Back ground for the prsentation

MAY 31, 2008

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 1. RENAL PARENCHYMAL DISEASE E.G ACUTE NEPHRITIS,

CHR. GN ETC.2. RENOVASCULAR DISEASE E.G RAS, ATHEROSCLEROSIS

ETC3. CO-ARCTATION OF AORTA 4. 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 HYPERTENSIONFINDINGS 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 HYPERTENSIONRARE CAUSE OF HYPERTENSION

1 -2 % OF SECONDARY HTNIN MAJORITY

1. MINERALOCORTICOID EXCESS EG PRIMARY HYPERALDOSTERONISM

2. PHEOCROMOCYTOMA3. GLUCOCORTICOID EXCESS EG CUSHINGS

SYNDROME OTHER CONDITIONS1. ESTROGEN – INDUCED HYPERTENSION2. PREGNANCY - INDUCED HYPERTENSION3. HYPERPARATHYROIDISM4. HYPOTHROIDISM5. ACROMEGALY6. CONGENTIAL ADRENAL HYPERPLASIA7. LIDDLE SYDROME 8. RENIN SECRETING TUMORS

PHEOCROMOCYTOMASYMPATHOCHROMAFFIN (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 RARE0.1% OF HYPERTENSIVE PATIENTS

IMPORTANT TO DETECT BECAUSEHTN CURABLEUNTREATED – RISK OF LETHAL HTN5-10% MALIGNANTCLUE TO PRESENCE OF FAMILIAL & AUTOSOMAL

SYNDOME MEN-2A HYPERPARATHRODISM MEDULALLARY CA THYROID 2B MUCOSAL NEUROMAS, MEDULLARY CA THYROID

DIAGNOSIS 1. CLINICAL SUSPICION2. BIOCHEMICAL CONFIRMATION3. ANATOMICAL LOCALIZATION

CLINICAL 1. PAROXYSMM SYMPTOMS HEADACHE, DIAPHORESIS , PALPITATIONS

PPTED BY VARIETY OF STIMULIPOSITIONAL CHANGESEMOTIONAL STRESSABDOMINAL PRESSUREDIRECT PRESSURE ON TUMORSMEDICATIONS

2. LABILE OR PAROXYSMAL HTN3. F/H

METABOLIC FEATURES – SIGNS OF HYPERCATABOLISM METABOLIC RATEPROFUSE SWEATINGHYPERGLYCAEMIA (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 MEDULLAE99% ABDOMEN REMAINDER – MEDIASTINUMLOCALIZED CT

MRI (IODOBENZYLGUANADINE SCINTIGRAPHY)

RULE OF 10%MULTIPLEBILATERALMALIGNANT

TYROSINE

DIHYDROXY PHENYLALANINE

(DOPA)

CATHACHOLAMINES

3 – METHOXY 4 HYDROXY

MANDELIC ACID VMA

HYDROXYLATED

DECARBOXYLATED

DEGRADED

TREATMENT

SURGICAL – EXPERIENCED SURGEONSPRE 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 & ALDOSTERONEECF VOLUME

(VOMITING / DIARREHA)

PERFUSION OF KIDNEYS

(CIRRHOSIS, HF, RAS)

OEDEMA (SPIRONALATONE)

EXCESS OF ALDOSTERONE

ECF EXPANSIONHTN

MARKED SUPPRESSON OF

RENIN SECRETION

2/3 ADENOMA< 2CM

BILATERAL HYPERPLASIA

CLINICAL

HYPERTENSIONHYPOKALAMIA

NA ECF

VASCULAR RESISTANCEMUSCULAR WEAKNESS

CRAMPSPOLYURIA

DIAGNOSIS HYPERTENSIONSPONTANEOUS HYPOKALAMIA

URINARY POTASSIUM > 30 MMOL 24 HR RENAL POTASSIUM WASTING

RENIN ALDOSTERONE

SCREENINGPLASMA POTASSIUM (NOT ON DIURETICS)

PLASMA ALDOSTERONE / PLASMA ACTIVITY RATIO< 30 NOT IRY> 50 CERTAINLY IRY

ALDOSERONE SUPPRESSIN2 LITER 0.9% SALINE I/V OVER 4 HOURS WITH PATIENT

SUPINE NORMAL PLASMA ALDOSTERONE < 4MG/DL.

DDINCIDENTAL ADRENAL NODULES

IRY DIAGNOSED BY ENDOCRINE TESTING NOT RADIOLOGY

ADRENAL VENOUS ALDOSTERONE MEASUREMENTS

TREATMENTRESECTION

GLUCORTICOID EXCESS

HYPERCORTISOLISMCUSHING SYNDROMEACTH DEPENDENT

PITUITARY DEPENDENTCUSHING DISEASE) 65%

ECTOPIC ACTH PRODUCING 10%

ACTH ADMINISTRATION

NON -ACTH DEPENDENT

ADRENAL 25%

ADENOMA HYPERPLASIA

CARCINOMA

CORTICOSTEROID ADMINISTRATION

CUSHING’S SYNDROMECUSHING’S SYNDROME

HYPERCOTISOLISMHYPERCOTISOLISMCUSHINGOID FACIESCUSHINGOID FACIESCENTRAL OBESITYCENTRAL OBESITYPROXIMAL MUSCLE WEAKNESSPROXIMAL MUSCLE WEAKNESSECCHYMOSESECCHYMOSESSTRIAESTRIAEHYPERTENSIONHYPERTENSIONGLUCOSE INTOLERANCE GLUCOSE INTOLERANCE

DIAGNOSIS

1. CIRCADIAN RHYTHM2. 24 HR URINARY COTRISOL3. ACTH4. LOW DOSE DEYAMETHASONE5. HIGH DOSE DEXAMETHASONE TEST

IMAGING

SURGICAL

ENDOCRINE HYPERTENSIONRARE CAUSE OF HYPERTENSION

1 -2 % OF SECONDARY HTNIN MAJORITY

1. MINERALOCORTICOID EXCESS EG PRIMARY HYPERALDOSTERONISM

2. PHEOCROMOCYTOMA3. GLUCOCORTICOID EXCESS EG CUSHINGS

SYNDROME OTHER CONDITIONS1. ESTROGEN – INDUCED HYPERTENSION2. PREGNANCY - INDUCED HYPERTENSION3. HYPERPARATHYROIDISM4. HYPOTHROIDISM5. ACROMEGALY6. CONGENTIAL ADRENAL HYPERPLASIA7. LIDDLE SYDROME 8. RENIN SECRETING TUMORS

CASE 167 year old woman is referred to you by a 67 year old woman is referred to you by a

psychiatrist to rule out an organic cause for psychiatrist to rule out an organic cause for “panic attacks”“panic attacks”

She is somewhat anxious appearing and She is somewhat anxious appearing and complains of severe “pounding” headaches, two complains of severe “pounding” headaches, two to three times a week episodes of “breaking out to three times a week episodes of “breaking out in sweats,” palpitations, and nausea.in sweats,” palpitations, and nausea.

Her BP in clinic is 150/100. She says, “That Her BP in clinic is 150/100. She says, “That must be a mistake, because at the psychiatrist’s must be a mistake, because at the psychiatrist’s office they checked me and I was much lower office they checked me and I was much lower than that.” On exam, she is diaphoretic and her than that.” On exam, she is diaphoretic and her heart rate is tachycardic but regular. heart rate is tachycardic but regular.

CASE 2

19 MALE – ATTENDED OPUNCONTROLLED BP 180 / 120INVESTIGATIONS DONE AT

ABBOTABADHB 13.6 GS.CREATININE 0.8 mEqECG

25MAK-AKU 2008

26MAK-AKU 2008

INVESTIGATION DONE AT AKUH

K+ 2.32.62.4

RENIN 0.9 n/ml.hr ALDOSTERONE 60 n/dl

CT SCAN

OPERATED

THIS PATIENT HAS A BP 155/110

TAKE HOME MESSAGE

EARLY, ABRUPT, RESISTANT, HYPERTENSION THINK ABOUT SECONDARY HYPERTENSION.

PAROXYSMAL HYPERTENSION, SWEATING, PALPITATIONS, HEADACHE PHEOCHROMOCYTOMA

MOST OF THE CAUSES ARE TREATABLE.

THANKYOU THANKYOU FOR YOUR ATTENTION FOR YOUR ATTENTION

31MAK-AKU 2008