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Step One Prep > Growth Adaptations, Cellular Injury, and Cell Death > Flashcards

Growth Adaptations, Cellular Injury, and Cell Death Flashcards

1
Q

Barret esophagus

A

acid refulx from the stomach causes the normally nonkeratinizing squamous epithelium (suited for friction of food bolus) of the esophagus to undergo metaplasia to nonciliated, mucin-producing columnar epithelium (suited for stomach acid) of the stomach

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2
Q

cellular injury

A

stress can be so severe that it exceeds the cells ability to adapt

likelihood of injury depends on type of stress, severity of stress, and type of cell affected

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3
Q

dysplasia

A

disordered cell growth

generally refers to proliferation of precancerous cells

often arises from longstanding pathologic hyperplasia (ex. endometrial hyperplasia) or metaplasia (Barrett esophagus)

REVERSIBLE with alleviation of inciting stress

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4
Q

mechanism of decreased organ size

A

decreased stress on an organ leads to decreased organ size

atrophy

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5
Q

carcinoma

A

result of longstanding dysplasia

IRREVERSIBLE

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6
Q

causes of ischemia

A
  1. decreased arterial perfusion (ex. atherosclerosis)
  2. decreased venous drainage (ex. Budd-Chiari syndrome - caused by polycythemia vera or lupas anticoagulant)
  3. shock - systemic hypotension resulting in decreased tissue perfusion
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7
Q

keratomalacia

A

metaplasia

switch from thin squamous lining of conjunctiva to startified keratinized squamous epithelium

caused by Vit A deficiency

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8
Q

progression of metaplasia

A

with persistent stress, metaplasia can progress to dysplasia and eventually to cancer

ex. Barrett esophagus to adenocarcinoma of the esophagus

EXCEPTION: apocrine metaplasia of the breast does not incresae risk of cancer

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9
Q

hypoxemia - V/Q mismatch

A

blood bypassses oxygenated lung (ex. right to left shunt) or oxygenated air can’t reach blood (ex. atelectasis)

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10
Q

cervical intraepithelial neoplasia

A

dysplasia

precursor to cervical cancer

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11
Q

aplasia

A

failure of cell production during embryogenesis

ex. unilateral renal agenesis

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12
Q

pathogenic hyperplasia

A

hyperplasia occuring due to underlying pathology

can progress to dysplasia and eventually cancer

EXCEPTION: benign prostatic hyperplasia - doesn’t increase risk for prostate cancer

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13
Q

causes of hypoxia

A
  1. ischemia
  2. hypoxemia
  3. decreased O2 carrying capacity
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14
Q

mechanism of decrease in number of cells

A

apoptosis

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15
Q

mechanism of hyperplasia

A

production of new cells from stem cells

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16
Q

metaplasia

A

change in stress on an organ leads to changhe in cell type - new cell type is better able to handle the new stress

generally a change from one type of surface epithelium to another (squamous, columnar, transitional - urogenital)

ex. Barrett esophagus

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17
Q

hypoxemia - hypoventilation

A

increased PACO2 causes decreased PAO2

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18
Q

ischemia

A

decreased blood flow through an organ

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19
Q

cell injury - severity of stressor

A
  1. slowly developing ischemia = atrophy (cell adaptation)
    ex. renal artery atherosclerosis
  2. acute ischemia = cell injury
    ex. renal artery embolus
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20
Q

common causes of cell injury

A

inflammation, nutritional deficiency or excess, hypoxia, trauma, and genetic mutation

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21
Q

mechanism of hypertrophy

A

gene activation to produce new proteins (increase cytoskeleton production)

production of organelles (to support increased size of cell)

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22
Q

hypoxemia - diffusion deficit

A

thicker diffusion barrier results in PAO2 not being able to push as much O2 into the blood

causes decreased PaO2

ex. interstitial pulmonary fibrosis

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23
Q

hypertrophy

A

increase in size of existing cells

permanent tissues (cardiac muscle, skeletal muscle, and nerve) can only undergo hypertrophy

ex: cardiac myocytes undergo hypertrophy only in response to systemic hypertension

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24
Q

cell injury - type of cell affected

A
  1. neurons are highly susceptible to ischemia - will undergo cell injury in ischemic situation
  2. skeletal muscle is more resistant to ischemic injury
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25
Q

hypoplasia

A

decrease in cell production during embryogenesis resulting in a relatively small organ

ex. streak ovary in Turner syndrome

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26
Q

hypoxemia

A

low partial pressue of O2 in the blood (PaO2 <90%)

normal: FiO2 - PAO2 - PaO2 - SaO2

     atmosphere  alveolar    arterioles   Hb saturation
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27
Q

mechanism of decrease in size of cells

A
  1. ubuquitin-proteosome degradation of cytoskeleton (ubiquitin-tagged intermediate filaments destroyed in proteosome)
  2. autophagy of cellular components (generation of autophagic vacuoles- fuse with lysosomes whse hydrolytic enzymes break down cellular components)
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28
Q

Mechanisms of increased organ size

A

an increase in stress leads to an increase in organ size

hyperplasia

hypertrophy

generally occur together (ex: uterus during pregnancy) except in permanent tissues = only hypertrophy

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29
Q

hyperplasia

A

increase in number of cells

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30
Q

metaplasia of mesenchymal tissue

A

bone, blood vessels, fat, cartilage

ex. myositis ossificans - connective tissue within muscle changes to bone during healing after a trauma (x-ray will show distinct separation of bone section - if connected to existing bone = osteosarcoma)

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31
Q

atrophy

A

decrease in size and number of cells

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32
Q

hypoxia

A

low O2 delievery to a tissue = imparied oxidative phosphorylation (O2 os the final electron acceptor in electron transport chain of oxidative phosphorylation) = decreased ATP production = cell injury

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33
Q

Vitamin A deficiency

A

can result in metaplasia

Vit A necessary for differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye

with Vit A deficiency - squamous lining of conjunctiva undergoes metaplasia to stratified keratinizing squamous epithelium

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34
Q

mechanism of metaplasia

A

reprogramming of stem cells, which then produce the newcell type

REVERSIBLE with removal of the stressor (ex. treat gastroesophageal reflux to reverse Barrett esophagus)

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35
Q

hypoxemia - high altitude

A

decreased FiO2

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36
Q

cell injury - type of injury

A

certain stressors are more likely to result in cell adaptation than injury

37
Q

anemia

A

decrease in RBC mass

PaO2 normal, SaO2 normal - less Hb, but remaining Hb still binds O2 normally

38
Q

CO poisoning

A

PaO2 normal, SaO2 decreased - CO binds Hb with 100X affinty than O2

less O2 is able to bind Hb = decreased saturation

exposure = smoke from fire, car exhaust, gas heaters

39
Q

classic finding of CO poisoning

A

cherry red appearance of skin

40
Q

early sign of CO exposure

A

headache (late exposure = coma and death)

41
Q

Methemoglobinemia

A

Fe2 iron in heme is oxidized to Fe3 - can’t bind O2

SaO2 decreased

42
Q

mechanism of methemoglobinemia

A

oxidant stress (sulfa and nitrate drugs)

seen in newborns

43
Q

classic finding of methemoglobinemia

A

cyanosis with chocolate-colored blood

44
Q

treatment for methemoglobinemia

A

intravenous methylene blue - reduces Fe3 back to Fe2

45
Q

damaging results of low ATP (hypoxia)

A
  1. NA/K pump dysfunction - buildup of sodium, and thus water, in the cell (cell swelling)
  2. Ca2 pump dysfunction - buildup of Ca2 in cytosol (normally kept out of cytosol) = inappropriate enzyme activation
  3. forces anaerobic glycolysis - lactic acid buildup results in low pH (denatures proteins and precipitates DNA)
46
Q

initial phase of cellular injury

A

REVERSIBLE

hallmark of reversible injury = cell swelling

47
Q

results of reversible cellular injury

A

cell swelling

causes loss of microvilli and membrane blabbing

swelling of RER results in disassociation of ribosomes, and thus decreased protein production

48
Q

late phase of cellular injury

A

IRREVERSIBLE

hallmark of irreversible injury = membrane damage

49
Q

result of plasma membrane damage due to irreversible cellular damage

A
  1. cytosolic enzymes leak into serum
    * **test for cardiac enzymes in serum to confirm myocardial infarction
  2. additional calcium entering the cell
50
Q

result of mitochondrial membrane damage due to irreversible cellular damage

A
  1. loss of electron transport chain (on inner mito membrane)

2. cytochrome C leaking into cytosol = apoptosis

51
Q

result of lysosomal membrane damage due to irreversible cellular damage

A

hydrolytic enzymes leak into cytosol - activated by high intracellular calcium

52
Q

end result of irreversible cellular injury

A

cell death

53
Q

morphologic hallmark of cell death

A

loss of nucleus

54
Q

mechanism of loss of the nucleus during cell death

A
  1. pyknosis - nuclear condensation
  2. karyorrhexis - fragmentation
  3. karyolysis - dissolution
55
Q

mechanisms of cell death

A
  1. necrosis

2. apoptosis

56
Q

necrosis

A

“cell murder” - always from an external pathological process

death of a large group of cells followed by acute inflammation

57
Q

types of necrosis

A
  1. coagulative necrosis
  2. liquefactive nécrosais
  3. gangrenous necrosis
  4. caseous necrosis
  5. fat necrosis
  6. fibrinoid necrosis
58
Q

coagulative necrosis

A

tissue dies, but general structure remains/ cell structure remains (cells lose nucleus) - structure remains by coagulation of proteins

CHARACTERISTIC OF ISCHEMIC INFARCTION IN ANY ORGAN EXCEPT THE BRAIN

59
Q

characteristics of ischemic infarction

A

area of infarcted tissue is wedge-shaped and pale (point of wedge points to focus of vascular occlusion)

60
Q

red infarction

A

arises if blood reenters a loosely organized tissue

ex. pulmonary or testicular infarction (testicle twists and collapses vein = blood can’t circulate and tissue dies)

61
Q

liquefactive necrosis

A

necrotic tissue becomes liquefied

62
Q

mechanism of liquefactive necrosis

A

enzymatic lysis of cells and protein results in liquefaction

CHARACTERISTIC OF BRAIN INFARCTION, ABCESS, and PANCREATITIS

63
Q

mechanism of liquefactive necrosis in brain infarction

A

proteolytic enzymes from mircoglial cells liquefy the brain

64
Q

mechanism of liquefactive necrosis in abscess

A

proteolytic enzymes from neutrophils liquefy tissue

65
Q

mechanism of liquefactive necrosis in pancreatitis

A

proteolytic enzymes from pancreas liquefy parenchyma

66
Q

gangrenous necrosis

A

coagulative necrosis that resembles mummified tissue (dry gangrene)

CHARACTERISTIC OF ISCHEMIA OF THE LOWER LIMB

67
Q

wet gangrene

A

gangrenous necrosis with superimposed infection of dead tissue - liquefactive necrosis ensues

68
Q

caseous necrosis

A

soft and friable necrotic tissue with “cottage cheese-like” appearance

combination of coagulative ad liquefactive necrosis

CHARACTERISTIC OF GRANULOMATOUS INFLAMMATION DUE TO TB OR FUNGAL INFECTION

69
Q

fat necrosis

A

necrotic adipose tissue with chalky-white appearance due to deposition of calcium

CHARACTERISTIC OF TRAUMA TO FAT (breast) and PANCREATITIS-MEDIATED DAMAGE OF PERIPANCREATIC FAT

70
Q

mechanism of fat necrosis

A

fatty acids released by trauma (breast) or lipase (pancreastitis) join with calcium via a process called saponification

71
Q

saponification

A

dystrophic calcification: necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate (process of fat necrosis)

NORMAL SERUM LEVELS/DEAD TISSUE

72
Q

metastatic calcification

A

occurs with high serum calcium or phosphate levels lead to calcium deposition in normal tissues

ex. hyperparathyroidism leading to nephrocalcinosis

HIGH SERUM LEVELS/NORMAL TISSUE

73
Q

fibrinoid necrosis

A

necrotic damage to blood vessel wall

CHARACTERISTIC OF MALIGNANT HYPERTENSION AND VASCULITIS

74
Q

mechanism of fibrinoid necrosis

A

leaking of proteins (fibrin) into vessel wall results in bright pink staining of wall microvilli

75
Q

apoptosis

A

“cell suicide” - ATP dependent, genetically programmed cell death involving single cells or small groups of cells (necrosis involves large groups of cells)

ex. endometrial shedding during menstrual cycle; removal of cells during embryogenesis; CD8 T-call mediated killing of virally infected cells

76
Q

morphology of apoptotic cells

A
  1. dying cell shrinks = cytoplasm becomes more eosinophilic
  2. nucleus condenses and fragments in organized manner
  3. apoptotic bodies fall from the cell and are removed by macrophages

NOT FOLLOWED BY INFLAMMATION

77
Q

mechanism of apoptosis

A

mediated by caspases that activate proteases and endonucleases

  • proteases break down cytoskeleton
  • endonucleases break down DNA
78
Q

activation of caspases - intrinsic pathway

A

caused by cellular injury, DNA damage, decreased hormonal stimulation - leads to inactivation of Bcl2 (Bcl2 stabilizes mito membrane)

lack of Bcl2 allows cytochrome c to leak from inner mito matrix into cytoplasm = activates aspases

79
Q

activation of caspases - extrinsic pathway

A
  1. FAS ligand binds FAS death receptor (CD95) on target cell and activates caspases = negative selection of thymocytes in thymus
  2. tumor necrosis factor (TNF) binds TNF receptor on target cell and activates caspases
80
Q

activation of caspases - cytotoxic T cell pathway

A

perforins secreted by cytotoxic T-cell create pores in membranes of target cells

granzyme from CD8 T cell enters pores and activates caspases

CD8 T-cell killing of virally infected cells

81
Q

pre-eclampsia

A

increased pressure (generally third trimester) causes fibrinoid necrosis in placental vessels

82
Q

free radicals

A

chemical species with an unpaired electron in outer orbit

unpaired electrons cause damage

83
Q

physiologic generation of free radicals

A

occurs during oxidative phosphorylation

cytochrome c oxidase transfers electrons to oxygen (terminal electron acceptor)

partial reduction of O2 yields .O2- (super oxide), H2O2 (hydrogen peroxide), and .OH (hydroxyl radicals)

84
Q

pathogenic generation of free radicals

A
  1. ionizing radiation - H2O hydrolyzed to .OH
  2. Inflammation - NADPH oxidase generates superoxide during oxygen-dependent killing by neutrophils
  3. metals (copper and iron) - Fe2+ generates hydroxyl free radicals via fenton reaction (iron usually bound when in blood to prevent this)
  4. drugs and chemicals - P450 system of liver metabolizes drugs (ex. acetaminophen) generating free radicals (leads to liver necrosis)
85
Q

most damaging free radical

A

hydroxyl radicals

86
Q

hemochromatosis

A

iron buildup = free in blood generates free radicals = damage

87
Q

Wilson’s disease

A

copper buildup = pathologic generation of free radicals

88
Q

mechanism of injury via free radicals

A
  1. peroxidation of lipids
  2. oxidation of DNA and proteins (particularly indicated in oncogenesis)

***both processes indicated in aging and oncogenesis

89
Q

mechanism of elimination of free radicals

A
  1. antioxidants (glutathione and vitamins A,C,E)
  2. enzymes
    -superoxide dismutase (mito) = superoxide to hydrogen
    peroxide
    -glutathione peroxidase (mito) = 2GSH + free radical =
    GSSG and H20
    -catalase (peroxisomes) = H2O2 = O2 and H2O
  3. metal carrier proteins = carry free iron and copper in the blood to prevents oxidation reactions
    -transferrin and ceruloplasmin

Step One Prep (2 decks)

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