Материал: MasterPass _ Pharmacology in 7 Days for Medical Students

PHARMACOLOGY IN 7 DAYS FOR MEDICAL STUDENTS

•For supraventricular tachycardia (SVT): Verapamil.

•For ventricular tachycardia (VT): Lignocaine; phenytoin.

Digoxin toxicity: indications of digoxin-binding antibody fragment9

1Reserved for very severe cases:

•Patients who have taken a large overdose (≥10 mg in adults and ≥4 mg in children).

•Serum digoxin level >13nmol/L.

•Serum K+ level >5mmol/L.

•Presence of life-threatening arrhythmias (2nd or 3rd degree AV block; VT; VF).

Aspirin/salicylate toxicity

It could be mild (called salicylism) or severe.

Mild toxicity: features

•GI: N, V.

•Respiratory: Hyperventilation (salicylate toxicity → metabolic acidosis → hyperventilation).

•CNS: Headache; dizziness; tinnitus (ringing of ears).

Severe toxicity: features

Symptoms of mild toxicity are followed by restlessness, delirium, hallucinations, convulsions and coma. The usual cause of death is respiratory failure.

Lethal dose

In children: ≥10 gm

In adults: 300 mg/kg

Investigations

1Serum salicylate levels (levels of >70 mg/dl indicate severe intoxication).

2Arterial blood gases (to determine pH): It will initially show respiratory alkalosis (d/t hyperventilation) followed by metabolic acidosis (d/t drug itself).

Treatment

Mild cases:

1Symptomatic.

2Alkaline diuresis (NaHCO3 added in dextrose water → alkalisation of urine → increasing the urinary pH enhances the elimination of salicylate).

Severe cases:

1Haemodialysis.

2Mechanical ventilation (if pulmonary oedema develops).

3Intravenous mannitol (if cerebral oedema develops).

Acetaminophen (paracetamol) toxicity

Acetaminophen is acted upon by cytochrome P450 mixed-function oxidase to form a toxic intermediate (called N-acetyl-p-benzoquinoneimine). In therapeutic doses, this

9Normally given as I/V infusion over 30 minutes. In cases of cardiac arrest, it can be given as I/V bolus. It freely filters through the kidneys and thus can be given even in CRF patients.

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MISCELLANEOUS

toxic intermediate conjugates with hepatic glutathione to form non-toxic mercapturic acid. In lethal doses, all available glutathione reserves of the liver are depleted and the toxic intermediate combines with the essential hepatic cell proteins, resulting in cell death/hepatic necrosis – a potentially life-threatening condition (renal tubular necrosis can also occur → acute renal failure).

In patients who are already suffering from some chronic liver disease, the glutathione reserves may be subnormal so that even near-normal doses of paracetamol may cause hepatic necrosis.

Treatment

If given within 10 hours of paracetamol toxicity, N-acetylcysteine, which contains sulfhydryl groups to which the toxic intermediate can bind, is life-saving.

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Important tables

Table 7.1 Important receptors and their agonists and antagonists

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