Salicylates Flashcards
how do peak levels change in OD
normally peaks in 30ming in OD peaks 4-6hrs after very delayed
effervescent effect on absorption
pushes the agent into the small intestine where drug is always absorbed the most
effect of Vd in OD
normally small, increased
effect on protein binding in OD
normally high, decreases
how are salicylates eliminated
first order kinetics
5 pathways of metabolism
liver metabolism
renal elimination depends on urine pH
effect on half life in OD
increased from 2 to 18-26
bc changes to zero order kinetics - michealis menton
why does OD lead to decreased protein bindin and increased tissue binding
michalis menten
metabolism pathways become saturated
toxic doses
150-200 mg/kg = mild intoxication
300-500mg/kg = severe
500 = lethal
>100mg/kg/d for > 2d = chronic intoxication
severe toxicity in acut serum levels
> 90-100mg/dL
or >60 with acidosis and altered mental status?
chronic therapeutic values
10-30mg/dL
central stimulation of respiratory center causes
hyperventilation
respiratory alkalosis
dehydration
intracellular effects
interference with krebs cycle and uncoupling of oxidative phosphorylation - lactic acid accumulation
increased fatty acid metabolism
metabolic acidosis
hyper and then hypoglycemia
explain why hyper and hypo glycemia occur
first mobolizationof glycogen stores causes hyper then theres glycogen depletion and inhibition of gluconeogenesis
GI effects
hemorragic gastritis
renal effects
tubular damage
proteinuria
hepatic effect
salicylate induced hepatitis
ototoxicity
tinnitus
hearing loss
acute toxicity signs and symptoms
vomitng hyperpnea tinnitus lethargy mixed respiratory alkalosis and metabolic acidosis coma seizure hypoglycemia hyperthermia cerebral and pulmonary edema
characteristics of chronic toxicity
100mg/kg/d for 2 days elderly slow onset less severe appearance often misdiagnosed
chronic toxicity presentation
hearing loss and tinnitus NV dyspnea, hyperventialtion hyperthermia neurologic cerebral and pulmonary edema more common
acute vs chronic poisoning
acute is generally younger, intentional, easily recognized, suicidal, marke serum elevation, mortality uncommon, not many disease states
chronic opposite
lab tests for management
salicylate
ABG
electrolytes
possible interventions
gastric emptying activated charcoal sodium bicarb urinary alkalinization hemodialysis hemoperfusion MDAC continuous venovenous hemofiltration
can we use emesis
no cause cna have a coma or seizure
how to use sodium bicarb
correct metabolic acidemia bringing ph to 7.4
continuous titration over 4-8hrs
treat hypokalemia
indications for hemodialysis
acute ingestion serum levels higher than 100mg/dL with severe acidosis or other manifestations of toxicity
chronic intoxication serum levels >60mg/dL
renal failure
deterioration