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First Aid - USMLE Step 1 > Pathology - Cellular Injury > Flashcards

Pathology - Cellular Injury Flashcards

1
Q

cellular adaptations

A

*reversible changes that can be physiologic (eg. uterine enlargement during pregnancy) or pathologic (eg. myocardial hypertrophy secondary to systemic HTN).
*if stress is excessive or persistent, adaptations can progress to cellular injury (eg. significant LV hypertrophy → myocardial injury → heart failure)

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2
Q

hypertrophy

A

*increased structural proteins and organelles →increase in SIZE of cells
*ex. cardiac hypertrophy

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3
Q

hyperplasia

A

*controlled proliferation of stem cells and differentiated cells → increase in NUMBER of cells
*excessive stimulation → pathologic hyperplasia, which may progress to dysplasia and cancer

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4
Q

atrophy

A

*decrease in tissue mass due to decrease in SIZE and/or NUMBER of cells
*causes include disuse, denervation, loss of blood supply, loss of hormonal stimulation, poor nutrition

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5
Q

metaplasia

A

*reprogramming of stem cells → replacement of one cell type by another that can adapt to a new stressor
*usually due to exposure to an irritant (such as gastric acid or tobacco smoke)
*may progress to dysplasia → malignant transformation with persistent insult

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6
Q

dysplasia

A

*disordered, precancerous epithelial cell growth
*characterized by:
-a loss of uniformity of cell size and shape (pleomorphism)
-loss of tissue orientation
-nuclear changes
*usually preceded by persistent metaplasia or pathologic hyperplasia

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7
Q

reversible cell injury (mechanisms)

A

*decreased ATP → decreased activity of Ca2+ and Na+/K+ ATPase pumps → cellular swelling
*ribosomal/polysomal detachment → decreased protein synthesis
*plasma membrane changes
*nuclear changes
*rapid loss of function
*myelin figures

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8
Q

irreversible cell injury (mechanisms)

A

*breakdown of plasma membrane → cytosolic enzymes leak outside of cell; influx of Ca2+ → activation of degradative enzymes
*mitochondrial damage/dysfunction → loss of electron transport chain → decreased ATP
*rupture of lysosomes → autolysis
*nuclear degradation: pyknosis (nuclear condensation) → karyorrhexis (nuclear fragmentation) → karyolysis (nuclear dissolution)
*amorphous densities/inclusions in mitochondria

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9
Q

apoptosis

A

*ATP-dependent cell death
*intrinsic, extrinsic, and perforin/granzyme B pathways →activate caspases (cytosolic proteases) → cellular breakdown

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10
Q

intrinsic (mitochondrial) pathway of apoptosis - overview

A

*involved in tissue remodeling in embryogenesis
*occurs when a regulating factor is withdrawn from a proliferating cell population and/or **after exposure to injurious stimuli

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11
Q

intrinsic (mitochondrial) pathway of apoptosis - regulation

A

*regulated by Bcl-2 family of proteins
*Bax and Bak are proapoptotic
*Bcl-2 and Bcl-xL are antiapoptotic

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12
Q

intrinsic (mitochondrial) pathway of apoptosis - regulation: Bax and Bak proteins

A

*PROAPOPTOTIC
*form pores in the mitochondrial membrane → release of cytochrome C from inner mitochondrial membrane into the cytoplasm → activation of caspases

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13
Q

intrinsic (mitochondrial) pathway of apoptosis - regulation: Bcl-2 and Bcl-xL proteins

A

*ANTIAPOPTOTIC
*Bcl-2 keeps the mitochondrial membrane impermeable, preventing cytochrome C release
*Bcl-2 overexpression (eg. follicular lymphoma t[14;18]) → caspase activation → tumorigenesis

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14
Q

extrinsic (death receptor) pathway of apoptosis

A

*ligand receptor interactions: FasL binding to Fas (CD95) or TNF-alpha binding to its receptor
*Fas-FasL interaction is necessary in thymic medullary negative selection

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15
Q

perforin/granzyme B pathway of apoptosis

A

*release of granules containing perforin and granzyme B by immune cells (cytotoxic T cells and natural killer cells) → perforin forms a pore for granzyme B to enter the target cell

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16
Q

necrosis - overview

A

*exogenous injury → plasma membrane damage → intracellular components leak → cell undergoes enzymatic degradation and protein denaturation → local inflammatory reaction

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17
Q

coagulative necrosis - seen in

A

*ischemia/infarcts to most tissues (EXCEPT brain)

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18
Q

coagulative necrosis - due to

A

*ischemia or infarction
*injury denatures enzymes → proteolysis blocked

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19
Q

coagulative necrosis - histology

A

*preserved cellular architecture (cell outlines seen), but cell nuclei disappear
*increased cytoplasmic binding of eosin stain (→ increased eosinophilia; red/pink color)

20
Q

liquefactive necrosis - seen in

A

*bacterial abscesses
*CNS infarcts

21
Q

liquefactive necrosis - due to

A

*neutrophils release lysosomal enzymes that digest the tissue

22
Q

liquefactive necrosis - histology

A

*early: cellular debris and macrophages
*late: cystic spaces and cavitation (CNS)
*neutrophils and cell debris seen with bacterial infecion

23
Q

caseous necrosis - seen in

A

*tuberculosis (TB)
*systemic fungi (eg. Histoplasma capsulatum)
*Nocardia

24
Q

caseous necrosis - due to

A

*macrophages wall of the infection microorganism → granular debris

25
Q

caseous necrosis - histology

A

*fragmented cells and debris surrounded by lymphocytes and macrophages (granuloma)
*cheese-like gross appearance

26
Q

fat necrosis - seen in

A

*enzymatic, acute pancreatitis (saponification of pancreatic fat)
*nonenzymatic trauma (eg. injury to breast tissue)

27
Q

fat necrosis - due to

A

*damaged pancreatic cells release lipase, which breaks down triglycerides
*liberated fatty acids bind calcium → saponification (chalky-white appearance)

28
Q

fat necrosis - histology

A

*outlines of dead fat cells without peripheral nuclei
*saponification of fat (combined with Ca2+) appears dark blue on H&E stain

29
Q

fibrinoid necrosis - seen in

A

*immune vascular reactions (eg. polyarteritis nodosa)
*nonimmune vascular reactions (eg. hypertensive emergency, preeclampsia)

30
Q

fibrinoid necrosis - due to

A

*immune complex deposition (type III hypersensitivity reaction) and/or plasma protein (eg. fibrin) leakage from damaged vessel

31
Q

fibrinoid necrosis - histology

A

*vessel walls contain eosinophilic layer of proteinaceous material

32
Q

gangrenous necrosis - seen in

A

*distal extremity and GI tract, after chronic ischemia

33
Q

gangrenous necrosis - due to

A

*dry = due to ischemia
*wet = due to superinfection

34
Q

gangrenous necrosis - histology

A

*dry: coagulative
*wet: liquefactive superimposed on coagulative

35
Q

ischemia - overview

A

*inadequate blood supply to meet demand
*mechanisms include:
-decreased arterial perfusion
-decreased venous drainage
-shock

36
Q

regions most vulnerable to hypoxia/ischemia and subsequent infarction

A
  1. brain (ACA, MCA, PCA boundary areas)
  2. heart (subendocardium of LB)
  3. kidney (straight segment of proximal tubule, thick ascending limb)
  4. liver (area around central vein / zone III)
  5. colon (splenic flexure, rectosigmoid junction)
37
Q

types of infarct: red infarct

A

*occurs in venous occlusion and tissues with multiple blood supplies (eg. liver, lung, intestine, testes) and with reperfusion
*reperfusion injury is due to free radicals

38
Q

types of infarct: pale infarct

A

*occurs in solid organs with a single (end-arterial) blood supply (eg. heart, kidney)

39
Q

free radical injury - overview

A

*free radicals damage cells via membrane lipid peroxidation, protein modification, DNA breakage
*initiated via radiation exposure, metabolism of drugs, redox rxns, nitric oxide, transition metals, WBC oxidative bust

40
Q

elimination of free radicals

A

*free radicals can be eliminated by scavenging enzymes (catalase, superoxide dismutase, glutathione peroxidase), spontaneous decay, antioxidants (vitamins A, C, E), and certain metal carrier proteins

41
Q

ionizing radiation therapy

A

*ionizing radiation causes DNA and cellular damage both directly and indirectly through production of free radicals
*stem cells of rapidly regenerating tissues are the most susceptible to radiation injury

42
Q

amyloidosis - overview

A

*extracellular deposition of protein in abnormal fibrillar form (beta-pleated sheet configuration) → cell injury and apoptosis
*manifestations vary depending on involved organ:
-renal = nephrotic syndrome
-cardiac = restrictive cardiomyopathy
-GI = hepatosplenomegaly
-neuro = peripheral neuropathy

43
Q

amyloidosis - histology

A

*amyloid deposits are visualized by:
-Congo red stain (red/orange on nonpolarized light)
-apple-green birefringence on polarized light
-H&E stain (amorphous pink)

44
Q

AL amyloidosis

A

*fibril protein = AL (from Ig Light chains)
*seen in plasma cell dyscrasias (eg. multiple myeloma)

45
Q

AA amyloidosis

A

*fibril protein = AA (serum Amyloid A)
*seen in chronic inflammatory conditions (eg. rheumatoid arthritis, IBD, familial Mediterranean fever, protracted infection)

46
Q

AF amyloidosis

A

*fibril protein = transthyretin (TTR)
1. sporadic (wild-type TTR) - slowly progressive, associated with aging; mainly affects the heart
2. hereditary (mutated TTR) - familial amyloid polyneruopathy and/or cardiomyopathy

First Aid - USMLE Step 1 (6 decks)

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