SYSTEMIC HYPERTENSION Hypertension (HT) = pathologically  blood pressure Blood pressure:Systolic /diastolic pressure Normal blood pressure (adults) : < 140 mm Hg/90 mm Hg Borderline HT: mm Hg/ mm Hg Definite HT:> 160 mm Hg/95 mm Hg

The kidney and blood pressure Role in regulation of blood pressure - Renin-angiotensin system (juxtaglomerular apparatus). - Production of a variety of vasodepressor or antihypertensive substances (prostaglandin, NO). Renal diseases may cause systemic HT. HT may cause renal damage.

Classification  Essential vs secondary HT  Benign vs malignant HT Essential HT % of cases. Pathogenetic mechanisms multifactorial and poorly understood. Secondary HT % of cases. Hypertension due to a recognisable disease.

Diseases associated with secondary HT: 1) Renal diseases - Renal parenchymal diseases (see later). - Renovascular HT = systemic HT due to stenosis of a renal artery (  ischaemia  release of renin).

2) Endocrine - Adrenocortical hyperfunction/tumour (Cushing, Conn) - Exogenous glucocorticoids - Pheochromocytoma - Acromegaly - Hyperthyroidism - Pregnancy-induced

3) Cardiovascular - Coarctation of aorta

4) Neurogenic - Increased intracranial pressure - Acute stress

Pathogenetic factors in essential HT Arterial blood pressure = cardiac output (*) x peripheral vascular resistance (**) Blood pressure will rise if either (*) or (**) is increased

Essential hypertension is associated with: -  peripheral vascular resistance (pathogenesis poorly understood) - Sodium and water retention   blood volume,  cardiac output

A high salt intake correlates with  prevalence of essential HT. Genetic factors: -  Sensitivity of some individuals to a high salt intake. - High prevalence in blacks.

Benign HT - moderate increase in blood pressure. - long clinical course. - little clinical effects in early stages. Malignant HT - diastolic pressure > 130 mm Hg - severe impact on cardiovascular system, kidneys and central nervous system.

Malignant HT: - May arise in previously normotensive individuals, but more commonly as a complication of benign HT. - Relatively uncommon (1-5% of hypertensive patients). - Aggressive treatment is required.

Complications of systemic HT  Cardiovascular  CNS  Renal

Cardiovascular  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.

 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 (of Bouchard) in brain.

CNS - 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).

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

VASCULITIS Inflammation of blood vessel walls. Types I, II, III and IV hypersensitivity reactions may contribute to the inflammation. Idiopathic OR Associated with autoimmune diseases/ infections/drug reactions.

The inflammation of the blood vessel walls may lead to: - Thrombus formation in vessels with ischaemic effects. -  Fragility of small vessels with petechial haemorrages (skin and other organs). - Weakening of vessel wall, with aneurism formation.

A. Arteritis associated with infection  Direct invasion of artery by microorganisms (usually bacteria) in septisaemia  weakening of arterial wall  mycotic aneurism, e.g. in brain.  Syphilitic aortitis - Aneurism of aortic arch in tertiary syphilis. - Involvement of coronary ostia  myocardial ischaemia. - Fibrosis of valve cusps  aortic insufficiency.

B. Polyarteritis nodosa (PAN) Medium to small arteries. Segmental lesions. Immune complex disease (type III hypersensitivity reaction). HbsAg + (30% of cases). Multisystem disease, excluding lungs. Ischaemic lesions. Renal involvement: haematuria, hypertension.

C.Hypersensitivity (leukocytoclastic) vasculitis Inflammation of venules, capillaries, arterioles of skin, but also other organs. Aetiology: - Reactions to certain infections - Foreign proteins ('serum sickness') - Drugs (aspirin, penicillin, sulphonamides) - Auto-immune diseases

Henoch-Schönlein purpera A variant of hypersensitivity vasculitis - skin (purpera) - abdomen (pain, vomiting, melena) - joints (arthritis) - kidneys (acute glomerulonephritis)

D. Giant cell (temporal) arteritis Temporal artery and branches of external carotid artery. 50 years. Unusual in blacks. Opthalmic branch of ECA  blindness.

E. Takayasu’s disease (pulseless disease) Young women. Idiopathic arteritis involving origins of branches of aortic arch. Complicated by fibrosis and thrombosis  weakening of radial pulse, dizziness, syncope.

E. Wegener’s granulomatosis Granulomatous vasculitis of upper and lower respiratory tracts, with involvement of glomerular vessels  acute glomerulonephritis.

F. Thromboangiitis obliterans (Buerger’s disease) Small and medium sized arteries and veins of extremities (lower extremities in particular). Males < 35 years Cigarette smokers. Gangrene of fingers / toes. Neutrophils in vessel wall, thrombi in vessel lumen.

Aneurisms Permanent, abnormal dilatation of a blood vessel due to weakening of the wall of the vessel. Aorta and its major branches. Less frequently: Large muscular arteries.

Complications: Alterations of blood flow distally Thrombosis and embolism Rupture Compression of adjacent structures

True aneurism: Composed of all layers of vessel. False aneurism: Traumatic rupture of vessel, and formation of blood-filled cavity by adventitial tissues.

 Atherosclerotic  Syphilitic  Dissecting  Berry  Mycotic

Atherosclerotic aneurism: Encroachment of atheroma on media  weakening of wall. Most common aneurism in Western World. Abdominal aorta, usually infrarenal. Rarely thoracic aorta, femoral / popliteal arteries. Males > 60 years. Mural thrombi  may embolise. Obliteration of branches of aorta  ischaemic effects.  Risk of rupture when > 6cm  intra-abdominal / retroperitoneal haemorrhage.

Syphilitic aneurism Complication of syphilitic aortitis (tertiary syphilis). > 50 years. Obliterative arteritis of vasa vasorum  aortitis  aneurism. Thoracic aorta. Aortic valvular incompetence, cardiac failure. Large (15 – 20cm). Compression of bronchus, oesophagus.

Dissecting aneurism Aetiopathogenesis: Degeneration of elastic and muscular tissue of the media of thoracic aorta ('medionecrosis'). Idiopathic. Some cases associated with Marfan’s syndrome or coarctation of the aorta. Higher incidence in pregnancy. Many patients are hypertensive. Intimal tear  blood enters the aortic wall.

Complications: Rupture: - into mediastinum - into pericardial sac (cardiac tamponade) - back into aorta  'double-barrelled aorta'. Encroachment on branches of aorta (coronary, renal, carotid arteries) with ischaemic effects.

Berry aneurisms Small saccular lesions of circle of Willis. Develop at sites of congenital weakness of media, at bifurcations of arteries. Rupture: -  Risk with hypertension. - Subarachnoid haemorrhage.