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Review of Respiratory Disorders from 2010 ABP Content Specs

Review of Respiratory Disorders from 2010 ABP Content Specs

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  • 1. Respiratory Disorders<br />
    • General Signs and Symptoms
    • 2. Stridor
    • 3. Know the ddx of congenital stridor
    • 4. Inspiratory stridor: Laryngomalacia, subglottic stenosis, vocal cord paralysis
    • 5. Expiratory stridor: tracheomalacia or lesions in the airway structures or thoracic cavity
    • 6. Biphasic: vascular rings and slings
    • 7. Know the different etiologies of stridor in children of different ages
    • 8. Birth: choanal atresia, laryngeal web or stenosis, vascular ring, vocal cord paralysis
    • 9. 4-6 weeks: laryngomalacia, tracheomalacia
    • 10. 1-4 years: croup, epiglottitis, foreign body aspiration
    • 11. >5 years: vocal cord dysfunction, exercise, peritonsillar abscess, anaphylaxis
    • 12. Know that endoscopy is the diagnostic tool of choice for laryngeal and vocal cord disorders
    • 13. Laryngomalacia will reveal an omega shaped epiglottis that prolapses during inspiration
    • 14. Paroxysmal vocal cord motion (PVCM)
    • 15. Understand the appropriate approach to the evaluation of congenital stridor
    • 16. Primary evaluation: thorough birth hx, current medical hx, , observation of breathing patterns in different positions, auscultation of the airway
    • 17. Secondary evaluation: can include radiography, spirometry, direct airway visualization (laryngoscopy)
    • 18. Know that vocal cord dysfxn may mimic asthma
    • 19. Also called paroxysmal vocal cord motion (PVCM) or laryngeal dyskinesia
    • 20. Differences between it and asthma: the dyspnea is primarily inspiratory, noise occurs on inspiration, does not respond to brochodilators, no hyperinflation on CXR, PFTs show a variable flattening of the inspiratory limb of the flow-volume curve (is the expiratory limb in asthma)
    • 21. Respiratory failure
    • 22. Know the clinical manifestations of acute hypercapnea: flushing, agitation, confusion, tachycardia, HA
    • 23. Look for a case where a pediatric patient is being under-ventilated, i.e. giving breaths at too slow a rate while being BVMed
    • 24. Know the potential risks and benefits of administering oxygen to children with chronic respiratory failure
    • 25. The respiratory drive of some of these patients is dependent on hypoxemia, and correcting the hypoxemia could lead to respiratory arrest; goal should be to use the lowest amount of supplemental O2 possible to maintain an SaO2 of 90%
    • 26. Know when to intubate and when to provide oxygen therapy in patients with respiratory failure of various etiologies
    • 27. Failure to respond to O2 administration indicates the need for more aggressive management such as BVM or intubationif there is a process that is affecting their neurologic or neuromuscular processes and interfering with their ability to generate adequate tidal volumes, then earlier intubation would be likely
    • 28. Cough
    • 29. Know the ddx of chronic cough in children of different ages
    • 30. Causes of chronic cough in kids with normal CXR:
    • 31. Upper airway cough syndrome (previously post nasal drip syndrome)
    • 32. Expect to find this in a kid over age 3 and with other sx of allergies
    • 33. Asthma
    • 34. GER
    • 35. (usually creates sx during the first few postnatal months and then resolves by age 12 mos)
    • 36. Tracheomalacia
    • 37. Habit-cough syndrome
    • 38. Vocal cord dysfxn
    • 39. Distinguish between clinical manifestations of psychogenic cough and those caused by cough of organic etiology
    • 40. Aka “habit cough syndrome”
    • 41. Usually begin with an uncomplicated URI, but the cough lingers for months to years; will see a repetitive coughm cessation during sleep, and a hacky/barky nature to the cough
    • 42. Recognize cough as a major and at times singular manifestation for asthma
    • 43. Understand the limited indications for cough suppressants
    • 44. Not better than placebo on several trials
    • 45. Best rec is to use saline nasal drops, suctioning
    • 46. Know the initial screening evaluation of chronic cough should include x-ray study if the chest, a sweat test, tuberculin skin test, and PFTs before resorting to other tests
    • 47. Know which conditions that occur in childhood impair the effectiveness of cough: CO, muscle weakness, vocal cord dysfunction, CNS disease, thoracic deformities, pain
    • 48. Exercise intolerance
    • 49. Know that exercise intolerance may reflect etiologies other than pulmonary disease: anemia, muscle weakness, deconditioning, cardiac disease, psychogenic causes
    • 50. Exercise intolerance = failure to tolerate physical exercise at the level that would be expected for the person’s age and condition
    • 51. Measured by the maximal oxygen consumption test
    • 52. Know that exercise intolerance may be a presenting sx of CLD (e.g. asthma, interstitial lung disease) or vocal cord dysfxn
    • 53. Asthma = shortness of breath, chest tightness, cough about 10-15 mins after beginning exertion, nighttime cough
    • 54. Vocal cord dysfxn= paradoxic adduction of vocal cords during inspiration, causing airway obstruction during exercise; also with inspiratory wheezing and throat tightness ; NO night time cough
    • 55. Apnea
    • 56. Distinguish between apnea and periodic breathing
    • 57. Apnea is defined as a cessation of respiration for more than 20secs or if for less than 20 secs is associated with cyanosis or bradycardia
    • 58. Know the difference between central and obstructive apnea
    • 59. Central sleep apnea is a problem in which they lack the ability to sense hypercapnea
    • 60. Obstructive sleep apnea = a disorder of breathing during sleep characterized by prolonged or partial airway obstruction or intermittent complete obstruction that disrupts normal ventilation during sleep and normal sleep patterns
    • 61. Habitual (nightly) snoring, often with intermittent pauses, gasps or snorts
    • 62. Sleep difficulty
    • 63. Daytime neurobehavioral problems
    • 64. Differentiate among obstructive, central, and mixed sleep-associated apnea
    • 65. Obstructive – see above
    • 66. Central – see above; myelomeningocele, hydrocephalus and Arnold- Chiari can be causes
    • 67. Mixed – combines aspects of OSA and CSA
    • 68. Know the testing procedures to evaluate the presence and degree of obstructive apnea on older children
    • 69. Overnight polysonmnography is the gold standard but isn’t very practical
    • 70. Overnight oximetry or nap time PSG (high specificities but low sensitivities)
    • 71. Know the ddx of central sleep apnea in infancy
    • 72. Have to differentiate it from apnea due to positions (neck overflexed), GER with reflex glottic closure and cessation of airflow, and mechanical obstruction of trachea or larynx
    • 73. Central apnea can be due to:
    • 74. Infection
    • 75. Prolonged hypoxemia (lung dz, anemia, PDA)
    • 76. Meds / CNS depressants
    • 77. ICH
    • 78. Hydrocephalus
    • 79. Electrolyte abns
    • 80. Hypoglycemia
    • 81. Hypo/hyperthermia
    • 82. Prematurity and immature resp drive
    • 83. Know the tx of idiopathic recurrent apnea in premature infants
    • 84. i.e. apnea of prematurity
    • 85. MUST rule out other treatable causes
    • 86. Treated with caffeine
    • 87. Understand the association between apnea and anemia in premature infants
    • 88. Anemia of prematurity can contribute to apnea of prematurity when profound (usually if hgb<7), but is a late phenomenon occurring 2-4 weeks after birth
    • 89. Wheezing
    • 90. Differentiate among the dxes responsible for persistent localized wheezes (e.g foreign body, malacia) versus diffuse or migratory wheezes
    • 91. Know the ddx of recurrent wheezing
    • 92. Asthma related causes and non-asthma related causes
    • 93. Kids who wheeze during infancy continue to wheeze after age 6 about 15% of the time; also about 15% of asthmatics will develop wheezing after age 6
    • 94. Non-asthma – foreign body, bronchiolitis obliterans, BOOP, bronchiectasis
    • 95. Know when to consider foreign body in the ddx of recurrent wheezing
    • 96. Age (older infants and toddlers), abrupt onset of symptoms especially if after eating “danger” foods (popcorn, nuts, hot dog), previously without sx or a long time since any respir probs
    • 97. If the hx strongly suggests FB aspiration, they need prompt rigid bronochoscopy; can’t often see the effects of the FB for up to 24 h after aspirated (air trapping)
    • 98. Contrary to popular belief, the aspiration of a small foreign body, including food, is as common in the left as the right mainstem bronchus in young children because the bifurcation of the trachea remains symmetric until the aortic knob grows larger in later childhood
    • 99. Complication= secondary bacterial pneumonia
    • 100. Tachypnea
    • 101. Know that respir rates vary with age and that normal variations occur with sleep, eating and activity in normal children
    • 102. Recognize that tachypnea is a sensitive indicator of respiratory disease
    • 103. Especially lower airway disease and should be looked at in context of other symptoms
    • 104. Hemoptysis
    • 105. Know the ddx of hemoptysis in children
    • 106. Most common etiologies are infection, foreign body and bronchiectasis
    • 107. More rare causes include vasculitides (HSP, Wegener’s, Goodpasture’s and SLE), congenital heart or lung defects,vneoplasm, AV malformation, hemangioma, trauma, PE and idiopathic
    • 108. Know the initial management of hemoptysis in children and adolescence
    • 109. Assess other signs and sx
    • 110. Get a CXR and if dx still not clear get a CT
    • 111. After bleeding is controlled a bronchoscopy with BAL is done; look for hemosiderin laden macrophages (are diagnostic for pulm bleeding, don’t usually appear until 3 days after bleed)
    • 112. Management is usually supportive, follow the ABCs of life support, might need embolotx of severe
    • 113. Cyanosis
    • 114. Know that cyanosis is not a sensitive indicator of oxyhemoglobin saturation (??)
    • 115. Know the common extrapulmonary causes of cyanosis: R to L shunt, methemoglobinemia
    • 116. The article cited only talks about methemoglobinemia; treat it with methylene blue
    • 117. Know how to validate and quantitate a clinical observation of cyanosis: ABG, oxyhemoglobin sat
    • 118. Clubbing
    • 119. Recognize D/Os commonly associated with digital clubbing
    • 120. Cyanotic heart disease (pulm atresia with unrepaired VSD and collateral pulmonary blood flow), chronic lung disease, biliary cirrhosis, infective endocarditis
    • 121. Upper airway
    • 122. General
    • 123. Croup
    • 124. Distinguish between viral and noninfectious croup
    • 125. Viral/infectious croup
    • 126. Usually parainfluenza
    • 127. Low grade fever, rhinorrhea, mild cough followed 1-3 days later by a harsh, nonproductive “barking” cough and inspiratory stridor
    • 128. Noninfectious/spasmodic croup
    • 129. The cough is similar in that it is barking and nonproductive, but there is no fever, rhinorrhea or other sx of infection; possibly allergic
    • 130. Know the appropriate management of croup
    • 131. Mainstay = cool mist therapy
    • 132. Some evidence that adding steroids to the mist can help decrease inflammation
    • 133. Moderate to severe croup can benefit from heliox and also racemic epi
    • 134. Know the clinical manifestations of laryngotracheobronchitis (croup)
    • 135. See above for infectious croup
    • 136. Epiglottitis
    • 137. Know how to tx a child with it
    • 138. Carefully
    • 139. Don’t examine them invasively, don’t send them to radiology
    • 140. Establish an airway (have anesthesia come ASAP) if looking crumpy
    • 141. Give abx, maybe steroids
    • 142. Differentiate the clinical and radiographic findings of viral croup from those of epiglottitis and bacterial tracheitis
    • 143. Viral croup: cough, runny nose, possible prior low grade fever, don’t appear toxic
    • 144. Epiglottitis: appear toxic, have inspiratory stridor, rarely a coughthumb sign; enlarged epiglottis protruding from the anterior wall of the hyopharynx
    • 145. Bacterial tracheitis: toxic appearing, high fever, tachypnea, brassy cough; imaging = subglottic narrowing and a ragged tracheal air column
    • 146. Know the risks of examination in a patient with suspected epiglottitis
    • 147. Increased swelling and collapse of airway
    • 148. Lower airway
    • 149. Vascular anomalies
    • 150. Recognize the variable presentation of vascular anomalies affecting the airway
    • 151. Vascular rings and slings; often present with stridor while feeding; biphasic stridor
    • 152. Congenital malformations
    • 153. Recognize that congenital malformations of the lung (e.g. hypoplastic left lung, cystic adenomatoid malformation) may cause respiratory signs and symptoms
    • 154. Pulmonary sequestration:
    • 155. Intrapulmonary is most common (75-90% of cases); it presents later in life and is usually associated with recurrent unilateral pneumonias, cough, wheezing, fevers
    • 156. Extrapulmonary are far less common and present in early infancy (prior to age 6 months) and in conjunction with other congenital abnormalities
    • 157. Bronchogenic cysts are usually asx and found incidentally on cxr; sometimes present as airway compression or infection
    • 158. Congenital cystic adenomatoid malformation (CCAM) is usually identified on prenatal ultrasound or present in the newborn period with respiratory distress; they may involve the entire lung, they may be associated with other abnormalities; if presenting later may do so with recurrent pneumonia, but would be earlier in life than a pulm sequestration
    • 159. Bronchiolitis I think I’m all set with bronchiolitis, thanks.
    • 160. Recognize the clinical manifestations of bronchiolitis
    • 161. Know the indications for hospitalization for a child with bronchiolitis
    • 162. Aspiration syndromes
    • 163. Know how to eval for a suspected foreign body aspiration
    • 164. See prior section
    • 165. Know the long term complications for FB aspiration
    • 166. Bacterial pneumonia os most common complication
    • 167. Can also get atelectasis and bronchiectasis
    • 168. Know the pulmonary complications of GER
    • 169. Wheezing, scarring of vocal cords…
    • 170. Know the possible radiographic manifestations of FB aspiration
    • 171. Lung remains inflated on expiratory films, might see the foreign body, might see atelectasis, air trapping
    • 172. Know that recurrent aspiration can recur with swallowing d/os independent of GER
    • 173. Swallowing dysfunction can be a cause
    • 174. Plan the management of a patient with FB aspiration
    • 175. See above under the wheezing part
    • 176. Understand that hydrocarbon pneumonitis may cause acute and chronic lung disease
    • 177. Hydrocarbons are mineral spirits, gasoline, turpentine, pine oil
    • 178. Acutely can cause aspiration, hypoxemia requiring O2 support, the resp sx usually resolve in 7 days
    • 179. Chronically can cause penumatoceles, pneumothorax, empyema, bacterial pna, respiratory distress syndrome
    • 180. May get proliferative alveolar thickening and that can cause permanent damage to pulm fxn
    • 181. Know that aspiration can occur despite the presence of a tracheostomy
    • 182. Bronchiectasis
    • 183. Know the ddx of it
    • 184. Bronchiectasis abnormal dilatation of the bronchi and bronchioles; may be localized or diffuse and the changes are irreversible
    • 185. Most common cause is CF
    • 186. Less common causes include allergic bronchopulmonary aspergillosis, primary ciliary dyskinesia, immunodeficiency and recurrent infections (TB, pertussis, measles); foreign body aspiration can be a cause as well
    • 187. Know that high res CT of the chest is useful to dx it in a child
    • 188. Tracheomalacia
    • 189. Know that it can occur as a complication of chronic mechanical ventilation in children
    • 190. High vent pressures can result in weakening or destruction of tracheal cartilage
    • 191. Know that tracheoesophageal fistula may result in tracheomalacia
    • 192. Can remain problematic despite repair of the fistula
    • 193. Know the clinical manifestations of tracheomalacia and laryngomalacia
    • 194. Laryngomalacia: most common cause of stridor in infants
    • 195. Occurs during inspiration due to collapse of supraglottic structures unable to remain open during times of increased intrathoracic pressure
    • 196. Exacerbated during times of crying or agitation; may be relieved when infant is in prone position
    • 197. Usually resolve spontaneously in the first postnatal year; should also consider other problems like GER that can exacerbate it, and tx those comorbid conditions
    • 198. Tracheomalacia
    • 199. Occurs during expiration due to collapse trachea during expiratory maneuvers
    • 200. Hallmark = expiratory wheeze
    • 201. Can be isolated or in association with other clinical entities like TEF or trisomy 21; can be acquired due to vents
    • 202. Differentiate between the two – see above
    • 203. Tracheitis
    • 204. Recognize the si/sx of bacterial tracheitis
    • 205. toxic appearing, high fever, tachypnea, brassy cough; imaging = subglottic narrowing and a ragged tracheal air column
    • 206. Know the clinical course of bacterial tracheitis, including biphasic illness, precipitous worsening, requirement for intubation, and relatively prolonged intubation
    • 207. Often have sx of a croup-like illness for a few days and then a sudden deterioration with spiking fevers, increased hoarseness, toxic appearance, stridor, rtx and decreased O2 sats
    • 208. Doesn’t respond to the usual txes for croup
    • 209. Know the tx of it
    • 210. Secure an airway; might need a prolonged intubation doe to need to get secrcxretions cleared and also due to degree of edema in the airway
    • 211. Start abx including coverage for staph (nafcillin)
    • 212. Know the microbiology of it
    • 213. Most commonly due to s. aureus
    • 214. Can also be due to parainfluenza, moraxella, nontypable h. flu and oral anaerobes
    • 215. Hemosiderosis
    • 216. Know that it is associated with hemoptysis
    • 217. Parenchymal
    • 218. Pneumonias
    • 219. Know the etiologies of pna in children of different ages
    • 220. AgePathogenComments3weeks to 3 monthsC. trachomatisRSVParainfluenzaS. pneumoBordatella pertussisVertical transmissionAfebrileInterstitial infiltrates on cxrBronchiolitis with wheezing most commonOnset usually late fallBronchiolitis or pneumoniaSeen fall through springMajor bacterial cause through childhoodTracheobronchitis with severe paroxysmal cough, no feverPneumonia occasionally seen; usually related to aspiration3 months to age 4 yrsRSV, parainfluenzae, human metapneumovirus, influenza, rhinovirusStrep pneumoMycoplasma pneumoniaMost toddler pneumonia is viralMajor treatable pathogen in this age groupPossible in all agesIncreased incidence in children approaching school age5yrs through adolescenceM pneumoniaC. pneumoniaS pneumoTBMajor treatable cause in school age children and adolescenceAlso an important cause, similar clinical presentation to mycoplasmaStill an important causeComplications, especially empyema, often ensuePrimarily in areas or populations of high TB prevalenceHigher risk at puberty and in pregnancy
    • 221. Know the major acute and chronic complications of pneumonia, including empyema, sepsis, ptx, bronchopleural fistula, and pneumatoceles
    • 222. Necrotizing pna: rare; liquefaction and necrosis of lung tissue due to toxins of highly virulent organisms
    • 223. Lung abscess: usually develop after an aspiration event, frequently involve mouth organisms like streps, anaerobes, gram negative rods
    • 224. Empyema: kids usually present wih persistent fever, decreased appetite, fatigue, chest pain and some degree of respiratory distress; usually requires surgical intervention of some kind (chest tube, VATS)
    • 225. Bronchopleural fistula: development of a connection between the bronchial tree and the pleural space. Is associated with a pretty high morbidity and mortality (30-70%) and requires surgical repair. Usually seen in a very sick kids, if on a vent would likely have an air leak
    • 226. Know the clinical manifestations of pnas with different etiologies
    • 227. SyndromeTypcal causeAge groupTypical clinical featuresBacterial (suppurative)Pneumococcus, othersAll ages; younger children (<6mos) more commonAbrupt onset, high fever, ill/toxic appearance, more focal findings on exam, chest/abd pain, focal infiltrate if CXR is obtainedAtypical – infancyC. trachomatis<3mostachypnea, mild hypoxemia, lack of fever; wheezing, interstitial infiltrates on CXRAtypical – older childrenMycoplasma>5ygradual onset, low grade fever, diffuse exam findings, diffuse infiltrates if CXR obtainedViralMultiple All ages; 3mos – 5yrs more commonProminent URI sx, low grade or absent fever, diffuse findings/wheezes on exam, possible diffuse interstitial infintrates if CXR obtained
    • 228. Know the lab tests for pneumonia, including x-ray study of the chest, blood cx, CBC, urine antigen detection studies, serology for mycoplasma, sputum cx
    • 229. Rarely need lab if patient going to be managed as outpt
    • 230. If being managed inpt the recs are for getting CBC, blood cx, chem panel; sputum cx of possible to test for bacterial pathogens; nasopharyngeal secretions can be tested for viral resp tract pathogens
    • 231. Mycoplasma, chlamydophila and legionella can be determined serologically
    • 232. Legionella and pneumococcal infections are detactable with urine antigen testing
    • 233. Know the sequelae of pna and manage appropriately
    • 234. ?
    • 235. Know the methods of prevention and/or control of pna
    • 236. Good hygiene
    • 237. Breastfeeding
    • 238. Immunization with Hib, pertussis and heptavalent pneumococcal vaccines
    • 239. If kid is older than 2 and has risk facrots then needs the 23-valent pneumococcal polysaccharide vaccine
    • 240. Flue shots
    • 241. Know which organisms are likely to cause the pleural and parenchymal complications of pneumonia
    • 242. Usually s. pneumo
    • 243. GAS (strep pyogenes) can cause pneumatoceles
    • 244. S. aureus can cause pneumatoceles, ptx, abscesses, empyema
    • 245. Know that invasive studies (bronch, lung aspiration, open bx) may be indicated in pts with acute pna
    • 246. Know the ddx of recurrent pna
    • 247. Recurrent pna = more than one radiographically confirmed episode in a year, or more than three episodes in a lifetime, with clinical or radiographic resolution between episodes
    • 248. Ddx includes anatomic lesions, i.e. vascular rings, cysts, pulmonary sequestration; resp tract disorders like CF, GER, aspiration, and immune disorders
    • 249. Know that congenital lesions of the lung may mimic pna
    • 250. Know the significance of pna in a child with NM dz
    • 251. More likely to get aspiration pneumonia
    • 252. Know the tx of pna in a child with NM dz
    • 253. Cover for causes of aspiration pneumonia (ampicillin, ampicillin-sulbactam, clindamycin); probably needs to be admitted
    • 254. Diaphragmatic hernia – covered in GI section
    • 255. Recognize the clinical manifestations of it
    • 256. Know the appropriate therapy
    • 257. Know the initial stabilization maneuvers for a newborn infant with DH
    • 258. Know that DH is associated with persistent pulmonary htn, and sybsequent abnormalities including poor growth, tracheomalacia and developmental delay
    • 259. Know that pulm hypoplasia is associated with DH
    • 260. Trauma
    • 261. Know how to evaluate a child with sx following a chest wall trauma
    • 262. Know how to stabilize a child with respiratory sx following a chest wall trauma
    • 263. Drowning, near drowning, and acute respiratory distress syndrome
    • 264. Know the clinical manifestations of ARDS
    • 265. Tachypnea, decreased lung compliance, worsening hypoxemia leading to respiratory muscle fatigue
    • 266. Disgnostic triad = noncardiogenic pulmonary edema, impaired oxygenation, bilateral pulmonary infiltrates
    • 267. Know the natural hx of ARDS
    • 268. Three stages:
    • 269. Exudative stage – rapid development of respiratory failure; characterized by profound hypoxemia and atelectasis, sometimes resolves in 3-7 days, but can progress to
    • 270. Inflammatory stage – fibrosing alveolitis and surfactant deficiency; characterized by persistent hypoxemia, decreased lung compliance, and development of pneumothoraces
    • 271. Resolution – may eventually recover normal lung function; final stage consists of resolution of hypoxemia and improved lung compliance;c omplete resolution may take 6-12 months but some develop lifelong restrictive lung disease, lung cysts, or decreased exercise tolerance
    • 272. Know the pulmonary sequelae of ARDS
    • 273. Pulmonary fibrosis
    • 274. Reactive airway disease
    • 275. Severe chronic lung disease (rare)
    • 276. Know that ARDS has multiple etiologies
    • 277. Know that a pt with minimal sx following a near drowning may later develop sx that require hospitalization
    • 278. Know that ARDS may result from a near drowning after a period of initial recovery
    • 279. Know the major causes of death in children with ARDS: sepsis, extrapulmonary multiorgan failure, air leaks
    • 280. Newborn infants
    • 281. Bronchopulmonary dysplasia (chronic lung disease of infants)
    • 282. Recognize that infants with BPD are prone to cor pulmonale and recurrent wheezing with infections
    • 283. Recognize that failure to thrive and severe respiratory infections are common in infants with BPD
    • 284. Recognize that aversive oral motor behavior is associated with BPD, thereby limiting ways to feed such infants
    • 285. Other – not BPD
    • 286. Know the specific radiographic findings in idiopathic neonatal RDS (see below)
    • 287. Differentiate between normal results of a newborn cxr and the radiographic findings that reflect MAS (see below)
    • 288. Differentiate between the normal results of a newborn cxr and the radiographic patterns that reflect pna
    • 289. RDS: underinflation, “ground glass” appearance, air bronchograms
    • 290. TTN: fluid in horizontal fissure, adequate lung expansion with perihilar and central vascular prominence
    • 291. MAS: patchy areas of diffuse atelectasis, focal areas of air trapping, increased lung volumes
    • 292. Pna:
    • 293. Recognize that CLD may result from MAS
    • 294. Asthma
    • 295. CF
    • 296. Know which vitamins are fat soluble and therefore are usually insufficient in children with CF
    • 297. Understand the inheritance of CF
    • 298. Autosomal recessive
    • 299. Must have two mutations on both copies of the CFTR gene in order to be affected
    • 300. For a healthy person whose parents are known carriers, the risk of being a carrier of a mutated CFTR gene is 2/3
    • 301. Of the 4 possible outcomes from that person’s parents, one in four would have two mutated genes, and hence not be “healthy” so they are taken out of the equation on this tricky little scenario (question 2010: 151)
    • 302. Know the association of rectal prolapse and CF
    • 303. Accounts for about 10% of all reported cases of RP during infancy and early childhood
    • 304. RP occurs in about 20% of patients with CF between age 6months and 3 years
    • 305. This was in question 2010: 225, and the scenario was of a child whose weight/height were mismatched, had chronic constipations, and experienced the rectal prolapse after being txed for constipation and passing soft stools – these were supposed the be the CF “red flags”
    • 306. Know the neonatal non-pulmonary manifestations of CF: meconium ileus, meconium peritonitis, prolonged jaundice
    • 307. Mec ileus thick mec obstruction in the distal ileum, usually presents as a small bowel obstruction; consider in newborn with delayed passage of stool and bile stained emesis; abd film may show stacked loops of variably dilated bowel, soap suds bubbly like appearance of the mec (often in the RLQ); distal bowel with paucity of bowel gas
    • 308. Mec peritonitis bowel obstruction leading to perf and spillage of mec into the abd cavity; it often calcifies and forms a “pseudocyst” that can be seen on abd films
    • 309. Prolonged jaundice
    • 310. Know the manifestations of CF in infancy: hypoproteinemia, anemia, steatorrhea, recurrent pulmonary sx, hypochloremic alkalosis
    • 311. Know that hemoptysis and ptx can be potentially life threatening complications of CF
    • 312. Primary ciliary dyskinesia (dysmotile cilia syndrome)
    • 313. Know that otitis media, dextrocardia, and/or bronchiectasis may be due to PCD
    • 314. Note that in question 2007:143 the vignette was a boy who had chronic infections, cludding, cough, nasal polyps, rhinorrhea and a “point of maximal impulse displaced t the right” this was supposed to be the clue to dextrocardia and therefore the PCD rather than CF
    • 315. Extrapulmonary
    • 316. Pleural fluid
    • 317. Understand the etiologies of pleural fluid accumulations
    • 318. Transudates = plasma ultrafiltrates that usually result from renal and liver dz or CHF
    • 319. Exudates = inflammatory processes, like pna, malignancy, trauma, systemic inflammatory dz, impaired lymphatic drainage
    • 320. Empyema is a type of exudate and is characterized by the presence of WBCs, a positive gram stain, or frank pus
    • 321. Exudates have LOW pH (b/c of bacterial glucose consumption)LDH will be 2-3x the serum values, and high protein vaues (>3g/dL)
    • 322. 70% of peduatric pleural effusion are parapneumonic effusions
    • 323. Pleural effusions are seen in up to 40% af bacterial pnas, and about 50% of those will progress to empyema
    • 324. Know the characteristics of pleural fluid due to chylothorax
    • 325. Pneumothorax, pneumomediastinum
    • 326. Know the si/sx of ptx
    • 327. Know the appropriate tx for a child with ptx
    • 328. Know that asthma may be associated with either of these
    • 329. Know that ptx is a complication of rescusitation and mechanical ventilation
    • 330. Thoracic deformities
    • 331. Recognize the association between scoliosis and restrictive pulmonary disease
    • 332. Scoliosis can restrict the thoracic cavity, thereby causing a restrictive lung dz
    • 333. Recognize that severe progressive neuromuscular disease of any etiology can produce serious restrictive pulmonary disease
    • 334. Recognize that pectus excavatum is not usually associated with any pulmonary disease or exercise limitation
    • 335. Pulmonary htn and cor pulmonale
    • 336. Know that oxygenation may decrease during normal abnormal sleep, which may cause pulmonary hypertension or exacerbate existing cor pulmonale
    • 337. Know that PHTN is potentially reversible
    • 338. Treatment is aimed at the underlying disease in cases of secondary PH
    • 339. Treatment is sx management and treatment of pulm vasculopathy in idiopathic PH
    • 340. Know the situations in which PHTN and or pulmonale may occur
    • 341. PPHN
    • 342. CHD
    • 343. Lung disease that causes chronic hypoxia (leads to remodeling of the pulmonary vascular wall)
    • 344. Thrombotic or embolic disease
    • 345. Idiopathic
    • 346. Sleep disorders (see prior sections on OSAS, also, its kind of common sense)
    • 347. Know the respiratory and non-respiratory conditions that may cause sleep disorders
    • 348. Understand the sx that reflect poor sleep quality in children
    • 349. Know the appropriate eval of suspected OSA in children
    • 350. Know that children with severe OSA due to upper airways obstruction are at significant risk for resp distress postoperatively (due to post op airway selling, post op obstructive pulmonary edema)
    • 351. SIDS
    • 352. Recognize a child with an ALTE
    • 353. ALTE is an episode that is frightening to the observer and that is characterized by some combination of apnea (centrally or occasionally obstructive), color change (usually cyanotic or pallid but occasionally erythematous or plethoric), marked change in muscle tone (usually marked limpness), choking or gagging
    • 354. Know the appropriate management of a child with ALTE
    • 355. Get a good hx, full PE to assess the severity of the event
    • 356. Article recommends screening for GER, UA and cx, brain neuroimaging, pneumogram, and WBC count
    • 357. Know the risk factors for SIDS- got it.
    • 358. Know the ddx of ALTE in infants includes infection, metabolic abnormality, GER, aspiration, cardiac dysrhythmia, seizures, nonaccidental trauma, apnea of infancy
    • 359. Recognize the limitation of apnea monitors in following infants with ALTEs
    • 360. Diagnostic testing – prior sections pretty much cover this
    • 361. PFTs
    • 362. Know what spirometry measures
    • 363. Oximetry
    • 364. Know the correlation between PaO2 and oxyhemoglobin saturation
    • 365. Understand the value and limitations of pulse ox in caring for children with acute pulmonary dz
    • 366. Blood gas analysis
    • 367. Recognize the limitations of cap blood gas testing
    • 368. Imaging
    • 369. Recognize intrathoracic airway obstruction by x-ray study of the chest
    • 370. Recognize atelectasis by x-ray study of the chest