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GI COPY Flashcards

1
Q

What is a bowel/intestinal obstruction? What are the three key types? Of these three types, which is the most common? How serious are they?

A
  • A bowel obstruction is an arrest of the onward propulsion of intestinal contents. 3 types:
  • Small bowel obstruction
  • Large bowl obstruction
  • Pseudo-obstruction
  • Small bowel obstructions are the most common (60-75%)
  • All intestinal obstuctions can be serious and potentially fatal
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2
Q

What are the three big causes (90% of cases) of intestinal obstruction?

A
  • Adhesions (small bowel)
  • Hernias (small bowel)
  • Malignancy (large bowel)
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3
Q

Describe the aetiology of small bowel obstruction. What are these due to?

A
  • ADHESIONS (~60%) - usually due to previous abdo/pelvic surgery, but can be caused by previous abdo infections, e.g. peritonitis
  • Hernias - due to intestinal contents being unable to pass through a strangulated loop
  • Malignancy
  • Crohn’s disease
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4
Q

Describe the pathophysiology of small bowel obstruction.

A
  • Obstruction of the bowel leads to distension above the blockage due to a build up of fluid & contents
  • This causes increased pressure which pushes on the blood vessels within the bowel wall causing them to become compressed
  • These compressed vessels cannot therefore supply blood resulting in ischaemia & necrosis, and eventually perforation
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5
Q

What is the clinical presentation of small bowel obstruction?

A
  • Pain - INITIALLY COLICKY BUT THEN DIFFUSE. Pain is higher in the abdomen than LBO
  • Profuse vomiting following pain. Vomiting OCCURS EARLIER IN SBO THAN LBO
  • Abdominal distension - but less than LBO
  • INCREASED BOWEL SOUNDS (TINKLING from AIR/FLUID)
  • Tenderness - suggests strangulation/risk of perforation
  • Constipation with no passage of gas occurs late in SBO
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6
Q

What are the investigations for small bowel obstruction? What is diagnostic?

A
  • ALL bowel obstructions are are diagnosed first by abdo X-ray and then by a confirmatory CT scan
  • Abdominal X-ray (1st line):
  • Key finding = DISTENDED LOOPS OF BOWEL proximal to obstruction
  • Shows central gas shadows that completely cross the lumen
  • Non-contrast CT = Gold standard. Accurately localises the obstruction
  • Examination of hernia orifices and rectum
  • FBC
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7
Q

Describe the management for small bowel obstruction.

A
  • DECOMPRESSION OF THE BOWEL:
  • ‘Drip and suck’ - Nil by mouth and IV fluids with Nasogastric (NG) tube. If this fails, then surgery
  • Aggressive fluid resuscitation
  • Analgesia & anti-emetics for symptoms
  • Antibiotics
  • Surgery to remove obstruction - usually laparotomy (open)
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8
Q

Why are large bowel obstructions less common than small bowel obstructions?

A

Because the lumen is much larger and can distend more, therefore is harder to block

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9
Q

What is the aetiology of large bowel obstruction?

A
  • MALIGNANCY (90%). More common in the EU/West than Africa
  • VOLVULUS = rotation/twisting of the bowel on its mesenteric axis. Sigmoid colon is the most common place for this to occur as it has a mesentery
  • Diverticulitis
  • Crohn’s disease
  • Intussusception = when the bowel rolls inside of itself. Almost exclusively in neonates/infants as they have ‘softer’ bowels
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10
Q

Describe how Crohn’s disease can cause intestinal obstruction.

A

Crohn’s disease -> fibrosis -> contraction -> obstruction

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11
Q

Describe how Diverticular disease can cause intestinal obstruction.

A

Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction

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12
Q

What is the clinical presentation of large bowel obstruction?

A
  • Abdominal pain = MORE CONSTANT AND DIFFUSE THAN SBO. Usually occurs lower in abdomen, especially LIF
  • Abdominal distension - MUCH MORE THAN SBO
  • Normal bowel sounds initially, then increased and eventually silent as no movement
  • Palpable mass, e.g hernia. Most common in LIF
  • VOMITING OCCURS MUCH LATER THAN SBO, AND MAY BE ABSENT
  • CONSTIPATION EARLIER THAN IN SBO
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13
Q

What are the investigations for large bowel obstruction? What is diagnostic?

A
  • Abdominal X-ray (1st line):
  • Peripheral gas shadows proximal to blockage, but doesn’t show rectum hence why DRE is essential. Caecum and ascending colon will be distended
  • CT = gold standard
  • Digital rectal exam (DRE):
  • Empty rectum
  • Hard, compacted stools
  • Might be blood
  • FBC
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14
Q

What is the management for large bowel obstruction?

A

EXACTLY THE SAME AS SMALL BOWEL OBSTRUCTION:

  • DECOMPRESSION OF THE BOWEL:
  • ‘Drip and suck’ - Nil by mouth and IV fluids with Nasogastric (NG) tube. If this fails, then surgery
  • Aggressive fluid resuscitation
  • Analgesia & anti-emetics for symptoms
  • Antibiotics
  • Surgery to remove obstruction - usually laparotomy (open)
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15
Q

What is pseudo-bowel obstruction?

A

Bowel obstructions that present identically to SBOs or LBOs, dependent on the location (can present as both at the same time if whole bowel is obstructed), although a blockage cannot be found

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16
Q

What is the best way to manage a pseudo-bowel obstruction?

A

Treat the underlying cause

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17
Q

What is oesophageal cancer? What are the two main histological types? Describe these two types.

A
  • Oesophageal cancer = rare malignancy of oesophageal epithelium
  • Two main types:
  • Adenocarcinoma = most common in the developed world. Typically found in the lower 1/3 of the oesophagus. Often caused by Barrett’s oesophagus but smoking is also a risk factor
  • Squamous cell carcinoma = most common in the developing world. Typically found in the upper 2/3 of the oesophagus. Most common risk factors are smoking and alcohol ingestion
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18
Q

What are the risk factors for oesophageal adenocarcinoma?

A
  • Barrett’s oesophagus
  • GORD
  • Smoking
  • Achalasia
  • Obesity
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19
Q

What are the risk factors for oesophageal squamous cell carcinoma?

A
  • Alcohol
  • Smoking
  • Achalasia
  • Obesity
  • Low fruit/veg/fibre/vit A/C
  • Hot drinks
  • Plummer-Vinson syndrome
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20
Q

What is the clinical presentation of oesophageal cancer?

A
  • PROGRESSIVE DYSPHAGIA - solids then liquids
  • Vomiting
  • Anorexia and weight loss
  • Odynophagia, hoarseness, melaena, cough
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21
Q

What are the investigations for oesophageal cancer?

A
  • Upper GI endoscopy and biopsy (1st line)
  • CT scan or endoscopic ultrasound (staging)
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22
Q

Describe the management of oesophageal cancer.

A
  • Medically fit and metastases = surgical resection and then adjuvant chemotherapy
  • Medically unfit and metastases = palliative care. Stents can help with dysphagia
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23
Q

What is gastric/stomach cancer? What are the two histological types?

A
  • Gastric cancer = aggressive adenocarcinoma arising from gastric mucosa
  • Two types:
  • Type 1 (intestinal/differentiated, 70-80%)
  • Type 2 (diffuse/undifferentiated, 20%)
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24
Q

What are the risk factors, histology, appearance and location of type 1 (intestinal/differentiated) gastric cancer?

A
  • Risk factors: male, H.PYLORI, chronic and atrophic gastritis, older age, diet (nitrates and nitrosamines), smoking, alcohol
  • Histology: glandular epithelium
  • Appearance: large, irregular (polyploid/ulcerated with heaped up edges)
  • Location: antrum and lesser curvature
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25
Q

What are the risk factors, histology, appearance and location of type 2 (diffuse/undifferentiated) gastric cancer?

A
  • Risk factors: blood type A, genetic, younger age, diet (nitrates, nitrosamines), smoking, alcohol
  • Histology: poorly differentiated, signet ring cells
  • Appearance: GASTRIC LINITIS. Submucosa invasion. No movement on barium swallow (late sign)
  • Location: anywhere, especially cardia (defective adhesion because of CDH-1 mutation = defective E-cadherin = increased ability to invade and spread
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26
Q

A mutation in what gene can cause familial diffuse gastric cancer? What is performed in this instance?

A

CDH1 - 80% chance of gastric cancer.
Prophylactic gastrectomy is done in these patients

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27
Q

What is the clinical presentation of gastric cancer?

A
  • Often late presentation:
  • Anorexia, nausea, weight loss, anaemia, dysphagia, vomiting
  • Haematemesis
  • Malaena
  • Epigastric pain - better with ant-acids
  • Paraneoplastic syndromes, e.g. polycythaemia
  • Metaplastic signs, e.g. Krukenberg tumour
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28
Q

What are the investigations for gastric cancer? When would the endoscopy be urgent?

A
  • Gastroscopy with biopsy: 8-10 biopsies
  • CT/MRI/PET
  • Endoscopic USS. 2 week wait for endoscopy if upper abdominal mass consistent with stomach cancer and: dysphagia of any age, >55 + weight loss with upper abdominal pain, reflux or dyspepsia. Consider non-urgent endoscopy if haematemesis, treatment resistant dyspepsia, upper abdominal pain + anaemia
  • Laparoscopy final line
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29
Q

What is the management for proximal and distal gastric cancer? What do we have to give to the patient for the rest of their lives after this type of surgery?

A
  • Nutritional support
  • Proximal gastric cancer with no spread: 3 cycles of chemo and then a full gastrectomy. Lymph node removal too
  • Distal gastric cancer with no spread: 3 rounds of chemotherapy and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too
  • Gastrectomy = lack of intrinsic factor = give vitamin B12 to prevent pernicious anaemia
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30
Q

What vitamin supplement will a patient need following gastrectomy?

A

They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia

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31
Q

What is the epidemiology of colorectal cancer? What are the risk factors?

A
  • 3rd most common cancer in Western world, 4th leading cause of cancer deaths in the US
  • Risk factors:
  • Family history of bowel cancer
  • FAMILIAL ADENAMATOUS POLYPOSIS (FAP) (autsomal dominant)
  • HEREDITARY NONPOLYPOSIS COLORECTAL CANCER (HNPCC) - also known as LYNCH SYNDROME
  • IBD (Crohn’s or ulcerative colitis)
  • Increased age
  • Diet (high in red and processed meat and low in fibre)
  • Obesity and sedentary lifestyle
  • Smoking
  • Alcohol
  • Radiotherapy
  • Hormonal factors; nulliparity, late first pregnancy, early menopause
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32
Q

Where do colo-rectal cancers most commonly occur?

A

Rectum (38%) and sigmoid colon (20%)

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33
Q

Give three signs of rectal cancer.

A
  • Change in bowel habit, e.g. more frequent and loose stools
  • Rectal bleeding
  • Unexplained weight loss
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34
Q

Give 4 signs of left-sided colon cancer.

A
  • Change in bowel habit (more loose/frequent stools)
  • Abdominal pain
  • Abdominal mass upon inspection
  • Rectal bleeding
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35
Q

Give 4 signs of right-sided colon cancer.

A
  1. Abdominal pain
  2. Abdominal mass upon inspection
  3. Unexplained weight loss
  4. Change in bowel habit (more frequent and loose stools)
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36
Q

What are the investigations for colo-rectal cancer? What is FIT used for?

A
  • Colonoscopy - gold standard
  • Flexible sigmoidoscopy, barium enema, CT colonography
  • Faecal immunochemical test - look for amount of human haemoglobin in the stool. Used for patients who do not meet the specific criteria for a two week wait referral:
  • >50 with unexplained weight loss and no other symptoms
  • <60 with a change in bowel habit
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37
Q

How do we grade colo-rectal tumours?

A

USED to be Dukes’ classification but has been replaced by TNM staging

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38
Q

Describe Dukes’ classification system.

A
  • Dukes A – confined to mucosa and part of the muscle of the bowel wall
  • Dukes B – extending through the muscle of the bowel wall
  • Dukes C – lymph node involvement
  • Dukes D – metastatic disease
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39
Q

Describe TNM staging.

A
  • T for Tumour:

TX – unable to assess size

T1 – submucosa involvement

T2 – involvement of muscularis propria (muscle layer)

T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa

T4 – spread through the serosa (4a) reaching other tissues or organs (4b)

  • N for Nodes:

NX – unable to assess nodes

N0 – no nodal spread

N1 – spread to 1-3 nodes

N2 – spread to more than 3 nodes

  • M for Metastasis:

M0 – no metastasis

M1 – metastasis

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40
Q

Describe the treatment for colo-rectal cancer.

A
  • Caecal, ascending or proximal transverse colon = right hemicolectomy
  • Distal transverse, descending colon = left hemicolectomy
  • Sigmoid colon = high anterior resection
  • Upper rectum = anterior resection (TME)
  • Low rectum = anterior resection (low TME)
  • Anal verge = abdomino-perineal resection of rectum
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41
Q

Familial adenomatous polyposis (FAP) is a risk factor for colo-rectal cancer. What is FAP? Describe the investigations and management.

A
  • (FAP) = autosomal dominant condition involving malfunctioning of the tumour suppressor genes called adenomatous polyposis coli (APC). It results in many polyps (adenomas) developing along the large intestine. These polyps have the potential to become cancerous (usually before the age of 40)
  • Colonoscopy every 1-2 years, beginning at 10-12 years of age
  • Patients have their entire large intestine removed prophylactically to prevent the development of bowel cancer (panproctocolectomy)
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42
Q

Hereditary nonpolyposis colorectal cancer (HNPCC) is a risk factor for colo-rectal cancer. What is it? Describe its investigations and management.

A
  • HNPCC (a.k.a. Lynch syndrome) is an autosomal dominant condition that results from mutations in DNA mismatch repair (MMR) genes. Patients are at a higher risk of a number of cancers, but particularly colorectal cancer. Unlike FAP, it does not cause adenomas and tumours develop in isolation
  • Colonoscopy every 1-2 years, beginning at 20-25 years of age. After surgery, sigmoidoscopy every 1-2 years if subtotal colectomy was performed, or colonoscopy if segmental resection was performed
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43
Q

What is gastro-oesophageal reflux disease (GORD)? Why is the oesophagus more sensitive to acid than the stomach?

A
  • GORD is where acid from the stomach refluxes through the lower oesophageal sphincter (due to dysfunction) and irritates the lining of the oesophagus
  • The oesophagus has a squamous epithelial lining, whereas the stomach has a columnar epithelial lining, so the oesophagus is more sensitive
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44
Q

What are the risk factors for GORD?

A
  • Lifestyle factors: obesity, smoking, alcoholism, fat rich diet, caffeine
  • Medications, e.g. antihistamines, CCBs, antidepressants - inhibit the strength at which the LOS can contract
  • Hiatus hernia = lowers LOS pressure = increase reflux
  • Pregnancy
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45
Q

What is the clinical presentation of GORD?

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

  • Heartburn (retrosternal chest pain) - related to meals, worse when lying, relieved by antacids
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating
  • Unexplained weight loss, anaemia, dysphagia, upper abdo mass, persistent vomiting (red flags)
  • Nocturnal cough
  • Hoarse voice
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46
Q

What are the investigations for GORD? What are the key red flag features for an urgent referral?

A
  • Clinical diagnosis
  • First line = therapeutic challenge = give PPI = will get better
  • Gold standard = oesophageal manometry = 24hr of pH and pressure montoring
  • X-ray with barium contrasts = shows stenosis and ulcers
  • Endoscopy to assess for peptic ulcers, oesophageal or gastric malignancy. Red flags for urgent referral:
  • DYSPHAGIA (difficulty swallowing)
  • >55
  • Weight loss
  • Epigastric pain / reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin (anaemia)
  • Raised platelets
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47
Q

Describe the management for GORD.

A
  • Conservative:
  • Quit smoking
  • Reduce alcohol
  • Weight loss
  • Avoid heavy meals before bed time and stay upright after meals rather than lying flat
  • Medical:
  • PPIs (first line) and H2 receptor antagonists (second line, e.g. ranitidine) - both decrease acidification of gastric acid secretions
  • Surgical:
  • GOLD STANDARD = Nissen Fundoplication = upper part of stomach wrapped around LOS = strengthens sphincters, prevents acid reflux
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48
Q

What are the complications of GORD?

A
  • Barrett’s oesophagus (pre-malignant condition). This is because the cells try to adapt - stratified squamous to simple columnar
  • Oesophageal adenocarcinoma
  • Oesophagitis
  • Oesophageal strictures
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49
Q

What is Helicobacter pylori? Where does it live? What does it cause?

A
  • H. pylori is a gram negative aerobic bacteria. It lives in the stomach. It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid
  • It also produces ammonia to neutralise the stomach acid, which directly damages the epithelial cells
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50
Q

What are the complications of Helicobacter pylori infection?

A
  • Peptic ulcers
  • Gastric carcinomas
  • Gastritis
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51
Q

What are the investigations for Helicobacter pylori infection?

A
  • Urea breath test using radiolabelled carbon 13
  • Stool antigen test
  • Rapid urease test can be performed during endoscopy. Also known as a CLO test (Campylobacter-like organism test). It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more alkali giving a positive result on when the pH is tested
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52
Q

What is the treatment for a Helicobacter pylori infection?

A
  • TRIPLE THERAPY:
  • Proton pump inhibitor, e.g. omeprazole
  • 2 antibiotics, e.g. amoxicillin and clarithromycin for 7 days
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53
Q

What is Barrett’s oesophagus? What is it caused by? What is it classified as? What is it a risk factor for? What is its pathology?

A
  • Barret’s oesophagus = metaplasia of lower oesophagus epithelium from stratified squamous to simple columnar
  • It is caused by the constant reflux of acid
  • It is classified as a ‘premaligant’ condition. It is a risk factor for adenocarcinoma of the oesophagus
  • Pathology = squamous - metaplasia (goblet cells) - dysplastic (precancer) - neoplastic (cancer)
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54
Q

What are the risk factors for Barrett’s oesophagus?

A
  • GORD
  • Male (7:1)
  • Caucasian
  • FHx
  • Hiatus hernia
  • Obesity
  • Smoking
  • Alcohol
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55
Q

What is the clinical presentation of Barrett’s oesophagus?

A

CLASSIC HISTORY - middle aged caucasian male with a long history of GORD and dysphagia

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56
Q

What are the investigations for Barrett’s oesophagus?

A
  1. Upper GI endoscopy (oesophago-gastro-duodenoscopy)
  2. Biopsy
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57
Q

What is the management for Barrett’s oesophagus?

A
  1. Lifestyle: weight loss, smoking cessation, reduce alcohol, small meals, avoid hot drinks/alcohol/eating <3 hrs before bed, avoid certain drugs (nitrates, anticholinergics, TCAs, NSAIDs, K+ salts, alendronate)
  2. Endoscopic Surveillance with Biopsies
  3. High dose PPI if non-dysplastic
  4. Low grade dysplasia - radiotherapy with endoscopic mucosal resection
  5. Severe (high grade dysplasia): radiotherapy with oesophagectomy
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58
Q

What are oesophageal varices? What are their potential complications?

A
  • Dilated veins at sites of portosystemic anastomosis (left gastric + inferior oesophageal veins)
  • As these vessels are thin and not meant to transport higher pressure blood, they can easily RUPTURE = haematemesis OR rupture = blood digested = malaena
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59
Q

What are the prehepatic, hepatic and post-hepatic causes of oesophageal varices?

A
  • Pre-hepatic = portal vein thrombosis/obstruction
  • Hepatic = cirrhosis, schistosomiasis
  • Post-hepatic = Budd-Chiari, RHF, constrictive pericarditis, compression
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60
Q

What is the clinical presentation of oesophageal varices?

A
  • Haematemesis and/or melena
  • Epigastric discomfort
  • Sudden collapse - Sx haemodynamic instability
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61
Q

What are the investigations for oesophageal varices?

A

1ST LINE/GOLD STANDARD: upper GI endoscopy

  • FBC, U+E, clotting (INR), LFTs
  • CXR/ascitic tap/further Ix for PHT
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62
Q

How do we treat oesophageal varices?

A
  • GOLD STANDARD - ENDOSCOPIC THERAPY: BAND LIGATION OR SCLEROTHERAPY
  • Small oesophageal varices = watch and wait
  • ABCDE
  • Medical for medium to large = beta blocker to reduce CO -> reduce portal pressure and band ligation
  • Acute bleeding = ROCKALL SCORE (predicition of re-bleeding and mortality)
  • Nitrate to reduce portal pressure
  • Terlipressin – analogue of ADH -> reduce portal pressure
  • Surgical:
  • Band ligation
  • Transjugular intrahepatic portosystemic shunt (TIPSS)
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63
Q

What is a Mallory-Weiss tear? What is it pathophysiology?

A
  • Haematemesis from tear in oesophageal mucosa
  • Pathophysiology: severe vomiting = sudden increase in intra-abdominal pressure = partial laceration at gastro-oesophageal junction = bleeding from mucosa
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64
Q

What are the risk factors for a Mallory-Weiss tear?

A
  • Alcoholism
  • Hypermesis gravidarum
  • Gastroenteritis
  • Bulimia
  • Chronic cough
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65
Q

What is the clinical presentation of a Mallory-Weiss tear?

A
  • Haematemesis
  • Malaena
  • Sx of hypovolaemic shock
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66
Q

What are the investigations for a Mallory-Weiss tear?

A
  • Rockall score (assess blood loss: <3 = low risk)
  • Endoscopy
  • FBC, U+E, coagulation studies, haematocrit
  • ECG + cardiac enzymes
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67
Q

What is the treatment for a Mallory-Weiss tear?

A
  • ABCDE
  • Urgent endoscopy
  • Anti-emetics if N+V persists
  • PPI to suppress acid
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68
Q

What is Boerhaave syndrome? What is it caused by? What are the main symptoms?

A
  • Rupture through the oesophagus
  • Caused by an increased intraoesophageal pressure and a negative intrathoracic pressure
  • Meckler’s triad: vomiting, chest pain and subcutaneous emphysema
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69
Q

What is achalasia? What is its pathophysiology? How is it different to oesophageal carcinomas?

A
  • Rare disorder that makes it difficult for food to pass through oesophagus (LOS won’t relax)
  • Degeneration of ganglion cells = oesophageal smooth muscle fibres fail to relax = oesophageal sphincter remains closed/fails to open
  • Will affect solids at the SAME POINT it affects liquids as it is a MOTILITY problem. In carcinomas, it will be PROGRESSIVE DYSPHAGIA (important)
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70
Q

What are the signs and symptoms of achalasia?

A
  • Dysphagia affecting solids and liquids AT THE SAME POINT
  • Heartburn
  • Weight loss
  • Coughing while lying horizontally
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71
Q

What are the investigations for achalasia?

A
  • Barium swallow X-ray and continuous fluoroscopy - normal peristalsis not seen
  • Oesophageal endoscopy with or without endoscopic ultrasound
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72
Q

What is the treatment for achalasia?

A
  • Medications: CCBs for mild to moderate, nitrates effective before dilation occurs, PPIs effective after surgery
  • Gold standard = Laparoscopic Heller myotomy = oesophageal dilation via surgical cleaving of muscle
  • Endoscopic myotomy
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73
Q

What are the three main types of ischaemic bowel disease? What do they affect?

A
  • Ischaemic bowel diseases can be classified into 3 main types:
  • Acute mesenteric ischaemia
  • Chronic mesenteric ischaemia
  • Ischaemic colitis
  • Acute & chronic mesenteric ischaemia almost always affect the small bowel, whereas ischaemic colitis affects the large bowel
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74
Q

Where does the bowel get the majority of its blood supply from? Which areas are most susceptible to ischaemia?

A
  • The bowel mostly gets its blood supply from the superior & inferior mesenteric arteries
  • “Watershed areas” like the splenic flexure + caecum are the most susceptible to ischaemia
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75
Q

What is mesenteric ischaemia? What is its aetiology?

A
  • Mesenteric ischemia occurs when narrowed or blocked arteries restrict blood flow to your small intestine
  • Aetiology:
  • Superior mesenteric artery (SMA) THROMBOSIS
  • SMA EMBOLISM (DUE TO AF)
  • Mesenteric vein thrombosis - typically young patients who are in hypercoaguable states
  • Non-occlusive disease, e.g. poor blood flow, poor cardiac output
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76
Q

What is the clinical presentation of mesenteric ischaemia?

A
  • Classical triad:
  • Acute, severe abdo pain - usually constant & central
  • No abdo signs on exam
  • Rapid hypovolaemia > shock
  • The symptoms are often way out of proportion with clinical signs
  • IF YOU SEE AF WITH SEVERE ABDOMINAL PAIN, THINK AMI
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77
Q

What is the difference between chronic mesenteric ischaemia and AMI in terms of presentation? What is chronic mesenteric ischaemia described as?

A

Chronic mesenteric ischaemia is very similar to AMI, except the symptoms are on a lower level & persist for much longer. It is described as “abdominal angina”

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78
Q

What are the investigations for mesenteric ischaemia?

A
  • Bloods = ^^Hb due to blood loss and persistent metabolic acidosis due to ischaemia
  • ABDOMINAL X-RAY = used to rule out bowel obstruction
  • Laparoscopy = used to visualise the necrosis
  • CT/MRI ANGIOGRAPHY = non-invasive way to look at arteries to see blockages, but is a difficult scan to perform
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79
Q

Describe the management of mesenteric ischaemia.

A
  • FLUID RESUSCITATION
  • Antibiotics - Metronidazole, Gentamicin
  • IV HEPARIN TO REDUCE CLOTTING
  • Surgery to remove necrotic bowel
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80
Q

What are the complications of mesenteric ischaemia?

A
  • Sepsis
  • Peritonitis
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81
Q

What is ischaemic colitis? What is its aetiology?

A
  • Ischaemic colitis = inflammation of the large intestine resulting from a lack of blood flow
  • Aetiology:
  • Thrombosis
  • Emboli
  • Low flow states
  • Low cardiac output/arrhythmias
  • Surgery
  • Vasculitis
  • Coagulation disorders
  • Oral contraceptive pill
  • Idiopathic
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82
Q

What is the clinical presentation of ischaemic colitis?

A
  • SUDDEN ONSET LIF PAIN
  • Passage of bright red blood
  • SIGNS OF HYPOVOLAEMIC SHOCK
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83
Q

What are the investigations for ischaemic colitis?

A
  • Urgent CT to rule out perforation
  • Flexible sigmoidoscopy w/ biopsy - will show epithelial cell apoptosis
  • Colonoscopy w/ biopsy = Gold standard = only done AFTER patient has fully recovered to exclude the formation of a strictures at the site and to confirm mucosal healing
  • Barium enema
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84
Q

Describe the management for ischaemic colitis.

A
  • Most patients will be fine with only symptomatic treatment
  • Fluid replacement
  • Antibiotics = reduce infection risks due to translocation of bacteria across the drying bowel wall
  • Strictures at the disease site are common
  • Gangrenous ischaemic colitis = peritonitis & hypovolaemic shock, will require surgical intervention
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85
Q

What is Coeliac’s disease? What is it an intolerance to? What does it cause?

A
  • Inflammation of the mucosa of the upper small bowel in response to GLUTEN (general name for proteins found in wheat)
  • AUTOIMMUNE - T cell mediated
  • Intolerance to PROLAMIN (in wheat, barley, rye, oats) - component of gluten protein
  • Causes VILLOUS ATROPHY, which leads to MALABSORPTION
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86
Q

What is the epidemiology of Coeliac’s disease?

A
  • 1% of the UK population (yet only 25% diagnosed)
  • Males and females equally
  • Any age, peaks in infancy and 40-60 years
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87
Q

What are the risk factors for Coeliac’s disease?

A
  • FAMILY history - 10% risk in 1st degree relatives
  • HLA associated - HLA-DQ2 and HLA-DQ8
  • Other AUTOIMMUNE diseases, e.g T1DM
  • IgA deficiency
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88
Q

What is the pathophysiology of Coeliac’s disease?

A
  • ALPHA-GLIADIN is resistant to digestion from protease enzymes (pepsin & chymotrypsin) in small intestine lumen
  • Passes through damaged epithelial wall, into cells
  • Deaminated by tissue TRANSGLUTAMINASE
  • Interacts with antigen-presenting cells via HLA-DQ2 or HLA-DQ8
  • These activate gluten-sensitive CD4+ T-CELLS
  • T-cells produce pro-inflammatory cytokines -> inflammatory cascade
  • Causes VILLOUS ATROPY and CRYPT HYPERPLASIA
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89
Q

What does villous atrophy lead to?

A

Villous atrophy leads to MALABSORPTION

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90
Q

What is the clinical presentation of Coeliac’s disease?

A
  • Steatorrhoea + stinking stools - inability to properly absorb fat from diet
  • Anaemia - due to inability to absorb B12, folate, iron
  • Weight loss, fatigue & weakness, diarrhoea, abdominal pain, bloating, N+V
  • Aphthous ulcers
  • Angular stomatitis
  • Osteomalacia - decreased absorption of Vitamin D
  • Failure to thrive (children)
  • Dermatitis herpetiformis:
  • Raised red patched of skin
  • B​listers, burst with scratching
  • Elbows, knees, buttocks, torso, scalp
  • Deposition of IgA in skin
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91
Q

What are the complications of Coeliac’s disease?

A
  • Most patients who follow a strict diet recover, but a few are non-responsive
  • ANAEMIA
  • Osteoporosis
  • Hyposplenism
  • Neuropathies
  • Increased risk of MALIGNANCY:
  • T-cell lymphoma = increased T-cells in GI wall
  • Gastric, oesophageal, small bowel, colorectal cancer = increased cell turnover
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92
Q

What are the investigations for Coeliac’s disease?

A
  • Serum antibody testing = FIRST LINE:
  • IgA TISSUE TRANSGLUTAMINASE (tTG) (can also test for IgA anti-endomysial antibody (EMA) = less sensitive)
  • Very high sensitivity & specificity, false negatives in IgA deficiency, offered to people with other autoimmune diseases
  • Positive/negative with high index of suspicion = biopsy
  • Duodenal BIOPSY = GOLD STANDARD:
  • Endoscopically, required for definite diagnosis
  • Postive findings: villous atrophy, crypt hyperplasia, increased epithelial WBCs
  • FBC: low Hb, low folate, low ferritin, low B12, ~50% have mild anaemia
  • Genetic testing: HLA-DQ2 and HLA-DQ8 genotyping
  • DEXA scan - because of the increased risk of osteoporosis
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93
Q

What is the management for Coeliac’s disease? What is the main reason for recurrence?

A
  • Lifelong GLUTEN-FREE DIET:
  • Avoid foods containing wheat, barley, rye, oats
  • GLUTEN-FREE FOOD are now more available
  • Poor compliance is the main reason for recurrence
  • Symptoms and serology used to monitor response and compliance
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94
Q

What is inflammatory bowel disease? What are the two major forms? What is the general pathophysiology? Which group are the most affected?

A
  • Inflammatory bowel disease = a term used to mainly describe two CHRONIC and AUTOIMMUNE conditions:
  • ULCERATIVE COLITIS
  • CROHN’S DISEASE
  • Mucosal immune system responds inappropriately to luminal antigens, e.g. bacteria when they enter mucosa via leaky epithelium
  • Jewish people are the most affected group
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95
Q

What is ulcerative colitis? Describe it on a macroscopic and a microscopic level.

A
  • Ulcerative colitis = inflammation of colon, ulcers are present
  • MACROSCOPIC:
  • ONLY COLON affected
  • STARTS AT RECTUM, can progress as far as ileocaecal valve
  • CIRCUMFERENTIAL AND CONTINUOUS inflammation – no skip lesions
  • ULCERS + PSEUDO-POLYPS in severe disease
  • MICROSCOPIC:
  • MUCOSA ONLY inflamed - no deeper (not transmural)
  • CRYPT ABCESSES
  • Depleted goblet cells
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96
Q

What is the cause of ulcerative colitis? What are the risk factors?

A
  • Cause: “Inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
  • Risk factors:
  • Family history
  • NSAIDS
  • Chronic stress + depression
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97
Q

What is the epidemiology of ulcerative colitis?

A
  • Highest prevalence in northern Europe & North America
  • Affects males + females equally
  • Presentation mostly at 20-40 YEARS
  • Higher incidence than Crohn’s
  • SMOKING IS A PROTECTIVE FACTOR against UC
  • Incidence is 3x higher in non-smokers
  • Symptoms may relapse on stopping smoking
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98
Q

What are the symptoms of ulcerative colitis?

A
  • Remissions + exacerbations
  • Abdo pain – lower left quadrant
  • Abdo cramps/discomfort
  • Episodic or chronic diarrhoea: blood and mucus, urgency, frequency relates to severity, night & day in severe attacks
  • Systemic symptoms in attacks: fever, anorexia, malaise, weight loss
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99
Q

What are the signs of ulcerative colitis?

A
  • Might be no signs
  • Acute, severe UC = fever, tachycardia, tender, distended abdomen
  • Extraintestinal signs = clubbing, oral aphthous ulcers, nutritional deficits
  • Extraintestinal complications
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100
Q

What are the complications of ulcerative colitis in the colon, skin, joints, eyes, and liver?

A
  • Colon: blood loss, perforation, toxic dilatation, colorectal cancer
  • Skin: erythema nodosum (tender red bumps, symmetrically on shins), pyoderma gangrenosum (painful ulcers on skin)
  • Joints: ankylosing spondylitis, arthritis (HLA-B27 associated)
  • Eyes: iritis, uveitis, episcleritis
  • Liver: fatty change, chronic pericholangitis, sclerosing cholangitis
  • Venous thromboembolism
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101
Q

What are the investigations for ulcerative colitis?

A
  • Blood tests: raised WCC, raised platelets, raised CRP + ESR
  • Anaemia: normocytic of chronic disease most likely
  • pANCA may be POSITIVE (it’s negative in Crohn’s)
  • Liver biochemistry may be abnormal
  • Hypoalbuminaemia - in severe disease
  • COLONOSCOPY - BIOPSY = GOLD STANDARD. Sigmoidoscopy - diagnosis, full colonoscopy - to define extent, once controlled
  • Stool samples = to exclude C.diff, Campylobacter + others
  • Faecal calprotectin - indicates IBD if raised, doesn’t differentiate UC and Crohn’s
  • Abdominal X-ray = to exclude colonic dilatation. Also useful when UC is too severe for colonoscopy
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102
Q

Describe the management for ulcerative colitis.

A
  • Aiming to induce REMISSION

SULFASALAZINE, mesalazine, olsalazine (all used in mild to moderate cases). Oral – FIRST LINE for left sided/extensive. Rectal (suppository) – for proctitis (inflammation of rectal lining)

  • Mild/moderate: ORAL PREDNISOLONE (glucocorticoid steroid). SECOND LINE – if they don’t respond to a 5-ASA. Also used in severe cases
  • Severe with systemic features: IV Hydrocortisone, ciclosporin, infliximab
  • Maintaining remission: 5-ASA or azathioprine if still relapsing on 5-ASA
  • SEVERE cases with NO RESPONSE to treatment = surgery:
  • Colectomy:
  • Whole colon removed
  • Ileoanal anastomosis OR ileostomy -> stoma
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103
Q

What is Crohn’s disease? Describe its macroscopic and microscopic features.

A
  • Crohn’s disease = inflammation in the GI tract
  • MACROSCOPIC:
  • Affects ANY PART of GI tract – MOUTH TO ANUS - especially terminal ileum & proximal colon
  • NON-CONTINUOUS inflammation – SKIP LESIONS
  • Cobblestone appearance – ulcers + fissures in mucosa
  • MICROSCOPIC:
  • TRANSMURAL inflammation – through all layers of bowel wall
  • GRANULOMAS - non-caseating
  • Increased chronic inflammatory cells + lymphoid hyperplasia
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104
Q

What is the cause of Crohn’s disease? What are its risk factors?

A
  • Cause: inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
  • Risk factors:
  • Family history
  • Stronger genetic association than UC
  • Smoking - 2-4x risk
  • NSAIDs - exacerbate it
  • Chronic stress + depression - triggers flares
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105
Q

What is the epidemiology of Crohn’s disease?

A
  • Highest prevalence in northern Europe & north America
  • Affects females more than males
  • Presentation mostly at 20-40 years
  • Lower incidence than UC
106
Q

What are the symptoms of Crohn’s disease in the small bowel and colon?

A
  • Small bowel:
  • ABDOMINAL PAIN
  • WEIGHT LOSS
  • Terminal ileum - RIGHT iliac fossa pain mimicking appendicitis - less common
  • Colon:
  • BLOODY DIARRHOEA = URGENCY
  • PAIN ON DEFECATION
  • Systemic symptoms on attack: fever, anorexia, malaise, fatigue
107
Q

What are the signs of Crohn’s disease?

A
  • Bowel ulceration
  • Abdominal tenderness
  • Abdominal mass
  • Perianal disease
  • Extraintestinal signs:
  • Clubbing
  • ORAL APHTHOUS ULCERS - more common than in UC
  • Skin, joint + eye problems
108
Q

What are the complications of Crohn’s disease?

A
  • Bowel:
  • Malabsorption, either from Crohn’s or following surgery -> malnutrition
  • Small bowel obstruction
  • Toxic dilatation
  • Bowel perforation
  • Abscess formation
  • Fistula formation
  • Sclerosing cholangitis
  • Colorectal cancer
  • Anaemia
  • Iron/folate deficiency
  • Perianal disease: abscesses, fistulae, skin tags, fissures
  • Amyloidosis (systemic) = rare
  • Venous thromboembolism
  • Extra-intestinal complications are rarer than in UC
109
Q

Describe the classification system for Coeliac’s disease.

A

MARSH CLASSIFICATION:

  • Marsh 1 - solely intraepithelial lymphocytes with NO crypt hyperplasia
  • Marsh 2 - intraepithelial lymphocytes and crypt hyperplasia
  • Marsh 3a - intraepithelial lymphocytes and partial/mild villous atrophy
  • Marsh 3b - intraepithelial lymphocytes and subtotal/moderate villous atrophy
  • Marsh 3c - intraepithelial lymphocytes and total villous atrophy
110
Q

What are the investigations for Crohn’s disease?

A
  • Blood tests: raised WCC, raised platelets, raised CRP & ESR
  • Anaemia: normocytic of chronic disease. Iron, folate or B12 deficiency
  • Liver biochemistry may be abnormal
  • Hypoalbuminemia – in severe disease
  • pANCA NEGATIVE
  • COLONOSCOPY - BIOPSY = GOLD STANDARD. Granulomatous transmural inflammation
  • Stool samples = to exclude C.diff, Campylobacter & others
  • Faecal calprotectin = indicates IBD if raised, doesn’t differentiate UC & Crohn’s
  • Small bowel imaging = to detect proximal disease, e.g. capsule endoscopy
  • Abdominal X-Ray
  • MRI – strictures & fistulae
  • Ultrasonography
111
Q

Describe the management of Crohn’s disease.

A
  • Aiming to induce remission
  • Mild/moderate:
  • ORAL PREDNISOLONE = glucocorticoid steroid - FIRST LINE. 2nd line = 5-ASA
  • Severe disease:
  • IV hydrocortisone
  • Smoking cessation
  • Correct iron/folate/B12 deficiencies
  • Antibiotics for perianal disease, e.g. Metronidazole
  • Liquid enteral nutrition
  • If not responsive to steroids:
  • ANTI-TNF ANTIBODIES, e.g. infliximab, adalimumab
  • Maintaining remission:
  • AZATHIOPRINE (1st line)
  • Methotrexate (if intolerant to azathioprine
  • Infliximab/Adalimumab (if resistant to immunosuppressives)
  • Surgery:
  • Resection of worst affected areas of bowel. Up to 80% require 1+ operation. Never fully cures, so kept to a minimum. Recurrence is almost inevitable in remaining bowel. Short bowel syndrome - lifelong (diarrhoea, malabsorption)
  • Indications: failure of medical therapy, obstruction from strictures, istulae, abscesses, perianal disease, toxic dilatation & perforation
  • Temporary ileostomy - allows time for affected areas to rest
112
Q

What is irritable bowel syndrome (IBS)? What is its epidemiology?

A
  • IBS = mixed group of abdominal symptoms with NO ORGANIC CAUSE
  • Epidemiology:
  • Age of onset <40 years
  • More common in FEMALES than males
  • 1 IN 5 in western world
113
Q

The pathophysiology of IBS is not completely understood. Describe some of the different theories.

A
  • Disorders of intestinal motility
  • Enhanced visceral perception
  • Disfunction of brain-gut axis
  • Microbial dysbiosis (imbalance)
114
Q

Describe the risk factors for IBS.

A
  • Biologically female
  • GI infections
  • Previous severe long-term diarrhoea
  • Anxiety and depression
  • Psychological stress, trauma, abuse
  • Eating disorders
115
Q

What are the three types of IBS?

A
  • IBS-C – with constipation
  • IBS-D – with diarrhoea
  • IBS-M – mixed, with alternating constipation & diarrhoea
116
Q

When should a diagnosis of IBS be considered?

A
  • A diagnosis of IBS should be considered if patients report ANY of (ABC):
  • Abdominal pain/discomfort
  • Bloating
  • Change in bowel habit
117
Q

What is the diagnosis criteria for IBS? What are the other symptoms?

A
  • Diagnosis criteria:
  • ABDOMINAL PAIN/DISCOMFORT associated with 2+ of:
  • RELIEVED BY DEFECATION
  • ALTERED STOOL FORM
  • ALTERED BOWEL FREQUENCY
  • Other symptoms:
  • Urgency
  • Incomplete evacuation
  • Abdominal bloating/distension
  • Mucus in rectum & stool
  • Worsening of symptoms after food
  • Abdominal tenderness
118
Q

IBS is a multi-system disorder. Give some other symptoms.

A
  • Painful periods
  • Bladder symptoms: frequency, urgency, nocturia, incomplete emptying
  • Back pain
  • Joint hypermobility
  • Fatigue
  • Nausea
119
Q

How long do the symptoms of IBS last for? What are symptoms exacerbated by?

A
  • Symptoms are chronic – 6+ months
  • Symptoms are exacerbated by:
  • Stress
  • Menstruation
  • Gastroenteritis
  • Food
120
Q

What are the differential diagnoses for IBS?

A
  • Coeliac disease
  • Lactose intolerance
  • Bile acid malabsorption
  • Inflammatory bowel disease (IBD)
  • Colorectal cancer
  • GI infection
  • Pancreatic insufficiency
121
Q

Compare ulcerative colitis and Crohn’s disease.

A
  • Ulcerative colitis: colon only, continouous lesions (circumferential), only mucosal inflammation, lower RIGHT quadrant pain, pseudo-polyps, crypt abcesses, depleted goblet cells, mucus + blood in stools
  • Crohn’s disease: whole GI tract, skip lesions - non-continuous, transmural inflammation, lower LEFT quadrant pain, granulomatous inflammation, cobblestone appearance, blood in stools
122
Q

What are the red flags for colon cancer?

A
  • Unexplained weight loss
  • Bleeding on defecation/wiping
  • Abdominal/rectal mass
  • Raised inflammatory markers
  • Anaemia
  • Family history
  • Aged over 50
  • Nocturnal symptoms
123
Q

What are the investigations for IBS?

A
  • Blood tests: FBC – anaemia, ESR & CRP – inflammation, tTG/EMA – Coeliac’s disease
  • Faecal calprotectin – raised in IBD
  • Colonoscopy – IBD, colorectal cancer
124
Q

What is the management for mild IBS?

A
  • Education & reassurance
  • Dietary modification: regular meals or small frequent meals. Plenty of fluids. Avoid caffeinated, alcoholic, fizzy drinks
  • Keep a food diary - identify trigger foods
  • Avoid fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs): found to cause IBS symptoms. Include apples, cherries, peaches, lactose, legumes, green vegetables (broccoli, sprouts, cabbage, peas), artificial sweeteners
125
Q

What is the management for IBS-C?

A
  • SOLUBLE FIBRE:
  • Dissolves in water
  • Broken down by bacteria
  • Softens stool
  • Barley, oats, beans, prunes, figs
126
Q

What is the management for IBS-D?

A
  • AVOID INSOLUBLE FIBRE:
  • Makes diarrhoea worse
  • Doesn’t dissolve in water
  • Passes through gut unchanged
  • Bulks up faeces
  • Increases gut motility
  • Cereals, whole-wheat bread, lentils, apples, avocados
127
Q

What is the management for moderate IBS?

A
  • Pharmacotherapy:
  • For pain/bloating:
  • ANTISPASMODICS - mebeverine, buscopan
  • For diarrhoea:
  • LOPERAMIDE (IMODIUM)
  • For constipation:
  • LAXATIVES: macrogol, docusate, senna. Linactolide (12 months constipation not relieved by 2 different max. dose laxative classes). Prucalopride (alternative when other laxatives fail)
128
Q

What is the management for IBS patients who haven’t responded to the aforementioned treatments? How about in severe IBS?

A
  • TRICYCLIC ANTIDEPRESSANTS, e.g. amitriptyline, nortriptyline. Warn about drowsiness. Take about 4-6 weeks to have an effect. Dampen down gut severity
  • If tricyclic antidepressants aren’t tolerated, move to SSRIs - consider side effects. Can be used in conjunction with psychological therapies, e.g. CBT
  • For severe IBS: refer to PAIN TREATMENT CENTRE
129
Q

What is the function of the appendix? Where is it located?

A
  • The appendix is a vestigial organ with disputed functionality
  • It is located at McBurney’s point which lies 2/3rds of the way from the umbilicus to the anterior superior iliac spine
130
Q

What is acute appendicitis? What is its epidemiology?

A
  • Acute appendicitis = sudden inflammation of the appendix
  • Epidemiology:
  • Appendicitis can occur at any age, although its highest incidence is ~10-20yrs
  • Appendicitis is the most common surgical emergency and is commonly examined
131
Q

What is the aetiology of acute appendicitis?

A
  • Most commonly, acute appendicitis occurs because of an obstruction within the appendix, however this obstruction can arise in many different ways:
  • FAECOLITHS
  • Bezoars/foreign bodies
  • Trauma
  • Intestinal worms
  • Lymphoid hyperplasia
132
Q

What is the pathophysiology of acute appendicitis?

A

The obstruction of the appendix results in the invasion of gut organisms into the appendix wall. This leads to inflammation, necrosis and eventually perforation

133
Q

What is the clinical presentation of acute appendicitis?

A
  • EARLY PAIN/DISCOMFORT AROUND THE UMBILICUS THAT MIGRATES TO THE RIGHT ILIAC FOSSA. As the inflammation of the appendix progresses, it irritates the overlying peritoneum causing severe, localised pain at MCBURNEY’S POINT
  • GUARDING
  • Tender mass in RIF
  • PYREXIA
  • Anorexia
  • NAUSEA AND VOMITING
  • Rosving’s sign - left lower-quadrant palpated = right lower-quadrant pain
  • Moving/coughing causes pain due to peritonism
  • You can get chronic (grumbling) appendicitis, but this is not examined and presents with milder symptoms
134
Q

What are the differential diagnoses for acute appendicitis?

A
  • Acute Crohn’s disease
  • Ectopic pregnancy
  • UTI
  • Diverticulitis
  • Perforated ulcer
  • Food poisoning
  • Constipation
  • Strangulated hernia
135
Q

What are the investigations for acute appendicitis? What is diagnostic?

A
  • Blood tests: RAISED WCC (+/- ^neutrophils), RAISED CRP & ESR
  • Ultrasound: can detect an inflamed appendix, may show an appendiceal mass
  • CT = GOLD STANDARD = highly sensitive & specific
  • Pregnancy test to exclude ectopic pregnancy
  • Urinalysis to exclude UTI
136
Q

Describe the management of acute appendicitis.

A
  • APPENDICECTOMY = GOLD STANDARD. This is a laparoscopic (keyhole) procedure in most cases, however in severe cases laparotomy (open) surgery is required
  • IV antibiotics & fluids both pre & post-operatively, e.g. metronidazole, cefuroxime
137
Q

What are the complications of acute appendicitis?

A
  • PERFORATION
  • Appendix mass - small bowel & omentum adhere to appendix
  • Appendiceal abscess
  • ADHESIONS
  • Pelvic inflammatory disease (PID)
138
Q

What is peptic ulcer? What are its risk factors?

A
  • Peptic ulcer = break in the lining of the gastric or duodenal mucosa = chronic mucosal ulceration of stomach/duodenum
  • Risk factors:
  • H.pylori infection (most common) - increased gastric acid secretion, decreases duodenal HCO3- secretion
  • NSAIDS - particularly low dose aspirin corticosteroids
  • Zollinger-Ellison syndrome (tumour that causes hypergastrinaemia)
  • Physiological stress
139
Q

What is the clinical presentation of peptic ulcer? How can we differentiate between a peptic and duodenal ulcer based on the pain?

A
  • Up to 70% asymptomatic
  • ROUND, CIRCULAR, CLEANED OUT BASE = peptic ulcer
  • Epigastric burning pain - may mimic MI. Usually occurs few hours after meal, worsens at night . Peptic ulcer = pain increases when eating and goes 2-3 hours later. Duodenal ulcer = pain decreases when eating and comes 2-3 hours later
  • Nausea and vomiting
140
Q

What are the investigations for peptic ulcer disease?

A
  • Duodenal ulcer = H.pylori test (faecal antigen test or urease breath test). No PPIs and antibiotics within 2 and 4 weeks respectively - 1st line
  • Peptic ulcer = upper GI endoscopy with biopsy (if >55 or red flags present) - 1st line and gold standard
141
Q

Describe the management for peptic ulcer disease.

A
  • Lifestyle modification (weight loss, smoking cessation etc.)
  • Treat cause (stop NSAIDS and/or eradicate H.pylori - PPIs, clarithromycin, amoxicillin). If no PPI then H2 receptor antagonists
  • Re-scoped 6-8 weeks after treatment to see if healed
  • Surgery: endoscopic ligation/coagulation of bleeding ulcers
142
Q

What are the complications of peptic and duodenal ulcer?

A
  • Bleeding
  • Perforation
  • Gastric cancer
143
Q

What is the pathology, risk factors, presentation and complications of gastric ulcers?

A
  • Gastric ulcers:
  • Pathology: lesser curvature of gastric antrum
  • Risk factors: H.pylori infection, smoking, drugs (NSAIDS, SSRIs, corticosteroids, bisphosphonates)
  • Presentation: epigastric pain - worse on eating, relieved by antacids
  • Complications: haemmorrhage, perforation, gastric outflow obstruction, malignancy
144
Q

What is the pathology, risk factors, presentation and complications of duodenal ulcers?

A
  • Duodenal ulcers:
  • Pathology: more common than gastric ulcers, 1st part of duodenum
  • Risk factors: H.pylori, smoking, drugs, alcohol
  • Presentation: epigastric pain - before meals and at night, relieved by eating or milk
  • Complications: haemorrhage, perforation, gastric outflow obstruction, malignancy
145
Q

What is gastritis? What are the two types?

A
  • Gastritis: inflammation of the stomach’s mucosal lining
  • Two types:
  • Acute gastritis
  • Atrophic gastritis (chronic gastritis)
146
Q

What is the aetiology of acute and atrophic gastritis?

A
  • Acute: aspirin + NSAIDS (inhibit COX-1 = less prostaglandins = increase in acidity due to less bicarbonate release), H.pylori (releases urease and protease), alcohol, stress
  • Atrophic: infectious or autoimmune (damage to parietal cells = less intrinsic factor = less vitamin B12 absorption = pernicious anaemia)
147
Q

What is the clinical presentation of gastritis?

A
  • May be asymptomatic
  • Epigastric pain
  • N + V
  • Mucosal ulcers
148
Q

What are the investigations for gastritis?

A
  • If H.pylori risk factors: H.pylori faecal antigen test (first line) H.pylori urea breath test (first line but not as important)
  • Endoscopy and biopsy (GOLD STANDARD)
149
Q

Describe the management for gastritis (can also be called stomach flu).

A
  • Encourage fluid intake, small light non-fatty meals (mild treatment)
  • Addressing cause, e.g. NSAIDs (PPI or H2 receptor antagonist to decrease acidity of the stomach) (moderate to severe treatment)
  • H.pylori eradication (triple therapy: PPI (omeprazole, given to reduce the side effects of antibiotics, e.g. ulcers), clarithromycin, amoxicillin) (moderate to severe treatment)
  • Correction of vitamin deficiency
150
Q

What do these terms mean:

a) diverticulum
b) diverticulosis
c) diverticulitis
d) diverticular disease
e) Meckel’s diverticulum?

A

a) diverticulum = outpouching of gut mucosa (gaps in wall of gut where blood vessels penetrate. Very common in those >50 years. Can be true (all layers) or false (mucosa and submucosa)
b) diverticulosis = presence of multiple diverticula
c) diverticulitis = inflammation/infection of diverticulum
d) diverticular disease = diverticula are symptomatic
e) Meckel’s diverticulum = common congenital abnormality of GI tract. 2-3% of the population. Usually asymptomatic

151
Q

What is Meckel’s diverticulum caused by? Is it a true or false diverticula? What are the symptoms? What is the key investigation?

A
  • Meckel’s diverticulum is caused by incomplete obliteration of the vitelline duct
  • True diverticula of all 3 layers of the small intestines
  • Usually asymptomatic but can get painless bleeding due to ulcer caused by heteroscopic gastric tissue
  • Investigation: 99M TECHNETIUM PERTECHNETATE - MECKEL’S SCAN (nuclear medicine scan)
152
Q

Where are diverticula most likely to occur? Why?

A

Sigmoid colon - it has the smallest luminal diameter and the highest pressure

153
Q

What are the risk factors for diverticulitis? What are the complications?

A
  • Risk factors: low fibre diet, obesity, smoking and NSAIDS
  • Complications: strictures (intestinal obstruction), fistula formation, e.g. bladder communication
154
Q

What is the clinical presentation of diverticulitis?

A
  • LIF pain with tenderness
  • Palpable LIF mass
  • Constipation
  • Tachycardia
  • Fever
155
Q

What are the investigations for diverticulitis? What would they show?

A
  • Bloods - raised WCC, ESR + CRP
  • Imaging: erect CXR, AXR and CT scan with contrast. May show:
  • Pneumoperitoneum
  • Dilated bowel loops
  • Obstruction
  • Abcess
156
Q

Describe the management for diverticulitis.

A
  • Oral/IV antibiotics - ciprofloxacin, metronidazole
  • Analgesia + liquid diet +/- fluid resus
  • Surgical resection - rare cases
157
Q

What are the risk factors for diverticular disease? What is the presentation?

A
  • Risk factors: low fibre diet, obesity and age (>40)
  • Presentation: altered bowel habit, abdominal pain, bleeding PR
158
Q

What are the investigations for diverticular disease?

A
  • Abdominal CT scan
  • Colonoscopy
  • FBC
159
Q

Describe the management of diverticular disease.

A
  • High fibre diet and fluids +/- laxatives
  • Surgery
160
Q

What colour does E.coli show on MacConkey agar? What are its commonly associated diseases? What are the different types?

A
  • Pink colonies on MacConkey agar (lactose-fermenting)
  • Commonly associated diseases: genitourinary tract infections (leading cause of cystitis, pyelonephritis, prostatitis), intra-abdominal infections (enteric infections, abcesses, cholecystitis, spontaneous bacterial peritonitis), meningitis (in neonates)
  • Different types: Enteroinvasive (EIEC), Enterotoxigenic (ETEC), Enteropathogenic (EPEC), Enterohaemorrhagic (EHEC)
161
Q

What are the signs and symptoms of EIEC, EHEC, ETEC, and EPEC?

A
  • EIEC (enteroinvasive E.coli) = dystentery, mimics shigellosis; bloody diarrhoea, abdominal pain, tenesemus
  • EHEC (enterohaemorrhagic E.coli) = BLOODY DIARRHOEA AND SHIGA-LIKE TOXIN, malaise, fever
  • ETEC = watery diarrhoea (Travellers’ diarrhoea), nausea, abdominal pain
  • EPEC = fever, watery diarrhoea - can last >2 weeks, typically affects children
162
Q

Describe the treatment for E.coli.

A
  • Antimicrobial treatment (UTIs, pneumonia, meningitis, intra-abdominal infections, sepsis)
  • Antidiarrhoeal medications - contraindicated in children and EIEC infections
  • EHEC - antibiotics contraindicated - can increase the risk of HUP and TTP complications
  • ETEC - antibiotics useful; reduce diarrhoea duration
163
Q

What are the risk factors and complications of C.difficile?

A
  • Risk factors: antibiotic exposure, previous hospitalisation (increased risk for infection), children with neutropenia
  • Complications:
  • Multiple relapses, dehydration (due to diarrhoea)
  • GI complications: toxic megacolon, colon perforation, intussusception, pneumatosis, ascites
  • Extraintestinal complications: splenic abcess, osteomyelitis
164
Q

What are the signs and symptoms of C.difficile?

A
  • Watery diarrhoea (most common) with mucus and blood
  • Abdominal distension, cramps
  • Malaise
  • Fever
165
Q

What is the treatment for C.difficile? What are the complications?

A
  • C.difficile = DIFFICULT to treat:
  • Mild disease: oral metranidazole
  • Severe disease: oral vancomycin
  • Complications: combination of oral vancomycin, IV metronidazole
  • Surgery: colectomy
166
Q

What is pseudomembranous colitis?

A

Pseudomembranous colitis refers to swelling or inflammation of the large intestine (colon) due to an overgrowth of Clostridioides difficile (C.difficile) bacteria. This infection is a common cause of diarrhoea after antibiotic use

167
Q

What are haemorrhoids? What are the two types?

A
  • Haemorrhoid: anal cushions hypertrophy due to supportive tissue deterioration
  • Two types:
  • Internal: affecting haemorrhoidal venous cushions above the dentate line, 4 grades
  • External: affecting haemorrhoidal venous cushions below the dentate line
168
Q

What are the complications of signs and symptoms of haemorrhoids?

A
  • Itching
  • Bleeding associated with bowel movement
  • Pain
  • Mucous discharge
169
Q

What are the investigations for haemorrhoids?

A
  • Anoscopic examination
  • Colonoscopy/flexible sigmoidoscopy
170
Q

Describe the treatment for haemorrhoids.

A
  • Medications: stool softeners, topical + systemic analgesics
  • Surgery: sclerotherapy, rubber band ligation
  • Increase fibre and fluid intake
171
Q

What are anal fistulae? What are the different types?

A
  • Anal fistula = abnormal connection between anal canal and perianal skin
  • Different types:
  • Intersphincteric
  • Transsphinteric
  • Suprasphinteric
  • Extrasphinteric
172
Q

What are the signs and symptoms of anal fistulae?

A

Skin excorations, pus/serous fluid/faeces draining from the skin-opening, bleeding, itching, pain, redness, swelling

173
Q

What are the investigations and treatment for anal fistulae?

A
  • Investigations: anal examination - delineate course of fistula
  • Treatment: surgery - drain infection, eradicate fistulous tract, preserve anal sphincter function, avoid recurrences
174
Q

What are anal fissures? What are the risk factors?

A
  • Anal fissure = small tear in the anal mucosa
  • Risk factors: low fibre diet, diarrhoea, previous anal surgery
175
Q

What are the signs and symptoms of anal fissures?

A
  • Midline tear
  • Pain during bowel movements
  • Blood on toilet paper
176
Q

What are the investigations for anal fissures?

A
  • Clinical diagnosis
  • Anal manometry
177
Q

Describe the treatment for anal fissures.

A
  • Medications: stool softeners, topical nitrates/CCBs
  • Surgery: sphincterotomy
  • Proper anal hygeine, fibre supplementation
178
Q

What is a perianal abcess?

A

Perianal abcess is a superficial infection that appears as a tender red lump under the skin near the anus. The infection occurs when bacteria gets trapped in the crypt glands that line the anal canal

179
Q

What is a pilonidal sinus? When does it need to be treated?

A

A pilonidal sinus is a small hole or tunnel in the skin at the top of the buttocks, where they divide (the cleft). It does not always cause symptoms and only needs to be treated if it becomes infected

180
Q

For the following features, state whether they belong to IBS, UC, Crohn’s or Coeliac’s:

1) Continuous lesions
2) Can be managed with TCAs or SSRIs
3) Transmural lesions
4) Nocturnal diarrhoea
5) Villous atrophy
6) Mucoid diarrhoea
7) Dermatitis herpetiformis
8) pANCA positive IBD
9) Smoking is a protective factor for this disease
10) tTG & EMA positive
11) Has 3 distinct sub-types
12) Can use methotrexate to maintain remission

A

1) Continuous lesions - UC
2) Can be managed with TCAs or SSRIs - IBS
3) Transmural lesions - Crohn’s
4) Nocturnal diarrhoea - IBD, not IBS
5) Villous atrophy - Coeliac’s
6) Mucoid diarrhoea - UC
7) Dermatitis herpetiformis - Coeliac’s
8) pANCA positive IBD - UC
9) Smoking is a protective factor for this disease - UC
10) tTG & EMA positive - Coeliac’s
11) Has 3 distinct sub-types - IBS
12) Can use methotrexate to maintain remission - Crohn’s

181
Q

A patient presents to you in your GP practice. She tells you that she has had diarrhoea, abdominal pain and some bloating for months now, maybe even years. After asking her a few questions you ascertain that her stool is quite pale and often floats, it also has a rather vile stench. Looking at her past history, you notice she is known to have Hashimoto’s thyroiditis.

What investigation should be offered to her to definitively confirm her most likely diagnosis?

A) Genetic testing

B) Colonoscopy + biopsy

C) Duodenal biopsy

D) DEXA scan

E) Serum antibody testing

A

C) Duodenal biopsy

182
Q

A woman presents to you with LLQ abdo pain with episodes of bloody & mucoid diarrhoea. You send him for a colonoscopy + biopsy; his results come back showing continual inflammatory lesions extending from the rectum.

What is the first line management to induce remission in this patient?

A) Prednisolone

B) Azathioprine

C) Infliximab

D) Olsalazine

E) Hydrocortisone

A

D) Olsalazine

183
Q

A 13 year-old child presents to you in A&E with severe pain and vomiting. The pain has migrated over the last few hours from a dull ache around their umbilicus to what is now a sharp pain in the RLQ over McBurney’s point. Upon examination, you elicit guarding and rebound tenderness in this area.

Which of the following is the least common cause of acute appendicitis?

A) Trauma

B) Metastases

C) Intestinal worms

D) Bezoars

E) Lymphoid hyperplasia

A

B) Metastases

184
Q

An elderly gentleman presents to A&E with constant pain throughout his abdomen as well as lots of distension. You find out he has not passed wind or emptied his bowels in 3 days. You listen to his abdomen as hear no bowel sounds. He is known to have bowel cancer.

Which of the following is the 1st line investigation used to confirm a diagnosis of a bowel obstruction?

A) MRI

B) Abdo x-ray

C) Ultrasound

D) CT

E) ERCP

A

B) Abdominal X-ray

185
Q

The abdominal x-ray you ordered before comes back showing peripheral gas shadows proximal to a blockage as well as severe distension of the caecum and ascending colon. Your consultant doesn’t congratulate you on your fast actions and diagnostic skills, instead he treats you to a question:

“What is the most common cause of large bowel obstructions in the UK?”

A) Sigmoid volvulus

B) Adhesions

C) Intussusception

D) Hernias

E) Malignancy

A

E) Malignancy

186
Q

A 52 year-old woman presents to you in your GP clinic complainging of 10 days of quite severe vomiting and diarrhoea. You start to think about what are the most common causes of diarrhoea as you need to decide if you prescribe her something else alongside loperamide.

Which of the following are the most common cause of diarrhoea in adults?

A) Norovirus

B) Campylobacter jejuni

C) Rotavirus

D) E. Coli

E) Salmonella

A

A) Norovirus

187
Q

Salma, a 65 year old lady, presents with lower abdominal pain.

  1. What are some differential diagnoses?
  2. She has been passing small amounts of blood whilst defecating. What would be your primary diagnosis?
  3. Her observations show that she is pyrexic and has tachycardia. What is now the primary diagnosis?
  4. On examination the pain is localised to the LIF, with guarding and tenderness. What investigation is now contraindicated?
  5. How would you treat this condition?
A
  1. Appendicitis, Diverticulitis, Peritonitis, GU Issues, Bowel Cancer
  2. Bowel Cancer
  3. Diverticulitis
  4. Colonoscopy, due to increased risk of perforation
  5. Oral/IV Antibiotics, Analgesia, Fluid Resus, Liquid Diet
188
Q

Tariq, 54 yrs old, brought to A&E vomiting blood.

  1. List 4 differentials.
  2. 3 medications that can cause upper GI bleeding?
  3. Diagnostic Ix used?
  4. Oesophageal varices is found on your investigation, what may be the cause?
  5. How can you treat?
A
  1. Mallory-Weiss tear, oesophageal ulcer, PUD, gastritis, oesophageal rupture, cancer
  2. NSAIDS, SSRIs, bisphosphonates
  3. OGD + Biopsy
  4. Liver Disease, Portal Hypertension/PVT, cirrhosis, BCS, constrictive pericarditis, RHF
  5. ABCDE, Rockfall Score (Prediction of Rebleeding and Mortality), Bleeding Varices - Terlipressin + Prophylactic Antibiotics (Ciprofloaxcin), Balloon tamponade (Sengstaken-Blakemore tube), Endoscopic Banding, TIPS, Bleed Prevention - BB + Endoscopic Banding. Cirrhosis = screening endoscopy
189
Q

A patient drinks 4 pints (568ml=1 pint) of beer (4%) a day, and 2 standard (175ml) glasses of red wine (13%) on Saturday and Sunday additionally. How many units of alcohol is he drinking per week? (round up to nearest whole number)

A. 73 units

B. 62 units

C. 94 units

D. 57 units

E. 49 units

A
  • Beer: 4% x 568ml x 4 x7 ÷ 1000 = 63.6
  • Wine: 13% x 175ml x 2 x 2 ÷ 1000 = 9.1
  • Total no. of units per week = 72.7 (73)
190
Q

A 16 year old girl is admitted with vomiting and abdominal pain. She reports taking 20 paracetamol tablets after her boyfriend split up with her. Which one of the following test results would you NOT expect to see?

A. Metabolic acidosis

B. A prolonged prothrombin time

C. A raised creatinine

D. Hyperglycaemia

E. ALT 1000

A

D. Hyperglycaemia - causes hypoglycaemia

191
Q

83 year old lady complains of being tired all the time. She has had long-term epigastric pain. She is generally unwell with a fever and malaise. She has had diarrhoea on and off for 6 months.

What do they most likely have?

a) Coeliac’s disease
b) Pancreatitis
c) Infective diarrhoea
d) Autoimmune gastritis
e) IBD
f) Tropical spure

A

d) Autoimmune gastritis

192
Q

32 year old lady is rushed into A+E because she has diffuse abdominal pain. O2 saturations are 91%, heart rate is 178b.p.m. She has a duodenal ulcer. What is your management plan?

a) PPI for 1 month
b) IV antibiotics
c) Admit to sugery
d) Endoscopy

A

c) Admit to surgery

193
Q

Allan came to A+E with central chest pain. He has anxiety and was worried he was having a heart attack. He explains he has had fever for the past 5 days with diarrhoea but the chest pain has been worsening. His flatmate has also had diarrhoea for a week. His ECG is normal. You do an endoscopy and diagnose with gastritis. What treatment is most appropriate?

a) Encourage fluid intake
b) Encourage fluid intake with antimotility agents
c) PPI for 4 weeks
d) Clarithromycin + amoxicillin + PPI

A

a) Encourage fluid intake. A = mild gastritis treatment, B = contraindicated as it’s an infective cause, C = treatment for GORD, D = treatment for H.pylori if gastritis is severe

194
Q

You are an FY1. A 41 year old has had a recent endoscopy result back. The endoscopy result shows moderate gastritis and a test for H.pylori was positive. How long is the sick note for?

a) Miss work until 1 week with no diarrhoea symptoms
b) Miss work until 2 days without diarrhoea
c) After 2 days without diarrhoea he needs a negative stool sample and 24 hours after that he needs another negative stool sample before returning
d) FY1s can’t write sick notes

A

A. C = for E.coli

195
Q

Simon has come to collect his endoscopy results. They describe the following: Brunner’s gland hypertrophy with scarring of the base of the lesion. What is the diagnosis?

a) Barrett’s oesophagus
b) Oesophageal dysplasia
c) Peptic ulcer
d) Duodenal ulcer

A

d) Duodenal ulcer

196
Q

A 24 year old has persistent GORD. He has taken on board lifestyle changes. He has been taking his PPIs. He isn’t taking any NSAIDs but still gets frequent burning in his chest and his pain is relieved by eating, so he has put on a lot of weight.

An endoscopy confirms he has duodenal ulcers. What further test should be done?

a) Serum gastrin
b) Serum cholecystekinin
c) 24 hour pH monitoring
d) Therapeutic challenge
e) Barium contrast X-ray

A

a) Serum gastrin. A = Zollinger-Ellinson - PPI resistant ulcers with GORD, C = he halready has GORD, D = PPIs already tried, E = would show stenosis but stenosis isn’t associated with ulcers

197
Q

A 27 year old male with fever, abdominal cramps and diarrhoea comes to your GP practice. He has a proven duodenal ulcer which and was previously treated for H.pylori infection. You want to test for H.pylori to see if the treatment worked. What test will you do?

a) Stool test
b) Urease breath test
c) Endoscopy
d) Blood test

A

b) Urease breath test

198
Q

Simon comes to the GP as he has had epigastric pain for 2 weeks. The pain decreases when eating and increases 2-3 hours later. What is the first line investigation?

a) Endoscopy
b) Barium swallow
c) Faecal antigen test
d) Urea breath test

A

c) Faecal antigen test. A = first line for peptic ulcers, C = first line for duodenal ulcers, D = used to confirm absence of H.pylori

199
Q

Ryan has a peptic ulcer. He had PPIs for 1 month and had a rescoping of his ulcer. It was not healed. What is the most appropriate action (THIS MEANS WHAT IS THE BIGGEST RISK TO HIM/WHAT NEEDS DOING ASAP)?

a) Biopsy
b) Test for H.pylori
c) Try PPI for 4 more weeks
d) Change to H2 antagonist

A

a) Biopsy. A = peptic ulcer with weight loss so malignancy more likely, B = duodenal ulcers and gastritis are more likely than H.pylori, C = reasonable but not

200
Q

What are the microscopic changes seen in persistent GORD?

a) Squamous - dysplastic - metaplasia - neoplastic
b) Squamous - metaplastic - neoplasia - dysplastic
c) Squamous - metaplasia - dysplastic - neoplastic
d) Squamous - dysplastic - neoplastic - metaplastic

A

c) Squamous - metaplasia - dysplastic - neoplastic

201
Q

Katie is a 93 year old patient living in a care home. She has been sent to A+E as she has dysphagia and can no longer tolerate any oral food or liquids. She initially couldn’t eat solids thus survived on liquids but now she is having trouble swallowing liquids. She has no signs of weight loss and no lymphadenopathy.

What is the most likely diagnosis?

a) Achalasia
b) Oesophageal cancer
c) Benign oesophageal growth
d) GORD

A

b) Oesophageal cancer

202
Q

June is an 84 year old lady. She has had trouble swallowing solid food for 2 weeks. The consultant performs an endoscopy. He sees a narrowing in the oesophagus. What is the most likely cause of the narrowing?

a) Oesophageal cancer
b) Benign oesophageal cancer
c) Hiatus hernia
d) Barrett’s oesophagus
e) Achalasia

A

b) Benign oesophageal cancer

203
Q

A 75 year old man is admitted with abdominal pain and vomiting, and had not opened his bowels for 5 days. Examination revealed a distended abdomen with tympanic percussion and tinkling bowel sounds. He has no past medical history. His AXR is shown below. What is the most likely underlying diagnosis?

A. Colorectal cancer

B. Adhesions

C. Constipation

D. Sigmoid volvulus

E. Hernia

A

D. Sigmoid volvulus

204
Q

A 74 year old man presents with a change in bowel habit and anaemia. Colonoscopy and subsequent CT showed below. What is the Duke stage of his cancer?

A. Dukes A

B. Dukes B

C. Dukes C

D. Dukes D

A

D. Dukes D

205
Q

Which one of the following is FALSE regarding colorectal cancer?

A. Bowel cancer screening is offered to people aged 55 or over

B. The majority of cancers occur in the proximal colon

C. FAP and HNPCC are two inherited causes of colon cancer

D. Proximal cancers usually have a worse prognosis

E. Patients with PSC and UC have an increased risk of developing colon cancer

A

B. The majority of cancers occur in the proximal colon

206
Q

A 50 year old man presents with dysphagia. Which one of the following suggests a benign nature of his disease?

A. Weight loss

B. Dysphagia to solids initially then both solids and liquids

C. Dysphagia to solids and liquids occurring from the start

D. Anaemia

E. Recent onset of symptom

A

C. Dysphagia to solids and liquids occurring from the start

207
Q

. A 32 year old lady complains of a 6 month history of bloating and diarrhoea. What is the most likely diagnosis based on the small bowel histology?

A. Crohn’s disease

B. Ulcerative colitis

C. Microscopic colitis

D. Coeliac disease

E. Irritable bowel syndrome

A

D. Coeliac disease

208
Q

A 19 year old girl presents with abdominal pain and loose stool. Which of the features suggest that she has irritable bowel syndrome?

A. Anaemia

B. Nocturnal diarrhoea

C. Weight loss

D. Blood in stool

E. Abdominal pain relieved by defaecation

A

E. Abdominal pain relieved by defaecation

209
Q

Which statement is true regarding Helicobacter pylori?

A. It is a gram positive bacteria

B. HP prevalence is similar in developing and developed countries

C. 15% of patients with a duodenal ulcer are infected with H. Pylori

D. PPIs should be stopped 1 week before a H. Pylori stool antigen test

E. It is associated with an increased risk of gastric cancer

A

E. It is associated with an increase in the risk of gastric cancer

210
Q

Which of the following features best distinguishes Ulcerative colitis from Crohn’s disease?

A. Ileal involvement

B. Continuous colonic involvement on endoscopy

C. Non-caseating granuloma

D. Transmural inflammation

E. Perianal disease

A

B. Continuous colonic involvement on endoscopy

211
Q

A 68 year old lady presents with abdominal pain and distention. She last opened her bowels 5 days ago. She has a poor appetite and has lost some weight recently. Her PMH includes an abdominal hysterectomy and diverticulosis. She drinks 20 units of alcohol a week and smokes 5 a day. Examination reveals a distended abdomen with tympanic percussion throughout. There is a small left groin lump with a cough impulse. Which one of the following is NOT likely to be the cause of her abdominal pain and distention?

A. Colon cancer

B. Adhesions

C. Ascites

D. Diverticulitis

E. Strangulated hernia

A

C. Ascites

212
Q

A 71 year old man was admitted to hospital with pneumonia after he returned from a cruise holiday in the Mediterranean Sea. He was treated with a week of augmentin (co-amoxiclav) for his pneumonia. On day 7 of his admission, he started having diarrhoea 10 times a day without any blood. He feels unwell and dehydrated. He had a flexible sigmoidoscopy which showed this. What is the likely organism responsible for his diarrhoea?

A. Norovirus

B. Escherichia coli

C. Giardia lamblia

D. Clostridium difficile

E. Salmonella enteritidis

A

D. Clostridium difficile

213
Q

A 23 year old man was brought in at 2am with RIF pain and was diagnosed with acute appendicitis. He was stable and was scheduled for appendicectomy in the morning. During the ward round, he acutely deteriorated. He was immediately brought to theatre for a perforated appendix. What clinical signs would you NOT expect to see?

A. Fever

B. Tinkling bowel sounds

C. Tachycardia

D. Rebound tenderness

E. Guarding

A

B. Tinkling bowel sounds

214
Q

Mary comes to A+E with haematemesis. Her observations are taken showing the following:

Respiratory rate = 19, HR = 120, BP = 135/88

What is the most urgent course of action next?

a) Rockall score
b) Terlipressin
c) Endoscopy
d) Fluids

A

c) Endoscopy

215
Q

June is in her second trimester. She already has a diagnosis of hyperemesis gravidarum and comes to the GP with slight haematemesis. What is the most likely cause of her haematemesis?

a) Portal hypertension
b) Repeated sickness
c) Chronic cough
d) Alcohol abuse
e) GORD

A

b) Repeated sickness

216
Q

Ruben is a 1 year old boy who has had a terrible chest infection. It has caused repeated coughing attacks. His cough is now getting better but he has been regurgitating blood when bottle fed. What is the most appropriate action?

a) PPI
b) Resus
c) Anti-emetics
d) Nothing

A

d) Nothing

217
Q

A 32 year old man comes into A+E. He has a history of hepatitis caused by alcohol abuse. He is heavily intoxicated and has slurred speech with stumbling when walking. He begins vomiting excessively and whilst at first there was no blood there now is. What is the most likely diagnosis?

a) GORD
b) Stroke
c) Oesophageal varices
d) Mallory-Weiss tear

A

d) Mallory-Weiss tear

218
Q

A 42 year old man has an endoscopy due to his dysphagia. The endoscopy showed a dilated oesophagus with distal stenosis. A diagnosis of achalasia is made. Following surgery what is the most common complication?

a) Mallory-Weiss syndrome
b) Gastric carcinoma
c) Perforation
d) GORD

219
Q

28 year old weightlifter comes to the GP with retrosternal pain. This pain came on after a workout. Bowel sounds can be heard over her left lung base and her x-ray shows a retrocardiac mass. What is the most likely diagnosis?

a) Costochondritis
b) GORD
c) Focal lesions with normal adjacent mucosa in distal oesophagus = aka Mallory-Weiss tear
d) Perforation
e) Pulmonary embolism

A

c) Focal lesions with normal adjacent mucosa in distal oesophagus = aka Mallory-Weiss tear

220
Q
A

E. Sigmoid volvulus

221
Q
A

A. Hepatic vein

222
Q
A

C. Cleared previous infection

223
Q
A

A. Transmural inflammation

224
Q
A

B. Lipase inhibition

225
Q
A

B. Cholangiocarcinoma of the pancreatic head

226
Q
A

D. Ascending cholangitis

227
Q
A

D. Acute mesenteric ischaemia

228
Q
A

D. Coeliac disease

229
Q
A

D. Acute diverticulitis

230
Q
A

E. Duodenal ulcer

231
Q
A

B. 30% of bile is reabsorbed by the enterohepatic circulation

232
Q
A

B. Difficulty swallowing solids and liquids from the start

233
Q
A

D. AST/ALT ratio <1

234
Q
A

C. Pernicious anaemia

235
Q
A

C. Murphy’s sign

236
Q
A

C. Cholecystokinin

237
Q
A

B. CT abdomen

238
Q

A 42-year-old gentleman presents with a 3-week history of epigastric pain which is worse after eating, particularly fatty meals. He takes regular ibuprofen for back pain and has a history of allergic reaction to flucloxacillin. Given the likely diagnosis, what would be the most appropriate management plan?

a) Refer for cholecystectomy
b) 7 days PPI + clarithromycin and amoxicillin
c) 7 days PPI + clarithromycin and metronidazole
d) 2 months PPI e.g. omeprazole

A

C) 7 days PPI + clarithromycin and metronidazole

239
Q

A 42-year-old gentleman presents with a 3-week history of epigastric pain which is worse after eating, particularly fatty meals. He takes regular ibuprofen for back pain and has a history of allergic reaction to flucloxacillin. Given the likely diagnosis, what would be the most appropriate management plan?

What else would you consider in this man’s treatment?

A

Note – you would do a nitrogen breath test first

You would want to look for alternatives to the NSAID or at least prescribe gastric protection

240
Q

A 22-year-old female attends A&E with diarrhoea, worsening over the past week. She has passed water stool 10 times in the past 24 hours and reports the presence of blood. She has to rush to the toilet but sometimes feels the need to open her bowels without being able to pass any stool. On examination she is tachycardic and appears drowsy. Given the likely diagnosis, what is the most appropriate management?

a) Rectal sulfasalazine
b) Oral sulfasalazine
c) Oral prednisolone
d) IV prednisolone

A

D) Oral prednisolone. This is severe UC (severe as ≥10 per day, UC indicated by bloody diarrhoea and tenesmus) so high-dose IV steroids should be started as soon as possible

241
Q

A young man phones you at the GP with a 48 hour history of diarrhoea – he reports watery stools, abdominal cramps and nausea, but is otherwise well and coping at home. He returned from a backpacking tour around Asia yesterday. What is the most appropriate advice?

a) An anti-motility drug such as loperamide
b) Immediate metronidazole
c) Increase oral fluid intake; watch and wait
d) Immediate admission for IV fluid resuscitation

A

C) Increase oral fluid intake; watch and wait.

Traveller’s diarrhoea is most likely to be E. coli and therefore the most appropriate treatment is supportive.

He is managing at home so admission probably isn’t necessary, metronidazole would be used for e.g. Giardia but that has a longer, drawn out course.

Generally try to avoid antimotility in diarrhoea ESPECIALLY if it might be E.coli.

242
Q

A 22-year-old man presents to your GP surgery with recurrent episodes of abdominal pain and non-bloody diarrhoea around 6-times a day. You investigate and his faecal calprotectin is raised at 312. Which of the following would indicate a diagnosis of Crohn’s disease?

a) Non-granulomatous inflammation
b) Continuous inflammation with no skip lesions
c) Inflammation affects mucosa only
d) Inflammation beyond the ileocecal valve
e) Goblet cell depletion

A

d) Inflammation beyond the ileocaecal valve.

Crohn’s disease is characterised by transmural (full-thickness) inflammation of anywhere within the GI tract, there are skip lesions and no goblet cell depletion.

Answers A, B, C and E are characteristic of Ulcerative Colitis

243
Q

A 30 year old man presents with difficulty swallowing. He struggles with tough solid foods like steak and bread, but is generally ok with liquids and soups. He gets lots of regurgitation and heartburn with it. More info:

Trialled PPIs - didn’t help

No fevers, weight loss, night sweats etc

Does cough at night

CXR shows very dilated oesophagus

Small/absent gastric bubble

Barium swallow: slow movement within oesophagus

As this progresses, the patient may be at risk of aspiration pneumonia

What does this patient have?

A

This patient has achalasia. Dysphagia affecting solids more than liquids. No apparent underlying cause. REGURGITATION RATHER THAN REFLUX

244
Q

A 60-year-old lady presents to your GP surgery with episodes of abdominal pain and bloating. This is triggered by certain foods. She has lost a little bit of weight, but has no fevers or night sweats. On asking, you find that her stools are smelly and hard to flush. She has a history of Sjogren’s syndrome and type 1 Diabetes.

a) What is your differential diagnosis?
b) What foods might trigger this?
c) Which initial investigation would be most appropriate, and what should the patient do in the 6-weeks leading to this?
d) What might you see on biopsy?
e) What is the management for this condition?

A

a) Coeliac disease
b) Bread, pasta. Anything containing whear, rye, barley, or oats
c) Anti-tTG antibody. Patient must keep gluten in diet 6 weeks prior to this
d) Villous atrophy, crypt hyperplasia
e) Lifelong gluten-free diet

245
Q

A 48-year-old man presents to A&E with severe epigastric pain and haematoschezia. He feels faint and appears pale. He has had this pain on and off before, but has never coughed up blood before. The pain is relieved by eating. He has a PMH of GORD. What is your differential diagnosis and which artery is likely the source of the bleed?

a) Gastric ulcer, gastroduodenal artery
b) Barrett’s Oesophagus, oesophageal arteries
c) Duodenal ulcer, gastroepiploic artery
d) Duodenal ulcer, gastroduodenal artery
e) Mallory Weiss Tear, oesophageal arteries

A

d) Duodenal ulcer, gastroduodenal artery.

This man has a duodenal ulcer with an acute bleed: a posterior duodenal wall ulcer may erode into the gastroduodenal artery!

You can differentiate between a gastric and duodenal ulcer by how it relates to eating: pain relieved with meals suggests duodenal; worse with meals suggests gastric.

Despite the history of GORD, this presentation is too acute to be Barrett’s oesophagus.

A Mallory-Weiss tear is a tear of the mucosa in the lower oesophagus and is preceded by a history of forceful coughing or vomiting

246
Q

A 62 year old male patient arrives to your GP clinic complaining of a relapse of heartburn. They were having trouble eating, but had lost significant weight.

PMHx: diverticulitis, angina, depression, hiatus hernia, GORD

SHx: Smoker, 20 units of alcohol per week

Which of the following is not a risk factor for oesophageal cancer?

a) Barret oesophagus
b) Achalasia
c) Diverticulitis
d) Hiatal hernia
e) Angina

247
Q

Chloe is an 8-year-old girl who presents to A&E with severe abdominal pain. Her mum tells you she first started getting a tummy ache 4 hours ago, but began crying with the pain around half and hour ago. It started in the middle but now it is worst in the right lower quadrant. She feels sick but hasn’t been sick. What is the gold standard for management of Chloe’s condition?

a) Laparoscopic cholecystectomy
b) Fluids and antibiotics
c) Laparoscopic appendicectomy
d) Ultrasound scan abdomen
e) Antiemetics for the nausea

A

c) Laparoscopic appendicectomy.

Chloe has appendicitis: Generalised abdominal pain localising to McBurney’s Point in the RIF. The Gold Standard for management is a laparoscopic appendicectomy.

Laparoscopic cholecystectomy is the Gold Standard for management of cholecystitis, which would present similarly but localise to RUQ, not RLQ.

Ultrasound scan abdomen would be an investigation, not management, and the other options are forms of symptomatic / conservative management

248
Q

A young person presents to your GP clinic complaining of a 4 day history of diarrhoea, a fever and abdominal pain.

a. Name 1 pathogenic causes of diarrhoea
b. Name 1 non-infectious diseases which may present with diarrhoea
c. Name 1 other causes of diarrhoea which are not related to disease or infection

A

a) E.coli
b) IBS
c) Medication related

249
Q

Which of the following statements is most applicable to coeliac disease?

a) Characterised by enhanced gastric acid production
b) Two peaks of incidence at ~2months and ~40 years of age
c) Transmural areas of inflammation on biopsy
d) Associated with HLA-DQ2/DQ8
e) SBR may be raised on bloods

A

d) Associated with HLA-DQ2/DQ8.

A = GORD, C = Crohn’s, E = Jaundice.

2 month old babies don’t eat gluten - so it must be D!

250
Q

Trevor is a 28 year old man who has recently had an endoscopy for inflammatory markers present in his bloodwork, and diarrhoea. On endoscopy skip lesions were found, and transmural inflammation.

What is the first line treatment for this patient?

a) Oral prednisolone
b) Methotrexate
c) Infliximab
d) Mercaptopurine
e) Azathioprine

A

a) Prednisolone

251
Q

Haemorrhoids are swollen veins in the anus and lower rectum. They are similar to varicose veins, and are very common. Which of the following features would indicate that the haemorrhoids are internal, rather than external?

a) Painless bleeding with bowel movements
b) Itching and irritation in anal region
c) Pain and discomfort
d) Swelling around your anus
e) Bleeding

A

a) Painless bleeding with bowel movements. A and C both involve pain and are mutually exclusive (i.e., both cannot be true) - therefore the answer must be A or C by default. A = Applies to internal haemorrhoids only: external = painful. A is the single best answer as it is the differentiating feature

252
Q

Julie is a 59-year-old lady who presents with left lower quadrant abdominal pain associated with nausea. It started a few days ago, and is constant and persistent. She last opened her bowels 5 days ago, and her LLQ is soft and tender on examination. Julie has a high BMI, a low fibre diet, and an 18-pack-year smoking history. What might you see on a CT scan?

a) Ascites
b) Inflamed and infected pouches of the sigmoid
c) Appendiceal inflammation
d) Haemoperitoneum
e) Free gas within peritoneal cavity

A

b) Inflamed and infected pouches of the sigmoid. Julie has diverticulitis:

Management:

  • If uncomplicated / mild infection: PO antibiotics & liquid diet
  • If complicated: IV antibiotics, drain any abscesses
  • Surgery may be indicated if:

Complicated, recurrent, immunocompromised

Primary bowel resection with anastomosis

Bowel resection with colostomy

253
Q

You are on F1 on the geriatric ward. You have been asked by a nurse to review a patient who has become acutely unwell. The patient was in the ward for treatment of cellulitis. They have watery diarrhea that contains blood and intense abdominal pain and a temperature of 39.2 degrees. The nurse reports that a few other patients have been complaining of malaise and abdominal cramping.

What is the first line treatment for this patient?

a) 500mg Metronidazole IV TD 10 days
b) 250mg Clarithromycin BD 5 days
c) 200mg Fidaxomicin PO BD 10 days
d) 125mg Vancomycin QD PO 10 days
e) 500mg Amoxicillin TD PO 5 days

A

d) 125mg Vancomycin QD PO 10 days

254
Q

Which of the following is the least appropriate with regards to irritable bowel syndrome?

a) Group of abdominal symptoms with no apparent organic cause
b) Abdominal pain relieved by defecation
c) Loperamide is an appropriate treatment for IBS-related constipation
d) Low-FODMAP diet is advisable
e) Patient may have mucus in stools

A

c. Loperamide is an appropriate treatment for IBS-related constipation.

Answers A, B, D and E are all correct. Loperamide, whilst used in the management of IBS, is an anti-motility drug - you don’t want to give this to a constipated patient! It is used to treat diarrhoea. Senna and Movicol are appropriate for IBS-related constipation. Buscopan is an antispasmodic used to treat pain

255
Q

Perianal disorders are those that affect the area around the anus. Which of the following best describes a pilonidal sinus?

a) Rectal mucosa protrusion through the anus causing a dragging sensation
b) Tear in the squamous lining of the anal canal causing pain
c) A track communicating between skin and rectum or anal canal causing discharge
d) Abnormal pocket in the skin near the tailbone containing hair and skin debris
e) Swollen veins that protrude inside the rectum

A

d) Abnormal pocket in the skin and rectum or anal canal causing discharge.

A = rectal prolapse

B = anal fissure

C = fistula

D = pilonidal sinus

E = internal haemorrhoids

256
Q

Gastritis is inflammation of the lining of the stomach. Which of the following would be the least appropriate management option?

a) Clarithromycin, Amoxicillin, and Metronidazole
b) Omeprazole
c) Ranitidine
d) Ibuprofen
e) Gaviscon

A

d) Ibuprofen

A = appropriate for H.pylori infection, which is a cause of gastritis

B = PPI - blocks acid production and promotes healing

C = H2 receptor antagonist - reduces acid production

D = NSAIDs - can damage the gastric mucosa by suppressing prostaglandin synthesis, impair barrier properties of mucosa and reduce mucosal blood flow

E = Antacid - neutralise acid, appropriate symptom relief

257
Q

Barry is a 57 year old man with a 15 year history of Gastro-oesophageal Reflux Disease. On endoscopy you notice his oesophageus is red, so you decide to biopsy. What cells are likely to be present?

a) Stratified squamous non-keratinising epithelium
b) Simple columnar epithelium with goblet cells
c) Simple squamous epithelium
d) Stratified squamous keratinising epithelium
e) Pseudostratified ciliated columnar epithelium

A

b) Simple columnar epithelium with goblet cells

258
Q

A 22 month old child is brought into A+E by their parents. The parents report that the child suddenly started screaming, pulling their knees to their stomach. They appear to be in great abdominal pain. On examination their stool contains blood and mucus. The x-ray shows large dilated loops of bowels.

a) What is the diagnosis of this child?
b) What is the most likely cause of this diagnosis?
c) How would you manage this?

A

a) Bowel obstruction
b) Intussusception
c) Conservative management - treat the symptoms

IV fluids, nasogastric suction

Surgery if persists

259
Q

Mesenteric ischaemia and ischaemic colitis are two conditions affecting blood flow within the gastrointestinal tract.

a) What is the main difference between these conditions?
b) List some risk factors for ischaemic colitis.
c) What are some potential complications of mesenteric ischaemia?
d) How might you investigate if you suspected ischaemic colitis? How does this differ from mesenteric ischaemia?
e) For which of these conditions may you treat surgically with a stent?

A

a) Mesenteric ischaemia → narrowed / blocked arteries restrict blood flow to small intestine. Ischaemic colitis → temporary restriction of blood supply to the large intestine due to vasoconstriction or low pressure flow
b) Demographic: Age (>60), Sex (F>M). Clotting Abnormalities: i.e., Factor V Leiden. High Cholesterol → Atherosclerosis → Vessel narrowing. Reduction of blood flow → HF, Low BP, Shock, DM, RA. Prev abdo surgery → scar tissue. Heavy exercise → may lead to reduced colonic blood flow. Surgery involving the aorta
c) Sepsis, bowel necrosis (→ short bowel syndrome), death, fear of eating, unintentional weight loss
d) CT Abdomen (rule out other things such as IBD), Colonoscopy, Stool culture (rule out infection). Investigate with angiography, doppler ultrasound
e) Mesenteric ischaemia (surgical management of ischaemic colitis may involve bowel resection due to necrosis or blockage, or repairing a hole in the colon)

260
Q

Jerry is a 54-year-old man who is blue-lighted into A&E with haematemesis. His son tells you that his stools have been darker in colour, and he lost consciousness before the ambulance arrived. His skin has a yellow tinge. His son confides in you that Jerry has had a drinking problem for some years now. You suspect a rupture of oesophageal varices.

a) What are oesophageal varices?
b) What is causing Jerry’s stools to be dark?
c) What is the likely cause in Jerry’s case?
d) What else could cause oesophageal varices?

A

a) Abnormal, enlarged veins in the oesophagus that develop when normal blood flow to the liver is blocked by a clot/scar tissue
b) The bleeding varices can result in swallowing large amounts of blood, which can cause black, tarry stools

261
Q

Millie is a 19-year-old girl with a past medical history of Bulimia Nervosa. She presents to A&E with upper abdominal pain and significant haemoptysis. What is the likely cause of the haemoptysis in Millie’s case, and what other symptom might she have?

a) Lung cancer, ipsilateral anhidrosis
b) Mallory-Weiss tear, bloody stools
c) Gastric ulcer, left upper quadrant pain
d) Oesophageal varices, chest pain
e) Hiatus hernia, reflux

A

b) Mallory-Weiss tear, bloody stools

A = Lung cancer, ipsilateral anhidrosis

→ No symptoms of cancer or Horner’s syndrome

B = Mallory-Weiss tear, bloody stools

→ Correct answer - fits clinical picture and history

C = Gastric ulcer, left upper quadrant pain

→ May occur as complication but no history of reflux

D = Oesophageal varices, chest pain

→ Would be a more acute picture

E = Hiatus hernia, reflux

→ No symptoms of heartburn, reflux or feeling of fullness

Phase 2a (25 decks)

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