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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

DNA laddering?

A 
Sensitive indicator of apoptosis
During karyorrhexis (nuclear fragmentation): endonucleases clear at internucleosomal regions yielding fragments in multiples of 180bp
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2
Q

Radiation therapy induces?

A

Apoptosis, rapidly dividing cells are most susceptible

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3
Q

Pro-apoptoic factors

A

BAX and BAK

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4
Q

BAX and BAK increase leads to?

A

Increased mitochondrial permeability and cytochrome C release

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5
Q

Anti-apoptotic factors

A

Bcl-2

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6
Q

Bcl-2 increase leads to?

A

Decreased cytochrome C release by binding to and inhibiting Apaf-1

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7
Q

Function of Apaf-1?

A

Induces activation of caspases

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8
Q

What happens when Bcl-2 is over expressed?

A

Apaf-1 is overly inhibited leading to decrease in caspase activation and tumorigenesis (Follicular lymphoma)

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9
Q

Ligand receptor interactions involved in extrinsic pathway apoptosis

A

FasL binding to Fas (CD95)

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10
Q

Immune cell release what to acitivate the extrinsic pathway apoptosis?

A

cytotoxic T cell release of perforin and granzyme B

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11
Q

Fas-FasL interactions are necessary for?

A

Thymic medullary negative selection

When Fas-FasL bind, they induce other Fas around them to activate FADD which activates caspases

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12
Q

Defective Fas-FasL interactions contribute to?

A

Autoimmune disorders

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13
Q

What type of necrosis is seen in brain infarcts?

A

Liquefactive

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14
Q

Liquefactive necrosis due to

A

Neutrophil releasing lysosomal enzymes that digest the tissue (enzymatic degradation then protein denaturing)
Brain infarcts: liquefactive due to high fat content

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15
Q

Coagulative necrosis due to

A

Ischemia or infarction; proteins denature, then enzymatic degradation

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16
Q

Caseous necrosis due to

A

Macrophages wall off the infecting microorganism–>granular debris

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17
Q

Fat necrosis due to

A

Damaged cells release lipase, which breaks down fatty acids in cell membranes–>vessel wall damage

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18
Q

Fibrinoid necrosis due to

A

Immune complexes combine with fibrin–>vessel wall damage

Vessel walls are thick and pink on histology

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19
Q

Gangrenous necrosis due to

A

Distal extremity after chronic ischemia
Dry: ischemia (coagulative)
Wet: superinfection (liquefactive)

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20
Q

Is ATP depletion reversible with O2 or irreversible?

A

Reversible

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21
Q

Is cellular/mitochondrial swelling (decreased ATP->decr. activity of Na/K pumps) reversible with O2 or irreversible?

A

Reversible

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22
Q

Is lysosomal rupture reversible with O2 or irreversible?

A

Irreversible

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23
Q

Is nuclear pyknosis, karryorrhexis, karyolysis reversible with O2 or irreversible?

A

Irreversible

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24
Q

Is plasma membrane damage (degradation of membrane phospholipid) reversible with O2 or irreversible?

A

Irreversible

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25
Q

Is decreased glycogen reversible with O2 or irreversible?

A

Reversible

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26
Q

Is fatty change reversible with O2 or irreversible?

A

Reversible

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27
Q

Is ribosomal/polysomal detachment reversible with O2 or irreversible?

A

Reversible

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28
Q

Is membrane blebbing reversible with O2 or irreversible?

A

Reversible

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29
Q

Is nuclear chromatin clumping reversible with O2 or irreversible?

A

Reversible

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30
Q

Is mitochondrial permeability/vacuolization; phospholipid-containing amorphous densities within mitochondria

A

Irreversible

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31
Q

Which area is most susceptible to ischemia in the brain?

A

ACA/MCA/PCA boundary areas

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32
Q

Which area is most susceptible to ischemia in the heart?

A

subendochondral

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33
Q

Which area is most susceptible to ischemia in the kidney?

A

Straight segment of proximal tubule (medulla)

Thick ascending limb (medulla)

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34
Q

Which area is most susceptible to ischemia in the liver?

A

Area around central vein (zone 3)

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35
Q

Which area is most susceptible to ischemia in the colon?

A

Splenic flexure, rectum (watershed zones)

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36
Q

Which organs get pale infarcts?

A

Heart, kidney, spleen

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37
Q

Which areas get red infarcts?

A

Venous occlusions
Tissues with multiple blood supplies: lungs, liver, intestine
Reperfusion: due to damage to free radicals

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38
Q

Chromatolysis

A

Axonal injury (changes reflect ^ in protein synthesis:
Round cellular swelling
Displavement of the nucleus to the periphery
Dispersion of Nissl substance throughout the cytoplasm

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39
Q

Dystrophic calcification

A

Ca2+ deposited into abnormal tissues secondary to injury or necrosis

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40
Q

Examples of dystrophic calcification

A

Calcific aortic stenosis, TB, lequefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi, schistosomiasis, Monckeberg arteriolosclerosis, congenital CMV+toxoplasmosis, psammomma bodies

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41
Q

Metastatic calcification

A

Widespread deposition of Ca2+ into normal tissue secondary to hypercalcemia or high calcium-phosphate product levels

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42
Q

Examples of metastatic calcification

A

Ca2+ predominantly deposits into kidney, lung, gastric mucosa (these tissues lose acid quickly, ^pH favors deposition)

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43
Q

Calcium levels in patients with metastatic and dystrophic calcification

A

Metastatic: not normocalcemia
Dystrophic: normocalcemia

44
Q

Proteins involved in margination and rolling of WBC

A

E-selectin
P-selectin
GlyCAM1, CD34

45
Q

Proteins involved in tight binding of WBC

A

ICAM1

VCAM1

46
Q

Proteins involved in diapedesis of WBC

A

PECAM1

47
Q

Proteins involved in migration of WBC

A

Chemotactic products: C5a, IL-8, LTB4, kallikrein, platelet activating factor

48
Q

What is the defective on the WBC in leukocyte adhesion deficiency type 1

A

CD18 integrins: LFA1, MAC-1

49
Q

What part of the WBC binds to E/P-selectins

A

Sialyl-lewis (during margination/rolling) (lewis=leukocyte)

50
Q

What part of the WBC binds to GlyCAM/CD34

A

L-selectin “leukocyte-selectin”

51
Q

What part of the WBC binds to ICAM1

A

CD11/CD18 integrins: LFA1/MAC1 (I=leukocyte)

52
Q

What part of the WBC binds to VCAM1

A

VLA-4 integrin (I=leukocyte)

53
Q

How do free radicals damage cells?

A

Membrane lipid peroxidation
Protein modification
DNA breakage

54
Q

Scavenging enzymes purpose and types

A

Eliminate free radicals.
Catalase
Superoxide dismutase
Glutathoine peroxidase

55
Q

Types of free radical elimination

A

Scavenging enzymes
Spontaneous decay
Antioxidants (Vit. A, C, E)
Certain metal carrier proteins (transferrin, ceruloplasmin)

56
Q

Free radical injury due to carbon tetrachloride

A

Liver necrosis (fatty change)

57
Q

Free radical injury due to acetaminophen overdose

A

Fulminant hepatitis, renal papillary necrosis

58
Q

Free radical injury due to iron overload

A

Hemochromatosis

59
Q

Free radical injury due to reperfusion injury

A

Esp. due to thrombolytic therapy

60
Q

Tissue mediators that facilitate angiogenesis

A

VEGF
TGF-B
FGF

61
Q

Tissue mediators that facilitate tissue remodeling

A

Metalloproteinases

62
Q

Tissue mediators that stimulate cell growth

A

EGF (via tyrosine kinases (EGFR))

63
Q

Tissue mediators that stimulate vascular remodeling and smoother muscle cell migration

A

PDGF

64
Q

Tissue mediators that stimulate fibroblast growth for collagen synthesis

A

PDGF (TGF-B stimulates fibrosis)

65
Q

Tissue mediators that stimulate cell cycle arrest

A

TGF-B

66
Q

PDGF role

A

Activated platelets and macrophages secrete to:
Induce remodeling and smooth muscle cell migration
Stimulates fibroblast growth for collagen synthesis

67
Q

FGF role

A

Stimulates angiogenesis

68
Q

EGF role

A

Stimulates cell growth via tyrosine kinases

69
Q

TGF-B role

A

Angiogenesis, fibrosis, cell cycle arrest

70
Q

Metalloproteinases role

A

Tissue remodeling

71
Q

VEGF role

A

Stimulates angiogenesis

72
Q

1st phase of wound healing

A

0-3 days. Inflammatory: clot formation, increase vessel permeability and PMN migration, macrophages clear out debris

73
Q

2nd phase of wound healing

A

3 days-weeks. Proliferative: Deposition of granulation tissue and collagen, angiogenesis, wound contraction (myofibroblasts)

74
Q

3rd phase of wound healing

A

1 week-months. Remodeling: Type III collagen replaced by type 1 collagen
^ tensile strength of tissue

75
Q

Granulomatous disease mechanism

A

Th1 cells secrete IFN-g, activating macrophages

TNF-a from macrophages induces and maintains granuloma formation

76
Q

What should you always test for being starting anti-TNF therapy?

A

Tuberculosis (TNF-a breaks down the granuloma and can cause full dissemination of the disease)

77
Q

Examples of disease with granulomas

A 
Bartonellas
Listeria
M. Leprae
M. tuberculosis
Treponema pallidum (tertiary)
Schistosomiasis
Fungal infections
Sarcoidosis
Berylliosis
Eosinophlic granulomatosis with polyangitis (Churg-strauss)
Granulomatosis with polyangitis (Wegeners)
Crohn diease
Foreign device
78
Q

Exudate contents

A

Cellular, protein rich, ^specific gravity (1.020+)

79
Q

Reasons for exudate

A

Lymphatic obstruction
Inflammation/ infection
Malignancy

80
Q

Transudate contents

A

Hypocellular, protein-poor, decrease specific gravity (less than 1.012)

81
Q

Reasons for transudate

A

Increased hydrostatic pressure
Decreased oncotic pressure (cirrhosis, nephrotic syndrome)
Na+ retention

82
Q

ESR measures what?

A

Products of inflammation coat RBCs and cause aggregation. The denser the RBC, the faster it falls

83
Q

Elevated ESR associated with

A 
Most anemia
Infection
Inflammation (termporal arteritis)
Cancer
Pregnancy
Autoimmune disorders (SLE)
84
Q

Decreased ESR associated with

A 
Sickle cell anemia
Polycythemia
HF
Microcytosis
Hypofibrinogenemia
85
Q

AL amyloidosis consists of

A

Ig Light chains (aL for light chain)

Multiple myeloma or other plasma cell disorders

86
Q

AA amyloidosis consists of

A

serum Amyloid A (AA)

Seen in chronic inflammatory conditions: RA, IBD, spondyloarthropathy, protracted infection

87
Q

Dialysis related amyloidosis consists of

A

Fibrils composed of B2-microglobulin in patients with ESRD

88
Q

Heritable amyloidosis consists of

A

Heterogenous group of disorders: familiar amyloid polyneuropathies
Transthyretin gene mutation

89
Q

Age-related (senile) systemic amyloidosis

A

Deposition of normal transthyretin in myocardium

Slow cardiac progression than AL

90
Q

Amyloidosis on histology

A

Congo red stains with apple green birefringence

91
Q

Lipofuscin

A

Signs of normal aging
Yellow-brown wear and tear pigment
Oxidation and polymerization of autophagocytoseed organellar membranes
Autopsy of elderly person will reveal deposits in heart colon, liver, kidney, eye etc.

92
Q

P-glycoprotein aka

A

Multidrug resistance protein 1 (MDR1)

93
Q

What is the function of MDR1/P-glycoprotein?

A

A function of cancer cells that is used to pump out toxins including chemotherapy (ATP dependent)

94
Q

What type of protein is MDR1/P-glycoprotein?

A

ATP-dependent protein efflux pump

95
Q

What cancer classically has MDR1/P-glycoprotein?

A

Adrenal cell carcinoma

96
Q

Anaplasia

A

Loss of structural differential and function of cells
Resemblings primitive cells of same tissue
May see giant cells with single large nucleus

97
Q

Desmoplasia

A

Fibrous tissue formation in response to neoplasm

Ex. linitis plastica in diffuse stomach cancer)

98
Q

Cancer grade

A

Degree of cellular differentiation and mitotic activity on histology

99
Q

Cancer stage

A

Degree of localization/spread based on primary lesion
TNM: Tumor size, node involvement, metastases
**Best indicator of prognosis!!

100
Q

Most carcinomas spread?

A

Lymphatically

101
Q

Most sarcomas spread?

A

Hematogenously

102
Q

Hamartoma definition and example

A

Disorganized overgrowth of tissues in their native location

Ex. Peutz-Jeghers polyps

103
Q

Choristoma definition and example

A

Normal tissue in a foreign location

Gastric tissue located in the small bowel in Meckel diverticulum

104
Q

Cachexia definition

A

Weight loss, muscle atrophy, and fatigue that occurs in chronic disease (cancer, AIDS, heart failure, TB)

105
Q

What mediates cachexia

A

TNF-a (also IFN-g, IL-1, IL-6)

Pathology (5 decks)

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