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Pathology of Heart Disease Flashcards

(66 cards)

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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
What parts of the heart does the left main to the left circumflex coronary arteries supply
The Lateral LV
26
What parts of the heart does the Right coronary artery supply
- Posterior wall LV, - Posterior 1/3 IV septum - Posterior RV
27
A blockage in the left main coronary artery causes what kind of Myocardial infarction
Massive anterolateral MI
28
A blockage in the left anterior descending coronary artery causes what kind of Myocardial infarction
Anteroseptal MI
29
A blockage in the left circumflex coronary artery causes what kind of Myocardial infarction
Lateral MI
30
A blockage in the right coronary artery causes what kind of Myocardial infarction
Posterior/inferior MI
31
Describe the 2 types of valvular heart disease
Stenosis - Failure of valve to open fully preventing forward flow Regurgitation - failure of valve to close allowing backward flow
32
What is infective endocarditis and what causes it
Colonisation of heart valves by infectious agents that requires bacteraemia/septicaemia
33
How does infective endocarditis present itself clinically
Fever and changing heart murmurs
34
What are some risk factors (epidemiology) that contributes to Infective endocarditis
* Congenital heart disease * Rheumatic heart disease * Artificial valves * Floppy mitral valve/calcified aortic valve * Immunodeficiency * Immunosuppression * Intravenous drug abuse
35
What complications can occur with congenital heart disease
Shunts, obstruction of failure VSD - ventricular septal defect 33% ASD - Atrial septal defect 5%
36
What causes can there be for congenital heart disease
genetic and environmental influences like drugs and infections e.g. rubella
37
Describe the factors and onset of subacute infective endocarditis
- Background of valvular/congenital heart disease | - Insidious onset
38
What types of organisms can cause subacute IE and name one
low virulence organisms e.g. strep viridans
39
Describe the vegetations associated with subacute IE
Vegetations less bulky and inflammation less destructive
40
What is a vegetation in the heart
an infected mass
41
What do acute IE patient usually have wrong with their heart
Nothing lol usually a normal heart
42
What kind of organisms can cause acute IE and name a few
Virulent organisms e.g. Staph aureus nd fungi
43
Describe the vegetations associated with acute IE
Bulky vegetations with rapid severe necrotising inflammation
44
Describe the morphology of IE
Friable, bulky, usually bacteria laden vegetations - Single or multiple - 1mm to several cms - May perforate/erode leaflet
45
What cardiac complications can arise as a result of IE
Valvular insufficiency Valvular stenosis Myocardial abscess Suppurative pericarditis Dehiscence of artificial valve Emboli to coronary arteries
46
What are the potential systemic embolic complications that can occur with left heart IE
Brain Spleen Kidneys etc embolisms
47
What are the potential systemic embolic complications that can occur with right heart IE
Lungs | Possibly with secondary abscess formation
48
What renal complications can occur with IE
- Embolic infarction - Embolic infection (secondary abscesses) - Focal glomerulonephritis - Diffuse glomerulonephritis
49
What is glomerluonephritis
Glomerulonephritis is damage to the tiny filters inside your kidneys
50
Describe what acute rheumatic fever is and how it occurs
- Recurrent inflammatory disease in childhood - Follows pharyngeal infection by group A streptococcus - Immunologically mediated not direct bacterial invasion
51
What can acute rheumatic fever lead to
Chronic valve disease
52
What are the symptoms of acute rheumatic fever
``` Fever Migratory polyarthritis (large joints) Pancarditis Subcutaneous nodules Erythema marginatum Sydenhams chorea ```
53
Describe the pathology/histology sorta thing of acute rheumatic fever
- Small friable vegetations on valves (endocardium) | - Microscopy shows: aschoff bodies in myo- and pericardium
54
What are aschoff bodies
Small collections of epithelioid macrophages i.e. mini granulomas
55
What are the symptoms of chronic rheumatic fever and how do they occur
Stenosis - fibrous scarring of calcification of valves with bridges between commissures Regurgitation - fibrous scarring of chordae tendinae
56
What changes are there to the heart morphology and histology 0-12 hours after an MI
none
57
What changes are there to the heart morphology and histology 12-24 hours after an MI
Macroscopic - pale and blotchy | Microscopic - Bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis, intracellular oedema
58
What changes are there to the heart morphology and histology 24-72 hours after an MI
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
What changes are there to the heart morphology and histology 3-10 days after an MI
Macroscopic - Soft, yellow-brown with hyperaemic border | Microscopic - Replacement of infarcted area by granulation tissue
60
What changes are there to the heart morphology and histology weeks-months after an MI
Macroscopic - White, fibrous scar | Microscopic - Collagenous scar tissue
61
What are the short term complications of an MI
* dysrhythmias/arhythmia (sudden death) * cardiogenic shock * cardiac rupture – ventricular free wall with haemopericardium * septal rupture * papillary muscle failure * pericarditis * DVT
62
What can happen if the mural myocardium ruptures in an MI
Blood passes through the ventricular wall into the pericardial sac Pericardial sac is distended with blood, heart action is impeded and = death
63
What can happen if the papillary muscles rupture in an MI
Sudden incompetence of the mitral valve = serious aggravation of cardiac pumping load = acute failure and often death
64
What can happen if the inter ventricular septum ruptures in an MI
Rapid combined ventricular failure = death
65
What are the long term complications of an MI
* LV failure * aneurysm * Dressler’s syndrome (auto-immune) * recurrent infarction * sudden death/arrhythmia
66
When does chronic rheumatic fever tend to occur
after 10 years or more of the acute illness

FHHD (21 decks)

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