small bowel Flashcards

1
Q

duodenal atresia: what is it? who is at risk?

A

congenital failure of the small bowel to cannulize. associated with Down.

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2
Q

clinical features of duodenal atresia

A

polyhydramnios (we resorb amnitic fluid by swallowing and digesting it- w/o that ability, we see polyhydramnios)
bilious vomiting
distension of the stomach and distention of the duodenom. in between the, is the tight pyloric sphincter- double bubble sign.

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3
Q

what is meckel’s diverticulum? cause?

A

outpouching of all 3 layers of the bowel wall (true diverticulum). It may contain ectopic acid-secreting gastric mucosa or pancreatic tissue.
arises due to a failure of the vitelline duct to involute.
remember, yolk sac feeds the midgut through the vitelline duct in the early embryo. forms at wk 4 and involutes by wk 7. persistence = meckel’s diverticulum

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4
Q

what are some clinical manifestations of failure of the vitelline duct to close?

A

passing meconium through the umbiligus (no closure of the vitelline duct at all)
partial closure of the vitelline duct: feels like there is stool caught in the Mecke’s diverticulum on palpation of the umbilical area

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5
Q

What are some important clinical and epidemiological facts about Meckel’s diverticulum?

A

2% of the population (most common congenital anomoly of the GI tract)
2 inches long, usually in small bowel 2 feet from the ileocecal valve.
usually asymptomatic, but if it does present, it usually does so in the first 2 yrs of life.
may have 2 types of epithelia (gastric/pancreatic)

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6
Q

How does meckel’s divertuculm present? How is it diagnosed?

A

usually asymptomatic, but may present with bleeding, volvulus, intussusception or obstruction near the terminal ileum in the first 2 yrs of life. you can have heterotopic gastric mucosa that makes acid –> ulcer –> bleeding
diagnosed with a pertechnetate study for uptake by ectopic gastric mucosa

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7
Q

volvulus: definition

A

twisting of bowel along its mesentery. results in obstruction and disruption of the blood supply (infarction).

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8
Q

volvulus: locations

A

sigmoid colon in eldery and cecum in young adults (in FA, midgut is most common in infants and kids)

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9
Q

intussusception definition and most common location

A

telescoping of proximal segment into a distal segment
can cause infarction or obstruction. infarction can present with “current jelly” stools.
commonly occurs at the ileocecal junction.

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10
Q

intussusception causes

A

associated with a leading edge that drags the bowel with it.
in kids, most common cause is idiopathic or lymphoid hyperplasia. terminal ileum is dragged into the cecum because of the thickness of the wall
in adults, most common cause is tumor

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11
Q

small bowel infarction: definition and types; most common locations.

A

small bowel very susceptible to ischemic injury becasue it requires so much O2. Small bowel infarction may be transmural infarction or mucosal infarction
commonly seen at the splenic flexure and the distal colon.

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12
Q

transmural small bowel infarction: causes

A

infarction: transmural infartion occurs with emobolism/thrombosis of the SMA or thrombosis of the vein. causes of embolism: Afib, or vasculitis (PAN). Vein thrombosis may be from polycythemia vera, or lupus anticoagulant.

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13
Q

mucosal small bowel infarction causes

A

mucosa is furthest from the blood supply- infarction with marked hypotension

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14
Q

clinical features of small bowel infarction

A

abdominal pain, bloody diarrhea, decr. bowel sounds

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15
Q

definition of celiac disease. genetic associations, affected locations.

A

immune medated damage of small bowel villi due to gluten exposure. associated w/ DQ2 and DQ8. decreased mucosal absorption primarily affects the distal duodenum and/or proximal jejunum.

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16
Q

what is the pathophysiology of celiac disease

A

gluten is present in wheat and grains and causes a hypersensitivity. most pathogenic part is gliadin, which is deaminated by tissue transglutamidase. altered gliadin is presented by APS to helper T cells by MHC type II molecules.

17
Q

Associated findings with celiac disease. what is the cause?

A

dermatitis herpetiformis. due to deposition of IgA at the tips of the dermal papillae that destroys the connection btw the dermis and the epidermis at that point- causes herpes-like vesicles

18
Q

lab findings for celiac

A

IgA Abs against endomysium, tissue transglutamidase, or gliadin.
some of the pts are deficient in IgA, however, so you should also look for IgG abs against things.

19
Q

histo findings in celiac

A

duodenal biopsy: flattening of villi, hyperplasia of crypts, and lymphocytes, esp. in the lamina propria of the epithelium.
remember that most damage is in the duodenum, while the jejunum and ileum are less involved.

20
Q

complications of celiac

A
  1. small bowel carcinoma

2. T-CELL lymphoma (EATL: enteropathy associated T cell lymphoma)