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Diseases of the blood vessels by Dr. Maruf Raza, Assistant Professor of Pathology, Noakhali Medical College

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  1. 1. Diseases of The Blood Vessels Prepared by DR. MARUF RAZA Based on Robbins and Cotran, 8th.
  2. 2. DISEASES OF BLOOD VESSELS By two principal mechanisms:  Narrowing or complete occlusion of the lumen.  Weakening of the walls leading to dilatation or rupture.
  4. 4. HYPERTENSIVE VASCULAR DISEASE  Essential Hypertension  Secondary Hypertension  Accelerated or Malignant Hypertension
  5. 5. 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
  6. 6. Secondary Hypertension  Renal Acute glomerulonephritis Chronic renal disease Polycystic disease Renal artery stenosis  Endocrine Adrenocortical hyperfunction Exogenous hormone Pheochromocytoma Acromegaly Thyroidism (Hypo and Hyper) Pregnancy-induced  Cardiovascular Coarctation of aorta Polyarteritis nodosa (or other vasculitis)  Neurologic
  7. 7. Renal Mechanism of Blood Pressure Control  Renin Angiotensin Mechanism  GFR (Increases reabsorption of NA)  Vascular Relaxing Factor (NO, PG)  Natriuretic Factors (Inhibit NA reabsorption)
  8. 8. 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.
  9. 9. 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.
  10. 10. Risk Factors for Atherosclerosis Major Nonmodifiable  Increasing age  Male gender  Family history  Genetic abnormalities Potentially Controllable  Hyperlipidemia  Hypertension  Cigarette smoking  Diabetes
  11. 11. 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
  12. 12. Pathogenesis of Atherosclerosis
  13. 13. Composition of Atheromatous Plaque Cells: Smooth muscle, Macrophages, T cells ECM: Collagen, Elastic fibres, Proteoglycans Lipids: Intra and Extracelluar
  14. 14. Complication/Fate/Consequences
  15. 15. Complication of Atheromatous Plaque  Rupture, Ulceration or Erosion  Hemorrhage into the plaque  Atheroembolism  Aneurysm formation
  16. 16. Aneurysm Localized abnormal dilatation of a blood vessels
  17. 17.  True Aneurysm Involves 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
  18. 18. VASCULITIS Vasculitis Is the vessel wall inflammation. Mostly involves small vessels, from arterioles to capillaries to venules
  19. 19. Classification  Large vessel vasculitis Giant cell arteritis Takayasu arteritis  Medium vessel Vasculitis Polyarteritis nodosa Kawasaki disease  Small vessel Vasculitis Wegener Granulomatosis Microscopic Polyangitis
  20. 20. Vascular Tumors Benign Neoplasms Hemangioma Capillary hemangioma Cavernous hemangioma Pyogenic granuloma (lobular capillary hemangioma) Lymphangioma Glomus tumor Intermediate-Grade Neoplasms Kaposi sarcoma Hemangioendothelioma Malignant Neoplasms Angiosarcoma Hemangiopericytoma
  21. 21. Further Reading  Wegener Granulomatosis  Thromboangitis Obliterance(Burger Disease)  Hemangioma  Thrombophlebitis and Phlebothrombosis
  22. 22. Thank You All
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