Respiratory Flashcards
1
Q
Conducting portion
A
Tubes to transport and condition air
2
Q
Respiratory portion
A
Membranes for gas exchange
3
Q
R lung (lobes and fissures)
A
3 lobes 2 fissures (oblique and horizontal)
4
Q
L lung (lobes and fissures)
A
2 lobes 1 fissure (oblique)
5
Q
Where does the trachea bifurcate?
A
Carina
6
Q
Functions of thoracic cage (x 2)
A
Protection
Respiratory movements
7
Q
Functions of fluid film (x 2)
A
Aid sliding
Create surface tension
8
Q
What does increased surface tension help?
A
Inspiration
9
Q
Pressures in inspiration
A
Pb > Pa
10
Q
Pressures in expiration
A
Pb
11
Q
Quiet inspiratory muscles (x 2)
A
Diaphragm
External intercostals
12
Q
Increasing effort inspiratory muscles (x 4)
A
Diaphragm
External intercostals
Accessory
Neck/Shoulder girdles
13
Q
Quiet expiratory muscles (x 1)
A
Elastic recoil of tissues
14
Q
Increasing effort inspiratory muscles (x 2)
A
Internal intercostals
Abdominal wall
15
Q
What type of pressure does expansion exert on the intrapleural space?
A
Negative
16
Q
Tidal volume (TV)
A
Volume of air in and out in normal breathing (6-7 ml/kg)
17
Q
Inspiratory reserve volume (IRV)
A
Deepest possible inspiration (3000 ml)
18
Q
Expiratory reserve volume (ERV)
A
Deepest possible expiration (1500 ml)
19
Q
Residual volume (RV)
A
Air remaining in the lungs after ERV (1000ml)
20
Q
Why is there a residual volume?
A
Due to the rigidity of the thorax and pleural attachments
21
Q
Total lung capacity (TLC)
A
TV + IRV + ERV + RV
22
Q
Vital capacity (VC)
A
TV + IRV + ERV
23
Q
Functional residual capacity (FRC)
A
ERV + RV
24
Q
Restrictive lung disease
A
Lower RV, TLC, VC and FRC
FVC/FEV1 > 0.7
25
Obstructive lung disease
Higher RV, TLC (emphysema) and FRC
Lower TLC (COPD)
FVC/FEV1
26
When is compliance reduced?
Fibrosis and circumferential burns
27
When is compliance increased?
Emphysema
28
When will alveoli be poorly ventilated?
When closing capacity > FRC
29
Surface tension =
Energy needed to maintain gas-liquid interface
30
How is PE minimised?
By forming a sphere -> reduces SA : vol
31
Which cells make surfactant?
Type 2 alveolar cells
32
Functions of surfactant (x 5)
```
Reduce surface tension
Increase compliance
Prevent atelectasis
Aid alveolar recruitment
Minimise fluid
```
33
Why is it important that surfactant becomes more dispersed as volume increases?
Helps to equalise pressure
34
How is energy used in inspiration?
To overcome elasticity stored as PE
35
In what form is energy dissipated in expiration?
Heat
36
Rate of oxygen uptake is proportional to...
Area x change in pressure
37
Rate of oxygen uptake is dependent on...
Physiochemical properties of the gas
| Nature of the membrane
38
Pressure gradient
The difference in partial pressure of gas in alveolus and blood
39
Partial pressure
The pressure a gas would exert if it were the only gas in a mixture
= P x fractional constant
40
Why is pp inversely proportional to solubility?
As fewer molecules are available to exert a pressure
41
Why is CO2 transport more efficient than O2?
Because CO2 is 24 times more soluble
42
Alveolar fibrosis
Thickening of the alveolar wall
43
Pneumonia
Alveolar consolidation
44
Pulmonary oedema
Frothy secretions
45
Interstitial oedema
Fluid around alveoli
46
Emphysema
Alveolar-capillary destruction
47
Atelectasis
Alveolar collapse
48
How are airways kept patent?
Through continuous muscle activity
49
Pharyngeal dilator reflex
P receptor -> brainstem -> muscle
50
Sleep disordered breathing
No pharyngeal contraction -> periods of airway destruction -> lack of deep sleep
51
What is sleep disordered breathing associated with?
Obesity
Hypertension
Drugs
Alcohol
52
Which cells produce airway lining fluid?
Ciliated epithelial cells
53
What is airway lining fluid produced in response to?
Irritation
Smoke
Pollution
54
Functions of airway lining fluid (x 2)
Humidifies alveoli
| Forms part of the airway defence
55
What are cilia inhibited by?
Smoke, anaesthetic, pollution and infection
56
What determines where a particle is deposited?
Size
57
Non-immune pulmonary defences
Physical barrier and removal
Chemical inactivation
Alveolar macrophages
58
Immune pulmonary defences
Humoral (IgA, IgE and IgG)
| Cell-mediated
59
In what two forms is O2 carried?
Dissolved in the blood and combined with haemoglobin
60
How many O2 molecules can each haemoglobin carry?
4 (4 chains)
61
In which form of haemoglobin can O2 access the binding site?
R State (not in T state)
62
Thalassemia
Absent globin chain
63
HbS (Sickle Cell)
Defective globin chain
64
Methaemoglobin
Defective Fe atom
65
CO Hb
Wrong ligand (CO)
66
In which 3 forms is CO2 carried?
Dissolved in plasma
In carbamino compounds
As bicarbonate
67
Respiratory alkalosis
Low PCO2
Normal HCO3-
Due to hyperventilation
68
Respiratory acidosis
High PCO2
High HC03-
Due to ventilatory failure
69
Metabolic alkalosis
Normal PCO2
High HCO3-
Due to loss of H+
70
Metabolic acidosis
Low PCO2
Low HCO3-
Due to renal failure/shock/diabetic ketoacidosis
71
When do lung buds form?
Week 1
72
When do main and secondary bronchi form?
Week 5
73
When do tertiary bronchi form?
Week 6
74
When do terminal bronchioles form?
Week 16
75
When do respiratory bronchioles form
Week 26
76
When do alveoli form?
Week 36
77
What are tracheoesophageal fistulas (TOF)?
Incomplete division of foregut into oesophageal and tracheal portions
- most common with oesophageal atresia
78
What is oesophageal atresia?
When the upper oesophagus end abruptly, and the lower forms a fistula with the trachea -> milk regurgitated and acid into trachea
79
Pseudoglandular lung maturation
5-17 weeks
| Resp tree -> terminal bronchioles
80
Canicular lung maturation
16-25 weeks
| Terminal bronchioles -> resp bronchioles -> alveolar duct
81
Terminal sac lung maturation
26 weeks - birth
Formation of primitive alveoli, blood-air barrier and surfactant film
Foetus can survive
82
Alveolar lung maturation
36 weeks - 8 years
83
What is pulmonary agenesis?
When the lung bud fails to split-
- bi (incompatible with life)
- uni (prompts respiratory stress)
84
What is pulmonary hyperplasia?
All components are present, but are underdeveloped
85
What is respiratory distress?
Damage to alveolar lining -> laboured/fast breathing and chronic lung injury
86
Treatment of RDS
Glucocorticoid and surfactant therapy
87
Differences between apical and basal alveoli
Apical are
- 4 x larger
- better ventilated
- less expanded
88
Hydrostatic pressure
Force exerted by the weight of fluid due to gravity (greatest at bottom)
89
What are the 3 lung zones?
Dead space, recruitment and distension
90
Ventilation-perfusion mismatch
Ideally 1, but 3.3 at apex and 0.6 at base
91
Anatomical dead space
Conducting airways- no gas exchange
92
Alveolar dead space
Unperfused alveoli
93
Physiological dead space
Anatomical + alveolar
94
Shunt
Where deoxygenated blood reaches the L side by bypassing the lungs or failing to be oxygenated eg pneumothorax
95
How does the medulla oblongata function as a respiratory centre?
Dorsal respiratory group (DRG) fires on inspiration
| Ventral RG fires on inspiration and expiration
96
How does the pons function as a secondary respiratory centre?
It regulates the medulla- apneustic centre stimulates DRG and pneumotaxic centre inhibits insp neurones in VRG
97
Oxygen cascade
Humidification -> alveolar gas -> alveolar-capillary diffusion -> ventilation-perfusion mismatch/shunt -> tissue diffusion -> diffusion in cell
98
Oxygen delivery
Amount of O2 leaving the heart in a minute
| = O2 content x CO
99
Oxygen consumption (VO2)
Amount of O2 used in a minute
100
Respiratory exchange ration/quotient
CO2 production : O2 consumption (should be 1)
101
How does oxygen generate energy?
Glyolysis
Tricarboxylic acid cycle
Oxidative phosphorylation
102
When does cellular hypoxia occur?
When there is insufficient O2 to mitochondria
103
What are the 3 causes of cellular hypoxia?
Anoxic (lack of O2)
Stagnant (poor blood supply)
Anaemia (lack of haemoglobin)
104
What is VO2 max?
The plateaued VO2. An indicator of fitness and anaerobic threshold
105
How are changes to normal respiration controlled?
Neural input
Proprioreceptors
Changes in arterial blood gases
Temperature regulation
106
Responses to altitude (x5)
```
Hyperventilation
Better unbinding of O2
Polycythaemia
HCO3- excretion
Duiresis/hyponatraemia
```
107
What are the symptoms of acute mountain sickness?
Headache, nausea, vomiting, loss of appetite, difficulty sleeping/exercising, amnesia and dizziness
108
Effects of diving
Compression of lungs, chest and abdomen
Increased pressure in pleural cavity
Reduced volume of O2 and blood
Increased pp of O2
109
Treatments of dry cough
Cough suppressants
Stop smoking
Opioids/non-opioids
Sedatives
110
Treatments of productive cough
Expectorants and mucolytics
111
Selective B2 antagonists
Inhalers or nebulisation
Short (salbutamol) or long-lastin (salmeterol)
SE= palpitation, tachycardia, tremor and restlessness
