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PATH > Q1 Exam 1 > Flashcards

Q1 Exam 1 Flashcards

1
Q

pyknosis

A

irreversible condensation of chromatin in the nucleus

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2
Q

karyorrhexis

A

nuclear fragmentation

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3
Q

karyolysis

A

extremely pale nucleus (can even later disappear entirely)

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4
Q

what differs with necrosis vs apoptosis?

A

necrosis- swelling and inflammation, cell pops
apoptosis- cell shrinks, no inflammation, releases apoptotic bodies with cell membrane intact

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5
Q

initiator caspases

A

extrinsic - caspase 8
intrinsic - caspase 9

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6
Q

executioner caspases

A

caspase 3, 6, 7, 12

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7
Q

7 signs of necrosis

A

eosinophilia, glassy appearance, cytoplasmic vacuolation, karyolysis, ghost cells, nearby leukocytes, dystrophic calcification

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8
Q

labile cells

A

continuously cycling cells, typically stem cell pool present, ex. mouth, skin, gut and bladder, bone marrow

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9
Q

quiescent tissue

A

stable cells, divide infrequently but can be stimulated to divide (in G0), ex. most cells in the body

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10
Q

permanent cells

A

non dividing tissues, have very little regenerative capacity, ex. neurons, cardiac muscle, and photoreceptors

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11
Q

causes of pathologic atrophy

A

abnormal decrease in functional demand, denervation, starvation

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12
Q

causes of pathologic hyperplasia and hypertrophy

A

abnormal increase in functional demand, excessive hormonal stimulation, or reactive/inflammatory

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13
Q

concentric hypertrophy

A

heart hypertrophy from the outside toward the lumen

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14
Q

eccentric hypertrophy

A

circumference gets bigger, not wall thickness (addition of sarcomeres in series)

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15
Q

cavitation

A

results from significant damage to the brain

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16
Q

anthracosis

A

black carbon pigment found in the lung, associated with air pollutants

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17
Q

tyrosinase

A

copper containing enzyme that oxidizes tyrosine to melanin

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18
Q

lipofuscin

A

endogenous yellow brown pigment, “wear and tear” pigment formed from autophagocytosis that accumulates naturally over time

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19
Q

ceroid

A

endogenous yellow green pigment that is bad for cells, can accumulate with specific pathologic conditions

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20
Q

jaundice

A

yellow pigmentation due to presence of bilirubin

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21
Q

hematin

A

brown pigment that is an artifact of formic acid and heme

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22
Q

gout pathogenesis

A

absence of enzyme uricase cannot convert uric acid to allantoin

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23
Q

amyloidosis

A

deposits accumulate often secondary to inflammation because of acute phase proteins (stains with congo red and apple green bioflumaofn (idk))

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24
Q

calcinosis circumscripta

A

localized calcium deposits, purple crystals under HE

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25
Q

major structural component of extracellular matrix

A

type 1 collagen

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26
Q

4 causes of edema

A

increased permeability, increased hydrostatic pressure (hepatic and heart failure, RAAS), decreased osmotic pressure, decreased lymphatic drainage

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27
Q

canine congenital lymphedema

A

abnormal development of lymphatic vessels leads to interstitial swelling and edema

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28
Q

hyperemia vs congestion

A

increase of blood volume in tissue due to: arteriolar dilation vs impaired outflow (respectively)

29
Q

virchow’s triad

A

endothelial injury, alterations in blood flow, hypercoagulability

30
Q

what are the vitamin K dependent factors in the coagulation cascade

A

10, 9, 7, 2

31
Q

plasmin

A

digests fibrin clots and prevents blood clots from forming badly

32
Q

antithrombin III

A

coagulation inhibitor produced by endothelium and hepatocytes

33
Q

petechial hemorrhage

A

less than 2mm in diameter

34
Q

ecchymotic hemorrhage

A

2-10mm in diameter

35
Q

purpuric hemorrhage

A

mix of petechial and ecchymotic

36
Q

arterial thrombus vs venous thrombus

A

arterial- laminated appearance, deposition of fibrin and platelets from rapid flow
venous- dark and gelatinous containing a lot of erythrocytes because slow flow

37
Q

how can you tell the difference between acute and chronic infarcts

A

acute- red and swollen, beginning of necrosis
chronic- pale shrunken and firm

38
Q

5 signs of infection

A

swelling, redness, pain, heat, loss of function

39
Q

what activates neutrophils and endothelial cells for the leukocyte adhesion cascade

A

il1, 6, 8, TNFa, C3a, C5a

40
Q

postive and negative APP

A

c-reactive protein+, SAA+, albumin-

41
Q

transudate

A

little protein and few cells, clear and watery

42
Q

exudate

A

rich in protein or cells

43
Q

hypersensitivity 1

A

igE from allergen

44
Q

hypersensitivity 2

A

igG and igM (IMHA) reacts to own cells

45
Q

hypersensitivity 3

A

igG and igM to a soluble antigen, causes necrotizing vasculitis

46
Q

hypersensitivity 4

A

T lymphocyte mediated, contact dermatitis, johnes, forms granulomas

47
Q

myeloperoxidase

A

enzyme in neutrophils that contributes to necrosis and liquefaction

48
Q

how fast do abcesses form

A

2-3 days for sterile and weeks for septic

49
Q

nodular granuloma

A

cells arranged in discrete masses, TH1 based

50
Q

diffuse granuloma

A

cells dispersed in sheets, TH2 based often intracellular bacterial burden (johnes)

51
Q

FIP immune component

A

pyogranulomatous vasculitis

52
Q

phases of wound healing

A

hemostasis, inflammation, proliferation, maturation (TGFb critical)

53
Q

primary vs secondary intention wound healing

A

primary- edges apposed, heals rapidly

54
Q

bovine lymphosarcoma cause

A

bovine leukemia retrovirus

55
Q

hamartoma vs choristoma

A

disorganized tissue in normal location (often benign) vs. disorganized in abnormal location (often malignant)

56
Q

sheets

A

common in round cell tumors

57
Q

packets

A

common in neuroendocrine

58
Q

nests

A

cells form encapsulated clumps, common in invasive carcinomas

59
Q

cords

A

cells form branching chains, common in epithelial tumors

60
Q

lobules

A

cells form inside bands of connective tissue, common in some epithelial tumors

61
Q

why do carcinomas tend to use the lymphatic system to spread

A

they tend to form larger neothrombi and thus need the larger gaps in lymphatic valves

62
Q

atrial natriuretic peptide

A

promotes renal sodium and water excretion and stimulates vasodilation

63
Q

disseminated intravascular coagulopathy

A

initiated by diffuse endothelial damage and platelet activation, small blood clots form inside blood vessels everywhere, causes abnormal bleeding and ischemic injury

64
Q

ARDS

A

damaged vessels allow leakages of fibrin and fluid which can damage hyaline membranes in the lungs

65
Q

neurogenic shock pathogenesis

A

autonomic system triggered but SNS tone is lost, PNS dominates, vasodilation and bradycardia causes hypoperfusion

66
Q

three stages in development of shock

A

compensation (RAAS), progression (acidosis), and irreversible ischemic necrosis

67
Q
A
68
Q

Common staging of tumors

A

T0-4 for size, N0-3 for lymph node involvement, M0-3 for metastasis

PATH (13 decks)

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