Secondary hypertension
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SECONDARY HYPERTENSION. DEFINITION. Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes or mendelian (monogenic) forms are not present High BP – repeatedly measured BP exceeding 140/90 mmHg, i.e. a systolic BP above 140 and/or diastolic BP above 90.

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SECONDARY HYPERTENSION

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SECONDARY HYPERTENSION


DEFINITION

  • Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes or mendelian (monogenic) forms are not present

  • High BP – repeatedly measured BP exceeding 140/90 mmHg, i.e. a systolic BP above 140 and/or diastolic BP above 90


Aetiology of Hypertension

  • Primary – 90-95% of cases – also termed “essential” of “idiopathic”

  • Secondary – about 5% of cases

    • Renal or renovascular disease

    • Endocrine disease

      • Phaeochomocytoma

      • Cushings syndrome

      • Conn’s syndrome

      • Acromegaly and hypothyroidism

    • Coarctation of the aorta

    • Iatrogenic

      • Hormonal / oral contraceptive

      • NSAIDs


Aetiology of Hypertension

  • Primary – 90-95% of cases – also termed “essential” of “idiopathic”

  • Secondary – about 5% of cases

    • Renal parenchymal (2-5%)

      or renovascular disease

    • Endocrine disease

      • Phaeochomocytoma

      • Cushing syndrome

      • Conn syndrome

      • Acromegaly and hypothyroidism

    • Coarctation of the aorta

    • Iatrogenic

      • Hormonal / oral contraceptive

      • NSAIDs


Renal parenchymal disease

  • Acute and chronic glomerulonephritis

  • Polycystic kidney disease

  • Diabetic nephropathy

  • Pyelonephritis

  • Obstructive uropathy

  • Neoplasms

  • Renal trauma

  • Radiation nephritis


Renal parenchymal disease

CIN – chronic interstitial nephritis; APKD – adult-onset polycystic kidney disease; MCN - minimal change nephropathy; MGN – membranous glomerulonephritis; DN – diabetic nephropathy; MPGN – membranoproliferative glomerulonephritis; FSGN – focal segmental glomerulonephritis


Candidate pathophysiologic mechanisms related to hypertension in parenchymal renal disease


Hypertension in parenchymal renal disease: major target organ manifestations


Hypertension in parenchymal renal disease


Hypertension in parenchymal renal disease:CONCLUSIONS

  • Hypertension may result from renal disease that reduces functioning nephrons;

  • Evidence shows a clear relationship between high blood pressure and end-stage renal disease;

  • BP should be controlled to 130/85 mmHg (125/75 mmHg in patients with proteinuria in excess of 1g/24 h)


Aetiology of Hypertension

  • Primary – 90-95% of cases – also termed “essential” of “idiopathic”

  • Secondary – about 5% of cases

    • Renal parenchymal

      or renovascular disease (0.3-3%)

    • Endocrine disease

      • Phaeochomocytoma

      • Cushings syndrome

      • Conn’s syndrome

      • Acromegaly and hypothyroidism

    • Coarctation of the aorta

    • Iatrogenic

      • Hormonal / oral contraceptive

      • NSAIDs


RENAL ARTERY STENOSIS(RAS)

  • Atherosclerotic RAS (>90% of cases): involves the ostium and the proximal portion of the main renal artery with plaque extending into the perirenal aorta

  • Fibromuscular dysplasia (10% of cases): typically seen in young and middle-aged females. As opposed to atherosclerotic RAS, fibromuscular dysplasia typically affects the distal two thirds of the main renal artery


RENAL ARTERY STENOSIS:screening and diagnostic studies

  • Renal duplex sonography

  • Magnetic resonance angiography

  • Renal artery arteriography

  • Captopril renography


RENAL ARTERY STENOSIS:renal duplex sonography

Stenoses over 60%:

  • Peak systolic velocity (PSV) >150-180 cm/sec

  • Renal-aortic ratio >3.5

    Prognostic value:

  • Resistance index (RI):

    RI=(1-EDV)/PSVx100;

    if RI>80 no benefit after revascularization


RENAL ARTERY STENOSIS:MR angiography

Strong sides:

  • Provides images of the renal arteries, 3D-reconstruction, plaque characterization and hemodynamic information

  • Gadolinium (contrast agent): non-nephrotoxic

    Weak sides: high cost and limited availability


RENAL ARTERY EVALUATION:MR angiography (3D-reconstruction)


RENAL ARTERY EVALUATION:contrast angiography (the “gold” standard)

Fibromuscular dysplasia:

“string of beads” appearance

Atherosclerotic RAS with

poststenotic dilatation


What is your diagnosis ?


RENAL ARTERY STENOSIS:treatment

  • BP control

  • Antiplatelet, lipid-lowering therapy, and beta-blockers, if appropriate

  • No ACE-inhibitors in severe RAS !


RENAL ARTERY STENOSIS:treatment

Percutaneous or surgical revascularization, if:

● Resistant or poorly controlled hypertension and unilateral or bilateral renal artery stenosis

● Renal artery stenosis and recurrent flash pulmonary edema for which there is no readily explainable cause

● Chronic renal failure and bilateral renal artery stenosis or renal artery stenosis to asolitary functioning kidney

● Sonographic renal longitudinal length >7cm


Aetiology of Hypertension

  • Primary – 90-95% of cases – also termed “essential” of “idiopathic”

  • Secondary – about 5% of cases

    • Renal or renovascular disease

    • Endocrine disease

      • Phaeochomocytoma (0.1-0.6 %)

      • Cushings syndrome

      • Conn’s syndrome

      • Acromegaly and hypothyroidism

    • Coarctation of the aorta

    • Iatrogenic

      • Hormonal / oral contraceptive

      • NSAIDs


PHEOCHROMOCYTOMA“frequently searched for, but rarely found”

  • About 90 % of pheochromocytomas are located within the adrenal glands;

  • 10% are bilateral;

  • 10% are malignant;

  • 10% are extra-adrenal;

  • Extra-adrenal pheochromocytomas develop in paraganglion chromaffin tissue of the sympathetic nervous system; of them, 40% are not diagnosed, 5% are multiple;

  • overall, nearly 98% of pheochromocytomas are found in the abdomen


PHEOCHROMOCYTOMA“the great mimic”

Frequency of signs and symptoms (%) of pheochromocytoma


PHEOCHROMOCYTOMAdiagnostic techniques

  • Biochemical tests

  • High pressure liquid chromatography:

  • Plasma catecholamines: noradrenaline, adrenaline;

  • Free plasma fractionated metanephrines: normetanephrine, metanephrine;

  • Urinary catecholamines (24h)

  • Urinary fractionated metanephrines (24h)

  • Spectrophotometry:

  • Total metanephrines (24h urine);

  • Vanillylmandelic acid(24h urine)


PHEOCHROMOCYTOMA

Sensitivity and specifity of biochemical tests for diagnosis of pheochromocytoma


PHEOCHROMOCYTOMAimaging techniques

  • Duplex sonography;

  • Magnetic resonance imaging (MRI);

  • Computed romography (CT);

  • 123I – meta-iodo-benzyl-guanidine scanning (123I-MIBG)


PHEOCHROMOCYTOMA

Sonography :

  • Sonographic appearances are those of a well-defined homogeneous hypoechoic mass in approximately 50 pet cent of patients.

  • However the mass may be complex or even cystic (16 pet cent) and hyperechoic to the renal parenchyma (approximately 20 pet cent).


PHEOCHROMOCYTOMA

MRI (coronal and sagittal sections):

  • Magnetic resonance (MR) imaging is equally sensitive to CT and lends itself to in vivo tissue characterization, which is not possible with CT;

  • MR imaging is nearly 100% sensitive and around 70% specific.

  • Preferred for the localisation of extra-adrenal tumours or tumours during pregnancy, in children, or in patients with allergies to contrast


PHEOCHROMOCYTOMA

CT:

  • accurately detects tumors larger than 1.0 cm and has a localization precision of approximately 98%, although it is only 70% specific;

  • since CT scanning and MRI have similar sensitivities (90–100%) and specificities (70–80%), MRI is the preferred procedure


PHEOCHROMOCYTOMA

123I-MIBG scanning:

  • increased specificity (95–100%), as compared with CT or MRI;

  • provides both anatomic and functional characterization;

  • Relevant in patients with multiple, extra-adrenal, malignant (metastatic) tumors


PHEOCHROMOCYTOMA: laparoscopic removal

Preoperative Management (10-14 days)

  • Purpose:to prevent catecholamine induced, serious, and potentially life-threatening complications during surgery, including hypertensive crises, cardiac arrhythmias, pulmonary oedema, and cardiac ischemia;

  • BP should be reduced to below 160/90 mm Hg for at least 24h;

  • orthostatic hypotension should be present, but blood pressure in the upright position should not fall below 80/45 mm Hg;

  • there should be no more than one ventricular extrasystole every 5 min;

  • and the electrocardiogram should show no S-T segment changes and T-wave inversions for 1 week;


PHEOCHROMOCYTOMA:

Management

  • Phenoxybenzamine, a long acting alpha-adrenergic blocker, is the mainstay of medical treatment to control BP. A total dose of 1 mg/kg is sufficient in most patients.

  • An alpha-blocker Doxazosin in increasing doses from 1 to 16 mg once a day.

  • A beta-adrenoceptor blocker (eg,propranolol 40 mg three times daily or atenolol 25–50 mg once daily) could be included after several days of alpha-adrenergic blockade.

  • Adequate salt and fluid intake lowers the risk of orthostatic hypotension.


PHEOCHROMOCYTOMA:

Management

  • Should substantial rises in blood pressure still take place during surgery, these can be controlled by bolus or by continuous infusion of phentolamine, sodium nitroprusside, or a shortacting calcium antagonist (eg, nicardipine);

  • Tachyarrhythmias can be treated by infusion of a shortacting -adrenoceptor blocker (eg, esmolol).


PHEOCHROMOCYTOMA

Sensitivity and specifity of biochemical tests for diagnosis of pheochromocytoma


Conn’s Syndrome (primary hyperaldosteronism)

  • Should be considered in any hypertensive pt with muscle weakness, polydipsia, andor hypokalemia;

  • 75% - adrenal adenoma;

  • 25% - adrenal hyperplasia

  • Rarely – adrenocortical cancer


Primary Hyperaldosteronism

  • Screening for hyperaldosteronism should include plasma aldosterone and plasma renin activity

    measured in morning samples

  • Plasma aldosterone:renin ratio: normally <20;

    diagnostic cut-off value >30;

  • Aldosterone excretion rate during salt loading, captopril, or spironolactone test (the captopril test may be less useful in blacks because of the high prevalence of low plasma renin activity)

  • Adrenal CT, MRI


Primary Hyperaldosteronism

Should be differentiated from

  • Secondary hyperaldosteronism in patients with renal failure, CHF, essential hypertension

  • Monogenic forms of hypertension (pseudohyperaldosteronism):

  • Liddle’s syndrome (autosomal-dominant disorder, characterized by low-renin, low-aldosterone, low-potassium volume-expanded hypertension)

  • Gordon’s syndrome (autosomal-dominant disorder, characterized by low-renin, low-aldosterone, high-potassium volume-expanded hypertension)


Primary Hyperaldosteronism

TREATMENT

1. Medical

  • Spironolactone, a competitive aldosterone antagonist

  • Amiloride, a potassium-sparing diuretic

  • Glucocorticoids (in glucocorticoid-remediable form)

    2. Surgical, if appropriate


Aetiology of Hypertension

  • Primary – 90-95% of cases – also termed “essential” of “idiopathic”

  • Secondary – about 5% of cases

    • Renal or renovascular disease

    • Endocrine disease

      • Phaeochomocytoma

      • Cushing’s syndrome (0.1-0.6%)

        Conn’s syndrome

      • Acromegaly and hypothyroidism

    • Coarctation of the aorta

    • Iatrogenic

      • Hormonal / oral contraceptive

      • NSAIDs


Cushing’s Syndrome

  • Hypertension occurs in about 80% of patients;

  • Urinary free cortisol

  • If 24h UFC>100 µg/ml: measure plasma ACTH


Hypothyroidism

  • Both hypertension (particularly diastolic) and hypotension are common;

    Hyperthyroidism

  • Accompanied by systolic hypertension, especially in the elderly;

    Acromegaly

  • 25-50% exhibit elevated blood pressure


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