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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

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Conditions leading to secondary hypertension

•Renal artery stenosis

•Chronic renal disease

•Hyper aldosteronism

•Stress

•Sleep apnea

•Hyper or hypothyroidism

•Pheochromocytoma

•Pre eclampsia

•Aortic co-arctations

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Hyperthyroidism Lability, irritability, palpitations, muscle weakness, weight loss, diarrhea, heat intolerance, menstrual irregularity

Tremor, fine hair, onycholysis, lid lag, proptosis, tachycardia, atrial fibrillation, wide pulse pressure.

Elevated thyroid hormones, suppressed thyrotropin.

Cushing’s syndrome Weakness, weight gain, amenorrhea

Moon facies, acne, supraclavicular fat pad, purple stria on abdomen/thighs, edema

Increased plasma cortisol, increased urinary 17-keto and hydroxysteroids

Coarctation of the aorta

Usually no suggestive clues on history. Occassionally a history of epistaxis, intermittent claudication, dizziness, or headaches.

Diminished pulse/ blood pressure in vessels distal to coarctation (femoral, sometimes left brachial)

Electrocardiogram shows left ventricular hypertrophy, chest radiograph may show notching of lower rib borders, angiography is diagnostic

Hyperparathyroidism Muscle weakness, nausea, anorexia, constipation, weight loss, polyuria, polydipsia, deafness, parasthesias, bone pain. Suggested by triad of peptic ulcer, urinary calculi, and pancreatitis.

Band keratitis, hypotonia, weakness

Hypercalcemia, hypophosphatemia, hypercalciuria, elevated alkaline phosphatase

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.

Varies. Weakness, anorexia, weight changes, edema, palpable enlarged kidneys

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.

  ©2006 UpToDate® • www.uptodate.com Licensed to Babu Shersad

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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

3. Patients with refractory HTN

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A.Primary Hyper aldosteronism (Conn's Disease) 1.Solitary adrenal adenomas (80-90%) 2.Bilateral adrenal hyperplasia (10-20%)

a.Idiopathic hyper aldosteronism b.Accounts for 50% of cases at some referral centers

3.Adrenal Carcinoma (rare) 4.Unilateral Adrenal Hyperplasia (very rare)

B.Secondary Hyperaldosteronism 1.Hypertensive States

a.Primary reninism (rare renin producing tumor) b.Secondary reninism due to decreased renal perfusion

2.Edematous States a.Cirrhosisb.Nephrotic

Types and causes:

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A.Serum Electrolytes 1.Serum Potassium decreased (Hypokalemia) 2.Serum Sodium increased (Mild) 3.Metabolic Acidosis

B.Aldosterone to PRA ratio over 20-25 1.Definitely significant if ratio >100 2.Aldosterone high and plasma renin low

C.Saline suppression 1.IVF: 300-500 cc/hour for 4 hours 2.Normal response

a.Aldosterone usually under 0.28 b.Renin usually suppressed

Diagnostic findings:

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•Adrenal Adenoma

•Renal Artery Stenosis

•Reno vascular Hypertension

•Adrenal Carcinoma

•Conn’s syndrome

•Cushings syndrome

•Hypertension & Hypertension, Malignant

•Hypokalemia & metabolic Alkalosis

•Eclampsia

•Carcino Adrenal Surgery

•Bartter Syndrome

•C-11 hydroxylase deficiency & C-17 hydroxylase deficiency

•Encephalopathy, Hypertensive

•Pre eclampsia (Toxemia of Pregnancy)

Differential diagnosis

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Differential Diagnosis: Hypertension with hypokalemia

A.Cushing’s Disease

Low Aldosterone and Low Plasma Renin

A.Renal Artery Stenosis or other renal cause

High Aldosterone and High Plasma Renin

But what a physician should always rule out are:

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Points to remember

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These are a must (Rule of 9)

ECG

Urine analysis

Blood glucose (9 to 12 hr fasting)

Hematocrit

Serum potassium

Serum creatinine

Serum calcium

Lipid profile (LDL & HDL with triglycerides) (9 to 12 hr fasting)

Albumin creatinine ratio

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Appropriate BP measurement

With verification in the contra-lateral arm

Examination of optic fundi

BMI

Auscultation of carotid, abdominal and femoral bruits

Examination of heart, lungs and kidneys

Seek abnormal aortic pulse

Examination of edema and abnormal pulses in the lower extreme ties

Neurological examination

Proper physical evaluation is a must :

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All references from: Joint National Committee’s 7th Report, Mayo Clinic & American Heart Association

This is where the world is heading to

“Did you hear about the baby born in the high tech delivery room?”“It was cordless!”

“No matter how hi-tech we go but a proper detection and evaluation is a must for an exact clinical diagnosis”

It is high time for us physicians to find every possible way

to treat a patient for his/her root sickness.

Like I say, “things happen for a reason, believe….”

Thank you