Vascular pathology/ Blood vessels diseases.pptx

Vascular pathology is a subdivision of pathology that focuses on diseases of the blood vessels, including arteries, veins, and capillaries. Understanding vascular pathology is crucial for diagnosing and treating various cardiovascular diseases and conditions.

Types of Vascular Disease
A. Atherosclerosis
- Definition: A chronic inflammatory disease characterized by the buildup of plaques (atheroma) within arterial walls.
- Pathogenesis: Begins with endothelial injury due to risk factors like hypertension, hyperlipidemia, and smoking. This leads to lipid accumulation, inflammatory cell recruitment, and formation of fibrous caps.
- Consequences: Can result in ischemic heart disease, stroke, and peripheral artery disease.

B. Aneurysms
- Definition: Localized dilatation of a blood vessel due to weakening of the vessel wall.
- Types:
- Aortic Aneurysm: Focal dilation of the aorta, can be thoracic or abdominal.
- Berry Aneurysm: Small saccular aneurysms located at the bifurcations of cerebral arteries.
- Complications: Rupture leading to massive hemorrhage, thrombosis, and embolism.

C. Vasculitis
- Definition: Inflammation of blood vessels, which can result in vessel wall damage and disruption of blood flow.
- Types: Includes large-vessel vasculitis (like Giant Cell Arteritis), medium-vessel vasculitis (Kawasaki disease), and small-vessel vasculitis (ANCA-associated vasculitis).
- Symptoms: Can include fever, malaise, weight loss, and specific organ-related symptoms depending on the vessels affected.

D. Thrombosis and Embolism
- Thrombosis: Formation of a blood clot within a blood vessel, which can obstruct blood flow.
- Venous Thrombosis: Often occurs in the deep veins (DVT), leading to complications like pulmonary embolism.
- Arterial Thrombosis: Can lead to acute coronary syndrome or stroke.
- Embolism: A particle (such as a thrombus, fat globule, or air bubble) travels through the bloodstream and lodges in a vessel, causing blockage.

E. Phlebothrombosis and Varicose Veins
- Phlebothrombosis: Formation of a thrombus in a vein without prior inflammation.
- Varicose Veins: Dilated, tortuous veins usually in the lower extremities, resulting from valve insufficiency and increased venous pressure.

Peripheral Artery Disease (PAD)
- Definition: Atherosclerosis of peripheral arteries, leading to decreased blood flow to limbs.
- Symptoms: Claudication (pain during walking), rest pain, and ulceration.

2. Risk Factors
- Lifestyle (smoking, diet, physical inactivity)
- Medical history (hypertension, diabetes, hyperlipidemia)
- Genetic predisposition

3. Diagnosis
- Imaging: Ultrasound (Doppler), CT angiography, MRI angiography, and conventional angiography.
- Blood Tests: Lipid profiles, inflammatory markers, and clotting studies.

1. VASCULAR PATHOLOGY Pathology & Microbiology-II Dr. Aneeka Ehsan (PT)

2. CONTENTS Introduction Blood pressure regulation Arteriosclerosis Atherosclerosis Aneurysms and dissection Vasculitis and its types

3. INTRODUCTION Vessels are the tubes by which blood is distributed to and from the organs. Obstruction or occlusion of vessels leads to ischemia of the organs, which causes cell death (necrosis). The most common cause of obstruction or occlusion of vessels is  arteriosclerosis   (“hardening of the arteries”).

4. BLOOD PRESSURE REGULATION Low blood pressure (hypotension) results in: inadequate organ perfusion, organ dysfunction, and sometimes tissue death. high blood pressure (hypertension) causes: vessel and end-organ damage and is one of the major risk factors for atherosclerosis.

5. ARTERIOSCLEROSIS “Hardening of the arteries”   Causes : high cholesterol, high blood pressure, diabetes, and certain genetic influences. Arteriosclerosis-related disease involving plaque buildup in the coronary, peripheral, or carotid arteries is also known as  atherosclerosis .

6. ATHEROSCLEROSIS A chronic inflammatory condition that involves the buildup of plaque in your arteries. This plaque is made of substances such as cholesterol and fat. Accumulation of plaque -> narrowing of arteries -> decreased flow of oxygen-rich blood to the vital organs.

7. Pathogenesis Endothelial Injury : Damage to the endothelium (inner lining of blood vessels) due to factors like hypertension, high cholesterol, smoking, or diabetes. Lipid Accumulation : LDL cholesterol penetrates the damaged endothelium and accumulates in the intimal layer of the artery. Inflammatory Response : Macrophages migrate to the site, engulfing oxidized LDL particles, and transform into foam cells, leading to local inflammation. Plaque Formation : Accumulation of foam cells, lipids, and other cell debris forms a fatty streak. Smooth muscle cells proliferate and migrate, creating a fibrous cap over the lipid core.

8. Pathogenesis - Plaque Stability and Complications : Plaques can become stable or unstable. Unstable plaques may rupture, leading to thrombosis (blood clot formation) and potentially resulting in heart attack or stroke. - Narrowing of Arteries : As plaques grow, they narrow the arterial lumen, restricting blood flow and causing symptoms such as angina or intermittent claudication. - Calcium Deposits : Over time, plaques may calcify, further stiffening the arteries and contributing to cardiovascular disease.

9. ANEURYSMS AND DISSECTIONS Aneurysm:  A localized bulge in the wall of the aorta due to weakness in the aortic wall. Or, Congenital or acquired dilations of blood vessels or the heart. “True” aneurysms involve all three layers of the artery (intima, media, and adventitia). Dissection:  A tear in the inner lining of the aorta that allows blood to flow between the layers of the aortic wall, creating a false lumen.

10. AORTIC ANEURYSM Abnormal dilation or bulging of the aorta. Types : Thoracic Aortic Aneurysm (TAA) : Located in the chest. Abdominal Aortic Aneurysm (AAA) : Located in the abdomen. Causes : Atherosclerosis, hypertension, genetic conditions, and trauma. Risk Factors : Older age, smoking, family history, high cholesterol, and male gender. Symptoms : Often asymptomatic; potential symptoms include back pain, chest pain, or a pulsating sensation.

11. CLINICAL CONSEQUENCES Rupture : Risk of life-threatening hemorrhage, leading to rapid exsanguination. Pain and Discomfort : Chronic pain or discomfort in the chest, back, or abdomen. Thromboembolism : Potential for blood clots to form, leading to stroke or other organ damage. Compression of Surrounding Structures : This may cause difficulty swallowing, hoarseness, or respiratory issues due to pressure on nearby structures. Progressive Expansion : Risk of growth over time, increasing the likelihood of rupture.

12. AORTIC DISSECTION A serious condition where the inner layer of the aortic wall tears, allowing blood to flow between layers. Types : Stanford Type A : Involves the ascending aorta. Stanford Type B : Involves the descending aorta. Causes : Hypertension, connective tissue disorders (e.g., Marfan syndrome), trauma, and invasive medical procedures. Risk Factors : Same as aortic aneurysms, especially hypertension and family history. Symptoms : Sudden severe chest or back pain, often described as "tearing"; may also include dizziness or a feeling of impending doom.

13. CLINICAL CONSEQUENCES Cardiovascular Complications : Possible aortic rupture, leading to massive internal bleeding. Organ Ischemia : Reduced blood flow to vital organs can cause ischemia, potentially leading to organ failure. Stroke : Increased risk of stroke due to dissection-related emboli. Aortic Regurgitation : Damage to aortic valves can lead to significant heart failure. Life-Threatening Emergency : Requires urgent intervention due to rapid deterioration of the patient's condition.

14. VASCULITIS I nflammation of the blood vessels. Inflammation can cause the walls of the blood vessels to thicken, which reduces the width of the passageway through the vessel. If blood flow is restricted, it can result in organ and tissue damage. Vasculitis might affect just one organ or several. Types include : Large vessels vasculitis Medium vessels vasculitis Small vessels vasculitis

15. TYPES OF VASCULITIS There are many types of vasculitis, and most of them are rare. Giant Cell Arteritis Takayasu Arteritis : Affects the aorta; leads to reduced blood flow. Kawasaki Disease Polyarteritis Nodosa : Affects medium arteries; linked to hepatitis B. Granulomatosis with Polyangiitis : Affects small vessels; respiratory and kidney involvement. Microscopic Polyangiitis : Small vessel vasculitis; causes kidney and lung issues. Eosinophilic Granulomatosis with Polyangiitis : Small vessels; asthma and eosinophilia present. Bechet's Disease : Systemic; recurrent ulcers and multi-system involvement. Hypersensitivity Vasculitis : Reaction to drugs/infections; skin rashes common. Cryoglobulinemic Vasculitis : Small vessels; linked to cryoglobulins and hepatitis C.

16. GIANT CELL ARTERITIS Giant cell arteritis (GCA) is a systemic vasculitis affecting large and medium-sized arteries, primarily the temporal arteries. M ost common in individuals over 50 years old; more prevalent in women. Exact cause unknown; thought to involve an autoimmune response.

17. AUTOIMMUNE RESPONSE Immune Activation : CD4+ T cells activate and infiltrate the walls of arteries. Cytokine Release : Release of pro-inflammatory cytokines (e.g., IL-6, IL-1 β) exacerbates inflammation. Giant Cell Formation : Fusion of macrophages leads to multinucleated giant cells in arterial walls. Endothelial Damage : Inflammation damages the endothelium, causing arterial narrowing or occlusion. Vascular Injury : Results in symptoms like headaches, vision loss, and possible complications (e.g., stroke). Potential Triggers : May include infections, genetic predisposition, and environmental factors.

18. KAWASAKI DISEASE A vasculitis affecting medium-sized arteries, primarily in children. Most common in children under 5 years; more prevalent in boys. Exact cause unknown; hypothesized to involve an autoimmune response post-infection. Complications : Risk of coronary artery aneurysms and myocarditis. Treatment : High-dose intravenous immunoglobulin (IVIG) and aspirin to reduce inflammation and prevent heart complications.

19. PATHOGENESIS Immune System Activation : Triggered by infectious agents ( virus, bacteria) or environmental factors in genetically predisposed individuals. Cytokine Release : Pro-inflammatory cytokines (e.g., IL-1, IL-6) are released, leading to systemic inflammation. Vascular Inflammation : Affects medium-sized arteries, particularly coronary arteries, resulting in vasculitis. Endothelial Damage : Inflammation damages endothelial cells, leading to necrosis and vasculitis. Aneurysm Formation : Severe inflammation can lead to coronary artery dilation and aneurysm formation. Immune Response : Activation of B cells and plasma cells produces antibodies, contributing to ongoing inflammation. Resolution and Sequelae : Incomplete resolution can cause long-term cardiac complications.