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CSI > Case 8 > Flashcards

Case 8 Flashcards

1
Q

How can Mr Muller’s symptoms be described?

A

Reflux and dyspepsia

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2
Q

What is dyspepsia?

A

Recurrent epigastric pain, heartburn or symptoms of acid regurgitation, with or without bloating, nausea or vomiting

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3
Q

What are underlying causes of dyspepsia?

A

Oesophageal reflux

Gastroenteritis

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4
Q

In addition to dyspepsia, what are other symptoms a patient with oesophageal reflux may experience?

A

Belching, excess salivation known as water brash

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5
Q

In addition to dyspepsia, what are other symptoms a patient with gastroenteritis may experience?

A

Fever, vomiting and diarrhoea

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6
Q

What are a list of differentials for dyspepsia?

A 
Coeliac disease
Inflammatory bowel disease
GORD
Gastritis
Pancreatitis
Medication side effects
Functional dyspepsia
Gallbladder disease
Gastroenteritis
Stress
Peptic ulcer disease
Coronary heart disease
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7
Q

What are the 5 most likely diagnosis for Mr Muller?

A 
GORD
Functional dyspepsia
Gastritis
Stress
Peptic ulcer disease
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8
Q

What is functional dyspepsia?

A

Most common cause of dyspepsia

Its where an individual suffers symptoms of dyspepsia but routine investigations do not reveal causative abnormalities

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9
Q

What is gastritis?

A

Inflammation of the gastric mucosa

Often resolves by itself

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10
Q

Whats is the overlap between functional dyspepsia and gastritis?

A

In functional dyspepsia, endoscopy often reveals an element of gastritis
However even if gastritis is resent it doesn’t correlate with the degree of symptoms which is why its called functional dyspepsia

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11
Q

What can cause gastritis?

A

Gastritis can be symptomatic and problematic e.g. when caused by infection, medications e.g NSAIDs (effect integrity of mucous lining of stomach), or alcohol excess

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12
Q

What can gastritis lead to?

A

Stomach ulceration

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13
Q

What can stress be associated with?

A

Can be associated with functional dyspepsia, overt gastritis, peptic ulceration

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14
Q

What is oesophagitis?

A

Reflux irritates the oesophagus

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15
Q

What is peptic ulcer disease?

A

Gastric ulceration or duodenal ulceration

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16
Q

How would gallbladder disease present?

A

Dyspepsia

Pain would be more colicky in nature

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17
Q

What is colicky pain?

A

Intermittent, spasmodic pain that occurs when a hollow tube contracts to try and relieve obstruction
Eg. gallstones cause colicky pain along with renal stones and intestinal obstruction

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18
Q

How does pancreatitis present?

A

Associated with signs and symptoms of pancreatic insufficiency e.g steatorrhea or diabetes

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19
Q

What are risk factors Mr Muller has for coronary disease?

A

Stress
Smoking history
Angina pain can present as dyspepsia

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20
Q

What term is given to signs or symptoms with a more serious underlying pathology?

A

Red Flag symptoms

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21
Q

Why is the concept of red flags useful?

A

Help bus risk stratify so we can differentiate between more innocent symptoms and possible dangerous underlying pathology.
This allows those that need it to get early investigation and management

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22
Q

What are important red flags?

A

Back pain- spinal cord compression? malignancy? infection?
Red flags for back pain: previous cancer, bladder/bowel dysfunction, fever

Headaches- meningitis? intracerebral tumour? infection? acute bleed?
Red flags for headache: meningism (meninges irritated- raised inter-cranial pressure or sudden/severe headache)

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23
Q

What red flags make a doctor suspicious for upper GI cancer?

A

Mass
Dysphagia
Weight Loss

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24
Q

Where can you find red flag features?

A

Referral guidelines

E.g. NICE guidlines

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25
Q

What is the term given for vomiting blood?

A

Haematemesis

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26
Q

In the NICE guidelines, what are the refer outlines for suspected upper GI cancer?

A

Urgent referral: upper abdominal mass consistent with stomach cancer

Urgent upper GI endoscopy: dysphagia, weightloss, upper abdominal pain, reflux, dyspepsia

Non-urgent upper GI endoscopy: haematemesis
- if over 55: treatment resistant dyspepsia, abdominal pain with low Hb, low platelet count with nausea/vomiting/weight-loss/reflux/dyspepsia/abdominal pain, nausea and vomiting with weight loss/reflux/dyspepsia/upper abdominal pain

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27
Q

What are 7 investigations the GP should carry out for Mr Muller at initial presentation of symptoms?

A 
Test for H. Pylori
FBC
LFTs
Alcohol history
Medication history
Weight
ECG
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28
Q

What are benefits of an ECG?

A

Quick and non-invasive
Ideally during pain (to see if associate with cardiac ischaemia)
Might highlight abnormalities

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29
Q

What are benefits of measuring weight?

A

Simple an free
Monitering
BMI

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30
Q

What is the importance of taking an alcohol history?

A

Above the limit? (Recommend is 14 units per week)
Clinical consequences- e.g alcoholic gastritis or liver damage
Offer support

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31
Q

What’s the importance of taking a medication history?

A

Include over the counter
Those that relax the oesophageal sphincter e.g. Ca channel blockers and nitrates
Those that affect gastric mucosa e.g. NSAIDs and aspirin

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32
Q

Why is it important to test for H. Pylori?

A

Common is dyspepsia
Gastric, peptic ulcer diseases and gastric malignancies (inc. adenocarcinoma, MALT lymphoma)
Highly prevalent (~50% of population have it living in their stomachs))

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33
Q

Why is it important to take a FBC?

A 
Anaemia- due to occult blood loss and cancer can impact RBC production through interference with erythropoietin production
High platelets (thrombocytosis)-  no of cancer can cause this due to release of cytokines which promote platelet production
34
Q

What is the significance of taking liver function tests (LFTs)?

A

Biliary disease?
Alcohol-induced changes?
Opportunistic

35
Q

When would we use stool tests?

A

Diarrhoea
Recent travel
Suspected gastroenteritis

36
Q

When is an abdominal radiograph used?

A

In an acute setting when looking for intestinal obstruction or perforation
Don’t show subtle findings

37
Q

When would you do a rectal examination?

A

To look for upper GI bleeding- can identify presence of malaena

38
Q

What is malaena?

A

Dark and offensive smelling faeces containing digested blood from upper GI tract

39
Q

What is the site of infection of H. Pylori?

A

The stomach- has HCl which H. Pylori can survive in

40
Q

How is H. Pylori infect the stomach?

A

H. Pylori s ingested
H. Pylori synthesises urease which catalyses a reaction to neutralise the acid surrounding it
Uses flagella to propel itself and is guided by chemotactic gradient towards the stomach lining

41
Q

What is the role if urease?

A

Converts urea into ammonia and CO2

42
Q

What is the role of urease?

A

Converts urea into ammonia and CO2

Ammonia is basic and neutralises HCl

43
Q

What happens when H. Pylori reaches the mucous layer?

A

pH is very neutral close to surface of epithelial cells- this is where it needs to get
It has special molecules e.g. LPS/BabA which help it to adhere to cells on the stomach lining once its reached here
This process is not harmful to the human host

44
Q

What toxins does H. Pylori release once its adhered?

A

cagA- Disrupts the tight junctions between cells in the stomach lining leading to inflammation- gastritis

vacA- Causes cells in stomach lining to undergo apoptosis and die

45
Q

What is the effect of the toxins H. Pylori releases?

A

Toxins disrupt the continuity of the stomach lining and cause underlying cells to now be exposed to corrosive effects of HCl which can lead to ulcers

46
Q

How do different strains of H. Pylori differ?

A

Not all strains cause gastritis or ulcers
More than 50% of the world population have H.Pylori in their stomachs- not all these people suffer from upper GI problems

47
Q

What tests can be carried out to test for H. Pylori?

A

Carbon 13 urea breath test- probes for H. Pylori protein
Stool antigen test- Probes for H.Pylori protein
Serum serology test- Probes for human protein
CLO test- probes for H. Pylori protein

48
Q

What are advantage and disadvantages of carbon-13 urea breath test?

A

A:

  • non invasive, simple and safe
  • high sensitivity and specificity
  • can be used for diagnosis and as a test of cure

D:

  • Requires specialist analysing equipment, samples may need sending away
  • If patient is on ABs or PPIs results may be falsely negative
  • Requires fasting conditions
49
Q

What are advantage and disadvantages of stool antigen test?

A

A:

  • non-invasive, simple, safe
  • highly sensitive and specific
  • can be used for diagnosis ad theoretically as a test of cure

D:

  • pateints might prefer other tests
  • samples need refrigeration
  • If patient is on ABs or PPIs results may be falsely negative
  • Sufficient evidence lacking for use of test of cure
50
Q

What are advantage and disadvantages of serum serology test?

A

A:

  • Cheap and widely available
  • Maybe useful for diagnosing patient the is newly infected

D:

  • IgM poorly sensitive for new infection
  • IgG does not tell you if infection is current (as will remain positive after infection cleared)
  • Cannot test for cure
51
Q

What are advantage and disadvantages of CLO test?

A

A:
High sensitivity and specificity
- Instantaneous results

D:

  • If patient is on ABs or PPIs results may be falsely negative
  • Invasive
52
Q

Why do NICE guidelines recommend a carbon-13 urea test or stool antigen test be used initially to test for H. Pylori?

A

They highly specific and sensitive
They’re non-invasive, simple and safe
Stool antigen test was chosen fr Mr Muller as c13 urea breath test requires specialist equipment

53
Q

What cells secrete HCl

A

Parietal cell lines gastric gland- it secretes HCl

54
Q

How is HCl produced?

A

CO2 from capillaries/ interstitial fluid moves into parietal cell
CO2 combines with water to form H+ and HCO3- via carbonic anhydrase
K+ moves in from lumen and H+ moves out into lumen via gastric H+/K+ ATPase
K+ moves in from capillaries/ interstitial fluid into parietal cell
Cl- moves into cell as HCO3- moves out of cell
Cl- moves into lumen via chloride channel

55
Q

What receptors are found on the parietal cell and what is their role?

A

ACh receptor
H2 receptor (histamine receptor)- initiate signalling cascade that result in getting proton pump from cytoplasm to the apical cell membrane
Gastrin receptor

56
Q

Where to drugs which reduce HCl production act?

A

Act on the proton pump- proton pump inhibitors
Act of H2 receptor- H2 antagonists
Act on HCl- acid-base neutralisation

These drugs are known as antacids

57
Q

What is the effect of PPIs?

A

Reduce production of HCl- 80% of acid is blocked by PPIs
Have weak antibacterial effects against H. Pylori
Have anti-urease activity and anti- ATPase activity

58
Q

Whats the most effective way to treat H Pylori infection?

A

Couple PPIs with antibiotics

By suppressing acid secretion, PPIs cause ABs to concentrate enhancing their effect

59
Q

What are examples of antacid drugs?

A

PPIs: omeprazole, Lansoprazole
H2 antagonists: Cimetidine, Ranitidine
HCl neutralisers: Magnesium carbonate, aluminium hydroxide

60
Q

What was Mr Muller treated with?

A

Omeprazole, Amoxicillin, clarithromycin

Re-tested with carbon-13 breath test

61
Q

How are carbon-13 breath test false negatives avoided?

A

Nice recommends the test is proceeded by at least 2 weeks of no PPIs and four weeks of no ABs

62
Q

Wta is a hiatus hernia?

A

It’s where part of the abdominal viscera herniates through the oesophageal opening in the diaphragm.

63
Q

What are risk factors for a hiatus hernia?

A

Male gender, obesity, age, pregnancy, genetic predisposition

64
Q

What causes a hiatus hernia?

A

Widening of the diaphragmatic hiatus
Pulling up of the stomach (eg due to oesophageal shortening)
Pushing up of the stomach (eg due to increased intra-abdominal pressure)

65
Q

What does a hiatus hernia lead to?

A

Leads to the function og the lower oesophageal sphincter to be compromised and anti-reflux barrier to be lost allowing stomach contents to be refluxed into the oesophagus

66
Q

What are the 2 variants of a hiatus hernia?

A

Sliding and rolling

67
Q

Whats the difference between a sliding and rolling hiatus hernia?

A

Sliding: 85-95% of causes, GOJ moves upwards, predominantly causes GORD

Rolling: 5-15% of causes, GOJ remains in place, a portion of the stomach, bowel, pancreas or spleen herniates into chest next to the GOJ

68
Q

What is ideal treatment for non-acidic reflux?

A

Alginate medication e.g. gaviscon
Alginates precipitate into a gel which reacts with stomach contents to form a foamy raft that floats onto of stomach contents
This can act as a physical barrier to reflux or will preferentially reflux into into the oesophagus into the irritating stomach contents

69
Q

What is important about identifying Barrett’s oesophagus?

A

A small proportion of those with Barrett’s oesophagus will go on to develop oesophageal cancer (~1-5%)

70
Q

What are the different tissues along the GI tract?

A

Oesophagus- stratified squamous epithelium
Stomach- columnar tissue with gastric pits and glands (foveolar cels, parietal cells, g cells and chief cells)
Small intestine- Columnar tissue (enterocytes, goblet cells)
Large - columnar epithelium

71
Q

What happens in barrettes oesophagus?

A

Squamous epithelium undergoes metaplasia to columnar epithelium

Intestinal metaplasia is characterised by columnar epithelium and distinct intestinal- type goblet cells

72
Q

How does the Barretts mucosa differs in appearance to the normal oesophageal mucosa?

A

Barretts mucosa is more red and velvety

73
Q

What is cardiac metaplasia?

A

Cardiac refers to the cardia part of the stomach

Cardiac metaplasia is sometimes considered as a precursor of intestinal metaplasia

74
Q

Why is Barrett oesophagus a problem?

A

Metaplasia leads to the excessive production of growth signals in a non-native location.
These metaplastic cells are vulnerable to developing architectural and cytological abnormalities- leads to dysplasia

75
Q

What do we call a group of high grade dysplasia cells that hasn’t extended beyond their original location?

A

Carcinoma in situ
Intra-epithelial neoplasia
Stage 0 cancer

76
Q

What happens if dysplasia cells extend beyond their original location?

A

Become an invasive carcinoma

In a patient who has Barretts oesophagus this leads to oesophageal cancer

77
Q

What are 6 suggestion that should be given to Mr Muller?

A
  • Raise 1 end of bed by 10-20cm (gravity limits reflux)
  • Try to lose weight (excess weight on abdomen can increase abdominal pressure and reflux)
  • Try to find ways to relax (stress affects brain-gut axis, stress my lower o- sphincter, slow gastric emptying, affect inflammatory pathways)
  • Do not eat 3-4 hours before bed (gives stomach time to digest)
  • Do not smoke (nicotine relaxes lower o-sphincter)
  • Do not drink too much alcohol (chronic alcohol may damage gastric mucosa and increase acid production, inhibit gastric emptying, effect function of los)
78
Q

What are common food triggers for acid reflux?

A

Spicy food
Acidic fruits
Coffee

79
Q

Whats the difference between squamous cell carcinoma and adenocarcinoma?

A

Squamous cell carcinoma: a subtype of oesophageal cancer, occurs at any level
Adenocarcinoma: occurs in inferior 1/3 of oesophagus, related to Barretts oesophagus

80
Q

What is oesophageal varicose?

A

Abnormally dilated sub-mucosal veins in the anastomosis between the systemic and portal circulation
This can cause portal hypertension

CSI (10 decks)

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