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Cardiovascular > Ischaemic heart disease and atherosclerosis > Flashcards

Ischaemic heart disease and atherosclerosis Flashcards

1
Q

What is atherosclerosis?

A

The build-up of plaque in arteries

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2
Q

Give 7 risk factors for atherosclerosis

A
  1. Increasing age
  2. Tobacco smoking
  3. High serum cholesterol
  4. Obesity
  5. Diabetes
  6. Hypertension
  7. Family history
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3
Q

Describe the distribution of atheroscleroic plaques

A
  • Within peripheral and coronary arteries
  • Focal distribution along the artery length
  • Distribution may be governed by haemodynamic factors
  • The LAD and right coronary arteries commonly develop atherosclerosis
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4
Q

Describe the structure of a plaque

A

It is a complex lesion with a mixture of cell types - lipid, necrotic core, connective tissue, fibrous ‘cap’

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5
Q

How do atherosclerotic plaques form?

A
  1. Endothelial injury leads to endothelial dysfunction
  2. Chemoattractants attract leukocytes
  3. Leukocytes accumulate and migrate into the vessel wall so inflammation occurs
  4. LDLs can pass through the arterial wall in excess and accumulate in the intima
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6
Q

Name the inflammatory cytokines found in plaques

A 
• Interleukins
	IL-1 (key one)
	IL-6
	IL-8
• Interferons 
	IFN-γ (a very strong pro-inflammatory agent)
• TGF-β (involved in wound healing)
• C reactive protein (linked with IL-6)
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7
Q

Describe the steps in the adhesion cascade of leukocyte recruitment

A
  1. Capture – 1st interaction of the leukocyte with the vessel wall/endothelial cell
  2. Rolling – cell slows down as it rolls along the vessel wall
  3. Firm adhesion to the vessels wall
  4. Transmigration across endothelial cells
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8
Q

In the adhesion cascade, what do selectins mediate?

A

The initial steps of the rolling stage

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9
Q

In the adhesion cascade, what do integrins and chemoattractants mediate?

A

Firm adhesion to the vessels wall and transmigration across endothelial cells

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10
Q

What are the key steps in the disease progression of atherosclerosis?

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaques/advanced lesions
  4. Plaque rupture
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11
Q

When do fatty streaks appear in atherosclerosis?

A

At a very early age (<10yrs)

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12
Q

What do fatty streaks consist of?

A

Aggregations of lipid-laden macrophages and T lymphocytes within the intimal layer of the vessel wall

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13
Q

What are intermmediate lesions composed of?

A
  • Foam cells
  • Vascular smooth muscle cells
  • T lymphocytes
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14
Q

What are foam cells?

A

Lipid laden macrophages

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15
Q

What are fibrous plaques/advanced lesions composed of?

A
  • Smooth muscle cells
  • Lipid core
  • Necrotic debris
  • Macrophages and T lymphocytes
  • Foam cells
  • RBCs
  • Fibrin
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16
Q

What is the dense fibrous cap of atherosclerotic plaques made of?

A

Extracellular matrix proteins including collagen (strength) and elastin (flexibility)

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17
Q

How does plaque rupture occur?

A
  1. The plaque is constantly growing and receding
  2. The fibrous cap needs to be resorbed and redeposited in order to be maintained
  3. If balance shifts e.g. in favour of inflammatory conditions (increased enzyme activity) then the cap becomes weak and the plaque ruptures
  4. Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessel within the plaque
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18
Q

How would you treat coronary artery disease?

A
  • Percutaneous coronary intevention (PCI)
  • Aspirin
  • Statins
  • Antiplatelets e.g. clopidogrel/ticagrelor
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19
Q

Define angina

A

A condition marked by severe chest pain due the mismatch of oxygen supply and demand to the heart

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20
Q

Give 3 reasons for oxygen demand and supply imbalance to the heart

A
  1. Impaired blood flow by proximal arterial stenosis
  2. Increased distal resistance e.g. left ventricular hypertrophy
  3. Reduced oxygen-carrying capacity of blood e.g. anaemia
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21
Q

How is Ohm’s law applied relating to the biology of IHD and angina?

A

Pressure driving blood = blood flow x resistance from plaques and vessels

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22
Q

How is Poiseuille’s equation applied relating to the biology of IHD and angina?

A
  • Change in pressure is inversely proportional to the 4th power of the radius
  • Nothing happens until the diameter of stenosis reaches 70% then there is rapid demand
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23
Q

Give some predisposing factors to IHD and angina

A
  • Smoking
  • Sedentary lifestyle
  • Obesity
  • Hypertension
  • Diabetes mellitus
  • Family history
  • Genetics
  • Age
  • Hypercholesterolaemia
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24
Q

Give 6 supply conditions which would exacerbate IHD/angina

A
  1. Anaemia
  2. Hypoxemia
  3. Polycythaemia
  4. Hypothermia
  5. Hypovolaemia
  6. Hypervolaemia
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25
Q

Give 5 demand conditions which would exacerbate IHD/angina

A
  1. Hypertension
  2. Tachyarrhythmia/tachycardia
  3. Valvular heart disease
  4. Hyperthyroidism
  5. Hypertrophic cardiomyopathy
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26
Q

Give 3 environmental factors which would exacerbate IHD/angina

A
  1. Cold weather
  2. Heavy meals
  3. Emotional stress
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27
Q

Give 5 cardiac symptoms which may suggest angina/IHD

A
  1. Chest pain
  2. Breathlessness
  3. Fluid retention
  4. Palpitations
  5. Syncope/pre-syncope
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28
Q

Describe features which suggest ischaemic heart pain

A
  • Character = heavy, crushing
  • Location = in the middle of the chest
  • Provoking factors = cold weather, big meal, exercise
  • Relieving factors = rest, GTN spray
  • Associated symptoms = breathlessness
  • Associated risk factors = smoking, etc.
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29
Q

Give 7 differential diagnoses of IHD/angina

A
  1. Pericarditis/myocarditis
  2. PE
  3. Chest infection/pleurisy
  4. Dissection of the aorta
  5. Gastro-oesophageal problems e.g. reflux, spasm, ulceration
  6. MSK problems
  7. Psychological – anxiety
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30
Q

How would you treat angina/IHD?

A
  • Reassure patient
  • Tackle key lifestyle factors e.g. smoking, weight
  • Advice for emergency situations
  • Medication and drugs
  • Revascularisation
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31
Q

Name some types of drugs/medication that you might give in IHD/angina

A
  • Aspirin
  • Beta blockers (most effective)
  • Nitrate (GTN spray)
  • Calcium channel blockers
  • Statins
  • ACE inhibitors
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32
Q

What types of revascularisation may be used in IHD/angina?

A
  • Percutaneous coronary intervention (PCI)

* Coronary artery bypass graft (CABG)

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33
Q

How would you diagnose IHD/angina?

A
  • Exercise testing - Monitor ECG when the patient walks on a treadmill
  • Myoview scan (aka perfusion scan) - IV radiolabelled agent is injected and dark spots indicate ischaemia/infarction
  • CT coronary angiogram
  • Stress echo (rare to do as it requires a highly skilled person to perform in)
  • Perfusion MRI
  • Invasive coronary angiography
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34
Q

What is unstable (crescendo) angina?

A
  • Either: Angina of recent onset (<24hrs)

* Or: Cardiac chest pain with crescendo pattern

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35
Q

How does unstable angina differ from stable angina?

A

Unstable may be more severe and occurring on minimal exertion or even at rest

36
Q

How would you diagnose unstable angina?

A
  • History
  • ECG
  • Troponin (no significant rise in unstable angina)
37
Q

What is a STEMI?

A

• ST-elevation myocardial infarction:

  • Complete occlusion of a major coronary artery previously affected by atherosclerosis
  • Causes full thickness damage of the heart muscle
  • Can usually be diagnosed on ECG at presentation
  • Will produce a pathological Q wave sometime after MI so also known as Q wave infarction
38
Q

What is an NSTEMI?

A

• Non-ST elevation myocardial infarction:

  • Complete occlusion of a minor or partial occlusion of a major coronary artery previously affected by atherosclerosis
  • Retrospective diagnosis made after troponin results and sometimes other investigation results
  • Causes partial thickness damage of the heart muscle
  • AKA non-Q wave infarction
39
Q

What would you see on an ECG for a STEMI?

A
  • ST segment elevation

* Pathological Q wave sometime after the MI

40
Q

What would you see on an ECG for an NSTEMI?

A

ST depression and/or T wave inversion

41
Q

Describe the 5 types of MI

A
  • Type 1: spontaneous MI with ischaemia due to a primary coronary event e.g. plaque rupture/erosion, fissuring or dissection
  • Type 2: MI secondary to ischaemia due to increased oxygen demand or decreased supply
  • Types 3-5: MI due to sudden cardiac death, related to PCI and related to CABG respectively
42
Q

What are risk factors for unstable angina?

A

Same as for stable angina:

  • Smoking
  • Sedentary lifestyle
  • Obesity
  • Hypertension
  • Diabetes mellitus
  • Family history
  • Genetics
  • Age
  • Hypercholesterolaemia
43
Q

How would you diagnose acute coronary syndromes?

A
  • 12 lead ECG
  • Biochemical molecules
  • Chest X ray
44
Q

Which biochemical molecules can be used in diagnosis of acute coronary syndromes?

A
  • Troponin T and I
  • CK-MB
  • Myoglobin
45
Q

How are Troponin T and I useful in diagnosis of acute coronary syndromes?

A
  • They are markers of myosin contraction

* They are the most sensitive and specific markers of myocardial necrosis but not specific to ACS

46
Q

How do serum levels of Troponin T and I change during and after an acute coronary syndrome?

A

Serum levels increase in 3-12hrs from chest pain onset, peak at 24-48hrs, then fall back to normal over 5-14 days

47
Q

What might you look for in a chest X-ray for chest pain/suspected ACS?

A
  • Cardiomegaly
  • Pulmonary oedema
  • Widened mediastinum (aortic rupture)
48
Q

How would you treat an acute coronary syndrome?

A
  • Pain relief e.g. GTN spray, IV opioid
  • Anti-emetic
  • Oxygen if hypoxic
  • Antiplatelets e.g aspirin, P2Y12 inhibitors, glycoprotein IIb/IIIa antagonists
  • Other medications e.g. beta blockers, statins, ACE inhibitors
  • Revascularisation e.g. PCI, CABG
  • Risk factor modification e.g. stop smoking, lose weight
49
Q

Describe the anatomy of the pericardium

A

• Two continuous layers
• The visceral layer is adherent to the epicardium
The parietal layer is fibrous and about 2mm thick
• 50ml of serous fluid between the layers - lubricant
• Great vessels lie within, LA is mainly outside

50
Q

What is the parietal layer of the pericardium made out of?

A

Acellular collagen and elastin fibres

51
Q

How does the pericardium promote cardiac efficiency?

A

It limits dilation, maintains ventricular compliance and distributes hydrostatic forces

52
Q

Why does the pericardium only have a small reserve volume?

A

It initially stretches a bit but becomes stiff at higher tensions

53
Q

What is cardiac tamponade?

A

A clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise

54
Q

How does the pericardium adapt in chronic pericardial effusion and what effect does it have?

A

Elastin and collagen are layered down so the pericardium becomes more elastic so there is no collapse of the RA since the pressure equalises

55
Q

Define acute pericarditis

A

Acute inflammation of the pericardium with or without effusion

56
Q

Who is acute pericarditis most commonly seen in?

A

Young, previously healthy, adult patients, more commonly men than women

57
Q

What is the most common infectious cause of acute pericaditis?

A

Viral causes

58
Q

Give some viral causes of acute pericarditis

A
  • Enteroviruses e.g. coxsackieviruses & echoviruses

* Adenoviruses

59
Q

What is the main bacterial cause of acute pericarditis?

A

Mycobacterium tuberculosis (other bacteria are rare)

60
Q

What is the main fungal cause of acute pericarditis and who would it be seen in?

A

Histoplasma spp. - most likely to be seen in immunocompromised patients

61
Q

Give 6 non-infectious causes of acute pericarditis

A
  1. Autoimmune
  2. Neoplastic
  3. Dressler’s syndrome
  4. Traumatic and iatrogenic
  5. Metabolic
  6. Other
62
Q

Give 4 autoimmune causes of acute pericarditis

A
  1. Sjörgren’s syndrome
  2. Rheumatoid arthritis
  3. SLE
  4. Systemic vasculitis
63
Q

What is a neoplastic cause of acute pericarditis?

A

Secondary metastatic tumours, usually from breat or lung cancers

64
Q

What is Dressler’s syndrome?

A

A type of pericarditis where there is an immune system response after cardiac/pericardium injury

65
Q

Are early onset or delayed onset trauma causes of acute pericarditis more common?

A

Delayed onset

66
Q

What are traumatic/iatrogenic causes of acute pericarditis?

A

• Early onset (rare):
 Direct injury - penetrating thoracic injury or oesophageal perforation
 Indirect injury - non-penetrating thoracic injury or radiation
• Delayed onset (common):
 Pericardial injury syndromes (common)
 Iatrogenic trauma e.g. PCI or pacemaker lead insertion

67
Q

Give 2 metabolic causes of acute pericarditis

A
  1. Uraemia

2. Myxoedema

68
Q

Give 4 other causes of acute pericarditis which don’t come under specific categories

A
  1. Amyloidosis
  2. Aortic dissection
  3. Pulmonary artery hypertension
  4. Chronic heart failure
69
Q

Give some clinical presentation features of acute pericarditis

A
  • Chest pain
  • Dyspnoea
  • Cough
  • Hiccups
  • Pericardial friction rub present on auscultation
  • Fever and lymphocytosis if cause is viral/bacterial
  • Tachycardia
70
Q

What might be features of chest pain in acute pericarditis?

A
  • Severe, sharp & pleuritic (without constricting crushing character of ischaemic pain)
  • Rapid onset
  • Worse on inspiration or lying flat - relieved by sitting forward
  • Left anterior chest or epigastrium
  • Radiates to arm, more specifically the trapezius ridge
71
Q

In acute pericarditis, what is the most important differential to rule out?

A

Myocardial infarction

72
Q

Give some differential diagnoses of acute pericarditis

A
  • MI
  • Pleurisy
  • Gastro-oesophageal reflux
  • Pancreatitis
  • Angina
  • PE
  • Aortic dissection
  • Pneumonia
  • Costochondritis
  • Pneumothorax
  • Herpes zoster (shingles)
73
Q

How would you diagnose acute pericarditis?

A
  • Clinical exam
  • ECG
  • CXR
  • Bloods
  • Echocardiogram
74
Q

What would you see on an ECG for acute pericarditis?

A
  • Saddle shaped ST elevation
  • Diffuse ST segment elevation - present in all leads
  • PR depression
  • An ECG is diagnostic for acute pericarditis
75
Q

What might you see on an chest X-ray for acute pericarditis?

A
  • May show cardiomegaly due to effusion but often normal

* Pneumonia is common with bacterial pericarditis

76
Q

What bloods might you do and what might you see for acute pericarditis?

A
  • FBC: increased WCC, elevated troponin suggests myopericarditis
  • ESR/CRP: high ESR indicated autoimmune
77
Q

Why might you do an echocardiogram inacute pericarditis?

A

To confirm if there is effusion/cardiomegaly on a CXR

78
Q

How would you treat acute pericarditis?

A
  • Restrict physical activity until symptom resolution and improvement in ECG and CRP
  • NSAIDs
  • Colchicine for 3 weeks (limited by nausea and diarrhoea)
79
Q

What is the 5 year mortality rate for mild/moderate peripheral artery disease?

A

25%

80
Q

What is the 5 year mortality rate for severe peripheral artery disease?

A

75%

81
Q

Give some complications of atherosclerotic plaques

A
  • Progression (increase in size etc. leading to narrowing and occlusion)
  • Haemorrhage
  • Plaque rupture/fissure
  • Overlying thrombosis
  • Dissection
  • Aneurysm
  • Oxygen supply/demand imbalance
82
Q

Give some organ-specific symptoms of peripheral artery disease

A 
• Stress-induced physiological malformation
- Exercise induced angina
- Intermittent claudication
• Structural and functional breakdown
- Ischaemic cardiac failure
- Critical limb ischaemia
- Vascular dementia
• Infarction
- Gangrene
83
Q

Give some common clinical presentations of peripheral artery disease

A

• Intermittent claudication
• Critical leg ischaemia
- Rest pain, ulceration, gangrene
• Acute limb ischaemia (embolism or thrombosis)
- 6 Ps
• Cardiac artery disease
- Stroke, transient ischaemic attack, amaurosis fugax (temporary, painless vision loss in one or both eyes)
• Abdominal aortic aneurysm (AAA)
- Usually asymptomatic until rupture occurs

84
Q

Give 3 causes of aortic aneurysm

A
  1. Peripheral artery disease
  2. Collagen disorers e.g. Marfan’s
  3. Arteriomegaly
85
Q

Where is the commonest aortic aneurysm site?

A

The infrarenal aorta

86
Q

How would you investigate peripheral artery disease?

A
  • Blood glucose
  • Lipids
  • Vasculitic screen
  • Blood pressure
  • Vessel imaging (duplex, CT/MR angiography)
87
Q

How would you treat peripheral artery disease?

A
  • Risk factor modification
  • Revascularisation for ‘critical ischaemia’ e.g. bypass, stents
  • Amputation if revascularisation fails
  • Replace artery segments at risk of aneurysm rupture/stent the artery

Cardiovascular (5 decks)

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