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