Pathology of Hypertension

“Smile, smile at your wife, smile at your husband, smile at your children, smile at stranger, smile at each other, it doesn't matter who it is - and that will help you to grow up in greater love for each other." Mother Teresa 1910-1997, Roman Catholic Missionary Pathology of Hypertension: Dr. Venkatesh M. Shashidhar. Associate Professor of Pathology Fiji School of Medicine Hypertension - Introduction • • • • • • • • Silent Killer – painless – complications dizziness, headache, and visual difficulties, It is the leading risk factor – MI, DM, Stroke Responsible for the majority of office visits, Number one reason for drug prescription. 25% of population, <35% aware, <5% ..! Complications bring to diagnosis but late… Chronic, end organ & vascular damage Introduction • • • • • “Sustained increase in blood pressure” Systolic >140, Diastolic > 90 mm of Hg* Normal* < 130 <85 (120/80 +/- 10/5) Mild + 20, Moderate +40 Severe +80 Malignant - > 210/120 Regulation of BP: BP = Cardiac Output x Peripheral Resistance • Endocrine Factors – Renin, Angiotensin, ANP, ADH, Aldosterone. • Neural Factors – Sympathetic & Parasympathetic • Blood Volume – Sodium, Mineralocorticoids, ANP • Cardiac Factors – Heart rate & Contractility. Etiologic Classification: • Primary/Essential Hypertension (95%) • Secondary Hypertension (5-10%) – Renal – GN, RAS, Renin tumors – Endocrine – Cushing, OCP, Thyrotoxicosis Myxdema, Pheochromocytoma, Acromegaly. – Vascular – Coarctation of Aorta, PAN, Aortic insufficiency. – Neurogenic – Psychogenic, Intracranial pressure, olyneuritis etc. Etiology: • Secondary - Known abnormal control. – Renal disorders – Renin-Angiotensin. Sodium retention, ADH, Aldosterone. – Cushings, Pheochromocytoma, • Essential - Etiology is multifactorial. – Increased peripheral resistance (sympathetic tone) – stress, hormonal, neural. – Genetic, familial, life style. Pathogenesis of Renovascular HTN: GFR Renin by JGA Aldosterone Sodium Retention Blood Volume Angiotensin II Vasoconstriction  P. Resistance Hypertension Malignant Hypertension: • • • • • • • Rapidly progressive end organ damage. May complicate any type of HTN. Artery necrosis with thrombosis. Rapidly developing renal failure. Hypertensive encephalopathy. Left ventricular failure. less time  No hypertrophy …! Morphology: • Large Blood Vessels – Macroangiopathy. – Atherosclerosis and its complications. • Small Blood Vessels – Microangiopathy. – Hyperplastic arteriolosclerosis. (thick arterioles) • Heart – LVH, Hypertensive cardiomyopathy IHD, MI. • Kidney – Benign nephrosclerosis. • Eyes: – Hypertensive retinopathy • Brain: – Haemorrhage, infarction, – splinter hemorrhages & Lacunar infarcts. Pathogenesis of vascular changes. •Arteriolosclerosis •Rupture •Aneurysm •Rupture. Left Ventricular Hypertrophy: Left Ventricular Hypertrophy Hyperplastic Arteriolosclerosis: Narrow Lumen Onion Skin Thickening Of arterioles. Necrotizing arteriolitis: Thrombosis Fibrinoid Necrosis Subarachnoid Haemorrhage: Cerebral Blood vessels Special features: • Thin walled* • End arteries* • Cong. Aneurisms Cerebral Infarction (Stroke) : Haemorrhagic Necrosis Lacunar Infarct: • Chronic hypertension • Arteriolosclerosis of deep penetrating arterioles of brain stem. • Single or multiple cavitary infarcts – lacunes. • Lenticular nucleus, thalamus • Slit Haemorrhages. Benign Nephrosclerosis: Leathery Granularity due to minute scarring Cerebral Infarction: Renal Causes : • • • • • • Renal artery atherosclerosis Polycystic Disease Glomerulonephritis (A/C) Renal artery stenosis Renal vasculitis – SLE Renin producing tumors. Polycystic Kidney -> Renal Artery stenosis - Atrophy Leathery Granularity Benign Nephrosclerosis Normal Retina - Fundoscopy Hypertensive Retinopathy: • Arteriosclerosis cause the arteriole light reflex to become broad and dull – silver wire • Generalized or focal retinal arteriolar constriction – pale. • Superficial flame-shaped hemorrhages. • Small white foci of retinal ischemia (cotton-wool spots). • Yellow hard exudates, due to lipid deposition deep in the retina. Hypertensive Retinopathy: • Grade I – Thickening of arterioles. • Grade II – Focal Arteriolar spasms. Vein constriction. (AV nipping) • Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool (ischemia) and hard waxy exudates (lipid deposition). • Grade IV - Papilloedema Conclusions: • • • • • • • • Persistent increased blood pressure (140/90) 95% Essential, 5% secondary - Renovascular Benign and Malignant types (>120Diastolic) Vessel damage & Arteriolosclerosis Complicates - Atherosclerosis, Diabetes, IHD Ischemia or Infarction in end organs. Kidney, Brain, Heart & Eyes. Nephrosclerosis, renal damage, IHD, MI, Stroke & Retinopathy. Self Assessment Questions: • Define essential, hypertension? • Briefly describe pathogenesis of renal damage in hypertension. • Classify hypertension, briefly describe pathogenesis in each? • Summarize common complications of hptn? • What is nephrosclerosis? Briefly describe its pathogenesis? • What is meant by malignant hypertension? Briefly describe clinical and pathological features? • What are lacunar infarcts? arteriolosclerosis? • How does hptn causes stroke? Damage heart?