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Core Conditions - Abdominal > GI Key OSCE Overview > Flashcards

GI Key OSCE Overview Flashcards

1
Q

What is coeliac disease?

In what type of person is it a common presentation?

A

it is an autoimmune condition in which an individual becomes sensitive to gluten

  • it is a common presentation in young Caucasians with general non-specific diarrhoea
  • there is often abdominal discomfort too - this could be pain or bloating
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2
Q

What are the most common symptoms of coeliac disease?

A
  • chronic diarrhoea
  • abdominal distention
  • malabsorption (which can lead to constant fatigue)
  • crampy abdominal pains
  • loss of appetite
  • weight loss
  • dermatitis herpetiformis
  • some people may be asymptomatic
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3
Q

What is dermatitis herpetiformis and why does it have this name?

A
  • pruritic papulovesicular lesions which present in a symmetrical distribution
  • often present on the elbows, knees and buttocks
  • it resembles herpes simplex
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4
Q

What increases the genetic risk of coeliac disease?

What other autoimmune conditions is it associated with?

A
  • HLA-DQ2 (95%) and HLA-DQ8 (80%)
  • it is associated with dermatitis herpetiformis and other autoimmune conditions
  • this includes type 1 diabetes, autoimmune hepatitis and autoimmune thyroid disease
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5
Q

What do investigations and examinations tend to show in someone with coeliac disease?

A
  • examination and imaging tends to be unremarkable
  • blood tests will show iron-deficiency anaemia
  • patient may also be vitamin D deficient due to malabsorption and diarrhoea
    • this contributes to constant fatigue
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6
Q

What happens when someone with coeliac disease eats gluten?

How does this lead to iron-deficiency anaemia?

A
  • when gluten is consumed, an abnormal immune response leads to the production of autoantibodies
  • these can attack various different organs
  • in the small bowel, autoantibodies cause an inflammatory reaction that leads to shortening of the villi
    • this is villous atrophy
  • this means that less nutrients can be absorbed, leading to anaemia
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7
Q

What are the first line investigations for someone with suspected coeliac disease?

A

ANTIBODY TESTS

  • these are used to identify the presence of any antibodies against gluten
  • tissue transglutaminase (tTG) IgA antibodies
    • this is highly sensitive and highly specific
  • endomysial IgA antibodies
    • ​this is to exclude a selective IgA deficiency which could produce a false negative to tTG
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8
Q

What is the gold standard test to diagnose coeliac disease?

What must the patient do prior to this test?

A

duodenal biopsy during endoscopy

  • if the patient is on a gluten-free diet, they need to resume consumption of gluten >/= 6 weeks before the test
  • otherwise they will not form antibodies against gluten and their bowels will look normal
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9
Q

What 3 features are looked for on a biopsy in coeliac disease?

A
  • blunted villi as a result of subtotal villus atrophy
  • crypt hyperplasia
  • increased intra-epithelial lymphocytes & infiltration of lamina propria lymphocytes
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10
Q

What is meant by villous atrophy?

A
  • this occurs when the finger-like villi of the small intestine erode away to leave a virtually flat surface
  • this leads to reduced absorption of nutrients from the diet
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11
Q

What is crypt hyperplasia and why does it occur in coeliac disease?

A
  • the crypts are the site of epithelial stem cells in the intestine
  • to replace the loss of enterocytes, the number of actively dividing cells in the crypts increases
  • there is elongation of the crypts of Lieberkühn
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12
Q

What is the first stage in the management of coeliac disease?

A

starting a gluten-free diet

this involves avoiding:

  • wheat
    • e.g. pasta, bread, pastry
  • barley
    • ​e.g. beer
  • rye
  • people with coeliac disease have variable tolerance to oats
    • ​some people can eat these and some need to avoid them
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13
Q

Despite having a gluten-free diet, what can people with coeliac disease still eat?

A
  • whisky as this contains malted barley
  • rice
  • potatoes
  • corn / maize
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14
Q

What are the other stages involved in the management of coeliac disease?

A
  • check for nutritional deficiencies
    • iron, vitamin D, vitamin B12, folate
  • offer the pneumococcal vaccine, followed by a booster every 5 years
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15
Q

Why is the pneumococcal vaccine offered to patients with coeliac disease?

A
  • coeliac disease is associated with functional hyposplenism
  • the spleen is not functioning as well as normal
  • patients are at increased risk of serious infections from encapsulated bacteria
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16
Q

What is meant by inflammatory bowel disease (IBD)?

A
  • this is an umbrella term for 2 conditions - Crohn’s & UC
  • it is characterised by chronic inflammation of the GI tract, with unknown aetiologies
  • prolonged inflammation results in damage to the GI tract
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17
Q

What are the non-specific symptoms associated with inflammatory bowel disease (IBD)?

A
  • diarrhoea
  • abdominal pain
  • PR bleeding / bloody stools
    • ​this is much more common in ulcerative colitis than Crohn’s
  • weight loss
  • fatigue
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18
Q

What % of IDB is either Crohn’s or UC?

What is the other %?

A
  • 90% of IBD is either Crohn’s or UC
  • 10% is indeterminate colitis
    • ​patient has symptoms and diagnostic test results that show IBD, but do not definitively place them into Crohn’s or UC
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19
Q
A
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20
Q

Which parts of the GI tract are affected in Crohn’s disease?

A
  • affects the entire GI tract
  • produces patchy inflammation throughout small and large bowel
  • it is characterised by the presence of skip lesions
    • lesion in one part of the bowel, skip some bowel and then a lesion further on
  • there is usually involvement of the distal ileum / ileocaecal junction
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21
Q

What type of inflammation is present in Crohn’s disease?

A

transmural inflammation

  • this describes inflammation across all layers of the GI tract
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22
Q

What is involved in the pathophysiology of ulcerative colitis?

A
  • this only affects the large bowel / colon
  • there is continuous and uniform inflammation in the large bowel
  • sometimes it can extend to the caecum & ileum, but it often does not progress this far
  • it continues distally from the anus
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23
Q

What type of inflammation is present in ulcerative colitis?

A

inflammation does not go past the submucosa

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24
Q

What are the risk factors for inflammatory bowel disease that are the same for both Crohn’s and UC?

A
  • age of onset - there is a biphasic distribution
    • it is more common between 15 to 30 and 50 to 80
  • Jewish > white > black / hispanic
  • positive family history
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25
Q

How does smoking impact inflammatory bowel disease?

A
  • smoking INCREASES the risk of Crohn’s disease
  • smoking DECREASES the risk of ulcerative colitis
  • if someone has many vague symptoms and a strong smoking history, it is more likely to be Crohn’s disease
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26
Q

What are other risk factors that are specific for Crohn’s disease?

A
  • refined sugar-rich diet
  • oral contraceptive pill
  • not being breastfed as a child
  • NSAID use
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27
Q

What are other risk factors that are specific to ulcerative colitis?

A
  • NSAID use
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28
Q

What acronym can be used to remember presenting features that occur in both Crohn’s and UC?

A

the acronym DWARF can be used

  • D - Diarrhoea
    • UC is more likely to have bloody diarrhoea
  • W - Weight loss
  • A - Abdominal pain
    • in Crohn’s, this is a crampy RLQ pain (over ileocaecal valve)
    • in UC, this pain starts as crampy and becomes very severe
  • R - Rectal bleeding
  • F - Fatigue
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29
Q

What are some presenting features that are specific to Crohn’s disease?

A
  • aphthous ulcers
    • ​ulcers in the mouth as Crohn’s can affect the entire GIT
  • arthritis (in 20% cases)
  • cutaneous lesions
    • erythema nodosum
    • pyoderma gangrenosum
  • features indicating fistulae
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30
Q

What are some presenting features that are specific to ulcerative colitis?

A
  • arthritis / ankylosing spondylitis
    • this is less likely than in Crohn’s
  • fever
  • cutaneous lesions
    • erythema nodosum
    • pyoderma gangrenosum
  • episcleritis / uveitis
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31
Q

Why is fistulae formation a risk in Crohn’s disease?

A
  • Crohn’s disease can affect all layers of the GI tract
  • fistulas form between 2 epithelial surfaces
  • an ulcer/sore forms on the epithelial surface of the gut and extends through the entire thickness of the bowel wall
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32
Q

What is erythema nodosum?

A
  • it is a panniculitis - an inflammatory disorder affecting subcutaneous fat
  • it presents as tender red nodules on the anterior shins
  • the nodules are due to inflammation of fat cells under the skin
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33
Q

What is pyoderma gangrenosum?

A
  • an inflammatory skin disease where painful pustules or nodules become ulcers, which progressively grow
  • it is an enlarging ulcer, but is not infective
  • it is a full thickness ulcer with blue undermined borders
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34
Q

What investigations are performed in primary care for suspected Crohn’s disease?

A
  • comprehensive blood panel
  • stool sample testing

this is to rule out infection with Yersinia enterocolitica

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35
Q

What are the investigations performed for UC in primary care?

A
  • comprehensive blood panel
  • stool sample testing

this is to look for the presence of faecal calprotectin

  • this is a sensitive marker for inflammation of the GI tract
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36
Q

What is the importance of testing for faecal calprotectin in primary care?

A
  • this is used to distinguish between inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS)
  • it is a sensitive marker for inflammation of the GI tract that will be raised in IBD
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37
Q

What is the gold standard diagnostic test for Crohn’s disease and ulcerative colitis?

A

Crohn’s disease:

  • this can be diagnosed based on colonoscopy

Ulcerative colitis:

  • colonoscopy alone is not sufficient to diagnose Crohn’s
  • a biopsy is also needed
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38
Q

What does Crohn’s disease look like on colonoscopy?

A
  • it has a characteristic cobblestone appearance
  • there will be skip lesions
  • there may also be ulcerations and strictures
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39
Q

What does ulcerative colitis look like on colonoscopy?

A
  • there tends to be white plaques of ulceration
    • these would be biopsied
  • there are sometimes polyps
  • more severe cases are associated with erosions, ulcers and spontaneous bleeding
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40
Q

What are the 4 stages of treatment escalation in inflammatory bowel disease?

A
  • supportive treatment
  • treatment to induce remission
  • maintenance treatment
  • surgery
  • you need to first induce remission of the inflammation and then try to maintain this remission
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41
Q

What supportive treatment is recommended in Crohn’s disease?

A

smoking cessation

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42
Q

What is the stepwise approach to achieving remission in Crohn’s disease?

A
  • start with a corticosteroid such as prednisolone or budesonide
  • aminosalicylate (5-ASA) such as mesalazine
  • azathioprine / mercaptopurine
  • methotrexate
  • monoclonal antibodies such as Infliximab / adalimumab
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43
Q

What is involved in the maintenance treatment of Crohn’s disease?

A
  • azathioprine / mercaptopurine
  • methotrexate
    • methotrexate is needed to induce remission
    • this is used in people who are intolerant to thioprines
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44
Q

When is surgery considered in Crohn’s disease?

A
  • it is considered in patients where the disease is limited to the distal ileum
    • this means that all of the diseased area can be removed
  • need to balance between the risks and benefits, plus the risk of recurrence
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45
Q

What treatments are involved in the stepwise approach to the remission of ulcerative colitis?

A
  • topical aminosalicylate (5-ASA)
  • oral 5-ASA
  • topical / oral corticosteroids
  • immunomodulative therapies
    • anti-TNFa (infliximab / adalimumab)
    • anti-integrin (vedolizumab)
    • janus kinase inhibitors
46
Q

What treatments are involved in the maintenance of ulcerative colitis remission?

A
  • topical / oral 5-ASA
  • oral azathioprine / mercaptopurine
47
Q

What treatment is given for acute severe admission of ulcerative colitis?

A
  • when UC flares up, this is known as fulminant colitis
  • IV corticosteroids / ciclosporin will reduce the inflammation
  • surgical intervention, which is curative in UC
48
Q
A
49
Q

What are the acute complications of Crohn’s disease?

A
  • intestinal obstruction
  • sinus tracts
    • ​this is fistula formation but when the sinus develops into fascia / tissue / muscle rather than just into epithelium
  • toxic megacolon
50
Q

What is toxic megacolon?

In what IBD is this more common?

A
  • IBDs cause the colon to expand, dilate and distend
  • when this happens, the colon traps all the gas and faecal material and this cannot pass out of the body
  • peristalsis / bowel movements are still occurring
  • this can lead to rupture of the colon, which is life threatening
51
Q

What are the chronic complications of treatment for Crohn’s disease?

A
  • pregnancy - methotrexate, which is used in treatment, is teratogenic
  • anaemia
  • malabsorption ./ short bowel syndrome
    • having a shorter bowel following surgery means patient is absorbing less nutrients & water
    • this leads to imbalanced U&Es
52
Q

What are the acute complications of ulcerative colitis?

A
  • fulminant colitis
  • toxic megacolon
    • this is more likely to occur in UC than Crohn’s
53
Q

What is meant by fulminant colitis?

A
  • this occurs in about 10% of patients with UC when they have:
  • more than 10 stools per day
  • continuous bleeding
  • abdominal pain
  • distention
  • acute, severe toxic symptoms such as fever and anorexia
54
Q

What are the chronic complications of ulcerative colitis?

A
  • colonic adenocarcinoma
    • colonoscopy surveillance is 10 years post-onset to look for any changes
  • primary sclerosing cholangitis
55
Q

What is primary sclerosing cholangitis?

A

a long-term progressive disease of the liver and gallbladder

it is characterised by inflammation and scarring of the bile ducts

the bile ducts eventually become blocked, meaning that bile can build up in the liver and cause damage

56
Q

What is the mean age of onset for colorectal carcinoma?

A
  • the mean age of onset is 67
  • 60-70% of cases affect the colon and 20-30% are rectal
57
Q

What are the 3 pathways by which colorectal cancer can develop?

A
  • chromosomal instability
    • occurs through oncogene and tumour suppressor gene mutations
  • CpG island methylator phenotype
    • ​promoter methylation epigenetically silences tumour suppressor and mismatch repair genes
  • microsatellite instability
    • ​this involves inactivated mismatched repair genes
58
Q

What gene can usually be involved in the chromosomal instability pathway leading to colorectal carcinoma?

A
  • APC is a tumour suppressor gene
  • if it becomes mutated, this leads to epithelial dysplasia
  • this then leads to adenoma and then carcinoma
59
Q

What familial condition is mutations in the APC gene linked to?

A

familial adenomatous polyposis

this involves numerous small polyps developing in the epithelium of the large intestive

60
Q

What syndrome is CpG island methylator phenotype linked to?

A

it is linked to serrated polyposis syndrome that usually affects the proximal colon

this leads to the presence of serrated polyps in the colon and increases risk of colorectal cancer

61
Q

What syndrome is microsatellite instability linked to?

A

Lynch syndrome (also known as HNPCC)

this is a hereditary predisposition to colorectal cancer, in which patients are more likely to get cancer before the age of 50

62
Q

What are the risk factors for colorectal cancer?

A
  • increasing age
  • family history of:
    • polyps / colorectal cancer (<30%)
    • Lynch syndrome (<3%)
    • FAP (1%)
  • PMH of polyps, chronic IBD or acromegaly
  • obesity, smoking & diet
    • ​particularly a diet high in saturated animal fats, red meat
  • abdominal radiotherapy or ureterosigmoidostomy
63
Q

What are the key features to pick out in the history of someone with colorectal carcinoma?

A
  • PR bleeding (this is the major red flag)
  • any change in bowel habit
    • diarrhoea
    • rectal or stool bleeding / presence of mucus
    • tenesmus
  • FLAWS
    • ​fever, lethargy, appetite change, weight loss, night sweats
  • right-sided disease tends to have an iron-deficiency anaemia presentation, rather than changes in bowel habit
64
Q

How do 20% of colorectal cancer cases present acutely?

A

they may present as emergency obstruction, haemorrhage or perforation

there is a risk of peritonitis (inflammation of the peritoneum) with perforation

65
Q

What are the clinical features of colorectal cancer that will be present on examination?

A
  • clinical features of anaemia
    • conjunctival pallor / pale skin
    • cold peripheries
    • fatigue
  • when digital rectal exam is done there will be an abdominal or rectal mass
  • if there are metastases there may be hepatomegaly, ascites or palpable abdominal masses
66
Q

What test is done in the GP surgery when there is suspected colorectal cancer?

A

FIT (faecal immunochemical) test to detect for blood in the stool

if this is positive, there is a 2 week wait referral pathway for suspected cancer

67
Q
A
68
Q

What components are looked at in the FBC of someone with suspected colorectal cancer?

A

FBC is done to identify the type / presence of anaemia

  • haematocrit
  • haemoglobin
  • MCV
  • Fe studies
  • not CEA !!!
69
Q

When is a CEA blood test done in colorectal cancer?

A
  • this is not sensitive or specific enough to be used as a marker for colorectal cancer
  • this is used when there is a confirmed diagnosis of CRC
  • it is used to test how well treatment is working for certain types of cancer
70
Q

What does the CEA test look for?

A
  • CEA stands for carcinoembryonic antigen
  • carcinoembryonic antigens are proteins that are produced by certain types of cancers, particularly colorectal cancer
  • in response to antigens, the body produces antibodies to fight them
71
Q

What is the gold standard treatment for diagnosing colon cancer?

A

colonoscopy and biopsy

  • biopsy is needed for histological confirmation
  • CT / MRI can be used to identify large tumours for staging
72
Q

What is the surgical management for colorectal cancer?

A
  • localised CRC is treated with surgical resection
  • laparoscopic resection is being increasingly used
    • shorter post-op pain
    • shorter hospital stay
    • shorter recovery period
  • rectal cancer is more complex
    • ​this depends on staging and location but often a total mesorectal excision is done
73
Q

When do chemotherapy and radiotherapy tend to be used to treat colorectal cancer?

A
  • it depends on tumour staging
  • later stages often require chemotherapy as adjuvant therapy
  • chemotherapy is more commonly used in colon cancer
  • radiotherapy is more commonly used to treat rectal cancer, alongside surgical resection
74
Q

What mutation makes colorectal cancers much more resistant to chemotherapy?

A

BRAF V600E mutations

75
Q

What is currently involved in the colorectal cancer screeing programme in the UK?

A
  • people >60 are invited to take part in screening
  • a FIT test will be sent to the home address
  • if this comes back as positive, then the person is invited for a colonoscopy
76
Q

What are the main risk factors for peptic ulcer disease?

A
  • the most common is H. pylori
  • medications
    • NSAIDs
    • steroids
    • bisphosphonates (used to treat osteoporosis / bone diseases)
    • SSRI
  • Zollinger-Ellison syndrome
77
Q

What is Zollinger-Ellison syndrome?

A
  • there is the presence of a neuroendocrine tumour, called a gastrinoma
  • gastrinomas secrete the hormone gastrin
  • this causes the stomach to produce too much acid, resulting in the formation of peptic ulcers
78
Q

What are the symptoms of peptic ulcer disease?

A
  • burning epigastric pain
  • nausea and/or vomiting
  • if there is bleeding, there will be haematemesis and or/melaena
  • if there is bleeding, there will be anaemia
    • this presents as tiredness / lethargy
79
Q

How is the burning epigastric pain different in gastric and duodenal ulcers?

A
  • the pain is worse after eating if there is a gastric ulcer
  • the pain is relieved by eating if it is a duodenal ulcer
80
Q

What is haematemesis and what does it suggest?

A

this is the vomiting of blood

it is different to haemoptysis, which is the coughing up of blood

if it has a “coffee ground” appearance, this is typically associated with upper GI bleeding

81
Q

What is melaena?

A

dark black faeces that have a tarry appearance

this is associated with upper GI bleeding

82
Q

What are the clinical signs of peptic ulcer disease?

What about if there is a bleed?

A
  • pallor
  • epigastric tenderness
  • if bleeding and patient is in shock, there will be tachycardia and hypotension
  • if bleeding, there may be melaena on PR examination
83
Q

What 3 non-invasive blood tests are done in suspected peptic ulcer disease?

A
  • FBC to check for anaemia
  • U&Es which could identify either dehydration or upper GI bleed
  • CRP / ESR
84
Q

What could U&E abnormalities show in peptic ulcer disease?

A

a urea level of > 7 mmol/L can indicate that the patient is either dehydrated or there is an upper GI bleed

urea will not be high in a lower GI bleed

85
Q

What is the first line test in a haemodynamically stable patient with suspected peptic ulcer disease?

What is the gold-standard test?

A
  • first line tests are stool antigen or urea breath tests
    • this is to detect the presence of H. pylori
  • the gold standard test is upper GI endoscopy and biopsy
    • ​this is not routinely performed in a non-bleeding ulcer
86
Q

What instructions are given to patients prior to having an upper GI endoscopy and biopsy for peptic ulcer disease?

A
  • if they are taking a PPI, this needs to be stopped 2 weeks prior to the procedure
  • the PPI could mask the presence of an ulcer
87
Q

When might Zollinger-Ellison syndrome be suspected?

What is the test for this?

A
  • ZE syndrome is suspected when the patient is resistant to all treatment given for peptic ulcer disease
    • i.e. does not respond to PPIs
  • a fasting gastrin level is measured
88
Q

What is involved in the conservative treatment for peptic ulcer disease?

A

removing any risk factors

this includes stopping taking NSAIDs

89
Q

What is involved in the management of peptic ulcer disease in H. pylori positive patients?

A

this involves triple eradication therapy

  • PPI + clarithromycin + amoxicillin

OR

  • PPI + clarithromycin + metronidazole (if penicillin allergy)
90
Q

What are the stages involved in the treatment of someone with peptic ulcer disease who has had an acute upper GI bleed?

A
  • whenever someone is haemodynamically unstable, the first step is the ABCDE approach
  • then first line treatment is endoscopic intervention (diagnostic and therapeutic)
    • mechanical - clipping +/- adrenaline
    • thermal coagulation + adrenaline
    • sclerotherapy + adrenaline
  • a high dose IV PPI is given after endoscopy
91
Q

What is the mnemonic to remember the causes of acute pancreatitis?

What are the most important / common causes?

A

I GET SMASHED

  • I - Idiopathic
  • G - Gallstones
  • E - Ethanol
  • T - Trauma
  • S - Steroids
  • M - Mumps
  • A - Autoimmune conditions
  • S - Scorpion stings
  • H - Hypercalcaemia, hyperlipidaemia, hypothermia
  • E - ERCP
  • D - Drugs
    • e.g. azathioprine
    • diuretics
    • valproate
  • the most important / common causes are alcohol and gallstones
92
Q

What are the symptoms of acute pancreatitis?

A
  • anorexia
  • nausea and/or vomiting
  • severe epigastric pain that may radiate through to the back
93
Q

What are the signs of acute pancreatitis?

A
  • epigastric tenderness
  • low grade fever / signs of shock
  • bluish discolouration around the umbilicus (Cullen’s sign) or flank (Grey-Turner’s sign)
94
Q

What other condition might you be worried about when there is epigastric pain that radiates to the back?

A

this could also be a sign of abdominal aortic aneurysm

95
Q

What are the first line investigations for acute pancreatitis?

What other investigations might be done?

A

First line investigations:

  • serum amylase and serum lipase
    • lipase of more sensitive and more specific than lipase
  • if gallstone is suspected, then an ultrasound is also done

Other investigations:

  • FBC, U&Es, LFTs
  • MRCP if a gallstone is confirmed
  • CT scan
96
Q

What criteria is used to assess the severity of acute pancreatitis?

A

the modified Glasgow Criteria (PANCREAS)

  • P - PaO2
    • less than 8 kPa
  • A - Age
    • age > 55 years
  • N - Neutrophils
    • neutrophils > 15 x 109 mmol/L
  • C - Calcium
    • calcium < 2 mmol/L
  • R - Renal function
    • urea > 16 mmol/L
  • E - Enzymes
    • LDH > 600 iu/L or
    • AST > 100 iu/L or
    • ALT > 100 iu/L
  • A - Albumin
    • albumin < 32 g/L
  • S - Sugar
    • glucose > 10 mmol/L
97
Q

Using the Glasgow criteria, how is severe pancreatitis diagnosed?

A

if there are 3 or more of any of the criteria, this is severe pancreatitis and the patient goes to ICU

98
Q

If no gallstone is identified, what is the treatment for acute pancreatitis?

A

treatment is supportive and involves:

  • oxygen if sats < 94%
  • IV fluids
  • analgesia
  • antiemetic if patient is vomiting
  • antibiotics
  • nutritional support
    • this can be oral, enteral or parenteral
99
Q

What is the treatment for acute pancreatitis if a gallstone is identified?

A
  • after MRCP, if LFTs do not spontaneously resolve then an ERCP is performed
  • a stent is left in place for 6 weeks
  • there is also supportive treatment
100
Q

What are the local complications of acute pancreatitis?

A
  • peripancreatic fluid collections
  • pleural effusions (exudative)
  • pancreatic pseudocyst
  • pancreatic necrosis
  • pancreatic abscess
  • haemorrhage
101
Q

What is an acute peripancreatic fluid collection?

How is it usually treated?

A

this involves a collection of fluid around the inflamed pancreas

  • this is an early complication of acute pancreatitis that tends to develop in the first 4 weeks
  • there is no necrosis involved
  • they result from pancreatic inflammation and/or rupture of one of the small pancreatic side ducts
  • most resolve so do not require aspiration / drainage
102
Q

What is a pancreatic pseudocyst and how is this different to a peripancreatic fluid collection?

A
  • this involves a collection of peripancreatic fluid** that is walled off by **fibrous or granulation tissue
  • the fluid is rich in pancreatic enzymes, blood and necrotic tissue
  • it typically occurs 4 weeks or more after acute pancreatitis
103
Q

What is the main systemic complication of acute pancreatitis?

A

acute respiratory distress syndrome

this has a very high mortality rate

104
Q

What are the 4 different causes of chronic pancreatitis?

A

Metabolic / toxic:

  • alcohol (80% of cases)
  • haemochromatosis

Obstruction:

  • gallstone
  • cystic fibrosis

Tumour

Idiopathic (autoimmune)

105
Q

What are the symptoms of chronic pancreatitis?

A
  • dull epigastric pain
  • nausea and/or vomiting
  • steatorrhoea
    • foul-smelling stools which are difficult to flush
  • features of diabetes including polydipsia and polyuria

chronic pancreatitis is characterised by a triad of epigastric pain + steatorrhoea + diabetes

106
Q

What are the clinical signs of chronic pancreatitis?

A
  • epigastric tenderness
  • weight loss and lethargy
107
Q

What blood tests and functional tests are performed in the investigation of chronic pancreatitis?

A

Blood tests:

  • LFTs are done as an AST : ALT ratio > 2 indicates alcoholic liver disease
  • HbA1c is performed to investigate for diabetes

Functional tests:

  • faecal elastase - a REDUCTION indicates chronic pancreatitis
    • the pancreas makes elastase and it is poorly functioning in this condition
108
Q

What imaging investigations are performed in chronic pancreatitis?

A
  • first line is ultrasound scan
  • CT scan
  • abdominal X-ray may show calcifications of the pancreas
109
Q

What is the treatment for chroinic pancreatitis?

A

treatment is conservative and involves:

  • smoking and alcohol cessation
  • a low fat but high calorie diet with fat-soluble vitamins
    • it needs to be high calorie as the patient cannot reabsorb much of the energy from their diet
    • they also cannot digest fat
110
Q

What are the medical treatments for chronic pancreatitis?

A
  • analgesia for associated pain
  • a pancreatic enzyme supplement, such as Creon
111
Q

What are the complications of chronic pancreatitis?

A
  • malabsorption
  • diabetes mellitus
  • pseudocyst of the pancreas
  • carcinoma of the pancreas

Core Conditions - Abdominal (13 decks)

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