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systemic hypertension( htn)

SYSTEMIC HYPERTENSION( HTN)
SYSTEMIC HYPERTENSION( HTN)

systemic hypertension( htn)

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Definition.

Is the disorder characterized by sustained elevation of systemic arterial blood pressure.

Usually equal or above a systolic of 140mmhg and a diastolic pressure of 90mmhg.

• This diseases is a significant risk factor of cardiovascular diseases and a major causes of heart failure, renal failure, and stroke

Risk factors for HTN

• Genetic factor • Age

• Salt intake

• Tobacco

• Obesity

• Stress

• Sedentary life style • Male gender

• Black race

Etiological classification

(i)Primary htn (essential hypertension) This is the type of hypertension whose

etiology is unknown. Incidence is 90% More common in adult

(ii)Secondary htn

This is the type of hypertension with the specific causes.

Incidence is 5% to 10 %

• i. e Endocrine diseases; eg cushing disease, aldosteronism, pregnancy, coarctation of aorta.

• renal diseases eg; renal vascular or renal parenchyma diseases, renin secreating tumour

pathogenesis

• Hypertension represents an inbalance in the factors that controls

➢Cardiac output

➢Peripheral  resistance

➢Sodium hemostasis

Kidney influences blood pressure through several mechanism

• The renin-angiotensin-aldosterone system.

Is the major blood pressure mechanism.

Activation of the system result in an increase in systemic blood pressure.

The system act follows:

a) Renin is released by juxtaglomerularcells under the stress of decreased afferent arteriolar pressure,

decreased sodium delivery to the distal tubule or direct sympathetic stimulation

b) Renin cleaves angiotensinogen, a circulating 2-globulin produced in the liver to form angiotensin-1, which is further modified to potent vasoconstrictor angiotensin-2 by angiotensin converting enzymes by single passage through the lungs.

• Angiotensin II also stimulate the production of aldosterone by the adrenal cortex.which inturn results in increases in renal reabsoption of Na+.

• It also stimulate renin released by increasing activity of the sympathetic neurosystem

Symptoms

• Headache (occipital, common in the morning)

• Tinnitus

• Vertigo

• Altered vision

• Buzzing or hissing in the ears

• lightheadedness

Hypertensive urgency

• Severely elevated BP 180/120 mmhg without impending or progressive end organ damage

Hypertensive emergency:

Severely elevated BP 180/120mmhg with impending or progressing end organ damage eg.loss of vision, severe headache, chest pain , confusion/altered level of consciousness, reduced urine

output.

Diagnosis

• Hypertension is diagnosed on the basis of a persistently high blood pressure. Traditionally, this requires three separate sphygmomanometer.

Initial assessment of the hypertensive people should include a complete history and physical examination.

– Need for several BP readings with the 24- hour ambulatory blood pressure monitors and home blood pressure machines

• Urine for protein • Ecg

• Rbg

• Urea

• Creatinine

• And electrolytes.

 

treatment

Non – pharmacological therapy

• Lifestyle modification:

➢Weight Reduction; Maintain ideal body weight BMI 18.5 – 24.9kg/m2

➢Adopt DASH* eating plan; Consume a diet rich in fibre – fruits, vegetable, unrefined carbohydrate and low fat dairy products with reduced content of saturated and total fat

➢ Reduce dietary sodium intake no more than 1000mmmol/l (2.4gm sodium or 6gm

sodium chloride

➢ Physical Activity; Engage in regular activity such as a brisk walking at least 30min/day most days a week

➢Stop using all tobacco products

➢Moderation of alcohol consumption; Limit consumption to no more than 2 drinks per day in men and no more than one drink per day in Women and light person

*DASH – Dietary Appropriate to Stop Hypertension

Pharmacological therapy

• First line treatment without compelling indications:

• Low Dose Thiazide diuretics + Potassium sparing e.g. Bendroflumethiazide 2.5 – 5mg/d, Hydrochlothiazide 12.5 -25mg/d + Spironolactone 25mg daily

Second line

• Calcium channel blockers such as nifedipine and amlodipine block L-type calcium channels and are effective arterial vasodilators.

• Beta Blockers

Eg; Propranolol , Atenolol ,Metoprolol, Carvedilol .

• Direct arterial vasodilators such as hydralazine have relatively limited use. Neither has much effect on venous tone. The mechanism of action of hydralazine is not known.

• Renin-angiotensin system (RAS) blockers comprise two broad categories: angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin type 1 receptor blockers (ARB’s).

ACE inhibitors like captopril, enalapril

• ACE inhibitors like captopril, enalapril, and lisinopril decrease the conversion of angiotension I to angiotensin II

• ACE inhibitors are associated with a definite improvement in renal function in patients with diabetes and it has been shown that renal injury due to long-standing diabetes is reduced. Diabetics who do not have a contraindication for this class of drugs should be taking them for renal protective purposes.

• Angiotensin receptor blockers (ARB’s) like losartan and valsartan cause arteriolar vasodilation by blocking the effects of angiotensin II at the angiotensin Type I receptor. Since the mechanism is essentially the same as for the ACE inhibitors, the indications and contraindications are the same. The blockade is downstream, so bradykinin is not elevated, and this class of drugs is not associated with a cough

Complication of HTN

• Cerebrovascular diseases • Renal failure

• Heart failure

• Coronary artery diseases

Prognosis

• Most individuals diagnosed with hypertension will have increasing blood pressure (BP) as they age. Untreated hypertension is notorious for increasing the risk of mortality and is often described as a silent killer

• Mild to moderate hypertension, if left untreated, may be associated with a risk of atherosclerotic disease in 30% of people and organ damage in 50% of people within 8-10 years after onset.

• Death from ischemic heart disease or stroke increases progressively as BP increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in BP above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

• The morbidity and mortality of hypertensive emergencies depend on the extent of end-organ dysfunction on presentation and the degree to which BP is controlled subsequently

-With BP control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%

• In the Framingham Heart Study, the age-adjusted risk of congestive heart failure was 2.3 times higher in men and 3 times higher in women when the highest BP was compared to the lowest BP

• The Framingham Heart Study found a 72% increase in the risk of all-cause death and a 57% increase in the risk of any cardiovascular event in patients with hypertension who were also diagnosed with diabetes mellitus

• Nephrosclerosis is one of the possible complications of long-standing hypertension. The risk of hypertension-induced end-stage renal disease is higher in black patients, even when blood pressure is under good control

• Furthermore, patients with diabetic nephropathy who are hypertensive are also at high risk for developing end-stage renal disease.

• Clinical trials have demonstrated the following benefits with antihypertensive therapy :

– Average 35-40% reduction in stroke incidence

– Average 20-25% reduction in myocardial infarction

– Average reduction in heart failure >50% in heart failure