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Chapter 4 of 8

Endocrine & Metabolic Drugs

Insulin preparations are categorized by onset and duration: rapid-acting lispro, aspart, and glulisine; short-acting regular insulin; intermediate-acting NPH; and long-acting glargine, detemir, and degludec. Metformin works primarily by reducing hepatic gluconeogenesis through AMPK activation and, importantly, does not cause hypoglycemia as monotherapy. It is contraindicated when eGFR falls below 30 because of lactic acidosis risk, which is the most feared adverse effect.

SGLT2 inhibitors such as empagliflozin, dapagliflozin, and canagliflozin block glucose reabsorption in the proximal convoluted tubule, producing glucosuria, modest glycemic control, weight loss, and meaningful cardiovascular and renal protection. Their side effects include genitourinary infections, euglycemic diabetic ketoacidosis, and volume depletion. GLP-1 receptor agonists (semaglutide, liraglutide) augment glucose-dependent insulin secretion, suppress glucagon, slow gastric emptying, and produce substantial weight loss, with gastrointestinal side effects and a small pancreatitis risk being the main drawbacks.

Thyroid storm is a hypermetabolic crisis managed with a multi-pronged approach: a beta-blocker (typically propranolol) to control adrenergic symptoms, a thionamide such as PTU or methimazole to block new thyroid hormone synthesis, iodine (Lugol's solution) given after the thionamide to block thyroid hormone release via the Wolff-Chaikoff effect, and corticosteroids to impair peripheral T4-to-T3 conversion and address relative adrenal insufficiency, alongside fever control and supportive care.

All chapters
  1. 1Analgesics, Anti-inflammatories & Gout Therapy
  2. 2Anticoagulation & Antithrombotic Therapy
  3. 3Cardiovascular Drugs
  4. 4Endocrine & Metabolic Drugs
  5. 5Anti-infectives
  6. 6CNS, Autonomic & Neuromuscular Pharmacology
  7. 7Anesthesia, Pain Management & Local Anesthetics
  8. 8Chemotherapy, Biologics & Specialty Drugs

Drill it

Reading is not remembering. These come from the Usmle Step 1 High Yield Pharmacology deck:

Q

Mechanism of acetaminophen toxicity?

Hepatic CYP2E1 oxidizes APAP → toxic NAPQI metabolite. Glutathione normally detoxifies; in overdose glutathione is depleted → centrilobular hepatic necrosis.

Q

Antidote for acetaminophen overdose?

N-acetylcysteine — replenishes glutathione.

Q

Aspirin mechanism?

Irreversible COX-1 / COX-2 inhibitor → ↓ thromboxane A₂ in platelets (antithrombotic) + ↓ prostaglandins (analgesic, antipyretic, anti-inflammatory).

Q

Aspirin overdose acid-base picture?

Mixed: respiratory alkalosis (early — direct medullary stimulation) + anion-gap metabolic acidosis (later — uncoupled oxidative phosphorylation).