Week 2 - CVS Flashcards
MI/IHD, Atherosclerosis, Aneurysms
1
Q
What is the best way to salvage ischaemic myocardium and how?
A
Rapid reperfusion:
- thrombolysis
- PTCA +/- stenting
- CABGs
*Keep in mind re-perfusion injury!
2
Q
What is atherosclerotic plaque separation caused by?
A
Proteolytic enzymes
3
Q
What are the 3 types of aortic dissection classifications?
A
- Debakey I –> whole aorta
- Debakey II –> ascending only
- Debakey III –> descending only
- Type A Stanford = Debakey I and II
- Type B Stanford = Debakey III
4
Q
What is the most important cause of aneurysms?
A
Atherosclerosis
5
Q
Where are berry aneurysms common?
A
Cerebral arteries
- haemorrhage (rupture)
- stroke (thromboembolism)
6
Q
What are complications of aneurysms?
A
- mural thrombosis/embolism –> COMMONEST
- fatal hemorrhage (if rupture)
- surrounding organ compression
- ischaemic organ damage!
7
Q
What is the pathogenesis of aneurysms?
A
Cystic medial degeneration
8
Q
What are vasa vasorum?
A
small blood vessels that supply wall of blood vessels
9
Q
What is an aneurysm and its types?
A
Abnormal dilatation of an artery
- True (all layers involved) –> saccular/berry; fusiform
- False (not truly enlarged - escaped blood causes bulge) –> hematoma; dissecting
10
Q
Which cardiac marker is best for lab evaluation of an MI?
A
Troponins I + T
- increased within 2-4hrs
- peak @48hrs
- remain elevated for 7-10 days
11
Q
What are the MI markers?
A
- myoglobin
- troponin I + T
- CK + CK-MB
- lactate dehydrogenase
12
Q
What are chronic complications of MI?
A
- chronic IHD - CHF
- arrhythmias
- ventricular aneurysm
- mural thrombosis
- papillary muscle contraction –> Mitral regurgitation
13
Q
What are acute complications of MI?
A
- heart failure
- arrhythmias
- CHF
- cardiogenic shock
- pericarditis
- mural thrombosis
- myocardial wall rupture –> tamponade (3-10days)
- papillary muscle rupture –> mitral regurgitation
14
Q
Which coronary arteries are commonly affected by infarction?
A
- LAD (ant/septum) –> 50% (most commonly affected)
- RCA (posterior) –> 30%
- Left marginal (L circumflex) (lateral) –> 20%
15
Q
What are the 3 types of myocardial infarcts?
A
- Sub-endocardial
- partial obstruction
- NSTEMI - Transmural
- complete obstruction
- STEMI - Multiple Small (Microscopic)
- small vessels affected
- normal ECG
- gives rise to chronic IHD
16
Q
Where in the artery is an atheroma located within?
A
Tunica Intima
17
Q
Compare the 3 types of aneurysms
A
- Berry
- from one side of artery producing a ‘fruit-like bulge’
- common in cerebral arteries - Fusiform
- whole circumference of artery dilates due to AS plaque with inflammation weakening the arterial wall - Dissecting
- plaque ruptures in middle, blood rushes inside splitting wall into 2 layers (blood between tunica intima and media)
- common in aorta; blood enters ruptured plaque
18
Q
What are the complications of atherosclerosis?
A
- ischaemia/infarction of organ supplied
- progressive block
- thrombosis/thromboembolism
- aneurysm
- rupture –> haemorrhage
- MACROANGIOPATHY
19
Q
What is the pathogenesis of atherosclerosis?
A
- Endothelial injury
- LDL entry and oxidation in intima
- Oxidised LDL causes adhesion and entry of monocytes/T-cells across endothelium via pro-inflammatory mediators
- Monocytes –> macrophages which consume large amounts of LDL –> Foam cells
- Foam cells release cytokines which cause inflammation and smooth muscle cell/fibroblast proliferation –> fibrous cap formation
20
Q
Compare the 2 types of plaques
A
Unstable Plaque (10%):
- large lipid core
- severe inflammation (IFN-gamma) –> M1
- thin fibrous cap
- low SMC
- rapid change
- pain at rest (unstable angina)
Stable Angina (90%):
- small lipid core
- low inflammation (IL-4/IL-13) –> M2
- thick fibrous cap
- high SMC
- slow progressive
- pain on exertion (stable angina)
21
Q
True or False?
Unstable plaque cannot regress back to stable plaque
A
False
- atheroma plaque = balance between inflammation and healing
- increased inflamm. = unstable
- increased healing = stable
- with modifications of risk factors, unstable plaque can –> stable (and vice versa)
22
Q
What are the 2 pathways of macrophage activation?
A
- Classic Path
- Th1 –> IFN-gamma –> M1 - Alternate Path
- Th2 –> IL-4/IL-13 –> M2
23
Q
Where does plaque accumulation start in BVs and why?
A
At the bifurcation of arteries
- due to increased trauma here from blood hitting this area with increased force
24
Q
What are the risk factors for atherosclerosis?
A
- Non-modifiable
- age, male, family history, genetics - Modifiable
- hyperlipidemia, HTN, smoking, DM, lifestyle - Additional
- CRP, hyperhomocysteinemia, metabolic syndrome, pro-coagulants
25
What are the clinical manifestations associated with unstable plaque?
- unstable angina
- acute MI
- sudden cardiac death
26
What is the earliest microscopic feature in atheroma formation?
Foam cells
27
Outline gross and microscopic changes to heart post-MI
```
Gross:
<4hrs - none
4-12hrs - occasional dark mottling
12-24hrs - dark mottling
1-3days - mottling + yellow tan centre
3-7days - pale/yellow centre with hemorrhagic border
7-10days - max. yellow tan + red margins
1-3wks - red-grey depressed borders, thin (loss of tissue mass)
>3wks - small silvery white scar
```
Micro:
<4hrs - none (loss of LDH/glycogen - special stain*)
4-12hrs - oedema, hemorrhage, beginning of necrosis
12-24hrs - coagulative necrosis, contraction bands, oedema, hemorrhage, neutrophils, pyknosis of nuclei
1-3days - necrosis, loss of nuclei, interstitial neutrophils
3-7days - dead myocytes, dying neutrophils, phagocytosis by macrophages
7-10days - macrophages, granulation tissue
1-3wks - no muscle, new BVs, granulation, fibroblasts (collagen), macrophages
>3wks - dense fibrosis (collagen scar), NO inflammation
28
What is granulation tissue?
Collective term for structure composed of new BVs and collagen fibres formed in the healing process approximately 7-10 days post-MI
29
When is the most dangerous time during healing post-MI for rupture of ventricular walls to occur and why?
Between 3-7days
-macrophages are present and begin phagocytosing dead debris (neutrophils and dying myocytes) --> thus potentially thinning the wall to the point of rupture --> CARDIAC TAMPONADE
30
What is Metabolic Syndrome X?
Collection of disorders that occur together and increase the risk of developing T2DM and CVD. Dx. is made when a person has >/= 3 of:
- central obesity
- HTN
- increased triglycerides
- increased LDLs/decreased HDLs
- increased BSLs
31
Where do coronary arteries arise from and when do they receive blood supply?
- from behind the the cusps of aortic valve
| - receive blood during DIASTOLE, from L+R coronary sinuses
32
What are gross and microscopic features of chronic IHD?
Gross:
- LV dilatation and hypertrophy
- myocardium will show multiple grey-white scars (old MIs)
- evidence of atherosclerosis
- patchy white scars in endothelium --> mural thrombi
Micro:
- myocyte hypertrophy and vacuolisation
- fibrosis
33
What is the commonest cause of clinical angina?
Decreased coronary blood flow (90%)
| -90% of this is atherosclerosis
34
What are contraction bands and when do they occur?
- bright, eosinophilic bands of condensed contractile proteins that run at right angles to the long axis of the cardiac myocyte
- occur after acute MI (12-24hrs)
35
What are the stages of AS plaques?
Foam cells --> fatty streak --> intermediate lesion --> atheroma --> fibrous plaque --> complicated lesion/rupture
36
What is cystic medial degeneration?
- elastic fibre degeneration
- small cyst-like spaces of necrosis in media
- commonest pathogenesis of aortic aneurysms
- caused by atherosclerosis
- separation of media tissue by elastic fragmentation forming cleft-like spaces in media
37
What is IHD?
Primarily a consequence of inadequate coronary perfusion relative to myocardial demand --> angina pectoris
38
What % of the coronary artery is required to be occluded to cause symptoms?
- <70% = asymptomatic
- >70% = critical stenosis (symptomatic on exertion - stable angina)
- >90% = symptomatic at rest - unstable angina
39
What is collateral perfusion?
Remodelling of coronary vessels over time to provide compensatory blood flow for at-risk areas
40
After how long does loss of function and necrosis occur with lack of O2?
loss of function --> 1-2mins
| necrosis --> 20-40mins
41
What is the pathogenesis of ischaemic pain in cell injury/inflammation?
-decreased oxidative phosphorylation = decreased ATP = increased anaerobic glycolysis = increased lactic acid = decreased pH --> PAIN
42
What are the CXR findings of cardiac failure?
```
A - alveolar bat wings
B - kerley B lines
C - cardiothoracic ratio > 50%
D - dilated upper lobe vessels
E - pleural effusion
```
43
What is Nutmeg liver?
Passive venous congestion of liver, characteristic of RHF
44
Give examples of ischaemic vs. non-ischaemic causes of cardiac pain.
Ischaemic:
- stable angina
- unstable angina
- MI
Non-ischaemic:
- myocarditis
- pericarditis
- aortic dissection
45
Outline management process for ACS pts.
M - morphine/fentanyl (analgesia)
O - oxygen if hypoxic
N - nitrates if pain not controlled by opioids
A - aspirin ASAP
L - leads (ECG)
I - IV access + blood tests taken (cardiac markers)
S - streptokinase (+ other thrombolytics)
A - anti-platelet therapy as required
*Re-perfusion Tx. if pts. present within 12hrs of symptom onset
