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Histopathology > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

1
Q

What is atherosclerosis?

A

A chronic inflammation of the intima in the large arteries, characterised by intimal thickening and lipid accumulation

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2
Q

Explain the pathogenesis of atherosclerosis

A

1) Endothelial injury
2) LDL enter the intima and is trapped
3) LDL is converted into oxidised LDL and causes inflammation
4) Macrophage recruitment to take up the oxidised LDL and convert into foam cells
5) Foam cells apoptose and become the cholesterol core of the plaque
6) Vascular smooth muscle becomes the fibrous cap of the plaque

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3
Q

Where is atherosclerosis more likely to occur?

A

Near the roots of branches, as there is turbulent flow here, which is more atherogenic.

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4
Q

What is the fate of atherosclerotic plaques?

A

Obstruction:

  • They can stenose an artery
  • > 70% stenosis to cause symptoms (angina etc.)

Acute Plaque Change:

  • Rupture
  • Erosion
  • Internal haemorrhage
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5
Q

What are the risk factors for atherosclerosis?

A

Non-modifiable:

  • Age
  • Gender
  • Familial history (genetics)

Modifiable:

  • Type 2 Diabetes Mellitus
  • Hypercholesterolaemia
  • Hypertension
  • Smoking
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6
Q

What coronary arteries are most commonly affected by atherosclerosis?

A
  • Right coronary
  • Left mainstem
  • Left anterior descending
  • Left circumflex
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7
Q

What types of angina are there? How do you differentiate them?

A

Stable
- On exertion

Unstable
- On rest

Prinzmetal
- Due to coronary artery spasm

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8
Q

What is ischaemic heart disease?

A

This is a collection of diseases caused by an imbalance of demand and supply of blood to the heart.

  • Angina pectoris
  • Chronic ischaemic heart disease
  • Myocardial infarction
  • Sudden cardiac death
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9
Q

What is a myocardial infarction?

A

Ischaemia of the cardiac muscle leads to necrosis and death. Irreversible damage occurs if this goes on for longer than 20-40 minutes.

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10
Q

What is the epidemiology surrounding myocardial infarction?

A

Half of all MI-related deaths occur before they reach the hospital

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11
Q

What are the complications of myocardial infarction?

A

Mechanical:

  • Contractile dysfunction, leading to cardiogenic shock
  • Congestive cardiac failure
  • Cardiac rupture of free wall, septum or papillary muscle
  • Ventricular aneurysm, increasing the likelihood of thrombi

Arrhythmias:

  • VF can occur in the first 24 hours and commonly causes sudden cardiac death
  • Electric instability is a common complication of MIs

Pericardial:

  • Post-MI pericarditis (Dresser’s Syndrome): fever, chest pain and effusion
  • Pericardial effusion +/- tamponade
  • Fibrinous pericardium

Mural thrombus:

  • Can occur in ventricular aneurysms
  • Can dislodge and spread to brain or other tissues
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12
Q

What are the histological findings of myocardial infarction?

A

0 - 6 hours: no changes
6 - 24 hours: oedema, loss of nuclei, necrotic cell death
1 - 4 days: infiltration of macrophages
5 - 10 days: removal of debris
1 - 2 weeks: granulation tissue, new blood vessels
Weeks - months later: strengthening, scar tissue

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13
Q

When are cardiac muscle ruptures most likely to occur after a myocardial infarction?

A

Within the first 10 days; this is due to the weakened wall with macrophage infiltration. As scar tissue begins to develop, the scar tissue is far more fibrous and strong, and this occurs later.

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14
Q

What is reperfusion injury?

A

As the tissue may be necrotic, reperfusion quickly can cause inflammation, calcium overload and a ‘stunned’ myocardium

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15
Q

What is the definition of sudden cardiac death?

A

Cardiac death in a previously asymptomatic patient, or death within one hour of symptoms onset.

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16
Q

What is heart failure?

A

Insufficiency of the heart s a pump

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17
Q

What are the common causes of heart failure?

A
  • Ischaemic heart disease
  • Valvular disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
  • Arrhythmias
18
Q

What are the complications of heart failure?

A
  • Sudden cardiac death
  • Systemic emboli (DVT and PE)
  • Pulmonary oedema (with infection)
  • Hepatic cirrhosis (nutmeg liver)
19
Q

What is the pathophysiology associated with cardiac failure?

A

Either:

  • Cardiac damage reduces output, and activates the RAS system to retain water and salt, causing fluid overload.
  • Cardiac damage causes a decreases stroke volume, and baroreceptors maintain the perfusion.
20
Q

What are the symptoms of heart failure?

A

Left sided:

  • Pulmonary oedema
  • SOB, orthopnoea, PND, wheeze, fatigue

Right sided:
- hepatomegaly, peripheral oedema, ascites

21
Q

What is cardiomyopathy?

A

Non-ischaemic damage to the myocytes; it can be dilated, hypertrophic or restrictive.

22
Q

Describe dilated cardiomyopathy and its causes.

A

It is a dilation of the cardiac sections, caused idiopathically, by alcohol, myocarditis or even in peripartum.

23
Q

Describe restrictive cardiomyopathy and its causes.

A

It is a restriction on the contractility of the heart, usually caused by amyloidosis or sarcoidosis.

24
Q

Describe hypertrophic cardiomyopathy and its causes. What can it cause?

A

It is a hypertrophy of the cardiac walls (commonly the septum or the left ventricle. It is commonly caused by mutations in the beta myosin heavy chain gene, inherited in an autosomal dominant pattern.

It can cause sudden cardiac death. and outflow tract obstruction (HOCM).

25
Q

Describe the epidemiology and symptoms of acute rheumatic fever.

A

It occurs between 5-15 years, and is a multisystem disease affecting:

  • Heart: pancarditis
  • Skin: erythema marginatum
  • Joints: arthritis
  • CNS: Sydenham’s chorea

It usually develops after a streptococcal throat infection

26
Q

How is rheumatic heart disease diagnosed?

A

A group A strep infection + 2 major criteria/1 major and 2 minor

Major criteria: CASES

  • Carditis
  • Arthritis
  • Sydenham’s chorea
  • Erythema marginatum
  • Subcutaneous nodules

Minor criteria:

  • Fever
  • Raised ESR or CRP
  • Previous rheumatic fever
  • Prolonged PR
27
Q

What types of vegetative endocarditis are there? Briefly describe them

A

Rheumatic heart disease
- Antigenic mimicry, small warty vegetation

Infective endocarditis
- Infective cause, large irregular masses on valves

Non-bacterial thrombotic endocarditis
- DIC/hypercoagulation, small bland vegetations

Libman-Sacks endocarditis
- Associated with SLE, small warty sterile vegetations

28
Q

What are the risk factors for infective endocarditis?

A
  • Dental work/poor dental hygiene
  • IVDU
  • Soft tissue infection
  • Cannulae/lines
29
Q

What are the causative organisms in acute infective endocarditis and subacute infective endocarditis?

A

Acute:

  • Staphylococcus aureus
  • Streptococcus pyogenes

Subacute:

  • Streptococcus viridans
  • Staphylococcus epidermis
  • HACEK (haemophilus, aggregobacter, cardiobacter, eikenella, kingella)
30
Q

What are the clinical features?

A
  • Fever
  • New murmur
  • Immune phenomena (roth spots, oslers nodes_
  • Thromboembolic phenomena (janeway lesions, splinter haemorrhages)
31
Q

What valves are usually affected in infective endocarditis?

A

Mitral/aortic, unless IVDU (tricuspid)

32
Q

What is the diagnostic criteria for infective endocarditis?

A

Duke’s Criteria: 2 major, 1 major and 3 minor, 5 minor

Major:

  • 2 positive usual cultures, 12 hours apart
  • Positive echo

Minor:

  • Positive bacterial culture
  • Risk factors
  • Fever above 38 degrees
  • Thromboembolic phenomena
  • Immune phenomena
33
Q

How do you treat infective endocarditis?

A

Treat with broad spectrum antibiotics until culture is obtained

Acute:

  • Flucloxacillin (MSSA)
  • Rifampacin, vancomycin and gentamicin (MRSA)

Subacute
- Benzylpenicillin and gentamicin

34
Q

What is the main cause for aortic stenosis?

A

Calcification (old age)

Other: endocarditis, valvular disease

35
Q

What are the main causes for aortic regurgitation?

A

Endocarditis, connective tissue disease

36
Q

What valve does rheumatic fever usually affect?

A

Mitral

37
Q

What is chronic rheumatic valve disease?

A

Predominantly left sided, and mostly mitral (M>A>T>P). There is also thickening and shortening of the chordae tendinae

38
Q

What is the difference between true and false aneurysms? Name some causes

A

True: all layers of the vessel wall
False: not all layers

Caused: weak wall

  • Congenital (Marfan’s)
  • Atherosclerosis
39
Q

What is pericarditis?

A

Inflammation on the pericarditis, caused by:

  • Infarction
  • Granulomatous
  • Haemorrhage
40
Q

What is a pericardial effusion?

A

Fluid in the pericardial sac, usually caused by chronic heart failure. Can be blood from a ruptured myocardial wall, as a result of an MI.

Histopathology (21 decks)

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