Small Intestine Flashcards

1
Q

Describe the management of enterocutaneous fistulae

A

S- Sepsis

S- Skin

N- Nutrition (and electrolytes!)

A- Anatomy of the fistula

P- Planning of corrective surgery

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2
Q

Features of Crohns

Macroscopic

Endoscopic

Microscopic

A

Macroscopic

  • Skip lesions/Discontinuous
  • Distribution anywhere in the GI tract
  • Transmural- fat wrapping occurs

Endoscopic

  • Linear ulcers- progress to additional transverse sinuses and subsequent cobblestone appearance
  • Skip lesions

Microscopic

  • Transmural lymphoid infiltrates
  • Sarcoid-like non caseating granulomas
    • 50%
  • Paneth cell hyperplasia is also common
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3
Q

Crohns distribution

A

55% SB and colon

30% SB only

15% Colon only

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4
Q

Classification of EC fistulae

A

Category

Low<200mL

Intermediate 200-500mL

High>500mL

Anatomy

site of defect in viscus e.g Jejunal, gastric etc

Etiology

IBD

Radiation

Iatrogenic

Foreign body

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5
Q

Spontaneous EC Fistula resolution timing

A

90% that close will do by 1 month

10% in months 1-3

None over 3 months

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6
Q

What is blind loop syndrome

A

Rare disorder secondary to bacterial overgrowth in areas of SB stasis

diarrhoea

steatorrhoea

Megaloblastic anaemia

Abdominal pain

Fat soluble vitamin deficiencies

B12 supplementation and Abx can resolve this temporarily

Surgical correction needed long term

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7
Q

Complications of jejunal diverticulosis

A

Bleeding

Enterolith formation

Perforation

Blind loop syndrome/malabsorption

Chronic pain

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8
Q

Malignancies with a preponderence for small bowel mets

A

Intraabdominal/transcoelomic/Local invasion (most common cause of SB malignancy)

Ovarian

Gastric

Cervical

Renal

Pancreas

Colon

Extraabdominal (rare)

Melanoma (most common)

Breast

Lung

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9
Q

SB GIST

  • Origin
  • Cellular markers
  • Mutation
  • Growth and Metastasis
  • Adjuvant treatment
A

Origin

  • Mesenchymal
  • interstitial cells of Cajal

Cellular markers

  • CD117 (molecular component of c-kit)
    • ~85%
  • DOG1 (Discovered on GIST-1)
    • ~100%
  • PKC-theta (Protein Kinase C- theta)
    • ~100%

Mutation

  • c-kit (of which the CD117 molecule is a component) present in most (~85%)
    • position of c-kit mutation is important
      • exon 11, codon 557/558 due to high recurrence risk
    • Of those tumours without c-kt mutation many will have a PDGFRA mutation
  • 10-15% wild type
    • NF-1
    • Carney complex and Carney-Stratakis syndrome
      • Succinate dehydrogenase

Growth and metastasis

  • Invade locally, spread haematogenous- liver, lung, bone

Adjuvant (or neoadjuvant) treatment

  • c-kit is a receptor tyrosine kinase
    • Tyrosine kinase inhibitors are the agent of choice
  • 3 years of adjuvant Imatanib is standard of care for intermediate to high risk disease
    • induces cellular quiescence rather than demise
  • TKI’s also have demonstrable antitumour activity in most tumours with PDGFRA mutations
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10
Q

How are GISTs risk stratified

What is the risk of progressive disease

A
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11
Q

Crohns perianal manifestations

A

Fissures

Fistulas

Abscesses

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12
Q

Cholecystokinin

A

Secreted by I cells in the duo and jej

  • Response to lipid, protein and carb in duo

Actions

  • Pancreatic enzyme release
  • Relaxation of SOD
  • GB contraction
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13
Q

Secretin

A

Secreted by S cells in Duo

  • Response to low pH

Actions

  • Secretion of Bicarb and water from pancreas
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14
Q

GIP

A

Gastric inhibitory polypeptide

Secreted by K cells in duo and jej

Acts to

  • reduce gastric acid production
  • Increase insulin release
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15
Q

Intestinal Malrotation

A

Normal rotation is counter clockwie (as the surgeon looks down on the abdomen

  • 270 degrees

Non rotation is more common but not usually symptomatic

Ix-

  • UGI series- bird beak at D3 with displaced ligament of Trietz
  • USS- Alteration of usual SMA/SMV relationship

Management:

  • Ladds procedure
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16
Q

How are GI neuroendocrine neoplasms subclassed

What genetic markers is each associated with

A

NENs are subdivided into:

  • neuroendocrine tumours (NET)
    • referring to well differentiated tumours
      • MEN1, DAXX, ATRX
      • grade low, int, high subtypes
  • neuroendocrine carcinoma (NEC)
    • referring to poorly differentiated tumours
      • ​TP53, RB1
      • Small cell, large cell subtypes
  • mixed adenoneuroendocrine carcinoma (MANEC)
    • Features of neuroendocrine and epithelial derived malignancy
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17
Q

Carcinoid syndrome

A

Carcinoid syndrome is classically characterised by:

  • flushing (70%)
  • diarrhoea (50%)
  • intermittent abdominal pain (40%)

Due to the secretion of bioactive amines, most commonly serotonin, directly into the systemic circulation from either metastatic neuroendocrine tumour to liver or less commonly retroperitoneum.

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18
Q

Carcinoid crisis

A

Characterised by:

  • profound flushing
  • bronchospasm
  • tachycardia
  • labile blood pressure

Caused by:

  • release of high levels of serotonin or other bioactive amines, such as histamine.

Can be precipitated by:

  • induction of anaesthesia
  • intraoperative tumour handling
  • invasive techniques such as tumour ablation.
  • histamine releasing drugs (e.g morphine)
  • sympthomimetic drugs (e.g adrenaline)

It is critical that patients with known carcinoid syndrome or at those at risk of carcinoid crisis are managed appropriately in the perioperative period.

  • octreotide and its analogues
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19
Q

Carcinoid heart disease

A

Seen in 20% of patients with carcinoid syndrome

Fibrosis of the right-side heart valves caused by many years of high serotonin levels

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20
Q

Perioperative octreotide in GI NETs

A
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21
Q

Grading of GI NETs

A
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22
Q

Describe the surgical management of intestinal malrotation

A

Ladds procedure has 5 steps

  1. Counter clockwise detorsion
  2. Division of Ladds bands
  3. Elongation of the mesentary
  4. Appendicectomy
  5. Placement of bowel to right and colon to left
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23
Q

What are the tumour markers for NETs

Why are they elevated in NET

What factors might falsely elevate each

A

Chromogranin A

  • granins are proteins involved in exocytosis of secretory vesicles
  • found in both functional and non functional NETs
    • higher with higher secretion (volume or function)
  • also elevated by:
    • PPI use
    • CHF
    • CRF

5-HIAA (5-hydroxyindoleacetic acid)

  • degradation product of serotonin
    • Direct assay of serotonin is difficult
    • Serotonin produced by >70% of NETS
  • also elevated by
    • chocolate, caffeine, nuts, nicotine, banana
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24
Q

Diagnostic imaging for GI NETs

A

Imaging for GI NETs may be either radiological or endoscopic

  • Radiology
    • CT is the most useful modality
      • Mesenteric disease is a common feature
        • spiculated/stellate mesenteric mass
      • Primary tumour
      • Mucocoele of appendix
    • PET
      • Gallium Dotatate (GaTate)
        • Gallium 68 labelled rapidly cleared novel somatostatin analogue
      • The most sensitive investigation for metastatic disease
    • Somatostatin receptor scintigraphy
      • Previously used
      • Long imaging protocol (2 days)
      • Accuracy improved by SPECT but now superceeded by GaTate PET
    • MRE
      • More accurate than WCE for identifying (and localising) small intestinal primaries
  • Endoscopy
    • Allows direct visualisation
      • Limited by access to OGD and colonoscopy distributions
    • WCE is part of the diagnostic work up of the SB
      • cannot identify exact site
      • May cause luminal obstruction
25
Q

What staging systems are used for GI neurgoendocrine neoplasms (NENs)

How do they differ

A

ENETS

  • European Neuroendocrine Tumour Society
    • Covers all NENs
      • NETs
      • NECs

AJCC/UICC

  • American Joint Cancer Committee/ Union for International Cancer Control
    • Covers only NETs

There are some also specific differences in T staging of appendix and stomach NETs

26
Q

Small bowel NETs

epidemiology

A

NETs are the most common SB primary tumour

The majority have lymph node metastasis at the time of initial diagnosis

  • Interestingly there does not appear to be a relationship between size and grade and the risk of nodal spread as is seen in appendiceal NETs

Primaries are often small at diagnosis

  • 30% have multifocal small bowel primary
27
Q

What genes are associated with Crohns disease

what is the mechanism of action

A

NOD2

  • decreased paneth cell antimicrobial action

CARD15

  • impaired NF-kB

Many others

  • HLA, MHC
28
Q

What grading system can be used to classify the phenotype of crohns

A

The Vienna classification was modified to the montreal system to include under 16 as an additional age group

Age at diagnosis

  • A1: <16 (Vienna<40)
  • A2: 16-40 (Vienna >40)
  • A3 >40 (No corresponding Vienna group)

Location

  • L1: TI
  • L2: colon
  • L3: ileocolonic
  • L4: upper GI tract (L4 can also be used when occuring concurrent with another distribution)

Behaviour

  • B1: non stricturing
  • B2: stricturing
  • B3: penetrating
    • the suffix modifier “p” is used where concurrent perianal disease exists
29
Q

ECCO surgery in UC guidelines.

admission of patients with acute severe UC

A
30
Q

ECCO surgery in UC guidelines.

Who should care for patients with acute severe UC

A
31
Q

ECCO surgery in UC guidelines.

What is the recommended initial management of patients with acute severe UC

A
32
Q

ECCO surgery in UC guidelines.

Monitoring and escalation of initial treatment in UC

A
33
Q

ECCO surgery in UC guidelines.

When should a second external pathologist be involved

A
34
Q

ECCO surgery in UC guidelines.

Managing low grade dysplasia

A
35
Q

ECCO surgery in UC guidelines.

Managing high grade dysplasia

A
36
Q

ECCO surgery in UC guidelines.

What is the recommended operation in UC with dysplasia (anywhere in the colon)

A
37
Q

ECCO surgery in UC guidelines.

Steroids in UC: how long is too long?

A

In acute UC the response should be assessed on day 3 and care escalated

in chronic UC:

38
Q

ECCO surgery in UC guidelines.

surgery in anti-TNF therapy

A
39
Q

ECCO surgery in UC guidelines.

What should be done with the rectum in panproctocolectomy for acute UC

A
40
Q

ECCO surgery in UC guidelines.

laparoscopic vs open surgery for acute severe UC

A
41
Q

ECCO surgery in UC guidelines.

choice of pouch construction

A
42
Q

ECCO surgery in UC guidelines.

In patients who are not candidates for restorative procedures following proctocolectomy what procedures are recommended

A

total colectomy, with (preferably intersphincteric) proctectomy, and end ileostomy with or without Kocks pouch

43
Q

ECCO surgery in UC guidelines.

Is total colectomy and ileorectal anastomosis a reasonable alternative

A
44
Q

ECCO surgery in UC guidelines.

Should patients have a diverting loop ileostomy?

A

yes

45
Q

ECCO surgery in UC guidelines.

Sexual function in UC surgery

A
46
Q

ECCO surgery in UC guidelines.

Oncological surgery in dysplasia

A
47
Q

What are the cell types found in the SB intestinal mucosa

Where is the site of cellular proliferation

A

The site of cellular proliferation is the crypts

Four cell types are found

  • Absorptive enterocytes (95%)
  • Paneth cells (do not migrate from the crypts)
  • Goblet cells
  • Enteroendocrine cells
48
Q

How can the jejunum and ileum be clinically differentiated

A

Two main differences

  • the vasculature of the mesentary
    • jejunum has 1-2 arcades with long straight vasarectae
    • ileum has 4-5 arcades and short vasa rectae
  • the mucosa
    • jejunal mucosa is thickened and palpably mobile within the bowel lumen
49
Q

Where is iron absorbed

A

duodenum

50
Q

Where is calcium absorbed

A

Duodenum and proximal jejunum

51
Q

Intussusceptum

A

The part of an intussusception which passes into the intussuscipiens

52
Q

Intussuscipiens

A

The part of the intussusception which receives the intussusceptum

53
Q

Crohns disease severity: clinical assessment

A

Crohns disease severity index (CDAI)

  • score from 0-1100
    • stratified into
      • mild < 150
      • mild to moderate 150-220
      • moderate to severe 220-450
      • severe > 450
  • components
    • stool number (and use if loperamide)
    • pain
    • general wellbeing
    • extraintestinal manifestations
    • mass on exam
    • weight off baseline by percentage
    • perianal disease
    • fever
    • anaemia
54
Q

crohns severity: endoscopic

A

Crohns Disease- Simple Endoscopic Score

  • components
    • ulcer type
    • ulcer size
    • ulcerated surface %
    • affected surface %
    • stenoses
  • stratified into
    • remission
    • mild activity
    • moderate activity
    • severe activity
55
Q

Crohns disease severity: imaging

A

MRE based severity scores have high accuracy for assessing extent and severity of disease

there are no validated USS and CT scores

56
Q

How should the severity of crohns disease be assessed

A

By a combined assessment of clinical, endoscopic and imaging scores

  • Clinical by Crohns Disease Activity Index
  • Endoscopic by Simple Endoscopic Score if Crohns Disease
  • Imaging graded score by MRE
57
Q

How should the severity of UC be assessed

A

By endoscopic and clinical severity

  • clinical severity by Truelove and Witt score
  • endoscopic by Ulcerative Colitis Endoscopic Index of Severity (UCEIS)
    • this score is the only validated score in UC and is more accurate than the Mayo score for predicting need for colectomy
58
Q

UC endoscopic severity score

A

Ulcerative Colitis Endoscopic Index of Severity (UCEIS)

  • 0-8 points
    • vascular pattern (0-2)
    • bleeding (0-3)
    • erosions (0-3)
  • this score is recommended over the Mayo score by ECCO as it is the only validated score of endoscopic severity, it is easy to calculate with low inter-observer variability and predicts colectomy more accurately
59
Q

What tests should be done in suspected carcinoid syndrome

A

CT chest, abdomen and pelvis

Serum chromogranin A

Urinary 5HIAA

Echo

Dotatate PET