Colon conditions Flashcards
Define IBS
Functional bowel disorder defined as:
recurrent episodes of abdominal pain/discomfort (in the absence of detectable structural pathology) for > 6 months
Relieved by defecation or associated with altered bowel frequency/stool form.
State bowel dysfunctions that must be associated with abdominal pain to diagnose IBS
Abdo pain should be accompanied by at least two of the following:
- Altered stool passage i.e. straining, urgency, incomplete evacuation
- Abdominal bloating, distension, tension or hardness
- Symptoms made worse by eating
- Passage of mucus
ABC- abdo pain, bloating, change in bowel habits
Give some risk factors for IBS
- physical and sexual abuse
- PTSD
- age <50 years
- female sex- 2:1 female/male ratio
- previous enteric infection
- family history
Explain the aetiology of IBS
UNKNOWN
Believed to be a disorder of altered gastrointestinal motility.
Multiple contributing causes, including:
- visceral sensory abnormalities
- gut motility abnormalities
- psychosocial factors (e.g. stress)
- food intolerance (e.g. lactose)
- inflammatory or immune basis
Summarise the epidemiology of IBS
- COMMON
- 10-20% of adults
- More common in females (2:1 ratio)
Recognise the presenting symptoms of IBS
6+ months history of abdominal pain
- Pain is often colicky
- It is in the lower abdomen
- Relieved by defecation or passing of flatus
Altered bowel frequency (> 3 motions per day or < 3 motions per week)
- Abdominal bloating/distension
- Change in stool consistency
- Worsening of symptoms after food
- Passage with urgency or straining
- Tenesmus
Other symptoms: nausea, bladder symptoms, back ache
Symptoms are CHRONIC and exacerbated by stress, menstruation or gastroenteritis (post-infection IBS)
Recognise the signs of IBS on physical examination
Usually NORMAL on examination
Sometimes the abdomen may appear distended and be mildly tender on palpation in one or both iliac fossae
Identify appropriate investigations for IBS
Mostly clinical but need to exclude organic pathology
- FBC- check for anaemia/abnormalities (would suggest non-IBS)
- Fecal occult blood test- abnormalities sugest IBD/ca
-
Serologic tests for celiac disease
- IgA human anti-tissue transglutaminase (anti-tTG)
-
Faecal calprotectin/lactoferrin, CRP
- postive in IBD
- Ultrasound: exclude gallstone disease
- Urease breath test: exclude dyspepsia due to Helicobacter pylori
- Endoscopy: if other pathologies suspected
List some dietary modifications for IBS
AVOID: fibre, lactose, fructose, wheat, starch, caffeine, alcohol, fizzy drinks
For constipation: increase soluble fibre, bisacodyl and sodium picosulfate
State some medical treatment for different IBS symptoms
Bloating/colic:
- antispasmodics
- buscopan- hyoscyamine
- dicycloverine
Constipation:
- prokinetic agents: domperidone, metaclopramide (reduce N+V)
- laxatives: ispaghula, lactulose, movicol
Diarrhoea:
- loperamide
- colestyramine
Psychological symptoms/vixercal hypersensitvity:
- paroxetine
- citalopram
What else may be recommended for IBS patients other than medical therapy?
Hypnotherapy and CBT
Identify the possible complications of IBS
- Physical and psychological morbidity
- Increased incidence of colonic diverticulosis
Summarise the prognosis for patients with IBS
- Chronic relapsing and remitting course of disease
- Often exacerbated by psychosocial stresses
State the key pathological differences between Crohn’s and UC:
- Immune cells involved
- Gut layers affected
- Regions of gut affected
- Pattern of inflammation
- Histological features
Immune cells involved:
-
Crohn’s = Th1 mediated (main cytokine = TNF-a)
- Florid T cell expansion
- abnormal T cell apoptosis
-
UC = Th2 mediated (main cytokine = IL13)
- normal T cell apoptosis
Gut layers affected:
- Chron’s = all layers (transmural)
- UC = mucosa/submucosa
Regions of gut affected:
- Chron’s = entire GI tract; terminal ileum most common site
- UC = only colon affected; rectum involved in virtually all patients
Pattern of inflammation:
- Chron’s = patchy, skip lesions common
- UC = continuous proximal spread from rectum, decreased haustra
Histological features:
- Chron’s = cobblestone mucosa, creeping fat serosa, deep fissuring ulcers and fistulas
- UC = pseudopolyps, no serosal involvement, shallow ulcers
What might you see in microscopy of UC versus Chron’s
Chron’s = non-caseating granulomas
UC = crypt abscesses
What is the term for UC when it:
- is only in the rectum
- is only in the descending colon
- is affecting the entire colon
rectum = proctitis
descending colon = left-sided colitis
entire colon = pan-colitis
WHich IBD can be cured fully?
UC- surgery is curative
proctocolectomy with ileostomy – surgical removal of colon, rectum and anal canal
or ileo-anal pouch formation
Define Chron’s disease
Disorder of unknown aetiology characterised by transmural inflammation of any or all parts of the entire GI tract from mouth to perianal area
What causes:
- intestinal obstruction
- fistulae
in chrons?
- Transmural inflammation → fibrosis → obstruction.
- The inflammation can also result in sinus tracts that burrow through and penetrate the serosa → perforations and fistulae
Where is Chron’s most comoonly found?
40% terminal ileum
perianal also common
What does the pathophysiology of Chron’s disease indicate as its cause?
Indicates a role for infectious, immunological, environmental, dietary, and psychosocial factors….
…in a genetically and immunologically susceptible person
Describe the development of Chron’s lesions
- Starts as inflammatory infiltrate around crypts
- develops into ulceration of superficial mucosa
- Inflammation progresss to involve deeper layers
- eventually forms non-caseating granuloma
- granulomas involve all layers of the intestinal wall and the mesentery and regional lymph nodes.
Describe what you would see on endoscopy of Chron’s
Early endoscopic findings: hyperaemia and oedema of the inflamed mucosa.
Progresses to discrete deep ulcers located transversely and longitudinally, creating a cobblestone appearance.
These lesions are separated by healthy areas known as skip lesions
Define fistula
abnormal fusion between a hollow tubular organ and the body surface, or between two hollow/tubular organs
Summarise the epidemiology of Crohn’s disease
- Highest incidence of CD is in northern climates and in developed countries,
- UK prevalence: 50-80/100,000
- The peak age of onset: 15-40 years
What are the presenting symtoms of Crohn’s
-
Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)
- right iliac fossa if terminal ileum involved
- Diarrhoea
- Anorexia, weight loss, malnutrition, nausea, fatigue
- Fever
- Symptoms of complications –
- eye disease (uveitis)
- joint disease (seronegative arthritis)
- skin disease (erythema nodosum)
- anaemia
What are the signs of Crohn’s on examination?
- Weight loss
- Clubbing
- Signs of anaemia
- Aphthous ulcers in mouth
- Perianal lesions: skin tags, fistulae, abscesses, scarring, or sinuses
Signs of complications: Uveitis, erythema nodosum, pyoderma gangrenosum
How does diarrhoea differ between Chron’s and UC?
Crohn’s = diarrhoea with mucus and bleeding
UC = very bloody diarrhoea (inflammation is in rectum/sigmoid colon)
What blood investigations would you do for suspected Chron’s? What wuld be a positive result?
-
FBC-
- anaemia due to: chronic inflammation/blood loss, iron/B12/folate malabsorption
- leukocytosis
- thrombocytosis- active inflammation
-
Iron studies
- (serum iron, serum ferritin, total iron binding capacity [TIBC], transferrin saturation)
- Low due to bleeding/malabsorption
-
Comprehensive metabolic panel (CMP)/LFTs:
- hypoalbuminaemia
- hypocholesterolaemia
- hypocalcaemia
-
CRP, ESR
- elevated
- Serology to exclude Y enterocolitica, a bowel pathogen that causes an acute ileitis.
What other non-invasive investigations would you carry out in suspected Crohn’s? what would they show?
-
Stool microscopy and culture
- See absence of infectious elements eg C. Difficile
- exclude infective colitis
-
Plain abdominal X-ray
- Good to assess severity
- would see: small bowel or colonic dilation; calcification; sacroiliitis; intra-abdominal abscesses
-
Small bowel follow through
- xray with barium contrast
-
CT abdo w/contrast
- Localisation
- Diagnose fistulae, abscesses, and other extra-mural complications
- MRI if young patient/CT contrast contraindicated
What 3 specific diagnostic markers would you see in a small bowel follow through of a Chron’s patient?
- Fibrosis/strictures (string sign of Kantor - part of the intestine looks like a piece of string, showing incomplete filling of the intestinal lumen)
- Deep ulceration (rose thorn ulcers)
- Cobblestone mucosa
What invasive investigations would oyu do for suspeted Chron’s? what is the positive result?
-
Colonoscopy- definitive test to diagnose CD
- see: aphthous ulcers, hyperaemia, oedema, cobblestoning, skip lesions
-
Tissue biopsy
- transmural involvement with non-caseating granulomas
- for monitoring malignancy and disease progression
-
OGD
- to differentiate from PUD
- see aphthous ulcers; mucosal inflammation
State the extraintestinal manifestations common to UC and CD and those which are specific
Both:
- Aphthous ulcers mouth
- Uveitis, iritis
- Seronegative arthritis, spondyloarthropathy
- Erythema nodosum, pyoderma gangrenosum
- Thromboembolic disease
UC:
- Increased risk of gallstones
CD:
- Association with primary sclerosing cholangitis
Generate a management plan for acute exacerbation of Crohn’s disease
- Fluid resuscitation, may also be on oral iron
- IV/oral corticosteroids- prednisolone, budenoside
-
5-ASA analogues
- mesalazine is absorbed in small bowel and colon
- olsalazine requires activation by colonic flora so absorbed in colon only
- Analgesia
- Parenteral nutrition may be necessary
- Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb
Describe the long-term management plan for Crohn’s disease
- Oral corticosteroids- budesonide
-
5-ASA analogues -
- decreases the frequency of relapses (mild-moderate disease)
- More commonly used in UC
-
Immunosuppression- steroid-sparing agents
- (e.g. azathioprine, 6-mercaptopurine, methotrexate)
- reduces the frequency of relapses
-
Anti-TNF agents:
- (e.g. infliximab and adalimumab)
- very effective at inducing and maintaining remission.
- Usually reserved for refractory Crohn’s.
What are 5-ASA analogues? give an example
Aminosalicylates e.g. mesalazine
Give examples of immunsoupressants used in Crohn’s disease (steroid sparing agents)
azathioprine, 6-mercaptopurine, methotrexate
For mildly active-moderate disease, which steroids would be used for:
- iliocaecal
- colonic
…inflammation?
For iliocaecal inflammation: budesonide
For colonic inflammation: prednisolone
What is the only lifestyle modification shown to have an effect in preventing the recurrence of Crohn’s disease?
Smoking cessation
When is surgeyr indicated in Crohn’s? What are the options?
Medical treatment fails, stricture forms
Failure to thrive in children in the presence of complications
Involves resection of affected bowel and stoma formation -
NOTE: there is a risk of disease recurrence and short bowel syndrome
Possible GI complications for Crohn’s?
- obstruction (due to stricture)
- intra-abdominal sepsis
- abscess
- Fistulae (between bowel, bladder, vagina)
- Perianal fistulae and abscesses
- toxic megalcolon
- anaemia, malabsorption
- short bowel syndrome
- malignancy
- methotrexate-associated: hepatotoxicity/ pulmonary fibrosis/ myelosuppression
- metabolic bone disease due to: corticosteroid therapy, malabsorption, inflammation
What are the presenting symptoms of UC?
- Bloody diarrhoea
- History of cramping lower abdominal pain
- Mucus discharge, faecal urgency and rectal tenesmus
- Presence of extraintestinal manifestations:
- erythema nodosum
- acute arthropathy
- arthritis and spondylitis
Anorexia, weight loss, malnutrition, anaemia, nausea, fatigue
What would a barium enema show in UC?
Mucosal ulceration with granular appearance and filling defects (due to pseudopolyps)
Narrowed colon
Loss of haustral pattern - leadpipe appearance
How would you manage moderate to severe UC?
- Oral steroids- prednisolone
- Oral and/or rectal 5-ASA- mesalazine
- Immunosuppression - infliximab, cyclosporin
- (anti-TNF monoclonal antibody)
What are the 2 main surgical procedures to treat UC?
Proctocolectomy with ileostomy – surgical removal of colon, rectum and anal canal
Ileo-anal pouch formation
Define diverticular disease/diverticulosis/diverticulitis
Diverticulosis:
Herniation of the mucosa and submucosa through the muscular layer of the colonic wall
Diverticular disease:
Diverticulosis associated with complications e.g. haemorrhage, infection, fistulae
Diverticulitis:
Acute inflammation and infection of colonic diverticulae
Describe the Hinchey Classification of Acute Diverticulitis
Stage I: small or confined pericolic or mesenteric abscess.
Stage II: large paracolic abscess often extending into pelvis.
Stage III: perforated diverticulitis where a peri-diverticular abscess has perforated resulting in purulent peritonitis.
Stage IV: perforated diverticulitis where there is free perforation and is associated with faecal peritonitis.
Explain the aetiology/pathogenesis of diverticular disease
- A low-fibre diet increases intestinal transit time and decreases stool volume
- Results in increased intraluminal pressure and colonic segmentation
- Leads to the herniation of the mucosa and submucosa
- Occurs between the tenia coli at presumed sites of weakness where the vasa recti penetrate the colonic wall.
What are the presenting symptoms of diverticular disease?
80-90% asymptomatic
-
Left lower quadrant abdominal pain- common, may be mild in uncomplicated disease
- guarding
- tenderness
- Leukocytosis
- Low grade pyrexia
- PR bleeding- less common, if acute. Profuse, arterial, painless
-
Bloating, constipation
- may alternate with episodes of diarrhoea
What are some signs that there may be diverticular fistulation?
pneumaturia, faecaluria, recurrent UTI
State the appropriate investigations for ACUTE diverticular disease and what you would see
-
FBC with differential
- see polymorphonuclear leukocytosis
- raised CRP
- check clotting and cross-match if bleeding
- culture if signs of septic
-
CT abdomen
- thickening of bowel wall, mass, abscess, streaky mesenteric fat
- may show gas in the bladder in cases of fistula
State the appropriate investigations for chronic/sub-acute diverticular disease
NOT when acute → perforation
Barium enema w/contrast
- when initial acute symptoms have resolved- confirmation
Flexible Sigmoidoscopy and Colonoscopy:
- Diverticulae can be visualised
- Other pathology (e.g. polyps and tumours, ischaemia) can be excluded
How would diverticulitis be managed?
- Analgesia
- IV antibiotics- if no improvement after 72 hours oral
- Low residue diet/bowel rest
- IV fluids/rehydration
- Abscesses may be drained by radiologically sited drains
What surgical procedures are considered for refractive/recurrent/complicated diverticulitis?
Hartmann’s procedure- proctosigmoidectomy and stoma formation
One-stage resection + anastomosis
- risk of leak
- with/without defunctioning stoma
Laparoscopic drainage, peritoneal lavage and drain placement can be effective
Define volvulus
Rotation of a loop of bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia.
Identify appropriate investigations for volvulus
-
FBC, ABG
- lactic acidosis with resp alkalosis leading to low pCO2
- due to inappropriate bowel perfusion
-
AXR (and CXR if perforation suspected)
- distended bowel loops above volvulus
- HORSESHOE SIGN
-
GI contrast series
- either upper GI or enema (lower GI)
-
CT abdomen w/contrast
- IV contrast shows no contrast in SMA
- oral contrast shows no contrast beyond duodenum
Define perineal abscess
pus collection in the perineal region
Define perineal fistula
an abnormal chronically infected tract communicating between the perineal skin and either the anal canal or the rectum
Explain the aetiology of perineal abscess/fistula
- 90% cases: perianal fistula forms as a consequence of perianal abscess
- Blockage of anal duct → fluid stasis → infection and abscess
- Common causative organisms:
- E. coli
- Bacteriodes spp.
- Enterococcus spp..
Describe the Goodsall rule
The Goodsall rule can be used clinically to predict the trajectory of a fistula tract, depending on the location of the external opening:
- External opening posterior to the transverse anal line – fistula tract will follow a curved course to the posterior midline
- External opening anterior to the transverse anal line – fistula tract will follow a straight radial course to the dentate line
Describe the treatment of perianal abscesses and fistulae
Requires SURGICAL treatment:
Open Drainage of Abscess, or
-
Fistulotomy (superficial disease)
- Opening tract by cutting through skin and subcutaneous tissue
- Allows to heal by secondary intention
- care to prevent sphincter damage
-
The placement of a seton (high tract disease)
- non-absorbable suture that is threaded through the fistula
- allows drainage of the localised infection and slow healing
may need MULTIPLE operations
