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DIT topics > cell biology: cell injury and death > Flashcards

cell biology: cell injury and death Flashcards

1
Q

physiologic causes of apoptosis

A

embryogenesis
cell break down (menstruation)
maintain constant cell number (immature lymphocytes)

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2
Q

pathologic causes of apoptosis

A

DNA damage: radiation, hypoxia
misfolded proteins: gene mutation, free radicals
infection: HIV

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3
Q

histology of apoptosis

A

cell shrinks
eosinophilic cytoplasm
pyknosis: nucleus shrinks (basophilic)
karyorrhexia: nuclear fragmentation
karyolysis: nuclear fading d/t dissolution of chromatin
membrane blebbing
apoptotic bodies (cytoplasm) → phagocytosed

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4
Q

does apoptosis cause inflammation

A

NO - phagocytes pick up debris

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5
Q

does necrosis cause inflammation

A

YES - intracellular contents leak out causing inflammation

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6
Q

coagulative necrosis looks like

A

gelatinous

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7
Q

liquefactive necrosis looks like

A

viscous fluid

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8
Q

caseous necrosis looks like

A

clumpy cheese

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9
Q

coagulative necrosis occurs in

A

heart, liver, kidney: end-artery supply

low O2 → infarction → coag necrosis

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10
Q

liquefactive necrosis occurs in

A

brain

bacterial infection, pleural effusion

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11
Q

caseous necrosis occurs in

A

TB

systemic fungi

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12
Q

fatty necrosis occurs in

A

activated lipase → fatty necrosis
pancreatitis: saponification
breast trauma

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13
Q

fibrinoid necrosis occurs in

A

autoimmune mediated vascular damage: henoch-schonlein purpura, churg-strauss syndrome
malignant hypertension

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14
Q

dry gangrenous necrosis occurs in

A

arterial occlusion →ischemia of toes, feet

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15
Q

wet gangrenous necrosis occurs in

A

bacterial infection → limbs, GI tract

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16
Q

cellular by-products released in serum when injured:

cardiac myocytes

A

cardiac troponin I
creatine kinase
creatine kinase-MB
myoglobin

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17
Q

cellular by-products released in serum when injured:

skeletal muscle

A

aldolase
creatine kinase
myoglobin (can cause renal failure)

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18
Q

cellular by-products released in serum when injured:

hepatocytes

A

AST/ALT
alkaline phosphatase
GGT: gamma-glutamyl-transpeptidase

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19
Q

cellular by-products released in serum when injured:

salivary gland cells

A

amylase

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20
Q

cellular by-products released in serum when injured:

pancreatic exocrine cells

A

amylase

lipase

21
Q

cellular by-products released in serum when injured:

RBCs

A

heme → bilirubin

22
Q

enzymes that protect against free radical damage (cause free radical degradation)

A 
catalase
superoxide dismutase (SOD)
glutathione peroxidase
spontaneous decay
antioxidants: vitamin A,C, E
23
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
ATP depletion from ↓O2/nutrients or toxins (cyanide)

A

reversible

24
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
cellular/mito swelling: ↓ ATP, ↓Na/K ATPase activity

A

reversible

25
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
nuclear chromatin clumping

A

reversible

26
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
↓glycogen

A

reversible

27
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
fatty change of liver: hepatocyte damage, little acetaminophen overdose

A

reversible

28
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
ribosomal detachment ↓ protein synthesis

A

reversible

29
Q 
reversible (with O2/nutrients) or irreversible cause of cell injury?
nuclear pyknosis (condense chromatin), karyorrhexis (nucleus fragmentation), karyolysis (dissolution of chromatin)
A

irreversible

30
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
lysosomal rupture

A

irreversible

31
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
plasma membrane damage - degrade phospholipids

A

irreversible

32
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
Ca2+ influx or ↓O2 or mutation in mito gene → ↑mito permeability → caspase activation

A

irreversible

33
Q

red (hemorrhagic) infarcts occurs in

A

loose tissue + collateral blood supply or after thrombolytic treatment (reperfusion injury >3 hrs after MI/stroke)
liver, lung, intestine, BRAIN

34
Q

pale infarcts occurs in

A

solid tissue with single blood supply (no re-vascularization)
heart, kidney, spleen

35
Q

pathophysiology of red infarct

A

obstruction → ischemia → infarction → reperfusion → free radical damage → more damage

36
Q

what is an infarction?

A

TISSUE DEATH caused by lack of O2 (hypoxia) usually due to lack of blood flow (ischemia)

37
Q

how can Ca2+ influx cause cell injury?

A 
↑ mito permeability 
activate:
phospholipase
protease
endonuclease
ATPase
38
Q

how can oxidative stress (free radicals) cause cell injury?

A

membrane lipid peroxidation

protein modification/DNA damage

39
Q

causes of oxidative stress

A 
radiation
metabolism of drugs
redox reaction
nitric oxide
transition metals: iron, copper
leukocyte oxidative burst (kills bacteria!)
iron overdose 
reperfusion injury after thrombolytic treatment (occurs if tx given >3 hrs after stroke/MI)
40
Q

what is pyknosis?

A

nuclear shrinks (basophilic)

41
Q

what is karyorrhexia?

A

nuclear fragmentation

42
Q

what is karyolysis?

A

dissolution of chromatin

43
Q

reversible (with O2/nutrients) or irreversible cause of cell injury?
nuclear changes: pyknosis, karyorrhexis, karyolysis

A

irreversible

44
Q

what does catalase do?

A

H202 → O2 + H20

in peroxisome!

45
Q

what does superoxide dismutase do?

A

O2 free radicals → H202

46
Q

what does glutathione peroxidase do?

A

free radical breakdown

47
Q

what is necrosis?

A

response to cell injury

enzyme + protein degradation → leaks out of cell → inflammation

48
Q

what is inflammation and its classic findings?

A 
method to repair cell damage
rubor (redness)
dolor (pain)
calor (heat)
tumor (swelling)
loss of function

DIT topics (115 decks)

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