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INTERNAL MEDICINE - Secondary Hypertension
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INTERNAL MEDICINE - Secondary Hypertension


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  • 1. INTERNAL MEDICINE: Secondary HypertensionnianderthalNOTES
  • 2. SECONDARY HYPERTENSIONDEFINITION:-the elevation of blood pressure due to a specific underlying disorderCAUSES (Include but not limited to):-Renal Parenchymal Diseases-Primary Aldosteronism-Cushing’s Syndrome-Pheochromocytoma
  • 3. Renal Parenchymal Diseases-RENAL DISEASE IS THE MOST COMMON CAUSE OF SECONDARY HYPERTENSION-Hypertension is MORE SEVERE in GLOMERULAR DISEASES than in Interstitial Diseases-Proteinuria >1000 mg/day and an active urine sediment are indicative of PRIMARY RENAL DISEASE
  • 4. Renovascular Hypertension-hypertension due to obstruction of a renal artery-potentially curable form-mechanism is related to activation of the renin- angiotensin system-Females 8x > Males-Patients at risk: 1. Older arteriosclerotic patients with plaque on renal artery, frequently at its origin 2. Patients with fibromuscular dysplasia
  • 5. Renovascular Hypertension-Histologic Variants of Fibromuscular Dysplasia: 1. Medial Fibroplasia – MOST COMMON 2. Perimedial Fibroplasia 3. Medial Hyperplasia 4. Intimal Fibroplasia*Fibromuscular dysplasia lesion are bilateral and affect more distal portions of the renal artery
  • 6. Renovascular Hypertension-S/Sx: -abdominal or flank bruit that extends throughout systole into diastole-Treatment: -Renal Vascular repair: pts with long-standing HTN, advanced renal insufficiency, DM are LESS LIKELY to benefit -ACE inhibitors/ARBs: decrease GFR in stenotic kidneys causing renal arteriolar vasodilation; cause progressive renal insufficiency in pts w/ bilateral renal artery stenosis or renal artery stenosis on a solitary kidney BUT insufficiency is REVERSIBLE IF DRUG is DISCONTINUED
  • 7. Renovascular Hypertension-Treatment: -Percutaneous Transluminal Renal Angioplasty (PTRA) -intial treatment of choice in pts w/ Fibromuscular Disease-LAB/Imaging: -OIH scan / DTPA scan before and after a single dose of ACEi to assess renal blood flow and GFR, respectively -Doppler Ultrasound -Gadolinium-contrast magnetic resonance angiography – proximal > distal renal artery - Contrast Angiography – “GOLD STANDARD” for detecting Renal Artery Lesions; NEPHROTOXIC ( to patients with DM, w/ pre-existing Renal Insufficiency)
  • 8. Renovascular Hypertension-Prognosis: -Patients with fibromuscular disease have more favorable outcomes than patients with atherosclerotic lesions, owing to younger age, shorter duration of HTN and less systemic disease
  • 9. Primary Aldosteronism-DEFINITION: excess aldosterone production-potentially curable form of HTN-HTN is mild to moderate, but occasionally severe-increased aldosterone production is INDEPENDENT of the renin-angiotensin system and the consequences are: 1. sodium retention 2. hypertension 3. hypokalemia 4. low PRA
  • 10. Primary Aldosteronism-Risk Factors: -30s-50s -pts taking diuretics-S/Sx: -asymptomatic (most) -polyuria -polydipsia -paresthesias or muscle weakness -hypertension- mild-moderate, occasionally severe
  • 11. Primary Aldosteronism-LAB/Imaging: 1. Serum potassium concentration -SIMPLEST SCREENING TEST -can be normal initially in some pts with aldosterone secreting adenoma 2. Plasma Aldosterone to Plasma Renin Activity (PA/PRA) ratio -ambulatory pts in the morning - >20 PA/PRA ratio -90% have aldosterone secreting adenoma -affected by drugs: -Aldosterone antagonists – increases aldosterone -ARBs and ACEi – increases renin
  • 12. Primary Aldosteronism-LAB/Imaging: 3. CT/MRI -should be carried out in all patients diagnoses with primary aldosteronism 4. Adrenal Scintigraphy -if CT/MRI does not detect adenoma
  • 13. Primary Aldosteronism-Diagnosis: -confirmed by demonstrating FAILURE TO SUPPRESS plasma aldosterone to <277 pmol/L after IV infusion of 2L of isotonic saline over 4h
  • 14. Primary Aldosteronism-Etiology: -aldosterone producing adrenal adenoma -unilateral, <3cm in diameter -biosynthesis is more responsive to ACTH -Hypertension responsive post surgery -adrenocortical hyperplasia -bilateral -biosynthesis is more responsive to angiotensin -Hypertension NOT responsive post surgery
  • 15. Primary Aldosteronism-Etiology: -adrenal carcinoma -produce other adrenal steroids -ectopic malignancy -e.g. ovarian arrhenoblastoma
  • 16. Primary Aldosteronism-Treatment: 1.Surgery -should be undertaken only after BP has been controlled and hypokalemia corrected -HYPOaldosteronism may occur 3 months post operation during this time Potassium should be monitored, and HYPERkalemia should be treated with potassium-wasting diuretics and fludrocortisone 2. Aldosterone antagonists 3. Potassium-sparing diuretics
  • 17. Primary Aldosteronism-Treatment: 4. Glucocorticoids / Spironolactone -for rare, monogenic, autosomal dominant form of the disease characterized by moderate to severe HTN
  • 18. Cushing’s Syndrome-Hypertension occurs in 75-80% of patients-MECHANISM: -stimulation of mineralocorticoid receptors by cortisol and increased secretion of adrenal steroids -can be seen in patients taking exogenous glucocorticoids
  • 19. Cushing’s Syndrome-Lab/Imaging: 1. 24-h urine excretion rate of free cortisol 2. Overnight Dexamethasone suppression tes-Treatment: -appropriate therapy depends on etiology
  • 20. Pheochromocytoma-DEFINITION: catecholamine secreting tumors that are located in the adrenal medulla -autosomal dominant -can be associated with multiple endocrine neoplasias (MEN) type 2A and type 2B-PARAGANGLIOMA: -tumor in extra-adrenal paraganglion tissue
  • 21. Pheochromocytoma-MECHANISM: -related to increased circulating catecholamines, and may secrete other vasoactive substances -RARITY: epinephrine is secreted predominantly and causes HYPOtension rather than HYPERtension
  • 22. Pheochromocytoma-Lab/Imaging: 1. Catecholamine in Urine or Plasma 2. Genetic screening
  • 23. MISCELLANEOUS CAUSES OF HYPERTENSION1. Obstructive Sleep Apnea -severity of HTN correlates with severity of sleep apnea -should be considered in drug-resistant patients and with history of snoring -Dx: confirmed by Polysomnography -Rx: Weight loss, Continuous Positive Airway Pressure (CPAP)
  • 24. MISCELLANEOUS CAUSES OF HYPERTENSION2. Coarctation of the Aorta -MOST COMMON CONGENITAL CARDIOVASCULAR CAUSE OF HYPERTENSION -occurs in 35% of pts with Turner’s Syndrome -Patients with less severe lesions may not be diagnosed until young adulthood -S/Sx: diminished and delayed femoral pulses, systolic pressure gradient between the right arms and legs
  • 25. MISCELLANEOUS CAUSES OF HYPERTENSION2. Coarctation of the Aorta -Dx: Chest X-ray and transesophageal echocardiogram -Tx: Surgical repair, Balloon angioplasty (with or without cardiovascular stent)3. Thyroid diseases -Hypothyroidism: mild diastolic hypertension -Hyperthyroidism: systolic hypertension
  • 27. MONOGENIC HYPERTENSION-recognized by their characteristic phenotypes and Dx confirmed by genetic analysis-inherited defects in adrenal steroid biosynthesis and metabolism result in MINERALOCORTICOID-INDUCED HYPERTENSION and HYPOKALEMIA
  • 28. MONOGENIC HYPERTENSION DEFICIENT PHYSIOLOGIC EFFECT CLINICAL MANIFESTATION ENZYME17a- Decreased sex hormone and -no sexual maturationhydroxylase cortisol -males: pseudohermaphroditism -females: primary amenorrhea, absent secondary sexual characteristic11B- Salt-retaining adrenogenital -virilization and ambiguous genitaliahydroxylase syndrome resulting in -penile enlargement decreased cortisol synthesis, -precocious puberty increased mineralocorticoids -short stature and shunting of the steroid -PRESENTING Sx: acne, hirsutism, biosynthesis in the androgen menstrual irregularities pathway -HTN: less common in late-onset11B- Impaired ability to metabolize -HTNhydroxysteroid cortisol to cortisone (inactivedehydrogenase metabolite); can be acquired due to licorice-containing glyccherizic acid
  • 29. MONOGENIC HYPERTENSION-LIDDLE’S SYNDROME: -results from constitutive activation of amiloride sensitive epithelial sodium channels on the distal renal tubule resulting in EXCESS SODIUM REABSORPTION-HYPERTENSION IN PREGNANCY -exacerbated due to activation of mineralocorticoid receptors by progesterone