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![The American Heart Association has recommended guidelines to define normal and high
blood pressure[5]
:
• Normal: Systolic lower than 120 mm Hg, diastolic lower than
80 mm Hg
• Elevated BP: Systolic 120-129 mm Hg, diastolic lower than 80
mm Hg
• Hypertension Stage 1: Systolic 130-139 mm Hg, diastolic 80-
89 mm Hg
• Hypertension Stage 2: Systolic 140 mm Hg or greater,
diastolic 90 mm Hg or greater](https://image.slidesharecdn.com/secondaryhypertension-240807173016-661e9da7/75/SECONDARY-HYPERTENSION-pptxcivil-service-nepal-2-2048.jpg)
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SECONDARY HYPERTENSION.pptxcivil service nepal
- 1. SECONDARY HYPERTENSION Dr Rifat Siddiqui FCPSResident Internal Medicine
- 2. The American HeartAssociation has recommended guidelines to define normal and high blood pressure[5] : • Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg • Elevated BP: Systolic 120-129 mm Hg, diastolic lower than 80 mm Hg • Hypertension Stage 1: Systolic 130-139 mm Hg, diastolic 80- 89 mm Hg • Hypertension Stage 2: Systolic 140 mm Hg or greater, diastolic 90 mm Hg or greater
- 4. Who are atrisk? • Advancing Age • Sex (men and postmenopausal women) • Family history of cardiovascular disease • Sedentary life style & psycho-social stress • Smoking ,High cholesterol diet, Low fruit consumption,high salt inake • Obesity & wt. gain • Co-existing disorders such as diabetes, and hyperlipidaemia • High intake of alcohol
- 5.
- 9. TYPES OF HYPERTENSION: •Essential hypertension • 90% • No underlying cause • Secondary hypertension (10%) • Underlying cause
- 10. When to suspectsecondary hypertension clinicallly? • Absence of family history of hypertension • Severe hypertension > 180/110 mm Hg with onset at age < 20 years, or > 50 years • Difficult-to-treat or resistant hypertension with significant end-organ, damage features • Presents with combination of pain (headache), palpitation, pallor, and perspiration - 4 P's of phaeochromocytoma • Persons with Short and thick neck - Obstructive Sleep Apnoea • Polyuria, nocturia, proteinuria or hematuria - indicative of renal diseases
- 11. Contd.. •Absence of peripheralpulses, brachiofemoral delay and abdominal or peripheral vessel bruits • History of polycystic renal disease or palpable enlarged, kidneys • Cushingoid features, multiple neurofibromatosis • Significant elevation of plasma creatinine with use of, ACE inhibitors • Hypertension in children • History of snoring, daytime somnolence, obesity
- 12. Blood Pressure Determinants: • Cardiacoutput: Increased with renal salt/water retention • Total peripheral resistance: Key vessels: arterioles Increased by vasoconstrictors (i.e. catecholamines) Increased by sympathetic nervous system, BP = CO X TPR
- 13. Causes of secondaryhypertension: RENAL DISEASE: • Renal parenchymal disease: • Polycystic disease • Chronic nephritis • Glomerulonephritis • Diabetic nephropathy • Hydronephrosis • Reno-vascular disease • Renin producing tumor • Primary sodium retention
- 14. • VASCULAR CAUSE: Coarctationof aorta • Neurological : • Increased intracranial pressure • Porphyria • Familial dysautonomia (Riley Day) • Lead poisoning • Guillain-Barre syndrome
- 15. ENDOCRINE: • Hypothyroidism • Hyperthyroidism •Adrenal: • Cushing's syndrome • Congenital adrenal hyperplasia • Primary aldosteronism • Pheochromocvtoma • Hypercalcemia • Carcinoid • Extra-adrenal • Exogenous hormones: • Estrogen • Mineralocorticoids • Sympathomimetics • Tyramine + MAO inhibitors
- 16. • DRUGS/TOXINS • PREGNANCY •STRESS: • Postoperative • Burn • Pain • Hypoglycemia • Alcohol withdrawal
- 17. There are twoforms of kidney diseases causing hypertension a) Renal parenchymal & b) Renovascular causes • Renal parenchymal diseases : • Chronic glomerulonephritis • Chronic interstitial nephritis • Pyelonephritis • Nephrocalcinosis • Neoplasms • Glomerulosclerosis • Analgesic nephropathy • Polycystic kidney disease • Obstructive nephropathy
- 18. RENOVASCULAR HYPERTENSION • Etiology: •Atherosclerosis • Takayasu's arteritis • Fibromuscular dysplasia • Other causes: • Aortic/renal dissection • Thrombotic/cholesterol emboli • Post transplantation stenosis • Post radiation
- 19. Renal Artery Stenosis: • Vasculardisease of renal arteries • Decreased blood flow to kidneys • Key exam finding: renal bruit
- 20. Renal artery stenosiscontd.. • Increased renin, salt-water retention =HTN • Often unilateral stenosis • Normal kidney compensates • Results: No signs of volume overload
- 21. ADPKD Autosomal dominant polycystic kidney disease •Genetic disorder • Mutations of PKD1 or PKD2 • Presents in adulthood with HTN and renal cysts • Increased RAAS activity
- 22. Fibromuscular Dysplasia: • Vasculardisease - obstruction to flow, • Common among women, • Often occurs in 40s-50s, • Non-atherosclerotic, non-inflammatory, • Often involves medial layer fibroplasia, • Stenosis and aneurysms of vessels ("string of beads"), • Most common in renal and carotid arteries, • Can lead to renal artery stenosis
- 23. Coarctation of aorta: consistsof localized narrowing of the aortic arch, just distal to the origin of the left subclavian artery. Congenital defect, male>female Clinical presentation: •Differential systolic BP in arms and legs •May have differential BP in arms if defect is proximal to Left, subclavian artery •Diminished/absent femoral artery pulse •Often asymptomatic •Associated with Turners syndrome, bicuspid Aortiv valve
- 25. Primary Aldosteronism: • Excessivelevels of aldosterone secretion, • Not due to increased activity of RAAS system, • Adrenal adenoma (Conn's syndrome), • Bilateral idiopathic adrenal hyperplasia • Increased Na reabsorption distal nephron • Incr ECV -> incr CO – Hypertension • Increased K excretion -> hypokalemia
- 26. Primary Aldosteronism contd.. •Clinical features, • Resistant hypertension • Hypokalemia • Normal volume status on physical exam, • Diagnosis • Renin-independent aldosterone secretion • Low plasma renin activity • High aldosterone levels • Drugs of choice: Spironolactone/Eplerenone Aldosterone antagonists
- 27. Liddle Syndrome: • Geneticdisorder, •Increased activity of ENaC • Similar clinical syndrome to hyperaldosteronism: Hypertension Hypokalemia, • Aldosterone levels low
- 28. Pheochromocytoma •Catecholamine-secreting tumor • Epinephrine,norepinephrine, dopamine • Usually arises from adrenal gland and unilateral • Triad: Palpitations, headache, episodic sweating • Most patient have hypertension • Diagnosis: Catecholamines breakdown products, • Metanephrines • Vanillylmandelicacid (VMA)
- 29. Cushing's Syndrome: • Excesscortisol • Often from steroid administration • Other causes, •Cushing's Disease (pituitary oversecretes ACTH) • Tumors (i.e. small cell lung cancer secretes ACTH) • Adrenal tumor secretes cortisol, • Cortisol -> hypertension Increased vascular sensitivity to adrenergic agonists
- 30. Obstructive Sleep Apnea: • Sleep-relatedbreathing disorder • Apnea during sleep • Polysomnography is diagnostic • Often associated with hypertension • Treatment may reduce BP • Use of c-pap improves hypertension.
- 31. DRUGS CAUSING HYPERTENSION: •NSAIDs • Estrogens • Wt loss agents: sibutramine,phentermine • Immunosuppressants: cyclosporine, tacrolimus,steroids • Antiparkinsonian: bromocriptine • MAOinhibitors: phenelazine • Anabolic steroids: testosterone • Stimulants: nicotine, amphetamines • Sympathomimetics
- 32. NSAIDs: Ibuprofen, naproxen, indomethacin,ketorolac, diclofenac • Nonsteroidal anti-inflammatory drugs, • Inhibit cyclooxygenase in kidneys, • Decrease synthesis of prostaglandins, • PGE-2: renal vasodilator
- 33. ORAL CONTRACEPTIVE PILLS: •Estrogen & progesterone analogs • Cause mild increase in blood pressure
- 34. Pseudoephedrine : • Nasaldecongestant • Alpha-1 agonist • vasoconstriction– decrease nasal blood flow
- 35. Evaluating secondary causesof hypertension: Causes Diagnostic evaluation OSA Sleep study Hyperaldosteronism Plasma aldosterone level Renovascular(renal artery stenosis or FMD) Renal artery duplex doppler ultrasound, CT or MRA Primary kidney disease or nephrotic syndrome Renal USG, lab tests to discern underlying cause Hyperthyroidism TFT Cushing syndrome Dexamethasone suppression test, 24h urine free cortisol Pheochromocytoma 24h urine metanephrines, abdominal cross-sectional imaging Coarction of aorta Echocardiography, CT or MRA
- 36. Management of secondaryhypertension: • Withdraw/replace BP-raising medications • Management of endocrine causes typically requires specialist involvement • Consider revascularization for renovascular hypertension • Anti-hypertensive therapy will frequently be required
- 37. OTHER TYPES OFHYPERTENSION: • WHITE COAT HYPERTENSION: High blood pressure readings are found when measured by the physician, but not when the patient measures at home. Evidence of anxiety-induced, sympathetic phenomena such as tachycardia, perspiration, cold, hands, tremor, and/or pupil dilation will usually be present
- 38. Isolated systolic hypertension: • It's not uncommon to have either a systolic, number that's elevate while the diastolic, number remains normal. It's less common for patients to have, elevated diastolic number. This condition, known as isolated systolic hypertension.
- 39. Persistent Hypertension • Characterizedby a diastolic blood, pressure above 110 to 120 mm Hg. • It results when hypertension is, unresponsive to treatment and become a, truly severe emergency condition as the, pressure continues to rise unchecked.
- 40. Malignant Hypertension: • Severeelevation of bp (diastolic greater thn 120) • Rare form ,often fatal • Rapidly progressive over 1 to 2 years • Renal failure, retinal haemorrhages , ischaemia
- 41. Resistant hypertension: • Bloodpressure that remains above goal inspite of the concurrent use of three antihypertensive agents of different classes including a diuretic. All agents should prescribed at optimal dose amounts.
- 42. Refractory hypertension: • Refractoryhypertension (RfHTN) is defined as blood pressure (BP) that is uncontrolled despite using 5 ≥ antihypertensive medications of different classes, including a long-acting thiazide diuretic and a mineralocorticoid receptor antagonist.
- 43. Hypertensive urgency: • Severehypertension without end organ damage. • Usually greater than 180/120
- 44. Hypertensive Emergency: • Severehypertension with end organ damage. • BP usually >180/120 • Patient longstanding HTN, stops meds • Neurologic impairment • Retinal hemorrhages, encephalopathy • Renal impairment • Acute renal failure, • Hematuria, proteinuria, • Cardiac ischemia • Associated with MAHA • Endothelial injury-thrombus formation
- 46. Control of hypertension: •Non pharmacological measures: 1. Weight reduction 2. Dietary sodium reduction 3. Vegetarian and vegan diet 4. The DASH diet 5. Reduction of alcohol consumption 6. Smoking cessation 7. Exercise
- 47. Control of HTNcontd.. • Pharmacological measures: 1. Beta blockers 2. Thiazides 3. Calcium blockers 4. Dihydropyridines 5. Non-dihydropyridines 6. ACEi/ARB
- 48. • Discontinue offendingmedications if possible • Renal artery stenosis: management may include antihypertensives and/or angioplasty and stenting • FMD :therapy with ACE inhibitor or ARB, angioplasty may be necessary • Hyperaldosteronism: Spironolactone, ACE inhibitor and/or ARB; surgery may be, curative in cases of adrenal adenoma
- 49. • Liddle syndrome:Low sodium diet and triamterene or amiloride • Gordon syndrome :Low sodium diet and thiazide diuretics • Phaeochromocytoma : Adrenalectomy and combined alpha/beta blockers • Obstructive sleep apnea : weight loss and CAP while sleeping • Aortic coarctation: may require surgery • Renal parenchymal disease : • Treatment depends on the type of disease • ACE inhibitors and/or ARBs are usually recommended for BP control and renoprotection
- 50. • REFERENCES: • MANUALOF HYPERTENSION of the European Society of Hypertension • UpToDate • Harrison’s principles of internal medicine