First Medical Center health with us 1 An unusual cause of Hypertension Adrenal Glands Disorders Case Presentation by: Dr. Babu Dr. Babu Shersad MD, MACP Shersad MD, MACP American Board Certified Internal Medicine & American Board Certified Internal Medicine & Nephrology Nephrology Venue : Dubai Sheraton Creek Date: 12/12/06 Credit Hours : 180 minutes (3hrs.) Approved by: Department of Health Dubai First Medical Center
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First Medical Center health with us1 An unusual cause of Hypertension Adrenal Glands Disorders Dr. Babu Shersad MD, MACP Case Presentation by: Dr. Babu.
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First Medical Center health with us 1
An unusual cause of Hypertension Adrenal Glands Disorders
Case Presentation by: Dr. Babu Shersad Dr. Babu Shersad MD, MACPMD, MACP
American Board Certified Internal Medicine & American Board Certified Internal Medicine & NephrologyNephrology
Venue : Dubai Sheraton Creek
Date: 12/12/06
Credit Hours : 180 minutes (3hrs.)
Approved by: Department of Health Dubai
First Medical Center
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Anatomy of the talk
1. Case study
2. Hypertension and what is secondary Hypertension?
3. Causes and Evaluation- ABCDE molecule
4. Hyper aldosteronism
5. Differential diagnosis
6. Rule of 9
7. Points to remember
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Hypertension:
Pre Hypertension:• blood pressure 120/80 mmHg to 139/89 mmHg
• not a disease category
Hypertension:• blood pressure of 140/90 mmHg or above
• three readings 6 hours apart
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A quick review on Hypertension
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Secondary hypertension
“Hypertension secondary to underlying, identifiable & often reversible cause”
Why did I choose to talk on this topic?15 – 25 % of hypertensive cases constitute secondary HT
Client report:42 year old teacher with HT X 15 years.Referred for quadriparesis possibile plasma pheresis Admission work up:
Serum potassium 1.80 mmol /lSerum bicarbonate 28 mmol / l
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Diagnosis of Secondary Hypertension : “ABCDE” moleculeA - Accuracy, Apnea and AldosteronismB - Bruits & bad kidneys (Renal parenchymal disease)C - Catecholamine, Co arctations & Cushing’s syndromeD - Drugs & Diet E - Erythropoietin & Endocrine disorders
Hyperaldosteronism Often none. Weakness, paralysis, paresthesias
Weakness. Chvostek’s or Trousseau’s sign
Hypokalemia or low-normal potassium
Renal parenchymal disease.
Varies, from none to overt uremia. May have history of previous renal disease, diabetes, previous urinary tract infections, abdominal surgeries, prostate disease, or family history of polycystic kidney or other renal disease. Many drugs can cause or worsen renal disease.
Urinalysis may reveal blood, protein or leukocytes. Sediment examination may reveal casts, oval fat bodies, or dysmorphic cells; however, completely bland sediment does not exclude renal disease Proteinuria should be quantified with 24-hour urine. Electrolytes reveal elevated blood urea nitrogen or creatinine in many, although calculation of creatinine clearance may be needed in the elderly or in patients with low muscle mass to identify those with normal serum creatinine but reduced glomerular filtration rate. Renal ultrasound, renal biopsy, and urine electrolytes may assist.
Clinical features of the different causes of secondary hypertension Condition History Physical
ExaminationLaboratoryFindings
Pheochromocytoma Paroxysmal hypertension, dizziness, palpitations, headache, nausea, vomiting, “sense of doom,” worse with abdominal manipulations, postcoital, or with abdominal torsion, episodes of hyper- or hypotension related to anesthesia or surgery. Can have paroxysmal hypertension with beta blockade. Family or personal history suggestive of multiple endocrine neoplasia syndrome.
Flushing or pallor, tachycardia, bounding pulses. May be normotensive or hypertensive on presentation; usually hypertensive during paroxysms; abdominal palpation may incite paroxysm.
Elevated urine and plasma catecholamines.
Renal artery stenosis Usually hypertension is severe, resistant to drug treatment, and often presents relatively acutely in previously normotensive individuals. Age usually <35 or >55. May have history of renal insufficiency, particularly after administration of an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Often a history of vascular disease.
Abdominal bruit or bruits across other vascular beds suggestive of vascular disease.
Duplex ultrasound or angiogram of the renal vessels.Laboratory data may confirm presence of renal insufficiency, often with bland urine.
Hypothyroidism Dry skin, hair loss, weight gain, constipation, cold intolerance, cognitive slowing, menstrual irregularity. May be asymptotic in elderly.
Round full face, slow speech, hoarseness, muscle weakness, delayed relaxation on reflex testing, cold skin, coarse brittle hair, normal or faint cardiac impulse, cardiac enlargement, bradycardia, edema.
Low thyroid hormone levels, high thyrotropin
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Adrenal Gland Disorder : Hyper aldosteronism
“over production of aldosterone independent of renin-angiotensin regulator system”
“Increased urinary excretion of potassium signals hyper-aldosteronism which should be
suspected in all hypertensive patients with unprovoked hypokalemia”
“fluid retention and increased blood pressure, weakness, and, rarely, periods
of paralysis”
It leads to …..
Remember…..
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Signs & Symptoms:
•Weakness
•Tingling and muscle spasm
•Periods of temporary paralysis
•Thirsty
•Fontal headache
•polyuria & polydypsia
•Abdominal distension
•Ileus from hypokalemia
•Findings related to complications of HTN
•Chvostek’s or Trousseau’s sign
•“ Aldosterone escape” - due to spontaneous natruesis and diuresis
that occurs in these patients (no signs of edema)
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Some times the clinical presentation of Hyper
aldosteronism is not distinctive,the common clinical
scenarios are:
1. Patients with spontaneous or unprovoked hypokalemia, especially if the patient is also hypertensive
2. Patients who develop severe and/or persistent hypokalemia in the setting of low-to-moderate doses of potassium-wasting diuretics