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NBME 21 > Pathology > Flashcards

Pathology Flashcards

1
Q

neurons most vulnerable to hypoxic-ischemic insults

A

purkinje cells of cerebellum

pyramidal cell of hippocampus and neocortex (zones 3, 5, 6)

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2
Q

histology of caseous necrosis

A

fragmented cells and debris surrounded by lymphocytes and macrophages (granuloma)

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3
Q

what is primary systemic amyloidosis associated with

A

plasma cell dycrasias (MM)

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4
Q

what is secondary systemic amyloidosis

A

systemic deposition of serum amyloid A (AA)

seen in chronic inflammatory conditions (RA, IBD, familiar mediterranean fever, protracted infection, cancer)

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5
Q

Fever mechanism

A
  1. pyrogens (LPS) induce macrophages to release IL-1 and TNF
  2. increase COX in perivascular cells of hypothalamus
  3. increase PGE2
  4. increase temp set point
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6
Q

which bcl-2 proteins are proapoptotic

A

BAX
BAK
form pores in mitochondrial membrane –> release cytochrome C (inner mito) into cytoplasm –> activation of capsases

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7
Q

the two pathways of extrinsic (death receptor) path

A
  1. ligand receptor interactions (FasL binding to Fas [CD95] or TNF alpha bind to receptor)
  2. immune cell (cytotoxic T-cell release of perforin and granzyme B)
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8
Q

Fas-FasL interaction is necessary in

A

thyme medullary negative selection

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9
Q

What kind of necrosis is seen with distal extremity and GI tract after chronic ischemia

A

gangrenous

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10
Q

caseous necrosis is d/t

A

macrophages

-wall off infecting microorganism –> granular debris

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11
Q

How is apoptosis different from necrosis

A

apoptosis does not have local inflammatory reaction

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12
Q

area of liver most vulnerable to ischemia

A

area around central vein (zone III)

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13
Q

histology of wet gangrene

A

liquefactive superimposed on coagulative

liquefactive: neutrophils and cell debris seen with bacterial infection
coagulative: preserved cell structure w/no nuclei, increased eosin staining, PMNs later to clean up

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14
Q

what does bcl-2 do

A

keeps mitochondrial membrane impermeable

prevents cytochrome C from leaking

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15
Q

what is primary systemic amyloidosis

A

systemic deposition of AL amyloid derived from Ig light chain

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16
Q

acute phase proteins are notably induced by

A

IL-6

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17
Q

rubor (redness) and color (warmth) is mediated by

A 
histamine
PG
bradykinin
NO
vasodilation (SM relaxation)
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18
Q

MC see coagulative necrosis in what organs

A 
heart
liver
spleen
kidneys
organs that use a lot of oxygen
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19
Q

Aschoff bodies in acute rheumatic heart disease is an example of what kind of necrosis

A

fibrinoid necrosis
(type II hypersensitivity)
lymphocytes in heart muscles layers

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20
Q

what does fat necrosis look like on H&E stain

A

dark blue

-saponification of fat with Ca

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21
Q

familial ventricular endomyocardium deposition of amyloid causes

A

restrictive cardiomyopathy and arrhythmia

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22
Q

what kind of necrosis do you see in brain infarcts and pancreas

A

liquefactive

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23
Q

tumor (swelling) is mediated by

A 
endothelial contraction
leukotrienes C4, D4, E4
histamine
serotonin
increase vascular permeability and interstitial oncotic pressure
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24
Q

what kind of necrosis will you see in immune vascular reactions (PAN)

A

fibrinoid necrosis

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25
Q

what is familial mediterranean fever

A

AR
dysfunction of neutrophils
acute fever and serousal inflammation
high SAA during attacks that deposit as AA amyloid

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26
Q

opsonin
fixes complement and facilitates phagocytosis
measured clinically as nonspecific sign of ongoing inflammation

A

CRP (positive, upregulated)

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27
Q

definition of pseudocyst (seen in pancreas)

A

cavity of fluid lined by necrotic tissue

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28
Q

intrinsic and extrinsic apoptosis mediated by

A

capsases (cytosolic proteases)

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29
Q

Part of kidney most vulnerable to ischemia

A

straight segment of proximal tubule (medulla)

thick ascending limb (medulla)

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30
Q

GI manifestations of systemic amyloidosis

A

macroglossia
hepatomegaly
malabsorption from bowel thickening

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31
Q

histology of dry gangrene

A

same as coagulative

  • preserved cell architecture
  • nuclei disappear
  • increase cytoplasmic binding of eosin stain
  • neutrophils will come in to clean up later on
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32
Q

liquefactive necrosis histology

A

early: cellular debris and macrophages
late: cystic spaces and cavitation (brain), neutrophils and cell debris seen with bacterial infection

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33
Q

MC organ affected by amyloid

A

kidney

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34
Q

general characteristics of reversible cell injury

A
  • ribosomal/polysomal detachment (decrease protein synthesis)
  • plasma membrane changes (blobbing)
  • nuclear changes (chromatin clumping)
  • rapid loss of function (myocardial cells are non contractile after 1-2 min of ischemia)
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35
Q

general characteristics of irreversible cell injury

A
  • mitochondrial damage/dysfunction
  • rupture of lysosomes –> autolysis
  • nuclear degradation
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36
Q

Intrinsic pathway regulated by what family of proteins

A

bcl-2

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37
Q

neurologic manifestations of systemic amyloidosis

A

neuropathy

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38
Q

examples of localized amyloidosis

A 
alzheimer dz
T2DM
medullary thyroid cancer
isolated atrial amyloidosis
systemic senile (age related) amyloidosis
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39
Q

autoimmune lymphoproliferative syndrome is caused by

A

defective Fas-FasL interactions

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40
Q

MSK manifestations of systemic amyloidosis

A

carpal tunnel syndrome

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41
Q

amyloidosis Dx requires

A

biopsy

abdominal fat pad or rectum are easy

42
Q

transudate is d/t

A

increase hydrostatic pressure (HF, Na retention)

decrease oncotic pressure (cirrhosis, nephrotic syndrome)

43
Q

MC type of necrosis

A

coagulative

  • seen in ischemia/infarcts (except in brain)
  • injury denatures enzymes (proteolysis blocked)
44
Q

Where do you see caseous necrosis (cottage cheese)

A

TB
systemic fungi (histoplasma capsulatum)
nocardia

45
Q

Definition of a cyst

A

cavity of fluid lined by epithelium

46
Q

histology of coagulative necrosis

A
  • preserved cell architecture
  • nuclei disappear
  • increase cytoplasmic binding of eosin stain
  • neutrophils will come in to clean up later on
47
Q

area of colon most vulnerable to ischemia

A

splenic flexure

rectum

48
Q

When do red infarcts occur

A

venous occlusion
tissues with multiple blood supplies (liver, lung, intestine, testes)
reperfusion (after angioplasty)

49
Q

apoptotic cell characterized by

A

ATP dependent programmed cell death
eosinophilic cytoplasm
basophilic nucleus
pyknosis (nuclear condensation)
karyorrhexis (nuclear fragmentation)
DNA laddering (fragments in multiples of 180 bp)
cell membrane typically intact w/o significant inflammation

50
Q

beta 2 microglobulin is associated with

A

supports MHC class I transmembrane function

51
Q

histology of fat necrosis

A

outlines of dead fat cells w/o peripheral nuclei

52
Q

what are the two inherited amyloidoses

A

familial amyloid cardiomyopathy (5% in AA)
familial amyloid poly neuropathies
both mutated transthyretin (ATTR)

53
Q

lipofuscin is formed by

A

oxidation and polymerization of autophagocytosed organelles membranes

54
Q

what cell predominates the late stages of acute inflammation

A

macrophages
peak 2-3 days after onset
influence outcomes by secreting cytokines

55
Q

where do you see systemic senile amyloidosis

A

cardiac ventricles
increased transthyretin (TTR, normal wild type)
cardiac dysfunction more insidious than in AL amyloidosis
asymptomatic

56
Q

what coats RBCs during inflammation

A

fibrinogen
makes them less negative and stick together
increases ESR

57
Q

Biochemical basis of reversible cell injury

A

decrease ATP –> decrease activity of calcium and Na/K pumps –> cellular swelling (earliest) –> mitochondrial swelling

58
Q

what kind of necrosis will you see in hypertensive emergency and preeclampsia (non-immune vascular reaction)

A

fibrinoid necrosis

59
Q

deposition of beta 2 micro globulin in joints

A

dialysis-related amyloidosis

60
Q

pale infarcts occur when

A

solid organs with single blood supply (heart, kidney)

61
Q
  • tissue remodeling in embryogenesis
  • withdrawn regulating factor from proliferating cell population
  • after exposure to injurious stimuli (radiation, toxins, hypoxia)
A

intrinsic pathway (mitochondrial)

62
Q

fibrinoid necrosis is d/t

A
  • immune complex deposition (type III)

- plasma protein (fibrin) leakage from damaged vessel

63
Q

which bcl-2 proteins are antiapoptotic

A

bcl-2

bcl-xL

64
Q

what triggers activation of capsases in intrinsic pathway

A

cytochrome C release from inner mitochondrial

65
Q

over expression of bcl-2 is associated with what cancer

A

follicular lymphoma t[14, 18]

-decrease capsize activation = tumorigenesis

66
Q

on H& E stain, calcium deposits appear

A

basophilic

67
Q

what kind of necrosis do you see in bacterial abscesses

A

liquefactive

68
Q

characteristics of dysplasia

A

disordered precancerous epithelial cell growth
not truly adaptive response
-loss of uniformity (pleomorphism)
-loss of tissue orientation
-nuclear changes (increase nuclear:cytoplasm ratio, clumped chromatin)

69
Q

AL deposition

A

primary systemic amyloidosis

70
Q

nuclear changes in irreversible cell injury

A

nuclear degradation

  1. pyknosis (nuclear condensation)
  2. karyorrhexis (nuclear fragmentation caused by endonuclease by endonuclease mediated cleavage
  3. karyolysis (nuclear dissolution)
71
Q

Coagulation factor
promotes endothelial repair
correlates with ESR
acute phase reactant

A

fibrinogen (positive, upregulated)

72
Q

necrosis seen with traumatic injury

A

non enzymatic fat necrosis

-injury to breast tissue

73
Q

wet gangrene is d/t

A

superinfection

74
Q

cardiac manifestations of systemic amyloidosis

A

restrictive cardiomyopathy

arrythmia

75
Q

biochemical basis of irreversible cell injury

A

breakdown plasma membrane –> cytosolic enzymes leak into serum (troponin) –> influx of Ca –> activation of degradative enzymes

76
Q

reduction conserves amino acids for positive reactants

A

albumin (negative, down regulated)

acute phase reactant

77
Q

organs with amyloid deposition can only be cured with

A

transplant

cannot be removed

78
Q

isolated atrial amyloidosis commonly seen in

A

normal aging
increase risk of a-fib
increased ANP

79
Q

What is amyloid

A

misfiled protein that deposits in extracellular space and damages tissues

80
Q

examples that decrease ESR

A 
-sickle cell (altered shape)
polycythemia (increase RBC "dilute" aggregation factors)
-HF
-microcytosis
-hypofibrinogenemia
81
Q

acute phase proteins are made by

A

the liver in both acute and chronic inflammation

82
Q

Alzheimer dz is d/t

A

increased beta-amyloid protein

cleaved from amyloid precursor protein (APP)

83
Q

serum amyloid A

A

secondary systemic amyloidosis

84
Q

amyloid tends deposits around

A

blood vessels

85
Q

histology of fibrinoid necrosis

A

vessel walls are thick and pink

86
Q

amyloid in DM is d/t

A

deposition of amylin in pancreatic islets

will see increased islet amyloid polypeptide (IAPP)

87
Q

Dolor (pain) is mediated by

A

bradykinin
PGE2
histamine
sensitization of sensory nerve endings

88
Q

attack of increased SAA and deposition of AA amyloid

A

familial mediterranean fever

89
Q

Why doesn’t the brain experience coagulative necrosis

A

less fibroblasts

90
Q

Dry gangrene is d/t

A

ischemia

91
Q

mutations in Fas causes

A

increase numbers of circulating self-reacting lymphocytes d/t failure of clonal deletion

92
Q

liquefactive necrosis is d/t

A 
neutrophil release (heterolysis)
lysosomal enzymes that digest tissue (autolysis)
93
Q
  • decrease in tissue mass d/t decrease in size
  • increase cytoskeleton degradation via ubiquitin-proteasome path and autophagy, decrease protein synthesis
  • apoptosis
A

atrophy

94
Q

renal manifestations of systemic amyloidosis

A

nephrotic syndrome

95
Q

Exudate is due to

A

lymphatic obstruction
inflammation/infection
malignancy

96
Q

SAA is an example of an

A

acute phase reactant

increased in chronic inflammation, malignancy, familial mediterranean fever

97
Q

what is lipofuscin

A

“wear and tear” pigment
yellow-brown
associated with normal aging
see in heart, colon, liver, kidney, eye, other

98
Q

what is dialysis related amyloidosis

A

systemic amyloidosis with deposition of beta 2 micro globulin

seen in ESRD and/or long term dialysis

99
Q

necrosis seen in acute pancreatitis

A

enzymatic fat necrosis

  • saponification of peripancreatic fat
  • damaged pancreatic cells release lipase –> breaks down TG
  • liberated FA’s bind Ca = saponification (chalky white appearance)
100
Q

hematologic manifestations of systemic amyloidosis

A

easy bruising

splenomegaly

NBME 21 (13 decks)

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