Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying primary cause. It is much less common than the other type, called essential hypertension, affecting only 5% of hypertensive patients. It has many different causes including endocrine diseases, kidney diseases, and tumors. It also can be a side effect of many medications.
|Classification and external resources|
Renovascular hypertension (I15.0)Edit
It has two main causes: fibromuscular dysplasia and atheromatous stenosis. Also diabetes
- See main article at Renovascular hypertension.
Other well known causes include diseases of the kidney. This includes diseases such as polycystic kidney disease which is a cystic genetic disorder of the kidneys, PKD ,which is characterized by the presence of multiple cysts (hence, "polycystic") in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain. It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, renal insufficiency and renal pain. Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.
Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system.
Also, some renal tumors can cause hypertension. The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms' tumor, and renal cell carcinoma, all of which may produce renin.
Hypertension secondary to other renal disorders (I15.1)Edit
- Chronic renal failure
- Kidney disease / renal artery stenosis – the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration. Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated.
- Renal segmental hypoplasia (Ask-Upmark kidney)
Hypertension secondary to endocrine disorders (I15.2)Edit
- Neurogenic hypertension – excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from chronic high activity of the sympathoadrenal system, the sympathetic nervous system and the adrenal gland. The specific mechanism involved is increased release of the "stress hormones", epinephrine (adrenaline) and norepinephrine which increase blood output from the heart and constrict arteries. People with neurogenic hypertension respond poorly to treatment with diuretics as the underlying cause of their hypertension is not addressed.
- Pheochromocytoma – a tumor which results in an excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction
- Hyperaldosteronism (Conn's syndrome) – idiopathic hyperaldosteronism, liddle's syndrome (also called pseudoaldosteronism), glucocorticoid remediable aldosteronism
- Cushing's syndrome – an excessive secretion of glucocorticoids causes the hypertension
Congenital adrenal hyperplasia, a group of autosomal recessive disorders of the enzymes responsible for steroid hormone production, can lead to secondary hypertension by creating atypically high levels of mineralocorticoid steroid hormones. These mineralocorticoids cross-react with the aldosterone receptor, activating it and raising blood pressure.
- 17 alpha-hydroxylase deficiency causes an inability to produce cortisol. Instead, extremely high levels of the precursor hormone corticosterone are produced, some of which is converted to 11-Deoxycorticosterone (DOC), a potent mineralocorticoid not normally clinically important in humans. DOC has blood-pressure raising effects similar to aldosterone, and abnormally high levels result in hypokalemic hypertension.
- 11β-hydroxylase deficiency, aka apparent mineralocorticoid excess syndrome, involves a defect in the gene for 11β-hydroxysteroid dehydrogenase, an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone. At high concentrations cortisol can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension. This effect can also be produced by prolonged ingestion of liquorice (which can be of potent strength in liquorice candy), by causing inhibition of the 11β-hydroxysteroid dehydrogenase enzyme and likewise leading to secondary apparent mineralocorticoid excess syndrome. Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present. Cortisol induced hypertension cannot be completely explained by the activity of Cortisol on Aldosterone receptors. Experiments show that treatment with Spironolactone (an inhibitor of the aldosterone receptor), does not prevent hypertension with excess cortisol. It seems that inhibition of nitric oxide synthesis may also play a role in cortisol induced hypertension.
Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not. GRA appears to be the most common monogenic form of human hypertension.
Another adrenal related cause is Cushing's syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands. Cushing's syndrome can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH). More than 80% of patients with Cushing's syndrome develop hypertension., which is accompanied by distinct symptoms of the syndrome, such as central obesity, lipodystrophy, moon face, sweating, hirsutism and anxiety.
Neuroendocrine tumors are also a well known cause of secondary hypertension. Pheochromocytoma (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).
Other secondary hypertension (I15.8)Edit
- Hormonal contraceptives
- Neurologic disorders
- Obstructive sleep apnea
- Liquorice (when consumed in excessive amounts)
- Pregnancy: unclear cause.
- Cancers: tumours in the kidney can operate in the same way as kidney disease. More commonly, however, tumors cause inessential hypertension by ectopic secretion of hormones involved in normal physiological control of blood pressure.
- Drugs: In particular, alcohol, nasal decongestants with adrenergic effects, NSAIDs, MAOIs, adrenoceptor stimulants, and combined methods of hormonal contraception (those containing ethinylestradiol) can cause hypertension while in use.
- Malformed aorta, slow pulse, ischemia: these cause reduced blood flow to the renal arteries, with physiological responses as already outlined.
- Anemia: unclear cause.
- Fever: unclear cause.
- White coat hypertension, that is, elevated blood pressure in a clinical setting but not in other settings, probably due to the anxiety some people experience during a clinic visit.
- Perioperative hypertension is development of hypertension just before, during or after surgery. It may occur before surgery during the induction of anesthesia; intraoperatively e.g. by pain-induced sympathetic nervous system stimulation; in the early postanesthesia period, e.g. by pain-induced sympathetic stimulation, hypothermia, hypoxia, or hypervolemia from excessive intraoperative fluid therapy; and in the 24 to 48 hours after the postoperative period as fluid is mobilized from the extravascular space. In addition, hypertension may develop perioperatively because of discontinuation of long-term antihypertensive medication.
Medication side effectsEdit
Certain medications, including NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Other medications include extrogens (such as those found in oral contraceptives with high estrogenic activity), certain antidepressants (such as venlafaxine), buspirone, carbamazepine, bromocriptine, clozapine, and cyclosporine. High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called rebound hypertension. The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose. Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and methyl-dopa.
Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.
Another common and under-recognized sign of hypertension is sleep apnea, which is often best treated with nocturnal nasal continuous positive airway pressure (CPAP), but other approaches include the Mandibular advancement splint (MAS), UPPP, tonsillectomy, adenoidectomy, septoplasty, or weight loss. Another cause is an exceptionally rare neurological disease called Binswanger's disease, causing dementia; it is a rare form of multi-infarct dementia, and is one of the neurological syndromes associated with hypertension.
Because of the ubiquity of arsenic in ground water supplies and its effect on cardiovascular health, low dose arsenic poisoning should be inferred as a part of the pathogenesis of idiopathic hypertension. Idiopathic and essential are both somewhat synonymous with primary hypertension. Arsenic exposure has also many of the same signs of primary hypertension such as headache, somnolence,  confusion, proteinuria  visual disturbances, and nausea and vomiting 
Due to the role of intracellular potassium in regulation of cellular pressures related to sodium, establishing potassium balance has been shown to reverse hypertension. 
The ABCDE mnemonic can be used to help determine a secondary cause of hypertension
- A: Accuracy, Apnea, Aldosteronism
- B: Bruits, Bad Kidney
- C: Catecholamines, Coarctation of the Aorta, Cushing's Syndrome
- D: Drugs, Diet
- E: Erythropoietin, Endocrine Disorders 
- Ecder T, Schrier RW (April 2009). "Cardiovascular abnormalities in autosomal-dominant polycystic kidney disease". Nature Reviews Nephrology. 5 (4): 221–28. doi:10.1038/nrneph.2009.13. PMC . PMID 19322187.
- Gross P (May 2008). "Polycystic kidney disease: will it become treatable?". Polskie Archiwum Medycyny Wewnȩtrznej. 118 (5): 298–301. PMID 18619180. Retrieved 2009-06-19.
- Masoumi A, Reed-Gitomer B, Kelleher C, Schrier RW (2007). "Potential pharmacological interventions in polycystic kidney disease". Drugs. 67 (17): 2495–510. doi:10.2165/00003495-200767170-00004. PMID 18034588.
- Chapman AB (May 2007). "Autosomal dominant polycystic kidney disease: time for a change?". Journal of the American Society of Nephrology : JASN. 18 (5): 1399–407. doi:10.1681/ASN.2007020155. PMID 17429048. Retrieved 2009-06-19.
- Chapman AB (July 2008). "Approaches to testing new treatments in autosomal dominant polycystic kidney disease: insights from the CRISP and HALT-PKD studies". Clinical Journal of the American Society of Nephrology. 3 (4): 1197–204. doi:10.2215/CJN.00060108. PMID 18579674. Retrieved 2009-06-19.
- Berthoux FC, Mohey H, Afiani A (January 2008). "Natural history of primary IgA nephropathy". Seminars in Nephrology. 28 (1): 4–9. doi:10.1016/j.semnephrol.2007.10.001. PMID 18222341. Retrieved 2009-06-19.
- D'Cruz D (February 2009). "Renal manifestations of the antiphospholipid syndrome". Current Rheumatology Reports. 11 (1): 52–60. doi:10.1007/s11926-009-0008-2. PMID 19171112.
- Licht C, Fremeaux-Bacchi V (February 2009). "Hereditary and acquired complement dysregulation in membranoproliferative glomerulonephritis". Thrombosis and Haemostasis. 101 (2): 271–78. doi:10.1160/th08-09-0575. PMID 19190809. Retrieved 2009-06-19.
- Textor SC (May 2009). "Current Approaches to Renovascular Hypertension". The Medical Clinics of North America. 93 (3): 717–32, Table of Contents. doi:10.1016/j.mcna.2009.02.012. PMC . PMID 19427501. Retrieved 2009-06-19.
- Voiculescu A, Rump LC (January 2009). "[Hypertension in patients with renal artery stenosis]". Der Internist (in German). 50 (1): 42–50. doi:10.1007/s00108-008-2198-5. PMID 19096816.
- Kendrick J, Chonchol M (October 2008). "Renal artery stenosis and chronic ischemic nephropathy: epidemiology and diagnosis". Advances in Chronic Kidney Disease. 15 (4): 355–62. doi:10.1053/j.ackd.2008.07.004. PMID 18805381. Retrieved 2009-06-19.
- Méndez GP, Klock C, Nosé V (December 2008). "Juxtaglomerular Cell Tumor of the Kidney: Case Report and Differential Diagnosis With Emphasis on Pathologic and Cytopathologic Features". Int. J. Surg. Pathol. 19 (1): 93–98. doi:10.1177/1066896908329413. PMID 19098017.
- Samuel J Mann (2003). "Neurogenic essential hypertension revisited: the case for increased clinical and research attention". American Journal of Hypertension. 16 (10): 881–88. doi:10.1016/S0895-7061(03)00978-6.
- Giacchetti G, Turchi F, Boscaro M, Ronconi V (April 2009). "Management of primary aldosteronism: its complications and their outcomes after treatment". Current Vascular Pharmacology. 7 (2): 244–49. doi:10.2174/157016109787455716. PMID 19356005.
- Bailey MA, Paterson JM, Hadoke PW, et al. (January 2008). "A Switch in the Mechanism of Hypertension in the Syndrome of Apparent Mineralocorticoid Excess". Journal of the American Society of Nephrology. 19 (1): 47–58. doi:10.1681/ASN.2007040401. PMC . PMID 18032795.
- Vantyghem MC, Marcelli-Tourvieille S, Defrance F, Wemeau JL (October 2007). "11beta-hydroxysteroide dehydrogenases. Recent advances". Annales d'endocrinologie (in French). 68 (5): 349–56. doi:10.1016/j.ando.2007.02.003. PMID 17368420.
- Atanasov AG, Ignatova ID, Nashev LG, et al. (April 2007). "Impaired protein stability of 11beta-hydroxysteroid dehydrogenase type 2: a novel mechanism of apparent mineralocorticoid excess". Journal of the American Society of Nephrology. 18 (4): 1262–70. doi:10.1681/ASN.2006111235. PMID 17314322. Retrieved 2009-06-19.
- Johns C (January 2009). "Glycyrrhizic acid toxicity caused by consumption of licorice candy cigars". Canadian Journal of Emergency Medical Care. 11 (1): 94–96. PMID 19166646.
- Sontia B, Mooney J, Gaudet L, Touyz RM (February 2008). "Pseudohyperaldosteronism, liquorice, and hypertension". Journal of Clinical Hypertension. 10 (2): 153–57. doi:10.1111/j.1751-7176.2008.07470.x. PMID 18256580.
- Whitworth, Judith (Dec 2015). "Cardiovascular Consequences of Cortisol Excess". Vasc Health Risk Manag. 1 (4): 291–99. PMC . PMID 17315601.
- Escher G (April 2009). "Hyperaldosteronism in pregnancy". Therapeutic Advances in Cardiovascular Disease. 3 (2): 123–32. doi:10.1177/1753944708100180. PMID 19171690. Retrieved 2009-06-19.
- Sukor N, Mulatero P, Gordon RD, et al. (August 2008). "Further evidence for linkage of familial hyperaldosteronism type II at chromosome 7p22 in Italian as well as Australian and South American families". Journal of Hypertension. 26 (8): 1577–82. doi:10.1097/HJH.0b013e3283028352. PMID 18622235. Retrieved 2009-06-19.
- Omura M, Nishikawa T (May 2006). "[Glucocorticoid remediable aldosteronism]". Nippon Rinsho (in Japanese). Suppl 1: 628–34. PMID 16776234.
- Luft FC (October 2003). "Mendelian Forms of Human Hypertension and Mechanisms of Disease". Clinical Medicine & Research. 1 (4): 291–300. doi:10.3121/cmr.1.4.291. PMC . PMID 15931322. Retrieved 2009-06-19.
- Nicod J, Dick B, Frey FJ, Ferrari P (February 2004). "Mutation analysis of CYP11B1 and CYP11B2 in patients with increased 18-hydroxycortisol production". Molecular and Cellular Endocrinology. 214 (1–2): 167–74. doi:10.1016/j.mce.2003.10.056. PMID 15062555. Retrieved 2009-06-19.
- McMahon GT, Dluhy RG (2004). "Glucocorticoid-remediable aldosteronism". Cardiology in Review. 12 (1): 44–48. doi:10.1097/01.crd.0000096417.42861.ce. PMID 14667264. Retrieved 2009-06-19.
- Ziaja J, Cholewa K, Mazurek U, Cierpka L (2008). "[Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas]". Endokrynologia Polska (in Polish). 59 (4): 330–39. PMID 18777504.
- Astegiano M, Bresso F, Demarchi B, et al. (March 2005). "Association between Crohn's disease and Conn's syndrome. A report of two cases". Panminerva Medica. 47 (1): 61–4. PMID 15985978.
- Pereira RM, Michalkiewicz E, Sandrini F, et al. (October 2004). "[Childhood adrenocortical tumors]". Arquivos Brasileiros de Endocrinologia e Metabologia (in Portuguese). 48 (5): 651–58. doi:10.1590/S0004-27302004000500010. PMID 15761535. Retrieved 2009-06-19.
- Kievit J, Haak HR (March 2000). "Diagnosis and treatment of adrenal incidentaloma. A cost-effectiveness analysis". Endocrinology and Metabolism Clinics of North America. 29 (1): 69–90, viii–ix. doi:10.1016/S0889-8529(05)70117-1. PMID 10732265.
- Kumar, Abbas, Fausto. Robbins and Cotran Pathologic Basis of Disease, 7th ed. Elsevier-Saunders; New York, 2005.
- Dodt C, Wellhöner JP, Schütt M, Sayk F (January 2009). "[Glucocorticoids and hypertension]". Der Internist (in German). 50 (1): 36–41. doi:10.1007/s00108-008-2197-6. PMID 19096817.
- Yudofsky, Stuart C.; Robert E. Hales (2007). The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences (5th ed.). American Psychiatric Pub, Inc. ISBN 1-58562-239-7.
- Kassim TA, Clarke DD, Mai VQ, Clyde PW, Mohamed Shakir KM (December 2008). "Catecholamine-induced cardiomyopathy". Endocrine Practice. 14 (9): 1137–49. PMID 19158054. Retrieved 2009-06-19.
- Chobanian AV, et al. (2003). "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report". JAMA. 289 (19): 2560–72. doi:10.1001/jama.289.19.2560. PMID 12748199.
- Varon J, Marik PE (2008). "Perioperative hypertension management". Vasc Health Risk Manag. 4 (3): 615–27. PMC . PMID 18827911.
- Simone Rossi, ed. (2006). Australian medicines handbook 2006. Adelaide: Australian Medicines Handbook Pty Ltd. ISBN 0-9757919-2-3.[page needed]
- White WB (May 2009). "Defining the problem of treating the patient with hypertension and arthritis pain". The American Journal of Medicine. 122 (5 Suppl): S3–9. doi:10.1016/j.amjmed.2009.03.002. PMID 19393824. Retrieved 2009-06-18.
- Mackenzie IS, Rutherford D, MacDonald TM (2008). "Nitric oxide and cardiovascular effects: new insights in the role of nitric oxide for the management of osteoarthritis". Arthritis Research & Therapy. 10 Suppl 2 (Suppl 2): S3. doi:10.1186/ar2464. PMC . PMID 19007428. Retrieved 2009-06-18.
- Berenbaum F (2008). "New horizons and perspectives in the treatment of osteoarthritis". Arthritis Research & Therapy. 10 Suppl 2 (Suppl 2): S1. doi:10.1186/ar2462. PMC . PMID 19007426. Retrieved 2009-06-18.
- Akinbamowo AO, Salzberg DJ, Weir MR (October 2008). "Renal consequences of prostaglandin inhibition in heart failure". Heart Failure Clinics. 4 (4): 505–10. doi:10.1016/j.hfc.2008.03.002. PMID 18760760. Retrieved 2009-06-18.
- Lowenstein J (January 1980). "Drugs five years later: clonidine". Annals of Internal Medicine. 92 (1): 74–77. doi:10.7326/0003-4819-92-1-74. PMID 6101302.
- Robertson JI (January 1997). "Risk factors and drugs in the treatment of hypertension". Journal of Hypertension Supplement. 15 (1): S43–6. doi:10.1097/00004872-199715011-00006. PMID 9050985.
- Schachter M (August 1999). "Moxonidine: a review of safety and tolerability after seven years of clinical experience". Journal of Hypertension Supplement. 17 (3): S37–9. PMID 10489097.
- Schäfer SG, Kaan EC, Christen MO, Löw-Kröger A, Mest HJ, Molderings GJ (July 1995). "Why imidazoline receptor modulator in the treatment of hypertension?". Annals of the New York Academy of Sciences. 763: 659–72. doi:10.1111/j.1749-6632.1995.tb32460.x. PMID 7677385. Retrieved 2009-06-18.
- Larsen R, Kleinschmidt S (April 1995). "[Controlled hypotension]". Der Anaesthesist (in German). 44 (4): 291–308. doi:10.1007/s001010050157. PMID 7785759.
- Scholtysik G (March 1986). "Animal pharmacology of guanfacine". The American Journal of Cardiology. 57 (9): 13E–17E. doi:10.1016/0002-9149(86)90717-4. PMID 3006469.
- Myers MG (January 1977). "New drugs in hypertension". Canadian Medical Association Journal. 116 (2): 173–76. PMC . PMID 343894.
- van Zwieten PA, Thoolen MJ, Timmermans PB (1984). "The hypotensive activity and side effects of methyldopa, clonidine, and guanfacine". Hypertension. 6 (5 Pt 2): II28–33. doi:10.1161/01.hyp.6.5_pt_2.ii28. PMID 6094346.
- Kang A, Struben H (November 2008). "[Pre-eclampsia screening in first and second trimester]". Therapeutische Umschau. Revue Thérapeutique (in German). 65 (11): 663–66. doi:10.1024/0040-5918.104.22.1683. PMID 18979429.
- Marik PE (March 2009). "Hypertensive disorders of pregnancy". Postgraduate Medicine. 121 (2): 69–76. doi:10.3810/pgm.2009.03.1978. PMID 19332964. Retrieved 2009-06-18.
- Mounier-Vehier C, Delsart P (April 2009). "[Pregnancy-related hypertension: a cardiovascular risk situation]". Presse Médicale (Paris, France : 1983) (in French). 38 (4): 600–08. doi:10.1016/j.lpm.2008.11.018. PMID 19250798. Retrieved 2009-06-18.
- Pack AI, Gislason T (2009). "Obstructive sleep apnea and cardiovascular disease: a perspective and future directions". Progress in Cardiovascular Diseases. 51 (5): 434–51. doi:10.1016/j.pcad.2009.01.002. PMID 19249449. Retrieved 2009-06-20.
- Silverberg DS, Iaina A, Oksenberg A (January 2002). "Treating Obstructive Sleep Apnea Improves Essential Hypertension and Quality of Life". American Family Physician. 65 (2): 229–36. PMID 11820487.
- Tomimoto H, Ihara M, Takahashi R, Fukuyama H (November 2008). "[Functional imaging in Binswanger's disease]". Rinsho Shinkeigaku (in Japanese). 48 (11): 947–50. doi:10.5692/clinicalneurol.48.947. PMID 19198127.
- Arsenic trioxide drugs dot com
- atsdr-medical management guidelines for arsenic trioxide
- Arsenic Author: Frances M Dyro, MD, Chief of the Neuromuscular Section, Associate Professor, Department of Neurology, New York Medical College, Westchester Medical Center
- Addison WL (March 1928). "The Use of Sodium Chloride, Potassium Chloride, Sodium Bromide, and Potassium Bromide in Cases of Arterial Hypertension which are Amenable to Potassium Chloride". Can Med Assoc J. 18 (3): 281–85. PMC . PMID 20316740.
- Williams B et al.; British Hypertension Society; Michael Sutters, MD (2006). "Secondary Hypertension". Hypertension Etiology & Classification - Secondary Hypertension. Armenian Medical Network. Retrieved 2007-12-02.