2. Recognize by Hx

3. Recognize recurrent bacterial infections as a manifestation of quantitative or qualitative leukocyte disorders

4. Know that children with severe neutropenia may become infected with their own skin and bowel flora

5. The most common offending organisms are staph aureus and gram-negative bacteria

6. Recognize by PE

7. Recognize palpable bruises in areas not exposed to trauma as distinctly abnormal

8. Recognize mucosal ulcerations as a sign of neutropenia

9. Mucosal ulcerations and also gingival inflammation

10. Distinguish between bruising due to TCP and normal bruising in an active child

11. Bruises seen in normal active children are usually pretibial; bruises seen on kids with TCP are often on the arms and trunk as well as the legs

12. Recognize that child abuse may be a cause of bruising in a child with a normal platelet count

13. Bruises related to abuse tend to be more generalized and do not have associated petechiae or TCP

14. Recognize that vasculitic disorders my be a cause of bruising or purpura in a child with a normal (or increased) platelet count

15. Know that TCP or functional plt disorders may cause bruising, petechiae, epistaxis, or GI bleeding but rarely cause deep muscle or joint bleeding

16. Deep muscle or joint bleeding are indicative of hemophlia and other blood coagulation disorders

17. Formulate the ddx for a pt with a purpuric rash

18. Recognize that children with hemihypertrophy and somatic overgrowth syndromes should be periodically evaluated for the development of embryonal tumors

19. This includes Beckwith-Wiedman

20. Patients with these syndromes have a high incidence of Wilms and hepatoblastoma

21. Surveillance for development of Wilms include following serum AFP levels, US for microscopic hematuria, and also abd u/s q3months until age 5years

22. WAGR syndrome: Wilms, aniridia, GU abnormalities, retardation)

23. Interpretation of lab results

24. Recognize the physiologic anemia of infancy and understand that further lab eval is not necessary

25. Nadir is reached at about age 2 months with avg hgbs of about 9-11

26. At birth there is a drop in epo production due to the dramatic increase in arterial PaO2

27. Fun fact: RBC lifespan during the first 6-8 weeks of life is 90 days, then increases to the usual 120 day lifespan after that age

28. Understand the concept of physiologic anemia

29. Know that Fe deficiency anemia and thalassemia minor are the most common causes of microcytic anemia

30. Know that a total leukocyte count and leukocyte differential count are needed to dx neutropenia

31. May have a normal WBC count but an ANC in the neutropenic range

32. Know that neutropenia is usually defined as a neutrophil count <1000

33. Mild neutropenia = ANC 1000-1500

34. Moderate neutropenia = ANC 500-1000

35. Severe neutropenia = ANC <500

36. Recognize that bleeding time is a test of platelet function and blood vessel function

37. Also know that we don’t do this test anymore

38. Recognize that TCP is defined as a plt count <150

39. Understand the normal variation in hgb concentration and MCV during childhood

40. MCV falls during the first 6-12 months to an approx nadir of ~77 and then rises through rest of childhood and adolescence

41. Hgb initially falls, as above

42. In the rest of childhood it keeps up with growth, gradually increasing; then in adolescence it further increases so that male > female hgb (due to androgen)

43. Erythrocyte disorders

44. Nutritional anemias

45. Understand that Fe deficiency anemia causes nonhematologic effects such as behavior and learning disturbances

46. Unclear whether these effects are reversible with Fe treatment; goal of Fe tx is to try and prevent them from occurring in the first place

47. These effects can occur even without presence of anemia; so if the hgb is normal but the MCV is low, need to tx with Fe

48. Know that dietary deficiency is the most common cause of Fe deficiency anemia in young children

49. Dietary iron is absorbed in the duodenum

50. The presence of acidic foods enhances the absorption of iron

51. Human milk has less iron than formuka, but it is mush more well absorbed

52. Heme iron (i.e. from meats and shellfish_ is better absorbed than non-heme iron (from grains, vegtables, etc)

53. Calcium inhibits Fe absorption

54. Know that cow milk contains very little bio-available iron and that an infant with Fe deficiency anemia often drinks large amount of cow milk

55. Very important to get a good dietary hx

56. Understand the need to look for bleeding as a cause of Fe deficiency anemia in a child with a normal diet

57. Look for melena, hematochezia, heavy menses; also check for fecal occult blood

58. Know how to dx Fe deficiency anemia

59. Microcytosis

60. Elevated RDW; decreased retic, RBC number and mean cellular hgb

61. More advanced tests: ferritin (total body iron stores) may be low, but in cases of acute illness it may be elevated as it is an acute phase reactant; TIBC may me elevated; transferring saturation is low

62. Mentzer index = MCV/RBC; if it is >13 it is indicative of Fe deficiency, if <13 it is indicative of a thalassemia (but this is only a screen)

63. Know that tx for Fe deficiency with Fe sulfate should continue after the hgb concentration has returned to normal

64. Should see increases in MCV, hgb and retic counts in about 1-4 weeks, and these should be checked in that timeframe to see if there is a result of the Fe tx

65. Usual dose is 6mg/kg/day of elemental Fe and it can be in divided doses. Giving it with vitamin C can help improve absorption

66. Reason for continuing the tx beyond the initial improvement is to replenish iron stores and prevent repeat problems

67. Know that IM injxns or erythrocyte infusions are not appropriate for a child with routine nutritional Fe deficiency

68. Recognize vit B12 or folate as a cause of macrocytic anemia

69. Macrocytosis = MCV >100

70. Megaloblastic = presence of macro-ovalocytes snd hypersegmented neutrophils

71. B12 associated sx

72. Glossitis (smooth painful tongue)

73. Neurologic sx including ataxia, paresthesias and difficulty walking as well as decreased reflexes, dimished vibratory and positon sense

74. Altered mental status in late stages

75. Document the dx of B12 or folate deficiency with specific measurement of serum B12 concentration or serum or erythrocyte folic acid concentrations before beginning replacement tx

76. Regarding folate, the RBC / erythrocyte folate level is the one to check because the serum folate level is variable and may not acutely reflect that folate status

77. Know that B12 deficiency may occur following small bowel resection or as a result of a maternal vegan diet in a child who is exclusively breastfed

78. If there are gut probs in the patient, think B12

79. Remember intrinsic factor (made in the parital cells) required to absorb the B12 in the ileum. Also requires transcobalamin II within the cells to be converted to active form

80. Congenital pernicious anemia = abnormal or deficient IF; usually declares itself in first year of life

81. Juvenile pernicious anemia= anti-IF autoantibodies; presents later than congenital

82. Also note that PPIs and metformin are two common meds that can lead to B12 deficiency

83. Know that ingestion of goat milk as a principal source of nutrition in infancy is a cause of folate deficiency

84. Hemolytic anemias

85. Know that G6PD is a common X-linked disorder

86. Hence males more affected than females

87. Know that sudden onset of pallor and anemia may be a manifestation of G6PD deficiency

88. Indicates an acute hemolytic process

89. Should also be considered in any newborn who manifests jaundice in the first 24 horus after borth, is jaundce depiste being exclusively formula fed, or has a fam hx of RBC disorders

90. Know that causes of hemolysis in pts with G6PD and manage appropriately

91. Main thing is to avoid agents of oxidative stress

92. Meds: sulfonamides, antimalarial drugs, nitrofurantoin, cipro

93. Also illnesses can increase the oxidative stress and led to more hemolysis

94. Tx = supportive care, giving PRBCs if needed

95. Be aware of the clinical differences in the forms of G6PD seen in patients with different ethnic backgrounds

96. More severe in those of Asian and Meditarranean descent, and they need to avoid the meds above, as well as ASA and APAP

97. Understand that sickle cell disease can be dxed at birth

98. Newborn screen

99. Know that kids with SCD are particularly vulnerable to death from overwhelming bacterial sepsis and require early evaluation and tx when febrile

100. Clinical guidelines for intervention:

101. All pts with SCD who develop fver >101 is mandated and administration os a 3rd generation cephalosporin (ceftriaxone, cefotaxime) plus clinda or vanco for severe infections is the current practice (Per PIR article, 2007)

102. The spleen is the first organ to experience major damage in SCD; therefore infection w encapsulated orgaisms (strep penumo) is especially concerning

103. Recognize the findings of an enlarged spleen and worsening anemia as indicative of sequestration crisis in SCD

104. Understand that immediate intervention with IVFs and/or blood is the tx for acute sequestration crises

105. Recognize painful swelling of the hands or feet as a manifestation of SCD in young children

106. Understand the use of ppx penicillin in kids with SCD

107. Due to loss of functional spleen and susceptibility to strep pneumo

108. Main rec is to start by age 3months and continue it up to age 5years

109. Growing resistance PCN and cephalosposins, hence tx as above

110. Recognize increasing pallor, decreased hgb concentration, and a decreased retic count as findings in an aplastic crisis in SCD

111. Know that acute chest syndrome and painful crises are common manifestations of SCD

112. Acute Chest = radiographic appearance of a new pulmonary infiltrate along with a fever

113. Can be due to infection, VOC, fat embolism

114. Tx = broad spectrum abx, including a cephalosporin and a macrolide, as well as oxygen, hydration, incentive spriometry and early intervention with simple transfusion tx for associated hypoxia or hct <18%

115. Painful crises are most common cause of hospitalization

116. Frequent admissions for pain crises (>6/year) are a known risk factor for early death in SCD

117. Management should include aggressive pain management with age appropriate patient controlled analgesia (morphine or hydromorphone), NSAIDs (ibup or ketorolac), hydration, PT, and ancillary therapies like guided therapy/relaxation, etc

118. Know that thalassemia major usually presents as a severe hypochromic, microcytic anemia with enlargement of the liver and/or spleen

119. Recognize the association of cholelithiasis in patients with SCD

120. 42% of patients with Hb-SS have cholelithiasis by dolescence.

121. Cholecystectomy is only indicated if they hav suffer abd pain or cholestatic jaundice due to common duct obstruction; if they get cholecystitis then they are txed with abx and supportive care and have elective cholcystectomy weeks after the acute event

122. Know that priapism os a common manifestsation of SCD

123. Understand the complications of erythrocyte infusion in a child with autoimmune hemolytic anemia

124. The transfused erythrocytes will also be destroyed

125. Know that ABO incompatibility may cause anemia in a first born child, but Rh incompatibility rarely does

126. Know that progressive and severe anemia may occur at 4-8 weeks of age in infants with severe Rh or ABO incompatibility

127. Aplastic and hypoplastic erythrocyte disorders

128. Distinguish between that clinical characteristics of Diamond Blackfan syndrome and transient erythroblastopenia of childhood

129. TEC: usually occurs around age 2; rarely in the first year after birth

130. PE findings normal other than pallor and other si/sx of anemia

131. Possible h/o recent viral illness

132. Other labs usually WNL

133. Tx with transfusion of hgb <5

134. DBA: often dxed in first year of life

135. Associated PE findings include abn facies, thumb abnormalities, congenital heart diseases

136. Lab with macrocytic anemia and reticulocytopenia

137. Have insensitivity to epo

138. Know the signs, symptoms and lab findings of transient erythroblastopenia of childhood

139. See above

140. Understand the role of erythrocyte transfusions in transient erythroblastopenia of childhood

141. Only for hgb <5; usually not needed if >5

142. Therapeutic Approaches

143. Understand the risk of transmitting infectious diseases during blood transfusions

144. HIV: about 1 in 2.1 million

145. HCV: about 1 in 1.9 million

146. HBV: about 1 in 200,000

147. Recognize that erythrocyte transfusions may be associated with hemolytic, febrile and urticarial reactions

148. Febrile nonhemolytic transfusion reaction (FNHTR)

149. Occur in about 0.2% of transfusions and are likely due to cytokine release from the donor blood WBCs; can be minimized with leukocyte reduced blood

150. Premed with APAP does not decrease its incidence

151. Urticarial reactions/Allergic reactions

152. About 0.4% of transfusions

153. If occurs need to give antihistamines and hold the transfusion; if the sx resolve quickly then the transfusion can likely be resumed

154. Premed with antihistamines does not reduce incidence

155. Kids with h/o allergic reactions may do better with plasma reduced PRBCs or washed RBCs

156. Hemolytic reactions: can be immediate or delayed

157. Immediate: due to high-titer Abs and usually due to ABO incompatible blood

158. Si/sx = fever, chills, N/V, abd or back pain, tachycardia and hypotension

159. Must immediately stop the transfusion and give supportive care for hemolysis and possibl DIC, shock, renal failure

160. Delayed: due to primary immunization or due to anamnestic response from a low level alloantibody

161. Primary usually happen about 2-3 weeks after transfusion with si/sx of hemolysis

162. Anamnestic usually happen with days and can have same si/sx as immediate reactions, although more mild but may still need supportive care

163. Understand the role of erythrocyte transfusions in the management of anemia

164. See examples in prior sections

165. Understand the role of erythropoietin in the management of anemia or renal failure and chronic inflammatory disease

166. This is all up for debate

167. It might be helpful for those with CKD who would have reduced levels of epo due to their kidney probs, but what the actual role and benefit can be is currently being questioned (my editorialization)

168. Leukocyte disorders

169. Quantitative leukocyte disorders

170. Recognize that congenital neutropenia may be persistent or cyclical, and manage appropriately

171. Cyclical neutropenia:

172. Usually cycles of about 21 days; often with fevers and mouth ulcers during the nadir of the WBC count

173. Neutropenia often lasts 3-4 days

174. Dx can be difficult b/c by the time they present they may have a nrmal or near normal WBC count; therefore if it suspected, they will need to have their counts checked 2-3 times a week for 4-6 weeks in order to determine if there is a cycle

175. Does not appear to be a risk factor for myelodysplasia or AML

176. During the nadir of the WBC count they may benefit from GCSF

177. Persistent: severe congenital neutropenia; multiple varieties

178. Presentation may be with umbilical infection, pyoderma, oral ulcers, pulmonary infections or perineal infections

179. ANC often less than 500

180. GCSF is used to support them

181. Have a higher risk of developing myelodyplastic syndromes and AML

182. Recognize neutropenia as a sign of overwhelming bacterial sepsis

183. Can be sign of overwhelming bacterial sepsis (basically consumptive)

184. Understand that neutropenia may be drug induced and, if so, should lead to d/c of the drug

185. Leading offenders include Anagelsics/NSAIDs, certain abx (chloramphenical, sulfa, pcn), anticonvulsants (phenytoin, carbamazepine), PTU, procainamide, quinidine, cimetidjne, ranitidine

186. Recognize that common viral infections may cause transient neutropenia that does not require specific tx

187. Consider a f/u CBC after the condition has resolved in order to see that it has improved

188. Qualitative leukocyte disorders

189. Recognize that a child with recurrent bacterial infections and a normal neutrophil count may have abnormal neutrophil function

190. Therapeutic approaches

191. Understand the role of growth factors in the tx of neutropenia

192. Platelet disorders

193. Quantitative platelet disorders

194. Know that TCP in a newborn infant may be a sign of bacterial sepsis and, in an ill child, should lead to appropriate culture and antibiotic therapy

195. Usually have TCP due to platelet destruction caused by vasculitis, endotoxin, immune complexes or DIC

196. Plt transfusions are recommended when the count is <10, whenthere is difficult to control bleeding or when an invasive procedure is planned

197. Recognize that a hx of medications should be part of the eval of a child with tcp

198. Valproic acid and other anticonvulsanrs are notable for causing TCP

199. Recognize that the presence of TCP in a newborn infant with microcepahly a=or other congenital abnormalities may be due to a congenital viral infection such as CMV

200. Recognize TCP, eczematoid rash and recurrent infections as signs of Wiskott-Aldrich syndrome

201. Know that a rapidly enlarging hemangioma should lead to a plt count to check for TCP

202. Manage the TCP associated with TAR syndrome

203. Maintain plts >15,000 with plt transfusions

204. The TCP is usually self-limited and resolves by age 2 years

205. Need to avoid trauma and elective surgeries until the TCP resolves

206. Genetics consults are recommended and need to address recurrence risks

207. Note: the TCP is not responsive to steroids or IVIg, it is actually due to a hyporegenerative marrow; don’t need to do a bone marrow bx

208. Know that ITP is characterized by a low plt count and normal or increased production of plts in the marrow

209. This is the most common cause of isolated TCP in otherwise well children

210. Bone marrow bx isn’t part of the work up, and should only be considered with referral to a hematologist

211. Understand that most children with ITP will recover in less than one year without tx

212. Tx is available, but do not alter the natural hx of acute ITP, neither preventing its progression to chronicity or accelerating disappearance of the offending antibody

213. Know that the common presenting sx of ITP is increased bruising

214. Usually a sudden onset of petechiae and bruising in a previously healthy child; may also have some mucosal bleeding

215. Know that corticosteroids and IVIg usually increase the plt count in children with ITP but do not alter the natural course (e.g. length of the dz)

216. Steroids help raise the count faster than no tx, and IVIg helps raise the count faster than steroids

217. No data show that drug treatment helps prevent serious bleeding, including ICH

218. Note, British panels recommend observation, American panels recommend intervention; overall more study is needed per the PIR article

219. Understand that ASA or other drugs that interfere with plt fxn should not be given to children w ITP or other qualitative or quantitative plt d/os

220. Recognize persistent or severe HA as a sign if ICH in ITP

221. Need to have imaging and get drug tx promptly

222. Know that splenectomy is not appropriate tx at the onset of ITP in a child who is not having major bleeding problems

223. 5-10% of patients will not respond to the splenectomy and there is no way to predict it

224. Usually viewed as a last resort

225. Know that a mother with ITP may have an infant with TCP and know how to manage the infant

226. Usually these are “well” infants, they rarely have bleeding probs

227. If they do have bleeding issues then IVIg is the tx of choice, and the TCP usually resolves after several months (the maternal ab has to be catabolized by the infant’s system before they can fully recover)

228. Recognize that multiple sibs with neonatal TCP suggests isoimmune TCP

229. Know that TCP due to maternal ITP or isoimmune TCP usually resolves within 6-12 weeks

230. Plan the appropriate management of a pt with ITP

231. Do not give platelets as a standard, first line tx!!!

232. See above for other txes

233. Pancytopenia

234. Decreased Production

235. Understand that aplastic anemia and childhood leukemia may both present with purpura, pallor, and fever

236. Know that the absence of blasts in the peripheral blood of a patient with pancytopenia does not rule out the dx of leukemia

237. Coagulation Disorders

238. Congenital bleeding and thrombotic disorders

239. Know that excessive bleeding after circumcision may be the first sign of a congenital coagulation factor deficiency

240. Indentify prothrombin time and partial thromboplastin time as important parts of the evaluation of a pt with increased bruising

241. Prolonged PT = abnormal Factor VII

242. Prolonged PTT = abnormal Factor VIII, IX, XI

243. Both prolonged = abnormal Factor V, Factor X, prothrombin, fibrinogen

244. Know that a child born to the daughter of a person with hemophilia should be tested for that particular bleeding disorder

245. A child whose maternal grandparent has hemophilia needs to be checked

246. Carrier females have a 50% chance of passing the affected chromosome to male offspring

247. Know that HA is an important sx of intracranial bleeding and requires early assessment and tx

248. Understand that serious head trauma in a person with hemophilia requires careful assessment and early replacement tx even in the absence of neurologic abnormalities

249. Recognize bleeding in the forearm of a person with hemophilia as an emergency because of the danger of nerve compression

250. Know that femoral or jugular venipunctures should be avoided in the person with hemophilia who has not received replacement tx

251. Know that some kids with hemophilia have a negative family hx for bleeding disorders

252. Recognize that partial thromboplastin time is often normal in patients with vWF disease, but the bleeding time is commonly prolonged

253. Recognize that a manifestation of vWF in girls may be heavy menstrual bleeding

254. Recognize that a strong fam hx of PE or DVT may suggest a congenital hypercoagulable d/o

255. Understand the usefulness of DDAVP in the tx of a pt with hemophilia or vWF

256. DDAVP increases levels of vWF in the plasma and also causes a 2-4fold increase in factor VIII activity

257. Peak hours can be reached within one hour of treatment, making it useful for surgical prophylaxis

258. Acquired bleeding and thrombotic disorders

259. Identify the need for measuring PT, PTT and plt count as part of the eval for DIC in a child with sepsis and purpura

260. Prolonged PT/PTT

261. Decreased platelets

262. Decreased fibrinogen; serial measurement of fibrinogen is a sensitive and specific test for DIC

263. Increased FDP/d-dimer

264. Peripheral smear will show evidence of intravascular hemolysis, like fragmented, burr, or helmet shaped cells

265. Tx of DIC = find and treat the sause of the shock; acidosis and hypoxemia worsen DIC; may need to give platelets, cryoprecipitate or FFP to stop hemorrhaging.

266. Recognize purpura as an indication of bacterial sepsis in a febrile child

267. Neoplastic disorders

268. Hematologic malignancies

269. Recognize bone pain as a symptom of leukemia

270. Presentation with fever and bone pain is most common in younger children

271. The bone pain is due to marrow expansion and occurs in about 1/3 of kids with ALL

272. When presents with bone pain, may have an insidious onset with initially nl blood counts

273. Failure of NSAIDs and refusal to walk necessitate consideration of leukemia, particularly if the use of corticosteroids is considered

274. Understand that most patients with ALL will be cured of their disease using current tx strategies

275. 75-50% of kids with ALL and nearly 50% of kids with AML are cured

276. Identify the CNS and testes as important sites of relapse of ALL

277. CNS: all regimens now have prophylactic tx of the CNS because systemic chemo may not cross the BBB

278. Testes: therapy in males in prolonged for 1 year, which helps negate the risk of testicular recurrence

279. Identify Down syndrome as a disease with an increased risk of leukemia

280. Recognize the need to evaluation of supraclavicular LN enlargement

281. Worrisome and should prompt a throough eval for a cause, with malignancy high on the ddx

282. Low threshold for excisional bx

283. ID the CXR as an important part of the initial eval of the pt with unexplained LAD

284. Know that overwhelming sepsis is a serious complication in patients with Hodgkin dz who have undergone splenectomy, and know that such patients should be evaluated thoroughly if fever develops

285. Solid tumors

286. Understand that a neuroblastoma usually presents as a nontender abd mass

287. Solid, often fixed, painful or painless, irregularly shaped masses that cross the midline

288. Understand that urinary catecholamine excretion is increased in most patients with nboma and that tests for urinary VMA and HVA are appropriate screening tests for this kind of tumor

289. Know that Wilms tumor is associated with hemihypertrophy and/or aniridia

290. WAGR (Wilms, aniridia, GU abnormalities, Retardation)

291. Understand that Wilms usually presents as an abd mass and may cause htn and hematuria

292. Does NOT cross the midline (diff from nboma)

293. Htn in about 25% of cases, due to increase rennin activity

294. Understand the px of Wilms

295. Cure rate of about 85-90%

296. Recognize the si/sx of craniopharyngioma

297. Confined to sella tucica: usually clinical manifestations due to pituitary-hypothalamic involvement (short stature due to GH deficiency) and visual field defects due to pressure on optic chiasm,may also have other si of pituitary dysfxn like DI, hypothyroid, precocious puberty

298. If extands through the diaphragm sella, it may compress the third ventricle and cause sx of increased ICP like HA, vomiting and papilledma

299. Other sx can include alterations in personality, lethargy, hyperactivity, irritability, forgetfulness

300. Recognize the presenting si of brain tumor (eg, headache, deteriorating school performance, ataxia, emesis)

301. School age children: declining academic performance, fatigue, behavioral changes and vague HA, especially in the occipital or frontal region; over time the HA may be worse in the AM and lethargy and vomiting may develop; also horizontal diplopia and papilledema

302. Infants: irritability, anorexia, FTT, developmental regression can be signs. Macrocephaly, splitting of cranial sutures, bulging anterior fontanelle

303. “Setting sun” sign can be seen with attendant hydrocephalus (downward deviation of eyes)

304. Supratentotial lesions: hemiparesis, hemisensory loss, hyperreflexia, sz, visual complaints

305. Infratentorial: ataxia, hemiparesis, hyperreflexia, cranial neuropathies, but NOT seizures

306. Know that the presenting sx of osteosarcoma is usually bone pain or swelling

307. Systemic sx are rare

308. Occurs in the long bones near the growth plates

309. Identify the clinical and laboratory features of osteoid osteoma

310. Common benign bone tumor, occurs in those age 5-20 yrs (usually)

311. Usually present with gradually increasing sharp focal pain that is worse at the end of day or at night.

312. Pain usually no related to activity, it responds dramatically to NSAIDs

313. Normal lab findings

314. Plain films reveal a small spherical or round lytic lesion surrounded by soft tissue edema and reactive bone formation

315. Recognize the clinical manifestations of histiocytosis syndromes of childhood

316. Oncologic emergencies

317. Differentiate the clinical manifestations of spinal cord compression (eg, from a tumor) from those of other myelopathies and eval appropriately

318. Identify varicella as a life threatening illness in a pt receiving hemotx, and know that varicella Ig should be given immediately after exposure to varicella

319. Recognize the need for immediate eval of a febrile child who is neutropenic as a result of chemotx

320. Therapeutic considerations

321. Understand the gonadal effects associated with the use of chemotx drugs

322. Understand the effects of cranial irradiation on growth hormone secretion

323. Can diminish GH secretion, and replacement tx may be indicated

324. Be familiar with the late sequelae of cancer and cancer tx

325. Good tables in article, will try and copy into this