Secondary HT Flashcards
Causes of secondary HT
o 5-10% HT cases
Causes: RECAPS ABCDEF • Renal disease (ex: renal artery stenosis) • Estrogens and eclampsia • Coarctation of aorta • Aldosteronisms • Pheochromocytoma • Sleep apnea • Alcoholism • Brain lesions • Cushings syndrome • Drugs • Endocrine diseases • Fat
Describe the pathology and pathogenesis of blood pressure elevation in unilateral renal artery stenosis and chronic kidney disease
Mechanisms kidneys cause HT:
1) Retain Na+
• Liddle’s syndrome: genetic overexpression of epithelium Na+ channels → excessive Na+ reabsorption, volume expansion, HT
• Re-set pressure-natriuresis relationship
• Relationship between amount of pressure in renal artery and amount of Na+ excreted:
• Retain Na+ = increases intravascular volume → increased CO (raises BP) → increased blood flow to most organs = autoregulation of flow by vasoconstriction (raises BP)
• Visa versa (higher BP increases Na+ excretion)
2) Release renin
• Renin-secreting tumors (hemangiopericytomas or Wilm’s tumors)
• Seen in children
o Increase adrenergic nerve traffic
Indications for renal HT:
o HT before age 25 or after age 50
o Severe HT and pressure rose rapidly
o Pressure difficult to control with ordinary doses
o Renal function worsens (especially with BP drugs)
o Pain over kidneys
o Atherosclerosis elsewhere
o Recurrent pulmonary edema without obvious cause
Renal artery stenosis
o Causes HT in 1-3% patients
o Not always a cause of HT because need right effect on blood flow
• Slight stenosis: not decrease blood flow due to autoregulation (dilation) to compensate
• More stenosis (autoregulatory capacity exceeded): renal artery causes renin release → HT
• Too much stenosis: kills kidneys = no renin release!
o Result: need physiologically significant stenosis: 75-90% decrease in diameter
o Causes:
• Atherosclerosis = most common cause; usually affects >1 site
• Fibromuscular dysplasia= young-middle aged females; due to spotty CT overgrowth; sting of beads appearance on angiogram
• Neurogibromatosis = in children
• Others: emboli, inflammatory lesions, extrinsic pressure from tumors or cysts, post-transplantation kinking, trauma
Chronic kidney disease
o Kidneys unable to excrete Na+ → HT
o Cycle: HT → nephrosclerosis → worsening HT and renal function
Primary aldosteronism
Identify the diagnostic hallmarks of renal artery stenosis
Abdominal bruits (both systolic and diastolic)
Angiogram = gold standard, but invasive and uses contrast
• Artery with significant stenosis (diameter reduced by 75% or more)
• Post-stenotic dilation
• Collateral arteries
• Affected kidney is smaller
Renogram +/- ACE-I
• Look for delayed appearance and wash-out of dye
• Use ACE-I to accentuate differences (since RAAS may compensate for stenosed artery)
Measure renal vein renin levels
• Assesses significance of renal artery stenosis
• (NOTE: peripheral vein renins not helpful because many clinical states causing increased renin)
Other tests: CT angiography, MRI angiography, ultrasound
Describe the principal therapies for renal artery stenosis
Percutaneous transluminal renal angioplasty (balloon dilation and stent)
Vascular surgery used when:
• Stenosis at aortic root of renal arteries
• Unable to pass balloon through lesion
• Stenosis beyond reach of balloon catheters
Medical therapy
• Unilateral stenosis: ACE-I and ARB
• Bilateral stenosis: ACE-I and ARBs contraindicated because block efferent vasoconstriction maintaining GFR
Describe the principal therapies for primary aldosteronism
Increased secretion of aldosterone not accompanied by elevated renin
• Have low renin even with salt restriction
o Common causes: adrenal adenomas and adrenal hyperplasia
Pathogenesis:
• Aldosterone → Na+ reabsorption, K+ and H+ excretion → increased blood volume, CO, peripheral resistance
• Mineralocorticoid escape: elevated aldosterone → increased EC volume → new equilibrium reached (no further Na+ retention occurs)
• But: continued loss of K+
Clinical findings: • HT • Weakness • Muscle cramps • NO edema
Lab findings: • High blood and urine aldosterone • Low plasma renin • High urine K+ excretion • Low serum K+ • Alkalosis (due to H+ excretion)
Best screening test = Alosterone/renin ratio
• When <20 = unlikely cause of HT
Imaging:
• MRI and CT to localize adenomas
• Iodocholesterol scans
Describe the pathology and pathogenesis of hypertension in coarctation of the aorta
Congenital narrowing of aorta
• Increased resistance → HT
• RAAS stimulated → HT
Clinical findings:
• Young patients with HT
• BP lower in legs compared to arms
• Pain or weakness in less during exercise
• Systolic murmur over chest
• Large intercostal arteries → bruits in chest wall
• Chest x-ray:
• “3-sign” = dents on left side of aortic shadow
• Notching on underside of ribs from enlarged collateral vessels
Describe the pathology and pathogenesis of hypertension in pheochromocytoma
Clinical signs: • Headache • Sweating • Palpitations • Anxiety/nervousness/tremor • Pallor • Nausea/vomiting • Often associated with neurofibromatosis (see café-au-lait spots, etc.)
Pathogenesis:
• Tumors (often in adrenal medulla) secrete bursts of catecholamines → increase CO and peripheral resistance
Lab tests:
• Measure catcholamines or metabolites (especially good = metanephrines) in 24-hr urine sample
• If measure urinary vanillylmandelic acid (product of catecholamine metabolism) = can be falsely elevated by vanilla containing foods
Imaging:
• CT or MRI
• Scintigraphy (nuclear scanning)
Describe the pathology and pathogenesis of estrogens and eclampsia
o Only about 5% women sensitive to estrogen
Estrogen mechanisms:
• Na+-retaining effects
• Stimulate hepatic synthesis of renin substrate
• Increase sensitization of peripheral vessels to catcholamines
Pre-eclampsia: • Late (>20 weeks) HT (>90 diastolic) • Edema • Proteinuria (>300 mg/day) • Decreased renal function • CNS or visual changes • Pulmonary edema
Eclampia: • Late HT • General edema • Proteinuria • Convulsions • Coma
Describe the pathology and pathogenesis of sleep apnea
o About 50% with sleep apnea also have HT
Sleep apnea and HT more common in: • Obese • Alchohol abusers • Males • Elderly
Pathogenesis:
• Hypoxia → Periodic stimulation of sympathetic NS
o Treat with positive pressure mask → rapid decrease in BP
Describe the pathology and pathogenesis of alcoholism
o Dose related: >3 drinks/day
o Alcohol withdrawal → elevated BP (resembles pheochromocytoma attack, often accompanied by low K+)
Describe the pathology and pathogenesis of brain lesions
o Increased intracranial pressure → triggers sympathetic nerves → HT
o Clinical signs: slow pulse, high systolic pressure, wide pulse-pressure
Describe the pathology and pathogenesis of Cushings syndrome
o Excessive amount of glucocorticoids (cortisol)
o From primary adrenal tumors making cortisol or pituitary tumors making ACTH
o Also from exogenous glucocorticoid medications: prednisone, dexamethasone
o Clinical signs: moon face, acne, purple striae on abdomen, diabetes, HT
List drugs that can raise BP
o Sympathomimetics: nasal decongestants, stimulatnts for ADHD, appetite suppressants with amphetamine-like actions, bronchodilators
o Cocaine = vasoconstrictive effect
o Ergot alkaloids = vasoconstrictive effect
o Cyclosporine = nephrotoxic
o MOI in presence of foods high in tyramine = block sympathomimetic degradation
o Erythropoietin
o Glucocorticoids
Describe the pathology and pathogenesis of endocrine diseases
Hyperthyroidism • Increased systolic pressure • Decreased diastolic pressure • Rapid pulse rate • Treat with beta-blocker (ex: propranolol)
Hypothyroidism
• Increased diastolic pressure
Hyperparathyroidism:
• Revealed by blood Ca2+ level
Describe the effect of visceral fat on BP
o See decreased BP with weight loss before IBW reached
