Hypertensive vascular disease By: Dr. S.Homathy
Normal vessels • Main components of vascular walls are • Intima – endothelial cells • Media – smooth muscle cells (SMC) • Adventitia – extra cellular matrix (ECM) + vasavasorum + nerve fibres.
Vascular system • Arterial system • Venous system • Lymphatic system
Large arteries Large veins Medium arteries Medium veins Small arteries Small veins Arterioles Collecting venules Post capillary venules Capillaries
Types of arteries Based on their size and structural features • Large / Elastic arteries • Aorta and its large branches ( subclavian, common carotid, iliac) • Medium / Muscular arteries • Coronary arteries • Renal arteries • Small arteries (<2mm), arterioles (20-100m) Note- Arterioles are the principal points of physiologic resistance to blood flow. • Capillaries(7-8m) have one cell thick wall and large cross sectional area – useful in exchange of diffusible substances
Features of veins • Large diameter - 2/3 of systemic blood is in venous system • Large Lumina • Thinner and less organized walls • Valves to prevent reverse flow Veins are predisposed to • Irregular dilation • Compression • Easy penetration by tumors
Lymphatics • Thin walled endothelium lined channels • Serve as a drainage system for retaining interstitial tissue fluid to blood • Important pathway for disease dissemination – bacteria, tumour cells
Functions of endothelial cells • Maintenance of permeability barrier • Elaboration of anticoagulant and antithrombotic molecules • Elaboration of prethrombotic molecules • Extra cellular matrix production • Modulation of blood flow and vascular reactivity • Regulation of inflammation and immunity • Regulation of cell growth • Oxidation of LDL
Functions of SMCs • Vasoconstriction/dilation in response to normal/pharmacologic stimuli • Synthesize collagen, elastin and proteoglycans • Elaborate growth factors and cytokines • Migrate to the intima and proliferate after injury
Vascular disorders Vascular abnormalities cause clinical disease by two mechanisms • Narrowing or completely obstructing the Lumina • Progressively- atherosclerosis • Precipitously – thrombosis or embolism • Weakening of the walls-leading to dilation or rupture
Vascular disease • Congenital anomalies • Arteriovenous fistula – some times causes high-out put cardiac failure • Arteriosclerosis • Atherosclerosis • Monckeberg medial calcific sclerosis • Arteriolosclerosis • Hypertensive vascular disease • Aneurysms and dissections • Inflammatory vascular disease.
Hypertensive vascular diseases • Hypertension - Elevated blood pressure • DBP >90mmHg • SBP >140mmHg • Affect both the function and structure of blood vessels
HT is a risk factor for • atherosclerosis (AS) • Coronary heart disease • Cerebrovascular accident • Also cause • cardiac hypertrophy and Heart failure (hypertensive heart disease) • Aortic dissection • Renal failure
Will discuss about • Normal blood pressure control • Possible mechanisms of hypertension • Pathologic changes in small blood vessels
Normal blood pressure control BP = Cardiac out put × Peripheral resistance Blood volume Sodium Mineralocorticoids ANP
Physiological mechanisms to maintain normal blood pressure • Autonomic nervous system response • Hormonal responses • Capillary shift mechanism • Kidney and fluid balance mechanisms
Peripheral resistance is regulated predominantly at the level of the arterioles. • It is influenced by neural and hormonal inputs
Autonomic nervous system • Most rapidly responding regulator of blood pressure • Control BP by changing blood distribution in the body and by changing blood vessel diameter • Sympathetic and parasympathetic activity will affects veins, arteries and heart • Receives continuous information from the baroreceptors in carotid sinus and the aortic arch
This information is relayed to the brainstem to the vasomotor centre • Vasomotor centre is a cluster of sympathetic neurons found in medulla • It sends efferent motor fibers that innervate smooth muscles of blood vessels • A decrease in blood pressure causes activation of the sympathetic nervous system resulting in increased contractility of the heart and vasoconstriction
Hormonal mechanisms • They act in various ways including • Vasoconstriction • vasodilatation • alteration of blood volume
Kidneys and adrenals are central plyers in blood pressure regulation • They interact with each other to modify vessel tone and blood vessel through vrious ways.
The principal hormones raising blood pressure are • adrenaline and noradrenaline secreted from the adrenal medulla in response to sympathetic nervous system stimulation • They increase cardiac output and cause vasoconstriction • Renin and angiotensin production is increased in the kidney when stimulated by hypotension
Capillary fluid shift mechanism • Exchange of fluid that occurs across the capillary membrane between the blood and the interstitial fluid • Low blood pressure results in fluid moving from the interstitial space into the circulation helping to restore blood volume and blood pressure.
Kidney and fluid balance mechanism • Regulate the blood pressure by • increasing or decreasing the blood volume - changing the GFR leading to increase or decrease reabsorption of Na • through renin-angiotensin system –influences both peripheral resistance and sodium homeostasis • Secretion of vasodepressor or antihypertensive substances (prostaglandins and nitric oxide)
Risk factors of hypertension • Genetic factors • Environmental factors • Diet – excessive salt consumption • Lifestyle – stressful, physical inactivity • Weight – obesity • Alcohol – increased intake • Oral contraceptives
Classification of hypertension • Benign hypertension • Malignant hypertension Based on severity • Diastolic HT • systolic HT Based on type. • Primary • Secondary Based on aetiology
Benign hypertension • Usually asymptomatic • Most cases discovered when pressure is measured at a routine medical examination • Affects heart and arteries of all sizes • It causes • IHD • Heart failure • CVA • acceleration of renal disease • Malignant HT
Malignant hypertension • Develop in previously normotensive persons often superimposed in preexisting benign HT • DBP >120mmHg + renal failure + retinal hemorrhages and exudates with or without papilledema • It also causes • Cardiac failure • CVA • Hypertensive encephalopathy
Etiological classification of hypertension • Essential hypertension – 95%, idiopathic, combine with long life unless complications develops • Secondary hypertension – 5-10% • Renovascular disease/ renal parenchymal disease • AGN • CRF • Renal artery stenosis • Polycystic kidney disease • Renin producing tumors
Endocrine • Adrenocorticalhyperfunction • Cushing’s syndrome • Primary aldosteronism • Congenital adrenal hyperplasia • Exogenous hormones • Oestrogens –OCP • Drug activate renin – angiotesin – aldosterone system • Glucocorticoids • Mineralocorticoids • Sympathomimetics
Phaeochromocytoma • Acromegaly • Hypothyroidism / Hyperthyroidism • DM
Cardiovascular • Coarctation of aorta • Rigidity of the aorta • Increased cardiac output • Neurogenic • Increased intracranial pressure • Acute stress • Psycogenic
Essential hypertension • HT occurs when the relationship between blood volume and total peripheral resistance is altered. • Pathogenesis is uncertain • Multifactorial etiology Genetic factors Environmental factors +
Genetic factors • Blood pressure tends to run in families • children of hypertensive parents tend to have higher BP than age matched children of people with normal BP. • Fetal factors • Low birth weight is associated with subsequent high BP • May be due to fetal adaptation to intrauterine undernutrition with long term changes in blood vessel structure • Insulin resistance • An association between diabetes and hypertension has long been recognized.
Genetic factors • Defects in the renal sodium homeostasis • Inadequate sodium excretion • Salt and water retension • Increase plasma and ECF volume • Increased cardiac output and peripheral vasoconstriction • Increased blood pressure. • Functional vasoconstriction • Defects in the vascular smooth muscle growth and structure.
Environmental factors • Diet – excessive salt consumption • Lifestyle – stressful, physical inactivity • Weight – obesity • Alcohol – increased intake • Environmental factors affect the variables that control BP in the genetically predisposed individuals • In essential HT both increased blood volume and increased peripheral resistance contribute to increased BP.
Humoral mechanism • The autonomic nervous system, • renin – angiotensin • naturetic peptides • play a role in the physiological regulation of short term changes in blood pressure • & have been implicated in the pathogenesis of essential hypertension. • However there is no convincing evidence that the above systems are directly involved in the maintenance of hypertension.
Currently favored hypothesis is that high dietary intake of sodium in a genetically predisposed individuals. Failure of excretion by kidney in the face of prolonged high sodium level Increase in naturetic factors One of this factor inhibits Na+-K+-ATP ase Intracellular Ca2+ concentration increases Vasoconstriction in vascular SMC
Secondary hypertension • Renal diseases • Account for over 80% of the cases • Common causes are • diabetic nephropathy, • chronic glomerulo nephritis, • adult polycystic kidney disease • renovascular diseases • HT can itself causes or worsen renal disease • Mechanism of BP elevation is primarily due to sodium and water retention, • although there can be inappropriate elevation of plasma renin level.
Clinical symptoms of HT • Mild hypertensive patients are usually asymptomatic • High levels of BP may be associated with • Headache • Epistaxis • Nocturia • Malignant HT may be present with • Severe headache • Visual disturbances • Fits • Transient loss of consciousness
Breathlessness may be present owing to LVH or cardiac failure • Patients may present with the symptoms of complications of hypertension. • Attacks of • Sweating • Headache • Palpitation
Vascular pathology in hypertension • Accelerates atherogenesis • Degenerative changes in large and medium arteries leads to • aortic dissection • cerebrovascularhaemorrhages • Small vessel changes • Hyaline arteriolosclerosis • Hyperplasticartriolosclerosis
Hyaline arteriolosclerosis High BP • leakage of plasma components across vascular endothelium • excessive ECM production by SMCs secondary to • chronic hemodynamic stress of HT • Metabolic stress in DM • Accentuates EC injury
Morphology • Homogenous, pink, hyaline thickening of the walls of arteriole with • loss of underlying structural detail • narrowing of the lumen. • Major morphologic characteristic of benign nephrosclerosis.