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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
foam cells rupture, releasing lipids into extracellular space, may crystalize into...
cholesterol clefts
26
seen in renal diseases with heavy protein loss; increased reabsorption into proximal tubules; fusion of pinocytotic vesicles to make phagolysosomes
reabsorption droplets in proximal renal tubules (reversible)
27
synthesis of excessive amounts of normal secretory protein (immunoglobulins by plasma cells)
russell bodies (prtn accumulation)
28
characteristially seen in alchoholic liver disease (prtn accumulation)
mallory body or alchohol hyaline - this is a type of cell injury
29
eosinophilic intracytoplasmic inclusions composed of cytoskeletal filaments in damaged liver cells
mallory bodies/ alcoholic hyaline
30
aid in proper folding and transport; repair misfolded proteins; facilitate degradation of damaged prtn
chaperones
31
marks abnormal prtn for degradation by proteosomal complex
ubiquitin
32
responses to unfolded/misfolded prtns
1) increased synthesis of chaperones 2) decreased translation of prtns 3) activation of ubiquitin-proteasome pathway 4) activation of capsases --> apoptosis
33
what is "ER stress"
protein folding demand is greater than capacity
34
cell responses to ER stress
1) failure to adapt and apoptosis | 2) cellular adaptation with decreased prtn syntheis and increased prodution of chaperones
35
alpha1-antitrypsin deficiency
anti-protease deficiency | -too many proteases cause damage in this disease
36
red globules on PAS stain
alpha-1 antitrypsin deficiency
37
orange-red deposits on congo red stain
amyloidosis
38
glassy, pink homogenous appearance on H&E
hyaline cartilage
39
what might be some intracellular causes of hyaline change
protein droplets in tubules, russell bodies, mallory alcoholic hyalin, viral inclusions
40
what might be some extracellular causes of hyaline change
``` collagenized scar damaged glomeruli halline arteriosclerosis atherosclerosis amyloid ```
41
appearance of glycogen deposits
clear cytoplasmic vacuoles
42
glycogen seen in the cytoplasm of renal tubular epithelium, hepatocytes, cardiac myocytes, beta cells of islets of langerhans
diabetes mellitus
43
myocardial fibers full of glycogen
Pompe disease (glycogen storage disease)
44
most common exogenous pigment
carbon
45
darkened LNs and lung tissue
anthracosis
46
process of carbon pigment accumulation
- inhaled, picked up by macrophage and transported through the lymphatics to regional lymph nodes - heavy accumulation can be toxic: emphysema or fibroblastic rxn
47
coal workers pneumoconiosis
heavy accumulation of carbon
48
localized exogenous pigmentation of skin in dermal macrophages
tattooing
49
brownish-yellow granular intracellular material, usually in perinuclear area
lipofuscin
50
wear and tear pigment
lipofuscin
51
marker of past free radical injury; probably derived from subcellular membrane lipid peroxidation
lipfuscin
52
brownish grossly; "brown atrophy of heart"
lipofuscin
53
brown-black pigment formed in melanocytes by oxidation of tyr to dihydroxyphenyalanine
melanin
54
endogenous screen against UV-radiation
melanin
55
where does melanin accumulate?
basal keratinocytes in skin or dermal macrophages
56
spitz nevus in child
dark mole
57
hemoglobin-derived, golden-yellow-brown granular or crystalline pigment in which form iron is stored in cells
hemosiderin
58
aggregates of ferritin micelles
hemosiderin
59
heart failure cells
hemosiderin laden macrophages in pulmonary alveoli
60
systemic overload of iron
hemosiderosis- deposition of iron in man organs and tissues
61
causes of hemosiderosis
- increased absorption of dietary iron - impaired use of iron - hemolytic anemia - transfusions
62
coarse, golden granular pigment, intracytoplasmic ID with prussian blue
hemosiderin
63
what are some potential complications of hemosiderosis
liver fibrosis heart filaure diabetes mellitus
64
gut absorbs a lot of iron
hemochromatosis
65
hemoglobin derived, but contains no iron
bilirubin
66
cuased by excess bilirubin
jaundice
67
normal serum calcium; local process calcification
dystrophic calcification
68
calcification type seen in atherosclerotic plaques, aging or damaged heart valves, areas of necrosis
dystrophic calcification (cyrstallin calcium phosphate)
69
deposition of calcium salts in vital tissues in association with a defect in calcium metabolism characterized by hypercalcemia
metastatic calcification
70
causes of hypercalcemia
- cancer destroying bone - high PTH - Vitamin D related disorders
71
seen mainly in intertistial tissue of blood vessels, kidney, lungs and gastric mucosa
metastatic calcification
72
which type of calcification usually is associated with dysfunction
dystrophic metatstatic usually no dysfunction

Pathology I (12 decks)

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