Pharmacology of the Airways Flashcards Preview

CARDIO-RESPIRATORY > Pharmacology of the Airways > Flashcards

Flashcards in Pharmacology of the Airways Deck (13)
1

What type of stimulation causes bronchodilation?

Sympathetic (adrenergic) stimulation

2

What type of stimulation causes bronchoconstriction?

Parasympathetic (cholinergic) stimulation

3

Explain how beta blockers (beta-1 receptor antagonists) can trigger asthma or bronchospasm

Blocking beta-1 receptors affects the heart, but bronchial smooth muscle has beta-1 receptors (cause bronchodilation) and therefore, due to a lack of specificity, the beta blockers may block these receptors also and cause bronchoconstriction, especially at high doses

4

Explain how COX blockers can trigger asthma or bronchospasm

Cyclo-oxygenase blockers (e.g. aspirin and NSAIDS) cause a relative increase in arachidonic acid --> increases leukotriene production --> leukotrienes mediate inflammation --> COX-blocking drugs may be associated with bronchospasm in susceptible individuals

5

Describe how an individual becomes sensitised to an allergen at the beginning of asthma development

Antigen engulfed by dendritic cells --> activation --> columnar epithelia also recognise allergen and stimulate secretions of lymphocytes --> lymphocytes condition activated dendritic cells to produce chemokines to attract CD4 T cells (helper) --> dendritic cells activate CD4 cells into Th2 cells --> Th2 cells stimulate plasma cell production via IL-3 and IL-4 on B cells --> promotes IgE antibody production (allows class switch) --> IgE binds to mast cell receptors via Fc portion of antibody --> forms IgE-mast cell complexes --> these respond to allergens and cause mast cell degranulation

6

Outline the mechanism of mast cell activation upon re-exposure to an allergen in asthma

Allergen re-exposure --> allergen binds to allergen-specific IgE-mast cell complexes --> cross-linking in FcԑR binding two aspects together --> intracellular signalling --> mast cell activation and degranulation --> inflammatory mediators --> synthesis of newly formed mediators

7

Describe the mediators that are released from mast cells in degranulation (as in asthma)

Histamine (vasodilation and increased vascular permeability --> mediates inflammation), proteases (degradation of endothelium, eosinophil and neutrophil chemotactic factors), prostaglandins (vasodilation), and leukotrienes (increased vascular permeability and increased mucus secretion)

8

Describe the late phase reactions in asthma responses

Activated mast cells secrete TNFα (tumour necrosis factor alpha) which activates the endothelium at the site of exposure to the allergen causing expression of adhesion molecules that promote migration of leukocytes from the blood. At this point chemotactic factors are also secreted by activated dendritic cells which causes the later recruitment of eosinophils, neutrophils, basophils and T cells to the site and this causes further inflammation

9

Describe how beta-2 agonists can be used in the treatment of asthma

Beta-2 agonists mimic the sympathetic nervous system and cause the bronchodilation from activation of this receptor in the bronchial smooth muscle

10

Describe how steroids can be used in the treatment of asthma

Used as an anti-inflammatory to prevent distended airways and small lumen

11

Describe how mast cell stabilisers can be used in the treatment of asthma

Stabilise mast cells through the use of leukotriene agonists, in order to prevent degranulation

12

Describe how monoclonal anti-IgE antibodies can be used in the treatment of asthma

To prevent the presentation of IgE so complexes cannot be formed that respond to allergens in asthma

13

Describe how anti-muscarinics can be used in the treatment of asthma

They block the parasympathetic nervous impact on the beta-2 adrenergic receptors in the bronchial smooth muscle, and therefore inhibit bronchoconstriction