ESSENTIAL (PRIMARY) HYPERTENSION

 ESSENTIAL (PRIMARY) HYPERTENSION

AETIOLOGY:

ESSENTIAL (PRIMARY) HYPERTENSION is still far from clear.However, the following factors are important:

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  1. Family history is usually seen in several members of the same family
  1. Genetic factor: Homozygos or the dominant gene is usuallyseen to be severely affected than the heterozygos. Genetic factor is very important.
  2. Age: Essential hypertension is commonly seen in the aged individuals near about 40 years but varies from 25 years to 55 years. Hypertension in the young (below 20 years) always indicates secondary hypertension.
  3. Sex: Commonly seen in males.
  4. Structural changes in arterioles: Thickening of the arteriolar wall and narrowing of the lumen lead to resistance in the blood flow.
  5. Salt intake: If the salt intake is more than average, hypertension may result. Na intake is as important as Cl intake. However, excessive salt intake with genetic predisposition is very important.
  6. Race: It is said to be common in American Negroes and Japanese.
  7. Influence of sympathetic nervous system: Excessive sympathetic nervous activities may result in hypertension. It has an important role in young hypertensives who usually exhibit tachycardia and high output. But there is poor correlation between plasma catecholamine and BP. In adrenergic hyperactivity insensitivity of the bioreflexes may play a role.
  8. Neurogenic hypertension: Lesion of the carotid sinus and aortic baroreceptor may lead to hypertension.
  9. Psychic factor: It acts via the neural pathway.
  10. Renin angiotensin system: Renin is secreted from the juxta glomerular cells surrounding the afferent arteriole from various stimuli, e.g., diminished renal perfusion, diminished blood volume, diminished catecholamines, increased sympathetic activity, arteriolar stretching, hypokalaemia, etc. Renin acts on Angiotensinogen or renin substrate to convert it to Angiotensin I. This is acted upon by Angiotensin II. This is a potent vasoconstrictor and stimulate aldosterone release from Adrenal gland. Though this system has an important bearing on regulating blood pressure yet possibly it has no primary role in the pathogenesis of essential hypertension.ESSENTIAL (PRIMARY) HYPERTENSION

12.Defect in natriuresis: In presence of elevated BP, high serum Nat or blood volume normal individual will have increased natriuresis. In hypertensives this Nat excretion ability is diminished, so this results in increased blood volume and high BP.

  1. Intracellular Nat and Cat: In essential hypertension intracellular Nat and Ca are elevated. The latter is responsible for increase of smooth muscle tone of vessels
  2. Miscellanious Excessive alcohol, smoking, steroids and NSAID, low potassium intake, exercise, Polycythemia etc.

CLINICAL FEATURES:

Onset is insidious. Symptoms are usually variable and at times very vague. There may be no symptom and the disease is diagnosed accidentally during routine examination. If present they are the following:ESSENTIAL (PRIMARY) HYPERTENSION

  1. Pulsating headache often occipital and occurs particularly in the morning
  2. Easy fatiguability.
  3. Insomnia.
  4. Dizziness.
  5. Lack of concentration.
  6. Loss of memory
  7. Occasional palpitation.
  8. Breathlessness.

At later stages as different target organs of the body are involved various additional symptoms may develop usually as a part and parcel of complications which are mentioned below. Symntoms of associated diseases may also be present.

 Cerebral Arteriosclerosis…

This may give rise to:

  1. Hypertensive encephalopathy.
  2. Cerebral and subarachnoid haemorrhage.
  3. Cerebral thrombosis.
  4. TIA.
  5. Insanity and dementia.
  6. Convulsive seizure.
  7. Arteriosclerotic Parkinsonism.

Retinal Arteriosclerosis…

This may give rise to:

  1. Dimness of vision.
  2. Hypertensive retinopathy consisting of the following four stages (Keith, Wagener).

Grade I: Thickening of the arterial wall and increased light reflex (silver wire arteries). Narrowing of the arterioles. Grade II: Reduction of arterial calibre in comparison to that of the vein (altered arteriovenous ratio) and arteriovenous nipping.

Grade III: Exudates and haemorrhages.

Grade IV: Papilloedema. This is a common finding in accelerated or malignant hypertension.

Coronary Arteriosclerosis….

(See Ischaemic heart disease):

This may give rise to:

  1. Acute left ventricular failure.
  2. Angina pectoris.
  3. Coronary thrombosis.
  4. Various other features, including hypertrophy.

Renal Arteriosclerosis

This may give rise to:

  1. Uraemia.
  2. Haematuria in malignant hypertension due to arteriolar necrosis.
  1. Polyuria.
  2. Nocturia.

Arteriosclerosis of limb vessels

This may give rise to:

  1. Ischaemic limb pain.
  2. Intermittent claudication.
  3. Gangrene (dry).

GENERAL  SURVEY

Age: Usually above 40 years

Sex: Usually males.

Robust build with short neck. Tortuous temporal artery may be present. BP above 140/90 mm of Hg.

Carotid dance may be present but not very common due to thickening of arterial wall.

Pulse rate may be slow at times, due to Marey’s reflex; volume is high, bounding in character; wall is thick (Whip cord).

.ESSENTIAL (PRIMARY) HYPERTENSION.