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Y5 Gastrointestinal System > List I - Core Conditions > Flashcards

List I - Core Conditions Flashcards

1
Q

What is malnutrition?

A
  • NICE define malnutrition as the following:
  • BMI of <18.5; or
  • Unintentional weight loss of >10% within the last 3-6 months; or
  • BMI of <20 and unintentional weight loss >5% within the last 3-6 months
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2
Q

Who is at risk of malnutrition?

A
  • Around 10% of patients aged over 65 years are malnourished, vast majority are living independently
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3
Q

Which tool can be used to screen for malnutrition?

A
  • Malnutrition Universal Screen Tool (MUST) tool
  • Should be completed on admission to hospital, nursing or care home or if there is concern - thin, elderly with pressure sores
  • Takes into account BMI, recent weight change and the presence of acute disease
  • Stratifies patients into low, medium and high risk
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4
Q

How is malnutrition managed?

A
  • Following points are recommended by NICE:
  • Dietician support if the patient is high risk
  • Food first approach with clear instructions e.g. add full fat cream to mashed potato, rather than just prescribing oral nutritional supplements such as Ensure
  • If ONS are used they should be taken between meals, rather than instead of meals
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5
Q

What is oesophagitis and reflux?

A
  • Symptoms of oesophagitis secondary to refluxed gastric contents
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6
Q

What is dyspepsia?

A
  • Term used to describe a complex of upper GI tract symptoms which are typically present for 4 or more weeks, including upper abdominal pain or discomfort, heart burn, acid reflux, nausea and/or vomiting
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7
Q

What is GORD?

A
  • Usually a chronic condition where there is reflux of gastric contents (particularly acid, bile, and pepsin) back into the oesophagus, causing predominant symptoms of heart burn and acid regurgitation
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8
Q

What atypical symptoms may be associated with GORD?

A
  • Affecting the oropharynx and/or respiratory tract, such as hoarseness, cough, asthma and dental erosions in some people
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9
Q

What does ‘proven GORD’ mean?

A
  • Endoscopically determined reflux disease, which may be due to:
  • Oesophagitis, when oesophageal inflammation and mucosal erosions are seen
  • Endoscopically negative reflux disease (or non-erosive reflux disease) when a person has symptoms of GORD but endoscopy is normal (seen in up to 2/3 of people)
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10
Q

What is the mechanism of GORD?

A
  • Thought to be a combination of mechanisms, such as transient relaxation (reduced tone) of the lower oesophageal sphincter, increased intra-gastric pressure (straining and coughing), delayed gastric emptying, and impaired oesophageal clearance of acid
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11
Q

What are the risk factors for developing GORD?

A
  • Stress and anxiety
  • Smoking and alcohol
  • Trigger foods, such as coffee and chocolate which may reduce lower oesophageal tone, and fatty foods which delay gastric emptying
  • Obesity
  • Drugs the decrease LOS pressure such as alpha blockers, anti-cholinergics, benzodiazepines, beta-blockers, bisphosphonates, calcium channel blockers, corticosteroids, NSAID’s, nitrates, theophyllines and tricyclic antidepressants
  • Pregnancy (hormonal changes are thought to decrease LOS pressure in some women)
  • Hiatus hernia (may lower LOS tone)
  • Family history
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12
Q

What are the risk factors for developing Barrett’s oesophagus?

A
  • Male gender
  • Long duration and/or increased frequency of GORD symptoms
  • Previous oesophagitis or hiatus hernia
  • Previous oesophageal stricture or ulcers
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13
Q

What are the complications of GORD?

A
  • Oesophageal ulcers
  • Oesophageal haemorrhage
  • Anaemia due to chronic blood loss (usually secondary to severe oesophagitis)
  • Oesophageal stricture (severe oesophagitis can lead to fibrosis and narrowing of the oesophageal lumen)
  • Aspiration pneumonia
  • Barrett’s oesophagus
  • Oral problems such as dental erosions, gingivitis and halitosis
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14
Q

What is the prognosis of oesophagitis?

A
  • Annual risk of recurrence of untreated GORD symptoms is 50%, and the lifetime risk of recurrence is 80%
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15
Q

How should oesophagitis be managed?

A
  • Assess for any symptoms suggesting a complication
  • Offer self management advice - NHS leaflet on heart burn and GORD
  • Offer advice on lifestyle measures that may improve symptoms
  • Lose weight if overweight or obese
  • Avoid trigger foods, coffee, chocolate, tomatoes
  • Eat smaller meals and 3-4 hours before going to bed
  • Stop smoking
  • Reduce alcohol
  • Sleep with head of bed raised
  • Assess for stress and anxiety
  • Ask about OTC meds
  • Review any regular meds
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16
Q

What is the management for a person with proven GORD?

A
  • Full dose PPI for 4 weeks to aid healing
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17
Q

What is the management for a person with proven severe oesophagitis?

A
  • Offer full dose PPI for 8 weeks to aid healing
  • Offer full dose PPI long term as maintenance treatment
    (Do not arrange testing for H. Pylori infection)
  • Advise the person for follow up appointment if there are refractory or recurrent symptoms following initial management
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18
Q

What is the management for a person with endoscopically negative reflux disease?

A
  • Full dose PPI for 1 month
  • If responsive then offer low dose treatment, possibly on an as required basis, with a limited number of repeat prescriptions
  • If no response then H2RA or prokinetic for one month
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19
Q

What is dysphagia?

A
  • Difficulty swallowing - many different causes
  • Oesophageal cancer
  • Oesophagitis
  • Oesophageal candidiasis
  • Achalasia
  • Pharyngeal pouch
  • Systemic sclerosis
  • Myasthenia gravis
  • Globus hystericus
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20
Q

How does oesophageal carcinoma present?

A
  • Dysphagia may be associated with:
  • Weight loss
  • Anorexia
  • Vomiting during eating

PMH

  • Barrett’s oesophagus
  • GORD
  • Excessive smoking
  • Alcohol use
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21
Q

What is the referral criteria for urgent 2 week endoscopy?

A

Suspected oesophageal or stomach cancer

  • Urgent (within 2 weeks) to assess for oesophageal cancer in people with:
  • Dysphagia
  • Aged 55 and over with weight loss and any of the following:
  • Upper abdominal pain
  • Reflux
  • Dyspepsia
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22
Q

What is the referral criteria for non urgent endoscopy?

A

Suspected oesophageal or stomach cancer

  • Non-urgent direct access upper GI endoscopy for people with:
  • Haematemesis
  • People aged 55 or over with treatment resistant dyspepsia
  • Upper abdominal pain with low haemoglobin levels or
  • Raised platelet count with any of the following:
  • Nausea
  • Vomiting
  • Weight loss
  • Reflux
  • Dyspepsia
  • Upper abdominal pain or
  • Nausea or vomiting with any of the following:
  • Weight loss
  • Reflux
  • Dyspepsia
  • Upper abdominal pain
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23
Q

What are the symptoms suggestive of an upper GI cancer?

A
  • Appetite loss
  • Weight loss
  • Upper abdominal mass
  • Abdominal pain
  • Back pain with weight loss
  • Diabetes (new onset) with weight loss
  • Diarrhoea or constipation
  • Jaundice
  • Nausea or vomiting
  • Dyspepsia (with raised platelet count or nausea or vomiting, age 55 and over
  • Dysphagia
  • Haematemesis
  • Haemoglobin levels low with upper GI pain
  • Platelet count raised
  • Reflux
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24
Q

What is the most common type of oesophageal cancer?

A
  1. Adenocarcinoma

2. Squamous cell carcinoma

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25
Q

What is the prognosis of oesophageal cancer?

A
  • 5 year survival rate is 15%
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26
Q

What is the location of adenocarcinoma if it is oesophageal?

A
  • Low third of oesophagus - near the gastro-oesophageal junction
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27
Q

What are the risk factors for adenocarcinoma if it is oesophageal?

A
  • GORD
  • Barrett’s oesophagus
  • Smoking
  • Achalasia
  • Obesity
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28
Q

What is the location of squamous cell carcinoma if it is oesophageal?

A
  • Upper two thirds of the oesophagus
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29
Q

What are the risk factors for squamous cell carcinoma if it is oesophageal?

A
  • Smoking
  • Alcohol
  • Achalasia
  • Plummer-Vinson sydrome
  • Diets rich in nitrosamines
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30
Q

How is diagnosis of oesophageal carcinoma made?

A
  • Upper GI endoscopy is first line test
  • Staging is done with CT chest, abdomen and pelvis
  • If CT does not show metastatic disease, then local stage may be more accurately assessed by use of endoscopic USS
  • Staging laproscopy is performed to detect occult peritoneal disease
  • PET CT is performed in those with negative laparoscopy
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31
Q

What are the treatment options for oesophageal carcinoma?

A
  • Surgical resection if possible
  • Most standard is the Ivor-Lewis type oesophagectomy:
  • Involves the mobilisation of the stomach and division of the oesophageal hiatus
  • Abdomen is closed and a right sided thoracotomy performed, stomach is brought to the chest and the oesophagus mobilised further
  • Intrathoracic oesophagogastric anastomosis is constructed
  • Alternative surgical strategies include a transhiatal resection (for distal lesions), a left thoracoabdominal resection (difficult access due to thoracic aorta) and a total oesophagectomy (McKeown) with a cervical oesophagogastric anastomosis
  • Biggest risk is an anastomotic leak, with an intrathoracic anastomosis this will result in mediastinitis - high mortality
  • McKeown technique has an intrinsically lower systemic insult in the event of anastomotic leakage
  • In addition to surgery, most patients are treated with adjuvant chemotherapy
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32
Q

What is a hiatus hernia?

A
  • A hiatus hernia describes the herniation of part of the stomach above the diaphragm.
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33
Q

What are the two types of hiatus hernia?

A
  • Sliding (A) accounts for 95% of hiatus hernia, the gastrooesophageal junction moves above the diaphragm
  • Rolling (B) (paraoesophageal): the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
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34
Q

What are the investigations for hiatus hernia?

A
  • OGD is gold standard
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35
Q

What is the conservative management of hiatus hernia?

A 
Weight loss
Stop smoking 
Stop/reduce alcohol
Lose weight
PPI prescription
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36
Q

When is surgery for hiatus hernia indicated?

A
  • Indicated when:
  • Remaining symptomatic despite conservative measures including medication
  • Increased risk of strangulation
  • Nutritional failure due to outlet obstruction
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37
Q

What are the surgical options for hiatus hernia?

A

Types of surgery:

  • Cruroplasty – hernia is reduced from the thorax to the abdomen and the hiatus reapproximated to size – large defects require mesh to strengthen the repair
  • Fundoplication – gastric fundus is wrapped around the lower oesophagus and stitched in place – strengthens the lower oesophagus and keep the GOJ in place below the diaphragm
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38
Q

What are the features of peptic ulcer disease?

A
  • Epigastric pain
  • Nausea
  • Gastric ulcers
  • Epigastric pain worsened by eating
  • Duodenal ulcers
  • More common than gastric ulcers
  • Epigastric pain when hungry, relieved by eating
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39
Q

What are the risk factors for peptic ulcer disease?

A
  • Helicobacter pylori is associated with the majority:
  • 95% of duodenal ulcers
  • 75% of gastric ulcers
  • Drugs
  • NSAIDs
  • SSRIs
  • Corticosteroids
  • Bisphosphonates
  • Zollinger-Ellison syndrome: rare cause characterised by excessive levels of gastrin, usually from gastrin secreting tumour
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40
Q

What are the investigations for H. pylori?

A
  • Urease breath test or stool antigen test should be first line
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41
Q

What is the management of H. pylori?

A
  • If negative - then PPI’s should be given until the ulcer is healed
  • If positive for H. Pylori, then eradication therapy should be given
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42
Q

What is the eradication therapy for H. Pylori?

A
  • 7 day course
  • PPI + amoxicillin + (clarithromycin or metronidazole)
  • If penicillin allergic: PPI + metronidazole + clarithromycin
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43
Q

What are the complications of peptic ulcer disease?

A
  • Acute bleeding

* Perforation

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44
Q

Which artery is commonly a source of significant gastrointestinal bleeding occurring as a complication of peptic ulcer disease (duodenal)?

A
  • Gastro-duodenal artery
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45
Q

What is the most common features of acute bleeding from peptic ulcer disease?

A
  • Haematemesis
  • Malaena
  • Hypotension
  • Tachycardia
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46
Q

How should patients with acute bleeding from peptic ulcer disease be managed?

A
  • A to E assessment
  • IV PPI
  • Endoscopy is first line intervention
  • If this fails then most patients have:
  • Urgent interventional angiography with transarterial embolization or surgery
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47
Q

What is the presentation of patients with peptic ulcer disease (perforation)?

A
  • Symptoms develop suddenly
  • Epigastric pain, later becoming more generalised
  • Patients may describe syncope
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48
Q

What are the investigations for patients with perforation secondary to peptic ulcer disease?

A
  • Diagnosis is largely clinical
  • Plain film x-rays are the first form of imaging to obtain
  • Upright (erect) chest x-ray is usually required when a patient presents with acute upper abdominal pain
  • This is a useful test as approximately 75% of patients with a perforated peptic ulcer will have free air under the diaphragm ‘pneumoperitoneum’
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49
Q

How common is gastric cancer?

A
  • 700,000 new cases of gastric cancer worldwide each year
  • Overall incidence is decreasing, but incidence of tumours arising from the cardia is increasing
  • Peak age = 70-80 years
  • More common in Japan, China, Finland and Colombia than the West
  • More common in males 2:1
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50
Q

What is the histology of gastric cancer?

A
  • Signet ring cells may be seen in gastric cancer
  • They contain a large vacuole of mucin which displaces the nucleus to one side
  • Higher number of signet ring cells are associated with worse prognosis
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51
Q

What is gastric cancer associated with?

A
  • H. Pylori infection
  • Blood group A: gAstric cAncer
  • Gastric adenomatous polyps
  • Pernicious anaemia
  • Smoking
  • Diet: salty, spicy, nitrates
  • May be negatively associated with duodenal ulcer
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52
Q

What are the features of gastric cancer?

A
  • Dyspepsia
  • Nausea and vomiting
  • Anorexia and weight loss
  • Dysphagia
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53
Q

What are the investigations associated with gastric cancer?

A
  • Diagnosis: endoscopy with biopsy

* Staging: CT or endoscopic ultrasound - endoscopic USS has recently been shown to be superior to CT

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54
Q

How are tumours of the gastro-oesophageal junction classified?

A
  • Type 1
  • True oesophageal cancers and may be associated with Barrett’s oesophagus
  • Type 2
  • Carcinoma of the cardia, arising from the cardiac type epithelium or short segments with intestinal metaplasia at the oesophagogastric junction
  • Type 3
  • Sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric cancer
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55
Q

What is the treatment for gastric cancer?

A
  • Proximally sited disease greater than 5-10cm from the OG junction may be treated by sub total gastrectomy
  • Total gastrectomy if tumour is <5cm from OG junction
  • For type 2 junctional tumours (extending into the oesophagus) oesophagogastrectomy is usual
  • Endoscopic sub mucosal resection may play a role in early gastric cancer confined to the mucosa and perhaps the sub mucosa (this is debated)
  • Lyphadenectomy should be performed
  • A D2 lyphadenectomy is widely advocated by the Japanese, the survival advantages of extended lyphadenectomy have been debated, however overall recommendation is that D2 nodal dissection be undertaken
  • Most patients will receive chemotherapy either pre or post operatively
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56
Q

Which gastric condition is associated with para-proteinaemia?

A
  • Gastric MALT lymphoma
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57
Q

What is associated with gastric MALT lymphoma?

A
  • H. Pylori infection in 95% of cases
  • Good prognosis
  • If low grade then 80% respond to H. pylori eradication
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58
Q

What are the presenting features of pancreatic cancer?

A
  • Classically painless jaundice
  • Pale stools
  • Dark urine
  • Pruritis
  • Cholestatic liver function tests
  • Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
  • Patients typically present in non-specific way with anorexia, weight loss, epigastric pain
  • Loss of exocrine function e.g. steatorrhoea
  • Loss of endocrine function e.g. diabetes mellitus
  • Atypical back pain is often seen
  • Migratory thrombophlebitis Trousseau sign is more common than with other cancers
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59
Q

What are the investigations for pancreatic cancer?

A
  • USS - sensitivity 60-90%
  • High resolution CT scanning is the investigation of choice if the diagnosis is suspected
  • Imaging may demonstrate the double duct sign
  • Presence of simultaneous dilation of the common bile and pancreatic ducts
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60
Q

What is the management of pancreatic cancer?

A
  • Less than 20% are suitable for surgery at diagnosis
  • Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of the pancreas
  • Side effects of the Whipple’s include dumping syndrome and peptic ulcer disease
  • Adjuvant chemotherapy is usually given following surgery
  • ERCP is often used for palliation
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61
Q

What is coeliac disease?

A
  • Autoimmune condition causing sensitivity to the protein gluten
  • Repeated exposure leads to villous atrophy which can in turn cause malabsorption
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62
Q

What are the signs and symptoms of coeliac disease?

A

Signs and symptoms

  • Chronic or intermittent diarrhoea
  • Failure to thrive or faltering growth
  • Persistent unexplained GI symptoms including vomiting and nausea
  • Prolonged fatigue
  • Sudden unexpected weight loss
  • Unexplained iron deficiency anaeamia or other anaemia
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63
Q

What are the complications of coeliac disease?

A
  • Anaemia – iron, folate, B12 (folate deficiency more common than B12 deficiency in coeliac disease)
  • Hyposplenism
  • Osteoporosis, osteomalacia
  • Lactose intolerance
  • Enteropathy associated T cell lymphoma of small intestine
  • Subfertility
  • Rare: oesophageal cancer
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64
Q

What are the associated complications of coeliac disease?

A
  • Associated conditions
  • Dermatitis herpetiformis
  • Other AI conditions T1DBM, AI hepatitis
  • HLA-DQ2 95% and HLA-DQ8 80%
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65
Q

How is testing for coeliac disease done?

A
  • Diagnosis is made by a combination of serology and endoscopic intestinal biopsy
  • Patients who are already taking a gluten free diet should reintroduce gluten for at least 6 weeks prior to testing
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66
Q

What is serology testing for coeliac disease?

A
  • Tissue transglutaminase (TTG) antibodies (IgA) are first choice according to NICE
  • Endomyseal anti-body (IgA)
  • Need to look for selective IgA deficiency which would give a false negative result
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67
Q

What is endoscopic intestinal biopsy for coeliac disease?

A
  • ‘Gold standard’ - should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis
  • Traditionally done in the duodenum but jejunal biopsies are also sometime performed
  • Findings supportive of coeliac disease:
  • Villous atropy
  • Crypt hyperplasia
  • Increase in intraepithelial lymphocytes
  • Lamina propria infiltration with lymphocytes
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68
Q

What is the management of people with coeliac disease?

A
  • Gluten free diet
  • Notable foods which are gluten free include:
  • Rice
  • Potatoes
  • Corn (maize)
  • Gluten containing cereals include:
  • Wheat: bread, pasta, pastry
  • Barley: beer
  • Rye
  • Oats - some patients with coeliac disease appear to be able to tolerate oats
  • TTG may be checked to check compliance with a gluten free diet
  • Immunisation
  • Patients with coeliac disease often have a degree of functional hyposplenism
  • For this reason, all patients with coeliac disease are offered the pneumococcal vaccine - UK recommends all people with coeliac disease to be vaccinated against pneumococcal infection and have a booster every 5 years
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69
Q

What is the pathophysiology of acute pancreatitis?

A
  • Auto-digestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
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70
Q

What are the features of acute pancreatitis?

A
  • Severe epigastric pain that may radiate through to the back
  • Vomiting is common
  • Examination may reveal epigastric tenderness, ileus and low grade fever
  • Peri-umbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare
  • Rare features associated with pancreatitis include:
  • Ischaemic (Purtscher) retinopathy - may cause temporary or permanent blindness
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71
Q

What are the causes of pancreatitis?

A

I GET SMASHED

  • Iatrogenic
  • Gall stones **
  • ETOH **
  • Trauma
  • Scopion bite!
  • Mumps
  • Auto-immune
  • Steroids
  • Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
  • ERCP
  • Drugs (azathioprine, mesalazine, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

NB Pancreatitis is 7 times more likely in someone taking mesalazine than sulfasalazine

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72
Q

What are the investigations for acute pancreatitis?

A
  • Serum amylase - raised in 75%, typically > 3 times the upper limit of normal (other causes of raised amylase include: pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis
  • Serum lipase - more sensitive and specific than serum amylase, longer half life so may be useful for late presentations > 24 hours
  • Diagnosis of acute pancreatitis can be made without imaging if characteristic pain and amylase/lipase > 3 times normal level
  • However early USS imaging is important to assess the aetiology as this may affect management - e.g. patients with gallstones/biliary obstruction
  • Other options include contrast enhanced CT
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73
Q

Which scoring systems are used for assessing acute pancreatitis?

A
  • Ranson score
  • Glasgow score
  • APACHE II

Features vary but common ones include:

  • Age >55 years
  • Hypocalcaemia
  • Hyperglycaemia
  • Hypoxia
  • Neutrophilia
  • Elevated LDH and AST
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74
Q

What are the potential complications of acute pancreatitis?

A
  • Local
  • Peri-pancreatic fluid collections
  • Pseudocysts
  • Pancreatic necrosis
  • Pancreatic abscess
  • Haemorrhage
  • Systemic
  • Acute respiratory distress syndrome
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75
Q

How should acute pancreatitis be stratified to manage care?

A
  • Mild - no organ failure or local complications
  • Moderately severe - transient organ failure, possible local complications
  • Severe - persistent >48 hours, possible local complications
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76
Q

What is the approach to care of someone with acute pancreatitis?

A
  • Fluid resuscitation - aggressive early hydration with crystalloids, in severe cases 3-6 litres of third space fluid loss may occur
  • Aim for a urine output of >0.5 mls/kg/hr
  • May also help relieve pain by reducing lactic acidosis
  • Analgesia - IV opioids are normally required
  • Nutrition - patients are routinely made nil by mouth unless there is a clear reason e.g. vomiting
  • Enteral nutrition should be offered to anyone with moderately severe or severe acute pancreatitis within 72 hours of presentation
  • NICE state do not offer prophylactic antimicrobials
  • Potential indications include infected pancreatic necrosis
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77
Q

What is the role of surgery for a person with acute pancreatitis?

A
  • If due to gall stones patients should undergo early cholecystectomy
  • Patients with obstructed biliary system due to stones should undergo early ERCP
  • Patients who fail to settle with necrosis and have worsening organ dysfunction may require debridement, fine needle aspiration is still used by some
  • Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy
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78
Q

What is spontaneous bacterial peritonitis?

A
  • Form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis
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79
Q

What are the features of SBP?

A
  • Ascites
  • Abdominal pain
  • Fever
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80
Q

How is SBP diagnosed?

A
  • Paracentesis - neurophil count > 250 cells/ul

* Most common organism found on ascitic fluid culture is E.coli

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81
Q

What is the management of SBP?

A
  • IV ceftriaxone is usually given
  • Antibiotic propylaxis should be given to patients with ascites if:
  • Patients have had an episode of SBP
  • Patients with fluid protein <15 g/l and either a Child-Pugh score of at least 9 or hepatorenal syndrome
  • NICE recommend
  • Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved
  • Alcoholic liver disease is a marker of poor prognosis in SBP
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82
Q

What is peritonitis?

A
  • Inflammation of the thin layer of tissue that lines the inside of the stomach called the peritoneum
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83
Q

What is an inguinal hernia?

A
  • Inguinal hernia – found supero-medial to the pubic tubercule
    Account for 75% of abdominal wall hernias
    Men have a 25% lifetime risk of developing an inguinal hernia
    May be classified as being direct or indirect, distinction between the two rests on their relation to Hesselbach’s trinagle
    Boundaries of Hesselbach’s Triangle
    Medial: Rectus abdominis
    Lateral: Inferior epigastric vessels
    Inferior: Inguinal ligament
    Inferior epigastric vessels – Indirect hernias will be lateral to the vessels whilst direct hernias will be medial to the vessels
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84
Q

What is a direct inguinal hernia?

A
  • Direct 20% – within the triangle
    Bowel enters through the inguinal canal ‘directly’ through a weakness in the posterior wall of the canal, termed Hesselbach’s triangle
    More common in older patients due to laxity of abdominal wall or significant increase in intra-abdominal pressure
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85
Q

What is an indirect inguinal hernia?

A
  • Indirect 80% – outside the triangle
    Bowel enters through the inguinal canal via the deep inguinal ring
    Arise from incomplete closure of the processus vaginalis, an outpouching of peritoneum allowing for embryonic testicular descent, therefore are usually deemed congenital in origin
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86
Q

What is a femoral hernia?

A
  • Found infero-lateral to the pubic tubercule (and medial to the femoral pulse)
  • More common in women, particularly multiparous ones
  • High risk of obstruction and strangulation
  • Surgical repair is required
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87
Q

What is the management of a fermoral hernia?

A

All femoral hernias should be managed surgically, ideally within 2 weeks of presentation, due to the high risk of strangulation.

Two different approaches can be taken with the femoral hernia surgical reduction:
• Low approach – the incision is made below the inguinal ligament, which has the advantage of not interfering with the inguinal structures but does result in limited space for the removal of any compromised small bowel
• High approach – the incision is made above the inguinal ligament is the preferred technique in an emergency intervention due to the easy access to compromised small bowel
• The operation involves reducing the hernia and then narrowing the femoral ring with sutures medially between the pectineal and inguinal ligaments or with a mesh plug

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88
Q

What is an umbilical hernia?

A
  • A paraumbilical hernia is a herniation occurring through the linea alba around the umbilical region* (not through the umbilicus itself).
  • They are also typically secondary to raised chronic intra-abdominal pressure and present as a lump around the umbilical region.
  • They are extremely common, with risk factors including obesity and pregnancy.
  • Generally they contain pre-peritoneal fat although they can occasionally contain bowel. Whilst they are a fairly common presentation in general surgery, they do not commonly strangulate
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89
Q

What is the presentation of a patient with gallstones?

A
  • Colicky right upper quadrant pain occurs postprandially
  • Symptoms are usually worst following a fatty meal when cholecystokinin levels are highest and gallbladder contraction is maximal
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90
Q

What are the investigations for gallstones?

A
  • Abdominal USS
  • Liver function tests

2nd MRCP
3rd ERCP

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91
Q

What are the different types of gall stone disease?

A
  • Biliary colic
  • Acute cholecystitis
  • Gall bladder abscess
  • Cholangitis
  • Gall stone ileus
  • Acalculous cholecystitis
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92
Q

What are the features of biliary colic?

A
  • Colicky abdominal pain

* Worse after meals - fatty foods

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93
Q

What is the management of biliary colic?

A
  • If imaging shows gallstones and history is compatible, then cholecystectomy
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94
Q

What are the features of acute cholecystitis?

A
  • Right upper quadrant pain
  • Fever
  • Murphy’s sign
  • Occasionally deranged LFT’s (especially Mirizzi syndrome)
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95
Q

What is the management of acute cholecystitis?

A
  • USS and cholecystectomy (ideally within 48 hours of presentation)
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96
Q

What are the features of a gall bladder abscess?

A
  • Usually prodromal illness and right upper quadrant pain
  • Swinging pyrexia
  • Patient may be systemically unwell
  • Generalised peritonism not present
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97
Q

What is the management of gall bladder abscess?

A
  • USS +/- CT scanning
  • Ideally surgery
  • Sub-total cholecystectomy may be needed if Calot’s triangle is hostile
  • If unfit, percutaneous drainage may be considered
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98
Q

What are the features of cholangitis?

A
  • Patient severely septic and unwell
  • Jaundice
  • Right upper quadrant pain
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99
Q

What is the management of cholangitis?

A
  • Fluid resuscitation
  • Broad spectrum intravenous antibiotics
  • Correct any coagulopathy
  • Early ERCP
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100
Q

What are the features of gallstone ileus?

A
  • Patients may have a history of previous cholecystitis and known gallstones
  • Small bowel obstruction (may be intermittent)
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101
Q

What is the management of gallstone ileus?

A
  • Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction
  • The fistula between the GB and duodenum should not be interfered with
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102
Q

What are the features of acalculous cholecystitis?

A
  • Patients with intercurrent illness e.g. diabetes, organ failure)
  • Patients systemically unwell
  • GB inflammation in the absence of stones
  • High fever
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103
Q

What is the management of a patient with acalculous cholecystitis?

A
  • If patient is fit then cholecystectomy

* If unfit then percutaneous cholecystectomy

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104
Q

What is the name of gallstones in the common bile duct?

A
  • Choledocholithiasis
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105
Q

What are the four main risk factors for biliary colic?

A
  • Fat
  • Female
  • Fertile - pregnant
  • Forty

Other notable risk factors include:

  • Diabetes
  • Crohin’s disease
  • Rapid weight loss
  • Drugs: fibrates, COCP
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106
Q

What is the pathophysiology of biliary colic and gallstone related disease?

A
  • Occur due to increased cholesterol, reduced bile salts and biliary stasis
  • Pain occurs due to the GB contracting against a stone lodged in the cystic duct
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107
Q

What is acute cholecystitis?

A
  • Inflammation of the gallbladder

- Number of different pathological classifications including oedematous, necrotizing, supparative and chronic

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108
Q

What are the causes of acute cholecystitis?

A
  • Most commonly gallstones 90-95%
  • In a minority of people, blockage to the part of the biliary system such as the GB neck or cystic duct by gallstone causes symptoms (pain, inflammation in the GB wall, and infection) which if untreated can progress to cholecystitis
  • Approximately 5% presenting with acute cholecystitis do not have gallstones
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109
Q

What are the risk factors for developing gallstones?

A
  • Obesity
  • Increasing age
  • Female gender
  • Higher levels of triglycerides and lower levels of LDL’s
  • Weight cycling (up and down)
  • DBM
  • COCP
  • HRT
  • Smoking
  • Crohn’s disease
  • Genetic and ethnic factors
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110
Q

What are the risk factors for acalculous cholecystitis?

A
  • Trauma
  • Burns
  • Immobility
  • Starvation
  • Sepsis
  • Acute renal failure
  • DBM
  • Vascular disease
  • TPN
  • Narcotic analgesics
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111
Q

How common is acute cholecystitis?

A
  • Most common complication in people with gallstone disease
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112
Q

What are the complications of acute cholecystitis?

A
  • Necrosis of GB
  • Perforation of GB
  • Biliary peritonitis
  • Peri-cholecystic abscess
  • Fistula (GB to duodenum)
  • Jaundice (due to inflammation of adjoining biliary ducts - Mirizzi’s syndrome)
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113
Q

How is a diagnosis of acute cholecystitis made?

A
  • Suspect in a person with the following symptoms:
  • Sudden onset constant, severe pain in the RUQ lasting several hours
  • Anorexia, nausea, or vomiting
  • Fever
  • Tenderness in the RUQ +/- Murphy’s sign
  • Referred pain to the shoulder
  • Hx gallstones
  • Look for signs which could indicate a complication
  • RUQ palpable mass
  • Fever
  • Jaundice
  • More severe localised or generalised tenderness
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114
Q

What are the differential diagnoses for acute cholecystitis?

A
  • Gall stones
  • GORD
  • Acute cholangitis
  • Acute pancreatitis
  • Hepatitis
  • Malignancy
  • Appendicitis
  • Right lower lobe pneumonia
  • ACS
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115
Q

What is the management from primary care for acute cholecystitis?

A
  • Urgently admit to hospital for
  • Confirmation of the diagnosis, including abdominal USS, WCC, CRP, amylase
  • Monitoring of basic observations
  • Treatment - IV fluids, antibiotics, analgesia
  • Surgical assessment for cholecystectomy
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116
Q

What is portal hypertension?

A
  • Increase in the BP in the portal vein, which carries the blood from the bowel and spleen to the liver
  • One of the consequences of chronic liver disease
  • Pressure in the portal vein may rise because there is a blockage, such as a blood clot, or because the resistance in the liver is increased because of scarring (fibrosis) or cirrhosis
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117
Q

What are the symptoms of portal hypertension?

A
  • Portal hypertension and its consequence of bleeding varices are usually seen in people with moderately advanced liver disease
  • May be other features such as ascites (fluid in the stomach) and encephalopathy (disturbance of brain function as a result of disordered liver function)
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118
Q

What is the pressure definition of portal hypertension?

A
  • > 12mmHg
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119
Q

What are the three main areas of the hepatic portal system that can connect to the systemic venous system and can be affected due to portal hypertension?

A
  • Inferior portion of the oesophagus
  • Superior portion of the anal canal
  • Round ligament of the liver
120
Q

What are the consequences of portal hypertension on the inferior portion of the oesophagus?

A
  • Oesophageal varices - most common consequence
121
Q

What are the consequences of portal hypertension on the superior portion of the anal canal?

A
  • Haemorrhoids
122
Q

What are the consequences of portal hypertension on the round ligament of the liver?

A
  • Capute medusa
123
Q

What is the consequences of portal hypertension on the spleen?

A
  • Congestive splenomegaly
  • Anaemia
  • Leukopenia
  • Thrombocytopenia
124
Q

What is the endothelial consequence of portal hypertension?

A
  • Endothelial cells lining the blood vessels release more nitric oxide
  • NO makes peripheral arteries dilate which makes BP drop, this stimulates release of aldosterone from the adrenal glands which tells the kidneys to retain sodium and water
  • In time, the plasma volume expands so much that fluid in the blood vessels is more likely to get pushed into tissues and across tissues into large open spaces like the peritoneal cavity - leading to ascites
  • Ascitic fluid can become infected with bacteria SBP
125
Q

What is the medical treatment for portal hypertension?

A
  • Propanolol

- Reduces venous pressure and prevents compication

126
Q

What is the treatment for ascites?

A
  • Sodium restriction
  • Diuretics
  • Reduce fluid overload
127
Q

What is the treatment for bleeding oesophageal varices?

A
  • A to E assessment and management
  • Ideally resuscitation prior to endoscopy
  • Correct clotting FFP, vitamin K
  • Vasoactive agents:
  • Terlipressin or Octreotide
  • Prophylactic IV antibiotics
  • Endoscopy for band ligation
  • Sengstaken-Blakemore tube if uncontrolled haemorrhage
  • TIPPS if the above measures fail - connects the hepatic vein to the portal vein - can lead to an exacerbation of hepatic encephalopathy
128
Q

What are the different types of viral hepatitis?

A
  • ABCDE
129
Q

What are the features of hepatitis A?

A
  • Typically benign, self limiting disease with serious outcome very rare
  • Incubation period 2-4 weeks
  • RNA picornavirus
  • Transmission by faecal oral spread, often in institutions
  • Doesn’t cause chronic disease
130
Q

What are the symptoms of hepatitis A?

A
  • Flu-like prodrome
  • RUQ pain
  • Tender hepatomegaly
  • Jaundice
  • Cholestatic LFT’s
131
Q

Who should be vaccinated for hepatitis A?

A
  • People travelling to regions high or intermediate prevalence, if aged > 1 year old
  • People with chronic liver disease
  • Patients with haemophilia
  • MSM
  • IVDU
  • Occupational risk
132
Q

What are the features of hepatitis B?

A
  • Double stranded DNA hepadnavirus and is spread through exposure to infected blood or body fluids, including vertical transmission from mother to child
  • Incubation period is 6-20 weeks
  • Complications include:
  • Chronic hepatitis (5-10%) - ground glass hepatocytes may be seen on light microscopy
  • Fulminant liver failure (1%)
  • Hepatocellular carcinoma
  • Glomerulonephritis
  • Polyarteris nodosa
  • Cryobulinaemia
133
Q

What are the symptoms of hepatitis B?

A
  • Fever
  • Jaundice
  • Elevated liver transaminases
134
Q

Who should be vaccinated for hepatitis B?

A
  • Children born in the UK as part of normal vaccination schedule (2, 3, 4 months)
  • At risk workers - e.g. healthcare, IVDU, sex workers, etc
  • Contains HBsAg absorbed onto aluminium hydroxide adjuvant and is prepared from yeast cells using recombinant DNA technology
  • Around 10-15% of adults fail to respond or respond poorly to 3 doses of the vaccine - risk factors include age over 40 years, obesity, smoking, alcohol excess and immunosuppression
135
Q

What is the treatment of hepatitis B?

A
  • Pegylated interferon-alpha 1st line (used to be the only treatment) - it reduces viral replication in up to 30% of chronic carriers
  • Better response is predicted by being female <50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy
  • Other treatments include:
  • Tenovir
  • Entecavir
  • Telbivudine
136
Q

What are the features of hepatitis C?

A
  • RNA flavivirus
  • Incubation period 6-9 weeks
  • Transmission
  • Needle stick 2%
  • Vertical from mother to child - 6% risk is higher in presence of HIV
  • Breast feeding is not contraindicated
  • Sexual intercourse transmission - 5%
  • No vaccine exists
  • Complications include
  • Rheumatological problems such as arthralgia, arthritis
  • Eye problems such as Sjorgren’s syndrome
  • Cirrhosis
  • Hepatocellular cancer
  • Cryoglobulinaemia
  • Porphyria
  • Membranoproliferative glomerulonephritis
137
Q

What are the symptoms of hepatitis C?

A
  • Transient rise in serum aminotransferases / jaundice
  • Fatigue
  • Arthralgia
138
Q

What are the investigations for hepatitis C?

A
  • HCV RNA is the investigation of choice to diagnose acute infection
  • Patients will eventually develop anti-HCV antibodies and clear the virus but the anti-bodies will remain
139
Q

What is the treatment of hepatitis C?

A
  • Aims of treatment are for sustained virological response (SVR)
  • Defined as undetectable serum HCV RNA six months after the end of therapy
  • Currently a combination of protease inhibitors (e.g. daclatasvir etc) with or without ribavirin are used
140
Q

What are the complications of hepatitis C treatment?

A
  • Ribavirin - haemolytic anaemia, cough
  • Women taking ribavirin should not become pregnant within 6 months of stopping as it is teratogenic
  • Interferon alpha - side effects - flu like symptoms, depression, fatigue, leukopenia, thrombocytopenia
141
Q

What are the features of hepatitis D?

A
  • Single stranded RNA virus that is transmitted parenterally
  • It is an incomplete RNA virus that requires hepatitis B surface antigen to complete its replication and transmission cycle
  • Transmitted in a similar way to hep B (exchange of bodily fluids) - patients may be infected with hep B and D at the same time
  • Co-infection - Hep B and D at the same time
  • Super infection - Hep B surface antigen postive patient subsequently develops a hep D infection
  • Super infection is associated with risk of fulminant hepatitis, chronic hepatitis status and cirrhosis
142
Q

How is diagnosis of hepatitis D made?

A
  • Reverse polymerase chain reaction of hepatitis D RNA
143
Q

What are the features of hepatitis E?

A
  • RNA hepevirus
  • Spread by faecal-oral route
  • Incubation 3-8 weeks
  • Common in Central and South East Asia, North and West Africa and in Mexico
  • Cause a similar disease to hepatitis A, but carries significant mortality (about 20%) during pregnancy
  • Does not cause chronic disease or an increased risk of hepato-cellular cancer
144
Q

What is liver cirrhosis?

A
  • Develops progressively as a result of damage to the liver progressively usually over a number of years
  • Normal smooth liver structure becomes distorted, with nodules surrounded by fibrosis - affects the liver’s synthetic, metabolic and excretory actions
145
Q

How can liver cirrhosis be categorised?

A
  • Compensated - when the liver can still function effectively and there are few or no, noticeable clinical symptoms
  • Decompensated - when the liver is damaged to the point it cannot function adequately and overt clinical complications (jaundice, ascites, variceal haemorrhage and hepatic encephalopathy) are present
  • Events causing decompensation include infection, portal vein thrombosis and surgery
146
Q

What are the risk factors for cirrhosis?

A
  • Alcohol misuse
  • Hepatitis B and C
  • Obesity (BMI of 30 kg/m2 or more) or T2 DBM

Less common causes of cirrhosis include:

  • Autoimmune liver disease (AI hepatitis, PBC, PSC)
  • Genetic conditions (haemochromatosis, Wilson’s disease, alpha-1 anti-trypsin deficiency, cystic fibrosis)
  • Long term medication such as methotrexate
  • Budd-Chiari syndrome or veno-occlusive disease
  • Sarcoidosis and glycogen storage disease
147
Q

What are the major complications of cirrhosis?

A
  • Ascites
  • Hepatic encephalopathy
  • Haemorrhage from oesophageal varices
  • Infection
  • Others including:
  • Hepato-renal syndrome
  • Hepatocellular carcinoma
  • Portal vein thrombosis
  • Cardio-vascular complications including circulatory changes such as decreased BP and cirrhotic cardiomyopathy
148
Q

What is the prognosis of cirrhosis?

A
  • Once cirrhosis has occurred it is usually considered irreversible
  • People may show no symptoms for many years (compensated)
  • Once people start to show complications such as jaundice, ascites, variceal haemorrhage, or hepatic encephalopathy arise due to portal hypertension and/or hepatocellular failure - this marks a transition from compensated to decompensated
  • Prognosis can be managed to a certain extent by life style changes such as:
  • Treatment of underlying cause e.g. stop drinking alcohol, treat hepatitis
149
Q

When should you suspect liver cirrhosis?

A
  • Palpable left lobe of the liver, hepatomegaly, splenomegaly
  • Presence of stigmata of chronic liver disease (spida naevi, palmar erythema, white nails, muscle wasting)
  • Features of severe liver impairment and signs of decompensated liver disease such as:
  • Jaundice (examine the sclera under natural light_
  • Abnormal bruising
  • Peripheral oedema
  • Ascites
  • Sepsis
  • Variceal bleeding
  • Encephalopathy - asterixis
150
Q

What is the LFT picture in a person with known chronic liver disease?

A
  • Low platelet count
  • Elevated AST: ALT ratio
  • High bilirubin
  • Low albumin
  • Increased prothrombin time or INR
151
Q

What should be offered to diagnose cirrhosis?

A
  • Offer transient elastography to diagnose cirrhosis for:
  • People with hepatitis C infection
  • Men who drink over 50 units of alcohol per week and women who drink over 35 units per week and have done so for several months
152
Q

What is transient elastography?

A
  • Brand name ‘Fibroscan’
  • Uses a 50-MHz wave passed into the liver from a small transducer on the end of an ultrasound probe
  • Measures the stiffness of the liver which is a proxy for fibrosis
153
Q

what further investigations should be done for a patient with alcoholic liver disease?

A
  • NICE recommend doing an upper endoscopy to check for varices in patients with a new diagnosis of cirrhosis
  • Liver USS every 6 months (+/- alpha feto protein) to check for hepato-cellular cancer
154
Q

What is non-alcoholic fatty liver disease?

A
  • NAFL is liver disease largely caused by obesity
  • Spectrum of disease ranging from:
  • Steatosis - fat in the liver
  • Steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH)
  • Progressive disease may cause fibrosis and liver cirrhosis
155
Q

What is thought to be the mechanism leading to steatosis?

A
  • NAFLD is thought to be the hepatic manifestation of the metabolic syndrome and hence insulin resistance is thought to be the key mechanism leading to steatosis
156
Q

What is non-alcoholic steatohepatitis (NASH)?

A
  • Term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse
  • Relatively common (3-4% of the population)
157
Q

What are the associated factors with NAFLD?

A
  • Obesity
  • T2 DBM
  • Hyperlipidaemia
  • Jejunoileal bypass
  • Sudden weight loss/starvation
158
Q

What are the presenting features of NAFLD?

A
  • Usually aysmptomatic
  • Hepatomegaly
  • ALT is typically greater than AST
  • Increased echogenicity on USS
159
Q

What are the NICE guidelines on the management of NAFLD?

A
  • No evidence to support screening
  • If found incidentially - typically asymptomatic fatty changes on liver USS:
  • Enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis
160
Q

In the absence of an ELF test what other assessments can be used for NAFLD?

A
  • FIB4 score
  • NALFD fibrosis score
  • Combine these scores with a FibroScan
  • This combination has an excellent accuracy in predicting fibrosis
161
Q

What is the mainstay of management for NAFLD?

A
  • Lifestyle changes
  • Weight loss in particular
  • Monitoring
  • Ongoing research into gastric banding and insulin sensitising drugs e.g. metformin, pioglitazone
162
Q

What is ascites?

A
  • Ascites is the abnormal accumulation of fluid in the abdomen
163
Q

How can the causes of ascites be categorised?

A
  • According to the serum-ascites albumin gradient (SAAG)
  • <11g/L or
  • > 11g/L
164
Q

What are the causes of ascites with a SAAG >11g/L (indicates portal hypertension) ?

A
  • Liver disorders are the most common cause:
  • Cirrhosis
  • Acute liver failure
  • Liver metastases
  • Cardiac
  • Right heart failure
  • Constrictive pericarditis
  • Other causes
  • Budd-Chiari syndrome
  • Portal vein thrombosis
  • Veno-occlusive disease
  • Myxoedema
165
Q

What are the causes of ascites with a SAAG <11g/L ?

A
  • Hypoalbuminaemia
  • Nephrotic syndrome
  • Severe malnutrition e.g. Kwashiorkor
  • Malignancy
  • Peritoneal carcinomatosis
  • Infections
  • Tuberculous peritonitis
  • Other causes
  • Pancreatitis
  • Bowel obstruction
  • Biliary ascites
  • Post operative lymphatic leak
  • Serositis in connective tissue diseases
166
Q

What is the management of ascites?

A
  • Reducing dietary sodium
  • Fluid restriction sometimes recommended if the sodium is <125 mmol/L
  • Aldosterone antagonists e.g. spironolactone
  • Loop diuretics are often added in patients who don’t respond to aldosterone agonists
  • Drainage of tense ascites (therapeutic abdominal paracentesis)
  • Large volume paracentesis for the treatment of ascites requires albumin cover - reduces paracentesis induced circulatory dysfunction and mortality
  • Prophylactic antibiotics to reduce the risk of SBP - NICE recommend prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litres or less until the ascites has resolved
  • Transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
167
Q

What are the potential consequences of large volume (>5L) paracentesis induced circulatory dysfunction?

A
  • Associated with a high rate of ascites recurrence
  • Development of hepatorenal syndrome
  • Dilutional hyponatraemia
  • High mortality rate
168
Q

What are the features of Crohn’s disease?

A
  • Weight loss, lethargy, diarrhoea +/- bloody, abdominal pain, perianal disease e.g. skin tags or ulcers
  • Raised inflammatory markers, increased faecal calprotectin, anaemia, low B12 and vitamin D
  • Mouth to anus skip lesions, inflammation to all layers of bowel commonly affects the terminal ileum,
  • Goblet cells, granulomas, bowel obstruction, fistulae
    (Erythema nodosum, pyoderma gangrenosum IBD)
169
Q

What are the investigations for Crohn’s disease?

A
  • Colonoscopy – deep ulcer’s skip lesions
  • Small bowel enema – for examination of the terminal ileum, strictures Kantor’s string sign, proximal bowel dilation, rose thorn ulcers, fistulae
170
Q

What is the histological appearance of Crohn’s disease?

A
  • Inflammation in all layers from mucosa to serosa, goblet cells, granulomas
171
Q

What is the medical management of Crohn’s disease?

A
  • Patients should be advised to stop smoking (but may help UC)
  • Inducing remission – glucocorticoids (oral, topical or IV)
    Budesonide is an alternative
    Azathioprine or mercaptopurine may be used as an add on medication to induce remission (not monotherapy)
    Infliximab used for refractory disease and fistulating Crohn’s
    Metronidazole is used for peri-anal disease
  • Maintaining remission – azathioprine or mercaptopurine, methotrexate second line, mesalazine should be considered if the patient has had surgery
    80% of patients will eventually have surgery
172
Q

What needs to be assessed for a patient with Crohn’s disease before starting azathioprine or mercaptopurine?

A
  • Need to assess thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine – risks bone marrow suppression
173
Q

What is the indication for surgery in Crohn’s disease?

A
  • Due to common structuring in the terminal ileum – ileocaecal resection – however due to common recurrence sub-total colectomy and panproctocolectomy are done to treat the disease
174
Q

What are the features of ulcerative colitis?

A
  • Bloody diarrhoea, urgency, tenesmus, abdominal pain left lower quadrant – 15-25 and 55-65 years
  • Submucosa ulceration, preservation of adjacent mucosa, pseudopolyps, crypt abscesses, depletion of goblet cells and mucin from gland epithelium, lead pipe appearance of colon on barium enema, loss of haustral markings
175
Q

What are the extra intestinal features of UC?

A
  • Extra intestinal – Uveitis, episcleritis, erythema nodosum, primary sclerosing cholangitis, arthritis, (ankylosing spondylitis, pyoderma gangrenosum IBD)
176
Q

What criteria can be used to stratify the severity of UC?

A

Truelove & Witts – Stratifies Severity

  • Mild - <4 stools per day without blood, no systemic disturbance, normal ESR and CRP
  • Moderate – 4-6 stools per day with minimal systemic disturbance
  • Severe - >6 stools per day containing blood, evidence of systemic disturbance e.g. fever, tachycardia, abdominal tenderness, distention or reduced bowel sounds, anaemia, hypoalbuminaemia
177
Q

What is the approach to the management of UC exacerbations?

A
  • Mild to moderate – topical (rectal) aminosalicylates (mesalazine) 4 weeks, if remission not achieved add topical or oral corticosteroids
  • Extensive disease – topical (rectal) aminosalycylate and a high dose oral aminosalycylate, remission not achieved in 4 weeks stop topical and offer high dose oral aminosalycylate and oral corticosteroids
  • Severe colitis – should be treated in hospital, IV steroids are first line, IV ciclosporin may be used if steroid are contraindicated

If no improvement after 72 hrs, consider adding ciclosporin to IV corticosteroids or consider surgery

178
Q

What is the approach to maintaining remission of UC?

A
  • For maintaining remission
  • Following a severe relapse or >= 2 exacerbations in the past year
  • Oral azathioprine or oral mercaptopurine
  • Need to assess thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine – risks bone marrow suppression
179
Q

What is diverticulosis?

A
  • Multiple outpouchings of the bowel wall – commonly in the sigmoid colon – due to increasing age and low fibre diet
180
Q

What are the presenting features of diverticulitis?

A
  • Left iliac fossa pain and tenderness, anorexia, nausea, vomiting and diarrhoea
    Features of infection (pyrexia, #WCC, #CRP)
181
Q

What is the approach to the management of diverticulitis?

A
  • Mild attacks can be treated with oral antibiotics
  • More significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given
182
Q

What are the features of acute appendicitis?

A
  • Most common acute abdominal condition requiring surgery, most common in young people age 1-20 yrs
  • RIF abdominal pain, McBurney’s point, Rovsing’s sign, vomiting once or twice, mild pyrexia 37.5-38c, anorexia
  • Typically raised inflammatory markers, neutrophilia in 80-90%
183
Q

What is the approach to the management of acute appendicitis?

A

Investigations
* PT in females, USS scan to rule out other pelvic organ pathology in females, presence of free fluid should always raise suspicion, CT scan is useful but not always common

Treatment

  • Appendicectomy can be performed via either an open or laparoscopic approach
  • Prophylactic IV antibiotics to reduce wound infection
  • Perforated appendix require abdominal lavage
  • In older patients, need to be aware of underlying possible caecal malignancy or perforated sigmoid diverticular disease
184
Q

What is the mechanism of small bowel obstruction?

A
  • In small bowel obstruction, the passage of food, fluids and gas, through the small intestines becomes blocked.
  • Adhesions (e.g. following previous surgery) are the most common cause of small bowel obstruction, followed by hernias
185
Q

What are the clinical features of small bowel obstruction?

A
  • Diffuse, central abdominal pain
  • Nausea and vomiting - typically bilious vomiting
  • ‘Constipation’ with complete obstruction and lack of flatulence
  • Abdominal distension may be apparent, particularly with lower levels of obstruction
  • ‘Tinkling’ bowel sounds (more common in early bowel obstruction)
186
Q

What imaging should be used for small bowel obstruction?

A
  • Abdominal x-ray generally first-line imaging for suspected small bowel obstruction distended small bowel loops with fluid levels
  • Considered dilated if small bowel is >3cm diameter
  • CT is the definitive investigation and is more sensitive, particularly in early obstruction.
187
Q

What is the initial approach to the management of small bowel obstruction?

A
  • NBM
  • IV fluids
  • NG ‘Ryalls’ tube with free drainage
  • Some may improve, others may require surgery
188
Q

What is the mechanism of large bowel obstruction?

A
  • In large bowel obstruction, the passage of food, fluids and gas, through the large intestines becomes blocked.
  • Causes include:
  • Tumour this accounts for 60% of cases of large bowel obstruction
  • Obstruction is the initial presenting complaint of colonic malignancy approximately 30% of cases this is particularly the case in more distal colonic and rectal tumours, as these tend to obstruct earlier due to the smaller lumen diameter
  • Volvulus
  • Diverticular disease
189
Q

What are the clinical features of large bowel obstruction?

A
  • Absence of passing flatus or stool
  • Abdominal pain
  • Abdominal distention
  • Nausea and vomiting are late symptoms that may suggest a more proximal lesion
    peritonism may be present if there is associated bowel perforation
190
Q

What are the investigations for large bowel obstruction?

A
  • Abdominal x-ray still commonly used first-line - normal diameter limits are 10-12 cm for caecum, 8 cm for ascending colon, and 6.5 cm for recto-sigmoid - diameter greater than this is diagnostic of obstruction
    presence of free intra-peritoneal gas indicates colonic perforation
  • CT scan - high sensitivity and specificity for identifying obstruction (over 90% each) as well as identifying the aetiology of obstruction itself
191
Q

What is the management of large bowel obstruction?

A

Initial steps:

  • NBM
  • IV fluids
  • Nasogastric tube with free drainage
  • Urgency of management depends on whether perforation is suspected - if the cause of obstruction itself does not require surgery, conservative management for up to 72 hours can be trialled, after which further management may be required if there is no resolution
  • Around 75% will eventually require surgery
  • IV antibiotics will be given if perforation suspected or surgery planned

Surgery

  • If there is any overt peritonitis or evidence of bowel perforation, emergency surgery is necessary
  • Irrigation of the abdominal cavity, resection of perforated segment and ischaemic bowel, and address the underlying cause of the obstruction itself
192
Q

What is a paralytic ileus?

A
  • Paralytic ileus is a common complication after surgery involving the bowel, especially surgeries involving handling of the bowel. There is no peristalsis resulting in pseudo-obstruction.
  • Paralytic ileus can also occur in association with chest infections, myocardial infarction, stroke and acute kidney injury.
  • Deranged electrolytes can contribute to the development of paralytic ileus, so it is important to check potassium, magnesium and phosphate. As the bowel is not functioning as normal it is better to replace electrolytes intravenously.
193
Q

How should patients with ileus be managed?

A
  • Keep the patient NBM
  • Monitor fluid balance
  • Monitor for bowel sounds until present
  • Daily bloods
  • Encourage mobilisation
  • Reduce opiate analgesia as tolerated
194
Q

What are the different types of colorectal carcinoma?

A
  • It is currently thought there are three types of colon cancer:
  • Sporadic (95%)
  • Hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
  • Familial adenomatous polyposis (FAP, <1%)
195
Q

What is thought to be the pathophysiology of sporadic colonic cancer?

A
  • Studies have shown that sporadic colon cancer may be due to a series of genetic mutations. For example, more than half of colon cancers show allelic loss of the APC gene. It is believed a further series of gene abnormalities e.g. activation of the K-ras oncogene, deletion of p53 and DCC tumour suppressor genes lead to invasive carcinoma
196
Q

What is the cause of HNPCC leading to colonic cancer?

A
  • HNPCC, an autosomal dominant condition, is the most common form of inherited colon cancer.
  • Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive.
  • Currently seven mutations have been identified, which affect genes involved in DNA mismatch repair leading to microsatellite instability.
    The most common genes involved are:
    MSH2 (60% of cases)
    MLH1 (30%)
  • Patients with HNPCC are also at a higher risk of other cancers, with endometrial cancer being the next most common association, after colon cancer
197
Q

What criteria are used to aid the diagnosis of HNPCC colonic cancers?

A
  • The Amsterdam criteria are sometimes used to aid diagnosis:
  • At least 3 family members with colon cancer
  • The cases span at least two generations
  • At least one case diagnosed before the age of 50 years
198
Q

What is the mechanism of FAP leading to colonic cancers?

A
  • FAP is a rare autosomal dominant condition which leads to the formation of hundreds of polyps by the age of 30-40 years.
  • Patients inevitably develop carcinoma - It is due to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene (APC), located on chromosome 5.
  • Genetic testing can be done by analysing DNA from a patient’s white blood cells.
  • Patients generally have a total colectomy with ileo-anal pouch formation in their twenties.
199
Q

What other types of cancer are people with FAP at risk of developing?

A
  • Patients with FAP are also at risk from duodenal tumours.
  • A variant of FAP called Gardner’s syndrome can also feature osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin
200
Q

How common is colorectal cancer?

A
  • Colorectal cancer is the third most common type of cancer in the UK and the second most cause of cancer deaths.
  • Annually there are about 150,000 new cases diagnosed and 50,000 deaths from the disease.
Location of cancer (averages)
rectal: 40%
sigmoid: 30%
descending colon: 5%
transverse colon: 10%
ascending colon and caecum: 15%
201
Q

What is the approach to the treatment of colonic cancer?

A
  • Cancer of the colon is nearly always treated with surgery.
  • Stents, surgical bypass and diversion stomas may all be used as palliative adjuncts. * Resectional surgery is the only option for cure in patients with colon cancer. The procedure is tailored to the patient and the tumour location. The lymphatic drainage of the colon follows the arterial supply and therefore most resections are tailored around the resection of particular lymphatic chains (e.g. ileo-colic pedicle for right sided tumours).
  • Some patients may have confounding factors that will govern the choice of procedure, for example a tumour in a patient from a HNPCC family may be better served with a panproctocolectomy rather than segmental resection.
202
Q

What is the approach to the treatment of rectal cancer?

A
  • The management of rectal cancer is slightly different to that of colonic cancer.
  • This reflects the rectum’s anatomical location and the challenges posed as a result.
  • Tumours located in the rectum can be surgically resected with either an anterior resection or an abdomino-perineal excision of rectum (APER).
  • The technical aspects governing the choice between these two procedures can be complex to appreciate and the main point to appreciate for the exam is that involvement of the sphincter complex or very low tumours require APER.
203
Q

What is ABC in the context of irritable bowel syndrome?

A
  • Diagnosis should be considered if the patient has had the following for at least 6 months:
  • Abdominal pain, and/or
  • Bloating, and/or
  • Change in bowel habit
204
Q

How can diagnosis of IBS be confirmed?

A
  • Diagnosis should be confirmed if the patient has abdominal pain relieved by defaecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms:
  • Altered stool passage (straining, urgency, incomplete evacuation)
  • Abdominal bloating (more common in women than men), distention, tension or hardness
  • Symptoms made worse by eating
  • Passage of mucus
205
Q

What are the primary care investigations for IBS?

A
  • Primary care investigations
  • FBC
  • ESR/CRP
  • Coeliac disease screen (tissue transglutaminase antibodies)
206
Q

What are the red flag symptoms to ask about in anyone with features of IBS?

A
  • Red flag features should be enquired about:
  • Rectal bleeding
  • Unexplained/unintentional weight loss
  • Family history or bowel or ovarian cancer
  • Onset after 60 years of age
207
Q

What is the dietary advice for people with IBS?

A
  • Dietary advice
  • Have regular meals, take time to eat
  • Avoid missing meals or long gaps between eating
  • Drink at least 8 cups of fluid per day – water and non-caffeinated drinks
  • Restrict to 3 cups tea/coffee per day
  • Reduce fizzy drinks
  • Reduce intake of high fibre food and resistant starch
  • Limit to 3 portions of fresh fruit per day
  • For wind and bloating increase intake of oats e.g. porridge and linseeds
208
Q

What is the first line treatment offered to people with IBS?

A
  • First line pharmacological treatment according to symptoms:
  • Pain – antispasmodic agents
  • Constipation – laxatives but avoid lactulose
  • Diarrhoea – loperamide is first line
  • Patients with constipation not responding to conventional laxatives linaclotide may be considered, if:
  • Optimal or maximum tolerated doses of previous laxatives from different classes have not helped
  • Constipation for at least 12 months
209
Q

What is the second line treatment for people with IBS?

A
  • Second line pharmacological treatment
  • Low dose TCA’s e.g. amitriptyline 5-10mg are used in preference to SSRI’s
    Consider CBT referral if not responding to pharmacological treatments after 12 months
210
Q

What are the features of a rectal prolapse?

A
  • Associated with childbirth and rectal intussceception.
  • May be internal or external
  • Associated with CF – due to bulky stools
211
Q

What are the management options for rectal prolapse?

A
  • Conservative - monitor

* Surgical – rectopexy

212
Q

What are haemorrhoids?

A
  • Painless rectal bleeding is the most common symptom
  • Pruritus
  • Pain: usually not significant unless piles are thrombosed
  • Soiling may occur with 3rd or 4th degree piles
213
Q

What types of haemorrhoids are there?

A
  • Internal
    Originate below the dentate line
    Prone to thrombosis, may be painful
  • External
    Above dentate line
    Do not cause pain
214
Q

What are the management options for haemorrhoids?

A
  • Soften stools – increase dietary fibre and fluid intake
  • Topical local anaesthetics and steroids for symptomatic relief
  • Rubber band ligation – superior to injection scleropathy
  • Surgery reserved for large symptomatic haemorrhoids not responding to outpatient treatment
  • Newer treatments include: Doppler guided haemorrhoid artery ligation, stapled haemorrhoidopexy
215
Q

What is a peri-anal abscess?

A
  • Collection of pus within the subcutaneous tissue of the anus that has tracked from the tissue surrounding the anal sphincter
216
Q

Which bacteria are involved in peri-anal abscess?

A
  • E.Coli

* Staph aureus

217
Q

What imaging can be done for a peri-anal abscess?

A
  • MRI or trans-perineal USS

* MRI gold standard but not commonly used unless IBD or complicated

218
Q

How is a peri-anal abscess treated?

A
  • Usually managed with incision and drainage
  • Left open or packed for 3-4 weeks
  • Antibiotics if there is systemic upset
219
Q

What are the causes of a peri-anal fissure?

A
  • Constipation
  • IBD esp. Crohn’s
  • STI’s
220
Q

What are the features of a peri-anal fissure?

A
  • Painful, bright red bleeding

* 90% occur posterior midline

221
Q

How should a peri-anal fissure be managed?

A

<6 weeks = acute
++fibre and ++fluid intake
Bulk forming laxatives – Fybogel
Analgesia

> 6 weeks = chronic
Continue with above measures
Topical GTN is first line
If not effective after 8 weeks – surgical sphinctorectomy or botulinum toxin

222
Q

What is a volvulous?

A
  • Volvulus may be defined as torsion of the colon around it’s mesenteric axis resulting in compromised blood flow and closed loop obstruction
223
Q

What is a sigmoid volvulous?

A
  • Sigmoid volvulus (around 80% of cases) describes large bowel obstruction caused by the sigmoid colon twisting on the sigmoid mesocolon
224
Q

What is associated with sigmoid volvulous?

A
  • Older patients
  • Chronic constipation
  • Chagas disease
  • Neurological conditions e.g. Parkinson’s disease, Duchenne muscular dystrophy
  • Psychiatric conditions e.g. schizophrenia
225
Q

What are the presenting features of sigmoid volvulous?

A
  • Constipation
  • Abdominal bloating
  • Abdominal pain
  • Nausea/vomiting
226
Q

How is a diagnosis of sigmoid volvulous made?

A
  • Usually diagnosed on the abdominal film
    sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign
  • Caecal volvulus: small bowel obstruction may be seen
227
Q

What is the management of volvulous?

A
  • Sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion
  • Caecal volvulus: management is usually operative. Right hemicolectomy is often needed
228
Q

What is the appearance of the sigmoid volvulous on abdominal x-ray?

A
  • Coffee bean sign
229
Q

What is achalasia?

A
  • Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated.
  • Achalasia typically presents in middle-age and is equally common in men and women
230
Q

What are the clinical features of achalasia?

A
  • Dysphagia to both liquids and solids
  • Typically variation in severity of symptoms
  • Heart burn
  • Regurgitation of food – cough, aspiration pneumonia
  • Malignant change in small number of patients
231
Q

What are the investigations for achalasia?

A
  • Oesophageal manometry – excessive LOS tone which doesn’t relax on swallowing, considered most important test
  • Barium swallow – shows grossly expanded fluid level, bird’s beak appearance
232
Q

What is the management of achalasia?

A
  • Balloon dilation 1st line – better recovery, lower risk than surgery
  • Surgery – Heller cardiomyotomy if persistent or recurrent symptoms
  • Intra-sphincteric injection for high risk patients with botulinum toxin
  • Calcium channel blockers or nitrates have a role but limited by side effects
233
Q

What is dyspepsia?

A
  • The term ‘dyspepsia’ is used to describe a complex of upper gastrointestinal tract symptoms which are typically present for four or more weeks, including upper abdominal pain or discomfort, heartburn, acid reflux, nausea and/or vomiting
234
Q

What are the causes of dyspepsia?

A
  • GORD - most common
  • Peptic ulcer disease (gastric or duodenal ulcers)
  • Functional dyspepsia (non-ulcer dyspepsia)

Other causes include:

  • Barrett’s oesophagus
  • Upper GI malignancy
235
Q

How common is dyspepsia?

A
  • Symptoms can occur in about 40% of the population each year
  • 5% of the population are referred to the GP each year
236
Q

What is the urgent management for patients who are experiencing associated symptoms of dyspepsia?

A
  • All patients with the following:
  • Dysphagia
  • Upper abdominal mass consistent with stomach cancer
  • Patients aged >= 55 years with weight loss AND any of the following:
  • Upper abdominal pain
  • Reflux
  • Dyspepsia

Should have an urgent (within 2 weeks) endoscopy

237
Q

What is the non-urgent management for patients who are experiencing associated symptoms of dyspepsia?

A
  • Patients with haematemesis
  • Patients aged >=55 years who have got:
  • Treatment resistant dyspepsia or
  • Upper abdominal pain with low haemoglobin levels or
  • Raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
  • Nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

Should have a non-urgent (within 6 weeks ??) endoscopy

238
Q

How should patients with dyspepsia who do not meet the referral criteria be managed (undiagnosed dyspepsia)?

A
  1. Review medications for possible causes of dyspepsia
  2. Lifestyle advice
  3. Trial of full dose PPI for one month OR test and treat approach for H. Pylori
    - If symptoms persist after either of the above approaches then the alternative approach should be tried
239
Q

How should H. Pylori be tested?

A
  • Initial diagnosis: NICE recommend using a carbon 13 urea breath test or a stool antigen test or laboratory serology where its performance has been locally validated
  • Test of cure - No need to check for H. Pylori eradication if symptoms have resolved following test and treat
  • However if repeat testing is required should use carbon-13 urea breath test
240
Q

What is chronic pancreatitis?

A
  • Inflammatory condition which ultimately can affect both exocrine and endocrine functions of the pancreas
  • Around 80% of cases are due to alcohol excess - 20% of cases unexplained
241
Q

Other than alcohol, what are the causes of chronic pancreatitis?

A
  • Genetic - CF, haemochromatosis

* Ductal obstruction - tumours, stones, structural abnormalities including pancreas divisum and annular pancreas

242
Q

What are the clinical features of chronic pancreatitis?

A
  • Pain - typically worse 15 to 30 minutes following a meal
  • Steatorrhoea - symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
  • DBM - typically occurs more than 20 years after symptoms begin
243
Q

What investigations can be done for chronic pancreatitis?

A
  • Abdominal x-ray shows pancreatic calcification in 30% of cases
  • CT is more sensitive at detecting pancreatic calcification. Sensitivity is 80%, specificity is 85%
  • Functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive
244
Q

What is the management of chronic pancreatitis?

A
  • Conservative - stop drinking alcohol
  • Medical
  • Pancreatic enzyme supplements
  • Analgesia
  • Antioxidants - limited evidence
245
Q

What is a subphrenic abscess?

A
  • Localised collections of pus, usually underneath the right or left hemi-diaphragm
  • Other sites include the lesser sac beneath the liver and the hepato-renal pouch
  • Usually a result of a breach in the integrity of the peritoneum
  • Sub phrenic abscesses are the most common intra-abdominal abscess
246
Q

What is the aetiology of a subphrenic abscess?

A
  • Acute appendicitis
  • Perforated peptic ulcer
  • Perforated GB, producing a right sided subphrenic abscess and biliary surgery
  • Bowel surgery and subsequent peritoneal faecal contamination

Other causes include infection for example haematoma after a splenectomy

247
Q

What is the clinical presentation of a subphrenic abscess?

A
  • One who develops features of toxicity 2 to 21 days after making an initial recovery from an episode of peritonitis or an operation:
  • Swinging fever
  • Malaise, nausea, weight loss
  • Upper abdominal pain that radiates to the shoulder tip
  • SOB due to lower lobe lung collapse or development of a pleural effusion
248
Q

How is subphrenic abscess diagnosed?

A
  • USS or abdominal CT: localises collections of pus
  • WCC often a leucoytosis of around 20,000
  • Chest x-ray
  • High diaphragm on the affected side
  • May be gas and fluid beneath the diaphragm
  • If there is a pleural effusion then this is seen on chest x-ray
249
Q

How is a subphrenic abscess managed?

A
  • Drainage - can use USS or via open operation
  • If the abscess is diagnosed early and has no air or fluid level then this may be treated with broad spectrum antibiotics e.g. gentamicin, benzylpenicillin and metronidazole
  • If symptoms persist for more than 5 days then conservative management should be abandoned and abscess drainage performed
250
Q

What is the most common organism found in a pyogenic liver abscess?

A
  • Staphylococcus aureus in children

* Escherichia coli in adults

251
Q

What is the management of a pyogenic liver abscess?

A
  • Drainage (typically percutaneous) and antibiotics
  • Amoxicillin + ciprofloxacin + metronidazole
  • If penicillin allergic: ciprofloxacin + clindamycin
252
Q

What are the most common primary liver tumours?

A

Most common

  • Cholangiocarcinoma
  • Hepatocellular carcinoma

Others

  • Hepatoblastoma
  • Sarcomas (rare)
  • Lymphomas
  • Carcinoids (most often secondary)
  • Overall metastatic disease accounts for 95% of all liver malignancies making primary liver tumours comparitively rare
253
Q

What are the features of hepatocellular carcinoma?

A
  • Account for 75% of primary liver tumours
  • Occur on a background of chronic inflammatory activity
  • Most cases arise in cirrhotic livers or those with chronic hepatitis B infection
  • Majority of patients 80% present with existing liver cirrhosis, with a mass discovered on screening USS
254
Q

How is diagnosis of hepatocellular carcinoma made?

A
  • CT/MRI
  • AFP elevated in almost all cases
  • Biopsy should be avoided
  • Cases of doubt CT and AFP measurements are the preferred strategy
255
Q

What is the treatment for hepatocellular carcinoma?

A
  • Staging with liver MRI, chest, abdo, pelvis CT
  • Surgical resection is the mainstay of treatment in operable cases
  • Transplant is a consideration if resection is possible
  • Survival - poor prognosis 15% at 5 years
256
Q

What are the features of cholangiocarcinoma?

A
  • Second most common type of primary liver malignancy
  • Arise in the bile duct - 80% of tumours arise in the extra hepatic biliary tree
  • Most patients present with jaundice at this stage most will have disease that is not resectable
257
Q

What is the main risk factor for cholangiocarcinoma?

A
  • Primary sclerosing cholangitis

* Typhoid and liver flukes are also major risk factors in deprived countries

258
Q

How is cholangiocarcinoma diagnosed?

A
  • Typically an obstructive picture on liver function tests
  • CA 19-9, CEA and CA125 often elevated
  • CT/MRI are the main imaging methods of choice
259
Q

What is the treatment of cholangiocarcinoma?

A
  • Surgical resection offers the best chance of cure
  • Local invasion of peri-hilar tumours is a particular problem and this coupled with lobar atrophy will often contra indicate surgical resection
  • Palliation of jaundice is important, although metallic stents should be avoided in those considered for resection
260
Q

What is the prognosis for cholangiocarcinoma?

A
  • Poor - 5-10% 5 year survival
261
Q

What is acute liver failure?

A
  • Rapid onset of hepatocellular dysfuntion leading to a variety of systemic complications
262
Q

What are the causes of acute liver failure?

A
  • Paracetamol overdose
  • Alcohol
  • Viral hepatitis (A or B)
  • Acute fatty liver of pregnancy
263
Q

What are the clinical features of acute liver failure?

A
  • Jaundice
  • Coagulopathy - raised prothrombin time
  • Hypoalbuminaemia
  • Hepatic encephalopathy
  • Renal encephalopathy
  • Renal failure is common (hepato-renal syndrome)
264
Q

What is important to be aware of when assessing synthetic function of the liver?

A
  • LFT’s do not always accurately reflect the synthetic function of the liver
  • Best assessed by looking at the prothrombin time and albumin level
265
Q

What is hepatic encephalopathy?

A
  • Excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut
  • Often associated with acute liver failure, may also be associated with chronic disease
  • Has also been associated with transjugular intrahepatic portosystemic shunting (TIPPS)
266
Q

What are the clinical features of hepatic encephalopathy?

A
  • Confusion, altered GCS
  • Asterix: liver flap, arrhythmic negative myoclonus with a frequency of 3-5 Hz
  • Constructional apraxia - inability to draw a 5 pointed star
  • Triphasic slow waves on EEG
  • Raised amonia level
267
Q

What is the grading system for hepatic encephalopathy?

A

West-Haven Criteria

  • Grade I - irritability
  • Grade II - confusion, inappropriate behaviour
  • Grade III - incoherent, restless
  • Grade IV - coma
268
Q

What are the precipitating factors for hepatic encephalopathy?

A
  • Infection e.g. spontaneous bacterial peritonitis
  • GI bleed
  • Post TIPPS
  • Constipation
  • Drugs: sedatives, diuretics
  • Hypokalaemia
  • Renal failure
  • Increased dietary protein
269
Q

What is the approach to the management of hepatic encephalopathy?

A
  • Treat any underlying precipitant cause
  • NICE recommend lactulose first line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
  • Lactulose - promotes excretion of ammonia and increasing metabolism of ammonia by gut bacteria
  • Anti-biotics such as rifiximin are thought to modulate gut flora resulting in decreased ammonia production
  • Other options include embolisation of portosystemic shunts and liver transplant in selected patients
270
Q

What is hepato-renal syndrome?

A
  • Most accepted theory is that vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance - results in under filling of the kidneys
  • This is sensed by the juxtaglomerular apparatus which then activates the RAAS system, causing renal vasoconstriction which is not enough to counter balance the effects of the splanchnic vasodilation
271
Q

How is HRS categorised?

A
  • Type 1 HRS
  • Rapidly progressive
  • Doubling of serum creatinine to >221mmol/L or a halfing of creatinine clearance to less than 20ml/min over a period of <2 weeks
  • Very poor prognosis
  • Type 2 HRS
  • Slowly progressive
  • Poor prognosis, but patients may live for longer
272
Q

What is the management of HRS?

A
  • Vasopressin analogues - terlipressin to cause vasocontriction of the splanchnic circulation
  • Volume expansion with 20% albumin
  • TIPPS
273
Q

What types of polyposis are there?

A
  • Familial adenomatous polyposis
  • MYH associated polyposis
  • Peutz-Jeghers syndrome
  • Cowden disease
  • HNPCC (Lynch syndrome)
274
Q

What are the features of FAP?

A
  • Mutation of APC gene
  • 80% cases dominant
  • Typically over 100 colonic adenomas
  • Cancer risk of 100%
  • 20% are new mutations
275
Q

What is the management of FAP?

A
  • Annual flexible sigmoidoscopy (if known)

* Polyps found = resectional surgery and pouch vs sub total colectomy

276
Q

What are the features of MYH associated polyposis?

A
  • Biallelic mutation of mut Y human homolgue on chromosome 1p, recessive
  • Multiple polyps, right side more common than in FAP
  • 100% cancer risk by age 60
277
Q

What is the management of MYH polyposis?

A
  • Once identified, resection and ileoanal pouch reconstruction is recommended
  • Regular colonoscopy
  • Associated with increased risk of breast cancer
278
Q

What are the features of Peutz-Jeghers syndrome?

A
  • STK11 (LKB1) mutation on chromosome 19
  • Multiple benign intestinal hamartomas
  • Episodic obstruction and intussusception
  • Increased risk of GI cancers (colorectal and gastric)
279
Q

What is the management of Peutz-Jeghers sydrome?

A
  • Annual examination
  • Pan-intestinal endoscopy every 2-3 years

Associations
* Malignancies at other sites - classical pigmentation pattern

280
Q

What are the features of Cowden disease?

A
  • Mutation of PTEN gene on chromosome 10q22, dominant
  • Macrocephaly
  • Multiple intestinal harmartomas
  • Multiple trichilemmomas
  • 89% risk of cancer at any site
  • 16% risk colorectal cancer
281
Q

What is the approach to management of Cowden disease?

A
  • Targeted individualised screening

Associations

  • Breast cancer risk (81%)
  • Thyroid cancer and non-toxic goitre
  • Uterine cancer
282
Q

What are the clinical features of HNPCC (Lynch syndrome)?

A
  • Germline mutations of DNA mismatch repair genes
  • Colo rectal cancer 30-70%
  • Enometrial cancer 30-70%
  • Gastric cancer 5-10%
  • Scanty colonic polyps may be present
  • Colonic tumours likely to be right sided and mucinous
283
Q

What is the approach to management of HNPCC (Lynch syndrome)?

A
  • Colonoscopy every 1-2 years from age 25
  • Consideration of prophylactic surgery
  • Extra colonic surveillance recommended due to increased risk of developing
284
Q

What are the features of an epigastric hernia?

A
  • Lump in the midline between umbilicus and the xiphisternum
  • Most common in men aged 20-30 years
  • Through the fibres of the linea alba
  • RF’s – raised intra-abdominal pressure, pregnancy, ascites
285
Q

What are the features of anal carcinoma?

A 
* Relatively rare 1.5/100,000
Older age 85-89 yrs average
Risk factors
-	HPV 16&18 – MSM
-	HIV +ve with immunosuppressive medication
-	Smoking
Features, subacute onset of:
-	Peri-anal pain and bleeding
-	Palpable lesion
-	Faecal incontinence
286
Q

What is a peri-anal haematoma?

A
  • Wrongly called a thrombosed or external pile
  • Collection of blood within the skin around the anus usually caused by minor trauma
  • Typical history is of a moderate sized swelling at the anal verge which is tense and intensely painful
287
Q

What is the management of a peri-anal haematoma?

A
  • Conservative
  • Leave alone and will resolve by itself in a couple of weeks but pain and swelling through this time, stool softeners and analgesia
  • Surgical
  • Local anaesthetic surgical excision, wound is left open to allow drainage
288
Q

What is a fistula-in-ano?

A
  • Usually due to previous ano-rectal abscess

Intersphincteric, transphincteric, suprasphincteric and extra-sphincteric

289
Q

What is the imaging used for fistula in ano?

A

Imaging
Fistulography – if extrasphincteric fistula suspected
Endoanal USS – determine complexity of the fistula
MRI – gold standard for fistula-in-ano imaging

290
Q

What is the management of fistula in ano?

A
  • Fistulotomy - setons, fibrin glue, anal fistula plug
291
Q

What is re-feeding syndrome?

A

Describes the metabolic abnormalities which occur on feeding a person following a period of starvation. Occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. Metabolic consequences include:
- Hypophosphataemia
- Hypokalaemia
- Hypomagnesaemia – can lead to torsades de points
- Abnormal fluid balance
Overall can lead to organ failure.

292
Q

What are the potential causes of hypophosphataemia?

A
  • Alcohol excess
  • Acute liver failure
  • DKA
  • Refeeding syndrome!
  • Primary hyperparathyroidism
  • Osteomalacia
293
Q

What are the consequences of hypophosphataemia?

A
  • RBC haemolysis
  • WC and platelet dysfunction
  • Muscle weakness and rhabdomyolysis
  • CNS dysfunction
294
Q

How is risk of re-feeding syndrome assessed?

A

In order to reduce the risk, patients at risk of refeeding syndrome may be identified by the following:

High risk if one or more:
- BMI <16 kg/m2
- Unintentional weight loss >15% over 3-6 months
- Little nutritional intake >10 days
- Hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
If two or more of the following:
- BMI <18.5 kg/m2
- Unintentional weight loss >10% over 3-6 months
- Little nutritional intake >5 days
- History of alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

295
Q

What is the management of re-feeding syndrome?

A
  • NICE recommend that if a patient hasn’t eaten for >5 days, aim to re-feed at no more than 50% of requirements for the first 2 days
  • Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
  • Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and supplements
  • Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)

Y5 Gastrointestinal System (4 decks)

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