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Goljan Lecture Notes > Chapter 2: Cellular Reaction to Injury > Flashcards

Chapter 2: Cellular Reaction to Injury Flashcards

1
Q

MCC of ischemia

A

thrombus in muscular artery

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2
Q

2nd MCC of tissue hypoxia

A

hypoxemia

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3
Q

Ventilation defects

A

Respiratory distress syndrome

Creates an intrapulmonary shunt

If give 100% O2, pO2 did not increase –> SHUNT

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4
Q

Perfusion defects

A

PE

Increase in dead space

If give 100% O2, pO2 did GO UP

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5
Q

3 things to remember for CO

A
  1. decrease in O2 saturation
  2. left shift in O2 sat. curve
  3. blocks cytochrome oxidase
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6
Q

The 3 C’s for cytochrome oxidase

A
  1. cytochrome oxidase
  2. cyanide (blocks cyt oxidase)
  3. CO (blocks cyt oxidase)
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7
Q

Left shift in Hb curve

A

CO, methemoglobin, HbF, decrease in 2, 3- BPG, alklalosis

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8
Q

Uncoupling agents

A

Dinitrylphenol (chemical for preserving wood)
Alcohol
Salicylates

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9
Q

Additional risk/sign of uncoupling agent

A

hyperthermia

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10
Q

What happens when there is respiratory acidosis?

A

Hb stays same
O2 saturation decreased
partial pressure of O2 decreased (d/t pO2 decreased)

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11
Q

What happens when there is anemia?

A

only Hb is affected

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12
Q

What happens when there is CO/methemoglobin?

A

Hb normal
O2 sat decreased
pO2 normal

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13
Q

Tx for CO poisoning

A

100% O2

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14
Q

Tx for methemoglobin

A

IV methaline blue or vitamin C

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15
Q

MC cancer from radiation

A

leukemia d/t hydroxyl free radicals

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16
Q

MCC drug induced fulminant hepatitis

A

Tylenol OD

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17
Q

Coagulation necrosis results from

A

Sudden cutoff of blood supply to an organ (ischemia)

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18
Q

Gangrenous necrosis types

A

wet and dry

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19
Q

MCC nontraumatic amputation

A

diabetes d/t enhanced atherosclerosis (esp. popliteal artery)

DRY gangrene

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20
Q

Wet gangrene complicated by…

A

infective heterolysis –> liquefactive necrosis

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21
Q

Good consistency = pale infarct

A

coagulation necrosis

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22
Q

Loose consistency of tissue

A

hemorrhagic infact

bowel, testes, ESP. lungs

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23
Q

MCC of bowel infarction

A

adhesions from previous surgery

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24
Q

2nd MCC of bowel infarction

A

small bowel trapped in indirect hernial sac

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25
Q

Liquefactive necrosis

A

think neutrophils!

occurs in the BRAIN

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26
Q

Caseous (Cheesy consistency) necrosis

A

mycobacterial infection or fungal infection ONLY

lipids in cell wall –> cheesy appearance

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27
Q

enzymatic fat necrosis

A

unique to pancreas!

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28
Q

traumatic fat necrosis

A

usually breast tissue or adipose tissue
NOT cancer (cancer is usually painless while this is usually painful)
Can result in calcifications

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29
Q

Fibrinoid necrosis is the result of what kind of damage?

A

Immunologic damage

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30
Q

What are examples of fibrinoid necrosis?

A

Henoch-Scholein purpura
Rheumatic fever
Rheumatoid arthritis

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31
Q

MCC fatty change in liver?

A

alcohol

32
Q

Zone in liver affected by yellow fever

A

Zone 2

33
Q

Zone in liver affected by acetaminophen OD?

A

Zone 3 (around central vein) b/c gets least amount of O2 –> cannot combat free radical injury

34
Q

2 types of metabolic acidosis seen in alcoholics

A
  1. lactic acidosis (b/c driving pyruvate into lactate)

2. increased synthesis of ketone bodies b/c excess acetyl CoA

35
Q

What is the main ketoacid?

A

beta hydroxybutyric acid

36
Q

Why does alcohol produce fatty change?

A

In glycolysis, around run 4, get intermediates dihydroxyacetone phosphate (NADH rxn) and is forced to come glycerol 3-phosphate –> makes TGs

*basically increased VLDL

37
Q

What is the mechanism for Kwashiorkor Syndrome?

A

Decreased protein intake –> cannot make apolipoproteins to put around VLDL to get it out of the liver and into the bloodstream –> accumulation of VLDL in liver –> fatty liver and protuberant belly

38
Q

Dystrophic calcification means…

A

tissue gets damaged –> abnormal calcification

39
Q

What is an example of dystrophic calcification?

A

enzymatic fat necrosis

40
Q

MCC aortic stenosis

A

bicuspid aortic valve –> hemolytic anemia

41
Q

Metastatic calcification in cases of…

A

hypercalcemia

hyperphosphatemia

42
Q

MCC hypercalcemia (outside of the hospital)

A

hyperparathyroidism

43
Q

MCC hypercalcemia (inside the hospital)

A

malignancy induced hypercalcemia

44
Q

Difference b/t dystrophic and metastatic calcification

A

Dystrophic calcification puts calcium into damaged tissue while metastatic calcification puts calcium into NORMAL tissue

45
Q

What does high levels of phosphate in blood do?

A

Drives calcium into the cells –> very bad

This is why pts with kidney failure need dialysis

46
Q

What causes spherocytosis?

A

Defect in spectrin protein –> no biconcave disc shape

47
Q

What are examples of ubiquintation?

A 
Mallory bodies (liver)
Lewy bodies (Parkinson's Dz)
neurofib tangles (Alheimers Dz and Jacob Crutzfelt)
48
Q

What are the different cell types and describe them?

A

Labile - cell division is via a stem cell
Stable - in resting, G0 phase
Permanent - can no longer get into the cell cycle, permanently differentiated

49
Q

What is the most variable stage of the cel cycle?

A

G1 phase

50
Q

Does glucagon or insulin phosphorylate or dephosphorylate?

A

Glucagon is a phosphorylator while insulin is a dephosphorylator.

51
Q

What is the key area to control in the cell cycle?

A

transition from G1 to S phase

52
Q

Rb suppressor gene is located on which chromosome?

A

chromosome 13

53
Q

What is the function of the Rb protein?

A

prevents the cell from going from the G1 to the S phase

54
Q

p53 is located on which chromosome?

A

chromosome 17

55
Q

No. 1 most important gene in cancer

A

p53

56
Q

What changes occur in the cell during the S phase?

A

Everything doubles

2N => 4N

57
Q

What occurs during G2 phase?

A

when tubular is made

58
Q

What drugs act on S phase?

A

Ergot alkaloids

Methotrexate

59
Q

What drugs act on G2 phase?

A

Etoposide

Bleomycin

60
Q

What drugs act on M phase?

A

Gresiofulvin
Paclitaxel
Vincristine and Vinblastine
Colchicine

61
Q

HIV + person with dyspnea and white out of the lung on a drug –> ends up with cyanosis. Which drug is it?

A

Dapsone

62
Q

What kind of growth alteration occurs in hydronephrosis?

A

Compression atrophy b/c of increased pressure on the cortex and medulla –> produces ischemia –> decreased blow flow and atrophy of renal tubules

63
Q

What is the mechanism of atrophy in Lou Gehrig’s disease?

A

knock off neurons to the muscle –> no stimulation –> atrophy

64
Q

What are causes of atrophy to the brain?

A

atherosclerosis (MC)

degeneration of neurons (Alzheimers Dz, related to beta amyloid protein which is toxic to neurons)

65
Q

What change in the adrenal cortex results from hypopituitarism?

A

Adrenal cortex atrophy

66
Q

What happens to the thyroid if you take too much thyroid hormone?

A

atrophy of thyroid b/c no TSH

67
Q

Definition of hypertrophy

A

Increase in SIZE, not number

68
Q

Definition of hyperplasia

A

Increase in NUMBER

69
Q

Definition of metaplasia

A

replacement of one adult cell type by another

e.g. mucosal cells replace squamous cells of lower esophagus –> Barretts esophagus (precursor to adenocarcinoma)

70
Q

Name examples of metaplasia

A
  1. mucosal cells replace squamous cells of lower esophagus –> Barretts esophagus (precursor to adenocarcinoma)
  2. Lining of mainstream of bronchus (ciliated columnar, pseudo stratified columnar –> turns into squamous)
  3. goblet cells in the stomach –> precursor to adenocarcinoma
71
Q

MCC adenocarcinoma of the stomach

A

H. pylori

72
Q

MC precursor lesion to endometrial carcinoma

A

d/t unopposed estrogen

73
Q

Does prostatic hyperplasia lead to cancer?

A

NO

74
Q

What is the process of cancer formation?

A

metaplasia –> dysplasia –> cancer

75
Q

What two parasites cause cancer and how?

A
  1. clonesis sinesis –> cholangiocarcinoma (Chinese liver fluke)
  2. shistosoma hematoabia –> bladder cancer by causing the transitional epithelium to undergo squamous metaplasia
76
Q

What is the precursor lesion for squamous cell carcinoma?

A

actinic keratosis

Goljan Lecture Notes (4 decks)

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