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Flashcards in Toxicology Deck (52)
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Initial eval of pt presenting w/ overdose?

- ABCs
- ABGs
- IV access
- tx coma promptly:
glucose,narcan, if ETOHism suspected: thiamine
- maintain circ: crystalloid, if that doesnt work: swan to check PCWP (worry about over hydration and pulm edema)
- tx seizures: diazepam, if fails: phenobarbital
- cardiac monitoring and pulse Ox


Triad of opioid overdose?

- CNS depression
- miosis
- respiratory depression


When should emesis be induced?

- only in pts w/ intact gag reflex
- may have limited efficacy if more than 1 hr since ingestion
- most useful if initiated at home w/in few minutes of ingestion
- not indicated in ED for drugs not absorbed by charcoal (iron, lithium)
- don't induce emesis if caustics or low viscosity hydrocarbons have been ingested
- don't induce if rapid acting convulsants have been ingested (amphetamine, cocaine, TCAs, strychnine)
- ipecac syrup 30 ml for adults, 15 ml for kids followed by 1-2 liters of water until they vomit


When is a gastric lavage done?

- suspected serious ingestions when emesis has failed
- pt is lethargic or otherwise uncooperative
- when gag reflexed is markedly depressed
- pts have ingested rapid acting convulsants
- place pt in L lateral decubitus position w/ head down (protect airway)
- use large bore NG or OG tube at least 36Fr
- use tap water or saline at body temp in 250ml increments and continue until fluid returns clear and free of pil fragments


Use of activated charcoal in decontamination?

- following emesis or lavage give 50-100g charcoal as slurry by mixing w/ equal amts of water
- can give b/f or after lavage/emesis: however need residual charcoal left in gut
- mix charcoal w/ sorbitol to improve taste and cathartic action
- charcoal has great adsorptive properties and binds most poisions (EXCEPT: potassium, alcohols, iron, lithium - PAIL)
- if ingested dose of poison known- give at least 10x that wt in activated charcoal


When is whole bowel irrigation useful?

- w/ sustained release and enteric coated tabs
- golytely 1-2 L/hr until rectal effluent is clear


Lab studies for toxicology?

- ABGs
- draw blood for chem 7 and calc anion and osmolar gap
- obtain EKG and monitor for wide QRS or prolonged QT
- CXR looking for pulmonary edema
- flat plate of abdomen looking for radiopaque pills (high false neg)
- urine for tox screen
- draw and hold serum tox screens


1st order kinetics?

- fixed percentage of toxin is removed per unit time (barbs)


zero order kinetics?

- fixed amt of toxin removed per unit time (alcohol)
- many times in OD situations - elimination pathways are saturated and drug which normally has 1st order kinetics develops zero order


toxins w/ large volumes of distribution (tissue bound not plasma bound) are not efficiently removed by?

- dialysis or diuresis


Use of hemodialysis?

- toxin must be relatively water soluble and not protein bound
- toxin is removed from blood into dialysate soln across semipermeable membrane
- drugs need to have small vol of distribution and slow rate of intrinsic clearance
- indicated for: MELS - methanol, ethylene glycol, lithium, and salicylate


When is hemoperfusion preferred?

- advantage over hemodialysis: drug or toxin is in direct contact w/ adsorbent material - quick, can be used w/ activated charcoal
- drugs need to have small vol of distribution and slow rate of intrinsic clearance
- high MW, poor water solubility, plasma binding proteins not limited factors
- commonly assoc w/ thrombocytopenia and won't correct lyte imbalances, or adjust pH


Hemoperfusion is useful for what drugs?

-Tricyc antidepressants
- paraquat
- ethchlorvynol
- phenobarbital
- theophylline
- digitoxin


Antidotes for common ODs?

- APAP: acetylcysteine
- anticholinergics: physostigmine (also tx myasthenia gravis)
- benzos: Flumazenil (danger - can cause seizures, is a GABA antagonist)
- cyanide: Na nitrate and Na thiosulfate
- methanol/polyeth glycol (antifreeze): ethanol
- narcotics: naloxone


Most common cause of change in osmolar gap?

- ethanol


What occurs in APAP overdose?

- active ingredient in many OTC preps
- tylenol w/ mixed ODs (lortab, vicodin, darvocet)
- one of metabolites are very hepatotoxic:
saturates glutathione detoxification system, accum in liver and causes delayed hepatotoxicity 24-72 hrs post ingestion
- toxic dose is over 140 mg/kg (lower in pt w/ chronic liver disease, or alcoholism)
- draw up an APAP level


Tx of APAP overdose?

- decontaminate and give activated charcoal
- est severity:
amt ingested, best level is 4 hrs post ingestion
- ***acetylcysteine therapy:
subs for glutathione and binds to metabolite
- 140 mg/kg orally of 10-20% soln and follow up w/ 70 mg/kg dose q 4-8 hrs or until tylenol level is 0
- key: must be given EARLY - don't wait for initialy level, must be given w/in 12-16 but preferably w/in 8-10 hrs


Effects of cocaine/amphetamines?

- all are CNS stim and cause sympathetic hyperactivity
- some may produce sig vasoconstriction and cause HTN and bradycardia
- HTN may be accompanied by ventricular arrhythmias
- seizure and hyperthermia may produce rhabdo and myoglobinuria


Sxs of cocaine overdoses?

- euphoria
- excitement
- restlessness
- toxic psychosis
- seizures
- tachycardia
- hyperthermia
- possible MI (prinzmental angina)


Dx and Tx of cocaine/amphetamine overdose?

- dx: sig toxicity will always have sxs, short half lives and peak effects occur w/in 12 hrs
GI decontamination as indicated, severe agitation or psychosis: diazepam - tx seizures, if DBP over 120 or HTN encephalopathy: nitroprusside
- if tachycardia/vent arrhythmias: BBs
- monitor temp and EKG - may need CT of head
- don't acidify urine: myogloburia and ARF (rhabdo)


Anticholinergics that are used? Sxs?

- atropine, scopolomine, belladona, many antihistamines, TCAs
- seen in plants: jumsonweed, nightshade, amanita muscaria mushrooms
- block cholinergic receptors both centrally and peripherally
- sig poisoning always has some

delerium, blurred vision, mydriasis, hallucinations, coma, dry mucous membranes, inhibition of sweating, hyperthermia, tachycardia
- hot as a hare, red as a beet, dry as a bone, blind as a bat and as mad as a hatter


Tx of OD of anticholinergics?

- supportive care
- GI decontamination
- physostigmine slowly IV (only reserved for severe sxs):
must have atropine ready, pt must be on cardiac monitor, ***never use w/ tricyclic overdose, asthma, or mechanical bowel or bladder obstruction
- peak effects may be delayed due to sig delayed gastric emptying and slowed peristalsis through GI


MOA of anticoags and OD?

- warfarin MC used
- super warfarins (brodifacoum and indanediones) commony rodenticides
- inhibit blood clotting by blocking vit K dependent clotting factors
- only synthesis of new clotting factors affected - may be seen 8-12 hrs after ingestion
- peak effects are not seen for 1-2 days due to long half life of other clotting factors (24-60 hrs)
- warfarin highly bound to albumin w/ half life of 35 hrs/metabolized by the liver
- super anticoag may produce severe bleeding disturbances for several weeks to months following single overdose


S/S of anticoag toxicity?

- ecchymosis
- hematuria
- uterine bleeding
- melena
- epistaxis
- gingival bleeding
- hemoptysis
- hematemesis


Tx of anticoag toxicity?

- supportive therapy/GI decontamination
- obtain baseline PT and repeat in 24-48 hrs, vita K 1-2 mg can restore clotting factors in 6-8 hrs, in emergency give FFP!


Where is arsenic found?

- insecticides, rodenticides, wood preservatives contain trivalent arsenic
- shellfish may contain pentavalent arsenic (less toxic) which can cause + urine arsenic level but not assoc w/ clinical toxicity
- highly toxic arsine gas is produced by burning arsenic containing ores and is used in electronic industry
- arsenic is well absorbed from resp and GI tract and avidly binds w/ tissue proteins and accum in tissues
- lethal doses of trivalent arsenic is about 100-200 mg in an adult


S/S of acute arsenic ingestion?

- crampy abd pain, vomiting, profuse watery diarrhea, burning mucosa, conjunctivitis, tremor and seizurse
- garlic odor may be on pts breath
- periorbital edema after 1-2 days


S/S of chronic arsenic ingestion?

- peripheral and sensory neuropathy, malaise, anorexia, alopecia, anemia, stomatitis


S/S of arsine gas inhalation?

- highly toxic and causes rapid intravascular hemolysis and renal failure
- other sxs: usually not seen due to speed of onset of acute sxs


Tx of arsenic toxicity?

- 24 hr urine aresnic levels most useful for monitoring response to chelation therapy, false + levels are possible from eating shellfish
- tx:
*acute ingestion: GI decontamination w/ lavage and charcoal, admin dimercaperaol (BAL) for 5 days
* chronic ingestion: penicillamine
* arsine gas inhalation: transfusion may be necessary and adequate hydration to prevent renal hemaglobin deposition
- chelation therapy is of no value in acute exposure to arsine gas


Most likely hx of CO poisoning?

- in winter, has poorly fxning heating system
- wake up in morning w/ HAs and is tired, and then feels better at work


Can pulse ox be used to access O2 in CO poisoning?

- no!! will be falsely high - binds to Hgb just like O2
- binds to Hgb 230-270x stronger than O2
binds w/ myoglobin 20-25x stronger than O2
- imposes chemical anemia in pt


Testing for pts w/ CO poisoning?

- minimal sxs: no loss of consciousness, awake and cooperative reqr minimal testing and therapy: COHgb level adn EKG
- pts w/ moderate to severe sxs: COHgb, ABG, chem 7, serum lactate, CBC, EKG, serum CK-MB, troponin, urine myoglobin, and CXR (any pt w/ persistent dyspnea)
- tx primarily 100% FiO2 for 4 hrs (half life of COHgb is 15 min w/ 100% FiO2 at 2.5 atm (HBO) or 60 min when breathing 100% FiO2


S/S of CO poisoning?

- high O2 extracting organs (heart/brain) quickly become dysfxnl form CO intoxication
- CNS: fatigue, malaise, flulike, nausea, confusion, loss of memory, emotional lability, dizziness, paresthesias, weakness, vomting, lethargy, somnolence, stroke, coma, seizures, resp arrest
- cardio: chest pain, myocardial ischemia, palpitations, dysrhythmias, poor cap refill, hypotension, cardia arrest
- more severe in pts w/ comorbidities of trauma, drug ingestion, burns, myocardial ischemia, cerebrovascular dz, or smoke inhalation


Indications for referral to HBO for CO poisoning?

- AMS or abnormal neuro exam
- hx of LOC or near-syncope
- hx of seizure
- coma
- hx of hypotension during or shortly after exposure
- myocardial ischemia
- hx of prolonged exposure
- preg w COHgb levels over 15%
- persistent acidosis (relative)
- concurrent thermal or chemical burns (relative)


Digitalis toxicity can come from?

- digoxin, digitoxin, foxglove, oleander, lily of the valley and some rodenticides
- all contain cardiac glycosides:
enhance cardiac contractilty, slow AV conduction, enhance automaticity
- digoxin: has large vol of distribution and half life of 40 hrs and is excreted unchanged in urine
- digitoxin: has small vol of distribution, highly protein bound, undergoes extensive enterohepatic recirculation: half life is 7 days


S/S of digitalis toxicity?

- anorexia, N/V/D, abd pain, blurred vision, color vision disturbance
- EKG shows toxic effects of 3rd degree AV block, bradycardia, ventricular ecotype, or paroxysmal atrial tachycardia w/ AV block
- acute ingestion of an overdose is often assoc w/ hyperkalemia
- all suspected ODs get admitted to monitored bed


Tx of digitalis toxicity?

- if hyperkalemia severe (over 7) tx but use glucose + insulin therapy and not NaHCO3+CaCl therapy (may kill pt)
- for sx brady, 2nd or 3rd degree AV block - give aropine many need pacer
- for ventricular ectopy: lidocaine
- avoid d/c countershock and only if absolutely necessary use lowest voltage possible
- dialysis or hemoperfusion is of no use in digoxin overdose due to large vol of distribution
- digitalis specific Fab frag abs (digibind) - indicated for any pt w/ severe arrhythmias or severe hyperkalemia
- toxicity reversed in 5-10 min and digitalis-digibind complex excreted in urine


Sxs of ethanol toxicity? Tx?

- CNS depressant
- metabolized by alcohol dehydrogenase (fixed rate, zero order kinetics)
- metabolized at rate of 7-10 g/hr
- sxs: ataxia, dysarthria, depressed sensorium, nystagmus
- tx is supportive
- watch BG as ETOH inhibits gluconeogenesis
- give thiamine 100 mg IM/IV to prevent wernickes


Mushroom toxicity - sxs?

- poisoning is baded on their toxins
- most are GI irritatns and cause mild GI sxs in most cases
- severe gastroenteritis, hepatic or renal failure
- muscarine: salivation, miosis, bradycardia, diarrhea (tx is atropine and supportive)
- Psilocybin: sxs are hallucinations
- ibotenic acid and muscimol - sxs: are anticholinergic - mydriasis, tachycardia, hyperpyreixa, delerium (Tx is supportive)

- most of these tx: are supportive


MOA of opiates?

- mult forms from propoxyphene (Darvon) - heroin. Dextromethorphan is a form that is overlooked
- act on CNS receptors causing sedation, hypotension, bradycardia, hypothermia, resp depression
- most have half life of 3-6 hrs except propoxyphene (12-15 hrs) and methadone (15-20 hrs)
*** opiate intoxication should be considered in any pt who is unconscious from unknown cause


S/S of opiate toxicity?

- pinpoint pupils
- dx confirmed w/ toxic levels of opiates are found in urine or if pt awakens w/ admin of naloxone IV
- clonidine overdose may appear identical to opiate overdose, but they won't respond to naloxone


Tx of opiate OD?

- tx: IV naloxone 0.2-2 mg repeate 3-4x if no response and opiate OD is suspected
- propoxyphene OD is particularly resistant to naloxone
- naloxone: half life only 1 hr and effects last only 2-3 hrs, need repeated doses!!
- acute withdrawal syndrome: may be precipitated in chronic opiate users, but not life threatening
- admit all who respond to naloxone unless it is a heroin overdose:
heroin overdose: can safely be d/c if they are asx 3 hrs after last naloxone dose


Where are organophosphates found? MOA?

- cholinesterase inhibitors found in may insectasides (carbamates) - weed sprayers, home insecticides, bug bombs, flea collars
- also used as chemical warfare: nerve agents
- VX nerve gas- most lethal chemical known to man
- MOA: inhibit cholinesterase, allowing accum of ACh at muscarinic and nicotinic receptors at neuromuscular junctions
- all organophosphates are rapidly absorbed from intact skin, GI tract and resp tract


What does the mnemonic DUMBELS stand for? Sxs?

- Diarrhea
- Urination
- Miosis
- Bronchospasms
- Excitation
- Lacrimation
- Salivation

- hyperactive bowel sounds, lethargy, muscle fasiculations, seizures
- may have profound bradycardia (muscarinic effect) or tachycardia (nicotinic effect)
- death is caused by respiratory arrest


Tx of organophosphate toxicity?

- initially: decontamination and aggressive airway management due to sig secretions and bronchospasms
- atropine IV in large doses
- Pralidoxime (2-PSM chloride): competitively inhibits binding of organophosphates to ACh



- AKA as crystal or angel dust
- smoked, snorted, ingested or injected
- sympathomimetic, hallucinogenic, dissociative agent
- rapid Onset of action when smoked or snorted: rarely serious overdose by this route as they self titrate
- ingestion of 20-25 mg PCP can cause serious intoxication
- very large vol of distribution w/ half life of several days, elim primarily by metabolism


Sxs of PCP toxicity? Tx?

- severe, paranoid, bizarre violent behavior or quiet stupor
- vertical and horizontal nystagmus (mult-direction), HTN, tachycardia, hyperthermia, marked muscle rigidity, dystonias, seizures
- tx: aimed at limiting seizures and violence using diazepam or haloperidol
- monitor and prevent rhabdo


Major tricyclics used? MOA?

- Amitriptyline (Elavil), imiparamine (Tofranil), Doxepin (Adapin, sinequan)
- maprotiline tetracycline antidepressant
- analongs of phenothiazines w/ complex effects: anticholinergic, alpha adrenergic receptor blocking, quinidine like activity on the heart
- well absorbed and very highly tissue bound, huge vol of distribution
- half lives: 10-30 hrs
- avg toxic dose: 5 mg/kg w/ severe poisoning at 10-20 mg/kg
- probably single worst OD to try to care for w/ absolute worst outcomes


Sxs of TCA toxicity?

Anticholinergic effect:
mydriasis, dry mouth, tachycardia, agitation, hallucinations
- onset of coma may be rapid
- frequently totally refractory seizures
- cardiac manifestations: most dramatic, life-threatening, and difficult to manage:
quinidine like slowing of conduction seen by widening of QRS more than 100 ms and prolong QT and PR intervals, varying degrees of AV block and V tach are common, Torsade de pointes may occur, profound hypotension due to decreased contractility and vasodilation occurs and is often cause of death
- dx usually based on hx, relevant PE findings, widening QRS and prolong QT


What are the 3 Cs of tricyclic toxicity?

- cardiac abnorm, convulsions and coma
- can confirm dx by quantitative serumassays but there is no clear correlation b/t drug level and severity of toxicity


Tx of TCA toxicity?

- critical!
- GI decontamination (don't induce emesis): emesis can precipitate seizures and coma, gastric lavage and instill charcoal
- ALL must have cont. cardiac monitoring
- tx seizures w/ diazepam or phenytoin (DON'T use physostigmine as some recommend - 80% chance of death)
- sinus tach usually benign (physostigmine and propranolol will worsen conduction abnormalities and should never be used)
- Vent. arrhythmias and conduction defects may respond to NaHCO3 (50-100 mEq IV):
lidocaine, phenytoin
- hypotension: NaHCO3 and crystalloid - if no response place swan to prevent iatrogenic pulm edema