Intestinal obstruction


Clinical manifestations: abdominal pain and distension, vomiting, constipation
Usually requires surgical intervention for mechanical obstruction or severe infarction
1. Hernias



Acquired hernias most commonly occur anteriorly (inguinal/femoral canals or umbilicus)
Usually small bowel loops, but also can be large bowel or omentum
Can block venous drainage  oedema  inc hernia size  permanent entrapment
(incarceration) and arterial and venous compromise (strangulation)  infarction
2. Adhesions


Causes: surgery, infection, peritoneal inflammation (eg. endometriosis)
Fibrous bridges can create closed loops  other viscera become entrapped if they slide through
 internal herniation
3. Volvulus



Complete twisting of a loop of bowel about its mesenteric base of attachment  RARE
Luminal and vascular compromise  present with features of obstruction and infarction
Sigmoid colon > caecum > small bowel > stomach > transverse colon
4. Intussusception

= when a segment of intestine, constricted by a wave of peristalsis, telescopes into the
immediately distal segment
o The invaginated segment is propelled by peristalsis and pulls the mesentery along
5. Tumours and infarction

Only 10-15% of small bowel obstructions
Ischaemic disease




Mucosal infarction Vs mural infarction (mucosa + submucosa) Vs transmural infarction
Causes of transmural: atherosclerosis, aortic aneurysm, hypercoagulable states, OCP,
embolisation
Causes of mucosal or mural infarction (ie. hypoperfusion): cardiac failure, shock, dehydration
Pathogenesis:
1. Initial hypoxic injury  epithelial cells are relatively resistant to transient hypoxia
2. Reperfusion injury  initiated by restoration of blood supply; can trigger multi-organ
failure



Most common at ends of arterial supply (splenic flexure > sigmoid colon and rectum)
Morphology:
o Lesions are often segmental and patchy
o Haemorrhagic, ulcerated mucosa
o Oedematous bowel wall
Clinical features:
o Usually older people with cardiac/vascular disease
o Acute transmural infarction: sudden, severe abdominal pain and tenderness (+ nausea,
vomiting, bloody diarrhoea, grossly melanotic stool)  can progress to shock
o Peristaltic sounds reduce or disappear; muscular spasm causes rigid abdominal wall
Malabsorption



Presents most commonly as chronic diarrhoea
Can also show weight loss, anorexia, abdominal distention, borborygmi, muscle wasting,
steatorrhoea, other symptoms of specific vitamins not being absorbed
While one step in absorption may be most affected, >1 is usually affected  therefore all
malabsorptive diseases resemble each other
1. Cystic fibrosis


Intestinal chloride ion secretion defect  defective bicarbonate, Na+ and H2O secretion 
defective luminal hydration
Duct obstruction  low-grade chronic autodigestion of the pancreas  exocrine pancreatic
insufficiency
2. Celiac disease




Immune-mediated enteropathy
Pathogenesis:
o Gluten degraded to gliaden
o IL-15 expression by epithelial cells
o CD8+ cells activated and proliferate
o NKG2D expression (NK cell marker)
o Killing of cells expressing MIC-A (a HLA-I-like protein expressed in response to stress)
o Also CD4+ effects
Morphology: 2nd portion of duodenum or proximal jejunum
o Histopathology: inc CD8+ T cells (intraepithelial lymphocytosis) + crypt hyperplasia +
villous atrophy
o Also possibly limited differentiation of absorptive enterocytes (due to high turnover)
o Increased plasma cells, mast cells and eosinophils
 Esp in upper part of lamina propria
Clinical features:



o 30-60 year olds; no gender preference but more commonly noticed in women
o Often atypical presentations; Can also be silent or latent disease
o Anaemia, chronic diarrhoea, bloating, chronic fatigue
o Associated with dermatitis herpetiformis, lymphocytic gastritis and lymphocytic colitis
Ix: IgA against tissue transglutaminase or IgA/IgG to deamidated gliadin
Tx: gluten-free diet  but hard to adhere to
Complications: higher rate of malignancy (eg. enteropathy-associated T-cell lymphoma)
3. Tropical Sprue



Malabsorptive, generally endemic to the tropics
Histology: similar to celiac disease, but total villous atrophy is uncommon; usually distal bowel
No definitive causative organism identified
4. Autoimmune enteropathy



Severe persistent diarrhoea and autoimmune disease in young children
IPEX = immune dysregulation + polyendocrinopathy + enteropathy + x-linked disorder
o Due to germ-line FOXP3 mutation  severe form of disease
o FOXP3 mutation causes defective T-cell regulatory function
Tx: immunosuppressive drugs (cyclosporine), BM transplant (if severe)
5. Lactase deficiency


Biopsy generally unremarkable
Congenital Vs acquired
o Congenital: mutated lactase gene; autosomal recessive
o Acquired: down-regulation of lactase gene expression
6. Abetalipoproteinemia
 Rare autosomal recessive disease
 Inability to secrete triglyceride-rich lipoproteins
1. Mutation in microsomal triglyceride transfer protein  catalyzes transport of triglycerides,
cholesterol esters and phospholipids
2. Therefore chylomicrons cannot be assembled  triglycerides accumulate within epithelial cells
 Ie. transepithelial transport failure  malabsorption
 Clinical: failure to thrive, diarrhoea, steatorrhoea, complete absence of all plasma lipoproteins
containing apolipotrotein B, deficiency of fat-soluble vitamins and lipid membrane defects (burr
cells present in peripheral blood smears)
7. Crohn disease
8. Pancreatic insufficiency