Peds- Pulm

Lung anatomy
 Trachea- primary bornchius- secondary-tertiary- bronchiole- Terminal Bronchiole to
Alveoli
 Alveoli:
o Surfactant: coast alveolie walls, redcued the surface tension so that minimal
pressure is needed in the lung to keep alveoli open
o Site of O2 and CO2 gas exchange
Lung development
 24 wks—fetus starts to form alveoli
 30-32 wks—fetus’ lung are still developing
 36 wks/full term= complete production of surfactant
At birth
 Amniotic fluid is removed: through the trachea via pulm lphyatics and bld vessels
 Surfactant def increase effort needed to keep alveoli open & for gas exchange to occur
o DOL#3 point of adequate surfactant production
Infants
 resting oxygen consumption2x that of an adult’s
 Chest wall: muscles are less developed and fatigue faster
APNEA- cessation of breathing
 Central apnea lack of resp effort (age: wks-months of life)
o Cause: meds, tomors, increase ICP, Arnold-chiari malform, mitochondrial metab d.o
 Obstructive apnea total airway obstruction
 Mixed--> central and obstructive apnea
 Criteria
o Pauses lasting > 15 seconds
o * pauses of 10 seconds are normal

HYALINE MEMRBANE DISEASE aka RDS

 One of most common problems of premature babies
 Cause: not enough surfactant
 Epidemiology
o >50% of preemies born before 28 ws gestations
o Less then 1/3 of those norn bw 32-35 wks
 Increased risk if..
o Preemi > FT
o More so in white, male babies
o C section
o Sold stress—bc will suppress surfactant production
o Infants of DM moms
o Babiues with patent ductors arteriosus
  Sx: cyanosis, falring nostils, grunting noises, retractions
 Dx:
o Appearance, color and breath effort
o CXR—“ground glass” appearance aka reticulogranular pattern
o Bld gas
o eg
 Tx
o Endotracheal ET tube
o Some preemies need to be put on mechanical ventilator
 Complication: Cor Pulmonale
o Oxy
o CPAP
o Artificial surfactant
 Complications
o air leaks of the lung tissues such as:
 pneumomediastinum - air leaks into the mediastinum (the space in the
thoracic cavity behind the sternum and between the two pleural sacs
containing the lungs).
 pneumothorax - air leaks into the space between the chest wall and the
outer tissues of the lungs.
 pneumopericardium - air leaks into the sac surrounding the heart.
 pulmonary interstitial emphysema (PIE) - air leaks and becomes trapped
between the alveoli, the tiny air sacs of the lungs.
o chronic lung disease, sometimes called bronchopulmonary dysplasia
o
BRONCHECTASIS aka Obstructive lung dz
o “ectasis”—expansion or dilation
o Destruction of resp muscle and elastic tissue causingLocalized, irreversible dilation of part of
bronchial tree
o Bronchi are easily collapsible- therefore—obstructive
o Etiology—pathogens that lie at the lower resp tract
o Step pneumo, stpah aureus, H. Influ, pseudomonas aureginosa
o Types of Obstructive lung dz
o Bronchectasis
o Emphysema
o Bronchitits
o Asthma/COPD
o CF
PECTUS EXCAVATUM aka Cobbler’s chest, Sunken cheat or funnel chest
 Most common congential deformity of the anterior chest wall
 Sign: caved in, sunken appearance of the chest
  Can be congenital or not develop until puberty
 Can be just cosmetic, or pathological if it impairs heart/lung function
 Etiology: 37% genetic link
 Increased risk if already dx with Marfan’s syndrome

PECTUS CARINATUM aka pigeon chest

 Epidemiology: 1/400 ppl
o Carninatum is less common that excavatum
o Males > F; 4:1
 Protrusion of the sternum bc of over growth of the cartilage
 Cause:
o 1. Post open hear surgery and cartilage over groms- least lielys
o 2. Congenital: becomes promnents around 2-3 y.o
o 3. Growth spurt in males aroun 11-14 y.o—MOST commonly

BRONCHIOLITITS
o Infection of the bronchiolies
o Epidemiology
o Mostly seen in Infants and young kids—< 2y.o
o Peak age – 3-6 months
o Increased risk if
o Males
o Children NOT breastfed
o Babies who live in crowded conditions
o Early day care
o Cigg smoke exposure
o Px: some can have an increased risk of asthma later on
o EtiologyViral infections..
o RSV #1 viral cause
o Rhinovirus
o Flu
BACTERIAL TRACHEITIS
o Upper airway infection caused by obstruction
o Ddx: Epitglottis and Croup
o often mis-dx as Croup (both have barking cough, stridor and fever)
 BUT tracheitis will not respond to Croup Tx
 Croup is way more common than tracheitis
o Pathology:
o Inflamm of larynx, trachea and bronchi with major site of dz at Cricoid cartilage
(narrowest part of the trachea)
 o Etiology
o Viruses—Most commonly that cause parainfluenza viruses
o Bacteria—Staph areus or strep pyogenes
o Trauma due to previous intubation
o Epidemiology: mostly in peds; M> F
o Dx: failed tx of croup; culture
o Sx
o Fevers, stridor, tachypnea, resp distress (retractions/dyspnea/nasal flaring/cyanosis),
high WBC, barky cough, sore throat
o Pertinent negatice NO drooling, NO position of comfort
o Tx:
o stabilize air way
o Abx: 3rd gen cephalo (cefotaxime, ceftriaxone); Penicillianse resistant PCN (oxacillim,
nafcillin); clinda IV
 MRSA- used vanco
o Tracheostomy- rarely done, only if scarring to trachea has caused narrowing of airway
Croup: aka laryngotracheitis and laryngotracheobronchitis
o a common, primarily pediatric viral respiratory tract illness.
 Pathology:: mostly affects larynx and trachea but may extend to bronchi
 most common etiology for hoarseness, barking cough, and onset of acute stridor in febrile
children
 epidemiology: M>F; < 3y.o
 etiology
o #1 virus= parainfluenza viruses
o Bacterial= influenza A, Mycoplasa penumo, Diptheria
 #1 entry site: Nasopharynx
 early sx: nonspecific respiratory symptoms,
o rhinorrhea, sore throat, and cough, low-grade fever
 later sx (after 1-2 days)
o hoarseness, “seal-like” barking cough, and inspiratory stridor develop
o In mild cases, respiratory sounds at rest are normal; however, mild expiratory
wheezing may be heard.
 Croup is primarily a clinical diagnosis, with the diagnostic clues based on presenting history
and physical examination findings.
o CXR:
 steeple sign, which signifies subglottic narrowing; whereas the lateral neck
view may reveal a distended hypopharynx (ballooning) during inspiration
 Treatment:
o corticosteroids and nebulized epinephrine; steroids
o If severe enough, may need to do a tracheotomy

SPASMODIC CROUP aka laryngismus stridulus

o Non -nfectious d.o (as opposed to Croup)
 o Etiology: may be allergic rather than infectious
o Sx: alwas occurs at night and reoccurs in children
o Signs: subglottic edema occurs without inflammation
INFLUENZA
o Vacinations
o HiB against H. Infu B; ages 2,4,6 and 15 m/o
 If > 5y/o—do not need it unless immunocomp
o Flu Vaccine- annualy
 IM shot—only if not allergic to eggs and doesn’t have fever
 Nasal spray: NOT if allergic to eggs, fever, or asthma
o Sx: typical flu sx.. but in peds add—conjunctivis, rhinitis and GI sx
o Dx: diagnosing influenza A and B is a
o viral culture of nasopharyngeal samples and/or throat samples
o Enzyme-linked immunosorbent assay (ELISA)
o Rapid influenza diagnostic tests (RIDTs)[1]
o
o Tx: supportive
AVIAN INFLUENZA
o Tx:
o Oseltamivir
o Zanamivir

PERTUSIS aka whooping cough aka 100 day s cough

o Etiology: Bordetella Pertusis- very contagious
o Vaccines:Dtap 2,4,6, 15 m/o and 4-6 y.o
o Sx:
o uncontrollable cough that makes it hard to breath
o Whooping sound- deep breathes taken b.w coughs
o Fainting/vomiting after coughing
o Dx: Culture
o Tx: oxy tent, IVF, abx: Erythromycin

VOCAL CORD PARALYSIS

o Etiology
o Birth – common congenital defect of larynx= b/l scarring
o CNS abnormalities: Chirari malformations, ICP
o Cardiac surgery scarring—causes u/l vocal cord scarring
o Sx: occur by 2 m/o
o U/L aspiration, transient stridor, weak/breathy cry
o B/L paralysis: aspiration, blue spells, stridor, SOB
 oTx—usually only if breathing is compromised
o U/L: inject filler material into affected/weaker cord; restoring function to the nerve of
vocal cord
o B/L: tracheostomy tube, surgery to increase opening in back of larynx (posterior
laryngeal airway)
PENUMONOA
o Epidemiology
o Can occur at any age but more common in kids
o Makes up 13% of all infectious illness of infant < 2 y.o
o Etiology
o Bacteria:
 Grp B strep= #1 cause transmitted through utero; most common in 1-3 m/o
 Listeria, E.coli, Klebsiella pnemo
 Mycoplasma penumo= #1 cuase in in older kids/adolescents
o Viral: #1 is RSV
o Sx in infants: poor feeding, cough (#1),tachypnea, reatractions, hypoxemia, fever
o Sx in adolescents: same as above Plus.. h.a, pleuritic chest pain, abd pain, N/V/D, otits
o Dx:
o Look at respiration rate
 Children younger than 2 months: Greater than or equal to 60 breaths/min
 Children aged 2-11 months: Greater than or equal to 50 breaths/min
 Children aged 12-59 months: Greater than or equal to 40 breaths/min
o 02sat%
o CXR, cbc, u/s (new data shows how effective u/s are for dx and may replace CXR)
o Tx
o Tx resp distress
o Abx
 Standard of care: high dose Amoxicillin
 2nd or 3rd cephalo
 Macrolides
o Vaccines
o The pneumococcal conjugate vaccine (PCV13) is recommended for all children younger
than 59 months old.
o The 23-valent polysaccharide vaccine (PPVSV) is recommended for children 24 months
or older who are at high risk of pneumococcal disease.

RESPIRATORY SYNCYTIAL VIRUS (RSV)

o Adult sx: cold-like sx—runny nose, cough, h.a, sore thrat, fever
o Complications or RSV: when Infants/children with lung/heat dz get RSV= serious illness
o Highly contagious ** almost ALL ids are infected by RSV 1x by 2 y.o
 o RSV can lead to..
o Pneumonia, bronchiolitis
FOREIGN BODY ASPIRATION
 Age: most common < 4 y.o
 Location: most likely in tracheobronchial tree or RIGHT lung
 Sx: strifor, bloody sputum, u/l absence of breath sounds
 Dx: CXR, rigid bronchoscopy
OBSTRUCTIVE SLEP APNEA
 Complications
o FTT, cor pulmonale, poor school performance
 Increased risk if..
o Obese , tonsil and adenoid hypertrophy, craniofacial abn, neuromusc dz
 Dx: sleep study
 Tx; CPAP
 Sx: daytime slepiness

LARYNGOMALACIA
 “malacia”- state of abnormal softening
 #1 congential anomaly of the larynx
 Patho: the laryngeal cartilage and tracheal rings are less rigid=floppy airway
 Sx:
o obstructive airway- bc floppy airway caused collapse of the supraglottis during
inspiration
o turbulent air flow- bc of obstruction of supraglottis due to floppy laryngeal cartilage and
tracheal rings
o Stridor:** a sx of the UPPER air ways
 High pitch inspiratory sound, more severe the obstruction= higher the pitch
 Alleviating factors: stridor improves in prone position
BRONCHIOLITIS
 Epidemiology
o Mostly in kids <2 y.o; mostly in winter
 Pathology: obstruction of airway due to inflamed bronchioles
 Bronchioles (smaller airways <2mm close to the alveoli)
o are free of mucous glands and cartilage
 Sx inflammation at bronchioles causes
o congestion of mucosa, and edema of submucosa
o destroyed cilia
 Px: 25-50% will develop asthma
 Rare complications
o bronchiectasis- dilated bronchi, irreversible damage, impaired mucociliary clearance
 o bronciolitis obliterans- hypertrophy of epithelium of medium & large bronchi with
cellular infiltration of airway walls, muscle & elastic tissue destruction, fibrosis
 MAS- Meconium Aspiration Syndrome
o ** most common and dangerous neonatal aspiration!!
o 2% of babies who have meconium-stained amniotic fluid aspirate it
o A fetus can release meconium into their amniotic fluid and in period of hypoxia the
stressed fetus will have deep gasping respirations leading to MAS
o Complications
 Atelectasis: Collapse or obstruction of the Lung
 In MAS- it refers to blockage of air flow
 Overexpansion: one way valve- so only lets air in and not out
 Air-leak syndrome: pneumothorax or pneumomediastinum
 Pulmonary HTN: transient repsonce to hypocxia or acidosis
 Meconium pneumonitis: inflammatory response to bile salts & other irritating
chemicals in meconium
 Alveoli instability bc meconium impairs surfactant functions (an acquired
form of ARDS)
 Chronic lung dz:
o Occurs in premature infants who require treatment with oxygen or mechanical
ventilation from birth
o Criteria: child neds supplemental oxy at 36 wks AND abnormalities on CXR
 BronchioPulmonary dysplasia BPD
o This is a chronic lung dz (criteria s above)
o Causes:
 1. Immature lung architecture stretched or distorted during mechanical
ventilation or with spontaneous breaths
 2. Oxygen toxicity causes injury due to inadequate antioxidant defenses of the
premature lung
 3. Excessive pulmonary blood flow from L to R shunting through PDA or
excessive fluid may compound injury
o Histopathology- areas of cystic destruction alternating with areas of fibrosis and
atelectasis
o Effects
 *Insufficient amounts of functional surfactant leads to alveolar instability and
collapse
 *High pressure needed to reopen the collapsed alveoli
 TTN- Transient Tachypnea of the Newborn aka Wet Lungs, Aka type II resp distress synd
o MOST COMMON RESP DISTRESS IN A TERM NEWBORN (1% of all newborns)
o Px: most make a full recovery with no long term issues
o Etiology: delayed clearance of lung fluid by the cells lining the resp tract
 Surfactant insuff. Can be mild or cal lead to RDS
 o Pathology: Amniotic fluid removed through trachea & reabsorbed via pulmonary
lymphatics & blood vessels
 extra fluid in the lungs remains or the fluid is cleared too slowly so the baby
breathes faster and harder to get enough oxygen into the lungs.
o Risk factors for TTN
 C section – eso if without labor
 Mom never going through Labor the pressure of passing through the birth
canal, squeezes some of the fluid out of the lungs. Also, the hormonal changes
during labor lead to absorption of some fluid
 Mom with DM
 Mom with asthma
 Baby is small for gestational age/ or preemies
o Sx:
 Tachypnea > 60 bpm
 Retractions, nasal flaring, cyanosis, grunting on exhale
o Dx: CXR to r.o pneumonia ; pulse ox, CBC
o Tx: NICU, oxy mas, CPAP, ventilator (if severe), IVF
o Px: most make a full recovery with no long term issues
 Within 24-48 hrs—breathing with TTN improves/normal
 Within 72 hrs- usually all sx resolved
 ALTE- acute life threatening event
o Any event in which changes a baby’s behavior and can threaten a baby’s life
o Sx: apnea, color change, limpness, choking, gagging
o Etiology: 0.05-1%
 SIDS- Sudden Infant death syndrome
o The unexpected death in a baby < 1 y.o
o Cause are still unknown even after a autopsy
o Incidence is highest in…
 Boys >> girls
 Babies of young mothers
 Impoverished, smoking mothers
 Preemies, low birth wt
 AA and native americans
 Druggy moms
 Age: mostly occurs in age 2-4 motnhs
 Winter
 If sibling died from SIDS, have a 3-5x increased risk
o Etiology—UNKNOWN but have some theories
 Brain stem cellular abn
 Maturational delay of cardioresp control
 Prolonged QT interval
  CO2 rebreathing
 KARTAGENER SYNDROME--Immotile Cilia syndrome
o Etiology: inherited—AR
o 50% of ppl with primary ciliary dyskinesia have Kartagener’s synd
o Sx: Triad
 Situs inversus- reversal of internal organs
 Bronchiectasis- destruction and widening of the large airways
 Sinusitis
 ** also assoc with otitis media, and infertile males
 CYSTIC FIRBOSIS aka Mucoviscidosis
o Inherited AR; Chrom 7, long (q) arm
 Need both CFTR genes to not work to be dx with CF
 Most common Mutation: deletion of F508= loss if a.a. phenylalanine
 Accounts for 2/3 of all cases world wide, and 90% of causes in US
 There are 1500 other types of mutations
 Depending on how the mutation affects CFTR gene= the severity of CF
o Epidemiology: : 1/3,200 Caucasians
 Most common in Cuacasiosn
o Etiology
 Mutation of both CFTR genes (on chrom 7) which is needed to form the
protein--CFTR cystic fibrosis transmembrane regulator
 CFTR protein is needed to regulate Chloride channels movement of Cl and Na
ions across epithelial membranes (i.e. the lungs)
 Chloride channels- regulate our sweat, digestive fluids and mucous
o Pathology: abnormal transport of Cl and Na across the epithelium
 This leads to thick, viscous secretions
o Target organs: lungs, pancreas, liver, intestines
 CF sx
o Lung and sinuses Sx
 build up of mucous leads to decrease in muco-ciliary clearance which leads to
inflammation and eventually infection/injury/structural changes
 early lung sx: cough, copious phlegm production, decrease exercise, pneumo
 late lung sx: architectural changes to the lung (bronchiectasis), hemoptysis,
pulm HTN, heart failure hypoxia,
 Lung infection- Most common organisms to infect the lung area
 Common Bacteria: Staph Aureus, H. Influ, Pseudomonas aeruginosa
 Common Fungus: Aspergillus Fuigatus
 Chronic Sinus infections- nasal polys, h/a
 Burkholderia cepacia infection- leads to rapid lung infection/declin and death

o #1 cause of death on CF pts cardiorespiratory complications 80%
o GI sx
 Meconium Ileus (5-10%)
 Rectal prolapse -10% - protrusion of the internal rectal membranes
 Pancreatitis- bc (like the lungs) the secretions (digestive juices) from the
pancreas becomes thickened= clog pancreatic ducts= pancreatitis (adolescents)
 A. block the digestive enzymes from entering the duodenum=
malabsorption of nutrients=hypoproteinemia=edema
 B. steatorrhea---difficulties absorbing fat soluble vitamin D,A,K,E
 CFRD- CF related Diabetes- due to damage of the pancreas and islets of
Langehands (make insulin)
 Adults GI sx: intussusception, constipation, heart burn, distal intestinal
obstruction syn (thickened feces=intestinal blockage)
o Liver sx
 Cirrhosis via--Blocked bile ducts
 Liver failure= fails to rid bld of toxins and make clotting factors
o Infertility—
 97% of men are infertile but NOT sterile
 Most can have kids if assiseted with repro techniques
 #1 type--Congenital Absence of the Vas deferens (connects the testes to the
ejaculatory duct of the penis)

o CF signs
 Clubbing of fingers and toes—hypoxia
 FTT
o Complications
 Cyst and fibrotic tissue forms in the targeted organs
o Dx:
 genetic testing Before birth
 New born screening at birth; needs to be confirmed with a sweat test
 For the most part- CF is not a routine new born screen in most states
 sweat testing early childhood- or parnets make the dx bc their child “tastes
salty”
 MOST COMMON DX TEST
 ** prior to newborn screening—CF was dx when a newborn failed to pass
meconium aka Meconium Ileus ( in 5-10% of CF babies)
o Px: infants born 70 yrs ago would most likely die before their 1 st birthday, today CF pts
are living until about 40
o Tx:
 Resp therapy- life long
 chest physiotherapy (CPT)- percuss areas of chest to lossen up
secretions
  ThAIRapy Vdest and intrapulmonary percussive ventilator- devivces that
recreate percussion to loosen up secretions
 BiPAP
 Lung transplantation and gene therapy- aim to cure some aspects of CF
 Abx- even as a prophylaxis
 Rx: Aerosolized DNase--thin mucous; bronchiodilators
 Pancreas tx—enzyme replacemenst, high cal diet, 2x fat soluble vit
 Psych tx

ATHSMA

o Chronic Obstructive / inflamm disorder

o Sx:
o Wheezing, -A musical, high-pitched whistling sound produced by airflow turbulence i
 one of the most common symptoms of asthma
o coughing- non productive; can be worsened at night or with exercise
o SOB
o Chest tightness
o Acute episodes: breathless, cannot tal in sentences, sit upright, retractions, nasal flaring
o Severe episodes:
o RR>30; Hr> 120; suprasternal retractions, accessory muscles, Sp02 on RA <91%
o Pulsus paradoxus- systolic bld pressure drops > 10 mmHG
o Feel “tired”—bad sign, pt getting fatigued from trying to breath
o
o
o Status asthmaticus- recurrent asthma attacks
o Sx: paradoxical tharcoabd movements, absent wheezing (when severe), bradycardia (severe
hypoxemia),
o Poorer px when
o Bradycardic (severe hypoxemia); tired; Pulsus paradoxus,
o Classifications….
o Intermittent:
o Frequency < 2 days/wk
o Night time awakenings
 0-4 y.o= 0 xs; OR >5 y/o= <2x/month
o SABA usage: < 2 days/ wk
o Interference with daily activities: None
o Lung Function test > 80% FERV1/FVC
o Risk of Exacerbation needeing corticosteroids 0-1 yr
o Mild:
o Frequency > 2 days/wk
 o Night time awakenings
 0-4 y.o= 1-2 x’s/mo; OR >5 y/o= 3-4 x’s/mo
o SABA usage: >2 days/ wk
o Interference with daily activities Minor
o Lung Function test > 80% FERV1/FVC
o Risk of Exacerbation needing corticosteroids
 0-4 y.o: >2 x’s in 6 mo OR > 4 wheezing episodes per 1 yr lasting > 1 day
 > 5 y/o: >2 x’s/yr
o Moderate:
o Frequency Daily
o Night time awakenings
 0-4 y.o= 3-4 x’s/mo; OR >5 y/o= >1x /wk
o SABA usage: Daily
o Interference with daily activities Some
o Lung Function test 60-80% FERV1/FVC
o Risk of Exacerbation needing corticosteroids
 0-4 y.o: >2 x’s in 6 mo OR > 4 wheezing episodes per 1 yr lasting > 1 day
 > 5 y/o: >2 x’s/yr
o Severe:
o Frequency throughout the day
o Night time awakenings
 0-4 y.o= >1 x’s/wk; OR >5 y/o= often; 7x’s/wk
o SABA usage: several x’s/day
o Interference with daily activities extreme
o Lung Function test <60% FERV1/FVC
o
o Risk of Exacerbation needing corticosteroids
 0-4 y.o: >2 x’s in 6 mo OR > 4 wheezing episodes per 1 yr lasting > 1 day
 > 5 y/o: >2 x’s/yr
o
o Dx:
o Pulm function test
o Exdercixe challenge: spirometry of baseline, then at 60% HRmax
o FeNO- fraction of exhaled NO—noninvasive marker of airway inflamm
o Allergy testing
o Tx: while figuring out management- should f.u with pt q 2-6 wks; once controlled- f/u q 1-6 mo
o A pt is well controlled if use SABA inhaler  < 2 days/w

TREATMENT OF ASTHMA

o Progression of asthma management…..

 1. SABA- everyone gets this; if used >2x/wk; add long acting
2. Low dose ICS
3. Medium dose ICS orrr can add LABA to low dose ICS

o Short acting/Rescue Meds…

o 1. SABA--SHORT ACTING BETA 2 AGONISTS—rescue inhales
o A. Albuterol
 1. Proventil
 2. Ventolin
 ADR: tachycardia, skeletal muscle tremor, dizziness, nausea / vomiting,
palpitations
o B. Levalbuterol (Xopenex)
o 2. Anticholinergics (Ipratropoium) ** no always included in astha acute management
o MOA: bronchiodialtor – concern is that is only reverses the cholinergically mediated
bronchiospasm
o Atrovent HFA or neb ipratropium bromide
o COmbivent- ipratropium bromide (anticholinergic)/abludterol (SABA)
o More so used for COPD in adults; bc most asthma’s bronchiospasms are not cholinergically
mediated
o Long acting Inhalers does NOT rescue the pt!!—takes too long!!
o 1. Corticosteroid
o NOT a rescue
o DOES suppress the dz and ODES reverse inflamm
o Safe long term
o Names of commonly used long acting
 A. Budesonide DPI, Pulmicort Flehaler (inhaler)
 B. Budesonide nebs , Pulmicort Respules (neb)
 C. Fluticasone propronate, Flovent
o ADR of Steroids- tend to cause over growth of any organism- but specially Fungi!!
 Tx: after inhaled steroids– just rinse mouth and spits
o Tips: children should use spacers to ensure they are getting most of the meds
o 2. Mast cell stabilizers- not used as often as corticosteroids
o A. Cromolyn:
 Croolyn sodium (Intal)= nebulizer or inhaler
 Nasalcrom= Nasal spray
o B. Nedrocromil (Tilade)= inhaler or neb
o MOA: used to stabilize an immune mediatied or allergy related asthma
 Basophils and mast cells release histamine; this med prevents mast cells from
releasing histamines and thus prevent the asthmatic response
 Note: takes a few wks for this to start working (2 wks will se benefits; but need
4-6 wks to see max benefit)
o 3. Immunomodulators
o Indicated for use if..
 MUST be > 12 y.o to use this
 ICS not doing the trick
o Product Omalizuman (Xolair); Anti-IgE
o Who can prescribe this Pulmonologist – bc pt needs to be monitored whiel admitting this
med bc anaphylactic shock is possible
o 4. Long acting beta 2 agonist- sympathomimetic LABA
o MOA: bronchodilators
o LABA can be added to ICS after ICD dose has been maximized
o Indications: use when ICS is not enough
o Products: salmeterol xinofoate (Serevent Diskus)
o Note ..
 For asthma—use ICS thennn use LABA
 For COPD (adults)—use LABA thennn ICS
o Contraindications:
 Cardiac arythmias – tachy or heart  bc LABA increase HR (sympathomimetic)
 Narrow angle glaucoma—sympathomitic will vasoconstrics
o ADR: tachy, skel muscle tremoe, hypoK, prolonged QT interval, dizzy, N/V/, paryngitis
o drug rxns in adults: may counteract the benefits of BB
o 5. Combo products Corticosteroid + LABA
o Advair—Fluticasone Propionate + Salmeterol Xiafoate
o Symbicort= Budesonide ( ICS) + Formoterol (symbicort)
o Dulera= mometasone + formoterol
o 6. Methylxanthine
o Product: Theophylline SR
o MOA: smooth muscle relaxation, increases diaphragm contracabilty and mucocilary clearance,
Bronchiodilation
o Used more so for COPD—bc decrease diaphragmatic fatigue
o 7. LTRA- Leukotriene modifiers
o Product: Montelukast Sodium (Singulair)
o MOA: affects mast cells
 Leukotriene receptor antagonist
o ADR: may be some correlation bw Singulair and Suicide
o Severe cases
o 1. Systemic Corticosteroids
o Want to limit this bc of ADR assoc with long term use
o 2. Can give IV corticosteroids (when admitted)
o 3. Mg Sulfate IV
o Used in the ER in combo with systemic steroids
 o Improve bronchodilation and improve airflow.
o
o Evaluation if asthma is being managed well
o 1. Using SABA < 2x/wk
o 2. FEV1 > 80% predicted max

TUBERCULOSIS

o BACTERIAL: Mycobacterium Tb; acid fast bacteria

o Spread: prsn to prsn through resp droplets
o Note: children are less likely to spread TB- bc they usually have the less infectious type
o Tb found in kids is mostly seen in
o Kids < 5 y.o OR adolescents > 10 y.o
o Young children are at high risk for TB complications than adults
o i.e. Disseminated TB and TB meningitis
o Latent TB: mycoplasma is in body, however subsided by the healthy immune system
o Active TB: when bacteria is able to multiply bc pt in immunocompromised
o Kids are more likely to become active TB than adults
o Dx in kids is harder than adults bc..
o 1. Hard to get a sputum sample from them
o 2. Lab test to find TB in sputum—kids have smaller amount of the Tb bacteria
o ** therefore, Tb dx in kids is usually made WIHTOUT lab confirmation
o Dxing TB in kids
o 1. Clinical sx
o 2. (+) TST test or (+) TB bld test (IGRA) or interferon gamma release assay
 When children are latent or asx; this is the only diagnosable entity
 TST is preferred for IGRA test in kids < 5 y.o
 Note: prior BCG vaccine will show a false positive on TST but NOT on IGRA bld test
 Note: if either is (+).. does not differentiate if it is latent or active tb
o 3.CXR
o 4. Hx of contacts with an infectious TB personm
o TB sx
o Cough, lethargy, fever, night sweats, FTT
o , icterus, hepatosplengomegaly, tachypnea, lymphadenopathy
o Endocrachial dz with Lympohadenopathy = most common sx
o pleural effusions= more common in adolescents
 chest pain, that increases with deep inspiration, SOB, fever
o WHO SHOULD BE TX FOR LATENT TB….

Groups Who Should be Given High Priority for Latent TB Infection Treatment
People who have a positive IGRA result or
a TST reaction of 5 or more millimeters
 HIV-infected persons
 Recent contacts of a TB case
 Persons with fibrotic changes on
chest radiograph consistent with old
TB
 Organ transplant recipients
 Persons who are immunosuppressed
for other reasons (e.g., taking the
equivalent of >15 mg/day of
prednisone for 1 month or longer,
taking TNF-α antagonists)
People who have a positive IGRA result or a TST
reaction of 10 or more millimeters
 Recent immigrants (< 5 years) from high-
prevalence countries
 Injection drug users
 Residents and employees of high-risk
congregate settings (e.g., correctional
facilities, nursing homes, homeless
shelters, hospitals, and other health care
facilities)
 Mycobacteriology laboratory personnel
 Children under 4 years of age, or children
and adolescents exposed to adults in high-
risk categories

o Latent TB Med types..

o Note: these 3 drugs are available in diff regimens based on the pt
 isoniazid (INH)—most common for peds
 rifampin (RIF)
 rifapentine (RPT)
o In Peds use..
 9 months of Isonizid
o This regimen is very effective and is the preferred regimen for HIV-infected
people taking antiretroviral therapy, and children aged 2–11 years of age.

o Active TB first-line med types
 Isoniazid (INH)
 rifampin (RIF)
 ethambutol (EMB)
o  pyrazinamide (PZA)
o Initiation pahse 2 months
o Continuation phase either 4 or 7 months; with a totally or 6 or 9 months of tx
depending on the pt
o The 4-month continuation phase should be used in the large majority of patients.
o The 7-month continuation phase is recommended only for three groups:
 patients with cavitary pulmonary tuberculosis caused by drug-susceptible organisms
and whose sputum culture obtained at the time of completion of 2 months of
treatment is positive;
 patients whose initial phase of treatment did not include PZA;
 and patients being treated with once weekly INH and rifapentine and whose sputum
culture obtained at the time of completion of the initial phase is positive.

o TB Vaccine BCG Bacille Calmette-Guérin

o Extremely rare to be given in U.S.
 o It IS gevein if…
 Child is TST neg and is constantly being exposed, i.e. cannot be separated from
adults who are not txed effectively or
 Have TB strains resistant to isoniazn and rifampin

PULMONARY HTN

 MOA: not enough vessels in lung or vessels become narrowed or blocked causing BP to rise to
push bld through these vessels
 1. Idiopathic pulm HTN IPH
o Can be genetic BMPR2 gene
 2. Secondary pulm HTN
o Due to: congentical hert abn, lung dz, preemi lung issues, abn function of left ventricle,
SCD, etc..
 Sx: fainting, SOB, fatigue, dizzy, low BP, edema, tachycardia
 Dx: do echo, CTs PFT, to dx the underlying issue
 Acute tx:
o Inhaled oxy, iNO (inhaled Nitric oxide), SABA, anticoag (prevent clots), diuretics,
o Artrial septostomy- surgery done when all else has failed
 Prevents R ventrivle from working so hard againt the pulm pressure
 Hole put in heart to redirect from directly from R to L ventricle
o Lung transplanmt

COR PULMONALE

 High risk peds pt has cystic fibrosis

 Pathology
o some pulmonary dz leads to pulm HTN and increased pulm vascular resistance PVR
which causes Right ventricle to pump hard and soon fail leading to ---Right heart failure,
i.e. Cor Pulmonale
o it is NOT the result of some primary congintalt heart defect

 most common etiology
o ARDs- for 2 rsns
 1. Pathological features of virus 2. Mechanical ventialion (needs higher
transpulmonary pressure)
 In the case of ARDS--, cor pulmonale is associated with increased possibility of
right-to-left shunt through the patent foramen ovale and carries a poorer
prognosis
o Pulm Embolism- suddeen increase in pulm resistant leading to increased n RV
o Increase bld viscosity, obstructive lung dzs
 Chronic cor pulmonlae RVH
 Acte cor pulmmonale RV dilation