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GI Flashcards

1
Q

which organs does GALD not impact

A

spleen, lymph nodes and bone marrow are relatively spared from deposits

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2
Q

When is the ideal time for the kasai procedure

A

30-45 days. follow bilirubin levels for need for hepatic transplant

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3
Q

between duodenal atresia and ileal atresia, what is the etiology?

A

Duodenal atresia: failure to recanalize
obliteration of lumen should be 6-7 wks, recanalization 8-10w
Jejunal -ileal atresia: ischemia (Ilial, Ischemia) - this is more common than duondenal atresia

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4
Q

what does maternal intrahepatic cholestasis put the fetus at risk for?

A

many pulm things: RDS, MAS, bile acid pneumonia

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5
Q

what is an obese mother’s placenta at risk for?

A

hypermature (increased villi), large, decreased perfusion

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6
Q

most common cause of flank mass?

A

hydronephrosis

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7
Q

where is copper absorbed

A

stomach

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8
Q

what is absorbed in the jejunum

A

fat, protein, carbs

Fe, Mg, Ca

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9
Q

What is absorbed in the ileum

A

B12, bile salts, Zn

fat and fat soluble vitamins

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10
Q

what is absorbed in the colon

A

water and electrolytes

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11
Q

what is neonatal hemochromatosis

A

aka GALD - maternal alloab against baby hepatocytes. deposition of Fe in liver and other tissues.
Dx: anemia, low plts, low fib. High ferritin, high lfts
Bx: salivary gland or liver bx
presents with liver failure and cardiac impairment, or iufd, iugr, pt delivery

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12
Q

what is hemophagocytic lymphohistocytosis (HLH)

A

abnormality of hyperactive T cells and macrophages, where macrophages are phagocytosing hematopoietic precursors (imagine wbc and rbc)

dx: anemia, low plts and neutropenia. low fib, high ferritin, high lfts
dx: hemophagocytosis in BM, spleen and ln tissue

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13
Q

what are the lengths of the different FA

A

short : <6 C
medium 6-12 C
long: 13-21 C

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14
Q

what does CCK do

A

released by small intestine

stimulates pancreatic enzyme secretion and contracts gall bladder

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15
Q

what does gastrin do

A

gastric acid secretion

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16
Q

what does secretin do

A

released by duodenum

stimulates liver bile production, pancreas to release bicarb and inhibits gastric acid

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17
Q

what does motilin do

A

released by small intestine, increases motility and gastric emptying

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18
Q

what does glucose dependent insulinotropic peptide do

A

released by jejunum, post-prandial release of insulin

19
Q

what does neurotensin do

A

released by ileum, inhibits gastric secretion and increases motility

20
Q

what trace elements should you remove in renal dysfunction

A

chromium and selenium (think music, kidneys are headphones)

21
Q

which trace elements should you remove in cholestasis

A

manganese and copper

22
Q

what is manganese involved in

A

cho metabolism and bone structure

23
Q

what is selenium involved in

A

glutamine peroxidase. deficiency cause cardiac problems

24
Q

what is chromium involved in

A

glucose levels through insulin metabolism

25
Q

what is the treatment of choledochal cyst and risks after treatment

A

prompt surgical removal of cyst, anastamose hepatic ducts to pancreatic duct and remove the cyst. Still at risk for malignancy even after, so need careful lifelong surveillance. Increased risk of malignancy if had cyst drainage via cystenterostomy. If surgery needs to be delayed, can place a drain and start abx.

26
Q

what is a choledochal cyst and how does it present

A

anomaly of bile duct, can involve intra or extrahepatic. 75% involved CBD. More common in females and asian populations. Present with increased d. bili. Juncture of pancreatic duct and CBD may be abnormal, allowing for pancreatic reflux which can cause inflammation and malignancy.

27
Q

what other anomalies is duodenal atresia associated with

A

congenital heart disease (30%), Tri 21 and other GI anomalies

28
Q

how does duodenal atresia present

A

in utero, 75% with polyhydramnios, 20% noted on prenatal US, 80% are atretic after ampula so present with bilious vomiting

29
Q

where and how does gi duplication present

what is treatment

A

MC in small intestine (40%) - mc in ileum > colon (15%)
can be cystic or tubular
cystic: can be a lead point for volvulus
tubular: can retain intestinal contents and cause obstruction
with gastric mucosa: can ulcerate
treatment: resection and f/u for pancreatitis, bleeding, malignancy

30
Q

how does biliary atresia present

A

more common in females and asians
presents with elevated d. bili, jaundice beyond 2nd week, acholic stools after 1st week, dark urine (from d bili) and gi sx and hsm after 4th week

31
Q

when should the kasai procedure be performed and what is the success rate

A

ideally before 2 months, 30-50% success rate but may still need liver transplant

32
Q

what is allagile syndrome

A

AD intrahepatic hypoplasia of biliary ducts

  • mutation in JAG and NOTCH gene
  • Triangular facies, Posterior embryotoxon (iris strands), butterfly vertebrae, renal disease, Cardiac defects (peripheral pulmonic stenosis, tetralogy of Fallot), Direct hyperbilirubinemia, May have acholic stool, elevated ALT, bile acids and GGT
33
Q

In NEC, what goes up, what goes down?

  • microbio diversity
  • protebacteria
  • firmicutis
A

decreased: microbio diversity and firmicutis
increased: proteobacteria

34
Q

what is nec totalis, what are treatment options, and what are sequelae?

A

Nec totalis: widespread disease with <25% viable bowel
either resect all necrotic bowel and have diversion, OR divert and then come back later 6-8w for bowel
almost all have SBS and long term TPN dependence

35
Q

What are risk factors for inguinal hernias?
When is the best time to treat?
What is normal descent process of testes?
What is incarceration vs strangulation?

A

Risk factors include PT (40% in 24w vs 4% in 32w), bw (40% in Elbw vs 4% in term), male (3-5x), ab pressure, constipation, cld and dex.

Controversial about when to treat but >55w Pma associated with less recurrence and need for vent support without increasing risk of incarceration.

At 8-15w descend from diaphragm to abdomen when and contents reenter. At 25-35w descend to scrotum when it gets developed.

Incarceration is difficult to reduce, (80% should be reducible) and strangulation is loss of blood flow (20% risk)

36
Q

Gastroschisis: more common in which pregnancies? Presentation?

Over how much time do you reduce contents? What is ideal abd pressure?

A

More common in younger moms (Omphalocele Older). Over all gastroschisis is mc and wall defect. Almost always to the right of the umbillicus. Babies frequently sga.

Reduce over 3-5d. And pressure should be 15-20mmhg. Takes 4-6 weeks for bowel improvement.

Closed gastroschisis is where defect narrows in utero —> strangulation —> atresia

37
Q

What is a “giant omphalocele”?

What is an important genetic association?

A

Greater than 5cm and with liver. Commonly have Pulm hypoplasia.

12% with omphalocele have BW.

38
Q

what is the most common late complication of NEC and where is it located?

A

intestinal strictures, usually in left colon (not TI! even though this is most common site of NEC)

39
Q

what is a good vs bad LHR. when is it most accurate

A

<25% lung to head ratio is assc with <30% survival, vs >50% LHR assc with >85% survival.
most accurate at 22-26w ega.

40
Q

what length of bowel is normal in pt and term, what is pathalogic for SBS?

A

PT: 100cm, Term 160cm

<25% is associated with SBS, <75cm at risk for SBS

41
Q

if you can’t pass an OG beyond what depth do you worry about TEF?

A

10cm

42
Q

what are complications of TEF?

A

1) esophageal peristalsis
2) esophageal dysmotility
3) GERD
4) leak (most resolve spontaneously but can result in stricture)
5) stricture (more common if gap >2.5 cm)
6) recurrence (usually at 2-18 m and in spot of leak or original fistula pouch)
7) asthma

43
Q

what conditions are associated with hirschsprungs?

A

wardenburg, slo, cchs

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