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Pathology Exam I > Cellular Adaptations and Accumulations II > Flashcards

Cellular Adaptations and Accumulations II Flashcards

1
Q

What are subcellular responses to injury

A

distinctive alterations involving only subcellular organelles and cytosolic proteins

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2
Q

lysosomes

A

vesicles filled with a variety of hydrolytic enzymes

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3
Q

primary lysosomes

A

small membrane bound vesicles budding from golgi appartus

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4
Q

secondary lysosomes

A

formed when primary lysosomes fuse with pinocytic or phagocytic vesicles. also called phagolysosomes

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5
Q

heterophagy

A

materials from extracellular environment taken up through endocytosis

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6
Q

residual bodies

A

undigested materials/lipids

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7
Q

hereditary lysosomesal storage disorders

A

abnormal accumulations of intermediated metabolites

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8
Q

what happens when smooth ER undergoes hypertophy

A

becomes more efficient

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9
Q

What can cause mitochondrial to enlarge, have abnormal shapes

A

EtOH liver disease, nutritional deficiency

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10
Q

What is the cytoskeleten made of

A

thin filaments, microtubules, intermediate filaments

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11
Q

Thin filaments

A 
actin, myosin.
function in movement, phagocytosis
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12
Q

microtubules

A

function is motility, phagocytosis, mitotic spindle

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13
Q

intermediate filaments

A

form intracellular scaffolid, maintain cellular architecture, can accumulate and be pathologic

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14
Q

Cytoskeletal prteins

A

active participants in signal transduction

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15
Q

intracellular accumulation

A

manifestation of metabolic derangement, storage of some product by individual cells

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16
Q

What are the 3 categories of intracellular accumulations

A

normal endogenous substance that metabolism can’t remove
normal or abnormal endogenous substance that accumulates after some defect
abnormal exogenous substance that get’s deposited and can’t be removed

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17
Q

What are mechanisms of intracellular accumulations

A

abnormal metabolism
alteration in protein folding/transport
deficiency of critical enzyme
inability to degrade phagocytosed particles

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18
Q

steatosis (fatty change)

A

abnormal accumulations of triglycerides within parenchymal cells

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19
Q

What causes steatosis

A

toxins, protein malnutrition, diabetes, obesity, anoxia, EtOH

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20
Q

Atherosclerosis

A

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

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21
Q

What happens when foam cells rupture

A

release lipids into extracellular space, may crystallize into cholesterol clefts

22
Q

What do protein accumulations look like

A

pink droplets in cytoplasm, can be extracellular

23
Q

What can cause protein accumulatiosn

A

reabsorption droplets in proteinuria, synthesis of excessive amounts of protein, defects in protein folding

24
Q

Russell bodies

A

synthesis of immunoglobulins by plasma cells, happen in protein accumulation

25
Q

Mallory body

A

alcoholic hyalin, seen in alcoholic liver disease, due to protein accumulation

26
Q

chaperones

A

aid in proper folding and transport, repair misfolded proteins, facilitate degradation of damaged protein

27
Q

ubiquitin

A

marks abnormal protein for degradation by proteosomal compelx

28
Q

Partially folded intermediates are ____ to aggregate formation or entanglement

A

vulnerable

29
Q

What happens to protein folding with ER stress

A

protein folding demand is higher than protein folding capacity

30
Q

What is ER stress induced by

A

unfolded and misfolded proteins

31
Q

What does alpha1 antitrypsin deficiency look like histologically

A

red globules on PAS stain

32
Q

What does amyloidosis look like histologially

A

orange red deposits on congo red stain

33
Q

Examples of intracellular stuff that can undergo hyaline change

A

protein droplets in tubules
Russell bodies
Mallory alcoholic hyalin
viral inclusions

34
Q

Examples of extracellular stuff that can undergo hyaline change

A

collagenized scar, damged glomeruli, hyaline artheriosclerosis, atherosclerosis, amyloid

35
Q

What happens histologically to glycogen in diabetes patients

A

glycogen can be seen in cytoplasm of renal tubular epitherlium, hepatocytes, cariac mycoytes, beta cells of islets of langerhans

36
Q

What does mycardium look like in pompe disease

A

fibers are full of glycogen

37
Q

What is the most common exogenous pigment

A

carbon

38
Q

anthracosis

A

darkered LN and lung tissue due to carbon

39
Q

When carbon is inhaled, what does it get picked up by?

A

macrophages

40
Q

What can melanin accumulate

A

basal keratinocytes in skin or dermal macrophages

41
Q

hemosiderain

A

hemoglobin-derived, golden yellow to brown, pigment that sores iron

42
Q

hemosiderosis

A

way too much iron

43
Q

What are some things that can cause hemosiderosis

A

increased iron in diet
impaired use of iron
hemolytic anemias
transfusions

44
Q

How can we identify hemosiderosis in lab

A

prussian blue stain

45
Q

what is jaundice caused by

A

excess bilirubin

46
Q

Dystrophic calcifation

A

occurs in injured or dying tissues, can cause organ dysfunction, seen in atherosclerotic plaques, aging, or damaged heart valves

47
Q

metastatic calcification

A

increased serum calcium

48
Q

What can cause hypercalcemia

A

cancer destroys bone
high PTH level
Vitamin-D disorder

49
Q

pathologic dystrophic

A

forms crystalline calcium phosphate, can lead to further dysfunction

50
Q

heterotopic bone

A

may form in foci of calcification

Pathology Exam I (11 decks)

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