Lecture Content im shit at

Question 1

What is arteriosclerosis?

Answer 1

A group of conditions where arteries become stiff and lose flexibility.

Question 2

What are the 3 main types of arteriosclerosis?

Answer 2

Atherosclerosis, arteriolosclerosis, and Monckeberg’s medial calcification.

Question 3

What are the 3 layers of a blood vessel wall?

Answer 3

Tunica intima (inner), tunica media (middle), tunica adventitia (outer).

Question 4

Which layer is affected in atherosclerosis?

Answer 4

The tunica intima (inner layer).

Question 5

Which arteries does atherosclerosis mainly affect?

Answer 5

Large and medium arteries like coronary, aorta, carotid, femoral, cerebral.

Question 6

What causes atherosclerosis?

Answer 6

High LDL, low HDL, smoking, diabetes, hypertension, poor diet, genetics

Question 7

Is atherosclerosis fast or slow?

Answer 7

Very slow; often develops silently over years.

Question 8

What is the earliest visible change in atherosclerosis?

Answer 8

Fatty streaks (Type II).

Question 9

What is a complicated plaque?

Answer 9

Advanced stage (Type VI) with damage like bleeding, rupture, or clot formation.

Question 10

What happens to monocytes in early plaque formation?

Answer 10

They enter the intima, turn into macrophages, and eat lipids to become foam cells.

Question 11

What role do smooth muscle cells play?

Answer 11

They move into the intima, take up lipids, and help build the plaque.

Question 12

What is a fatty streak?

Answer 12

A buildup of foam cells in the vessel wall—can be reversed early on.

Question 13

What is a fibrous cap?

Answer 13

Collagen and other proteins that form a “shell” over a maturing plaque.

Question 14

What are 4 outcomes of plaque progression?

Answer 14

Calcification – hardened arteries

Cholesterol emboli – bits break off into the blood

Thrombosis – clot formation over plaque

Haemorrhage – bleeding inside the plaque

Question 15

What symptoms come from narrowed arteries?

Answer 15

Chest pain (angina)

Leg pain on walking (claudication)

Brain fog or stroke symptoms

Question 16

What are serious complications of full blockage?

Answer 16

Heart attack (MI)

Stroke

Gangrene (limb death)

Question 17

What vessels are affected in arteriolosclerosis?

Answer 17

Small arteries and arterioles (esp. kidneys, retina, gut).

Question 18

What causes arteriolosclerosis?

Answer 18

Mainly high blood pressure (hypertension), and diabetes.

Question 19

What is hyaline arteriolosclerosis?

Answer 19

Wall thickening due to protein buildup; looks pink and glassy under microscope.

Question 20

What is malignant arteriolosclerosis?

Answer 20

Severe type seen in dangerous high blood pressure → kidney damage, ischemia.

Question 21

What is Monckeberg’s calcification?

Answer 21

Calcium builds up in the tunica media, not the intima.

Question 22

Does it block blood flow Monckeberg’s Medial Calcification?

Answer 22

No—vessel stays open, so usually no symptoms unless paired with atheroma.

Question 23

Who is affected by Monckeberg’s?

Answer 23

Older adults (>50), men and women equally.

Question 24

monckeburgs Which arteries are usually involved?

Answer 24

Medium muscular arteries—like femoral, radial, ulnar.

Question 25

Which lifestyle habits increase risk atherosclerosis?

Answer 25

Smoking, poor diet, no exercise, stress.

Question 26

Which medical conditions increase risk atherosclerosis?

Answer 26

Diabetes, hypertension, obesity.

Question 27

What are harmful blood lipid levels?

Answer 27

High LDL, low HDL.

Question 28

What inflammatory marker is associated?

Answer 28

High C-reactive protein (CRP).

Question 29

What is the role of endothelial cells in healthy arteries?

Answer 29

They form a barrier and regulate blood flow, clotting, and inflammation.

Question 30

How are endothelial cells involved in atherosclerosis?

Answer 30

They become dysfunctional, letting in lipids and allowing immune cells to stick and enter the wall.

Question 31

What happens to LDL in the vessel wall?

Answer 31

It becomes oxidised, which triggers inflammation and attracts immune cells.

Question 32

How do monocytes contribute to atherosclerosis?

Answer 32

They enter the intima, turn into macrophages, and eat oxidised LDL.

Question 33

What do macrophages become when they engulf too much LDL?

Answer 33

Foam cells

Question 34

What do foam cells create in early plaque formation?

Answer 34

Fatty streaks

Question 35

Where do SMCs come from, and what do they do?

Answer 35

From the tunica media; they migrate to the intima and produce collagen, forming the fibrous cap.

Question 36

Can smooth muscle cells also become foam cells?

Answer 36

Yes – they can engulf lipids and contribute to plaque bulk.

Question 37

What is the role of T cells in plaques?

Answer 37

They release cytokines that increase inflammation and can worsen plaque instability.

Question 38

What do fibroblasts do in plaques?

Answer 38

Produce collagen and extracellular matrix, contributing to the fibrous cap.

Question 39

When do platelets become involved in atherosclerosis?

Answer 39

When the fibrous cap ruptures, exposing the lipid core → platelets stick and form a thrombus.

Question 40

What life-threatening event can this thrombus cause?

Answer 40

Heart attack or stroke

Question 41

Are neutrophils always involved in atherosclerosis?

Answer 41

Not early on, but they can appear during plaque rupture, releasing enzymes that worsen damage.

Question 42

What do smooth muscle cells do in plaques?

Answer 42

Move from media into intima Proliferate Take up lipids Produce collagen (→ fibrous cap) Can also become foam cells

Question 43

What do foam cells and dead tissue create inside plaques?

Answer 43

A soft lipid core full of debris and cholesterol.

Question 44

What do fibroblasts and SMCs produce?

Answer 44

Collagen, elastin, and matrix → forms fibrous cap over plaque.

Question 45

What is the first event in plaque formation?

Answer 45

Endothelial dysfunction, often from high BP, LDL, smoking.

Question 46

What does the immune response do next?

Answer 46

Brings in monocytes → foam cells form → fatty streak develops.

Question 47

How does a fatty streak turn into a mature plaque?

Answer 47

Smooth muscle cells migrate + proliferate Fibrous cap forms Foam cells die, forming necrotic core

Question 48

What new structure can form in advanced plaques?

Answer 48

New blood vessels (angiogenesis) to feed the plaque.

Question 49

What is a thrombus?

Answer 49

A blood clot that forms on the surface of a plaque after rupture.

Question 50

How does a thrombus form in atherosclerosis?

Answer 50

The fibrous cap ruptures The lipid core is exposed to blood This activates platelets and clotting, leading to thrombus formation

Question 51

What is the danger of a thrombus?

Answer 51

It can block the artery completely → causes heart attack, stroke, or sudden death.

Question 52

What is an embolus?

Answer 52

A piece of plaque or clot that breaks off and travels through the bloodstream.

Question 53

What happens when an embolus lodges in a smaller vessel?

Answer 53

It causes a blockage (embolism) → can lead to infarction (tissue death).

Question 54

What is a cholesterol embolus?

Answer 54

A small piece of cholesterol crystal or plaque material that breaks off and travels downstream → can damage kidneys, brain, or limbs.

Question 55

What does "superimposed thrombosis" mean?

Answer 55

It means a clot has formed on top of an existing plaque — often the final event before infarction.

Question 56

What are possible clinical outcomes of embolism from an atherosclerotic plaque?

Answer 56

Ischemic stroke (if embolus goes to brain) Renal infarct Acute limb ischemia

Question 57

What is arteriolosclerosis?

Answer 57

Arteriolosclerosis is the thickening and hardening of the walls of small arteries and arterioles, usually due to high blood pressure or diabetes. It reduces blood flow to tissues, especially in organs like the kidneys, retina, and brain.

Question 58

What is oedema?

Answer 58

Accumulation of abnormal amounts of fluid in extravascular and intercellular tissue spaces.

Question 59

What are the two main types of oedema?

Answer 59

Localised and generalised.

Question 60

What regulates capillary fluid exchange?

Answer 60

Blood hydrostatic pressure (BHP), blood osmotic pressure (BOP), interstitial fluid hydrostatic pressure (IFHP), and interstitial fluid osmotic pressure (IFOP).

Question 61

Which pressures cause fluid to leave the capillary?

Answer 61

BHP and IFOP.

Question 62

Which pressures cause fluid to enter the capillary?

Answer 62

BOP and IFHP.

Question 63

What causes increased blood hydrostatic pressure (BHP)?

Answer 63

Impaired venous return (e.g., DVT, heart failure, pregnancy, long flights).

Question 64

How does right ventricular failure cause oedema?

Answer 64

Increases BHP in systemic veins → fluid pushed into tissues.

Question 65

How does left ventricular failure cause oedema?

Answer 65

Increases BHP in pulmonary circulation → pulmonary oedema.

Question 66

What causes decreased blood osmotic pressure (BOP)?

Answer 66

Low albumin due to nephrotic syndrome, liver disease, malnutrition.

Question 67

How does nephrotic syndrome cause oedema?

Answer 67

Proteinuria → hypoalbuminaemia → ↓ BOP → generalised oedema.

Question 68

What increases capillary permeability?

Answer 68

Inflammation, trauma, allergies, anaphylaxis.

Question 69

How can lymphatic obstruction cause oedema?

Answer 69

Impaired drainage → fluid accumulation (e.g., post-surgery, filariasis).

Question 70

How does salt and water retention contribute to oedema?

Answer 70

Activates RAAS → aldosterone → sodium/water retention → increased volume and pressure.

Question 71

What causes generalised oedema?

Answer 71

Systemic issues like low albumin (e.g., starvation, renal or liver disease) or widespread ↑ venous pressure (e.g., congestive heart failure).

Question 72

What causes localised oedema?

Answer 72

Obstruction or inflammation in a specific region (e.g., DVT in one leg, trauma).

Question 73

What is peripheral oedema?

Answer 73

Oedema in dependent parts of the body, e.g., ankles, sacrum.

Question 74

What is pulmonary oedema?

Answer 74

Fluid in alveolar spaces of lungs (often due to LVF), causes dyspnoea and cough.

Question 75

What is cerebral oedema?

Answer 75

Fluid accumulation in brain tissue, may be localised (tumour) or generalised (trauma, encephalitis).

Question 76

What is ascites?

Answer 76

Localised oedema in the abdominal cavity.

Question 77

What is pleural effusion (hydrothorax)?

Answer 77

Localised oedema in the thoracic cavity.

Question 78

What is angioneurotic oedema?

Answer 78

Allergic oedema of skin or mucosa, can obstruct airways and be life-threatening.

Question 79

What is haemostasis?

Answer 79

The physiological process that prevents blood loss.

Question 80

What are the five stages of haemostasis?

Answer 80

Vasoconstriction, platelet plug formation, coagulation, clot retraction, clot dissolution.

Question 81

What is fibrinolysis?

Answer 81

Breakdown of fibrin clot by plasmin to restore blood flow.

Question 82

What is haemorrhage?

Answer 82

Blood loss from the circulation into tissues or externally.

Question 83

What is the difference between internal and external haemorrhage?

Answer 83

Internal stays in the body; external leaves the body (e.g., GI bleed, menstruation).

Question 84

What happens with significant blood loss?

Answer 84

Hypovolaemia → ↓ BP → ↓ cardiac output → organ failure → possible death.

Question 85

What factors influence the outcome of haemorrhage?

Answer 85

Rate of loss, volume lost, site of bleeding.

Question 86

What are signs of hypovolaemic shock?

Answer 86

Dizziness, tachycardia, cold skin, confusion, fainting, low urine output.

Question 87

What causes defects in platelets?

Answer 87

Low count (thrombocytopoenia) or poor function (thrombasthenia) due to drugs, infection, bone marrow issues.

Question 88

What causes vessel wall defects?

Answer 88

Infections, drugs, collagen diseases (e.g., scurvy, SLE), skin diseases.

Question 89

What congenital coagulation disorders cause bleeding?

Answer 89

Haemophilia A (factor VIII), Haemophilia B (factor IX), von Willebrand’s disease.

Question 90

What acquired coagulation disorders cause bleeding?

Answer 90

Liver disease, Vitamin K deficiency, anticoagulants, malnutrition.

Question 91

Define petechiae.

Answer 91

Small pinpoint haemorrhages in skin/mucosa.

Question 92

Define purpura.

Answer 92

Slightly larger areas of bleeding in skin/mucosa.

Question 93

Define haematoma.

Answer 93

Large area of haemorrhage ("bruise").

Question 94

Define ecchymosis.

Answer 94

Large subcutaneous haematoma.

Question 95

Define haemarthrosis.

Answer 95

Bleeding into a joint.

Question 96

Define haemothorax.

Answer 96

Bleeding into the thoracic cavity.

Question 97

Define haemoperitoneum.

Answer 97

Bleeding into the abdominal cavity.

Question 98

Define haemopericardium.

Answer 98

Bleeding into the pericardial cavity → can cause tamponade.

Question 99

What causes colour changes in a bleeding area?

Answer 99

Breakdown of haemoglobin in extravasated (leaked) blood.

Question 100

What colour indicates the presence of oxygenated haemoglobin in tissue?

Answer 100

Bright red.

Question 101

What colour indicates deoxygenated haemoglobin?

Answer 101

Cherry red (or dark red).

Question 102

What colour is associated with bilirubin during haemoglobin breakdown?

Answer 102

Orange-yellow.

Question 103

What colour is associated with biliverdin in tissue?

Answer 103

Greenish.

Question 104

What colour is caused by haemosiderin deposition?

Answer 104

Brownish.

Question 105

What is haemosiderin and what happens to it?

Answer 105

It is the final insoluble breakdown product of haemoglobin; taken up by macrophages.

Question 106

Why does extravasated blood trigger inflammation?

Answer 106

The presence of blood in tissues excites an inflammatory response.