pharmacology

Question 1

c1 esterase inhibitor does what?

Answer 1

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

Question 2

what cytokines mediate angiodemia?

Answer 2

bradykinin, c3a, c5a

Question 3

zidovudine moa

Answer 3

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

Question 4

difference between NRTI and NNRTI

Answer 4

former requires phosphorylatoin by host cell kinases

Question 5

anthracycline (doxorubicin) moa

Answer 5

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

Question 6

foscarnet moa

Answer 6

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

Question 7

isoniazid SE

Answer 7

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

Question 8

penicillin moa

Answer 8

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

Question 9

sulfonamide moa

Answer 9

antimetabolites that compete with PABA for incorporation into FA

Question 10

trimethoprime moa

Answer 10

inhibit dihydrofolate reductase

Question 11

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

Answer 11

4 to 5 half lives

Question 12

oral metronidazole + ETOH leads to

Answer 12

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

Question 13

BZD should not be used with

Answer 13

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

Question 14

chlamydia interesting fact

Answer 14

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

Question 15

enterococci achieve aminoglycoside resistance via what mechanism?

Answer 15

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

Question 16

tetracycline mechanism of resistance

Answer 16

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

Question 17

fluoroquinolone mechanism of resistance

Answer 17

mutations in DNA gyrase or topoisomerase genes

Question 18

AD therapies (3)

Answer 18

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

Question 19

tachyphylaxis: 2 examples

Answer 19

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

Question 20

rebound rhinorrhea

Answer 20

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

Question 21

low Vd (3-5 L) drug characteristics

Answer 21

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

Question 22

medium Vd (14-16 L) drug characteristics

Answer 22

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

Question 23

large Vd (41 L) drug characteristics

Answer 23

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

Question 24

carbamazepine indications and SE

Answer 24

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

Question 25

ethosuximide moa, rx

Answer 25

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

Question 26

beta blocker moa

Answer 26

inhibiting the NT-receptor interaction at the synapses

Question 27

bradykinin is

Answer 27

potent vasodilator

Question 28

myoclonic seizures pw, rx

Answer 28

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)

Question 29

myoclonic seizure vs tourette syndrome

Answer 29

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

Question 30

restless leg syndrome more common in, rx

Answer 30

iron deficiency, CKD, DM; dopamine agonist

Question 31

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

Answer 31

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

Question 32

why not use NE instead of Epi in anaphylactic reaction?

Answer 32

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

Question 33

why epi in anaphylxis

Answer 33

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

Question 34

dobutamine moa

Answer 34

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

Question 35

anticholinergic SE

Answer 35

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

Question 36

HIV meds: protease inhibitor (indinavir) SE

Answer 36

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

Question 37

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

Answer 37

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

Question 38

liver failure after general anesthesia

Answer 38

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

Question 39

CMV retinitis occurs when, rx?

Answer 39

AIDS pt <50 count; ganciclovir

Question 40

anticholinergic toxocity

Answer 40

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

Question 41

acyclovir undergoes what in virus-infectec cell?

Answer 41

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

Question 42

high lipophilicity allows what?

Answer 42

entry into hepatocytes and CNS

Question 43

hepatic clearance: drug characteristics

Answer 43

high lipophilicity and high volume of distribution

Question 44

enterobius vermicularis rx

Answer 44

albendazole, with pyrantel pamoate as an alternative in pregnant patients

Question 45

efficacy

Answer 45

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

Question 46

potency

Answer 46

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)

Question 47

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

Answer 47

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

Question 48

competitive antagonism

Answer 48

reversible (ionic) and irreversible (covalent)

Question 49

isoniazid metabolism moa

Answer 49

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