

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

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

36

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

Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

37

Appears as round or oval masses with intensely eosinophilic cytoplasm, nuclei with various stages of chromatin condensation and aggregation, karyorrhexis.

Apoptotic cell(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20

37

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

Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

38

Membrane bound vesicles of cytosol and organelles quickly extruded and phagocytosed without eliciting inflammatory response.

Apoptotic bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20

38

This type of inflammation is manifested by the presence of large amounts of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid.

Suppurative (purulent) inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

39

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

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

39

Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci.

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

40

Focal, intracellular fat deposits creating alternating bands of yellowed myocardium with alternating bands of darker red-brown uninvolved heart or "tigered effect".

Fatty change of the heart(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24

40

It is an excavation of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of inflammatory necrotic tissue.

Ulcer(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

41

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

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

41

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

Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

42

Eosinophilic cytoplasmic inclusion in liver cells composed of aggregated intermediate filaments which resist degradation. Seen in patients woth alcoholic liver disease.

Mallory body / "alcoholic hyalin"(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25

42

Complement fragments which are anaphylotoxins.

C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

43

Aggregated protein inclusions that contain microtubule-associated proteins and neurofilaments, reflecting disrupted neuronal cytoskeleton.

Neurofibrillary tangles in Alzheimer's disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26

43

Complement fragment which aids in opsonization.

C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

44

An insoluble brownish-yellow granular intracellular material that accumulates as a function of age and atrophy. Appears as perinuclear electron-dense granules on electron microscopy.

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

44

Membrane attack complex

C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

45

A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture.

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

45

It is the cytolytic endproduct of the complement cascade, which forms a transmembrane channel causing osmotic lysis of target cells.

Membrane attack complex (C5b,C6-9)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

46

Refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction.

Fat necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11

46

Enzyme blocked by NSAIDS.

Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47

47

A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called "fibrinoid" (fibrin-like) by pathologists.

Fibrinoid necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11

47

Enzyme inhibited by glucocorticoids

Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47

48

Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue.

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

48

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

Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

49

This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.

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

49

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

Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

50

Major cytokines in acute inflmmation.

TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

51

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

Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49

52

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

53

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

Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53

54

Macrophages in the liver

Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

55

Macrophages in the spleen and lymph nodes

Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

56

Macrophages in the CNS

Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

57

Macrophages in the lungs

Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

58

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

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

59

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

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

60

Acid-fast bacilli in macrophages, noncaseating granulomas

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

61

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

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

62

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

63

Noncaseating granulomas with abundant activated macrophages

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

64

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

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

65

Cells with pink, granular cytoplasm with indistinct boundaries.

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

66

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

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

67

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

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

68

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

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