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STEP 2 Pulmonary > Pulm. Asth nsaid,GERD,anaph, asthma vs COPD (10-28) (2) > Flashcards

Pulm. Asth nsaid,GERD,anaph, asthma vs COPD (10-28) (2) Flashcards

1
Q

aspirin/nsaids.
It is a pseudoallergic reaction to NSAIDs.
not mediated by what?

A

These are NOT IgE-mediated reaction

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2
Q

aspirin/nsaids.
in what comorbids?

A

Asthma
Chronic Rhinosinusitis with nasal polyposis
Chronic urticaria

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3
Q

aspirin/nsaids.
pathophysiology?

A

Aspirin blocks the COX pathway, leading to overstimulation of leukotriene (ie, proinflammatory) pathway

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4
Q

aspirin/nsaids. onset?

A

Patient presents with symptoms within 30 minutes to 3 hours after NSAID ingestion

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5
Q

aspirin/nsaids.
3 groups of symptoms?

A

Asthmatic (Cough, Wheezing, Chest tightness)

Nasal and ocular symptoms (Nasal congestion, Rhinorrhea, Periorbital edema)

Facial flushing

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6
Q

aspirin/nsaids. treatment?

A

Management of asthma and chronic rhinosinusitis

Avoidance of NSAIDs

Desensitization of NSAIDs (if it is necessary)

Leukotriene inhibitors (eg, zileuton) and leukotriene receptor antagonist (eg, montelukast) can also improve respiratory and nasal symptoms

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7
Q

aspirin/nsaids. differentiatials?

A

Anaphylaxis
i. Skin involvement is seen in anaphylaxis
ii. NSAIDs can worsen anaphylaxis by resulting in non-immunologic mast cell activation

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8
Q

arachidonic pathway.
membrane phospholipids by phospholipase A2 –> arachidonic –> 2 ways: 5lipoxygenase or COX.

5lipoxygenase –> ?

A

Leukotriene A4 –>
a) LTB4 (chemotaxis)
b) LTC4, D4, E4 (bronchospasm, incr. permeability)

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9
Q

arachidonic pathway.
membrane phospholipids by phospholipase A2 –> arachidonic –> 2 ways: 5lipoxygenase or COX.

COX –>? this way is inhibited by aspirin and redirected to lipoxygenase pathway.

A
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10
Q

GERD in asthma. what mechanism?

A

GERD is common in asthma patients and can exacerbate asthma symptoms through microaspiration of gastric contents, leading to:
a. inr. vagal tone
b. Bronchial reactivity

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11
Q

GERD on resp. presentation?

A

a. Sore throat
b. Morning hoarseness
c. Worsening cough only at night
d. Increased need for albuterol inhaler following meals
e. Dysphagia
f. Chest pain/heartburn
g. Sensation of regurgitation

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12
Q

GERD.treatment?

A

PPI

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13
Q

Atelectasis in asthma.
mechanism?

A
  1. Asthma exacerbation leads to mucus hypersecretion (eg, dark colored sputum), which can result
    in formation of a mucus plug in the airways
  2. This mucus plug blocks the airway, leading to atelectasis of the lung of the affected side
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14
Q

Anaphylaxis table.
triggers?

A

Food (eg nuts, fish)
Medications (eg beta lactam, abs)
Insect stings

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15
Q

Anaphylaxis table.
cardiovascular manifestation?

A

Vasodilation –> hypotension and tissue edema
Tachycardia

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16
Q

Anaphylaxis table.
respiratory manifestation?

A

Upper airway edema –> stridor and hoarseness
Bronchospasm –> wheezing

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17
Q

Anaphylaxis table.
cutaneous manifestation?

A

urticarial rash, pruritus, flushing

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18
Q

Anaphylaxis table.
GI manifestation?

A

nausea, vomiting, abdominal pain

19
Q

Anaphylaxis table.
Treatment. 3

A

Intramuscular epinephrine
Airway management and volume resuscitation
Adjunctive therapy (antihistamines, glucocorticoids)

20
Q

Asthma and COPD diff. table.

Differentiating between the two is important as therapeutic approach is different in both:

A

Inhaled corticosteroids are the primary long-term intervention for asthma

Long-acting anticholinergic inhaler is preferred for COPD

21
Q

Long-acting anticholinergic inhaler is preferred for ?

A

COPD

22
Q

Inhaled corticosteroids are the primary long-term intervention for ?

A

asthma

23
Q

Asthma and COPD diff. table.
what test used to differentiate?

A

The differentiating test is spirometry before and after administration of a bronchodilator (usually albuterol)

24
Q

Asthma and COPD diff. table.
spirometry with bronchodilator. what result in asthma?

A

If patient has asthma, there will be complete restoration of normal airflow after bronchodilator administration

25
Q

DLCO decreases in COPD due to
alveolar destruction but increases (or
stays normal) in asthma due to
increased thoracic blood flow caused
by negative intrathoracic pressures
during inspiration

A

.

26
Q

Asthma vs COPD table.

Asthma FVC?

A

normal/decreased

27
Q

Asthma vs COPD table.

COPD FVC?

A

normal/decreased

28
Q

Asthma vs COPD table.

late-stage COPD FVC?

A

decr (1 arrow) /very decr (2 arrows)

29
Q

Asthma vs COPD table.

Asthma FEV1?

A

decr

30
Q

Asthma vs COPD table.

COPD FEV1?

A

decr.

31
Q

Asthma vs COPD table.

late-stage COPD FEV1?

A

very decr (2 arrows)

32
Q

Asthma vs COPD table.

Asthma FEV1/FVC?

A

decr.

33
Q

Asthma vs COPD table.

COPD FEV1/FVC?

A

decr

34
Q

Asthma vs COPD table.

late stage COPD FEV1/FVC?

A

very decr (2 arrows)

35
Q

Asthma vs COPD table.

Asthma bronchodilator response?

A

reversible

36
Q

Asthma vs COPD table.

COPD bronchodilator response?

A

partially reversible/nonreversible

37
Q

Asthma vs COPD table.

late stage COPD bronchodilator response?

A

usually nonreversible

38
Q

Asthma vs COPD table.

asthma xray?

A

normal

39
Q

Asthma vs COPD table.

COPD xray?

A

normal

40
Q

Asthma vs COPD table.

late-stage COPD xray?

A

hyperinflation, loss of lung markings

41
Q

Asthma vs COPD table.

asthma DLCO?

A

normal/INCR.

42
Q

Asthma vs COPD table.

COPD DLCO?

A

normal/DECR.

43
Q

Asthma vs COPD table.

late stage COPD DLCO?

A

decreased (1 arrow)

44
Q

DLCO wtf?

A

diffusion capacity of the lung for carbon monoxide

STEP 2 Pulmonary (30 decks)

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