Secondary HTN 5-10% of all HTN - PowerPoint Presentation

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Secondary HTN

5-10% of all HTN

More common in subgroup of resistant HTN

May be progressive, intermittent or curable

Staging is similar to essential HTN

CLASSIFICATION

1- Renal disorders:

Renal parenchymal ( acute or chronic GN,

tubulointerstitial

diseases, AKI, CKD, ADPKD

, obstructive nephropathy )

Renovascular

diseases

Renin

producing tumors

Genetic diseases affecting tubular transport

(

Liddle’s

syndrome)

Endocrine disorders

A: Excess

mineralocorticoid

Primary

hyperaldosteronism

Apparent

mineralocorticoid

excess

Congenital adrenal hyperplasia

Liqurice

ingestion

Exogenous

mineralocorticoid

Ectopic ACTH secretion

Pseudohyperaldosteronism

Endocrine disorders

B- Other endocrine disorders

Pheochromocytoma

Cushing syndrome

Hypothyroidism

Hyperthyroidism

Acromegaly

Carcinoid

tumors

Drugs

Esterogen

containing contraceptives

Sympatomimetics

Glucocorticoids

NSAIDs

Ciclosporine

MAO inhibitors

Amphetamines

Cocain

Na-bicarbonate

Pregnancy

Pre-

eclampsia

(

eclampsia

)

Gestational HTN

Super-imposed HTN

Miscellaneous

Coarectation

of Aorta

Obstructive sleep apnea

↑ICP or spinal injury

Volume overload

Anemia

Fever

Thyrotoxicosis

Aortic regurgitation

A-V fistula

Acute intermittent

porphyria

Alcohol withdrawal

Primary hyperaldosteronism

Autonomous

Ald

secretion with suppressed

renin

level

Renal Na⁺ retention with↑ urinary K⁺ and H⁺ loss

↑total Na⁺ content

 HTN

Account for 0.1% of HTN papulation

The most common endocrine HTN

Often asymptomatic

↓K⁺, metabolic

alkalosis,mild

Na⁺↑ (in essential HTN treated with diuretic Na is low-normal )

Primary hyperaldosteronism

Ethiology

:

Conn’s syndrome(adrenal adenoma ) 70%

Bilateral adrenal hyperplasia ~ 30%

Glucocorticoid

remediable

aldosteronism

Aldosterone

producing carcinoma

Primary hyperaldosteronism

Diagnosis:

K⁺ is screening test

Only 50-80% have

hypokalemia

Renal K⁺ wasting (urine K> 30

meq

/day)

Ald

/renin ratio is highOral salt loading or

salin

load test

Fludrocortsone

suppression test (4 days )

Adrenal CT or MRI

 > 1.5 cm

Adrenal vein sampling is occasionally necessary

Primary

hyperaldosteronism

Treatment:

Spironolacton

50-100mg initially

Eplerenon

is an alternative

Add

amiloride

5-20 mg if hypokalemia persistsSurgery for adenoma > 30

 adenoma

Ald

/PRA 15-30

 hyperplasia

<15 Rules out the diagnosis

Glucocorticoid

remediable

aldosteronism

Very rare

autosomal

dominant

11

β

hydroxylase ectopic production

Present with HTN at a young age with positive family historyCongenital adrenal hyperplasia: is a very rare autosomal recessive

Secondary

hyperaldosteronism

Caused by ↑

renin

level

Often due to renal

hypoperfusion

:

Renal artery

stenosisRenal infarction (atheroemboli )

Cirrhosis

Nephrotic

syndrome

Page kidney

Renin

secreting tumor ( very rare )

Renavascular

HTN

Renal infarct

Acute GN

Diuretic use

Coarectation

of aorta

Renin

producing tumor

PRA↑ & PAC↑

Primary

aldosteronism

Bilateral adrenal hyperplasia

Aldosterone producing carcinoma

PRA

↓

& PAC↑

PRA↓ & PAC↓

Liddle’s

syndrome

Liqurice

ingestion

Exogenous

mineralocorticoid

Cushing syndrome

Cushing syndrome

HTN in 80% of cases

Diagnosis by overnight

dexamethasone

supression

test :

Plasma

cortisol

level> 5μg/dl at 8 AM

Pheochromocytoma

Very rare < 0.1% of HTN

papulation

Adenoma of adrenal medulla

Can arise in extra-adrenal

chromafin

cells

Postural hypotension may be present

MIBG scan may localize the Tumor

A successful pregnancy rules it outWeight loss is very common

Pheochromocytoma

10% is malignant

10% extra adrenal

10% bilateral

10% extra abdominal

10% with MEN

10% is

macroadenoma

50%

only episodic HTN

Pheochromocytoma

Plasma

methanephrin

is 99% sensitive & 89% specific

Plasma

cathecolamine

is 85% sensitive & 80% specific

Urinary VMA is 63%sensitive & 94% specific

Coarectation of Aorta

In children and young adults

Women> men

Never be malignant