Pathology Part 1 Flashcards
1
Q
Features of acute asthma
A
Worsening dyspnoea, wheeze and cough that is not responding to salbutamol
Maybe triggered by a respiratory tract infection
2
Q
Why is a normal CO2 in acute asthma not a good sign?
A
Indicates exhaustion and should, therefore, be classified as life-threatening.
3
Q
Moderate acute asthma attack features
A
PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm
4
Q
Severe acute asthma attack features
A
PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm
5
Q
Life-threatening acute asthma attack features
A
PEFR < 33% best or predicted Oxygen sats < 92% Silent chest, cyanosis or feeble respiratory effort Bradycardia, dysrhythmia or hypotension Exhaustion, confusion or coma
6
Q
The classification of acute asthma
A
Moderate
Severe
Life-threatening
7
Q
When is a chest x-ray indicated in acute asthma attacks?
A
life-threatening asthma
suspected pneumothorax
failure to respond to treatment
8
Q
When is hospital admission indicated in acute asthma attacks?
A
- Life-threatening asthma attack
- Severe asthma features if they don’t respond to initial treatment
- Previous near-fatal asthma attack
- Pregnancy,
- Presentation at night
9
Q
When is oxygen indicated in acute asthma attacks?
A
Acutely unwell should be started on 15L of supplemental via a non-rebreathe mask, which can then be titrated down to a flow rate where they are able to maintain a SpO₂ 94-98%.
10
Q
Criteria for discharge after acute asthma attacks
A
Stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
Inhaler technique checked and recorded
PEF >75% of best or predicted
11
Q
Management of acute asthma attacks
A
- SABA
- All patients given 40-50mg of prednisolone orally (PO) daily, continued for at least five days or until the patient recovers from the attack
- Nebulised ipratropium bromide given 3rd line if needed
- IV magnesium sulphate
- IV aminophylline after consultation with senior medical staff
12
Q
Acute bronchitis
A
A type of chest infection which causes inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.
13
Q
Leading cause of acute bronchitis
A
Viral infection
14
Q
How long does acute bronchitis last?
A
Usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time.
15
Q
Features of acute bronchitis
A
Typically present with an acute onset of:
> cough: may or may not be productive
> sore throat
> rhinorrhoea
> wheeze
> Low grade fever (may/may not be present)
16
Q
Chest examination findings in acute bronchitis
A
Majority of patients with have a normal chest examination, however, some may have Low-grade
fever & Wheeze
17
Q
Differentiating acute bronchitis from pneumonia
A
Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
Examination: No other focal chest signs in acute bronchitis other than wheeze. Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
18
Q
Investigations in acute bronchitis
A
Typically a clinical diagnosis
19
Q
Management of acute bronchitis
A
- analgesia
- good fluid intake
- consider antibiotic therapy
- doxycycline first-line - cannot be used in children or pregnant women - amoxicillin is alternative
20
Q
When is antibiotic therapy indicated in acute bronchitis?
A
- Systemically very unwell
- Pre-existing co-morbidities
- CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
21
Q
What antibiotic is first line in acute bronchitis?
A
Doxycycline - cannot be used in children or pregnant women - amoxicillin is alternative
22
Q
Features Acute exacerbation of COPD
A
- Increase in dyspnoea, cough, wheeze
- Increase in sputum suggestive of an infective cause
- May be hypoxic and in some cases have acute confusion
23
Q
The most common bacterial organisms that cause infective exacerbations of COPD
A
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
24
Q
Most common bacteria that causes infective exacerbations of COPD
A
Haemophilus influenzae
25
Management of infective exacerbations of COPD
Increase frequency of bronchodilator use and consider giving via a nebuliser
Prednisolone 30 mg daily for 5 days
Give oral antibiotics if sputum is purulent or signs of pneumonia - amoxicillin or clarithromycin or doxycycline first-line
26
When are antibiotics indicated in infective exacerbations of COPD?
Give oral antibiotics if sputum is purulent or signs of pneumonia - amoxicillin or clarithromycin or doxycycline first-line
27
What are the first-line antibiotics for infective exacerbations of COPD?
Amoxicillin or clarithromycin or doxycycline first-line
28
Acute respiratory distress syndrome (ARDS)
Caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli - life-threatening condition where the lungs cannot provide the body's vital organs with enough oxygen.
29
Causes of Acute respiratory distress syndrome (ARDS)
```
infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
cardio-pulmonary bypass
```
30
Features of Acute respiratory distress syndrome (ARDS)
```
> Acute onset and severe
> dyspnoea
> elevated respiratory rate
> bilateral lung crackles
> low oxygen saturations
```
31
Key investigations in Acute respiratory distress syndrome ARDS
A chest x-ray and arterial blood gases
32
Management of Acute respiratory distress syndrome ARDS
1. ITU
2. Oxygenation/ventilation to treat the hypoxaemia
3. Treat underlying cause e.g. antibiotics for sepsis
4. Strategies such as prone positioning and muscle relaxation shown to improve outcome in ARDS
33
Adult respiratory distress syndrome
Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia (PaO2/FiO2 ratio < 200) in the absence of evidence for cardiogenic pulmonary oedema.
34
Adult respiratory distress syndrome causes
Sepsis
Direct lung injury
Trauma
Acute pancreatitis
Long bone fracture or multiple fractures (through fat embolism)
Head injury (causes sympathetic nervous stimulation which leads to acute pulmonary hypertension)
35
The two stages of Adult respiratory distress syndrome
Early stages consist of an exudative phase of injury with associated oedema.
The later stage is one of repair and consists of fibroproliferative changes. Subsequent scarring may result in poor lung function.
36
Features of Adult respiratory distress syndrome
Acute dyspnoea and hypoxaemia hours/days after event
Multi organ failure
Rising ventilatory pressures
37
Management of Adult respiratory distress syndrome
> Treat the underlying cause
> Antibiotics (if signs of sepsis)
> Negative fluid balance i.e. Diuretics
> Recruitment manoeuvres such as prone ventilation, use of positive end expiratory pressure
38
Allergic bronchopulmonary aspergillosis
Results from an allergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.
39
Allergic bronchopulmonary aspergillosis features
1. Bronchoconstriction: wheeze, cough, dyspnoea.
2. Patients may have a previous label of asthma
3. Bronchiectasis (proximal)
40
Investigations in Allergic bronchopulmonary aspergillosis
> eosinophilia
> flitting CXR changes
> positive radioallergosorbent (RAST) test to Aspergillus
> positive IgG precipitins (not as positive as in aspergilloma)
> raised IgE
41
Management Allergic bronchopulmonary aspergillosis
1. oral glucocorticoids
| 2. itraconazole as a second-line agent
42
Three main types of altitude-related disorders
Acute mountain sickness (AMS), which may progress to High altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE).
43
Features of Acute mountain sickness
Develop gradually over 6-12 hours and potentially last a number of days:
> headache
> nausea
> fatigue
44
HAPE/HACE features
Some people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions
> HAPE presents with classical pulmonary oedema features
> HACE presents with headache, ataxia, papilloedema
45
Management of high altitude pulmonary oedema (HAPE)
1. descent
2. nifedipine, dexamethasone, acetazolamide,
3. phosphodiesterase type V inhibitors*
4. oxygen if available
46
Management of high altitude cerebral oedema (HACE)
1. descent
| 2. dexamethasone
47
Alpha-1 antitrypsin (A1AT) deficiency
Common inherited condition caused by a lack of a protease inhibitor normally produced by the liver.
The role of A1AT is to protect cells from enzymes such as neutrophil elastase. It classically causes emphysema in patients who are young and non-smokers.
48
What disease does Alpha-1 antitrypsin (A1AT) deficiency cause?
Causes emphysema (i.e. chronic obstructive pulmonary disease) in patients who are young and non-smokers.
49
The role of Alpha-1 antitrypsin
To protect cells from enzymes such as neutrophil elastase.
50
Inheritance of Alpha-1 antitrypsin (A1AT) deficiency
Autosomal recessive
51
Features of Alpha-1 antitrypsin (A1AT) deficiency
1. Usually have PiZZ genotype
2. Panacinar emphysema, mostly in lower lobes of lungs
3. Liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
52
Investigations in Alpha-1 antitrypsin (A1AT) deficiency
1. A1AT concentrations
| 2. spirometry: obstructive picture
53
Management of Alpha-1 antitrypsin (A1AT) deficiency
1. no smoking
2. supportive: bronchodilators, physiotherapy
3. IV alpha1-antitrypsin protein concentrates
4. Lung volume reduction surgery
5. lung transplantation
54
Normal PaO2 levels
Pa02 on air should be >10 kPa
| Less than this is hypoxaemic
55
Acidaemic and alkalaemic pH
Acidaemic (pH <7.35)
| Alkalaemic (pH >7.45)
56
PaCO2 > 6.0 kPa
Suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
57
PaCO2 < 4.7 kPa
Suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)
58
Bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l)
Suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
59
Bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)
Suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)
60
Low pH + high PaCO2
Acidosis
61
High pH + low PaCO2
Alkalosis
62
Low pH + low bicarbonate
Acidosis
63
High pH + high bicarbonate
Akalosis
64
Asbestos
Can cause a variety of lung disease from benign pleural plaques to mesothelioma.
65
Pleural plaques
Benign and do not undergo malignant change. They, therefore don't require any follow-up. Most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
66
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
67
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis.
A chronic lung condition that is caused by prolonged exposure to high concentrations of asbestos fibers in the air.
68
Lung changes in Asbestosis
Typically causes lower lobe fibrosis
69
Asbestosis features
As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.
70
Mesothelioma
A malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form. Mesothelioma can occur even with very limited exposure to asbestos
71
Features of Mesothelioma
1. progressive shortness-of-breath
2. chest pain
3. pleural effusion
72
Aspiration pneumonia
A pneumonia that develops as a result of foreign materials gaining entry to the bronchial tree, usually oral or gastric contents such as food and saliva.
73
Risk factors for the development of aspiration pneumonia
```
Poor dental hygiene
Swallowing difficulties
Prolonged hospitalization or surgical procedures
Impaired consciousness
Impaired mucociliary clearance
```
74
Lung changes in Aspiration pneumonia
The right middle and lower lung lobes are the most common sites affected, due to the larger calibre and more vertical orientation of the right main bronchus.
75
Most common bacteria to cause infection in Aspiration pneumonia
Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
76
Most common chronic respiratory disorder encountered in clinical practice
Asthma
77
Asthma
Defined as a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity. Symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction.
78
Risk factors for Asthma
1. personal or family history of atopy
2. Maternal smoking, viral infection during pregnancy 3. Low birth weight
4. Not being breastfed
5. Maternal smoking around child
6. Exposure to high concentrations of allergens
7. Air pollution
8. 'hygiene hypothesis'
79
Patients with asthma also suffer from other IgE-mediated atopic conditions; what are they?
1. atopic dermatitis (eczema)
| 2. allergic rhinitis (hay fever)
80
Occupational asthma
Type of asthma caused by exposure to inhaled irritants in the workplace. Diagnosed by observing reduced peak flows during the working week with normal readings when not at work.
81
Symptoms and signs of asthma
1. cough: often worse at night
2. dyspnoea
3. 'wheeze', 'chest tightness'
4. expiratory wheeze on auscultation
5. reduced peak expiratory flow rate (PEFR)
82
Spirometry
Test which measures the amount (volume) and speed (flow) of air during exhalation and inhalation.
Categorizes respiratory disorders as either obstructive or restrictive.
83
FEV1
Forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration
84
FVC
Forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration
85
Typical spirometry results in asthma
FEV1 - significantly reduced
FVC - normal
FEV1% (FEV1/FVC) < 70%
86
Investigations in asthma patients over 17
Spirometry with a bronchodilator reversibility test
All patients should have a FeNO test
Chest x-ray: particular in older patients or those with a history of smoking
87
Short-acting beta-agonists (SABA)
Salbutamol
88
Inhaled corticosteroids (ICS)
Beclometasone
Dipropionate
Fluticasone
Propionate
89
Long-acting beta-agonists (LABA)
Salmeterol
90
Leukotriene receptor antagonists
Monteleukast
91
Maintenance and reliever therapy (MART)
A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required.
92
Side effects of Short-acting beta-agonists (SABA)
> Trembling, particularly in the hands.
> Nervous tension.
> Headaches
> Suddenly noticeable heartbeats (palpitations)
> Muscle cramps
93
Inhaled corticosteroids (ICS) side effects
Candidiasis and stunted growth in children
94
LABA side effects
```
Shaking of a part of your body that you cannot control
headache
nervousness
dizziness
cough
```
95
Investigations in asthma patients under 16
All patients should have spirometry with a bronchodilator reversibility (BDR) test
FeNO test should be requested if there is normal spirometry or obstructive spirometry with a negative bronchodilator reversibility (BDR) test
96
Management of asthma
```
> SABA
> SABA + low-dose ICS
> SABA + low-dose ICS + LTRA
> SABA + low-dose ICS + LABA
> Continue LTRA depending on response to LTRA
> SABA +/- LTRA
> Switch ICS/LABA for a low-dose ICS MART
> SABA +/- LTRA + medium-dose ICS MART
> SABA +/- LTRA + high-dose ICS MART
```
97
Low dose ICS
<= 400 micrograms budesonide or equivalent
98
Moderate dose ICS
400 micrograms - 800 micrograms budesonide or equivalent
99
High dose ICS
> 800 micrograms budesonide or equivalent
100
Common chemicals that cause occupational asthma
```
ocyanates - spray painting and foam
moulding using adhesives
platinum salts
soldering flux resin
glutaraldehyde
flour
epoxy resins
proteolytic enzymes
```
101
Atelectasis
A common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.
A complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid. Atelectasis is one of the most common breathing (respiratory) complications after surgery
102
Atelectasis features
Should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively
103
Atelectasis management
> positioning the patient upright
| > chest physiotherapy: breathing exercises
104
Most common causes of bilateral hilar lymphadenopathy
Sarcoidosis and tuberculosis
105
All causes of bilateral hilar lymphadenopathy
```
> lymphoma/other malignancy
> pneumoconiosis e.g. berylliosis
> fungi e.g. histoplasmosis, coccidioidomycosis
> Sarcoidosis
> Tuberculosis
```
106
Bronchiectasis
Describes a permanent dilatation of airways secondary to chronic infection or inflammation
107
Causes of Bronchiectasis
Post-infective: tuberculosis, measles, pertussis, Pneumonia
Cystic fibrosis
Bronchial obstruction e.g. lung cancer/foreign body
Immune deficiency: selective IgA, Hypogammaglobulinaemia
Allergic bronchopulmonary aspergillosis (ABPA)
Yellow nail syndrome
108
Management of Bronchiectasis
Physical training (e.g. inspiratory muscle training)
Postural drainage
Antibiotics for exacerbations + long-term rotating antibiotics in severe cases
Bronchodilators in selected cases
Immunisations
Surgery in selected cases (e.g. Localised disease)
109
Most common organisms isolated from patients with bronchiectasis
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
110
Most common bacteria isolated from patients with bronchiectasis
Haemophilus influenzae
111
Chest drain
A tube inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity.
112
Chest drain indications
```
> Pleural effusion
> Empyema
> Haemothorax
> Haemopneumothorax
> Chylothorax
> Pneumothorax not suitable for conservative management or aspiration
```
113
Chest drain contraindications
1. INR > 1.3
2. Platelet count < 75
3. Pulmonary bullae
4. Pleural adhesions
114
Insertion of chest drain
Patient should be positioned in a supine position or at a 45º angle.
Forearm may be positioned behind the patient's head to allow easy access to the axilla.
Identify the 5th intercostal space in the midaxillary line.
115
Chest drain complications
1. Failure of insertion
2. Bleeding
3. Infection
4. Penetration of the lung
5. Re-expansion pulmonary oedema
116
Re-expansion pulmonary edema
Uncommon complication following drainage of a pneumothorax or pleural effusion. Symptoms include cough, chest discomfort and hypoxemia; if the edema is severe, shock and death may ensue.
117
How to prevent re-expansion pulmonary oedema
Recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours).
118
When are large bore chest drains used?
Trauma and haemothorax drainage
119
When are smaller diameter chest drains used?
Pneumothorax or pleural effusion drainage
120
Differentials for Chest x-ray: cavitating lung lesion findings
```
Abscess
Squamous cell lung cancer
Tuberculosis
Wegener's granulomatosis
Pulmonary embolism
Rheumatoid arthritis
Aspergillosis, histoplasmosis, Coccidioidomycosis
```
121
Common causes of lobar collapse
1. Lung cancer
2. Asthma (due to mucous plugging)
3. Foreign body
122
Most common cause of lobar collapse in older adults
Lung cancer
123
The general signs of lobar collapse on a chest x-ray
1. Tracheal deviation towards the side of the collapse
2. Mediastinal shift towards the side of the collapse
3. Elevation of the hemidiaphragm
124
Chest x-ray findings for lung metastases
Multiple, round well-defined lung secondaries are often referred to as 'cannonball metastases'. Commonly seen with renal cell cancer but may also occur secondary to choriocarcinoma and prostate cancer.
125
Causes of actual mediastinal widening
```
vascular problems: thoracic aortic aneurysm
lymphoma
retrosternal goitre
teratoma
tumours of the thymus
```
126
How can nasogastric tube position be assesed?
Chest x ray
127
Complications of misplaced nasogastric tubes
Aspiration pneumonia and death
128
Chest x-ray pulmonary oedema changes
1. interstitial oedema
2. bat's wing appearance
3. upper lobe diversion (increased blood flow to the superior parts of the lung)
4. Kerley B lines
5. pleural effusion
129
Chest x-ray: white lung lesions causes
```
consolidation
pleural effusion
collapse
pneumonectomy
specific lesions e.g. tumours
fluid e.g. pulmonary oedema
```
130
Trachea pulled toward the white-out (Chest x-ray: white lung lesions)
Pneumonectomy
Complete lung collapse
Pulmonary hypoplasia
131
Trachea pushed away from white-out (Chest x-ray: white lung lesions)
Pleural effusion
Diaphragmatic hernia
Large thoracic mass
132
Trachea central in white lung lesion findings
Consolidation
Pulmonary oedema (usually bilateral)
Mesothelioma
133
Cardiac causes of finger clubbing
Cyanotic congenital heart disease
Bacterial endocarditis
Atrial myxoma
134
Respiratory causes of finger clubbing
```
Lung cancer
Cystic fibrosis
Bronchiectasis
Abscess
Empyema
Tuberculosis
Asbestosis, mesothelioma
```
135
Coal workers' pneumoconiosis
An occupational lung disease caused by long term exposure to coal dust particles. Commonly experienced by those who have been involved in the coal mining industry and severity is linked to the extent of exposure.
136
Pathophysiology of Coal workers' pneumoconiosis
Dust reaches the terminal bronchioles and is engulfed by alveolar and interstitial macrophages.
Dust particles are then moved by the macrophages via the mucociliary elevator and removed from the body as mucus.
In coal miners who are exposed over many years, the system is overwhelmed and the macrophages begin to accumulate in the alveoli, which starts an immune response, causing damage to the lung tissue.
137
The two presentations for Coal workers' pneumoconiosis
Simple pneumoconiosis:
| Progressive Massive Fibrosis
138
Simple pneumoconiosis
Commonest type of pneumoconiosis
Patients are often asymptomatic
Increases the risk of lung diseases
May lead to Progressive Massive Fibrosis (PMF)
Pneumoconiosis is one of a group of interstitial lung disease caused by breathing in certain kinds of dust particles that damage your lungs
139
Commonest type of pneumoconiosis
Simple pneumoconiosis
140
Progressive Massive Fibrosis
Round fibrotic masses most commonly in the upper lobes.
The exact pathogenesis is not known.
Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
141
Progressive Massive Fibrosis symptoms
Often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
142
Coal workers' pneumoconiosis
Chest x-ray: upper zone fibrosis
Spirometry: restrictive picture on lung function tests
143
Pneumoconiosis
Accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis.
144
Most common cause of COPD
Smoking
145
Causes for COPD
```
Smoking
Alpha-1 antitrypsin deficiency
Cadmium (used in smelting)
Coal
Cotton
Cement
Grain
```
146
What is COPD?
Refers to a group of diseases that cause airflow blockage and breathing-related problems. It includes emphysema and chronic bronchitis.
147
COPD features
Cough: often productive
Dyspnoea
Wheeze
Severe cases, right-sided heart failure
148
Investigations in COPD
1. Spirometry (obstructive picture)
2. Chest x-ray
3. Full blood count
4. Body mass index (BMI) calculation
149
Chest x-ray changes in COPD
> hyperinflation
> bullae
> flat hemidiaphragm
> also important to exclude lung cancer
150
Stage 1 COPD (mild)
FEV1/FVC < 0.7
| FEV1 of predicted >80%
151
Stage 2 COPD (moderate)
FEV1/FVC < 0.7
| FEV1 of predicted = 50-79%
152
Stage 3 COPD (severe)
FEV1/FVC < 0.7
| FEV1 of predicted 30-49%
153
Stage 4 COPD (very severe)
FEV1/FVC < 0.7
| FEV1 of predicted <30%
154
General management for all COPD patients
> Smoking cessation advice
> Annual influenza vaccination
> One-off pneumococcal vaccination
> Pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD
155
First line management for COPD
SABA or SAMA
156
Second line management for COPD patients
Breathless or have exacerbations despite SAMA/SABA the next step is determined by whether the patient has 'asthmatic features/features suggesting steroid responsiveness'
No asthmatic features/features suggesting steroid responsiveness
add LABA + LAMA - already taking a SAMA, discontinue and switch to a SABA
Asthmatic features/features suggesting steroid responsiveness
LABA + inhaled corticosteroid (ICS)
157
Third line treatment for COPD in patients with and without asthma features
LABA + LAMA + ICS
158
When is oral prophylactic antibiotic therapy recommeneded in COPD patients?
Patients should not smoke, have optimised standard treatments and continue to have exacerbations
159
What antibiotic is used for oral prophylactic antibiotic therapy in COPD patients?
Azithromycin
160
When are mucolytics indicated in COPD?
Should be 'considered' in patients with a chronic productive cough and continued if symptoms improve
161
Anion gap calculation
(Na+ + K+) - (Cl- + HCO3-)
162
Normal chloride ion levels
The normal range = 10-18 mmol/L
163
Normal anion gap ( = hyperchloraemic metabolic acidosis) causes
1. Bicarbonate loss: diarrhoea, fistula
2. Renal tubular acidosis
3. Drugs: e.g. acetazolamide
4. Ammonium chloride injection
5. Addison's disease
164
Raised anion gap causes
1. Lactate: shock, hypoxia
2. Ketones: diabetic ketoacidosis, alcohol
3. Urate: renal failure
4. Acid poisoning: salicylates, methanol
165
Metabolic alkalosis
A rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate.
166
Causes of metabolic alkalosis
```
Vomiting / aspiration
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
Congenital adrenal hyperplasia
```
167
Mechanism of metabolic alkalosis
Activation of RAAS is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality
168
Causes of Respiratory acidosis
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose
169
Causes of Respiratory alkalosis
```
> Anxiety leading to hyperventilation
> Early salicylate poisoning*
> Stroke, subarachnoid haemorrhage,
> encephalitis
> Pregnancy
> Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude
```
170
Respiratory alkalosis mechanism
Hyperventilation resulting in excess loss of carbon dioxide - result in increasing pH
171
Respiratory acidosis mechanism
Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
172
Methylxanthines (e.g. theophylline) mechanism of action
Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP
173
Monteleukast, zafirlukast mechanism of action
Blocks leukotriene receptors
174
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
An ANCA associated small-medium vessel vasculitis
175
Another name for Eosinophilic granulomatosis with polyangiitis
Churg-Strauss syndrome
176
Features of Eosinophilic granulomatosis with polyangiitis
```
asthma
blood eosinophilia
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%
```
177
Extrinsic allergic alveolitis
A condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles. Thought largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.
178
Classifications of Extrinsic allergic alveolitis
1. bird fanciers' lung
2. farmers lung
3. Malt workers' lung
4. mushroom workers' lung
179
Cause of farmers lung (Type of EAA)
Spores of Saccharopolyspora rectivirgula from wet hay
180
Cause of Malt workers' lung (type of EAA)
Aspergillus clavatus
181
Causes of mushroom workers' lung (type of EAA)
Thermophilic actinomycetes*
182
Acute presentation of EAA
Occurs 4-8 hrs after exposure
dyspnoea
dry cough
fever
183
Chronic presentation of EAA
```
Occurs weeks-months after exposure
lethargy
dyspnoea
productive cough
anorexia and weight loss
```
184
Investigations in EAA
Imaging: upper/mid-zone fibrosis
Serologic assays - specific IgG antibodies
Blood: NO eosinophilia
185
EAA chest x-ray changes
Upper/mid-zone fibrosis
186
Management of EAA
1. avoid precipitating factors
| 2. oral glucocorticoids
187
Granulomatosis with polyangiitis (Wegener's granulomatosis)
An autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.
188
Features of Granulomatosis with polyangiitis (Wegener's granulomatosis)
1. Epistaxis, sinusitis, nasal crusting
2. Dyspnoea, haemoptysis
3. Rapidly progressive glomerulonephritis
4. Saddle-shape nose deformity
189
Another name for Granulomatosis with polyangiitis
Wegener's granulomatosis
190
Investigations in Granulomatosis with polyangiitis
cANCA positive in > 90%, pANCA positive in 25%
Renal biopsy - epithelial crescents in Bowman's capsule
191
Management of Granulomatosis with polyangiitis
> steroids
> cyclophosphamide (90% response)
> plasma exchange
192
Renal biopsy findings in Granulomatosis with polyangiitis
Epithelial crescents in Bowman's capsule
193
Idiopathic pulmonary fibrosis
A chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis, IPF is used when no underlying cause exists.
194
Epidemiology of Idiopathic pulmonary fibrosis
Typically seen in patients aged 50-70 years and is twice as common in men.
195
Features of Idiopathic pulmonary fibrosis
Progressive exertional dyspnoea
Bibasal fine end-inspiratory crepitations
Dry cough
Clubbing
196
Investigations in Idiopathic pulmonary fibrosis
Restrictive results on spirometry
Impaired gas exchange: reduced TLCO
Imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - 'ground-glass' - later progressing to 'honeycombing') may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
ANA positive in 30%,
197
Imaging findings in Idiopathic pulmonary fibrosis
Bilateral interstitial shadowing (typically small, irregular, peripheral opacities - 'ground-glass' - later progressing to 'honeycombing') may be seen on a chest x-ray
High-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
198
Management of Idiopathic pulmonary fibrosis
Pulmonary rehabilitation
| Many patients will require supplementary oxygen and eventually a lung transplant
199
Klebsiella pneumoniae
A Gram-negative rod that is part of the normal gut flora. Can cause a number of infections in humans including pneumonia and urinary tract infections.
200
Features of Klebsiella pneumonia
More common in alcoholic and diabetics
May occur following aspiration
'red-currant jelly' sputum
Often affects upper lobes
201
Small cell lung cancer features
Usually central
ADH → hyponatraemia
ACTH → Cushing's syndrome & can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome
202
Squamous cell lung cancer features
Parathyroid hormone-related protein secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH
203
Adenocarcinoma features
Gynaecomastia
| HPOA
204
Investigations for lung cancer
```
Chest x-ray
CT
Bronchoscopy
PET scanning
Bloods
```
205
When is PET scanning used in lung cancer?
Typically done in non-small cell lung cancer to establish eligibility for curative treatment
206
When is bronchoscopy used in lung cancer?
Allows a biopsy to be taken to obtain a histological diagnosis sometimes aided by endobronchial ultrasound
207
Lung cancer: non-small cell management
Only 20% suitable for surgery
Mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement
Curative or palliative radiotherapy
Poor response to chemotherapy
208
Lung cancer classifications
Small cell lung cancer (SCLC)
| Non-small cell lung cancer (NSCLC)
209
Non-small cell lung cancer (NSCLC) further classifications
```
adenocarcinoma
squamous
large cell
alveolar cell carcinoma
bronchial adenoma
```
210
Most common type of lung cancer
Adenocarcinoma
211
What lung cancer is seen in non-smokers?
Adenocarcinoma & alveolar cell carcinoma
212
Acronym for causes of upper zone fibrosis
```
C - Coal worker's pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
```
213
Fibrosis predominately affecting the lower zones
idiopathic pulmonary fibrosis
most connective tissue disorders
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis
214
What drugs cause lung fibrosis of lower lungs?
amiodarone, bleomycin, methotrexate
215
Contents of Superior mediastinum
```
Superior vena cava
Brachiocephalic veins
Arch of aorta
Thoracic duct
Trachea
Oesophagus
Thymus
Vagus nerve
Left recurrent laryngeal nerve
Phrenic nerve
```
216
Contents of middle mediastinum
```
Pericardium
Heart
Aortic root
Arch of azygos vein
Main bronchi
```
217
Contents of Anterior mediastinum
Thymic remnants
Lymph nodes
Fat
218
Contents of Posterior mediastinum
```
Oesophagus
Thoracic aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves
```
219
Mesothelioma
A cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure.
220
Microscopic polyangiitis
A small-vessel ANCA vasculitis
221
Non-invasive ventilation - key indications
1. COPD with respiratory acidosis pH 7.25-7.35
2. Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
3. Cardiogenic pulmonary oedema unresponsive to CPAP
222
Predisposing factors for Obstructive sleep apnoea/hypopnoea syndrome
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan's syndrome
223
Assessment for sleepiness in Obstructive sleep apnoea/hypopnoea syndrome
Epworth Sleepiness Scale
| Multiple Sleep Latency Test (MSLT)
224
Diagnosis of Obstructive sleep apnoea/hypopnoea syndrome
Sleep studies (polysomnography
225
Management of Obstructive sleep apnoea/hypopnoea syndrome
> Weight loss
> CPAP
> DVLA should be informed
226
Oxygen dissociation curve
Describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration
227
The L rule in Oxygen dissociation curve (shifts to left)
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature
228
Oxygen dissociation curve (shifts to right?
Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG*
Raised temperature
229
What does it mean when the Oxygen dissociation curve shifts to the right?
Raised oxygen delivery
230
What does it mean when the Oxygen dissociation curve shifts to the left?
Lower oxygen delivery
231
Oxygen saturation targets
Acutely ill patients: 94-98%
| Patients at risk of hypercapnia (e.g. COPD patients): 88-92%
232
Pleural effusion classifications
Transudate
| Exudate
233
Pleural effusion
Build-up of excess fluid between the layers of the pleura outside the lungs. The pleura are thin membranes that line the lungs and the inside of the chest cavity and act to lubricate and facilitate breathing.
234
Transudate causes of pleural effusions
```
(< 30g/L protein)
heart failure
hypoalbuminaemia
hypothyroidism
Meigs' syndrome
```
235
Most common transudate cause of pleural effusion
Heart failure
236
Exudate causes of pleural effusions
```
Exudate (> 30g/L protein)
infection: pneumonia, TB, subphrenic abscess
connective tissue disease: RA, SLE
neoplasia: lung cancer, mesothelioma, metastases
pancreatitis
pulmonary embolism
Dressler's syndrome
yellow nail syndrome
```
237
Most common exudate cause of pleural effusion
Pneumonia
238
Exudate protein concentration
(> 30g/L protein)
239
Transudate protein concentration
(< 30g/L protein)
240
Features of Pleural effusions
Dyspnoea, non-productive cough or chest pain
Classic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion
241
Pleural aspiration for pleural effusions
Ultrasound is recommended to reduce the complication rate
A 21G needle and 50ml syringe should be used
Fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
242
Managing patients with recurrent pleural effusions include
recurrent aspiration
pleurodesis
indwelling pleural catheter
drug management to alleviate symptoms
243
Investigations for pleural effusion
Posterioranterior (PA) chest x-rays
Ultrasound
Contrast CT
Pleural aspiration
244
Heavy blood staining in pleural effusion causes
Mesothelioma, pulmonary embolism, tuberculosis
245
Low glucose pleural effusion causes
rheumatoid arthritis, tuberculosis
246
Raised amylase pleural effusion causes
pancreatitis, oesophageal perforation
247
Pleural infection management
All patients with a pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling
if the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage
if the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed
248
Most common type of pneumonia
Bacterial
249
Causes of pneumonia
Bacterial, viral & fungal
250
Pneumonia
Describes any inflammatory condition affecting the alveoli of the lungs, but in the vast majority of patients this is secondary to a bacterial infection.
251
Idiopathic interstitial pneumonia
A group of non-infective causes of pneumonia - Examples include cryptogenic organizing pneumonia which describes a form of bronchiolitis that may develop as a complication of rheumatoid arthritis or amiodarone therapy.
252
Community-acquired pneumonia (CAP)
Develop pneumonia within the community, i.e. outside of hospital
253
Signs and symptoms of pneumonia
```
Cough
Sputum
Dyspnoea
Pleuritic chest pain
Fever
Tachycardia
Reduced oxygen saturations
Reduced breath sounds
Bronchial breathing
```
254
Chest x-ray changes in pneumonia
Consolidation
255
Investigations in Pneumonia
```
Chest x-ray - consolidation
Full blood count - Neutrophilia in bacterial infections
Urea and electrolytes
CRP - raised in response to infection
Arterial blood gases
```
256
Management of Pneumonia
1. Antibiotics: treat underlying infection
2. Oxygen therapy if hypoxaemic
3. IV fluids if hypotensive/dehydration
257
CURB-65
Risk stratification process using a scoring system called CURB-65 - grades the severity of community-acquired pneumonia and risk of death
258
CURB65 calculation
C Confusion (abbreviated mental test score <= 8/10)
U Urea > 7
R Respiration rate >= 30/min
B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65 Aged >= 65 years
259
Management of Pneumonia depending on CURB65 score
Home-based care for patients with a CRB65 score of 0 - oral amoxicillin is generally used first-line
Hospital assessment for all other patients, particularly those with a CRB65 score of 2 or more.
260
Risk factors of Pneumothroax
Pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
Connective tissue disease: Marfan's syndrome, rheumatoid arthritis
Ventilation
261
Symptoms of Pneumothorax
```
> dyspnoea
> chest pain: often pleuritic
> sweating
> tachypnoea
> tachycardia
```
262
Primary pneumothorax management
If the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
Otherwise, aspiration should be attempted
If this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
263
Primary Pneumothorax
Primary if there is no underlying lung disease and secondary if there is.
264
Secondary pneumothorax management
If the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
Otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted.
All patients should be admitted for at least 24 hours - if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
265
Contraindications after treated for pneumothroax
1. Smoking
2. Fitness to fly - may travel 2 weeks after successful drainage if there is no residual air.
3. Scuba diving
266
Restrictive lung disease
FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
267
Obstructive lung disease
FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced
268
Obstructive lung disease causes
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans
269
Restrictive lung disease causes
```
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity
```
270
Expiratory reserve volume
maximum volume of air that can be expired at the end of a normal tidal expiration
271
Inspiratory reserve volume (IRV)
maximum volume of air that can be inspired at the end of a normal tidal inspiration
272
Tidal volume (TV)
volume inspired or expired with each breath at rest
273
Residual volume (RV)
volume of air remaining after maximal expiration
increases with age
274
Functional residual capacity (FRC)
the volume in the lungs at the end-expiratory position
| FRC = ERV + RV
275
Vital capacity (VC)
maximum volume of air that can be expired after a maximal inspiration
4,500ml in males, 3,500 mls in females
Decreases with age
276
Total lung capacity (TLC)
The sum of the vital capacity + residual volume
277
Centor criteria
presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough
278
Sarcoidosis
A multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent
279
Sarcoidosis features
```
Erythema nodosum
bilateral hilar lymphadenopathy,
swinging fever
polyarthralgia
dyspnoea
non-productive cough
malaise
weight loss
Hypercalcaemia
```
280
Why is there hypercalcaemia in sarcoidosis?
Macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
281
Lofgren's syndrome
An acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis
282
Mikulicz syndrome
There is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma
283
Heerfordt's syndrome
(uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis
284
Investigations in Sarcoidosis
A chest x-ray
Spirometry: may show a restrictive defect
Tissue biopsy: non-caseating granulomas
285
Sarcoidosis stages on chest x-ray
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis
286
Indications for steroids in Sarcoidosis
Chest x-ray stage 2 or 3 disease who are symptomatic.
Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
Hypercalcaemia
Eye, heart or neuro involvement
287
Silicosis
A fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing TB (silica is toxic to macrophages).
288
Occupations at risk of silicosis
mining
slate works
foundries
potteries
289
Features of silicosis
fibrosing lung disease
| 'egg-shell' calcification of the hilar lymph nodes
290
What is a disease that can develop with silicosis?
TB (silica is toxic to macrophages).
291
Tension pneumothorax
May occur following thoracic trauma when a lung parenchymal flap is created. This acts as a one way valve and allows pressure to rise.
The trachea shifts and hyper-resonance is apparent on the affected side.
292
Treatment of Tension pneumothorax
Treatment is with needle decompression and chest tube insertion.
293
Features of tension pneumothorax
The trachea shifts and hyper-resonance is apparent on the affected side.
294
Transfer factor
Describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion.
295
Causes of a lower TLCO
```
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
```
296
Causes of a raised TLCO
```
asthma
Wegener's, Goodpasture's
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise
```
