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SECONDARY HYPERTENSION HYPERTENSION THAT RESULTS FROM AN UNDERLYING, IDENTIFIABLE, OFTEN CORRECTABLE CAUSE 5-10 %

SECONDARY HYPERTENSION INCIDENCE < 5% CLINICAL IMPORTANCE UNLIKE ESSENTIAL HYPERTENSION – INCURABLE LIFE LONG DISORDER SECONDARY HYPERTENSION – CURABLE BY REMOVING THE UNDERLYING CAUSE CAUSES RENAL PARENCHYMAL DISEASE E.G ACUTE NEPHRITIS, CHR. GN ETC. RENOVASCULAR DISEASE E.G RAS, ATHEROSCLEROSIS ETC CO-ARCTATION OF AORTA ENDOCRINE CAUSES

RISK FACTORS FOR SECONDARY HYPERTENSION POOR RESPONSE TO THERAPY I.E. RESISTANT HYPERTENSION WORSENING OF CONTROL IN PREVIOUSLY STABLE HYPERTENSIVE PATIENT STAGE 3 HYPERTENSION ( SYSTOLIC BLOOD PRESSURE >180 mm Hg OR DIASTOLIC BLOOD PRESSURE >110 MM HG) ONSET OF HYPERTENSION IN PERSON YOUNGER THAN 20 OR OLDER THAN 50 YRS SIGNIFICANT HYPERTENSIVE TARGET ORGAN DAMAGE LACK OF FAMILY HISTORY OF HYPERTENSION FINDINGS ON HISTORY, PHYSICAL EXAMINATION OR LABORATORY TESTING THAT SUGGEST A SECONDARY CAUSE

ENDOCRINE HYPERTENSION ENDOCRINE HYPERTENSION IS AN UNCOMMON CAUSE OF RAISED BLOOD PRESSURE. IT ACCOUNTS FOR LESS THAN 2% OF ALL CASES, BUT BECAUSE HYPERTENSION AFFECTS OVER 10% OF THE POPULATION, A SIGNIFICANT NUMBER OF PATIENTS HAVE AN UNDERLYING ENDOCRINE CAUSE TO EXPLAIN THEIR HIGH BLOOD PRESSURE.

ENDOCRINE HYPERTENSION RARE CAUSE OF HYPERTENSION 1 -2 % OF SECONDARY HTN IN MAJORITY 1 . MINERALOCORTICOID EXCESS EG PRIMARY HYPERALDOSTERONISM 2. PHEOCROMOCYTOMA 3. GLUCOCORTICOID EXCESS EG CUSHINGS SYNDROME OTHER CONDITIONS ESTROGEN – INDUCED HYPERTENSION PREGNANCY - INDUCED HYPERTENSION HYPERPARATHYROIDISM HYPOTHROIDISM ACROMEGALY CONGENTIAL ADRENAL HYPERPLASIA LIDDLE SYDROME RENIN SECRETING TUMORS

PHEOCROMOCYTOMA SYMPATHOCHROMAFFIN (SYMPATHOADRENAL) SYSTEM PROTOTYPE NEUROENDOCRINE SYSTEM TWO COMPONENTS SYMPATHETIC NERVOUS SYSTEM (POST GANGLIONIC NEUROINES) VAST MAJORITY RELEASE NOREPINEPHRINE (NORADRENALINE) CROMAFFIN TISSUES INCLUDING ADRENAL MEDULAE – MAJOR SOURCE OF CIRCULATING EPINEPHRINE (ADRENALINE) NOREPINEPHRINE + EPINEPHRINE + DOPAMINE = CATECHOLAMINES

“ PHEOCHROMOCYTOMAS ARE TUMORS THAT PRODUCE, STORE AND SECRETE CATECHOLAMINES.” “ THE CLASSIC SYMPTOMS OF PHEOCHROMOCYTOMA INCLUDE HEADACHE, DIAPHORESIS, PALPITATIONS, AND PAROXYSMAL HYPERTENSION.”

CATHACHOLAMINE PRODUCTING TUMOURS CHROMAFFIN CELLS LABILE HYPERTENSION PAROXYSMAL SYMPTOMS RARE 0.1% OF HYPERTENSIVE PATIENTS IMPORTANT TO DETECT BECAUSE HTN CURABLE UNTREATED – RISK OF LETHAL HTN 5-10% MALIGNANT CLUE TO PRESENCE OF FAMILIAL & AUTOSOMAL SYNDOME MEN-2A HYPERPARATHRODISM MEDULALLARY CA THYROID 2B MUCOSAL NEUROMAS, MEDULLARY CA THYROID

DIAGNOSIS CLINICAL SUSPICION BIOCHEMICAL CONFIRMATION ANATOMICAL LOCALIZATION CLINICAL PAROXYSMM SYMPTOMS HEADACHE, DIAPHORESIS , PALPITATIONS PPTED BY VARIETY OF STIMULI POSITIONAL CHANGES EMOTIONAL STRESS ABDOMINAL PRESSURE DIRECT PRESSURE ON TUMORS MEDICATIONS 2. LABILE OR PAROXYSMAL HTN 3. F/H METABOLIC FEATURES – SIGNS OF HYPERCATABOLISM  METABOLIC RATE PROFUSE SWEATING HYPERGLYCAEMIA (GLYCOSURIA) WEIGT LOSS (INSPITE OF GOOD APPT) ORTHOSTATIC HYPERTENSION + HYPERGLYCAEMIA + ERHROCYTOSIS

BIOCHEMICAL 24 HOUR URINE FOR CATHACHOLAMINE / VMA (PREFERABLE CATHACHRAMMES) > 90% VALUES – TWICE NORMAL AVOID HTNSIVES (CLONIDINE) AVOID FALSE +VE PLASMA CATECHOLAMINES LOCALIZATION 90% ADRENAL MEDULLAE 99% ABDOMEN REMAINDER – MEDIASTINUM LOCALIZED CT MRI (IODOBENZYLGUANADINE SCINTIGRAPHY) RULE OF 10% MULTIPLE BILATERAL MALIGNANT

TYROSINE DIHYDROXY PHENYLALANINE (DOPA) CATHACHOLAMINES 3 – METHOXY 4 HYDROXY MANDELIC ACID VMA HYDROXYLATED DECARBOXYLATED DEGRADED

TREATMENT SURGICAL – EXPERIENCED SURGEONS PRE OP CONTROL OF BP ( α – ADRENERGENIC) ANTAGONIST E.G. PHENOXY BENZAMINE, PRAZOSIN). PREVENT CATASTROPHIC RISE IN BP DURING SURGICAL HANDLING OF TUMOR SUCCESSFUL RESECTION. PROMPT RESOLUTION OF HYPERTENSION MOST GRATIFYING

HYPERALDOSTERISM PRIMARY SECONDARY BOTH RENIN & ALDOSTERONE ECF VOLUME (VOMITING / DIARREHA)  PERFUSION OF KIDNEYS (CIRRHOSIS, HF, RAS) OEDEMA (SPIRONALATONE) EXCESS OF ALDOSTERONE ECF EXPANSION HTN MARKED SUPPRESSON OF RENIN SECRETION 2/3 ADENOMA < 2CM BILATERAL HYPERPLASIA

CLINICAL HYPERTENSION HYPOKALAMIA  NA  ECF VASCULAR RESISTANCE MUSCULAR WEAKNESS CRAMPS POLYURIA

DIAGNOSIS HYPERTENSION SPONTANEOUS HYPOKALAMIA URINARY POTASSIUM > 30 MMOL 24 HR  RENAL POTASSIUM WASTING RENIN  ALDOSTERONE  SCREENING PLASMA POTASSIUM (NOT ON DIURETICS) PLASMA ALDOSTERONE / PLASMA ACTIVITY RATIO < 30 NOT IRY > 50 CERTAINLY IRY ALDOSERONE SUPPRESSIN 2 LITER 0.9% SALINE I/V OVER 4 HOURS WITH PATIENT SUPINE NORMAL PLASMA ALDOSTERONE < 4MG/DL.

DD INCIDENTAL ADRENAL NODULES IRY DIAGNOSED BY ENDOCRINE TESTING NOT RADIOLOGY ADRENAL VENOUS ALDOSTERONE MEASUREMENTS TREATMENT RESECTION

GLUCORTICOID EXCESS HYPERCORTISOLISM CUSHING SYNDROME ACTH DEPENDENT PITUITARY DEPENDENT CUSHING DISEASE) 65% ECTOPIC ACTH PRODUCING 10% ACTH ADMINISTRATION NON -ACTH DEPENDENT ADRENAL 25% ADENOMA HYPERPLASIA CARCINOMA CORTICOSTEROID ADMINISTRATION

CUSHING’S SYNDROME HYPERCOTISOLISM CUSHINGOID FACIES CENTRAL OBESITY PROXIMAL MUSCLE WEAKNESS ECCHYMOSES STRIAE HYPERTENSION GLUCOSE INTOLERANCE

DIAGNOSIS CIRCADIAN RHYTHM 24 HR URINARY COTRISOL ACTH LOW DOSE DEYAMETHASONE HIGH DOSE DEXAMETHASONE TEST

CASE 1 67 year old woman is referred to you by a psychiatrist to rule out an organic cause for “panic attacks” She is somewhat anxious appearing and complains of severe “pounding” headaches, two to three times a week episodes of “breaking out in sweats,” palpitations, and nausea. Her BP in clinic is 150/100. She says, “That must be a mistake, because at the psychiatrist’s office they checked me and I was much lower than that.” On exam, she is diaphoretic and her heart rate is tachycardic but regular.

CASE 2 19 MALE – ATTENDED OP UNCONTROLLED BP 180 / 120 INVESTIGATIONS DONE AT ABBOTABAD HB 13.6 G S.CREATININE 0.8 mEq ECG MAK-AKU 2008

INVESTIGATION DONE AT AKUH K+ 2.3 2.6 2.4 RENIN 0.9 n/ml.hr ALDOSTERONE 60 n/dl CT SCAN OPERATED

TAKE HOME MESSAGE EARLY, ABRUPT, RESISTANT, HYPERTENSION THINK ABOUT SECONDARY HYPERTENSION. PAROXYSMAL HYPERTENSION, SWEATING, PALPITATIONS, HEADACHE PHEOCHROMOCYTOMA MOST OF THE CAUSES ARE TREATABLE.

THANKYOU FOR YOUR ATTENTION MAK-AKU 2008

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