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Pathoma: Growth adaptations, cell injury and death Flashcards

1
Q

Hypertrophy

A

increase in size of the organ

involves gene activation, protein synthesis, and production of organelles

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2
Q

Hyperplasia

A

increase in number of cells in the organ

involves the production of new cells from stem cells

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3
Q

Permanent Tissues

A

Cardiac muscle
skeletal muscle
nerve

cannot make new cells
undergo hypertrophy only

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4
Q

Pathologic hyperplasia progresses to

A

dysplasia and eventually cancer

exception - benign prostatic hyperplasia, does not increase the risk for prostate cancer

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5
Q

Atrophy

A

decrease in stress leads to decrease in organ size by a decrease in size and number cells

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6
Q

what process decreases the number of cells in atrophy

A

apoptosis

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7
Q

what processes decreases the cell size in atrophy

A

ubiquitin-proteasome degradation of cytoskeleton - intermediate filaments of cytoskeleton are tagged with ubiquitin and destroyed by proteasomes
autophagy of cellular components - generation of autophagic vacuoles - fuse with lysosomes whose hydrolytic enzymes breakdown cellular components

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8
Q

metaplasia

A

change in stress on an organ leads to a change in cell type - most commonly one epithelium to another better able to handle the new stress

occurs via reprogramming stem cells
may be reversible by treating stressor

persistent stress - can progress to dysplasia and eventually cancer

Barrett’s Esophagus

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9
Q

Barrett’s Esophagus

A

esophagus normally lined by nonkeratinizing squamous epithelium - can handle friction of food bolus
acid reflux from the stomach causes metaplasia to nonciliated, mucin-producing columnar cells- better able to handle stress of acid

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10
Q

Vitamin deficiency that can lead to metaplasia

A

vitamin A
necessary for differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye
vit A deficiency can cause goblet cell/columnar epithelium of conjunctiva to undergo metaplasia into keratinizing squamous epithelium
dry eyes (xerophtalmia) can lead to destruction of the cornea and blindness

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11
Q

What condition occurs in response to healing in trauma that causes mesenschymal tissues to undergo metaplasia

A

myositis ossificans

connective tissue within muscle changes to bone during healing after trauma

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12
Q

Dysplasia

A

disordered cellular growth

most often refers to proliferation of precancerous cells

often arises from longstanding pathologic hyperplasia or metaplasia

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13
Q

Aplasia

A

failure of cell production during embryogenesis

ex. unilateral renal agenesis

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14
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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15
Q

Common causes of cell injury

A 
inflammation
nutritional deficiency or excess
hypoxia
trauma
genetic mutations
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16
Q

hypoxia

A

low oxygen delivery to tissue
oxygen is the final electron acceptor in the electron transport chain of oxidative phos
decreased oxygen impairs ox phos, resulting in decreased ATP production
lack of ATP leads to cell injury

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17
Q

causes of hypoxia

A

ischemia
hypoxemia
decreased oxygen carrying capacity of blood

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18
Q

ischemia

A

decreased blood flow through an organ

decreased arterial perfusion - atherosclerosis
decreased venous drainage - Budd-Chiari syndrome
Shock - generalized hypotension -> poor tissue perfusion

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19
Q

hypoxemia

A

low partial pressure of oxygen in the blood - PaO2 decreased PaO2
hypoventilation - increased PaCO2 -> decreased PaO2
diffusion defect - PaO2 not able to push as much O2 into the blood due to a thicker diffusion barrier (interstitial pulmonary fibrosis)
V/Q mismatch - blood bypasses oxygenated lung or oxygenated air cannot reach blood

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20
Q

decreased O2 carrying capacity

A

hemoglobin loss or dysfunction

anemia - normal PaO2
carbon monoxide poisoning - PaO2 normal - cherry red appearance of skin, early sign is HA
Methemoglobinemia - iron in heme is oxidized to Fe3+ which cannot bind oxygen - PaO2 normal - seen in oxidant stress - cyanosis with chocolate colored blood - Tx is intravenous methylene blue which helps reduce Fe3+ back to Fe2+

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21
Q

hallmark of reversible cellular injury

A

cellular swelling - cytosol swelling results in loss of microvilli and membrane blebbing
swelling of the rough ER results in dissociation of ribosomes and decreased protein synth

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22
Q

Hallmark of irreversible cellular injury

A

membrane damage - results in cytosolic enzymes leaking into the serum (cardiac troponin), additional calcium entering cell

End result is cell death

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23
Q

Mitochondrial Membrane Damage

A

results in loss of the electron transport chain (inner mito membrane), cytochrome c leaking into cytosol (activates apoptosis)

24
Q

lysosomal membrane damage

A

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

25
Mechanisms of cell death
necrosis and apoptosis
26
morphologic hallmark of cell death
loss of nucleus occurs via nuclear condensation (pyknosis) fragmentation(karyorrhexis) and dissolution (karyolysis)
27
Necrosis
death of large groups of cells followed by acute inflammation never physiologic
28
Coagulative Necrosis
necrotic tissue that remains firm organ structure is preserved but nucleus disappears characteristic of ischemic infarction of any organ except the brain often wedge-shaped and pale red infarction arises if blood re-enters loosely organized tissue
29
Liquefactive Necrosis
necrotic tissue that becomes liquefied enzymatic lysis of cells and protein results in liquefaction characteristic of - brain infarction - proteolytic enzymes from microglial cells liquefy the brain abscess - proteoplytic enzyes from neutrophils liquefy tissue pancreatitis - proteolytic enzymes from pancreas liquefy parenchyma
30
Gangrenous Necrosis
coagulative necrosis that resembles mummified tissue - dry gangrene characteristic of ischemia of lower limb and GI tract if superimposed infection of dead tissues occurs then liquefactive necrosis ensues - wet gangrene
31
Caseous Necrosis
soft and friable necrotic tissue with cottage cheese-like appearance combination of coag and liquefactive necrosis characteristic of granulomatous inflammation due to tuberculous or fungal infection
32
Fat Necrosis
necrotic adipose tissue with chalky-white appearance due to deposition of calcium characteristic of trauma to fat and pancreatitis-mediated damage of peripancreatic fat FA released by trauma or lipase join with calcium via a saponification
33
Saponification
dystrophic calcification in which calcium deposits on dead tissues necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate
34
Metasstatic calcification
high serum calcium or phosphate levels lead to calcium deposition in normal tissues
35
Fibrinoid Necrosis
necrotic damage to blood vessel wall leaking proteins into vessel wall results in bright pink staining of the wall microscopically characteristic of malignant hypertension and vasculitis
36
Apoptosis
programmed cell death ATP (energy) dependent endometrial shedding during menstrual cycle removal of cells during embryogenesis CD8+ T cell-mediated killing of virally infected cells
37
Morphology of Apoptosis
dying cell shrinks - cytoplasm becomes more eosinophilic nucleus condenses and fragments apoptotic bodies fall from the cell and are removed by macrophages - not followed by inflammation
38
Apoptosis is mediated by
caspases - which activate proteases and endonucleases proteases break down cytoskeleton endonucleases break down DNA
39
Caspases are activated by
intrinsic and extrinsic pathway
40
intrinsic mitochondrial pathway
cell injury - DNA damage - or decreased hormonal stimulation leads to inactivation of Bcl2 lack of Bcl2 allow cytochrome c to leak from the inner mitochondrial matrix into the cytoplasm and activate caspases
41
extrinsic receptor - ligand pathway
FAS ligand binds FAS death receptor (CD95) on target cell - activates caspases TNF binds TNF receptor on target cell - activates caspases
42
Cytotoxic CD8+ T cell -mediated apoptotic pathway
perforins secreted by CD8+T cell create pores in membrane of target cell granzyme from CD8+ T cell enters pores and activates caspases CD8+ T-cell killing of virally infected cells is an example
43
pathologic generation of free radicals occurs with
ionizing radiation - water hydrolyzed to hydroxyl free radical inflammation - NADPH oxidase generates superoxide ions during oxygen dependent killing by neutrophils metals - copper and iron drugs and chemicals - p450 system of liver metabolizes drugs, generating free radicals
44
free radicals cause cellular injury via
peroxidation of lipids and oxidation of DNA and proteins | DNA damage is implicated in aging and oncogenesis
45
Elimination of Free radicals
antioxidants - glutathione and vit A, C, E Enxymes - superoxide dismutase - mito - glutathione peroxidase - mito - catalase - peroxisomes Metal Carrier Protiens - transferrin and ceruloplasmin
46
Carbon Tetrachloride - CCl4
organic solvent used in dry cleaning converted to CCl3 free radical by p450 system of hepatocytes causes cell injury with swelling of RER -> ribosomes detach, impairing protein synthesis decreased apolipoproteins lead to fatty change in the liver
47
reperfusion injury
return of blood to ischemic tissue results in production of O2 derived free radicals which further damage tissue leads to rise in cardiac enzymes (troponin) after reperfusion of infarcted myocardial tissue
48
amyloid
misfolded protein that deposits in the extracellular space thereby damaging tissues multiple proteins can be deposited as amyloid - Beta pleated sheets - congo red staining and apple - green birefringence
49
Primary systemic amyloidosis
systemic deposition of AL amyloid - derived from immunoglobulin light chain associated with plasma cell dyscrasias (mult. myeloma)
50
Secondary systemic amyloidosis
systemic deposition of AA amyloid - derived form serum amyloid-associated protein (SAA) - acute phase reactant that is increased in chronic inflammatory states - malignancy and familial Mediterranean fever
51
Familial Mediterranean Fever
AR episodes of fever and acute serosal inflammation high SAA during attacks deposits as AA amyloid in tissues
52
Localized Amyloidosis
senile cardiac amyloidosis - non-mutated serum transthyretin deposits in the heart - usually asymptomatic
53
Familial amyloid cardiomyopathy
mutated serum transthyretin deposits in the heart leading to restrictive cardiomyopathy
54
Amylin (derived from insulin) deposits where
islets of pancreas in DM
55
Alzheimer Amyloid are derived from
Beta amyloid precursor protein -> AlphBeta amyloid -> deposits in brainformin amyloid plaques gene for APP is on chromosome 21
56
Dialysis associated amyloidosis
Beta2 - macroglobulin deposits in joints
57
medullary carcinoma of the thyroid
calcitonin (produced by tumor cells) deposits within the tumor (tumor cells in an amyloid background)

neuro (18 decks)

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