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SYSTEMIC HYPERTENSION
Hypertension (HT) = pathologically blood pressure
Blood pressure : Systolic /diastolic pressure
Normal blood pressure (adults) : < 140 mm Hg/90 mm Hg
Borderline HT : 140 - 160 mm Hg/90 - 95 mm Hg
Definite HT : > 160 mm Hg/95 mm Hg
The kidney and blood pressure
• Role in regulation of blood pressure
- Renin-angiotensin system (juxtaglomerular
apparatus).
- Production of a variety of vasodepressor or
antihypertensive substances (prostaglandin, NO).
• Renal diseases may cause systemic HT.
• HT may cause renal damage.
Classification
Essential vs secondary HT
Benign vs malignant HT
• Essential HT
90 - 95% of cases.
Pathogenetic mechanisms multifactorial and poorly
understood.
• Secondary HT
5 - 10% of cases.
Hypertension due to a recognisable disease.
Diseases associated with secondary HT:
1) Renal diseases
- Renal parenchymal diseases (see later).
- Renovascular HT = systemic HT due to
stenosis of a renal artery ( ischaemia
release of renin).
2) Endocrine
- Adrenocortical hyperfunction/tumour (Cushing,
Conn)
- Exogenous glucocorticoids
- Pheochromocytoma
- Acromegaly
- Hyperthyroidism
- Pregnancy-induced
3) Cardiovascular
- Coarctation of aorta
4) Neurogenic
- Increased intracranial pressure
- Acute stress
Pathogenetic factors in essential HT
Arterial blood pressure
= cardiac output (*)
x
peripheral vascular resistance (**)
Blood pressure will rise if either (*) or (**)
is increased
Essential hypertension is associated with:
- peripheral vascular resistance
(pathogenesis poorly understood)
- Sodium and water retention
blood volume, cardiac output
A high salt intake correlates with prevalence of
essential HT.
Genetic factors:
- Sensitivity of some individuals to a high salt
intake.
- High prevalence in blacks.
Benign HT
- moderate increase in blood pressure.
- long clinical course.
- little clinical effects in early stages.
Malignant HT
- diastolic pressure > 130 mm Hg
- severe impact on cardiovascular system,
kidneys and central nervous system.
Malignant HT:
- May arise in previously normotensive individuals, but
more commonly as a complication of benign HT.
- Relatively uncommon (1-5% of hypertensive
patients).
- Aggressive treatment is required.
Complications of systemic HT
Cardiovascular
CNS
Renal
Cardiovascular
Heart
- Increased workload on left ventricle
Left ventricular hypertrophy
left ventricular failure.
- Greater thickness of left ventricle
decreased perfusion and ischaemia of
subendocardial region of myocardium.
Arteries
- Accelerated atherogenesis.
- risk of developing aortic dissecting aneurism.
Arterioles: Arteriolosclerosis
- Benign HT:
Deposition of eosinophilic (‘hyaline’) material in vessel
walls due to influx of plasma proteins.
- Malignant HT:
Thickening of intima.
Necrosis of vessel walls ('fibrinoid' necrosis) and
formation of micro-aneurisms (of Bouchard) in brain.
CNS
- Rupture of micro-aneurisms of small penetrating
arteries Intracerebral haemorrhage.
- Risk of cerebral infarction due to atherosclerosis