Secondary Hypertension

In about 5-10% cases, hypertension can be shown to be a consequence of a specific disease or abnormality. The causes are listed as follows:

Causes of Secondary Hypertension:

(A). Coarctation of Aorta

1. Renal disease: Parenchymal renal disease
Eg: Glomerceloneptiritis, chronic pyclonephritis

- Collagen vascular diseases
- Polycystic kidney disease
- Renal artery stenosis.

2. Endocrine disorders

- Phaeochromacytoma
- Cushing’s syndrome
- Conn’s syndrome (primary hyperaldosternonism)
- Acromegaly
- Primary hypothyroidism
- Congenital adrenal hyperplasia

3. Alcohol

4. Drugs

– Oral contraceptive’s containing Oestrogens, Anabolic steroids,
- Corticosteroids, Non-sterridal anti-inflammatory, Carbenoxolone

5. Pregnancy: Pre

- Edamptic toxaemia

These conditions give an insight into the possible mechanisms by which hypertension may be caused. In the case of phaeochromocytoma, it results from an increased cardiac output and raised peripheral resistance due to excessive catecholamines.

Conn’s syndrome is associated with sodium retention and probably an alteration in the reactivity of vascular smooth muscle. Renal causes of hypertension are also often associated with sodium retention and in many cases with high plasma concentrations of rennin,

Which causes the production of the potent production of the potent vascoconstriction agent angiontensin II. The latter stimulates aldosterone secretion and thus also encourages sodium retention.

In majority of the patients with hypertension, although some of these mechanisms may be operating, it is not possible to define a specific underlying causes and they are said to have essential hypertension.

In 70 percent of such patients another member of the family is affected. Essential hypertension is especially frequent some races, particularly American blacks and Japanese and it is common in countries where there is high salt intake.

Long standing hypertension causes important structural changes in peripheral resistance vessels and kidneys. These changes may lead to an increase in peripheral vascular resistance and further rise in blood pressure.

Hence, the factors that cause a rise in blood pressure, hence the factors that cause a rise in blood pressure may differ from those that sustain high blood pressure once it is established.

The principal cause of severe pulmonary hypertension in adults is an increase in pulmonary vascular resistance. In infancy another important cause is an increased pulmonary blood flow resulting from left to right shunting, as in atrial and ventricular septal defects and is persistent ductus arteriosus.

While this is initially reversible when the shunt is corrected, prolonged exposure of a child’s lungs to pulmonary hypertension causes irreversible vascular damage, and a rise in pulmonary vascular resistance perpetuates the hypertension.

Any cause of left sided cardiac failure may produce pulmonary hypertension, but it is most prominent when there has been a very gradual rise in left atrial pressure as in some cases of mitral stenosis.

The combined burden of a raised left atrial pressure and an increased pulmonary vascular resistance may produce secondary right heart failure. Provided the left failure is relieved, eg, by mitral valvotomy, the pulmonary hypertension will usually regress.

Pulmonary vasoconstriction in response to hypoxia is to some extent a protective reflex, which will divert blood flow away from poorly ventilated alveoli.

It may be responsible however for the chronic pulmonary hypertension seen in some people who live at high altitude, and for the pulmonary hypertension and right heart failure associated with chronic alveolar hypoventilation.