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Semester 2: Cardiorespiratory Fitness > PBL Topic 2 Case 5 > Flashcards

PBL Topic 2 Case 5 Flashcards

1
Q

Identify two adhesion molecules involved in the development of an atheroma

A
  • ICAM-1

- E-Selectin

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2
Q

What causes expression of adhesion molecules in the development of an atheroma?

A
  • Damage to the vascular endothelium

- For example increased blood pressure

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3
Q

What is the effect of adhesion molecules in the development of atheroma?

A
  • Decrease nitric oxide release

- Increased adhesion of particles

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4
Q

Identify how foam cells are produced and explain their effect in the development of an atheroma

A
  • Adhesion of monocytes and LDLs
  • Differentiation of monocytes into macrophages
  • Macrophages engulf LDL to form foam cell
  • Which form a visible fatty streak
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5
Q

How does the formation of a visible fatty steak result in vessel occlusion?

A
  • Proliferation of fatty streak to form a plaque

- Plaque bulges into lumen

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6
Q

How does hardening of the arteries occur in atherosclerosis?

A
  • Fibroblasts deposit connective tissue

- Calcifications

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7
Q

Explain how the presence of the plaque may result in thrombus or embolus formation

A
  • Rupturing of plaque causes rough surface
  • Which attracts platelets
  • Deposition of fibrin
  • Trapping of red blood cells
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8
Q

How is cholesterol transported from the liver?

A
  • As low density lipoproteins

- Composed of 50% cholesterol and 20% protein

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9
Q

How is cholesterol transported back to the liver?

A
  • As high density lipoproteins

- Composed of 50% protein and 20% cholesterol

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10
Q

Explain the process by which cells take up cholesterol

A
  • Receptor Mediated Endocytosis
  • LDL binds to receptors
  • Clathrin coated pits pinch off to form clathrin coated vesicles
  • Vesicles are delivered to endosomes
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11
Q

Identify five risk factors for atherosclerosis

A
  • Hypertension
  • Familial Hypercholesterolemia
  • Smoking and Alcohol Consumption
  • Diet and Physical Inactivity
  • Family History
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12
Q

What is an aneurysm?

A
  • Permanent dilation of a vessel

- Due to loss of elastic tissue

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13
Q

Where are atherosclerotic aneurysms typically located?

A
  • Lower abdominal aorta

- Iliac arteries

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14
Q

What are the clinical effects of atherosclerotic aneurysms?

A
  • Pulsatile abdominal mass
  • Lower limb ischaemia
  • Rupture, with massive retroperitoneal haemorrhage
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15
Q

When does ischaemia occur?

A
  • When there is an imbalance between the supply of oxygen and the metabolic demands of the tissues
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16
Q

Identify three causes of ischaemic heart disease

A
  • Atherosclerosis
  • Shock
  • Stenosis
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17
Q

When does coronary heart disease develop?

A
  • When the vessel is more than 75% occluded
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18
Q

When does reversible ischaemia of coronary vessels develop?

A
  • When ATP levels are low and anaerobic glycolysis has ceased
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19
Q

When does angina occur?

A
  • Lack of blood supply

- Results in lack of contractility

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20
Q

Identify three characteristics of stable angina

A
  • Central chest pain
  • Precipitated by exertion
  • Relived by rest
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21
Q

Identify two characteristics of angina on an ECG

A
  • ST depression

- T wave inversion

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22
Q

Identify five pieces of lifestyle advice for a patient suffering from angina

A
  • Smoking cessation
  • Regular exercise
  • Avoiding severe unaccustomed exertion
  • Aim for ideal bodyweight
  • Sublingual nitrates
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23
Q

Identify an example of a potassium channel activator

A
  • Nicorandil
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24
Q

Identify three examples of calcium channel antagonists

A
  • Nicardipine
  • Nifedipine
  • Verapamil
  • Diltiazem
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25
Q

Explain the mechanism of action of calcium channel antagonists

A
  • Inhibit L-type calcium channels
  • Reducing myocardial contractility and blood pressure
  • Reducing oxygen demand of myocardium
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26
Q

Identify three side effects of calcium channel antagonists

A
  • Flushing
  • Peripheral Oedema
  • Headache and Dizziness
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27
Q

Identify an example of an If channel antagonist and explain its effect

A
  • Ivabradine

- Induces bradycardia by modulating ion channels in the sinus node

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28
Q

When is PCI carried out?

A
  • Single vessel disease
  • Multi-vessel < 65 years
  • Suitable anatomy
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29
Q

Outline the procedure of PCI

A
  • Guidewire passed across stenosis
  • Ballon inflation to dilate stenosis
  • Stent insertion to maximise dilation
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30
Q

Identify three drugs that are combined with PCI to improve patient outcome

A
  • Aspirin
  • Heparin
  • IIB/IIIa Receptor Antagonists
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31
Q

Identify two examples of drug-eluting stents

A
  • Cypher Stent, contains sirolimus, an immunosuppressant agent
  • Taxus Stent, contains paclitaxel, a mitotic inhibitor
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32
Q

Identify the main complication of PCI

A
  • Occlusion
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33
Q

Outline the evidence base of PCI

A
  • Stents (drug-eluting) result in lower rates of stenosis
  • More effective in alleviating angina than medical therapy
  • Does not reduce mortality
  • Carries risk of procedure-related MI
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34
Q

When is CABG carried out?

A
  • Unsuitable anatomy
  • Multi-vessel > 65 years
  • Diabetes
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35
Q

Outline the procedure of CABG

A
  • Bypassing coronary stenosis

- Using internal mammary arteries, radial arteries of reversed segments of saphenous vein

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36
Q

Identify three drugs that are combined with CABG to improve patient outcome

A
  • Aspirin

- Clopidogrel

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37
Q

Which type of graft is more patent following surgery?

A
  • Arterial grafts
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38
Q

Outline the evidence base of CABG

A
  • Superior to medical treatment in terms of survival
  • Most effective in left main coronary artery
  • Reduced need for repeat procedure compared to PCI
  • Better survival rates in patients with diabetes compared to PCI
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39
Q

Briefly outline unstable angina

A
  • Deterioration of stable angina

- Symptoms occurring at rest

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40
Q

Briefly outline refractory angina

A
  • Revascularisation is not possible

- Angina is not controlled by medical therapy

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41
Q

Briefly outline variant (Prinzmetal’s) angina

A
  • Angina without provocation
  • Characteristic ST elevation
  • More common in women
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42
Q

Briefly outline Cardiac Syndrome X

A
  • Angina of unknown cause (normal exercise test and angiography)
  • More common in women
43
Q

Identify four classes of angina

A
  • Class 1: Angina with strenuous activity
  • Class 2: Angina with normal activity
  • Class 3: Angina with gentle activity
  • Class 4: Angina at rest
44
Q

Outline the pathophysiology of myocardial infarction

A
  • Cessation of blood flow with exception of collateral flow
  • Stagnant Blood
  • Engorged vessels and bluish-brown hue due to de-oxygenation
  • Fluid leak and oedema
  • Death of cardiac muscle cells
45
Q

How many millilitres of oxygen is required for each 100 grams of cardiac muscle?

A
  • 1.3 ml
46
Q

Identify four causes of death after MI

A
  • Decreased cardiac output resulting in shock
  • Damming of blood resulting in pulmonary oedema
  • Sudden ventricular fibrillation
  • Rupture of the infarcted area resulting in cardiac tamponade
47
Q

What is a STEMI?

A
  • Myocardial Infarction with ST elevation

- Occlusion involves entire thickness of the myocardium

48
Q

What is an NSTEMI?

A
  • Myocardial Infarction without ST elevation

- Occlusion involves subendocardial zone of myocardium

49
Q

What is the difference between unstable angina and NSTEMI?

A
  • In NSTEMI there is an occluding thrombus
  • Resulting in myocardial necrosis
  • And a rise in serum troponin or CK-MB
50
Q

Identify the five types of myocardial infarction

A
  • Type 1: Ischaemia due to primary coronary event such as a plaque erosion/rupture
  • Type 2: Ischaemia due to increased oxygen demands such as coronary embolism, anaemia, hypertension
  • Type 3: Sudden cardiac death
  • Type 3: PCI
  • Type 5: CABG
51
Q

Identify signs and symptoms of a STEMI

A
  • Chest pain that radiates to left arm, neck or jaw
  • That does not respond to GTN
  • Autonomic symptoms such as paleness and clamminess
  • Thready pulse with hypotension, bradycardia or tachycardia
52
Q

How would you identify an anterior wall MI using ECG?

A
  • ST elevation in V1-V3
53
Q

How would you identify an inferior wall MI using ECG?

A
  • ST elevation in leads II, III and aVF
54
Q

How would you identify a posterior wall MI using ECG?

A
  • ST depression in V1-V3
  • Dominant R wave
  • ST elevation in V5-V6
55
Q

How would you identify a lateral wall MI using ECG?

A
  • ST elevation in leads I, aVL and V5-V6
56
Q

How would you identify an anterolateral wall MI using ECG?

A
  • ST elevation in leads I, aVL and V2-V6

- Inverted T waves in leads I, aVL and V3-V6

57
Q

Identify the different types of troponin

A
  • Troponin T: attaches complex to tropomyosin
  • Troponin C: Binds calcium during excitation-contraction coupling
  • Troponin I: Inhibits myosin binding site on actin
58
Q

What limits the accuracy of CK-MB as a biochemical marker in MI?

What is its alternative use as a biochemical marker?

A
  • Low levels of CK-MB in the serum of normal individuals and in patients with significant skeletal muscle damage,
  • Reinfarction as levels drop back to normal after
    36–72 hours.
59
Q

What is the Killip classification used for?

A
  • To assess patients with heart failure post MI
60
Q

Describe the Killip Classification rankings

A
  • 1: No crackles and no third heart sound
  • 2: Crackles in <50% of the lung fields or a third heart sound
  • 3: Crackles in >50% of the lung fields
  • 4: Cardiogenic Shock
61
Q

Identify three causes of mitral regurgitation following MI

A
  • Left ventricular dysfunction and dilation
  • MI of inferior wall causing dysfunction of papillary muscle
  • MI of papillary muscles
62
Q

What is the TIMI score?

A
  • Used to determine likelihood of ischaemic events in patients with unstable angina or NSTEMI
  • Risk factors include age, coronary artery disease, aspirin use, severe angina, ST deviation
63
Q

What is the GRACE score

A
  • Used to predict mortality risk in STEMI and NSTEMI

- Based on age, heart rate, systolic pressure, serum creatinine and Killip score

64
Q

What is the role of aspirin

A
  • Anti platelet

- NSAID

65
Q

Explain how aspirin results in platelet actication

A
  • Inhibition of COX-1

- Inhibited production of thromboxane A2 and platelet activating factor

66
Q

Identify adverse effects of aspirin

A
  • Gastrointestinal effects
  • Postural encephalitis (Reye’s syndrome)
  • Risk of bleeding if given with warfarin
67
Q

What is the role of ticagrelor?

A
  • Anti-platelet
68
Q

Outline the mechanism of action of ticagrelor

A
  • Blocks ADP receptors

- As ADP is used in activation of platelets

69
Q

Identify two side effects of ticagrelor

A
  • Dyspnoea

- Bleeding

70
Q

Identify the mechanism of action of atorvastatin

A
  • Inhibition of HMG-CoA reductase
  • Reduced hepatic cholesterol synthesis
  • Increased LDL receptor synthesis
71
Q

Identify three adverse effects of atorvastatin

A
  • Gastrointestinal disturbance
  • Myalgia
  • Raised concentrations of liver enzymes in the plasma
72
Q

What is the active principle in Glyceryl Trinitrate?

A
  • Nitric Oxide
73
Q

Explain how GTN results in vasodilation

A
  • Activation of Guanylyl Cyclase
  • Conversion of GTP to cGMP
  • Activation of protein Kinase G
  • Phosphorylation of proteins
  • Inhibition of Ca2+ induced smooth muscle contraction
74
Q

Identify three effects of GTN

A
  • Decreased afterload and preload
  • Dilation of collateral vessel
  • Antiatherosclerotic characteristics
75
Q

How is GTN administered and why?

A
  • Sublingual spray

- To avoid first-pass metabolism

76
Q

Identify two side effects of GTN

A
  • Headache

- Postural hypotension

77
Q

What is referred pain?

A
  • Pain felt in a part of the body that is remote from the tissue causing the pain
78
Q

Where pain of acute myocardial ischaemia referred to?

A
  • Skin areas supplied by intercostobrachial nerve (T2)
  • Neck and jaw
  • Epigastrium (T7,T8,T9 dermatomes)
79
Q

Chest Pain:

How would this present in: Acute coronary syndrome?

A
  • Central crushing chest pain
  • Radiating to left arm / jaw
  • Duration of more than 20 minutes
  • Associated with sweating / clamminess / nausea / shortness of breath
  • Symptoms are worsened by expiration and improved with GTN spray
80
Q

Chest Pain:

How would this present in: Stable angina?

A
  • Central chest pain
  • Radiating to left arm / jaw
  • Duration less than 20 minutes with full resolution
  • Associated with shortness of breath
  • Often triggered by exertion and resolved with GTN spray / rest
81
Q

Chest Pain:

How would this present in: Pericarditis?

A
  • Central chest pain
  • Worsened by lying flat and improved leaning forwards
  • Patient may have had multiple episodes in the past
82
Q

Chest Pain:

How would this present in: Aortic dissection?

A
  • Central chest / abdominal pain that is ‘tearing’ in nature
  • Radiating through to the back
  • May have associated syncope/ dizziness due to haemodynamic instability
83
Q

Chest Pain:

How would this present in: Pneumonia

A
  • Sharp chest pained worsened by inspiration

- Associated with cough, shortness of breath, fever, malaise

84
Q

Chest Pain:

How would this present in: Spontaneous Pneumothorax

A
  • Sudden onset of sharp chest pain that is pleuritic in nature
  • Associated with shortness of breath
85
Q

Chest Pain:

How would this present in: Pulmonary Embolism

A
  • Sudden onset of chest pain associated with shortness of breath
86
Q

Chest Pain:

How would this present in: GI Reflux

A
  • Epigastric chest pain that is burning in nature and worsened by lying flat
87
Q

Chest Pain:

How would this present in: Oesophageal Spasm

A
  • Epigastric chest pain with no associated shortness of breath
  • That is relieved by GTN spray, hence can be confused with ACS.
88
Q

Which genes are affected in FH?

A
  • LDL Receptor Gene

- Apo B100

89
Q

How many people are estimated to be heterozygous for a mutation in the LDLR gene?

A
  • 1 in 500
90
Q

Identify the four main classes of mutations of the LDL receptor

A
  • Reduced biosynthesis
  • Reduces transport to cell surface
  • Abnormal binding of LDL
  • Abnormal internalisation of LDL
91
Q

Identify two clinical features of FH

A
  • Corneal arcus

- Xanthelasma (xanthoma when larger and nodular)

92
Q

When is FH diagnosed?

A
  • Total cholesterol level greater than 7.5 mmol/L

- Family history (cascade testing)

93
Q

Outline the mechanism of action of ezetimibe?

A
  • Reduces intestinal cholesterol absorption

- By inhibiting intestinal mucosal transporter NPC1L1

94
Q

What are healthy total cholesterol levels?

A
  • < 5 mmol/L
95
Q

What are healthy LDL-C levels?

A
  • < 3 mmol/L
96
Q

What are healthy HDL-C levels?

A
  • > 1 mmol/L
97
Q

What should the ratio of total cholesterol to HDL be?

A
  • 4.5
98
Q

What is the role of psychology in coronary heart disease assessed in terms of?

A
  • Beliefs about CHD
  • Psychological impact of MI
  • Predicting and changing risk factors
  • Patient rehabilitation
99
Q

How can the Health Belief Model be applied to CHD?

A

Susceptibility: Belief that they will not have a heart attack

Severity: Belief that lots of people recover from heart attack and thus heart attacks are not that severe.

Costs: Belief that interventions to reduce the risk of coronary heart disease, such as exercise, would require a lot of effort

100
Q

What are predictors of non-attendance in cardiac rehabilitation programmes?

A
  • Age
  • Income
  • Poor Health Beliefs
101
Q

Stress management involves teaching individuals about what?

A
  • Theories of stress
  • Encouraging people to be aware of the factors that can trigger stress
  • Teaching people to reduce stress, including ‘self-talk’, relaxation-techniques and general lifestyle approaches such as time management and problem solving.
  • Stress management appears to reduce some of the risk factors for CHD, including raised blood pressure, blood cholesterol and type A behaviour.
  • Stress management reduces angina, which in turn could reduce the occurrence of myocardial infarctions.
102
Q

Outline Leventhal’s Self-Regulatory Model

A
  • Illness is dealt with in the same way as any other problem
  • Interpretation, coping and appraisal
  • Until equilibrium is attained
103
Q

What is Cardiac Rehabilitation?

A
  • Sum of activities required to influence underlying cause of CHD
  • To improve physical, mental and social conditions
  • Using a multidisciplinary approach
104
Q

Briefly outline the Evidence Base for Cardiac Rehabilitation

A
  • Reduction in cardiovascular mortality (besides those with recurrent MI)
  • Reduction in acute hospital admissions (including those with recurrent MI)
  • Different models of CR delivery are equally effective
  • Importance of early CR

Semester 2: Cardiorespiratory Fitness (18 decks)

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