PAEDIATRICS

SMAHRT NOTES
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1. Infant mortality Rate [21, 11]
Ans.
𝑁𝑜. 𝑜𝑓 𝑑𝑒𝑎𝑡ℎ𝑠 𝑖𝑛 𝑡ℎ𝑒
1𝑠𝑡 𝑦𝑒𝑎𝑟 𝑜𝑓 𝐿𝑖𝑓𝑒
Infant mortality rate (IMR) = 𝑥 1000
𝑁𝑜.𝑜𝑓 𝐿𝑖𝑣𝑒 𝑏𝑖𝑟𝑡ℎ𝑠
As per 2016 data, IMR in India is 34 per 1000 live births
IMR indicates the availability, utilization and effectiveness
of perinatal care
Causes of infant Mortality
Preventive and social measures to ↓IMR:
1. Prenatal nutrition – given if the mother is malnourished
2. Prevention of infection – by immunization under Universal Immunization Programme.
3. Promote Breast-feeding – it is a safeguard against GIT & respiratory infections and PEM.
4. Growth monitoring – All infants should be weighed periodically (at least once a month) and their
growth charts maintained. These charts help to identify children at risk of malnutrition early.
5. Family planning – Family limitation and spacing of births contribute to lowering of IMR.
6. Sanitation - infants and young children gets exposed to infections through contaminated food and
water, lack of hygiene, flies, poor housing etc.
7. Provision of primary health care with a view of detecting mothers with "high-risk factors"
8. Socio-economic development – Ex: improvement of nutritional standards, provision of safe water and
basic sanitation, improvement of housing conditions, etc.
9. Education - esp. female literacy. Educated women generally do not have early pregnancies, are able
to space their pregnancies, have better access to information related to care of their children.
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2. National Rural Health Mission [10]
Ans.
NATIONAL RURAL HEALTH MISSION:
» Was Launched on 5th April, 2005.
» The mission seeks to improve rural health care
delivery system.
» Aim of NRHM is to provide accessible, affordable,
accountable, effective and reliable primary health
care, and bridging the gap in rural health care through
creation of a cadre of Accredited Social Health Activist
(ASHA).
» It is an instrument to integrate multiple vertical
programmes along with their funds at the district
level. Ex: RCH II; NVBCP; NLEP; RNTCP; NPCB etc.
Major initiatives under NRHM
1. : 1 ASHA for 1000 population. In
tribal, hilly and desert areas the norm could be relaxed to one ASHA per habitation.
2. : It is a registered
society whose members act as trustees to manage the affairs of the hospital.
3. The SCs are far better equipped now with BP measuring
equipment, Hb measuring equipment, stethoscope, weighing machine etc.
4.
5. Under the scheme, cash assistance is provided to eligible pregnant
women for giving birth in a government health facility. {to ↓ MMR}
6. this entitles all pregnant women delivering in public
health institutions to absolutely free and no expense delivery, including caesarean section
7. (NMMUs)
8. – Currently, 32 states/UTs have the facility where people can dial 108
or 102 telephone number for calling an ambulance.
9. (MCTS) – for ensuring delivery of services like timely
antenatal care, institutional delivery and postnatal care for the mother, and immunization .
Some of the New initiatives taken since 2011:
a. Home delivery of contraceptives (condoms, OCPs, emergency contraceptive pills) by ASHA.
b. Involving ASHA in Home Based Newborn Care
c. Rashtriya Bal Swasthya Karyakram (RBSK) - for early detection and management of 4 Ds i.e.,
Defects at birth, Diseases, Deficiencies, Development delays.
d. Free drugs and free diagnostic service
e. Mother and Child Health Wings (MCH Wings) - have been sanctioned in public health facilities with
high bed occupancy to cater to the increased demand for services
f. Reproductive, Maternal, Newborn, Child and Adolescent Health Services (RMNCH+A).
g. Kilkari
h. Launch of Nationwide anti-TB drug resistance survey – to estimate the burden of MDR-TB within
the community. It is the biggest ever such survey in the world
i. Kala- azar elimination plan: for UP, Bihar, West Bengal and Jharkhand was launched
With the advent of the National Urban Health Mission, the NRHM is now called as National Health
Mission (NHM).
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1) Define neonatal mortality rate & write 4 leading causes of neonatal mortality in India [03]
Ans.
 Neonatal Mortality Rate:
 Causes:
1. Define growth and development. Enumerate the factors affecting growth & development. How do
you evaluate short stature? [14, 12, 11]
a. Causes of short stature [15, 10]
b. Name the anthropometric parameters for growth assessment [12]
c. Describe 5 important nutritional causes of growth retardation [08]
d. Describe the evaluation of physical growth and development of children from birth till one year of age [07]
Ans.
» Growth refers to a net increase in the size or mass of tissues. It is largely attributed to
multiplication of cells and increase in the intracellular substance. {Quantity}
» : Other GENES
 Phenotype—Transmission of parental traits to offspring is genetically
determined
 Race—Growth potential of children from various racial groups are different.
Genetic
 Sex— Growth spurt occurs earlier in girls
factors:
 Biorhythm & maturation—Daughters often reach menarche at a similar age
as their mother
 Genetic disorders—Turners syndrome, Down syndrome
▪ Maternal malnutrition, anemia, tobacco, & alcohol abuse
Prenatal period  IUGR.
Environmental
▪ PIH, preeclampsia also retard fetal growth
factors
Children suffering from protein energy malnutrition, anemia,
Postnatal period
and vitamin deficiencies
▪ Socioeconomic level - Children from families with high socioeconomic status
suffer from fewer infections because of better hygienic living conditions
Social factors
▪ Emotional factors—Children from broken homes and orphans lack
emotional support and love from the family
Endocrinal
GH, Thyroxine, Androgens & Insulin
factors
Nutritional Over-nutrition; Malnutrition; Vitamin Deficiencies; Mineral deficiencies
factors {Calcium, iodine, Iron, Zinc etc.}
Others:
 Trauma to epiphysis can retard growth
 Infections and infestations can retard growth
 Drugs—Androgenic hormones can accelerate growth
 Cultural factors—Child rearing and feeding practices affect growth
» Development refers to maturation of functions like acquisition of a variety of skills for optimal
functioning of the individual (Quality)
»
Pre-natal factors – IQ of parents, maternal health, maternal drug or alcohol abuse, malnutrition,
stress etc.
Neonatal risk factors – LBW, Neonatal seizures, infections etc.
Post Neonatal factors: nutritional deficiency, endocrine deficiency (Ex: hypothyroidism) etc.
Social factors: Parenting, Poverty, Violence and abuse
» :

Weight

 Length is for children < 2 years of age (via infantometer)

 standing height is for children above 2 years of age (via Stadiometer)
Length/Height
 Expected height between 2—12 years in cm (Weech formula) =
(Age in years × 6) + 77
Head  Measured through Occipital protuberance and supraorbital ridge
circumference  Dine’s formula for head circumference = ( Length/2) +9.5 ± 2.5
Chest Measured Midway between inspiration and expiration at the level of nipples
circumference Used to check relative brain growth by comparing with head circumference
Mid arm  MAC is relatively constant between 16.5 and 17.5 cm between 6 months and 5 years
circumference {Age independent}
(MAC)  Measured with Shakir tape {Green yellow & Red Zone}
Skin fold
Triceps skinfold is measured using Harpenden skin-fold calliper
thickness

:
Short stature is defined as
 Height/length for age below 3rd centile (OR)
 Height/length more than 2SD below the median height B- HCG
for that age & sex according to the population standard
:
: 👇🏻

Accurate height measurement – via either infantometer or

Stadiometer
Determine body proportions: By measuring US—LS ratio
▪ Increase in US:LS ratio—Rickets, achondroplasia, untreated
congenital hypothyroidism
▪ Decrease in US:LS ratio—Spondyloepiphyseal dysplasia,
vertebral anomalies TB
Assessment of height velocity: If height velocity is low,
pathological cause of short stature should be suspected
Plot height in growth charts expressed in centile or SD.
Compare with Child’s own genetic potential by measuring the
Mid parental height (MPH)
SMR stage should be assessed in older children
 :
Essential tests for short stature: ESI
 Complete hemogram with ESR
 Bone age
 Urine analysis including microscopy, osmolality and pH
 Stool examination for parasites, steatorrhea, and occult blood
 Blood – urea, creatinine, venous gas, calcium, phosphate, alkaline phosphatase, fasting glucose,
albumin, and transaminase
Specific tests:
▪ Serum thyroxine and TSH to rule out hypothyroidism
▪ Karyotype to rule out turner syndrome in girls
Invasive tests
Celiac serology (anti-endomysial or anti-tissue transglutaminase antibodies) & duodenal biopsy
GH stimulation test with clonidine or insulin and serum IGF-1 level estimation
: it depends on the etiology
General measures
▪ Intake of balanced diet with macro- and micronutrients
▪ Zinc supplementation
Specific treatment
Levothyroxine for hypothyroidism
Limb lengthening procedure for skeletal dysplasia
GH replacement therapy for GH deficiency
Monitoring the height of child.
Familial and constitutional stunting— Diagnosis of Exclusion; Monitor Continuously till puberty;
No specific treatment required
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1) Important milestones till 2 years of age [21]

a. Language milestones till 4 years of age [19]
b. Developmental milestones in a 9-month-old child [14]
c. Mention the normal milestones achieved by one year old infant [11]
d. Assessment of the appropriateness of growth in a one-year-old [09]
e. Describe the gross motor, fine motor, personal, social & language milestones in a 9-month-old child [03]
Ans.

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2) Definition and causes of microcephaly in children [12, 08, 07]
Ans.
Definition: Head circumference <3rd centile or < –3 SD below the mean for age and sex
 TORC

RAZ

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3) Proportionate dwarf [04] RAO _ C
a. Disproportionate short stature – causes [09]
Ans.
Proportionate dwarfism is caused by genetic risk factors and
systemic conditions that affect growth potential
Causes:
Management {Refer 1st LQ}

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1. Causes of Macrocephaly [11]

Ans.
1) Breath Holding Spells & it’s treatment [21, 20, 14, 04]
Ans.
Breath-holding spells are reflex events typically initiated by a provocation that causes anger,
frustration or pain making the child cry.
The crying stops at full expiration, and the child becomes apneic and cyanotic or pale or
unconscious.
In prolonged events, brief tonic-clonic movements may happen.
Time of onset: Breath-holding spells are rare before 6 months of age, peak at 2 years and abate by
5 years of age.
DDx: seizures and cardiac arrhythmias {long QT syndrome}.
 The history of a provoking event and stereotyped pattern of events help in distinguishing
breath-holding spells from seizures. In relevant clinical scenarios, seizures and cardiac
arrhythmias including should be ruled out.
Management:
Reassure the parents
Advise the family to be consistent in handling the child, to remain calm during the event, turn him
sideways so that secretions can drain and avoid picking the child up (since this decreases blood
flow to the brain).
The family should avoid exhibiting undue concern nor give into the child's demands, if the spell
was provoked by anger or frustration.
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2) C/F & Mx of Attention Deficit/Hyperactivity [21]
Ans.
Attention deficit/hyperactivity disorder (ADHD) is a neurobehavioral disorder defined by symptoms of
inattention, hyperactivity, and impulsivity.
Etiology: ADHD is multifactorial in origin, with genetic, neural, and environmental contributions
Clinical Features
» ADHD is diagnosed clinically by History - Information should be gathered from the family and the
school via ADHD-specific rating scales {Ex: Conners’ Rating Scales or the Vanderbilt Rating Scales}.
» A physical examination is essential to identify medical (e.g., neurologic, genetic) or developmental
problems (e.g., cognitive impairment, language disorder, learning disability, autism spectrum
disorder) that may underlie, coexist, or provide an alternative explanation for the child’s
behaviours.
» : failing to pay close attention to details, appearing to not listen
when spoken to directly, failing to follow through on instructions or finish assigned work, having
difficulty sustaining attention during tasks or play, having difficulty organizing tasks or activities,
avoiding or disliking activities that require sustained mental effort (e.g., schoolwork), frequently
losing things required for tasks and activities, becoming easily distracted, and experiencing
frequent forgetfulness in daily activities.
» : being restless, leaving a seat when expected to remain seated,
running or climbing excessively in inappropriate situations, having difficulty in playing quietly,
acting as if “driven by a motor,” and talking excessively.
» : blurting out answers before a question has been completed,
having difficulty awaiting his or her turn, and causing frequent interruptions or intrusions
Diagnosis:
⇨ Diagnosis of children up to the age of 16 years requires the presence of at least 6 symptoms of
inattention or 6 symptoms of hyperactivity-impulsivity for at least 6 months in two or more
environments
⇨ Children 17 years of age and older must exhibit at least 5 symptoms of inattention or at least 5
symptoms of hyperactivity-impulsivity.
Laboratory and imaging studies – Consider thyroid function studies, blood lead levels, genetic studies,
and brain imaging studies if indicated by medical history, environmental history, or physical
examination.
Management
 Children with ADHD respond to behavioural management – Maintain Daily behaviour report cards.
 Medications:
Stimulant medications Non-stimulant medications
Examples Methylphenidate or Atomoxetine (norepinephrine-reuptake
amphetamine compounds inhibitor), guanfacine, or clonidine (α-agonists)
Indications They are the first-line agents for They are helpful in situations such as
treatment of ADHD nonresponse to stimulant medications etc.
Side ↓ Appetite, sleep disturbance & ▪ GIT symptoms with atomoxetine
effects sudden cardiac death ▪ Sedation with α-agonists
DDx:
Medical Conditions: seizure disorders, substance use, hyperthyroidism, lead intoxication, and
sensory deficits
Genetic Conditions: Fragile X, 22q11.2 deletion syndrome, and neurofibromatosis 1.
Psychological Conditions: Chaotic living situations or psychological stress (e.g., bullying, abuse)
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3) Pica [19, 14, 13, 09]
Ans.
▪ Pica is the persistent ingestion of non-nutritive substances such as plaster, charcoal, paint and soil
for at least 1 month, inappropriate to the child’s development level and cultural practice.
▪ It is common in children less than 5 years of age.
▪ a/w Poor socioeconomic status, malnutrition and iron deficiency.
▪ Predisposing Factors: Developmental delay, psychosocial stress (maternal deprivation, parental
neglect and abuse) and other behavioural disorders.
▪ Children with pica are at increased risk for lead poisoning and parasitic infestations.
▪ Management: Behaviour modification, alleviating the psychosocial stress, screening for lead
poisoning, deworming and iron supplementation.
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4) Thumb sucking [14, 13, 09]
Ans.
 This entity is normal in infants and toddlers.
 Time of onset: It peaks by 18-21 months of age and usually disappears by the age of 4 years.
 Its persistence in older children is socially unacceptable and can lead to dental malalignment.
 In children below 4 years, parents should be reassured.
 Beyond 4 years of age, the child should be motivated to refrain from this habit. Both positive and
negative reinforcements can be used.
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5) Principles of growth and development [03]
Ans.
Principles of Growth Principles of Development
Development in one field does not run parallel with
 Growth is a continuous and
another field (dissociation)
orderly process
Development is intimately related to the maturation of
 Growth pattern of every
nervous system
individual is unique
Development is a continuous process, starting in utero and
 General growth pattern in
progressing in an orderly, predictable manner until
human beings is cephalocaudal
maturity
and distal to proximal
The sequence of attainment of milestones is same in all
 Sequence of growth is the same
children e.g.,: All babies stand before they walk, reach for
but the pace of development
objects before they can start transferring them
can be non-uniform
Time and manner of attainment of milestones are variable
 Each fetal and infantile growth
Process of development progresses in a cephalocaudal
spurt is a biological process
direction (head control → trunk control → lower limb
 At puberty growth spurt occurs
control)
due to neurohumoral
The controls of limbs proceed in proximo-distal fashion
stimulation of hypophysis by
(Shoulder control → hand control → finger control)
the hypothalamus.
Certain primitive reflexes have to be lost before relevant
 Various tissues of the body
milestones are attained e.g., palmar grasp is lost before
grow at different rates
voluntary grasp is attained.
 Somatic growth curve is
Initial disorganized mass activity is gradually replaced by
“Sigmoid” shaped
more specific and voluntary activity.
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1. List red flag signs of Autism [17, 15]

Ans.

BSC
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2. Asymmetric Tonic Neck Reflex [07]
Ans.
Asymmetric Tonic Neck Reflex {ATNR} is one of the primitive reflexes
Persistence of ATNR is a feature of Cerebral palsy
: passive head turning to the side
: limbs extend on the same body side to which the head was turned; Limbs on the
opposite side flexes
during 13th week in utero & remain active till 6 mon of infant life
Fully present at birth; participate in the birth process
1) Etiology, C/F {incl. ECG changes} & Mx of Hyperkalemia [21, 16, 14, 08, 07]
Ans. is defined as existing when serum K+ is > 5 mmol/L.
Causes of HYPERkalaemia
 Haemolysis during venepuncture or in vitro – Release of intracellular K+
1) Artefactual during sample collection
 Thrombocytosis/leucocytosis
- Dietary Potassium
2) Increased intake
- Potassium-containing intravenous fluids
▪ Acidosis
3) Redistribution ▪ Insulin deficiency & severe hyperglycaemia
From cells (flux of ▪ β – blockers
K+ into PLASMA) ▪ Hyperkalaemic periodic paralysis
▪ Rhabdomyolysis, Severe haemolysis & Tumour lysis syndrome
↓GFR – Acute kidney injury & chronic kidney disease
↓ Mineralocorticoid receptor activation – seen in:
Addison’s disease & Congenital adrenal hyperplasia
ACE inhibitors & ARBs {↓ Aldosterone levels}
Calcineurin inhibitors, Spironolactone & Eplerenone {block the
mineralocorticoid receptor}
4) Reduced urinary Heparin {inhibits aldosterone production}
excretion
↓ Renin production – can occur due to: NSAIDs & β-blockers
Tubulointerstitial diseases – Interstitial nephritis, Diabetic nephropathy &
Obstructive uropathy
Others:
▪ Amiloride – Blocks K+ exchange in distal tubule
▪ Gordon’s syndrome – ↓ K+ secretion in the renal tubules
Clinical features
⇨ Mild to moderate hyperkalaemia (< 6.5 mmol/L) is usually
asymptomatic
⇨ In severe cases muscular weakness & cardiac arrest occurs.
⇨ Electrocardiogram (ECG) changes:
Management
 Treatment of hyperkalaemia depends on its severity and the
rate of development
 Mild to moderate hyperkalaemia (< 6.5 mmol/L) can be
treated with a reduction of potassium intake and correction
of predisposing factors
 Treatment of severe hyperkalaemia

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2) Causes of Hyponatremia [19]
Ans.

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3) 3 causes of Metabolic Acidosis in children and treatment [08]
Ans.

Identify & treat the cause first.

Shock should be treated with aggressive fluid therapy and adequate oxygenation.
Vasoactive agents (dopamine, dobutamine) should be added only after volume replacement as
they can worsen acidosis.
Routine IV sodium bicarbonate for metabolic acidosis is not recommended.
Sodium bicarbonate is indicated in the following situations:
- When pH is below 7.15
- In cases of Salicylate poisoning
- Inborn errors of metabolism
Amount of Sodium bicarbonate is calculated using the formula: HCO3– deficit (mEq) = 0.5 × body
weight (Kg) × (desired—actual serum HCO3–)
Potassium supplementation to prevent hypokalemia in cases such as DM
Calcium gluconate therapy if Hypocalcemia is precipitated by correction of metabolic acidosis
In severe cases of metabolic and respiratory acidosis, THAM (Tris-hydroxymethylaminomethane) is
more effective buffer used at a dose (mL) = weight (kg) × base deficit, over 3 × 6 h because it
neutralizes acid without releasing CO2
1. Describe the clinical features, complications and Mx of a 2-year-old child with severe PEM. [13]
a. C/F & Mx of marasmus. [21]
b. List all 4 criteria to define SAM in children as per WHO. Write the etiology of malnutrition &
outline the hospital management of SAM. [18]
c. Age independent criteria for assessment of PEM in children. [17]
d. Wellcome classification of PEM [14, 13]
e. PEM – Define & Classify. How do you manage a case of kwashiorkor? [10]
f. Dietary Mx of PEM [03]
Ans.
➢ PEM stands for Protein-Energy Malnutrition; It’s a Clinical syndrome due to lack of appropriate
amount of proteins, energy, vitamins, and other nutrients required by the body to maintain
homeostasis and normal organ function
➢ Causes of PEM
 Nutritional Factors: ↓intake of food (Low quantity, Low Quality)
 Social factors: Low socioeconomic status, Large families, Working mother etc.
 Infections – they form a vicious circle with malnutrition – Ex: Diarrhea, pneumonia, TB etc.
➢ Classification of PEM:
Clinical Classification – Kwashiorkor & Marasmus
1) Kwashiorkor is a severe form of undernutrition occurs due to low protein/energy ratio.
2) Marasmus is caused by inadequate intake of both protein and energy.
Anthropometric Classification –
 Ex: WHO classification, Gomez Classification, IAP classification etc.
 The 3 anthropometric indices - weight-for-age, height/length-for-age, weight-for-height/length
are used to identify 3 nutrition conditions: underweight, stunting and wasting.
 In WHO classification – SAM (Severe acute malnutrition) among children 6-59 months of age is
defined by any of the following 3 criteria:
a) Weight-for-height < -3 SD on WHO growth standards
b) Presence of bipedal edema
c) MUAC < 11.5 cm
Wellcome Classification of PEM:
➢ Assessment of PEM in Children: It involves various
techniques such as:
: It is the simplest and the most
practical method. It detects signs associated with states of malnutrition. Signs used in nutritional
surveys are classified into 3 categories as those:
a) not related to nutrition, e.g., alopecia, pyorrhoea,
pterygium etc.
b) that need further investigation, e.g., malar
pigmentation, corneal vascularization, etc.
c) known to be of utmost value, e.g., angular stomatitis,
Bitot's spots, etc.
 : weight, height, MUAC, chest & head circumference, skin fold
thickness – are recorded over a period of time to observe the
patterns of growth and development, and how individuals deviate
from the normal pattern.

 Laboratory tests – Ex: Hb estimation, Stool & urine tests

 Biochemical tests: they measure individual nutrient
concentration in body fluids (e.g., serum iron).
:
➢ Clinical features of PEM
Marasmus is characterized by severe form of wasting
Severe marasmus is typical form of severe acute malnutrition (SAM)
Clinical Features Kwashiorkor Marasmus
Deficiency of Proteins Calories
Child Appearance Dull, disinterest, apathetic ALERT, irritable
Face Bloated (moon) face Shrivelled (monkey) face {due to
loss of buccal pad of Fat}
Hair changes Lustreless, sparse, Flag sign Thin, silky texture
Skin changes Flaky paint dermatoses Loose skin of buttocks
Liver enlargement & Mental
changes Present No
Fat Retained Loss of subcutaneous fat
Muscle wasting Masked (by edema) Obvious
Edema Present {pitting} No
Serum proteins & cholesterol Normal
Urinary nitrogen Raised
Appetite Poor Good
Growth failure Moderate SEVERE
Prognosis Bad Good
➢ Management:
The treatment involves 10 steps
in 2 phases of treatment;
which lasts
2−7 days followed by
which BMW
might take several weeks to
months
➢ Complications of SAM: B/L pitting
edema, LRTI, Severe Pallor, severe
dehydration, convulsions etc.

RUTF
Family counsel
community health worker
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1) Rickets – Causes, Dx & Rx [19, 13, 08]
a. Bony changes in Rickets. [21]
b. Clinical features of Vitamin D deficiency. [11]
c. Biochemical and radiological features in nutritional rickets. [07]
d. Radiological features of nutritional rickets and scurvy. [06]
Ans. Rickets is a disease of the growth plate characterized by deficient mineralization
As it is a disorder of growing bones, it invariably presents by 18 months of age
:
Vitamin D deficiency – poor sunlight exposure, inadequate dietary intake, deficient
hydroxylation in cirrhosis & renal failure.
Deficient Vitamin D action – seen in Vitamin D resistant ricket
Hypophosphatemia – seen in renal tubular acidosis, Antacids etc.
Defective mineralisation – Ex: osteogenesis imperfecta, fibrogenesis imperfecta etc.
There are two types of rickets i.e., Type I and Type II.
In Type I, there is either a deficiency of vitamin D or a defect in its
metabolism.
Type II Rickets – occurs due to a deficiency of phosphates or a
defect in its metabolism
:
Bone deformities: C2D2F
Knock knees, bow legs
and coxa vara are
common deformities
in older children
:
 Most are diagnosed by
classical radiological
features— cupping,
splaying and flaying of the metaphysis
 Laboratory tests
 ALP;
 Low 25(OH)D3 & Decrease in Serum phosphorus
 PTH level is ↑ in hypocalcemic rickets and normal in
hypophosphatemic rickets

: 👉🏻

:
 Conservative
methods: Mermaid
splints or orthopaedic shoes for correction of knee deformities.
 Operative methods: Corrective osteotomies, depending upon the nature of deformities, are performed.
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1. Hind milk [20]
Ans.
Mature milk consists of Foremilk & Hindmilk
Foremilk is the milk secreted during initial part of breastfeeding. It contains more water content
which satisfies thirst of the baby
is secreted during part of breastfeeding. It is rich in fat and satisfies of the
baby
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2. Hypervitaminosis D. [20]
Ans.
 Toxicity of vitamin D which occur at doses between 2,000 and 3,000 IU/day {10,000 IU/day in adults}
for several months
 It leads to 'idiopathic hypercalcemia' in infants – anorexia, vomiting, hypertension, renal
insufficiency and failure to thrive
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3. Prevention of malnutrition at family level. [16]
Ans.
Action at the family level – Nutrition education.
 Both the husband and the wife need to be educated on the selection of right kinds of foods
within the limits of their purchasing power.
 Attention should also be focused on the nutritional needs of expectant and nursing mothers
 Knowledge of the "package" of mother and child health, family planning and immunization
services.
----------------------------------------------------------------------------------------------------------------------------------------
4. Differentiate between stunting and wasting. [06]
Ans.
Wasting Stunting
Denotes Acute Malnutrition Denotes CHRONIC malnutrition
Low WFH {weight-for-height} Low {height-for-age}
1. Clinical features of Vitamin A deficiency. [16, 13]
a. Vitamin A prophylaxis. [14, 12]
b. Ocular manifestations of Vitamin A deficiency (WHO classification) [09]
Ans.
Clinical features
Night blindness – earliest symptom of xerophthalmia in children.
Conjunctival Xerosis: It consists of one or more patches of dry,
lustreless, non-wettable conjunctiva.
Bitot’ s spot: It is an extension of the xerotic process. The Bitot’ s
spot is a raised, silvery white, foamy, triangular patch of
keratinised epithelium, situated on the bulbar conjunctiva
Corneal xerosis: cornea lacks lustre.
Corneal ulceration/keratomalacia ➔ stromal defects ➔ blindness.
Corneal scars: Healing of stromal defects results in corneal
scars of different densities and sizes.
Xerophthalmic Fundus: It is characterized by typical seed-
like, raised, whitish lesions scattered uniformly over the
pan of the fundus at the level of optic disc
Prevention and control of xerophthalmia
1) Short-term action: administration of large doses of vitamin A orally. Under National Immunization
Schedule, Vitamin A is given as:
 1 lac IU at 9 months age (along with measles vaccine)
 2 lac IV every six months thereafter, till the age of 5 years (at 18, 24, 30, 36, 42, 48, 54, 60 months)
2) Medium-term action: promote regular and adequate intake of vitamin A enriched foods
3) Long-term action: These are measures aimed at elimination of factors contributing to ocular
disease, e.g., persuading people to consume green leafy vegetables or other vitamin A rich foods;
promotion of breast-feeding for as long as possible; etc.
----------------------------------------------------------------------------------------------------------------------------------------
2. Hypervitaminosis A. [11]
Ans.
Toxicity of vitamin A which occur at doses > 50,000 IU / day for several months in form of fish liver
oil, therapeutic vitamin preparations or, in adolescents, as retinol or retinoic acid for acne etc.
Clinical Feature:
 Pseudotumor cerebri (vomiting, irritability, bulging fontanel, diplopia, headache)
 Dermatitis, alopecia, hepatosplenomegaly + hyperostosis
 Fetal anomalies in pregnant women
The WHO recommends that vitamin A intake during pregnancy should not exceed 3000 µg daily or
7500 µg every week
1. Advantages of breast feeding & the disadvantages of artificial feeding? [21, 18, 12, 06]
a. Benefits of exclusive breast feeding. [21, 05]
b. List all points of good attachment of Breast feeding. [17] or Enlist 4 of the 10 steps for successful breast feeding. [06, 04]
c. Colostrum. [16]
d. List anti-infective factors in human milk. [15]
e. Immunological benefits of exclusive breast feeding. [08]
f. Antimicrobial factors in breast milk. [04]
Ans. Breast milk contains necessary nutrients to sustain appropriate growth and development during
the first 6 months of life in term infants
Breastfeeding should be initiated within half an hour after vaginal delivery and within 4 h after
caesarean delivery
Exclusive breastfeeding: Giving a breastfeeding baby no other food or drink, including water (with
the exception of prescribed drugs) during first 6 months of age
It Protect against common childhood infections and reduction in infant and under 5 mortality rates.
Breast milk is with no risk of infection
Improves bonding between mother and baby
Breastfed babies are protected against diabetes, heart disease, allergic disorders etc.
Reduces postpartum bleeding, prevents anemia in mother in addition to contraceptive effect
Protective factors {Anti-infective Factors} in Breast milk:
—Protects against amoeba and giardia infection
—Protects against malaria
—Surface protection to respiratory tract and GIT
—Ensures absorption of iron and makes it unavailable for microorganisms.
Bacteriostatic, inhibits Escherichia coli.
—Colonization of lactobacillus
—Precursor of tryptophan which is a neurotransmitter
: Phosphorus ratio >2; Ensures good calcium absorption
: Promotes brain growth, reduces dyslexia/hyperactivity.
—Binds to thyroxine, Vitamin D, and B12
—Promotes growth, neurotransmitters
Signs of Good attachment for Breastfeeding:
▪ Lips are everted
▪ Mouth wide open
▪ Chin touching breast
▪ Lower areola not visible
Colostrum:
 Initial 40–50 mL of yellowish milk
 Rich in protein and
 Contains more Sodium, proteins, and immunoglobulins
when compared to mature breast milk
 Contains less fat and lactose when compared to mature
breast milk
Disadvantages of artificial feeding: --------------------
 The 10 steps to successful breastfeeding: {to be followed in maternity hospitals/nursing homes}
1) Written breastfeeding policy should be available
2) All healthcare professionals should be trained to acquire skills necessary to implement this
policy.
3) All mothers should be educated about advantages of breastfeeding.
4) Mothers should receive help to initiate breastfeeding within 30 min of birth.
5) Mothers should be shown how to breastfeed and how to maintain lactation if they have to be
separated from their babies.
6) Newborn infants should not be given any food or drink other than breastmilk (Exclusive breastfeeding).
7) Practice ‘rooming in’ and allow mothers and infants to remain together—24 h a day.
8) Mothers should be motivated to breastfeed on demand.
9) No artificial teats or pacifiers should be given to infants.
10) Breastfeeding support groups should be fostered and mothers should be referred to these
groups on discharge.
----------------------------------------------------------------------------------------------------------------------------------------
2. Define pre-term baby. Discuss the factors affecting prematurity. Name the complication of
prematurity. [11, 06]
a. Late complications in preterm children. [07]
Ans.
: Babies born in <37
completed weeks (259 days)
: 👉🏻

:
  length of hospital stay.
 Hypothermia – due to less fat & surface area
 Asphyxia – due to
anatomical and
RBL I
functional immaturity.
 Hypoglycemia {due to
lack of glycogen stores
in liver} & Jaundice
{hepatic immaturity}
 Patent DA
 Long term
Complications: Poor
Growth, Cerebral
palsy, hearing loss,
chronic lung disease &
ADHD.

----------------------------------------------------------------------------------------------------------------------------------------
3. Discuss the known causes of Intrauterine Growth Retardation (IUGR), the various complications
that are anticipated in a full-term low birth weight neonate and steps to prevent these
complications. [09, 08]
 a. Immediate and long term handicaps of intrauterine growth retarded babies. [16]
b. Definition of low birth weight, small for date and preterm baby. [14]
c. Mention 4 Important complications of small for gestational age infants [04]
Ans.
: birth wt. 2.5 kg or less
: Small for gestational age (SGA): It is a statistical definition and denotes
weight of infant being < 2 standard deviation or less than the 10th percentile of the population norms
(plotted on intrauterine growth chart).
SGA and IUGR are considered
synonymous

👉🏻

:
Antenatal period: Chronic fetal
distress, fetal death
Intranatal—Hypoxia & acidosis
Immediately after birth: Asphyxia,
RDS, Hypoglycemia, Hypothermia,
anemia, Multiorgan failure, 
perinatal morbidity and mortality
Late Complications: mental retardation, risk of metabolic syndrome in adult life: obesity, HTN,
DM and CHD.
----------------------------------------------------------------------------------------------------------------------------------------

1. Kangaroo mother care. [21, 18]

Ans.
Kangaroo mother care (KMC) refers to a specialized care given preterm and LBW infants by placing
them in skin to skin with the mother or other caregivers
Components:
Kangaroo position - Skin to skin contact in vertical position
under mother’s clothes and between her breasts. Mother is
in semi-reclining position to avoid gastric reflux in infant
Kangaroo nutrition - Exclusive breastfeeding
Kangaroo discharge {Early home discharge} and follow up
Duration of KMC
 Start with short sessions
 Gradually transition from conventional to continuous KMC
 Mother can sleep with baby in KMC position
----------------------------------------------------------------------------------------------------------------------------------------
2. Approach to a child with Jaundice. [20]
a. Causes of Neonatal Hyperbilirubinemia. [19]
b. List the causes of jaundice in the first week of life and outline important points to differentiate physiological
from pathological jaundice in newborn. [18, 16]
c. Causes & Management of Neonatal Jaundice. [13, 11, 05]
d. Pathological Jaundice of Newborn. [11] List the causes of jaundice appearing on the first postnatal day [03]
Ans.
Jaundice implies Hyperbilirubinemia
: 👉🏻

occurs due to functional

immaturity of the
neonates to handle the
production of bilirubin
due to enterohepatic
circulation, fetal
erythrocyte breakdown,
decreased hepatic excretion and immature hepatic conjugation.
is arbitrarily defined as serum bilirubin exceeding 5 mg/ dL on day 1, 10
mg/dL on day 2, 15 mg/dL on day 3 and thereafter.

 Kramer’s rule: Used for clinical assessment of

jaundice👉🏻
 Total and direct bilirubin
 Mother and baby blood group – to r/o Rh
isoimmunisation
 Hb & PCV
 Peripheral blood smear (for RBC shape and evidence of hemolysis)
 G6PD assay
 Thyroid profile, Evaluate for cholestasis, urine culture etc.
– Phototherapy and exchange transfusion are treatment of choice
Phototherapy consists of compact florescent lamps in wave length range of 460 to 490 nm – Side
effects are: water loss, Diarrhea, Bronze baby syndrome (when used in conjugated jaundice)
Double volume exchange transfusion (DVET) should be done if values exceed the age specific cut
off – Side effects are: Hypoglycemia, Hypocalcemia, Hypokalemia & Sepsis.
Drugs – not used routinely:
Oral Phenobarbitone—Induces enzymes required for bilirubin conjugation
Heavy metals—Inhibits hemoxygenase enzyme and reduces hemoglobin break down
----------------------------------------------------------------------------------------------------------------------------------------
3. Baby Friendly Hospital Initiative. [19, 07]
Ans.
BFHI was launched to ensure that all maternal–child health services in healthcare facilities are
made breastfeeding friendly and support for breastfeeding becomes a vital point of their program
as a standard for care.
This program was started by UNICEF and WHO in Ankara, Turkey in the year 1991
Healthcare facility should implement “The Ten Steps to Successful Breastfeeding” to be qualified as
“baby friendly” hospital {refer 1st LQ}
Health care staff working in MCH services should be trained to offer skilled support for initiation
and continuation of exclusive breastfeeding.
Low-cost breastmilk substitutes, feeding bottles or teats should not be allowed inside the facility.
Establishment of community outreach support systems for breastfeeding mothers.
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4. Respiratory distress syndrome – C/F & Mx [18]
a. Prevention of hyaline membrane disease. [05]
Ans.
Hyaline Membrane Disease {aka Resp. Distress Syndrome} in newborn is the presence of one or
more of the following features: Respiratory rate > 60/min, Chest retractions & Grunt.
This usually affects preterm neonate whose lungs are deficient in surfactant.
Clinical Features:
 Usually presents within the first 6 h of delivery
 Most commonly seen in premature infants as rapid and shallow respirations
 Tachypnea
 Retractions with grunting and cyanosis
 Decreased air entry
 Downe and Silverman scoring are done to objectively quantify ‘work of breathing’
Management: Chest x ray is the IOC – it reveals low volume lungs; Treatment is supportive
 Prevent or treat hypothermia—Infant should be placed in incubator or radiant warmer
 Respiratory distress—Requires Early Continuous positive airway pressure (CPAP)
 Provide warm humidified oxygen in order to maintain oxygen saturation of 89 -93%
 Mechanical ventilation and surfactant are indicated in
infants with severe Respiratory failure
 Surfactant administration through INSURE (Intubate –
surfactant-extubate)/MIST (Minimally invasive surfactant therapy) reduces occurrence of BPD
Prevention of HMD:
 Antenatal assessment of lung maturity – with Lecithin: Sphingomyelin ratio
 Antenatal corticosteroids to pregnant women between 24 weeks and 34 weeks of gestation with
threatened preterm labor.
 Course: 2 doses of betamethasone (12 mg IM) at 24-hourly interval or 4 doses of dexamethasone
(6 mg IM) at 12-hourly intervals
 Antenatal steroids are contraindicated in Maternal fever & Chorioamnionitis
----------------------------------------------------------------------------------------------------------------------------------------
5. Apgar score. [15,13]
Ans.
It is an objective method of evaluating baby’s condition after birth
APGAR stands for:
A-Appearance (Skin colour)
P-Pulse (Heart Rate)
G-Grimacing (Reflex)
A-Activity (Tone) and
R-Respiration (Chest movement)
APGAR Scoring is done 1 and 5 min after birth
APGAR score is not used to initiate the
resuscitation but to check its response.
If 5-minute APGAR score is <7, scoring should be repeated every 5 min till 20 min
----------------------------------------------------------------------------------------------------------------------------------------
6. Birth injuries & their causes [14, 12]
a. Cephalhematoma. [21, 12]
Ans.
 Birth injuries is an impairment of the infant’s body function or structure due to adverse influences
that occurred at birth
Causes of Birth injuries: Fetal macrosomia; Cephalopelvic disproportion; Very low birth weight
infant; Prolonged or obstructed labor; Shoulder dystocia; Instrumental delivery (forceps or
ventouse); Abnormal presentation (breech); Manipulative delivery (IPV); Precipitate labor
Examples of Birth Injuries: Cephalohematoma, Caput succedaneum, Subaponeurotic hemorrhage/
subgleal bleed, Brachial palsy, Clavicle fracture etc.
: it is a collection of blood under the periosteum (Subperiosteal location) of the
skull bones.
Clinical Features:
 Swelling appears after 4−8 h of birth and reaches maximum size by 3rd day
 Swelling is U/L, does not cross the suture line & has well-defined margin
 Swelling is: fluctuant, irreducible, non-pulsatile in size during crying
Treatment:
No specific treatment is required. Resolves spontaneously over a period of time {till 3rd month}
Reassurance to the parents
Complications: Risk of jaundice & secondary infections
----------------------------------------------------------------------------------------------------------------------------------------
7. Step wise management of an asphyxiated newborn. [03]
Ans.

----------------------------------------------------------------------------------------------------------------------------------------
1. Hypoglycemia in a newborn baby. [21]
Ans.
Definition: Blood glucose less than 40 mg/dL in general,
regardless of the gestational age
Clinical Features
 Approximately 50% cases present with symptoms.
 Symptoms: irritability, poor feeding, jitteriness, lethargy,
tachycardia, tremors and sweating
Treatment:
 In Asymptomatic neonates – determine the risk &
initiate early feeding
 Treatment in symptomatic neonates:
Immediate therapy: Bolus dose of 10% Dextrose, 2 ml/kg (IV)
Maintenance therapy: Glucose infusion rate (GIR) of 4–10 mg/kg/minute
IV glucose is gradually tapered and switched to oral feeding under glucose monitoring
 In refractory hypoglycemia, not responding to IV glucose therapy, steroids are indicated.
Prednisone, 1-2 mg/kg/day or hydrocortisone, 5 mg/kg, every 12 h is used
Steroids peripheral glucose utilization and gluconeogenesis
 2 line drugs – Glucagon & Diazoxide
nd

----------------------------------------------------------------------------------------------------------------------------------------
2. Prevention & treatment of Hypothermia in the new born. [19, 14]
Ans.
Prevention of Hypothermia: Reduce the heat loss by conduction, convection and radiation
Treatment of Hypothermia:
 For Mild to Moderate hypothermia: Immediate skin to skin contact
with mother; Radiant warmer or convection warmed incubator;
Frequent feedings
 For Severe hypothermia
 Requires incubator, thermostatically controlled heated mattress at 37–38°C
 Fast rewarming till 34°C and then slow rewarming.
 Monitor axillary temperature every half hour till it reaches 36.5°C, then hourly for next 4 h, 2
hourly for 12 h thereafter and 3 hourly as a routine.
 Oxygen, empirical antibiotics and IV fluids
 Vitamin K if bleeding is present
 FFP, Exchange transfusion if DIC is present
----------------------------------------------------------------------------------------------------------------------------------------
3. Prevention of hemorrhagic disease of newborn. [05]
Ans.
Hemorrhagic Disease of Newborn (Vitamin K deficiency bleeding) – All babies should receive vitamin
K prophylaxis, particularly breastfed babies. Either single IM dose or multiple oral doses required
1. Pneumonia – Etiology, clinical features, complications & management. [21, 11]
a. Treatment of a child with severe pneumonia. [19]
b. Hemophilus influenzae Pneumonia. [14]
c. Clinical features and etiology of Bacterial pneumonia. [05]
Ans.
Any infection of the lung parenchyma is known as pneumonia.
Viruses are the most common cause in younger children, while
bacteria are commoner in older children.
:
Risk Factors: LBW; Malnutrition; Vitamin A deficiency; Passive
smoking; Large family size; overcrowding etc.
:

: Empyema; Pyo-pneumothorax; Pericarditis;

Metastatic abscess; Pleural
thickening
:
Chest X-ray findings
CBP & Serologies
Mainstay of
management are antibiotics and supportive therapy
All non-severe pneumonias > 3 months of age – 1st line Abx is Amoxicillin – given for 5 days
For age less than 3 months – 1st line Abx are Cefotaxime/Ceftriaxone ± Aminoglycosides.
Azithromycin for Atypical pneumonia – caused by Mycoplasma – it is a/w Cervical
lymphadenopathy & hemolytic anemia
Swine flu is treated with Oseltamivir.
Supportive therapy:
Oxygen—if cyanosis or respiratory distress
IV fluids to maintain hydration.
Empyema —Intercostal drainage
----------------------------------------------------------------------------------------------------------------------------------------
2. Causes of wheezing in a child? How will you manage a child with acute severe asthma? [16]
a. Status asthmaticus & it’s Mx [21, 04]
b. Treatment of acute exacerbation of asthma. [16, 14, 06]
c. Four clinical types of childhood Asthma. [07]
Ans.
Causes of Wheezing in a child:
Bronchial asthma is a chronic inflammatory airway
disease, resulting in episodic airflow obstruction

(Acute Severe Asthma): When an attack of asthma is prolonged with severe

intractable wheezing, it is known as acute severe asthma.

Humidified oxygen inhalation.

Nebulized β2-adrenergic agonist (salbutamol 5mg/ terbutaline 10 mg) + anticholinergic agent
(ipratropium bromide 0.5 mg). Salbutamol/terbutaline 0.4 mg i.m./s.c. may be added, since inhaled
drug may not reach smaller bronchi due to severe nar-rowing/ plugging with secretions
Systemic Glucocorticoids: Hydrocortisone 200 mg IV stat followed by 100 mg 6th hourly
(or)
Oral Prednisolone 30-60 mg/day depending on the patient’s condition.
IV Fluids to correct dehydration
K+ supplements to correct hypokalemia caused due to repeated doses of salbutamol/terbutaline.
Sodium bicarbonate to treat acidosis
Intubation and mechanical ventilation, if needed
Antibiotics to treat infection (since Upper respiratory tract infection is the most common precipitant of status asthmaticus).

NSAIDs like aspirin, ibuprofen, diclofenac, etc. (Paracetamol can be used).

β- Adrenergic blockers.
Cholinergic agents.
----------------------------------------------------------------------------------------------------------------------------------------
3. Acute upper respiratory infection in a child – etiology, C/F & Mx. [10]
a. Causes of Acute respiratory insufficiency and management. [09]
b. Case Management Plan of Acute Respiratory Infections (ARI) in ARI Control Programme. [07]
Ans.
ARI Control Programme: Govt. of India started – 1990; Now it’s a part of IMCI; Crux of the program is
to diagnose and treat children with symptoms and signs of ARI at the community level by training the
field workers & early referral if needed.
Causes of Acute respiratory insufficiency:

Management plans of Acute Respiratory Infections as

per ARI: 👇🏻
----------------------------------------------------------------------------------------------------------------------------------------

1. Clinical features and management of Croup. [21, 09]

Ans.
Croup {aka Acute laryngotracheobronchitis} is an inflammatory condition of the larynx, trachea and
bronchi
AETIOLOGY: To begin with, it is viral in origin (parainfluenza type I and II) but soon bacterial (G+ve)
invasion takes place. Male children are more often affected
PATHOLOGY: The loose areolar tissue in the subglottic region swells up and causes respiratory
obstruction and stridor. This, coupled with thick tenacious secretions and crusts, may completely
occlude the airway.
CLINICAL FEATURES
o Disease starts as upper respiratory infection with hoarseness and croupy cough + mild fever.
o This may be followed by difficulty in breathing and inspiratory type of stridor.
o The characteristic “Barking” cough
o Steeple Sign on AP view of Neck X-Ray – {subglottic tracheal narrowing produces the shape of a
church steeple within the trachea itself}
TREATMENT
1) Hospitalisation – Administer inhalation anaesthesia (sevoflurane) and oxygen to the patient, secure
i.v. line and then perform laryngoscopy to make the diagnosis. Take laryngeal swabs for culture and
sensitivity tests and intubate the patient.
2) Antibiotics like ampicillin are effective against secondary bacterial infections.
3) Humidification helps to soften crusts and tenacious secretions which block tracheobronchial tree.
4) Parenteral fluids – to combat dehydration.
5) Steroids, e.g., hydrocortisone 100 mg i.v. may be useful to relieve oedema.
6) Racemic adrenaline administered via a respirator is a bronchodilator and may relieve dyspnoea
7) Tracheostomy is done if intubation is required beyond 72 h.
----------------------------------------------------------------------------------------------------------------------------------------
2. Bronchiolitis – Etiology, clinical features & treatment. [20, 14, 13, 12, 04]
a. Acute Bronchiolitis. [10]
b. Causes of acute viral bronchiolitis. [06]
Ans.
Bronchiolitis is inflammation and narrowing of bronchial tree,
secondary to acute lower respiratory tract infection
:
 H/o upper respiratory tract infection. Fever is mostly low grade (38.5–39°C)
 Fast breathing and oral intake are the typical presenting complaints.
 Severe cases may present with irritability, dyspnea and cyanosis.
 On examination – signs of respiratory distress seen  tachypnea, usage of accessory muscles,
respiratory effort indicated by nasal flaring, tracheal tugging, subcostal & intercostal retractions
 On auscultation – fine crackles or overt wheezes, with prolongation of the expiratory phase.
 Severe obstruction to airflow can increase the severity of wheezing  impending respiratory
failure
 Systemic symptoms are usually absent
: Foreign body aspiration; GERD; Congenital malformation of respiratory tract—
{Vascular rings, Bronchomalacia}
:
Hospitalize & start humidified oxygen + Frequent nasal & oral suctioning relieves upper respiratory
obstruction
Nebulization with hypertonic 3% saline and racemic epinephrine
Bronchodilators in severe cases
Antiviral Therapy: Aerosolized Ribavirin
IV fluids to maintain hydration {avoid oral fluids – risk of aspiration}
In cases of Respiratory failure - CPAP or assisted ventilation
----------------------------------------------------------------------------------------------------------------------------------------
3. Outline drug treatment of childhood tuberculosis as per Revised National Tuberculosis Control
Program. [17]
Ans.

---------------------------------------------------------------------------------------------------------------------------------------
4. Primary complex. [04]
Ans
 It is seen in TB which is a chronic granulomatous disease
 Primary complex – aka Ghon complex denotes the healing of Ghon focus {gray-white lesion with
cheesy white appearing center} in cases of Primary Pulmonary TB who have Good Cell Mediated
Immunity.
 Site: Lungs (Upper lobe - Lower part; Lower lobe – Upper part)
 Ghon complex = Ghon focus + lymphadenopathy
 Ghon complex undergoes progressive fibrosis, followed by radiologically detectable calcification
(Ranke complex)
----------------------------------------------------------------------------------------------------------------------------------------
5. Causes of recurrent respiratory tract infection. [03]
Ans.

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1. Mantoux Test & it’s Interpretation [21, 09, 05]

a. Interpretation of Tuberculin test. [15]
Ans.
{Mantoux test}: PPD (Purified protein derivative antigen): It is a purified preparation of
the active tuberculoprotein
 0.1 mL of PPD containing 1 TU is injected intradermally into flexor surface of forearm. [TU= Tuberculin Unit].
 Reading is taken after 48-72 hours. At the site of inoculation, an induration surrounded by
erythema is produced. If the width of the induration is:
a. ≥ 10 mm: Positive.
b. 6-9 mm: Equivocal/doubtful reaction
c. < 5 mm: -ve.
 Interpretation of Result:
▪ +ve in adults: indicates present/past exposure to TB bacilli
▪ +ve in children → indicates active infection and used as diagnostic marker
▪ False-positive: after – BCG vaccination & NTM infection
▪ False-negative in early or advanced TB, miliary TB, decreased immunity (HIV-infected people)
----------------------------------------------------------------------------------------------------------------------------------------
2. Define tachypnoea as used in ARI programme. [04]
Ans.
1) What are the causes of Proteinuria in a child? How do you manage a child with Nephrotic
Syndrome? [19, 15, 12, 11, 10]
a. Complications of Nephrotic Syndrome [20]
b. Treatment of Freshly diagnosed Nephrotic Syndrome in a child of 15 kg body weight
[18]
c. Pathogenesis, Dx & Mx of Minimal Lesion Idiopathic Nephrotic Syndrome [17, 05]
d. Specific Mx of Nephrotic Syndrome [03]
Ans.
Cause of Proteinuria: 👉🏻
is a glomerular disease characterised
by the classic tetrad of findings: (>
3.5g/day or > 4mg/kg/hr in child), ,

 Peripheral edema – Initially it is noted in the dependent areas such as the lower extremities, but
later becomes generalized. Early morning facial puffiness is seen in most patients
 Dyspnea – due to pulmonary edema and pleural effusion.
 Ascites may be present.
 Patients are more prone to infection due to loss of immunoglobulins and complements in the
urine.
 Patients also have hypercoagulable state due to urinary losses of antithrombin III, protein C,
protein S. and increased platelet activation. Patients are prone to renal vein thrombosis and other
venous thrombo-emboli.
 Microcytic hypochromic anemia may result from loss of transferrin in the urine.
 Vit D deficiency may result from loss of cholecalciferol binding protein.
 : 👉🏻

 Urine analysis – shows heavy proteinuria + hematuria

 Serum albumin – low (<3 g/dl)
 Serum anticoagulants and complement – decreased.
 Blood sugar and glycosylated hemoglobin – to r/o
diabetes
 ANA & ANCA – to r/o collagen vascular disease &
vasculitis
 Total cholesterol and LDL-cholesterol – Increased
 Urea & Creatinine – may be elevated if there is renal
failure

Protein Loss – replace with  dietary intake; ACEI & ARBs will also help to  proteinuria.
Edema – dietary salt + thiazide and loop diuretics.
Hyperlipidemia – Exercise + Dietary modification + Statins.
Hypercoagulable State – Start Anticoagulation therapy at least 3-6 months
Treatment of the Underlying Cause – Example:
 Minimal change disease responds to steroids.
 Membranous nephropathy responds to alternating monthly corticosteroids and monthly oral
chlorambucil over 6 months.
:
❖ Coronary atherosclerosis (due to Hyperlipidemia)
❖ Infections: esp. staphylococci and pneumococci due to loss of immunoglobulins in the urine.
❖ Loss of Complements (esp. C3b) → ↑risk of pneumococcal infections
❖ Loss of Transferrin → Fe Def. anemia
❖ Thrombotic complications: due to loss of endogenous anticoagulants (e.g., antithrombin III) in the
urine.
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1. Nocturnal enuresis [19, 18, 16, 12, 10]

a. Causes, types and treatment of Enuresis [15]
Ans.
Involuntary urination is referred to as enuresis.
Classification of enuresis:
 Primary (90%) and secondary
 Nocturnal and diurnal (while awake)
: Involuntary voiding in the night beyond the age of 5 years
(Primary) or loss of acquired urinary continence after at least 3 months of dryness (Secondary).
:
 Genetic – Family history is positive in 50 % cases
 Approximately 60% cases occur in boys
 Psychological factors; Giggle and stress incontinence;  bladder irritability;
 Organic causes—spina bifida, ectopic ureter
 Polyuria; Micturition deferral (waiting till last minute to pass urine)
— UTI; Diabetes insipidus; Diabetes mellitus; Worm infestations etc.
– Combined approach
Reassure parents – Most cases resolve spontaneously with age
Rule out secondary causes (UTI, DM, diabetes insipidus)
Conditioning therapy—Alarm therapy (treatment of choice)
Motivational therapy – star chart; rewarding (positive re-enforcements)
General measures:
▪ No punishment
▪ Child should void before retiring to bed
▪ No fluids for 1–2 h before going to bed
▪ Thick clothes to cover urinary area
▪ Bladder strengthening exercises
Pharmacological treatment – Second line treatment
 Oral desmopressin – DOC
 Oxybutynin – for Age >6 years
 Other Drugs: Imipramine; Tolterodine
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2. Complications & Mx of acute glomerulonephritis [19, 11, 04]
a. Urinary findings in post- streptococcal acute glomerulonephritis [12]
b. Life threatening complications of Acute Post Streptococcal glomerulonephritis [08]
Ans.
Acute glomerulonephritis/Acute Nephritis/Acute nephritic syndrome is characterized by rapid onset
hematuria, proteinuria, associated with hypertension, edema and renal insufficiency.
 MCC is Postinfectious GN in children
 Complications:
 Management:
Urine analysis reveals dysmorphic RBC cells,
RBC cast, polymorphonuclear leukocytes and
proteinuria
(Investigations same as Nephrotic Syndrome)
Evidence of prior streptococcal infection required for confirming diagnosis - ASO & Anti-DNase

▪ Diet – avoid sodium, fluids, protein & potassium diet

▪ Daily weight monitoring & Fluid restriction {Hypervolemia  worsen hypertension  left ventricular failure
 precipitate pulmonary edema}
▪ Diuretics – Furosemide (2–4 mg/kg) in presence of pulmonary edema
▪ For HTN – give Antihypertensives {beta blockers, ACE inhibitors and nifedipine}
▪ In cases of Left ventricular failure – IV furosemide + Urgent dialysis
▪ Systemic Antibiotics: Penicillin course for 10 days to limit the spread of nephritogenic strains
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3. Mx of acute renal failure [15, 10]
Ans.
Sudden worsening in kidney function resulting in the inability to maintain fluid & electrolyte
homeostasis is referred to as ARF
Investigations:
» Urine analysis: {Urine microscopy in acute renal failure}
 Urine is acellular – Pre-renal AKI
 Pigmented "muddy brown" granular casts &
casts containing tubule epithelial cells are
characteristic of ATN {Renal AKI}
 RBC casts – Glomerular injury
 Abundant uric acid crystals – acute urate
nephropathy
 Hemoglobinuria or myoglobinuria – Renal
failure due to hemolysis & rhabdomyolysis.
 Eosinophiluria – Allergic interstitial nephritis
» Renal ultrasound – to detect hydronephrosis
» Coagulation profile
» Renal biopsy
» CT angiography
Management 👉🏻
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4. Approach to child with hematuria [14]
a. Causes of hematuria [09]
Ans.

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5. Clinical features and Dx of Urinary Tract Infection (UTI) in infancy and childhood [13, 05]
Ans.
– depends on age & severity:
 In neonates: Sepsis with
fever, vomiting, diarrhea,
Jaundice, Poor weight gain
and lethargy
 In older children:
Unexplained fever;
Frequency and urgency of
micturition; Foul smelling
urine & Hypogastric pain
Diagnosis of UTI:
 Gold standard test: Urine Culture – Clean catch sample showing > 105 CFU/mL is considered as
significant bacteriuria
 Asymptomatic bacteriuria—Absence of symptoms with significant bacteriuria
 Imaging studies (Ultrasound, DMSA, micturating cystourethrogram) are indicated in first episode of
culture positive UTI under the age of 1 year and recurrent UTI in older children
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1) Enumerate causes of Anasarca [15]

Ans.

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2) Side effects of steroid therapy [14, 08]
Ans.
Steroid toxicity—
Cushingoid facies
Fluid retention
Hypokalemia SHOCSi
Hypertension
Gastritis
Infections – due to immune-suppression and
Osteoporosis
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3) Name the complications of renal failure [12]
Ans.

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4) Furosemide [12]
Ans. It is a Loop Diuretic (High-Ceiling Diuretic)
:
 Edema: During the initial stages of renal, hepatic and cardiac oedema, loop diuretics are
preferred. Loop diuretics can also be used in cerebral oedema but i.v. mannitol is the preferred drug
 IV furosemide, along with isotonic saline (to prevent volume depletion), is used in
Hypercalcaemia as it promotes the excretion of Ca2+ in urine.
 Acute pulmonary oedema
 Hypertension: a/w CCF/renal failure and in hypertensive emergencies. Furosemide is not preferred in
uncomplicated primary hypertension because of its short duration of action
 To prevent volume overload, furosemide is administered during blood transfusion
:
➢ Electrolyte disturbances: due to excretion of Na, K, Ca & Mg in urine
 Hypokalemia
 Hyponatremia
 Hypocalcemia
 Hypomagnesaemia – can predispose to arrythmias
➢ Metabolic disturbances:
 Hyperglycaemia {due to insulin secretion}
 Hyperuricaemia {due to  renal excretion of uric acid} – may precipitate attack of gout
 Hyperlipidemia: {due to  plasma triglycerides and LDL cholesterol}
➢ Ototoxicity: manifests as deafness, vertigo and tinnitus and is due to damage to hair cells in inner ear. The
symptoms are usually reversible on stoppage of therapy.
➢ Hypersensitivity – Skin rashes, eosinophilia, photosensitivity, etc. may occur
➢ Diuretics should be avoided in Pregnancy as they  placental perfusion by  blood volume which can cause
fetal death.
1. How do you classify Anaemia in children? Describe Iron deficiency Anaemia – causes, C/F, lab
diagnosis, management & preventive strategies. [21, 16, 06]
a. Enumerate the causes of Anaemia in children. [14, 12]
b. Peripheral smear findings in iron deficiency anemia. [10]
c. Peripheral blood smear picture of Nutritional Anemias. [08]
d. Risk factors and diagnosis of Iron deficiency anemia. [06]
Ans.
Anemia is defined as reduced amount of hemoglobin & in oxygen carrying capacity of RBCs
WHO criteria for diagnosing Anemia (Hemoglobin cut off below which a person is anaemic)
 Children 6 months–5 years < 11 gm/dL
 Children 6–14 years < 12 gm/dL

:
Fatigue, pallor; Alopecia, koilonychia; Pica; Plummer-Vinson
syndrome
IDA also impairs cognitive abilities and can affect mental,
social and emotional development
 As iron is a cofactor for many enzymes in cellular metabolic pathways, IDA can depress immunity
and predispose to secondary infections.
:
:
Hemoglobin, hematocrit (PCV) & Reticulocyte count: decreased
↓ in MCV, MCH & MCHC; ↑ In RDW
RBCs: microcytic, hypochromic, ring/pessary cells, anisocytosis & poikilocytosis (pencil/cigar
shaped cells).
WBCs & Platelets: Normal
Serum Iron Profile:
▪ Reduced: Serum iron, ferritin
& % transferrin saturation
▪ Increased: TIBC, TFR
(transferrin receptor) and red
cell protoporphyrin.
BM Findings
Cellularity: Moderately
hypercellular
M:E ratio: varies from 2:1 to 1:2 (normal 2:1 to 4:1).
Erythropoiesis: Hyperplasia and micronormoblastic maturation.
Myelopoiesis & Megakaryopoiesis: Normal
Absence of bone marrow iron: “Gold standard” test, demonstrated by ve Prussian blue reaction.

 Identify & treat the cause

 Dietary counselling
 Oral therapy – Ferrous sulfate on empty stomach is most effective and started at 3–6 mg/kg/ day
in 3 divided doses for 4–6 months.
Side-effects: Nausea, vomiting, diarrhea, constipation, abdominal cramps, staining of teeth and
tongue and discoloration of stools
 Parenteral therapy {in cases of intolerance to oral iron} – IV iron sucrose is safe and effective.
 Blood transfusions – rarely needed – Ex: severe anemia with congestive cardiac failure
:
Exclusive breastfeeding for 6 months
Timely introduction of complementary feeding at 6 months
Iron supplementation for preterm/ LBW infants from 2 months
Restrict cow’s milk consumption
Intake of green leafy vegetables and sprouting green grams
Periodic deworming in endemic areas
Iron supplements for susceptible infants and children and at puberty, especially in girls
National Nutritional Anemia Control Program recommends 20 mg of iron and 100 µg of folic acid
daily for 100 days every year
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2. Beta Thalassaemia – Etiopathogenesis, clinical features and management [05]
a. Peripheral blood smear findings of a child with Thalassemia major. [18]
Ans.
β-Thalassaemia is an Inherited disorder
which occurs due to mutations impairing
the synthesis of β-chains of globin.
β globin gene is present on
chromosome 11
:
 Absence of β-globin chain →
absence of synthesis of HbA
→microcytic hypochromic RBC
 Unpaired and excess α-chains
aggregate into insoluble
precipitates → bind to and
damage the membrane of
erythroid precursors → erythroid
precursors fail to mature → Marked erythroid hyperplasia in the bone Marrow.
 Extravascular hemolysis: RBCs with β-chain inclusions are removed by macrophages of spleen.
 γ globin chain synthesis continues even 6 months after birth and combines with α-globin →
↑↑ HbF.
 Extramedullary hematopoiesis: in liver and spleen → hepatosplenomegaly.
 Expansion of marrow may cause erosion of existing cortical bone & subsequent new bone
formation. In the bones of the face & skull, this gives rise to Hair on end (“crew-cut”)
appearance on x-ray.
:
Age: Infants develop moderate to severe anemia {severe pallor} 6-9 months after birth.
Icterus - due to iron overload and liver dysfunction
Bone changes: Distortion of skull and facial bones  Thalassemic facies & malocclusion of the jaw.
Thalassemic (chipmunk face) facies—prominent forehead, cheekbones & upper jaw; Depressed
nasal bridges
Hepatosplenomegaly
Cachexia in severe cases
:
Peripheral Blood Smear
RBCs – Microcytic hypochromic anemia; Many
target cells; Anisopoikilocytosis; Basophilic
stippling; Nucleated red cell precursors
(normoblasts)
WBCs: Leukocytosis with mild left shift
Platelets: Normal
Serum haptoglobin - 
X-ray skull shows hair on end appearance
Hb electrophoresis - HbF 👉🏻
HPLC – used for confirmation of Diagnosis
:
Correction of anemia—packed red cell transfusions
Hydroxyurea—15–20 mg/kg /day used to HbF and
reduce need for blood transfusion in other thalassemic
states
 Future treatment—Gene replacement therapy, intrauterine BMT
Management of Complications like:
Iron overload—treated with chelation therapy with Desferrioxamine
Blood transfusion related reactions and infections {Hep B, Hep C, HIV, malaria, CMV etc.}
Hypersplenism – splenectomy
Osteoporosis; osteopenia; Gall stones
Extramedullary hematopoiesis
Psychological complications
Prevention of disease by antenatal diagnosis and genetic counselling
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3. How do you investigate and manage ABO hemolytic disease of newborn? [03]
a. Rh iso-immunization – Prevention & Investigative workup of cord blood at birth. [07]
Ans.

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1. Treatment of acute immune thrombocytopenic purpura. [20, 13]

a. Immune thrombocytopenic purpura – Etiology, Clinical features & management [05]
Ans.

Immune thrombocytopenic purpura (aka Idiopathic Thrombocytopenic Purpura) (ITP)

– occurs due to Autoantibody mediated destruction of platelets causing thrombocytopenia.
Sex: F>M
Etiology: Primary or secondary.
 Primary or idiopathic: No known risk factors.
 Secondary: Seen with SLE, HIV or CLL.
Pathogenesis:
 Production of autoantibodies (IgG) against platelet
membrane glycoproteins IIb-IIIa or Ib-IX.
 Autoantibody coated platelets are phagocytosed and
destroyed in spleen.
C/P: Bleeding manifestations such as petechiae, ecchymoses; Easy bruising, nosebleeds, and bleeding
from gums; Melena, hematuria or excessive menstrual flow.
Diagnosis:
Peripheral smear: Low platelet count with large platelets (megathrombocytes).
Bone marrow: raised megakaryocytes.
PT & PTT: Normal
Tests for platelet autoantibodies.
Complications: Subarachnoid hemorrhage & intracerebral hemorrhage.
Management
Children with active bleeding should be given IV immunoglobulin 1 g/kg/day for 1–2 days
Prednisolone 1–4 mg/kg/day for 2–4 weeks then tapered
Dexamethasone at 20 mg/m2 over 4 days every 3 weeks for 4–6 courses.
Routine Platelet transfusion should be avoided {done only in serious hemorrhages}
Refractory cases—immunosuppressive drugs like vincristine, cyclosporine, azathioprine, rituximab
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2. Classify Hemolytic anaemias and how do you manage hemolytic anemias. [15, 11]
a. Peripheral smear picture in common hemolytic anaemias. [06]
Ans.

Investigations of Hemolytic anemias:

Fall in Hb
Signs of Fall in Haptoglobin (seen in intravascular hemolysis)
erythrocyte Increased unconjugated bilirubin in blood
destruction Increased stercobilinogen in stool causing dark-colored stool
Increased urobilinogen in urine leading to high-colored urine
Peripheral
Signs of  Reticulocyte count; nucleated red cells; Large RBCs
Blood
erythropoiesis
Bone Marrow Erythroid hyperplasia; iron stores (because of iron released from heme
after hemolysis).
 In Peripheral smear - spherocyte, sickle cell, target cell, acanthocyte, malarial
Specific to
parasite, Bite cells {in G6PD deficiency} etc.
etiology
 Coomb’s test
Management of Hemolytic anemias:
Maintain fluid balance and renal output during and after hemolysis
Blood transfusions – In acute anemia
Transfused RBCs can also undergo hemolysis if pathology persists.
Autoimmune hemolytic anemia (AIHA) is treated with corticosteroids (prednisolone 1–2
mg/kg/day) and tapered over months after hemolysis has resolved
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3. Thrombocytopenia – Causes & Clinical features. [13, 10]
Ans.

Clinical Features – Bleeding manifestations such as petechiae, ecchymoses; Easy bruising, nosebleeds,
and bleeding from gums; Melena, hematuria or excessive menstrual flow
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4. Hemophilia A. [09]
Ans.
It is the MC hereditary cause of serious bleeding with an abnormality of the intrinsic coagulation
pathway
Cause: Sporadic or germ line mutations causing factor VIII deficiency
Inheritance of the Disease:
▪ X-linked recessive disease.
▪ Genes for factor VIII are located on the long arm of the X-chromosome.
▪ Males with a defective factor VIII gene (hemophiliac gene) on their single X chromosome (X H)
suffer from hemophilia.
▪ Heterozygous females are carriers and do not express the full clinical disease because of the paired
normal X-chromosome.
Genetic alterations: deletions, inversions, point mutations and insertions
Clinical Presentation:
1) Easy bruising, massive hemorrhage after trauma or operative procedures.
2) Spontaneous bleeding into joints (hemarthrosis).
Differential Diagnosis: Hemophilia B; Von Willebrand disease
Lab Investigations to confirm Dx
Bleeding time: Normal
Clotting time: ↑
Platelet count: Normal
 Prothrombin time: Normal
Activated partial thromboplastin time (APTT): ↑ (normal 30–40 seconds)
Factor VIII assay: ↓; Essential for the Dx & to assess the severity of disease {Normal range for factor VIII:
45–158 IU/dL}

Fibrinogen assay: Normal

FDP: Negative
Detection of carriers: By DNA markers
Complications due to Hemophilia: Anemia, intramuscular hematomas & Joint deformities
Management
 Appropriate factor replacement; Gene therapy
 Physiotherapy to prevent chronic joint disease
 Counselling for injury prevention
 Desmopressin, synthetic analogue of vasopressin – induce factor VIII levels and is tried in mild cases
 Acute bleeds should be treated early (within 2 h if possible) – via Cryoprecipitate & fresh frozen
plasma {Cryoprecipitate doesn’t contain factor IX so it cannot be used in hemophilia B}
 Avoid IM injection & arterial puncture
Complications following the therapy
 Viral hepatitis: Hepatitis B, C & D in patients who received multiple transfusions of
FFP/cryoprecipitate.
 AIDS: In individuals who received fresh frozen plasma (FFP) or cryoprecipitate, when screening
tests for HIV were not available
 Development of antibodies against factor VIII, following infusions of recombinant factor VIII makes
further management difficult.
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1. Peripheral smear in Megaloblastic anaemia. [19]

Ans.
Peripheral Blood
Hb & PCV Reduced
Red cell
↑ MCV; ↑ MCH & normal MCHC
indices:
Normal. High reticulocyte count is
Reticulocyte
seen on 7th day following vitamin
count
B12 therapy
Peripheral
Pancytopenia
smear
 Macrocytic and oval (egg-
shaped macro-ovalocytes)
 Lack central pallor
RBCs  Anisopoikilocytosis
 Evidence of dyserythropoiesis:
Basophilic stippling, Cabot ring
and Howell Jolly bodies
leukopenia & Hyper segmented
WBCs
neutrophils
Platelets ↓↓

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2. Peripheral smear findings in acute lymphatic Leukemia. [11]
Ans.

Peripheral Blood in ALL

Hb Reduced
Total WBC Markedly raised, ranging from
Count: 20 × 109/L to 200 × 109/L
Peripheral smear
RBCs Normocytic normochromic type of anemia
  Total WBC count
 Differential count: More than 20%
lymphoblasts.
 Morphology of lymphoblasts:
 larger than lymphocyte.
WBCs
 High N:C ratio
 Nucleus with condensed chromatin and
nucleoli are either absent or
inconspicuous.
Scant agranular basophilic cytoplasm
Platelets ↓↓
1) A one and half year-old child is brought to the emergency department with h/o loose motion and
vomiting for 3 days. His weight is 7 kg
Tabulate signs of mild and some dehydration as per WHO integrated management of neonatal
and Childhood illness guidelines
Outline management of dehydration in the above child [17]
a. Severe dehydration in a 2-year-old child. [21]
b. Management of acute watery diarrhea. [16]
c. Principles and management of dehydration. [12, 10]
d. A nine-month-old infant presents with acute watery diarrhea – causes, complications & Mx [09]
e. Triaging & Mx of Diarrhoeal dehydration. [07]
f. Clinical features of severe diarrhoeal dehydration and its management. [06]
g. Management of severe dehydration (plan C in DTTU management). [05]

Ans. – Definition: Change in consistency and frequency of stools;

Liquid or watery stools occurring > 3 times a day, without any visible blood & Persisting for < 14 days
Signs of Dehydration: thirst and irritability; Sunken eyes; Dry tongue; Depressed fontanelle if open;
Delayed Skin pinch test; Passing urine at longer intervals
Principles of management
1) Rehydration and maintaining good hydration
2) Ensure adequate feeding
3) Oral supplementation of zinc and probiotics
4) Early recognition of danger signs and treatment of complications

 Can be treated at home

Plan A  Ask the mother to Give more fluids & continue breastfeed
 Bring the child back in case of danger signs
▪ Provide daily requirement of Fluids
▪ 75 mL/kg of ORS given over 4 hours and child is
Plan B
reassessed  successful  treat as NO dehydration
▪ If ORT is not successful then treat as severe dehydration
 Rehydrate the child with IV fluids {Ringer lactate is preferred}
 Total of 100 mL/kg of fluid bolus is given as:
Plan C
1) Infants < 1 year—30 mL/kg body weight within first 1 hour, followed by 70 mL/kg
body weight over next 5 hours
 2) Older children > 1 year—30 mL/kg body weight within half an hour, followed by
70 mL/kg body weight over next 2.5 hours
 Child is monitored every 15–30 min for pulses, blood pressure, urine output and
hydration status
 After bolus the child should be reassessed:
 Persistence of dehydration—repeat IV infusion
 Hydration improved but some dehydration is present—discontinue iv fluids, ORS
given as in plan B
 No dehydration—discontinue iv fluids, treatment plan A is followed
:
Promote Early feeding – it  stool volume and prevents malnutrition; Avoid Fiber rich diet
Breastfeeding should be continued –  risk of persistent diarrhea
During recovery, at least 125% of RDA of nutrients should be supplemented
– Zinc is given as sulphate or acetate or gluconate at a dose of 20 mg/kg/day
for children > 6 months and 10 mg/kg for infants < 6 months for 14 days.
Acute Diarrhea are self-limiting in most of the cases and does not require any routine antibiotics
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1. Diagnosis and management of Typhoid {Enteric} fever. [19, 16, 15, 12]
a. Typhoid vaccine - types, dose schedule and age of vaccination [17]
b. Choice of antibiotics for treatment of multidrug resistant typhoid fever. [07]
Ans. Enteric fever, was also called as Typhoid, is a systemic infection caused by Salmonella typhi or
paratyphi A & B (aka Eberthella typhi).
Clinical Features:
» Step ladder pattern of Fever – a/w headache, myalgia
st
1 week » GI upset – Constipation {due to swelling of lymphoid tissue around ileocecal junction} is
followed by Diarrhea {“pea soup” appearance of stools}, vomiting
• Rose spots on trunk
• Abdominal distension, Hepatosplenomegaly & mild jaundice
End of 1st week
• GI upset
• Bronchitis, Cough and epistaxis occur
End of 2nd Week Complications, delirium, coma & death (if untreated)
Investigations:
Treatment:
– Prevention & Control:
Proper sanitation practices – hand washing techniques & safe disposal of excreta
Safe and clean drinking water & food hygiene practices
Health education for endemic areas Vaccine Age & Dose
Vaccines for typhoid – for people traveling to >5 yrs & ORAL
1. Ty21a
3 doses: 1,3,5 days
endemic area or in contact with case/carrier.
>1 yr. & SC/I.M (0.5ml)
2. ViCPS
dose
DOC – Fluoroquinolone >5yrs & Parenteral
3. Vi-rEPA
Case of MDR – Azithromycin 1g OD for 7 days doses
Case of Quinolone resistance – Ceftriaxone 1-2g iv/i.m.
for 10 days
Paracetamol for fever, headache & myalgia
 Severe case of typhoid – Dexamethasone
 Chronic carrier – Antibiotic therapy for 6 weeks [Ampicillin + Probenecid]
Ideal management for carrier: Cholecystectomy + Ampicillin
 Supportive measures – good nutrition & hydration
 Disinfection protocol: 5% cresol x 2 hours
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2. Causes of hepatosplenomegaly in a 8 month old child. [10]
Ans.

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1. Oral rehydration solution (ORS). [21]

Ans.

The aim of oral fluid therapy is to prevent dehydration & reduce mortality
Oral fluid therapy is based on the observation that glucose given orally ↑the intestinal absorption
of salt and water, and is capable of correcting the electrolyte and water deficit.
Indications of ORS: To treat acute diarrhoeas due to all aetiologies, in all age groups, and in all
countries.
 Composition of ORS:
Inclusion of trisodium citrate in place of sodium bicarbonate made
the product more stable and it resulted in less stool output
especially in high-output diarrhoea as in cholera, probably because
of direct effect of trisodium citrate in increasing intestinal
absorption of sodium and water
If the WHO mixture of salts is not available, then: a simple
mixture consisting of table salt (1 level teaspoon) and
sugar (6 level teaspoon) dissolved in 1 litre of drinking
water may be safely used until the proper mixture is
obtained.
The earlier the treatment is instituted the better it is for
the patient
Advantages of ORS: The introduction of oral rehydration fluid has not only reduced the cost of
treatment, but also made possible treatment of patients in their own homes by primary health
workers or relatives of patient
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2. Mention four causes of constipation in children. [13]
Ans.

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3. Composition of super ORS. [03]
Ans.
1) A 2 years old child is brought to the paediatric Out patient department with history of fever and
maculopapular rashes all over the body for last 3 day
 List important causes of the above condition
 Briefly write C/F, complications and prevention of Measles. [16, 15, 09, 06]
 MMR vaccine. [20] Measles Vaccine. [14]
 Neurological complications of Measles. [10, 07]
Ans.
Etiology of Measle
 Causative Agent: Measles is
caused by an RNA
paramyxovirus.
 Infective material: Secretions of the nose, throat and respiratory tract of a case of measles during
the prodromal period and the early stages of the rash.
 Period of Communicability: 4 days before and 4 days after the appearance of the rash.
 Incubation period: 10 days from exposure to onset of fever, and 14 days to appearance of rash
Clinical features There are 3 stages in the natural history of measles,
– fever, nasal discharge, Koplik’s spots {seen 2 days after the onset
of fever} on buccal mucosa etc.👉🏻
– maculopapular rash.
 Rash starts behind the ears, then spreads to face, trunk, extremities, palms & soles
 The rash starts disappearing after 4-5 days in the same order in which it appeared.
- The child will have lost weight, growth retardation etc.
Measles tends to be very severe in the malnourished child
Epidemics of measles are common in India during winter and
early spring (January to April).
Complications – mainly seen in malnourished and
immunocompromised children 👉🏻
Treatment: No specific antiviral; Entirely supportive therapy
 Antipyretic for fever
 Adequate fluids
 Bed Rest
 Treatment of complications—e.g., Antibiotics if bronchopneumonia or otitis media

Prevention and Control of measles

Measles vaccination (Active Immunisation) – Only live attenuated vaccines are recommended for use;
The vaccine is presented as a freeze-dried product & is sensitive to sunlight
Indications: At the age of 9 months; (can be lowered to 6 months if there is measles outbreak in the
community)
Route of administration: single subcutaneous dose of 0.5 ml
Side Effects: mild '"measles" illness (fever and rash) 5 to 10 days after immunization;
Toxic shock syndrome (TSS) can occur when measles vaccine is contaminated
 Immunity –appears to be of long duration, probably for life.
Contraindications: pregnant women, People with a history of an anaphylactic reaction to the
vaccine, persons who are severely immunocompromised etc.
COMBINED VACCINE: Measles vaccine can be combined with other live attenuated vaccines such as
mumps, and rubella vaccines (MMR vaccine), measles, mumps, rubella and varicella (MMRV), and
measles and rubella (MR) , and such combinations are also highly effective.
Immunoglobulin (Passive Immunisation): The dose recommended by WHO is 0.25 ml per kg of body
weight. It should be given within 3- 4 days of exposure.
Eradication of measles - requires achieving an immunization coverage of at least 96 % of children
under one year of age
Outbreak control measures: Isolation for 7 days after onset of rash, Immunization of contacts within 2
days of exposure is essential to limit the spread
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1. Strategies to reduce mother to child transmission of HIV infection. [17]

Ans.
Early Cord Clamping
Education about the disease
Take precautions while using blood/blood products
Screening blood/blood products: Use sterile injection equipment; No sharing of needles by drug
users
Antenatal mothers – check HIV status & start anti-retroviral therapy
For HIV positive women presenting directly in labour:
 Immediate Maternal ART (Tenofovir + Lamivudine + Efavirenz)
 For infant: Daily Nevirapine syrup for 6–12 weeks
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2. List warning signs of Dengue fever. [15]
a. Dengue hemorrhagic fever – etiology, clinical features and management. [05]
Ans.
Dengue fever is an Acute viral infection caused by dengue virus {ssRNA; Flaviviridae}

 Primary dengue infection occurs when a person is infected with dengue virus for the first time
 Secondary dengue infection: a more severe form of dengue may appear due to infection with
another serotype.
 Antibody Response Against
Dengue: 2 types of Abs –
neutralizing and non-
neutralizing antibodies.
» The neutralizing antibodies
neutralize the infective
serotype
» The non-neutralizing
antibodies are produced
following the 1st serotype
infection, can bind to a 2nd
 serotype during secondary dengue infection; but instead of neutralizing, it protects it from immune
system by inhibiting the B cell activation against the 2nd serotype. This phenomenon is called
Antibody Dependent Enhancement (ADE).
» Among all the serotypes combinations, ADE is remarkably observed when serotype 1 infection is
followed by serotype 2.
 The course of dengue illness can be divided into 3 phases – Febrile phase, Critical phase & Recovery
phase.
 : CBP of the patient should be done at 1st visit.
Management of Dengue Fever:
 Give fluids – Ex: ORS with electrolytes & sugar to replace losses from fever and vomiting.
 Give paracetamol for high fever. Tepid sponge if the patient still has high fever. Do not give Aspirin,
Ibuprofen or other NSAIDs as these drugs may aggravate gastritis or bleeding.
 Instruct the care-givers that the patient should be brought to hospital immediately if there is no improvement.
Management of DHF Grade I & II: Hospitalize the patient & Look for signs of shock. Give IV fluid
therapy.
Management of DHF Grade III & IV: same as DHF II + Oxygen should be given to all patients in shock.

Loss of blood (overt blood) ≥ 10 %

Refractory shock despite adequate fluid administration and declining haematocrit.
If fluid overload is present packed cells are to be given.
In case of massive bleeding, Prolonged shock etc.
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3. Diagnosis and management of neonatal Sepsis. [15]
a. Early onset sepsis. [10]
Ans.
Systemic bacterial infections are known by generic term Neonatal sepsis which incorporates
septicemia, pneumonia and meningitis.
Neonatal sepsis is of two types:
:
It is a type of neonatal sepsis in which clinical  72 h or more
symptoms appear less than 72 hrs after birth.  Etiology: caused by the organisms
Etiology: it caused by organisms prevalent in the thriving in the external environment.
maternal genital tract or in the delivery area.  Predisposing factors: LBW; Not
Predisposing factors: LBW; Foul smelling liquor; Breastfed; Use of IV fluids; Superficial
Multiple per vaginal examinations; Maternal Fever etc. infections (pyoderma, umbilical
Clinical Presentation: MC is Pneumonia followed by sepsis)
septicemia & meningitis.  Manifests with vague and ill-defined
Treatment: supportive care & specific antimicrobial symptoms – require high index of
therapy suspicion
Diagnosis of neonatal sepsis:
 Blood culture and other septic screening tests – to start specific antimicrobial therapy
 CRP; ESR
 Lumbar puncture performed in all cases of late onset neonatal sepsis
 PCR
Treatment:
Supportive care:
Provide warmth and ensure normal temperature
 Start oxygen by hood or mask.
Assess peripheral perfusion by palpating peripheral pulses.
 If perfusion is poor, infuse NS or ringer lactate 10ml/ kg over 5-10 min.
 Dopamine and dobutamine may be required to maintain normal perfusion
In hypoglycemia, infuse 10% glucose 2ml/kg stat.
Add potassium to IV fluids once normal flow of urine has been documented
Enteral feeds should be initiated early if there is no
abdominal distension and baby is hemodynamically
stable. Feed mothers’ milk
Administer vitamin K 1mg intramuscularly
Transfuse packed cells, if baby has low hematocrit (less
than 35-40%).
Specific Care:
Antimicrobial therapy constitutes the mainstay of
treatment of sepsis.
In cases of very neonate suspected of sepsis, do not
wait for sensitivity report; start on 👉🏻
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4. Differential diagnosis of acute flaccid paralysis {at least 4 causes}. [17, 12, 09, 04]
Ans.

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5. Clinical features {at least 4} of congenital rubella syndrome. [05, 04]
22
Ans.
The classical triad of congenital rubella syndrome consists of deafness, cataract and congenital
heart disease.
Delayed manifestations such as diabetes mellitus and renal disease can also occur
 Transmissibility is highest in the first trimester; The fetus is completely spared if infection occurs
beyond 16 weeks.
Diagnosis: Demonstrate positive rubella IgM in cord or neonatal blood
No treatment exists
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6. Complications of Chickenpox. [04]
Ans.

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7. Treatment of Pinworm infestation. [03]
Ans.
is also called as pin worm or threadworm.
Prevention: By improving personal hygiene such as proper washing of
bed clothes and hand washing
Treatment: 👉🏻

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1. Mention 4 clinical manifestations of Ascaris Lumbricoides. [21, 14]

Ans.
Affect Due to Migrating Larva
1. Pulmonary symptoms: Migrating larvae in lungs provoke hypersensitivity response. Symptoms
include cough, chest discomfort and fever.
2. Loeffler’s Syndrome: In severe cases, patients develop dyspnea and a transient patchy
infiltrates seen on chest X-ray along with peripheral eosinophilia
Affect Due to Adult worm:
 Asymptomatic
 Malnutrition and growth retardation
 Intestinal complications: small bowel obstruction → Pain, perforation, intussusception, or
volvulus
 Extraintestinal complications: larger worms can enter and occlude the biliary tree → biliary colic,
cholecystitis, pancreatitis, or (rarely) intrahepatic abscesses. Wandering worms may migrate to
pharynx and can cause respiratory obstruction or may block the eustachian tube.
  Allergic manifestations like fever, urticaria, angioneurotic edema and conjunctivitis may occur
due to toxic fluid (ascaron or ascarase) released by the adult worm
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2. Complications of Diphtheria. [12]
Ans.

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3. Clinical features of Malaria. [11]
Ans.
Type of Malaria Periodicity of fever
Paroxysms of fever
Benign tertian malaria every 3rd day
{high grade,
Malignant tertian malaria every 3rd day
intermittent} with
Ovale tertian malaria every 3rd day
paroxysms of fatigue
Benign quartan malaria every 4th day
is classical for malaria
Quotidian malaria recurs every day
 Fever is often accompanied by prodromal features like headache, lethargy, nausea, vomiting,
musculoskeletal pain and rarely diarrhea.
 Classical signs on examination include pallor, jaundice and hepatosplenomegaly
 Features of Severe malaria: Cerebral malaria, Severe shock like state (Algid malaria),
Hemoglobinuria (Black water fever) etc.
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4. 4 reasons why poliomyelitis is globally eradicable. [07]
Ans.
a) Poliovirus causes acute, non-persistent infections
b) People are the only reservoir
c) Virus is transmitted only by infectious people or their waste
d) Immunization with polio vaccine interrupts virus transmission
e) Survival of virus in the environment is finite
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5. 3 microscopic differences between plasmodium vivax and falciparum. [07]
Ans.

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6. Post-exposure prophylaxis of Rabies. [04]
Ans.
Postexposure prophylaxis (PEP) = local wound care + both active and passive immunization.
Local Treatment: clean the wound, scrub with soap and water and apply antiseptics. Bite wounds are not
sutured immediately.
Passive Immunization: Human rabies immune globulin (HRIG) & Equine rabies immunoglobulin (ERIG)
Active Immunization (Rabies Vaccine): 2 types of Vaccines – Neural & non-neural.
 : They are poorly immunogenic and encephalitogenic; hence
not used.
 Cell line derived, they are the recommended vaccine
currently – Ex: Purified Vero cell (PVC) & Human diploid cell (HDC).
National Guideline on Rabies Prophylaxis: Regimens:
Site of Injection:
1) Deltoid region is ideal site. Gluteal region is not recommended because fat retards the
absorption of antigen
2) Infants and young children: Anterolateral part of the thigh is the preferred site
----------------------------------------------------------------------------------------------------------------------------------------
7. Drug therapy of a child with uncomplicated malaria. [04]
Ans.
1) Approach to a child with stridor [16]
Ans.
Stridor is noisy respiration produced by turbulent airflow through
the narrowed air passages. It may be heard during inspiration,
expiration or both.
AETIOLOGY
1. : Choanal atresia in newborn.
2. : Macroglossia due to cretinism, haemangioma, dermoid
at base of tongue, lingual thyroid.
3. : Micrognathia, Pierre-Robin syndrome. Here, stridor
is due to falling back of tongue.
4. : Congenital dermoid, adenotonsillar hypertrophy,
retropharyngeal abscess & tumours.
5. .

Vascular rings, oesophageal

Laryngeal web,
Atresia, stenosis, atresia, tracheo-oesophageal
1) Congenital laryngomalacia, cysts,
tracheomalacia fistula, congenital goitre,
subglottic stenosis
cystic hygroma
Epiglottitis,
Retropharyngeal and Retro-
2) Inflammatory Laryngotracheitis, Tracheobronchitis
oesophageal abscess
Diphtheria, Tuberculosis
Haemangioma, Juvenile
3) Neoplastic multiple papillomas & Tumours of trachea Masses in neck
carcinoma in adults
Injuries of larynx, foreign
Foreign body, stenosis
bodies, oedema following FB oesophagus (secondary
4) Traumatic trachea (e.g., following
endoscopy, or prolonged tracheal compression)
prolonged intubation).
intubation
5) Neurogenic Laryngeal paralysis
MANAGEMENT OF STRIDOR
Clinical Evaluation:
Stridor is a physical sign & not a disease. Attempt should always be made to discover the
cause.
1. Time of onset – To find whether cause is congenital or acquired.
2. Mode of onset – Sudden onset (foreign body, oedema), gradual and progressive (laryngomalacia,
subglottic haemangioma, juvenile papillomas).
3. Duration – Short (foreign body, oedema), long (laryngomalacia, subglottic haemangioma, anomalies
of tongue and jaw).
4. Relation to feeding – Aspiration in laryngeal paralysis, oesophageal atresia, laryngeal cleft, vascular
ring, foreign body oesophagus.
5. Cyanotic spells – Indicate need for airway maintenance.
6. Aspiration or ingestion of a foreign body.
7. Laryngeal trauma – Blunt injuries to larynx, intubation, endoscopy.
 Stridor is always associated with respiratory distress
1) Recession in suprasternal notch, intercostal spaces & epigastrium during inspiratory efforts.
2) Note if stridor is inspiratory, expiratory or biphasic – Indicates the probable site of obstruction.
3) Note associated characteristics of stridor:
a. Snoring or snorting sound → nasal or nasopharyngeal cause.
b. Gurgling sound and muffled voice → pharyngeal cause.
c. Hoarse cry or voice → laryngeal cause.
4) A/w fever indicates infective condition, e.g., acute laryngitis, epiglottitis, diphtheria etc.
5) Stridor of laryngomalacia, micrognathia & macroglossia – disappears when baby lies in prone
position.
6) Sequential auscultation with stethoscope over the nose, open mouth, neck and the chest help to
localize the probable site of origin of stridor.
7) In adults, indirect laryngoscopy can be done easily while infants and children require flexible
fibreoptic laryngoscopy.
Investigations – History and clinical examination will dictate the type of tests required
X-ray lateral and PA view of neck & chest help in diagnosing the foreign bodies of the airway.
CT scan with contrast – to rule out congenital vascular anomalies compressing the trachea or bronchi, e.g., anomalous
innominate artery, double aortic arch etc.
Oesophagogram with contrast – to rule out tracheobronchial fistula, oesophageal atresia et.
Direct laryngoscopy & bronchoscopy:
Done in OT under general anaesthesia with full preparation tp deal with respiratory distress.
After a quick direct laryngoscopy, bronchoscope is inserted to examine the air passage from the
subglottis to bronchi for any obstruction.
Secretions can be collected for culture and sensitivity.
Crusts and foreign body, if any, can be removed.
Treatment: Once the diagnosis has been made, treatment of exact cause can be planned.
1. Pneumococcal vaccine – types, indications and dosage schedule. [21, 18, 16]
Ans.
Pneumococcal vaccine – 2 types:
–
Min. age 6 weeks
Indications: 👉🏻
Dosage Schedule: 👇🏻

Single dose can be administered (6-18 years of age) in children with asplenia, cochlear implant,
CSF leak etc.
– Min. age 2 years; not routinely used
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2. National Immunization Schedule. [21, 19, 12]
Ans.

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3. DPT vaccine. [14, 13]
Ans.
is combined vaccine – it consists of (diphtheria toxoid}, (Whole cell} and (tetanus toxoid}
Diphtheria toxoid is used for vaccination.
Pertussis component (in DPT) acts as adjuvant
Administration of DPT:
 : 5 doses →
 : IM at anterolateral aspect of thigh, (gluteal region is not
preferred as fat may inhibit DPT absorption).
AEFI of DPT:
 Mild: Fever and local reaction (swelling & indurations).
 Severe: Whole cell killed vaccine of pertussis is encephalitogenic. Hence, DPT is not recommended after 6 years of age.
Contraindication to DPT: Hypersensitivity to previous dose & Neurological disorders
Storage: +2° to +8° C
Vaccine is not effective for:
 Prevention of cutaneous diphtheria
 Elimination of carrier state
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4. Hepatitis B vaccines. [12, 06]
Ans.
Perinatal transmission accounts for 30%–50% of all Hepatitis B carrier states.
Plasma derived and yeast derived recombinant HBsAg vaccines are used
Dose: 10 µg in children (0.5 mL) less than 10 years; 20 µg (1.0 mL) for older persons
Schedule — At Birth, 1, 6 & 12 months or At Birth, 6 weeks, 6 month or 0, 2, 6, & 12th month
Mode of Administration—Intramuscular in the anterolateral thigh and never in the gluteal region;
Storage—2–8˚C
Vaccination in child born to a hepatitis B positive mother:
 The newborn must receive both the 1st dose of Hepatitis B Vaccination + Hepatitis B
immunoglobin within 24 h of birth.
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5. Haemophilus influenzae type b preventive vaccines. [10, 07, 05]
Ans.
Diseases caused by H. influenza: Meningitis, Bacteremia, Epiglottitis, Pneumonia, Septic arthritis
etc.
Conjugated Vaccines are used – Ex:
Dosage and Mode of Administration: 0.5 mL IM
Schedule:

Storage: 2–8°C

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6. Japanese B encephalitis vaccine [06]
Ans.
 Live attenuated vaccine: It is cell line derived most commonly from primary hamster kidney cell
lines
It is manufactured in China, but now licensed in India
Schedule: Two doses; 1st at 9 - 12 months of age and 2nd at 16 - 24 months
 Inactivated vaccines are mouse brain derived and formalin inactivated; manufactured in India.
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1. Bacille Calmette Guerin Vaccine. [16, 11]

a. Complications of BCG Vaccination. [04]
Ans.
BCG is available in two forms:
a. Liquid (fresh) form: It is less stable
b. Lyophilized (freeze-dried) form: It is more stable and is recommended for use.
:
✓ Dose and strength: 0.1 mL containing 0.1 mg TU
✓ Alcohol should not be used to wipe the skin
✓ Site: above the insertion of left deltoid.
✓ Route: ID by using a 26-gauge tuberculin syringe
Phenomena after BCG: Papule {2-3 weeks} → Shallow ulcer {5-6 weeks} → Permanent tiny scar {6-12 weeks} → Mantoux test +ve {8-14 weeks}.
Immunity lasts only for 15-20 years.
:
 Most Common: Ulceration at the vaccination site and regional lymphadenitis.
 Rarely, keloid or lupus lesion, and osteomyelitis
 Very rarely, non-fatal meningitis, progressive tuberculosis and disseminated infection.
:
If not given at birth it can be given later, maximum up to 2 years.
Onco TICE strain of BCG has been tried as an adjunctive therapy in bladder carcinoma
: HIV-positive child, Child borne to AFB positive mother, Child with low
immunity, Generalized eczema & Pregnancy.
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2. Rota virus vaccines - types, dose schedule and age of vaccination. [15]
Ans.
Rota virus vaccine is an oral, live vaccine
2 types: Human Monovalent & Human Bovine Pentavalent 👉🏻
Dosage and Schedule: 1st dose should be given within 12 weeks
 RV1- two doses: 10wks –14wks
 RV5 - three doses: 6wks—10wks—14wks
Mode of administration: 1ml orally
Adverse Effects: risk of intussusception
Contraindication: h/o allergy, h/o intussusception
Upper age limit:
 For initiation – within 15 wks of age
 For completion -- within 32 wks of age
----------------------------------------------------------------------------------------------------------------------------------------
3. Tabulate advantages and disadvantages of oral and Inactivated polio vaccine. [15]
Ans.

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4. National Immunization Day. [11]
Ans.
 National Immunization Day is on March 16th
 It is celebrated to acknowledge and appreciate the hard work of frontline health care workers to
ensure the vaccination of every child.
 India vaccinates over 30 million pregnant women & 26 million children each year under Universal
Immunisation Programme
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5. Prevention of hepatitis A. [05]
Ans.
Mode of Transmission: fecal-oral route (MC). Rarely by sexual (homosexuals through orogenital
contact) and parenteral routes (infected blood products or needle pricks).
Hepatitis A is the most common cause of acute viral hepatitis in children.
Hepatitis A vaccine:
Dosage and Mode of Administration—2 Primary Doses (720 EU in adults and 360 EU/mL in
children) and a Booster Dose after 6–12 Months administered intramuscularly.
Storage at +2 to +8 0˚C;
Duration of protection: 10 years after the Booster
1. Write Clinical manifestations and Diagnosis of acute rheumatic fever. How do you manage
rheumatic carditis? [04]
a. Prevention of Rheumatic disease/fever – incl Primary and secondary prophylaxis [19, 18, 16, 14, 08]
b. Modified Jones criteria for Rheumatic disease/fever [13, 10]
Ans.
Rheumatic fever is a febrile disease affecting connective tissues initiated by infection of the throat by
group A beta haemolytic streptococci.
Jones criteria:
 Major: Migratory polyarthritis of the large oints; ancarditis; Subcutaneous odules; rythema
marginatum; ydenham chorea
 Minor: Fever; Arthralgia; WBC, ↑ acute phase reactants in blood; 1st degree AV block;

DIAGNOSIS: Evidence of a preceding Group A streptococcal infection, with 2 major or 1 major & 2
minor manifestations
PREVENTION:
1. : Identify all "high-risk" groups
→ treat them with Penicillin {single IM injection of 1.2
MU of benzathine benzyl penicillin for adults and 6 lakh units for
children is adequate, or oral penicillin (Penicillin V or G) should be
given for 10 days}. For patients with allergy to
penicillin, erythromycin is the drug of choice.
2. - to prevent the
recurrences of RF give 1 IM injection of
benzathine benzyl penicillin (1.2 million units in adults
and 600,000 units in children) every 3 weeks for at least 5 years or until the child reaches 18 years whichever is
later.
3. – Ex: Improvements in socioeconomic conditions (particularly better housing)
4. Jai Vigyan Mission Mode project is being carried out on various aspects of RF and RHD.
5. : Periodic surveys should be carried out on the prevalence of RHD in school children.
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1) VSD – Haemodynamics, C/F & Mx [21, 06]

Ans.
: VSD is the most common congenital heart
disease in which there is a defect in ventricular septum
either in the small membranous part or the large muscular
part.
: 👉🏻
The magnitude of the left to right shunt in VSD
depends on the Size of the defect & the level of PVR
Systole  L to R shunt {blood from the LV enters the PA through RV}  blood enters the lung,
delivered back to left atrium and LV.
 Thus, LV volume over load occurs in VSD, with dilated PA and LA. T
RV remains normal in size, till the onset of pulmonary hypertension.

– Treat CCF with diuretics (furosemide/ potassium sparing diuretics) + ACE inhibitors &
treat anemia till spontaneous closure occurs.
:
For large VSD – Surgical closure is done within the first 6 months of life
Children with PAH – Surgical closure is done by 1 year of age.
Surgery is contraindicated in children with right to left shunt.
Complications of Surgery: RBBB, left anterior hemi block and the residual VSD
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2) Cyanotic spells in a case of Tetralogy of Fallot’s – C/F, Complications & Mx [19, 15, 14, 13, 07, 05]
a. Radiological findings in Tetralogy of Fallot’s [12]
b. Tetralogy of Fallot [11]
c. Cyanotic spells [10]
d. Mention two drugs used in cyanotic spells [04]
Ans.
The 4 components of tetralogy of Fallot (TOF) are: 1) VSD 2) Overriding aorta 3) Right ventricular out
flow tract obstruction 4) Right ventricular hypertrophy (RVH)

Mild (RVOT) obstruction—Often presents with an isolated murmur (Pink tetralogy).

Severe obstruction (PS) presents with cyanosis, left lower parasternal heave, S 2—loud and single
(due to anterior position of the aorta and soft closure of the pulmonary valve).
Intensity of the murmur is inversely proportional to the degree of obstruction
Pan digital clubbing
 – seen in TOF in children < 2 years of age.
▪ Events like waking up in the morning or exertion (excessive crying/straining for defecation) which
decreases the systemic vascular resistance, initiates the spell.
▪ Child Starts crying → becomes more hyperpneic and restless → deepening of cyanosis
(disappearance of heart murmur) → Gasping respiration → syncope may follow → severe spells
can lead to convulsions or hemiparesis. This vicious cycle continues if not intervened
▪ Toddlers assume squatting to relieve these symptoms

 Hypoxic spells and Squatting.

 Cerebral abscesses from septic emboli, cerebral thrombosis/stroke due to dehydration
and bacterial endocarditis may occur.
 Polycythemia {erythropoietin stimulation due to low arterial oxygen saturation.} Though they
have polycythemia, smear shows microcytic RBCs due to relative iron deficiency.
 Bleeding disorder, gout.

 For cyanotic spells – Knee-chest position, vasoconstrictors

 Correct iron-deficiency anemia

▪ Corrective Surgery: Patch closure of the VSD and RV muscle bundle resection + trans pulmonary
valve annulus patch or pulmonary valvotomy at 6–12 months of life.
▪ Palliative Surgery – Blalock–Taussig shunt

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3) C/F & Mx of Congestive Heart Failure in children [15, 12]
a. Mention the '4’prongs for the treatment of Congestive Heart Failure (CHF) in children [14]
Ans.

The 4 prongs are:

a) Reducing cardiac work,
b) Augmenting myocardial
contractility,
c) Improving cardiac
performance
d) Correcting the underlying
cause
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4) Treatment of Patent Ductus Arteriosus [09]
Ans.
Asymptomatic small PDA – follow up for 6 months for spontaneous closure.
– Indomethacin/ ibuprofen for symptomatic PDA
– if medical management fails
▪ Surgical ligation is done commonly by posterolateral thoracotomy approach
– indicated in symptomatic PDA with CCF – Gianturco stainless steel
coils/Amplatzer duct occluder are used for closure  Injury to recurrent laryngeal nerve, phrenic
nerve or thoracic duct is a known complication of this procedure.
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5) Classification of Congenital Cyanotic Heart Diseases [08]

Ans.
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1. Name the complication of cyanotic heart diseases [10]
a. 4 complications of congenital cyanotic heart diseases [06]
Ans.
 Hypoxic spells {in cyanotic HD}.
 Cerebral abscesses from septic emboli, cerebral thrombosis/stroke due to dehydration and
bacterial endocarditis may occur.
 Polycythemia {erythropoietin stimulation due to low arterial oxygen saturation.} Though they
have polycythemia, smear shows microcytic RBCs due to relative iron deficiency.
 Bleeding disorder, gout.

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2. Drug treatment of Hypertensive Emergencies [08]
Ans.
1. Diabetic ketoacidosis – C/F & Mx [21, 07]
Ans.
DKA is an acute complication of DM consisting of
Hyperglycemia, ketosis & Acidemia

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2. Delayed puberty and its etiology [16]
Ans.
Delayed puberty is defined as failure to develop
secondary sexual characteristics by 2 SD beyond the
mean age of onset for that population
----------------------------------------------------------------------------------------------------------------------------------------
3. Newborn with Hypothyroidism – C/F, inv. & Tt [16, 09]
a. ' Congenital Hypothyroidism [11]
b. Investigations for suspected neonatal hypothyroidism [08]
c. Treatment of cretinism or congenital hypothyroidism [07]
Ans.
Congenital hypothyroidism is the most common preventable cause of mental retardation in children.

 Thyroid dysgenesis is the most common etiology. Exact cause of dysgenesis is not known. Genetic
and Immunological factors play a role.
 Approximately 98% of cases occur sporadically while 2% are familial.
 Other causes: Dyshormonogenesis, Deficiency of Iodine, Congenital anomalies of thyroid gland,
Pituitary & hypothalamic dysfunction
 Associated syndromes: Pendred Syndrome {SNHL & goiter} & Kocher Debre Semelaigne
syndrome.
Most affected infants are asymptomatic at birth. Symptoms evolve during the first
few months
 activity, hypotonia, hoarse cry, wide anterior fontanelle, prolonged hyperbilirubinemia and
passage of stools or constipation; delayed dentition, poor feeding, short stature.
 Examination reveals coarse facial features, large protruding tongue, umbilical hernias and mottled,
cold and dry skin (Cutis marmoratus).
 Cretinism develops in untreated children myxedema, severe mental retardation, developmental
delay, growth failure and goiter.

Neonatal Screening: total or free T4 and TSH levels.

Epiphyseal dysgenesis: Absent distal femoral and proximal tibial epiphysis in term babies.
Imaging: Ultrasound examination to rule out ectopic thyroid in lingual or sublingual areas.
Down syndrome, Pituitary dwarfism & Mucopolysaccharidosis

Immediate exogenous replacement of thyroid hormone regardless of the etiology.

Drug of choice is synthetic oral levothyroxine (Eltroxin). It is started at a dose of 10-15 mcg/kg/day
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1. Undescended testis [15]

Ans.
▪ It results from arrest of descent of the testis in some part along its pathway to the scrotum.
▪ Bilateral undescended testis is called cryptorchidism (means hidden testis).
▪ Complications of undescended testis: Sterility; Torsion testis; indirect inguinal hernia; Epididymo-
orchitis; Testicular atrophy; Malignant transformation to seminoma
1. Convulsions in children / neonate – causes, inv. & Mx algorithm. [21, 17, 13]
a. 4 causes of neonatal convulsions [21, 05]
b. Causes of seizures in a child. How do you manage a child with Status Epilepticus? [19, 15, 11]
c. Convulsions in a 2-day old neonate – Causes, inv. & Tt. [09]
Ans.
Definition: A seizure is a brief syndrome of manifestations resulting from abnormally increased
neuronal firing in the brain.

Etiology of neonatal convulsions:

– Intrauterine infections, Bacterial meningitis, tuberculous meningitis,
aseptic meningitis, cerebral malaria, tetanus, Reye’s syndrome.
- Dyselectrolytemia (hypocalcemia, hypomagnesemia).
- Neoplasm, brain abscess, tuberculoma, cysticercosis.
- AV malformations, intracranial thrombosis, and hemorrhage.
, sequelae of birth trauma, birth asphyxia, grey matter degeneration,
storage disorders.
- Phenothiazines, salicylate, phenytoin, carbon monoxide, lead.

- Status epilepticus is seizure activity not resolving spontaneously, or recurrent

seizure with no recovery of consciousness in between

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2. Pyogenic meningitis in infant – etiology, C/F, Complications {at least 4} & Treatment [16, 14, 04]
a. CSF picture in acute bacterial & TB meningitis [15, 13, 09, 07, 06]
b. Choice of antibiotics in the treatment of childhood pyogenic meningitis [07]
Ans.
Bacterial infections causing inflammation of meninges is referred to as Pyogenic meningitis.
It is more common in neonates and infants than older children because of immature immune system.
:

» Refusal to feed
» Projectile
vomiting, shrill cry Signs of Meningeal irritation:
and bulging Neck stiffness, Kernig sign, Limited
fontanelle extension of knee & Brudzinski sign –
Hips and knees flex with passive neck
» Seizures, altered flexion
sensorium Papilledema, hypertension
progressing to with bradycardia due to ICP
coma Photophobia Tache Cerebrale –Flushing seen
» Myalgia, arthralgia with scratching of Abdominal skin

» Poor cry, lethargy

& Drowsiness

Seizures (MC), Increased ICP, cranial nerve palsies, stroke, SIADH, cerebral or cerebellar herniation
and thrombosis of the dural venous sinuses.
Subdural effusions in infants (seen in H. influenza & Pneumococcus)
Thrombocytosis, eosinophilia and anemia
Pericarditis or arthritis
Hydrocephalus, Ventriculitis, Arachnoiditis
MC sequelae of bacterial meningitis – Sensorineural hearing loss
Long term neurological complications – hemiplegia, aphasia, ocular palsies, SNHL & mental
retardation
– Based on choice of antibiotic & duration of therapy
Meningococcal or  Penicillin 400, 000 - 500,000 units/kg/day every 4th hourly.
pneumococcal  Cefotaxime 150-200 mg/kg/day every 8th hourly.
meningitis  Ceftriaxone 100-150 mg/kg/day every 12th hourly.
Ceftriaxone / Cefotaxime / Combination of Ampicillin (300mg/kg/day
H. influenzae meningitis
q6h) and Chloramphenicol (100mg/kg/day)
Vancomycin is the treatment of choice if Penicillin or Methicillin
Staph meningitis
resistance is suspected
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3. TB meningitis in children – C/F, Dx & Mx [14, 13, 05]
Ans. Caused by M. tuberculosis
: untreated case classically goes through 3 stages
a) Prodromal stage or Stage of invasion: low grade fever, Irritability, head banging & photophobia
b) Stage of meningitis
c) Stage of coma: Dilated pupils, nystagmus,
Cheyne-stokes breathing etc.
: Lumbar puncture–CSF examination
▪ Mantoux test may be positive. If negative
does not rule out diagnosis
▪ Chest X ray to look for pulmonary TB.
▪ CT and MRI show inflammatory granulomas, hypodense lesions or infarcts and hydrocephalus.
▪ BACTEC & PCR
:
Antitubercular therapy - for at least 12 months.
At least 4 anti-tubercular drugs should be used for initial 2 months:
Isoniazid (5mg/kg/day, max 300 mg)
Rifampicin (10mg/kg orally, max 600 mg)
Pyrazinamide (30mg/kg/day orally)
Ethambutol (15-20 mg/kg/day)
Streptomycin (30-40 mg/kg/day)
Steroids - parenteral dexamethasone 0.15mg/kg, every 6 hr IV, Change to oral prednisolone once
brain edema settles.
Symptomatic therapy of ICP, seizures, Dyselectrolytemia should be done.
Ventriculocaval shunt - for increasing hydrocephalus.
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1. Simple febrile convulsion – Define, C/F, Dx and management [21, 18, 14, 12, 10]
a. Febrile seizures [21]
b. Emergent management of Febrile Seizure [17]
Ans.
This term denotes seizures associated with fever due to extracranial source.
– Febrile seizure is a familial disorder. Positive family history seen in 1/3 rd cases.

Up-rolling of eyes, fixed gaze & tonic movements of limbs.

Clinical examination should be focused at Ruling out meningeal infection, ICT, focal deficits etc.

To identify the cause of fever - Blood, Urine culture, serology, CBP {based on DDx of fever}
Neuroimaging if focal seizures or focal deficits detected on examination
LP & EEG

Immediate therapy – for children with active seizures – IV or

rectal diazepam is the first choice (0.3mg/kg/dose)  intubate
if necessary
Long term therapy – to prevent recurrences. 👉🏻
Antiepileptic therapy is not required as long-term prophylaxis against simple febrile seizures
In cases of parental anxiety, Intermittent diazepam prophylaxis can be given during febrile
episodes (Dose - 0.3 mg / kg / dose every 8 – 12 hours)
Antipyretic measures and seizure prophylaxis reduces but does not completely prevent the
recurrence of seizures
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2. Hydrocephalous – causes {at least 4} & C/F [20, 19, 14, 06]
Ans.
Hydrocephalous refers to enlargement of the head secondary to accumulation of CSF in the
intracranial spaces.
The cause may be due to increased production, decreased clearance of CSF or both.
Type of
Hydrocephalous
Causes
Occurs due to obliteration of subarachnoid cisterns or dysfunctional arachnoid villi
Non-obstructive » Post hemorrhagic (MCC)
or communicating » Meningitis
hydrocephalus » Achondroplasia
» Choroid plexus papilloma
Occurs due to obstruction within the ventricular system
Obstructive or
Aqueductal stenosis (MCC)
non-
Infections (Toxoplasma, neurocysticercosis, mumps)
communicating
Arnold Chiari and Dandy-walker anomalies
hydrocephalus
Mass lesions - Abscess, hematoma, tumors etc.
Clinical features
Congenital hydrocephalus either presents immediately after birth or after few weeks
Acquired hydrocephalus develops much later often in association with risk factor like post-
meningitic sequelae.
Classical presentation: Excessive increase in head size, protruding forehead along with wide and
bulging fontanels. Cranial sutures open up and scalp veins become dilated and more prominent.
‘Sunset sign’. Percussion of the head
reveals cracked pot resonance
(Macewen sign). Transillumination of
cranium may be positive.
Features of ICP seen in older children
{anterior fontanelle closes} – Irritability,
seizures, papilledema, spasticity, ataxia, urinary incontinence & progressive mental deterioration
can occur.
Lumbar puncture is contra-indicated in OBSTRUCTIVE hydrocephalous– risk of herniation of the
brainstem and cerebellar tonsils
Lumbar puncture is of diagnostic & therapeutic value for communicating hydrocephalus.
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3. Spastic cerebral palsy [11]
Ans.
Spastic CP (Pyramidal CP) – it is the MC type of CP which
manifest with increased tone causing Hemiplegia,
Mono/Di/Tri/Quadriplegia
Diagnosis: History and physical examination, MRI or CT of
brain, Ophthalmic evaluation, Hearing tests, Speech and
language evaluation, Psychological educational evaluation,
EEG
Treatment
 Multidisciplinary approach – treatment of CP involves:
general paediatrician, occupational therapists, speech-
language therapist, orthopaedist, psychiatrist or
neurologist, and social support services
 Parent counselling
 Drugs –
 Muscle relaxants {Baclofen, dantrolene sodium and Benzodiazepines} to relieve spasticity
 Anticonvulsants – for epilepsy
 Botulinum toxin injections + stretching and/or serial casting to treat joint deformities and
improves the motor function
 Physiotherapy – most important part of treatment - Children are trained to relax the spastic
muscles, helping the children to stand and walk on their own
 Surgical procedures - Orthopaedic surgery to correct the deformities – Ex: Tendoachilles
lengthening etc.
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4. Prevention of neural tube defects [08, 07]
Ans.
Neural tube defects (NTD) are the MC congenital anomalies of the CNS resulting from failure of
spontaneous closure of neural tube between 3rd and 4th week of fetal life.
- Periconceptional folic acid supplementation to all pregnant mothers in a
dose of 0.4 mg /day

Mothers’ previous pregnancy with neural tube defects should receive 4 mg/ day
Folate supplementation should be started two months before expected conception till first 3
months during pregnancy.
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1) Preventable causes of Mental Retardation [19, 08]

Ans.

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2) Erb’s palsy [16]
Ans. Erb’s palsy (C5–C7)
aeroplane splint
Most common brachial plexus injury
Risk factors: Macrosomic babies, Shoulder dystocia
Involved hand is adducted, internally rotated, forearm extended and pronated (Policeman’s or
Waiters tip posture)
Moro’s, biceps and radial reflexes are absent, but grasp reflex is present. {refer ortho notes for Mx}
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3) Absence attacks [11]
Ans.
Absence seizures are brief seizures characterized by sudden discontinuation of the activity being
performed with starring spell, eye fluttering or rhythmic movements.
Etiology: Childhood absence epilepsy (CAE), Juvenile absence epilepsy (JAE), and juvenile
myoclonic epilepsy (JME); Lennox-Gastaut syndrome.
More common in Girls
EEG is the main diagnostic tool – it shows characteristic 3 Hz spike and slow wave discharge
 Drug of choice – Valproate (previously Ethosuximide)
Older terms for absence Seizures:
 Pyknolepsy – {pyknos, in Greek means “very frequent”}
 Petit mal seizure
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4) Carbamazepine [10]
Ans.
 MOA: Like phenytoin, carbamazepine slows the rate of recovery of Na+ channels from inactivation,
thereby reduces neuronal excitability.
 Uses:
1) DOC in GTCS and partial (SPS and CPS) seizures.
2) DOC in the treatment of trigeminal neuralgias. It inhibits high frequency discharges. The other
drugs useful are phenytoin, gabapentin, TCAs (amitriptyline), etc.
3) It is used in the treatment of acute mania and bipolar disorder.
 Precautions:
1) Carbamazepine induces the metabolism of phenytoin, phenobarbitone, sodium valproate & OC
pills & hence the effects of these drugs are reduced.
2) INH & Erythromycin inhibit carbamazepine metabolism, so carbamazepine toxicity may occur
 Adverse Effects: CNS Depression, Megaloblastic & Aplastic anemia, osteomalacia, Teratogenicity
{Cleft Lip & palate; Spina bifida}, Exfoliative Dermatitis (Steven Johnson Syndrome), ↑ADH
secretion (dilutional hyponatremia) etc.
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5) Pseudoparalysis — causes [09]
Ans.
Pseudoparalysis refers to the inability to move a part of the body owing to factors, as pain, other than
those causing actual paralysis
: Acute osteomyelitis, toxic synovitis of hip or knee, sprain, unrecognised
trauma etc.
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6) Causes of benign intracranial hypertension in children [03]
Ans.
This condition is characterized by raised intracranial pressure
without any biochemical or cellular changes in CSF.

Causes of benign intracranial hypertension

 MD VPUN
1. Discuss DDx of fever with rash in 1 year old child. How do you treat Kawasaki disease? [20]
Ans.
Differential Diagnosis of Fever with Rash
Type of Rash Seen in
▪ Measles ▪ EBV ▪ Roseola infantum
Macular/ ▪ Rubella ▪ CMV ▪ Erythema infectiosum
maculopapular ▪ Dengue ▪ HIV ▪ Scrub typhus
rash ▪ Drug Rash ▪ Chronic Hep-B ▪ 2° syphilis
▪ Lupus ▪ Chikungunya ▪ M. pneumoniae
Diffuse erythema
 Scarlet fever  Toxic epidermolysis
with peeling  Kawasaki Disease
 SJS  Toxic shock syndrome
(desquamation)
Vesicular rash » Varicella » Enteroviral Infections » Herpes simplex
HEV {Hand-foot-mouth disease}
Petechial + Dengue hemorrhagic
Meningococcemia, Henoch Schönlein purpura
purpuric rash fever, Chickenpox
Urticarial rash Scabies, insect bites Cutaneous larva migrans Pediculosis & strongyloides
Nodular rash Molluscum contagiosum erythema nodosum Cryptococcosis

Kawasaki disease is an acute febrile mucocutaneous lymph node syndrome mainly affecting infants
and young children

CRASH + Burns 🔥

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1. Down’s syndrome (& it’s genetic basis) [15, 11, 08]

a. Antenatal Diagnosis of Down Syndrome. [21]
Ans.
Down’s syndrome is the most common chromosomal disorder. The extra 21st chromosome could be
either maternal or paternal in origin
Advanced maternal age increases the risk of Down’s syndrome.
Cytogenetics—3 mechanisms are known
Nondisjunction in the first meiotic division of gametogenesis {95%}
 Robertsonian translocation in about 5% of cases
Mosaicism in about 1% of cases
Clinical features: Children are mentally retarded with low IQ
: Flat face and occiput, with a low-bridged nose, ↓ interpupillary distance & oblique
palpebral fissures; Epicanthal folds of the eyes {mongolism}
 Enlarged and malformed ears
 Prominent tongue (macroglossia), which lacks a central fissure & protrudes through an open
mouth
 Speckled appearance of the iris (Brushfield spots)
: shorter bones of the ribs, pelvis, & extremities {short stature}
: broad and short with a Simian crease (a single transverse crease across the palm). The fifth
finger curves inwards.
: esophageal/duodenal stenosis or atresia, imperforate anus and Hirschsprung disease
(megacolon).
Congenital cardiac anomalies {ASD, VSD, tetralogy of fallot & PDA}
Men are sterile because of spermatogenesis arrest
Susceptible to serious infections due to defective immunity.
: Antithyroid antibodies hypothyroidism.
: risk of both ALL & AML
:
▪ Atlantoaxial instability {excess movement due to laxity of either bone or ligament}  abnormal
gait, restricted neck mobility, torticollis, etc
▪ Alzheimer disease at younger age.
Prenatal diagnosis
Fetal karyotype by chorionic villus sampling or amniocentesis
Screening with maternal serum markers (AFP levels)
Triple test, Quadruple test, and PAPP-A {Pregnancy Associated Plasma Protein-A} levels
Ultrasonography for nuchal fold thickness
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1. Problems in a child with cleft palate [09]

Ans.
KDT
• Speech is defective especially in cleft palate, mainly to phonate B, D, K, P, T and G
• Bacterial contamination of upper respiratory tract with recurrent infection
BPG
• Small maxilla with crowded teeth, absent/poorly developed upper lateral incisors
• Chronic otitis media with deafness may occur
• Swallowing difficulties to certain extent and speech problems
• Cosmetic problems (Hypoplasia of Maxilla)
1. Treatment of scabies [08]
Ans.
1. Kerosene oil poisoning [21, 13, 09]
a. Principles of management of accidental poisonings [08]
Ans.
: Accidental ingestion {children}; Transdermal absorption & IV drug abusers.
:
Violent coughing, flushing of the face and vomiting following ingestion.
kerosene odour from mouth and vomitus.
Older children often complain of headache, abdominal pain abdominal distension, dry throat and
difficulty in swallowing. Fever is very common.
In severe cases – CNS problems like restlessness, convulsion and coma occur
– Basilar infiltrates and emphysematous changes. Rarely pleural effusion
and pneumatoceles can be seen.
:
Hospitalise  Preserve airway  Oxygen and respiratory support with β-agonists.
Patients should be put on left lateral position to avoid aspiration.
Removal of contaminated dressings prevent ongoing dermal absorption.
Gastric lavage & Emesis are contraindicated due to the risk of aspiration.
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2. Organophosphorus poisoning [13]
Ans.
: OP compounds {attach to esteratic site of ChE & form covalent bonds} irreversibly inhibit
cholinesterases and cause accumulation of ACh at muscarinic and nicotinic sites. All organophosphorus (OP)
compounds except echothiophate have no therapeutic applications. Echothiophate is rarely used in resistant cases of glaucoma.

Muscarinic effects: Profuse sweating, salivation, irritation of eyes, lacrimation, tracheobronchial

secretions, bronchospasm, vomiting, abdominal cramp, miosis, bradycardia, hypotension, cardiac
arrhythmias, involuntary urination & defecation.
Nicotinic effects: Twitching, fasciculations, muscle weakness & paralysis (due to prolonged depolarization).
Central effects: Headache, restlessness, confusion, convulsions, coma & death are usually due to
resp. failure.
. OP poisoning can be diagnosed by:
 History of exposure.
 Characteristic signs and symptoms.
 ↓cholinesterase activity in blood.
:
:
1. Remove the Contaminated clothes; wash skin with soap & water.
2. Gastric lavage should be continued till the returning fluid is clear
3. Airway should be maintained
4. If necessary, Artificial respiration should be given
5. Supportive measures—maintain BP, hydration, Diazepam should be used cautiously by slow IV
inj. to control convulsions.
:
1. is the 1st Drug to be given in OP poisoning -
 It competitively blocks the muscarinic effects of OP compounds (competitive antagonism).
 Inject Atropine 2mg IV stat & should be repeated every 5-10 min doubling the dose, if required,
till the patient is fully atropinized (fully dilated & non-reactive pupils, tachycardia, etc.).
2. Atropine is not effective for reversal of neuromuscular paralysis.
Neuromuscular transmission can be improved by giving
cholinesterase reactivators such as pralidoxime, obidoxime, etc.
MOA: OP compounds inactivate ChE by phosphorylating esteratic
site of the enzyme. Oximes bind with high affinity to anionic site,
dephosphorylate the enzyme, and reactivate it. Early
administration of oximes is necessary before the phosphorylated enzyme undergoes aging (loses
alkyl groups) and becomes resistant to reactivation.
Pralidoxime is administered IV slowly in a dose of 1-2 g.
Oximes are ineffective as an antidote to carbamate anti-ChEs (physostigmine, neostigmine,
carbaryl, propoxur) in which case the anionic site of the enzyme is not free to provide
attachment to it. It is rather contraindicated in carbamate poisoning, because not only it does
not reactivate carbamylated enzyme, it has weak anti-ChE activity of its own.
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1) Mx of Snake Bite [21]

Ans.
:
Alleviate anxiety & fear {MCC of death is fear}
Wash the wound with soap and water / KMNO4
Immobilize the limb – to prevent spread of venom
Sutherland wrap is applied to occlude veins & lymphatics {except in viper bite to avoid local necrosis}
:
Secure IV line
Remove Sutherland bandage
Inj. TT, 0.5 mL IM
Inj. { olyvalent nti-snake enom} – to neutralize the toxic effects of snake venom
Dosage: lyophilized powder is diluted in 500 ml normal saline and infused in 1 hour.
Minimal symptoms (only local signs, no systemic signs) – 5 Vials
Moderate (moderate local & systemic signs) – 10 Vials
Severe (severe local & systemic signs) – 15 Vials
If signs of paralysis seen  Inj. Neostigmine 1.5 mg
Inj. Atropine 0.6 mg to counteract muscarinic effects of Neostigmine
If clotting abnormalities seen – Inj. Heparin 1000-5000 units
Antibiotics, Pain killers {PCM} & Surgical debridement of wound
Hemodialysis and other supportive measures
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2) Neurotoxic Snake Envenomation [19]
Ans.
Neurotoxic envenomation treatment
Mechanical ventilation in patients with bulbar and respiratory paralysis
 Neostigmine (0.05 mg/kg) ½ hrly for five doses & then every 2-6 hrly
General Supportive measures
Broad spectrum antibiotics
Prophylaxis against tetanus and gas gangrene.
FFP, platelets and Packed cell transfusion
Restriction of fluids, electrolytes and dialysis in Acute renal injury
Surgical debridement in case of gangrene.