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Pathology > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Cell injury results when

A

cells are stressed so much that they are no longer able to adapt, or when cells are exposed to damaging agents they suffer from abnormal changes within

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2
Q

Cell response to injury depends on

A

dose, duration, & type of injury

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3
Q

Major causes of cell injury

A

Lack of oxygen, physical agents & trauma, chemical agents & drugs, infectious agents, immunologic reactions, genetic defects, nutritional imbalances

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4
Q

5 major biochemical mechanisms of cell injury

A
  1. Influx of calcium into cell & loss of calcium homeostasis
  2. Mitochondrial damage
  3. Depletion of ATP
  4. Accumulation of oxygen-derived free radicals (oxidative stress)
  5. Defects in membrane permeability
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5
Q

Increase in intracellular calcium causes

A

Increased mitochondrial permeability (decrease ATP)

Activation of cellular enzymes - membrane & nuclear damage

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6
Q

Mitochondria is damaged by

A

Increase Ca in cytosol, oxidative stress, & lipid breakdown products

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7
Q

Necrosis can be caused by

A

Decreased oxygen supply, toxins, radiation

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8
Q

Apoptosis can be caused by

A

Decreased survival signals & DNA or protein damage

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9
Q

Lack of oxygen or interference with the phosphorylation pathway cause

A

ATP levels in the cell to decrease (because of decrease in oxidative phosphorylation)

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10
Q

Decreased ATP causes

A

Can’t pump Na out of cell, so water enters cell causing swelling of the cell & blebbing of outer membrane
Increase in intracellular Ca, activates enzymes causing membrane damage
Switch to anaerobic glycolysis causes build up of lactic acid (lower pH) & DNA clumping
Ribosome detachment reduces protein synthesis

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11
Q

Oxidative stress

A

Accumulation of damage caused by oxygen-derived free radicals

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12
Q

Peroxidation of membranes

A

Damage lipid membranes & forms more peroxides

Caused by oxygen-derived free radicals

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13
Q

Protein oxidation causes

A

loss of enzymatic activity & abnormal folding

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14
Q

DNA oxidation causes

A

DNA damage/ single stranded breaks & mutations

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15
Q

Respiratory burst

A

Digestion of bacteria by neutrophils using HOCl & OH radicals

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16
Q

Problems with respiratory burst pathway cause

A

people to die at young age from infection

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17
Q

Respiratory burst pathway

A

NADPH oxidase converts oxygen into oxygen radical (can activate neutrophil granules to degrade bacteria)
SOD converts oxygen radical into H2O2 which is converted into HOCl by myeloperoxidase & OH radical by Fe2+

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18
Q

Damage to membrane permeability causes

A

Activation of phospholipases in cytosol

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19
Q

Reversible cell injury

A

damage not too severe, cells can repair themselves

20
Q

Irreversible cell injury

A

Point of no return

Cells can’t recover from accumulated damage & die

21
Q

Reversible cell changes

A

Swollen mitochondria & ER
Clumping of chromatin but nuclei still in tact
Membrane blebs

22
Q

Irreversible cell changes

A

Swelling of ER & loss of ribosomes
Lysosome rupture
Nuclear condensation (break apart, dissolve, no nuclei)
Swollen mitochondria with amorphous densities

23
Q

Necrosis

A

cell death resulting from exogenous or endogenous damage not controlled by cell
Damage to membrane results in leaking cell contents

24
Q

Apoptosis

A

Programmed cell death can be result of external or internal cell damage, physiologic or developmental
Cell fragmentation & phagocytosis - doesn’t leak

25
Q

Types of necrosis

A

coagulative, liquefactive, caseous, enzymatic fat, fibrinoid, & gangrenous

26
Q

Coagulative necrosis

A

Death due to ischemia, hypoxia, reperfusion injury in most organs except brain
Basic outline of cell preserved but with no nuclei

27
Q

Liquefactive Necrosis

A

Tissue degrades & liquifies - loss of cells & tissue structure (looks granular)
Occurs often in brain because of no connective framework
Abscesses - center made of enzymatic digested neutrophils & cells (pus)

28
Q

Caseous Necrosis

A

Accumulation of mononuclear cells that mediate chronic inflammatory reaction & granuloma formation
Grayish, white or yellow & soft, cheese-like
Few organisms such as TB & fungi

29
Q

Enzymatic fat necrosis

A

Fat digested due to action of lipases
Fatty acids released react with calcium - form soap-like, white, chalky substance
See material in fat cells
In pancreatitis (enzymes leak out & digest tissue & body fat) & inflammation in fat

30
Q

Fibrinoid Necrosis

A

Injury in blood vessels with accumulation of plasma proteins
Depositing in blood vessel wall attracts complement that cause necrosis

31
Q

Gangrenous Necrosis (gangrene)

A

Generalized necrosis - Not specific pattern of cell death
Limb or bowel that has died because loss of circulation
If also have bacterial infection called wet gangrene

32
Q

Ischemia

A

Caused by reduction of available oxygen

When leads to tissue death - have heart attack, stroke, etc.

33
Q

Reperfusion

A

Blood flow/oxygenation of tissue is restored

Leads to large amount of ROS damage

34
Q

Stages of Apoptosis

A

Signaling pathways commit cell to death
Intracellular signals further commit cell to apoptotic pathway (initiator caspases)
Execution phase - execution caspases catabolize cytoskeleton & activate endonucleases which cause DNA breakdown
Removal of dead cells by macrophages

35
Q

Intrinsic apoptosis pathway

A

Regulated by things within cell (growth factor withdrawal, DNA damage, protein misfolding, ER stress, etc.)
Activates family of Bcl-2 family protein sensors (some proapoptotic, some antiapoptotic)

36
Q

Bax & Bak

A

Proapoptotic Bcl-2 proteins
Intrinsic pathway
Dimerize & form holes in mitochondria - allows Cytochrome C to leak out

37
Q

Cytochrome C

A

From mitochondria
Intrinsic pathway
When leaks out, activates initiator caspases which stimulate executioner caspases

38
Q

Bcl-2 & Bcl-x

A

Antiapoptotic

Block Bax & Bak and other pro-apoptotoic proteins

39
Q

Extrinsic Pathway

A

Regulated by receptors from signals outside cell

TNF receptor & Fas ligand - when activated, activate Adapter proteins

40
Q

Adapter proteins

A

Extrinsic pathway

Activate initiator caspases

41
Q

Executioner caspases

A

breakdown cytoskeleton & fragment DNA

42
Q

Apoptotic body

A

Degraded DNA & proteins packaged into apoptotic bodies & sent to phagocytes

43
Q

Intrinsic & extrinsic pathways converge on

A

Initiator caspases

44
Q

p53 activates

A

Proapoptotic forms if there are a lot of mistakes made during cell replication
Stimulates Bax & Bak

45
Q

Necrosis features

A

Enlarged cell, condensed/degraded nuclei, disrupted plasma membrane, cell contents may leak out, frequent inflammation, pathologic role

46
Q

Apoptosis features

A

Reduced cell, fragmented nucleus, Intact plasma membrane, intact cell contents, no inflammation, physiologic & pathologic role

47
Q

Zone of liver most likely to get liver necrosis from drug overdose

A

Zone 3

Least oxygenated & have least nutrients

Pathology (6 decks)

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