Medical Toxicology III

jmanderson's version from 2016-03-12 00:50

envenomation toxins


Question Answer
what are the poison snakes in the US?Pit vipers (rattlesnakes, copperheads, and cottonmouths)
T/F: when treating pit viper bites, you keep calm and seek medical care, antivenom is 99% effective if administered with 2 hours and apply a tourniquet.FALSE, do NOT apply a tourniquet
antidote for pit viper bitesAntivenin (Crotalidae) polyvalent immune Fab (CRO-FAB)
A person comes in with extreme pain, N&V, fever, dizziness, headache, numbness, tingling and sweating from PTEROIS venom, what animal stung them?lionfish
A person comes in with erythema, burning pain, hypersensitivity and inflammation from CNIDARIAN VENOM, what animal stung them?Venomous cnidarian (jellyfish)
Tx jellyfish sting?rinse w/ sea-water or vinegar, soak in hot water, use hydrocortisone or diphenhydramine for itching
T/F: the antidote for brown recluse bites is antiveninFALSE, there is no antidote for brown recluse
black widow mechanism of toxicity and treatmentLATROXIN, causes pore formation in presynaptic nerve terminals increasing intracellular Ca2+ and neurotransmitter release => treat with ANTIVENIN
mechanism of toxicity of pit viper bitesCROTALIDAE venom => Local; severe pain, bruising and swelling. Systemic; N&V, muscle fasciculations, paralysis and COAGULOPATHY

environmental toxins


Question Answer
carbon monoxide mechanism of toxicityBinds to the oxygen-binding site on hemoglobin with a ~200-250 times greater affinity than oxygen forming CARBOXYHEMGLOBIN (causing hypoxia)
source of carbon monoxide poisoningbyproducts of incomplete combustion (car exhaust, residential, fire)
leading cause of poising in US?carbon monoxide
carbon monoxide toxicity clinical featuresComa, metabolic acidosis, retinal hemorrhages
carbon monoxide toxicity antidote100% oxygen
cyanide mechanism of toxicityhigh affinity for CYTOCHROME C OXIDASE (cellular hypoxia and lactic acidosis), high affinity for METHEMOGLOBIN forming CYANMETHEMOGLOBIN
cyanide toxicity clinical featuresBITTER ALMOND ODOR, seizures, coma, abnormal ECG
cyanide toxicity antidote1st sodium nitrite or inhaled amyl nitrate => 2nd sodium thiosulfate or Hydroxocobalamin
MOA sodium nitriteregenerate active cytochromes and oxidize hemoglobin to the more cyanide-reactive METHEMOGLOBIN (forming cyanmethemoglobin)
MOA sodium thiosulfateconverts cyanomethemoglobin to the more easily excreted THIOCYANATE ion

drug toxicities 1


Question Answer
acetaminophen mechanism of toxicityoxidation of CYP2E1 forms of N-acetyl-p-benzoquinoneimine (NAPQI) => glutathione depletion, mitochondrial damage
chronic alcohol use will increase toxicity of acetaminophen by inducing …….CYP2E1
acetaminophen toxicity clinical featuresMild anorexia, nausea, vomiting, delayed jaundice, hepatic and renal failure, RUQ tenderness (MOST COMMON SIGN)
most common sign of acetaminophen toxicity (occurs 1—2 days in)?RUQ tenderness
acetaminophen toxicity antidoteN-acetylcysteine (NAC)
what time frame are blood levels useful when monitoring acetaminophen OD severity?after 4 hours, before 24 hours
what population is ASA contraindicated in and why?Contraindicated in children with viral infections: REYE’S SYNDROME (an often fatal, fulminating hepatitis with cerebral edema)
what type of kinetics does ASA have at LOW doses?FIRST-order (rate of elimination is proportional to the drug concentration => higher concentration = faster elimination)
what type of kinetics does ASA have at HIGH doses?ZERO-order (constant amount of the drug is eliminated per unit time)
alicylates (ASA) toxicity clinical featuresConfusion, lethargy, coma, seizures, hyperventilation, hyperthermia, dehydration, hypokalemia, anion gap metabolic acidosis, TINNITUS
alicylates (ASA) toxicity antidoteSODIUM BICARBONATE (correct metabolic acidosis and alkalinize urine to increase excretion), HEMODIALYSIS
anticholinergic toxicity clinical featuresFlushed skin, anhidrosis, blurred vision, confusion, delirium tachycardia, mydriasis, dry mouth, urinary retention, decreased GI motility and coma
anticholinergic toxicity antidotePhysostigmine (CAN GET INTO THE BRAIN)
BBs toxicity clinical featuresBradycardia, hypotension, cardiac conduction block and seizures
BBs toxicity antidoteGlucagon (increases inotropy and chronotropy of heart)
digitalis toxicity clinical featuresVomiting, hyperkalemia (hypokalemia may increase toxicity), sinus bradycardia, AV block, atrial tachycardia, ventricular arrhythmia and ventricular tachycardia
digitalis toxicity antidoteAnti-digitalis Fab fragment (DigiFab), normalize potassium, lidocaine, magnesium
opioid toxicity clinical featuresPinpoint pupils, respiratory depression, bradycardia, hypotension, hypothermia, nausea, vomiting, sedation and coma
opioid toxicity antidoteNaloxone, naltrexone

drug toxicities 2


Question Answer
benzo toxicity clinical featuresRespiratory depression, hypotension, hypothermia, stupor and coma
benzo toxicity antidoteFlumazenil
TCA toxicity clinical featuresAnticholinergic, sedation, hypotension, cardiotoxicity, conduction blockade, QRS interval widening, ventricular tachycardia and arrhythmias
TCA toxicity antidoteNaHCO3, manage seizures, hyperthermia and arrhythmia
heparin toxicity clinical featuresHemorrhage, thrombocytopenia and hyperkalemia
heparin toxicity antidoteProtamine
warfarin toxicity clinical featuresHemorrhage, hemoptysis, excessive bruising, blood in the urine and stool
warfarin toxicity antidoteFresh frozen plasma (FFP), vitamin K (phytonadione)
tPA toxicity clinical featuresHemorrhage
tPA toxicity antidoteAminocaproic acid
theophylline toxicity clinical featuresTachycardia, hypotension, hypokalemia , tremor, vomiting, hyperglycemia and seizures
theophylline toxicity antidoteβ-blockers

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