cell biology: cell injury and death Flashcards by L W

Q

physiologic causes of apoptosis

A

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

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Q

pathologic causes of apoptosis

A

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

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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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Q

does apoptosis cause inflammation

A

NO - phagocytes pick up debris

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Q

does necrosis cause inflammation

A

YES - intracellular contents leak out causing inflammation

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Q

coagulative necrosis looks like

A

gelatinous

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Q

liquefactive necrosis looks like

A

viscous fluid

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Q

caseous necrosis looks like

A

clumpy cheese

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Q

coagulative necrosis occurs in

A

heart, liver, kidney: end-artery supply

low O2 → infarction → coag necrosis

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Q

liquefactive necrosis occurs in

A

brain

bacterial infection, pleural effusion

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Q

caseous necrosis occurs in

A

TB

systemic fungi

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Q

fatty necrosis occurs in

A

activated lipase → fatty necrosis
pancreatitis: saponification
breast trauma

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Q

fibrinoid necrosis occurs in

A

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

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Q

dry gangrenous necrosis occurs in

A

arterial occlusion →ischemia of toes, feet

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Q

wet gangrenous necrosis occurs in

A

bacterial infection → limbs, GI tract

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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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Q

cellular by-products released in serum when injured:

skeletal muscle

A

aldolase
creatine kinase
myoglobin (can cause renal failure)

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Q

cellular by-products released in serum when injured:

hepatocytes

A

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

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Q

cellular by-products released in serum when injured:

salivary gland cells

A

amylase

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Q

cellular by-products released in serum when injured:

pancreatic exocrine cells

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A

amylase

lipase

Q

cellular by-products released in serum when injured:

RBCs

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A

heme → bilirubin

Q

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

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A

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

Q

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

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A

reversible

Q

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

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A

reversible

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

reversible

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

reversible

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

reversible

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

reversible

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

irreversible

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

irreversible

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

irreversible

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

irreversible

red (hemorrhagic) infarcts occurs in

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

pale infarcts occurs in

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

pathophysiology of red infarct

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

what is an infarction?

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

how can Ca2+ influx cause cell injury?

``` ↑ mito permeability activate: phospholipase protease endonuclease ATPase ```

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

membrane lipid peroxidation | protein modification/DNA damage

causes of oxidative stress

``` 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) ```

what is pyknosis?

nuclear shrinks (basophilic)

what is karyorrhexia?

nuclear fragmentation

what is karyolysis?

dissolution of chromatin

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

irreversible

what does catalase do?

H202 → O2 + H20 | in peroxisome!

what does superoxide dismutase do?

O2 free radicals → H202

what does glutathione peroxidase do?

free radical breakdown

what is necrosis?

response to cell injury | enzyme + protein degradation → leaks out of cell → inflammation

what is inflammation and its classic findings?

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