Y Lecture 12: Cardiovascular Flashcards
What are the 3 stages of atheroma development?
- Raised lesion
- Soft lipid core
- White fibrous cap
Recall the 7 steps of atheroma pathophsyiology
- 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
What % atheroma of a vessel lumen is considered ‘critical stenosis’?
70%
What is prinzmental angina?
Coronary artery spasm
Which parts of the cardiac muscle are affected by an infarction of the LAD?
Anterior wall of left ventricle, anterior septum and apex
Which parts of the cardiac muscle are affected by an infarction of the RCA?
Posterior wall of left ventricle, posterior septum and posterior wall of right ventricle
Which parts of the cardiac muscle are affected by an infarction of the LCx?
Lateral wall of left ventricle
What are the 4 most important complications of MI?
- Contractile dysfunction (eg cardiogenic shock) 2. Arrhythmia3. Myocardial rupture4. Pericarditis
What is Dressler’s syndrome?
Pericarditis occuring weeks-months post-MI
What is the average time between MI and myocardial rupture?
4-5 days
What is the prognosis of papillary muscle rupture following MI?
Rubbish - very high mortality
What is the most common cause of sudden cardiac death?
Lethal arrhythmia
What is restrictive cardiomyopathy?
Normal size heart but with large atria - may be due to amyloidosis
Recall 3 possible causes of aortic regurgitation
Infective endocarditis
Marfan’s
Ankylosing spondylitis
What is Monckeberg atherosclerosis?
Focal calcification of the media of small-medium sized vessels; no associated inflammation
What histological findings would be found within 6 hours of an MI?
Normal histology and normal CK-MB
What histological findings would be found 6 -24 hours following an MI?
Loss of nuclei
Homogenous cytoplasm
Necrotic cell death
What histological findings would be found 1-4 days following an MI?
Infiltration of polymorphs and macrophages
What histological findings would be found 5-10 days following an MI?
Removal of debris
What histological findings would be found 1-2 weeks following an MI?
Granulation tissue
New blood vessels
Myofibroblasts
Collagen synthesis
What histological findings would be found in the months following an MI?
Strengthening, de-cellularising scar tissue
Recall the possible complications of MI
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
What types of cardiomyopathy can be caused by sarcoidosis?
Dilated and restrictive
Which type of cardiomyopathy is associated with alcohol misuse?
Dilated
Is the pathology of cardiomyopathy systolic or diastolic dysfunction ina) dilated CMb) hypertrophic CMc) restrictive CM?
Dilated: systolicHypertrophic and restrictive: diastolic
What is the HOCM?
Hypertrophic obstructive CM = septal hypertrophy resulting in an outflow tract obstruction
What mutation is associated with Hypertrophic CM?
Beta-myosin heavy chain(Beta-HMC - HMC is HCM rearranged)
Recall the major criteria for Rheumatic fever diagnosis
CASES Carditis Arthritis Sydenham's chorea Erythema marginatum Subcutaneous nodules
What is the main pathogen in rheumatic fever?
Lancefield group A strep
How is ‘antigenic mimicry’ involved in rheumatic heart fever?
Cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens
How are vegetations seen on heart valves in rheumatic fever described?
Small and warty, “verrucae”
What is Libman-Sacks endocarditis
Unknown pathogenesis - associated with SLE and anti-phospholipid syndrome
Differentiate the likely causative organisms in acute vs subacute infective endocarditis
Acute: Staph aureus/ pyogenes
Subacute: strep viridans/ epidermis/ HACEK/ coxiella/ candida/ mycoplasma
Recall the major and minor Duke criteria for infective endocarditis
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
How many of Duke’s criteria are needed for diagnosis of infective endocarditis?
2 major
1 major and 3 minor
5 minor
What abnormality in the mitral valve might be caused by rheumatic fever vs IE?
RhF: mitral stenosis
IE: mitral regurgitation
