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SP - Week 8 (Respiratory) > Asthma > Flashcards

Asthma Flashcards

1
Q

Asthma attack symptoms?

A
  1. Coughing
  2. Wheezing
  3. Shortness of breath
  4. Tightness in chest
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2
Q

Two main phases of asthma attacks :

A

 Immediate
 Late (or delayed) phase

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3
Q

Asthmatics have what cells

A

Asthmatics have activated T cells
 T-helper (Th2) profile of mechanisms
cytokine production
 Mechanism of activation not
fully understood
- Allergens are one of the mechanisms

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4
Q

Asthma includes:

A
  1. Inflammation
  2. Bronchial Hypersensitivity
  3. Reversible Airway Obstruction
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5
Q

What happens to T cell lymphocytes in asthma

A

 Allergen interacts with dendritic cells and CD4+ T
cells
 Development of Th0 lymphocytes
 Development of Th2 lymphocytes:
1. Generate cytokines that switch B cells/plasma cells to the production and release of immunoglobulin IgE
2. Generate cytokines, which promote differentiation and activation of eosinophils
3. Release cytokines that induce expression of IgE receptors on mast cells and eosinophils

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6
Q

IMMEDIATE PHASE

A

Inhaled allergen cross-links IgE
molecules on mast cells

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7
Q

Degranulation is what

A

Degranulation: release of mediators

   - Powerful bronchoconstrictors (e.g. leukotrienes (LK), histamine)
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8
Q

Other stimuli for mast cell degranulation

A

 Noxious gases
 Airway dehydration
 Drugs (any drug; aspirin and other NSAIDs:
LK-mediated)

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9
Q

When does the immediate phase occur in allergic asthma?

A

-In allergic asthma, the immediate phase
occurs abruptly

  • Setting the stage for the delayed phase
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10
Q

Delayed phase is ?

A

May be nocturnal

Progressing inflammatory reaction via eosinophils

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11
Q

Damage and loss of epithelium
Leads to…

A

Bronchial hyper-reactivity

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12
Q

Growth factors released act on … meaning there’s …

A

smooth muscle cells
 Hypertrophy and hyperplasia

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13
Q

Name the 4 Bronchodilators

A

•β2 agonists
• LK antagonists/LOX inhibitors
• Methylxanthines
• Muscarinic receptor antagonists

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14
Q

Anti-inflammatory drugs

A

• Glucocorticoids
• Biological therapy

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15
Q

β2 -ADRENOCEPTOR AGONISTS MoA

A

Main bronchodilators
-Relieve bronchospasm and breathlessness

Dilate the bronchi by a direct action on the β2-adrenoceptors of smooth muscle
- cAMP-PKA pathway activation via Gs-coupled
receptors

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16
Q

Anti - inflammatory effects of Beta 2 agonists

A

 Inhibit mediator release from mast cells
 Inhibit TNF-α release from monocytes
 Increase mucus clearance by action on cilia

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17
Q

Route of Admin. Of β2 agonists

A

Given by inhalation (b/c you’re increasing amount of drug delivered in resp. System as you decrease Adv. effects systematically)
 Aerosol -> Metered-dose inhaler
 Powder
 Nebulized solution

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18
Q

Other RoA of β2 agonists

A
  1. Oral
  2. By injection
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19
Q

Short-acting adrenergic β2 agonists (SABA)
Exs.

A

salbutamol (albuterol),
metaproterenol, terbutaline

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20
Q

Duration of axn for SABA
+ onset

A

 Duration of action is 3–5 h
 Fast onset of action (about 5 minutes)

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21
Q

When is SABA used?

A

 May be used on an ‘as needed’ basis
(reliever)
 Bronchodilator of choice in acute asthma

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22
Q

Guidelines regarding SABA

A

Use ICS with SABA

23
Q

Longer-acting adrenergic β2 agonists (LABA)
Exs.

A

-terol

salmeterol and formoterol

24
Q

Durn of axn for LABA + when is it given?

A

 Duration of action is 8–12 h
 Given regularly (controller)

25
LABA is adjunctive therapy with? And when used together ?
ICS= inhaled corticosteroids When used together, reduce dose of ICS (to reduce AE of steroids)
26
CI of LABA
Lack of evidence for LABA use in children <5 years
27
AE of LABA Most common + other
-Commonest adverse effect is tremor - Other unwanted effects 1. Tachycardia (caution for those with CV disease) 2. Cardiac dysrhythmia (caution for those with CV disease) 3. Anxiety 4. Headache 5. In High doses : Hypokalemia + Lactic acidosis
28
CYSTENEIL LEUKOTRIENES Are!?
 Potent spasmogens of bronchial muscle  Increase mucus secretion (can contribute to airway obstrxn) Can contribute to bronchial hyperactivity
29
CYSTENEIL LEUKOTRIENES receptors
Receptors: CysLT1 and CysLT2  Expressed in respiratory mucosa and infiltrating inflammatory cells  Functional significance is unclear
30
CYSTENEIL LEUKOTRIENE ANTAGONISTS Exs.
Montelukast and zafirlukast
31
CYSTENEIL LEUKOTRIENE ANTAGONISTS MoA + in mild asthma?
Decrease early and late responses to allergens Relax the airways in mild asthma  Less effective than salbutamol (additive actions)
32
CYSTENEIL LEUKOTRIENE ANTAGONISTS Clinical use + they’re not used for?
 Adjunct to treatment (w/ ICS + LABA)  Alternative to ICS for chronic asthma but Less efficacious  Also useful in exercise-induced asthma So used for chronic tx BUT Does not offer acute relief & Neither does zileuton
33
CYSTENEIL LEUKOTRIENE ANTAGONISTS RoA
Taken by mouth: tablets, granules
34
CYSTENEIL LEUKOTRIENE ANTAGONISTS Montelukast and zafirlukast AE + CI
Generally well tolerated  Adverse effects: headache, GI disturbances, hepatotoxicity  Increase risk of respiratory tract infections
35
Be aware of!!! (For montelukast + zafirlukast)
Neuropsychiatric events (aggressive behaviour, depression, hallucinations + suicidal behaviour)
36
Which is the LOX inhibitor ? And how do we use it
Zileuton : LOX inhibitor Adjunctive to steroids
37
When do we use Zileuton?
- in More severe asthma than DOESNT respond to 1st or 2nd tx
38
METHYLXANTHINES exs.
-phylline Theophylline-oral (also used as aminophylline- IV)
39
Theophylline/ aminophylline MoA
PDE IV inhibition:  Bronchodilator!  Anti-inflammatory action
40
In methylxanthines, there’s competitive antagonism between
Adenosine A1 (Gi-linked) and A2 (Gs-linked) receptor This may contribute to the side effects and the bronchodilation
41
Theophylline clinical uses
- given to pts whose asthma doesn’t respond enough to β2 adrenoceptor agonist, WITH STEROIDS - WITH OTHER BRONCHODILATORS & STEROIDS in COPD - IV ( as aminophylline, a mix of theophylline with ethylenediamine to increase its water solubility) in acute severe asthma.
42
Theophylline AE
1. Nausea, diarrhea 2. Insomnia, nervousness 3. Serious dysrhythmias, which can be fatal 4. Seizures, which can be fatal 5. Dose optimization by plasma level monitoring It has a narrow therapeutic index
43
PK: half-life increased By what?
1. liver dx 2. Cardiac dx 3. CYP450 inhibitors These lead to severe toxicity
44
PK.: half-life decreased by what factors ?
• heavy cigarette smoking • CYP450 inducers These lead to severe toxicity
45
Anti- inflammatory drugs
-.1. Glucocorticoids 2. Biological therapy
46
What are Glucocorticoids? And what’re they used for
- they’re NOT BRONCHODILATORS - prevent progression of chronic asthma - effective in acute severe asthma
47
GLUCOCORTICOIDS exs.
MAIN anti - inflammatory drugs in asthma for ALL ages -one, -ide Beclometasone, budesonide, fluticasone, mometasone, ciclesonide, flunisolide
48
GLUCOCORTICOIDS RoA + when is it effective
 Given by inhalation with a metered-dose or dry powder inhaler  Full effect on bronchial hyper-responsiveness attained only after weeks or months of therapy
49
MoA of Glucocortocoids:
 Bind to nuclear receptors  Affect transcription of a number of genes  Acute effects attributed to mechanisms independent of transcription
50
Serious AE are uncommon w/ inhaled steroids
 Oropharyngeal candidiasis  Sore throat and croaky voice  Use of ‘spacing’ devices reduce these problems  Regular high doses can produce some adrenal suppression !! Oral glucocorticoids may have many adverse effects (Oral- only given for chronic severe pts when other txs have failed)
51
Clinical uses in asthma: of glucocorticoids
- pts who need regular bronchodilators should be considered for glucocorticoid tx (w/ low-dose inhaled beometasone) - more severely affected pts. are treated w/ high-potency inhaled drugs (fluticasone) - pts. W/ acute asthma exacerbation need IV hydrocortisone and oral prednisolone -chronic tx w/ oral prednisolone , w/ inhaled bronchodilators + steroids, is required by some severe asthma pts.
52
Severe Acute Asthma tx
- it’s a medical emergency Tx; 1. Oxygen 2. Nebulised salbutamol 3. IV hydrocortisone 4. Followed by course of oral prednisolone ( also needed at any stage of severity of clinical condition is deteriorating rapidly to “ rescue” )
53
Additional measures occasionally used, when asthma is more severe:
1. Nebulised ipratropium (short-acting antimuscarinic) 2. IV salbutamol 3. IV aminophylline 4. Abx (if bacterial infxn is present)

SP - Week 8 (Respiratory) (3 decks)

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