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Phase 1 finale > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the path of air from trachea?

A

Trachea bifurcates at T4 - lobar bronchi - segmental bronchi - terminal bronchioles - respiratory bronchioles - alveolar ducts - alveolar sacs

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2
Q

What is the function of pleural fluid?

A

It allows optimal expansion and contraction of the lungs during breathing. It acts as a lubricant, reducing friction between the parietal and visceral layer.

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3
Q

What is the conducting zone of your respiratory tract?

A

From nasopharynx to terminal bronchioles

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4
Q

What is the respiratory zone of your respiratory tract?

A

From respiratory bronchioles to alveolar sacs

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5
Q

Where is the epithelium change in the respiratory tract?

A

It is respiratory epithelium up till the terminal bronchioles which are lined by simple cuboidal (to columnar) epithelium onwards.

Alveolar ducts are simple squamous epithelium

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6
Q

What is respiratory epithelium?

A

Pseudostratified ciliated columnar epithelium with goblet cells

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7
Q

What is boyle’s law?

A

At a fixed temperature, the volume of gas is inversely proportional to the pressure exerted by the gas.

P1V1 = P2V2

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8
Q

What are the pontine and medullary respiratory centres?

A

Pontine-
Pneumotaxic- smooths transition from inspiration to expiration (inhibits inspiration) –> Acts on VRG to cause expiration

Apneustic- Fine tunes inspiratory signals

Medullary centres-
Ventral respiratory group (VRG) - involved in both inspiratory and expiratory phases of breathing

Dorsal respiratory group (DRG) - mainly responsible for initiating and coordinating inspiration.

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9
Q

Where do the intercostal nerves arise from?

A

T1-T11

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10
Q

What are the 3 lung receptors?

A

Slow adapting stretch receptors, rapid adapting stretch receptors and J receptors

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11
Q

What are the slow adapting stretch receptors in the lungs?

A

Found in smooth muscles in the airway

They respond to distension.

When they are activated (during inspiration), they act to inhibit inspiration (transitioning to expiration) - Hering-Breuer reflex.

Myelinated

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12
Q

What are the rapid adapting stretch receptors (irritant receptors) in the lungs?

A

Found between the airway epithelium

They respond to irritants

By causing bronchoconstriction (can also cause cough reflex)

Myelinated

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13
Q

What are the J receptors of the lungs?

A

Located in the alveolar walls, in close proximity to the capillaries

Respond to increased lung interstitial pressure caused by fluid (pulmonary oedema) or alveolar hyperinflation –> they stimulate respiratory centres resulting in rapid and shallow breathing

Non-myelinated

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14
Q

How many more times does CO have an affinity for haemoglobin compared to oxygen?

A

200

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15
Q

What is V/Q mismatch?

A

V- ventilation
Q- Perfusion

This can cause hypoxia (oxygen deficiency in tissues)

Occurs when parts of the lungs receive oxygen but there is not enough blood to absorb it.

You can have alveoli that are ventilated- but not perfused (due to pulmonary embolism- a fragment of blood clot is lodged, blocking blood supply to the lungs, forms dead space)
OR
Alveoli that are perfused- but not ventilated (Pulmonary oedema) - blood will be shunted from places with no ventilation to alveoli with oxygen

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16
Q

What happens when dead space is created by a pulmonary embolism?

A

There will be local bronchoconstriction– to divert air to other sites which are better perfused.

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17
Q

What happens when pulmonary oedema occurs, resulting in alveoli that are perfused not being ventilated?

A

There will be hypoxic pulmonary vasoconstriction to divert blood to better ventilated areas

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18
Q

What is the bohr effect?

A

It describes hemoglobin’s lower affinity for oxygen secondary to increases in the partial pressure of CO2, decreased pH, increased temperature and increased 2,3 DPG

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19
Q

What causes the oxygen dissociation curve to shift to the right and what does this mean?

A

Increased temperature, decreased pH, increased PaCO2, increased 2,3 DPG

These factors decrease the affinity of hemoglobin for oxygen, causing more unloading/dissociation of oxygen into tissues thus leading to less hemoglobin saturation at the same Partial pressure of oxygen compared to normal circumstances.

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20
Q

What shifts the oxygen dissociation curve to the left?

A

Decreased temperature, increased pH, decreased PaCO2, decreased 2,3 DPG

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21
Q

What is the carbon dioxide distribution in the blood?

A

10% plasma
23% bound to haemoglobin
65% as bicarbonate (from dissociation equation, via carbonic anhydrase)

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22
Q

What is the normal pH range of the body?

A

7.35 - 7.45

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23
Q

What is the carbonic anhydrase equation?

A

H20 + CO2 – (with Carbonic anhydrase forms) H2CO3 – HCO3- + H+. REVERSIBLE REACTIONS

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24
Q

What is the formula for alveolar gas equation?

A

PAO2 = PiO2 - PaCO2/0.8

big A = alveolar

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25
Q

What is lung compliance and what is it determined by?

A

Compliance- how easily the lungs will expand

Determined by
Elasticity of lung tissue- increased elasticity, increased compliance

Surface tension (produced by type 2 pneumocytes) - increased surfactant decreases surface tension, increasing compliance

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26
Q

What is hypoxia and what are its causes?

A

Defined as inadequate oxygen delivery to tissues

Causes include
- Hypoventilation (increased PaCO2)
- Diffusion impairment - (due to thickening of membrane through which diffusion occurs)
- Shunting - perfusing unventilated alveoli
- V/Q mismatch
- Hypoxemia (decrease in partial pressure of oxygen in the blood)

SAME CAUSES AS TYPE 1 RESPIRATORY FAILURE

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27
Q

What is the main constitution of the respiratory drive?

What is the most common cause?

A

Hypercapnia - high levels of Co2 (high PaCO2)

Hypoventilation is the main cause

28
Q

Differences between type 1 and type 2 respiratory failure

A

Type 1 - Low PaO2 and low/normal PaCO2
Type 2- Low PaO2 and high PaCO2

Type 1- The respiratory system is unable to provide an adequate supply of oxygen to the body leading to hypoxemia (pulmonary oedema, pneumonia COPD, asthma, ARDS)

Type 2- The respiratory system is unable to remove sufficient carbon dioxide from the body leading to hypercapnia - impaired ventilation(COPD, severe asthma

Type 1 - Typically caused by V/Q mismatch, shunting, diffusion impairment
Type 2- Typically caused by inadequate alveolar ventilation due to respiratory muscle weakness

Type 1- treatment focuses on improving oxygenation
Type 2- treatment focuses on improving ventilation

29
Q

Causes of Type 2 respiratory failure

A

Increased airway resistance

Respiratory muscle weakness

Reduced breathing effort (obesity)

Excess workload

Decrease in area of lung available for gas exchange (chronic bronchitis)

30
Q

What is FEV1. What is it usually in relation to FVC?

A

It is the volume of air you can forcibly expire in the first second. FEV1 is About 75-80% of FVC

31
Q

What is peak expiratory flow?

A

The maximal flow of air as it is expired with maximum effort after maximum inspiration

32
Q

What is the difference between airway obstruction and airway restriction?

A

Obstruction- Flow abnormality, limitation of airflow in and out of the lungs
Restriction- Problem with the volume, a decrease in total volume of air the lungs are able to hold

Obstruction- FEV1/FVC is less than 0.7 (indicates blockage somewhere)
Restriction- FVC is less than 0.8

Obstruction- COPD, Asthma
Restriction- Pulmonary fibrosis

33
Q

What is the total lung capacity? Definition and volume

A

The total volume of air the lungs can hold.
5 litres

34
Q

What is the Inspiratory reserve volume? Definition and volume

A

Inspiratory reserve volume (IRV)- The amount of air that can be forcibly/maximally inhaled after a normal tidal volume. (used during deep breathing) normal adult value is 2000ml

35
Q

What is the expiratory reserve volume? Definition and volume

A

Expiratory reserve volume (ERV)- The amount of air that can be forcibly/maximally exhaled after a normal tidal volume (1250ml) → Reduced with obesity.

36
Q

What is tidal volume? Definition and volume

A

Tidal volume (TV)- The amount of air that can be inhaled or exhaled in one respiratory cycle. 500ml

37
Q

What is residual volume? Definition and volume

A

Residual volume(RV)- Volume of air remaining in the lungs after forced exhalation. Average 1250ml

38
Q

What is vital capacity? Definition and volume

A

Vital capacity(VC)- The amount of air exhaled with maximum effort after maximum inspiration.(ERV+TV+IRV)- assesses strength of thoracic muscles and pulmonary function

3750ml

39
Q

What is inspiratory capacity? Definition and volume

A

Inspiratory capacity(IC)- The maximum volume of air that can be inhaled following a normal tidal expiration. Tidal volume + Inspiratory reserve volume

2500ml

40
Q

What is functional residual capacity? Definition and volume

A

Function residual capacity(FRC)- Volume of air in the lungs at the end of normal tidal expiration. (bottom of tidal volume)- RV+ERV

2500ml

41
Q

Qualities of an ageing lung

A

Decreased compliance due to decreased lung elasticity
Delayed hypercapnea/hypoxia response
Increased V/Q mismatch
Decreased immunity response
Decreased FEV1/FVC ratio

42
Q

What are the key mediators in innate immunity? Describe them a little

A

Neutrophils- inflammatory mediators produced in bone marrows
70% of all white blood cells

Macrophages (smaller proportion)

43
Q

What is the process of innate immunity?

A

1) When a threat is identified, neutrophils are recruited

2) They are activated by cytokines and adhere at the site of infection (chemotaxis)

3) Phagocytosis and bacterial killing

44
Q

What is the process of adaptive immunity?

A

T cells are involved in direct pathogen killing
Cytotoxic T cells (CD-8) - involved in pathogen killing
Helper T cells (CD-4)- induce other cell activation (macrophages, B cells)

B cells differentiate into plasma cells which secrete antibodies. A small proportion develop into memory cells which provide long lasting immunisation.

45
Q

What are the most common immunoglobuilins?

A

GAMED
G- IgG - most abundant - bacterial and viral infections
A- IgA- Secreted in breast milk and mucosa (defends mucosal surfaces)
M- IgM- The FIRST antibody produced in response to a foreign pathogen
E- IgE- Antibodies produced in response to allergies
D- IgD- B cell activation

46
Q

What are the non immune barriers of host defence in the lungs?

A

Respiratory epithelium- acts as a barrier and goblet cells produce mucus

Mucus- provides lubrication and protection via the mucocilliary escalator

Cough reflex- (During inspiration, epiglottis and vocal cords close, abdominal muscles contract and internal intercostals contract to increase intrathoracic pressure for expulsion of air)

47
Q

What are the immune barriers of host defence in the lungs?

A

Alveolar macrophages - 93% of all macrophages in the lung

Phagocytose swiftly.
If pathogen attack is too strong, they respond by recruiting neutrophils. - causes inflammatory response

48
Q

What are hypersensitive reactions?

A

An exaggerated immune response to an antigen which would not normally trigger an immune response

49
Q

Type 1 hypersensitivity

A

Antibody- IgE mediated
Timing- Immediate (within an hour)
Causes- inflammatory response
Examples- ANAPHYLAXIS, hayfever

  • Occurs when an individual is sensitised to a specific allergen. Upon re-exposure to the allergen, IgE antibodies are produced, triggering the release of histamine (from mast cells)
50
Q

Type 2 hypersensitivity

A

Antibody- IgM, IgG,
CYTOTOXIC response
Timing - Hours to days
Examples- Goodpasture syndrome

  • categorised by the binding of IgM or IgG to antigens on the surface of target cells. It triggers an immune response that results in the destruction of the cell via the complement system. (opsonization, inflammation, phagocytosis, lysis)
  • Body can also make antibodies that attack host cells (lungs, kidneys, etc)
51
Q

Type 3 hypersensitivity

A

Antibody- IgG
(antigen-antibody complex) IMMUNE COMPLEX FORMATION
Timing- 7-21 days
Examples- farmer’s lung, malt worker’s lung

Immune complex activates complement system (may release oxygen free radicals)

Type 2 involves - membrane bound antigens
Type 3- soluble antigens
but both involve complement system

52
Q

Type 4 hypersensitivity

A

T cells
Timing- Days to weeks
DELAYED RESPONSE
Examples- tuberculosis

Upon exposure to the antigen, sensitised T cells release cytokines which activate immune cells such as macrophages. Delayed hypersensitvity

53
Q

What are the neurotransmitters and receptors involved in parasympathetic stimulus to the bronchioles? What does this cause?

A

Parasympathetic stimulation via vagus nerve causes bronchoconstriction

At the ganglion, acetylcholine acts on N2 receptors at the target organ,
Ach acts on M3 receptors on smooth muscle (cardiac muscle, glands)

54
Q

What are the neurotransmitters and receptors involved in sympathetic stimulation to the bronchioles? What does this cause?

A

Sympathetic stimulation via the sympathetic chain causes bronchodilation

At the ganglion, acetylcholine acts on N2 receptors, at the target organ,
Noradrenaline on b2 receptors on smooth muscle (cardiac muscle, glands)

55
Q

What are the neurotransmitters and receptors involved in somatic stimulation of skeletal muscles?

A

Acetylcholine acts directly on N1 receptors on the target organ (skeletal muscles)

56
Q

What is the atmospheric pressure in kilopascals at sea level?

A

100 kpa

57
Q

How to calculate pressure of inspired gas?

Calculate it when altitude is 0m

A

Pressure of inspired gas = atmospheric pressure (kpa) x fraction of inspired gas

So the pressure of inspired oxygen at 1 atmosphere= 100 Kpa x 0.21 (natural air contains 20-21% oxygen) = 21 Kpa at sea level

58
Q

Pressure of inspired gas = atmospheric pressure x fraction of inspired gas

How does increasing elevation affect this?

A

Fraction of inspired gas stays the same (0.21-natural air 21% oxygen)

Pressure of inspired oxygen falls

59
Q

What is the normal physiological response to an increase in elevation?

A

Hypoxia → leads to hyperventilation → which increases minute ventilation → causing a decrease in PaCO2 → Initial alkalosis (excess base or acid caused by low level of carbon dioxide in the blood) pH rises → Tachycardia is a result of hyperventilation

Acute mountain sickness- needs to descend

60
Q

What is decompression sickness?

A

When a diver ascends too rapidly, tiny bubbles of nitrogen form in the tissues.

61
Q

1 atmosphere is equivalent to how many bars, millibars, metres of sea water, psi?

A

1 atmosphere = 1 bar = 1000 millibars =101 kpa =14 psi = 10m of sea water

62
Q

For every 10m that you dive, how much does the pressure increase?

A 46 year old diver, spent 3 hours diving, using a 30% oxygen system at 130m of depth. What is the pressure of oxygen they were breathing?

A

1 atmosphere

Pressure of inspired oxygen= 0.3 (percent of oxygen) x 14 (14 atmospheres)= 4.2 atmospheres of oxygen

63
Q

Where does the trachea start and end?

A

C6 - T4/5

64
Q

What is an acinus of the alveoli?

A

A functional unit running out from the terminal bronchiole that is supplied with air by one terminal bronchiole.

65
Q

What is dead space? What kind of dead space is there and how much volume is it?

A

Dead space- Refers to the volume of air that does not participate in gas exchange/ventilation. (it includes the air in the nose, pharynx, trachea and bronchioles)

Anatomic dead space (mentioned above) has approx 150ml and the alveolar dead space has about 25ml (as not every set of alveoli that receive gas are perfused with blood) so in the lungs, there is a total of 175ml of dead space not contributing to ventilation (physiological dead space-total dead space).

66
Q

What is the most common mutation in cystic fibrosis?

A

Delta F508
CFTR gene

67
Q

Laplace’s law

A

The tension in the wall of a structure is directly proportional to the pressure inside the structure and its radius. (increased pulmonary surfactant, reduces surface tension. Decreased radius reduces surface tension- as it increases surfactant concentration)

P= 2T/r

Phase 1 finale (16 decks)

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