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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
Where are most drugs metabolized?
liver
26
Wat are the different metabolism kinetics?
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
27
What is important about the metabolism of acetaminophen?
small amt metabolized to NAPQ1 = hepatotoxic glutathione = sulfur donor key to elimination of this NAC is a sulfur donor = antidote
28
Where are most drugs eliminated?
renal
29
What is clearance?
removal of drug from plasma per unit time | blood flow important to clearance rate
30
What can enhance elimination?
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
What are indications for enhanced elimination of poisons?
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
What are the ideal agents for hemodialysis?
small volume of distribution, low molecular weight, low protein binding methanol, salicylate, ethylene glycol, lithium ion
33
What is the clinical presentation of acetaminophen overdose? How is it treated?
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
What are the pharmacokinetics of acetaminophen?
rapid absorption, charcoal important, small volume of distribution may allow for dialysis, longer half life in overdose
35
What are indications for different levels of treatment of acetaminophen toxicity?
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
What are the different forms of NAC that can be used?
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
What types of patients are more sensitive to acetaminophen poisoning?
pts w induced cytochrome p450 2E1 - alcohol, cbzp, dilantin, isoniazid, phenobarbital pts w reduced glutathione stores - malnutrition, wasting
38
When can the acetaminophen nomogram not be used?
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
How is salicylate toxicity assessed?
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
What is the treatment of salicylate toxicity?
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
What are indications for hemodialysis w salicylate toxicity?
really ugly high levels cerebral or pulmonary edema persistent metabolic acidosis *renal failure
42
What are the different phases of iron intoxication?
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
What is the assessment of pts w iron toxicity?
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
What is the most important prognostic indicator in pts w iron toxicity?
presence or absence of anion gap metabolic acidosis
45
What are the pharmacokinetic considerations in iron toxicity management?
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
What are the indications for use of deferoxamine in iron toxicity?
metabolic acidosis | vomiting, toxic appearance, levels greater than 500, signs of shock, hypotension, GI bleeding
47
What is the presentation of CO poisoning?
non-specific, flu-like, looks like everything else - can be dangerous b/c hard to diagnose
48
What is the pathophysiology of CO poisoning?
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
What is the key to diagnosing CO toxicity?
carboxyhemoglobin level greater than 25% | but levels don't always correlate w toxicity!
50
What is the treatment of CO poisoning?
remove pt from exposure distribution not a target metabolism and elimination - hyperbaric oxygen therapy!
51
What are indications for hyperbaric oxygen therapy in CO poisoning?
pregnant, coma, ischemia, neurologic deficits | may decrease neurologic sequelae but conflicting studies
52
What are the forms of cyanide and how does it cause poisoning?
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
What is the key for cyanide diagnosis?
arterial blood gas for acidosis - good and fast
54
How does detox of cyanide work?
combo w sulfur to form thiocyanate
55
What is the treatment of cyanide poisoning?
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
What are the adverse effects with TCAs?
anticholinergic toxidrome alpha-blocking activity --> hypotension quinidine like effects = conduction disturbances GABA inhibition --> seizure activity think 3 C's = coma, conduction, convulsions
57
What EKG changes are seen with TCAs?
widened QRS, prominent S waves in leads I and aVL | R wave in lead aVR shows right axis tilt
58
What are the key points to assessing TCA toxicity?
acute overdose happens VERY rapidly | use clinical symptoms and EKG - urine screens take too long
59
What are the pharmacokinetic keys to treating TCA toxicity?
absorption: charcoal (not MDAC) distribution: large volume of d - can't be dialyzed, sodium bicarb may limit binding to Na channels
60
What is the treatment of TCA toxicity?
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
What is an example of an amphetamine?
MDMA (ecstacy, XTC, the love drug) = mood enhancing
62
What is the pharmacology of amphetamines?
based on phenylethylamine structure readily absorbed across most membranes w rapid effects weak bases
63
What is the pathophysiology and clinical presentation of amphetamine toxicity?
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
What are some effects of mood enhancing amphetamines?
``` seretonin syndrome (rigidity, hyperreflexia, hyperprexia) rebound phase of prolonged sleep and voracious eating ```
65
What is the treatment of amphetamine toxicity?
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
What are the big 3 toxic alcohols?
ethylene glycol isopropanol methanol
67
What is the clinical presentation of alcohol toxicity?
depends on alcohol and its metabolite acetone --> CNS depression, gastritis, asphyxia oxalic acid --> renal failure, severe acidosis methanol, formic acid --> ocular toxicity, acidosis
68
What is the assessment of alcohol toxicity?
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
What are the pharmacokinetic considerations in treatment of alcohol toxicity?
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
Who gets fomepizole and who gets alcohol to treat poisoning?
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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