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(Phase 2) YLL Pharmacology AY24/25 > CVS - Hypertension & Antihypertensives > Flashcards

CVS - Hypertension & Antihypertensives Flashcards

1
Q

Name one effect of ACE inhibitors?

A

Inhibits the conversion of Ang I to Ang II.

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2
Q

Name 3 clinical uses of ACE inhibitors?

A

Hypertension, heart failure, post-myocardial infarction

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3
Q

Name a common adverse effect of ACE inhibitors.

A

Dry cough.

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4
Q

How do the “sartans” class of antihypertensives work?

A

Block the action of Ang II on AT1 receptors.

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5
Q

What is the main difference between ACE inhibitors and AT1 blockers regarding their adverse effects?

A

Compared to ACE inhibitors, AT1 blockers has Less/no dry cough

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6
Q

Name 4 clinical uses of beta-blockers?

A

Hypertension, cardiac failure, post-myocardial infarction, anxiety disorders.

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7
Q

Name 3 adverse effects of beta-blockers.

A

Bradycardia, hypotension, reduced exercise capacity.

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8
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit Na+/Cl- cotransporter in distal convoluted tubule.

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9
Q

Name 4 clinical uses of thiazides?

A

Hypertension (preferred), congestive heart failure, nephrolithiasis due to idiopathic hypercalciuria, nephrogenic diabetes insipidus.

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10
Q

What are common adverse effects of thiazide diuretics?

A

Hypokalemia, hyperuricemia, hyperglycemia, hyponatremia.

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11
Q

What is the MOA of Calcium channel blockers?

A

Inhibit L-type calcium channels, reducing intracellular calcium, leading to vasodilation.

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12
Q

What are clinical uses of Calcium channel blockers?

A

Hypertension, angina, arrhythmias, Raynaud’s phenomenon.

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13
Q

Name an adverse effect of Calcium channel blockers.

A

Peripheral edema, constipation, reflex tachycardia.

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14
Q

How do alpha-adrenoceptor antagonists lower blood pressure?

A

Block ?1-receptors, causing vasodilation.

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15
Q

What are the clinical uses of alpha blockers?

A

Hypertension, benign prostatic hyperplasia.

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16
Q

Name an adverse effect of alpha blockers.

A

Postural hypotension, reflex tachycardia.

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17
Q

What is the MOA of centrally acting ?2 agonists?

A

Stimulate ?2 receptors in CNS, reducing sympathetic outflow.

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18
Q

What are the clinical uses of centrally acting ?2 agonists?

A

Hypertension, especially with renal disease.

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19
Q

Name an adverse effect of centrally acting ?2 agonists.

A

Sedation, dry mouth, rebound hypertension.

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20
Q

How do vasodilators like hydralazine work?

A

Directly relax arterial smooth muscle.

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21
Q

What are the clinical uses of hydralazine?

A

Hypertension, especially in pregnancy, heart failure.

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22
Q

Name an adverse effect of hydralazine.

A

Headache, tachycardia, fluid retention, lupus-like syndrome.

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23
Q

How do diuretics assist in blood pressure control?

A

Reduce blood volume and cardiac output.

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24
Q

What is the MOA of loop diuretics like furosemide?

A

Inhibit Na+/K+/2Cl- cotransporter in the loop of Henle.

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25
Q

What are clinical uses of loop diuretics?

A

Congestive heart failure, hypertension, edema.

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26
Q

Name an adverse effect of loop diuretics.

A

Electrolyte imbalance, dehydration, ototoxicity.

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27
Q

How do potassium-sparing diuretics work?

A

Block Na+ channels or aldosterone receptors in distal tubules and collecting ducts.

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28
Q

What are the clinical uses of potassium-sparing diuretics?

A

Hypertension, edema, in combination with thiazides or loop diuretics.

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29
Q

Name an adverse effect of potassium-sparing diuretics.

A

Hyperkalemia, metabolic acidosis.

30
Q

What is hypertension?

A

Hypertension is a condition where blood pressure is consistently too high.

31
Q

Identify two major consequences of hypertension.

A
  • Congestive heart failure - Myocardial infarction
32
Q

What formula represents arterial blood pressure?

A

Arterial Blood Pressure ? Cardiac Output x Peripheral Resistance

33
Q

What is the role of heart contractility in blood pressure regulation?

A

Heart contractility affects cardiac output, which influences blood pressure.

34
Q

How does arteriolar tone influence blood pressure?

A

Arteriolar tone affects peripheral resistance, thus impacting blood pressure.

35
Q

Define preload in the context of cardiac function.

A

Preload is the stretching of cardiac muscles before contraction, associated with ventricular filling.

36
Q

What is afterload in cardiac terms?

A

Afterload is the force against which the heart must contract to eject blood, associated with peripheral resistance.

37
Q

What are the clinical uses of Angiotensin Converting Enzyme Inhibitors (ACE-I)?

A
  • Hypertension - Cardiac failure - Post-myocardial infarction - Renal insufficiency
38
Q

List four adverse effects of ACE inhibitors.

A
  • Severe hypotension - Acute renal failure - Hyperkalemia - Angioedema and dry cough
39
Q

Why are ACE inhibitors contraindicated in pregnancy?

A

They can cause fetal harm and should therefore be avoided during pregnancy.

40
Q

What are Ang II type 1 (AT1) blockers and give examples.

A

AT1 blockers are drugs that inhibit angiotensin II’s effects on AT1 receptors, e.g., Valsartan, Losartan.

41
Q

List two adverse effects of AT1 blockers.

A
  • Less/no dry cough compared to ACE inhibitors - Contraindicated in pregnancy
42
Q

What is the mechanism of action of beta-blockers in cardiac myocytes?

A

Beta-blockers block ?1 receptors in cardiac myocytes, leading to decreased contractility.

43
Q

List the main types of beta-blockers.

A
  • Non-Selective (e.g., Propranolol) - Cardioselective (e.g., Atenolol) - Mixed (e.g., Nebivolol)
44
Q

What are the clinical uses of beta-blockers?

A
  • Hypertension - Cardiac failure - Post-myocardial infarction - Abnormal heart rhythms - Anxiety disorders
45
Q

Identify six adverse effects of beta-blockers.

A
  • Hypotension - Bradycardia - AV nodal block - Reduced exercise capacity - Bronchoconstriction - CNS effects (e.g., vivid dreams, depression)
46
Q

What is the action of thiazide diuretics on the distal convoluted tubule?

A

Thiazides inhibit NaCl reabsorption and enhance Ca2+ reabsorption in the distal convoluted tubule.

47
Q

List the clinical uses of thiazide diuretics.

A
  • Hypertension - Congestive heart failure - Nephrolithiasis due to hypercalciuria - Nephrogenic diabetes insipidus
48
Q

What are the adverse effects of thiazide diuretics?

A
  • Hypokalemic metabolic alkalosis - Hyponatremia - Hyperuricemia - Hyperglycemia - Hyperlipidemia - Hypercalcemia
49
Q

Explain the mechanism of thiazide-induced hypokalemia.

A

Thiazides increase aldosterone-mediated K+ and H+ ion excretion in the collecting duct, leading to hypokalemia.

50
Q

What role does the renin-angiotensin system (RAS) play in blood pressure regulation?

A

RAS regulates blood pressure through vasoconstriction and aldosterone-mediated sodium and water retention.

51
Q

Describe the mechanism of action of calcium channel blockers in vascular smooth muscle.

A

Calcium channel blockers inhibit calcium entry into vascular smooth muscle cells, leading to vasodilation.

52
Q

How do beta-blockers reduce blood pressure?

A

Beta-blockers reduce blood pressure by decreasing cardiac output and inhibiting renin release.

53
Q

What is the mechanism of action of diuretics in treating hypertension?

A

Diuretics lower blood pressure by reducing blood volume and cardiac output.

54
Q

How does sympathetic nervous system activity affect blood pressure?

A

Increased sympathetic activity raises blood pressure by increasing heart rate, cardiac output, and vasoconstriction.

55
Q

Explain the role of ?1-adrenergic receptors in blood pressure regulation.

A

?1-Adrenergic receptors mediate vasoconstriction, increasing peripheral resistance and blood pressure.

56
Q

How do thiazide diuretics affect calcium reabsorption in the distal convoluted tubule?

A

Thiazides enhance calcium reabsorption, reducing urinary calcium excretion.

57
Q

What is the mechanism of thiazide diuretics in reducing hypertension?

A

Thiazides inhibit Na+/Cl- cotransport in the distal convoluted tubule, leading to diuresis and reduced blood volume.

58
Q

Describe the impact of beta-blockers on ?1 and ?2 adrenergic receptors.

A

Beta-blockers block ?1 receptors in the heart (reducing contractility) and ?2 receptors in bronchial smooth muscle (leading to bronchoconstriction).

59
Q

How do alpha-adrenergic antagonists reduce blood pressure?

A

Alpha-adrenergic antagonists block ?1 receptors on vascular smooth muscle, reducing vasoconstriction and peripheral resistance.

60
Q

What are the clinical indications for using alpha-adrenergic antagonists?

A

Indicated for hypertension and symptomatic relief of urine retention due to benign prostate hyperplasia.

61
Q

Explain the mechanism of beta-blocker-induced bronchoconstriction.

A

Beta-blockers block ?2 receptors in bronchial smooth muscle, reducing bronchodilation and potentially causing bronchoconstriction.

62
Q

Why are NSAIDs contraindicated with thiazide diuretics?

A

NSAIDs reduce renal prostaglandin synthesis, which can interfere with the antihypertensive action of thiazides.

63
Q

What are the adverse effects associated with alpha-adrenergic antagonists?

A

Common adverse effects include reflex tachycardia, palpitations, orthostatic hypotension, depression, urinary frequency, and flushing.

64
Q

How do thiazide diuretics lead to hypokalemia?

A

Thiazides increase aldosterone-mediated K+ excretion, leading to hypokalemia.

65
Q

Explain how thiazide diuretics can cause hyponatremia.

A

Thiazides decrease sodium reabsorption, leading to lower circulating sodium levels and potential hyponatremia.

66
Q

Why can thiazide diuretics lead to hyperglycemia?

A

Thiazide-induced hypokalemia impairs insulin secretion, leading to hyperglycemia.

67
Q

How do thiazide diuretics contribute to hyperuricemia?

A

Thiazides increase urate reabsorption in the proximal tubule, leading to hyperuricemia and an increased risk of gout.

68
Q

What are second-line antihypertensive drugs?

A

Second-line drugs include hydralazine, mineralocorticoid receptor antagonists, and alpha-adrenergic antagonists.

69
Q

Describe the mechanism of action of hydralazine.

A

Hydralazine directly vasodilates arterioles, reducing peripheral resistance and blood pressure.

70
Q

What is the primary action of mineralocorticoid receptor antagonists?

A

They block aldosterone receptors, preventing sodium and water retention and reducing blood pressure.

71
Q

How do alpha-blockers affect renal blood flow and glomerular filtration rate (GFR)?

A

Alpha-blockers do not affect renal blood flow

(Phase 2) YLL Pharmacology AY24/25 (36 decks)

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