Toxicology

Question 1

What are the cellular effects of Dig toxicity?

Answer 1

Increase in intracellular Ca
Increased vagal tone - bradycardia
Increased automaticity in all cardiac tissues except the SA node, leading to dysrrhythmias

Question 2

Toxic causes of bradycardia and hypotension?

Answer 2

CCB
Beta blockers
Clonidine
Opiates
Cholinergic

Question 3

After an acute Dig ingestion, when should a blood level be drawn?

Answer 3

6 hours post, if time known, as it distributes to the tissues (lipophilic)

Question 4

Why is hyperkalemia common in acute Dig ingestion?

Answer 4

Dig blocks the Na/K ATPase receptor.

Is a marker of high mortality if >5.5

Question 5

Compare and contrast acute vs chronic digoxin toxicity

Answer 5

Acute: lower mortality, often younger, more bradycardias, healthy, do well without Digibind
Chronic: elderly, higher mortality, ventricular dysrrhythmias, often need Digibind, underlying comorbidities increased mortality

Question 6

Arrhythmias that are specific for Dig toxicity? (not pathognomonic)

Answer 6

Afib with slow ventricular rate
Atrial tachycardia with block
Bidirectional ventricular tachycardia
Nonparoxysmal junctional tachycardia (rate 70-130bpm)

Question 7

Indications for Digibind in adults?

Answer 7

Ventricular dysrhythmias (more than PVCs)
Hemodynamically significant bradycardia, no change with Atropine
Potassium > 5
Progressive rhythm disturbances or rising potassium
Coingestion of cardiotoxins (CCB, BB, TCA)
Ingestion of plant form with ventricular dysrhythmias
Acute ingestion >10mg plus any of the above
Dig concentration >6 plus any of the above

Question 8

What is the proposed mechanism for high-dose insulin therapy in CCB and BB overdoses?

Answer 8

When stressed, cardiac myocytes switch from free FA metabolism to glucose utilization. Insulin promotes glucose uptake by myocytes.

Question 9

High dose insulin therapy regimen?

Answer 9

Bolus insulin regular 1U/kg with Dextrose 1 amp

Infusion: 0.5-1U/kg/hr with 0.5mg/kg/hr dextrose

Question 10

EKG findings in BB toxicity?

Answer 10

Bradycardia
1st degree AVB
Wide QRS, Ventricullar arrhythmias (only with ones that have membrane stabilizing effects, sodium channel blockade)

Question 11

Describe the mechanism of action of Digoxin

Answer 11

Blocks the ATPase pump, thereby increasing intracellular Na.
This decreases efflux of Ca through the Ca/Na exchanger (usually Ca out, Na in).
Increased intracellular Ca –> increased contractility

Question 12

Describe the breakdown of methanol

Answer 12

Methanol to formaldehyde by ADH (alcohol dehydrogenase)

Formaldehyde to formic acid by aldehyde dehydrogenase

Question 13

Two main complications of severe methanol toxicity?

Answer 13

1. optic neuropathy

2. putaminal necrosis

Question 14

Characteristic CNS changes at an anatomic level with methanol toxicity?

Answer 14

Bilateral, symmetrical putaminal hypodensities, hemorrhages, or cystic lesions. (basal ganglia)
Necrosis in subcortical white matter cells, anterior horn cells, and cerebellum.

Question 15

Describe the latency period in relation to methanol toxicity. How does this affect your diagnosis?

Answer 15

There is a latency period from conversion of methanol to formic acid, on average 12 - 24 hours. May be shorter with large ingestions or longer with co-ingestion of EtOH.
This means acidosis and WAGMA may not be present early with a serious ingestion, takes time for formic acid to build up. Additionally, Osmolar gap will only be high early on, as methanol is osmotically active, not formic acid.

Question 16

Describe the breakdown of ethylene glycol.

Answer 16

ethylene glycol to glycoaldehyde by ADH
glycoaldehyde to glycolic acid by aldehyde dehydrogenase
glycolic acid to glycoxylic acid by LDH
glycoxylic acid to oxalic acid (only ~2%, can deposit in tissues as crystals with calcium)