1. iBSc: Question 1
By Alan McLeod

2. Getting the best marks
Read the whole question – a latter section may give you a clue about an earlier one. To see how many points you need look at the marks allocated – for example a 3 point question is generally looking for 3 salient points If giving a list answer put the best answers first – examiners will not usually mark answers too far down a list
Always write something – it may get you part of a mark and is anonymised so no one will think you are stupid!
If you genuinely have no clue then re-write the question to see if this sparks some ideas.
If not then move on and come back at the end. And remember – always write something.
Good luck!

3. Question 1
Mr Smith, a 68 year old smoker, presents to A+E with a 2 hour history of severe crushing chest pain.
Q1.1
List 5 differentials for chest pain (5)

4. Your SHO asks you to do an ECG and cardiac specific bloods
Question 1
Your SHO asks you to do an ECG and cardiac specific bloods
Q1.2
What ECG changes might you expect if the cause is STEMI or NSTEMI? (3)
Q1.3
What cardiac specific blood tests would you request? (2)

5. Question 1
After ECG and blood tests, Mr Smith is diagnosed with STEMI caused by occlusion of one of his coronary vessels
Q1.4
Label these vessels (4)

6. The loss of blood supply can damage cardiac muscle
Question 1
The loss of blood supply can damage cardiac muscle
Q1.5
List differences between cardiac and skeletal muscle (3)

7. In this case, atherosclerotic disease is to blame.
Question 1
In this case, atherosclerotic disease is to blame.
Q1.5
Describe a model for the formation of atherosclerotic plaques (5)
Q1.6
List 2 modifiable and 2 non-modifiable risk factors for atherosclerotic disease (2+2 = 4 pts)

8. A D B C Endocardium Fold E Question 1.7
Lable these layers of cardiac muscle and other tissues
Note that the two layers of pericardium are one continuous membrane folded over.

9. Question 1
In this patient’s notes is a letter from his GP stating that Mr Smith is ‘non-compliant with smoking cessation measures’.
Q1.8
Describe compliance and concordance (2)
33 marks total for question 1

10. The Answers
View these on ‘note view’ rather than on full screen – additional notes are provided for some slides

11. Generating Differentials: I’D GET VINO…
Infectious / inflammatory D
Degenerative G
Genetic / Idiopathic E
Endocrine T
Trauma V
Vascular
Iatrogenic / ingested N
Neoplastic O
Organs

12. Causes of Chest Pain I D G E T V N O Infectious / inflammatory
Pneumonia, pleurisy, Costochondritis D
Degenerative G
Genetic / ideopathic E
Endocrine T
Trauma
Fractured rib, pulled muscle, pneumothorax V
Vascular
Myocardial infarction, angina, aortic dissection, PE
Iatrogenic / ingested
Surgical scar N
Neoplastic
Bony mets O
Organs / other
Oesophagus (spasm, reflux), heart (pericarditis)
Lung, Aorta, bones, muscle, cartilage, anxiety

13. STEMI and NSTEMI A: Normal ECG B: ST Elevation C: ST Depression
ST elevation in response to Isoelectric line (I)
ST Segment A I P T
QRS B C

14. Evolution of ECG Changes in STEMI
Minutes to hours
Peaked T waves
Hours
ST elevation
Hours to days
T wave inversion
Loss of R wave
Days
Pathological Q wave
NSTEMI will show: horizontal ST wave depression and deep, symmetrically inverted T waves

15. Cardiac Enzymes
Troponin T and I
These are contractile proteins of the myofibril. The cardiac isoforms are very specific for cardiac injury and are not present in serum from healthy people.
Rises hours after injury,
Peaks in hours
- cTnI stays elevated for 5-10 days,
- cTnT for 5-14 days
Creatine Kinase (creatine phosphokinase)
This enzyme is found in heart muscle (CK-MB), skeletal muscle (CK-MM), and brain (CK-BB).  Creatine kinase is increased in over 90% of myocardial infarctions. However, it can be increased in muscle trauma, physical exertion, postoperatively, convulsions, delirium tremens and other conditions.
Time sequence after myocardial infarction
begins to rise 4-6 hours
- peaks 24 hours
- returns to normal in 3-4 days
Creatine Phosphokinase Isoenzymes
MM fraction  - skeletal muscle
- MB fraction - heart muscle
- BB fraction – brain
MB fraction
Rises and returns to normal sooner than total CK
- Rises in 3-4 hours 
- Returns to normal in 2 daysCK - MB subforms
This test is becoming more popular. MB2 is released from heart muscle and converted in blood to MB1. A level of MB2 equal or greater than 1.0 U/L and an MB2/MB1 ratio equal or greater than 1.5 indicates myocardial infarction.
Myoglobin
Found in striated muscle. Damage to skeletal or cardiac muscle releases myoglobin into circulation.
Rises fast (2 hours) after myocardial infarction
- Peaks at hours
- Returns to normal in hours
Have false positives with skeletal muscle injury and renal failure.
Lactic Dehydrogenase
- This enzyme is no longer used to to diagnose myocardial infarction.

16.
Right: Right Ventricle, most of Right Atrium, Part of Left Atrium Left: Left Ventricle, part of Right atrium, most of Left atrium Left circumflex: Left margin of heart and its entire posterior wall, Left atrium, posterior IV septum LAD: Anterior 2/3 of IV septum, anterior portion of LV, whole apex

17.
SA Node: Right 51-65%, Left 35-45%, Bilateral <10% AV Node: Right 80-90%, Left 10-20% ALL HIGHLY VARIABLE!!!

18. Plaque Formation
From Stevens and Lowe, Pathology

19. Plaque Formation
From Stevens and Lowe, Pathology

20. Plaque Formation
From Stevens and Lowe, Pathology

21. Plaque Formation
From Stevens and Lowe, Pathology

22. Plaque Anatomy Plaque Anatomy (early) Free Lipid Foam cells
Increased myointimal cells
Collagen
Disruption of internal elastic lamina
Plaque Anatomy (later)
Collagen cap
Extracellular lipid mass
Foam cells
Myointimal cells
Disrupted internal elastic lamina
Pressure atrophy of muscle  collagenous replacement

23. Atheroma – Risk factors
Non-preventable
Increasing age
Male sex
Family history
Preventable
Hyperlipidaemia
LDL and Cholesterol
Hypertension
Diastolic most important
Diabetes
Smoking
Males have a higher risk generally but this tends to equalise later as women pass through the menopause
Hyperlipidaemia: direct correlation with levels of LDL and cholesterol. Less association with VLDL and triglyceride.
Elevated HDL levels are protective – this is the basis of mild alcohol intake being cardioprotective as this favours higher LDL levels.

24. Muscle Comparison Skeletal Cardiac Smooth Voluntary Involuntary
Striated
Non-striated
Multinucleated
Mononucleated
Unbranched
Branched
No gap junctions
Gap junctions
In contrast to skeletal muscle, cardiac muscle requires both extracellular calcium and sodium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in cardiac muscle cells is derived from the entry of sodium ions across the sarcolemma in apostive feedback loop. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur under normal excitation-contraction (EC) coupling to cause contraction. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which initiates contraction by allowing the contractile proteins, myosin and actin to associate through cross-bridge formation. Cardiac muscle is intermediate between smooth muscle, which has an unorganized sarcoplasmic reticulum and derives its calcium from both the extracellular fluid and intracellular stores, andskeletal muscle, which is only activated by calcium stored in the sarcoplasmic reticulum.

25. Layers of the Heart Fibrous Pericardium
Parietal Layer of Serous Pericardium
Myocardium
Pericardial Space
Endocardium
Fold
Visceral Layer of Serous Pericardium
Layers of the Heart
Note that the two layers of pericardium are one continuous membrane folded over.

26. Health Behaviour Compliance Adherence Concordance
Extent to which patient’s behaviour matches recommendations from the prescriber
Adherence
Extent to which the patient’s behaviour matches agreed recommendations from the prescriber.
Concordance
Extent to which the patient’s behaviour matches agreed recommendations from the prescriber after exploring and discussing the patients beliefs, views and opinions.

27. The End
The slides here should allow you to mark your own work – remember 1 mark per answer up to the maximum for the question. Multiply by 3 to get percentage points. I assume a 60% pass mark. Sorry but I am unable to give further advice on answers due to time constraints.