Small Bowel

Question 1

Pathophysiology of Adhesions?

Answer 1

• balance between fibrin deposition and degradation is critical
• peritoneal injury -> repair response including inflammation, fibrin deposition at
  site of injury (starts within hrs and peaks at day 4-5) -> neutrophil, macrophage infiltration, phagocytosis of dead tissue, O2 free radicals, and recruitment of mesothelial cells, fibrinolysis by tPA -> mesothelial cells aggregate on surface of injury to form small islands that proliferate to re-epithelialise the injured area (5-7 days)
• adhesions form if fibrinolysis is incomplete, ingrowth of fibroblasts, deposition of collagen connective tissue scar and capillaries
• surgery reduces fibrinolytic activity by increased levels of plasminogen activator inhibitors and reducing tissue O2
• fibrinolysis can also be impaired by thermal injury, ischaemia, foreign bodies, blood, bacteria
• genetics may also play a role

Question 2

Features of strangulated obstructed bowel?

Answer 2

1. Constant non cramping abdominal pain
2. tachycardia/fever
3. Localised peritonism
4. Leukocytosis
5. Lactate
   6, CT findings (late) -> pneumatosis intestinal, portal venous gas

Question 3

Small bowel embryology?

Answer 3

Physiological herniation
During 4-8th week embryonic cavity can’t accommodate rapidly -> expanding GIT => primary intestinal loop buckling into yolk stalk around axis of SMA outside of the abdomen

Rotation: Bowel then rotates by twisting 90 degrees counterclockwise due to
● Faster growth of proximal bowel (duodenojejunal loop) vs distal bowel (caecocolic loop)
● Rapid growth of liver

Retraction and further rotation
The primary loop grows until 8-10th week and then returns to abdomen where there is an additional 180-degree counterclockwise rotation
Total rotation = 270 degrees

Fixation
Once rotated, it is fixed to posterior abdomen -> proximal part (ligament of treitz) is fixed to retroperitoneum early, whereas fixation of colon is gradual and complete at near term

Normal rotation and fixation => wide-based mesentery that extends from ligament of treitz to ileocaecal valve

Question 4

Rigler’s Triad?

Answer 4

Signs of SBO
Pneumobilia (air in biliary tree) → 30-60%
Stone may be visible if calcified (<15%)

Gallstone Ileus

Question 5

Small bowel adenocarcinoma is often diagnosed late. 50% are diagnosed with advanced disease, 1/4 have distant mets and 1/3 have nodal involvement. What are the familial syndromes associated with this condition?

Answer 5

FAP -> duodenal adenomas and adenocarcinoma (1/10000 APC gene mutation. Codes APC protein which is a tumour suppressor protein that antagonised the Wnt signalling pathway

HNPCC (Lynch) - adenocarcinoma throughout small bowel. Defect in mismatch repair -> microsatellite instability

coeliac disease

Peutz Jegher - STK11 gene -> multiply cancers. Characterised by hemartomatous polyps in the GIT, hyperpigmented macule on the lips and melanosis to the oral mucosa

Question 6

Management of Small bowel Adenocarcinoma?

Answer 6

D1/2 tumours- pancreaticoduodenectomy
D3/4 tumours - segmental resection preferred
Jejunal/ileal - wide segmental bowel resection with mesentery
distal ileal - ileocolic

Unresectable/metastatic

• Chemotherapy
• consider palliative resection for bleeding or obstruction
• Consider intestinal bypass or endoscopically placed stent
• consider metastectomy
• consider cytoreductive surgery and bypass

Question 7

Prognosis of small bowel adenocarcinoma

Answer 7

5YS
Stage 1 - 65%
Stage 2 - 48%
Stage 3 - 35%
Stage 4 - 4%

Question 8

Staging of small bowel Adenocarcinoma?

Answer 8

T1: submucosa A - lamina propria B- submucosa
T2 - Muscularis propria
T3 Subserosa
T4 other organs

N 1: 1-2 nodes
N2: >2 nodes

Stage

1: T1/2
2: T3/4
3: N1
4: M1

Question 9

Mechanism of paradoxical acuduria?

Answer 9

1. In GOO/duodenal obstruction there is non-bilious projectile vomiting which causes gastric HCl loss. Consequently there is hypochloremic metabolic alkalosis.
2. Initially, urine containing less chloride and more bicarbonate as the form of sodium bi-carbonate. That means,in response to metabolic alkalosis kidney excretes more sodium bicarbonate to reduce blood alkalinity as compensatory mechanism.
3. Urinary loss of sodium bicarbonate causes hyponatremia. so this hyponatremic phase is followed by aldosterone mediated sodium retention phase. (RAAS) This phase allows more sodium and water reabsorption in exchange of hydrogen and potassium ion.
4. Hypokalemia develops and the body excretes H+ instead of K+ making the urine acidic-> So, the patient develops hypokalaemia and urine becomes acidic due to presence of hydrogen ions.
5. Why this is called paradoxical aciduria?
   Because in the presence of metabolic alkalosis kidney should have produced alkaline urine.

Question 10

Criteria for diagnosing primary GI lymphoma?

Answer 10

1. No peripheral or mediastinal lymphadenopathy
2. Normal WCC/smear
3. Tumours involvement predominantly in GI tract
4. No evidence of liver or spleen involvement

Question 11

Risk factors for small bowel lymphoma

Answer 11

1. autoimmune disease/HIV/ long standing immunosuppression
2. Crohns
3. Radiation therapy
4. Nodular lymphoid hyperplasia
5. Helicobacter pylori (MALT lymphoma) - may also respond to eradication

Question 12

Hereditary GIST is a rare autosomal dominant disease due to germline mutation of KIT or PDGFRA. It is associated with NF1

What is Carney’s triad?

Answer 12

GIST, paraganglionoma, pulmonary chondroma (rare benign tumour of the lung)

Paraganglionoma is a rare neuroendocrine neoplasm. In the adrenal gland it is a phaeochromocytoma. All contain neurosecretory granules but only 1-3% secrete hormones such as catecholamines

Question 13

Hereditary GIST is a rare autosomal dominant disease due to germline mutation of KIT or PDGFRA. It is associated with NF1

What is Carne- Stratakis dyad?

Answer 13

GIST

Paraganglionoma

Question 14

What is the call of GI bleeding in Meckel’s Diverticulum?

Answer 14

Meckels often contain ectopic tissue as they are lined by pluripotent stem cells.

50% contain gastric mucosa
5% pancreatic
Can also contain colonic or duodenal

Gastric secretions from gastric heterotrophic mucosa ulcerate ill mucosa opposite diverticulum on the mesenteric border.
Occurs in 25-50% of complicated meckels

Question 15

What is a Little hernia?

Answer 15

Meckel’s diverticulum incarcerated within a hernia Littre hernia

Usual sites of Littre hernia are: inguinal (50%), umbilical (20%), and femoral (20%)

Question 16

Pathophysiology of Angiodysplasia

Answer 16

o Ectatic, thin-walled vessels lined by endothelium alone +/- small
amounts of smooth muscle
o Associated with tortuous, dilated submucosal veins
o Small arteriovenous communications often present
o Pathogenesis uncertain may develop due to recurrent low-grade
obstruction of submucosal veins at level of muscularis propria results in dilation and tortuosity of draining vessels (submucosal vessels, venules, superficial capillaries)

Question 17

Nutrition in enterocutaneous fistula?

Answer 17

Baseline nutritional requirements for pts with ECF may be 1-2.5x more than normal esp if large open wounds, ongoing infection or high output

o Low output approx. 20-30kcal/kg/day with 1-1.5gkg/day of protein
o High output approx. 25-35kcal/kg/day with 1.5-2.5gkg/day of protein
o Vitamins and trace elements (vit C, zinc, copper, selenium) increase healing

Question 18

Fistulas are unlikely to close if…

Answer 18

Unlikely to close if: = Pram has NO FRIENDS
o Proximal fistula 
o Nutrition poor 
o Output high
o Foreign body
o Radiation
o Inflammation (Crohn’s)/Infection (TB, diverticulitis) 
o Epithelialization
o Neoplasia
o Distal obstruction
o Short (<2cm), wide (>1cm2) track

Question 19

Describe the absorption of Carbohydrates?

Answer 19

Polysaccharides digested by amylase to disaccharides

Dissachardies are hydrolysed into monosaccharides at the brush border and then absorbed by active transport - SGLT 1, GLUT 2, GLUT 5

Question 20

Describe the absorption of proteins?

Answer 20

Denatures in the stomach then digested by pancreatic proteases at the duodenal brush border - trypsin, chymotrypsin and elastase

Absorbed by sodium mediated active transport

Question 21

Describe the absorption of fats?

Answer 21

Triglycerides are emulsified by bile to form micelles + broken down into monoglycerides and free fatty acids by lipase

Absorbed at brush border and packaged again as triglycerides into chylomicrons and moved into the lymphatics

Short and medium chain fatty acids van be water soluble and directly absorbed into blood stream

Question 22

Water, electrolytes and vitamins in the bowel?

Answer 22

7 L of fluid produced, 6L reabsorbed before the IC valve, 800mL absorbed by the colon. 200mL in faeces

Water is absorbed by following the osmotic gradient formed by the active transport of sodium, glucose and amino acids

Most electrolytes are absorbed by active transport at the cell surface - sodium mostly by ileum and colon.

Fat soluble vitamins are absorbed with chylomicrons

Water soluble vitamins are absorbed by active transport, diffusion and facilitated transport.

Question 23

Describe the physiology of vitamin B12

Answer 23

Binds to intrinsic factor (produced in the stomach) to protect it from proteolysis and taken up by translocation as a complex in the terminal ileum