Hypertension PDF

HYPERTENSION Dr. Abdul Rehman  Learning Outcomes Define hypertension Enlist types and causes of hypertension Benign and Malignant hypertension Etiopathogenesis of hypertension Hypertension associated vascular morphology Complications of hypertension...

HYPERTENSION Dr. Abdul Rehman  Learning Outcomes Define hypertension Enlist types and causes of hypertension Benign and Malignant hypertension Etiopathogenesis of hypertension Hypertension associated vascular morphology Complications of hypertension Etone repting strains 11Thnov weaving  BLOOD VESSELS Vascular disease develops through two principal mechanisms: Narrowing or complete obstruction of vessel lumen – acute or progressive Weakening of vessel walls – dilation, rupture  NORMAL BLOOD VESSELS: General architecture and cellular composition of blood vessels are the same throughout CVS The vessel wall consists of endothelial cells (ECs), smooth muscle cells (SMCs) & extracellular matrix (ECM)  includes elastin, collagen & proteoglycans The vessel wall consists of three concentric layers 1. Intima consist of 3 layers vessel wall 2. Media intima 3. Adventitia Adventitia These layers vary depending upon the tissue requirements & hemodynamic forces Vessel wall cosist of Endothelial cell smooth muscle cell Elastin belgerman cellularmatrixincludescollagen Media Extra proteoglycans Adventitia  am Variation in thickness & composition of various layers  Blood Pressure Regulation Blood pressure is a function of cardiac output and a peripheral vascular resistance  influenced by multiple genetic & environmental factors CARDIAC OUTPUT: stroke volume & heart rate Stroke volume – Na conc. & Myocardial contractility Heart rate – α- & β-adrenergic systems PERIPHERAL VASCULAR RESISTANCE: Arterioles – neural & humoral inputs Arterioles Normal vascular tone – a balance between vasoconstrictors & vasodilators Autoregulation - blood flow  vasoconstriction Fine tuning – tissue pH & hypoxia  Blood Pressure Regulation DO 0 calculate Blood pressure How to Cardiac output prepheral vascular Humantheneral  vasoornstrian a Elan Farently Interaction of factors released from kidneys, adrenals & myocardium kidney Adrenal Renin-angiotensin system myocardium Release of Renin  o 1. Low B.P. in afferent arterioles O 2. levels of circulating catecholamines 3. Low Na levels in distal convoluted tubules Fauseton Vasodilators – prostaglandins, NO low BP Adrenal aldosterone cicatehamin's Myocardial natriureteric peptide INA in distal convoluted tubules Interplay of Renin, Angiotension, Aldosterone & ANP HYPERTENSIVE VASCULAR DISEASE Hypertension (increased blood pressure) 111ms – a sustained diastolic pressure > 90 mm Hg 8 or a sustained systolic pressure >140 mm Hg About 25% of individuals in general population are hypertensive Pathological effects of hypertension  Stroke  Coronary heart disease  Cardiac hypertrophy & heart failure  Aortic dissection dementia  Multi-infarct dementia Multiinfarct  Renal failure failure Renal Types and Causes of Hypertension O O All cases have primary hypertension is due secondaryhypertension Renal arterystenosis Renal vaults Risk Factors of Primary HTN MALIGNANT HYPERTENSION: Rapidly rising blood pressure that, if untreated, leads to death within 1-2 years Severe HTN ( systolic pressure > 180 mm Hg or D O diastolic pressure > 120 mm Hg), renal failure & retinal hemorrhages & exudates f T.in i exudate a Mostly superimposed on preexisting “benign” hypertension Malignanthypertension blood pressure if Rapidlyrising untreated It years Mechanisms of Primary Hypertension alteration in renalN1homeostasis in vascular resistance mechanism it self is antown Specific triggers are unknown no specifictrigger Alteration in Renal Ns homeostasis It appears that alterations in renal Na homeostasis and increased vascular resistance contribute to vassitive primary hypertension REDUCED RENAL SODIUM EXCRETION: redeemed E Increased volume and cardiac output Increasedvolume cardiac output INCREASED VASCULAR RESISTANCE: Vasoconstriction or structural changes in vessel Increase walls of vasterresisture vasoconstriction or structural changes In Westfall GENETIC FACTORS: ogenpolymorphism Angiotensin Angiotensin 11 linked to specific angiotensinogen polymorphisms & angiotensin II receptor variants Single gene disorders cause rare but severe forms of hypertension 1. Gene defects affecting enzymes involved in aldosterone metabolism (aldosterone synthase, 11β- hydroxylase, 17α-hydroxylase)  increased aldosterone secretion Is 2. Mutations affecting proteins that influence Na resorption  increased distal tubular resorption of Na ENVIRONMENTAL FACTORS: Stress – Obesity – Smoking - Lack of exercise Heavy salt consumption Mechanisms of Primary Hypertension Finance  HYPERTENSIVE VASCULAR MORPHOLOGY Accelerates atherogenesis Degenerative changes in the walls of large & medium sized arteries – aortic dissection, cerebrovascular hemorrhage pegenerativechangesintayem.li E'Hamage Associated with two forms of small blood vessel disease: 1) Hyaline arteriolosclerosis I eating small 2) Hyperplastic arteriolosclerosis tightens atheroma thorough Hyperpl dissection arteriolo  sclerosis Hyaline Arteriolosclerosis Associated with benign hypertension IIe Marked by thickening of arteriolar walls Benignhypertension Homogeneous pink hyaline material Loss of underlying structural details homogenous Narrowed arteriolar lumen Leakage of plasma proteins across endothelium Excessive ECM synthesis Elderly & Diabetes pattern leakage of of thickening plasma proteins across endothelium arteritis  Hyperplastic Arteriolosclerosis O Characteristic of severe “malignant” HTN talignant nypd “Onion skin”, concentric, laminated wall thickening Arteriolar luminal narrowing Laminations  SMC with thickened basement membrane o_ Malignant HTN Necrotizing arteriolitis (fibrinoid necrosis whereae raise  Hypertensive Vascular MORPHOLOGY Fenton Hyperplastic arteriolocos began Fibrinoid e on_mines Complications of Hypertension Questions??