Toxicology Flashcards

1
Q

Initial eval of pt presenting w/ overdose?

A
  • 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
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2
Q

Triad of opioid overdose?

A
  • CNS depression
  • miosis
  • respiratory depression
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3
Q

When should emesis be induced?

A
  • 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
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4
Q

When is a gastric lavage done?

A
  • 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
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5
Q

Use of activated charcoal in decontamination?

A
  • 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
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6
Q

When is whole bowel irrigation useful?

A
  • w/ sustained release and enteric coated tabs

- golytely 1-2 L/hr until rectal effluent is clear

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7
Q

Lab studies for toxicology?

A
  • 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
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8
Q

1st order kinetics?

A
  • fixed percentage of toxin is removed per unit time (barbs)
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9
Q

zero order kinetics?

A
  • 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
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10
Q

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

A
  • dialysis or diuresis
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11
Q

Use of hemodialysis?

A
  • 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
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12
Q

When is hemoperfusion preferred?

A
  • 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
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13
Q

Hemoperfusion is useful for what drugs?

A

TRI PEP-TD

  • Tricyc antidepressants
  • paraquat
  • ethchlorvynol
  • phenobarbital
  • theophylline
  • digitoxin
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14
Q

Antidotes for common ODs?

A
  • 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
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15
Q

Most common cause of change in osmolar gap?

A
  • ethanol
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16
Q

What occurs in APAP overdose?

A
  • 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
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17
Q

Tx of APAP overdose?

A
  • 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
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18
Q

Effects of cocaine/amphetamines?

A
  • 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
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19
Q

Sxs of cocaine overdoses?

A
  • euphoria
  • excitement
  • restlessness
  • toxic psychosis
  • seizures
  • HTN
  • tachycardia
  • hyperthermia
  • possible MI (prinzmental angina)
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20
Q

Dx and Tx of cocaine/amphetamine overdose?

A
  • dx: sig toxicity will always have sxs, short half lives and peak effects occur w/in 12 hrs
    -tx:
    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)
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21
Q

Anticholinergics that are used? Sxs?

A
  • 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

-sxs:
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

22
Q

Tx of OD of anticholinergics?

A
  • 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
23
Q

MOA of anticoags and OD?

A
  • 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
24
Q

S/S of anticoag toxicity?

A
  • ecchymosis
  • hematuria
  • uterine bleeding
  • melena
  • epistaxis
  • gingival bleeding
  • hemoptysis
  • hematemesis
25
Q

Tx of anticoag toxicity?

A
  • 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!
26
Q

Where is arsenic found?

A
  • 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
27
Q

S/S of acute arsenic ingestion?

A
  • 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
28
Q

S/S of chronic arsenic ingestion?

A
  • peripheral and sensory neuropathy, malaise, anorexia, alopecia, anemia, stomatitis
29
Q

S/S of arsine gas inhalation?

A
  • highly toxic and causes rapid intravascular hemolysis and renal failure
  • other sxs: usually not seen due to speed of onset of acute sxs
30
Q

Tx of arsenic toxicity?

A
  • 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
31
Q

Most likely hx of CO poisoning?

A
  • in winter, has poorly fxning heating system

- wake up in morning w/ HAs and is tired, and then feels better at work

32
Q

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

A
  • 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
33
Q

Testing for pts w/ CO poisoning?

A
  • 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
34
Q

S/S of CO poisoning?

A
  • high O2 extracting organs (heart/brain) quickly become dysfxnl form CO intoxication
    Sxs:
  • 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
35
Q

Indications for referral to HBO for CO poisoning?

A
  • 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)
36
Q

Digitalis toxicity can come from?

A
  • 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
37
Q

S/S of digitalis toxicity?

A
  • 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
38
Q

Tx of digitalis toxicity?

A
  • 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
39
Q

Sxs of ethanol toxicity? Tx?

A
  • 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
40
Q

Mushroom toxicity - sxs?

A
  • 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
41
Q

MOA of opiates?

A
  • 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
42
Q

S/S of opiate toxicity?

A
  • 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
43
Q

Tx of opiate OD?

A
  • 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
44
Q

Where are organophosphates found? MOA?

A
  • 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
45
Q

What does the mnemonic DUMBELS stand for? Sxs?

A

DUMBELS:

  • 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
46
Q

Tx of organophosphate toxicity?

A
  • 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
47
Q

MOA of PCP?

A
  • 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
48
Q

Sxs of PCP toxicity? Tx?

A
  • 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
49
Q

Major tricyclics used? MOA?

A
  • 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
50
Q

Sxs of TCA toxicity?

A

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

51
Q

What are the 3 Cs of tricyclic toxicity?

A
  • 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

52
Q

Tx of TCA toxicity?

A
  • 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