DNB June 2022 Paper - Solution

DTaP Paediatrics/ Dr. A.K.
Saini Page |1
DNB PAEDIATRICS
(Session: - JUNE 2022)
Paper – 1st
DTaP Pediatrics / Dr. A. K. Saini

DTaP Paediatrics/ Dr. A.K. Saini Page |2
Paper 1
Q. 1) IRON metabolism?
Ans. IRON metabolism

Q. 2) METHODS OF DISINFECTION ?
Ans.

Q. 3) Childhood Diabetes management ?
Ans. TYPE OF Diabetes :-
Type 1 Diabetes –
Cannot make enough insulin, because the body’s own immune system destroys the beta
cells of the pancreas. Not clear exactly what triggers this destruction.
Type 1 diabetes can only be treated with injectable insulin. Oral antidiabetic drugs do not
help in T1D. Treatment with insulin is essential for survival and normal health, because
the body cannot make enough. The child can become very sick (diabetic ketoacidosis) or
even die if insulin doses are missed or too little. This is not an addiction.
Type 2 Diabetes –
Insulin demand is high, and even though insulin is produced, it is less effective: “insulin
resistance”.
Obesity and a family history of T2D increase the risk.

T2D is less common in adolescents, but is more severe than in adults, and must be taken
seriously.
It can be managed effectively by healthy eating and other lifestyle modifications, as well
as by metformin (an antidiabetic drug) in the early stages.
Diagnostic criteria for diabetes and prediabetes are defined per the American Diabetes
Association (ADA) 2021 guidelines:-
Type :-
M/C form in this age-group remains type 1 diabetes - immune mediated.
Type II diabetes, although rare, is on the increasing trend in our country.
Type III diabetes includes other forms such as –
Monogenic diabetes/maturity-onset diabetes of the young (MODY),
cystic fibrosis-related diabetes (CFRD),
fibrocalculous pancreatic diabetes (FCPD),
drug-induced diabetes, and
lipodystrophic diabetes, which are also being recognized.
Factors that favor diagnosis of non-type 1 diabetes mellitus (T1DM) are as follows:-
Overweight/obesity
Presence of hyperlipidemia at onset
Absence of ketosis

Family history of early onset diabetes in preceding two generations
Medications—steroids and immunosuppressants
THERAPY GOALS:-
Maintain a good “time in range” (70% and above) defined as percentage of time the blood
glucose (BG) values lie in target range of 70–180 mg/dL.
Prevention of acute complications such as diabetic ketoacidosis (DKA) and hypoglycemia.
Prevention of long-term complications and achieving good quality of life.
Achieve normal growth and development.
MANAGEMENT OF CHILDHOOD DIABETES :-
Pillars
[1] Medical nutrition therapy
[2] Physical activity
[3] Glucose monitoring
[4] Insulin therapy
Medical nutrition therapy

There is no special diet in diabetes.
Encouraged for healthy diet with limited intake of snacks, sweeteners, and high glycemic
index carbohydrates.
Balanced diet by plate method as below:
1/3rd high-quality high-fiber rich carbohydrates,
1/3rd of fruits and vegetable
1/3rd protein.
Carbohydrate content of food can be calculated as “carb count” which helps to titrate

insulin therapy.
One carbohydrate exchange equals = 15 g carbohydrate.
Dietary options become challenging for a patient with a coexistent celiac disease where
food should be made gluten free and with a low glycemic index.
PHYSICAL ACTIVITY :-
Regular fitness and physical activity regime -> Good metabolic control.
Parents encourage the child for such as walking, running, dancing, using stairs often, and
playing in open grounds.
Participate in all sports but should be educated to check BG before exercise and preferably
consume a snack if BG is low, to avoid hypoglycemia.
BLOOD GLUCOSE MONITORING:-
An essential pillar of management in diabetes.
Easiest way to monitor is using a hand-held glucometer to check BG daily.
An ideal BG log should record premeal and 2-hour postmeal BG values at least thrice a
day.

Additional testing should be done before a planned physical activity, at bedtime, and if
the child develops any uneasiness or discomfort.
Continuous glucose monitoring system (CGMS) –

Simplified the glucose monitoring.
This device places a sensor over the skin to measure the glucose level in the interstitial
fluid at frequent intervals.
Readings from the sensor can be read real time or as records which can show fluctuations
(both hypo- and hyperglycemia) that would have gone unnoticed on timed-finger prick
checking.
Sensors usually last 5–14 days, and may need calibration with finger-prick values of a
glucometer.
CGMS log also helps to calculate the “time-in-range” that is defined as -> the
percentage of time when the BG remained between 70 and 180 mg/dL.
An optimum value is 70% or more.
At present, CGMS of Medtronic, Dexcom, and Abbott are available in India.
Target BG profile –
INSULIN THERAPY: -
Insulin should be started soon after diagnosis of diabetes.
Multiple daily injections Insulin Therapy with the basal-bolus regime are preferred.

Poorer metabolic control with premixed twice daily insulin in adolescents makes them
unsuitable for use in children.
Regular or rapid/ultra-rapid-acting insulin are administered preprandial timed as per
the onset and peak of action.
Basal insulin are given once (or twice) a day and timed at a fixed schedule in a day,
usually night.
Regime is personalized to suit the child’s meal and activity pattern, and convenience.
Insulin Administration –
Syringes, pens, or advanced technology like insulin pumps.
Insulin syringes:
One should use U-100 syringes with U-100 vials (100 units of insulin/mL) and
U-40 syringes with U-40 vials (40 units of insulin/mL).
The attached needles are 6 or 8 mm long.
Regular and neutral protamine Hagedorn (NPH) insulin are usually available in 40
IU/mL strength, while insulin analogs are usually 100 IU/mL.

DTaP Paediatrics/ Dr. A.K. Saini P a g e | 10
Instructed to check the strength of insulin vial before use.
Insulin pen:
Reusable or Disposable (more expensive);
Typically have 1-unit increments (0.5 unit increments also available).
They are easy to carry and convenient.
Pen needles are 4, 5 or 6 mm long.
Insulin pump:
Delivers short-acting or regular insulin using a battery-operated pump over 24 hours
to provide a basal continuous supply.
Additional top-up boluses of insulin can be given using the same device for mealtime.
The insulin goes through a flexible catheter and a cannula directly into subcutaneous fat
over abdomen or gluteal area.
Expensive and require operational expertise.
Insulin Dose –
If presenting as DKA ->> a dose of 0.05–0.1 unit/kg/hour of short-acting insulin is
given as an i.v. infusion, following which insulin requirement may be as high as 2–3
units/kg/day for the first few days.
Typically, as the patient enters the honeymoon phase, the dose comes down to 0.5
units/kg/day or less.
Following this, 0.7–1.5 U/kg/day is the usual dose with 40% as basal and 60% as
boluses for 3 meals.
The dose and distribution may vary depending on age and puberty.
Change the place of the injection by 2–3 cm daily—“site rotation”. Repeated injections on

the same site harden the skin (lipohypertrophy)—the pain is less, but insulin is not
absorbed evenly, so blood sugars fluctuate.
Insulin sensitivity factor (ISF) 
Extent to which the BG is expected to drop (in mg/dL) with 1 unit of regular insulin
or rapid-acting analog.
This factor can be derived by dividing a constant factor (1,700) by the patient’s total daily
dose (TDD).
Insulin-to-carbohydrate ratio (ICR) 
(or the grams of carbohydrate for which 1 unit of rapid- or short-acting insulin is
needed) is calculated by dividing the constant 500 by the TDD.
The amount of carbohydrate being consumed can be titrated for premeal insulin dose as
per the ICR, i.e., to calculate the amount of insulin needed for the amount of carbohydrate.
The BG logs can be analyzed with ICR and ISF to optimize insulin dosage and meal
patterns.
Intelligent use of these ratios helps with better glycemic control.
FOLLOW UP :-
Monitor growth (anthropometry)—3–6 monthly
Check insulin dose prescribed and compliance to same
Examine—site of injection, method, and complications at local site
Check record book which should contain date and time of:-
Glucose levels—crosscheck with glucometer
Carbohydrate intake—diet plan being followed to be reviewed for balanced diet,
carb counts if available to titrate premeal short-acting insulin

Insulin dosage—whether doses adjusted as per self-monitoring of blood glucose
(SMBG)/carbohydrate intake
Note of special events affecting glycemic control (e.g., illness and exercise)
Hypoglycemic episodes, describing of severity and potential alterations in the usual
routine to help explain the cause for the event
Blood glucose logs for “Time-in-Range”—to be reviewed at each visit
Hemoglobin A1C (HbA1C) monitoring every 3 months
Explain symptoms of hypoglycemia such as lethargy, increased irritability, excessive
sweating, tremors, and its prevention and treatment
Inform SICK DAY management:-
Do not omit insulin
When unwell frequent random BG and ketone (urine or blood) monitoring is needed,
usually 2–3 hourly. Top-up insulin is often needed.
Calculate TDD.This is the sum of all insulin being given in a day. To give extra dose of
rapid-acting or regular insulin subcutaneous.
If BG < 80 mg/dL: Regular insulin should be omitted. Frequent feeds in small quantities
should be given with 2–3 hourly BG monitoring. Basal insulin should be given. If urine
ketones are positive, basal insulin can be reduced by 30%.
Hospitalize: If child is drowsy, vomiting more than three times, not tolerating oral feeds,
develops fast breathing, and has significant abdominal pain.

Q. 4) PATHOPHYSIOLOGY OF DKA ?
Ans.

Q. 5) BILIRUBIN METABOLISM ?
Ans.

Q. 6) GRADE approach of level of evidence?
Ans.
GRADE (Grading of Recommendations, Assessment, Development and Evaluation) :-
This approach allows systematic review producers and users to apply semi-objective
judgments on factors that may limit the quality of evidence in the review.
Key factors used are –
Study limitations (viz., risk of bias),
Inconsistency (due to heterogeneity),
Indirectness,
Imprecision, and
Publication bias.
A detailed explanation of the GRADE approach is outside the scope of this article.
It does not downgrade lower-level evidence when deciding recommendations provided
the results are consistent.
For example, a strong recommendation (grade A) is given to both level I evidence as well
as consistent evidence from Levels II, III and IV studies.
Consistent level 2 or 3 studies and extrapolation from level 1 studies are given grade B.

Level 4 studies and extrapolation from level 2 or 3 studies are allotted grade C.
Level 5 evidence and inconsistent or inconclusive studies from any level are the lowest
grade (grade D).
Key Points
GRADE provides a framework for assessing quality that encourages transparency and an
explicit accounting of the judgments made.
GRADE distinguishes between quality assessment conducted as part of a systematic
review and that undertaken as part of guideline development.
The optimal application of GRADE requires systematic review of the impact of alternative
management strategies on all patient-important outcomes.
Information about study limitations, imprecision, inconsistency, indirectness, and
publication bias is necessary for decision makers, clinicians, and patients to understand
and have confidence in the assessment of quality and estimate of effect size.
Q. 7 ) The Fetal to Neonatal Circulatory Transition & Changes after birth ?
Ans. In the fetal circulation, the right and left ventricles exist in a parallel circuit, as opposed
to the series circuit of a newborn or adult.
In the fetus, the placenta provides for gas and metabolite exchange. Because the lungs do
not provide gas exchange, the pulmonary vessels are vasoconstricted, diverting blood
away from the pulmonary circulation.
3 cardiovascular structures unique to the fetus are important for maintaining this parallel
circulation: -
Ductus venosus
Foramen ovale

Ductus arteriosus
Umbilical venous partial pressure of oxygen (PO2), the highest O2 level provided to the
fetus, is only 30-35 mm Hg.
Approximately 50% of the umbilical venous blood enters the hepatic circulation, Rest
bypasses the liver and joins the inferior vena cava (IVC) via the ductus venosus, where it
partially mixes with poorly oxygenated IVC blood derived from the lower part of the fetal
body.
This combined venous blood flow (PO2 of 26-28 mm Hg) enters the right atrium and is
preferentially directed by a flap of tissue at the right atrium–IVC junction, the eustachian
valve, across the foramen ovale to the left atrium. This is the major source of left
ventricular (LV) blood flow.
LV blood -> ascending aorta, supplies predominantly the fetal upper body and brain.
Fetal superior vena cava (SVC) blood, which is considerably less oxygenated (PO2 of
12-14 mm Hg) than IVC blood, enters the right atrium and preferentially flows across
the tricuspid valve-> Into the RV -> ejected into the pulmonary artery (PA).
Because the pulmonary arterial circulation is vasoconstricted, only approximately 5%
of right ventricular (RV) outflow enters the lungs. The major portion of this blood
bypasses the lungs and flows right-to-left through the ductus arteriosus into the
descending aorta to perfuse the lower part of the fetal body, including providing flow
to the placenta via the 2 umbilical arteries.
Upper part of the fetal body (including the coronary and cerebral arteries and those to
the upper extremities) is perfused exclusively from the LV with blood that has a slightly
higher PO2 than the blood perfusing the lower part of the fetal body, which is derived
mostly from the RV.

From the ascending aorta (ONLY 10% of fetal cardiac output) flows all the way around
the aortic arch (aortic isthmus) to the descending aorta.
Total fetal cardiac output—(combined output of both LV+RV ) —is approximately 450
mL/kg/min.
Approximately 65% of descending aortic blood flow returns to the placenta, remaining
35% perfuses the fetal organs and tissues.
In Human fetus, RV output is probably closer to 1.3 times LV flow.
Thus, during fetal life the RV is not only pumping against systemic blood pressure, but
also performing a slightly greater volume of work than the left ventricle. Thus the RV
wall is as thick as the LV wall during fetal and immediate neonatal life.
Blood flow is important determinant of growth of fetal cardiac chambers, valves, and
blood vessels.
Narrowing (stenosis) of an upstream structure such as the mitral valve, flow
downstream into the left ventricle is limited and LV growth may be compromised, which
may be a cause of hypoplastic left heart syndrome (HLHS)
Stenosis of a downstream structure such as the aortic valve can disrupt flow into the left
ventricle and also potentially lead to HLHS.
In many cases of HLHS there is a separate defect in the LV cardiomyocytes themselves
(i.e., cell-autonomous defect).
The Transitional Circulation
At birth, mechanical expansion of the lungs and an increase in arterial PO2 -> result
in a rapid decrease in pulmonary vascular resistance (PVR).

Concomitantly, removal of the low-resistance placental circulation -> leads to an increase
in systemic vascular resistance (SVR).
Output from RV flows entirely into the pulmonary circulation, and because PVR becomes
lower < SVR, Shunt through the ductus arteriosus reverses and becomes left to right.
Over several days the high arterial PO2 constricts and eventually closes the DA ->
becomes the ligamentum arteriosum.
Increased volume of pulmonary blood flow -> LA from the lungs -> increases LV volume
and pressure sufficiently to close the flap of the foramen ovale functionally, although
the foramen may remain patent, on probing, for several years.
Removal of the placenta -> Results in closure of the (DV) ductus venosus.
The left ventricle is now coupled to the high resistance systemic circulation, and its wall
thickness and mass begin to increase. In contrast, the right ventricle is now coupled to the
low resistance pulmonary circulation, and its wall thickness and mass decrease.
The Left ventricle, now deliver the entire systemic cardiac output (approximately 350
mL/kg/min), an almost 200% increase in output, -> Achieved through a combination of
hormonal and metabolic signals, including an increase in the level of circulating
catecholamines and in the density of myocardial β-adrenergic receptors.
Because the ductus arteriosus and foramen ovale do not close completely at birth, they
may remain patent in certain congenital cardiac lesions.
Patency of these fetal pathways may either provide a –
Lifesaving pathway for blood to bypass a congenital defect, eg.
Patent ductus in pulmonary atresia or coarctation of aorta,
Foramen ovale in transposition of great vessels.
Additional stress to the circulation, eg.

Patent ductus arteriosus in premature infant,
Pathway for right-to-left shunting in infant with pulmonary hypertension.
Prostaglandin E1 – Maintain PATENT these fetal pathways.
Indomethacin - hasten their closure. This pharmacology explains why Indomethacin
and similar drugs are contraindicated during the third trimester.
Q. 8 ) types of Study design ?
Ans.
Q. 9) DEVELOPMENT OF DIAPHRAGM, TRACHEA, ESOPHAGUS AND TYPE OF TOF WITH
DIAGRAM?
Ans. DIAPHRAGM

• Diaphragm is the dome-shaped musculotendinous partition that separates the
thoracic and abdominal cavities.
• The pericardial and pleural cavities are above (or cranial to) it, whereas the
peritoneal cavity is below (caudal to) it.
• Diaphragm is mesodermal in origin. 4 mesodermal components contribute for its
development.

The components are: –
1) Septum transversum is the most important component and it contributes for the
unpaired anterior and median part that includes central tendon, esophageal and
vena caval openings.
a. Liver develops in the caudal part of septum transversum. Cranial part form the
diaphragm.
2) Pleuroperitoneal membranes form the paired dorsolateral part of diaphragm.
3) Ventral and dorsal mesenteries of esophagus form the irregular dorsal median part
that fuses with septum transversum and pleuroperitoneal membranes.
4) Mesoderm of body wall including mesoderm around dorsal aorta that fuses with
pleuroperitoneal membranes.
TRACHEA
The trachea develops from the intermediate part of laryngotracheal tube that lies
between the points of its bifurcation into bronchial or lung buds and the larynx.
With the caudocranial extension of tracheoesophageal septum, the trachea elongates.
At birth the bifurcation of trachea lies at the level of lower border of 4th thoracic
vertebra.
Developmental components of trachea:
– The endoderm of laryngotracheal diverticulum forms the lining epithelium and glands
of trachea.
– The cartilage, muscle, and connective tissue of trachea develop from splanchnopleuric
mesoderm surrounding laryngotracheal tube.

ESOPHAGUS
• The esophagus is developed from the part of the foregut between the pharynx and the
stomach.
• It is at first short but elongates with the formation of the neck, with the descent of the
diaphragm, and with the enlargement of the pleural cavities.
• The musculature of the esophagus is derived from mesenchyme surrounding the
foregut. Around the upper two-thirds of the esophagus, the mesenchyme forms striated
muscle. Around the lower one-third, the muscle formed is smooth (as over the rest of the
gut).
Q. 11) management approach in prolonged jaundice in new born ?
Ans. Prolonged jaundice –
Generally, persistence of significant jaundice for more than 2 wk in term and more
than 3 weeks in preterm babies is taken as PJ.

Most of these babies do well without any specific intervention or investigation.
First and foremost step to manage an infant with PJ is to rule out cholestasis.
Yellow colored urine is a reasonable marker for cholestasis; however the urine color
could be normal during initial phase of cholestasis.
PJ with normal colored urine can be considered to have unconjugated
hyperbilirubinemia.
If the infant has dark colored urine, the infant should be managed as per cholestasis
guidelines.
Thyroid screen can be considered in such infants at this stage if routine metabolic screen
for hypothyroidism has not been carried out at birth.
G6PD level, thyroid screen, ABO of infant & mother if not done earlier should performed
to delineate possible cause.
infants having TSB in phototherapy range should be started on phototherapy.
The adequacy of breastfeeding should be assessed by history, observation of
breastfeeding session, and degree of weight loss.

Q. 12) current recommendation for management of diaphragmatic hernia ?
Ans. Therapeutic approach to congenital diaphragmatic hernia (CDH) has shifted from one

of immediate repair to management of pulmonary hypertension, physiologic stabilization,
and delayed surgical repair.

Algorithm of prenatal management of CDH. US ultrasound, LHR lung area-to-head
circumference ratio, FLV fetal lung volume, SVD spontaneous vaginal
delivery, FETO fetal endoscopic tracheal occlusion
Lung hypoplasia, remodeled pulmonary vasculature, and ventricular dysfunction all
contribute to the high morbidity and mortality associated with CDH.
Delivery Room Management –
The infant’s heart rate, preductal and postductal saturations, and blood pressure (invasive
or non-invasive) need to be monitored.
The key principles of successful delivery room resuscitation and stabilization are the
avoidance of high airway pressures and high oxygen concentration as this will facilitate in
minimizing ventilation-induced lung injury.
After delivery, the infant should be intubated immediately without bag and mask
ventilation.
Ventilation by bag and mask may cause distention of the stomach and must be avoided as
it may limit expansion of the hypoplastic lung.
Ventilation in the delivery suite may be done with a ventilation bag or Neopuff with a peak
pressure as low as possible, preferably ≤25 cm of H2O to avoid lung damage.
Oxygen saturations—the goal is to achieve acceptable preductal saturations levels of 80–
95 %. FiO2 should be started at 1.0 and then adjusted downwards to achieve SpO 2 targets.
Immediate placement of oro- or nasogastric tube with continuous or intermittent suction
will help to decompress the bowel and facilitate lung expansion.
A central or peripheral venous line should be inserted to allow for administration of fluids
and inotropes if necessary.
Arterial line is to be placed for monitoring of blood pressure and for blood sampling after
initial stabilization.
Arterial blood pressure to be maintained at acceptable levels for gestational age. In case of
hypotension or poor perfusion volume bolus (NaCl 0.9 % at 10–20 ml/kg) should be
administered and inotropes should be considered.
No routine use of surfactant in either term or premature infants is recommended as
surfactant therapy is associated with higher mortality rate, greater use of ECMO, and more
chronic lung disease with CDH.
Algorithm of postnatal management of CDH. OI oxygenation
index, ECMO extracorporeal membrane oxygenation. The algorithm is by no means
a complete representation of postnatal management of CDH, as the therapy for CDH
is still evolving.
Surgical Repair
Most surgeons wait for a few days for the period of stabilization to occur prior to surgery.
Standard surgical approach to repair the diaphragmatic defect consists of the subcostal
incision with removal of the abdominal contents from the thorax and complete
closure of the defect.
For defects that are too large to be closed by primary repair, a number of reconstructive
techniques such as prosthetic patches have been evolved to close the gap, and this can
be accomplished by synthetic non-absorbable material (Gore-Tex) or by natural
absorbable patch (Surgisis).
Approximately half of all the repairs that require some type of patch may result in
recurrent diaphragmatic herniation.
Minimally invasive surgery techniques for repair of CDH is gaining popularity; But
significantly higher recurrence risk of herniation.
Even though early repair of CDH in neonates on ECMO can be accomplished, CDH repair
after ECMO therapy is associated with improved survival compared to repair on ECMO
after controlling for factors associated with severity of CDH.
Q. 13) JSSK ?
Ans. Government of India has launched Janani Shishu Suraksha Karyakaram (JSSK) on 1st
June, 2011.
The scheme is estimated to benefit more than 12 million pregnant women who access
Government health facilities for their delivery.
Moreover it will motivate those who still choose to deliver at their homes to opt for
institutional deliveries.
It is an initiative with a hope that states would come forward and ensure that benefits
under JSSK would reach every needy pregnant woman coming to government
institutional facility.
All the States and UTs have initiated implementation of the scheme.
in 2014, the programme was extended to all antenatal & post-natal complications of
pregnancy and similar entitlements have been put in place for all sick newborns and
infants (up to one year of age) accessing public health institutions for treatment.
The following are the Free Entitlements for pregnant women:
Free and cashless delivery

Free C-Section
Free drugs and consumables
Free diagnostics
Free diet during stay in the health institutions
Free provision of blood
Exemption from user charges
Free transport from home to health institutions
Free transport between facilities in case of referral
Free drop back from Institutions to home after 48hrs stay
The following are the Free Entitlements for Sick newborns till 30 days after birth.This
has now been expanded to cover sick infants:
Free treatment
Free drugs and consumables
Free diagnostics
Free provision of blood
Exemption from user charges
Free Transport from Home to Health Institutions
Free Transport between facilities in case of referral
Free drop Back from Institutions to home
Q.14) malaria surveillance ?
Ans .
India moved towards global commitment for malaria elimination and endorsed a plan to

eliminate malaria throughout the region by 2030.
WHO has developed the Global technical strategy for malaria under the National
framework for malaria elimination in India 2016-2030 to eliminate malaria (zero
indigenous cases) throughout the entire country by 2030, and maintain malaria-free
status and prevent its re-introduction.
DISEASES BURDEN AND SURVEILLANCE –
Odisha - Durgama Anchalare Malaria Nirakaran (DAMaN) initiative and compre-hensive
case management of malaria.
Strengthening Malaria Diagnosis –
Accurate diagnosis is the key to success in the elimination goal.
P. falciparum and P. vivax cause the majority of cases.
Microscopy has always been the gold standard method but it requires highly skilled
microscopist with genuine knowledge of different stages of Plasmodium species with
capability to read low-density parasitemia - fulfilling such a requirement in rural India is
a daunting task, as a consequence, more than a quarter of malaria cases are missed by
microscopy.
RDTs used where microscopy is not feasible.
P. falciparum histidine-rich protein 2 (PfHRP2) antigen ->> P. falciparum - >90% RDTs.
Deletions of the Pfhrp2 gene in the parasite, fluctuation in the expression level of
Plasmodium Lactic Dehydrogenase (pLDH), and prozone phenomena are the major
problems leading to inaccurate diagnosis of plasmodium species.
Other potential biomarkers such as heme detoxification protein, apical merozoites
surface protein Pf34, Glutamate dehydrogenase, and hypnozoites-based serological
marker should be validated to strengthen the RDT tool.

Molecular methods - Polymerase chain reaction (PCR) - particularly low-density
infection.
Methods like conventional PCR, nested PCR, qPCR, multiplex PCR, and Loop-mediated
isothermal amplification (LAMP) are less frequently used techniques due to longer time
required, need for advanced equipment, expensive reagents and experienced personnel,
and difficultly in organizing in most field conditions.
A hemozoin-based magneto-optical detection device (Gazelle) may prove an
alternative to RDT for accurate diagnosis in the field.

Q. 15) National Immunisation Schedule ?
Ans.
National immunisation schedule :-

IAP immunisation schedule :-

Q. 16) Risk bias and confounding factor in clinical study ?
Ans.
Bias
• Bias:  Is any ‘systematic error’ in an epidemiological study, occurring during data
collection, compilation, analysis and interpretation.
Biases are of 3 types:
Subject bias: Error introduced by study subjects. Eg.
Hawthorne effect
Recall bias
Investigator bias: Error introduced by investigator –
Selection bias
Analyzer bias: Error introduced by analyzer
Important Types of Biases in Epidemiological Studies -
Apprehension bias: Certain levels (pulse, blood pressure) may alter systematically from
their usual levels when the subject is apprehensive.
Attention bias (Hawthorne effect): Study subjects may systematically alter their
behaviour when they know they are being observed.
Berkesonian bias (Admission rate bias): Bias due to hospital cases and controls being
systematically different from each other.
Interviewer bias: Interviewer devotes more time of interview with cases as compared to
controls
Lead time bias (Zero time shift bias): Bias of over-estimation of survival time, due to
backward shift in starting point, as by screening procedures.

Memory/ Recall bias: Cases are more likely to remember exposure more correctly than
controls
Neymann Bias (Prevalence-incidence bias): Bias due to missing of fatal cases, mild/
silent cases and cases of short duration of episodes from the study.
Selection bias (Susceptibility bias): Groups to be compared are differentially
susceptible to the outcome of interest, even before the experimental maneuver is
performed
Confounding:
Any factor associated with both exposure and outcome, and has an independent
effect in causation of outcome is a confounder.
It is found unequally distributed between the study and control groups
Is associated with both exposure and outcome
Has an independent effect in causation of outcome (thus is a risk factor itself).

Q. 17) management of persistent pulmonary hypertension ?
Ans. Management
Goals of therapy in PPHN are to promote lung recruitment, pulmonary vasodilation,
improve oxygenation and provide adequate oxygen delivery to the tissues while
minimizing oxidative stress and free radical injury.
Supportive Therapies –
Maintaining normal body temperature, glucose level, ionic calcium and sedation/
analgesia are important for optimal outcomes in patients with PPHN.
Lung Recruitment –
A common cause of failure to respond to treatment in (HRF) Hypoxic Respiratory Failure
with impaired oxygenation and ventilation is inadequate lung recruitment.
Optimizing lung recruitment with the use of PEEP to achieve lung expansion to functional
residual capacity (FRC) approximately 8–9 ribs expansion on anteroposterior chest X-
ray) often ensures adequate lung recruitment.
Underinflation and overinflation increase PVR due to the mechanical effects on the extra-
alveolar and intra-alveolar pulmonary blood vessels.
Atelectasis increases intrapulmonary right to  left shunting leading to worsening
hypoxia and hypercarbia.

Overinflation can impede venous return and cause systemic hypotension.
Oxygenation –
Oxygen is a potent vasodilator and hypoxia causes pulmonary vasoconstriction.
Supplemental O2 should be provided to achieve PaO2 between 50 and 80 mmHg.
Hyperoxia (PaO2 > 100 mmHg) does not enhance pulmonary vasodilation and increases
the formation of oxygen free radicals that increases pulmonary arterial contractility and
impairs vasodilator response to iNO.
Optimal saturation target range for patients with PPHN is not known.
Targeting a lower limit of preductal SpO2 of 92% Or 93% provides a buffer to hypoxic
pulmonary vasoconstriction and an upper limit of 97% ensures the optimal balance of
pulmonary vasodilation and minimizes adverse effects from oxidative stress.
Adequacy of tissue o2 delivery  by pulse oximetry and blood gas monitoring for acidosis.
Near infrared spectroscopy (NIRS)  is a non-invasive assessment of oxygen
delivery and is commonly used in postoperative management of congenital heart
disease. Although not routinely used in the management of PPHN, there may be benefit
to the use of NIRS in the presence of PPHN associated with hypoxic ischemic
encephalopathy.
Surfactant Replacement Therapy
Surfactant inactivation occurs with MAS, pneumonia and sepsis.
Surfactant therapy leads to improvement in oxygenation by improving V/Q matching and
decreases intrapulmonary shunting.
In newborn infants with parenchymal lung disease, surfactant replacement prior to
initiation of iNO improves outcome and reduces the need for extracorporeal membrane
oxygenation (ECMO).
Inhaled Nitric Oxide (iNO) –
Inhaled nitric oxide remains the only United States Food and Drug Administration
(FDA)-approved pulmonary vasodilator for infants with PPHN.
iNO is produced by the endothelial cells and causes pulmonary vasodilation through
generation of cyclic guanosine monophosphate (cGMP).
iNO causes selective vasodilation of the pulmonary circulation as it diffuses from the
alveolus into the smooth muscle cells and causes pulmonary vasodilation.
iNO is inactivated by hemoglobin in the circulation and hence has minimal systemic
vasodilator effect.
iNO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated
alveoli and decreases intrapulmonary right-to-left shunting and improves V/Q matching
(microselective effect).
iNO is usually initiated when the oxygenation index reaches 15–25.
Starting dose of iNO is usually 20 ppm.
Higher doses (80ppm) do not enhance pulmonary vasodilation and may increase the
incidence of side effects.
Clinical response is defined as an improvement in PaO2 by at least 20 mm Hg following
initiation of iNO.
In infants who fail to respond to iNO after optimizing lung recruitment, ventilation and
hemodynamic support, it is important to discontinue iNO to prevent downregulation of
endogenous NO pathway and prevent injury by formation of peroxynitrite.
Once oxygenation response is achieved, iNO dose can be weaned in decrements of 5 ppm
till 5 ppm is reached and by 1 ppm subsequently.
It is important to monitor methemoglobin and nitrogen dioxide levels at initiation and


daily during treatment with iNO. Once oxygenation response is achieved, iNO dose can be
weaned in decrements of 5 ppm till 5 ppm is reached and by 1 ppm subsequently.
It is important to monitor methemoglobin and nitrogen dioxide levels at initiation and
daily during treatment with iNO. The approach to weaning iNO used-
Guidelines for initiation and weaning iNO =
Recommended starting dose of iNO is 20 parts per million (ppm).
Improvement in PaO2 ≥ 20 mm Hg or hemoglobin saturation by pulse oximetry ≥ 5% is
considered complete response.
In patients who fail to respond iNO, measures needed to optimize of lung recruitment and
hemodynamics need to be undertaken.
iNO should be discontinued if there no response.

In responders wean FiO2 initially while maintaining PaO2 between 60 and 80 mm Hg.
Once PaO2 is stable and FiO2 is below 0.6, start weaning iNO by 5 ppm every 4 h till 5
ppm. Below 5 ppm wean iNO by 1 ppm every 4 h.
During weaning >5% drop in pulse oximetry or sustained increase in FiO2 > 0.15 to
maintain PaO2 > 60 mm Hg is considered weaning failure, and previous dose of iNO
should be resumed.
Weaning should be resumed once stable.
Monitor methemoglobin levels at baseline, 2 and 8 h following initiation and every 48 h
thereafter.
Prostaglandins –
Prostacyclins  Mainstay of therapy for pulmonary hypertension in adults.
Evidence for use in newborns with PPHN is limited.
Prostaglandins cause activation of adenylate cyclase increasing the cAMP levels in the
vascular smooth muscle cells leading to pulmonary vasodilation.
Intravenous prostacyclins can lead to systemic hypotension and worsening of VQ
mismatch.
Inhaled PGI2 by nebulization has been shown to be effective in infants who had poor
response to Ino.
Phosphodiesterase Inhibitors –
Cyclic mononucleotides cGMP and cAMP are degraded by phosphodiesterase (PDE)
enzymes in the pulmonary artery smooth muscle cells.
Milrinone is a PDE3A inhibitor and  enhances cAMP levels in the arterial smooth
muscle cells and cardiac myocytes resulting in vasodilation and inotropy.
Milrinone is administered as a loading dose of 50 µg/kg/min given over 30 min 

followed by 0.33 µg/kg/min as a continuous infusion.
Dose may be titrated up to 1 µg/kg/min with close monitoring of systemic blood pressure.
Sildenafil –
PDE5 inhibitor, which decreases breakdown of cGMP resulting in pulmonary
vasodilation.
Sildenafil may be used in combination with iNO, or may be used alone to prevent rebound
PH following withdrawal of iNO.
Hyperoxic ventilation increases PDE5, and PDE5 inhibitors may be particularly effective
in patients who have been exposed to hyperoxic ventilation.
Typical dose of intravenous sildenafil is a Loading dose of 0.42 mg/kg over 3 h
followed by 0.07 mg/kg/h.
The starting dose of oral sildenafil is 0.5 mg/kg/dose every eight hourly and can be
increased to a maximum of 3–8 mg/kg/day, divided every 6–8 h.
Phosphodiesterase inhibitors dilate the pulmonary vasculature irrespective of ventilation
status and could cause V/Q mismatch leading to worsening oxygenation.
Systemic vasodilation and hypotension are particularly common during initiation of
therapy, hence intravascular volume status should be optimized, and blood pressure
monitored closely during treatment with phosphodiesterase inhibitors.
Inotropes
Sedation/Paralysis
Nutrition
Acid–Base Balance
Extracorporeal Membrane Oxygenation (ECMO)

Newer agents such as –
L-Citrulline,
Endothelin receptor antagonists,
Soluble guanylyl cyclase stimulators and activators,
Rho kinase inhibitors,
Peroxisome proliferator activated receptor gamma (PPAR 7) agonists, and
Antioxidants
PATHOPHYSIOLOGY OF PPHN :-


DTaP PAEDIATRICS
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DTaP Paediatrics/ Dr. A.K.

(Session: - JUNE 2022)

DTaP Pediatrics / Dr. A. K. Saini

Ans. IRON metabolism

DTaP Pediatrics / Dr. A. K. Saini

DTaP Pediatrics / Dr. A. K. Saini

Q. 3) Childhood Diabetes management ?

Ans. TYPE OF Diabetes :-

Obesity and a family history of T2D increase the risk.

DTaP Pediatrics / Dr. A. K. Saini

as by metformin (an antidiabetic drug) in the early stages.

Association (ADA) 2021 guidelines:-

M/C form in this age-group remains type 1 diabetes - immune mediated.

Type II diabetes, although rare, is on the increasing trend in our country.

Type III diabetes includes other forms such as –

Monogenic diabetes/maturity-onset diabetes of the young (MODY),

cystic fibrosis-related diabetes (CFRD),

fibrocalculous pancreatic diabetes (FCPD),

drug-induced diabetes, and

lipodystrophic diabetes, which are also being recognized.

Presence of hyperlipidemia at onset

DTaP Pediatrics / Dr. A. K. Saini

Family history of early onset diabetes in preceding two generations

Medications—steroids and immunosuppressants

glucose (BG) values lie in target range of 70–180 mg/dL.

Prevention of acute complications such as diabetic ketoacidosis (DKA) and hypoglycemia.

Prevention of long-term complications and achieving good quality of life.

Achieve normal growth and development.

MANAGEMENT OF CHILDHOOD DIABETES :-

[1] Medical nutrition therapy

[2] Physical activity

[3] Glucose monitoring

[4] Insulin therapy

Medical nutrition therapy

Balanced diet by plate method as below:

1/3rd high-quality high-fiber rich carbohydrates,

1/3rd of fruits and vegetable

DTaP Pediatrics / Dr. A. K. Saini

One carbohydrate exchange equals = 15 g carbohydrate.

playing in open grounds.

consume a snack if BG is low, to avoid hypoglycemia.

BLOOD GLUCOSE MONITORING:-

An essential pillar of management in diabetes.

Easiest way to monitor is using a hand-held glucometer to check BG daily.

DTaP Pediatrics / Dr. A. K. Saini

the child develops any uneasiness or discomfort.

Continuous glucose monitoring system (CGMS) –

fluid at frequent intervals.

percentage of time when the BG remained between 70 and 180 mg/dL.

An optimum value is 70% or more.

At present, CGMS of Medtronic, Dexcom, and Abbott are available in India.

Insulin should be started soon after diagnosis of diabetes.

DTaP Pediatrics / Dr. A. K. Saini

unsuitable for use in children.

Regular or rapid/ultra-rapid-acting insulin are administered preprandial timed as per

the onset and peak of action.

Syringes, pens, or advanced technology like insulin pumps.

U-40 syringes with U-40 vials (40 units of insulin/mL).

The attached needles are 6 or 8 mm long.