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Questions and Answers

What are the three main components of atherosclerotic plaques?

The three main components of atherosclerotic plaques are smooth muscle cells, macrophages and T cells; extracellular matrix, including collagen, elastic fibers, and proteoglycans; intracellular and extracellular lipid.

Which of the following is NOT a clinical feature of Takayasu Arteritis?

  • Involvement of the renal arteries leads to systemic hypertension (correct)
  • Involvement of the more distal aorta may lead to claudication of the legs
  • Reduced blood pressure and weak pulses in the carotids and the upper extremities
  • Nonspecific symptoms such as fatigue, weight loss, and fever
  • Ocular Disturbances including visual defects, retinal hemorrhages, and total blindness
  • Pulmonary artery involvement can cause pulmonary hypertension
  • Narrowing of the coronary Ostia may lead to myocardial infarction
  • The balance of collagen degradation and synthesis is altered by inflammation and associated proteases in aneurysm development.

    True

    Which of the following is considered a primary cause of hyperlipidemia?

    <p>Nephrotic Syndrome</p> Signup and view all the answers

    What are the two most important causes of endothelial dysfunction?

    <p>The two most important causes of endothelial dysfunction are hemodynamic disturbances and hypercholesterolemia.</p> Signup and view all the answers

    Which type of aneurysm is also known as a 'pseudo-aneurysm?'

    <p>false aneurysm</p> Signup and view all the answers

    What is the most common cause of death from aortic dissection?

    <p>The most common cause of death from aortic dissection is rupture of the dissection into the pericardial, pleural, or peritoneal cavities.</p> Signup and view all the answers

    Hypertension is a major risk factor for both aortic dissection and atherosclerosis.

    <p>True</p> Signup and view all the answers

    What are the two main classifications of aortic dissections?

    <p>Aortic dissections are generally classified into two types: type A and type B.</p> Signup and view all the answers

    Which of the following is NOT a common complication of an abdominal aortic aneurysm (AAA)?

    <p>Involvement of the renal arteries leading to systemic hypertension</p> Signup and view all the answers

    What is characteristic of 'classic' Kaposi's Sarcoma?

    <p>Seen in older men of Mediterranean descent</p> Signup and view all the answers

    Angiosarcoma can arise in the setting of lymphedema.

    <p>True</p> Signup and view all the answers

    Which of the following is a common complication of varicose veins?

    <p>All of the above</p> Signup and view all the answers

    What are the two main types of vasculitis?

    <p>The two main types of vasculitis are noninfectious vasculitis and infectious vasculitis.</p> Signup and view all the answers

    Which of the following is a classic symptom of giant cell (temporal) arteritis?

    <p>All of the above</p> Signup and view all the answers

    Kawasaki Disease is a self-limited condition primarily affecting children.

    <p>True</p> Signup and view all the answers

    What is the leading cause of acquired heart disease in children?

    <p>Kawasaki disease is the leading cause of acquired heart disease in children.</p> Signup and view all the answers

    Which of the following best describes the primary cause of microscopic polyangiitis?

    <p>Anti-neutrophil cytoplasmic antibodies (ANCAs)</p> Signup and view all the answers

    What is the main cause of noninfectious vasculitis?

    <p>The main cause of noninfectious vasculitis is a local or systemic immune response.</p> Signup and view all the answers

    Which of the following is associated with Wegener granulomatosis?

    <p>All of the above</p> Signup and view all the answers

    Thromboangiitis obliterans (Buerger's disease) is primarily associated with heavy cigarette smoking.

    <p>True</p> Signup and view all the answers

    What is the most serious complication of deep venous thrombosis (DVT)?

    <p>The most serious complication of deep venous thrombosis (DVT) is pulmonary embolism.</p> Signup and view all the answers

    What is the main cause of essential hypertension?

    <p>Idiopathic (unknown)</p> Signup and view all the answers

    Hypertension is a major risk factor for the development of left ventricular hypertrophy and heart failure.

    <p>True</p> Signup and view all the answers

    What is the primary mechanism of action of natriuretic peptides in the heart?

    <p>Natriuretic peptides are released from the heart in response to volume expansion, and they primarily inhibit sodium reabsorption in the distal renal tubules.</p> Signup and view all the answers

    Hyperplastic arteriolosclerosis is more commonly seen in patients with benign hypertension compared to malignant hypertension.

    <p>False</p> Signup and view all the answers

    What is the microscopic finding in hyaline arteriolosclerosis?

    <p>The microscopic finding in hyaline arteriolosclerosis is a thickening of the arteriolar wall with deposition of pink, hyaline material.</p> Signup and view all the answers

    Which of the following is NOT a common manifestation of a superior vena cava syndrome?

    <p>Lower extremity edema</p> Signup and view all the answers

    Study Notes

    Vascular Pathology

    • This is a study of diseases affecting blood vessels.
    • There are various types of blood vessels that have different layers and functions

    Blood Vessel Structure

    • Large Vein: Tunica externa, Tunica media, Tunica intima (endothelium)
    • Medium-Sized Vein: Tunica externa, Tunica media, Tunica intima (endothelium)
    • Venule: Tunica externa, endothelium
    • Elastic Artery: Internal elastic layer, Tunica media, Tunica externa, endothelium, tunica Intima
    • Muscular Artery: Tunica externa, Tunica media (smooth muscle cells), Tunica Intima, endothelium
    • Arteriole: Smooth muscle cells (tunica media), Endothelium, Basement membrane
    • Capillary: Endothelial cells, Basement membrane

    Types of Blood Vessels

    • Large (Elastic) Arteries: Aorta and its branches (common carotid, iliac artery). The media contains elastin for expansion during systole and recoil during diastole, resulting in pulsatile flow.
    • Medium (Muscular) Arteries: Coronary, popliteal, and renal artery. The media is primarily smooth muscle cells, enabling regulation of regional blood flow and pressure.
    • Small Arteries/Arterioles: Composed of smooth muscle cells, these are the principal locations of physiological resistance to blood flow.
    • Capillaries: Have thin walls and slow blood flow; the site of exchange between blood and tissues
    • Venules/Veins: Veins are characterized by larger diameters, lumens and thinner walls. They return interstitial tissue fluid and inflammatory cells to the bloodstream, with potential for disease dissemination.

    Congenital Abnormalities

    • Berry Aneurysms: Occur in cerebral vessels and can cause fatal intracerebral hemorrhage if ruptured.
    • Arteriovenous Fistula: Direct connections between arteries and veins without capillaries. Can lead to intracerebral hemorrhage, high-output cardiac failure (large or multiple fistulas).
    • Fibro muscular dysplasia: Focal thickening of medium- and large-sized arteries (including renal, carotid, splanchnic, and vertebral vessels). The cause is unknown.

    Vascular Diseases:

    • Sclerosis: Hardening of the arteries due to thickening and loss of elasticity.
      • Atherosclerosis: Clinically significant disease of large and medium-sized arteries, characterized by atheroma (plaque) formation. Patches of atherosclerotic disease affect the wall of the vessel and often appear eccentrically on a cross section.
      • Arteriolosclerosis: Affects the small arteries and arterioles, can have Hyaline and hyperplastic variants; most commonly linked to hypertension and diabetes mellitus.
      • Mönckeberg medial sclerosis: Not clinically significant, involves calcification of the walls of muscular arteries, typically involving the internal elastic membrane, most often in older persons.

    Atherosclerosis Theories

    • Insudation hypothesis: Lipid infiltration from plasma.
    • Encrustation hypothesis: Small initial mural thrombi.
    • Monoclonal hypothesis: Smooth muscle cell proliferation from one or two cells.
    • Reaction to injury hypothesis: Smooth muscle cell proliferation due to factors released by platelets and monocytes.
    • Intimal cell mass hypothesis: Smooth muscle cell proliferation.

    Atherosclerosis Risk Factors

    • Constitutional: Genetics (familial hypercholesterolemia) age (more prevalent in the 40s-60s, but can appear younger), gender (males tend to have it earlier in life)
    • Modifiable: Hyperlipidemia (excess cholesterol in blood); high LDL, low HDL. Hypertension, Smoking, Diabetes mellitus.
    • Additional: Inflammation (C-reactive protein), Hyperhomocystinemia, Lipoprotein (a) level

    Atherosclerosis Pathogenesis

    • Endothelial injury and dysfunction, leading to increased vascular permeability
    • Accumulation of lipoproteins (LDL and oxidized forms)
    • Monocyte adhesion to endothelium, followed by migration into the intima to become macrophages then foam cells.
    • Platelet adhesion to the vessel wall, inducing further smooth muscle cell proliferation and ECM production
    • Smooth muscle cell proliferation, extracellular matrix production, and recruitment of T cells (inflammatory cells).
    • Lipid accumulation both extracellular and within cells (macrophages and smooth muscle).

    Vascular Pathologies: Morphology

    • Fatty streaks: Lipid-filled foamy macrophages.
    • Atherosclerotic plaque (fibrolipoid): Intimal thickening with lipid accumulation; form plaques, appear white-yellow.
    • Complicated plaques: Red-brown, ulcerated plaques superimposed by thrombosis, hemorrhage, emboli, or aneurysms

    Aortic Aneurysms

    • An aneurysm is a weakness of vessel wall. Either a true aneurysm (involves wall of artery) or false (pseudo) aneurysm (extravascular hematoma). Common areas include abdominal and thoracic regions.
    • Types: Saccular (outpouching), Fusiform (diffuse dilation),
    • Atherosclerotic aneurysm: Commonly found in abdominal aorta.
    • Causes: Atherosclerosis, hypertension.
    • Other causes: Trauma, Vasculitis, congenital defects, infections, connective tissue disease (Marfan syndrome).

    Pathogenesis of Aneurysms

    • Altered balance of collagen synthesis and degradation due to inflammation and increased proteases like MMPs.
    • Vasoconstriction from atherosclerotic plaque buildup, ischemia, or inadequate connective tissue synthesis (as in Marfan syndrome). These can all lead to progressive weakening and dilation of the vessel wall.

    Classifications by Etiology

    • Congenital, Traumatic, Mycotic, Atherosclerotic, Syphilitic, Idiopathic, inflammatory.

    Aortic Dissections

    • Dissection occurs where blood separates the laminar planes of the vessel's media to form a blood-filled channel.
    • Causes: Hypertension, degenerative changes in the media, connective tissue disorders (Marfan syndrome)
    • Types (Stanford or DeBakey): Proximal (ascending aorta and descending aorta) or Distal (below subclavian artery)

    Complications of Vascular Disease

    • Rupture into cavities (most common cause of death in many cases)
    • Cardinal issues; Myocardial infarction, Cerebrovascular accident, Peripheral vascular disease, Spinal cord damage
    • Others; Hemorrhage, Embolism

    Vascular Tumors (Benign and Malignant)

    • Hemangioma: Common tumor of blood-filled vessels (capillary, cavernous, juvenile hemangiomas). Often spontaneously regress.
    • Lymphangioma: Tumor of lymphatic vessels (simple or cavernous/cystic hygroma).
    • Intermediate grade: Kaposi Sarcoma (caused by HHV-8)
    • Malignant: Angiosarcoma (from endothelial cells).

    Vascular Pathology in Hypertension

    • Hypertensive arteriolosclerosis: Hyaline (commonly due to age related issues) and hyperplastic (usually in malignant hypertension) are the two common forms that involve thickening of the vessel walls.

    Vasculitis

    • Inflammation of vessel walls. Causes include immune-mediated inflammation (immune-complex deposition, ANCA, auto-reactive T cells) or direct invasion by infection.
    • Types: Large-vessel vasculitis (Takayasu arteritis, temporal/giant cell arteritis); Medium-vessel vasculitis (polyarteritis nodosa, Churg-Strauss syndrome, Wegener's granulomatosis); Small-vessel vasculitis (HenochSchönlein purpura, hypersensitivity vasculitis/vasculopathy, microscopic polyangiitis)

    Special Topics

    • Kawasaki Disease: Acute, febrile illness affecting medium-sized arteries, often with coronary artery involvement.
    • Thromboangiitis obliterans: Also known as Buerger's disease, typically found in heavy cigarette smokers.
    • Raynaud phenomenon: Exaggerated vasoconstriction of arteries and arterioles in the extremities.
    • Myocardial vessel vasospasm: Excessive constriction of coronary arteries and myocardial arterioles, may result in MI.

    Other topics

    • Lymphangitis: Infection of lymphatic vessels, leads to inflammation of the vessels and surrounding areas.
    • Lymphedema: Accumulation of fluid in lymphatic tissue

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