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pharm unit 6 > Clinical Toxicology 1 and 2 > Flashcards

Clinical Toxicology 1 and 2 Flashcards

1
Q

Opioid toxidrome:

A
  1. altered mental status
  2. Vitals: decreased RR, slight decreases in HR, BP, temp;
  3. Pinpoint pupils
  4. Decreased bowel sounds
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2
Q

List some opioids

A
  1. Heroin (injected, ingested, smoked)
  2. Fentanyl (injected or ingested)
    Also codeine, hydrocodone, meperidine, oxycodone, methadone, buprinorphine (agonist/antagonist)
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3
Q

How to deal with opioid toxidrome:

A
  1. Remove obstructive process
  2. Assess and protect if necessary
  3. IV fluids in sick patients
  4. O2 100%
  5. Dextrose/thiamine (look for altered mental status with hypoglycemia); also think about thiamine
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4
Q

Naloxone properties; what is the possible withdrawal?:

A
  1. Comp mu, delta, kappa opioid receptor antagonist
  2. depressed RR best predicts response
  3. Higher doses required for SYNTHETIC opioids
  4. Could precipitate withdrawal IF TOLERANT!!
  5. Half life of 15 min;
    flu-like symptoms (N/V, diarrhea), piloerection, yawning, irritability, but NORMAL MENTAL STATUS (15-30 min)
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5
Q

Natural, semi-synthetic, and synthetic opioids:

A

Natural: morphine, codeine;
Semi-synthetic: heroin, hydromorphone, oxycodone
Synthetic: meperidine, methadone, fentanyl, also buprinorphine

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6
Q

Other opioid receptor antagonists and properties:

A

Nalmefene and naltrexone;

differ in pharmacokinetics, may produce a PROLONGED withdrawal state (N/V, piloerection/yawning)

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7
Q

Benzo toxidrome; benzo uses:

A
  1. DEPRESSED mental status
  2. NORMAL vitals
  3. Other sedative hypnotics can cause respiratory depression;
    benzo can treat toxins causing CNS stimulation and anticholinergic toxins
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8
Q

Some key sedative hypnotics:

A

Benzos: diazepam, lorazepam, midazolam, roofies (rohypnol)
gamma-hydroxybutyrate: chloral hydrate, methaqualone, etomidate, propofol, ethanol
Barbituates: phenobarbitol, amobarbital

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9
Q

Treatment of benzos:

A
  1. ABC’s, substrates
  2. supportive care
  3. consider FLUMAZENIL (comp non-selective benzodiazepine receptor antagonist)
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10
Q

Dangers of flumazenil:

A
  1. can precipitate acute withdrawal
  2. seizures possible in mixed OD
  3. not uniform in reversal of RD
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11
Q

For any person who tries to harm themselves, what should we do?

A

APAP (acetaminophen) level

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12
Q

For acetaminophen toxicity, what would you expect at each stage?

A

1: .5-24 hrs (asymp, or mild GI irritation)
2: 24-72 hrs (LFT and renal function abnormalities w/w/o RUQ pain); can revert to normal
3: (72-96 hrs): hepatic necrosis w/w/o renal failure but can revert to normal
4: (4 days to 2 wks): can progress to liver failure, transplant, death, or go to normal

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13
Q

How can one treat APAP poisoning? Mech of this antidote:

A

N-ACETYLCYSTEINE (best if given within 8 hrs of overdose); good for all stages of poisoning (if we’re forced to use the accessory P450 pathways);
sulfhydryl groups supplied, antioxidant for microcirculation improvement, glutathione supplied, decrease cerebral edema and improve CO to help with liver regen

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14
Q

NAC indicated when

A
  1. you know level and known time of ingestion over Rumack-Matthew nomogram
  2. Patient showing signs of hepatotoxicity
  3. APAP level won’t be available within 8 hrs of ingestion
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15
Q

Some newer prognosis criteria for acetaminophen toxicity:

A

Think serum lactate and serum phosphate being high (e.g. 2-3 days after overdose)

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16
Q

TCA toxidrome:

A
  1. ANTICHOLINERGIC
  2. Catechol reuptake inhibitor
  3. Alpha adrenergic blocker (hypotension)
  4. GABA antagonist (seizures)
  5. KILLED by NA CHANNEL BLOCKER QUALITIES (phase 0 slowed and QRS complex widened, leading to seizures if more than .1 sec, or dysrhythmias if more than .16 sec)
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17
Q

Antidote to TCA toxidrome:

A

Nabicarb (alkalinization can reduce TCA affinity to its receptor in the myocardium; Na is competitive!!)

18
Q

Anticholinergic toxidrome:

A

Mydriasis, dry flushed skin, decreased bowel sounds, urinary retention, increased temp, altered mental status (confusion, hallucinations, seizures)

19
Q

Examples of antiCh:

A
  1. atropine
  2. diphenhydramine (has anti-Ch and antihistamine effects)
  3. Scopolamine
  4. Meclizine
  5. TCA’s

SAD MatT

20
Q

Antidote to antiCh; toxicity:

A

Physostigmine (antiChase);

  1. contraindicated after TCA EXPOSURE
  2. Muscarinic and nicotinic excess seen if used in a pt not anti-Ch
  3. Rapid administration results in seizures (SLOW!!)
21
Q

When is physostigmine indicated?

A
  1. Pure antiCh poisoning
  2. CNS and PNS manifestations
  3. No ECG findings suggesting TCA exposure (b/c of contraindicatino)
22
Q

Ch toxidrome:

A

miosis, salivation, lacrimation, urination, defecation, CNS excitation, bronchorrhea/spasm, fasciculations

23
Q

Ch agents:

A
  1. Anticholinesterases: nerve gases (sarin), organophosphates, carbamates; physostigmine and neostigmine
  2. Cholinomimetics: bethanecol
24
Q

Antidote(s) for Ch:

A

ATROPINE (could need very high doses);

PRALIDOXIME: enzyme regenerator and can decreases atropine requirement, serving as only drug for MUSCARINIC effects

25
Q

Osmolal gap over 50 indicates

A

toxic alcohol unless proven otherwise

26
Q

For toxic alcohol poisoning, what can cause issues? How to treat?

A 
Formic acid (high AG metabolic acidosis), glycolate (can kill), and oxalate (precipitates in tubules as stones leading to ATN);
Fomepizole, if not ethanol;

also, remove toxin and metabolites through hemodialysis;
indications: methanol or ethylene glycol levels 25-50, metabolic acidosis, coma, hemodynamic instability

27
Q

With both bradycardia and hypotension, what is in the differential?

A
  1. Beta-blockers
  2. CCB’s
  3. Alpha-2 agonist (clonidine, guanfacine)
  4. Digoxin

ABCD

28
Q

CCB causes; what phase of contraction does it affect?

A
  1. peripheral vasodilation (decrease the PVR)
  2. decreases sinus rate
  3. shows AV conduction;
    phase 2 primarily, with slowed inward Ca current
29
Q

Pathophys of CCB overdose:

A
  1. Decreased ventricular contractility (neg inotrope)
  2. Sinus node depression leading to brady (neg chronotrope)
  3. AV node depression leads to various blocks (hypotension)
  4. vasodilation leads to HYPOTENSION
30
Q

Actions against CCB overdose and the diagnostics:

A
  1. IV, monitor
  2. decrease absorption (activated charcoal, whole bowel irrigation);
    diagnostics are lytes, EKG, Ca and Mg
31
Q

Specific treatment/antidote for CCB overdose:

A
  1. Ca salts
  2. Glucagon
  3. High dose insulin euglycemia
  4. Amrinone (phosphodiesterase inhibitor)
  5. Vasopressors (alpha-1, beta-1): dopamine, NE
  6. Lipid emulsion
32
Q

Beta-blocker OD:

A
  1. Think propanolol (membrane stabilizing activity with fast Na channel blocker activity and increased QRS)
  2. Lipophilic: leads to mental status depression and seizures
33
Q

Clonidine OD (or guanfacine) and toxidrome:

A
  1. alpha-2-agonist: decreases CNS symp output
  2. alpha-1 agonist (any cross-reactivity);
    bradycardia, pinpoint pupils, CNS depression

Count Bowling Pins

34
Q

Acute digoxin toxicity:

A

N/V, HYPERKALEMIA (predict death in people, especially if over 5.5);
also hypotension, bradycardia, dysrhythmia, death

35
Q

Treatment of acute digoxin toxicity:

A

Digibind:digoxin specific FAB fragments (Fc fraction cleaved)

36
Q

Cocaine/amphetamine toxicity:

A
  1. CNS stim, agitation, hallucinations, seizures;
  2. increased muscle activity: increased temp, CK, kidney injury

CHASe the TiCK

37
Q

PCP/Ketamine/DM toxicity:

A

low: euphoria;
medium: agitation, anesthesia, increased strength;
high: CNS anesthesia (preserve respiratory drive, and worry about nystagmus)

38
Q

Synthetic marijuana:

A
  1. Upwards of 60 times as potent as THC
  2. Hyperadrenergic findings, seizures, paranoia

SHoP for marijuana

39
Q

LSD/psilocybin:

A
  1. alterations in perceptions and hallucinations
  2. adverse effects related to EXPERIENCE
  3. psychiatric illness
40
Q

Treatment of cocaine/amphetamines, PCP/ketamine, synthetic marijuana, LSD/psilocybin:

A

Sedation/restraint/cooling;

look for any other injuries

pharm unit 6 (8 decks)

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