Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MD Y1S1 > Cardio Path > Flashcards

Cardio Path Flashcards

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

Organising anteroseptal transmural myocardial infarct with biventricular dilatation and thrombosis

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

Lines of Zahn, organisation of thrombus

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

Fate of thrombus

A
  1. Resolution/dissolution
  2. Emboli formation
  3. Organisation and recannalisation (return of blood flow)
  4. Propogation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Anti-mortum vs post-mortum clot

A

Antimortum:

  • lines of zahn
  • attached to vessel wall
  • firm but frailable

Postmortum:

  • No lines of zahn
  • not attached to vessel wall
  • rubbery, gelatinous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
A

Saddle embolism

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

Pulmonary embolism and infarction with fibrinous pleurisy

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

DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Reperfusion injury

A

blood and O2 –> free radicals and ROS –> increased inflammatory response

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

signs of coagulative necrosis on histology

A
  • no nuclei
  • retention of cellular architechture
  • eosinophilic cytoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What stage of myocardial infarct?

A

Swelling and increased opacity of tissue due to coagulative necrosis

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

What stage of MI?

A

Inflammatory response to area of infarction

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

What stage of MI?

A

Ingrowth of granulation tissue

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

What stage of MI?

A

Formation of mature scar tissue

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

Severe myocardial ischaemia with multiple foci of old and recent infarction. Cardiac hypertrophy and dilatation.

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

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.

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

Hypertrophy, rupture of papillary muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A

Concentric hypertrophy

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

Atherosclerosis - cholesterol clefts, fibrous cap, foam cells, lipid deposits

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

Hyperplastic arterioloscerosis due to malignant hypertension

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

Hyaline arterioloscerosis due to HTN or DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A

Monkeburg arterioloscerosis - calcification in media due to ageing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
A

Fusiform aneurysm and mural thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
A

Aortic dissection

26
Q
A

Dissecting aneurysm of the aorta. Left ventricular hypertrophy suggests pre-existing arterial hypertension, a common factor predisposing to the development of aortic dissection

27
Q
A

Transmural infarct

–> whole wall

–> complete occlusion

–> STEMI

28
Q
A

Subendocardial infarct

–> due to global HTN, shock, anaemia

–> NSTEMI

29
Q

0-24hrs post MI

A
  • No visible changes 0-4hrs
  • Coag necrosis 4-24hrs
  • Risk of arrhythmia
30
Q

24-72hrs post MI

A
  • Neutrophil infiltration
  • Infarcted region on heart looks pale
  • Risk of arrhythmia
31
Q

3-7 days post MI

A
  • Early granulation tissue
  • Macrophages remove debris as well as structural components
  • Risk of wall/septal/papillary muscle rupture
32
Q

>2 months post MI

A
  • Dense collagen scar
  • Risk of ventricular aneurysm
33
Q
A

Severe atheroma with thrombus formation

34
Q
A

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.

35
Q
A

Cardiac aneurysm with mural thrombosis due to old supero- lateral infarct. Acute infarct involving interventricular septum. Cardiac hypertrophy and dilatation.

36
Q
A

Acute subendocardial myocardial infarction

37
Q
A

Myocardial infarct with papillary muscle rupture

38
Q
A

Marked concentric hypertrophy of left ventricle and area of myocardial fibrosis

39
Q
A

Transmural, anteroseptal, myocardial infarct, 24 hours old, with marked thinning of the infarcted ventricular wal

40
Q
A

Rupture of papillary muscle complicating acute myocardial infarction.

41
Q
A

Transposition of great vessels with ventricular septal defect

42
Q
A

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.

43
Q
A

Infective endocarditis. There are large vegetations on both the mitral and aortic valves

44
Q
A

Infective endocarditis complicating rheumatic mitral stenosis. Note the vegetation on the posterior leaflet of the mitral valve.

45
Q

Jones criteria for RHD

A

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
46
Q
A

Congenital bicuspid aortic valve, with secondary degenerative changes typical of calcific aortic stenosis.

47
Q
A

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.

48
Q
A

Aschoff nodules. These lesions are rarely seen today, but are a classical feature of acute rheumatic carditis

49
Q
A

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

50
Q
A

Left ventricular hypertrophy, as well as enlargement of both ventricular chambers consistent with cardiac failure. A large and easily recognisable anteroseptal infarct.

51
Q
A

Acute pulmonary interstitial oedema

52
Q
A

Cor pulmonale

53
Q
A

Dilated cardiomyopathy

54
Q
A

Nutmeg liver –> due to hepatic venous congestion

55
Q
A

Calcific aortic stenosis

56
Q
A

Tetrology of Fallot

57
Q
A

Infective endocarditis. There are large vegetations on both the mitral and aortic valves

58
Q
A

Fibrous scarring of heart valves due to past, chronic, proliferative inflammation in rheumatic fever.

59
Q
A

Hemosiderin-laden macrophages (“heart failure cells”). The presence of these cells is diagnostic for previous episodes of pulmonary oedema.

60
Q
A

MD Y1S1 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions