1
Q
What are the two major patterns of MI?
A
- Transmural (usually STEMI)
2. Subendocardial (usually NSTEMI)
2
Q
What conditions are characterised as acute coronary syndromes and which ones are characterised as chronic coronary syndrome?
A
ACS: 1. Unstable angina 2. Myocardial infarction 3. Sudden cardiac death CCS: 1. Stable angina 2. Chronic myocardial ischemia
3
Q
Histological features 1 day post MI
A
Irreversible injury: Key: - Eosinophilic - Hemorrhagic, therefore RBCs Other: - Coagulative necrosis - Breakdown of nuclei - Disarray - Not many inflammatory cells
4
Q
Histological features 3-7 days post MI
A
Acute inflammation:
- Neutrophils
5
Q
Histological features 1-2 wks post MI
A
Early granulation tissue:
- Complete disarray
- Fibroblasts (main cell). These won’t appear earlier.
- Macrophages
- Capillaries
- Lymphocytes
6
Q
Histological features 6-8 wks post MI
A
Scar tissue:
- No structure, just scar tissue
- Scattered fibroblasts
- Eosinophilic
7
Q
Gross pathology of MI 3-10days post event
A
- Pale (coagulative necrosis)
- Thin (after some time)
- Fibrous
8
Q
Supply of the LAD
A
- Anterior 2/3 of septum
- Anterior wall of LV
9
Q
Supply of left circumflex
A
- Lateral wall of LV
10
Q
Supply of right coronary artery
A
- SA/AV node
- Posterior 1/3 of septum
- Right ventricle
11
Q
Complications of MI
A
Immediate: 1. Arrhythmias 2. Acute cardiac failure 3. Cardiogenic shock Days: 1. Mechanical complications (papillary muscle or wall rupture, acquired VSD) 2. Infarct expansion 3. Pericarditis 4. Arrhytmias 5. Mural thrombus formation 6. Progressive cardiac failure Weeks-months 1. LV aneurysm and thombus formation 2. Chronic cardiac failure - this is KEY 3. Arrhythmias (hear block, sick sinus syndrome)
12
Q
Complications of MI
A
Immediate: 1. Arrhythmias 2. Acute cardiac failure 3. Cardiogenic shock Days: 1. Mechanical complications (papillary muscle or wall rupture, acquired VSD) 2. Infarct expansion 3. Pericarditis 4. Arrhythmias 5. Mural thrombus formation 6. Progressive cardiac failure Weeks-months 1. LV aneurysm and thombus formation 2. Chronic cardiac failure - this is KEY 3. Arrhythmias (hear block, sick sinus syndrome)
13
Q
Complications of MI
A
Immediate: 1. Arrhythmias 2. Acute cardiac failure 3. Cardiogenic shock Days: 1. Mechanical complications (papillary muscle or wall rupture, acquired VSD). N.B. Ventricular septal defect. 2. Infarct expansion 3. Pericarditis 4. Arrhythmias 5. Mural thrombus formation 6. Progressive cardiac failure Weeks-months 1. LV aneurysm and thombus formation 2. Chronic cardiac failure - this is KEY 3. Arrhythmias (hear block, sick sinus syndrome) N.B. At all stages there is the possibility of arrhythmia and cardiac failure (acute -> progressive -> chronic)
14
Q
Most common problem post MI
A
Chronic ischemic heart disease
15
Q
Causes of sudden cardiac death
A
- Fatal tachyarrhythmia (often can be idiopathic). Can be the 1st manifestation of ischemic heart disease
- Acute MI
16
Q
What is an aneurysm
A
- Bulge/dilation of lumen in blood vessel wall. Not dissection, because blood still contained in lumen
- Caused by weakening in MEDIA
17
Q
What is an aneurysm
A
- Bulge/dilation of lumen in blood vessel wall. Not dissection, because blood still contained in lumen
18
Q
2 types of true aneursym
A
- Saccular (one side)
2. Fusiform (both sides)
19
Q
What is false aneurysm
A
Pocket of blood but not in lumen (in layers of vessel). This is different from dissection, because dissection is not just one pocket, it also tears through media and tracks up the vessel.
20
Q
2 types of true aneursym
A
- Saccular (one side bulges)
2. Fusiform (both sides bulge)
21
Q
Causes of aneurysms
A
Key: 1. Congenital e.g. Berry aneurysm 2. Atherosclerotic Others: 3. Inherited 4. Infectious
22
Q
3 key examples of aneurysm:
A
- AAA (fusiform)
- Berry (saccular). Major cause of subarachnoid haemorrhage
- LV (complication of MI -> weakening of wall)
23
Q
2 key causes of aortic dissection
A
- Connective tissue diseases (e.g. Marfan’s due to Fibrillin 1 defect)
- Hypertension (most COMMON)
24
Q
Where do dissections often occur?
A
- Arch of aorta
25
2 key causes of aortic dissection
1. Connective tissue diseases (e.g. Marfan's due to Fibrillin 1 defect)
2. Hypertension
26
Major complications of aortic dissection
1. Acute aortic regurgitation
2. Haemopericardium
3. Haemoperitoneum
4. Haemothorax
5. Hypotension and shock
6. Mesenteric and renal ischaemia
Pain is described as 'tearing' that goes all the way to the back.
27
Different types of embolism
1. Thromboembolism
2. Atheroembolism
3. Fat and marrow embolism
4. Air and gas embolism
28
Most common cause of PE
| Most common outcome of PE
DVT (>98%)
| Minor and clinically silent (75)
29
Different types of embolism
1. Thromboembolism
2. Atheroembolism
3. Fat and marrow embolism (e.g. due to trauma or surgery of long bones)
4. Air and gas embolism (often iatrogenic)
30
Risk factors for DVT
1. Increasing age
2. Family history
3. Prolonged immobility --> stasis
4. Cancer
5. High oestrogen
6. Smoking
31
Most common outcome of PE
Minor and clinically silent (75)
32
Causes of infective endocarditis
Acute
- can be v. dangerous (50% mortality)
- common is Staph. aureus
Subacute
- better prognosis but harder to pick up (non-specific)
Other:
- Can dislodge from heart and go to brain
33
Changes that occur in lung with lobar pneumonia
```
Lobar:
1. Congestion (vascular engorgement, many RBCs, intra-alveolar fluid with numerous bacteria but few neutrophils)
2. Red hepatisation
3. Grey hepatisation
4. Resolution (macrophages, fibroblasts)
Broncho:
- Patchy consolidation
- Bilateral
- Basal (secretions pool down due to gravity)
```
34
Changes that occur in lung with lobar pneumonia
Lobar:
1. Congestion (vascular engorgement, many RBCs, intra-alveolar fluid with numerous bacteria but few neutrophils)
2. Red hepatisation (neutrophils are key, RBCs, fibrin). Red colour mainly due to vascular dilation.
3. Grey hepatisation
4. Resolution (macrophages, fibroblasts)
Broncho:
- Patchy consolidation
- Bilateral
- Basal (secretions pool down due to gravity)
35
What is atypical pneumonia and how does it present?
- "Walking pneumonia" - symptoms more mild than lobar pneumonia
- moderate amounts of sputum
- no physical findings of consolidation
- moderate elevation of WCC
- lack of alveolar exudate
36
Risk factors for lung cancer
1. Smoking
2. Asbestos (and other inhaled particles)
3. Ionising radiation
4. Genetic
37
Major subdivisions of cancer
1. Small cell carcinoma (20-25%)
2. Non small cell carcinoma (70-75%)
These are differentiated based on presentation and treatment (small cell is more systemic with worse prognosis)
38
Who is more likely to get adenocarcinoma?
- This is least associated with smokers, however the majority of cases are still in smokers.
- Female
- Asian ethnicity
39
Who is more likely to get adenocarcinoma? *not as common MCQs
- This is least associated with smokers, however the majority of cases are still in smokers.
- Female
- Asian ethnicity
40
Who is more likely to get adenocarcinoma? *Adenocarcinoma are not as commonly examined in MCQs
- This is least associated with smokers, however the majority of cases are still in smokers.
- Female
- Asian ethnicity
41
Classical clinical vignette of squamous cell carcinoma:
1. Male
| 2. Smoking history
42
Classical clinical vignette of small cell carcinoma
1. Smoker
2. Metastatic at diagnosis
3. Sensitive to chemo/radiotherapy
4. Dismal prognosis
43
What is paraneoplastic syndrome?
Clinical manifestation of cancer not caused by local invasion or mass effects, but by the secretion of humeral factors. Key things to know:
- Small cell lung cancer associated with SIADH and Cushing's syndrome
- Squamous cell carcinoma associated with hypercalcaemia
44
What is the most common cause of heart failure?
Ischemic heart disease, of which the main cause is atherosclerosis in coronary arteries.
45
Most common cause of sudden cardiac death?
Acute MI --> acute electrical instability -> VF
Cardiac pathology
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