GI and Nutrition Flashcards
FAP = Familial Adenomatous polyposis
numerous (>100) adenomatous polyps in intestines. Risk colorectal cancer, hepatoblastoma, medulloblastoma. Epidermoid cysts.
8-year-old girl who has hyperpigmented macules in her mouth and a history of GI bleeds. Her dad and brother have something similar. What type of cancer is she at risk for?
Peutz Jeghers syndrome
- mucocutaneous hyperpigmented macules + GI polyps (benign, in small intestine, can have bleeding/intuss)
- inherited cancer syndrome AD for colorectal ca
- annual upper and lower endoscopy by age 8 or if symptoms
- polyps present while young
button battery ingestion
if < 12 hr, can do honey or sucralfate
emergent removal within 2 hr if esophageal or gastric (<5 yr and >20mm)
GI Complications of CF
- exocrine pancreatic insufficiency
- pancreatitis
- CF related diabetes d/t damage to pancreas
- meconium ileus in younger pt
- distal intestinal obstructive syndrome (DIOS) in older pt (obstruction, RLQ pain and palpable mass)
FPIES
- diagnosis gold standard: oral food challenge by allergist
- Age 2-7 mos with intro solids or formula
- Milk, soy, rice, oat egg (classic is rice)
- sx: profuse vomiting, pallor and/or lethargy, diarrhea (no resp or rash sx) very severe vomiting
- may need anti-emetic and IV fluids d/t dehydration
- eliminate trigger food
- no need to eliminate from maternal diet
- refer to allergist
- oral food challenge can be done to see if they’ve outgrown (usually by age 3-5 yrs) - try 12-18. mo later
- don’t need stool tests, imaging or endoscopy
- no epi pen needed
Infant Dyschezia
ROME criteria
- < 9 mo
- straining prior to defecation with crying, facial discoloration for >10 mins before successful or unsuccessful passage of stool
- no other health problems
- NOT constipation
Reassurance
Rumination disorder
- repeated regurgitation of food 1+ month
- often daily, not in sleep
- usually presents at 3- 12 mo
- treatment behavioural and gum chewing
how many ml in oz
1 oz = 30 ml
formula is 20cal/ oz or 0.67 cal/mil
NAFLD
- chronic hepatic steatosis
- start screening in age 9-11 for all obese children or overweight with other obesity risk problems (Ex. diabetes, OSA). Screen q2-3 yr
- screen with ALT (>2x ULN for >3m)
- liver US is not used for NAFLD - you would need elastography
don’t do US
management
- counsel on diet and exercise
- rpt labs q1-6 mo
- r/o other liver problems if symptomatic or red flags
Pediatric acute liver failure
INR >1.5 not correcting with vitamin K and encephalopathy OR >2 without encephalopathy
with signs of liver damage, no chronic liver problem
hepatoblastoma associated geentic conditions
beckwith wiedemann or other hemiphyperplasia or overgrowth syndromes
screen with AFP
AXR and AUS
celiac long term complication
lymphoma
EoE diagnosis
EGD and biopsy (>15 eosinophils per HPF or signs of eosinophilic inflammtion
don’t need PPI response for diagnosis
Management
- dietary management (2-6 food elimination)
- PPI can be used for symptoms
- swallowed steroids x 6-8 weeks
H pylori
- don’t do urea breath test if you think theres an ulcer from h pylori
Diagnosis
- upper endoscopy with biopsy (2 weeks post PPI, 4 weeks post abx)
Oral rehydration therapy
15 min to 30 min after administration of oral ondansetron.
Mild: ORS 50ml/kg over 4h
Mod: ORS 100ml/kg over 4h
Severe: IV 20-40ml/kg x1h
Galactossemia
What is it: inability to convert galactose into glucose (missing GALT enzyme), and this causes galactose to build up in the body ( brain, liver and other tissues)
Inheritance pattern: AR
Age of Onset: first few DOL/ within a few days of starting formula (may be delayed by soy formula use)
Presentation: jaundice, vomiting,diarrhea, hepatomegaly, poor feeding, lethargy, E.coli sepsis, cataracts
Labs: hypoglycemia, increased plasma galactose, hyperbilirubinemia, abnormal LFTs, metabolic acidosis, glycosuria, hemolytic anemia
Dx: SHOULD BE PICKED UP ON NMS, , elevated galactose, reduced GALT enzyme activity, increased plasma amino acids and molecular genetic testing
Tx: immediate removal of galactose (all dairy) while you do confirmatory testing
Outcomes: if not treated (with dietary modification) then liver failure, sepsis, and neonatal death, despite treatment- there is an increased risk of DD, speech problems and abnormalities of motor function. Almost all females will have premature ovarian insufficiency
Crohn’s
Crohns
“Gum to Bum”
Abdominal Pain
Diarrhea
Perianal disease
Weight loss, growth failure
Involves any part of GI tract
Skip lesions
Rectal Sparing
Fistula, Abscess, Stricture
Linear ulcers
Transmural involvement
protein losing enteropathy diagnosis
stool A1AT
Ulcerative Colitis
Rectal bleeding
Bloody diarrhea
Abdominal pain
NO perianal disease
Risk for toxic megacolon
Colon only
Continuous (Paintbrush)
No rectal sparing
No fistula, abscess, stricture
Inflammation limited to mucosa
No granulomas or Crypts
risk of primary sclerosis cholangitis
short stature, neutropenia, bone marrow failure, pancreatic insuff
schwachman diamond syndrome
high a1at in the stool
protein losing enteropathy
high fecal elastase
pancreatic insufficiency
- CF
- Schwachman diamond
- chronic pancreatitis
most common cause of low weight and poor growth in IBD
poor nutritional intake
genetic mutation of the polyposis syndromes
autosomal dominant
