An unusual cause of Hypertension : Adrenal Glands Disorders

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Transcript An unusual cause of Hypertension : Adrenal Glands Disorders

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An unusual cause of Hypertension
Adrenal Glands Disorders
Case Presentation by: Dr. Babu Shersad MD, MACP
American Board Certified Internal Medicine & Nephrology
Venue : Dubai Sheraton Creek
Date: 12/12/06
Credit Hours : 180 minutes (3hrs.)
Approved by: Department of Health Dubai
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Anatomy of the talk
1.
2.
3.
4.
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6.
7.
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Case study
Hypertension and what is secondary Hypertension?
Causes and Evaluation- ABCDE molecule
Hyper aldosteronism
Differential diagnosis
Rule of 9
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 /l
Serum bicarbonate 28 mmol / l
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Diagnosis of Secondary Hypertension : “ABCDE” molecule
A - Accuracy, Apnea and Aldosteronism
B - Bruits & bad kidneys (Renal
parenchymal disease)
C - Catecholamine, Co arctations &
Cushing’s syndrome
D - 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)
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
Electrocardiogram shows left
ventricular hypertrophy, chest
radiograph may show notching of
lower rib borders, angiography is
diagnostic
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
Examination
Laboratory
Findings
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.
Dry skin, hair loss, weight gain,
constipation, cold intolerance,
cognitive slowing, menstrual
irregularity. May be asymptotic in
elderly.
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.
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
Hypothyroidism
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Adrenal Gland Disorder : Hyper aldosteronism
“over production of aldosterone independent of reninangiotensin regulator system”
Remember…..
“Increased urinary excretion of potassium
signals hyper-aldosteronism which should be
suspected in all hypertensive patients with
unprovoked hypokalemia”
It leads to …..
“fluid retention and increased blood
pressure, weakness, and, rarely, periods
of paralysis”
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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
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(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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Types and causes:
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.Cirrhosis
b.Nephrotic
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Diagnostic findings:
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
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Differential diagnosis
•Adrenal Adenoma
•Eclampsia
•Renal Artery Stenosis
•Carcino Adrenal Surgery
•Reno vascular
Hypertension
•Bartter Syndrome
•Adrenal Carcinoma
•C-11 hydroxylase deficiency &
C-17 hydroxylase deficiency
•Conn’s syndrome
•Encephalopathy, Hypertensive
•Cushings syndrome
•Hypertension &
Hypertension,
Malignant
•Pre eclampsia (Toxemia of
Pregnancy)
•Hypokalemia &
metabolic Alkalosis
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But what a physician should always rule out are:
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
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Points to remember
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These are a must (Rule of 9)

ECG
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Urine analysis

Blood glucose (9 to 12 hr fasting)
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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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Proper physical evaluation is a must :

Appropriate BP measurement
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With verification in the contra-lateral arm
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Examination of optic fundi
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BMI
Auscultation of carotid, abdominal and
femoral bruits
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Examination of heart, lungs and kidneys
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Seek abnormal aortic pulse
Examination of edema and abnormal
pulses in the lower extreme ties
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
Neurological examination
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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
All references from: Joint National Committee’s 7th Report, Mayo Clinic & American Heart
Association
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