Atherosclerosis Flashcards
(106 cards)
1
Q
What is the definition of atheroma?
A
Formation of a focal elevated lesion (plaque) win the intima of large and medium-sized arteries
2
Q
Describe the general progression of atheroma formation?
A
- Fatty streak
- Early atheromatous plaque
- Fully developed atheromatous plaque
3
Q
What structures can rim the intima?
A
Foamy macrophages
4
Q
What is the nature of atheroma that leads to occlusion of vessels?
A
Highly thrombogenic
5
Q
What is arteriosclerosis?
A
Non-atheromatous disease - age related loss of compliance of elastic fibres of arteries
6
Q
What comprises a fatty streak?
A
Lipid laden macrophages - look like a yellow smear
7
Q
What are the constituents of a fully atheromatous plaque?
A
Central lipid core capped with fibrous material and covered by a endothelial layer
8
Q
What is the physiological change in arteriosclerosis?
A
Smooth muscle hypertrophy, apparent reduplication of elastic laminae, intimal fibrosis leads to decrease in vessel diameter
9
Q
What is the general aetiology of atheroma?
A
Hypercholeterolaemia
10
Q
What are the typical signs of hyperlipidaemia?
A
Biochemical evidence - LDL, HDL total cholesterol and TAGs
Corneal arcus
Tendon xanthomata
11
Q
What is the two step process to developing an atheromatous plaque?
A
- Endothelial injury
2. Chronic inflammation and healing response of the vascular wall
12
Q
Risk factors of atheroma are?
A
Smoking Hypertension Diabetes mellitus Male Elderly
13
Q
What are some less strong risk factors for developing atheroma?
A
Obesity
Sedentary lifestyle
Low-Socioeconomic status
Low birthweight
14
Q
Normal blood flow is described as what?
A
Laminar
15
Q
What two abnormal blood flow patterns are there?
A
Stagnation and turbulence
16
Q
What can abnormal blood flow precede?
A
Thromboembolism, atheroma, hyperviscosity, spasm, vasculitis and vascular steal
17
Q
What is vascular steal?
A
Reduction in blood flow to tissue as a result of abnormal blood flow
18
Q
What is Virchow’s Triad?
A
A set of three conditions for the development of thromboembolism
19
Q
What does Virchow’s Triad consist of?
A
- Changes in blood vessel intima
- Changes in blood constituents
- Changes in the pattern of blood flow
20
Q
What is thrombosis?
A
The formation of a solid mass from the constituents of blood within the vascular system during life
21
Q
What is the pathogenesis of thrombosis?
A
- Endothelial injury
- Stasis or turbulent blood flow
- Hypergoaculability of blood
22
Q
What do the consequences of thrombosis depend on?
A
Site, extent and collateral circulation
23
Q
What are the common clinical outcomes of thrombosis?
A
DVT, Ischaemic limb and MI
24
Q
What is embolism?
A
Movement of abnormal material in the bloodstream and its impaction in a vessel; blocking its lumen
25
What is an embolus?
Detached intravascular solid, liquid or gaseous mass
26
Most emboli are dislodged thrombi; what are these known as?
Thromboemoli
27
List a few types of emboli
```
Systemic/arterial
Venous embolism
Fat embolus
Gas embolus
Air embolus
```
Tumour, trophoblast, septic material, amniotic fluid, bone marrow, foreign bodies
28
What is the pathophysiology of SIHD?
Due to a mismatch between the demand for O2 by the myocardium and supply
29
What causes SIHD?
Reduced blood flow in coronary arteries
Reduced oxygen tension
Pathological increase in O2 demand
30
What are common, infrequent and rare cases of reduced blood flow in coronary arteries?
Common - Atherosclerosis
Infrequent - Coronary artery spasm
Rare - Coronary inflammation/arthritis
31
What could cause reduced oxygen tension?
Anaemia
32
What could cause a pathological increase in O2 demand?
Left ventricular hypertrophy and thyrotoxicosis
33
What are a few examples of modifiable risk factors for SIHD?
Smoking, diet, hyperlipidaemia, hypertension, diabetes
34
What are a fe non-modifiable risk factors for SIHD?
Age, sex, genetics
35
What is the defining clinical presentation of SIHD?
Retro-sternal dull chest pain with potential radiation into the left axilla and neck
36
What are the five relevant investigations for SIHD?
```
Blood tests
CXR
ECG
ETT
Myocardial perfusion imaging
```
37
What would you look for in a full blood test?
Electrolytes, thyroid and liver function, fasting glucose, FBC and lipid profile
38
What would you look for in an ECG?
Pathological Q-waves - Prior MI
High voltage/lateral ST-depression (strain pattern) - LVH
39
What would you look for in an ETT?
ST depression strain pattern for positive test
40
What does myocardial perfusion imaging help distinguish?
Between ischaemia and MI
41
If it is not possible to get the patient to exercise, how can stress be induced?
Adenosine
42
What is the role of treatment in the SIHD?
1. Halt progression
2. Relieve symptoms
3. Regression of disease
4. Prevent MI
43
What is the drug regimen for treatment of SIDH?
1. Beta-blocker
2. Aspirin
3. Statin
4. CCB
5. Nitrate
6. Nicroandil
44
What do beta-blockers do?
Slow heart rate
45
What does aspirin do?
Anticoagulant
46
What do statins do?
Reduce blood cholesterol
47
What do CCBs do?
Rate limiting and vasodilator types
48
What is the rebound phenomenon?
Sudden cessation of beta-blockers precipitates MI
49
Why don't we use immediate release nefidipine?
Has significant ADRs such as stroke, arrhythmias and MI
50
What do nitrates do?
Vasodilation
51
What does nicorandil do?
Vasodilator (potassium channel opener)
52
What interventions are used for the treatment SIHD?
Cardiac angiography (PCI) and stenting or Coronary Artery Bypass Graft (CABG)
53
What is the definition of myocardial infarction?
Myocardial necrosis due to ischaemia
54
Describe the prevalence of MI in Scotland in regards to mortality
Second biggest killer
55
What is the typical presentation of an acute MI?
- Looks very unwell
- Often no specific features
- Check: Heart rate, blood pressure and murmurs/crepitations
56
What are the characteristics of a STEMI?
Initial ECG shows STEMI
Three days proceeding will show pathological Q-waves
57
What are the characteristics of a NSTEMI?
Intimal ECG shows NSTEMI
Three days proceeding shows no pathological Q-waves
58
How is diagnosis of MI made using biomarkers?
Detection of cardiac death using troponin
59
What non-cardiac causes of elevated troponin are there?
Pulmonary embolism, sepsis, renal failure and sub-arachnoid haemorrhage
60
What is the goal of pharmacological treatment of ACS?
Increased myocardial oxygen supply
Decrease myocardial oxygen demand
61
How can pharmacology decrease myocardial oxygen demand?
Decree heart rate, blood pressure, preload and contractility
62
What is the pharmacology regimen for treatment of ACS?
1. Aspirin
2. Fondaparinux/LMW heparin
3. IV nitrates
4. Beta-blockers
5. Statins
6. Analgesia
(7. GPIIbIIIa receptor blockers)
63
How is aspirin given in the treatment of ACS and in combination with what?
High initial dose of aspirin and given with clopidogrel
64
What is the pharmacological action of GPIIbIIa receptor blockers?
Anti-coagulant
65
What is the indication for PCI in regards to NSTEMIs?
If they are likely to suffer subsequent cardiac events
66
What is the nature of STEMIs that means it requires PCI within two hours?
Highly thrombogenic
67
If it is not possible to undergo percutaneous cardiac intervention, what other procedure may be done?
Thrombolysis
68
What is the definition of ischaemia?
Relative lacking go blood supply to tissues/organs leading to inadequate oxygen supply to meet the needs of the tissue
69
What is the definition of hypoxia?
Normal inspired O2 but abnormal level in tissues
70
What are the different types of hypoxic hypoxia?
Type a - Low inspired O2
Type b - Normal inspired O2 but low PaO2
71
What is the definition of infarction?
Necrosis due to ischaemia
72
What is the relationship between atheroma and ischaemia?
Atheroma causes a reduction in blood flow, causing ischaemia to tissues detail to the atheroma
73
What are the consequences of ischaemia?
Reduced oxygen delivery which eventually leads to infarction
74
Outline the process of ischaemia to infarction
```
Seconds - anaerobic ATP depletion
<2mins - loss of myocardial contractility
<30mins - irreversible damage
<40mins - necrosis
>1hr - injury to microvasculature
```
75
What is the process of infarction within 24 hours?
Early coagulation necrosis, oedema and haemorrhage, neutrophil infiltration
76
What is the process of infarction within 1 week?
Loss of striations, disintegration of dead myofibres, dying neutrophils and early phagocytosis
77
What is the process of infarction within 2 weeks?
Granulation tissue deposition at margins penetrating in and collagen deposition
78
What is the process of infarction within 2 months?
Increased collagen deposition and decreased cellularity
79
What is the process of infarction beyond two months?
Dense collagenous scarring
80
What are the two types of infant?
Subendothelial and transmural
81
What is transmural infarction?
Full thickness of myocardium
82
What is sub-endothelial infarction?
Ischaemic necrosis mostly limited to a zone just under the endothelial lining of the heart
83
What are prognostic differences for transmural vs sub-endothelial infarction?
Slightly better to have sub-endothelial
84
What are the two consequences of infarction?
Loss of myocardial contractility and injury to the microvasculature
85
What is the reparative process of infarction?
1. Cell death
2. Acute inflammation
3. Macrophage phagocytosis of dead cells
4. Granulation tissue
5. Collagen deposition (fibrosis)
6. Scar formation
86
What are the two types of necrosis?
Colliquitive and coagulative
87
Where does colliquitive necrosis occur?
Occurs in brain
88
Where does coagulative necrosis occur?
Heart and lungs
89
What are some major risk factors for stroke?
Hypertension, diabetes, stress, diet etc .
90
What is the acute treatment for stroke?
Thrombolysis
91
What is primary prevention of stroke?
Preventing a stroke from happening having never suffered one before
92
What is secondary prevention?
Preventing a stroke having suffered one before
93
What approaches to secondary prevention of stroke are there?
Pharmacological:
- Aspirin and clipidogrel
- Statins
- Blood pressure medication
Surgical
-Carotid endarterectomy
94
What investigations are carried out on a stroke patient?
Blood tests
ECG
Imaging including CT, MRI and carotid doppler
95
What are the benefits of using CT over MRI?
CT is quick and shows up blood
MRI is slow af and expensive and claustrophobic
96
What is the benefit of MRI over a CT in regards to stroke?
Shows up ischaemic stroke better than CT does
97
What is claudication?
Limb pain exacerbated by physical activity
98
When does claudication resolve?
On rest
99
Claudication is the most common manifestation of what diseases?
Peripheral arterial disease
100
What is the clinical presentation of aneurysmal disease?
Not symptomatic unless enlargement of vessel compresses other anatomy
Usually incidental finding
Symptomatic on rupture
101
What two circulatory systems supply the brain?
The carotid and vertebra-basilar system
102
What does the carotid system supply?
Most of the hemispheres and cortical deep white matter
103
What does the vertebra-basilar system supply?
The brain stem, cerebellum and occipital lobes
104
What are the stroke subtypes?
TACS - Total anterior circulation
PACS - partial anterior circulation
LACS - lacunar stroke
POCS - posterior circulation
105
Surgery for carotid artery stenosis is called what?
Carotid endarterectomy
106
Surgical bypass for limb arteries require what three things
Inflow, conduit and outflow
