Table of contents:

1. Secondary hypertension
2. Primary or secondary?
3. What causes may lie behind secondary hypertension?
4. Symptoms of the disease
5. Obstructive sleep apnoea

Secondary hypertension

Arterial hy pertension is divided into primary and secondary hypertension. Primary hypertension is much more commonly diagnosed, whose pathogenesis is heterogeneous and multifactorial. Its components include genetic, environmental and lifestyle factors that interact to disrupt the function of one or more systems involved in regulating blood pressure, with the result that blood pressure values are set at a higher level. Secondary hypertension developing in the course of other diseases is much rarer. Thus, unlike primary hypertension, which is a disease entity in itself, secondary hy pertension is a response to disrupted mechanisms in the course of various disease entities.

Primary or secondary?

Differences exist not only in the pathogenesis itself, but also in the treatment, course and diagnosis. Diagnosis is often difficult and requires a multi-stage diagnosis. In primary hypertension, the situation is somewhat simpler and the scenario is usually that the patient has his or her blood pressure measured during a visit to the general practitioner, where a diagnosis is made and treatment is implemented, which, with some discipline on the part of the patient, allows proper blood pressure control. Primary hypertension is usually asymptomatic, especially in the early stages, and often co-exists with obesity, excessive salt intake, an unhealthy lifestyle, lack of exercise and long-term chronic stress. The essential role of genetic factors is emphasised, although a clear cause for the development of hypertension can never really be determined. Secondary hy pertension is characterised by sudden increases in blood pressure, the symptoms are more severe and pharmacotherapy often does not have the intended effect. This is all due to the fact that the underlying cause of hypertension is another disease. In the general practitioner's office, it is often diagnosed as primary hypertension and only after difficulties with therapy is the diagnosis deepened. Secondary hypertension can affect patients of different ages. Quite often it affects young people, in whom primary hypertension is rather rare.

What causes may lie behind secondary hypertension?

Renal causes - this is how they are often abbreviated by doctors who diagnose secondary hypertension - nephrologists or hypertensiologists. By what mechanism does hypertension occur? In this situation, the culprit is the well-known atherosclerosis. Unfortunately, it does not spare the renal arteries either, where, as in many other vessels, cholesterol is deposited, consequently leading to their narrowing. The stenosis impairs blood flow to the kidneys, which react to the reduced blood perfusion by secreting various compounds, including a substance called renin. Under its influence, a cascade of production of further compounds is triggered, the high concentration of which has the effect of, among other things, constricting the vessels at the periphery and retaining more sodium in the body. The mechanism has many components, but ultimately there is a pathological increase in pressure, which adversely affects other organs and systems of our body.

This hypertension is characterised by resistance to treatment, high pressure values and organ complications. Diagnosis is based on imaging studies of the renal arteries (Doppler, CT scan, MRI and arteriography of the renal arteries). Treatment often includes surgical intervention, which involves unblocking the renal arteries by using stents to dilate the arterial lumen. Another cause may be secondary hyperaldosteronism (Conn's syndrome). The essence of this entity is an excessive amount of aldosterone, a hormone involved in mineral metabolism. Its high concentration causes salt retention in the body. This translates into increased blood pressure. The sources of excessive aldosterone production can vary.

Diagnosis of hypertension, photo: panthermedia

The most common include adrenocortical adenoma and bilateral adrenal hyperplasia. Rarer causes include familial type 1 and 2 hyperaldosteronism, aldosterone-secreting adrenocortical carcinoma, aldosterone-secreting ectopic tumour (e.g. kidney, ovary). Diagnosis involves specialised endocrinological investigations, which most often require hospitalisation and daily aldosterone determinations. The next step is imaging studies to localise the lesions responsible for the excessive production of the hormone. Treatment consists of the administration of drugs to reduce the aldosterone concentration in the blood, while in some cases surgical intervention is required. In the case of pheochromocytoma, another possible culprit of secondary hypertension, there is excessive production of catecholamines by the tumour mass.

Symptoms of the disease

Typical symptoms of this disease are paroxysmal increases in blood pressure, which can last from a few minutes to several hours. The elevations are accompanied by headaches, palpitations and a feeling of anxiety. Diagnosis is based on the determination of urinary concentrations of adrenaline, noradrenaline derivatives (catecholamines). When values are high, imaging studies look for the tumour responsible for the excessive production of these compounds. Treatment consists of surgical removal of the tumour, together with pharmacotherapy to protect the patient from high blood pressure spikes and organ damage as a consequence of prolonged, severe hypertension. Another syndrome in the course of which hypertension may develop is Cushing's syndrome. This is a clinical syndrome resulting from an excess of glucocorticosteroids (CSCs) - hormones produced by the adrenal cortex. There are several causes of this syndrome. As in hyperaldosteronism, excess GCSs may be related to a tumour in the adrenal cortex that secretes these compounds in excess. Another cause is located at the level of the pituitary gland, which controls various organs in the body and may, in a sense, 'force' the adrenal cortex to increase steroid production. These mechanisms result in the production of compounds (GCS) that are also involved in mineral metabolism. A disturbance in the concentration of individual minerals carries over to a disturbance in the mechanisms that control blood pressure. Diagnosis is multistage and requires consultation in an endocrinology department. The same is true for treatment, which depends on the cause and severity of the symptoms. Excess steroids strongly affect not only blood pressure, but also carbohydrate metabolism, the cardiovascular system and blood composition.

Obstructive sleep apnoea

It is important to promptly recognise and implement appropriate therapy to avoid multi-organ complications. Another disease that is quite often overlooked is obstructive sleep apnoea (ESRS). Its course is characterised by repeated episodes of upper airway closure at the level of the pharynx with subsequent apnoea and shortness of breath. This then compromises blood oxygenation and results in frequent awakenings during sleep. Faced with such a situation, sleep and therefore proper rest is not possible. Hypoxaemia (low oxygen concentration in the blood) causes excessive activation of the sympathetic nervous system, which then translates into increased blood pressure. Factors that contribute to obstructed breathing are obesity (excessive neck circumference), long uvula, hypertrophy of the palatine tonsils, curvature of the nasal septum, drinking alcohol (especially before bed), smoking, hypothyroidism.

During the day, drowsiness, headache, memory impairment, difficulty concentrating, emotional disturbances prevail. At night, there is increased snoring alternating with apnoea, increased sweating, awakenings with a feeling of breathlessness, palpitations, dry mouth upon awakening. The diagnosis is based on an assessment of daytime sleepiness according to the Epworth Sleepiness Scale (ESS) and a detailed sleep study - polysomnography, one component of which is an assessment of the number of apnoeas during sleep. Treatment is mainly based on lifestyle changes: reducing body weight, increasing physical activity and, in the case of ENT causes, septoplasty (straightening of the nasal septum), tonsillectomy (removal of the tonsils) and uvulopalatoplasty (plasty of the soft palate) are carried out.