Respiratory system: Cells of respiratory system Flashcards
(34 cards)
Mucus ( function, secreted by who? consists of what?)
function: protection –> trapping + destroy of bacteria, chemicals etc.
Shifted out by cilia in Metachronal movements
Secreted by Submucosal glands and Goblet cells
Two phases: one more liquid (closer to cilia) and one further away (thicker)
–> Gel like structure because of glycoproteins called mucins
Respiratory endothelial cells Function
Endothelial
- A physical barrier, ciliated cells –> shift mucus out
- secrete mucins, salts, and water –> components of mucus
Goblet cells in respiratory endothelium function and location
In larger (most abundant/significant) middle and smaller airways
20% of endothelium
Secret mucus
Non-ciliated secretory bronchiolar epithelial cell (other Names, location, function)
Clara cells, Club cells
replace goblet cells in smaller airways (ca. 20% of all cells)
Function:
- secretion
- detoxification
- repair + progenitor (vorfahre) cells
Type 1 Pneumocytes
in alveoli
Gas exchange
very very thin with large surface are –> 96% of alveolar surface area
Type 2 Pneumocytes
Secrete Surfactant –> prevent alveoli from collapsing
barrier inside epithelium
stemm cells –> can differentialte into type 1 in damage
like clubb cells –> also detoxification
Respiratory smooth muscle cell function
under Endothelium
Function:
- structure
- tone
- little secretion (can be modified in inflammation –> NO, prostaglandins, chemokines, cytokines)
Respiratory Interstitial cells
include –> alveolar epithelial cells, ECM etc –> form support network
Stroma cells: produce ECM –> collagen and elastin –> elasticity and compliance
decide to repair damage ( can lead to fibrosis if too much)
Changes in Epithelium in lung disease (Smoking)
- more goblet cells (doubles at least) –> more, thicker secretion in order to try to clear chemicals
- less ciliated cells –> no clearance of mucus possible
- The function of ciliated cells: asynchronous etc –> don`t work properly
–> Stenotic airways (damage to alveoli, normally alveoli keep the airway open)
–> Leads to obstruction of airways (also inflammation, try to repair with fibrosis –> irreversible damage)
Changes to Alveoli/Pneumocytes in Lung disease / Smoking (Alveolar fibrosis + Emphysema)
In Emphysema: too many holes in lung cells (starts in the center of alveolar sac –> gets destroyed–> attempt of reparation with fibrotic tissue –> Emphysema
Alveolar fibrosis:
Normally: Type 2 cells differentiate into type 1 cells when type 1 cell damage
in smokers/fibrosis: No differentiation + excessive ECM –> fibrosis
Changes to immune cells in lung disease / smoking
Macrophages and neutrophils increase up to 10 times + relation changes
in respiratory unit: increase in neutrophils compared to macrophages
in airways this change is even more significant
Which regulatory and inflammatory agents do the airway epitheilal cells produce?
- NO (–> speed up Celia?)
- CO (–> killing bacteria)
- Chemokines
- Cytokines
- Arachidonic acid metabolies
- Proteases
How do cilia clear mucus?
They beat in a highly syncronised way –> metachronically
to clear mucus out
What are the typical layers and components of an airway?
What are the functions of Airway smooth muscle?
To control/determine
- Secretions (e.g. inflammatory mediators, cytokines, chemokines in inflammation)
- Tone (via relaxation and contraction)
- Structure (e.g. proliferation/hypertrophy)
Explain the secretory airway smooth muscle function in inflammation
Where do the bronchial arteries arise from?
Bronchial arteries arise from many sites on:
aorta, intercostal arteries and others
How does blood from the airways return to the heart?
Blood returns from tracheal circulation via systemic veins
Blood returns from bronchial circulation to both sides of the heart via bronchial and pulmonary veins
What is the function of the tracheobronchial circulation?
- Good gas exchange (airway tissues and blood)
- Contributes to the warming of inspired air
- Contributes to humidification of inspired air
- Clears inflammatory mediators
- Clears inhaled drugs (good/bad, depending on the drug)
- Supplies airway tissue and lumen with inflammatory cells
- Supplies airway tissue and lumen with proteinaceous plasma (‘plasma exudation’ – next slide)
Where does plasma exudation in the airway occur?
How can it be stimulated?
Plasma exudation occurs in the post-capillary venules e.g. as a feature of asthmah
It is stimulated by
- C-fibre (nerves)
- and inflammatory mediators
How is contraction of the human airway achieved?
Explain the cholinergic mechanism of the airway
Via parasympathetic control of the vagus nerve
How is relaxation of the human airway achieved?
- Sympathetic NS–> Adrenals –> Adrenaline
- NO relaxation (via spinal cord)
What is the cause for asthma to occur?
What are its characteristics?
An overresponsiveness to stimmuli leading to
- Airflow obstruction varies over short periods of time and is reversible (spontaneously or with drugs)
- Dyspnoea, wheezing and cough(varying degrees - mild to severe)
- Airway inflammation leading to re-modelling
What are the structural changes in the airway in asthma?
- Mucus plug –> Lumen is blocked
- Epithelial fragility –> m
- Goblet cell hyperplasia
- Thicker basement membrane
- Increase in SM
- Increase in Submucosal gland (hypertrophy)
- Vasodilation
- The cellular infiltrate–> inflammatory cells in mucus and submucosal)
