Clinical Toxicology 1 and 2

Question 1

Opioid toxidrome:

Answer 1

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

Question 2

List some opioids

Answer 2

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

Question 3

How to deal with opioid toxidrome:

Answer 3

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

Question 4

Naloxone properties; what is the possible withdrawal?:

Answer 4

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)

Question 5

Natural, semi-synthetic, and synthetic opioids:

Answer 5

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

Question 6

Other opioid receptor antagonists and properties:

Answer 6

Nalmefene and naltrexone;

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

Question 7

Benzo toxidrome; benzo uses:

Answer 7

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

Question 8

Some key sedative hypnotics:

Answer 8

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

Question 9

Treatment of benzos:

Answer 9

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

Question 10

Dangers of flumazenil:

Answer 10

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

Question 11

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

Answer 11

APAP (acetaminophen) level

Question 12

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

Answer 12

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

Question 13

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

Answer 13

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

Question 14

NAC indicated when

Answer 14

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

Question 15

Some newer prognosis criteria for acetaminophen toxicity:

Answer 15

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

Question 16

TCA toxidrome:

Answer 16

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)

Question 17

Antidote to TCA toxidrome:

Answer 17

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

Question 18

Anticholinergic toxidrome:

Answer 18

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

Question 19

Examples of antiCh:

Answer 19

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

SAD MatT

Question 20

Antidote to antiCh; toxicity:

Answer 20

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!!)

Question 21

When is physostigmine indicated?

Answer 21

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

Question 22

Ch toxidrome:

Answer 22

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

Question 23

Ch agents:

Answer 23

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

Question 24

Antidote(s) for Ch:

Answer 24

ATROPINE (could need very high doses);

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

Question 25

Osmolal gap over 50 indicates

Answer 25

toxic alcohol unless proven otherwise

Question 26

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

Answer 26

``` 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

Question 27

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

Answer 27

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

Question 28

CCB causes; what phase of contraction does it affect?

Answer 28

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

Question 29

Pathophys of CCB overdose:

Answer 29

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

Question 30

Actions against CCB overdose and the diagnostics:

Answer 30

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

Question 31

Specific treatment/antidote for CCB overdose:

Answer 31

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

Question 32

Beta-blocker OD:

Answer 32

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

Question 33

Clonidine OD (or guanfacine) and toxidrome:

Answer 33

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

Question 34

Acute digoxin toxicity:

Answer 34

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

Question 35

Treatment of acute digoxin toxicity:

Answer 35

Digibind:digoxin specific FAB fragments (Fc fraction cleaved)

Question 36

Cocaine/amphetamine toxicity:

Answer 36

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

Question 37

PCP/Ketamine/DM toxicity:

Answer 37

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

Question 38

Synthetic marijuana:

Answer 38

1. Upwards of 60 times as potent as THC 2. Hyperadrenergic findings, seizures, paranoia SHoP for marijuana

Question 39

LSD/psilocybin:

Answer 39

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

Question 40

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

Answer 40

Sedation/restraint/cooling; | look for any other injuries