Respiratory Flashcards
1
Q
Name a disease that is responsible for reversible airway obstruction.
A
Asthma.
2
Q
What intrinsic factors can affect pneumonia? (triggers)
A
Cold temperature, infection, stress, exercise, various pollutants.
3
Q
What can cause acute airway obstruction?
A
- Swallowing or inhaling object
- Asthma
- Allergic reaction
- Some infections
4
Q
What can chronic obstructive pulmonary disease be sub-divided into?
A
- Chronic bronchitis.
2. Emphysema.
5
Q
Is chronic bronchitis reversible?
A
Chronic bronchitis is irreversible.
6
Q
What is the clinical diagnosis of chronic bronchitis?
A
A persistent cough and sputum for >3 months in 2 consecutive years.
7
Q
What is the effect of chronic bronchitis on lung function?
A
- Reduced FEV1/FVC ratio.
- Reduced PEFR.
- Increased TLCO.
8
Q
What can cause chronic bronchitis?
A
It is often tobacco smoking induced and can be aggravated by pollution and infections.
9
Q
What can happen over time in a patient with chronic bronchitis?
A
The patient might become hypercapnic, hypoxic and have progressive right sided cardiac failure (cor pulmonale) due to pulmonary vasoconstriction. There is fibrosis and tissue destruction.
10
Q
What is the pathology of emphysema?
A
Irritants and chemicals trigger inflammatory mediators to release matrix destructive enzymes -> elastin destruction and enlargement of alveolar air spaces -> air trapping.
11
Q
What can cause emphysema?
A
It is often tobacco smoking induced. It can also be associated with alpha-1-antitrypsin deficiency and coal dust exposure.
12
Q
What is bronchiectasis?
A
Permanent dilation of bronchi due to obstruction and inflammation this leads to a build-up of excess mucus and predisposes someone to chest infections.
13
Q
What is the effect of interstitial lung disease on lung volumes?
A
Reduced TCO, VC and FEV1. FEV1/FVC ratio and PEFR is normal.
14
Q
Give an example of a chronic interstitial lung disease.
A
Interstitial pneumonia, sarcoidosis, rheumatoid.
15
Q
What is the pathology of interstitial lung disease?
A
inflam => Increased fibrous tissue within the lung parenchyma => increased stiffness and decreased expansion (permanent damage)
16
Q
What is the treatment for interstitial lung disease?
A
generally poor prognosis and damage is irreversible
- remove or treat underlying cause (drug induced)
- oxygen if hypoxic at rest
- stop smoking
- pneumococcal and flu vaccine
- pirfenidone (antifibrotic)
- Lung transplant
17
Q
What is idiopathic pulmonary fibrosis?
A
Progressive fibrosis in the alveoli that limits the patients ability to respire.
18
Q
What is the name of the lung disorder group that reflects inhaled dust/toxins?
A
Pneumoconiosis.
19
Q
Give an example of a pneumoconiosis?
A
Coal worker’s pneumoconiosis, silicosis, asbestos exposure, extrinsic allergic alveolitis.
20
Q
Pneumoconiosis: What is silicosis?
A
Silicosis often reflects silica exposure and may occur in grinding related occupations and mining practices.
21
Q
What does someone with silicosis have an increased risk of developing?
A
TB.
There is a borderline increased risk of cancer.
22
Q
Pneumoconiosis: What might be the consequences of asbestos exposure?
A
- Lung cancer.
- Persistent pleural effusion.
- Diffuse pleural fibrosis.
- Diffuse interstitial lung fibrosis.
23
Q
If the trachea, bronchi and bronchioles are involved in a disease process, is this likely to be an obstructive or a restrictive disease?
A
Obstructive.
24
Q
If the lung parenchyma are involved in a disease process, is this likely to be an obstructive or a restrictive disease?
A
Restrictive.
25
If the chest wall is involved in a disease process, is this likely to be an obstructive or a restrictive disease?
Restrictive.
26
What happens to the FEV1, FVC and FEV1/FVC ratio in an obstructive lung disease?
- FEV1 is < 80% predicted.
- FVC is normal.
- FEV1/FVC ratio < 0.7.
27
What happens to the FVC and FEV1/FVC ratio in a restrictive lung disease?
- FVC reduced.
| - FEV1/FVC ratio normal.
28
Give an example of a reversible obstructive lung disease.
Asthma.
29
Give an example of an irreversible obstructive lung disease.
COPD.
30
What is the affect of COPD on residual volume and total lung capacity?
RV and TLC are increased.
31
Give an example of a restrictive lung disease.
Pulmonary fibrosis.
32
How would you describe the PEF for asthma.
Variable.
33
What factors can commonly exacerbate asthma?
1. Cold weather.
2. Exertion.
3. Fumes.
4. Often worse at night.
34
Define inspiratory reserve volume (IRV).
The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.
35
Define expiratory reserve volume (ERV).
The additional volume of air that can be forcibly exhaled after a tidal volume expiration.
36
Define forced vital capacity (FVC).
The maximum volume of air that can be forcibly exhaled after maximal inhalation.
37
Define total lung capacity.
The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.
38
Define residual volume (RV).
The volume of air remaining in the lungs after a maximal exhalation.
39
Define functional residual capacity (FRC).
The volume of air remaining in the lungs after a tidal volume exhalation.
40
Define tidal volume (TV).
The volume of air moved in and out of the lungs during a normal breath.
41
Define FEV1.
The volume of air that can be forcibly exhaled in 1 second.
42
What is a normal tidal volume?
500ml.
43
What equation can be used to work out FRC?
FRC = ERV + RV.
44
Define peak expiratory flow (PEF).
The greatest rate of airflow that can be obtained during forced expiration. Age, sex and height can all affect PEF.
45
What is the transfer coefficient?
The ability of O2 to diffuse across the alveolar membrane.
46
How can you find the transfer coefficient?
Low dose CO is inspired, the patient is asked to hold their breath for 10s at TLC, the amount of gas transferred is measured.
47
What is consolidation on a CXR?
Regions of the lung filled with liquid e.g. pulmonary oedema. The areas appear white - dense.
48
What are the possible complications of bronchoscopy?
Pneumonia and pneumothorax.
49
Give 2 early symptoms and 2 late symptoms of lung cancer.
1. Early: change in cough, wheeze, hemoptysis.
| 2. Later: weight loss, lethargy.
50
If a chronically breathless patient is wheezing, what is the likely cause?
Obstruction.
51
If a chronically breathless patient is NOT wheezing, what is the likely cause?
Restriction? Are there crackles on auscultation?
52
Give examples of non-respiratory causes of breathlessness.
Heart disease, anaemia.
53
Give 3 signs of infection.
1. If the patient has a temperature.
2. Increased neutrophils.
3. Increased CRP.
54
What is ANCA?
Anti-neutrophil cytoplasmic antibody.
| - Auto-immune disorder.
55
What is the mechanism of ANCA?
ANCA activates neutrophils and monocytes. The neutrophils adhere to endothelial cells, there is degranulation and free radicals are released. The free radicals damage the endothelium. There is further neutrophil recruitment = +ve feedback. This can result in inflammation of the vessel wall - vasculitis.
56
What disease can be caused by ANCA?
ANCA associated vasculitis.
57
What are common affects of rheumatoid arthritis on the lung?
1. Pleural effusion.
2. Fibrosing alveolitis.
3. Airway disorders e.g. bronchiolitis and bronchiectasis.
58
What is Guillain Barre syndrome?
Demyelinating polyneuropathy.
| It can present 6 weeks after flu/CMV.
59
Immune mediated damage: what is the mechanism behind tissue damage in chronic infection?
The infection won't clear.
There is chronic neutrophil recruitment and persistent cellular activation. Pro-inflammatory mediators are released = tissue damage.
60
Give an example of a disease where there is tissue damage due to chronic infection.
COPD.
61
Give examples of diseases where there is an excessive immune response.
1. ARDS.
| 2. Asthma.
62
Give an example of a disease where there is a failure to control the immune response.
Alpha 1 antitrypsin disease: emphysema.
63
Name 2 upper respiratory tract infections.
1. Common cold: caused by rhinovirus.
| 2. Sore throat: caused by adenoviruses, EBV.
64
What viruses can cause pneumonia?
Adenoviruses, influenza A and B, measles, VZV.
65
Which influenza pathogen is commonly behind severe and extensive outbreaks? Why?
Influenza A; it replicates a lot and mutations are common.
66
How can influenza virus be transmitted?
- Aerosol: coughing and sneezing, inhale particles.
| - Droplet: hand to hand.
67
What is the reproduction number?
The average number of secondary cases generated from a primary case.
68
Give an example of a disease with a high reproduction number.
Measles.
69
What is the treatment for influenza?
Supportive care! Antiviral medications might be used to reduce the risk of transmission.
70
Define outbreak.
occurrence of disease cases in excess of normal expectancy
71
Define epidemic.
More cases in a region/country.
72
Define pandemic.
Epidemics that span international boundaries.
73
What can mast cell mediators affect?
Release of histamines
| Airways and blood vessels. They can result in bronchoconstriction and vasodilation.
74
How would you describe the airways in asthma?
Hyper-reactive. This leads to inflammation.
75
What is allergic asthma?
When an innocuous allergen triggers an IgE mediated response. The immune recognition processes are faulty and so there is increased IgE, IL-3,4 and 5 production.
76
What is non-allergic asthma?
Airway obstruction induced by exercise, cold air and stress.
77
Describe the process of IgE binding to and activating mast cells.
IgE binds to the high affinity receptor on the mast cell surface. There is cross-linking and biochemical cascades => release of proinflammatories (histamines, eosinophil activators, proteases)
78
What might be released on mast cell degranulation?
1. Histamines
2. Eosinophil activators
3. Proteases
4. Cytokines
79
what are interleukins responsible for in IgE reaction
- Pro-inflammatory and eosinophil survival
- Increases the number of mast cells
- IgE synthesis
80
Which lung mast cell mediators are responsible for bronchoconstriction?
histamine.
81
Which lung mast cell mediators are responsible for inflammation?
histamine and cytokines.
82
Which lung mast cell mediators are responsible for airway remodelling?
cytokines and enzymes.
83
Give 3 reasons why the airways hyper-reactive in asthmatics?
1. Inflammatory infiltrate.
2. Eosinophils.
3. Epithelium destruction gives easier access to bronchoconstrictors.
84
What are the 2 principles of asthma treatment?
1. Alleviate symptoms.
| 2. Target inflammation.
85
What broad class of drugs are commonly used to alleviate symptoms?
Bronchodilators.
86
What broad class of drugs are commonly used to target inflammation?
Steroids.
87
Name 3 types of bronchodilators that are commonly used.
1. Beta agonists.
2. Muscarinic antagonists.
3. Methylxanthines.
88
What makes LABA long acting?
They have increased lipophilicity.
89
What type of beta adrenergic receptors are found in the lungs?
Beta 2.
90
Where are beta 1 adrenergic receptors found?
In the heart.
91
Where are beta 3 adrenergic receptors found?
In adipose tissue.
92
Where are anti-inflammatory steroids produced?
Adrenal cortex.
93
Where in the adrenal cortex are mineralocorticoids produced and give an example of one.
- Zona glomerulosa.
| - Aldosterone.
94
Where in the adrenal cortex are glucocorticoids produced and give an example of one.
- Zona fasciculata.
| - Cortisol
95
How do glucocorticoids work?
They interfere with gene transcription.
96
Give 2 effects of hydrocortisone.
1. Metabolic.
| 2. Anti-inflammatory.
97
Give 3 potential side effects of prolonged hydrocortisone use.
(Steroid)
- Muscle wasting.
- Osteoporosis.
- Increased risk of infection.
- weight gain
- stomach ulcers
98
What are the main cells responsible for inflammation in asthma?
Mast cells and eosinophils.
99
What are the main cells responsible for inflammation in COPD?
Neutrophils and macrophages.
100
Describe the mechanism behind aspirin induced asthma.
Aspirin inhibits COX. There is an increase in arachidonic acid. This is shunted and there is increased leukotriene production = INFLAMMATION!
101
How does anti IgE therapy work?
Ab binds to and neutralises free IgE; this prevents IgE binding and results in decreased mast cell sensitisation. Allergens are unable to activate mast cells.
102
What is the advantage of having inhaled medications in the management of asthma?
Inhaled medications are more likely to reach the target sites and there is reduced chance of side effects.
103
Name 5 groups of people who might be at increased risk on pneumonia.
1. The elderly.
2. Children.
3. People with COPD.
4. Immunocompromised people.
5. Nursing home residents.
104
Describe in 3 steps the pathogenesis of pneumonia.
1. Bacteria translocate to normally sterile distal airway.
2. Resident host defence is overwhelmed.
3. Macrophages, chemokines and neutrophils produce an inflammatory response
4. sputum fills airways and alveoli
105
What can cause pneumonia to be severe?
1. Excessive inflammation.
2. Lung injury.
3. Resolution failure.
106
Describe the process of pneumonia resolution?
Bacteria are cleared and inflammatory cells are removed by apoptosis.
107
What protective features does the respiratory tract have against pathogens?
Teeth, commensal bacteria, swallowing reflex - epiglottis closes respiratory tract, mucociliary escalator, coughing and sneezing etc.
108
What symptoms might you see in someone with pneumonia?
- Productive cough.
- Sweats.
- Fever.
- Breathlessness.
- Pleuritic chest pain.
- Myalgia, headache, arthralgia suggests atypical pneumonia.
109
What signs might you see in someone with pneumonia?
- Fever.
- Signs of lung consolidation - bronchial breath sounds and dull to percuss.
- Pleural effusion - stony dull percussion.
- Crackles and wheeze.
- Abnormal vital signs (tachypnoea, tachycardia, hypoxia, hypotension)
110
What investigations might you do on someone to determine whether or not they have pneumonia?
- CXR (consolidation)
- FBC (raised WBC)
- U+E (raised urea)
- CRP (raised)
- Microbiology: sputum culture, blood culture, serology etc.
111
How can pneumonia be prevented?
- Children are given PCV.
- Smoking cessation is encouraged.
- Influenza vaccines are given to children and the elderly.
112
What is CURB65 used for?
It is a way of assessing the severity of community acquired pneumonia (CAP). It predicts mortality.
113
What does CURB65 stand for?
```
Confusion.
Urea (>7)
RR (>30/min)
BP (<90/60)
Age >65.
```
114
Why is CRB65 often used in the community?
Because facilities to measure urea are often not available.
115
Name 2 bacteria that are common causes of pneumonia?
1. Streptococcus pneumoniae.
| 2. Haemophilus influenzae.
116
Describe s.pneumoniae.
Gram positive cocci chain. Alpha haemolytic and optochin sensitive.
117
Describe haemophilus influenzae.
Gram negative bacilli.
118
What antibiotic would you give to someone with haemophilus influenzae?
Co-amoxiclav or doxycycline.
119
What groups of people may develop pneumonia caused by klebsiella pneumoniae?
- Homeless people.
- Alcoholics.
- People in hospital.
120
What kind of bacteria is klebsiella pneumoniae?
Gram negative bacilli.
121
What can be a sign of effusion on a CXR?
Lots of consolidation.
122
What is empyema?
Pockets of pus that have collected in a body cavity e.g. in the lungs.
123
Give 3 signs of empyema.
1. WBC/CRP don't settle with antibiotics.
2. Pain on deep inspiration.
3. Pleural collection.
4. recent pneumonia
124
What is the usual treatment for empyema?
1) Empirical IV Abx (amoxicillin)
2) chest tube drainage
3) supportive care (analgesics)
125
Name 3 groups of people who might be at risk of hospital acquired pneumonia.
1. Elderly.
2. Ventilator associated.
3. Post operative patients.
126
What is bronchiolitis?
Airway obstruction caused by inflammation of the bronchioles and increased mucus secretions. It is caused by RSV infection.
127
What can cause bronchiolitis?
Respiratory syncytial virus (RSV).
128
In what group of people is bronchiolitis common?
Children (infants under 1)
129
What is the difference between bronchitis and bronchiolitis?
- Bronchiolitis: inflammation of bronchioles and increased mucus secretion due to RSV infection.
- Bronchitis: inflammation of bronchi epithelium due to irritants and chemicals.
130
What investigations might you do in someone you suspect to have infective bronchitis?
- CXR (often normal).
| - Viral and bacterial swabs.
131
What is the usual cause of infective bronchitis?
- Mainly viral!
| - Acute bronchitis can be caused by adenoviruses.
132
Is infective bronchitis normally caused by bacterial or viral infection?
Viral.
133
Is pharyngitis normally caused by bacterial or viral infection?
Viral e.g. rhinovirus, adenovirus etc.
134
What bacteria might sometimes cause pharyngitis?
Streptococcus pyogenes.
135
What is the Centor criteria used for?
It determines the likelihood that a sore throat is bacterial.
will Abx be beneficial
136
What signs make up the Centor criteria?
1. Tonsillar exudate.
2. lymphadenopathy
3. Fever (>38°C).
4. Absence of cough.
(3 or 4 of these = 50% chance of bacterial infection).
137
Is sinusitis usually bacterial or viral?
Viral.
138
What type of bacteria is Bordetella pertussis?
Gram negative bacilli.
139
What are the symptoms of whooping cough in adults? how long does it last
- low grade fever, mild dry cough
- progresses after a week: more sever coughing fits, inspiratory whoop
- usually resolves within 8 weeks but can last months
140
What agar would you culture bordetella pertussis on?
Bordet Gengou agar.
141
What antibiotics might you use in someone with bordetella pertussis infection?
Clarithromyocin or azithromycin
142
When is someone vaccinated against bordatella pertussis?
A child is vaccinated at 8, 12 and 16 weeks and at 3 years 4 months with dTaP vaccine.
pregnant women
143
What causes Croup?
Parainfluenza virus
respiratory syncytial virus (RSV)
144
In which group of people is Croup common?
Children (6 months - 2 years)
145
What is croup?
Acute larygnotracheobronchitis - trachea, bronchi and larynx are all affected.
146
Malignant bronchial tumours can be divided into two groups; what are they?
1. Non small cell cancer.
| 2. Small cell cancer.
147
Which type of malignant bronchial tumour fits into TNM staging?
Non small cell cancer.
148
Which type of malignant bronchial tumour tends to have a worse prognosis?
Small cell cancer.
149
Give 5 causes of lung cancer.
1. SMOKING!
- Occupational:
2. Asbestos exposure.
3. Radon exposure.
4. Coal tar exposure.
5. Chromium exposure.
150
Give 3 main cell types that make up non small cell lung cancer?
1. Squamous cell (20%).
2. Adenocarcinoma (40%).
3. Large cell.
151
How does PET scanning work?
FDG is taken up by rapidly dividing cells. Tumours therefore appear 'hot' on the scan. PET scans are functional rather than anatomical.
152
What does TNM stand for?
1. T: tumour (T1-4).
2. N: nodal involvement (N0-3).
3. M: metastases (M0-1).
- Increased staging = decreased survival.
153
Give 6 symptoms of local disease lung cancer.
1. Chest pain.
2. Wheeze.
3. Breathlessness.
4. Cough.
5. Haemoptysis.
6. Recurrent chest infections.
154
Give 6 symptoms of lung cancer that has metastasised.
1. Bone pain, especially waking up in the night from pain.
2. Headache.
3. Seizures.
4. Neurological deficit.
5. Hepatic and/or abdominal pain.
6. Weight loss.
155
Name 5 places that lung cancer might metastasise to.
1. Bone.
2. Brain.
3. Liver.
4. Lymph nodes.
5. Adrenal glands.
156
What are paraneoplastic syndromes?
Disorders triggered by immune response to a neoplasm.
157
Give 5 examples of paraneoplastic syndromes.
1. Finger clubbing.
2. Anorexia.
3. Weight loss.
4. Hypercalcemia.
5. Hypernatremia.
158
What investigations might you do on someone to determine whether they have lung cancer?
- CXR.
- CT scan.
- Bronchoscopy.
- bronchoscopy or percutaneous biopsy
- histological diagnosis
159
What tests might you do on a patient to determine whether they're fit for operation?
1. ECG.
2. Lung function tests.
3. Determine performance status.
160
It is important to ask a patient if they've had any previous cancers. Name 5 cancers that can spread to the lung.
1. Breast.
2. Prostate.
3. Kidney.
4. Melanoma.
5. Lymphoma.
161
Give an example of a malignant pleural tumour.
Mesothelioma.
162
What can cause pleural tumours?
Occupational - asbestos exposure!
163
Give 5 potential consequences of asbestos exposure.
1. Plaques.
2. Effusion.
3. Asbestosis.
4. Mesothelioma.
5. Bronchial carcinoma.
164
What are signs and symptoms of mesothelioma?
1. Breathlessness.
2. Chest pain.
3. Weight loss.
4. Sweating.
5. Abdominal pain.
165
What investigations might you do on someone to determine whether they have mesothelioma?
- CXR.
- CT scan.
- Pleural biopsy.
166
What is the treatment for mesothelioma?
1. Symptom control.
2. Palliative chemotherapy or radiotherapy.
3. Radical surgery (removal of tumour blood supply).
167
How does the treatment differ between local and systemic lung cancer?
- Local: surgery and radiotherapy.
| - Systemic: chemotherapy.
168
What is the difference between radical radiotherapy and palliative radiotherapy?
1. Radical: daily treatments for 4-6 weeks.
| 2. Palliative: the patient attends the minimum number of visits possible to control symptoms.
169
Give 5 side effects of radiotherapy.
1. Fatigue.
2. Anorexia.
3. Cough.
4. Oesophagitis.
5. Systemic symptoms.
170
What are the 3 main aims of palliative chemotherapy?
1. Relieve symptoms.
2. Improve quality of life.
3. Shrink tumours.
171
Give 4 side effects of chemotherapy.
1. Alopecia.
2. Nausea/vomiting.
3. Peripheral neuropathy (nerve damage in extremities).
4. Constipation or diarrhoea
5. infertility
6. tumour lysis syndrome (increases uric acid)
172
What does pleural fluid contain?
Proteins e.g. albumin, globulin.
173
What is the function of the pleura?
It allows movement of the lung and lung expansion against the chest wall.
174
What produces and reabsorbs pleural fluid?
The parietal pleura.
175
Name 2 diseases associated with the pleura.
1. Pleural effusions.
| 2. Pneumothorax.
176
Give 5 potential causes of pleural effusion?
1. Malignancy (exudate).
2. Infection (exudate).
3. Inflammation (exudate).
4. Heart/renal failure (transudate).
5. Hypoalbuminemia (transudate).
177
How might you diagnose pleural effusion?
1. Take a good history.
2. pleural ultrasound
3. Thoracentesis - can tell you transudates v exudates.
178
What is a pneumothorax?
Air in the pleural space (space which separates lung from chest wall) which can lead to partial of complete lung collapse.
179
What are the three main types of pneumothorax?
| aetiology
1. Traumatic e.g. stab wound.
2. Spontaneous: can be primary (PSP) or secondary (SSP).
3. Iatrogenic.
180
What is the treatment for a traumatic pneumothorax?
insert large bore cannula into 2nd intercostal space in midclavicular line (on side of pneumothorax)
181
what is tension pneumothorax
trauma creates one way valve (only lets air in to pleural space) => air drawn in in inspiration and trapped in expiration => pneumothorax gets larger => increase pressure => mediastinum moves across => major vessels kink => cardiorespiratory arrest
182
What does the medulla detect?
The pH (H+ conc) of the CSF.
183
What do carotid and aortic bodies detect?
Chemoreceptors respond to increased CO2 and decreased O2.
184
What is type 1 respiratory failure?
Hypoxia - decreased PaO2.
| PaCO2 is normal or slightly low due to hyperventilation.
185
What is type 2 respiratory failure?
Hypoxia and hypercapnia - decreased PaO2 and increased PaCO2.
There is alveolar hypoventilation.
186
Give 3 signs of hypercapnia.
1. Bounding pulse.
2. Flapping tremor.
3. Confusion.
4. hyperventilation
187
What can cause type 1 respiratory failure?
1. Airway obstruction.
2. Failure of O2 to diffuse into the blood.
3. V/Q mismatch.
4. Alveolar hypoventilation.
188
What can cause type 2 respiratory failure?
Alveolar hypoventilation.
189
Give examples of diseases that obstruct the airway and so could lead to type 1 respiratory failure.
1. COPD.
2. Obstructive sleep apnoea.
3. Asthma.
(Can't get O2 in but can get CO2 out).
190
Name 5 things that lead to alveolar hypoventilation and so could cause type 1 and type 2 respiratory failure.
1. Opiates.
2. Emphysema.
3. Obesity.
4. Neuromuscular weakness e.g. MND.
5. Chest wall deformity.
191
Give examples of diseases that lead to a failure of O2 to diffuse into the blood and so could cause type 1 respiratory failure.
1. Emphysema.
| 2. ILD e.g. IPF, sarcoidosis.
192
Give examples of diseases that lead to V/Q mismatch and so could cause type 1 respiratory failure.
1. Cardiac failure.
2. PE (dead space, V/Q = ∞)
3. Shunt (V/Q = 0)
4. Pulmonary hypertension.
193
What treatments might be given for V/Q mismatch?
Ventilation support e.g. CPAP and BIPAP.
194
COPD is an umbrella term. What 2 diseases does it include?
1. Chronic bronchitis.
| 2. Emphysema.
195
What is chronic bronchitis?
Exposure to irritants and chemicals e.g. smoke -> hypertrophy and hyperplasia of mucus secreting glands -> increased mucus -> airway obstruction. Neutrophil and macrophage involvement -> bronchi become inflamed.
196
How is airway obstruction defined by spirometry?
- FEV1 < 80% predicted.
| - FEV1/FVC < 0.7.
197
What are the main causes of COPD?
SMOKING!
| Genetics, socio-econonomic factors, occupation and the environment can all contribute to COPD too.
198
Would a patient with emphysema be a 'pink puffer' or a 'blue bloater'?
They would be a 'pink puffer'.
These patients often present with symptoms of weight loss; breathlessness; barrel chest; pursed lip breathing; CO2 retention.
199
Would a patient with chronic bronchitis be a 'pink puffer' or a 'blue bloater'?
They would be a 'blue bloater'.
These patients often present with symptoms of chronic cough, phlegm, cor pulmonale, hypoxia and hypercapnia, wheeze, crackles and cyanosis.
200
Aside from COPD, what might be a differential diagnosis for breathlessness?
1. Heart failure.
2. PE.
3. Pneumonia.
4. Lung cancer.
201
Shortness of breath can lead to exercise limitation. Give 3 potential consequences of this.
1. Muscle wasting.
2. Depression and anxiety.
3. Disability.
202
A young person presents to you with breathlessness, wheeze and cough. There appears to be inflammation of the airways. When you do a spirometry test the results are variable. You ask the patient to do a peak flow diary and the results of this show diurnal variation. Is the patient likely to have asthma or COPD?
They are likely to have asthma!
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are variable is a large indication that this person has asthma!
The patient is also young and COPD tends to be more common in older people.
203
An older person presents to you with breathlessness, wheeze and cough. There appears to be inflammation and fibrosis of the airways and also alveolar disruption. You ask the patient to do a peak flow diary and the results of this are all abnormal. Is the patient likely to have asthma or COPD?
They are likely to have COPD!
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are consistently abnormal is a large indication that this person has COPD; in asthma there would be diurnal variation. Fibrosis and alveolar disruption are also signs of COPD and the fact that the patient is an older patient also makes COPD the more likely diagnosis.
204
What are the treatments for COPD?
1. Smoking cessation!
2. Pulmonary rehabilitation.
3. SABA/LABA for symptom relief.
4. ICS.
205
Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD?
Advantages:
1. Improve Q.O.L.
2. Improve lung function.
3. Reduce the likelihood of exacerbations.
Disadvantages:
1. There is an increased risk of pneumonia.
206
Define exacerbation.
An acute event characterised by worsening symptoms beyond normal day to day variation. It often leads to a change in medication.
207
Give 5 potential consequences of exacerbations of COPD/asthma.
1. Worsened symptoms.
2. Decreased lung function.
3. Negative impact on Q.O.L.
4. Increased mortality.
5. Huge economic cost.
208
What is the likely cause for an exacerbation of COPD?
Viral infection e.g. RSV, influenza, parainfluenza, rhino and coronaviruses.
209
What is the treatment for an exacerbation of COPD?
1. Oxygen.
2. Bronchodilators.
3. Systemic steroids.
4. Antibiotics if there is breathlessness and sputum production.
210
What are the aims of treatment for exacerbations of COPD?
1. Minimise the impact of the current exacerbation.
| 2. Prevent subsequent exacerbations.
211
Give 3 ways in which subsequent exacerbations be prevented.
1. Smoking cessation.
2. Vaccination.
3. LABA/LAMA/ICS.
212
Secretion of which hormones might result in paraneoplastic changes?
1. PTH.
| 2. Increased ADH (SIADH).
213
Why is the prognosis for small cell lung cancer normally very poor?
Small cell cancers often metastasise and so prognosis is poor.
214
Describe mycobacterium tuberculosis.
1. Acid fast bacilli.
2. Has a waxy capsule (so gram stain not effective)
3. It grows slowly + high oxygen demand (so hard to culture and treat)
4. It can resist phagolysosomal killing resulting in granulomatous disease.
215
What mycobacterium can cause abdominal tuberculosis?
Mycobacterium bovis.
| - Can be found in unpasteurised milk.
216
Where are a high proportion of cases of TB found?
The indian sub continent e.g. India, Bangladesh, Pakistan etc.
217
Give 5 risk factors for TB.
1. If you live in a high prevalence area.
2. IVDU.
3. Homeless.
4. Alcoholic.
5. HIV+
6. contact with active TB (family, healthcare worker)
218
How is TB transmitted?
Aerosol transmission - mycobacterium TB bacilli are inhaled and enter the lung.
219
describe primary TB
initial contact with alveolar macrophage => uses macrophage to proliferate => taken to lymph nodes => cell mediated immunity
220
describe latent TB
- immune system encapsulates site of infection (granuloma) to slow progression
- provides area for TB to grow + block from systemic infection => latent, dormancy
221
TB disease: Where in the lung is a granuloma cavity most likely to develop?
Most likely to develop in the apex of the lung as there is more air and less blood supply/immune cells.
222
Presentation of TB: what systemic symptoms might you see?
1. Weight loss.
2. Night sweats.
3. Anorexia.
4. Malaise.
223
Presentation of TB: what pulmonary TB symptoms might you see?
1. Cough.
2. Haemoptysis.
3. Chest pain.
4. Breathlessness.
224
What might you see on a CXR taken from someone with TB?
1) Primary: pleural effusion
2) nodular consolidation with cavitation
3) disseminated miliary (millet seeds)
225
Name 6 places where TB might spread to?
1. Bone and joints - pain and swelling.
2. Lymph nodes - swelling and discharge.
3. CNS - TB meningitis.
4. Miliary TB - disseminated.
5. Abdominal TB - ascites, malabsorption.
6. GU TB - sterile pyuria, WBC in GU tract.
226
What test might you do to diagnose latent TB?
Mantoux test - stimulates type 4 hypersensitivity reaction.
looks for prev immune response to TB: +ve indicates previous vaccination/latent/active
227
What drugs are given in the treatment of TB?
Rifampicin (6 months).
Isoniazid (6 months).
Pyrazinamide (2 months).
Ethambutol (2 months).
228
TB treatment: which 2 drugs are taken for the entire 6 months?
1. Rifampicin.
| 2. Isoniazid.
229
TB treatment: which 2 drugs are taken for only the first 2 months?
1. Pyrazinamide.
| 2. Ethambutol.
230
TB treatment: How long do you take Rifampicin for?
6 months.
231
TB treatment: How long do you take Isoniazid for?
6 months.
232
TB treatment: How long do you take Pyrazinamide for?
2 months.
233
TB treatment: How long do you take Ethambutol for?
2 months.
234
Give 3 potential side effects of Rifampicin.
1. Red urine.
2. Hepatitis.
3. Drug interactions; rifampicin is an enzyme inducer.
235
Give 2 potential side effects of Isoniazid.
1. Hepatitis.
| 2. peripheral Neuropathy.
236
Give 3 potential side effects of Pyrazinamide.
1. Hepatitis.
2. Gout.
3. Rash.
237
Give 1 potential side effect of Ethambutol.
1. Optic neuritis.
238
Compliance in taking TB medication is critical. Why?
Resistance and relapse may be likely if the patient is non-compliant.
239
Why does TB treatment need to last for 6 months?
TB treatment lasts for at least 6 months to ensure all the dormant bacteria have 'woken up' and been killed.
240
What is the acronym commonly used for the drugs taken in TB treatment?
;)
```
HRZE.
HR = 6 months.
ZE = 2 months.
- H - isoniazid.
- R - rifampicin.
- Z - pyrazinamide.
- E - ethambutol.
```
241
TB treatment: Give 4 factors that can increase the risk of drug resistance?
1. If the patient has had previous treatment.
2. If they live in a high risk area.
3. If they have contact with resistant TB.
4. If they have a poor response to therapy.
242
What are the problems associated with drug resistance in TB treatment?
1. TB becomes more difficult to treat.
2. Medication course > 20 months.
3. Increased risk of side effects.
4. Increased relapse rate.
243
How can TB be prevented?
1. Active case finding - reduce infectivity.
2. Detect and treat latent TB.
3. Vaccination - BCG.
244
What are interstitial lung diseases?
Diseases of the alveolar/capillary interaction. There is often scarring around the alveoli and so an increased diffusion pathway for gaseous exchange.
245
What are the 5 major categories of interstitial lung disease?
1. Associated with systemic diseases e.g. rheumatological.
2. Environmental aetiology e.g. fungal, dusts.
3. Granulomatous disease e.g. sarcoidosis.
4. Idiopathic e.g. IPF.
5. Other.
246
Give 4 major signs and symptoms of interstitial lung disease.
1. Cough.
2. Breathlessness.
3. Finger clubbing.
4. Evidence of systemic disease.
247
Would pulmonary function tests taken from someone with interstitial lung disease show a restrictive or obstructive pattern?
They would be restrictive!
| There is decreased gas transfer and a reduction in PaO2.
248
Who does idiopathic pulmonary fibrosis usually effect?
It tends to be a disease of the elderly.
249
Give 3 signs/symptoms of IPF.
1. Dyspnoea on exertion.
2. Dry cough.
3. Elderly effected.
250
What is IPF?
A disease characterised by chronic inflammation and permanent scarring in the alveoli. Respiratory ability is affected. Chest infection and hypoxic damage are likely.
251
Give 4 risk factors for IPF.
1) age
2) male
3) family history
4) smoking
252
What treatment is used in IPF?
acute, ongoing
- Acute: prednisolone
| - Ongoing: anti fibrotic therapy (pirfenidone)
253
What is the general treatment for all interstitial lung disease?
prognosis ?
generally poor prognosis as damage irreversible
1. Steroids
ongoing
1. Remove the exposure! oxygen if hypoxic, stop smoking
3. pulmonary rehab (strengthen other muscles)
2. pneumococcal and flu vaccine
254
What kind of disease is sarcoidosis?
where typically affected ?
- It is a granulomatous disease!
| - It can affect any organ system but typically affects the lungs + lymph nodes.
255
Is sarcoidosis a restrictive or obstructive disease?
Pulmonary function tests would show restrictive patterns.
256
What is the usual treatment for sarcoidosis?
acute: prednisolone
ongoing: ongoing steroids (oral prednisolone)
257
# Define bronchiectasis.
explain briefly
- Irreversible and abnormal dilation of the bronchi with chronic inflammatory and fibrotic changes.
- inflam => bronchial wall oedema and increased mucus prod => bronchioles damaged + dilated => further inflam
258
Describe the pathogenesis of bronchiectasis.
Failed mucocilliary clearance and impaired immune function mean => microbe can easily invade => infection => inflam => lung damage => bronchitis => bronchiectasis => fibrosis.
259
What can cause bronchiectasis?
aetiology
anything that causes chronic inflam
1. recurrent and/or sever infections
2. immunodeficiency (HIV)
3. genetic (CF)
4. COPD
5. Idiopathic ! (50% of patients)
260
Which bacteria might cause bronchiectasis?
1. Haemophilus influenzae.
2. Pseudomonas aeruginosa.
3. Staphylococcus aureus.
261
Give 6 symptoms of bronchiectasis.
1. Chronic productive cough.
2. Recurrent chest infections.
3. Dyspnoea and wheeze.
4. Recurrent exacerbations.
5. Chest pain.
6. Haemoptysis.
262
What investigations might you do on someone to determine whether they have bronchiectasis?
- High resolution CT scan
- CXR
- Sputum culture + sensitivity
263
What is the treatment/management for bronchiectasis?
- daily airway clearance
| - Abx (amoxicillin)
264
Describe the pathogenesis of cystic fibrosis.
There is a defect in chromosome 7 coding CFTR protein. Cl- transport is affected and there is production of thickened mucus secretions.
265
How is cystic fibrosis passed on?
It is an autosomal recessive condition.
| 1 in 25 people are carriers.
266
A common mutation in which gene can cause CF?
CFTR protein
267
Give 6 potential complications of CF.
1. Malnutrition due to malabsorption.
2. Respiratory failure and cor pulmonale.
3. Weight loss and growth retardation.
4. Infertility, very common in males due to defect in vas deferens.
5. Diabetes mellitus due to pancreatic insufficiency.
6. Delayed puberty.
7. Breathlessness
8. Finger clubbing.
9. Frequent respiratory infections (-> bronchiectasis).
10. Salty sweat
268
What is the management of CF?
1. Prevention e.g. vaccination.
2. bronchodilator (salbutamol)
4. Enzyme supplements for pancreatic insufficiency.
5. prophylactic Abx (flucloxacillin)
6. Physical therapies e.g. airway clearance and exercise.
7. High cal diet
269
Define pulmonary hypertension.
- mPAP > 25mmHg.
| => Secondary RV failure.
270
What can cause an increase in mPAP?
| mean pulmonary arterial pressure
Increased resistance to flow.
| Increased flow rate.
271
Give 5 causes of pulmonary hypertension.
1. Hereditary.
2. Idiopathic.
3. Drug use.
4. HIV infection.
5. Pulmonary hypertension secondary to left heart disease (valvular, systolic/diastolic dysfunction).
272
Give 5 symptoms of pulmonary hypertension.
```
Initial symptoms:
1. Dyspnoea on exertion.
2. Lethargy.
3. Fatigue.
4. Syncope.
Symptoms as RV failure develops:
1. Pulmonary oedema.
2. Abdominal pain.
```
273
What investigations might you do in someone to determine whether they have pulmonary hypertension?
1. Right heart catheterisation (diagnostic)
2. ECG - see if there's RV hypertrophy.
3. CXR - enlarged proximal pulmonary arteries.
4. transthoracic doppler Echocardiography.
274
What might you notice in the ECG take from someone with pulmonary hypertension?
There might be signs of RV hypertrophy.
275
What might you notice in a CXR take from someone with pulmonary hypertension?
There might be enlarged proximal pulmonary arteries which taper distally.
276
Describe the usual treatment for someone with pulmonary hypertension.
1. Initial treatment is O2.
2. Warfarin (due to risk of thrombosis).
3. Diuretics (for oedema).
4. Ca2+ blockers (pulmonary vasodilators).
5. Treat underlying cause.
277
Why might someone with pulmonary hypertension experience peripheral oedema?
Blood accumulates in the pulmonary artery. The RV experiences a greater afterload and works harder to get blood out of the ventricle and into the pulmonary artery. There is RV hypertrophy and right heart failure. This results in peripheral oedema.
278
Pulmonary embolism: where might an emboli arise from?
Emboli often arise from a dislodged DVT - from iliofemoral veins.
279
What is the consequence of a small, peripheral PE?
Infarction!
| There is ventilation but no perfusion; dead space.
280
What is the consequence of a large, central PE?
Ischaemia!
| There is resistance to flow which can also result in RHF.
281
What are symptoms of a small, peripheral PE?
- Breathlessness.
| - Pleuritic chest pain.
282
What are symptoms of a large, central PE?
- Severe central chest pain.
| - Pale and sweaty.
283
What investigations might you do in someone to determine whether they have PE?
- CXR.
- ECG.
- D-dimer.
- V/Q lung scan - shows ventilated areas with perfusion defects.
- CTPA - can detect emboli.
284
What is D dimer?
A small protein fragment found after a blood clot is degraded by fibrinolysis.
285
The Wells scoring system is used to work out the probability of a person having a PE. Name 5 factors that the scoring system uses.
1. Clinical signs/symptoms of DVT.
2. HR > 100bpm.
3. Recent immobilisation.
4. Previous DVT/PE.
5. Haemoptysis.
6. Malignancy.
Score >4 - PE likely.
286
Describe the treatment for PE.
1) unfractioned heparin
2) thrombolysis (alteplase)
3) switch heparin to DOAC (apixiban)
287
What diseases might be in the differential diagnosis of PE?
1. Asthma.
2. COPD.
3. Pneumonia.
4. MI.
288
What is pulmonary vasculitis?
Inflammation of the pulmonary arterial wall.
289
Why are immunosuppressants given as treatment to people with pulmonary vasculitis?
Pulmonary vasculitis is autoimmune associated.
290
What 2 categories can asthma be divided into?
1. Allergic asthma (extrinsic); atopic. IgE and mast cell involvement.
2. Non allergic asthma (intrinsic).
291
Describe asthma.
An inflammatory disease characterized by hyper-responsive airways. Airway obstruction is reversible. There is inappropriate smooth muscle contraction.
292
Extrinsic asthma: what happens when IgE binds to mast cells?
Vasoactive substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion.
293
What occupations may be associated with an increased risk of developing asthma?
1. Paint sprayers - exposure to fumes.
2. Animal breeders.
3. Bakers.
4. Laundry workers.
294
What are the symptoms of asthma?
1. Breathlessness.
2. Diurnal variation - often worse in the morning.
3. Cough.
4. Episodic wheeze.
5. Chest tightness.
295
What investigations might you do on someone to determine whether they have asthma?
1. PEFR.
2. Spirometry should show an obstructive pattern; FEV1 < 80%, FEV1/FVC < 0.7, PEFR - variable.
3. Test for atopy; RAST, skin prick test.
3. CXR.
4. Eosinophil count.
5. O2 saturation.
296
How can reversibility be tested in asthma?
When given a beta agonist there will be a 400ml increases in FEV1 OR a 20% improvement in PEFR.
297
Describe the management/treatment of asthma.
- SABA (salbutamol)
- add ICS (budesonide/formoterol)
- add leukotriene receptor antagonists (montelukast)
- switch SABA to LABA
- MART therapy (LABA + ICS)
- increase ICS dose (to moderate)
- increase ICS dose (to high)
298
Give 5 side effects of systemic steroids.
1. Diabetes.
2. Osteoporosis.
3. Hypertension.
4. Oral candida (oral steroids).
5. Skin thinning.
299
What 4 measurements can be used to diagnose acute severe asthma?
RR? HR? PEFR?
1. RR > 25.
2. HR > 110.
3. PEFR 35-50% predicted.
4. Unable to complete a sentence in one breath.
300
What is the first line treatment for acute severe asthma?
- Nebulised salbutamol with oxygen.
- oral steorids (prednisolone)
- abx if evidence of infection.
301
Respiratory immunity: describe the innate immune response.
Mucous, mucociliary escalator, macrophages and neutrophils all play a role in the innate immune response. Cough reflex and epiglottis closing off trachea on swallowing.
302
Respiratory immunity: describe the adaptive immune response.
- B cells produce mainly IgG and IgA antibodies.
| - T cells - CD4, CD8 and regulatory.
303
How can neutrophils destroy bacteria?
Neutrophil bactericidal functions include ROS, proteases and NETs.
304
What can affect cilia function?
- Infection.
| - Primary dyskinesia.
305
What are the 3 types of immunosuppression?
1. Granulocyte defect - associated with chemotherapy.
2. B cell defect - associated with rituximab and hematological malignancy.
3. T cell defect - associated with immunosuppression/HIV.
All result in an increased risk of infection.
306
What is a granulocyte immunodeficiency defect associated with?
Chemotherapy.
307
What is a T cell defect associated with?
Immunosuppression and HIV.
308
What is a B cell defect associated with?
Rituximab and hematological malignancy. There is an increased risk of encapsulated bacteria infection e.g. H.influenzae.
309
Define neutropenia.
A disease characterised by having an abnormally low concentration of neutrophils in the blood.
310
What can cause neutropenia?
Often iatrogenic causes e.g. chemotherapy.
311
Give 4 examples of iatrogenic immunosuppression.
1. Corticosteroid use.
2. Chemotherapy.
3. Immune suppression after organ transplant.
4. Rituximab.
312
Give 4 examples of non-specific immunosuppression.
1. Malnutrition.
2. Alcohol.
3. Sepsis.
4. Trauma.
313
How can illness be prevented in the immunocompromised?
1. Hand hygiene.
2. Education e.g. avoid live vaccines.
3. Isolation.
4. Screen for TB before anti TNF therapy.
5. PCP prophylaxis of < CD4 count.
314
Describe the usual presentation of pulmonary infection in the immunocompromised?
1. Pyrexia.
2. Lethargy.
3. Cough.
4. Breathlessness.
5. Hypoxic.
315
An immunocompromised person presents with a rapid onset pulmonary infection. Is this likely to have a bacterial or viral cause?
Rapid onset is likely to be bacterial.
316
An immunocompromised person presents with a slow onset pulmonary infection. Is this likely to have a bacterial or viral cause?
Slow onset is likely to be CMV, aspergillus or cryptococcus.
317
Describe the signs and symptoms of PCP.
- Progressive breathlessness and dry cough.
- Lymphopenia typical (CD4<200).
- Hypoxia.
318
What is the usual treatment for PCP?
High dose co-trimoxazole.
| Consider secondary prophylaxis.
319
Who might be at risk of CMV?
Transplant recipients or HIV patients.
320
Define CF.
An autosomal recessive disease resulting in abnormal exocrine gland function.
321
The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a neonate likely to be colonised with?
s.aureus.
322
The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a child likely to be colonised with?
h.influenzae.
323
The airways in a person with bronchiectasis often become chronically colonised. What is the airway of an adult likely to be colonised with?
pseudomonas aeruginosa.
324
Name 3 less common 'atypical' pathogens that can be responsible for causing pneumonia.
1. Mycoplasma pneumoniae.
2. Chlamydia psittaci/pneumoniae.
3. Coxiella burnetti.
4. Legionella pneumophilia.
325
How can less common 'atypical' pathogens responsible for causing pneumonia be identified?
They are hard to grow in culture and so serology and antigen tests are often used.
326
What antibiotic might be used against less common 'atypical' pathogens responsible for causing pneumonia?
Macrolides like clarithromyocin as they are often resistant to beta lactams.
327
A special culture medium is needed to grow TB. What is the medium called?
Lowenstein Jensen Slope.
328
Lowenstein Jensen Slope is a medium used to grow TB. What is special about this medium?
1. It contains growth factors that promote mycobacterial growth.
2. It contains small amounts of penicillin that prevent pyogenic bacteria growth.
329
What might a lymph node biopsy from someone with TB show?
Caseating granuloma.
330
Name a disease that causes a reduction in TLCO.
Asthma.
331
What is TLCO?
The extent to which O2 passes from the alveoli into the blood.
332
What 3 factors can affect TLCO?
1. Alveoli/capillary interaction.
2. Hb concentration.
3. Cardiac output.
333
Is a substantial smoking history needed to establish a diagnosis of COPD?
Although smoking is a major risk factor for COPD, there are many other causes and so a substantial smoking history isn’t necessary for a diagnosis of COPD.
334
Give 3 factors that can be used to establish a diagnosis of COPD?
1. Progressive airflow obstruction.
2. FEV1/FVC ratio < 0.7.
3. Lack of reversibility.
335
How long is the treatment for an idiopathic pulmonary embolism?
At least 6 months.
336
How much fluid is contained within the healthy pleural space?
15ml.
337
Which chromosome codes or CFTR?
Chromosome 7.
338
Name ion that CFTR transports.
1. Chloride.
339
Give 3 radiological indications for bronchoscopy.
1. Lobar collapse.
2. Presence of a mass.
3. Persistent consolidation.
340
Give 3 non-radiological indications for bronchoscopy.
1. Hemoptysis.
2. Cough.
3. Wheeze.
4. Stridor.
341
What percentage of asthma is thought to be caused by occupational factors?
10%.
342
Deficiency of what protease inhibitor can cause emphysema?
Alpha 1 anti-trypsin deficiency.
343
What is the function of alpha 1 anti-trypsin?
It inhibits proteases.
344
What can inactivate alpha 1 anti-trypsin?
Tobacco smoke.
345
What type of T lymphocyte is involved in COPD?
CD8+.
346
What type of T lymphocyte is involved in asthma?
CD4+.
347
What are the symptoms of COPD?
1. Breathlessness.
2. Wheeze.
3. Chronic cough.
4. Sputum.
348
What does a patients' PaO2 have to be less than in order for them to qualify for home O2?
PaO2 < 7.3kPa when breathing room air.
349
Describe the pathophysiology of chronic bronchitis.
Exposure to irritants and chemicals e.g. smoke -> hypertrophy and hyperplasia of mucus secreting glands -> increased mucus -> airway obstruction. Neutrophil and macrophage involvement -> bronchi become inflamed.
350
What are the 3 characteristic features of asthma?
1. Airflow obstruction.
2. Hyper-responsive airways to a range of stimuli.
3. Bronchial inflammation.
351
Define atopy.
The tendency to develop IgE mediated responses to common aeroallergens.
352
Describe the process of airway remodelling in asthma.
1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen.
2. Deposition of collagen below the BM thicken the airway wall.
3. Eosinophils also play a role in remodelling.
353
Give 3 histo-pathological changes that occur in asthma.
1. Basement membrane thickening.
2. Epithelium metaplasia; increased no. of goblet cells leads to mucus hypersecretion.
3. Increase in inflammatory gene expression on many cell types.
354
What are the signs of asthma?
1. Secretions.
2. Obstructive spirometry.
3. Variable PEFR.
4. Reversibility when given beta-2-agonist, FEV1 > 20%.
5. Diurnal variation.
355
What is hypersensitivity pneumonitis (EAA)?
Inhalation of organic dusts leads to a type 3 hypersensitivity reaction; there is an inflammatory response in the alveoli and small airways.
356
Name a cause of hypersensitivity pneumonitis (EAA).
1. Farmer's lung; due to mouldy hay and aspergillus spores.
| 2. Bird fancier's lung; due to proteins present in bird faeces.
357
What can happen if exposure is persistent in someone with farmer's lung?
Progressive fibrosis can occur. There may be signs of weight loss, dyspnoea and cough too.
358
What are occupational lung disorders?
Lung disorders due to a response to inhaling something at work e.g. fumes, dust, gas, aerosol.
359
-
-
360
Give an example of an occupational asthma.
Baker's asthma; flour being the harmful allergen.
361
How might you diagnose someone with having occupational asthma?
1. Do a PEFR test at their place at work and take a history to determine whether their symptoms are worse at work.
2. Serum immunology looking for IgE to a particular workplace allergen.
362
Bronchiectasis is a disease characterised by irreversible dilation of the bronchi. True or False: spirometry shows an obstruction pattern.
True!
Even though bronchi are dilated there is chronic inflammation, scarring and thickening of the bronchi wall which result in airway obstruction.
363
Give 5 signs of sarcoidosis.
1. Bi-lateral hilar lymphadeonopathy (BHL).
2. Erythema nodosum.
3. Uveitis.
4. Non productive cough, SOB, wheeze.
5. Metabolic affect of sarcoidosis = hyperacalcaemia -> nephrocalcinosis.
6. Arthalgia.
7. Hepatosplenomegaly.
8. Neurological: inflammation of the meninges and seizures.
9. Heart block.
10. Lung fibrosis.
11. Finger clubbing is rare!
364
Give 5 signs of pulmonary hypertension.
1. RV hypertrophy (ECG).
2. Loud pulmonary secondary sound.
3. Right parasternal heave.
4. Enlarged proximal pulmonary arteries (CXR).
5. In advanced disease there are signs of RHF, elevated JVP, hepatomegaly and pleural effusion etc.
365
What is Wegener's granulomatosis?
Vasculitis of unknown aetiology. It commonly involves the upper airway and endo-bronchi.
366
What are the symptoms of wegener's granulomatosis?
1. Rhinorrhoea.
2. Nasal mucosa ulceration.
3. Cough.
4. Haemoptysis.
5. Pleuritic chest pain.
367
What would serum tests for someone with Wegener's granulomatosis show?
- C-ANCA and anti-PR3 positive.
368
How would you treat a pleural effusion with a transudate cause e.g. heart/renal failure?
You would treat the underlying cause e.g. the heart failure.
369
What are the symptoms of wegener's granulomatosis?
1. Rhinorrhoea.
2. Nasal mucosa ulceration.
3. Cough.
4. Haemoptysis.
5. Pleuritic chest pain.
370
What would serum tests for someone with Wegener's granulomatosis show?
- C-ANCA and anti-PR3 positive.
371
How would you treat a pleural effusion with a transudate cause e.g. heart/renal failure?
You would treat the underlying cause e.g. the heart failure.
372
How would you treat a pleural effusion with an exudate cause e.g. inflammation?
Drainage.
373
What is the function of inositol trisphosphate?
Inositol trisphosphate (IP3) increases free cytosolic Ca2+ by releasing Ca2+ from intracellular compartments. Ca2+ activates MLC kinase = bronchial smooth muscle contraction.
374
What does activation of the M3 receptor cause?
1. Bronchoconstriction.
2. Vasodilation.
3. Glandular secretions.
375
What is the treatment for someone with mild pneumonia (a CURB65 score of 0-1)?
PO amoxicillin.
376
Where should someone with mild pneumonia (a CURB65 score of 0-1) be treated?
In the community.
377
What is the treatment for someone with moderate pneumonia (a CURB65 score of 2)?
PO amoxicillin and clarithromyocin.
378
Where should someone with moderate pneumonia (a CURB65 score of 2) be treated?
In hospital.
379
What is the treatment for someone with severe pneumonia (a CURB65 score of >3)?
IV co-amoxiclav and clarithromyocin.
380
Where should someone with severe pneumonia (a CURB65 score of 3) be treated?
In hospital.
381
Where should someone with severe pneumonia (a CURB65 score of >4) be treated?
In hospital, consider admission to critical care.
382
A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L.
a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient.
a) Their CURB65 score is 5.
b) This patient should be treated in hospital and admitted to critical care.
c) The patient should be given IV clarithromyocin and co-amoxiclav.
383
Give 2 potential complications of pneumonia.
1. Empyema.
| 2. Lung abscess.
384
Describe the pathophysiology of a tension pneumothorax.
A pleural tear creates a 1-way valve through which air passes in inspiration -> increased intra-pleural pressure -> respiratory distress, shock and cardiac rest.
385
What is the treatment for a tension pneumothorax?
Immediate needle decompression.
386
Give 5 risk factors for PE.
1. Obesity.
2. Recent surgery.
3. Malignancy.
4. Immobility.
5. OCP/HRT.
387
When looking to diagnose IPF, what 3 findings would you look for on pulmonary function tests?
1. Reduced TLCO.
2. Restrictive spiromerty: low FEV1 and FVC but normal ratio.
3. Low/normal PaO2.
388
In what two types of interstitial lung disease will neutrophil levels be raised?
IPF and DIP.
389
A patient presents with breathlessness. On examination they have absent breath sounds and their chest produces a stony dull sound on percussion. They have a PMH of heart failure. What is the likely cause of their symptoms?
Pleural effusion.
390
Give 3 pulmonary symptoms of sarcoidosis.
- Cough.
- SOB.
- Wheeze.
391
What is the effect of sarcoidosis on the skin?
Erythema nodosum.
392
What is the effect of sarcoidosis on the eyes?
Uveitis.
393
Give a metabolic effect of sarcoidosis.
Hypercalcaemia.
394
What is the effect of sarcoidosis on bone?
Arthralgia.
395
What is the effect of sarcoidosis on the liver?
Hepatosplenomegaly.
396
Give a neurological effect of sarcoidosis.
- Inflammation of the meninges.
| - Seizures.
397
Give 2 diseases that might be in the differential diagnosis of sarcoidosis.
1. Lymphoma.
| 2. Pulmonary TB.
398
A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?
Bronchiectasis.
399
Why does someone with chronic bronchitis develop cor pulmonale?
There is pulmonary vasoconstriction in the lungs in an attempt to shunt blood to better ventilated alveoli -> pulmonary hypertension -> RHF -> cor pulmonale.
400
Give 5 signs of chronic bronchitis.
1. Chronic productive cough.
2. Wheeze and crackles.
3. Hypoxic and hypercapnic.
4. Cyanosis.
5. Vasoconstriction -> pulmonary hypertension -> cor pulmonale.
401
Give 5 signs of emphysema.
1. Pursed lip breathing.
2. SOB.
3. Barrel chest.
4. Weight loss.
5. CO2 retention.
402
Give 4 signs of a large PE.
1. Shocked.
2. Central cyanosis.
3. Raised JVP.
4. Accentuation of second heart sound.
403
Infection with a gram negative bacteria is a particular concern in patients with CF. What is this organism and how can infection be prevented?
- Pseudomonas Aeruginosa.
| - Nebulised anti-pseudomonal antibiotic therapy and regular sputum cultures.
404
A patient comes in with bilateral lymphadenopathy. Give 3 conditions that you would include in your differential diagnosis?
1. Local infection e.g. tonsilitis/TB.
2. Lymphoma.
3. Sarcoidosis.
405
Why does TB cause hypercalcaemia?
Granulomatous diseases -> increased vitamin D production and so increased bone resorption, increased absorption from gut and increased re-absorption from kidney.
This is also seen in sarcoidosis.
406
What syndrome may result from an apical lung cancer affecting the T1 nerve root?
Horner's syndrome.
407
Give 5 signs of Horner's syndrome.
1. Anhydrosis.
2. Miosis - pupil constriction.
3. Ptosis.
4. Loss of ciliospinal reflex.
5. Enophthalmos - backwards displacement of the eyeball.
408
Is TLC increased or decreased in restrictive lung diseases?
TLC is decreased.
409
Is TLC increased or decreased in obstructive lung diseases?
TLC is increased.
410
State the name of the pathological lesion that characterises primary tuberculosis?
Ghon complex.
411
State two socioeconomic factors that are associated with an increased prevalence of tuberculosis.
1. Overcrowding.
2. Poverty.
3. Lower socio-economic class.
412
State why cystic fibrosis increases the viscosity and tenacity of the bronchial mucus?
Failure to excrete Cl- leads to Na+ retention. This then leads to H2O retention.
413
Which type of NSCC is most common in smokers?
Squamous cell carcinoma.
414
From what cells are SCC derived from and what is the significance of this?
Neuroendocrine cells.
Can secrete peptide hormones such as ACTH, PTHrP, ADH and HCG.
415
A man with squamous cell carcinoma complains of a dull ache in his back, being very thirsty, and tired. What is the cause of these symptoms?
Squamous cell carcinomas can release PTHrP.
