Tissue Responses to Injury & Adaptations Flashcards

1
Q
  • here for the Liz brain *
A

hehe haha

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2
Q

define labile cells

A

continuously cycling - regenerative

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3
Q

list examples of labile cells

A

mouth/skin/bladder epithelium
bone marrow cells

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4
Q

define stable cells

A

quinescent aka divide infrequently
can be stimulated to divide (in G0 until stim to G1)

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5
Q

list examples of stable cells

A

liver
renal tubules
fibroblasts
endothelial cells
chondrocytes
osteocytes of CT

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6
Q

define permanent cells

A

non-dividing - can NOT be replaced when lost

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7
Q

list examples of permanent cells

A

neurons
cardiac muscle
photoreceptors in retina

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8
Q

define atrophy

A

reduction in function mass/size of cell/tissue/organ

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9
Q

define hypertrophy

A

increase in SIZE
* since it’s a party

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10
Q

define hyperplasia

A

increase in NUMBER of cells

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11
Q
  • again, here for Liz brain *
A
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12
Q

if the middle image is a normal uterus, is the R image hypertrophy OR hyperplasia?

A

hypertrophy - pregnancy

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13
Q

___ is the mechanism for cell loss of physiological atrophy (apoptosis or necrosis)

A

apoptosis

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14
Q

list causes of pathological atrophy

A

vascular/ischemic
tissue destruction (pressure, inflamed, necrosis)
endocrine (corticosteroid drugs)
denervation of skeletal muscle
starvation
decreased functional demand (fracture)

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15
Q

ID the pathology

A

renal cortical/medullary atrophy
* hydronephrosis

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16
Q

describe the pathogenesis of hydronephrosis

A

transitional cell carcinoma in bladder -> blocking of ureter flow -> increase pressure in renal pelvis -> renal cortical/medullary atrophy -> hydronephrosis

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17
Q

list some causes of pathological hyperplasia and hypertrophy

A

abnormal increase in functional demand
excessive hormone stim
response to inflammation or trauma

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18
Q

ID the pathology
which side is normal?

A

R side normal
L side hypertrophic cardiomyopathy

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19
Q

define erosion

A

damage to tissue, BUT basement membrane stays intact

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20
Q

define ulceration

A

damage where basement membrane becomes compromised, so tissue/cells replaced by fibrous tissue (scaring)

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21
Q

erosion or ulceration?

A

erosion

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22
Q

erosion or ulceration?

A

ulceration

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23
Q

what’s the most common causes of stricture in esophagus?

A

circumferential erosion
ulceration via pressure necrosis

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24
Q

ID pathology

A

perforation - peritonitis
result of stomach ulcer

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25
Q

how does the heart and skeletal muscle respond to stress/injury?

A

reversible changes - atrophy and hypertrophy
* cardiac cells do fibrosis/scar instead of regeneration

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26
Q

define concentric hypertrophy of the heart

A

thickening from the outside, towards the lumen

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27
Q

define eccentric hypertrophy of the heart

A

addition of sarcomeres next to one another to enlarge and dilate a heart chamber (wall thinning)

28
Q

what process is being shown in the R image?

A

fibrosis - cardiac cells are permanent so death results in fibrous CT taking its place

29
Q

list the key forms of injury to bone

A

fracture
resorption
necrosis (due to infection, inflame, hypoxia)

30
Q

list key responses to bone injury

A

alter shape/mass
regeneration (form woven bone)
periosteum forms

31
Q

list key forms of neurologic injury

A

compression
necrosis
degeneration

32
Q

list key responses to neuronal injury

A
  • cavitation NOT fibrosis
    very minimal regeneration
33
Q

define exogenous pigment

A

pigment taken from external source

34
Q

define endogenous pigment

A

pigment produced by cell

35
Q

define hematogenous pigments

A

hemoglobin
parasite hematin
bilirubin

36
Q

exogenous pigment examples

A

anthracosis (carbon) - black lung, near highway, heavy smoker owner

37
Q

endogenous pigment examples

A

melanin
lipofuscin (wear and tear, age indication)
ceroid (vit E deficiency)

38
Q

ID the pigment type

A

exogenous - anthracosis within lung

39
Q

ID the pigment type

A

endogenous - melanin (black/brown)

40
Q

how does copper deficiency effect melanin?

A

melanin is formed via tyrosine oxidation, which requires copper-containing tyrosinase

41
Q

define lipofuscin
what type of pigment?

A

endogenous pigment
yellow/brown color, not harmful
associated with aging
result of autophagocytosis accumulation in cells aka partially metabolized protein and lipid

42
Q

define ceroid
what type of pigment?

A

endogenous pigment
yellow/green color
deleteriois effect to cells
accumulate as a specific pathologic condition (vit E deficiency)

43
Q

ID the type of pigment

A

endogenous - lipofuscin

44
Q

define jaundice/icterus

A

pigmentation due to bilirubin presence
yellow color
hematogenous pigment

45
Q

define hematin pigment

A

brown color
artifact from formic acid and heme
* can also be linked to liver flukes present

46
Q

ID the pigment type

A

icterus

47
Q

ID pigment type

A

hematin - due to liver flukes

48
Q

what is gout?

A

accumulation of gout crystals (tophi) aka uric acid in either articular or visceral form

49
Q

how does gout occur?

A

absence of enzyme uricase
* prevents uric acid from becoming allantoin

50
Q

what are gout crystals commonly surrounded by?

A

inflammation - befringement in polarized light

51
Q

ID the pathology

A

gout crystals - kidney

52
Q

define amyloid

A

pathogologic protein based material
extracellular accumulation - compresses surrounding tissue

53
Q

list examples of localized amyloid

A
54
Q

list examples of generalized amyloid

A
55
Q

ID the pathology
which is normal?

A
56
Q

ID the pathology AND the stain used

A

amyloid
congo red stain

57
Q

ID the pathology AND the stain used

A

amyloid
apple green birefringence by polaarized light

58
Q

ID the pathology

A
59
Q

define dytrophic calcification

A

blood Ca levels seem normal
localized

60
Q

define calcinosis circumscripta

A

necrosis, inflammation, dystrophic calcification in dog

61
Q

ID the pathology

A

calcium salts

62
Q

define metastatic calcification

A

hypercalcemia - secondary to renal failure, lymphoma

63
Q

ID the pathology

A

mucosal calcification

64
Q

ID the pathology

A

pink inclusion within nucleus

65
Q

ID the pathology

A

inclusion