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Year 4 > Surgery - Colorectal > Flashcards

Surgery - Colorectal Flashcards

1
Q

What are the peaks of incidence of IBD

A

2 peaks
10-40yrs
50-70yrs

Crohn’s more common than UC

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2
Q

What effect does smoking have in IBD?

A

Smoking ?helps UC

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3
Q

What is the pathophysiology of IBD

A

autoimmune, inappropriate response to gut flora in genetically susceptible individuals

  • immunological
  • environmental
  • genetics
  • diet
  • psychosocial
  • genetics
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4
Q

At the level of the colon describe the differences between UC and CD

A

UC:

  • colon and rectum only
  • continuous
  • mucosa only
  • reduced goblet cells
  • polyps and crypt abscesses

CD:

  • anywhere mouth to anus (commonly TI)
  • skip lesions
  • transmural
  • normal goblet cells
  • granulomas and fistulas

Fistulas = entero-enteric, colovesicle, colovaginal, enterocutaneous

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5
Q

What are the GI and extra-GI features of IBD?

A

GI: abdo pain, weight loss, tenesmus (UC), blood in stool, anal strictures, finger clubbing

Extra-GI: erythema nodosum, pyoderma gangrenosum, oral ulcers, finger clubbing, enteropathic arthritis

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6
Q

What is Truelove and Witts score?

A

Used to assess the severity of a UC flare

  • no. bloody stools, HR, temp, Hb, ESR/CRP
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7
Q

What investigations are carried out for IBD/and IBD flare?

A 
Bloods: FBC, ESR/CRP, U&E, LFT, INR, ferritin, TIBC, B12, folate
Blood cultures
Stool microbiology (exclude infection)
Stool cultures (?C.Diff)
Faecal calprotectin (will always be raised acutely)
Colonoscopy and biopsy
Capsule endoscopy
CTMRI
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8
Q

What are the treatments for CD?

A

Acutely: fluids, nutrition, prophylactic heparin, smoking cessation

Medical =

  • steroids
  • biologics
  • thiopurines (steroid sparing anti-inflammatories e.g. mercaptopurine/azathioprine)
  • 5-ASA (steroid sparing anti-inflammatory chemically related to aspirin)
  • METHOTREXATE

Surgery = resection, stricturoplasty, perianal drainage

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9
Q

What are the treatments for UC?

A

Acutely: fluids, nutrition, prophylactic heparin, smoking cessation

Medical =

  • steroids
  • biologics
  • thiopurines (steroid sparing anti-inflammatories e.g. mercaptopurine/azathioprine)
  • 5-ASA (steroid sparing anti-inflammatory chemically related to aspirin)

Surgery = resection, stricturoplasty, perianal drainage

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10
Q

What are complications of IBD?

A
  • NSAIDs can exacerbate disease
  • bowel obstruction
  • toxic dilatation
  • fistulae
  • cancer
  • malnutrition
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11
Q

What are the causes of bowel obstruction?

A 
Mechanical = structural pathology blocks intestinal contents passing
Functional = no mechanical blockage, due to -> inflammation, electrolyte imbalances, recent surgery (ileus)
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12
Q

Name causes of SB obstruction

A

adhesions from previous surgery (75%)
hernias
cancers/growth

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13
Q

Name causes of LB obstruction

A

cancers
diverticular strictures
rare (hernias/volvulus)

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14
Q

Why does third-spacing occur in bowel obstruction

A

Occluded bowel segment -> proximal dilatation -> increased peristalsis, increased hydrostatic pressure and large fluid movements into the bowel

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15
Q

What is volvulus and how is it managed?

A 
Twisting of bowel on its mesentery
common areas:
- sigmoid (coffee bean sign)
- caecum
Increased risk of ischaemia and perforation
- Treat by deflating through anal canal
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16
Q

What are the S/Sx of bowel obstruction?

A

Abdominal pain (crampy)
Vomiting (gastric contents -> bilious -> faecal)
Abdo distension
Complete constipation
O/Ex: scars from previous surgery, absence of bowel sounds

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17
Q

How is potential bowel obstruction investigated?

A

Bloods: FBC, U&E, CRP, LFT, G&S/CM
Venous blood gas: ?high lactate, assess degree of metabolic derangement (e.g. dehydration and vomiting)
Imaging: AXR, CT (erect CXR ?perforation)

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18
Q

What are features of SB obstruction on AXR?

A
  • dilatation >3cm
  • central swelling
  • valvulae conniventes/plicae circularis (completely across diameter)
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19
Q

What are features of LB obstruction on AXR?

A
  • dilatation >7cm (>9 in caecum)
  • peripheral location
  • haustral lines visible (half way)
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20
Q

How is bowel obstruction managed?

A
  • urgent A-E and fluid resuscitation
  • conservative: drip and suck (NG tube and IV fluids), catheter, analgesia, anti-emetics
  • surgery (usually laparoscopic) if = ischaemia, closed loop obstruction, strangulation, pt has a virgin abdomen
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21
Q

What are complications of bowel obstruction?

A

Bowel ischaemia
Perforation and faecal peritonitis
Dehydration and AKI

22
Q

Name three inherited bowel genetic conditions and describe them

A

1) FAP (familial adenomatous polyposis)
- APC mutations, many polpys develop and 100% pts have CRC by 40yrs, get prophylactic colectomy

2) HNPCC (hereditary non-polyposis colorectal cancer)/Lynch syndrome
- MMR mutation, quick progression of adenoma -> carcinoma sequence, Lynch 2 associated with endometrial/gastric/breast cancer

3) Peutz-Jeghers syndrome
- SKT11 mutation, mucosal hyperpigmentation, polyps, intusseption and haemorrhage

23
Q

What are symptoms of a R sided CRC?

A

anaemia
weight loss
abdominal pain

24
Q

What are symptoms of a L sided CRC?

A

tenesmus
altered bowel habit
blood/mucous PR
PR mass

25
Q

Describe the staging methods of CRC

A

TNM

Duke's:
A) confined to the bowel wall
B) through the bowel wall
C) through the bowel wall + LN involvement
D) distant metastases
26
Q

How is suspected CRC investigated?

A

1) Examination (abdo + PR)
2) Bloods - FBC, LFT, haematinics, tumour markers (CEA, AFP)
3) Imaging - CXR (mets), liver USS (mets), CT/MRI (staging), barium enema (apple core)
4) Endoscopy - flexible sigmoidoscopy/colonoscopy

27
Q

What are the treatment options for CRC

A

Surgery +/- neoadjuvant chemo

Palliative bypass, stenting also options

28
Q

Describe a right hemicolectomy

A

removal of caecum and ascending colon

29
Q

Describe a left hemicolectomy

A

removal of splenic flexure and descending colon

Usually an anastomosis and no stoma needed

30
Q

Describe an anterior resection

A

For rectal/sigmoid disease
Removal of sigmoid colon and rectum
May anastomose end of descending colon to anal stump but put on a stoma at first to allow anastomosis to heal, then later reverse the stoma in a few months

31
Q

Describe an AP (abdominal perineal) resection

A

Removal of sigmoid colon, rectum and anus

Formation of an end colostomy

32
Q

Describe a Hartmann’s procedure

A

Usually performed for an obstructing cancer/diverticular disease
Resection of sigmoid colon +/- rectum (with rectum it is called a procto-sigmoidoscopy)
Can be temporary or permanent
Distal anal end can be stitched closed if permanent, or can be brought to the surface creating a mucous fistula

33
Q

Describe the screening process for CRC

A

1) FOB testing: 50-74yr olds (2 yrly)
- ~70-80% sensitivity

3) new Q-FIT (quantitative faecal IHC testing)
- will have ~90% sensitivity

34
Q

What are the 4 layers of the colon?

A

Mucosa
Submucosa
Muscularis propria/externa
Serosa/adventitia

35
Q

Describe diverticular disease and its causes

A

the clinical state relating to symptoms caused by colonic diverticulae

Diverticular disease = altered bowel habit, L colic (relieved by defectation), nausea, flatulence
Diverticulitis = impacted faeces causes infection, LIF tenderness, pyrexia and localised peritonitis

Can be congenital or acquired
Rare <60yrs
Due to genetics + low fibre diet and environmental factors (NSAID use, collagen structure)

36
Q

How is diverticular disease investigated?

A

Colonoscopy (gold standard for diagnosis, but NOT used in acute setting)
Bloods - FBC, CRP, ESR, amylase (raised), G&S, CM
Imaging - CT abdo, erect CXR (perf?), AXR (obstruction?)

37
Q

What staging system is used for Diverticular disease and describe it

A

Hinchey classification - looks at the degree of infective complications with diverticular disease and the need for surgery

1A - phlegmon
1B - pericolic abscess
2 - pelvic abscess

(surgery rarely needed and CT-guided percutaneous drainage sufficient)

3 - generalised purulent peritonitis
4 - generalised faecal peritonitis

(need surgery)

38
Q

How is diverticular disease managed?

A

High fibre diet
Hospital admission if uncontrolled pain and fluids not tolerated
Medical: NMB, IV fluids, analgesia, laxatives, antibiotics
Surgery: if perforation/strictures/obstruction/haemorrhage -> usually Hartmann’s procedure to resect the diseased bowel

39
Q

What is ano-rectal sepsis

A

due to a perianal abscess

40
Q

What is fistula-in-ano

A

Formation of an anal fistula between the bowel & skin in the perineal/perianal area

41
Q

Name the 6 types of anal fistula

A

Named based on the tissues through which they track

  • submucosal
  • inter-sphincteric
  • transphincteric (high or low)
  • supratransphincteric
  • extratransphincteric
42
Q

How is ano-rectal sepsis managed?

A

Antibiotics (manage symptoms but will not cure underlying disease)
Surgical
- Drainage
- Lateral internal sphincterotomy (to reduce internal pressure and allow fissure to heal)
- Fissurectomy (removal of tract)
- Anal advancement flap (avoids need to cut sphincter muscles and less risk of incontinence)

43
Q

Describe the types of colonic polyps

A

Pedunculated (on a stalk)
Sessile (flat)
Or can be a combination of both

44
Q

How do colonic polyps present?

A 
Normally asymptomatic and found on imaging/scopes
Can present with:
- bleeding
- mucous discharge
- prolapse (if low in the rectum)
45
Q

How are colonic polyps investigated:

A 
Colonoscopy
Genetic mutation testing:
APC gene = FAP
MMR gene = HNPCC
STK11 gene = Peutz-Jeghers syndrome
46
Q

Describe haemorrhoids and risk factors for developing them:

A

XS amounts of the normal endovascular cushions consisting of:

  • anorectal mucosa
  • submucosal tissue
  • mucosal blood vessels (small arterioles and veins)

Common in young adults and RFx include:

  • constipation
  • pregnancy
  • chronic straining
  • irregular bowel habits
  • obesity
  • genetics (absence of valves in haemorrhoid veins)
47
Q

How are haemorrhoids described

A

Classified by dentate line as internal/external
(dentate line divides lower 1/3rd anal canal from upper 2/3rds)
- typically occur in the same location as the main anal blood vessel pedicles:
11 o’clock
3 o’clock
7 o’clock

48
Q

How might haemorrhoids present?

A 
Internal = painless bleeding and itch
External = bleeding, swelling, mucous, painful!
49
Q

How can haemorrhoids be managed?

A

Medical (diet, high fibre, creams)

Surgical (banding, HALO = haemorrhoid artery ligation operation, stapled anopexy, haemorrhoidectomy)

50
Q

Describe causes of rectal bleeding

A

Anorectal = bright red blood on paper/in stool

  • haemorrhoids
  • fissures
  • proctatisis (rectal inflammation)
  • rectal prolapse

Rectosigmoid = darker blood with clots

  • rectal tumour
  • proctocolitis
  • diverticular disease
51
Q

What is a pilonidal sinus and how it is caused?

A

A sinus existing in the midline of the buttock clefts
Usually contains - hair, secretions, debris
Lateral tracts may run into neighbouring buttock tissue

Commonest in men/hirsute people
Often precipitated by long periods of sitting:
- lorry drivers
- computer operators

Year 4 (28 decks)

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