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Goljan Pathology - High Yield Facts > Cell injury > Flashcards

Cell injury Flashcards

1
Q

PO2

A

driving force for diffusion of O2 into tissue

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2
Q

SaO2

A

percent heme groups occuied by O2

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3
Q

Cyanosis

A

decreased O2 saturation

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4
Q

O2 content

A

1.34 x Hb x SaO2 + PaO2

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5
Q

Oxygen

A

eceton acceptor in oxidative pathway

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6
Q

Hypoxia

A

inadequate O2 leads to ATP depletion

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7
Q

Ischemia

A

decreased arterial (or venous) blood flow

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8
Q

Respiratory acidosis

A

retention of CO2 always decreases PaO2

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9
Q

Ventilation defect

A

impaired delivery of O2 to alveoli; intrapulmonary shunting of blood (e.g., RDS)

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10
Q

Perfusion defect

A

absent blood flow to alveoli; increased alveolar dead space e.g., pulmonary embolus)

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11
Q

Diffusion defect

A

O2 cannot cross alveolar-capillary interface; interstitial lung disease (e.g., sarcoidosis)

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12
Q

Methemoglobin

A

decreased SaO2; heme Fe +3; oxidizing agents (sulfur/nitro drugs); Rx with IV methylene blue

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13
Q

Clinical methemogloinemia

A

cyanosis not corrected by O2; chocolate colored blood`

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14
Q

Carbon monoxide

A

decreased SaO2; left-shift O2 binding curve; inhibits cytochrome oxidase

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15
Q

Causes carbon monoxide poisoning

A

car exhaust, space heaters, smoke inhalation

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16
Q

S/S carbon monoxide poisoning

A

headache; cherry red color skin

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17
Q

Cyanide

A

inhibits cytochrome oxidase; systemic asphyxiant

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18
Q

Carbon monoxide + cyanide poisoning

A

house fires

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19
Q

left-shifted O2

A

decreased 2,3 BPG, carbon monoxide, alkalosis, HbF, methemoglobin, hyothermia

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20
Q

right-shifted O2

A

increased 2,3 BPG, high altitude, acidosis, fever

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21
Q

high altitude

A

respriratory alkalosis enhances glycolysis; increased systhesis 2,3 BPG

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22
Q

Mitochondrial poisons

A

damages membrane and drains off protons; alcohol salicylates

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23
Q

Uncoupling agents in mitochondria

A

drain off protons; dinitrophenol, thermogenin (brown fat)

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24
Q

Complication mitochondrial poisons/uncoupling agents

A

hyperthermia

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25
Q

Decreased ATP

A

impaired Na+/K+ ATPase pump (cellular swelling); reversible

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26
Q

Anaerobic glycolysis

A

ATP synthesis in hypoxia; lactate decreases intracellular pH, denatures proteins

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27
Q

Irreversible injury hypoxia

A

membrane/mitochondrial damage

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28
Q

Mitochondrial damage

A

release cytochrome c activates apoptosis

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29
Q

Irreversible injury hypoxia

A

increases cytosolic Ca2+ activates phospholipase, proteases, endonuclease

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30
Q

Free radicals

A

unpaired electron in outer orbit; damage cell membranes and DNA

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31
Q

Free radicals

A

superoxide, hydroxyl, peroxide, drugs (acetaminophen)

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32
Q

Superoxide dismutase

A

neutralizes superoxide

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33
Q

Glutathione

A

neutralizes peroxide, drug FRs

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34
Q

Catalase

A

neutralizes peroxide

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35
Q

Lipofuscin

A

indigestible lipid of lipid peroxidation; brown pigment increased in atrophy and FR damage

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36
Q

Reperfusion injury in heart

A

superoxide FRs + calcium

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37
Q

Mitochondrial injury

A

cytochrome c in cytosol initiates apoptosis

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38
Q

SER hyperplasia

A

alcohol, barbiturates, phenytoin

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39
Q

Complications SER hyperplasia

A

increases drug metabolism (e.g., oral contraceptives); decreased vitamin D

40
Q

Chediak-Higashi

A

membrane protein defect in transferring lysosomal enzymes to phagocytic vacuoles

41
Q

Chediak-Higashi

A

AR; giant lysosomes

42
Q

I cell disease

A

absent enzyme marker in Golgi apparatus (mannose-6-phosphate); empty lysosomes

43
Q

Rigor mortis

A

stiff muscles after death due to ATP depletion

44
Q

Fatty change in liver

A

MCC alcohol (increase in NADH); DHAP –>G3P –> TG

45
Q

Fatty change in liver

A

increase VLDL pushes nucleus to side

46
Q

Causes fatty change

A

increase synthesis of TG/FAs, decrease beta-oxidation FAs/ synthesis apoproteins/ release VLDL

47
Q

Fatty change in kwashiorkor

A

decrease synthesis of apoproteins

48
Q

Ferritin

A

primary iron storage protien; soluble in blood; serum level reflects marrow storage iron

49
Q

Hemosiderin

A

insoluble ferritin degradation product visible with Prussian blue stain

50
Q

Atrophy

A

reduction in cell/tissue mass by either loss or cell shrinkage

51
Q

Brain atrophy

A

ischemia; Alzhemier’s

52
Q

Exocrine gland atrophy in CF

A

duct obstruction by thick secretions

53
Q

Labile cells

A

stem cells (skin, marrow, GI tract)

54
Q

Stable cells

A

in Go phase (smooth muscle, hepatocytes); can enter cell cycle (growth factors, hormones)

55
Q

Permanent cells

A

cannot replicate; cardiac/striated muscle; neurons

56
Q

Hypertrophy

A

increase in cell size (structural components, DNA)

57
Q

LVH

A

increased preload (valve regurgitation), increased afterload (HTN, aortic stenosis)

58
Q

RVH

A

pulmonary hypertension

59
Q

Bladder smooth muscle hypertrophy

A

prostate hyperplasia constricts urthra

60
Q

Removal of kidney

A

hypertrophy of remaining kidney

61
Q

Hyperplasia

A

increase in number of cells

62
Q

Endometrial hyperplasia

A

unopposed estrogen (obesity, taking estrogen)

63
Q

RBC hyperplasia

A

increased EPO (blood loss, ectopic secretion, high altitude)

64
Q

Prostate hyperplasia

A

increased dihydrotestosterone

65
Q

Gynecomastia

A

hyperplasia male breast tissue; normal in newborn, adolescent, elderly

66
Q

Metaplasia

A

one adult cell type replaces another cell type

67
Q

Squamous metaplasia in bronchus

A

smoking

68
Q

Intestinal metaplasia in stomach

A

Paneth cells, goblet cells; H. pylori chronic atrophic gastritis

69
Q

Squamous metaplasia bladder

A

Schistosoma hematobium infection

70
Q

Barrett’s esophagus

A

glandular metaplasia of distal esophagus; due to GERD

71
Q

Dysplasia

A

atypical hyperplasia or metaplasia are precursors for cancer

72
Q

Squamous dyplasia in cervix

A

HPV

73
Q

Squamous dysplasia in bronchus

A

smoking

74
Q

Necrosis

A

death of groups of cells

75
Q

Coagulation necrosis

A

preservation of structural outline (due to increase lactic acid)

76
Q

Infarction

A

pale (e.g., heart, kidney); hemorrhagic (e.g., lung, small bowel); dry gangrene

77
Q

Liquefactive necrosis

A

brain infarct, bacterial infections; wet gangrene

78
Q

Caseous necrosis

A

variant coagulation necrosis; granulomas due to TB/systemic fungi

79
Q

Granulomas

A

acticated macrophages (epitheliod cells); multinucleated giant cells; CD4 T cells

80
Q

Epitheliod cells

A

gamma-interferon releaed by CD4 T cells activates macrophages

81
Q

Multinucleated giant cells

A

fusion of epitheliod cells

82
Q

Granulomas

A

type 4 HSR

83
Q

Enzymatic fat necrosis

A

associated with pancreatitis; soap formation (Ca2+ & fatty acids)

84
Q

Fibrinoid necrosis

A

necrosis of immune reactions (immune vasculitis/endocarditis)

85
Q

Postmortem necrosis

A

autolysis; no inflammatory reaction

86
Q

Dystrophic calcification

A

calcification of damged tissue; normal serum calcium

87
Q

Dystrophic calcification

A

pancreatitis; atheroscelerotic plaque

88
Q

Metastatic calcification

A

calcification of normal tissue; increased seum calcium or phosphorus

89
Q

Nephrocalcinosis

A

metastatic calcification of collecting tubule basement membranes

90
Q

S/S nephrocalcinosis

A

polyuria due to nephrogenic diabetes insipidus; renal failure

91
Q

Apoptosis

A

gene regulated individual cell death

92
Q

Signals activating apoptosis

A

mullerian inhibitory factor, tumor necrosis factor, hormone withdrawal

93
Q

Signal modulators of apoptosis

A

P53 suppressor gene, BCL-2 genes

94
Q

BCL-2 genes

A

anti-apoptosis gene; prevents cytochrome c from leaving mitochondria

95
Q

Caspases

A

responsible for enzymatic cell death in apoptosis; proteases and endonucleases

96
Q

Marker of apoptosis

A

esoinophilic cytoplasm, pyknotic (ink dot) nucleus

97
Q

Apoptosis

A

loss Mullerian epithlium in male fetus; thymus involution; killing cancer cells

Goljan Pathology - High Yield Facts (20 decks)

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