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Systems 1a Revision Decks > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

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

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2
Q

Describe the general progression of atheroma formation?

A
  • Fatty streak
  • Early atheromatous plaque
  • Fully developed atheromatous plaque
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3
Q

What structures can rim the intima?

A

Foamy macrophages

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4
Q

What is the nature of atheroma that leads to occlusion of vessels?

A

Highly thrombogenic

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5
Q

What is arteriosclerosis?

A

Non-atheromatous disease - age related loss of compliance of elastic fibres of arteries

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6
Q

What comprises a fatty streak?

A

Lipid laden macrophages - look like a yellow smear

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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

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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

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9
Q

What is the general aetiology of atheroma?

A

Hypercholeterolaemia

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10
Q

What are the typical signs of hyperlipidaemia?

A

Biochemical evidence - LDL, HDL total cholesterol and TAGs

Corneal arcus

Tendon xanthomata

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11
Q

What is the two step process to developing an atheromatous plaque?

A
  1. Endothelial injury

2. Chronic inflammation and healing response of the vascular wall

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12
Q

Risk factors of atheroma are?

A 
Smoking
Hypertension
Diabetes mellitus 
Male
Elderly
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13
Q

What are some less strong risk factors for developing atheroma?

A

Obesity
Sedentary lifestyle
Low-Socioeconomic status
Low birthweight

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14
Q

Normal blood flow is described as what?

A

Laminar

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15
Q

What two abnormal blood flow patterns are there?

A

Stagnation and turbulence

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16
Q

What can abnormal blood flow precede?

A

Thromboembolism, atheroma, hyperviscosity, spasm, vasculitis and vascular steal

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17
Q

What is vascular steal?

A

Reduction in blood flow to tissue as a result of abnormal blood flow

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18
Q

What is Virchow’s Triad?

A

A set of three conditions for the development of thromboembolism

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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
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20
Q

What is thrombosis?

A

The formation of a solid mass from the constituents of blood within the vascular system during life

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21
Q

What is the pathogenesis of thrombosis?

A
  • Endothelial injury
  • Stasis or turbulent blood flow
  • Hypergoaculability of blood
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22
Q

What do the consequences of thrombosis depend on?

A

Site, extent and collateral circulation

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23
Q

What are the common clinical outcomes of thrombosis?

A

DVT, Ischaemic limb and MI

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24
Q

What is embolism?

A

Movement of abnormal material in the bloodstream and its impaction in a vessel; blocking its lumen

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25
Q

What is an embolus?

A

Detached intravascular solid, liquid or gaseous mass

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26
Q

Most emboli are dislodged thrombi; what are these known as?

A

Thromboemoli

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27
Q

List a few types of emboli

A 
Systemic/arterial 
Venous embolism 
Fat embolus 
Gas embolus 
Air embolus

Tumour, trophoblast, septic material, amniotic fluid, bone marrow, foreign bodies

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28
Q

What is the pathophysiology of SIHD?

A

Due to a mismatch between the demand for O2 by the myocardium and supply

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29
Q

What causes SIHD?

A

Reduced blood flow in coronary arteries

Reduced oxygen tension

Pathological increase in O2 demand

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30
Q

What are common, infrequent and rare cases of reduced blood flow in coronary arteries?

A

Common - Atherosclerosis

Infrequent - Coronary artery spasm

Rare - Coronary inflammation/arthritis

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31
Q

What could cause reduced oxygen tension?

A

Anaemia

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32
Q

What could cause a pathological increase in O2 demand?

A

Left ventricular hypertrophy and thyrotoxicosis

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33
Q

What are a few examples of modifiable risk factors for SIHD?

A

Smoking, diet, hyperlipidaemia, hypertension, diabetes

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34
Q

What are a fe non-modifiable risk factors for SIHD?

A

Age, sex, genetics

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35
Q

What is the defining clinical presentation of SIHD?

A

Retro-sternal dull chest pain with potential radiation into the left axilla and neck

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36
Q

What are the five relevant investigations for SIHD?

A 
Blood tests
CXR
ECG
ETT
Myocardial perfusion imaging
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37
Q

What would you look for in a full blood test?

A

Electrolytes, thyroid and liver function, fasting glucose, FBC and lipid profile

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38
Q

What would you look for in an ECG?

A

Pathological Q-waves - Prior MI

High voltage/lateral ST-depression (strain pattern) - LVH

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39
Q

What would you look for in an ETT?

A

ST depression strain pattern for positive test

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40
Q

What does myocardial perfusion imaging help distinguish?

A

Between ischaemia and MI

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41
Q

If it is not possible to get the patient to exercise, how can stress be induced?

A

Adenosine

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42
Q

What is the role of treatment in the SIHD?

A
  1. Halt progression
  2. Relieve symptoms
  3. Regression of disease
  4. Prevent MI
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43
Q

What is the drug regimen for treatment of SIDH?

A
  1. Beta-blocker
  2. Aspirin
  3. Statin
  4. CCB
  5. Nitrate
  6. Nicroandil
44
Q

What do beta-blockers do?

A

Slow heart rate

45
Q

What does aspirin do?

A

Anticoagulant

46
Q

What do statins do?

A

Reduce blood cholesterol

47
Q

What do CCBs do?

A

Rate limiting and vasodilator types

48
Q

What is the rebound phenomenon?

A

Sudden cessation of beta-blockers precipitates MI

49
Q

Why don’t we use immediate release nefidipine?

A

Has significant ADRs such as stroke, arrhythmias and MI

50
Q

What do nitrates do?

A

Vasodilation

51
Q

What does nicorandil do?

A

Vasodilator (potassium channel opener)

52
Q

What interventions are used for the treatment SIHD?

A

Cardiac angiography (PCI) and stenting or Coronary Artery Bypass Graft (CABG)

53
Q

What is the definition of myocardial infarction?

A

Myocardial necrosis due to ischaemia

54
Q

Describe the prevalence of MI in Scotland in regards to mortality

A

Second biggest killer

55
Q

What is the typical presentation of an acute MI?

A
  • Looks very unwell
  • Often no specific features
  • Check: Heart rate, blood pressure and murmurs/crepitations
56
Q

What are the characteristics of a STEMI?

A

Initial ECG shows STEMI

Three days proceeding will show pathological Q-waves

57
Q

What are the characteristics of a NSTEMI?

A

Intimal ECG shows NSTEMI

Three days proceeding shows no pathological Q-waves

58
Q

How is diagnosis of MI made using biomarkers?

A

Detection of cardiac death using troponin

59
Q

What non-cardiac causes of elevated troponin are there?

A

Pulmonary embolism, sepsis, renal failure and sub-arachnoid haemorrhage

60
Q

What is the goal of pharmacological treatment of ACS?

A

Increased myocardial oxygen supply

Decrease myocardial oxygen demand

61
Q

How can pharmacology decrease myocardial oxygen demand?

A

Decree heart rate, blood pressure, preload and contractility

62
Q

What is the pharmacology regimen for treatment of ACS?

A
  1. Aspirin
  2. Fondaparinux/LMW heparin
  3. IV nitrates
  4. Beta-blockers
  5. Statins
  6. Analgesia
    (7. GPIIbIIIa receptor blockers)
63
Q

How is aspirin given in the treatment of ACS and in combination with what?

A

High initial dose of aspirin and given with clopidogrel

64
Q

What is the pharmacological action of GPIIbIIa receptor blockers?

A

Anti-coagulant

65
Q

What is the indication for PCI in regards to NSTEMIs?

A

If they are likely to suffer subsequent cardiac events

66
Q

What is the nature of STEMIs that means it requires PCI within two hours?

A

Highly thrombogenic

67
Q

If it is not possible to undergo percutaneous cardiac intervention, what other procedure may be done?

A

Thrombolysis

68
Q

What is the definition of ischaemia?

A

Relative lacking go blood supply to tissues/organs leading to inadequate oxygen supply to meet the needs of the tissue

69
Q

What is the definition of hypoxia?

A

Normal inspired O2 but abnormal level in tissues

70
Q

What are the different types of hypoxic hypoxia?

A

Type a - Low inspired O2

Type b - Normal inspired O2 but low PaO2

71
Q

What is the definition of infarction?

A

Necrosis due to ischaemia

72
Q

What is the relationship between atheroma and ischaemia?

A

Atheroma causes a reduction in blood flow, causing ischaemia to tissues detail to the atheroma

73
Q

What are the consequences of ischaemia?

A

Reduced oxygen delivery which eventually leads to infarction

74
Q

Outline the process of ischaemia to infarction

A 
Seconds - anaerobic ATP depletion 
<2mins - loss of myocardial contractility 
<30mins - irreversible damage 
<40mins - necrosis 
>1hr - injury to microvasculature
75
Q

What is the process of infarction within 24 hours?

A

Early coagulation necrosis, oedema and haemorrhage, neutrophil infiltration

76
Q

What is the process of infarction within 1 week?

A

Loss of striations, disintegration of dead myofibres, dying neutrophils and early phagocytosis

77
Q

What is the process of infarction within 2 weeks?

A

Granulation tissue deposition at margins penetrating in and collagen deposition

78
Q

What is the process of infarction within 2 months?

A

Increased collagen deposition and decreased cellularity

79
Q

What is the process of infarction beyond two months?

A

Dense collagenous scarring

80
Q

What are the two types of infant?

A

Subendothelial and transmural

81
Q

What is transmural infarction?

A

Full thickness of myocardium

82
Q

What is sub-endothelial infarction?

A

Ischaemic necrosis mostly limited to a zone just under the endothelial lining of the heart

83
Q

What are prognostic differences for transmural vs sub-endothelial infarction?

A

Slightly better to have sub-endothelial

84
Q

What are the two consequences of infarction?

A

Loss of myocardial contractility and injury to the microvasculature

85
Q

What is the reparative process of infarction?

A
  1. Cell death
  2. Acute inflammation
  3. Macrophage phagocytosis of dead cells
  4. Granulation tissue
  5. Collagen deposition (fibrosis)
  6. Scar formation
86
Q

What are the two types of necrosis?

A

Colliquitive and coagulative

87
Q

Where does colliquitive necrosis occur?

A

Occurs in brain

88
Q

Where does coagulative necrosis occur?

A

Heart and lungs

89
Q

What are some major risk factors for stroke?

A

Hypertension, diabetes, stress, diet etc .

90
Q

What is the acute treatment for stroke?

A

Thrombolysis

91
Q

What is primary prevention of stroke?

A

Preventing a stroke from happening having never suffered one before

92
Q

What is secondary prevention?

A

Preventing a stroke having suffered one before

93
Q

What approaches to secondary prevention of stroke are there?

A

Pharmacological:

  • Aspirin and clipidogrel
  • Statins
  • Blood pressure medication

Surgical
-Carotid endarterectomy

94
Q

What investigations are carried out on a stroke patient?

A

Blood tests
ECG
Imaging including CT, MRI and carotid doppler

95
Q

What are the benefits of using CT over MRI?

A

CT is quick and shows up blood

MRI is slow af and expensive and claustrophobic

96
Q

What is the benefit of MRI over a CT in regards to stroke?

A

Shows up ischaemic stroke better than CT does

97
Q

What is claudication?

A

Limb pain exacerbated by physical activity

98
Q

When does claudication resolve?

A

On rest

99
Q

Claudication is the most common manifestation of what diseases?

A

Peripheral arterial disease

100
Q

What is the clinical presentation of aneurysmal disease?

A

Not symptomatic unless enlargement of vessel compresses other anatomy

Usually incidental finding

Symptomatic on rupture

101
Q

What two circulatory systems supply the brain?

A

The carotid and vertebra-basilar system

102
Q

What does the carotid system supply?

A

Most of the hemispheres and cortical deep white matter

103
Q

What does the vertebra-basilar system supply?

A

The brain stem, cerebellum and occipital lobes

104
Q

What are the stroke subtypes?

A

TACS - Total anterior circulation
PACS - partial anterior circulation
LACS - lacunar stroke
POCS - posterior circulation

105
Q

Surgery for carotid artery stenosis is called what?

A

Carotid endarterectomy

106
Q

Surgical bypass for limb arteries require what three things

A

Inflow, conduit and outflow

Systems 1a Revision Decks (22 decks)

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