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Block 11 - Multisystems > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What substances are used in the general management of poisoning?

A

DON’T

dextrose, O2, naloxone, thiamine

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2
Q

What is the role of dextrose in the management of poisoning?

A

increases blood sugar, b/c hypoglycemia can cause coma or stupor = empirical treatment

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3
Q

What is the role of oxygen in the management of poisoning?

A

continuously assess airway since ongoing absorption of poison can disrupt consciousness
pulse ox not accurate if CO poisoning or methemoglobinemia - use cooximetry

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4
Q

What is the role of naloxone in the management of poisoning?

A

give just enough to reverse resp dep (.2 mg intervals)
may limit to pts w RR less than 12, mitotic pupils, and circumstantial evidence of opioid abuse
beware of withdrawal

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5
Q

What is the role of thiamine in the management of poisoning?

A

100 mg IVP for anyone w altered mental status with signs of Wernicke’s, malnourishment, hx of alcoholism, prolonged vomiting, chronically ill
IV thiamine is safe - only 1% with AEs

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6
Q

What is ipecac?

A

syrup for decontamination - proven to be ineffective
AE of lethargy can be confused w poison’s effects, complicating dx
may delay or reduce effectiveness of other treatments
acts locally by irritating gastric mucosa and centrally to stimulate medullary chemoreceptor trigger zone - but vomiting doesn’t guarantee removal of poison

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7
Q

What is the role of gastric lavage in decontamination?

A

current lit suggests not a lot or only w/i one hour but research is flawed
truth: consider for anyone w massive ingestions, early presentation, severely ill w/o antecedent vomiting, substances not bound to charcoal, if pts ingested substance that delays gastric emptying or forms bezoar

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8
Q

What are substances not bound to charcoal?

A 
mnemonic is CHARCOAL
caustics/corrosives
heavy metals
alcohol
rapid onset/absorption (CN, liquids)
chlorine, iodine
others (insoluble in tablet form or bezoar)
aliphatics
laxatives, lithium
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9
Q

What are toxins that form bezoars?

A 
mnemonic = BIGMESS
barbiturates
iron
glutethamide
meprobamate
enteric coated tablets
salicylates
sustained release products
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10
Q

What are the pros and cons of giving activated charcoal for decontamination?

A

pros: superior to ipecac-induced emesis and gastric lavage at preventing absorption in volunteer studies
cons: some drugs not bound to it, severe complications inc aspiration
uncertainties: many overdose cases involve inaccurate hx

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11
Q

What are the recommendations for giving activated charcoal for decontamination?

A

give to most oral drug overdoses
exceptions = drug not bound to AC, child ingestion of small amount and known entity, known benign ingestion, risk of aspiration, drug already absorbed (greater than 2 hrs for most)

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12
Q

What is multiple dose activated charcoal?

A

select group w enteroenteric or enterohepatic re-circulation - phenobarbitol, cbzp, theophylline, ASA, dapsone and quinine
caution: aspiration, ileus, obstipation, and electrolyte abnormalities from multiple dose sorbitol admin

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13
Q

What is the role of whole bowel irrigation in decontamination?

A

admin of 2L/hr in adults, 0.5 L/hr in child of PEG-ELS solution via NGT to flush out GI tract
given to body packers: pts who ingested sustained release preps (theophylline, verapamil, bupropion)
pts who ingested substances that form bezoars (iron, lead, large amts ASA)

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14
Q

What are toxidromes?

A

collection of symptoms characteristic for specific agent groups
management of any toxidrome is same regardless of agent

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15
Q

What are the different toxidromes?

A

sympathomimetic, anticholinergic, cholinergic, opioid, sedative-hypnotic

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16
Q

What are the symptoms of anticholinergic and sympathomimetic toxidromes and how can you tell the difference between them?

A

both have increased HR and BP and pupil size, agitated mental status, hyperthermia
anticholinergic only has hypoactive bowel sounds and possible increased bladder size
anticholinergic has dry skin, sympathomimetic has wet

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17
Q

What is the opioid toxidrome?

A

depressed mental status, miosis, decreased respirations

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18
Q

What is the cholinergic toxidrome?

A 
muscarinic = DUMBELS = diarrhea, urination, miosis, bronchorrhea, emesis, lacrimation, salivation
nicotinic = days of the week = mydriasis, tremor, weak, HTN, fasciculations
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19
Q

What is the sedative hypnotic toxidrome?

A

mental status depression

rarely bradypnea, hypotension, ataxia, hyporeflexia

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20
Q

What is the salicylates toxidrome?

A

SOB, increased breathing, N/V, tinnitus/hearing changes, diaphoresis, dizzy, respiratory alkalosis w metabolic acidosis

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21
Q

What are the principles of absorption in toxicology?

A

usually first order kinetics = concentration dependent
decreased by charcoal, gastric emptying, catharsis, WBI
faster if liquid form, non-ionized, small molecular size

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22
Q

What is the antidote for acetaminophen poisoning and how is it delivered?

A

N-acetyl cysteine

orally! - want first pass to concentrate it in the liver

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23
Q

What are factors affecting drug distribution?

A

protein binding, size, lipophilicity

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24
Q

What are examples of small and large volume of distributions?

A

small is less than 1 L/kg (water, stays in IV space and interstitium)
large is greater than 3-4 L/kg (lipids, enter cells), not in plasma and not amenable to being removed by hemodialysis

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25
Q

Where are most drugs metabolized?

A

liver

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26
Q

Wat are the different metabolism kinetics?

A

first order: steady fraction removed per unit time, enzymes not saturated, complete after 5 half lives
zero order: steady absolute amt removed per unit time, enzyme saturated
michaelis-menton: rate of elimination varies w drug concentration, high concentrations saturates enzyme and causes zero order, opposite at lower concentrations

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27
Q

What is important about the metabolism of acetaminophen?

A

small amt metabolized to NAPQ1 = hepatotoxic
glutathione = sulfur donor key to elimination of this
NAC is a sulfur donor = antidote

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28
Q

Where are most drugs eliminated?

A

renal

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29
Q

What is clearance?

A

removal of drug from plasma per unit time

blood flow important to clearance rate

30
Q

What can enhance elimination?

A

alkaline diuresis - urine pH to 8 increases excretion of weak acids like phenobarbital and aspirin
acid diuresis - excretion of weak bases like amphetamine, rarely used b/c of acute renal failure
hemodialysis
pulse doses of activated charcoal for some drugs

31
Q

What are indications for enhanced elimination of poisons?

A

drug has small volume of distribution
metabolites, if toxic, must also be removed
supportive care measures not sufficient
toxicity must be reversible and plasma concentration-dependent

32
Q

What are the ideal agents for hemodialysis?

A

small volume of distribution, low molecular weight, low protein binding
methanol, salicylate, ethylene glycol, lithium ion

33
Q

What is the clinical presentation of acetaminophen overdose? How is it treated?

A

maybe no acute symptoms, maybe depression, N/V
3-8 days later - fulminant hepatic failure w centrolobular necrosis - level 4 hrs after ingestion determines risk on nomogram
need to replenish glutathione stores - oral or IV NAC

34
Q

What are the pharmacokinetics of acetaminophen?

A

rapid absorption, charcoal important, small volume of distribution may allow for dialysis, longer half life in overdose

35
Q

What are indications for different levels of treatment of acetaminophen toxicity?

A

if PT greater than number of hrs from time of ingestion - transplant likely
no LFT elevation 36 hrs out - unlikely to develop toxicity - just use NAC

36
Q

What are the different forms of NAC that can be used?

A

IV = acetadote - FDA approved but more expensive

new oral regimen - treat for 36 hrs from ingestion and stop if no evidence of liver injury (normal LFTs)

37
Q

What types of patients are more sensitive to acetaminophen poisoning?

A

pts w induced cytochrome p450 2E1 - alcohol, cbzp, dilantin, isoniazid, phenobarbital
pts w reduced glutathione stores - malnutrition, wasting

38
Q

When can the acetaminophen nomogram not be used?

A

time of ingestion unknown
pt is detoxing from alcohol or routinely takes isoniazid or anticonvulsants
ER tylenol or coingestion of drugs that delay gastric emptying - do two APAP levels

39
Q

How is salicylate toxicity assessed?

A

must assess level and clinical symptoms at same time
level drawn from blood - if decreasing could be due to renal elimination OR movement into central compartments (CNS) which means pts actually getting worse

40
Q

What is the treatment of salicylate toxicity?

A

charcoal decreases absorption - repeated doses for delayed absorption
distribution not a target
metabolism and elimination: MDAC, ion trapping w sodium bicarb (alkalinize urine), hemodialysis
continue until all symptoms gone

41
Q

What are indications for hemodialysis w salicylate toxicity?

A

really ugly high levels
cerebral or pulmonary edema
persistent metabolic acidosis
*renal failure

42
Q

What are the different phases of iron intoxication?

A

phase 1: corrosive stage (30 min-2 hrs) - vomiting, diarrhea, ab pain, hematemesis, lethargy, shock, hypotension, metabolic acidosis
phase 2: recovery (2-24 hrs) - apparent recovery due to redistribution of iron into cells
phase 3: metabolic acidosis (12-48 hrs) - shock, coma
phase 4: hepatic (2-4 hrs) - hepatic necrosis, bleeding diathesis
phase 5: GI (2-4 wks) - gastric scarring, pyloric stenosis, achlorhydria, hepatic cirrhosis

43
Q

What is the assessment of pts w iron toxicity?

A

no GI symptoms make toxicity unlikely
radiograph may show tablets/bezoars
serum levels: draw 4-6 hrs after ingestion - 500-1000 associated w severe toxicity

44
Q

What is the most important prognostic indicator in pts w iron toxicity?

A

presence or absence of anion gap metabolic acidosis

45
Q

What are the pharmacokinetic considerations in iron toxicity management?

A

no metabolism

absorption: charcoal not helpful, bezoars are problem, WBI is key
distribution: chelation w deferoxamine must occur BEFORE movement into cells (once TIBC saturated)
elimination: IV deferoxamine, turns urine red - stop when symptoms better, acidosis resolved, urine clear

46
Q

What are the indications for use of deferoxamine in iron toxicity?

A

metabolic acidosis

vomiting, toxic appearance, levels greater than 500, signs of shock, hypotension, GI bleeding

47
Q

What is the presentation of CO poisoning?

A

non-specific, flu-like, looks like everything else - can be dangerous b/c hard to diagnose

48
Q

What is the pathophysiology of CO poisoning?

A

binds hemoglobin more avidly than oxygen
shifts oxygen dissociation curve to the left - decreases off loading of oxygen
causes myocardial depression
binds cytochrome oxidase in ETC - cells can’t use oxygen
all leads to hypoxia and metabolic acidosis

49
Q

What is the key to diagnosing CO toxicity?

A

carboxyhemoglobin level greater than 25%

but levels don’t always correlate w toxicity!

50
Q

What is the treatment of CO poisoning?

A

remove pt from exposure
distribution not a target
metabolism and elimination - hyperbaric oxygen therapy!

51
Q

What are indications for hyperbaric oxygen therapy in CO poisoning?

A

pregnant, coma, ischemia, neurologic deficits

may decrease neurologic sequelae but conflicting studies

52
Q

What are the forms of cyanide and how does it cause poisoning?

A

salt, hydrogen cyanide (gas, smoke)
small amount can kill you
stops cytochrome oxidase fxn - total body anaerobic metabolism, ischemia of everything, rapid severe metabolic acidosis

53
Q

What is the key for cyanide diagnosis?

A

arterial blood gas for acidosis - good and fast

54
Q

How does detox of cyanide work?

A

combo w sulfur to form thiocyanate

55
Q

What is the treatment of cyanide poisoning?

A

supportive care
absorption: if oral exposure, give charcoal
distribution not a target
metabolism and elimination: high flow oxygen, the cyanide kit = two nitrites (oxidize hemoglobin to methemoglobin which binds CN but can be toxic itself) and IV sodium thiosulfate

56
Q

What are the adverse effects with TCAs?

A

anticholinergic toxidrome
alpha-blocking activity –> hypotension
quinidine like effects = conduction disturbances
GABA inhibition –> seizure activity
think 3 C’s = coma, conduction, convulsions

57
Q

What EKG changes are seen with TCAs?

A

widened QRS, prominent S waves in leads I and aVL

R wave in lead aVR shows right axis tilt

58
Q

What are the key points to assessing TCA toxicity?

A

acute overdose happens VERY rapidly

use clinical symptoms and EKG - urine screens take too long

59
Q

What are the pharmacokinetic keys to treating TCA toxicity?

A

absorption: charcoal (not MDAC)
distribution: large volume of d - can’t be dialyzed, sodium bicarb may limit binding to Na channels

60
Q

What is the treatment of TCA toxicity?

A

maintain perfusion - treat cardiovascular effects - sodium bicarb in boluses until CV status stable then continuous infusion until QRS normalizes
benzos to aggressively treat seizures
NE for hypotension
NO physostigmine, flumazenil or class 1A antiarrhythmics

61
Q

What is an example of an amphetamine?

A

MDMA (ecstacy, XTC, the love drug) = mood enhancing

62
Q

What is the pharmacology of amphetamines?

A

based on phenylethylamine structure
readily absorbed across most membranes w rapid effects
weak bases

63
Q

What is the pathophysiology and clinical presentation of amphetamine toxicity?

A

alpha agonist, reuptake of neurotransmitter decreased –> sympathomimetic toxidrome and CNS stimulation
seretonin increased by mood enhancing only (ecstasy)
tachy and HTN, diaphoresis, irritable, tremor, bruxism, hyperacitivyt, confusion, chest pain, aggression, dehydration, mild hyperthermia, delirium, seizures, ventricular dysrhythmias, rhabdo, cerebral edema

64
Q

What are some effects of mood enhancing amphetamines?

A 
seretonin syndrome (rigidity, hyperreflexia, hyperprexia)
rebound phase of prolonged sleep and voracious eating
65
Q

What is the treatment of amphetamine toxicity?

A

charcoal if drug taken orally and its early
distribution and metabolism not treatment targets
elimination: urine alkalinization if rhabdo to decrease renal failure
IV fluids, agitation control (benzos, restraint), cooling measures

66
Q

What are the big 3 toxic alcohols?

A

ethylene glycol
isopropanol
methanol

67
Q

What is the clinical presentation of alcohol toxicity?

A

depends on alcohol and its metabolite
acetone –> CNS depression, gastritis, asphyxia
oxalic acid –> renal failure, severe acidosis
methanol, formic acid –> ocular toxicity, acidosis

68
Q

What is the assessment of alcohol toxicity?

A

H&P unreliable, manifest too late
anyone w severe anion gap metabolic acidosis w single digit sodium bicarb withOUT DKA considered to have EG or ME on board
isopropyl alcohol doesn’t cause acidosis
*osmolar gap coupled w anion gap raises suspicion
calcium oxalate crystals maybe from EG

69
Q

What are the pharmacokinetic considerations in treatment of alcohol toxicity?

A

rapidly absorbed, doesn’t bind charcoal
small Vd –> dialysis
folic acid - enhances metabolism in ME toxicity
thiamine, pyridoxine, Mg - enhance metabolism to less toxic metabolites of EG
competitive inhibition of alcohol dehydrogenase = Fomepizole

70
Q

Who gets fomepizole and who gets alcohol to treat poisoning?

A

fomepizole for anyone with: EG level more than 20, ME more than 10, hx of ingestion with greater than 5-10 osmolar gap, pH t have fomepizole

Block 11 - Multisystems (29 decks)

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