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Secondary hypertension

 

Secondary hypertension

Secondary hypertension
Classification and external resources
ICD-10 I15
ICD-9-CM 405

Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying secondary 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.

Contents

  • Types 1
    • Renovascular hypertension (I15.0) 1.1
    • Hypertension secondary to other renal disorders (I15.1) 1.2
    • Hypertension secondary to endocrine disorders (I15.2) 1.3
    • Other secondary hypertension (I15.8) 1.4
    • Adrenal 1.5
    • Kidney 1.6
    • Medication side effects 1.7
    • Pregnancy 1.8
    • Sleep disturbances 1.9
    • Arsenic exposure 1.10
    • Potassium deficiency 1.11
  • Diagnosis 2
  • References 3
  • External links 4

Types

Renovascular hypertension (I15.0)

It has two main causes: fibromuscular dysplasia and atheromatous stenosis. Also diabetes

Hypertension secondary to other renal disorders (I15.1)

Hypertension secondary to endocrine disorders (I15.2)

Other secondary hypertension (I15.8)

Adrenal

A variety of adrenal cortical abnormalities can cause hypertension, In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.[5]

Another related disorder that causes hypertension is apparent mineralocorticoid excess syndrome which is an autosomal recessive disorder that results from mutations in the gene encoding 11β-hydroxysteroid dehydrogenase, an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone.[6] At high concentrations cortisol can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension.[7] 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.[8][9][10] Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present.[9] 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.[11]

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.[12][13][14][15][16] GRA appears to be the most common monogenic form of human hypertension.[17]

Compare these effects to those seen in Conn's disease, an adrenocortical tumor which causes excess release of aldosterone,[18] that leads to hypertension.[19][20][21]

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).[22] More than 80% of patients with Cushing's syndrome develop hypertension.,[23] which is accompanied by distinct symptoms of the syndrome, such as central obesity, lipodystrophy, moon face, sweating, hirsutism and anxiety.[24]

Kidney

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 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.[25][26][27][28] 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.[29] Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.[30][31][32]

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.[33][34][35]

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.[36]

Neuroendocrine tumors are also a well known cause of secondary hypertension. Pheochromocytoma[37] (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).

Medication side effects

Certain medications, including NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension.[38][39][40][41][42] 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.[3] High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called rebound hypertension.[43][44][45][46][47][48][49] 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[50] and methyl-dopa.[49]

Other herbal or "natural products" which have been associated with hypertension include ma huang, St John's wort, and licorice.[3]

Pregnancy

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy.[51] 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.[52][53]

Sleep disturbances

Another common and under-recognized sign of hypertension is sleep apnea,[54][55] 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.[56]

Arsenic exposure

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, [57] confusion, proteinuria [58] visual disturbances, and nausea and vomiting [59]

Potassium deficiency

Due to the role of intracellular potassium in regulation of cellular pressures related to sodium, establishing potassium balance has been shown to reverse hypertension. [60]

Diagnosis

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 [61]

References

  1. ^ Office of Public Affairs (13 October 2003). "NewYork Weill Cornell Research Highlights Need To Focus on Frequently Neglected Neurogenic Hypertension: Closer Analysis Can Pinpoint True Cause of Hypertension and Direct Successful Management: Not All Hypertension Should Be Treated with the Same Drug". The New York Weill Cornell Medical Center. Retrieved 29 January 2013. In this form of "neurogenic" hypertension, blood pressure elevation is caused by increases in cardiac output and constriction of systemic arteries due to increased epinephrine (adrenaline) and norepinephrine production—the so-called "stress" hormones. 
  2. ^ Samuel J Mann (2003). "Neurogenic essential hypertension revisited: the case for increased clinical and research attention".  
  3. ^ a b c 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".  
  4. ^ Varon J, Marik PE (2008). "Perioperative hypertension management". Vasc Health Risk Manag 4 (3): 615–27.  
  5. ^ Giacchetti G, Turchi F, Boscaro M, Ronconi V (April 2009). "Management of primary aldosteronism: its complications and their outcomes after treatment".  
  6. ^ Bailey MA, Paterson JM, Hadoke PW, et al. (January 2008). "A Switch in the Mechanism of Hypertension in the Syndrome of Apparent Mineralocorticoid Excess".  
  7. ^ Vantyghem MC, Marcelli-Tourvieille S, Defrance F, Wemeau JL (October 2007). "11beta-hydroxysteroide dehydrogenases. Recent advances".  
  8. ^ 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".  
  9. ^ a b Johns C (January 2009). "Glycyrrhizic acid toxicity caused by consumption of licorice candy cigars".  
  10. ^ Sontia B, Mooney J, Gaudet L, Touyz RM (February 2008). "Pseudohyperaldosteronism, liquorice, and hypertension".  
  11. ^ Whitworth, Judith (Dec 2015). "Cardiovascular Consequences of Cortisol Excess". Vasc Health Risk Manag 1 (4): 291–299.  
  12. ^ Escher G (April 2009). "Hyperaldosteronism in pregnancy".  
  13. ^ 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".  
  14. ^ Omura M, Nishikawa T (May 2006). "[Glucocorticoid remediable aldosteronism]".  
  15. ^ Luft FC (October 2003). "Mendelian Forms of Human Hypertension and Mechanisms of Disease".  
  16. ^ Nicod J, Dick B, Frey FJ, Ferrari P (February 2004). "Mutation analysis of CYP11B1 and CYP11B2 in patients with increased 18-hydroxycortisol production".  
  17. ^ McMahon GT, Dluhy RG (2004). "Glucocorticoid-remediable aldosteronism".  
  18. ^ Ziaja J, Cholewa K, Mazurek U, Cierpka L (2008). "[Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas]".  
  19. ^ Astegiano M, Bresso F, Demarchi B, et al. (March 2005). "Association between Crohn's disease and Conn's syndrome. A report of two cases".  
  20. ^ Pereira RM, Michalkiewicz E, Sandrini F, et al. (October 2004). "[Childhood adrenocortical tumors]".  
  21. ^ Kievit J, Haak HR (March 2000). "Diagnosis and treatment of adrenal incidentaloma. A cost-effectiveness analysis".  
  22. ^ Kumar, Abbas, Fausto. Robbins and Cotran Pathologic Basis of Disease, 7th ed. Elsevier-Saunders; New York, 2005.
  23. ^ Dodt C, Wellhöner JP, Schütt M, Sayk F (January 2009). "[Glucocorticoids and hypertension]".  
  24. ^ Yudofsky, Stuart C.; Robert E. Hales (2007). The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences (5th ed.). American Psychiatric Pub, Inc.  
  25. ^ Ecder T, Schrier RW (April 2009). "Cardiovascular abnormalities in autosomal-dominant polycystic kidney disease".  
  26. ^ Gross P (May 2008). "Polycystic kidney disease: will it become treatable?".  
  27. ^ Masoumi A, Reed-Gitomer B, Kelleher C, Schrier RW (2007). "Potential pharmacological interventions in polycystic kidney disease".  
  28. ^ Chapman AB (May 2007). "Autosomal dominant polycystic kidney disease: time for a change?".  
  29. ^ Chapman AB (July 2008). "Approaches to testing new treatments in autosomal dominant polycystic kidney disease: insights from the CRISP and HALT-PKD studies".  
  30. ^ Berthoux FC, Mohey H, Afiani A (January 2008). "Natural history of primary IgA nephropathy".  
  31. ^ D'Cruz D (February 2009). "Renal manifestations of the antiphospholipid syndrome".  
  32. ^ Licht C, Fremeaux-Bacchi V (February 2009). "Hereditary and acquired complement dysregulation in membranoproliferative glomerulonephritis".  
  33. ^ Textor SC (May 2009). "Current Approaches to Renovascular Hypertension".  
  34. ^ Voiculescu A, Rump LC (January 2009). "[Hypertension in patients with renal artery stenosis]".  
  35. ^ Kendrick J, Chonchol M (October 2008). "Renal artery stenosis and chronic ischemic nephropathy: epidemiology and diagnosis".  
  36. ^ 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): 93–8.  
  37. ^ Kassim TA, Clarke DD, Mai VQ, Clyde PW, Mohamed Shakir KM (December 2008). "Catecholamine-induced cardiomyopathy".  
  38. ^ Simone Rossi, ed. (2006). Australian medicines handbook 2006.  
  39. ^ White WB (May 2009). "Defining the problem of treating the patient with hypertension and arthritis pain".  
  40. ^ 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".  
  41. ^ Berenbaum F (2008). "New horizons and perspectives in the treatment of osteoarthritis".  
  42. ^ Akinbamowo AO, Salzberg DJ, Weir MR (October 2008). "Renal consequences of prostaglandin inhibition in heart failure".  
  43. ^ Lowenstein J (January 1980). "Drugs five years later: clonidine".  
  44. ^ Robertson JI (January 1997). "Risk factors and drugs in the treatment of hypertension".  
  45. ^ Schachter M (August 1999). "Moxonidine: a review of safety and tolerability after seven years of clinical experience".  
  46. ^ Schäfer SG, Kaan EC, Christen MO, Löw-Kröger A, Mest HJ, Molderings GJ (July 1995). "Why imidazoline receptor modulator in the treatment of hypertension?".  
  47. ^ Larsen R, Kleinschmidt S (April 1995). "[Controlled hypotension]".  
  48. ^ Scholtysik G (March 1986). "Animal pharmacology of guanfacine".  
  49. ^ a b Myers MG (January 1977). "New drugs in hypertension".  
  50. ^ 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.  
  51. ^ Kang A, Struben H (November 2008). "[Pre-eclampsia screening in first and second trimester]".  
  52. ^ Marik PE (March 2009). "Hypertensive disorders of pregnancy".  
  53. ^ Mounier-Vehier C, Delsart P (April 2009). "[Pregnancy-related hypertension: a cardiovascular risk situation]".  
  54. ^ Pack AI, Gislason T (2009). "Obstructive sleep apnea and cardiovascular disease: a perspective and future directions".  
  55. ^ Silverberg DS, Iaina A and Oksenberg A (January 2002). "Treating Obstructive Sleep Apnea Improves Essential Hypertension and Quality of Life". American Family Physician 65 (2): 229–36.  
  56. ^ Tomimoto H, Ihara M, Takahashi R, Fukuyama H (November 2008). "[Functional imaging in Binswanger's disease]".  
  57. ^ Arsenic trioxide drugs dot com
  58. ^ atsdr-medical management guidelines for arsenic trioxide
  59. ^ Arsenic Author: Frances M Dyro, MD, Chief of the Neuromuscular Section, Associate Professor, Department of Neurology, New York Medical College, Westchester Medical Center
  60. ^ 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): 281–5.  
  61. ^ 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. 

External links

  • CVPhysiology
  • CNN
  • Mayo Clinic
  • Hypertension Types
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