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CVS II > Atheroma, Infarction, Preventation > Flashcards

Atheroma, Infarction, Preventation Flashcards

1
Q

Key components of atheromatous plaques?

A

Necrotic core (inner)
Cellular layer
Fibrous cap

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2
Q

Components of necrotic core?

A

dead cellular tissue, lipid, cholesterol clefts, fibrin, foam cells, cell debris

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3
Q

Where does the necrotic core lie?

A

between media+intima

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4
Q

Components of cellular layer?

A

foam cells, migrating SM cells, macrophages, lymphocytes, less connective tissue

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5
Q

Components of fibrous cap?

A

SM cells + collagen

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6
Q

Where does the fibrous cap lie?

A

below endothelium if stable plaque

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7
Q

Stages of atheromatous plaques?

A
  • initial lesion
  • fatty streak
  • intermediate lesion
  • atheroma
  • fibroatheroma
  • complicated lesion
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8
Q

What’s initial lesion

A
  • isolated foam cells
  • macrophage infiltration in intima builds up
  • lipid accumulation
  • fatty streak
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9
Q

How does fatty streak grow?

A

from intracellular lipid accumulation

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10
Q

What’s intermediate lesion

A

intracellular lipid accumulation

small intracellular lipid pools

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11
Q

Describe atheroma

A

intracellular lipid accumulation

core of extracellular lipid

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12
Q

Describe fibroatheroma

A

single/multiple lipid cores

calcified

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13
Q

How does fibroatheroma grow?

A

increased SM + collagen

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14
Q

What’s complicated lesion

A

surface defect
hematoma-haemorrhage
thrombosis

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15
Q

How does complicated lesion grow?

A

hematoma/thrombosis

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16
Q

At 20 what’s the sig coronary atherosclerosis?

A

20%

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17
Q

At 20-29 what’s the sig coronary atherosclerosis?

A

50%

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18
Q

At 30-39 what’s the sig coronary atherosclerosis?

A

65%

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19
Q

Common sites of plaque build up?

A 
Circle of Willis
Carotid arteries
Coronary arteries
Aorta
Iliac arteries
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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
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21
Q

eg of inflammatory mediators (IM)?

A

LDL + Angiotension II

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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
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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
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24
Q

Describe maturation of plaque

A
  • SM + foam cell becomes apoptotic
  • releases lipid forms necrotic core
  • matrix breakdown forms fibrous cap
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25
Q

Describe calcification + instability of plaque

A
  • foam cells release calcium deposits

- unstabilises plaque

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26
Q

Describe rupture of plaque

A
  • endothelial breaks
  • vWf exposed to active platelets + TF activates coagulation cascade
  • thrombosis in coronary artery
  • MI
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27
Q

Describe rupture of plaque

A
  • endothelial breaks
  • vWf exposed to active platelets + TF activates coagulation cascade
  • thrombosis in coronary artery
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28
Q

What’s occlusive thrombosis + eg?

A

blocks artery eg MI

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29
Q

What’s thromboembolism + eg?

A

thrombus moves eg ischaemic stroke

30
Q

What’s peripheral vascular disease + eg?

A

less blood flow to legs so wounds don’t heal eg critical limb ischaemia

31
Q

What’s aneurysm + eg?

A

wall weakness eg AAA

32
Q

Causes of chest pain?

A 
Broken rib
Collapsed lung
Nerve infection (shingles)
“Pulled” muscle
Infection
Heart burn (hernia)
Pericarditis
Blood clot in the lungs (PE)
Angina
MI
33
Q

What’s stable cardiac angina?

A

atheroma which permanently limits blood flow

34
Q

What’s unstable cardiac angina?

A

transient thrombosis where rupture causes thrombosis which is cleaned up by fibrolytic system

35
Q

What’s MI?

A

COMPLETE blockage of coronary artery

36
Q

ECG of MI?

A

ST elevation

37
Q

Why are there elevated cardiac troponins released during MI?

A

necrosis

38
Q

Treatment of Acute Coronary Syndromes?

A 
PHARMACOLOGICAL:
General myocardial oxygenation
Antiplatelet/Antithrombotic
Analgesia
Myocardial energy consumption
Coronary vasodilatation
Anticoagulation
Thrombolysis
Plaque stabilization
SURGERY:
Reperfusion
Re-vascularisation
39
Q

Time frames for Acute Coronary Syndromes treatment?

A

Arrival to ECG: 10 min
Door-to-needle for thrombolysis: 20 min
Door-to-balloon time for PCI: 60 min

40
Q

Treatment of MI?

A 
SURGERY:
Balloon angioplasty
Stent
Coronary bypass
PHARMACOLOGICAL
41
Q

What are the pharmacological treatments for MI + ischaemic stroke?

A

tPA + bacterial activator, streptokinase for therapeutic thrombolysis

42
Q

Describe how tPA works?

A
  • allows plasminogen -> plasmin

- lyse fibrin to get D dimers

43
Q

How are D dimers generated?

A

when cross-linked fibrin is degraded

44
Q

How are FDP (Fibrin degradation products) generated?

A

when non-cross linked fibrin or fibrinogen is broken down

45
Q

Complications of MI?

A 
Acute pump failure
Conduction problems – arrhythmia
Papillary damage – valve dysfunction
Mural thrombosis - stroke
Wall rupture
Chronic pump failure – myocardial fibrosis/scarring
46
Q

Long term management after MI?

A 
❌🚬
 🏃‍♂️
 Diabetes management
 ❌🍔
 Blood pressure control
 Lipid management
 Management of heart failure or LV dysfunction
 Prevention of sudden death
47
Q

eg of CVD?

A 
coronary heart disease (CHD) 
cerebrovascular disease
peripheral arterial disease
rheumatic and congenital heart diseases 
venous thromboembolism
lymphatic disease
48
Q

CVD mortality in men vs women?

A

men: 25%
women: 17%

49
Q

Define primary prevention

A

lowering the risk of disease occurring

50
Q

Define secondary prevention

A

lowering the risk of disease recurring

51
Q

Where does 80% CVD mortality occur?

A

in developing nations

52
Q

Why’s CVD worldwide predicted to increase?

A

as the prevalence of risk factors rises in previously low-risk countries

53
Q

What does primary prevention prevent?

A
  • risk factors
  • oxidative + mechanical stress + inflammation
  • early tissue dysfunction
  • atherothrombosis + progresive CVD
  • MI, stroke, renal/peripheral arterial insufficeincy
54
Q

What does secondary prevention prevent?

A
  • MI, stroke, renal/peripheral arterial insufficeincy
  • pathological remodelling
  • target organ damage
  • end-organ failure
  • death
55
Q

Where’s early deaths from CVD (<75) most common?

A

north England, central Scotland, south Wales

56
Q

Where’s highest rate of CVD decline?

A

deprivation from low socioeconomic communities

57
Q

Direct healthcare costs of CVD per year?

A

£9 billion

58
Q

CVD cost to the UK economy per year (including premature death, disability, informal costs) ?

A

£19 billion

59
Q

How much MI is preventable?

A

90%

60
Q

Risk factors of CVD?

A

🚬
Abnormal lipid profile (apolipoprotein ratio apoB/apoA-I)
Hypertension
Diabetes mellitus
Abdominal obesity (abdominal fat is a stronger predictor than BMI)
Psychosocial (stress)

61
Q

Protective factors of CVD?

A

Regular 🍎 + 🥦
🏃‍♂️
Moderate 🥤

62
Q

Non-modifiable risks of CVD?

A

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
Q

Management of CVD?

A 
❌🚬
🏃‍♂️
Diet + weight reduction
Lipid management
BP control
Diabetes management
64
Q

Dietary targets to prevent CVD?

A
  • 🍎🥦🥜 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
Q

Consequences of improving lipid profiles by daily statins?

A

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
Q

When is drug treatment for hypertension used?

A

systolic pressure above 160 /diastolic above 100 mmHg

67
Q

Link between diabetes + CVD risk?

A

Risk from diabetes is as great as having previous history of CVD

68
Q

2 approaches to primary prevention?

A

Individual: clinician tailors care to individual patient needs + risk factors
Population: increased public awareness - or law used to reduce risk factors

69
Q

How each approach of primary prevention contributes to decline in UK CHD events?

A

42% of decline from interventional approaches (both primary and secondary)
58% from population-level approaches influencing smoking + hypertension

70
Q

Issues with secondary prevention + eg?

A

failure of the medical profession to engage with patients

eg 1 in 7 patients were advised to attend smoking cessation clinics

71
Q

What does class I level A mean + eg?

A

benefit&raquo_space;> risk with large studies

Dietary interventions to lower LDL-C + lower BP

72
Q

What does class IIb level B mean + eg?

A

no benefit/harm with single studies

HbA1C testing of asymptomatic patients w/o diagnosis of diabetes + genomic testing

CVS II (19 decks)

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