Adrenergic Agonists And Antagonists

Simple Notes

1. Adrenergic Agonists (Sympathomimetics)

• Drugs that stimulate adrenergic receptors (α, β) → mimic effects of sympathetic nervous system (“fight or flight”).
• Effects: ↑ HR, ↑ BP, bronchodilation, pupil dilation.
• Examples:
  • Epinephrine (used in anaphylaxis, cardiac arrest)
  • Albuterol (β₂ agonist for asthma, COPD)

2. Adrenergic Antagonists (Sympatholytics)

• Block adrenergic receptors → oppose sympathetic action.
• Effects: ↓ HR, ↓ BP, bronchoconstriction.
• Examples:
  • Propranolol (nonselective β-blocker → HTN, arrhythmia)
  • Prazosin (α₁-blocker → HTN, BPH)

3. Cholinergic Drugs (Parasympathomimetics)

• Stimulate muscarinic or nicotinic receptors → mimic parasympathetic activity (“rest and digest”).
• Effects: ↑ salivation, ↑ GI motility, pupil constriction, ↓ HR.
• Examples:
  • Pilocarpine (glaucoma → ↑ aqueous humor outflow)
  • Bethanechol (urinary retention → stimulates bladder)

4. Anticholinergic Drugs

• Block acetylcholine receptors → oppose parasympathetic activity.
• Effects: Dry mouth, constipation, urinary retention, ↑ HR, pupil dilation.
• Examples:
  • Atropine (bradycardia, eye exams → pupil dilation)
  • Ipratropium (inhaler for COPD/asthma)

5. Insulin

• Hormone from pancreatic β-cells → lowers blood glucose by promoting cellular uptake & storage (glycogen, fat, protein).
• Types:
  • Rapid-acting (Lispro, Aspart)
  • Short-acting (Regular insulin)
  • Long-acting (Glargine, Detemir)
• Uses: Type 1 DM (always), Type 2 DM (if uncontrolled), DKA, HHS.

6. Acidosis

• pH < 7.35
• Can be respiratory (↑ CO₂ from hypoventilation, COPD) or metabolic (↑ acid or ↓ HCO₃⁻ from DKA, renal failure).
• Symptoms: Confusion, weakness, Kussmaul breathing (if metabolic).

7. Alkalosis

• pH > 7.45
• Respiratory: hyperventilation (↓ CO₂, e.g., panic attack).
• Metabolic: ↑ HCO₃⁻ (vomiting, diuretics).
• Symptoms: Muscle cramps, tetany, arrhythmias.

8. Compensation

• Body’s attempt to restore normal pH when acid–base balance is disturbed.
• Respiratory compensation: lungs alter CO₂ (fast, minutes).
• Metabolic compensation: kidneys alter H⁺/HCO₃⁻ (slow, hours–days).
• Example:
  • Metabolic acidosis (DKA) → lungs hyperventilate (Kussmaul breathing) to blow off CO₂.
  • Respiratory alkalosis (hyperventilation) → kidneys excrete HCO₃⁻.

9. Kussmaul Breathing

• Deep, labored, rapid breathing seen in metabolic acidosis (especially DKA).
• Purpose: blow off CO₂ to reduce acidity.

10. DKA (Diabetic Ketoacidosis)

• Seen mostly in Type 1 DM due to absolute insulin deficiency.
• Pathophysiology:
  • No insulin → ↑ lipolysis → ↑ ketone production → metabolic acidosis.
• Key Features: Polyuria, polydipsia, abdominal pain, fruity breath, Kussmaul breathing.
• Labs: Hyperglycemia (>250), metabolic acidosis, ketones in urine/blood.
• Treatment: IV fluids, IV insulin, electrolyte correction (esp. K⁺).

11. HHS (Hyperosmolar Hyperglycemic State)

• Seen mostly in Type 2 DM.
• Pathophysiology:
  • Enough insulin to prevent ketones, but not enough to control glucose.
• Key Features: Severe hyperglycemia (>600), dehydration, altered mental status, no significant acidosis.
• Treatment: IV fluids, insulin, treat underlying cause (infection, MI, etc.).