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76 Cards in this Set

  • Front
  • Back
FDA categories for drug use in pregnancy
A - controlled studies show no risk. fetal harm is small. e.g. potassium chloride

B- no evidence of risk in humans.

C- risk cannot be ruled out. animal studies show adverse effect or no studies available

D - positive evidence of human fetal risk.

X- contraindicated in pregnancy. e.g. triazolam/flurazepam/temazepam, accutane (isotretinoin)
classification of adverse reactions
-extension effects - dose related and predictable
-side effects - dose dependent and predictable
-idiosyncratic reactions - unpredictable
-drug allergy - unpredictable, independent
extension effects
arise from an extension of the therapeutic effect.

mechanism based.

e.g. insult to lower blood glucose cuases hypoglycemia
% of drugs ok to use in pregnancy
pharmacokinetic drug interactions can result in
elevated drug concentrations (due to reduced elimination rates or protein-bound drug displacement) leading to toxicity
causes decreases in plasma concentratoins (via more rapid drug elimination or decreased drug absorption) leading to levels below therapeutic effectiveness.
pharmacodynamic drug interactions at the receptor level can result in
phamcologic or physiolgoic enhancement
or antagonism of drug action
which pateints are high risk for drug-drug interactions
-pts in high risk clinical situations (dependent on drug treatment, acute illness, unstable disease)
-pts with renal/hepatic disease
-pts with multiple preswcribing physicians
PK interactions
which drugs have narrow therapeutic index
means they need to be monitored carefully in plasma

insulin and warfarin

-aminoglycoside Ab
-cancer chemotherapeutics
-HIV agents
-immunosupressants (cyclosporine
-neuromuscular blocking agents
PK interactions with absorption
decreases in motility --> lower peak plasma drug levels

increases in absorption less important

physiochemical inactivatoin via changes in pH or formation of insoluble complexes reduces bioavailability
PK distribution interactions
protein bindingdisplacement interactions.

competitive binding increases free drug

cellular distribution interactions
PK metabolism interactions
inducers (increase metaboilc rate) causing subtherapeutic levels

inhibitors (decreased metaboilc rate) causing increased toxic levels of drug

most interactions occur via CYP
PK excretion interactions
most in KIDNEYS
change in GFR (glomerular filtration rate)
change in tubular secretion
change in urine pH
Pharmacodynamic interactions
-antagonistic effects
-synergisitc or additive therapeutic efects
-synergistic or additive side effects
-indirect pharmacodynamic effect
pharmaceutic interactions
when 2 drugs mixed in same IV fluid
chemical inactivation or precipitation via pH changes or alteration of vehicle
single most important determinant of poisoning outcomes is
supportive care

-cardiopulmonary support and protection of airway
-assess electrolytes, acid-base balance and fluids
-CNS precautions
-renal function (direct drug toxicity and indirect hypotension renal failure)
study of absorption, distribution and elimination of toxic parent compounds and metaboic products that aids in predictino of amt of toxin that reaches site or injury and the resulting damage.

-absorption (bioavailability F)
-volume of distribution (Vd)
-clearance (metabolism/excretion)
absorption in toxicokinetics
large amt of ingested drug may slow tablet dissolution

alter GI emptying

injure GI tract --> altered absorption --> delayed peak effect
clearance (metabolism / excretion)
important to know contribution of kidney and liver to elimiantion fo toxin to plan treatment strategy
half life in toxicokinetics
the published values are for therapeutic doses

half life may be PROLONGED in toxic overdoses due to saturation of the elimination mechanisms
general treatment strategies for poisoning
-prevent / decrease absorption
-inhibit toxication (prevent conversion to toxic species)
-enhance metabolism (detox)
-increase elimination of toxin (decrease rate out)

prevention of absorption
-emesis (ipecac, apomorphine)

-gastric lavage

-chemical adsorption. activated charcoal
local irritation and CNS stimulation of chemoreceptor zone

effective orally but must be given BEFORE charcoal

emesis after 15-30 minute lag, repeat after 20 minutes
not recommended in children, rarely used at all

dopamine agonist, produces emesis by stimulation of chemoreceptor zone
respiratory depressnat, toxic in children

-comatose patient (lack of gag reflex --> risk of aspiration)
-ingestion of corrosive poisons (strong acids or alkalis)
-ingestion of CNS stimulatn such as strychnine (risk of seizures)
ingestion of petroleum distillate (risk of pneumonitis)
pregnancy category C
gastric lavage
most rapid and complete method of emptying stomach

lavage + emesis removes only about 30% of most oral poisons

-washing of stomach contents with saline and removal via nasogastric tube
-best within 60 minutes of poison ingestion
activated charcoal
binds drug in gut to limit absorption
-effective without prior gastric emptying and can reduce eliminatino half lives of drugs that have been given IV
(back diffusion of drug from blood with ion-trapping in the stomach)
osmotic cathartics
decrease time of toxin in GI tract (via osmotic laxative effect)
indicated if toxin ingestion is > 60 min

-magnesium citrate/sulfate
-sodium solfate
-polethylene glycol
sorbitol with charcoal
osmotic cathartic given together to prevent briquet formation
magnesium sulfate/citrate
osmotic cathartic (decrease time of toxin in GI tract)
avoid in renal disease or poisonings with nephrotoxic agents
sodium sulfate
osmotic cathartic (decrease time of toxin in GI tract.
avoid use of sodium containing cathartics in CHF or hypertension (systemic absorption --> fluid overload)
inhibition of toxication
methanol/ehtylene glycol

methanol metabolized --> formic acid (retinal damage & blindness)

ethylene glycol metaboilzed --> oxalic acid (insoluble crystals in kidney - acute kidney failure)

treatment - correction of metabolic acidosis with NaHCO3, removal of parent compounds and metabolites with
hemodialysis, and suppression of production of production of toxic metabolites by inhibiting the rate limiting enzyme (alcohol dehydrogenase) with ethanol (competitive inhibitor) or fomepizole (specific inhibitor of alcohol dehydrogenase)
ethanol as an inhibitor of toxication
substrate and a competitive inhibitor of alcochol dehydrogenase
fomepizole as an inhibitor of toxication
specific inhibitor of alcohol dehydrogenase
enhancement of detoxification is a method to treat toxic levels of
acetaminophen toxicity
toxic single dose > 10-20 g will saturate phase II metabolic pathways leading to increased formation of phase I hepatotoxic metabolite
deplete glutathione stores availble for detoxification

hepatocellular injury
cyanide toxicity
cyanide binds ferric ions in cytochrome oxidase

cellular respiration
cytotoxic hypoxia
lactic acidosis
treatment of acetaminophen toxicity
-gastric lavage
-supportive theray
-N-acetylcysteine (precursor for glutathione synthesis and nucleophile to capture the electrophilic heatotoxic metabolite)
treatment of cyanide toxicity
hydroxocobalimin (vitamin b12 precursor that binds cyanide to make cyanocobalamin)
enhancement of elimination
-extracorporeal removal
-enahnced metabolism
-enhanced renal excretion
-chelation of heavy metals
extracorporeal removal
method to enhance elimination

-hemodialisis/peritoneal dialysis (blood pumped through filter)

-hemoperfusion (bloodpumped through column of adsorbent material)
hemodialysis / peritoneal dialysis
blood pumped through filter

-effective for toxins with small Vd
-toxins should have low protein binding capacity
-helps in correction of fluid and electrolyte imbalance
if drug is outside plasma, large Vd, would hemodialysis /peritoneal dialysis be useful
no because hemodialysis useful for toxins with small Vd
blood pumped through column of adsorbent material.
-useful for high MW toxins with poor water solubility
-risks: bleeding (removal of platelets) and electrolyte distubances
enhanced metabolism
method to enhance elimination

-induction of cytochrome p450 is NOT REALISTIC due to delay (1-3 days for onset of action)
-enhancement of detoxificatoin metaboilc pathways with N-acetylcysteine in acetaminophen toxicity and thiocyanate in cyanide poisoning
-inhibition of metabolism to block formation of toxic metabolistes (e.g. inhibition of alcohold dehydrogenase in methanol or ethylene glycol toxicity)
N acetylcysteine
enhances detoxification of metabolic pathways in acetaminophen toxicity
enhances detox metabolic pathways in cyanide poisoning
enhancement of renal excretion
method of enhancment of elimination in toxic
-forced diuresis
-block reabsorption from kidney
-block active reabsorption
forced diuresis
normal saline plushigh efficacy diuretics (furosemide)
-small effect with danger of fluid overload (worsens pulmonary function)
-protects kidney (beneficial effect)
block reabsorption from kidney
prevention of passive reabsorption via alteration of urinary pH and ion trapping
-make urine more basic (with NaHCO3) then trap weak acids like aspirin
-make urine more acidic(with NH4Cl or ascorbic acid) then trap weak bases
chelation of heavy metals
-enhances elimination of toxins (increase renal excretion) and inactivate toxin (decreases ability to interact with and damage target tissue)
normal physiology of chelation of heavy metals
heavy metals coordinate covalent bonds with protein side chain nucleophiles
mechanism of toxicity in of heavy metals
enzyme inhibition


alteration of membrane structure
treatment of heavy metal toxicity
give chelating agent to complex with free metal ions.
this promotes dissociation of metals from intracellular macromolecules.
chelating agents
chelating agents
-treats mercury poisoning
-treats lead poisoning (Ca-Na2-EDTA)

better at preventing binding to sulfhydryl groups than reactivating them.
treat Cu++ toxicity (Wilsons disease)

treats mercury and lead poisoning
rheumatoid arthritis (uncertain mechanism) and cystinuria)
treat children with elevated blood lead levels

mercury poisoning
useful to metals more tightly bound than Ca++

treats lead intoxification

not useful for mercury toxicity
Ca Na2-EDTA is not useful to treat
mercury toxicity
treats acute iron intoxication, chronic iron overload, possible use for Al+++chelation in dialysis patients
narcotics (opiates)
nerve gas/insecticides
nerve gas/insecticides
digoxin Fab (digibind)
oral anticoagulants
vitamin K analogs
methanol,ethylene glycol
ethanol, 4-methylpyrazole
iron salts
arsenic, gold, mercury
lead (also mercury)
succimer, Ca(Na)2EDTA
copper, lead, gold, mercury
carbon monoxide
methylene blue