Chronic hypertension causes: Difference between revisions
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==Causes== | ==Causes== | ||
Patients presenting with high BP must conduct a complete work-up before the diagnosis of essential hypertension is considered | Patients presenting with high BP must conduct a complete work-up before the diagnosis of essential hypertension is considered. 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 name="pmid17462751">{{cite journal| author=Chiong JR, Aronow WS, Khan IA, Nair CK, Vijayaraghavan K, Dart RA et al.| title=Secondary hypertension: current diagnosis and treatment. | journal=Int J Cardiol | year= 2008 | volume= 124 | issue= 1 | pages= 6-21 | pmid=17462751 | doi=10.1016/j.ijcard.2007.01.119 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17462751 }} </ref>. Further work-up may be necessary if the above raised the suspicion of secondary hypertension. | ||
===Primary 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 | 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 name="pmid17462751">{{cite journal| author=Chiong JR, Aronow WS, Khan IA, Nair CK, Vijayaraghavan K, Dart RA et al.| title=Secondary hypertension: current diagnosis and treatment. | journal=Int J Cardiol | year= 2008 | volume= 124 | issue= 1 | pages= 6-21 | pmid=17462751 | doi=10.1016/j.ijcard.2007.01.119 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17462751 }} </ref>. | ||
The prevalence of primary hypertension is much more common than secondary hypertension, where only 5-10% of hypertension cases are diagnosed as secondary hypertension | 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 name="pmid12537168">{{cite journal| author=Onusko E| title=Diagnosing secondary hypertension. | journal=Am Fam Physician | year= 2003 | volume= 67 | issue= 1 | pages= 67-74 | pmid=12537168 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12537168 }} </ref>. The classical age range of primary hypertension is 30-55 years<ref name="pmid11509166">{{cite journal| author=Dosh SA| title=The diagnosis of essential and secondary hypertension in adults. | journal=J Fam Pract | year= 2001 | volume= 50 | issue= 8 | pages= 707-12 | pmid=11509166 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11509166 }} </ref>, but age alone should never warrant an insufficient work-up by healthcare providers for patients suspected to have primary hypertension. | ||
===Secondary Hypertension=== | ===Secondary Hypertension=== | ||
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====Apnea:==== | ====Apnea:==== | ||
Obstructive sleep apnea (OSA) is a respiratory disease due to repetitive narrowing or collapse of the upper airway during sleep | Obstructive sleep apnea (OSA) is a respiratory disease due to repetitive narrowing or collapse of the upper airway during sleep<ref name="pmid18250206">{{cite journal| author=Eckert DJ, Malhotra A| title=Pathophysiology of adult obstructive sleep apnea. | journal=Proc Am Thorac Soc | year= 2008 | volume= 5 | issue= 2 | pages= 144-53 | pmid=18250206 | doi=10.1513/pats.200707-114MG | pmc=PMC2628457 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18250206 }} </ref> 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 name="pmid10593319">{{cite journal| author=Victor LD| title=Obstructive sleep apnea. | journal=Am Fam Physician | year= 1999 | volume= 60 | issue= 8 | pages= 2279-86 | pmid=10593319 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10593319 }} </ref>. 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:==== | ==== Aldosterone:==== | ||
Primary (hyporeninemic) and secondary (hyperreninemic) hyperaldosteronism result in excess sodium and water retention with excretion of potassium | Primary (hyporeninemic) and secondary (hyperreninemic) hyperaldosteronism result in excess sodium and water retention with excretion of potassium<ref name="pmid9854120">{{cite journal| author=Ganguly A| title=Primary aldosteronism. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 25 | pages= 1828-34 | pmid=9854120 | doi=10.1056/NEJM199812173392507 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9854120 }} </ref>. 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 name="pmid7923898">{{cite journal| author=Gordon RD, Stowasser M, Tunny TJ, Klemm SA, Rutherford JC| title=High incidence of primary aldosteronism in 199 patients referred with hypertension. | journal=Clin Exp Pharmacol Physiol | year= 1994 | volume= 21 | issue= 4 | pages= 315-8 | pmid=7923898 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7923898 }} </ref>. 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:==== | ==== 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 | 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 name="pmid12196346">{{cite journal| author=Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC et al.| title=Distinct renal injury in early atherosclerosis and renovascular disease. | journal=Circulation | year= 2002 | volume= 106 | issue= 9 | pages= 1165-71 | pmid=12196346 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12196346 }} </ref> and fibromuscular dysplasia in younger patients (Ref: 22286647) are common etiologies. Definitive diagnosis is made by Magnetic Resonance angiography (MRA) and renal arteriography<ref name="pmid11416635">{{cite journal| author=Wofford MR, King DS, Wyatt SB, Jones DW| title=Secondary Hypertension: Detection and Management for the Primary Care Provider. | journal=J Clin Hypertens (Greenwich) | year= 2000 | volume= 2 | issue= 2 | pages= 124-131 | pmid=11416635 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11416635 }} </ref>. Other diagnostic methods include duplex ultrasound scanning<ref name="pmid22595689">{{cite journal| author=AbuRahma AF, Srivastava M, Mousa AY, Dearing DD, Hass SM, Campbell JR et al.| title=Critical analysis of renal duplex ultrasound parameters in detecting significant renal artery stenosis. | journal=J Vasc Surg | year= 2012 | volume= 56 | issue= 4 | pages= 1052-9, 1060.e1; discussion 1059-60 | pmid=22595689 | doi=10.1016/j.jvs.2012.03.036 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22595689 }} </ref>, and captopril-augmented radio-isotopic renogram<ref name="pmid10482969">{{cite journal| author=Aitchison F, Page A| title=Diagnostic imaging of renal artery stenosis. | journal=J Hum Hypertens | year= 1999 | volume= 13 | issue= 9 | pages= 595-603 | pmid=10482969 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10482969 }} </ref>. Treatment is targeted at the etiology and is driven by the baseline patient condition, comorbidities, and expected outcome. | ||
==== Bad Kidney:==== | ==== 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 | 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 name="pmid11866231">{{cite journal| author=Soergel M, Schaefer F| title=Effect of hypertension on the progression of chronic renal failure in children. | journal=Am J Hypertens | year= 2002 | volume= 15 | issue= 2 Pt 2 | pages= 53S-56S | pmid=11866231 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11866231 }} </ref>. 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:==== | ====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 | 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. | ||
Diagnostic value of plasma and urinary catecholamines is of less major importance due to the very short half-life of catecholamines. Treatment is by surgical resection of the secreting tumor.<ref name="pmid11903030">{{cite journal| author=Lenders JW, Pacak K, Walther MM, Linehan WM, Mannelli M, Friberg P et al.| title=Biochemical diagnosis of pheochromocytoma: which test is best? | journal=JAMA | year= 2002 | volume= 287 | issue= 11 | pages= 1427-34 | pmid=11903030 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11903030 }} </ref> | |||
==== Coarctation:==== | ==== Coarctation:==== | ||
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====Cushing’s Syndrome:==== | ====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 | 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 name="pmid3397172">{{cite journal| author=Imai Y, Abe K, Sasaki S, Minami N, Nihei M, Munakata M et al.| title=Altered circadian blood pressure rhythm in patients with Cushing's syndrome. | journal=Hypertension | year= 1988 | volume= 12 | issue= 1 | pages= 11-9 | pmid=3397172 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3397172 }} </ref>. Although an ideal diagnostic test is not considered yet available, clinicians often utilize 24-hour urinary cortisol excretion<ref name="pmid3958132">{{cite journal| author=Contreras LN, Hane S, Tyrrell JB| title=Urinary cortisol in the assessment of pituitary-adrenal function: utility of 24-hour and spot determinations. | journal=J Clin Endocrinol Metab | year= 1986 | volume= 62 | issue= 5 | pages= 965-9 | pmid=3958132 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3958132 }} </ref>, low-dose dexamethasone suppression test<ref name="pmid14315650">{{cite journal| author=NUGENT CA, NICHOLS T, TYLER FH| title=Diagnosis of Cushing’s Syndrome; Single Dose Dexamethasone Suppression Test. | journal=Arch Intern Med | year= 1965 | volume= 116 | issue= | pages= 172-6 | pmid=14315650 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14315650 }} </ref>, late evening serum or salivary cortisol <ref name="pmid9709931">{{cite journal| author=Raff H, Raff JL, Findling JW| title=Late-night salivary cortisol as a screening test for Cushing's syndrome. | journal=J Clin Endocrinol Metab | year= 1998 | volume= 83 | issue= 8 | pages= 2681-6 | pmid=9709931 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9709931 }} </ref>, and CRH after dexamethasone test for the diagnosis of the syndrome and the various entities causing it<ref name="pmid8386285">{{cite journal| author=Yanovski JA, Cutler GB, Chrousos GP, Nieman LK| title=Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states. | journal=JAMA | year= 1993 | volume= 269 | issue= 17 | pages= 2232-8 | pmid=8386285 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8386285 }} </ref>. | ||
====Drugs:==== | ====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 | 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 name="pmid12537168">{{cite journal| author=Onusko E| title=Diagnosing secondary hypertension. | journal=Am Fam Physician | year= 2003 | volume= 67 | issue= 1 | pages= 67-74 | pmid=12537168 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12537168 }} </ref>. | ||
==== Diet:==== | ==== 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 ( | 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 name="pmid11136953">{{cite journal| author=Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D et al.| title=Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 1 | pages= 3-10 | pmid=11136953 | doi=10.1056/NEJM200101043440101 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11136953 }} </ref>. 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 name="pmid11136953">{{cite journal| author=Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D et al.| title=Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 1 | pages= 3-10 | pmid=11136953 | doi=10.1056/NEJM200101043440101 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11136953 }} </ref>. | ||
====Erythropoietin:==== | ====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 | 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 | ||
====Endocrine: ==== | <ref name="pmid10213636">{{cite journal| author=Vaziri ND| title=Mechanism of erythropoietin-induced hypertension. | journal=Am J Kidney Dis | year= 1999 | volume= 33 | issue= 5 | pages= 821-8 | pmid=10213636 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10213636 }} </ref>. 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 | 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. 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 name="pmid22145139">{{cite journal| author=Chopra S, Cherian D, Jacob JJ| title=The thyroid hormone, parathyroid hormone and vitamin D associated hypertension. | journal=Indian J Endocrinol Metab | year= 2011 | volume= 15 Suppl 4 | issue= | pages= S354-60 | pmid=22145139 | doi=10.4103/2230-8210.86979 | pmc=PMC3230087 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22145139 }} </ref>. | ||
==Complete List of Causes by Organ System== | ==Complete List of Causes by Organ System== |
Revision as of 20:18, 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. 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[1]. 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[1].
The prevalence of primary hypertension is much more common than secondary hypertension, where only 5-10% of hypertension cases are diagnosed as secondary hypertension[2]. The classical age range of primary hypertension is 30-55 years[3], 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[4] 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[5]. 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[6]. 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[7]. 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[8] and fibromuscular dysplasia in younger patients (Ref: 22286647) are common etiologies. Definitive diagnosis is made by Magnetic Resonance angiography (MRA) and renal arteriography[9]. Other diagnostic methods include duplex ultrasound scanning[10], and captopril-augmented radio-isotopic renogram[11]. 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[12]. 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.
Diagnostic value of plasma and urinary catecholamines is of less major importance due to the very short half-life of catecholamines. Treatment is by surgical resection of the secreting tumor.[13]
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[14]. Although an ideal diagnostic test is not considered yet available, clinicians often utilize 24-hour urinary cortisol excretion[15], low-dose dexamethasone suppression test[16], late evening serum or salivary cortisol [17], and CRH after dexamethasone test for the diagnosis of the syndrome and the various entities causing it[18].
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[2].
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[19]. 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[19].
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
[20]. 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. 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[21].
Complete List of Causes by Organ System
Causes in Alphabetical Order
References
- ↑ 1.0 1.1 Chiong JR, Aronow WS, Khan IA, Nair CK, Vijayaraghavan K, Dart RA; et al. (2008). "Secondary hypertension: current diagnosis and treatment". Int J Cardiol. 124 (1): 6–21. doi:10.1016/j.ijcard.2007.01.119. PMID 17462751.
- ↑ 2.0 2.1 Onusko E (2003). "Diagnosing secondary hypertension". Am Fam Physician. 67 (1): 67–74. PMID 12537168.
- ↑ Dosh SA (2001). "The diagnosis of essential and secondary hypertension in adults". J Fam Pract. 50 (8): 707–12. PMID 11509166.
- ↑ Eckert DJ, Malhotra A (2008). "Pathophysiology of adult obstructive sleep apnea". Proc Am Thorac Soc. 5 (2): 144–53. doi:10.1513/pats.200707-114MG. PMC 2628457. PMID 18250206.
- ↑ Victor LD (1999). "Obstructive sleep apnea". Am Fam Physician. 60 (8): 2279–86. PMID 10593319.
- ↑ Ganguly A (1998). "Primary aldosteronism". N Engl J Med. 339 (25): 1828–34. doi:10.1056/NEJM199812173392507. PMID 9854120.
- ↑ Gordon RD, Stowasser M, Tunny TJ, Klemm SA, Rutherford JC (1994). "High incidence of primary aldosteronism in 199 patients referred with hypertension". Clin Exp Pharmacol Physiol. 21 (4): 315–8. PMID 7923898.
- ↑ Chade AR, Rodriguez-Porcel M, Grande JP, Krier JD, Lerman A, Romero JC; et al. (2002). "Distinct renal injury in early atherosclerosis and renovascular disease". Circulation. 106 (9): 1165–71. PMID 12196346.
- ↑ Wofford MR, King DS, Wyatt SB, Jones DW (2000). "Secondary Hypertension: Detection and Management for the Primary Care Provider". J Clin Hypertens (Greenwich). 2 (2): 124–131. PMID 11416635.
- ↑ AbuRahma AF, Srivastava M, Mousa AY, Dearing DD, Hass SM, Campbell JR; et al. (2012). "Critical analysis of renal duplex ultrasound parameters in detecting significant renal artery stenosis". J Vasc Surg. 56 (4): 1052–9, 1060.e1, discussion 1059-60. doi:10.1016/j.jvs.2012.03.036. PMID 22595689.
- ↑ Aitchison F, Page A (1999). "Diagnostic imaging of renal artery stenosis". J Hum Hypertens. 13 (9): 595–603. PMID 10482969.
- ↑ Soergel M, Schaefer F (2002). "Effect of hypertension on the progression of chronic renal failure in children". Am J Hypertens. 15 (2 Pt 2): 53S–56S. PMID 11866231.
- ↑ Lenders JW, Pacak K, Walther MM, Linehan WM, Mannelli M, Friberg P; et al. (2002). "Biochemical diagnosis of pheochromocytoma: which test is best?". JAMA. 287 (11): 1427–34. PMID 11903030.
- ↑ Imai Y, Abe K, Sasaki S, Minami N, Nihei M, Munakata M; et al. (1988). "Altered circadian blood pressure rhythm in patients with Cushing's syndrome". Hypertension. 12 (1): 11–9. PMID 3397172.
- ↑ Contreras LN, Hane S, Tyrrell JB (1986). "Urinary cortisol in the assessment of pituitary-adrenal function: utility of 24-hour and spot determinations". J Clin Endocrinol Metab. 62 (5): 965–9. PMID 3958132.
- ↑ NUGENT CA, NICHOLS T, TYLER FH (1965). "Diagnosis of Cushing's Syndrome; Single Dose Dexamethasone Suppression Test". Arch Intern Med. 116: 172–6. PMID 14315650.
- ↑ Raff H, Raff JL, Findling JW (1998). "Late-night salivary cortisol as a screening test for Cushing's syndrome". J Clin Endocrinol Metab. 83 (8): 2681–6. PMID 9709931.
- ↑ Yanovski JA, Cutler GB, Chrousos GP, Nieman LK (1993). "Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states". JAMA. 269 (17): 2232–8. PMID 8386285.
- ↑ 19.0 19.1 Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D; et al. (2001). "Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group". N Engl J Med. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. PMID 11136953.
- ↑ Vaziri ND (1999). "Mechanism of erythropoietin-induced hypertension". Am J Kidney Dis. 33 (5): 821–8. PMID 10213636.
- ↑ Chopra S, Cherian D, Jacob JJ (2011). "The thyroid hormone, parathyroid hormone and vitamin D associated hypertension". Indian J Endocrinol Metab. 15 Suppl 4: S354–60. doi:10.4103/2230-8210.86979. PMC 3230087. PMID 22145139.