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PLE Pathology > Cellular Responses To Stress > Flashcards

Cellular Responses To Stress Flashcards

1
Q

Hypertrophy involves growth of which cellular structure

A

Cytoskeleton, plus extra organelles

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2
Q

Hypertrophy, hyperplasia, or both

  1. Uterus
  2. Cardiac Myocytes
  3. Skeletal Muscle
  4. Nerve
A
  1. Both

2,3,4 - hypertrophy only (permanent cells no stem cell)

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3
Q

Physiologic vs pathologic hyperplasia

A

Physio - pregnancy

Pathologic - cancer precursor (except BPH)

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4
Q

Stimulus for atrophy

A

Decrease in organ stress

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5
Q

Mechanisms of atrophy

A
  1. Apoptosis - decrease cell number

2. Decrease in cell size - degradation of cytoskeleton, autophagy

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6
Q

Mechanism of degradation of cytoskeleton (name)

A

Ubiquitin-proteosome degradation
Ubiquitin - marker
Proteosome - destroyes proteins

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7
Q

TRUE OR FALSE

Metaplasia is reversible?

A

TRUE - remove driving force to return cell growth type to normal. Reprogramming of stem cells

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8
Q

TRUE OR FALSE

All metaplasia progress to cancer if left untreated

A

FALSE - exception is Apocrine Metaplasia (breast)

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9
Q

Deficiency of which vitamin can cause metaplasia

A

Vitamin A - keratomalacia

Metaplasia of conjunctiva – thickening

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10
Q

Mesenchymal tissue undergoing metaplasia

A

Myositis ossificans - production of bone in skeletal muscle

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11
Q

TRUE OR FALSE Dysplasia is reversible

A

TRUE

Carcinoma is the one which is ireeversible

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12
Q

Aplasia vs Hypoplasia

A

Aplasia - failure of development

Hypoplasia - decrease cell production, small organ

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13
Q

Classic finding of exposure to this poison is cherry red skin with headache in early exposure

A

Carbon Monoxide

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14
Q

Condition when iron is oxidized to ferric ion Fe3+, which cannot.bind O2, leading to cyanosis with chocolate colored blood

A

Methemoglobinemia

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15
Q

Cellular findings in reversible injury

A

Cellular swelling - hallmark (failure of Na K pump)

Loss of microvilli, blebbing, RER swellimg

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16
Q

Cellular features of irreversible cellular injury

A

Membrane damage (hallmark)

Plasma membrane, leak of intracellular content
Mitochondrial membrane - inefficient O2 use
Lysosome membrane

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17
Q

What substance in the mitochondria when released triggers apoptosis?

A

Cytochrome C

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18
Q

Morphologic hallmark of cell death

A

Loss of nucleus

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19
Q

Nucleus shrinks

A

Pyknosis

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20
Q

Breaking up of nucleus into small pieces

A

Karyorrhexis

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21
Q

Breaking down of nuclear fragments to basic building blocks

A

Karyolysis

22
Q

TRUE OR FALSE

Necrosis is always pathologic

A

True

23
Q

Necrosis where tissue remains firm, and cell retains shape and organ structure is preserved, but nuclei disappear

A

Coagulative Necrosis

24
Q

Ischemic infarction of organs except brain is what type of necrosis

A

Coagulative

25
Q

TRUE OR FALSE

All infarcts are pale colored

A

FALSE

Red infarction can happen (when vein is blocked but not artery.) Ex. Testis

26
Q

Necrosis with enzymatic lysis of cells

A

Liquefactive necrosis

27
Q

Three major examples of liquefactive necrosis

A

Brain infarct
Absess
Pancreatitis (of panc tissue)

28
Q

Logic behind liquefactive necrosis of brain

A

Microglial cells contain enzymes which destroy brain tissue when they die

29
Q

Necrosis resembling mummified tissue

A

Gangrenous necrosis

30
Q

What is wet gangrene

A

Gangrenous necrosis with superimposed infection, making it liquefactive

31
Q

Necrosis which is combination of coagulative and liquefactive, characteristic of granulomatous infection

A

Caseous necrosis

32
Q

Necrosis of adipose tissue with chalky white apperance from deposition of calcium. What is process of deposition

A

Fat necrosis

Saponification

33
Q

Dystrophic calcification vs metastatic calcification

A

Dystrophic - normal serum Ca, reacts with dead tissue

Metastatic -high serum Ca and PO4 3-, deposits in tissue

34
Q

Necrotic damage to blood vessel wall

A

Fibrinoid necrosis

35
Q

Three conditions associated with fibrinoid necrosis

A

Malignant hypertension
Vasculitis
Preeclampsia

36
Q

Morphological changes in apoptosis

A

Nucleus shrinks, apoptotic bodies fall off from cell, no inflammation

37
Q

Enzymes that mediate apoptosis

A

Caspases

Activate protease(cytoskeleton) and endonuclease (DNA)

38
Q

Three pathways of apoptosis

A

Intrinsic mitochondrial pathway - cell damage, dna damage, decreased hormones, cytochrome C leaks

Extrinsic receptor-ligand pathway - ligand binds to cell and activate apoptosis

Cytotoxic CD8 T cell pathway - through perforins and granzymes

39
Q

Molecule which stabilizes mitochondrial membrane. This is knocked out during apoptosis

A

Bcl2

40
Q

Most damaging free radical

A

OH.

Hydroxyl ion

41
Q

Reaction name where ion generates free radicals

A

Fenton reaction

42
Q

Mechanisms of free radical damage

A

Peroxidation of lipids

Oxidation of dna and proteins

43
Q

Mechanisms of eliminating free radicals

A

Antioxidants
Metal carrier proteins - bind metals to prevent reactions
Free radical scavenging enzymes

44
Q

Three enzymes in charge of destroying reactive oxygen species

A

Superoxide dismutase - superoxide
Catalase - peroxide
Glutathione peroxidase - hydroxyl

45
Q

Mechanism of free radical injury of carbon tetrachloride

A

Breakdown to free radical CCl3. – attack liver cells and disrupts protein synthesis

46
Q

Mechanism of reperfusion injury

A

Infarction –> cell membrane damage –> enzyme leakage,

Return of blood brings inflammatory cells and Oxygen in contact with dead tissue, and this creates free radicals and do more damage

Intracellular Ca overload, complement activation

47
Q

Misfolded proteins that deposit in extracellular space

A

Amyloid

48
Q

Stains which detect amyloid

A

Congo red

Apple green birefringence

49
Q

Primary vs secondary amyloidosis

A

Primary - systemic deposition of AL amyloid from Ig light chain
Secondary - systemic deposition of AA amyloid from SAA (which is an acute phase reactant)

50
Q

Plasma cell dyscrasia is associated with which amyloidosis

A

Primary

51
Q

Most commonly involved organ in amyloidosis and classic presentation

A

Kidney - nephrotic syndrome

PLE Pathology (10 decks)

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