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Secondary hypertension
Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which has a specific and identifiable underlying primary cause. It is much less common than essential hypertension, affecting only 5-10% of hypertensive patients. It has many different causes including obstructive sleep apnea, kidney disease, endocrine diseases, and tumors. The cause of secondary hypertension varies significantly with age. It also can be a side effect of many medications.
The cause of secondary hypertension are numerous (obstructive sleep apnea, kidney disease, endocrine diseases, tumors, medication side effect, Etc.) and etiologies varies significantly with age.
Obstructive sleep apnea (OSA) is one of the most common causes; 30-50% of patients who have OSA have co-morbid secondary hypertension. OSA is prevalent in older adults and should be considered in cases of resistant hypertension, hypertension refractory to appropriate aggressive medical therapy. OSA remains an under-diagnosed cause of secondary hypertension, likely secondary many risk factors associated with OSA such as obesity, advanced age, and cigarette smoking are shared with primary hypertension. The intermittent hypoxia and resultant hypercapnia that is characteristic of OSA leads to activation of the sympathetic nervous system and leads to elevated blood pressure. As with all cases of secondary hypertension, the goal of treating patients with hypertension due to OSA is addressing the underlying cause. Therefore, weight loss and nocturnal nasal continuous positive airway pressure (CPAP) are mainstays in treating hypertension secondary to OSA. Other approaches include the mandibular advancement splint (MAS), UPPP, tonsillectomy, adenoidectomy, or septoplasty.
Obstruction of the renal arteries supplying the kidney that result in elevated blood pressure 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. There are two main causes of renovascular hypertension: renal artery stenosis and fibromuscular dysplasia.
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.
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, chronic kidney disease and kidney pain. Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.
Hypertension is common in chronic kidney disease.
Certain medications, including NSAIDs (ibuprofen aka Motrin) and steroids can cause hypertension. Other medications include estrogens (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.
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Secondary hypertension
Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which has a specific and identifiable underlying primary cause. It is much less common than essential hypertension, affecting only 5-10% of hypertensive patients. It has many different causes including obstructive sleep apnea, kidney disease, endocrine diseases, and tumors. The cause of secondary hypertension varies significantly with age. It also can be a side effect of many medications.
The cause of secondary hypertension are numerous (obstructive sleep apnea, kidney disease, endocrine diseases, tumors, medication side effect, Etc.) and etiologies varies significantly with age.
Obstructive sleep apnea (OSA) is one of the most common causes; 30-50% of patients who have OSA have co-morbid secondary hypertension. OSA is prevalent in older adults and should be considered in cases of resistant hypertension, hypertension refractory to appropriate aggressive medical therapy. OSA remains an under-diagnosed cause of secondary hypertension, likely secondary many risk factors associated with OSA such as obesity, advanced age, and cigarette smoking are shared with primary hypertension. The intermittent hypoxia and resultant hypercapnia that is characteristic of OSA leads to activation of the sympathetic nervous system and leads to elevated blood pressure. As with all cases of secondary hypertension, the goal of treating patients with hypertension due to OSA is addressing the underlying cause. Therefore, weight loss and nocturnal nasal continuous positive airway pressure (CPAP) are mainstays in treating hypertension secondary to OSA. Other approaches include the mandibular advancement splint (MAS), UPPP, tonsillectomy, adenoidectomy, or septoplasty.
Obstruction of the renal arteries supplying the kidney that result in elevated blood pressure 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. There are two main causes of renovascular hypertension: renal artery stenosis and fibromuscular dysplasia.
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.
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, chronic kidney disease and kidney pain. Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.
Hypertension is common in chronic kidney disease.
Certain medications, including NSAIDs (ibuprofen aka Motrin) and steroids can cause hypertension. Other medications include estrogens (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.