Antihypertensives Flashcards
What is the medical definition of hypertension?
High blood pressure (BP) >130/80 mmHg.
Why is hypertension dangerous?
It can damage vital organs like the brain (stroke), heart (heart disease), kidneys, and retina.
What is primary (essential) hypertension and how is it managed?
Hypertension with no known cause, accounting for 90% of cases.
Antihypertensive agents.
What is secondary hypertension and how can it be treated?
Hypertension caused by renal or endocrine disorders, accounting for 10% of cases.
By addressing the underlying cause.
What is malignant hypertension, its risk, and how is it treated?
A severe, rapidly progressing form of hypertension.
It can lead to retinal or renal damage.
With aggressive medical intervention.
How does relaxation of vascular smooth muscle affect blood pressure?
It reduces peripheral resistance, leading to vasodilation.
How does reducing sympathetic activity lower blood pressure?
Decreased epinephrine (EPI) and norepinephrine (NE) reduce vasoconstriction and heart rate.
How do changes in sodium and water balance lower blood pressure?
Decreasing sodium retention lowers blood volume, reducing blood pressure.
What is the site of action for Clonidine?
CNS (Vasomotor Center).
How does Clonidine reduce sympathetic activity?
It stimulates α2 receptors, reducing NE and EPI release, leading to decreased blood pressure.
What is the site of action for Mecamylamine?
Sympathetic Ganglia.
How does Prazosin lower blood pressure?
It causes vasodilation by blocking α1 receptors, reducing peripheral resistance.
What is the mechanism of Mecamylamine?
Blocks nicotinic receptors, preventing sympathetic transmission to the heart and vessels.
What is the result of Mecamylamine’s action?
Decreased cardiac output and vasodilation.
What receptor does Prazosin block?
α1 receptors on blood vessels.
What are the two types of beta blockers?
Specific β1 blockers and Non-Specific β1/β2 blockers.
Where do specific β1 blockers act?
Heart and kidney (juxtaglomerular cells).
How do specific β1 blockers reduce blood pressure?
By decreasing heart rate, contractility, and renin release.
Why are β1-selective blockers preferred for asthmatics and diabetics?
They lack β2 effects, avoiding bronchoconstriction and worsening peripheral vascular disease.
What additional effect do non-specific β1/β2 blockers have?
They can cause bronchoconstriction due to β2 blockade.
What is the unique feature of beta blockers with ISA?
They have partial agonist activity, causing less cardiac depression.
When are beta blockers with ISA preferred?
In patients with bradyarrhythmias or diminished cardiac reserve.
Where does Hydralazine, Minoxidil, and Sodium Nitroprusside act?
Vascular smooth muscle.
How does Hydralazine cause vasodilation?
It decreases intracellular Ca++ release from the sarcoplasmic reticulum.
What is the mechanism of Sodium Nitroprusside?
It releases nitric oxide (NO), reducing Ca++ levels and causing rapid vasodilation.
How does Minoxidil induce vasodilation?
It opens K+ channels, maintaining polarization and minimizing Ca++ influx.
When is Sodium Nitroprusside used?
In hypertensive emergencies.
What are the dental implications of Calcium Channel Blockers (CCBs)?
Xerostomia and gingival enlargement.
Where do Calcium Channel Blockers act?
Heart and vascular smooth muscle.
How do Calcium Channel Blockers reduce muscle contraction?
They block Ca++ entry via L-type channels.
Which Calcium Channel Blocker is most selective for cardiac muscle?
Verapamil.
What is the effect of Verapamil?
Decreases heart contraction and rate.
Which Calcium Channel Blocker affects both the heart and vasculature?
Diltiazem (Dilacor XR).
Where do Thiazide Diuretics act?
Kidney (Distal Tubule).
Which CCBs mainly cause vasodilation?
Dihydropyridines (e.g., Amlodipine, Nifedipine).
How do Thiazide Diuretics lower blood pressure?
By promoting sodium and water excretion; may also act as a vasodilator.
What is a common side effect of Thiazide Diuretics?
Potassium deficiency.
What is the site of action for ACE Inhibitors?
Renin-Angiotensin System.
How do ACE Inhibitors reduce blood pressure?
By blocking the conversion of Angiotensin I to Angiotensin II (a potent vasoconstrictor).
What is the key advantage of ARBs and Losartan over ACE Inhibitors?
They do not cause cough.
What is the mechanism of action of Losartan?
Competitive antagonist at angiotensin II (AT1) receptors located in vascular tissue
What is the primary effect of Losartan?
Lowers blood pressure.
What is Hyzaar®?
Losartan + Hydrochlorothiazide, used for enhanced blood pressure control.
What is the mechanism of action of Aliskiren?
Direct renin inhibitor—prevents renin from binding to angiotensinogen.
What compensatory mechanism can beta blockers trigger?
They reduce heart rate but may increase peripheral resistance.
Why is combination therapy often used for blood pressure control?
Single-drug therapies can trigger compensatory physiological responses that counteract their effects.
How can diuretics activate a compensatory response?
They reduce blood volume but can stimulate the renin-angiotensin system.
What is the benefit of combining a Beta Blocker with a Diuretic?
It offsets compensatory renin release.
How does an ACE Inhibitor + Thiazide Diuretic combination help?
It enhances blood pressure control while preventing hypokalemia.
What is the advantage of combining a Calcium Channel Blocker with an ACE Inhibitor?
It provides both vasodilation and renin system inhibition.
