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Antihypertensives
Hypertension;
high blood pressure that stays elevated over time.
•
Can lead to coronary artery disease, heart failure, stroke, CKD, retinopathy, Afib, aneurysms
•
90% essential or idiopathic HTN
•
Risk factors: age, obesity, physical inactivity, high-sodium, excess alcohol, smoking, family history
•
Goal of therapy directed at decreasing cardiac output and TPR
•
Mechanisms involved in increasing BP
BP; force of blood passing through arteries,veins,capilleries.
•
Barorecetors; pressure sensitive nerve endings,detect pressure changes in arterial only. *relays signal to
•
medulla:regulates force/speed of heart contraction.
medulla oblongata; regulates-force/speed of heart contractions
•
(RAAS) Renin-angiotensin-aldosterone system; (hormonal response), long term BP
maintenance, angiotensin, aldosterone
decrease in BP leads to decrease in blood flow to kidneys.
•
Juxtaglomerular Cells respond to release the enzyme RENIN
•
Renin converts the inactive plasma protein angiotensin (in liver) into angiotenisn I.
•
Angiotensin I is converted in the lungs to angiotensin II.
•
Angiotensin II stimulated the adrenal cortex to release aldosterone.
•
Aldosterone directs the kidney to reabsorb more sodium and Secrete K
•
which leads to increased retention of Water.
•
Water follows sodium back into the Extracellular fluid.
•
Beta blockers
They work by blocking the effects of the hormone epinephrine and norepinephrine.
•
They Reducing blood pressure.
•
They Decrease heart rate.
•
Beta-1 receptors; located primarily in the heart. (Acebutolol, Bisoprolol, Esmolol, Metoprolol)
•
Beta-2 receptors; located in the smooth muscle of lungs, uterus, and other organs.
•
Nonselective beta blockers; means that it will affect both beta-1 and beta-2 receptors. (Nadolol,
•
Propranolol, Timolol, Carvedilol, Labetalol )
Clinical indications: HTN (less CO, less b1-mediated renin release) HF, angina pectoris, MI,
•
supraventricular tachycardia, hyperthyroidism, glaucoma
Adverse effects
Cardiovascular inhibition- bradycardia, low BP, AV block, HF exacerbation
•
CNS- lethargy, insomnia, seizures
•
Dyslipidemia w/ metoprolol
•
Erectile dysfunction
•
Masked hypoglycemia (caution in DM)
•
Asthma/COPD exacerbations (nonselectives-B2 blockade)
•
Must be tapered over weeks to avoid withdrawal-angina, MI
•
ACE inhibitors
Name; captopril, enalapril, lisinopril, benazepril, ramipril.
•
Mechanism;
inhibit the conversion of angiotensin-1 to its more active from (angiotensin-2).
•
ACE inhibitors counteract or inhibit all of the pharmacological effects of angiotensin-2, so they cause
•
vasodilation, decrease aldosterone levels, Na+ & fluid wasting & K+ retention.
found mainly in the lungs
•
Reduces Na+ and H20 reabsorption in the kidneys
•
Increase renal blood flow
•
Inhibits aldosterone release
•
Decreases vasoconstriction
•
Decreases BP
•
ARBs ( Losartan, candesartan, valsartan)
ARBs block the action of angiotensin II, alowing the blood vessels to widen, thus making it easier for the heart
•
to pump blood.
Mechanism;
Selectively block binding of angiotensin II to AT1 receptor.
•
Effects similar to ACE inhibitors but ARBs do not increase bradykinin.
•
Clinical:
Hypertension, Heart Failure, Chronic Kidney Disease
•
Effects;
Hperkalemia, decrease GFR, Hypotension, teratogen.
•
Aliskiren
Mechanism;
Aliskiren is a direct inhibitor of renin, blockers conversion of angiotensinogen to angiotensin 1.
•
Clinical:
Hypertension
•
Effects;
Hperkalemia, decrease GFR, Hypotension, angioderma.
•
CCBs
A2-agonists aka Sympatholytics
adrenergic receptor
•
located in postganglionic sympathetic nerve endings
•
Inhibits release of norepinephrine; dilates blood vessels; produces hypotension; decreases gastrointestinal
•
motility and tone.
Clonidine;
For refractory HTN
•
Adverse: CNS depression, bradycardia, hypotension, respiratory depression, miosis, rebound HTN with
•
abrupt cessation
Methyldopa
For HTN in pregnancy (alternatives: Nifedipine, Labetalol, Hydralazine
•
Adverse: hemolytic anemia, drug-induced lupus, hyperprolactinemia
•
antihyperlipidemics
Drugs that control lipids in the blood.
•
two lipids that are found in blood (Cholesterol and Triglycerides)
•
hyperlipidemia; Elevation of plasma cholesterol and/or TAGs and Low HDL levels.
•
atherosclerosis; A disorder where lipid deposits accumulate in the linings in blood vessels. It slowly
•
degeneates the body and blocks blood flow.
Drugs; Bile Salts, Cholestyramine, Colestipol, Atorastati, Lovastatin
•

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Antihypertensive & Antihyperlipidemic .pdf

  • 1. Antihypertensives Hypertension; high blood pressure that stays elevated over time. • Can lead to coronary artery disease, heart failure, stroke, CKD, retinopathy, Afib, aneurysms • 90% essential or idiopathic HTN • Risk factors: age, obesity, physical inactivity, high-sodium, excess alcohol, smoking, family history • Goal of therapy directed at decreasing cardiac output and TPR • Mechanisms involved in increasing BP BP; force of blood passing through arteries,veins,capilleries. • Barorecetors; pressure sensitive nerve endings,detect pressure changes in arterial only. *relays signal to • medulla:regulates force/speed of heart contraction. medulla oblongata; regulates-force/speed of heart contractions • (RAAS) Renin-angiotensin-aldosterone system; (hormonal response), long term BP maintenance, angiotensin, aldosterone decrease in BP leads to decrease in blood flow to kidneys. • Juxtaglomerular Cells respond to release the enzyme RENIN • Renin converts the inactive plasma protein angiotensin (in liver) into angiotenisn I. • Angiotensin I is converted in the lungs to angiotensin II. • Angiotensin II stimulated the adrenal cortex to release aldosterone. • Aldosterone directs the kidney to reabsorb more sodium and Secrete K • which leads to increased retention of Water. • Water follows sodium back into the Extracellular fluid. • Beta blockers They work by blocking the effects of the hormone epinephrine and norepinephrine. • They Reducing blood pressure. • They Decrease heart rate. • Beta-1 receptors; located primarily in the heart. (Acebutolol, Bisoprolol, Esmolol, Metoprolol) • Beta-2 receptors; located in the smooth muscle of lungs, uterus, and other organs. •
  • 2. Nonselective beta blockers; means that it will affect both beta-1 and beta-2 receptors. (Nadolol, • Propranolol, Timolol, Carvedilol, Labetalol ) Clinical indications: HTN (less CO, less b1-mediated renin release) HF, angina pectoris, MI, • supraventricular tachycardia, hyperthyroidism, glaucoma Adverse effects Cardiovascular inhibition- bradycardia, low BP, AV block, HF exacerbation • CNS- lethargy, insomnia, seizures • Dyslipidemia w/ metoprolol • Erectile dysfunction • Masked hypoglycemia (caution in DM) • Asthma/COPD exacerbations (nonselectives-B2 blockade) • Must be tapered over weeks to avoid withdrawal-angina, MI • ACE inhibitors Name; captopril, enalapril, lisinopril, benazepril, ramipril. • Mechanism; inhibit the conversion of angiotensin-1 to its more active from (angiotensin-2). • ACE inhibitors counteract or inhibit all of the pharmacological effects of angiotensin-2, so they cause • vasodilation, decrease aldosterone levels, Na+ & fluid wasting & K+ retention. found mainly in the lungs • Reduces Na+ and H20 reabsorption in the kidneys • Increase renal blood flow • Inhibits aldosterone release • Decreases vasoconstriction • Decreases BP • ARBs ( Losartan, candesartan, valsartan) ARBs block the action of angiotensin II, alowing the blood vessels to widen, thus making it easier for the heart • to pump blood. Mechanism; Selectively block binding of angiotensin II to AT1 receptor. • Effects similar to ACE inhibitors but ARBs do not increase bradykinin. • Clinical: Hypertension, Heart Failure, Chronic Kidney Disease • Effects; Hperkalemia, decrease GFR, Hypotension, teratogen. • Aliskiren Mechanism; Aliskiren is a direct inhibitor of renin, blockers conversion of angiotensinogen to angiotensin 1. • Clinical: Hypertension • Effects; Hperkalemia, decrease GFR, Hypotension, angioderma. • CCBs
  • 3. A2-agonists aka Sympatholytics adrenergic receptor • located in postganglionic sympathetic nerve endings • Inhibits release of norepinephrine; dilates blood vessels; produces hypotension; decreases gastrointestinal • motility and tone. Clonidine; For refractory HTN • Adverse: CNS depression, bradycardia, hypotension, respiratory depression, miosis, rebound HTN with • abrupt cessation Methyldopa For HTN in pregnancy (alternatives: Nifedipine, Labetalol, Hydralazine • Adverse: hemolytic anemia, drug-induced lupus, hyperprolactinemia • antihyperlipidemics Drugs that control lipids in the blood. • two lipids that are found in blood (Cholesterol and Triglycerides) • hyperlipidemia; Elevation of plasma cholesterol and/or TAGs and Low HDL levels. • atherosclerosis; A disorder where lipid deposits accumulate in the linings in blood vessels. It slowly •
  • 4. degeneates the body and blocks blood flow. Drugs; Bile Salts, Cholestyramine, Colestipol, Atorastati, Lovastatin •