Obstructive lung diseases (rowley) Flashcards

1
Q

What is the definition of asthma?

A
  • reversible airway obstruction
  • airway inflammation
  • increased airway responsiveness to a variety of stimuli
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2
Q

What gender more likely to develop asthma in middle age?

A

Females

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3
Q

What is the role of smooth muscle innervation as it relates to asthma?

A

PS contraction - narrows airway

SS relaxation- relaxes airway smooth muscle (minor)

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4
Q

What encompasses the Early Asthmatic Response?

A

minutes-2 hrs

Mast cell and mediators! blocked by B ag and cromlyn

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5
Q

What up with the late asthmatic response?

A

only in 50%, usually occurs within 6-8 hrs and can last 24 hrs. mediates by remaining inflammatory cells (bronchial hyperreactivity!) NOT related to mast cells! antihistamine won’t do anything

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6
Q

What’s the stimulus that causes bronchial hyperreactivity in asthma?

A

NONSPECIFIC!! not an allergen! histamine/methacoline used clinically

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7
Q

Airway inflammation leads to airway obstruction via?

A

smooth muscle activation (bronchospasm)
vascular congestion/bronchial edema
accumulation of airway secretions, mucus casts, cellular debris

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8
Q

What are the PFT changes in asthma between attacks?

A

normal!!!

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9
Q

WHat are the pft changes during an asthma attack?

A

obstructive pattern! Decreased FEV1, FVC and FEV/FVC ratio! increased RV and FRC

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10
Q

What do we see grossly in asthmatic lungs?

A

hyperinflation! airway is narrowed so can’t get air out of lungs so hyperinflate! also because of air trapping

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11
Q

What role does asthma have on lung compliance?

A

DECREASES!! increased airway resistance causes hyperinflation of lungs, causes flattened diaphragm. work of breathing increases because lungs are stiffer and need more pressure to effect change in lung volume

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12
Q

Does asthma cause alterations in gas exchange?

A

During attacks, VQ mismatch! So, hypoxemia and increased dead space

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13
Q

What is the presentation of a moderate asthmatic?

A

Appears in distress! wheezes, tachypnea, tachycardia, diaphoresis, accessory muscle use.

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14
Q

What ABGs of a moderate asthmatic during an attack?

A

mild- respiratory alkalosis (dec co2) mod- mild hypoxemia, pco2 decreased or normal

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15
Q

What is the presentation of severe asthmatic attack?

A

chest is QUIET because not moving air!! fatigue/somnolence, cyanotic

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16
Q

What ABGs of severe asthmatic attack?

A

severe hypoxemia! respiratory acidosis! (increase PCO2, decrease PO2)

17
Q

How do we classify someone with intermittent asthma?

A

smptoms less than 2 days a week, awake less than 2x month, use beta agonist less than 2x/week, lung function normal (rule of 2s)

18
Q

What is the MAIN goal of asthma treatment?

A

TREAT THE INFLAMMATION!! can’t just give albuterol! treating the bronchospasm won’t fix the inflammation

19
Q

What is the mainstay treatment for asthma?

A

corticosteroids b/c of their broad anti-inflam action.
inhaled for chronic- fluticasone/budesonide
oral/iv for exacerbation- prednisone, methylprednisolone

20
Q

What are three contributors to the pathogenesis of COPD?

A

role of inflammation, role of oxidative stress, role of amplification

21
Q

In what COPD do we see increased lung compliance?

A

emphysema

22
Q

What is the definition of bronchiectasis?

A

chronic, irreversible dilation and distortion of bronchi caused by inflammatory destruction of bronchial walls

23
Q

What are some potential etiologies for bronchiectasis?

A

infections, immotile cilia syndrome (kartageners), hpogammaglobulinemia (inc freq infections), cystic fibrosis, allergic bronchopulmonary aspergillosis

24
Q

what is the specific spectrum that presents with allergic bronchopulmonary aspergillosis?

A

episodic wheezing, febrile episodes, expectoration of mucous plugs, peripheral blood eosinophilia, intermittent pulmonary infiltrations