1. Hypertension

2. definition
The level of BP at which the benefits of treatment outweigh the costs and hazards

3. Aetiology of Hypertension
Primary – 90-95% of cases – also termed “essential” of “idiopathic”
Secondary – about 5% of cases
-Renal disease : Parenchymal renal disease, particularly glomerulonephritis Renal vascular disease
-Alcohol ,Obesity, Pregnancy (pre-eclampsia)
-Endocrine disease : Phaeochromocytoma , Cushing’s syndrome , Primary hyperaldosteronism (Conn’s syndrome) , Acromegaly , Primary hypothyroidism , Thyrotoxicosis , Congenital adrenal hyperplasia •
-Drugs : e.g. Oral contraceptives containing oestrogens, anabolic steroids, corticosteroids, NSAIDs, carbenoxolone,
- coarctation of the aorta

4. Approach to newly diagnosed hypertension
Hypertension is predominantly an asymptomatic condition and the diagnosis is usually made at routine examination or when a complication arises.

5. The objectives of the initial evaluation of a patient with high BP readings are: •
To obtain accurate, representative BP measurements
To identify contributory factors and any underlying cause (secondary hypertension)
To assess other risk factors and quantify cardiovascular risk
To detect any complications (target organ damage) that are already present
To identify comorbidity that may influence the choice of antihypertensive therapy.

6. History
Family history, lifestyle (exercise, salt intake, smoking habit) and other risk factors should be recorded.
A careful history will identify those patients with drug- or alcohol-induced hypertension and may elicit the symptoms of other causes of secondary hypertension, such as phaeochromocytoma (paroxysmal headache, palpitation and sweating, or complications such as coronary artery disease (e.g. angina, breathlessne

7. Examination
Left ventricular hypertrophy (apical heave), accentuation of the aortic component of the second heart sound, and a fourth heart sound.
Radio-femoral delay (coarctation of the aorta;
Enlarged kidneys (polycystic kidney disease), Abdominal bruits (renal artery stenosis) and the Characteristic facies and habitus of Cushing’s syndrome secondary hypertension.
Risk factors, such as central obesity and hyperlipidaemia .
Most abnormal signs are due to the complications of hypertension.

8. Target organ damage
Central nervous system Stroke is a common complication of hypertension and may be due to cerebral haemorrhage or infarction. TIAs are more common in hypertensive patients. Subarachnoid haemorrhage is also associated with hypertension.
Hypertensive encephalopathy is a rare condition characterised by high BP and neurological symptom.

9. Heart
CAD The excess cardiac mortality and morbidity associated with hypertension are largely due to a higher incidence of coronary artery disease.
LVH
Atrial fibrillation
Heart failure

10. Hypertensive retinopathy
Grade 1 Arteriolar thickening, tortuosity and increased reflectiveness (‘silver wiring’)
Grade 2 Grade 1 plus constriction of veins at arterial crossings (‘arteriovenous nipping’)
Grade 3 Grade 2 plus evidence of retinal ischaemia (flame-shaped or blot haemorrhages and ‘cotton wool’ exudates)
Grade 4 Grade 3 plus papilloedema.

11. Hypertension: investigation of all patients
Urinalysis for blood, protein and glucose
Blood urea, electrolytes and creatinine
Blood glucose
Serum total and HDL cholesterol
Thyroid function tests
12-lead ECG (left ventricular hypertrophy, coronary artery disease.
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12. Hypertension: investigation of selected patient
Chest X-ray: to detect cardiomegaly.
Ambulatory BP recording
Echocardiogram
Renal ultrasound
Renal angiography: renal artery stenosis
Urinary catecholamines: to detect possible phaeochromocytoma
Urinary cortisol : Cushing’s syndrome
Plasma renin activity and aldosterone

13. Management
The sole objective of antihypertensive therapy is to reduce the incidence of adverse cardiovascular events, particularly coronary artery disease, stroke and heart failure.

14. Threshold for intervention >140/90
Treatment targets <140/90

15. Antihypertensive drugs
Thiazide and other diuretics
ACE inhibitor
Angiotensin receptor blockers
Calcium channel antagonists.
Beta-blockers
Other drugs. vasodilators

16. Non-drug therapy
Correcting obesity, reducing alcohol intake, restricting salt intake, taking regular physical exercise and increasing consumption of fruit and vegetables can all lower BP.
Moreover, quitting smoking, eating oily fish and adopting a diet that is low in saturated fat may produce further reductions in cardiovascular risk.

17. white coat’ hypertension
Sphygmomanometry, particularly when performed by a doctor, can cause an unrepresentative surge in BP which has been termed ‘white coat’ hypertension, and as many as 20% of patients with apparent hypertension in the clinic may have a normal BP when it is recorded by automated devices used at home.

18. Malignant’ or ‘accelerated’ phase hypertension
Very high BP and rapidly progressive end organ damage, such as retinopathy (grade 3 or 4), renal dysfunction (especially proteinuria) and/or hypertensive encephalopathy)or Left ventricular failure.

19. Practical point
Emergency treatment of accelerated phase or malignant hypertension, lowering BP too quickly may compromise tissue perfusion (due to altered autoregulation) and can cause cerebral damage, including occipital blindness, and precipitate coronary or renal insufficiency. Even in the presence of cardiac failure or hypertensive encephalopathy, a controlled reduction to a level of about 150/90 mmHg over a period of 24–48 hours is ideal.

20. Follow-up
For patients with BP stabilised by management, follow up should normally be three monthly (interval should not exceed 6 months), at which the following should be assessed by a trained nurse:
*   Measurement of BP and weight  *   Reinforcement of non-pharmacological advice *   General health and drug side-effects  *   Test urine for proteinuria (annually)