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small bowel Flashcards

1
Q

what 2 types of ischaemia are there

A

mesenteric arterial occlusion

non occlusive perfusion insufficiency

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2
Q

what can cause ischaemia

A 
mesenteric artery atherosclerosis
thromboembolus from heart 
shock
strangulation
drugs e.g cocaine
hyperviscosity
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3
Q

which part of the small bowel is most metabolically active and therefore most sensitive to ischaemia

A

mucosa

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4
Q

what is Meckel’s diverticulum

A

incomplete regression of vietello intestinal duct

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5
Q

how can a Meckel’s diverticulum mimic appendicitis

A

it may contain heterotropic gastic mucosa which can release acid
it can cause bleeding, perforation or diverticulitis which mimicks appendicitis
commonly asymptomatic

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6
Q

are primary tumours of the small bowel common

A

no they are very rare

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7
Q

what type of tumours can you get in the small bowel

A

lymphomas
carcinomas
carcinoid tumours

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8
Q

what are carcinomas of the small bowel associated with

A

crohns disease and coeliac disease

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9
Q

what is coeliac disease and how does it affect enterocytes

A

autoimmune disease

abnormal reaction to a constituent of wheat flour, guten which damages enterocytes and reduced absorptive capacity

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10
Q

coeliac disease has an association to what gene

A

HLA-B8

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11
Q

what are some of the compliation with coeliac disease

A

T cell lymphoma of the GI tract
increased risk of small bowel carcinoma
Gall stones
ulcerative jejenoilleitis

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12
Q

what is the suspected component of gluten that is toxic

A

gliadin

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13
Q

what happens to the cells in coeliac disease

A

increasing loss of enterocytes
loss of villus structure SA, reduction in absorption and a flat duodenal mucosa
inflammation in lamina propria
increased intraepithelial lymphocytes

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14
Q

what are metabolic effects of coeliac disease

A

malabsorption of all nutrients
steatorrhoea (excess fat in faeces)
reduced pancreatic secretion and bile flow-gallstones

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15
Q

in terms of pathology what happens in acute appendicitis

A

acute inflammation (neutrophils)
mucosal ulceration
serosal congestion, exudate
pus in lumen

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16
Q

which has a lower protein content exudate or transudate

A

transudate

17
Q

in non occlusive ischaemia when does most damage occur

A

after reperfusion

18
Q

when would you get type 1 intestinal failure

A

self-limiting short term

post operative ileus

19
Q

when would you get type 2 intestinal failure

A

prolonged, associated with sepsis and metabolic complications. often reated to abdominal surgery with complications

20
Q

what types of diseases are associated with type 3 intestinal failure

A 
short gut syndrome 
crohn's disease
neoplasia
vascular 
mechanical 
radiation enteritis 
dysmotility
21
Q

what is short bowel syndrome

A

unsufficient length of small bowel to meet nutritional needs without artificial nutritional support

22
Q

how is PN given

A

PICC peripheraly inserted central catheter

23
Q

what are some of the compilations of parenteral nutrition

A 
sepsis 
SVC thrombosis 
line fracture 
line leakage 
line migration 
metabolic bone disease
nutrient toxicity/insufficiency eg.manganese
liver disease
24
Q

what are some indications for oral nutritional supplemements

A 
disease related malnutrition 
intractable malabsorption 
per-operative preparation of malnourished patients
dysphagia 
proven IBD
post total gastrectomy 
SBS
bowel fistulae
25
Q

what are some contra-indications for ETF

A 
lower gastrointestinal obstruction 
prolonged intestinal ileus 
severe diarrhoea or vomiting 
high enterocutaneous fistula 
intestinal ischaemia
26
Q

what is re-feeding syndrome

A

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

27
Q

what is APR

A

abdominoperineal resection

28
Q

what is the difference in parenteral and enteral feeding

A

parenteral feeding supplies nutrients directly into the blood
enteral feeding-liquid food through a catheter directly into GI tract

29
Q

when would you give enteral feeding

A

impaired ingestion, inability to intake adequate nutrients orally, impaired digestion, absorption and metabolism

30
Q

when would you give parenteral feeding

A

short bowel syndrome, sever acute pancreatitis, small bowel ischaemia, intestinal atresia, severe liver failure, bone marrow transplant, acute resp failure

31
Q

what are some contraindications for ETF

A 
lower gastrointestinal obstruction 
prolonged intestinal ileus 
severe diarrhoea or vomiting 
high enterocutaneous fistula 
intestinal ischaemia
32
Q

what are some of the metabolic results of re-feeding syndrome

A 
hypokalaemia
hypophosphataemia 
hypomagnesia 
altered glucose metabolism 
fluid overload
33
Q

what are some of the physical consequences of re-feeding syndrome

A 
arrhythmias 
altered level of consciousness
seizure
resp failure 
cardiovascular collapse 
death
34
Q

how is re-feeding syndrome linked to insulin

A

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

GI (13 decks)

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