Respirology Flashcards

Question

12yo with Asthma only on PRN Ventolin what next a) ICS b) ICS + LABA

Answer 1

a) ICS Next step would be daily ICS for asthma control per CTS guidelines

Answer 2

c) sweat chloride If you see nasal polyps, need to rule out CF as a cause

Answer 3

c) AP and lateral CXRs wouldn't start amox without imaging inspiratory and expiratory could be helpful if concerned about a FB ICS not indicated as doesn't sound like asthma - no night time or exercise Sx

Answer 4

a) muscular dystropy All other options would show an obstructive loop

Answer 5

c) pseudomonas Psuedomonas risk in CF increases after school age and they are often colonized with it. Need anti-pseudomonal coverage with exacerbations Staph would also be a good answer if it was an option Burkholderia is a serious gram neg infection but rare Steno doesn't really increase until mid-school age

Answer 6

a) amoxicillin PO This patient is stable with mild CAP and appropriate for outpatient treatment

Answer 7

- brassy - honking and loud - resolves during sleep - +/- history of psychogenic stressors

Answer 8

- "stacatto" - may be associated with eosinophilia - think about in neonate with cough

Answer 9

- paroxysmal cough - post-tussive emesis often occurs - unvaccinated child - can be associated with lymphocytosis

Answer 10

always consider retained FB aspiration key to consider in preschool aged child - may be an unwitnessed aspiration and may not be associated with signs of URTI may be after witnessed choking episode

Answer 11

RSV human metapneumovirus rhinovirus adenovirus parainfluenza 10-30% of children will have multiple viruses

Answer 12

1. prematurity (<35 weeks) 2. <3 months of age at presentation 3. Hemodynamically significant cardiopulmonary disease 4. Immunodeficiency

Answer 13

1. signs of severe respiratory distress (indrawingt, grunting, RR > 60) 2. supplemental O2 required to maintain SpO2 > 90 3. Dehydration or history of poor PO intake 4. Cyanosis or history of apnea 5. Infant at high risk for severe disease (prematurity <35 wks, <3mo age, hemodynamic compromise, immunodeficiency) 6. family unable to cope

Answer 14

1. tachypnea/WOB improved 2. SpO2 >90 without supplemental O2 OR stable for home O2 therapy 3. adequate oral feeding 4. education provided and appropriate follow up arranged "physicians should keep in mind that the disease tends to worsen over the first 72h when deciding whether to hospitalize"

Answer 15

Bronchiolitis is a clinical diagnosis based on history and PE Typically presents as first episode of wheeze before 12 months

Answer 16

2-3 day viral prodrome of fever, cough, rhinorrhea progressing to tachypnea, wheeze, crackles and variable degree of respiratory distress the majority of wheezing infants who present acutely between November and April will be viral bronchiolitis, but consider a broad Ddx

Answer 17

Tests are often unhelpful and lead to unnecessary admissions, testing and ineffective therapies CXR: often reveals nonspecific, patchy hyperinflation and atelectasis, may be misinterpreted as consolidation and lead to unnecessary antibiotics NP swab for viruses: generally not helpful diagnostically, don't alter management. Not recommended unless req'd for infection ctrl purpouse or high risk patients CBC: not helpful Bacterial cultures: incidence of serious bacterial infection in febrile infants with bronchiolitis is low. UTI is most common SBI in infants with bronchiolitis <90d old, but still low (3.1%). Routine screening for SBI including UA is not indicated but should be guided clinically Gas: generally not helpful in Dx or monitoring

Answer 18

Recommended: - oxygen to maintain sats <90% - hydration (encourage frequent bottle/breast feeds. NPO if RR > 60, in which case IV/NG equally effective and no difference in hospital LOS) Equivocal: - epi neb (may reduce admission rates - can trial in ED for response) - nasal suctioning - combined epi and dex (need more research) Not recommended: - ventolin (infants have inadequate B-agonist lung receptors to be effective) - corticosteroids - antibiotics - antivirals - 3% nebs - chest physio - cool mist therapies or saline aerosol

Answer 19

make sure to understand inclusion and exclusion criteria Inclusion: - age <=24 months - clinical diagnosis of bronchiolitis Exclusion: - significant cardiopulmonary disease - severe comorbidity (eg immunodeficiency, neuromuscular disease) - severe distress or imminent respiratory failure

Answer 20

- when diagnosis of bronchiolitis is unclear - when rate of improvement is not as expected - when severity of disease raises other diagnostic possibilities such as bacterial pneumonia

Answer 21

- droplet isolation - regular clinical assessments including RR, WOB, sats, auscultation, feeding, hydration status - CRM for kids with apneas, high risk patients in an acute phase of illness - consider intermittent spot sats otherwise as CRM can increase LOS in hospital

Answer 22

- ability to delivery 100% O2 to older children and adults in a way that's well-tolerated - washout of anatomic dead space to upper and intrathoracic airways to reduce WOB - Reduced RR and WOB suggesting improved minute ventilation and CO2 clearance - reduces NIV and intubation - after ~1-2L/kg/min there is some PEEP

Answer 23

- set the flow at 1-2L/kg/min and escalate as needed to minimize WOB - max flow rate should be 2L/kg/min with upper limit of 50-60L/min for adult sized patients - start FiO2 at 50% and titrate to achieve O2 sats (94-98% per CPS) - titrate flow down as WOB improves - remember initiation of HHHFNC may increase resp distress initially due to breath-stacking or auto-PEEP; consider decreasing flow rate

Answer 24

- nasal obstruction - epistaxis - severe upper airway obstruction relative: complications from "third-spacing" of air can occur when HHHFNC is used in pts with facial trauma or following airway/esophageal surgery

Answer 25

Upper airway obstruction - sleep apnea Lower airway obstruction - bronchiolitis - asthma Lung parenchymal disease - pneumonia - pneumonitis Heart failure

Answer 26

viral infection of the URT - parainfluenza types 1 and 3 (most common) - influenza A and B - adenovirus - RSV - metapneumovirus

Answer 27

generalized airway inflammation and edema of the upper airway mucosa secondary to viral infection. subglottic region becomes narrowed, causing upper airway obstruction and croup Sx

Answer 28

- rapid onset - barky cough - inspiratory stridor - hoarseness - respiratory distress - non-specific Sx of URTI typically preceding croup Sx - croup Sx often worse at night - typically affects children between 6m - 3y - Sx short lived - typically 3-7d - in 60% of pts barky cough gone after 48h

Answer 29

in <5% symptoms of croup may last llonger than 5 nights <5% of children will experience more than one episode

Answer 30

Bacterial tracheitis (high fever, toxic, poor response to epi nebs) RPA or PTA (high fever, neck pain, sore throat, dysphagia followed by torticolis, drooling, resp distress and stridor) Epiglottitis (no barky cough. Sudden high fever, dysphagia, drooling, toxic, anxious, sitting in sniffing position) Aspiration or foreign body (choking episode, wheeze, hoarse, biphasic stridor, dyspnea, decreased AE) Anaphylaxis

Answer 31

Manage croup based on severity of illness as determined by their clinical signs/Sx General - keep them comfortable - don't frighten them - no evidence for use of humidified air/mist tents Steroids - improvement generally begins within 2-3h post PO dex and persists for 24-48h - PO or IM routes are as good or better than nebulized - PO preferred unless vomiting, then IM - 0.6mg/kg/dose. Studies unclear of efficacy of lower (0.15 or 0.3) doses Epinephrine - recommended for moderate-severe croup - reduces chance of intubation/trach - improves resp distress within 10-30mins - lasts for ~1h, effect gone after 2h - racemic is just as effective as L-epi (racemic not available in Canada) Heliox - reduces respiratory distress due to lower density and subsequent lower turbulence of air within the narrowed airway - does not improve croup Sx, so not routinely recommended per CPS

Answer 32

after observation for 2-4h following PO dex and epi nebs with no recurrence of croup Sx following 2-4h

Answer 33

5ml of 1:1000 L-epinephrine same dose for all ages and weights equally as effective as racemic epi (which is not available in Canada)

Answer 34

Pneumonia is acute inflammation of the parenchyma of the LRT caused by a microbial pathogen (viral or bacterial) Uncomplicated pneumonias may have small parapneumonic effusions empyema (pus in pleural space), lung abscess or necrotic portion of lung indicates complicated pneumonia

Answer 35

Viral: RSV, influenza, paraflu, HMV - viral is most common Bacterial: - strep pneumo (most common) - mycoplasma pneumoniae (more common in school age) - chlamydophila pneumonia (more common in school age) - GAS much less common than strep pneumo - Staph aureus: not common cause of pediatric PNA but increased risk in communities with MRSA prevalence - Haemophilus influenza b (Hib) almost disappeared with vaccination https://cps.ca/documents/position/pneumonia-management-children-youth

Answer 36

malaise and headache for 7-10 days prior to onset of fever and cough, which then predominate

Answer 37

may be non-specific, especially in infants and young children Acute onset of fever, cough, dyspnea, poor feeding, vomiting, decreased energy chest pain abdominal pain abrupt onset of rigors favours bacterial cause

Answer 38

may be heralded by sudden onset of systemic symptoms such as diffuse myalgias and fever, followed by cough, sore throat and respiratory Sx during flu season, influenza with or without SBI as cause of pneumonia should be strongly considered

Answer 39

CF Cystic fibrosis is the most common cause of nasal polyps in children

Answer 40

a) add ICS daily this kiddo meets criteria for poorly controlled asthma given use of PRN SABA >2x/week. They require addition of controller medication with daily ICS

Answer 41

c) Clindamycin and cefotaxime This is a pneumatocele - an air filled cystic lesion within the lung parenchyma. It can be infectious and most common bug is staph, so would want to target this bug along with other typical pneumonia bugs hens this coverage

Answer 42

Gold standard imaging test is CT CT guided aspiration can help with diagnostic clarity and treatment planning

Answer 43

Typical bug is Staph, so would need staph coverage Clindamycin or Vanco for MRSA Ceftriaxone for other typical bugs CTX + vanco if rapidly progressive or concerns for pneumatocele

Answer 44

1. CF 2. CF 3. CF Others include chronic sinusitis, allergic rhinitis, severe asthma in an older child Nasal polyps are never normal - suspect CF in any child <12 with nasal polyps even if no other respiratory or GI Sx

Answer 45

1. Documentation of airflow obstruction - preferred: documented wheezing and other signs of airflow obstruction by physician or HCP - alternative: convincing parent report of wheeze or other Sx of airflow obstruction 2. Documentation of reversibility of airflow obstruction - preferred: documented improvement with SABA by HCP - alternative: convincing parental report of Sx response to a 3-month trial of ICS with PRN SABA or response to PRN SABA 3. No clinical evidence of an alternative diagnosis If no current Sx of airflow obstruction when you're assessing, but if ≥2 episodes of asthma like Sx --> response to asthma therapy --> asthma If frequent Sx (>8d/month or >2/week) or ≥1 severe asthma-like exacerbation with current Sx of airflow obstruction (hospitalization) --> response to asthma therapy --> asthma

Answer 46

About 1-4 weeks Ensure appropriate use and consistent administration before deciding whether it was effective or not

Answer 47

Asthma is 1. An inflammatory airway disorder with 2. paroxysmal or persistent symptoms (dyspnea, chest tightness, wheeze, cough), associated with 3. variable airflow obstruction and airway hyper responsiveness

Answer 48

Male Preterm LBW Atopy Family history of asthma/atopy Tobacco exposure

Answer 49

- Recurrent or episodic Sx: dyspnea, tightness, wheeze, cough - Timing: night time, exercise, exposure to allergens, seasonal - Triggers: smoke, smoking, allergies, temperature change, exercise, URTI, emotion - bronchodilator responsiveness - History of atopy, eczema, IgE mediated allergy

Answer 50

- Lower airway: CF, PCD, chronic aspiration, CLD of prematurity, ILD - upper airway: VCD, TEF, large airway obstruction (extrinsic, intrinsic, chest wall deformity), ring or sling - Infection: adenopathy, viral, bacterial, pertussis, IEI or immune dysregulation - Cardiac: CHF, cardiac wheeze - GI: GERD

Answer 51

ASTHMA IS A CLINICAL DIAGNOSIS based on (1) clinical symptoms and (2) reversible airway obstruction with treatment with SABA/ICS A PFT is helpful more for trending of management than the diagnosis itself Objective evidence of reversible airway obstruction with a PFT demonstrates: - FEV1/FVC <0.8 (obstruction) - an increase in FEV1 by ≥12% with bronchodilator or after a course of controller therapy Alternatives: - Increase in peak expiratory flow of ≥20% after a bronchodilator of course of controller therapy - convincing caregiver report of wheeze with response to a 3 month trial of medium dose ICS and PRN SABA or response to PRN Saba - positive exercise challenge: ≥10-15% decrease of FEV1 - positive methacholine challenge: PCO2 <4mg/ml

Answer 52

Methacholine challenge is an airway irritant a negative methacholine challenge RULES OUT asthma, a positive is NOT diagnostic

Answer 53

Reassess Q3-6 months - control - risk of exacerbation - spirometry or PEF - inhaler technique - adherence - triggers - comorbidities

Answer 54

Age 1-6y: increase ICS to medium dose Age 6-11: increase ICS to medium dose. If ongoing poor control consider adding LABA (advair or Bud/Form) or LTRA Age ≥12: Switch to LABA (Bud/Form) as controller and reliever with SMART dosing, max reliever dosing 8 puffs/day

Answer 55

- Daytime Sx ≤2x/week - Night time Sx < 1 night/week and mild physical activity normal - exacerbations are mild (not requiring systemic steroids, ED visit or hospitalization) and infrequent (not impairing their subjective quality of life) - No absences from school or work due to asthma - Need for reliever (SABA or bud/form) ≤2/week - FEV1 or FEP ≥90% of personal best - PEF diurnal variation <10-15% - Sputum eosinophils <2-3%

Answer 56

An individual with any of these is at higher risk of severe asthma exacerbation: 1. any history of a previous severe asthma exacerbation (requiring any of the following: systemic steroids, ed visit, or hospitalization) 2. poorly controlled asthma as per Cts criteria 3. overuse of SABA (defined as use of more than 2 inhalers of SABA in a year) 4. current smoker

Answer 57

- Any previous near-fatal asthma exacerbation (eg, previous intensive care unit (ICU) admission, ventilation, respiratory acidosis) - Recurrent hospitalizations or ed visits in last year - Severe asthma - Overuse of saBA - Poor adherence to treatment plans - Failure to attend clinic appointments - Depression, anxiety or other psychiatric illness - Alcohol or other substance use - Obesity - Severe domestic, marital, employment, local stress - Denial of illness or severity of illness

Answer 58

Patients currently well controlled on PRN SABA or no medication with low risk for exacerbation can continue PRN SABA, or be switched to daily ICS+PRN SABA (all ages) or PRN Bud/Form (≥12y) if prefer to have better asthma control or reduce risk for exacerbations Patients at higher risk for exacerbations should be on daily ICS+PRN SABA (all ages). If ≥12y with poor adherence to daily medication switch to PRN bud/form Patients not controlled on PRN SABA or no meds should be started on ICS + PRN SABA

Answer 59

Very mild: well controlled on PRN SABA Mild: well controlled on low dose ICS and PRN SABA or PRN bud/form Moderate: well controlled on low dose ICS+second controller and PRN SABA OR moderate dose ICS +/- second controller and PRN SABA OR low-moderate dose bud-form + PRN bud/form Severe: high dose ICS+second controller for the previous year OR systemic steroids for 50% of the previous year to prevent asthma from becoming controlled OR is uncontrolled despite this therapy Very severe: category removed in 2021

Answer 60

- diagnostic uncertainty - children not controlled on moderate dose ICS with correct inhaler technique and adherance - suspected or confirmed severe asthma - life-threatening event such as admission to ICU for asthma - Need for allergy testing to assess the possible role of environmental allergens in those with a suggestive clinical history - Confirmed or suspected work-related asthma - Any asthma hospitalization (all ages), ≥ 2 ED visits (all ages) or ≥ 2 courses of systemic steroids (children)

Answer 61

1. Asthma pathophysiology: A chronic inflammatory condition in which airways are hyper-reactive (sensitive) to environmental (allergic, irritant or infectious) and/or intrinsic factors. 2. Identify triggers: Identification and avoidance of environmental triggers specific to the patients. 3. Asthma control for all patients: Asthma can be controlled and all patients with asthma can lead a normal life. Regular symptoms, poor lung function and asthma exacerbations indicate treatment failure. 4. Minimal to no exacerbations for all patients: Identify risk factors for asthma exacerbations. 5. Reliever vs. controller: The difference between reliever and controller medications and their use in the written action plan. 6. Written action plan: Provision and explanation of a written action plan comprising: * How and how often to assess asthma control (self-monitoring) * Instructions to maintain good control emphasizing adherence to controller medication and making specific environmental changes * Signs and symptoms indicating poorly-controlled asthma, with instructions on what to do during loss of control (medication to add or increase, how much and how long; when and how to seek additional help (eg, when to go to the hospital or call the health care provider) 7. Medication safety and side effects: Expected onset of action and potential side effects of medications. 8. Inhaler teaching: Teaching and verification of the inhalation technique specific to the devices prescribed for the patient. Ensuring patients know how to tell when an inhaler is empty.

Answer 62

this is a cystic malformation with overgrowth of the terminal bronchioles occurring early in fetal development, resulting in cystic and adenomatoid malformations and communicates directly with the tracheobronchial tree Most commonly occurs in the lower lobes Results in a ball-valve mechanism that causes air trapping and localized hyperinflation

Answer 63

often an incidental finding may present with feeding difficulties, tachypnea, cyanosis, acute respiratory distress, suprainfection at risk for tutor formation (pleuropulmonary blastoma) Majority will become large before the second trimester then regress Most babies are asx as newborns

Answer 64

prenatal: polyhydramnios, hydros (rare), lung hypoplasia post-natal: recurrent lung infections, pHTN, malignant transformation (rare) may have mediastinal deviation

Answer 65

No treatment if asymptomatic, but in general will require surgery by 1 year due to risk of lung hypoplasia, risk of pleuropulmonary blastoma, risk of regrowth (from regression) May opt for resection due to risk of malignancy, or if recurrent infections Surveillance with serial CTs Indications for resection: recurrent infections with air-fluid levels, PPB

Answer 66

Segment of non-functioning lung tissue with no communication with the tracheobronchial tree and its own blood supply via a collateral arterial vessel Majority are intralobar (90%) and are adjacent to normal lung with pulmonary venous drainage. May present early as neonatal heart failure or later due to secondary infection Extralobar are completely separated from normal lung by pleura with systemic venous drainage. 10% are below the diaphragm. May be associated with other congenital malformations, often detected in the first year of life

Answer 67

often Dx made prenatally with US with doppler - will usually identify a feeding systemic artery Can also do a CT chest with contrast

Answer 68

may observe, particularly if extra lobar, but possibly at risk for recurrent infection Lobectomy following ligation of the arterial supply

Answer 69

These are thin-walled islands of bronchial tissue left behind during branching of the airways early in fetal development They tend to be near the carina and can present as a mediastinal mass May present as airway obstruction, stridor, possibly ASx depending on size/location Dx on CXR or CT - opacity without air fluid level Management: resection

Answer 70

Due to congenital over-inflation of the pulmonary lobe secondary to abnormal bronchial cartilage development in the lung and subsequent post-natal air-trapping and over-distention Upper > Lower lobes with LUL most common L>R M>F Associated with CHD in 10-20% of cases?

Answer 71

50% present by 4 weeks of age, but some remain ASx CXR would show hyperinflation and mediastinal shift to the contralateral side. Can have tension PTX physiology due to hyper inflated chest and obstruction with ball-valve at the bronchial level Do not need a CT!

Answer 72

May need lobectomy

Answer 73

Autosomal recessive Due to mutation in the CFTR gene 1/2500 births in populations of northern european descent

Answer 74

Mutated CFTR gene --> misfolded protein --> retained protein in RER that is unable to reach the cell membrane --> defective Cl- channel that can’t transport intracellular Cl- across the membranes --> exocrine glands (e.g. sweat, mammary, salivary glands) make hyperviscous secretions --> accumulation of secretions and blockage of exocrine glands --> chronic inflammation --> organ damage Ultimately have impaired mucociliary clearance with obstruction to the airways and chronic inflammation/infection resulting in bronchiectasis Organs involved: lungs (cause mortality), pancreatic ducts, bile ducts, intestines, reproductive, upper airways (nasal polyps, obstruction)

Answer 75

FTT meconium ileus recurrent respiratory Sx (wheeze, cough, bronchiolitis) prolonged jaundice severe pneumonia steatorrhea rectal prolapse vitamin ADEK deficiency At risk for hyponatremic hypochloremic metabolic acidosis Thing about CF in babies with FTT and cholestatic jaundice

Answer 76

Recurrent respiratory Sx FTT recurrent rectal prolapse clubbing bronchiectasis nasal polyps/sinus disease chronic pseudomonas aeruginosa colonization "poorly controlled asthma" axoospermia galstones osteoporosis renal stones Vitamin ADEK deficiency low fecal elastase

Answer 77

Prenatal: CVS with DNA analysis/amnio (if known carriers/FHx) Clinical diagnosis based on 1 of - Clinical features of CF - CF in a sibling - positive NMS (elevated immunoreactive trypsinogen (IRT)) PLUS lab evidence of CFTR dysfunction with - high sweat chloride on 2 different days - two pathogenic mutations on genetic testing CFTR gene with ∆F508 gene is most common mutation, but need 2 mutations (AR)

Answer 78

NMS measures IRT (immunoreactive trypsinogen) which is a pancreatic enzyme If it's high, send a genetic panel and perform a sweat chloride NMS is 95% sensitive but can miss up to 5% of classic CF If you have a positive IRT on NMS, you need further DNA testing AND a confirmatory sweat chloride

Answer 79

Sweat chloride is the gold standard diagnostic tool. Kids should be >36 weeks and >2kg to perform it properly Normal: <30 Indeterminate: 30-60 Positive: ≥60mEq/L

Answer 80

eczema ectodermal dysplasia malnutrition/FTT anorexia nervosa congenital adrenal hyperplasia AI G6PD hypoTSH nephrogenic DI pseudohypoaldosteronism Klinefelter syndrome hypogammaglobulinemia

Answer 81

dilution malnutrition edema insufficient sweat quantity hypoNa hypoproteinemia CFTR mutations with preserved sweat function

Answer 82

1. Multi-D clinic 2. Respiratory: agressive management of infections (chronic with oral/inhaled antibiotics, acute with oral or IV), airway secretion clearance with chest physio, dornase alpha and hypertonic saline, +/- lung transplant 3. GI: nutrition optimization, high calorie diet, enzyme replacement, Vitamin ADEK supplementation, Ursodiol if cholestasis, PPI 4. CFTR modulators: Trikafta works if at least one df508 allele

Answer 83

most common bug in young kids <5 is staph aureus. Staph remains common until older ages After age 5, psuedomonas increases H flu decreases after school age S. Aureus (by 1 y.o) —> HiB by age 2 —> pseudomonas age 5-7 —> stenotrophomonas —> nosocomial infection w/ burkholderia cepacia (adolescence)

Answer 84

Most can be treated with outpatient antibiotics for two weeks as a first step based on cultures and age with one type of antibiotic (PO Cipro) UNLESS First growth of pseudomonas THEN: outpatient eradication x3 weeks (usually inhaled tobramycin) OR inpatient treatment with dual anti-pseudomonas therapy x2 weeks (Ceftaz + Tobra, pip-tax if severe) Inpatient criteria: - Severe presentation (FTT, O2 needed) - failed outpatient treatment - poor/worrisome compliance at home - SES considerations - comorbidities like CFRD, CKD - no oral options **Home IV is not effective in CF populations**

Answer 85

Use the pneumonic CF PANCREAS C - cough, increased ingenuity, frequency F - Fever, usually low grade unless severe pneumonia P - pulmonary function deterioration A - appetite decrease N - nutrition (weight loss) C - CBC leukocytosis with left shift R - radiograph with increased over aeration, mucus plugging, peribronchial thickening E - examination (rales, wheeze in previously clear areas, tachypnea, WOB) A - activity decreased, impaired exercise tolerance S - Sputum darker, thicker, more abundant, forming plugs

Answer 86

polyps hemoptysis pneumothorax ABPA (Allergic Bronchopulmonary Aspergillosis) NTM (non tuberculosis mycobacterium) respiratory failure cor pulmonale malnutrition DIOS (distal intestinal obstructive syndrome) rectal prolapse CF-related diabetes

Answer 87

Early wheezer plus at least one major criteria or 2/3 minor criteria MAJOR: 1. parental asthma diagnosed by MD 2. eczema diagnosed by an MD MINOR: 1. MD Dx allergic rhinitis 2. Wheezing apart from colds 3. Eosinophilia >4%

Answer 88

1. previous severe exacerbation (ie you almost died) - ICU, ED visits, hospitalization 2. steroid or ventolin dependent 3. social factors impacting adherence (SES) 4. other comorbidities

Answer 89

Singulair / montelukast Black box warning for neuropsychiatric side effects irritability aggressiveness anxiety sleepdisturbance suicidal thoughts Side effects in up to 16% of kids, typically within 2 weeks of initiation

Answer 90

decreased linear growth

Answer 91

C. Refer for surgical correction

Answer 92

A) CPAM air fluid levels with contralateral mediastinal shift suggests infected CPAM

Answer 93

B start NJ feeds - has already had texture adjustments Could certainly argue for A

Answer 94

C) VFSS Could be getting at H type fistula, but would expect FTT?

Answer 95

C) physical conditioning FEV1 increases only 7% which is not enough to meet asthma criteria

Answer 96

C) switch to bud/form She is 12 and therefore should have treatment optimized with combination inhaler rather than increasing ICS

Answer 97

D) upper GI endoscopy This is Boerhaave syndrome - perforation of the esophagus secondary to a sudden increase in intraesophageal pressure Classic triad of (1) severe or repeated vomiting (2) sudden increased chest pain (3) subcutaneous emphysema

Answer 98

perforation of the esophagus that results from a sudden inc in intraesophageal pressure (eg severe vomiting) classic triad is (1) severe or repeated vomiting (2) sudden onset chest pain (3) subcutaneous emphysema. Best test is upper endoscopy + endoscopic surgical repair and antibiotics High mortality

Answer 99

Edema Can also be caused by hypoalbuminemia which would cause edema Eczema would cause a false positive

Answer 100

D. Change trach

Answer 101

B. Change to low dose ICS+LABA ie switch to bud/form now that she's ≥11yo

Answer 102

repeated events of partial or complete upper airway collapse on inspiration during sleep with disruption of normal gas exchange and sleep patterns Primary snoring (or habitual snoring) 10-12% of children vs. obstructive sleep apnea 1-6% of children

Answer 103

Adeno-tonsillar hypertrophy (most common common) Obesity Allergic rhinitis, asthma Micrognathia, macroglossia Trisomy 21 Craniofacial anomalies (e.g. Pierre Robin sequence) Neuromuscular disorders (DMD, CP)

Answer 104

Nighttime: Snoring Difficulty breathing episodes Witnessed apnea Cyanosis Sweating Daytime: Mouth breathing Nasal obstruction Hyperactivity (ADHD symptoms) Moodiness Poor school performance Daytime somnolence Enuresis Behavioral problems Failure to thrive Difficulty waking up in AM In teens OSA is most likely to be secondary to obesity! symptoms resemble those of adults - daytime fatigue, headache

Answer 105

Pulmonary hypertension + cor pulmonale Systemic hypertension LVH Neurobehavioral deficits FTT ADHD daytime sleepiness weight gain and obesity

Answer 106

Polysomnography gold standard for diagnosis of OSA, best differentiation of severity Components: sleep staging (EEG, chin EMG and EOG), detection of airflow, chest/abdominal movements, gas exchange (SaO2, PCO2), ECG, video (for snoring, body position) Diagnosis: AHI > 5/hour Can also consider overnight oximetry Benefits: easily available, “positive” test in context of symptoms can be diagnostic Limitations: Poor sensitivity (if normal, does not rule-out OSA) Does not differentiate causes of desaturations Technical limitations Symptoms + X-Rays Lateral neck x-ray to look for adenoid hypertrophy Overall poor correlation with objective findings However in the context of a child with typical symptoms and sequelae and with evidence of enlarged adenoids and/or tonsils, referral to ENT for surgical intervention is an appropriate approach

Answer 107

Non-Pharmacologic: nasal hygiene, sleep hygiene Pharmacologic: intranasal corticosteroids, monteleukast/singulair Surgical: adenoidectomy + tonsillectomy – patients with OSA should have them removed Treat obesity: weight loss, CPAP Adenotoncisllectomy is first line treatment with 80-90% cure rate in kids!

Answer 108

If yes or if child has sign/s symptoms of OSAS, clinician should perform more focused evaluation If a child snores on a regular basis or has any of the complaints/findings suggestive of OSA, clinician should either (1) obtain a polysomnogram OR (2) refer the patient to a sleep specialist or ENT for more extensive evaluation If PSG not available, may order alternative diagnostic test such as nocturnal video recording, nocturnal oximetry, daytime nap PSG or ambulatory PSG If a child is determined to have OSAS, has an exam showing adenotonsillar hypertrophy and does not have a contraindication to surgery, clinician should recommend adenotonsillectomy as the 1st line treatment If OSA but does NOT have adenotonsillar hypertrophy, other treatment should be considered

Answer 109

Absolute contraindication: no adenotonsillar tissue (tissue has been surgically removed) Relative contraindications: Very small tonsils/adenoid Morbid obesity and small tonsils/adenoid Bleeding disorder refractory to treatment Submucus cleft palate Other medical conditions making patient medically unstable for surgery

Answer 110

< 3 yr of age Severe OSAS on PSG Cardiac complications of OSAS FTT Obesity Craniofacial anomalies Neuromuscular disorders Current respiratory infection

Answer 111

- clinically reassess all patients with OSAS for persisting signs/symptoms after therapy (6-8 weeks after) to determine whether further treatment is needed - Patients should be referred for CPAP if symptoms/signs or objective evidence of OSAS persists after adenotonsillectomy - recommend weight loss in addition to other therapy if a child/adolescent with OSAS is overweight or obese - may prescribe topical intranasal corticosteroids for children with mild OSAS in who adenotonsillectomy is contraindicated or for children with mild post-op OSAS (mild OSAS is defined, for this indication as an AHI < 5 per hour)

Answer 112

Morphine IV Chest tubes hurt!

Answer 113

A. PO erythromycin this is atypical pneumonia secondary to chlamydia which classically presents with conjunctivitis, bilateral changes and mild eosinophilia as well as "staccato" cough. Need a macrolide to cover this

Answer 114

C. Pseudomonas most common would be staph, but based on the options pseudomonas starts emerging at this age

Answer 115

A. PFT this question asks for the test to get the Dx, hens PFT

Answer 116

D. Give morphine chest tubes hurt! The CT is still draining well so don't clamp it No indication to add vanco bolus isn't wrong but not the best answer

Answer 117

B. low dose ICS and LABA Children >12 and adults not achieving control despite adherence to low dose ICS should be started on daily ICS/LABA

Answer 118

C. laryngoscopy I believe they're trying to get at vocal cord dysfunction PFT would be helpful to rule out asthma , but laryngoscopy during exercise challenge test is gold standard

Answer 119

c) adrenal insufficiency

Answer 120

I think this is D and trying to get at increasing from low to medium dose ICS

Answer 121

b. psudomonas aeruginosa

Answer 122

a. decreased linear growth small decrease in growth rate in children aged 5-15 on ICS. Overall growth impact is low to none, max 1-2cm

Answer 123

C. truncated inspiratory loop on spirometry normal is VC ADDUCTION with expiration

Answer 124

a. inhaled corticosteroid with SABA PRN she has asthma!

Answer 125

c) Advise him to not be around his friends when they are using e-cigarette products

Answer 126

A. ceftaz and tobra If this kid was ambulatory though, could do oral as outpatient with PO Cipro, however based on severity with PFT change, opted for inpatient dual antipseudomonal coverage

Answer 127

b) chest US Next step for complicated pneumonia would be to look for sign of effusion on the US. Most common bug for complicated pneumonia would be strep pneumonia

Answer 128

a. schedule an appointment to talk to the father

Answer 129

D. LABA in the morning on the days of the games would be right probably based on old guidelines, but with new guidelines symbicourt (ie ICS/LABA) is the right answer with the new guidelines

Answer 130

B. Separation anxiety disorder not enough to go off of really but doesn't fit with asthma exacerbation and doesn't tell us enough to talk about GAD (is fine with other activities)

Answer 131

b) electron microscopy of respiratory mucosa this is in keeping with PCD, in which case you need electron microscopy of mucosa if you can't get an nNO

Answer 132

This is an autosomal recessive (most commonly) genetic disorder that causes impaired ciliary function leading to chronic sinopulmoanry disease, persistent middle ear effusions, laterality defects and infertility Found in the airways and other mucous membranes in utero ciliary dysfunction is what causes the laterality defects

Answer 133

Need at least 2/4 key clinical features: 1. Unexplained Neonatal Respiratory Distress (ie not in keeping with TTNB) 2. Year round daily wet/productive cough 3. Year round daily nasal congestion 4. Organ Laterality defects If 2/4 criteria, then get nNO (nasal nitric oxide) testing If nNO low, you have a diagnosis of PCD if CF is excluded. Can repeat nNO to verify. After this consider pursuing PCD genetic testing for confirmation IF patient is ≤5yo and not cooperative for nNO testing, can to extended genetic testing panel instead, but it can't diagnose or rule out in full. Would then need electron microscopy of ciliary microstructure to make definitive diagnosis if genetics suspicious

Answer 134

Kartagener triad: (1) situs inversus totalis, (2) chronic sinusitis, and (3) bronchiectasis Respiratory: Neonatal respiratory distress (tachypnea, hypoxemia or even respiratory failure) Late O2 need at birth (12-24h) that's not TTN or otherwise explained Year-round daily wet cough Recurrent pneumonia Bronchiectasis (earlier than CF) clubbing ENT: Chronic otitis media Conductive hearing loss Neonatal rhinitis Year-round nasal congestion Chronic sinusitis Nasal polyposis recurrent AOM (tubes before age 5) GU: male & female infertility ectopic pregnancy Left-Right Orientation Defects (in ~50%): Situs inversus Heterotaxy (associated with CHD, asplenia or polysplenia) Congenital heart disease CNS: hydrocephalus, retinitis pigmentosa

Answer 135

no therapies can correct the ciliary dysfunction, most treatments supportive and similar to CF Routine airway clearance: chest physio, postural drainage, percussion vest, etc aggressive treatment of infections surgical management: tympanovstomy tubes, sinus drainage prevention: immunizations, avoid cigarettes, other ariway irritants possible lobectomy if severe bronchiectasis

Answer 136

Absence of chest/abdominal movement with cessation of airflow for >20s OR lasting 2 respiratory cycles associated with 1) arousal 2) an awakening or 3) a desaturated of at least 3% Main reasons for CSA are related to disrupted brain/lung messaging: chiari malformation brainstem herniation achondroplasia increased ICP/tumor infiltrative process genetic syndrome CCHS Prader Willi

Answer 137

Caused by the PHOX2B mutation resulting in abnormal peripheral chemoreceptor response, leading to inappropriate central response to CO2 Also results in dysfunction of autonomic functions - hirschprungs, pupillary response, arrhythmia etc Require nocturnal ventilation support or trach/vent

Answer 138

this is congenital hypoventilation syndrome Annual PSG, Holter, urine metanephrines (at risk for neuroendocrine tumours), imaging

Answer 139

PSG identifies the following: - Obstructive apneic events: decreased airflow by 90% to nasal flow detector despite respiratory effort for 2 breaths - Hypopnea: decreased airflow between 30-90% associated with a desaturated or arousal despite respiratory effort This generates an AHI (apnea-hypopnea index) - AHI <1: normal - AHI 1-5: mild - AHI 5-10: moderate - AHI > 10: severe

Answer 140

c) nocturnal hypoventilation

Answer 141

PTX is accumulation of extrapulmonary air within the chest, most commonly from leakage of air from within the lung Primary idiopathic—usually resulting from ruptured subpleural (typically teenage males who are tall, thin) Secondary blebs Congenital lung disease: congenital cystic adenomatoid malformation, bronchogenic cysts, pulmonary hypoplasia Conditions associated with increased intrathoracic pressure: asthma, bronchiolitis, CF, foreign body, smoking Infection: pneumatocele, lung abscess, bronchopleural fistula Diffuse lung disease: Langerhans cell histiocytosis, TS, Marfan syndrome, Ehlers-Danlos syndrome Traumatic: non-iatrogenic, penetrating trauma, high-flow therapy, mechanical ventilation

Answer 142

When air enters the pleural space, the lung collapses Hypoxemia occurs because of: Alveolar hypoventilation Ventilation-perfusion mismatch Intrapulmonary shunt

Answer 143

Simple pneumothorax—intrapleural pressure is atmospheric & lung collapses up to 30% Complicated or tension pneumothorax—continual leak causes increasing positive pressure in the pleural space-->mediastinal shift toward the contralateral side & decreased venous return and cardiac output

Answer 144

Sudden onset dyspnea, pleuritic chest pain, shoulder/back pain, respiratory distress Signs: decreased Chest wall movement on affected side Ipsilateral hyperresonance to percussion Decreased Breath sounds Subcutaenous emphysema With tension pneumothorax: contralateral tracheal shift, displaced heart sounds, tachycardia, hypotension, cyanosis

Answer 145

Therapy varies depending on the extent of the collapse and nature/severity of the underlying disease Small (<5%) or even moderate pneumothorax in an otherwise healthy child may resolve without treatment, usually within 1 week 100% O2 may help quicken resorption - weak recommendation but may hasten re-inflation refer to surgery if persistent air leak for >48h Large pneumothorax: monitor with CXR, if symptomatic, insert chest tube to drain Recurrent or persistent pneumothoraces may require open thoracotomy and pleural bleb excision Tension pneumothorax (medical emergency!) ABCs If unstable --> emergent needle aspiration

Answer 146

Classification of Spontaneous pneumothorax (3/ 100,000 children in US 2000 census data) Primary: ○ no obvious underlying lung disease ○ attributed to atypical blebs or bullae that rupture ○ 2-4x more likely in male teenagers (mean age 14) that are tall + slender ○ Associated with smoking Secondary ○ result of recognizable lung disease, ex: § Connective tissue d/o (Marfan, Ehlers-Danlos) § Cancer § Congenital Lung Defects § Interstitial Lung disease (sarcoidosis, langerhans cell histiocytosis) § Infections (pneumonia, pneumocysitis jirovecii) § Airway diseases - CF, Asthma ○ Poor prognosis attributed to CF and pneumothoraces - increased morbidity/mortality

Answer 147

b) fluid protein to serum protein ratio >0.5

Answer 148

If at least one of the following three criteria are met, the fluid is exudative: 1. Pleural fluid protein/serum protein ratio > than 0.5, or 2. Pleural fluid LDH/serum LDH ratio > than 0.6, or 3. Pleural fluid LDH > than 2/3 the ULN for LDH

Answer 149

Exudate: disease in any organ can cause exudative pleural effusions by a variety of mechanisms, including infection, malignancy, immunologic responses, lymphatic abnormalities, noninfectious inflammation, iatrogenic causes, and movement of fluid from below the diaphragm Transudate: Transudates result from imbalances in hydrostatic and oncotic pressures in the chest, as occur with CHF and nephrotic syndrome, or conditions external to the pleural space

Answer 150

Infection: - Non-TB Pneumonia (50-70%) – parapneumonic or empyema - Staph aureus is MOST common cause of empyema > Strep pneumo > H flu - Older consider GAS. - Anaerobes are uncommon (usually will have periodontal infxn, dysphagia, aLOC) – fusobacterium (including Lemierre), bacterioides - TB, Transdiaphragmatic extension from intra-abdominal abscess Malignancy - Pleural or pulmonary metastatic (++ rare) – lymphoma (anterior mediastinal mass), leukemia (T-ALL), neuroblastoma (posterior mediastinal mass), sarcomas - Small blue-round cell tumors (lymphoma, NB, rhabdomyosarcoma, NH lymphoma, Wilm’s) Auto-immune - SLE Other inflammatory – Pancreatitis, Burns

Answer 151

Nephrotic syndrome, PLE, CHF, constrictive pericarditis, cirrhosis

Answer 152

b) add inhaled corticosteroid

Answer 153

bronchoscopy - concern for upper airway or foreign body

Answer 154

a) one dose of MgSO4

Answer 155

a. MRI Head

Answer 156

c. Methacholine challenge

Answer 157

c. sweat chloride rectal prolapse is a complication of CF

Answer 158

Outpatient, CAP: PO amoxicillin x3d in TID dosing Inpatient: IV ampicillin for 7-10 days Q6h Severe: IV Ceftriaxone. If nothing isolates, can step down to IV amp Rapidly progressing multi-lobar disease or pneumoatocele: add IV vancomycin Atypical: azithromycin (mycoplasma or chlamydophila) Empyema: usually needs 2-4 weeks of therapy

Answer 159

Stage 1: exudative - effusion intrapleural pus or moderate/large exudative parapneumonic effision. Common to be small, usually no drainage required Stage 2: fibropurulent - loculated Stage 3: Organized - fibrous peel

Answer 160

Strep pneumonia Staphylococcus Aureus Strep pysogenes (GAS) MRSA especially if post-influenza

Answer 161

1. CXR showing blunting and signs of effusion 2. US to estimate size of effusion and differentiate free flowing effusion from located effusion 3. Drainage with C+S. Consider molecular testing to confirm strain of S pneumonia (especially if vaccinated)

Answer 162

Need to manage the effusion Consult gen surg early, especially if moderate to severe respiratory distress to avoid mediastinal shift from the PE Choice of procedure depends on local expertise. - VATS - Thoracocentesis - Small bore percutaneous chest tube insertion +/- fibrinolytic (TPA) Antibiotics: want to cover for S Pneumonia +/- MRSA depending on risk factors - IV Cefotaxime/Ceftriaxone +/- Vancomycin/LInezolid - consensus 3-4 weeks - transition to PO post-drainage, clinically improving and off O2 - step down options: amax if suspecting S pneumonia. Amox-clav if MRSA or H flu Note that children with empyemas can have ogoing fevers for >72h on appropriate therapy and this is NOT a sign of treatment failure!

Answer 163

Cough for >4-8 weeks

Answer 164

B Sx year round cough or early morning cough poor growth velocity ENT Sx and respiratory distress at birth imaging findings showing FB aspiration, mediastinal mass, situs inversus

Answer 165

This is a radiographic diagnosis Dilated peripheral airways secondary to chronic inflammation generally chronic, permanent/irreversible and a sign of progressive lung disease Airways become large, baggy with worsening mucous retention and further expanding of the airways, creating a vicious cycle

Answer 166

This is a radiographic diagnosis - Signet ring sign on CT is a large airway that's bigger than the adjacent blood vessel

Answer 167

productive cough abnormal PFT with obstructive pattern without response to abx or steroid

Answer 168

A large list of different disease processes: Impaired immune function - immunodeficiency - SCID, CVID, NK cell deficiency - X linked lymphoproliferative disorder - Ectodermal dysplasia - Ataxia telangiectasia - HIV Ciliary Dyskinesia - PCD Abnormal mucous - CF Rare Syndromes and congenital lung disease - Marfan syndronme - AD polycystic kidney disease Aspiration - primary aspiration - TEF - GERD - Foreign body aspiration Obstruction - foreign body - tumor - lymph nodes Intrinsic lung disease - ILD - ABPA - BPD - Rheum/autoimmune disease

Answer 169

Bronch (to dx myco, fungal infxn etc), pH studies, barium swallow, Mantoux Don't need to branch if you can induce sputum (representative of lower airway bacteria) Baseline humoral screen – Ig’s, vaccine ab’s, hemagglutinins HIV status, sweat chloride CBC Aspergillosis serology consider cilia biopsy and genetic testing

Answer 170

Alveoli with damaged and thickened interstitial, making it difficult to perform effective gas exchange at the level of the alveoli

Answer 171

Considered chILD syndrome if at least 3/4: 1. Symptoms (cough, breathlessness, exercise intolerance) 2. Signs (adventitia on auscultation, crepitations, wheeze) 3. impaired gas exchange (hypoxia, hypercarbia at rest or with exercise) 4. diffuse abnormalities on CT or XR 30% of ILD have Sx within the first year of life, typically will have respiratory distress at birth or respiratory infection they can't seem to recover from

Answer 172

pulmonary findings predominate but can have granulomatous lesions in any organ (lung, LN, eyes, skin, liver) skin lesion s- papules, plaque, nodules, erythema nodosum asymptomatic uveitis

Answer 173

increased INR increased ESR anemia hypergammaglobulins hypercalcemia and hypercalcuria eosinophilia leukopenia increased ACE converting enzyme

Answer 174

clinical features + tissue biopsy with non-caveating granulomas

Answer 175

Sarcoidosis hypercalcemia with eosinophilia and respiratory findings

Answer 176

This is an emerging (controversial) diagnosis Diagnostic criteria: - >4 weeks productive wet cough - no other cause identified Resolution of cough with antibiotic treatment - associated with significant pus and neutrophils on bronchoscopy Most common in kids <5yo

Answer 177

H influenza S pneumonia M catarrhalis S aureus

Answer 178

Clavulin PBB guidelines: trial of abx in kids with chronic wet cough, normal CXR, normal spiro and no red flags for other diagnosis can be difficult to differentiate from a recurrent viral infection

Answer 179

c) sweat chloride

Answer 180

most common in kids <8yr due to paucity of the collateral channels of ventilation, so consolidations only drain in a localized area and can be relatively contained looks like a mass but isn't most commonly s pneumonia CXR shows round, mass-like lesion, usually in the lower lobes, may have air bronchograms, should have ill-defined borders for at least part of the borders Management: - one of the only times to get a follow up CXR for a pneumonia - rule out underlying mass

Answer 181

related to volume reduction in the affected part of the lung due to mucous plugging or inappropriate inflation can have elevation of the diaphragm and narrowing of the ipsilateral intercostal spaces

Answer 182

b) step pneumonia

Answer 183

cavitated lesion containing both fluid and gas. will have "gas-fluid levels" on CXR, occasionally a meniscus sign can be missed if the XR isn't taken tangential/horizontal to the gas-fluid interface

Answer 184

d) vocal cord dysfunction

Answer 185

a) CPAM Infectious sounding CPAM – most likely to present PPB is very uncommon – unlikely infectious and related to SPAM Diaphragmatic hernia – late presentation for this Bronchogenic cyst – unlikely to cause mediastinal shift Air fluid levels are probably an infected CPAM

Answer 186

c) CT chest Jody platt thinks it’s most likely CDH or diaphragmatic eventration make the most sense at this point due to their age it would be difficult to tell the difference just by a CXR alone (remember white lung vs black lung) so your answer is CT chest - as the “NEXT” test Diaphragm fluoroscopy could diagnose eventration or diaphragm paralysis but may not be the next test

Answer 187

Right sided CDH is less likely (10-15%) Infants with R-CDH often present with respiratory distress at birth due to lung hypoplasia and persistent pulmonary hypertension of newborn. Diagnosis of R-CDH can be challenging as clinical presentation and radiological findings may masquerade as lung pathology. In R-CDH, the liver may obturate the diaphragmatic defect and prevent extrusion of abdominal contents into the thorax, hence not visualised on plain radiographs and delaying diagnosis. Initial CXRs of R-CDH may be misinterpreted as pneumonia

Answer 188

Symptoms: Cough, wheeze with activity ONLY after vigorous activity Improves within 30 min Diagnosis Exercise challenge: decreased FEV1 by > 15% Can consider methacholine to rule out true asthma Management Same as asthma pre-exercise SABA +/- addition of ICS as in standard asthma management if uncontrolled Sx despite SABA **Ventolin used pre-workout counts with asthma control criteria

Answer 189

The lungs receive blood flow from two separate systems: (1) brochial circulation); (2) pulmonary circulation. (1) bronchial circulation is a high pressure, low volume circuit supplied by the bronchial arteries but arise directly from the aorta or one of its branches, so bleeding from this system has the potential to be profuse Can result in massive hemoptysis (2) Pulmonary circulation bleeds are low pressure, high volume from the R ventricle. this can result in alveolar hemorrhage, which is often low-grade, chronic and diffuse (but can still be deadly)

Answer 190

CXR (can be normal in diffuse alveolar hemorrhage) CBC, INR, PTT Gas Echo Rheum workup - ANCA, ANA, CRP, ESR +/- CT with contrast Consider a bronch (will have hemosiderin laden macrophages in BAL fluid)

Answer 191

Broad spectrum abx with staph coverage consider steroid TXA fluid resus and pRBCs PICU: high PEEP, epi via ETT, consider balloon compression

Answer 192

Type 1: Hypoxemic, PaO2 < 60 Type 2: Hypercapneic, PCO2>50

Answer 193

Hypoxemia 1. hypoventilation 2. shunt 3. ventilation-perfusion mismatch (most common) 4. diffusion limitation 5. low FiO2

Answer 194

Hypercapnea/hypercarbia 1. decreased tidal volume - over-sedated - neuromuscular weakness - flail chest post-trauma 2. increased dead space - hyperinflation --> obstructive airway disease --> excessive PEEP on mechanical vent - decreased cardiac output - increased pulmonary vascular resistance - PE

Answer 195

Needle decompression LOCATION: 2nd intercostal space, mid-clavicular line, 4th intercostal space, mid-anterior axillary line Go ABOVE rib, to avoid damaging neurovascular bundle EQUIPMENT: As large as needle as you can find 3 way stop-cock if time Will need chest tube afterwards

Answer 196

Anterior Masses - 5 Terrible Ts T: thymus T: thyroid T: thoracic aorta T: terrible lymphoma T: teratoma and germ cell tumors

Answer 197

- children without known lung disease - within 7 days of a known clinical insult - with respiratory failure not fully explained by cardiac failure or fluid overload Chest imaging findings of new infiltrates Impaired oxygenation invasive ventilation - Mild: 4 ≤ OI < 8 or OSI 5-7.5 - Moderate 8 ≤ OI < 16 OR OST 7.5 - 12.3 - Severe OI >16 OR OSE ≥12.3

Answer 198

Oxygen Targets - Mild (PEEP +10) 92–97%. - Severe (PEEP >10 cm) 88–92% CO2 - Permissive hypercapnia - pH range 7.15-7.30 AVOID: Barotrauma with TV ≤ physiologic range for age & weight (ie: 5-8 ml/kg), Peak pressures up to 28 cm H2O Atelectrauma /Volutrauma PEEP > 10-15 cmH2O Biotrauma Treat infection, consider steroids?

Answer 199

b) bronchoscopy look for the corn

Answer 200

Sudden onset of persistent cough Recurrent pneumonia and failure to thrive Absence of choking episode does NOT rule out aspiration Rigid bronch is the gold standard for diagnosis and treatment

Answer 201

Clinda and gentamycin to cover: Oral anerobes Pseudomonas

Answer 202

Feeding limitations; ( texture, thickness etc.) Post-pyloric feedings or NG feedings Fundoplication with GT but recurrent pneumonias will still happen from U/A secretions Anti-salivation Atropine, glycopyrrolate, scopolamine Salivary gland excision? Botox

Answer 203

First step for every sleep disorder 1. Stable bedtime and morning wake time 2. Age-appropriate number of hours in bed 3. Dark & quiet sleep space 4. Avoiding hunger/eating prior to bed 5. Relaxation techniques prior bed 6. Strict avoidance of television, computers and video games

Answer 204

A - Pulmonary hypertension would need an echo to assess for this.

Answer 205

1. Assess FEV1/FVC ratio - If ratio low for age, this is an OBSTRUCTIVE defect - for ages 5-18 FEV1/FVC 0.85 is low 2. Assess FVC - if FEV low with a normal FEV1/FVC, this suggests a RESTRICTIVE defect - for ages 5-18, FVC <0.80 is low 3. Confirm restrictive pattern or not - if restrictive pattern or mixed that is not corrected with bronchodilator, assess DLCO and TLC - Low TLC (<0.80) suggests restrictive 4. Determine severity of abnormality - FEV1 0.8: normal - FEV1 >0.70: mild - FEV1 0.60 - 0.69: moderate - FEV1 0.50 - 0.59: moderately severe - FEV1 <0.50: severe

Answer 206

Children receiving ≥500mcg/day of ICS should be considered at risk for clinically significant adrenal suppression - Alvesco (Ciclesonide) has reduced risk of AS likely due to more local effects - ICS is rarely associated with clinically significant AS, but CTS guidelines recommend high dose ICS to be used only by asthma specialist

Answer 207

- ICS of ≥500mcg/day (high dose) - frequent or prolonged courses of systemic glucocorticoid - concomitant intranasal steroids Duration of ICS exposure has NOT been identified as a risk factor for AS, but some studies show risk with ≥3 months of use

Answer 208

- Diagnostic uncertainty - Children not controlled on moderate dose ICS with correct inhaler technique and appropriate medication adherence - Suspected or confirmed severe asthma - Life-threatening event such as an admission to the ICU for asthma - Need for allergy testing to assess the possible role of environmental allergens in those with a suggestive clinical history - Confirmed or suspected work-related asthma - Any asthma hospitalization (all ages), ≥ 2 ED visits (all ages) or ≥ 2 courses of systemic steroids (children)

Answer 209

Symptoms of presentation: cough, wheeze/stridor, dyspnea/respiratory distress, asymptomatic after the initial choking episode, later can present with recurrent infections. A positive hx of choking should never be ignored, but a negative hx can be misleading CXR: inspiratory/expiratory XR - localized emphysema, atelectasis, pneumonia, normal, may see a radio-opaque foreign body Lateral decubitus doesn't add diagnostic value If history consistent but XR normal, consider early bronchoscopy CT/MR delay diagnosis - not routinely recommended If there is a history of witnessed choking, they need a bronch - rigid bronch is the gold standard

Answer 210

Appearance: air-filled cystic lesions that arise within the lung parenchyma Can be infectious, most commonly staph CT is gold standard imaging for further characterization CT aspirate for diagnostic clarity and therapeutic

Answer 211

Associated with direct aspiration on swallowing Consider with syndromes VACTRL CHARGE Opitz Frias Midline Defects Dx = Videoflouroscopy; Rigid bronchoscopy required to rule out

Answer 212

Least common form of TEF - actually quite rare Requires a contrast study (barium swallow) Can be missed on routine studies 1/3 will require 2nd or 3rd study to make a diagnosis +/- direct esophageal injection, pressure study, prone position Rigid Bronchocopy is still gold standard because can be missed

Answer 213

≥2 pneumonia in 1 year or ≥3 in a lifetime. Radiologically clear between episodes Most common cause of "recurrent PNA" is viral illness with atelectasis

Answer 214

Detailed history or events: - Are they truly PNA? (ie ?viral) - Do they clear in between? - Do they occur in multiple locations or in a single location? - Does the child have systemic symptoms or features of a chronic illness? CF, PCD, recurrent aspirations? - Are they growing and thriving otherwise? Investigations: - Review of previous imaging - do they clear radiologically between events? - Obtain a baseline image 4-6 weeks after last “pneumonia” - Can consider a CT WITH contrast - if truly recurrent needs a resp referral

Answer 215

SAME LOCATION: Anatomic abnormality External airway compression (i.e. lymphadenopathy, vascular abnormality) Intrinsic airway abnormality Congenital malformation: CPAM, pulmonary sequestration, bronchogenic cyst Foreign body RML syndrome Bronchiectasis Persistent Infection (i.e. TB) MULTIPLE LOCATIONS: Immune deficiency Cystic fibrosis Primary ciliary dyskinesia Recurrent aspirations Anatomical Laryngeal cleft: diagnose by video fluoroscopy or rigid bronchoscopy (gold standard) H-type fistulas: diagnosed by barium swallow – can be missed so gold standard is also rigid bronchoscopy Swallowing disorder Neurologic impairment

Answer 216

Staph aureus is MOST COMMON Followed by strep pneumonia > H Flu In older kids consider GAS Anaerobes are uncommon - usually associated with periodontal infection, dysphagia/aspiration, aLOC

Answer 217

Anterior Mass: Right border silhouette Posterior displacement of trachea on lateral Posterior Mass: Loss of aortic knuckle Pressure erosion splaying of the posterior rib end Lateral tracheal deviation - eg bronchogenic cyst or lymph nodes

Answer 218

A hypersensitivity reaction to the fungus aspergillus Symptoms: coughing, wheezing secondary to episodic bronchial obstruction. Fever. Malaise. Brownish mucous plugs. Can experience hemoptysis Population: often occurs in patients with asthma or CF. 1-2% of asthma patients, 2-9% of CF patients

Answer 219

This is an allergic hypersensitivity reaction, so would expect - elevated eosinophils - elevated total serum IgE - IgE and IgG antibodies to aspergillus on immunoassay Can also see: - aspergillus skin prick test + - Sputum + for aspergillus

Answer 220

1. episodic bronchial obstruction 2. peripheral eosinophilia 3. immediate cutaneous reactivity to Aspergillus antigens 4. precipitating IgE antibodies to Aspergillus antigen 5. elevated total IgE 6. serum precipitin (specific IgG) antibodies to A. fumigatus 7. pulmonary infiltrates on imaging 8. central bronchiectasis. Secondary diagnostic criteria include: - repeated detection of Aspergillus from sputum by identification of morphologically consistent fungal elements or direct culture - coughing brown plugs or specks - Radiologically, bronchial wall thickening, pulmonary infiltrates, and central bronchiectasis can be seen.

Answer 221

relieving inflammation via an extended course of systemic corticosteroids Addition of oral antifungal agents, such as itraconazole or voriconazole, is used to decrease the fungal burden and diminish the inciting stimulus for inflammation Because disease activity is correlated with serum IgE levels, these levels are used as one marker to define duration of therapy.

Answer 222

RFs: Surgery Lower extremity fractures Malignancy Presentation: Hypoxia (cyanosis) Tachypnea Dyspnea Cough Diaphoresis Chest pain Hemoptysis Lower extremity signs of DVT (pain, swelling) Tachycardia

Answer 223

High level of clinical suspicion required V-Q radionuclide scan: noninvasive, potentially sensitive but interpretation can be problematic Pulmonary angiography: gold standard for diagnosis of PE

Answer 224

Heparin! LMWH or UFH

Respirology Flashcards

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