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Body systems- respiratory > Physiology of the airway > Flashcards

Physiology of the airway Flashcards

1
Q

When the mouth is open for breathing- what muscles contract and relax

A
  • Tongue contracted
  • Pharynx is relaxed
  • Flops backwards when breathing
  • Tonic and phasic muscle activity
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2
Q

What is phasic activity?

A

dPhasic activity that happens as phases- inspiration/ expiration

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3
Q

What is tonic activity?

A

Tonic is when it happens all the time

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4
Q

What is the pharyngeal dilator reflex?

A

Airway has pressure receptors that detect when P drops- by airway being too narrow. Pressure receptors to brain stem via afferent (trigeminal nerve). Brain to pharyngeal muscle contraction via efferent (vagus nerve).

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5
Q

Sleep disordered breathing- snoring

A

Snoring (25%)- when the reflex isn’t working well enough- Snore is soft palete flapping backwards and forwards very quickly

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6
Q

Sleep disordered breathing- apnoea

A

Sleep apnoea (10%)- lack of breathing- airway blocks and air can’t get through- number of times a person stops breathing per hour

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7
Q

Sleep disordered breathing- clinical features

A 
Clinical features:
•	Snoring
•	Daytime somnolence
•	Associated with:
-obesity- related to sleep apnoea- can diagnose with the size of the neck as more fat tissues in the neck
-hypertension
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8
Q

Sleep disordered breathing- treatment

A

Treatment:
• Weight loss
• CPAP- continuous positive airway pressure- keeps air at a higher P than atm P

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9
Q

When are the control of the muscles often poor

A

During sleep or with sedative drugs

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10
Q

What is airway lining fluid produced by?

A

Epithelial and goblet cells

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11
Q

What do goblet cells produce?

A

Goblet cells- produce mucus – present in large number in the airways
Mucin protects the lungs.

Goblet cells release mucin granules.

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12
Q

What are mucin granules released in response to?

A
  • airway irritation
  • tobacco smoke
  • infection
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13
Q

How many layers do cilia cells have?

What is the lower layer made of?

A

Movement- 2 layers- periciliary and mucous

Periciliary layers (salt layer)- water with salt

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14
Q

What is cilia inhibited by?

A
  • Tobacco smoke
  • Inhaled anaesthetics
  • Air pollution
  • Infections
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15
Q

How do cilia cells working?

A

Recovery and effective stroke of cilia cells.

Muco-ciliary escalate- pushing against gravity- towards the larynx so that you can get cough it out

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16
Q

Airway lining fluid- function- humidification

A
  • Nose breathing better than mouth breathing
  • Affected by breathing pattern
  • Heat and moisture exchanger- when dry air passes the fluid water evaporates into the gas mixture. Cause the heat from the fluid to be lost. When air is expired the warm air heats up the lining fluid causing condensation. If this exchange didn’t occur, litres of water would be lost from expired air.
  • ‘Active’ control of periciliary layer
17
Q

Airway lining fluid- function- airway defence

A
  • Muco-ciliary escalator

* Expectoration- coughing out mucus which have moved up the top of the airway

18
Q

Why is nose breathing better than mouth breathing?

A

Nose breathing better than mouth breathing as air has further to go and there is less turbulence - more air comes into contact with mucus so better humidified
To humidify- water evaporates from the linings

19
Q

What does the perciliary secrete?

A

Periciliary layer secretes chloride, decreasing water potential, causing water to move in via osmosis- controlling water loss- gel layer thickness controls water loss

20
Q

What are the clinical features of CF?

A
  • Autosomal recessive inheritance
  • (1 in 2500 births)
  • Abnormal cystic fibrosis transmembrane regulator protein
  • Progressive lung infection and destruction
  • Affects all systems with epithelial surfaces
21
Q

How does CF occur?

A

CFTR protein on epithelial cells that controls the airway lining fluid

Mutation of the CFTR gene can lead to CF- some mild, some severe

22
Q

Inhaled particles- very large ones

A

Deposited- Nose and pharynx
Mechanism- Inertial impaction
Examples- Pollen and sawdust

23
Q

Inhaled particles- large ones

A

Deposited- Large airways
Mechanism- Inertial impaction
Examples- Fungal spores

24
Q

Inhaled particles- small ones

A

Deposited- Bronchioles
Mechanism- Sedimentation
Examples- Particulate pollution, stone dust, asbestos

25
Q

Inhaled particles- very small

A

Deposited- Exhaled
Mechanism- Diffusion
Examples- Smoke (including cigarettes)

26
Q

Inhaled drug delivery- Large

A

Site of deposition- Pharynx/large airways

Potential uses- Hay fever

27
Q

Inhaled drug delivery- Medium

A

Site of deposition- Small airways

Potential uses- Athsma, COPD

28
Q

Inhaled drug delivery- Small

A

Site of deposition- Alveolus

Potential uses- Absorption into blood

29
Q

Pulmonary defences-second function of airway lining- non-immunological systems

A

Physical barrier and removal- catch it and cough it- how we deal with most of what we inhale- gel present stops pathogens in.

Whilst pathogen stuck to the mucus- chemicals in mucus by epithelium to help damage the pathogen.

30
Q

Pulmonary defence- chemical inactivation

A
  • Lysozyme- breaks down cells- bacterial cells
  • Protease enzymes e.g. elastase (& anti-protease system)- breaks down proteins- pathogen must have protein in it- will break pathogenic cell down- We have cells if protease gets through to our cilia cells- will damage epithelial cells- so lungs produce anti protease to prevent damage to yourself- Inherited disease- don’t produce anti protease – can cause emphysema
  • Antimicrobial peptides e.g. human b defensins- antibiotics against certain bacteria in the lungs
31
Q

Pulmonary defences- immunological systems- Humoral?

A

Humoral:

  • IgA (nose and large airways)
  • IgG (small airways)
  • IgE (allergic disease)
32
Q

Pulmonary defences- immunological systems- Cell-mediated cells?

A

Cell-mediated:

  • Epithelial cells
  • Macrophages
33
Q

Pulmonary defences- immunological systems- pathology?

A
  • Neutrophils (infection)- standard inflammatory cells

* Eosinophils (allergy)

34
Q

What harmful things do we breathe in?

A

Carbon monoxide- decrease oxygen carriage
Nitrogen oxides- airway irritation and asthma
Ozone-airway irritation and cough
Particulate matter- lung and systemic inflammatory response

35
Q

What are the sources for harmful things in air?

A

Indoor – cooking (gas or wood)

Outdoor – vehicles & power stations

36
Q

What are the associated risks of breathing harmful things?

A
  • Asthma
  • Pneumonia
  • Stroke
  • Heart attack
  • T2 diabetes

Body systems- respiratory (10 decks)

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