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Year 1 LSS > Respiratory system: Cells of respiratory system > Flashcards

Respiratory system: Cells of respiratory system Flashcards

1
Q

Mucus ( function, secreted by who? consists of what?)

A

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

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2
Q

Respiratory endothelial cells Function

A

Endothelial

  1. A physical barrier, ciliated cells –> shift mucus out
  2. secrete mucins, salts, and water –> components of mucus
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3
Q

Goblet cells in respiratory endothelium function and location

A

In larger (most abundant/significant) middle and smaller airways

20% of endothelium

Secret mucus

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4
Q

Non-ciliated secretory bronchiolar epithelial cell (other Names, location, function)

A

Clara cells, Club cells

replace goblet cells in smaller airways (ca. 20% of all cells)

Function:

  • secretion
  • detoxification
  • repair + progenitor (vorfahre) cells
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5
Q

Type 1 Pneumocytes

A

in alveoli

Gas exchange

very very thin with large surface are –> 96% of alveolar surface area

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6
Q

Type 2 Pneumocytes

A

Secrete Surfactant –> prevent alveoli from collapsing

barrier inside epithelium

stemm cells –> can differentialte into type 1 in damage

like clubb cells –> also detoxification

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7
Q

Respiratory smooth muscle cell function

A

under Endothelium

Function:

  • structure
  • tone
  • little secretion (can be modified in inflammation –> NO, prostaglandins, chemokines, cytokines)
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8
Q

Respiratory Interstitial cells

A

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)

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9
Q

Changes in Epithelium in lung disease (Smoking)

A
  • 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)

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10
Q

Changes to Alveoli/Pneumocytes in Lung disease / Smoking (Alveolar fibrosis + Emphysema)

A

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

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11
Q

Changes to immune cells in lung disease / smoking

A

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

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12
Q

Which regulatory and inflammatory agents do the airway epitheilal cells produce?

A
  • NO (–> speed up Celia?)
  • CO (–> killing bacteria)
  • Chemokines
  • Cytokines
  • Arachidonic acid metabolies
  • Proteases
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13
Q

How do cilia clear mucus?

A

They beat in a highly syncronised way –> metachronically

to clear mucus out

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14
Q

What are the typical layers and components of an airway?

A
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15
Q

What are the functions of Airway smooth muscle?

A

To control/determine

  1. Secretions (e.g. inflammatory mediators, cytokines, chemokines in inflammation)
  2. Tone (via relaxation and contraction)
  3. Structure (e.g. proliferation/hypertrophy)
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16
Q

Explain the secretory airway smooth muscle function in inflammation

A
17
Q

Where do the bronchial arteries arise from?

A

Bronchial arteries arise from many sites on:

aorta, intercostal arteries and others

18
Q

How does blood from the airways return to the heart?

A

Blood returns from tracheal circulation via systemic veins

Blood returns from bronchial circulation to both sides of the heart via bronchial and pulmonary veins

19
Q

What is the function of the tracheobronchial circulation?

A
  • 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)
20
Q

Where does plasma exudation in the airway occur?

How can it be stimulated?

A

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
21
Q

How is contraction of the human airway achieved?

Explain the cholinergic mechanism of the airway

A

Via parasympathetic control of the vagus nerve

22
Q

How is relaxation of the human airway achieved?

A
  1. Sympathetic NS–> Adrenals –> Adrenaline
  2. NO relaxation (via spinal cord)
23
Q

What is the cause for asthma to occur?

What are its characteristics?

A

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
24
Q

What are the structural changes in the airway in asthma?

A
  • 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)
25
Q

What is the major inflammatory cell in Astma?

A

Eosinophil

26
Q

What is the role of surfactant in the alveoli?

A

surfactant is the thin liquid lining the alveoli and preventing it from collapsing

27
Q

How do the ciliated cells in the epithelium of the lung changes in smokers?

What can this lead to?

A

The mucus clearing is not as effective –>

  • The movement is asynchronous
  • They grow further down the lung and block smaller airways

This can lead to fibrosis:

via obstruction –> Bronchitis –> More mucus production –> thicker mucus –> inflammation –> Fibrosis

28
Q

How do the goblet cells in the airway in smokers and COPD change compared to a non-smoker?

A

Goblet cells (normally 20%) double at least!

This leads to an increased, thick secretion

29
Q

How are small airways normally kept open?

A

Via alveoli

–> But can get stenotic in COPD and smoking –> no air can get through

30
Q

Where do Club cells in the airway occur?

What is their function?

A

Replace Goblet cells in the smaller airways

  • secrete
  • Normally 20%
  • Detoxification
  • Repair
31
Q

What is the function of Stoma cells in the alveoli?

A

They secrete ECM

–> Collagen, Elastin. and divide to repair damage

32
Q

Explain How where which type of leukocyte in the airway occurs and how these proportions change in smoking

A

In Respiratory unit:

10% Neutrophils, 90% Macrophages

Smoking: 30%N, 70% M

In Airways:

30% Neutrophils, 70% Macrophages

Smoking: 70% N, 30% Macrophages

–> Both cell types can be up to 10 folds increased in smoking

33
Q

Which effects do Oxidants secreted by Neutrophils and Macrophages have?

A

They secrete oxidants:

Good: Antimicrobial

But: Also Oxidants –> break down of tissue + mediation of chronic inflammation

34
Q

What are the two acini of a submucosal gland?

What does each secrete?

A

Mucous cells secrete mucus

Serous cells secrete antibacterials

(e.g. lysozyme)

Glands also secrete water and salts

(e.g. Na+and Cl-)

Year 1 LSS (12 decks)

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