RM Week 10 Asthma Flashcards by Adam Little

What are the type/s of innervation to the smooth muscle of the airways?

Parasympathetic
Nonadrenergic NonCholinergic (NANC)
*sympathetic nerves do not supply the bronchial smooth muscle

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What type of airway is most likely to collapse and why?

Bronchiole/small airways

They have no cartilage support and rely on smooth muscle tone to remain open

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How can adrenergic control be exerted on bronchial smooth muscle?

By action of catecholamines (noradrenaline)

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What adrenoreceptors are found on bronchial smooth muscle?

B1, B2 and A1

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What is the result of noradrenaline binding to B2 receptor on smooth muscle?

Has an inhibitory effect on the smooth muscle, causes it to relax. Overall causes relaxation of the bronchial smooth muscle and increased diameter of the airway lumen

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What occurs when norepinephrine binds with alpha 1 receptors?

Contraction of bronchial smooth muscle

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What is the mechanism of action of NE on B2 receptors

The receptor is G Protein Coupled receptor, which when activated causes activation of adenylate cyclase, forming cAMP - which goes on to inhibit calcium entry into cell which stops contraction

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Apart from smooth muscle, what other cells present in the lung have B2 receptors on them?

Sub mucosal glands and mast cells, epithelial and endothelial cells

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Is B1 or B2 receptors most abundant in the lungs? What is a general ratio of the difference in numbers?

B2 more abundant

3:1

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What effect does parasympathetic stimulation have on the airway wall?

Constriction

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What is the type of receptor and what is the neurotransmitter that acts on the receptor?

Muscarinic type 3 receptor

Acetylcholine (ACh) neurotransmitter

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Apart from bronchoconstriction, what are other effects of Stimulation of muscarinic receptors within the lungs?

Increased glandular secretion
Increased viscosity of mucus
Histamine release increased

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How is it suggested that NANC aids in bronchodilation?

Vasoactive intestinal peptide, Nitric Oxide and ATP possible neurotransmitters
NANC innervates smooth muscle and releases ligand which reduces calcium in the cells and prevents contraction

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What is asthma?

Narrowing airways and inflammation of airway walls due to increased responsiveness to various stimulus by tracheobronchial tree

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What is a key feature of asthma?

Chronic inflammation of airways which over time leads to damage to normal function - which can amplify further hypersensitivity reactions

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What are the 2 basic classifications of asthma and how are they different?

Extrinsic and intrinsic
Extrinsic triggered by exposure to an extrinsic allergen (from outside the body)
Intrinsic is where the cause is not due to an external allergen

What are the different classes of intrinsic asthma?

Atopic and occupational

What is the most common form of asthma?

Atopic (allergic)

What is the cause of atopic asthma?

Type 1 hypersensitivity reaction to an allergen, following presensitisation

What is presensitisation?

Antigen (that the body doesn’t like) is presented to the the Type 2 T Helper Cell. Produces cytokines that turn on B cells which produce IgE antibodies for the antigen. These antibodies are loaded onto mast cells. There is no reaction the first time the body encounters the antigen, but the next time there will be reaction

What are the 3 phases of a type 1 hypersensitivity reaction

Presensitisation
Initial (early) phase
Late phase

What occurs in the early phase response to an allergen which the body is already sensitised to?

Binding of antigen to mast cell antibodies leads to degranulation reaction, which releases chemical mediators
Leads to increased increased mucus production, opening of mucosal tight junctions (causing greater exposure of antigen to mast cells) and direct stimulation of parasympathetic nerves which cause bronchoconstriction

What occurs in the late phase response?

Release of inflammatory mediators from mast cells, and granulocytes leading to the recruitment of leukocytes, injury to the epithelia and mucociliary escalator and increased airway responsiveness

Why are eosinophils of particular importance in late phase response?

They produce major basic protein and cationic proteins which are toxic to epithelial cells. Epithelial and endothelial cells then release inflammatory mediators which makes the situation worse. Bronchoconstriction results from the proteins released from eosinophils

Why is there dyspnea in asthma?

Hypertrophied smooth muscle airways constrict and narrow airways, creating more resistance and airway friction Hypertrophy of mucus gland an increased mucus secretion further narrows airways Mucus is thick and slow to move

Clinical symptoms of asthma?

Unpredictable, disabling attacks of severe dyspnea (accompanied by coughing/wheezing) Virtually symptomatic between attacks Reduction in all indices of expiration flow (FEV1, PEFR, FEV1/FVC) Increased residual volume

What response does an asthmatic have on a flow volume test following administration of a bronchodilator?

Improvement of FEV1/FVC because it should widen airways and lower resistance to allow a better outflow of air during expiration

What happens to the equal pressure point in asthma?

It moves lower into the bronchioles. The narrowing of airways increases resistance and friction of air. Because there is more friction it means that the air is not getting through, and more effort is required to push it though. But the more effort means more pushing from the accessory muscles, which causes dynamic airway compression.

What is occupational asthma and how is it different to atopic asthma?

Exposure to allergen occurs due to nature of work and could be avoided altogether removing self from that environment. Can either be a hypersensitivity reaction or liberation of bronchoconstrictors which doesn't have any IgE

What is the most common cause of idiosyncratic asthma?

Respiratory tract infection, generally viral

How does idiosyncratic asthma bring about bronchoconstriction?

Viral induced inflammation of respiratory mucosa lowers threshold for stimulation of sub epithelial vagal receptors

Would IgE have to be present in idiosyncratic asthma?

What are the two treatment aims for asthma?

Reverse/prevent bronchodilation (bronchodilators) | Halt inflammatory response (anti-inflammatory drugs)

What is the main role of B2 agonists in the treatment of asthma?

The mimicking of adrenaline action on the smooth muscle -> bronchodilation

What other positive affects does B2 agonists have to prevent asthmatic response?

Stimulate mucus clearance | Inhibit mediator release from mast cells, neutrophils and eosinophils (which also have B2 receptors)

What role do corticosteroids have on preventing asthmatic response?

Inhibition of mast cell activity prevents the degranulation reaction Block chemotactic mediators from recruiting more WBCs Enhance beta receptor expression/function Disrupt activity/transcription of cytokines Prevent inflammatory mediators released from epithelium

In what way would anticholinergics benefit an asthmatic, and why is it considered inferior to B2 agonist?

Muscarinic antagonists prevent parasympathetic stimulation and bronchoconstriction of airway smooth muscle. Inferior because it doesn't block the part of the response mediated by immune cells which can directly stimulate bronchoconstriction