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Pathology Exam 1 > Cell Injury & Death > Flashcards

Cell Injury & Death Flashcards

1
Q

define hyperplasia

A

increase in cell number

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2
Q

define hypertrophy

A

increase in cell size

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3
Q

define atrophy

A

decrease in cell size and number

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4
Q

define metaplasia

A

adult cell changes into another cell type

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5
Q

T/F hyperplasia and hypertrophy both can be physiological or pathological

A

True

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6
Q

during atrophy, how are proteins degraded?

A
  • cytoskeleton broken down by proteasome
  • cellular components are “self-eaten” (autophagy)
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7
Q

examples of metaplasia

A
  • smokers from resp. epith. to squam. epith.
  • gastric reflux from squam. epith. to gastric/intestinal eptih.
  • vitamin A deficiency = squamous lining begins to keratinize
  • myositis ossificans = m tissue changing to bone after trauma
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8
Q

what is hypoxia caused by

A
  • ischemia
  • hypoxemia
  • decreased O2 carrying capacity of blood
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9
Q

what is ischemia

A

decreased blood flow to a tissue/organ
- shock = generalized drop in BP causing poor tissue perfusion

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10
Q

what is hypoxemia

A

low partial P of Oxygen (PaO2) in arterial blood

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11
Q

what causes hypoxemia

A
  • high altitude = decreased PaO2
  • hypoventilation = increased PaCO2 –> decreased PaO2
  • diffusion defect
  • blood bypasses the lung or oxygenated air can’t reach the blood
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12
Q

what is anemia

A

decrease in RBC mass - PaO2 and SaO2 are normal

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13
Q

what can cause decreased OXYGEN carrying capacity

A

anemia
carbon monoxide poisoning
methemoglobinemia

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14
Q

does CO or OXYGEN bind Hb better

A

CO binds better = carbon monoxide poisoning

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15
Q

what is methemoglobinemia

A

iron in heme is oxidized to F3+ which can’t bind O2

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16
Q

what are the four general mechanisms that lead to cell injury

A
  • ATP depletion and production of ROS
  • Ca2+ influx into cytoplasm
  • cell mem. damage
  • DNA damage and protein misfolding
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17
Q

what happens in the cell when there is decreased ATP

A
  1. Na+K+ pump stops working –> increased Na+ and water in the cytosol = cell swelling
  2. Ca2+ pump stops working –> increased Ca2+ in cytosol
  3. switch to anaerobic glycolysis –> lactic acid buildup lowers the pH = denatures protein and precipitates DNA
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18
Q

three things ROS can cause

A
  • peroxidized lipids –> membrane damage
  • oxidation of DNA –> mutations
  • oxidation of proteins –> protein breakdown/misfolding
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19
Q

how are ROS made

A
  • during mitochondrial respiration due to imperfect rx of OXYGEN to water which forms (superoxide) O2-
  • in phagosome of phagocytes as part of the respiratory (oxidative) burst
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20
Q

what does superoxide get converted to and by what

A

converted to hydrogen peroxide by superoxide dismutase

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21
Q

what can superoxide combine with and what does that produce

A

nitric oxide (NO) —> peroxynitrite ONOO-

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22
Q

what can hydrogen peroxide be converted to and by what

A

converted to hypochlorite (HOCl) by myeloperoxidase

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23
Q

damage caused by ROS is called what

A

oxidative stress

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24
Q

free radicals and ROS decay spontaneously and are broken down by what

A
  • superoxide dismutase
  • glutathione peroxidases in cytoplasm and catalase in peroxisome both convert hydrogen peroxide to water
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25
Q

what do antioxidants do

A

block free radical formation or scavenge them

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26
Q

ischemia causes release of what

A

intracellular Ca2+ stores into the cytosol then later influx across the plasma membrane

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27
Q

what happens when there is elevated cytosolic Ca2+

A
  • activates enzymes which damage membranes, proteins, DNA and ATP
  • can also induce apoptosis by activation of caspases and increasing mitochondrial permeability (cytochrome c release)
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28
Q

what does plasma membrane damage lead to

A
  • cytosolic enzymes leaking into serum (e.g. cardiac troponin)
  • calcium influx
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29
Q

what does mitochondrial membrane damage lead to

A
  • loss of ETC
  • cytochrome c leaking into cytosol (activates apoptosis)
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30
Q

what does lysosome membrane damage lead to

A

hydrolytic enzymes leaking into the cytosol which are activated by high intracellular calcium

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31
Q

define hydropic degeneration

A

accumulation of water droplets in cytoplasm. causes organs to appear pale/swollen

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32
Q

define fatty change (degeneration)

A

in cells involved in fat metabolism - lipid vacuoles in cytoplasm. cause organs to appear yellow/greasy

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33
Q

T/F for reversible injury if the stimulus is removed, the tissues return to normal

A

T

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34
Q

what are two examples of reversible cell injury

A
  • hydropic degeneration
  • fatty change
35
Q

what are two predictors of irreversible injury

A
  • cell can no longer make ATP
  • membranes lose their integrity
36
Q

T/F cells lost function after they change morphology or die

A

False. Cells lose their function long before they change morphology or die

37
Q

what are the two main mechanisms of cell death

A

necrosis and apoptosis

38
Q

what is the main histologic change in cell death

A

loss of the nucleus

39
Q

what are the three ways a cell can lose its nucleus

A
  • condensation (pyknosis)
  • fragmentation (karyorrhexis)
  • dissolution (karyolysis)
40
Q

what are the three main types of necrosis

A

coagulative, liquefactive, and caseous

41
Q

define necrosis

A

death of a group of cells –> release of cellular components –> acute inflammatory response

42
Q

define coagulative necrosis

A

cell shape and organ structure preserved due to coagulation of proteins but nucleus disappears

43
Q

coagulative necro pattern is seen when

A

with ischemic infarction (obstruction of blood leading to cell/tissue death) of any organ except the brain

44
Q

clinical feature of coagulative necro

A
  • area of infarcted tissue is pale and wedge-shaped (pointing to focus of vascular occlusion)
  • red infarction arises if blood re-enters a loosely organized tissue (pulmonary or testicular infarction)
45
Q

define liquefactive necro

A

necrotic tissue becomes liquefied: enzymatic lysis of cells and protein results in liquefaction

46
Q

liquefactive necro is characteristic of what

A
  • brain infarction = proteolytic enzymes from microglial cells liquefy the brain
  • abscess = proteolytic enzymes from neutrophils liquefy tissue
47
Q

gangrenous necro is a type of which necro

A

coagulative necro

48
Q

gangrenous necro resembles what kind of tissue

A

mummified tissue (dry gangrene)

49
Q

gangrenous necro is characteristic of what

A

ischemia of lower limb and GI tract

50
Q

with gangrenous necro, if superimposed infection of dead tissues occur, what happens next

A

liquefactive necro ensues (wet gangrene)

51
Q

define caseous necro

A

soft and friable with cheese-like appearance

52
Q

caseous necro is characteristic of what

A
  • tuberculosis
  • deep fungal infections
53
Q

what happens to tissue architecture during caseous necro

A

tissue architecture replaced by define foci of granulomatous inflammation (contain granulomas)

54
Q

define fat necro

A

focal areas of fat destruction from trauma or enzymatic breakdown

55
Q

ex. of fat necro

A

acute pancreatitis releases pancreatic enzymes:
—> break down membranes and fats of adjacent adipose tissue in the peritoneum
—> fatty acids released combine with Ca2+ to form chalky white areas (fat saponification)

56
Q

define fibrinoid necro

A

necrosis of a vessel wall leading to leakage of fibrin and other proteins into the wall which stains bright pink on H&E

57
Q

what is fibrinoid necro caused by

A

immune reactions (vasculitis) and malignant hypertension
- (inflammatory response to blood vessel itself)

58
Q

define apopto

A

ATP dependent “programmed” cell death of a single or small group of cells

59
Q

purpose of apoptosis is to eliminate what

A
  • unneeded structures- embryogenesis, stopping the immune response
  • old, non-functional cells - intestine turnover, menstrual cycle
  • potentially harmful cells - virus-infected, cancer cells
  • cells with DNA damage that can’t be repaired - radiation, drugs etc.
60
Q

what is apopto initiated by

A

caspases which activate endonucleases (degrade DNA) and proteases (degrade cytoskeleton)

61
Q

what happens during apopto as the dying cell shrinks

A
  • cytoplasm becomes more eosinophilic and the nucleus condenses and fragments
  • fragments of the cell break off with intact cell membranes
  • phagocytes engulf the fragments
62
Q

is there an inflammatory response to apopto?

A

little to no inflammatory response

63
Q

what are the two kinds of apopto

A

intrinsic (mitochonndrial) and extrinsic (death receptor)

64
Q

what initiates the intrinsic apopto pathway

A

cell injury, DNA damage or lack of growth signals

65
Q

intrinsic pathway steps

A
  • decrease in BCL-2 protein family (anti-apoptotic)
  • which allows cytochrome c to leak from the mitochondria into the cytoplasm
  • activates caspases leading to apoptosis
66
Q

extrinsic apopto pathway cells express what

A

death receptors
- TNF receptor family
- Fas (CD95)

67
Q

extrinsic apopto pathway steps

A

Fas ligand (FasL), mainly on activated T cells, binds to Fas and activated caspases leading to apopto

68
Q

how are intracellular accumulations acquired?

A
  • inadequate removal of nermal substance from cell
  • genetic or acquired defect in protein folding or transport
  • enzyme deficiency leads to accumulation of metabolites
  • accumulation of exogenous substances
69
Q

pigments can be ____ or _____

A

exogenous or endogenous colored substances

70
Q

what is the most common exogenous pigment

A

carbon. in coal dust and urban air. aggregates in the lung

71
Q

what are the four pigments that we need to know

A

-carbon
-lipofuscin
- melanin
- hemosiderin

72
Q

define lipofuscin

A

‘wear and tear’ brownish-yellow complex of lipid and protein

73
Q

what is lipofuscin derived from

A

previous free radical damage of membranes

74
Q

how does lipofuscin accumulate

A

with age or atrophy in heart, liver and brain

75
Q

what is melanin

A

brown/black pigment made by melanocytes that screens against UV damage

76
Q

what is hemosiderin

A

golden yellow/brown, hemoglobin derived pigment present where there is excess of iron

77
Q

what is pathologic calcification

A

abnormal tissue deposition of calcium salts

78
Q

if pathologic calcification occurs in dead or dying tissues they are called what

A

dystrophic calcifications

79
Q

if pathologic calcification occurs in normal tissues they are called what

A

metastatic calcifications

80
Q

what are metastatic calcifications caused by

A

elevated calcium caused by:
- renal failure
- increased PTH
- bone destruction
- vitamin D disorders

81
Q

what slows cell aging

A

calorie restriction and physical activity

82
Q

why do cells age

A
  • accumulation over time of unrepaired DNA damage
  • decreased cellular replication
  • defective proteins
  • increasing inflammation
83
Q
A
83
Q
A

Pathology Exam 1 (5 decks)

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