Asthma presentation

1. BRONCHIAL ASTHMA

2. • The most common chronic respiratory disease in the
world
• > 330m globally (WHO, 2022)
• 7.5% (4M)of Kenyan population living with asthma
• World over the disease is underdiagnosed and
undertreated- high levels of morbidity and avoidable
deaths
• Burden increasing

3. OUTLINE
• Definition, description and diagnosis
• Assessment of asthma
• Treating asthma
• Medications and strategies or symptom control and risk
reduction
• Management of worsening asthma and exacerbations
• Asthma and COPD

4. • A heterogeneous disease , characterized by chronic
airway inflammation.
• Defined by the hx of respiratory symptoms: sob, chest
tightness and cough that vary over time and intensity ,
together with variable expiratory airflow limitation
• Airflow limitation may later become persistent
• Majority of asthma deaths occur in low and middle income
countries

5. Risk factors
• Genetics –asthma tends to run in families
– ADAM33, IL18R1, IL33,IL2RB,IL10, TGFB1
• Atopy
• AHR
• Male gender in early life, female in late life
• b/feeding for <6months
• Diet : high salt diet and diet low in antioxidant vitamins e.g. vit C
• Obesity
• Exposure to tobacco smoke
• Viral infections in early childhood

6. Pathogenesis and pathophysiology
• A wide array of inflammatory cells
is involved in the asthmatic
inflammation :mast cells,
eosinophils, epithelial
cells,macrophages, activated T
lymphocytes
• Airway cells (fibroblasts,
endothelial/epithelial cells)
• Basement membrane thickening,
airway smooth muscle
hyperplasia and hypertrophy,
increase in mucus producing
elements:goblet cells and
submucosa glands

7. • Chronic airway inflammation is
associated with increased bronchial
hyperresponsiveness which leads
to bronchospasms and typical
signs on exposure to allergens
• In chronic asthma, airflow limitation
may be only partially reversible
because of airway remodeling
(hypertrophy and hyperplasia of
smooth muscle, angiogenesis, and
subepithelial fibrosis) that occurs
with chronic untreated disease

8. Asthma Phenotypes
• These are recognizable clusters of demographic , clinical and or
pathophysiological characteristics (traits)
• Allergic asthma::The most easily recognized asthma. Often commences
in childhood and is associated with past/family hx of allergic diseases –
eczema, allergic rhinitis, food/drug allergy. Sputum b4 treatment reveals
eosinophilic airway inflammation. Usually responds well to ICS treatment
• Non allergic asthma: Not associated with allergy. Cellular sputum profile
may be neutrophilic , eosinophilic or contain few inflammatory cells .
Patient demonstrate a lesser short time response to ICS

9. • Adult/late onset asthma.Some patients esp women
present with asthma for the first time in adult life. They
often need higher doses of ICS and are relatively
refractory to corticosteroid treatment. R/o occupational
asthma
• Asthma with persistent airflow limitation: occur in some
patients with long standing asthma. Due to airway wall
remodeling
• Asthma with obesity :

10. Occupational asthma
• Occupational rhinitis may precede asthma by upto 1 year
• 5-20% of new cases of adult onset asthma can be
attributed to exposure
• Focused hx on symptoms at work vs away from work
• PEF at work and away from work

11. Obesity and asthma
dashed arrows changes seen after weight loss

12. Symptoms that increase the probability of
asthma
• Patients experience more than one of (wheeze, sob,
cough,chest tightness)
• Symptoms often worse at night or early morning
• Symptoms vary over time and intensity
• Triggered by viral infections, exercise, allergen exposure,
laughter, fumes, strong smells

13. Diagnosis
• Based on
– the history of xstic symptom patterns
– evidence of variable expiratory airflow limitation- documented
from bronchodilator reversibility testing or other tests
• Test before treating wherever possible. Its more difficult to
confirm the diagnosis once control has improved

14. Diagnosis
• PFT: FEV1/FVC <0.75
• Bronchodilator response improves by 12% / 200ml
• PEF variability >10% or greater between morning and
evening/ work and off-work
NORMAL lung function but the clinical suspicion still
high?
• AHR challenge test
– FEV1 drop by >20% with only small doses of inhaled
bronchoconstrictor: Methacoline, histamine, mannitol,

15. Role of biomarkers
-fraction of exhaled NO (FENO) and CO(FECO)
• Non invasive –hand held gadgets
• Evaluates airway inflammation in asthma
– Determine the likelihood of steroid responsive asthmatic
– Monitor the adequacy of the controller ICS dose
– Indicate poor adherence to therapy
– To indicate poor inhaler technique
• Stool microscopy for helminths
– Systemic helminths like AL trigger asthma like symptoms

16. Diagnostic criteria
• 1. Symptoms
• 2. confirmed variable reversibility”: Documented excessive variability in lung function. One or more of:
– Positive BD responsiveness (Reversibility) test: Increase in FEV1 of >12% or 200ml. Change measured 10-15 min
after 200-400mcg salbutamol
– Excessive variability in twice daily PEF over2 weeks. Average daily diurnal PEF variability >10% . (Days High-
Low/mean of days highest and lowest)x 100
– Increase in lung function after 4 weeks of treatment: FEV1 by >12% from baseline after 4 weeks of ICS
– Positive exercise challenge test: Fall in FEV1 of >10% and > 200ml from baseline
– Positive bronchial challenge test: Fall in FEV1 from baseline of>20% with methacoline

17. OTHER TESTS
• Allergy tests : measurement of (Specific)sIgE or skin prick
testing
• Imaging

18. Stepping down ICS to help confirm the dx
of asthma
• Document patients current status and asthma control
• Choose a suitable time :no infection ,not pregnant, not travelling
• Provide a written asthma action plan
• Reduce ICS by 25-50%
• Revisit 4 weeks, review response
• If symptoms , and coupled with variable expiratory airflow
limitation=confirm asthma.
• If no consider ceasing ICS, repeat PFT in 2-3 weeks , fllup for
atleast 12 months

19. Severity of asthma

20. Ddx
• Chronic upper airway cough syndrome
• Bronchiectasis
• Primary ciliary dyskinesia
• CHD
• Bronchopulmonary dysplasia
• A1ATD
• Inhaled FB
• Copd
• Medication related cough

21. • Severity of asthma tells us about asthma control
– So What is meant by Asthma control?

22. • The extent to which the manifestations of asthma can be
observed in the patient
• Described in terms of both Symptom control and future
risk domains
– Mr X has good asthma control but she is at increased risk of
future exacerbations becauses of previous hx of the same in
the last 1 year…, currently smoking…, poor medication
adherence …, etc

23. Assessment of asthma control
• Assess symptom control and future risk of adverse
outcomes
– Assess treatment issues :inhaler technique , written asthma
action plan
– Assess multimorbidity: Rhinnitis, rhinosinnusitis, GER,
obesity, OSA, depression

24. Refer to BOX 2.2
• GINA assessment of asthma in adults , adolescents and children 6-11 yrs

25. • The average rate of FEV1 decline in non smokers healthy
adults is 15-20ml/year
• Asthmatics may have an accelerated decline and develop
airflow limitation that is not fully reversible

26. Treatment
• Goals :
• Achieve good control of symptoms
and maintain normal activity levels
• Minimize the risk of asthma related
deaths, exacerbations, persistent
airflow limitation and side effects
Key points
• ICS are the cornerstone of
managing asthma to achieve
control
• Oral short acting bronchodilators
, cough mixtures, mucolytics
arent recommended in asthma
mx
• A spacer device can be used in any
age group for those not able to use
pMDIs directly, and all children
<5yrs

27. Types of inhaler devices
• Pressurized MDI
• Breath accentuated MDIs
• Dry powder inhalers
• Soft mist inhalers
• Nebulized or wet aerosols
• Spacer devices

28. • Refer to box 3-1. Communication strategies for health care providers

29. GINA 2023 STARTING TREATMENT
• Refer to “GINA 2023 STARTING TREATMENT” box 3-12
• Track 1 and Track 2

30. …Step 5
• Tropium e.g spiriva
• Tripple inhaler for >18yrs beclometasone /formoterol/glycopyrronium;
mometasone/indacaterol/glycopyrronium
• Add on azithromycin 500mgx3/week if persistent attacks despite high
dose ICS-LABA.Check sputum for atypical mycobacteria, ECG
QTc(and recheck after a month on treatment, risk of antimicrobial
resistance.Diarrhoea common. Treat for atleast 6 months
• Add on biologic therapy
– antiIgE (Omalizumab) with severe allergic asthma
– Antiinterleukin-5/5R: s/c mepolizumab; iv reslizumab; or s/c benralizumab for
severe eosinophilic asthma
– Antiinterleukin 4R alpha
– Antithymic stromal lymphopoietin

31. …step 5
• Bronchial thermoplasty: Reduces smooth muscle mass –
longterm effects not known
• As last resort add on low dose oral corticosteroid
<7.5mg/day pdl , Often associated with substantial side
effects

33. Doses
• Refer to Box 3-14. Low, medium and high daily metered doses of
inhaled corticosteroids (alone or with LABA)

34. WHY ICS containing meds should be
commenced from the time of diagnosis
• Reduces risk of severe exacerbations and ED visists or
hospitalization by 65% compared with SABA only
treatment
• Leads to greater improvement in lung function than if
symptoms have been present for more than 2-4 years
• Increases early resolution of symptoms for occupational
asthma and improvement of lung function

35. Dust mites
• microscopic arachnids that have lived on earth for millions of years.
• Feed mostly on dander (i.e. dead skin cells) and thrive in warm, humid
conditions.
• Depending on your home’s environment, millions of dust mites can be present.
• A mattress alone typically contains hundreds of thousands of them.
• The mites themselves aren’t harmful,. But the proteins found in their feces are
considered the most important inducers of allergenic diseases worldwide.”

36. Aspirin exacerbated respiratory disease
(AERD)
• Previously Aspirin induced asthma
• Starts with nasal congestion and anosmia, and progress to chronic
rhinosinusitis with nasal polyps that regrow rapidly after surgery.
• Asthma and hypersensitivity to aspirin and NSAIDs develop
subsequently
• Following ASA ingestion or NSAID an AAA develops within minutes
to 1-2 hrs
• Usually accompanied by rhinorrhea, nasal obstruction, conjunctival
irritation, scarlet flush of head and neck,then to severe
bronchospasms , shock,LOC and respiratory arrest

37. Management of acute exacerbations
• May be the first presentation
• Focused clinical assessment to determine severity
• Vital signs is a must
• Mainstay of treatment include assess need for o2, use inhaled or
nebulized BD and systemic cortosteroids
• Non responders: second line therapy: Parenteral magnesium
sulphate, salbutamol or aminophylline in an ICU setup
• Fllup within 48-72 hrs of discharge
• Discharge with asthma action plan

38. • Change in patients usual status characterised by increase
in symptoms of SOB , cough, wheezing or chest tightness
unresponsive to usual effective therapy and which may
necessitate care in emergence room or hospital ward

39. Goals of treating asthmatic attack
• Rapid alleviation of hypoxia
• Relieve airway obstruction
• Prevent worsening
• Prevent relapse
• Restore lung function to normal or previous best

40. Relieving symptoms
• Beta adrenoceptor agonist: salbutamol,fenoterol,
terbutaline,formoterol
• Anticholinergics :ipratropium , oxitropium
• Magnesium sulphate

41. • 5-10 puffs of SABA through pMDI and a volume spacer
• Admin with nebulizer should be reserved for severe
exacerbations esp those who appear exhausted, drowsy,
confused, silent chest. Always use oxygen as the driving gas
• Assess response every 15-30mins and repeat at similar intervals
until response is obtained
• Add anticholinergics if SABA not effective
• Iv aminophylline should be reserved for above treatment non
responders
• Adrenaline should be reserved for those who didn’t respond to
aminophylline
• IV Mgso4 as an adjuvant where usual treatment is not working
• Oral corticosteroids at 0.5-1mg/kg pdl upto 40mg max.For 5 days
or until 2 days after attack resolves

42. • Chest physiotherapy, mucolytics and mucokinetic agents,
cough mixtures and antihistamines are also not needed in
the management of patients with asthma attacks and may
in fact be dangerous.

43. Techniques
• Turbuhaler
• The diskus
• pMDIs

44. CHRONIC OBSTRUCTIVE PULMONARY DISEASE

45. • A heterogeneous lung condition characterized by chronic
respiratory symptoms (dyspnea, cough, sputum
production and/or exacerbations) due to abnormalities of
the airways (bronchitis,bronchiolitis) and/or alveoli
(emphysema) that cause persistent, often progressive,
airflow obstruction.

46. • Patients typically present with a combination of s/s of
chronic bronchitis, emphysema and reactive airway
disease
– Cough, usually worse in the mornings and productive of a small
amount of colorless sputum
– Breathlessness: The most significant symptom, but usually
does not occur until the sixth decade of life
– Wheezing: May occur in some patients, particularly during
exertion and exacerbations

47. PE
• Sensitivity of PE findings in mild-moderate COPD is
relatively poor
• Barrel chest
• Wheeze
• Diffuse decreased breath sounds
• Hyperesonance
• Prolonged expiration

48. COPD. chronic bronchitis or emphysema
Chronic bronchtis
• May be obese
• Cough with expectoration
• Use of accessory muscles
• Wheeze
• May be very thin with barrel chest
• Little or no cough or expectoration
• Pursed lips and use of accessory
muscles
• Hyperesonant and wheezing
• Distant heart sounds

49. Risk factors
• Gene environment interaction occurring over lifetime of
the individual that can damage the lungs and or alter their
normal development / aging process
• Main exposure: Tobacco smoking / inhalation of toxic
substances from household and outdoor
• Mutation of SERPINA1 gene
• Smoking in pregnancy –alter fetus lung growth

50. • Biomass exposure
• Occupational exposures : pesticides, inorganic dusts,
• Air pollution: Particulate matter, heavy metals, green
house gases
• Asthma
• Severe childhood respiratory infections –reduced lung
function in adulthood-particularly with P. aeruginosa
• Sex : changing trends in prevalence

51. • Iv drug use-pulmonary vascular damage resulting from
insoluble filler e.g. cotton fibers, talc , cellulose)
• Immunodeficiency syndromes
• Connective tissue disorders: Cutis laxa, marfan
syndrome , Ehlers-Danlos syndrome

52. • Presence of non fully eversible airflow obstruction
(FEV1/FVC < 0.7 post-bronchodilation) measured by
spirometry confirms the diagnosis of COPD

53. Pathophysiology
• COPD is characterized by increased numbers of macrophages in large airways, small
peripheral airways, lung parenchyma and pulmonary vessels, together with increased
activated neutrophils and increased lymphocytes.
• These inflammatory cells, together with epithelial cells and other structural cells release
multiple inflammatory mediators:-human leukocyte elastace, matrix metalloproteinases-
• which attract inflammatory cells from the circulation, amplify the inflammatory process,and
induce structural changes (via growth factors)

54. Structural changes
• There is compelling evidence for an imbalance in the
lungs of COPD patients between proteases derived from
inflammatory and epithelial cells that break down
connective tissue components and antiproteases that
counterbalance this action
• Repeated injury of the airway wall-excessive production of
muscle and fibrous tissue

55. • Airflow obstruction
• Hyperinflation-loss of elastic recoil and expiratory flow
obstruction
• Pulmonary gas exchange abnormalities V/Q mismatch
• Pulmonary hypertension
•

56. Dx
• A diagnosis of COPD should be considered in any patient
with dyspnea, chronic cough or sputum production, a
history of recurrent lower respiratory tract infections
and/or a history of exposure to risk factors for the
disease,
• but spirometry showing post- bronchodilator FEV1/FVC <
0.7 is mandatory to establish the Dx of COPD

57. C/F
• Typically complain of
– dyspnea, wheezing, chest tightness, fatigue, activity limitation,
and/or cough with or without sputum production,
– and may experience exacerbations: acute events characterized
by increased respiratory symptoms

58. • Small quantitity, tenacious Sputum
• Fatigue
• Weigh loss, muscle mass loss, anorexia-severe disease

59. Ddx
• Asthma
• Congestive heart failure
• Bronchiectasis
• Tuberculosis

60. Medical history
• ► Exposure to risk factors, such as smoking
and environmental exposures
(household/outdoor).
• ► Past medical history, including early life
events (prematurity, low birthweight,
maternal smoking during pregnancy, passive
smoking exposure during infancy), asthma,
allergy, sinusitis, or nasal polyps;
• respiratory infections in childhood; HIV;
tuberculosis.
• ► Family history of COPD or other chronic
respiratory disease.
• ► Pattern of symptom development: COPD
typically develops in adult life
• ► History of exacerbations or previous
hospitalizations for respiratory disorder.
• ► Presence of comorbidities, such as heart
disease, osteoporosis, musculoskeletal
disorders, anxiety and
• depression, and malignancies that may
also contribute to restriction of activity.
• ► Impact of disease on patient’s life,
including limitation of activity, missed work
and economic impact, effect on family
routines, feelings of depression or anxiety,
wellbeing, and sexual activity.
• ► Social and family support available to the
patient.
• ► Possibilities for reducing risk factors,
especially smoking cessation

61. Role of spirometry in COPD
• Diagnosis
• Assessment of severity
• Followup

62. GOLD grades and severity of airflow obstruction in
COPD (based on post-BD FEV1)
In COPD FEV1<70%
• GOLD 1 mild FEV1 >80% predicted
• GOLD 2 moderate 50 %- 80%
• GOLD 3 Severe 30%- 50% predicted
• GOLD 4 very severe <30% predicted

63. Prevention
• Reduce exposure to risk
• Smoking cessation
• Household and outdoor air pollution
• Vaccinations :cov2, etc

64. Pharmacological treatment
Refer to GOLD 2023 guidelines
– Dyspnoea scale (mMRC) table 2.7
– CAT assessment figure 2.2

65. Refer to GOLD 2023 guidelines
– Gold ABE tool figure 2.3
– Algorithms for the assessment, initiation and follow-up management of pharmacological
treatment. “Initial pharmacological treatment figure4.2”

66. • Group A: LABA preferably, or SABA if very occasional
breathlessness
• Group B:
• Cochrane systematic review and network meta-analysis comparing dual
combination therapy versus mono long- acting bronchodilators showed that the
LABA+LAMA combination was the highest ranked treatment group to reduce COPD
exacerbation

67. • Use of LABA-ICS in COPD is not encouraged. If there is
an indication for an ICS, then LABA+LAMA+ICS has been
shown to be superior to LABA+ICS and is therefore the
preferred choice (esinophil >300c/ul
• Short acting rescue BD should be prescribed to all for
immediate symptom relief
• If COPD patients have asthma, they should be treated as
asthma (ICS)

68. ECOPD
• On monotherapy BD? Escalate to LABA+LAMA
• Further exacerbations? Escalate to LABA+LAMA+ICS
• Further exacerbations?
– Add roflumilast
– Add macrolide

69. • COPD , no features of asthma and well controlled on
LABA/ICS? Ct mx. If they have exacerbations
– Eosinophils>100c/ul: LABA+LAMA+ICS
– Eosinophil <100c/ul: LABA+LAMA

70. • Followup on response
• Chest physiotherapists

71. • long-term oxygen therapy:
– for patients with a PaO2 of less than 55 mm Hg
– a PaO2 of less than 59 mm Hg with polycythemia, or cor
pulmonale
– Maintain PaO2 @ 60-65mmhg

72. BRONCHIOECTASIS

73. • Common disease
• Usually sec to infectious process
• Leading to abnormal and permanent distortion of one or
more of bronchi
• Can be categorised as COPD manifested by inflamed and
easily collapsible airways
• Leads to airflow obstruction, sob,impaired clearance of
secretions and occasional haemoptysis

74. • Usually focal process involving a lobe, a segment or a
subsegment of the lung
• Its rarely diffuse involving both lungs, as such most often
in association with systemic disease such as cystic
fibrosis and/or sinopulmonary disease

75. • Antibiotics and chest physiotherapy are the mainstay Rx
modalities.
• Additional mx of underlying conditions
• Sx is an adjunct therapy

76. Pathophysiology
• Abnormal dilatation of the proximal and medium sized
bronchi
• Acquired, congenital
• Caused by weakening and destruction of the muscular
and elastic components of bronchial wall
• Transmural inflammation, edema, scarring and ulceration

77. • Acquired is due to an infection, drainage impairment,
airway obstruction, and or defect in host defense
• Tissue also destroyed by neutrophilic
proteases,cytokines,NO, free O2 radicals
• Impaired secretion clearance
• Colonization and infection
• Purulent expectorations
• Vicious cycle

78. Etiology
• Primary infections
• Bronchial obstruction
• Aspiration
• Cystic fibrosis
• Primary ciliary dyskinesia
• Allergic Broncho-Pulmonary
Aspagillosis
• Immunodeficiency states
• Congenital anatomic defects
• A1ATD
• Idiopathic inflammatory diseases
• Toxic gas exposure
• Autoimmune disease

79. • Primary infections typical offending
organisms
– Klebiella spp
– Staph aureus
– MTB
– M pneumoniae
– Virus Measles, pertusis,influenza,
herpes simplex, adenovirus
Bronchial obstruction:
– Endobronchial tumors
– Broncholithiasis
– FB aspiration
– Right middle lobe syndrome-abnormal
angulation of the lobar bronchus at its
origin

80. • Young syndrome- bronchioectasis
and obstructive azoospermia
• ABPA- a hypersensitivity reaction to
inhaled Aspergillus antigen.
Suspect in productive cough who
also have a long hx of asthma type
like symptoms that do not respond
to conventional therapy
Congenital anatomic defects
• Williams-Campbell
syndrome:congenital cartilage
deficiency from lobar to 2nd
generation segmental airways
• Mounier-Kuhn
syndrome(tracheobronchomegally)-
dilatation of the trachea and bronchi
• Yellow nail syndrome –exudative
pleural effusions

81. Autoimmune diseases
• RA
• Sjogren syndrome
• Ankylosing spondylitis
• SLE
• Inflammatory bowel disease
• Sarcoidosis
• Marfan syndrome-weakness of the
CT
AD-PCK: Is a ciliopathy
• Traction bronchioectasis: distortion
of the airways sec to mechanical
traction of the bronchi from fibrosis
of the surrounding lung
parenchyma
• Toxic gases esp chlorine and
ammonia

82. CF
• History: Cough and daily
mucopurulent sputumlasting
months to years
• Dry bronchiectasis: A rare variant.
Presents as episodic haemoptysis
with little to no sputum. Usually a
sequalae of TB and is found in
upper lobes
• Total daily sputum:
– <10ml-mild
– 10-150 moderate
– >150ml severe
• Hemoptysis occurs in 56-92% of
bronchioectasis. Mild
• Dyspnoea
• Wheezing
• Pleuritic chest pains
• Fatigue -73%
• Weight loss-increased caloric
needs
• Fever-acuteinfection
• Urinary incontinence esp in women
?cause

83. PE
• Wheeze and crepts -73%
• Digital clubbing-2-3%
• Cyanosis
• Wasting
• Weight loss
DDX
• A1ATD
• Aspiration pneumonia
• Asthma
• Bronchitis
• Copd
• Emphysema
• GERD
• TB

84. Workup
• HRCT scan
• Sputum analysis
• CBC: Anaemia, high WBC,
Eosinophilia?ABPA, Polycythemia
• A1ATD
• Autoimmune screening
• PFT: usually unresponsive to BD
• Bronchoscopy
• Radiography: PA and Lateral in all
patients
• Electron microscopy- ciliary
dyskinesia

85. Rx
GOAL
• Improve symptoms
• Reduce complications
• Control exacerbations
• Reduce morbidity and mortality
• Antibiotics and Chest physiotherapy
• BD
• Dietary supplementation
• Oxygen and surgical therapies
•

86. Acute exacerbations? Give
antibiotics 7-10/7
• Amoxicillin
• Cephalosporin: 2nd gen
• Fluoroquinolones
Moderate to severe: Iv
antibiotics
• Aminoglycosides
• 3rd gen cephalosporin
• Fluoroquinolones
• Inhaled Tobramycin is the doc in
pseudomonas spp
MAC in bronchiectasis?
• 3-4 drug treatment regimen with
clarithromycin/rifampin/ethambutol/
streptomycin 18-24 months

87. Supportive treatment
• Smoking
• Second hand smoke
• Adequate nutrition
• Immunization

88. Bronchial hygiene
• Postural drainage and percussion
• Devices to assist mucus clearance:
incentive spirometry
• Nebulization with7% Nacl-
• Mucolytics not universally beneficial
• Hydration to maintain viscidity of
secretions
• Bronchodilators, including beta-
agonists and anticholinergics, may
help patients with bronchiectasis,
presumably reversing
bronchospasm associated with
airway hyperreactivity and
improving mucociliary clearance.
• High-quality, large, randomized
clinical trials of bronchodilator
treatment in bronchiectasis have
not been performed.
• Surgical consideration

89. Gidelines by european respiratory society
Minimun set of tests:
• CBC
• ABPA
• Treat exacerbation with 10-14/7
course antibiotics
• Inhaled corticosteroids not
suggested unless in asthma or
COPD
• Long term antibiotic rx for
bronchiectasis with 3 and above
exacerbations
• P aeruginosa: inhaled antibiotic
• No response or CI , not tolerated?
Azithromycin/erythromycin
• Macrolides even if no
pseudomonas
• Resp physiotherapy 1-2x/week

90. OSA

91. • Read and make notes on Obstructive sleep apnea