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HYPERTENSION

HYPERTENSION. Roll No. : 46, 47, 48, 49, 50 Teacher In charge : Dr. G.S. Ranga. Determinants of arterial pressure. What is HYPERTENSION ?. Transitory or sustained elevation of systemic arterial blood pressure to a level likely to induce cardiovascular damage or other adverse consequences.

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HYPERTENSION

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  1. HYPERTENSION Roll No. : 46, 47, 48, 49, 50 Teacher In charge : Dr. G.S. Ranga

  2. Determinants of arterial pressure

  3. What is HYPERTENSION ? Transitory or sustained elevation of systemic arterial blood pressure to a level likely to induce cardiovascular damage or other adverse consequences

  4. Classification of hypertension

  5. Etiology of Hypertension There are two types on the basis of etiology: • Primary hypertension– 90-95% of cases – also termed “essential” of “idiopathic” • Secondary hypertension– about 5% of cases

  6. Primary (Essential) hypertension • Cause unknown • Tends to be familial • Is a polygenic disorder; different patients carry different subsets of genes associated with obesity, dyslipidemia, insulin resistance, etc, • Consequence of interaction between environment and genetic factors

  7. Risk factors for essential hypertension • Old age • Smoking • Obesity • Excessive intake of salt • Alcohol consumption • Stress • Family history • Low dietary intake of vitamin D, calcium and potassium

  8. Secondary hypertension • A specific underlying disorder is the cause of hypertension • Accounts for only 5 – 10% cases

  9. Causes of secondary hypertension • Metabolic syndromes • Dyslipidemia • Insulin resistance • Renal parenchymal or renovascular disease • Obstructive sleep apnea • Preeclampsia and eclampsia • Neurogenic causes • Acute increased intracranial pressure • Acute spinal cord section • Endocrine disease • Phaeochomocytoma • Cusings syndrome • Conn’s syndrome • Acromegaly , hypothyroidism and hyperthyroidism • Coarctation of the aorta • Mendelian forms of hypertension • Iatrogenic • Hormonal / oral contraceptive • NSAIDs

  10. PATHOGENESIS OFHYPERTENSION Roll no. 47 – Mohit Chhabra

  11. Vascular Regulatory Mechanisms • Local Regulation– Autoregulation, Vasodilator metabolites, Localized vasoconstriction • Endothelial factors– NO, Endothelins, Prostacyclins and Thromboxane A2 • Systemic regulation by hormones– Kinins, Natriuretic hormones (ABC), circulating vasoconstrictors (vasopressin, norepinephrine, angiotensin II). • Vasoconstrictiveinfluences: Ion transport/ Endothelial factors

  12. Vascular Regulatory Mechanisms Increased Na+-H+ activity in the vessel wall Increased intracellular Na+ Increased intracellular pH Increased smooth muscle contractility and vasoconstriction

  13. Regulatory Mechanisms of the Autonomic Nervous System: Baroreceptors • Baroreceptors monitoring the arterial circulation are present in the carotid sinus and the aortic arch. • Stimulated by distention/raised BP • Increased baroreceptor discharge inhibits tonic discharge of the sympathetic nervous system

  14. Action of Baroreceptors

  15. Regulatory Mechanisms of the Autonomic Nervous System Inhibition of RVLM/ Vasomotor Center Inhibited β receptors in heart Inhibited α receptors on blood vessels Decreased HR & CO Decreased PVR Lowered Blood Pressure

  16. Regulatory Mechanisms of the Kidney • Kidney regulates BP by two main mechanisms: • Regulation of sodium and water homeostasis • Renin-Angiotensin-Aldosterone-System • Significant renal impairment is associated with hypertension in large part due to disturbance in sodium handling. • Reduced renal perfusion leading to raised BP, relates to the activity of the Renin-Angiotensin-Aldosterone System.

  17. Sodium Homeostasis

  18. Renin-Angiotensin-Aldosterone System • There are 3 major stimuli for renin secretion: • Decreased NaCl transport to the macula densa • Decreased stretch within the renal afferent arteriole (Baroreceptor mechanism) • Stimulation of β1 adrenoreceptors in JG cells • Other stimulatory factors – Prostaglandins • Other inhibitory factors – Angiotensin II, Vasopressin

  19. Renin-Angiotensin-Aldosterone Axis Increased activity of the renin-angiotensin-aldosterone axis is not invariably associated with hypertension

  20. Renin-Angiotensin-Aldosterone System • The main effector molecules of RAAS are Angiotensin II and Aldosterone. • Angiotensin II acts on AT1 receptors: • In the adrenal cortex to release Aldosterone which increases Na+ reabsorption by epithelial sodium channel (ENaC) on the collecting duct with resultant hypokalemia and alkalosis to maintain electric neutrality. • In the arterioles to cause vasoconstriction • AT2 receptor antagonizes AT1 by causing vasodilation and sodium excretion.

  21. Pathogenesis of Essential Hypertension Main factors involved in the pathogenesis of hypertension are: • Genetic factors • Environmental and lifestyle influences • Impact of fetal and infant growth • Prehypertension • Renal mechanisms • Vascular mechanisms • Neurohumoral control systems

  22. Genetic Factors Lancet, 349, 1353-7 It is more likely that essential hypertension results from interactions of mutations or polymorphisms at several loci that influence blood pressure

  23. Environmental & Lifestyle Influences • Dietary salt intake influences not only blood pressure but also cardiovascular disease outcomes. Sodium balance has an impact on blood pressure. • Visceral adiposity seems important in defining the relationship between blood pressure and obesity. • Alcohol intake – Intervention trials confirm that blood pressure falls when alcohol is withdrawn from heavy drinkers. • Clear cut association between obstructive sleep apnea and hypertension. • Psychosocial stress and blood pressure.

  24. Impact of fetal and infant growth • Association between low birth weight and risk of developing hypertension. • Inverse relationship between birth weight & gestational age with systolic BP.

  25. Prehypertension • Annual rate of progression to hypertension is higher amongst pre-hypertensives. • Prehypertension is also more common in people with diabetes

  26. Pathogenesis of Secondary Hypertension • For most forms underlying pathways are well understood: * http://books.google.co.in/books?id=QfsjuUncJE0C&pg=PA147&lpg=PA147&dq=AGN+and+hypertension&source=bl&ots=MEsoSD5bTf&sig=lN_zKxoD1j5hXR7nKiGSZFlgCPs&hl=en&ei=VzOCTtYHo6mIB9avpf0O&sa=X&oi=book_result&ct=result&resnum=4&ved=0CDcQ6AEwAw#v=onepage&q=AGN%20and%20hypertension&f=false

  27. SOURCES • Harrison’s Principles of Internal Medicine, 18/e • Robbins and Cotran Pathologic Basis of Disease, 8/e • Oxford Textbook of Medicine, 5/e • Ganong’s Review of Medical Physiology, 23/e • Principles of Pharmacology by KK Sharma, 2/e

  28. DIAGNOSIS OF HYPERTENSION Roll no. 48 – MohitGarg

  29. History • A complete history should be taken which assess the following points: • Duration • Previous therapies • Family history of hypertension and cardiovascular diseases • Dietary and psychosocial history • Other risk factors : weight change, dyslipidemia, smoking, diabetes and physical activity • Evidence of secondary hypertension: spells of sweating, palpitations, tremors, erratic sleep and snoring etc.

  30. Physical Examination • Body habitus, including weight and height. • At the initial examination, blood pressure should be measured in both arms • Heart rate • The neck should be palpated for an enlarged thyroid gland, and patients should be assessed for signs of hypo- and hyperthyroidism • Examination of blood vessels • Kidneys of patients with polycystic kidney disease may be palpable in the abdomen. • The physical examination also should include evaluation for signs of CHF and a neurologic examination.

  31. Physical Examination • Measured using a sphygmomanometer • Seated quietly for 5 minutes • Centre of the cuff at the level of the heart. • Width of the bladder cuff should equal at least 40% of the arm circumference • the length of the cuff bladder should be enough to encircle at least 80% of the arm circumference • Inflate 20-30 mmHg above loss of radial pulse • Deflate at 2mmHg per second

  32. Classification of hypertension

  33. Laboratory Tests

  34. COMPLICATIONS OF HYPERTENSION Roll no. 49 – MohitSharma

  35. Complications of Hypertension CNS - Stroke, retina damage • Damage Heart - CHF, MI, Sudden death, angina Kidneys - renal failure, proteinuria Peripheral Vascular disease

  36. Cardiovascular complications Heart - Increased workload on left ventricle  Left ventricular hypertrophy  left ventricular failure. - Greater thickness of left ventricle  decreased perfusion and ischaemia of subendocardial region of myocardium.

  37. Consequences of Hypertension • Cardiac - LVH

  38. Arteries - Accelerated atherogenesis. -  risk of developing aortic dissecting aneurism. Arterioles: Arteriolosclerosis - Benign HT: Deposition of eosinophilic (‘hyaline’) material in vessel walls due to influx of plasma proteins. - Malignant HT: Thickening of intima. Necrosis of vessel walls ('fibrinoid' necrosis) and formation of micro-aneurisms in brain.

  39. CNS Complications: • - Rupture of micro-aneurisms of small penetrating • arteries  Intracerebral haemorrhage. •  Risk of cerebral infarction due to atherosclerosis • of circle of Willis. • Acute malignant HT: ‘Hypertensive encephalopathy’ • due to cerebral oedema (headache, nausea and vomiting, • visual disturbances, seizures and disturbances of • consciousness).

  40. Consequences of Hypertension - CNS

  41. Peripheral vascular disease Classical presentation : Intermittent claudication (aching pain in calves or buttocks while walking that is relived by rest) Ankle-brachial index: -Ratio of SBP ankle to arm - <0.90 : diagnostic

  42. Peripheral Vascular Disease

  43. Renal complications Arteriolosclerosis  Ischaemic sclerosis of glomeruli and tubular atrophy. Proteinuria and microscopic haematuria, especially in malignant HT .

  44. Consequences of Hypertension -Kidney

  45. Consequences of Hypertension - Retina Factors responsible: -Vasoconstriction -Vascular leakage: lead to flame shaped retinal hmg & retinal edema -Arterioloscelerotic changes

  46. Grading- Hypertensive retinopathy Grade 1: subtle broadening of the arteriolar light reflex, mild generalized arteriolar attenuation, particularly of small branches, and vein concealment Grade 2: obvious broadening of the arteriolar light reflex and deflection of veins at arteriovenous crossings (Salus sign) Grade 3: -‘Copper-wiring’ of arterioles -Banking of veins distal to arteriovenous crossings (Bonnet sign) -Tapering of veins on both sides of the crossings (Gunn sign) and right-angled deflection of veins. Grade 4: ‘Silver-wiring’ of arterioles & papilloedema associated with grade 3 changes

  47. Consequences of Hypertension - Retina

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