Vascular Structure & Arteriosclerosis Flashcards

Question

What is structure of Atherosclerosis?

Answer 1

1. Fibrous Cap (Top purple-pink layer) What it is: A protective “lid” made of: * Smooth muscle cells * Macrophages (immune cells) * Foam cells (lipid-filled macrophages) * Collagen & elastin (fibrous proteins) * Lymphocytes (immune cells) * Neovascularization (tiny new blood vessels) Why it matters: * This cap tries to contain the plaque underneath. * If it ruptures, the contents can spill into the blood and trigger a clot (thrombus) → leads to heart attacks or strokes. ⸻ 2. Necrotic Center (Yellow, mushy middle) What it contains: * Dead cells * Cholesterol crystals * Foam cells (macrophages stuffed with fat) * Cell debris * Calcium deposits Why it matters: This is the core of the plaque — messy, inflammatory, and dangerous. * It’s full of things that irritate the vessel wall. * If exposed (from a cap rupture), it strongly activates blood clotting. ⸻ 3. Media (Bottom layer with wavy black line) What it is: The muscular middle layer of the artery. Why it matters: * Atherosclerosis mainly affects the intima (inner layer), but it can also damage the media, weakening the vessel wall. * Over time, you can lose smooth muscle cells, making the artery less flexible. * If this plaque ruptures, it can cause a thrombus (clot) to suddenly form. * That can completely block an artery, leading to myocardial infarction (heart attack) or stroke.

Answer 2

🧠 Here’s the progression: 1. Endothelial injury/dysfunction → starts the whole process. 2. Lipid accumulation (LDL sneaks into the intima). 3. Inflammation kicks in → monocytes come in, become foam cells. 4. Fatty streaks form (earliest visible sign). 5. Smooth muscle cells migrate & proliferate. 6. Fibrous cap forms over a lipid core → now this is called a classic atheroma. ⸻ 🔹 So technically: * Atheroma = the specific type of plaque that develops during the later stages of atherosclerosis. * Atherosclerosis = the disease process that leads to atheroma formation. 🧬 Clinical context: * A patient “has atherosclerosis” → means they have developed one or more atheromas. * When a plaque ruptures or blocks flow → we usually mean a complicated atheroma. - involves large and medium sized arteries abdominal aorta, coronary artery, popliteal artery, and internal carotid artery are commonly alfected.

Answer 3

Hypertension It is a major risk factor, probably because it causes vessel wall damage due to increased pressure. Increases the risk of IHD by 60% Hyperlipidemia Hypercholesterolemia is major risk factor LDL transports cholesterol to peripheral tissue whereas HDL transports cholesterol from the periphery to the liver for excretion in bile. Hence high levels of HDL correlates with reduced risk Cigarette smoking One or more packs of cigarette /day increases the risk of ischemic heart disease to 70% to 80% Diabetes mellitus – induces hypercholesterolemia and marked increase in the risk of atherosclerosis 🧠 Step 1: Understand Insulin’s Normal Role in Lipid Metabolism Under normal (non-diabetic) conditions, insulin helps regulate lipid metabolism: * It inhibits lipolysis (fat breakdown) in adipose tissue. * It promotes fat storage and lipoprotein lipase (LPL) activity, helping clear triglycerides from the blood. * It helps the liver handle cholesterol and fat more effectively. ⸻ 🚨 Step 2: In Diabetes (Especially Type 2), Insulin Function Is Impaired * Insulin resistance = cells don’t respond well to insulin. * This means insulin can’t inhibit lipolysis, so fat breakdown goes unchecked. * That leads to more free fatty acids (FFAs) in the blood. ⸻ ⚙️ Step 3: Liver Overload & Dyslipidemia With all those free fatty acids: * The liver turns FFAs into triglycerides and VLDL (very-low-density lipoprotein). * This increases circulating VLDL and LDL (bad cholesterol). * At the same time, HDL (good cholesterol) often goes down. ⸻ 🔬 Step 4: Abnormal Lipid Profile in Diabetes This is called diabetic dyslipidemia, and it typically shows: * ⬆️ Triglycerides * ⬆️ VLDL * ⬆️ Small, dense LDL (which is more atherogenic) * ⬇️ HDL So even if total cholesterol isn’t extremely high, the type of lipids present are particularly damaging to blood vessels. ⸻ 💥 End Result: Hypercholesterolemia & Atherosclerosis Risk * High levels of LDL and low HDL accelerate atherosclerosis. * Small dense LDLs are more likely to penetrate the endothelium, get oxidized, and start plaque formation.

Answer 4

* Increasing age– progresses with age and manifests in middle age (40- 60years) * Gender – * Males are at increased risk. * Premenopausal women are relatively protected except if they are associated with hypertension, hyperlipidemia and diabetes * After menopause females also have increased risk. * Genetic factors- family history and familial clustering of other established risk like hypertension or diabetes or hyperlipidemia

Answer 5

🧠 Atherosclerosis in Simple Steps 🟡 Step 1: LDL (Low-Density Lipoprotein) enters the intima * LDL is a type of cholesterol that normally travels in the bloodstream. * If there’s damage or dysfunction in the endothelium (the inner lining of blood vessels), LDL can sneak into the intima (the innermost layer of the artery wall). ⸻ 🔥 Step 2: LDL gets oxidized * Once inside the intima, LDL gets oxidized — like it’s getting rusty. * Oxidized LDL is harmful and acts like a distress signal. ⸻ 🧲 Step 3: Inflammation is triggered * Oxidized LDL attracts immune cells: * Monocytes (a type of white blood cell) cross the endothelium and enter the vessel wall. * They turn into macrophages (big eaters). ⸻ 🍔 Step 4: Foam cell formation * The macrophages engulf (eat) the oxidized LDL. * When they eat too much, they turn into foam cells — these are the hallmark of early atherosclerotic plaque (fatty streaks). ⸻ 💣 Step 5: Cytokine release and smooth muscle involvement * Foam cells and other immune cells release cytokines (chemical messengers). * These cytokines: * Promote inflammation * Stimulate smooth muscle cells to migrate from deeper layers into the intima * Encourage more plaque buildup ⸻ 🧱 Eventually: Plaque Formation * Over time, a plaque forms, made of: * Foam cells * Cholesterol * Cell debris * Smooth muscle * A fibrous cap that covers it all ⸻ 🧬 Side Notes from the Slide: * LDL brings cholesterol into tissues (bad when it ends up in artery walls). * HDL removes cholesterol from tissues and returns it to the liver for excretion (this is why HDL is “good cholesterol”). ⸻ 🔑 Key Point: Atherosclerosis is a chronic inflammatory response to oxidized LDL in the artery wall — it’s not just about cholesterol being high, but also how your body responds to it.

Answer 6

🧱 First, what are smooth muscle cells (SMCs)? * They are muscle cells found mainly in the media layer (the middle layer) of your blood vessels. * Their job is to contract and relax to control blood pressure and flow. ⸻ 🏃🏽‍♀️ What does “migrate into the intima” mean? * Your blood vessel has layers: 1. Intima = inner lining 2. Media = middle layer (where SMCs usually live) 3. Adventitia = outer layer * During atherosclerosis: * The immune system and damaged cells release cytokines and growth factors (chemical messengers). * These signals tell smooth muscle cells in the media: “Hey, something’s wrong! Come up here to help!” * So the SMCs migrate upward into the intima — the layer where the plaque is forming. ⸻ 🛠️ Why do they move there? Once in the intima, the smooth muscle cells: * Multiply (proliferate) * Make extracellular matrix (collagen, proteoglycans, etc.) * Help form the fibrous cap over the atherosclerotic plaque ⸻ 🧠 Why is this important? * The fibrous cap helps stabilize the plaque. * But too much smooth muscle and matrix can also narrow the blood vessel, contributing to stenosis (blockage). ⸻ Summary: “Stimulate smooth muscle cells to migrate into the intima” means the smooth muscle cells move from their usual place in the media into the inner lining of the artery, where they contribute to the plaque structure and healing response — but can also make things worse by narrowing the vessel.

Answer 7

🧪 1. Endothelial Injury – The Trigger What causes it? * Smoking * High blood pressure (hypertension) * High cholesterol (especially LDL = “bad cholesterol”) * Diabetes What happens? * The endothelium (the smooth inner lining of blood vessels) gets injured. * This damage makes the vessel wall leaky and dysfunctional. ⸻ 🛠 2. Endothelial Dysfunction * Increased permeability: LDL cholesterol can now leak into the vessel wall (intima). * White blood cells (monocytes) stick to the endothelium and move into the wall (called adhesion and emigration). ⸻ 🧟 3. Monocytes → Macrophages * Once inside, monocytes turn into macrophages (the body’s clean-up crew). * These macrophages get activated and start gobbling up the LDL. ⸻ 🧴 4. Foam Cell Formation & Smooth Muscle Involvement * Macrophages and smooth muscle cells both start eating the LDL. * They fill up with fat and become foam cells — a key part of the fatty streak. * Meanwhile, growth factors like PDGF (platelet-derived growth factor) and FGF (fibroblast growth factor) are released. * These signals recruit smooth muscle cells from the deeper layer (media). * Smooth muscle cells migrate into the intima and proliferate (multiply). ⸻ 🟡 5. Fatty Streak → Fibrofatty Atheroma * Now you have a visible fatty streak: a yellowish line under the endothelium. * Smooth muscle cells make extracellular matrix (ECM) like collagen → helps build a fibrous cap over the lipid core. * Over time, this becomes a fibrofatty plaque (atheroma). ⸻ 🧭 6. Collateral Circulation in Slow Plaques * If this process happens slowly, the body may grow new blood vessels (called collaterals) to help reroute blood around the blockage. * This is protective, and why some people with slow plaque buildup may not feel symptoms until late.

Answer 8

💢 Atherosclerosis: Step-by-Step 1. Normal Artery * A healthy artery has: * A lumen (the open space where blood flows) * Endothelium (the thin inner lining of the vessel) * Smooth muscle in the wall (provides structure and control of diameter) ⸻ 2. Endothelial Dysfunction * This is the first step toward disease. * Caused by things like: * Smoking * High blood pressure * High cholesterol * Diabetes * The endothelium becomes damaged, and starts to act abnormally: * Becomes “leaky” * Allows LDL cholesterol to slip into the wall * Expresses signals that attract monocytes (a type of white blood cell) ⸻ 3. Fatty Streak Formation * Monocytes enter the vessel wall and turn into macrophages. * These macrophages eat up the oxidized LDL and become foam cells (fatty, bloated cells). * The collection of foam cells forms a fatty streak — a flat yellow lesion. * These fatty streaks are common even in teenagers and are the earliest visible lesion of atherosclerosis. ⸻ 4. Smooth Muscle Migration * In response to injury and inflammation, growth factors like PDGF and cytokines cause smooth muscle cells (SMCs) to: * Leave their usual place in the deeper wall layer (media) * Migrate into the intima (inner wall layer) ⸻ 5. Fibrous Plaque Formation * The migrated SMCs: * Proliferate (multiply) * Produce extracellular matrix (ECM) like collagen * This forms a fibrous cap over the fatty core. * You now have a mature atherosclerotic plaque, which: * Narrows the lumen (reducing blood flow) * Can rupture, causing clots (→ heart attack or stroke)

Answer 9

Increased total cholesterol and decreased HDL cholesterol -

Answer 10

🧠 Atheroma: Key Points 🔴 What is it? * Pathognomonic lesion of atherosclerosis — meaning it’s the defining feature. * A raised focal lesion located in the intima (innermost layer) of an artery. * Appears as a necrotic, yellow, soft core of lipids (mainly cholesterol and cholesterol esters). * Covered by a white, firm fibrous cap (mainly collagen) → This cap stabilizes the plaque. ⸻ 🧬 Composition of an Atheroma 1. Cells: * Smooth muscle cells (migrated from deeper layers) * Macrophages (turned into foam cells after engulfing LDL) * Lymphocytes and other leukocytes (inflammatory role) 2. Extracellular Matrix (ECM): * Collagen * Elastic fibers * These form the fibrous cap that covers the lipid core 3. Lipids: * Intracellular lipids (within foam cells) * Extracellular lipids (in the necrotic lipid core) ⸻ 📍 Where do atheromas form? * Elastic arteries (e.g., aorta, carotid, iliac) * Large & medium-sized muscular arteries (e.g., coronary, popliteal) These are the vessels most affected by high pressure and turbulence, which explains why they’re common sites for atherosclerosis.

Answer 11

🔬 What are they? Foam cells are: * Macrophages (or sometimes smooth muscle cells) that have engulfed large amounts of oxidized low-density lipoprotein (oxLDL). * Called “foamy” because under a microscope, their cytoplasm appears bubbly or foamy due to the accumulation of lipid droplets. ⸻ 🧪 How do they form? 1. Endothelial injury (from smoking, hypertension, diabetes, etc.) makes the vessel wall permeable. 2. LDL particles enter the intima and become oxidized. 3. Monocytes are attracted to the site and migrate into the intima → they differentiate into macrophages. 4. These macrophages engulf oxLDL using scavenger receptors. 5. As they fill with lipids, they turn into foam cells. ⸻ 🧱 Why are they important? * Foam cells are the earliest visible lesion of atherosclerosis → they make up the fatty streak. * They secrete inflammatory cytokines, which: * Attract more immune cells * Stimulate smooth muscle cell migration and proliferation * Eventually contribute to the necrotic core of an atheroma when they die. ⸻ 🔁 Summary: Foam cells = macrophages full of oxidized LDL → early building blocks of atherosclerotic plaques.

Answer 12

🧠 Key Points from the Slide Title: “Stenosis of medium-sized vessels” 🔹 Stenosis = narrowing of blood vessels due to plaque buildup (atheroma), which limits blood flow. ⸻ 📍 Conditions by Vessel Type 1. Peripheral vascular disease (PVD) * Affects lower extremity arteries (e.g., popliteal artery). * Symptoms: Claudication (pain in legs when walking), poor wound healing, cold limbs, limb ischemia. * Seen in the legs → as shown in the bottom left image of the slide. 2. Angina (coronary arteries) * Coronary artery stenosis limits blood supply to the heart. * Stable angina: chest pain with exertion. * Unstable angina: chest pain at rest; may indicate an impending heart attack. 3. Ischemic bowel disease (mesenteric arteries) * Involves mesenteric arteries (blood supply to the intestines). * Causes abdominal pain after eating, weight loss, and in severe cases, bowel infarction. Atherosclerotic stenosis of medium-sized arteries causes major clinical syndromes like leg pain (PVD), chest pain (angina), and abdominal pain (bowel ischemia) due to reduced oxygen delivery to tissues ** There are no symptoms until there is 70% stenosis!

Answer 13

You’re asking about plaque rupture, especially at the “neck” of an atheroma, and how that triggers a thrombotic cascade, ultimately leading to myocardial infarction (MI) or stroke. ⸻ 🧠 Understanding Plaque Rupture at the Neck ✅ Key Terms * Fibrous cap: The protective covering over the atheromatous core. * Necrotic core: Soft, lipid-rich center of the plaque filled with cholesterol, dead cells, and debris. * Plaque neck: Thinnest and most vulnerable part where the fibrous cap is weakest — prone to rupture. ⸻ 🧨 Step-by-Step Process: Plaque Rupture & Thrombosis 1. Plaque growth over time * Cholesterol builds up in the intima. * Inflammation recruits macrophages, forming foam cells. * A necrotic lipid core develops, with a thin fibrous cap over it. 2. Weakest Point: The Neck * The “neck” is the thinnest part of the cap, under high shear stress. * Chronic inflammation weakens it further (macrophages release MMPs → degrade collagen). 3. Rupture of Fibrous Cap * The cap breaks open, especially at the neck. * This exposes the thrombogenic necrotic core to the bloodstream. 4. Thrombotic Cascade is Triggered * Platelets stick to exposed material. * Tissue factor (TF) from the core activates the coagulation cascade. * Rapid clot formation (thrombus) occurs on top of the ruptured plaque. 5. Occlusion of Vessel * The thrombus can partially or fully block the artery. * Depending on the site: * Coronary artery → MI (heart attack) 🫀 * Cerebral artery (e.g., MCA) → Stroke 🧠

Answer 14

A thrombus is: * A solid mass of blood components (fibrin, platelets, red/white cells), * That forms inside a blood vessel or the heart, * While the person is alive, * And it adheres to the vessel wall. So, while it is a blood clot, the term “thrombus” is more specific: It refers to a pathological (abnormal) clot that can block blood flow and cause disease like MI or stroke. * Thrombus = pathological → can obstruct blood flow. * If it breaks off, it becomes an embolus, which can travel and block other vessels. ⸻ 🔁 Quick Recap: A thrombus is a specific type of blood clot that forms inside a vessel, is pathological, and can lead to serious conditions like MI, stroke, or DVT.

Answer 15

1. Endothelial Injury * Damage to the inner lining of a blood vessel (endothelium). * Most important factor in arterial thrombosis. * Causes: * Atherosclerotic plaque rupture * Hypertension * Trauma * Surgery * Smoking 👉 Why it matters: When the fibrous cap ruptures (like at the neck of a plaque), the necrotic core is exposed. This triggers platelet activation and the coagulation cascade, leading to thrombus formation — and potentially a myocardial infarction (MI). ⸻ 2. Abnormal Blood Flow * Either stasis (sluggish flow) or turbulence. * Stasis → mostly in veins (e.g., deep vein thrombosis - DVT). * Turbulence → mostly in arteries (e.g., around plaques or valve defects). 👉 Slowed or disturbed flow brings platelets in contact with endothelium more frequently and prevents natural anticoagulants from working effectively. ⸻ 3. Hypercoagulability * Increased tendency for blood to clot. * Inherited (e.g., Factor V Leiden, Protein C deficiency) or acquired (e.g., cancer, pregnancy, oral contraceptives, COVID-19). 👉 These conditions tip the balance toward clotting, even without vessel injury.

Answer 16

🔹 1. Necrotic Core Exposure (Plaque Rupture) * A mature atherosclerotic plaque has a lipid-rich, necrotic core (dead cells, cholesterol). * It is normally covered by a fibrous cap. * Rupture at the plaque “neck” (usually the weakest point) exposes the necrotic core to the blood. ⸻ 🔹 2. Platelet Adhesion * The necrotic core contains collagen, tissue factor, and other pro-thrombotic materials. * When exposed to blood, platelets immediately stick (adhere) to this area. * Platelets then activate and release chemicals to recruit more platelets. ⸻ 🔹 3. Coagulation Cascade Activation * Tissue factor from the necrotic core activates the coagulation cascade. * This leads to conversion of fibrinogen → fibrin, forming a fibrin mesh over the platelets. ⸻ 🔹 4. Thrombus Formation * The result is a thrombus (blood clot) made of: * Platelets * Fibrin * Red blood cells * This partially or completely blocks the artery, stopping blood flow. ⸻ 🚨 End Result: * If this happens in a coronary artery → Myocardial infarction (heart attack) * If in a cerebral artery → Stroke

Answer 17

🧠 1. Early Atheroma (Early Lesion) * Stage: Early * Features: * Starts with endothelial dysfunction (e.g., from high LDL, smoking, hypertension). * LDL cholesterol accumulates in the intima → becomes oxidized. * Monocytes → macrophages → foam cells form (from eating oxidized LDL). * A fatty streak begins to form. ⸻ 🛡️ 2. Stabilized Plaque (Stable Plaque) * Stage: Late but not dangerous (yet). * Features: * Thick fibrous cap (protective layer over the lipid core). * Small lipid pool. * Fewer inflammatory cells. * Lumen is preserved (still enough blood flow). * Risk: Low risk of rupture. * Clinical consequence: Can cause chronic symptoms like angina (stable). ⸻ ⚠️ 3. Vulnerable Plaque (Unstable Plaque) * Stage: Late and dangerous. * Features: * Thin fibrous cap (easily ruptures). * Large lipid pool. * Many inflammatory cells (macrophages, T cells). * Releases enzymes that weaken the cap. * Risk: High risk of rupture → thrombosis. * Clinical consequence: Can cause acute MI or stroke. ⸻ 💥 4. Plaque Rupture with Thrombosis * If a vulnerable plaque ruptures, the necrotic core is exposed. * Platelets adhere → thrombus forms → artery gets partially or totally blocked. * Leads to myocardial infarction (heart attack) if in coronary artery. ⸻ ✅ Healed Rupture * Sometimes, a plaque ruptures but doesn’t completely block the vessel. * Healing leads to a fibrotic scar, but causes narrowing of the lumen (chronic ischemia possible).

Answer 18

Plaque rupture with embolization happens mainly in arteries affected by atherosclerosis, where fatty plaques build up inside the vessel walls. Here’s why cholesterol clefts appear in this context: 1. Plaques contain cholesterol crystals: Atherosclerotic plaques have a core made of lipids, including cholesterol in crystal form. 2. Plaque rupture exposes the core: When the plaque’s fibrous cap breaks (ruptures), the inner core—rich in cholesterol crystals—gets exposed to the bloodstream. 3. Cholesterol crystals are released: Some of these crystals can break off or embolize (travel downstream as tiny particles). 4. In tissue samples, cholesterol crystals dissolve during processing: So under the microscope, instead of seeing the crystals themselves, pathologists see cholesterol clefts—the empty spaces left behind after the crystals dissolve. In short: The cholesterol clefts are the microscopic evidence of where cholesterol crystals were in the ruptured plaque and embolized material. In simple terms: When pathologists see cholesterol clefts in embolized tissue, they know “this came from a ruptured plaque.”

Answer 19

* When the wall weakens (due to damage or disease), it can balloon out — this ballooning is called an aneurysm. * Aneurysms are dangerous because they can rupture, causing severe bleeding.

Answer 20

1. Atherosclerosis starts in the intima: * Plaques form in the intimal layer, where lipids, inflammatory cells, and smooth muscle cells accumulate. * The intima is normally very thin, so when plaques develop, they thicken this layer. 2. Plaque grows and affects underlying layers: * As the plaque enlarges, it can compress or distort the media (the middle muscular layer). * The phrase “plaque is thicker than the remaining media” means the plaque mass in the intima is bigger than the thickness of the media next to it. * Sometimes, especially in severe disease or aneurysms, the media becomes thinned, damaged, or atrophied due to the disease process. 3. Why mention the media? * Pathologists compare the plaque thickness to the media thickness to emphasize how much the plaque is growing. * In aneurysms, the media is often weakened or lost, which is why the plaque’s size relative to the media matters. ⸻ Summary: * The plaque itself is in the intima (where atherosclerosis happens). * The media underneath can become thinned, damaged, or compressed. * Saying the plaque is thicker than the remaining media highlights the extent of disease and wall weakening. An aneurysm is a localized, abnormal dilation (ballooning) of a blood vessel wall. Think of it like a weak spot on a worn-out tire that bulges outward. Over time, if that bulge gets too large, it can burst (rupture) — which is very dangerous, especially in large vessels like the aorta. ⸻ ✅ Why does an aneurysm happen? The key reason is weakening of the vessel wall, especially the media layer, which is responsible for giving the artery its strength and elasticity. ⸻ ✅ What is the media and why is it important? The media is the middle layer of the artery wall. It contains smooth muscle cells and elastic fibers — these give the artery strength and allow it to stretch and recoil. * When the media is healthy, the vessel can withstand pressure. * When the media is damaged or thinned, the wall becomes weak and can bulge outward, forming an aneurysm. ⸻ ✅ So, why is the media weakened or lost in atherosclerosis-related aneurysms? 1. Inflammation: Chronic inflammation from atherosclerosis leads to the release of enzymes that break down the media’s elastic tissue and muscle. 2. Ischemia of the media: The vasa vasorum (tiny blood vessels that supply the outer parts of large arteries) can be blocked by plaque. That starves the media of nutrients and oxygen, leading to degeneration. 3. Mechanical stress from the plaque: Large plaques press on and distort the underlying media. 4. Proteolytic enzymes: Macrophages in plaques release enzymes (like matrix metalloproteinases) that degrade the extracellular matrix of the media. ⸻ 🧠 Bottom line: * Aneurysm = bulging of artery wall due to loss or weakening of the media. * Atherosclerosis plays a key role by damaging the media indirectly, even though it starts in the intima.

Answer 21

🔹 1. Atherosclerotic Stenosis * Stenosis means narrowing of the blood vessel. * As the plaque enlarges, it narrows the vessel lumen, restricting blood flow. * This can lead to chronic ischemia (reduced oxygen delivery) to tissues, such as: * Angina (chest pain from coronary artery narrowing) * Claudication (leg pain from peripheral artery disease) ⸻ 🔹 2. Acute Plaque Changes These are dangerous and sudden events involving the plaque surface: * Rupture: Fibrous cap tears, exposing inner contents. * Ulceration or erosion: Damage to the plaque surface. * This exposes thrombogenic material (like collagen and lipids) to blood → triggers thrombosis (clot). * The resulting clot can fully or partially block the vessel, causing: * Myocardial infarction (heart attack) * Stroke * Sudden cardiac death ⸻ 🔹 3. Hemorrhage into Plaque * Bleeding inside the plaque can occur if: * The fibrous cap ruptures * Fragile new blood vessels (from neovascularization) within the plaque burst * This leads to a hematoma, which expands the plaque, further narrowing the artery. ⸻ 🔹 4. Atheroembolism * When a plaque ruptures, debris (cholesterol crystals, necrotic material) can break off into the bloodstream. * These microemboli travel to smaller vessels, where they block blood flow, causing tissue damage. * Under the microscope, cholesterol clefts may be seen in embolized tissue — a hallmark of atheroembolism. ⸻ 🔹 5. Aneurysm Formation * Long-standing atherosclerosis damages the media (middle layer of vessel wall): * Ischemia from blocked vasa vasorum * Inflammation and matrix degradation * This causes loss of elastic tissue → wall weakens → vessel balloons out (aneurysm). * Risk: Rupture, which can be life-threatening (especially in the aorta). ⸻ 🔹 6. Calcification * Over time, dystrophic calcification can occur in plaques. * This is the deposition of calcium salts in damaged or necrotic tissues, even when blood calcium is normal. * It makes arteries harder and less flexible (like in peripheral artery disease or “hardening of the arteries”).

Answer 22

“Steal” Concept: * Blood is stolen from the brain (via the basilar and vertebral arteries) and diverted into the arm. * This leads to vertebrobasilar insufficiency (reduced blood flow to brainstem/posterior brain). Symptoms (due to vertebrobasilar ischemia): These often occur with arm exertion: * Dizziness / Vertigo * Ataxia (loss of coordination) * Visual disturbances * Syncope (fainting) * Confusion, aphasia * Headache * Motor deficits (e.g., weakness) * Arm claudication (pain or fatigue with arm use) * Arm weakness, especially on the side of the occlusion

Answer 23

- narrowing of small arterioles 1. hyaline 2. hyperplastic

Answer 24

What is Arteriosclerosis? Arteriosclerosis is a general term that means “hardening of the arteries.” It refers to thickening, hardening, and loss of elasticity of arterial walls. This process reduces the ability of blood vessels to expand and contract, which can impair blood flow. It can affect small, medium, or large arteries and is commonly associated with aging, hypertension, and vascular disease.

Answer 25

1. Atherosclerosis * Affects: Large and medium-sized arteries (e.g., aorta, coronary, carotid arteries) * Cause: Accumulation of lipids, cholesterol, inflammatory cells, and fibrous tissue in the intima (innermost layer) * Forms plaques that narrow the vessel and may rupture, leading to heart attacks, strokes, and aneurysms 📌 Key feature: Atheromatous plaque with lipid core and fibrous cap 🔬 Complications: Thrombosis, embolism, aneurysm, stenosis ⸻ 2. Arteriolosclerosis * Affects: Small arteries and arterioles, especially in hypertension and diabetes * Has two subtypes: * Hyaline arteriolosclerosis: pink, glassy thickening of arteriolar walls (seen in benign hypertension or diabetes) * Hyperplastic arteriolosclerosis: concentric, “onion-skin” thickening (seen in malignant hypertension) 📌 Key feature: Thickening of arteriolar walls → narrowed lumen → ischemia 🔬 Seen in: Kidneys, retina, and other small vessels ⸻ 3. Monckeberg Medial Calcific Sclerosis (less clinically significant) * Affects: Medium-sized muscular arteries * Calcification of the media layer (not the intima), usually no narrowing of the lumen * Often an incidental finding in elderly patients on X-ray

Answer 26

* Appearance: Homogeneous, pink, glassy (hyaline) thickening of the arteriolar wall seen under the microscope. * Cause: Leakage of plasma proteins and increased extracellular matrix from smooth muscle cells. * Associated with: * Benign hypertension * Diabetes mellitus * Effect: Narrowing of the lumen → reduced blood flow → ischemia (e.g., in the kidneys → nephrosclerosis) * Benign hypertension is chronic and mild-to-moderate. * Over time, the constant elevated pressure causes: * Leakage of plasma proteins into the vessel wall * Increased matrix production by smooth muscle cells * This results in slow, progressive thickening of the arteriolar wall with hyaline (glassy pink) material. ✅ It’s a slow process, so organs suffer from gradual ischemia (e.g., chronic kidney disease).

Answer 27

* Appearance: “Onion-skin” concentric, laminated thickening of arteriolar walls (due to smooth muscle cell proliferation and basement membrane duplication). * Associated with: * Malignant hypertension (severe, rapidly progressive) * Effect: Markedly narrowed lumen → acute ischemia → can lead to fibrinoid necrosis and acute organ damage (e.g., kidneys) * Malignant hypertension is severe and rapid-onset, with very high BP (often >180/120 mmHg). * The intense pressure triggers: * Proliferation of smooth muscle cells * Duplication of basement membranes * This leads to onion-skin-like concentric thickening, which rapidly narrows the lumen. * It may also cause fibrinoid necrosis (vessel wall death due to pressure and inflammation). ❗ Because it’s so sudden, it causes acute organ damage — especially in the kidneys (→ acute renal failure), brain (→ encephalopathy), or retina (→ papilledema, hemorrhages).

Answer 28

* Smooth muscle cells are normally found in the tunica media (middle layer) of arteries and arterioles. * In hyperplastic arteriolosclerosis, due to very high blood pressure (malignant hypertension), these cells: * Multiply rapidly (proliferate) * Lay down more layers of themselves and basement membrane * This creates multiple concentric layers around the lumen → “onion-skin” appearance on histology. ⸻ 🧪 Why does this happen? * Malignant hypertension causes: * Mechanical stress on vessel walls * Endothelial injury * Growth signals that tell smooth muscle cells to proliferate and repair the damage * But instead of normal healing, this leads to excessive, maladaptive wall thickening ⸻ 🔁 Consequence: * The lumen narrows dramatically, reducing blood flow * Can also lead to fibrinoid necrosis if the pressure is extremely high * End result = acute end-organ ischemia (especially in kidneys, brain)

Answer 29

🔬 What happens in hyaline arteriolosclerosis? * The walls of small arteries and arterioles become thickened with homogeneous pink (hyaline) material. * This material is made of: * Plasma proteins that leak into the vessel wall * Increased extracellular matrix from smooth muscle cells * The vessel lumen becomes narrowed. ⸻ 🧠 So what’s the consequence? When the lumen narrows, less blood can flow through the arteriole. Over time, this causes chronic underperfusion (ischemia) of the tissues that depend on that blood supply. ⸻ 🔻 End-organ ischemia means: Organs like the kidney, brain, retina, and heart get less oxygen and nutrients. Examples: * Kidney: Glomerular ischemia → chronic kidney disease (nephrosclerosis) * Brain: Small vessel disease → lacunar infarcts → vascular dementia * Retina: Retinal microvascular damage → visual changes * Heart: Reduced perfusion → myocardial ischemia ⸻ ⚠️ Why is this dangerous? * The process is slow and silent, but over years, it leads to irreversible tissue damage and organ failure.

Answer 30

🩺 Malignant Hypertension (rapidly progressive, very high blood pressure is Hyperplastic). * Consequence: Acute ischemic injury → acute renal failure (malignant nephrosclerosis). ⸻ Why? * In malignant hypertension, there is: * Severe, sudden elevation of blood pressure * This causes hyperplastic arteriolosclerosis (onion-skin thickening) and fibrinoid necrosis of arterioles in the kidney. * The injury leads to multiple tiny petechial hemorrhages on the kidney surface. * These hemorrhages give the kidney a “flea-bitten” or “pinpoint” appearance grossly. ⸻ Clinical picture: * Rapidly progressive acute kidney injury (acute renal failure) * Symptoms of malignant hypertension (headache, visual disturbances, encephalopathy) * Can lead to malignant nephrosclerosis Why Not Hyaline Arteriolosclerosis for Acute Renal Failure and Flea-Bitten Kidneys? 1. Nature of the Injury * Hyaline arteriolosclerosis causes gradual, chronic thickening of small arterial walls. * This leads to slow narrowing of the lumen and chronic ischemia. * The damage accumulates over years, causing progressive organ dysfunction (like chronic kidney disease), not sudden failure. 2. No Vessel Necrosis or Hemorrhage * Hyaline arteriolosclerosis does not cause: * Fibrinoid necrosis of vessel walls * Acute rupture or bleeding into the kidney cortex * Because of this, you don’t get the tiny petechial hemorrhages (the “flea bites”) on the kidney surface. 3. Clinical Course * Patients with hyaline arteriolosclerosis usually develop slowly progressive renal insufficiency over many years. * This contrasts with malignant hypertension, where the kidney injury is sudden, severe, and accompanied by hemorrhage.

Answer 31

* Fibrinoid necrosis = acute, inflammatory, destructive. Think of it like the vessel wall being ripped apart by pressure or immune attack. * Hyaline arteriosclerosis = slow, passive thickening of the vessel wall from protein seepage and pressure over time. So yes — they are different processes, though both affect arterioles and both can impair blood flow and cause end-organ ischemia.

Answer 32

🩸 When endothelial cells are damaged… 1. Exposure of subendothelial collagen * Collagen is normally hidden under intact endothelium. * Injury (like from hypertension, smoking, or high LDL) exposes it. * This triggers: * Platelet adhesion * Coagulation cascade * Release of inflammatory signals ⸻ 2. Platelets & damaged endothelium release PDGF (Platelet-Derived Growth Factor) * PDGF recruits and activates vascular smooth muscle cells (SMCs) from the media layer. * These SMCs migrate into the intima (the inner layer of the vessel wall). ⸻ 3. Smooth Muscle Cells (SMCs) proliferate and change phenotype * They shift from a contractile to a synthetic phenotype. * They start: * Making extracellular matrix (ECM) — like collagen, elastin, and proteoglycans * Contributing to intimal thickening and fibrous cap formation in atherosclerosis ⸻ 4. ECM (extracellular matrix) builds up * The ECM stabilizes the lesion but also narrows the vessel lumen. * It makes the plaque fibrotic and less elastic. * Excessive ECM contributes to vascular stiffness and ischemia. ⸻ 🧠 Why this matters: This process is central to atherosclerosis, restenosis after angioplasty, and vascular remodeling in chronic hypertension.

Answer 33

🩺 Essential vs Secondary Hypertension 1. Essential Hypertension (a.k.a. Primary Hypertension) * ~90–95% of all hypertension cases * No identifiable single cause * Thought to be due to a combination of: * Genetics * Diet (high salt intake) * Obesity * Sedentary lifestyle * Neurohormonal dysregulation * Renal sodium handling issues ⸻ Pathophysiology of Essential Hypertension: Here’s how it develops step-by-step: 1. Kidneys retain sodium → blood volume increases → ↑ cardiac output 2. Body senses the increased pressure and vasoconstriction kicks in to “compensate” 3. Over time, cardiac output normalizes, but systemic vascular resistance remains elevated 4. Chronic vasoconstriction → structural changes in vessels (arteriolar thickening, decreased compliance) 5. End result = persistently high BP ⸻ 🔁 Where pressure natriuresis fits in: Normally, as BP rises, kidneys should excrete more sodium (pressure natriuresis) → this helps lower blood volume and BP. But in essential hypertension: * The pressure-natriuresis mechanism is impaired. * The kidneys require a higher BP to excrete the same amount of sodium. * This shifts the pressure-natriuresis curve to the right. 🧠 The body maintains a higher blood pressure as the new baseline just to get rid of sodium properly. ⸻ 2. Secondary Hypertension * ~5–10% of hypertension cases * Caused by an identifiable underlying condition

Answer 34

❄️ What is Raynaud’s Phenomenon? Raynaud’s is a vasospastic disorder that affects small arteries and arterioles, typically in the fingers and toes. It causes episodic color changes in response to cold or stress: 1. White (pallor) – vasoconstriction, ↓ blood flow 2. Blue (cyanosis) – prolonged lack of oxygen 3. Red (hyperemia) – reperfusion as vessels relax ⸻ 🔵 Primary Raynaud’s Phenomenon * Also called Raynaud’s disease or idiopathic Raynaud's * No associated underlying disease * Most common type (especially in young women) * Usually symmetric, mild, and non-progressive * Normal nailfold capillaries * Negative ANA and other autoimmune markers ⚠️ Complications: * Rarely leads to tissue damage or ulcers ⸻ 🔴 Secondary Raynaud’s Phenomenon * Occurs secondary to another disease, often autoimmune * More severe and may cause ulceration, ischemia, or gangrene * Often asymmetric or one-sided * Abnormal nailfold capillaries may be visible (with capillaroscopy) * Positive autoimmune labs are common (e.g., ANA, anti-centromere) 💡 Common associated diseases: * CREST syndrome (a limited form of systemic sclerosis) * Calcinosis * Raynaud’s phenomenon * Esophageal dysmotility * Sclerodactyly * Telangiectasia * Systemic sclerosis * Lupus (SLE) * Mixed connective tissue disease * Rheumatoid arthritis * Sjögren’s syndrome * Vasculitides

Answer 35

- hypertension - hyperlipidemia - diabetes mellitus - smoking

Answer 36

- increased plasma renin - unilateral atrophy of affected kidney (due to narrowed renal artery that can be from atherosclerosis, this can lead to hypertension through RAAS activation)

Answer 37

1. atherosclerosis (ELDERLY MALES) 2. Fibromuscular Dysplasia (YOUNG FEMALES)

Answer 38

- thickening of large and medium sized muscular arteries - Renal arteries can develop stenosis - there is a BEADED (string of beads) appearance and can lead to aneurysms or dissections

Answer 39

- calcium deposits in muscular arteries (uterine and radial) - no clinical consequence (Lumen is NOT narrowed) - calcification can be seen in X-ray - this is dystrophic calcificaiton (tissue damange but Calcium levels are normal)

Answer 40

- hypertensive crisis (hyperplastic arteriosclerosis) that is without signs of acute organ damage and with signs of acute organ damage - remember that acute means FAST ONSET, and chronic means benign (takes longer)

Vascular Structure & Arteriosclerosis Flashcards

(65 cards)