Chest pain

62 year old gentleman presents to A&E with chest pain

Differential Diagnosis

What are the differential diagnosis for chest pain?

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A good way of thinking of about this is to list the structures are in the location.

  • Heart: Acute Coronary Syndrome*, Angina, Aortic Aneurysm / Dissection*
  • Lungs: Pulmonary Embolism*, Pneumonia
  • Gastro intestinal: Oesphageal disease / GORD, Peptic ulcer
  • Musculoskeletal

A good differential list should always contain common condition and also *ones not to miss (these sohuld be ruled out first).

Taking a history

What key questions in the history will help you narrow down your differentials?

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Asking about the pain is the first key area, think "SOCRATES":

  • Site - May hint at the structures, but remember visceral pain may be difficult to localise
  • Onset - Immediate onset points to a vascular cause
  • Character - 'Tearing' pain may point to aortic dissection
  • Radiation - Jaw or arm pain may indicate ACS
  • Associated symptoms - Shortness of breath worse on inspiartion might lead you to PE
  • Timings - Associated with food may be GI related
  • Exacerbating or relieving factors - Relieved with GTN may indicate cardiac cause
  • Severity - helps differentials and choice of analgesia

In an acute setting a full history may be inappropriate to obtain before doing an ABCDE assessment. A focused history including past medical / surgical history, medications (including allergies) and family history may be relevant.

History

Brian Grant is a 62 year old gentleman with pain in his central chest that came on two hours ago. The pain is crushing in nature and radiates to his left arm and his jaw. He feels nauseated with the pain and has some shortness of breath. The pain that he experiences gets worse on exertion. he describes the pain as the worst he has ever felt and expresses a deep concern about his impending doom.

Mr Grant has a history of angina and takes GTN spray for attacks which of late have become increasingly frequent and have begun to trouble him at rest. He also has type two diabetes which was diagnosed 2 years ago and is controlled entirely through diet. He takes no regular medication (except the GTN spray) and has no allergies.

He has no significant family history and lives with his wife who is fit and well, he drinks a moderate amount of alcohol and smokes ten cigarettes per day with 20 pack years under his belt.

Mr Grant is mobile and has previously been in good health other than the comorbidities listed.

History

Apart from the pain, what are the other important points from the history that point towards Acute Coronary Syndrome?

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  • Past medical history of angina
  • Past medical history of type 2 diabetes
  • Smoker

Aetiology

What causes Acute Coronary Syndrome? What are the risk factors?

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Acute Coronary Syndrome (ACS) is a medical emergency where the heart muscle is at risk of damage due to iscaemic heart disease. It is an umbrella term that encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) or ST-elevated myocardial infarction (STEMI).

Atheroma is the cause, and it's super-easy to remember the risk factors as they spell 'ATHEROMA' (I wonder if this is how it got its name?):

  • Age > 60 years
  • Tobacco - smoking
  • Hyperglycaemia - diabetes, hypergylicaemia increases the endothelial damage
  • Ethanol - alcohol
  • Reduced physical activity / obesity
  • Male
  • Arterial hypertension

Key Concept: Atheroma

The easiest way to think about atheroma is the 4 layers, 4 stages of development and 4 outcomes.

4 layers

Always start with the normal when thinking of pathology. The 4 layers of the arterial are:

  • Lumen - (okay not truly a layer, but let's not forget it!)
  • Intima - endothelium, sub-endothelium, internal elastic lamina
  • Media - smooth muscle, external elastic lamina
  • Adventitia

4 stages of atheroma development

  • Damage - endothelial cells damaged by hypertension and diabetes
  • Fatty streak - LDL (lipids in the blood) enters the intima and is phagocytosed by macrophages (foam cells). Oxidation of LDL causes fatty streak.
  • Lipid plaque - fibroblasts stimulated to secrete collagen. The lumen becomes narrowed and media is invaded
  • Ulceration - collagenous cap forms, large extracellular lipid may calicify and occlude in situ. Turbulent blood exposes collagen and predisposes to thrombus formation.

On a global scale this may cause arteriosclerosis; thick hardening of the arteries due to atheroma.

4 outcomes

  • Occlusion - extracellular lipid may occlude in situ or thrombosis ma occur
  • Dissection - bleeding (fissure) into a plaque
  • Embolism - exposure of collagen creates thromboembolism
  • Aneurysm - loss of elastin may give rise to ballooning of artery

Assessing an unwell patient

Given the high suspicion of ACS how would you assess this patient?

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At medical school we're frequently asked questions by senior doctors like 'A patient comes with a headache - what would you do for them?' or 'A patient has chest pain - what would you do next?'. They are usually asking for something specific but in truth all these questions have only two possible answers:

  1. Take a full history and examination
  2. ABCDE assessment

Which approach to take clearly is dictated by how unwell the patient is, how likely they are to deteriorate or how time sensitive the investigations / management are.

In the case of our patient Mr Grant we've taken a brief history (perhaps too detailed at this stage!) and because we suspect Acute Coronary Syndrome then we should approach this patient with an ABCDE assessment.

Examination

Mr Grant is sat up on an A&E trolley, he is pale and short of breath. He still has some chest pain which he scores as 4/10.

Call for help with any acutely unwell patient.

ABCDE approach

What interventions would you like to have done during your ABCDE approach?

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It is important when taking an ABCDE approach to a patient that you correct abnormal findings before reassessing and moving on.

Always ask for "High flow oxygen - 15 litres through a non-rebreather mask" when assessing an acutely unwell patient - you can always reduce it later, i.e. if you are concerned about CO2 retention in COPD patients. It is important in this patient as he has tachynopea and is desaturating.

A chest x-ray would is indicated to look for signs of fluid overload and rule our consolidation / other primary lung pathology. An ABG is a useful investigation for acidosis / alkolisis, quick electrolytes / lactate values and obtaining accurate oxygen and cardon dioxicde levels.

An ECG is critically important for anyone presenting with chest pain. During OSCE stations is may sound obvious to list IV access as part of your interventions, but it is important and a good reminder to mention which bloods and to take cultures if you are concerned about infection.

ABCDE approach

What is the most likely cause for tachypnoea and desaturations? Would you give fluids?

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Pulmonary oedema from acute heart failure is the most likely cause. When part of a coronary artery becomes occluded the tissue supplied by that artery begins to fail.

The heart failure can be due to 3 main things; poor muscle contractility (most common), arryhtmias (from damage to electrical conduction) or valve problems (damage to the papillary muscles).

If part of the muscle in the left ventricle becomes damaged then blood is unable to be pumped effectively from it (and it's ejection fraction falls). The result is that blood backs up in the pulmonary veins leading to pulmonary hypertension, this increased hydrostatic pressure forces fluid from the blood stream into the alveolar spaces in the lungs, impairing gas exchange and leading to desaturation.

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Investigations

Mr Fence has a set of bloods taken.

FBCValueNormal range
WBC12.844.5 - 13.5 x 10^9 /L
RBC4.094.0 - 6.0 x 10^12 /L
Hb90 *130-150 g/L
MCV78 *90 - 120 fL

* denotes abnormal result

U&E: NAD

LFT: NAD

Glucose: 4.9 mmol/L (Normal range: 4.4 - 6.1 mmol/L).

Data interpretation

What do these blood results indicate? What would we see in folate & B12 deficiencies?

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The results show a microcytic anaemia (small cells, but normal in number).

  • Commonly related to iron deficiency and blood loss.
  • Consider also anaemia of chronic disease, thallasaemia and sideroblastic anaemia (bonus points if you thought of any of these!).

Blood loss in the GI tract is either:

  • Visible - for bleeding to be seen it must be a lower GI bleed (or a massive upper GI bleed!); haemorrhoids, inflammatory bowel disease, left-sided bowel malignancy, prolapse and ulceration, diverticulosis.
  • Occult - blood would be mixed in with the stool if it is from higher up in the GI tract; gastric / duodenal ulcer, inflammatory bowel disease (Crohn's), right sided malignancy.

Key Concept: Anaemia

The best way to picture anaemia is to think of what goes into making a red blood cell.

Haemoglobin is a protein with iron molecules at it's core. Red blood cells are packed full of haemoglobin, so it makes sense that if iron stores are low then each red blood cell becomes smaller and this manifests as a microcytic anaemia.

Folate and B12 are building blocks of DNA and so are needed to replicate, therefore deficiencies in these will decrease the number of cells, meaning each cell ends up having more haemoglobin and is therefore macrocytic (larger cells).

Guidelines

What should be the next step for this patient? Is there a guideline that could assist?

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Urgent 2 week referral for colonoscopy for any of the following:

  • Age 40+ with new bowel symptoms
  • Rectal bleeding and persistent change in bowel habit for > 6 weeks
  • Iron-deficiency anaemia
  • Palpable mass (abdominal or rectal).

So which of these does our patient have?

Worryingly he has 3 out of the 5; remember any one of these would merit an endoscopy.

You may find it useful to read the full NICE guidline.

Demographics

What would be your top differentials if the patient was 25 years old?

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We'd worry more about an inflammatory or infective process, although remember that certain genetic conditions predispose to early onset bowel cancer. Bonus points for naming some.

Key Concept: Inflammatory Bowel Disease

Inflammatory Bowel Disease (IBD) is a chronic inflammatory autoimmune condition that has two major sub-types: Ulcerative Colitis and Crohn's disease.

The main two symptoms are bleeding per rectum and diarrhoea.

Other symptoms/signs that are included in IBD include:

  • Low grade fever
  • Malaise (a term for 'generally unwell')
  • Abdominal pain
  • Loss of weight without intention

Note: all these symptoms would have been uncovered with our abdominal history we covered above.

Ulcerative Colitis and Crohn's disease are closely related and both have similar treatments (immunosuppression medication), so why do you need to know the differences? Well because it always comes up in exams.

Ulcerative ColitisCrohn's
GeneticsDRB-1DQ4 DR7
AetiologyTwo peaks: 20-25; 50-60 M=FOne peak: 40-60 F>M
PathologyStarts at rectum, pseudopolyps due to recovering ulcers, mucosa only affected, loss of goblet cells, thin wallsAnywhere from mouth to anus, full thickness granulomatous inflammation, cobblestone appearance with skipped lesions, most common site is terminal ileum
SequelaeSignficant increase in colorectal cancer riskFistulas, strictures and bowel obstruction, abscess, mile increase in colorectal cancer

Management

Mr Fence went to hospital for a colonoscopy which revealed several polyps in the ascending and transverse colon and a large mass in the caecum of the colon. This was biopsied and found to be malignant.

Pathology

What is a polyp? Does it need to be removed?

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Bowel polyps are small growths on the inner lining of the colon (large bowel) or rectum. They are common, affecting 15-20% of the UK population, and don't usually cause symptoms.

Bowel polyps are not usually cancerous, although if they're discovered they'll need to be removed, as some will eventually turn into cancer if left untreated.

You can read more about polyps at NHS choices.

Key Concept: Dysplasia

It is important to understand the link between dysplasia and malignancy.

Histology of a polyp on a stalk (pedunculated) areas 1, 2 &3 from bottom up representing normal dysplastic and neoplastic regions.

Concluding the case

After Mr Fence had his colonoscopy he was informed that it was a cancerous growth. The fact that Mr Fence's cancer was confined to his colon (that it had not metastasised), him being a fit and healthy man for his age, it was advised that he have surgery to remove the caecum, the ascending colon and the hepatic flexure.

To learn more about types of operations done please visit: Cancer Research UK.

Self-assessment

What is the order of the layers of the gastrointestinal wall?

Different pathological processes affect different layers, so make sure you're familiar with the normal structure.

What does microcytic hypochromic anaemia mean?

Think about what goes into making a red blood cell.

Which of these complications are most likely to arise from Ulcerative Colitis?

You can reason this question out by knowing two things, that Crohn's disease can be inflammation anywhere from mouth to anus and that it is full thickness inflammation. Small bowel obstruction for example is much more likely from Crohn's strictures as the lumen of the small intestine is much thinner (around half the size) of the large bowel.

A single mutation in which gene is responsible for the dominantly heritable familial adenomatous polyposis colorectal cancer?

All of these markers are involved somehow in cancer, do you know what cancer they're involved in?

True or False: Polyps are very likely to be cancerous?

A simple way of remembering is that 10% polyps will turn cancerous within 10 years.

What is the most common Histology for a colorectal cancer cell?

Remember it is glandular epithelium in the GI tract because of it's secretory nature, therefore an 'adenocarcinoma'.

What is the name of the lymphoid tissue in the large bowel?

This is important as it can be a site of lymphoma.

Which of the following symptoms would require an urgent 2 week referral for colonoscopy?

The correct NICE guidelines are covered above.

What is the definition of Diverticulitis?

Diverticulosis is merely the presence of outpouching, which can lead to diverticulitis - inflammation in these pouches.

------- is the name of the process used to tell how far along a cancer is.

Be sure that you know concepts like this.

Answered: 2/10 Score: 50%

Objectives

Wow! You made it all the way to the end. These are the objectives you will have picked up along the way.

  1. Describe the Aetioogy of colorectal carcinoma
  2. Describe the morphology of colorectal cancer
  3. Describe the normal histology of the GI tract
  4. Describe the pathological consequences of colorectal carcinoma
  5. Describe the pathological change of the histology in neoplasia of the colon
  6. Define Inflammatory Bowel Disease
  7. Indicate the difference in pathology between Crohn's disease and Ulcerative Colitis
  8. Describe additional manifestations of inflammatory bowel disease