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BOD I > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

-itis

A

inflammation

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2
Q

-osis

A

degeneration

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3
Q

–oma, -trophy, -plasia

A

disorders of growth

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4
Q

-opathy

A

uncertain pathogenesis

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5
Q

what causes enlargement of cells

A

glycogen
hypertrophy of organelles
storage changes/error in metabolism (e.g. lysosomal storage disease

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6
Q

hyaline

A

homogenous, glossy appearance
describes IC proteins depositions (russel bodies, metal inclusions, viral inclusions)
describes EC protein deposits (edema fluid, fibrin, amyloid)

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7
Q

causes of amyloid

A

EC protein deposits composed of protein fibrils in beta pleated sheet

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8
Q

AA Amyloid

A

serum amyloid A

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9
Q

AL Amyloid

A

Ig light chains

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10
Q

AF Amyloid

A

prealbumin

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11
Q

endocrine amyloid

A

hormone and hormone-like proteins

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12
Q

type of amyloid in glomeruli in dogs, hepatic sinusoids in birds

A

AA amyloid

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13
Q

type of amyloid in lymphoid follicles

A

AL amyloid

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14
Q

type of amyloid in pancreatic islets or renal medulla in cats

A

endocrine amyloid

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15
Q

biochemical features of amyloid

A

insoluble
indigestable

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16
Q

morphological features of amyloid

A

amorphous
hyaline
extracellular
stains red/orange with congo red
stains green with Thioflavine T

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17
Q

Some parenchymal cells have a few small round, perfectly clear cytoplasmic spaces

A

reversible fatty change

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18
Q

All parenchymal cells contain a very large, perfectly clear, round cytoplasmic space

A

irreversible fatty degeneration

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19
Q

Some parenchymal cells have modest cytoplasmic swelling

A

reversible hydropic change

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20
Q

All parenchymal cells are markedly swollen

A

irreversible hydropic degeneration

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21
Q

pyknosis

A

shrinkage, clumping of nuclear chromatin

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22
Q

karyorrhexis

A

nuclear fragmentations

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23
Q

karyolysis

A

nuclear fading

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24
Q

Pro-Oxidants

A

xanthine oxidase
fenton & haber weiss reactions
superoxide anion, singlet oxygen
hydroxyl radical
nitric oxide
hydrogen peroxide

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25
Q

anti-oxidants

A

superoxide dismutase & catalase
glutathione peroxidase/reductase
vitamins A,C,E
transferrin, lactoferrin, ceruloplasmin

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26
Q

ATP depletion role in cell injury

A

affects membrane transport, protein synthesis, lipogenesis, phospholipid turner, and metabolism

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27
Q

Ca influx role in cell injury

A

activates enzymes (phospholipases, proteases, ATPases, endonucleases)

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28
Q

mitochondrial injury role in cell injury

A

mitochondrial permeability transition –> signal for apoptosis

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29
Q

membrane damage/increased permeability role in cell injury

A

ATP depletion, Ca activates phospholipases and direct damage by toxins/viral proteins/complement/perforins/chemical/physical agents

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30
Q

ROS role in cell injury

A

damage membranes, proteins and nucleic acids

31
Q

dry gangrene causes

A

frostbite or intoxicants

32
Q

wet gangrene causes

A

digested/liquified by environmental flora

33
Q

two concurrent processes of necrosis

A
  1. enzymatic digestion
  2. protein denaturation
34
Q

necrosis features

A

karyolysis
adjacent tissue unaffected
RBC intact
inflammation
passive, degradative
tissue response
membrane injury and organelle damage

35
Q

causes of metastatic mineralization

A

hypervitamin D
renal disease
primary hyperparathyroidism
hyperadrenocorticism
paraneoplastic syndromes (PTHrP)

36
Q

where is metastatic mineralization commonly found

A

gastric mucosa
blood vessels
lungs
kidney

37
Q

are thrombi dystrophic or metastic mineralization

A

dystrophic due to presence of platelets and fibrin

38
Q

apoptosis features

A

pyknosis & karyorrhexis
no inflammation
active process
no tissue response
DNA damage, no organelle damage
increased cytoplasmic eosinophilia
forms apopotic bodies

39
Q

what intiiates apoptosis

A

extrinsic pathway
intrinsic pathway
perforin/granzyme pathway

40
Q

increased apoptosis results in…

A

neurodegenerative disorders
exacerbation of damage in ischemic injury
virus-induced lymphocyte depletion in acquired immunity deficiency syndromes

41
Q

decreased apoptosis results in…

A

neoplasia
autoimmune diseases

42
Q

breakdown products of lipids, granular golden brown; usually microscopic

A

lipofuscin

43
Q

dark, gross appearance, primarily in the lungs, urban environments, incidental

A

carbon

44
Q

incidental pigmentation of tissues in pigmented animals; commonly affects pleura and meninges

A

melanin

45
Q

postmortem production of hydrogen sulfide by bacteria with rxn with Fe in hemoglobin to form insoluble iron sulfide

A

pseudomelanosis

46
Q

yellow pigment from wound, bruising

A

hematoidin

47
Q

lighter brown granular pigment, represents accumulations of Fe & apoferritin

A

hemosiderin

48
Q

greenish-brown pigment usually not granular, seen within hepatocytes/bile canaliculi/renal tubular epithelium; may be bright yellow and stain all tissues in hemolytic anemia (jaundice)

A

bilirubin

49
Q

pinpoint hemorrhage, up to 1mm, capillary injury, petechiation

A

petechia

50
Q

larger hemorrhage, up to a few cm, paintbrush appearance

A

ecchymosis

51
Q

petechiae and ecchymoses on mucous membranes

A

purpura

52
Q

focal hemorrhage which produced mass-like lesion

A

hematoma

53
Q

causes of hemorrhage

A

local - trauma, hypoxia, degenerative conditions
systemic - coagulopathies, metabolic,, neoplastic, or infectious diseases

54
Q

consequences of hemmorhage

A

primary - shock, space occupying lesions with disastrous consequences in CNS/pericardial sac
secondary - resorption of fluid, RBC lysis and phagocytosis, fibrinolysis, scarring

55
Q

local edema causes

A

venous obstruction
lymphatic obstruction
inflammation or vascular injury

56
Q

generalized edema causes

A

cardiac edema (increased hydrostatic pressure)
renal failure (decreased plasma oncotic pressure)
hepatic failure (decreased plasma oncotic pressure)

57
Q

physioloical (eating, exercise) & pathological (inflammaltion/injury)

A

active hyperemia

58
Q

pathological (heart failure, mechanical, gravity - recumbent animals)

A

passive hyperemia

59
Q

acute passive hyperemia

A

sudden occlusion (torsion, strangulation)
anoxia

60
Q

chronic passive hyperemia

A

long standing interference, not complete ischemia (heart failure)
hypoxia

61
Q

best to worst fates of thrombi

A

fibrinolysis
organization and recanalization
propagation
embolism

62
Q

antemortem clots vs postmortem

A

antemortem - attached to endothelium, lesion
postmortem - not attached to endothelium, incidental, no lesion

63
Q

pale, dry, fibrin and platelets, firm thrombi

A

arterial thrombi

64
Q

large, dark red, shiny, cranberry sauce-like thrombi with RBC

A

venous thrombi

65
Q

a raised infarction is _______

A

acute

66
Q

a depressed infarcation is _____

A

chronic

67
Q

pale, light, anemic infarct is due to ____

A

arterial occlusion

68
Q

dark, hemorrhagic infarct in tissues with dual circulation is due to _____

A

venous occlusion

69
Q

how do you distinguish between an old infarct and new one

A

old has scar tissue, appears paler than adjacent tissue and smaller volume due to scarring

70
Q

consequences of infarction

A

necrosis

71
Q

which tissues are the most vulnerable to infarcts? least vulnerable?

A

most vulnerable - single perfusion organs - brain, heart, renal cortex
least vulnerable - dual blood supply organs - liver & lungs - must occlude both bronchial a. and pulmonary a. for lungs and both hepatic a. and portal v. for liver

72
Q

pro-coagulant factors for hemostasis

A

endothelial cells only:
VWF
collagen
ADP and TXA2
tissue factor
Ca2+
clotting factors
platelet-activating factor
plasminogen activator inhibitor (PAI)
alpha2 antiplasmin

73
Q

anti-coagulants factors for hemostasis

A

endothelial cells & blood proteins involved:
covering thrombogenic subendothelial collagen
NO and PGI2
Antithrombin III
Thrombomodulin
Plasminogen activators (t-PA and urokinase-like PA)
antithrombins & protein C&S

BOD I (7 decks)

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