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Y3 - presentations based > Chest pain > Flashcards

Chest pain Flashcards

1
Q

Give a DDx of chest pain by category:

1) CVS
2) GI - no key things for this one
3) Resp
4) MSK
5) Other

A

1)

  • IHD
    • Angina pectoris (stable angina)
    • ACS (MI or unstable angina)
  • Aortic dissection
  • Thoracic aortic aneurysm
  • Pericarditis
  • Cocaine induced coronary spasm

2)

  • Oesophageal spasm
  • Oesophagitis
  • Gastritis
  • Peptic ulcer disease
  • Acute pancreatitis
  • Cholecystitis
  • Boerhave’s perforation

3)

  • Pulmonary Embolism
  • Pneumonia
  • Pneumothorax

4)

  • MSK INFLAMMATION (note this is THE most likely diagnosis - most common). Caused by…..
    • ….Costochondritis (Tietze’s syndrome)
    • Strain (e.g. due to coughing)

5)

Anxiety

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2
Q

20F on COCP with chest pain - how does this narrow down the original DDx and what might you think to be mroe likely?

A
  • Less likely to suffer from diseases of old age e.g.
    • IHD:
  • ACS (MI)
  • Angina (stable / unstable)
  • Myopericarditis
  • Thoracic aortic dissection
  • Thoracic aortic aneurysm
  • More likely:
  • PE (the OCP is thrombogenic)
  • Pneumothorax (especially in tall and thin patients)
  • Cocaine-induced coronary spasm - more common in young patients for obvious reasons
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3
Q

List the causes of chest pain that are medical / surgical emergencies and require immediate attention

A
  1. ACS (MI, unstable angina)
  2. Aortic dissection
  3. Thoracic aortic aneurysm
  4. Pneumothorax
  5. PE
  6. Boerhaave’s perforation
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4
Q

What are some common investigations carried out for chest pain, including all the different blood test stuff?

A
  • ECG
  • Blood tests:
  • Troponin
  • Serum cholesterlol
  • FBC
  • U&E
  • Inflammatory markers - CRP, WCC
  • Imaging - erect CXR m

SECOND LINE

  • D-dimer
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5
Q

TROPONIN

1) What are the considerations in troponin measurement in terms of timing of when the levels are measured?
2) What is a good alternative to troponin and why is it useful? Why is troponin more useful than it?
3) What does an elevated troponin suggest ?
4) When else should you take a raised troponin result with a grain of salt?

A

1)

  • Measured 3 hrs after the episode of chest pain at least due to delayed response - it takes time to rise
  • Must take serial measurements of troponin - otherwise how can you tell whether this level is rising or falling on the patient?

2)

  • CK-MB
  • (Creatinine Kinase)
  • Useful because it is elevated much more rapidly than troponin is (less of a delay than the 3 hours delay in troponin) and also it falls off much quicker unlike troponin which remains elevated up to 7 days after the infarct so it can be measured to give an indication of recurrence
  • However, it is less specific and sensitive to cardiac damage

3)

  • Very sensitive and specific to CARDIAC DAMAGE due to…
  • MI
  • Unstable angina
  • Cocaine induced coronary artery spasm
  • Aortic dissection causing ischaemia
  • Myopericarditis
  • Hypertrophic cardiomyopathy
  • HF
  • Cardiac trauma from surgery or RTA
  • PE

4)

  • Troponin is renally excreted, so in renal failure you may fail to properly excrete troponin so it may appear elevated and be a false positive
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6
Q

1) What can serum cholesterol in the blood tests tell you that is important in the investigation of chest pain?
2) What might interfere with the results for serum cholesterol levels? Therefore what consideration must be made when thinking about measuring it?

A

1)

  • Raised serum cholesterol (hypercholesterolaemia) is a risk factor for CVS disease

2)

  • MI weirdly reduces the serum cholesterol levels and both LDL and HDL within 24 hours and it doesn’t normalise until a few months
  • Therefore if you want an accurate reading, it must be done within 24 hours of the episode of chest pain (in case the cause is MI and interferes with the results)
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7
Q

What can FBC in the blood tests tell you that is important in the investigation of chest pain?

A
  • Anaemia
  • Anaemia will exacerbate any deficiency of cardiac perfusion, resulting in ischaemic heart disease (ACS - MI and unstable angina or angina pectoris - stable angina)
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8
Q

What can U&E in the blood tests tell you that is important in the investigation of chest pain?

A
  • K+ levels - this may be the cause of the arrythmia
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9
Q

What can raised inflammatory markers in the blood tests tell you that is important in the investigation of chest pain?

A
  • Raised CRP and raised WCC
  • Could suggest pericarditis
  • Could suggest aortic dissection and MI which both cause inflammation
  • Could suggest Bornholm’s disease (secondary to Coxsackie B virus)
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10
Q

What can capillary glucose levels in the blood tests tell you that is important in the investigation of chest pain?

A
  • Significant increase in the risk of CVS disease with DM, particularly if untreated
  • Diabetics more likely to suffer from silent infarcts (MI without chest pain)
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11
Q

What can serum amylase levels in the blood tests tell you that is important in the investigation of chest pain?

A
  • Excludes potential acute pancreatitis as the cause of the central chest pain
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12
Q

1) What are elevated d-dimers useful for in chest pain investigation?
2) Why must you be wary of diagnosing those conditions alone based upon the d-dimer, what else could affect the d-dimer?

A

1)

  • PE or DVT exclusion only
  • I.e. if d-dimer is not raised - then its not PE or DVT
  • However it is NOT diagnostic of PE or DVT -

2)

  • Elevated d-dimers are simply symptomatic of breakdown of a fibrin clot due to any cause such as recent surgery or trauma, and are therefore not diagnostic of DVT or PE alone
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13
Q

What is the imaging used to diagnose or exclude aortic dissection?

A
  • CT angiography of the chest
  • Transoesophageal echo
  • Both to look for a false lumen
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14
Q

What is the imaging used to diagnose or exclude pneumothorax?

A
  • CXR - does it show absence of lung markings or tracheal deviation - if yes then its pneumothorax
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15
Q

What is the imaging / investigation used to diagnose or exclude PE?

A
  • D-dimer to exclude but NOT diagnostic
  • CTPA
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16
Q

What is the imaging used to diagnose or exclude Boerhaave’s perforation?

A
  • CXR after a gastrograffin swallow
17
Q

What is the common management for ACS (MI + angina)?

Exclude the additional treatments in MI in your answer

A
  • MONABASH
  • Morphine + metoclopramide (anti-emetic)
  • Oxygen (up to 94%)
  • Nitrates (GTN) to vasodilate to lower preload and therefore reduce myocardial work and therefore myocardial oxygen demand
  • Antiplatelets - aspirin and clopidogrel (ADP receptor antagonist)
  • Beta-blockers - to reduce myocardial oxygen demand
  • ACE inhibitors - reduces ATII induced vasoconstriction, thereby improving blood flow through coronary arteries and also reduces afterload in general - thereby reducing myocardial work and thus myocardial oxygen demand . Prevents post-infarct ventricular remodelling that could result in arrythmia and
  • Statins - improves endothelial function, modulate inflammation, maintain atherosclerotic plaque stability and prevent thrombus formation
  • Heparin (LMWH OR fondaparinux etc) - prevents coronary thrombosis
18
Q

1) What is the acute management for STEMI?
2) What is the acute managemenr for NSTEMI?
3) What is the long-term management for MI of any kind?

A

1)

  • MONABASH
  • Morphine + metoclopramide (anti-emetic)
  • Oxygen (up to 94%)
  • Nitrates (GTN)
  • Anti-platelets - aspirin and clopidogrel
  • Beta-blockers
  • ACE inhibitors
  • Statins
  • Heparin (LMWH OR fondaparinux etc)
  • URGENT PCI (percutaneous coronary intervention)
  • Thrombolysis - streptokinase etc

2)

SAME AS ABOVE EXCEPT

  • No need for thrombolysis - evidence suggests it doesn’t work in NSTEMI

3)

  • Lifestyle changes - smoking cessation, low-salt, exercise, weight loss
  • Anti-HTN - ACEi, CCB, thiazide diuretics
  • Reduce thromboembolic risk: low dose aspirin for life, and an ADP receptor inhibitor (e.g. clopidogrel, ticagrelor) for 1yr
19
Q

Beta-blockers are one of the many drugs used to treat ACS such as MI and angina. When are they contra-indicated?

A
  • Heart failure
  • Asthma
  • Heart block
  • Arrythmia
  • Cardiogenic shock
20
Q

When is ACEi (long-term anti-HTN control) use contra-indicated in STEMI patients?

A
  • In patients with renal failure where creatinine > 150 micromol/L
21
Q

What are the common complications of MI?

A
  • DARTH VADER
  • Death
  • Arrythmia
  • Rupture (either of the septum or outer walls)
  • Tamponade
  • Heart failure
  • Valve disease
  • Aneurysm
  • Dressler’s syndrome (autoimmune pericarditis 2-10 weeks post-MI)
  • Embolism
  • Reinfarction
22
Q

How are gallstones diagnosed - first investigation?

A
  • U/s
23
Q

1) What can oesophageal spasm often be secondary to, and thus how is it often treated?
2) How can oesophageal spasm be diagnosed / excluded?

A

1)

  • Oesophageal spasm secondary to reflux
  • Therefore, often treated with PPIs such as omeprazole

2)

  • Barium swallow / oesophageal manometry
24
Q

What are the characteristic changes seen in an ECG in MIs?

A
  • ST elevation - STEMIs
    • IMPORTANT NOTE: this is often with reciprocal ST depression in other leads
    • IMPORTANT NOTE: sometimes ST depression may be actual ST elevation in a posterior MI disguised as ST depression (since its reversed) and not actual ST depression - therefore if there is ST depression in the anterior leads, this may either be ischaemia (as suggested by taking ST depression at face value) OR posterior infarction. You can differentiate between the 2 based upon the R-waves - more prominent in posterior MI than in ischaemia
    • NSTEMI - no ST elevation
  • Tented T-waves in affected leads (due to localised hyperkalaemia following myocyte ischaemia)
  • T-wave inversion
  • Q-waves
25
Q

What should you be thinking of in tall, thin patients who present with chest pain?

A
  • Tall, thin → risk factor for pneumothorax
  • Marfan’s → risk factor for thoracic aortic aneurysm
26
Q

What risk factors are there that can be taken from the history that should alert you to the possibility of PE as the cause of chest pain?

A
  • Recent travel
  • Recent surgery
  • Malignancy
27
Q

What are the characteristic features on an ECG for pericarditis / myocarditis?

A
  • Saddle-shaped ST elevation in a number of leads not conforming to the territory of a single coronary artery (remember how you can map which coronary artery is affected based on in which leads there is ST elevation)
28
Q

Nausea and vomiting are most commonly associated with which type of MI, and why?

Important note - therefore MI does not always present with nausea and vomiting so beware

A
  • Inferior MI
  • Due to the Bezold-Jarisch reflex - don’t need to remember the name but remember the logic…
  • Infarction of the inferior myocardium irritates the diaphragm, resulting in vomiting via the vagal afferent
29
Q

What GI cause of chest pain can confusingly cause resp signs and symptoms, and what are the signs and symptoms it can cause?

A
  • Boerhaave’s perforation
  • Dyspnoea
  • Consolidation
  • Pleural effusion
30
Q

What 2 causes of chest pain often also cause nausea and vomiting and in what pattern?

A
  • MI (especially inferior MIs) - pain then vomiting
  • Boerhaave’s perforation - this is a perforation of the oesophagus due to forceful vomiting so vomiting and then pain
31
Q

Detail the mechanism of action of the following anti-platelet drugs

1) Aspirin
2) Clopidogrel (and prasugrel and ticagrelor)
3) Abciximab and tirofiban
4) Bivalirudin

A

1)

  • Aspirin - irreversible inhibitor of COX which synthesises TXA (platelet aggregator) - therefore reduces platelet aggregation. Irreversible since platelts have no nuclei so can’t synthesise new COX enzymes) - therefore

2)

  • Clopidogrel - irreversibly blocks the ADP receptor on platelet cell membranes that prevents them binding fibrinogen and hence inhibits platelet aggregation

3)

  • Abciximab and tirofiban both reversibly block fibrinogen binding to the glycoprotein IIb/IIIa receptors on platelet cell membranes that mediate platelet membrane. Abciximab is a monoclonal antibody

4)

  • DTI (direct thrombin inhibitor) and is sometimes used as an alternative to heparin (an indirect thrombin inhibitor)
32
Q

1) What is the gold-standard investigation for angina?
2) What are some alternatives to this gold-standard investigation?

A

1)

  • Exercise tolerance test
  • ECG and BP measured
  • ST depression greater than or equal to 2mm - typical symptoms of exertional angina
  • ST elevation greater than or equal to 1mm - indicates stenosis of the coronary arteries

2)

  • Stress echocardiogram - for people who can’t exercise due to severe arthritis, PVD etc. Stress induced using dobutamine and infarcted myocardium will be hypokinetic in response to stress
  • Myocardial scan
  • CT coronary angiography
  • Angiography / angioplasty
33
Q

What ECG abnormalities would you expect in a patient who suffered a full-thickness MI 2 years previously? What is the basis for these changes?

A
  • Pathological Q-waves
34
Q

1) What 2 things are used to exclude PE?
2) If PE cannot be excluded, and is a possibility, what are the next steps in investigation / management?

A

1)

  • D-dimer
  • Wells’ score

2)

  • CTPA immediately
  • Start LMWH
35
Q

What may chest pain brought on by lying down be?

A
  • Decubitus angina
36
Q

What is decubitus angina?

A
  • A form of angina which is characteristically brought on by laying down

Y3 - presentations based (6 decks)

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