Lecture 9: Asthma Flashcards
(93 cards)
1
Q
Are beta-blockers a good treatment for asthmatics?
A
No!
2
Q
What type of disorder is asthma?
A
A chronic inflammatory disorder of the airways
3
Q
Explain how asthma starts off acute and becomes chronic
A
- Asthma starts off acute because originally mast cells are activated and explode releasing mediators of inflammation that trigger the body so it can be ready next time the allergen is present
- After mast cells get activated, immune system takes over which makes it chronic
4
Q
What 6 types of cells are involved in asthma?
A
Mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells
5
Q
What are 4 symptoms of asthma?
A
Wheezing; breathlessness; chest tightening; coughing
6
Q
When are the symptoms of asthma typically the worst?
A
At night or in the early morning
7
Q
True or false: asthma symptoms are often reversible spontaneously or with treatment
A
True
8
Q
What age group is asthma most common?
A
Children
9
Q
True or false: children with asthma typically have it in adulthood as well
A
False, up to 70% of children with asthma will have markedly improved or non-existent symptoms by early adulthood
10
Q
What are some predictors of adult asthma persistence?
A
- Diagnosis during school age
- Presence of atopy (genetic tendency to develop allergic diseases)
- Bronchial hyper-reactivity
11
Q
What are 2 non-modifiable risk factors for asthma?
A
- Genetics (genes predisposing for atopy or BHR)
- Gender (males in childhood and females in adulthood)
12
Q
What are 6 modifiable risk factors for asthma?
A
- Low socioeconomic status
- Family size
- Obesity
- Exposure to secondhand smoke in utero and/or at a young age
- Respiratory syncytial virus
- Decreased exposure to childhood infectious agents
13
Q
What are 6 potential triggers of an asthmatic attack?
A
1) Respiratory tract infections
2) Allergens
3) Environment
4) Exercise
5) Emotions
6) Drugs/preservatives
14
Q
Describe the bronchial tubes of a non-asthmatic person
A
Muscle around the bronchial tubes are relaxed and tissue is thin, allowing for easy airflow
15
Q
Describe the bronchial tubes of an asthmatic person
A
Muscles of bronchial tubes tighten and thicken, and air passages become inflamed and mucous-filled, making it difficult for air to move
16
Q
What does spirometry measure?
A
How an individual inhales/exhales volumes of air as a function of time
17
Q
What is FVC?
A
- Forced vital capacity
- Maximum amount of air forcibly expired after maximum inspiration
18
Q
What is FEV1?
A
- Forced expiration volume in 1 second
- Volume of gas exhaled during first second
19
Q
What is a normal FEV1/FVC ratio?
A
0.75 - 0.8
20
Q
What is conclusive of an FEV1/FVC ratio below 70%?
A
Airway obstruction
21
Q
What does peak expiratory flow (PEF) measure?
A
Maximum speed of expiration
22
Q
What is peak expiratory flow useful for?
A
Monitoring therapy
23
Q
What do airway responsiveness tests measure?
A
Sensitivity to certain “triggers” such as methacholine, histamine, cold air, or exercise
24
Q
When is airway responsiveness testing necessary?
A
If original pulmonary function tests are inconclusive but symptoms suggest asthma
25
What are the 4 main pathophysiological events that lead to obstruction of the airways (aka asthma)?
1) Bronchial hyper-responsiveness
2) Airway inflammation (acute and chronic)
3) Airway remodeling
4) Airway obstruction
26
What does bronchial hyper-responsiveness cause?
Increased tendency of bronchospasms
27
How does the degree of bronchial hyper-responsiveness vary?
Among patients and at different points within individuals (seasonal)
28
Describe the sensitization phase of airway inflammation
- Exposure to allergen mobilizes production of specific IgE antibodies against the allergen
- IgE antibodies bind to mast cells
29
Describe the early phase of airway inflammation
Re-exposure to same allergen triggers that specific IgE antibody on the mast cell to bind to allergen and form a cross-linked complex, triggering mast cell to explode and release pro-inflammatory mediators causing muscle contraction, mucous release, and vasodilation, ultimately causing a restricted airway
30
Describe the last phase of airway inflammation
- Recruitment of more immune system mediators of inflammation
- T cells activate, which in turn activate B cells that develop into plasma cells that produce IgE antibodies against the initial allergen
31
How does chronic airway inflammation occur and what does it result in?
- Occurs from repeated exposure to allergen
| - Results in permanent inflammation of respiratory system even though symptoms are episodic
32
What are 5 clinical consequences to chronic airway inflammation?
1) Increased bronchial hyper-reactiveness to physical, chemical, and pharmacological stimuli
2) Non-specific BHR and increased risk of exacerbations
3) Increased symptoms and worsening of airway obstruction
4) Increased mucous production and thickening
5) Decreased clearance of allergen from mucosal lining of airways
33
How do tissues respond to injury?
Acute inflammation
34
Why does airway remodeling occur?
Asthma is a chronic inflammatory process that is subject to pathological healing
35
What does airway remodeling lead to?
Fibrosis and increased size and number of smooth muscle cells and mucous glands
36
What are 3 causes of airway obstruction?
1) Mucous production
2) Smooth muscle of airways
3) Neuronal control and neurogenic inflammation
37
What is the lung's main defense against external pathogens and irritants?
Mucous
38
How is mucous produced?
By goblet cells and bronchial epithelial tissue
39
What is different about mucous in asthmatics?
Tends to be more viscous
40
How is smooth muscle arranged in airways?
Wrapped around airways in spiral formation
41
What are airways innervated by?
Sympathetic, parasympathetic, and afferent sensory neurons
42
What do cholinergic pathways cause?
Bronchoconstriction
43
What do adrenergic pathways cause?
- Norepinephrine binds to alpha receptors and causes bronchoconstriction
- Epinephrine binds to beta receptors and causes bronchodilation
44
What do afferent pathways cause?
Neurogenic inflammation/BHR
45
True or false: neuronal pathways are pretty much independent of each other and don't affect others pathways
False, changes in the function of one neuronal pathway may have a significant effect on the function of another pathway
46
How is asthma diagnosed?
- Symptomatic presentation
- Family history
- Measurement of lung function
- Airway responsiveness testing
- Allergy testing to assess triggers
47
What do relievers do for asthma?
Act quickly to reverse bronchoconstriction and relieve symptoms
48
What are examples of relievers for asthma?
- Rapid-acting beta2-agonists
- Inhaled anticholinergics
- Short-acting theophylline
49
What do inhaled steroids do for asthma?
Suppress inflammation
50
How often are controllers used for asthma and why?
Daily, continuously to prevent symptoms and flare ups
51
What are examples of controllers for asthma?
- Inhaled and systemic glucocorticoids
- Leukotriene modifiers
- Long-acting beta2-agonists combined with ICS
- Sustained-release theophylline
52
Would a rapid-acting beta2-agonist be a better reliever or controller of asthma?
Reliever
53
Would an inhaled anticholinergic be a better reliever or controller of asthma?
Reliever
54
Would a short-acting theophylline be a better reliever or controller of asthma?
Reliever
55
Would a long-acting beta2-agonist mixed with ICS be a better reliever or controller of asthma?
Controller
56
Would an inhaled glucocorticoid be a better reliever or controller of asthma?
Controller
57
Would a leukotriene modifier be a better reliever or controller of asthma?
Controller
58
Would a sustained-release theophylline be a better reliever or controller of asthma?
Controller
59
What are the 2 main treatment targets of asthma?
Bronchoconstriction and inflammation
60
Where are mast cells found?
Throughout walls of respiratory tract
61
Are there more mast cells in patients with or without asthma?
With
62
What does allergen exposure do to mast cells?
Degranulates mast cells, causing allergen to bind to cell-bound IgE, resulting in mast cells releasing bronchoconstrictors and eosinophil and neutrophil chemotactic factors
63
What are examples of bronchoconstrictors released by mast cells?
Histamine, leukotrienes, prostaglandin D2, or platelet activating factor
64
What do eosinophil and neutrophil chemotactic factors do?
Attract more mast cells to the area they are released
65
What do activated eosinophils do?
Release inflammatory mediators such as leukotrienes and granule proteins to injure airway tissue
66
What do T-lymphocytes do?
Release cytokines that mediate allergic inflammation
67
What causes increased TH2 activity?
TH1/TH2 imbalance
68
What do macrophages do in normal airways?
Engulf and digest bacteria and other foreign material
69
What do macrophages release?
- Inflammatory mediators such as platelet activating factor and leukotrienes
- Neutrophil and eosinophil chemotactic factor which amplify the inflammatory process
70
How can epithelial cells be activated?
By IgE-dependent mechanisms, viruses, pollutants, or histamine
71
What is the function of epithelial cells?
Participate in mucocilliary clearance and removal of noxious agents
72
What happens to epithelial cells in chronic asthma?
Epithelial shedding which causes increased airway responsiveness and decreased clearance of noxious agents
73
What are the 3 main mediators of inflammation?
1) Histamine
2) Arachadonic acid
3) Platelet activating factor
74
What releases histamine?
Lung mast cells
75
What does histamine do?
- Induces smooth muscle constriction and bronchospasm
| - May take part in mucosal edema and mucous secretion
76
How is arachadonic acid metabolized?
By cyclooxygense
77
What does arachadonic acid form after it is metabolized?
Prostaglandins and thromboxanes
78
What do prostaglandin D2 and F2a cause?
Bronchoconstriction
79
What does prostacyclin (PGI2) cause?
Vasodilation and edema
80
What does thromboxane A2 cause?
Bronchoconstriction in late asthmatic response, airway inflammation, and BHR
81
What does platelet activating factor do?
Mediates bronchospams, inflammation, anaphylaxis, sustained induction of BHR, edema, and eosinophils chemotaxis
82
Where is platelet activating factor produced?
In neutrophils, monocytes, and macrophages
83
How are leukotrienes formed?
By arachadonic acid metabolized by 5-lipooxygenase
84
What can metabolism of arachadonic acid by 5-lipooxygenase lead to?
Excess production of the leukotrienes LTC4, LTD4, and LTE4
85
What do the cysteinyl leukotrienes (LTC4, LTD4, and LTE4) promote?
Bronchospasms, histamine release from mast cells, mucous secretion, and airway edema
86
Where are cysteinyl leukotrienes released?
From mast cells and eosinophils
87
True or false: 5-lipooxygenase inhibitors are not readily used
True
88
What does montelukast/Singulair do?
Inhibits physiologic actions of LTD4 at the CysLT1 receptor
89
What are aspirin and ibuprofen considered and what do they do?
- Cox 1 and Cox 2 non-selective inhibitors
| - Block PGE1 and PGE2
90
True or false: it is possible for asthmatics to develop aspirin/ibuprofen sensitivity or intolerance
True
91
What is a better option for asthmatics than aspirin or ibuprofen and why?
Cox 2 selective inhibitors because they don't affect PGE1 and PGE2
92
What are the 3 best medications for acute asthma attacks?
1) Beta agonists
2) Smooth muscle relaxants
3) Oral corticosteriods
93
What are the 2 best medications for prophylactic asthma attacks?
1) Anticholinergic medications
| 2) Inhaled corticosteroids
