L11.2 Smooth muscles in the respiratory system Flashcards
1
Q
How many generation of branches of airways are there?
A
- 23 generations of airway, doubles at each branching
- gen 0 = trachea
- gen 1 = 2 main bronchi
- gen 2-4 = large bronchi
- gen 5-11 = small bronchi
- gen 12-23 = bronchioles
2
Q
How are the number of airways determined?
A
- # of airway = 2generations
3
Q
Movement of air through the airways
A
- Conducting airway → air diiffusion at exchange
- Parenchyma → gas movement by bulk
4
Q
Resistance of airways
A
- 50% resides in nose, pharynx, larynx
- Nose
- resistance 2x higher than mouth → reflex switch breathing through mouth in exercise
- Vocal folds of larynx
- Come tgt to form “expiratory brake” to prevent too-rapid collapse of lungs by maintaining intramural pressure
- ↓cross sectional area → ↑resistance
- ∴trachea and bronchi (low generation of branches) → ↑resistance
- Resistance increases till 3rd generation, then starts decreasing (due to increase SA)
5
Q
Why/how do you cough?
A
- S.M in airways facilitate coughing → to remove foreign object obstructing the airways by coughing
6
Q
Resistance of small bronchi/bronchioles
A
- Generation 7-14 → small cross-sectional area, some contribution to resistance
- Resistance is variable
- No support of cartilage, and with presence of SM
7
Q
Resistance beyond 16 generation
A
- Rapid ↑ in airway numbers → ↑x-sectional area → ↓resistance
8
Q
Airway smooth muscles
A
- More prominent in lower airways
- No cartilage in small airways → SM contraction → collapses small airways
- Tube narrows and shortens
9
Q
Silent zone of airways
A
- FEV1.0 used to measure airflow through airways
- Contributed to by LARGE airways ONLY
- Drug which treats smaller airways will not see change in FEV1.0
- COPD is a silent disease because it is not picked up by such measures and largely affects the smaller airways
10
Q
ASM morphology
A
- Cytosol rich in contractile myofilament
- Actin-myosin of SM show great plasticity
- When ASM contracts, ASM shortens in a way that doesn’t lose volume, just becomes squat
11
Q
ASM of asthmatic patients
A
- More prominent SM
- More mediators activating SM
- Muscles acts on mucus gland → excessive mucus which contributes to further narrowing of airway
- ↑globet cell (secrete mucus)
- ↑mucosal vascularity
12
Q
Bronchial thermoplasty
A
- kills SM for severe asthmatics
13
Q
Effectiveness of b-agonists on asthma
A
- b-agonist → treats spasms BUT vascular inflammation and mucus obstruction not treated
14
Q
ASM dysfunction
A
- Contributes to wall vol in airway remodelling and inflammation
- Prolif and migrate SM
- Secretion of cytokines, extracellular matrix proteins (i.e. collagen)
15
Q
Do ASM matter?
A
- Asthmatic patients have more SM mass, but SM proliferation is not increased
- SM secretes cytokines and is proinflammatory
- ↓Cytokine mediators after thermoplasty → removing SM
- Removal of SM → improves asthma (in initial trials)
17
Q
Inflammatory mechanism
A
- Mast cells activated
- Mast cells release mediators that activate ASM (LT most important)
- Over time → other cells activated
- Communicate via cytokines (e.g. T cells prod GM-CSF → ↑eosinophils survival)
18
Q
Actions of important agonists
A
- LTD/E4 are potent contractile agents in SM (much more significant than histamine)
- Causes persistent activation of SM in airways
