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Hypertension Dr.Hassan H Alwafi MBBS, Demonstrator Department of Clinical Pharmacology UQU

Hypertension Dr.Hassan H Alwafi MBBS, Demonstrator Department of Clinical Pharmacology UQU. Hypertension The Silent Killer. Hypertension is the term used to describe high blood pressure .

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Hypertension Dr.Hassan H Alwafi MBBS, Demonstrator Department of Clinical Pharmacology UQU

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  1. Hypertension Dr.Hassan H Alwafi MBBS, Demonstrator Department of Clinical Pharmacology UQU

  2. Hypertension The Silent Killer • Hypertension is the term used to describe high blood pressure. • Blood Pressure: is a measurement of the force against the walls of your arteries as the heart pumps blood through the body. • Blood pressure management includes systolic and disystoliccomponents, and both are important determining an individual’s cardiovascular risk.

  3. Determinants of Arterial Pressure Mean arterial pressure = CO X TPR (blood volume & arterial diameter). Mechanisms of Controlling CO and TPR 1-Neural Sympathetic & parasympathetic nervous system. 2. Hormonal Renal: Ang II Adrenal: Catecholamine’s& Aldosterone. 3-Local factor artery & vein. CRITICAL POINTS! 1. These organ systems and mechanisms control physical factors of CO and TPR 2. Therefore, they are the targets of antihypertensive therapy.

  4. Etiology : • Primary hypertension (90-95%) *Essential hypertension. • SECONDARY HYPERTENSION *Renal disease. *Endocrine disease. *Vascular disease. *Drug. Sympathomimetic Amine- Estrogen-Cyclosporine-Erythropoietin,NSAID- and steroid

  5. Hypertension Complications: (The risk of complication is related to the level of BP elevated) • Aneurysm: Hypertension symptoms weaken blood vessel walls, which can result in an aneurysm. This bulge in the blood vessel can rupture, causing internal bleeding. A ruptured aneurysm is a life-threatening event. • Atherosclerosis. • Coronary Artery Disease. • Heart Failure. • Kidney Complications: total renal failure, Kidney aneurysms and renal tissue scarring. • cerebral hemorrhage /infarction. • Vision Loss: The small blood vessels in the eyes can be damaged as a result of high blood pressure, causing nerve damage or bleeding. Blurred vision can occur, as can - 

  6. Symptom: Most of the time, there are no symptoms. Symptoms that may occur include: -Confusion -Fatigue -Headache -Irregular heartbeat -Nose bleeding -Vision changes

  7. Diagnoses: • Blood pressure should be measured by using sphygmomanometer. 2. Check for possible secondary cause by (Taking history, blood Test, Echo, ECG, Urinalysis,& Ultrasound of the kidney )

  8. Treatment: • The goal of treatment is to reduce blood pressure to lower risk of complications. • Treatment of hypertension includes both pharmacological and Non-pharmacological treatment.

  9. General Treatment Strategy of Hypertension • 1-Diagnosis. • 2-Primary or secondary hypertension. • 3-Secondary > treat underlying cause. • 4-Primary> initiate life style modification. • 5->Pharmacological treatment

  10. Pharmacological Treatment: • A large selection of antihypertensive drug is available. • It’s important to use drug that minimize patient Side effects. • Many patient need combination of drug to achieve adequate blood pressure.

  11. Antihypertensive Medication Classes of Antihypertensive Agents 1-Diuretics 2-Peripheral a-1 adrenergic antagonist . 3-Central sympatholytic (a-2Agonist). 4-B-Adrenergic Antagonists. 5-Anti-angiotensin Drugs. 6-Ca++ Channel Blockers. 7-Vasodilator. CRITICAL POINTS: Each designed for specific control system Often used in combination .

  12. 1-Diuretics 1-Site of Action: Renal Nephron. 2-Mechanism of action: Increase (urine excretion & Na excretion) . Decrease (extracellular fluid and plasma volume). 3-Effect on Cardiovascular System: Acute decrease in CO. Chronic decrease in TPR.

  13. 1-Diuretics1st line 1. Thiazides hydrochlorothiazide (HydroDIURIL, Esidrix); chlorthalidone (Hygroton) 2. Loop diuretics furosemide (Lasix); bumetadine (Burmex); ethacrynic acid (Edecrin) 3-K+ Sparing amiloride (Midamor); spironolactone (Aldactone); triamterene (Dyrenium)

  14. Diuretics (cont) 4. Adverse Reactions dizziness. electrolyte imbalance/depletion. hypokalemia.(thiazide) hyperkalemia (k sparing ) hyperlipidemia.(thiazide) hyperglycemia (Thiazide). gout.(Thizide) gynecomastia (k sparing ) 5. Contraindications hypersensitivity. compromised kidney function. cardiac glycosides (K+ effects). hypovolemia. hyponatremia

  15. Diuretics (cont) Therapeutic Considerations : Thiazides (most common diuretics for HTN). Generally start with lower potency diuretics. Generally used to treat mild to moderate HTN. Use with lower dietary Na+ intake. and K+ supplement or high K+ food. K+ Sparing (week diuretic >combination with other agent). Loop diuretics (severe HTN, or with CHF ) Osmotic (HTN emergencies).

  16. 2-Peripheral a-1 Adrenergic Antagonists Drugs: prazosin (Minipres); terazosin (Hytrin) 1-Site of Action-:- Peripheral arterioles, smooth muscle 2- Mechanism of Action Competitive antagonist at a-1 receptors on vascular smooth muscle .. 3- Effects on Cardiovascular System Blocking -receptors on vascular smooth muscle allows muscle relaxation, dilation of vessel, and reduced resistant

  17. Peripheral a-1 Adrenergic Antagonists, con. 4. Adverse effects nausea; drowsiness; postural hypotension; 1st dose syncope 5. Contraindications Hypersensitivity 6. Therapeutic Considerations -useful with diabetes, asthma, and/or hypercholesterolemia -use in mild to moderate hypertension -often used with diuretic, antagonist

  18. 3-Central Sympatholytic (a-2 Agonists) Drugs: clonidine (Catapres), methyldopa (Aldomet) 1. Site of Action: CNS medullary cardiovascular centers” 2-Mechanism of Action : CNS a-2 adrenergic stimulation >Decreased norepinephrine release 3-Effects on Cardiovascular System : Stimulation of a-2 receptors in the medulla decreases peripheral Sympathetic activity reduces tone, vasodilation and decreases TPR

  19. Central Sympatholytic (a-2 Agonists); cont. 4. Adverse Effects dry mouth; sedation; impotence; 6. Therapeutic Considerations third line; methyldopa drug of choice for pregnancy prolonged use--salt/water retention, add diuretic

  20. 4- B- Adrenergic Antagonists. Drugs: propranolol (Inderal); metoprolol (Lopressor) atenolol (Tenormin); nadolol (Corgard); pindolol(Visken) 1-Site of action: 2-Mechanism of Action competitive antagonist at b- adrenergic receptors. .3-Effects on Cardiovascular System . Cardiac--  HR,  SV CO . Renal--  Renin  Angiotensin II  TPR

  21. b-Adrenergic Antagonists, cont 4. Adverse Effects oadema ; postural hypotension fatigue; exercise intolerance; 5. Contraindications asthma; diabetes; bradycardia; hypersensitivity 6. Therapeutic Considerations Selectivity nadolol (Corgard) non selective, but 20 hr 1/2 life metoprol(Lopresor) b-1 selective, 3-4 hr 1/2 life Risky in pulmonary disease even selective b-1 Use post myocardial infarction- protective Use with diuretic to prevent reflex tachycardia . Mixed a/b blocker available (labetalol)(Trandate, Normodyne) decreases TPR (), prevents reflex tachycardia ()

  22. 2. Ang II Receptor Antagonists losartan (Cozaar); candesartan (Atacand); valsartan (Diovan) 5-Anti-Angiotensin II Drugs Angiotensin II Formation Angiotensin Converting Enzyme- Inhibitors ) quinapril (Accupril); fosinopril (Monopril); moexipril (Univasc); lisinopril (Zestril, Prinivil); benazepril (Lotensin); captopril (Capoten Angiotensinogen Ang I ACE Lung VSM Brain Kidney Adr Gland  AT1 Ang I Ang II ACE AT2  Ang II Renin

  23. . Effects on Cardiovascular System a. Renal 1. Maintenance of normal GFR 2. Reduces plasma vasopressin and aldosterone Decreased CO b. Cardiac 1. Decreased Ang II and Norepinephrine effects Decreased SymNS influence; Decreased CO c. Vascular 1. Decreased Ang II Decreased TPR- due to Ang II

  24. Anti-Angiotensin II Drugs, cont 4. Adverse Effects a. hyperkaelemia b. altered gustatory sensation c. angioedema- sudden edema skin/ mucous membranes; etiology unknown d. cough- increase bradykinin / prostaglandins a. 5. Contraindications pregnancy; hypersensitivity; bilateral renal stenosis 6. Therapeutic Considerations a. use with diabetes or renal insufficiency 1. Ang II contributes to decreased renal function b. use in heart failure 1. Ang II contributes to ventricular remodeling c. usually used with diuretic, additive with thiazide 1. Decreases sodium retention by reducing aldosterone d. used where diuretic or b-blocker contraindicated or ineffective Enalapril, iv for hypertensive emergency

  25. 6- Ca++ Channel Blockers 1-Site of Action- Vascular Ca++ Channel Blockers smooth muscle 2-Mechanism of Action- Blocks Ca++ channel decreases/prevents contraction 3- Effect on Cardiovascular system Vascular relaxation Decreased TPR

  26. Ca++ Channel Blockers, cont. 4. Adverse Effects a. most associated with excessive vasodilation 1. mild to moderate edema 2. flushing 3. tachycardia- Nifedipine- due to reflex SymNS activation aggravates angina 4. bradycardia- Diltiazem, verapamil 5. Contraindications Congestive heart failure; pregnancy and lactation; Post-myocardial infarction 6. Therapeutic Considerations verapamil >interactions w/ cardiac glycosides

  27. 7- Vasodilators Drugs: hydralazine (Apresoline); minoxidil (Loniten); nitroprusside (Nipride); diazoxide (Hyperstat I.V.); fenoldopam (Corlopam) 1-Site of Action: vascular smooth muscle 2-Effect on cardiovascular system:vasodilation > decrease TPR

  28. 5. Therapeutic Considerations Nitroprusside- IV only Hydralazine- safe for pregnancy diazoxide- emergency use for severe hypertension. Vasodilators, Cont 4. Adverse Effects reflex tachycardia Increase SymNS activity (hydralazine, minoxidil,diazoxide) lupus (hydralazine) hypertrichosis (minoxidil) cyanide toxicity (nitroprusside)

  29. Summary Important PointsHypertensive Agents Each class of antihypertensive agent: 1. has as specific mechanism of action, 2. acts at one or more major organ systems, 3. on a major physiological regulator of blood pressure, 4. reduces CO and/or TPR to lower blood pressure, 5. has specific indications, contraindications, and therapeutic advantages and disadvantages associated with the mechanism of action.

  30. Treatment of hypertensive emergencies • Goal: produce a rapid but well controlled fall in BP. • Context: hypertensive encephalopathy, eclampsia, pheo, hypertension with pulmonary oedema, aneurism, subarachnoid hemorrhage etc.. • Labetalol iv (alpha & beta blocker) • I.vnitroprusside • I.v. nitroglycerine • hydralazine iv or im (eclampsia) • iv phentolamine or phenoxybenzaminepo (pheo)

  31. hypertensive emergency • Hypertensive EmergencyA hypertensive emergency exists when blood pressure reaches levels that are damaging organs. Hypertensive emergencies generally occur at blood pressure levels exceeding 180 systolic OR 120 diastolic, but can occur at even lower levels in patients whose blood pressure had not been previously high.

  32. http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/AboutHighBloodPressure/Hypertensive-Crisis_UCM_301782_Article.jsphttp://www.heart.org/HEARTORG/Conditions/HighBloodPressure/AboutHighBloodPressure/Hypertensive-Crisis_UCM_301782_Article.jsp • The Washington manual of medical therapeutic / • Clinical pharmacy and therapeutic /

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