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IK1 - LSS > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

What are the functions of the respiratory system?

A
  • gas exchange
  • host defence
  • metabolism of endogenous and exogenous molecules
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2
Q

What is the health burden of respiratory disease?

A

1 in 5 people in the UK die from respiratory disease

Most common = lung cancer, pneumonia &

COPD 1 in 8 admissions are due to COPD

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3
Q

What are common symptoms associated with lung disease?

A
  • shortness of breath
  • cough
  • sputum production
  • blood stained sputum (haemptysis)
  • chest pain
  • hypersomnolance
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4
Q

Give examples of infectious lung disease?

A
  • TB - infective bronchitis
  • pneumonia
  • empyema
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5
Q

Give examples of pulmonary vascular disease?

A

pulmonary emboli, pulmonary hypertension

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6
Q

Give example of some localised obstructive airway disease.

A

Sleep apnoea, laryngeal carcinoma, thyroid enlargement, vocal cord dysfunction, tumours, foreign bodies, bronchopulmonary dysplasia

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7
Q

Give examples of some generalised obstructive airway disease.

A

Asthma, COPD, cystic fibrosis, obliterative bonchiolitis

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8
Q

Give examples of some small lung disorders (restrictive) that occur within the lung.

A

Sarcoidosis, asbestos exposure, extrinsic allergic alveolitis

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9
Q

Give examples of some small lung disorders (restrictive) that occur outside of the lung.

A

Pleural effusions, pneumothorax, scoliosis, respiratory muscle weakness and obesity

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10
Q

What is dyspnoea?

A

Dyspnoea is a sensation of difficult, laboured or uncomfortable breathing

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11
Q

What is the role of nasal cavities?

A

Filtering air, conserving heat and water from expired air while warming and humidifying inspired air.

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12
Q

Why do we switch to breathing through our mouths when exercising?

A

Due to the complex structure of the nasal cavities breathing through our nose has a high resistance to airflow so when breathing demands go up we switch to breathing through our mouths which has a lower resistance.

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13
Q

What features are in place in the respiratory system to prevent airway or alveolar collapse?

A
  • in alveoli surfactant acts as a lubricant protecting against collapse
  • in the trachea and large bronchi cartilaginous c-rings hold the airways open
  • In branching bronchi as cartilaginous components decrease till they are not present smooth muscle increases holding airways open.
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14
Q

How does blood circulate through the pulmonary system?

A

deoxygenated blood enters right atrium → right ventricle → contraction forces blood into pulmonary trunk → travels through left and right pulmonary arteries → goes through arterioles → alveolar capillaries where gas exchange occurs → oxygenated blood travels through venules → pulmonary veins → blood enters left atrium

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15
Q

What is minute ventilation?

A

The volume of air expired in one minute or per minute

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16
Q

What is alveolar ventilation?

A

The volume of air reaching the respiration zone

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17
Q

What is hyper/hypopnoea?

A

Increased/decreased depth of breathing

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18
Q

What is tidal volume? What is it roughly when at rest for a 70kg man.

A

Tidal volume (TV or Vt) is the volume of air inspired and expired during regular breathing.

  • 500mL for a 70kg man at rest
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19
Q

What is inspiratory reserve volume? What would it be for a 70kg man at rest? Why do we need it?

A

The inspiratory reserve volume (IRV) is the volume of air that can be inspired after a tidal inspiration.

  • around 2.7 L for a 70kg man

this is needed for coughing and exercise

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20
Q

What is expiratory reserve volume? What would it be for a 70kg man at rest?

A

Expiratory reserve volume (ERV) is the volume of air that can be expired after a tidal expiration.

  • approximately 1.3L in a 70kg man
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21
Q

What is residual volume? What is the approximate value for healthy adults?

A

Residual volume (RV) is the volume of air that cannot be emptied from the lungs, no matter how hard you expire. This is fixed because of the lung-chest wall interface

  • approximately 1.2L in healthy adults This residual volume helps to maintain open distal airways
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22
Q

What is total lung capacity? What volume do you combine to calculate it (equation)?

A

Total lung capacity = the maximum capacity of the lungs (around 6L in 70kg man)

Total lung capacity = RV + IRV+ TV +ERV

  • residual volume + inspiratory reserve volume + tidal volume + expiratory reserve volume
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23
Q

What is functional residual capacity? How would you calculate it from volumes?

A

Functional residual capacity = The volume of air in the lungs following a tidal expiration at rest. The capacity represents the “default” volume of the lungs, when the lung recoil inwards and the chest recoil outwards are in equilibrium

Function residual capacity = RV + ERV

  • residual volume + expiratory residual volume
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24
Q

What is the inspiratory capacity? How would you calculate it from volumes?

A

Inspiratory capacity = the maximum volume of air the lungs can draw in from the equilibrium functional residual capacity point

Inspiratory capacity = TV +IRV

  • tidal volume + inspiratory reserve volume
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25
Q

What is the vital capacity? How would you calculate it from volumes?

A

Vital capacity = The volume of air between the maximum and minimum achievable volumes

Vital capacity = TLC - RV OR IRV + TV + ERV

  • total lung capacity - residual volume
  • the critical value of 1L is used to assess whether a patient can maintain spontaneous ventilation or requires assistance
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26
Q

What factors can effect lung volumes and capacities?

A

Body size, gender, fitness, disease and age

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27
Q

What is the conducting zone? What make up the conducting zone?

A

The conducting zone is as inspired air passes through velocity decreases and surface area increases. Important in defence, speech and preparation for gas exchange. Trachea, main bronchi, bronchi, bronchioles and terminal bronchioles

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28
Q

What is the respiratory zone? What makes up the respiratory zone?

A

Here the surface area is used for gas exchange. Made up of alveolar ducts and sacks

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29
Q

What is anatomical dead space?

A

Areas that aren’t involved in gas exchange. Anatomical dead space includes conducting airways and upper respiratory tract. To measure this a dilution test is needed. Note that intubation increases this

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30
Q

What is alveolar dead space?

A

Areas of respiratory tissue (i.e. alveoli) that are unable to participate in gas exchange. Death of alveolar usually due to absent/inadequate blood flow. in a healthy lung this is almost 0

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31
Q

What is the physiological dead space?

A

The alveolar dead space + anatomical dead space

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32
Q

What is transpulmonary pressure?

A

the difference between the alveolar sacs and pleural cavity

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33
Q

What is transthoracic pressure?

A

difference between pleural cavity and atmosphere

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34
Q

What is transrespiratory pressure?

A

the difference between alveolar sacs and atmosphere

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35
Q

What sort of pressure breathing is normal breathing?

A

negative pressure breathing When inspiring the movement of the diaphragm and intercostal muscles causes pleural pressure to decrease and the visceral pleura is pulled out inflating the lung

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36
Q

What can be measured from a volume- time curve?

A

The test allows you to measure forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) This allows calculation of FEV1/FCV ratio which can used to diagnose pathologies FET = forced expiratory time which is the time taken to expel all lungs from air (not commonly used)

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37
Q

What would you expect to see on volume - time curve from someone with obstructive lung disease in comparison to a normal individual?

A

In obstructive lung disease:

  • FEV1 would be much lower
  • FET much higher
  • FVC lower
  • FEV1/FVC low

This is all due to narrow airways

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38
Q

What would you expect to see on volume - time curve from someone with restrictive lung disease in comparison to a normal individual?

A

In restrictive lung disease:

  • FVC is lower
  • FEV1 is relatively high (just a little lower than normal)
  • FEV1/FVC is normal
  • they don’t have narrow airways but their thorax expansion is limited
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39
Q

What would the flow-volume loop of someone with mild obstructive disease look like compared to normal?

What changes to volumes may there be and why?

A

flow -volume loop: displaced to the left, indented exhalation curve

RV and TLC are elevated

This is due to milk breakdown of lung parenchymal tissue and hyperinflation of lungs. Mild ‘coving’ of expiration suggest obstruction of small airways

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40
Q

What are the phases shown on this Flow-volume loop? (labelled A-F)

A

A = gentle tidal inspiration

B = gentle expiration caused by passive recoil of lung

C = moderate inspiration to total lung capacity

D = maximal expiration (phase 1)

E = maximal expiration (phase 2) - as airways empty the rate of expiartin slows steadily untl residual volume has been reached

F = ispiration to total lung capacity (mediated by inspiratory muscles)

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41
Q

What would the flow-volume loop of someone with restrictive disease look like compared to normal?

What changes to volumes may there be and why?

A

Flow - volume loop: displacement to the right and narrower curve

narrow x-axis difference indicating decreased TLV. there is impaired flow rates for inspiration and expiration

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42
Q

What would the flow-volume loop of someone with severe obstructive disease look like compared to normal?

What changes to volumes may there be and why?

A

Flow -volume loop: The curve would be shorter, displaced to the left and indentented expiration curve

Rv is larger and coving is more pronounced. There is a decreasing peak expiratory flow rate due to increasing narrow airways

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43
Q

What would the flow-volume loop of someone with variable extra-thoracic disease look like compared to normal?

What changes to volumes may there be and why?

A

Flow-volume loop: blunted inspiration curve, but otherwise normal.

the inspiratory curve is flattened due to obstruction outside of the throax (maybe in upper airway)

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44
Q

What would the flow-volume loop of someone with variable intra-thoracic disease look like compared to normal?

What changes to volumes may there be and why?

A

Flow-volume loop: blunted expiratory curve, but otherwise normal

Obstruction within thorax e.g in trachea that prevents expiration

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45
Q

What would the flow-volume loop of someone with fixed airway obstruction look like compared to normal?

What changes to volumes may there be and why?

A

Flow -volume loop: has blunted inspiration and expiration

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46
Q

What is ventilation - perfusion ratio (V/Q)?

A

The ideal circumstance where blood only goes to areas that are being ventilated.

  • The ratio denotes the volume of ventilation per litre of perfusion
  • high ratio is associated with poorly perfused areas
  • Low ratio with poorly ventilated areas

This is a measure of the wasted ventilation (alveoli ventilated with no blood supply) and wasted perfusion (perfused non-ventilating alveoli)

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47
Q

What is Fick law?

A

Molecules diffuse from regions of high concentration to low concentration at a rate proportional to the concentration gradient, the exchange surface area and the diffusion capacity of the gas, and inversely proportional to the thickness of the exchange surface

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48
Q

What are the standard oxygen blood gases at different part of the circulatory system?

  • alveolar, arteriole, tissue and venous
A

Alveolar: 13.5 kPa

Arteriole: 13.3 kPa

Tissue: 5.3 kPa

Venous: 5.3 kPa

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49
Q

What are the standard carbon dioxide blood gases at different part of the circulatory system?

  • alveolar, arteriole, tissue and venous
A

Alveolar: 5.3 kPa

Arteriole: 5.3 kPa

Tissue: 6.1 kPa

Venous: 6.1 kPa

50
Q

What role does 2,3 - DPG have?

A

2,3 - DPG can bind to haemoglobin. When ATP is produced in large amounts (very metabolically active) 2.3 -DPG is produced.

it binds to haemoglobin and ersults in squeezing as much oxygen out of the haemoglobin. 2,3 - DPG decreases he affinity for oxygen

51
Q

What is cooperativity?

A

It is what happens to haemoglobin. On binding to an intialy oxygen it’s conformation changes and it’s affinity for oxygen increases.

52
Q

What is methaemoglobin?

A

HbA but the haem group has been oxidised to Fe3+ so it can’t bind to oxygen

53
Q

What would lead to a left shift of the oxygen dissociation curve?

A

In conditions where there is a high oxygen environment there is a shift to the left meaning there is increased affinity for loading.

Other factors leading to it:

  • decreased temperature
  • alkalosis
  • hypocapnia
  • decreased 2,3 - DPG
54
Q

What would lead to a rightwards shift of the oxygen dissociation curve?

A

In conditions associated with low oxygen environment.

These are:

  • increased temperature
  • acidosis
  • hypercapnia
  • increased 2,3 - DPG
55
Q

In a healthy individual what is P50 value?

P50 - the PO2 corresponding with 50% saturation

A

P50: 3.3 kPa

56
Q

What leads to an upwards shift of the oxygen dissociation curve?

A

Polycythaemia (concentration of RBC is much higher) leads to an upwards dissociation. So for a given PO2 there is no change in HbO2 saturation but marked increase in blood oxygen content.

  • INCREASED OXYGEN-CARRYING CAPACITY
57
Q

What leads to a downwards shift of the oxygen dissociation curve?

A

Anaemia leads to downwards shift so it markedly reduces the OXYGEN-CARRYING CAPACITY of the blood.

  • note these patients may still have a normal pulse oximetry because they can fully saturate their Hb
58
Q

What happens to the oxygen dissociation curve in the presence of carbon monoxide?

A

There is a downwards and leftwards shift of the curve. This is because haemoglobin has a higher affinity for CO than oxygen.

So the number of binding sites available for oxygen is reduced so oxygen content falls. additionally binding to Co pushes Hb into a tense state reducing its ability to release oxygen.

59
Q

How does fetal heamoglobin differ to adult haemoglobin?

A

Foetal haemoglobin has a greater affinity for oxygen than adult haemoglobin. This is because it needs to bind to oxygen already bound to the mothers Hb. The P50 is around 2.4 kPa

60
Q

In what way does the parasympathetic innervate the respiratory system?

A

Parasympathetic pathway leads to constriction of the ariways via the vagus nerve.

  • also innervates the submucosal glands and smooth muscle cells
61
Q

How does the sympathetic system innervate the respiratory system?

A

Via the cervical thoracic ganglion and leads to relaxation of airways.

it also stimulates nitric oxide production leading to further dilation

62
Q

Where are goblet cells found and what is their function? What are the components of their secretions?

A

Goblet cells are found in the large, central and small airways making up around 20% of epithelial cells. Their function is to synthesis and secrete mucus

The mucus contains:

  • mucin proteins, proteolgycans, glycosaminoglycans → mucus has elasticity
  • serun-dervied proteases helping to combat micro-oragnsism and phagocytic proteases
    • aided by anti proteases formed in epithelial
  • antioxidants countering inhaled oxidants and through released by actvated phagocytes
63
Q

How does the number of goblet cells in a smoker compare to that in a non-smoker?

A

Smoekrs have an increase of at least double in the number.

this leads to more and thicker mucus, smoke is trapped by microorganisms are too so there is an increased risk of respiratory infections

64
Q

Where are ciliated cells found? What is their function?

A

Ciliated cells are found in the large, central and small airways making up 80% of epithelial cells. They tips are in the sol phase of mucus so they can push the mucus to the epiglottis to be swallowed by beating metasynchronously

65
Q

How does the prevalence and function of ciliated cells differ in:

a) smoker vs non-smoker
b) someone with COPD and someone without

A

a) smokers have depleted numbers and they beat asynchronously so inefficient clearing. they are alsod found in the broncjioles.
- unable to clear mucus leads to infection and airway obstruction
b) mucus can become trapped due to the narrowing of airways. alveoli are then broken down by enzymes and inflammatory cells → reduced peripheral gas exchange

66
Q

What three conditions make up COPD (chronic obstructive pulmonary disease)

A
  1. chronic bronchitis - effects large and central airways (bronchi not bronchioles) mainly. Lots of mucus - goblet cell hyperplasia
  2. small airway disease - effects bronchioles and non cartilaginous regions where they become blocked from mucus due to narrowing/stenosis. Airways become hypertrophic leading to narrowing
  3. emphysema - effects respiratory bronchioles. destruction of respiratory tissue by proteolytic enzymes leads to loss of ECM → loss of SA, elastic recoild and vascularisation → gas exchange is compromised
67
Q

Where are clara cells found and how does their abundance change as you move distally through respiratory system? What is their function?

A

Clara cells are non-ciliated secretory epithelum found in large, central and small airways as well as bronchi and bronchioles.

  • abundance increases as you most distally so bronchi and bronchioles are enriched with them

FUNCTION: xenobiotic metabolism (breakdown foreign compounds)

  • contains Phase I and Phase II enzymes
  • Phase I: designed to metabolism compounds to format to allow phase II to neutralise toxin
    • often convert pro-carcinogens into carcinogens
  • Phase II: neutralisation
68
Q

Alveolar walls are made of type I and type II epithelial cells. Describe what each cell type does.

A

type I epithelium

makes up most of the surface area. They are very thin allowing gas exchange to occur

Type II epithelium

They are more abundant but make up less of the surface area. They synthesis and secrete phospholipid rich solution (pulmonary surfactant) They also synthesis and secrete anti-proteases

  • they are the precursor to type I - divide and differeniate to replace any lost/damaged
69
Q

What do alveolar macrophages do? How do they differ in abundance in a smoker vs a non-smoker?

A

They make up 90% of phagocytic celels in lungs and found in higher proportions in the lower airways,

  • scavenging cells: phagocytose debris & micro-organism
  • send “messages” to blood/lymphatic systen to trigger immune response to infection or toxin
  • make proteases to digest debris
  • make oxidants to kill pathogens, also make some anti-oxidants to counter effects

in smokers there is a 5-10 fold increase

70
Q

Where are polymorphonuclear neutrophils found? What do they do? Difference in smokers?

A

They are found throughout the airway though only 5% in the lower airways. They store high levels of potent proteases in granules whicha released on activation

in smokers there is a 5-10 fold increase (may also occur in infection)

71
Q

What are the different types of lung cancer? are the small cell or non-small cell?

A

non-small cell carcinoma:

  • squamous cell carcinoma
  • adenocarcinoma
  • large cell carcinoma

small cell carcinoma

72
Q

What happens in squamous cell carcinoma? What proportion of lung cancer does it account for? Is it small cell or non-small cell? Does it have an association with smoking?

A

Proportion of lung cancers: 25-40%

Strong association to smoking

NON-SMALL CELL CARCINOMA

Mainly in central airways and distant spread occurs later than in adenocarcinome

→ smoking leads to irritation so tougher epithelium develops i.e. ciliated to squamous. Squamous acquire mutations leading to dysplasia and further mutations allow cancer to develope and eventual spread

73
Q

What happens in adenocaricoma? What proportion of lung cancer does it account for? Is it small cell or non-small cell? Does it have an association with smoking?

A

Proportion of lung cancer: 25-40%

Most common cancer in non-smokers

non-small cell carcinoma

Forms in the glandular epithelium. It usually has a prescursor lesion and occurs in the periphery with multicentric nature.

alveolar wall thicken with atypical cells. these increase in size and mutate to produce enzymes that degrade stroma leading to formation of fibrous tissue and inflammation. extrathoracic metastases are common and early

SMOKERS: K ras mutation

NON-SOMKERS: EFGR mutation/amplification

74
Q

What is large cell carcinoma?

A

They present as poorly differentiated tumours comprised of large cells. No histological evidence of glandular or squamous differentiation with a poor prognosis as it grows and spreads rapidly

non-small cell carcinoma

75
Q

What happens in small cell carcinoma? What proportion of lung cancer does it account for? Is it small cell or non-small cell? Does it have an association with smoking?

A

Proportion of lung cancer: 20-25%

It is a small-cell carcinoma which is rare in non smokers as it has a very strong association with smoking.

VERY AGGRESIVE BEHAVIOUR, worst prognosis of all lung cancers usually.

usually central. Associated with paraneoplastic syndromes. usually grow so fast they out grow their blood supply and become necrotic

76
Q

What 3 things would you do to diagnose lung cancer?

A
  1. cytology
  2. histology
  3. other special techniques such as gene profiling
77
Q

What are paraneoplastic syndomes? Give examples of those that may occur with lung cancer?

A

Paraneoplastic syndromes is where the tumour cells express substances expressed by the tissue from which the tumour arose

  • inappropriate ADH secretion leading to low sodium often seen in small cell carcinoma
  • adrenocorticotrophin hormone leading to cushings and associated with small cell
78
Q

What are the 3 mechanisms that interact to control breathing in the awake state?

A
  1. metabolic controller in the medulla which responds to Co2 production/demand - INVOLUNTARY
  2. behavioural control in the cortex which allows voluntary control of breathing for talking, singing etc
  3. reflex control
79
Q

Where is the carotid body found? through which nerve does it send impulses to the brain?

A

Found at the bifurcation of the common carotid into internal and external branches. Acts as a chemoreceptor detecting pH changes in response to oxygen and carbon dioxide levels in the blood. ilicits fast response as it is hyperperfused so can detect small changes.

signal via glossopharyngeal nerve

80
Q

What happens to:

  • acid production
  • acid elimination
  • base productioin
  • base elimination

during acidosis?

A

Acid production: increased

acid elimination; decreased

base production: decreased

base elimination: increased

81
Q

What happens to:

acid production

acid elimination

base production

base elimination

in alkalosis?

A

acid production: decreased

acid elimination: increased

base production: increased

base elimination: decreased

82
Q

What is influenza?

A

Haemophilus influenza is the most common cause of airway infections. Bacteria have hair like projections that anchor them to epithelial cells. They can stimulate more mucus production to which bacteria can stich to.

  • exoproducts which impair mucociliary clearance
  • enzymes: break down local immunoglobulins
  • exoprodcuts impairing WBC
  • avoids immune surveillance
83
Q

What are irritant receptors? where are they found? what are the 3 main types?

A

Irritant receptor stimulation leads to reflexes such as coughing or sneezing. Most are located on the posterior wall of the trachea, some by the main carina and branching points of large airways. there are fewer in the lung periphery and non in the bronchioles

  1. c-fibre receptors
  2. Rapidly adapting stretch receptors
  3. slow adapting stretch receptors
84
Q

Describe C-fibre receptors

A

They have free nerve endings and are present in the upper respiratory tract. They have small unmyelinated fibres resulting in slow conduction and respond to chemical irritant and inflammatory mediators

They release neuropeptide inflammatory mediators: substance P, neurokinin A and Calcitonin Gene related peptide

85
Q

Describe rapidly adapting stretch receptors.

A

They are myelinated leading to rapid conduction. They are present in: naso-pharynx, larynx, trachea and bronchi.

mechanical and chemical irritants are stimulin as are inflammatory mediators

86
Q

Describe slow adapting stretch receptors

A

Located in the airway smooth muscle they are myelinated so conduct quickly. Predominantly in the trachea and main bronchi and respond to lung inflation (mechanoreceptors)

87
Q

What happens when a irritant receptor is stimulated to generate a cough?

A

irritant receptor is stimulated ⇒ sensory information goes via vagus nerve ⇒ to brainstem to the cough centre (medullary cough pattern generator) ⇒ stimulation of muscles needed to cough

88
Q

What are the mechanics of coughing? Name the 3 phases.

A
  1. inspiratory phase
  2. Glottis closure
  3. expiratory phase

The inspiratory phase opens trachea. During the act of coughing there is an increase in intrapulmonary pressure which compresses the posterior membrane of the traceha so the trachea narrows into a crescent shape. this increases flow and contributes to the sound created

89
Q

What is cough hypersensitivity syndrome?

A

Those who are cough senstivie react to a low concentration of capsaicin leading to a cough. triggers may include laughing, deep breathing and smells.

management: increases voluntary control through speech pathology management.
medicines: amitriptyline, gabapentin and opiates

90
Q

Describe pneumonia

A

It is an infection of the alveoli and is serious. there is a 5% mortality for those admitted to hospital.

Symptoms: cough, sputum, fever, dyspnoea, pleural pain and headache

The alveoli fill with inflammatory cells, fibrin, cell debris and bacteria and is commonly caused by streptococcus pneumonia

91
Q

What is primary ciliary dyskinesia?

A

Rare autosomal recessive condition with incomplete penetrance. the cilia do not beat will together so there is inefficient mucus clearance.

The cilia can either be immotile or move in a slow disturbed fashion.

92
Q

What is bronchiectasis?

A

these are patients who usually have a history of breathing difficultes as an infant, recurrent chest infections as a child. Often suffer from fatigue and difficulty breathing - the aim of treatment is to remove phlegm which is done through physiotherapy

93
Q

What are some causes of chronic bonchial sepsis?

A

Congenital, mechanical obstruction, inflammatory pneumonitis, fibrosis, post-infective, immunological, imparied mucociliary clearance and immun deficiency

94
Q

Why is the protease - anti protease balance?

A

Damage caused by inflammation is largely due to this balance. Phagocytes release proteases in killing pathogesns and some of these spill into surroundings.

  • in a normal lung anti-proteases will neutralise these and stop damage
  • in chronic inflammationthere are so many neutrophils that the amount of proteases overwhelms anti-proteases. there are free proteases sitting around leading to damage to the lung tissue
95
Q

What happens in negative pressure breathing?

A

Air is drawn into the lungs from a neutral pressure to a low/negative pressure.

diaphragm contracts compressing abdominal cavity and decompressing the thoracic cavity ⇒ intrapleural pressure decreases from -5cmH2O to -8cn H2O ⇒ the lung expands ⇒ alveolar pressure decreases and air flows in until alveolar pressure returns to 0 cmH2O

a negative transmural pressure will cause air flow into the lung

96
Q

What happens during expiration?

A

The diaphragm relaxes and the elastic recoil of the lung increases alveolar pressure ⇒ air flows out of the lungs down the pressure gradient

positive transmural pressure will cause air flow out of the lungs

97
Q

What is compliance? What is the equation to calculate compliance?

A

COMPLIANCE describes the propensity for the lungs and chest wall to stretch and distort out of shape.

A greater change in volume per unit of pressure reflects a higher degree of compliance.

compliance is most applicable to changing lung volume away from FRC

compliance = change in volume/change in pressure

98
Q

What is elastance? How do you calculate elastance?

A

Elastance describes the tendency of the lungs to recoil to their original volume after removal of inspiratory forces.

a greated change in pressure per unit volume reflects a higher degree of elastance. it is most applicable in changing lung volume towards FRC.

Elastance = change in pressure/change in volume

99
Q

What does surfactant do?

A
  • helps prevent collapse in small alveoli
  • increases compliance by reducing surface tension
  • reduces ‘the work of breathing’

The polar phospholipids migreat to the surface and arrange themselves with hydrophobic in fluid and hydrophilic in air. This interrupts the attraction of water molecules and reduced surface tension in alveoli.

It regulates size of alveoli. Large alveoli ⇒ large air-fluid interface & surface area ⇒ less concentrated. In smaller alveoli a greated pressure isneeded. Increasing surface tension by the lower surfactant concentration hinders more compliant alveoli expansion allowing the small alveoli to expand THIS ALLOWS LUNGS TO EXPAND AS ONE

100
Q

What is the oxygen cascade?

A

The pxygen cascade is the partial pressure of oxygen that decreases rom atmospheric air to respiring tissue that facilitates movement of oxygen.

101
Q

What are the four determinants for the effectiveness of the oxygen cascade?

A
  1. alveolar ventilation
  2. Ventilation-perfusion matching: if you are ventilating airways that aren’t perfused ⇒ inefficient gas exchange. perfusing non ventilated ares don’t increase saturation
  3. Diffusion capacity: disease that causes parenchyma leading it to thicken so less efficient gas exchange
  4. Cardiac output: increase CO there is more blood going to lungs and greater oppertunity to oxygenate so increase O2 delivery
102
Q

What is the oxygen partial pressure going from atmosphere to cells?

A

Atmospheric (21.3 kPa) → upper airways (20 kPa) → alveolus (13.5 kPa) → post-alveolar capillary (13.5 kPa) → pulmonary veins (13.3 kPa) → systemic artery (13.3. kPa) →cells (5.3 kPa)

103
Q

What happens during exercise to the oxygen dissociation curve and how does this occur?

A

During exercise cellular mechanism increases → an increase in CO2 produces → increased PO2 → decreased pH withhin tissues (carbonic acid formation) → mild acidosis and hypercapnia → shift of oxygen dissociation curve to the right (improving oxygen unloading)

  • increased CO2 is detected by chemoreceptors in medulla
  • should oxygen supply go below 4.5 kPa in the alveolus then anaerobic respiration takes over
104
Q

What is the ventilatory response to exercise?

A

Initially the respiration rate increases. It can then remain stable for a long time because an increase in tidal volume is more efficient at increasing ventilation then increasing respiration rate.

once tidal volume starts to plateau the respiratory rate states to increase again.

105
Q

What initially happens when you increase altitude?

A

The air becomes thinner which reduces atmospheric PO2 →decreasing alveolar O2 so there is a reduced concentration gradient →slower diffusion of oxygen into capillaries

Low PaO2 instimulates ventilation (hypobaric hypoxia) Hyperventilation → more Co2 expired →PaCO2 falls → rise in PH alkalosis →ODC shifts to the left. This stops main stimulus for increased ventilation

106
Q

What are the 2 challenges to altitude?

A
  1. Hypoxia: much less oxygen in the ambient air
  2. Thermal stress (cold)
  3. Solar radiation
  4. hydration
  5. dangerous
107
Q
A
108
Q

What are 2 compensatory mechanisms for respiratory alkalaemia caused by increasing altitudde?

A
  • Renal compensation by bicarbonate excretion which helps return pH to normal and ODC shifts to normal place
  • increased production of 2,3 - DPG to improve oxygen unloading in tissues
109
Q

What causes chronic symptoms of allergy?

A

T helper 2 cell activation to release cytokines and chemokines

110
Q

What is the mechanism of allergy?

A

Goes via helminth response route. An allergen comes into comtact with epithelial via toll-like and NOD-like receptors. Epithelial →secrete IL-25 and IL-33 →stimulate innate immune system.

Secretion of IL4 and IL-13 → these stimulate IgE production by B cells and IL-5 stimulates eosinophils →proliferation of mast cells and Th2 cells.

Acute allergy symptoms cause by mast cells. Mast cells have IgE coated cell membranes and when the allergen reaches the IgE the mast cells release granules containing histamines which lead to symptoms

111
Q

What are symptoms of anaphylaxis? What is the pathophysiology?

A

The massive release of histamine causes relaxation of vascular smooth muscle and contraction of non-vascular smooth muscle. It causes vasodilation and so fluids rapidly leave the circulation resulting in dramatic hypotension. Narrows airways via oedema and bronchoconstriction

Seizures, dizzy, unconcious, swlling, tingling, arrhytmia, vomiting, anxiety

112
Q

What is the treatment for anaphylaxis?

A

Iv fluids and adrenaline

113
Q

What are the functions of pulmonary circulation?

A

gas exchange

metabolism of vasoactive substances

filtration of blood

114
Q

What are the three pulmonar shunts?

A
  1. Bronchial circulation has a shunt where there is mixing of venous and oxygenated blood. Blood leaves the thoracic artery and resturns via pulmonary veins
  2. Foramen Ovale (foetal circulation) between 2 atria of the heart
  3. Ductus arteriosus (foetal) links the pulmonary artery bifurcation to the proximal descending aorta (normally fuses in first few days of life)
115
Q

What are the four forces involed in pulmonary fluid balance?

A
  1. capillary hydrostatic pressure
  2. intersitial hydrostatic pressure
  3. plasma protein oncotic
  4. interstital protein oncotic pressure
116
Q

What are the four mechanisms by which fluid accumulation occurs in the pulmonary system?

A
  • increasing the intravascular hydrostatic pressure
    • ​mitral valve stenosis & heart failure
  • reducing the oncotic pressure
    • ​hyproproteinaemia, protein-losing nephropathies, liver cirrhosis
  • increasing the intersitial oncotic pressure​​
    • pulmonary endothelial damage, infection
  • blocked lymphatic system
    • ​cancer
117
Q
A
118
Q

How is breathing controlled in the asleep state?

A

During REM sleep SO2 and PaO2 drop a little.

CO2 increase when you sleep is vital to be able to breath at night

Co2 threshold is reached and is communicated to the respiratory centre (Pre-Botzinger Complex). The respiratory centre sends impulses to the respiratory muscles to stimulate breathing

119
Q

What is central sleep apnoea?

A

When CO2 is prevented from reaching the apnoeic threshold then the individual will not breath while asleep. (congenital central hypoventilation syndrome)

Chemo-sensitivity is affected. it’s very rare and treated by ventilation at night

120
Q

What is obstructive sleep apnoea?

A

When patients sleep muscle function is lost. The patients ariway may close a little and if they can’t breath sufficiently the oxygen level falls and CO2 rises. Eventually the hypoxia or hypercapnia will wake patient allowing clearing/opening of airways

IK1 - LSS (5 decks)

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