Chronic hypertension causes: Difference between revisions
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==Complete List of Secondary Causes of Hypertension <ref>isbn=140510368X Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:85</ref><ref>isbn=1591032016 Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:194-195</ref>== | ==Complete List of Secondary Causes of Hypertension <ref>isbn=140510368X Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:85</ref><ref>isbn=1591032016 Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:194-195</ref>== | ||
==Most common== | |||
* [[Anxiety]] | |||
* [[Arteriosclerosis]] | |||
* [[Congenital adrenal hyperplasia]] | |||
* [[Essential hypertension]] | |||
* [[Glucocorticoids]] | |||
* [[Glomerulonephritis]] | |||
* [[Gestational hypertension]] | |||
* [[Increased salt intake]] | |||
* [[Metabolic syndrome]] | |||
* [[Obesity]] | |||
* [[Renal failure]] | |||
* [[Sleep apnea]] | |||
* [[Stress]] | |||
* [[White coat hypertension]] | |||
==By organ system== | ==By organ system== |
Revision as of 19:29, 7 July 2012
Hypertension Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor-In-Chief: Taylor Palmieri
Hypothesized Underlying Causes of Primary Hypertension
Salt sensitivity
Sodium is the environmental factor that has received the greatest attention. Approximately 60% of the essential hypertension population is responsive to sodium intake. This is due to the fact that increasing amounts of salt in a person's bloodstream causes the body to draw in more water, increasing the pressure on the blood vessel walls. In addition to sodium, choride plays an important role as it causes volume expansion increasing blood pressure as sodium with combined with other anions does not increase blood pressure.[1] Also salt sensitivity is known to be increased with increasing age, obesity, in African americans and in the metabolic syndrome.[2]
Mechanisms
The proposed mechanism for salt-sensitvity is incraesed salt intake over a long period of time leads to impaired excretion of salt which causes hypertension. There may be several other pathways involved in the pathophysiology of salt-sensitivity leading to hypertension. Salt-sensitive patients are known to have a dysregulated renin-angiotensin pathway and patients show an abnormal vascular response to angiotensin II[3]. Increased sodium re absorption, though not well understood, is mostly related abnormalities across Na-H proximal tubule channels, Na-K-Cl co-transporter across the thick ascending limb, Na-Cl distal tubule co-transporter and epithelial Na channels. Dietary deficiency in potassium is also known to trigger increased sodium sensitivity in patients in particular African-Americans, but the mechanism is still not clearly determined.
Role of renin
Renin is a hormone secreted by the juxtaglomerular cells of the kidney and linked with aldosterone in a negative feedback loop. The range of renin activity observed in hypertensive subjects tends to be broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than Caucasians and may explain why they tend to respond better to diuretic therapy than drugs that interfere with the renin-angiotensin system.
High Renin levels predispose to Hypertension: Increased Renin --> Increased Angiotensin II --> Increased Vasoconstriction, Thirst/ADH and Aldosterone --> Increased Sodium Reabsorption in the Kidneys (DCT and CD) --> Increased Blood Pressure.
Insulin resistance
Insulin is a polypeptide hormone secreted by the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. Insulin resistance and/or hyperinsulinemia have been suggested as being responsible for the increased arterial pressure in some patients with hypertension. This feature is now widely recognized as part of syndrome X, or the metabolic syndrome.
Sleep apnea
Sleep apnea is a common, under-recognized cause of hypertension.[4] It is best treated with UPPP, tonsilectomy, adenoidectomy, sinus surgery, or weight loss, nocturnal nasal positive airway pressure, or the Mandibular advancement splint (MAS).
Genetics
Hypertension is one of the most common complex disorders, with genetic heritability averaging 30%. Data supporting this view emerge from animal studies as well as in population studies in humans. Most of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each have an elevated blood pressure as one of their phenotypic expressions.
More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing.
Causes of Secondary Hypertension
Only in a small minority of patients with elevated arterial pressure, can a specific cause be identified. These individuals will probably have an endocrine or renal defect that, if corrected, could bring blood pressure back to normal values. Common causes include:
- Renal hypertension
- Hypertension produced by diseases of the kidney. This includes diseases such as polycystic kidney disease or chronic glomerulonephritis. 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.
- Adrenal hypertension
- Hypertension is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.
- In patients with pheochromocytoma increased secretion of catecholamines such as epinephrine and norepinephrine by a tumor (most often located in the adrenal medulla) causes 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).
- Diet
- The North American diet that is high in fat and salt has been proven to exacerbate hypertension. A study in the U.S. found that patients placed on a strict vegetarian diet showed a significant benefit to their condition over the one year. Certain medications, especially NSAIDS (Motrin/ibuprofen) and steroids can cause hypertension. Imported licorice (Glycyrrhiza glabra) inhibits the 11-hydroxysteroid hydrogenase enzyme (catalyzes the reaction of cortisol to cortison) which allows cortisol to stimulate the Mineralocorticoid Receptor (MR) which will lead to effects similar to hyperaldosteronism, which itself is a cause of hypertension.
- Age
- Over time, the number of collagen fibers in artery and arteriole walls increases, making blood vessels stiffer. With the reduced elasticity comes a smaller cross-sectional area in systole, and so a raised mean arterial blood pressure.
Complete List of Secondary Causes of Hypertension [5][6]
Most common
- Anxiety
- Arteriosclerosis
- Congenital adrenal hyperplasia
- Essential hypertension
- Glucocorticoids
- Glomerulonephritis
- Gestational hypertension
- Increased salt intake
- Metabolic syndrome
- Obesity
- Renal failure
- Sleep apnea
- Stress
- White coat hypertension
By organ system
By alphabetical order
References
- ↑ Kurtz TW, Al-Bander HA, Morris RC (1987). ""Salt-sensitive" essential hypertension in men. Is the sodium ion alone important?". N. Engl. J. Med. 317 (17): 1043–8. PMID 3309653. Unknown parameter
|month=
ignored (help) - ↑ Obarzanek E, Proschan MA, Vollmer WM; et al. (2003). "Individual blood pressure responses to changes in salt intake: results from the DASH-Sodium trial". Hypertension. 42 (4): 459–67. doi:10.1161/01.HYP.0000091267.39066.72. PMID 12953018. Unknown parameter
|month=
ignored (help) - ↑ Chamarthi B, Williams JS, Williams GH (2010). "A mechanism for salt-sensitive hypertension: abnormal dietary sodium-mediated vascular response to angiotensin-II". J. Hypertens. 28 (5): 1020–6. doi:10.1097/HJH.0b013e3283375974. PMID 20216091. Unknown parameter
|month=
ignored (help) - ↑ Silverberg DS, Iaina A and Oksenberg A (2002). "Treating Obstructive Sleep Apnea Improves Essential Hypertension and Quality of Life". American Family Physicians. 65 (2): 229–36. PMID 11820487. Unknown parameter
|month=
ignored (help) - ↑ isbn=140510368X Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:85
- ↑ isbn=1591032016 Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:194-195