1 / 33

Endocrine Hypertension

Endocrine Hypertension. Essential hypertension 92-94% Secondary hypertension 6-8% Renal 4-5% Miscellaneous ~2% Endocrine 1-2% Primary hyperaldosteronism 0.3-15% Cushing ’ s syndrome <0.1% Pheochromocytoma <0.1%.

hien
Télécharger la présentation

Endocrine Hypertension

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Endocrine Hypertension Essential hypertension 92-94% Secondary hypertension 6-8% Renal 4-5% Miscellaneous ~2% Endocrine 1-2% Primary hyperaldosteronism 0.3-15% Cushing’s syndrome <0.1% Pheochromocytoma <0.1%

  2. Endocrine Hypertension Mineralocorticoid excess Cushing’s syn. Pheochromocytoma

  3. Sympathetic Nervous System

  4. Epinephrine Norepinephrine Tyrosine Hydroxylase COMT AADC Metanephrine Normetanephrine Dopamine β Hydroxylase MAO PNMT Vanylmandelic Acid (VMA) CA Synthesis & Metabolism APUD cells

  5. Pheochromocytoma • ~ 0.1% or less of hypertension • Extraadrenal- Paraganglioma “10% Tumor” Bilateral Extra-adrenal Familial(? ~20%) Malignant

  6. Pheochromocytoma Symptoms During paroxysm:Between attacks: Headache Sweating Sweating Cold hands & feet Palpitations Weight loss Tremor Constipation Chest pain Abdominal pain Nausea, vomiting

  7. Pheochromocytoma Signs: • Increased blood pressure • Orthostatic hypotension • Tachycardia

  8. Pheochromocytoma Familial forms: (germ-line mutations autosomal dominant) Syndromic- Multiple Endocrine Neoplasia Type 2 (A & B) Multiple Endocrine Neoplasia Type 1 (rarely) von Hippel-Lindau disease Neurocutaneous syndromes (NF1) Non- syndromic SDHB, C, D; TEM127

  9. When to Suspect a Pheochromocytoma? • Episodic HTN accompanied by the classical triad • Refractory HTN • Labile HTN • Severe pressor response to surgery etc. • Familial Hx associated with Pheo • Incidental adrenal mass • HTN at a young age • Takotsubo cardiomyopathy

  10. MEN2 MEN 2A MEN 2B Familial Medullary Thyroid Carcinoma (FMTC) קרצינומה מדולארית של בלוטת התריס פאוכרומוציטומה היפרפרהטירוידיזם 10-20% 40-50% 90% 40-50% 100% 90%

  11. MEN2b מראה מרפנואידי נוירומות בריריות

  12. Von-HippelLindau Disease • Renal cell carcinoma • Retinal angioma • Cerebellar or spinal hemangioblastoma • Pheochromocytoma-7-19%.

  13. Pheochromocytoma-Biochemical Diagnosis • 24 hour urine collection for free CATs • epinephrine and norepinephrine • Sensitivity ~70% • 24 hour urine collection for CAT metabolites (METS) • metanephrine, normetanephrine and acid • More specific, sensitivity >90% • Urinary CATS + METS • Sensitivity > 95% • Plasma free metanephrines. • Highest sensitivity > 95%

  14. Pheochromocytoma imaging Only after the Dx of pheo is biochemically confirmed!! • CT • MRI • I123MIBG • PET-18FDG • Octreoscan or 68Ga-DOTATATE-PET

  15. Malignant pheo- 68Ga-DOTATATE Scan

  16. Pheochromocytoma- Therapy Surgical resection of tumor- • If localized to adrenal- laparoscopic adrenalectomy Prior to surgery- • Hypertension: α-blockade (phenoxybenzamine, doxasocin, phentolamine) • Tachycardia- β-blockade (only after α blockade)

  17. Mineralocorticoid excess

  18. Kidney 11 β HSD type 2 cortisol cortisone ANDROSTENDIONE Biosynthesis and action of Aldosterone Glomerulosa

  19. Renin-Angiotensin- Aldosterone Regulatory System ↑ACTH Sympathetic stimulation

  20. Mineralocorticoid Excess Hyperaldosteronism Primary Secondary Apparent MC excess ↓PRA and ↓ PAC

  21. Hyperaldosteronism DD: Primary-PRA Secondary- PRA 1. Renal Artery Stenosis(atherosclerosis, fibromuscular dysplasia). 2. Primary tumor of the JGA

  22. Primary Aldosteronism • Described by Conn in 1955. • Hypertension, hypokalemia, metabolic alkalosis. • Prevalence: 5-15% of patients with hypertension.

  23. Causes of Primary Aldosteronism Aldosterone Producing Adenoma (APA) ~30% Idiopathic/hyperplasia (IHA) ~ 70% AdrenocorticalCarcinoma rare

  24. Clinical Presentation Hypertension Moderate to severe (APA>hyperplasia) Refractory to medications K on low dose diuretics End-organ damage(aldosterone, HTN) LVH Micro and macro vascular disease

  25. Clinical Presentation • Laboratory K, ↔K Metabolic alkalosis Mild Na • Symptoms related to hypokalemia Neuromuscular Nephrogenic DI (polyuria & nocturia)

  26. Screening for Primary Hyperaldosteronism • Hypertension and hypokalemia(including patients treated with low dose diuretics). • Severe, resistant, or relatively acute hypertension, age<30. • An adrenal incidentaloma

  27. Diagnosis: • Screening test • Confirmatory testing • Determine the subtype

  28. Screening Tests for Primary Aldosteronism: PAC/PRA(PAC >20 ng/dl, PRA<1 ng/ml/h) • >30 suggestive; >50 diagnostic • Morning, ambulatory, paired, random PAC and PRA. • Serum K levels should be normalized • Not under beta blockers and spironolactone (preferably also w/o ACE inhibitors).

  29. Diagnosis • Confirmatory tests: Saline infusion test-non suppressed aldo. 24 hour urinary aldosterone • Determining subtype: Posture test- normal response: elevation of Aldo IHA- normal response APA- no elevation

  30. Imaging • Only after biochemical Dx(2-10% nonfunctioning adenomas on CT). • Abdominal spiral CT • In patients > 40 years of age-Selective adrenal venous sampling

  31. Treatment • APA- Unilateral total adrenalectomy • IHA- Medical management (aldactone, amiloride, aplerenone)

  32. >30

  33. Other Causes for Endocrine HTN • Hypothyroidism –diastolic HTN • Hyperthyroidism- systolic HTN • Acromegaly- salt retention • Hyperparathyroidism

More Related