iBSc: Question 1 By Alan McLeod

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!

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)

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)

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)

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)

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)

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.

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

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

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

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

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

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

Cardiac Enzymes http://classes.kumc.edu/son/nurs420/unit5/cardiac_enzymes.htm 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 2 - 6 hours after injury, Peaks in 12 - 16 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 6 - 8 hours
- Returns to normal in 20 - 36 hours Have false positives with skeletal muscle injury and renal failure. Lactic Dehydrogenase - This enzyme is no longer used to to diagnose myocardial infarction.

http://perfline.com/student/vessel.html 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

http://perfline.com/student/vessel.html SA Node: Right 51-65%, Left 35-45%, Bilateral <10% AV Node: Right 80-90%, Left 10-20% ALL HIGHLY VARIABLE!!!

Plaque Formation From Stevens and Lowe, Pathology

Plaque Formation From Stevens and Lowe, Pathology

Plaque Formation From Stevens and Lowe, Pathology

Plaque Formation From Stevens and Lowe, Pathology

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

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.

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.

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.

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.

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.