Cardio Path Flashcards
Organising anteroseptal transmural myocardial infarct with biventricular dilatation and thrombosis
Lines of Zahn, organisation of thrombus
Fate of thrombus
- Resolution/dissolution
- Emboli formation
- Organisation and recannalisation (return of blood flow)
- Propogation
Anti-mortum vs post-mortum clot
Antimortum:
- lines of zahn
- attached to vessel wall
- firm but frailable
Postmortum:
- No lines of zahn
- not attached to vessel wall
- rubbery, gelatinous
Saddle embolism
Pulmonary embolism and infarction with fibrinous pleurisy
DVT
Reperfusion injury
blood and O2 –> free radicals and ROS –> increased inflammatory response
signs of coagulative necrosis on histology
- no nuclei
- retention of cellular architechture
- eosinophilic cytoplasm
What stage of myocardial infarct?
Swelling and increased opacity of tissue due to coagulative necrosis
What stage of MI?
Inflammatory response to area of infarction
What stage of MI?
Ingrowth of granulation tissue
What stage of MI?
Formation of mature scar tissue
Severe myocardial ischaemia with multiple foci of old and recent infarction. Cardiac hypertrophy and dilatation.
Old and recent myocardial infarction with extensive left ventricular mural thrombosis. Note the pericarditis associated with the recent infarct, and the lines of Zahn in the thrombus.
Hypertrophy, rupture of papillary muscle
Concentric hypertrophy
Atherosclerosis - cholesterol clefts, fibrous cap, foam cells, lipid deposits
Hyperplastic arterioloscerosis due to malignant hypertension
Hyaline arterioloscerosis due to HTN or DM
Monkeburg arterioloscerosis - calcification in media due to ageing
Atherosclerotic plaque complicated by the formation of an occlusive thrombosis in the vessel. The thrombosis is reorganising. It is likely to be due to rupture of the plaque.
Fusiform aneurysm and mural thrombus
Aortic dissection
Dissecting aneurysm of the aorta. Left ventricular hypertrophy suggests pre-existing arterial hypertension, a common factor predisposing to the development of aortic dissection
Transmural infarct
–> whole wall
–> complete occlusion
–> STEMI
Subendocardial infarct
–> due to global HTN, shock, anaemia
–> NSTEMI
0-24hrs post MI
- No visible changes 0-4hrs
- Coag necrosis 4-24hrs
- Risk of arrhythmia
24-72hrs post MI
- Neutrophil infiltration
- Infarcted region on heart looks pale
- Risk of arrhythmia
3-7 days post MI
- Early granulation tissue
- Macrophages remove debris as well as structural components
- Risk of wall/septal/papillary muscle rupture
>2 months post MI
- Dense collagen scar
- Risk of ventricular aneurysm
Severe atheroma with thrombus formation
Dissecting aneurysm of the aorta. Note involvement of subclavian arteries and tear in anterior part of outer wall of aneurysm just above aortic valve. This resulted in haemorrhage into the pericardial cavity.
Cardiac aneurysm with mural thrombosis due to old supero- lateral infarct. Acute infarct involving interventricular septum. Cardiac hypertrophy and dilatation.
Acute subendocardial myocardial infarction
Myocardial infarct with papillary muscle rupture
Marked concentric hypertrophy of left ventricle and area of myocardial fibrosis
Transmural, anteroseptal, myocardial infarct, 24 hours old, with marked thinning of the infarcted ventricular wal
Rupture of papillary muscle complicating acute myocardial infarction.
Transposition of great vessels with ventricular septal defect
Atrial septal defect visible here in the wall of the left atrium. There is enlargmenet of the right atrium and the pulmonary outflow tract reflecting increased blood in the right heart because of the left to right shunt across the ASD.
Infective endocarditis. There are large vegetations on both the mitral and aortic valves
Infective endocarditis complicating rheumatic mitral stenosis. Note the vegetation on the posterior leaflet of the mitral valve.
Jones criteria for RHD
Strep A infection PLUS 2 major/1 major and 2 minor/3 minor criteria
Major criteria:
- Carditis
- Polyarthritis
- Chorea
- Erythema Marginatum (redness of skin/mucous membranes)
- Subcutaneous nodules
Congenital bicuspid aortic valve, with secondary degenerative changes typical of calcific aortic stenosis.
There is concentric LHV, consistent with some degree of aortic stenosis, and the aortic valve shows some thickening of the free edge of at least one leaflet. The mitral valve orifice is markedly narrowed, and the free edges of the leaflets appear thickened. These changes are typical of rheumatic heart disease.
Aschoff nodules. These lesions are rarely seen today, but are a classical feature of acute rheumatic carditis
While this specimen shows both some left ventricular hypertrophy and a dilated cardiac chamber, the reason for this is apparent in the perforations within the leaflets of the aortic valve
Left ventricular hypertrophy, as well as enlargement of both ventricular chambers consistent with cardiac failure. A large and easily recognisable anteroseptal infarct.
Acute pulmonary interstitial oedema
Cor pulmonale
Dilated cardiomyopathy
Nutmeg liver –> due to hepatic venous congestion
Calcific aortic stenosis
Tetrology of Fallot
Infective endocarditis. There are large vegetations on both the mitral and aortic valves
Fibrous scarring of heart valves due to past, chronic, proliferative inflammation in rheumatic fever.
Hemosiderin-laden macrophages (“heart failure cells”). The presence of these cells is diagnostic for previous episodes of pulmonary oedema.
