2. SECONDARY HYPERTENSION
DEFINITION:
-the elevation of blood pressure due to a specific
underlying disorder
CAUSES (Include but not limited to):
-Renal Parenchymal Diseases
-Primary Aldosteronism
-Cushing’s Syndrome
-Pheochromocytoma
3. Renal Parenchymal Diseases
-RENAL DISEASE IS THE MOST COMMON CAUSE
OF SECONDARY HYPERTENSION
-Hypertension is MORE SEVERE in GLOMERULAR
DISEASES than in Interstitial Diseases
-Proteinuria >1000 mg/day and an active urine
sediment are indicative of PRIMARY RENAL
DISEASE
4. Renovascular Hypertension
-hypertension due to obstruction of a renal artery
-potentially curable form
-mechanism is related to activation of the renin-
angiotensin system
-Females 8x > Males
-Patients at risk:
1. Older arteriosclerotic patients with plaque on
renal artery, frequently at its origin
2. Patients with fibromuscular dysplasia
5. Renovascular Hypertension
-Histologic Variants of Fibromuscular Dysplasia:
1. Medial Fibroplasia – MOST COMMON
2. Perimedial Fibroplasia
3. Medial Hyperplasia
4. Intimal Fibroplasia
*Fibromuscular dysplasia lesion are bilateral and
affect more distal portions of the renal artery
6. Renovascular Hypertension
-S/Sx:
-abdominal or flank bruit that extends throughout
systole into diastole
-Treatment:
-Renal Vascular repair: pts with long-standing HTN,
advanced renal insufficiency, DM are LESS LIKELY to
benefit
-ACE inhibitors/ARBs: decrease GFR in stenotic kidneys
causing renal arteriolar vasodilation; cause progressive
renal insufficiency in pts w/ bilateral renal artery
stenosis or renal artery stenosis on a solitary kidney
BUT insufficiency is REVERSIBLE IF DRUG is
DISCONTINUED
7. Renovascular Hypertension
-Treatment:
-Percutaneous Transluminal Renal Angioplasty (PTRA)
-intial treatment of choice in pts w/ Fibromuscular
Disease
-LAB/Imaging:
-OIH scan / DTPA scan before and after a single dose of ACEi
to assess renal blood flow and GFR, respectively
-Doppler Ultrasound
-Gadolinium-contrast magnetic resonance angiography –
proximal > distal renal artery
- Contrast Angiography – “GOLD STANDARD” for detecting
Renal Artery Lesions; NEPHROTOXIC ( to patients with DM,
w/ pre-existing Renal Insufficiency)
8. Renovascular Hypertension
-Prognosis:
-Patients with fibromuscular disease have
more favorable outcomes than patients with
atherosclerotic lesions, owing to younger age,
shorter duration of HTN and less systemic
disease
9. Primary Aldosteronism
-DEFINITION: excess aldosterone production
-potentially curable form of HTN
-HTN is mild to moderate, but occasionally severe
-increased aldosterone production is INDEPENDENT
of the renin-angiotensin system and the
consequences are:
1. sodium retention
2. hypertension
3. hypokalemia
4. low PRA
11. Primary Aldosteronism
-LAB/Imaging:
1. Serum potassium concentration
-SIMPLEST SCREENING TEST
-can be normal initially in some pts with aldosterone
secreting adenoma
2. Plasma Aldosterone to Plasma Renin Activity (PA/PRA) ratio
-ambulatory pts in the morning
- >20 PA/PRA ratio -90% have aldosterone secreting
adenoma
-affected by drugs:
-Aldosterone antagonists – increases aldosterone
-ARBs and ACEi – increases renin
12. Primary Aldosteronism
-LAB/Imaging:
3. CT/MRI
-should be carried out in all patients
diagnoses with primary aldosteronism
4. Adrenal Scintigraphy
-if CT/MRI does not detect adenoma
13. Primary Aldosteronism
-Diagnosis:
-confirmed by demonstrating FAILURE TO
SUPPRESS plasma aldosterone to <277 pmol/L
after IV infusion of 2L of isotonic saline over 4h
14. Primary Aldosteronism
-Etiology:
-aldosterone producing adrenal adenoma
-unilateral, <3cm in diameter
-biosynthesis is more responsive to ACTH
-Hypertension responsive post surgery
-adrenocortical hyperplasia
-bilateral
-biosynthesis is more responsive to angiotensin
-Hypertension NOT responsive post surgery
16. Primary Aldosteronism
-Treatment:
1.Surgery
-should be undertaken only after BP has been
controlled and hypokalemia corrected
-HYPOaldosteronism may occur 3 months post
operation during this time Potassium should be
monitored, and HYPERkalemia should be treated with
potassium-wasting diuretics and fludrocortisone
2. Aldosterone antagonists
3. Potassium-sparing diuretics
17. Primary Aldosteronism
-Treatment:
4. Glucocorticoids / Spironolactone
-for rare, monogenic, autosomal dominant
form of the disease characterized by moderate
to severe HTN
18. Cushing’s Syndrome
-Hypertension occurs in 75-80% of patients
-MECHANISM:
-stimulation of mineralocorticoid receptors by
cortisol and increased secretion of adrenal
steroids
-can be seen in patients taking exogenous
glucocorticoids
20. Pheochromocytoma
-DEFINITION: catecholamine secreting tumors
that are located in the adrenal medulla
-autosomal dominant
-can be associated with multiple endocrine
neoplasias (MEN) type 2A and type 2B
-PARAGANGLIOMA: -tumor in extra-adrenal
paraganglion tissue
21. Pheochromocytoma
-MECHANISM:
-related to increased circulating
catecholamines, and may secrete other
vasoactive substances
-RARITY: epinephrine is secreted predominantly
and causes HYPOtension rather than
HYPERtension
23. MISCELLANEOUS CAUSES OF
HYPERTENSION
1. Obstructive Sleep Apnea
-severity of HTN correlates with severity of
sleep apnea
-should be considered in drug-resistant
patients and with history of snoring
-Dx: confirmed by Polysomnography
-Rx: Weight loss, Continuous Positive Airway
Pressure (CPAP)
24. MISCELLANEOUS CAUSES OF
HYPERTENSION
2. Coarctation of the Aorta
-MOST COMMON CONGENITAL
CARDIOVASCULAR CAUSE OF HYPERTENSION
-occurs in 35% of pts with Turner’s Syndrome
-Patients with less severe lesions may not be
diagnosed until young adulthood
-S/Sx: diminished and delayed femoral pulses,
systolic pressure gradient between the right
arms and legs
25. MISCELLANEOUS CAUSES OF
HYPERTENSION
2. Coarctation of the Aorta
-Dx: Chest X-ray and transesophageal
echocardiogram
-Tx: Surgical repair, Balloon angioplasty (with
or without cardiovascular stent)
3. Thyroid diseases
-Hypothyroidism: mild diastolic hypertension
-Hyperthyroidism: systolic hypertension
26. MISCELLANEOUS CAUSES OF
HYPERTENSION
4. Acromegaly
5. Hypercalcemia
-MOST COMMON ETIOLOGY IS PRIMARY
HYPERPARATHYROIDISM
27. MONOGENIC HYPERTENSION
-recognized by their characteristic phenotypes
and Dx confirmed by genetic analysis
-inherited defects in adrenal steroid biosynthesis
and metabolism result in
MINERALOCORTICOID-INDUCED
HYPERTENSION and HYPOKALEMIA
28. MONOGENIC HYPERTENSION
DEFICIENT PHYSIOLOGIC EFFECT CLINICAL MANIFESTATION
ENZYME
17a- Decreased sex hormone and -no sexual maturation
hydroxylase cortisol -males: pseudohermaphroditism
-females: primary amenorrhea, absent
secondary sexual characteristic
11B- Salt-retaining adrenogenital -virilization and ambiguous genitalia
hydroxylase syndrome resulting in -penile enlargement
decreased cortisol synthesis, -precocious puberty
increased mineralocorticoids -short stature
and shunting of the steroid -PRESENTING Sx: acne, hirsutism,
biosynthesis in the androgen menstrual irregularities
pathway -HTN: less common in late-onset
11B- Impaired ability to metabolize -HTN
hydroxysteroid cortisol to cortisone (inactive
dehydrogenase metabolite); can be acquired
due to licorice-containing
glyccherizic acid
29. MONOGENIC HYPERTENSION
-LIDDLE’S SYNDROME:
-results from constitutive activation of
amiloride sensitive epithelial sodium channels
on the distal renal tubule resulting in EXCESS
SODIUM REABSORPTION
-HYPERTENSION IN PREGNANCY
-exacerbated due to activation of
mineralocorticoid receptors by progesterone