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75 Cards in this Set

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what are the most common ingestants in the US
Analgesics: APAP, salicylates, NSAIDS.
what are the most common fatal OD in the US
Sedative/hypnotics/antipsychotics
what are the forms of toxic reaction mechanisms
1. affect the acquisition of or utilization of oxygen (e.g. hydrogen sulfid or CO or methemoglobin forms)
2. if it affects oxygen, is this effect mediated locally (e.g. simple asphyxiant like methane displacing alveolar oxygen) or does it affect systemic processes (HCN)
3. toxin depletes glucose or other essential substrates
4. cause cellular injury via free radical formation and lipid peroxidation (e.g. acetaminophen forming a reactive elctrophile NAPQI)
5. does the toxin result in formation of a metabolite that is more toxic than parent compound (ethylene glycol to glycolic acid or methanol to formic acid)
6. does the toxin reveal an underlying metabolic or enzymatic defect (G-6-PD)
how does APAP cause damage
forms NAPQI via CYP2E1 which is detoxified endogenoously by scavenger of glutathione (binds to glutathione sulfur). in OD glutathione reserves are depleted and the toxic metabolite binds to hepatic macromolecules. main site of organ injury is the liver.
what is the antidote for APAP
NAC (N-acetylcysteine) promotes additional glutathione synthesis and may offer a substitute target for NAPQI
what is methemoglobinemia
Fe3+ hemoglobin formed from oxidizing Fe2+ state Hb
what is the antidote for methemoglobinemia
methylen blue is an antidote that reduces methemoglobin back to functional Hb. but b/c methylene blue needs to be reduced by NADPH which is made by G6PD, the antidote doesn't work for people with a G6PD deficiency
what are methemoglobin formers
numerous agents, mainly organic nitrite and nitrate compounds
what's bad about Gyromitra mushrooms
hydrazines in mushrooms inhibiti pyridoxing phosphokinase = no pyridoxine for GABA channel synthesis = seizures
what's the gyromitra mushroom cure
pyridoxine vit B6 antidote. (hydrazines in mushrooms inhibit pyridoxine phosphokinase = no pyridoxine for GABA channel synthesis = seizures)
what does INH OD do
INH inhibits pyridoxine phosphokinase = no pyridoxine for GABA channel synthesis = seizures
INH OD antidote
pyridoxine vit B6. INH inhibits pyridoxine phosphokinase = no pyridoxine for GABA channel synthesis = seizures
what is the most common cause of drug-induced seizures
alcohol (ethanol) withdrawal (others causes include cocaine, MDMA, INH)
how do you treat alcohol seizure withdrawal
thiamine then dextrose
MOA for black widow spider venom
black widow aka latrodectus spider = alpha latrotoxin which binds to presynaptic cation channel = opens them = influx= ACh release. reuptake is also inhibited
crotalinae (pit vipers) and elapidae (coral snakes) venom MOA
inhibit ACh release same as botulinum toxin
botulinum toxin MOA
cleaves vesicle attachment proteins = inhibit ACh release
Neuroleptic malignant syndrome major criteria
DA antagonism is MOA
1. recent use of antipsychotic drug or other DA alterer
2. fever w/o any other cause
3. muscle rigidity
4. elevated CK (muscle fiber damage)
5. autonomic instability (2 or more of sweating, tachycardia, elevated or depressed BP)
drugs that cause NMS
DA antagonism. recent use of antipsychotic drug or other DA alterer. ziprasidone, haloperidol, fluphenazine
Serotonin syndrome criteria
1. cog/behav: confusion, disorientation, agitation, coma
2. autonomic dysfunction: hyperthermia, diaphoresis (too much sweat), tachycardia, tachypnea
3. neuromuscular: myoclonus, hyperreflexion, muscle rigidity, tremors
what causes serotonin syndrome
SSRI + MAOI
SSRI + dextromethorphan
paroxetine + meperidine (demerol, an opioid analgesic drug
SSRI + CAD
SSRI (e.g. venlafaxine which is a very potent SSRI))
what are two things that cause hair loss
radiation and thallium can cause alopecia
what causes miosis
opiates/opioids and organophosphate insecticides
what causes mydriasis
anticholinergics, cocaine and amphetamines. (cocaine blocks reuptake of NE, amphetamines cause NE release)
what are some things that case bradycardia
calcium channel antagonist OD, beta-blocker OD, organophosphate insecticide
bradycardia is a a part of the chlinergic toxidrome
cholinergic toxidrome mechanism and symptoms
too much ACh. DUMBBBBEL
diarrhea, urination , miosi, bradycardia, bronchorrhea, bronchoconstriction, bradynea, emesis (vomiting), lacrimation
you can die from the Bs
what is the antidote for the cholinergic toxidrome
atropine, muscarinic antagonist which treats bradycardia from any cause cause it stops vagal influence on SA node
what can tachycardia be caused by
amphetamines, cocaine, and other sympathomimetics and tricyclic antidepressantts
how do tricyclic antidepressants cause tachycardia
poison sodium channel causing wide QRS (widened ro delayed depolarization) on ECG and also poison the K channel leading to QTc prolongation (prolonged repolarization)
what is the anticholinergic toxidrome
dry as a bone( dry mouth & skin); red as a beet (flushed skin); blind as a bat (dilated pupils and loss of accommodation); mad as a hatter (central anticholinergic mania); hot as hades (hot, dry skin less able to release heat); full as a flask (urinary retention and full bladder)
what is the antidote for anticholinergic toxidrome
pysostigmine salicylate which crosses BBB and is a reversible acetylcholinesterase inhibitor.
what are some untoward effects of physostigmine salicylate
may induce arhythmias so administer slowly and put on heart monitor. short duration of action = may have to readminister. should not be used with TC antidep OD because can cause lethal arrhythmias
what causes cholinergic toxidrome
organophosphate can cause it
what is the opiate toxidrome
pinpoint pupils (miosis), respiratory depression, CNS depression
what is opiate toxidrome caused by
opiates like heroin, codeine, diphenoxylate, propoxyphone
what is opiate toxidrome antidote
naloxone.
activated charcoal indication
no data that says that helps poisoing. don't give to person wwho can't protect their own airway.
what are some causes of anion gap metabolic acidosis
M (methanol); U (uremia); D (diabetic ketoacidosis (also alcoholic)); P (Phenols); I (iron, INH, inborn errors, inhaled solvents (toluene); L (lactic acidosis from shock, sepsis, etc, E (ethylen glycol, ethanol), S (salicylates)
what is anion gap formula
Na - (Cl- + CO2); normal is 14. if higher than 1 this means there are too many anions floating around in the blood
what is osmolarity formula
2Na + BUN/2.8 + BS/18. this is the calculated osm. what the person should have
what is osmolar gap
its used to estimate blood level of toxin that exerts osmotic force (ie how much drug is in the blood). osmolar gap = [measured osm]-[calculated osm]
how do you use osmolar gap to estimate the drug concentrations in a patient's blood
Level (mg/dL) = osmolar gap x MW/10
what can cause false positive THC
efavirenz
what can cause false positive amphetamines
sympathomimetics like cold medicine
what can cause false positive PCP
diphenydramine
what is acetaminophen metabolism like
metabolized mostly by glucoronidation and sulfation but the minor metabolic pathway via CYP2E1 forms the toxic metabolite
are salicylates easily dialyzable?
yes b/c MW less than 500 and Vd is low
what is the MOA of salicylate OD
interfere with kreb cycle = limit ATP production; affect proton porter function in mitochondria b/c they uncouple oxphos in OD (=hyperpyrexia). form organic acids = anion-gap metabolic acidosis.
what is iron OD overdose
deferoxamine mesylate chelates iron
what is iron MOA
when free in the blood it catalyzes redox reaction causing lipid peroxidation + free radical formation
what does deferoxamine do to you adverse effect?
vin rose color urine. chronic use has high frequency hearing loss, visual loss as well as yersinia sepsis and mucormycosis (fungal infection)
what are some neural tube defect causes
carbamazepine (CBZ) and valproic acid (VPA) can lead to neural tube defects so theya re teratogenic
what does digoxin MOA
works on Na+/K+ ATPase pump and poisons it in OD thus leading to hyperkalemia
what is used as a digoxin antidote
Fab antibody can be used as an antidote
what does beta-blocker OD do
it can cause bradycardia, hypotension, and low blood glucose
how do you treat beta-blocker OD
glucagon which bypasses blocked beta receptor to increase cyclic AMP which enhances calcium flux thru calcium channels and increases the rate and strength of myocardial contraction. treats hypoglycemia because it stimulates heaptic gluconeogenesis and glycogenolysis
what is methanol's OD MOA?
formic acid
what is methanol OD cure?
formic acid formation can be prevented by inhibiting ADH with fomepizole or ethanol. prevents formation of toxic metabolites thus buying time while the parent molecule is excreted unchanged or removed by hemodialysis
what is ethylene glycol's MOA
forms toxic metabolite glycolic acid, glycoxylic acid and oxalic acids =severe metabolic acidosis and renal toxicity. oxalate complexes wtih serum and tissue calcium = hypocalceia
ethylene glycol antidote
glycolic acid formation can be prevented by inhibiting ADH with fomepizole or ethanol. prevents formation of toxic metabolites thus buying time while the parent molecule is excreted unchanged or removed by hemodialysis
what does isopropanol cause
it cause ketosis not metabolic acidosis. alcohol dehydrogenase makes acetone from isopropanol. acetone and increasing ketosis.
wwhat makes you at risk for aspiration pneumonitis
aliphatic hydrocarbons.
what makes you at risk for leukemia
aromatic hydrocarbons
what does toluene cause
distal renal tubular acidosis and brain atrophy
what is CO MOA
hypoxia via interfering with Hb function
what is CN mechanism
hypoxia from poisoning cytochromes
what is cyanide #1 choice antidote
hydroxocobalamin whihc attracts cyanide to form cyanocobalamin
how do you treat snakebites
Fab antivenom
what do brown recluse spider bites cause
loxoscleles are dermonnecrotic
what quality does lionfish marine toxin have
heat labile
what does ciguatera poisoning lead to
cold-hot temperature sensation reverseal
what is the MOA of most mushroom fatalities in north america
cyclopeptide species such as amantin phalloides have amanitin toxin which inhibits RNA polymerase II leading to decrease in mRNA and protein transcription leading to cell death
what are the most common pathogens for food poisoning
staphylococci, campylobacter, and salmonella.
what food poisoning is especially toxic
E. coli 0157:H7 can cause hemolytic uremic syndrome which is due to verotxoin causing blood vessel damage, hemolysis and kidney failure
what is botulism classic dx criteria
descending paralysis; classic emg finidng is brief, small, abundant motor unit action potentials after repetitive stimulation