Respiratory Flashcards
1
Q
Define asthma
A
Chronic inflammatory airway disease characterised by intermittent reversible airway obstruction, bronchial hyper-responsiveness and inflammation
2
Q
What is the aetiology of asthma?
A
Multi-gene association interacting with environmental exposure
- Initial trigger leads to the release of inflammatory mediators
- Activation and migration of other inflammatory cells.
- Th2 lymphocytic response - release of interleukins, chemokines etc.
- Inflammatory cells move to the airway, causing changes in the epithelium, airway tone, hyper-secretion of mucus, mucociliary function alteration and increased smooth muscle responsiveness.
Acute: SM contraction leading to bronchoconstriction Mucus hypersecretion Oedema Airway obstruction
Chronic:
Proliferation of SM cells and fibroblasts causing airway remodelling
3
Q
What are the risk factors of asthma?
A
Family history Atopic history - eczema, dermatitis, allergic rhinitis Obesity GORD Nasal polyposis
Exposure to allergens/precipitants: Cats Dogs Cockroaches Dust mites Fungal spores Tobacco smoke Fumes from chemicals eg bleach Pollen from trees, weeds, and grass. Viral infections - rhinovirus, influenza Bacterial infections - Mycoplasma pneumoniae, chlamydia pneumoniae Cold Exercise Extreme emotion
4
Q
Summarise the epidemiology of asthma
A
Affects 10% of adults and 5% of children
Prevalence is increasing
Highest hospitalisation rates and asthma deaths were amongst black patients
5
Q
What are the presenting symptoms of asthma?
A
Cough
Wheeze
SOB/dyspnoea precipitated by allergen exposure
Chest pain/tightness
Nocturnal symptoms
Worse at night
Variation in symptoms (episodic history) - sometimes fine and sometimes symptomatic
Previous hospitalisation for asthma
6
Q
What are the signs on physical examination of asthma?
A
Nasal polyps/congestion Polyphonic high-pitched expiratory wheeze Tachypnoea Prolonged expiratory phase Hyperinflated chest Chest may be silent in severe asthma
7
Q
What are the appropriate investigations for asthma?
A
Forced Expiratory Volume in 1 second/Forced Vital Capacity - <80% of predicted
FEV1 <80% of expected
PEFR - variation >20% over 3 days a week over several weeks. >20% increase following bronchodilator therapy
ACUTE: Peak flow Pulse oximetry ABG CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax). Normal or hyperinflated. May show signs of infection. FBC - raised WCC if infective exacerbation CRP U&Es Blood and sputum cultures
CHRONIC:
Peak flow monitoring - often shows diurnal variation with a dip in the morning
Pulmonary function test
Bloods - Eosinophilia, IgE level, Aspergillus antibody titres
Skin prick tests - identify allergens
8
Q
What is the management of an acute exacerbation of asthma?
A
ABCDE and necessary resuscitation
Monitor O2 sats, ABG, PEFR and U&Es (K+ lowered by bronchodilators)
High-flow oxygen (get to 94-98%)
Salbutamol nebulizer (5 mg initially continuously, then 2-4 hourly)
Nebulised Ipratropium bromide (0.5 mg QDS)
Steroid therapy: 100-200 mg IV hydrocortisone. THEN, 40 mg oral prednisolone for 5-7 days
If no improvement - IV magnesium sulphate
Consider IV aminophylline infusion
Consider IV salbutamol
May need ITU and ventilation if fatiguing.
- Normal PCO2 is a BAD SIGN as they should be hyperventilating and blowing off their CO2 (PCO2 should be low)
Treat underlying cause (e.g. antibiotics if it is an infective exacerbation)
DISCHARGE when: PEF > 75% predicted Diurnal variation < 25% Inhaler technique checked Stable on discharge medication for 24 hours Patient owns a PEF meter Patient has steroid and bronchodilator therapy Arrange follow-up
9
Q
What is the management of chronic asthma?
A
Start on the step that matches the severity of the patient’s asthma
- Inhaled short-acting beta-2 agonist used as needed eg SALBUTAMOL
If needed > 1/day then move onto step 2 - SABA + regular inhaled low-dose steroids (400mcg/day)
- SABA + low-dose steroids + inhaled long-acting beta-2 agonist
If inadequate control with LABA, increase steroid dose (800 mcg/day)
If no response to LABA, stop LABA and increase steroid dose (800 mcg/day) - Increase inhaled steroid dose (2000 mcg/day)
Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet) - Add regular oral steroids
Maintain high-dose oral steroids
Refer to specialist care
10
Q
What are the possible complications of asthma?
A
Exacerbations Airway remodelling Oral candidiasis secondary to incorrect use of inhaled corticosteroids Growth retardation Chest wall deformity – Harrison’s sulcus Recurrent infections Pneumothorax Respiratory failure Death
11
Q
What is the prognosis of asthma?
A
Patients with well-controlled asthma have the same life expectancy as patients without
Many children improve as they get older
Adult-onset asthma is usually chronic
12
Q
Define COPD
A
A chronic progressive lung condition that is characterised by irreversible airflow obstruction which encompasses emphysema and chronic bronchitis.
13
Q
What is emphysema and describe its aetiology?
A
Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles
Destruction and enlargement of alveoli due to elastin breakdown, causing loss of the elastic traction that keeps small airways open in expiration.
14
Q
What is chronic bronchitis and describe its aetiology?
A
Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
Narrowing of the airways due to bronchiole inflammation and bronchi with mucosal oedema, mucous hypersecretion (increased goblet cell size and number) and squamous metaplasia
15
Q
What are the causes/risk factors of COPD?
A
CIGARETTE SMOKING Advanced age White ancestry Air pollution Occupational exposure (dust, traffic fumes, sulphur dioxide) Male sex Developmentally abnormal lung Genetic disorders eg alpha-1 antitrypsin deficiency (common cause in young, non-smokers)
16
Q
Summarise the epidemiology of COPD
A
More common in those over 65 years old
Slightly higher prevalence in men
Very common - prevalence up to 8%
17
Q
What are the presenting symptoms of COPD?
A
Chronic cough and white frothy sputum production (often in morning) Progressively worsening SOB Fatigue Wheeze Reduced exercise tolerance History of smoking
18
Q
What are the signs on physical examination of COPD?
A
Barrel chest Hyper-resonance on auscultation Quiet breath sounds, prolonged expiration, crepitations Wheeze Coarse crackles Tachypnoea Tchycardic Asterixis Cyanosis Clubbing Use of accessory muscles Bounding pulse
In late stages, signs of right heart failure i.e. raised JVP, ankle oedema, RV heave
19
Q
What are appropriate investigations for COPD?
A
Spirometry - FEV1/FVC <0.7
Pulse oximetry - low O2 sats (88-90%)
CXR - hyperinflation (>6 anterior ribs visible, flat hemidiaphragms)
ECG - risk factors for COPD similar to those of IHD
Alpha-1 antitrypsin
Acute presentation:
ABG - PaCO2 >50mmHg +/- PaO2 <60mmHg suggests respiratory insufficiency
FBC - increased WCC and haematocrit, raised Hb (secondary polycythaemia)
Sputum culture
20
Q
What is the management of an acute exacerbation of COPD?
A
Short acting bronchodilator
Systemic corticosteroid which is transferred to inhaled corticosteroid
Airway clearance techniques (respiratory physio to clear sputum)
Supplementary O2 - 24% via non-variable flow Venturi Mask (aim for 88-92% O2 sats)
Antibiotics if infectious exacerbation
Non-invasive positive pressure ventilation if respiratory insufficiency (BiPAP)
Prevent infective exacerbations: pneumococcal & influenza vaccination
21
Q
What is the management of COPD?
A
Short or long-acting bronchodilator (SABA or LABA, anti-cholinergics eg ipratropium bromide via inhaler or nebs)
If LABAs used >2 exacerbations per year - use steroids (oral eg prednisolone or inhaled eg budesonide)
Patient education and prophylactic vaccination
Smoking cessation
Pulmonary rehabilitation
Long term O2 therapy
22
Q
What are possible complications of COPD?
A
Cor pulmonale - R sided heart failure secondary to long-standing COPD (chronic hypoxia - pulmonary vasoconstriction - pulmonary hypertension) Recurrent pneumonia Pneumothorax Respiratory failure Anaemia Secondary polycythaemia
23
Q
What is the prognosis of COPD?
A
Variable prognosis dependent on genetic predisposition, environmental exposure, comorbidities
High level of morbidity
Three-year survival rate 90% if <60 years old, FEV1>50% predicted
Three-year survival rate 75% if >60 years old and FEV1 40-49% predicted.
24
Q
Define acute respiratory distress syndrome
A
Syndrome of acute and persistent lung inflammation with increased vascular permeability due to non-cardiogenic pulmonary oedema.
25
What are the four characteristics of Acute Respiratory Distress syndrome?
1. Symptoms occur within 1 weeks of insult
2. CXR shows diffuse bilateral opacities
3. Pulmonary oedema cannot be explained by heart failure (no clinical evidence for increased left atrial pressure so PCWP <18mmHg)
4. PaO2:FiO2 < 300mmHg (hypoxaemia regardless of level of positive-end expiratory pressure)
26
Summarise the aetiology of acute respiratory distress syndrome
Systemic inflammation causes cytokines secretion leading to damage to alveolar or capillary endothelium.
Increases permeability of membrane, leading to fluid moving into alveoli - PULMONARY OEDEMA.
Fluid prevents normal gas exchange and surfactant is diluted leading to eventual alveolar collapse - DECREASED LUNG COMPLIANCE.
27
What are risk factors for acute respiratory distress syndrome?
```
Sepsis - pneumonia, UTI, infected intravenous line
Acute pancreatitis
Burns injury
Trauma
Near drowning
DIC
Toxic smoke inhalation
Aspiration of gastric contents
Transfusion
Drug overdose/reaction
Transplantation
```
28
Summarise the epidemiology of acute respiratory distress syndrome
Annual UK incidence ~ 1 in 6000
Critical illness, cigarette smoking and alcohol use are predisposing factors.
Most common cause is sepsis
29
What are the presenting symptoms of acute respiratory distress syndrome?
```
Severe shortness of breath
Rapidly worsening respiratory failure
Cough
Respiratory distress
Dyspnoea
```
30
What are the signs on physical examination of acute respiratory distress syndrome?
```
Cyanosis
Tachypnoea
Hypoxaemia
Diffuse crackles on auscultation - widespread inspiratory crepitations
Tachycardia
Signs are BILATERAL
```
31
What are the appropriate investigations for acute respiratory distress syndrome?
CXR - will show bilateral opacities if ARDS
ABG - low PaO2 - HYPOXAEMIA
Investigations to determine cause:
Sputum culture - positive for infectious agent if sepsis is cause
Blood culture - test for any underlying infection causing sepsis
Urine culture - test for any underlying infection eg UTI causing sepsis
Amylase and lipase - raised if acute pancreatitis is underlying cause
Bloods - FBC, U&E, LFT, ESR/CRP, clotting
Investigations to rule out cardiogenic pulmonary oedema:
Serum BNP - raised if due to heart failure
Echo - if due to heart failure would show decreased ejection fraction or abnormal relaxation of myocardium
Pulmonary artery catheterization: PCWP <18 mmHg (if higher suggests heart failure as cause of pulmonary oedema due to raised pulmonary BP)
32
Define pulmonary embolism
Occlusion of the pulmonary vasculature (usually pulmonary arteries) by a venous thromboembolus usually from the deep veins of the lower limbs.
33
Summarise the aetiology and risk factors of pulmonary embolism
VIRCHOW'S TRIAD
A venous thromboembolus travels through the circulation to the pulmonary vasculature where it causes an occlusion
Usually from a DVT in the lower limb.
Most PEs originate from the veins above the knee
Rarely from right atrium in patients with AF
Other embolising agents: amniotic fluid, air, fat, tumour, septic emboli (from Right Sided Endocarditis)
```
Risk factors:
Bed ridden >3 days
Recent surgery <12 weeks
Recent long haul flight or care journey
Sedentary lifestyle
OCP
Genetic coagulation disorders - factor V leiden, protein C deficiency
Trauma
Pregnancy
Obesity
Active cancer
Smoking
Varicose veins
Previous or FHx of DVT or thromboembolic event
```
34
Summarise the epidemiology of pulmonary embolism
Relatively common especially in hospitalised patients
| Occur in 10-20% of people with confirmed proximal DVT
35
What are the presenting symptoms of pulmonary embolism?
Small PE - asymptomatic
```
Sudden onset, severe, PLEURITIC chest pain
Chest pain better on leaning forwards
Dyspnoea
Cough
Haemoptysis
Fatigue
Fever
Feeling of apprehension
```
```
Large (or proximal):
Shock
Syncope
Acute right heart failure
Sudden death
```
Symptoms of DVT:
Unilateral, painful, erythematous swelling of leg
36
What are the signs on physical examination of pulmonary embolism?
Small: often no clinical signs, however, the earliest signs are tachycardia and tachypnoea
```
Moderate:
Tachypnoea
Tachycardia
Pleural Rub
Hypoxaemia
```
Massive PE:
Shock (increased HR and RR, decreased BP)
Cyanosis
Signs of Right Heart Strain (increased JVP, Left parasternal heave, accentuated S2 heart sound)
Multiple small recurrent:
Signs of pulmonary HTN and right heart failure
37
What are the appropriate investigations for a pulmonary embolism?
Wells Score: should be calculated in patients with suspected PE
CTPA - direct visualisation of of thrombus in pulmonary artery - DIAGNOSTIC!!
Ventilation-Perfusion (V/Q) Scan - area is ventilated but NOT perfused. If negative, excludes PE
D-dimer - elevated
ECG - sinus tachycardia, right axis deviation, RBB
CXR: often normal, but done to exclude other DDx
Echo: may show right heart strain
Doppler USS Lower Limbs: to examine for venous thrombosis
ABG - respiratory alkalosis
38
What is the management of a pulmonary embolism?
DVT prevention:
Compression stockings
Regular calf exercises in periods of immobility
Heparin prophylaxis i.e. pre-surgery
Early mobilisation and hydration post-surgery
Prevention of further PE:
Anticoagulation eg warfarin, heparin
Surgically place filter in IVC
If Haemodynamically stable:
Respiratory Support: Supplemental high concentration O2 (Target saturations 94-8%)
Anticoagulation with heparin or LMW heparin
Change to oral warfarin therapy (INR 2-3) for a minimum of 3 months
Analgesia
```
If Haemodynamically Unstable:
Resuscitate: give O2 and IV fluid
Thrombolysis i.e. Alteplase
Vasoactive agents for Hypotension i.e. noradrenaline
Anticoagulation i.e. LMWH
```
Thrombectomy if needed
39
What are the possible complications of pulmonary embolism?
```
Sudden cardiac death
Cardiac arrest
Right heart failure
Pulmonary hypertension
Recurrent venous thromboembolism
Pulmonary infarction
```
40
Summarise the prognosis of pulmonary embolism
30% mortality in untreated (8% in those with treatment due to recurrent emboli)
Patients have an increased risk of future thromboembolic events
41
Define sarcoidosis
A chronic granulomatous disorder of exclusion which commonly affects the lungs, skin and eyes. It is associated with the formation of non-caseating granulomas and accumulation of lymphocytes and macrophages.
42
Summarise the aetiology and risk factors of sarcoidosis
Aetiology is unknown
```
Risk factors:
African American
Scandinavian origin
Age 20-40 years
Female
Family history of sarcoidosis
Recent infection with mycobacterium tuberculosis or borrelia burgdorferi
```
43
Summarise the epidemiology of sarcoidosis
Higher incidence in those of Scandinavian descent
Women are more likely to have eye and neurological involvement and have erythema nodosum
Men are more likely to be hypercalcaemic
44
What are the presenting symptoms of sarcoidosis?
```
Fever
Weight loss
Fatigue
Dyspnoea
Visual changes - blurred vision
Non-productive cough
Wheezing (bronchospasm due to airway hyperactivity)
Red, painful eye
Arthralgia (pain in knees, ankles and wrists)
```
45
What are the signs on physical examination of sarcoidosis?
Rhonchi (bronchospasm due to airway hyperactivity)
Arthralgia with NO synovial thickening on examination
Lymphadenopathy - enlarged, non-tender (cervical, submandibular nodes involved)
Photophobia (usually indicated uveitis)
Tender Erythema nodosum (on lower extremities)
Lupus pernio (hardened plaques with discolouration of nose, cheeks, lips & ears)
Conjunctival Nodules (with ocular involvement)
Facial Palsy
Arrhythmias
46
What are the appropriate investigations of sarcoidosis?
CXR: BILATERAL HILAR LYMPHADENOPATHY and non-caseating granulomas
Hilar and/or paratracheal adenopathy with upper lobe predominant, bilateral infiltrates; pleural effusions (rare) and egg shell calcifications (very rare) may be seen
Bloods:
Calcium - elevated as macrophages produce this
ACE - elevated as T cells produce this
Serum Urea & Creatinine (may be elevated)
Liver Enzymes (elevated)
Pulmonary Function: monitoring, persistent decline in FVC indicates disease progression
ECG: to exclude or confirm cardiac involvement
CT
Bronchoalveolar Lavage - increased T cells
Biopsy - shows non-caseating granulomas
47
Define tuberculosis
Tuberculosis is an infectious granulomatous disease caused by mycobacterium tuberculosis that mainly affects the lungs. It can remain latent in patients for a long time.
48
Explain the aetiology and risk factors of tuberculosis
TB is caused by mycobacterium tuberculosis and is passed via inhalation of aerolised droplets containing mycobacterium
Mycobacterium Tuberculosis is an intracellular organism that survives after being phagocytosed in macrophages.
```
Risk factors:
Immunosuppression eg HIV
Iatrogenic immunosuppression eg corticosteroid use
Living in or visiting an endemic country
Systemic diseases - COPD, diabetes, end-stage renal disease
Age extremes
Exposure to infectious TB case
IV drug use
Apical fibrosis
Silicosis
```
49
Summarise the epidemiology of tuberculosis
9th leading cause of death worldwide
Leading cause of death from a single infectious agent
More than half of all cases were in either India, Indonesia, China, the Phillipines or Pakistan
Most common in Asian patients
2 billion people are infected worldwide
50
What are the presenting symptoms of tuberculosis?
Primary TB is often asymptomatic
Most patients have mild flu-like symptoms
```
Fever
Weight loss
Night sweats
Cough
Haemoptysis
Fatigue
Loss of appetite
```
Rare: dyspnoea, pleuritic chest pain
51
What are the signs on physical examination of tuberculosis?
```
Lymphadenitis
Anorexia
Abnormal chest auscultation - crackles, bronchial breath sounds
Clubbing
Erythema Nodosum
```
If leads to systemic miliary TB - signs and symptoms of other organs affected eg hepatomegaly if hepatitis caused
52
What are the appropriate investigations for TB?
PPD intradermal skin test/tuberculin/mantoux test:
Tuberculin injected between layers of dermis
Immune reaction with 48-72 hours if previously infected (large area of induration)
Interferon gamma release assay - looks for evidence in blood of mycobacterium
CXR - fibronodular opacities in upper lobes with or without cavitation. Ghon complex (ghon focus and caseating hilar lymph node), calcification, hilar lymphadenopathy
Sputum sample/bronchoalveolar lavage - staining, culture, PCR - positive for acid-fast bacilli
FBC - high WBC, low Hb
Nucleic Acid Amplification Test (NAAT) - positive for mycobacterium tuberculosis
Sputum acid-fast bacilli smear: +ve for acid-fast bacilli
53
Define bronchiectasis
An obstructive lung disorder characterised by chronic dilation of the bronchi and bronchioles with mucuous plugging of the airways, due to recurrent infections.
54
Summarise the aetiology of bronchiectasis
Chronic lung inflammation leads to fibrosis and permanent dilation of the bronchi. This leads to pooling of mucus, which predisposes to further cycles of infection, damage and fibrosis of bronchial walls resulting in progressive bronchial damage
Primary ciliary dyskinesia - unable to clear mucous leading to recurrent pneumonia
Cystic fibrosis - thick mucuous leading to recurrent pneumonia
Tumour in or outside airway causing airway obstruction
Foreign object lodged in the airway causing obstruction preventing mucociliary clearance
Idiopathic (50%)
Post infectious: pneumonia, Pertussis, TB
Immunodeficiency: HIV
α1-antitrypsin deficiency
Connective tissue disorders: Rheumatoid arthritis, Sjogren’s Syndrome
IBD: UC or Crohns
55
Summarise the epidemiology of bronchiectasis
Most often arises in childhood
| Incidence decreases with the use of antibiotics
56
What are the presenting symptoms of bronchiectasis?
```
Chronic cough
Cough productive of thick cloudy/opaque sputum or yellow/green if infection
Cough and sputum production worsened by lying flat or on side
Recurrent infections
Wheeze
Shortness of breath
Fever
Fatigue
Weight loss
Haemoptysis
Pleuritic chest pain
```
57
What are the signs on physical examination of bronchiectasis?
Fever
Clubbing
Wheeze
Use of accessory muscles
Tachypnoea
Coarse crepitations – usually at lung bases and shifts on coughing
Inspiratory squeaks and crackles (quite characteristic of bronchiectasis if present)
58
What are the appropriate investigations for bronchiectasis?
```
Pulmonary function tests - show obstructive lung pattern:
Decreased lung capacity
Decreased ability to force air out
Reduced FEV1
Increased RV/TLC
```
CT - shows dilated bronchi and bronchioles with thickened walls - DIAGNOSTIC
CXR: dilated bronchi, fibrosis, atelectasis, pneumonic consolidations (may be NORMAL)
Genetic testing for PCD, CF
Serum alpha 1 antitrypsin
Sputum sample, culture and sensitivity during exacerbation - PSEUDOMONAS AERUGINOSA is most often causative, haemophilus influenzae, staph aureus, streptococcus pneumoniae, Klebsiella, mycobacteria
59
Explain the management of bronchiectasis
Flu vaccination, maintain hydration
Acute exacerbations:
TWO IV ANTIBIOTICS that cover Pseudomonas aeruginosa - amoxicillin or clarithromycin
Prophylaxis:
Antibiotics in patients with frequent exacerbations (> 3 times a year) - Long-term macrolide azithromycin
```
Inhaled Corticosteroids (e.g. fluticasone): reduces inflammation and volume of sputum (does NOT affect the frequency of exacerbations or lung function)
Bronchodilators considered in patients with responsive disease i.e. salbutamol, ipratropium
```
Physiotherapy - sputum and mucus clearance
Bronchial artery embolisation: if life-threatening haemoptysis due to bronchiectasis
Surgical: localised resection, lung or heart lung transplantation
60
What are the possible complications of bronchiectasis?
Pulmonary hypertension
Right ventricular hypertrophy (leading to cor pulmonale)
Recurrent chest infections and pneumonias
Massive haemoptysis
Respiratory failure
Empyema
61
Summarise the prognosis of bronchiectasis
Irreversible
Periods of symptom control and periods of acute exacerbations
Often associated with other respiratory problems
Most patients continue to have symptoms after 10 years
62
Define pneumothorax
Air accumulation in the pleural space
Tension pneumothorax: air entry to the pleural space occurs but a flap of tissue prevents air exit, leading to a medical emergency
63
Summarise the aetiology of pneumothorax
Primary spontaneous pneumothorax:
In patients with no underlying respiratory conditions and no precipitating trauma or event
Rupture of bullae
Often in tall, thin, young males after holding breath
Secondary spontaneous pneumothorax:
Develops in individuals with underlying respiratory disease eg COPD, asthma, cystic fibrosis, Marfan's, lung cancer, emphysema
Traumatic pneumothorax:
Following puncture of parietal pleural eg rib fracture, gunshot, stab, post-medical procedure
Tension pneumothorax:
Develops from traumatic or spontaneous pneumothorax
One way valve made from tissue, preventing air exit
64
Summarise the epidemiology of pneumothorax
Annual incidence: 9/100,000
Mainly in 20-40 year olds
4 times more common in males
More common in smokers
65
What are the presenting symptoms of pneumothorax?
If small spontaneous pneumothorax, could be asymptomatic
Pleuritic chest pain
Dyspnoea
Sudden onset
Tension pneumothorax: laboured respiration, rapid shallow breathing
66
What are the signs on physical examination of pneumothorax?
```
Tachypnoea
Tachycardia
Ipsilateral hyperexpansion of the chest
Ipsilateral reduced breath sounds
Ipsilateral hyperresonance on percussion
Ipsilateral decreased vocal fremitus
Sweating
```
```
Tension Pneumothorax:
Severe Respiratory Distress
Tachycardia
Hypotension
Cyanosis
Distended Neck Veins
Tracheal Deviation to contralateral side
```
67
What are the appropriate investigations for pneumothorax?
Chest X-Ray:
See outline of collapsed lung
No pulmonary vessel markings outside the collapsed lung outline
Flattening of hemidiaphragm
Deepening of costophrenic angle
Tension pneumothorax - trachea and mediastinal deviation away
Use expiratory film - makes small pneumothoraces more obvious
Fluid level seen if blood present
CT Chest: More sensitive than CXR, useful in patients with underlying respiratory disease, useful in differentiating pneumothorax from bullous emphysema
Other: Chest US, Bronchoscopy, ABG (to determine if there is hypoxaemia particularly in secondary disease)
68
What is the management of pneumothorax?
Supplemental oxygen
Primary spontaneous pneumothorax <2cm - discharge and repeat CXR in 1-2 weeks
Primary spontaneous pneumothorax >2cm - aspiration with large bore cannula, chest drain if unsuccessful
Secondary pneumothorax <2cm - aspiration with large bore cannula
Secondary pneumothorax >2cm - chest drain
Follow up with CXR 2 hours and 2 weeks later
Needle aspiration = 2nd ICS at MCL above rib
Chest drain = 4th or 5th ICS at anterior axillary line
Stop needle aspiration if patient coughs or resistance felt
69
What are the possible complications of pneumothorax?
Recurrent Pneumothoraxes
Bronchopleural Fistula
Re-expansion pulmonary oedema
70
Summarise the prognosis of pnuemothorax
After one spontaneous pneumothorax at least 20% have another
Recurrent pneumothoraces more common if secondary spontaneous pneumothorax
Frequency increases with repeated pneumothoraxes
71
Define mesothelioma
An aggressive epithelial neoplasm arising from the lining of the lung, abdomen, pericardium, or tunica vaginalis, which is highly associated with exposure to asbestos.
72
Define the aetiology of mesothelioma
Mesothelioma is heavily associated with asbestos exposure, with a latency period of 20-40 years between exposure and development of disease.
Often construction workers - insulation, roof tiles, painting
Other possible aetiologies:
Exposure to radiotherapy
Genetic predisposition - BAP 1 mutation
Simian virus 40 (SV-40)
73
Summarise the epidemiology of mesothelioma
More common in males
More common in elderly 60-90 years old
More common in Caucasians
74
What are the presenting symptoms of mesothelioma?
```
Shortness of breath
Dry, non-productive cough
Chest pain
Haemoptysis if invades blood vessels
Constitutional symptoms: fatigue, fever, sweats, weight loss
```
Abdominal distension and pain if it spreads to abdomen
75
What are the signs on physical examination of mesothelioma?
Weight loss
Diminished breath sounds
Dullness to percussion
76
What are the appropriate investigations of mesothelioma?
CXR - may show pleural thickening, pleural effusion of pneumothorax, reduced lung volume, parenchymal changes i.e. lower zone linear interstitial fibrosis (asbestos exposure)
CT: pleural thickening and/or discrete pleural plaques, pleural and/or pericardial effusions; enlarged hilar and/or mediastinal lymph nodes; chest wall invasion and/or spread along needle tracts can occur
Pleural biopsy and staining - shows increased calretinin
Chest MRI
PET scan
Metabolic panel - usually normal
FBC - usually normal, if low Hb and platelets and elevated WCC then advanced disease
77
Define asbestosis
Diffuse intersitial fibrosis of the lung due to exposure to asbestos, which occurs >10 years after exposure.
78
Summarise the aetiology of asbestosis
Caused by chronic lung disease caused by inhalation of asbestos fibres
Risk factors:
Occupational exposure (asbestos miners, aircraft & auto mechanics, boiler operators, building construction workers)
Cigarette smoking
79
Summarise the epidemiology of asbestosis
Latency period of around 20 years from first time of exposure
Patients usually present at around > 50 years old
In the UK 5,000 asbestos related deaths per year
80
What are the presenting symptoms of asbestosis?
```
SOB on exertion
Persistent dry, non-productive cough
Appetite loss
Weight loss
Chest tightness or pain
```
81
What are the signs on physical examination of asbestosis?
Crackles
| Clubbing
82
What are the appropriate investigations of asbestosis?
CXR - diffuse interstitial lung fibrosis, particularly lower zone. Pleural thickening, pleural plaques
Pulmonary function tests - non specific. Restrictive picture (decrease FVC, FEV1, TLC, normal FEV1/FVC). If chronic exposure and also smoking, could be obstructive
CT - more specific
Biopsy
Bronchial lavage containing asbestos particles
83
Define obstructive sleep apnoea
Episodes of partial or complete upper airway obstruction during sleep, leading to cessation of breathing, oxyhaemoglobin desaturations and wakening from sleep.
84
Summarise the aetiology of obstructive sleep apnoea
Narrowing of the upper airway during sleep due to collapse of soft tissues of pharnyx due to decreased tone of pharyngeal dilators
```
Obesity
Oropharyngeal narrowing
Severe overbite and other maxillomandibular abnormalities
Adenoid or tonsil swelling
Allergy-induced inflammation
Macroglossia
Male
Post-menopause
Hypothyroidism
PCOS
Marfan's syndrome
Alcohol and sedative use
```
85
Summarise the epidemiology of obstructive sleep apnoea
More common with increasing age
More common in men
COMMON:
5-10% of men > 35 years old
2-15% of women > 35 years old
86
What are the presenting symptoms of obstructive sleep apnoea?
```
Excessive daytime tiredness
Lack of concentration
Loud snoring prior to apnoea reported by partner
Waking during the night/restless sleep
Episodes of gasping during the night
Headaches during the day (morning headaches) due to sleep deprivation
Irritability and mood changes
Dry mouth
```
87
What are the signs on physical examination of obstructive sleep apnoea?
```
Overweight
Large neck circumference - >42cm males, >40cm females
Macroglossia
Maxomandibbular abnormalities
Enlarged tonsils
Long or thick uvula
Retrognathia (pulled back jaws)
Hypertension
```
88
What are the appropriate investigations for obstructive sleep apnoea?
```
Sleep study/polysomnography:
EEG
Airflow
EMG
Pulse oximetry
Capnography
Heart rate
Respiratory effort
```
Bloods: TFT’s (rule out hypothyroid as sleepiness cause), ABG
Epworth sleepiness scale
89
Define pneumonia
Infection and inflammation of the alveoli in the lungs caused by a microbe with consolidation and interstitial lung infiltrates
90
Summarise the aetiology of pneumonia
CAP:
Streptococcus pneumoniae
Haemophilus influenza
Moraxella catarralis
HAP:
Staphylococcus aureus
Pseudomonas aeurginosa
Klebsiella
```
Atypical pneumonia:
Mycoplasma pneumoniae
Chlamydia psittaci
Chlamydia pneumoniae
Legionella pneumophila
```
91
What are the risk factors of pneumonia?
```
Age >65 years old
Hospital admission
Immunocompromise
Smoking
Travel
COPD
Alcohol
```
92
Summarise the epidemiology of pneumonia?
Annual incidence rate is approximately 6 cases per 1000 people in individuals aged 18–39 years
93
What are the presenting symptoms of pneumonia?
```
Productive cough - purulent yellow sputum
Dyspnoea
Pleuritic chest pain
Fever
Chills
Rigors
Fatigue
```
```
Atypical:
Dry cough
Headache
Myalgia
Diarrhoea
```
Older patients: confusion, worsening of underlying disease
94
What are the signs on physical examination of pneumonia?
```
Tachycardia
Tachypnoea
Reduced chest expansion
Reduced breath sounds
Dull percussion note
Increased vocal fremitus
Increased tactile fremitus
Cyanosis
Bronchial breath sounds
Bibasal inspiratory coarse crackles
Low oxygen saturations
```
95
What are the appropriate investigations for pneumonia?
FBC - elevated WBC
CRP/ESR - elevated
Sputum culture
CXR:
Bronchopulmonary pneumonia - patchy areas throughout the lung
Lobar - consolidation localised to a zone
Atypical - reticular markings around perihilar region
96
What is the management of pneumonia?
```
Acute:
Sit patient up and give O2
Fluids
CPAP if required
Surgical drainage if abscess or empyema
```
```
Antibiotics:
Usually give amoxicillin and chlarithromycin
Typicals - amoxicillin or co-amoxiclav
Atypicals - chalrithromycin
Staph - flucloxacillin and gentamycin
MRSA = vancomycin
```
97
What are the possible complications of pneumonia?
```
Pleural effusion
Pneumatoceles
Lung abscess
Sepsis
Empyema
Necrotising pneumonia
Pneumothorax
ARDS
```
98
What is the prognosis of pneumonia?
Most people with pneumonia improve after three to five days of antibiotic treatment, but a mild cough and fatigue can last longer.
Pneumonia can also be fatal.
```
Mortality evaluated with CURB-65 score
C - confusion <8 AMTS
U - urea >7mmol/L
R - respiratory rate >30
B - blood pressure <90/60mmHg
>65 years old
```
```
0-1 = outpatient, low risk
2 = intermediate risk, short stay
3-5 = high risk, inpatient +/- ITU
```
