HYPERTENSION

Hypertension: Elevated arterial BP
- Rise in systolic pressure > in men
- 20-30% if adult population
- Rates are higher in black Africans

High BP 130-139/ 85-89

Hypertension
Grade 1: 140-149/ 90-99
Grade 2: 160-179/100-109
Grade 3: >180/ >10

Isolated systolic Hypertension
Grade 1: 140-149/ <90
Grade 2: >160/ <90

Causes:
Essential: idiopathic 90% of people with hypertension
1. Genetic
2. Fetal factors: Low birthweight associated with high BP. Fetal adaptation to intrauterine undernutrition with long-term changes in vessel structure or function of crucial hormone systems
3. Environment
a. Obesity
b. Alcohol: small amts good though
c. Sodium intake
d. Stress: however, chronic stress is not proven to be a cause
4. Humoral mechanism: ANS, as well as rennin-angiotensin etc has a role in physiological regulation of BP short-term.
5. Insulin resistance: hyperinsulinaemia, glucose intolerance, reduced levels of HDL cholesterol, hypertriglyceridaemia, central obesity (metabolic syndrome)

Secondary: has specific cause
1. Renal diseases: Na, H20 retention, plasma rennin elevation
2. Endrocrine: Conn’s syndrome, adrenal hyperplasia, phaeochromocytoma, Cushing’s syndrome, acromegaly
3. Congenital CV: coarctation of aorta
4. Drugs: monoamine oxidase inhibitors, consuming tyramine-containing foods etc
5. Pregnancy: Usually resolves after delivery. Pre-eclmapsia: pregnancy-induced hypertension with proteinuria.

Pathophysiology
- Causes changes in large arteries. Thickening of media, increase in collagen & secondary deposition of calcium. Loss of arterial compliance. Atheroma develop in large arteries due to interaction of mechanical stress & low-growth factors. Endothelial dysfunctions with alternations in NO & endothelins.
- Chronic hypertension: cardiac output normal, increased peripheral resistance (small arteries and arterioles have structural changes) Increase wall thickness with reduced lumen diameter.
- Left ventricular hypertrophy: increased peripheral vascular resistance, increased LV load
- Renal vasculature affected: reduced renal perfusion, glomerular filtration rate, reduction in sodum, water excretion. Activation of rennin-angiotensin system with further sodium, water retention.

Complications
Cerebrovascular disease, CAD, renal failure, peripheral vascular disease, stroke
Malignant hypertension: BP rises rapidly, severe. (Diastolic >120) Fibrinoid necrosis of vessel wall, if untreated, death by renal failure, heart failure, aortic dissection or stroke. High risk of cerebral oedema and haemorrhage.

Investigations
ECG, Urine stix test for blood & prot, fasting blood for lipids & glucose, serum urea, creatinine, electrolytes

Treatment:
Non-Pharmacological
Weight reduction
Low-fat, saturated fat diet
Low sodium diet
Limited alcohol consumption
Exercise
Increase fruit & vege
Stop smoking & increase oily fish consumption

Pharmacological
1. ACE-inhibitors or angiotensin receptor antagonist: block conversion of angiotensin 1 to 2 (vasoconstrictor), block degradation of bradykinin (vasodilator) OR block receptors for angiotensin 2, no effect on bradykinin (no cough)
2. beta-blockers: change effects of sympathetic nervous and rennin-angiotensin, reduce force of cardiac contraction & HR
3. calcium-channel blockers: arteriolar dilatation, reduce force cardiac contraction
4. diuretic

Note: Cannot reduce blood too rapidly as it may lead to cerebral, renal, retinal or myocardia infarct

Source: K & C