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55 Cards in this Set

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