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MM Pharmacology > Pharmacology Synopses 3 > Flashcards

Pharmacology Synopses 3 Flashcards

1
Q

can’t make hemoglobin chain, anemia, kidney makes excess EPO

A

iron overload

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2
Q

causes hematopoiesis in liver, skull and spleen, requires chelating

A

excess EPO

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3
Q

effective at binding Fe, but short half-life, requires pump

A

deferoxamine

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4
Q

genetic disease that increases Cu, causing abd pain, vomiting, convulsions, diarrhea

A

Wilson’s, treat with penicillamine

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5
Q

Mad hatter (paranoia, renal tox), Methyl, Minimata disease

A

inorganic mercury

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6
Q

what causes rebound after lead chelating?

A

lead stored in bone

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7
Q

most toxic arsenic metabolite

A

methylarsonous

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8
Q

universal methylator, needs folate to function

A

SAM

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9
Q

less toxic arsenic, renallly excreted

A

DMA

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10
Q

more folate means more methylation, means

A

more renal elimination, less blood arsenic

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11
Q

arsonous is ____, arsonic is ____

A

poisonous, picnic

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12
Q

causes skin lesions, blackfoot

A

arsenic toxicity

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13
Q

can lead penetrate blood-brain barrier?

A

yes

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14
Q

bioavailability of ingested lead

A

10.00%

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15
Q

increases Pb bioavailability by upregulating nonselective divalent metal transporter DMT

A

iron deficiency

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16
Q

toxic effects: encephalopathy, seizures, learning disabilities, chronic kidney disease

A

lead

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17
Q

organic source of Hg

A

Top-level predatory fish

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18
Q

Can Hg levels in mother effect fetus?

A

yes

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19
Q

asymptomatic mothers, physically deformed/mentally handicapped children, extremity sensory disturbance, hearing impairment, vision

A

methyl mercury (fetal transmission)

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20
Q

methyl mercury stays in

A

hair

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21
Q

found in drinking water, non-toxic version in fish

A

arsenic

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22
Q

heavy metal that causes cancers, stroke, neuropathy, MI

A

arsenic

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23
Q

lessened by selenium and folate in diet

A

arsenic toxicity

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24
Q

20 year epigenetics due to fetal transmission

A

arsenic toxicity

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25
Q

two null alleles, no enzyme for metabolizing omeprazole, a pump inhibitor. Less drug required to treat ulcers

A

CYP2C1923

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26
Q

CYP2C1923 occurs in 13-20% of

A

Asians

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27
Q

more than 2 alleles, increased metabolic activity requires higher doses of some drugs

A

CYP2D6*2xN

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28
Q

CYP2D6*2xN occurs in 30% of

A

Ethiopians/Saudis

29
Q

deletion that effects nicotine metabolism

A

CYP2A6del

30
Q

CYP2A6del occurs in 15% of

A

Asians

31
Q

Warfarin, Atomoxitine, 6MP/azathioprine, Tamoxifen, Abacavir

A

genetic testing suggested

32
Q

magnitude and effect of DDI is greater in

A

extensive and ultrarapid metabolizers: more enzyme to inhibit

33
Q

omeprazol has ____ DDIs in Caucasians than in Asians

A

greater

34
Q

not stored, synthesized as needed

A

eicosanoids

35
Q

housekeeping, found in platelets

A

COX1

36
Q

inducible by inflammation, found in endothelial cells

A

COX2

37
Q

generated by endothelial cells, dilation, anti-platelet, GI protective

A

prostacyclin (PGI2)

38
Q

generated in platelets, causes clotting, constriction

A

thromboxane (TXA2)

39
Q

dilation, GI protection, inhibits inflammation, causes fever and pain

A

prostaglandin (PGE2)

40
Q

PGE2 binds to EP3 to

A

cause fever

41
Q

cytosolic enzymes that insert molecular oxygen into fatty acid backbone

A

lipoxygenase

42
Q

converts arachidonic acid into LTA4 to initiate synthesis of leukotrienes

A

5-lipoxygenase

43
Q

vasoconstrictors that activate neutrophils, inflammation, edema and asthma

A

leukotrienes

44
Q

found in neutrophils, causes them to stick and migrate into tissues

A

LTB4

45
Q

inhibit COX, inhibiting prostaglandins, prostacyclins, and thromboxane

A

NSAIDS

46
Q

inhibiting prostaglandins (and capillary permeability, infiltration of leukocytes)

A

Anti-inflammatory

47
Q

inhibiting PGE2 synthesis

A

Anti-pyretic

48
Q

inhibiting PGs sensation effects inside and outside of CNS

A

Analgesic

49
Q

PG inhibitition in gut prevents

A

EP3 activation, causes GI bleeding

50
Q

PG inhibition in the kidney prevents

A

normal blood flow, causes acute kidney injury

51
Q

associated with polyps and eosinophils, generation of leukotrienes, can cause anaphylaxis

A

aspirin sensitivity

52
Q

what if a patient wants analgesics and anti-platelet effects?

A

aspirin before NSAID, or aspirin + acetominophen

53
Q

rhinitis, edema, bronchial asthma, urticaria, anaphylaxis

A

histamine effects in immune response

54
Q

exocytose histamine in response to IgE, through Ca mechanism

A

mast cells and basophils

55
Q

in response to gastrin and vagal stimulation, histamine is release and

A

stimulates H+ secretion by parietal cells in the gastric epithelium

56
Q

stimulates wakefulness in the hypothalamus and pain/itch at peripheral nerve endings

A

histamine in central and peripheral neurons

57
Q

common target for antihistamines, involved in most systemic effects

A

H1

58
Q

stimulates gastric secretion from parietal cells

A

H2

59
Q

within the nervous system

A

H3

60
Q

all histamine receptors are

A

G-protein coupled

61
Q

H1 & H2 effects on vaso, BP

A

dilation, lower BP

62
Q

H1 effects on capillary permeability

A

increase, leading to edema

63
Q

H1 effects on bronchii and bronchial secretion

A

constriction and increased secretion, leading to bronchial asthma

64
Q

H1 effects on cutaneous nerve endings

A

increase itch and pain sensation

65
Q

H2 effect on parietal cells

A

stimulate H+ secretion by parietal cells

66
Q

H1 effect in hypothalamus

A

increase wakefulness

67
Q

H1 & H2 effects on HR and cardiac arrhythmias (at high concentrations)

A

increase HR and cardiac arrhythmias

68
Q

H1 receptor antagonists are actually reverse agonists because

A

they stabilize the inactive form of the receptor

69
Q

difference between first and second generation H1 antagonists

A

second can’t cross BBB, no CNS effects

MM Pharmacology (5 decks)

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