front 1 Bronchiolitis pathopysiology | back 1 viral induced inflammation of small, distal airways; bronchiolar obstruction from sloughed epithelial cells, leukocytes and mucus; RSV most common cause |
front 2 Bronchiolitis clinica presentation | back 2 Age <2; antecedent nasal congestion, rhinorrhea, cough, wheezing and crackles, tachypnea, retractions (peak severity days 3-5) |
front 3 Bronchiolitis radiographic findings | back 3 bilateral hyperinflation, increased interstitial markings and peribronchial cuffing |
front 4 Bronchiolitis treatment | back 4 supportive |
front 5 Bronchiolitis complications | back 5 apnea (<2 months old), resp failure |
front 6 Bronchiolitis prevention | back 6 nirsevimab for all children under 8 months old |
front 7 Transposition of great vessels is | back 7 a congenital defect that typically presents within the first 24 hrs of life w/ cyanosis and a single loud S2 |
front 8 Hypertrophic cardiomyopathy in infants of diabetic mothers pathogenesis | back 8 maternal hyperglycemia leading to fetal hyperglycemia and hyperinsulinemia; increased glycogen and fat deposition in interventricular septum leading to LVOT obstruction |
front 9 Hypertrophic cardiomyopathy in infants of diabetic mothers clinical findings | back 9 often asymptomatic but may have resp distress and/or hypotension; systolic ejection murmur |
front 10 Hypertrophic cardiomyopathy in infants of diabetic mothers imaging | back 10 CXR: cardiomegaly ECHO: increased thickness of interventricular septum and decreased LV chamber size |
front 11 Hypertrophic cardiomyopathy in infants of diabetic mothers treatment | back 11 IV fluids and beta blockers to increase LV blood volume |
front 12 Hypertrophic cardiomyopathy in infants of diabetic mothers prognosis | back 12 spontaneous regression age 1 |
front 13 Psychogenic pseudosyncope | back 13 a type of conversion disorder characterized by an apparent loss of consciousness w/o impaired cerebral perfusion. Prolonged duration of unconsciousness, absence of objective physical findings, and high frequency of episodes are common. They'll say stuff like "I felt my head throbbing after I hit the floor." or "I felt weak before I passed out" |
front 14 Cataplexy | back 14 an emotionally triggered, sudden loss of muscle control, can mimic syncope; however, it typically occurs in pts w/ narcolepsy, who usually have other symptoms such as excessive daytime sleepiness. The episodes are brief. |
front 15 Causes of acquired QT prolongation | back 15 macrolides and fluoroquinolones, odansetron and them, azoles (fluconazole), antipsychotics, TCAs, SSRIs, some opioids (methadone, oxycodone), quinidine (class Ia antiarrythmics), dofetilide, sotalol (class III antiarrythmics), electrolytes abnormalities (decreased Mg, K, and Ca) |
front 16 Congenital causes of QT prolongation | back 16 Romano-Ward syndrome, Jervell and Lang-Nielsen syndrome |
front 17 Tof can present with | back 17 hypercyanotic tet spells due to RVOT obstruction and right to left shunting in the setting of exertion of agitation. Squatting increases afterload, which increases blood flow across the RVOT, which in turn improves cyanosis |
front 18 Isolated ASD | back 18 an acyanotic lesion that causes a wide and fixed splitting of S2 and a systolic ejection murmur due to increased blood flow across the pulmonic valve |
front 19 Partial anomalous pulmonary venous return | back 19 drainage of some but not all pulmonary veins into the right sided circulation typically demonstrating a step-up in oxygen saturation from the inferior vena cava to the right atrium. Other clinical findings include right-sided cardiac enlargement and signs of pulmonary HTN (exertional dyspnea) |
front 20 Trisomy 18 (Edwards syndrome) | back 20 characterized by micrognathia, microcephaly, rocker bottom feet, overlapping fingers, and absent palmar creases. Ventricular septal defect in common in these pts w/ a holosystolic murmur |
front 21 Peripheral cyanosis in children mechanism | back 21 increased tissue oxygen extraction |
front 22 Peripheral cyanosis in children typical causes | back 22 vasomotor instability, cold exposure, low cardiac output, venous obstruction |
front 23 Peripheral cyanosis in children features | back 23 finger, toe, perioral cyanosis, cool extremities, does not improve with oxygen |
front 24 Central cyanosis in children mechanism | back 24 decreased systemic O2 sat |
front 25 Central cyanosis in children typical causes | back 25 pulm disease, cyanotic heart disease |
front 26 Central cyanosis in children features | back 26 diffuse and/or mucosal cyanosis, warm extremities, may improve w/ O2 |
front 27 Pathologic murmurs history | back 27 infants: poor weight gain, resp distress, difficult feeding older children: exertional fatigue, chest pain, syncope fam Hx of SCD of CHD |
front 28 Pathologic murmurs characteristics | back 28 holosystolic or diastolic, harsh, grade at least 3 intensity, intensity persists w/ standing and valsalva maneuver |
front 29 Pathologic murmurs other findings | back 29 central cyanosis, loud fixed, or single S2, weak femoral pulses, hepatomegaly |
front 30 Pathologic murmurs management | back 30 EKG and ECHO |
front 31 Benign murmurs history | back 31 asymptomatic, normal growth, no significant family history |
front 32 Pathologic murmurs characteristics | back 32 early or midsystolic, musical or vibratory, grade 1-2 intensity, decreases or disappears w/ standing and valsalva maneuver |
front 33 Pathologic murmurs other findings | back 33 normal vitals, normal S1 and S2, symmetric pulses |
front 34 Pathologic murmurs management | back 34 reassurance |
front 35 Persistent pulm HTN of the newborn pathogenesis | back 35 abnormal persistent of increased fetal pulm vascular resistance, right to left shunting across ductus arteriosus |
front 36 Persistent pulm HTN of the newborn risk factors | back 36 lung hypoplasia (congenital diaphragmatic hernia), meconium aspiration syndrome, infection (neonatal pneumonia) |
front 37 Persistent pulm HTN of the newborn examination | back 37 decreased postductal relative to preductal O2 sat, resp distress and cyanosis, prominent S2 |
front 38 Persistent pulm HTN of the newborn treatment | back 38 O2 and ventilation, inhaled nitric oxide (pulm dilator) |
front 39 Infection control isolation precautions airborne | back 39 tuberculosis, varicella, SARS, measles |
front 40 Infection control isolation precautions contact | back 40 VRE, MRSA, E coli O157:H7, scabies, RSV, C. diff |
front 41 Infection control isolation precautions droplets | back 41 mycoplasma pneumonia, influenza, Hib, neisseria meningitidis, adenovirus |
front 42 Krabbe disease | back 42 galatocerebridase deficiency, AR, presents early in infancy w/ developmental regression, hypotonia, and areflexia |
front 43 Hurler syndrome | back 43 lysosomal hydrolase deficiency, presents at age 6 months to 2 yrs w/ coarse facial features, inguinal or umbilical hernias, corneal clouding, and hepatospenomegaly |
front 44 Once Guillian Barre syndrome is suspected in a hemodynamically stable patient... | back 44 assess pulm function w/ spirometry. FVC and negative inspiratory force monitor resp muscle strength and serial pulm function testing should be performed given the potential for rapid progression of disease |
front 45 Guillian Barre syndrome CSF | back 45 WBC: 0-5 Glucose: 40-70 Protein: 45- 1,000 |
front 46 Viral Meningitis CSF | back 46 WBC: 10-500 Glucose: 40-70 Protein: <150 |
front 47 Tuberculous Meningitis CSF | back 47 WBC: 100-500 Glucose: <45 Protein: 100-500 |
front 48 Bacterial Meningitis CSF | back 48 WBC: >1000 Glucose: <40 Protein: >250 |
front 49 Congenital Toxoplasmosis | back 49 chorioretinitis, obstructive hydrocephalus, parenchymal calcifications |
front 50 Congenital Syphilis | back 50 osteoarticular destruction (Hutchinson teeth, saddle nose), hepatosplenomegaly, jaundice, rhinitis, and rash |
front 51 Congenital Rubella | back 51 cataracts, sensorineural hearing loss, PDA |
front 52 Congential CMV | back 52 sensorineural hearing loss, hydrocephalus ex vacuo, and periventricular calcifications |
front 53 Retinal detachment typically presents with | back 53 acute vision loss, floaters, and flashes of light. Funduscopic exam shows a retinal tear and/or elevation |
front 54 Open-angle glaucoma causes | back 54 painless loss of peripheral vision and presents in late adulthood. Funduscopic exam shows optic nerve cupping |
front 55 Vitamin A deficiency causes | back 55 xerophthalmia, characterized by excessive dryness of the cornea and conjunctivae, and night blindness |
front 56 Retinitis Pigmentosa etiology | back 56 genetic mutation causing loss of photoreceptors, progressive retinal degeneration, symptom onset from age 10 through adulthood |
front 57 Retinitis Pigmentosa clinical features | back 57 night blindness, progressive visual field loss (midperiphery), decreased visual acuity (late finding) |
front 58 Retinitis Pigmentosa Funduscopic findings | back 58 retinal vessel attenuation, optic disc pallor, abnormal retinal pigmentation |
front 59 Retinitis Pigmentosa prognosis | back 59 most are legally blind by age 40 |
front 60 Most infants with congenital syphilis | back 60 asymptomatic at birth; those with symptoms typically have rhintis (snuffles), hepatomegaly, and a maculopapular rash |
front 61 Use of lisinopril during pregnancy can cause | back 61 fetal renal failure and associated oligohydramnios that results in pulm hypoplasia, growth restriction, and limb defects (Potter sequence) |
front 62 To minimize risk of congenital malformation, pts who require antiepileptics during pregnancy should be | back 62 titrated to the lowest dose for seizure control prior to conception and started on high dose (4mg) folic acid supplementation |
front 63 Fetal hydantoin syndrome | back 63 microcephaly, cleft lip and palate, cardiac defects, hypoplasia of nails and phalanges, wide anterior fontanelle, due to in utero exposure to an antiepileptic (phenytoin, carbamazepine, valproate) |
front 64 Erb-Duchenne palsy | back 64 involves the 5th, 6th, and sometimes 7th cranial nerves |
front 65 Erb-Duchenne palsy management | back 65 observation and physical therapy b/c up to 80% of pts have spontaneous recovery within 3 months |
front 66 Neonatal HSV infection skin, eye, and mouth clinical findings | back 66 mucocutaneous vesicles, keratoconjunctivitis |
front 67 Neonatal HSV infection CNS clinical findings | back 67 seizures, fever, lethargy, temporal lobe hemorrhage/edema |
front 68 Neonatal HSV infection disseminated clinical findings | back 68 sepsis, hepatitis, pneumonia |
front 69 Neonatal HSV infection Dx | back 69 viral surface cultures: HSV PCR (blood, CSF) |
front 70 Neonatal HSV infection treatment | back 70 acyclovir |
front 71 Newborns thermoregulatory center | back 71 underdeveloped and are at risk for hypothermia. Skin to skin contact prevents heat loss. You could also swaddle w/ warm blankets and place under a radiant warmer. |
front 72 Newborns underdeveloped thermoregulatory center vitamin K injection and ophthalmic erythromycin ointment | back 72 postpone for an hour |
front 73 Asymmetric fetal growth restriction onset | back 73 2nd/3rd trimester |
front 74 Asymmetric fetal growth restriction etiology | back 74 uteroplacental insufficiency, maternal malnutrition |
front 75 Asymmetric fetal growth restriction clinical features | back 75 head-sparing growth lag |
front 76 Asymmetric fetal growth restriction management | back 76 monitor/treat complications (hypoglycemia, hypothermia, polycythemia and hypocalcemia) |
front 77 Symmetric fetal growth restriction onset | back 77 1st trimester |
front 78 Symmetric fetal growth restriction etiology | back 78 chromosomal abnormalities, congenital infection |
front 79 Symmetric fetal growth restriction clinical features | back 79 global growth lag |
front 80 Symmetric fetal growth restriction management | back 80 monitor or treat complications (hypoglycemia, hypothermia, polycythemia and hypocalcemia) |
front 81 Neonatal complications of diabetes during pregnancy | back 81 hypoglycemia, polycythemia (low iron), hypocalcemia and hypomagnesemia, hyperbilirubinemia, congenital anomalies, macrosomia (w/ brachial plexus injury or clavicle fracture), resp distress syndrome, hypertrophic cardiomyopathy |
front 82 Pts w/ cryptorchid testes are at risk of | back 82 testicular cancer (dysgerminoma, gonadoblastoma), due in part to an increase in intraabdominal temperature that causes abnormal spermatogenesis and aberrant germ cell differentiation |
front 83 Androgen insensitivity syndrome pathophysiology | back 83 x-linked mutation in androgen receptor |
front 84 Androgen insensitivity syndrome management | back 84 gender identity/assignment counseling: gonadectomy (malignancy prevention) |
front 85 Fibrocystic change in breast and juvenile fibroadenoma both typically present in the | back 85 upper outer quadrant of the breast after menarche |
front 86 Primary amenorrhea | back 86 absence of menarche in a girl at least 13 years old w/ no secondary sexual characteristics, or a girl at least 15 years old w/ secondary sexual characteristics. If pelvic US shows uterus, test FSH levels and that'll give you your answer |
front 87 First line treatment for symptomatic fused labia due to labial adhesions | back 87 topical estrogen |
front 88 Balantis | back 88 inflammation of the glans penis |
front 89 Balanoposthitis | back 89 inflammation of the glans penis and foreskin |
front 90 Balantis and Balanoposthitis causes | back 90 irritation, infection, trauma |
front 91 Balantis and Balanoposthitis evaluation | back 91 KOH microscopy for suspected candida infection STI screen if urethral discharge present |
front 92 Balantis and Balanoposthitis management | back 92 foreskin hygiene, sitz baths, topical treatment, diabetes 2 screening for candida infection w/o risk factors |
front 93 Hydrocele | back 93 fluid collection within the tunica vaginalis, which surrounds the testis. Should spontaneously resolve by 1 y/o and can safely be monitored during that period |
front 94 Cryptorchidism risk factors | back 94 prematurity, small for gestational age |
front 95 Cryptorchidism clinical features | back 95 empty, poorly rugated scrotum on affected side(s) +/- inguinal fullness/mass |
front 96 Cryptorchidism management | back 96 orchiopexy and 6-12 months |
front 97 Cryptorchidism complications | back 97 inguinal hernia, testicular torsion, infertility, testicular cancer |
front 98 If neither testicle is palpated in the groin area a difference of sex development is of primary concern; | back 98 evaluate 17-hydroxyprogesterone level and electrolytes. Perform karyotype and pelvic US |
front 99 First step in management of hypospadias | back 99 urologic evaluation b/c most cases require surgical correction. Circumcision is deferred until after evaluation b/c the foreskin may be required for hypospadias repair |
front 100 Hypospadias pathogenesis | back 100 failure of urethral folds to fuse |
front 101 Hypospadias clinical features | back 101 ventrally displaced urethral meatus, dorsal hooded foreskin, +/- underdeveloped penis and glans, +/- penile curvature (chordee) |
front 102 Other Hypospadias management | back 102 +/- karyotype, pelvic US if severe |
front 103 Mastoiditis is a complication of | back 103 acute otitis media most commonly due to strep pneumo |
front 104 Mastoiditis treatment | back 104 IV antibiotics, drain via tympanostomy or mastoidectomy |
front 105 Young children w/ stroke symptoms | back 105 headache, seizure, in addition to focal neurological deficits |
front 106 Young children w/ stroke management | back 106 urgent MRI/MR angio to confirm Dx and determine eligibility for potenital reperfusion therapies |
front 107 Sydenham Chorea etiology | back 107 autoimmune complication that can occur months after GAS infection |
front 108 Sydenham Chorea pathogenesis | back 108 molecular mimicry btw anti-GAS antibodies and neuronal antigens in basal ganglia |
front 109 Sydenham Chorea clinical features | back 109 involuntary jerky movements, hypotonia, emotional lability, obsessive complusive behaviors, +/- sx of acute rheumatic fever |
front 110 Sydenham Chorea Dx | back 110 GAS test w/ throat culture, ASO and Anti-DNAse B titers, ECHO and EKG |
front 111 Sydenham Chorea treatment | back 111 abx and antidopaminergics (haloperidol) |
front 112 Chiari I malformation etiology | back 112 displacement of the cerebellar tonsils through the foramen magnum |
front 113 Condition commonly associated w/ Chiari I malformation | back 113 syringomyelia |
front 114 Chiari I malformation presentation | back 114 although frequently asymptomatic, presentation may occur in adolescence/adulthood w/ occipital headache exacerbated by activity and valsalva maneuvers |
front 115 Chiari II malformation etiology | back 115 herniation of cerebellum through foramen magnum |
front 116 Chiari II malformation clinical findings | back 116 obstruction of cerebrospinal fluid flow through 4th ventricle, lateral ventricular dilation, myelomeningocele |
front 117 3 year milestone gross motor | back 117 walks up stairs w/ alternating feet, rides tricycle |
front 118 3 year milestone fine motor | back 118 dresses w/ help, uses fork, copies circle |
front 119 3 year milestone language | back 119 says at least 3-word sentences, speech 75% intelligible |
front 120 3 year milestone social/cognitive | back 120 knows age/sex, plays w/ other children |
front 121 30 months milestone gross motor | back 121 jumps |
front 122 30 months milestone fine motor | back 122 removes clothes, turns pages |
front 123 30 months milestone language | back 123 says at least 50 words |
front 124 30 months milestone social/cognitive | back 124 follows 2-step command, knows 1 color |
front 125 2 year milestone gross motor | back 125 runs, kicks ball, walks up stairs |
front 126 2 year milestone fine motor | back 126 uses spoon |
front 127 2 year milestone language | back 127 says 2-word phrases |
front 128 2 year milestone social/cognitive | back 128 knows 2 body parts, parallel play |
front 129 18 month milestone gross motor | back 129 walks easily, climbs on/off chair |
front 130 18 month milestone fine motor | back 130 scribbles, feeds w/ fingers |
front 131 18 month milestone language | back 131 says at least words in addition to mama and dada |
front 132 18 month milestone social/cognitive | back 132 follows 1-step command w/o gesture, imitates |
front 133 15 month milestone gross motor | back 133 takes a few steps |
front 134 15 month milestone fine motor | back 134 stacks 2 blocks |
front 135 15 month milestone language | back 135 says 1 or 2 words plus mama and dada |
front 136 15 month milestone social/cognitive | back 136 follows 1-step command w/ gesture, points to get something, shows affection |
front 137 1 year milestone gross motor | back 137 pulls to stand, cruises |
front 138 1 year milestone fine motor | back 138 pincer grasp |
front 139 1 year milestone language | back 139 says mama and dada, understands no |
front 140 1 year milestone social/cognitive | back 140 plays pat-a-cake, looks for hidden object |
front 141 Glaucoma in children pathophysiology | back 141 optic neuropathy +/- increased IOP |
front 142 Causes on increased IOP in glaucoma in children | back 142 impaired drainage of intraocular fluid, primary anatomic abnormaility (angle dysgenesis), Sturge-Weber syndrome, tumor, trauma, infection involving the angle, corticosteroid induced |
front 143 Glaucoma in children key features | back 143 tearing, photophobia, blepharospasm, enlarged cornea or globe, optic nerve cupping, increased IOP on tonometry |
front 144 Glaucoma in children management | back 144 surgery +/- pressure-reducing eye-drops |
front 145 Fragile X syndrome inheritance | back 145 X-linked dominant, remember they exhibit self-injurious behavior like hand-biting |
front 146 Signs concerning for pathologic microcephaly | back 146 neuro abnormalities like hypotonia and developmental delay, dysmorphic features, rapidly decreasing head circumference percentiles (ie curve crossing multiple major percentiles) |
front 147 Maternal Risk factors for SIDS | back 147 substance use (cigs, alc, drugs) |
front 148 Infant Risk factors for SIDS | back 148 prematurity or low birth weight, sleep environment (prone/side-sleep position, soft sleep surface, loose bedding, bed-sharing), smoke exposure |
front 149 Dilated cardiomyopathy is a features of | back 149 Duchenne muscular dystrophy |
front 150 Rett disorder epidemiology | back 150 greater incidence in girls, onset age 6-18 months |
front 151 Rett disorder pathophysiology | back 151 initially normal development followed by loss of speech, loss of purposeful hand use, and gait abnormalities |
front 152 Rett disorder additional findings | back 152 microcephaly, seizures, breathing abnormalities, sleep disturbance, autistic features |
front 153 Rett disorder etiology | back 153 MECP2 gene mutations |
front 154 Rett disorder neuropathology | back 154 deceleration of brain growth |
front 155 Rett disorder prognosis | back 155 middle aged life expectancy, decreased mobility, seizures, resp difficulties |
front 156 Tay-Sachs pathology | back 156 B- hexosaminidase A deficiency |
front 157 Tay-Sachs epidemiology | back 157 AR, Ashkenazi Jews, onset 2-6 months old |
front 158 Tay-Sachs clinial features | back 158 loss of motor milestones: hypotonia, feeding difficulties, cherry-red macula, hyperreflexia |
front 159 Niemann-Pick Disease pathology | back 159 sphingomyelinase deficiency |
front 160 Niemann-Pick Disease epidemiology | back 160 AR, Ashekensazi Jews, onset 2-6 months |
front 161 Niemann-Pick Disease clinical features | back 161 loss of motor milestones, hypotonia, feeding difficulties, cheery-red macula, hepatospenomegaly, areflexia, fatal by age 3 |
front 162 Subgaleal hemorrhage location | back 162 btw periosteum and gala aponeurotica |
front 163 Subgaleal hemorrhage clinical features | back 163 can expand over days, soft, fluctuant, diffuse, crosses sutures, +/- overlying bruising |
front 164 Subgaleal hemorrhage prognosis | back 164 can cause life-threatening blood loss |
front 165 Cephalohematoma location | back 165 subperiosteal (btw skull and periosteum) |
front 166 Cephalohematoma clinical features | back 166 present hours after birth, firm, nonfluctuant, does not cross sutures, overlying skin is normal, forceps or vacuum assisted delivery increases risk |
front 167 Cephalohematoma prognosis | back 167 increased hyperbilirubinemia risk, resorbs within a month |
front 168 Caput succedaneum location | back 168 subcutaneous |
front 169 Caput succedaneum clinical features | back 169 present at birth, soft and boggy, crosses sutures, overlying skin is normal |
front 170 Caput succedaneum prognosis | back 170 self-resolves in days |
front 171 You can also see periungal fibromas in a pt w/ | back 171 tuberous sclerosus complex |
front 172 Wilson disease pathogenesis | back 172 AR mutation of ATP7B --> hepatic copper accumulation --> leak rom damaged hepatocytes --> deposits in tissues (basal ganglia, cornea) |
front 173 Wilson disease clinical findings | back 173 Hepatic: acute liver failure, chronic hepatitis, cirrhosis Neuro: parkinsonism, gait disturbance, dysarthria Psych: depression, personality changes, psychosis |
front 174 Wilson disease Dx | back 174 decreased ceruloplasmin and increased urinary copper excretion, kayser-fleischer rings on slit lamp exam, increased copper on liver biopsy |
front 175 Wilson disease treatment | back 175 chelators (D-penicillamine, trientine), zinc (interferes w/ copper absorption) |
front 176 Ataxia-telangiectasia | back 176 AR disorder where defective DNA repair results in cerebellar ataxia, oculocutaneous telangiectasias, and recurrent sinopuml infection. Lymphoid tissue is often small/nonpalpable due to lymphopenia |
front 177 Gastroesophageal reflux pathogenesis | back 177 immature lower esophageal sphincter |
front 178 Gastroesophageal reflux clinical findings | back 178 spit up, normal weight gain, no pain/back-arching |
front 179 Gastroesophageal reflux management | back 179 upright positioning after feeds, burping during feeds, frequent, small volume feeds, vitamin D, supplements |
front 180 Beckwith-Wiedemann syndrome is associated with | back 180 omphalocele |
front 181 Mild dehydration | back 181 presents w/ history of decreased intake or increased fluid loss w/ minimal or no clinical symptoms |
front 182 Moderate dehydration | back 182 presents w/ decreased skin turgor, dry mucous membranes, tachycardia, irritability, a delayed capillary refill (2-3 seconds) and decreased urine output |
front 183 Severe dehydration | back 183 presents w/ cool, clammy skin, delayed capillary refill, (>3 seconds), cracked lips, dry mucous membranes, sunken eyes, sunken fontanelle (if still present), tachycardia, lethargy, and minimal or no urine output. Pts can present w/ hypotension and signs of shock |
front 184 Eosinophilic esophagitis pathogenesis and epidemiology | back 184 Th2-mediated inflammatory response triggered by food antigen exposure, comorbid atopy (asthma, eczema, food allergy, allergic rhinitis) common |
front 185 Eosinophilic esophagitis presentation in toddler | back 185 feeding difficulties (solid food refusal), weight loss |
front 186 Eosinophilic esophagitis presentation in school-aged children | back 186 abdominal pain, vomiting |
front 187 Eosinophilic esophagitis presentation in adolescents | back 187 dysphagia, heartburn, food impaction |
front 188 Eosinophilic esophagitis Dx | back 188 endoscopy and esophageal biopsy (eosinophils: at least 15/hpf), exclusion of alternate Dx (achalasia, infection) |
front 189 Eosinophilic esophagitis treatment | back 189 elimination from diet, PPIs, topical glucocorticoids, feeding therapy |
front 190 Hirschsprung disease | back 190 typically presents in neonates w/ decreased stooling, increased rectal tone, and signs of intestinal obstruction (bilious emesis, abdominal distention, dilated bowel loops). Contrast enema is performed to identify the level of obstruction |
front 191 Shiga toxin-producing E. coli pathogenesis | back 191 ingestion of contaminated/undercooked beef or contact w/ farm animals, invasion of intestinal epithelial cells, production of toxin |
front 192 Shiga toxin-producing E. coli clinical features | back 192 watery to bloody diarrhea within 3 days, NO high fever |
front 193 Shiga toxin-producing E. coli Dx | back 193 multiplex stool PCR testing, stool toxin assay, stool culture |
front 194 Shiga toxin-producing E. coli management | back 194 supportive care (aggressive fluids), avoidance of antibiotics and antidiarrheals |
front 195 Shiga toxin-producing E. coli complications | back 195 HUS (may develop 1-2 weeks after diarrhea onset) |
front 196 Campylobacter gastroenteritis epidemiology | back 196 most commonly transmitted via undercooked poultry |
front 197 Campylobacter gastroenteritis clinical features | back 197 fever, abdominal pain, diarrhea (mucoid +/- blood), pseudoappendicitis (RLQ pain due to acute ileocecitis) |
front 198 Campylobacter gastroenteritis treatment | back 198 supportive care (sx usually self-limited <7 days) |
front 199 Campylobacter gastroenteritis treatment | back 199 abx only in severe of high-risk cases |
front 200 Campylobacter gastroenteritis complications | back 200 Guillan Barre syndrome, reactive arthritis |
front 201 Meconium Ileus pathophysiology | back 201 inspissated stool causes obstruction at terminal ileum, strong association w/ CF |
front 202 Meconium Ileus clinical features | back 202 failure to pass meconium within 24hrs of birth, abdominal distention, no stool in rectal vault, +/- bilious emesis |
front 203 Meconium Ileus work-up | back 203 X-ray: dilated loops of small bowel Contrast enema: microcolon dx eval for CF via sweat test |
front 204 Meconium Ileus treatment | back 204 hyperosmolar enema, +/- surgical management |
front 205 Infant dyschezia resolves spontaneously by age | back 205 9 months |
front 206 Management of necrotizing enterocolitis immediate interventions | back 206 discontinuation of enteral feeds, nasogastric decompression, blood cultures, and empiric abx, IV fluid repletion |
front 207 Management of necrotizing enterocolitis monitoring | back 207 serial CBC and electrolytes, serial abdominal exams and imaging |
front 208 Management of necrotizing enterocolitis indications for surgery | back 208 bowel perf, clinical deterioration, despite medical management (suggestive of bowel necrosis) |
front 209 Management of duodenal atresia | back 209 discontinue enteral feeds, NG tube decompression, and surgical repair |
front 210 Cyclic vomiting syndrome history | back 210 personal or family hx of migraines, episodes often have identifiable trigger (infection, stress) |
front 211 Cyclic vomiting syndrome symptoms | back 211 stereotypical vomiting episodes: acute onset of nausea, abdominal pain/headache, vomiting, self-limited, lasting 1-2 days btw episodes: usually asymptomatic, often regular intervals (2-4 weeks) |
front 212 Neonatal sepsis etiology | back 212 group B strep, E. coli, listeria (age <7 days) |
front 213 Neonatal sepsis clinical features | back 213 temp instability (fever, hypothermia), CNS signs (lethargy, irritability, apnea), poor feeding, resp distress (tachypnea, grunting), jaundice |
front 214 Neonatal sepsis evaulation | back 214 inflammatory markers (CRP, ANC, procalcitonin), blood, urine, and CSF cultures |
front 215 Neonatal sepsis treatment | back 215 parenteral abx (ampicillin and gentamicin) |