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YR5 Histopathology > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

What is this?

A

Atherosclerosis

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2
Q

What is atherosclerosis?

A

An arteriosclerosis characterized by atheromatous deposits in + fibrosis of the inner layer of the arteries.

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3
Q

What is atherosclerosis characterised by?

A

Intimal lesions- Atheroma (atheromatous plaques) that protrude into vessel lumen.

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4
Q

What is this?

A

Atherosclerosis

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5
Q

What is an atheromatous plaque?

A

Raised proliferation of endothelium

Soft lipid core

White fibrous cap

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6
Q

What are the 7 main risk factors for atherosclerosis?

A

Age

Sex

Genetics

Hyperlipidaemia

HTN

Smoking

Diabetes Mellitus

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7
Q

How do the number of risk factors affect the risk of getting atherosclerosis?

A

2 RFs increase risk 4-fold

3 RFs increase risk 7-fold

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8
Q

What is the pathogenesis of atherosclerosis according to the response to injury hypothesis?

A
  1. Endothelial injury, disrupted flow, increased permeability
  2. LDL accumulation
  3. Monocyte adhesion to endothelium
  4. Monocyte migration into intima -> macrophages + foam cells
  5. Platelet adhesion
  6. Factor release from activated platelets
  7. Induces smooth muscle cell recruitment, proliferation, ECM production + T cell recruitment
  8. Lipid accumulation: extra + intracellular, macrophages + smooth muscle cells
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9
Q

What is this?

A

Atherosclerosis - smooth muscle proliferation

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10
Q

What is a fatty streak?

A

Earliest lesion

Lipid filled foamy macrophages

No flow disturbance

In ~all children >10yrs

Relationship to plaques uncertain

Same sites as plaques

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11
Q

What characterises an atherosclerotic plaque?

A

Patchy: cause local flow disturbances

Only involve a portion of wall

Rarely circumferential

Appear eccentric

Composed of cells, lipid, matrix

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12
Q

What is this?

A

Atherosclerotic plaque

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13
Q

What are 2 consequences of atheromas?

A

Stenosis

Acute plaque changes

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14
Q

What is stenosis?

A

Critical stenosis: demand > supply

Occurs at ~70% occlusion (or diameter <1mm)

Causes “stable” angina

Can lead to Chronic IHD

Acute plaque rupture can occur

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15
Q

What is this?

A

Plaque disruption Type 11 eccentric ragged stenosis

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16
Q

What is this?

A

Normal coronary artery

No atherosclerosis

Widely patent lumen that carries as much blood as the myocardium requires.

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17
Q

What are the acute plaque changes that can occur?

A

Rupture: Exposes prothrombogenic plaque contents

Erosion: Exposes prothrombogenic subendothelial basement membrane

Haemorrhage into plaque: Increase size

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18
Q

What characterises vulnerable plaques?

A

Large lipid core

Thin fibrous cap

Large inflammatory infiltrate

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19
Q

What is the mechanism for a rupture of a vulnerable plaque?

A

Adrenaline increases BP + causes vasoconstriction.

Increases physical stress on plaque.

Hence emotional stress increases risk of sudden death.

Circadian periodicity to sudden death (6am-noon).

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20
Q

How do vulnerable plaques contribute to plaque growth?

A

Not all rupture causes occlusion.

Plaque disruption with platelet aggregation + thrombosis probably common.

Important mechanism for plaque growth.

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21
Q

What can vasoconstriction be due to?

A

Adrenergic agonists

Platelet contents

Reduced endothelial relaxing factors

Mediators from perivascular cells

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22
Q

What is this?

A

Coronary atherosclerotic plaque with a yellow core of lipid separated from the lumen by a fibrous cap.

Opposite core = arc of normal vessel wall

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23
Q

What is ischaemic heart disease?

A

Group of conditions resulting from myocardial ischaemia.

Imbalance of supply to demand for oxygenated blood.

Less nutrients + less waste removal.

Therefore less well tolerated than pure hypoxia.

90% myocardial ischaemia due to reduced blood flow due to atherosclerosis.

Long silent progression prior to Sx

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24
Q

What is this?

A

IHD

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25
What is this?
IHD
26
List 4 presentations of IHD
Angina pectoris Myocardial infarction Chronic IHD with heart failure Sudden cardiac death
27
What is the epidemiology of IHD?
500,000 deaths yearly USA 50% fall in death rate since 1963 (peak) Fall due to prevention + tx But aging population
28
What is the predominant pathogenesis of IHD? What is this due to?
Insufficient coronary perfusion relative to myocardial demand Due to chronic progressive atherosclerotic narrowing of epicardial coronary arteries + variable superimposed plaque change, thrombosis + vasospasm.
29
Where do plaques usually occur in IHD?
1st few cm of LAD or LCX Entire length RCA
30
What is the pathogenesis of acute coronary syndrome?
Stable plaque becomes unstable. Due to rupture, erosion, haemorrhage Generally leads to superimposed thrombus which increases occlusion.
31
What is angina pectoris?
Transient ischaemia not producing myocyte necrosis.
32
What are the different types of angina?
Stable, Prinzmetal, Unstable **Stable** comes on with exertion, relieved by rest, no plaque disruption. **Prinzmetal:** Uncommon, due to artery spasm
33
What is unstable angina pectoris?
Unstable more frequent, longer onset with less exertion/ at rest. Disruption of plaque. Superimposed thrombus. Possible embolisation or vasospasm. Warning of impending infarction.
34
What is a myocardial infarction? What is the incidence?
Death of cardiac muscle due to prolonged ischaemia. 5/1000 yearly UK (STEMI). IHD most common cause death postmenopausal women.
35
What is the pathogenesis of artery occlusion in MI?
Sudden change to plaque Platelet aggregation Vasospasm Coagulation Thrombus evolves
36
What is the myocardial response to an MI?
Myocardial blood supply compromised leading to ischaemia Loss of contractility within 60s Therefore HF can precede myocyte death Potentially reversible Irreversible after 20-30m
37
What are common sites of occlusion in an MI?
**LAD:** 50%, ant wall LV, ant septum, apex **RCA:** 40%, post wall LV, post septum, post RV **LCx:** 20%, lat LV not apex
38
What is the evolution of changes after an MI?
**\< 6h:** Normal histology + CK-MB **6–24h:** Loss of nuclei, homogenous cytoplasm, necrotic cell death. **1-4d:** Infiltration of polymorphs then macrophages (clear up debris). **5-10d:** Removal of debris. **1-2w:** Granulation tissue, new blood vessels, myofibroblasts, collagen synthesis. **Weeks-months:** Strengthening, decellularising scar.
39
What is this?
MI, 3–7 days
40
What is this? What can be seen?
MI 1-3 days. Coagulation necrosis Loss nuclei + striations Neutrophils +++
41
What is this? What can be seen?
MI 10-14 days Granulation tissue Macrophages.
42
What is this? At what time point?
MI \>2 months old Lots of fibrosis + scar formation
43
What are clinical features of an MI?
Common in elderly + diabetes mellitus 10 – 15% asymptomatic Cardiac enzymes (High CK, Troponin) Subendocardial infarct may not cause usual ST changes.
44
What is a reperfusion injury?
Clinical importance uncertain Due to oxidative stress, Ca overload, inflammation Arrhythmias common Biochemical abnormalities last days -\> weeks Thought to cause “stunned myocardium” – reversible cardiac failure lasting several days.
45
What are 7 short term complications of MI?
**Contractile dysfunction → Cardiogenic shock** **Arrhythmia: conduction disturbance- bradycardia, SVT** **Myocardial rupture: LV free wall most common at ~4-5d** **Pericarditis (Dressler syndrome): 2-3d after MI** **RV infarction** **Infarct extension: new necrosis adjacent to old** **Infarct expansion: necrotic muscle stretches → mural thrombus**
46
What is this?
Dressler syndrome
47
What is the mortality associated with an MI?
Total mortality = 30% in 1 year. 3-4% mortality per year after
48
What is chronic ischaemic heart disease?
Progressive heart failure due to ischaemic myocardial damage. May not be have had prior infarction. Can arise with severe obstructive coronary artery disease. Enlarged heavy heart, hypertrophied, dilated LV. Atherosclerosis Maybe mural thrombi Fibrosis
49
What is sudden cardiac death?
Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1hr) after onset of Sx. Usually due to lethal arrhythmia Usually on background of IHD (90%)
50
Which conditions are associated with sudden cardiac death?
Acute myocardial ischaemia is usual trigger. Usually causes electrical instability at sites distant from conduction system often near scars from old MIs. Other conditions also associated e.g. Aortic stenosis, mitral valve prolapse, pulmonary HTN.
51
What is cardiac failure? What are the two types of cardiac failure?
End point of many conditions. Congestive Heart Failure (L+R). * **Left sided:** SOB, pulmonary oedema * **Right sided:** Peripheral oedema
52
What is this?
Pulmonary oedema due to left sided heart failure.
53
What are causes of heart failure?
Ischaemic heart disease Valve disease HTN Myocarditis Cardiomyopathy Left sided heart failure (Right)
54
What are complications associated with heart failure?
Sudden Death Arrhythmias Systemic emboli Pulmonary oedema with superimposed infection
55
What is the histopathology of heart failure?
Dilated heart, Scarring + thinning of the walls. **Microscopy:** Fibrosis + replacement of ventricular myocardium.
56
What are the types of cardiomyopathy?
Dilated Hypertrophic Restrictive (Too thin, too thick, too stiff)
57
What is dilated cardiomyopathy?
Progressive loss of myocytes. Dilated heart.
58
What are causes of dilated cardiomyopathy?
**Idiopathic** **Infective:** Viral myocarditis **Toxic:** Alcohol, chemotherapy (adriamycin, daunorubicin), cobalt, iron **Hormonal:** Hyper-, hypo- thyroid, diabetes, peri-partum (?). **Genetic:** Haemochromatosis, Fabry’s, McArdle’s. **Immunological:** Myocarditis incl. Viral (hypersensitivity component)
59
What is hypertrophic cardiomyopathy?
LV hypertrophy Familial in 50% (AD, variable penetrance) Beta-myosin heavy chain Thickening of septum narrows left ventricular outflow tract.
60
What is restrictive cardiomyopathy?
Impaired ventricular compliance Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis Normal size heart, big atria
61
What is chronic rheumatic valvular disease?
Sequelae of rheumatic fever. Predominantly left-sided valves (almost always mitral). * Mitral \> Aortic \> Tricuspid \> Pulmonary * Mitral alone 48%, Mitral + aortic 42% Thickening of valve leaflet, especially along lines of closure. Fusion of commissures. Thickening, shortening + fusion of chordae tendineae.
62
What is calcific aortic stenosis?
Commonest cause aortic stenosis Occurs in 70-80s. Calcium deposits outflow side cusp impairs opening. Orifice compromised. Outflow tract obstruction.
63
What are causes of aortic regurgitation?
**Rigidity:** Rheumatic, degenerative **Destruction:** Microbial endocarditis **Disease of aortic valve ring:** Results in dilitation. Valve insufficient to cover increased area.
64
What are 4 conditions associated with aortic regurgitation?
Marfan's Syndrome Dissecting aneurysm Syphilitic aortitis Ankylosing spondylitis
65
What are the two main categories of aneurysms?
**True:** All layers wall **False:** Extravascular haematoma
66
What are 4 causes of aneurysms?
Weak wall Congenital e.g. Marfans Atherosclerosis Hypertension
67
Which lipids are good and which are bad?
LDL = BAD HDL = GOOD
68
What 7 less obvious risk factors contribute to atherosclerosis?
Inflammation: pro inflammatory state Metabolic syndrome: HTN, hyperlipidaemia Lipoprotein a: RF for Cerebrovascular + cardiovascular disease Haemostasis: procoagulation Lack of exercise Stress Obesity: HTN, DM, low HDL
69
What is the response to injury hypothesis?
Chronic inflammatory + healing response of arterial wall to endothelial injury.
70
Why are there many asymptomatic potential victims in atherosclerosis?
Majority of plaques show only mild-moderate luminal stenosis prior to acute change
71
How does vasoconstriction contribute to risk of disruption of a vulnerable plaque?
Reduced luminal size increases local mechanical forces
71
How does vasoconstriction contribute to risk of disruption of a vulnerable plaque?
Reduced luminal size increases local mechanical forces
72
Describe the impact of IHD worldwide
Leading cause of death worldwide for M+F (7million/year).
73
In general, what amount of stenosis is required to cause symptoms?
75% = Sx precipitated by exercise Vasodilation cannot compensate above this 90% = pain at rest
74
List 3 long term complications of MI
Ventricular aneurysm → thrombus, HF, arrhythmia Papillary muscle rupture Chronic IHD: progressive late HF
75
What is this? How common is it?
Ventricular aneurysm Very rare
76
What is this?
Papillary muscle rupture

YR5 Histopathology (27 decks)

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