exam 1 - respiratory Flashcards

1
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Extracted Text

A

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2
Q

epiglottitis

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-MC associated with Haemophilus influenzae; streptococcal species in immunized patients
-Sudden onset of high fever, dysphagia, drooling, muffled voice, inspiratory retractions, cyanosis, and soft stridor
-Pts sit in “sniffing dog” position (neck hyperextended, chin stretched forward)
-Progression to total airway obstruction may occur and result in respiratory arrest
-Definitive dx: Direct inspection of epiglottis (OR during intubation) > cherry-red and swollen epiglottis
-Imaging: Lateral neck radiograph > “thumbprint” sign caused by swollen epiglottis
-Treatment:
-Endotracheal intubation to establish airway
-Blood and epiglottis cultures performed
-IV antibiotics (ceftriaxone or equivalent cephalosporin) x 2-3 days, followed by PO abx x 10 days
-Extubation within 1-2 days, when reduction in size of epiglottis is evident

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3
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laryngomalacia

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-Congenital disorder in which the cartilaginous support for the supraglottic structures is underdeveloped
-Manifests as inspiratory stridor in infants, usually within the first 6 weeks of life -> Stridor worse with supine positioning, increased crying, URIs, and feeding
-Typically, benign and resolves by 2 years of age
-Treatment:
-Mild (no stridor at rest, no retractions): Treatment usually not needed
-Severe (stridor at rest, retractions, OSA, increased work of breathing, feeding difficulties, FTT): Laryngoscopy > surgical supraglottoplasty (remove excess tissue)

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4
Q

croup

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-MCC is parainfluenza virus serotypes; children 6 months – 5 years in fall and early winter
-Edema in the subglottic space accounts for predominant signs of upper airway obstruction (inflammation of entire airway is typically present)
-Prodrome of URT symptoms, followed by barking cough, laryngitis, and stridor
-Mild: Stridor only with agitation
-Worsening obstruction: Stridor at rest, retractions, air hunger, cyanosis, hypoxemia
-Imaging: Not indicated (possible in atypical presentations to rule out other causes)

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5
Q

croup tx

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-Mild croup: Supportive, hydration; with or w/o dexamethasone
-expose child to cold moist air
-Dexamethasone: 0.15-0.6 mg/kg PO/IV x 1 dose
-Alternative/adjuvant therapy: Prednisolone (1 mg/kg) QD x 3 days and/or inhaled budesonide
-Severe/stridor at rest: Nebulized racemic epinephrine (diluted in sterile saline!)
-give dexamethasone too (prevents rebound)
-Sx resolution within 3-4 hours of glucocorticoids/nebulized epinephrine -> safely discharged without fear of rebound
-If recurrent doses of nebulized epinephrine treatments required > admission for observation, supportive care, and repeat steroid dosing/neb treatments as needed
-Impending respiratory failure > intubation with endotracheal tube, with extubation within 2-3 days

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6
Q

asthma

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-Chronic airway inflammation with hx of respiratory symptoms such as wheeze, SOB, chest tightness, and cough
-Vary over time and in intensity, along with variable expiratory limitation
-MC chronic ds of childhood (6.2 million children in U.S.)
-M > F, black children > Hispanic and non-Hispanic white children, low socioeconomic status
-Up to 80% of kids develop sx prior to 5 years of age
-Approx 40% of infants/young children who have wheezing with viral infections in first few years of life will have continuing asthma through childhood
-Strongest predisposing factor is atopy (personal or familial)
-Sensitization to inhalant allergens increases over time
-Principal allergens: Perennial (dust mite, animal dander, cockroach, soil mold)
-Triggers (besides allergens): Tobacco smoke exposure, exercise, cold air, pollutants, chemical odors, and rapid changes in barometric pressure
-Shedding of airway epithelium, edema, mucus plug formation, mast cell activation, and collagen deposition beneath basement membrane
-Inflammatory cell infiltrates > bronchial hyperresponsiveness, airflow limitation, disease chronicity
-Airway wall remodeling/irreversible changes

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7
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asthma sx

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-Dx based largely on judgment and assessment, activity limitation, and quality of life
-Wheezing is most characteristic sign -> Also, “chest congestion,” prolonged cough, exercise intolerance, dyspnea, and recurrent bronchitis/PNA
-Auscultation: Prolonged expiratory phase with wheezing
-Increased severity: High-pitched wheeze with diminished breath sounds
-Severe obstruction: No wheeze because of poor air movement
-Flaring of nostrils, intercostal and suprasternal retractions, use of accessory muscles
-Cyanosis of lips/nail beds with underlying hypoxia
-Tachycardia/pulsus paradoxus
-Agitation/lethargy may be signs of impending respiratory failure

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8
Q

asthma: lab findings: Airflow assessment

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-Spirometry
-FEV1 (forced expiratory volume in 1 second) and FEV1/FVC (forced vital capacity – volume exhaled in 1 breath) – Diminished
-Emphasis placed on documenting excessive variability in lung function
-Following treatment administration, + exercise challenge test, + bronchoprovocation test, variation in lung function between visits
-PEFR monitoring: Children with moderate to severe asthma, history of severe exacerbations, or poor perception of airflow limitation/worsening condition
-Body box plethysmography to determine lung volume measurements
-RV, FRC, and TLC usually increased in asthma (air trapping/hyperinflation), VC is decreased
-Infants sedated with compression techniques/forced oscillation

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9
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asthma: lab findings: bronchial hyperresponisveness

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-To stimuli such as inhaled pharmacologic agents (histamine, methacholine, and mannitol) or physical stimuli (exercise/cold)
-Mannitol bronchoprovocation approved by FDA
-Simulates airway responses to specific physiologic situations by creating an osmotic effect within the airway, subsequently resulting in an inflammatory response
-Typically note a 15-20% drop in FEV1 (depending on agent/stimulus)

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10
Q

other findings in asthma

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-Pulsus paradoxus
-Early findings: Hypoxemia, normal PaCO2, respiratory alkalosis
-Later findings:
-< 91% and respiratory acidosis indicative of significant obstruction
-With metabolic acidosis > impending respiratory failure
-Hypercapnia once FEV1 < 20% predicted value
-PaO2 < 60 mmHg, PaCO2 > 60 mmHg/rising > 5 mmHg/hour: Relative indications for mechanical ventilation in a child with status asthmaticus
-Imaging: Not indicated

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11
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asthma assessment

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-Severity directs level of initial therapy
-2 general categories: Intermittent and persistent (mild, moderate, severe)
-Most accurate in pts not receiving controller therapy
-Already on therapy -> classified according to level of med requirement to maintain control
-Control refers to degree to which symptoms, ongoing functional impairments, and risk of adverse events minimized/goals of therapy met
-Performed at every visit
-Categorized as “well-controlled,” “not well-controlled,” and “very poorly controlled”

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12
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asthma: assessment (risk)/step of therapy

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13
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asthma: control assessment (impairment)

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14
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asthma: control assessment (risk)/recommended action

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15
Q

asthma: stepwise management approach

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16
Q

asthma: pharm therapy

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-Long-term controller medications and quick-relief medications (SABAs)
-Long-term: Anti-inflammatory agents (inhaled corticosteroids, leukotriene modifiers), long-acting bronchodilators (and LAMAs), and biologics
-Inhaled corticosteroids (ICS)
-Most potent inhaled anti-inflammatory agents
-Low-dose ICS can provide adequate control, but some patients may need higher doses (step up) due to variable responsiveness -> Greater risks for systemic adverse effects with higher doses
-Early intervention can improve control and prevent exacerbations, but do not prevent development of persistent asthma/alter course
-Delivered in different devices – MDI, dry powder inhaler (DPI), and nebulized aerosol suspensions
-ICS + LABA (salmeterol, formoterol, and vilanterol)
-LABAs are beta-agonists
-Latest guidelines > preference of ICS-LABA as maintenance therapy (Step 3 and above)
-Formoterol tends to be the preferred add-on LABA
-Quick onset of action
-Found to reduce exacerbations and provide control at relatively low-maintenance ICS dose requirement
-Leukotriene antagonists (montelukast, zafirlukast)
-Monotherapy or add-on therapy (alternate/in addition to LABA)
-Long-acting muscarinic antagonists (tiotropium)
-Approved for QD maintenance (6 years and older) as an add-on to ICS-LABA
-Can be added to an ICS as independent adjunct only if LABA cannot be used in certain individuals (unable to tolerate/use drug/device or have contraindications to LABA)

17
Q

asthma: pharm therapy: biologics and theophylline

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-Biologics (omalizumab, mepolizumab, dupilumab)
-Moderate-severe asthma, symptoms inadequately controlled with medium-high dose ICS
-Effective at reducing exacerbations, improving lung function and symptom control, and decreasing oral corticosteroid use
-Theophylline, PO corticosteroids rarely utilized

18
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asthma: pharm therapy: SABAs

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-Quick relief medications: SABAs (albuterol, levalbuterol, pirbuterol, terbutaline)
-Nebulizer, MDI, DPI
-Better to use PRN versus regularly
-Anticholinergics (ipratropium), systemic corticosteroids (prednisone, prednisolone, methylprednisolone) as supplements

19
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asthma: monitoring

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-Regular follow-up visits are important to assess degree of control and consider appropriate adjustments in therapy
-At each step, patients should be instructed to avoid/control exposure to allergens, irritants, or other factors that contribute to asthma severity
-Consider referral to specialist:
-< 5 years: Moderate, persistent; Step 3 or 4 care; considered for Step 2
-> 5 years: Step 4 or higher; considered for Step 3
-Considered for allergen immunotherapy or biologic consideration

20
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asthma: exercise-induced bronchospasm

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-Occurs minutes after vigorous activity, peaks 5-10 minutes after stopping, resolves over 20-30 minutes
-Tx prior to physical activity or exercise usually effective (if only manifestation despite being otherwise “well-controlled”)
-SABAs, LTRAs, cromolyn, or nedocromil
-SABA + cromolyn or nedocromil even more effective
-Salmeterol and formoterol may block bronchospasm up to 12 hours; montelukast up to 24 hours
-Promote extended warm-up period

21
Q

asthma: acute exacerbation

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-Home
-SABA, 2-6 puffs from MDI, every 20 minutes, up to 3 times; or via nebulizer
-Improvement > continue every 3-4 hours x 1-2 days
-Failed completion of improvement > SABA + PO corticosteroid
-Marked distress > ED or 911 for assistance
-Office/ED
-PFTs (when feasible), pulse oximetry -> Maintain oxygen > 90%
-FEV1 or PEFR > 40%: SABA (nebulizer or inhaler) x 3 doses in first hour; with or without PO corticosteroids
-FEV1 or PEFR < 40%: High-dose SABA + ipratropium bromide q 20 minutes x 3 doses; supplemental oxygen PRN; corticosteroids
-Impending/ongoing respiratory arrest > intubated/ventilated with 100% oxygen, IV corticosteroids, ICU admission
-ICU admission: FEV1 or PEFR < 25%, less than 10% improvement after treatment/values that fluctuate widely

22
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asthma: acute exacerbation: pt discharge

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-Sustained response of bronchodilator therapy of at least 1 hour or greater than 70% of predicted/personal best and oxygen saturation > 90% in room air
-Action plan given, reviewed
-Inhaled SABA and PO corticosteroid x 3-10 days
-F/U and specialist recommendations provided

23
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bronchiolitis/respiratory syncytial virus

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-Ds of small bronchioles with increased mucus production and occasional bronchospasm, sometimes leading to airway obstruction
-MC in infants and young children; potentially life-threatening -> Leading cause of hospitalization of infants
-MCC is respiratory syncytial virus (RSV), though other viruses may cause
-Extremely contagious via contact with infected respiratory secretions
-Incubation of 4-6 days
-Presents as a progressive respiratory illness similar to common cold (rhinorrhea and cough)
-Young infants may not have a prodrome – apnea may be first sign!
-Progresses over 3-7 days to noisy, raspy breathing with audible wheezing
-EDUCATE THE PARENT IT WILL GET WORSE BEFORE IT GETS BETTER
-Bronchiolar obstruction: Prolonged expiratory phase, nasal flaring, intercostal retractions, suprasternal retractions, air trapping
-Auscultation: Diffuse wheezes and crackles
-More severe disease: Grunting, cyanosis

24
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bronchiolitis/respiratory syncytial virus dx and tx

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-Laboratory/Imaging Studies
-Pulse oximetry - 90-91%
-Rapid viral diagnosis of NP secretions via PCR (not necessary for diagnosis)
-CXR: Lung hyperinflation/flattened or depressed diaphragms, areas of increased density
-Treatment
-Supportive therapy: Respiratory monitoring, fever control, hydration, upper airway suctioning, supplemental oxygen
-Hospitalization: Respiratory distress, hypoxemia, apnea, inability to tolerate oral feeding, high-risk children
-Abx, bronchodilators, corticosteroids, chest physiotherapy, and hypertonic saline seldom effective

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bronchiolitis/respiratory syncytial virus: complications and prevention
-Complications/Prognosis -Most hospitalized children show improvement in 2-5 days with supportive treatment alone -Tachypnea, hypoxia > rapid progression to respiratory failure > assisted ventilation -Incidence of asthma higher in children hospitalized for bronchiolitis as infants -Mortality rate highest among infants with pre-existing cardiopulmonary or immunologic impairment -Prevention: -Monthly injections of palivizumab (RSV-specific monoclonal antibody), just before onset of RSV season (December through March in U.S.) -Indicated for infants with prematurity (< 29 weeks gestation), chronic lung disease of prematurity, hemodynamically significant cyanotic and acyanotic congenital heart disease in first year of life
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influenza
-MC A/H1N1, A/H2N2, and B; isolated avian and swine outbreaks -Infection rates in children > adults – initiate community outbreaks -Incubation period is 2-7 days, spread via respiratory droplets -Sudden onset high fever, severe myalgia, headache, and chills -> Overshadow coryza, pharyngitis, and cough -Fever, diarrhea, vomiting, and abdominal pain are common in young children -Infants may develop a sepsis-like illness and apnea -Acute illness lasts 2-5 days, viral shedding may persist for several weeks in children -Testing: PCR has highest specificity and sensitivity (nearly 100%)
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influenza tx, complications, prevention
-Treatment -Supportive care, management of pulmonary complications (bacterial superinfection) -Antivirals: Useful if within 48 hours of symptom onset (oseltamivir) x 5 days -Discuss side effects with parents! -Complications/Sequelae -LRT symptoms MC in children < 5 years -Hospitalizations MC in children < 2 years -Secondary bacterial infections (lungs, ears, sinuses) -Encephalitis, myositis -Prevention -Trivalent and quadrivalent vaccines (IIV or LAIV) recommended for all individuals 6 months and older -Prophylaxis with oseltamivir used in select cases of children > 3 months; inhaled zanamivir in children > 5 years
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pertussis (whooping cough)
-Caused by Bordetella pertussis (only infects humans, transmitted via coughing) -Incubation period 7-10 days, patients most contagious during the first 2 weeks of cough -Peaks among those less than 6 months of age (too young for complete immunization + most likely to have severe complications) -Catarrhal stage: 1-2 weeks -Non-specific signs (low-grade fever, nasal congestion) -Paroxysmal stage: 3-4 weeks duration -Coughing occurs in paroxysms during expiration (to dislodge plugs of necrotic bronchial epithelial tissues and thick mucus) -Forceful inhalation against narrowed glottis that follows = “whoop” -Convalescent stage: 1-2 weeks -Gradual resolution of symptoms
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pertussis (whooping cough): dx and tx
-Dx: -Isolation of B. pertussis or detection of nucleic acids (PCR) -Culture from NP swabs or aspirates -Lymphocytosis present in 75-85% of infants and young children, but not diagnostic -Radiograph: Segmental lung atelectasis, perihilar infiltrates -Treatment -Macrolides (azithromycin, clarithromycin, erythromycin)! -Complications/Prognosis: -MC is PNA (primary or secondary) -Other complications: Atelectasis, free air (from paroxysms), epistaxis, hernias, retinal/subconjunctival hemorrhage, OM, sinusitis
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viral pneumonia
-Common cause of CAP in children < 2 years -MCC: Human rhinovirus, adenovirus, parainfluenza, influenza, coronavirus, and human metapneumovirus -URI commonly precedes onset of lower respiratory disease -Wheezing/stridor may be more prominent than in bacterial PNA -Cough, respiratory distress, rales, decreased breath sounds more non-specific -Dx: -Fluorescent antibody, ELISA, and/or PCR only if it will change management, for high-risk patients, or for epidemiology/infection control -Imaging not indicated in B/L, symmetrical findings on exam, no significant distress, no temperature -Findings non-specific: Hyperinflation, peribronchial cuffing, increased interstitial markings, and subsegmental atelectasis -Tx: -supportive; no evidence to support use of antibiotics
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bacterial pneumonia
-CAP is MCC of childhood mortality worldwide -MCC of bacterial PNA in children of all ages is Streptococcus pneumoniae -Usually follows a lower respiratory tract infection -Compromised pulmonary defense systems increase risk of PNA -Abnormal mucociliary clearance, impaired cough function, immunocompromised state, aspiration of oral secretions, or intake and malnutrition -Hallmarks: Fever, tachypnea, and cough -Respiratory distress and hypoxemia are signs of more severe disease -Auscultation: Focal crackles or decreased breath sounds in setting of consolidation/effusion
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bacterial pneumonia: labs and tx
-Dx: -CXR: Indicated for those hospitalized or to assess for complications -Lab studies only for hospitalized patients -Blood cultures, inflammatory markers, CBC (for complications) -Sputum cultures -Tx: -< 4 weeks of age: Ampicillin + aminoglycoside -4-12 weeks of age: Hospital admission, IV ampicillin x 7-10 days -> Similar for 3-6 months -> 6 months of age: High-dose amoxicillin (divided into 2 or 3 doses, daily) x 7 days -Additional therapy: Oxygen, hydration/electrolyte supplementation, and nutrition
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mycoplasma pneumonia
-MC in children > 5 years of age, long incubation (2-3 weeks), onset of symptoms is slow Clinical Manifestations -Fever, headache, cough, chest pain, malaise -Cough dry at onset, sputum production later -Sore throat, OM, OE, and bullous myringitis may occur -Rales, decreased breath sounds, or dullness to percussion may be present -Diagnosis -PCR is gold standard for diagnosis -CXR: Interstitial or bronchopneumonic infiltrates -Treatment: Macrolide x 5-10 days, supportive measures
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cystic fibrosis
-Autosomal recessive -chronic sinopulmonary infections, malabsorption, and nutritional abnormalities -Defect in gene that encodes epithelial chloride channel called the CF transmembrane conductance regulator (CFTR) protein -Alters salt and water movement across cell membrane -> abnormally thick secretions in various organs -One of MC lethal genetic ds in U.S. (1:3000 Caucasian, 1:9,200 Hispanic) -Most develop obstructive lung ds assoc with chronic infection and progressive loss of pulmonary function
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cystic fibrosis sx
-Approx 15% of newborns with CF are born with meconium ileus -Severe intestinal obstruction resulting from inspissation (high viscosity) of tenacious (adherent) meconium in terminal ileum -Virtually diagnostic -> further testing always indicated regardless of screening results -FTT due to malabsorption from exocrine pancreatic insufficiency (failure of pancreas to produce sufficient enzymes to digest fats and protein) -Failure to gain wt despite good appetite -Frequent, bulky, foul-smelling, oily stools -Hypoproteinemia, anemia, deficiency of fat-soluble vitamins (ADEK) -Severe dehydration and hypochloremic alkalosis, bronchiectasis, nasal polyps, chronic sinusitis, rectal prolapse, or unexplained pancreatitis or cirrhosis -Respiratory symptoms: Productive cough, wheezing, recurrent PNA, progressive obstructive airway disease, exercise intolerance, dyspnea, or hemoptysis -Infections with S. aureus and H. influenzae (first few months), then P. aeruginosa -Chronic infection -> airflow obstruction and progressive airway/lung destruction -> bronchiectasis and lung function decline -Pulmonary exacerbations: Increased cough and sputum production, decreased exercise tolerance, malaise, wt loss, and decrease in measures of lung function -> tx -> Abx and augmented airway clearance
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cystic fibrosis dx and tx
-Diagnosis -All states in U.S. perform newborn screening for CF -> Measure immunoreactive trypsin (IRT), a pancreatic enzyme most with CF have an elevated IRT -+ screen -> confirmation via sweat testing and/or mutation analysis -Sweat chloride concentration > 60 mmol/L following an abnormal newborn screen or when obtained for clinical symptoms or family history of CF -Genotyping that reveals two disease-causing CFTR mutations -Treatment (multidisciplinary by accredited CF foundation) -GI: Pancreatic enzyme supplementation, high calorie/protein/fat diet, daily multivitamins (ADEK), salt supplementation -Respiratory: Airway clearance therapy and aggressive abx use -Inhaled hypertonic saline, inhaled abx (tobramycin, aztreonam), PO azithromycin, bronchodilators, anti-inflammatories -Protein-rescue therapies (CFTR modulators – 4 currently FDA-approved) -Directly target underlying defects in CFTR -Approval in younger age ranges > life expectancy to increase (median 40 years of age)
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foreign body aspiration
-Significant cause of death each year -6mo–3yo at highest risk -Typically lodges in supraglottic airway (protective mechanisms -> laryngospasm), smaller objects (coins) my pass glottis and obstruct trachea -Acute onset, inability to vocalize/cough (complete obstruction) and cyanosis with marked distress -Progressive cyanosis -> LOC -> seizures -> bradycardia -> cardiopulmonary arrest -Drooling, stridor, ability to vocalize (partial obstruction) -Lower respiratory tract: Asymmetrical physical findings – decreased breath sounds, localized wheezing, recurrent PNA in one location (chronic cough is suspicious as well) -Diagnosis: Gold-standard is rigid or flexible bronchoscopy (rigid is standard for removal) -Treatment -Prevention is key! ->Counsel parents on age-specific, safe foods and toys -Upper airway obstruction: -Partial: Cough reflex to remove FB -Complete: BLS/PALS guidelines! -Never blind sweeps -Open airway with jaw thrust – FB visualized > remove -If becomes unresponsive > CPR (chest compressions may help to dislodge FB) -Lower airway FB: -Rigid bronchoscopy under general anesthesia -Followed by B-adrenergic neb treatments + chest physiotherapy -Complications: Failure to identify FB > bronchiectasis, lung abscess
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test
know if pt is well controlled or not - should we step up? -place a dx (severity of asthma)