Lecture 10: Lung development and surfactant part 2 Flashcards
Why are there bubbles in olympic diving?
Breaks the surface tension to reduce possibility of injury
What’s the necessity of lowering surface tension?
Otherwise the tension development is to high for us to generate enough work of breathing to adequately overcome.
If the surface of the liquid lining the lung was plasma the pressure required to maintain lung volume would be 6x higher then the norm
Pulmonary Surfactant
Produced by our lungs
95% phospholipids
5% proteins
Although small amounts of proteins, if some are absent it can lead to terminal defects
Site of surfactant Synthesis
Type II alveolar cells
Have Lamellar bodies (look like an onion cut in two), due to the highly organised packaging of the phospholipids and proteins, similar to the membranes of cells.
What is the make up of a Pulmonary surfactant phospholipid and how does that support its function?
-Non-polar tail (fatty portion), that’s hydrophobic
Carbon chain length up to 18
-Polar Head, Hydrophillic
SO they favour the surface environment.
Surfactant proteins, Similarities and differences between them?
Four Proteins: SP-A, B, C, D
SP-A and D
SP-A and SP-D: Large hydrophillic which favour the aqueous environment.
-host defence, ST reduction, regulate surfactant synthesis
D) Doesn’t exhibit SPA’s effect on surface tension
SP-B and C
SP-B and SP-C: Small lipophillic proteins that favour the surface or lipid environment which the phospholipids are found
B) Formation of tubular myelin.
B&C)formation and stabilisation of phospholipid monolayer (break up phospholipids) this is done most effectively by SP-B
Formation of the phospholipid Monolayer
1) Lammelar body (SPA, SPB and calcium) excreted to the liquid surface of the lung, forms Tubular Myelin (fine mesh)
2) SPA, SPB and SPC break it up to form the phospholipid monolayer at the surface
Degradation of the phospholipids
The PL’s expand and collapse, bang into each other, leading to mechanical destruction, so have a turnover rate of 3-11 hours.
1) Taken up/endocytosed and repackaged by Type II cells.
2) Transported towards ciliated airways, due to surface tension escalator
3) Degradation by extracellular enzymatic activity: proteases in the lungs
4) Macrophage phagocytosis: due to non-specific immune response and due to phagocytosis of surfactant itself
5) Epithelial Reabsorption into either lymph or blood
So if PL production is impaired (sepsis), then your work of breathing is higher
Surface tension Elevator
Low ST at the bottom and a high ST at the top. Things move towards higher ST
How does surfactant actually work?
Water molecules are attracted to each other, Surfactant interfere with that.
A monoclonal layer of surfactant DON’T ATTRACT EACH OTHER, thereby there is no tension, and there is a marked reduction in the desire of that surface to collapse.
This makes it easier to expand and to remain a constant, so the pressure of FRC
How much does Surfactant reduce surface tension
From 70 mN/m to 10mN/m, the means a 6-7x reduction in the work of breathing and pressures required to maintain the lung
Breathing in and out
Expand surface : Molecules move in, Surface tension increase
compress: Molecules move out
Still requires energy, but not as much ( not energy independent)
Sighing, expands the lungs, reduces ST and allows for more surfactant
Compliance
Pressure required to expand the lung by and given pressure
C = V/P
Determined by:
- Elasticity of lung tissue
- Surface tension of the air-liquid interface in the alveoli
Saline vs air compliance graph shows the importance of ST
Around the working regions of the lung (FRC) the ST is the most important factor of lung elasticity.
La place’s Law
The pressure of holding a bubble open related to tension and radius.
P= 2T/r
The smaller the radius the much higher the pressure. We get around the very small radius of the alveoli by reducing the tension in the lining of the lung
Surfactant and fluid balance.
Reduces the tendancy for fluid to be ‘sucked’ into the airspace, due to the high surface tension causing a negative pressure.
Host Defences
Surface tension gradients move particulate matter towards ciliated regions
Both SP-A and SP-D act to bind to pathogens to promote the action of macrophages in the immune response.
Reduces formation of Liquid plugs
stops forming and helps to break up.
Diseases/ conditions with impaired Pulmonary Surfactant
Complications of prematurity
-NRDS
Infectious Lung DIsease:
- pneumonia
- HIV
- pulmonary oedema
Obstructive Lung Diseases:
- Asthma
- Bronchiolitis
- COPD
Congenital Diseases:
- Cystic Fibrosis
- Surfactant protein B deficiency
Non-specific Resp Diseases:
-ARDS
Transition from liquid to air Breathing
Surfactant from week 24 onwards. High mortality rate.
The amount of surfactant rapidly increases post 34 weeks, so survival increases.
Neonatal Respiratory Distress Syndrome
De-lamination of the alveoli. The pressure required to change lung volume caused mechanical damage to the babies lungs, 5x harder work of breathing.
As diaphragm goes down, chest collapses.
