PNEUMONIA IN CHILDREN

What is pneumonia?
- Inflammation of lung tissue due to an infectious agent that stimulates a response resulting in
damage to lung tissue
- UNICEF 2015 - leading cause of mortality in children <5 years old

Etiology What are possible causes of pneumonia?

- Aspiration
- Lipoid pneumonia
- Hypersensitivity reactions
- Drugs
- Radiation-induced
- Infection - difficult to determine/inaccurate tests

Viral pathogens are usually common in?

- Most common in 1 month to <5 year old children and usually resolve
in 3 days.

Which viral pathogens are most common in <2 year old children?
- RSV → bronchiolitis
- Rhinoviruses → do not cause severe pneumonia

What are other examples of viral pathogens capable of causing

pneumonia?
- influenza, human metapneumovirus, parainfluenza, adenoviruses,
enteroviruses

Which bacterial pathogen is common in 3 week to 4 year old children?

- S. pneumoniae

Bacterial pathogens common in children more than 5 years old:

- M. pneumoniae
- C. pneumoniae

Major causes of hospitalization and deaths in developing countries:

- S. pneumoniae
- H. influenzae
- S. aureus

Which bacterial pathogens are to be considered if with HIV?

- M. tuberculosis
- non-TB mycobacteria
- Salmonella
- E. coli
- P. jiroveci
- CMV

Pathogenesis What kind of defense mechanisms does the lower RT have?

- Mucociliary clearance
- Macrophages
- Secretory IgA
- Clearing of the airways by coughing

Pneumonia occurs when there is disruption of the ecosystem. The

lower RT is the site for dynamic interactions between?
- Pneumonia pathogens
- Resident microbial communities
- Host immune defenses

Viral Pneumonia - can predispose to secondary bacterial infection

Virus not removed by cough → spread of infection ℅ direct injury of the
respiratory epithelium → swelling, abnormal secretions, cellular debris →
airway obstruction → (if complete,) atelectasis, interstitial edema, hypoxemia
 Bacterial superinfection is usually preceded by?
- viral or M. pneumoniae infections

When does bacterial superinfection usually happen?

- Impairment of cough reflex
- Interruption of mucociliary clearance d/t destroyed epithelium

How does prior viral infection enhance bacterial adherence?

- Altered host defenses
- Induction of receptors on exposed surfaces
- Changes in extracellular environment - modify bacterial flora

Pathogenesis for bacterial pneumonia occurs via:

- Colonizing the trachea → access to the lungs
- Direct seeding from bacteremia

M. pneumoniae MOA:
- Inhibits ciliary action

How does S. pneumoniae spread infection?

- Local edema aiding in proliferation → focal lobar involvement

What are usually involved in Group A Streptococcus infection?

- More diffuse lung involvement + interstitial pneumonia
- Necrosis of tracheobronchial mucosa → exudate, edema, local
hemorrhage
- Pleural involvement likely

Manifests as confluent bronchopneumonia which is often unilateral

and occurs resulting in pneumatoceles, empyema, bronchopulmonary
fistula.
- S. aureus

When is pneumonia considered recurrent?

- 2 or more episodes in a year
- 3 or more episodes ever

Clinical Manifestations What are the typical upper RT infection symptoms that manifest
preceding pneumonia?
- Rhinitis, cough

What is the most consistent clinical manifestation in viral pneumonia?

- Tachypnea

Auscultation of the chest in viral pneumonia may reveal?

- Crackles, wheezing

What are typical symptoms found in bacterial pneumonia?

- Sudden high fever, cough, chest pain

Abdominal pain is usually present and consistent in?

- Lower lobe pneumonia

When children lie on one side with the knees drawn up to the chest,
this is to:
- Minimize pleuritic pain, improve ventilation

These symptoms may be found early in the course of pneumonia:

- Diminished breath sounds
- Scattered crackles
- Rhonchi

Development of increasing consolidation or complications of

pneumonia include:
- Pleural effusion or empyema
- Dullness on percussion
- Diminished breath sounds
Diagnosis Chest radiograph (PAL) view

Viral
- hyperinflation with bilateral interstitial infiltrates and peribronchial
cuffing

Pneumococcal
- lobar consolidation

Bacterial
- 15,000-40,000/mm3 and predominance of polymorphonuclear
leukocytes
- Large pleural effusion, lobar consolidation, high fever at the onset of
the illness
- Definitive diagnosis = isolation of bacterial organism

M. pneumoniae
- cold agglutinins titers > 1:64

GAS pneumonia
- Antistreptolysin O, anti-DNase B titers

Other biomarkers: CRP, PCT, lipocalin-2, TNF-related apoptosis-inducing

ligand

Treatment Mildly ill children

- High doses of Amoxicillin (90mg/kg/day orally divided twice daily)
- Alternatives: Cefuroxime or Amoxicillin/Clavulanate

School-aged children and adolescents (M. pneumoniae, C. pneumoniae

suspected)
- Macrolide Azithromycin
- Alt: Clarithromycin or Doxycycline - 8 yo and above

Adolescents
- Levofloxacin or Moxifloxacin (Fluoroquinolone)

Fully immunized against HIb and S. penumoniae, not severely ill

- Ampicillin or Penicillin G
- Children who do not meet these criteria → Ceftriaxone or
Cefotaxime

Staphylococcal pneumonia
- Include Vancomycin or Clindamycin

M. pneumoniae or C. pneumoniae
- Include a Macrolide

Antibiotics duration: until Px has been afebrile for 72 hours

- 10 days of compliance (5 days if Azithromycin)
- 5-7 days of compliance if managed OPD

Reduce mortality:
- oral Zinc (10mg/kg/day for <12 mo., 20mg/kg/day for >12 mo. for 7
days)

Prognosis Uncomplicated type improve within 48-72 hours of initiation of antibiotics

Complications Most common causes of parapneumonic effusions and empyema:

- S. aureus, S. pneumoniae, S. pyogenes

Pleural fluid → gram stain, bacterial culture

Small (<1 cm on lateral decubitus radiograph), free-flowing parapneumonic

effusions - antibiotic therapy only

Large effusions, especially if purulent (empyema) - drained

Prevention PCV
Influenza vaccine - administered to >6 mos of age
Vaccination for Hib, pertussis, measles

Pneumonia Clinical
Features
Bacterial Viral, Mycoplasma, Mycoplasmal
Chlamydia

Fever, chills, Wheezing Headache, malaise,

abdominal pain, chest non-productive cough,
pain , productive low-grade fever
cough

Tachypnea - more sensitive and specific

2-12 months ≥ 50
1-5 years ≥ 40
>5 years ≥ 30

PCAP PCG Clinical Questions

1) What clinical signs and
symptoms will accurately
diagnose CAP?
Cough or fever, plus any of the following:
1. Tachypnea
2. Retractions or chest indrawing
3. Nasal flaring
4. O2 saturation <95% at room air
5. Grunting, head bobbing

2) What clinical and ancillary

parameters will determine the
need for admission?

3) What diagnostic aids will Routine diagnostic aids are not suggested
confirm the presence of Left to the discretion of the clinician based on her assessment
nonsevere CAP in an
ambulatory setting?

4) What diagnostic aids will ● Chest radiograph - initial diagnostic

confirm the presence of severe ● Point-of-care chest ultrasonography (POCUS)
CAP in a hospital setting? ● PCT
● Sputum gram stain and culture - not routinely
● CBC, ABG, serum electrolytes

5) What clinical and ancillary Both severe and nonsevere pneumonia:

parameters will determine the ● Elevated WBC, CRP, PCT
need for antibiotic treatment?
6) What empiric treatment is
effective if a bacterial etiology
is considered?
7) Will the addition of a
macrolide to standard empiric
regimen improve outcome?
8) What treatment is effective if
a viral etiology is considered?
9) What clinical and ancillary
parameters will determine a
good response to current
therapeutic management?
10) What should be done if a
● Alveolar infiltrates (CXR)
● Unilateral, solitary lung consolidation and/or air
bronchograms and/or pleural effusion (UTZ)
A. Non-severe PCAP, regardless of immunization status
against S. pneumoniae and/or Hib
● Amoxicillin trihydrate 40mg/kg/day Q8 for 7 days
or 80-90 mg/kg/day Q12 for 5-7 days
● Amoxicillin-Clavulanate 80-90 mg/kg/day Q12 for 5-7
days
or Cefuroxime 20-30 mg/kg/day Q12 for 7 days (if with
high-level penicillin-resistant pneumococci)
B. Severe PCAP, regardless of immunization status against
S. pneumoniae
● Penicillin G 200,000 units/kg/day Q6 (with complete HiB)
or Ampicillin 200 mg/kg/day Q6 (if with
no/incomplete/unknown Hib vaccination)
● Cefuroxime 100-150 mg/kg/day Q8
or Ampicillin-sulbactam 200 mg/kg/day Q6 (if with
resistance)
● ADD Clindamycin 20-40 mg/kg/day Q6-Q8 (Staph is
highly suspected)
or Vancomycin 40-60 mg/kg/day Q6-Q8 (life threatening
case)
C. With hypersensitivity to Penicillin
● Non-type 1 hypersensitivity
○ Cefuroxime PO 20-30 mg/kg/day
or IV 100-150 mg/kg/day Q8
○ Ceftriaxone 75-100 mg/kg/day Q12-Q24
● Type 1 hypersensitivity
○ Azithromycin 10 mg/kg/kg/day PO
or IV Q24 for 3 days
or 10 mg/kg/kg/day (Day 1)
then 5 mg/kg/kg/day Q24 (Day 2-5)
○ Clarithromycin 15 mg/kg/day Q12 for 7 days
○ Clindamycin 10-40 mg/kg/day PO
or 20-40 mg/kg/day IV Q6-Q8
● Atypical pathogen suspected
○ Add a macrolide
● Uncomplicated bacterial CAP
○ 7-10 days
Not considered in the empiric treatment of bacterial CPAP
Macrolide resistance is possible
Oseltamivir immediately within 36 hours of laboratory-confirmed
influenza infection
A. In non-severe PCAP
● Clinical stability for the past 24 hours:
○ Improvement of cough or normalization of core
body temperature in the absence of pyretics
(within 24-72 hours of initiation)
B. In severe PCAP
● Clinical stability for the past 24 hours:
○ Absence or resolution of hypoxia, danger signs,
tachypnea, fever, tachycardia
○ Resolving or improving radiologic pneumonia
○ Resolving or absent chest UTZ findings
○ Normal or decreasing CRP, PCT
A. In non-severe PCAP and not improving or is worsening:
patient is not responding to the
current therapeutic
management?
*14:1 Amoxicillin:Clavulanate
If with severe pneumonia, there
may be an underlying septicemia
or bacteremia → blood culture
(sputum, bronchoalveolar lavage,
or FT aspirates)
10) What clinical parameters
will determine that switch
therapy can be considered in
the management of severe
CAP?
Switch therapy involves
discontinuation of IV antibiotics to
oral form once px fulfills criteria →
11) What adjunctive treatment is
effective for CAP?
Standard care in PCAP:
O2 and hydration
● Consider diagnostic evaluation for presence of:
○ Coexisting or other etiologic agents
○ Resistant etiologic agent
○ Other diagnosis:
■ pleural effusion
■ Necrotizing pneumonia
■ Lung abscess
○ Asthma
○ Pulmonary tuberculosis
● If started with standard dose Amoxicillin 40-50 mg/kg/day:
○ Increase dose to 80-90 mg/kg/day Q12
or Amoxicillin/Clavulanate* 80-90 mg/kg/day Q12
or Cefuroxime 20-30 mg/kg/day
● If started with high-dose Amoxicillin,
Amoxicillin-Clavulanate, or Cefuroxime:
○ Parenteral antibiotics
● If adding a macrolide:
○ Azithromycin 10 mg/kg/day QD for 3 days
or 10 mg/kg/day (day 1) → 5 mg/kg/day (day 2-5)
or Clarithromycin 15 mg/kg/day Q12 (atypical
pathogen is suspected)
B. Severe PCAP and not improving or is worsening:
● Consider diagnostic evaluation for presence of:
○ Coexisting or other etiologic agents
○ Resistant etiologic agent
○ Other diagnosis
■ Acute respiratory failure
■ Pleural effusion
■ Pneumothorax
■ Necrotizing pneumonia
■ Lung abscess
○ Asthma
○ Pulmonary TB
○ Sepsis
C. Diagnostic evaluations considered in treatment failure of
severe PCAP:
● Cultures
● Nucleic acid amplification test
● Serology
● Imaging modalities
● Biomarkers
D. Referral to a specialist
Considered in bacterial CAP when ALL of the following are
present:
● Current parenteral antibiotics have been given for at least
24 hours
● Afebrile for at least 8 hours without antipyretics
● Able to feed w/o vomiting or diarrhea
● Clinical improvement as defined by ALL of the ff:
○ Absence of hypoxemia, danger signs, tachypnea,
fever, tachycardia
Vitamin A - measles pneumonia
Bronchodilators - in the presence of wheezing
Not considered: zinc, Vitamin D, microkinetic, secretolytic,
mucolytic agents
Insufficient evidence: oral folate, probiotics, vitamin C, virgin
coconut oil, nebulization with saline
12) What interventions are ● Vaccination:
effective for prevention of CAP? ○ Pneumococcus
○ Hib
○ Pertussis
○ Measles
○ Influenza
● Breastfeeding
● Avoidance of environmental tobacco smoke or indoor
Confusing, bale maka help biomass fuel exposure
prevent ang zinc and vit. D pero ● Zinc supplementation
indi sila ka adjunctively treat? And ● Insufficient evidence: Vitamin A, C, D
vice versa sa Vitamin A?
 TUBERCULOSIS

TB infection

- Previously known as latent TB infection

- Persistent immune response to stimulation by antigens
- First contact with TB antigen
- Initial stage: exposure to other px with disease and cavitations, high risk of getting infected
- No symptoms, but at risk for TB disease
- No gold standard test of direct identification of infection

EPIDEMIOLOGY ● Include 0-14 YO only (>15 YO same tx as adult)

● 4 countries for 44% TB = IPIS (India, PH, Indonesia, South Africa)
● PH: #4 high TB burden, #7 MDR-TB burden
● most at risk for TB disease and infection = 0-4 YO
● TB disease - 1 YR after TB infection
● Children <2 YO, especially 0-1 YO, with TB are susceptible to developing the
following:
○ Disseminated Disease
○ Tuberculosis Meningitis
● Exposed Infant (0-1 YO), with TB infection, no TPT = 18% TB disease in 2
years
● 2-5 YO = 19% TB disease in 2 years
● TPT effectiveness for children and adolescent with infection = 91%

PATHOGEN ● M. tuberculosis - red in AFB, gram ghost, Yellow orange fluorescence,

obligate aerobe, ~18 hrs doubling time, non-motile
● Others: M. avium, M. intracellulare (MAC), M. bovis

DIAGNOSIS ● TB culture - gold standard

● Others: Acid fast staining, GeneXpert, TB lamp, Xpert Ultra

Presumptive PTB

1. Cough/wheeze =/> 2 wks, unexplained (unresponsive to antibiotics or bronchodilator tx, B2

agonist)
2. Fever =/> 2 wks, exclude malaria or pneumonia
3. Weight loss
4. Decrease playfulness/activity (added criteria, in contact with known TB case)
Note: any 1 or more of the top 3 = presumptive TB

- If child has CXR of Pulmonary TB

● Not routinely recommended except with TB household contact
● I: 3 YO, recurrent pneumonia, fever, weight loss, dec. act., parents have tb, multiple
index case
- Identified PTB, ask HE and exposure to TB cases for DR-TB
 Presumptive EPTB

● Gibbus deformity - recent onset, vertebral TB

● Non-painful, enlarged cervical lymphadenopathy, w/ or w/out fistula
● Neck stiffness, drowsiness suggestive of meningitis, Sub-acute onset or raise intracranial P
● Pleural effusion
● Pericardial effusion
● Distended abdomen w ascites
● Enlarged joint, non painful
● Tuberculin hypersensitivity

Clinically Diagnosed Pulmonary or ETB

● >15 YO, persistent signs and symptoms

● Not bacteriologically confirmed
● Dx is thru clinical findings, CXR, Biopsy/tissue
● Sputum/nonsputum specimen is negative for TB in Smear, Culture, Rapid tests (GeneXpert,
Line probe assay, TB Lamp)

Bacteriologically Confirmed Pulmonary or ETB

● Sputum/nonsputum specimen is positive for TB in Smear, Culture, Rapid tests

● Culture is gold standard
● (GeneXpert, Line probe assay, TB Lamp)

Approach to Dx:
1. Collection
a. Gastric lavage - can’t cough’, use NSS, but since parents are against it, mostly
children are clinically dx
b. Sputum - 10-18 YO, can cough effectively, culture or GeneXpert
c. TST - if uncertain results
2. Screening
a. MTB detected = px is BCTB
b. MTB not detected/ can’t expectorate = request XRay
i. If strongly suggestive of TB = CDTB
ii. negative/uncertain
● no Primary Complex in CXR, but with lymphadenopathies =
suspect TB
● uncertain, px is symp = broad spectrum antibiotics and follow up
(2 wks)
○ After 2 wks = symp persists + contact w confirmed TB
case = CDTB
■ Not in contact = perform TST (+ CDTB, - with
persistent symp = specialist)
Exposure to household contact: 1 or more nights, frequent/extended daytime periods during
3 mos start of tx os source case
IGRA AND TST are not required prior to TPT in ff:
● PLHIV
● <5 YO in contact with BCPTB
● >/=5 YO in contact with BCPTB + risk factors:
○ smoking, alcohol consumption
○ diabetics
○ immunocompromised
○ living with multiple TB px
○ Undernutrition
TPT (TB Preventive Treatment)
● Make sure PX does not have active TB!
● Recommended for the ff:
○ known and household contacts of BCPTB
○ PLHIV
○ TB infections in children <5 YO, no active disease
○ others who don’t have active disease
3HR is more commonly used for children.
3HP is recommended but rifapentine is not available in PH.
1HP is for HIV px.

Monitoring and Management

● Check for adverse effects:
○ for hepatotoxicity (SGPT is monitored taking TB tx) - Pyrazinamide and Isoniazid
○ =/> 10 YO w liver problems = monitor SGPT
○ reddish/orange urine and stool = rifampicin
○ jaundice due to hepatitis, joint problems
● uninterrupted anti-TB med with comprehensive patient-centered care (individualized)

TX for Drug-Susceptible TB:

Regimen 1 (2HRZE/4HR)
- PTB/EPTB (except CNS, bones, joints)
- Rif sensitive MTB
- Rif indeterminate MTB
- New PTB or new EPTB (except CNS, bones,
joints)
- with positive SM/TB lamp
- or clinically dx
- Xpert not done
- XPert is MTB not detected
Regimen 2 (2HRZE/10HR)
- EPTB of CNS, bones, joints
- MTB, RIF sensitive
- MTB, Rif indeterminate
- New EPTB CNS, bones, joints
- with positive SM/TB lamp
- or clinically dx
- Xpert not done
- XPert is MTB not detected
- 6 mos = DS-TB, 12 mos = severe DS-EPTB
- 9-20 mos DR-TB
TB Treatment Outcomes
Cured BC MDR-TB/RR-TB, complete tx, no failure, 3 or more negative cultures (30
days apart)

Treatment complete without failure, no record 3 or more cultures taken at least 30 days apart are
negative

Treatment failed ● tx terminated/ permanent regimen change

● lack of evidence at least 2 negative cultures, not followed by positive
culture by end of extended intensive phase (6 mos) of shorter regimen
● positive sputum smear confirmed by 2 consecutive samples after 6
mos tx
● culture reversion in continuation phase after conversion to negative
● evidence of addtl acquired resistance of fluoroquinolone/ 2nd line
injectable drugs
● adverse drug reaction due to switching to new regimen

Died dies from any reason during tx

Lost to Follow Up tx was interrupted for at least 2 consec months, or px diagnosed with active TB,
not started tx

Not evaluated no tx outcomes assigned, “transferred out” cases to another tx unit, tx outcome
is unknown
 TUBERCULOSIS IN ADULTS
Red/orange colored urine - Rifampin
CYP450 inducer - Rifampin
Peripheral neuropathy secondary to b6 deficiency - Isoniazid
Increase uric acid : gout - pyrazinamide
Optic neuritis - Ethambutol
Hepatotoxicity - Isoniazid, pyrazinamide, rifampin
World TB day - March 24
Drug which shortens the duration of treatment - Pyrazinamide
significant tobacco smoking history for Tb risk - 10 pack years smoker
Structures that reduce the permeability of cell wall - Arabinogalactan and peptidoglycan
Initiates pathogen to host interaction and facilitates the survival of M. tuberculosis within
macrophages - Lipoarabinomannan
Drug contraindicated to pregnant women - Pyrazinamide
Characteristic lesion of TB - Caseous Necrosis
TB of the spine - Pott’s Disease
Drug which shortens the duration of treatment - Pyrazinamide
small, bilateral, scattered white lesions in CXR - Miliary TB
granulomatous primary lesion of TB - Ghon focus
For intolerance to pyrazinamide/ pregnancy - stop Z → triple treatment (HRE) + prolong
continuation phase to 7 months (add 3 months)
TPT regimen contraindicated for pregnant women - 3HP
combination of Ghon focus and lymph node involvement - Ghon complex
Most severe complication of TB - fungal infection
Recommended diagnostic for TB - Nucleic acid amplification technology (Xpert MTB/RIF
assay)
Drugs with bad effects to the heart and liver- delamanid, linezolid, and levofloxacin
new all-oral combination of drugs given in 4 months - Bedaquiline (B), Pretomanid (Pa) and
Linezolid (L)
In pregnancy, the continuation phase is prolonged for how many months? - 7 months
Duration of initial phase and continuation phase - 2 months initial phase + 4 months
continuation = 6 months
HRZE - Isoniazid, Rifampicin, Pyrazinamide, Ethambutol
What TPT regimen is taken weekly - 3HP / 3 months weekly Isoniazid + Rifapentine (not
Rifampicin)

Mycobacterium tuberculosis (MTB) Infection

Characteristics Non spore, obligate aerobe, AFB positive, Rod shaped, Gram neutral, size 0.5 µm by 3
µm

Transmission Droplet nuclei → cough, sneezing, speaking

Smallest droplet (<5-10 µm in diameter) - suspends in air for hours/days
3000 nuclei per cough

Determinants of likelihood of transmission:

1. Intimacy and duration
2. Degree of infectiousness
- Cavitary disease is more likely infectious
3. Shared environment

Patient likelihood of transmissibility:

1. Sputum smear-POSITIVE cases
2. CAVITARY pulmonary disease
 3. NON-infectious
a. Culture negative pulmonary TB
b. Extrapulmonary TB

Clinical Primary TB Secondary TB/ Post primary TB

- Children in first few years of life - Adults
- Immunocompromised - Reactivation
- Lymph nodes or mid-lower lobes - (+) reinfection
- (+) immunocompromised
- (+) age
- (+) co-infection ex. HIV

Pathogenesis Droplet nuclei + acid fast bacilli MTB infects host→ Passes through the 1st line of defense
( trapping in upper airways and expelled by ciliated mucosal cells) → reach the alveoli →
activates cell-mediated immunity → calls help from myeloid dendritic cells + alveolar
macrophages → MTB cells will clump on the macrophage and kill it → MTB grow inside
macrophage → the dead macrophage is cleaned up by another macrophage→However,
the increasing number of bacteria inside the dead macrophage means that the new
macrophage is even more likely to die than the first one → continuation of infection cycle
→ GRANULOMA formation

MACROPHAGE-ACTIVATING RESPONSE:
- Cell mediated immunity → caseous necrosis
- Presence of Ghon focus and Ghon complex
- Healed lesions → possible calcification (white lesion on CXR)

DELAYED TYPE HYPERSENSITIVITY:

- Cavitary Lesions - more infectious than non-cavitary

- Associated with active TB
- Miliary TB or disseminated TB or tuberculous meningitis
- hematogenous / contiguous spread

LATENT TB INFECTION
- persistent immune response to stimulation by MTB antigens with no evidence of
clinically manifesting active TB
- Asymptomatic + Clear CXR + Negative sputum test and GeneXpert
- Most Filipinos → POSITIVE Tuberculin Skin Test ( TST)
 Clinical PRIMARY DISEASE
Manifestations - Children
- Occur soon after infection
- Asymptomatic OR w/ Fever and occasional pleuritic chest pain ONLY
- Ghon focus and ghon complex

Lesion Ghon Focus Ghon Complex

Features - Granulomatous primary lesion Ghon focus + lymph node involvement

- Peripheral location Possible pleural reaction and thickening
- TRANSIENT hilar/ Regional lymphadenopathies
paratracheal Caseating tissue
lymphadenopathies
- Small calcified nodules -
Healed lesion

POST-PRIMARY (ADULT-TYPE) DISEASE

- Reactivation or Secondary TB
- Lesions are localized to the APICAL and POSTERIOR segments of the UPPER
lobes
- small infiltrates to extensive cavitary disease
- lesions become fibrotic and may later calcify, but cavities persist in other parts.
- Diurnal fever can last up to 2 weeks
- Defervescence → night sweats
- weight loss, anorexia, malaise, and weakness, hemoptysis, cough and
purulent sputum

POST-TB COMPLICATIONS
- Bronchiectasis
- Alveolar damage
- URTI → LRTI → Exacerbation
- Fungal Infections - most severe complication
- Aspergillomas and Chronic Pulmonary Aspergillosis

Diagnosis 1. High Index of SUSPICION

2. HIGH RISK Population
3. CXR or CT → upper-lobe infiltrates w/ cavities
4. Nucleic acid amplification technology (Xpert MTB/RIF assay)
- Recommended diagnostic for TB
5. AFB microscopy
6. Molecular tests
7. Rapid Culture
8. Drug Susceptibility Testing (DST)
9. Tuberculin Skin Testing (TST) - uses purified protein derivative (PPD)
10. IFN- γ Release Assays (IGRA) - whole blood testing
- Turnaround time = 5 days
- 8k - expensive

Treatment AIMS OF TREATMENT

- prevent morbidity and death
- preventing recurrences and emergence of drug resistance
- interrupt transmission

CLASSIFICATION
1. New - never had tx / less than 1 month of anti-TB therapy
2. Retreatment - has been treated for at least one month
a. Relapse - declared cured/ treatment completed BUT with recently
diagnosed ACTIVE TB
 b. Retreatment after failure - treated but failed recent course based on
POSITIVE SM (in 5 months follow up or later) or clinically diagnosed does
not show clinical improvement
c. Treatment after lost to follow-up - treated but did not complete therapy + lost
to follow up for at least 2 months
d. Previous treatment outcome unknown - Previously treated but whose
outcome in the most recent course is unknown
e. Unknown previous TB treatment history - but whose outcome in the most
recent course is unknown OR previous treatment history is unknown

TB PREVENTIVE THERAPY (TPT)

Regimen Dosing and Duration Notes

3HP - Isoniazid + Rifapentine Regimen of choice

- Once Weekly Can be initiated w/o baseline Lung
function tests
CI in pregnant women

3HR - Isoniazid + Rifampicin

- Daily

4R - Rifampicin ONLY Preferred if 3HP is not available/

- Daily Contraindicated

6H - Isoniazid ONLY
- Daily

PREVENTIVE THERAPY ELIGIBILITY USING TUBERCULIN SKIN TEST/ IGRA

- Risk factors to note:
- PLHIV
- Diabetes
- Smokers
- Immune suppressive medical conditions
- Malnourished
- Multiple people with TB in same household
- Index case → refers to the first confirmed case of tuberculosis within a household

Eligible Require TST/IGRA NOT Eligible

(TST/IGRA not required) (TPT if Positive only)

- PLHIV regardless of - Contacts of CD-TB

contact (>= 1 years - Household contact index case (except
old) of BC-TB index <5 years old)
case + WITHOUT
- Household contact TB risk factors - Contacts of
of BC-TB index - Close contact of MDR-TB or RR-TB
case + TB risk BCTB index case index case
factors (>= 5 years
old) - Patients on
- < 5 yo household dialysis, with
contact of BC-TB silicosis, preparing
index for organ / blood
transplant.

- Patients w/
anti-TNF treatment
PULMONARY TUBERCULOSIS REGIMEN

RECOMMENDED TREATMENT FOR TB PATIENTS

Regimen Eligibility

(1) 2HRZE + 4HR *DOES NOT involve the CNS, bones, joints*

New or retreatment PTB or EPTB w/

*DOES NOT involve the 1. Final Xpert results:
CNS, bones, joints* ● MTB, RIF sensitive
● MTB, RIF indeterminate

New PTB or EPTB w/

1. Positive SM/ TB LAMP
OR
2. Clinically Diagnosed : Xpert was not done /Xpert resul
MTB not detected

(2) 2HRZE+ 10HR New or retreatment of EPTB of CNS, bones, joints w/:
1. Final Xpert results:
● MTB, RIF sensitive
* EPTB of CNS, bones, ● MTB, RIF indeterminate
joints*
New EPTB of CNS, bones, joints w/
- Longer duration 1. Positive SM/ TB LAMP
of treatment (12 OR
months) 2. Clinically Diagnosed : Xpert was not done / Xpert resu
MTB not detected

DRUG DOSING

Daily Dosage

Drug Adult Pediatric

(mg/kg) (mg/kg)

H - Isoniazid 5 10

R - Rifampicin 10 15

Z - Pyrazinamide 25 35

E - Ethambutol 15 20
 TREATMENT INDICATIONS

Patient Regimen

New case + POSITIVE smear/ culture 2HRZE + 4HR (Regimen 1)

New case + NEGATIVE culture

Pregnant 2HRE + 7HR

OR
2HRZE + 4HR
(According to WHO and International Union Against
TB and Lung Disease)

Resistance/ Intolerance to 2HRE + 7HR

Pyrazinamide(Z)

Resistance/ Intolerance to Isoniazid (H) 6RZEQ

(chang to Quinolone)

MDR TB or Resistance to Rifampicin ( R ) - 4-month BPAL treatment

regimen

Drug DRUG – RESISTANT TB

Resistance - Primary drug resistance - infected by resistant strain
- Acquired Drug resistance - develops during the course of treatment for TB.

Drug Resistance Classification Resistance to

Isoniazid-resistant TB - Isoniazid ONLY

RR-,MDR - TB - (at least) Isoniazid AND Rifampin

(Rifampicin Resistant or
Multi-drug Resistant TB)

XDR TB - Aminoglycosides, Rifampicin, Isoniazid, or

Quinolones
(Extensively Drug-Resistant TB)

- Regimen for drug-resistant TB is usually for 18 months + at least 5-6 kind of

drugs
- Drugs with bad effects to the heart and liver: delamanid, linezolid, and
levofloxacin
- it has to be given 12-18 months
- The government will launch a 4-month BPAL treatment regimen for MDR-TB but
it is important to be vigilant of the relapse and reinfection. - Bedaquiline (B),
Pretomanid (Pa) and Linezolid (L)
 LUNG CANCER
I. Epidemiology
- Most common cause of cancer death in americans
- 40-80 years old; median age has been descending (20-30 yo at Stage IV)
- Lung cancer - #1 cause of cancer-related mortality
II. Risk Factors
- Cigarette smoking (10-fold increased risk of developing lung cancer)
- Cigarette smoking exposure (environmental smoke, biomass fuels, second-hand smoke)
- Radon exposure
- Occupational exposure (asbestos, etc)
- Cancer history (first-degree relatives)
- Disease history
III. Pathology
- Lung cancer – tumors arising from the respiratory epithelium (WHO)
- Classified into:
o Small-cell lung cancer (SCLC)
o Non-SCLC
§ Squamous cell CA
§ Adenocarcinoma
§ Large-cell CA
- Most predominant subset before smoking cessation programs: squamous cell CA
- Most predominant subset now: adenocarcinoma

Small Cell Lung Cancer

- Highly aggressive malignancy

- Paraneoplastic syndrome – common in pt with SCLC
o May be associated as the first sign of recurrence
- Cell characteristics:
o Cytoplasm: scant
o Borders: ill-defined
o Nuclear chromatin: finely granular
o Nucleoli: absent or inconspicuous
o Mitotic count: high
o Neuroendocrine markers: CD56, NCAM, synaptophysin, chromogranin

Non-SCLC

A. Squamous Cell Carcinoma B. Adenocarcinoma

- Bronchial epithelial cells - Glandular

- Most commonly associated with tobacco use
- Cell characteristics:
o Cytoplasm: eosinophilic, keratinized,
with nests and keratin pearls
o Immunohistochemical marker: p63
§ Member of p53 family
§ Mutation will result to SCC
o Immunohistochemical marker: p40
- Never smokers or former light smokers (<10
pack-year history), women, and younger
adults (<60 years)
- Cell characteristics:
o Cytoplasm: abundant mucin
o Nuclei: small, basally-oriented
(rosette-forming, palisading)
o Immunohistochemical marker: TTF I
(Thyroid Transcription Factor I) or
Napsin A
- Adenocarcinoma in situ (<3 cm)
o Caught in stages III/IV
o Minimally invasive; pure lepidic growth
≤5 mm invasion
 o 5-year disease-free survival with
complete tumor resection
- Invasive adenocarcinoma
o 70-90% of resected lung
adenocarcinomas
o Patterns:
§ Lepidic – favorable prognosis
§ Acinar
§ Papillary
§ Solid – poor prognosis

IV. Immunohistochemistry
- Utilize lineage-specific markers for the exclusion of metastatic origin of the tumors

Nap-A TTF-1
Primary lung adenocarcinoma + +
Primary lung squamous CA - -
Primary SCLC - +

- TTF1 can also be positive with neuroendocrine tumors present

- Considering adenocarcinoma → request TTF1
- Rule out SCC → (-) TTF1

V. Molecular Pathogenesis
- Hallmark Capabilities of All Cancer Cells
o Self-sufficiency in growth signals
o Insensitivity to antigrowth signals
 o Evading apoptosis
o Limitless replicative potential
o Sustained angiogenesis,
o Tissue invasion and metastasis
- Driver mutations – initiation and maintenance of tumor cells
o Most common in NSCLC:
§ KRAS – men, European, smokers, with squamous histology
§ EGFR – women, Asians, never-smokers, Pt with adenocarcinoma

VI. Screening
- Low-dose CT (LDCT) – recommended screening test for lung cancer, expensive, not covered by
Philhealth
Benefits of Lung Cancer Risks of Lung Cancer Patients Not Eligible for
Screening Screening Screening

o Dec. lung cancer mortality
o Improved quality of life
o Discovery of other significant
occult health risks
o Earlier detection, higher
survival rate
o Futile detection of indolent o Symptoms of lung cancer
disease o Previous lung cancer
o Quality of life (anxiety about o Functional status and/ or
comorbidity that would prohibit
test findings) curative intent treatment
o Physical complications from o Low ECOG (Eastern
diagnostic workup Cooperative Oncology Group)
o False-positive results score [No use/not beneficial]
o False-negative results
o Unnecessary testing and
procedures
o Radiation exposure
o Cost
o Incidental lesions
VII. Clinical Manifestations
Lung Cancer Metastatic Disease

Cough – irritation of airways Spread of tumor in the thorax:

Horner’s syndrome
Hemoptysis – endobronchial masses - Enophthalmos, ptosis, miosis, anhidrosis

Dyspnea – may be the only clinical manifestation
Over half of all patients diagnosed with lung
cancer present locally advanced or metastatic
disease at the time of diagnosis.
Pancoast (or superior sulcus tumor) syndromes:
- shoulder pain that characteristically
radiates in the ulnar distribution of the
arm, often with radiologic destruction of
the first and second ribs
- involvement of the 8th cervical, 1st and 2nd
thoracic nerves

Extrathoracic metastatic disease at autopsy in:

- >50% pt with squamous cell CA
- 80% pt with adenocarcinoma and
large-cell CA
- >95% pt with SCLC

VIII. Diagnosis
- Tissue biopsy – gold standard
- Sputum cytology – least invasive; not as good
- Transthoracic needle aspiration (TTNA) - may have poor surgical yield; seek help from both
radiologist and pathologist for a frozen section of biopsy (rapid onsite cytology)
 MEMORIZE NI KUNO

IX. Staging
- Classified in terms of:
o Tumor size
o Regional lymph nodes involved
o Degree of metastasis

Anatomic Staging Physiologic Staging

o Determination of the location of the tumor and o Assessment of a patient’s ability to withstand
possible metastatic sites various antitumor treatments
o NSCLC: all should undergo CT, PET, or o Presence of comorbid conditions
preferably PET-CT o OK for pneumonectomy: FEV1 > 2L or >80%
o SCLC: PET-CT and MRI o OK for lobectomy: FEV1 > 1.5L
§ Otherwise wedge or anatomic
segmental resection
o All should be assessed for CV risk
§ NO for thoracic surgery
· MI within the past 3 months
· Uncontrolled arrhythmias
· FEV1 < 1L
· CO2 retention (resting PCO2 >
45mmHg)
· DLCO < 40%
· Severe pulmonary hypertension
 Staging of Non-Small-Cell Lung Cancer
Tumor-Node-Metastasis (TNM) International Staging System for NSCLC

MEMORIZE MAN NI KUNO

 Staging of Small Cell Lung Cancer

o Both Veterans Administration system and the American Joint Committee on Cancer/ International
Union Against Cancer eighth edition system (TNM) be used to classify
o Veterans Administration system – a distinct two-stage system dividing patients into those with
limited-or extensive-stage disease
§ Limited Stage
· Confined to the ipsilateral hemithorax and can be encompassed within a tolerable radiation
port
· Ex. Contralateral supraclavicular nodes, recurrent laryngeal nerve involvement, SVC
obstruction
§ Extensive Stage
· Overt metastatic disease; organs cannot be encompassed safely or effectively within a
single radiation therapy port
· Ex. Cardiac tamponade, malignant pleural effusion, bilateral pulmonary parenchymal
involvement

X. Risk Stratification
Actual risks affected by parameters defined
here and:
o Patient factors (comorbidities, age)
o Structural aspects (center, volume,
specialization)
o Process factors (management of
complications
o Surgical access (thoracotomy vs
minimally invasive)
XI. Physiologic Evaluation
A. Cardiac Algorithm B. ECOG Score

- Eastern Cooperative Oncology Group (ECOG)

Score
- Assesses disease progress, how dx affects daily
living abilities, and appropriate treatment and
prognosis

XII. Treatment
NSCLC

Stage III NSCLC

 Stage IV (palliative)

Without Driver Mutations With Driver Mutations

SCLC

Principles of Palliative Care (ATS 2007)

- Centered on the patient and on the patient’s family
- Right of competent adult patients to determine their goals of care
- Identification and respect on patient’s preference (values, goals, priorities)
- Encourages family support and involvement
- Should begin when a patient becomes symptomatic
- ALL patients with chronic, life-threatening, critical illnesses should have access to palliative
care
- Bereavement of the family is integral part
- Health care providers should have appropriate level of competence
- Psychological and emotional needs should be acknowledged
- Respect on cultural and spiritual values
 COPD
What age does the FEV1 normally decline into 30 mL/yr? 25 yrs old

How many times does FEV1 decline in smokers in comparison to the normal population?
Decline in FEV1 for smokers = x5 than normal = 30 mLx 5 = 150 mL/yr

What is the cut off age for COPD to appear? 40 yrs old “disease of the elderly”

Accelerated Decline in FEV1 is noted in the ff;

○ Alpha-1 antitrypsin deficiency
○ childhood illness that affect lung growth
○ lung maturity not on time

What are the indicators of COPD during diagnosis?

Persistent/progressive dyspnea, recurrent wheeze, recurrent LRTI, history of risk factor
(smoking etc)

COPD-G (Genetics) ● Alpha-1 antitrypsin deficiency

COPD-D (lung dev) ● premature birth

● low birthweight

COPD-C (cigarette) ● in utero/passive smoking exposure

● vaping
● cannabis

COPD-P (pollution) ● household/air pollution, occupational hazards

COPD-I (infections) ● childhood infections

● TB-associated COPD
● HIV-associated COPD

COPD-A (+asthma) ● childhood asthma

COPD-U ● unknown

In performing Spirometry:
● Expiratory time/volume should be free from irregularities
● pause between inspiration & expiration should be less than 1 sec
● recording until volume plateau is reached ~>15s in severe
● FVC and FEV1 should vary no more than 5%/ 150 mL from 3 curves
● FEV1/FVC from largest sm of FVC and FEV1
● Dosage protocols:
○ 400 mcg SABA
○ 160 mcg SA anticholinergic
○ or combined
● FEV1 is measured
○ 10-15 mins after SABA
○ 30-45 mins after SA anticholinergic/combi
● Being on bronchodilator tx is not CI.

What confirms the presence of non-fully reversible airflow obstruction? FEV1/FVC <0.7
What is the FEV1/FVC ratio if the FEV1 is 1.8L and the FVC is 3.2L?
● 1.8/3.2 = 0.56 below 0.7 - there is airflow obstruction
Role of Spirometry in COPD:
- diagnosis
- assessment of severity of obstruction (prognosis)
- GOLD Grades
- GOLD 1: mild = more than or equal to 80%
- GOLD 2: moderate = 50 - 79%
- GOLD 3: severe = 30 - 49%
- GOLD 4: very severe = less than 30%
- Modified MRC Dyspnea Scale
- Grade 0 = breathless with strenuous act
- Grade 1 = short of breath walk on slight hill
- Grade 2 = walk slower than others, have to stop for breath
- Grade 3 = stop for breath in every 100 m on level
- Grade 4 = breathless to leave house/dressing
- CAT Assessment
- follow up assessment

Flow for GOLD ABE Assessment Tool

1. Spirometry confirmed dx: FEV1/FVC <0.7
2. Assessment of Airflow (GOLD 1-4)
3. Assessment of Symptoms/ Risk for Exacerbations (per yr)
a. E = 2 or more moderate exacerbations, 1 or more lead to hospi
i. LABA + LAMA*
ii. if eosino 300 or more, LABA+LAMA+ICS
iii. nonpharma: smoking cessation, pulmo rehab, physical act., vax
b. A = 0-1 moderate exacerbations, no hospi, mMRC: 0-1, CAT <10
i. A bronchodilator
ii. nonpharma: smoking cessation, physical act., vax
c. B = 0-1 moderate exacerbations, no hospi, mMRC: 2 or more, CAT 10 or more
i. LABA + LAMA*
ii. nonpharma: smoking cessation, pulmo rehab, physical act., vax
iii.

This procedure is beneficial for patients if they demonstrate FEV1= 15% - 45% and evidence of
hyperinflation in CT. Endobronchial Valve Therapy
What is the recommended dose of CT scan for lung cancer screening for patients with COPD
due to smoking? Annual low-dose CT Scan

Management of COPD
Diagnosis Initial Assessment Initial Review Adjust
Management

symptoms GOLD 1-4 Stop smoking Sympt pharmaco

risk factors GOLD ABE Vax Exacerbations nonpharma
spirometry Exacerbation hx Active lifestyle Smoking stat review
Smoking stat 1’ pharmaco Exposure to risks
Blood eosino count Self mngmt inhaler technique
a1-antitrypsin Manage comorb Inhaler Adherence
comorbidities Pulmo rehab
Self mngmt
Oxygen, NIV, LV
Vax
⬇️
manage comorb
spirometry (annual)
T or F
1. Smoking cessation intervention should be done in all people with COPD. T
2. It is important to systematically identify all tobacco users every other visit. F. - every visit
3. Strongly urge all tobacco users to quit and determine their willingness and rationale to
quit. T
4. Scheduling for follow up contact can be done in person or via telephone. T
5. There is a strong dose-response relation between intensity of tobacco dependence
counseling and its effectiveness. T
6. More than 1 device type can be used ideally as an inhalation device. F - only 1 ideally

What are the examples of first line pharmacotherapies for tobacco dependence?
Varenicline, nortriptyline, nicotine gum, nicotine inhaler, nicotine patch

Vaccinations for Stable COPD:

● Influenza vax
● SARS CoV2
● 1 dose PCV20 or 1 dose PCV15 & PPSV23
● Pneumococcal (reduce CAP/exacerbations)
● RSV Vax >60 YO, Chronic Heart/Lung Disease
● TdaP vax for pertussis not vax in adolescence and Zoster for shingles >50YO

If initial tx is not appropriate:

● Check adherence, inhaler technique, interfering comorb
● consider predominant treatable trait (dyspnea vs exacerbations)

Appropriate Inhalation Device Choice:

● Dry powder inhalers - forceful deep breath
● Metered-dose inhalers/ soft mist inhalers - slow and deep breath
● Nebulizer for unable to use MDI
● Smart inhalers if there are issues with adherence or inhalation technique

Follow-up nonpharma tx:

1. If response is appropriate, maintain + offer influenza vax, self management + smoking
cessation, ensure exercise program maintenance and adequate sleep and diet
2. if not: consider predominant trait:
Adv COPD = end of life and palliative care support
Oxygen therapy
- long term administration increase survival in pc with severe chronic resting arterial
hypoxemia but in stable COPD, it does not lengthen time of death
- Arterial hypoxemia: PaO2 less or equal to 55 mmHg or SaO2 <88% or PaO2 >55% with
RHF or erythrocytosis - tx by supplement O2 to keep SaO2 90% and above, recheck in
60-90 days
Ventilatory Support
- long term noninvasive ventilation for severe chronic hypercapnia and hospitalization for
ARF

Bronchodilators
● Inhaled bronchodilators over oral bronchodilators
● Combi of SAMA + SABA than monotherapy
● LABA + LAMA than short acting agents except for those with occasional dyspnea
● LAMA over LABA on exacerbation reduction
● for persistent dyspnea = single long acting bronchodilator into 2

LABA + ICS
CI: repeated pneumonia events, blood eosino <100 cells/uL, mycobacterial infection history
I: hist of hospi for exacerbations, 2 or more mod. Exacerbations, blood eosino >300 cells/uL,
concomitant asthma
Other Pharma Tx:
Alpha 1 antitrypsin augmentation therapy: IV slow down emphysema progression
Antitussives: no conclusive evidence for COPD
Vasodilators: worsen oxygenation
Opioids: low dose long acting oral and parenteral for dyspnea with severe disease
Pulmonary HPN Therapy: drugs for 1’ PHPN are not for PHPN 2’ to COPD

Additional notes from Harrison:

Chronic Obstructive Pulmonary Disease
● airflow limitation, not fully reversible
● 4th leading cause of death
● affects >16 million in US
What are the pulmonary diseases that are included in COPD in varying degrees?
1. Emphysema - destruction/enlargement of alveoli
2. Chronic bronchitis - chronic cough and phlegm
3. Small airway disease - narrowed small bronchioles
Is chronic bronchitis without chronic airflow obstruction included within COPD?
- No, COPD is present only if there is chronic airflow limitation obstruction.
Risk Factors (CAI-O-HA-Pα = “kay-o ha pa”)
Cigarette smoking major risk factor
dec. FEV1 in dose-dependent with pack years

Airway Responsiveness hyperresponsiveness, obstruction, pulmonary symp. similar to

asthma

Infections exacerbations (childhood/adult)

Occupational exposures dust at work, coal & gold mining, cotton textile
cadmium exposure: reduced FEV1, FEV1/FVC, DLCO

HA - Hangin = Air increased symptoms in urban areas

pollution use of biomass combustion for COPD in women

Passive/2nd Hand maternal smoking - reduced lung growth

Smoke in utero tobacco smoke - reduced postnatal pulmonary function
passive exposure: reductions in pulmonary function

α1 antitrypsin (α1AT) reduced or absence of any α1AT production

deficiency

Pathophysiology
● Airflow Obstruction
○ reduced cross sectional area - less elastic recoil, increase airflow resistance -
decrease in flow - decreased lung volume
○ Early stages of COPD = “scooped-out” lower part in flow-volume curve
○ Advanced stages = entire curved has decreased expiratory flow
● Hyperinflation
○ ”air trapping” (inc RV; inc ratio of RV to TLC; increased tTLC in late stage)
○ Compensatory mechanism to preserve maximum expiratory airflow
○ Advantages:
■ lung volume increase - elastic recoil increase, decrease airflow resistance
○ Disadvantages: push diaphragm in flattened position
■ decrease zone of apposition between diaphragm and abdominal wall,
positive abdominal pressure during inspiration is not applied well
■ Flat diaphragm = Shorter muscle fibers, generate less inspiratory P
■ need to generate greater tension to produce tidal breathing
● note the Laplace’s law, p=2t/r
● Gas Exchange
○ FEV1 <50% - Pao2 remains near normal until
○ FEV1 <25% - PaCO2 may or not elevate
○ Predicted FEV1 <25%, Pao2 <55 mmHg - cor pulmonale and RV failure
○ even much lower ~50%, normal Pao at rest

What is the difference of asthma from COPD in terms of FEV1?

In COPD, reduced FEV1 seldom shows large responses to inhaled bronchodilators.
 ASTHMA IN CHILDREN
Asthma in Pediatrics Part 1

Pathological changes in asthma encompass the entire respiratory tract except? - Lung
parenchyma
Asthma phenotype which is less sensitive to corticosteroids? - neutrophilic pattern in severe
asthma / Non-allergic
Cytokines associated with increased IgE formation? - IL-4 and IL-13
What type of lymphocytes predominates in normal airways? - Th1 cells
Cytokines associated with eosinophilic inflammation? - IL-5
Gold standard diagnostic test for asthma? - Spirometry
What is the predicted PEFR of px, Reiven, 6 years old, height of 110 cm. ? - (110 + 170)x
+175= 225
Common cause of bronchiolitis in infants? - RSV
GINA & PAPP recommend what sport for asthmatic patients? - swimming
What is the characteristic of the curve of a person with asthma in spirometry? - Scooping
What phenotype of asthma responds to ICS in higher doses and can be refractory? - Adult
onset asthma
An FEV1 measurement of how much relative to the predicted value is evidence of airway
obstruction? - <80% of the predicted value
Increased levels of FeNO can be a marker of what? - eosinophilic airway inflammation
What is the NORMAL" Daily diurnal PEF variability" in Adults and Children? - Adults: <10% ;
Children: <13%
In a patient with good reversibility, what is the expected improvement in lung function after
inhaling salbutamol? - increase in FEV1 by >12% and in PEF >200 mL from baseline
What is the medication used in assessing therapeutic response to controller treatment when
diagnosing <6 years old? - Low-dose ICS w/ as needed SABA
Mhayven, 5 years old, Female, cough and wheezing >3 episodes this year, and occasional
symptoms between episodes. Determine the asthma category. - Suspected Asthma
What is the normal FEV1/FVC (6 -18 years old) ? - usually >0.90
How long should SABA and LABA be withheld prior to bronchodilator reversibility test? - SABA
>= 4 hrs, LABA >= 15 hrs
Expected value for Positive BD reversibility test (6-18 years old)? - Increase in FEV1 of >12%
predicted
Expected result for excessive variability in twice-daily PEF over 2 weeks? - Average daily
diurnal PEF variability >13%
Expected result in positive Exercise challenge test? - Fall in FEV1 of >12% predicted or PEF
>15%
Excessive variation in lung function between visits. - Variation in FEV1 of >12% or PEF of
>15% between visits
ASTHMA PHENOTYPES
Types Allergic Non allergic Adult onset Persistent Athma w/
airflow obesity
limitations

Features Childhood Obese, Adults, Late onset, Long standing Prominent

onset, Hx of Smokers common in asthma, respiratory
atopy, eczema, women, Non persistent/ symptoms
Food/drug allergic partially
allergy reversible

Pathophysiology Eosinophilic Neutrophilic, Paucigranuloc Airway wall Less

inflammation Eosinophilic, ytic remodeling eosinophilic
Paucigranuloc
ytic

ICS response Responsive Less short- Higher dose - -

term response ICS, refractory

INCREASED PROBABILITY of DECREASED PROBABILITY of having ASTHMA

having ASTHMA

1. More than 1 episode of 1. Isolated cough

character symptom
2. Symptoms vary over time
and intensity
3. Triggered by something
2. Chronic sputum production
3. Shortness of breath w/ dizziness,
light-headedbess or paresthesia
4. Chest pain
5. Exercise induced dyspnea and NOISY inspiration

Diagnostics:
1. Spirometry - GOLD STANDARD
2. Peak Flow Meter
3. Radiography (not routine - just for RULING OUT)
4. Allergic testing

DIAGNOSTIC PARAMETERS
1. Forced Expiratory Volume in 1 sec (FEV1) - “Spirometry “
- GOLD STANDARD parameter to assess severity of obstruction
- Test validity: if the FEV1 is within 5% on 3 attempts, then the highest effort of the
3 is used
- Less than <80% = obstruction
- Asthmatic curve : SCOOPING
- Feasible in children >6 years old
2. Peak Expiratory Flow Rate (PEFR) - “Peak flow meter”
- Less sensitive than the 1st
- Predicted NORMAL PEFR for Filipino Children (6 -17 years old)
Formula :
- MALES : (Height in cm - 100) x 5 + 175
- FEMALES : (Height in cm - 100) x 5 + 170
- % PEFR
Formula: ACTUAL / PREDICTED x 100
3. Bronchial Provocation Test
- “Methacholine challenge”
4. Fraction of exhaled Nitric oxide (FeNO)
- Marker of eosinophilic airway INFLAMMATION
5. Allergy test / Skin prick test - NOT helpful in diagnosis of asthma
CONCEPTS

1. Variability
- Improvement and deterioration of symptoms

2. Daily diurnal variability

- Average daily diurnal PEF variability -Asthmatic Adults: >10% and asthmatic Children: >13%
- Formula PEF variability
= (Day’s highest PEF - Day’s lowest PEF) / (mean of the day’s highest and lowest PEF)

(Note: calculated from twice daily readings (best if 3 each time), averaged over 2 weeks.)

3. Reversibility
- “Responsiveness”
- Rapid improvement in FEV1 after inhalation of 200-400 mcg Salbutamol OR more sustained improvements over days or weeks after use of ICS
- Results:
1. increase or decrease in FEV1 >12% and >200ml, from baseline
OR
2. change in PEF of at least 20%

Population Diagnostic Criteria (GINA guidelines)

<6 years old Approach to Diagnosis

- “CLINICAL”
- “Probability-based”

CLINICAL COMPONENTS:
1. Symptom patterns (cough, wheezing, breathlessness, nocturnal/daytime
symptoms)
2. Risk Factors ( hx of atopy, allergic rhinitis, food/medication therapy)
3. Therapeutic response to controller treatment
- Low-dose ICS w/ as needed SABA → improvement/worsening during
8-12 weeks of tx
4. Exclusion of alternate diagnosis

PROBABILITY BASED APPROACH

 Asthma Categories
( < 6 years old)

Less likely Suspected More likely

Symptoms <10 days Symptoms >10 days Symptoms >10 days

2-3 episodes/ year >3 episodes/ year OR >3 episodes/ year OR

severe/night episodes severe/night episodes

No symptoms between OCCASIONAL symptoms REGULAR symptoms

episodes between episodes between episodes

(+) allergic sensitization,

allergic dermatitis, food
allergy or family hx of
asthma

Adjunct to assist in diagnosis

1. Spirometry - Lung function test
2. Plain CXR - “exclusion of other diagnosis”
3. Allergic sensitization tests - NOT REQUIRED but helpful if considering
immunotherapy

6-18 years old 2 KEY DIAGNOSTIC FEATURES:

1. History of VARIABLE respiratory symptoms

2. CONFIRMED variable expiratory airflow limitation
(picture below)
4 CLINICAL PATTERNS AND DIAGNOSTIC PATHWAYS ( please read the pathways )

(-) available
(+) not available

(1) Initial presentation of symptoms + Steroid naive

1. For patients with symptoms → (-) spirometry → ambulatory → responsive

to EMPIRIC therapy→ Asthma diagnosis is likely
2. For patients with symptoms → (+) spirometry → (+) PEF with
reversibility test→ results support asthma → Diagnose/Treat ASTHMA
3. For patients with symptoms → (+) spirometry → (-) PEF with reversibility
test → EMPIRIC therapy + repeat tests on diff occasion → results
support ASTHMA dx → treat for ASTHMA

(2) On controllers + Variable symptoms ; w/o variable airflow limitation

- REPEAT Spirometry : either after withholding bronchodilators or during symptoms

1. Variability of FEV1 & bronchodilator reversibility → FEV1 <70% →

consider Step-up ICS (3 months)
2. Variability of FEV1 & bronchodilator reversibility → FEV1 >=70% → N/A
Bronchial Provocation test → trial Step-down ICS
3. Variability of FEV1 & bronchodilator reversibility → FEV1 >=70% →
POSITIVE Bronchial Provocation test →continue controller therapy
4. Variability of FEV1 & bronchodilator reversibility → FEV1 >=70% →
NEGATIVE Bronchial Provocation test →Step-down therapy + search
alternative dx.

(3) On controllers + Few symptoms; Normal pulmonary function test; NO variable

airflow limitation

- Bronchodilator test (BD) if feasible

- Trial : Stop controller treatment
 1. NORMAL BD test → alternate diagnosis
2. (-) BD test → STOP controller Treatment → Symptoms RECUR and
Lung function DECLINE→ Asthma confirmed → STEP-UP therapy
3. (-) BD test → STOP controller Treatment → NO CHANGE in Symptoms
and Lung function (at lowest ICS) → TRIAL STOP controller and
MONITOR + search for alternative Dx

(4) On controllers + Persistent shortness of breath & airflow limitation

- Stepping up controller treatment (3 months)
- Improvement of symptoms and PFT = Asthma
- No response to treatment = RESUME previous treatment
Bronchial Asthma
Definition
- chronic inflammation of the airways → episodic airflow obstruction
- “Airway hyper responsiveness ( AHR) “ → provocates exposures
History
- Wheeze, shortness of breath, chest tightness and cough
- Vary over time and in intensity - VARIABILITY
Pathophysiology
- Histology
(1) Thickening of the basement membrane
(2) Occlusion of the airway lumen - MUCUS PLUG
(3) Vasodilation and angiogenesis
- Airway mucosa is infiltrated by : activated eosinophils, T lymphocytes, and mast cells
- “AHR”
- Cells involved in Airway inflammation
- Mast cells
- Release bronchoconstrictor mediators
- Activated by “IgE dependent” mechanism
- histamine, prostaglandin D2, and cysteinyl-leukotrienes
- cytokines, chemokines, growth factors, and neurotrophins
- Macrophages
- Activated by allergens via LOW-AFFINITY IgE Receptors (FcεRII)
- Also release anti-inflammatory mediators ( ex. IL10)
- Dendritic cells
- Antigen-presenting cells (APCs)
- Immature dendritic cells
- Promote Th2 cell differentiation
- Requires IL-12 and TNF-a → promote Th1 response
- Cytokine thymic stromal lymphopoietin (TSLP) - instructs
dendritic cells to release chemokines → Th2 attraction into
airways
- Eosinophil
- FEATURE of asthmatic airways
- Role in development of AHR
- Neutrophil
- SPUTUM and AIRWAYS → in px w/ severe asthma exacerbations
- Not responsive to - ICS
- Lymphocytes
- Role in release of specific patterns of CYTOKINES
- Recruitment and survival of EOSINOPHILS and MAST cells

- Th2 cells in “ Th2 asthma phenotype” release the following

cytokines:
(1) IL-5 - eosinophilic inflammation
(2) IL-4 and IL-13 - increased IgE formation
- Natural killer CD4+ T lymphocytes express high levels of IL-4.
- Regulatory T cells (Treg) - role in determining expression of other
t-cells
- Structural Cells
- Epithelial, Fibroblasts, smooth muscle cells
- Inflammatory Mediators
- Mast cell derived : histamine, prostaglandin D2, and cysteinyl-leukotrienes
- Contract airway + Increased microvascular leak + Increase airway
mucus + attract Inflammatory cells
- Cytokines
- Th2 cytokines : IL-4, IL-5, IL-9, and IL-13 → mediate allergic
inflammation
- TNF-α and IL-1β → amplify inflammatory response ; associated with
severe disease.
- TSLP → mediate release of chemokines that attract Th2 cells
- IL-10 and IL-12 → ANTI-INFLAMMATORY meaning DEFICIENT in
asthma
- Chemokines
- Eotaxin (CCL11) Selectively attractant to eosinophils via CCR3,
- CCL17 (TARC) and CCL22 (MDC) - attract Th2 cells via CCR4
- Oxidative Stress - RELATED TO DISEASE SEVERITY
- Increased concentrations of 8-isoprostane (a product of oxidized
arachidonic acid)
- Increased ethane (a product of lipid peroxidation)
- Nitric Oxide
- Produced by “NO” synthases
- In asthmatics , NO level is HIGH in expired air due to eosinophilic
inflammation. — principle used in Fractional Exhaled NO (FENO)
- Transcription Factors
- Nuclear factor-κB (NF-κB) and activator protein-1 - Inflammation
- nuclear factor of activated T cells (NFAT) and GATA-3 - regulate
expression of cytokines in Th2 and ILC2 cells
- EFFECTS OF INFLAMMATION
1. Airway epithelial shedding
2. Fibrosis
a. Type 3 and 5 collagen deposition
3. Airway smooth muscle
a. Hypertrophy and hyperplasia (PDGF and endothelin-1)
4. Vascular responses
a. Angiogenesis
b. Leakage
5. Mucus Hypersecretion
a. “Mucous plug”
b. Hyperplasia of glands - increased goblet cells
c. Induced by IL-13
6. Neural Regulation
a. Inflammatory products → hyperalgesic nerves
b. Neurotrophins → proliferation and sensitization of airway
nerves
c. Substance P → inflammatory effects
- AIRWAY REMODELING
1. Increased airway smooth muscle
2. Fibrosis
3. Angiogenesis
4. Mucus hyperplasia
- PHYSIOLOGY
- Bronchoconstriction + airway edema; vascular congestion; luminal
occlusion => LIMITATION OF AIRFLOW → Reduction in FEV1,
 FEV1/FVC ratio, and PEF => meaning “Increased AIRWAY
RESISTANCE”
- LOW Arterial PCO2 - due to increased ventilation

- AIRWAY HYPERRESPONSIVENESS
- Increased AHR = iIncreased FREQUENCY of symptoms = Increased
Bronchoconstrictor RESPONSIVENESS

ASSESSMENT OF ASTHMA

Level of asthma control:

1. SYMPTOM CONTROL
2. FUTURE RISK of adverse outcomes

Asthma Severity:

● Retrospective assessment of at least 2-3 months

● Control of symptoms and exacerbations
● Dependent on the compliance and technique

●Assess symptom control for atleast 4

Assess asthma control= symptom control weeks
and future risk of adverse outcomes ● Identify other factors for exacerbations
● Assess other factors for airflow
limitation.
How to measure lung function?
● From start of treatment, then after 3- 6
months, after that 1-2 years.

Assess treatment issues ● Technique

● Adherence
● Side effects
● Attitudes regarding the goals for
medications.

Assess comorbidities What are the common causes of

microaspiration that can contribute to
poor asthma control?
● Rhinitis
● Rhinosinusitis
● GER

GINA assessment to asthma control: out of 4 questions:

0- well controlled
1-2 - partly controlled
3-4 - uncontrolled asthma can have risks for exacerbations

Potentially modifiable risk factors for flare ups:

● Medications
○ High SABA use
○ Inadequate ICS
○ Poor adherence
○ Incorrect inhaler technique
 ● Other medical conditions:
○ Obesity
○ Chronic rhinitis
○ GERD
○ Food allergy
○ Pregnancy
● Exposures:
○ Smoking
○ E-cigs
○ Allergen exposure
○ Air pollution
● Major physical and socio economic problems
● Lung function
○ Low FEV1
○ Less than 60% predicted
○ High response to BD
● Type 2 inflammatory markers
○ High eosinophils
○ Elevated FENO
● Others:
○ Intubation
○ More than one exacerbation event in 12 months

Risk factors for developing persistent airflow limitation

History Preterm

Low birth weight

Greater infant weight gain

CHRONIC mucus hypersecretion

medications Lack ICS

exposures Tobacco

Occupational exposures

Noxious substances

Investigations Low initial FEV1, sputum or blood eosino

Severe asthma VS Uncontrolled Asthma

What are the common problems?

● Poor technique
● Poor adherence
● Incorrect diagnosis
● Comorbidities that complicates the condition
● Ongoing exposure to sensitizing irritant
Steps to investigate a patient with poor control

1. Watch the patient using inhaler

2. Confirm the diagnosis
3. Remove risk factors
4. Assess and manage comorbidities
5. Consider treatment set-up
6. Refer to specialist

TREATING ASTHMA

Patient-doctor relationship

● Establish good communication skills

● Assess the health literacy if the patient can assets can understand what you are saying

How to have good communication?

● Congenial demeanor
● Allow the patient to express their goals
● Empathy reassurance
● Give encouragement and reassurance
● Personalized your information
● Provide feedback
How to reduce the impact of low health literacy?
● Arrange information from most important up to the least
● Speak slowly
● Simplify
● Illustrate
● Repeat to check understanding
● Pay attention to non-verbal understanding

Key points:
● Adults and adolescents - SABA long term use is not recommended. It is not for
maintenance; can kill.
● Adults and adolescents- take ICS containing treatment to reduce exacerbation.
● Treatment for adults shows two tracks-
○ TRACK 1- LOW DOSE ICS-FORMOTEROL ( BASTA MAY EXACERBATION)
○ TRACK 2- SABA RELIEVER
NOTE: BEFORE STEPPING UP, CHECK GID IF COMPLIANT AND TAMA ANG
TECHNIQUE!!!

GINA TREATMENT FOR ADULTS AND ADOLESCENTS >12 YEARS

● Track 1
○ ICS-FORMOTEROL better than SABA because this reduces that risks
● Track 2
○ Less effective than the track 1
○ back -up only
○ Used if good adherence si patient sa controller
○ No exacerbations more than 12 months
○ At step 5, anti TSLP can be added

Good asthma control for 3 months, OK to step down, provide action plan, do not
completely remove ICS upon stepping down. Amat amat lang.

Categories of asthma medications

Controller Contains ICS

Reduce airway inflammation

Maintenance

Dose should be optimized

Early initiation leads to better improvement’

If px is not taking ICS, greater chance of REMODELING that leads

to long term decline in lung function

Please remove exposures!

Reliever For breakthrough symptoms

Add-on For px with severe asthma

Px with persistent symptoms

Included in step-up
Before starting controller:
● Secure diagnosis for asthma
● Look for the level of risks
● Consider the choice for available treatment options and adherence
● Technique
● Follow up
After starting:
● Monitor stability
● Check adherence

GINA guidelines:
Initial asthma treatment 6-11 years

Symptoms Initial treatment

Infrequent asthma symptoms SABA as needed

Symptoms needing reliever (occurs twice a Low dose ICS with as needed SABA
month)

Troublesome asthma (4-5 times a week) Low dose ICS-LABA with as needed
SABA

Medium dose ICS with as need SABa

Very low dose ICS-formoterol maintenance

and reliever

Initial asthma presentation Regular comptroller with MEDIUM dose

ICS-LABA with as needed SABA
MANAGEMENT;
● Wheezing episodes in young children should be treated initially with inhaled short-acting
beta2- agonists (SABA), regardless of the dx. But it should be more than 1 year to be
effective.
● PMDI with spacer and mask for <3 years old

ASSESSMENT AND MANAGEMENT OF ASTHMA FOR CHILDREN 5 YEARS AND

YOUNGER

Inhaler device
● Cornerstone for treatment for 5 years and younger
● Tidal breathing during administration using spacer
● 5-10 breath
● Delay between actuating the pMDI into the spacer and inhalation may reduce the
amount of drug available.
● This varies between spacers, but to maximize drug delivery, inhalation should start as
soon as possible after actuation.
● If you are using mask, it should fit tightly into the face
● Nebulizers are variable alternative
PREFERRED AND ALTERNATIVE DEVICE FOR AGE

0-3 YR?

PREFERRED : PMDI + spacer with mask

ALTERNATIVE: nebulizer with face mask

4-5 yr?

PREFERRED : PMDI + spacer with mouthpiece

ALTERNATIVE: nebulizer with face mask

MANAGEMENT OF EXACERBATIONS OF ASTHMA

TAKE NOTE:
● Timing
● Severity
● Symptoms of anaphylaxis
● Risk factors
● Current reliever and controlle rmedications
● Vital signs
● Factors that may complicate
<90% O2 sat, need aggressive therapy

Management (refer to figure below)

CLINIC
MILD Phrase
100-120 bpm
90-95 O2 sat
PEF >50% predicted or best

SEVERE Words
Hunched forward
Agitated
RR >30
HR>120 bpm
O2 sat <90
PEF <50

LIFE THREATENING Drowsy

Confused
Silent chest
 ER

Notes: Ipratropium bromide added with salbutamol every 20 min for 1 hour in severe cases.
Assigning exacerbation severity
For discharge:
1. O2 sat >94%
2. PEF >75%
3. Not in respiratory distress
4. On discharge med for 12 to 24 hours
5. Stable on a 4-hourly inhaled SABA treatment
6. Can demonstrate inhaler use correctly
7. Understand treatment prescribed and signs of worsening asthma.
SPECIFIC IMMUNOTHERAPY IN ASTHMA

Desensitization- when adjunct therapy is not responsive to the pharmacologic treatment

Immunotherapy-
- part of long term management
- Anaphylaxis can develop
- Not possible to avoid allergens
- Reduces the degree of allergy therefore it reduces the severity of the diseases
- Avoidance of triggers
- Suppression of the disease with medications
-
High quality extracts in safe doses:
● House Dust mites
● Animal dander
● Molds
● Pollens: grass, weed, tree

Indications for Immunotherapy

● Px must have IgE sensitivity to allergens
● Should be severe enough
● Progression to allergic rhinitis to asthma
● Unable to control symptoms
● In maintenance medication
● To improve efficacy
● Patient should be compliant to past medications
● 1-2 years of drastic reduction of symptoms
● To re-evaluate if there’s no efficacy seen after a year.

ASTHMA TRIGGERS

Predisposing factors
● Atopy
● gender
Tiggers
● Domestic Allergens
○ House dust mites
○ Animal allergens
○ Insect allergens
○ Mold allergens
● Pollens
○ Higher density of pollen in the afternoon
○ From picnics
● Food additives and drugs
○ LEAST COMMON TRIGGER
● Pollution
● Smokin
● Respiratory and viral infections
○ NUMBER 1 TRIGGER in infants
● Weather changes
● Extreme emotion
● Exercise
 Control measures and their relative efficacy

Definitely useful Impermeable pillow cases

Should be washed with >60 degrees C
water

Probably useful Remove the carpets, drapes, house dust

mites

Carpet not the same as linoleum

Possibly useful Vacuum

Air filter

Unlikely useful acaracide

For patient who are into sports:

● Medication should be correct in timing
● Warm up before actual intense sports
● Sport that should have warm, humid air
○ Swimming- least asthmogenic
● Running and bike- most asthmogenic

Consensus recommendation for exercise induced asthma

● Inhaled short or long-acting B2 agonist (recommended)

○ Oral can slo be given in sub for inhaled given at least 1 hour before exercise

Asthma action plan

● Joint preparation by the patient and doctor
● Updated to the changes
 ASTHMA IN ADULTS

What is asthma?
● Heterogeneous disease- meaning more causes
● Characterized by airway obstruction
● TETRAD of symptoms:
○ Wheeze
○ Chest tightness
○ Difficulty in breathing
○ Cough- diurnal (less frequent during the day; frequent at night)
■ Asthma
■ Upper airway cough syndrome
■ GERD/TB
How to diagnose and manage?
● Different symptoms, different way to manage
● Different genetic composition, different response to meds
● Can vary depending on the severity

COPD ASTHMA

20-pack year smoker Persistent if not treated

Mostly in 40 years of age Most occur in childhood

Downward trend of progmosis Reversible coz of meds

Improved when smoking is reduced

Does not imporved in MEDS FOR ASTHMA

NOTE: they can overlap if the px has asthma and a smoker at the same time

Severe asthma can lead to silent chest; indicative of TOTAL OBSTRUCTION

CHRONIC INFLAMMATION + AIRWAY HYPERRESPONSIVENESS = RECURRENT

EPISODES OF TETRAD

EPIDEMIOLOGY
● 300 million with 4.3% prevalence
● Ph is 2nd in most deaths in the world
○ Poverty
○ Most reliance in Beta-2 agonist (can be deadly ex. salbutamol)
○ More prevalent in children than adults, but more severe in adults
○ Inhaled corticosteroids reduce mortality
How does asthma develop?
● Genetics
● Risk genes and atopy
○ TRIAD
■ Asthma
■ Eczematous dermatitis
■ Rhinitis
○ Exposure and RF:
■ Prenatal
■ Childhood
■ Adult
 ● Can be symptomatic or asymptomatic
● Can have exacerbations when there are triggers

Exposures and Risk factors for development

● Allergen exposure
○ Most important
○ Will only affect people with predisposition with atopy
○ If not, teh wala
● Occupational
● Air pollution
● Infections
● Tobacco
● Obesity
● Diet
● Fungi in allergic airway mycoses
● Acute irritants and reactive airway dysfunction
● High intensity exercise

AIRWAY AND ASTHMA

PATHOPHYSIOLOGY

Bronchioles
● More prone because it is the narrowest
● Most airway resistance
● Asthma is severe in terminal bronchioles
● May constrict due to muscle contraction where they may close or collapse and fail to
exchange

NOTES: AIRWAY HYPERRESPONSIVENESS IS THE HALLMARK FOR ASTHMA

Triggers of airway narrowing:

● Allergens
○ HOUSE DUST MITES- primary reason
○ Grass common in the PH
■ Carabao and Bermuda
● Irritants
● Viral infections
● Exercise in cold dry air
● Air pollution
● Drugs
● Occupational exposures
● Hormonal changes
○ in menstrual period
● Pregnancy

Asthma pathology
● Denuded epithelium ( thickened)
● Increased gland size
● Increase mucus secretion
● Small airways
NOTES: if asthma is not controlled, can get severe
Long term changes in asthma

Increased sputum
Goblet and mucous gland hyperplasia Airway narrowing
Airway wall thickness

Inflammation/fibrosis products
Increased smooth muscle mass Asthma severity
Airway narrowing
AHR

Airway wall edema

Angiogenesis Mediator delivery
- increase in the number of cells = increase
in blood vessels ( support the needs of
the cells) prolonged

AHR
Epithelial alteration Decreased protective barrier

permanent
Subepithelial fibrosis

Mediators of inflammation
 IL4, IL5, IL13
Cytokines

Leukotrienes, Prostaglandins
Fatty acid mediator

Tested via FeNO

Nitric oxide

Caused by over O2 increase in O2 therapy

Reactive oxygen species (ROS)

Refer to picture:
Chemokines
Type 2 inflammation

1. (Th2 cell)- major mediator of inflammation in asthma

2. Trigegred by thymic stromal lipoprotein
3. Then TSL triggers antigens
4. Th2 cells will release the mediators
5. IL-4, 5, 13 – will trigger mucus secretion brought about
by specifically, IL-13
6. IL-4 will trigger B cells.
7. B cells will trigger mast cells to produce GM-CSF,
leukotrienes, PGD2, histamine, and another set of
cytokines: IL-3, 4, 5 and 9 (Most important: histamine
and leukotrienes)
8. IL-3, 4, 5 and 9- trigger contraction,
hyperresponsiveness, smooth muscle proliferation
9. IL-5 will trigger eosinophils.
10. Eosinophils will increase AHR and inflammation.

CONCORDANT and DISCORDANT

Concordant:
● airway dysfunction = level of inflammation
Discordant:
OA-
● Low inflammation, OA ang symptoms
● Low eosinophil, early onset symptoms
● Females can be OA

NONCHALANT:
● High inflammation, chill lang symptoms
● High eosinophil, late onset symptoms
● Males are chill

Is it asthma;

Two features:

1. History of respiratory symptoms that vary over time and intensity

2. Variable expiratory airflow limitation
PFT- test done in clinical trials but make sure that the patient is NOT GRABE.

History of respiratory symptoms

● Always follow TETRAD

● Generally more than one
● Can vary
● Triggers
○ Exercise
○ Laughter
○ Allergens
○ cold , dry air
● Can worsen with viral infections
● History of reactions to medications

Physical Exam
● Often normal as seen in atopy
● Allergic rhinitis with pale nasal mucus membranes
● Nasal polyps
○ This should be removed
● Wheezing on expiration (less during inspiration)
○ If mild, no wheeze; but if fast, can be heard
○ More wheeze=severe;
○ SILENT:DANGER!!!
● Acute asthma attack
○ Tachypnea and tachycardia
○ Accessory muscles can be observed
○ 5 minutes golden time to gain access to air, if not: DANGER!!

Evidence of Variable Expiratory Airflow Limitation

● confirmed at least once by a reduced FEV1/FVC ratio (normally >0.75-80 in adults)

● Asthma if FEV1 increase after bronchodilator (>200ml and >12%), and PEF >10%
● For 4 weeks of treatment
● Asthma with viral infections can result to absence of bronchodilator reversibility

Obstructive= FEV1 FVC ratio, DECREASED

Restrictive = FEV1 FVC ratio, NORMAL

Air trapping- severe form of asthma

Spirometry: GOLD STANDARD: Pulmonary Function Test or Spirometry

Before administration of bronchodilating agents, FEV1 is decreased, and diaphragm is flat due to air
trapping
Peak flow Meter

● Twice daily for 2 weeks

● ADULTS – average Diurnal variability in PEF by >10% (over 2 weeks)
● IF THERE is CHANGE= ASTHMA
● IF NO CHANGE= COPD

Bronchoprovocation test
● Done only in hospital for safety
● Use of direct stimuli:
○ Methacholine
○ Mannitol
○ Histamine
○ Hypertonic saline
○ Challenge with exercise and/or cold, dry air

Adjunct tests

● Eosinophil counts
● IgE, skin tests, and radioallergosorbent tests
● nitric oxide (FeNO), inflam= asthma
● Chest radiography- for air trapping
● Sputum analysis- presence of eosinophils and neutrophils
If there is no confirmed alternative dx, always go with trial treatment for likely diagnosis

PHARMACOTHERAPY OF ASTHMA

Reliever (rescue medications) ADD on therapies

Controller Medication:

● Used for regular ● Provided to all patients ● considered when

maintenance for as-needed relief of patients have persistent
treatment. breakthrough symptoms and/or
symptoms, including exacerbations despite
● They reduce airway
during worsening optimized treatment with
inflammation, control asthma or high dose controller
symptoms, and reduce exacerbation. medications.
future risks.
Asthma treatment bottomline
● Inhalant is superior to oral
● Direct to airways, less adverse effects

Four components of asthma care

● Develop patient/doctor relationship

○ Educate
○ Involve family
○ Prepare a written personal action plan
○ To enhance compliance
○ Avoid RFs
○ To understand the difference between controller and reliever meds

● Identify and reduce exposure to Risk

● Control asthma using meds to decrease severity NOT TO CURE

● Continue exercise but should be appropriate to condition
● Take rapid-acting beta agonist prior to strenuous
exercise
● Annual flu vax for moderate to severe patients
● Reduce exposure to allergens
Assessing patient with asthma

Asthma control ● Symptom control

● Modify risk factors
● Measure lung function before start treatment course 3-6
months later, and then periodically

● Rhinitis, GERD, obesity, OSA, depression, anxiety

Comorbidities

Treatment issues ● Side effects

● Check inhaler technique and timing

NOTE: puff should be in slow inhalation to create laminar

flow

Management to asthma

Assess, adjust, review of response (cycle)

ASSES - Diagnosis
- Symptom control
- RFs
- Inhaler techniques
- Adherence
- Patient preferences

ADJUST - Medications
- Non-pharmacological strategies
- Treatment of modifiable risk factors

RESPONSE
- effectiveness and side-effects

LONG-TERM GOALS - Reduce the burden of the for exacerbations, side effects
and death
Risk Factors for Poor Asthma

Medications
- ICS not prescribed
- Poor adherence
- Incorrect inhaler technique
- High SABA use

Comorbidities
- Obesity
- Chronic rhinosinusitis
- GERD
- Food allergies
- Anxiety, depression
- Pregnancy

Exposures
- Smoking
- Allergen
- Air pollution

Lung function
- Low FEV1, especially if <60% predicted
- Higher reversibility

Independent risk factors

- History of intubation or admission to intensive care for
asthma
- Having 1 or more severe exacerbations in the last 12
months

● Periodic assessment of the diagnosis every 1-2 years

● Measure FEV1 at start of treatment, after 3-6 months of controller treatment
NOTE

- Over-reliance on SABA at the expense of ICS controller therapy was associated with an
increased risk of asthma-related death.
- Inhaled corticosteroids are the specific medications to be titrated in asthma and not the
bronchodilators

● Low dose ICS reduced asthma hospitalizations and death

● Low dose ICS is very effective in:
○ preventing severe exacerbations
○ reducing symptoms
○ Improving lung function
○ preventing exercise-induced bronchoconstriction
STEPS

STEP 1-2: LOW DOSE ● symptoms less than twice a month and NO
ICS-FORMOTEROL TAKEN AS exacerbation risk factors
NEEDED FOR SYMPTOM RELIEF ● Step down treatment for patients whose asthma is well
(TRACK 1) controlled on

Other options:

● Step 1: Low-dose ICS taken whenever SABA is taken

● Step 2: Leukotriene receptor antagonists (LRTAs)
○ Less effective than regular ICS
● Step 2: Daily low dose ICS-LABA
● SABA as needed from the old guidelines

Check:
STEP 3: LOW DOSE
ICS-FORMOTEROL ● adherence
MAINTENANCE AND RELIEVER ● Technique
THERAPY (TRACK 1) ● environmental exposures
● comorbidities

Preferred controller:

● Low-dose ICS-formoterol maintenance and

reliever therapy (MART)

Alternative:

● Low-dose ICS-LABA maintenance plus

as-needed SABA

Other options:

● Medium dose ICS

● Low dose ICS plus LTRA
● ICS formoterol reduces severe AE by 60% and ER visit
by 65%

Preferred controller:
STEP 4: MEDIUM DOSE
ICS-LABA MAINTENANCE AND ● Medium dose ICS-LABA maintenance and reliever
RELIEVER THERAPY (TRACK 1)
Other options:

● Medium or high dose ICS-LABA with as needed SABA

● Add-on tiotropium by mist inhaler for patients >= 6

years with a history of exacerbation
● Add-on LTRA

Add-on treatments:
STEP 5: REFER FOR ● Tiotropium by mist inhaler
PHENOTYPIC INVESTIGATION +/- ● For severe allergic asthma: anti-IgE (SC
ADD-ON TREATMENT omalizumab, >= 6 years)
Other options:
● Low dose ICS

Reliever will still be low dose ICS-formoterol

Reviewing response and adjusting treatment

Should be seen 1-3 months after, then follow-up 3-12 months after:
● Pregnancy: every 4-6 weeks

Controlled, then titrate

STEP Up

Sustained step-up for at least 2-3 months Asses if:

● Incorrect inhaler technique

● Poor adherence
● smoking
● Has Comorbidities

Short term step up 1-2 weeks

During viral infection or allergen exposure

Step down asthma treatment

● Consider if good control is achieved
● Be sure that:
○ No respiratory infection
○ No planned travel
○ No pregnancy
● Document baseline status
● Step down through available formulations to reduce the ICS dose by 25-50% at 2-3 month
intervals

Asthma action plan inclusions:

● Usual asthma medications

● When and how to increase medications and start ICS
● How to access medical care
Color codes:

● Green: 80-100% of personal best

○ Means Go zone
○ Use preventive medicine
● Yellow: 50-80% of personal best
○ Means Caution zone
○ Add quick-relief medicine
● Red: <50% of personal best
○ Means Danger zone
○ Get help from a doctor

Patients at risk for greater asthma flare ups

● Review patient’s understanding

● Modifiable risk factors for exacerbations
● Choice of treatment track
● technique skills
● Adherence
● Written action plan

Managing asthma exacerbations:

● Assess exacerbation severity while starting SABA and oxygen

● Assess alternative causes of dyspnea
● Arrange immediate transfer
● Start treatment with repeated doses of SABA, early ICS, and oxygen.
● Titrate oxygen and maintain SpO2 93-95%

PLEASE: DO NOT routinely prescribe antibiotics.

Special Considerations:

Pregnancy - Close follow-up and medication adjustments

- Down Titration has low priority
- Treat exacerbations aggressively

Obesity
- Same treatment
- Weight loss to improve control

Surgery
- Evaluate lung function
- Ensure that controller therapy maintained
- If on long-term high dose ICS, or > 2 weeks OCS in the past 6
months, give intraoperative hydrocortisone

Rhinitis, nasal polyps

- Treatment to improve symptoms

Occupational asthma
- Same treatment principles
- Consult asthma specialist
 OSA
Short questionnaire to assess daytime sleepiness? - Epworth Sleepiness Scale
There are 4 stages of sleep: N1, N2, N3, REM
What stage is considered the restorative stage? - N3
Is PSG type 3 also known as Home Sleep Attended Studies or Portable Monitoring? - Yes.
How long is the duration of the sleep cycle? - 90-120 minutes
In evaluation of OSA, what symptom has the greatest specificity? - Witnessed apnea
In evaluation of OSA, what symptom has the greatest sensitivity? - Chronic Snoring
pCO2 levels in Sleep-related Hypoventilation syndrome? - >55mmHg for >=10 minutes
In type 3 PSG, what is the only clue for obstructive events during sleep? - O2 desaturation
In evaluation of OSA, the presence of what symptom suggests the need for a sleep study? -
Excessive daytime sleepiness
Epworth sleepiness scale: what score indicates a need for further evaluation? - >= 11
PSG type used in clinical trials? - Type 2
Questionnaire indicated for Pre-operative Patients? - STOP BANG
Awake Hypoventilation: what are the pCO2 levels? - pCO2 >= 45mmHg
What is the best documented risk factor for hypoventilation disorders? - Obesity
Standard initial treatment of choice for moderate to severe and possible mild OSA in adults: -
CPAP
Sleep apnea is associated with 2 mental health conditions: - Anxiety and Depression
Recommendations for napping? - 30 minutes a day before 3 PM
What was the definitive surgical procedure for OSA before CPAP was invented? -
Tracheostomy
Questionnaire used to categorize individuals into risk groups for OSA? - Berlin Questionnaire
Sleep Disorder Obstructive Sleep Apnea (OSA) Obesity Hypoventilation Syndrome (OHS) Sleep-related Hypoventilation Syndrome

DEFINITION Repetitive episodes of complete (apnea) or partial The only category of hypoventilation syndrome that Insufficient ventilation → Hypercapnia
(hypopnea) upper airway obstruction during sleep. is diagnosed with awake pCO2.

90% of OHS px have OSA

PATHO Sleep onset → loss of neuromuscular compensation
PHYSIOLOGY + dec. pharyngeal muscle activity → AIRWAY
COLLAPSE → Apnea / hypopnea → hypoxia &
hypercapnia → Inc. Ventilatory Effort → AROUSAL
→ Restored muscle activity → airway opens →
Hyperventilate → sleep onset
“ Fragmented Sleep”
Leptin Resistance + Inc. Mechanical work & Weak
respiratory muscles + OSA or Upper Airway
Obstruction → Blunted ventilatory Response →
CHRONIC HYPERCAPNIA
“Leptin resistance” → hypoventilation ; leptin is a
stimulant of ventilation and hunger suppressant.
“Fat deposition” → Decrease FRV and ERV
(1) Accessory muscle atonia (REM) Sleep + (2)
Inc. upper airway resistance due to Gravity +
(3) Dec. Ventilatory Response to CO2 or O2
—-> HYPOVENTILATION
Sleep-related Hypoventilation:
- pCO2: >55mmHg for >=10 min
- >=10 mmHg increase in pCO2 during
sleep

“Breathing abnormalities” → OSA or Upper airway

resistance

RISK FACTORS Obesity

Old Age
Male
Familial and Genetic
Post Menopause
African-American / Asian
Alcohol & Smoking
Hypothyroidism

DIAGNOSTICS The clinical Triad: DIAGNOSTIC CRITERIA:

1. Witnessed apnea 1. Hypoventilation during wakefulness (pCO2

2. Excessive daytime sleepiness >= 45 mmHg)
3. Chronic snoring 2. BMI > 30
3. Hypoventilation not due to other
disorders
 CLINICAL TOOLS AND QUESTIONNAIRES
APNEA-HYPOPNEA INDEX (AHI)
*should NOT be used to diagnose OSA if without
Polysomnography
Body weight AHI
Berlin Questionnaire
10% increase 32% increase
- categorize individuals into risk groups for
OSA
10% decrease 26% increase
Categories:
(1) 2 or more positive response to Qs (there is 5% difference in AHI)
1-6 : WEIGHT LOSS = is NOT a CURE
(2) 2 or more positive response to Qs
7-9
(3) 1 or more positive response and or
a BMI >35
POLYSOMNOGRAPHY
Epworth Sleepiness Scale
- Assess excessive daytime sleepiness - End Tidal Carbon Dioxide instead of
- DOES NOT rule in OSA ABG since px is asleep
- Positive : >= 11 - Hypnogram is the summary of results
- X axis = time
- Y axis = events/stages
STOP BANG Questionnaire

- Snore, Tired, Observed apnea, Pressure of

blood, BMI, Age, Neck, Gender
- Indicated or Pre-operative Patient

Risk No. of YES

Low 0-2

Intermediate 3-4

High 5-8 qs.

(either of the 4)
2 or more STOP qs + male
 2 or more STOP qs + BMI>35
kg/m2

2 or more STOP qs + neck circum.

17in/ 43cm (male) or 16in /41cm
in females

Classification of Scores
Tool Scores

Low Moderate/High

Berlin 1 Category At Least 2

categories

Epworth <11 At least 11

STOP BANG <3 At least 3

POLYSOMNOGRAM (PSG)

Type Description

1 Complete PSG + In-lab attendants

(GOLD STANDARD)

2 w/o in-lab attendants

3 (min. 4 variables)

2 Respiratory variables + O2 sat. +

ECG

4 (min. 1 channel)
O2 sat. + Flow or Chest movement
TREATMENT/ Goals
MANAGEMENT
1. Improve symptoms, quality of life, sexual intimacy
2. DECREASE AHI to <5/hr w/o DESAT or AROUSAL
3. Improve Comorbidities
4. Prevent and Minimize Cardiovascular diseases and TRAFFIC Incidents

CPAP or Continuous Positive Airway Pressure

● Moderate to Severe OSA in adults – CPAP

● Mild OSA - mild CPAP
● Napping for around 30 min. - Not required
● If patient needs higher pressure (around 50) - Bi-Level PAP

DENTAL/ ORAL APPLIANCE

● Mild to Moderate OSA and alternative to Severe OSA- Custom fitted titratable oral appliance
● “Boil and Bite” method -NOT RECOMMENDED

SURGERY

● Definitive treatment prior to invention of CPAP -Tracheostomy

● Tonsillectomy - NOT ENOUGH, CPAP therapy more beneficial
● Maxillomandibular Advancement - increases airway but very traumatic
● Uvulopalatopharyngoplasty - “cave-like” airway, very bloody and traumatic, rarely done (severe
cases; can’t tolerate CPAP)

HYPOGLOSSAL NERVE STIMULATION

● Stimulation is SUFFICIENT enough to evoke response from nerve but MILD enough not to
disturb sleep

POSITIONAL THERAPY

● High Back Rest Lateral Position

● Tennis Balls, Vests, Positional Alarms, Orthopedic Pillow
● POOR LONG TERM compliance
 OXYGEN THERAPY
● NOT RECOMMENDED - prolongs apneic episodes

BEHAVIORAL/ LIFESTYLE
● Weight Loss
● Avoid Alcohol
● Avoid Sedatives - except if psychiatric meds
● Proper Sleep Hygiene

FOLLOW UP
● First 2 Weeks of PAP
● Assess compliance and improvement of symptoms

EXTRAS Parameters:

(1) Apnea
- Cessation of airflow >= 10s
- Drop of 90% of baseline in Peak thermal sensor excursion
- +/- desaturation or cortical arousal
- Drop in O2
- No flow in nose/mouth
(2) Hypopnea
- Partial obstruction : there is still airflow
- Drop of >30% of baseline in nasal pressure transducer (airflow)
- Decreased airflow >= 10s
- >=3% O2 desaturation from baseline OR arousal
(3) Respiratory Effort Related Arousal (RERA)
- Increasing respiratory effort or flattening of the inspiratory portion of nasal pressure -
lasting >10s
- “Esophageal Manometry” - not always available
(4) Respiratory Disturbance Index (RDI)
- No of events per hour of sleep
- RDI = Apnea + Hypopnea + RERA / Total Sleep Time
- Severity in Adults::
Normal : <5/hr
Mild : 5-14/hr
Moderate: 15-30/hr
Severe: >30/hr
 PULMONARY REHABILITATION

Pulmonary Rehabilitation Comprehensive intervention based on Components: Exercise Limitations:

Thorough patient assessment - Exercise training - Ventilatory
followed by patient tailored therapies that - Education (COPD,bronchiectasis)
include (but not limited to - Breath retraining - Gas Exchange
- Exercise - Psychological support - Respiratory Muscle problem
- Training - Nutritional advice (sarcopenia; loss of body
- Education - Outcome assesment mass)
- Behavior change - Cardiac
- Psychological impact (more
Designed to improve the physical and psychiatric than psychological)
psychological condition of people with - Lower limb dysfunctions
CRD and to promote the long-term
adherence to health- enhancing
behaviors ( ATS-ERS Statement 2013)

Goals: Indications: Contraindications:

- Alleviate symptoms - Severe dyspnea/fatigue - Unstable angina
- Increase exercise capacity - Decreased exercise - Arrhythmia
- Increase ADL tolerance/ability /physical - Unstable bone fracture
- Improve Quality of life activity levels - Communicable infectious
- Behavioral change - Difficulty in performing disease (during covid they use
- Decision making activities of daily living youtube
It cannot cure the disease but only - Impaired health status - Unstable psychiatric condition
manage the symptoms - Decreased occupational posing harm to self or others
performance or ability
- Frequent or increased
medical resource utilization
- Difficulty coping with or
managing the disease
- Recovery from COPD
exacerbation (later decline

Assessment Necessary to determine Severity of
respiratory impairment
- Clinical history
- Review of records
- Educational assessment
- Physical exam
Other assessments:
- Respiratory muscle strength
- Peripheral muscle strength
- ADL
- Health status
- Cognitive function
- Psychological Status
- Nutritional status
- Body composition
Stress testings
- Physical performance test to
measure activity limitation
- Can also check how far the
disease has progressed
Quality of LIFE
Questionnaires (divided into)
- Genre specific
- Diseases specific
- CRDQ
- SGRQ
lung function due to COPD)
- Preparation for or recovery
from lung transplantation
- Nutritional depletion
SGRQ
- 50 items
- 10-15 mins
- Self administered
- Symptoms (frequency and
severity)
- Activity
- Impact (social,
psychological)
CDRQ
-20 questions (four domains)
- 15-30mins
-interviewer administered
-20 questions (four domains)
- 8-10 mins
-self administered
- Dyspnea
- Fatigue
- Emotional function
- Mastery of disease
Standardized dyspnoea domain
available
1. Feeling emotional
(angry/upset)
2. Taking care of basic needs
3. Walking
4. Chores
5. Social activities
Same scoring method for individual
/ standardized dyspnoea items
- 8 minutes to complete
 Chronic Respiratory Disease
Questionnaire (CRDQ
or CRQ) –
St George's Respiratory
Questionnaire (SGRQ) – disease specific
Settings:
- Outpatient
- Inpatient
- Home (for px with financial
problems)
- Community
- technology/remote
Education Education on self management
- Normal pulmonary anatomy and
physio
- Pathophysio of chronic resp
diseases
- Communicating with the health
care provider
- Interpretation of medical testing
- Breathing strategies
- Secretion clearance techniques
- Role and rationale for
Total score can also be calculated Total score can be calculated from
from all three components with: Four components
0 - no health impairment
100 - maximum impairment
- Sensitive and responsive to
change after PR
- Sensitive and responsive to
change after PR (Self
- Clinically significant change administered = more
(a reduction of 4 U has been identified
as the minimum clinically significant
responsive)
change) - Measures clinically significant
change ( a change of 0.5 U has been
identified as the minimum clinically
- Available in many significant change)
languages - Available in many languages
- Reliability and validity - Reliability and validity widely
widely tested tested
Topics concerning advance care
planning
● Prognosis
● Patient autonomy in medical
decision-making
● Life-sustaining treatments
● Advance directives documents
● Surrogate decision-making
● Durable powers of attorney for
health care
 medications (inc. oxygen therapy) ● Discussing advance care
- Effective use of respiratory planning with health care
devices professionals and family caregivers
- Benefits of exercise and physical ● Process of dying
activities ● Prevention of suffering
- Energy conservation during
activities of daily living
- Healthy food intake
- Irritant avoidance
- Early recognition and treatment of
exacerbations
- Leisure activities
- Coping with chronic lung disease

Exercise training ● Cornerstone of pulmonary rehabilitation Benefits Components:

● Best available means of improving
muscle function in
COPD
● Improved oxidative capacity
● Reduced ventilatory requirement
● Increased motivation for exercise
beyond the
rehabilitation environment
● Reduced mood disturbance
● Less symptom burden
● Improved cardiovascular function
- Increased fat free mass
- Normalizes proportion of T1
fibers
- Increases cross sectional
area of muscle fibers
- Increases capillary contacts
to muscle fibers
- Increases capacity of
oxidative enzymes
- Increases glutathione levels
- Normalize the pH
- Lower extremity exercises
- Arm exercises
- Ventilatory muscle training
Types:
- endurance/aerobic
- Interval
- strength/resistance
- Balance
- Others: whole-body vibration,
neuromuscular electrical
stimulation. Yoga, Tai Chi

Lower extremity exercises

- Walking
- Treadmill
- Stationary bike
- Stair climbing
- Sit and stand
 Some px are given supp o2.

Upper extremity exercises:

- Arm cycle ergometer (alt for
stationary bike)
- Unsupported arm lifting
- Weights

Inspiratory Muscle Training Resistive IMT Threshold IMT

- Increase strength and endurance
to reduce dyspnea in COPD Px breathes through handheld Px breathes through a device with a
device with which resistance to valve which opens at a given pressure
flow can be gradually increased

Chest Physical therapy and breath

retraining

1.Pursed lip breathing

- shifts breathing pattern and inhibits
dynamic airway collapse

2.posture techniques
-forward leaning reduces effort, elevating
depressed diaphragm by shifting
abdominal contents

3.diaphragm breathing
-px with extreme trapping and
hyperinflation have increased WOB

4.Postural draining (Cystic fibrosis)

-px who produce more than 30cc/day
Psychological considerations - 40 percent of COPD px have
symptoms of depression or
anxiety
- Associated with significantly
worse functional capacity
- Screening should be part of initial
assessment
- Incorporation of breathing training
and coping strategies for
recognition and management of
anxiety can reduce panic attacks

Nutritional interventions - Associated with increased Supplementation:

morbidity and mortality - Energy dense food (milk)
- High calorie req from exercise - well - distributed during the
training in rehab day
- Decreased intake - Small frequent meals
(dyspnea)=impaired energy
balance
- Imbalance in protein synthesis
and breakdown
- Loss of fat and weight loss (bmi
<21)
- Depletion of FFM or lean body
mass

DURATION OF REHABILITATION - Max (can be extended) 6 weeks

- There can be a plateau
- Daily to weekly
- 10-45 mins per session
- Other considerations
- Bronchodilator (SABA)
- O2 therapy
Outcome assessment 1. Providing patients with
opportunity to give feedback
about the program is a useful
measure of quality control
2. Patient feedback also allows
coordinators to evaluate the
components of pulmonary rehab
that patients find most useful
3. The questionnaires should also
provide patients with variety of
answering options
4. Exercise capacity measurements

EXAMPLES OF OUTCOME MEASUREMENT SCALES/TEST

ASSESSMENT FOR
PULMONARY REHABILITATION

Laboratory measures of exercise - Incremental

performance cardiopulmonary exercise
testing
- Endurance testing at

Functional exercise - 6-minute walk test

capacity - Incremental walk and
endurance shuttle walk
tests
- Muscle strength
(dynamometry)
- Timed up and go testing
- Sit-to-stand testing
-Dowel lifting
- Balance assessment
Exertional dyspnea Borg scale or visual
analogue scale during
exercise testing

Dyspnea w/ daily - Modified Medical

activities Research Council
questionnaire
- Baseline and transitional
dyspnea indices
- San Diego shortness of
breath questionnaire

Health status Chronic respiratory

disease questionnaire
- St. George's respiratory
questionnaire
- Medical outcomes study
short form
- COPD assessment test
- Other disease relevant

Functional performance - Pulmonary function

status scale
- Pulmonary function
status and dyspnea
questionnaire

Physical activity - PROActive instrument

- Activity monitors/
accelerometers

Nutritional status or body -Body mass index BMI

composition - Body composition using
bioelectrical impedance or dual
energy X-ray
absorption
 Additional important - Fatigue
patient centered - Cognition
outcomes - Disease exacerbations
- Use of tobacco or vaping
products
- Patient self-efficacy,
coping style, and
knowledge
- Patient satisfaction with
PR program

Additional important - Hospitalization and

health system outcomes urgent healthcare visits
- PR program quality
metrics
- Program costs

IV. STRUCTURE OF PULMONARY 1. Proper patient *Exercise training Outcome

REHABILITATION PROGRAM selection *Caloric Assessment:
2. Patient Supplementation Symptoms
assessment *Strength Exercise Exercise
3. Individualization *Self Education Performance
of program Management Quality of Life
*Psychological
Aspects:
depression and
anxiety