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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