Asthma and COPD

ASTHMA AND COPD
Assistant Professor Carmen Elena Pleşoianu, MD, PhD, FESC

Life long learner
Neuroplasticity
”Neurons that fire together, wire together”
Life long learner
Neural net = Safety net

AGENDA
I. GENERAL DATA
II. PHYSIOPATHOLOGY
III. DIAGNOSTIC
IV. MANAGEMENT
Asthma - definition
• chronic inflammatory disease of the airways of unknown etiology

• characterized by distinct components:
1. recurrent episodes of airway obstruction - resolves spontaneously
/ result of treatment
2. airway hyperresponsiveness = exaggerated bronchoconstrictor response to
stimuli that have little or no effect in normal subjects
• Pathology: diffuse narrowing of the airways, reversible spontaneous/

treatment
• Clinical manifestations: paroxysmal dyspnea + wheezing + coughing
Asthma - epidemiology & burden of disease
• extremely common disorder

• Incidence 4 -5 % → ≥10% (in adult population)
• onset at any time throughout life (most cases < 40 years)
• boys > girls; women slightly > men
• “industrialized” lifestyle → greatest incidence
Asthma - classification
• Extrinsic asthma after exposure to a specific (known) allergen

- personal / family history of allergy
- skin testing
- IgE ↑ in serum
- + reaction to provocation tests (antigen inhallation)
• Intrinsic asthma no identifiable reason
I. Mild Intermitent ≤1 attack/w

II. Mild Persistent >1 attack/w, <1/day
III. Moderate Persistent daily attacks
IV. Sever Persistent continual daytime
symptoms
Risk factors and triggers
1. Allergens (pneumallergens: house dust mites - main species are

identified as Dermatophagoides, pollen, mold spores, animal
allergens; etc)
2. Farmacological stimuli
- aspirin-exacerbated asthma (+NSAIDs)
- Beta-blockers
- bisulfite food additives
3. Environmental stimuli and pollutants
(smoke, odors, cold air, weather….)
4. Occupational allergens (Occupational A: isocyanates, anhydrides,
amines, metals, drugs, plastics, dyes: spray painting, foundry,
manufacturing, chemical, etc)
5. Infections
6. Effort (exercise-induced asthma)
7. Emotional Stress
AGENDA
I. GENERAL DATA
II. PHYSIOPATHOLOGY
III. DIAGNOSTIC
IV. MANAGEMENT
Pathology
Airway obstruction induced
by:
1. smooth muscle constriction

(most widely accepted explanation for the acute
reversible airway obstruction)
2. edema and hyperemia of

the mucosa (airway wall is
thickened)
3. hyperviscous mucus (thick,

sticky)
↓
↑ resistance to airflow → abnormalities in arterial blood gas

(exp>insp) composition (hypoxemia = low arterial PO2 &
hipocapnia = low arterial PCO2)
Pathology
1. Tonicity of the
bronchal smooth
muscle = maintained by
the balance between br-
constriction and br-
dilation (Ca pump)
2. Airway
hyperresponsiveness =
exaggerated
bronchoconstrictor
response to stimuli that
have little or no effect in
normal subjects
Pathology
1. Allergy
• Immune type I response
(immediate) by specific
stimulation (antigen) / non-
specific (nonimmunological) of
the IgE on the surface of
Mastocytes → degranulation →
mediators of inflammation (H,
serot, bradik, leucotriene)
→ br-constriction + edema and
hyperemia of the mucosa ±
mucus
• Immune type III response

Pathology
2. Chronic inflammation of the submucosa
The chronic airway narrowing (airway wall remodeling) that occurs in
many patients with asthma likely results from the actions of
inflammatory cells in the asthmatic airway.
- inflammatory cells: Mast cells, Eosinophils, Lymphocites

(TH2 phenotype)
- inflamatory mediators:
• cytokines (interleukin-4, -5, -13)
• Histamine (Mast cells)
• Leukotrienes (Mast cells, Eosinophils, alveolar
macrophages)
Mediators of the Acute Asthmatic Response: Acetylcholine, Histamine,

Leukotrienes
AGENDA
I. GENERAL DATA
II. PHYSIOPATHOLOGY
III. DIAGNOSTIC
IV. MANAGEMENT
Diagnosis - clinical manifestations
A = episodic disease, asymptomatic between crises
• Typical: short crisis (min-h), patient seems to recover completely after

an attack
• 3 Elements: 1. dyspnea – acutely onset

2. wheezing
3. cough
• Personal atopic history (rhinitis, conjunct)
• Identification of a provoking stimulus through careful questioning
helps establish the diagnosis of asthma and may be therapeutically
useful if the stimulus can be avoided.
Diagnosis - physical examination
• Rapid respiratory rate = 25 - 40/min,
exp>insp
• Prolonged expiration + Wheezing
• accessory muscles
• hyperinflated chest, hyperresonance
• Wheezing, rhonchi = suggestive of

free secretions in the airway lumen (!!!
The absence of breath sounds → severe airflow
obstruction)
• Cyanosis = hypoxia, late, severe

Physical examination - status asthmaticus
• severe state, > 24 h, refractory to bronchodilatatory

• life threatening by duration & gravity
• causes: - respiratory infection
- inhalatory sympathomimetics abuse
- sudden stop of CS
- psychological factors
• Anxiety, cianosis, tahycardia
• Extreme thoracic distension (thorax blocked in insp)
• Prolonged expiration
• MV ↓
• Dyspnea ↓ as PaCO2 ↑
• Severely modified gas exchange: hypoxemia, hypercapnia, respiratory
acidosis → metabolic
• Heart: tahycardia, RV hypertrophy, paradoxical pulse
Diagnosis: laboratory findings
• Pulmonary function
findings
Obstructive Ventilatory
Defect
(↓FEV1, ↓FVC, ↑RV)
- reversibility after broncho-
dil
(≥12% increase FEV1) =
“bronchodilator response”
Patient undergoing a SPIROMETRY

• Sputum:
macroscopy – clear/opaque, viscous
microscopy (Gram-stained and Wright-stained sputum
smear)– E, Charcot-Leyden crystals, Curshmann spirals, Creola bodies;
PN, bact.
• Chest radiography
normal/hyperinflation/
complications
• Arterial blood gases (ABG)
hypoxemia and hypocapnia + respiratory alkalemia
Normal CO2 + metabolic acidosis = severe obstruction, overcoming of

compensatory mechanisms
• Other blood findings
- blood eosinophilia
- ↑serum levels of immunoglobulin E (IgE)
• EKG
- sinus tachycardia
- +/- right axis deviation, right bundle branch block (~P pulmonale~)
Differential Diagnosis
• Cardiac asthma
• Chronic bronchitis
• Spontaneous pneumothorax
• Pulmonary embolism
• Carcinoid syndrome
• Laryngeal/ tracheal obstruction
• Hyperventilation
Complications
• Pneumothorax
• Pneumonia (infection of the lungs)
• a collapse of part or all of the lung.
• respiratory failure
• status asthmaticus (severe asthma attack that do not
respond to treatment)
AGENDA
I. GENERAL DATA
II. PHYSIOPATHOLOGY
III. DIAGNOSTIC
IV. MANAGEMENT
Treatment - goals
• Control of symptoms = ↓resistance to airflow
• Prevention of exacerbations =
Allergen Removal + Desensitization
Vaccination against seasonal influenza and
pneumococcal disease is recommended in patients with
asthma.
Treatment
• Symptomatic treatment = ↓ resistance to airflow
1. For acute asthmatic airway obstruction (asthma attack

treatment)
2. Controller treatments (prevent acute airway narrowing)
between the attacks
Treatment
I. Bronchodilator drugs
II. Antiallergic drugs
III. Corticosteroids
IV. fluidifiant and expectorant drugs
V. ATB
VI. Immunotherapy
- the “desensitization” therapies = Allergen immunotherapy
- Monoclonal Antibody Treatment
Treatment
V. ATB
VI. Immunotherapy
B2 agonists
= adrenalin derivates
Action: ↑AMPc
Classification:
• short-acting beta agonists (SABAs)*: effect onset in 5-15’→Δt=4-6h)
SALBUTAMOL (ALBUTEROL)
FENOTEROL
TERBUTALINA
• long-acting beta agonists (LABAs)**: 9-12 h
SALMETEROL – albuterol derivate
FORMOTEROL
BAMBUTEROL
*inhalers – 1-2 puffs every 4-6 h, ≤ 8 puffs/d
**Inhalers – 1-2 puffs every 12 h
beta2 agonists
Anticholinergics
= atropin derivates
Action: ↓ GMPc
Preparate:
IPRATROPIUM BROMID (Atrovent)
TIOTROPIUM BROMID (Spiriva)
Prevent cholinergic mediated bronchoconstriction

Metered dose inhaler, 2puffs every 4-6 h
Methylxanthines
= teophylline derivate
Action: bronchodilation by phosphodiesterase inhibition →↑cAMP
AMINOFILINA = ethylene-diaminated teophylline
tb 100 mg, tb. Retard 200, 250, 300 mg
f 240 mg
Adm: iv 6mg/kg in 20 min….piv 0,2-0,9mg/kg/h
po every 6-8 h (≤10 mg/kg/zi)
Toxicity - plasma levels for therapeutic effects 10 - 20 μg/mL
Theophylline has anti-inflammatory, immunomodulatory, and bronchoprotective

effects that potentially contribute to its efficacy as a prophylactic anti-asthma drug
Treatment
V. ATB
VI. Immunotherapy
Antiallergic drugs
• Inh. of mast cell degranulation (mbr. stabilizers):

SODIUM CROMOGLICATE (Intal, Lomudal)
NEDOCROMIL (Tilade)
• Antileukotrienes:
ZILEUTRON (Zyflo), MONTELUKAST
Treatment
V. ATB
VI. Immunotherapy
Corticosteroids
Beneficial effects by multiple mechanisms:

Reduction of inflammation in the bronchial wall
Stabilizes lysosomal membrane
↓the histamine and leukotriene deposits in cells
↓ the no. of active inflammatory cells from the bronchial wall
Indications
1. Asthma attack
2. Long - term control
3. Bronchial hypersecretion + obstruction
Corticosteroids
• iv: HHC: 2-4 mg/kg….3 mg/kg/6 h

Methyl-Prednisolon (Solu-Medrol): 125mg/6 h
Δt = 24-72 h
• po: PDN 40-60 mg/d (x1 or x 2/d = 2/3+1/3)
Δt = 4-7 days……↓tapered to zero during 7 - 14 d.
patients who cannot stop taking steroids = 5-20mg/zi (alternate-day
administration of oral steroids is preferable to daily treatment)
• inhaled steroids: BECLOMETHASONE, BUDESONIDE,

FLUTICASONE, BETAMETHASONE…. 1-2 puf x 4/d
Monoclonal Antibody Treatment
• = form of immunotherapy that uses monoclonal antibodies (mAb)

to bind monospecifically to certain cells or proteins
• Omalizumab = humanized murine monoclonal antibody that binds

circulating IgE, associated with decreased serum
free (not total) IgE levels
Adm: a monthly subcutaneous dose
• Mepolizumab = humanized monoclonal antibody directed against
IL-5
Adm: a monthly subcutaneous dose
Treatment
Asthma medications - generally divided into two categories:
1. Quick relief (reliever medications)
2. Long-term control (controller medications)

Treatment – quick relief medications
- used to relieve acute asthma exacerbations and to prevent exercise-

induced bronchoconstriction (EIB) symptoms
1. short-acting beta agonists

2. Aminophylline (iv)
3. systemic corticosteroids (which speed recovery from acute
exacerbations)
Treatment – long-term control medications
1. long-acting beta agonists

2. inhaled corticosteroids
3. long-acting anticholinergics
4. Methylxanthines
5. leukotriene receptor antagonists
6. combination inhaled corticosteroids and long-acting beta agonists

Treatment – crisis
• Mild attack:
β2 sympathomimetic inhaler 1-2 puffs - may be repeated after 15’
• More severe attack – no normalization inhaled β2 sympathomimetic
MYOFILIN iv 6 mg/kg in 20' + HHC 3 mg/kg
• Persistence of dyspnoea → the patient is hospitalized
MYOFILIN piv 0.2-0.9 mg/kg/h (≤10 mg/kg/day)
+
HHC iv 3 mg/kg every 6 hours or Methyl Prednisolone 125 mg every 6 h
Treatment – status asthmaticus
Status Asthmaticus = medical emergency → intensive care admission
• Oxygen therapy on mask/ nasal tube assisted ventilation (IOT)

• MYOPHILIN piv
• Corticosteroids iv high doses (e.g. HHC ≤ 1000mg/day)
• ADRENALINE sc
• Antibiotics - broad spectrum, iv
• Hydration of the patient
• Monitoring: ECG, BP, FR, SaO2, diuresis
Treatment – steps
ICS = inhaled corticosteroid

LABA = long-acting beta2 agonist
LTRA = leukotriene receptor antagonist
OCS = oral corticosteroid
Chronic obstructive pulmonary disease
(COPD)
GLOBAL INITIATIVE FOR CHRONIC OBSTRUCTIVE LUNG DISEASE (GOLD):
TEACHING SLIDE SET

2021
This slide set is restricted for academic and educational purposes only.
Use of the slide set, or of individual slides, for commercial or
promotional purposes requires approval from GOLD.
© 2020 Global Initiative for Chronic Obstructive Lung Disease

FEV1= Forced Expiratory
Volume in one second –
how much air a person can
exhale forcefully in one
second after taking a deep
breath

FEV1 = Forced Expiratory Volume in one second = how much air a person can exhale forcefully in one second after taking a deep breath
FVC = Forced Vital Capacity = the maximum amount of air a person can exhale forcefully and completely after taking a deep breath
* MRC Dyspnea Scale= Modified British Medical Research Council Dyspnea Scale

SABA = Short - Acting Beta 2 Agonists
LABA = Long - Acting Beta 2 Agonists
SAMA = Short - Acting Anticholinergics
LAMA = Long - Acting Anticholinergics
ICS = Inhaled Corticosteroids

SABA = Short - Acting Beta 2 Agonists
LABA = Long - Acting Beta 2 Agonists
SAMA = Short - Acting Anticholinergics
LAMA = Long - Acting Anticholinergics
SABA = Short - Acting Beta 2
Agonists
LABA = Long - Acting Beta 2
Agonists
SAMA = Short - Acting
Anticholinergics
LAMA = Long - Acting
Anticholinergics

Life long learner
Neuroplasticity
”Neurons that fire together, wire together”

Asthma and COPD

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ASTHMA AND COPD

Assistant Professor Carmen Elena Pleşoianu, MD, PhD, FESC

Neural net = Safety net

• chronic inflammatory disease of the airways of unknown etiology

• Pathology: diffuse narrowing of the airways, reversible spontaneous/

• extremely common disorder

• Extrinsic asthma after exposure to a specific (known) allergen

I. Mild Intermitent ≤1 attack/w

1. Allergens (pneumallergens: house dust mites - main species are

1. smooth muscle constriction

2. edema and hyperemia of

3. hyperviscous mucus (thick,

↑ resistance to airflow → abnormalities in arterial blood gas

• Immune type I response

• Immune type III response

- inflammatory cells: Mast cells, Eosinophils, Lymphocites

Mediators of the Acute Asthmatic Response: Acetylcholine, Histamine,

A = episodic disease, asymptomatic between crises

• Typical: short crisis (min-h), patient seems to recover completely after

• 3 Elements: 1. dyspnea – acutely onset

• Prolonged expiration + Wheezing

• hyperinflated chest, hyperresonance

• Wheezing, rhonchi = suggestive of

• Cyanosis = hypoxia, late, severe

• severe state, > 24 h, refractory to bronchodilatatory

Patient undergoing a SPIROMETRY

Normal CO2 + metabolic acidosis = severe obstruction, overcoming of

• Other blood findings

• Control of symptoms = ↓resistance to airflow

• Symptomatic treatment = ↓ resistance to airflow

1. For acute asthmatic airway obstruction (asthma attack

Prevent cholinergic mediated bronchoconstriction

Toxicity - plasma levels for therapeutic effects 10 - 20 μg/mL

Theophylline has anti-inflammatory, immunomodulatory, and bronchoprotective

• Inh. of mast cell degranulation (mbr. stabilizers):

Beneficial effects by multiple mechanisms:

• iv: HHC: 2-4 mg/kg….3 mg/kg/6 h

• inhaled steroids: BECLOMETHASONE, BUDESONIDE,

• = form of immunotherapy that uses monoclonal antibodies (mAb)

• Omalizumab = humanized murine monoclonal antibody that binds

Asthma medications - generally divided into two categories:

1. Quick relief (reliever medications)

2. Long-term control (controller medications)

- used to relieve acute asthma exacerbations and to prevent exercise-

1. short-acting beta agonists

1. long-acting beta agonists

6. combination inhaled corticosteroids and long-acting beta agonists

Status Asthmaticus = medical emergency → intensive care admission

• Oxygen therapy on mask/ nasal tube assisted ventilation (IOT)

ICS = inhaled corticosteroid

TEACHING SLIDE SET

© 2020 Global Initiative for Chronic Obstructive Lung Disease

© 2020 Global Initiative for Chronic Obstructive Lung Disease

© 2020 Global Initiative for Chronic Obstructive Lung Disease

© 2020 Global Initiative for Chronic Obstructive Lung Disease

© 2020 Global Initiative for Chronic Obstructive Lung Disease

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