Pediatrics2 Flashcards

1
Q

The most common congenital heart defect

A

VSD

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2
Q

Inv for congenital CHF

A
Echo
ECG
CXR
Pre- and post-ductal O2 saturation
4limb BP
Hyperoxia test
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3
Q

Amount of deoxyhemoglobulin causing cyanosis

A

30 d/dL

O2 sat <75%

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4
Q

Snowman heart

A

Total anomalous pulmonary venous return

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5
Q

Egg-shaped heart

A

Transposition of great arteries

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6
Q

Boot-shaped hearts

A

TOF

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7
Q

Types of STD

A
Ostium premium (common in DS)
Ostium secundum (most common)
Sinus venosus
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8
Q

Natural Hx of ASD

A

80-100% spontaneous closure rate if diameter < 8 mm

If remains patent: CHF and pulmonary HTN

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9
Q

Clinical presentation of ASD

A

Asymptomatic in childhood
If large: HF

2-3/6 pulmonary outflow murmur

Widely split and fixed S2

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10
Q

Inv in ASD

A

ECG: RAD, mild RVH, RBBB

CXR: increased pulmonary vasculature, cardiac enlargement

Echo: test of choice

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11
Q

Mx of ASD

A

Elective surgical/catheter closure between 2-5 yr of age

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12
Q

Clinical presentation of VSD

A

Small:
Asymptomatic

Early systolic/holosystolic murmur at LLSB, thrill

ECG: normal

CXR: normal

Echo: confirms Dx

Mod-large VSD:
CHF by 2 mo, late 2° pHTN

Holocystolic murmur at LLSB, mid-diastolic rumble at apex

ECG: LVH, LAH, LVH

CXR: increased pulmonary vasculature, cardiomegaly, CHF

Echo: diagnostic

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13
Q

Mx of VSD

A

Small:
Closes spontaneously

Mod-large:
Mx CHF
Surgical closure by 1yr

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14
Q

Functional and anatomical closure of PDA

A

F: within 15 h of birth

A: within first days

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15
Q

Natural Hx of PDA

A

Spontaneous closure common in premature, less common interm

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16
Q

Clinical presentation of PDA

A

Asymptomatic
Or
Bounding pulses, wide pulse pressure, hyperactive precordium.

Continuous machinery murmur at left infraclavicular area

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17
Q

Inv in PDA

A

ECG:left arterial enlargement, LVH, RVH

CXR: nl or mildly enlarged heart, increased pulmonary vasculature, prominent pulmonary artery

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18
Q

Mx of PDA

A

Indomethacin for premature

Catheter/surgical closure if:
Persistent beyond 3 mo
Respiratory compromise
FTT

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19
Q

Sx of obstructive cardiac lesions

A
Decreased U/O
Palloe
Cool extremities
Poor pulses
Shock
Sudden colapse
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20
Q

Coarctation of aorta associations

A

Turner

Bicuspid aortic valve

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21
Q

Coarctation Sx

A

Blood pressure discrepancy between upper and lower extremities (esp if > 20)

Deminished/delayed femoral pulses, relative to brachial

Systolic murmur with late peak at: apex, left axilla, left back

If severe: shock in neonate with PDA closure

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22
Q

Inv of coarctation

A

ECG: LVH

Echo/MRI for Dx

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23
Q

Mx of coarctation

A

PG to keep PDA patent

Surgical correction in neonate

Balloon arterioplasty in older children

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24
Q

Aortic stenosis Sx

A

Asymptomatic
Or
CHF
Exertional chest pain, syncope, sudden death

SEM at RUSB

Aortic ejection click at apex (if valvular)

Echo for Dx

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25
The most common type of aortic stenosis
Valvular
26
Mx of aortic stenosis
Valvular: balloon valvuloplasty Sub/supra-valvular: surgery Exercise restriction
27
Pulmonary stenosis, most common type
Valvular
28
Pulmonary stenosis Sx
If critical: Dependent on PDA Hypoxia, cyanosis Wide split S2 on expiration SEM at LUSB Pulmonary ejection click if valvular
29
Associations of PS
TF Congenital rubella Noonan
30
Inv for PS
ECG: RVH CXR: post-stenotic dilation of the main pulmonary artery Echo
31
Mx of PS
Surgery if critically ill or symptomatic older infants/children
32
Wide split S2 in
ASD: Fixed, wide PS: Wide in expiration
33
Characteristic features of non-cyanotic heart defects
ASD: Wild split and fixed S2 VSD: Early systolic/holosystolic murmur at LLSB Mid-diastolic rumble at apex PDA: Bounding pulses, wide pulse pressure, precordial hyperactivity Continuous machinery murmur at left infraclavicular area Coarctation: BP discrepancy between upper and lower extremities (>20), diminished/delayed femoral pulses Systolic murmur at apex, axilla, back AS: Syncope, exertional chest pain SEM at RUSB, click at aoex PS: Wide split S2 SEM at LUSB ejection click
34
Hyperoxic test
Performed in cyanosis (O2 sat <75%) Differentiates between cardiac and other causes of cyanosis Obtain Rt radial ABG in room air(preductal) Repeat after child inspires 100% O2 If PaO2 improves to >150, cyanosis less likely cardiac in origin
35
Pre-, post-ductal pulse oximetry
If > 5% difference= suggests R to L shunt
36
TOF Sx
Peak Dx :2-4 mo Initially no cyanosis (L to R shunt) Later, R to L shunt and cyanosis Hypoxic tet spells: During exertional states: => increase in R to L shunting => paroxysms of rapid and deep breathing, irritability, crying, increasing cyanosis, decreased intensity of murmur May lead to: decreased LOC, seizures, death Single loud S2 SEM at LSB
37
Inv for TOF
ECG: RAD, RVH CXR: boot-shaoed heart, decreased pulmonary vasculature, Rt aortic arch Echo
38
Mx of tet spells
O2 Knee-chest position Fluid bolus Morphine Propranolol
39
Tx of TOF
Surgical repair at 4-6 mo Earlier if marked cyanosis or tet spell
40
Transposition of great arteries Sx
PDA closure causes rapid deterioration: severe hypoxemia, acidosis, death If VSD present: no prominent cyanosis. But CHF within first weeks of life
41
Inv for TGA
ECG: RAD, RVH, CXR: egg-shaped heart, narrow mediastinum Echo
42
Mx of TFA
PGE1 infusion Then balloon atrial septoplasty Arterial switch surgery performed in 1st 2 wks
43
Mx of total anomalus pulmonary venous return
Surgery, urgent if severe cyanosis
44
Epstein anomaly associations
Maternal Li an BDZ in T1
45
Ebstein anomaly
Septal and posterior leaflets if tricuspid valve are malformed and displaced into the RV RV dysfunction Functional PS TR WOW
46
congenital heart defect with potential for coronary ischemia
Truncus arteriosus Tx: surgery within first 6 wk
47
Most common cause of death from CHD in first month of life
Hypoplastic left heart syndrome
48
Mx of hypoplastic left heart syndrome
Intubate, Correct metabolic acidosis IV PGE1 Surgical palliation/heart transplant
49
Heart anomalies depending on PTA
Hypoplastic left heart syndrome TGA Coarctation of aorta
50
Uncommon CHF Sx in children
Orthopnea PND Dependent edema
51
Key features of CHF
Tachycardia Tachypnea Cardiomegaly Hepatomegaly
52
Inv for CHF
CXR ECG Echo CBC, lytes, BUN, Cr, LFT
53
Mx of CHF
Setting up O2 Sodium and water restriction Increased caloric intake Diuretics Afterload reduction (ACEI) BB Dig rarely Correction of underlying
54
Tachycardia in infants
>150
55
Pediatric ECG findings that may be normal
HR >100 Shorter PR interval, QT interval, QRS duration Inferior and lateral small Q waves RV larger than LV in neonates RAD Large precordial R waves Upright T waves Inverted T waves in the anterior precordial leads
56
Benign PVC features
Single Uniform Disappear with exercise No associated structural lesion
57
Causes of PAC
``` Normal variant Or Lyte disturbances Hyperthyroidism Cardiac surgery Dig toxicity ```
58
SVT in children
HR > 220 in infants HR > 180 in children P absent or abnormal No beat-to-beat variability Narrow QRS PR indeterminable
59
How to differentiate sinus tachycardua from SVT
Slow the sinus rate by vagal massage, BB to identify P wave
60
Congenital heart block
Mother SLE, Anti-RO, anti-La Dx in utero (hydrops) Tx: pace maker
61
Innocent murmur characteristics
Asymptomatic SEM < 3/6 Soft, blowing, vibratory Physiologic S2 No extra sounds Varies with change in position
62
Pathological murmur
Sx/signs of cardiac disease All: Diastolic Pansystolic Continuous (except venous hum) 3/6 or more Fixed split or single S2 May have other sounds/clicks Unchanged with position change
63
Innocent heart murmur locations
LLSB: Still (flow across pulmonic valve leaflets) LUSB: Pulmonary ejection Peripheral pulmonic stenosis Supraclavicular: Supraclavicular arterial bruit (carotid) Infraclavicular: Venous hum
64
Definition of global developmental delay
Performance significantly below average in two or more domains of development (gross motor, fine motor, speech/language, cognitive, social/personal, activities of daily living) in a child 5 yr of age
65
Inv for global developmental delay (GDD)
Neurodevelopmental assessment Neuroimaging Vision and hearing test EEG Sleep study OT, PT, SLP assessments Psychosocial evaluation Lead level, CBC, ferritin, TSH Glucose, Lytes, lactate, ammonia, liver function, pyruvate, alb, TG, aa, urine organic acids, acylcarnithines, CPK Genetic: microarray, fragile X testing, testing for inborn errors of metabolism
66
Mx of global developmental delay
Depends on specific area of delay Speech and language therapy for language delay OT/PT for motor delay Early intervention services
67
Intellectual disability definition
State of functioning that begins in childhood Limitation in intelligence and adaptive skills IQ< 70 Often preceded by Dx of GDD
68
Areas of adaptive functioning deficit in itellectual disability
``` At least 2 of: Communication Self-care Home-living Social skills Self-direction Academic skills Work Leisure Health Safety ```
69
Classification of intellectual diabilities
Mild 50-70 Moderate 35-49 Severe 20-34 Profound <20
70
Inv for intellectual disability
Standardized psychology assessment (IQ, measure of adaptive functioning) Vision Hearing Neurologic Genetic/metabolic testing
71
Mx of intellectual disability
Main objective: enhance adaptive functioning level Community-based Tx, Early intervention Individual/family therapy Behavior management services Therapy services: OT, SLP Medications Education: life skills, vocational training, communication skills, family education Psychosocial support, respite care
72
Language delay definition
At least 1 SD below mean of age on standardized testing Types: Expressive Receptive Both M>F
73
RFs for SNHL
Genetics syndromes/family history Congenital (TORCH) Craniofacial abnormalities <1500 g birthweight Hyperbilirubinemia/kernicterus Asphyxia/low APGAR Bacterial meningitis, viral encephalitis
74
RFs for language delay
``` FHx Male Prematurity LBW Hearing loss ```
75
Inv for language delay
Language specific screens: The Early Language Milestone CAT/CLAMS, MCHAT... Developmental evaluation Refer to audiologist if needed CBC, lead level Genetic, metabolic W/U
76
Mx of language delay
Multidisciplinary Early intervention services Special education services SLP, OHNS, dental professionals, general support services Prevention: Parents can read aloud to their child Engage in dialogue reading Avoid baby talk Narrates daily activities
77
Best prognosis among etiologies of speech delay
Developmental speech delay
78
Persistence of language delay beyond this age is likely to persist into adulthood
5 yr
79
The effect of bilingualism on language delay
No effect
80
Specific learning disorder
Specific and persistent failure to acquire academic skills despite conventional instructions, adequate intelligence, and sociocultural opportunity Types: Dyslexia Dyscalculia Writing
81
Psychiatrist comorbidities associated with specific learning disorders
``` Anxiety Dysthymia Conduct disorder Major depressive disorder Oppositional defiance disorder ADHD ```
82
Possible etiologies of specific learning disorder
``` Turner Kleinfelter Prematurity LBW Birth trauma/hypoxia CNS damage Hypoxia Environmental toxins FAS Psychosocial deprivation Malnutrition ``` POOR VISUAL ACUITY IS NOT A CAUSE
83
RFs for specific learning disorders
Positive family history Prematurity Developmental/mental health conditions Neurologic disorders CNS infection/irradiation/traumatic injury
84
Inv for specific learning disorder
Psychoeducational assessment Scores on achievement tests on reading, writing or math, > 2 SD below that expected for age, education, IQ Evaluate: attention, memory, expressive language, coordination skills
85
Mx of Specific learning disorder
Quality instruction for specific learning disability Modification of the curriculum Providing accommodations Grade retention in certain students Specialized education placements
86
Most common preventable cause of intellectual disability
Fetal alcohol spectrum disorder
87
3 facial features of fetal alcohol syndrome
Flattened philtrum Thin upper lip Short palpebral fissures
88
Criteria for Dx of FAS
Growth deficiency: LBW, decelerating weight over time Characteristic facial features ``` CNS dysfunction: 3 or more of: Motor skills Neuroanatomy/neurophysiology Cognition Language Academic achievement Memory Attention Executive function Affect regulation Adaptive behavior Social skills Social communication Microcephaly ```
89
Criteria for Dx of ARBD (alcohol related brain-damage)
``` Congenital anomalies including: Cardiac Skeletal Renal Ocular Auditory ```
90
Criteria for diagnosis of ARND (alcohol-related Neurodevelopmental disorder)
CNS dysfunction similar to FAS Behavioral and cognitive abnormalities
91
Mx of FASD
Early diagnosis is essential Patients and their families should be linked to community resources and services to improve outcome
92
DM Dx in children (1 or 2)
1. Symptoms + random BS> 11.1 2. Two of: Fasting glucose > 7 2 h OGTT > 11.1 Random glucose > 11.1 3. One of the following on 2 separate occasions: Fasting glucose >7 2h OGTT > 11.1 Random > 11.1 Random glucose is not appropriate for confirmation
93
Mx of DM1
``` Diet: Consistent levels of carbs Avoiding food with high glycemic index Exercise Yearly influenza vaccine Blood glucose monitoring ``` Screen for complications: Ophthalmology assessment Microalbuminuria BP Screen for concurrent AI disorders, mental health issues, hyperlipidemia
94
Extensive activity involving legs in DM1 pts
May cause prolonged hypoglycemia
95
Tx of DKA
``` ABC 100% O2 Admit Monitor Correct fluid ECG ( for abn T) Ins (1st SC, then IV) Correct lytes Identify/treat participating event Avoid complications Low threshold to investigate and treat cerebral edema (CT, MRI, mannitol) Frequent BG, lyte, fluid monitoring) ```
96
Tx of hypoglycemia in DM1
Dextrose Glucagon Glucose
97
RFs for DM2
``` Obesity FHx Female PCOS Hyperglycemia exposure in utero Certain ethnic groups ```
98
Breastfeeding effect on risk of Childhood DM2
Reduces the risk
99
Inv for DM
FPG If very obese with multiple RFs: OGTT
100
Mx of DM2
``` Ins if severe metabolic decompensation: DKA A1C > 9% Unclear Dx (DM1/DM2) Random BG > 14 ``` Can wean off ins later ``` Initially LSM for 3-6 mo: Diet Wt loss Physical activity (at least 60 min/d) Screen time < 2h/d +/- metformin ``` HbA1c target: < 7% If target not achieved with LSM: Metformin (1st line. Could start at Dx) Glimepiride Insulin Screening: Same as DM1 Also: PCOS, NAFLD annually
101
DM2 monitoring
A1c q 3 mo ``` Finger-stick blood glucose if: On meds with risk of hypoglycemia If changing med regimen If have not met Tx goals If intercurrent illness ```
102
A1c target in different age ranges
<6 yr : <8% 6-12 yr: <7.5% >12 yr: <7%
103
Definition of short stature
Ht < 3rd percentile
104
Poor growth evidences
Growth deceleration: Ht crosses major percentile lines Growth velocity < 25th percentile
105
RFs for GH deficiency
Previous head trauma Hx of intracranial bleed or infection Head surgery/RT FHx Breech delivery
106
Inv for short stature
Mid-parental Ht AP Xray of left hand and wrist GH testing Other inv guided by Hx and PEx
107
Requirements for GH therapy for short stature
GH shown to be deficient by 2 different stimulation tests: Arginin Ins Glucagon Growth velocity < 3rd percentile or height << 3rd percentile Bone Xray shows unfused epiphyses/delayed bone age
108
DDx of proportional (upper body/lower body) short stature with normal growth velocity
Constitutional growth delay Familial
109
Constitutional growth delay
Delayed puberty May have family Hx of delayed puberty May need short-term: androgen/estrogen Delayed bone age Mid-parental height is often nl
110
Familial short stature
Normal bone age Tx not indicated FHx of short stature
111
DDx of proportionate short stature with slow growth velocity
``` Endocrine: GH deficiency Hypothyroidism/Hyperthyroidism Hypercortisolism Hypopituitarism Adrenal insufficiency ``` ``` Chronic disease: Cyanotic CHD Celiac IBD CF Chronic infections CRF ``` Psychosocial neglect: Decreased Ht and Wt (and HC if severe)
112
Tall stature
Ht > 2 SD above the mean for a given age, sex, race
113
Tall stature DDx
Constitutional/familial ``` Endocrine: Hyperthyroidism Gigantism Precocious puberty Beckwith-Wiedemann ``` ``` Genetic: Homocystinuria Kleinfelter Marfan Sotos ```
114
Questions to ask when short stature:
IUGR? Proportional? Velocity? Bone age?
115
The most common cause of congenital hypothyroidism
Thyroid gland dysgenesis
116
Causes of transient hypothyroidism
Maternal: Antibody mediated Iodine deficiency Prenatal exposure to anti-thyroid medications Neonatal: Neonatal iodine deficiency or excess Congenital liver hemangiomas Certain gene mutations
117
Screening for congenital hypothyroidism
Screen all neonates: TSH or free T4 ``` Repeat screening at 2 wk if: Preterm LBW Infant in NICU Specimen collection < 24 h of life Multiple births ``` If abn results: Confirm with serum levels from venupuncture
118
Inv for congenital hypothyroidism
``` Primary: Radioisotop scanning/thyroid U/S Tg Maternal anti-thyroid ab Urinary iodine ``` Secondary: MRI Gene analysis Eye exam (optic nerve hypoplasia)
119
Time to normalize thyroid hormone in congenital hypothyroidism
Within 2 wk to avoid cognitive impairment
120
Prognosis of congenital hypothyroidism
Excellent if treated within 1-2 mo Permanent developmental delay and/or disability, intellectual impairment, poor growth, hearing loss if treatment started after 3-6 mo of age
121
The most common cause of 46 XX DSD
Virilizing CAH
122
Inv for ambiguous genitalia
``` Lytes Renin Karyotyping 17-OH-prog Androgen FSH LH Abdominal U/S (uterus, ovaries, testicles) ```
123
Mx of ambiguous genitalia
Avoid announcement of probable sex Avoid use of personal pronouns Continuous psychosocial support for parents and child Elective surgical reconstruction
124
CAH Sx
Classic deficiency with salt-wasting: Inadequate aldosterone => FTT, hyperK, hypoNa, acidosis, hypoglycemia Classic deficiency without salt-wasting: Female: amenorrhea, precocious puberty, PCO, hirsutism Male: hyperpigmentation, penile enlargement, rapid growth, accelerated skeletal maturation, Non-classic: Mild androgen excess=> virilization, addisonian crises
125
Inv in CAH
Newborn screening ``` 17-OH-prog ACTH Lytes ABG Aldosterone, Renin activity ``` U/S
126
Mx of CAH
Correct fluid, lytes, glucose Hydrocortisone Fludrocortisone Extra glucocorticoids in times of stress Psychosocial support
127
Age of puberty onset in girls
8-13 yr
128
Onset of puberty in males
9-14 yr
129
Puberty sequence in males
Testicular enlargement Penile enlargement Pubarche Growth spurt
130
When should organic causes be excluded in puberty onset disorder?
Late puberty in girls and early puberty in boys
131
Gynecomastia during puberty
In 50% of males Self-limited Evaluate if any mass or discharge
132
Definitiin of precocious puberty
2° sexual characteristics 2-2.5 SD before population mean Boys< 9 yr Girls< 8 yr F> M
133
Percentage if idiopathic precocious puberty in M and F
F: 90% M: 50%
134
DDx of central precocious puberty
Idiopathic/constitutional CNS disturbances: tumor, ICP, infection... NF Primary severe hypothyroidism
135
DDx of peripheral precocious puberty
``` Tumors CAH Exogenous steroids Hypothyroidism McCune-Albright Aromatase excess ```
136
Normal growth velocity
Prepubertal: 4-6 cm/y Puberty: Girls: 6-8 cm/h Boys: 8-10 cm/h
137
Inv for precocious pubeety
Initial: Bone age FSH, LH, testo, estradiol, 17-OH-prog, DHEA-S, TSH 2° tests: MRI head, pelvic U/S, B-hCG, GnRH, ACTH
138
Mx of precocious puberty
Indication for medical intervention: Rapid advancement Early age Risk of compromise of final adult height Psychological ``` If central: GnRH agonist (luprolide) ``` If peripheral: Treat underlying Decrease production of hormones/block effect (Ketoconazole, spironolactone, tamoxifen, anastrozole) Surgical intervention
139
Definition of delayed puberty
Failure to develop 2° sexual characteristics by 2-2.5 SD beyond population mean Male: lack of testicular enlargement by 14 Females: lack of breast development by 13, no menarche by 16/within 5 yr of puberty onset M>F
140
Causes of delayed puberty
Central: Constitutional Hypogonadotropic hypogonadism ``` Peripheral: Hypergonadotropic hypogonadism: Primary gonadal failure Gonadal damage Turner AIS Hormone deficiency ```
141
Inv for delayed puberty
Initial: Bone age Estradiol, testo, FSH, LH, TSH, free T4, IGF-1 CBC, lytes, BUN, Cr, LFT, liver enzymes, ESR, CRP, U/A, 2° tests: MRI head, pelvic U/S, karyotype, IBD panel, celiac panel, LH following GnRH
142
Mx of delayed puberty
Underlying Hormonal replacement
143
Red flags in vomiting
``` Bilious Bloody Projectile Abdominal distention and tenderness High fever Dehydration ```
144
Vomiting without diarrhea
Most likely not gastroenteritis
145
Inv for vomiting
CBC Lytes, BUN, Cr, amylase, lipase, glucose In risk child add: ESR, VBG Blood/stool C&S Imaging
146
TEF time of presentation
Soon after birth
147
Inv for TEF
NG CXR upper GI series with water-soluble contrast
148
Pyloric stenosis time of presentation
2-4 wk
149
Pyloric stenosis inv
U/S Upper GI study if U/S not helpful Lytes ABG
150
Arching of back is sign of
GERD
151
Inv for GERD
Empiric acid suppression pH monitoring study Upper GI studies Endoscopy
152
Mx of vomiting in children
Rehydration Underlying ``` Antiemetic if > 2yr and severe vomiting: Promethazine Prochlorprazine Metoclopramide Ondansetron ```
153
Prevalence of GERD in infants
50%
154
Vomiting in GERD
Soon after feeding Non-bilious Rarely contains blood Small volume < 30 ml
155
Inv for GERD
NON IF THRIVING CHILD Upper GI radiology Esophageal pH Bx Endoscopy
156
Mx of GERD
Infants: Thickened feeds Frequent and smaller feeds Elevation of head Change formula to hydrolyzed protein or aa Mothers exclude milk and egg from diet (if BF) Older children/adolescents: same as adults Medical: Short-term parenteral feeding (to enhance wt gain) Ranitidine PPI If gastroparesis: Domperidone Metoclopramide
157
Diarrhea definition
Infants: Increased stool frequency to twice as often per day Children: 3+ loose or watery stool per day Acute: <2wk Chronic >2 wk
158
Inv for acute diarrhea
Stool C&S, O&P, microscopy (WBC) C. Difficile toxin Electron microscopy for viruses B/C, U/C Blood work
159
Inv for chronic diarrhea
Serial Wt and Ht, growth percentile If thriving: Stool culture, stool reducing substances If red flags present: Stool: consistency, pH, reducing substances, microscopy, occult blood, O/P, C/S, C.difficile toxin, 3d fecal fat, a-1-antitrypsin clearance, elastase U/A, U/C CBC, diff, ESR, CRP, smear, lytes, protein, alb, carotene, Ca, PO4, Mg, Fe, ferritin, folate, fat-soluble vitamins, PTT, INR Sweat chloride, celiac screen, thyroid function, urine VMA, HVA, HIV test, lead levels CXR, Upper GI series, follow through Endoscopy, small bowel Bx
160
Diarrhea red flags
``` Bloody stool Fever Petechia/purpura Signs of severe dehydration Chronic skin rash Wt loss/ FTT Other serious infections ```
161
Inv for gastroenteritis
Not usually required in young children Stool analysis: WBC/RBC: bacterial/parasitic pH <6, reducing substances: viral etiology
162
Viral gastroenteritis features
Associated with URTI Resolves in 3-7 d Slight fever, malaise, vomiting, vague abd pain
163
Bacterial gastroenteritis features
Severe abd pain High fever Bloody diarrhea
164
RFs for gastroenteritis
Daycare Young age Sick contact ImmComp Travel Poorly cooked/refrigerated meat or food AB
165
Mx of gastroenteritis
Address dehydration Early refeeding Ondansetron: If mild-mod dehydration, failed ORT, significant vomiting AB, anti-parasitic therapy when indicated Notify public health if needed Promote regular hand washing Rota vaccine ANTIDIARRHEAL MEDS NOT INDICATED
166
When to return to school after gastroenteritis
24 h after the last episode of diarrhea
167
The most common cause of chronic diarrhea during infancy
Toddler’s diarrhea
168
Onset and resolution of toddler’s diarrhea
Onset: 6-36 mo Cessation: 2-4 yr
169
Sx of Toddler’s diarrhea
Excess juice intake Disaccharide malabsorption +/- Undigested food particles in stool Excoriated diaper rash
170
Mx of toddler diarrhea
Reassurance ``` 4Fs: Adequate fiber Normal fluid intake 35-40% fat Discourage excess fruit juice ```
171
Lactose intolerance types
1°: Older children. Crampy abd pain with loose stool 2°: Older infants. Persistent diarrhea due to decreased lactase production post viral/bacterial infection, celiac disease, IBD.
172
Dx of lactase deficiency
Trial of lactose-free diet Acid pH of stool Positive reducing sugars Positive breath hydrogen test (if > 6mo)
173
Mx of lactase deficiency
Lactose-free diet Soy formula Lactase-containing tablets/capsules/drops
174
Usual age of celiac presentation
6-24 mo, but any age
175
Pathophysiology of milk allergy vs cow’s milk protein allergy
Milk allergy: IgE mediated Cow’s milk protein allergy: non-IgE, more common
176
Milk allergy Sx
Within hours of exposure Urticaria, pruritis Wheeze, cough
177
Sx of cow’s milk protein allergy
= food protein induced proctocolitis of infancy 2-8 mo of infancy Proctocolitis: mild diarrhea, small amounts of bloody stools Enterocolitis: vomiting, diarrhea, anemia, hematochezia, constipation Enteropathy: chronic diarrhea, hypoalbuminemia,
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Inv for milk allergy or cow’s milk protein allergy
Gold std: food challenge Skin prick test Allergen-specific IgE Patch testing
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IgA and celiac
IgA deficiency is more prevalent in celiac disease So order IgA level along with IgA-anti-tTG
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Forbidden in celiac:
Barley Rye Oat Wheat
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Mx of milk allergy
Stop exposure
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Mx of cow’s milk protein allergy
Stop, reintroduce milk at 6-8 mo >90% will outgrow intolerance by 1 yr Casein hydrolysate formula Or Mother may sequentially remove: cow’s milk protein, all bovine protein, soy protein, legumes, (7d washout) and continue BF with adequate Ca and VitD
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Definition of constipation
< 3 stool/wk Hard pellet-like
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Time of constipation onset in infants
When introducing cow’s milk after breast milk due to high fat and solute and lower water content
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Time of constipation onset in toddlers/older children
During toilet training Or Starting school
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Mx of constipation
Education: Explain the mechanism Clean out: PEG 3350 flakes, picosalax, PEGlyte ``` Maintenance: Adequate fluid Adequate dietary fibre Stool softening (PEG3350, mineral oil) Appropriate toilet training technique (3-10 min, 1-2 x/d) ``` Children should be treated for at least 6 mo Regular F/U with ongoing support/encouragement
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RFs for intussusception
CF GJ tube (jejunum) M> F Most common age: 3-12 mo
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Triad of intissusception
Abd pain Palpable mass Apple currant jelly stool Often preceded by URTI
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Dx of intussusception
U/S Air enema (75%also curative)
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Mx of intussusception
Air enema Reduction under hydrostatic pressure Surgery (rarely needed)
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Chronic abd pain prevalence
10% of school children Peak: 8-10 y F> M Definition: > 3 yr 3 mo 3 episodes of severe pain
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Dx of functional abd pain requires:
No alarming Sx Normal PEx Normal S/E
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Alarming Sx for chronic abd pain
Age < 5 yr Involuntary wt loss Deceleration of linear growth GI blood loss Significant vomiting Chronic severe diarrhea Persistent upper or right lower quadrant pain Pain away from midline Pain awakens child at night Unexplained fever Anemia Rash Joint pain Travel Hx FHx of IBD Abn/unexplained physical exam findings
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Characteristics of chronic abd pain
Clusters of vague, crampy pain Periumbilical, epigastric Seldom awakens Less common on weekends Aggravated by exercise Alleviated by rest Psychological factors related to onset and maintenance School avoidance Dx of exclusion
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Psychiatric comorbidities of chronic abd pain
``` Anxiety Somatoform Mood Learning disorder Sexual abuse Eating disorders Elimination disorders ```
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Inv for chronic abd pain
FOB Others based on Hx, PEx
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Mx of chronic abd pain
Continue to attend school Mx any emotional/family problems Counseling CBT Trial of high fiber diet Trial of lactose free diet If dyspepsia: acid reduction therapy If pain: Anti spasmodic agents, smooth muscle relaxants If altered bowel habits: Non-stimulating laxatives, antidiarrheal Amitriptyline Reassurance
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Course of chronic abd pain
Resolves in 30-50% within 2-6 wk of Dx 30-50% will have functional pain as adults
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Most common cause of chronic lower GIB
Fissure
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Inv for lower GIB
Stool (C&S, C.difficile toxin) U/A, microscopy CBC, smear, diff, ESR, CRP, lytes, urea, Cr, INR, PTT, alb, iron studies, amoeba titers Abd Xray Meckel scan
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Mx of lower GIB
ABC NPO NGT Once stable, endoscopy and/or surgery as indicated
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Age and Hb level in physiologic anemia
8-12 wk 100 g/L Earlier and more exaggerated if premature
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Most common cause of childhood anemia
IDA
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Age of Iron reserves exhaustion in term and preterm infants
Term: by 6 mo Preterm: 2-3 mo
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Age of iron deficiency anemia
6mo-3yr 11-17yr
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RFs for IDA
Premature LBW Low SES Whole cow milk in first year of life Age> 6 mo: <2 servings/d iron-fortified cereals, red meat, legumes Age <12 mo: low-iron formula (<10 mg/L), primary diet of cow, goat, soy milk Age 1-5 y: > 16-20 oz/d of non-fortified milk Repeated blood sampling Cow’s milk-induced colitis
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Inv for anemia
CBC, retic count Mentez index (MCV/RBC) PBS Iron studies
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Mentez index
To differentiate IDA from thalassemia If > 13: IDA IF < 13: thalassemia
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Initial therapy for IDA
Trial of iron therapy Encourage diverse balanced diet Limit homogenized milk to 16-20 oz/d Oral iron therapy: 4-6 mg/kg/d elemental iron, divided bid/tid x 3mo
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Normal MCV in children
70 + age until 80
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Prevention of IDA
BF terms: Start Iron supplementation (1 mg/kg/d) at 4-6 mo Continue until able to eat at least 2 feed/d of iron-rich foods Non BF terms (<50% of diet): Iron-fortified formula from birth Premature infant: Iron supplements from 1mo through to 1 yr of age No cow’s milk until 9-12 mo Early introduction of red-meat and iron-rich vegetables
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Universal Hb screening at:
9 mo
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Total daily iron should be:
6-12 mo: 11 mg 1-3 yr: 7 mg
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Response to iron therapy
Increased retic count: day 2-3 Peak retic: day 5-7 Increased Hb in: 4-30 d Repletion of iron stores: 1-3 mo Repeat Hb level after 1 mo of treatment
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Sx of vitamin K deficiency
Generalized bleeding GIB Intracranial hemorrhage (Within few days after birth)
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Prevention of vitamin K deficiency
IM injection at birth Or Oral: birth, 2-4 wk, 6-8 wk (higher risk of hemorrhage)
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Human milk vitamin K
Small amount
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Platelet function activity in vWD
Distorted (Increases)
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Most common cause of thrombocytopenia in children
ITP
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Peak age of ITP
2-6 y M=F
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Which blood disorder protects against malaria?
G6PD deficiency
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Sx of ITP
1-3 wk after viral infection Sudden onset Petechia, purpura, epistaxis Otherwise well child No LAP/HSM
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Clinically significant bleeding happent in what percent of ITP pts?
3%
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Indications for MBA/Bx in ITP
Atypical presentation > 1 cell-line abnormal HSM
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Mx of ITP
Spontaneous recovery in >70% within 3 wk Tx with IVIg or prednisone if: Mucosal bleeding Internal bleeding Plt < 10 At risk of significant bleeding (surgery, dental, concomitant vasculitis or coagulopathy) If life-threatening bleed: Additional plt transfusion Emergent splenectomy Avoid contact sport/ ASA, NSAIDs
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Persistent or chronic ITP definition
Persistent >3 mo Chronic >12 mo Mx: re-evaluate Treat if symptomatic
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IVIg vs prednisone for ITP
IVIg: more rapid plt increase
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Anti D in IVP
A single dose of anti-D can be used as first line treatment in Rh positive, non-splenectomized children requiring Tx
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The most common type of pediatric malignancy
Leukemia> Followed by: brain tumor> lymphoma
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Inv for generalized LAP
``` CBC diff B/C Uric acid, LDH ANA, RF, ESR EBV, CMV, HIV serology Toxo titer Fungal serology CXR TB Bx ```
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Inv for regional LAP
Period of observation if asymptomatic Trial of oral AB U/S Bx if: >6 wk and or constitutional symptoms
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Most common cause of acute bilateral cervical LAP
Viral
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Age of leukemia
2-5 y
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Mist common type of leukemia
ALL
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Hyperleukocytosis
WBC >100,000 Medical emergency Respiratory/neurological distress Risk of: ICH Pulmonary leukostasis syndrome Tumor lysis syndrome
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Tx of leukemia
Fluid Allopurinol/raspuricase FFP, plt Induction chemo Combination chemo Allogenic SCT (if high-grade, recurrent) Supportive care NO RBC TRANSFUSION UNLESS SYMPTOMATIC (then very small volumes)
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Risk stratification in leukemia is based on
WBC and age Also CNS/testicular disease Immunophenotype Cytogenetics Most important prognostic factor: Initial response to therapy
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Age of Hodgkin
15-34 >50
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NHL age
Peak 7-11 y
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Most common presentation of hodgkin lymphoma
Persistent, painless, firm, cervical or supraclavicular LAP
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Back pain children
Must always be investigated
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Prognosis of lymphoma
Hodgkin: >90% 5 yr survival NHL: 75-90% 5yr survival
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Prognosis of leukemia
ALL, 80-90% 5yr survival AML 50-60%
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Age of wilms Dx
2-5 yr | M=F
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Most common presentation of Wilm’s tumor
Unilateral abdominal mass
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Mx of Wilm’s
Staging Nephrectomy Chemo Radio
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Prognosis of wilm’s
90% long-term survival
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The most common cancer occurring in the first year of life
Neuroblastoma
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Most common site of neuroblastoma
Adrenal gland
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Sx of neuroblastoma mets
``` Bone pain Limp Periorbital ecchymoses Abd pain Emesis Fever Wt loss Anorexia Hepatomegaly Blueberry muffin skin nodules ```
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Opsimyoclonus
Paraneoplastic manifestation of neuroblastoma
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Mx of neuroblastoma
``` Surgery RT Chemo Autologous SCT Immunotherapy ```
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Good prognostic factors in neuroblastoma
Age<18 mo Lower stages Posterior mediastinum and neck Low serum ferritin More differentiated histology Aneuploidy Absent MYCN oncogene amplification
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Definition of fever of unknown origin
Daily or intermittent fevers For at least two consecutive weeks Uncertain cause
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Fever in neonate. Next step?
Admit Full SWU Empiric AB
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Fever in child 1-3 mo, next step?
If non-toxic, reliable F/U, low-risk Rochester criteria: Partial SWU + AB May consider treatment as outpt Or Consider observation without AB All others: Admit Full SWU Empiric AB
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Infans with low risk of serious bacterial infaction according to Rochester criteria
``` Clinically well WBC 5-15 Band<1.5 U/A <10 WBC Stool (if diarrhea) <5 WBC Born > 37 wk Home with mom No hospitalization No prior AB No prior Tx for unexplained hyperBil No chronic disease ```
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Partial SWU includes
CBC, diff Urine R&M, S&C Blood S&C LP CXR (if respiratory Sx) Stool S&C (if GI Sx)
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Fever in child 3 mo- 3 yr
If toxic: Admit Full SWU Empiric AB If non-toxic and no focus: If T < 39: Urine R&M Observe If T > 39: CBC, urine R&M Blood S&C
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If a child 3 mo-3 yr, non toxic, no focus, T > 39 °, next step?
Urine R and M CBC ``` If WBC > 15000: Blood C&S Urine C&S If no source found: amoxi or ceftriaxone Acetaminophen ``` ``` If WBC < 15000: Blood C&S Observe Acetaminophen F/U in 24 h ```
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Most common age of AOM
18 mo-6 yr
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Etiology of refractory AOM
Non-typeable HI
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RFs for AOM
Prolonged bottlefeeding while lying down Short duration of breast-feeding Pacifier use Second hand smoke Crowded living condition FHx of otitis media Orofacial abnormalities Immunodeficiency Ethnicity (first nations, inuit)
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Most important diagnostic criteria for AOM
Bulging TM
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Tx of AOM
1st line: Amoxicillin 75-90 mg/d divided into 2 doses If allergic: macrolide, TMP-SMX 2nd line: Amoxi-clav Cephalosporin: cefixime, ceftriaxone, cefuroxime, cefaclor Also: Antipyretics/analgesics Decongestants
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Unresponsive AOM definition
Sx, signs, otoscopic findings persist beyond 48 h of AB Tx
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Etiology and Tx of otitis-conjunctivitis Sx
Etiology: HI, M. Catarrhalis Tx: Amoxicillin-clavulanate Cephalo: cefixime, ceftriaxone, cefuroxime, cefaclor
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Prevention of AOM
Parent education Vaccines (pneumococcal, influenza) Surgery: Tympanostomy tube Adenoidectomy
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Indications of AB therapy in AOM
``` > 6mo with: Moderate-severe otalgia Irritable, Difficulty sleeping, Poor response to antipyretic Otalgia for at least 48 h T: 39 or higher ``` If no severe signs or symptoms: Either AB or observation with close F/U Begin AB if no improvement after 48-72 h of Sx onset
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Role of prophylactic AB in recurrent AOM
None
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Indication of tympanostomy
3 episodes of AOM in 6 mo or 4 episodes in 1 yr (one in last 6 mo)
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AOM without MEE or AOM with MEE but without bulging or Mildly erythematous TM Mx?
Consider viral Reassess in 24-48 h
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Most common cause of pediatric hearing loss
Otitis media with effusion (no inmflammation)
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RFs of OME
Same as AOM
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The most reliable finding in OME with pneumatic otoscopy
Immobility
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Tx of OME
Expectant: 90% improve within 3 mo Audiogram Myringotomy +/- ventilation tube +/- adenoidectomy (if enlarged, or on insertion of 2nd set of tubes after first set falls out) Ventilation tube
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Parvovirus risk of transmission after Sx begin
Low
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Parvo virus transmission mode
Respiratory secretions Blood
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Onset of rash in erythema infectiosum
10-17 d after symptoms
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Which rash may recur with sunlight or exercise?
Parvo B19
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Viruses causing Gianotti-Crosti
EBV | Hep B
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Gianotti-Crosti resolution
3-12 wk
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HFMD communicability
Usually 1-7 d after Sx | May be up to month
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HSV incubation
1-26 d
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Measles communicability
4 d before and after rash
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Mx of unimmunized contacts of measles
Vaccine within 72 h of exposure Or IgG within 6 d of exposure Respiratory isolation
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Confirmation of Dx of enteroviruse infections
Viral culture from nasopharynx and rectal swabs
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Reseola infantum rash starts at
Neck and trunk
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Nagayama spots
Enanthema of roseola Erythematous papules on soft palate and uvula
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Rubella communicability
7days before to 7 days after eruptions
291
Rubella rash starts at
Face
292
Varicella communicability
1-2 d pre-eruption to 5d post eruption
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Viral rash with risk of necrotizing fasciitis
Varicella
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Viral infections with risk of DIC
HSV, varicella