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

1. Diseases of The Blood
Vessels
Prepared by
DR. MARUF RAZA
Based on
Robbins and Cotran, 8th.

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.

3. STRUCTURE/HISTOLOGY

4. HYPERTENSIVE VASCULAR
DISEASE
 Essential Hypertension
 Secondary Hypertension
 Accelerated or Malignant Hypertension

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. 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. 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. 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. 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. Risk Factors for Atherosclerosis
Major
Nonmodifiable
 Increasing age
 Male gender
 Family history
 Genetic abnormalities
Potentially Controllable
 Hyperlipidemia
 Hypertension
 Cigarette smoking
 Diabetes

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. Pathogenesis of Atherosclerosis

14. Composition of Atheromatous
Plaque
Cells: Smooth muscle, Macrophages, T cells
ECM: Collagen, Elastic fibres, Proteoglycans
Lipids: Intra and Extracelluar

15. Complication/Fate/Consequences

16. Complication of Atheromatous
Plaque
 Rupture, Ulceration or Erosion
 Hemorrhage into the plaque
 Atheroembolism
 Aneurysm formation

17. Aneurysm
Localized abnormal dilatation of a blood vessels

18.  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

19. VASCULITIS
Vasculitis Is the vessel wall inflammation.
Mostly involves small vessels, from arterioles to
capillaries to venules

20. Classification
 Large vessel vasculitis
Giant cell arteritis
Takayasu arteritis
 Medium vessel Vasculitis
Polyarteritis nodosa
Kawasaki disease
 Small vessel Vasculitis
Wegener Granulomatosis
Microscopic Polyangitis

21. 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

22. Further Reading
 Wegener Granulomatosis
 Thromboangitis Obliterance(Burger
Disease)
 Hemangioma
 Thrombophlebitis and Phlebothrombosis

23. Thank You All