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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

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
TRUE OR FALSE | All infarcts are pale colored
FALSE Red infarction can happen (when vein is blocked but not artery.) Ex. Testis
26
Necrosis with enzymatic lysis of cells
Liquefactive necrosis
27
Three major examples of liquefactive necrosis
Brain infarct Absess Pancreatitis (of panc tissue)
28
Logic behind liquefactive necrosis of brain
Microglial cells contain enzymes which destroy brain tissue when they die
29
Necrosis resembling mummified tissue
Gangrenous necrosis
30
What is wet gangrene
Gangrenous necrosis with superimposed infection, making it liquefactive
31
Necrosis which is combination of coagulative and liquefactive, characteristic of granulomatous infection
Caseous necrosis
32
Necrosis of adipose tissue with chalky white apperance from deposition of calcium. What is process of deposition
Fat necrosis Saponification
33
Dystrophic calcification vs metastatic calcification
Dystrophic - normal serum Ca, reacts with dead tissue | Metastatic -high serum Ca and PO4 3-, deposits in tissue
34
Necrotic damage to blood vessel wall
Fibrinoid necrosis
35
Three conditions associated with fibrinoid necrosis
Malignant hypertension Vasculitis Preeclampsia
36
Morphological changes in apoptosis
Nucleus shrinks, apoptotic bodies fall off from cell, no inflammation
37
Enzymes that mediate apoptosis
Caspases Activate protease(cytoskeleton) and endonuclease (DNA)
38
Three pathways of apoptosis
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
Molecule which stabilizes mitochondrial membrane. This is knocked out during apoptosis
Bcl2
40
Most damaging free radical
OH. Hydroxyl ion
41
Reaction name where ion generates free radicals
Fenton reaction
42
Mechanisms of free radical damage
Peroxidation of lipids | Oxidation of dna and proteins
43
Mechanisms of eliminating free radicals
Antioxidants Metal carrier proteins - bind metals to prevent reactions Free radical scavenging enzymes
44
Three enzymes in charge of destroying reactive oxygen species
Superoxide dismutase - superoxide Catalase - peroxide Glutathione peroxidase - hydroxyl
45
Mechanism of free radical injury of carbon tetrachloride
Breakdown to free radical CCl3. -- attack liver cells and disrupts protein synthesis
46
Mechanism of reperfusion injury
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
Misfolded proteins that deposit in extracellular space
Amyloid
48
Stains which detect amyloid
Congo red | Apple green birefringence
49
Primary vs secondary amyloidosis
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
Plasma cell dyscrasia is associated with which amyloidosis
Primary
51
Most commonly involved organ in amyloidosis and classic presentation
Kidney - nephrotic syndrome

PLE Pathology (10 decks)

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