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Pathology I > 5: cellular adaptations and accumualtions > Flashcards

5: cellular adaptations and accumualtions Flashcards

1
Q

distinctive alterations involving only subcellular organelles and cytosolic prtns

A

subcellular response

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2
Q

lysosomal catabolism

A

subcellular response

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3
Q

induction(hypertrophy) of smooth ER

A

subcellular response

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4
Q

mitochondrial alterations

A

subcellular response

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5
Q

cytoskeletal abnormalities

A

subcellular response

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6
Q

how does a primary lysosome become a secondary lysosome?

A

primary lysosomes budding from the golgi apparatus fuse with pinocytic or phagocytic vesicles from the PM to form secondark lysosomes aka phagolysosomes

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7
Q

undigested lipids and other materials

A

form residual bodies

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8
Q

what organelle synthesizes phospholipids and detoxifies?

A

smooth ER

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9
Q

smooth ER response to barbiturates and p-450 mixed function oxidase system

A

smooth ER undergoes hypertrophy and becomes more efficient

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10
Q

enlarged, abnormal mitochondrial shapes

A

seen in ETOH liver

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11
Q

ragged red fiber mitochondria

A

mitochondrial myopathies (genetic disease)

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12
Q

thin filaments example

A

acin, myosin, movement, phagocytosis

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13
Q

microtubules example

A

motility
phagocytosis
mitotic spindle

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14
Q

intermediate filaments example

A

intracellular scaffold, maintain cellular architecture, accumulate and be pathologic

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15
Q

4 mechanisms of intracellular accumulations

A

1) abnormal metabolism
2) alterations in protein folding and transport
3) deficiency of critical enzymes
4) inability to degrade phagocytosed particles

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16
Q

fatty liver

A

normal substance; metabolic rate inadequate to remove it

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17
Q

cuases of steatosis/fatty change

A 
toxins
protein malnutrition 
diabetwes
obesity
anoxia 
alcohol
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18
Q

most common cause of steatosis in industrialized nations

A

alcohol and diabetes

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19
Q

foam cells

A

atherosclerosis

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20
Q

xanthomas

A

hyperlipidemic state

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21
Q

cholesterolosis

A

gall stones

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22
Q

niemann-pick disease, type C

A

lysosomal storage disease

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23
Q

found at sites of cell injury secondary to phagocytosis of cholesterol from injured cells membranes

A

inflammation and necrosis

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24
Q

in plaques, smooth muscle cells and macrophages within intimal layer of aorta and large arteries fill with lipid vacuoles (foam cells). aggregates produce yellow, cholesterol laden atheromas

A

atherosclerosis

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25
Q

foam cells rupture, releasing lipids into extracellular space, may crystalize into…

A

cholesterol clefts

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26
Q

seen in renal diseases with heavy protein loss; increased reabsorption into proximal tubules; fusion of pinocytotic vesicles to make phagolysosomes

A

reabsorption droplets in proximal renal tubules (reversible)

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27
Q

synthesis of excessive amounts of normal secretory protein (immunoglobulins by plasma cells)

A

russell bodies (prtn accumulation)

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28
Q

characteristially seen in alchoholic liver disease (prtn accumulation)

A

mallory body or alchohol hyaline

  • this is a type of cell injury
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29
Q

eosinophilic intracytoplasmic inclusions composed of cytoskeletal filaments in damaged liver cells

A

mallory bodies/ alcoholic hyaline

30
Q

aid in proper folding and transport; repair misfolded proteins; facilitate degradation of damaged prtn

A

chaperones

31
Q

marks abnormal prtn for degradation by proteosomal complex

A

ubiquitin

32
Q

responses to unfolded/misfolded prtns

A

1) increased synthesis of chaperones
2) decreased translation of prtns
3) activation of ubiquitin-proteasome pathway
4) activation of capsases –> apoptosis

33
Q

what is “ER stress”

A

protein folding demand is greater than capacity

34
Q

cell responses to ER stress

A

1) failure to adapt and apoptosis

2) cellular adaptation with decreased prtn syntheis and increased prodution of chaperones

35
Q

alpha1-antitrypsin deficiency

A

anti-protease deficiency

-too many proteases cause damage in this disease

36
Q

red globules on PAS stain

A

alpha-1 antitrypsin deficiency

37
Q

orange-red deposits on congo red stain

A

amyloidosis

38
Q

glassy, pink homogenous appearance on H&E

A

hyaline cartilage

39
Q

what might be some intracellular causes of hyaline change

A

protein droplets in tubules, russell bodies, mallory alcoholic hyalin, viral inclusions

40
Q

what might be some extracellular causes of hyaline change

A 
collagenized scar
damaged glomeruli
halline arteriosclerosis
atherosclerosis
amyloid
41
Q

appearance of glycogen deposits

A

clear cytoplasmic vacuoles

42
Q

glycogen seen in the cytoplasm of renal tubular epithelium, hepatocytes, cardiac myocytes, beta cells of islets of langerhans

A

diabetes mellitus

43
Q

myocardial fibers full of glycogen

A

Pompe disease (glycogen storage disease)

44
Q

most common exogenous pigment

A

carbon

45
Q

darkened LNs and lung tissue

A

anthracosis

46
Q

process of carbon pigment accumulation

A
  • inhaled, picked up by macrophage and transported through the lymphatics to regional lymph nodes
  • heavy accumulation can be toxic: emphysema or fibroblastic rxn
47
Q

coal workers pneumoconiosis

A

heavy accumulation of carbon

48
Q

localized exogenous pigmentation of skin in dermal macrophages

A

tattooing

49
Q

brownish-yellow granular intracellular material, usually in perinuclear area

A

lipofuscin

50
Q

wear and tear pigment

A

lipofuscin

51
Q

marker of past free radical injury; probably derived from subcellular membrane lipid peroxidation

A

lipfuscin

52
Q

brownish grossly; “brown atrophy of heart”

A

lipofuscin

53
Q

brown-black pigment formed in melanocytes by oxidation of tyr to dihydroxyphenyalanine

A

melanin

54
Q

endogenous screen against UV-radiation

A

melanin

55
Q

where does melanin accumulate?

A

basal keratinocytes in skin or dermal macrophages

56
Q

spitz nevus in child

A

dark mole

57
Q

hemoglobin-derived, golden-yellow-brown granular or crystalline pigment in which form iron is stored in cells

A

hemosiderin

58
Q

aggregates of ferritin micelles

A

hemosiderin

59
Q

heart failure cells

A

hemosiderin laden macrophages in pulmonary alveoli

60
Q

systemic overload of iron

A

hemosiderosis- deposition of iron in man organs and tissues

61
Q

causes of hemosiderosis

A
  • increased absorption of dietary iron
  • impaired use of iron
  • hemolytic anemia
  • transfusions
62
Q

coarse, golden granular pigment, intracytoplasmic ID with prussian blue

A

hemosiderin

63
Q

what are some potential complications of hemosiderosis

A

liver fibrosis
heart filaure
diabetes mellitus

64
Q

gut absorbs a lot of iron

A

hemochromatosis

65
Q

hemoglobin derived, but contains no iron

A

bilirubin

66
Q

cuased by excess bilirubin

A

jaundice

67
Q

normal serum calcium; local process calcification

A

dystrophic calcification

68
Q

calcification type seen in atherosclerotic plaques, aging or damaged heart valves, areas of necrosis

A

dystrophic calcification (cyrstallin calcium phosphate)

69
Q

deposition of calcium salts in vital tissues in association with a defect in calcium metabolism characterized by hypercalcemia

A

metastatic calcification

70
Q

causes of hypercalcemia

A
  • cancer destroying bone
  • high PTH
  • Vitamin D related disorders
71
Q

seen mainly in intertistial tissue of blood vessels, kidney, lungs and gastric mucosa

A

metastatic calcification

72
Q

which type of calcification usually is associated with dysfunction

A

dystrophic

metatstatic usually no dysfunction

Pathology I (12 decks)

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