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FHHD > Pathology of Heart Disease > Flashcards

Pathology of Heart Disease Flashcards

1
Q

Name 3 types of heart disease

A
  • Ischaemic Heart Disease
  • Valvular Heart Disease
  • Congenital Heart Disease
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2
Q

Describe what ischaemic heart disease is briefly

A

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

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3
Q

Describe the different aetiologies of ischaemic heart disease

A
  • 95% caused by atheroma of the coronary arteries

- Build up of lipid with subsequent mural changes in large and medium sized arteries

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4
Q

Name some of the risk factors of Ischaemic heart disease

A
  • Hypertension
  • hyperlipidaemia
  • smoking
  • diabetes mellitus
  • Age
  • gender
  • familial predisposition
  • obesity
  • insufficient exercise
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5
Q

Describe the pathogenesis of Ischaemic heart disease

A

Following injury to the endothelium:

  • Encrustation (rokitansky) - platelet thrombi formation
  • Imbibition (Virchow) - low grade inflammation leads to increase in plasma filtration
  • Reaction to injury (Ross and Glomset) - increased permeability with smooth muscle accumulation
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6
Q

What are complications that can arise as a result of atherosclerosis

A
  • Calcification
  • Rupture
  • Ulceration
  • Haemorrhage
  • Thrombosis
  • Aneurysm
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7
Q

Ischaemic heart disease is most common in men or women? and at what ages for each gender?

A

More common in men
Men - 55-64 years
Women - 70-80 years

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8
Q

What clinical syndromes can arise as a result of ischaemic heart disease

A
  • Sudden death
  • Myocardial infarction
  • Angina - stable and unstable
  • Chronic Ischaemic heart disease
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9
Q

How can sudden death happen from IHD

A

Due to arrhythmias

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10
Q

What are the symptoms of stable angina and when does it tend to occur

A
  • crushing central chest pain

* occurs after exercise

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11
Q

What causes stable angina and what relieves stable angina

A
  • relieved by rest or vasodilators

* caused by low flow in coronary arteries

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12
Q

What complication can arise from stable angina

A

• may result in minor patchy fibrosis

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13
Q

Describe the clinical features/complications of unstable angina

A
  • sudden onset
  • increasing intensity
  • may progress to MI or sudden death
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14
Q

How does unstable angina respond to rest and drugs

A

• may be unresponsive to rest/drugs

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15
Q

What does acute myocardial infarctions result from

A

Result from acute thromboses due to plaque disruption.

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16
Q

What are the 2 patterns of infarction

A
  • Transmural

- Subendocardial

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17
Q

What part of the heart is affected by transmural infarctions

A

• Whole thickness of myocardium

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18
Q

What causes transmural infarctions

A

• Caused by arterial occlusion

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19
Q

Describe the blood flow in transmural infarctions

A

• flow often re-established but persistent occlusion result in fatal outcome

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20
Q

What wave on an ECG elevates on transmural infarctions

A

the ST wave

STEMI - ST segment elevation myocardial infarction

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21
Q

What part of the heart is affected by subendocardial infarctions

A

Confined to the inner third of the ventricle and well defined area

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22
Q

What causes subendocardial infarctions

A

Caused by rapid lysis of occlusive thrombus

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23
Q

How is the ECG affected by subendocardial infarctions

A

NSTEMI

Non ST elevation on ECG

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24
Q

What parts of the heart does the left main coronary artery branching to the left anterior descending supply

A
  • Anterior LV wall,
  • Anterior 2/3 interventricular septum
  • Anterior RV
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25
Q

What parts of the heart does the left main to the left circumflex coronary arteries supply

A

The Lateral LV

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26
Q

What parts of the heart does the Right coronary artery supply

A
  • Posterior wall LV,
  • Posterior 1/3 IV septum
  • Posterior RV
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27
Q

A blockage in the left main coronary artery causes what kind of Myocardial infarction

A

Massive anterolateral MI

28
Q

A blockage in the left anterior descending coronary artery causes what kind of Myocardial infarction

A

Anteroseptal MI

29
Q

A blockage in the left circumflex coronary artery causes what kind of Myocardial infarction

A

Lateral MI

30
Q

A blockage in the right coronary artery causes what kind of Myocardial infarction

A

Posterior/inferior MI

31
Q

Describe the 2 types of valvular heart disease

A

Stenosis - Failure of valve to open fully preventing forward flow
Regurgitation - failure of valve to close allowing backward flow

32
Q

What is infective endocarditis and what causes it

A

Colonisation of heart valves by infectious agents that requires bacteraemia/septicaemia

33
Q

How does infective endocarditis present itself clinically

A

Fever and changing heart murmurs

34
Q

What are some risk factors (epidemiology) that contributes to Infective endocarditis

A
  • Congenital heart disease
  • Rheumatic heart disease
  • Artificial valves
  • Floppy mitral valve/calcified aortic valve
  • Immunodeficiency
  • Immunosuppression
  • Intravenous drug abuse
35
Q

What complications can occur with congenital heart disease

A

Shunts, obstruction of failure
VSD - ventricular septal defect 33%
ASD - Atrial septal defect 5%

36
Q

What causes can there be for congenital heart disease

A

genetic and environmental influences like drugs and infections e.g. rubella

37
Q

Describe the factors and onset of subacute infective endocarditis

A
  • Background of valvular/congenital heart disease

- Insidious onset

38
Q

What types of organisms can cause subacute IE and name one

A

low virulence organisms e.g. strep viridans

39
Q

Describe the vegetations associated with subacute IE

A

Vegetations less bulky and inflammation less destructive

40
Q

What is a vegetation in the heart

A

an infected mass

41
Q

What do acute IE patient usually have wrong with their heart

A

Nothing lol usually a normal heart

42
Q

What kind of organisms can cause acute IE and name a few

A

Virulent organisms e.g. Staph aureus nd fungi

43
Q

Describe the vegetations associated with acute IE

A

Bulky vegetations with rapid severe necrotising inflammation

44
Q

Describe the morphology of IE

A

Friable, bulky, usually bacteria laden vegetations

  • Single or multiple
  • 1mm to several cms
  • May perforate/erode leaflet
45
Q

What cardiac complications can arise as a result of IE

A

Valvular insufficiency
Valvular stenosis
Myocardial abscess Suppurative pericarditis Dehiscence of artificial valve Emboli to coronary arteries

46
Q

What are the potential systemic embolic complications that can occur with left heart IE

A

Brain
Spleen
Kidneys etc embolisms

47
Q

What are the potential systemic embolic complications that can occur with right heart IE

A

Lungs

Possibly with secondary abscess formation

48
Q

What renal complications can occur with IE

A
  • Embolic infarction
  • Embolic infection (secondary abscesses)
  • Focal glomerulonephritis
  • Diffuse glomerulonephritis
49
Q

What is glomerluonephritis

A

Glomerulonephritis is damage to the tiny filters inside your kidneys

50
Q

Describe what acute rheumatic fever is and how it occurs

A
  • Recurrent inflammatory disease in childhood
  • Follows pharyngeal infection by group A streptococcus
  • Immunologically mediated not direct bacterial invasion
51
Q

What can acute rheumatic fever lead to

A

Chronic valve disease

52
Q

What are the symptoms of acute rheumatic fever

A 
Fever
Migratory polyarthritis (large joints) 
Pancarditis
Subcutaneous nodules
Erythema marginatum
Sydenhams chorea
53
Q

Describe the pathology/histology sorta thing of acute rheumatic fever

A
  • Small friable vegetations on valves (endocardium)

- Microscopy shows: aschoff bodies in myo- and pericardium

54
Q

What are aschoff bodies

A

Small collections of epithelioid macrophages i.e. mini granulomas

55
Q

What are the symptoms of chronic rheumatic fever and how do they occur

A

Stenosis - fibrous scarring of calcification of valves with bridges between commissures

Regurgitation - fibrous scarring of chordae tendinae

56
Q

What changes are there to the heart morphology and histology 0-12 hours after an MI

A

none

57
Q

What changes are there to the heart morphology and histology 12-24 hours after an MI

A

Macroscopic - pale and blotchy

Microscopic - Bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis, intracellular oedema

58
Q

What changes are there to the heart morphology and histology 24-72 hours after an MI

A

Macroscopic - Soft, pale and yellow
Microscopic - Coagulative necrosis with loss of nuclei and striations, beginning of acute inflammatory response with heavy interstitial neutrophil infiltrate

59
Q

What changes are there to the heart morphology and histology 3-10 days after an MI

A

Macroscopic - Soft, yellow-brown with hyperaemic border

Microscopic - Replacement of infarcted area by granulation tissue

60
Q

What changes are there to the heart morphology and histology weeks-months after an MI

A

Macroscopic - White, fibrous scar

Microscopic - Collagenous scar tissue

61
Q

What are the short term complications of an MI

A
  • dysrhythmias/arhythmia (sudden death)
  • cardiogenic shock
  • cardiac rupture – ventricular free wall with haemopericardium
  • septal rupture
  • papillary muscle failure
  • pericarditis
  • DVT
62
Q

What can happen if the mural myocardium ruptures in an MI

A

Blood passes through the ventricular wall into the pericardial sac
Pericardial sac is distended with blood, heart action is impeded and = death

63
Q

What can happen if the papillary muscles rupture in an MI

A

Sudden incompetence of the mitral valve = serious aggravation of cardiac pumping load = acute failure and often death

64
Q

What can happen if the inter ventricular septum ruptures in an MI

A

Rapid combined ventricular failure = death

65
Q

What are the long term complications of an MI

A
  • LV failure
  • aneurysm
  • Dressler’s syndrome (auto-immune)
  • recurrent infarction
  • sudden death/arrhythmia
66
Q

When does chronic rheumatic fever tend to occur

A

after 10 years or more of the acute illness

FHHD (21 decks)

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