Based on 2010 Content Specs

2. Acute

3. Know the evaluation of a patient with acute abd pain

4. Need to do more extensive evaluation beyond the H/P if they have si/sx suggestive of a potential surgical emergency, i.e.

5. Appendicitis: tenderness localized to RLQ

6. SBO: absent bowel sounds, abd distention

7. Perforated viscus: rigid abd, distention, fever, toxicity

8. Malrotation: diffuse tenderness, abd distention

9. Intussusception: severe crampy abd pain,alternating with periods of relief

10. Peritonitis: fever, toxicity, diffuse abd tenderness

11. Understand the mechanism of injury by which NSAIDs may produce GI sx

12. Erosive gastritis

13. Recognize appendicitis as a cause of acute abd pain

14. Know the lab eval of appendicitis

15. Although fatigue and anorexia are often the initial sx

16. Abdominal CT is the most sensitive and specific test for dx of appendicitis; debate about whether or not rectal contrast is needed

17. No blood tests are particularly god in terms of sensitivity and specificity

18. Fatigue, anorexia, indigestion or periumbilical pain that gradually moves to the RLQ, fever (often 100-102 degrees), N/V then occur

19. Pain that suddenly resolved indicates rupture; pain will recur in short order

20. Recognize the si, sx and lab findings of acute pancreatitis in children

21. Sx: epigastric pain and vomiting

22. Si: epigastric tenderness on palpation; if more severe case may have signs of intravascular volume depletion

23. Lab: elevated amylase and lipase; more severe may have hyperglycemia, hypocalcemia, high BUN and cre, low Hct and coagulopathy

24. Formulate a ddx for chronic or recurrent pancreatitis in children

25. CF

26. Hereditary pancreatitis

27. Anatomic lesions

28. Recognize the presence of intussusception

29. Occurs when a part of the intestine “telescopes” into an adjoining segment of bowel. Can drag mesentery in along with it, leading to venous obstruction, edema of the bowel. The edema can then eventually lead o arterial obstructionischemiaperforation

30. Usually occurs between age 2 months and 5 years; peak is age 4-10 months

31. Presents with abd pain, vomiting and bloody stools; currant jelly stools can occur days after the initial abd pain; if an infant they may have episodes where they draw up the legs, scream, and then after awhile they go back to normal – this is b/c it can be episodic in nature but then eventually it gets constant

32. During an episide you might be able to feel the sausage shaped mass in the upper abd

33. Diagnostic and therapeutic test of choice is the air-contrast enema, it will actually reduce the intussusception 90% of the time without needing surgery; but don’t do it if they have peritonitis, instead they need surgery

34. Recognize the presence of malrotation

35. Most commonly caused by nonrotation; in this case the cecum is on the left side and the small intestine is all on the right side of the superior mesenteric artery. Leads to a short mesentery and minimal fixation of the bowel to the posterior peritoneal cavity. The duodenum is small and it fuses with the colon via a common mesentery around the superior mesenteric artery. Adhesions known as Ladd bands fix the mesentery to the right abdominal wall.

36. 90% of cases present in the first year of life; often in the first month of life

37. Presents as an acute process with episode of bilious emesis due to an acute midgut volvulus; later signs include rectal bleeding, hematemesis, palpable bowel loops, and a distended abdomen with possible respiratory compromise and systemic shock

38. Radiographs will often show a gasless colon with the “double bubble” sign due to duodenal obstruction

39. Recognize the presence of volvulus

40. Is a twisting of the intestine causing obstruction

41. Malrotation disorders set up the situation for a volvulus to occur

42. On imaging will see the bird beak sign (do and upper GI series); If it is only partially obstructed there may be a corkscrew pattern visible

43. Requires surgery a Ladd procedure must be done

44. Recognize the likely sites of injury following blunt abd trauma

45. Most likely to injure the liver and spleen

46. Formulate a management plan for a patient with post op intestinal obstruction

47. Chronic

48. Know the uses and abuses of anticholinergic drugs in the tx of GI dz

49. Know the ddx of recurrent abd pain in an 11 year old girl

50. Recognize the clinical manifestations of chronic recurrent abd pain

51. Plan the management of patients with chronic recurrent abd pain

52. If it is one of the functional bowel disorders then tha management is usually aimed at txing the symptoms

53. Plan the eval of a child with chronic recurrent abd pain

54. Need to look for red flag symptoms:

55. Weiht loss, unexplained fevers, pain radiating to the back, bilious emesis, hematemesis, hematochezia/melena, chronic diarrhea, GI blood loss, oral ulcers, dysphagia, unexplained rashes, nocturnal sx, arthritis, anemia/pallor, delayed puberty, decel of linear growth velocity, family h/o inflammatory bowel dz

56. Any of these require further evaluation to look for an organic cause prior to a dx with a functional bowel disorder assocated with abdominal pain or discomfort

57. Know how to recognize and manage irritable bowel syndrome

58. IBS = abdominal pain or discomfort that is relieved with defecation and is associated with either a change in frequency or consistency of the stool

59. Management is initially addition of a fiber supplement, which can help in 50% of cases. Other txes are antispasmodics (hyoscyamine), antidiarrheals (loperamide), cholestyramine, probiotics. Second line therapies include psychotherapy, CBT, hypnosis

60. Recognize the role of lactose intolerance in recurrent abd pain

61. Lactose breath hydrogen test can be used to diagnose

62. Abdominal mass

63. Formulate an age appropriate ddx for an abd mass in a pediatric patient

64. Vomiting

65. GI and non-GI causes of vomiting

66. Understand the age related ddx of vomiting

67. Newborn:

68. Intestinal atresia / webs bilious, depending on level of lesion

69. May occur at level of esophagus, duodenum or jejunum

70. Meconium ileusbilious

71. Strongly associated with CF; need to get genetic testing

72. HIrschspring Dz bilious or nonbilious

73. Hx of non-passage of stools in nursery suggestive; may need bx of rectum or colon and it would show a lack of ganglion cells

74. NEC bilious or nonbilious

75. Plain films may show intestinal pneumatosis

76. Inborn errors of metabolismbilious or nonbilious

77. May have acidosis or hypoglycemia

78. Age up to 3 months

79. Pyloric stenosisnonbilious

80. Hypochloremic metabolic acidosis

81. Malrotation with midgut volvulus bilious

82. May have plain films that show air fluid levels, paucity of gas in the distal bowel

83. Needs surgical consultation

84. Inborn errors of metabolismbilious or nonbilious

85. May have a normal newborn schrren

86. See above

87. Milk/soy protein allergy bilious or nonbilious; may have gross or occult blood

88. May have h/o extreme fussiness

89. May have fecal occult blood positive

90. GERnonbilious; may have gross or occult blood

91. Emesis usually w/in 30mins of feeding

92. Sx worse in the supine or flat position

93. Child abuse nonbilious

94. Check for anterior fontanelle fullness and si/sx of CNS bleeding; may need imaging

95. Age 3-12 months

96. Gastroenteritisnonbilious initially, may progress to bilious

97. Stool studies may help establish offending pathogen

98. Intussusception bilious

99. May have abd distention

100. Plain films with air fluid levels, paucity of distal bowel gas

101. Currant jelly stools

102. Need suegical consult

103. May be able to reduce by a contrast enema

104. Child abusenonbilious

105. See above

106. Intracranial mass lesionnonbilious

107. May have fullness of anterior fontanelle; CNS imaging may be diagnostic

108. Understand the significance of bilious vomiting

109. Usually pathologic, often indicates some type of an obstruction

110. Indicates a problem beyond the ampulla of Vater

111. Know the management of a newborn with bilious vomiting

112. See above

113. Know the eval and management of a 3 week old infant with projectile vomiting

114. Think of the above possible issues

115. Vomiting from infectious and noninfectious causes

116. Understand that vomiting may be a sx of a systemic illness

117. Like UTI, sepsis, inborn error of metabolism; especially true in newborns

118. Toxic ingestions

119. Structural causes of vomiting

120. Recognize the clinical findings of pyloric stenosis

121. Presentation at age 2-6 weeks with persistent projectile vomiting

122. Hypochloremic metabolic alkalosis, hypokalemia

123. Know the clinical situations in which duodenal atresia may occur

124. More common in trisomy 21

125. Double bubble sign

126. Presents in newborn period; due to a failure of canalization of the duodenum

127. Know the eval and management of a 2 y/o child with the acute onset of vomiting and obstruction

128. Think of gastroenteritis

129. Also think of intussusception, toxic ingestions, foreign bodies

130. Know the presenting si and sx of an antral web

131. D/Os associated with chronic vomiting

132. Plan the eval of a child with cyclic vomiting

133. By definition, cyclic vomiting comes in recurrent episodes of N/V without an identifiable cause, and has

134. 3 or more episodes of recurrent vomiting

135. intervals of normal health between episodes

136. episodes that are stereotypic with regard to sx onset and duration

137. lack of lab or radiographic evidence to support an alternative dx

138. During an episode, to establish the dx must rule out other pathology. Need to check for intraabd pathology, CNS pathology

139. During an episode it is helpful to check lytes, and get some metabolic studies (ammonia, urine organic acids, acylcarnitine, plasma amino acids, pyruvate and lactate

140. TX: if older than age 5 often ppx with amitryptiline; if under age 5 cyproheptadine is of choice

141. Esophageal D/Os

142. Motility

143. Recognize that regurg is physiologic in a significant number of infants

144. Recognize the diffs between rumination and regurgitation

145. Rumination is a voluntary, habitual regurg of stomach contents into the mouth for self stimulation

146. Regurg is the passage of stomach contents into the oral pharynx. Not voluntary.

147. Trauma

148. Understand that corrosive esophageal burns after alkali ingestion can occur in the absence of mouth burns (see Poisonings_

149. Know how to dx GER (see other sections)

150. Know the sx of an esophageal foreign body

151. GI sx can include dysphagia, excessive drooling, poor feeding, vomiting, gagging, retching, anorexia, neck or throat pain, sensation of foreign body in the throat, refusal to eat or drink

152. Respiratory sx can be caused due to the object compressing on the posterior tracheal wall or larynx. It could produce cough, stridor, wheezing, choking

153. Know the tx of same

154. Make sure the airway is controlled

155. If there are any sx it needs to be removed

156. If there are no sx, then monitoring the patient and getting a repeat film 12-24 hours later to see if it is moving can be done

157. If it is sharp it should probably be removed pretty quickly

158. Button batteries need to come out immediately due to the high risk of complications (corrosion, tissue damage)

159. GER

160. Recognize the sx and complications of GER (e.g. poor growth, pain, anemia, dystonic movements)

161. Know how to eval a patient who has GER

162. If they have persistent reflux (more than 3 months) or complicated reflux (having hematemsis or respiratory sx) then they need more involved workup

163. Includes GI films to r/o malrotation and hiatal hernia; pH probe or esophageal impedance, gastric emptying scan, esophageal motility eval, upper endoscopy w or w/o bx

164. Know the tx for GER

165. Know the px of GER

166. It is often physiologic and does not cause other problems

167. Often peaks at age 4-6 months

168. Most babies (90-95%) will outgrow it by age 12 months

169. Know how to tx significant GER

170. GER itself usually does not need direct tx since it is physiologic, parental reassurance is what AAP wants with otherwise healthy babies

171. Formula can be thickened as a means to address the vomiting; addition of 1-2 tbs of rice cereal per oz of formula is the recipe in medstudy; note that this can cause some other feeding probs

172. Don’t give meds if otherwise uncomplicated GER. If pharmacologic tx is done, start with an H2 blocker or a PPI. If there are more severe and persistent complications, especially respiratory, then apparently okay to start with PPI

173. Surgical tx is a final option (note that in this case the kis has GERD, not just GER)

174. Know the association between GER and respiratory sx

175. Hoarseness, laryngitis, cough, pneumonia and apnea

176. Diarrhea

177. Diarrhea caused by infectious mechanisms

178. Plan the eval of a patient with suspected giardiasis

179. Stool O/P, ELISA and direct fluorescence antibodies can be used to detect and diagnose

180. Giardia antigen based tests are more sensitive than the stool O/P

181. Know the common etiologic agents of infectious diarrhea in children

182. Infants and ToddlersChildren age 5 to 12 yearsAdolscentsRotavirusNorwalk virusNorwalk and Norwalk-likeEnteric adenovirusGiardiaCampylobacterSalmonellaEPECETECShigellaEHECEHECCampylobacterETECSalmonellaYersiniaSalmonellaShigellaGiardiaCampylobacter

183. Recognize the si/sx of enteropathogenic E. coli infxn

184. Severe acute watery diarrhea, vomiting

185. Acute and chornic, epidemic and endemic diarrhea in infants (<6mos of age)

186. Recognize the si/sx of campylobacter diarrhea

187. Distinguish between salmonella and shigella with regard to pathophys and sx

188. Shigella is often more severe due to systemic invasion by the shiga toxin; produces neurologic sx including seizures

189. Salmonella can cause high fevers as well as bloody stools, but the severity of illness is not usually as bad

190. Tidbits on shigella:

191. Humans are the only natural host

192. Antimicrobial tx IS indicated

193. Kids can’t go back to school until they have a negative stool culture

194. Plan the tx for a pt with e coli diarrhea

195. Correct fluid and electrolytes, give supportive care

196. DO NOT GIVE ANTIMICROBIALS until you have a negative shiga toxin test and only if the sx are protracted or the kid isn’t getting better

197. Recognize the clinical si and lab findings associated with e coli O157:H7 infxn

198. Important to know that the shiga-toxin producing e. coli (STEC, formerly known as EHEC) cannot ferment sorbitol and to culture it you have to use MacConkey agar; therefore know that a special test has to be ordered if this infection is suspected and then it has to be verified often by a state lab

199. Remember it causes HUS (TCP, hemolytic anemia, nephropathy) and therefore those lab problems

200. Illness often biphasic, starts off as a bad diarrhea and then the next phase is more systemic, possibly more severe diarrhea (this is when the HUS would be seen)

201. Typical incubation period of 3-5 days but can be as long as 8 days

202. Not only due to undercooked hamburger. Also associated with unpasteurized milk and apple cider as well as petting zoos and dairy farms

203. Diarrhea caused by noninfectious mechanisms

204. Recognize the sx, available tests and tx of milk protein intolerance

205. Recognize that colitis in a breastfed infant is a possible manifestation of food allergy secondary to allergens in the mother’s diet

206. Know the ddx of noninfectious intractable diarrhea in infancy

207. Enteric infection and associate compromise in food intake and absorption lead to a variable loss of digestive and absorptive capacity in infants; a milder form is transient lactose intolerance (post0infectious lactose intolerance)

208. DDX:

209. Immunodeficiency dz, CF, celiac dz, congenital short gut, congenital chloride diarrhea, congenital sodium diarrhea, VIPoma, acrodermatitis enteropathica, autoimmune enteropathy

210. Per Nelson’s “common” are postinfectious secondary lactose deficiency, cow’s milk.soy protein intolerance, celiac dz, CF and AIDS enteropathy

211. Chronic nonspecific diarrhea

212. Understand the dx and px of chronic nonspecific diarrhea of early childhood (toddler’s diarrhea)

213. Onset at age 6-18 months; have multiple (6-12/day) loose, explosive bowel movements containing food particles; growth is normal as long as not on a restricted diet

214. Tx = reassurance, lifestyle modifications (reducing intake of high carb load beverages) and avoidance of restrictive diets

215. Recognize that poor growth, fever, melena are incompatible with the dx of chronic nonspecific diarrhea

216. Understand that extremely low fat diets, sorbitol, fruit juices, and excessive water consumption may cause chronic nonspecific diarrhea

217. Protracted diarrhea

218. Know that malnutrition, chronic infection, systemic disease and immunodeficiency are predisposing factors to the development of diarrhea

219. Plan the initial eval of an infant with protracted diarrhea

220. Understand the importance of enteral nutrition in txing protracted diarrhea

221. Constipation

222. Know the complications of Hirschsprung disease

223. Enterocolitis; usually occurs at age 2-4 weeks and is characterized by explosive foul smelling stool with a fever, abd distentions; diarrhea may be bloody

224. Intestinal obstruction

225. Know how to distinguish between simple constipation and Hirschsprung dz in the newborn period

226. Simple constipation: child will have passed meconium as expected; normal caliber stools; frequent encopresis; usually no associated anomalies; abundant stool in the vaut

227. Hirschprung: failure to pass meconium in first 24 hours; “pencil thin” stools; no encopresis; associated with other anomalies (Down syndrome); absence of stool in rectal vault

228. Know the clinical manifestations of Hirschsprung dz

229. See above

230. Recognize the si/sx of fecal overflow incontinence

231. Know the action of laxatives, stool softeners and lubricants

232. Recognize the role of rectal bx in a infant with suspected Hirschsprung dz

233. Often diagnostic

234. Jaundice

235. Neonatal and infancy

236. See “fetal and newborn” section

237. Recognize cholecystitis in children

238. Keep in mind the entitity chronic acalculous cholecystits as well as gallbladder dysmotility

239. Sx will be same as for cholecystitis but with basically normal labs as well as US. Need to get a nuclear med GB emptying scan to check for it

240. Recognize the si/sx of biliary atresia

241. Persistent jaundice with conjugated hyperbilirubinemia

242. If progresses without tx it can cause liver to be firm and palpable, eventually the spleen to be palpable

243. Know the dx tests for biliary atresia

244. DISIDA or other hepatobiliary nuc med scan

245. Know the management of biliary atresia

246. Needs surgical tx, fairly high number progress to liver failure, need transplant

247. Children and adolescents

248. Know how to eval a child with conjugated hyperbili

249. Know the lab findings of hepatitis

250. Recognize the si/sx of Wilson dz

251. Recognize the si/sx of infectious hepatitis

252. Recognize the si/sx of liver dz due ti alpha 1 antitrypsin deficiency

253. Recognize the si and sx of cholelithiasis and choledocolithiasis

254. GI bleeding