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home - Small Bowel - Miscellaneous - Small Bowel Pathology Presentations Written by Dr Sebastian Zeki
Knowledge


Defines the pathophysiology of fluid and nutrient malabsorption,
including causes, e.g. anatomical and functional short bowel
syndrome, high output stomas, enterocutaneous fistulae and
pancreatic insufficiency

Knows how to investigate patients with malabsorption
Describes the clinical consequences of malabsorption, including
malnutrition, fluid and electrolyte disturbance and micronutrient
deficiency and anaemia and how to manage these

Describes all other causes of anaemia, including bone marrow
disorders and haemolysis

Describes the metabolism, absorption and bioavailability of iron, B12
and folate and clinical conditions and diets associated with their
deficiency

Skills
Identifies and appropriately investigates clinical features suggestive of
malabsorption

Manages fluid, electrolyte and micronutrient disturbances associated
with short bowel syndrome or high output stomas

Uses the appropriate investigations for the different types of anaemia
Behaviours
Takes a careful clinical approach to managing patients with
malabsorption and anaemia. Explains plan of management clearly to
patients and their relatives.

Small Bowel Pathology Presentations

Rule out fixed lesions-Show dismotility -Rule out secondary causes Causes of obstruction: Adhesions (15% of laparotomy pts get this within 2 years). Cancer. Crohn's. Hernia. Pseudo obstruction. Non-ulcerative Coeliac sprue Tropical sprue Menetriers Whipple's SLE Eosinophilic gastroenteritis Lymphatic problems (ie lymphangiectasia) Increased RAP Whipple's Mesenteric LN obstruction (TB/sarcoid/lymphoma/RPF). Protein losing enteropathy Oedema/ hypoprotaenaemia/ low albumin/ diarrhoea Enteral protein loss/ alpha1 antitrypsin in stool Upper GI endoscopy Gastrinoma Menetrier’s disease Mucosal hyperplasiaReduction in or absence of parietal cellsReduced acid secretionSerum gastrin normal or slightly elevated Mucosal hyperplasiaIncreased number of parietal cellsIncreased acid secretionSerum gastrin normal Normal gastric appearance Normal duodenum Abnormal duodenum Colonoscopic radiography Small bowel biopsy Crohn’s diseaseUlcerative colitisNeoplasms Intestinal lymphangiectasia Exudative gastropathy Dysmotility problems Written by Dr Sebastian Zeki Secondary Dysmotility causes: TCI. Clonidine. Opiates. Anti-Parkinson's. Venothiazine. DM/TSH increase or decrease/decrease PTH. Chagas. Paraneo plastic pseudo-obstruction. Parkinson's. Spinal chord injury. MD. RA. Amiloidosis. Coeliac sprue. Radiation enteritis. Jejunoileal bypass. Anorexia and bulimia. Diffuse lymphoid inflammation. Primary Dysmotility Causes: Familial. Visceral myopathy (1,2,3). Visceral neuropathy (1,4). Non-familial. Visceral myopathy. Visceral neuropathy. Mechanical Small Bowel Presentations Mucosal phase A. Brush border hydrolysis 1. Congenital disaccharidase defect Sucrase-isomaltase deficiency 2. Acquired disaccharidase defect Lactase deficiency B. Epithelial transport 1. Nutrient-specific defects in transport Hartnup's disease 2. Global defects in transport Celiac sprue Postabsorptive, processing phase A. Enterocyte processing Abetalipoproteinemia B. Lymphatic Intestinal lymphangiectasia Phase and nature of malabsorptive defect Example Luminal phase A. Substrate hydrolysis 1. Digestive enzyme deficiency Chronic pancreatitis 2. Digestive enzyme inactivation Zollinger-Ellison syndrome 3. Dyssynchrony of enzyme release, inadequate mixing Post Billroth II procedure B. Fat solubilization 1. Diminished bile salt synthesis Cirrhosis 2. Impaired bile secretion Chronic cholestasis 3. Bile salt de-conjugation Bacterial overgrowth 4. Increased bile salt loss Ileal disease or resection C. Luminal availability of specific nutrients 1. Diminished gastric acid Atrophic gastritis - vitamin B12 2. Diminished intrinsic factor Pernicious anemia - vitamin B12 3. Bacterial consumption of nutrients Bacterial overgrowth - vitamin B12 Small Bowel Malabsorption Small Intestinal UlcerationSmall intestine ulceration.Medication induced.KCL/NSAID.Systemic disease related.Vasculitic/ischaemia/infection/inflammatory (Crohn's/SLE).Increased acidity - ZE, Meckel's.Tumours.Ulcerative jejunoileitis. UlcerativeCrohn’sCancerPMC Process1. Bowel dilates2. Bacterial overgrowth Therefore faeculent vomiting3. Bowel wall oedema4. Bowel loses absorptive ability so more fluid accumulates5. Wall oedema gets so bad that transudative loss into the peritoneal cavity occurs6. Oedema then compromises gut blood supply7. Strangulatio and necrosis occur (this increases mortality from 5 to 37%)- at this point pain may progress from colicky to constant. Lactate is senstive but not specific marker of strangulationTreatment of SBO“never let the sun rise or set on a small bowel obstruction”- maximum 12 to 24hours observation. If no improvement then for theatreBowel obstruction in patients with cancer - surgery has inpatient mortality of 35%, succesful relief of 70%, non-opersative manage-ment success is about 30%Early post-operative obstruction- usually treat conservatively as will settle