Module 2 - Respiratory system Flashcards

1
Q

Respiration

A

External: Movement of gases between environment and cells of body

Internal: Movement of gases from lungs, through the blood stream to the cells

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2
Q

Ventilation

A

Exchange of air between atmosphere and lungs

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3
Q

Divisions of respiratory system

A

Upper: nose, pharynx and associated structures
Lower: Larynx, trachea, bronchi and lungs

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4
Q

Pharynx (Adenoid)

A

Location: behind the nasal cavity and mouth extending downwards to the esophagus and larynx

Two pathways: toward esophagus and into trachea

Function:
1. Passageway for air and food
2. Plays a role in Sound production (phonation)
3. Protection against aspiration
4. Immune function
5. Does not take part in digestion but creates an entry route for food.
6. Opens to both digestive and respiratory passages
7. Respiratory passages closed during swallowing

Three regions;
1. nasopharynx
2. oropharynx
3. laryngopharynx

Example: when we swallow, the trachea moves upwards, epiglottis closes the opening to the larynx. If food doesnt go into esophagus, it is likely to go into trachea

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5
Q

Larynx

A

Location: In throat between pharynx and trachea
Function:
1. Prevents foods and liquids from entering the airway during swallowing.
2. Voice production
3. Protects lower respiratory tract
4. Controls breathing

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6
Q

Trachea

A

Location: Runs from end of larynx (C6) to T4/T5 whereby it bifurcates into the primary bronchi.

Structure: Flexible, slightly rigid tube in mediastinum. Lots of cartilage.

Function:
1. Filter, warm and humidify air

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7
Q

Role of Cilia

A

Hair-like, made of specialised protein structures, can move rhythmically.

Function: Move microbes and debris up and out of airways. If they do not work, this can cause mucus to build up, leading to breathing problems and infection.

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8
Q

Pleural Membranes

A
  1. Visceral Pleura: Covers surface of lungs.
    Function:
    - protects from friction
    - maintains shape
    - prevents lung collapse
    - synchronising movement with chest wall
  2. Parietal Pleura: lines thoracic cavity
    Function:
    - covers not only lungs, but heart and major blood vessels
    - protects from friction
    - maintains integrity of pleural cavity
  3. Pleural Cavity: contains pleural fluid - 25mL
    Function:
    - creates a moist and slippery surface for easy sliding and reduces friction
    - holds lungs tight agains thoracic wall
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9
Q

Pleural Sac and Fluid

A
  • creates a moist, slippery surface so opposing membranes can slide across each other as lungs move within thorax
  • holds lungs tight against thoracic wall
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10
Q

Pleural Fusion

A

Fluid builds up due to injury or infection leading to movement of interstitial fluid into the sac. Does not impact friction but impacts how much lungs can expand and therefore efficiency of gas exchange.

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11
Q

Bronchial circulation

A

Part of systemic circulation. Consists of tiny bronchiole arteries and veins that supply bronchi and bronchioles of the lung

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12
Q

Lungs

A

Structure: Divides into left and right side. Division point is called the carina. 3 major lobes on right (Superior, Middle and Inferior) and 2 major lobes on left (Superior and Inferior).

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13
Q

Bronchioles

A

Structure: smallest branches found deep within lungs, lack cartilage, have smooth muscle in walls, allowing them to constrict and dilate to regulate flow.

Function:
1. Deliver air to the exchange surfaces of the lungs

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14
Q

How does the body change amount of air entering the alveoli?

A
  1. Broncho constriction
  2. Broncho dilation
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15
Q

Alveolus

A

Pockets that air moves into for gas exchange

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16
Q

Perfusion (Q)

A

delivering blood to alveoli to pick up oxygen and drop carbon dioxide

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17
Q

Alveolar Pneumocytes

A

Type 1:
- simple squamous (squished/flat) epithelial cells
- form walls of respiratory membrane
- one layer for easy gas exchange due to less distance

Type 2:
- simple cuboidal epithelial cells
- produce surfactant

Alveolar Macrophages:
- Resident immune cells
- Phagocytose pathogens

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18
Q

Muscles of Inhalation

A
  • Sternocleidomastoid
  • Scalenes
  • External intercostals
  • Diaphragm
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19
Q

Muscles of Exhalation

A

-Internal intercostals
- External oblique
- Internal oblique
- Transversus abdominus
- Rectus abdominis

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20
Q

Eupnoea

A

Quiet breathing at rest. Can be diaphragmatic or costal.

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21
Q

Diaphragmatic vs costal

A

Diaphragmatic; deep breathing. contraction of the diaphragm
Costal; shallow breathing. External intercostal muscles contract

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22
Q

Hypereupnea

A

Fast forced breathing.

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23
Q

Inspiration

A

Accessory muscles assist external intercostal muscles to elevate the ribs and enlarge the thorax

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24
Q

Exhalation

A

Internal intercostal muscles depress the ribs

Abdominal muscles compress abdominal contents & reduce the volume of the thoracic cavity

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25
Q

Three types of pressure

A
  1. Intrapulmonary pressure
  2. Intrapleural pressure
  3. Transpulmonary (transmural)
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26
Q

Intrapulmonary pressure

A

Alveolar pressure

Inspiration, leads to increase in lung volume, decrease in pressure - less than the atmosphere

Expiration, leads to decrease lung volume, increase in pressure

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27
Q

Intrapleural pressure

A

Lower than the intrapulmonary and atmospheric pressures.
* Keep the lungs inflated and allows them to adhere to the chest wall, enabling efficient breathing.
* ↑ lung volume, smaller intrapleural space, increase in pressure
* ↓ lung volume, larger intrapleural space, decrease in pressure

28
Q

Transpulmonary (transmural)

A

Always positive because the pressure inside the lungs is normally higher than the pressure in the pleural cavity. Leads changes in lung size.
* TP (transpulmonary) =AP (Intrapulmonary) -IP (Intrapleural)

29
Q

Distensibility

A

How much the lung and chest wall can stretch

30
Q

Airway Resistance

A

The resistance (opposition/hindrance) to the flow of air through the respiratory tract during the process of breathing. It’s a measure of how much effort is required to move air in and out of the lungs.

Related to
* Length
* Radius
* Cross-sectional area of the airways
* Bronchodilation
* Bronchoconstriction
* Density, viscosity (does not really change too much)
* Velocity of the gas

31
Q

High compliance vs Low compliance

A

High compliance: lungs and chest wall expand easily with each breath in, so it takes less effort to breathe.

Low compliance: they’re stiffer and it takes more effort to fill them with air.

32
Q

Role of pressure gradient & airway resistance

A

Air flow is the volume of air flowing through the lungs at any point in time

It is directly proportional to the pressure gradient between the external atmosphere & alveoli, & inversely proportional to resistance of airway passages

–> Respiratory airways cause resistance to air flow during inhalation and exhalation. The pressure gradient is necessary to transport the air from the mount (or nose) to pulmonary alveoli.

33
Q

Air Flow

A

F ∝ ΔP / R where F= air flow
* The volume of air that moves into or out of the lungs at any given point in time.

ΔP= pressure gradient
* The difference in air pressure between two points e.g., external atmosphere and
the alveoli

R= resistance
* the opposition or difficulty that the air encounters as it moves through the airway
passage

34
Q

Elastic Recoil

A

After we take a breath in, the lungs want to return to their normal state. The chest wall also has elastic recoil, but outwards, counteracting the inward elastic recoil of the lungs. This is the opposite of compliance.

Example:
Thin elastic band Easily stretched (compliance) BUT
not great recoil!

Thick elastic band Not easily stretched (low compliance)
BUT
good recoil!

35
Q

Summary of inspiration

A
  1. Inspiration muscles contract (diaphragm descends, ribcage rises)
  2. Thoracic cavity volume increases
  3. Lungs are stretches, intrapulmonary volume increases
  4. Intrapulmonary pressure drops to -1mm Hg
  5. Air (gases) flows into lungs down its pressure gradient until intrapulmonary pressure is 0, which is equal to atmospheric pressure
36
Q

Summary of Expiration

A
  1. Inspiration muscles relax (diaphragm rises, ribcage descends due to recoil of costal cartilage)
  2. Thoracic cavity volume decreases
  3. Elastic lungs recoil passively, intrapulmonary volume decreases
  4. Intrapulmonary pressure rises to +1mm Hg
  5. Air (gases) flows out of lungs down its pressure gradient until intrapulmonary pressure is 0, which is equal to atmospheric pressure
37
Q

Boyle’s Law

A

the volume of a gas and pressure are inversely proportional at a given temperature (e.g., body temperature).

  • little space, a lot of pressure
  • big space, less pressure
  • gases move from high to low pressure
38
Q

How does the alveoli remain open?

A
  1. Transmural Pressure Gradient: The pressure inside the alveoli (the air you’ve breathed in),
    compared to the pressure in the pleural space (less than atmospheric pressure).
  2. Pulmonary Surfactant: Reduces the surface tension within the alveoli
  3. Alveolar interdependence
    If one alveolar in the middle is collapsing, those around it can stop this from happening due to their shared walls and connective tissue.
39
Q

What promotes the alveolar to collapse?

A
  1. Alveolar Surface Tension: The inward pull due to the polar water molecules.
  2. Elasticity of stretch pulmonary connective tissue: Recoil of the lungs and chest wall.
40
Q

Gas Exchange

A

The exchange of oxygen (O2) and carbon dioxide (CO2) between the external environment and the body’s cells through the respiratory system.

41
Q

Why do we need gas exchange?

A

Cellular respiration so we can create ATP and a byproduct is CO2. If we dont exhale Co2, our blood can become acidic.

42
Q

External Respiration

A
  • Occurs in the lungs
  • Oxygen (O2) is delivered from the
    alveoli to the pulmonary capillary
  • Carbon dioxide (CO2) is delivered to
    the alveoli from the pulmonary capillary
43
Q

Internal Respiration

A
  • Occurs at the cellular level
  • Oxygen (O2) is delivered from the
    bloodstream to the body’s tissues and cells.
  • Carbon dioxide (CO2) produced by cellular
    metabolism, moves from the cells into the bloodstream
44
Q

Fick’s Law of diffusion

A

The shorter the distance through which diffusion must take place, the greater the rate of diffusion.
The greater the surface area across which diffusion can take place, the greater the rate of diffusion

45
Q

Surfactant

A
  • A detergent-like mixture of phospholipids, surfactant proteins, and neutral lipids - it is amphiprotic (some of it is non-polar and another part is polar).
  • Decreases water cohesiveness
  • Reduces surface tension of alveolar fluid, & reduces tendency to recoil (alveolar collapse)
46
Q

Dalton’s Law

A

Each gas has its own partial pressure, based upon its concentration in the solution. The sum of these is the overall pressure. i.e., the total pressure of the air in your lungs is the sum of the pressures each of these gases would exert if they were alone.

47
Q

Henry’s Law

A

the amount of dissolve gas in a liquid (blood) is proportional to the partial pressure above the liquid.

48
Q

Gas exchange by diffusion: ventilation, diffusion coupling

A

Gas exchange: O2& CO2 need to move between lungs & other body cells transported in blood & exchanged by passive diffusion
1. Partial pressure gradient (Dalton’s and Henry’s Law)
2. Thickness & surface area of exchange membranes (Fick’s Law)
3. Ventilation-perfusion coupling (V/Q), we want to have appropriate amount of gases moving in alveoli to match amount of blood leaving through capillaries

49
Q

Summary: Gas transport

A

O2 in
1. Ventilation of the lungs.
2. Diffusion of oxygen from the alveoli into the blood in the pulmonary capillaries.
3. Perfusion of systemic capillaries with oxygenated blood.
4. Diffusion of oxygen from systemic capillaries into the cells.

CO2 out (essentially the reverse!)
1. Diffusion of carbon dioxide from the cells into the systemic capillaries.
2. Perfusion of the pulmonary capillary bed with deoxygenated blood.
3. Diffusion of carbon dioxide into the alveoli.
4. Removal of carbon dioxide from the lung by ventilation.

50
Q

Gas Transport: Haemoglobin

A

Haemoglobin (Hb) molecule consists of four protein chains called globins. Each globin chain is attached to a heme group that contains an iron atom. Each iron atom has the capacity to bind with one molecule of oxygen.

51
Q

Factors that influence respiration

A
  1. Haldane Effect: The binding or release of one oxygen molecule changes the conformation or shape of the haemoglobin molecule, making it easier for the subsequent oxygen molecules to be released.
    - In the tissues:
    Oxygen is released from haemoglobin, increased capacity to bind with carbon dioxide and protons (forming bicarbonate), removes these from tissues.
    - In the lungs:
    Oxygen binds to haemoglobin, decreased capacity to bind with carbon dioxide and protons, release to be exhaled
  2. pH:
    The Bohr effect:
    A lower pH (more acidic conditions), increase of O2 from hemoglobin, promotes CO2 binding.
  3. Temperature
    * Higher temperatures promote the release of O2
    * ↑ oxygen to actively metabolizing tissues, where heat is generated
52
Q

Regulation of breathing

A
  • Respiratory muscles contract only when stimulated by nerves
  • Rhythmic breathing is established by cyclic neural activity from the brainstem to respiratory muscles (although origin of this rhythm not well understood)
  • Maintains breathing & reflex adjustments when required
  • Can be voluntarily modified
53
Q

ANS

A
  • preganglionic fibres in the PNS are much longer, therefore the nerve fibres coming into the body are longer and the ganglion is closer to organ itself. Length of the preganglionic fibre is related to speed of response, the sympathetic is responsible for stressful situation, so the fibre is shorter, whereas PNS is rest and digest.
54
Q

Central regions of respiratory regulation in the brain

A
  1. Dorsal Grouo
  2. Pons respiratory Centre (located in regions superior to medulla, important for connecting with higher brain centres, like the hypothalamus)
  3. Ventral respiratory group
55
Q

Afferent Signalling to medulla oblongata

A

Respiratory centres are sensitive to excitatory & inhibitory stimuli:

  • Chemical factors: arterial CO2, H+, O2 via central & peripheral chemoreceptors
  • Inflation reflex: stretch receptors signal respiratory centres via vagal nerve
    afferents to end inspiration & lungs recoil
  • Pulmonary irritants: mucus, dust, fumes stimulate bronchiole receptors that
    communicate with respiratory centres via vagal nerve afferents, like Reflex constriction, cough, sneeze
  • Higher brain centres: hypothalamus (emotions & pain) & motor cortex (voluntary
    control)
56
Q

Efferent responses activate..?

A
  1. Activates SNS: releases noradrenaline which increases rate and depth of respiration
  2. Activates PNS: returns us to base line after stress and reduces heart rate
57
Q

Three types of Chemoreceptors

A
  1. Carotid body chemoreceptors
  2. Aortic body chemoreceptors
  3. Central chemoreceptors
58
Q

Regulation of breathing during exercise

A

If we have a decrease in Co2 in our blood and its in our arterioles it’s going to be PA (pressure arterioles). Our left ventricle is pushing the blood our the aorta, lots of blood flow, this is where chemoreceptors quickly detect decrease in CO2, afferent signal off to the brain stem, interpreted in brain stem, send signals off to the lungs, if we have too much CO2 we compensate by increasing O2, to do this we increase ventilation (respiration), we do this by increasing depth of breathing using our sympathetic nervous system, chemo signalling slows down as we return to homeostasis.

59
Q

Stretch receptors

A

Located in the walls of the airways in the lungs, these receptors detect the degree of lung inflation. Nerve impulses via the vagus nerve. Prevent lungs from over stretching.

60
Q

Regulation of breathing

A
  1. Depth of breathing:
    * How much air is inhaled or exhaled during a single breath (tidal
    volume).
    * Determined by degree of neuronal stimulation from respiratory
    centres
    ↑ stimulation of inspiratory neurons
    ↑ force of respiratory muscle contraction resulting in greater thoracic expansion
  2. Rate of breathing:
    * The number of breaths taken in a minute
    * Determined by how long the inspiratory neurons are active.
    * If they’re active for a more extended period, inhalation will last
    longer, leading to a slower breathing rate
    * If they’re active for a shorter time, the breathing rate will be faster.
61
Q

Respiratory Diseases

A
  1. Obstructive Sleep Apnoea
  2. Cystic Fibrosis
  3. Asthma
    4.
62
Q

Obstructive Sleep Apnoea

A

Upper airway obstruction during sleep.

Can be caused by:
* Neck circumference, caused by a number of factors such as
– Excess weight (10% weight gain ↑ risk by x 6)
– Obstruction due to muscles or glands – Anatomy
* Hypothyroidism
* Excess growth hormones
* Smoking
* Alcohol or drug abuse

Consequences:
* Increased risk of
– Hypertension
– Stroke
– Heart attack
– Diabetes
– GORD
– Heart failure
– Arrythmias

Treatment:
Most common is CPAP (continuous positive airway pressure) Mild air pressure to keep breathing airways open during sleep

63
Q

Cystic Fibrosis

A

CFTR gene mutation causes defect in CFTR channel. Unable to transfer chloride across. This changes how much Na moves across. Change in Na = change in water movement: consequence = dehydration of mucus  mucus becomes really sticky and so radius of air ways becomes smaller (bronchoconstriction). Dehydration of mucus also causes impaired cilia – unable to filter well – and any pathogens that enter will get stuck in the mucus like glue causing increased risk of infection. CF also causes chronic inflammation. When there is lots of inflammation tin airway lots of immune cells come in which can be good to fight infection but they also damage epithelial cells which triggers more immune cells to come in and so damaged more epithelial cells. This continuous inflammation of airways can lead to coping mechanisms such as build-up of fibrosis and stiffening of air ways impacting how wellt he airways inflate and deflate.

Treatment:
Pancreatic enzyme supplements, high-calorie diet, aerosolised DNAse, antibiotics, chest physio, lung transplantation

64
Q

Asthma

A
  • Chronic inflammatory disorder of the airways
  • Inflammation results from hyperresponsiveness of the airways
  • Can lead to obstruction and status asthmaticus
    Symptoms include: expiratory wheezing
  • Dyspnoea
  • Tachypnoea
  • Cough
  • Chest tightness
    Peak flow meters used to monitor
65
Q

Nociceptors

A

Sensory nerve endings that respond to noxious or harmful stimuli.

Activated by inhaled irritants:
* Chemicals
* Temperature Extremes
* Mechanical Injury
* (and Inflammation)

Activation results in sensations of pain or discomfort and might induce reflexes like constriction, cough, sneeze.

66
Q

Obstructive and Restrictive Pulmonary Diseases

A

Obstructive:
Conditions where airflow is impeded, making it hard to exhale all the air in the lungs.
Narrowing or blockage of the airways.
e.g.,
* Chronic Bronchitis
* Emphysema
* Collectively called Chronic Obstructive Pulmonary Disorder (COPD)
* Asthma

Restrictive:
Conditions where the lungs cannot fully expand in volume.
Often due to stiffness in the lungs or weakness in the chest wall muscles.
e.g.,
* Pulmonary fibrosis
* Sarcoidosis
* Chest wall deformities.