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176 Cards in this Set
- Front
- Back
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What drug will treat spasticity in MS without total muscle weakness (dantrolene) or sedation (benzodiazepines)?
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baclofen
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What enzyme maintains no spontaneous depolarization at phase 4?
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Na/K ATPase
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What are the adverse effects of Digoxin?
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Spontaneous phase IV premature ventricular contractions (PVCs)
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What is sildenafil’s MOA?
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Blocks PDE that breaks down cGMP (can’t take if pilot)
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Why can’t you use sildenafil and nitrates at the same time?
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Both maintain dilation so patient would stroke out or have an MI
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What is the tx for terminal CHF?
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aminorane/milinerone
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DOC for hyperprolactinemia
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Bromocriptine
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DOC for neonatal apnea? Why?
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Theophylline/aminophyline...b/c PDE Inhibitors
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What drugs stop seizures b/c increased chloride conductance?
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Benzodiazepines
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What cardiac drug prevents automaticity and stops PVCs?
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Procanamide, dispyramide and quinidine (“PQD for PVCs”)
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What blocks the 5HT receptors in the chemotrigger zone/
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Odansetron
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If a pt buys an OTC drug for heartburn and gets constipated what does it contain?
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Al
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If a pt buys an OTC drug for heartburn and gets diarrhea, what does it contain?
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Mg
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DOC for absence seizures?
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Ethosuximide
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What is the DOC to maintain BP at the same level during operations for pts at hypotensive risk (i.e. GSW)?
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Ketamine (NMDA blker, anesthetic)
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What is the DOC to prevent the contraction of skeletal muscle during malignant hyperthermia?
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Dantrolene
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If you don’t want SE of weakness (muscle) but want to get rid of spasticity, the DOC is?
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Baclofen
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If a pt is taking erythromycin for an infection and suddenly presents w/ drug toxicity of a previous Rx, why?
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b/c erythromycin inhibits CYP450, therefore the metabolism of the drugs decreases and the drugs stay in the system longer
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If a pt is takin cimetidine for heartburn and suddenly presents w/ drug toxicity of a previous rx?
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b/c cimetidine inhibits cyp 450
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What is the DOC to tx Hereditary Angioedema (due to a deficit in C1 esterase inhibitor), which is charac. By perifpheral edema, abdominal pain, and potentially lethal laryngoedema?
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Stanolozol (anabolic steroid androgen)
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What does the x-axis represent on a Scatchard plot?
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Number of receptors
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What does increased slope indic. on a Scatchard plot?
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Increased affinity. Decreased slope indicates decreased affinity
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What do you need to take into account if given p.o. trying to calc loading dose?
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Bioavailability must be taken into account if p.o., =1 if i.v.
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What does the size of the loading dose depend on?
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Vd
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What does the size of the maintenance dose depend on?
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Clearance
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What are the important CYP450 inhibitors? CYP450 inducers?
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CYP450 Inhibitors: cimetidine, ketoconazole, isoniazide, erythromycin, ETOH (acute), grapefruit juice (flavenoids)!
CYP450 inducers: phenobarbitol, rifampin, pheytoin, carbamazepine, ETOH (chronic), Cigarette smoke (benzopyrene), Dioxin (in agent orange), DDT (insecticide), Polychlorinated biphenyls (PCB’s) |
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Renal Clearanec of overdoses of acetaminophen or iron can be inc by?
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making urine more alkaline w sodium bicarb (quickly), acetazolamide (overtime)
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Renal clearance of basic drugs can be inc by?
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making the urine more acidic w ammonium chloride
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What are two S/E of pilocarpine?
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miosis (can’t see at night), and contraction of ciliary musc (near sight)
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What is the DOC to prevent muscarinic S/E?
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Atropine
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How do you dx Myasthenia gravis?
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edrophonium, is it tertiary or quaternary? (quaternary)
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How do you tx myasthenia gravis?
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Neostigmine (4*) or pyridostigmine (3*)
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how do you tx organophosphate poisoning?
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atropine and pralidoxime (2-PAM)
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What the sx of organophosphate poisoning?
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lacrimation, salivation, miosis, dyspnea, skeletal myscle fasciculations (N2), bronchconstriction, urinary incontinence and pulmonary edema
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What are the S/E of a muscarinic antagonist?
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mydriasis, dry mouth, dry eyes, dry nose, slow bowels, urinary retention
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What is the effect of trimethapham on the heart?
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blocks both bradycardia and tachycardia, bc trimethaphan is a ganglionic blocking drug
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What are two uses for acetazolamide?
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used to alkalinize the urine, used to tx altitude sickness, causes metabolic acidosis which stim respiration
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What is the DOC for treating Tape worms?
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Niclosamide (“tape and nickels are both flat”)
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What is Praziquantal’s MOA?
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The mechanism of praziquantal is UNKNOWN! (used as DOC from most trematode (fluke) and many cestode infections. Trematodes/flues move about the body, there are blood flukes and liver flukes, etc)
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What is mebendazole and other –bendazoles’ MOA?
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Mebendazole inhibits protein function in the worms. Binds to tubulin and inhibits glucose uptake, it can abe given orally and very little is absorbed from the GI tract.
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What is the DOC for the treatment of roundworm and pin worms?
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The “-bendazoles” such as Mebendazole and thiabendazole
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What is the DOC for River Blindness?
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Ivermectin
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What is the DOC for Tematodes (flukes = Schistosoma)*?
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Praziquantal. (“fluky word, z and q, for fluke). Praziquanantal is also used for mixed infestations (tape and fluke worm) or if the worm type is unknown
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What is that DOC for Taenia Solium?
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Taenia Solium is the Pork Tapeworm. It causes cystercosis---treat it with albendazole.
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What do you use to determine whether a pin worm infestation has occurred in a child?
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The cellophane tape test
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What do you treat pin worms with?
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Tx w/ mebendazole or pyrantel pamoate
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What is the DOC for Giardia, Trichomonas and C. difficile (i.e. the flagellated bugs)?
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Metronidazole.
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What is the DOC for the following clinical presentation: person going to a foreign country and eating at a street vendor and getting sick?
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Metronidazole for the treatment of Entmoeba histolytica
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What is a key drug interaction (toxicity) with metronidazole?
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MAJOR TOXICITY WITH ETOH!! Causes a disulfiram-like rxm w/ ETOH.
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What is the MOA of disulfiram?
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Blocks acetaldehyde dehydrogenase which causes acetaldehyde to build up after EtOH ingestion---makes the pt. sick (like rxn of metronidazole’s rxn w/ EtOH)
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What is the DOC for pneumocystis carninii pneumonia?
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Trim-sulfa (antifungal drugs are not used for PCP)
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What is the secondary DOC for pneumocystis carninii pneumonia?
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Pentamidine isethionate
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What is a bad side effect of Primaquine and the sulfonamides in patients with Glucose-6-Phosphate dehydrogenase deficiency?
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Causes acute hemolysis (hemolytic anemia) b/c RBC’s need G6PDH to make NADPH and protect themselves from oxidation by other products.
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What is the MOA for Primaquine?
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Unknown
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What is Primaquine the DOC for?
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Anti-malarial. Effective against liver forms (exoerythrocytic) and kills gametocytes. Often used for prophylaxis. Used to tx Plasmodium vivax and P. ovale strains.
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What is true about many malarial strains with regards to chloroquine?
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Many malarial strains are resistant
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What is the DOC for prophylaxis of malaria in chloroquine-resistant areas?
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Mefloquine
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What is the DOC for treatment of malaria in chloroquine-resistant areas?
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Sulfadoxine-pyrimethamine
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What is the DOC for HSV?
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Acyclovir
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What is the MOA for the DOC for HSV?
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Acyclovir’s MOA is: Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase. The first stem in activation of HSV is catalyzed by viral thymidine kinase, thus it is only activated in viral cells and not in host cells.
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Do you tx everything related to HSV with Acyclovir?
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No, tx keratoconjunctivitis with trifluridine
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What is the DOC for CMV?
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Ganciclovir
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What is the MOA for AZT?
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Inhibits viral DNA polymerase (=reverse transcriptase)
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What is the DOC for Coccidioides immitis and Aspergillis?
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Amphotericin B
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What is the MOA of Amphotericin B?
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Binds ergosterol (unique to fungi) to form membrane pores that allow leakage of electrolytes and disrupt homeostasis. “AmphoTERicin “tears” holes in the fungal membrane by forming pores.
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What is fungi’s resistance mechanism?
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Decreases ergosterol or changes ergosterol’s structure to prevent binding
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**What is a key SE of Amphotericin B? How to do you tx this bad SE?
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It is nephrotoxic. Tx nephrotoxicity with mannitol.
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How is Amphotericin B given?
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It is not absorbed from the GI tract, so it must be given intravenously or topically
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What is the MOA of the anti-fungal ketoconazole? And what is it used for?
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Inhibits fungal CYP450 and blocks ergosterol synthesis and cell wall formation. Don’t use ketoconazole w/ Ampho B b/c keoconazole stops the synthesis of the site where Ampho B acts.
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If you see + silver stain?
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Think PCP. The DOC is Trim-Sulfa
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What is the DOC from ring worm and athletes foot? (dematophytes w/ hyphae)
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Griseofulvin
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What is the MOA of Griseofulvin?
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Disrupts mitotic spindles (disrupts microtubules)
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What type of organisms is Penicillins the DOC for?
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Gram + organisms...(Cocci: Strep pneumo, viridans, syogenes, group B strep; enterococcus faecalis’, Staph aureus, epi, sapro; Rods: Clostridium, Listeria, Bacillus)
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What is penicillins MOA?
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Bind penicillin-binding-proteins to inhibit transpeptidation and inhibit cell wall syntehesis
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How are penicillins eliminated?
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By renal excretion
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How can you increase the half-life of penicillin and therefore prolong its action?
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Add Probenicid. Probenicid inhibits renal clearance of penicillins and increases their half-life
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What do clavulanate, sulfbactam and tazobactam have in common?
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They all inhibit beta-lactamases
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What are the penicillins that are resistant to beta lactamases?
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Methicillin, nafcillin, oxacillin, cloxacillin and dicloxacillin.
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What effect does cilastatin have on imipenem?
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It decreases the renal clearance of imipenem and thus increases the half-life of imipenem (which is beta-lactamase resistant).
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What is the MOA of cephalosporin?
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Same MOA, therefore if the pt has resistance or allergy to PCN, don’t give a cephalosporin b/c will probably have an allergy to that too.
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Who should you not use tetracycline on?
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Pregnant women or kids b/c it chelates calcium…use a macrolide (azithromycin, clarithromycin or erythromycin—Azi usu. Best)
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What is Tetracyclin’s bioavailability decreased by?
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Milk and food
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What are SE of Tetracyclin?
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Rash w/ sunlight
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How do you Tx MRSA?
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Clindamycin or Trim-Sulfa
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Use of *Vancomycin?
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i.v. for MRSA in hospital
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Is *Vancomycin bacteriocidal or bacteriostatic? *Aminoglycosides?
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Vanc: -cidal, *aminoglycosides (gentamycin)—cidal
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What is the major toxicity of *aminoglycosides (gentamycin)?
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Ototoxic (additive w/ furosemide), nephrotoxic (additive w/ Ampho B)
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What is Trim-Sulfa’s MOA?
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Sulfamethoxazole and sulfadoxine inhibit Dihydropteroate Synthase; Trimethoprim, pyrimethamine and methotrexate inhibit DHT reductase. Net effect, no synethesis of pyrimidines and purines, no syn. of methionine, glycine and serine, b/c all these things need THF (folate).
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What is the DOC for Community Acquired Pneumonia out-pt tx?
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*Macrolides (erythromycin, azithromycin, clarithromycin)
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What is the DOC for solo prophylaxis against TB?
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Isoniazide. Usu given in combo w/ Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazide (“RESPIre”)
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What are the SE of isoniazide?
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Causes Hepatic Damage and Vit B loss. Vit B loss will cause sensory and motor peripheral neuropathy in alcoholics b/c they are malnourished. (alcoholic—think 6 pack—and Vit B6 def if they get TB and have to take INH)
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What is the MOA of the *fluoroquinolones (Ciprofloxacin, norfloxacin, --oxacins, etc)?
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Inhibit DNA gyrase which forms negative supercoils
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Methods of resistance***: Where is resistance to beta-lactam drugs usually found and what method to the bugs use?
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Usu found in Gram + bugs ((Cocci: Strep pneumo, viridans, syogenes, group B strep; enterococcus faecalis’, Staph aureus, epi, sapro; Rods: Clostridium, Listeria, Bacillus). Method: production of beta-lactamases by bacteria
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Method of resistance for MRSA?
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Change binding sites of the penicillin-binding-proteins. These bugs are resistant to all penicillins and cephs.
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Gram – organisms:
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Cocci: Neisseria meningitides, N. gonorrhoea, Haemophilus influenzae, Pasteurella (animal bites), Brucella, Bordetella pertussis; Rods: Klebsiella, E. coli, Enterobacter, Shigella, Salmonella, Proteus, Pseudomonas
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Tx for hypochromic, microcytic anemia?
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Hypochromic, microcytic anemia is Fe-deficient anemia---this will look like small, pale RBC’s on smear. Tx w/ Ferrous Iron and Vit C (which increases Iron absorption)
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How do you tx an iron overdose (death in kids)?
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Deforroxamine**. We have no mechanism of iron excretion
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How do you tx acetomenophen toxicity in kids?
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N-Acetyl Cysteine
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What is the cause of normochromic, macrocytic (megaloblastic) anemia and how do you tx?
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Folate or B12 deficiency. If Folate def (no neuro sympt, all blood lines effected), tx w/ folate. If B12 def (neuro sympt. b/c B12 is req for myelin syn, all blood cell lines effected), tx. w/ a cobalamin
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What would be the drug used by an athlete who has a Hct of 59?
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EPO…Epoetin-alpha (Darbapoetin)
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How does aspirin have an antithrombotic effect?
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Preventing synthesis of Thromboxane-2
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What are two drugs that could be used in pts who develop a hypersensitivity to apririn?
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Ticlopidine and clopidegrel
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What is the speed of effect of unfractioned heparin?
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INSTANTLY EFFECTIVE anticoagulant
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What is the MOA for Heparin?
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Catalyzes the activation of antithrombin III, decreases thrombin and Xa.
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What are the clotting factors, hemostatic effect and platelet effect for Heparin, LMW-heparin, and Warfarin?
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Heparin: clotting factors 2, 9-12; increases aPTT; Increased BT
LMW-Heparin: clotting factor 10 (converts prothrombin to IIa); has no effect on aPTT or PT/INR; Increases BT {intrinsic pthwy} Warfarin: clotting factors 2, 7, 9, 10; increases PT/INR, increases aPTT (at high doses, over dose or toxicity); increased BT {Extrinsic pathway} |
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What is the only antagonist for heparin?
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Protamine sulfate, rapidly reverses heparinization
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When pt is given heparin w/ no increase in aPTT means that?
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They have decreased Antithrombin III
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What is the DOC for pts w/ atrial fibrillation b/c they develop microthrombi?
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Warfarin
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What is Warfarin’s MOA? How do you reverse it?
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Interferes w/ normal synthesis and y-carboxylation of Vit K-dependent clotting factors II, VII, IX and X and protein C and S. Reverse w/ Vit K, fresh frozen plasma, factor IX concentrate.
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What is a SE of tPA and streptokinase?
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Bleeding. Streptokinase is self-activated and is not selective and therefore digests all clotting factors. Both are used to tx
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What is the MOA for statins?
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Inhibition of the hepatic HMG CoA reductase
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What are the SE of statins?
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Myositis/myopathy can progress to rhabdomyolysis (muscle release of myoglobin); increased myoglobin→ myoglobulinemia→stops up renal tubules→acute renal failure.
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How should you tx rhabdomyolisis?
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Mannitol and fluids to increase flow thru kidneys→develop osmotic diuresis
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What are the DOC for tx Triglycerides? What is their MOA?
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Gemfibrozil and fenofibrate. Makes LDL bigger so harder to oxidize
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What is the effect of nitrates on the veins?
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Cause venodilation→decreases venous return→decreased preload and increased capacitance
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What is the major problem w/ nitrates?
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SE, tolerance is a major problem.
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What effect do ACE inhibitors (captopril, enalapril, lisinopril) and ARB (angiotensin II receptor blockers: candesartan, eprosartan, losartan, irbesartan, telmisartan, valsartan) have on blood vessels?
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Blanced veno-arteriolar dilation (preload/afterload)
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What is the DOC to tx a pt in heart failure?
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Digoxin
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Possible adverse side effect of succinylcholine?
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hyperkalemia is a big risk in patients with burns and denervation due to an increase in N2-rec density
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What is difference between depolarizing and non-depolarizing drugs?
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competitive vs. non-competitive, non-com= MEP is depolarized then repolarized but still refractory, com= MEP is NOT depolarized therefore no stimulatory effects (no fasciculations) by occupying nicotinic Type 2 receptors
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How do you inhibit NE/Epi synthesis?
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with metyrosine, inhibits tyrosine hydroxylase—the rate limiting step in E syn
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Patient in shock why would you choose DA over Epi?
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DA increases RBF/mesenteric BF via beta mediated inc in contractility of heart whereas Epi dec blood to kidney. Give DA and can save renal function
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How is NE different in effects from other adrenergic agonists in terms of effect on HR?
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NE dec HR by baroreflex by:
Vasoconstriction->inc TPR & BP->reflex inc parasympathetic to heart->dec HR |
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MAO-A and MAO-B metabolize catecholamines, which ones?
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MAO-A=NE and Serotonin, MAO-B=DA
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What is the second messenger for beta receptors?
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cAMP
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S/E in non-selective vs selective beta agonists?
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isoproterenol (non-selective)= bronchodilation w. inc in HR
albuterol, terbutaline (beta 2 selective)= bronchodilation w. less inc in HR |
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If you treat a pt with reserpine will indirect adrenergic agonists have an effect?
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No effect b/c depletes NE, only directly acting agonists will maintain an effect
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Pt comes to the hospital, looks wide awake on on-edge, he is easily agitated by the pesky questions the nurses keep asking and thinks they are out to get him, his HR and BP are elevated then he drops to the floor with convulsions, what do you treat him with?
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tx amphetamine OD psychosis with chlorpromazine
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What are the 3P’s? (a-blockers)
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phentolamine, prazosin, phenoxybenzamine
phenoxybenzamine-only on that is irreversible blocker phentolamine- tx pt with pheo before surgery to dec BP, epi reversal prazosin- no effect on HR phentolamine, PBZ- increase HR via baroreflex |
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major s/e of ALL alpha blockers
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orthostatic hypotension
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What will Epi do to particular organ systems and why?
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will interact with predominant receptor in the system
-alpha- VC skin, GI, kidney -B2- inc. blood, skeletal, and liver -If block alpha- then B2 is only being stimulated which causes V.D, hypotension, and a dec. in BP., if block beta- then only stim alpha causes HTN, inc BP |
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What is the MOA of beta blockers?
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dec O2 demand by dec HR, dp/dt, DBP via cardioselective or nonselective beta blocker
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S/E of timolol?
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Timolol is a nonseletive beta blocker used to dec IOP, if it enters the circ causes bradycardia and bronchoconstriction, do NOT use propanolol it will anesthetize the cornea
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What happens if you block beta receptors for a long time then take the pt off the Rx, why?
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up-regulates receptors which inc. the number of receptors so if you discontinue the B blocker there will be too many receptors and you will have a B block withdrawal which might cause angina or migraines
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What is the cheese rxn?
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inhibition of MAO-A in gut wall allows dietary tyramine to enter the circulation; tyramine releases NE to cause HT and tachycardia
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How do phenelzine and tranylcypromine work?
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inhibit MAO-A and MAO-B which decreases the degradation of DA, and DA makes people happy!!!
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Why are alpha-methyldopa and clonidine unique?
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these are centrally acting alpha2 agonists in the CNS, think of it as “fake NE” going to the brain, the brain thinks that there is plenty of NE around so in response decreases sympathetic outflow, dec NE which in turn dec rennin and HR
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S/E of alpha-methyldopa?
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hepatitis, “flu” syndrome, + coombs test
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Difference between clonidine withdrawal and beta blocker withdrawal?
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clonidine= sweating, inc HR, abrupt return of BP to HT value, abdominal pain, tremor, HA
beta-blocker= inc HR w/ palpitations but NO tremor, sweating, abdominal pain or inc in BP |
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Do arterial vasodilators work on veins?
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NO, hydralazine, minoxidil, diazoxide dilate resistance vessels causes a huge inc in CO and dec in cardiac afterload, have no effect on veins
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What is the major side effect of hydralazine? How do you treat it?
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SLE—arthralgia, arthritis, fever, malar rash, +ANA, glomerulonephritis
Tx w. dec hydralazine and give steroids (steroids end in –sone or –lone) |
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What is sodium nitroprusside used for and how does it work?
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used for HT emergency, works as a balanced vasodilator via release of NO, so CO does NOT change in normotensive pt, in pt w/ CHF-> dec preload & afterload-> inc CO
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What do diltiazam and verapamil do, how do you remember them?
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like on valentines day (VD) verapimil and diltiazam (VD) cause arteriolar vasodilation (VD)
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A patient is taking an ACE inhibitor develops a cough, what do you do?
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discontinue ACE inhibitor (“-il”) and start on angiotensin receptor blocking drug (losartan), why? B/c does not interfere with bradykinin like ACEI
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how do you increase renal clearance of a drug?
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make urine more alkaline= acetazolamide or Na Bicarb- inc renal clearance of acidic drugs
-make urine more acidic= ammonium chloride= inc renal clearance of basic drugs (ex. Amphetamine)—may be a question with a kid who ingested amphetamines |
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What is the major side effect of hydralazine? How do you treat it?
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SLE—arthralgia, arthritis, fever, malar rash, +ANA, glomerulonephritis
Tx w. dec hydralazine and give steroids (steroids end in –sone or –lone) |
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What is sodium nitroprusside used for and how does it work?
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used for HT emergency, works as a balanced vasodilator via release of NO, so CO does NOT change in normotensive pt, in pt w/ CHF-> dec preload & afterload-> inc CO
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What do diltiazam and verapamil do, how do you remember them?
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like on valentines day (VD) verapimil and diltiazam (VD) cause arteriolar vasodilation (VD)
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A patient is taking an ACE inhibitor develops a cough, what do you do?
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discontinue ACE inhibitor (“-il”) and start on angiotensin receptor blocking drug (losartan), why? B/c does not interfere with bradykinin like ACEI
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how do you increase renal clearance of a drug?
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make urine more alkaline= acetazolamide or Na Bicarb- inc renal clearance of acidic drugs
-make urine more acidic= ammonium chloride= inc renal clearance of basic drugs (ex. Amphetamine)—may be a question with a kid who ingested amphetamines |
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What is the major side effect of hydralazine? How do you treat it?
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SLE—arthralgia, arthritis, fever, malar rash, +ANA, glomerulonephritis
Tx w. dec hydralazine and give steroids (steroids end in –sone or –lone) |
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What is sodium nitroprusside used for and how does it work?
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used for HT emergency, works as a balanced vasodilator via release of NO, so CO does NOT change in normotensive pt, in pt w/ CHF-> dec preload & afterload-> inc CO
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What do diltiazam and verapamil do, how do you remember them?
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like on valentines day (VD) verapimil and diltiazam (VD) cause arteriolar vasodilation (VD)
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A patient is taking an ACE inhibitor develops a cough, what do you do?
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discontinue ACE inhibitor (“-il”) and start on angiotensin receptor blocking drug (losartan), why? B/c does not interfere with bradykinin like ACEI
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how do you increase renal clearance of a drug?
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make urine more alkaline= acetazolamide or Na Bicarb- inc renal clearance of acidic drugs
-make urine more acidic= ammonium chloride= inc renal clearance of basic drugs (ex. Amphetamine)—may be a question with a kid who ingested amphetamines |
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What is the major side effect of hydralazine? How do you treat it?
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SLE—arthralgia, arthritis, fever, malar rash, +ANA, glomerulonephritis
Tx w. dec hydralazine and give steroids (steroids end in –sone or –lone) |
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What is sodium nitroprusside used for and how does it work?
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used for HT emergency, works as a balanced vasodilator via release of NO, so CO does NOT change in normotensive pt, in pt w/ CHF-> dec preload & afterload-> inc CO
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What do diltiazam and verapamil do, how do you remember them?
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like on valentines day (VD) verapimil and diltiazam (VD) cause arteriolar vasodilation (VD)
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A patient is taking an ACE inhibitor develops a cough, what do you do?
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discontinue ACE inhibitor (“-il”) and start on angiotensin receptor blocking drug (losartan), why? B/c does not interfere with bradykinin like ACEI
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how do you increase renal clearance of a drug?
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make urine more alkaline= acetazolamide or Na Bicarb- inc renal clearance of acidic drugs
-make urine more acidic= ammonium chloride= inc renal clearance of basic drugs (ex. Amphetamine)—may be a question with a kid who ingested amphetamines |
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What are the differences between furosemide and hydrochlorothiazide?
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furosemide –
increases urinary excretion of everything (Ca2+ included) causes K+ wasting causes secondary hyperaldosteronism, which furthers K+ loss used to treat acute pulmonary edema via PG mechanism used to treat hypercalcemia s/e: bilateral hearing loss potentiated with gentamicin use, hypokalemia (skeletal muscle cramping) with alkalosis, dilutional hyponatremia, hyperuricemia and Lithium toxicity HCTZ – increases Na+ excretion by enhancing the efficiency of reabsorption in the PT of the kidney to 85% (normal is 65%), therefore, the kidney sends less water downstream to be lost. decreases excretion of Ca2+ (opposite of furosemide), used in hypercalcinuria to prevent kidney stones. urine is always hypertonic → dilutional hyponatremia NB: hypokalemia from furosemide and HCTZ prevented by K+ sparing diuretic drugs, ACEI, beta-blockers, and sometimes K+ supplements |
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patient tx with OCP: 19-nortestosterone stimulates hair growth.
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spironolactone prevents this because it is a partial agonist at androgen-R
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patient with adrenal tumor:
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Dr. K said it is important to be able to distinguish between these 3 types of adrenal tumors:
1) Pheochromocytoma – secretes epi → HTN with headache, sweating, hyperglycemia, tremor, constipation, and increased urinary catecholamines - treat with an α-blocker and a nonselective β-blocker 2) Cushings Syndrome – secretes cortisol → no suppression with dexamethasone, moon facies, hyperglycemia, HTN, hypokalemia, increased excretion of 17-hydroxysteroids in urine - in reality you would want to do surgery, but if your only option were medical therapy, treat with ketoconazole or *aminoglutethamide* - causes a medical adrenalectomy 3) Conn’s Syndrome – HTN, hypokalemia, decreased plasma renin activity, excretion of 17-hydroxysteroids in the urine will be normal - treat with spironolactone |
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How do you tx addison’s dz?
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Treat Addison’s Dz with hydrocortisone and fludrocortisone bc have to replace glucocorticoids and mineralocorticoids
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Explain the kinetics of Digoxin
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has a narrow therapeutic window
is 100% cleared by the kidneys cholestyramine is a bile-acid resin, so it binds the steroid ring of digoxin and prevents GI absorption |
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How would this effect an elderly person taking it or someone w dec GFR?
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elderly, dec Vd so dec loading dose, dec GFR->dec maintenance dose
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How does Digoxin cause automaticity?
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inhibits Na-K ATPase which inc dp/dt but dec resting memb pot and dec pumping of Na causes automaticity in fast fibers bc leads to low K (potentiates inhibition of ATPase), low Mg/high Ca (Ca overload inside cells causes automaticity)
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How does digoxin act in CNS to inc vagal tone?
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-inc vagal tone, dec HR, atrial contraction, and AV conduction
DOC for keeping the ventricular rate slow in a patient with atrial fibrillation |
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What effect does quinidine have on an action potential?
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blocks Na+ channels in fast fibers → decreases Phase 4 automaticity, decreases Phase ) slope (slowed conduction velocity = widened QRS)
blocks K+ channels → prolongs repolarization (moves Phase 3 to the right of the diagram, increases QT interval) can have an atropine-like action (ACh-R antagonist) at the AV node (vagal control slows it down) resulting in increased conduction and tachycardia -DOC for atrial and ventricular dysrhythmias |
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Clinical: treat the atropine-like effect of quinidine with verapamil or diltiazem
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ok.
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Why does procainamide cause SLE in some patients?
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bc these pts are slow acetylators, inactive acetylase enzyme
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If you are treating a pt with a local anesthetic and they begin to have seizures, what drug are you using and how do you tx S/E?
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you are using lidocaine, tx with benzodiazepine works to increase GABA-A - blocks Na+ channels in fast fibers
used to prevent PVC’s in ischemic tissue mediated Cl- conductance |
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What are the major S/E of amiodarone?
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pulmonary fibrosis, hypo-, hyperthyroidism; smurf man!
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What is the MOA of verapamil?
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blocks L-type Ca2+ channels at SA and AV nodes and cardiac myocytes
treats AVNRT |
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Clinical: verapamil can be used to treat A fib in patients WITHOUT heart failure because it will slow ventricular rate and improve AV filling
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do NOT give it to a patient with heart failure because it will decrease contractility, making the heart failure worse. If the patient has heart failure, use digoxin
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If a patient has aspirin hypersensitivity what can you use to tx after an MI or stroke?
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-ticlopidine, clodpidogrel– antagonists of platelet purinergic (ADP) –R
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