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Pre Neet Pediatrics Taruna Mehra PDF
Pre Neet Pediatrics Taruna Mehra PDF
Pediatrics
Taruna Mehra
MBBS MD PEDIATRICS (MAMC)
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All rights reserved. No part of this book may be reproduced in any form or by any means
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Why should I change anything in your life till the time you decide to
change yourself…
Quran
All the best may God help you cross the bridge
Taruna Mehra
“Do not count the days make the days count”
jaypeemcqproduction@gmail.com
so as to help us in further improvement of this book in
the subsequent edition.
Contents
Developmental Milestones
Contd...
2 Pre-NEET Pediatrics
Contd...
Secondary teeth
Mand, 8-10 yr
3
4 Pre-NEET Pediatrics
Weight of child
Weight for age (%): 100
Weight of normal child of same age
Advantages Disadvantages
• Classification is easy to compute as • Some normal children may be
weight is a widely recorded parameter classified as 1st degree malnutrition
because a cut-off point of 90
percent of reference is high.
• Classification has prognostic values • Does not distinguish between
for hospitalized patients (This is sudden acute episode of
because the cut off values were set malnutrition and along standing
during a study of risk of death chronic malnutrition as observation
based on weight for age at admission only consider weight for age
to a hospital unit) measurements.
Infancy
0-6 months 118
7-12 months 108 } K.Cal/kg/day
Children
1- 3 years 12.03 1240 5.1
4- 6 years 18.87 1690 7.0
7 - 9 years 26.37 1950 8.1
8 Pre-NEET Pediatrics
Protein
Total 1% 4% (too much)
Casein 0.5% 3% (too much)
Amino acids
Cystine Enough for growing brain Not enough
Taurine Enough for brain, retina
and bile acid conjugation
Fat
Total 4% (average) 4%
Saturation of fatty acids Enough unsaturated Too much saturated
Linoleic acid (essential) Enough for growing brain Not enough
Cholesterol Enough Not enough
Lipase to digest fat Present None
Lactose 7% (enough) 4.5%
Salts (mEq/1)
Sodium 6.5 (correct amount) 25 (too much)
Chloride 12 (correct amount) 29 (too much)
Potassium 14 (correct amount) 35 (too much)
Minerals (mEq/Il)
Calcium 350 (correct amount) 1,400 (too much)
Phosphate 150 (correct amount) 900 (too much)
Iron Small amount, but well- Small amount,
absorbed (enough) poorly absorbed
(not enough)
Vitamin Enough Extra needed
Pediatrics in Last Minutes 9
Bone-Age
Endocrine Disorders
• Hypothyroidism
• Steroid therapy and Cushing’s disease
• Hypogonadism (including Turner’s syndrome)
• Hypopituitarism - panhypopituitarism, growth hormone deficiency,
Laron dwarfism
Chromosome disorders
• Trisomy 21, Trisomy 18
• Hyperthyroidism
• Idiopathic sexual precocity
• Intracranial masses in the region of the hypothalamus (haniartoma,
astrocytoma, optic chiasm glioma, hydrocephalus, encephalitis)
Congenital Disorders
• McCune Albright syndrome: polyostotic fibrous dysplasia with
precocious puberty
• Cerebral gigantism (Soto’s syndrome)
• Lipodystrophy
• Pseudohypoparathyroidism
• Acrodysostosis
• Weaver smith syndrome
• Marshall syndrome
D/D of Rickets
Serum Ca Serum Serum Serum Serum
P043 Alkaline Parathormone HCO 3
phosphatase
Enuresis
• Enuresis is defined as the voluntary or involuntary repeated
discharge of urine into clothes or bed after a developmental age
when bladder control should be established (mostly mental age
of 5 years).
• Diagnosis of enuresis requires voiding of urine twice a week for
3 consecutive months or clinically significant distress in child’s
life as a result of wetting.
• Enuresis is more common in males than females
• Most common cause of diurnal enuresis is micturition deferral
(waiting until the last minute to void).
12 Pre-NEET Pediatrics
Treatment
Hormonal agents
• Corticosterojds Growth retardation, cleft palate and lip
• Diethyl stilbestrol (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)
• Anti-thyroid drugs Neonatal hypothyroidism and goiter
• Clomiphene NTD, multiple gestation, Down’s syndrome
• Synthetic Masculinization in female fetus, hypospadias
progestins
Antibiotics
• Chloramphenicol ‘Gray baby syndrome’ (peripheral vascular collapses)
• Sulphonamides Kernicterus, Methemoglobenemia
• Tetracyclines Dental discoloration (yellow) and deformity, Inhibition of
bony growth, cataracts,
• Aminoglycosides Fetal ototoxicity due to eighth N. damage
• Anti-malarials Intra-uterine death
• Quinine, Retinopathy, congenital deafness, comeal opacities
chloroquine
Psychiatrics drugs and substances of abuse
• Lithium Ebstien’s anomaly
• LSD (lysergic “fractured chromosomes” anomaly in fetus, stunted growth
acid diethylamide)
• Alcohol Foetal alcohol syndrome: prenatal-onset growth deficiency,
developmental delay, facial dysmorphism (short palpebral
fissures, ptosis, strabismus, ear abnormality, long philtrum
with a thin upper lip), multiple joint anomalies and cardiac
defects (ASD>VSD); mental subnormality
Contd...
14 Pre-NEET Pediatrics
Contd...
• Heroin Irritability, hyperactivity, tremors
• Cocaine Abruptio placentae, preterm labour, cerebral infarction
• Beta-blockers Foetal bradycardia
Anticoagulants
• Vitamin K Hyperbilirubinemia (hemolysis) and kernicterus
(large dose)
• Warfarin Conradi’s syndrome: skeletal and facial anomalies,
chondrodysplasia punctata, haemorrhage
• Aspirin Haemorrhagic disease of newborn
Other Drugs
• Cytotoxic drugs Multiple foetal malformations and abortion
• Isotretinoin CNS defects, facial palsy, deafness, cardiac defects
• Oxygen in high Retrolentalfibroplasia and blindness (>35%)
concentrations
• Thalidomide Phocomelia (seal limbs), cardiac malformations
• Thiazide diuretics Neonatal thrombocytopenia
• ACE inhibitors Renal tubular dysgenesis, lung hypoplasia, anuria,
oligohydramnios
• Misoprostol Mobius syndrome, arthrogryposis
(prostaglandin)
• Vitamin D William syndrome (infantile hypercalcemia,
supravalvular aortic stenosis, elfin facies)
Drugs taken during perinatal/neonatal period and their effects on the neonate
• Oxytocin (used for induction of labour) Hyperbilirubinemia in babies
• Prolonged cortisone Adrenal crisis in infants
• NSAIDS Premature closure of ductus
arteriosus
• Dexamethasone Periventricular leuocmalacia
Medications to baby
• Chloramphenicol Grey baby syndrome
• Erythromycin Pyloric stenosis
• Vitamin K Bleeding, hepatotoxicity
Pediatrics in Last Minutes 15
Disease Outcome/Comment
Bronchial asthma IUGR; Feal goiter and hypothyroidism (due to drugs-
beta agonists)
Chronic cardiac disease IUGR, abortion, asphyxia, prematurity
Chronic Crenal disease IUGR, prematurity
Hypertension Placental vasculopathy, IUGR
Thyroid disorders Maternal hypothyroidism may cause congenital
hypothyroidism (TSH does NOT cross placental, barrir
but LATS does)
SLE Congenital complete heart block, IUGR
Smoking 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
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.
Pediatrics in Last Minutes 17
DO NOT Resuscitate if
APGAR Score
0 1 2
Birth Trauma
Caput succedaneum Cephalhematoma
• Present at birth; • Seen at 2-4 days old;
• May extend over suture lines; • Limited by suture lines;
• Diffuse, ecchymotic, oedematous • Normal overlying skin;
overlying skin;
• Disappears spontaneously within • Reabsorbed over 2 weeks to 3
24hrs after birth; months; can calcify;
• No treatment needed • May require phototherapy for
jaundice
1. # Clavicle MC bone fractured due to birth trauma; appears at 1-20+ days
2. Sternomastoid tumor appears at 7-20+ days. Intrauterine posture is also a
cause. Located at junction of upper and middle third of muscle. Disappears by
6 months of age.
3. Brain MC internal organ to be injured during birth; next MC is liver
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
— Incidence is 1%, also a/w DM, prematurity, asphyxia.
• Cord clamping
— Early cord clamping done in
– Prematurity, Rh incompatibility, birth asphyxia, IUGR,
baby of diabetic mother.
— Delayed cord Clamping done in
– Prematurity and cord around neck
• Cord blood is useful for
— Estimation of TSH, T3 and T4; in screening of congenital
hypothyroidism (TSH levels > 50micrU/ml in cord blood are
diagnostic of neonatal hypothyroidism).
— Screening for inborn errors of metabolism/tandem mass
spectroscopy (TMS); e.g., in PKU, cystic fibrosis, G6PD
deficiency.
— Sampling of and infant born to Rh positive mother: or study of
blood group, Rh type, serum bilirubin, Coomb’s test.
Pediatrics in Last Minutes 19
Neonatal sepsis
• Early onset neonatal sepsis occurs within 72 hours of life and
is caused by organisms prevalent in the maternal genital tract or
in the labour room. Group B Streptococci are the MC organisms
(kelbsiella, E.coli and S.aureus are MC in India).
• Late onset neonatal sepsis is a nosocomial infection acquired
from the nursery or lying in ward and occurs 72 hours after
birth. Gram negative bacilli are MC organisms.
• Sepsis screen includes (usually 2 markers are considered
significant)
a. ANC<1000
b. Leucopenia < 5000/mm3
c. Band cell to neutrophil ratio or I:T ratio (immature to total
polymorphs) > 0.2 (band cells > 20%)
d. CRP> 8microgm/ml is positive
e. Micro ESR> 15 mm/first hour
f. Presence of > 5 PMN/hpf in gastric aspirate (limited utility in
blood stained or meconium stained liquor)
• Other markers - procalcitonin and cytokines
• Blood culture is confirmatory
• Listeria infection may produce preterm delivery,
intrauterine death
• Early conjugated hyperbilirubinemia with bilirubin > 0.5
mg/dl is noted in neonatal sepsis.
• 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
ROP screening criteria
• All infants born at d” 32 weeks.
• All infants with birth weight d” 1500 grams
• Very sick babies who require ventilatory support, multiple blood
transfusions.
Prematurity + oxygen toxicity predisposes to
• Retinopathy of prematurity (ROP)
• Bronchopulmonary dysplasia (BPD)
Antenatal steroid therapy (ANS)
• It is a/w reduced incidence of RDS/HMD, NEC
Postnatal corticosteroids
• Useful in prevention of HMD, BPD, but recent data are
inconclusive and not recommended anymore.
• They have some therapeutic utility in management of sclerema
neonatorum
Excess administration of vitamin E is a/w
• Intracranial hemorrhage
• NEC
Deficiency of Vitamin E is a/w
• ROP
• BPD
• Hemolytic anemia
Pediatrics in Last Minutes 21
Contd...
Pediatrics in Last Minutes 23
Contd...
Erythroblastosis Fetalis
• Haemolytic disease of the newborn (erythroblastosis fetalis)
is caused by blood group incompatibility between the mother and
fetus.
• Maternal IgG crosses the placenta and destroys fetal erythrocytes.
• An Rh - mother carrying an Rh + fetus is at highest risk
• Risk increases when fetal blood crosses into the maternal
circulation as in abortion, ectopic pregnancy, amniocentesis and
motor vehicle accidents.
• Affected neonates present with: anemia, hvperbilirubinemia
hepatosplenomegaly, pulmonary edema and ascites.
• The direct Coombs’ test is positive.
• Treat with exchange transfusions (see below).
• Prevent disease with anti-Rh IgG injections for high-risk mothers
at 28 weeks of delivery, and at any other time of exposure to fetal
blood.
Congenital Defects
• Cardiac (VSD, ASD, TGA Coarctation of aorta)
• Neural tube defect
• Holoprosencephaly
• Sacral agenesis (most specific)
• Hydronephrosis
• Renal agenesis
• Duodenal atresia
• Anorectal malformations
General
• Macrosomia
• Normal head size
• Increased subcutaneous fat
• Birth trauma
• Hairy pinna
Other
• Renal vein thrombosis
• Respiratory distress syndrome
• Polycythemia
• Small (lazy) left colon syn.
Cardiovascular
• Cardiomegaly
• Transient hypertonic cardiomyopathy
• Persistent fetal circulation
Metabolic
• Hypoglycemia
• Hypocalcemia
• Hypomagnesemia
• Hyperbilirubinemia
Pediatrics in Last Minutes 25
Neonatal Hypoglycemia
The whole blood glucose level of < 40 mg/dL indicates hypoglycemia
1. Transient hypoglycemia
• Prematurity; small for date infants; infant of diabetic mother;
smaller of twins.
2. Persistent hypoglycemia
• Hyper-insulinemia, Nesidioblastosis, Adenoma of beta cells,
Beckwith syndrome, leucine sensitivity.
• Deficiency of hormones such as glucagons, growth hormone,
epinephrine, ACTH.
• Deficiency of substrate as in ketotic hypoglycemia and Maple
syrup urine disease.
• Disorders of carbohydrate metabolism such as glycogen
storage disease, galactosemia, and fructose intolerance.
3. Other etiologies
• Idiopathic; Sepsis; Drugs (maternal tolbutamide); liver disease
(reye syndrome), carcinoma etc.
26 Pre-NEET Pediatrics
Head Malformations
1. Anencephaly: Due to failure of closure of the rostral neuropore
2. Holoprosencephaly: Incomplete separation of the cerebral
hemispheres. Seen in Patau’s 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. Shapiro’s syndrome: Agenesis of corpus callosum
Torch Infections
Infection Description Treatment Prevention
Contd...
Pediatrics in Last Minutes 27
Contd...
Infection Description Treatment Prevention
Perinatal Tuberculosis
• True congenital TB is rare. Congenital TB in a neonate is acquired
28 Pre-NEET Pediatrics
Apt Test
• The Apt test is most commonly used in cases of vaginal bleeding
late during pregnancy (antepartum hemorrhage) to determine if
the bleeding is from the mother or the fetus.
• Exposing the blood to NaOH (alkali) will denature the adult but
not the fetal hemoglobin. The fetal hemoglobin will appear pinkish
color under the microscope while the adult hemoglobin will appear
as a yellow - brownish color. - Positive test à Blood is of fetal
origin. - Negative test à Blood is of maternal origin.
• The Apt test can be used after birth (post partum hemorrhage) if
the newborn has bloody vomiting, bloody stool, or active bleeding
from nasogastric tube. A positive Apt test would mean that the
blood is either due to GI or pulmonary bleeding from neonate. A
negative Apt test would indicate that the blood is of maternal
30 Pre-NEET Pediatrics
Hematopoesis in Fetus
• The anatomic sites of hematopoesis undergo developmental
changes during embryonic and fetal life.
• RBC formation can be observed within the developing blood
vessels of the yolk sac at 2 weeeks of gestation.
• By 8 weeks of gestation the site of RBC formation begins to shift
to the sinusoids of the liver, where granulocyte precursors and
megakaryocytes are also seen. Hematopoesis in the liver is
maximal till 20-24 weeks and declines thereafter.
• Hematopoesis in the bone marrow is evident by the 4th month of
gestation and this becomes the predominant site of hematopoesis
during the rest of gestation and later.
Pediatrics in Last Minutes 31
Contd...
Key:
• CCF = congestive cardiac failure;
• CHD = Conegnital heart disease;
• FTI' = failure to thrive;
• TE = Infective endocarditis;
• LVH = left ventricular hypertrophy;
• PS = Pulmonary stenosis;
• RDS = respiratory distress syndrome;
• RVH = right ventricular hypertrophy;
• SBE = subacute bacterial endocarditis.
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 Minor
Systolic murmur, Systolic murmur < grade III
grade III or more, Abnormal 2 heart sound
especially with thrill Abnormal ECG
Diastolic murmur Abnormal X Ray
Cyanosis Abnormal BP
Congestive cardiac failure
Presence of one major or two minor criteria are essential for
indicating the presence of heart disease.
B. Laboratory
Essential criteria i. Acute phase reactants;
Evidence of recent leukocytosis, elevated
streptococcal sedimentation rate and C
infection as indicated reactive protein
by ii. Prolonged PR interval in the
electrocardiogram
a. Increased antistreptolysin
'O' titer
b. Positive throat culture
c. Recent scarlet fever
Pediatrics in Last Minutes 39
Contd...
regurgitation early-mid
diast
Mitral stenosis Apex Low pitched, None
raid diast.
Rumble
Mitral Apex Blowing, Left axilla
regurgitation holosystolic Lung fields
ASD Left 2nd ICS Harsh, SEM
VSD LLSB Harsh, None
Holosystolic
PDA Left 2nd - 3rd ICS Continuous Lung fields
Respiratory Infections
Croup (laryngo Acute epiglotitis
tracheobronchitis) (emergency)
Etiology MC parainfluenza virus MC by H. inflenzae type b.
Presenting 1; also by RSV
age 3 months to 3 years 3-7 years
Clinically Prodrome with URI Rapid onset (4-12 hours); high
symptoms for fever, dysphagia, drooling,
1-7 days; low muffled voice, stridor patients
grade fever, ins may be in "sniffing" position
Contd...
Pediatrics in Last Minutes 41
Contd...
• 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
Pediatrics in Last Minutes 43
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
• 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
Simple benign febrile Atypical complex
convulsions febrile convulsions
• Fits occur within • Anything different from features
24 hours of onset offever of simple febrile convulsions are
• Last < 10 minutes and atypical fits. Presence of family
are usually single per h/o epilepsy, neurodevelopmental
febrile episode retardation and atypical episodes
• Convulsions are increase risk of febrile episodes and
generalized subsequent epilepsy.
• No post-i ctal neurological
deficit
• Family history may be
present.
Treatment Prophylaxis
• Antipyretics (paracetamol, • Intermitent diazepam, clabazam,
ibuprofen AVOID aspirin midazolam- most desirable.
due to risk of Reye's
syndrome)
• Hydrotherapy, tepid sponging • Continuous prophyl axis - in form of
oxygen. antiepileptic drug therapy is
advocated
• IV diazepam in event of failure of intermittent
or phenobarbitone for therapy, especially in recurrent
control of seizures, atypical seizures or family h/o
epilepsy (valproate or
phenobarbitone).
Pediatrics in Last Minutes 47
Neisseria meningitides
Penicillin - sensitive Penicillin G or ampicillin
Penicillin - resistant Ceftriaxone or cefotaxime
Streptococus pneumoniae
Penicillin - sensitive Penicillin G (Ceftriaxone or cefotaxime)
Penicillin - intermediate Vancomycin
Gram-negative bacilli (except Ceftriaxone or cefotaxime
Pseudomonas spp.)
Pseudomonas aeruginosa Ceftazidime or Cefepime or Meropenam
Staphylococci spp.
Methicillin-sensitive Nafcillin
Methicillin-resistant Vancomycin
Listeria monocytogenes Ampicillin + gentamicin
Haemophilus influenzae Ceftriaxone or cefotaxime
Streptococcus agalactiae Penicillin G or ampicillin
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.
Pediatrics in Last Minutes 49
Mental Retardation
• MR - Abnormalities in intellectual/adaptive function.
• Age on onset before 18 years/age of maturity
• Most common cause = Chronic anomalies (Down's syndrome)
• Most common cause in males = Down's syndrome (mild - to -
moderate MR)
• Most common cause of severe MR in males = Fragile X syndrome
– Normal = 90 - 120
– Borderline = 70 - 90
– Mild = 51 - 70/ 50 -70
– Moderate = 36 - 50/ 35 - 50 (trainable)
– Severe = 21 - 35 (able to guard cannot manage self)
– Profound = <20 (unable to guard self)
– Severe and
profound MR = custodial
Spread
• By airborne droplets from nose and throat secretions, usually 4
days before and 5 days after the appearance of the rash.
• Secondary attack rate is 80%.
Age
• Children 6 months -3 years of age in developing countries and
older children (>5 years) in developed countries.
Immunity
• One attack of measles generally confers life long immunity.
• Maternal antibodies protect in infants up to 6 month of age.
Nutrition
• Mortality 400 times higher in the malnourished child (also vit A.
deficiency) and also these children excrete measles virus for longer
periods indicating prolonged risk to themselves and, of spread to
others.
Prodromal Symptoms
• Last 2-3 days, cough, coryza, conjunctivitis, fever, conjunctivae
look glassy, and then the semilunar fold swells (Meyer's sign).
Pediatrics in Last Minutes 51
Koplik's Spots
• Are 1-2 mm bluish-white spots on a red base on the buccal mucosa
opposite the first/second lower molars, pathogenomic of measles,
generally seen during the first 2 days of symptoms and are often
fading as the rash appears
Comby's Sign
• Thin, whitish patches on the gums and buccal mucosa formed of
degenerated squamous epithelium.
Rash
• On the fourth/fifth day, the macular rash appears consisting of
discrete lesions that begins behind the ears and become confluent
as rash spreads from hairline downward, sparing palms and soles;
• Rash and fever disappear in 3-4 days signalling the end of the
disease. Prolonged fever suggests a complication of measles. The
entire illness lasts about 10 days.
Complications
• Respiratory: otitis media, pneumonia, fatal giant cell pneumonitis
in the immunosuppressed, flare up of primary TB.
• Neurological: febrile fits, meningitis, encephalitis, subacute
sclerosing panencephalitis (late and rare):
• Digestive: resistant diarrhoea, achlorhydria, hepatitis, appendicitis
(due to lymphoid tissue blocking the lumen of the appendix);
• Miscellaneous: myocarditis, glomerulonephritis, thrombocytopenic
purpura, tuberculin anergy, keratoconunctivitis sicca, intrauterine
infection may cause fetal malformations.
Diagnosis
• Serology for measles IgM antibody. Warthin-Finkleday cells are
multinucleate giant cells with inclusion bodies in the nucleus and
cytoplasm, found in respiratory and lymphoid tissues,
pathognomonic of measles.
52 Pre-NEET Pediatrics
Prevention
• Measles vaccine: a live attenuated, tissue-culture vaccine presented
as freezdried product.
• WHO recommends immunization at 9 months of age. 0.5ml SC
injection, reconstituted vaccine should be kept on ice and used
within 1 hour. 5-10 days after immunization, a mild 'measles' illness
(fever and rash) may occur - self limiting.
• Immunity develops 11-12 days after vaccination. Susceptible
contacts over 9-12 months age, may be protected against measles
with measles vaccine, provides this is given within 3 days of
exposure.
Presentation
• Postauricular, cervical and suboccipital lymphadenopathy (may
appear as early as 7 days before the appearance of the rash).
• Macular rash spreads from hairline downwards, clearing as it
spreads. The rash disappears aitogether bythe third day. -
Forschemier's Spots
• (palatal petechiae), also seen in scarlet fever and infectious
mononucleosis.
Test
• The most widely used serological diagnostic test is the
haemagglutination inhibition test.
Treatment
• Usually none needed, self limiting
Pediatrics in Last Minutes 53
Complications
• Arthritis especially among women, encephalitis, thrombocytopenic
purpura, malformations in utero.
• Infection during the first 4 weeks of pregnancy: Cataract in 70%;
during weeks 4-8: patent ductus arteriosus; during weeks 8-12:
deafness.
Prevention
• Live attenuated RA 27/3 vaccine, produced in human diploid
fibroblast; seroconversion occurs in more than 95%; pregnancy
is considered a contraindication to rubella immunization.
Presentation
– Incubation period =14 to 16 days.
– Prodromal stage consists of fever, malaise and shivering.
– Rash comes on the day the fever starts. It is centri petal in
distributiort,first appears on the trunk where it is abundant
and then on the extremities. Mucosal surfaces are also
involved, but palms and soles are unaffected.
– The rash advances quickly through the stages of macule,
papule, vesicle, pustule and scab (pleomorphic rash)
Complications
– Secondary bacterial infection of the rashes; varicella
pneumonia; haemorrhages into the lesion; encephalitis, acute
cerebellar ataxia; purpura fulminans; arthritis; glomeru-
loniphritis; Reye's syndrome.
Treatment
– Symptomatic and supportive, since this is a self-limiting
condition. Aspirin should NOT be used as it may increase the
risk of developing Reye's syndrome.
Prevention
– Varicella zoster immunoglobulin, 1.25 to 5 ml given within 72
hours of exposure will modify or prevent the disease.
– Live attenuated chicken pox vaccine is now available.
Pediatrics in Last Minutes 55
Precocious Puberty
• Precocious puberty is defined as the onset of secondary sexual
characters before 8 yr of age in girls and 9 yr in boys.
• True (central) precocious puberty (gonadotropin dependant) is
due to hypothalamic-pituitary-gonadal activation. Caused by
– Idiopathic
– Organic brain lesions: brain tumours, severe head trauma,
hydrocephalus, hypothalamic hamartoma, CNS infections.
– Hypothyroidism, prolonged and untreated.
• Precocious pseudopuberty (peripheral, gonadotropin
independent): here secondary sex characters appear but there is
no activation of hypothalamic-pituitary-gonadal axis. Caused by
– Females: Congenital adrenal hyperplasia, Hypothyroidism,
Exogenous estrogen, McCune Albright syndrome, Aromatase
excess syndrome.
– Males: Congenital adrenal hyperplasia, Hypothyroidism,
Exogenous androgens, Activating LH receptor mutations,
HCG-secreting tumour.
Neuroblastoma
• MC tumour of adrenal medulla but can occur anywhere along
sympathetic chain; affects children <5 years.
• Risk factors: N-myc oncogene; Neurofibromatosis, tuberous
sclerosis, pheochromocytoma, Hirschsprung's disease.
• Clinically: abdominal mass, hepatomegaly, leg edema, periorbital
bruising.
• 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.
Contd...
58 Pre-NEET Pediatrics
Contd...
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)
Pediatrics in Last Minutes 61
Contd...
Disease Deficient enzyme Accumulating
metabolites
Sulfatidoses
• Metachromatic Arylsulfatase A Sulfatide
leukodystrophy
• Krabbe disease
• Gaucher disease Galactosylceramidase Galactocerebroside
• Fabry's disease Glucocerebrosidase Glucocerebroside
• Niemann- - Galactosidase A Ceramide trihoxoside
Pick disease Sphingomyelinase 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 – Adrenoleuco- – Canavans disease
leucodystrophy dystrophy
– Krabbe 's disease – Pelizaeus- – Alexander disease
Merzhacher
disease
• Symptoms vary according to the specific type of leucodystrophy
and may be difficult to recognize in the early stages of the disease.
Canavan's Disease
• Autosomal recessive disorder
• Caused due to deficiency of the enzyme N-Aspertoacylase.
• This leads to accumulation of N-Acetyl aspartic acid in brain and
urine.
Pediatrics in Last Minutes 63
Adrenoleucodystrophy
• X-linked recessive disorder
• Caused due to deficiency of Acyl-CoA synthetase.
• Onset is about 5-10 years
• Main symptoms are ataxia, spasticity, motor deficits, cortical
blindness.
• Marocephaly is not a key feature
Metachromatic leucodystrophy
• Autosomal recessive disorder
• Caused due to Arylsulfatase A deficiency
• Onset is in the 2nd year.
• Symptoms are inco-ordination, especially gait disturbance, then
general regression, optic atrophy, combined upper and lower
motor neuron signs.
• Marocephaly usually late.
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
• Wolman disease is very rare, with only 50 reports of the disease
published in the worldwide medical literature. It is an autosomal
recessivedisease and affects both males and females.
• The disease affects the breakdown and use of fats and cholesterol
in the body and belongs to a family of disorders called lipid storage
disorders.
• Wolman disease is caused by mutations in the LIPA gene. The
LIPA gene encodes for an enzyme called lysosomal acid lipase
which is found in the lysosomes. It breaks down fats such as
cholesteryl esters and triglycerides so that they can be used by the
body.
64 Pre-NEET Pediatrics
Clinical Features
• In affected individuals harmful amounts of lipids accumulate in
the spleen, liver, bone marrow, small intestine, adrenal glands
and lymphnodes.
• In addition to fat deposits, calcium deposits in the adrenal gland
are also seen.
• Infants with wolman disease are healthy and active at birth but
soon develops signs and symptoms of the disorder. These may
include
– Enlarged liver and spleen
– Poor weight gain
– Low muscle tone
– Jaundice
– Vomiting
– Dianthoea
– Developmental delays
– Anemia (low amount of iron in blood) poor absorption of
nutrients from food.
• Children affected by this condition develop severe malnutrition
and generally do not survive past early childhood.
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.
Treatment
• Currently there is no cure for wolmans disease so treatment focuses
on management of symptoms. If the adrenal gland is not making
enough hormones and steroids, replacement steroids and
hormones can be given.
Pre NEET Pediatric
INCLUDING RECENT ALL INDIA AND AIIMS TOPICS
QUESTIONS
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. Autosomal dominant
b. Mito chondrial
c. Autosomal recessive
d. X-linked dominant
Q 20. A newborn is born to a HIV positive woman an ART. He was
given Nevirapine at birth. Which of the following statements regarding
future management is false?
a. Start Cotrimoxazole prophylaxis at 1 month till HIV infection
can be ruledout.
b. Advise exclusive top feeding or exclusive breast feeding
c. Perform DNA PCR for HIV at 6-8 wks of age.
d. Do not give OPV and BCG at birth.
Questions 71
d. Cutaneous Vasoconstriction
Q 3. Due to advances in Cancer treatment the prognosis of which of
the following has become better?
a. Glioblastoma multiforme
b. Esophageal carcinoma
c. ALL in children
d. Cholangio carcinoma
Q 4. A newborn baby presented with profuse bleeding from the
umbilical stump after birth. Rest of the examination and PT, APTT
are within normal limits. Most probable diagnosis is:
a. Factor X deficiency
b. Glanzmann thrombasthenia
c. Van Willebrand disease
d. Bernard Soullier disease
Q 1. A 1 year old girl presents with fever since 24 hrs and on and off
coughing. She is passing foul-smelling bulky stools and had 4 attacks
of bronchitis in past. The girl is suspected of having:
a. Cystic fibrosis
b. Maple synp urine disease
c. Phenylketonuria
d. Impaired glucoronidization
Q 2. A 2 yrs old boy keeps on looking at his own hands and does not
respond on calling. His mother development is otherwise normal,
probable diagnosis would be:
a. Autism
b. Depression
c. ADHD
d. Schizophrenia
Q 3. Regarding parenteral nutrition of newborns, 20% intralipid has
are the following advantage over 10% intralipid solution except
a. Reduced phospholipids
b. Increased EFA (essential fatty acids)
Questions 75
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
ANSWERS
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. Cardiopulmonary–Tacypnea, Tacycardia, cyanosis and
cardiomegally.
2. CNS–Lethargy, 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
Trophic feeds are Minimal (sub nutritional) feeds (5–10 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.
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
• Usually discovered as a mass on plain radiography, CT or MRI
• Tumor markers including catecholamine metabolites homovanillic
acid (HVA), VMA (vanillylmandelic acid) are elevated in urine in
95% of cases.
• Biopsy from tumor tissue.
Treatment
1. Low risk
– Localized tumor: Treatment surgery survival rate 98%.
2. Intermediate risk
84 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
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.
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 µg/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.
88 Pre-NEET Pediatrics
Metabolism
• After absorption, lead is disseminated throughout the body. Mostly
it accumulates in bone and resides for years.
• About 97% in blood is bound on or in Red blood cells.
• The heme pathway is susceptible to lead inhibitory effects.
• Neurotransmitter release is adversely affected by lead.
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 µg/dL)
– Reversible fanconi syndrome.
4. Hemolytic anemia
Drug Treatment
A child with a venous BLL 45 µg/dL or higher should be treated. Children
with BLL of 44-70 µg/dL may be treated with a single drug, preferably
DMSA.
Those with BLL of 70 µg/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
Differential Diagnosis
• Protein losing enteropathy
• 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 2-
3 wks is recommended. Skin biopsy is not mandatory for diagnosis.
Henoch: Schonlein purpura
90 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
• S. Phosphate high in chronic renal failure
• S. Parathyroid hormone normal in hypophosphatemic rickets.
Answers 91
Hyphosphosphatemic Rickets
• Most common form of refractory rickets, inherited as
a. X-linked dominant: Most common
Mutations in the PHEX gene
(chromosome Xp22.1)
This gene is a regulator of FGF - 23
production by osteocytes.
b. Autosomal dominant
c. Autosomal recessive
d. Autosomal recessive with hypercalciuria
Remember
In hypophosphatemic rickets, symptoms of hypocalcemia (tetany, muscle
weakness) are absent.
Dental abnormalities are common in hypophosphatemic x linked
rickets.
92 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 cyst-
ourethrogram (VCUG)
Answers 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.
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.
Investigations
Lumbar puncture is recommended in children <1yr of age after their
first febrile seizure or if clinical signs and symptoms suggest meningitis
Treatment
• Rectal Diazepam/ Midazolam/ Lorazepam given at time of Seizure.
• Febrile status epilepticus - I/V phenobarbitone/ phenytoin/ valproate.
• Intermittent oral Diazepam/ Clobazam/ Clonazepam can be given
along with anti pyretics during febrile illness to reduce the risk of
seizure.
• Chronic antiepileptic therapy - may be considered for children with
a high risk for later Epilepsy.
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
98 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
• Autosomal dominant inheritance
• Cardinal features: Skin lesion, Convulsions and mental retardation
• Skin lesions: Hypopigmented ash leaf shaped macules, adenoma
sebacum (angiofibromas) shagreen patches, subungal fibroma
In infancy, myoclonic jerks often occur (West syndrome) - Drug of choice
Vigabatrine
Ataxia - Telengiectasia
• An autosomal recessive inherited disease (mapped to Chr. 11q)
• Usually manifests with progressive cerebellar ataxia, Oculocutaneous
telengiectasia, Choreoathetosis, pulmonary and sinus infections,
immune deficiency and lymphorecticular malignancies.
• feto protein is almost always elevated.
Neuro-imaging reveals cerebellar atrophy.
Treatment is Symptomatic
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
• Syringomyelia is a cystic cavity within the spinal cord that may/
may not communicate with the CSF pathways.
• Syringobulbia exists when the cystic cavity extends into the medulla.
• Communicating syringomyelia is frequently associated with Chiari
type I malformation.
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.
100 Pre-NEET Pediatrics
4. Medulloblastoma
• CNS tumors are the second most common malignancy in childhood
after leukemias.
– <1 yr: Supratentorial tumors predominate
– 1-10 yr: Infratentorial tumors predominate
– >10 yrs: Supratentorial tumors again predominate with diffuse
astrocytomas most common.
Medulloblastoma is a cerebellar tumor which occurs predominantly in
males and at a median age of 5-7 yr of age.
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.
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.
102 Pre-NEET Pediatrics
HIV in Newborn
HIV-1 and HiV-2 are members of the Retroviridae family.
HIV-2 is a rare cause of infection in children. It is most prevalent in
Western and southern Africa.
Transmission of HIV1 occurs via sexual contact, parenteral exposure
to blood, or vertical transmission from mother to child. Vertical
transmission can occur intrauterine (before birth), intrapartum during
birth), or through breast feeding (after delivery)
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.
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.
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.
Differentiating Features of Floppy Infant According to the Site of Involvement
106
EMG - Electromyography
NCS - Nerve conduction studies
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.
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.
2. Oxygen administration
3. Morphine subcutaneous at dose not exceeding 0.2 mg/kg
4. Intravenous soda bicarbonate if metabolic acidosis present
5. 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.
112 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. Sensitivity 98-100%
4. Specificity 88%
5. Tubular mass in longitudinal views
6. 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
114 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
• In 21 OH, 3 OH dehydrogenase deficiency
• Salt wasting crisis + female virilization
• In 11 hydroxylase, deficiency and 17 hydroxylase deficiency
• Hypertension present
• 11 hydroxylase female virilization (female pseudo
hermaphroditism)
• 17 hydroxylase male external genitalia feminization (male pseudo
hema phroditism)
26. Ans is c. A correct B wrong
(Ref: Nelson 18th, Pg. 609)
Feature of conjugated hyperbilirubenemia on the 3rd day accompanied
by sepsis and positive reducing substance in urine suggest diagnosis of
galactosemia.
The term Galactosemia generally designates the deficiency of
galactose - I phosphate uridyl transferase deficiency.
Without the transferase enzyme, the infant is unable to metabolize
galactose - I phosphate, the accumulation of which results in injury to
kidney, liver and brain.
Clinical Manifestations
In newborn or young infants, jaundice, hepatomegally, vomiting,
hypoglycaemia, cataracts, sepsis (esp. E coli) are main clinical features.
Symptoms improve when milk is temporarily withdrawn and replaced
with lactose free nutrition.
Diagnosis
Positive reducing substances in urine (Galactosuria)
Direct enzyme assay using erythrocytes
Treatment
Elimination of galactose from the diet reverses the growth failure,
Cataracts, renal and hepatic dysfunction.
Galactokinase Deficiency
The deficient enzyme is galactokinase, which catalyzes the phosphorylation
of galactose.
116 Pre-NEET Pediatrics
Clinical Features
Infants show conjugated Hyperbilirubenemia, yellow urine, clay colored
stools. Infants with EHBA are often full term and look apparently healthy
except for jaundice.
Those with neonatal hepatitis are small for date and show increased
association with infections and genetic abnormalities.
Answers 117
Hepatitis B
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 hemo-
concentration 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.
120 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 Non-
immune 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
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.
122 Pre-NEET Pediatrics
Surfactant Indications
i. Moderate to severe RDS-Rescue treatment
ii. All neonates less than 29 weeks irrespective of presence or absence
of RDS - Prophylactic treatment.
Answers 123
2. Ans is a. Shivering
(Ref: O.P. Ghai 7th, Pg. 115-118, Meharban Singh 7th, Pg. 200-206)
Definitions
• Hypothermia: Axillary temperature of baby < 36.50C
– Cold stress - 36.0 36.40C
– Moderate hypothermia - 32-35.90C
– Severe hypothermia - <320C
• Hyperthermia: Axillary temperature of baby >37.50C.
• Thermoneutral environment: The narrow range of environmental
temperature at which baby can maintain normal baby temperature
with minimal oxygen consumption. This is also called as the zone
of thermal comfort.
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.
Management
Cold Stress/ Moderate Hypothermia
• Skin to skin contact
• Regular temperature monitoring
• Supportive measures - Feeding, Monitor vitals.
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.
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
Prognostic Factors
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 ½ 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.
128 Pre-NEET Pediatrics
Clinical Presentation
• Umbilical stump bleeding
• Poor wound healing
• Infertility, abortion among affected females.
Lab Findings
• Prolonged bleeding time, prolonged aPTT.
• Normal platelet count (except 2B disease or platelet type disease)
130 Pre-NEET Pediatrics
Classification
I. Type I - VWF is quantitatively reduced
II. Type II - VWF is qualitatively abnormal
III. Type III - VWF is absent
Treatment
Desmopressin used in type I disease releases VWF from endothelial
cells.
Bernard-Soulier Syndrome
• Caused by absence or severe deficiency of VWF receptor (GPIb
complex) on platelet membrane.
• This is characterized by thrombocytopenia, giant platelets, prolonged
BT, absent ristocetin induced platelet aggregation but normal
aggregation to other agonists.
Glanzmann Thrombasthenia
• Caused by deficiency of platelet fibrinoger receptor IIb/IIIa.
• Characterized by prolonged BT, normal platelet count, normal sized
platelets, abnormal aggregation with all agonists except restocetin.
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
Management
1. Respiratory: Airway clearance techniques, antibiotics and anti-
inflammatory 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)
132 Pre-NEET Pediatrics
Autistic Disorder
Diagnosis
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.
Other Infant Tumors
• The most common intrarenal neoplasm manifesting at birth is
congenital mesoblastic nephroms followed by Wilm's tumor.
• Wilms tumor or nephroblastoma, is the most common intra
abdominal tumor of childhood but is relatively rare in the neonatal
period.
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.
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
Prevention
• Dose for primary prevention is 0.4 mg folate per day.
• A mother who has previously delivered a child with NTD should
receive 4 mg per day of folic acid in subsequent pregnancies.
Duration of supplementation is 2 months before and 3 months
after conception.
• Hydrocephalus in association with a type II Chiari malformation
develops in at least 80% of patients with myelomeningocele.
Generally, the lower the deformity the less likely is the risk of
hydrocephalus.
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.
138 Pre-NEET Pediatrics
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. All symptomatic patients
ii. Asymptomatic patients with pulmonary: Systemic blood food (Qp,
Qs ratio) of at least 2:1 or those with right ventricular enlargement.
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
140 Pre-NEET Pediatrics
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).
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
Genetics
The HPRT gene has been localized to the long arm of the X-
Chromosome. 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.
144 Pre-NEET Pediatrics
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
• 1st trimester: Nuchal translucency and nasal bone
• 2nd trimester: Increased nuchal fold thickness (measured over
occiput), short femur and humerus length and duodenal atresia.
Diagnosis
1. VDRL (Venereal disease research laboratory) tests are sensitive non-
treponemal 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.
148 Pre-NEET Pediatrics
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
• Most cases of congenital hypothyroidism are not hereditary and
result from thyroid dysgenesis (accouting for 80-85% cases). Most
common dysgenesis is an ectopic gland. Thyroid peroxidase defects
Answers 149
Laboratory Findings
• Newborn screening is done by heel prick between 2 and 5 days of
life (Raised TSH, low T4 level).
• Retardation of bone age at birth can be shown in about 60% of
congenital hypothyroidism infants. The distal femoral epiphyses,
normally present at birth is after absent.
• The epiphysis often have multiple foci of ossification (epiphyseal
dysgenesis), deformity ("beaking") of the 12th thoracic or 1st or 2nd
lumbar vertebra is common.
• Treatment: Levothyroxine is the treatment of choice
• Neonates - Initial starting dose is 10-15 µg/kg/d
• Children - 4 µg/kg/24 hr
• Adults - 2 µg/kg/24 hr
6. Ans is b. Sickle cell anemia
(Ref: Nelson 19th, Pg. 1662)
• G6Pd and hereditary spherocytosis can cause episodic anemia with
jaundice since birth.
• Our choice here is sickle cell anemia as it never manifests in first 6
month of life.
• Beta globin disorders such as sickle cell disease or beta-thalassemia
major do not become apparent clinically until several months of
age, when the switch from Haemoglobin F to haemoglobin A
synthesis reveals the defect.
• Moreover sickle cell anemia usually presents with anemia, fever
(infections), acute splenic sequestration, dactylitis , stroke etc.
150 Pre-NEET Pediatrics
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. Splenectomy is not indicated.
2. Glucocorticoids for acute hemolytic episodes
3. Prolonged anticoagulant therapy
4. Bone marrow transplantation
5. Eculizumab, monoclonal antibody against complement proteins
C5, stabilized haemoglobin levels and decrease the rate of hemolysis.
Previous Year’s Questions of
DNB
QUESTIONS
PAEDIATRICS 2010
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)
154 Pre-NEET Pediatrics
PAEDIATRICS 2009
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 down’s 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)
Previous Year’s Questions of DNB 157
PAEDIATRICS 2007
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)
160 Pre-NEET Pediatrics
PAEDIATRICS 2006
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
PAEDIATRICS 2004
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. Gilbert’s 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)
Previous Year’s Questions of DNB 167
PAEDIATRICS 2003
C. Pulmonary stenosis
D. Left ventricular hypertrophy
Ans. is A. ASD
(Ref: Nelson 19th, Pg. 1573)
Q 6. In Down’s 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. Addison’sdisease
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)
Previous Year’s Questions of DNB 169
PAEDIATRICS 2002
C. Diphtheria
D. Pertussis
Ans. is B. Measles
(Ref: Nelson 19th, Pg. 1072)
Q 6. Casoni’s test is diagnostic of:
A. Echinococcus granulosum
B. Toxoplasmosis
C. Toxocariasis
D. Syphilis
Ans. is A. Echinococcus granulosum
PAEDIATRICS 2001
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)
C. Verapamil
D. Triamterene
Ans. is A. Acetazolamide
(Ref: O.P. Ghai 7th, Pg. 55
PAEDIATRICS 2000
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. Addison’s disease
C. McCune Albright syndrome
D. Neuroblastoma
Ans. is C. McCune Albright syndrome
(Ref: Nelson 19th, Pg. 1892)