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MM Pharmacology > Pharmacology Synopses 3 > Flashcards

Pharmacology Synopses 3 Flashcards

(69 cards)

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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
two null alleles, no enzyme for metabolizing omeprazole, a pump inhibitor. Less drug required to treat ulcers
CYP2C19*2*3
26
CYP2C19*2*3 occurs in 13-20% of
Asians
27
more than 2 alleles, increased metabolic activity requires higher doses of some drugs
CYP2D6*2xN
28
CYP2D6*2xN occurs in 30% of
Ethiopians/Saudis
29
deletion that effects nicotine metabolism
CYP2A6del
30
CYP2A6del occurs in 15% of
Asians
31
Warfarin, Atomoxitine, 6MP/azathioprine, Tamoxifen, Abacavir
genetic testing suggested
32
magnitude and effect of DDI is greater in
extensive and ultrarapid metabolizers: more enzyme to inhibit
33
omeprazol has ____ DDIs in Caucasians than in Asians
greater
34
not stored, synthesized as needed
eicosanoids
35
housekeeping, found in platelets
COX1
36
inducible by inflammation, found in endothelial cells
COX2
37
generated by endothelial cells, dilation, anti-platelet, GI protective
prostacyclin (PGI2)
38
generated in platelets, causes clotting, constriction
thromboxane (TXA2)
39
dilation, GI protection, inhibits inflammation, causes fever and pain
prostaglandin (PGE2)
40
PGE2 binds to EP3 to
cause fever
41
cytosolic enzymes that insert molecular oxygen into fatty acid backbone
lipoxygenase
42
converts arachidonic acid into LTA4 to initiate synthesis of leukotrienes
5-lipoxygenase
43
vasoconstrictors that activate neutrophils, inflammation, edema and asthma
leukotrienes
44
found in neutrophils, causes them to stick and migrate into tissues
LTB4
45
inhibit COX, inhibiting prostaglandins, prostacyclins, and thromboxane
NSAIDS
46
inhibiting prostaglandins (and capillary permeability, infiltration of leukocytes)
Anti-inflammatory
47
inhibiting PGE2 synthesis
Anti-pyretic
48
inhibiting PGs sensation effects inside and outside of CNS
Analgesic
49
PG inhibitition in gut prevents
EP3 activation, causes GI bleeding
50
PG inhibition in the kidney prevents
normal blood flow, causes acute kidney injury
51
associated with polyps and eosinophils, generation of leukotrienes, can cause anaphylaxis
aspirin sensitivity
52
what if a patient wants analgesics and anti-platelet effects?
aspirin before NSAID, or aspirin + acetominophen
53
rhinitis, edema, bronchial asthma, urticaria, anaphylaxis
histamine effects in immune response
54
exocytose histamine in response to IgE, through Ca mechanism
mast cells and basophils
55
in response to gastrin and vagal stimulation, histamine is release and
stimulates H+ secretion by parietal cells in the gastric epithelium
56
stimulates wakefulness in the hypothalamus and pain/itch at peripheral nerve endings
histamine in central and peripheral neurons
57
common target for antihistamines, involved in most systemic effects
H1
58
stimulates gastric secretion from parietal cells
H2
59
within the nervous system
H3
60
all histamine receptors are
G-protein coupled
61
H1 & H2 effects on vaso, BP
dilation, lower BP
62
H1 effects on capillary permeability
increase, leading to edema
63
H1 effects on bronchii and bronchial secretion
constriction and increased secretion, leading to bronchial asthma
64
H1 effects on cutaneous nerve endings
increase itch and pain sensation
65
H2 effect on parietal cells
stimulate H+ secretion by parietal cells
66
H1 effect in hypothalamus
increase wakefulness
67
H1 & H2 effects on HR and cardiac arrhythmias (at high concentrations)
increase HR and cardiac arrhythmias
68
H1 receptor antagonists are actually reverse agonists because
they stabilize the inactive form of the receptor
69
difference between first and second generation H1 antagonists
second can't cross BBB, no CNS effects

MM Pharmacology (5 decks)

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