Congestion and Hemorrhage Flashcards

Question

What is Hyperemia?

Answer 1

- active process where arteriolar dilation (at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow - tissue turns red due to increased delivery of oxygenated blood

Answer 2

- it is a passive process resulting from reduced venous outflow of blood from a tissue - it can be systemic (such as in cardiac failure) or localized in an isolated venous obstruction - congested tissue become cyanotic and become reddish-blue in colour due to red cell stasis and the presence of deoxygenated hemoglobin - edema can happen due to the increased hydrostatic pressure resulting from the congestion

Answer 3

First: What is chronic passive congestion? - This happens when blood backs up into an organ (like the lungs or liver) over a long time. - Usually due to heart failure, where the heart can’t pump blood forward well. - So the blood sits still in the veins of the organ = “passive” congestion. What happens to the tissue? 1. Chronic hypoxia - Because blood is backed up, oxygen can’t get delivered well. - The tissue becomes low on oxygen (hypoxic) for a long time. - This can cause tissue injury and eventually scarring (fibrosis) — this is ischemic damage. 2. Capillary rupture - The tiny blood vessels (capillaries) can burst from the pressure. - This leads to tiny spots of bleeding in the tissue (hemorrhagic foci = small bleeds). 3. Red blood cells leak out - When the capillaries burst, RBCs leave the blood vessels and enter the tissue. 4. Macrophages clean it up - The body sends immune cells (macrophages) to clean up the spilled red blood cells. - These cells break down the hemoglobin from the RBCs and store the iron as hemosiderin. - The iron-filled macrophages are called “hemosiderin-laden macrophages” — a key sign of chronic congestion. Summary — in simple terms: In long-term blood backup (like from heart failure): - The tissue doesn’t get enough oxygen → injury + scarring - Blood vessels may burst → small bleeds - Red blood cells leak out - Macrophages eat up the RBCs → store iron → we see hemosiderin in those cells

Answer 4

💔 What causes this? * Congestive heart failure (CHF) or mitral stenosis makes it hard for blood to flow out of the left side of the heart. * So blood backs up into the lungs, causing chronic pulmonary congestion. 🫁 What happens in the lungs over time? 1. Septa thicken and become fibrotic * The septa are the thin walls between alveoli (air sacs). * When lungs are congested with blood for a long time: * The septa get stretched and damaged * The body responds by laying down scar tissue (fibrosis) * So they look thick and fibrotic (stiff) 2. Red blood cells leak into alveoli * The high pressure in lung capillaries causes tiny capillaries to burst. * Red blood cells leak into the alveoli. 3. Macrophages come in and clean up * These immune cells eat the red blood cells. * As they break them down, they store the iron from hemoglobin as a golden-brown pigment called hemosiderin. 4. These macrophages are called: “Heart failure cells” * Why? Because they’re seen in heart failure. * They sit in the alveoli, loaded with iron (hemosiderin). So in simple words: In chronic heart failure or mitral valve problems, blood gets stuck in the lungs. The pressure bursts small vessels, red blood cells leak into the air spaces, and cleanup cells (macrophages) eat them up. These macrophages store iron from the blood and become heart failure cells. Over time, lung tissue becomes stiff and scarred.

Answer 5

- Hemosiderin-laden macrophages - Hemosiderin deposition causes BROWN induration (spots) in the lung. This shows chronic passive congestion of the lungs due to left sided heart failure - Prussian Blue stain will be (+) because Hemosidrin contains Iron

Answer 6

First: What’s hepatic congestion? * “Hepatic” = liver * “Congestion” = too much blood stuck in the liver * This happens in right-sided heart failure, where the blood backs up into the liver through the central veins (since the heart isn’t pumping it out well) Step-by-step: 1.Blood backs up into the liver (via central vein) 2.This blood spreads into sinusoids (tiny liver blood channels) 3. Sinusoids get swollen (distended) from the pressure 4. Zone 3 (center area) is furthest from oxygen → gets the least oxygen. - So those hepatocytes die = ischemic necrosis You also get bleeding = centrilobular hemorrhagic necrosis 5. Zone 2 (middle cells) get some oxygen, but not enough → They get fatty change (cells swell with fat because they’re stressed) 6.Zone 1 (outer ring) is closest to oxygen → So those cells are mostly okay When blood backs up into the liver (like in heart failure), it puts pressure on the inside parts of the liver lobule. The very center cells (Zone 3) don’t get enough oxygen and die. The middle cells get stressed and fatty, and the outermost ones usually stay normal. The liver ends up swollen and damaged in a patchy way.

Answer 7

Right-Sided Heart Failure: What Happens? 🚫 The Problem: * The right ventricle can’t pump blood effectively into the lungs. * So blood starts to back up before the right heart — that means in the veins that bring blood back to it. Where does that backed-up blood go? It flows backward into the: 1. Superior vena cava (SVC) → → congestion in the head, neck, arms → jugular vein distension, maybe swelling in the face 2. Inferior vena cava (IVC) → → congestion in the lower body → legs and feet swell, and… 3. Hepatic veins → Liver → the liver gets engorged with blood Why the liver is affected: * The hepatic veins drain into the IVC, which leads into the right atrium. * If the right heart is failing, there’s backpressure in the IVC → hepatic veins → liver fills up with blood and gets congested. So yes: * Right heart failure = backup into the venous system * This affects arms, legs, neck, AND the liver * That’s why you get: * Peripheral edema (legs, feet) * Jugular venous distension (JVD) * Hepatomegaly (big, congested liver) * Ascites (fluid in belly due to liver congestion)

Answer 8

What’s happening inside the liver? Remember the liver lobule zones? * Zone 3 (central lobule) — closest to the central vein, farthest from oxygen * These areas are hit hardest when blood flow backs up So what happens over time? 1. Chronic backup of blood into the central veins (because of heart failure) 2. Central parts of the lobules (Zone 3) are always congested with blood 3. Not enough oxygen gets in → cell death (necrosis) occurs in that area 4. Dead tissue shrinks = it becomes slightly depressed 5. Meanwhile, the outer parts of the lobule (Zone 1) are still normal-looking What does it look like? “Nutmeg liver” * On the surface, the liver looks like a cut nutmeg seed * You see: * Dark red-brown spots = congested/dead central areas (Zone 3) * Paler tan areas = healthy outer liver zones (Zone 1) It’s a patchy appearance due to this uneven Chronic right-sided heart failure keeps sending blood backward into the liver. The central parts of the liver lobules drown in blood, die, and shrink, while the outer parts stay okay. This creates a mottled appearance called nutmeg liver — like red and tan spots on the liver surface. flow and damage.

Answer 9

The liver is made of many little hexagon-shaped lobules, each with: * A central vein in the middle (drains blood out of the liver) * Portal triads (portal vein + hepatic artery + bile duct) at the corners (bring blood into the liver) Blood flows from the portal triads → through sinusoids → to the central vein. So: * The central area (Zone 3) gets blood last and has the least oxygen * When blood backs up from heart failure, that area is hit hardest * This leads to cell death (necrosis) around the central vein = central lobular necrosis 👉 Why? Because those cells are starved of oxygen due to poor flow and backup In less damaged zones (like mid-zones or periportal areas), the liver cells don’t die — they get stressed. * Instead of dying, they accumulate fat inside → this is fatty change or steatosis * So you’ll see clear bubbles inside liver cells on microscope slides = lipid droplets

Answer 10

Located at the edge of each lobule and contains: 1. Portal vein (bringing nutrient-rich blood from intestines) 2. Hepatic artery (bringing oxygen-rich blood from aorta) 3. Bile ductule (draining bile out of liver) These three structures make up the portal triad — they’re not as damaged in congestion, because they’re closest to the blood supply

Answer 11

- leaking or extravasation of blood due to vessel rupture

Answer 12

- pinpoint hemorrhage, usually in skin or conjunctiva - 1-2 mm in size - rupture of capillaries - may be produced by microemboli from infected heart valves (bacterial endocarditis): Infected heart valves can release tiny clumps of bacteria and clotted blood (microemboli) into the bloodstream, which travel to small blood vessels (like in the skin, eyes, or nails) and block or damage them, causing capillary bleeding → petechiae. - often associated with clotting disorders or severe infections

Answer 13

- 0.2 to 1.0cm - diffuse superficial hemorrhage - larger than petechae "patches" not "pinpoint" - can be seen in conditions like vasculitis or coagulation disorders

Answer 14

- subcutaneous hemorrhages over 1.0cm to 2.0cm - can be raised or flat - usually from trauma, but not always - most common in arms, legs, thin skin - purple at first, turns green, then yellow before resolving. This is due to the oxidation of bilirubin released from hemoglobin of degraded erythrocytes. example: black eye

Answer 15

* Ecchymosis means blood has leaked under the skin, forming a large discoloration (usually >1 cm). * A bruise is a type of ecchymosis that’s caused by trauma or injury (like bumping into something). So: ✅ Every bruise = ecchymosis ❌ Not every ecchymosis = bruise, because some ecchymoses happen without trauma — like from a bleeding disorder or illness. Example: * You hit your leg → bruise = ecchymosis. * You have low platelets and get random skin discoloration = ecchymosis, but not a bruise.

Answer 16

Bleeding from the nose

Answer 17

- hemorrhage into soft tissue, collection of blood from broken blood vessel - may be from trauma or spontaneous (aneurysm) - usually a larger SINGLE lesion, if it is MULTIPLE think of ecchymosis A hematoma is usually a single, localized collection of blood under the skin or in tissue (like a lump or bump). It often forms in one spot, often after trauma or injury. * Ecchymosis refers to flat skin discoloration from blood leaking under the skin, and when you see multiple patches or spread-out areas, we think of ecchymoses, not just a single hematoma. 🩸 So, “single lesion” makes us think of a localized hematoma, while “multiple lesions” makes us think of scattered ecchymoses, which often suggest a bleeding problem. In short: * Single = hematoma (local lump) * Multiple = ecchymoses (flat patches of bleeding) Subungual = hematoma under nails - hematoma is bleeding (large) in space or tissue

Answer 18

A perirenal hematoma is when blood collects around the kidney (in the space outside the kidney but inside the surrounding capsule). It can happen spontaneously (without trauma), or from injury. What causes spontaneous perirenal hematoma? The most common causes are: 1. Tumor bleeding – especially: * Angiomyolipoma (a benign kidney tumor made of blood vessels, muscle, and fat) * Renal cell carcinoma (a type of kidney cancer) 2. Polyarteritis nodosa – a rare condition where small/medium blood vessels become inflamed and can rupture. What happens during it? * A blood vessel ruptures near the kidney. * Blood leaks out and pools around the kidney. * This causes pain (usually in the flank), and may lead to: * Drop in blood pressure * Visible blood in urine (hematuria) * Shock if bleeding is severe

Answer 19

Vomiting of blood

Answer 20

Coughing of blood

Answer 21

tarr-coloured, partly digested blood in stool Hematochezia - blood bright in stool

Answer 22

Bleeding into joint space

Answer 23

- blood in the pericardial sac around the heart (a form of effusion) - can cause pericardial/cardiac tamponade and death

Answer 24

1. ruptured ventricle after a myocardial infarction 2. aortic dissection (described as tearing/ripping chest pain radiating to the back)

Answer 25

- weakened wall from the death of myocytes and inflammation without established fibrosis can happen most MI - this can cause ventricular rupture 3-7 days most MI, this is why patients are hospitalized for several days afterwards - blood can fill the pericardial cavity once ventricle ruptures or there is an aortic dissection

Answer 26

Cardiac tamponade = fluid (usually blood) builds up in the sac around the heart (pericardium) and squeezes the heart so it can’t pump properly.

Answer 27

What is an aortic dissection? * The aorta is the large blood vessel that carries blood from your heart to your body. * It has three layers. * In an aortic dissection, the inner layer (intima) tears, and blood gets in between the layers, creating a false channel or false lumen. What do you mean by proximal dissection? * A proximal dissection means the tear starts near the heart, usually in the ascending aorta (the first part that comes out of the heart). * This is dangerous, because it’s very close to the heart and the pericardial sac So how does this cause cardiac tamponade? * If the dissection spreads and ruptures through the outer wall of the aorta (the adventitia), it can leak blood into the pericardium (the sac around the heart). * This causes cardiac tamponade — where blood squeezes the heart so it can’t fill or pump properly. What does “post-aortic dissection” mean? * It just means what happens after an aortic dissection. * For example, complications like: * Tamponade * Organ damage * Ongoing high blood pressure * Or even chronic dissection (where the false lumen stays open)

Answer 28

- Passive hyperemia happens due to impaired venous outflow, leading to accumulation of deoxygenated blood in an organ. For example, thrombosis of hepatic veins obstructs blood outflow resulting in passive congestion - Active hyperemia happens with increased arterial blood flow, this can happen bececause of exercise or inflammation and is not associated with venous congestion or thrombosis

Answer 29

- Passive Hyperemia (aka Congestion) * Cause: Impaired venous outflow → blood can’t leave. * Example: Heart failure, venous thrombus. * Mechanism: Blood backs up in the veins and capillaries → accumulation of deoxygenated blood → tissue looks blue-purple (cyanotic), swollen. * Key feature: Passive — due to backup, not demand. - Thrombosis in the Hepatic veins (**Budd-Chiari syndrome)** causes obstruction of blood outflow, leading to passive congestion. - The livers centrolobulars areas are closest to the central veins which suffer most from congestion, leading to sinusoidal dilation, and eventually hepatocyte death and liver fibrosis. - Passive Hyperemia can also include DVT in the legs (obstruction of deep veins) with resulting edema

Answer 30

- often seen in elderly patients after a fall, or patients on anticoagulation therapy - between the dura mater and brain - symptoms: somnolence (drowsiness), headache, confusion, loss of conciousness - caused by tearing of the bridging veins in the brain leading to slow bleeding (unlike arterial fast bleed in epidural hematoma)

Answer 31

- excess blood in vessels due to venous outflow obstruction

Answer 32

- heart failure cells - increased pressure causes RBC to be pushed through vascular wall and engulfed by macrophages - alveoli contain numerous macrophages laden with hemosiderin (HF cells) in chronic passive congestion of lungs due to LS HF

Answer 33

- this is a fluid accumulation in the alveoli that is low in protein and is a result of increased hydrostatic pressure or decreased oncotic pressure in the capillaries - if a patient suffers from MI, that can likely lead to heart failure where LV is not pumping properly. This causes backup of blood in the pulmonary circulation and increasing pulmonary hydrostatic pressure which leaks fluid into the alveoli causing pulmonary edema (pink frothy fluid, crackles). - since the fluid leaks out due to pressure alone (from the HF after MI), and it is not due to inflammation or injury to the alveolar walls, the fluid is TRANSUDATE and not EXUDATE (protein rich). - Transudative pulmonary edema is hallmart of heart failure ***

Answer 34

- exudate is rich in proteins, inflammation or injury, because inflammation causes increased vascular permeability to allow protein leakage - seen in pneumonia or actute respiratory distress syndrome (ARDS)

Answer 35

In heart failure, particularly left-sided or congestive heart failure, both pulmonary edema and pleural effusions can happen at the same time, and they’re both primarily due to the same core issue: Elevated hydrostatic pressure in the pulmonary and systemic circulation. ⸻ 💥 Here’s the connection: 🫁 Pulmonary Edema * Cause: ↑ hydrostatic pressure in the pulmonary capillaries (from blood backing up due to poor left ventricular function). * Effect: Fluid leaks into alveoli → shortness of breath, crackles, hypoxia. 🫁 Pleural Effusion (TRANSUDATIVE / EXUDATIVE) * Cause: That same ↑ hydrostatic pressure affects the pleural capillaries (especially in the parietal pleura) and can also reflect systemic venous congestion. * Effect: Fluid collects in the pleural space, particularly on the right side (for reasons we covered: lymphatic drainage, hepatic ascites, etc.). ⸻ ✅ Bottom Line: In heart failure, pulmonary edema and pleural effusion are both driven by fluid overload from increased vascular pressures — they’re separate spaces, but symptoms often appear together.

Answer 36

- no - acute LV failure after MI causes venous congestion in the pulmonary capillary bed and increased hydrostatic pressure leading to pulmonary edema by Transudation into the alveolar space (bat wing appearance) - neutriphils and fibrin would be seen in acute inflammation (pneumonia) - fibrosis and hemosiderin-filled macrophages (HF cells) will be seen in LONG STANDING LV failure

Congestion and Hemorrhage Flashcards

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