Histopathology 6 - Vascular and Cardiac pathology Flashcards

1
Q

What are the 3 stages of atheroma development?

A
  1. Raised lesion
  2. Soft lipid core
  3. White fibrous cap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Recall the 7 steps of atheroma pathophsyiology

A
  1. Endothelial injury
  2. LDL enters intima and gets trapped in intimal space
  3. LDL is converted into oxidised LDL –> inflammation
  4. Macrophages take up OxLDL via scavenger receptors –> foam cells
  5. Foam cell apoptosis –> inflammation and cholesterol deposition to form plaque core
  6. Endothelium expresses more adhesion molecules –> more macrophages and T cells enter plaque
  7. VSMCs form fibrous cap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes prinzmental angina?

A

Coronary artery spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Lateral wall of left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 4 most important complications of MI?

A
  1. Contractile dysfunction (eg cardiogenic shock)
  2. Arrhythmia
  3. Myocardial rupture (occurs at day 4-5)
  4. Pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Dressler’s syndrome?

A

Pericarditis occuring weeks-months post-MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the average time between MI and myocardial rupture?

A

4-5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the prognosis of papillary muscle rupture following MI?

A

Rubbish - very high mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the most common cause of sudden cardiac death?

A

Lethal arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is restrictive cardiomyopathy?

A

When there is impaired ventricular compliance (contractibility)

Normal size heart but with large atria - may be due to amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Recall 3 possible causes of aortic regurgitation

A

Infective endocarditis
Marfan’s
Ankylosing spondylitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Monckeberg atherosclerosis?

A

Focal calcification of the media of small-medium sized vessels; no associated inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Normal histology and normal CK-MB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What histological findings would be found 6 -24 hours following an MI? (3)

A
  • Loss of nuclei
  • Homogenous cytoplasm
  • Necrotic cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Infiltration of polymorphs and macrophages (to clear up debris)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Removal of debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

Granulation tissue
New blood vessels
Myofibroblasts
Collagen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Strengthening, de-cellularising scar tissue

22
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

23
Q

What types of cardiomyopathy can be caused by sarcoidosis?

A

Dilated and restrictive

24
Q

Which type of cardiomyopathy is associated with alcohol misuse?

A

Dilated

25
Q

Is the pathology of cardiomyopathy systolic or diastolic dysfunction in

a) dilated CM
b) hypertrophic CM
c) restrictive CM?

A

Dilated: systolic

Hypertrophic and restrictive: diastolic

26
Q

What is the HOCM?

A

Hypertrophic obstructive CM = septal hypertrophy resulting in an outflow tract obstruction (usually get LV hypertrophy)

27
Q

What mutation is associated with Hypertrophic CM?

A

Beta-myosin heavy chain

(Beta-HMC - HMC is HCM rearranged)

28
Q

Recall the major criteria for Rheumatic fever diagnosis

A

CASES

Carditis
Arthritis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules

29
Q

What is the main pathogen in rheumatic fever?

A

Lancefield group A strep

30
Q

How is ‘antigenic mimicry’ involved in rheumatic heart fever?

A

Cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens

31
Q

How are vegetations seen on heart valves in rheumatic fever described?

A

Small and warty, “verrucae”

32
Q

Differentiate the likely causative organisms in acute vs subacute infective endocarditis

A

Acute: Staph aureus/ pyogenes

Subacute: strep viridans/ epidermis/ HACEK/ coxiella/ candida/ mycoplasma

33
Q

Recall the major and minor Duke criteria for infective endocarditis

A

Major:

+ve blood culture growing typical IE organism OR 2 +ve cultures >12hrs apart

Minor:

  • RF (prosthetic valve, IVDU, congenital valve abnormalities)
  • Fever >38
  • Thromboembolic phenomena
  • Immune phenomena
  • Pos BCs not meeting major criteria
34
Q

How many of Duke’s criteria are needed for diagnosis of infective endocarditis?

A

2 major

1 major and 3 minor

5 minor

35
Q

What abnormality in the mitral valve might be caused by rheumatic fever vs IE?

A

RhF: mitral stenosis

IE: mitral regurgitation

36
Q

Features of Vulnerable atheromatous Plaques

A
  • Lots of foam cells or extracellular fluid
  • Thin fibrous cap
  • Few smooth muscle cells
  • Clusters of inflammatory cells
37
Q
A
38
Q

What is angina pectoris?

A

Transient ischaemia that does NOT produce myocyte necrosis

39
Q

Immune cell progression in myocardial infarctoin

A
  • day 1-3: neutrophils eating damaged myocardium
  • day 10-14: macrophages
  • after 2 months: scarring
40
Q

What can happen when blood re-enters area of myocardial necrosis?

A

Reperfusion Injury

  • oxidative stress, calcium overload and inflammation can cause further injury
41
Q

Congestive heart failure meaning

A

when it affects both sides of the heart

42
Q

Effect of L heart failure

A

SOB, pulmonary oedema (affects the lungs)

43
Q

Effect of R heart failure

A

peripheral oedema, nutmeg liver

44
Q

Most common cause of right-sided heart failure

A

Left-sided heart failure

45
Q

Aetiology of dilated cardiomyopathy

A

progressive loss of myocytes (get big/dilated heart)

46
Q

What precedes rheumatic fever?

A

streptococcal throat infection (2-4 weeks before)

47
Q

Tx of rheumatic heart fever

A

Benzylpenicillin

48
Q

MOST COMMON cause of aortic stenosis

A

Calcific Aortic Stenosis

49
Q

True vs false aneurysm

A
  • True- involves all layers of the wall
  • False- extravascular haematoma (i.e. a rupture and haematoma that forms)
50
Q

Which site is more likely to have dissecting aneurysm, and which is more likely to have rupturing aneurysm?

A
  • Dissecting: aortic arch
  • Rupturing: abdo aorta (AAA)