Beruflich Dokumente
Kultur Dokumente
Pediatrics
Taruna Mehra
MBBS MD PEDIATRICS (MAMC)
Dedication
I dedicate my work to my teachers,my parents
and most importantly my patients.
Preface
Why should I change anything in your life till the time you decide to
change yourself
Quran
With the challenging task ahead in month of November and December
with all the major exams within a period of 20 days, the committee
has decided to release Pre NEET Pediatrics inclusive of DNB questions
and important last minute revision points so that you are confident in
attempting maximum questions in all the exams.This book has been
written keeping in mind that maximum time taken to revise pediatrics
is less than one day.
All the best may God help you cross the bridge
Taruna Mehra
Do not count the days make the days count
Contents
1. Pediatrics in Last Minutes ..........................
1 65
66 77
78 150
PEDIATRICS
in Last Minutes
Developmental Milestones
Age
Gross motor
Fine motor
Language
1 mo
2 mo
Holds head in
No longer
midline. Lifts
clenches fist
chest when prone tightly, follows
objects past
midline
3 mo
Head holding
achieved
Social
Regards face
intently
Smiles after
Recognize
being stoked or parent, social
talked to
smile
Reaches for
familiar people
or objects,
anticipates
feeding
Follows moving
objects in a
circular fashion,
converges and
focuses
Coos (produces
vowel sounds
in a musical
fashion), laughs
aloud
Grasps objects/
rattle crudely
Enjoys looking
Orients to
around
voice/bell
environment
(localizes
laterlly);
"ahgoo", razzes
6 mo
Transfers
objects from
one hand to
another
Babbles
Stranger
anxiety, smiles
back at mirror
image of self
Responds to
name, says
mama/dada
(non-specific)
Responds to
social play,
plays pat-acake, starts to
explore
environment
(9-10 mo)
9 mo
Takes foot to
mouth, lifts head
and upper chest
with support
Uses pincer
Sits unassisted (8
grasp, probes
mo), Crawls,
with forefinger,
cruises, pulls to
holds feeding
stand
bottle
Contd...
Pre-NEET Pediatrics
Contd...
Age
Gross motor
Fine motor
Language
Social
Understands to
some "mama"
12 mo
15 mo Walks well
without support,
Walks backwards
and sideways
18 mo Starts to run,
climb stairs with
help
2 yrs
Makes a tower
of 6-7 cubes,
turns one page
of a book at a
time, may draw
horizontal line
Points to at
least one
named body
part, simple
2 word
sentences
(2 words at 2
years)
Follows 2-step
commands
3 yrs
Pedals tricycle,
jumps with both
feet off ground,
can alternate feet
when climbing
stairs
Make a tower of
9-10 cubes,
draws (copies) a
circle
Uses plurals, 3
word
sentences (3
word at
3 years)
Dresses and
undresses
partially
buttons/
unbuttons
4 yrs
Hops, alternates
feet going
downstairs (At 4
yr hop off the
floor)
Draws (copies)
a Cross
Knows colours
Buttons
clothing fully,
plays with other
children
5 yrs
Jumps on one
foot, heel to toe
walk
Draws (copies)
a Square
Dresses
without
supervision
Max, 10-12 mo
Mand, 3-4 mo
4-5mo
18-21mo
24-30mo
Birth
30-36mo
Max, 7-9 yr
Mand, 8-10 yr
Lateral incisors
Cuspids (canines)
Firstpremolars (biscuspids)
Secondmolars (biscuspids)
First molars
Secondmolars
Third molars
fetal mo
fetal mo
fetalmo
fetal mo
fetal mo
3-4mo
5th
5th
6th
5th
6th
Central incisors
Secondary teeth
Primary Teeth
Central incisors
Lateral incisors
Cuspids (canines)
Firstmolars
Second molars
18-25 yr
14-16yr
9-10yr
12-14yr
12-13yr
12-15yr
10-11yr
9-10yr
1824 mo
1824 mo
3036 mo
2430 mo
36 mo
Complete At
Calcification
Begins At
17-22 yr
12-13yr
6-7yr
10-12yr
10-11yr
11-l2yr
8-9yr
7-8yr
68 mo
811 mo
1620 mo
1016 mo
2030 mo
17-22 yr
12-13yr
6-7yr
11-13yr
10-12yr
9-11yr
7-8 yr
6-7yr
57 mo
710 mo
1620 mo
1016 mo
2030 mo
78 yr
89 yr
11l2 yr
1012 yr
1012 yr
67 yr
7-8 yr
911 yr
1012 yr
1113 yr
Mandibular
Age at Shedding
Mandibulaur Maxillary
Age at Eruption
Maxillary
Pre-NEET Pediatrics
Height
Head circumference
Pre-NEET Pediatrics
SD score -2 to -3
(70-79% of expected)
SD score -2 to -3
(85-89% of expected)
Severe undernutrition
SD score <-3
(<70%
of
expected)
SD score <-3
(<85% of expected)
Dugdales
Raos
Kanawati
MAC
(1-5 years)
Normal
Severely
malnourished
0.88-0.97
0.15-0.16
0.32-0.33
<0.79
<0.14
d0.25 cm
>13.5
<12.5 cm
Weight of child
100
Weight of normal child of same age
Disadvantages
Infancy
0-6 months
7-12 months
Children
1- 3 years
4- 6 years
7 - 9 years
118
108 } K.Cal/kg/day
12.03
18.87
26.37
1240
1690
1950
5.1
7.0
8.1
Pre-NEET Pediatrics
Protein
Total
Casein
Amino acids
Cystine
Taurine
Fat
Total
Saturation of fatty acids
Linoleic acid (essential)
Cholesterol
Lipase to digest fat
Lactose
Salts (mEq/1)
Sodium
Chloride
Potassium
Minerals (mEq/Il)
Calcium
Phosphate
Iron
Vitamin
Human
None
Antibodies, Leukocytes,
Lactoferrin Bifidus factor,
Others
Cow
Likely
Not active
1%
0.5%
4% (too much)
3% (too much)
Not enough
4% (average)
Enough unsaturated
Enough for growing brain
Enough
Present
7% (enough)
4%
Too much saturated
Not enough
Not enough
None
4.5%
25 (too much)
29 (too much)
35 (too much)
Enough
Bone-Age
Bone age is delayed compared to chronological age:
10
Pre-NEET Pediatrics
Endocrine Disorders
Hypothyroidism
Steroid therapy and Cushings disease
Hypogonadism (including Turners syndrome)
Hypopituitarism - panhypopituitarism, growth hormone deficiency,
Laron dwarfism
Chromosome disorders
Bone dysplasias
Malformation syndromes
11
Hyperthyroidism
Idiopathic sexual precocity
Intracranial masses in the region of the hypothalamus (haniartoma,
astrocytoma, optic chiasm glioma, hydrocephalus, encephalitis)
Congenital Disorders
D/D of Rickets
Serum Ca
Serum
P043
Serum
Alkaline
Serum
Serum
Parathormone HCO 3
phosphatase
Normal
9-10.5 mg/dl
3-4.5mg/dl
30-120 IU
10-55 units
Hypophosphatemic
Rickets
Vit D dependent
Rickets
Hyperparathyroidism
Nutritional rickets
Renal tubular
acidosis (distal)
21-30
meqlL
N
N/ (7.5-8)
N/
/N
N
N
Enuresis
12
Pre-NEET Pediatrics
Treatment
13
Corticosterojds
Diethyl stilbestrol
Anti-thyroid drugs
Clomiphene
Synthetic
progestins
Chloramphenicol
Sulphonamides
Tetracyclines
Aminoglycosides
Anti-malarials
Quinine,
chloroquine
Adverse effects
Anticonvulsants
Fetal hydantoin syndrome (microcephaly, cleft palate,
hypoplastic changes, IUGR)
Spina bifida, ? NTD
Relatively safe
Neural tube defect (1-2%), hypospadias, microstomia,
developmental delay.
Hormonal agents
Growth retardation, cleft palate and lip
(used as morning-after pill) Vaginal adenosis in female
offspring in adolescence Clear cell vaginal
adenocarcinoma in teenagers In male offspring (risk of
testicular cancer in later life)
Neonatal hypothyroidism and goiter
NTD, multiple gestation, Downs syndrome
Masculinization in female fetus, hypospadias
Antibiotics
Gray baby syndrome (peripheral vascular collapses)
Kernicterus, Methemoglobenemia
Dental discoloration (yellow) and deformity, Inhibition of
bony growth, cataracts,
Fetal ototoxicity due to eighth N. damage
Intra-uterine death
Retinopathy, congenital deafness, comeal opacities
14
Pre-NEET Pediatrics
Contd...
Heroin
Cocaine
Beta-blockers
Vitamin K
(large dose)
Warfarin
Aspirin
Other Drugs
Cytotoxic drugs
Isotretinoin
Oxygen in high
concentrations
Thalidomide
Thiazide diuretics
Neonatal thrombocytopenia
ACE inhibitors
Misoprostol
(prostaglandin)
Vitamin D
Drugs taken during perinatal/neonatal period and their effects on the neonate
Oxytocin (used for induction of labour)
Hyperbilirubinemia in babies
Prolonged cortisone
NSAIDS
Dexamethasone
Periventricular leuocmalacia
Medications to baby
Chloramphenicol
Erythromycin
Vitamin K
Pyloric stenosis
Bleeding, hepatotoxicity
15
SLE
Smoking
Outcome/Comment
IUGR; Feal goiter and hypothyroidism (due to drugsbeta agonists)
IUGR, abortion, asphyxia, prematurity
IUGR, prematurity
Placental vasculopathy, IUGR
Maternal hypothyroidism may cause congenital
hypothyroidism (TSH does NOT cross placental, barrir
but LATS does)
Congenital complete heart block, IUGR
IUGR/LBW; Sudden infant death syndrome (SIDS);
Increased ororfacial clefts in the fetus. Developmental
lag for first few years of life: adverse effects on
language skills and visual and spatial abilities.
NEONATOLOGY
Five Cleans of Intranatal Care
Clean hands
Clean delivery surface
Clean blade
Clean cord
Clean tie (for cord)
16
Pre-NEET Pediatrics
Begin PPV with oxygen concentration between room air and 100%
oxygen
Increase oxygen concentration up or down to achieve saturation
between 90 and 95%
If heart rate does not response by increasing rapidly to 100 per
minute, correct any ventilation problem and use 100% oxygen
Regarding PPV
LMA should NOT be used
In the setting of meconium stained amniotic fluid
When chest compression is required
In VLBW babies
For delivery of medications
Naloxone NOT to be given by ET route; epinephrine preferably by
intravenous route only
Capnography (exhaled CO2) recommended for confirming ET
tube placement.
Normal APGAR sore = 8-10 at minute after birth; <7 indicates
asphyxia.
NO NEED for resuscitation if these 5 criteria are fulfilled by
newborn:
Full term, crying, clear of meconium, pink, good muscle tone.
2 absolute indications for bag and mask ventilation are
Apnea at birth; HR < 100/minute.
Absolute contraindications for bag and mask ventilation are:
Diaphragmatic hernia, meconium aspiration.
Indications to start chest compression are:
HR < 60; ventilate with oxygen for a full 30 seconds initially
and proceed with chest compressions if the HR remains <60/
mm.
Indications for endotracheal intubation are:
Prolonged PPV; Ineffective bag and mask ventilation;
Diaphragmatic hernia, meconium aspiration.
17
DO NOT Resuscitate if
When gestation birth weight or congenital anomalies are a/w
almost certain death (class Ha)
Anencephaly
Chromosomal anomalies incompatible with life (e.g., trisomy 13)
APGAR Score
Appearance (Colour)
Blue or pale
Body pink,
Pink
extremities
blue
Pulse (Heart rate)
<100
> 100
No Response
Grimace
Cries, Coughs
Flaccid
Some
Actively
flexion
moving
(Reflex stimulation)
or Sneezes
extremities
Respiratory effort (not rate)
Slow
Good crying
irregular
Onset
Fully developed at
Persist till
Palmar grasp
28 wk
32 wk
2-3 months
32 wk
36 wk
Less
prominent after
1 month
Moro (extenson of
28-32 wk
37 wk
5-6 months
35 wk
7-8 months
1 month
10-11 months
6-7 months
Persists
throughout life
18
Pre-NEET Pediatrics
Birth Trauma
Caput succedaneum
Present at birth;
May extend over suture lines;
Diffuse, ecchymotic, oedematous
overlying skin;
Disappears spontaneously within
24hrs after birth;
No treatment needed
Cephalhematoma
Seen at 2-4 days old;
Limited by suture lines;
Normal overlying skin;
Umbilical Cord
Usually cord is cut 2.5 inches or 6 cm from the umbilical base.
Contains 2 arteries and 1 vein.
Single umbilical artery
Is a/w genitourinary anomalies (MC), CVS anomalies,
esophageal atresia, trache-esophageal fistula, imperforate
anus
19
Neonatal sepsis
20
Pre-NEET Pediatrics
Preterm babies
Can tolerate hypoxia for longer periods without sequelae
Suffer more periventricular ischemia as cortical vessels are
more superficial
Periventricular insults are more common than term babies
Term babies
Suffer more cortical ischemia and infarcts
It may lead to multifocal necrosis, porencephalic cyst,
hydrencephaly
Postnatal corticosteroids
21
Type I
Type II
Gilbert syndrome
Diffuse hepatocellular disease
Conjugated hyperbilirubinemia.
(Autosomal Recessive)
Rotors syndromeQ
(Autosomal Recessive)
Biliary atresia
Hypothyroidism
Gilberts syndrome
22
Pre-NEET Pediatrics
24-48hrs
48-72hrs
72hrs
20
25
25
Healthy baby
Phototherapy
Exchange
transfusion
Sick baby
Phototherapy Exchange
transfusion
<1000
1001-1500g
1501-2000g
2001-2500g
Term babies
5-7
7-10
10-12
12-15
11-13
13-15
15-18
18-20
4-6
6-8
8-10
10-12
10-12
11-13
13-15
15-18
>2500g
15-18
20-25
12-15
18-20
Immune
Rh incompatability
Non-immune
Anemia
Cardiac dysarrhythmias
Vascular
Lymphatic
CNS
Thoracic
23
Contd...
Teratomas
Tumor & storage diseases
Chromosomal
Bone diseases
Congenital infections
Others
Erythroblastosis Fetalis
24
Pre-NEET Pediatrics
General
Macrosomia
Normal head size
Other
Cardiovascular
Cardiomegaly
Transient hypertonic cardiomyopathy
Persistent fetal circulation
Metabolic
Hypoglycemia
Hypocalcemia
Hypomagnesemia
Hyperbilirubinemia
25
Less common
stressed.
Infection
Necrotizing enterocolitis
Uncommon
Uncommon
Neonatal Hypoglycemia
The whole blood glucose level of < 40 mg/dL indicates hypoglycemia
1. Transient hypoglycemia
3. Other etiologies
Idiopathic; Sepsis; Drugs (maternal tolbutamide); liver disease
(reye syndrome), carcinoma etc.
26
Pre-NEET Pediatrics
Hypoxic-ischaemic
encephalopathy
Birth injury (cerebral contusion)
First day hypocalcemia
(normal phosphate)
Pyridoxine dependency
Accidental injection of
local anesthetic
Intracranial haemorrhage
Tetany
Hypoglycemia
Narcotic withdrawal
Meningitis
TORCH infections
Head Malformations
1. Anencephaly: Due to failure of closure of the rostral neuropore
2. Holoprosencephaly: Incomplete separation of the cerebral
hemispheres. Seen in Pataus syndrome.
3. Porencephaly Cysts or cavities in the brain may result from
developmental defect or acquired lesions including infarction of
tissue
4. Lissencephaly: Bat like brain with no cerebral convolutions and a
poorly formed sylvian fissure due to faulty neuroblast migration
(agyria). Hypoplasia of optic nerves and microphthalmia are
common.
5. Schizencephaly: Unilateral or bilateral cleft in the cerebral
hemispheres, microgyria.
6. Scaphocephaly: MC type of cranoisynostosis.
7. Encephalocele: Is a malformed diverticulum of CNS tissue
extending through a defect in the cranium.
8. Shapiros syndrome: Agenesis of corpus callosum
Torch Infections
Infection
Description
Treatment
Prevention
Toxoplasmosis
3Cs Convulsions,
intracranial Calcification,
Chorioretinal scar,
hydrocephalus Ring
enhancing lesions on
head CT
Deafness (MC)
Bluberry muffin rash,
Pyrimethamine,
sulfadiazine,
spiramycin
Avoid exposure to
cats and cat feces
during pregnancy;
avoid raw
undercooked meat
None
Immunize mother
prior to pregnancy
Rubella
Contd...
27
Contd...
Infection
Description
Treatment
Prevention
Avoid exposure
Perform a
Caesarean section
if mother has active
lesions at time of
delivery
Treat seropositive
mothers with
penicillin
Perinatal Tuberculosis
28
Pre-NEET Pediatrics
by transplacental transmission through a lesion in the placenta or
ingestion of infected liquor.
Management
If the child has clinical features of perinatal TB
29
Apt Test
30
Pre-NEET Pediatrics
origin, suggesting that the neonate swallowed or aspirated maternal
blood, either during delivery or during breast feeding (from breast
fissures). Kleihauer Betke test (KB test)
The KB test is the standard test for detecting fetal - maternal
hemorrhage. It is used to measure the amount of fetal hemoglobin
transferred from a fetus to a mothers blood stream.
It is usually performed on Rh(-ve) mothers to determine the
required dose of Rho (D) immunoglobulin to inhibit formation of
Rh antibodies in the mother and prevent Rh hemolytic disease in
future Rh - positive children.
A standard blood smear is prepared from the mothers blood and
exposed to an acid bath. This removes adult hemoglobin, but not
fetal hemoglobin, from the red blood cells. Subsequent staining
makes fetal cells (containing HbF) appear rose pink, while adult
red cells are only seen as ghosts.
KB test quantifies the fetal - maternal hemorrhage.
Apt test
Hematopoesis in Fetus
31
32
Pre-NEET Pediatrics
Functional closure of foramen ovale occurs very
quickly.
The blood reaching the right atrium through IVC and SVC is
emptied into the right ventricle from where it is pumped into
pulmonary trunk.
The left venthcle pumps it out for distribution in the body for
oxygenation of the tissues.
Tetralogy of Fallot
Truncus arteriosus
Tricuspid atresia
TAPVR
S-I-M 5Ts
33
Anatomy/ Symptoms
Signs
Ventricular
septal defect
(MC Cong
HD)
ASD
90% in membranous
part of septum; 70-80%
have spontaneous
closure
In infants FTT, CCF.
MC cong. Heart
disease complicated
by IE
34
Pre-NEET Pediatrics
Anatomy/Symptoms
Coarctation of aorta
(COA)
Supravalvular:
asymptomatic,
a/w Williams syn.
Infantile aortic
stenosis proximal to
insertion of ductus
(preductal)
Adult: postductal,
MC coarctation
is just below
origin of left
subclavian A.
A/w HTN in upper
extremities, weak
pulses in lower
extremities
A/w Turner syn.
Signs
Thrill over
suprasternalnotch/
carotids, ejection
systolic murmur
maximal in 2nd
right I/C space
with neck radiation
Pulse: radiofemoral
delay
Elevated upper limb
BP
Palpable arterial
pulsations in
interscapular region
(Suzzman's sign)
Anatomy/Symptoms
Signs
Transposition of
great arteries
(TGA)
Tetralogy of
Fallot
(Pulmonary
stenosis, RVH,
Infant: progressively
deeper cyanosis,
weeks or few
months old.
Anatomy/Symptoms
Overriding of
aorta, VSD)
-
Eisenmenger's
syndrome
Cyanotic spells
from infundibular
spasm.
Childhood: squatting
after exertion to
overcome
dyspnea, SBE,
cerebral abscesses,
polycythemia.
CCF is very RARE.
Squatting cause
compression of
femoral arteries
increase pressure
threby decrease
the right to left shunt
and directing more
blood from the
RV to the lungs
Signs
at third left interspace.
Uncorrected VSD,
- Loud P2
ASD, PDA
increase pulmonary
vascular resistance
due to arteriolar
thickening
progressive
pulmonary hypertension.
As pulmonary resistance
increase the shunt
reverses from
L R to R L
shunt which causes
late cyanosis (clubbing
and polycythemia)
35
36
Pre-NEET Pediatrics
Anatomy/Symptoms
Signs
Truncus
arteriosus
Total anom
alous
pulmonary
venous
connection
(TAPC)
- Newborn: obstructed
venous return
simulates
RDS. Onset 2
months to 2
years. Breathless,
FTT
Key:
CCF
CHD
FTI'
TE
LVH
PS
RDS
RVH
SBE
=
=
=
=
=
=
=
=
=
Minimal cyanosis,
Bounding pulse, Single
S2, short systolic murmur
Cyanosis NOT improved
in 100% oxygen. Poor
pulse. Loud S2. Murmur
often absent, tachypnea,
right ventricular heave.
CXR: pulmonary edema
with Snowman heart
(figure of 8 heart of
'cottage leaf')
37
Disorder
Rubella
Turner's syndrome
Infant of diabetic mother
Wiliam's syn.
Marfan's syn.
Down's syn.
22q11 syn.
Defect
PDA
COA
TGV
Supravalvular AS
Aortic insufficiency
Ostium primum ASD, VSD, AV
septal defect (endocardial cushion
defect)
Truncus arteriosis, TOF
38
Pre-NEET Pediatrics
NADAs Criteria
The Assessment of a child for the presence or absence of heart disease
can be done with the help of some guidelines suggested by NADA.
These guidelines are called NADA 's criteria.
Major
Systolic murmur,
grade III or more,
especially with thrill
Diastolic murmur
Cyanosis
Congestive cardiac failure
Minor
Systolic murmur < grade III
Abnormal 2 heart sound
Abnormal ECG
Abnormal X Ray
Abnormal BP
Minor Criteria
1. Carditis
2. Arthritis
3. Subcutaneous nodules
4. Chorea
5. Erythema marginatum
A.
i.
ii.
iii.
Essential criteria
Evidence of recent
streptococcal
infection as indicated
by
a. Increased antistreptolysin
'O' titer
b. Positive throat culture
c. Recent scarlet fever
Clinical
Fever
Arthralgia
Previous rheumatic fever
or rheumatic heart
disease
B. Laboratory
i. Acute phase reactants;
leukocytosis, elevated
sedimentation rate and C
reactive protein
ii. Prolonged PR interval in the
electrocardiogram
39
Anatomy involved
Result
Indicated for
BlalockTaussig
shunt
Waterston
shunt
Subclavian artery
to ipsilateral
pulmonary artery
Aorta to right
pulmonary artery
Rashkind
procedure
Balloon atria
septostomy
BlalockHanlon
procedure
Balloon
angioplasty
Operative
atrial
septostomy
Valves and
vessels
Increased
pulmonary
blood flow
Increased
pulmonary
blood flow
Increased
atrial
mixing
Increased
atrial
mixing
Dilation
of valves/
vessels
Decreased
pulmonary
blood flow
Tetralogy of Fallot
Pulmonary valve atresia
Tetralogy of Fallot
pulmonary
valve atresia
Tricuspid atresia
Transposition of
great arteries
Tricuspid atresia
Transposition of
great arteries
Pulmonary
Pulmonary
artery banding artery
Fontan
procedure
Mustard
procedure
Norwood
procedure
Corrective procedures
Right atrium
Atrium
to pulmonary
functions
artery
as right
anastomosis
ventricle
Intera-atrial
RV remains
baffle
systemic
arteries
ventricle
A complex two
stage procedure
Pulmonary valve
stenosis, Aortic
valve stenosis
Endocardial
cushing
defect, Single
ventricle
Tricuspid atresia single
ventricle, pulmonary
atresia
Transposition of great
vessels
Loudest
Right 3rd ICS
Quality
Harsh, SEM
Radiation
Carotids
MLSB
Harsh, SEM
Low pitched,
Lungfields
Little to none
Contd...
40
Pre-NEET Pediatrics
Contd...
Procedure
Anatomy involved
regurgitation
Mitral stenosis Apex
Mitral
regurgitation
ASD
VSD
Apex
PDA
Result
Indicated for
early-mid
diast
Low pitched,
raid diast.
Rumble
Blowing,
holosystolic
Harsh, SEM
Harsh,
Holosystolic
Continuous
None
Left axilla
Lung fields
None
Lung fields
Autosomal dominant:
Marfan's - aortic and mitral valve incompetence, dilatation of
the ascending aorta
Holt - Oram - VSD, ASD
Noonan's - PSASD cardiomyopathy
Autosomal recessive:
Pompe's (Type II A glycogen storage disease) - cardiomyopathy
Ellis - VanCreveld - AVSD, common atrium
X-linked:
Duchenne Muscular Dystrophy - cardiomyopathy
Polygenic inheritance:
Well described for PDA with a recurrence risk of 2.5 inn siblings
(recurrence risk increased to 10% if > than one family member
affected).
Respiratory Infections
Etiology
Presenting
age
Clinically
Croup (laryngo
tracheobronchitis)
Acute epiglotitis
(emergency)
MC parainfluenza virus
1; also by RSV
3 months to 3 years
Prodrome with URI
symptoms for
1-7 days; low
grade fever, ins
MC by H. inflenzae type b.
3-7 years
Rapid onset (4-12 hours); high
fever, dysphagia, drooling,
muffled voice, stridor patients
may be in "sniffing" position
Contd...
41
Contd...
X-ray
Treatment
Croup (laryngo
tracheobronchitis)
Acute epiglotitis
(emergency)
Cystic fibrosis
HIV infection
Metabolic: Glucose-6-phosphate deficiency, Adrenal insufficiency,
Nephrogenic Diabetes Insipidus, Mucopolysaccharidoses,
Fucidosis
Intussusception
Telescoping of a bowel segment into itself may - edema, arterial
occlusion, gut necrosis and death.
42
Pre-NEET Pediatrics
Volvulus
Incomplete fixation to the posterior abdominal wall, causing
a malrotated gut to twist on itself.
Affects children 0-2 years;
Sudden onset of pain, distension, peritonitis, "bird's beak" on
X- ray,
Treat with surgery immediately since gut may necrose due to
superior mesenteric artery occlusion.
Necrotising enterocolitis
Intestinal necrosis occurring primarily in watershed
distributions,
Affects children 0-2 months;
Prematurity and congenital heart disease are risk factors;
Fever, rectal bleeding, air in bowel wail (pneumatosis
intestinalis) and/or hepatobiliary/ portal air;
Treat with NPO, IV fluids and antibiotics.
Meckel's diverticulum
A remnant of omphalomesenteric duct that persists as an
outpouching of the distal ileum; can contain ectopic gastric
mucosa
Affects children 0-2 years;
Rule of 2s for Meckel's diverticulum =2% of population
affected (MC GI tract abnormality; remnant of
omphalomesenteric duct), 2 inches long, within 2 feet of
ileocolic junction, presents in the first 2 years of life.
Meckel's diverticulum can cause intussusception, obstruction
or volvulus;
Use Meckel scan (technetium radionucide scan) to detect
gastric mucosa;
Treat with surgery
Meconium ileus
In cystic fibrosis, meconium plug obstructs intestine preventing
stool passage.
Affects children 0-2 weeks; may cause late feculent vomiting,
rectal prolapse
43
Pyloric stenosis
obstruction;
Duodenal
atresia
Tracheoesopha
geal fistula
Hirschsprung's
disease
44
Pre-NEET Pediatrics
45
Also Know
Infrequent relapses: If a patient gets 3 or less relapses in a year
Frequent relapses: If a patient has 4 or more relapses in a year
Steroid dependent: When relapse occurs within 2 weeks of
discontinuation of drugs
HSP
TTP
ITP
MC age
Children
Children
Young
adults
Children or
adults
Previous infection
Diarrhea
(EHEC,
Shigella)
URI
None
Viral (esp. In
children)
RBC count
Platelet count
Peripheral smear
Hemolysis
Hemolysis
Kidney effects
ARF,
hematuria
Hematuria
ARF,
proteinuria
None
Treatment
Supportive*
Supportive
Plasmapheresis,
NSAIDs;
No
platelets**
Steroids***,
splenectomy if
drugs fail
Key differential
points
Age,
diarrhea
Rash,
abdominal
pain,
arthritis,
melema
CNS
changes,
age
Antiplatelet
antibodies
Key
HUS = Haemolytic uremic syndrome; HSP = Henoch-Scholnlein
purpura; Ti? = Thrombotic thrombocytopenic purpura; ITP =
Idiopathic thrombocytopenic purpura; ARF = Acute renal failure;
46
Pre-NEET Pediatrics
Febrile Convulsions
Atypical complex
febrile convulsions
Prophylaxis
Intermitent diazepam, clabazam,
midazolam- most desirable.
Symptoms
Diagnosis
Treatment
Absence
seizures
Multiple brief
staring episodes
Generalized
3-Hz spike
and wave
pattern on
EEG
Ethosuximide
Infantile
spasms
(West
syndrome)
Affects infants
<1 year,
'jackknife
spasms',
developmental
regression
Hypsarrythmia on
EEG.
A/w tuberous
sclerosis
ACTH
Lennox
Gastaut
syndrome
First seizure
between 1-7
years of age;
multiple
progressive
difficult to treat
type seizures
with GTCS
and drop attacks
Atypical spike
and wave
pattern in
frontal region
on EEG
No effective
treatment
Juvenile
mycolonic
epilepsy
Affects healthy
adolescents;
myoclonic
jerks in
early morning
hours upon
wakening
Positivefamily
history
Easily treated
with a variety of
antiepileptic
medications
Benign
partial
epilepsy
Partial seizures
during
wakefulness
(oral, vocal)
Classic interictal
spikes
from the
centrotemporal,
(rolandic) region
Seizures usually
disappear by
adolescence
Landau
Klefner
syndrome
Normal children
and lose
language
between
3- 6 years;
often confused
with autism
Bilateral temporal
spike and sharp
waves on EEG.
Antiepileptic
medications
47
48
Pre-NEET Pediatrics
Antibiotic
Neisseria meningitides
Penicillin - sensitive
Penicillin - resistant
Penicillin G or ampicillin
Ceftriaxone or cefotaxime
Streptococus pneumoniae
Penicillin - sensitive
Penicillin - intermediate
Gram-negative bacilli (except
Pseudomonas spp.)
Pseudomonas aeruginosa
Staphylococci spp.
Methicillin-sensitive
Methicillin-resistant
Listeria monocytogenes
Haemophilus influenzae
Streptococcus agalactiae
CLINICAL MANIFESTATIONS OF CP
A. Spastic CP
MC type, 65%
May be diplegia, hemiparesis or quadriplegia
Stretch tendon reflexes always brisk
Variable degrees of mental, visual and behavioral problems
Seizures are common
B. Hypotonic or Atonic CP
Patients are atonic or hypotonic
Tendon reflexes are normal, or brisk & Babinski response is
(+)
Severely mentally retarded
C. Extrapyramidal CP
Dyskinesia such as athetosis, choreiform movements, dystonia,
tremors and rigidity are seen.
Arms, leg, neck and trunk may be involved.
Mental retardation and hearing deficits may be present.
Cerebellar involvement occurs in less then 5% of cases.
49
Mental Retardation
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Pre-NEET Pediatrics
Measles
Scarlet fever
Rubella (German measles)
Duke's disease (scarlantinella)
Erythema infectiosum
Exanthem subitum (Roseola
infantum)
Spread
Age
Immunity
Nutrition
Prodromal Symptoms
51
Koplik's Spots
Comby's Sign
Rash
Complications
Diagnosis
52
Pre-NEET Pediatrics
Prevention
Presentation
Forschemier's Spots
Test
Treatment
53
Complications
Prevention
Adults with fifth disease often have arthritis, and fetal hydrops
can develop in association with this condition in pregnant women.
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Pre-NEET Pediatrics
Presentation
Complications
Treatment
Prevention
55
Infectious periods
5 days before rash to 6 days after last crop
2-3 weeks (shorter with antibiotic therapy)
3 days before salivary swelling to 7 days after
7 days before onset of rash to 4 days after
From onset of prodromal symptoms to 4 days after onset of
rash
Scarlet fever 10-21 days after onset of rash (shortened to 1 day by penicillin)
Whooping cough 7 days after exposure to 3 wks after onset of symptoms
(shortened to abt 7 days by antibiotics)
Precocious Puberty
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Pre-NEET Pediatrics
Neuroblastoma
HVA in urine
Treatment localized tumours cured with excision; chemotherapy
and radiotherapy can be used as adjunct. Good prognosis if
diagnosed <1 year of age. Shimada classification is used.
Neuroblastoma
Age in years
2-5
Health
Well
Clinical
Swollen abdomen
Mass
Lobulated
Crosses midline
Rare
Common
Bilateral
Rare
Occasional
Renal pelvis
Grossly distorted
Lungs
Ultrasound
Metastases
Calcification found
57
Blast cells
Myeloperoxidase negative
3 % blasts myeloperoxidase
Myeloperoxidase positive
positive
M2 AML with maturation
M3 Acute promyelocytic
58
Pre-NEET Pediatrics
Contd...
Class
Blast cells
leukemia
Myeloperoxidase positive
M4 Acute myelomonocytic
leulcemia
59
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Pre-NEET Pediatrics
3. Miscellaneous types
Associated with glycogen storage in many organs and death
in early life.
Examples:
i. Type II glycogenosis - Acid maltase deficiency (Pompe 's
disease)
61
Deficient enzyme
Sphingolipidoses
GM1, gangliosidosis
GM2, gangliosidosis
i. Tay-sachs disease
ii. Sandoff disease
-galactosidase
GM1 ganglioside
Hexosaminidase - subunit GM2 ganglioside
Hexosaminidase - subunit GM2 ganglioside
Glycogenosis type II
Pompe disease
- 1,4, glucosidase
Glycogen
- 1, Iduranidase
Induronate sulfatase
Sulfoiduranate sulfatase
Dermatan sulfate
Heparan sulfate
Mycopolysaccharidose
MPS I (Hurler)
MPS II (Hunter)
Scheie syndrome
Accumulating
metabolites
Contd...
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Pre-NEET Pediatrics
Contd...
Disease
Deficient enzyme
Accumulating
metabolites
Sulfatidoses
Metachromatic
leukodystrophy
Krabbe disease
Gaucher disease
Fabry's disease
NiemannPick disease
Arylsulfatase A
Sulfatide
Galactosylceramidase
Glucocerebrosidase
- Galactosidase A
Sphingomyelinase
Galactocerebroside
Glucocerebroside
Ceramide trihoxoside
Sphingomyelin
Others
Wolman disease
Acid lipase
Cholesterol ester,
triglyceride
LEUCODYSTROPHY
Leucodystrophy refers to progressive degeneration of the white
matter of the brain due to imperfect growth or development of
the myelin sheath, the fatty covering that acts as an insulator
around nerve fibre.
Myelin which lends its color to the white matter of the brain, is a
complex substance made up of at least ten different chemicals.
The leucodystrophy are a group of disorders that are caused by
genetic defects in how myelin produces or metabolizes these
chemicals.
Each of the leucodystrophies in the result of a defect in the gene
that controls one (and only one) of the chemicals.
Specific leucodystrophies include:
Metachromatic
leucodystrophy
Krabbe 's disease
Adrenoleucodystrophy
PelizaeusMerzhacher
disease
Canavans disease
Alexander disease
Canavan's Disease
63
Adrenoleucodystrophy
Metachromatic leucodystrophy
Krabbe leucodystrophy
Autosomal recessive
Caused due to deficiency of Beta-galactosidase deficiency
Onset is in the first 6 months of life
Optic atrophy, spasticity
Head often small
Wolman's Disease
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Pre-NEET Pediatrics
A shortage of lysosomal acid lipase leads to accumulation of
triglycerides, cholesteryl esters and other fats within the cells of
the affected individuals. This accumulation as well as malnutrition
caused by the body's inability to use lipids properly result in signs
and symptoms of wolmans disease.
Clinical Features
Diagnosis
X-Ray Findings of Wolman Disease
Characteristic pattern of calcification (outlining the outline of
the cortex of both the glands) in enlarged but normally shaped adrenal
glands.
65
Treatment
QUESTIONS
CLINICAL QUESTIONS AND QUESTION BASED ON
EXPECTED NEET PATTERN
Q 1. A neonate delivered at 37 wks of gestation with a birth weight of
1.9 kg develops intolerance to feed/ lethargy/abdominal distension on
2nd day. Sepsis screens is negative. Physical examination is
unremarkable. PCV is observed to be 72%. Which of the following
represents with best management option:
a. Hydration with IV fluids
b. Partial exchange transfusion
c. Presumptive treatment for sepsis
d. Medical management for intestinal obstruction
Q 2. A premature baby born at 33 wks of gestation with a birth weight
of 1500 gm has stable vitals. Which of the following you will choose
as initial feeding method of choice:
a. Intravenous fluids
b. Intravenous fluids and oral feeding
c. Orogastric tube/ alternate oral route
d. Total parenteral nutrition
Q 3. A 2 yrs old male child presents to paediatric emergency
department with history of fever x 2 wks. He has received multiple
antibiotics. Blood tests for Typhoid, Malaria, Dengue are all negative.
He however had sterile pyuria in one of reports (urine C/s - sterile).
BCG scar is indurated and H/o conjunctivitis, chelitis and erythematous
rash over body for initial 5 days of illness is obtained the most likely
treatment of choice is:
a. Cyclosporin
b. Prednosolone
c. Methotrexate
d. IvIg
Questions
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Questions
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Q 18. A 5 months old formula fed infant has been brought with
complaints of watery diarrhoea of 2 days duration and irritability of
one day. Physical examination reveals a markedly irritable child with
a rather doughy skin and rapid pulse, borderline CFT. Which of the
following statements is true?
a. Give I/V bolus of normal saline
b. Give I/V bolus of ringer lactate
c. Calculate water deficit and replace over 24 hrs at a rate of
0.5 meq/L/hr.
d. Treat as any dehydration and give moderate dehydration
correction.
Q 19. Study the following inheritance pattern
Which of the following statements is true?
a.
b.
c.
d.
Autosomal dominant
Mito chondrial
Autosomal recessive
X-linked dominant
Questions
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Pre-NEET Pediatrics
b. Send PT, aPTT and give Inj Vit K
c. Do urgent USG and perform hydrostatic reduction.
d. Do urgent USG and prepare for urgent laparotomy
Q 25. A 8 day old breast fed male baby presents with vomiting, poor
feeding and loose stools. On examination the heart rate is 190/min,
blood pressure 50/30 mmHg, respiratory rate 72 breaths/ minute and
capillary refill time of 4 sec. Investigations show Hb 15 gm/dL, SNa+
- 120 meq/L K+ - 6.8 meq/L, Cl- 81 meq/L, bicarbonate 15 meq/L,
creatinine 0.6 mg/dL. The most likely diagnosis is:
a. 21 hydroxylase deficiency
b. 3- hydroxy steroid deficiency
c. 11 hydroxylase deficiency
d. Aldosterone synthase deficiency
Q 26. A. Assertion: A 8 day old child presents yellow sclera, whitish
stool and turmeric colour urine with reducing substance positive on
3rd day of septicaemia on broad spectrum antibiotics.
R. Reasoning: This is a case of severe sepsis and antibiotics should be
immediately upgraded
a. A and R both correct and R is explanation of A
b. A and R both correct but R is not explanation of A
c. A correct R wrong
d. A wrong R correct
Q 27. A: Assertion: A 1 month baby presents with history of jaundice,
turmeric colored urine and pale stools since birth. Examination reveals
liver span of 10 cm TORCH IgM is positive for Rubella.
R: Reasoning: A liver biopsy should be done to differentiate neonatal
hepatitis from biliary atresia
a. A and R both correct and R is explanation of A
b. A and R both correct but R is not explanation of A
c. A correct R wrong
d. A wrong R correct
Q 28. 30 yr old lady delivered a healthy baby at 37 wk of gestation,
she was positive for HBSAg but negative for HBCAg. Which of the
following is the most appropriate treatment for the baby:
a. Both active and passive immunization soon after birth
b. Passive immunization soon after birth and active immunization
at 1 yr of age.
c. Only passive immunization soon after birth
d. Only active immunization soon after birth
Questions
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Pre-NEET Pediatrics
d. Cutaneous Vasoconstriction
Questions
75
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Pre-NEET Pediatrics
b. S. Alkaline phosphatase
c. S. LDH
d. Lead levels in blood
Q 10. A child who can use 4-5 words including meaningful nouns
and represent his ideas mostly by non-verbal communication then
what is his probable age?
a. 15 months
b. 18 months
c. 24 months
d. 12 months
Q 11. All of the following can occur in a neonate for heat production
except:
a. Shivering
b. Universal flexion like a fetus
c. Breakdown of brown fat with adrenaline secretion
d. Cutaneous vasoconstriction
Q 12. A down's child mentally retarded, a/e
a. Deleted 21
b. Trisomy 21
c. Robert Sonian
d. Mosaic
Questions
77
ANSWERS
CLINICAL QUESTIONS AND QUESTIONS BASED ON
EXPECTED NEET PATTEN
1. Ans. is b. Partial exchange transfusion
(Ref: Nelson 18th, Pg. 1773, Meharban Singh 7th, Pg. 305)
This is a case of neonatal polycythemia which is symptomatic in
the form of lethargy and GIT manifestations
The management of choice for such a case is partial exchange
transfusion.
The diagnosis of polycythemia is made when venous or central
hematocrit is greater than 65%
Etiology
1. Delayed clamping of cord
2. Twin-twin transfusion syndrome. Causes polycythenia in the recipient
twin
3. Infants of diabetic mother
4. Intra uterine growth retarded babies due to chronic placental
insufficiency.
5. Rare causes: Cyanotic congenital heart disease, Cretinism, Trisomy
13,18 and 21, Beckwtih-Wiedemann syndromes, dehydration.
Clinical Features
1. CardiopulmonaryTacypnea, Tacycardia, cyanosis and
cardiomegally.
2. CNSLethargy, hypotonia, poor feeding, seizures, irritability.
3. Transient renal failure due to reduced perfusion of kidneys.
4. Hyperbiliribenemia
5. Thrombotic complications including renal vein thrombosis
6. Hypoglycemia, hypocalcemia, hypomagnesemia
Answers
79
Treatment
80
Pre-NEET Pediatrics
No proper sucking
efforts
No propulsive gut motility
Intravenous fluids
3032 wks
(12001500)
Oro-gastric
Or Naso - gastric
feeds
3234 wks
(15001800 gm)
Spoon, paladay
Or cup feeding
Breast feeding
Trophic feeds are Minimal (sub nutritional) feeds (510 ml/kg/d) used in
preterm babies with a gestation of <32 wks or birth weight <1500 gm
to harness its trophic benefits on the immature gastro intestinal tract of
the baby.
3. Ans is d. IvIg
(Ref: Nelson 19th, Pg. 863-865)
This is most likely a case of Kawasaki disease (KD) formerly known as
mucocutaneous lymph node syndrome and infantile polyarteritis nodosa.
The characteristic BCG scar induration, conjunctivitis, skin rash
and fever not responding to antibiotics point to diagnosis.
Classic clinical criteria for Kawasaki disease are:
Fever persisting at least 5 days and presence of at least 4 principal
features:
a. Changes in extremities
i. Acute: Erythema of palms, soles, edema of hands, feet.
ii. Subacute: Periungual peeling fingers, toes in weeks 2 and 3
b. Polymorphous exanthema
c. Bilateral bulbar conjunctival injection without exudate
Answers
81
Etiology
The cause of KD remains unknown, but certain epidemiologic and clinical
features support an infectious origin KD is a vascultis that predominantly
affects the medium sized arteries especially the coronary arteries.
In the absence of treatment, KD can be divided into 3 clinical
phases
1. The acute febrile phage: lasts 1-2 wks
2. The subacute phase: associated with desquamation,
thrombocytosisand development of coronary aneurysms and
generally lasts about 2 wk.
3. The convalescent phase: begins when all clinical signs of illness
have disappeared and continues until ESR returns to normal (about
6 8 wk after onset of illness)
Convalescent Stage
Aspirin 3-5 mg/kg until 6-8 wk after illness onset.
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Pre-NEET Pediatrics
4. Ans is b. Pyeloplasty
(Ref: Nelson 18th, Pg. 2237, Paediatric Nephrology 5th, Pg. 446-448)
The child in question is presenting with characteristic feature of PUJ
obstruction (dilated renal pelvis with normal ureters).
Epidemiology
Left side is involved more commonly than right (Bilateral = 10%)
Male more commonly involved than females (M:F = 2:1)
Management
Answers
83
Clinical Manifestations
1. Localized disease: asymptomatic mass or mass related symptoms,
including spinal cord compression, bowel obstruction, SVC
syndrome.
2. Metastatic disease: Fever, Bone pain, cytopenias, orbital proptosis,
subcutaneous nodules, periorbital ecchymosis.
3. Most common sites of metastasis are lymph nodes, bones (long),
skill, bone marrow, liver and skin. Lung and brain metastasis are
rare.
Diagnosis
Treatment
1. Low risk
Localized tumor: Treatment surgery survival rate 98%.
2. Intermediate risk
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Pre-NEET Pediatrics
Necrotizing Enterocolitis
Vanous predisposing factors are:
Prematurity (especially <34 wks)
Perinatal hypoxia
Active resuscitation
RDS/ apnea
Assisted ventilation
Acidosis/ Hypoxia/ Shock
Umbilical artery catheterization
Use of H2 blockers
Answers
85
Signs
Radiology
Treatment
IA (Suspected
NEC)
Lethargy apnea,
bradycardia,
elevated
pre-gavage
residuals,
emesis,
guaic positive
stool
Normal or
intestinal
dilation,
mild illeus
NPO,
Antibiotics
IB (Suspected
NEC)
Same as above
+ bright red
blood per rectum
Same as above
+ absent bowel
sounds
Same as
above
Same as
above
Same as
above +
pneumatosis
intestinalis
Same as
above
IIA (Definite
NEC)
IIB (Definite
NEC)
Same as above
+ mild
thrombocytopenia,
acidosis +
abdominal
cellulites
Same as IIA
+ portal vein
gas
Same +
Sodabicarbonate for
acidosis
IIIA (Advanced
NEC)
Same as IIB
+ DIC, neutropenia + signs
of peritonitis
Same as IIB
+ definite
ascitis
Same as
above +
assisted
ventilation
paracentesis
IIIB (Advanced
NEC)
Same as IIIA
Same as
IIIA + pneumo
peritoneum
Same as IIIA
+ Surgical
intervention
(Laparotomy)
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Pre-NEET Pediatrics
In ELBW (<1000 gm) or unstable babies, peritoneal drainage is
established under local anaesthesia and laparotomy is delayed for
stage IIIB.
Clinical Features
Usually there is mild cold for a few days before the child develops a
brassy cough and inspiratory stridor. The condition may worsen to
severe respiratory distress and cyanosis,
Croup is a clinical diagnosis and does not require a radiograph of
the neck. However, characteristic "Steeple sign" (Subglottic narrowing)
may be seen on PA view of neck.
Moderate
Severe
General
appearance
Happy
Irritable
Agitated or altered
sensorium
Stridor
Stridor on coughing
or no stridor
at rest
Stridor at rest,
gets worse on
agitation
Respiratory
distress
No distress
Oxygen
saturation
>92% in room
air
Management
Mild cases can be managed on ambulatory basis with symptomatic
treatment for fever Antibiotics have no role.
Moderately severe patient may need hospitalization and treatment
with racemic epinephrine diluted with water.
Answers
87
Differential Diagnosis
1. Epiglottitis: H. Influenza type B is the most frequent causative agent.
a. Clinical features: High fever with difficulty in swallowing. He
often sits up leaning forwards and saliva dribbling from his
chin.
b. Diagnosis: Direct laryngoscopy where epiglottis appears angry
red.
c. Management: Hospitalization, Humidified oxygen, fluids,
antibiotics (ampicillin/chloramphenicol/ceftriaxone)
Ventilation.
2. Spasmodic croup: Occurs in children between 1 and 3 yrs. Usually
no prodromal symptoms, sudden onset brassy cough and noisy
breathing, usually in early hours of morning. Pathogenesis is
unknown.
Treatment: Racemic epinephrine and steroids are helpful.
8. Ans is a. EDTA
(Ref: Nelson 19th P. 2450)
The child in question is presenting with signs and symptoms of plumbism
as suggested by blue line on gums (Bertonian line), gastrointestinal
manifestations like constipation and symptoms of lead encephalopathy
(seizures, drowsiness).
As the patient in question in presenting with encephalopathy, he is
likely to have blood levels >70 g/dL and hence, EDTA is the single
most important agent for treatment.
Lead Poisoning
Lead is a heavy metal that is purely a toxicant in humans. Lead poisoning
may occur in utero, because it readily crosses the placenta from maternal
blood. The spectrum of toxicity is similar to that experienced by children
after birth.
Major sources of exposure include lead based paints, batteries;
cable sheathing, cosmetic, plastic, toys, mineral supplements.
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Metabolism
Clinical Symptoms
1. GIT symptoms: anorexia, abdominal pain, vomiting, constipation
2. CNS symptoms: related to cerebral edema and increased intracranial
pressure.
Headache, Lethargy, Seizures, Papilledema, Coma.
3. Renal tubular dysfunction at high levels (>100 g/dL)
Reversible fanconi syndrome.
4. Hemolytic anemia
Drug Treatment
A child with a venous BLL 45 g/dL or higher should be treated. Children
with BLL of 44-70 g/dL may be treated with a single drug, preferably
DMSA.
Those with BLL of 70 g/dL or greater require 2 drug treatment.
1. EDTA + DMSA / BAL for those without encephalopathy
2. EDTA and BAL for those with encephalopathy
9. Ans. is a. No IgG deposits or C3 deposits on renal biopsy
(Ref: Nelson 19th, Pg. 1804 Paediatric Nephrology 5th, Pg. 195)
This girl is having generalized edema, grade 3 proteinuria, Fatty + hyaline
casts. This is a case of minimal change Nephrotic syndrome.
IgA nephropathy and Alport's syndrome present with acute nephritic
syndrome rather than nephrotic syndrome.
Nephritic syndrome is characterized by massive proteinuria (3+ 4+ protein), Hypoalbuminemia (<2.5 gm/dL) Hypercholestrolemia,
edema.
Answers
89
Mesangial proliferation
Membranous nephropathy
Membranoproliferative glomerulonephritis
Differential Diagnosis
Hepatic failure
Heart failure
Protein malnutrition
Chronic glomenlonephritis
Treatment
Children with onset of uncomplicated nephritic syndrome between 1-8
yr of age are likely to have steroid responsive MCNS (Minimal change
NS)and steroids therapy may be initiated without a diagnostic renal
biopsy. Children with features that make MCNS less likely (Gross
hematuria, hypertension, renal insufficiency, hypo-complementenia, age
<1 yr or >8yr) should be considered for renal biopsy before treatment.
About 90% children with MCNS respond to initial steroid therapy.
The initial episode is treated with prednisolone, 2 mg/kg/d for 6 wks.
Thereafter, the dose of prednisolone is reduced to 1.5 mg/kg given on
alternate days as a single morning dose for 6 more weeks.
Further prolongation of alternate day prednisolone therapy for 6
months may be beneficial in reducing the risk of subsequent relapses.
10. Ans. is b. Short course of steroids
(Ref: Paediatric Nephrology 5th, Pg. 155-157)
This is a classical case presentation of Henoch - Schonlein purpura
with skin, joint, GIT and renal manifestation. Use of oral steroids for 23 wks is recommended. Skin biopsy is not mandatory for diagnosis.
Henoch: Schonlein purpura
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Pre-NEET Pediatrics
(Anaphylactoid purpura)
It is the most common systemic small vessel vasculitis in children. It
occurs frequently between 3 and 10 yrs.
Diagnosis
Presence of purpura (commonly palpable) or petechiae with lower limb
predominance and one of the four following criteria:
1. Abdominal pain
2. Arthritis/ arthralgia
3. Renal: involvement (proteinuria or hematuria or presence of RBC
casts)
4. Histopathology showing Leukocytoclastic vasculitis with
predominant IgA deposits in skin or proliferative glomerulonephritis
with predominant IgA deposits in mesangium on kidney biopsy.
Treatment
1. Joint symptoms only: Rest, analgesia
2. GIT manifestations, orchites, marked subcutaneous edema ' steroids
(prednisolone x 2-3 wks)
3. Severe Nephritis or nephritic syndrome, pulmonary hemorrhage
'steroids and cytotoxic drugs.
11. Ans. is b. Oral phosphate and Vit D supplements
(Ref: Paediatric Nepthrology 5th, Pg. 324-335)
Remember
Answers
91
Hyphosphosphatemic Rickets
Remember
In hypophosphatemic rickets, symptoms of hypocalcemia (tetany, muscle
weakness) are absent.
Dental abnormalities are common in hypophosphatemic x linked
rickets.
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Pre-NEET Pediatrics
Treatment
1. Phosphate supplements (Joulie solution: Sodium phosphate,
phosphoric acid)
2. Vitamin D supplementation (except hypercalciuric variety)
Vesicoureteral Reflux
Retrograde flow of urine from the bladder to the ureter and renal pelvis
is called vesicuureteral reflux.
Reflux is usually congenital and affects approximately 1% of
children. Reflux predisposes to renal infection, reflux nephropathy (renal
insufficiency).
Classification
Based on appearance of urinary tract on a contrast voiding cystourethrogram (VCUG)
Answers
1. Grade I
2. Grade II
93
:
:
Treatment
With bladder growth and maturation there is a tendency for reflux to
resolve over time especially lower grades.
Grade 5 reflux rarely resolves.
Surgical correction of VUR also advised for
1. Multiple recurrences of UTI while on prophylaxis
2. Non compliance to medical management
3. Parental preference for surgery
4. Appearance of new renal scars during medical therapy.
Age (yr)
Scarring
Initial
Treatment
I - II
Any
+/-
Antibiotic
Prophylaxis
III - IV
0-5
+/-
Antibiotic
Prophylaxis
III - IV
6 - 10
+/-
Unilateral
Antibiotic
prophylaxis
Bilateral
Surgery
Prophylaxis
<1
+/-
Antibiotic
1-5
(-)
Unilateral
Antibiotics
prophylaxis
Bilateral
V
>1 yr
(+)
Surgery
Surgery
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Hyponatremia
Alkalosis
Hypochloremia
S.K+ 3 meq/L
S.Na+ 125 meq/L
PH 7.46
S.CI-88 meq/L
BARTTER SYNDROME
It is an autosomal recessive disorder, characterized by hypokalemia,
metabolic alkalosis, hyperreninemia and hyperaldosteronism, normal
blood pressure and urinary wasting of K+, Na+ and Cl-.
Clinical features include failure to thrive, polyuria and polydipsia
with recurrent episodes of dehydration, muscle weakness and cramps in
older children.
Molecular defect is in the thick ascending limb of Henle. Tubular
losses of K+, Na+, Cl- and water lead to volume contraction that in
turn causes secondary hyperaldosteronism.
Bartter syndrome should be differentiated from non renal causes of
chloride loss such as vomiting, cystic fibrosis. In these conditions the
urinary chloride concentration is in variably below 10meq/L.
Therapy: Potassium supplementation and Indomethacin (cyclo oxy
genase inhibitor decrease elevated prostaglandins that are responsible
for polyuria).
GITELMAN SYNDROME
Hypokalemia, metabolic alkalosis and hypomagnesemia are chief
abnormalities.
The combination of Hypocalciuria with renal magnesium wasting
distinguishes Gitelman from Bartter syndrome
Answers
95
Clinical Features
Generally milder symptoms. Appear in older children. There are episodes
of muscular weakness, cramps, fatigue, vomiting, tetany, polyuria and
growth retardation are mild.
Molecular defect is in the apical thiazide sensitive, sodium chloride
co-transporter (NCCT) in distal tubule. Features of Gitelman syndrome
mimic Chronic thiazide administration.
Treatment is with supplementation of potassium and magnesium
chloride.
14. Ans is b. Long term phenytoin is required
(Ref: Nelson 19th, Pg. 2017-18)
This is a case of recurrent febrile seizure which can be treated with
intermittent clobazam and paracetamol. The risk of epilepsy is 4%.
Considering this to be a low intermediate risk, EEG and neuroimaging
may be considered. But certainly long term phenytoin therapy is not
required unless EEG/ Neuroimaging turn out to be abnormal.
Febrile Seizures
Febrile Seizures are seizures that occur between the age of 6 months - 5
yrs with a temperature of 380C or higher, that are not the result of CNS
infection or any metabolic imbalance and that occur in the absence of
a history of prior afebrile seizures.
A simple febrile seizure - generalized, usually tonic clonic associated
with fever, lasting for a maximum of 15 min and not recurrent within a
24 hr period.
A complex febrile seizure is more prolonged >15 min, is focal, and/
or recurs within 24 hours.
Minor
Fever 38-390C
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1%
33%
29%
18%
11%
4%
Investigations
Lumbar puncture is recommended in children <1yr of age after their
first febrile seizure or if clinical signs and symptoms suggest meningitis
Treatment
15. Ans is d. EEG in this condition shows a 4-6/ sec irregular spike
and wave pattern, which is enhanced by photic stimulation.
(Ref: Nelson 18th, Pg. 2463)
This is a classical case presentation of juvenile myoclonic epilepsy (JANZ
syndrome). It begins usually between ages of 12-16 yrs. Patients note
frequent myoclonic jerks on awakening. A few years later, early morning
GTCS develop in association with myoclonus. EEG shows a 4-6/sec
irregular spike and wave pattern, which is enhanced by photic stimulation.
Drug of choice is Valproate and not carbemazepine. This is required
lifelong. Discontinuation of drug causes a high rate of recurrence of
seizures.
Other types of Myoclonic Epilepsies are:
1. Benign myoclonus of infancy: EEG is normal, No anticonvulsant
are required.
Answers
97
Neurofibromatosis
Inheritance is autosomal dominant
There are 2 types
1. Type I (Von Recklinghausen disease/ Peripheral NF1)
2. Type II (Central NF)
NF1: Deletion of NF gene on chromosome 17
NF2: Gene is probably located on Chr. 22
NF1: 2 or more of the following are present:
1. 6 or more Cafe-au-lait spots, each over 5 mm in diameter
before puberty or over 15 mm diameter in older persons.
2. 2 or more neurofibromas or one plexiform neuroma
3. Axillary/ Inguinal freckling
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Pre-NEET Pediatrics
4. Optic glioma
5. 2 or more Lisch nodules, dysplasia of sphenoid bone
6. A first degree relative with NF1
NF 2 - Presence of Bilateral auditory neuroma, unilateral auditory
neuroma along with a first degree relative with meningioma, schwanomas
or juvenile posterior subcapsular lenticular opacity.
Tuberous Sclerosis
Ataxia - Telengiectasia
Treatment is Symptomatic
17. Ans is d. Medullobastoma
(Ref: Nelson 18th, Pg. 2452, 2427)
Options a,b,c are congenital conditions whose presentations vary as
follows:
Answers
99
1. Chiari Malformation
Type I:
Typically produces symptoms during adolescence /adult life.
Patient complains of recurrent headache, urinary frequency and
progressive lower limb spasticity.
The deformity consists of displacement of the cerebellar tonsils
into the cervical canal. It is usually not associated with
hydrocephalus.
Type II:
Characterized by progressive hydrocephalus with a
myelomeningocele.
Usually presents in childhood with gait abnormality, spasticity
and incoordination. The deformity consists of elongation of
4th ventricle with displacement of inferior vermis, pons and
medulla into cervical canal.
3. Syringobulbia
Clinical Feature
It may rarely produces symptoms during childhood due to its slow
evolution.
Asymmetric loss of pain and temperature sensation with preservation
of light touch can occur (due to disruption of lateral spinothalamic
tracts)
Later, upper motor signs develop as cavity impinges on the
corticospinal tract.
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4. Medulloblastoma
Clinical Features
1. Increased ICP (ie. Headache, Nausea, Vomiting, Hypertension)
2. Cerebellar dysfunction (ataxia, poor balance, dysmetria)
Medulloblastoma is the childhood brain tumor that most
commonly metastasizes extraneuronally.
Medulloblastoma is sensitive to both chemotherapy and radiation theray
with surgery as the starting point of treatment.
Answers
101
Clinical Features
Doughy abdomen
CNS feature: irritability, lethargy, seizures (due to brain hemorrhage).
Fever
Thrombotic complications (secondary to dehydration and
hypercoagulability with hypernatremia)
Treatment
1. Restoration of Intravascular volume: Normal saline bolus.
2. Calculation of deficit and replacement over 24-48 hrs
Goal- decrease S. Sodium by <12 meq/L every 24 hr, a rate of 0.5
meq/L/hr
3. Peritoneal dialysis: Acute severe hypernatremia
19. Ans is d. X-linked dominant
(Ref: Nelson 19th, Pg. 388)
It is an X linked dominant pattern of inheritance
The features which suggest the X-linked dominant pattern are:
A single abnormal X Chromosome is sufficient to express the disease.
All of the female offsprings of a diseased male XY will receive the
abnormal X chromosome and express the disease, whereas none
of the male offspring to the diseased father will have the disease (as
sons don't receive X chromosome from father).
A diseased mother can transmit the abnormal
X chromosome to both daughter and sons equally.
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Answers
103
Diagnosis
All infants born to HIV infected mother test antibody positive at birth
because of passive transfer of maternal HIV antibody across the placenta.
Therefore HIV EIISA (based on antibody) is done at 18 months of age
(By this time, almost all infants loose maternal antibody). Specific viral
diagnostic assays, such as HIV DNA or RNA PCR, HIV Culture or HIV
P24 antigen are essential for diagnosis of infant HIV infection.
HIV DNA PCR is method for diagnosis. 2 positive HIV DNA PCR
(1st performed at 6-8 wks of age) confirm HIV infection.
HIV P24 antigen assay is the less sensitive, HIV culture is technically
complex, expensive and time consuming (2-4 wks compared to 2-3
days with PCR) and with HIV RNA assays, data results are limited.
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Cotrimoxazole Prophylaxis
1. All HIV exposed infants starting at 4-6 wks of age and continued
till HIV infection can be excluded.
2. All HIV infected infants <1yr should receive prophylaxis regardless
of symptoms or CD4 percentage.
3. After 1 yr of age, prophylaxis is recommended for symptomatic
children or children with CD4 <25%.
Immunization: Symptomatic HIV infected children should not be given
OPV and BCG.
Breast feeding: According to WHO 2001, when replacement feeding is
available, avoidance of breast feeding by HIV infected mothers is
recommended. Otherwise, exclusive breast feeding is recommended
keeping in mind that mixed feeding during this period carries a 70%
greater risk of transmission.
21. Ans is b. Statement A is true while statement B is false.
(Ref: O.P. Ghai 7th, P. 573)
Statement 'A' is a classical example of spinal muscular atrophy (SMA)
while statement 'B' is EMG finding of myasthenia gravis.
1. Infant has areflexia (absent reflexes) but Deep tendon reflexes are
preserved in myasthenia gravis.
2. Myasthenia (congenital) does not present in the intrauterine life (so
does not cause polyhydramnios)
Hence, statement A is true but B is false.
Answers
105
Floppy Infant
He/she is an infant with marked hypotonia of the muscles and variable
associated weakness.
Common causes are:
1. CNS (Central nervous system)
Perinatal asphyxia, neonatal encephalopathy, cerebral palsy
(atonic type), Down syndrome, Inborn errors of metabolism
(amino aciduria, mucopolysaccharidosis, cerebral lipidosis)
2. Spinal cord: Anterior horn cell disease: SMA, polio
3. Peripheral Nerves: Familial dysautonomia, hereditary motor sensory
neuropathy
4. Myoneural junction: Neonatal myasthenia gravis, infantile botulism
5. Muscles: Muscualr dystrophies, congenital myopathies, polymyositis,
glycogen storage disease
6. Miscellaneous : PEM, hypothyroidism, rickets, Prader willi syndrome,
Ehler Danbos syndrome.
Clinical Features
Delayed motor milestones frequent, respiratory infections.
Antenatal H/O polyhydramnios, decreased fetal movements.
Clinical Examination
Frog like postures, diminished resistance to passive movements, excessive
joint mobility.
+++
Variable
Central
Anterior
horn cell
Peripheral
nerve
Neuromuscular
junction
Muscle
EMG - Electromyography
Extent of
weakness
Site of
involvement
++
++
++
+++
Arms
+++
++
+++
+++
Legs
>
<
> or =
> or =
Proximal
Vs distal
weakness
Decreased
Normal
Decreased/
absent
Absent
Normal/
increased
DTR
Short
duration
polyphasic
potentials
Decremental
response on
repetitive
stimulation
Abnormal
CNS
denervation
potentials
Denervation
potentials,
fasciculation's
Normal
EMG
Characteristic
Normal
Denervation
pattern
Neurogenic
atrophy
Normal
Muscle Biopsy
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Answers
107
Types
1. SMA type I: Werdnig Hoffmann disease. A classical patient presents
within first 6 months and is never able to sit. More than 90% die by
10 yr of age.
2. Type II: Manifest by first yr of age, unaided sitting is possible but
walking is not achieved. More than 90% survive beyond 10 yrs.
3. Type III: Kugelberg-Welander disease, can achieve walking without
aids.
4. Type IV: Presents after 30 yrs
Severity is variable
Lifespan is unaffected
The heart is not involved in SMA. Intelligence is normal.
22. Ans is b. Emergency atrial septostomy
(Ref: Avery 8th, Pg 841, Cloherty 5th, Pg. 428)
This is a classical case presentation of hypoplastic left heart syndrome
(ductal dependent lesion) which fails to respond to medical therapy. In
these neonates, in order to benefit from a PGE1 infusion, there must be
a patent foramen ovale to allow effective systemic blood flow (pulmonary
venous return) to cross the atrial septum and enter the systemic vascular
bed through the ductus. In these neonates, emergent balloon dilation of
atrial septum may be necessary. After a period of stabilization, corrective
surgery (Norwood procedure followed by a fontan operation later in
childhood) is planned.
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Pre-NEET Pediatrics
Of the four, critical aortic stenosis manifests shortly after birth with
signs of CHF, gallop rhythm, murmur and poor perfusion. In other
three left sided lesions, most common presentation is shock (poor
perfusion) in first 1-2 wks of life.
Answers
109
ii.
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Pre-NEET Pediatrics
Treatment: Reassurance
Atropine (by blocking the vagus nerve) may be tried in refractory cases.
Clinical Manifestations
1. Acyanotic/pink tetralogy of fallot: when obstruction to right
ventricular outflow is mild-moderate and a balanced shunt across
the VSD, the patient is not cyanotic.
2. Ductal dependent pulmonary blood flow in infants.
3. Older children: presentation with cyanosis, clubbing and dyspnea
on exertion.
Signs
1. Prominent left anterior hemi thorax in older children (due to long
standing right ventricular hypertrophy)
2. A systolic thrill/ systolic murmur in left sternal 3rd - 4th parasternal
space. It is caused by turbulence through right ventricular outflow
tract. It loudness directly proportional to severity of pulmonary
stenosis but it can become less prominent with severe obstruction
and hypercyanotic spell.
3. Single 2nd heart sound or soft pulmonary component.
Chest X-ray "Coeur in Sabot" (Boot shaped heart) due to cardiac apex
elevation (due to right ventricle hypertrophy) pulmonary oligemia.
Answers
2.
3.
4.
5.
111
Oxygen administration
Morphine subcutaneous at dose not exceeding 0.2 mg/kg
Intravenous soda bicarbonate if metabolic acidosis present
Intravenous phenylephrine - increase systemic vascular resistance,
decrease right ' left shunt and improves symptoms.
Surgical Management
1. Palliative surgery - Blalock - Taussig shunt (systemic to pulmonary
artery shunt) performed to augment pulmonary artery flow.
Indication: Infants with less severe cyanosis without cyanotic
spells and with good growth.
Modified Blalock Taussig Shunt between subclavian artery and
pulmonary artery.
Waterson shunt between ascending aorta to main pulmonary artery.
Pott's Shunt: descending aorta to pulmonary artery.
2. Corrective surgery
a. Electively between 4-6 months of age in case of less severe
cyanosis without spells
b. Immediately in infants with severe cyanosis (marked right
ventricular outflow obstruction).
24. Ans is d. Do urgent USG and prepare for urgent laparotomy
(Ref: Nelson 19th, Pg. 1288-1289)
This is a classical presentation of Intussusception and in view of X-ray
features of peritoneal irritation (ascites with distended bowel loops),
hydrostatic reduction should not be attempted.
This is not a case of simple gastroenteritis because in enteritis, the
pain is less severe, there is diarrhea which is not the case in this clinical
problem.
Similarly Vit K deficiency is less likely as bleeding per rectum is
painless and there are no associated symptoms of excessive crying and
vomiting in Vit K deficiency.
Intussusception
It occurs when a portion of the alimentary tract is telescoped into an
adjacent segment.
The upper portion of bowel, the intussusceptions, invaginates into
the lower, the intussuscipiens.
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Pre-NEET Pediatrics
Clinical Features
Suddent onset in a previous well child of severe paroxysmal colicky
pain or episodes of excessive crying. Child may initially be comfortable
between paroxysms but progressively becomes weak and lethargic.
Vomiting occurs in most cases stools of normal appearance with
sometimes passage of blood.
Eventually a shock like states with fever develop.
Classic Triad
Pain, a palpable sausage shaped abdominal mass, and bloody or currant
jelly stool is seen in <15% of patients.
Abdomen Palpation
Usually (about 70% cases) reveals a slightly tender sausage shaped
mass, presence of bloody mucus on rectal examination supports the
diagnosis of Intussusception.
Diagnosis
Ultrasound
3.
4.
5.
6.
Sensitivity 98-100%
Specificity 88%
Tubular mass in longitudinal views
A doughnut or target appearance in transverse images.
Management
Immediate reduction of acute intussusceptions. In patients with prolonged
intussusception and signs of shock, peritoneal irritation, intestinal
Answers
113
Horizontal Enzymes
3 3- hydroxystroid dehydrogenase
2 21 - hydroxylase
1 11 - hydroxylase
Vertical Enzymes
All starting with "17"
4
- 17 hydroxylase
5
- 17, 20 lyase
6
- 17 hydroxy steroid dehydrogenase
* 7 - Cholestrol desmolase
* 8 - Aldosterone synthase
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Pre-NEET Pediatrics
1. 21 - Hydroxylase Deficiency
More than 90% of CAH are caused by 21-hydroxylase deficiency.
Enzyme '2' in diagram is required for synthesis of Aldosterone and
cortisol. In its absence, progesterone and metabolites are diverted to
production of androgens.
a. Deficiency of mineralo corticoid ' salt losing - hypotension,
hyponatremia, hyperkalemia, acidosis
b. Excess androgens - Virilization of female. In males, there will
be precocioius puberty due to androgen excess.
2. 11 - Hydroxylase Deficiency
Enzyme '1' in diagram is required for cortisol synthesis
In its absence
a. Excess DOC (Deoxy corticosterone) ' mineralo corticoid '
Hypertension
b. Excess androgens ' Virilization of female, precocious puberty in
males
4. 17 - Hydroxylase Deficiency
Enzyme '4' in diagram
Required for cortisol, Sex hormone synthesis in its absence, all
pregnenolone is converted to mineralocorticoid. So there will be:
a. Excess of mineralocorticoid ' Salt retention, hypertension
b. No androgens ' Feminization of external male genitalis, females
development will be normal.
Answers
115
Summary
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Answers
117
Incubations period
Hepatitis B
Perinatal Transmission of HBV
Most important risk factor that determines perinatal transmission ie.
HBeAg. HBSAg. Carrier mother who are HBeAg positive almost
invariably (>90%) transmit Hep B to their offspring, whereas carrier
mothers with anti HBe rarely (10-15%) infect their offspring.
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Anti HBS
Anti HBe
HBe Ag
Anti HBe
Interpretation
+
-
IgM
IgM
+
+/-
+/-
IgG
IgG
+
+
IgG
-
+/-
Acute infection
Acute infection,
anti BHC
window
Chronic
infection,
high infectivity
Chronic
infection,
low infectivity
Recovery
Immunization
Dengue Fever
Dengue fever is caused by 4 antigenic types of dengue virus (member of
family flaviviridae) spread through the bite of A.aegypti in Asia.
It is characterized by biphasic fever, myalgia, arthralgia and rash.
Answers
119
Clinical Features
Typically, after an incubation period of 4-6 days the patients may develop
abrupt onset high grade fever, facial fushing and headache. There may
be vomiting, pain abdomen associated with tender hepatomegally. Nearly
all patient have some hemorrhagic phenomenon. After subsidence of
fever, some children may show varying degrees of peripheral circulatory
falure
The presence of thrombocytopenia with concurrent hemoconcentration and evidence of plasma leak differentiate DHF from
dengue fever.
Hemo concentration - hematocrit elevated at least 20% above
baseline
Thrombocytopenia - <1Lakh cells/ mm3
Plasma leakage - Presence of pleural effusion on chest x-ray or
hypoalbuminemia
DHF with hypotension is called dengue shock syndrome.
Treatment
In hospital all children without hypotension should be given Ringer's
lactate infusion at rate of 7 ml/kg over 1hr. This is tapered to 3 ml/kg/hr
for 24-48 hrs if hematocrit decreases, and vital parameters improve.
But if hemocrit is rising and vitals dont' show improvement, fluids infusion
rate is increasd. (till 15 ml/kg/hr)
In children with hypotension, Ringer lactate boluses are given. If
hematocrit, and BP fall despite boluses, Blood is transfused.
Majority of patients recover in 24-48 hrs without sequelae.
30. Ans is b. -Thalassemia
(Ref: Nelson 18th, Pg. 2037)
Out of the given 4 types of haemolytic anemia only -Thalassemia is
able to give rise to such a severe presentation at birth. In all other
conditions, the newborn is either normal or has mild jaundice.
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Pre-NEET Pediatrics
Thalassemia
Thalassemia are genetic disorders in globin chain production (Autosomal
recessive). Adult haemoglobin is a tetramer, composed of 2 globin
chains and 2 globin chains.
Thalassemia is caused by deficient synthesis of chain with
normal chain synthesis.
Thalassemia is cause by deficient chain with normal chain
synthesis
Thalassemia - complete absence of chain
+ Thalassemia - Partial reduction chain
Most common type of genetic abnormality in Thalessemia is
point mutation ie. Nonsense and in Thalessemia is deletion of
globin genes.
In Thalassemia, excess of globin. Chains form Bart's haemoglobin
(4) infetal life and chains for HbH (4) after birth. Barts
haemoglobin in unable to release oxygen to tissues and hence,
causes severe hypoxia and extravascular hemolysis and causes Nonimmune Hydrops in the fetus.
Thalassemia
There are 3 forms of Thalassemia
1. Thalassemia major (Cooley's anemia)
Homozygous for Thalassemia genes.
Severe transfusion dependent
Manifesting at 6-9 months as haemoglobin synthesis switches
from HbF to HbA.
2. Thalassemia Minor ( Thalassemia trait)
Individual has only one copy of Thalassemia genes
(Heterozygous)
Mildest form - patient are usually asymptomatic
3. Thalassemia intermedia
Condition intermediate between major and minor
Individuals may rarely need occasional transfusion
Answers
121
Genetics
HbF
HbA2
T. Major
T. Intermedia
T. Minor (trait)
Homogygous
30-90%
<3.5%
Double heterozygotes
20-100%
<3.5%
Heterozygotes
0-5%
3.6-8%
Incidence
Its incidence is inversely related to gestational age and birth weight. It
occurs in 60-80% of infants <28 wk of gestational age, in 15-30% of
those between 32 and 36 wk, and rarely in those >37 wk.
Diagnosis
Age of onset: Presents usually within minutes of birth.
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Pneumonia
ARDS
HMD (Hyaline membrane disease)
Pulmonary consolidation
Alveolar proteinosis
Sarcoidosis
Lymphoma
Prevention
Administration of antenatal corticosteroids reduces the incidence of
RDS, IVH, NEC, early onset sepsis and developmental delay.
Drug Regimens
Treatment
CPAP indication: If oxygen saturation cannot be kept >85% at inspired
oxygen concentrations of 40-70% or greater.
Surfactant Indications
i.
ii.
Answers
123
2. Ans is a. Shivering
(Ref: O.P. Ghai 7th, Pg. 115-118, Meharban Singh 7th, Pg. 200-206)
Definitions
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Pre-NEET Pediatrics
Metabolic Thermogenesis
Non-Shivering thermogenesis, as result of metabolism of brown fat, is
the most important source of heat production in newborn.
The fetal brown fat is laid down mostly during the third trimester of
pregnancy and is located at the nape of the neck, interscapular region,
axillae, groin, around the Kidneys and adrenals. This fat is metabolically
very active in view of a large number of mitochondria and increased
vascularity. Lipolysis of this fat release fatty acids which are locally
consumed for generation of heat.
Answers
125
Management
Cold Stress/ Moderate Hypothermia
Severe Hypothermia
Incubator/ Radiant warmer
Regular temperature monitoring
Supportive measures: Oxygen, antibiotics (if sepsis suspected), saline
bolus (if hypotension present), Prewarmed IV fluids, Inj. Vit K, Monitor
Vitals.
3. Ans is c. All in children
(Ref: O.P. Ghai 7th, Pg. 580-584, Nelson 19th, Pg. 1732-1737)
The Leukemias are the most common malignant neoplasms in childhood,
accounting for about 31% of all malignancies that occur in children
<15 yrs of age.
ALL (Acute Lymphoblastic Leukemia) accounts for about 77%
of cases of childhood Leukemia.
The Leukemias are a group of malignant diseases in which genetic
abnormalities in a hematopoietic cell give rise to an unregulated clonal
proliferation of cells.
Down syndrome
Fanconi anemia
Bloom syndrome
Diamond - Blackfan anemia
Schwachman - diamond syndrome
Kostmann syndrome
Neurofibromatosis type I
Ataxia - telongiectasia
Severe combined immune deficiency
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Environmental Factors
Ionizing radiation
Alkylating agents
Nitrosourea
Benzene exposure
Epipodophyllotoxin
Diagnosis
Peripheral blood picture that indicates bone marrow failure -anemia,
thrombocytopenia, elevated WBC count with/without leukemic cells
(atypical lymphocytes).
ALL is diagnosed by a bone marrow evaluation that demonstrates
>25% of bone marrow cells as lymphoblasts.
Classification
Based on
1. Morphology
2. Immunopheno type
Leukemia
Prognostic Factors
Good Prognosis
Bad Prognosis
3. Girls-Sex
4. B-cell Leukemia
T-cell Leukemia
6. Hyperdiploidy
Hypodiploidy
7. Trisomy 4 and 10
8.
Answers
127
Management
Treatment of ALL is divided into 4 stages
i. Induction therapy (to attain remission)
ii. CNS prophylaxis
iii. Intensification (consolidation)
iv. Maintenance therapy
Average duration of treatment in ALL ranges between 2-2 yrs.
1. Induction therapy: Lasts 4-6 weeks. Current induction regime
includes vincristine, prednisolone, L-asparaginase and an
anthracycline.
2. CNS prophylaxis: Essential to eradicate Leukemic cells which
have passed the blood brain barrier. It comprises cranial irradiation
with Intrathecal methotrexate. Other alternative regimen includes
use of methotrexate, hydrocortisone, cytarabine.
3. Intensification therapy: It comprises intensified treatment after
remission induction to tackle problem of drug resistance. Commonly
used agents include methotrexate, L-asparaginase,
Cyclophosphamide, Cytarabine and Epipodophyllotoxin.
4. Maintenance therapy: This is required to prevent relapse. It is
continued for an additional 2-2.5 years after induction remission.
The main agents used include 6-mercaptopurine daily and
methotrexate once a week given orally
Relapse
Early bone marrow relapse before completing maintenance therapy has
the worst prognosis while late relapses after maintenance therapy have
a better prognosis.
Relapse in extramedullary sites especially testes is more favourable.
The treatment of relapse must be more aggressive than the first line
therapy.
* Glioblastoma multiforme (grade IV) is an aggressive form of
astrocytoma with poor prognosis. Pilocytic astrocytoma is with good
prognosis.
* Esophagealcarcinoma and Cholangio carcinoma usually remain
asymptomatic for a very long time. By the time they are detected these
malignancies would have already spread. So the only treatment that
can be offered is palliation.
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Abnormal aPTT
Normal PT
Hemophilia A and B,
Von willebrand disease
Abnormal PT
Normal aPTT
Anti-coagulant
therapy (eg:
Warfarin)
F Vll deficiency
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129
Clinical Presentation
Lab Findings
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Classification
I.
II.
III.
Type
Type
Type
I
II III -
Treatment
Desmopressin used in type I disease releases VWF from endothelial
cells.
Bernard-Soulier Syndrome
Glanzmann Thrombasthenia
Answers
131
Pathogenesis
CF epithelial cells especially the respiratory tract are unable to secrete
chloride ions which leads to excessive sodium and water reabsorption.
This leads to viscous desiccated secretions that cause airway obstruction.
In sweat glands, the main function to absorb rather than secrete chloride
not done, consequently sodium levels are elevated in sweat.
Diagnosis
History of CF in sibling or
Identification of 2 CF mutations or
Management
1. Respiratory: Airway clearance techniques, antibiotics and antiinflammatory agents.
2. Nutritional: Increasing caloric intake, supplement fat soluble
vitamins (A, D, E in twice the recommended doses), replace
pancreatic enzymes.
2. Ans is a. Autism
(Ref: Nelson 19th, Pg. 101)
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Delayed
and
disorde
redcommunication
Atypical
social
interaction
Restricted
range of
interests
Onset
before
3 yr
of age
Similar to
autism
except
language
skills
relatively
intact.
Usually
not
cognitively
delayed.
Almost, always
affects girls
in skills
between 6-18
months of age.
Clinically
significant
regression
in skills
bowel
and bladder
control,
play motor
skills) before
10 yrs
of age
Features of 1 of
the other
autism
spectrum
disorders,
but insufficient
for a specific
diagnosis
Autistic Disorder
Diagnosis
DSM IV criteria for Autistic disorder
(A) A total of six (or more) items from (1), (2), and (3) with at least 2
from (1) and one each from (2) and (3)
(1) Qualitative impairment in social interaction, as manifested by least
2 of the following:
a. Marked impairment in the use of non-verbal behaviours like eye
eye gaze, facial expression, body postures, and gestures to regulate
social interaction.
b. Failure to develop peer relationships approximate to developmental
level.
Answers
133
c.
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Complications of PN
1. Cholestasis: as a result of hepatic dysfunction (Reduced bile flow
and bile salt formation).
2. Metabolic bone disease
3. Azotemia, hyperammonemia, hyperchloremic metabolic acidosis
seen especially with amino acid intakes >4 gm/kg/dl.
4. Sepsis: associated with decreased Lipoprotein lipase activity. During
sepsis, lipid infusion is limited to 2 gm/kg/dl if triglyceride> 150 mg/
dL
Answers
135
5. Hyperlipidemia/hypertriglyceridemia
6. Indirect hyperbilirubinemis - due to displacement of bilirubin from
albumin binding sites by free fatty acids.
4. Ans is d. Sacrococcygeal teratoma
(Ref: Avery 8th, Pg. 1454)
Sacrococcygeal Teratoma
Sacrococcygeal teratoma is the most common solid tumor in newborn,
although it is rarely malignant.
Females are affected 2-4 times more frequently than males.
In most cases, the tumor manifests as a mass protruding between the
coccyx and rectum.
Most benign teratomas produce no functional difficulties.
Bowel/bladder dysfunction, painful defection and vascular/ lymphatic
obstruction suggest that the lesion is malignant.
Treatment
It is primarily surgical if age adjusted AFP and HCG levels are normal.
Chemotherapy (using Cisplatin and/ Bleomycin) + Surgery are used for
malignant sacrococcygeal tumors.
Congenital Leukemia
Rarely occurs during the 1st month of life. Most of neonatal cases arise
from the myeloid lineage. Trisomy 21 is particularly associated with
AML in newborns.
The chemotherapy regimens used in infants with myeloid leukemia
are identical to those used in older children.
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CNS Tumours
CNS malignancies are rare in newborn. Most of brain tumors are
supratentorial half of them are gliomas. Infants with primitive
neuroectodermal tumors and ependymoma have poor prognosis.
Hepatoblastoma
Uncommon in infants and children. The most common malignant
neoplasm involving the liver in infancy is "Metastatic neuroblastoma".
The most common benign hepatic neoplasm in neonate are
mesenchymal hamartomas and hemangiomas.
Hereditary conditions with associated tumors
1. Ataxia - telangiectasia - Leukemia, lymphoma
2. Beckwith - Wiedemann syndrome - Wilm's tumor, hepatoblastoma,
Rhabdomyosarcoma
3. Bloom syndrome - Leukemia
4. Denys - Drash syndrome - Familial Wilms tumor
5. Fanconi anemia - Leukemia
6. Klinefelter syndrome - Teratoma, leukemia, Breast cancers
7. Li-fraumeni syndrome - Sarcoma, CNS, Breast tumors
8. Neurofibroatosis - Glioma, leukemia, sarcoma
9. Trisomy 18 - Wilms tumor
10. Von hippel landau syndrome - Non Hodgkin lymphoma
11. WAGR syndrome - Wilms tumor
12. X-linked lymphoproliferative disorder - EBV lymphomas
Answers
137
Prevention
Treatment
The defects which are covered by skin do not need urgent treatment but
others should be closed soon after birth because they are likely to get
infected.
The Sac should be kept covered with a Sterile Saline - moistened gauze
sponge to prevent infection and fluid loss. After repair of a
myelomeningocele, most infants require a shunting procedure for
hydrocephalus.
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Clinical Manifestations
A child with an ASD is most often asymptomatic However, a history of
exercise intolerance, easy fatigability and recurrent pneumonias
accentuated may be obtained with large left to right shunts.
Auscultatory signs include a normal or accentuated 1st Heart sound;
wide, fixed splitting of the 2nd sound a pulmonary systolic ejection
murmur (due to increased flow of blood across right ventricular outflow
tract into pulmonary artery), a short mid diastolic murmur produced by
increased volume of blood flow across tricuspid valve.
The chest X-ray shows varying degree of enlargement of the right
ventricle and atrium, depending on the size of the shunt. The pulmonary
artery is enlarged and pulmonary vascularity is increased.
Treatment
Surgical closure usually after 1st year and before entry into school.
Answers
139
Indications
i.
ii.
Complications
Infective endocarditis is extremely rare and antibiotic prophylaxis is not
recommended.
* Partial anomalous pulmonary venous return (one or several
pulmonary veins returning anomalously to superior or inferior vena
cava, right atrium or the coronary (sinus)may be associated with
ASD (mostly of sinus venosus type)
* Scimitar syndrome: an anomalous pulmonary vein draining into
the inferior vena cava visible on CXR as a crescentic shadow of
vascular density along right border of the cardiac silhouette.
7. Ans is a. Can be seen after ventouse delivery
(Ref: Meharban Singh 7th, Pg. 254-272, Nelson 19th, Pg. 602-613)
Jaundice is observed during the 1st wk of life in approximately 60% of
term infants and 80% of preterm infants.
Although bilirubin may have a physiologic role as an antioxidant,
elevations of indirect, unconjugated bilirubin are potentially neurotoxic.
The conjugated form is not neurotoxic, direct hyperbilirubinemia
indicates a potentially serious hepatic disorders or a systemic illness.
Physiological Jaundice
In term babies, it appears after 36 hrs of age. Maximum intensity is
seen on the 4th day, S. Bilirubin does not exceed 15 mg/dL and jaundice
disappears by 10 days of life.
In preterm babies, the maximum intensity of jaundice is reached
on the 5th or 6th day, S. Bilirubin may go upto 15 mg/dL and it may
persist upto 14 days.
The etiology of physiologic jaundice appears to be over production
due to polycythemia, poor hepatic uptake, conjugation and excretion
of bilirubin.
Pathological jaundice: when jaundice in the newborn does not conform
to criteria described for physiological jaundice, it is designated as
pathological.
Cephalohematoma or significant bruising attributable to ventouse
delivery is a major risk factor for development of pathological
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Answers
141
Hypoglycemia in Newborn
Definition is controversial, however most workers agree that blood glucose
level of less than 40 mg/100mL (irrespective of period of gestation), if
associated with symptoms of hypoglycaemia or if confirmed on repeat
analysis in asymptomatic babies, is indicative of hypoglycaemia (1.0
mmd/L or glucose is equivalent to 18.02 mg/dL).
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3. Miscellaneous Conditions
Inborn errors of metabolism (glycogen storage disease,
galactosemia, fructose intolerance, CAH, cretinism)
Congenital Hypo pituitarism
Maternal therapy with Blockers (propanolol), Chlorpropamide
Exchange transfusion with heparinised blood/ACD/CPD blood.
Management
Answers
143
Genetics
The HPRT gene has been localized to the long arm of the XChromosome. The disorder appears in males, occurrence in females is
extremely rare and ascribed to non-random inactivation of the normal
X Chromosome.
The mechanism whereby HPRT leads to the neurologic and
behaviour symptoms is unknown but they are not caused by
hyperuricemia or excess hypoxanthine as patients with partial HPRT
deficiency do no self injure themselves.
Diagnosis
The presence of dystonia along with self-mutilation of mouth and fingers
suggests Lesch-Nyhan disease. Serum levels of uric acid >4-5 mg uric
acid/dL and a urine uric acid, creatinine ratio of 3:4 or more are highly
suggestive of HPRT deficiency.
The definitive diagnosis requires an analysis of the HPRT enzyme.
Treatment
Medical management of this disorder focuses on the prevention of renal
failure by pharmacologic treatment of hyperuricemia with high fluid
intake along with alkali and allopurinol.
Bone marrow transplantation (BMT) has been carried out in several
patients, based on the possibility that the CNS damage is produced by
a circulating metabolic toxin.
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Down Syndrome
This is the most common disorder occurring with a frequency of 1:800
- 1:1000 newborns.
Chromosome number 21 is present in triplicate, the origin of extra
chromosome 21 is mostly from the mother (97%). The risk in newborn
is 1:1550 if maternal age is between 15 and 29 years, 1:800 at 30-34
yrs, 1:270 at 35-39 yrs, 1:100 at 40-44 yrs and 1:50 after 45 yrs.
Cytogenetics
In approximately 95% of the cases of Down syndrome there are 3
copies of Chromosome 21.
Approximately 1% of Trisomy 21 are mosaics (with some cells
having 46 Chromosomes).
4% have translocation that involves Chromosome 21. Majority of
translocations are fusions at centromere between Chromosomes
13,14,15,21 and 22 called as Robert Sonian translocation. Translocation
(21,21) Carriers have a 100% recurrence risk and other Robert Sonian
translocations have a 5-7% recurrence risk when transmitted by females.
It is not possible to distinguish the phenotypes of persons with full
trisomy 21 and those with a translocation while patients who are mosaics
tend to have a milder phenotype.
Answers
145
Prenatal Diagnosis
Initial Screening - PAPP-A, free hCG in first trimester
Second trimester (Quad testing) - S.FP, hCG, Unconjugated estriol
and inhibin A.
Inhibin A, hCG (Both with 'h'spelling have high levels in Down's
syndrome. Rest all are decreased.
(i.e. PAPP-A, S.FP, Unconjugated estriol)
Ultrasound Findings
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147
Diagnosis
1. VDRL (Venereal disease research laboratory) tests are sensitive nontreponemal tests that detect antibodies against phospholipid antigens
on the treponema surface that cross react within the mammalian
cardiolipin - lecithin - cholesterol antigens. Titres increase with active
disease and decline with adequate treatment.
False positive VDRL: Infectious mononucleosis, connective tissue
disease, pregnancy.
False negative VDRL: Prozone effect (excess antibody), early
primary syphilis, latent syphilis, late congenital syphilis).
2. Treponemal antibody tests: TPHA (T. Pallidum hemagglutination
assay), FTA-abs (Fluorescent treponemal antibody absorption) test.
These tests become positive soon after initial infection and usually
remain positive for life, even with adequate therapy.
They are useful for diagnosis of a 1st episode of syphilis and for
distinguishing false positive result of VDRL but cannot accurately
identify length of time of infection, response to therapy or
reinfection.
Treatment
Congenital syphilis: Aqueous crystalline penicillin I/V for 10 days.
3. Ans is c. Vein of galen malformation
(Ref: Nelson 18th, Pg. 1988, 2511)
Arterio venous malformations result from failure of normal capillary
bed development between arteries and veins during embryogenesis. AV
malformations produce abnormal shunting of blood, causing vessel
expansion, a space occupying effect or rupture and intracerebral bleeding.
The vein of galen is an arterio venous malformation that is located
under cerebral hemisphere and drains the anterior and central regions
of the brain into the sinuses of posterior cerebral fossa.
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Genetics
Most PCD cases are autosomal recessive though there are reported
cases of Autosomal dominant and X-linked modalities. Austosomal
dominant and x-linked modalities.
5. Ans is b. Primary hypothyroidism
(Ref: Nelson 19th, Pg. 1895-1903)
Both choices A and C are similar - Both cause hyperthyroidism with a
high T4 level.
Choice D, TSH resistance is a very rare condition and many reported
cases showed normal T4 level.
Hypothyroidism
Answers
149
Laboratory Findings
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Clinical Manifestations
1. Nocturnal and morning hemoglobinuria is a classic finding in adults.
However, chronic hemolysis (intravascular) is more common in PNH,
despite its name.
2. Thrombocytopenia and leukopenia are after seen.
3. Thrombosis and thromboembolic phenomena are sometimes seen
(due to altered glycoproteins on the platelet surface and resultant
platelet activation).
4. Hypoplastic or a plastic pancytopenia may follow/precede the onset
of PNH
5. PNH rarely progresses to acute myelogenous leukemia
Lab Findings
1. Acidified serum hemolysis (Ham) test or sucrose lysis test. These
tests activate the alternative and classic pathways of complement
lysis, respectively.
2. Flow cytometry is the diagnostic test of choice for PNH. It uses anti
CD59 for RBCs and anti CD55, anti CD59 for granulocytes.
Treatment
1.
2.
3.
4.
5.
DNB
QUESTIONS
PAEDIATRICS 2010
Q 1. Earliest indication of sexual maturation in a girl is:
A. Menarche
B. Pubarche
C. Thelarche
D. Maturation of breasts
Ans. is C. Thelarche
(Ref: O.P. Ghai 7th, Pg. 498)
Q 2. Epiphyseal dysgenesis is a pathognomonic feature of:
A. Hypoparathyroidism
B. Hyperparathyroidism
C. Hypothyroidism
D. Hyperthyroidism
Ans. is C. Hypothyroidism
(Ref: Nelson 19th, Pg. 1899)
Q 3. Commonest cause of stridor in a new born is:
A. Laryngomalacia
B. Foreign body
C. Meconium aspiration
D. Recurrent laryngeal nerve palsy due to birth
Ans. is A. Laryngomalacia
(Ref: O.P. Ghai 7th, Pg. 340)
Q 4. Precocious puberty is seen in:
A. Hyperthyroidism
B. Addisons disease
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153
C. Hypomagnesiumia
D. Hypocalcemia
Ans. is A. Hypoglycemia
(Ref: O.P. Ghai 7th, Pg. 156)
Q 10. Which of the following is not used a in term baby as
vigorous:
A. Color
B . Heart rate
C. Respiratory effort
D. Muscle tone
Ans. is A. Color
(Ref: O.P. Ghai 7th, Pg. 100)
Q 11. Early neonatal sepsis in india is most commonly due
to:
A. Escherichia coli
B . Group-B Stretococci
C. Staphylococci
D. Pseudomonas
Ans. is A. Escherichia coli
(Ref: O.P. Ghai 7th, Pg. 136)
Q 12. A neonate with recurrent infection and abscess was
diagnosed with Kostmann syndrome. Treament is:
A. G-CSF
B. GM-CSF
C. Antithymocyte globulin+cyclosporin
D. Antithymocyte globulin+cyclosporin +GM-CSF
Ans. is A. G-CSF
(Ref: Nelson 19th, Pg. 750)
Q 13. Aniridia is associated with:
A. Hepatoblastoma
B. Medulloblastoma
C. Nephroblastoma
D. Retinoblastoma
Ans. is C. Nephroblastoma
(Ref: Nelson 19th, Pg. 1758)
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PAEDIATRICS 2009
Q 1. Commonest cause of heart failure in infancy is:
A. Myocarditis
B. Rheumatic fever
C. Cardiomyopathy
D. Congenital heart disease
Ans is D. Congenital heart disease
(Ref: O.P. Ghai 7th, Pg. 372)
Q 2. Congenital long QT syndrome is associated with
neonatal:
A. Sinus bradycardia
B. Sinus tachycardia
C. Supra ventricular. tachycardia
D. Ventricular tachycardia
Ans. is A. Sinus bradycardia
(Ref: Nelson 19th, Pg. 1617)
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C. Fibrointimal hyperplasia
D. Polyarteritis Nodosa
Ans. is A. Takayasu Aortoarteritis
(Ref: Paediatric Nephrology 5th, Pg. 162)
Q 8. Drug of choice for Rheumatic fever prophylaxis in
penicillin allergic patient:
A. Erythromycin
B. Clindamycin
C. Vancomycin
D. Gentamycin
Ans. is A. Erythromycin
(Ref: Nelson 19th, Pg. 924)
Q 9. Common to both acute and chronic malnutrition is:
A. Weight for age
B. Weight of height
C. Height for age
D. BMI
Ans. is A. Weight for age
(Ref: O.P. Ghai 7th, Pg. 62)
Q 10. Essential criteria for TOF includes all, except:
A. Valvular stenosis
B. Infundibular stenosis
C. Over riding of aorta
D. RVH
Ans. is A. Valvular stenosis
(Ref: O.P. Ghai 7th, Pg. 408)
Q 11. All of the following are features of downs syndrome,
except:
A. Increased PAPPA
B. Increased free beta HCG levels
C. Absent nasal bone
D. Abnormal ductus venous flow velocity
Ans. is A. Increased PAPPA
(Ref: IAP textbook of Pediatrics 4th, Pg. 995)
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PAEDIATRICS 2007
Q 1. Earliest indication of sexual maturation in a girl is:
A. Menarche
B. Pubarche
C. Thelarche
D. Maturation of breasts
Ans. is C. Thelarche
(Ref: O.P. Ghai 7th, Pg. 498)
Q 2. The first permanent teeth to erupt are usually the:
A. Lateral incisors
B. Central incisors
159
C. Second molars
D. First molars
Ans. is D. First molars
(Ref: O.P. Ghai 7th, Pg. 4)
Q 3. Blood specimen for neonatal thyroid screening is
obtained on:
A. Cord blood
B. 24 hours after birth
C. 48 hours after birth
D. 72 hours after birth
Ans is C. 48 hours after birth
(Ref: O.P. Ghai 7th, Pg. 483)
Q 4. Treatment of choice for thalassemia major is:
A. Blood transfusion and iron therapy
B. Folic acid and desferrioxamine
C. Blood transfusion and desferrioxamine
D. Iron, blood transfusion and desferrioxamine
Ans. is C. Blood transfusion and desferrioxamine
(Ref: O.P.Ghai 7th, Pg. 309)
Q 5. One of the intestinal enzymes that is generally deficient
in children following an attack of severe infectious enteritis
is:
A. Lactase
B. Trypsin
C. Lipase
D. Amylase
Ans. is A. Lactase
(Ref: O.P. Ghai 7th, Pg. 266)
Q 6. Sure sign of CCF in a infant is:
A. Basal crepts
B. JVP
C. Pedal oedema
D. Liver enlargement
Ans. is D. Liver enlargement
(Ref: O.P. Ghai 7th, Pg. 375)
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161
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PAEDIATRICS 2006
Q 1. Commonest cause of meningitis in postneonatal period
is:
A. Mycobacterium tuberculosis
B. Staph. aureus
C. Str. pneumonae
D. Klebsiella
Ans is C. Str. Pneumonae
(Ref: O.P. Ghai 7th, Pg. 536)
Q 2. Epiphyseal dysgenesis is a pathognomonic feature of:
A. Hypoparathyroidism
B. Hyperparathyroidism
C. Hypothyroidism
D. Hyperthyroidism
Ans. is C. Hypothyroidism
(Ref: Nelson 19th, Pg. 1899)
Q 3. In Downs syndrome, following congenital defect is
common:
A. PDA
B. PS
163
C. ASD
D. VSD
Ans. is C. ASD
(Ref: IAP textbook of Pediatrics 4th, Pg. 994)
Q 4.Craniotabes is found in children with the following
conditions except:
A. Rickets
B. Hydrocephalus
C. Syphilis
D. Kernicterus
Ans. is D. Kernicterus
(Ref: Nelson 19th, Pg. 200)
Q 5. Commonest haematological malignancy in children is:
A. CLL
B. AML
C. CML
D. ALL
Ans. is D. ALL
(Ref: Nelson 19th, Pg. 1732)
Q 6. Commonest cause of stridor in a new born is:
A. Laryngomalacia
B. Foreign body
C. Meconium aspiration
D. Recurrent laryngeal nerve palsy due to birth
Ans. is A. Laryngomalacia
(Ref: O.P. Ghai 7th, Pg. 340
PAEDIATRICS 2005
Q 1. The most important cause of under 5 mortality is:
A. Diarrhoea
B. Malnutrition
C. Respiratory infections
D. Trauma
Ans. is C. Respiratory infections
(Ref: O.P. Ghai 7th, Pg. 356)
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165
PAEDIATRICS 2004
Q 1. Craniotabes is found in children with the following
conditions except:
A. Rickets
B. Hydrocephalus
C. Syphilis
D. Kernicterus
Ans. is D. Kernicterus
(Ref: Nelson 19th, Pg. 200)
Q 2. In minimal change disease, correct is:
A. Most cases recover spontaneously
B. 20% go to CRF
C. 20% develop local glomerulosclerosis
D. 90% cases best respond to short course of steroid therapy
Ans. is D. 90% cases best respond to short course of steroid therapy
(Ref: Nelson 19th, Pg. 1803)
Q 3. Commonest haematological malignancy in children is:
A. CLL
B. AML
C. CML
D. ALL
Ans. is D. ALL
(Ref: Nelson 19th, Pg. 1732)
Q 4. Metabolic acidosis is accompanied with:
A. Acetazolamide
B. Phenformin
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C. Verapamil
D. Triamterene
Ans. is A. Acetazolamide
(Ref: O.P. Ghai 7th, Pg. 55)
Q 5. The commonest cause of death in diphtheric child is:
A. IIIrd nerve palsy
B. Myocarditis
C. Tonsillitis
D. Septicemia
Ans. is B. Myocarditis
(Ref: IAP textbook of Pediatrics 4th, Pg. 364)
Q 6. Unconjugated hyperbilirubinemia in newborn is caused
by following, except:
A. Breast milk jaundice
B. Galactosemia
C. Sphereocytosis
D. Gilberts syndrome
Ans. is B. Galactosemia
(Ref: Nelson 19th, Pg. 1376)
Q 7. Commonest cause of meningitis in postneonatal period
is:
A. Mycobacterium tuberculosis
B. Staph. aureus
C. Str. pneumoniae
D. Klebsiella
Ans. is C. Str. Pneumonia
(Ref: Nelson 19th, Pg. 2087)
Q 8. Sure sign of CCF in a infant is:
A. Basal crepts
B. JVP
C. Pedal oedema
D. Liver enlargement
Ans. is D. Liver enlargement
(Ref: O.P. Ghai 7th, Pg. 375)
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PAEDIATRICS 2003
Q 1. Epiphyseal dysgenesis is a pathognomonic feature of:
A. Hypoparathyroidism
B. Hyperparathyroidism
C. Hypothyroidism
D. Hyperthyroidism
Ans. is C. Hypothyroidism
(Ref: Nelson 19th, Pg. 1899)
Q 2. Commonest cause of systemic hypertension in children
is:
A. Coarctation of aorta
B. Acute glomerulonephritis
C. Nephrotic syndrome
D. Lactic acidosis
Ans. is B. Acute glomerulonephritis
(Ref: O.P. Ghai 7th, Pg. 434)
Q 3. Organism in bronchiolitis is:
A. Adeno virus
B. Influenza virus
C. Rhino virus
D. RSV
Ans. is D. RSV
(Ref: Nelson 19th, Pg.1456)
Q 4. Steroids is useful in:
A. Post-streptococcal glomerulonephritis
B. Membranous glomerulonephritis
C. Rapidly progressing glomerulonephritis
D. Minimal change type
Ans. is D. Minimal change type
(Ref: Nelson 19th, Pg. 1803)
Q 5. Not seen in Fallots tetralogy:
A. ASD
B. VSD
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C. Pulmonary stenosis
D. Left ventricular hypertrophy
Ans. is A. ASD
(Ref: Nelson 19th, Pg. 1573)
Q 6. In Downs syndrome, following congenital defect is
common:
A. PDA
B. PS
C. ASD
D. VSD
Ans. is C. ASD
(Ref: IAP textbook of Pediatrics 4th, Pg. 994)
Q 7. Following are causes of Pan systolic murmur, except:
A. MR
B. MS
C. VSD
D. TR
Ans. is B. MS
(Ref: Nelson 19th, Pg. 1556, 1627, 1628)
Q 8. Precocious puberty is seen in:
A. Hyperthyroidism
B. Addisonsdisease
C. McCune Albright syndrome
D. Neuroblastoma
Ans. is C. McCune Albright syndrome
(Ref: Nelson 19th, Pg. 1892)
Q 9. Craniotabes is found in children with the following
conditions, except:
A. Rickets
B. Hydrocephalus
C. Syphilis
D. Kernicterus
Ans. is D. Kernicterus
(Ref: Nelson 19th, Pg. 1072)
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PAEDIATRICS 2002
Q 1. The commonest cause of death in diphtheric child is:
A. IIIrd-nerve palsy
B. Myocarditis
C. Tonsillitis
D. Septicemia
Ans. is B. Myocarditis
(Ref: IAP textbook of Pediatrics 4th, Pg. 364)
Q 2. Best method of diagnosis of childhood HIV:
A. CD 4 cell counts
B. P24 antigen
C. ELISA
D. Anti HlV antibody
Ans. is B. P24 antigen
(Ref: Nelson 19th, Pg. 1167)
Q 3. Hyaline membrane is seen in all of the following
conditions, except:
A. Radiation pneumonitis
B. Viral pneumonitis
C. Uremic pneumonitis
D. Staphylococcal bronchopneumonia
Ans. is D. Staphylococcal bronchopneumonia
Q 4. Attainment of weight is a preschool normal child is:
A. 2-2.5 Kg
B. 3-3.5 Kg
C. 4-4.5 Kg
D. 5-5.5 Kg
Ans. is B. 3-3.5 Kg
(Ref: IAP textbook of Pediatrics 4th, Pg. 84)
Q 5. Subacute sclerosing panencephalit is complication of:
A. Pneumonia
B. Measles
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C. Diphtheria
D. Pertussis
Ans. is B. Measles
(Ref: Nelson 19th, Pg. 1072)
Q 6. Casonis test is diagnostic of:
A. Echinococcus granulosum
B. Toxoplasmosis
C. Toxocariasis
D. Syphilis
Ans. is A. Echinococcus granulosum
PAEDIATRICS 2001
Q 1. A child with diarrhoea has deep and rapid respiration.
Diagnosis is:
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis
D. Respiratory acidosis
Ans. is B. Metabolic acidosis
(Ref: Nelson 19th, Pg. 231)
Q 2. The percentage rise in length of infant in first year of life
is:
A. 20%
B. 30%
C. 40%
D. 50%
Ans. is D. 50%
(Ref: IAP textbook of paediatrics 4th, Pg. 84)
Q 3.The most important cause of under 5 mortality is:
A. Diarrhoea
B. Malnutrition
C. Respiratory infections
D. Trauma
Ans. is C. Respiratory infections
(Ref: O.P. Ghai 7th, Pg. 350)
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Q 9. At what age does a child sees the toy hidden and then
again hides it and gives to mother if she asks for:
A. 6 months
B. 8 months
C. 10 months
D. 12 months
Ans. is D. 12 months
(Ref: Forfar 6th, Pg. 119)
Q 10. Commonest nephrotic syndrome in child:
A. Minimal change
B. Chronic glomerulonephritis
C. Hemolytic uremic syndrome
D. Congenital
Ans. is A. Minimal change
(Ref: Nelson 19th, Pg. 1804)
Q 11. Commonest haematological malignancy in children
is:
A. CLL
B. AML
C. CML
D. ALL
Ans. is D. ALL
(Ref: Nelson 19th, Pg. 1732)
Q 12. A six years old girl child presents with spotting, no
secondary sexual characteristic present. Cause can be:
A. Menarche
B. Foreign body
C. Gonococcal infection
D. Haemorrhagic disease
Ans. is B. Foreign body
(Ref: For far 6th, Pg. 1152)
Q 13. Metabolic acidosis is accompanied with:
A. Acetazolamide
B. Phenformin
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C. Verapamil
D. Triamterene
Ans. is A. Acetazolamide
(Ref: O.P. Ghai 7th, Pg. 55
PAEDIATRICS 2000
Q 1. Not seen in Fallots tetralogy:
A. ASD
B. VSD
C. Pulmonary stenosis
D. Left ventricular hypertrophy
Ans. is A. ASD
(Ref: Nelson 19th, Pg. 1573)
Q 2. Congestive heart failure in children is best diagnosed
by:
A. Tachycardia and tender hepatomegaly
B. JVP
C. JVP + pedal edema
D. Hypotension
Ans. is A. Tachycardia and tender hepatomegaly
(Ref: O.P. Ghai 7th, Pg. 375)
Q 3. APGAR score of a child born blue with HR 70/ mt. floppy
with feeble cry with grimacing on nasal suction is:
A. 3
B. 2
C. 4
D. 5
Ans is A. 3
(Ref: Nelson 19th, Pg. 536)
Q 4. In Downs syndrome, following congenital defect is
common:
A. PDA
B. PS
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Pre-NEET Pediatrics
C. ASD
D. VSD
Ans. is C. ASD
(Ref: IAP textbook of paediatrics 4th, Pg. 994)
Q 5. Following is cause of pan systolic murmur:
A. MR
B. MS
C. VSD
D. ASD
E. TR
Ans. is A. MR, C. VSD & E. TR
(Ref: Nelson 19th, Pg. 1556, 1627, 1628)
Q 6. In hyperparathyroidism, seen is:
Ca++
PO4-
A.
B.
C.
D.
Ans is A.
(Ref: Nelson 19th, Pg. 1921)
Q 7. Precocious puberty is seen in:
A. Hyperthyroidism
B. Addisons disease
C. McCune Albright syndrome
D. Neuroblastoma
Ans. is C. McCune Albright syndrome
(Ref: Nelson 19th, Pg. 1892)