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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
Q

The most common type of aortic stenosis

A

Valvular

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26
Q

Mx of aortic stenosis

A

Valvular: balloon valvuloplasty

Sub/supra-valvular: surgery

Exercise restriction

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27
Q

Pulmonary stenosis, most common type

A

Valvular

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28
Q

Pulmonary stenosis Sx

A

If critical:
Dependent on PDA
Hypoxia, cyanosis

Wide split S2 on expiration
SEM at LUSB
Pulmonary ejection click if valvular

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29
Q

Associations of PS

A

TF
Congenital rubella
Noonan

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30
Q

Inv for PS

A

ECG: RVH

CXR: post-stenotic dilation of the main pulmonary artery

Echo

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31
Q

Mx of PS

A

Surgery if critically ill or symptomatic older infants/children

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32
Q

Wide split S2 in

A

ASD:
Fixed, wide

PS:
Wide in expiration

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33
Q

Characteristic features of non-cyanotic heart defects

A

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

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34
Q

Hyperoxic test

A

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

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35
Q

Pre-, post-ductal pulse oximetry

A

If > 5% difference= suggests R to L shunt

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36
Q

TOF Sx

A

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

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37
Q

Inv for TOF

A

ECG: RAD, RVH

CXR: boot-shaoed heart, decreased pulmonary vasculature, Rt aortic arch

Echo

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38
Q

Mx of tet spells

A

O2

Knee-chest position

Fluid bolus

Morphine

Propranolol

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39
Q

Tx of TOF

A

Surgical repair at 4-6 mo

Earlier if marked cyanosis or tet spell

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40
Q

Transposition of great arteries Sx

A

PDA closure causes rapid deterioration: severe hypoxemia, acidosis, death

If VSD present: no prominent cyanosis. But CHF within first weeks of life

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41
Q

Inv for TGA

A

ECG: RAD, RVH,

CXR: egg-shaped heart, narrow mediastinum

Echo

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42
Q

Mx of TFA

A

PGE1 infusion

Then balloon atrial septoplasty

Arterial switch surgery performed in 1st 2 wks

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43
Q

Mx of total anomalus pulmonary venous return

A

Surgery, urgent if severe cyanosis

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44
Q

Epstein anomaly associations

A

Maternal Li an BDZ in T1

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45
Q

Ebstein anomaly

A

Septal and posterior leaflets if tricuspid valve are malformed and displaced into the RV

RV dysfunction

Functional PS

TR

WOW

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46
Q

congenital heart defect with potential for coronary ischemia

A

Truncus arteriosus

Tx: surgery within first 6 wk

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47
Q

Most common cause of death from CHD in first month of life

A

Hypoplastic left heart syndrome

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48
Q

Mx of hypoplastic left heart syndrome

A

Intubate,
Correct metabolic acidosis
IV PGE1
Surgical palliation/heart transplant

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49
Q

Heart anomalies depending on PTA

A

Hypoplastic left heart syndrome

TGA

Coarctation of aorta

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50
Q

Uncommon CHF Sx in children

A

Orthopnea

PND

Dependent edema

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51
Q

Key features of CHF

A

Tachycardia
Tachypnea
Cardiomegaly
Hepatomegaly

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52
Q

Inv for CHF

A

CXR
ECG
Echo
CBC, lytes, BUN, Cr, LFT

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53
Q

Mx of CHF

A

Setting up
O2
Sodium and water restriction
Increased caloric intake

Diuretics
Afterload reduction (ACEI)
BB
Dig rarely

Correction of underlying

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54
Q

Tachycardia in infants

A

> 150

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55
Q

Pediatric ECG findings that may be normal

A

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

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56
Q

Benign PVC features

A

Single
Uniform
Disappear with exercise
No associated structural lesion

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57
Q

Causes of PAC

A 
Normal variant 
Or
Lyte disturbances
Hyperthyroidism
Cardiac surgery
Dig toxicity
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58
Q

SVT in children

A

HR > 220 in infants
HR > 180 in children

P absent or abnormal

No beat-to-beat variability

Narrow QRS

PR indeterminable

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59
Q

How to differentiate sinus tachycardua from SVT

A

Slow the sinus rate by vagal massage, BB to identify P wave

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60
Q

Congenital heart block

A

Mother SLE,

Anti-RO, anti-La

Dx in utero (hydrops)

Tx: pace maker

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61
Q

Innocent murmur characteristics

A

Asymptomatic

SEM

< 3/6

Soft, blowing, vibratory

Physiologic S2

No extra sounds

Varies with change in position

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62
Q

Pathological murmur

A

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

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63
Q

Innocent heart murmur locations

A

LLSB:
Still (flow across pulmonic valve leaflets)

LUSB:
Pulmonary ejection
Peripheral pulmonic stenosis

Supraclavicular:
Supraclavicular arterial bruit (carotid)

Infraclavicular:
Venous hum

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64
Q

Definition of global developmental delay

A

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

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65
Q

Inv for global developmental delay (GDD)

A

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

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66
Q

Mx of global developmental delay

A

Depends on specific area of delay

Speech and language therapy for language delay

OT/PT for motor delay

Early intervention services

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67
Q

Intellectual disability definition

A

State of functioning that begins in childhood

Limitation in intelligence and adaptive skills

IQ< 70

Often preceded by Dx of GDD

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68
Q

Areas of adaptive functioning deficit in itellectual disability

A 
At least 2 of:
Communication
Self-care
Home-living
Social skills
Self-direction
Academic skills
Work
Leisure
Health
Safety
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69
Q

Classification of intellectual diabilities

A

Mild 50-70

Moderate 35-49

Severe 20-34

Profound <20

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70
Q

Inv for intellectual disability

A

Standardized psychology assessment (IQ, measure of adaptive functioning)

Vision

Hearing

Neurologic

Genetic/metabolic testing

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71
Q

Mx of intellectual disability

A

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

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72
Q

Language delay definition

A

At least 1 SD below mean of age on standardized testing

Types:
Expressive
Receptive
Both

M>F

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73
Q

RFs for SNHL

A

Genetics syndromes/family history

Congenital (TORCH)

Craniofacial abnormalities

<1500 g birthweight

Hyperbilirubinemia/kernicterus

Asphyxia/low APGAR

Bacterial meningitis, viral encephalitis

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74
Q

RFs for language delay

A 
FHx
Male
Prematurity
LBW
Hearing loss
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75
Q

Inv for language delay

A

Language specific screens: The Early Language Milestone

CAT/CLAMS, MCHAT…

Developmental evaluation

Refer to audiologist if needed

CBC, lead level

Genetic, metabolic W/U

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76
Q

Mx of language delay

A

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

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77
Q

Best prognosis among etiologies of speech delay

A

Developmental speech delay

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78
Q

Persistence of language delay beyond this age is likely to persist into adulthood

A

5 yr

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79
Q

The effect of bilingualism on language delay

A

No effect

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80
Q

Specific learning disorder

A

Specific and persistent failure to acquire academic skills despite conventional instructions, adequate intelligence, and sociocultural opportunity

Types:
Dyslexia
Dyscalculia
Writing

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81
Q

Psychiatrist comorbidities associated with specific learning disorders

A 
Anxiety
Dysthymia
Conduct disorder
Major depressive disorder
Oppositional defiance disorder
ADHD
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82
Q

Possible etiologies of specific learning disorder

A 
Turner
Kleinfelter
Prematurity
LBW
Birth trauma/hypoxia
CNS damage
Hypoxia
Environmental toxins
FAS
Psychosocial deprivation
Malnutrition

POOR VISUAL ACUITY IS NOT A CAUSE

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83
Q

RFs for specific learning disorders

A

Positive family history

Prematurity

Developmental/mental health conditions

Neurologic disorders

CNS infection/irradiation/traumatic injury

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84
Q

Inv for specific learning disorder

A

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

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85
Q

Mx of Specific learning disorder

A

Quality instruction for specific learning disability

Modification of the curriculum

Providing accommodations

Grade retention in certain students

Specialized education placements

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86
Q

Most common preventable cause of intellectual disability

A

Fetal alcohol spectrum disorder

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87
Q

3 facial features of fetal alcohol syndrome

A

Flattened philtrum

Thin upper lip

Short palpebral fissures

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88
Q

Criteria for Dx of FAS

A

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
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89
Q

Criteria for Dx of ARBD (alcohol related brain-damage)

A 
Congenital anomalies including:
Cardiac
Skeletal
Renal
Ocular
Auditory
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90
Q

Criteria for diagnosis of ARND (alcohol-related Neurodevelopmental disorder)

A

CNS dysfunction similar to FAS

Behavioral and cognitive abnormalities

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91
Q

Mx of FASD

A

Early diagnosis is essential

Patients and their families should be linked to community resources and services to improve outcome

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92
Q

DM Dx in children (1 or 2)

A
  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

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93
Q

Mx of DM1

A 
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

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94
Q

Extensive activity involving legs in DM1 pts

A

May cause prolonged hypoglycemia

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95
Q

Tx of DKA

A 
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)
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96
Q

Tx of hypoglycemia in DM1

A

Dextrose

Glucagon

Glucose

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97
Q

RFs for DM2

A 
Obesity
FHx
Female
PCOS
Hyperglycemia exposure in utero
Certain ethnic groups
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98
Q

Breastfeeding effect on risk of Childhood DM2

A

Reduces the risk

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99
Q

Inv for DM

A

FPG

If very obese with multiple RFs:
OGTT

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100
Q

Mx of DM2

A 
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

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101
Q

DM2 monitoring

A

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
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102
Q

A1c target in different age ranges

A

<6 yr : <8%

6-12 yr: <7.5%

> 12 yr: <7%

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103
Q

Definition of short stature

A

Ht < 3rd percentile

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104
Q

Poor growth evidences

A

Growth deceleration:
Ht crosses major percentile lines
Growth velocity < 25th percentile

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105
Q

RFs for GH deficiency

A

Previous head trauma

Hx of intracranial bleed or infection

Head surgery/RT

FHx

Breech delivery

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106
Q

Inv for short stature

A

Mid-parental Ht

AP Xray of left hand and wrist

GH testing

Other inv guided by Hx and PEx

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107
Q

Requirements for GH therapy for short stature

A

GH shown to be deficient by 2 different stimulation tests:
Arginin
Ins
Glucagon

Growth velocity < 3rd percentile or height &laquo_space;3rd percentile

Bone Xray shows unfused epiphyses/delayed bone age

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108
Q

DDx of proportional (upper body/lower body) short stature with normal growth velocity

A

Constitutional growth delay

Familial

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109
Q

Constitutional growth delay

A

Delayed puberty

May have family Hx of delayed puberty

May need short-term: androgen/estrogen

Delayed bone age

Mid-parental height is often nl

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110
Q

Familial short stature

A

Normal bone age

Tx not indicated

FHx of short stature

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111
Q

DDx of proportionate short stature with slow growth velocity

A 
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)

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112
Q

Tall stature

A

Ht > 2 SD above the mean for a given age, sex, race

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113
Q

Tall stature DDx

A

Constitutional/familial

Endocrine:
Hyperthyroidism
Gigantism
Precocious puberty
Beckwith-Wiedemann
Genetic:
Homocystinuria
Kleinfelter
Marfan
Sotos
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114
Q

Questions to ask when short stature:

A

IUGR?

Proportional?

Velocity?

Bone age?

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115
Q

The most common cause of congenital hypothyroidism

A

Thyroid gland dysgenesis

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116
Q

Causes of transient hypothyroidism

A

Maternal:
Antibody mediated
Iodine deficiency
Prenatal exposure to anti-thyroid medications

Neonatal:
Neonatal iodine deficiency or excess
Congenital liver hemangiomas
Certain gene mutations

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117
Q

Screening for congenital hypothyroidism

A

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

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118
Q

Inv for congenital hypothyroidism

A 
Primary:
Radioisotop scanning/thyroid U/S
Tg
Maternal anti-thyroid ab
Urinary iodine

Secondary:
MRI
Gene analysis
Eye exam (optic nerve hypoplasia)

119
Q

Time to normalize thyroid hormone in congenital hypothyroidism

A

Within 2 wk to avoid cognitive impairment

120
Q

Prognosis of congenital hypothyroidism

A

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
Q

The most common cause of 46 XX DSD

A

Virilizing CAH

122
Q

Inv for ambiguous genitalia

A 
Lytes
Renin
Karyotyping
17-OH-prog
Androgen
FSH
LH
Abdominal U/S (uterus, ovaries, testicles)
123
Q

Mx of ambiguous genitalia

A

Avoid announcement of probable sex

Avoid use of personal pronouns

Continuous psychosocial support for parents and child

Elective surgical reconstruction

124
Q

CAH Sx

A

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
Q

Inv in CAH

A

Newborn screening

17-OH-prog
ACTH
Lytes
ABG
Aldosterone, Renin activity

U/S

126
Q

Mx of CAH

A

Correct fluid, lytes, glucose

Hydrocortisone

Fludrocortisone

Extra glucocorticoids in times of stress

Psychosocial support

127
Q

Age of puberty onset in girls

128
Q

Onset of puberty in males

129
Q

Puberty sequence in males

A

Testicular enlargement
Penile enlargement
Pubarche
Growth spurt

130
Q

When should organic causes be excluded in puberty onset disorder?

A

Late puberty in girls and early puberty in boys

131
Q

Gynecomastia during puberty

A

In 50% of males

Self-limited

Evaluate if any mass or discharge

132
Q

Definitiin of precocious puberty

A

2° sexual characteristics 2-2.5 SD before population mean

Boys< 9 yr

Girls< 8 yr

F> M

133
Q

Percentage if idiopathic precocious puberty in M and F

A

F: 90%

M: 50%

134
Q

DDx of central precocious puberty

A

Idiopathic/constitutional

CNS disturbances: tumor, ICP, infection…

NF

Primary severe hypothyroidism

135
Q

DDx of peripheral precocious puberty

A 
Tumors 
CAH
Exogenous steroids
Hypothyroidism
McCune-Albright
Aromatase excess
136
Q

Normal growth velocity

A

Prepubertal: 4-6 cm/y

Puberty:
Girls: 6-8 cm/h
Boys: 8-10 cm/h

137
Q

Inv for precocious pubeety

A

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
Q

Mx of precocious puberty

A

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
Q

Definition of delayed puberty

A

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
Q

Causes of delayed puberty

A

Central:
Constitutional
Hypogonadotropic hypogonadism

Peripheral:
Hypergonadotropic hypogonadism:
Primary gonadal failure
Gonadal damage
Turner
AIS
Hormone deficiency
141
Q

Inv for delayed puberty

A

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
Q

Mx of delayed puberty

A

Underlying

Hormonal replacement

143
Q

Red flags in vomiting

A 
Bilious
Bloody
Projectile
Abdominal distention and tenderness
High fever
Dehydration
144
Q

Vomiting without diarrhea

A

Most likely not gastroenteritis

145
Q

Inv for vomiting

A

CBC
Lytes, BUN, Cr, amylase, lipase, glucose

In risk child add:
ESR, VBG
Blood/stool C&S
Imaging

146
Q

TEF time of presentation

A

Soon after birth

147
Q

Inv for TEF

A

NG
CXR
upper GI series with water-soluble contrast

148
Q

Pyloric stenosis time of presentation

149
Q

Pyloric stenosis inv

A

U/S

Upper GI study if U/S not helpful

Lytes

ABG

150
Q

Arching of back is sign of

151
Q

Inv for GERD

A

Empiric acid suppression

pH monitoring study
Upper GI studies
Endoscopy

152
Q

Mx of vomiting in children

A

Rehydration

Underlying

Antiemetic if > 2yr and severe vomiting:
Promethazine
Prochlorprazine
Metoclopramide
Ondansetron
153
Q

Prevalence of GERD in infants

154
Q

Vomiting in GERD

A

Soon after feeding

Non-bilious

Rarely contains blood

Small volume < 30 ml

155
Q

Inv for GERD

A

NON IF THRIVING CHILD

Upper GI radiology
Esophageal pH
Bx
Endoscopy

156
Q

Mx of GERD

A

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
Q

Diarrhea definition

A

Infants:
Increased stool frequency to twice as often per day

Children:
3+ loose or watery stool per day

Acute: <2wk
Chronic >2 wk

158
Q

Inv for acute diarrhea

A

Stool C&S, O&P, microscopy (WBC)

C. Difficile toxin

Electron microscopy for viruses

B/C, U/C

Blood work

159
Q

Inv for chronic diarrhea

A

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
Q

Diarrhea red flags

A 
Bloody stool
Fever
Petechia/purpura
Signs of severe dehydration
Chronic skin rash
Wt loss/ FTT
Other serious infections
161
Q

Inv for gastroenteritis

A

Not usually required in young children

Stool analysis:
WBC/RBC: bacterial/parasitic
pH <6, reducing substances: viral etiology

162
Q

Viral gastroenteritis features

A

Associated with URTI

Resolves in 3-7 d

Slight fever, malaise, vomiting, vague abd pain

163
Q

Bacterial gastroenteritis features

A

Severe abd pain

High fever

Bloody diarrhea

164
Q

RFs for gastroenteritis

A

Daycare

Young age

Sick contact

ImmComp

Travel

Poorly cooked/refrigerated meat or food

AB

165
Q

Mx of gastroenteritis

A

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
Q

When to return to school after gastroenteritis

A

24 h after the last episode of diarrhea

167
Q

The most common cause of chronic diarrhea during infancy

A

Toddler’s diarrhea

168
Q

Onset and resolution of toddler’s diarrhea

A

Onset: 6-36 mo

Cessation: 2-4 yr

169
Q

Sx of Toddler’s diarrhea

A

Excess juice intake

Disaccharide malabsorption

+/- Undigested food particles in stool

Excoriated diaper rash

170
Q

Mx of toddler diarrhea

A

Reassurance

4Fs:
Adequate fiber
Normal fluid intake
35-40% fat
Discourage excess fruit juice
171
Q

Lactose intolerance types

A

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
Q

Dx of lactase deficiency

A

Trial of lactose-free diet

Acid pH of stool

Positive reducing sugars

Positive breath hydrogen test (if > 6mo)

173
Q

Mx of lactase deficiency

A

Lactose-free diet

Soy formula

Lactase-containing tablets/capsules/drops

174
Q

Usual age of celiac presentation

A

6-24 mo, but any age

175
Q

Pathophysiology of milk allergy vs cow’s milk protein allergy

A

Milk allergy: IgE mediated

Cow’s milk protein allergy: non-IgE, more common

176
Q

Milk allergy Sx

A

Within hours of exposure

Urticaria, pruritis

Wheeze, cough

177
Q

Sx of cow’s milk protein allergy

A

= 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,

178
Q

Inv for milk allergy or cow’s milk protein allergy

A

Gold std: food challenge

Skin prick test

Allergen-specific IgE

Patch testing

179
Q

IgA and celiac

A

IgA deficiency is more prevalent in celiac disease

So order IgA level along with IgA-anti-tTG

180
Q

Forbidden in celiac:

A

Barley
Rye
Oat
Wheat

181
Q

Mx of milk allergy

A

Stop exposure

182
Q

Mx of cow’s milk protein allergy

A

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

183
Q

Definition of constipation

A

< 3 stool/wk

Hard pellet-like

184
Q

Time of constipation onset in infants

A

When introducing cow’s milk after breast milk due to high fat and solute and lower water content

185
Q

Time of constipation onset in toddlers/older children

A

During toilet training

Or

Starting school

186
Q

Mx of constipation

A

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

187
Q

RFs for intussusception

A

CF

GJ tube (jejunum)

M> F

Most common age: 3-12 mo

188
Q

Triad of intissusception

A

Abd pain

Palpable mass

Apple currant jelly stool

Often preceded by URTI

189
Q

Dx of intussusception

A

U/S

Air enema (75%also curative)

190
Q

Mx of intussusception

A

Air enema

Reduction under hydrostatic pressure

Surgery (rarely needed)

191
Q

Chronic abd pain prevalence

A

10% of school children

Peak: 8-10 y

F> M

Definition:
> 3 yr
3 mo
3 episodes of severe pain

192
Q

Dx of functional abd pain requires:

A

No alarming Sx

Normal PEx

Normal S/E

193
Q

Alarming Sx for chronic abd pain

A

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

194
Q

Characteristics of chronic abd pain

A

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

195
Q

Psychiatric comorbidities of chronic abd pain

A 
Anxiety
Somatoform
Mood
Learning disorder
Sexual abuse
Eating disorders
Elimination disorders
196
Q

Inv for chronic abd pain

A

FOB

Others based on Hx, PEx

197
Q

Mx of chronic abd pain

A

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

198
Q

Course of chronic abd pain

A

Resolves in 30-50% within 2-6 wk of Dx

30-50% will have functional pain as adults

199
Q

Most common cause of chronic lower GIB

200
Q

Inv for lower GIB

A

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

201
Q

Mx of lower GIB

A

ABC

NPO

NGT

Once stable, endoscopy and/or surgery as indicated

202
Q

Age and Hb level in physiologic anemia

A

8-12 wk

100 g/L

Earlier and more exaggerated if premature

203
Q

Most common cause of childhood anemia

204
Q

Age of Iron reserves exhaustion in term and preterm infants

A

Term: by 6 mo

Preterm: 2-3 mo

205
Q

Age of iron deficiency anemia

A

6mo-3yr

11-17yr

206
Q

RFs for IDA

A

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

207
Q

Inv for anemia

A

CBC, retic count
Mentez index (MCV/RBC)
PBS
Iron studies

208
Q

Mentez index

A

To differentiate IDA from thalassemia

If > 13: IDA
IF < 13: thalassemia

209
Q

Initial therapy for IDA

A

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

210
Q

Normal MCV in children

A

70 + age until 80

211
Q

Prevention of IDA

A

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

212
Q

Universal Hb screening at:

213
Q

Total daily iron should be:

A

6-12 mo: 11 mg

1-3 yr: 7 mg

214
Q

Response to iron therapy

A

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

215
Q

Sx of vitamin K deficiency

A

Generalized bleeding

GIB

Intracranial hemorrhage

(Within few days after birth)

216
Q

Prevention of vitamin K deficiency

A

IM injection at birth
Or
Oral: birth, 2-4 wk, 6-8 wk (higher risk of hemorrhage)

217
Q

Human milk vitamin K

A

Small amount

218
Q

Platelet function activity in vWD

A

Distorted (Increases)

219
Q

Most common cause of thrombocytopenia in children

220
Q

Peak age of ITP

221
Q

Which blood disorder protects against malaria?

A

G6PD deficiency

222
Q

Sx of ITP

A

1-3 wk after viral infection

Sudden onset

Petechia, purpura, epistaxis

Otherwise well child

No LAP/HSM

223
Q

Clinically significant bleeding happent in what percent of ITP pts?

224
Q

Indications for MBA/Bx in ITP

A

Atypical presentation

> 1 cell-line abnormal

HSM

225
Q

Mx of ITP

A

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

226
Q

Persistent or chronic ITP definition

A

Persistent >3 mo

Chronic >12 mo

Mx:
re-evaluate
Treat if symptomatic

227
Q

IVIg vs prednisone for ITP

A

IVIg: more rapid plt increase

228
Q

Anti D in IVP

A

A single dose of anti-D can be used as first line treatment in Rh positive, non-splenectomized children requiring Tx

229
Q

The most common type of pediatric malignancy

A

Leukemia>

Followed by: brain tumor> lymphoma

230
Q

Inv for generalized LAP

A 
CBC diff
B/C
Uric acid, LDH
ANA, RF, ESR
EBV, CMV, HIV serology
Toxo titer
Fungal serology
CXR
TB
Bx
231
Q

Inv for regional LAP

A

Period of observation if asymptomatic

Trial of oral AB

U/S

Bx if:
>6 wk and or constitutional symptoms

232
Q

Most common cause of acute bilateral cervical LAP

233
Q

Age of leukemia

234
Q

Mist common type of leukemia

235
Q

Hyperleukocytosis

A

WBC >100,000

Medical emergency

Respiratory/neurological distress

Risk of:
ICH
Pulmonary leukostasis syndrome
Tumor lysis syndrome

236
Q

Tx of leukemia

A

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)

237
Q

Risk stratification in leukemia is based on

A

WBC and age

Also
CNS/testicular disease
Immunophenotype
Cytogenetics

Most important prognostic factor:
Initial response to therapy

238
Q

Age of Hodgkin

A

15-34

> 50

239
Q

NHL age

A

Peak 7-11 y

240
Q

Most common presentation of hodgkin lymphoma

A

Persistent, painless, firm, cervical or supraclavicular LAP

241
Q

Back pain children

A

Must always be investigated

242
Q

Prognosis of lymphoma

A

Hodgkin:
>90% 5 yr survival

NHL:
75-90% 5yr survival

243
Q

Prognosis of leukemia

A

ALL,
80-90% 5yr survival

AML
50-60%

244
Q

Age of wilms Dx

A

2-5 yr

M=F

245
Q

Most common presentation of Wilm’s tumor

A

Unilateral abdominal mass

246
Q

Mx of Wilm’s

A

Staging
Nephrectomy
Chemo
Radio

247
Q

Prognosis of wilm’s

A

90% long-term survival

248
Q

The most common cancer occurring in the first year of life

A

Neuroblastoma

249
Q

Most common site of neuroblastoma

A

Adrenal gland

250
Q

Sx of neuroblastoma mets

A 
Bone pain
Limp
Periorbital ecchymoses 
Abd pain
Emesis
Fever
Wt loss
Anorexia
Hepatomegaly
Blueberry muffin skin nodules
251
Q

Opsimyoclonus

A

Paraneoplastic manifestation of neuroblastoma

252
Q

Mx of neuroblastoma

A 
Surgery
RT
Chemo
Autologous SCT
Immunotherapy
253
Q

Good prognostic factors in neuroblastoma

A

Age<18 mo

Lower stages

Posterior mediastinum and neck

Low serum ferritin

More differentiated histology

Aneuploidy

Absent MYCN oncogene amplification

254
Q

Definition of fever of unknown origin

A

Daily or intermittent fevers

For at least two consecutive weeks

Uncertain cause

255
Q

Fever in neonate. Next step?

A

Admit

Full SWU

Empiric AB

256
Q

Fever in child 1-3 mo, next step?

A

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

257
Q

Infans with low risk of serious bacterial infaction according to Rochester criteria

A 
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
258
Q

Partial SWU includes

A

CBC, diff

Urine R&M, S&C

Blood S&C

LP

CXR (if respiratory Sx)

Stool S&C (if GI Sx)

259
Q

Fever in child 3 mo- 3 yr

A

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

260
Q

If a child 3 mo-3 yr, non toxic, no focus, T > 39 °, next step?

A

Urine R and M
CBC

If WBC > 15000:
Blood C&amp;S
Urine C&amp;S
If no source found: amoxi or ceftriaxone
Acetaminophen
If WBC < 15000:
Blood C&amp;S
Observe
Acetaminophen
F/U in 24 h
261
Q

Most common age of AOM

A

18 mo-6 yr

262
Q

Etiology of refractory AOM

A

Non-typeable HI

263
Q

RFs for AOM

A

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)

264
Q

Most important diagnostic criteria for AOM

A

Bulging TM

265
Q

Tx of AOM

A

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

266
Q

Unresponsive AOM definition

A

Sx, signs, otoscopic findings persist beyond 48 h of AB Tx

267
Q

Etiology and Tx of otitis-conjunctivitis Sx

A

Etiology:
HI, M. Catarrhalis

Tx:
Amoxicillin-clavulanate
Cephalo: cefixime, ceftriaxone, cefuroxime, cefaclor

268
Q

Prevention of AOM

A

Parent education

Vaccines (pneumococcal, influenza)

Surgery:
Tympanostomy tube
Adenoidectomy

269
Q

Indications of AB therapy in AOM

A 
> 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

270
Q

Role of prophylactic AB in recurrent AOM

271
Q

Indication of tympanostomy

A

3 episodes of AOM in 6 mo or 4 episodes in 1 yr (one in last 6 mo)

272
Q

AOM without MEE or
AOM with MEE but without bulging or
Mildly erythematous TM
Mx?

A

Consider viral

Reassess in 24-48 h

273
Q

Most common cause of pediatric hearing loss

A

Otitis media with effusion (no inmflammation)

274
Q

RFs of OME

A

Same as AOM

275
Q

The most reliable finding in OME with pneumatic otoscopy

A

Immobility

276
Q

Tx of OME

A

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

277
Q

Parvovirus risk of transmission after Sx begin

278
Q

Parvo virus transmission mode

A

Respiratory secretions

Blood

279
Q

Onset of rash in erythema infectiosum

A

10-17 d after symptoms

280
Q

Which rash may recur with sunlight or exercise?

281
Q

Viruses causing Gianotti-Crosti

282
Q

Gianotti-Crosti resolution

283
Q

HFMD communicability

A

Usually 1-7 d after Sx

May be up to month

284
Q

HSV incubation

285
Q

Measles communicability

A

4 d before and after rash

286
Q

Mx of unimmunized contacts of measles

A

Vaccine within 72 h of exposure

Or

IgG within 6 d of exposure

Respiratory isolation

287
Q

Confirmation of Dx of enteroviruse infections

A

Viral culture from nasopharynx and rectal swabs

288
Q

Reseola infantum rash starts at

A

Neck and trunk

289
Q

Nagayama spots

A

Enanthema of roseola

Erythematous papules on soft palate and uvula

290
Q

Rubella communicability

A

7days before to 7 days after eruptions

291
Q

Rubella rash starts at

292
Q

Varicella communicability

A

1-2 d pre-eruption to 5d post eruption

293
Q

Viral rash with risk of necrotizing fasciitis

294
Q

Viral infections with risk of DIC

A

HSV, varicella

Med (25 decks)

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