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pharmacology Flashcards

1
Q

c1 esterase inhibitor does what?

A

inhibit kalikrein, which has two functions (convert kininogen to bradykinin and convert plasminogen to plasmin)

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2
Q

what cytokines mediate angiodemia?

A

bradykinin, c3a, c5a

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3
Q

zidovudine moa

A

NRTI, binds to reverse transcriptase and incorporated into viral genome as a thymidine analog with an azido group in place of a 3’ OH group, impairing elongation

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4
Q

difference between NRTI and NNRTI

A

former requires phosphorylatoin by host cell kinases

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5
Q

anthracycline (doxorubicin) moa

A

intercalate between bases, causing defective base pairing and splitting of the DNA strands

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6
Q

foscarnet moa

A

pyrophosphate analog that does not require intracellular activation, directly inhbitis both DNA polymerase in HSV and reverse transcriptase in HIV; rx for AIDS pt with acyclovir-resistant herpesvirus or ganciclovir-resistant CMV virus

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7
Q

isoniazid SE

A

directly hepatotoxic in 10-20 percent, transient increases in liver enzymes, fever, GI sx (most itmes, return to baseline with continued treatment); can also cause peripheral neuropathy if pyridoxine is not administered

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8
Q

penicillin moa

A

structural analog to D-ala-D-ala that inhibit transpeptidaseby binding to its active site

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9
Q

sulfonamide moa

A

antimetabolites that compete with PABA for incorporation into FA

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10
Q

trimethoprime moa

A

inhibit dihydrofolate reductase

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11
Q

how long does it take continuous infusion of a drug metabolized by first-order kinetics to reach steady state concentration?

A

4 to 5 half lives

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12
Q

oral metronidazole + ETOH leads to

A

disulfiram-like effects (flushing, HA, N/V, ab cramps)

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13
Q

BZD should not be used with

A

ETOH, barbs, neuroleptics, first generation antihistamines (chlorpheniramine, diphenhydramine, promethazine, hydroxyzine - all act on central/peripheral H1 receptors)

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14
Q

chlamydia interesting fact

A

lack peptidoglycan within cell wall; thus, not effectively treated by penicillin or cephalosporin

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15
Q

enterococci achieve aminoglycoside resistance via what mechanism?

A

aminoglycoside-modifying enzymes that transfer different chemical groups (acetyl, adenyl , phosphate groups) to antibiotic molecule outside the bacterium, impairing its ability to bind to ribosomes; plasmid transferred

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16
Q

tetracycline mechanism of resistance

A
  1. synthesis of protein that allows ribosome to translate despite drug; 2. decreasing intracellular concentrtions by increased efflux or decreased influx
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17
Q

fluoroquinolone mechanism of resistance

A

mutations in DNA gyrase or topoisomerase genes

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18
Q

AD therapies (3)

A
  1. cholinesterase inhibitor (donepezil), 2. antioxidants (vita E), and 3. NMDA receptor antagonist (memantine)
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19
Q

tachyphylaxis: 2 examples

A

nitroglycerine and alpha-adrenergic agonists (phenylephrine, xylometazoline, oxymetazoline)

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20
Q

rebound rhinorrhea

A

alpha-adrenergic agonists vasoconstrict nasal mucosa, causing decongestation; however, afte ra couple days, lose their effect 2/2 decreased production of endogenous NE that results in relative vasodilation and subsequent edema and congestion

21
Q

low Vd (3-5 L) drug characteristics

A

large molecular weight, bound extensively to plasma proteins, hydrophilic (plasma)

22
Q

medium Vd (14-16 L) drug characteristics

A

small molecular weight (pass through endothelial junctions), but hydrophlic (plasma plus interstitial volume)

23
Q

large Vd (41 L) drug characteristics

A

small molecular weight and hydrophobic (plasma, interstitial, intracellular volume)

24
Q

carbamazepine indications and SE

A

simple, complex patial seizures, GTC seizures, mood stabilizer, trigeminal neuralgia; blocks voltage-gated Na channels in cortical neurons; BM suppression, hepatotoxic, SIADH

25
Q

ethosuximide moa, rx

A

blocks T-type Ca channels, decreases Ca current in thalamic neurons; absence seizures

26
Q

beta blocker moa

A

inhibiting the NT-receptor interaction at the synapses

27
Q

bradykinin is

A

potent vasodilator

28
Q

myoclonic seizures pw, rx

A

repeitive seizures that are brief, symmetric, muscular contractions with loss of body ton, in the morning, precipitated by stress and sleep deprivation; valproic acid (affecting GABA/NMDA receptors, NA/K channels)

29
Q

myoclonic seizure vs tourette syndrome

A

tourette: nonrhythmic, suppressible, and preceded by urge (rx with haloperidol)

30
Q

restless leg syndrome more common in, rx

A

iron deficiency, CKD, DM; dopamine agonist

31
Q

malaria caused by p. vivax and p. ovale moa, rx

A

latent hepatic infection (hypnozoites) with lysis of infected hepatocytes releasing merozoites into bloodstream that infect erythrocytes (trophozoites) and cause lysis (relapsing fevers, sweating); chloroquine eliminates plasmodia from the bloodstream, primaquine must be used to eradicate infection in liver

32
Q

why not use NE instead of Epi in anaphylactic reaction?

A

NE has predominantly alpha-1 adrenergic effect that can cause intense vasoconstriction, but limit cardiac output; and no effect on beta-2 receptor so no bronchodilator action

33
Q

why epi in anaphylxis

A

alpha-1 vasoconstriction, beta-1 increase in cardiac contractility, and beta-2 bronchodilatoin

34
Q

dobutamine moa

A

primary beta-1 adrenergic action that can cause increased cardiac output without its other effects

35
Q

anticholinergic SE

A

mainly muscarinic: inhibition of eccrine sweat glands can result in fever and compensatory cutaneous vasodilation and inhibition of pupillary constrictor causes pupillary dilation

36
Q

HIV meds: protease inhibitor (indinavir) SE

A
  1. lipodysrophy (increased deposition of fat on back/abdomen); 2. hyperglycemia; 3. inhibition of P-450
37
Q

HIV pt on protease inhibitor needs mycobacteria treatment: rifampin or rifabutin

A

rifabutin, rifampin is a 450 inducer that decreases amount of the protease inhibitor

38
Q

liver failure after general anesthesia

A

halogenated inhalation-related hepatitis (2 days to 4 weeks); light microscopy: widespread centrilobular hepatic necrosis, high mortality rate

39
Q

CMV retinitis occurs when, rx?

A

AIDS pt <50 count; ganciclovir

40
Q

anticholinergic toxocity

A

dry mouth, dilated pupils, flushed skin, fever, confusion

41
Q

acyclovir undergoes what in virus-infectec cell?

A

monophosphorylatoin by viral thymidine kinase (rate-limiting step); EBV/CMV have a different thymidine kinase so it cannot convert acyclovir to its active triphosphate form

42
Q

high lipophilicity allows what?

A

entry into hepatocytes and CNS

43
Q

hepatic clearance: drug characteristics

A

high lipophilicity and high volume of distribution

44
Q

enterobius vermicularis rx

A

albendazole, with pyrantel pamoate as an alternative in pregnant patients

45
Q

efficacy

A

intrinsic ability of drug to elicit an effect (maximum ceiling of activity with respect to a particular pharmacodynamic end point)

46
Q

potency

A

dose of drug needed to produce a given effect, primarily affected by the affininty of the drug for its receptor and the amount of drug that is able to reach the target tissue, measured by ED50 (lower = more potent)

47
Q

First-generation AP SE: low potency (chlorpromazine, thioridazine) vs high potency (haloperidol, fluphenazine)

A

low potency: sedation,anticholinergic, and orthostatic hypotension (alpha-1-blockade); high potency: EPS/neurologic

48
Q

competitive antagonism

A

reversible (ionic) and irreversible (covalent)

49
Q

isoniazid metabolism moa

A

acetylation (slow vs fast acetylators); slow aceylators are at increased risk for SE

step 1 (17 decks)

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