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Histopathology > Y Lecture 12: Cardiovascular > Flashcards

Y Lecture 12: Cardiovascular 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 injury2. LDL enters intima and gets trapped in intimal space3. LDL is converted into oxidised LDL –> inflammation4. Macrophages take up OxLDL via scavenger receptors –> foam cells5. Foam cell apoptosis –> inflammation and cholesterol deposition to form plaque core6. 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. Arrhythmia3. Myocardial rupture4. 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

Rubbish - 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 and normal CK-MB

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 and 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
CcfEffusion (pericardial) 
Mural thrombus
Aneurysm (ventricular)
(K)ontractile dysfunction
Early pericarditis
Rupture of venticular wall
Elevation of ST segment
Dressler's syndrome

• Contractile dysfunction – 40% infarct-> cardiogenic shock with 70% mortality rate
• Arrhythmia due to myocardial irritability & conduction disturbance
• Myocardial rupture - free wall most common, septum less common, papillary muscle least common.
(At mean 4-5days, range 1-10 days)

  • Pericarditis (Dressler syndrome) 2nd or 3rd day
  • RV infarction
  • Infarct extension – new necrosis adjacent to old
  • Infarct expansion – necrotic muscle stretches ->mural thrombus
  • Mural thrombus
  • Ventricular aneurysm, late -> thrombus, heart failure, arrhythmia, do not rupture
  • Papillary muscle rupture
  • Chronic Ischaemic Heart Disease (Chronic IHD) = progressive late heart failure
  • Bowel ischaemia
  • Papillary muscle rupture
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 ina) dilated CMb) hypertrophic CMc) restrictive CM?

A

Dilated: systolicHypertrophic and 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 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

What is Libman-Sacks endocarditis

A

Unknown pathogenesis - associated with SLE and 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 apartMinor: - 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

Histopathology (10 decks)

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