Hypertension

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Hypertension may be classed as primary or may be secondary to a known cause.
Primary (essential) hypertension is elevation of blood pressure with age, but with no apparent cause.
It accounts for over 90% of all cases and is usually seen after the age of 40 years.
The phenotype of high blood pressure in essential hypertension is the result of interactions between genetic predisposition, obesity, alcohol consumption, physical activity and other, as yet, unidentified factors.
Accounting for about 10% of all cases, secondary hypertension is due to an identifiable cause, the most common of which is renovascular disease that elevates blood pressure by activation of the renal-angiotensin-aldosterone system.

Depending on the clinical course of disease, both primary and secondary hypertension can be classified into two types.
With benign hypertension there is stable elevation of blood pressure over many years, and with
accelerated hypertension blood pressure elevation is severe and becomes worse over a short period of time.
Factors that regulate blood pressure}

Blood pressure can be elevated by increasing cardiac output or by increasing peripheral vascular resistance. The former is raised by increasing the blood volume or by increasing cardiac contractility and rate, and the latter may be increased by humoral, neural and autoregulatory factors.

Artery wall thickening and hyaline arteriolosclerosis are features of benign hypertension.
In benign hypertension, vessel changes develop gradually in response to a persistent stable elevated blood pressure.

These degenerative changes in the walls of small vessels such as arterioles lead to reduction in effective lumen, with consequent tissue ischaemia, and to increased fragility of vessels in the brain, predisposing to haemorrhage.

There is hypertrophy and thickening of muscular media, thickening of elastic lamina, fibroelastic thickening of the intima, and reduction in the size of of the vessel lumen.

There is hyaline wall thickening (hyaline arteriolosclerosis), increased rigidity (with limited capacity for expansion and constriction), and reduction of lumen size.

Destruction of small vessel walls is seen in malignant hypertension.
When the blood pressure rises suddenly and markedly, acute destructive changes occur in the walls of small blood vessels, together with proliferative reparative responses in the walls of small arteries.
These changes lead to cessation of blood flow through the small vessels,with multiple foci of tissue necrosis, e.g. in the glomeruli in the kidney.

Loose myxomatous fibrous intimal proliferation can be seen, together with reduction of lumen and normal media.
Hypertension mainly affects the heart, brain, kidneys and aorta.

The pathological consequences of hypertension are seen in four main tissues:
•Heart. With increasing pressure, the left ventricular myocardium undergoes hypertrophy.
Since hypertension is usually associated with increased severity of atherosclerosis, coronary blood flow may be insufficient, leading to ischaemic heart disease.
Left ventricular failure is a common result of hypertensive heart disease.

•Brain. Hypertensives are particularly prone to developing massive intracerebral haemorrhage due to rupture of intracerebral blood vessels.
Small vessel damage within the cerebral hemispheres produces microinfarcts in the form of small areas of brain destruction filled with fluid (hypertensive lacunae).

•Kidney. Arteriolosclerosis leads to progressive ischaemia of the nephron, with eventual destruction
of glomeruli, and atrophy of the associated tubular system. This disease is slowly progressive, as
individual nephrons are picked off one at a time.
When sufficient nephrons have been rendered non-functional through ischaemia, the patient develops
slowly progressive chronic renal failure. When hypertension has produced significant nephron
ischaemia, the kidney is said to have developed benign hypertensive nephrosclerosis.
It is a common and important cause of chronic renal failure in the middle-aged and elderly population.

•Aorta. Hypertension predisposes to development of severe atheroma, abdominal aortic aneurysms, and
dissections.
Hypertrophy of a cardiac muscle.
Transverse slices of a normal heart and a heart with hypertrophy of the left ventricle.

•Intracerebral haematoma.
A large haematoma effaces the basal ganglia, with compression of adjacent brain. Blood has ruptured into the ventricles.

•Aortic aneurysm.
The abdominal aorta, between the origin of the renal arteries above, and the bifurcation into iliac arteries below, is distended by a thin-walled fusiform aneurysm with large amounts of laminated thrombus
in the aneurysm cavity.

The abdominal aorta, between the origin of the renal arteries above, and the bifurcation into iliac arteries below, is distended by a thin-walled fusiform aneurysm with large amounts of laminated thrombus in the aneurysm cavity.
Secondary hypertension accounts for less than 10% of cases In a minority of cases, some structural abnormality is considered to be responsible for the development of systemic hypertension. For example,
stenosis of one renal artery (usually at its origin) by atherosclerosis can produce hypertension, treatable by surgery.
Associated with a rise in renin and angiotensin II levels in the circulation from the ischaemic
kidney, the hypertension can be cured in the early stages by removal of the affected kidney.

Hypertension is also a feature of diffuse renal disease such as glomerulonephritis and pyelonephritis.
The hypertension is transient in the initial acute phase of glomerular diseases (e.g. acute nephritic syndrome),but is permanent in chronic diffuse renal disease.

Phaeochromocytoma, an adrenaline-noradrenaline
(epinephrine-norepinephrine)-secreting tumour, usually of the adrenal medulla, produces hypertension that is initially paroxysmal.

Coarctation of the aorta is a congenital malformation in which there is increased peripheral resistance due to a structural narrowing of the aorta.
In such cases the hypertension is not truly systemic as it affects only the arterial system proximal to the coarctation and, thus, mainly the arms, head and neck.

Hypertension is a feature of adrenal cortical diseases, conditions associated with excess production of glucocorticoids and mineralocorticoids by the adrenal cortex (Cushing's syndrome and Conn's syndrome).

It is also a feature of pre-eclampsia, may be seen in association with endocrine disorders such as thyrotoxicosis, acromegaly and, occasionally, hypothyroidism, or there may be a neurogenic cause such as raised intracranial pressure.

Pulmonary arterial hypertension is usually due to disease in the lung or left side of the heart.
Most pulmonary hypertension is 'secondary' in that it develops as a consequence of one of two types of raised pressure in the pulmonary capillary bed.
Pulmonary capillary pressure may be raised due to raised pressure in the left atrium and left ventricle. This back pressure is the result of inadequate emptying of the left heart chambers (left heart failure), the increased pressure in these chambers being reflected along the pulmonary veins and into the pulmonary capillary beds (pulmonary congestion).
Important causes are left ventricular failure due to hypertensive or ischaemic heart disease, aortic
valve stenosis, and mitral valve stenosis (leading to left atrial failure).
Alternatively, pulmonary capillary pressure may be raised due to destruction
of the pulmonary capillary bed as a result of primary lung diseases.
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