small bowel Flashcards
what 2 types of ischaemia are there
mesenteric arterial occlusion
non occlusive perfusion insufficiency
what can cause ischaemia
mesenteric artery atherosclerosis thromboembolus from heart shock strangulation drugs e.g cocaine hyperviscosity
which part of the small bowel is most metabolically active and therefore most sensitive to ischaemia
mucosa
what is Meckel’s diverticulum
incomplete regression of vietello intestinal duct
how can a Meckel’s diverticulum mimic appendicitis
it may contain heterotropic gastic mucosa which can release acid
it can cause bleeding, perforation or diverticulitis which mimicks appendicitis
commonly asymptomatic
are primary tumours of the small bowel common
no they are very rare
what type of tumours can you get in the small bowel
lymphomas
carcinomas
carcinoid tumours
what are carcinomas of the small bowel associated with
crohns disease and coeliac disease
what is coeliac disease and how does it affect enterocytes
autoimmune disease
abnormal reaction to a constituent of wheat flour, guten which damages enterocytes and reduced absorptive capacity
coeliac disease has an association to what gene
HLA-B8
what are some of the compliation with coeliac disease
T cell lymphoma of the GI tract
increased risk of small bowel carcinoma
Gall stones
ulcerative jejenoilleitis
what is the suspected component of gluten that is toxic
gliadin
what happens to the cells in coeliac disease
increasing loss of enterocytes
loss of villus structure SA, reduction in absorption and a flat duodenal mucosa
inflammation in lamina propria
increased intraepithelial lymphocytes
what are metabolic effects of coeliac disease
malabsorption of all nutrients
steatorrhoea (excess fat in faeces)
reduced pancreatic secretion and bile flow-gallstones
in terms of pathology what happens in acute appendicitis
acute inflammation (neutrophils)
mucosal ulceration
serosal congestion, exudate
pus in lumen
which has a lower protein content exudate or transudate
transudate
in non occlusive ischaemia when does most damage occur
after reperfusion
when would you get type 1 intestinal failure
self-limiting short term
post operative ileus
when would you get type 2 intestinal failure
prolonged, associated with sepsis and metabolic complications. often reated to abdominal surgery with complications
what types of diseases are associated with type 3 intestinal failure
short gut syndrome crohn's disease neoplasia vascular mechanical radiation enteritis dysmotility
what is short bowel syndrome
unsufficient length of small bowel to meet nutritional needs without artificial nutritional support
how is PN given
PICC peripheraly inserted central catheter
what are some of the compilations of parenteral nutrition
sepsis SVC thrombosis line fracture line leakage line migration metabolic bone disease nutrient toxicity/insufficiency eg.manganese liver disease
what are some indications for oral nutritional supplemements
disease related malnutrition intractable malabsorption per-operative preparation of malnourished patients dysphagia proven IBD post total gastrectomy SBS bowel fistulae
what are some contra-indications for ETF
lower gastrointestinal obstruction prolonged intestinal ileus severe diarrhoea or vomiting high enterocutaneous fistula intestinal ischaemia
what is re-feeding syndrome
potentially fatal shifts in fluids and electrolytes and distrubances in organ function that may result form rapid initiation of refeeding after a period of under nutrition
what is APR
abdominoperineal resection
what is the difference in parenteral and enteral feeding
parenteral feeding supplies nutrients directly into the blood
enteral feeding-liquid food through a catheter directly into GI tract
when would you give enteral feeding
impaired ingestion, inability to intake adequate nutrients orally, impaired digestion, absorption and metabolism
when would you give parenteral feeding
short bowel syndrome, sever acute pancreatitis, small bowel ischaemia, intestinal atresia, severe liver failure, bone marrow transplant, acute resp failure
what are some contraindications for ETF
lower gastrointestinal obstruction prolonged intestinal ileus severe diarrhoea or vomiting high enterocutaneous fistula intestinal ischaemia
what are some of the metabolic results of re-feeding syndrome
hypokalaemia hypophosphataemia hypomagnesia altered glucose metabolism fluid overload
what are some of the physical consequences of re-feeding syndrome
arrhythmias altered level of consciousness seizure resp failure cardiovascular collapse death
how is re-feeding syndrome linked to insulin
during refeeding insulin is secreted in response to increasing blood sugars which results in increased glycogen, fat and protein synthesis
this requires phosphates, magnesium and potassium which are already depleted and the stores rapidly become used up
