Transcript Document

SYSTEMIC HYPERTENSION
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
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
90 - 95% of cases.
Pathogenetic mechanisms multifactorial and poorly
understood.
• 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).
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 .