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Neontal boards J > GI/Bili > Flashcards

GI/Bili Flashcards

1
Q

What is Liley curve

A

measures amniotic fluid concentration of bilirubin by means of spectrophotometry.

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2
Q

What is the most common condition requiring surgery in infancy

A

pyloric stenosis

Associated with T21

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3
Q

Possible cause of breastmilk jaundice

A
  • Mutations in the UGT1A1 gene
  • High levels of beta-glucuronidase.

consider other non-hemolytic causes of prolonged hyperbilirubinemia, need not investigate for them unless jaundice does not resolve by 12 weeks of age

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4
Q

Factors that worsen normal physiologic jaundice (5)

A
  1. prematurity
  2. sequestered blood
  3. delayed establishment of feedings
  4. maternal meds
  5. DDC
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5
Q

Duration of breastmilk jaundice

A

normalize over 4-12 weeks

can reach 20-30 mg/dl by 2 weeks

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6
Q

Causes of pathologic jaundice

Onset before 24 hrs, inc >0.5 mg/dl/hr (>5mg/dl/day), Jaundice > 8 day for term 14 days preterm, DB >1mg/dl

A
  1. Increased production
    * hemolytic
    * enzyme def- G6PD, PK
    * membrane defect
  2. decreased clearance: gilbert
  3. impaired conjugation: crigler-najjar
  4. increased enterohepatic circulation:breastmilk and breastfeeding jaundice
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7
Q

Long term consequences of kernicterus

A
  • extrapyramidal (choreoathetosis)
  • Sensorineural hearing loss
  • gaze palsies
  • dental dysplasia

greatest risk with rapid rate of increase

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8
Q

Phototherapy depends on (4)

A
  1. spectrum of light- blue (460-490 nm)
  2. irridiation- 30uW/cm2
  3. surface exposed
  4. distance of infant from light- 12-16 in/30-40 cm
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9
Q

It significantly increases surface area of the small intestine

A

Villi and microvilli

covered by columnar epithelial cells at tips- absorbtive cells, crypts- secretory

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10
Q

Part of the bowel that mainly absorbs calcium and iron

A

Duodenum

  • 80-100% absorb calcium via active transport
  • Also initiates digestion
  • production of GI hormones
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11
Q

Parts of the bowel that absorbs calcium

A
  1. Duodenum via active transport
  2. Jejunum via concentration gradient
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12
Q

What are the location of nutrient absorption in the bowel

A
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13
Q

Specialized function of the distal ileum

A

Absorption of:
1. Vit B12 (needs intrinsic factor)
2. Zinc
3. Bile acid

Bile salts: not reabsorbed can cause diarrhea and impair Na and H2O

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14
Q

what GI hormone cause delayed in gastric emptying

A

glucagon peptide I and petide YY

stimulated by lipids in the ileum

longer transit time, nutrient absorption in small intestine

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15
Q

Function of the ileocecal valve

A
  1. regulates fluids, electrolytes, nutrient
  2. Prevents reflux of colonic material incl bacteria
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16
Q

Greatest absorption of water and sodium in the GI tract

A

Colon

tightest intrercellular junction and slowest transt time

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17
Q

morbidities/ complication of short bowel syndrome

A
  1. catheter related blood stream infection- E coli and enterococci
  2. Cholestasis
  3. Growth failure
  4. Small bowel bacterial overgrowth (SBBO)

CLABSI- d/t leaky gut mucosal barrier

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18
Q

Strategies to reverse cholestasis

A
  1. lipid reduction (1mg/kg 1-3/wk)
  2. lipid modification (SMOF/omegaven)
  3. advancement enteral feeds

Lipid supplement cannot be stopped d/t risk essential FA def

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19
Q

Antibiotic therapy for SBBO

A

Metronidazole
Ciprofloxacin

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20
Q

Red flags for cholestasis (3)

A
  1. jaundice >2 weeks
  2. hepatomegaly
  3. pale stools/diarrhea

Obtain fractionated bilirubin

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21
Q

Identifiable causes of cholestasis

A
  • from most common
    1. biliary atresia
    2. genetic/metabolic: A1AT, alagille synd, CF
    3. Idiopathic/transient neonatal cholestasis
    4. PNAC
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22
Q

Direct bilirubin level assoc with cholestasis

A
  • first 5 days: >0.3-0.4 mg/dl
  • 10% of TB
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23
Q

Differential for GGT >150 U/L

A
  1. Biliary atresia
  2. choledochal cyst
  3. A1AT def
  4. CF
24
Q

Differential for GGT <125 U/L

A
  1. PFIC (progressive familial intrahepatic cholestasis I, II)
  2. Inborn errors of bile acid synthesis
  3. panhypopit
25
Q

Ideal timing for kasia procedure

A

Done before 30-45 days

chances for post-op bile flow, avoid/delay liver transplant

26
Q

Evaluation for cholestasis

A
27
Q

Most frequent indication for pediatric liver transplant

A

Biliary Atresia

28
Q
  • AR d/o associated with cholestasis
  • Have hepatocyte retention of polymers mutant Z protein
  • risk for early emphysema
A

A1AT deficiency

29
Q
  • AD d/o associated with cholestasis
  • Mutation with Jagged1 gene
  • Clinical features:
    * bile duct paucity
    * cong heart dis (right sided)
    * dysmorphic facies- triangular face, broad forehead, deep set eyes, sm pointed chin
    * ocular post embryotoxon
    * butterfly vertebrae
    * renal anomalies
A

Alagille syndrome

30
Q

What is the hallmark of clinical surgical abdominal emergencies

A

Bilious emesis

31
Q

What is the most common site of gastric perforation

A

Greater curvature

Abd XR: pneumoperitoneum, NG in the pelvis

Sx Acute abdomen, lethargy, apnea, RDS, bloody output from NG
Mx: Exlap, gastrostomy

32
Q

It is due to lack of recanalization of duodenum

A

Duodenal atresia

  • normally happens 8-10 weeks GA
  • Dx: Abd XR: double bubble (distended stomach and prox duodenum); +/- bilious output
  • Mx: gastric decompression, TPN, ECHO
  • Repair not an emergency
33
Q

It is the most severe complicaion of intestinal malrotation

A

Midgut volvulus

  • Incidence highest first 2 months
  • Sx: feeding intolerance and bilious emesis, bloody stools, late abd distension
  • pathophysiology: obstruction and vascular compromise
34
Q

What is the normal location of:
a. duodenojejunal junction
b. ilocecal valve

A

a. Left upper quadrant
b. right lower quadrant

In malrotaton: duodenojejunal: midabdomen, ileocecal valve: RUQ

35
Q

Gold standard Dx for malrotation/ volvulus

A

UGI
(corkscrew sign)

Ultrasound: whirlpool sign by superior mesenteric vessels

36
Q

What are the steps of the Ladd procedure

A
  1. Devolvulizing the midgut
  2. Adhesiolysis- separate duodenaljejunal junc and ileocecal
  3. Verticalizing the duodenum
  4. Performing appendectomy
  5. Replacement of the small bowel on the right hemi-abdomen and the colon on the left hemi-abdomen

done when no sigificant ischemia

37
Q

What is pathology in small bowel atresia

A

Vascular occlusion
* can involve mesentery based on extent

38
Q

True or false:
Passage of meconium rules out small bowel atresia

A

False
* Its commonly seen symptom failure to pass meconium

Factor associated with inc M&M prematurity, other malformation, multiple atresia (can lead to short bowel)

39
Q

What is the common site for spontaneous perforation (SIP)

A

terminal ileum

Dx: Abd XR pneumoperitoneum w/o NEC

No reason, no vascular compromise
More common in males
risk factor: perinatal use and postnatal indomethacin, preeclampsia

40
Q

Goal mgt of SIP

A

for <1kg: Percutaneous drain at bedside to:
1. release pressure- eliminate hypoperfusion
2. outlet spilled intestinal content

For >1kg: Laparotomy (Primary closure vs temp ostomy)

Long term consequence: enterocutaneous fistula, stricture

41
Q

True or false: NEC exclusively occurs in preterm infants

A

False
* 5% of preterm<30 wks
* 10% of term (from hypoperfusion- CHD, sepsis)

findings: intestinal ischemia leading to damage to intestinal mucosa, bacterial invasion, sepsis
- poor mucin production overpermeability of intercellular junction
- risk factors: H2 blockers, nonhuman milk, hyperosomolar meds/formula

42
Q

NEC staging and mgt

A
43
Q

What are the parameters to determine need for exploration (SIP/NEC)

A
  1. worsening acidosis
  2. inc need cario-resp support
  3. worsening coagulopathy
  4. inc erythema/ bluish discoloration

Rationale: ischemic (not necrotic) intestinal tissue keeps the patient in a vicious circle

44
Q

Signs of esophageal atresia

A

early postnatal period:
* difficult feeding
* excessive oral secretions
* cyanosis/ apnea during feeds

Prefer Dx test: flexible esophagoscopy/ bronchoscopy
UGIS after surgical repair- leak and stricture

45
Q

Ultrasound finding for hypertrophic pyloric stenosis

A

Thickness: 3mm
Length: 15 mm

46
Q

What are the functions of the GI tract

A
47
Q

What is the GI cellular origin and function

function at maturity

A

Endoderm: digestion and absorption
Mesoderm: muscle
Ectoderm: enteric nervous system-Auerbach plexus is between muscle layers, Meissner plexus adjacent mucosal layer.

48
Q

What are the sections of the GI tract embryologically

A

common sources of blood supply, innervation, and lymphatic drainage with those derived from the same precursor
Foregut: celiac artery
Midgut: superior mesentery artery
Hindgut: inferior mesentery artery

49
Q

What are the ultrasound findings of biliary atresia

A
  • sclerosed bile ducts
  • absence of a gallbladder
  • “triangular cord” sign
50
Q

Findings in chylous ascites

A
  • milky fluid
  • elevated triglyceride
  • cell count with lymphocyte predominance
  • low glucose.
51
Q

Predictors of outcome of CDH

A

1.Degree of pulmonary hypoplasia
* Lung to head ratio (<0.6)
* Observed vs expected total lung volume
2. Pulmonary hypertension
3. involvement of the liver
4. Prematurity

52
Q

Delivery room mgt of CDH

A
  1. place a NGT soon after delivery for decompression of the stomach and intestines
  2. prompt intubation for respiratory distress

Goals in vent setting: PIP<25, preductal sats >70%

53
Q

What are the fetal predictors of outcome of CDH

A
  1. Associated anomalies
  2. Extent of lung hypoplasia
  3. Position of the liver- liver up worst prognosis, highly predictive of ECMO

LHR and survival
* >1.35- 100%
* 1.35-0.6 - 61%
* <0.6- no survival

observe/expectrd LHR
<25% severe, survival 10%liver up, 25% liver down
<15 with liver up 100 mortality

54
Q

long term complications of CDH

A
  1. sev pulm hypoplasia
  2. pulm htn
  3. chronic lung disease
  4. neuro cog delay
  5. hearing loss- can be late
  6. chest wall deformity
  7. scoliosis
  8. poor growth
  9. hernia reoccurence
55
Q

What is the most common primary hepatic malignancy in childhood

A

Hepatoblastoma

  • usually isolated, but may be associated with Beckwith-Wiedemann syndrome, isolated hemihyperplasia, familial adenomatous polyposis coli, or trisomies.
  • Treatment with initial surgical resection versus neoadjuvant chemotherapy is determined by risk stratification based on extent, location, and histology.
56
Q

What is the serum marker for hepatoblastoma

A

Serum α1-fetoprotein (AFP)

can be a useful marker for response to treatment

useful marker for response to treatment

57
Q

How does phototherapy work for hyperbilirubinemia

A
  1. structural/geometric isomerization- Lumirubin- irreversible excreted via bile and urine (major contributor to the lowering of total serum bilirubin)
  2. Photo isomerization- reversible (hydrophilic, reduce the exposure of the brain to the toxic, lipid-soluble configuration).
  3. Photo oxidation

Neontal boards J (19 decks)

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