Asthma (Exam III) Flashcards

1
Q

Where is the point of maximum airway resistance?

A

Medium-sized Bronchi

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2
Q

What are the 3 basic functions of the conducting zone of the lungs?

A
  1. Warm air
  2. Trap Debris
  3. Produce Mucus
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3
Q

Which portion of the ANS directly innervates the bronchiole smooth muscle?
Which portion indirectly affects bronchiole tone?

A
  • PSNS = direct innervation w/ vagus nerve
  • SNS = indirect control of tone (think epi)
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4
Q

What is the transition structure from the conducting zone of the airways to the respiratory zone of the airways?

A

Terminal bronchioles

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5
Q

What pathophysiologies are the components of COPD?

A

Chronic Bronchitis + Emphysema

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6
Q

What characterizes the alveoli of someone who has Emphysema?

What usually causes Emphysema?

A
  • The alveoli have enlarged and have ↓ surface area.
  • Smoking
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7
Q

What is the most common chronic disease in children?

Can children grow out of it?

A

Asthma, and yes, most children grow out of it.

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8
Q

What are 3 hypotheses for increasing prevalence of asthma around the world?

A
  1. Infant second-hand smoke
  2. Worsening air quality
  3. Hygiene hypothesis
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9
Q

What are general symptoms of asthma?
When are symptoms generally worse?

A
  • Dyspnea, wheezing, coughing, chest tightness
  • Symptoms usually worse at morning and at night.
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10
Q

What histological change contributes to worse COPD symptoms in the morning?

A
  • Columnar Epithelial Cells → COPD → Squamous Epithelial Cells.
  • This change results in ↓ mucus and ↓ cilia causing mucus to settle deep in the lungs.
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11
Q

Which two measurements are used in the diagnosis of asthma?

A

Forced Expiratory Volume (FEV) & Peak Expiratory Flow (PEF)

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12
Q

Which two measurements are used in the diagnosis of asthma?

A

Forced Expiratory Volume (FEV) & Peak Expiratory Flow (PEF)

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13
Q

Which two drugs are used to provoke a fall in forced expiratory volume after being inhaled?

A

Histamine and methacholine

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14
Q

What are the two major categories of asthma treatment?

A
  1. Short Term: sympathomimetics (β₂-agonists)
  2. Longer Term: Anti-inflammatories (Corticosteroids)
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15
Q

Is α-1 stimulation beneficial in asthma treatment?

A

Yes, vasoconstriction of pulmonary arteries decreases congestion.

need to verify, he later says it makes things worse

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16
Q

What are the two sources of pathogenesis in asthma?

A
  • Intrinsic = genetic
  • Extrinsic = Type I Hypersensitivity Reaction (Allergen)
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17
Q

Degranulation of what cell is responsible for the release of inflammatory mediators?

A

Mast Cells

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18
Q

What inflammatory mediators are released from mast cell degranulation?

What response does cytokine release (from inflammatory mediators) cause?

A
  • Histamines, Leukotrienes, & Prostaglandins.
  • Diffuse response: bronchoconstriction, vascular leakage, mucus secretion, itching, anaphylaxis, etc.
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19
Q

What inflammatory mediator is responsible for attracting WBC’s for the later reaction?

A

PGD₂

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20
Q

What causes the late reaction of an immunologic hypersensitivity reaction? How much later does this usually occur?

A
  • WBCs (T-lymphocytes, Eosinophils, & Neutrophils)
  • 2-8 hours after initial event.
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21
Q

Which inflammatory mediator is considered the “slower-reacting” cytokine?

A

Leukotrienes

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22
Q

Describe the hypersensitivity reaction.

A
  1. Dendritic cell interacts w/ antigen.
  2. MCHII presents antigen to T-Helper 2 cell
  3. T-Helper

(needs work)

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23
Q

Briefly describe the early reaction portion of a hypersensitivity reaction.

A
  1. Allergen triggers IgE antibodies on Mast cell
  2. Mast cell degranulates & releases inflammatory mediators
  3. Histamine, LTC4, PGD₂ produce bronchostriction (and inflammation to a lesser degree).
24
Q

Does a late reaction have the same intensity as an early reaction?

A

Yes

25
Q

What characterizes the late reaction portion of a hypersensitivity reaction?

A
  1. Allergen triggers Mast cell
  2. Mast cell releases pro-inflammatory cytokines
  3. Cytokines + PGD₂ = release of WBC’s = ↑ inflammatory response.
26
Q

What cells produce mucus?
What is the normal composition of mucus?
What is the composition of mucus in asthma?

A
  • Goblet and Columnar Epithelial Cells
  • 95% H₂O, 5% glycoproteins
  • 90% H₂O, 10% glycoproteins
27
Q

What structure maintains the normal resting tone of airway smooth muscle?
What ANS receptors are the primary receptors of bronchostriction?

A
  • Vagal Nerve
  • M3 Receptors
28
Q

What is Croup?
Who is most often affected?
What is the hall-mark sign?
Does this condition resolve on its own or require treatment?

A
  • Acute laryngotrachobronchitis
  • Children (6 months - 5 years)
  • Barking, seal-like, cough.
  • Usually self-resolving, can require nebulized epi in severe cases.
29
Q

What occurs with mucus specifically when one has chronic bronchitis?

A
  • ↑ Number of mucus glands
  • ↑ Size of mucus glands
  • Thicker mucus
30
Q

What β₂-agonists should be known?

A

Terbutaline, albuterol, metaproterenol, salmeterol, etc.

31
Q

What would β₂-agonist toxicity cause?

A

Skeletal muscle tremor

32
Q

When would nebulized epinephrine be utilized?

Is nebulized epi primarily used in children or adults?

A
  • In a severe acute asthma attack.
  • Primarily in children
33
Q

What potent nebulized bronchodilator can cause arrhythmias and is potentially the cause of ↑ mortality rates?

A

Isoproterenol

34
Q

Which drug is the most widely used SAβ₂A bronchodilator?

A

Albuterol, similar efficacy to isoproteronol w/ less side effects.

35
Q

What two LAβ₂A’s should be known?
What is their duration of action and what makes them long acting?

A
  • Salmeterol & Formoterol
  • 12 hours, high lipid solubility
36
Q

Which particle size from nebulizers is effective at actually delivering medicine?
How much dose is usually lost and what happens to the other sized particles?

A
  • Medium-sized particles
  • 80-90% of dose is usually breathed back out via small particles or deposited in the mouth via large particles.
37
Q

Which methylxanthine is best for asthma?

A

Theophylline

38
Q

What is the essential mechanism of action for methyxanthines?

A

Phosphodiesterase inhibition (PDE blocked from breaking down cAMP = ↑ cAMP = bronchodilation)

39
Q

When does Theophylline become toxic?

A

> 20mg/L

40
Q

What methylxanthine requires peak/trough monitoring?

A

Theophylline

41
Q

Why would ipratropium bromide be preferred over atropine?

A
  • More selective so no CNS effects.
42
Q

What drugs does ipratropium bromide combine well with?

A

β₂ agonists = synergistic

43
Q

Give the general duration of action of atropine, tiotropium, and ipratropium in order of shortest to longest.

A
  1. Atropine (shortest)
  2. Ipratropium Bromide
  3. Tiotropium (Longest)
44
Q

What condition is less responsive to corticosteroids?

A

COPD

45
Q

What is the use of corticosteroids for asthma?
What is their general mechanism of action?

A
  • Anti-Inflammatory = prevention of acute attacks.
  • Inhibition of production of cytokines & inhibition of lymphocytic and eosinophilic airway inflammation.
46
Q

How do glucocorticoids work?

A
  • Inhibition of immune response by blocking transcription/translation.
47
Q

What are some bad side effects of corticosteroid use?

A
  • ↑ osteoporosis w/ long term therapy
  • ↓ rate of growth in children
  • fluid retention
48
Q

What nasty side effect occurs from oral corticosteroid use?

A

Oropharyngeal Candidiasis (fungus)

49
Q

What long term effects are hopefully seen with usage of inhaled corticosteroids for asthma?

A
  • ↓ symptoms
  • ↑ lung function
  • ↓ oral steroids
  • ↓ bronchial activity.
50
Q

What drugs are available for refractory asthma symptoms not well treated with long-term inhaled corticosteroid use?
How do these work?
Why are these not prescribed more often?

A
  • Anti-IgE monoclonal antibodies.
  • IgE MABs work by binding to mast cell receptors and preventing antigen binding.
  • MABs are expensive.
51
Q

What two ways do Leukotriene pathway inhibitors work?

A
  • Inhibition of 5-Lipoxygenase pathway (zileuton)
  • Inhibition of LTA4 receptor binding (Montelukast)
52
Q

What would be a good choice of drug for mild asthma?

A
  • Albuterol (β receptor agonist as needed)
53
Q

What would be a good choice for moderate asthma with nocturnal symptoms?

A
  • Anti-inflammatories like an inhaled corticosteroid or inhaled Cromolyn
  • Oral Leukotriene receptor antagonists.
54
Q

Is Cromolyn used for asthma now-a-days? What is its mechanism of action?

A
  • Utilized for more for eyes
  • Mast cell degranulation inhibitor
55
Q

Increased levels of Annexin-1 (from glucocorticoid administration) is associated with what two things?

A
  • Phospholipase A2 suppression
  • Leukocyte response inhibition