Gastroenterology

Question 1

Define Crohn’s disease

Answer 1

Crohn’s disease is a form of inflammatory bowel disease characterised by transmural (causes bowel wall to thicken) inflammation of the gastrointestinal tract (anywhere from mouth to anus), with the terminal ileum and colon most commonly affected.

Question 2

Describe the epidemiology of Crohn’s disease

Answer 2

Epidemiology Jewish people, less common than UC, smoking increases risk 2-4x, more females than males, age 20-40

Question 3

Describe the aetiology of Crohn’s disease

Answer 3

• Environmental factors e.g. smoking
• Genetic factors e.g. CARD15/NOD2 mutation
• Pathogens e.g. Mycobacterium paratuberculosis, Pseudomona and Listeria species

Question 4

Describe the risk factors for Crohn’s disease

Answer 4

• Family history
• Smoking
• NSAIDs may exacerbate
• Stress and depression

Question 5

Describe the pathophysiology of Crohn’s disease

Answer 5

Dysfunctional unregulated inflammatory response which causes tissue damage. Inflammation starts in the mucosa and progresses to involve deeper layers and forms granulomas (large masses of immune cells) and ulcers. The granulomas extend to involve all layers of the GI wall (transmural).

Question 6

Describe the clinical manifestations of Crohn’s disease

Answer 6

Follows a relapsing and remitting course

• Signs
  
  • Abdominal tenderness
  • Fever
  • Rectal examination: blood, skin tags, erythema, fissures, fistulas, ulceration
  • Aphthous mouth ulcers
• Symptoms
  
  • Diarrhoea
  • Abdominal pain (most commonly in RLQ where the ileum is)
  • Bloody stools: more common in ulcerative colitis
  • Delayed puberty and failure to thrive: in children
  • Weight loss
  • Systemic symptoms:
    
    • Anorexia
    • Fever
    • Malaise
    • Lethargy

Question 7

Describe some extra-intestinal manifestations of Crohn’s disease

Answer 7

More common in patients with colitis and peri-anal disease

• Cutaenous
  
  • Erythema nodosum - inflammatory disorder affecting subcutaneous fat.
  • Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
• Musculoskeletal
  
  • Pauci-articular arthritis: asymmetrical
  • Osteoporosis
  • Axial arthritis
  • Polyarticular arthritis: symmetrical
  • Clubbing
  • Sacroiliitis
  • Ankylosing spondylitis
• Eyes
  
  • Episcleritis - inflammation of your episclera
  • Uveitis - eye inflammation
  • Conjunctivitis
• Hepatobiliary
  
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
  • Gallstones
• Other
  
  • Calcium oxalaterenal stones

Question 8

Describe the primary investigations for Crohn’s disease

Answer 8

1st line FBC: raised WCC, platelets, CRP&ESR, anaemia. Faecal calprotectin raised (indicates IBD). pANCA negative. Stool samples (rule out infection). LFTs: hypoalbuminemia. Low iron, vitamin B12 and folate (B9) levels.

Question 9

What is the gold standard investigation for Crohn’s disease

Answer 9

Colonoscopy and biopsy (granulomatous transmural inflammation. Skip lesions, cobblestone appearance. Strictures “string sign”)

Question 10

What are other investigations to consider for Crohn’s disease

Answer 10

Imaging: abdominal USS/x-ray/MRI (strictures and fistulae)

Question 11

What are the differential diagnosis for Crohn’s disease

Answer 11

Ulcerative colitis, irritable bowel syndrome, diverticulitis, indeterminate/infectious/radiation colitis

Question 12

Describe the general advice for Crohn’s disease

Answer 12

• General advice
  
  • Advice regarding smoking cessation is extremely important
  • There is some evidence to suggest that use of NSAIDs or the combined oral contraceptive pillmayincrease the risk of relapse. May consider ceasing use.

Question 13

Describe the management for Crohn’s disease

Answer 13

For remission:
Mild to moderate disease: 1. oral corticosteroids (prednisolone).
Severe disease: IV hydrocortisone. If steroids don’t work add TNF-a inhibitor (infliximab) or immunosuppressants (azathioprine, methotrexate)
Maintaining remission: azathioprine, mercaptopurine
Surgery if no response to treatment: resection or worst affected bowel, temporary ileostomy (allows time for affected areas to rest). Surgery is not curative for Crohn’s as entire bowel is affected.
Also: stop smoking, replace iron/B12/folate deficiencies, antibiotics for perianal disease

Question 14

Describe the management for maintaining remission for Crohn’s disease

Answer 14

Patients can either have no treatment, or pharmacological therapy depending on their risk of relapse. Glucocorticoids should not be offered

1st line:Azathioprine or Mercaptopurine

2nd line:Methotrexate, Infliximab, Adalimumab

Post-surgery: consider azathioprine, with or without methotrexate

Question 15

Describe the complications for Crohn’s disease

Answer 15

Bowel: obstruction, malabsorption, toxic megacolon, perforation, fistula, colorectal cancer. Perianal disease. Extraintestinal: Oral aphthous ulcers, uveitis, episcleritis, erythema nodosum, pyoderma gangrenosum, arthritis, ankylosing spondylitis

Question 16

Describe the prognosis for Crohn’s disease

Answer 16

This is a life-long condition, and most people will require medical management indefinitely.

There are multiple genetic and environmental factors that will determine the frequency of flare-ups and subsequent remission length.

Question 17

Crohn’s NESTS

Answer 17

No blood or mucus
Entire GI tract
Skip lesions on endoscopy
Terminal ileum most affected and transmural inflammation
Smoking is a risk factor

Question 18

Define ulcerative colitis

Answer 18

Type of inflammatory bowel disease. Inflammation of the walls of the colon and rectum, and ulcers, with periods of exacerbation and remission. CLOSE UP: Continuous inflammation (no skip lesions), Limited to colon and rectum, Only superficial mucosa affected, Smoking is protective, Excrete blood and mucus, Use aminosalicylates, Primary Sclerosing Cholangitis

Question 19

Describe the epidemiology of ulcerative colitis

Answer 19

• Ulcerative colitis has a bimodal age distribution at approximately 15-25 and 55-70 years of age.
• Prevalence = 100-200/100,000
• Highest incidence and prevalence in Northern Europe, UK and North America
• Affects caucasians and eastern European Jews most
• Is 3 times more common in NON-SMOKERS

Question 20

Describe the risk factors of ulcerative colitis

Answer 20

• Family history
• HLA-B27
• Caucasian
• Non-smoker
• NSAIDs- associated with flares
• Chronic stress and depression - associated with flares

Question 21

Describe where ulcers tend to form in ulcerative colitis

Answer 21

UC is a type of inflammatory bowel disease that tends to form ulcers along the inner-surface or lumen of the large intestine, including both the colon and the rectum.

These ulcers are spots in the mucosa and submucosa where the tissue has eroded away and left behind open sores or breaks in the membrane.

Question 22

Describe the origin of ulcerative colitis

Answer 22

Environmental factors like diet and stresswere once thought to be the culprit but now it’s thought that these are more secondary. UC is now thought to be autoimmune in origin.

Question 23

Describe the pathophysiology of ulcerative colitis

Answer 23

Inappropriate autoimmune response against colonic flora in genetically susceptible individuals. T cells destroy cells lining the colon which leaves behind eroded areas called ulcers.

Question 24

Describe the clinical manifestations of ulcerative colitis

Answer 24

• Signs
  
  • Abdominal tenderness
  • Fever - in acute UC
  • Tachycardia - in acute severe UC
  • Fresh blood on rectal examination
• Symptoms
  
  • Diarrhoea
  • Blood and mucus in stool
  • Urgency and tenesmus (cramping rectal pain)
  • Abdominal pain: particularly in left lower quadrant
  • Weight loss and malnutrition
  • Fever and malaise during attacks

Question 25

Describe what extra-intestinal manifestations may occur with ulcerative collitis

Answer 25

• Cutaenous
  
  • Erythema nodosum - inflammatory disorder affecting subcutaneous fat.
  • Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
• Musculoskeletal
  
  • Pauci-articular arthritis: asymmetrical
  • Osteoporosis
  • Axial arthritis
  • Polyarticular arthritis: symmetrical
  • Clubbing
  • Sacroiliitis
  • Ankylosing spondylitis
• Eyes
  
  • Episcleritis - inflammation of your episclera
  • Uveitis - eye inflammation
  • Conjunctivitis
• Hepatobiliary
  
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
• Other
  
  • Cholangiocarcinoma
  • Aphthous oral ulcer
  • Nutritional deficits

Question 26

Define fulminant disease in relation to ulcerative colitis

Answer 26

• Fulminant refers to an abrupt and severe onset of a UC flare
• Suggested byoneof the following:
  
  • > 10 bowel movements per day
  • Continuous bleeding
  • Abdominal tenderness and distention
  • Toxicity
  • Colonic dilation
  • The need for blood transfusion

Question 27

Describe the primary investigations for ulcerative colitis

Answer 27

• Faecal calprotectin: will be raised; a marker of inflammation in the gastrointestinal tract and helps differentiate from irritable bowel syndrome
• FBC:leukocytosis during a flare; may demonstrate anaemiafrom PR bleeding
• LFTs:should be checked every 6-12 months to screen for PSC; low albumin may suggest protein-losing enteropathy
• CRP/ESR: raised during acute inflammation of the bowel (flare)
• Colonoscopy and biopsy: GOLD STANDARD and allows for biopsy
  
  • Red and raw mucosa with widespreadshallow ulceration
  • No inflammation beyond the submucosa, unless fulminant disease
  • Lamina propria inflammatory cell infiltrates
  • Pseudopolyps: mucosa adjacent to ulcers is preserved, which has the appearance of polyps
  • Crypt abscessesdue to neutrophil migration through gland walls
  • Goblet cell depletion, withinfrequentgranulomas

Question 28

Describe the differential diagnosis of ulcerative colitis

Answer 28

Alternative causes of diarrhoea should be excluded e.g. Salmonella spp,
Giardia intestinalis and rotavirus

Question 29

What is the management for ulcerative colitis dependent upon

Answer 29

Depends on the location and severity of disease.

Question 30

Describe the general management for ulcerative colitis

Answer 30

• Mild = 1st line aminosalicylate and 2nd line corticosteroids
• Severe = 1st line IV corticosteroid and 2nd line IV ciclosporin
• Colectomy may be required: leaves patient with J-pouch (can be reversed) or ileostomy.
  
  • J- pouch: ileoanal anastomosis, colon removed and rectum fused to ileum
  • Ileostomy: colon and rectum are removed and the ileum brought out on
    to the abdominal wall as a stoma
• Maintenance = aminosalicylate, azathioprine, mercaptopurine
• Biologics = may be considered in patients who are intolerant/ not responding to immunomodulation e.g. infliximab, adalimumab, golimumab

Question 31

Describe the complications of ulcerative colitis

Answer 31

• Toxic megacolon: this is an acute form of colonic distension and patients can become septic and perforate. Requires supportive care, bowel rest, NG decompression and antibiotics. Requires a colectomy if no improvement within 24-48 hours
• Perforation: associated with high mortality
• Colonic adenocarcinoma
• Strictures and obstruction:bowel loops can develop strictures following chronic inflammation and this can lead to bowel obstruction
• Extraintestinal manifestation (refer to signs^)

Question 32

Describe the prognosis of ulcerative colitis

Answer 32

There does not appear to be an increased rate of mortality in patients with ulcerative colitis. However, the most common cause of death is toxic megacolon. Furthermore, colonic adenocarcinomas develop in 3-5% of patients

Question 33

Describe the UC CLOSEUP pneumonic for UC

Answer 33

C–Continuous inflammation

L–Limited to colon and rectum

O–Only superficial mucosa affected

S–Smoking is protective

E–Excrete blood and mucus

U–Useaminosalicylates

P–Primary Sclerosing Cholangitis

Question 34

Describe the symptomatic differences and similarities between UC and Crohn’s disease

Answer 34

UC and Crohn’s both have abdominal pain.

UC has bloody diarrhoea whereas Crohn’s disease is usually non-bloody diarrhoea

UC involves mucus and weight loss

Crohn’s disease involves significant weight loss and aphthous ulcers

Question 35

Describe the impact smoking has on UC and Crohn’s disease

Answer 35

UC smoking reduces risk

Crohn’s disease smoking increases risk

Question 36

Describe the differences in pathology between UC and Crohn’s disease

Answer 36

UC starts in the rectum and spreads proximally towards the ileocaecal valve. Never spreads into the small bowel or anus.

Crohn’s disease is any part of the GI tract and skip lesions may be seen. Tends not to involve the rectum

Question 37

Where is the most common location for both UC and Crohn’s disease

Answer 37

UC rectal involvement is almost universal

Crohn’s disease is terminal ileum

Question 38

Describe the differences in endoscopic findings between UC and Crohn’s disease

Answer 38

UC - shallow ulcers with pseudopolyps

Crohn’s disease - mucosal inflammation, deep ulcers, skip lesions and cobblestone mucosa

Question 39

Describe the difference in histology between UC and Crohn’s disease

Answer 39

UC - mucosal and submucosal ulceration only. Crypt abscess with neutrophil infiltration

Crohn’s disease - transmural inflammation, granulomas and goblet cells

Question 40

Describe the difference in specific extra-intestinal features between Crohn’s and UC

Answer 40

UC - primary sclerosing cholangitis and cholangiocarcinoma (can occur in Crohn’s disease but is much rarer)

Crohn’s disease - gallstones due to reduced bile reabsorption. Calcium oxalate renal stones

Question 41

What are the shared extra-intestinal features between UC and Crohn’s disease

Answer 41

Arthritis, uveitis, episcleritis, erythema nodosum, pyoderma gangrenosum

Question 42

Describe the different complications of UC and Crohn’s disease

Answer 42

UC - toxic megacolon and strictures

Crohn’s disease - fissures, fistulas and strictures

Question 43

What are the risks of colorectal cancer for UC and Crohn’s disease

Answer 43

UC - marked increase

Crohn’s disease - slight increase

Question 44

Describe the impact surgery has on UC and Crohn’s disease

Answer 44

UC- curative

Crohn’s disease - for complications such as strictures

Question 45

Define irritable bowel syndrome

Answer 45

Irritable bowel syndrome (IBS) is a chronic condition characterised by abdominal pain associated with bowel dysfunction. It is a functional bowel disorder (there is no identifiable organic disease underlying the symptoms).

• IBS-C - with constipation
• IBS-D - with diarrhoea
• IBS-M - with constipation and diarrhoea

Question 46

Describe the epidemiology of IBS

Answer 46

• It is very common and occurs in up to 20% of the population.
• Common, in western world around 1 in 5 report symptoms consistent with IBS
• It affects women more than men
• More common in younger adults <40 years

Question 47

Describe the exacerbating factors for IBS

Answer 47

• Acute gastroenteritis
• Stress
• Menstruation

Question 48

Describe the pathophysiology of IBS

Answer 48

Abdominal pain:

Patients have “visceral hypersensitivity,” which means that the sensory nerve endings in the intestinal wall have an abnormally strong response to stimuli like stretching during and after after a meal.

Abnormal bowel motility:

Eating FODMAPs (fermentable oligo-, di-, mono-saccharides and polyols) often trigger the symptoms. These unabsorbed short-chain carbohydrates act as solutes that draw water across the gastrointestinal wall and into the lumen.

In addition to triggering visceral hypersensitivity which causes pain, that excess water can also cause smooth muscle lining in the intestines to spasm, and create diarrhoea if the excess water is not reabsorbed back into the body.

In addition, the unabsorbed short-chain carbohydrates are often metabolised by gastrointestinal bacterial flora which produce gas that could trigger more bloating, spasm, or pain.

Question 49

Describe the clinical manifestations of IBS

Answer 49

Symptoms are chronic: >6 months

• Signs
  
  • General abdominal tenderness may be felt.
• Symptoms
  
  • Fluctuating bowel habit
  • Diarrhoea
  • Constipation
  • Incomplete evacuation
  • Urgency
  • Mucus PR
  • Abdominal pain
    
    • Pain worse after eating
    • Improved by opening bowels
  • Bloating

Question 50

Describe the diagnostic criteria for IBS

Answer 50

• Diagnostic criteriaAbdominal pain / discomfort:
  • Relieved on opening bowels, or
  • Associated with a change in bowel habit
  AND 2 of:
  • Abnormal stool passage
  • Bloating
  • Worse symptoms after eating
  • PR mucus

Question 51

What investigations may be done for IBS

Answer 51

• Exclude other pathology
  
  • Normal FBC, ESR and CRP blood tests
  • Faecal calprotectinnegative, excludes inflammatory bowel disease
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer is not suspected or excluded if suspected: colonoscopy

Question 52

What are the differential diagnosis for IBS

Answer 52

• Crohn’s disease
• Ulcerative colitis
• Coeliac disease
• Malignancies

Question 53

What is the lifestyle advice for IBS

Answer 53

• Adequate fluid intake
• Regular small meals
• Reduced processed foods
• Limit caffeine and alcohol
• Low “FODMAP” diet (ideally with dietician guidance)
• Increase fibre if constipation, reduce fibre if diarrhoea
• Avoid sorbitol sweeteners, if diarrhoea
• Eat oats and linseeds if there is a problem with wind
• Trial ofprobioticsupplements for 4 weeks
• Reduce stress
• Increase activity
• Weight loss if obese or overweight

Question 54

What is the pharmacological management for IBS

Answer 54

• First line
  
  • Loperamidefor diarrhoea
  • Laxatives for constipation.
    
    • Avoidlactuloseas it can cause bloating.
    • Linaclotideis a specialist laxative for patients with IBS not responding to first-line laxatives
  • Antispasmodics for cramps e.g.hyoscine butylbromide(Buscopan)
• Second line
  
  • Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night)
• Third line
  
  • SSRIs antidepressants

Question 55

What other options for management of IBS are there

Answer 55

• Peppermint oil can also be used as an antispasmodic
• Cognitive Behavioural Therapy (CBT) is also an option to help patients psychologically manage the condition and reduce distress associated with symptoms.

Question 56

Describe the prognosis for IBS

Answer 56

Patients with IBS have a normal life expectancy, and there are no long-term complications of their disease.

Question 57

When should other diagnoses be considered for IBS

Answer 57

• Age >60 years
• History <6 months
• Family history of cancer
• Anorexia
• Weight loss
• Waking at night with pain/ diarrhoea
• Mouth ulcers
• Abnormal CRP and ESR
• Malaena
• Rectal or abdominal mass

Question 58

Define coeliac disease

Answer 58

Coeliac disease is a systemic autoimmune disorder that affects the small intestine and is triggered by the ingestion of gluten peptides found in wheat, barley, rye and other related grains. Malabsorption is the hallmark of coeliac disease.

Previously known as coeliac sprue.

Question 59

Describe the epidemiology of Coeliac disease

Answer 59

• The estimated prevalence of coeliac disease in European populations is 1-2%, with a prevalence of 1% in the UK.
• Commoner if Irish
• Usually develops in early childhood but can start at any age. Another peak at 50-60 years.

Question 60

What are triggers for coeliac disease

Answer 60

Prolamin’s: gliadin in wheat, hordeins in barley and secalins in rye

Question 61

What are risk factors for coeliac disease

Answer 61

• Family historyof coeliac disease
• HLA-DQ2andHLA-DQ8:95% of patients have HLA-DQ2, and 80% have HLA-DQ8
• Autoimmunity:type 1 diabetes, autoimmune thyroid disease and autoimmune hepatitis
• IgA deficiency:allows increased gluten peptides to circulate in the submucosa
• Down’s syndrome
• Turner’s syndrome

Question 62

Describe the pathophysiology of Coeliac disease

Answer 62

Type 4 hypersensitivity reaction mediated by T cells.
Gluten breaks down to gliadin which triggers the immune system to produce IgA autoantibodies such as anti-tissue transglutaminase (anti-tTG), and anti-endomysial (anti-EMA) which target the epithelial cells of the small bowel causing villous atrophy, crypt hyperplasia, intraepithelial lymphocytes.

Question 63

Describe the clinical manifestations for coeliac disease

Answer 63

• Persistent abdominal symptoms:
  
  • Indigestion
  • Diarrhoea (watery) or steatorrhoea (pale, floating stools)
  • Abdominal bloating or discomfort
  • Constipation
• Prolonged fatigue
• Unexpected weight loss
• Failure to thrive in children
• Severe or persistent mouth ulcers
• Dermatitis herpetiformis: itchy vesicular skin eruption caused by IgA antibodies attacking tTG in the epidermis.
• Anaemia secondary to iron, B12 or folate deficiency
• Rarely coeliac disease can present withneurological symptoms:
  
  • Peripheral neuropathy
  • Cerebellar ataxia
  • Epilepsy

Question 64

Describe the gold standard investigations for coeliac disease

Answer 64

• Small bowel histology: endoscopy and duodenal biopsy is thegold-standarddiagnostic test
  
  • All patients with positive serology should be referred for biopsy
  • Classic findings include 1) villous atrophy; 2) crypt hyperplasia; 3) an increase in intraepithelial lymphocytes; 4) lamina propria infiltration with lymphocytes
  • The Marsh histological classification is used

Question 65

Describe the first line investigations for coeliac disease

Answer 65

If possible, patients should beona gluten-containing diet for 6 weeks prior to investigations.

ALL new cases of type 1 diabetes are investigated, even if they don’t have symptoms as the conditions are often linked.

- **Tissue transglutaminase antibodies (tTG; IgA) and total IgA:**
    - **First-line**serological test is for IgA antibodies against tTG
    - Total IgA must also be measured as a small proportion of patients are IgA deficient, which would give a false negative anti-tTG measurement
- **Endomysial antibodies (IgA):**
    - **Second-line**serological test and performed if anti-tTG is weakly positive
    - **Anti-tTG, endomysial, or gliadin (IgG) antibodies:**
    - If patients are**IgA deficient**, then IgG antibodies against tTG, gliadin or endomysium can be measured
- **Anti-casein antibodies**:
    - Also found in some patients

Question 66

What are other investigations to consider with coeliac disease

Answer 66

• FBC: typically a microcytic anaemia. Alternatively, folate or vitamin B12 deficiency can result in macrocytic anaemia
• Nutritional status:25-hydroxy vitamin D, calcium, iron studies, Vitamin B12, folate
• Skin biopsy:if there is evidence of possible dermatitis herpetiformis
• HLA testing:DQ2 or DQ8**testing is only performed in a specialist setting

Question 67

Describe the management for coeliac disease

Answer 67

Gluten-free diet: this involves the avoidance of the following

• Wheat: bread, pastry and pasta
• Rye
• Barley: beer (whisky is made using malted barley but issafeto drink as gluten is removed in the distillation process)
• Oats: this remains controversial but may be required in some patients

Dietary supplements:

• Patients should receive calcium, vitamin D and iron supplementationifthe patient’s diet is insufficient

Dietician input:

• Patients may be offered input regarding their diet and risks associated with non-compliance with dietary measures

Refer to a specialist:

• If symptoms persist despite a gluten-free diet or significant extra-intestinal manifestations, the patient may require referral to a gastroenterologist

Question 68

What other management steps may be taken for coeliac patients

Answer 68

Vaccinations:

• Due to functional hyposplenism, coeliac patients are at risk of pneumococcal infection so should all be offered vaccination, with a booster every 5 years;influenza vaccinationis offered on an individual basis

Question 69

Describe the management for coeliac disease

Answer 69

• Check-ups to instruct and monitor their gluten-free diet adherence.
• DEXA scan to monitor osteoporotic risk

Question 70

Describe the complications with coeliac disease

Answer 70

Osteopenia, anaemia, malignancy (T cell lymphoma, NHL), vitamin deficiency

Question 71

Describe the prognosis for coeliac disease

Answer 71

Coeliac disease generally has a very good prognosis, with theresolution of symptoms in up to 90% of patients on a gluten-free diet. Rates of adherence have improved with the increased availability of gluten-free products.

The 10-30% of patients that remain symptomatic often have other intolerances such as lactose, fructose, sucrose, or sorbitol intolerance.

1-2% have refractory coeliac disease.

The importance of a gluten-free diet must be emphasised to patients, as the risk ofmalignancynormalises after a few years of gluten restriction. Villous atrophy and immunology usually reverse on a gluten-free diet.

Question 72

Describe the layers of the GI tract

Answer 72

Normally, the wall of the entire gastrointestinal tract is made of 4 layers: the inner mucosa (innermost epithelial layer, a middle lamina propria, and outermost muscularis mucosa), the submucosa, a muscular layer, and an outer layer called the adventitia.

Question 73

Describe the composition of the stomach mucosa

Answer 73

• The epithelial layer is made up of cylindrical cells, which dive into the lamina propria, forming pits (gastric glands).
• Among the cylindrical gland cells, there are different types of secretory cells:
  
  • G cells: secrete gastrin
  • Parietal cells: secrete HCl
  • Chief cells: secrete pepsinogen
• There are also defence mechanisms:
  
  • Foveolar cells: secrete mucus containing bicarbonate
  • Rich in vessels: to get access to O2 and bicarbonate from the blood supply

Question 74

Describe the composition of oesophageal mucosa

Answer 74

• Made up of stratified squamous epithelium, which is better equipped to resist abrasion from food going down.
• Epithelium doesn’t have defence mechanisms, like the stomach - so it’s more susceptible to acid damage.
• Defence mechanism of the oesophagus:
  
  • Lower oesophageal sphincter: opens to pass food to stomach and closes to prevent acid reflux.
  • Saliva also helps to neutralise the acidity

Question 75

Define gastro-oesophageal reflux disease (GORD)

Answer 75

Reflux of stomach contents into the oesophagus.

Question 76

Describe the epidemiology of GORD

Answer 76

In Western European and Northern American populations, the estimated prevalence is as high as 10-20%.

Question 77

Describe the aetiology of GORD

Answer 77

• Lower oesophageal hypotension
• Oesophageal dysmotility
• Gastric acid hypersecretion

Question 78

Describe the risk factors of GORD

Answer 78

• High BMI
• Genetic association
• Pregnancy
• Smoking
• NSAIDs, caffeine & alcohol
• Other medication (may lower LOS pressure) e.g. antihistamines, calcium channel blockers, antidepressants, benzodiazepines, and glucocorticoids.
• Hiatus hernia: part of the upper stomach pushes up through the diaphragm (lowering pressure of LOS)
• Scleroderma: muscle of the lower oesophageal sphincter is replaced by connective tissue, so it can’t contract properly.
• Zollinger-Ellison syndrome: increased gastrin causes increased HCl secretion

Question 79

Describe the pathophysiology of GORD

Answer 79

Physiology:

Normally the oesophagus propels food into the stomach by peristalsis. At the gastro-oesophageal junction, a sphincter relaxes to allow food to enter the stomach. This is known as thelower oesophageal sphincter(LOS). After entry, the sphincter contracts to prevent reflux of stomach contents.

If the LOS relaxes inappropriately (becomes loose due to drop in pressure), stomach content willwash back into the oesophagus. This is a normal physiological response in most people. The episodes are brief and do not causes symptoms.

Pathology:

When the pressure of the LOS gets lower, reflux persists for longer, becoming pathological. Persistentacid reflux damages the oesophageal mucosa, causing local inflammation, or oesophagitis. This in turn, causes oedema and erosion of the mucosa, which leads to more complications.

As the epithelium is damaged, it is replaced by scar, making the walls thicker and the lumen narrower (oesophageal stenosis).

As it’s damaged, there may also be a change in the cells of the epithelium (Barret’s oesophagus), and may even eventually lead to adenocarcinoma.

Question 80

Describe the clinical manifestations of GORD

Answer 80

• Heartburn
  
  • Usually worse when lying down and after meals
• Regurgitation
• Dyspepsia
• Chest pain/ retrosternal or epigastric pain
• Bloating
• Dysphagia(difficulty swallowing)
• Odynophagia(painful swallowing)
• Nausea and/or vomiting
• Water brash: mouth fills with saliva
• Cough: reflux goes into the respiratory tract
• Hoarse voice: reflux goes into the respiratory tract

Question 81

Describe the investigations for GORD

Answer 81

• Can be diagnosed based on clinical presentation and based on whether PPI trial would resolve the symptoms
• pH monitoring
  
  • 24-hour pH monitoring: small tube inserted through the nose and positioned in lower oesophagus. Can be combined with high resolution manometry (assesses motor abnormalities of the oesophagus).
  • Wireless pH capsules testing: insertion of pH capsule at gastro-oesophageal junction during endoscopy. Carry recording device to capture episodes. Will naturally fall off wall of oesophagus and pass through GI tract.
• Endoscopy
  
  • Able to diagnose the presence of oesophagitis, Barrett’s oesophagus or an alternative diagnosis (i.e. oesophageal/gastric malignancy).
  • Usually reserved for patients with red flags symptoms, suspected complications, symptoms refractory to treatment or those being considered for surgery.

Question 82

Describe the red flags for GORD

Answer 82

• New onset dyspepsia(>55 years)
• Weight loss
• Dysphagia
• Upper abdominal pain
• Nausea and vomiting
• Symptoms refractory to treatment
• Anaemia
• Raised platelet count

Question 83

Describe the differential diagnosis of GORD

Answer 83

• Functional heartburn
• Achalasia(failed relaxation of LOS)
• Eosinophilic oesophagitis
• Peptic ulcer disease
• Non-ulcer dyspepsia
• Malignancy
• Pericarditis
• Ischaemic heart disease

Question 84

Describe the lifestyle changes patients need to make with GORD

Answer 84

• Weight loss
• Smoking cessation
• Dietary modification: Smaller meals. Reduce tea, coffee, alcohol, spicy foods, fizzy drinks, chocolate
• Patients should avoid eating within two hours of sleep
• Patients should elevate the head of the bed

Question 85

Describe the medical and surgical management for GORD patients

Answer 85

• Medical
  
  • PPI: prevent acid production within the stomach through inhibition of H+/K+ ATPases in parietal cells.
  • H2 receptor antagonist e.g. ranitidine: reduces stomach acid
  • Antacids e.g. gaviscon: neutralise stomach acid
• Surgical
  
  • Nissen fundoplication: wrapping the fundus of the stomach around the lower oesophagus to tighten the sphincter
    
    • SE: dysphagia, gas-bloat syndrome (inability to belch/vomit), new-onset diarrhoea

Question 86

Describe the complications for GORD

Answer 86

Oesophageal:

• Typical reflux syndrome
• Reflux chest-pain syndrome
• Reflux oesophagitis(inflammation and damage of oesophageal mucosa, which can lead to ulcers, bleeding and peptic stricture formation.)
• Reflux stricture(narrowing of oesophagus, can cause dysphagia. May require dilatation or stenting.)
• Barrett’s oesophagus(premalignant condition in the oesophagus due to columnar metaplasia)
• Oesophageal adenocarcinoma

Extra-oesophageal:

• Reflux cough syndrome
• Reflux laryngitis syndrome: reflux goes all the way up to throat and down the larynx
• Reflux asthma syndrome
• Reflux dental erosion syndrome: acid refluxes far enough to erode the teeth enamel
• Proposed associations: idiopathic pulmonary fibrosis, sinusitis, etc

Question 87

Describe the prognosis for GORD

Answer 87

Most patients respond to treatment with proton-pump inhibitors (PPIs). Maintenance PPI therapy is recommended for those who have symptoms when the PPI is discontinued, as well as for those with erosive oesophagitis and Barrett’s oesophagus.

Most patients relapse off PPI therapy but this has to be balanced with the risk of long-term drug use.

Oesophageal adenocarcinoma may be a serious though rare complication of GORD.

Question 88

Define Barret’s oesophagus

Answer 88

Barrett’s oesophagus describes metaplasia (transformation of one differentiated cell type to another differentiated cell type) of the lower oesophageal lining from stratified squamous epithelium to mucous secreting columnar epithelium with goblet cells.

Barrett’s is classified as short segment (< 3 cm) and long segment (> 3 cm).

Question 89

Describe the epidemiology of Barret’s oesophagus

Answer 89

• Around 1 in 10 patients who experience GORD have Barrett’s oesophagus on endoscopy
• Estimated to affect 0.9-10% of the general population
• M>F
• More common in Caucasians

Question 90

Describe the risk factors for Barret’s oesophagus

Answer 90

• Gastro-oesophageal reflux disease:the single greatest risk factor for developing Barrett’s oesophagus
• Age
• Male sex
• Caucasian
• Smoking
• Obesity
• Family history

Question 91

Describe the pathophysiology of Barret’s oesophagus

Answer 91

The lower oesophagus marks the junction between oesophagus and stomach. Tonic contractions of the lower oesophageal sphincter, coupled with extrinsic compression of the right crus of the diaphragm, are important toprevent acidic stomach content from entering the oesophageal lumen.

These mechanisms are not perfect and a small amount of reflux of stomach content (i.e. the refluxate) is common, but usually not associated with symptoms. Prolonged exposure to the refluxate can lead to symptomaticgastro-oesophageal reflux disease, oesophagitis and erosions.

In addition, chronic damagecan lead to transformation of normal squamous epithelium into metaplasticcolumnar epithelial cells (Barret’s oesophagus)

Metaplasia is an adaptive response to acid in order to protect the oesophageal wall, however, it also predisposes to subsequent dysplasia and oesophageal adenocarcinoma.

Adenocarcinoma may occur through further reflux-associated DNAdamage, genetic alterations and uncontrolled cellular proliferation.

Question 92

Describe the clinical manifestations of Barret’s oesophagus

Answer 92

No specific symptoms or signs associated with Barrett’s oesophagus. It is typically diagnosed on endoscopy for upper gastrointestinal (GI) symptoms.

• Symptoms of GORD
  
  • Heartburn:
    
    • ‘Burning’ epigastric and retrosternal chest pain
    • Worse with spicy meals and lying flat
    • Wakes the patient up from sleep
  • Indigestion (dyspepsia)
  • Regurgitation: sour taste in mouth
  • Chest discomfort
  • Hoarseness of voice
  • Cough: reflux-induced
  • Dysphagia: suggestive of stricture or malignancy in context of BO

Question 93

Describe the investigations for Barret’s oesophagus

Answer 93

Upper GI endoscopy (OGD) and biopsy:

• Typically performed in patients with chronic GORDandadditional risk factors such as age and obesity
• On endoscopy,normalstratified squamous epithelium is smooth and pale but, in Barrett’s, the squamocolumnar junction ispink-red
• Biopsy isdiagnosticand reveals metaplasia fromsquamous to glandular columnar epitheliumin the distal oesophagus, which resembles the cardia of the stomach or small intestine, withgoblet cellsand abrush border
• Biopsies should be quadrantic and at 2cm intervals (Seattle protocol): increases chance of detection

Question 94

Describe the prague criteria classification for Barret’s oesophagus

Answer 94

The Prague criteria refers to the endoscopic description of BO, which is divided into two components:

• Circumferential (C) extent: maximal circumferential height of BO
• Maximal (M) length: refers to the longest segment of BO

and length:

• Short segment Barrett’s(< 3cm)
• Long segmentBarrett’s(> 3cm)

Question 95

Describe the management for underlying reflux

Answer 95

• Management of underlying reflux
  
  • Lifestyle changes:weight loss, smoking cessation, alcohol abstinence
  • Proton pump inhibitor:omeprazole or lansoprazole; usually high dose

Question 96

Describe the management for non-dysplastic Barrett’s oesophagus

Answer 96

Repeat surveillance endoscopy: at least every 5 years or sooner depending on the length of oesophagus affected (usually every 3-5 years)

Question 97

Describe management for low-grade dysplasia

Answer 97

• Repeat endoscopy: every 6 months
• Endoscopic therapy:radiofrequency ablation (to destroy epithelium and replace with new cells) or mucosal resection may be considered if high-grade dysplasia develops. If there is no longer any dysplasia over 2 consistent endoscopies, the patient can be followed-up under the non-dysplastic pathway.

Question 98

Describe the management for high-grade dysplasia

Answer 98

• Radiofrequency ablation:typically for flat lesions
• Endoscopic mucosal resection:typically for raised lesions

Question 99

Describe the management for adenocarcinoma

Answer 99

Oesophagectomy: surgical intervention is indicated in non-metastatic disease

Question 100

Describe the complications with Barrett’s oesophagus

Answer 100

• Associated with a50-100 foldincreased risk of oesophageal adenocarcinoma.
• Endoscopic complications: oesophageal rupture, or stricture development

Question 101

Describe the prognosis for Barrett’s oesophagus

Answer 101

Oesophageal adenocarcinoma is unfortunately associated with a poor prognosis as it is often detected at an advanced stage. This explains the rationale behind surveillance of patients with Barrett’s oesophagus.

It is estimated that up to 13% of patients with Barrett’s oesophagus will develop oesophageal adenocarcinoma.

Question 102

Describe the anatomy of the oesophagus

Answer 102

The oesophagus is a long tube going from the pharynx to the stomach, and it’s connected to the pharynx through the upper oesophageal sphincter, and to the stomach through the lower oesophageal sphincter.

Both relax during swallowing to allow the passage of food or liquids.

Additionally, the lower oesophageal sphincter is tightly closed between meals to prevent acid reflux.

The oesophageal wall has four layers - the adventitia; the muscular layer; the submucosa and the mucosa.

The mucosa comes into direct contact with food, and it protects the oesophageal wall from friction.

The mucosa also has three layers of its own: stratified squamous epithelium; the lamina propria; and the muscularis mucosae.

Finally, at the lower esophageal sphincter, the squamous epithelium joins the columnar gastric epithelium to form the gastroesophageal junction.

Question 103

Define malignant oesophageal tumours

Answer 103

Oesophageal cancer is when malignant or cancerous cells arise in the oesophagus. It is divided into adenocarcinoma and squamous cell carcinoma.

Question 104

Describe the epidemiology of malignant oesophageal tumours

Answer 104

• M>F
• Occurs mainly in those aged 60-70 years. Peak incidence around 80 years of age
• Adenocarcinoma is the commonest type in the Western world, whilst SCC is more common in countries such as Japan.

Question 105

Describe the general risk factors for malignant oesophageal tumours

Answer 105

• Age > 60
• Smoking
• Achalasia

Question 106

Describe the risk factors for adenocarcinoma

Answer 106

• Barret’s oesophagus:metaplasia from squamous epithelium to mucus-secreting columnar epithelium secondary toGORD
• Obesity
• Male sex
• Smoking
• Rare causes:coeliac disease and scleroderma

Question 107

Describe the risk factors for squamous cell carcinoma

Answer 107

• Smoking:more associated with SCC
• Alcohol
• Achalasia
• Plummer-Vinson syndrome: rare disease characterised by difficulty swallowing, iron-deficiency anaemia, glossitis, cheilosis and oesophageal webs.
• Palmoplantar keratoderma: thick patches of skin develop on the hands and feet.
• Hot beverages
• Nitrosamines(dietary)
• Caustic strictures: strictures caused by caustic ingestions e.g. household bleach

Question 108

Describe the pathophysiology of squamous cell carcinoma

Answer 108

Arises from squamous epithelium.

Most often in the upper two thirds.

When this epithelium is repeatedly exposed to risk factors like alcohol, cigarette smoke, or hot fluids, it gets damaged, so the squamous cells divide to replace the old damaged cells.

With each division, there is a risk that a mutation can occur. Mutations can occur in tumour suppressor genes or proto-oncogenes.

When this happens, squamous cells start dividing uncontrollably, and more mutations accumulate with each division.

Eventually, these mutations might make the cells malignant.

Question 109

Describe the pathophysiology of oseophageal adenocarcinomas

Answer 109

Adenocarcinoma arises from columnar glandular epithelium.

Most often in the lower third of the oesophagus.

Most frequently, adenocarcinoma develops as a consequence of GORD

With GORD, the lower oesophageal sphincter is weaker than normal, and it allows acid from the stomach to go back up into the oesophagus after meals.

The presence of acid in the oesophagus can lead to Barrett’s oesophagus, which is when the squamous epithelium lining the oesophagus undergo metaplasia.

Over time, mutations might accumulate in either tumour suppressor genes or proto-oncogenesthat control the division of thesemetaplastic cells, ultimately resulting in a malignant tumour.

Question 110

Describe the clinical manifestations of malignant oesophageal tumours

Answer 110

Patients often present late and have unresectable disease on presentation.

• Signs
  
  • Lymphadenopathy
  • Vocal cord paralysis
  • Melaena on digital rectal examination: due to bleeding oesophageal cancer
• Symptoms
  
  • Progressive dysphagia (solids then liquids): most common feature
  • Regurgitation
  • Pyrosis (heartburn)
  • Pain in chest or back
  • Odynophagia
  • Weight loss and anorexia
  • Hoarseness: with recurrent laryngeal nerve involvement
  • Vomiting

Question 111

Describe the investigations for malignant oesophageal tumours

Answer 111

• 1st line
  
  • Upper GI endoscopy (OGD) and biopsy: first-line investigation and allows for visualisation of masses and biopsy
• Staging investigations
  
  • Barium swallow: to see strictures
  • CT chest, abdomen and pelvis (CAP): first-linestaginginvestigation in order to detect metastatic disease
  • Endoscopic ultrasound (EUS):NICE suggests considering staging ultrasound to guide further management. It can aid detection of local invasion and lymphatic spread
  • Staging laparoscopy: NICE suggests considering staging laparoscopy to guide further management. It may aid in detecting occult peritoneal disease
  • PET CT: offered to all patients with oesophageal cancer who are suitable for curative surgery to rule out metastasis
  • HER2 testing: patients with HER2-positive metastatic oesophageal cancer may be responsive to trastuzumab(Herceptin)
• StagingStaged using TNM

Question 112

Describe the management for localised adenocarcinomas

Answer 112

• Endoscopic mucosal resection:only for very early lesions or for Barrett’s oesophagus
• Ivor Lewis oesophagectomy:the most common procedure and performed forlower thirdlesions. The stomach is mobilised into the thorax with the formation of an intrathoracic oesophagogastric anastomosis. Involves a lateral thoracotomy (incision to chest), and laparotomy (incision to abdomen)
• McKeown oesophagectomy:performed forproximaltumours. The stomach is mobilised into the thorax with the formation of a cervical oesophagogastric anastomosis. Involves an incision in the neck, lateral thoracotomy, and laparotomy
• Transhiatal oesophagectomy:carried out fordistaltumours. The stomach is mobilised into the thorax with the formation of a cervical oesophagogastric anastomosis. Involves an incision in the neck and laparotomy
• Chemotherapy:offered toallsurgical patients preoperatively (neoadjuvant) and may be given post-operatively (adjuvant)

Question 113

Describe the management for squamous cell carcinoma

Answer 113

Radical chemoradiotherapy: localised SCC can be treated with curative chemoradiotherapy, although surgical resection may be offered

Question 114

Describe the management for advanced or metastatic disease

Answer 114

• Palliation: stenting for dysphagia
• Chemotherapy or chemoradiotherapy: platinum-based agents
• Trastuzumab (Herceptin): for HER2 positive metastatic oesophageal cancer, in combination with chemotherapy

Question 115

Describe the complications with malignant oesophageal tumours

Answer 115

Cancer-related:

• Tracheo-oesophageal or broncho-oesophageal fistula: when the cancer invades and perforates the entire oesophageal wall, it can invade the trachea in front of it, forming a fistula. This can cause pulmonary aspiration of oesophageal contents, which may cause symptoms like coughing and dyspnea.
• Aspiration pneumonia:oesophageal obstruction may result in aspiration
• Metastasis:lymph nodes, liver, lung, bones. If the cancer spreads to the diaphragm, it can cause hiccups.

Oesophagectomy-related:

• Anastomotic leak: A leak may result in mediastinitis, which is associated with considerable morbidity and mortality and can result in profound sepsis
  
  • Ivor-lewis oesophagectomy: potentially catastrophic if an anastomotic leak occurs, due to leakage of contents into the thorax (mediastinitis)
  • McKeown oesophagectomy: the complications of a leak are less severe as the anastomosis is in the neck so it does not result in mediastinitis
• Recurrent laryngeal nerve injury: proximity of this nerve to the oesophagus places it at risk, either due to invasion of the tumour or iatrogenic injury
• Delayed gastric emptying:thought to be caused by bilateral vagotomy (one or more branches of the vagus nerve are cut) during the procedure which impairs gastric motility

Question 116

Describe the prognosis of malignant oesophageal tumours

Answer 116

Unfortunately, the majority of oesophageal cancers are diagnosed at an advanced stage.

5-year survival is 15% but those who are diagnosed with early-stage disease have a survival rate of 55%

Question 117

Describe the epidemiology of benign oesophageal tumours

Answer 117

• Account for 1% of all oesophageal tumours
• Leiomyomas are most common
• Papillomas
• Fibrovascular polyps
• Haemangiomas
• Lipomas

Question 118

Describe the epidemiology of leiomyomas

Answer 118

Leiomyomas:

• Smooth muscle tumours arising from the oesophageal wall
• They are intact, well encapsulated and are within the overlying mucosa
• Slow growing

Question 119

Describe the clinical manifestations of benign oesophageal tumours

Answer 119

• Usually asymptomatic, found incidentally on barium swallow
• Dysphagia
• Retrosternal pain
• Food regurgitation
• Recurrent chest infections

Question 120

Describe the investigations for benign oesophageal tumours

Answer 120

• Endoscopy and biopsy: to rule out malignancy
• Barium swallow

Question 121

Describe the management for oesophageal tumours

Answer 121

• Endoscopic removal
• Surgical removal of larger tumours

Question 122

What is a barium swallow

Answer 122

Also called an esophagogram and is an imaging test that checks for problems in your upper GI tract

Question 123

What are the 4 regions of the stomach

Answer 123

The stomach has four regions: the cardia, the fundus, the body, and the pyloric antrum.

There’s also a pyloric sphincter at the end of the stomach, which closes while eating, keeping food inside for the stomach to digest.

Question 124

What are the 4 layers of the gastric wall

Answer 124

The gastric wall is made up of four layers:

The adventitia; the muscular layer; the submucosa; and the mucosa.

Question 125

Describe the layers of the mucosa

Answer 125

The mucosa has three layers of its own.

• The innermost layer is the epithelial layer and it absorbs and secretes mucus and digestive enzymes.
• The middle layer is the lamina propria and it has blood, lymph vessels, and mucosa associated lymphoid tissue, which are nodules of immune cells called lymphocytes, in charge of eliminating pathogens that could pass through the epithelial layer.
• The outermost layer of the mucosa is the muscularis mucosa, and it’s a layer of smooth muscle that contracts and helps with the break down food.

Question 126

Describe the epithelial layer of the stomach and the cells within it

Answer 126

The epithelial layer dips down below the surface of the stomach lining to form gastric pits. And these pits are contiguous with gastric glands below which contain various epithelial cell types, each secreting a variety of substances.

• Foveolar cells secrete mucus
• Parietal cells secrete hydrochloric acid
• Chief cells secrete pepsinogen
• G cells secrete gastrin

Question 127

Describe the types of gastric cancer

Answer 127

Gastric cancer is when malignant or cancerous cells arise in the stomach.

This cancer can appear in any part of the stomach and it’s classified into adenocarcinoma (most common), lymphoma, carcinoid tumour, and leiomyosarcoma; depending on the type of cells it originates from.

Question 128

Define gastric adenocarcinoma

Answer 128

Gastric adenocarcinomas arise from columnar glandular epithelium (adeno = gland)

Adenocarcinomas are divided into intestinal, or well-differentiated adenocarcinoma; and diffuse, or undifferentiated adenocarcinoma. Intestinal is the most common!

Question 129

Describe the epidemiology of gastric adenocarcinoma

Answer 129

• Gastric cancer is most common in Japan and is the 5th most common cancer worldwide.
• Other countries with a high incidence include China, Finland and Colombia.
• Whilst the overall incidence is decreasing, the incidence of tumours affecting the cardia is increasing.
• Currently, cancers of the antrum remain the commonest.
• M>F

Question 130

Describe the risk factors of gastric adenocarcinoma

Answer 130

Modifiable risk factors:

• H. pylori infection: commonest cause, accounting for 60% of cases
• Smoking
• Alcohol
• Diet: smoked and preserved foods (N-nitroso compounds), nitrosamines; salty and spicy foods
• Obesity

Non-modifiable risk factors:

• Male gender: gastric cancer is twice as common in males
• Increasing age: peak age of diagnosis is 70-80 years old
• Family history
• Pernicious anaemia: associated with a 2- to 3-fold increased risk of gastric cancer
• Blood type A
• Gastric adenomatous polyps: most common neoplastic polyp
• Lynch syndrome II: hereditary non-polyposis colorectal cancer
• Autoimmune gastritis: immune system attacks the parietal cells, causing inflammation
• Achlorhydria: decreased or lack of gastric acid production

Question 131

Describe the pathophysiology of intestinal type gastric adenocarcinoma

Answer 131

Most commonly caused by H.pylori

H.pylori releases virulence factors, such as cagA, that go inside the epithelial cells and cause extensive damage.

The immune system detects this damage and cause an inflammatory response within the gastric lining, causinggastritis. The infection persists, leading to chronic gastritis.

The normal epithelium of the stomach gets continuously damaged and repaired. Over time, the stomach cells in the epithelium undergo metaplasia. These metaplastic cells might accumulate mutations in the genes that are in charge of thecell cycle and cell division.

Tumor suppressor genes and proto-oncogenes can experience mutations and the metaplastic cells divide uncontrollably and may become malignant.

Intestinal types are well differentiated - meaning they resemble normal intestinal cells.

This type typically appears on the lesser curvature of the antrum as a large, irregular ulcer, with heaped up edges.

Question 132

Describe the pathophysiology of diffuse gastric adenocarcinoma

Answer 132

Appear in any part of the stomach

Mostly related to genetic mutations in the CDH1 gene, a tumor suppressor gene that codes for a membrane adhesion molecule called E-cadherin. Normally, E-cadherin helps epithelial cells stick to one another and it also transmits signals that control the progression of cell cycle.

When E-cadherin isn’t working properly, cells detach and starts dividing uncontrollably.

This type of adenocarcinoma has an increased ability to spread and invade adjacent structures, so it’s way more aggressive than the intestinal type.

This type can cause gastric linitis plastica, where the stomach wall grow thick and hard and look like a leather bottle, as the cancer invades the connective tissue of the submucosa.

Histologically, there’s ‘signet ring cells’: they look like a signet ring because the cytoplasm has giant vacuoles that push the nucleus to the edge of the cell.

Question 133

Describe the clinical manifestations of gastric adenocarcinoma

Answer 133

Early stages may be asymptomatic so many patients present late!

• Signs
  
  • Iron deficiency anaemia: koilonychia (spoon nails), pallor, angular cheilitis (swollen patches in corner of mouth)
  • Palpable mass
  • Melaena on digital rectal examination
  • Acanthosis nigricans: darkening of the skin at the axilla and other skin folds.
  • Troisier’s sign: an enlarged, hard Virchow’s node (left supraclavicular node)
  • Leser-Trelat sign: sudden onset seborrhoeic keratosis (brown patches on skin)
  • Polyarteritis nodosa: inflammation, weakening, and damage to small and medium-sized arteries.
  • Trousseau syndrome: blood clotting disorder
• Symptoms
  
  • Malaise
  • Loss of appetite
  • Anorexia and weight loss
  • Dyspepsia
  • Abdominal pain
  • Difficulty swallowing
  • Early satiety
  • Nausea and vomiting
  • May be malaena and haematamesis: if cancer ulcerates and bleeds

Question 134

What are the investigations for gastric adenocarcinoma

Answer 134

• 1st line
  
  • Upper GI endoscopy and biopsy: ulcer with heaped-up edges is a common presentation
• Staging investigations
  
  • CT chest, abdomen and pelvis (CAP): if biopsy reveals malignancy, CT imaging is usually the first-line staging investigation to detect metastatic disease
  • PET: offered after CT when metastatic disease is suspected and assists with staging
  • Staging laparoscopy:allpatients with potentially curable disease should have a staging laparoscopy to exclude occult peritoneal metastasis
  • Endoscopic ultrasound:assists with staging, particularly for patients where curative surgery is being considered; recent evidence suggests it may be superior to CT
  • HER2 testing: patients with HER2-positive metastatic gastric cancer may be responsive to trastuzumab(Herceptin)

Question 135

Describe the TNM classification of gastric adenocarcinoma

Answer 135

• TNM classification preferred for gastric tumoursT = tumour size and local extension, N = lymph node metastases, and M = distant metastases.Each of these categories have substages: T0 to T4, from N0 to N3, and M0 or M1, and the combinations of these substages determine the oesophageal cancerstage, from 0 to IV. The higher the number, the more the cancer has invaded and spread.e.g. T1N0M0 = invasion of submucosa but no spread to lymph nodes or distal organs

Question 136

Describe the Siewert’s classification for gastro-oesophageal tumours

Answer 136

Type 1 - carcinoma of the distal oesophagus associated with Barrett’s oesophagus, which infiltrates the GOJ from above and located 1-5cm above the gastric cardia

Type 2 - junctional carcinoma of the cardia. Located 1cm above or 2cm below the gastric cardia; true GOJ tumour

Type 3 subcardial cancer, which indiltrates the GOJ from below and is located 2-5cm below the gastric cardia

Question 137

Describe the differential diagnosis for gastric adenocarcinoma

Answer 137

• Peptic ulcer disease
• Oesophageal stricture
• Achalasia

Question 138

Describe the management for localised gastric adenocarcinoma

Answer 138

• Oesophagogastrectomy: for type 2 GOJ tumours that extend into the oesophagus
• Total gastrectomy: for proximal tumours within 5cm from the GOJ
• Sub-total gastrectomy: if the tumour is >5cm from the GOJ
• Endoscopic submucosal resection: if the tumour is early and confined to the mucosa this may be appropriate but remains controversial
• D2 lymph node dissection: should be considered inallpatients undergoing a curative gastrectomy
• Chemotherapy: offer chemotherapy before and after surgery toallpatients with gastric cancer

Question 139

Describe the management for advanced or metastatic gastric adenocarcinomas

Answer 139

• Chemotherapy or chemoradiotherapy: usually a combination of a platinum compound and fluorouracil
• Palliative gastrectomy
• Trastuzumab (Herceptin): for HER2 positive metastatic gastric cancer, in combination with chemotherapy

Question 140

Describe the complications with gastric adenocarcinoma

Answer 140

Cancer-related:

• Bleeding: patients may present with melaena from a bleeding gastric tumour
• Gastric outlet obstruction: tumour blocks the gastric outlet causing non-bilious post-prandial (after a meal) vomiting
• Perforation: ulceration of a neoplastic lesion can weaken the stomach wall and if left untreated could lead to perforation
• Metastasis: Virchow’s node (left supraclavicular node), lung, liver, peritoneum, ovaries (Krukenberg tumour)
• Leser-Trélat sign: seborrheic keratosis, or brownish spots all over the skin. Results from the stimulation of keratinocytes by growth factors produced by the gastric cancer cells.
• Polyarteritis nodosa: inflammation and necrosis of multiple medium-sized arteries, including those that supply the kidneys and the heart
• Trousseau syndrome: cancer cells stimulate vascular and inflammatory cells to release tissue factor, which then activates the coagulation cascade; therefore, there’s an increase in blood coagulability that leads to thrombosis, or generation of blood clots.
• Pseudoachalasia syndrome: if gastric cancer grows near the gastro-oesophageal junction, it can cause a stricture that makes it difficult for food and liquids to pass through from the oesophagus into the stomach

Question 141

Describe the complications of gastrectomy to treat gastric adenocarcinoma

Answer 141

• Malabsorption:
  
  • Vitamin B12 deficiency (reduced intrinsic factor)
  • Iron deficiency due to reduced conversion of Fe2+to Fe3+in the stomach and hence reduced absorption
• Small bowel bacterial overgrowth:post gastrectomy, a blind-ending bowel loop is created to allow the gall bladder to drain into. Bacterial overgrowth within this portion of the bowel can lead to malabsorption
• Dumping syndrome: occurs when sugar moves too quickly into the small bowel and associated with gastrectomy
  
  • Early dumping syndrome:occurs 30 mins after a meal as fluid moves into the intestine due to the high osmotic load, resulting in dizziness and palpitations
  • Late dumping syndrome: occurs 2 hours after a meal. As glucose is rapidly absorbed in the intestine, this causes reactive hyperinsulinaemia and subsequent hypoglycaemia

Question 142

Describe the prognosis for gastric adenocarcinoma

Answer 142

The 5-year survival for early localised disease is approximately 70%, which decreases to 5% for patients with metastatic disease.

Unfortunately, the majority of gastric cancers are at an advanced stage at diagnosis as it often presents with vague, non-specific symptoms. So is associated with poor prognosis.

Early gastric cancer has a 90% 5 year survival

Stage 1 has a 65% 5 year survival

Stage 2 has a 36% 5 year survival

Stage 3 has a 24% 5 year survival

Question 143

Describe lymphomas

Answer 143

• Lymphoma arises from lymphocytes found in MALT (mucosa-associated lymphoid tissue).
• These cells, more specifically B-cells, are in charge of recognising and responding to any pathogen that crossed past the epithelial layer.
• Infection e.g. chronic H.pyloriinfection, can cause excessive B-cellproliferation, which makes these cells more prone to have mutations and develop lymphoma.
• Histologically, it usually appears as diffuse lymphocytes surrounding the normal lymphoid nodules and epithelial cells.

Question 144

Describe carcinoid tumour

Answer 144

• Originates in the neuroendocrine cell e.g. G-cells of the stomach.
• It’s a well differentiated tumour, that usually appear as a protruding mass from the mucosa, called a polyp.
• Although it mainly appears in the stomach, it can also arise in other parts of the digestive tract like the intestine or the pancreas, which also have G-cells.

Question 145

Describe leiomyosarcoma

Answer 145

• Leiomyosarcoma arises from smooth muscle cells from the gastric wall.
• Extremely rare.
• Under the microscope, cancerous cells can look like spindle, epithelial, or undifferentiated cells.

Question 146

Describe the development of tumours in the small intestine

Answer 146

• Small intestine is relatively resistant to the development of neoplasia
• Quite a rare place for cancer to develop - 1% of all malignancies
• Adenocarcinoma is the most common tumour of the small intestine, accounting for up to 50% of primary tumours

Question 147

Describe where lymphomas are most commonly found

Answer 147

Lymphomas (Non-Hodgkin’s type- B or T cell origin) are most frequently found in the ileum and are less common than adenocarcinomas

Question 148

What are the risk factors of malignant small bowel tumours

Answer 148

• Coeliac disease
• Crohn’s disease

Question 149

Describe the clinical manifestations of malignant small bowel tumours

Answer 149

• Pain
• Diarrhoea
• Anorexia and weight loss
• Anaemia
• May be a palpable mass

Question 150

Describe the investigations for malignant small bowel tumours

Answer 150

• Ultrasound
• Endoscopic biopsy to histologically confirm diagnosis
• CT scan: may show small bowel wall thickening and lymph node involvement - seen in lymphoma

Question 151

Describe the management for malignant small bowel tumours

Answer 151

• Surgical resection
• Radiotherapy

Question 152

What is Peutz-Jeghers syndrome

Answer 152

• Due to germline mutation in tumour suppressor gene STK11
• Autosomal dominant condition with mucocutaneous pigmentation and hamartomatous (benign, local malformation of cells) GI polyps
• Polyps may occur anywhere in the GI tract – most common in small bowel
• May bleed or cause intussusception or may undergo malignant change

Question 153

What are the types of benign small bowel tumours

Answer 153

Small bowel cancer is very rare

• Peutz-Jeghers syndrome
• Adenomas, leiomyomas and lipomas are rare
• Familial adenomatous polyposis

Question 154

How is the large intestine subdivided

Answer 154

Intraperitoneal space - first part of the duodenum, small intestines, transverse colon, sigmoid colon and rectum

Retroperitoneal space - distal duodenum, ascending colon, descending colon and anal canal

Question 155

Define a colonic polyps

Answer 155

A colonic polyp is an abnormal growth of tissue projecting from the colonic mucosa.

Polyps range from a few millimetres to several centimetres and are single or multiple

Question 156

Describe the epidemiology of colonic polyps

Answer 156

Polyp presence increases with age and is rare before 30 yrs

Question 157

Describe the pathophysiology of colonic polyps

Answer 157

Mutations in genes e.g. APC gene or DNA repair genes, allow cells to grow unchecked and accumulate further mutations. As they replicate, a growth is formed, known as a polyp.

There are many different types of polyps, and some are more prone to become malignant; these are called pre-malignant or neoplastic polyps.

These pre-malignant polyps can be classified into adenomatous and serrated, according to how they look under the microscope.

Typically, adenomatous polyps have an APC mutation and the cells look like normal colonic mucosa cells, whereas serrated polyps have defects in DNA repair genes and have a saw-tooth appearance.

Question 158

Describe the clinical manifestations of colonic polyps

Answer 158

• Most polyps are asymptomatic and found by chance
• Polyps in the rectum or sigmoid colon often present with bleeding

Question 159

Describe the management of colonic polyps

Answer 159

Polyps are removed at colonoscopy to reduce development into cancer risk

Question 160

Define colorectal cancer

Answer 160

Colorectal carcinoma is a neoplastic growth in the colon or rectum. The majority are adenocarcinomas.

Question 161

Describe the TNM and Dukes’ staging used for colorectal cancer

Answer 161

TNM stage up to T1, N0,M0 = Duke’s stage A = Limited to the submucosa

TNM up to T4, N0M0 = Duke’s stage B = B1: limited to muscular layer B2: growth through serosal layer (transmural)

Any T, N1/N2, M0 = Duke’s stage C = local lymph node involvement

Any T, any N, M1 = Duke’s stage D = distant metastatic spread

Question 162

Describe the epidemiology of colorectal cancer

Answer 162

• Colorectal cancer is the fourth most common UK cancers, behind breast, prostate and lung.
• It is the most common type of cancer of the gastrointestinal tract.
• There are 42,300 new cases in the UK each year.
• 90% of cases are seen in those aged 50 years and above.
• M>F
• More common in Western countries than in Asia or Africa

Question 163

Describe the aetiology of colorectal cancer

Answer 163

• Around 95% are sporadic mutations
• Others can be due to inherited conditions
  
  • Familial adenomatous polyposis (FAP)
  • Hereditary non-polyposis colon cancer (HNPCC)/ lynch syndrome
  • Peutz-Jeghers syndrome (hamartomatous polyposis)

Question 164

What is the inheritance pattern for familial adenomatous polyposis (FAP) and hereditary non-poluposis colon cancer (HNPCC)

Answer 164

Autosomal dominant

Question 165

Describe the prevalence rate of FAP and HNPCC

Answer 165

FAP = 1% of all colorectal cancers

HNPCC = 5% of all colorectal cancers

Question 166

Describe the peak age of onset for FAP and HNPCC

Answer 166

FAP = 20-40 yrs old
HNPCC = >40 yrs old

Question 167

Describe the risk factors of colorectal cancer

Answer 167

• Increasing age
• Male
• Smoking
• Obesity
• Red or processed meats
• Diet low in fibre
• Inflammatory bowel disease
• Polyps
• Hereditary conditions:FAP, HNPCC, Peutz-Jeghers syndrome

Question 168

Describe the pathophysiology of colorectal cancer

Answer 168

• Most cases of colorectal tumours happen because of sporadic mutations
• A small number are caused by known inherited genetic mutations:
  
  • Adenomatous polyposis coli gene (APC) mutations:
    
    • APC is a tumour suppressor gene. Normally, the APC protein identifies when a cell is accumulating a lot of mutations and forces it to undergo apoptosis, or programmed cell death.
    • When the APC gene is mutated, the mutated bowel cells don’t die, and instead some start dividing uncontrollably, giving rise to polyps.
    • Over time, these polyps might accumulate more mutations in other tumour suppressor genes like the K-ras gene or the p53 gene, and ultimately it might might become a malignant tumour.
  • Genetic mutations in DNA repair genes (e.g. MLH-1 and MSH-2)
    
    • When DNA repair genes are mutated - cells accumulate mutations and over time can develop into polyps and eventually adenocarcinomas.
• Essentially, adenocarcinomas are the malignant evolution of polyps, and polyps arise when cells start dividing faster than usual.
• The rectum is the most common site (40%), followed by the sigmoid (30%), descending colon (5%), transverse colon (10%), and ascending colon and caecum (15%).
• Cancers can also metastasise depending on the stage of their disease. The most common site of metastasis for colon cancer is the liver, and for rectal cancer it’s the lungs.

Question 169

Describe the clinical manifestations of right sided colorectal cancer

Answer 169

Right-sided tumours are often asymptomatic, with the majority of patients presenting with incidental iron-deficiency anaemia.

• Signs
  
  • Iron deficiency anaemia: koilonychia, pallor, angular cheilitis
  • May be very largewithoutevident symptoms or signs
• Symptoms
  
  • Progressive change in bowel habit: diarrhoea or constipation; more prominent in left-sided tumours
  • Abdominal discomfort
  • Symptoms of large bowel obstruction: more common in left-sided tumours
  • Constitutional symptoms e.g. weight loss
  • Dyspnoea and fatigue

Question 170

Describe the clinical manifestations of left sided colorectal cancer

Answer 170

Left-sided tumours are particularly associated with a change in bowel habit and have higher rates of rectal bleeding and large bowel obstruction.

• Signs
  
  • Rectal mass
  • Anaemia is rare
• Symptoms
  
  • Progressive change in bowel habit: diarrhoea or constipation; more prominent in left-sided tumours
  • Abdominal discomfort
  • Symptoms of large bowel obstruction: more common in left-sided tumours
    
    • Obstruction causes colicky abdominal pain, constipation, blood-streaked stools if stool is passed, abdominal distension, vomiting (faeculent)
  • Constitutional symptoms e.g. weight loss
  • Rectal bleeding and tenesmus

Question 171

Describe the primary investigations for colorectal cancer

Answer 171

• FBC: may demonstrate microcytic anaemia(iron-deficiency)
• U&Es: renal function may be deranged in advanced pelvic disease
• LFTs: liver function may be deranged in metastatic disease
• Colonoscopy and biopsy: gold standard investigation for diagnosis, and may demonstrate an ulcerating lesion, mucosal lesion that narrows the bowel lumen, or a polyp
• CT colonography: CT with bowel prep and contrast to visualise the colon. Consider in patient less fit for colonoscopy
• CT chest, abdomen and pelvis (CAP): if a biopsy is diagnostic of malignancy, a CT CAP must be performed for staging.
• Carcinoembryonic antigen (CEA): a serum tumour marker used tomonitor disease progression; it isnotdiagnostic and should only be performed following confirmation of diagnosis

Question 172

What further investigations may be considered for colorectal cancer

Answer 172

MRI: may be used as an alternative to CT and is sometimes preferred for staging of rectal cancers. PET scan is not routine

Question 173

Describe the differential diagnosis for colorectal cancer

Answer 173

• IBS
• Ulcerative colitis
• Crohn’s disease
• Haemorrhoids
• Anal fissure
• Diverticular disease

Question 174

Describe the screening for colorectal cancer

Answer 174

• NHS home screening test to detect traces of blood in stool
  
  • The two types of test are the Faecal Occult Blood (FOB) test and Faecal Immunochemical Test (FIT)
• Screening sigmoidoscopy
  
  • Colonoscopy may be offered based on findings

Question 175

Describe the intial management for colorectal cancer

Answer 175

Iron replacement: should be started immediately for patients with iron deficiency anaemia whilst awaiting for further investigations

Question 176

Describe the elective treatment for colorectal cancer

Answer 176

• Neoadjuvant therapy:for locally advanced or metastatic tumours
  
  • Colon cancer:chemotherapy
  • Rectal cancer:radiotherapy (T3 and above) or chemoradiotherapy (rectal cancer is amenable to radiotherapy as it is an extraperitoneal structure)
• Surgical resection:for all stages of colorectal cancer
  
  • If the cancer is metastatic, the primary tumour, along with metastases to the liver and lung, can still be resected as this has been shown to improve survival
    Adjuvant chemotherapy:for locally advanced or metastatic tumours

Question 177

Describe the complications with colorectal cancer

Answer 177

Cancer-related

• Metastasis: most commonly to the liver, lung, and peritoneum
• Large bowel obstruction:colorectal cancer is the commonest cause; requiring resection in colon cancer or a defunctioning colostomy in rectal cancer

Treatment-related

• Surgical complications: such as anastomotic leak, perforation, sepsis. Rates of anastomotic leak are higher for left-sided tumours, which is why a Hartmann’s procedure is often performed

Question 178

Describe the prognosis for colorectal cancer

Answer 178

Early localised disease has a 5-year survival between 95% and 100%, whilst metastatic disease has a survival between 5% and 10%.

Serum CEA is used to monitor disease progression and the effectiveness of treatment.

Question 179

Describe the cell layers of the inner wall of the entire GI

Answer 179

The inner wall of the entire GIis lined with mucosa, which has three cell layers.

• The innermost epithelial layer absorbs and secretes mucus and digestive enzymes.
• The middle lamina propria contains blood and lymph vessels.
• The outermost muscularis mucosa, a layer of smooth muscle that contracts and helps break down food.

Question 180

Describe the regions of the stomach

Answer 180

In the stomach, there are four regions - the cardia, the fundus, the body, and the antrum. The epithelial layer in different parts of the stomach contains different proportions of gastric glands which secrete various substances.

Question 181

Describe the cells and their secretions of the cardia, fundus, body, antrum and duodenum

Answer 181

• The cardia contains mostly foveolar cells that secrete mucus
• The fundus and the body have mostly parietal cells that secrete hydrochloric acid and chief cells that secrete pepsinogen, an enzyme that digests protein.
• The antrum has mostly G cells that secrete gastrin in response to food entering the stomach. (These G cells are also found in the duodenum and the pancreas). Gastrin stimulates the parietal cells to secrete hydrochloric acid, and more broadly stimulates the growth of glands throughout the stomach.
• The duodenum also contains Brunner glands which secrete mucus rich in bicarbonate ions, to neutralise the acid.

Question 182

How else is stomach acid neutralised by the blood, duodenum and stomach

Answer 182

In addition, the blood flowing to the stomach and duodenum brings in even more bicarbonate which helps neutralise the hydrochloric acid.

The stomach and duodenum also secrete prostaglandins which stimulate mucus and bicarbonate secretion, vasodilate the nearby blood vessels allowing more blood to flow to the area, promote new epithelial cell growth, and also inhibit acid secretion.

Question 183

Define peptic ulcer disease

Answer 183

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter. Duodenal ulcers are more common than gastric ulcers.

Question 184

Describe the epidemiology of peptic ulcer disease

Answer 184

• M>F
• Estimated lifetime prevalence for men estimated at 11–20% and for women at 8–11%
• More common with increasing age
• More common in developing countries due to Helicobacter pylori

Question 185

Describe the aetiology of peptic ulcer disease

Answer 185

A result of an imbalance between factors promoting mucosal damage (gastric acid,H. pylori, NSAIDs) and those promoting gastroduodenal defence (prostaglandins, mucus, bicarbonate).

• H. pylori**:causes chronic inflammation which breaks down protective layer; responsible for themajority of peptic ulcers**(95% of duodenal ulcers and 75% of gastric ulcers).
• NSAIDs: inhibit cyclo-oxygenase (COX) resulting in reduced prostaglandin which normally reduces acid secretion and increases mucus production
• Other drugs: SSRIs, corticosteroids and bisphosphonates. These break down the protective layer.
• Smoking and alcohol: may lead to increased acid.
• Caffeine: may lead to increased acid.
• Stress: may lead to increased acid.
• Zollinger-Ellison syndrome:a gastrinoma (tumour) that results in numerous peptic ulcers due to elevated gastrin levels
• Blood type O
• Raised intracranial pressure:causes vagal stimulation which increases acid production (Cushing’s ulcer).
• Severe burn:hypovolaemia secondary to a burn causes reduced perfusion of the stomach leading to necrosis (Curling ulcer)

Question 186

Describe the pathophysiology of peptic ulcer disease

Answer 186

the protective layer of the stomach and duodenum is comprised of mucus and bicarbonate and secrete by stomach mucosa. NSAIDs and H. Pylori break down the protective layer by decreasing mucus production. an increase in stomach acid causes ulceration. Alcohol, caffeine, stress increase stomach acid.
Gastric ulcers - Lesser curvature of antrum. Duodenal ulcers - 1st part of duodenum

Question 187

Describe the clinical manifestations of peptic ulcer disease

Answer 187

• Signs
  
  • Evidence of bleeding
    
    • Hypotension and tachycardia (shock)
    • Melaena on rectal examination
  • Epigastric tenderness
  • Pallor, if anaemic
• Symptoms
  
  • ‘Burning’ epigastric pain
    
    • Pain relieved by eating and worse when hungry:duodenal ulcer
    • Pain worsened by eating:gastric ulcer
  • Nausea and vomiting
  • Haematemesis or melaena
  • Dyspepsia (indigestion)
  • Reduced appetite and weight loss
  • Anaemia: due to bleeding
  • Fatigue

Question 188

Describe the investigations for peptic ulcer disease

Answer 188

• No active bleeding
  
  • H. pyloribreath test and/or stool antigen
    
    • Breath test: measures CO2 in breath after ingesting C-urea
    • Stool antigen: monoclonal antibodies for detection of H. pylori
    • Patients must be PPI-free for 2 weeks and antibiotic-free for 4 weeks as this may give a false negative
    • Serology(for IgG) isonlyused if breath test and stool antigen are unavailable
  • Upper GI endoscopy and biopsy:
    
    • Gold standard diagnostic test for visualisation, and biopsy:
      
      • Excludes malignancy
      • Rapid urease test ‘clo test’: to check for H. pylori (H.pylori produces urease)
    • Notroutinely performed for non-bleeding ulcers
  • Fasting gastrin level: if suspected Zollinger-Ellison syndrome e.g. recurrent or treatment-resistant peptic ulcers
• If active bleeding
  
  • FBC: assess the extent of anaemia
  • U&Es: urea is raised in an upper GI bleed (protein in RBCs is digested into urea in the GI tract), whilst pre-renal acute kidney injury may also be present
  • LFTs and coagulation profile:**assess severity of liver disease
  • Venous blood gas: can be analysed within minutes and provides an estimate of the Hb. Also, a raised lactate suggests poor tissue perfusion and is associated with a significant bleed
  • Upper GI endoscopy and biopsy: diagnostic and therapeutic. All gastric ulcers should be biopsied as they can potentially be malignant
  • Erect CXR:if concerned about perforation, an erect CXR may demonstrate pneumomediastinum

Question 189

Describe the management for peptic ulcer disease

Answer 189

The core aspects of treating peptic ulcers are:

Stopping NSAIDs
Treating H. pylori infections with triple therapy
Proton pump inhibitors (e.g., lansoprazole or omeprazole)

Question 190

Describe the complications of peptic ulcer disease

Answer 190

• Perforation: life-threatening as ulcer penetrates the duodenum or stomach into the peritoneal cavity causing peritonitis. May also allow air to collect under the diaphragm and irritate the phrenic nerve causing referred shoulder pain. Requires surgical intervention!
• Gastric outlet obstruction/ pyloric stenosis: caused by obstruction of the pylorus due to an ulcer and subsequent scarring. Presents with abdominal pain, distension, vomiting and nausea after eating

Question 191

Describe the prognosis of peptic ulcer disease

Answer 191

ForH. pylori-negative peptic ulcers, if adequate acid suppression is offered thenmost duodenal ulcers heal in 4 weeks and gastric ulcers in 8-10 weeks.

For ulcers related to NSAID use, discontinuing NSAID use is associated with low ulcer recurrence. If NSAIDs continue, a PPI must be offered alongside it.

ForH. pylori-positive peptic ulcers, duodenal ulcer recurrence is 20% and gastric ulcer recurrence is 30% post-eradication

Question 192

Define appendicitis

Answer 192

Inflammation of the appendix located at McBurney’s point (2/3 between from umbilicus to ASIS)

Question 193

Describe the epidemiology of appendicitis

Answer 193

• Appendicitis is the most common acute abdominal condition in the UK requiring surgery
• The highest incidence is between 10-20 years of age
• M>F

Question 194

Describe the risk factors for appendicitis

Answer 194

• Young age:the highest incidence is between 10-20 years of age
• Male
• Frequent antibiotic use:causes an imbalance in gut flora and a modified response to subsequent infection which may trigger appendicitis
• Smoking

Question 195

Describe the aetiology of appendicitis

Answer 195

Faecolith (calcified faecal deposits) most common. Foreign bodies, intestinal worms/pinworm, lymphoid hyperplasia

Question 196

Describe the pathophysiology of appendicitis

Answer 196

Obstruction of the lumen of the appendix leads to stasis > bacterial overgrowth > inflammation. Obstruction leads to increased pressure in the appendix which can cause rupture.

Question 197

What are the key presentations of appendicitis

Answer 197

Central abdominal pain which migrates to the right iliac fossa, low-grade pyrexia and anorexia. 50% of patients present with this characteristic history.

Question 198

Describe the clinical manifestations of appendicitis

Answer 198

• Signs
  
  • Right iliac fossa tenderness: rebound tenderness (pain when pressure is taken off) or percussion tenderness (pain during percussion) suggests localised peritonism
  • Guarding
  • Tachycardia, hypotension and generalised peritonism: suggests perforation
  • Rovsing’s sign: pain in the right iliac fossa is worsened by pressing on left iliac fossa
  • Psoas sign: pain is worsened by extending the hip
  • Obturator sign: pain is worsened by flexing and internally rotating the hip
  • Digital rectal examination: not routinely performed but a boggy sensation suggests a pelvic abscess
• Symptoms
  
  • Periumbilical pain (referred pain) which migrates to the right iliac fossa (McBurney’s point)
  • Low-grade fever: > 38°C suggests alternative pathology e.g. mesenteric adenitis
  • Reduced appetite and anorexia
  • Nausea and vomiting: persistent vomiting is unusual
  • Diarrhoea: rare but may occur in pelvic appendicitis or due to a pelvic abscess

Question 199

What are the first line investigations for appendicitis

Answer 199

• FBC: leukocytosis and neutrophilia is seen in up to 90% of patients
• CRP and ESR: raised due to inflammation
• U&Es: acute kidney injury in dehydration secondary to vomiting, or in instances of perforation and sepsis
• Urinalysis: perform in all patients to exclude renal colic, a urinary tract infection or pregnancy in women; in appendicitis, there may be a mild leukocytosis without nitrates.
• Group & save: important to conduct prior to surgical intervention

Question 200

What is the gold standard investigation for appendicitis

Answer 200

Abdominal CT with contrast

Question 201

Describe the differential diagnosis for appendicitis

Answer 201

• Ectopic Pregnancy: serum or urine bHCG (pregnancy test) to exclude pregnancy is essential
• Ovarian Cysts: can cause pelvic and iliac fossa pain, particularly with rupture or torsion
• Meckel’s Diverticulum: malformation of thedistal ileumthat occurs in around 2% of the population. It is usually asymptomatic, however it can bleed, become inflamed, rupture or cause avolvulusorintussusception.
• Mesenteric Adenitis: inflamed abdominal lymph nodes. This presents with abdominal pain, usually in younger children. This is often associated with tonsillitis or an upper respiratory tract infection.
• UTI
• Diverticulitis
• Perforated ulcer
• Food poisoning
• Acute terminal ileitis (due to Crohn’s)

Question 202

Describe the management for appendicitis

Answer 202

• Initial management
  
  • Fluids: patients will require hydration due to fluid losses, as well as due to being nil-by-mouth prior to surgery
  • Analgesia: patients can be in considerable pain
  • Antiemetics: can be given for nausea and vomiting e.g. ondansetron
  • Preoperative IV antibiotics: prophylactic antibiotics are associated with reduced wound infection rates, e.g. ceftriaxone and metronidazole
• Definitive management
  
  • Prompt appendicectomy:laparoscopicappendicectomy is the treatment of choice, using a three-port approach. Occasionally, anopenapproach is required, with a 2-3 inch incision just below McBurney’s point. Significantabdominal lavageis required for perforated appendicitis
  • Postoperative antibiotics: usually given for only 24 hours, but occasionally patients are discharged on a brief course of oral antibiotics if the appendix was perforated or necrotic

Question 203

Describe the complications of appendicitis

Answer 203

Peritonitis if ruptured, appendix abscess, adhesions

Question 204

Describe the prognosis for appendicitis

Answer 204

Following surgery, the chance of death from appendicitis is very low. Most patients will leave the hospital in 1-3 days. Those who have a non-perforated appendix have a mortality rate of 0.08%, compared to 0.5% in those with perforation.

Question 205

Define bowel obstruction

Answer 205

Bowel obstruction is when the normal flow of contents moving through the intestines is interrupted. The causes can be either mechanical or functional (also called ileus)

Question 206

Describe the classifications for bowel obstruction

Answer 206

• According to site:
  
  • Large bowel or small bowel
• Extent of luminal obstruction:
  
  • Partial
  • Complete
• According to mechanism:
  
  • Mechanical: obstruction
  • Functional: lack of contraction
• According to pathology:
  
  • Simple: one obstructing point and no vascular compromise
  • Closed loop: obstruction at two points causing grossly distended bowel at risk of perforation
  • Strangulation: blood supply is compromised and patient is very ill. Sharp, constant and localised pain. Peritonism, fever, increase WCC and signs of mesenteric ischaemia are all features.

Question 207

Describe the aetiology of bowel obstruction

Answer 207

• Mechanical causes
• Small intestine (scar tissue post-surgery, hernia, gallstone ileus or meconium ileus)
• Large intestine (kinks in loop)
• Functional (infection, inflammation, postoperative ileus)

Question 208

Describe the pathophysiology of bowel obstruction

Answer 208

When there’s an obstruction, the bowel contents distal to the obstruction get passed; but proximal to the obstruction, gas and stool start to accumulate, causing the bowel to dilate, and therefore, the overall abdominal cavity to distend.

The accumulated gas and stool causes pressure inside the bowel lumen to increase, so the intestinal contents push towards the intestinal wall, compressing the mucosal blood and lymphatic vessels. Since the walls of veins and lymphaticsare weaker and easier to compress compared to arteries, venous and lymphatic drainage are the first ones to get blocked. The pressure pushes the water from these vessels into the surrounding tissue, leading to mucosal oedema. If pressure inside the lumen gets even higher, it also compresses mucosal arteries, leading to ischaemia or reduced blood flow to the intestinal wall. This also leads to hypoxia.

At the cellular level, this is accompanied by the production of reactive oxygen species; which can damage DNA, RNA, and proteins of the cells in the epithelial layer and lamina propria of the mucosa, leading to cell death, or mucosal infarction.

When the mucosa becomes damaged and capillary blood vessels in the lamina propria rupture, blood enters the bowel lumen. All this stool and blood in the lumen becomes a nutritious feast for bacteria that normally reside in the intestines, and they start growing out of control. These bacteria can then get into the intestinal wall, where they get attacked by macrophages rushing into the mucosa. These macrophages then release inflammatory cytokinese.g. tumor necrosis factor-alpha, which cause blood vessels to become more permeable to fluid and to more immune cells, further increasing mucosal oedema, inflammation, and damage.

The overall result is the compromised ability of the mucosa to absorb food and water, which may lead todehydration and loss of electrolytes, like sodium, potassium and chloride.

As all these lumen contents continues to build up, intraluminal pressure rises even higher, making the problem even worse. And if this pressure becomes high enough, even larger arteries get compressed, meaning that the arterial supply to more layers of the bowel wall is compromised. Bowel ischaemia and infarction extend from just the mucosa to all layers bowel wall, known as a transmural infarction.

This may result in perforation, and all the bacteria that have been accumulating inside the lumen, can now easily leak out, causing peritonitis. Large numbers of bacteria from the peritoneal cavity can sneak into the bloodstream, triggering sepsis.

Question 209

Define small bowel obstruction

Answer 209

Small bowel obstruction (SBO) is a mechanical or functional obstruction of the small intestine that prevents the normal passage of digestive contents.

It can be partial or complete.

Question 210

Describe the epidemiology of small bowel obstruction

Answer 210

• Accounts for 60-75% of intestinal obstruction
• A rare disease in those who have not had previous surgery.
• The risk can increase by at least twelve-fold in those with a history of abdominal surgery

Question 211

Describe the aetiology of small bowel obstruction

Answer 211

Adhesions from previous surgery (75%), hernias (10%), Crohn’s strictures, malignancy

Question 212

Define the pathophysiology of small bowel obstruction

Answer 212

Obstruction of bowel leads to distention above the blockage due to a build up of fluid and contents. This causes increased pressure which pushes upon blood vessels in the bowel wall causing them to be compressed. Compressed vessels cannot supply blood leading to ischaemia, necrosis and perforation.

Question 213

Describe the clinical manifestations of small bowel obstruction

Answer 213

Colicky central or generalised abdominal pain (higher up), abdominal distention (less severe than LBO), early onset vomiting first (bilious) followed by late onset constipation, ‘tinkling’ bowel sounds. Abdominal bloating, constipation and anorexia

Question 214

What is the gold standard investigation for small bowel obstruction

Answer 214

CT abdomen and pelvis with contrast

Question 215

Describe the first line investigations for small bowel obstruction

Answer 215

Abdominal x-ray – dilation of small bowel >3cm, coiled spring appearance (valvulae conniventes - due to mucosal folds on surface), dilated bowel loops and gas shadows (fluid and air accumulates in bowel)

Question 216

Describe the further investigations for small bowel obstruction

Answer 216

FBC, U&E imbalances, ABG (metabolic alkalosis, raised lactate)

Question 217

Describe the management for small bowel obstruction

Answer 217

Stable: ABCDE, ‘drip and suck’ – insert IV cannula > fluid resuscitation, nil-by-mouth, insert nasogastric tube to decompress stomach, catheter (monitor urine output), analgesia, antiemetics, antibiotics
Unstable: treat according to cause: laparotomy, adhesiolysis for lesions, hernia repair, tumour resections, bowel resection

Question 218

Describe the differential diagnosis for small bowel obstruction

Answer 218

Large bowel obstruction, pseudo-obstruction

Question 219

Describe the complications for small bowel obstruction

Answer 219

Necrosis, perforation, sepsis, aspiration pneumonia and short gut syndrome

Question 220

Describe the prognosis for small bowel obstruction

Answer 220

Small bowel obstruction is most commonly caused by adhesions. These patients are at risk of recurrent SBO, even after adhesiolysis. Recurrence occurs most commonly within 5 years but can occur decades later.

Question 221

Define large bowel obstruction

Answer 221

Large bowel obstruction (LBO) occurs due to mechanical or functional obstruction of the large intestine that prevents the normal passage of contents.

Question 222

Describe the epidemiology of large bowel obstruction

Answer 222

• Less common, accounting for only 25% of all intestinal obstruction due to larger lumen
• Large bowel obstruction is a common complication of colorectal cancer and can occur in up to 30% of patients
• Usually in people over 65 years old

Question 223

Describe the aetiology of large bowel obstruction

Answer 223

• Colorectal cancer most common cause
• Stricture
• Volvulus: torsion of the colon around itself and the mesentery (either sigmoid or caecal - less common)
• Hirschprung’s disease

Question 224

Describe the risk of large bowel obstruction

Answer 224

• Increasing age: usually in people over 65 years old
• Colorectal cancer:smoking, obesity, processed meat, inflammatory bowel disease
• Stricture:diverticulitis, inflammatory bowel disease, post-surgical bowel resection with anastomosis
• Volvulus

Question 225

Describe the pathophysiology of large bowel obstruction

Answer 225

Obstruction of bowel leads to distention above the blockage due to a build-up of fluid and contents. This causes increased pressure which pushes upon blood vessels in the bowel wall causing them to be compressed. Compressed vessels cannot supply blood leading to ischaemia, necrosis and perforation.

Question 226

What are the key presentations for large bowel obstructions

Answer 226

Continuous abdominal pain (lower down), severe abdominal distention, early onset constipation first followed by later onset vomiting (initially bilious then faecal), absent bowel sounds. Tachycardia and hypotension. Bloating, constipation and anorexia

Question 227

Describe the gold standard investigation for large bowel obstruction

Answer 227

CT abdomen and pelvis with contrast:gold standard imaging as it can identify dilated bowel loops, evidence of ischaemia and perforation, as well as the underlying cause

Question 228

Describe the first line investigations for large bowel obstruction

Answer 228

Abdominal x-ray – dilated large bowel >6cm, dilated caecum >9cm. Dilated bowel loops and gas shadows (fluid and air accumulates in bowel). Coffee bean sign (if sigmoid volvulus)
Digital rectal exam (empty rectum, hard compacted stools, maybe blood). X-ray doesn’t show rectum so DRE necessary

Question 229

Describe the further investigations for large bowel obstruction

Answer 229

FBC, U&E imbalances, ABG (metabolic alkalosis, raised lactate)

Question 230

What are the differential diagnosis for large bowel obstruction

Answer 230

Small bowel obstruction, pseudo-obstruction

Question 231

Describe the management for large bowel obstruction

Answer 231

Management Stable: ABCDE, ‘drip and suck’ – insert IV cannula > fluid resuscitation, nil-by-mouth, insert nasogastric tube to decompress stomach, catheter (monitor urine output), analgesia, antiemetics, antibiotics
Unstable: treat according to cause: laparotomy, adhesiolysis for lesions, hernia repair, tumour resections, bowel resection

Question 232

Describe the complications for large bowel obstruction

Answer 232

• Bowel ischaemia and perforation: twisting of the bowel compromises the blood supply and can lead to necrosis with eventual perforation
• Sepsis: perforation leads to faecal peritonitis and sepsis
• Aspiration pneumonia:the risk is reduced with NG tube decompression
• Dehydration: occurs due to ‘third-spacing of fluid’

Question 233

Describe the prognosis for large bowel obstruction

Answer 233

Early management reduces the likelihood of bowel ischaemia and subsequent surgical resection.

Overall prognosis also depends on the underlying cause. If a patient has bowel obstruction secondary to colorectal malignancy, they have a lower 5-year survival rate.

Question 234

Define pseudo-obstruction

Answer 234

Clinical picture mimicking colonic obstruction but with no mechanical cause.

Also known as Ogilvie syndrome.

Question 235

Describe the epidemiology of pseudo-obstruction

Answer 235

• Usually associated with recent severe illness or surgery.
• Often seen in the post-partum setting, particularly following caesarian section.

Question 236

Describe the aetiology of pseudo-obstruction

Answer 236

In more than 80% of cases its a complication of other conditions:

• Puerperium: the period after childbirth during which the mother’s reproductive organs return to their original non-pregnant condition.
• Postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic and neuro
• Intra-abdominal trauma
• Intra-abdominal sepsis
• Pelvic, spinal and femoral fractures
• Drugs e.g. opiates (particularly after orthopaedic surgery), antidepressants
• Cardiorespiratory and neurological disorders

Question 237

Describe the clinical manifestations of pseudo-obstruction

Answer 237

Rapid and progressive abdominal pain, abdominal distention, vomiting, constipation

Question 238

Describe the gold standard investigation for pseudo-obstruction

Answer 238

CT of abdomen and pelvis with contrast (no transition zone)

Question 239

Describe the first line investigations for pseudo-obstruction

Answer 239

Abdominal x-ray: megacolon distention >10cm

Question 240

Describe the management for pseudo-obstruction

Answer 240

Drip and suck, IV neostigmine, surgical decompression (caecostomy, ileostomy)

Question 241

Describe the complications with pseudo-obstruction

Answer 241

Weight loss: due to malabsorption in chronic pseudo-obstruction

Question 242

Define diverticulosis, diverticular disease and diverticulitis

Answer 242

• Diverticulosis:the presence of diverticula (out-pouching) in an asymptomatic patient
• Diverticular disease: where diverticula cause symptoms, such as intermittent lower abdominal pain, without inflammation and infection
• Diverticulitis:**where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding

Question 243

Describe the epidemiology of diverticular

Answer 243

• Diverticula are very common with increasing age, affecting 66% of patients over 80 years old. Peak age is 50-70 years old.
• 30% of Westerners have diverticulosis by age 60.
• 25% of patients with diverticulosis develop symptoms, whilst almost 80% of these people have an episode of diverticulitis.
• Mainly form in sigmoid colon but can also affect right colon, particularly in Asian people.

Question 244

Describe the risk factors for diverticula

Answer 244

• Increasing age:> 50 years; peak age is 50-70 years old
• Low dietary fibre
• Obesity: particularly in younger people
• Sedentary lifestyle
• Smoking:increases the risk of complicated diverticular disease
• NSAIDs:increases the risk of perforation in diverticulitis

High pressure in the colon

Question 245

Describe the pathophysiology of diverticula

Answer 245

High pressures in the colon + weak wall leads to outpouching of the colon wall forming diverticula. Most commonly in the sigmoid colon due to its smallest luminal diameter and high pressure. If faecal matter or bacteria gather in the diverticula this causes inflammation and can lead to rupture of blood vessels = diverticulitis.

Question 246

Describe the clinical manifestations of diverticular disease and diverticulitis

Answer 246

Diverticular disease: bowel habits changed (constipation), bloating/flatulence, LLQ pain, guarding and tenderness, nausea and vomiting
Diverticulitis: all of above + fever, blood in stool, tachycardia, palpable LIF mass

Question 247

What is the gold standard investigation for diverticula

Answer 247

Abdominal/pelvis CT with contrast (may show dilated bowel loops, obstruction, abscess)

Question 248

What are first line investigations for diverticula

Answer 248

Abdo examination: tenderness and guarding (peritoneum irritated), distended and tympanic to percussion (gas), bowel sounds diminished (colon not working well).
FBC: raised WCC, CRP, ESR. Colonoscopy

Question 249

Describe the management for diverticulosis, diverticular disease and diverticulitis

Answer 249

Diverticulosis = nothing, watchful waiting. Lifestyle modification (weight loss, smoking, fibre)
Diverticular disease = high fibre diet and fluids. Bulk-forming laxatives. Surgery if needed.
Diverticulitis = Abx (co-amoxiclav = amoxicillin/clavulanate) + paracetamol. Analgesia, IV fluid, liquid food.

Question 250

Describe the complications for diverticular disease

Answer 250

Infection > abscess, bowel perforation, peritonitis, haemorrhage, obstruction, fistulae into adjacent organs (vagina, bladder)

Question 251

What are the differential diagnosis for diverticular disease

Answer 251

Appendicitis, endometriosis, colorectal cancer, IBD

Question 252

Describe the prognosis for diverticulitis

Answer 252

It is estimated that 85% of people with uncomplicated diverticulitis will respond to medical treatment, whilst approximately 15% of patients will require surgical intervention.

Question 253

Define gastritis

Answer 253

Gastritis refers to inflammation of the lining of the stomach associated with mucosal injury.

Question 254

Describe the aetiology of gastritis

Answer 254

• Helicobacter pylori infection
• Autoimmune gastritis
• Viruses e.g. cytomegalovirus and herpes simplex
• Duodenogastric reflux - whereby bile salts enter stomach and damage mucin protection resulting in gastritis
• Specific causes e.g. Crohn’s (more common in children than adults)
• Mucosal ischaemia - reduced blood supply to mucosal cells can mean less mucin produced so acid can induce gastritis
• Increased acid - can overwhelm mucin resulting in gastritis, stress can increase acid production
• Aspirin and NSAIDs e.g. Naproxen
• Alcohol, smoking, caffeine - irritates and erodes stomach mucosa
• Extreme physiological stress e.g. shock, sepsis or burns

Question 255

Describe the risk factors for gastritis

Answer 255

• Alcohol
• NSAIDs
• H.pylori
• CMV and herpes
• Infectious: crowding and poor sanitation
• Autoimmune: HLA-DR3 and B8
• Reflux/hiatus hernia
• Granulomas e.g. in Crohn’s
• Zollinger-Ellison syndrome: tumours cause the stomach to produce too much acid
• Menetrier’s disease: massive overgrowth of mucous cells (foveola) in the mucous membrane lining the stomach

Question 256

Describe the pathophysiology of gastritis

Answer 256

H. Pylori causes inflammation. Alcohol increases gastric acid and irritates stomach. NSAIDs inhibit COX which inhibits prostaglandin synthesis which decreases mucus protective barrier production. Autoimmune gastritis attacks parietal cell and intrinsic factor antibodies which reduces B12 absorption.

Question 257

Describe the clinical manifestations of gastritis

Answer 257

• Nausea or recurrent upset stomach
• Vomiting
• Abdominal bloating
• Epigastric pain
• Indigestion
• Haematemesis/ malaena

Question 258

What is the gold standard investigation for gastritis

Answer 258

Endoscopy and biopsy (gastric mucosal inflammation and atrophy)

Question 259

What are the first line investigations for gastritis

Answer 259

Helicobacter pylori urea breath test, H. Pylori stool antigen test

Question 260

What are further investigations for gastritis

Answer 260

FBC: low Hb. Autoimmune: low vitamin B12, parietal cell/intrinsic factor antibodies

Question 261

What are the differential diagnosis for gastritis

Answer 261

• Peptic ulcer disease (PUD)
• GORD
• Non-ulcer dyspepsia
• Gastric lymphoma
• Gastric carcinoma

Question 262

Describe the management for gastritis

Answer 262

1st line – treat underlying cause.
H. Pylori eradication: triple therapy – proton pump inhibitor + 2 antibiotics for 7 days.
1st line – omeprazole, amoxicillin 1g, clarithromycin 500mg. if penicillin allergy, swap amoxicillin for 400mg metronidazole
NSAIDs/alcohol – stop. Autoimmune – IM vitamin B12 (cyanocobalamin)

Question 263

Describe the complications of gastritis

Answer 263

Peptic ulcers, achlorhydria (lack of HCl in stomach) , bleeding and anaemia (VB12 deficiency), MALT lymphoma, gastric cancer

Question 264

Describe the prognosis of gastritis

Answer 264

• Erosive gastritis: symptoms typically improve following discontinuation of or reduction in exposure to offending agent e.g. NSAIDs
• Helicobacter pylori infection: prognosis is good. An initial traditional triple therapy regimen may be inadequate, and patients may require an alternative quadruple bismuth-based regimen.
• Autoimmune gastritis: prognosis is excellent for B₁₂ deficiency following replacement therapy with cyanocobalamin. There is a small increased risk for the development of gastric adenocarcinoma and gastric carcinoids.

Question 265

Define diarrhoea

Answer 265

The abnormal passage of loose or liquid stool more than 3 times daily

Question 266

Describe the epidemiology of diarrhoea

Answer 266

2nd leading cause of child death globally

Question 267

Describe the aetiology of diarrhoea

Answer 267

1. Rotavirus – leading cause in children
2. Norovirus – leading cause in adults. Cruise ships, hotels, restaurants.
3. Traveller’s diarrhoea – most commonly enterotoxigenic E. coli or cholera
4. Bacteria – campylobacter jejuni (mc, undercooked chicken), E. coli (enterotoxigenic – watery, enterohaemorrhagic – bloody), salmonella enterica, shigella
5. Antibiotics – clostridium difficile infection. Cs: co-amoxiclav, clindamycin, ciprofloxacin, cephalosporins, clarithromycin
6. Parasites – giardia lamblia (mc), cryptosporidium
7. Non-infective: IBD, coeliac, IBS, malignancy

Question 268

What are the key presentations with diarrhoea

Answer 268

Diarrhoea loose liquid stools, vomiting, abdominal cramps.
Blood in stool = bacterial infection
Watery diarrhoea = viral, parasitic
Virus = fever, fatigue, headache, muscle pain
Traveller’s diarrhoea = fever, N+V, cramps, tenesmus, bloody stools during trip abroad
Rice-water diarrhoea = cholera
Guillain barre = campylobacter jejuni

Question 269

Describe the first line investigations for diarrhoea

Answer 269

Stool sample (microscopy, culture, toxin detection). FBC (raised CRP, ESR), blood culture.
Campylobacter jejuni: CCDA or PCR. Salmonella: pink with black centre on XLD. Shigella: pink on XLD.

Question 270

Describe the management for diarrhoea

Answer 270

Usually self-limiting. Isolation. Treat underlying cause. Fluid rehydration. Electrolyte replacement.
Medication for symptoms: antiemetics (metoclopramide), antidiarrheals (loperamide), broad spectrum Abx (ciprofloxacin, ceftriaxone)
Bacterial diarrhoea – metronidazole.

Question 271

Define acute diarrhoea

Answer 271

Acute diarrhoea is defined as that lasting less than 2 weeks

Question 272

Describe the aetiology of acute diarrhoea

Answer 272

• Usually due to infection e.g. travellers diarrhoeaSuspect gastroenteritis!

Question 273

Define chronic diarrhoea

Answer 273

Chronic diarrhoea is defined as lasting more than 2 weeks

Question 274

Describe the aetiology of chronic diarrhoea

Answer 274

Organic causes (associated with changes in the structure of an organ or tissue resulting in symptoms - increased stool weights) must be differentiated from functional causes (conditions in which there is no physical cause for symptoms - frequent passage of low volume and weight stools) such as irritable bowel syndrome (IBS)

Question 275

Describe the blood supply for the colon

Answer 275

The blood supply to the colon is primarily provided by the superior and inferior mesenteric arteries.

There are many branches that supply the colon. The areas they supply cross-over and they have a tendency to anastomose allowing for a degree of collateral supply. The supply is most precarious at so called ‘watershed’ areas, where such collaterals are limited - namely the splenic flexure and rectosigmoid junction.

Question 276

Define ischaemic colitis

Answer 276

Bowel ischaemia which affects the large bowel. This is mainly due to pathology in the inferior mesenteric artery territory and can range from mild ischaemia to gangrenous colitis.

Also known as chronic colonic ischaemia.

Question 277

Describe the epidemiology of ischaemic colitis

Answer 277

• Colonic ischaemia has an approximate incidence of 22.9 per 100,000 person-years
• The most common form of intestinal ischaemia
• Incidence increases with advancing age

Question 278

Describe the aetiology of ischaemic colitis

Answer 278

Intestinal ischaemia occurs when blood flow to the intestines (small and large bowel) is reduced and thereby insufficient for the needs of the intestines. The cause of insufficient blood flow varies and can be occlusive, or non occlusive (most common)

Thrombosis, embolism, surgery, vasculitis, coagulation disorders

Question 279

Describe risk factors for ischaemic colitis

Answer 279

• Older age
• Peripheral vascular disease
• Infective endocarditis
• Atrial fibrillation
• Atherosclerosis: smoking, HTN, hypercholesterolaemia, diabetes
• Previous MI: impaired ventricular wall motion results in thrombus formation and mesenteric embolisation
• Coagulation disorders
• Cocaine use: may cause IC in younger patients
• Vasculitis: may cause IC in younger patients
• Hypoperfusion:sepsis and trauma

Question 280

Describe the clinical manifestations for ischaemic colitis

Answer 280

• Signs
  
  • Abdominal tenderness
  • Peritonism
  • Haemodynamic instability
  • Pyrexia - shock
  • Tachycardia - shock
• Symptoms
  
  • Lower left side abdominal pain (may be crampy in nature)
  • Diarrhoea +/- blood
  • Haematochezia - passage of fresh blood through the anus
  • Fever

Question 281

What is the gold standard investigation for ischaemic colitis

Answer 281

Colonoscopy and biopsy

Question 282

What are the first line investigations for ischaemic colitis

Answer 282

Urgent CT contrast/angiography (rule out perforation). FBC: metabolic acidosis (raised lactate),

Question 283

What are the differential diagnosis for ischaemic colitis

Answer 283

Other causes of acute colitis e.g. IBD

Question 284

What is the management for ischaemic colitis

Answer 284

1st line – IV fluids, antibiotics (prophylactic- metronidazole and ciprofloxacin), anticoagulants, surgery if gangrenous

Question 285

What are the complications with ischaemic colitis

Answer 285

• Bowel infarction and perforation: ischaemia can result in necrosis and subsequent perforation. This can lead to peritonitis and profound sepsis
• Systemic inflammatory response syndrome (SIRS) progressing into a multi-organ dysfunction syndrome, mediated by bacteria translocation across the dying gut wall
• Strictures: patients with ischaemic bowel managed conservatively have a risk of developing strictures

Question 286

Describe the prognosis of ischaemic colitis

Answer 286

Most patients’ symptoms improve within 24 to 48 hours, with complete clinical recovery within 1 to 2 weeks

Mortality ~22%

Question 287

Describe the blood supply of the gut

Answer 287

• Foregut
  
  • Stomach and part of duodenum, biliary system, liver, pancreas
  • Celiac artery
• Midgut
  
  • Duodenum to 1sthalf of transverse colon
  • Superior mesenteric artery
• Hindgut
  
  • 2ndhalf of transverse colon to rectum
  • Inferior mesenteric artery

Question 288

Define mesenteric ischaemia

Answer 288

Type of ischaemic bowel disease affecting the small intestine. Can be acute or chronic

Question 289

Describe the epidemiology of mesenteric ischaemia

Answer 289

• Age: typically occurs in people > 40 years old, but can occur in younger patients depending on the cause
• Gender: chronic mesenteric ischaemia is 3 times more frequent in women

Question 290

Describe the aetiology of mesenteric ischaemia

Answer 290

Arterial

• Thrombosis - atherosclerotic plaque formation. The commonest cause.
• Embolism - most common cause usually due to atrial fibrillation or spontaneous rupture of an atheroma
• Other - vasculitides, external compression e.g. tumour, hernia, volvulus, intussuception (part of the intestine slides into an adjacent part of the intestine. This telescoping action often blocks food or fluid from passing through)

Venous

• Thrombosis - rare cause and patients usually have a history of hypercoagulability

Non-occlusive

• Hypoperfusion - multiple causes e.g. trauma, sepsis, and heart failure

Question 291

Describe the risk factors for mesenteric ischaemia

Answer 291

• Older age
• Atrial fibrillation: results in embolisation
• Atherosclerosis:smoking, HTN, hypercholesterolaemia, diabetes
• Previous MI: impaired ventricular wall motion results in thrombus formation and mesenteric embolisation
• Hypercoagulable state
• Infective endocarditis
• Vasculitis
• Hypoperfusion:sepsis and trauma

Question 292

Describe the pathophysiology of mesenteric ischaemia

Answer 292

Superior mesenteric artery most commonly affected
Acute: blockage of mesenteric arteries or veins supply small intestine.
Chronic: narrowing of GI blood vessels causing ischaemia to bowel

Question 293

Describe the clinical manifestations of mesenteric ischaemia

Answer 293

Triad: 1. central/RIF acute severe abdominal pain. 2. No abdominal signs on exam (tenderness, guarding). 3. Rapid hypovolemic shock. Abdominal bruit, haematochezia/melaena, nausea and vomiting, weight loss

Question 294

What is the gold standard test for mesenteric ischaemia

Answer 294

Contrast CT/CT angiogram (bowel wall thickening)

Question 295

Describe the investigations for mesenteric ischaemia

Answer 295

Contrast CT/CT angiogram, FBC and ABG (metabolic acidosis, raised lactate)

Question 296

Describe the management for mesenteric ischaemia

Answer 296

1st line – IV fluids, antibiotics, IV heparin to reduce clotting, surgery to remove necrotic bowel

Question 297

Describe the complications of mesenteric ischaemia

Answer 297

Bowel ischaemia > necrosis, perforation, sepsis, peritonitis

Question 298

Describe the prognosis for mesenteric ischaemia

Answer 298

Mortality of acute mesenteric ischaemia is high if left untreated, ranging from 50-80% with non-occlusive aetiology associated with a poorer prognosis.

The most important factor in increasing survival is an early diagnosis prior to the onset of bowel infarction. Chronic mesenteric ischaemia has a much better prognosis.

Question 299

Describe the differences in pathology between mesenteric ischaemia and ischaemic colitis

Answer 299

MI- affects small bowel due to embolus or thrombus

IC- affects large bowel and occurs in ‘watershed’ areas e.g. splenic flexure

Question 300

Describe the differences in presentation between mesenteric ischaemia and ischaemic colitis

Answer 300

MI - acute: severe, sudden abdominal pain; pain is disproportionate to clinical findings. chronic: colicky, post-prandial abdominal pain.

IC - transient, less severe abdominal pain with bloody diarrhoea

Question 301

Describe the difference in diagnostic tests between mesenteric ischaemia and ischaemic colitis

Answer 301

MI - CT angiogram or angiography

IC- colonoscopy

Question 302

Describe the management differences for mesenteric ischaemia and ischaemic colitis

Answer 302

MI- surgical emergency and anticoag

IC- conservative and surgery if conservative fails

Question 303

Define Mallory-Weiss tear

Answer 303

Tear of the oesophageal mucosal membrane due to sudden increases in intra-abdominal pressure

Question 304

Describe the epidemiology of MWT

Answer 304

• MWT accounts for up to 15% of cases of upper GI bleeding
• MWT is more common in men than in women
• The age of presentation may vary but is most common in people aged between 30 and 50 years

Question 305

Describe the risk factors of MWT

Answer 305

• Any condition that predisposes to retching or vomiting: such as gastroenteritis, bulimia, hyperemesis gravidarum
• Alcoholism: damages the gastric mucous membrane and also causes vomiting
• Chronic cough: often due to COPD, asthma, bronchiectasis
• Hiatus hernia
• Gastro-oesophageal reflux disease
• Trauma to chest or abdomen
• Transoesophageal echocardiography
• Heavy lifting or straining
• Male
• Aged 40-60 years

Question 306

Describe the pathophysiology of MWT

Answer 306

MWT is caused by a sudden rise in intra-abdominal and transmural pressure across the gastro-oesophageal junction secondary to vomiting and retching in the presence of a preexisting damaged gastric mucous membrane, which is often related to alcoholism. This causes a subsequent laceration resulting in an upper GI bleed that is usually self-limiting.

Question 307

Describe the clinical manifestations of MWT

Answer 307

Haematemesis after retching Hx, melaena, hypovolemic shock (hypotension, dizziness), dysphagia. No Hx of liver disease or portal hypertension

Question 308

What is the gold standard investigation for MWT

Answer 308

Endoscopy (tear or laceration)

Question 309

What are the first line investigations for MWT

Answer 309

1st line Endoscopy (tear or laceration). FBC, U&E, LFT, Coagulation screen, blood cross-matching and group. Rockall score – severity of upper GI bleeding

Question 310

What are the differential diagnosis for MWT

Answer 310

• Boerhaave’s syndrome: spontaneous perforation of the oesophagus, usually due to vomiting, which ruptures all the layers of the oesophageal wall (transmural). Boerhaave’s syndrome is a surgical emergency.
• Gastroenteritis
• Peptic ulcer
• Varices
• Cancer

Question 311

Describe the management for MWT

Answer 311

1st line – most resolve spontaneously.
ABCDE, blood transfusion, anti-emetic, endoscopy to stop bleeding, proton pump inhibitor. Surgical repair if endoscopic haemostasis has failed

Question 312

Describe the complications with MWT

Answer 312

• Rebleeding: usually occurs within the first 24 hours, but is rare after endoscopy
• Hypovolaemic shock: only occurs with life-threatening, persistent bleeds, which are very rare following MWT
• Oesophageal perforation: a rare complication
• MI

Question 313

Describe the prognosis of MWT

Answer 313

The prognosis associated with MWT is generally excellent.Bleeding often ceases spontaneouslyprior to arriving at the emergency department and almost always does so before endoscopy. Up to 15% of patients experience rebleeding, with the highest risk of rebleeding within the first 24 hours.

Alcoholism is a common underlying feature and requires recognition, and long-term support should be offered as appropriate.

Question 314

Define haemorrhoids

Answer 314

Haemorrhoids are normal spongy vascular structures in the anal canal that act as cushions for the stool as it passes through. Hemorrhoidal disease (simply know as haemorrhoids) is when haemorrhoids get disrupted, swollen and inflamed. Internal (above dentate line) and external (above dentate line)

Question 315

Describe the epidemiology of haemorrhoids

Answer 315

• Prevalence increases with age with a peak in 45-65 yr olds
• Equally common in both males and females

Question 316

Describe the aetiology of haemorrhoids

Answer 316

Haemorrhoids are often caused by chronically or recurrently increased abdominal pressure, from a variety of causes:

• Straining during bowel movements
• Chronic diarrhoea or constipation
• Congestion from a pelvic tumour, pregnancy, congestive cardiac failure and portal hypertension
• Anal intercourse

Question 317

Describe risk factors for haemorrhoids

Answer 317

Constipation, straining, coughing, heavy lifting, pregnancy, obesity, old age

Question 318

Describe the classification of internal haemorrhoids

Answer 318

Internal grades 1-4.
1: bleeding, no prolapse. 2: prolapse when straining and reduces when relaxing. 3: prolapse on straining, requires manual pushback. 4: permanently prolapsed

Question 319

Describe the clinical manifestations of haemorrhoids

Answer 319

Bright red bleeding on wiping, not in stool. Pruritis ani (itching), constipation, straining, lumps around or inside anus, perianal pain

Question 320

Describe the investigations for haemorrhoids

Answer 320

1st line External examination (see external haemorrhoids), digital rectal exam (DRE), proctoscopy (see internal haemorrhoids)

Question 321

Describe the differential diagnosis for haemorrhoids

Answer 321

Rectal bleeding: colorectal cancer, IBD, IBS.
Perianal disorders: anal fissure, anal fistula, perianal abscess

Question 322

Describe the management for haemorrhoids

Answer 322

Conservative: topical treatment, constipation – increase fluid, fibre, laxatives
1st and 2nd grade: rubber band ligation, infrared coagulation, injection scleropathy, bipolar diathermy
3rd and 4th grade: haemorrhoidectomy, stapled haemorrhoidectomy, haemorrhoidal artery ligation

Question 323

Describe the complications for haemorrhoids

Answer 323

• Anaemia due to chronic blood loss
• Strangulation if the blood supply to an internal haemorrhoid is cut off, leading to ischaemia
• Thrombosed haemorrhoids: blood pools inside a haemorrhoid and forms clots.

Procedure related:

• Rubber band ligation: pain, delayed haemorrhage if the rubber band dislodges, hemorrhoidal thrombosis, localised infection or abscess at the site of band ligation, sepsis, or urinary retention.
• Sclerotherapy: minor discomfort or bleeding with the injection, rectourethral fistulas, rectal perforations, and necrotising fasciitis, which can occur with misplaced injections into non-hemorrhoidal tissues or into the vasculature.
• Haemorrhoidectomy: infection, urinary retention mainly associated to spinal anaesthesia; urinary tract infection possibly secondary to urinary retention; fecal incontinence due to pain, anal spasm, and changes in sensation; anal stricture if too much anoderm is resected; and delayed haemorrhage due to sloughing of the primary clot, which usually occurs 7 to 16 days after the procedure.

Question 324

Define an anal fistula

Answer 324

An abnormal connection between the epithelial surface of the anal canal and skin - it is essentially a track that communicates between the skin and anal canal/rectum

Question 325

Describe the aetiology of anal fistulas

Answer 325

• Perianal sepsis
• Anorectal abscesses (70%)
• Crohn’s ulcerations (30%)
• TB
• Diverticular disease
• Rectal carcinoma
• Immunocompromise

Question 326

Describe the pathophysiology of anal fistulas

Answer 326

Blockage of deep intramuscular gland ducts is thought to predispose to the formation of abcesses, which discharge to form the fistula.

Question 327

Describe the clinical manifestations of anal fistulas

Answer 327

• Pain
  
  • Usually intermittent and during defecation, during sitting or activity.
• Malodorous discharge (bloody or mucus)
• Pruritus ani (itchy bottom)
• Perianal skin may be excoriated and inflamed
• Systemic abscess if it becomes infected

Question 328

What is the gold standard investigation for anal fistulae

Answer 328

Digital rectal exam

Question 329

What are the differential diagnosis for anal fistulae

Answer 329

Rectal bleeding: colorectal cancer, IBD, IBS. Perianal disorders: haemorrhoids, anal fissure, perianal abscess

Question 330

Describe the management for anal fistulae

Answer 330

1st line – surgical removal and drainage and treat with Abx if infected

Question 331

Define anal fissure

Answer 331

Painful tear in squamous lining of lower anal canal, distal to the dentate line resulting in pain on defecation.

Can be acute: <4-6 weeks

Or chronic: >6 weeks

Question 332

Describe the epidemiology of anal fissures

Answer 332

• 90% are posterior tears
• Anterior tears usually follow childbirth
• F>M

Question 333

Describe the aetiology of anal fissures

Answer 333

Constipation, anal trauma, Crohn’s, TB

Question 334

Describe the clinical manifestations of anal fissures

Answer 334

Extreme pain on defaecation (strong sensory supply), fresh blood on wiping or on stool, tearing sensation on passing stool

Question 335

What is the gold standard investigation for anal fissures

Answer 335

Digital rectal exam

Question 336

Describe the differential diagnosis for anal fissures

Answer 336

Rectal bleeding: colorectal cancer, IBD, IBS.
Blood on wiping: haemorrhoids, anal fistulae, perianal abscess

Question 337

Describe the management for anal fissures

Answer 337

1st line – stool softening: fluids and more fibre. Also topical creams, e.g., glyceryl trinitrate, diltiazem

Question 338

Describe the complications for anal fissures

Answer 338

The main complication of surgical treatment for anal fissures is fecal incontinence.

Question 339

Define a perianal abscess

Answer 339

Superficial infection that appears as a tender red lump under the skin near the anus. Most common anorectal abscess. Infection in anorectal tissue forming walled off collections of stool/bacteria abscess near the anus.

Question 340

Describe the epidemiology of perianal abscess

Answer 340

• Perianal abscesses make up 45% of anorectal abscesses (most common type)
• F>M
• 2-3 times more common in those who have anal sex

Question 341

Describe the aetiology of perianal abscesses

Answer 341

Anal fistula, Crohn’s, anal trauma (e.g., from anal sex)

Question 342

Describe the pathophysiology of a perianal abscess

Answer 342

An abscess forms when normal tissue is split apart and that new space is invaded by nearby pathogens like bacteria. This leads to an immune response.

Question 343

Describe the clinical manifestations of a perianal abscess

Answer 343

Constant perianal pain, perianal swelling, fever, pus in stool

Question 344

What is the gold standard investigation for a perianal abscess

Answer 344

Digital rectal exam

Question 345

Describe the differential diagnosis for perianal abscess

Answer 345

Rectal bleeding: colorectal cancer, IBD, IBS.
Blood on wiping: haemorrhoids, anal fistulae, anal fissure

Question 346

Describe the management for a perianal abscess

Answer 346

• Surgical excision and drainage
• Treatment with antibiotics

Question 347

Define a pilonidal sinus/abscess

Answer 347

Hair follicles get stuck under the skin in the natal cleft (butt crack) ~6cm above the anus, resulting in irritation and inflammation leading to small tracks which can become infected (abscess)

Question 348

Describe the epidemiology of pilonidal sinus/abscess

Answer 348

• M>F
• Commonly presents between 20-30 yrs

Question 349

What are the risk factors for a pilonidal sinus/abscess

Answer 349

• Obese caucasians and those from Asia, Middle East and Mediterranean are at increased risk
• Large amount of body hair
• Having deep gluteal clefts
• Sedentary job
• Family history
• Stiff hair

Question 350

Describe the pathophysiology of pilonidal sinus/abscess

Answer 350

Pilonidal disease is a common anal condition characterised by skin infection in the gluteal cleft. This is usually related to mechanical forces on the skin damaging and opening pores that collect loose hairs and debris, leading to hair follicle infection.

The ingrowing of hair excites a foreign body reaction and may cause secondary tracks to open laterally with or without abscesses, with foul-smelling discharge.

Question 351

Describe the clinical manifestations of pilonidal sinus/abscess

Answer 351

Swollen pus filled smelly abscess, sacrococcygeal discharge, pain, swelling and sinus tracts

Question 352

What is the gold standard for pilonidal sinus/abscess

Answer 352

Clinical examination

Question 353

Describe the management for pilonidal sinus/abscess

Answer 353

1st line – surgery (drainage). Area hygiene + antibiotics (co-amoxiclav). Hair removal