1. Classes of hypertension
1.1. Normal
1.1.1. 120/80
1.1.2. check every 2 years
1.2. prehypertension
1.2.1. 120-139
1.2.2. 80-89
1.2.3. check in one year
1.3. stage 1
1.3.1. 140-159
1.3.2. 90-99
1.3.3. confirm within 2 months
1.4. stage 2
1.4.1. >160
1.4.2. >100
1.4.3. Evaluate within 1 week to 1 month
1.4.4. should be treated at once if BP is greater than 180/110 mm Hg
2. non-pharmacological therapy
2.1. effective (alone) when diastolic BP is between 85 to 94
2.2. Reduction in salt intake
2.3. Weight reduction
2.3.1. every 1 Kg lower 2.5/1.5
2.4. Light physical exercise
2.4.1. 30 minutes brisk walking most days of the week reduces B.P by 4-9
2.5. dietary approaches to stop hypertension (DASH)
2.5.1. diet high in fruits, vegetables and low fat dairy products
2.5.2. significantly reduces BP in about 8 weeks
2.5.3. diet rich in potassium and calcium
2.5.3.1. Potassium
2.5.3.1.1. direct vasodilator
2.5.3.1.2. increases the synthesis of bradykinin and natriuretic peptide
2.5.3.2. Calcium
2.5.3.2.1. enhances the secretion of a vasodilator peptide: Calcitonin Gene Related Peptide (CGRP)
2.5.3.2.2. reduces the secretion of parathyroid hypertensive factor (PHF)
2.6. reduce alcohol intake
2.7. Cessation of smoking
2.8. Decrease caffeine intake
2.9. Psychological methods
2.9.1. meditation
2.9.2. relaxation
2.10. Lifestyle modification
3. guidelines
3.1. if not lowered to target limit within 3 to 6 months of lifestyle changes
3.1.1. start treatment
3.1.2. keep the lifestyle modifications
3.2. target
3.2.1. below 140/85 for non-diabetic
3.2.2. below130/80 in diabetic
3.3. British Hypertension Society: August 2011
4. Drugs
4.1. Diuretics
4.1.1. types
4.1.1.1. Thiazides
4.1.1.1.1. hydrochlorothiazide
4.1.1.1.2. chlorthalidone
4.1.1.1.3. indapamide
4.1.1.1.4. used in mild to moderate hypertension with normal renal function
4.1.1.2. Loop diuretics
4.1.1.2.1. furosemide
4.1.1.2.2. bumetanide
4.1.1.2.3. ethacrynic acid
4.1.1.2.4. used in acute edema due to congestive heart failure
4.1.1.3. Potassium sparing diuretics
4.1.1.3.1. spironolactone
4.1.1.3.2. triamterene
4.1.1.3.3. amiloride
4.1.1.3.4. used in hyper aldosteronism and heart failure
4.1.2. mechanism
4.1.2.1. decreasing vascular resistance because sodium makes smooth muscle more stiff
4.1.2.2. recent studies
4.1.2.2.1. activating ATP-regulated K+ channels in arterioles
4.1.2.2.2. leading to membrane hyper polarization, which opposes Ca2+ entry and inhibiting contraction
4.1.3. clinical use
4.1.3.1. at least as effective as BBs, CCBs, and ACE inhibitors in reducing CV outcomes
4.1.3.2. particularly effective in preventing stroke and HF
4.1.3.3. good for elderly
4.1.3.4. effectively lower B.P in most patients from 10-15
4.1.3.5. for mild to moderate hypertension
4.1.4. adverse effects
4.1.4.1. hypokalemia (except for potassium sparing)
4.1.4.1.1. problematic in patients with arrhythmia or acute MI
4.1.4.1.2. prevented with
4.1.4.2. hyponatremia if they have HF
4.1.4.3. others
4.1.4.3.1. hyperuricemia
4.1.4.3.2. hypercalcemia
4.1.4.3.3. hyperglycemia
4.1.4.3.4. male sexual dysfunction
4.2. Inhibitors of Renin Angiotensin System
4.2.1. Angiotensin converting enzyme (ACE) inhibitors
4.2.1.1. types
4.2.1.1.1. Sulphydryl group
4.2.1.1.2. Dicarboxyl group
4.2.1.1.3. Phosphorus containing drugs
4.2.1.1.4. all are equally effective. differ in potency, pro or active, and pharmacokinetics
4.2.1.2. other indications
4.2.1.2.1. cardiac failure
4.2.1.2.2. diabetic nephropathy
4.2.1.2.3. left ventricular systolic dysfunction
4.2.1.3. Mechanism
4.2.1.3.1. inhibits conversion of angiotensin I to angiotensin II
4.2.1.3.2. lead to accumulation of bradykinin, because angiotensin II degrades it
4.2.1.4. adverse effects
4.2.1.4.1. dry cough
4.2.1.4.2. hypotension
4.2.1.4.3. skin rash
4.2.1.4.4. protein urea
4.2.1.4.5. hyperkalemia
4.2.1.4.6. acute renal failure
4.2.1.4.7. abnormalities in taste
4.2.1.4.8. angioneurotic edema
4.2.1.4.9. fetal hypotension and renal failure
4.2.1.5. Interactions
4.2.1.5.1. NSAIDs
4.2.1.5.2. Antacids (containing aluminum and magnesium hydroxide)
4.2.1.5.3. azathioprine
4.2.1.5.4. digoxin and lithium
4.2.1.5.5. ARBs
4.2.2. Angiotensin receptor blockers (ARBs)
4.2.2.1. types
4.2.2.1.1. losartan
4.2.2.1.2. valsartan
4.2.2.1.3. candesartan
4.2.2.2. Mechanism
4.2.2.2.1. blocking the receptor for angiotensin II
4.2.2.3. Clinical use
4.2.2.3.1. if ACE didn't work, or if cough not tolerated
4.2.2.4. Side effects
4.2.2.4.1. hyperkalemia
4.2.2.4.2. muscular cramps
4.2.2.4.3. GIT complaints
4.2.2.4.4. headache and dizziness
4.2.2.5. Contraindications
4.2.2.5.1. hypersensitivity
4.2.2.5.2. pregnancy
4.2.2.6. interactions
4.2.2.6.1. lithium
4.2.2.6.2. Digoxin
4.2.2.6.3. Indomethacin
4.2.3. Renin Inhibitors
4.2.3.1. Aliskiren
4.3. Calcium Channel Blockers
4.3.1. Types
4.3.1.1. Phenyl alkyl amines
4.3.1.1.1. verapamil
4.3.1.2. Dihydropyridines
4.3.1.2.1. nifedipine
4.3.1.2.2. amlodipine
4.3.1.2.3. felodipine
4.3.1.2.4. cause reflex tachycardia
4.3.1.3. Benzothiazepines
4.3.1.3.1. diltiazem
4.3.1.4. All CCBs produce peripheral vasodilation and negative inotropic effect -> equally effective in lowering BP
4.3.2. Mechanism
4.3.2.1. blocking L type Ca+2 channels in blood vessels and myocardium
4.3.2.1.1. in smooth muscles
4.3.2.1.2. in cardiac cells
4.3.2.2. Ca+ is important for initiating contraction, but still the cells have stores inside
4.3.2.3. block contractile process, dilate arterioles, reduce peripheral vascular resistance and myocardial force of contraction, lowering the blood pressure
4.3.3. Clinical use
4.3.3.1. not first line for hypertension, but they're effective especially in African-American patients.
4.3.3.2. better used if you have CAD risks and diabetes
4.3.4. Side effects
4.3.4.1. constipation
4.3.4.2. flushing
4.3.4.3. edema
4.3.4.4. dizziness, headache and nausea
4.3.4.5. cough and wheezing
4.3.4.6. DHP produce reflex tachycardia
4.3.5. Interaction
4.3.5.1. digoxin and verapamil
4.3.5.1.1. digoxin toxicity
4.3.5.2. cimetidine
4.3.5.2.1. increased levels
4.3.5.3. cyclosporine
4.3.5.3.1. levels increased by Amlodipine and Diltiazem
4.3.5.3.2. CCBs inhibit the enzyme CYP 3A4 responsible for metabolism of cyclosporine
4.3.5.4. antifungal agents: itraconazole, fluconazole and ketoconazole
4.3.5.4.1. increase levels of CCBs
4.3.5.5. Cigarette smoke
4.3.5.5.1. reduce effects of nifedipine and verapamil
4.3.5.6. Rifampicin
4.3.5.6.1. increase CCB metabolism -> reduce efficacy
4.3.5.7. NSAIDs and oral anticoagulant
4.3.5.7.1. monitor symptoms of GIT haemorrhage
4.4. Sympatholytics or Sympathoplegic Agents
4.4.1. Centrally acting agents
4.4.1.1. types
4.4.1.1.1. methyldopa
4.4.1.1.2. clonidine hydrochloride
4.4.1.2. only used in particular situations due to potential adverse effects
4.4.1.2.1. during pregnancy
4.4.1.2.2. hypertensive urgency
4.4.1.3. adverse effects
4.4.1.3.1. sedation
4.4.1.3.2. dry mouth
4.4.1.3.3. mental depression
4.4.1.3.4. may cause sleep disturbances including nightmares
4.4.2. Ganglionic blocking agent
4.4.2.1. trimethaphan
4.4.2.2. only used in particular situations due to potential adverse effects
4.4.2.2.1. hypertensive emergencies
4.4.3. α Adrenergic Antagonist
4.4.3.1. types
4.4.3.1.1. prazosin
4.4.3.1.2. doxazosin
4.4.3.1.3. terazosin
4.4.3.1.4. phenoxybenzamine
4.4.3.2. indication
4.4.3.2.1. Use with with coexisting hyperlipidemia, benign prostatic hyperplasia
4.4.3.3. side effects
4.4.3.3.1. postural hypotension
4.4.3.3.2. nasal stuffiness
4.4.3.3.3. headache
4.4.3.3.4. failure of ejaculation in male
4.4.4. β Adrenergic Antagonists
4.4.4.1. types
4.4.4.1.1. propranolol
4.4.4.1.2. atenolol
4.4.4.1.3. metoprolol
4.4.4.2. indication
4.4.4.2.1. chronic hypertension associated with angina pectoris
4.4.4.2.2. first-line agents when there is coexisting coronary risk, MI, or heart failure
4.4.4.3. side effects
4.4.4.3.1. depression
4.4.4.3.2. sexual dysfunction
4.4.4.3.3. masking symptoms of hypoglycaemia in diabetes
4.4.5. Mixed Adrenergic Antagonists
4.4.5.1. labetalol
4.4.5.2. for urgency
4.5. Vasodilators
4.5.1. Arterial vasodilators
4.5.1.1. hydralazine
4.5.1.1.1. mechanism
4.5.1.1.2. indication
4.5.1.1.3. side effects
4.5.1.2. minoxidil
4.5.1.2.1. mechanism
4.5.1.2.2. Indication
4.5.1.2.3. side effects
4.5.1.3. Diazoxide
4.5.1.3.1. mechanism
4.5.1.3.2. indication
4.5.1.3.3. dose
4.5.1.3.4. side effects
4.5.1.4. all cause reflex tachycardia
4.5.2. Balanced vasodilator
4.5.2.1. sodium nitroprusside
4.5.2.1.1. for emergency
4.5.2.2. prazosin + ACEI