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MHD Exam 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

injury to a cell can disrupt…

A
  • the chemical processes of a cel

- directly damage components of the cell

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2
Q

8 categories of cell injury

A 
1 hypoxia
2 chemical
3 physical
4 biological (infectious disease)
5 Immunologic
6 genetic
7 nutritional
8 aging (degenerative)
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3
Q

living cells change in _____ and _____ when stressed/injured. These changes are clinically apparent as ______

A

1 structure and
2 function
3 symptoms

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4
Q

an inability to ____ leads to cell injury

A

adapt

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5
Q

irreversible injury can result in _____ or _____

A

necrosis or apoptosis

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6
Q

adaptation

A

process by which cells change in size, number, and appearance in response to changes in cell environment.
-Changes can be physiologic or pathologic

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7
Q

hyperplasia

A

increase in the number of cells - can be physiologic or pathologic

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8
Q

hypertrophy

A

increase in the size of a cell because of increased cellular substance
-can be physio or patho

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9
Q

atrophy

A

decrease in the size of a cell because of loss of cellular substance
-can be patho or physio

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10
Q

metaplasia

A

substitution of one type of an adult cell for another type of adult cell
- always pathologic

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11
Q

timeline of cell injury

A

1) reversible cell injury has a continuous decline in cell function until you get
2) cell death in which case it becomes irreversible cell injury
3) ultrastructural changes
4) light microscopic changes
5) gross morphological changes

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12
Q

vulnerable biochemical systems to cell injury

A
  • mitochondria
  • cellular calcium
  • integrity of membranes
  • integrity of genetic material
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13
Q

mitochondrial damage mechanism of cell injury

A
  • decrease ATP has multiple downstream effects

- increase reactive oxygen species damages lipids, proteins and DNA

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14
Q

Entry of calcium mechaism of cell injury

A
  • increase mitochondrial permeability

- activation of multiple cellular enzymes

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15
Q

mb damage mechanism of cell injury

A
  • plasma mb= loss of cellular components

- lysosomal mb- enzymatic digestion of cellular components

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16
Q

protein misfolding and DNA damage

A

activation of pro-apoptotic proteins

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17
Q

hypoxic injury model causes

A

ischemia, hypoxemia, or decreased oxygen carrying capacity

18
Q

hypoxic injury model effects

A
  • affects the mitochondria: decr oxidative p-lation and decr ATP causes…
    1) decr Na+ pump— influx of Ca2+, H2O, and Na+ and an efflux of K+ — ER swelling, cellular swelling, loss of microvilli, and blebs
    2) incr anaerobic glycolysis—- decr glycogen, incr lactic acid, decr pH — clumping of nuclear chromatin due to low pH
    3) Detachment of ribosomes– decr protein synthesis— lipid deposition
19
Q

Which enzymes does Ca activate?

A

1) phospholipase (decr phospholipids) and proteases (disrupt mb and cytoskeletal proteins) —- mb damage
2) endonuclease — nuclear damage
3) ATPase— decr ATP (also caused by incr mb permeability caused by Ca)

20
Q

altered mb permeability causes ______ to leak from cells which can be measured clinically

A

intracellular enzymes

21
Q

elevated CK or troponin

A

acute myocardial infarction

22
Q

elevated AST/ALT

A

hepatitis

23
Q

decreased ATP causes decreased intracellular oxygen which can be measured clinically via ___

A

lactic acid

24
Q

free radical

A

atom/s with a single unpaired electron in the outer orbit. They are chemically unstable and very reactive with components of the cell

25
Q

O2 superoxide removal

A

conversion to H2O2 by SOD

26
Q

H2O2 removal

A

decomposition to H2O by glutathione peroxidas and catalase

27
Q

pathologic effects of free radicals

A
  • lipid peroxidase = mb damage
  • protein modifications = breakdown and misfolding
  • DNA damage= mutations
28
Q

Carbon tetrachloride

A

converted to CCl3 in hepatocytes and causes lipid peroxidation and damage to cell structures

29
Q

reperfusion injury

A
  • return of blood/oxygen to ischemic tissue
  • oxygen derived free radicals produced
  • further injury to cells (can convert reversible injury to irreversible)
30
Q

morphology of REVERSIBLE cell injury chain of events

A
  1. cellular swelling
  2. steatosis (fatty change)
  3. myelin figures
  4. ER swelling (Na/K pumps = ineffective)
  5. Membrane blebs
31
Q

hallmark of irreversible injury

A
  • pyknosis = loss of nuclei
  • fragmentation of cells
  • leakage of contents
32
Q

pyknosis

A

cell damage causes loss of nuclei which look like little inkdots on H&E staining

33
Q

necrosis

A
  • sum total of morphological changes that occur in living tissue following cell death (so not a disease but a process found in many diseases)
  • includes structural changes of nucleus and cytoplasm of dead cell
  • CHARACTERIZED BY the presence of leukocytes (especially neutrophils) infiltrating dead tissue from adjacent living tissue
  • morphological changes occur as a result of enzymatic breakdown of cell and denaturation of proteins
34
Q

coagulation necrosis

A
  • pattern of necrosis associated with severe ischemia
  • in solid organs
  • histologically- ghost like remnants of intact cells which lack nuclei. the cell outline is preserved and the cytoplasm stains intense pink (eosinophilia)
  • macroscopically - tissue firm in early stages
  • ex. myocardial infarct, renal infarct
35
Q

liquefactive necrosis

A

-pattern of necrosis often associated with bacterial infections
-microscopic- bacteria release enzymes causing a rapid loss of cellular structure and a collection of liquid and amorphous debris
-macroscopic- creamy yellow material = abscess
-IMPORTANT** pattern of necrosis with brain hypoxia/infarct
-

36
Q

abscess

A

collection of neutrophils, dead cells, liquid

37
Q

caseous necrosis

A
  • pattern of necrosis associated with an inflammatory reaction called granuloma
  • histologically - amorphous, granular debris (dead cells) i the center of granulomatous cell reaction
  • macrocopically - necrotic tissue is soft, white, friable
38
Q

enzymatic fat necrosis

A

focal cell death in the pancreas and adjacent fat

-when peripancreatic adipose tissue is broken down, free fatty acids and calcium result

39
Q

gangrene

A

coagulation necrosis of an extremity, bowel, or gallbladder

40
Q

wet gangrene

A

if bacteria contaminate dying tissue, superimposing liquefactive necrosis, the process is referred to as wet gangrene

41
Q

apoptosis

A
  • regulated pattern of cell death characterized by nuclear condensation and fragmentation coupled with fragmentation of cytoplasm into apoptotic bodies
  • physiologic or pathologic
  • not associated with an inflammatory reaction - important distinction with necrosis
  • recognition, removal of dead cells by phagocytes
  • doesn’t usually spill its contents
  • often includes single cells and not the whole tissue
42
Q

where is apoptosis seen?

A
  • normal embryogenesis
  • hormone dependent physiological involution (menstrual cycle)
  • proliferating cell populations
  • DNA damage
  • infections
  • accumulation of misfolded proteins

MHD Exam 1 (6 decks)

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