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Life Sciences - Sem 2 > 4.4 Drugs for Asthma and COPD > Flashcards

4.4 Drugs for Asthma and COPD Flashcards

1
Q

Early phase asthma is associated with bronchospasms. What is the mechanism behind this?

A
  1. Allergen interaction with IgE on mast cells = release histamine, leukotriene, B4, and prostaglandin
  2. Other mediators release IL-4, IL-5, IL-14, macrophages, protein-1a, and TNF-a
  3. Various chemotaxis and chemokines attract leukocytes (eosinophils and mononuclear cells) preparing for late phase
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2
Q

Early phase asthma is associated with bronchospasms. What is the mechanism behind this?

A
  1. Allergen interaction with IgE on mast cells = release histamine, leukotriene, B4, and prostaglandin
  2. Other mediators release IL-4, IL-5, IL-14, macrophages, protein-1a, and TNF-a
  3. Various chemotaxis and chemokines attract leukocytes (eosinophils and mononuclear cells) preparing for late phase
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3
Q

Late phase asthma is associated with inflammation. What is the mechanism behind this?

A

Infiltration of cytokine TH2 lymphocytes + activation of eosinophils

Eosinophils release leukotienes, interleukins IL-3, IL-5, and IL-8, and toxic proteins

Growth factors released from inflammatory cells act on smooth muscle, causing hypertrophy and hyperplasia

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4
Q

According to the AMH, what medication would an asthmatic patient be taking at early phase and late phase?

A

Early = SABA when req. for symptom relief + low dose ICS

Late (if symptomatic) = ICS + LABA for maintenance and SABA when req. for symptom relief

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5
Q

Beta-2 adrenoreceptor agonists are used in treating early phase asthma. What are the two types of this drug + examples?

A
  1. Short-Acting Beta-2 Adrenoreceptor Agonist (SABA) = salbutamol
  2. Long-Acting Beta-2 Adrenoreceptor Agonist (LABA) = salmeterol and formoterol
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6
Q

How do beta-2 adrenoreceptor agonists work to relieve asthma symptoms?

A
  1. Adrenaline + noradrenaline (Ad + NAd) = natural mediators of SNS
  2. Ad +NAd activate beta-2 adrenoreceptors to relax bronchial smooth muscle
  3. Beta-2 adrenoreceptor agonists mimic Ad + NAd
  4. Ad = 20x more potent than NAd
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7
Q

What are the adverse effects of B2 agonists?

A

Common = tremor, increased heart rate / palpitations, headaches

Serious (at higher dose) = hypokalaemia (low plasma / potassium)

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8
Q

What is anaphylaxis?

A

Medical emergency

Bronchospasm + hypotension due to mast cell degranulation + histamine release

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9
Q

Adrenaline (epipen) is potentially life saving in the case of anaphylaxis. What is the mechanism behind it?

A

Adrenaline = non selective adrenoreceptor agonist

Alpha-1 activation = vasconstriction (restores BP)

Beta-2 activation = bronchodilation (reverse airway obstruction)

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10
Q

What are relievers and controllers?

A

Relievers = short acting agonist to relive symptoms (bronchodilators eg SABA)

Controllers = treatment of underlying causes (anti-inflammatories eg ICS or LABA)

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11
Q

What are exmaples of inhaled corticosteroids (ICS)?

A

Budesonide
Fluticasone

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12
Q

What are corticosteroids?

A

Mimic cortisol with minimal aldosterone activity

Glucocorticoids

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13
Q

Cortisol is an endogenous hormone which can regulate many physiological processes and one major immune system process. How do different levels of corticosteroids impact these processes?

A

Low levels = physiological concentrations = improve immune function

High levels = pharmacological concentrations = potent anti-inflammatory agents and immunosuppressants

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14
Q

Steroids act on nuclear receptors to alter gene transcription, this is a slower process than via other receptors. What are 4 common receptors and their activation time scales?

A
  1. Ligand-gated ion channels (ionotropic receptors) = milliseconds
  2. G protein coupled receptors = seconds
  3. Kinase-linked receptors = hours
  4. Nuclear receptors = hours
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15
Q

How do glucocorticoids (ICS) alter production and release of inflammatory mediators?

A
  1. Decrease production of prostanoids via suppression of COX II and arachidonic acid release
  2. Decrease production of cytokines
  3. Decrease histamine release + other mediators from basophils and mast cells
  4. Increase synthesis of anti-inflammatory factors
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16
Q

How do glucocorticoids alter the activity of inflammatory cells?

A
  1. Decrease egress of meutrophils from blood vessels = reduce activation of neutrophils. macrophages, and mast cells
  2. Decrease activation of T-helper cells and switch from Th1 to Th2 immune response
17
Q

What are the adverse effects of corticosteroids?

A

Common = oropharyngeal thrush and dysphonia

Systemic (high dose) = adrenal suppression, bone density loss, glaucoma, cataract pneumonia, skin thinning, impaired growth

18
Q

At high doses, corticosteroids may cause adrenal gland suppression. What does this mean and how does it happen?

A

Cortisol synthesis and release from adrenals is inhibited

Corticosteroids mimic cortisol so establish negative feedback from adrenal glands (think they don’t need to produce more even if they normally would)

Important to wean patients off corticosteroids in order to reactivate adrenal glands

19
Q

What are the two types of inhaled muscarinic acetycholine antagonistsm and what are examples of each?

A
  1. Short Acting Muscarinic Acetylcholine (SAMA) = Ipratopium
  2. Long Acting Muscarinic Acetylcholine (LAMA) = Tiotropium, Glycopyrrolate
20
Q

What medication might a patient with COPD be takinng in early and late phase exacerbations?

A

Early = SABA or SAMA for symptom relief

Late (if symptomatic) = LABA or LAMA

Later = LABA + LAMA + ICS

21
Q

Beta 2 agonists relieve asthma symptoms via G protein coupled receptros to affect relaxation pathways on the SNS. How does muscarinic acetylcholine relieve symptoms for COPD?

A

G protein couple receptors

Activates acetylcholine muscarinic receptors from PNS to affect contraction pathway

21
Q

Beta 2 agonists relieve asthma symptoms via G protein coupled receptros to affect relaxation pathways on the SNS. How does muscarinic acetylcholine relieve symptoms for COPD?

A

G protein couple receptors

Activates acetylcholine muscarinic receptors from PNS to affect contraction pathway

22
Q

What are the common adverse effects of muscarinic antagonists?

A

Dry mouth + throat irritation

23
Q

What is the treatment of allergic rhinitis?

A

Histamine receptor antagonist + corticosteroid

Examples = Cetirizine + Azelastine w/ fluticasone

24
Q

What is allergic rhinitis and why is it associated with asthma?

A

Local IgE mediated allergic condition to inhaled allergens

50-80% asthmatics ALSO have allergic rhinitis
20-30% of allergic rhinitis patients ALSO have asthma

Life Sciences - Sem 2 (27 decks)

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