Secondary hypertension can be caused by a number of diseases.
Renal causes (2.5-6%) of hypertension include the renal parenchymal diseases and renal vascular diseases, as follows:
Vascular causes include the following:
- Coarctation of aorta
- Collagen vascular disease
- Endocrine causes account for 1-2% and include exogenous or endogenous hormonal imbalances.
Exogenous causes include administration of steroids. The most common form of secondary hypertension is a renal cause (although the true prevalence of hyperaldosteronism is not clear).
- Another common cause is endocrine: oral contraceptive use. Activation of the renin-angiotensin-aldosterone system (RAAS) is the likely mechanism, because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives.
Approximately 5% of women taking oral contraceptives may develop hypertension, which abates within 6 months after discontinuation. The risk factors for oral contraceptive–associated hypertension include mild renal disease, familial history of essential hypertension, age older than 35 years, and obesity. It would be better to group oral contraceptives and steroids with drug-induced hypertension (see Table 1, below).
- Exogenous administration of the other steroids used for therapeutic purposes also increases blood pressure (BP), especially in susceptible individuals, mainly by volume expansion.
Nonsteroidal anti-inflammatory drugs (NSAIDs) may also have adverse effects on BP. NSAIDs block both cyclooxygenase-1 (COX-1) and COX-2 enzymes. The inhibition of COX-2 can inhibit its natriuretic effect, which, in turn, increases sodium retention.
NSAIDs also inhibit the vasodilating effects of prostaglandins and the production of vasoconstricting factors—namely, endothelin-1. These effects can contribute to the induction of hypertension in a normotensive or controlled hypertensive patient.
Endogenous hormonal causes include the following:
Neurogenic causes include the following:
- Brain tumor
- Bulbar poliomyelitis
- Intracranial hypertension
Drugs and toxins that cause hypertension include the following:
- Cyclosporine, tacrolimus
- Adrenergic medications
- Decongestants containing ephedrine
- Herbal remedies containing licorice (including licorice root) or ephedrine (and ephedra)
Other causes include the following:
- Hyperthyroidism and hypothyroidism
- Obstructive sleep apnea
- Pregnancy-induced hypertension
- Multiple studies have shown OSA to be an independent risk factor for the development of essential hypertension, even after adjusting for age, gender, and degree of obesity.
- Approximately half of individuals with hypertension have OSA, and approximately half with OSA have hypertension.
- Numerous studies have shown that treatment of OSA by continuous positive airway pressure (CPAP) or position therapy lowers the awake and 24-hour blood pressure levels. Unfortunately, most cases of OSA go undiagnosed.
There are several parts to making an accurate diagnosis of Secondary Hypertension.
A: ACCURACY, APNEA, And ALDOSTERONISM
The first, most practical step in evaluating an elevated blood pressure reading is to investigate its accuracy. A blood pressure cuff that is too small, tight-fitting sleeves that are not removed, or a brachial artery that is noncompressible because of calcification (sometimes seen in the elderly) can cause falsely elevated readings.
White-coat hypertension (blood pressure that is elevated in the physician's office but normal at other times) accounts for about 20 percent of patients with elevated readings. JNC-VI recommends confirming high blood pressure readings outside of the office setting.
Obstructive sleep apnea (OSA), a repetitive mechanical obstruction of the upper airway during sleep, is an independent risk factor for hypertension. At least one half of patients with OSA have hypertension. Treatment of OSA with surgery or nasal continuous positive air way pressure reduces hypertension in these patients.
Primary hyperaldosteronism is defined as overproduction of aldosterone independent of its usual regulator, the renin-angiotensin system. The resulting retention of excess salt and water suppresses renin levels.
Increased urinary excretion of potassium signals hyperal-dosteronism, which should be suspected in all hypertensive patients with unprovoked (i.e., not diuretic-induced) hypokalemia. The next diagnostic test should be demonstration of an elevated ratio of plasma aldosterone levels to plasma renin activity.
B: BRUITS, BAD KIDNEYS (RENAL PARENCHYMAL DISEASE)
Renovascular hypertension is defined as hypertension resulting from compromised arterial supply to the kidneys. About 65 percent of renovascular disease is secondary to atherosclerosis in the renal arteries, usually seen after age 50 in patients at risk for arterial compromise (e.g., smokers, patients with diabetes, and patients with known atherosclerotic disease). The remainder of patients will demonstrate fibromuscular dysplasia (FMD) and will tend to be younger (25 to 50 years of age) at the time of diagnosis.
Abdominal bruits heard in both systole and diastole is more suggestive of renovascular hypertension than systolic bruits alone.
Magnetic resonance angiography (MRA) is a more sensitive noninvasive imaging modality for detection of renal artery stenosis. MRA best delineates the proximal renal vasculature and is therefore useful as an initial diagnostic tool for patients suspected of having atherosclerotic renal artery stenosis. Patients suspected of having FMD, which tends to involve the distal renal artery, should undergo conventional angiography or computed tomographic angiography.
Another initial diagnostic test is the captopril-augmented radio isotopic reno-gram.But the disadvantage of this test is that this test is not as useful if stenosis is present bilaterally.
Duplex ultrasound scanning is another diagnostic option, but it can be limited by its dependence on operator skill and experience. Renal arteriography remains the gold standard for defining the vessel anatomy.
Diagnosis is based on loss of renal cortical function (demonstrated by elevated serum creatinine levels and decreased creatinine clearance), although it may be impossible to tell if the renal dysfunction is primary or secondary to the hypertension.
C: CATECHOLAMINES, COARCTATION, CUSHING'S SYNDROME
- Factors which suggest co-arctation of aorta include decreased lower-extremity (femoral) pulses with upper-extremity hypertension, dyspnea on exertion, and chest radiographic findings of notched ribs (from dilated collateral vessels) and dilation of the aorta above and below the constriction (the 3 sign).
- Cushing's Syndrome
- Diagnosis of Cushing’s syndrome is made via dexamethasone-suppression test.
D: DRUGS, DIET
Many prescription and nonprescription drugs can cause or exacerbate hypertension. The best way to come to come to a conclusion involves proper history taking about use of drugs and associated problems.
The dietary impact on blood pressure can be concluded by proper history taking about salt intake and amount other minerals that have a direct impact on blood pressure.
E: ERYTHROPOIETIN, ENDOCRINE DISORDERS
Order for serum erythropoietin levels in patients suspected to have elevated blood pressure due to erythropoietin based disorders.
Hypothyroidism can cause a more prominent rise in diastolic blood pressure than in systolic blood pressure. Conversely, hyperthyroidism causes a greater increase in systolic blood pressure. A thyroid-stimulating hormone level is the best diagnostic screening test for thyroid disorders.
Hyperparathyroidism (primary or secondary to chronic renal insufficiency) is a potentially reversible cause of hypertension.
Pregnancy-induced hypertension has an incompletely understood neurohumoral mechanism (possibly initiated by inadequate establishment of blood supply to the developing placenta) and occasionally can develop in the immediate postpartum period.
Pheochromocytoma is another endocrine cause of hypertension. The classic symptoms include headache, diaphoresis, palpitations, and paroxysmal hypertension. The usual screening test has been urinary measurement of catecholamine metabolites (vanillylmandelic acid, metanephrines, normetanephrines).
Acromegaly (elevated growth hormone) is a rare endocrine cause of hypertension. The diagnosis is on the basis of elevated IGF-1 levels.
Lifestyle modifications are necessary in order to cope with secondary hypertension.
Healthy eating, active living, and achieving a healthy weight have a major impact on prevention and management of hypertension.
More specifically, the risk factors of overweight, physical inactivity, and high sodium intake appear to be major independent contributors to hypertension. Indeed, clustering these risk factors into low-risk or high-risk groupings allows us to identify individuals at high or low risk of developing hypertension.
- The Canadian Hypertension Education Program (CHEP) recommends that “Hypertensive patients and normotensive individuals at increased risk of developing hypertension consume a diet that emphasizes fruits, vegetables and low-fat dairy products, dietary and soluble fibre, whole grains and protein from plant sources and that is reduced in saturated fat and cholesterol.”
- The DASH (Dietary Approaches to Stop Hypertension) diet which was developed specifically to address hypertension and traditionally referenced as the recommended dietary guideline along with other DASH-like diets.
The DASH diet is known to result in substantial reductions in blood pressure, even when sodium intake is not reduced.
Best practices and patient resources
Supporting patients who are making lifestyle changes aimed at preventing or managing hypertension calls for a comprehensive, structured, multidisciplinary, and sustained approach.
Clinicians can support self-management and help patients access ap¬propriate, culturally sensitive, clear, and affordable resources and supports in the community.
Healthy eating, sodium reduction, physical activity, healthy weight, moderate alcohol consumption, and stress management are the best recommendations that a health care physician can give to his patient.