Introduction to Respiratory system + Oedema Flashcards
what do we mean by conducting zone vs gas exchange zone in the respiratory system
conducting zones (nose to bronchioles) form a path for conduction of the inhaled gases {aka air’s journey to respiratory zone}
respiratory zone (alveolar duct to alveoli) where the gas exchange takes place
immune defences of lung
1) 1st line: Non-specific barriers
a) Skin and mucous membranes b) Cilia
2) 2nd line: Non-specific (i.e. innate immune system) immune cells
a) Patrolling leukocytes – phagocytic WBCs –**primarily macrophages** b) In response to bacterial infection - neutrophils
3rd line: specific, acquired immunity=B and T cells + antibodies
defense against pathogens starts in the nose:
[______ _____ ______] in nasal passages spin air flow into vortex - dust particles and some airborne pathogens are thrown outwards into mucous – trapped and destroyed.
○ nasal epithelium covered in mucus. Air taken in nasally passes over mucous covered surfaces.
○ Turbinate bones (conchae) in nasal passages spin air flow into vortex - dust particles and some airborne pathogens are thrown outwards into mucous – trapped and destroyed.
○ Mucous contains antibodies + antibiotic peptides which can kill/ immobilise pathogens
Mucous continuously secreted by goblet cells which are interspersed w epithelial cells. Epithelial cells have cilia on their surface; cilia move back + forth and transmit mucous containing immobilised pathogens back into throat where swallowed and most pathogens killed by stomach acid
mucus is continuously secreted by goblet cells which is moved by cilia; what kind of epithelium covers the respiratory tract up until the bronchioles
respiratory tract epithelium: ciliated pseudostratified columnar epithelium until bronchioles
this system of mucus being moved by cilia is called the mucociliary elevator
what is cystic fibrosis
- Autosomal recessive genetic disorder
- Abnormal function of epithelial chloride channel - mutation in CFTR gene; Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) – key role in maintaining lungs epithelia
N.B. In CF mucous is abnormally thick (due to genetic mutation), and difficult for cilia to move. People with CF require regular physiotherapy to ‘cough up’ and remove thick mucous decrease infection with pathogens
why do alveolar ducts have no mucus lining?
as it would impede gas exchange
what is the relationship between pressure of a gas and the volume it occupies
Boyle’s Law
= inverse relationship between pressure of a gas and the volume it occupies
so the smaller the volume the higher the pressure
what is quiet inspiration
Quiet inspiration {breathing}, aka eupnea, is breathing at rest and does not require the cognitive thought of the individual.
describe lung mechanics of inspiration + expiration
quiet inspiration:
* Diaphragm contracts {inferiorly} and moves downward, external intercostal muscles contract, rib cage expands/chest pulled outwards
- Increases thoracic cavity volume
- As a result, intrapleural pressure becomes more negative (decreases further below atmospheric pressure)
- Increase in negative intrapleural pressure increases the transpulmonary pressure, causing lungs and alveoli) to expand
- As alveoli expand, alveolar pressure drops below atmospheric pressure.
*This pressure difference causes air to flow into lungs until alveolar pressure equals atmospheric pressure
quiet expiration: (passive)
*External intercostal muscles relax and the inward elastic recoil of lungs results in decrease in lung volume
- Alveolar volume decreases, thoracic cavity volume decrease
*(pressure increases inside lungs)
Causes alveolar pressure> atmospheric pressure and air leaves the lungs until pressures equalise and no more air movement; atmospheric pressure in lungs high again as smaller volume
- Intrapleural pressure remains negative relative to atmosphere, but less negative than at end inspiration
Thus still positive transpulmonary pressure – alveoli do not completely collapse despite increased pressure within lung from lung elastic recoil decreasing lung volume
define the following:
*tidal volume
*total lung capacity
*residual volume
*lung compliance
*lung elastic recoil/ aka elastance
define the following:
*intrapulmonary pressure
* intrapleural pressure
* transpulmonary pressure
Intrapulmonary pressure: pressure inside alveoli/lungs
Intrapleural (pleural) pressure: pressure in pleural space between visceral and parietal pleura
(Intrapulmonary pressure)- (intrapleural pressure)
=Transpulmonary pressure (always +ve; enables alveoli to expand and keeps the alveoli expanded so they don’t collapse (regardless of pressure)
what connects lungs to chest wall
connects lungs to chest wall: PLEURA
pleura is the reason when we expand our ribcage, expands our lungs; as remember no muscles or ligaments or tendons that attach lungs to ribcage just pleura. The chest wall is connected to lungs because of the pleural seal {surface tension cuz of intrapleural fluid}
► Pleura: Each of a pair of serous membranes lining thorax and enveloping lungs. ► Parietal pleura lines the inside of each hemi-thorax (the bony thoracic cage, diaphragm & mediastinal surfaces) ► Visceral pleura lines the outside of lung. ► Intrapleural space = space between visceral and parietal pleura, (potential space; between the 2 serous membranes) - contains about 15 ml fluid N.B. Fluid in pleural space
lungs have a natural [__] elastic recoil
chest wall has a natural [___] elastic recoil
these 2 opposing forces create a negative pressure in the intrapleural space= stopping the lungs from COLLAPSING
lungs have a natural inwardelastic recoil
chest wall has a natural outward elastic recoil
these 2 opposing forces create a negative pressure in the intrapleural space; -ve pressure due to elastic recoil of lung pulling visceral pleura inward and chest wall elastic recoil pulling parietal pressure outward
*intrapleural pressure negative throughout expiration + inspiration [becomes even more -ve up until end of inspiration] relative to atmosphere and intra-alveolar pressure keeps alveoli/lungs from fully collapsing with each expiration
what is the functional residual capacity (FRC) of lungs
FRC/ Functional residual capacity= volume air at resting expiratory level
resting expiratory level (REL)= state of equilibrium maintained by
–lung collapse inwards (lung elastic recoil)
-chest wall pulls outwards (chest elastic recoil)
these FORCES are equal and opposite so chest balances out= no movement of chest wall
n.b. if condition where recoil too strong then FRC will be lower, if lung elastic recoil is too weak the FRC will be larger BOTH ARE PATHOLOGICAL AND BAD NEWS
Each alveolus consists of three types of cell populations (listed below) can you explain their functions?
- **Type 1 pneumocytes** (70% internal surface of alveolus) These cells are thin and squamous, ideal for gas exchange. They share a basement membrane with pulmonary capillary endothelium, forming the air-blood barrier where gas exchange occurs. These pneumocytes joined one another and other alveolar cells by tight junctions, forming an impermeable barrier to limit the infiltration of fluid into the alveoli. - **Type 2 pneumocytes **(7% of the internal surface of each alveolus) These cells have a mean volume that's half that of type I pneumocyte with apical microvilli. Within their cytoplasm are characteristic lamellar bodies containing a surfactant, a substance secreted that decreases the surface tension of alveoli - **Alveolar macrophages** (mononuclear phagocytes that are residents in alveoli) They derive from blood monocytes. The cell membrane of these cells can utilize a network of microtubules to change shape during chemotaxis or phagocytosis.
Functions:
Type I pneumocytes :
* Facilitate gas exchange
* Maintain ion and fluid balance within the alveoli
* Communicate with type II pneumocytes to secrete surfactant in response to stretch
Type II pneumocytes:
* Produce + secrete pulmonary surfactant - surfactant is a vital substance that reduces surface tension, preventing alveoli from collapsing.
* Expression of immunomodulatory proteins that are necessary for host defense
* Transepithelial movement of water
* Regeneration of alveolar epithelium after injury
Alveolar macrophages:
* they collect inhaled particles from the environment e.g. coal, silica, asbestos, microbes i.e. viruses, bacteria, fungi.
* have a receptor named toll-like receptor, which binds to another receptor on surface of microbial cells, the pathogen-associated molecular receptor. This interaction facilitates the phagocytosis of the pathogen and the secretion of pro-inflammatory cytokines to enhance the local immune response.
* Within the alveolar macrophage, engulfed microbes become fused with their lysosome to destroy the pathogen
