systemic hypertension hypertension (ht) = pathologically blood pressure blood pressure:systolic...
Embed Size (px)
Hypertension (HT) = pathologically blood pressure
Blood pressure : Systolic /diastolic pressure
Normal blood pressure (adults) : < 140 mm Hg/90 mm Hg
Borderline HT : 140 - 160 mm Hg/90 - 95 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
- Production of a variety of vasodepressor or
antihypertensive substances (prostaglandin, NO).
• Renal diseases may cause systemic HT.
• HT may cause renal damage.
Essential vs secondary HT
Benign vs malignant HT
• Essential HT
90 - 95% of cases.
Pathogenetic mechanisms multifactorial and poorly
• Secondary HT
5 - 10% 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).
- Adrenocortical hyperfunction/tumour (Cushing,
- Exogenous glucocorticoids
- Coarctation of aorta
- Increased intracranial pressure
- Acute stress
Pathogenetic factors in essential HT
Arterial blood pressure
= cardiac output (*)
peripheral vascular resistance (**)
Blood pressure will rise if either (*) or (**)
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
- Sensitivity of some individuals to a high salt
- High prevalence in blacks.
- moderate increase in blood pressure.
- long clinical course.
- little clinical effects in early stages.
- diastolic pressure > 130 mm Hg
- severe impact on cardiovascular system,
kidneys and central nervous system.
- May arise in previously normotensive individuals, but
more commonly as a complication of benign HT.
- Relatively uncommon (1-5% of hypertensive
- Aggressive treatment is required.
Complications of systemic HT
- 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.
- Accelerated atherogenesis.
- risk of developing aortic dissecting aneurism.
- 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.
- 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
Ischaemic sclerosis of glomeruli and
Proteinuria and microscopic haematuria,
especially in malignant HT .
Inflammation of blood vessel walls.
Types I, II, III and IV hypersensitivity reactions may contribute to the inflammation.
• Associated with autoimmune diseases/
The inflammation of the blood vessel walls may lead to:
- Thrombus formation in vessels with ischaemic
- Fragility of small vessels with petechial
haemorrages (skin and other organs).
- Weakening of vessel wall, with aneurism
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.
- Aneurism of aortic arch in tertiary syphilis.
- Involvement of coronary ostia myocardial
- Fibrosis of valve cusps aortic insufficiency.
B. Polyarteritis nodosa (PAN)
• Medium to small arteries.
• Segmental lesions.
• Immune complex disease (type III hypersensitivity
• 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.
- Reactions to certain infections
- Foreign proteins ('serum sickness')
- Drugs (aspirin, penicillin, sulphonamides)
- Auto-immune diseases
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
• 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
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.
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.
• Alterations of blood flow distally
• Thrombosis and embolism
• Compression of adjacent structures
Composed of all layers of vessel.
Traumatic rupture of vessel, and formation of blood-filled cavity by adventitial tissues.
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.
• Complication of syphilitic aortitis (tertiary syphilis).
• > 50 years.
• Obliterative arteritis of vasa vasorum
• Thoracic aorta.
• Aortic valvular incompetence, cardiac failure.
• Large (15 – 20cm).
• Compression of bronchus, oesophagus.
• Degeneration of elastic and muscular tissue of the
media of thoracic aorta ('medionecrosis').
• 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.
- 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.
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 .