1 / 64

Secondary Hypertension: Adrenal and Nervous Systems

Secondary Hypertension: Adrenal and Nervous Systems. Ανδρέας Πιτταράς Καρδιολόγος Clinical Hypertension Specialist ESH Υπερτασικό ιατρείο Τζάνειο νοσοκομείο Υπερηχοκαρδιογραφικό εργαστήριο ΝΜΥΑ ΙΚΑ. Adrenocortical Causes of Hypertension. The adrenal cortex can cause hypertension.

bisaacson
Télécharger la présentation

Secondary Hypertension: Adrenal and Nervous Systems

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. Secondary Hypertension: Adrenal and Nervous Systems Ανδρέας Πιτταράς Καρδιολόγος Clinical Hypertension Specialist ESH Υπερτασικό ιατρείο Τζάνειο νοσοκομείο Υπερηχοκαρδιογραφικό εργαστήριο ΝΜΥΑ ΙΚΑ

  2. Adrenocortical Causes of Hypertension

  3. The adrenal cortex can cause hypertension

  4. Pathways of adrenal steroidogenesis

  5. Algorithmic approach to mineralocorticoid-induced hypertension

  6. Hypertensive Syndromes Secondary to Hypersecretion of Deoxycorticosterone

  7. Abnormalities of steroid production

  8. Findings on physical examination

  9. 17 -hydroxylase deficiency syndrome

  10. Physical characteristics

  11. Hypertensive Syndromes Secondary to Cortisol Excess

  12. Causes of Cushing's syndrome

  13. Abdominal striae caused by excess cortisol production

  14. Ectopic adrenocorticotropic hormone excess

  15. Inferior petrosal sinus sampling for ACTH

  16. Inferior petrosal sinuses before and after oCRH

  17. OHSD deficiency syndromes

  18. Hypertensive Syndromes Secondary to Hypersecretion of Aldosterone

  19. Primary aldosteronism

  20. Primary aldosteronism can occur at all ages • Clinical clues to the presence of primary aldosteronism • Spontaneous hypokalemia • Diuretic-induced hypokalemia • Difficulty in maintaining a normal serum potassium while on diuretics despite concomitant use of potassium-sparing agents or KCl supplementation • Refractory hypertension • Family history of primary aldosteronism

  21. Serum potassium concentrations in primary aldosteronism

  22. Stimulated plasma renin activity in primary aldosteronism

  23. Aldosterone excretion rate

  24. Plasma aldosterone concentration

  25. Sensitivity and specificity of screening tests

  26. Biochemical confirmation of adenoma versus hyperplasia MEASUREMENTSADENOMABILATERAL HYPERPLASIA Serum potassium, mEq/L 3.03.0 Plasma 18-OHB, ng/dL 100100 Plasma aldosterone response to ambulation DecreaseIncrease Urinary 18-hydroxycortisol IncreaseNormal

  27. CT scan of normal adrenal glands

  28. CT scan of a right adrenal tumor

  29. Venography of a left adrenal tumor

  30. Diagnostic accuracy of iodocholesterol NP-59 scanning Diagnostic accuracy of imaging techniques in adrenocortical disorders TRUE POSITIVES, %DISORDERPATIENTS, nNP-59CT Cushing's syndrom289390 Primary aldosteronis588891 Nonfunctional tumors1310089

  31. Hemodynamic features of primary aldosteronism

  32. Diuretic therapy in patients with primary aldosteronism

  33. Relationship between plasma volume and arterial BP

  34. Calcium antagonists as alternatives to diuretics

  35. Surgery is indicated in patients with solitary adenomas

  36. Influence of the severity of hypertension on BP response after surgery

  37. Efficacy of long-term medical management of aldosterone-producing adenomas ELECTROLYTE LEVELS AT DIAGNOSIS ELECTROLYTE LEVELS AT LAST FOLLOW-UP PATIENT AGE y SEX FOLLOW-UP, y BLOOD PRESSURE AT PRESENTATION*, mm Hg MOST RECENT BLOOD PRESSURE*, mm Hg SODIUM POTASSIUM CHLORIDE CARBON DIOXIDE SODIUM POTASSIUM CHLORIDE CARBON DIOXIDE 1 65 M 5 170/94 120/80 145 3.1 105 30 140 5.2 110 28 2 69 M 12 164/65 157/86 141 3.2 98 35 141 3.9 104 30 3 63 M 11 178/96 130/95 141 2.9 100 28 144 4.0 107 26 4 43 F 8 180/104 124/82 140 3.0 98 31 137 4.1 105 25 5 39 F 5 184/132 128/80 141 3.9 102 29 140 3.7 106 28 6 76 M 9 174/100 116/74 143 2.9 104 29 139 4.7 103 23 7 68 M 6 180/105 195/76 140 3.1 98 32 142 4.2 109 28 8 69 M 5 190/95 130/70 144 2.9 103 29 140 4.1 104 21 9 59 M 7 180/116 145/99 144 2.4 102 35 139 4.3 104 30 10 55 M 8 180/110 140/74 145 3.0 102 30 142 4.6 104 30 11 59 M 6 165/102 112/68 142 3.0 106 30 142 4.8 108 30 12 50 M 6 177/117 115/80 144 3.1 102 31 143 4.5 104 27 13 44 M 6 160/110 130/82 141 3.0 106 29 140 4.3 103 29 14 54 F 8 160/98 142/60 144 3.4 106 29 142 4.7 108 25 15 52 F 13 150/104 104/76 142 3.3 105 24 137 4.4 106 25 16 52 F 5 168/102 128/91 143 2.7 102 32 141 3.6 106 32 17 54 F 17 180/110 101/71 143 3.0 105 33 139 4.4 101 30 18 59 M 8 176/116 158/78 142 2.6 106 29 138 4.6 101 27 19 44 F 9 190/122 122/78 142 2.6 98 32 137 3.6 98 26 20 61 F 14 160/110 144/72 145 2.9 103 35 140 3.7 113 29 21 68 F 5 166/108 111/78 143 2.6 103 30 146 4.5 108 26 22 66 M 11 178/108 150/92 141 3.0 101 31 142 3.8 102 26 23 73 M 10 178/100 107/66 143 3.8 99 31 143 4.8 105 24 24 56 M 15 200/125 128/85 141 3.2 102 32 139 4.6 102 26 *Blood pressure values are the average of at least three measurements. Levels are measured in millimoles per liter.

  38. Comparison of eplerenone and spironolactone

  39. Glucocorticoid-remediable aldosteronism

  40. Pheochromocytoma

  41. Important facts about pheochromocytomas • About 30% of pheochromocytomas reported in the literature are found either at autopsy or at surgery for an unrelated problem • 35% to 76% of pheochromocytomas discovered at autopsy are clinically unsuspected during life • The average age of diagnosis in those whose disease was discovered before death was 48.5 y, while the average in those diagnosed at autopsy was 65.8 y • Death was usually attributed to cardiovascular complications

  42. Pathologic features of pheochromocytoma

  43. Differential diagnosis of pheochromocytoma -Adrenergic hyperresponsiveness Acute state of anxiety Angina pectoris Acute infections Autonomic epilepsy Hyperthyroidism Idiopathic orthostatic hypotension Cerebellopontine angle tumors Acute hypoglycemia Acute drug withdrawal (Clonidine-Adrenergic blockade -MethyldopaAlcohol) Vasodilator therapy (Hydralazine, Minoxidil) Factitious administration of sympathomimetic agents Tyramine ingestion in patients on monoamine oxidase inhibitors Menopausal syndrome with migraine headaches

  44. Priorities for detection of pheochromocytoma • Patients with the triad of episodic headaches, tachycardia, and diaphoresis (with or without associated hypertension) • Family history of pheochromocytoma • Incidental suprarenal masses • Patients with a multiple endocrine adenomatosis syndrome, neurofibromatosis, or von Hippel-Lindau disease • Adverse cardiovascular responses to anesthesia, to any surgical procedure, or to certain drugs (eg, guanethidine, tricyclics, thyrotropin-releasing hormone, naloxone, or antidopaminergic agents)

  45. Supine resting plasma catecholamines

  46. Relationship between BP and plasma catecholamines

  47. Effect of clonidine on BP

More Related