SECONDARY HYPERTENSION

RIDO WANDRIVEL
DEFINISI DAN EPIDEMIOLOGI

hypertension due to an identifiable cause, which may be treatable with an intervention specific to the
cause

small fraction (5% to 15%) of hypertensive cases

prevalence varies by age, more common in younger persons

• with a prevalence close to 30% in those 18 to 40 years of age with hypertension

Extensive testing for secondary hypertension is not warranted in all patients with hypertension because
of cost, low yield, and the potential for false-positive results
KARAKTERISTIK PASIEN
COMMON CAUSE
COMMON CAUSE
RARE GENETIC CAUSE
ETIOLOGI BERDASARKAN USIA
EVALUATION OF
SUSPECTED SECONDARY
HYPERTENSION
EVALUATION OF
SUSPECTED SECONDARY
HYPERTENSION
HIPERTENSI RENOVASKULER

reversible cause
Etiologi
contribute to only 1% of mild hypertension cases
• Atherosclerotic renal artery stenosis (85%
• accounts for 10% - 45% of severe or malignant hypertension of patients)
cases in white patients • fibromuscular dysplasia (FMD)
• renal trauma
renal artery stenosis (RAS) • renal artery occlusion
• dissection, embolism, and/or
In young adults, especially women, can be caused thrombosis
by fibromuscular dysplasia
PATOFISIOLOGI

renal artery stenosis

unilateral and bilateral renal hypoperfusion

Activation of the renin–angiotensin–aldosterone system

increases in angiotensin II levels and secondary hyperaldosteronism

sodium and water retention and vasoconstriction

increase in blood pressure

DIAGNOSIS

 Diagnostic standard is angiography

 invasive and should not be used as an initial diagnostic
test
 Doppler ultrasonography
 Inexpensive, 75% sensitivity & 90% specificity

 magnetic resonance angiography (MRA) with

gadolinium contrast media and computed
tomography (CT) angiography
 equally accurate in visualizing stenosis and give better
sensitivity, specificity, and anatomic detail than Doppler
ultrasonography
PENATALAKSANAAN

medical therapy is equal to revascularization

• similar rates of blood pressure control and cardiovascular deaths, and without the associated
complications of surgery
Medical therapy
• angiotensin-converting enzyme inhibitors or angiotensin receptor blockers

In RAS secondary to fibromuscular dysplasia

• MRA or CT angiography.
• the cure rates for angioplasty and surgery are 36% and 54%
HIPERALDOSTERON PRIMER

 excess production of aldosterone independent of the renin-angiotensin system

 caused by
 Primer
 adrenal adenoma
 unilateral or bilateral adrenal hyperplasia
 adrenocortical carcinoma

 secondary to excessive growth hormone

 acromegaly

 The prevalence : 6% in patients with hypertension

DIAGNOSIS

 patients who are resistant to combined

antihypertensive medical treatment
 Hipokalemia
 urinary potassium test

 measurement of the ratio of the plasma aldosterone

concentration to plasma renin activity after potassium
repletion
ALUR DIAGNOSIS

Penatalaksanaan
 autonomous aldosterone secretion are aldosterone-
producing adenomas
 unilateral adrenalectomy

 idiopathic hyperaldosteronism due to bilateral

adrenal hyperplasia
 chronic mineralocorticoid antagonist therapy (i.e.
spironolactone, eplerenone)
OBSTRUCTIVE SLEEP APNEA

 leading treatable cause of secondary hypertension

 common in men 40 to 59 years of age who are obese and who snore, leading to apneic episodes
 Other symptoms
 headache, fatigue, daytime somnolence, confusion, difficulty concentrating, depression, personality changes, hypertension,
and cardiac arrhythmias
 Patients who are obese and who have signs or symptoms of OSA and hypertension should be assessed with
polysomnography
 standard diagnostic test, clinical assessment tools
PATOFISIOLOGI

obstructive sleep-disordered breathing

sympathetic activation
Efferent renal sympathetic nerve stimulation

endothelial dysfunction
increases in renin release from juxtaglomerular cells

increased endothelin release

renal sodium and water reabsorption
reduced nitric oxide production sodium and water retention vasoconstriction

systemic inflammation renal vascular resistance

increase blood pressure

PENATALAKSANAAN

 Patients with OSA retain sodium and do not respond to hypertensive medication
 Aldosterone antagonists

 Treatment of OSA may improve blood pressure control, sleep quality, day time sleepiness ,and mortality
 positive airway pressure
 mandibular devices
PHEOCHROMOCYTOMA

 paroxysmal elevations in blood pressure

 Other symptoms
 classic triad : headache, palpitations, and sweating

 Work up
 metanephrines in a 24-hour urine sample or by measuring plasma free metanephrines
 followed by CT if results are abnormal.
CUSHING SYNDROME

 classical features
 moon facies, central obesity, proximal muscle weakness, and ecchymosis

 Most cases are iatrogenic from prescribed corticosteroids

 Only 20% have hypertension
 tumors causing Cushing syndrome are rare, 80% or more of these patients develop hypertension

 First-line work up
 two of the following
 24-hour urinary free cortisol, low-dose dexamethasone suppression, or late-night salivary cortisol tests

 If any test result is abnormal or if there is a high suspicion of Cushing syndrome despite normal results, referral to an
endocrinologist is needed.
COARCTATION OF THE AORTA

 common cause of secondary hypertension in children, especially males, but may not be detected until adulthood
because it is often asymptomatic
 Classic signs of coarctation of the aorta
 upper extremity hypertension, delayed or decreased femoral pulses (brachial-femoral delay) and low or unobtainable blood
pressure in the lower extremities, and murmur
 chest radiography
 classic figure three sign or rib notching

 Pemeriksaan penunjung
 Transthoracic echocardiography in children
 MRA in adults

 Surgery is recommended for those with a transcoarctation pressure gradient of more than 30 mm Hg.
CHEMOTHERAPEUTIC AGENTS

 cause microvascular injury and those that inhibit

vascular endothelial growth factor.
TERIMA KASIH
INDIKASI EVALUASI
PASIEN DENGAN
HIPERTENSI
SEKUNDER