Q1 Exam 1 Flashcards
pyknosis
irreversible condensation of chromatin in the nucleus
karyorrhexis
nuclear fragmentation
karyolysis
extremely pale nucleus (can even later disappear entirely)
what differs with necrosis vs apoptosis?
necrosis- swelling and inflammation, cell pops
apoptosis- cell shrinks, no inflammation, releases apoptotic bodies with cell membrane intact
initiator caspases
extrinsic - caspase 8
intrinsic - caspase 9
executioner caspases
caspase 3, 6, 7, 12
7 signs of necrosis
eosinophilia, glassy appearance, cytoplasmic vacuolation, karyolysis, ghost cells, nearby leukocytes, dystrophic calcification
labile cells
continuously cycling cells, typically stem cell pool present, ex. mouth, skin, gut and bladder, bone marrow
quiescent tissue
stable cells, divide infrequently but can be stimulated to divide (in G0), ex. most cells in the body
permanent cells
non dividing tissues, have very little regenerative capacity, ex. neurons, cardiac muscle, and photoreceptors
causes of pathologic atrophy
abnormal decrease in functional demand, denervation, starvation
causes of pathologic hyperplasia and hypertrophy
abnormal increase in functional demand, excessive hormonal stimulation, or reactive/inflammatory
concentric hypertrophy
heart hypertrophy from the outside toward the lumen
eccentric hypertrophy
circumference gets bigger, not wall thickness (addition of sarcomeres in series)
cavitation
results from significant damage to the brain
anthracosis
black carbon pigment found in the lung, associated with air pollutants
tyrosinase
copper containing enzyme that oxidizes tyrosine to melanin
lipofuscin
endogenous yellow brown pigment, “wear and tear” pigment formed from autophagocytosis that accumulates naturally over time
ceroid
endogenous yellow green pigment that is bad for cells, can accumulate with specific pathologic conditions
jaundice
yellow pigmentation due to presence of bilirubin
hematin
brown pigment that is an artifact of formic acid and heme
gout pathogenesis
absence of enzyme uricase cannot convert uric acid to allantoin
amyloidosis
deposits accumulate often secondary to inflammation because of acute phase proteins (stains with congo red and apple green bioflumaofn (idk))
calcinosis circumscripta
localized calcium deposits, purple crystals under HE
major structural component of extracellular matrix
type 1 collagen
4 causes of edema
increased permeability, increased hydrostatic pressure (hepatic and heart failure, RAAS), decreased osmotic pressure, decreased lymphatic drainage
canine congenital lymphedema
abnormal development of lymphatic vessels leads to interstitial swelling and edema
hyperemia vs congestion
increase of blood volume in tissue due to: arteriolar dilation vs impaired outflow (respectively)
virchow’s triad
endothelial injury, alterations in blood flow, hypercoagulability
what are the vitamin K dependent factors in the coagulation cascade
10, 9, 7, 2
plasmin
digests fibrin clots and prevents blood clots from forming badly
antithrombin III
coagulation inhibitor produced by endothelium and hepatocytes
petechial hemorrhage
less than 2mm in diameter
ecchymotic hemorrhage
2-10mm in diameter
purpuric hemorrhage
mix of petechial and ecchymotic
arterial thrombus vs venous thrombus
arterial- laminated appearance, deposition of fibrin and platelets from rapid flow
venous- dark and gelatinous containing a lot of erythrocytes because slow flow
how can you tell the difference between acute and chronic infarcts
acute- red and swollen, beginning of necrosis
chronic- pale shrunken and firm
5 signs of infection
swelling, redness, pain, heat, loss of function
what activates neutrophils and endothelial cells for the leukocyte adhesion cascade
il1, 6, 8, TNFa, C3a, C5a
postive and negative APP
c-reactive protein+, SAA+, albumin-
transudate
little protein and few cells, clear and watery
exudate
rich in protein or cells
hypersensitivity 1
igE from allergen
hypersensitivity 2
igG and igM (IMHA) reacts to own cells
hypersensitivity 3
igG and igM to a soluble antigen, causes necrotizing vasculitis
hypersensitivity 4
T lymphocyte mediated, contact dermatitis, johnes, forms granulomas
myeloperoxidase
enzyme in neutrophils that contributes to necrosis and liquefaction
how fast do abcesses form
2-3 days for sterile and weeks for septic
nodular granuloma
cells arranged in discrete masses, TH1 based
diffuse granuloma
cells dispersed in sheets, TH2 based often intracellular bacterial burden (johnes)
FIP immune component
pyogranulomatous vasculitis
phases of wound healing
hemostasis, inflammation, proliferation, maturation (TGFb critical)
primary vs secondary intention wound healing
primary- edges apposed, heals rapidly
bovine lymphosarcoma cause
bovine leukemia retrovirus
hamartoma vs choristoma
disorganized tissue in normal location (often benign) vs. disorganized in abnormal location (often malignant)
sheets
common in round cell tumors
packets
common in neuroendocrine
nests
cells form encapsulated clumps, common in invasive carcinomas
cords
cells form branching chains, common in epithelial tumors
lobules
cells form inside bands of connective tissue, common in some epithelial tumors
why do carcinomas tend to use the lymphatic system to spread
they tend to form larger neothrombi and thus need the larger gaps in lymphatic valves
atrial natriuretic peptide
promotes renal sodium and water excretion and stimulates vasodilation
disseminated intravascular coagulopathy
initiated by diffuse endothelial damage and platelet activation, small blood clots form inside blood vessels everywhere, causes abnormal bleeding and ischemic injury
ARDS
damaged vessels allow leakages of fibrin and fluid which can damage hyaline membranes in the lungs
neurogenic shock pathogenesis
autonomic system triggered but SNS tone is lost, PNS dominates, vasodilation and bradycardia causes hypoperfusion
three stages in development of shock
compensation (RAAS), progression (acidosis), and irreversible ischemic necrosis
Common staging of tumors
T0-4 for size, N0-3 for lymph node involvement, M0-3 for metastasis
