Toxicology Flashcards
Cocaine
- MOA
- Clinical features
MOA: Inhibition of dopamine, serotonin and noradrenaline uptake –> increased dopamine in the synaptic cleft of the endogenous reward system
Inhibition of Na channels cause local anaesthetic action by blocking nerve action potential transmission
- Snorting can cause damage to the nasal vessels = nosebleeds
- Local vasoconstriction may cause ischaemic necrosis - perforated nasal septum
Cocaine Toxicity
vs
Cocaine Withdrawal
TOXICITY
- Euphoria, arousal
- Sweating
- Tachycardia, tachyarrhythmia
- HTN
- Chest pain/angina
- Mydriasis
- Malignant hyperthermia
- Sudden cardiac death
INTOXICATION TREATMENT:
- Benzodiazepines
- Control HTN, tachycardia, arrhythmias with non-selective alpha/beta antagonists such as labetalol
WITHDRAWAL
- Physiological crash: severe depression with suicidal ideation, constricted pupils, psychomotor agitation
- Depression
Complications of cocaine toxicity
COCAINE INDUCED VASOSPASM
- Decreased reuptake of noradrenaline –> increased a and B1 stimulation –> vasoconstriction and vasospasm –> myocardial infarction, cerebrovascular accident or ischaemic colitis
Tx: treat like STEMI, calcium channel blockers + a blockers can reduce vasospasm
RHABDOMYOLYSIS
- Risk of ATN due to myoclobinuria
Betel nut toxicity
Similar to cholinergic toxicity: salivation, lacrimation, urinary incontinence, sweating, diarrhea, emesis, facial flushing, and fever
- Can lead to oral cancer
Red back spider poisoning
Muscle fasciculations
Paralysis
Tachycardia
Lomotil - diphenoxylate/atropine
CNS depression
Miosis
Hypotension
Tricyclic antidepressants (TCA)
- MOA
- Side Effects
Example: Amitriptyline
MOA: inhibition of serotonin and norepinephrine reuptake in synaptic cleft → ↑ serotonin and norepinephrine levels
SE: TCASS
- Tremor
- Cardiovascular adverse effects: due to Na channel inhibition in myocardium - prolonged QT (predisposes to torsades), wide QRS
- Anticholinergic adverse effects: due to blockage of muscarinic cholinergic receptors
- Sedation
- Seizures
- Orthostatic hypotension
What are anticholinergic symptoms
- Cardiovascular: tachycardia, arrhythmia, hypotension
- CNS: confusion, hallucinations, sedation, coma, seizures
- Gastrointestinal: intestinal ileus, constipation
- Genitourinary: urinary retention
- General: xerostomia, mydriasis, hyperthermia, dry skin
TCA toxicity
The 3 C’s - convulsions, coma, cardiac conduction abnormalities (prolonged QTC)
- Most associated with anticholinergic syndrome
- Prolonged QT, arrythmias
- Seizures
- Coma
Prolonged QRS
Prolonged QTC
Treatment
- Supportive
- Activated charcoal
- Sodium bicarbonate for treatment and prevention of cardiac arrhythmia - monitor with ECG (QRS >100 or ventricular arrhythmias)
- Benzos for seizures
Which of the following predicts the risk of seizures and arrhythmias in TCA overdose? A. QRS >160 B. QTC >500 C. HR >100 D. PR >200 E. Right axis deviation
A. QRS >160
Organophosphate toxicity
- Irreversible inhibition of acetylcholinesterase –> increased acetylcholine levels –> activation of muscarinic and nicotinic acetylcholine receptors
- Life-threatening activation of the parasympathetic system
ACUTE CHOLINERGIC CRISIS DUMBBELLSS - Diarrhoea - Urination - Miosis - Bradycardia - Bronchospasm - Emesis - Lacrimation - Lethargy - Sweating - Lethargy
TREATMENT
- Atropine: reverses muscarinic effects
- Pralidoxime: treats neuromuscular dysfunction
What lithium level indicates lithium toxicity and what medications can precipitate it?
- Occurs at serum levels > 1.5
Medications that can precipitate lithium toxicity by increasing renal absorption of lithium:
- Thiazide diuretics
- NSAIDs except aspirin
- ACEi
- Other medications - tetracyclines, cyclosporines
Clinical features of lithium toxicity
LITHIUM
- Lithium can cause Irregular Thyroxine levels (hypo/hyperthyroidism)
- Heart (Ebstein anomaly)
- Nephrogenic diabetes insipidus
- Uncontrolled muscle movements (tremor)
