NEET PG Paediatrics Flashcards

24 sample cards from the Paediatrics deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. List the antigens in the pentavalent vaccine used in India's UIP.

   Pentavalent vaccine combines DPT (Diphtheria, Pertussis, Tetanus), Hepatitis B, and Haemophilus influenzae type b (Hib). In India's National Immunization Schedule it is given at 6, 10, and 14 weeks.

2. What is the Indian National Immunization Schedule at birth and at 6/10/14 weeks?

   At birth: BCG, OPV-0, and Hepatitis B birth dose. At 6, 10, and 14 weeks: Pentavalent, OPV, fIPV (inactivated polio), and Rotavirus; PCV is also given (6 & 14 weeks plus booster). Measles/MR is at 9-12 months.

3. Which vaccines are live-attenuated and what is the key contraindication?

   Live vaccines include BCG, OPV, measles/MR/MMR, rotavirus, varicella, and yellow fever. They are contraindicated in significant immunodeficiency and (with caution) pregnancy. Two live parenteral vaccines should be given the same day or separated by >= 4 weeks.

4. What is the stepwise pharmacologic management of childhood asthma per GINA?

   Reliever: as-needed SABA (or low-dose ICS-formoterol). Controllers step up: low-dose ICS, then low-dose ICS + LABA (or medium ICS), then medium/high ICS-LABA, then add-on (LAMA/biologics). Assess control, inhaler technique, and adherence before stepping up.

5. What clinical and spirometric features support a diagnosis of asthma in a child?

   Recurrent wheeze, cough (often nocturnal), breathlessness, and chest tightness, variable and reversible. Spirometry (usually feasible > 5 years) shows obstructive pattern with FEV1/FVC reduced and >= 12% improvement in FEV1 after bronchodilator (reversibility).

6. What is bronchiolitis: typical age, cause, and management?

   Bronchiolitis is a lower-respiratory viral illness in infants < 2 years (peak 2-6 months), most often caused by RSV. Features: coryza progressing to wheeze, fine crackles, respiratory distress, and feeding difficulty. Management is supportive (oxygen, hydration, nasal suction); bronchodilators/steroids are not routinely recommended.

7. How do you clinically distinguish bronchiolitis from infantile asthma/viral wheeze?

   Bronchiolitis: first episode in an infant < 2 years, prodromal coryza, diffuse crackles plus wheeze, RSV season, poor bronchodilator response. Recurrent wheezing episodes, family/personal atopy, and a good bronchodilator response favor asthma/viral-induced wheeze.

8. What is the genetic basis and inheritance of cystic fibrosis?

   Cystic fibrosis is autosomal recessive, caused by mutations in the CFTR gene on chromosome 7 (most common: delta-F508). Defective CFTR chloride channel produces thick secretions affecting lungs, pancreas, intestine, and sweat glands.

9. What is the diagnostic test for cystic fibrosis and its classic clinical features?

   Diagnosis: sweat chloride test (>= 60 mmol/L is positive), supported by genetic testing/newborn screen (raised immunoreactive trypsinogen). Features: recurrent pulmonary infections (Pseudomonas, Staph aureus), pancreatic insufficiency with steatorrhea, failure to thrive, meconium ileus, and male infertility.

10. What are the WHO classifications of malnutrition (SAM criteria)?

    Severe acute malnutrition (SAM): weight-for-height/length < -3 SD, OR MUAC < 11.5 cm (6-59 months), OR bilateral pitting pedal edema. Moderate acute malnutrition: weight-for-height between -2 and -3 SD or MUAC 11.5-12.5 cm.

11. Compare marasmus and kwashiorkor.

    Marasmus: severe wasting from total calorie deficit — marked muscle/fat loss, 'old man' face, weight < 60% expected, NO edema, alert/irritable, appetite preserved. Kwashiorkor: protein deficiency — generalized edema, hepatomegaly (fatty liver), 'flaky paint' dermatosis, hair changes, apathy, anorexia.

12. What are the steps of WHO management of severe acute malnutrition, including the danger of refeeding?

    Stabilization (manage/prevent hypoglycemia, hypothermia, dehydration, infection, electrolyte imbalance, micronutrients) then rehabilitation (catch-up growth with F-100/RUTF). Refeeding too fast causes refeeding syndrome (hypophosphatemia, hypokalemia, hypomagnesemia, cardiac failure) — start cautious feeding with F-75.

13. What is the most common congenital heart defect, and what murmur does VSD produce?

    Ventricular septal defect is the most common congenital heart defect. It causes a left-to-right shunt with a harsh holosystolic (pansystolic) murmur best heard at the left lower sternal border. Large VSDs cause heart failure and may progress to Eisenmenger syndrome.

14. What are the auscultatory hallmarks of an atrial septal defect?

    ASD produces a wide, fixed split S2 (does not vary with respiration) and a mid-systolic ejection murmur at the upper left sternal border (from increased pulmonary flow). Ostium secundum is the most common type; large shunts cause RA/RV enlargement and paradoxical embolism risk.

15. Describe the murmur and management of patent ductus arteriosus.

    PDA causes a continuous 'machinery' murmur at the left infraclavicular/upper left sternal area, wide pulse pressure, and bounding pulses. In preterms, indomethacin or ibuprofen (prostaglandin inhibitors) promote closure; symptomatic/persistent PDAs need catheter device or surgical closure.

16. What are the four components of Tetralogy of Fallot and its classic X-ray/echo signs?

    TOF = (1) VSD, (2) overriding aorta, (3) right ventricular outflow tract obstruction (pulmonary stenosis), (4) right ventricular hypertrophy. Chest X-ray shows a 'boot-shaped' heart (coeur en sabot) with decreased pulmonary vascularity; it is the most common cyanotic CHD beyond infancy.

17. What is a 'tet spell' and how is it managed acutely?

    A hypercyanotic (tet) spell is paroxysmal worsening cyanosis from increased RVOT obstruction/decreased SVR. Management: knee-chest position (increases SVR/venous return), oxygen, morphine, IV fluids, beta-blockers (propranolol/esmolol), and phenylephrine to raise SVR; correct acidosis. Definitive treatment is surgical repair.

18. What are the clinical features and classic findings of coarctation of the aorta?

    Coarctation causes upper-limb hypertension with weak/delayed femoral pulses (radio-femoral delay) and a BP gradient between arms and legs. Chest X-ray shows rib notching (collateral intercostal vessels) and a '3 sign'. Associated with bicuspid aortic valve and Turner syndrome.

19. Define a simple febrile seizure and its key reassuring features.

    A simple febrile seizure is a generalized (tonic-clonic), single seizure lasting < 15 minutes, not recurring within 24 hours, in a child 6 months-5 years with fever and no CNS infection or prior afebrile seizures. It has an excellent prognosis with low epilepsy risk.

20. What features define a complex febrile seizure?

    A complex febrile seizure has any of: focal onset/features, duration > 15 minutes, or recurrence within 24 hours (or within the same febrile illness). Complex features warrant closer evaluation and carry a slightly higher risk of subsequent epilepsy than simple febrile seizures.

21. What is the management approach to febrile seizures, including when to do a lumbar puncture?

    Most febrile seizures are self-limited; treat the fever and reassure, no long-term anticonvulsants for simple cases. Prolonged seizures: benzodiazepines (rectal/IV/buccal). Consider LP if meningeal signs, < 12 months with uncertain status, complex features, or pretreatment with antibiotics masking meningitis.

22. What is the allergic march and how are allergic rhinitis, conjunctivitis, and atopic dermatitis linked?

    The 'atopic march' is the typical progression of IgE-mediated allergic disease: atopic dermatitis (eczema) and food allergy in infancy, followed by allergic rhinitis and asthma in later childhood. Allergic rhinoconjunctivitis (sneezing, itchy nose/eyes, watery rhinorrhea, conjunctival itch/tearing) shares Th2-driven IgE pathophysiology.

23. Describe atopic dermatitis (eczema) distribution by age and first-line management.

    Atopic dermatitis: infancy — face, scalp, extensor surfaces; childhood/adult — flexural creases (antecubital/popliteal fossae). It is intensely pruritic and relapsing, often with raised IgE. Management: liberal emollients (skin barrier), topical corticosteroids for flares, trigger avoidance, and topical calcineurin inhibitors as steroid-sparing agents.

24. What is anaphylaxis, its most common food triggers in children, and first-line treatment?

    Anaphylaxis is a severe, rapid-onset IgE-mediated systemic reaction with airway/breathing/circulation compromise (urticaria, angioedema, wheeze, hypotension, vomiting). Common food triggers: milk, egg, peanut, tree nuts, fish, shellfish. First-line treatment is intramuscular adrenaline 0.01 mg/kg (anterolateral thigh), supine positioning, oxygen, and IV fluids — antihistamines/steroids are adjuncts only.

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