General - large bowel disease Flashcards

1
Q

Appendicitis

A

Inflammation of the appendix
Most commonly affects those in their second/third decade

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2
Q

Appendicitis pathophysiology

A

Typically caused by direct luminal obstruction, usually secondary to a faecolith, lymphoid hyperplasia, impacted stool or rarely a tumour
When obstructed, commensal bacteria in the appendix can multiply -> acute inflammation
Reduced venous drainage and localised inflammation can result in increased pressure within the appendix, in turn can result in ischaemia
Left untreated -> ischaemia within the appendiceal wall can result in necrosis -> perforation

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3
Q

Appendicitis risk factors

A

Family history
Ethnicity – more common in Caucasians
Environmental – summer

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4
Q

Appendicitis clinical features

A

Pain – initially peri-umbilical, classically dull and poorly localised, but later migrates to the right iliac fossa, where it is well-localised and sharp
Vomiting, anorexia, nausea, diarrhoea or constipation
Examination – rebound tenderness and percussion pain over McBurney’s point, guarding, severe cases
- Rovsing’s sign: RIF fossa pin on palpation of the LIF
- Psoas sign: RIF pain with extension of the right hip (appendix in a retrocaecal position)

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5
Q

Appendicitis investigations

A

Urinalysis, pregnancy test
Routine bloods – FBC, CRP, serum B-hCG if ectopic pregnancy has not been excluded
Imaging – ultrasound is first line if the differential includes gynaecological pathology, CT is able to delineate multiple differentials including GI and urological causes

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6
Q

Appendicitis management

A

Definitive treatment – laparoscopic appendicectomy
Appendix should routinely be sent to histopathology to look for malignancy

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7
Q

Appendicitis complications

A

Perforation – if left untreated can perforate and cause peritoneal contamination
Surgical site infection
Appendix mass
Pelvis abscess – fever with a palpable RIF mass, confirmed on CT scan, management is usually with abx and percutaneous drainage of abscess

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8
Q

Colorectal cancer aetiology

A

Originate from the epithelial cells, most commonly an adenocarcinoma
Develop via a progression of normal mucosa to colonic adenoma to invasive adenocarcinoma (adenoma carcinoma sequence)
Certain genetic mutations:
- Adenomatous polyposis coli (eg. FAP)
- Hereditary nonpolyposis colorectal cancer

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9
Q

Colorectal cancer risk factors

A

Increasing age
Male gender
Family history
Inflammatory bowel disease
Low fibre diet
High processed meat intake, smoking, excess alcohol

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10
Q

Colorectal cancer clinical features

A

Change in bowel habit, rectal bleeding, weight loss, abdominal pain and symptoms of anaemia
Right-sided colon cancers – abdominal pain, iron-deficiency anaemia, palpable in RIF, often present late
Left-sided colon cancers – rectal bleeding, change in bowel habit, tenesmus, palpable mass in LIF/PR exam

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11
Q

Colorectal cancer screening

A

Every 2 years to men and women aged 60-75 years
FIT test is used – utilises antibodies against human haemoglobin to detect blood in faeces
Positive samples – offered an appointment with a specialist nurse and further investigations via colonoscopy

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12
Q

Colorectal cancer investigations

A

Routine bloods – FBC, LFTs, clotting, CEA can be used to monitor disease progression
Imaging – gold standard for diagnosis is via colonoscopy with biopsy
Once diagnosis is made:
- CT chest/abdomen/pelvis to look for distal metastases and local invasion
- MRI rectum (for rectal cancers only)
- Endo-anal ultrasound (for early rectal cancers, T1/T2 only)
Biopsy samples will be assessed using TNM staging, histological subtyping, grading and assessment of lymphatic, perineural and venous invasion

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13
Q

Colorectal cancer surgical management

A

Mainstay of curative management
1) Right hemicolectomy/extended right hemicolectomy – surgical approach for caecal tumours/ascending colon tumours
2) Left hemicolectomy – surgical approach for descending colon tumours
3) Sigmoidcolectomy – sigmoid colon tumours
4) Anterior resection – high rectal tumours
5) Abdominoperineal resection – low rectal tumours
6) Hartmann’s procedure – used in emergency bowel surgery (eg. obstruction/perforation), involves a completed resection of the recto-sigmoid colon

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14
Q

Colorectal cancer chemotherapy

A

Indicated typically in patients with advanced disease
FOLFOX – folinic acid, fluorouracil & oxaliplatin
Newer biologic agents or immunotherapies

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15
Q

Colorectal radiotherapy

A

Can be used in rectal cancer, most often as neo-adjuvant treatment and can be given alongside chemotherapy
Particular use in patients with rectal cancers which look on MRI to have a ‘threatened’ circumferential resection = pre-operative long-course chemo-radiotherapy to shrink the tumour

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16
Q

Crohn’s disease pathophysiology

A

Any part of the GI tract, commonly targets the distal ileum/proximal colon
Characterised by transmural inflammation in the affected region of bowel, producing deep ulcers and fissures (‘cobblestone’ appearance), skip lesions
Non-caseating granulomatous inflammation
Fistulae commonly form

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17
Q

UC vs Crohn’s disease

A

Site involvement – large bowel in UC, entire GI tract in CD
Inflammation – mucosal only in UC, transmural inflammation in CD
Microscopic changes – crypt abcess formation, reduced goblet cells, non-granulomatous in UC, non-caseating granulomatous in CD
Macroscopic changes – continuous inflammation, pseudo polyps and ulcers may form in UC, skip lesions, fissures, deep ulcers, fistula formation in CD

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18
Q

Crohn’s disease risk factors

A

Strong family history
Smoking

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19
Q

Crohn’s disease clinical features

A

Episodic abdominal pain and diarrhoea – colicky pain and diarrhoea may contain blood/mucus
Systemic symptoms – malaise, anorexia and low-grade fever, malabsorption & malnourishment
Oral aphthous ulcers
Perianal disease

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20
Q

Crohn’s disease extraintestinal manifestations

A

MSK – enteropathic arthritis, nail clubbing or with metabolic bone disease
Skin – erythema nodosum, pyoderma gangrenosum
Eyes – episcleritis, anterior uveitis or iritis
Hepatobiliary – PSC, cholangiocarcinoma, gallstones
Renal – renal stones

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21
Q

Crohn’s disease investigations

A

Routine bloods
Faecal calprotectin, stool sample
Colonoscopy is gold standard investigation with biopsies taken to confirm the diagnosis
Imaging – CT scan abdomen pelvis in severe Crohn’s disease, MRI, EUA with proctosigmoidoscopy may be considered to examine and treat perianal fistulae present

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22
Q

Crohn’s disease management

A

Should be referred to a gastroenterologist
Inducing remission – fluid resus, nutritional support, prophylactic heparin, corticosteroid therapy as first line, immunosuppressive agents/biological agents can be trialled as rescue therapy if then needed
Maintaining remission – azathioprine, smoking cessation, colonoscopic surveillance is offered to people who have had the disease > 10 years with > 1 segment of bowel affected
Surgical management – failed medical management or severe complications

23
Q

Crohn’s disease complications

A

GI – fistula, stricture formation, recurrent perianal fistulae, GI malignancy
Extraintestinal – malabsorption, osteoporosis, increased risk of gallstones, increased risk of renal stones

24
Q

Diverticular disease

A

Diverticulum = outpouching of the bowel wall
Diverticulosis – presence of diverticula
Diverticular disease – symptoms arising from the diverticula
Diverticulitis – inflammation of the diverticula
Diverticular bleed – where the diverticulum erodes into a vessel & causes a large volume painless bleed

25
Diverticular disease pathophysiology
Aging bowel becomes weakened over time, movement of stool within the lumen will cause an increase in luminal pressure Results in an outpouching of the mucosa through the weaker areas of the bowel wall Bacteria can overgrow within the outpouchings, leading to inflammation -> can sometimes perforate
26
Diverticular disease risk factors
Age Low dietary fibre intake Obesity Smoking Family history NSAID use
27
Diverticular disease clinical features
Diverticulosis – asymptomatic and found incidentally during routine colonoscopy or CT imaging Diverticular disease – intermittent lower abdominal pain, typically colicky in nature & may be relieved by defecation (other symptoms – altered bowel habit, associated nausea and flatulence) Acute diverticulitis – acute abdominal pain, typically sharp in nature & normally localised in the LIF pain, worsened by movement Examination – localised tenderness, alongside features of systemic upset
28
Diverticular abscess
Diverticular abscess occurs as a sequelae in complicated diverticulitis Around <5cm can generally be managed conservatively with IV abx, if any bigger, then radiological drainage is first-line treatment Complicated multi-loculated abscesses will need surgical intervention (laparoscopic washout/Hartmann’s procedure)
29
Diverticular disease investigations
Lab tests – initial routine blood tests, group and save, VBG, urine dipstick Imaging – CT abdomen-pelvis is investigation of choice (thickening of colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, free air) Flexible sigmoidoscopy is a good initial approach (suspected uncomplicated diverticular disease)
30
Diverticular disease management
Uncomplicated diverticular disease – can be managed as an outpatient with simple analgesia and encouraging oral fluid intake Patients with diverticular bleeds – can often be managed conservatively as most cases will be self-limiting Those that fail to respond to conservative management may warrant embolization/surgical resection
31
Acute diverticulitis management
Most can be managed conservatively – abx, IV fluids and analgesia Symptoms typically improve within 2-3 after the initiation of treatment for uncomplicated cases Clinical deterioration should prompt repeat imaging to check for disease progression/complication
32
Diverticular disease surgical management
Required in those with perforation with faecal peritonitis or overwhelming sepsis Usually involves a Hartmann’s procedure (sigmoid colectomy with formation of an end colostomy) An anastomosis with reversal of colostomy may be possible may be possible at a later date
33
Diverticular disease complications
Diverticular stricture – following repeated episodes of acute inflammation, can result in large bowel obstruction, sigmoid colectomy is required Fistula formation – nearly always require surgical intervention - Colovesical fistula – gas bubbles in the urine (pneumoturia) - Colovaginal fistula – copious vaginal discharge or recurrent vaginal infections
34
Pseudo-obstruction
Disorder characterised by dilatation of the colon due to an adynamic bowel in the absence of mechanical obstruction Most commonly affects the caecum and ascending colon
35
Pseudo-obstruction pathophysiology
Thought to be due to an interruption of the autonomic nervous supply to the colon resulting in the absence of smooth muscle action in the bowel wall Variety of causes: - Electrolyte imbalance or endocrine disorders - Medication - Recent surgery, severe illness or trauma - Neurological disease
36
Pseudo-obstruction clinical features
Abdominal pain Abdominal distension Constipation Vomiting Examination – abdomen will be distended and tympanic
37
Pseudo-obstruction investigations
Initial blood tests should be performed to assess for biochemical/endocrine Plain abdominal films (AXR) – show bowel distension Should undergo CT abdomen-pelvis scan with IV contrast – will show dilatation of the colon
38
Pseudo-obstruction management
Most cases can be managed conservatively – patients should be made nil-by-mouth and started on IV fluids If patient is vomiting an NGT should be inserted to aid decompression Endoscopic decompression will be mainstay of treatment if not resolved in 24-48 hours -> insertion of a flatus tube & allows region to decompress, IV neostigmine may also be trialled if suitable Surgical management – non-responding cases may require segmental resection +/- anastomosis
39
UC pathophysiology
Characterised by diffuse continual mucosal inflammation of the large bowel beginning in the rectum and spreading proximally Backwash ileitis = distal ileum cab become affected in the ileocaecal valve is not competent Histological changes – non-granulomatous inflammation of the mucosa and submucosa, crypt abscesses and goblet cell hypoplasia
40
UC clinical features
Bloody diarrhoea PR bleeding, mucus discharge, increased frequency and urgency of defecation and tenesmus Systemic symptoms – malaise, anorexia and low-grade pyrexia Clinical examination – generally unremarkable
41
UC extra-intestinal manifestations
MSK – enteropathic arthritis, nail clubbing Skin – erythema nodosum (tender red/purple subcutaneous nodules, typically on the shins) Eyes – episcleritis, anterior uveitis or iritis Hepatobiliary – primary sclerosing cholangitis (chronic inflammation & fibrosis of the bile ducts)
42
UC investigations
Routine bloods Faecal calprotectin and stool sample Imaging – definitive diagnosis is via colonoscopy with biopsy (continuous inflammation with possible ulcers & pseudopolyps visible) Acute exacerbations – AXR or CT imaging - AXR features: mural thickening and thumbprinting; in chronic cases of UC a lead-pipe colon
43
UC management (inducing remission)
Aggressive fluid resus, nutritional support and prophylactic heparin Medical management – IV corticosteroid agents, immunosuppressive agents, biological agents
44
UC management (maintaining remission)
Remission of the disease can be maintained using immunomodulators, typically 5-ASAs eg. mesalazine/sulfasalazine or azathioprine Colonoscopic surveillance is offered to people who have had the disease for >10 years with >1 segment of bowel affected Referred to IBD-nurse specialists and patient-support groups
45
UC management (surgical management)
Indications: disease refractory to medical management, toxic megacolon or bowel perforation Elective causes – total proctocolectomy is curative (patient will require an end ileostomy) Many patients for disease control will initially undergo a subtotal colectomy with ileo-rectal anastomosis or panproctocolectomy with ileo-pouch anal anastomosis
46
UC complications
Toxic megacolon – present with severe abdominal pain, abdominal distension, pyrexia and systemic toxicity Colorectal carcinoma Osteoporosis Pouchitis
47
Volvulus
Twisting of a loop of intestine around its mesenteric attachment, resulting in a closed loop bowel obstruction Affected bowel can become ischaemic due to compromised blood supply Most volvuli occur at the sigmoid colon and are a common cause of large bowel obstruction
48
Volvulus risk factors
Increasing age Neuropsychiatric disorders Resident in a nursing home Chronic constipation/laxative use Male gender Previous abdominal operations
49
Volvulus clinical features
Clinical features of bowel obstruction Colicky pain, abdominal distension and absolute constipation occur earlier Rapidity of the onset (over a few hours) and degree of abdominal distension Examination – abdomen is often very tympanic to percussion
50
Volvulus investigations
Routine bloods CT scan abdomen-pelvis with contrast – much more sensitive and specific for bowel obstruction & also identifies the site and cause AXR – coffee-bean sign arising from the LIF, if the ileocaecal valve is incompetent – also show signs of small bowel dilatation
51
Volvulus conservative management
Most patients are treated conservatively initially with decompression by sigmoidoscope and insertion of a flatus tube Flatus tube is often left is situ for up to 24 hours after initial decompression to allow the continued passage of contents
52
Volvulus surgical management
Indications for surgery: colonic ischaemia/perforation, repeated failed attempts at decompression, necrotic bowel noted at endoscopy - Usually a Hartmann’s procedure Patients with recurrent volvulus – may choose to have an elective procedure to prevent further recurrence
53
Volvulus complications
Bowel ischaemia and perforation Risk of recurrence Complications from stoma Mortality from surgery