Atheroma, Infarction, Preventation Flashcards
(72 cards)
1
Q
Key components of atheromatous plaques?
A
Necrotic core (inner)
Cellular layer
Fibrous cap
2
Q
Components of necrotic core?
A
dead cellular tissue, lipid, cholesterol clefts, fibrin, foam cells, cell debris
3
Q
Where does the necrotic core lie?
A
between media+intima
4
Q
Components of cellular layer?
A
foam cells, migrating SM cells, macrophages, lymphocytes, less connective tissue
5
Q
Components of fibrous cap?
A
SM cells + collagen
6
Q
Where does the fibrous cap lie?
A
below endothelium if stable plaque
7
Q
Stages of atheromatous plaques?
A
- initial lesion
- fatty streak
- intermediate lesion
- atheroma
- fibroatheroma
- complicated lesion
8
Q
What’s initial lesion
A
- isolated foam cells
- macrophage infiltration in intima builds up
- lipid accumulation
- fatty streak
9
Q
How does fatty streak grow?
A
from intracellular lipid accumulation
10
Q
What’s intermediate lesion
A
intracellular lipid accumulation
small intracellular lipid pools
11
Q
Describe atheroma
A
intracellular lipid accumulation
core of extracellular lipid
12
Q
Describe fibroatheroma
A
single/multiple lipid cores
calcified
13
Q
How does fibroatheroma grow?
A
increased SM + collagen
14
Q
What’s complicated lesion
A
surface defect
hematoma-haemorrhage
thrombosis
15
Q
How does complicated lesion grow?
A
hematoma/thrombosis
16
Q
At 20 what’s the sig coronary atherosclerosis?
A
20%
17
Q
At 20-29 what’s the sig coronary atherosclerosis?
A
50%
18
Q
At 30-39 what’s the sig coronary atherosclerosis?
A
65%
19
Q
Common sites of plaque build up?
A
Circle of Willis Carotid arteries Coronary arteries Aorta Iliac arteries
20
Q
Major risk factors for atherosclerosis?
A
Age, genetics 🚬🥤💊🍔 Male + menopausal women Hyperlipidaemia Hypertension Diabetes mellitus Metabolic syndrome Systemic inflammation promotes atheroma eg rheumatoid arthritis + parasitic infections
21
Q
eg of inflammatory mediators (IM)?
A
LDL + Angiotension II
22
Q
Describe initiation
A
- oxidised LDL + angiotension II is an inflammatory mediator
- inflammation
- activates endothelial releases cytokines + adhesion molecules
- circulating monocyte lodges to endothelial cell
- monocyte moves into intima
- monocyte differentiates into tissue macrophage
23
Q
Describe plaque formation
A
- tissue macrophage takes up LDL
- becomes foam cell
- releases IM
- SM cells migrates into intima + profilerates
- releases elastic + collagen
24
Q
Describe maturation of plaque
A
- SM + foam cell becomes apoptotic
- releases lipid forms necrotic core
- matrix breakdown forms fibrous cap
25
Describe calcification + instability of plaque
- foam cells release calcium deposits
| - unstabilises plaque
26
Describe rupture of plaque
- endothelial breaks
- vWf exposed to active platelets + TF activates coagulation cascade
- thrombosis in coronary artery
- MI
27
Describe rupture of plaque
- endothelial breaks
- vWf exposed to active platelets + TF activates coagulation cascade
- thrombosis in coronary artery
28
What's occlusive thrombosis + eg?
blocks artery eg MI
29
What's thromboembolism + eg?
thrombus moves eg ischaemic stroke
30
What's peripheral vascular disease + eg?
less blood flow to legs so wounds don't heal eg critical limb ischaemia
31
What's aneurysm + eg?
wall weakness eg AAA
32
Causes of chest pain?
```
Broken rib
Collapsed lung
Nerve infection (shingles)
“Pulled” muscle
Infection
Heart burn (hernia)
Pericarditis
Blood clot in the lungs (PE)
Angina
MI
```
33
What's stable cardiac angina?
atheroma which permanently limits blood flow
34
What's unstable cardiac angina?
transient thrombosis where rupture causes thrombosis which is cleaned up by fibrolytic system
35
What's MI?
COMPLETE blockage of coronary artery
36
ECG of MI?
ST elevation
37
Why are there elevated cardiac troponins released during MI?
necrosis
38
Treatment of Acute Coronary Syndromes?
```
PHARMACOLOGICAL:
General myocardial oxygenation
Antiplatelet/Antithrombotic
Analgesia
Myocardial energy consumption
Coronary vasodilatation
Anticoagulation
Thrombolysis
Plaque stabilization
SURGERY:
Reperfusion
Re-vascularisation
```
39
Time frames for Acute Coronary Syndromes treatment?
Arrival to ECG: 10 min
Door-to-needle for thrombolysis: 20 min
Door-to-balloon time for PCI: 60 min
40
Treatment of MI?
```
SURGERY:
Balloon angioplasty
Stent
Coronary bypass
PHARMACOLOGICAL
```
41
What are the pharmacological treatments for MI + ischaemic stroke?
tPA + bacterial activator, streptokinase for therapeutic thrombolysis
42
Describe how tPA works?
- allows plasminogen -> plasmin
| - lyse fibrin to get D dimers
43
How are D dimers generated?
when cross-linked fibrin is degraded
44
How are FDP (Fibrin degradation products) generated?
when non-cross linked fibrin or fibrinogen is broken down
45
Complications of MI?
```
Acute pump failure
Conduction problems – arrhythmia
Papillary damage – valve dysfunction
Mural thrombosis - stroke
Wall rupture
Chronic pump failure – myocardial fibrosis/scarring
```
46
Long term management after MI?
```
❌🚬
🏃♂️
Diabetes management
❌🍔
Blood pressure control
Lipid management
Management of heart failure or LV dysfunction
Prevention of sudden death
```
47
eg of CVD?
```
coronary heart disease (CHD)
cerebrovascular disease
peripheral arterial disease
rheumatic and congenital heart diseases
venous thromboembolism
lymphatic disease
```
48
CVD mortality in men vs women?
men: 25%
women: 17%
49
Define primary prevention
lowering the risk of disease occurring
50
Define secondary prevention
lowering the risk of disease recurring
51
Where does 80% CVD mortality occur?
in developing nations
52
Why's CVD worldwide predicted to increase?
as the prevalence of risk factors rises in previously low-risk countries
53
What does primary prevention prevent?
- risk factors
- oxidative + mechanical stress + inflammation
- early tissue dysfunction
- atherothrombosis + progresive CVD
- MI, stroke, renal/peripheral arterial insufficeincy
54
What does secondary prevention prevent?
- MI, stroke, renal/peripheral arterial insufficeincy
- pathological remodelling
- target organ damage
- end-organ failure
- death
55
Where's early deaths from CVD (<75) most common?
north England, central Scotland, south Wales
56
Where's highest rate of CVD decline?
deprivation from low socioeconomic communities
57
Direct healthcare costs of CVD per year?
£9 billion
58
CVD cost to the UK economy per year (including premature death, disability, informal costs) ?
£19 billion
59
How much MI is preventable?
90%
60
Risk factors of CVD?
🚬
Abnormal lipid profile (apolipoprotein ratio apoB/apoA-I)
Hypertension
Diabetes mellitus
Abdominal obesity (abdominal fat is a stronger predictor than BMI)
Psychosocial (stress)
61
Protective factors of CVD?
Regular 🍎 + 🥦
🏃♂️
Moderate 🥤
62
Non-modifiable risks of CVD?
Age – risk of stroke doubles every decade after 55
Family history – direct blood relative has CHD or stroke before age 55 (65 for female). INTERHEART study says 10% of risk accounted by family history
Ethnicity – Pakistan, Bangladesh, Indian, African Caribbean
63
Management of CVD?
```
❌🚬
🏃♂️
Diet + weight reduction
Lipid management
BP control
Diabetes management
```
64
Dietary targets to prevent CVD?
* 🍎🥦🥜 2-3 servings daily
* ↓saturated FA, <10% of total energy via replacement by poly-unsaturated FA (PUFA).
* Use vegetable oils rich in PUFA + spreads (soybean, canola, extra-virgin olive oil)
* ↓refined grains + sugar 30-45 g wholegrain products fibre daily
* 1-2 servings oily 🐟 weekly (sardines, herring, tuna, salmon, mackerel, trout)
* ❌processed meat, ↓fresh red meat to 2-3 servings weekly
* ❌ trans unsaturated FA
* ❌coke
* ↓sodium <5 gr of salt daily
* 🥤2 glasses daily (20 gr alcohol) in men + 1 glass daily (10 gr alcohol) in women.
65
Consequences of improving lipid profiles by daily statins?
Cost – feasible at a population level?
Distract from simpler ways to lower lipids (diet/exercise)?
Compliance – would people adopt this approach of chronic drug administration?
66
When is drug treatment for hypertension used?
systolic pressure above 160 /diastolic above 100 mmHg
67
Link between diabetes + CVD risk?
Risk from diabetes is as great as having previous history of CVD
68
2 approaches to primary prevention?
Individual: clinician tailors care to individual patient needs + risk factors
Population: increased public awareness - or law used to reduce risk factors
69
How each approach of primary prevention contributes to decline in UK CHD events?
42% of decline from interventional approaches (both primary and secondary)
58% from population-level approaches influencing smoking + hypertension
70
Issues with secondary prevention + eg?
failure of the medical profession to engage with patients
| eg 1 in 7 patients were advised to attend smoking cessation clinics
71
What does class I level A mean + eg?
benefit >>> risk with large studies
| Dietary interventions to lower LDL-C + lower BP
72
What does class IIb level B mean + eg?
no benefit/harm with single studies
| HbA1C testing of asymptomatic patients w/o diagnosis of diabetes + genomic testing
