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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
hypoplasia
decrease in cell production during embryogenesis resulting in a relatively small organ ex. streak ovary in Turner syndrome
26
hypoxemia
low partial pressue of O2 in the blood (PaO2 <90%) normal: FiO2 - PAO2 - PaO2 - SaO2 atmosphere alveolar arterioles Hb saturation
27
mechanism of decrease in size of cells
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)
28
Mechanisms of increased organ size
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
29
hyperplasia
increase in number of cells
30
metaplasia of mesenchymal tissue
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)
31
atrophy
decrease in size and number of cells
32
hypoxia
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
33
Vitamin A deficiency
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
34
mechanism of metaplasia
reprogramming of stem cells, which then produce the newcell type REVERSIBLE with removal of the stressor (ex. treat gastroesophageal reflux to reverse Barrett esophagus)
35
hypoxemia - high altitude
decreased FiO2
36
cell injury - type of injury
certain stressors are more likely to result in cell adaptation than injury
37
anemia
decrease in RBC mass PaO2 normal, SaO2 normal - less Hb, but remaining Hb still binds O2 normally
38
CO poisoning
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
classic finding of CO poisoning
cherry red appearance of skin
40
early sign of CO exposure
headache (late exposure = coma and death)
41
Methemoglobinemia
Fe2 iron in heme is oxidized to Fe3 - can't bind O2 SaO2 decreased
42
mechanism of methemoglobinemia
oxidant stress (sulfa and nitrate drugs) seen in newborns
43
classic finding of methemoglobinemia
cyanosis with chocolate-colored blood
44
treatment for methemoglobinemia
intravenous methylene blue - reduces Fe3 back to Fe2
45
damaging results of low ATP (hypoxia)
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
initial phase of cellular injury
REVERSIBLE hallmark of reversible injury = cell swelling
47
results of reversible cellular injury
cell swelling causes loss of microvilli and membrane blabbing swelling of RER results in disassociation of ribosomes, and thus decreased protein production
48
late phase of cellular injury
IRREVERSIBLE hallmark of irreversible injury = membrane damage
49
result of plasma membrane damage due to irreversible cellular damage
1. cytosolic enzymes leak into serum * **test for cardiac enzymes in serum to confirm myocardial infarction 2. additional calcium entering the cell
50
result of mitochondrial membrane damage due to irreversible cellular damage
1. loss of electron transport chain (on inner mito membrane) | 2. cytochrome C leaking into cytosol = apoptosis
51
result of lysosomal membrane damage due to irreversible cellular damage
hydrolytic enzymes leak into cytosol - activated by high intracellular calcium
52
end result of irreversible cellular injury
cell death
53
morphologic hallmark of cell death
loss of nucleus
54
mechanism of loss of the nucleus during cell death
1. pyknosis - nuclear condensation 2. karyorrhexis - fragmentation 3. karyolysis - dissolution
55
mechanisms of cell death
1. necrosis | 2. apoptosis
56
necrosis
"cell murder" - always from an external pathological process death of a large group of cells followed by acute inflammation
57
types of necrosis
1. coagulative necrosis 2. liquefactive nécrosais 3. gangrenous necrosis 4. caseous necrosis 5. fat necrosis 6. fibrinoid necrosis
58
coagulative necrosis
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
characteristics of ischemic infarction
area of infarcted tissue is wedge-shaped and pale (point of wedge points to focus of vascular occlusion)
60
red infarction
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
liquefactive necrosis
necrotic tissue becomes liquefied
62
mechanism of liquefactive necrosis
enzymatic lysis of cells and protein results in liquefaction CHARACTERISTIC OF BRAIN INFARCTION, ABCESS, and PANCREATITIS
63
mechanism of liquefactive necrosis in brain infarction
proteolytic enzymes from mircoglial cells liquefy the brain
64
mechanism of liquefactive necrosis in abscess
proteolytic enzymes from neutrophils liquefy tissue
65
mechanism of liquefactive necrosis in pancreatitis
proteolytic enzymes from pancreas liquefy parenchyma
66
gangrenous necrosis
coagulative necrosis that resembles mummified tissue (dry gangrene) CHARACTERISTIC OF ISCHEMIA OF THE LOWER LIMB
67
wet gangrene
gangrenous necrosis with superimposed infection of dead tissue - liquefactive necrosis ensues
68
caseous necrosis
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
fat necrosis
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
mechanism of fat necrosis
fatty acids released by trauma (breast) or lipase (pancreastitis) join with calcium via a process called saponification
71
saponification
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
metastatic calcification
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
fibrinoid necrosis
necrotic damage to blood vessel wall CHARACTERISTIC OF MALIGNANT HYPERTENSION AND VASCULITIS
74
mechanism of fibrinoid necrosis
leaking of proteins (fibrin) into vessel wall results in bright pink staining of wall microvilli
75
apoptosis
"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
morphology of apoptotic cells
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
mechanism of apoptosis
mediated by caspases that activate proteases and endonucleases - proteases break down cytoskeleton - endonucleases break down DNA
78
activation of caspases - intrinsic pathway
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
activation of caspases - extrinsic pathway
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
activation of caspases - cytotoxic T cell pathway
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
pre-eclampsia
increased pressure (generally third trimester) causes fibrinoid necrosis in placental vessels
82
free radicals
chemical species with an unpaired electron in outer orbit unpaired electrons cause damage
83
physiologic generation of free radicals
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
pathogenic generation of free radicals
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
most damaging free radical
hydroxyl radicals
86
hemochromatosis
iron buildup = free in blood generates free radicals = damage
87
Wilson's disease
copper buildup = pathologic generation of free radicals
88
mechanism of injury via free radicals
1. peroxidation of lipids 2. oxidation of DNA and proteins (particularly indicated in oncogenesis) ***both processes indicated in aging and oncogenesis
89
mechanism of elimination of free radicals
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

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