Q1 Exam 1

Question 1

pyknosis

Answer 1

irreversible condensation of chromatin in the nucleus

Question 2

karyorrhexis

Answer 2

nuclear fragmentation

Question 3

karyolysis

Answer 3

extremely pale nucleus (can even later disappear entirely)

Question 4

what differs with necrosis vs apoptosis?

Answer 4

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

Question 5

initiator caspases

Answer 5

extrinsic - caspase 8
intrinsic - caspase 9

Question 6

executioner caspases

Answer 6

caspase 3, 6, 7, 12

Question 7

7 signs of necrosis

Answer 7

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

Question 8

labile cells

Answer 8

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

Question 9

quiescent tissue

Answer 9

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

Question 10

permanent cells

Answer 10

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

Question 11

causes of pathologic atrophy

Answer 11

abnormal decrease in functional demand, denervation, starvation

Question 12

causes of pathologic hyperplasia and hypertrophy

Answer 12

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

Question 13

concentric hypertrophy

Answer 13

heart hypertrophy from the outside toward the lumen

Question 14

eccentric hypertrophy

Answer 14

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

Question 15

cavitation

Answer 15

results from significant damage to the brain

Question 16

anthracosis

Answer 16

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

Question 17

tyrosinase

Answer 17

copper containing enzyme that oxidizes tyrosine to melanin

Question 18

lipofuscin

Answer 18

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

Question 19

ceroid

Answer 19

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

Question 20

jaundice

Answer 20

yellow pigmentation due to presence of bilirubin

Question 21

hematin

Answer 21

brown pigment that is an artifact of formic acid and heme

Question 22

gout pathogenesis

Answer 22

absence of enzyme uricase cannot convert uric acid to allantoin

Question 23

amyloidosis

Answer 23

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

Question 24

calcinosis circumscripta

Answer 24

localized calcium deposits, purple crystals under HE

Question 25

major structural component of extracellular matrix

Answer 25

type 1 collagen

Question 26

4 causes of edema

Answer 26

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

Question 27

canine congenital lymphedema

Answer 27

abnormal development of lymphatic vessels leads to interstitial swelling and edema

Question 28

hyperemia vs congestion

Answer 28

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

Question 29

virchow's triad

Answer 29

endothelial injury, alterations in blood flow, hypercoagulability

Question 30

what are the vitamin K dependent factors in the coagulation cascade

Answer 30

10, 9, 7, 2

Question 31

plasmin

Answer 31

digests fibrin clots and prevents blood clots from forming badly

Question 32

antithrombin III

Answer 32

coagulation inhibitor produced by endothelium and hepatocytes

Question 33

petechial hemorrhage

Answer 33

less than 2mm in diameter

Question 34

ecchymotic hemorrhage

Answer 34

2-10mm in diameter

Question 35

purpuric hemorrhage

Answer 35

mix of petechial and ecchymotic

Question 36

arterial thrombus vs venous thrombus

Answer 36

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

Question 37

how can you tell the difference between acute and chronic infarcts

Answer 37

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

Question 38

5 signs of infection

Answer 38

swelling, redness, pain, heat, loss of function

Question 39

what activates neutrophils and endothelial cells for the leukocyte adhesion cascade

Answer 39

il1, 6, 8, TNFa, C3a, C5a

Question 40

postive and negative APP

Answer 40

c-reactive protein+, SAA+, albumin-

Question 41

transudate

Answer 41

little protein and few cells, clear and watery

Question 42

exudate

Answer 42

rich in protein or cells

Question 43

hypersensitivity 1

Answer 43

igE from allergen

Question 44

hypersensitivity 2

Answer 44

igG and igM (IMHA) reacts to own cells

Question 45

hypersensitivity 3

Answer 45

igG and igM to a soluble antigen, causes necrotizing vasculitis

Question 46

hypersensitivity 4

Answer 46

T lymphocyte mediated, contact dermatitis, johnes, forms granulomas

Question 47

myeloperoxidase

Answer 47

enzyme in neutrophils that contributes to necrosis and liquefaction

Question 48

how fast do abcesses form

Answer 48

2-3 days for sterile and weeks for septic

Question 49

nodular granuloma

Answer 49

cells arranged in discrete masses, TH1 based

Question 50

diffuse granuloma

Answer 50

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

Question 51

FIP immune component

Answer 51

pyogranulomatous vasculitis

Question 52

phases of wound healing

Answer 52

hemostasis, inflammation, proliferation, maturation (TGFb critical)

Question 53

primary vs secondary intention wound healing

Answer 53

primary- edges apposed, heals rapidly

Question 54

bovine lymphosarcoma cause

Answer 54

bovine leukemia retrovirus

Question 55

hamartoma vs choristoma

Answer 55

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

Question 56

sheets

Answer 56

common in round cell tumors

Question 57

packets

Answer 57

common in neuroendocrine

Question 58

nests

Answer 58

cells form encapsulated clumps, common in invasive carcinomas

Question 59

cords

Answer 59

cells form branching chains, common in epithelial tumors

Question 60

lobules

Answer 60

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

Question 61

why do carcinomas tend to use the lymphatic system to spread

Answer 61

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

Question 62

atrial natriuretic peptide

Answer 62

promotes renal sodium and water excretion and stimulates vasodilation

Question 63

disseminated intravascular coagulopathy

Answer 63

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

Question 64

ARDS

Answer 64

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

Question 65

neurogenic shock pathogenesis

Answer 65

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

Question 66

three stages in development of shock

Answer 66

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

Question 68

Common staging of tumors

Answer 68

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