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Pathology of Hypertension

Pathology of Hypertension. Lecture for medical students.

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Pathology of Hypertension

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  1. Pathology of Hypertension Keep Smiling….!  “ It will help you to grow up in greater happiness & Love for each other." Mother Teresa 1910-1997, Roman Catholic Missionary

  2. Pathology of Hypertension: Dr. Venkatesh M. Shashidhar. Associate Professor & Head of Pathology Pathology of Hypertension: Dr. Venkatesh M. Shashidhar. Associate Professor & Head of Pathology

  3. Introduction <ul><li>“ Sustained increase in blood pressure” </li></ul><ul><li>Systolic >140, Diastolic > 90 mm of Hg* </li></ul><ul><li>Normal* < 130 <85 (120/80 +/- 10/5) </li></ul><ul><li>Mild + 20, Moderate +40 Severe +80 </li></ul><ul><li>Malignant - > 210/120 </li></ul> Introduction <ul><li>“ Sustained increase in blood pressure” </li></ul><ul><li>Systolic >140, Diastolic > 90 mm of Hg* </li></ul><ul><li>Normal* < 130 <85 (120/80 +/- 10/5) </li></ul><ul><li>Mild + 20, Moderate +40 Severe +80 </li></ul><ul><li>Malignant - > 210/120 </li></ul>

  4. Hypertension - Introduction <ul><li>Silent Killer – painless – complications </li></ul><ul><li>dizziness, headache, and visual difficulties, </li></ul><ul><li>It is the leading risk factor – MI, DM, Stroke </li></ul><ul><li>Responsible for the majority of office visits, </li></ul><ul><li>Number one reason for drug prescription. </li></ul><ul><li>25% of population, <35% aware…<5% ..! </li></ul><ul><li>Complications bring to diagnosis but late… </li></ul><ul><li>Chronic, end organ & vascular damage </li></ul> Hypertension - Introduction <ul><li>Silent Killer – painless – complications </li></ul><ul><li>dizziness, headache, and visual difficulties, </li></ul><ul><li>It is the leading risk factor – MI, DM, Stroke </li></ul><ul><li>Responsible for the majority of office visits, </li></ul><ul><li>Number one reason for drug prescription. </li></ul><ul><li>25% of population, <35% aware…<5% ..! </li></ul><ul><li>Complications bring to diagnosis but late… </li></ul><ul><li>Chronic, end organ & vascular damage </li></ul>

  5. Regulation of BP: <ul><li>BP = Cardiac Output x Peripheral Resistance </li></ul><ul><li>Endocrine Factors </li></ul><ul><ul><li>Renin, Angiotensin, ANP, ADH, Aldosterone. </li></ul></ul><ul><li>Neural Factors </li></ul><ul><ul><li>Sympathetic & Parasympathetic </li></ul></ul><ul><li>Blood Volume </li></ul><ul><ul><li>Sodium, Mineralocorticoids, ANP </li></ul></ul><ul><li>Cardiac Factors </li></ul><ul><ul><li>Heart rate & Contractility. </li></ul></ul> Regulation of BP: <ul><li>BP = Cardiac Output x Peripheral Resistance </li></ul><ul><li>Endocrine Factors </li></ul><ul><ul><li>Renin, Angiotensin, ANP, ADH, Aldosterone. </li></ul></ul><ul><li>Neural Factors </li></ul><ul><ul><li>Sympathetic & Parasympathetic </li></ul></ul><ul><li>Blood Volume </li></ul><ul><ul><li>Sodium, Mineralocorticoids, ANP </li></ul></ul><ul><li>Cardiac Factors </li></ul><ul><ul><li>Heart rate & Contractility. </li></ul></ul>

  6. Etiologic Classification: <ul><li>Essential (Primary) Hypertension (95%) </li></ul><ul><ul><li>Unknown etiology. Life style, genetic, … </li></ul></ul><ul><li>Secondary Hypertension (5-10%) </li></ul><ul><ul><li>Renal – GN, RAS, Renin tumors </li></ul></ul><ul><ul><li>Endocrine – Cushing, OCP, Thyrotoxicosis Myxdema, Pheochromocytoma, Acromegaly. </li></ul></ul><ul><ul><li>Vascular – Coarctation of Aorta, PAN, Aortic insufficiency. </li></ul></ul><ul><ul><li>Neurogenic – Psychogenic, Intracranial pressure, olyneuritis etc. </li></ul></ul> Etiologic Classification: <ul><li>Essential (Primary) Hypertension (95%) </li></ul><ul><ul><li>Unknown etiology. Life style, genetic, … </li></ul></ul><ul><li>Secondary Hypertension (5-10%) </li></ul><ul><ul><li>Renal – GN, RAS, Renin tumors </li></ul></ul><ul><ul><li>Endocrine – Cushing, OCP, Thyrotoxicosis Myxdema, Pheochromocytoma, Acromegaly. </li></ul></ul><ul><ul><li>Vascular – Coarctation of Aorta, PAN, Aortic insufficiency. </li></ul></ul><ul><ul><li>Neurogenic – Psychogenic, Intracranial pressure, olyneuritis etc. </li></ul></ul>

  7. Etiology: <ul><li>Secondary - Known abnormal control. </li></ul><ul><ul><li>Renal disorders – Renin-Angiotensin. Sodium retention, ADH, Aldosterone. </li></ul></ul><ul><ul><li>Cushings, Pheochromocytoma, </li></ul></ul><ul><li>Essential - Etiology is multifactorial. </li></ul><ul><ul><li>Increased peripheral resistance (sympathetic tone) </li></ul></ul><ul><ul><li>stress, hormonal, neural. </li></ul></ul><ul><ul><li>Genetic, familial, life style. </li></ul></ul> Etiology: <ul><li>Secondary - Known abnormal control. </li></ul><ul><ul><li>Renal disorders – Renin-Angiotensin. Sodium retention, ADH, Aldosterone. </li></ul></ul><ul><ul><li>Cushings, Pheochromocytoma, </li></ul></ul><ul><li>Essential - Etiology is multifactorial. </li></ul><ul><ul><li>Increased peripheral resistance (sympathetic tone) </li></ul></ul><ul><ul><li>stress, hormonal, neural. </li></ul></ul><ul><ul><li>Genetic, familial, life style. </li></ul></ul>

  8. Pathogenesis of Renovascular HTN:  GFR Renin by JGA Angiotensin II Vasoconstriction  P. Resistance Sodium Retention  Blood Volume Aldosterone Hypertension Pathogenesis of Renovascular HTN:  GFR Renin by JGA Angiotensin II Vasoconstriction  P. Resistance Sodium Retention  Blood Volume Aldosterone Hypertension

  9. Malignant Hypertension: <ul><li>Rapidly progressive end organ damage. </li></ul><ul><li>May complicate any type of HTN. </li></ul><ul><li>Artery necrosis with thrombosis. </li></ul><ul><li>Rapidly developing renal failure. </li></ul><ul><li>Hypertensive encephalopathy. </li></ul><ul><li>Left ventricular failure. </li></ul><ul><li>less time  No hypertrophy …! </li></ul> Malignant Hypertension: <ul><li>Rapidly progressive end organ damage. </li></ul><ul><li>May complicate any type of HTN. </li></ul><ul><li>Artery necrosis with thrombosis. </li></ul><ul><li>Rapidly developing renal failure. </li></ul><ul><li>Hypertensive encephalopathy. </li></ul><ul><li>Left ventricular failure. </li></ul><ul><li>less time  No hypertrophy …! </li></ul>

  10. . Morphology: <ul><li>Large Blood Vessels – Macroangiopathy. </li></ul><ul><ul><li>Atherosclerosis and its complications. </li></ul></ul><ul><li>Small Blood Vessels – Microangiopathy. </li></ul><ul><ul><li>Hyperplastic arteriolosclerosis. (thick arterioles) </li></ul></ul><ul><li>Heart </li></ul><ul><ul><li>LVH, Hypertensive cardiomyopathy  IHD, MI. </li></ul></ul><ul><li>Kidney </li></ul><ul><ul><li>Benign nephrosclerosis. </li></ul></ul><ul><li>Eyes : </li></ul><ul><ul><li>Hypertensive retinopathy </li></ul></ul><ul><li>Brain : </li></ul><ul><ul><li>Haemorrhage, infarction, </li></ul></ul><ul><ul><li>splinter hemorrhages & Lacunar infarcts. </li></ul></ul>

  11. . Pathogenesis of vascular changes. <ul><li>Arteriolosclerosis </li></ul><ul><li>Rupture </li></ul><ul><li>Aneurysm </li></ul><ul><li>Rupture. </li></ul>Ischemia, Aneurysm, Rupture

  12. 13. Left Ventricular Hypertrophy: Left Ventricular Hypertrophy

  13. 14. Hyperplastic Arteriolosclerosis: Onion Skin Thickening Of arterioles. Narrow Lumen

  14. 15. Nephrosclerosis in HPTN: Artery Sclerosis Artery Sclerosis PCT hydropic deg.

  15. 16. Nephrosclerosis in HPTN: Artery Sclerosis Glom. Sclerosis Artery Sclerosis PCT hydropic deg.

  16. 17. Necrotizing arteriole: Malignant HPTN Fibrinoid Necrosis Thrombosis

  17. 18. Subarachnoid Haemorrhage: <ul><li>Cerebral Blood vessels </li></ul><ul><li>Special features: </li></ul><ul><li>Thin walled* </li></ul><ul><li>End arteries* </li></ul><ul><li>Cong. Aneurisms </li></ul>

  18. 19. Cerebral Infarction (Stroke) : Haemorrhagic Necrosis

  19. 20. Lacunar Infarct: <ul><li>Chronic hypertension </li></ul><ul><li>Arteriolosclerosis of deep penetrating arterioles of brain stem. </li></ul><ul><li>Single or multiple cavitary infarcts – lacunes. </li></ul><ul><li>Lenticular nucleus, thalamus </li></ul><ul><li>Slit Haemorrhages. </li></ul>

  20. 21. Benign Nephrosclerosis: Leathery Granularity due to minute scarring

  21. 22. Cerebral Infarction:

  22. 23. Renal Causes : <ul><li>Renal artery atherosclerosis </li></ul><ul><li>Polycystic Disease </li></ul><ul><li>Glomerulonephritis (A/C) </li></ul><ul><li>Renal artery stenosis </li></ul><ul><li>Renal vasculitis – SLE </li></ul><ul><li>Renin producing tumors. </li></ul>Polycystic Kidney ->

  23. 24. Renal Artery stenosis - Atrophy Leathery Granularity Benign Nephrosclerosis

  24. 25. Normal Retina - Fundoscopy

  25. 26. Hypertensive Retinopathy: <ul><li>Arteriosclerosis cause the arteriole light reflex to become broad and dull – silver wire </li></ul><ul><li>Generalized or focal retinal arteriolar constriction – pale. </li></ul><ul><li>Superficial flame-shaped hemorrhages. </li></ul><ul><li>Small white foci of retinal ischemia (cotton-wool spots). </li></ul><ul><li>Yellow hard exudates, due to lipid deposition deep in the retina. </li></ul>

  26. 27. Hypertensive Retinopathy: <ul><li>Grade I – Thickening of arterioles. </li></ul><ul><li>Grade II – Focal Arteriolar spasms. Vein constriction. (AV nipping) </li></ul><ul><li>Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool (ischemia) and hard waxy exudates (lipid deposition). </li></ul><ul><li>Grade IV - Papilloedema </li></ul>

  27. 28. G Protien Polymorphisms in Metabolic Syndrome-X <ul><li>A common C825T polymorphism in the gene GNB3 , which encodes the β3 subunit of heterotrimeric G proteins, was identified in cell lines from patients with hypertension. The 825T allele is associated with increased intracellular signal transduction. Many population-based and case-control studies in different ethnicities have investigated an association between this polymorphism and hypertension, obesity, and atherosclerosis. A critical assessment of published studies suggests that 825T allele carriers have an increased risk for hypertension combined with features of the metabolic syndrome, such as dyslipidemia, hypercholesterolemia, insulin resistance, and obesity. It is anticipated that this polymorphism will be used in clinical practice to better characterize hypertension and for individualized treatment regimens. </li></ul>

  28. 29. Conclusions: <ul><li>Persistent increased blood pressure.. </li></ul><ul><li>95% Essential, 5% secondary - Renovascular </li></ul><ul><li>Benign and Malignant types (>120 Diastolic) </li></ul><ul><li>Vessel damage & Arteriolosclerosis </li></ul><ul><li>Complicates - Atherosclerosis, Diabetes, IHD </li></ul><ul><li>Ischemia or Infarction in end organs. </li></ul><ul><li>Kidney, Brain, Heart & Eyes. </li></ul><ul><li>Complications: Nephrosclerosis, renal damage, IHD, MI, Stroke & Retinopathy. </li></ul>

  29. 30. Self Assessment Questions: <ul><li>Define essential, hypertension? </li></ul><ul><li>Briefly describe pathogenesis of renal damage in hypertension. </li></ul><ul><li>Classify hypertension, briefly describe pathogenesis in each? </li></ul><ul><li>Summarize common complications of hptn? </li></ul><ul><li>What is nephrosclerosis? Briefly describe its pathogenesis? </li></ul><ul><li>What is meant by malignant hypertension? Briefly describe clinical and pathological features? </li></ul><ul><li>What are lacunar infarcts? arteriolosclerosis? </li></ul><ul><li>How does hptn causes stroke? Damage heart? </li></ul>

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