Histopathology 6 - Vascular and Cardiac pathology Flashcards

(46 cards)

1
Q

What are the 3 stages of atheroma development?

A
  1. Raised lesion
  2. Soft lipid core
  3. White fibrous cap
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2
Q

Are men or women more affected by atherosclerosis?

A

premenopausal women protected → post-menopausal women = >risk than men

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3
Q

Recall the 7 steps of atheroma pathophsyiology

A
  1. endothelial injury → LDL accumulation
  2. monocyte adhesion to endothelium
  3. monocyte migration into intima → macrophages & foam cells
  4. platelet adhesion → factor release → smooth muscle cell recruitment
  5. lipid accumulation → extracellular and intracellular macrophages and smooth muscle cells
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4
Q

What % atheroma of a vessel lumen is considered ‘critical stenosis’?

A

70%

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5
Q

What lesions can you visualise on histology in atherosclerosis?

A

1. Fatty streak

Lipid filled foamy macrophages, no flow disturbance

In virtually all children <10y/o

Relationship to plaques uncertain but same sites as plaques

2. Atherosclerotic plaque

Occur in points of disturbed flow - bifurcations, curvatures

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6
Q

What is prinzmental angina?

A

Coronary artery spasm

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7
Q

Where do plaques commonly form in angina?

A

first parts of LAD or LCx; or entire length of RCA

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8
Q

Which parts of the cardiac muscle are affected by an infarction of the LAD?

A

Anterior wall of left ventricle, anterior septum and apex

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9
Q

Which parts of the cardiac muscle are affected by an infarction of the RCA?

A

Posterior wall of left ventricle, posterior septum and posterior wall of right ventricle

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10
Q

Which parts of the cardiac muscle are affected by an infarction of the LCx?

A

Lateral wall of left ventricle

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11
Q

What are the 4 most important complications of MI?

A
  1. Contractile dysfunction (eg cardiogenic shock)
  2. Arrhythmia
  3. Myocardial rupture
  4. Pericarditis

D Death

A Arrhythmia

R Rupture (papillary muscle)

T Tamponade

H Heart Failure

V Valvular disease

A Aneurysm of ventricle

D Dressler’s syndrome (pericarditis; 2nd or 3rd day)

E Embolism (i.e. bowel ischaemia)

R Recurrence

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12
Q

What is Dressler’s syndrome?

A

Pericarditis occuring weeks-months post-MI

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13
Q

What is the average time between MI and myocardial rupture?

A

4-5 days

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14
Q

What histological findings would be found within 6 hours of an MI?

A

Normal histology and normal CK-MB

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15
Q

What histological findings would be found 6 -24 hours following an MI?

A

Loss of nuclei
Homogenous cytoplasm
Necrotic cell death

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16
Q

What histological findings would be found 1-4 days following an MI?

A

Infiltration of polymorphs and macrophages

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17
Q

What histological findings would be found 5-10 days following an MI?

A

Removal of debris

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18
Q

What histological findings would be found 1-2 weeks following an MI?

A

Granulation tissue
New blood vessels
Myofibroblasts
Collagen synthesis

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19
Q

What histological findings would be found in the months following an MI?

A

Strengthening, de-cellularising scar tissue

20
Q

Recall the possible complications of MI

A

Mnemonic = PACE MAKERED

Papillary muscle dysfunction
Arrhythmia
Ccf
Effusion (pericardial)

Mural thrombus
Aneurism (ventricular)
(K)ontractile dysfunction
Early pericarditis
Rupture of venticular wall
Elevation of ST segment
Dressler’s syndrome

21
Q

What is reperfusion injury?

A

oxidative stress, Ca2+ overload, inflammation

  • Arrhythmias common
  • Biochemical abnormalities last days to weeks
  • Thought to cause “stunned myocardium”: reversible cardiac failure lasting several days
22
Q

What is hibernating myocardium

A

chronic sublethal ischaemia causes lowered metabolism in myocytes is reversed with revascularisation

23
Q

What is a cause of sudden cardiac death?

A

lethal arrhythmia (from ischaemia-induced electrical instability)

Usually BG IHD (90%) although drugs such a cocaine may be the cause

Acute MI is usual trigger → electrical instability at sites distant from conduction system (near scars from old MIs)

24
Q

What is nutmeg liver a sign of?

A

peripheral oedema (hepatic venous congestion)

25
What are some histopathological features of heart failure?
Dilated heart, scarring and thinning of the walls Microscopy: fibrosis and replacement of the ventricular myocardium
26
What is dilated cardiomyopathy?
Progressive loss of myocytes Dilated heart
27
What is restrictive cardiomyopathy?
Too stiff Normal size heart but with large atria - may be due to amyloidosis/sarcoidosis
28
What are some causes of dilated cardiomyopathy?
* Idiopathic * Infective: viral myocarditis * Toxic: alcohol, chemotherapy (adriamycin, daunorubicin), Cobalt, iron * Hormonal: hyper/hypothyroid, diabetes, peri-partum * Genetic: haemochromatosis, Fabry’s, McArdle’s * Immunological: myocarditis; inc. viral
29
Which type of cardiomyopathy is associated with alcohol misuse?
Dilated
30
What types of cardiomyopathy can be caused by sarcoidosis?
Dilated and restrictive
31
What is the HOCM?
Hypertrophic obstructive CM = septal hypertrophy resulting in LVH -\> outflow tract obstruction
32
What mutation is associated with Hypertrophic CM?
Beta-myosin heavy chain | (Beta-HMC - HMC is HCM rearranged)
33
Is the pathology of cardiomyopathy systolic or diastolic dysfunction in a) dilated CM b) hypertrophic CM c) restrictive CM?
Dilated: systolic Hypertrophic and restrictive: diastolic
34
What is the main pathogen in rheumatic fever?
Lancefield group A strep
35
Recall the major criteria for Rheumatic fever diagnosis
CASES Carditis Arthritis Sydenham's chorea Erythema marginatum Subcutaneous nodules
36
How is 'antigenic mimicry' involved in rheumatic heart fever?
Cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens
37
How are vegetations seen on heart valves in rheumatic fever described?
Small and warty, "verrucae"
38
Which valve is most commonly affected by chronic rheumatic valvular disease?
Mitral \> Aortic \> Tricuspid \> Pulmonic L\>R (almost always mitral stenosis)
39
What histopathological changes might you see in chronic rheumatic valvular disease?
Thickening of valve leaflet, especially along lines of closure Fusion of commissures Thickening, shortening and fusion of chordae tendineae
40
What is the most common cause of aortic stenosis?
Calcium deposits in outflow side cusp which impair opening or orifice is compromised outflow tract obstruction
41
Recall 3 possible causes of aortic regurgitation
**Rigidity** RHD **Destruction:** IE **Disease of aortic valve ring**: dilatation → valve insufficient to cover increased area Marfan's Syndrome Dissecting aneurysm Syphilitic aortitis Ankylosing spondylitis
42
Which valves are most commonly affected in infective endocarditis?
Left-sided normally (as it is often the more ‘damaged valve’) Right-sided in IVDU (as it is the first valve the bacterium come across)
43
What abnormality in the mitral valve might be caused by rheumatic fever vs IE?
RhF: mitral stenosis IE: mitral regurgitation
44
Mechanism of action of statins
inhibit HMG-CoA reductase
45
True vs false cardiac aneurysm
True: all layers of the wall False: extravascular haematoma → aortic dissections
46
Recall 3 causese of aneurysms
weak wall of large arteries Marfan’s Atherosclerosis Hypertension