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Surgery Finals > Lower GI > Flashcards

Lower GI Flashcards

1
Q

What is a Meckel’s diverticulum?

A

Ileal remnant of the vitellointestinal duct which joins the yoke sac to the midgut lumen

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2
Q

What are the features of Meckel’s diverticulum (2’s)?

A
  • True diverticulum
  • 2 inches long
  • 2ft from the ileocaecal valve on the antimesenteric border
  • 2% of the population
  • 2% symptomatic
  • Contain ectopic gastric or pancreatic tissue
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3
Q

How does symptomatic Meckel’s present?

A
  • Rectal bleeding: from gastric mucosa
  • Diverticulitis mimicking appendicitis
  • Intussusception
  • Volvulus
  • Malignant change: adenocarcinoma
  • Raspberry tumour: mucosa protruding at umbilicus (vitello-intestinal fistula)
  • Littre’s hernia: herniation of Meckel’s
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4
Q

How is meckel’s diagnosed?

A

Tc pertechnecate scan - detects gastric mucosa and is positive in 70%

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5
Q

How is meckel’s managed?

A

Surgical resection

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6
Q

What is intussusception?

A

Where a portion of intestine (the intussusception) is invaginated into its own lumen (the intussuscipiens)

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7
Q

What are the causes of intussusception?

A
  • Hypertrophied Peyer’s patch (post viral)
  • Meckel’s
  • HSP
  • Peutz-Jeghers
  • Lymphoma
  • Leukaemia
  • Duplication cysts
  • Haemangioma of bowel
  • Inspissated meconium in CF
  • Intestinal luminal polyp
  • Nephrotic syndrome
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8
Q

How does intussusception present?

A
  • 6-12 months
  • Colicky abdominal pain:
    • Episodic inconsolable crying, drawing up legs
    • ± bilious vomiting
  • Redcurrant jelly stools
  • Sausage-shaped abdominal mass
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9
Q

How is intussusception managed?

A
  • Resuscitate, cross match, NGT
  • US and reduction by air enema
  • Surgery if not reducible by enema
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10
Q

Does intussusception happen in adults?

A

Rarely - if it does think of neoplasm as a lead point

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11
Q

What is mesenteric adenitis and what are the differentiating features for it?

A
  • Viral infection/URTI leads to enlargement of mesenteric lymph nodes -> pain, tenderness and fever
  • Differentiating features:
    • Post URTI
    • Headache and photophobia
    • Higher temperature
    • Tenderness is more generalised
    • Lymphocytosis
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12
Q

What kinds of neoplasms occur in the small bowel?

A
  • All quite rare
  • Benign: 35%
    • Lipoma
    • Leiomyoma
    • Neurofibroma
    • Haemangioma
    • Adenomatous polyps (FAP, Peutz-Jeghers)
  • Malignant: 65% (only 2% of GI malignancies)
    • Adenocarcinoma (40% of malignant tumours)
    • Carcinoid (40% of malignant tumours)
    • Lymphoma (especially coeliac disease: EATL)
    • GIST
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13
Q

How do small bowel neoplasms present?

A
  • Often non specific symptoms, so late
  • Nausea and vomiting, obstruction
  • Weight loss and abdominal pain
  • Bleeding
  • Jaundice from biliary obstruction or liver mets
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14
Q

What investigations should you do in a suspected small bowel cancer?

A
  • Imaging:
    • AXR (SBO)
    • Barium follow through
    • CT
  • Endoscopy
    • Push enteroscopy
    • Capsule endoscopy
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15
Q

What is Gardner’s syndrome?

A
  • Small bowel adenomas and carcinomas
  • Associated with skeletal abnormalities and desmoid tumours
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16
Q

Which cancers can cause secondary tumours in the small bowel?

A

Rarely - lung, breast, malignant melanoma

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17
Q

What are carcinoid tumours?

A

Diverse group of neuroendocrine tumours of enterochromaffin cell origin capable of producing 5HT.

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18
Q

Where might carcinoid tumours be derived from?

A
  • Foregut: respiratory tract
  • Midgut: stomach, ileum, appendix
  • Hindgut: colorectum
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19
Q

Which hormones can carcinoid tumours secrete?

A
  • 5-HT
    • Hindgut tumours rarely secrete 5HT
  • VIP
  • Gastrin
  • Glucagon
  • Insulin
  • ACTH
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20
Q

What does carcinoid syndrome suggest?

A

Bypass of firstpass metabolism - strongly associated with metastatic disease

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21
Q

Which MEN are carcinoid tumours associated with and how commonly?

A

10% part of MEN1

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22
Q

Where are carcinoid tumours found?

A
  • Appendix: 45%
  • Ileum: 30%
  • Colorectum: 20%
  • Stomach: 10%
  • Elsewhere in GIT
  • Bronchus: 10%
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23
Q

How do carcinoid tumours present?

A
  • Appendicitis
  • Intussusception or obstruction
  • Abdominal pain
  • Carcinoid syndrome
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24
Q

What are the features of carcinoid syndrome?

A
  • FIVE HT
  • Flushing: paroxysmal, upper body ± wheals
  • Intestinal: diarrhoea
  • Valve fibrosis: tricuspid regurg and pulmonary stenosis
  • Wheeze: bronchoconstriction
  • Hepatic involvement: bypassed first pass metabolism
  • Tryptophan deficiency: pellagra (3Ds)
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25
Q

What are the key investigations in a suspected carcinoid tumour?

A
  • Raised urine 5-hydroxyindoleacetic acid
  • Raised plasma chromogranin A
  • CT/MRI to find the primary
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26
Q

How do you treat carcinoid tumours?

A
  • Symptoms: octreotide or loperamide
  • Curative:
    • Resection: tumours are very yellow
    • Also give octreotide to avoid carcinoid crisis
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27
Q

What is a carcinoid crisis and how do you treat it?

A
  • Tumour outgrows blood supply or is handled too much and there is a massive mediator release
  • Features: vasodilatation, hypotension, bronchoconstriction, hyperglycaemia
  • Treat with high dose octreotide
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28
Q

What is the prognosis in carcinoid tumours?

A

Median survival is 5-8 years (~3 years if mets present)

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29
Q

What is the definition of acute appendicitis?

A

Inflammation of the vermiform appendix ranging from oedema to ischaemic necrosis and perforation

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30
Q

What is the epidemiology of appendicitis?

A
  • 6% lifetime incidence
  • Commonest surgical emergency
  • Rare <2 years
  • Maximal peak during childhood
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31
Q

What is the pathogenesis of acute appendicitis?

A
  • Obstruction of the appendix
    • Faeolith most commonly
    • Lymphoid hyperplasia post infection
    • Tumour e.g. caecal cancer, carcinoid
    • Worms e.g. Ascaris lumbicoides, schisto
  • Gut organisms -> infection behind obstruction
  • Leads to oedema, ischaemia, necrosis, perforation
    • Peritonitis
    • Abscess
    • Appendix mass
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32
Q

What is the pattern of abdominal pain in appendicitis and why?

A
  • Early inflammation -> appendiceal irritation
    • Visceral pain is not well localised compared to somatic pain
    • Nociceptive information travels in the sympathetic afferent fibres that supply the viscus
    • Pain referred to the dermatome corresponding to the spinal cord entry level of these sympathetic fibres
    • Appendix = midgut = lesser splanchnic T10/11 = umbilicus
  • Late inflammation -> parietal peritoneum irritation
    • Pain localised in RIF
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33
Q

What are the symptoms of appendicitis?

A
  • Colicky abdominal pain
    • Central then localised in RIF
    • Worse with movement
  • Anorexia (variable)
  • Nausea (vomiting rarely prominent but moeso if appendix is retroileal)
  • Constipation/diarrhoea ± mucus
  • Variable urinary symptoms (frequency/dysuria) if appendix is near ureter/bladder
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34
Q

What are the signs of appendicitis?

A
  • Low-grade pyrexia: 37.5-38.5
  • Raised HR, shallow breathing
  • Foetor oris + coated tongue
  • Guarding and tenderness at McBurney’s point
    • Positive cough/percussino tenderness
    • McBurney’s point = junction of the middle and outer thirds of a line joining the umbilicus to R ASIS
  • Appendix mass may be palpable in RIF
  • Pain PR suggests pelvic appendix
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35
Q

What are the eponymous signs of appendicitis?

A
  • Rovsing’s sign
    • Pressure in LIF -> more pain in RIF
  • Psoas sign
    • Pain on extending the hip: retrocaecal appendix
  • Cope sign
    • Flexion and internal rotation of the R hip causes pain
    • Appendix lying close to obturator internus
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36
Q

What are the differentials for acute appendicitis?

A
  • Surgical
    • Cholecystitis
    • Diverticulitis
    • Meckel’s diverticulitis
  • Gynae
    • Cyst accident: torsion, rupture, haemorrhage
    • Salpingitis/PID
    • Ruptured ectopic
  • Medical
    • Mesenteric adenitis
    • UTI
    • Crohn’s
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37
Q

What are the key investigations in acute appendix?

A
  • Principally clinical
  • Bloods: FBC, CRP, amylase, G+S, clotting
  • Urine
    • Sterile pyuria: may indicate bladder irritation
    • Ketones: anorexia
    • Exclude UTI
    • Beta HCG
  • Imaging
    • Ultrasound: exclude gynae pathology, visualise inflamed appendix
    • CT can be used
  • Diagnostic lap
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38
Q

How is acute appendicits managed?

A
  • Fluids
  • Antibiotics: cef 1.5g and met 500g IV TDS
  • Analgesia: paracetamol, NSAIDs, codeine phosphate
  • Certain diagnosis -> appendicectomy (open or lap)
  • Uncertain diagnosis -> active observation
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39
Q

What are the 3 most important complications of appendicitis?

A
  • Appendix mass
  • Appendix abscess
  • Perforation
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40
Q

What is an appendix mass and how is it managed?

A
  • Inflamed appendix with adherent covering of omentum and small bowel
  • Diagnose with US or CT
  • Initially antibiotics and NBM
  • Resolution of mass -> interval appendicectomy
  • Exclude a colonic tumour with colonoscopy
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41
Q

What causes an appendix abscess and how is it managed?

A
  • Results if appendix mass doesn’t resolve
  • Mass enlarges and patient deteriorates
  • Antibiotics and nil by mouth
  • CT guided percutaneous drainage
  • If no resolution surgery may involve right hemicolectomy
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42
Q

In which patients is a perforation a more common complication of appendicitis?

A
  • If a faecolith is present
  • Young children (as diagnosis often delayed)
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43
Q

What is the prevalence of UC and Crohn’s?

A

UC: 100-200/100,000

Crohn’s: 50-100/100,000

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44
Q

What is the peak age for UC and Crohn’s?

A

UC: 30’s

Crohn’s: 20’s

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45
Q

Are men or women more affected by IBD?

A

Women (just) for UC and Crohn’s

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46
Q

What is the concordance for UC and Crohn’s?

A

UC: 10%

Crohn’s: 70%

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47
Q

How does smoking affect UC and Crohn’s risk?

A

Current smoking is protective for UC. Smoking increases the risk of Crohn’s.

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48
Q

Which TH mediates Crohn’s and UC?

A

UC: TH2

Crohn’s: TH1/TH17

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49
Q

What locations are involved in UC and Crohn’s?

A

UC: Rectum + colon + backwash ileitis

Crohn’s: mouth to anus especially terminal ileum

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50
Q

What is the distribution of Crohn’s and UC?

A

UC: contiguous

Crohn’s: skip lesions

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51
Q

Do people get strictures in Crohn’s and UC?

A

UC: No

Crohn’s: Yes

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52
Q

What are the microscopic pathological features in Crohn’s and UC?

A

UC: mucosal inflammation, shallow, broad ulceration, marked pseudopolyps

Crohn’s: transmural inflammatino, cobblestone mucosa (deep, thin, serpiginous), marked fibrosis, granulomas, minimal pseudopolyps, fistulae

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53
Q

What are the systemic features in Crohn’s and UC?

A

Fever, malaise, anorexia, weight loss in active disease

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54
Q

What are the abdominal features in Crohn’s and UC?

A
  • UC: diarrhoea, blood ± mucus PR, abdominal discomfort, tenesmus, faecal urgency
  • Crohn’s: diarrhoea (not usually bloody), abdo pain, weight loss
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55
Q

What are the signs of UC and Crohn’s?

A

UC: fever, tender, distended abdo

Crohn’s: aphthous ulcers, glossitis, abdo tenderness, RIF mass, perianal abscesses, fistulae, tags, anal/rectal strictures

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56
Q

What are the extra abdominal features of UC and Crohn’s?

A
  • Skin: clubbing, erythema nodosum, pyoderma gangrenosum (esp UC)
  • Eyes: iritis, conjunctivitis, episcleritis, scleritis
  • Joints: arthritis (non deforming, asymmetrical), sacroiliitis, ank spond
  • HPB: PSC + cholangiocarcinoma (esp UC), gallstones (esp Crohn’s), fatty liver
  • Other: amyloidosis, oxalate renal stones (esp Crohn’s)
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57
Q

What are the complications of UC?

A
  • Toxic megacolon
    • >6cm, risk of perf
  • Bleeding
  • Malignancy
    • CRC in 15% with pancolitis for 20 years
  • Cholangiocarcinoma
  • Strictures causing obstruction
  • Venous thrombosis
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58
Q

What are the complications of Crohn’s?

A
  • Fistulae
    • Entero-enteric/colonic -> diarrhoea
    • Enterovesical -> frequency, UTI
    • Enterovaginal
    • Perianal -> “pepperpot” anus
  • Strictures -> obstruction
  • Abscesses
    • Abdominal
    • Anorectal
  • Malabsorption
    • Fat -> steatorrhoea, gallstones
    • B12 -> megaloblastic anaemia
    • Vit D -> osteomalacia
    • Protein -> oedema
  • Toxic megacolon and cancer can happen, but less than in UC
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59
Q

What are the complications of toxic megacolon?

A
  • Toxaemia
  • Anaemia from bleeding
  • Acute loss of water and electrolyte issues
  • Progressive abdominal distension
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60
Q

What investigations should you do in UC?

A
  • Bloods:
    • FBC (low Hb raised WCC)
    • LFT: low albumin
    • Raised CRP/ESR
  • Stool:
    • MCS: explude Campylobacter, Shigella, Salmonella
    • CDT: C diff can complicate or mimic
  • Imaging:
    • AXR: megacolon (>6cm), wall thickening
    • CXR: perforation
    • CT
    • Barium/gastrograffin enema
      • Lead pipe: no haustra
      • Thumbprinting: mucosal thickening
      • Pseudopolyps: regenerating mucosal island
  • Ileocolonoscopy + regional biopsy: Baron score
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61
Q

What are the Truelove and Witts Criteria?

A
  • Mild:
    • <4 motions, small PR bleed, apyrexic, HR<70, Hb>11, ESR<30
  • Moderate:
    • 4-6 motions, moderate PR bleed, T 37.1-37.8, HR 70-90, Hb 10.5-11
  • Severe:
    • >6 motions, large PR bleed, T>37.8, HR>90, Hb<10.5, ESR>30
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62
Q

What is the management for acute severe UC?

A
  • Resus: admit, IV hydration, NBM
  • Hydrocortisone: IV 100mg QDS + PR
  • Transfuse if needed
  • Thromboprophylaxis: LMWH
  • Monitoring:
    • Bloods: FBC, ESR, CRP, U+E
    • Vitals and stool chart
    • Twice daily examination
    • ± AXR
  • RCTs don’t show a benefit from Abx so only considered if megacolon, perf, uncertain Dx
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63
Q

What are the acute complications of severe UC?

A
  • Perforation
  • Bleeding
  • Toxic megacolon
  • VTE
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64
Q

What is the continuing therapy for acute severe UC?

A
  • If improving: switch to oral pred and 5-ASA, taper pred after a full remission
  • If no improvement, rescue therapy:
    • On day 3 a stool frequency of >8 or a CRP>45 predicts an 85% chance of needing a colectomy during the admission
    • Medical management: ciclosporin, infliximab or visilizumab (anti T cell)
    • Or surgery
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65
Q

How do you induce remission in mild/mod UC?

A
  • Oral therapy:
    • 1st line: 5-ASAs
    • 2nd line: pred
  • Topical therapy (mainly L sided disease)
    • Proctitis: suppositories
    • More proximal disease: enemas or foams
    • 5-ASAs ± steroids (prednisolone or budesonide)
  • Additional therapy: steroid sparing
    • Azathioprine or mercaptopurine
    • Infliximab for steroid dependent patients
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66
Q

How do you maintain remission in mild/mod UC?

A
  • 1st line: 5-ASAs PO - sulfasalazine or mesalazine
    • Topical therapy can be used in proctitis
  • 2nd line: azathioprine or mercaptopurine
    • Relapsed on ASA or are steroid dependent
    • Give 6-mercaptopurine ir azathioprine intolerant
  • 3rd line: infliximab/adalimumab
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67
Q

How common is the need for surgery in UC?

A
  • 20% need surgery at some point
  • 30% with colitis require surgery within 5 years
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68
Q

What are the indications for emergency surgery in UC?

A
  • Toxic megacolon
  • Perforation
  • Massive haemorrhage
  • Failure to respond to medical therapy
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69
Q

What procesdures are done in UC as emergency surgery?

A
  • Total/subtotal colectomy with end ileostomy ± mucus fistula
  • Followed after about 3 months be either:
    • Completion proctectomy and ileal pouch anal anastomosis (IPAA) or end ileostomy ileorectal anastomosis (IRA)
  • Panproctocolectomy + permanent end ileostomy
  • Acute colitis op mortality is 7% (30% if perforated)
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70
Q

What are the indications for elective surgery in UC?

A
  • Chronic symptoms despite medical therapy
  • Carcinoma or high grade dysplasia
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71
Q

Which procedures are done as elective surgery in UC?

A
  • Panproctocolectomy with end ileostomy or IPAA
  • Total colectomy with IRA
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72
Q

What are the possible surgical complications from UC operations?

A
  • Abdominal
    • SBO
    • Anastomotic stricture
    • Pelvic abscesses
  • Stoma: retraction, stenosis, prolapse, dermatitis
  • Pouch
    • Pouchitis (50%): metronidazole + cipro
    • Reduced female fertility
    • Faecal leakage
    • Renal calculi
    • Electrolyte imbalance
    • Psychological/sexual issues
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73
Q

What investigations should you do in Crohn’s?

A
  • Bloods
    • Severity markers: FBC (low Hb, raised WCC), LFT (low albumin), raised CRP/ESR
    • Haematinics: Fe, B12, folate
    • Blood cultures
  • Stool
    • MCS: exclude campylobacter, shigella, salmonella
    • CDT: C diff may complicate or mimic
  • Imaging
    • AXR: obstruction, sacrioileitis
    • CXR: perforation
    • MRI
      • Assess pelvic disease and fistula
      • Assess disease severity
    • Small bowel follow through or enteroclysis
      • Skip lesions
      • Rosethorn ulcers
      • Cobblestoning
      • String sign of Kantor: narrow terminal ileum
  • Endoscopy
    • Ileocolonoscopy + regional biopsy: investigation of choice
    • Wireless capsule endoscopy
    • Small bowel endoscopy
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74
Q

How should you assess a severe attack of Crohn’s?

A
  • Raised temp
  • Raised HR
  • Raised ESR
  • Raised CRP
  • Raised WCC
  • Low albumin
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75
Q

How do you manage a severe attack of Crohn’s?

A
  • Resus: admit, NBM, IV hydration
  • Hydrocortisone: IV + PR if recal disease
  • Abx: metronidazole PO or IV
  • Thromboprophylaxis: LMWH
  • Dietician review: elemental diet (liquid prep of amino acids, glucose and fatty acids), consider parenteral
  • Monitoring: vitals + stool chart, daily examination
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76
Q

What is the continuing therapy for a severe attack of Crohn’s?

A
  • Improvement: switch to oral therapy (40mg/d)
  • No improvement - rescue therapy
    • Discussion betweeen patient, doctor and surgeon
    • Medical: methotrexate ± infliximab
    • Surgical
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77
Q

How do you induce remission in mild/mod Crohn’s?

A
  • Supportive: high fibre diet, vitamin supplements
  • Oral therapy:
    • 1st line: ileocaecal: budesonide
      • Colitis: sulfasalazine
    • 2nd line: pred (tapering)
    • 3rd line: methotrexate
    • 4th line: infliximab or adalimumab
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78
Q

How do you manage perianal disease in Crohn’s?

A
  • Oral abx: metronidazole
  • Immunosuppression ± infliximab
  • Local surgery ± seton insertion
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79
Q

How do you maintain remission in Crohn’s?

A
  • 1st line: azathioprine or mercaptopurine
  • 2nd line: methotrexate
  • 3rd line: infliximab/adalimumab
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80
Q

How commonly do Crohn’s patients need surgery?

A
  • 50-80% need ≥1 operation in their life
  • Never curative
  • Should be as conservative as possible
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81
Q

What are the indications for surgery in Crohn’s?

A
  • Emergency
    • Failure to respond to medical therapy
    • Inestinal obstruction or perforation
    • Massive haemorrhage
  • Elective
    • Abscess or fistula
    • Perianal disease
    • Chronic ill health
    • Carcinoma
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82
Q

What procedures are done in Crohn’s?

A
  • Limited resection e.g. ileocaecal
  • Stricturoplasty
  • Defunction distal disease with temporary loop ileostomy
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83
Q

What complications do you get from Crohn’s surgery?

A
  • Stoma complications
  • Enterocutaneous fistulae
  • Anastomotic leak or stricture
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84
Q

What length of bowel causes short bowel syndrome?

A

<1-2m small bowel

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85
Q

What are the features of short gut syndrome?

A
  • Steatorrhoea
  • ADEK and B12 malabsorption
  • Bile acid depletion -> gallstones
  • Hyperoxaluria -> renal stones
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86
Q

What is the treatment for short gut syndrome?

A
  • Dietician
  • Supplements or TPN
  • Loperamide
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87
Q

Define “diverticulum”

A

Outpouching of tubular structure

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88
Q

Define “true” and “false” diverticulum

A

true = composed of complete wall e.g. Meckel’s

false = composed of mucosa only (pharyngeal, colonic)

89
Q

What is diverticular disease?

A

Symptomatic diverticulosis

90
Q

What is diverticulitis?

A

Inflammation of diverticula

91
Q

Who gets diverticular disease?

A

30% Westerner’s have diverticulosis by 60 years, F>M

92
Q

What is the pathophysiology of diverticular disease?

A
  • Associated with increased intraluminal pressure (low fibre diet -> no osmotic effect to keep stool wet)
  • Mucosa herniates through muscularis propria at points of weakness where perforating arteries enter
  • Most commonly located in sigmoid colon
  • Commoner in obese patients
93
Q

What is Saint’s triad?

A
  • Hiatus hernia
  • Cholelithiasis
  • Diverticular disease
94
Q

What are the symptoms of diverticular disease?

A
  • Aleterd bowel habit ± left sided colic, relieved by defecation
  • Nausea
  • Flatulence
95
Q

What is the treatment for diverticular disease?

A
  • High fibre diet
  • Mebeverine may help
  • Elective resection for chronic pain
96
Q

What is the pathophysiology of diverticulitis?

A

Inspissated faeces -> obstruction of diverticulum

97
Q

How does diverticulitis present?

A
  • Typically an elderly patient with a previous history of constipation
  • Abdo pain and tenderness - typically LIF, localised peritonitis
  • Pyrexia
98
Q

What investigations should you do in diverticulitis?

A
  • Bloods
    • FBC: raised WCC
    • Raised CRP/ESR
    • Amylase
    • G+S/cross match
  • Imaging:
    • Erect CXR: look for perf
    • AXR: fluid level/air in bowel wall
    • Contrast CT if complications
    • Gastrograffin enema
  • Endoscopy
    • Flexi sig
    • Colonoscopy: not in acute attack
99
Q

What grading system is used in diverticulitis?

A
  1. Small confined percolic abscesses = surgery rarely needed
  2. Large abscess extending into pelvis - may resolve without surgery
  3. Generalised purulent peritonitis - surgery needed
  4. Generalised faecal peritonitis - surgery needed
100
Q

How do you manage mild attacks of diverticulitis?

A

Can be treated at home with bowel rest (fluids only) and augmentin ± metronidazole

101
Q

When should you admit acute diverticulitis?

A
  • Unwell
  • Fluids can’t be tolerated
  • Pain can’t be controlled
102
Q

What is the medical management of acute diverticulitis?

A
  • NBM
  • IV fluids
  • Analgesia
  • Antibiotics: cefuroxime + metronidazole
  • Most cases settle
103
Q

What are the indications for surgery in diverticulitis and what procedure do you do?

A
  • Indications:
    • Perforation
    • Large haemorrhage
    • Stricture -> obstruction
  • Procedure is a Hartmann’s to resect the diseased bowel
104
Q

What are the complications of diverticular disease?

A
  • Perforation
  • Haemorrhage
  • Abscess
  • Fistulae
  • Strictures
105
Q

How does perforation present and what do you do about it?

A
  • Sudden onset pain (± preceding diverticulitis)
  • Generalised peritonitis and shock
  • CXR: free air under the diaphragm
  • Do a Hartmann’s
106
Q

What kind of haemorrhage do you get in diverticulitis and what do you do about it?

A
  • Sudden, painless, bright red PR bleed
  • Investigate: mesenteric angiography or colonoscopy
  • Treat:
    • Usually stops spontaneously
    • May need transfusion
    • Colonoscopy ± diathermy/adrenaline
    • Embolisation
    • Resection
107
Q

How does an abscess present in diverticulitis and what do you do about it?

A
  • Walled-off perforation
  • Swinging fever
  • Localising signs: e.g. boggy rectal mass
  • Leukocytosis
  • Treat: Abx + CT/US guided drainage
108
Q

What kind of fistulae do you get in diverticular disease?

A
  • Enterocolic
  • Colovaginal
  • Colovesicular: pneumaturia + intractable UTIs
109
Q

Why do you get strictures in diverticulitis?

A

Colon can heal with fibrous strictures after the diverticulitis

110
Q

How do you classify bowel obstruction?

A
  • Simple
    • 1 obstructing point and no vascular compromise
    • May be partial or complete
  • Closed loop
    • Bowel obstructed at 2 points
      • Left CRC with competent ileocaecal valve
      • Volvulus
    • Gross distension leading to perforation
  • Strangulated
    • Compromised blood supply
111
Q

What are the features of a strangulated bowel obstruction and what’s the risk?

A
  • Localised constant pain and peritonism
  • Fever
  • Raised WCC
  • Dies within 4-6 hours and ruptures
112
Q

What are the commonest causes of bowel obstruction?

A
  • SBO:
    • Adhesions: 60%
    • Hernia
  • LBO:
    • Colorectal neoplasia: 60%
    • Diverticular stricture: 20%
    • Volvulus: 5%
113
Q

What are the non-mechanical causes of bowel obstruction?

A
  • Post op
  • Peritonitis
  • Pancreatitis or any localised inflammation
  • Poisons/drugs: anti-AChM e.g. TCAs
  • Pseudo obstruction
  • Metabolic: hypokalaemia, hyponatraemia, hypomangnesaemia, uraemia
  • Mesenteric ischaemia
114
Q

What are the mechanical causes of bowel obstruction?

A
  • Intraluminal
    • Impacted matter: faeces, worms, bezoars
    • Intussusception
    • Gallstones
  • Intramural
    • Benign stricture (IBD, surgery, ischaemic colitis, diverticulitis, radiotherapy)
    • Neoplasia
    • Congenital atresia
  • Extramural
    • Hernia
    • Adhesions
    • Volvulus (sigmoid, caecal, gastric)
    • Extrinsic compression
      • Pseudocyst
      • Abscess
      • Haematoma
      • Tumour e.g. ovarian
      • Congenital bands (e.g. Ladd’s)
115
Q

How does bowel obstruction present?

A
  • Abdo pain (colicky, central)
  • Distension (moreso if lower obstructions)
  • Vomiting (early in high, late or absent in low)
  • Absolute constipation
116
Q

What examination findings suggest bowel obstruction?

A
  • Tachycardia (hypovolaemia, strangulation)
  • Dehydration, hypovolaemia
  • Fever (inflammation/strangulation)
  • Surgical scars
  • Hernias
  • Mass (neoplastic/inflammatory)
  • Bowel sounds (increased if mechanical, decreased in ileus)
  • PR: empty rectum, rectal mass, hard stool, blood from higher pathology)
  • Do a vaginal exam too
117
Q

How should you investigate bowel obstruction?

A
  • Bloods:
    • FBC (raised WCC)
    • U+E (dehydration, electrolyte abnormalities)
    • Amylase: increased in strangulation/perforation
    • VBG: raised lactate in strangulation
    • G+S, clotting
  • Imaging
    • Erect CXR
    • AXR ± erect film for fluid levels
    • CT: can show transition point
  • Gastrograffin studies
    • Loow for mechanical obstruction
    • Follow through or enema
    • Follow through may relieve mild mechanical obstruction esp adhesional
  • Colonoscopy
    • Can be used in some cases but there is a risk of perforation
    • May be used therapeutically to stent
118
Q

What are the AXR findings in small bowel obstruction?

A
  • ≥3 diameter
  • Central location
  • Valvulae coniventes - completely across
  • Absent LB gas
  • Many loops
  • Many, short fluid levels
119
Q

What are the AXR findings in large bowel obstruction?

A
  • ≥6cm diameter (caecum ≥9)
  • Peripheral
  • Haustra - partially across
  • LB gas present but not in rectum
  • Few loops
  • Few, long fluid levels
120
Q

What are the AXR findings in ileus?

A

Both small and large bowel may be visible but no clear transition point

121
Q

What is the initial therapy for bowel obstruction?

A
  • Resus - drip and suck
    • NBM
    • IV fluids: aggressive
    • NGT: decompress upper GIT, stops vomiting, prevents aspiration
    • Catheterise to monitor UO
  • Then
    • Analgesia (may need strong opioid)
    • Antibiotics (cef and met if strangulation/perforation)
    • Gastrograffin study (oral or via NGT)
    • Consider need for parenteral nutrition
122
Q

How should you monitor a patient with bowel obstruction?

A
  • Regular examination 4-6 hourly to make sure they’re not deteriorating
    • Distension
    • Pain/tenderness
    • Raised HR/RR
  • Repeat imaging and bloods
123
Q

How many patients with bowel obstruction need surgery?

A
  • Non operative Mx is successful in ~80% patients with SBO without peritonitis
  • LBO patients more likely to need surgery
124
Q

What are the indications for non surgical management of bowel obstruction?

A
  • Firm evidence there is no threat to the viability of the bowel
  • Incomplete obstruction in the small or large bowel with features suggesting non progression
  • Some instances of complete SBO e.g. adhesive obstruction
125
Q

What are the indications for surgical management of bowel obstruction?

A
  • Closed loop obstruction
  • Obstructing neoplasm (or other cause needing removal)
  • Strangulation/perforation -> sepsis, peritonitis
  • Failure of conservative management (up to 72 hours)
126
Q

What are the principles of surgical management of bowel obstruction?

A
  • Aim to treat the cause
  • Typically involves resection of the obstructing lesion
  • Colon hasn’t been cleansed so most surgeons use a proximal ostomy post resection
  • Patients with a substantial comorbidity or unresectable tumours may be offerd bypass procedures
  • Endoscopically placed expanding metal stents offer palliation or a briedge to surgery allowing optimisation
127
Q

What procedures are done to treat bowel obstruction?

A
  • Consent for possible resection ± stoma
  • SBO: adhesiolysis
  • LBO:
    • Hartmann’s
    • Colectomy + primary anastomosis and on table lavage
    • Palliative bypass procedure
    • Transverse loop colostomy or loop ileostomy
    • Caecostomy
128
Q

What is the most common location for volvulus?

A

Sigmoid - 80%

129
Q

What is the pathophysiology of sigmoid volvulus?

A
  • Long mesentery with a narrow base so predisposed to torsion
  • Usually due to sigmoid elongation secondary to chronic constipation
  • Increased risk in neuropsych patients - MS, PD, psychiatric (disease/treatment interferes with intestinal motility)
  • Closed loop obstruction
130
Q

How does sigmoid volvulus present?

A
  • Commoner in males
  • Often elderly, constipated, co-morbid patients
  • Massive distension with tympanic abdomen
131
Q

What is the AXR appearance in sigmoid volvulus?

A

Coffee bean sign

132
Q

What is the management for sigmoid volvulus?

A
  • Often relieved by sigmoidoscopy and flatus tube insertion
    • Monitor for signs of bowel ischaemia following decompression
  • Sigmoid colectomy occasionally required
    • Failed endoscopic decompression
    • Bowel necrosis
  • Often recurs so elective sigmoidectomy may be needed
133
Q

What is a caecal volvulus often associated with?

A

Congenital malformation where the caecum is not fixed in the RIF

134
Q

How is a caecal volvulus managed?

A
  • Only ~10% patients can be detorsed with a colonoscopy
    • Typically needs surgery
  • Right hemi with primary ielocolic anastomosis
  • Caecostomy
135
Q

What is the triad of gastrooesophageal obstruction?

A
  • Vomiting -> retching with regurgitation of saliva
  • Pain
  • Failed attempts to pass an NGT
136
Q

What are the risk factors for gastric volvulus?

A
  • Congenital
    • Bands
    • Rolling/paraoesophageal hernia
    • Pyloric stenosis
  • Acquired
  • Gastric/oesophageal surgery
  • adhesions
137
Q

What investigation findings suggest gastric volvulus?

A
  • Gastric dilatation
  • Double fluid level on erect films
138
Q

What is the management for a gastric volvulus?

A

Endoscopic manipulation or emergency laparotomy

139
Q

How does paralytic ileus present?

A
  • Reduced or absent bowel sounds
  • Mild abdo pain - not colicky
140
Q

What is paralytic ileus?

A

Adynamic bowel secondary to the absence of normal peristalsis - usually SBO

141
Q

What are the causes of paralytic ileus?

A
  • Post op
  • Peritonitis
  • Pancreatitis or any localised inflammation
  • Poisons/drugs: anti-AChM (e.g. TCAs)
  • Pseudo-obstruction
  • Metabolic: hypokalaemia, hyponatraemia, hypomagnesaemia, uraemia
  • Mesenteric ischaemia
142
Q

How do you prevent paralytic ileus?

A
  • Minimal bowel handling
  • Laparoscopic approach
  • Peritoneal lavage after peritonitis
  • Unstarched gloves
143
Q

How do you manage paralytic ileus?

A
  • Conservative ‘drip and suck’ management
  • Correct underlying causes (drugs, metabolic abnormalities)
  • Consider need for parenteral nutrition
  • Exclude mechanical cause if protracted
144
Q

What is Ogilvie’s syndrome?

A
  • Acute intestinal pseudo obstruction associated with massive dilatatoin
  • Usually of colon but also small intestine
  • Mechanical obstruction absent
  • Parasympathetic nerve dysfunction
145
Q

How does colonic pseudo obstruction present?

A
  • Clinical signs of mechanical obstruction
  • No obstructing lesion found
  • Usually distension only with no colic
146
Q

What are the causes of colonic pseudo obstruction?

A
  • Usually no cause found
  • But associated with:
    • Elderly
    • Cardiorespiratory disorders
    • Pelvic surgery e.g. hip arthroplasty
    • Trauma
147
Q

How should you investigate suspected pseudo obstruction?

A

Gastrograffin enema to exclude a mechanical cause

148
Q

How do you treat colonic pseudo obstruction?

A
  • Neostigmine: anticholinesterase
  • Colonoscopic decompression: 80% successful
149
Q

What is the epidemiology of colorectal ca?

A
  • 3rd commonest cancer
  • 2nd commonest cause of cancer deaths
  • Peaks in 60s
  • Rectal ca commoner in men
  • Westerners
150
Q

What are colonic adenomas?

A

Dysplastic epithelium - benign precursors to CRC

151
Q

How do you classify colonic adenomas?

A
  • Tubular: small, pedunculated, tubular glands
  • Villous: large, sessile, covered by villi
  • Tubulovillous: mixture
152
Q

How do colonic adenomas present?

A
  • Typically asymptomatic
  • LArge polyps can bleed causing IDA
  • Villous adenomas can cause hypokalaemia and hypoproteinaemia
153
Q

What factors increase the malignant potential of colonic adenomas?

A
  • Bigger
  • More dysplastic
  • Greater villous component
154
Q

What is APC and what is its role in CRC?

A
  • Negative regulator of beta catenin (component of WNT pathway)
  • APC binds to and promotes degradation of beta catenin
  • APC mutations -> increased beta catenin -> increased transcription of genes which promote cell proliferation
  • Proliferation leads to mutation of other genes which promote growth and prevent apoptosis e.g. KRAS (protooncogene) and p53 (TSG)
155
Q

What are the stages in the adenoma-carcinoma sequence?

A
  1. Mutation of one APC copy
  2. Mutation of second APC copy -> adenoma formation
  3. Additional mutations in adenoma -> malignant transformatone.g. KRAS, p53
156
Q

What are the aetiological factors in CRC?

A
  • Diet: low fibre and high refined carbohydrate
  • IBD: CRC in 15% of those with pancolitis for 20 years
  • Familial: FAP, HNPCC, Peutz-Jeghers
  • Smoking
  • Genetics
    • No relative: 1/50 risk
    • One 1st degree relative: 1/10 risk
  • NSAIDs/aspirin 300g/d protective
157
Q

What kinds of tumour are in the colon?

A

95% adenocarcinoma

Rest: lymphoma, GIST, carcinoid

158
Q

What location are colorectal tumours usually in?

A
  • Rectum 35%
  • Sigmoid 25%
  • Caecum and ascending colon 20%
  • Transverse 10%
  • Descending 5%
159
Q

What kinds of colorectal carcinomas are proximal and distal tumours?

A

Proximal: sessile or polypoid

Distal: annular stenosing

160
Q

How does colorectal carcinoma spread?

A
  • Local
  • Lymphatic
  • Blood (liver, lungs)
  • Transcoelomic
161
Q

Which presenting features are specific to left sided colorectal cancers?

A
  • Altered bowel habit (because stool is at least semisolid and calibre of bowel is less)
  • PR mass (60%)
  • Obstruction (25%)
  • Bleeding/mucus PR (rare)
  • Tenesmus
162
Q

What presenting features are common to both left and right sided colonic tumours?

A
  • Abdominal mass
  • Perforation
  • Haemorrhage
  • Fistula
163
Q

What are the examination findings suggestive of colorectal ca?

A
  • Palpable mass: per abdomen or PR
  • Perianal fistulae
  • Hepatomegaly
  • Anaemia
  • Signs of obstruction
164
Q

What investigations should you do in colorectal ca?

A
  • Bloods
    • FBC (Hb)
    • LFTs - mets
    • Tumour marker - CEA which is a useful marker of disease and emergence of recurrence
  • Imaging
    • CXR: lung mets
    • US liver: mets
    • CT and MRI (staging - MRI best for rectal ca and liver mets)
    • Endoanal US: staging rectal tumours
    • Ba/gastrograffin enema: apple core lesion
  • Endoscopy and biopsy
    • Flexi sig (65% tumours accessible)
    • Colonoscopy
165
Q

What is the staging system for colorectal carcinoma?

A

Dukes:

  • A = confined to bowel wall (90% 5 year survival)
  • B = through bowel wall but no lymph nodes (60% 5 year survival)
  • C = regional LNs (30% 5 year survival)
  • D = distant mets (<10% 5 year survival)
166
Q

What is the TNM staging for colorectal ca?

A
  • Tis: carcinoma in situ
  • T1: submucosa
  • T2: muscularis propria
  • T3: subserosa
  • T4: through the serosa to adjacent organs
  • N1: 1-3 nodes
  • N2: >4 nodes
167
Q

How do you grade colorectal ca?

A
  • Grading from low to high
  • Based on cell morphology
  • Dysplasia, mitotic index, hyperchromatism
168
Q

How many CRC patients can have surgery?

A

60%

169
Q

What are the principals of surgical management of CRC?

A
  • Excision depends on lymphatic drainage which follows arterial supply
  • Mobility of bowel and blood supply at cut ends is also important
  • Hartmann’s often used if obstruction
  • Laparoscopic approach is the standard
170
Q

How is rectal cancer managed surgically?

A
  • Neoadjuvant radiotherapy may be used to decrease local recurrence and increase survival
  • Anterior resection - tumours 4-5cm from the anal verge
    • Defunction with loop ileostomy
  • AP resection: <4cm from the anal verge
    • total mesorectal excision for tumours of the middle and lower third
      • Aims to decrease recurrence
      • Increased anastomotic leak and faecal incontinence
171
Q

How do you treat colonic cancers surgically depending on their location?

A
  • Sigmoid: high anterior resection or sigmoid colectomy
  • Left: left hemicolectomy
  • Transverse: extended right hemicolectomy
  • Caecal/right: right hemocolectomy
172
Q

What are the treatment options for colorectal cancer other than resections?

A
  • Local excision e.g. transanal endoscopic microsurgery
  • Bypass surgery: palliation
  • Hepatic resection: if single lobe mets only
  • Stenting: palliation or bridge to surgery in obstruction
  • Chemo
    • Adjuvant 5-FU for Dukes’ C decreases mortality by 25%
    • High grade tumour
    • Palliation of metastatic disease
173
Q

What are the 2 screening programmes for colorectal cancer?

A

Faecal occult blood testing and flexi sig

174
Q

How does the faecal occult blood screening programme work?

A
  • From 2006
  • 60-75 years
  • Homr FOB testing every 2 years (1/50 will be positive)
  • Colonoscopy if positive (1/10 have cancer)
  • Screening has decreased risk of dying from CRC by 25%
175
Q

How does the flexi sig screening programme for CRC work?

A
  • From 2011/12
  • 55-60 years
  • One only flexi sig
  • Decreased incidence by 33% and mortality by 43%
176
Q

What are the 3 main familial CRC syndromes?

A
  • Familial adenomatous polyposis (e.g. Gardener’s, Turcot’s)
  • Hereditary non polyposis colorectal cancer
  • Peutz-Jeghers syndrome
177
Q

How is FAP inherited?

A

Autosomal dominant - APC gene on 5q21

178
Q

How does FAP present?

A

100s-1000s of adenomas by ~16 years, mainly in the large bowel but also in the stomach and duodenum (near the ampulla)

179
Q

What is the risk with FAP?

A

100% get CRC often by 40

180
Q

What other congenital problem might FAP be associated with?

A

Congenital hypertrophy of the retinal pigment epithelium (CHPRE)

181
Q

What are hte features of attenuated FAP?

A

<100 adenomas, later CRC (>50)

182
Q

What are the features of Gardener’s syndrome?

A
  • Thyroid tumours
  • Osteomas of the mandible, skull and long bones
  • Dental abnormalities: supernumerary teeth
  • Epidermal cysts
183
Q

What are the features of Turcot’s syndrome?

A

CNS tumours (medullo and glioblastomas), adenomas

184
Q

What is the management plan for FAP?

A
  • Prophylactic colectomy befoer 20
  • Total colectomy and IRA
    • Requires life long stump surveillance
  • PRoctocolectomy and IPAA
  • Remain at risk of cancer in stomach and duodenum so they have regular endoscopic screening
185
Q

How is HNPCC inherited?

A

Autosomal dominant - mutation of mismatch repair enzymes e.g. MSH2 on chromosome 2p

186
Q

What is the commonest cause of hereditary CRC?

A

HNPCC - 3% of all CRC

187
Q

How does HNPCC present?

A
  • Lynch 1: right sided CRC
  • Lynch 2: CRC + gastric, endometrial, prostate, breast
188
Q

How do you diagnose HNPCC?

A

3-2-1 rule:

≥3 family members over 2 generations with one <50 years

189
Q

How is Peutz Jeghers inherited and what’s the mutation?

A

Autosomal dominant - STK11 mutation

190
Q

How does Peutz Jeghers present?

A
  • ~10-15 years
  • Mucocutaneous hyperpigmentation - macules on palms, buccal mucosa
  • Multiple GI hamartomatous polyps - intussusception, haemorrhage
  • Increased cancer risk - CRC, pancreas, breast, lung, ovaries, uterus
191
Q

What are the types of GI polyps?

A
  • Inflammatory
  • Hyperplastic
  • Hamartomatous
  • Neoplastic
192
Q

What is the aetiology of inflammatory polyps?

A

Regenerating islands of mucosa in UC

193
Q

What are the features of hyperplastic polyps?

A
  • Piling up of goblet cells and absorptive cells
  • Serrated surface architecture
  • No malignant potential
194
Q

What are the features of hamartomatous polyps?

A
  • Tumour like growths composed of tissues present at the site where they develop
  • Sporadic or part of familial syndromes
  • Juvenile polyp = solitary hamartoma in children (cherry on a stalk)
195
Q

What are the features of neoplastic polyps?

A
  • Tubular or villous adenomas
  • Usually asymptomatic
  • May have blood/mucus PR, tenesmus
196
Q

What are the faetures of juvenile polyposis?

A
  • Autosomal dominant
  • >10 hamartomatous polyps
  • Increased CRC risk: need surveillance and polypectomy
197
Q

What are the features of Cowden syndrome?

A
  • Autosomal dominant
  • Macrocephaly and skin stigmata
  • Intestinal hamartomas
  • Increased risk of extra intestinal Ca
198
Q

What are the causes of acute mesenteric ischaemia?

A
  • Arterial: thrombotic (35%), embolic (35%)
  • Non occlusive (20%)
    • Splanchnic vasoconstriction e.g. secondary to shock
  • Venous thrombosis (5%)
  • Other: trauma, vasculitis, strangulation
199
Q

How does acute mesenteric ischaemia present?

A
  • Nearly always small bowel
  • Triad:
    • Acute severe abdo pain ± PR bleed
    • Rapid hypovolaemia -> shock
    • No abdominal signs
  • Degree of illness may be greater than clinical signs
  • May be in AF
200
Q

How should you investigate suspected acute mesenteric ischaemia?

A
  • Bloods
    • High Hb: plasma loss
    • Raised WCC
    • Raised amyloase
    • Persistent metabolic acidosis - raised lactate
  • Imaging
    • AXR: gasless abdomen
    • Arteriography/CT/MRI angio
201
Q

What are the possible complications of mesenteric ischaemia?

A

Septic peritonitis, SIRS -> MODS

202
Q

How do you treat acute mesenteric ischaemia?

A
  • Fluids
  • Antibiotics: gent and met
  • LMWH
  • Laparotomy to resect necrotic bowel
203
Q

What is the cause of chronic small bowel ischaemia?

A

Atheroma + low flow state e.g. LVF

204
Q

How does chronic small bowel ischaemia present?

A
  • Severe, colicky, post prandial abdo pain - ‘gut claudication’
  • PR bleeding
  • Malabsorption
  • Weight loss
205
Q

How do you treat chronic small bowel ischaemia?

A

Angioplasty

206
Q

What is the cause of chronic large bowel ischaemia?

A

Follows low flow in IMA territory

207
Q

How does chronic large bowel ischaemia present?

A
  • Lower, left sided abdo pain
  • Bloody diarrhoea
  • Pyrexia
  • Tachycardia
208
Q

How should you investigate suspected chronic large bowel ischaemia?

A
  • Raised WCC
  • Barium enema: thumb printing
  • MR angiography
209
Q

What are the complications of chronic large bowel ischaemia?

A
  • May lead to peritonitis and septic shock
  • Strictures in the long term
210
Q

How do you manage chronic large bowel ischaemia?

A
  • Usually conservative: fluids and antibiotics
  • Angioplasty and endovascular stenting
211
Q

What are the common causes of lower GI bleeds?

A
  • Rectal: haemorrhoids, fissure
  • Diverticulitis
  • Neoplasm
212
Q

What are the less common causes of lower GI bleeds?

A
  • Inflammation: IBD
  • Infection: shigella, campylobacter, C diff
  • Polyps
  • Large upper GI bleed (15% of lower GI bleeds)
  • Angio: dysplasia, ischaemic colitis, HHT, AV malformation
  • Trauma
  • Solitary rectal ulcer
  • Fistula
  • Warts
213
Q

How should you investigate a lower GI bleed?

A
  • Bloods: FBC, U+E, LFT, cross match, clotting, amylase
  • Stool: MCS
  • Imaging
    • AXR, erect CXR
    • Angiography necessary if no source on endoscopy
    • Red cell scan
  • Endoscopy
    • 1st: rigid proctoscopy/sigmoidoscopy
    • 2nd: OGD
    • 3rd: colonoscopy: difficult in major bleeding
214
Q

How do you manage a lower GI bleed?

A
  • Resuscitate
  • Urinary catheter
  • Antibiotics if evidence of sepsis or perf
  • PPI if upper GI bleed possible
  • Keep bed bound: if need to pass stool, could be a large bleed leading to collapse
  • Stool chart
  • Diet: keep on clear fluids to allow colonoscopy
  • Surgery if unremitting or massive bleed
215
Q

What is the pathophysiology of angiodysplasia in the bowel?

A

Submucosal AV malformations - 70-90% are in the right colon and they can affect anywhere in the GIT

216
Q

How does angiodysplasia present?

A

Elderly, fresh PR bleeding

217
Q

How should you investigate suspected angiodysplasia?

A
  • Exclude other diagnoses: PR exam, barium enema, colonoscopy
  • Mesenteric angiography or CT angiography
  • Tc-labelled RBC scan: identify active bleeding
218
Q

How do you treat angiodysplasia?

A
  • Embolisation
  • Endoscopic laser electrocoagulation
  • Resection

Surgery Finals (12 decks)

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