pharmacology Flashcards
c1 esterase inhibitor does what?
inhibit kalikrein, which has two functions (convert kininogen to bradykinin and convert plasminogen to plasmin)
what cytokines mediate angiodemia?
bradykinin, c3a, c5a
zidovudine moa
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
difference between NRTI and NNRTI
former requires phosphorylatoin by host cell kinases
anthracycline (doxorubicin) moa
intercalate between bases, causing defective base pairing and splitting of the DNA strands
foscarnet moa
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
isoniazid SE
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
penicillin moa
structural analog to D-ala-D-ala that inhibit transpeptidaseby binding to its active site
sulfonamide moa
antimetabolites that compete with PABA for incorporation into FA
trimethoprime moa
inhibit dihydrofolate reductase
how long does it take continuous infusion of a drug metabolized by first-order kinetics to reach steady state concentration?
4 to 5 half lives
oral metronidazole + ETOH leads to
disulfiram-like effects (flushing, HA, N/V, ab cramps)
BZD should not be used with
ETOH, barbs, neuroleptics, first generation antihistamines (chlorpheniramine, diphenhydramine, promethazine, hydroxyzine - all act on central/peripheral H1 receptors)
chlamydia interesting fact
lack peptidoglycan within cell wall; thus, not effectively treated by penicillin or cephalosporin
enterococci achieve aminoglycoside resistance via what mechanism?
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
tetracycline mechanism of resistance
- synthesis of protein that allows ribosome to translate despite drug; 2. decreasing intracellular concentrtions by increased efflux or decreased influx
fluoroquinolone mechanism of resistance
mutations in DNA gyrase or topoisomerase genes
AD therapies (3)
- cholinesterase inhibitor (donepezil), 2. antioxidants (vita E), and 3. NMDA receptor antagonist (memantine)
tachyphylaxis: 2 examples
nitroglycerine and alpha-adrenergic agonists (phenylephrine, xylometazoline, oxymetazoline)
rebound rhinorrhea
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
low Vd (3-5 L) drug characteristics
large molecular weight, bound extensively to plasma proteins, hydrophilic (plasma)
medium Vd (14-16 L) drug characteristics
small molecular weight (pass through endothelial junctions), but hydrophlic (plasma plus interstitial volume)
large Vd (41 L) drug characteristics
small molecular weight and hydrophobic (plasma, interstitial, intracellular volume)
carbamazepine indications and SE
simple, complex patial seizures, GTC seizures, mood stabilizer, trigeminal neuralgia; blocks voltage-gated Na channels in cortical neurons; BM suppression, hepatotoxic, SIADH
ethosuximide moa, rx
blocks T-type Ca channels, decreases Ca current in thalamic neurons; absence seizures
beta blocker moa
inhibiting the NT-receptor interaction at the synapses
bradykinin is
potent vasodilator
myoclonic seizures pw, rx
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)
myoclonic seizure vs tourette syndrome
tourette: nonrhythmic, suppressible, and preceded by urge (rx with haloperidol)
restless leg syndrome more common in, rx
iron deficiency, CKD, DM; dopamine agonist
malaria caused by p. vivax and p. ovale moa, rx
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
why not use NE instead of Epi in anaphylactic reaction?
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
why epi in anaphylxis
alpha-1 vasoconstriction, beta-1 increase in cardiac contractility, and beta-2 bronchodilatoin
dobutamine moa
primary beta-1 adrenergic action that can cause increased cardiac output without its other effects
anticholinergic SE
mainly muscarinic: inhibition of eccrine sweat glands can result in fever and compensatory cutaneous vasodilation and inhibition of pupillary constrictor causes pupillary dilation
HIV meds: protease inhibitor (indinavir) SE
- lipodysrophy (increased deposition of fat on back/abdomen); 2. hyperglycemia; 3. inhibition of P-450
HIV pt on protease inhibitor needs mycobacteria treatment: rifampin or rifabutin
rifabutin, rifampin is a 450 inducer that decreases amount of the protease inhibitor
liver failure after general anesthesia
halogenated inhalation-related hepatitis (2 days to 4 weeks); light microscopy: widespread centrilobular hepatic necrosis, high mortality rate
CMV retinitis occurs when, rx?
AIDS pt <50 count; ganciclovir
anticholinergic toxocity
dry mouth, dilated pupils, flushed skin, fever, confusion
acyclovir undergoes what in virus-infectec cell?
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
high lipophilicity allows what?
entry into hepatocytes and CNS
hepatic clearance: drug characteristics
high lipophilicity and high volume of distribution
enterobius vermicularis rx
albendazole, with pyrantel pamoate as an alternative in pregnant patients
efficacy
intrinsic ability of drug to elicit an effect (maximum ceiling of activity with respect to a particular pharmacodynamic end point)
potency
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)
First-generation AP SE: low potency (chlorpromazine, thioridazine) vs high potency (haloperidol, fluphenazine)
low potency: sedation,anticholinergic, and orthostatic hypotension (alpha-1-blockade); high potency: EPS/neurologic
competitive antagonism
reversible (ionic) and irreversible (covalent)
isoniazid metabolism moa
acetylation (slow vs fast acetylators); slow aceylators are at increased risk for SE
