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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
hypertension is the result of interactions between genetic predisposition,
obesity, alcohol consumption, physical activity and other, as yet, unidentified
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
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
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.
is usually associated with increased severity of
atherosclerosis, coronary blood flow may be insufficient,
leading to ischaemic heart disease.
failure is a common result of hypertensive heart
•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
Hypertrophy of a cardiac muscle.
Transverse slices of a normal heart and a heart with hypertrophy
of the left ventricle.
A large haematoma effaces the basal ganglia, with compression of
adjacent brain. Blood has ruptured into the ventricles.
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
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
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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