PBL Topic 2 Case 5 Flashcards

(104 cards)

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
Explain the mechanism of action of calcium channel antagonists
- Inhibit L-type calcium channels - Reducing myocardial contractility and blood pressure - Reducing oxygen demand of myocardium
26
Identify three side effects of calcium channel antagonists
- Flushing - Peripheral Oedema - Headache and Dizziness
27
Identify an example of an If channel antagonist and explain its effect
- Ivabradine | - Induces bradycardia by modulating ion channels in the sinus node
28
When is PCI carried out?
- Single vessel disease - Multi-vessel < 65 years - Suitable anatomy
29
Outline the procedure of PCI
- Guidewire passed across stenosis - Ballon inflation to dilate stenosis - Stent insertion to maximise dilation
30
Identify three drugs that are combined with PCI to improve patient outcome
- Aspirin - Heparin - IIB/IIIa Receptor Antagonists
31
Identify two examples of drug-eluting stents
- Cypher Stent, contains sirolimus, an immunosuppressant agent - Taxus Stent, contains paclitaxel, a mitotic inhibitor
32
Identify the main complication of PCI
- Occlusion
33
Outline the evidence base of PCI
- 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
34
When is CABG carried out?
- Unsuitable anatomy - Multi-vessel > 65 years - Diabetes
35
Outline the procedure of CABG
- Bypassing coronary stenosis | - Using internal mammary arteries, radial arteries of reversed segments of saphenous vein
36
Identify three drugs that are combined with CABG to improve patient outcome
- Aspirin | - Clopidogrel
37
Which type of graft is more patent following surgery?
- Arterial grafts
38
Outline the evidence base of CABG
- 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
39
Briefly outline unstable angina
- Deterioration of stable angina | - Symptoms occurring at rest
40
Briefly outline refractory angina
- Revascularisation is not possible | - Angina is not controlled by medical therapy
41
Briefly outline variant (Prinzmetal's) angina
- Angina without provocation - Characteristic ST elevation - More common in women
42
Briefly outline Cardiac Syndrome X
- Angina of unknown cause (normal exercise test and angiography) - More common in women
43
Identify four classes of angina
- Class 1: Angina with strenuous activity - Class 2: Angina with normal activity - Class 3: Angina with gentle activity - Class 4: Angina at rest
44
Outline the pathophysiology of myocardial infarction
- 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
How many millilitres of oxygen is required for each 100 grams of cardiac muscle?
- 1.3 ml
46
Identify four causes of death after MI
- 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
What is a STEMI?
- Myocardial Infarction with ST elevation | - Occlusion involves entire thickness of the myocardium
48
What is an NSTEMI?
- Myocardial Infarction without ST elevation | - Occlusion involves subendocardial zone of myocardium
49
What is the difference between unstable angina and NSTEMI?
- In NSTEMI there is an occluding thrombus - Resulting in myocardial necrosis - And a rise in serum troponin or CK-MB
50
Identify the five types of myocardial infarction
- 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
Identify signs and symptoms of a STEMI
- 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
How would you identify an anterior wall MI using ECG?
- ST elevation in V1-V3
53
How would you identify an inferior wall MI using ECG?
- ST elevation in leads II, III and aVF
54
How would you identify a posterior wall MI using ECG?
- ST depression in V1-V3 - Dominant R wave - ST elevation in V5-V6
55
How would you identify a lateral wall MI using ECG?
- ST elevation in leads I, aVL and V5-V6
56
How would you identify an anterolateral wall MI using ECG?
- ST elevation in leads I, aVL and V2-V6 | - Inverted T waves in leads I, aVL and V3-V6
57
Identify the different types of troponin
- Troponin T: attaches complex to tropomyosin - Troponin C: Binds calcium during excitation-contraction coupling - Troponin I: Inhibits myosin binding site on actin
58
What limits the accuracy of CK-MB as a biochemical marker in MI? What is its alternative use as a biochemical marker?
- 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
What is the Killip classification used for?
- To assess patients with heart failure post MI
60
Describe the Killip Classification rankings
- 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
Identify three causes of mitral regurgitation following MI
- Left ventricular dysfunction and dilation - MI of inferior wall causing dysfunction of papillary muscle - MI of papillary muscles
62
What is the TIMI score?
- 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
What is the GRACE score
- Used to predict mortality risk in STEMI and NSTEMI | - Based on age, heart rate, systolic pressure, serum creatinine and Killip score
64
What is the role of aspirin
- Anti platelet | - NSAID
65
Explain how aspirin results in platelet actication
- Inhibition of COX-1 | - Inhibited production of thromboxane A2 and platelet activating factor
66
Identify adverse effects of aspirin
- Gastrointestinal effects - Postural encephalitis (Reye's syndrome) - Risk of bleeding if given with warfarin
67
What is the role of ticagrelor?
- Anti-platelet
68
Outline the mechanism of action of ticagrelor
- Blocks ADP receptors | - As ADP is used in activation of platelets
69
Identify two side effects of ticagrelor
- Dyspnoea | - Bleeding
70
Identify the mechanism of action of atorvastatin
- Inhibition of HMG-CoA reductase - Reduced hepatic cholesterol synthesis - Increased LDL receptor synthesis
71
Identify three adverse effects of atorvastatin
- Gastrointestinal disturbance - Myalgia - Raised concentrations of liver enzymes in the plasma
72
What is the active principle in Glyceryl Trinitrate?
- Nitric Oxide
73
Explain how GTN results in vasodilation
- 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
Identify three effects of GTN
- Decreased afterload and preload - Dilation of collateral vessel - Antiatherosclerotic characteristics
75
How is GTN administered and why?
- Sublingual spray | - To avoid first-pass metabolism
76
Identify two side effects of GTN
- Headache | - Postural hypotension
77
What is referred pain?
- Pain felt in a part of the body that is remote from the tissue causing the pain
78
Where pain of acute myocardial ischaemia referred to?
- Skin areas supplied by intercostobrachial nerve (T2) - Neck and jaw - Epigastrium (T7,T8,T9 dermatomes)
79
Chest Pain: How would this present in: Acute coronary syndrome?
- 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
Chest Pain: How would this present in: Stable angina?
- 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
Chest Pain: How would this present in: Pericarditis?
- Central chest pain - Worsened by lying flat and improved leaning forwards - Patient may have had multiple episodes in the past
82
Chest Pain: How would this present in: Aortic dissection?
- Central chest / abdominal pain that is ‘tearing’ in nature - Radiating through to the back - May have associated syncope/ dizziness due to haemodynamic instability
83
Chest Pain: How would this present in: Pneumonia
- Sharp chest pained worsened by inspiration | - Associated with cough, shortness of breath, fever, malaise
84
Chest Pain: How would this present in: Spontaneous Pneumothorax
- Sudden onset of sharp chest pain that is pleuritic in nature - Associated with shortness of breath
85
Chest Pain: How would this present in: Pulmonary Embolism
- Sudden onset of chest pain associated with shortness of breath
86
Chest Pain: How would this present in: GI Reflux
- Epigastric chest pain that is burning in nature and worsened by lying flat
87
Chest Pain: How would this present in: Oesophageal Spasm
- Epigastric chest pain with no associated shortness of breath - That is relieved by GTN spray, hence can be confused with ACS.
88
Which genes are affected in FH?
- LDL Receptor Gene | - Apo B100
89
How many people are estimated to be heterozygous for a mutation in the LDLR gene?
- 1 in 500
90
Identify the four main classes of mutations of the LDL receptor
- Reduced biosynthesis - Reduces transport to cell surface - Abnormal binding of LDL - Abnormal internalisation of LDL
91
Identify two clinical features of FH
- Corneal arcus | - Xanthelasma (xanthoma when larger and nodular)
92
When is FH diagnosed?
- Total cholesterol level greater than 7.5 mmol/L | - Family history (cascade testing)
93
Outline the mechanism of action of ezetimibe?
- Reduces intestinal cholesterol absorption | - By inhibiting intestinal mucosal transporter NPC1L1
94
What are healthy total cholesterol levels?
- < 5 mmol/L
95
What are healthy LDL-C levels?
- < 3 mmol/L
96
What are healthy HDL-C levels?
- > 1 mmol/L
97
What should the ratio of total cholesterol to HDL be?
- 4.5
98
What is the role of psychology in coronary heart disease assessed in terms of?
- Beliefs about CHD - Psychological impact of MI - Predicting and changing risk factors - Patient rehabilitation
99
How can the Health Belief Model be applied to CHD?
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
What are predictors of non-attendance in cardiac rehabilitation programmes?
- Age - Income - Poor Health Beliefs
101
Stress management involves teaching individuals about what?
- 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
Outline Leventhal's Self-Regulatory Model
- Illness is dealt with in the same way as any other problem - Interpretation, coping and appraisal - Until equilibrium is attained
103
What is Cardiac Rehabilitation?
- Sum of activities required to influence underlying cause of CHD - To improve physical, mental and social conditions - Using a multidisciplinary approach
104
Briefly outline the Evidence Base for Cardiac Rehabilitation
- 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