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BDS2; FHHD > SP3: Pathology of Heart Diseases > Flashcards

SP3: Pathology of Heart Diseases Flashcards

1
Q

What is ischaemic heart disease

A

Spectrum of disorders resulting from an imbalance between myocardial need for oxygen and adequacy of supply

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2
Q

What are the causes of ischaemic heart disease

A

Caused by atheroma of the coronary arteries which narrows the lumen due to lipid build up

By vasculitides and arterial vasospasm

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3
Q

What is atheroma/atherosclerosis

A

The is a disease of large and medium sized arteries where there is a build up of lipid and formation of atheromatous plaques

Children = fatty streaks
Adults = atheromatous plaques
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4
Q

What are the risk factors of ischaemic heart disease

A
  • hypertension
  • hyperlipidaemia
  • smoking
  • diabetes mellitus
  • older age
  • males
  • familial predispositions
  • obesity
  • insufficient excercise
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5
Q

What is encrustation

A

When platelet thrombi over injured endothelium

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6
Q

What is imbibition

A

When there is low grade inflammation leading to increased plasma filtration which means lipids flow into the subendothelial layer and accumilates

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7
Q

Outline the stages of atherosclerosis

A
  1. Turbulence (eddies in blood flow) causes platelets to adhere and dislodge endothelial cells. This increased exposure causes low grade inflammation with oedema.
  2. The fluid builds up in the internal elastic lamina and ruptures the internal elastic lamina
  3. Platelets aggregate and smooth muscle cells from the tunica media migrate through breaks in the internal elastic lamina, proliferate and produce collagen
  4. Smooth muscle cells take up fat and store it as droplets
  5. Smooth muscle cells overloaded with fat burst and release fat droplets
  6. Macrophages take up the fat droplets by phagocytosis
  7. Collagen increases and cellularity decreases this reduces the elasticity of the blood vessel wall (forms a relatively acellular plaque abundant in collagen)
  8. The centre becomes necrotic and calcified and this is the atherosclerotic plaque (vessels from vasa forum grow into this calcified region)
  9. Plaque eventually ruptures - risk of massive thrombus formation due to collagen exposure and stimulation of coagulation factors
  10. Eddies downstream from a plaque stenosis causes platelet thrombus formation and growth causing occlusion of the lumen leaned to a HEART ATTACK
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8
Q

What are the clinical syndromes of IHD

A
  • sudden death due to arrhythmias
  • myocardial infarction
  • angina
  • chronic IHD
  • cardiomegaly leads to heart failure due to accumulated myocardial damage
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9
Q

What is stable angina

A

Crushing central chest pain occurring after exercise relieved by vasodilators caused by low flow in coronary arteries

  • may result in minor patchy fibrosis
  • usually a stable plaque present
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10
Q

What is unstable angina

A

This has a sudden onset and increasing intensity which can also be unresponsive to drugs. It is associated with dynamic type 2 plaque; this could progress to MI or sudden death

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11
Q

What is an acute myocardial infarct

A

Heart attack resulting from acute thromboses due to plaque disruption and has the following patterns of infarction

  • regional transmural
  • regional subendocardial
  • circumferential subendocardial
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12
Q

What causes a regional transmural infarct

A 
Whole thickness of myocardium 
Type 2 plaque with thrombosis 
- most patients have arterial occlusion 
- flow can be re-established 
- persistent occlusion causes fatal outcome
- STEMI
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13
Q

What is a regional subendocardial infarct

A

Inner third of the venticle, well defined area
Rapid lysis of occlusive thrombus
Significant collateral supply to outer ventricle
- NSTEMI

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14
Q

What is a circumferential subendocardial infarct

A

General uderperfusion due to moderate hypotension with vessel disease or severe hypotension and normal vessels
- severe anaemia can also contribute

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15
Q

What are the short term complications of MI

A
  1. Dysrhythmias/arhythmia (sudden death)
  2. Cardiogenic shock (cannot perfuse peripheral organs)
  3. Left ventricular failure
  4. Cardiac rupture - haemopericardium (blood in pericardial sac of heart)
  5. Septal rupture (IV communication impaired)
  6. Papillary muscle failure = incompetence of mitrial and tricuspid valves causing regurgitation
  7. Pericarditis
  8. Mural thrombosis
  9. Deep vein thrombosis
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16
Q

What are the long term complications of MI

A
  1. Left ventricular failure
  2. Aneurysm
  3. Dressler’s syndrome (late onset of autoimmune pericarditis presenting with chest pain)
  4. Recurrent infarction
  5. Sudden death/ arrhythmia
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17
Q

What is stenosis

A

Failure of valve to open fully preventing forward flow - this is due to chronic cusp abnormality

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18
Q

What is regurgitation

A

Failure of valve to close allowing backflow - this is due to abnormality of cusp or supporting structures; acute or chronic

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19
Q

What is infective endocarditis

A

Colonisation of heart valves by infectious agent

  • requires bacteraemia/septicaemia - relevant in periodontitis because dental treatments causing injury to gums can allow bacteria to enter into bloodstream
  • it is predisposed by immunosuppression
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20
Q

What increases the risk of infective endocarditis

A 
Congential heart disease
Rheumatic heart disease
Artificial valves
Floppy mitrial valve/calcified aortic valve
Neutropenia
Immunodeficiency
Immunosupression
IV drug abuse
21
Q

What are the features of subacute IE

A

Has a background of valvular/congenital heart disease

  • insidious onset (gradual)
  • may recover with treatment (antibiotics)
  • low virulence organisms (strep. viridian’s)
  • vegetations are less bulky and inflammation is less destructive in the heart valves
22
Q

What are the features of acute IE

A

This usually occurs with a previously normal healthy heart in the elderly and IVDUs

  • virulent organisms (staph aureus, fungi)
  • high mortality
  • mitrial > aortic&raquo_space; tricuspid
  • bulky vegetations with severe necrotising inflammation
23
Q

What are the cardiac complications with IE

A 
valvular insufficiency 
valvular stenosis (not closing)
myocardial abcess
suppurative pericarditis 
dehiscence of artificial valve 
emboli to coronary arteries
24
Q

What are the systemic embolic complications of IE to the left side of the heart

A

Affects the

  • brain
  • spleen
  • kidneys
25
Q

What are the systemic embolic complications of IE to the right side of the heart

A

Affects the

  • lungs
  • possibly with secondary abscess formation
26
Q

What are the renal complications of IE

A
  • embolic infarction
  • embolic infection (secondary abscesses)
  • focal glomerulonephritis (blood in urine)
  • diffuse glomerulonephritis (blood in urine)
27
Q

What is acute rheumatic fever

A

A recurrent inflammatory disease in childhood following pharyngeal infection by group A streptococcus

  • immunologically mediated (host response)
  • usually resolves but can lead to chronic valve disease
  • small friable vegetations on valves

More common in underdeveloped countries

28
Q

What are aschoff bodies

A

result from inflammation in the heart muscle and are characteristic of rheumatic heart disease; they have many T-lymphocytes, plasma cells, activated macrophages = mini-granulomas; this leads to fibrosis due to thickened valvular tissue

29
Q

What are the symptoms of rheumatic fever

A
  • fever
  • migratory polyarthritis (in large joints)
  • pancarditis
  • subcutaneous nodules
  • erythema marginatum = rash on trunk (upper arms and lips showing red marks)
  • sydenhams chorea = (disorder of nervous systems causing rapid, irregular, and aimless involuntary movements of the arms and legs, trunk, and facial muscles)
30
Q

What is chronic rheumatic fever

A

10< years with acute

  • caused by organisation of endocardial inflammation
  • stenosis via fibrous scarring or calcification of valves with bridges between commissures
  • regurgitation via fibrous scarring of chordae tendinae
31
Q

What is a ventricular septal defect (and atrial)

A

When the left and right ventricles are connected by a hole (same for atrium)

Leads to shunts, obstruction or failure
Risk for infective endocarditis

32
Q

Outline pathogenesis of ischaemic heart disease

A
  1. Encrustation = formation of platelet thrombi over injured endothelium
  2. Imbibition = low grade inflammation leading to increased plasma filtration thus lipid flows into the sub endothelial layer and accumulates
  3. Reaction to injury = increased permeability and smooth muscle accumulation
  4. Monoclonal hypothesis = smooth muscle cels are genetically transformed and undergo proliferation, differentiating into a plaque
33
Q

What are the complications of atheroma formation

A
  1. Calcification
  2. Ulceration
  3. Fissuring
  4. Haemorrhage
  5. Thrombosis
  6. Aneurysm
34
Q

What are the different types of atheromatous plaques

A

Type 1 = static
Type 2 = dynamic
Concentric
Eccentric

35
Q

What happens when the following is the site of infarct:

Left main coronary artery

A

Massive anterolateral MI

36
Q

What happens when the following is the site of infarct:

Left anterior descending

A

Anteroseptal MI

37
Q

What happens when the following is the site of infarct:

Left circumflex

A

Lateral LV MI

38
Q

What happens when the following is the site of infarct:

Right coronary artery

A

Posterior/Inferior MI

39
Q

What macroscopic changes occur in ischaemic heart disease

A 
6-12 hrs = unapparent 
12-24 hrs = pallor
> 24 hrs = defined yellow softened area
5-7 days = red rim 
> 7 days = scar tissue
40
Q

What does the left main coronary artery branch into

A
  1. Left anterior descending (LAD) / Anterior inter ventricular artery (AIV)
  2. Left circumflex
41
Q

What does the left anterior descending / anterior inter-ventricular artery supply

A

Anterior left ventricular wall
Anterior right ventricular wall
Anterior 2/3 inter ventricular septum

42
Q

What does the left circumflex artery supply

A

Left atrium

Lateral walls of left ventricle

43
Q

What does the right coronary artery branch into

A
  1. Posterior descending (PDA) / Posterior inter ventricular artery (PIV)
  2. Acute marginal branch
44
Q

What does the posterior descending artery / posterior inter ventricular artery supply

A

Posterior ventricular walls

45
Q

What does the acute marginal branch supply

A

Myocardium of the right side of heart

46
Q

Two types of infective endocarditis

A

Acute and Subacute

47
Q

Outline morphology of infective endocarditis

A

Friable, bulky, bacteria-laden vegetations
Single/ multiple upto several cm big
May perforate or erode leaflet

48
Q

Outline pathology rheumatic heart disease

A

Small friable vegetations on valves (endocardium)

Aschoff bodies in myo- and pericardium

BDS2; FHHD (26 decks)

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