The document discusses secondary hypertension, defining it as elevated blood pressure due to an underlying disorder. The most common causes of secondary hypertension include renal parenchymal diseases, primary aldosteronism, Cushing's syndrome, pheochromocytoma, and renovascular hypertension. It provides details on the definition, causes, signs and symptoms, diagnostic tests, treatment options, and prognosis for each of these common causes of secondary hypertension.

1. INTERNAL
MEDICINE:
Secondary
Hypertension
nianderthalNOTES

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

10. Primary Aldosteronism
-Risk Factors:
-30s-50s
-pts taking diuretics
-S/Sx:
-asymptomatic (most)
-polyuria
-polydipsia
-paresthesias or muscle weakness
-hypertension- mild-moderate, occasionally
severe

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

15. Primary Aldosteronism
-Etiology:
-adrenal carcinoma
-produce other adrenal steroids
-ectopic malignancy
-e.g. ovarian arrhenoblastoma

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

19. Cushing’s Syndrome
-Lab/Imaging:
1. 24-h urine excretion rate of free cortisol
2. Overnight Dexamethasone suppression tes
-Treatment:
-appropriate therapy depends on etiology

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

22. Pheochromocytoma
-Lab/Imaging:
1. Catecholamine in Urine or Plasma
2. Genetic screening

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