secondary hypertension - medkorat.in.th · malignant ht •marked ht with retinal hemorrhages,...
TRANSCRIPT
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SECONDARY
HYPERTENSION
Grand round for Medical student
25 October 2013
By
Rungnapa Laortanakul, MD.
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OUTLINE
Primary aldosteronism
Pheochromocytoma
Cushing’s syndrome
Overview of HT
Secondary HT
Resistance HT
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HYPERTENSION
Definitions by JNC 7
BP based upon the average of two or more ...
•Pre HT : SBP 120 - 139 mmHg or DBP 80 - 89 mmHg
•HT stage 1 : SBP 140 - 159 mmHg or DBP 90 - 99 mmHg
•HT stage 2 : SBP ≥160 mmHg or DBP ≥100 mmHg
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MALIGNANT HT
• Marked HT with retinal hemorrhages, exudates, or
papilledema
• May also renal involvement "nephrosclerosis"
• Kidney injury, hematuria, and proteinuria
• Neurologic symptoms : ICH, SAH, or hypertensive
encephalopathy
• Usually associated with DBP > 120 mmHg
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HYPERTENSIVE
ENCEPHALOPATHY
•Presence of signs of cerebral edema
•Caused by breakthrough hyperperfusion from severe
and sudden rises in BP
• Insidious onset of headache, nausea, vomiting,
followed by nonlocalizing symptoms such as
restlessness, confusion, seizure, and coma.
"Reversible posterior leukoencephalopathy
syndrome"
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"REVERSIBLE POSTERIOR LEUKOENCEPHALOPATHY
SYNDROME"
CT - hypodensity in the posterior white matter
MRI (T2) - edema of the white matter of the parieto-occipital regions
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HYPERTENSIVE URGENCY
• Severe HT : DBP > 120 mmHg with asymptom
• No acute end-organ damage
• Little short-term risk
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PRIMARY (ESSENTIAL) HT
Atheroclerosis
• DM
• HT
• DLP
• Obesity
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SECONDARY HTGeneral clinical clues
• Severe or resistant hypertension
• An acute rise in BP developing in a patient with
previously stable values
• Age <30 years in non-obese, negative family history of
and no other risk factors (eg, obesity) for HT
• Malignant or accelerated hypertension
• Proven age of onset before puberty
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RESISTANT HT
• BP that remains above goal in spite of concurrent use of
3 antihypertensive agents of different classes
• One of three agents should be diuretic, and all agents
should be prescribed at optimal doses (50% or more of
maximum dose)
• Goal BP < 140/90 mmHg
The 2008 American Heart Association scientific statement
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Clinical features
suspected
Secondary HT
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Disorder Clinical feature
General
• Severe or resistant HT
• Acute rise BP with previously stable value
• Age < 30 years in non-obese with negative
family history and no other risk factor for HT
Renovascular
disease
• Acute elevation in S. Cr ≥ 30% after add ACE-I or ARB
• Mod to severe HT in Pt with diffuse atherosclerosis,
unilateral small kidney, or asymmetry in renal size of >
1.5 cm that cannot explained by another reason
• Mod to severe HT in Pt with recurrent episodes of flash
pulmonary edema
• Onset of stage 2 HT after age 55 years
• Abdominal bruit
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Disorder Clinical feature
Primary renal
disease• Elevated S. Cr
• Abnormal UA
Oral contraceptives • New elevation in BP temporally related to use
Sleep apnea
syndrome
• Obese who snore loudly while asleep
• Daytime somnolence, fatigue, and
morning confusion
Coarctation of the
aorta
• HT in the arms with diminished or delayed
femoral pulses and low or unobtainable BP in
the legs
• Left brachial pulse is diminished and equal to the
femoral pulse if origin of the left subclavian
artery is distal to the coarct
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Disorder Clinical feature
Primary aldosteronism• Unexplained hypokalemia with renal K loss
• More than one-half of Pts are normokalemia
Cushing's syndrome• Cushingoid facies, central obesity, proximal
muscle weakness, and ecchymoses
Pheochromocytoma • Paroxysmal elevations in BP
• Triad of headache
(pounding, palpitation, and sweating)
Hypothyroidism • Symptoms of hypothyroidism
Primary
hyperparathyroidism• Elevated serum calcium
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Endocrine
disease
Cardiovascular
disease
Other
Reno-vascular
disease
Secondary
hypertension
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Hypertension
with
hypo K
Reni
n
Aldosteron
e
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HYPERTENSION WITH HYPO K
• Hypo K with renal K loss
• 24-hours urine potassium
• Spot urine potassium concentration
• Urine potassium to creatinine ration
• Transtubular potassium gradient (TTKG)
Non renin-
aldosterone
Primary
hyperaldosteronism
Secondary
hyperaldosteronism
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NON RENIN-ALDOSTERONE
• Cushing's syndrome
• Licorice ingestion
• Certain forms of congenital adrenal hyperplasia (CAH)
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SECONDARY
HYPERALDOSTERONISM
• Renovascular disease
• Renin-secreting tumors
• Malignant HT
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PRIMARY
ALDOSTERONISM
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PRIMARY ALDOSTERONISM
• Disorder in which
aldosterone production
is inappropriately high
• Relatively autonomous
from the renin-
angiotensin system
• Nonsuppressible by
sodium loading
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PRIMARY ALDOSTERONISM
Most common subtypes
• Aldosterone-producing adenomas
• Bilateral idiopathic hyperaldosteronism
(bilateral adrenal hyperplasia)
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PRIMARY ALDOSTERONISM
Clinical features
•HT with hypoK
•Resistant HT
Laboratory
•Hypo K, metabolic alkalosis, mild hyper Na
• Muscle weakness
• Cardiovascular risk
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CASE DETECTION
• HT (by JNC 7) stage 2 (160–179/100–109 mmHg),
stage 3 ( >180/110 mm Hg)
• Drug-resistant HT
• HT spontaneous or diuretic-induced hypokalemia
• HT with adrenal incidentaloma
• HT and a family history of early-onset HT or CVA at
a young age < 40 yr
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Step of endocrine tests
• Signs and symptoms
• Labolatory tests
• Screening
• Confirmation
• Localized lesion : Imaging
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Screening test
• Plasma aldosterone concentration (PAC)
• Plasma renin activity (PRA)
• Plasma aldosterone to renin ratio (ARR)
= PAC / PRA
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MEASUREMENT OF THE ARR
• Correct hypo K
• Withdraw agents that markedly affect to ARR
• If necessary to HT control --> verapamil slow-release,
hydralazine, prazocin, doxazosin
• Collect blood mid-morning, after Pt has been up
(sitting, standing, or walking) for at least 2 hr.
• Maintain sample at room temperature
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ARR CUTOFF VALUES
• Recommend : plasma aldosterone to renin ratio (ARR)
to detect cases of primary aldosteronism
PAC >15 ng/dl, ARR > 30
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Confirmation tests
• Oral sodium loading
• Saline infusion or Saline loading test
• Fludrocortisone suppression
• Captopril challenge
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Saline loading test
• Infusion of 2 liters of 0.9% saline iv over 4 h
Post-infusion
• PAC < 5 ng/dl … PA unlikely
• PAC >10 ng/dl … Very probable sign of PA
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Step of endocrine tests
• Signs and symptoms
• Labolatory tests
• Screening
• Confirmation
• Localized lesion : Imaging
HT with hypo K
PAC, PRA
Saline loading test
CT adrenal glands
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CUSHING'S SYNDROME
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Normal
ACTH
NEJM 1995 Vol.332 NO 12
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CUSHING'S SYNDROME
ACTH-dependent
• Cushing's disease
• Ectopic ACTH syndrome
• Ectopic CRH syndrome
ACTH-independent
•Adrenal adenoma
•Adrenal carcinoma
•Micronodular hyperplasia
•Macronodular hyperplasia
Overproduction of deoxycorticosterone,
corticosterone, and cortisol
Pituitary
Adrenal
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ACTHACTHACTH
NEJM 1995 Vol.332 NO 12
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NEJM 1995 Vol.332 NO 12
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Features that best discriminate Cushing’s
syndrome; most do not have a high sensitivity
• Easy bruising
• Facial plethora
• Proximal myopathy (or proximal muscle weakness)
• Striae (especially if reddish purple and > 1 cm wide)
• In children, weight gain with decreasing growth velocity
J Clin Endocrinol Metab. May 2008, 93(5):1526–1540
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-11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) is a key enzyme in
cortisol metabolism
-11 beta-HSD type 1 : oxidize reaction, inactivate cortisol to cortisone
-11 beta-HSD type 2 : reverse (reductase) reaction, conversion of cortisone
to cortisol
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Step of endocrine tests
• Signs and symptoms
• Labolatory tests
• Screening
• Confirmation
• Localized lesion : Imaging
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Initial testing for Cushing’s syndrome
One of the following tests :
1. Urine free cortisol (UFC; at least two measurements)
2. Late-night salivary cortisol (two measurements)
3. 1-mg overnight dexamethasone suppression test (DST)
4. Longer low-dose DST (2 mg/d for 48 h)
J Clin Endocrinol Metab. May 2008, 93(5):1526–1540
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Normal
ACTH ACTH
NEJM 1995 Vol.332 NO 12
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Subsequent evaluation
for Cushing’s syndrome
• For the subsequent evaluation of abnormal initial
test results, recommend performing another
recommended test
• Suggest the additional use of the dexamethasone-
CRH test or the midnight serum cortisol test in
specific situations
J Clin Endocrinol Metab. May 2008, 93(5):1526–1540
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J Clin Endocrinol Metab. May 2008, 93(5):1526–1540
Cushing’s syndrome suspected
Exclude exogenous
glucocorticoid exposure
1. Urine free cortisol
2. Late-night salivary
cortisol
3. 1-mg overnight DST
4. Low-dose DST
(2 mg/d for 48 h)
1. Urine free cortisol
2. Late-night salivary cortisol
3. 1-mg overnight DST
4. Low-dose DST
(2 mg/d for 48 h)
5. dexamethasone-CRH test
6. midnight serum cortisol
Initial testing Subsequent testing
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1 mg dexamethasone
suppression test• 1 mg dexamethasone is usually given between 2300, and
cortisol is measured between 0800 the following morning
• Normal person : Post-dexamethasone serum cortisol <1.8 µg/dl
• Sensitivity rates >95% , Specificity rates 80%
Day 1 Dexamethasone (0.5)
2 tab oral at 23.00
Day 2 Morning cortisol 8.00
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Low dose dexamethasone
suppression test (LDDST)
• Dexamethasone (0.5 mg) 1 tab oral q 6 h (8 dose)
• Serum cortisol within 6 h after the last dose of dexamethasone
• Normal person : Post-dexamethasone serum cortisol <1.8 µg/dl
Day 1 12.00 18.00 24.00 Day2
06.00
Day 2 12.00 18.00 24.00 Day3
06.00
Morning cortisol 8.00
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ACTH level
• ACTH level < 5 pg/ml …
ACTH-independent CS >>> CT adrenal glands
• ACTH level > 20 pg/ml …
ACTH dependent CS >>> Pituitary or Ectopic ACTH
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Step of endocrine tests
• Signs and symptoms
• Labolatory tests
• Screening
• Confirmation
• Localized lesion : Imaging
HT with Cushingoid
appearance
1mg DST or UFC
LDDST or UFC
ACTH level
before CT adrenal
or MRI pituitary
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PHEOCHROMOCYTOMA
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PHEOCHROMOCYTOMA
“Pheochromocytoma"
• Catecholamine-secreting tumors
• Arise from chromaffin cells of the
adrenal medulla and the
sympathetic ganglia
“Catecholamine-secreting
paragangliomas"
• Extra-adrenal pheochromocytomas
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CLINICAL PRESENTATION
• Symptoms
o Classic triad : Paroxysm
Episodic headache, sweating, and tachycardia
• Discovery of an incidental adrenal mass
• Familial pheochromocytoma
VHL syndrome, MEN2, Neurofibromatosis type1, Familial paraganglioma
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Neurofibromatosis type1
• A syndrome caused by neurogenic tumors arising from neural sheath cells
located along peripheral and cranial nerves.
• Autosomal dominant
• Lisch nodules of the iris, schwannomas, café au lait macules, axillary
freckling, optic-nerve gliomas, astrocytomas, multiple neurofibromas, and
plexiform neurofibromas. N Engl J Med 2011; 365:2020
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Step of endocrine tests
• Signs and symptoms
• Labolatory tests
• Screening
• Confirmation
• Localized lesion : Imaging
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DIAGNOSTIC TESTS
• Urinary and plasma fractionated
metanephrines and catecholamines
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West J Med. 1992 April; 156(4): 399–407
Catecholamine biosynthesis
and metabolic degradation
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Catecholamine metabolites
• Vanillymandelic acid (VMA) has been shown to have
poor diagnostic sensitivity
• Fractionated catecholamine metabolites-metanephrine
and normetanephrine in the plasma or urine- are the
preferred screening tests for pheochromocytoma
Endocrinol Metab Clin North Am. 2011 Jun;40(2):279-94
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Radiologic tests
• CT and MRI adrenal glands
• About 10 percent of the tumors are extraadrenal
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Step of endocrine tests
• Signs and symptoms
• Labolatory tests
• Screening
• Confirmation
• Localized lesion : Imaging
HT with Paroxysm
Urinary fractionated
metanephrines x 2 days
CT or MRI adrenal
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Summary• Secondary HT should be suspected : Severe or resistant HT, Acute rise
BP with previously stable value, Age < 30 years in non-obese with
negative family history and no other risk factor for HT
• Approach : Cardiovascular, Renovascular, Renal parenchyma, Endocrine
disease, other
• Endocrine disease : Primary aldosteronism, Cushing’s syndrome, and
Pheochromocytoma
• Step of endocrine tests : signs&symptoms, screening test, confirmation
test, and imaging