Antihypertensive Drugs Flashcards
Classification of Blood Pressure Chart
Mechanisms of Hypertension
- Heart or pump-based HYPT- more common in young w/ hyperkinetic circulation (inc. SNS), inc. CO, PR normal
- Vascular-based HYPT- w/ inc. PR/vasoconstriction, normal CO
- Renal/volume-based HYPT- inc. Na/H2O/fluid retention, inc. renin-angiotensin activation/cardiac output/peripheral resistance
- Neuroendocrine dysfunction: hyperthyroidism, pheochromocytoma, hyperaldosteroidism
Step-Care Method of Treament for Hypertension
- Method of treatment where drug(s) are administered and combined in certain sequences so that the compensatory mechanisms are neutralized and that proper combinations of drugs have an additive hypotensive effect
STEP 1- DIURETIC or another drug which effectively reduces both compensatory mechanisms (beta blockers, ACE inhibitors, AT I blockers, calcium channel blockers)
STEP 2- Sympathoplegic agent
STEP 3- Vasodilator
Diuretics
- Thiazides: hydrochlorothiazide
- Loop diuretics: furosemide (LASIX)
- Potassium sparers: spironolactone, ameloride, triamterene
Hydrochlorothiazide Initial and Chronic Effects
Initial Effect- blood volume (decrease)
Chronic Effect- peripheral resistance (decrease)
Hydrochlorothiazide Effect on Compensatory Mechanisms
- Activation of renin-angiotensin system
Hydrochlorothiazide Dosage Regimen
- Low dose therapy- used in mild to moderate hypertension in pts. w/ normal cardiac and renal function
- Ceiling effect- higher doses are not more effective
Hydrochlorothiazide Adverse Effects
- Hypokalemia
- Increased plasma uric acid- gout
- Increased triglycerides and LDL’s
- Increased cholesterol
- Decreased HDL’s
- Hyperglycemia
- Allergic reactions, rash due to sulonamide component
Prazosin
- Reduces sympathetic activity
- Alpha-1 selective blocker; reduces arterial blood pressure by dilating resistance and capacitance vessels
- More effective when used in combination w/ a diuretic and beta blocker
- Produce less reflex tachycardia than non-selective alpha blockers
- Initial hypotension, declines w/ prolonged use
Beta Adrenergic Blockers
- Propanolol (non-selective beta blocker)
- Atenolol (selective beta-1 blocker)
- Metoprolol (selective beta-1 blocker)
Beta Adrenergic Blockers Mechanism of Antihypertensive Action
- Reducing renin secretion
- Lowering cardiac output and blood pressure
Beta Adrenergic Blockers Effect on Compensator Mechanisms
- Attenuates reflex tachycardia
Beta Adrenergic Blockers Potential Problems
- Congestive heart failure
- Bradycardia, arrhythmias
- Anginal attacks- abrupt withdrawal
- Respiratory distress
- CNS depression/disorientation
- Blood chemistry- TG, HDLP
- Mask symptoms of hypoglycemia (diabetics)
Mixed acting alpha/beta blockers
- Labetalol/ carvedilol
Labetalol
- Mixed acting alpha/beta blocker
Uses
- Pheochromocytoma and hypertensive emergency
Adrenergic Neuronal Blockers
- Reserpine
- Guanethidine
- Guanadrel
Reserpine
- Adrenergic Neuronal blocker
- Depletes NE from SNS nerve terminal vesicles
Guanethidine
- Adrenergic neuronal blocker
- Inhibits release of NE from SNS terminals
Guanadrel
- Adrenergic neuronal blocker
- Replaces NE from SNS vesicles and functions as “false transmitter”
Clonidine Site of Action
- Central adrenergic sympathoplegic drug (alpha-2 agonist)
- Site of action: alpha-2 adrenoreceptors in medulla of brain; pre and postsynaptic receptors
Clonidine MOA
- Reduce NE release via presynaptic alpha-2 receptor stimulation in both periphery and CNS; stimulates postsynaptic receptors in the medulla to inhibit pressor baroreceptor reflex (i.e., SNS activity)
Clonidine Main Pharmacologic Effects
- Reduces sympathetic tone; inc. parasympathetic tone