Page 265 - Concise Pathology for Exam Preparation ( PDFDrive )

250 SECTION II Diseases of Organ Systems

Clinical features:
• Presents with headache, dizziness, impaired vision, papilloedema and deranged
renal function
• Urine findings include haematuria and proteinuria
Gross pathology:
• If superimposed on pre-existing benign hypertension, kidneys are small, shrunken
and reduced in size.
• In the pure form, kidneys enlarge and show pin-point petechial haemorrhages on
the cortical surface (flea-bitten kidney) due to rupture of arterioles and glomerular
capillaries.
Microscopic findings:
• Necrotizing arteriolitis: Fibrinoid necrosis, a few acute inflammatory cells and small
haemorrhages
• Hyperplastic intimal sclerosis or onion-skin proliferation: Concentric laminar prolifera-
tion of smooth muscle cells, collagen and basement membrane material
• Ischaemic changes: Tubular loss, fine interstitial fibrosis and foci of infarction

Effects on CNS
• Stroke (cerebral haemorrhage and lacunar infarction)
• Carotid atheromas and transient ischaemic attacks
• Subarachnoid haemorrhage
• Hypertensive encephalopathy (neurological symptoms like disturbances in speech,
vision, paraesthesias, fits and loss of consciousness)
Effects on Retina (Hypertensive Retinopathy)
• Focal spasm of the arterioles followed by progressive sclerosis (arteriolar walls become
opaque with narrow light reflex)
• Chronic hypertension leads to intimal thickening, media wall hyperplasia and hyaline
degeneration of arterioles.
• Severe hypertension causes necrosis of vascular smooth muscle and endothelial cells result-
ing in exudate formation (“soft exudates” are ill-defined and result from microinfarctions;
whereas, “hard exudates” are due to leakage of protein from increased vessel permeability).
• Persistent increased pressure in the arterioles may result in formation of microaneu-
rysms which may rupture leading to ‘flame haemorrhages’.
• Impeded arteriolar circulation results in a compression of venules and ultimately dilata-
tion as arteriole and venous basement membranes are adherent with shared collagen
fibres at the crossing points.
• Development of a depression in the wall of the venule (arteriovenous nicking)
• Papilloedema (swelling of the optic disk)
Keith–Wagener–Barker classification of hypertensive retinopathy
Grade I: focal narrowing of the arterioles, mild arteriovenous nicking
Grade II: arteriole narrowing, copper wiring present, arteriovenous nicking more accentuated
Grade III: arteriole narrowing, silver wiring present, haemorrhages, soft and hard exudates,
disappearance of the vein under the arteriole, disk normal
Grade IV: arterioles are fine fibrous cords; same as grade III except papilloedema is present

Laboratory Work-Up of Essential Hypertension and Its
Consequences
• Heart disease, eg, ECG, chest X-ray for cardiomegaly and ECHO for left ventricular
hypertrophy
• Renal disease, eg, urine analysis, serum blood urea nitrogen (BUN), creatinine, renal
ultrasound and angiography
• Mineralocorticoid excess states, eg, serum electrolytes
• Pheochromocytoma, eg, urinary catecholamines
• Diabetes mellitus, eg, serum glucose
• Lipid abnormalities, eg, lipid profile

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