systemic hypertension hypertension (ht) = pathologically blood pressure blood pressure:systolic...

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 .