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Diseases of The Blood Vessels
Prepared by
DR. MARUF RAZABased on
Robbins and Cotran, 8th.
DISEASES OF BLOOD VESSELS
By two principal mechanisms:
Narrowing or complete occlusion of the lumen.
Weakening of the walls leading to dilatation or rupture.
STRUCTURE/HISTOLOGY
HYPERTENSIVE VASCULAR DISEASE
Essential Hypertension
Secondary Hypertension
Accelerated or Malignant Hypertension
Types and Causes of Hypertension
Essential Hypertension• 90% to 95% of cases• Gene defects affecting aldosterone metabolism• Mutations affecting sodium reabsorption
Secondary Hypertension• Organic or other identifiable causes
Malignant Hypertension
Secondary Hypertension Renal
Acute glomerulonephritisChronic renal diseasePolycystic diseaseRenal artery stenosis
EndocrineAdrenocortical hyperfunctionExogenous hormonePheochromocytomaAcromegalyThyroidism (Hypo and Hyper)Pregnancy-induced
CardiovascularCoarctation of aortaPolyarteritis nodosa (or other vasculitis)
Neurologic
Renal Mechanism of Blood Pressure Control
Renin Angiotensin Mechanism
GFR (Increases reabsorption of NA)
Vascular Relaxing Factor (NO, PG)
Natriuretic Factors (Inhibit NA reabsorption)
Arteriosclerosis
Arteriosclerosis means “hardening of the arteries” with arterial wall thickening and loss of elasticity.
Arteriolosclerosis affects small arteries and arterioles.
Monckeberg medial sclerosis characterized by calcific deposits in muscular arteries.
Atherosclerosis.
ATHEROSCLEROSIS
It is the intimal lesion called atheroma that protrude into vessel lumen
Arteries commonly affected:• Abdominal aorta• The coronary arteries• The popliteal arteries• The internal carotid arteries• Vessesle of the circle of willis.
Risk Factors for Atherosclerosis
Major
Nonmodifiable Increasing age Male gender Family history Genetic abnormalities
Potentially Controllable Hyperlipidemia Hypertension Cigarette smoking Diabetes
Lesser, Uncertain, or Nonquantitated
Nonmodifiable Obesity Physical inactivity Stress ("type A" personality) Postmenopausal estrogen deficiency High carbohydrate intake
Potentially Controllable Alcohol Lipoprotein Hardened (trans)unsaturated fat intake
Pathogenesis of Atherosclerosis
Composition of Atheromatous PlaqueCells: Smooth muscle, Macrophages, T cellsECM: Collagen, Elastic fibres, ProteoglycansLipids: Intra and Extracelluar
Complication/Fate/Consequences
Complication of Atheromatous Plaque
Rupture, Ulceration or Erosion
Hemorrhage into the plaque
Atheroembolism
Aneurysm formation
Aneurysm
Localized abnormal dilatation of a blood vessels
True AneurysmInvolves intact arterial wall or wall of heart
Atherosclerotic, Syphilitic aneurysm.
False Aneurysm
Defects in the vascular wall leading to extravascular haematoma
Ventricular rupture after Myocardial Infarction
VASCULITIS
Vasculitis Is the vessel wall inflammation.
Mostly involves small vessels, from arterioles to capillaries to venules
Classification Large vessel vasculitis
Giant cell arteritis
Takayasu arteritis
Medium vessel Vasculitis
Polyarteritis nodosa
Kawasaki disease
Small vessel Vasculitis
Wegener Granulomatosis
Microscopic Polyangitis
Vascular Tumors
Benign NeoplasmsHemangioma
Capillary hemangiomaCavernous hemangiomaPyogenic granuloma (lobular capillary hemangioma)
LymphangiomaGlomus tumor
Intermediate-Grade NeoplasmsKaposi sarcomaHemangioendothelioma
Malignant NeoplasmsAngiosarcomaHemangiopericytoma
Further Reading
Wegener Granulomatosis Thromboangitis Obliterance(Burger
Disease) Hemangioma Thrombophlebitis and Phlebothrombosis
Thank You All
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