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YR5 Histopathology > Histopathology 6 - Vascular and Cardiac pathology > Flashcards

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
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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
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3
Q

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

A

70%

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4
Q

What is prinzmental angina?

A

Coronary artery spasm

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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

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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

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7
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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8
Q

What are the 4 most important complications of MI?

A
  1. Contractile dysfunction (eg cardiogenic shock)
  2. Arrhythmia
  3. Myocardial rupture
  4. Pericarditis
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9
Q

What is Dressler’s syndrome?

A

Pericarditis occuring weeks-months post-MI

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10
Q

What is the average time between MI and myocardial rupture?

A

4-5 days

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11
Q

What is the prognosis of papillary muscle rupture following MI?

A

Very high mortality

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12
Q

What is the most common cause of sudden cardiac death?

A

Lethal arrhythmia

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13
Q

What is restrictive cardiomyopathy?

A

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

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14
Q

Recall 3 possible causes of aortic regurgitation

A

Infective endocarditis
Marfan’s
Ankylosing spondylitis

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15
Q

What is Monckeberg atherosclerosis?

A

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

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16
Q

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

A

Normal histology + normal CK-MB

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17
Q

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

A

Loss of nuclei
Homogenous cytoplasm
Necrotic cell death

18
Q

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

A

Infiltration of polymorphs + macrophages

19
Q

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

A

Removal of debris

20
Q

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

A

Granulation tissue
New blood vessels
Myofibroblasts
Collagen synthesis

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 + 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 + restrictive: diastolic

26
Q

What is the HOCM?

A

Hypertrophic obstructive CM = septal hypertrophy resulting in an outflow tract obstruction

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 + antibodies to streptococcal antigen cross-react with myocardial antigens

31
Q

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

A

Small + warty, “verrucae”

32
Q

What is Libman-Sacks endocarditis

A

Unknown pathogenesis - associated with SLE + anti-phospholipid syndrome

33
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

34
Q

Recall the major and minor Duke criteria for infective endocarditis

A

Major:
Pos BC growing typical IE organism OR 2 pos BCs >12hrs apart

Minor:

  • RF
  • Fever >38
  • Thromboembolic phenomena
  • Immune phenomena
  • Pos BCs not meeting major criteria
35
Q

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

A

2 major

1 major and 3 minor

5 minor

36
Q

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

A

RhF: mitral stenosis

IE: mitral regurgitation

37
Q

7 RF for atherosclerosis

A 
Age
Sex: M > F until menopause
FH
Hyperlipidaemia
HTN
Smoking 
T2DM
38
Q

How do multiple risk factors influence atherosclerosis risk?

A

Multiplicative effect

2 = 4 fold increase

39
Q

How do types of lipid vary?

A 
LDL = BAD
HDL = GOOD- helps mobilise cholesterol from plaques to liver
40
Q

What can HTN lead to for the heart?

A

LV hypertrophy

can lead to myocardial ischaemia itself

YR5 Histopathology (27 decks)

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