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Respiratory ESA 3 > Key facts > Flashcards

Key facts Flashcards

1
Q

<p>What are the conducting airways of the lungs?</p>

A

<p>Trachea -> Terminal bronchioles</p>

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2
Q

<p>What are the respiratory airways of the lungs?</p>

A

<p>Respiratory bronchioles -> Alveoli</p>

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3
Q

<p>What does the "Bucket handle" movement of the chest lead to?</p>

A

<p>Increased Lateral diameter</p>

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4
Q

<p>What does the "Pump handle" movement of the lead to?</p>

A

<p>Anterior-Posterior diameter increase</p>

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5
Q

<p>Name the 3 openings of the Diaphragm and their spinal levels</p>

A

<p>T8 - Vena Cava
T10 - Oesophagus
T12 - Aorta (aortic hiatus)</p>

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6
Q

<p>Where does the neurovascular bundle supply the rib run?</p>

A

<p>Along inferior of the bone (under the bone)</p>

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7
Q

What does the neurovascular bundle contain?

A

Intercostal vein, artery, nerve

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8
Q

What are the accessory muscles to breathing on inspiration?

A
  • SCM (COPD sign)

- Pec Major, Minor, Serratus anterior

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9
Q

What are the accessory muscles to breathing on expiriation?

A
  • Abdominal wall muscles

- Internal intercostal muscles

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10
Q

What does the Azygous system drain from and to?

A

From the intercostals, to the SVC

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11
Q

How many lobes do the right and left lungs have?

A 
R = 3
L = 2
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12
Q

What is the organisation of the Hilum of the lungs?

A

Bronchi top
Arteries middle
Veins bottom

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13
Q

What blood system supplies the Lungs?

A

Bronchial

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14
Q

What nerve supplies the smooth muscle of the lungs?

A

Vagus

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15
Q

What is the Tidal volume?

A

Amount of air that enters and exits with each breath

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16
Q

What is Boyle’s law?

A

Inverse relationship between pressure and volume of contained - if volume goes up, pressure goes down

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17
Q

How are the lungs attached to the external pleura? (parietal)

A

Surface tension via pleuritic fluid

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18
Q

What is the pressure within the pleura?

A

Negative

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19
Q

On all graphs, what does an upward deflection mean?

A

Inspiration

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20
Q

What is the Inspiratory Reserve Volume?

A

From tidal volume max inspiration to the top of the graph

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21
Q

What is the Vital Capacity?

A

IRV + TV + ERV

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22
Q

What is the Inspiratory Capacity?

A

IRV + TV

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23
Q

What is the Residual Volume?

A

Total Lung Capacity - VC

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24
Q

Define Compliance

A

Volume change per unit pressure change

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25
Q

What is Compliance determined by?

A

Elastic recoil of the lung

Surface tension of the lung

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26
Q

What does surfactant do to compliance?

A

Reduces surface tension, raises compliance

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27
Q

What is surfactant made by and at what age does it start being produced?

A

Type 2 pneumocytes start at 24 weeks, make enough by 35 weeks

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28
Q

What is the role of surfactant?

A

Increase compliance

Prevent small alveoli from collapsing into larger ones

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29
Q

How does surfactant prevent small alveoli from collapsing into larger ones?

A

Law of Laplace - Pressure = 2 x Surface Tension / Radius
Normally, smaller has larger pressure, so collapses into larger one.
In a larger alveoli, surfactant molecules are further apart, so they reduce surface tension less
In a smaller alveoli, surfactant molecules are closer together, so they reduce surface tension more
Therefore pressure in both is the same, despite volume difference

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30
Q

Where is the highest resistance in the airways?

A

Trachea, as going from larger to smaller

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31
Q

What prevents bronchi from collapsing inwards due to lack of cartilage?

A

“Radial traction” from alveoli

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32
Q

What is the relationship between Compliance and Elasticity?

A

Compliance = 1/Elasticity as the elastance PUSHES BACK IN, reducing the ability to push out

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33
Q

What are the two types of lung disease?

A

Obstructive

Restrictive

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34
Q

Describe how diffuse lung fibrosis occurs and what type of lung disease it is

A

Increased deposition of matrix eg. elastic fibres/ collagen in the interstitium of the lungs
Reduces compliance and increases elastic recoil, causes reduced filling
Restrictive disease

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35
Q

Give a cause of Diffuse Lung Fibrosis

A

Asbestosis

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36
Q

What is COPD?

A

Chronic Bronchitis and Emphysema

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37
Q

Describe the pathophysiology of Emphysema

A

Protease mediated destruction of elastin, leads to reduced alveolar SA, reduced radial traction of alveoli
Loss of elastic tissue leads to increased compliance - less able to get air out
Obstructive defect

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38
Q

Give one cause of Emphysema

A

Smoking

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39
Q

When is airway obstruction more significant? (inspiration or expiration?)

A

Expiration (no negative pressure in pleuritic space to keep airways open)

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40
Q

What is Atelectasis?

A

Lung collapse

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41
Q

Name 4 causes for Atelectasis

A

Pneumothorax, Pleural effusion, RDS, Resorption collapse due to blockage

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42
Q

Describe the pathophysiology of Respiratory Distress Syndrome

A

Reduced surfactant, therefore increased surface tension, therefore reduced compliance, therefore reduced filling, therefore difficulty breathing

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43
Q

What is the treatment for RDS?

A

Give mother corticosteroids before birth/ surfactant replacement therapy

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44
Q

What does SVP stand for?

A

Saturated water vapour constant = 6.28kPa

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45
Q

What is the equation for the amount of gas dissolved in a fluid?

A

Partial pressure of gas x solubility coefficient of the gas

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46
Q

What is the definition of partial pressure?

A

Pressure exerted by a gas when in solution (dissolved)

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47
Q

What is the partial pressure of O2 in the lungs?

A

13.3kPa

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48
Q

What is the partial pressure of CO2 in the lungs?

A

5.3kPa

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49
Q

What is the partial pressure of both CO2 and O2 in the lungs from the bloodstream?

A

6kPa

50
Q

What percentage of O2 is still bound in venous return?

A

67%

51
Q

What is the difference between hypoxia and hypoxaemia?

A 
Hypoxaemia = systemic reduction in O2 in the blood (like in anaemia)
Hypoxia = reduction in O2 in a tissue
52
Q

Where is an ABG taken from?

A

Radial artery needle puncture

53
Q

What is the normal respiration rate/minute?

A

12-20

54
Q

What is it called when the lungs constrict arteries in poorly perfused areas of the lung?

A

Hypoxic pulmonary vasoconstriction

55
Q

Why does significant V/Q mismatch make up for CO2 levels in the other lung, but not O2?

A

CO2 can be blown off through hyperventilation

O2 cannot be increased, as 13.3kPa already reached

56
Q

What is the carbonic acid equation?

A

CO2 + H2O -> H2CO3 -> H+ + HCO3-

57
Q

What determines blood pH?

A

HCO3- to H+ determines pH

58
Q

What controls pCO2 in the blood? What controls HCO3- levels in the blood?

A 
CO2 = lungs
HCO3- = produced constantly by the RBCs, but controlled by the kidneys
59
Q

What is the enzyme that converts CO2 and H2O to H+ and HCO3-?

A

Carbonic anhydrase

60
Q

Describe RBC HCO3- production

A

Carbonic anhydrase conversion of CO2 and H2O to HCO3- and H+
H+ binds to Hb
HCO3- exported

61
Q

The amount of H+ that Hb can carry is based on what?

A

Amount of O2 carried - this means that when O2 dropped off at muscles, more CO2 can be converted to HCO3- (buffering), since more H+ can be carried by Hb

62
Q

How can CO2 be carried back to the lungs?

A
  • H+ stored Hb
  • Carbamino compounds
  • Dissolved in blood
63
Q

What do Peripheral chemoreceptors detect and where are they? What nerves transmit to and from them?

A

O2 levels - carotid and aortic bodies

Glossopharyngeal and Vagus

64
Q

What do Central chemoreceptors detect and where are they?

A

CO2 levels via pH of CSF - in medulla of brain, choroid plexus cells - choroid plexus cells secrete HCO3- into the CSF, as the BBB is impermeable

65
Q

What does alkalosis cause? (not hypokalaemia)

A

Hypocalcaemia - leads to paraesthesia and tetany

66
Q

How do the kidneys controlled HCO3- levels?

A
  • 100% of HCO3- is reabsorbed in PCT (absorbed as H2O and CO2, then reabsorbed via Na+/HCO3- co-transporter)
  • In PCT - Amino acids converted to HCO3- and NH4+ (eg. glutamine)
  • In DCT - makes via CO2 + H2O - H+ buffered by phosphate and NH4+
67
Q

Explain why severe acidosis cannot be dealt with by the kidney

A 
Acidosis causes K+ to leave cells.
Acidosis causes K+ to leave PCT cells.
RECIPROCAL ION SHIFT.
Therefore, low H+ in kidney tubules, kidney thinks it's alkalotic, when it isn't.
Loses HCO3- - makes acidosis worse
68
Q

Explain the relevance of the anion gap

A

Gap between cations and anions
Gap is increased if anions not replaced by Cl-
IN ACIDOSIS:
If renal cause - no anion gap, as Cl- will replace due to anion exchanger
If non-renal cause, will have keto or lactic acidosis

69
Q

Give a cause of respiratory acidosis

A

High CO2, low O2
Type 2 respiratory failure
Severe COPD, severe asthma, respiratory distress from head injury or drug overdose
Hypoventilation

70
Q

Give a cause of respiratory alkalosis

A

Low CO2, low O2
Type 1 respiratory failure
Eg. everything

71
Q

Give a cause of metabolic acidosis

A

Increased anion gap: Ketoacidosis/Lactoacidosis

Normal anion gap: Kidney failure/ severe diarrhoea

72
Q

Give a cause of metabolic alkalosis

A

Increased HCO3- from stomach acid production

73
Q

What X-ray is done for lungs?

A

PA

74
Q

What is functional reserve volume?

A

RV + ERV

75
Q

What is FVC?

A

Forced vital capacity - total air breathed out after inhaling fully

76
Q

What is FEV1?

A

Total amount breathed out in 1 second

77
Q

What is the ratio used to check if restrictive/obstructive between FEV1 and FVC?

A

FEV1/FVC ratio

78
Q

What is the FEV1/FVC ratio for an obstructive disorder?

A

<70% - FEV1 down, FVC same

79
Q

What is the FEV1/FVC ratio for a restrictive disorder?

A

> 70% - FEV1 the same, FVC goes down

80
Q

What are the Flow-volume loop signs for restrictive and obstructive disorders?

A

Obstructive: scalloping
Restrictive: X-axis reduced (volume lower)

81
Q

Name 3 risk factors of PE

A

Pregnancy, COCP, DVT (immobilisation)

82
Q

What does PE lead to pathologically?

A

RV overload, respiratory failure due to V/Q mismatch

83
Q

What is the treatment for PE?

A

Oxygen, heparinisation, fibrinolytics

84
Q

Describe Type 1 vs Type 2 respiratory failure

A

Type 1 - Low O2, Low or Normal CO2

Type 2 - Low O2, High CO2

85
Q

What are the compensatory mechanisms for chronic hypoxaemia?

A
  • Increased EPO production
  • Increased 2,3-BPG production
  • Hypoxic pulmonary vasoconstriction
86
Q

List 2 Type 1 acute respiratory causes

A
  • Pneumonia, PE
87
Q

List 3 Type 1 chronic respiratory causes

A
  • Asthma, COPD, fibrotic lung disease,
88
Q

List 2 Type 2 acute respiratory causes

A
  • Narcotics, life threatening asthma
89
Q

List 1 Type 2 chronic respiratory causes

A

Chronic COPD

90
Q

Describe the pathophysiology of Asthma

A

Type 1 -> Type 4 hypersensitivity reaction

91
Q

Name 4 triggers of asthma

A

Pollen
Pets
Smoking
Dust mites

92
Q

Name 2 Asthma treatments

A
  • Corticosteroid inhaler (prednisolone)

- B2 agonist (salbutamol)

93
Q

Severe asthma vs life-threatening asthma

A

Severe: High resp rate, tachycardia, O2>92%

Life-threatening: Silent chest, low resp rate, O2 < 92%

94
Q

What is the treatment for life-threatening asthma?

A
  • Oxygen
  • Nebulised salbutamol
  • Ipratropium
  • Prednisolone
95
Q

What is Chronic Bronchitis?

A

Chronic mucous hypersecretion due to inflammation in upper airways - remodelling and narrowing + destruction of mucociliary escalator

96
Q

Name 3 early COPD signs

A

“Purse lip”
Accessory muscle usage
Hyperinflation

97
Q

How are pack years calculated?

A

1 pack year = 20 cigarettes/ day

98
Q

What is Bronchiectasis?

A

Chronic dilatation of bronchi, reduced mucous clearance, recurrent infections

99
Q

What can be seen on an X-ray in Bronchiectasis?

A

Signet-ring sign

100
Q

What are the symptoms of Bronchiectasis?

A

Chronic cough, sputum production, haemoptysis

101
Q

What are the causes of Bronchiectasis?

A

Infection: whooping cough, TB, influenza, lung scarring

102
Q

Name 3 LRT infections

A
  • Bronchitis
  • Pneumonia
  • Bronchiestasis
103
Q

What is pneumonia?

A

Lung parenchyma inflammation

Cellular exudate into alveolar spaces

104
Q

What are the most common organisms for hospital and community acquired pneumonias? What are their treatments?

A

Community: Strep pneumoniae - co-amoxiclav and
Hospital: Staph aureus - co-amoxiclav

105
Q

What type of Giant cells are present in TB?

A

Langerhans Giant Cells

106
Q

What tests are there for TB?

A

Tuberculin skin test
Interferon-Gamma test
Sputum and microscopy - only way of seeing if active infection

107
Q

What are the drugs to treat TB and how long are they taken for?

A 
RIZE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
6 months
108
Q

Where is the fluid build-up in a pleural effusion?

A

Under the lung

109
Q

What does a “bat-wing” appearance on an X-ray mean?

A

Congestive heart failure

110
Q

What are the “crackles” heard on auscultation?

A

Alveoli opening (snapping open)

111
Q

What type of breathing is normal?

A

Vesicular - not Bronchial

112
Q

What are the causes of primary and secondary pneumothoraxes?

A 
Primary: = bulla bursts
Secondary = secondary to lung disease
113
Q

Where is the chest drain placed in a normal pneumothorax?

A

5th mid axillary line

114
Q

Where is the CANNULA placed in a tension pneumothorax?

A

2nd mid clavicular line

115
Q

List the causes of pleural effusion and whether they are (lymphatic) absorptive failure or overproductive failures

A

Absorptive: Heart failure, Nephrotic syndrome
Overproduction: Infection from pneumonia

116
Q

What types of lung cancer are there?

A

Small cell, non-small cell - small cell most aggressive

117
Q

What is the minimum O2 the lungs need to be kept at to prevent damage?

A

8KPa

118
Q

Give 2 reasons why giving a patient with Chronic Hypoxia Oxygen is bad

A
  1. Will remove respiratory drive from peripheral chemoreceptors in carotid and aortic bodies
  2. Will lead to increased perfusion of poorly ventilated alveoli, removing the effect of hypoxic pulmonary vasoconstriction
119
Q

Where should a chest drain be inserted into a patient?

A

Just above the rib, avoid the neurovascular bundle

120
Q

Why is asthma worse at night?

A

Parasympathetic drive constricts the airways - rest and digest

121
Q

What is the main treatment for Small Cell lung cancer?

A

Chemo

122
Q

What is the main treatment for Non-Small Cell lung cancer?

A

Surgery

Respiratory ESA 3 (1 decks)

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