Unit 1 Respiratory 3: Pathophysiology

Question 1

What determines airway resistance?

Answer 1

Airway diameter

Question 2

What nerve supplies parasympathetic innervation to airway smooth muscles?

Answer 2

Vagus nerve (CN X)

Question 3

Describe the process of parasympathetic nervous system bronchoconstriction

Answer 3

Cholinergic nerve endings release Ach onto muscarinic-3 receptors.
M3 receptor is coupled to a Gq protein which is turned on and activates phospholipase C (PLC).
PLC activates inositol triphosphate (IP3) - the second messenger.
IP3 stimulates Ca+2 release from the sarcoplasmic reticulum.
Increased iCa+2 activates myosin light chain kinase, which enables contractile mechanism -> bronchoconstriction.

Question 4

How is the PNS bronchoconstriction pathway turned off?

Answer 4

When IP3 phophatase deactivates IP3 to IP2

Question 5

Besides PNS, what other mediators -> bronchoconstriction?

Answer 5

Mast cells are highly concentrated in smooth airway epithelium. Coughing, allergy, of infection activate IgE, cytokines and complement, which in turn amplify the inflammatory response.
Non-cholinergic c-fibers release chemicals that promote bronchoconstriction.

Question 6

How do circulating catecholamines -> bronchodilation?

Answer 6

Beta-2 receptor are well represented in airway smooth muscle, but there are SNS endings here, instead these receptors are activated by systemic catecholamines.
The B2 receptor is couple to a Gs protein, activation turns on the Gs protein and this activates adenylate cyclase.
Adenylate cyclase activates cAMP - the second messenger.
Along with protein kinase A, cAMP reduces Ca+2 release from the sarcoplasmic reticulum.
This reduces smooth muscle contraction and promotes bronchodilation.

Question 7

How is the bronchodilation via circulating catecholamines pathway turned off?

Answer 7

When phosphodiesterase 3 deactivates cAMP by converting it to AMP

Question 8

What affect does nitric oxide have on the bronchials?

Answer 8

It is a potent smooth muscle relaxant.
Non-cholinergic PNS nerves release vasoactive peptide onto airway smooth muscles, this increases NO production.
NO stimulates cGMP, which fosters smooth muscle relaxation and bronchodilation