ENDOCRINE HYPERTENSION

1. ENDOCRINE
HYPERTENSION
Dr.K.Naveen Kumar MD.,

2. CAUSES
 Adrenal dependent
 Thyroid dependent
 Parathyroid dependent
 Pituitary dependent

3. ADRENAL DEPENDENT
A. Pheochromocytoma
B.Primary aldosteronism (low renin high
aldosterone)
C.Hyperdeoxycorticosteronism (low renin low
aldosterone)
1.Congenital adrenal hyperplasia
11β-Hydroxylase deficiency
17α-Hydroxylase deficiency
2.Deoxycorticosterone-producing tumor
3.Primary cortisol resistance
4.Cushing's syndrome
continued......

4. D.APPARENT MINERALOCORTICOID EXCESS
(AME)/11β-HYDROXYSTEROID
DEHYDROGENASE DEFICIENCY (low renin
low aldosterone)
Genetic --- Type 1 AME,Type 2 AME
Acquired ---- Licorice or carbenoxolone
ingestion (type 1 AME), Cushing's
syndrome (type 2 AME)

5. THYROID DEPENDENT
 Hypothyroidism
 Hyperthyroidism
PARATHYROID DEPENDENT
Hyperparathyroidism
PITUITARY DEPENDENT
 Acromegaly
 Cushing's syndrome

6.  Pheochromocytoma
 Catecholamine secreting tumours include
adrenal pheochromocytoma and extra
adrenal paragangliomas
 Symptoms are due to the pharmacologic
effects of excess concentrations of
circulating catecholamines
 Signs and symptoms can be spell related
or due to chronic catecholamine excess

7. Spell related:
 Anxiety
 Diaphoresis
 Dyspnoea
 Epigastric and chest pain
 Pallor
 Palpitations
 Tremors

8. Chronic symptoms:
 Cold hands and feet
 Congestive heart failure
 Epigastric and chest pain
 Fever
 Headache
 Hyperglycemia
 Orthostatic hypotension
 Painless hematuria
 Palpitations
 Tremors
 Weight loss

9. Genetic and syndromic forms of
pheochromocytoma:
 MEN I
 MEN 2A &2B
 VHL
 Neurofibromatosis I
 Familial paragangliomas type 1,2,3,4

10. Pheochromocytoma should be suspected in
patients:
 Hyperadrenergic spells (e.g., self-limited
episodes of nonexertional palpitations,
diaphoresis, headache, tremor, or pallor)
 Resistant hypertension
 A familial syndrome that predisposes to
catecholamine-secreting tumors (e.g., MEN-2,
NF1, VHL)
 A family history of pheochromocytoma
 An incidentally discovered adrenal mass
 Hypertension and diabetes
 Onset of hypertension at a young age (e.g.,
younger than 20 years)
 Idiopathic dilated cardiomyopathy

12.  Treatment
 The treatment of choice for
pheochromocytoma is complete surgical
resection
 Most catecholamine-secreting tumors are
benign and can be totally excised
 Preoperative pharmacologic preparation is
indicated for all patients with catecholamine-
secreting neoplasms
CONTINUED

13.  Combined α- and β-adrenergic blockade is
one approach to control blood pressure and
prevent intraoperative hypertensive crises
 α-Adrenergic blockade should be started 7 to
10 days preoperatively to normalize blood
pressure and expand the contracted blood
volume
 After adequate α-adrenergic blockade has
been achieved, β-adrenergic blockade is
initiated, which typically occurs 2 to 3 days
preoperatively.

14.  Acute hypertensive crises may occur
before or during an operation, and they
should be treated intravenously with
sodium nitroprusside, phentolamine, or
nicardipine
 Sodium nitroprusside is an ideal
vasodilator for intraoperative
management of hypertensive episodes
because of its rapid onset of action and
short duration of effect

15.  Primary Aldosteronism
 Aldosterone-producing adenoma (APA)
 Bilateral idiopathic hyperplasia
 Primary (unilateral) adrenal hyperplasia
 Aldosterone-producing adrenocortical
carcinoma
 Glucocorticoid-remediable aldosteronism
 Ectopic aldosterone-producing adenoma
or carcinoma

16. When to suspect
hyperaldosteronismInvestigate for primary hyperaldosteronism
PAC>15ng/dl,,PRA<1ng/ml and PAC/PRA>20
Test for plasma aldosterone concentration(PAC),and plasma renin
activity(PRA)
Hypertension and hypokalemia,resistant hypertension,adrenal incidentaloma
and hypertension,hypertension in young,severe hypertension

17.  PAC/PRA ratio is widely accepted as the
screening test of choice for primary
aldosteronism.
 A high PAC/PRA ratio is a positive
screening test result, a finding that
warrants further testing.

18.  The diagnostic tests are
 1.oral sodium loading test
 2.IV saline infusion test
 3.Fludrocortisone supresssion test

19.  After the primary aldosteronism is
confirmed imaging and adrenal venous
sampling are required to distinguish
various causes of the condition

21.  Treatment.........
 For aldosterone producing adenoma and
unilateral hyperplasia,surgical treatment
is needed
 For bilateral hyperplasia,and
glucocorticoid remediable
hyperaldosteronism..potassium sparing
diuretics like spironolactone and
aldosterone antagonists like eplerenone
are to be given

22.  Glucocorticoid remediable
aldosteronism:
 There is a chimeric gene duplication in the
promotor sequence of CYP11B1 that
encodes for 11 B hydroxylase enzyme..
 Thus resulting ,mineralocorticoid secretion
under control of ACTH rather than the
normal secretagogue , angiotensin II.
 So,the aldosterone secretion here is
suppressed by glucocorticoid therapy

23.  Congenital adrenal hyperplasia
 Most common defect in this is 21A
hydroxylase
 But the enzyme defects that will cause
hypertension are 11B hydroxylase and
17A hydroxylase

25.  Deoxycorticosterone producing
tumour:
 DOC producing tumours are large and
malignant. A high level of plasma DOC or
urine tetrahydro DOC and a large adrenal
tumour on CT suggest the diagnosis
 Optimal treatment is complete surgical
resection

27.  Primary cortisol resistance:
 Increased cortisol secretion and plasma
cortisol concentrations without evidence of
Cushing's syndrome are found in patients
with primary cortisol resistance.
 Caused by defects in glucocorticoid receptors
and the steroid-receptor complex
 The treatment for this mineralocorticoid-
dependent hypertension is blockade of the
mineralocorticoid receptor with a
mineralocorticoid receptor-antagonist

28.  Apparent mineralocorticoid excess
syndrome:
 As a result of impaired activity of the microsomal
enzyme 11β-hydroxysteroid dehydrogenase type
2 (11β-HSD2), which normally inactivates
cortisol in the kidney by converting it to
cortisone.
 Two types of AME..type I and type II
 The diagnosis is confirmed by demonstrating an
abnormal ratio of cortisol to cortisone in a 24-
hour urine collection
 Treatment includes blockade of the
mineralocorticoid receptor with a
mineralocorticoid receptor-antagonist or
suppression of endogenous cortisol secretion
with dexamethasone.

29.  Liddle syndrome:
 Also called pseudohyperaldosteronism
 Caused by mutations in the β or g
subunits of the amiloride-sensitive
epithelial sodium channel
 Results in enhanced activity of the
epithelial sodium channel increased
sodium reabsorption, potassium wasting,
hypertension, and hypokalemia.

30.  Spironolactone is ineffective in these
patients
 Liddle's syndrome can easily be
distinguished from apparent
mineralocorticoid excess based on the
basis of good clinical response to
amiloride and triamterene

31.  Hyperthyroidism
 When there are excessive amounts of
circulating thyroid hormones , both
metabolic activity and sensitivity to
circulating catecholamines increase
 Thyrotoxic patients usually have
tachycardia, high cardiac output,
increased stroke volume, decreased
peripheral vascular resistance, and
increased systolic blood pressure

32.  Hypothyroidism
 The diastolic blood pressure will be high in
hypothyroid patients and it accounts for
about 1% of the diastolic hypertension in
general population
 Mechanisms include increased systemic
vascular resistance and extracellular
volume expansion.
 Treatment is replaement of thyroid
hormone

33.  Primary hyperparathyroidism
 Hypercalcemia is associated with an increased
frequency of hypertension
 The most common cause of hypercalcemia is
primary hyperparathyroidism
 The mechanisms are unclear because there is no
direct correlation with the elevated parathyroid
hormone or calcium levels
 The hypertension associated with
hyperparathyroidism can also result as a
complication of hypercalcemia-induced renal
impairment

34.  Acromegaly
 Hypertension occurs in 20% to 40% of
the acromegaly patients and is associated
with sodium retention and extracellular
volume expansion
 Pituitary surgery is the treatment of
choice; if necessary, it is supplemented
with medical therapy or irradiation or both
 If a surgical cure is not possible, the
hypertension usually responds well to
diuretic therapy

35. THANK YOU