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High Yield Pathoma > Ch. 1 Growth Adaptations, Cellular Injury, and Cell Death > Flashcards

Ch. 1 Growth Adaptations, Cellular Injury, and Cell Death Flashcards

1
Q

What are 3 types of permanent tissue that cannot make new cells and only undergo hypertrophy?

A

cardiac muscle, skeletal muscle, and nerves

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2
Q

What is a prime example of physiologic hyperplasia?

A

pregnancy

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3
Q

What is a notable exception of pathologic hyperplasia that does not progress to dysplasia or cancer?

A

BPH

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4
Q

What are the two methods of cell atrophy?

A

1) ubiquitin-proteosome degradation: intermediate filaments are tagged with ubiquitin and destroyed by proteosomes
2) autophagy of cellular components

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5
Q

How is Barrett esophagus an example of metaplasia?

A

The nonkeratinized squamous epithelium of the lower esophagus is constantly exposed to acid reflux from the stomach which reprograms the squamous epithelium into nonciliated, mucin-producing columnar cells that are seen in the stomach because these deal with acid better

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6
Q

Is metaplasia reversible or irreversible?

A

REVERSIBLE!

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7
Q

What is one example of metaplasia that does not progress to dysplasia?

A

apocrine metaplasia of the breast

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8
Q

How does vitamin A deficiency result in metaplasia?

A

it is important for specialized epithelium like conjunctiva; when it is deficient, the thin squamous lining undergoes metaplasia into stratified keratinizing squamous epithlium called KERATOMALACIA

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9
Q

What is myositis ossificans?

A

Skeletal muscle is injured and heals by forming born, or “ossifies”

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10
Q

What are two processes that can lead to dysplasia?

A

1) hyperplasia, i.e. CIN

2) metaplasia, i.e. Barrett

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11
Q

What is the difference between dysplasia and carcinoma?

A

dysplasia is reversible; cancer is not

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12
Q

What is a classic example of aplasia?

A

unilateral renal agenesis

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13
Q

What is a classic example of hyoplaisia?

A

streat ovary in Turner syndrome

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14
Q

How does slow ischemia compare to acute ischemia?

A

slow ischemia: atrophy

acute ischemia: injury

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15
Q

What is the difference between hypoxia and hypoxemia?

A

hypoxia: low O2 to injury –> low ATP
hypoxemia: low partial pressure of O2 in the blood
- hypoxemia is a type of hypoxia

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16
Q

What is an example of ischemia that occurs in veins?

A

Budd-Chiari syndrome: thrombosis of hepatic v.

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17
Q

What is the most common cause of Budd-Chiari syndrome?

A

polycythemia vera: high RBCs –> increased viscosity

-lupus is also another examaple - causes hypercoagulable state

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18
Q

What is the path of O2 flow into the RBCs?

A

FiO2 –> PAO2 –> PaO2 –> SaO2

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19
Q

How does hypoxemia occur in high altitude?

A

FiO2 is decreased

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20
Q

What decreases when PAC02 increases and what are examples?

A

PAO2 decreases

-hypoventilation, diffusion defect, V/Q mismatch

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21
Q

What is an example of decreased O2-carrying capacity with dysfunction or loss of Hb? How are PaO2 and SaO2 affected?

A

Anemia: decrease in RBC mass

-PaO2 and SaO2 are normal

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22
Q

What is SaO2?

A

ability of Hb to bind O2

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23
Q

What is the classic finding in CO poisoning? How are PaO2 and SaO2 affected?

A

cherry0red appearance of skin

  • PaO2 is normal
  • SaO2 is lower (bc less O2 bound to Hb)
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24
Q

What can lead to CO poisoning?

A

smoke from fires and exhaust from cars or gas heater

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25
Q

What is an early sign of CO poisoning?

A

headache

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26
Q

What state does iron bind O2?

A

Fe2+ (Fe2+ binds O2)

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27
Q

What is the pathophysiology of methemoglobinemia? Where is it seen?

A

Iron is oxidized to Fe3+ and can’t bind O2; SaO2 is decreased
-seen in oxidant stress or in newborns

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28
Q

What is the classic finding of methemoglobinemia?

A

cyanosis with chocolate-colored blood

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29
Q

What is the Tx for methemoglobinemia

A

IV methylene blue

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30
Q

How does low ATP d/t oxidative stress disrupt key cellular functions?

A
  1. Na+-K+ pump is disrupted so Na+ builds up in the cell and water follows leading to cell swelling
  2. Ca2+ pump failure results in Ca2+ buildup in cytosol - activates enzymes
  3. Aerobic glycolysis leads to lactic acid buildup and low pH which denatures proteins and precipitates DNA
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31
Q

What is the hallmark of reversible injury?

A

cell swelling

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32
Q

What is the hallmark of irreversible injury?

A

membrane damage

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33
Q

What does cell swelling in reversible injury lead to?

A

loss of microvilli, membrane blebbing, and swelling of RER –> ribosomes will pop off and will impair protein synthesis

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34
Q

What are the key consequences of membrane damage in irreversible injury?

A
  1. plasma membrane damage: cytosolic enzymes leaking into serum (i.e. cardiac troponin) and Ca2+ leaks into the cell
  2. mitochondrial membrane damage: loss of ETC and cytochrome c leaking into cytosol –> apoptosis
  3. lysosome membrane is damged so hydrolytic enzymes leak into cytosol which are activated by high IC Ca2+
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35
Q

What question are you trying to asking when measuring troponin levels after MI?

A

If there is irreversible injury to the cell marked by enzyme leaking into the serum

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36
Q

Where is the ETC?

A

inner mitochondrial membrane?

37
Q

What is the morphologic hallmark of cell death?

A

loss of nucleus

38
Q

What are the 3 phases of cell death nucleus loss

A
  1. pyknosis - nucleus shrinks
  2. karyorrhexis - fragmentation
  3. karyloysis - dissolution
39
Q

what kind of cell death is caused by death of large group of cells followed by acute inflammation d/t neutrophils?

A

necrosis

40
Q

What kind of necrosis occurs with firm necrotic tissue that preserves the cell shape and organ structure by coagulation of cellular proteins while nucleus disappears

A

coagulative necrosis

41
Q

Where does coagulative necrosis occur?

A

ischemic infarction of any organ except the brain

42
Q

What does the infarcted area look like in coagulative necrosis and why?

A

wedge-shaped and pale d/t branch points of vessels

43
Q

When does red infarction arise?

A

when blood re-enters a loosely organized tissue (i.e. pulmonary or testicular infarction)

44
Q

How does liquefactive necrosis occur and where is it seen?

A
  • enzymatic lysis of cells and protein
    1. brain: proteolytic enzymes from microglial cells
    2. abscess: protelytic enzymes from neutrophils
    3. pancreatitis: proteolytic enzymes from pancreas
45
Q

What is coagulative nerosis that resembles mummified tissue?

A

Dry gangrene

46
Q

Where is gangrenous necrosis most commonly seen?

A

lower limb and GI tract

47
Q

What is wet gangrene?

A

liquefactive necrosis on top of gangrenous necrosis d/t superimposed infection of dead tissues

48
Q

What is characterized by soft, friable necrotic tissue with “cottage cheese-like” appearance?

A

caseous necrosis

49
Q

what two types of necrosis make up caseous necroisis?

A

coag + liquefactive

50
Q

What is fat necrosis and where is it commonly seen?

A

necrotic adipose tissue with chalky-white appearnce d/t deposition of Ca2+
-characteristic of trauma to fat (i.e. breast) and pancreatitis-mediated damage of peripancreatic fat

51
Q

What is the pathophysiology of fat necrosis

A

fatty acids released by trauma or lipase combine with Ca2+ d/t saponification which is an example of dystrophic calcification

52
Q

What is dystrophic calcification?

A

Ca2+ deposits on dead tissue: necrotic tissue acts as a nidus for calcification in the setting of normal serum Ca2+ and phosphate

53
Q

What is metastatic calcification?

A

serum Ca2+ levels are elevated throughout the body

54
Q

What is fibrinoid necrosis and when is it found?

A
  • necrotic damage to blood vessel wall with bright pink staining
  • found in malignant HTN and vasculitis
55
Q

In what special circumstance might a middle aged woman present with fibrinoid necrosis?

A

pre-eclampsia: fibrinoid necrosis of the placenta

56
Q

What are some examples of apoptosis?

A

menstruation, removal of cells during embryogenesis, CD8+ T cell-mediated killing of virally infected cells

57
Q

What is the pathophysiology of apoptosis?

A

dying cell shrinks
nucleus condenses and fragments
apoptotic bodies fall from the cell and are removed by macrophages; NO inflammation present

58
Q

What is the key mediator of apoptosis and how does it function?

A

caspases

  • activate proteases: break down cytoskeleton
  • activate endonucleases: break down DNA
59
Q

How does intrinsic mitochondrial pathway activate caspases?

A

-cellular injury, DNA damage, or hormonal damage leads to inactivation Bcl2 which allows CYTOCHROME C to leak from inner mitochondiral matrix into cytplasm and activate caspases

60
Q

How does extrinsic receptor-ligand pathway activate caspases?

A

FAS ligand binds FAS death receptor (CD95) on target cell
TNF binds TNF receptor on target cell
*both of these processes activate caspases

-This is how autoreactive T cells die via negative selection

61
Q

How does cytotoxic CD8+ T cell-mediated pathway activate caspases?

A
  • Perforins create pores in membrane of target cell
  • Granzymes enter pores and activates caspases
  • i.e. CD8+ T-cell killing of virally infected cells
62
Q

What is a free radical?

A

A chemical species with an unpaired electron in their outer orbit

63
Q

How are free radicals generated in oxidative phsophorylation?

A

O2 –> O2- –> H2O2 –> OH –> H2O

64
Q

What is the most damaging free radical?

A

hydroxyl radical (*OH)

65
Q

How does oxygen generate superoxide free radical?

A

via NADPH oxidase enzyme

66
Q

How does iron generate free radicals?

A

Via Fenton Rxn: generates *OH radicals

67
Q

What are methods of generating free radicals?

A
  • ionizing radiation
  • inflammation
  • metals (copper and iron)
  • drugs and chemicals (acetominophen and CCL4)
68
Q

How doe free radicals cause damage?

A

peroxidation of lipids and oxidation of DNA and proteins

69
Q

What are 3 ways to eliminate free radicals?

A
  • antioxidants
  • metal carrier proteins
  • enzymes
70
Q

What are the 3 main enzymes involved in free radical elimination?

A
  1. SOD: O2 –> O2-
  2. catalase: O2- –> H2O2
  3. glutathoine peroxidase: H2O2 –> *OH
71
Q

How does CCl4 cause free radical injury?

A

CCl4 –> CCl3 in CYP450 in liver –> cell injury with swelling of rER –> decrease in protein synthesis –> decreased apoplipoproteins –> fatty change in liver (fat accumulates in cells)

72
Q

How does reperfusion injury cause free radical injury?

A

blood is returned to organ with dead tissue leading to increased oxygen and free radicals that will further damage the tissue

i. e. pt has MI and enzymes increase and continue to rise once blood is returned to tissue because oxygen rises and increases free radical injury
- O2 + inflammatory tisue –> increased generation of free radicals

73
Q

What is amyloid?

A

a misfolded protein that deposits in the extracellular space –> tissues become damaged

74
Q

What are two hallmarks of amyloid?

A
  • B-pleated configuration

- Congo red stain with apple green birefringence

75
Q

Where does amyloid often deposit?

A

around blood vessels

76
Q

What is primary amyloidosis?

A

systemic deposition of AL amyloid, derived from Ig light chain associated with plasma cell dyscrasias (lead to overproduced light chains)

77
Q

What is secondary amyloidosis?

A

systemic deposition of AA amyloid dervived from SAA which is an acute phase reactant increased in chronic inflammatory state, malignancy, and Familial Mediterranean fever

78
Q

What is Familial Mediterranean fever?

A

dysfunction of neutrophils (AR) - episodes of fever and acute serosal inflammation - can mimic MI or appendicitis
-high SAA during attacks deposit as AA amyloid

79
Q

What are the classic clinical findings of systemic amyloidosis?

A
  1. nephrotic syndrome - kidney most commonly involved
  2. restrictive cardiomyopathy or arrhtyhmia
  3. tongue enlargement, malabsorption, and HSmegaly
80
Q

How do you Dx amyloidosis?

A

tissue biopsy of abdominal fat pad and rectum

81
Q

Can amyloid be removed?

A

NO

82
Q

What is loclaized amyloidosis?

A

localized in a single organ

83
Q

What is senile cardiac amyloidosis?

A

non-mutated serum transthyretin deposits in the heart, usually asymptomatic, usually in elderly

84
Q

What is familial amyloid cardiomyopathy?

A

mutated serum transthyretin deposits in the heart that leads to restrictive cardiomyopathy

85
Q

What is Type ii DM?

A

Amylin (derived from insulin) deposits in the islets of pancreas

86
Q

How does amyloidosis present in Alzheimer?

A

AB amyloid depoist in brain, forming amyloid plaques derived from B-amyloid precursor protein (APP) which is on chr. 21 (early onset AD in Down syndrome pts)

87
Q

What is dialysis associated amyloidosis?

A

B2-microglobulin (part of MHC I) deposits in joints

88
Q

What is medullary carcinoma of the thyroid?

A

calcitonin deposits within the tumor (tumor cells in an amyloid background)
*thyroid is biopsied by fine needle aspiration

High Yield Pathoma (4 decks)

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