Respiratory system Flashcards
(216 cards)
1
Q
What is Boyle’s law?
A
If temperature is constant, pressure is inversely proportional to volume
2
Q
What is Charles’ law?
A
Pressure is proportional to absolute temperature (scale starts at absolute zero)
3
Q
What is Universal gas law?
A
Pressure x volume = gas constant x temperature (K)
4
Q
What is Partial pressure?
A
Pressure that each gas exerts on the mixture (each gas behaves differently)
Calculated as fraction of total pressure as volume fraction of gas in mixture
5
Q
What is Vapour pressure?
A
Pressure exerted by a gas in equilibrium with a solid or gas
6
Q
What is Saturated vapour pressure ?
A
When rate of molecules entering/ leaving water at the same time is equal
7
Q
What is Gas tension?
A
How readily a gas will leave the liquid
8
Q
What is Solubility?
A
Amount of gas that enters a liquid to establish a particular tension
9
Q
What is the equation for content?
A
Content = solubility x tension
10
Q
What is Tidal volume?
A
Amount of air that is displaced between normal inspiration and expiration, when extra effort is not applied
11
Q
What is Respiratory rate?
A
Number of breaths taken in a set time
12
Q
Is pulmonary circulation working under low or high resistance?
A
Low
Lots of capillaries connected in parallel
13
Q
Optimal ventilation/perfusion ratio?
A
0.8
14
Q
What is hypoxic pulmonary vasoconstriction?
A
Alveolar hypoxia results vasoconstriction of pulmonary vessels, and increased resistance means less flow to poorly ventilated areas
15
Q
What can chronic hypoxic vasoconstriction lead to?
A
Right ventricular failure, due to high afterload
16
Q
Define upper respiratory tract
A
Respiratory system that lies outside the thorax
Nasal cavity
Pharynx
Larynx
17
Q
Define lower respiratory tract
A
Part of respiratory system inside the thorax
18
Q
Which structures have cartilaginous rings and why?
A
Trachea and bronchi
To keep them open
19
Q
What are the functions of the nose?
A
Smell Respiration Filtration of dust Humidification of inspired air Reception and eliminations of secretions from paranasal sinuses and nasolacrimal ducts
20
Q
Where in the nose is the smell organ?
A
Olfactory area
21
Q
What are concha/ turbinates?
A
Structures in the nose that offer vast surface area for heat exchange
22
Q
Where do frontal sinuses drain into?
A
Through frontonasal duct into ethmoidal infundibulum, which drain into middle nasal recess
23
Q
What is Pneumothorax?
A
Air getting into the pleura, causing fluid surface tension to be broken and lungs to collapse
24
Q
What is lung compliance?
A
Stretchiness of the lungs
Volume change per unit pressure change
High compliance means easy to stretch
25
What is specific compliance?
Volume change per unit pressure change/ starting volume of lungs
26
What causes elastic properties of lungs?
Elastic tissue of lungs and surface tension forces of fluid lining alveoli
27
What is surface tension?
Interaction between molecules at surface of liquid lining alveoli, making surface resist stretching
Higher the surface tension, the harder lungs are to stretch
28
Where are surfactants produced?
Type 2 alveolar cells
29
What are surfactants?
Mixture of phospholipids and proteins with detergent properties that reduce the surface tension when lungs are deflated
30
What is Laplace's law?
Pressure if inversely proportional to the radius of the bubble
31
What is Poiseulle's law?
The resistance of a tube increases sharply with falling radius
32
Is resistance greater in the upper or lower respiratory tract?
Upper, as lower is connected in parallel
33
How does a spirometer work?
Patient fills lungs from atmosphere, and breathes out as fast and far as possible through spirometer
34
3 reasons why vital capacity can be less than normal
Filled normally in inspiration
Emptied normally in expiration
Both
35
What is forced vital capacity?
Maximum volume that can be expired from full lungs
36
What is forced expiratory volume in 1 second?
Volume expired in the first second of expiration from full lungs
37
What can you see on a vitolagraph during restrictive deficit?
FVC reduced
| FEV1 more than 70% of FVC
38
What can you see on a vitolagraph during obstructive deficit?
FEV1 reduced
| FVC relatively normal
39
How does helium dilution test work?
Helium is inert, colourless, odourless, tasteless and not toxic.
At the end of normal tidal expiration, patient is connected to a circuit, which is connected to a container with a gas mixture with a known helium concentration (C1) and volume (V1). Patient continues to breathe into container until equilibrium reached
New concentration of helium (C2) is found.
FRC and RV can be worked out
40
What does the Carbon Monoxide Transfer Factor measure?
Rate of transfer of CO from the alveoli to blood in ml per minute per kPa
Way of measuring diffusion capacity of lung, because amount transferred will depend on how well gas diffusion takes place
41
How do you carry out test to work out Carbon Monoxide transfer factor?
Patient performs full expiration, followed by rapid maximum inspiration of gas mixture composed of air, tiny fraction of CO and fraction of inert gas like helium.
Breath held for 10 seconds
Patient exhales, gas collected mid expiration, to gain alveolar sample.
Concentration of CO and inert gas measured
Carbon monoxide transfer factor calculated
42
Where do ethmoidal sinuses drain into?
Anterior → Ethmoidal Infundibulum → Middle Nasal Recess
Middle → Middle Nasal Recess
Posterior → Superior Nasal Recess
43
Where do sphenoid sinuses drain into?
They drain directly into the sphenoethmoidal recess
44
Where do Maxillary sinuses drain into?
They drain through the maxillary ostium into the middle nasal recess
45
What is the Pharynx divided into?
Nasopharynx
Oropharynx
Laryngyopharynx
46
What does the larynx connect?
Inferior oropharynx to trachea
47
Function of larynx
Protect air passage to prevent food entering trachea during swallowing
Phonation
48
Function of clara cells
secrete surfactant lipoproteins, so walls of bronchioles do not stick together during expiration
Also secrete protein CC16 - marker for bronchoalveolar damage or leakage across air-blood barrier
Lowered means lung damage
Increased means leakage
49
What are the types of cells + functions in the alveoli?
Type I Pneumocyte - simple squamous/ 90%/ permit gas exchange
Type II Pneumocyte - simple cuboidal/ 10%/ produce surfactant
Macrophages
50
How much do external intercostal muscles account for during quiet respiration?
30%
51
How much does the diaphragm account for during quiet respiration?
70%
52
Which muscles cause expiration during quiet breathing?
None
| Recoil of the lungs - passive
53
Which muscles cause inspiration during forced breathing?
```
Diaphragm
External intercostals
Sternocleidomastoid
Scalene
Pectoralis minor
Serratus anterior
```
54
Which muscles cause expiration during forced breathing?
Internal intercostals
Inner intercostals
Abdominal muscles
55
Factors affecting rate of gas exchange
Area available for exchange
Gradient of partial pressures
Diffusion distance
56
Normal pO2 and pCO2 in the alveoli
pO2 - 13.3kPa
| pCO2 - 5.2kPa
57
What is inspiratory reserve volume?
Extra volume that can be breathed in when extra force is applied
58
What is expiratory reserve volume?
Extra volume that can be breathed out when extra force is applied
59
What is residual volume?
Volume of air left after maximal expiration - measured by helium dilution
60
What is Vital capacity?
Biggest breath that can be taken in
Measured from maximal inspiration to maximal expiration
Usually 5L
61
What is functional residual volume?
Volume of air in lungs at resting expiratory level
Residual volume + expiratory reserve volume
Usually 2L
62
What is Inspiratory Capacity?
Biggest breath that can be taken in from resting expiratory level
Usually 3L
63
What is alveolar ventilation rate?
Amount of air reaching the alveoli
Pulmonary ventilation rate (tidal volume x RR) - dead space ventilation rate (dead space volume x RR)
64
What is serial dead space?
Air in conducting airways which does not take part in gas exchange.
First air in is first air out
150ml
65
Nitrogen wash out - steps for the experiment
1) Patient takes maximum inspiration of 100% Oxygen
2) Oxygen reaching alveoli will mix with alveolar air, resulting mix contains Nitrogen now
3) serial dead space air still only has O2
4) Exhale through one way valve, measuring % of nitrogen and air volume expired.
5) [Nitrogen] initially 0
6) When alveolar air is breathed out, [Nitrogen] increases until it reaches a plateau
66
What is alveolar dead space?
volume of air in alveoli not taking part in gas exchange
67
Physiological dead space equation?
anatomical dead space + alveolar dead space
68
What is a Pneumothorax?
Abnormal collection of air in the pleural space, leading to fluid surface tension in lungs to be lost, causing lungs to collapse
69
Define Lung compliance?
Stretchiness of the lungs
Lung volume change per unit pressure change
Greater the lung volume, the greater the compliance
70
If lungs can stretch easily, does it have high or low compliance?
High
71
Equation for Specific Compliance
Volume change per unit pressure change/ starting volume of lungs
72
What causes the elastic properties of the lungs?
Elastic tissue in lungs
| Surface tension forces of fluid lining alveoli
73
What is Surface tension?
Interaction between molecules on the surface of a liquid, making the surface resist stretching.
The higher the surface tension, the harder the lungs are to stretch
74
Define hypoxia
Fall in arterial pO2
75
Define hypercapnia
A rise in arterial pCO2
76
Define Hypocapnia
A fall in arterial pCO2
77
Define hyperventilation
Ventilation increases with no change in metabolism
78
Define Hypoventilation
Ventilation decreases with no change in metabolism
79
How does hyperventilation affect pCO2 and pH?
PCO2 decreases
| PH increases
80
How does hypoventilation affect pCO2 and pH?
PCO2 increases
| PH decreases
81
Describe the effects of acute hypoventilation
Hypercapnia and Respiratory acidosis
pH drops below 7.0
Enzymes denature
82
Describe the effects of acute hyperventilation
Hypocapnia and Respiratory alkalosis
pH rise above 7.6
Free calcium in blood falls enough to cause tetany. Ca2+ is only soluble in acid, so if pH rises, Ca2+ cannot stay in blood. Nerves become hyper-excitable
83
Define Respiratory acidosis
CO2 produced faster than it can be removed by the lungs.
| This causes alveolar CO2, and hence [Dissolved CO2] to increase greater than [HCO3}, producing fall in plasma pH
84
Define compensated respiratory acidosis
Respiratory acidosis persists, so kidneys reduce the excretion of HCO3 to restore the [Dissolved CO2] : [HCO3], which restores pH
85
Define Respiratory alkalosis
CO2 removed from lungs faster than it is made. This causes alveolar CO2 to decreases, causing [Dissolved CO2] : [HCO3] to be disturbed, causing plasma pH to increase
86
Define compensated respiratory alkalosis
Respiratory alkalosis persists, so kidneys excrete more HCO3, restoring [Dissolved CO2] : [HCO3], restoring pH
87
Define metabolic acidosis
Metabolic production of acid displaces HCO3 from plasma, causing pH to fall
88
Define compensated metabolic acidosis
The [Dissolved CO2] : [HCO3] to near normal by lowering pCO2 by the lungs increasing ventilation
89
Define metabolic alkalosis
Plasma [HCO3] rises, causing blood pH to rise
90
Define compensated metabolic alkalosis
The [Dissolved CO2] : [HCO3] to near normal by increasing pCO2 by the lungs decreasing ventilation
91
Describe the effects of upon ventilation of falling inspired pO2
detected by Peripheral Chemoreceptors located in Carotid and Aortic bodies, stimulated by decrease in O2 supply relative to usage.
Only respond to large O2 drops
Receptor stimulation causes:
Increase in tidal volume and respiration rate
Circulation changes directing more blood to kidney and brain
Heart rate increases
92
Describe the effects of upon ventilation of increasing inspired pCO2
Increasing arterial pCO2 is detected by Peripheral Chemoreceptors located in Carotid and Aortic bodies, but are insensitive.
Central Chemoreceptors in Medulla more sensitive, altering breathing.
Small rise in pCO2 leads to increased ventilation
Small drop in pCO2 leads to decreased ventilation
93
Where are peripheral chemoreceptors located?
In the Carotid and Aortic bodies
94
What are the functions of peripheral chemoreceptors?
Respond to large drops of arterial O2
Stimulation of the receptors:
o Increases the tidal volume and rate of respiration
o Changes in circulation directing more blood to the brain and kidneys
o Increased pumping of blood by the heart
95
Where are the central chemoreceptors located?
In the medulla of the brain
96
What are the functions of central chemoreceptors?
Detect changes in arterial pCO2
o Small rise in pCO2 → Increase Ventilation
o Small falls in pCO2 → Decrease Ventilation
Respond to pH changes of cerebro-spinal fluid (CSF)
97
What controls CSF [HCO3-]?
Choroid plexus cells
98
Define Hypoxia
Fall in arterial pO2
99
What causes respiratory failure?
Arterial pO2 falls below 8pKa while breathing at sea level
100
Describe the types of Respiratory failure?
Type I respiratory failure -
Arterial pO2 is low
Arterial pCO2 normal or low
Type II respiratory failure -
Arterial pO2 is low
Arterial pCO2 is high
101
List 5 factors that can lead to hypoxia
Low pO2 in inspired air - e.g. live in high altitude
Hypoventilation - neuromuscular problems
mechanical problems
hard to ventilate lungs
Diffusion impairment
Ventilation perfusion mismatch
Abnormal right to left cardiac shunt
102
Define Asthma
Chronic disorder characterised by airway wall inflammation and remodelling. It is a reversible airflow obstruction.
103
Describe the nature of airway obstruction in asthma
Airways have thickened smooth muscle and basement membranes.
Triggers cause the airway smooth muscle to contract, reducing airway radius, increasing resistance and reducing airflow.
104
What is the epidemiology of asthma?
```
Genetic risk
Airbourne allergens:
o House Dust Mite
o Pollens
o Air pollution
o Tobacco smoke (Pre-/post natal exposure, active)
```
105
What are the symptoms of Asthma?
```
Wheeze - expiratory polyphonic sound
Cough - during nights, exercise induced
Breathlessness - with exercise
Chest tightness
Variable airflow obstruction
```
106
What are the signs of Asthma?
Chest - Scars, deformity, barrel chest
General health - lethargy, eczema, hay-fever
Percussion - hyper-resonant
Auscultation - polyphonic wheeze
107
What tests would you do for a patient with asthma?
Spirometry - Low PEFR and Low FEV1/FVC ratio.
FEV1 increases by 12% with salbutamol
Chest X-ray - Rule out other causes
Allergy tests - Skin prick to aero-allergens
Blood IgE to specific aero-allergens
108
Describe the pathological changes in Asthma
Inflammation
Increase in mast cells, which release prostaglandins, histamine etc
Eosinophils - large number in bronchial walls
Dendritc Cells and Lymphocytes - Dendritic cells in charge of initial uptake and presentation of allergens to lymphocytes. T-helper lymphocytes (CD4) release cytokines that lead to activation of mast cells. Th2 phenotype favour antibody production by B lymphocytes to IgE.
Remodelling
Epithelium - stressed and damaged with loss of ciliated columnar cells
Basement membrane - collagen deposition cause thickening
Smooth muscle - hyperplasia
109
What are the precipitating factors for asthma?
Lack of treatment adherence
Respiratory Virus Infections associated with the common cold
Exposure to allergen or triggering drug (e.g. NSAID)
110
What is the treatment for Asthma?
Education - how to recognise, use medications properly
Primary intervention - stop smoking, weight loss, fresh air, reduce exposure to allergens
Pharmacological intervention - corticosteroids
β2-adrenoagonists - muscurinic antagonist
111
Define COPD (chronic obstructive pulmonary disease)
Chronic, slowly progressive disorder characterised by airflow obstruction, which does not changed markedly over several months.
112
What changes can you see in a Vitalograph in COPD?
Reduced FEV1
| Reduced FEV1: FVC
113
Describe epidemiology of COPD
Caused by the abnormal inflammatory response of the lung to noxious particles or gases, such as cigarette smoking and atmospheric pollutants.
Inherited deficiency of α1-antitrypsin causes emphysema
114
What are the symptoms of COPD?
o Productive Cough - White or clear sputum
o Wheeze
o Breathlessness
o Usually following many years of a smoker’s cough
115
What are the signs of COPD?
o May be no signs, or just quiet wheezes
o Hyperventilation with prolonged expiration - Expiratory airflow limitation
o Accessory muscles of respiration are used
o Hyperinflation of the lungs
116
Describe COPD assessment
o History - including MRC Dyspnoea scale
o Chest X-Ray - exclude other problems
o FEV1 reduced, Reduced FEV1/FVC ratio
o Other lung function tests - Lung volumes, loop
o High resolution CT scan - Detect emphysema
117
Outline oxygen therapy
Oxygen given to increase oxygen saturation and alleviate symptoms. It is a treatment for hypoxaemia, NOT breathlessness.
o Long term
o Portable
o Intermittent
118
Outline COPD management
Smoking cessation
Drug therapy - bronchodilators - β2-adrenoagonists
corticosteroid - immunosuppresant
Antibiotics - shortens exacerbation - given when sputum yellow/green
Oxygen therapy - increase blood O2
Pulmonary rehabilitation
α1-antitrypsin Replacement
Treat co-morbidities e.g. cardiac, depression
119
Name two common flora of the respiratory tract
```
Common
o Viridans streptococci
o Neisseria spp
o Anaerobes
o Candida spp
Less Common
o Streptococcus pneumonia
o Streptococcus pyogenes
o Haemophillus influenza
Other
o Pseudomonas
o E. coli
```
120
What are the natural defences of the respiratory system?
o Cough and sneezing reflex
o Muco-ciliary clearance mechanisms - Ciliated columnar epithelium and Nasal hars
o Respiratory mucosal immune system -Lymphoid follicles of the pharynx and tonsils, Alveolar macrophages and Secretary IgA and IgG
121
List the main infection diseases of the upper respiratory tract
```
o Rhinitis (common cold)
o Pharyngitis
o Epiglottitis
o Laryngitis
o Tracheitis
o Sinusitis
o Otitis media
```
122
State the organism commonly causes upper respiratory tract infections
```
Viruses:
o Rhinovirus
o Coronavirus
o Influenza/parainfluenza
o Respiratory Syncytial Virus (RSV)
```
Bacterial Super-Infection which are common with sinusitis and otitis mediia, leading to
• Mastoiditis
• Meningitis
• Brain abscess
123
Define pneumonia
Inflammation of the gas-exchanging region of the lung, usually due to infection (bacterial or viral)
or
Infection of the lung parenchyma
124
What is the difference between pneumonia and pneumonitis
Pneumonitis is not caused by bacteria or viruses but due physical or chemical damage
125
What are the differences between Lobar, broncho, aspiration, interstitial and chronic pneumonia?
Lobar Pneumonia - localised to a particular lobe/s of the lung due to Streptococcus pneumoniae
Broncho Pneumonia - diffuse and patchy. Infection starts in the airways and spreads to adjacent alveoli and lung tissue. Due to Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus, anaerobes, coliforms
Aspiration Pneumonia - food, drink, saliva or vomit aspiration. Organisms include oral flora and anaerobes.
Interstitial Pneumonia - Intersticium of the lung
Chronic Pneumonia - Inflammation that persists for an extended period of time
126
Describe the aetiology of community acquired pneumonia
```
Common Bacteria
o Streptococcus pneumoniae – 30%
o Haemophilus influenza – 13%
o Klebsiella pneumoniae
Atypical Bacteria
o Chlamydia pneumophilia - 10%
o Mycoplasma pneumoniae
o Legionella pneumophila
```
127
Describe the aetiology of hospital acquired pneumonia
o Gram –‘ve enteric bacteria - 10%
o Pseudomonas
o Staphylococcus aureus
o MRSA
128
List the aetiological clues for the common respiratory tract pathogens
S. pneumoniae - Elderly, co-morbidities, acute onset, high fever, Pleuritic chest pain
H. influenza - COPD
Legionella - Recent travel, younger patient, smokers, illness, multi-system involvement
Mycoplasma - Young, prior antibiotics, extra-pulmonary involvement (haemolysis, skin and joint)
S. aureus - Post-viral, Intra-Venous Drug User
Chlamydia - Contact with birds
Coxiella - Animal contact (sheep)
Klebsiella - Thrombocytopenia, leucopenia
S. milleri - Dental infections, abdominal source, aspiration
129
What are the symptoms of pneumonia?
```
o Fever, chills, sweats, rigors
o Cough
o Sputum - Clear / purulent / ‘rust coloured / haemoptysis
o Dyspnoea
o Pleuritic chest pain
o Malaise
o Anorexia and vomiting
o Headache
o Myalgia
o Diarrhoea
```
130
What are chest signs of pneumonia?
* Bronchial breath sounds
* Crackles
* Wheeze
* Dullness to percussion
* Reduced vocal resonance
131
When does hospital acquired pneumonia first present?
48 hours after hospital admission
132
What is the CURB 65 score?
Assess pneumonia severity. 2 or more of the following require hospital treatment
C – New mental Confusion
U – Urea > 7mmol/L
R – Respiratory rate > 30 per minute
B – Blood pressure diastolic
133
What do you find on laboratory investigations for pneumonia?
```
o Macroscopic - Sputum, purulent, blood stained
o Microscopy - Gram staining, Acid fast
o Culture - Bacteria and viruses
o PCR - Respiratory viruses
o Antigen detection - Legionella
o Antibody detection - Serology
```
134
What are the common pathogens causing pneumonia in immunosuppressed host?
o Virulent infection with common organism
Opportunistic pathogen:
• Viruses – Cytomegalovirus (CMV)
• Bacteria – Mycobacterium avium intracellulare
• Fungi – Aspergillus, candida, pneumocystis jiroveci
• Protozoa – Cryptosporidia, toxoplasma
135
What is the management for pneumonia?
o Oral fluid/IV fluids - Avoid dehydration
o Anti-pyretic drugs - Reduce fever and malaise
o Stronger analgesics - Deal with the pain (Pleuritic)
o Oxygen - If there is cyanosis
o Antibiotics
Community Acquired Pneumonia
The target organism is normally Pneumococcus, which is usually sensitive to Penicillin or related antibiotics.
Hospital Acquired pneumonia
The target organism is more likely to be Gram –‘ve, making it necessary to use antibiotics such as IV Co-Amoxiclav.
136
What are the outcomes of pneumonia?
o Resolution - Fibrous scarring
| o Complications - Lung abscess, bronchiectasis, empyema
137
What are the preventions of pneumonia?
o Immunization
• Flu vaccine – Given annually to high risk patients
• Pneumococcal vaccine – Two vaccines
o Chemoprophylaxis - Oral penicillin / erythromycin to patients with higher risk of lower respiratory tract infections e.g. immunodeficiency
138
Describe the microbiology of mycobacterium tuberculosis
Possess a lipid-rich cell wall that retains some dyes, even resisting decolourisation with acid (acid-fast).
139
What are the steps in the oxygen transport pathway from air to tissues
Air -> airways -> alveolar gas -> alveolar membrane -> arterial blood -> regional arteries -> capillary blood -> tissues
140
What are the managements for respiratory failure?
o Oxygen therapy
o Removal of secretions
o Assisted ventilation
o Treat acute exacerbations
141
What are the chronic effects of respiratory failure?
CO2 retention - CSF is acidic, which is corrected by chroid plexus. Initially corrected by kidney. Reduction of respiratory drive. Hypoxia persists.
Right Heart Failure (Cor pulmonare) - Effect of hypoxia on pulmonary arteries → Pulmonary hypertension
Chronic respiratory failure is severely disabling
142
What are the features of a lobar collapse?
Displacement of the horizontal fissure
If there is volume loss of the right upper lobe (e.g. collapse), the horizontal fissure is displaced upwards.
If there is volume loss of the right lower lobe (e.g. collapse), the horizontal fissure is displaced downwards.
143
What are the features of consolidation?
Alveoli and small airways fill with dense material, due to infection, fluid , blood or cells (cancer).
Area becomes dense and white. If the larger airways are spared, they are of relatively low density (blacker), known as air bronchogram and it is a characteristic sign of consolidation.
144
What are the features of space occupying lesions?
Mass in lungs e.g. squamous cell lung carcinoma
145
What are the features of pleural effusion?
Collection of fluid in the pleural space. Fluid gathers in the lowest part of the chest, according to the patient’s position.
If patient is upright in X-ray, a pleural effusion will obscure the Costophrenic angle/ Hemidiaphragm.
If patient is supine, pleural effusion layers along posterior aspect of the chest cavity, and is difficult to see on a chest X-Ray.
Pleural effusions appear on X-rays as uniformly white, with a concave area at the top, called the Meniscus sign.
146
What are the features of pneumothorax?
Air trapped in the pleural space. This may occur spontaneously, or as a result of underlying lung disease. Most common cause is trauma, with laceration of the visceral pleura by a fractured rib.
147
What are the features of tension pneumothorax?
If tracheal or mediastinal shift away from the pneumothorax, the pneumothorax is said to be under tension - medical emergency.
Trachea is pushed away by air in the pleural cavity.
148
What are the causes of trachael displacement?
Increases pressure or volume in one hemithorax will push the trachea and mediastinum away from that side.
(E.g. Tension pneumothorax, pleural effusion, tumour)
Any disease that causes volume loss in one hemithorax will pull the trachea over towards that side.
(E.g. collapsed lung, fibrosis)
149
What are the features of asbestos plaques?
Calcified asbestos related pleural plaques have a characteristic appearance.
Irregular, well defined and classically said to look like holly leaves.
150
What are the features of lung hyper-expansion?
Blunting of both costophrenic angles, and flattened hemidiaphragms.
151
What are the features of pneumoperitoneum?
Lungs normal, but air seen under the diaphragm.
| Sign of bowel perforation.
152
How do you work out the cardiothoracic ratio?
Widest part of heart and ribcage measured laterally. If heart is over 50% of the width of the thorax, it is enlarged.
153
What is interstitial space?
Potential space between alveolar cells and the capillary basement membrane, only apparent in disease states, when it may contain fibrous tissue, cells or fluid.
154
What is the pathophysiology of interstitial lung diseases?
o Development of fibrous tissue in Intersticium, making lungs less compliant, producing a restrictive ventilatory defect.
o Airway resistance is NOT increased. In fact, the FEV1/FVC ratio can be > 70%, due to the increased radial traction on the airway, which keeps the airway open.
o Lengthening of the diffusion path between alveolar air and blood impairs gas exchange, with oxygen uptake being affected selectively, as CO2 diffuses much more readily.
155
What are the symptoms of interstitial lung diseases?
Shortness of breath
Reduced exercise tolerance
Dry cough
156
What are the signs of interstitial lung diseases?
```
Tachypnoea
Tachycardia
Reduced chest movement (bilaterally)
Coarse crackles.
Cyanosis
Right heart failure
Clubbing in cryptogenic fibrosing alveolitis.
```
157
What are the causes of interstitial lung diseases?
```
Occupational
Treatment related
Connective tissue disease
Immunological
Idiopathic
```
158
List a number of occupational lung diseases and the environmental factors associated with each
Asthma - lab worker - rat urine
Diffuse fibrosis - railway construction - asbestos
Nodular fibrosis - Coal mine - coal dust
Alveolitis - Farmer - Fungal spores from hay
159
Describe the typical X-Ray picture of patients presenting with interstitial lung disease
Fibrosing Alveolitis - Small lungs
Micro-nodular shadowing (Lower lobes)
Ragged heart borders
Extrinsic Allergic Alveolitis (Acute) - Micro-nodular infiltrate, denser towards the hila.
Extrinsic Allergic Alveolitis (Chronic) - Almost normal, progressing to fibrosis in late disease
Sarcoidosis - Miliary and Nodular shadowing
Diffuse fibrosis
Asbestosis - Plaques
Fibrosis
Mesothelioma
160
What is the pleura?
Serous membrane consisting of a single layer of mesothelial cells with a thin layer of underlying connective tissue.
161
What is the pleural cavity?
Potential space between the two layers of pleura that are continuous at the hilum.
162
Describe the factors influencing the formation and reabsorption of pleural fluid
15ml turnover per day (Can increase to 300ml)
Produced by Capillary Filtration at the Parietal Pleura (Starling Forces)
• increased Lung interstitial fluid increase
• increased Hydrostatic Pressure (E.g. heart failure)
• increased Permeability (E.g. inflammation, spesis or malignancy)
• decreased Oncotic Pressure (E.g. liver failure)
Absorbed via lymphatic drainage
• decreased Lymphatic blockage
• increased Systemic venous pressure
163
Define pleural effusion
Any collection of extra fluid in the pleural space
Blood – Haemothorax
Chyle (Lymph with fats in it) – Chylothorax
Pus – Empyema
Serous Fluid – Simple Effusion
164
What is the difference between transudate and exudate?
Transudates have low protein content – 30g/Litre
165
What are the characteristics of a transudate?
Increased Hydrostatic Pressure
• Cardiac Failure
Decreased capillary Oncotic Pressure
• Hypoalbuminaemia
• Nephrotic Syndrome
Increased capillary Permeability
• Sepsis
166
What are the characteristics of an exudate?
Neoplasms
• Cancer involving pleural surface
• Secondary’s from breast, lung, ovarian, GI, lymphoma
• Primary tumour of pleura
Infection
• Pneumonia, TB
Immune Disease
• Connective tissue diseases (RA, SLE)
Abdominal Disease
• Pancreatitis (Diaphragmatic inflammation)
• Ascites (Transverse the diaphragm)
• Subphrenic abscess
167
What is pleuritis/ pleurisy?
Inflammation of the pleura
168
What are the characteristics of pleuritis?
o Sharp Pain on inspiration
o Pain worse with coughing, sneezing, laughing etc.
o Patients take small breaths, and hold affected side of chest
o Involvement of diaphragmatic pleura causes pain in the shoulder on the same side (Referred pain)
o Characteristic physical sign is Pleural Rub, a creaking noise heard through a stethoscope with respiratory movements
169
What are the causes of pleuritis?
Infection is the most common cause
• TB
• Pneumonia
Autoimmune
• SLE
• RA
Lung Cancer
Pneumothorax
Pulmonary Embolism
170
What is pleural fibrosis?
Unabsorbed pleural effusion may lead to fibrosis of the pleura.
Small degree of thickening has no effects, but wide spread fibrosis restricts expansion, with a measurable reduction in lung volumes and compliance.
171
What is the commonest pleural tumour?
Malignant mesothelioma
172
How do chest wall abnormalities affect breathing?
Deformation of the ribs, sternum and thoracic spine:
o Sternal abnormalities rarely produce functional impairment
o Scoliosis and kyphosis may produce significant function impairment of the thoracic cage
Acquired abnormalities:
o Trauma producing broken ribs, possible pneumothorax
o Some old patients may have had surgery for TB, designed to collapse their lung
173
How do muscles and neurological abnormalities affect breathing?
The muscles involved in breathing may be affected by generalised muscular diseases, such as muscular dystrophy or by neurological disease such as motor neurone disease or polio.
Muscle weakness produces respiratory failure with lower resistance to respiratory tract infections because of poor clearance of secretions.
174
Fibrosis alveolitis
Progressive inflammatory condition, unknown cause
o Histologically there are increase activated Alveolar Macrophages
• Attract Neutrophils and Eosinophils
• Local lung damage due to ROS and proteases
• Tissue destruction and fibrosis
o Patients report progressive shortness of breath on exercise, often with non-productive cough.
o Finger clubbing
o Chest X-Ray shows small lungs with micro-nodular shadowing predominating in the lower loves, with ragged heart borders
o Can be restrained by treatment with high dose oral steroids in the early stages, less effective once fibrosis has developed, effectiveness monitored by repeated lung function test
175
Sarcoidosis
Disease of unknown cause, characterise by Non-Caseating Granulomas (Non-necrotising) in multiple organs and body sites
o Most commonly in the lungs
o Fluid is collected by lavage of the airways, and alveoli contain lots of cells, including macrophages and lymphocytes
o Commoner in Afro-Caribbean and Asians than in Caucasians
• Genetic predisposition
o Highest incidence in 30’s and 40’s with more female cases
o Often asymptomatic, but may have Cough, breathlessness
o Grading system 0 – 4
o X-ray shows miliary and nodular shadowing and diffuse fibrosis
o Stages 1 – 3 steroids are usually effective in suppressing the disease
o Lung function tests show small lungs, reduced compliance and impaired gas transfer. May be evidence of air flow obstruction.
176
Extrinsic Allergic alveolitis
Inhalation of organic material triggers an allergic reaction in alveoli and bronchioles.
Acute
Sudden onset, rapidly progressing
o Farmer’s Lung
• Antigen = Thermophillic actinomycetes found in mouldy hay
• Influenza like illness 4-9 hours later with a dry cough and breathlessness on exertion
• Fine mid and late inspiratory crackles
• May be a wheeze
Chronic
Bird Fancier’s Lung
• Long Term Antigen Exposure = Pigeons / budgerigars
• Insidious malaise (feeling particularly unwell)
• Dry cough and breathlessness over months and years
• Inspiratory crackles
o No Finger clubbing
o Acute disease chest x-ray shows diffuse micro-nodular infiltrate denser towards the hila.
o Chronic disease chest x-ray may be almost normal, progressing to fibrosis in late disease.
o Lung function tests will show reduced compliance and reduced gas transfer.
177
Asbestosis
Inhalation of asbestos fibres, disease often develops long after the exposure.
o Asbestosis inhalation is associated with three forms of disease (along with a marked increase in lung cancer):
• Benign pleural plaques
• Asbestosis (pulmonary fibrosis)
• Mesothelioma
o Asbestos fibres that penetrate to the alveoli produce alveolitis
• Influx of macrophages produces characteristic asbestosis bodies
• Alveolitis progresses to fibrosis
o History of asbestos exposure
o Patient breathless on exertion and a dry cough.
o Inspiratory crackles at the lung bases, which rise as the disease advances.
o No treatment
o Lung function tests show small lungs, reduced compliance and impaired gas transfer
178
How is tuberculosis spread?
Person to person
| aerosol route
179
What do most infections of tuberculosis resolve in?
Local scarring
180
What are post-primary infections?
Development of tuberculosis beyond the first few weeks
May progress throughout the body (Miliary Spread). This may resolve spontaneously, or develop into localised infection (E.g. meningitis).
181
What is the pathology of tuberculosis?
The intense immune response causes local tissue destruction (Cavitation in the lung) and cytokine-mediated systemic effects (Fever and Weight loss).
TB may affect every organ of the body, mimicking both inflammatory and malignant diseases.
Untreated the infection follows chronic, deteriorating course.
Kidney infection may lead to signs of local infection, fever and weight loss, complicated by ureteric fibrosis and hydronephropathy.
The lumbosacral spine is a common site of bone infection – progression may cause vertebral collapse and nerve compression.
Inflammation of large joints may lead to destructive arthritis.
182
How does tuberculous meningitis present?
Fever and slowly deteriorating level of consciousness.
183
How does pulmonary tuberculosis present?
```
A chronic cough
haemoptysis
fever
weight loss
recurrent bacterial pneumonia
```
184
What is the host response to TB infection?
Mycobacterium Tuberculosis ingested by macrophages, but escapes from phagolysosome to multiply in cytoplasm.
It provokes an immune response, stimulating IL-12 release.
IL-12 drives IFN-γ and TNF-α release from NK and CD4 cells. These cytokines activate and recruit more macrophages to the site of infection, resulting in the formation of Granulomas.
185
What are primary changes in TB?
o Few Symptoms
| o Lymph nodes may become enlarged in young people
186
What are post-primary changes in TB?
o Cough (Not always productive)
o Fevers towards the end of the day or at night
o Weight loss and general debility
Chest X-Ray reveals pulmonary shadowing, which may be patchy solid lesions, cavitated solid lesions, streaky fibrosis or flecks of calcification.
187
What are the signs of respiratory TB?
```
Non-specific
Pallor
Fever
Weight Loss
Clubbing
Palpable lymph nodes
```
188
What are the symptoms of respiratory TB?
Primary usually asymptomatic
```
Tiredness and malaise
Weight loss and anorexia
Fever
Cough
Breathlessness
Haemoptysis occasionally
```
189
What are the Xray changes of respiratory TB?
```
Shadowing
Cavities
Consolidation
Calcification
Cardiomegaly
Miliary seeds
```
190
What is the clinical presentation of pleural tuberculosis?
More common in males, there are two mechanisms of pleural involvement. There is almost always some pulmonary disease present:
o Hypersensitivity response in primary infection
o Tuberculous empyema with ruptured cavity.
• Tuberculosis empyema has a tendency to burrow through the chest wall.
191
What is the clinical presentation of Lymph node tuberculosis?
More common in children, women and Asians. It is often painless, and occurs most commonly in the neck.
192
What is the clinical presentation of osteo-articular TB?
TB burrows into bone.
o Tuberculous Spondylitis
• Most common form of oesteoarticular TB
• Starts in sub-chondral bone and spread to vertebral bodies and joint space, before following the longitudinal ligaments, anterior and posterior to the spine.
• Mainly occurs in the lower thoracic and lumbar spine, but can be very high (Cervical tuberculosis)
• Parapledia and quadriplegia occurs in 25% of cases
o Poncet’s Disease
• Aseptic polyarthritis
• Knees, ankles and elbows
193
What is the clinical presentation of Miliary Tuberculosis?
o Bacilli spreading through the blood stream
o Either during primary infection or as reactivation
o Lungs are always involved
• Even spread throughout both lungs, as it is in the blood
• Many visible through the lungs on an X-Ray
o Headaches suggest meningeal involvement
o Few respiratory symptoms
o Ascites may be present
o Retinal involvement in children
194
Describe the diagnosis of TB
TB is diagnosed by:
o Clinical Features
• Cough, night fever, weight loss
o Radiological Features
• Shadowing, cavities, consolidation, cardiomegaly, miliary seeds
o Microbiology
• Identification of bacillus
• Direct smear and subsequent culture of the appropriate body fluid
• Important to isolate organism and determine its susceptibility to drugs
195
Describe the management of TB
```
Initial Phase (2 months):
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
```
Continuation Phase (4 months):
Rifampicin
Isoniazid
196
What reactions can follow from TB management drugs?
Rifampicin - Hepatitis, rash, flu-like symptoms, shock, ARF, thrombocytopenic purpura
Isoniazid - Rash, peripheral neuropathy, hepatitis
Pyrazinamide - Rash, hepatitis, arthralgia
Ethambutol - Optic neuritis
197
Describe the mechanisms of drug resistance in TB
There is a rising trend of Multidrug-Resistant TB (MDRTB). About one in a million bacilli are spontaneously resistant.
A case of MDRTB is suggested by a history of previous incomplete treatment, residence in a country with high incidence of MDRTB or failure to respond clinically to an adequate regimen.
A regimen of several drugs at once is used in an attempt to combat resistance.
198
Describe the role of BCG vaccination
Vaccination against tuberculosis that is prepared from a strain of the Attenuated Live Bovine Tuberculosis Bacillus.
The bacteria retain a strong enough antigenicity to act as a vaccine for human tuberculosis.
Issues
The vaccine has a variable efficacy, depending on genetic variation of populations and BCG strains.
Efficacy only lasts 15 years at most.
199
High risk groups of TB in UK
```
o HIV
o Silicosis
o Malnutrition
o Overcrowding - Prison’s, homeless shelters
o IV Drug abusers
o Chronic Lung Disease (Smokers)
o Ethnicity - Asians more likely
o Diabetes
```
200
Describe the relationship between TB and HIV infections
Higher risk in HIV infected patients - 20 - 37 times greater risk
TB is a leading cause of morbidity and mortality among HIV patients.
201
The public health issues surrounding a case of TB
If TB is suspected, contact is immediately made with TB radiology. The patient goes straight into a TB clinic, with no waiting times, and is given a questionnaire and sputum samples taken.
Treatment begins within 7 days.
202
Describe the incidence of lung cancer in different groups
Males
• Commonest male cancer
• Mortality rate is around 100 per 100,000
• Incidence slowly falling due to reduction in smoking
Females
• Exceeds breast cancer as a cause of death in women
• Mortality rate is around 40 per 100,000
• Incidence is steadily rising
Socio-economic groups
• Wide variation
• Rate three times higher in lowest compared with highest
203
Aetiological factors involved in lung cancers
```
Smoking
Asbestos exposure
Radon exposure
Genetic factors
Dietary factors
```
204
Symptoms reported by patients with lung cancer - primary tumour
```
Cough
Dyspnoea
Wheezing
Haemoptysis
Chest pain
Post-obstructive pneumonia
Weight loss
Lethargy / Malaise
```
205
Symptoms reported by patients with lung cancer - regional metastasis
Superior vena cava obstruction
Hoarseness (Left recurrent Laryngeal nerve palsy)
Dyspnoea (Phrenic nerve palsy)
Dysphagia
206
Symptoms reported by patients with lung cancer - distant metastasis
```
Bone pain / Fractures
CNS symptoms (Headache, double vision, confusion etc.)
```
207
Clinical signs for lung cancers
Paraneoplastic syndrome - presence of a symptom or disease due to the presence of cancer in the body, but not due to the local presence of cancer cells
```
Endocrine
• Hypercalcaemia
• Cushing’s syndrome
Neurological
• Encephalopathy
• Peripheral neuropathy
Skeletal
• Finger clubbing
Haematological
• Anaemia
• Thrombocytopenia
• Disseminated Intravascular Coagulation (DIC)
Other
• Nephrotic syndrome
• Anorexia or cachexia
```
208
Describe TNM staging
T – Size and position of tumour
o T1 – Cancer contained within lung ( 7cm diameter)
• Invading chest wall, mediastinal pleura, diaphragm, pericardium
• Complete lung collapse
• > 1 cancer nodule in the same lobe of lung
o T4
• Cancer invading mediastinum, heart, major blood vessel, trachea, carina, oesophagus, spine, recurrent laryngeal nerve
• Cancer nodules in more than one lobe of the same lung
N – Lymph node involvement
o N0 – No cancer in lymph nodes
o N1 – Cancer in lymph nodes nearest the affected lung
o N2 – Cancer in lymph nodes in mediastinum, on the same side
o N3 – Cancer in lymph nodes on the opposite side of the mediastinum / supraclavicular lymph nodes
M – Metastases
o M0 – No evidence of distal cancer spread
o M1 – Lung cancer cells in distant parts of the body, such as pleura, opposite lung, liver or bones etc
209
Describe number staging
Stage 1 – Small cancer, localised to one area of the lung
Stage 2 and 3 – Larger Cancer, may have grown into surrounding tissues (lymph nodes)
Stage 4 – Cancer has metastasised
210
What are the imagining techniques used to diagnose lung cancers?
```
First clinical suspicion
• Plain Chest X-Ray
Diagnosis and staging
• CT scan
• PET scan
• Isotope bone scan
```
There are two staging systems for Lung Cancer: Number and TMN
211
Common methods used to obtain material for histological diagnosis
bronchoscopy
needle biopsy of the lung
Surgical biopsy
212
What are the common classifications of lung tumours?
Non-Small Cell Lung Cancer
| Small Cell Lung Cancer
213
Describe the behaviour of different histological types and their relationship to prognosis and treatment
Non-Small Cell
o More than 2/3rds have inoperable disease at presentation
Small Cell
o ¾ have metastatic disease at presentation
```
Prognosis Depends On:
o Cell type
• Small Cell worse than Non-Small Cell
o Stage of disease
o Performance status
o Biochemical markers
o Co-morbidities
• E.g. Cardiac or chronic respiratory disease
```
214
Treatments for lung cancers
o Surgery
| • Mostly Non-Small Cell
215
What is the management of Non-Small Cell Lung Cancer?
o Palliative Radiotherapy for local symptoms
o Chemotherapy – 50 – 60% response rates.
o Combination Therapy – Important in locally advanced disease
o Targeted Agents – EGFR and VEGF
216
What is the management of Small Cell Lung Cancer?
o Rarely operable
o Combination Therapy – Responds well, adding ~1 year
o Palliative Chemotherapy for symptoms
o Death from cerebral metastases common
