In
only a small minority of patients with an elevated arterial pressure can be a
specific cause be identified. Yet these patients should not be ignored for at
least two reasons:
1. With correction
of the cause, their hypertension may be cured.
2. The secondary forms
may provide insight into the etiology of essential hypertension. Nearly all the
secondary forms are related to an alteration in hormone secretion and / or renal
function.
Hypertension
produced by renal disease is the result of either : - a derangement in the renal
handling of sodium and fluids leading to volume expansion or an alteration in
renal secretion of vasoactive materials resulting in a systemic or local change
in arteriolar tone.
The main subdivisions of renal hypertension are renovascular
hypertension including preclampsia and eclampsia, and renal parenchymal hypertension.
A simple explanation for renal vascular hypertension is that decreased
perfusion of renal tissue due to stenosis of a main or branch renal artery activates
the rennin antiotensin system.
Circulating angiotensin II elevates arterial
pressure by direct vasoconstriction, by stimulation of aldosterone secretion with
resultant sodium retention, and / or by stimulating the adrenergic nervous system.
In actual practice, only about one-half of patients with Reno vascular hypertension
have absolute elevations in rennin activity in peripheral plasma, although when
rennin measurements are referenced against an index of sodium balance, a much
higher fraction have inappropriately high values.
Hypertension
is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism
there is a clear relationship between the aldosterone induced sodium retention
and the hypertension.
Normal individuals given aldosterone develop hypertension
only if they also ingest sodium. Since aldosterone causes sodium retention by
stimulating renal tubular exchange of sodium for potassium,.
Hypokalemia
is a prominent feature in most patients with primary aldosteronism, and therefore,
the measurement of serum potassium provides a simple screening test.
The effect of sodium retention and volume expansion in chronically suppressing
plasma rennin activity is critically important for the definitive diagnosis.
In most clinical situations, plasma rennin activity and plasma or urinary
aldosterone levels parallel each other, but in patients with primary aldosteronism,
aldosterone levels are high and relatively fixed because of autonomous aldosterone
secretion, while plasma rennin activity levels are suppressed and respond sluggishly
to sodium depletion.
Primary aldosteronism may be secondary either to
a tumor or to a bilateral adrenal hyperplasia. It is important to distinguish
between these two conditions preoperatively, since usually the hypertension in
the latter is not modified by operation.
They
hypertension which occurs in up to one-third of patients with hyperparathyroidism
ordinarily can be attributed to renal parenchymal damage due to nephrolithiasis
and nephrocalcinosis.
However, increased calcium levels also can have a direct vasoconstrictive effect.
In some cases, the hypertension disappears when the hypercalcemia is corrected.
Thus paradoxically, the increased serum calcium level in hyperparathyroidism
raises blood pressure, while epidemiologic studies suggest thyroidism raises blood
pressure, while epidemiologic studies suggest that a high calcium intake lowers
blood pressure.
To further confuse the issue, calcium entry blocking
agents are effective antihypertensive agents. Additional studies are needed to
resolve these seemingly conflicting observations.
Thye
hypertension associated with coarctation may be caused by the constriction itself
of perhaps by the changes in the renal circulation which result in an unsual form
of renal arterial hypertension.
The diagnosis of coarctation is usually
evident from physical examinations. The neurological effects of long standing
hypertension may be divided into retinal and central nervous system changes.
Because the retina is the only tissue in which the arteries and arterioles
can be examined directly, repeated ophthalmoscopic examination provides the opportunity
to observe the progress of the vascular effects of hypertension.
Increasing
severity of hypertension is associated with focal spasm and progressive general
narrowing of the arterioles, as well as the appearance of hemorrhages, exudates
and papilledema.
The retinal lesions often produce scotomata, blurred
vision and even blindness. Central nervous system dysfunction also occurs frequently
in the patients with hypertension. Occipital headaches, most often in the morning
are amongst the most prominent early symptoms of hypertensions.
