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Inflammation (Phase II) > MoD > Flashcards

MoD Flashcards

1
Q

BCL-2 function

A

Main anti-apoptotic protein

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2
Q

Bim, Bid, Bad function

A

BH3 proteins: activate Bax/Bak channels (cause loss of cytochrome C, activation of capsases), also block BCL-2/BCL-X

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3
Q

Describe the extracellular apoptotic pathway

A

FasL (on T cells) binds to Fas, causing activation of “death receptors” in TNF family, leading to activation of caspases that degrade structural components of nuclear matrix. Fas can also activated Bid, inducing the intrinsic pathway.

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4
Q

Define Pyknosis. What broad change is it associated with?

A

Shrunken, hyper chromatic nucleus; necrosis

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5
Q

Define Karyolysis. What broad change is it associated with?

A

Fading of the nucleus; necrosis

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6
Q

Define Karyorrhexis. What broad change is it associated with?

A

Fragmentation of the nucleus; necrosis

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7
Q

List all changes associated with irreversible cell injury

A

Karyolysis, pyknosis, karyorrhexis, myelin figures, dilation of mitochondria (last 2 on EM)

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8
Q

What type of cellular adaptation precludes cell division? Give examples

A

Hypertrophy; uterine changes during pregnancy, cardiac myocytes (response to incr. workload)

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9
Q

What can cause atrophy? Give examples

A

Decr. inn., blood flow, hormonal stimulation, workload, nutrition, incr. pressure; old brain

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10
Q

What can cause hyperplasia? Give examples

A

Incr. hormonal or GF stimuli; endometrial changes in response to estrogen and lactating breast

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11
Q

What type of necrosis is uniquely associated with TB?

A

Caseous necrosis

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12
Q

Give an example of Fat necrosis

A

Pancreas: lipases split triglycerides into fatty acids which react with calcium to undergo saponification

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13
Q

Describe the mechanism of reperfusion injury

A

Restoration of blood flow causes surge in ROS and nitrogen, also inflammation (d/t hypoxic tissues expressing cytokines and adhesion molecules) with activation of the complement system

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14
Q

Describe abnormal intracellular accumulations seen in reperfusion injury

A

Exogenous substances like minerals, infectious agents; abnormal synthesis or metabolism of endogenous substances like A1AT, Mallory’s hyaline, neurofibrillary tangles in Alzheimers, amyloidosis

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15
Q

Describe the effect of mercuric chloride on GI intestinal cells

A

Incr. membrane permeability; can cause leakage of enzymes

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16
Q

Intracellular accumulations associated with hepatic steatosis

A

Triglycerides in hepatocytes

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17
Q

Intracellular accumulations associated with proteinuria

A

Protein droplets in tubules

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18
Q

Intracellular accumulations associated with A1AT deficiency

A

A1AT globules in liver

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19
Q

Diseases and deposition areas associated with “metastatic calcification”

A

Endocrine diseases (e.g. hypercalcemia caused by renal disease or parathyroid excess); areas of acid secretion like lung, kidney, stomach, pulm veins and systemic arteries

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20
Q

Gross and histologic hallmarks of acute inflammation

A

Edema; neutrophils

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21
Q

Phospholipase A2 function

A

Cleaves arachidonic acid from phospholipid cell membrane

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22
Q

PGI2 function

A

Vasodilation, incr. vasc permeability, pain (peripheral nerve ending sensitization), decr. platelet aggregation, “maintain GFR”

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23
Q

PGE2 function

A

Fever, vasodilation, incr. vasc permeability, pain (CNS + peripheral nerve ending sensitization), “maintain GFR,” “hyperalgesic”

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24
Q

Where does PGD2 come from? Effects?

A

Mast cells; vasodilation, incr. vasc permeability, attracts neutrophils

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25
Q

LTB4 function

A

Attracts and activates neutrophils, also neutrophil adhesion (up regulates interns on leukocytes) and transmigration, produces ROS, release of lysosomal enzyme

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26
Q

LTC4 function

A

Vasoconstriction, bronchospasm, incr. vasc permeability (via pericytes)

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27
Q

LTD4 function

A

Vasoconstriction, bronchospasm, incr. vasc permeability (via pericytes)

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28
Q

LTE4 function

A

Vasoconstriction, bronchospasm, incr. vasc permeability (via pericytes)

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29
Q

Cardinal signs of inflammation? What causes these? What are the mediators?

A

“Rubor and calor” (redness and pain), but also swelling (mediated by histamine); vasodilation; histamine, prostaglandins, bradykinin

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30
Q

Bradykinin function

A

Vasodilation, incr. vasc permeability, pain (via peripheral sensitization)

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31
Q

What 2 substances “do” pain

A

Bradykinin and prostaglandins (NOT histamine)

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32
Q

Where does histamine come from? What is histamine’s function?

A

Mast cells, basophils and platelets; vasodilation (by binding to H1 receptors), incr. vasc permeability (causes swelling associated with acute inflammation), release of P-selectin from W-P bodies (“rolling”), bronchospasm, mucous secretion, dermal edema (“wheal” formation)

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33
Q

Describe the mechanism behind fever incidence as it relates to acute inflammation

A

Pyrogens stimulate IL-1 and TNF release from macrophages, in turn stimulating COX in perivascular cells of the hypothalamus, leading to increased PGE2, which itself raises the temp set point

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34
Q

Where does IL-1 come from? What is IL-1’s function?

A

Dendritic cells and macrophages; one of the “main inflammatory cytokines” - fever (incr. COX activity), mast cell degranulation (acute inflammation), induces E-selectins (rolling), induces CAMs (adhesion), attracts leukocytes (by inducing chemokines), causes “left shift,” causes acute phase secretion of plasma proteins from liver, incr. serum amylase A (SAA), implicated in septic shock and toxic shock syndrome

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35
Q

What mediates vasodilation in acute inflammation?

A

NO

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36
Q

What mediates incr. vasc permeability specifically in acute inflammation?

A

Histamine

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37
Q

What stimuli can cause mast cell degranulation, as it pertains to acute inflammation?

A

C3a, C5a, IL-1, IL-8, cross-linking of surface IgE by antigen, neuropeptides (substance P), cold, heat, tissue trauma

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38
Q

Differentiate between lymphangitis and lymphadenitis

A

Lymphangitis is inflammation of the lymphatic system, lymphadenitis is inflammation of lymph nodes

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39
Q

Define transudate and give an example

A

Edema with low protein concentration and low specific gravity; ascites from liver damage

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40
Q

Define exudate and give an example

A

Edema with high protein concentration and high specific gravity; “empyema,” or pus in pleural spaces from pneumonia

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41
Q

What substances induce chemokines? What do chemokines do?

A

IL-1, TNF, microbial products like LPS; guide leukocytes through tissues

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42
Q

Alpha chemokines’ acronym? What cells do they attract?

A

CXC chemokines; neutrophils

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43
Q

Beta chemokines’ acronym? What cells do they attract?

A

CC chemokines; monocytes, basophils, eosinophils, lymphocytes

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44
Q

Gamma chemokines’ acronym? What cells do they attract?

A

C chemokines; lymphocytes

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45
Q

What are CXCR-4 and CCR-5? What disease are they associated with?

A

Chemokine receptors; HIV

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46
Q

IL-8 function

A

Attracts neutrophils (CXC chemokine), macrophage degranulation, prolongs inflammation (with macrophages)

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47
Q

What step of inflammation are selectins important to? List them all.

A

Rolling; P-selectin (from Weibel-Palade bodies/platelets and endothelial cells), L-selectin (from leukocytes), E-selectin (from endothelium, induced by TNF and IL-1)

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48
Q

What 4 chemical messengers bring neutrophils into the tissue during acute inflammation?

A

c5a, LTB4, IL-8 and bacterial products

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49
Q

What intracellular process is associated with Leukocyte activation?

A

Increase in cytosolic Ca++

50
Q

Describe the final step in acute inflammation with respect to the main cell type associated, and its potential effects

A

Macrophages; resolution and healing via IL-10 and TGF-b, prolonged inflammation via IL-8, abscess, chronic inflammation

51
Q

Characteristics of serous inflammation? Give an example

A

Non-infected fluid from blood plasma or mesothelial cells; blisters

52
Q

Characteristics of fibrinous inflammation? Give an example

A

Fibrinous exudate from extracellular deposition of fibrin, can be converted to scar tissue; meninges or pericardium

53
Q

Characteristics of suppurative inflammation? Give an example

A

Purulent (pus), characterized by neutrophils, liquefied debris of necrotic cells, edema, fluid; abscess (if surrounded by neutrophils, also can become walled off and invaded by connective tissue)

54
Q

What can prolong the neutrophil phase of acute inflammation?

A

Bacterial infections

55
Q

What cell type is associated with hypersensitivity reactions?

A

Eosinophils

56
Q

What cell type is increased by viral infections?

A

Lymphocytes

57
Q

List effects of the acute phase response in acute inflammation

A

Fever (via IL-1 and TNF), leukocytosis, “left shift” (also via IL-1 and TNF), incr. pulse and BP, decr. sweating, chills, rigor, release of liver plasma proteins such as hepcidin, SAA, CRP, fibrinogen (via IL-1, IL-6 and TNF)

58
Q

Clinical signs of septic shock? How is SIRS different?

A

Hypotension, diffuse intravascular coagulation (DIC), insulin resistance/hyperglycemia, metabolic acidosis; SIRS has similar presentation but no infectious cause

59
Q

List all cells associated with chronic inflammation

A

Macrophages (most important), lymphocytes, plasma cells (Ab production), eosinophils (immune reaction mediated by IgE), mast cells (release histamine and prostaglandin granules)

60
Q

Describe bi-directional action of lymphocytes and macrophages

A

Macrophages present antigens; activated T lymphocytes secrete chemokines that recruit macrophages

61
Q

2 ways macrophages get activated

A

By T cells; IL-4

62
Q

Difference between caseating and non-caveating granuloma

A

Non-caseating lacks central necrosis

63
Q

Defining characteristic of a granuloma

A

Presence of epithelioid histiocytes

64
Q

Examples of non-caseating granulomas

A

Crohn’s, sarcoidosis, foreign body, beryllium exposure

65
Q

Examples of caseating granulomas

A

TB, fungi

66
Q

What effect does serum Amyloid A (SAA) have in vivo? What is it stimulated by?

A

Severe chronic inflammation; IL-1 and TNF

67
Q

Major chronic inflammation cytokines (broadly)

A

IL-12, IFN-gamma

68
Q

Major acute inflammation cytokines (broadly)

A

IL-1, TNF

69
Q

IL-10 function

A

“Suppressive” - resolution after acute inflammation, inhibits Th1 cells (by antagonizing IFN-gamma)

70
Q

IL-4 function

A

Ig class switching/helps B cells make Ab (esp IgG1, IgE), incr. MHC II, T cell growth/survival, macrophage activation?

71
Q

IL-6 function

A

One of the “main inflammatory cytokines” - incr. sed rate (by stimulating CRP, fibrinogen from liver during the acute phase response), stimulates B cell differentiation into plasma cells (produce Ab), stimulates T cells differentiation into Th (secrete IL-17)

72
Q

IL-12 function

A

Converts CD4+ helper T cell to Th1 subtype in granuloma formation

73
Q

List examples of labile tissues

A

Skin (basal stem cells), GU, intestine (stem cells in crypts), bone marrow (CD34+ hematopoietic stem cells)

74
Q

List examples of stable tissues

A

Liver, kidney, lung, pancreas, adrenals

75
Q

List examples of permanent tissues

A

Myocardium, skeletal muscle, neurons

76
Q

Describe process/features of initial step of repair (wound healing)

A

Granulation tissue: fibroblasts, capillaries (nutrients), myofibroblasts (pull wound together), collagen III deposition which is replaced by collagen I (via collagenase, requires zinc cofactor)

77
Q

Within what time frame are macrophages usually present in wound healing?

A

3-7 days

78
Q

Within what time frame are neutrophils usually present in wound healing?

A

24 hrs

79
Q

Give examples of parenchymal fibrosis. What is the cause? What mediates this process?

A

Scleroderma, liver cirrhosis, constrictive pericarditis; repeated injurious stimuli; TGF-beta and myofibroblasts (for collagen deposition)

80
Q

What can cause delayed wound healing?

A

Bacterial infection (prolongs inflammation), vitamin C deficiency (required fro hydroxylation of proline), copper deficiency (Lysyl oxidase), zinc deficiency (cofactor for collagenase reaction)

81
Q

TGF-beta function

A

Resolution s/p acute inflammation; scar formation: production of collagen and fibronectin, inhibits metalloproteases (otherwise degrade ECM); “pleiotropic” (fx can be conditional)

82
Q

IFN-a function

A

Viral infection, incr. MHC I expression

83
Q

IFN-b function

A

Viral infection, incr. MHC I expression

84
Q

What cells produce IFN-gamma? What is IFN-gamma’s function?

A

Leukocytes and Th1 cells; “macrophage activation” (converts them to epithelioid histiocytes in granuloma formation), vasodilation, chronic inflammation, anti-bacterial, incr. expression of MHC I & II, inhibits Th2 proliferation

85
Q

What is the role of Serotonin specifically with respect to inflammation? What cells release Serotonin?

A

Vasoconstriction; platelets and neuroendocrine cells

86
Q

What does MCP-1 stand for? What kind of molecule is it?

A

Monocyte chemoattractant protein; chemokine

87
Q

FGF (fibroblast growth factor) function

A

Tissue repair (scar formation), angiogenesis, skeletal development

88
Q

What cells produce hepatocyte growth factor? What is its function? What receptor does it bind?

A

Mesenchymal cells, fibroblasts; cell migration, hepatocyte survival; MET (remember it’s over expressed in some tumors)

89
Q

PDGF function

A

Stimulates fibroblasts, endothelial cell and smooth m. proliferation; also stimulates wound contraction

90
Q

What conditions induce VEGF? What type of receptor does it bind? What effect does this have?

A

Hypoxia; tyrosine kinase; VEGF-A angiogenesis, VEGF-B embryonic angiogenesis, VEGF-C, -D, -E all do angiogenesis and lymphatics

91
Q

IL-17 function

A

Recruits neutrophils

92
Q

Factors in intrinsic (clotting) pathway and test used to assess function

A

II, V, VII, IX, XI, XII, fibrinogen; PTT

93
Q

Factors in extrinsic (clotting) pathway and test used to assess function

A

II, V, VII, X, fibrinogen; PT

94
Q

Thrombin function

A

Converts fibrinogen into cross linked fibrin

95
Q

Clotting factor deficiencies

A

Moderate to severe bleeding: V, VII, VIII, IX, X
Mild bleeding: XI
Thrombotic state: XII
Incompatible with life: Prothrombin

96
Q

Plasmin function (with respect to blood)

A

Breaks down fibrin (fibrinolytic cascade)

97
Q

D dimer

A

Indicative of thrombotic state (fibrinolytic product)

98
Q

Suppurative = ?

A

Supppurative = purulent = pus = pyogenic = dead neutrophils + liquefactive necrosis

99
Q

What area of the brain undergoes necrosis d/t herpes (“herpes encephalitis”)?

A

Temporal lobe destruction

100
Q

Supurative inflammation examples

A

Staphylococcal pneumonia, tissue abscesses (also strep, klebsiella)

101
Q

Mononuclear examples

A

Syphillis, tropheryma whipplei

102
Q

Cytopathic-cytoproliferative reactions examples

A

HPV, herpes

103
Q

Tissue necrosis examples

A

Clostridium perfringens, hep B

104
Q

Chronic inflammation/scarring examples

A

Liver cirrhosis

105
Q

Granulomatous inflammation examples

A

Schistosomiasis, (mycobacterium) TB

106
Q

What disease and clinical finding is associated with a pneumocytis Jiroveci infection?

A

AIDS (CD4+ helper T cell count < 200); diffuse bilateral infiltrates on CXR (fungal inf)

107
Q

Examples of Type III hypersensitivity diseases

A

SLE, rheumatoid arthritis, membranous glomerulonephritis

108
Q

Examples of T-cell mediated cytotoxicity diseases

A

Graft (and maybe transplant) rejection, viral infections, tumor surveillance

109
Q

Examples of type I hypersensitivity reactiosn

A

Asthma, hay fever

110
Q

What can cause an elevated sed rate?

A

If > 100 only neoplasm or temporal arteritis, but also elevated in RA, SLE, chronic inflammation, Sickle Cell Disease (really all anemia), and if elevated in stroke/CAD patients prognosis is poorer

111
Q

Neutropenia causes

A

Decr. production: cytotoxic drugs, radiation, (bone) marrow infiltrate
Decr. survival: Hypersplenism, incr. utilization
Decr. both: Megaloblastic anemia, drug reaction, infection, alcohol

112
Q

Lymphocytosis causes

A

Infectious: Pertussis, Brucellosis, viruses, fungus, TB, syphillis
Neoplastic: CLL causes wicked high levels

113
Q

Lymphocytopenia causes

A

Immunodeficiency (e.g. AIDS) or immunosuppression (e.g. drugs)

114
Q

Eosinophilia causes

A

Parasites, allergy, tumors, drug reactions

115
Q

Eosinopenia causes

A

Severe infection

116
Q

Monocytosis causes

A

Post-splenectomy, hematologic malignancies, TB, syphillis, endocarditis

117
Q

Monocytopenia causes

A

Aplastic anemia (decr. production of WBCs), hairy cell leukemia

118
Q

Basophilia causes

A

Allergic disorder, myeloproliferative disorder, hypothyroidism

119
Q

Basopenia causes

A

Hyperthyroidism (does it even exist?)

120
Q

What can cause an eosinophilic leukemoid reaction?

A

Children with parasitic infections

121
Q

Neutrophilic leukemoid reaction causes

A

Infection, hemolysis, hemorrhage, malignancy involving bone, burns, pregnancy

Inflammation (Phase II) (4 decks)

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