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55 Cards in this Set
- Front
- Back
volume of distribution = ?
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Vd = amount of drug in the body / plasma drug concentration
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clearance = ?
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Cl= rate elimination of a drug / plasma drug concentration
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half-life = ?
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half-life = (0.7 x Vd) / clearance
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loading dose = ?
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loading dose = (plasma drug concentration x volume of distribution) / bioavailability
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maintenance dose = ?
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maintenance dose = (plasma drug concentration x clearance) / bioavailability
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3 main drugs that undergo zero-order elimination
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phenytoin, ethanol, and aspirin
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rate of elimination is proportional to drug concentration
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first-order mechanics
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rate of elimination is constant regardless of drug concentration
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zero-order mechanics
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reactions in phase 1 mechanics
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reduction, oxidation, and hydrolysis
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reactions in phase 2 mechanics
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acetylation, glucuronidation, and sulfation
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neurotransmitter that provides sympathetic innervation to the adrenals and sweat glands
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ACh
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location of D1 versus D2 receptors
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D1- renal vascular smooth tissue
D2- brain |
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location of H1 versus H2 receptors
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H1- nose, respiratory tree
H2- stomach |
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location on B1 versus B2 receptors
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B1- heart
B2- lung |
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DOC for postoperative and neurogenic ileus and urinary retention
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bethanechol
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DOC to help diagnose asthma
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methacholine
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DOC for myasthenia gravis
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pyridostigmine
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anti-muscarinic used for Parkinsons
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benzotropine
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anti-muscarinic used for motion sickness
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scopolamine
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anti-muscarinic used for asthma
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ipratropium
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effect of atropine on the eye
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mydriasis and cycloplegia
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contraindications of atropine
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can not give atropine to infants (hyperthermia risk) or the elderly (may cause closed-angle glaucoma and increase risk for BPH)
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DOC to diagnose myasthenia gravis
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edrophonium
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antidote for acetaminophen toxicity
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N-acetylcysteine
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antidote for salicylate toxicity (i.e. aspirin)
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sodium bicarbonate, alkalinize the urine, dialysis
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antidote for amphetamine toxicity
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ammonium chloride, acidify the urine
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antidote for AChE inhibitors (i.e. physostigmine) or organophosphates (i.e. parathion)
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atropine or pralidoxime
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antidote for anticholinergic/antimuscarinic toxicity (i.e. atropine)
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physostigmine
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antidote for beta-blocker toxicity
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glucagon
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antidote for digitalis toxicity
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normalize K+, lidocaine, anti-digitalis antibodies, and magnesium
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antidote for iron toxicity
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deferoxamine
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antidote for lead toxicity
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EDTA, dimercaprol, or succimer
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antidote for mercury, arsenic, or gold
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dimercaprol or succimer
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antidote for copper toxicity
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penicillamine
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antidote for cyanide toxicity
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thiosulfate, nitrite
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antidote for methemoglobin toxicity
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methylene blue and vitamin C
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antidote for carbon monoxide toxicity
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100% oxygen and hyperbaric oxygen
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antidote for methanol or ethylene glycol (antifreeze) toxicity
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ethanol or fomepizole
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antidote for opioid toxicity
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naloxone or naltrexone
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antidote for benzodiazepine toxicity
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flumazenil
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antidote for TCA toxicity
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sodium bicarbonate
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antidote for heparin toxicity
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protamine
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antidote for warfarin toxicity
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vitamin K and fresh frozen plasma
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antidote for tPA or streptokinase toxicity
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aminocaproic acid
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antidote for theophylline toxicity
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B-blocker
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breakdown product of ethylene glycol
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oxalic acid
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breakdown product of methanol
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formaldehyde
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metabolic pathway of alcohol breakdown
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ethanol -> alcohol dehydrogenase -> acetaldehyde -> acetaldehyde dehydrogenase -> acetic acid
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which enzyme in the metabolic pathway of alcohol inhibits alcohol dehydrogenase
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fomepizole
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which enzyme in the metabolic pathway of alcohol inhibits acetaldehyde dehydrogenase
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disulfiram
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what is the metabolite in the metabolic pathway of alcohol that causes the nausea, vomiting, headache, ataxia, hypotension etc...
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acetaldehyde
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why do chronic alcohol ingestion cause lactic acidosis
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the metabolism of alcohol depletes NAD (therefore the NADH/NAD ratio increase) which is normally needed for the conversion of pyruvate into lactate
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CYP450 enzyme in alcohol metabolism
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CYP2E1
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why does alcohol precipitate acetaminophen toxicity
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normally, 95% of acetaminophen is metabolized by phase II enzymes and 5% is metabolized by CYP2E1
Normally, when that 5% gets metabolized by CYP2E1, it gets converted into NAPQI which is toxic and causes liver failure Overdosing on acetaminophen requires a much larger precentage to be metabolized by CYP2E1 thus creating more NAPQI and increasing the risk for liver failure and death Since alcohol is metabolized by CYP2E1, people taking even normal doses of acetaminophen but who are also chronic alcoholics will upregulate CYP2E1 and thus produce large amounts of NAPQI, thus increasing the risk for death |
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does salicylate toxicity cause alkalosis or acidosis
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intially, it causes a respiratory alkalosis (due to hyperventilation); shortly after, it causes a metabolic acidosis due to the accumulation of pyruvate and lactate (Krebs cycle)
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