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HARRISON'S PULMO > Asthma > Flashcards

Asthma Flashcards

1
Q

Peak age of asthma

A

3 years

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2
Q

Responsible for decreased mortality in patients with persistent asthma

A

ICS

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3
Q

Major risk factors for asthma deaths (3)

A
  1. poorly controlled disease with frequent use of bronchodilator inhalers
  2. lack of or poor compliance with ICS therapy
  3. previous admissions to hospital with near-fatal asthma.
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4
Q

Major risk factor for asthma

A

Atopy

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5
Q

Genetic predisposition in asthma

A

polymorphisms of genes on chromosome 5q, including the TH2 cells interleukin (IL)-4, IL-5, IL-9, and IL-13,
which are associated with atopy

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6
Q

Novel genes in asthma (3)

A

ADAM 33
DPP-10
ORMDL3

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7
Q

lack of infections in early childhood preserves the Th2 cell bias at birth, whereas exposure to infections and endotoxin results in a shift toward a predominant protective Th1 immune response.

A

Hygiene hypothesis

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8
Q

More severe, persistent asthma

A

Intrinsic asthma

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9
Q

Characteristics of intrinsic asthma

A 
Adult onset
Non-atopic
Concomitant nasa polyps
Aspirin-sensitive
More severe, persistent asthma
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10
Q

Most common allergens to trigger asthma

A

Dermatophagoides spp

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11
Q

Common triggers of ACUTE SEVERE EXACERBATIONS

A

Rhinovirus
RSV
Coronavirus

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12
Q

Mechanism is linked to hyperventilation

A

Exercise-induced asthma

increased osmolality in airway lining fluid and triggers mast cell mediator release, resulting in bronchoconstriction

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13
Q

Physiologic abnormality of asthma

A

Airway hyperresponsiveness

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14
Q

Important in initiating the acute bronchoconstrictor responses to allergens

A

Mast cells

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15
Q

Activated by allergens via low-affinity IgE receptors (FcεRII)

A

Macrophages

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16
Q

T helper phenotype

  1. in asthmatics
  2. In normal
A
  1. TH2

2. TH1

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17
Q

TH2 release the ff causing:

  1. IL-5
  2. IL-4, IL-13
A
  1. IL-5: eosinophilic inflammation

2. IL-4, IL-13: increases IgE formation

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18
Q

Major target cells for ICS

A

Epithelial cells

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19
Q

Mast cell-derived mediators that contract airway smooth muscle, increase microvascular leakage, increase airway mucus secretion, and attract other inflammatory cells

A

histamine
prostaglandin D2
cysteinyl-leukotrienes

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20
Q

Cytokines that amplify the inflammatory response

A

TNF-α and IL-1β

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21
Q

Anti-inflammatory cytokines deficient in asthma

A

IL-10, IL-12

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22
Q

Used in diagnosis and monitoring of asthmatic inflammation

A

FeNO

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23
Q

Airway nerves release this neurotransmitter which may have inflammatory effects

A

substance P

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24
Q 
True in asthma, except:
A. reduction in FEV1
B. Reduction in FEV1/FBC ratio
C. Increased peak expiratory flow (PEF)
D. increase in airway resistance.
A

C.

Should be Reduced PEF

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25
Q

Characteristic symptoms of asthma

A

Wheezing
Dyspnea
Coughing

26
Q

Reversibility in lung function test is demonstrated by

A

> 12% and 200-mL increase in
FEV 15 min
1. after an inhaled SABA; such as inhaled albuterol 400 μg
OR
2. Oral corticosteroids (prednisone or prednisolone 30–40 mg daily)

27
Q

Treatment:

increases intracellular cyclic adenosine monophosphate (AMP), which relaxes smooth muscle cells and inhibits certain inflammatory cells, particularly mast cells

A

B2 agonist

28
Q

Actions of B2-agonists, except:
A. reversing and preventing contraction of airway smooth muscle cells
B. inhibition of mast cell mediator release
C. Increase in plasma exudation
D. inhibition of sensory nerve activation

A

C.

Should be reduction in plasma exudation

29
Q

SABA duration of action

A

3-6 hours

30
Q

LABA duration of action

A

12 hours

Given BID (salmeterol, formoterol)

Given OD (indacaterol, olodaterol, vilanterol)

31
Q

Most common side effects of B2-agonists

A

Muscle tremor

Palpitations

32
Q

prevent cholinergic nerve-induced bronchoconstriction and mucus secretion

A

Muscarinic receptor antagonists

33
Q

Most common side effects of anticholinergics

A

Dry mouth

34
Q

inhibition of phosphodiesterases in airway smooth-muscle cells, which increases cyclic AMP

A

Theophylline

35
Q

Activated by theophylline which is a critical mechanism for switching off activated inflammatory genes and may therefore reduce corticosteroid insensitivity in severe asthma.

A

histone deacetylase-2 (HDAC2)

36
Q

Used in patients with severe exacerbation that are refractory to SABA

A

Aminophylline

37
Q

Most common side effects of theophylline

A

Nausea
Vomiting
Headaches

*due to phosphodiesterase inhibition

38
Q

Most effective controllers for asthma

A

ICS

39
Q

Effect/Action of ICS

A

switch off the transcription of multiple activated genes that encode inflammatory proteins such as cytokines, chemokines, adhesion molecules, and inflammatory enzymes.

40
Q

Timing of ICS

A

BID

41
Q

First line for persistent asthma

A

ICS

42
Q

Oral corticosteroids dosing for acute exacerbations

A

Prednisone or prednisolone 30-45 mg OD x 5-10 days

43
Q

are potent bronchoconstrictors; cause microvascular leakage and increase eosinophilic inflammation through the activation of cys-LT1-receptors.

A

Cysteinyl-leukotrienes

44
Q

effective in blocking trigger-induced asthma such as EIA and allergen- and sulfur dioxide-induced symptom

A

Cromones

45
Q

blocking antibody that neutralizes circulating IgE without binding to cell-bound IgE and, thus, inhibits IgE-mediated reactions

A

Omalizumab

46
Q

Anti-IL 5 used in asthma

A

Direct: Mepolizumab, resilizumab

Receptor: Benralizumab

47
Q

Treatment of Choi’s for all patients

A

ICS BID

48
Q

Clinical features of acute severe asthma

A

Increased ventilation
Hyperinflation
Tachycardia

49
Q

Mainstay of treatment in acute severe asthma

A

SABA via nebulizer or MDI with spacer

50
Q

Target SpO2 in acute severe asthma

A

> 90%

51
Q

Impending respiratory failure in acute severe asthma

A

PCO2 is normal or rises

*prophylactic intubation is indicated

52
Q

two major patterns of difficult asthma

A
  1. persistent symptoms and poor lung function, despite appropriate therapy
  2. normal or near normal lung function but intermittent, severe (sometimes life-threatening) exacerbations
53
Q

most common reason for poor control of asthma is poor adherence with medication

A

ICS

54
Q

Treatment: Severe premenstrual worsening of asthma unresponsive to corticosteroids

A

progesterone
OR
gonadotropin-releasing factors

55
Q

Persistent pattern of variability and may require OCS, or at times, continuous infusion of B2-agonists

A

Type 1 brittle asthma

56
Q

normal or near-normal lung function but precipitous, unpredictable falls in lung function that may result in death

A

type 2 brittle asthma

57
Q

Most effective therapy in brittle asthma

A

Subcutaneous epinephrine

58
Q

Treatment safe in pregnancy

A

SABA
ICS
Theophylline

59
Q

Improves lung function and reduces steroid resistance

A

Smoking cessation

60
Q

Results from an allergic pulmonary reaction to inhaled spores of Aspergillus fumigatus

A

Bronchopulmonary Aspergillosis

61
Q

Treatment for BPA that is beneficial in preventing exacerbations

A

Oral antifungal itraconazole

62
Q

Treatment for ACO

A

Triple therapy with ICS, LABA, LAMA

HARRISON'S PULMO (5 decks)

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