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Year 3 - Surgery > 3.04 General Surgery - Large Bowel Disease > Flashcards

3.04 General Surgery - Large Bowel Disease Flashcards

1
Q

What is the pathophysiology of appendicitis?

A

Luminal obstruction (e.g. faecolith, lymphoid hyperplasia, impacted stool, appendiceal tumour) causes commensal bacteria to multiple, resulting in acute inflammation.

Reduced venous drainage and localised inflammation results in increased pressure within the appendix, in turn resulting in ischaemia.

Untreated, ischaemia within the appendiceal wall results in necrosis and subsequent perforation.

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2
Q

Give the risk factors for acute appendicitis.

A
  • family history
  • ethnicity (Caucasian)
  • environmental (seasonal presentation in summer)
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3
Q

What are the clinical features of acute appendicitis?

A
  • peri-umbilical abdominal pain (visceral peritoneum inflammation), classically dull and poorly localised
  • right iliac fossa abdominal pain (parietal peritoneum inflammation), classically localised and sharp
  • vomiting
  • anorexia
  • nausea
  • diarrhoea
  • constipation

OE rebound tenderness and percussion pain over McBurney’s point; guarding; Rovsing’s sign +ve; Psoas sign +ve

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4
Q

Describe what constitutes a positive test result for

a) Rovsing’s sign

b) Psoas sign

A

a) RIF pain upon palpation of LIF

b) RIF pain with extension of right hip (suggests retrocecal position)

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5
Q

What are the differential diagnoses to acute appendicitis?

A

Gynaecological: ovarian cyst rupture; ectopic pregnancy; PID

Renal: ureteric stones; urinary tract infection; pyelonephritis

Gastrointestinal: IBD; Meckel’s diverticulum; diverticular disease

Urological: testicular torsion; epididymo-orchitis

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6
Q

How should suspected appendicitis be investigated?

A
  • urinalysis (exclude renal / urological cause)
  • pregnancy test if F of reproductive age
  • FBC & CRP
  • US / CT for imaging
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7
Q

How is acute appendicitis managed?

A

Laparascopic appendectomy is gold standard with appendix sent to histopathology to look for malignancy.

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8
Q

What are the complications of acute appendicitis?

A
  • perforation
  • surgical site infection
  • appendix mass
  • pelvic abscess
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9
Q

Which age group most commonly develops acute appendicitis?

A

20-30 years old

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10
Q

What is a diverticulum?

A

An outpouching of the bowel wall, most commonly found in the sigmoid colon.

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11
Q

Describe what is meant by:

a) diverticulosis

b) diverticular disease

c) diverticulitis

d) diverticular bleed

A

a) asymptomatic presence of diverticula

b) symptoms arising from the diverticula

c) inflammation of the diverticula

d) diverticula erodes into a vessel and causes a large volume, painless bleed

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12
Q

What is the pathophysiology of diverticular disease?

A

Aging bowel naturally weakens over time, resulting in outpouching of mucosa through weak areas.

Bacteria can overgrow, leading to inflammation of the diverticulum, which can sometimes perforate. Perforation can lead to peritonitis sepsis and death.

In chronic cases, fistulae can form, commonly colovesical or colovaginal.

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13
Q

Describe how diverticulitis is classified.

a) simple

b) complicated

A

a) no abscess or perforation

b) abscess +/- perforation

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14
Q

What are the risk factors for diverticular disease?

A
  • increasing age
  • low dietary fibre intake
  • obesity
  • smoking
  • family history
  • NSAID use
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15
Q

What are the clinical features of diverticulosis?

A

Asymptomatic and found incidentally during routine colonoscopy or CT imaging. Often no clinical significance.

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16
Q

What are the clinical features of diverticular disease?

A
  • intermittent lower abdominal pain
  • colicky
  • relieved by defecation
  • altered bowel habit
  • nausea
  • flatulence
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17
Q

What are the clinical features of acute diverticulitis?

A
  • acute LIF pain
  • sharp
  • worsened by movement

OE localised tenderness, anorexia, pyrexia, nausea.

If the diverticulum perforates, there will be signs of localised peritonism or generalised peritonitis.

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18
Q

What are the differential diagnoses for a patient presenting with lower abdominal pain and bowel symptoms?

A
  • inflammatory bowel disease
  • bowel cancer
  • mesenteric ischaemia
  • renal stones
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19
Q

What investigations are used to diagnose diverticulitis?

A
  • FBC, CRP and U&Es
  • Group & Save, VBG
  • urine dipstick to exclude urological causes
  • CT abdomen-pelvis

If uncomplicated diverticular disease, flexible sigmoidoscopy can be used to investigate.

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20
Q

How is diverticular disease managed?

A
  • simple analgesia
  • encourage oral fluid intake
  • regular colonoscopy to exclude masked malignancies

In cases of bleeds, blood products may be needed to resuscitate the patient.

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21
Q

How is acute diverticulitis managed?

A
  • antibiotics
  • intravenous fluids
  • analgesia

Surgical intervention if perforation with faecal peritonitis or overwhelming sepsis. Hartmann’s procedure (sigmoid colectomy with formation of end colostomy).

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22
Q

What are the complications of diverticular disease?

A
  • recurrence of diverticulitis
  • stricture formation
  • fistulae formation
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23
Q

What is a volvulus?

A

Twisting of a loop of intestine around its mesenteric attachment, compromising blood supply and leading to bowel necrosis and perforation.

Most commonly occurs at sigmoid colon.

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24
Q

Explain why sigmoid volvulus is the most common type.

A

Sigmoid colon has a long mesentery, which means that this segment bowel is more prone to twisting on its mesenteric base.

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25
Q

What are the risk factors for volvulus?

A
  • increasing age
  • chronic constipation
  • male gender
  • previous abdominal operations
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26
Q

What are the clinical features of volvulus?

A
  • bowel obstruction
  • colicky pain
  • abdominal distention
  • absolute constipation

OE tympanic to percussion

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27
Q

How is suspected sigmoid volvulus investigated?

A
  • routine bloods
  • CT abdomen pelvis with contract
  • AXR (coffee bean sign)
28
Q

How is sigmoid volvulus managed?

A
  • decompression by sigmoidoscope
  • insertion of flatus tube

Surgical indications (Hartmann’s procedure):
- colonic ischaemia / perforation
- repeated failed attempts at decompression
- necrotic bowel at endoscopy

29
Q

What are the main complications of sigmoid volvulus?

A
  • bowel ischaemia
  • bowel perforation
  • risk of recurrence
30
Q

What is pseudo-obstruction?

A

Dilatation of the colon due to an adynamic bowel, in the absence of mechanical obstruction.

Mostly affects the caecum and ascending colon.

31
Q

What is the pathophysiology of pseudo-obstruction?

A

Interruption of the autonomic nervous supply to the colon results in the absence of smooth muscle action in the bowel wall.

The colonic diameter widens, leading to an increased risk of toxic megacolon, ischaemia and perforation.

32
Q

What are some causes of pseudo-obstruction?

A
  • electrolyte imbalance (hypercalcaemia, hypomagnesaemia, hypothyroidism)
  • medication (opioids, CCBs, anti-depressants)
  • recent surgery
  • neurological disease (Parkinson’s disease, MS)
33
Q

What are the clinical features of pseudo-obstruction?

A

Presents similarly to mechanical bowel obstruction.

  • abdominal pain
  • abdominal distention
  • constipation
  • vomiting

OE abdomen is distended and tympanic. Focal tenderness indicates ischaemia and is a key warning sign.

34
Q

What are the clinical features of pseudo-obstruction?

A

Presents similarly to mechanical bowel obstruction.

  • abdominal pain
  • abdominal distention
  • constipation
  • vomiting

OE abdomen is distended and tympanic. Focal tenderness indicates ischaemia and is a key warning sign.

35
Q

What are the differentials for psuedo-obstruction?

A
  • mechanical obstruction
  • paralytic ileus
  • toxic megacolon
36
Q

How should pseudo-obstruction be investigated?

A
  • U&Es, Ca2+, Mg2+, TFTs
  • AXR to show bowel distension (looks same as mechanical obstruction)
  • abdominal-pelvic CT with IV contrast can differentiate between mechanical and pseudo-obstruction
37
Q

How is pseudo-obstruction managed?

A
  • NBM with IV fluids and nutritional support
  • NG tube if vomiting for decompression
  • endoscopic decompression
  • IV neostigmine
38
Q

What are the two main types of inflammatory bowel disease?

A
  • Crohn’s disease
  • ulcerative colitis
39
Q

What is the pathophysiology of Crohn’s disease?

A

Crohn’s can affect any part of the gastrointestinal tract, most commonly the distal ileum or proximal colon.

Appears to have a familial link and is associated with smoking.

Exact cause remains unknown.

40
Q

What are the characteristics of Crohn’s disease?

a) site involvement

b) inflammation

c) microscopic changes

d) macroscopic changes

A

a) can affect entire GI tract, most commonly ileum and proximal colon

b) transmural (affects all layers of the bowel)

c) granulomatous (non-caseating)

d) discontinuous inflammation (‘skip lesions’); fissures and deep ulcers (cobblestone appearance); fistula formation

41
Q

What are the risk factors for Crohn’s disease?

A
  • strong family history
  • smoking
42
Q

What are the intestinal clinical features of Crohn’s?

A
  • colicky abdominal pain
  • diarrhoea +/- blood and mucus
  • anorexia
  • fever
  • malabsorption and malnourishment
  • oral aphthous ulcers
  • perianal disease
43
Q

What are the extra-intestinal manifestations of Crohn’s disease?

A
  • enteropathic arthritis
  • nail clubbing
  • erythema nodosum
  • primary sclerosing cholangitis
  • renal stones
44
Q

How can Crohn’s disease be investigated?

A
  • FBC (anaemia), LFTs (hypoalbuminaemia indicative of systemic illness), CRP and WCC (inflammation)
  • faecal calprotectin
  • stool sample for any infective cause

Colonoscopy sits as GOLD STANDARD investigation, with biopsy to confirm the diagnosis.

45
Q

How can Crohn’s severity be assessed?

A

Montreal Score used to classify severity of Crohn’s based upon:
- age at diagnosis
- location
- behaviour of disease

46
Q

What imaging can be used to investigate Crohn’s?

A

Colonoscopy is the GOLD STANDARD imaging choice.

However, should not be used during an acute flare of CD due to risk of perforation. CT abdomen-pelvis or MRI can be used as alternative.

47
Q

How is Crohn’s managed?

A

Referred to gastroenterology for confirmation of diagnosis and treatment.

Acute attacks treated with fluid resuscitation, nutritional support, prophylactic heparin and anti-embolic stockings (IBD flares are prothombotic).

Corticosteroid therapy to induce remission. Infliximab can be used as rescue therapy.

Azathioprine to maintain remission. Smoking cessation advised.

Surgical management required in severe cases where medical management has failed.

48
Q

What are the complications of Crohn’s disease?

A
  • fistula formation
  • stricture formation
  • GI malignancy
  • malabsorption (growth delay in children)
  • osteoporosis (malabsorption or long-term steroid use)
  • increased risk of gallstones (reduced reabsorption of bile salts at terminal ileum)
  • increased risk of renal stones (reduced absorption of fats in small bowel)
49
Q

What is the pathophysiology of Ulcerative Colitis?

A

Exact aetiology is unknown, however seemingly an interaction between genetic factors and environmental factors.

Smoking is protective against UC.

50
Q

Outline the characteristics of ulcerative colitis.

a) site involvement

b) inflammation

c) microscopic changes

d) macroscopic changes

A

a) large bowel only*, continuous from the rectum

b) mucosa only

c) crypt abscess formation; reduced goblet cells; non-granulomatous

d) continuous inflammation (proximal from rectum); pseudopolyps and ulcers may form

*if iliocaecal valve is incompetent, may enter the terminal ileum

51
Q

What are the intestinal clinical features of ulcerative colitis?

A
  • bloody diarrhoea
  • frequency and urgency of defecation
  • tenesmus
  • malaise
  • anorexia
  • pyrexia

OE usually unremarkable unless severe exacerbation; severe abdominal pain may indicate toxic megacolon or colonic perforation.

52
Q

What are the extra-intestinal manifestations of ulcerative colitis?

A
  • enteropathic arthritis
  • erythema nodusum
  • primary sclerosing cholangitis
53
Q

What are the differentials to ulcerative colitis?

A
  • Crohn’s disease
  • malignancy
  • chronic infection
  • mesenteric ischaemia
  • coeliac disease
54
Q

How is ulcerative colitis investigated?

A
  • routine bloods (FBC, U&E, CRP, LFTs, clotting) to examine anaemia, low albumin (secondary to systemic illness) and evidence of inflammation
  • faecal calprotectin
  • stool sample for microscopy and culture
55
Q

What imaging is chosen to investigate ulcerative colitis?

A

Colonoscopy with biopsy.

AXR in acute exacerbations, or CT, to assess for toxic megacolon and/or bowel perforation.

56
Q

How is ulcerative colitis managed?

A

Referral to gastroenterology for diagnosis and initiation of treatment.

Acute attacks warrant aggressive fluid resuscitation, nutritional support and prophylactic heparin (due to prothrombotic state of IBD flares).

Corticosteroid and immunosuppressive agents to induce remission. Sulfasalazine can be used to maintain remission.

Colonic surveillance due to increase risk of colorectal malignancy.

57
Q

What is the most common subtype of colorectal cancer?

A
  • adenocarcinoma

Other types include lymphoma, carcinoid, and sarcoma.

58
Q

Outline the pathophysiology of colorectal cancer.

A

Progression of normal mucosa to colonic adenoma (polyps), to invasive adenocarcinoma.

Adenomas may be present for years before becoming malignant.

59
Q

Which genetic mutations are directly associated with colorectal cancer?

A
  • adenomatous polyposis coli (APC) (tumour suppressor gene)
  • hereditary nonpolyposis colorectal cancer (HNCC) (DNA mismatch repair gene)
60
Q

What are the risk factors for colorectal cancer?

A
  • increasing age
  • male gender
  • family history
  • IBD
  • low fibre diet
  • high processed meat intake
  • excess alcohol intake
  • smoking

Note approx. 75% of colorectal cancers are sporadic, and develop in people with no specific risk factors.

61
Q

What are the clinical features of colorectal cancer?

A
  • change in bowel habit
  • rectal bleeding
  • abdominal pain

Right sided colon cancer: abdominal pain, iron deficiency anaemia, palpable mass in RIF, often present late.

Left sided colon cancer: rectal bleeding, change in bowel habit, tenesmus, palpable mass in LIF or PR.

62
Q

According to NICE guidelines, when should a patient be referred for urgent investigation of suspected bowel cancer?

A
  • ≥40yrs with unexplained weight loss and abdominal pain
  • ≥50yrs with unexplained rectal bleeding
  • ≥60yrs with iron-deficiency anaemia or change in bowel habit
  • positive occult blood screening test
63
Q

What are the differentials for colorectal cancer?

A
  • IBD (usually presents younger; with diarrhoea containing blood and mucus)
  • haemorrhoids
64
Q

Describe the colorectal cancer screening programme in England and Wales.

A

Screening offered every 2 years to men and women aged 60-75yrs, using FIT test (antibodies detect Hb in faeces).

If any samples are positive, patients are offered investigation via colonoscopy.

65
Q

How is colorectal cancer investigated?

A
  • FBC (microcytic, iron-deficiency anaemia)
  • colonoscopy with biopsy GOLD STANDARD

For staging:

  • CT CAB
  • MRI rectum
  • endo-anal ultrasound

Note tumour marker CEA not used to make diagnosis but is associated with worse prognosis.

66
Q

How is colorectal cancer managed?

A

Surgery is mainstay of curative management:
- right hemicolonectomy (caecal tumour or ascending colon tumour)
- left hemicolonectomy (descending colon tumour)
- sigmoidectomy (sigmoid colon tumour)
- anterior resection )high rectal tumour)
- abdominoperineal resection (low rectal tumour)

Chemotherapy (FOLFOX; Folinic acid + Fluorouracil + Oxaliplatin) and radiotherapy.

Palliative care if advanced.

Year 3 - Surgery (30 decks)

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