Aeuology of essential hypertension is still far from clearHowever, the following factors are important
1. Family Nistory is usually seen in several members of the same family
2. Genetic facior Homozygos or the dominant gene is usual seen to be severely affected than the heterozygos. Genetic
factor is very important.
3. Age: Essential hypertension is commonly seen in the individuals near about 40 years but varies from 25 years t
55 years. Hypertension in the young (below 20 years always indicates secondary hypertension. Ser: Commonly seen in males
5. Structural changes in arterioles: Thickening of the arteriolar wall and narrowing of the lumen lead toresistance in the blood flow Aetiology
6. Salt intake: If the salt intake is more than average, hypertension may result. Nat intake is as important as Cl intake. However, excessive salt intake with genetic predisposition is very important.
7. Race: It is said to be common in American Negroes and Japanese
8. 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.
9. Neurogenic hypertension: Lesion of the carotid sinus andaortic baroreceptor may lead to hypertension.
10. Psychic factor: It acts via the neural pathway
11. 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 uponby Angiotensin II. This is a potent vasoconstrictor and
stimulate aldosterone release from Adrenal gland. Thoughthis system has an important bearing on regulating blood
pressure yet possibly it has no primary role in thepathogenesis of essential hypertension12. Defect in natriuresis: In presence of elevated BP, higlhserum Na+ or blood volume normal individual will haveincreased natriuresis. In hypertensives this Na excretion
ability is diminished, so this results in increased bloodvolume and high BP.13 Intracellular Na and Cat In essential hypertension
intracellular Na’ and Ca are elevated The lalter is responsible for increase of smooth muncle tone of vesnels14 Mixcellanious Escessive alcohol, smoking, steroids andNAID, l”w potassium intake, exervise. Illycythemia etc
Clinical Feoturess insiious. Symptoms are usually variahle and at timesvery vague There may he no ymptom and the diseuse
diagnosed accidentally during routine exnminntion. If presentthey are the following Pulsating hendache often occipital and occurs particuarly in the moning
2 Easy fatiguability
5. Lack of concentration
6. Loss of memory
7. Occasional palpitation
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 mentionedbelow. Symptoms 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.
5. Insanity and dementia.
6. Convulsive seizure
7. Arteriosclerotic Parkinsonism.
Retinal ArteriosclerosisThis may give rise to
1. Dimness of vision.
2. Hypertensive retinopathy consisting of the following four
stages (Keith, Wagener).
Grade 1: Thickening of the arterial wall and increased light
rellex (silver wire arteries), Narrowing of the arterioles
Grade Il: Reduction of arterial calibre in comparison to that
of the vein (altered arteriovenous ratio) and arteriovenous
Grade II: Exudates and haemorrhages.
Grade IV: Papilloedema. This is a common finding in
accelerated or malignant hypertension
(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 Arterio sclerosis This may give rise to
2. Haematuria in malignant hypertension due to arteriolarnecrosis
Arteriosclerosis of limb vesxela This may give rise to
1 Ischaemic limb pain
2. Intermittent elaudicution
Age: Usually above 40 years
Sex: Usually males.Robust build with short neck. Tortuous temporal artery maybe present. BP above 140/90 mm of HgCarotid dance may be present but not very common due to thickening of arterial wallPulse rate may be slow at times, due to Marey’s reflex volume is high, bounding in character, wall is thick (Whip cord) Examination of the Heart Apex beat may be more down, forceful and well sustained This is called heaving apex beat, which is a sign of left ventricular hypertrophy. This indicates hypertension of long duration.Over the mitral area 1st sound is loud and booming Sometimes there may be a soft systolic murmur due to dilatation of the heart or due to papillary muscle dysfunction. In about 5% of patients aortic diastolic murmur may be
present Aortic component of the second sound (A2) is accentuated and ringing in character. Rarely there may be a reversed
splitting of the second heart sound. There may be a systolic click and a systolic ejection murmur over the aortic area. S
may be audible. Examination of the Abdomen In cases of polycystic kidney, kidneys are palpable; in case ofhydronephrosis the affected kidney may be palpable and tenderness may be elicited over the renal angle or renal area
in cases of pyelonephritis Auscultation may reveal a systolic murmur over the aorta in cases of coarctation or over the renal artery due to renal artery stenosis. All these are included under causes of secondary hypertension. Sometimes over the aorta a systolic murmur may be audible due to gross aortic atherosclerosis which can be distinguished from murmurs of coarctation and
renal artery stenosis.