Diseases of Blood Vessels

<p>Cytokine activation (D)</p> Signup and view all the answers

<p>VCAM-1 (B)</p> Signup and view all the answers

<p>Production of LDL (D)</p> Signup and view all the answers

<p>Advanced glycosylation end products (C)</p> Signup and view all the answers

<p>Transforming growth factor beta (TGF-β) (D)</p> Signup and view all the answers

<p>Occurs in the chest portion of the aorta (C)</p> Signup and view all the answers

<p>Pulmonary hypertension (B)</p> Signup and view all the answers

<p>Cerebral aneurysm (A)</p> Signup and view all the answers

<p>Rupture leading to hemorrhage (C)</p> Signup and view all the answers

<p>Increase mean arterial pressure (A)</p> Signup and view all the answers

<p>Increased pulmonary capillary pressure (B)</p> Signup and view all the answers

<p>Femoral arteries (B)</p> Signup and view all the answers

<p>Dissections involve the separation of arterial wall layers (A)</p> Signup and view all the answers

<p>Increased ventricular volume (A)</p> Signup and view all the answers

<p>Development of ascites and fluid build-up (C)</p> Signup and view all the answers

<p>Inhibit sodium reabsorption (D)</p> Signup and view all the answers

<p>Immune complex deposition (B)</p> Signup and view all the answers

<p>Giant cell arteritis (A)</p> Signup and view all the answers

<p>Benign tumors (D)</p> Signup and view all the answers

<p>Diminished coronary perfusion (D)</p> Signup and view all the answers

<p>Even at rest (A)</p> Signup and view all the answers

<p>Ventricular septal defect (VSD) (D)</p> Signup and view all the answers

<p>Malaise (B)</p> Signup and view all the answers

<p>Hyperemic, central yellow-tan softening (D)</p> Signup and view all the answers

<p>Wegner's granulomatosis (C)</p> Signup and view all the answers

<p>Arrhythmias (A)</p> Signup and view all the answers

<p>Coarctation of the aorta (C)</p> Signup and view all the answers

<p>Rupture or fissuring of plaque (B)</p> Signup and view all the answers

<p>Type I Lesion (C)</p> Signup and view all the answers

<p>Neutrophils (C)</p> Signup and view all the answers

<p>Unknown in most cases (A)</p> Signup and view all the answers

<p>Increasing age (A)</p> Signup and view all the answers

<p>Essential hypertension (D)</p> Signup and view all the answers

<p>Large lipid cores (C)</p> Signup and view all the answers

<p>Endothelial injury (B)</p> Signup and view all the answers

<p>Type IV (C)</p> Signup and view all the answers

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

<p>Secondary hypertension (B)</p> Signup and view all the answers

<p>Family history (D)</p> Signup and view all the answers

<p>Stable plaques (C)</p> Signup and view all the answers

<p>Chronic inflammation (C)</p> Signup and view all the answers

<p>Aldosterone (C)</p> Signup and view all the answers

<p>Acute endocarditis leads to destruction of a normal heart valve. (C)</p> Signup and view all the answers

<p>Streptococcus viridans (C)</p> Signup and view all the answers

<p>They are foci of collagen surrounded by lymphocytes. (B)</p> Signup and view all the answers

<p>Chronic RHD leads to valvular thickening and retraction. (A)</p> Signup and view all the answers

<p>Chronic kidney disease (C)</p> Signup and view all the answers

<p>Hypersensitivity reaction to M proteins from streptococci. (D)</p> Signup and view all the answers

<p>Crural ulcer (A)</p> Signup and view all the answers

<p>It reduces deep venous pressure facilitating blood return. (D)</p> Signup and view all the answers

<p>Doppler ultrasound (C)</p> Signup and view all the answers

<p>Inflammation shifts from joint to joint over time (B)</p> Signup and view all the answers

<p>Septic infarcts in distant organs. (A)</p> Signup and view all the answers

<p>Superficial veins. (A)</p> Signup and view all the answers

<p>They are fragile and bulky. (B)</p> Signup and view all the answers

<p>Blood enters deep veins as superficial pressure decreases. (C)</p> Signup and view all the answers

<p>Localized inflammation along cardiac valves. (A)</p> Signup and view all the answers

A specialized lining in blood vessels that controls factors like permeability, coagulation, and blood flow.

Activated endothelial cells contribute to inflammation and blood clotting, while healthy ones prevent these.

A major process in atherosclerosis, it involves the buildup of cholesterol and other substances within the artery walls.

Vascular smooth muscle cells help regulate blood vessel diameter and synthesize important components of the vessel wall.

In response to injury, smooth muscle cells move from the outer layer to the inner layer of the vessel, contributing to the thickening of artery walls.

Blood vessels vary in structure and function based on their location and the demands of the tissue they serve.

Endothelial cells are dynamic and their function can change based on various stimuli, leading to different outcomes for blood vessel health.

Factors that trigger endothelial cell activation include inflammation, lipid products, advanced glycation end products, and viruses.

A buildup of fatty deposits, inflammation, and scar tissue within the inner lining of arteries, leading to narrowing and hardening of the vessels.

The process of atherosclerosis development, involving injury to blood vessel walls, inflammation, and accumulation of lipids.

An atheromatous plaque that has a thick fibrous cap, minimal lipid accumulation, and little inflammation.

An atheromatous plaque that has a thin fibrous cap, large lipid core, and significant inflammation.

The earliest visible lesion of atherosclerosis, characterized by subendothelial lipid-filled foamy cells.

The main components of an atherosclerotic plaque: cells, extracellular matrix, and lipids.

The rupture of a plaque, ulceration, erosion, bleeding into the plaque, thrombosis, or aneurysmal dilatation.

A sustained increase in blood pressure, often asymptomatic, affecting approximately 25% of the population.

Hypertension with an unknown cause, accounting for 95% of cases. It involves multiple factors like genetics and environment.

Hypertension caused by identifiable underlying medical conditions.

The renin-angiotensin system, prostaglandins & nitric oxide (NO), and sodium reabsorption.

A hormone that raises blood pressure by increasing peripheral resistance and blood volume.

A group of hormones that contribute to vasodilation, lowering blood pressure

Retention of sodium by the kidneys, leading to increased blood volume and blood pressure.

A major risk factor for atherosclerosis, heart failure, and kidney failure.

A group of disorders characterized by inflammation of blood vessel walls, often accompanied by systemic symptoms like fever, fatigue, and joint pain.

The process of immune complex deposition, where antibodies bind to antigens, forming complexes that deposit in blood vessel walls, triggering inflammation.

Autoantibodies targeting neutrophils, a type of white blood cell. These ANCAs can damage blood vessels, leading to vasculitis.

Antibodies that target endothelial cells, the cells lining blood vessels. These antibodies can damage the endothelium, contributing to vasculitis.

A type of vasculitis primarily affecting the temporal arteries, characterized by destructive giant cell granulomas.

A type of vasculitis affecting the arteries in the neck, specifically the carotid and subclavian arteries, leading to fibrosis and narrowing of the vessels.

A form of vasculitis affecting medium-sized arteries, often involving the renal arteries. Characterized by necrotizing fibrinous inflammation.

A type of vasculitis primarily affecting young children. It involves the coronary arteries.

A type of vasculitis involving small arterioles, capillaries, and venules. It can be seen in Henoch-Schonlein purpura and Churg-Strauss syndrome.

A type of vasculitis causing destruction, often involving the lungs and kidneys. It can present with granulomas, necrotizing vasculitis, and kidney inflammation.

A type of vasculitis affecting medium and small arteries, particularly the tibial and radial arteries. It's almost exclusively seen in heavy smokers.

Not true tumors but rather dilations of existing blood vessels.

Abnormal growths originating from blood vessels or lymphatic vessels. These tumors can be composed of endothelial cells, which line blood vessels, or other vascular wall cells.

A common type of benign vascular tumor, composed of endothelial cells.

A type of vascular neoplasm with an intermediate degree of malignancy. It can show locally aggressive behavior.

A highly malignant tumor originating from blood vessels. These tumors are solid and often lack regular vessel structures.

A localized, balloon-like bulge in an artery caused by weakening or destruction of the arterial wall.

A tear in the inner lining of an artery, allowing blood to enter the wall and separate the layers.

Aneurysm that occurs in the abdominal portion of the aorta.

Aneurysm that occurs in the chest portion of the aorta (above the diaphragm).

Aneurysms that occur in arteries other than the aorta and brain arteries.

A condition where the heart is unable to pump blood efficiently to meet the body's needs, resulting in fluid buildup and congestion.

The heart's ability to increase its output by stretching its muscle fibers, a temporary solution for heart failure.

The thickening of the heart muscle in response to increased workload, another temporary solution for heart failure.

The body's attempt to maintain blood pressure by activating hormones that constrict blood vessels and retain fluid.

The buildup of fluid in the lungs, a common complication of heart failure, making breathing difficult.

Infective endocarditis is a serious infection of the heart valves or inner lining of the heart caused by bacteria, fungi, or other microbes. It involves the formation of abnormal growths called vegetations on the heart valves, composed of blood clots, inflammatory cells, and the infecting organisms. These vegetations can damage the heart valves, leading to complications like heart failure, stroke, and even death.

Acute endocarditis is a rapidly progressing and severe form of infective endocarditis, typically caused by highly virulent bacteria. It affects previously healthy heart valves and can lead to death within days if not treated promptly.

Subacute endocarditis is a milder form of infective endocarditis that develops more gradually. It usually occurs on pre-damaged heart valves and progresses slowly, allowing for a higher chance of successful treatment.

Predisposing factors for infective endocarditis are conditions or situations that increase a person's risk of developing the infection. These factors include conditions that weaken the heart valves, damage the immune system, or make it easier for microbes to enter the bloodstream.

The most common cause of infective endocarditis is Streptococcus viridans, a type of bacteria commonly found in the mouth. Other common culprits include Staphylococcus aureus, especially in people with already damaged heart valves.

Microbial seeding refers to the process by which microbes enter the bloodstream and reach the heart valves. This can occur through various events like dental procedures, surgery, injections with contaminated needles, or infections in other parts of the body.

Rheumatic heart disease is an autoimmune reaction to a streptococcal infection (usually strep throat). This inflammation can damage the heart valves, potentially leading to chronic heart problems.

Aschoff bodies are characteristic inflammatory lesions found in the heart muscle during acute rheumatic fever. These lesions are composed of swollen collagen fibers surrounded by immune cells.

Pancarditis is inflammation of all three layers of the heart: the pericardium (outer layer), myocardium (muscle layer), and endocardium (inner lining). It can occur during acute rheumatic fever.

Chronic rheumatic heart disease is the long-term consequence of repeated or untreated rheumatic fever. It involves scarring and thickening of the heart valves, causing them to malfunction and leading to various heart problems.

Varicose veins are dilated, twisted, and enlarged superficial veins, primarily affecting the legs. These veins often become visible on the skin's surface.

The venous system is the network of veins that carry deoxygenated blood back to the heart. This system includes both superficial veins, closer to the skin's surface, and deep veins, located deeper within the muscles.

Muscle pumps are mechanisms that help move blood back to the heart, especially in the legs. As muscles contract and relax, they squeeze the deep veins, propelling blood upward against gravity.

Deep vein incompetency is a condition where valves in the deep veins malfunction, allowing blood to flow backward instead of upward. This can lead to blood pooling in the legs and varicose veins.

Venography is a medical imaging technique that uses a contrast dye to visualize the veins, allowing healthcare providers to assess vein health and identify problems like blockages or incompetent valves.