Gastrointestinal

Question 1

Define Chrons disease

Answer 1

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

Question 2

Epidemiology of Chrons

Answer 2

• Prevalence 100-200/100000
• Incidence 10-20/100000
• Highest incidence and prevalence in Northern Europe, UK and North America
• The disease has its peak onset in early life (20-40 years) with a second peak among the elderly (50-80)
• F>M

Question 3

Aetiology of Chrons

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

RF for Chrons

Answer 4

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

Question 5

Pathophysiology of Chrons

Answer 5

The immune system is thought to be triggered by some foreign pathogen e.g. Mycobacterium paratuberculosis, Pseudomona and Listeria species, in the gastrointestinal tract.

These pathogens are able to get through the wall due to some defect in the epithelial barrier.

The immune system targets the foreign pathogen but the immune response is large and uncontrolled and leads to the destruction of cells in the GI tract: T helper cells release cytokines which attract cells such as macrophages which release substances like proteases, platelet activating factor and free radicals. The immune cells invade deep into the mucosa and organise themselves into granulomas. Eventually ulcers form, which can go through all the layers. This is known as transmural.

It is thought one of the steps in the immune response is dysfunctional, which leads to the uncontrolled immune response. The dysfunctional step is thought to be due to genetics (frameshift mutation in NOD2/CARD15)

Crohn’s disease is characterised by skip lesions (occurs in patches) and can occur anywhere along the GI tract. It occurs most commonly in the terminal ileum and colon.

Explanation of symptoms:

Blood may appear in stools due to damaged intestinal walls and due to the damage, the intestines lose their ability to absorb water, causing diarrhoea.

If the small intestine is affected, it loses its ability to absorb nutrients, leading to malabsorption.

Question 6

Signs of Chrons

Answer 6

• Abdominal tenderness
• Fever
• Rectal examination: blood, skin tags, erythema, fissures, fistulas, ulceration
• Aphthous mouth ulcers

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 7

Symptoms of Chrons

Answer 7

• 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 8

Primary investigations for Chrons

Answer 8

• Primary investigations
  
  • 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;anaemia due to vitamin B12, folate or iron deficiency
  • Nutritional status:vitamin B12, folate, ferritin, and vitamin D may be low
  • CRP/ESR:CRP correlates with disease activity and should be measured in flares
  • U&Es: to assess for electrolyte disturbance and signs of dehydration
  • LFTs: a low serum albumin may indicate protein-losing enteropathy
  • Coeliac serology: to exclude coeliac disease
  • Stool microscopy and culture: to exclude infective gastroenteritis or pseudomembranous colitis (includingClostridium difficiletoxin)
  • Colonoscopy:investigation of choice and allows for biopsy
    
    • Mucosal inflammation, deep ulcers, skip lesions and cobblestone mucosa
    • Histology: transmural inflammation, granulomas and goblet cells

Question 9

Investigations to consider for Chrons

Answer 9

• CT abdomen pelvis:demonstrates inflammatory bowel changes and their distribution, as well the presence of fistulae or abscesses
• AXR:may show bowel inflammation (thumbprinting)
• MRI/US: shows small bowel disease activity and complications
• Serum antibody markers:to help differentiate UC and Crohn’s, particularly in the paediatric population
  
  • pANCA is more associated with ulcerative colitis
  • ASCA is more associated with Crohn’s disease

Question 10

Differentials for Chrons

Answer 10

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

Question 11

General management advice for Chrons

Answer 11

• 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 12

How to induce remission in Chrons

Answer 12

• Elemental diet: diet with nutrients in pre-digested form. May be used alone or in conjunction with medication to induce remission, particularly when there are concerns about steroids affecting growth in young people
• Glucocorticoids: first-line in inducing remission (e.g. budenoside in mild attacks, oral prednisolone in moderate-severe attacks or IV hydrocortisone in severe attacks )
• Immunosuppressants: azathioprine, mercaptopurine and methotrexate: used asadd-ontherapies in moderate attacks, but should not be used alone
  
  • Thiopurine methyltransferase (TPMT): assess levels before starting azathioprine or mercaptopurine
• Biological therapy (e.g. infliximab or adalimumab): used in refractory or fistulating disease, usually in combination with azathioprine or methotrexate
• Antibiotics e.g. metronidazole or ciprofloxacin: usually given for 1 month for isolated peri-anal disease

Question 13

How to maintain remission in Chrons

Answer 13

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 14

Surgery for Chrons (indications and types)

Answer 14

Not curative (unlike in UC), as Crohn’s can recur elsewhere along the GI tract.

• Indications for surgery
  
  • Poor response to drugs or nutritional treatment
  • Strictures
  • Abscesses and fistulae
  • Delayed growth in children
  • Malignancy
  • Emergency e.g. obstruction or perforation
• Types of surgery
  
  • Ileocaecal resection: healthy part of the bowel is then joined back with large colon
  • Partial right hemicolectomy: diseased portion of right colon removed
  • Colectomy with ileostomy: removal of colon and formation of stoma
  • Colectomy with ileo-rectal anastamosis: ending of ileum is attached to rectum
  • Panproctocolectomy and ileostomy: removal of rectum and colon and formation of stoma
  • Stricturoplasty: used to manage strictures
  • Abscess drainage
  • Resection of bowel section where fistulae have formed
  • Perianal fistula require drainage of infection and pus (using a seton suture)

Question 15

Complications of Chrons

Answer 15

Intestinal complications:

• Peri-anal abscess:peri-anal abscesses should be incised and drained under general anaesthetic due to the possibility of a fistula. Antibiotics are generally not required unless evidence of systemic infection
• Anal fissure:a small tear in the lining of the anus
• Anal fistula:an abnormal connection between 2 epithelial surfaces, e.g. from the anal canal to skin surface
• Strictures and obstruction:bowel loops can develop strictures following chronic inflammation and this can lead to bowel obstruction
• Perforation:chronic inflammation can weaken the bowel wall and predispose to subsequent perforation
• Malignancy: colorectal cancer and small bowel cancer
• Osteoporosis
• Anaemia and malnutrition
• Toxic dilatation of colon

Treatment complications:

• Infection:increased risk of opportunistic infections due to immunosuppressive therapy
• Myelosuppression:azathioprine and mercaptopurine require weekly FBC for the first month and then at least every 3 months after that
• Non-melanoma skin cancer: increased risk with thiopurines; people should be monitored for skin cancer and given appropriate sun protection advice

Question 16

Prognosis for Chrons

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

Mnemonic for Chrons

Answer 17

• Crohn’s (crows NESTS)
  
  • No blood or mucus (less common)
  • 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

Ulcerative colitis (UC) is a type of inflammatory bowel disease that characteristically involves the rectum and extends proximally to affect a variable length of the colon.

It never spreads proximally beyond the ileocaecal valve and is, therefore, confined to the large bowel. It does not affect the anus.

Question 19

Epidemiology of UC

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

RF for UC

Answer 20

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

Question 21

Pathophysiology of UC

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.

The pathology is not well understood.

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.

Cytotoxic T cells are often found in the epithelium lining the colon, and they may be responsible for destroying the cells lining the walls of the large intestine, leaving behind ulcers.

Some patients have p-ANCAs (perinuclear antineutrophilic cytoplasmic antibodies) in their blood - antibodies that target antigens in the body’s own neutrophils. Some theories suggest this may be partly due to an immune reactionto gut bacteria that have some structural similarity to our own cells, allowing antibodies to those gut bacteria, or p-ANCAs, to “cross-react” with neutrophils.

Patients also seem to have a higher proportion of gut bacteria that produce sulfides, and often high sulfide production is correlated with periods of active inflammation

The cause is ultimately some combination of environmental stimuli, perhaps the sulfide-producing bacteria, mixed with a genetic predisposition.

Question 22

Signs of UC

Answer 22

• Signs
  
  • Abdominal tenderness
  • Fever - in acute UC
  • Tachycardia - in acute severe UC
  • Fresh blood on rectal examination
• Extra-intestinal manifestations
  
  • 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 23

Symptoms of UC

Answer 23

• 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 24

What is fulminant disease

Answer 24

• 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 25

Primary Investigations for UC

Answer 25

• 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 26

Investigations to consider for UC

Answer 26

• Sigmoidoscopy: preferred to colonoscopy inacute flaresto avoid perforation; similar findings to colonoscopy but limited examination
• Abdominal X-ray:can assess for toxic megacolon, ‘lead-pipe’ appearance
• Stool microscopy and culture: to exclude infective gastroenteritis or pseudomembranous colitis
• Nutritional status: vitamin B12, folate, ferritin, and vitamin D may be low
• MRI/ CT abdomen and pelvis: helps assess the distribution of disease
• Barium enema:loss of haustrations, widespread superficial ulceration and ‘pseudopolyps’; may demonstrate a ‘lead-pipe’ colon in longstanding disease as the colon is narrowed and shortened
• Serum antibody markers:to help differentiate UC and Crohn’s disease, particularly in the paediatric population
  
  • pANCA is more associated with ulcerative colitis
  • ASCA is more associated with Crohn’s disease

Question 27

Differentials for UC

Answer 27

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

Question 28

General Management for UC

Answer 28

Depends on the location and severity of disease.

Generally,

• 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 29

Management for mild to moderate UC (proctatis)

Answer 29

• Induction of remission
  
  • First line: topical aminosalicylate (ASA); superior to rectal steroids or oral ASA
  • Second line(if remission not achieved within 4 weeks): add oral ASA
  • Third line: add topical or oral corticosteroid if remission still not achieved
• Maintenance of remission
  
  • Topical ASA (daily or intermittent)OR
  • Oral ASAwithtopical ASA (daily or intermittent)OR
  • Oral ASA alone: less effective than other two options

Question 30

Management of mild to moderate UC: proctosigmoiditis and left sided colitis (limited to splenic flexure)

Answer 30

• Induction of remission
  
  • First line: topical ASA
  • Second line(if remission not achieved within 4 weeks): add high-dose oral ASAORswitch to high-dose oral ASAandtopical corticosteroid
  • Third line: stop topical therapy and commence high-dose oral ASAandoral corticosteroid
• Maintenance of remission
  
  • Proctosigmoiditis:treat as for proctitis
  • Left-sided colitis:low maintenance dose of oral ASA

Question 31

Management of mild to moderate UC: extensive disease

Answer 31

• Induction of remission
  
  • First line:topical ASA and high-dose oral ASA
  • Second line(if remission not achieved within 4 weeks): stop topical therapy and commence high-dose oral ASAandoral corticosteroid
• Maintenance of remission
  
  • Low maintenance dose of oral ASA

Question 32

Management for acute severe UC (any site)

Answer 32

• Induction of remission
  
  • First line: admit to hospital and IV corticosteroid (or ciclosporin if steroids are contraindicated)
  • Second line:addIV ciclosporin if no improvement within 72h (or IV infliximab if ciclosporin is contraindicated)
  • Third line: Colectomy
• Maintenance of remission
  
  • Oral azathioprine or oral mercaptopurine
  • Consider oral ASA if the above are contraindicated

Question 33

Complications of UC

Answer 33

• 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 34

Prognosis for UC

Answer 34

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 35

UC mnemonic

Answer 35

• UC CLOSEUPC–Continuous inflammationL–Limited to colon and rectumO–Only superficial mucosa affectedS–Smoking is protectiveE–Excrete blood and mucusU–UseaminosalicylatesP–Primary Sclerosing Cholangitis

Question 36

Differences between UC and Chrons

Answer 36

Symptoms
UC - Abdo pain, bloody diarrhoea, mucus, weight loss
Chrons - Abdo pain, usually non bloody diarrhoea, significant weight loss, aphthous ulcers

Smoking
UC - Reduces risk
Chrons - Increases risk

Pathology
UC - Starts in the rectum and spreads proximally towards the ileocaecal valve. Never spreads into the small bowel or anus
Chrons - Any part of the GI tract and skip lesions may be seen

Most common location
UC - Rectal involvement is almost universal
Chrons - Terminal ileum

Endoscopic findings
UC - Shallow ulcers with pseudopolyps
Chrons - Mucosal inflammation, depp ulcers, skip lesions and cobblestone mucosa

Histology
UC - Mucosal and submucosal ulceration only. Crypt abscess with neutrophil infiltration
Chrons - Transmural inflammation, granulomas and goblet cells

Specific extra-intestinal features
UC - Primary sclerosing cholangitis and cholangiocarcinoma (can occur in Chrons but is much rarer)
Chrons - Gallstones: due to reduced bile reabsoprtion and calcium oxalate renal stones

Shared extra intestinal features
Arthritis, uveitis, Episcleritis, erythema nodosum, pyoderma gangrenosum

Complications
UC - Toxic megacolon and strictures
Chrons - Fissures, fistulas and strictures

Risk of colorectal cancer
UC - Marked increase
Chrons - Slight decrease

Surgery
UC - Curative
Chrons - For complications such as strictures

Question 37

Define IBS and its subtypes

Answer 37

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 38

Epidemiology of IBS

Answer 38

• 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 39

RF for IBS

Answer 39

Worsens symptoms:

• Acute gastroenteritis
• Stress
• Menstruation

Question 40

Pathophysiology of IBS

Answer 40

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 41

Signs of IBS

Answer 41

General abdominal tenderness may be felt.

Question 42

Symptoms of IBS

Answer 42

• Fluctuating bowel habit
• Diarrhoea
• Constipation
• Incomplete evacuation
• Urgency
• Mucus PR
• Abdominal pain
  
  • Pain worse after eating
  • Improved by opening bowels
• Bloating

Question 43

Diagnostic criteria for IBS

Answer 43

Abdominal 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 44

How to exclude other pathologies for IBS

Answer 44

• 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 45

Differentials for IBS

Answer 45

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

Question 46

Lifestyle advice for IBS

Answer 46

• Lifestyle advice
  
  • 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 47

Pharmacological management for IBS (1st, 2nd and 3rd line)

Answer 47

• 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 48

Other management for IBS

Answer 48

• 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 49

Prognosis for IBS

Answer 49

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

Question 50

When to consider other diagnoses for IBS

Answer 50

• 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 51

Define Coeliac

Answer 51

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 52

Epidemiology of Coeliac

Answer 52

• 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 53

Triggers of Coeliac

Answer 53

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

Question 54

RF for Coeliac

Answer 54

• 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 55

Pathophysiology of Coeliac

Answer 55

The most pathogenic component of gluten is gliadin.

Undigested gluten proteins, like gliadin, get to the small intestine, they meet the intestinal mucosa, lined with a layer of intestinal epithelial cells. Gluten proteins can then get across the gut epithelial cells, from the apical to the basolateral membrane, and get to the lamina propria.

Once there, an enzyme called tissue transglutaminase, or tTG, cuts off of an amide group from the protein. Deamidated gluten proteins are then eaten up by macrophages and served up on its MHC class IImolecules.

T helper cell recognise the gliadin and release inflammatory cytokineslike interferon gamma and tumour necrosis factor, which initiate inflammation directly damaging and destroying epithelial cells in the villi of the small intestine in the process.

The T helper cells also stimulate B cells to start producing antibodies, including:

• IgA: anti-tissue transglutaminase (anti-TTG), anti-endomysial (anti-EMA)
• IgG: deaminated gliadin peptides antibodies (anti-DGPs)

Finally, the T helper cells also recruit killer CD8+ T cells, which are drawn to and destroy cells undergoing inflammation.

Immune activation results in villous atrophy, lymphocyte accumulation and intestinal crypt hyperplasia, resulting in malabsorption. There are also numerous extraintestinal manifestations.

Question 56

Clinical manifestations of Coeliac

Answer 56

• 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 57

Investigations of Coeliac

Answer 57

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-lineserological 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-lineserological test and performed if anti-tTG is weakly positive
  • Anti-tTG, endomysial, or gliadin (IgG) antibodies:
  • If patients areIgA deficient, then IgG antibodies against tTG, gliadin or endomysium can be measured
• Anti-casein antibodies:
  
  • Also found in some patients
• 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 58

Other investigations to consider for Coeliac

Answer 58

• 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 59

Management for Coeliacs

Answer 59

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 60

Other management for Coeliacs

Answer 60

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 61

Monitoring for Coeliacs

Answer 61

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

Question 62

Complications of Coeliacs

Answer 62

• Dermatitis herpetiformis: may require treatment with dapsone
• Malignancy:increased risk of small bowel adenocarcinoma and enteropathy-associated T-cell lymphoma. The risk appears to normalise after a few years of gluten restriction
• Extra-intestinal malignancies: non-Hodgkin’s and Hodkin’s lymphoma, and oesophageal cancer (all are rare)
• Malabsorption-related:
  
  • Increased risk of osteoporosis: bone mineral density is usually checked after 1 year of a gluten-free diet in those who have other risk factors for osteoporosis
  • Calcium and vitamin D deficiency: may lead to secondary hyperparathyroidism and osteomalacia
  • Anaemia: microcytic anaemia (iron deficiency) or macrocytic anaemia (vitamin B12 / folate deficiency); folate deficiency is more common than vitamin B12 deficiency in coeliac disease
  • Peripheral neuropathy (B12/folate)
• Infection: hyposplenism is associated with coeliac disease and increases the risk of pneumococcal infection
• Lactose intolerance: due to gut damage secondary to coeliac disease; lactose intolerance is usually temporary following introduction of a gluten-free diet
• Subfertility and recurrent miscarriages
• Ulcerative jejunitis
• Coeliac crisis: a rare, life-threatening syndrome associated with significant metabolic derangements, presenting with severe diarrhoea and electrolyte disturbances

Question 63

Prognosis of Coeliacs

Answer 63

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 64

Physiology of gastric and oesophageal mucosa

Answer 64

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.

Stomach mucosa:

• 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

Oesophageal mucosa:

• 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 65

Define Gastro-oesophageal reflux disease (GORD)

Answer 65

Reflux of stomach contents into the oesophagus.

Question 66

Epidemiology of GORD

Answer 66

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

Question 67

Aetiology of GORD

Answer 67

• Lower oesophageal hypotension
• Oesophageal dysmotility
• Gastric acid hypersecretion

Question 68

RF for GORD

Answer 68

• 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 69

Pathophysiology of GORD

Answer 69

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 70

Clinical manifestations of GORD

Answer 70

• 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 71

Investigations of GORD

Answer 71

• 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 72

Red flags for GORD diagnosis

Answer 72

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

Question 73

Los Angeles classification of GORD

Answer 73

• Los Angeles classification
  
  • Grade A: ≥1 mucosal break, each ≤ 5mm
  • Grade B: ≥1 mucosal break > 5mm. Not continuous between top of mucosal folds.
  • Grade C: ≥1 mucosal break, continuous between top of mucosal folds, not circumferential
  • Grade D: mucosal breaks involving more thanthree quartersof luminal circumference.

Question 74

Reflux phenotyping for GORD

Answer 74

• Reflux phenotypingFour different phenotypes based on endoscopy findings and pH monitoring:
  • Erosive oesophagitis: erosions seen at gastroscopy
  • Non-erosive oesophageal reflux: normal gastroscopy, but pathological acid exposure on pH testing
  • Acid hypersensitive oesophagus: normal gastroscopy, non-pathological acid exposure on pH testing but temporal association of reflux events with symptoms
  • Functional heartburn: normal gastroscopy, non-pathological acid exposure on pH testing andno temporal association of reflux events with symptoms.

Question 75

Differentials for GORD

Answer 75

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

Question 76

Lifestyle Management of GORD

Answer 76

• 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 77

Medical management of GORD

Answer 77

• 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

Question 78

Surgical management of GORD

Answer 78

• 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 79

Complications of GORD

Answer 79

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 80

Prognosis of GORD

Answer 80

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 81

Define Barretts Oesophagus

Answer 81

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 82

Epidemiology of Barretts oesophagus

Answer 82

• 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 83

RF for Barretts oesophagus

Answer 83

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

Question 84

Pathophysiology of Barretts oesophagus

Answer 84

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 85

Clinical manifestations of Barretts oesophagus

Answer 85

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

Question 86

Investigations for Barretts oesophagus

Answer 86

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 87

Prague criteria for Barretts oesophagus

Answer 87

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 88

Management of underlying reflux

Answer 88

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

Question 89

Management of non-dysplastic Barretts oesophagus

Answer 89

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

Question 90

Management of low grade dysplasia in Barretts

Answer 90

• 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 91

Management of high grade dysplasia in Barretts

Answer 91

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

Question 92

Management of adenocarcinoma (Barretts)

Answer 92

Oesophagectomy: surgical intervention is indicated in non-metastatic disease

Question 93

Complications of Barretts

Answer 93

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

Question 94

Prognosis for Barretts

Answer 94

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 95

Physiology of the Oesophagus

Answer 95

• Oesophagus notesThe 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 96

Define malignant oesophageal tumours

Answer 96

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

Question 97

Epidemiology of malignant oesophageal tumours

Answer 97

• 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 98

RF for Malignant oesophageal

Answer 98

General risk factors

• Age > 60
• Smoking
• Achalasia

Risk factors for adenocarcinoma:

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

Risk factors for SCC

• 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 99

Pathophysiology of malignant oesophageal

Answer 99

Squamous cell carcinoma:

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.

Adenocarcinoma:

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 100

Signs of malignant oesophageal cancer

Answer 100

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

Question 101

Symptoms of oesophageal malignancy

Answer 101

• 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 102

1st line Investigations for oesophageal malignancy

Answer 102

Upper GI endoscopy (OGD) and biopsy: first-line investigation and allows for visualisation of masses and biopsy

Question 103

Staging investigations for oesophageal malignancy

Answer 103

• 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)

Question 104

Staging for oesophageal malignancy

Answer 104

Staged using TNM

Question 105

Management for localised malignant adenocarcinoma

Answer 105

• Localised adenocarcinoma
  
  • 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 106

Management for localised malignant squamous cell carcinoma of the oesophagus

Answer 106

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

Question 107

Management of advanced or metastatic oesophageal malignancy

Answer 107

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

Question 108

Cancer related complications of oesophageal malignancy

Answer 108

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.

Question 109

Oesophagectomy-related complications of oesophageal malignancy

Answer 109

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 110

Prognosis of oesophageal malignancy

Answer 110

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 111

Overview of Benign oesophageal tumours

Answer 111

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

Question 112

Pathophysiology of benign oesophageal tumour

Answer 112

Leiomyomas:

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

Question 113

Clinical manifestations of benign oesophageal tumour

Answer 113

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

Question 114

Investigations for benign oesophageal tumour

Answer 114

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

Question 115

Management of benign oesophageal tumour

Answer 115

• Endoscopic removal
• Surgical removal of larger tumours

Question 116

Physiology of the stomach

Answer 116

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.

The gastric wall is made up of four layers:

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

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.

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 117

Overview of gastric cancer

Answer 117

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 118

Define Gastric adenocarcinoma

Answer 118

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 119

Epidemiology of gastric adenocarcinoma

Answer 119

• 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 120

RF for gastric adenocarcinoma

Answer 120

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 121

Pathophysiology of Gastric adenocarcinoma

Answer 121

Intestinal type

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.

Diffuse type

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 122

Signs of gastric adenocarcinoma

Answer 122

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

Question 123

Symptoms of gastric adenocarcinoma

Answer 123

• 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 124

1st line investigations for gastric adenocarcinoma

Answer 124

Upper GI endoscopy and biopsy: ulcer with heaped-up edges is a common presentation

Question 125

Staging investigations for Gastric adenocarcinoma

Answer 125

• 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 126

Staging of Gastric adenocarcinoma

Answer 126

• 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 127

Differentials for Gastric adenocarcinoma

Answer 127

• Peptic ulcer disease
• Oesophageal stricture
• Achalasia

Question 128

Management for localised gastric adenocarcinoma

Answer 128

• Localised disease
  
  • 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 129

Management for advanced or metastatic gastric adenocarcinoma

Answer 129

• 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 130

Cancer related complications of gastric adenocarcinoma

Answer 130

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

Gastrectomy-related

• 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 131

Prognosis of gastric adenocarcinoma

Answer 131

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.

Question 132

Overview of Gastric Lymphoma

Answer 132

• 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 133

Overview of gastric carcinoid tumours

Answer 133

• 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 134

Overview of Gastric Leiomyosarcoma

Answer 134

• 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 135

Overview of Malignant small bowel tumours

Answer 135

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

Question 136

RF for malignant small bowel tumours

Answer 136

Coeliac and Chrons

Question 137

Clinical manifestations of Small bowel malignancies

Answer 137

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

Question 138

Investigations for small intestine malignancy

Answer 138

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

Question 139

Management of small intestine malignancy

Answer 139

• Surgical resection
• Radiotherapy

Question 140

Overview of Small bowel benign tumours

Answer 140

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

Question 141

Large intestine physiology

Answer 141

Large intestine can be thought of as having two spaces - the intraperitoneal space and the retroperitoneal space.

Intraperitoneal - First part of duodenum, small intestines, transverse colon, signmoid colon, rectum
Retroperitoneal - distal duodenum, ascending colon, descending colon, Anal canal

Question 142

Define Colonic polyps

Answer 142

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 143

Epidemiology of Colonic polyps

Answer 143

Polyp presence increases with age and is rare before 30 yrs

Question 144

Pathophysiology of colonic polyps

Answer 144

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 145

Clinical manifestations of colonic polyps

Answer 145

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

Question 146

Management of colonic polyps

Answer 146

Polyps are removed at colonoscopy to reduce development into cancer risk

Question 147

Define colorectal cancer

Answer 147

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

Question 148

Staging of Colorectal carcinoma

Answer 148

TNM and Dukes

Question 149

Epidemiology of Colorectal carcinoma

Answer 149

• 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 150

Aetiology of colorectal carcinoma

Answer 150

• 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 151

RF for colorectal carcinoma

Answer 151

• 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 152

Pathophysiology of colorectal carcinoma

Answer 152

• 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 153

General Clinical manifestation principles for colorectal carcinoma

Answer 153

Right-sided tumours are often asymptomatic, with the majority of patients presenting with incidental iron-deficiency anaemia. In contrast, left-sided tumours are particularly associated with a change in bowel habit and have higher rates of rectal bleeding and large bowel obstruction.

Question 154

Signs and symptoms of right sided colorectal carcinoma

Answer 154

• 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 155

Signs and symptoms of left sided colorectal carcinoma

Answer 155

• 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 156

Investigations for colorectal carcinoma

Answer 156

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

Question 157

Differentials for Colorectal carcinoma

Answer 157

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

Question 158

Screening for colorectal carcinoma

Answer 158

• 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 159

Initial management for colorectal carcinoma

Answer 159

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

Question 160

Elective treatment management for colorectal carcinoma

Answer 160

• 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

Question 161

Emergency treatment for large bowel obstruction or perforation

Answer 161

• Colon cancer: the two options are to stent or resect
  
  • Resection and anastomosis: a general rule is that right-sided (ileocolic) resections are safer than left-sided (colon-colon) resections, and anastomosis is usually possible, even in the emergency setting
  • Hartmann’s procedureis usually performed for obstructing sigmoid tumours, where anastomosis would be risky. It involves surgical resection of the rectosigmoid colon with closure of the anorectal stump and formation of an end colostomy which can be reversed at a later stage
• Rectal cancer: surgical resection mustnotbe performed in rectal cancer (unlike colon) until staging is complete due to the risk of a positive resection margin (cancer cells left behind) in an unstaged patient, as well as the high risk of anastomotic leak. Instead, adefunctioning loop colostomyis performed

Question 162

Complications of colorectal carcinoma

Answer 162

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 163

Prognosis of Colorectal carcinoma

Answer 163

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 164

Define peptic ulcer disease

Answer 164

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 165

Epidemiology of peptic ulcer disease

Answer 165

• 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 166

Aetiology of peptic ulcers

Answer 166

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 167

Pathophysiology of peptic ulcers

Answer 167

H.Pyori: release adhesions to help them adhere to the gastric foveolar cells and proteases that cause damage to the mucosal layer. Over time the damage erodes deeper into the mucosa, eventually causing ulcers.

NSAIDs: inhibit the enzyme cyclooxygenase which is involved in the synthesis of inflammatory prostaglandins. Overtime this leaves the mucosal layer susceptible to damage by ulcer formation.

Zollinger Ellison syndrome: a neuroendocrine tumor that is typically located in the duodenal wall or pancreas, and secretes abnormal amounts of gastrin. This stimulates parietal cells to release excess hydrochloric acid.

Peptic ulcers that result from any of these mucosa-damaging-mechanisms are usually small, round “punched out” holes in the mucosa.

• Gastric ulcers typically form in the lesser curvature of the antrum.
• Duodenal ulcers usually develop right after the pyloric sphincter and there’s usually Brunner gland hypertrophy - a consequence of the body trying to produce more mucus to protect the damaged area.

Typically, beneath the base is a layer of scar tissue and blood vessels, and occasionally the ulcers can bleed if the erosion goes deep.

• Gastric ulcers typically affect the left gastric artery
• Duodenal ulcers typically affect the gastroduodenal artery

Question 168

Signs of peptic ulcer disease

Answer 168

• Evidence of bleeding
  
  • Hypotension and tachycardia (shock)
  • Melaena on rectal examination
• Epigastric tenderness
• Pallor, if anaemic

Question 169

Symptoms of peptic ulcer disease

Answer 169

• ‘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 170

Investigations for peptic ulcer disease when theres no active bleeding

Answer 170

• 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

Question 171

Investigations for peptic ulcers with active bleeding

Answer 171

• 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 172

Differentials for peptic ulcers

Answer 172

• Gastric malignancyRed flag ALARM signs for cancer
  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset
  • Malaena or haematemesis
  • Swallowing difficulties (dysphagia)
• GORD
• Non-ulcer dyspepsia
• Gastritis

Question 173

Management for peptic ulcers that aren’t actively bleeding

Answer 173

First-line:

• Conservative:treat risk factors e.g. cease NSAIDs/ other drugs, smoking and alcohol
• H. pylorinegative:proton pump inhibitor (PPI) usually high dose initially for one month until the ulcer has healed; e.g. omeprazole. H2 antagonists may also be used to reduce acid release.
• H. pyloripositive:triple eradication therapy
  
  • Omeprazole, clarithromycin and amoxicillin
  • Omeprazole, clarithromycin and metronidazole, if penicillin-allergic

Second-line:

• Switch to alternative strategy:i.e. if the patient was trialled on a PPI, test them forH. pylori. If the patient was treated forH. pylori, trial them on a high dose PPI for a month

Question 174

Management for actively bleeding peptic ulcers

Answer 174

• IV crystalloid
• Blood transfusion: if significant acute blood loss suspected
• Upper GI endoscopy:diagnostic and therapeutic with one of the following suggested; adrenaline shouldnotbe used alone
  
  • Mechanical therapy (e.g. clipping) +/- adrenaline
  • Thermal coagulation with adrenaline
  • Sclerotherapy (fibrin or thrombin injection) with adrenaline
• High-dose IV PPI: administered post-endoscopy to reduce rebleeding. Shouldnotbe given before endoscopy as may mask bleeding

Second-line:

• Surgery or embolisation (blocking abnormal vessels) by interventional radiology: reserved for cases where adequate haemostasis is not achieved at endoscopy

Question 175

Complications of Peptic ulcer disease

Answer 175

• 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 176

Prognosis of peptic ulcer disease

Answer 176

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 177

Define and overview of Appendicitis

Answer 177

Acute appendicitis is an acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix.

The vermiform appendix may occupy avariety of positionsin relation to the caecum:

• Most commonly thedescending intraperitoneal or retrocaecal position
• Retrocaecal and pelvic appendicitis are often more difficult to distinguish clinically

Question 178

Epidemiology of Appendicitis

Answer 178

• 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 179

RF for Appendicitis

Answer 179

• 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 180

Pathophysiology of Appendicitis

Answer 180

Appendicitis describes acute inflammation and bacterial infection of the appendix. This occurs due toluminal obstructionby a faecolith (hard mass of stool), undigested seeds, foreign body, pinworm infection, lymphoid hyperplasia of Peyer’s patches, or fibrous strictures.

The appendix is always secreting mucus and fluids from its mucosa into its lumen to keep pathogens from entering the bloodstream and also to keep the tissue moist. This continues even with the obstruction. Fluid and mucus builds up, which increases the pressure in the appendix, it gets bigger and physically pushes on the afferent visceral nerve fibers nearby, causing abdominal pain.

Along with that, the flora and bacteria in the gut are now trapped, and intestinal bacteria that are usually kept in check in the gutare now free to multiply. This causes the immune systemto recruit white blood cells and pus starts to accumulate in the appendix.

If obstruction persists, the pressure in the appendix increases further. At a certain point, as it continues to swell up, it pushes on and compresses the small blood vessels that supply the appendix with blood and oxygen. Without O2 the cells in the walls of the appendix become ischaemic and die. The growing colony of bacteria can now invade the wall of the appendix.

The swelling may even continue to the point of rupture, allowing bacteria to escape. This can lead to peritonitis, abscess formation (due to pus and fluid), and even sepsis.

Mechanisms of pain in appendicitis:

• Peri-umbilical pain: inflammation of the appendix and visceral peritoneum irritates autonomic nerves of the embryological midgut → referred pain to the umbilical region
• Right iliac fossa pain: due to localised inflammation of the parietal peritoneum

Question 181

Key presentations of appendicitis

Answer 181

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

Question 182

Signs of Appendicitis

Answer 182

• 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

Question 183

Symptoms of Appendicitis

Answer 183

• 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 184

Primary investigations of appendicitis

Answer 184

• Primary investigations
  
  • 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 185

Further investigations for appendicitis

Answer 185

Imaging done mainly to confirm diagnosis and prevent removal of normal appendix!

• Abdominal ultrasound: preferred in children, pregnant, and breastfeeding women and may show a non-compressible inflamed appendix, however the appendix often cannot be visualised; sensitivity is 86% and specificity is 81%. Often used in female patients to exclude ovarian and gynaecological pathology.
• CT abdomen/pelvis with contrast: CT has a 95% sensitivity and specificity for appendicitis; becoming increasingly used as the first diagnostic test for appendicitis
• MRI abdomen/pelvis: mainly reserved for pregnant women when ultrasound is non-diagnostic
• Diagnostic laporoscopy: done to confirm diagnosis and then proceed to appendicectomy in same procedure

Question 186

Differentials for appendicitis

Answer 186

• 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 187

Initial and Definitive management of appendicitis

Answer 187

• 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 188

Complications of appendicitis

Answer 188

• Perforation (15-20%): if left untreated, there is a significant risk of appendiceal rupture, which will lead to sepsis and death if untreated
• Appendix Mass: occurs when theomentumsurrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa. This is typically managed conservatively with supportive treatment and antibiotics, followed by appendicectomy once the acute condition has resolved.
• Abscess: inflammation may cause the formation of a localised collection of pus in proximity to the appendix, which will require drainage. May also cause a subphrenic abscess (below diaphragm). Antibiotics alone may allow resolution.
• Complications of Appendicectomy
  
  • Bleeding, infection, pain and scars
  • Damage to bowel, bladder or other organs
  • Removal of a normal appendix
  • Anaesthetic risks
  • Venous thromboembolism (deep vein thrombosis or pulmonary embolism)

Question 189

Prognosis of appendicitis

Answer 189

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 190

Define bowel obstruction

Answer 190

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 191

Classification of bowel obstruction

Answer 191

• 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 192

Aetiology of bowel obstruction

Answer 192

Mechanical causes: caused by actual blockages in the large or small intestine, and it can be defined as partial or complete. Partial obstruction is when gas or liquid stool can pass through the point of narrowing, while complete obstruction is when nothing can pass.

Small intestine

• The most common cause in the small intestine is postoperative adhesions. After a surgery, the scar tissue that forms during the healing process can form fibrous bands that cause organs to attach to the surgical site or to other organs, causing the lumen of the bowel to get kinked or pinched tight in certain spots.
• Another cause of small intestinal obstruction is hernias, and they can occur when a portion of the bowel protrudes out of the abdominal cavity and can get trapped or tightly pinched at the point where it pokes out.
• Gallstone ileus - gallstone within lumen of small bowel
• Meconium ileus - in neonates, content of bowel is sticky = blockage

Large intestine:

• Most often due to a volvulus, which is when a loop of intestine twists upon itself, kinking off the lumen.
• Sometimes the volvuluscan occur around a mass like in colorectal cancer.

Both

• Inflammatory bowel disease which can cause strictures and adhesions
• Ingestion of a foreign body, which can get lodged along the GI tract
• Intussusception: a part of the intestine folds into the lumen of an adjacent section of bowel. This is the most common cause of obstruction in children under the age of 2.

Functional causes: causes disrupt peristalsis, which are the waves of contraction that move through the smooth muscles of the bowel wall that pushes food through the intestines.

• The most common one is postoperative ileus, which is transient paralysis of the smooth muscles in the intestinal wall, and it’s usually caused by trauma during surgery.
• Other causes include infection or inflammation, such as appendicitis or peritonitis, hypothyroidism, or electrolyte abnormalities e.g. hypokalaemia and hypercalcaemia, and various drugs e.g. opioids
• Hirschprung’s disease:
  
  • In neonates they are born without complete innervation of colon to rectum
  • Results in gut dilatation and the filling of faeces which remains since no ganglion cells to result in peristalsis and movement of contents - resulting in obstruction

Question 193

Pathophysiology of bowel obstruction

Answer 193

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 194

Define small bowel obstrcution

Answer 194

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 195

Epidemiology of small bowel obstruction

Answer 195

• 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 196

Aetiology of small bowel obstruction

Answer 196

Can be mechanical (obstruction) or functional (lack of contraction)

• Bowel adhesions: the most common cause, occurs due to previous abdominal surgery which leads to the formation of fibrous connective tissue between organs and tissue
• Incarcerated hernia: most commonly femoral and inguinal hernias
• Stricture formation: due to Crohn’s disease
• Intussusception: part of the bowel slides into another part, more common in children.
• Gallstone ileus - gallstone within lumen of small bowel
• Meconium ileus - in neonates, content of bowel is sticky = blockage
• Volvulus: a rare cause of SBO; commonly causes large bowel obstruction
• Ingestion of foreign body
• Paralytic ileus: functional obstructiondue to failure of peristalsis
  
  • Occurs post abdominal surgery
  • Can occur due to electrolyte imbalances, particularly hypokalemia and hypercalcaemia
  • Infection/ inflammation e.g. peritonitis, pancreatitis, appendicitis.
  • Spinal injury
  • Drugs e.g. TCAs

Question 197

Pathophysiology of small bowel obstruction

Answer 197

When peristalsis occurs against a mechanical obstruction, this results in the characteristic symptoms of abdominal pain, distention, and absolute constipation.

Dilation of the proximal bowel leads to compression of mesenteric vessels and mucosal oedema. This results in transudation of large volumes of electrolyte-rich fluid into the bowel (‘third-spacing’). Eventually, as arterial supply is compromised, bowel ischaemia occurs with risk of perforation and subsequent faecal peritonitis and sepsis

Question 198

Signs of small bowel obstruction

Answer 198

• Abdominal tenderness and distension: distension usually occurs with more distal obstruction and is less severe in SBO, compared to LBO
• Tinkling bowel sounds in mechanical obstruction/ absent bowel sounds may be present in functional obstruction
• Rectal examination:
  
  • The rectum may be empty
  • Blood suggests strangulation and ischaemia
• Tachycardia and hypotension:
  
  • Third-spacing of fluid
  • Significant hypotension may indicate ischaemia, perforation or sepsis

Question 199

Symptoms of SBO

Answer 199

• Colicky, central or generalised abdominal pain
  
  • Pain is located higher in SBO than in LBO - periumbilical and intermittent
  • Pain is usually less severe with ileus
• Nausea and vomiting: early symptoms in SBO and a late sign in LBO
• Abdominal bloating
• Constipation (may be absolute in distal obstruction): no passing of faeces or flatus; a late symptom in SBO
• Anorexia

Question 200

Investigations of SBO

Answer 200

• Primary investigations
  
  • Bloods:
    
    • FBC:elevated white cell count with neutrophilia
    • U&Es:assess for pre-renal acute kidney injury secondary to hypovolaemia (third spacing). Additionally, hypokalaemia is a cause of ileus
    • CRP:raised as part of the general inflammatory response
    • Group and save:patients may go for surgery and require blood products
    • Venous blood gas (VBG):to assess the degree of metabolic acidosis and lactate level, which may be suggestive of bowel ischaemia
  • Abdominal X-ray: first-line imaging and will reveal:
    
    • Dilated small bowel loops(>3cm)with fluid levels(suggesting mechanical obstruction)
    • OR generalised, uniform distention of the bowel suggesting functional bowel obstruction.
    • Free air under the diaphragm means there’s perforation, so emergency surgery is needed.
  • 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
• Other investigations to consider
  
  • Erect chest X-ray: may be considered to assess for pneumoperitoneum if concerned about perforation
  • Contrast studies: if the patient is not improving on conservative management, they can drink water-soluble contrast (e.g. gastrograffin) and have serial X-rays/ CT. If the contrast fails to reach the colon this is an indication for surgery

Question 201

Initial management of SBO

Answer 201

• Initial management
  
  • IV resuscitation: patients ‘third-space’ fluid into the lumen of the bowel segment proximal to the obstruction, resulting in hypovolaemia
  • Nasogastric (NG) tube: all patients with suspected bowel obstruction that are actively vomiting should have an NG (Ryle’s) tube inserted for abdominal decompression (suck out accumulating gas and fluid). The combination of IV fluids and NG tube insertion is known as‘drip’ (IV fluids) and ‘suck’ (NG tube)
  • IV antibiotics: patients receive broad-spectrum prophylactic antibiotics, typically if going for surgery to prevent wound infection, e.g. cefotaxime and metronidazole
  • Analgesia and anti-emetics

Question 202

Surgical and other management of SBO

Answer 202

• Emergency laparotomyto treat the underlying cause with bowel resection. Surgery is indicated in the following instances:
  
  • Evidence of bowel ischaemia regardless of the cause
  • A non-adhesional cause (e.g. strangulated hernia)
  • Failure of conservative management for adhesional obstruction e.g. worsening pain, lactate raised, bowel loop distension on imaging
• Adhesiolysis: performed for adhesional obstruction, and recurrent adhesional obstruction may require repeat adhesiolysis
• Other
  
  • Gastrograffin: as well as being diagnostic, evidence suggests that oral gastrograffin (e.g. 100ml with repeat abdominal X-rays) may be used therapeutically in adhesional obstruction. Gastrograffin may reduce the need for surgery when conservative treatment fails.

Question 203

Complications of SBO

Answer 203

• 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
• Short gut syndrome:in cases where the bowel has been resected due to infarction, there is a risk of malabsorption

Question 204

Prognosis for SBO

Answer 204

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 205

Define large bowel obstruction

Answer 205

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

Question 206

Epidemiology of LBO

Answer 206

• Less common, accounting for only 25% of all intestinal obstruction
• 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 207

Aetiology of LBO

Answer 207

• Colorectal cancer: most common cause
• Stricture: complication of diverticulitis, inflammatory bowel disease, or post-anastomosis
• Volvulus: torsion of the colon around itself and the mesentery. Results in compromised blood flow and a closed-loop obstruction
  
  • Sigmoid volvulustypically affects elderly patients, as well as those with chronic constipation or neuropsychiatric conditions, such as Parkinson’s disease and schizophrenia
  • Caecal volvulusis less common (20%). It is associated with adhesions, more common in females (e.g. pregnancy) and can occur at any age
• Hirschprung’s disease:
  
  • Neonates are born without complete innervation of colon to rectum
  • Results in gut dilatation and the filling of faeces which remains since no ganglion cells to result in peristalsis and movement of contents - resulting in obstruction

Question 208

RF for LBO

Answer 208

• 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 209

Pathophysiology of LBO

Answer 209

When peristalsis occurs against a mechanical obstruction, this results in the characteristic symptoms of abdominal pain, distention, and absolute constipation.

Dilation of the proximal bowel leads to compression of mesenteric vessels and mucosal oedema. This results in transudation of large volumes of electrolyte-rich fluid into the bowel (‘third-spacing’).

Eventually, as arterial supply is compromised, bowel ischaemia occurs with risk of perforation and subsequent faecal peritonitis and sepsis.

Question 210

Signs of LBO

Answer 210

Note: Large bowel has a larger lumen as well as circular and longitudinal muscles thus the ability of the large bowel to distend is much greater thus symptoms present slower and later than in SBO

• Signs
  
  • Abdominal tenderness and distention
  • Tinkling bowel sounds early on, absent later
  • Rectal examination: empty rectum, hard stools and blood
  • Tachycardia and hypotension
    
    • Third-spacing of fluid
    • Significant hypotension may indicate ischaemia, perforation or sepsis

Question 211

Symptoms of LBO

Answer 211

• Colicky, generalised abdominal pain
  
  • Pain is constant in LBO compared to SBO
• Bloating
• Constipation (may be absolute in distal obstruction): no passing of faeces or flatus
  
  • Occursearlierin LBO than in small bowel obstruction
• Vomiting:
  
  • May be faeculent in nature
  • Alatesymptom in LBO, occurs earlier in small bowel obstruction
• Anorexia

Question 212

All investigations for LBO

Answer 212

• Primary investigations
  
  • Bloods:
    
    • FBC:elevated white cell count with neutrophilia
    • U&Es:assess for pre-renal acute kidney injury secondary to hypovolaemia (third spacing)
    • CRP:raised as part of the general inflammatory response
    • Venous blood gas:to assess the degree of metabolic acidosis and lactate level, which may be suggestive of bowel ischaemia
    • Group and save:patients may go for surgery and require blood products
  • Abdominal X-ray:first-line imaging
    
    • Dilated large bowel may be visible (> 6cm in the colon; > 9cm in the caecum)
    • Sigmoid volvulus: a large, dilated loop of colon, with coffee bean sign
    • Caecal volvulus:small bowel obstruction may be seen (> 3 cm in the small bowel)
    • Free air under the diaphragm means there’s perforation, so emergency surgery is needed.
  • 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
• Investigations to consider
  
  • Erect chest X-ray: to assess for pneumoperitoneum if concerned about perforation
  • Contrast enema:a water-soluble contrast fluid, such as gastrografin, can be used to identify obstruction if the above investigations are equivocal
  • Colonoscopy: to investigate the cause, but beware of perforation.

Question 213

Initial management of LBO

Answer 213

• Initial management
  
  • IV resuscitation: patients ‘third-space’ fluid into the lumen of the bowel segment proximal to the obstruction, resulting in hypovolaemia
  • Nasogastric (NG) tube: all patients with suspected bowel obstruction that are actively vomiting should have an NG (Ryle’s) tube inserted for abdominal decompression (suck out accumulated fluid and gas). The combination of IV fluids and NG tube insertion is known as‘drip’ (IV fluids) and ‘suck’ (NG tube)
  • IV antibiotics: patients usually receive prophylactic antibiotics due to the risk of bacterial translocation across the inflamed bowel wall
  • Analgesia and anti-emetics

Question 214

Further management of LBO

Answer 214

• Treat the cause:
  
  • Colon cancer:stenting or surgical resection e.g. Hartmann’s procedure
  • Rectal cancer:defunctioning colostomy
  • Diverticular disease:Hartmann’s procedure or resection, with or without a stoma
  • Sigmoid volvulus: rigid sigmoidoscopy with flatus tube insertion. Sigmoid colectomy may be required
  • Caecal volvulus: usually requires surgery; right hemicolectomy is often performed
  • Unclear cause: exploratory laparotomy and remove any obstruction found
• Conservative: if CT does not demonstrate complicated features (e.g. ischaemia) and the patient is haemodynamically stable, they may be closely monitored and managed conservatively providing there is no evidence of an obstructing tumour or closed-loop bowel obstruction

Question 215

Complications of LBO

Answer 215

• 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 216

Prognosis of LBO

Answer 216

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 217

Define pseudo obstruction

Answer 217

Clinical picture mimicking colonic obstruction but with no mechanical cause.

Also known as Ogilvie syndrome.

Question 218

Epidemiology of PO

Answer 218

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

Question 219

Aetiology of PO

Answer 219

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 220

Clinical manifestations of PO

Answer 220

• Patients present with rapid and progressive abdominal distension and pain
• Similar presentation to mechanical obstruction

Question 221

Investigations for PO

Answer 221

X-ray shows a gas-filled large bowel

Question 222

Management of PO

Answer 222

• Treat underlying problem e.g. withdrawal of opiate analgesia
• Correct U&E
• IV Neostigmine - a cholinesterase inhibitor, may be given to encourage motility.
• Endoscopic colonic decompression can be used in those failing to respond.
• Those at increasing risk of or who have developed complications (e.g. necrosis, perforation) will typically need surgical management, if appropriate.

Question 223

Complications of PO

Answer 223

Weight loss: due to malabsorption in chronic pseudo-obstruction

Question 224

Define Diverticulosis, Diverticular disease and diverticuluitis

Answer 224

• 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 225

Epidemiology of Diverticulitis

Answer 225

• 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 226

RF for Diverticular disease

Answer 226

• 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

Question 227

Pathophysiology of Diverticular disease

Answer 227

• Colonic diverticulosis: is the formation of outpouchings (diverticula) in the wall of the colon, most frequently affecting the sigmoid due to its small diameter (small diameter = higher pressures).The diverticula can include all the layers, from mucosa to serosa, and these are true diverticula, and sometimes they only include the mucosa and submucosa which poke through the muscle layer. These are called pseudo or false diverticula as the the muscle layer isn’t included and the mucosa and submucosa are covered only by serosa.The formation of colonic diverticula is a result of high pressures that literally push the walls such that they bubble out and form these pouches.It is thought that the contractions in patients with diverticula are exaggerated or abnormal in some way, which causes an unequal distribution of pressure with some specific areas having really high pressures during contractions.Additionally, diverticula tend to form in the spots where the blood vessels that supply the intestinal walls traverses the muscle layer, this spot is slightly weaker, making it more likely for diverticula to form.As that diverticula forms, that blood vessel responsible for wall weakness becomes separated from the intestinal lumen only by mucosa, and is therefore subject to injury and predisposed to rupture, resulting in bleeding which can pass into stool.There are also other causes: things that affect stress or strength e.g. a low fibre diet or diet high in fatty foods and red meat.There are also genetic causes e.g. Marfan syndrome and Ehlers-danlos which are genetic disorders that affect connective tissue. Without strong connective tissue, diverticula can form.
• Diverticulitis: Inflammation can happen when fecal matter, or fecaliths, become lodged in the diverticula (less common) or more often due to erosion of the diverticular wall from higher luminal pressures.

Question 228

Signs of diverticular disease

Answer 228

• Pyrexia
• Left lower quadrant or iliac fossa tenderness and guarding: in diverticulitis
• Left iliac fossa tender mass: suggests an abscess (20%)
• Rigidity, guarding, rebound or percussion tenderness: suggests perforation
• Digital rectal examination: fresh blood and pelvic tenderness
• Tachycardia and hypotension: if septic

Question 229

Symptoms of diverticular disease

Answer 229

• Left lower quadrant pain: the sigmoid colon is most frequently affected, but the right colon can be affected in Asian patients. (Will be relieved after defecation in diverticular disease)
• Fresh rectal bleeding and mucus
• Constipation: may alternate between episodes of constipation (50%) and diarrhoea (25%)
• Urinary symptoms: such as frequency or urgency due to bladder irritation
• Nausea and vomiting: may be due to strictures or obstruction
• Flatulence: seen in diverticular disease
• Erratic bowel habits: seen in diverticular disease

Question 230

Primary investigations for diverticular disease

Answer 230

• FBC:anaemia, leukocytosis and neutrophilia
• U&Es:pre-renal acute kidney injury if significantly dehydrated or septic
• CRP and ESR:elevated
• Venous blood gas: raised lactate in significant PR bleed
• Blood cultures:if sepsis suspected
• CT abdomen/pelvis with contrast:modality of choice in patients with suspected acute diverticulitis and would demonstrate thickened bowel wall. Can also look for complications.
• Group and save: if PR bleeding is a feature, to ensure that crossmatching is possible if required

Question 231

Investigations to consider for diverticular disease

Answer 231

• Erect chest X-ray:may demonstrate a pneumoperitoneum if perforation is present
• Abdominal X-ray: often non-specific but may show dilated bowel loops or obstruction. May also show perforation (free air).
• CT angiogram:in cases of significant PR bleeding a CT angiogram would help to identify the bleeding point and allow embolisation
• Colonoscopy:should generally be avoided in acute diverticulitis due to the risk of perforation, and is used if the diagnosis is unclear or alternative pathology is suspected

Question 232

Management of diverticula

Answer 232

• Diverticulosis
  
  • Conservative: no further management is needed
• Diverticular disease
  
  • Conservative: patients may be advised to increase dietary fibre and take bulk-forming laxatives. Analgesia/ antispasmodic drugs should be prescribed if pain is present.
• Diverticulitis
  
  • Classification of diverticulitis for guiding managementHinchey classification is used for the classification of acute diverticulitis in order to guide management. Stage 3 and stage 4 require surgery.
  • Mild presentation: oral antibiotics, analgesia, low residue or liquid diet
  • Severe presentation:
    
    • Supportive management:NBM, IV fluids and analgesia
    • IV antibiotics:co-amoxiclav is typical but depends on local guidelines
    • Acute PR bleeding: transfuse blood products and arrange angiographic embolisation (blocks blood vessels) if available, otherwise, surgery is required
    • Surgery: if bleeding is not controlled or perforation is present, emergency surgical resection is required e.g. Hartmann’s procedure (removing the affected section of the bowel and creating an alternative path for faeces to be passed).
  • Diverticular abscess: radiological drainage or surgery
  • Recurrent diverticulitis: elective colonic resection

Question 233

Complications of diverticula

Answer 233

• Fistulae: pneumaturia, faecaluria, and recurrent urinary tract infections (colovesical fistula - colon and bladder fistula); the vaginal passage of flatus or faeces (colovaginal fistula - vagina and colon fistula). Requires surgery
• Abscess: suspect an abscess if there is no improvement within 48-72 hours of medical management. May also be a subphrenic abscess (below diaphragm). Antibiotics + drainage needed.
• Perforation: perforated sigmoid diverticulitis is a surgical emergency as it can rapidly result in peritonitis, profound sepsis and death; it usually requires Hartmann’s procedure
• Strictures: inflammation and fibrosis can cause strictures and patients can present with large bowel obstruction
• Haemorrhage: embolisation or colonic resection may be done if bleeding continues.

Question 234

Prognosis for diverticular disease

Answer 234

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 235

Define Gastritis

Answer 235

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

Gastropathy refers to epithelial cell damage and regeneration WITHOUT inflammation - commonest cause is mucosal damage associated with Aspirin/NSAIDs

Question 236

Classification of Gastritis

Answer 236

Gastritis can be classified basedupon location, timing or type of pathology:

• Antralorpangastritis
• Acuteorchronic gastritis
• Erosiveornon-erosive

Erosive gastritis accounts for 15-20% of Upper GI bleeding

Question 237

Aetiology of Gastritis

Answer 237

• 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 238

RF for Gastritis

Answer 238

• 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 239

Pathophysiology of Gastritis

Answer 239

• Acute = inflammation of the gastric mucosa
• Chronic = chronic inflammation → epithelial metaplasia, mucosal atrophy and gland loss. Metaplasia may also lead to dysplasia and so there is risk of cancer.
• Helicobacter pylori infection - most common cause:
  
  • Causes severe inflammatory response
  • Gastric mucus degradation and increased mucosal permeability, which is directly cytotoxic to the gastric epithelium: since H.pylori produces urease which converts urea to ammonia and CO2 which is toxic since ammonia and H+ (from HCl) form ammonium which damages gastric mucosa resulting in less mucous production.
• Autoimmune gastritis:Affects the fundus and body of the stomach leading to atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia (low RBCs due to low B12)
• Aspirin and NSAIDs e.g. Naproxen:Inhibit prostaglandins (which stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in less mucus production and thus gastritis

Question 240

Clinical manifestations of Gastritis

Answer 240

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

Question 241

Investigations for Gastritis

Answer 241

• Endoscopy - will be able to see gastritis
• Biopsy

Testing for H.pylori:

• ‘Clo test’ during biopsy to check for H.pylori presence
• H.pylori urea breath test
• H.pylori stool antigen test

Testing for autoimmune gastritis

• Look for anti-IF (intrinsic factor) antibody and anti-parietal cell antibodies
• Raised gastrin levels, reduced pepsinogen

Question 242

Differentials for Gastritis

Answer 242

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

Question 243

Management of Gastritis

Answer 243

• Remove causative agents such as alcohol/NSAIDs
• Reduce stress
• H2 antagonists e.g. ranitidine or cimetidine - to reduce acid release
• PPIs e.g. lansoprazole or omeprazole - to reduce acid release
• Antacids - neutralise acid to relieve symptoms
• If H. Pylori +ve:
  
  • Triple therapy:
    
    • PPI for acid suppression e.g. lansoprazole or omeprazole
    • Plus two of: metranidazole, clarithromycin, amoxicillin, tetracycline, bismuth
    • Quinolones e.g. ciprofloxacin, furozolidone and rifabutin are used when standard regimens have failed as ‘rescue therapy’
  • Eradication is confirmed by urea breath or stool antigen test
• Correct vitamin deficiencies for autoimmune gastritis

Question 244

Prevention of Gastritis

Answer 244

Give PPIs alongside NSAIDs - this also prevents bleeding from acute stress ulcers and gastritis which is often seen with ill patients - especially burns patients!

Question 245

Complications of gastritis

Answer 245

• Gastric cancers
• Achlorydria: lack of HCl in stomach
• Vitamin B12 deficiency

Question 246

Prognosis for gastritis

Answer 246

• 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 247

Define diarrhoea

Answer 247

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

Question 248

Pathophysiology of Diarrhoea

Answer 248

• Sudden onset of bowel frequency associated with crampy abdominal pains and a fever will point to an infective cause.
• Bowel frequency with loose, blood-stained stools will point to an inflammatory cause.
• Passage of pale, offensive stools that float often accompanied by a loss of appetite and weight loss point to steatorrhea
• Decreased stool consistency caused by:Water:Osmotic:
  • Large quantities of non-absorbed hypertonic substances in the bowel draw fluid into the intestine
  • Diarrhoea stops when the patient stops eating or the malabsorptive state is discontinued
  • Causes:
    
    • Ingestion of non-absorbable substances e.g. a laxative such as magnesium sulphate
    • Generalised malabsorption so that high concentrations of solute e.g. glucose remain in the lumen
    • Specific malabsorptive defect e.g. disaccharide deficiency
  Secretory - microscopic colitis:
  • There is active intestinal secretion of fluid and electrolytes as well as decreased absorption
  • Continues even when the patient fasts
  • Causes:
    
    • Enterotoxins e.g. E.coli and cholera toxin
    • Bile salts in colon following ileal disease, resection or idiopathic bile acid malabsorption
    • Fatty acids in colon following ileal resection
  Functional - Irritable Bowel SyndromeFat (steatorrhoea):
  • Characterised by increase gas, offensive smell and floating hard-to-flush stools
  • Giardiasis and coeliac disease can cause steatorrhoea
  Inflammatory discharge:
  • Damage to the intestinal mucosal cell leads to loss of fluid and blood and defective absorption of fluid and electrolytes
  • Causes:
    
    • Inflammatory e.g. UC or Crohn’s
    • Infective e.g. Shigella or Salmonella

Question 249

Define Acute diarrhoea

Answer 249

Acute diarrhoea is defined as that lasting less than 2 weeks

Question 250

Aetiology of acute diarrhoea

Answer 250

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

Question 251

Investigations for acute diarrhoea

Answer 251

• Stool MCS - establish the causative organism and antibiotic sensitivities.
• Flexible sigmoidoscopy with colonic biopsy is performed if symptoms persist and no diagnosis has been made

Question 252

Management of acute diarrhoea

Answer 252

• Treatment is symptomatic to maintain hydration with anti-diarrhoeal agents
  (Loperamide) for short-term relief and antibiotics for specific indications

Question 253

Define Chronic diarrhoea

Answer 253

Chronic diarrhoea is defined as lasting more than 2 weeks

Question 254

Aetiology of Chronic diarrhoea

Answer 254

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 255

Investigations of chronic diarrhoea

Answer 255

• Bloods -
  
  • Sometimes faecal markers of intestinal inflammation are used to differentiate functional disorders from organic disease
  • Low MCV and/or Fe deficiency e.g. in coeliac disease or colon cancer
  • High MCV if alcohol abuse or decreased B12 absorption e.g. coeliac disease or Crohn’s
  • Raised white cell count if parasites
  • Raised CRP, WCC and low albumin if C.diff
  • Raised ESR and CRP indicate infection, Crohn’s, UC or cancer
  • U&E: hypokalaemia in severe diarrhoea and vomiting
• Stool MCS - establish the causative organism and antibiotic sensitivities.
• Sigmoidoscopy with biopsy

Question 256

Management of chronic diarrhoea

Answer 256

• Treat cause
• Oral rehydration
• Anti-diarrhoeal e.g. loperamide or codeine phosphate

Question 257

Blood supply and anastamoses of the colon

Answer 257

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 258

Definition and overview of Ischaemic colitis

Answer 258

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 259

Epidemiology of ischameic colitis

Answer 259

• 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 260

Aetiology of ischaemic colitis

Answer 260

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)

Non-occlusive: reduced perfusion can be caused by

• Heart failure(low output state)
• Septic shock
• Vasopressors(e.g. noradrenaline, cause vasoconstriction)
• Recent CABG
• Renal impairment
• Peripheral vascular disease
• Cocaine use

Occlusive: blockage of vessels

Arterial:

• Thrombus
• Embolism (mainly due to AF - risk factor for left atrial thrombus that can lead to systemic embolism)
• Other: e.g. volvulus, tumours, hernias can cause external obstruction

Venous:

• Thrombus: impedes flow and causes stagnation leading to bowel wall oedema and eventual impairment of arterial supply

Question 261

RF for ischaemic colitis

Answer 261

• 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 262

Clinical manifestations of ischaemic colitis

Answer 262

There is a spectrum of disease from mild self-limiting insults to necrosis and bowel perforation.

• 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 263

Investigations for ischaemic colitis

Answer 263

• Bloods:
  
  • FBC: leucocytosis and neutrophilia. May be high Hb due to plasma loss. Anaemiaif bleeding.
  • U&Es: assess for pre-renal acute kidney injury due to hypovolaemia (‘third-spacing’ of fluid within the bowel lumen)
  • Venous blood gas: metabolic acidosis and raised lactate is suggestive of bowel ischaemia and necrosis
  • Coagulation screen: assess for possible hypercoagulability
• CT (typically with contrast) - bowel dilatation and thickening +/- surrounding fat stranding or free fluid. In fulminant disease with perforation, free air can be seen. Can also exclude other causes of acute abdomen.
• Abdominal x-ray: may show thumbprinting (thickening of large bowel)
• GI endoscopy: gold standard. direct visualisation and allows for biopsy.

Question 264

Differentials for ischaemic colitis

Answer 264

IBD

Question 265

Management of Ischaemic colitis

Answer 265

Varies depending on presentation. Many cases (particularly non-occlusive) will resolve with just supportive management. Other cases e.g. gangrenous ischaemic colitis require prompt resuscitation, resection and stoma formation.

• Supportive management
  
  • Nill-by-mouth. NG tube may be placed particularly in the presence of paralytic ileus.
  • IV fluid resuscitation and maintenance fluid
  • Broad spectrum antibiotics - especially essential in cases of perforation and peritonitis, due to increased risk of bacterial translocation across gut wall
  • IV unfractionated heparin/ LMWH heparin - anti-coagulation
  • Any underlying conditions should be treated
• Surgical intervention
  
  • Embolectomy
  • Thrombolysis
  • Mesenteric angioplasty and stenting
  • Laparotomy and resection of ischaemic/ necrotic segments
  • Stoma formation

Question 266

Complications of ischaemic colitis

Answer 266

• 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 267

Prognosis of Ischaemic colitis

Answer 267

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

Mortality ~22%

Question 268

Define Mesenteric Ischaemia

Answer 268

Bowel ischaemia which affects the small bowel. It refers to pathology affecting the superior mesenteric artery.

Question 269

Epidemiology of Mesenteric Ischaemia

Answer 269

• 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 270

Aetiology of Mesenteric Ischaemia

Answer 270

Mesenteric ischaemia may be caused by both acute or chronic processes and can hence present acutely or with gradual onset. Causes include:

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 271

RF for Mesenteric ischaemia

Answer 271

• 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 272

Pathophysiology of Mesenteric Ischaemia

Answer 272

Physiology:

Because the small intestine has a high demand for oxygen and nutrients to sustain digestion, it is highly susceptible to tissue injury from ischaemia. To reduce the risk of that happening, the mesenteric arteries branch and reconnect at points forming collateral circulation. This is protective because if blood flow is reduced in one pathway, then the tissue can still receive blood through another pathway.

Once the small intestines have gotten oxygenated blood, that blood leaves through the superior mesenteric vein.

Pathology:

Small bowel infarction happens when there’s a significant decrease in blood flow to the small intestine.

At the cellular level, ischaemic injury can lead to the production of reactive oxygen species which can damage DNA, RNA, and proteins in the cell, leading to cell death.

If blood flow returns to the tissue, it’s called reperfusion. Reperfusion can cause further injury - called reperfusion injury. The influx of oxygen into an already damaged cell can be overwhelming and can cause even more oxidative stress, which worsens the cell damage.

As damaged cells release reactive oxygen species, it triggers an inflammatory response which attracts immune cells, like neutrophils. The immune cells remove dead and damaged cells and release cytokinese.g. Tumour necrosis factor-alpha.

This causes blood vessels to become more permeable to fluid and more immune cells - resulting in bowel oedema or swelling of the small intestinal wall.

This can affect just the mucosal layer, called a mucosal infarct, or all layers, known as a transmural infarction.

Consequences:

• Ileus - food lingers and doesn’t get pushed along.
• Severe damage can cause a break in the epithelial lining of the small intestines, allowing bacteria in the lumen to get into the blood vessels in the wall.
• Bacteria can also cross the small intestinal wall and get into the peritoneal space, and from there get into lymphaticsor blood vessels. This can cause sepsis and septic shock. This can lead to organ failure and death.

Question 273

Signs and symptoms of mesenteric ischaemia

Answer 273

• Signs
  
  • Often no abdominal signs and pain is out of proportion to clinical findings
  • Absence of bowel sounds as motility decreases: late sign
  • Epigastric bruit on auscultation: in chronic ischaemia
  • Rectal exam: bleeding
  • Hypotensive and tachycardic - shock due to hypovolaemia
• Symptoms
  
  • Abdominal pain
    
    • Acute ischaemia: severe, out of proportion to abdominal signs
    • Chronic ischaemia: colicky, intermittent, post-prandial and described as ‘intestinal angina’
  • Nausea and vomiting
  • Diarrhoea
  • Fever
  • Weight loss: may be present with chronic ischaemia

Question 274

Investigations for mesenteric ischaemia

Answer 274

• ECG:atrial fibrillation is the most common cause of acute mesenteric ischaemia
• Bloods:
  
  • FBC: leucocytosis and neutrophilia. May be high Hb due to plasma loss. Anaemiaif bleeding.
  • U&Es: assess for pre-renal acute kidney injury due to hypovolaemia (‘third-spacing of fluid within the bowel lumen)
  • Venous blood gas: metabolic acidosis and raised lactate is suggestive of bowel ischaemia and necrosis
  • Coagulation screen: assess for possible hypercoagulability
• CT angiography: diagnostic test to assess for the site of the occlusion and the extent of ischaemia and necrosis. Visualizes blood flow through the small intestines.
• CT angiogram: can show bowel dilation, bowel wall thickening from oedema and inflammation and a gasless abdomen.
• Erect CXR: assess for pneumoperitoneum which would suggest perforation

Question 275

Management of Mesenteric ischaemia

Answer 275

Chronic mesenteric ischaemia can be managed by controlling cardiovascular risk factors and patients may be suitable for elective endovascular or open procedures.

Acute mesenteric ischaemia:

• Initial management
  
  • Bowel rest:patients are kept nil-by-mouth and have a nasogastric tube inserted for decompression
  • IV fluids: will aid bowel perfusion
  • IV broad-spectrum antibiotics: due to risk of bacterial translocation
  • IV heparin: anti-coagulation
  • Prompt laparotomy:in any patients with evidence of peritonism or infarction
• Definitive management
  
  • Endovascular revascularisation: may be considered in early disease or with partial vascular obstruction, but not if there is evidence of infarction
    
    • Embolectomycan be achieved endovascularly
    • Angioplastyin cases of thrombosis
  • Laparotomy: indicated if any evidence of significant ischaemia, infarction, or peritonism
    
    • Open embolectomy:surgical removal of the occluding embolism
    • Arterial bypass: performed if the embolus is not amenable to embolectomy or in cases where an arterial thrombus is the cause
    • Resectionof necrotic bowel

Question 276

Complications of mesenteric ischaemia

Answer 276

• 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 bacterial translocation across the dying gut wall
• Short bowel syndrome: following bowel resection, there is a risk of malabsorption due to lack of functional intestine
• Strictures: patients with ischaemic bowel managed conservatively have a risk of developing strictures

Question 277

Prognosis for Mesenteric ischaemia

Answer 277

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 278

Differences between mesenteric ischaemia and ischaemic colitis

Answer 278

Pathology
MI - Affects small bowel due to embolus or thrombus
IC - Affects large bowel and occurs in ‘watershed’ areas e.g. splenic flexure

RF
Increasing age, A fib, CVD RF, Endocarditis, Malignancy, Cocaine use, Vasculitis

Presentation
MI - Acute: severe sudden abdo pain, pain is disproportionate to clinical findings
Chronic: colicky, post-prandial abdo pain

IC - Transient, less severe abdo pain, with bloody diarrhoea

Diagnostic tests
MI - CT angiogram or angiography
IC - Colonoscopy (Gold standard), AXR

Management
MI - surgical emergency: endovascular therapy, embolectomy, bypass ir bowel resection, Anticoag
IC - Conservative, Surgery: if conservative management fails or peritonitis, perforation or ongoing bleeding

Outcomes
MI - Acute: high mortality if untreated
Chronic: manage CVD RF and elective revascularisation may be arranged
IC - Most patients symptoms improve with 24-48 hours, with complete clinical recovery within 1-2 weeks, overall mortality is 22%

Question 279

What is a Mallory-Weiss tear

Answer 279

Mallory-Weiss tear (MWT) refers to longitudinal lacerations limited to the mucosa and submucosa, at the border of the gastro-oesophageal junction.

Question 280

Epidemiology of MWT

Answer 280

• 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 281

RF for MWT

Answer 281

• 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 282

Pathophysiology of MWT

Answer 282

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 283

Classic presentations of MWT

Answer 283

The classic history of a Mallory Weiss tear is a patient with a background of alcohol excess presenting with episodes of violent retching or vomiting, followed by vomiting a small or moderate amount of fresh blood.

Question 284

Signs and symptoms of MWT

Answer 284

• Signs
  
  • Melaena on rectal examination: an uncommon feature
  • Features of shock: an uncommon feature
• Symptoms
  
  • Preceding retching and vomiting
  • Vomiting blood: usually a small to moderate volume of bright red blood, which is self-limiting
  • Melaena: rare
  • Epigastric pain

Question 285

Investigations for MWT

Answer 285

• 1st line
  
  • Upper GI endoscopy: gold-standard required for all patients as an inpatient or outpatient depending on the Glasgow Blatchford score
    
    • Usually shows a single longitudinal tear (there can be multiple tears) in the mucosa at the gastro-oesophageal junction
  • FBC: assess for anaemia secondary to bleeding; usually normal
  • U&Es: urea is raised in an upper GI bleed (protein in RBCs is digested into urea in the GI tract)
  • Coagulation profile: to assess an underlying coagulopathy contributing to bleeding
  • LFTs: typically normal but if deranged may raise the possibility of a variceal bleed
  • Erect CXR: performed to rule out oesophageal perforation or perforated peptic ulcer

Question 286

Differentials for MWT

Answer 286

• 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 287

Management for MWT

Answer 287

MWT can be self-limiting, so mild bleeding doesn’t require treatment. If bleeding is persistent or significant:

• 1st line
  
  • Upper GI endoscopy:diagnostic and therapeutic with one of the following suggested
    
    • Mechanical e.g. clipping +/- adrenaline
    • Thermal coagulation with adrenaline (use heat to seal off bleed)
    • Sclerotherapy with adrenaline (delivers medication to the tear to stop bleeding)
    • Variceal band ligation
  • High-dose IV proton pump inhibitor: administered post-endoscopy to reduce rebleeding; e.g. pantoprazole. Shouldnotbe given before endoscopy as may mask bleeding
  • Manage contributing factors: for example, offer a long-term proton pump inhibitor if there is evidence of GORD
• 2nd line
  
  • Surgical repair or interventional radiology: only performed if endoscopic haemostasis has failed or transmural oesophageal perforation is present; this is very rarely needed for MWT

Question 288

Complications of MWT

Answer 288

• 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

Question 289

Prognosis of MWT

Answer 289

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 290

Anus physiology

Answer 290

• The anus is the final 3 to 4 centimeters of theGI tract, and it extends from the rectum to the anal margin.
• The top and bottom of the anal canal are surrounded by the internal and the external anal sphincters, which are two muscular rings that control defecation.The internal sphincter is under involuntary control, while the external sphincter is under voluntary control.
• Within the anal canal, there are mucosal membrane infoldings that form the anal columns. At the base of these columns, there is the dentate or pectinate line, which divides the upper two thirds and lower third of the anal canal.
• Above the dentate line, the mucosa is lined by simple columnar epithelium, and below the dentate line, there’s the anoderm, which has no hair and sebaceous and sweat glands, and is lined by squamous epithelium.

Question 291

Define and overview of haemmorhoids

Answer 291

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.

Question 292

Classification of haemmorhoids

Answer 292

Internal haemorrhoids are ones above the dentate line, and external haemorrhoids are ones below the dentate line.

Internal haemorrhoidsare subclassified into four grades based on the degree of prolapse from the anal canal:

Grade I: no protrusion outside the anal canal.

Grade II: protrusion outside the anus during bowel movement, but they retract spontaneously.

Grade III: prolapsed haemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.

Grade IV: prolapsed haemorrhoids that cannot be manually pushed back in.

Question 293

Epidemiology of Haemorrhoids

Answer 293

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

Question 294

Aetiology of Haemorrhoids

Answer 294

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 295

RF for haemorrhoids

Answer 295

• Obesity
• Old age

Question 296

Pathophysiology of Haemorrhoids

Answer 296

• The normal/healthy anus is lined by discontinuous masses of spongy vascular tissue - the anal cushions, which contribute to anal closure
• They are attached by smooth muscle and elastic tissue but are prone to displacement and disruption, either singly or together
• The effects of gravity (erect posture), increased anal tone (possibly due to stress) and the effects of straining when defecating may make them become both bulky and loose, and so protrude to form piles
• They are very vulnerable to trauma (e.g. from hard stools) and bleed readily from the capillaries of the underlying lamina propria
• Since blood loss is from capillaries, it is bright red
• Since there are no sensory fibres above the dentate line (squamomucosal junction), piles are not painful unless they thrombus when they protrude and are gripped by the anal sphincter, blocking venous return
• External haemorrhoids are painful as there are sensory nerves below the dentate line
• There is a vicious circle; the vascular cushions protrude through a tight anus → become more congested and hypertrophy → protrude again more readily
• These protrusions may then strangulate

Question 297

Clinical manifestations of Haemorrhoids

Answer 297

• Internal haemorrhoids
  
  • Usually asymptomatic but can:
    
    • Get inflamed
    • Cause itching, burning, vague discomfort
    • Cause painless passage of bright red blood with a bowel movement
• External haemorrhoids
  
  • Painful, especially when associated with thrombosed haemorrhoids
  • Thrombosed external haemorrhoids are tender and have a purplish hue
  • Swelling in the affected area
  • Mucus discharge
  • Itching

Question 298

Investigations for Haemorrhoids

Answer 298

• Abdominal examination to rule out other disease
• Rectal exam
  
  • Prolapsing piles are obvious
  • Internal haemorrhoids are not palpable
• Internal haemorrhoids lie inside the rectum and so need proctoscopy
  
  • Internal haemorrhoids look like bulging purplish-blue veins
  • Prolapsed internal haemorrhoids appear dark pink, glistening, and are sometimes tender masses at the anal margin
• Further testing with flexible sigmoidoscopy or colonoscopy to exclude proximal pathology if >50 years old

Question 299

Differentials for Haemorrhoids

Answer 299

• Perianal haemotoma
• Anal fissure
• Abscess
• Tumour
• Proctalgia fugax: anal pain that doesn’t have a specific cause

Question 300

Management for Haemorrhoids

Answer 300

• 1st degree
  
  • Increase fibre and fluid intake
  • Stool softeners
  • Topical analgesia
  • Topical steroids for short periods
• 2nd and 3rd degree, or 1st degree of medical therapy failedNon-operative procedures:
  • Rubber band ligation
  • Sclerotherapy: injection of drugs causes coagulation
  • Infrared coagulation
  • Bipolar diathermy and direct current electrotherapy: local heat causes coagulation
• Surgery
  
  • Excisional haemorrhoidectomy
  • Stapled haemorrhoidopexy: removal of much of the abnormally enlarged haemorrhoidal tissue, followed by a repositioning of the remaining hemorrhoidal tissue back to its normal anatomical position.
• Management for prolapsed thrombosed piles
  
  • Analgesia
  • Ice packs
  • Stool softeners

Question 301

Complications of Haemorrhoids

Answer 301

• 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 302

Define Fistula

Answer 302

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 303

Aetiology of Fistula

Answer 303

Main causes:

• Perianal sepsis
• Abscesses
• Crohn’s
• TB
• Diverticular disease
• Rectal carcinoma
• Immunocompromise

Question 304

Pathophysiology of Fistula

Answer 304

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

Question 305

Clinical manifestations of fistula

Answer 305

• 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 306

Investigations for fistula

Answer 306

• In some cases, the internal opening can be palpated on digital rectal exam.
• MRI:
  
  • To exclude sepsis
  • To detect associated conditions e.g. Crohn’s or TB
  • Imaging will show air or contrast material in the fistula
• Endoanal ultrasound:
  
  • To determine tracks location and underlying causes

Question 307

Management for fistula

Answer 307

• Surgical - Fistulotomy (cutting along the whole length of the fistula to open it up so it heals as a flat scar) and excision
  
  • Low fistulae can be laid open as there is no risk of incontinence
  • High fistulae (that involve the continence muscles) require seton suture (surgical thread left in the fistula to keep it open allowing drainage), and this can be tightened over time to maintain continence
• Treat with antibiotics if infected

Question 308

Define fissure

Answer 308

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 309

Epidemiology of fissure

Answer 309

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

Question 310

Aetiology of fissures

Answer 310

Can be an isolated primary problem (resulting from anal trauma) in young middle-aged adults or can occur in association with Crohn’s or Ulcerative colitis (in which perianal abscesses and anal fistulae can complicate the fissure)

• Hard faeces (common cause)
• Rectal thermometers
• Enemas
• Endoscope
• Vaginal delivery
• Anal intercourse
• Rare causes:
  
  • Syphilis
  • Herpes
  • Trauma
  • Crohn’s
  • Anal cancer
  • Psoriasis

Question 311

Pathophysiology of fissures

Answer 311

An anal fissure is a tear to the anoderm, which contains many sensory receptors. This causes pain.

An anal fissure can also cause exposure of the internal sphincter muscle, leading to muscle spasms which can worsen the pain, restrict blood flow to the fissure by constricting the inferior rectal artery resulting in ischaemia and preventing healing of the fissure.

Most of the time, anal fissures are located in the posterior midline of the anal canal, and less often they can be in the anterior midline. Sometimes, there are fissures in both the anterior and posterior midline, and these are called “kissing fissures”.

Fissures in a lateral location are atypical and are more commonly due to a secondary cause, like Crohn’s disease, sarcoidosis, an infection such as HIV or syphilis, and anal cancer.

Question 312

Clinical manifestations of fissures

Answer 312

• Extreme pain - especially on defecation
• Bleeding
• Faecal impaction and constipation due to avoidance of toileting
• If chronic, there may be skin tags:
  
  • At distal end of the fissure, the tag is called a sentinel pile
  • At the proximal end of the fissure, the tag is called a hypertrophied anal papillae.

Question 313

Investigations and diagnosis of fissures

Answer 313

• Can usually be made on history alone
• Confirmed on perianal inspection
• Rectal examination (sometimes not possible due to pain and sphincter spasm)
• Individuals with rectal bleeding or an atypical location of the fissure should get further evaluation, including anoscopy, colonoscopy, or sigmoidoscopy to exclude secondary causes of an anal fissure or an alternative diagnosis like haemorrhoids.

Question 314

Management of fissures

Answer 314

• Increase dietary fibre and fluids
• Use of stool softeners
• Hygiene advice
• 1st line: Lidocaine ointment + GTN ointment or topical diltiazem
• 2nd line: Botulinum toxin injection (botox) and topical diltiazem
• Surgery if medication fails: lateral partial internal sphincterotomy (the internal sphincter is divided to lower its resting pressure, which helps improve blood supply to the fissure and allows faster healing).

Question 315

Complications of fissures

Answer 315

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

Question 316

Define Abscess

Answer 316

Superficial infection that appears as a tender red lump under the skin near the anus.

Question 317

Epidemiology of abscess

Answer 317

• 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 318

Aetiology of Abscess

Answer 318

• Anorectal abscesses usually caused by gut organisms
  
  • Rarely staphs or TB

Question 319

Pathophysiology of Abscess

Answer 319

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 320

Clinical manifestations of Abscess

Answer 320

• Painful swellings
• Tender
• Discharge

Question 321

Investigations for Abscess

Answer 321

• The diagnosis can usually be made by physical examination
• MRI
• Endoanal ultrasound

Question 322

Management of Abscess

Answer 322

• Surgical excision and drainage
• Treatment with antibiotics

Question 323

Define Pilonidal sinus/abscess

Answer 323

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 324

Epidemiology of Pilonidal abscess

Answer 324

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

Question 325

RF for pilonidal abscess

Answer 325

• 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

Question 326

Pathophysiology of Pilonidal abs

Answer 326

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 327

Clinical manifestations of Pilonidal Abscess

Answer 327

• Asymptomatic pilonidal cavity
• Acute abscess
  
  • Painful swelling over days
  • Pus filled with foul smell from abscess
  • Systemic signs of infection
• Chronic inflammation
  
  • Associated mucoid, purulent, or bloody drainage.
  • 4 in 10 have repeated recurrent pilonidal sinus
  • Infection never clears completely

Question 328

Investigations for Pilonidal abscess

Answer 328

Detected on clinical examination

Question 329

Management of Pilonidal Abscess

Answer 329

• Asymptomatic patients don’t require treatment
• Acute pilonidal abscess requires incision and drainage
• Chronic pilonidal disease and recurrent abscesses require:
  
  • Surgical excision, pus drainage destruction of all sinus tracts and skin pores of the involved area, trying to preserve as much normal tissue as possible to facilitate wound management.
  • Pre-op antibiotics
  • Complex tracks can be laid open and packed individually
  • Skin flaps can be used to cover defect
• Hygiene and hair removal advice (near sinus)