HYPERTENSION

By

J. Jayasutha

Dept of Pharmacy Practice

Definition

Persistent elevation of arterial blood pressure
Arterial blood pressure = cardiac output ×
Peripheral vascular resistance
 JNC 8 Classification
Category SBP mmHg DBP mmHg

Normal <120 and <80

Prehypertension 120–139 or 80–89

Hypertension, Stage 1 140–159 or 90–99

Hypertension, Stage 2 ≥160 or ≥100

 Classification

Primary hypertension Secondary hypertension

(90-95%) (5-10%)

No Known Cause
 Causes of Secondary
hypertension

 Renal artery stenosis

 Hyper- or
 Chronic renal disease
hypothyroidism
 Primary
hyperaldosteronism  Pheochromocytoma

 Stress  Preeclampsia

 Sleep apnea  Aortic coarctation

 Cushings syndrome

Pathophysiology of Hypertension

 Humoral mechanism
• Renin angiotensin aldosterone system
• Natriuretic hormone
• Insulin resistance and hyperinsulinemia
 Neuronal regulation
 Endothelial mechanism
 Peripheral autoregulatory components
 Electrolytes
Renin angiotensin aldosterone system

Reduced renal blood flow

Juxtraglomerular apparatus of kidney
Release renin
Angiotensinogen
Angiotensin I
Angiotensin II

Vasoconstriction Adrenal cortex
stimulation
Increased pheripheral resistance Increased aldosterone
Increased sodium and water retension
Fluid reabsorption
Increased Blood Pressure Increased blood volume



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Sympathetic Nervous system

Decrease in blood pressure

Increased sympathetic activity

Activation of β1 adrenoreceptor on heart &

Activation of α1 adrenoreceptor on smooth muscle

Cardiac Output Peripheral resistance

Hypertension

Clinical Presentation

 Headache
 Dizziness
 Blurred vision
 Nausea and vomiting
 Chest pain
 Shortness of breath

 Diagnosis

 Average of two or more readings taken at each of two or more

clinical encounters.

 As hypertension progresses, signs of end-organ damage begin

to appear
• Funduscopic examination
• Cardiopulmonary examination
• Peripheral vascular examination
• Patients with Cushing's syndrome may have the classic
physical features of moon face, hirsutism, and abdominal
striae
• Baseline hypokalemia suggest mineralocorticoid-induced
hypertension
 Typical tests performed in hypertension

System Tests

Microscopic urinalysis, proteinuria, serum BUN (blood urea nitrogen)

Renal
and/or creatinine

Endocrine Serum sodium, potassium, calcium, TSH (thyroid-stimulating hormone).

Fasting blood glucose, total cholesterol, HDL and LDL cholesterol,

Metabolic
triglycerides

Other Hematocrit, electrocardiogram, echo and chest radiograph

 Treatment

 Non Pharmacological
 Pharmacological
 Lifestyle Changes to Treat High Blood
Pressure



 Losing weight if you are overweight or obese

 smoking cessation

 Eating a healthy diet, including the DASH diet (eating more fruits,
vegetables, and low fat dairy products, less saturated and total
fat)

 Reducing the amount of sodium in your diet to less than 1,500

milligrams a day

 Getting regular aerobic exercise (such as brisk walking at least

30 minutes a day, several days a week)

 Limiting alcohol intake

 Pharmacological treatment of hypertension
Loop diuretics: Beta blockers Calcium channel Angiotensin II receptor
Bumetanide Atenolol blockers: antagonist
Ethacrynic acid Metoprolol Dihydropyridines: Candesartan
Furosemide Nadolol Amlodipine Eprosartan
Torsemide Oxprenolol Felodipine Irbesartan
Pindolol Isradipine Losartan
Thiazide diuretics: Propranolol Lercanidipine Olmesartan
Epitizide Timolol Nicardipine Telmisartan
Hydrochlorothia Nifedipine Valsartan
zide Alpha blockers: Nimodipine
chlorothiazide Doxazosin Nitrendipine Central alpha agonist
Bendroflumethia Phentolamine Non-dihydropyridines: Clonidine
zide Indoramin Diltiazem Guanabenz
Phenoxybenzamin Verapamil Methyldopa
Thiazide-like diuretics: e Moxonidine
Indapamide Prazosin ACE inhibitors
Chlorthalidone Terazosin Captopril Vasodilators
Metolazone Tolazoline Enalapril Sodium nitropruside
Fosinopril
Potassium-sparing Mixed alpha + beta Lisinopril Peripheral adrenergic
diuretics: blockers: Perindopril agonist
Amiloride Bucindolol Quinapril Reserpine
Triamterene Carvedilol Ramipril
Spironolactone Labetalol Trandolapril

Benazepril

 Diuretics
 Thiazide diuretics
• lower blood pressure initially by increasing sodium and
water excretion. This causes a decrease in extracellular
volume, resulting in a decrease in cardiac output and
renal blood flow

 A D R:hyp ok alemia, hyp eru ricemia, Hyp omag nesemia,

Hypercalcemia

 Loop diuretics cause decreased renal vascular resistance

and increased renal blood flow.

ADR: Hypercalcemia

 Potassium sparing diuretics reduce potassium loss in the

urine. ADR: Hyperkalemia

 Angiotensin converting enzyme (ACE) inhibitors:
Block production of the hormone angiotensin II, a compound in the
blood that causes narrowing of blood vessels and increases blood
pressure. By reducing production of angiotensin II, ACE inhibitors
allow blood vessels to widen, which lowers blood pressure and
improves heart output
Sideeffects: dry hacking cough, angioedema
 Angiotensin II receptor blockers (ARBs): Block the effects of
angiotensin II on cells in the heart and blood vessels. Similar to ACE
inhibitors, ARBs can widen blood vessels and lower blood press
Side effects — The main difference between ARBs and ACE inhibitors
is that ARBs do not produce cough.
 Dizziness, drowsiness, headache, nausea, dry mouth,
abdominal pain, or other side effects. Angioedema is less common
with ARBs than with ACE inhibitors

 Calcium channel blockers drugs reduce the amount of calcium that enters
the smooth muscle in blood vessel walls and heart muscle. Muscle cells
require calcium to contract. Thus, by inhibiting the flow of calcium across
muscle cell membranes, calcium channel blockers cause muscle cells to
relax and blood vessels to dilate, reducing blood pressure as well as
reducing the force and rate of the heartbeat.

Adverse effects:

 Dihydropyridines may develop headache, dizziness, flushing, nausea,

overgrowth of the gum tissue (gingival hyperplasia), or swelling of the
extremities (peripheral edema).

 Nondihydropyridines can occasionally cause the heart rate to slow too

much. Other side effects may include headache and nausea with diltiazem
or constipation with verapam

 Beta-blockers reduce heart rate and decrease the force of heart
contraction by blocking the action of adrenaline receptors.
 Beta blockers may worsen symptoms of asthma, other lung
diseases, or blood vessel disease outside the heart.I n addition, beta
blockers may mask symptoms of low blood sugar (hypoglycemia) in
people with diabetes who are treated with insulin. Beta blockers
can also cause fatigue, dizziness, insomnia, a decreased ability to
exercise, a slow heart rate, rash, and cold hands and feet due to
reduced blood flow to the limbs
 Alpha 1 receptor blockers: inhibit catecholamine uptake in smooth
muscle cells of the peripheral vasculature, resulting in vasodilation.
They do not alter alpha 1 receptor activity and therefore do not
cause reflex tachycardia.
 side effect is a first-dose phenomenon characterized by orthostatic
hypotension accompanied by transient dizziness or faintness,
palpitations, and even syncope within 1 to 3 hours of the first dose
or after later dosage increases.

 Central alpha 2 agonist: lower blood pressure primarily by
stimulating alpha 2 adrenergic receptors in the brain, which
reduces sympathetic outflow from the vasomotor center and
increases vagal tone. Stimulation of presynaptic alpha 2
receptors peripherally may contribute to the reduction in
sympathetic tone. Consequently, there may be decreases in
heart rate, cardiac output, total peripheral resistance,
plasma renin activity, and baroreceptor reflexes.

Side effects: Sedation and dry mouth

 Direct vasodilators relax (dilate) the blood vessels to
allow blood to flow under lower pressure.

Side effects: headache, weakness, nau sea,

constipation, swelling in the lower legs, and rapid
heartbeat.

 Reserpine depletes norepinephrine from sympathetic

nerve endings and blocks the transport of norepinephrine
into its storage granules. When the nerve is stimulated,
less than the usual amount of norepinephrine is released
into the synapse. This reduces sympathetic tone,
decreasing peripheral vascular resistance and blood
pressure.

Side effects: nasal stuffiness, increased gastric

acid secretion, diarrhea, and bradycardia.

Renin Inhibitors

 A selective renin inhibitor, aliskiren [a-LIS-ke-

rin] has been released for the treatment of
hypertension. Aliskiren directly inhibits renin
and, thus, acts earlier in the renin-angiotensin
-aldosterone system than ACE inhibitors or
ARBs. It lowers blood pressure about as
effectively as ARBs, ACE inhibitors, and
thiazides

 hyperkalemia

 Thank You