Hypertension Case Drugs

Question 1

Drug targets

Answer 1

Question 2

Antihypertensives

Answer 2

• Diuretics- thiazides; loops; K⁺-sparing; (acetazolamide)
• Renin inhibitor (-kiren)
• ACE inhibitors (-pril)
• Angiotensin Receptor Blockers (ARB) (-sartan)
• Calcium channel blockers (-dipine)
• β blockers (-lol)
• Centrally acting α₂ agonists (e.g., clonidine)
• Vasodilators
• nitroprusside = nitric oxide (NO) donor
• phentolamine = non-selective α-adrenergic antagonist
•prazosin = selective α₁-adrenergic antagonist
• hydralazine = ?
• minoxidil = potassium channel opener (KCO)

Question 3

Aliskiren

Answer 3

Question 4

Enalapril

Answer 4

Question 5

Valsartan

Answer 5

Question 6

Calcium channel blockers

Answer 6

• TARGET: all act on L-type channels (Cav1.x)
• CHEMISTRY: Three distinct structural groups

1. Phenylalkylamines
   • e.g., verapamil
   • ACTIVITY: Channel blocker (like LAs)
   • CLIN: antidysrhythmic
2. Benzothiazepines
   • e.g., diltiazem
   • ACTIVITY: Channel blocker (like LAs)
   • CLIN: angina
3. Dihydropyridines
   • e.g., amlodipine/nifedipine
   • ACTIVITY: Gating inhibitor
   • CLIN: hypertension / angina

Question 7

Anti-dysrhythmic

Answer 7

• Treatment of abnormal cardiac rhythms
• Vaughan-Williams Classification
• Class I: local anaesthetics e.g., lidocaine
• Class II: β blockers e.g., propranolol
• Class III: K+ channel blockers prolong repolarisation e.g., amiodarone
• Class IV: Ca2+ channel blockers e.g., verapamil

Question 8

Amlodipine

Answer 8

Question 9

Phentolamine

Answer 9

Question 10

B blockers

Answer 10

• Autonomic nervous system & RAAS
• α and β receptors
• β₁ receptors on heart (↑ rate and force of contraction) and JGA of kidney (renin secretion)
• NA acts as neurotransmitter
• β₂ receptors on smooth muscle → relaxation
• Adrenaline acts as hormone
• (β₃ receptors adipocytes (fat) → lipolysis)
• α receptors also influence physiological response to β blockers

PHYSIOLOGICAL HYPOTHESES
• No effect in normotensive subjects
• ↓ cardiac output
• ↓ peripheral vascular resistance
• Δ in baroreceptor sensitivity
• ↓ renin secretion (RAAS)
• ↓ sympathetic outflow from CNS
• Adaptive change: Δ receptor levels/↓ cardiac hypertrophy

Question 11

Atenolol

Answer 11

Question 12

Cocaine

Answer 12

• Local anaesthetic blocks VGNaCs → dysrhythmias
• Prevents neuronal uptake of noradrenaline through NET
• →↑sympathetic effects and release of adrenaline
• α → vasoconstriction →↑TPR →↑ABP
• + coronary vasoconstriction
• β₁ → cardiac stimulation →↑CO →↑ABP
• β₂ → vasodilation →↓TPR →↓ABP
• + coronary vasodilation

Question 13

Baxdrostat

Answer 13

Question 14

Treatment algorithm

Answer 14