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Cardiorespiratory > 9-asthma > Flashcards

9-asthma Flashcards

1
Q

what s the asthma?

A

A chronic inflammatory disease of the respiratory system characterized by bronchial hyperresponsiveness, episodic exacerbation (asthma attacks), and reversible airflow obstruction. Manifests with reversible cough, wheezing, and dyspnea.

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2
Q

the obstruction of asthma is due to a combination of what 3 factors?

A
  1. Mucosal inflammation with inflammatory cells, (eosinophils, mast cells and Th2 lymphocytes)
  2. Neural hyperresponsiveness
  3. Smooth muscle hypertrophy and thickening of the basement membrane, the space below the epithelium
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3
Q

how mucosal inflammation seen in asthma occurs?

A

Overexpression of Th2-cells → inhalation of antigen results in production of cytokines (IL-3, IL-4, IL-5, IL-13) → activation of eosinophils and induction of cellular response (B-cell IgE production) → bronchial submucosal edema and smooth muscle contraction → bronchioles collapse

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4
Q

what is the pathophysiology of asthma?

A
  • Inflammation of the airways with eosinophils, mast cells and lymphocytes
  • This immune dysregulation is driven by pollution, allergens and viruses
  • The inflammation leads to loss of the epithelium: ↑ mucus and bronchoconstriction (narrowing of the airway)
  • Intermittent/ episodic
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5
Q

asthma is drive by TH2 or TH1?

A

Asthma is generally characterized as an inflammatory disease driven by T-helper type 2 (Th2-cell) that manifests in individuals with a genetic predisposition

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6
Q

what are the typical features of inflammation seen in asthma?

A

The inflammation has typical features of an allergic response, such as the thickening of the basement membrane and the detection of eosinophils.

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7
Q

what level of the bronchial tree is mainly affected in asthma?

A

symptoms are primarily caused by inflammation of the terminal bronchioles, which are lined with smooth muscle but lack the cartilage found in larger airways.

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8
Q

endobronchial obstruction of asthma is caused by?

A
  • -Bronchospasm
  • -Mucosal edema
  • -Hypertrophy of smooth muscle cells
  • -Increased mucus production
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9
Q

what is the specific pathophysiology of allergic asthma

A

IgE-mediated type 1 hypersensitivity to a specific allergen; characterized by mast cell degranulation and release of histamine after a prior phase of sensitization

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10
Q

what is the specific pathophysiology of non-allergic asthma?

A
  • -Irritant asthma: irritant enters lung → ↑ release of neutrophils → submucosal edema → airway obstruction
  • -Aspirin-induced asthma: NSAID inhibition of COX-1 → ↓ PGE2 → ↑ leukotrienes and inflammation → submucosal edema → airway obstruction
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11
Q

what are the 2 principles of asthma treatment?

A
  1. Reduce inflammation (anti-inflammatory)

2. Open the airways(bronchodilation)

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12
Q

maintenance therapy of asthma consist of?

A

Inhaled corticosteroids (anti-inflammatory drugs) given by inhalers
e.g. Beclomethasone, budesonide, fluticasone
These are usually given along with Long-acting bronchodilator therapy
Long-acting β2 agonists (LABA) e.g. Salmeterol, formoterol

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13
Q

examples of long-acting β2 agonists

A

Salmeterol, formoterol

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14
Q

examples of inhaled glucocorticoids?

A

Beclomethasone, budesonide, fluticasone

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15
Q

what is the MOA of steroids in asthma?

A
  • -reduce mucous production by goblet cells
  • -restore epithelial cell growth
  • -increases numbers of beta receptors
  • -inhibits recruitment of inflammatory cells and reduce bronchial hyperactivity
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16
Q

acute symptoms of asthma are treated by what medications?

A
  • Inhaled short acting β2 agonists e.g. Salbutamol, Terbutaline
  • Inhaled anticholinergics e.g. Ipratropium
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17
Q

how anticholinergic drugs work in asthma?

A

inhibit Ach binding to muscarinic (M3) receptors

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18
Q

what are the symptoms of asthma?

A

• Cough (often nocturnal)
• Wheeze (intermittent)
• Shortness of breath (reversible)
• Typically the first onset in childhood
• A strong relationship with rhinitis and eczema (allergy
Persistent, dry cough that worsens at night, with exercise, or on exposure to triggers/irritants (e.g., cold air, allergens, smoke)
End-expiratory wheezes
Dyspnea
Chest tightness
Chronic allergic rhinitis with nasal congestion

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19
Q

what is the characteristic feature of cough of asthma

A

Persistent, dry cough that worsens at night, with exercise, or on exposure to triggers/irritants (e.g., cold air, allergens, smoke)

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20
Q

why the cough of asthma is worse at night?

A
  • Plasma adrenaline levels decrease 4 am
  • Plasma cortisol levels decrease 12 am
  • Nocturnal symptoms 2-3 am
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21
Q

what should be asked to reveal PMHx of a patient suspected to have asthma?

A
  • When was asthma diagnosed?
  • By whom? And How?
  • Impact of asthma
  • Progression over time
  • Days off work or school/ annum
  • Precipitating factors
22
Q

what are the common side effects of medications used in asthma?

A
  • Inhaled corticosteroids - oral candidiasis
  • β-agonists - tremor, palpitations, muscle cramps
  • Oral steroids – obesity, striae, myopathy, glaucoma, osteoporosis, PUD, diabetes, bruising
23
Q

on physical examination to what parameters attention should be kept?

A 
General inspection
•	Resp distress, accessory muscles, position
•	Speech
Vital Signs
•	RR
•	Peak flow
•	PR/ BP/ Pulses paradoxus
24
Q

what is the pulsus paradoxus

A

A physical examination finding in which there is a pathologic decrease (> 10 mm Hg) in systolic blood pressure during inspiration. Classically associated with cardiac tamponade and constrictive pericarditis, but can also be seen in noncardiac conditions (e.g., massive pulmonary embolism, hemorrhagic shock, obstructive sleep apnea, obstructive lung disease).

25
Q

what outpatient examinations should be done on a patient with asthma

A

1)Pulmonary function testing
• Spirometry (maybe normal when a patient is asymptomatic)
• Reversibility (pre and post bronchodilation - >15% improvement))
• Exercise testing (when symptoms are only exercise-related)
• Histamine challenge test (when spirometry is normal and the diagnosis isn’t clear)
2)CXR
3)Skin testing
4)Eosinophils
5)IgE/ RAST (to common antigens – HDM, dog, cat, aspergillus)

26
Q

what are the findings on the clinical examination of a patient with an asthma attack?

A

1) Auscultation (characteristic findings are usually only present during acute attacks)
- -Prolonged expiratory phase with wheezing (dry crackles)
- -Decreased breath sounds; possibly “silent chest”
- -Tachypnea
2) Percussion
- -Hyperresonant sound
- -Inferior displacement and poor movement of the diaphragm
3) In severe attacks
- -Altered level of consciousness
- -Cyanosis

27
Q

what is the inhaler Compliance Assessment (INCA) device

A

The Inhaler Compliance Assessment (INCA) device consists of a microphone, a battery, a memory card, an electronic real time clock and a microprocessor for recording audio when the patient uses their inhaler.

28
Q

So why do people not take their medicines?

A
  • Barriers
  • Beliefs
  • Comprehension
29
Q

what is the cough variant asthma?

A
  • -A form of asthma in which the predominant symptom is chronic, dry cough
  • -Other characteristic symptoms of asthma (e.g., wheezes, congestion, dyspnea) are absent.
30
Q

does characteristic findings on clinical examination present between asthma attacks?

A

no

31
Q

what is the first-line diagnostic test for asthma confirmation?

A

Pulmonary function testing (spirometry)

  • -First-line diagnostic test for confirmation of the diagnosis in patients ≥ 5 years of age.
  • -Shows signs of obstructive lung disease with increased airway resistance → ↓ FEV1, ↓ Tiffeneau index (FEV1/FVC ratio)
  • -Obstruction is reversible with bronchodilators → diagnostic confirmation via post-bronchodilator test
32
Q

what is the post-bronchodilator test?

A

A test used to distinguish asthma from other obstructive lung diseases if spirometry reveals findings of obstructive lung disease.Unlike in cases of COPD, obstruction in asthma is reversible with administration of bronchodilators and results in an increase of FEV1 of at least 12% and 200 mL from baseline.

33
Q

what is the methacholine challenge test?

A

Second-line diagnostic test if pulmonary function testing is nondiagnostic
Evidence of bronchial hyperresponsiveness after inhalation of methacholine
Positive if FEV1 reduced ≥ 20%

34
Q

chest X-ray in asthma is characteristic of?

A

1) Usually only indicated in patients with severe asthma to exclude differential diagnoses (e.g., pneumonia, pneumothorax)
2) Normal in mild cases
3) Signs of pulmonary hyperinflation in cases of severe asthma
- -Low, flattened diaphragm
- -Wide intercostal spaces
- -Barrel chest

35
Q

pulse oximetry and ABG in asthma are characterized by

A
  • -Blood gas analysis should be performed if oxygen saturation (SpO2) is < 94%.
  • -Findings on ABG
    1) Initially: ↓ pCO2, ↑ pH, ↓ pO2 leading to type 1 respiratory failure (A type of respiratory failure characterized by hypoxemia (↓ PₐO₂) and normocapnia or hypocapnia (↓ PₐCO₂) on arterial blood gas analysis.)
    2) Ultimately: severe respiratory distress: ↑ pCO2, ↓ pH, and ↓↓ pO2 leading to type 2 respiratory failure (A type of respiratory failure characterized hypercapnia (↑ PₐCO₂) and normoxemia or hypoxemia (↓ PₐO₂) on arterial blood gas analysis.)
36
Q

what are the characteristic lab findings in allergic asthma?

A
  • -Antibody testing, total IgE (increased), allergen-specific IgE (increased)
  • -CBC: possibly eosinophilia (This finding should raise suspicion of parasitic infection or Churg-Strauss syndrome.)
  • -Skin allergy tests: skin prick testing (SPT) or intradermal skin testing
37
Q

sputum sample of asthmatic patients is characteristic for?

A
  • -Curschmann spirals (whorled mucous plug in sputum that is formed by shed bronchial epithelium)
  • -Charcot-Leyden crystals (histopathologic finding in patients with eosinophilic inflammation and/or proliferation)
  • -and/or Creola bodies (aggregate of desquamated epithelial cells)
38
Q

what is the causal treatment of asthma?

A
  • -Avoid triggers
  • -Allergen immunotherapy in allergic asthma
  • -Early treatment of infections in infection-triggered asthma
  • -If GERD is suspected: proton pump inhibitors
39
Q

what are the leukotriene pathway modifiers used in asthma?

A

1) Montelukast and Zafirlukast
- -Leukotriene receptor antagonists (LTRAs): prevent leukotrienes from binding to their receptors
2) Zileuton
- -Inhibits 5-lipoxygenase → ↓ production of leukotrienes

40
Q

what are the indications of leukotriene pathway modifiers?

A

Long-term maintenance treatment (particularly in children)

Exercise-induced and aspirin-induced asthma

41
Q

examples of muscarinic antagonists used in asthma?

A
  • -Short-acting muscarinic antagonists (SAMA): ipratropium bromide
  • -Long-acting muscarinic antagonists (LAMA): tiotropium bromide
42
Q

how muscarinic antagonists work?

A

Competitively inhibit postganglionic muscarinic receptors in bronchial smooth muscle → bronchodilation

43
Q

what biological agents are used in asthma?

A

Omalizumab

Mepolizumab

44
Q

how does omalizumab work?

A

Anti-IgE antibody that binds to serum IgE

  • -Reduced serum levels of IgE prevent binding of IgE to high affinity IgE receptor (FcεRI) on mast cells and basophils → The inflammatory cascade triggering asthma is inhibited.
  • -Long-term reduction in serum IgE levels will reduce surface expression of IgE receptor on mast cells and basophils.
45
Q

how does theophylline work?

A

Inhibits phosphodiesterase (PDE) → ↑ cAMP levels → anti-inflammatory and mild bronchodilatory effect

46
Q

why the use of theophylline is limited?

A

cardiotoxic, neurotoxic

47
Q

what mast cell stabilizers are used in asthma?

A

Cromolyn sodium

Nedocromil sodium

48
Q

what are the uses of mast cell stabilizers?

A

Preventive treatment prior to exercise or unavoidable exposure to known allergens in patients ≥ 5 years old

49
Q

LABA, leukotriene pathway modifiers, theophylline, mast-cell stabilizers, biological agents are effective during acute asthma attacks. True/False

A

False

50
Q

what are the general principles of asthma long term management?

A
  • -Reduce the number of asthma attacks → Medical therapy is escalated or de-escalated depending on the patient’s individual needs.
  • -Self-monitoring for patients: peak flow meter to measure peak expiratory flow rate (PEFR)
  • —-Patients can avoid exacerbations with frequent PEFR measurements: PEFR decreases before symptoms appear → indicates insufficient medication regimen
  • -Influenza and pneumococcal vaccines are administered in all patients
51
Q

what is the status asthmaticus?

A

1) Definition: extreme asthma exacerbation that does not respond to initial treatment with bronchodilators
2) Clinical features
- -Initially: orthopnea, tachypnea, tachycardia, and cyanosis
3) Signs of imminent respiratory arrest
- -Drowsiness/confusion
- -Paradoxical thoracoabdominal movement
- -Bradycardia
- -Absent wheezing
- -Pulsus paradoxus

Cardiorespiratory (24 decks)

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