High-Yield One Liners in Pediatric Pulmonology

Difference between Pediatric Airway and Adult Airway

In Children

• The tongue is larger with respect to the oral cavity.
• Epiglottis in children is longer, larger, and abnormally shaped in many patients (omega-shaped).
• Excess omega-shaped epiglottis is a feature of laryngomalacia, but even certain asymptomatic and normal children can have an omega-shaped epiglottis.
• The larynx in children is placed higher and anteriorly at the level of the C2 vertebra.
• The narrowest part of the airway in children differs from that of adults.
• The subglottic area in front of the cricoid cartilage is the narrowest part of the airway in children.
• Pharynx and Larynx in children are narrower.

In Adults

• The narrowest part is the glottis area (vocal cords).

Why is the common cold so common?

Many stereotypes are present. If a person gets infected by the parainfluenza virus, the antibodies formed against this will not protect the body against another. Response in the form of IgA mediated, IgA-mediated response is short-lived

According to Nelson 21st edition

Azithromycin and cotrimoxazole are no longer indicated because of a high prevalence of antibiotic resistance in sinusitis.Therapy with antimicrobials is given for at least 10 days or 7 days after the resolution of symptoms. Decongestants, antihistamines, mucolytics, and intranasal corticosteroids are not recommended for the treatment of acute uncomplicated bacterial sinusitis in children.

Q. What is pleuropulmonary blastoma (PPB)?

Ans. 

• A malignant lesion associated with Type 4 CPAM.
• Resemble congenital pulmonary airway obstruction (CPAM).
• DICER-1 mutations are seen
• Sarcomatous/Malignant carcinomatous changes can develop rarely in other forms of CPAM
• All CPAM should be surgically resected before 1 year of age.

Types of Sequestration

Q. What is allergy sensitization?

Ans. Initially or after the first exposure to an allergen. Which leads to the production of IgE antibodies. These antibodies coat the mast cells and basophils.

AR and Bronchial Asthma

Up to 78% of patients with asthma have AR, 38% of patients with AR have asthma.

Aggravation of AR coincides with exacerbation of asthma, Treatment of nasal inflammation reduces bronchospasm, asthma-related emergency department visits, and hospitalization. Patients with AR have an overall three times higher risk of developing bronchial asthma later in life.

Key points regarding CFTR mutations

Severity according to the class

• Class I, II, III are severe
• Class IV, V, and VI are mild to moderate

Mutation types

• Overall, most common - Phe508del, also called ΔF508. (CLASS II)
• Most common in Ashkenazi Jews: Trp1282 X (W1282X). (CLASS I)
• Intestinal epithelial cells homozygous for Phe508del are unresponsive to the secretory effects of cholera toxin.
• CFTR mutations produce aberrantly greater negative potential differences across the respiratory epithelium.
• Non-CFTR modifier genes may also influence CF presentation.
• Chromosome 11 and chromosome 20 Polymorphisms may be related to lung severity.

Diagnostic criteria for cystic fibrosis

• Two factors must be fulfilled to diagnose cystic fibrosis (CF) (both)
• Clinical picture compatible with cystic fibrosis
• Laboratory evidence of CFTR (Cystic fibrosis transmembrane conductance regulator) dysfunction.
• One criterion from the clinical picture is compatible with cystic fibrosis + one criterion from laboratory evidence of CFTR dysfunction.

Diagnostic criteria in clinical picture compatible with cystic fibrosis

Clinical features suggestive of cystic fibrosis (respiratory, gastrointestinal, or genito-urinary features).

or

History of cystic fibrosis in a sibling.

or

A positive newborn screening test for cystic fibrosis.

Diagnostic criteria for laboratory evidence of CFTR dysfunction

• Two positive sweat chloride tests - done on two different days.
  • Screening test of choice (older children, adults)- sweat chloride test,
    • Check for chloride in sweat by pilocarpine iontophoresis.
    • Amount of chloride in the sweat sample- > 60 milliequivalents/ L → CFTR dysfunction.
• Two CFTR gene mutations are observed.
  • A single mutation may or may not be associated with cystic fibrosis.
• Abnormal nasal potential difference measurement.
  • Even a single abnormal Nasal potential difference measurement value → CFTR dysfunction

Drugs Causing Eosinophilic Pneumonias:

• Anti-inflammatory drugs like: Aspirin, Ibuprofen, Diclofenac, Naproxen, Piroxicam, Phenylbutazone, Sulindac and Tolfenamic acid
• Antibiotics: Penicillin, Sulphonamides (TMP-SMX),
• Minocycline, Nitrofurantoin, Ethambutol
  • Captopril
  • Carbamazepine
  • GM-CSF

AEP vs CEP: Key points to remember

Infections with a higher risk of pediatric bronchiectasis are:

• Streptococcus pneumoniae
• Moraxella catarrhalis
• Non- typeable Haemophilus influenzae
• Bordetella pertussis
• Post-measles
• RSV, adenovirus and Togavirus
• HIV
• Mycobacterium tuberculosis

MCQ Points 

• In contrast to GPA, the rhinitis is not destructive and nasal septal perforation does not occur in EGPA.
• Etiopathogenesis of EGPA is unknown.
• Many cases are associated with use of LTRAs (Leukotriene receptor antagonists): Montelukast and Zafirlukast.
• 40% cases are pANCA positive.
• New, effective steroid-sparing agent- Mepolizumab (Anti-IL5)
• In a patient of EGPA, presence of pleural effusion should raise suspicion for the presence of heart failure from cardiomyopathy.
• When the total IgE antibody in patients with cystic fibrosis exceeds 500 IU/mL (1,200 ng/mL), a strong clinical suspicion of ABPA is necessary.
• The absence of a positive skin prick test and intradermal test to A. fumigatus virtually excludes the diagnosis of ABPA.
• Asthma or CF: Refractories to treatment or recent worsening, consider ABPA.
  • Total serum IgE
  • Skin prick test: A. fumigatus
• The classic triad of Kartagener Syndrome:
  • Chronic rhinosinusitis
  • Situs Inversus Totalis
  • Bronchiectasis
• Prenatal diagnostic markers for PCD / Kartagener Syndrome:
  • Antenatal using ultrasound
    • Dilated ventricles in the brain
    • Situs inversus in a foetus

MCQ Pointers: Very Important

Infections

• Pneumonia in child aged 3 months to 3 years with NO FEVER - Chlamydia trachomatis
• Bacterial infection superimposed on the influenza virus - Staphylococcus aureus (measles and influenza).
• Pneumonia in cystic fibrosis is the most common cause overall (in adults) - Pseudomonas aeruginosa (Mucoid strains).
• In children with cystic fibrosis - Staphylococcus aureus > Pseudomonas aeruginosa
• The most common Fungal pneumonia in Cystic fibrosis - Aspergillus Fumigatus.
• Most severe/ fatal/ specific organism causing pneumonia in Cystic fibrosis - Burkholderia cepacia.

MCQ Example

Q. An 18-month child with fever, cough, mild chest indrawing and respiratory rate of 34/min presented to OPD. Which among the following is the appropriate therapy of choice?

1. Supportive therapy since no pneumonia
2. Oral Amoxicillin and review in 48 hours
3. Get CXR done and start Amoxicillin - Clavulanate
4. Give 1st dose of parenteral antibiotic and refer to higher center

Ans.

• The child is in the age group of 1-5 years.
• The respiratory rate in Tachypnea is ≥40 per minute.
• It is 34 per minute in the case mentioned in the question. So, no Tachypnea is present.
• The child in question has a fever, cough, and mild chest in drawing - diagnosed with pneumonia. Due to the absence of a dangerous sign, this is not a case of severe pneumonia.

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