Chronic hypertension causes: Difference between revisions
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===Secondary Hypertension=== | ===Secondary Hypertension=== | ||
Common causes of secondary hypertension are often memorized by the mnemonic ABCDE | Common causes of secondary hypertension are often memorized by the mnemonic ABCDE | ||
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{| border="1" align="right" style="wikitable" | |||
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|Mnemonic | |||
|Causes of Secondary Hypertension | |||
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|A | |||
|Accuracy, Apnea, Aldosteronism | |||
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|B | |||
|Bruit, Bad Kidneys | |||
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|C | |||
|Catecholamines, Coarctation, Cushing’s Syndrome | |||
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|D | |||
|Drugs, Diet | |||
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|E | |||
|Erythropoitin, Endocrine Disorders | |||
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====Accuracy:==== | ====Accuracy:==== | ||
Revision as of 19:46, 22 February 2013
Hypertension Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor-In-Chief: Taylor Palmieri
Overview
Causes
Patients presenting with high BP must conduct a complete work-up before the diagnosis of essential hypertension is considered (Ref: 17462751). Work-up includes, but is not limited to, a thorough medical history and physical examination, laboratory blood and urine testing, electrocardiogram, and radiological work-up (Ref: 17462751). Further work-up may be necessary if the above raised the suspicion of secondary hypertension.
Primary Hypertension
When a full evaluation yields no clear etiology for the hypertension, the latter is thus identified as primary or essential hypertension. It is considered a chronic disease that requires lifetime treatment and management. If an underlying disease is identifiable as the cause of hypertension, the latter is called secondary hypertension. Secondary hypertension is a potentially curable condition in most of the cases (Ref: 17462751).
The prevalence of primary hypertension is much more common than secondary hypertension, where only 5-10% of hypertension cases are diagnosed as secondary hypertension (Ref: 12537168). The classical age range of primary hypertension is 30-55 years (Ref: 11509166), but age alone should never warrant an insufficient work-up by healthcare providers for patients suspected to have primary hypertension.
Secondary Hypertension
Common causes of secondary hypertension are often memorized by the mnemonic ABCDE
Mnemonic | Causes of Secondary Hypertension |
A | Accuracy, Apnea, Aldosteronism |
B | Bruit, Bad Kidneys |
C | Catecholamines, Coarctation, Cushing’s Syndrome |
D | Drugs, Diet |
E | Erythropoitin, Endocrine Disorders |
Accuracy:
It refers to inappropriate technique to measure blood pressure. Re-measurement of blood pressures to ensure accuracy must always be performed as a first step when patients present with high blood pressure values. Appropriate measurement technique must be carefully followed. The physician in charge should check for the accuracy of home BP measurements.
Apnea:
Obstructive sleep apnea (OSA) is a respiratory disease due to repetitive narrowing or collapse of the upper airway during sleep (Ref: 18250206) leading to apnea, hypopnea, and decreased oxygen tension at night (Ref: 8872797). Symptoms and signs that might suggest OSA include daytime somnolence, obesity, snoring, and morning headaches (Ref: 10593319). Diagnosis is made by sleep study. Treatment relies basically on maintaining airway patency at night and includes, among others, the use of continuous positive airway pressure (CPAP).
Aldosterone:
Primary (hyporeninemic) and secondary (hyperreninemic) hyperaldosteronism result in excess sodium and water retention with excretion of potassium (Ref: 9854120). Patient profiles and treatment options differ significantly among the two categories. The most common cause of primary hyperaldosteronism is an aldosterone-producing adenoma, i.e. Conn’s Syndrome. Secondary hyperaldosteronism is due to overactive RAAS, as seen in renin-secreting tumors, renal artery stenosis, pheochromocytoma, and others. Diagnosis is made by measuring ratio of plasma aldosterone to plasma renin activity (Ref: 7923898). It is elevated in primary hyperaldosteronism and decreased/normal with elevated renin in secondary hyperaldosteronism. Treatment is etiology-dependent; including surgery for tumor resection and spironolactone, an aldosterone antagonist.
Bruit:
Renovascular hypertension is due to decreased blood supply to the kidneys secondary to renal artery stenosis. Atherosclerosis of the renal artery in older patients above 50 years of age (Ref: 12196346) and fibromuscular dysplasia in younger patients (Ref: 22286647) are common etiologies. Definitive diagnosis is made by Magnetic Resonance angiography (MRA) and renal arteriography (Ref: 11416635). Other diagnostic methods include duplex ultrasound scanning (Ref: 22595689), and captopril-augmented radio-isotopic renogram (Ref: 10482969) Treatment is targeted at the etiology and is driven by the baseline patient condition, comorbidities, and expected outcome.
Bad Kidney:
Renal parenchymal disease blunts the kidney’s physiological ability to maintain appropriate blood pressure. Significantly, hypertension is both a cause and a consequence of renal parenchymal disease; the two are closely associated and potentiate each other (Ref: 11866231). Diagnosis is made by demonstration of decreased GFR. The mechanisms by which renal parenchymal disease lead to the development of hypertension are many and include the activation of the local RAAS, vasoconstrictor cytokines, in addition to decreased GFR leading to inappropriate natriuresis for the BP level.
Catecholamines:
Catecholamine excess is witnessed in several non-disease states, such as acute stress, medications with sympathomimetic activity, and illicit drug use such as cocaine. Nonetheless, such conditions can be ruled out by mere history taking. Pheochromocytoma is a tumor of the adrenal gland leading to hypersecretion of epinephrine in most cases, should always be considered in the differential diagnosis of secondary hypertension, classically in young patients with the triad of intermittent hypertensive episodes causing headache, sweating, and tachycardia. Nonetheless, pheochromocytoma in older adults or a presentation with sustained hypertension is not uncommon. Diagnosis of pheochromocytoma remains controversial. The most applicable tests nowadays include measurement of plasma free metanephrines and urinary fractionated metanephrines (Ref: 11903030). Diagnostic value of plasma and urinary catecholamines is of less major importance due to the very short half-life of catecholamines (Ref: 11903030). Treatment is by surgical resection of the secreting tumor.
Coarctation:
Coarctation of the aorta is a congenital heart defect, caused by narrowing of a segment in the ascending or descending aorta. Diagnosis in neonates or infants usually starts with a suspicious physical examination of weak femoral pulses or asymmetrically brisk brachial pulses. Hypertension occurs as a result of decreased effective circulation at the level of the kidneys; the latter respond physiologically by increasing plasma volume causing hypertension in the upper extremities. Diagnosis is by CT angiography, but is usually achieved in neonates and infants by ultrasound of the heart and the great vessels. Definitive treatment is by surgical correction.
Cushing’s Syndrome:
An endocrine disorder caused by prolonged exposure to high endogenous or exogenous cortisol levels. Hypertension in Cushing ’s syndrome has been classically attributed to the mineralocorticoid effects of cortisol. It manifests as an absent fall of nocturnal blood pressure physiologically seen in normotensive subjects with associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (Ref: 3397172). Although an ideal diagnostic test is not considered yet available, clinicians often utilize 24-hour urinary cortisol excretion (Ref: 3958132), low-dose dexamethasone suppression test (Ref: 14315650), late evening serum or salivary cortisol (Ref: 9709931), and CRH after dexamethasone test for the diagnosis of the syndrome and the various entities causing it (Ref: 8386285).
Drugs:
An extensive list of drugs cause hypertension, such as immunosuppressive agents, non-steroidal anti-inflammatory drugs, oral contraceptive pills, some weight loss agents, stimulants, monoamine oxidase inhibitors, and sympathomimetics (Ref: 12537168).
Diet:
In addition to the association of obesity due to high-caloric diet with hypertension, the 2001 study “Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet” concluded that a high sodium diet above the recommended 100 mmol per day (2.4 g of sodium or 6 g of sodium chloride salt) is associated with hypertension (Ref: 11136953). As a result, reduction of sodium levels below 100 mmol per day and following the DASH diet (rich in vegetables, fruits, with low-fat dairy products) can significantly lower BP (Ref: 11136953).
Erythropoietin:
Elevated erythropoietin is typically seen in COPD patients who have functional anemia due to chronic hypoxia and in hematologic disorders such as polycythemia. The pathogenesis of erythropoietin-induced hypertension includes the increased hematocrit and blood viscosity, altered sensitivity to vasopressors, dysregulated vasodilatory factors, and vascular cell growth causing arterial remodeling and changes in arterial smooth musculature (Ref. 10213636). Diagnosis and treatment are etiology-dependent.
Endocrine:
In addition to the more common endocrine causes of hypertension such as hyperaldosteronism, Cushing’s syndrome, and pheochromocytoma, several other endocrine changes can cause hypertension. Both hypothyroidism and hyperthyroidism can cause hypertension by volume retention and by increased cardiac output, respectively (Ref: 22145139). Also, hyperparathyroidism and hypovitaminosis D can cause hypertension due to poorly understood mechanisms, where parathyroidectomy seems to significantly decrease blood pressure in patients with parathyroid disease and elevated BP (Ref: 22145139).
Complete List of Causes by Organ System
Causes in Alphabetical Order