wheezing and stridor Flashcards

1
Q

shortness of breath differential

A

lung cancer, asthma

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2
Q

clinical symptoms of copd

A

Dyspnea (at rest, with exertion)
Cough - with or without sputum
Wheezing
frequent chest illness/cold/bronchitis

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3
Q

Chronic inflammation of copd

A

Causes structural changes
Narrows small airways
Decreases lung elastic recoil

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4
Q

chronic bronchitis

A

chronic productive cough for 3 months in each of 2 successive years

Other causes of cough have been ruled out, may proceed or follow development of air flow limitiation obstruction

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5
Q

emphysema

A

pathologic term
Structural changes- Abnormal and permanent enlargement of airspaces distal to the terminal bronchioles, destruction of airspace walls without obvious fibrosis

Can be present in pts without air flow limitations

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6
Q

risk factors for copd

A

Host factors- Alpha 1 antitrypsin deficiency, airway hyperresponsiveness, lung growth impairment (low birth weight, childhood respiratory infections

Exposures- tobacco smoke, occupational dusts and chemicals, indoor airpollution, biomass fuels and ETs

Outdoor air pollution from inhaled particles, SES

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7
Q

Assessment of COPD

A

Symptoms- less symptoms or more symptoms based on modified medical research council dyspnea scale (mMRC) or COPD assessment test (CAT)

Grade of airflow limitation on post bronchodilator spirometry (low risk or high risk)

Number of exacerbations requiring a medication change (low risk or high risk)

Identification of comorbitidities that contribute to individual disease severeity

0- 4 (worst
Cat- 0 40(worst)

Airflow limitation
Grade 1 to 4 severe

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8
Q

Exacerbations

A

Acute events characterized by worsening of symptoms beyond normal-day to day variation and necessitating a change in medication (oral steroid and/or antibiotics)

Previous exacerbations predict future exacerbations

As airflow limitation worsens, exacerbation risk increases
Low risk of exacerbation <1 exacerbation/year and post-bronchodilator FEV1 >50% predicted

High risk of exacerbation >2 exacerbation/year and post bronchodilator FEV1<50 % predicted

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9
Q

treatment options for COPD

A
Self management education and smoking cessation
Bronchodilators
Inhaled corticosteroids
Pulmonary rehabilitation
Oxygen
Surgery
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10
Q

Drug names for COPD

A

Short acting B2 adrenergic agonists (SABA)- Albuterol

Short acting anticholinergic Antagonist- Ipratropium bromide

Long acting B2 adrenergic agonists (LABA)- salmeterol, formoterol

Long acting anticholinergic antagonist- tiotropium

Inhaled Corticosteroids- beclomethasone, fluticasone, and budesonide

Combined drugs- fluticasone/salmeterol, Budesonide/formoterol

Theophyllin (Tachycardia, many toxicity)
PDE4 inhibitor (roflumilast)

Other

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11
Q

managing acute exacerbations of COPD

A

Bronchodilators (SABA, short acting anticholinergic antagonists, combination)

Systemic corticosteroids- oral prednisone

Antibiotics- clinical improvement in pts with a moderate to severe exacerbation

Oxygen therapy

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12
Q

anticholinergics in COPD

A

anticholinergic drugs may be as effective as or even superior to B2 agonists

drugs inhibit vagally mediated airway tone, thereby producing bronchodilation

This effect is small in normal airway but it greater in airways of patients COPD

Which are structurally narrowed and have higher resistance to airflow because airway resistance is inversely related to the fourth power of the radius

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13
Q

Ipratropium bromide

A

Adverse effects- predictable consequences of muscarinic receptor (Dry mouth, constipation, blurred vision, dyspepsia, cognitive impairment)

Adverse effects and contraindications are of less concern with anticholinergics administered by inhalation

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14
Q

Wheezing

A

Congestion, rattling, wheezing stridor

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15
Q

Not all wheezes=Asthma, all wheezes=obstruction

A

continuous mucosal sound (multiple) that can be produced by oscillation of opposing walls of an airway that is narrowed almost to the point of closure

During inspiration or expiration (mostly expiration) from the large extrathoracic upper airway to the intrathoracic small airways

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16
Q

stridor

A

oscillation of a narrowed airway, obstruction of large airways, monophonic wheezing (loudest over anterior neck, typically high pitched), inspiratory/expiratory or both

17
Q

location determines the noise

A

the extrathoracic upper airway, which includes the nose, mouth, pharynx, larynx, and extrathoracic trachea

The intrathoracic central airway which included the intrathoracic trachea and bronchi at least 2 mm in diameter

The intrathoracic lower airways which include airways narrower than 2 mm in diameter

Stridor is from the top, wheexing from bottom

18
Q

Asthma

A

complex clinical syndrome characterized by variable airflow obstruction, airway inflammation, bronchial hyperresponsiveness

Pathophysiology- infiltration of airway by inflammatory cells, hypertrophy of airway smooth muscle, thickening of basement membrane (lamina reticularis), hyperplasia and hypertrophy of submucosal glands, goblet cell hyperplasia and hypertrophy, hyperplasia of microvascular dilation , loss of epithelial cells

19
Q

charcot leydin crystals

A

they consist of lysophospholipase, an enzyme synthesized by eosinophils, and are produced from the breakdown of these cells

They are indicative of a disease involving eosinophilic inflammation or proliferation often seen pathologically in patients with asthma

20
Q

Asthma time course

A

minutes- degranulation–>histaminine, leukotrienes, cytokines, proteases–> bronchoconstriction, immediate , early reaction–> chemotaxis, cell influx–> mediators–> late phase reactions inflammation

Hours–> secretion of cytokines, chemokines–> late phase reactions inflammtions

21
Q

LABAs

A

LABA may induce tolerance to the bronchodilating effect of SABA

Protective effect of LABA against a bronchoconstrictor stimulus is reduced with chronic use

LABA should not be used as a monotherapy

22
Q

steroids Adverse effects

A

Steroids inhibit ACTH and cortisol secretion by a negative feedback effect on the pituitary gland

Hypothalamic-pituitary andrenal axis suppression depends on dose

Significant suppression after short courses is usually not a problem, but prolonged suppression may occur after several months or years