CVS - Hypertension & Antihypertensives Flashcards
Name one effect of ACE inhibitors?
Inhibits the conversion of Ang I to Ang II.
Name 3 clinical uses of ACE inhibitors?
Hypertension, heart failure, post-myocardial infarction
Name a common adverse effect of ACE inhibitors.
Dry cough.
How do the “sartans” class of antihypertensives work?
Block the action of Ang II on AT1 receptors.
What is the main difference between ACE inhibitors and AT1 blockers regarding their adverse effects?
Compared to ACE inhibitors, AT1 blockers has Less/no dry cough
Name 4 clinical uses of beta-blockers?
Hypertension, cardiac failure, post-myocardial infarction, anxiety disorders.
Name 3 adverse effects of beta-blockers.
Bradycardia, hypotension, reduced exercise capacity.
What is the mechanism of action of thiazide diuretics?
Inhibit Na+/Cl- cotransporter in distal convoluted tubule.
Name 4 clinical uses of thiazides?
Hypertension (preferred), congestive heart failure, nephrolithiasis due to idiopathic hypercalciuria, nephrogenic diabetes insipidus.
What are common adverse effects of thiazide diuretics?
Hypokalemia, hyperuricemia, hyperglycemia, hyponatremia.
What is the MOA of Calcium channel blockers?
Inhibit L-type calcium channels, reducing intracellular calcium, leading to vasodilation.
What are clinical uses of Calcium channel blockers?
Hypertension, angina, arrhythmias, Raynaud’s phenomenon.
Name an adverse effect of Calcium channel blockers.
Peripheral edema, constipation, reflex tachycardia.
How do alpha-adrenoceptor antagonists lower blood pressure?
Block ?1-receptors, causing vasodilation.
What are the clinical uses of alpha blockers?
Hypertension, benign prostatic hyperplasia.
Name an adverse effect of alpha blockers.
Postural hypotension, reflex tachycardia.
What is the MOA of centrally acting alpha 2 agonists?
Stimulate alpha 2 receptors in CNS, reducing sympathetic outflow.
What are the clinical uses of centrally acting ?2 agonists?
Hypertension, especially with renal disease.
Name an adverse effect of centrally acting ?2 agonists.
Sedation, dry mouth, rebound hypertension.
How do vasodilators like hydralazine work?
Directly relax arterial smooth muscle.
What are the clinical uses of hydralazine?
Hypertension, especially in pregnancy, heart failure.
Name an adverse effect of hydralazine.
Headache, tachycardia, fluid retention, lupus-like syndrome.
How do diuretics assist in blood pressure control?
Reduce blood volume and cardiac output.
What is the MOA of loop diuretics like furosemide?
Inhibit Na+/K+/2Cl- cotransporter in the loop of Henle.
What are clinical uses of loop diuretics?
Congestive heart failure, hypertension, edema.
Name an adverse effect of loop diuretics.
Electrolyte imbalance, dehydration, ototoxicity.
How do potassium-sparing diuretics work?
Block Na+ channels or aldosterone receptors in distal tubules and collecting ducts.
What are the clinical uses of potassium-sparing diuretics?
Hypertension, edema, in combination with thiazides or loop diuretics.
Name an adverse effect of potassium-sparing diuretics.
Hyperkalemia, metabolic acidosis.
What is hypertension?
Hypertension is a condition where blood pressure is consistently too high.
Identify two major consequences of hypertension.
- Congestive heart failure - Myocardial infarction
What formula represents arterial blood pressure?
Arterial Blood Pressure ? Cardiac Output x Peripheral Resistance
What is the role of heart contractility in blood pressure regulation?
Heart contractility affects cardiac output, which influences blood pressure.
How does arteriolar tone influence blood pressure?
Arteriolar tone affects peripheral resistance, thus impacting blood pressure.
Define preload in the context of cardiac function.
Preload is the stretching of cardiac muscles before contraction, associated with ventricular filling.
What is afterload in cardiac terms?
Afterload is the force against which the heart must contract to eject blood, associated with peripheral resistance.
What are the clinical uses of Angiotensin Converting Enzyme Inhibitors (ACE-I)?
- Hypertension - Cardiac failure - Post-myocardial infarction - Renal insufficiency
List four adverse effects of ACE inhibitors.
- Severe hypotension - Acute renal failure - Hyperkalemia - Angioedema and dry cough
Why are ACE inhibitors contraindicated in pregnancy?
They can cause fetal harm and should therefore be avoided during pregnancy.
What are Ang II type 1 (AT1) blockers and give examples.
AT1 blockers are drugs that inhibit angiotensin II’s effects on AT1 receptors, e.g., Valsartan, Losartan.
List two adverse effects of AT1 blockers.
- Less/no dry cough compared to ACE inhibitors - Contraindicated in pregnancy
What is the mechanism of action of beta-blockers in cardiac myocytes?
Beta-blockers block ?1 receptors in cardiac myocytes, leading to decreased contractility.
List the main types of beta-blockers.
- Non-Selective (e.g., Propranolol) - Cardioselective (e.g., Atenolol) - Mixed (e.g., Nebivolol)
What are the clinical uses of beta-blockers?
- Hypertension - Cardiac failure - Post-myocardial infarction - Abnormal heart rhythms - Anxiety disorders
Identify six adverse effects of beta-blockers.
- Hypotension - Bradycardia - AV nodal block - Reduced exercise capacity - Bronchoconstriction - CNS effects (e.g., vivid dreams, depression)
What is the action of thiazide diuretics on the distal convoluted tubule?
Thiazides inhibit NaCl reabsorption and enhance Ca2+ reabsorption in the distal convoluted tubule.
List the clinical uses of thiazide diuretics.
- Hypertension - Congestive heart failure - Nephrolithiasis due to hypercalciuria - Nephrogenic diabetes insipidus
What are the adverse effects of thiazide diuretics?
- Hypokalemic metabolic alkalosis - Hyponatremia - Hyperuricemia - Hyperglycemia - Hyperlipidemia - Hypercalcemia
Explain the mechanism of thiazide-induced hypokalemia.
Thiazides increase aldosterone-mediated K+ and H+ ion excretion in the collecting duct, leading to hypokalemia.
What role does the renin-angiotensin system (RAS) play in blood pressure regulation?
RAS regulates blood pressure through vasoconstriction and aldosterone-mediated sodium and water retention.
Describe the mechanism of action of calcium channel blockers in vascular smooth muscle.
Calcium channel blockers inhibit calcium entry into vascular smooth muscle cells, leading to vasodilation.
How do beta-blockers reduce blood pressure?
Beta-blockers reduce blood pressure by decreasing cardiac output and inhibiting renin release.
What is the mechanism of action of diuretics in treating hypertension?
Diuretics lower blood pressure by reducing blood volume and cardiac output.
How does sympathetic nervous system activity affect blood pressure?
Increased sympathetic activity raises blood pressure by increasing heart rate, cardiac output, and vasoconstriction.
Explain the role of ?1-adrenergic receptors in blood pressure regulation.
?1-Adrenergic receptors mediate vasoconstriction, increasing peripheral resistance and blood pressure.
How do thiazide diuretics affect calcium reabsorption in the distal convoluted tubule?
Thiazides enhance calcium reabsorption, reducing urinary calcium excretion.
What is the mechanism of thiazide diuretics in reducing hypertension?
Thiazides inhibit Na+/Cl- cotransport in the distal convoluted tubule, leading to diuresis and reduced blood volume.
Describe the impact of beta-blockers on ?1 and ?2 adrenergic receptors.
Beta-blockers block ?1 receptors in the heart (reducing contractility) and ?2 receptors in bronchial smooth muscle (leading to bronchoconstriction).
How do alpha-adrenergic antagonists reduce blood pressure?
Alpha-adrenergic antagonists block ?1 receptors on vascular smooth muscle, reducing vasoconstriction and peripheral resistance.
What are the clinical indications for using alpha-adrenergic antagonists?
Indicated for hypertension and symptomatic relief of urine retention due to benign prostate hyperplasia.
Explain the mechanism of beta-blocker-induced bronchoconstriction.
Beta-blockers block ?2 receptors in bronchial smooth muscle, reducing bronchodilation and potentially causing bronchoconstriction.
Why are NSAIDs contraindicated with thiazide diuretics?
NSAIDs reduce renal prostaglandin synthesis, which can interfere with the antihypertensive action of thiazides.
What are the adverse effects associated with alpha-adrenergic antagonists?
Common adverse effects include reflex tachycardia, palpitations, orthostatic hypotension, depression, urinary frequency, and flushing.
How do thiazide diuretics lead to hypokalemia?
Thiazides increase aldosterone-mediated K+ excretion, leading to hypokalemia.
Explain how thiazide diuretics can cause hyponatremia.
Thiazides decrease sodium reabsorption, leading to lower circulating sodium levels and potential hyponatremia.
Why can thiazide diuretics lead to hyperglycemia?
Thiazide-induced hypokalemia impairs insulin secretion, leading to hyperglycemia.
How do thiazide diuretics contribute to hyperuricemia?
Thiazides increase urate reabsorption in the proximal tubule, leading to hyperuricemia and an increased risk of gout.
What are second-line antihypertensive drugs?
Second-line drugs include hydralazine, mineralocorticoid receptor antagonists, and alpha-adrenergic antagonists.
Describe the mechanism of action of hydralazine.
Hydralazine directly vasodilates arterioles, reducing peripheral resistance and blood pressure.
What is the primary action of mineralocorticoid receptor antagonists?
They block aldosterone receptors, preventing sodium and water retention and reducing blood pressure.
How do alpha-blockers affect renal blood flow and glomerular filtration rate (GFR)?
Alpha-blockers do not affect renal blood flow
