Respiratory Flashcards
1
Q
What is pneumonia?
A
Inflammation of the alveoli of the lungs, usually this is as a result of a bacterial infection
2
Q
What organisms commonly causes typical CAPs and what are the specific features seen in each?
A
- Streptococcus Pneumoniae – high fever, rapid onset, pleuritic chest pain and herpes labialis (cold sores on the lip)
- Haemophilus Influenza – common in COPD
- Staph Aureus – commonly following influenza infection
3
Q
What organisms commonly causes atypical CAPs and what are the specific features seen in each?
A
- Mycoplasma pneumoniae – dry cough, atypical chest signs, autoimmune haemolytic anaemia and/or thrombocytopenia, erythema multiforme and nodosum, often in younger patients – diagnosis from mycoplasma serology
- Legionella – hyponatraemia and lymphopenia, classically secondary to infected air conditioning units – diagnosis from urinary antigen
- Klebsiella Pneumoniae – typically following aspiration in alcoholics or diabetics, has a typical red-currant jelly sputum and most commonly affects the upper lobes.
- Pneumocystis Jiroveci – HIV patients, dry cough, exercise induced desaturations and absence of chest signs – manage with co-trimoxazole
- Chlamydia psittaci – causes psittacosis, suspect with a combination of fever and history of bird contact
4
Q
What organisms often cause hospital acquired pneumonia?
A
- Staph Aureus
- Enterobacteriaciae
- Pseudomonas species
- Haemophilus Influenzae
- Acinetobacter baumanii
- Fungal such as candida
5
Q
What are the clinical features of pneumonia?
A
Productive cough Dyspnoea Pleuritic chest pain or ache Fever Tachycardia Haemoptysis Dull to percussion Bronchial breathing Reduced breath sounds Crackly chest
6
Q
What investigations should be done in someone suspected of having a pneumonia?
A
Routine bloods – especially FBC, U&Es and CRP
CXR
ABG
Sputum sample
Pneumococcal and legionella urinary antigen test
7
Q
How should suspected pneumonia be assessed for management in the primary care setting?
A
CRB65 – Primary Care Confusions (AMTs < 8/10) Respiratory rate > 30 Blood pressure <90/60 Age of 65
0 = low risk
1 – 2 = intermediate risk
3-4 = high risk
Home based care for CRB65 of 0
Use clinical judgement for those with a score of 1
Hospital assessment if 2 or more
Point of care CRP test
< 20 – do not routinely offer antibiotics
20 – 100 – consider delayed antibiotics
> 100 – offer antibiotics therapy
8
Q
How is suspected pneumonia assessed for management in the secondary care setting?
A
CURB65 – secondary Care Confusions (AMTs < 8/10) Urea > 7 Respiratory rate > 30 Blood pressure <90/60 Age of 65
0 = treat in community
1 = safely managed in community if O2 sats > 92% and not bilateral or multi-lobar
2 or more = manage in hospital
3 or more = intensive care assessment
9
Q
What general management should be offered to patients with suspected pneumonia?
A
Oxygen as needed
Monitor urine output
Sepsis 6 if appropriate
10
Q
What antibiotics should be offered to patients with pneumonia?
A
If low severity CAP, then give 5-day course of amoxicillin or a macrolide, or tetracycline if pencilling allergic
If moderate severity CAP give 7-10-day course of dual antibiotic therapy – amoxicillin and a macrolide
If high severity CAP give 7-10-day course of dual antibiotic therapy – co-amoxiclav/tazocin and a macrolide
If HAP – give co-amoxiclav or cefuroxime within 5 days of admission. If more than 5 days after admission give Tazocin or ceftazidime or ciprofloxacin
11
Q
What is COPD?
A
Definition – COPD is airflow obstruction which is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.
COPD is umbrella term encompassing both emphysema and chronic bronchitis and patients may have features of both.
12
Q
What causes COPD?
A
Smoking
Alpha 1 antitrypsin deficiency
Occupational exposure such as coal dust, cadmium, cotton, cement, and grain
Pollution
13
Q
What are the clinical features of COPD?
A
Exertional breathlessness – purse lip breathing Chronic cough Excess sputum production Frequent respiratory infections Wheeze Right sided heart failure Smoker or ex-smoker
14
Q
What signs can be elicited in patients with COPD?
A
Bullae forming because of emphysema and destruction of alveoli
Hyperinflation
Cyanosis
Co2 retention (flap)
Cor pulmonale causing (right heart failure secondary to respiratory disease) – peripheral oedema, raised JVP, systolic parasternal heave and a loud P2
15
Q
What investigations should be done in patients with COPD?
A
Spirometry FEV1/FVC ratio < 70%. Stage 1, Mild – FEV1 > 80% Stage 2, Moderate – FEV1 = 50-79% Stage 3, Severe – FEV1 = 30-49% Stage 4, Very Severe – FEV1 < 30%
Chest X-ray – hyperinflation, bullae, flat hemidiaphragm and exclude lung cancer
ABG
FBC
Genetic test for alpha 1 antitrypsin deficiency
CT scan if considering for surgery
16
Q
What is the dyspnoea score?
A
- Not troubled by breathlessness except on strenuous exercise
- Short of breath when hurrying or walking up a slight hill
- Walks slower than contemporaries on level ground because of breathlessness or must stop for breath when waling at own pace.
- Stops for breath after walking about 100m or after a few minutes on level ground
- Too breathless to leave the house, or breathless when dressing or undressing.
17
Q
What is the general management of someone with COPD?
A
Smoking cessation and offering nicotine replacement therapy, varenicline or bupropion
Annual flue vaccine and one-off pneumococcal vaccine
Pulmonary rehabilitation
18
Q
What pharmacological management is offered to someone with COPD?
A
Short acting bronchodilators i.e. SABA (salbutamol) and/or SAMA (ipratropium)
Next you must determine whether patient has any asthmatic features or features suggesting they are likely to be steroid responsive:
• Any previous asthma diagnosis or atopy
• High blood eosinophil account
• Substantial variation in FEV1 over time (at least 400ml)
• Substantial diurnal variation in PEFR (at least 20%)
If they are like asthmatic or steroid responsive then switch to SABA + LABA (formoterol) + Inhaled corticosteroid, with the option of adding in a LAMA (tiotropium bromide) if still struggling (discontinue the SAMA if still on it). Use combined inhalers where possible.
If they do not have asthmatic features or are unlikely to be steroid responsive then switch to a LABA + LAMA and a SABA (discontinue the SAMA if still on it).
Oral theophylline can be added if patient is still breathless or if patient cannot use inhalers. Dose must be reduced if a macrolide or fluoroquinolone are co-prescribed.
19
Q
What antibiotics can be offered prophylactically to COPD patients and what criteria must be met first?
A
Antibiotic prophylaxis may be recommended in select patients, azithromycin is usually used but patients must not be smoking, and must have had a CT scan to exclude bronchiectasis and a sputum culture to exclude atypical infections and tuberculosis
20
Q
What drugs can we offer to help reduce the volume of sputum?
A
Mucolytics can be considered in chronic productive cough and continued if it improves symptoms, the most common drug used is carbocysteine.
21
Q
How should cor pulmonale be managed in COPD?
A
In cor pulmonale treat with diuretics and consider long term oxygen. Do not use ACEi, Ca+ blockers or alpha blockers.
22
Q
What are the last choice options for managing COPD
A
Long term oxygen therapy and lung volume reduction are last resorts
23
Q
Which COPD patients shoud be assessed for long term oxygen assessment?
A
Must be used for at least 15 hours a day and patients CAN NOT be smoking, cigarettes or e-cigarettes. Assess patient who have any of the following. Before commencing must make a risk assessment include risk of fire and risk of falls from equipment.
• Very severe airflow obstruction (FEV1 < 30%), consider if only severe (FEV1 30-49%)
• Cyanosis
• Polycythaemia
• Peripheral oedema or raised JVP
• Oxygen saturations = 92%
24
Q
How is someone assessed for long term oxygen therapy?
A
Assess by measured ABG on 2 occasions at least 3 weeks apart
Offer to those with pO2 < 7.3kPa
Offer to those with pO2 between 7.3-8kPa and one of the following
• Secondary polycythaemia
• Peripheral oedema
• Pulmonary hypertension
25
How does an exacerbation of COPD present?
Presentation – increased SOB, cough, wheeze, sputum, hypoxia, and confusion.
26
What often causes exacerbation of COPD?
Causes – can be non-infective but if infective then most commonly due to Haemophilus influenzae, others include strep pneumoniae and Moraxella catarrhalis. Viruses can also cause exacerbation and the most common cause is Rhinovirus.
27
How is exacerbation of COPD managed?
Treat with famous 5
• High flow oxygen by venturi mask 24% - use oxygen flow as instructed by mask
• Antibiotics (if infective cause) – amoxicillin/clarithromycin/doxycycline
• Nebulised Salbutamol
• Nebulised Ipratropium
• Corticosteroid – oral prednisolone 30mg for 5 days or IV hydrocortisone
• Oral theophylline with senior input
• NIV or BiPAP (Not CPAP which is better for HF and OSA)
28
Describe the systematic approach to interpreting an ABG
1. Check pH – is it alkalotic or acidotic
2. Check oxygen partial pressure and saturation to determine if arterial or venous
3. Check PaCO2 – does this match the pH
4. Check the HCO – does this match the pH
5. Check the lactate levels
6. Check Anion gap
7. Check everything else including electrolytes
29
What causes a metabolic acidosis?
Occurs due to a reduction in plasma bicarbonate levels by one of two mechanisms
1. Gain of strong acid e.g. ketones in DKA or lactate in sepsis
2. Loss of base e.g. from bowel in diarrhoea
30
How do we determine what has causes a metabolic acidosis?
This can be determined by calculating the anion gap. (Na + K) – (Cl + HCO), the normal range for the anion gap is 10-18mmol/L.
31
What does a normal anion gap in a metabolic acidosis suggest?
If the Anion gap is normal this suggests a hyperchloraemic metabolic acidosis i.e. bicarb has been lost and replaced with chloride ions.
Causes include:
• GI loss in diarrhoea, fistula, ureterosigmoidostomy
• Renal tubular acidosis
• Drugs such as acetazolamide
• Ammonium chloride injection
• Addison’s disease
32
What does a raised anion gap in a metabolic acidosis mean?
If the anion gap has been raised, then this suggests that bicarbonate has been used up by new acids and not replaced.
Causes include
• Lactate from shock or hypoxia or sepsis
• Ketones in DKA or alcohol
• Urate in renal failure
• Acid poisoning such as salicylates or methanol
33
Why does a metabolic alkalosis occur?
Occurs either due to an increase in plasma bicarbonate levels or a loss of hydrogen ions. This usually occurs in the kidney or the GI tract. Primarily this revolves around activation of the renin-angiotensin II-aldosterone system. Aldosterone causes reabsorption of Na in exchange for H+ in the kidneys. Fluid loss such as vomiting, and diuretics causes loss of Na and Cl which activates aldosterone causing a loss of H+. In hypokalaemia K+ inside cells is switched for H+.
34
What are the common causes of a metabolic alklaosis?
```
Causes:
• Vomiting/aspiration
• Diuretics
• Hypokalaemia
• Primary hyperaldosteronism
• Cushing’s syndrome
• Congenital adrenal hyperplasia
• Bartter’s syndrome
```
35
What is a respiratory acidosis?
Rise in CO2 that results in alveolar hypoventilation, renal compensation by increasing HCO can lead to a compensation respiratory acidosis.
36
What commonly causes a respiratory acidosis?
Causes
• COPD
• Decompensation respiratory conditions e.g. pulmonary oedema or asthma
• Sedative drugs such as opiates or benzodiazepines
37
What is a respiratory alkalosis?
Hyperventilation resulting in excess loss of CO2 resulting in an increase in pH.
38
What causes a respiratory alkalosis?
Causes
• Psychogenic – anxiety
• Hypoxia causing subsequent hyperventilation e.g. PE or high altitude
• Early salicylate poisoning (simulates the respiratory centre early but later on the acidic effect of salicylate causes a metabolic acidosis)
• CNS stimulation e.g. stroke, subarachnoid haemorrhage, and encephalitis
• Pregnancy
39
What is type 1 respiratory failure?
Gas exchange in the lungs in inadequate resulting in hypoxia, it is defined as a PaO2 < 8kPa with a normal or low PaCO2.
40
What causes type 1 respiratory failure?
```
This occurs primarily due to ventilation perfusion mismatching, hypoventilation, abnormal diffusion or right to left cardiac shunts.
Examples of V/Q mismatching:
• Pneumonia
• Pulmonary oedema
• Pulmonary embolism
• Asthma
• Emphysema
• Pulmonary fibrosis
• ARDS
```
41
What is type 2 respiratory failure?
Gas exchange in the lungs in inadequate resulting in hypoxia, it is defined as a PaO2 < 8kPa with a high PaCO2 >6kPa.
42
What causes type 2 respiratory failure?
Causes
This occurs due to alveolar hypoventilation with or without V/Q mismatching
• Pulmonary disease – asthma, COPD, pneumonia, pulmonary fibrosis and obstructive sleep apnoea
• Reduced respiratory drive – sedative drugs, CNS tumour or trauma
• Neuromuscular disease – cervical cord lesion, diaphragmatic paralysis, polio, myasthenia gravis and Guillain barre syndrome
• Thoracic wall disease – flail chest and kyphoscoliosis
43
How does respiratory failure present?
Hypoxia – dyspnoea, restlessness, agitation, confusion, central cyanosis, polycythaemia, pulmonary hypertension and cor pulmonale.
Hypercapnia – headache, peripheral vasodilation, tachycardia, bounding pulse, tremor/flap, papilloedema, confusion, drowsiness, and coma.
44
How should a suspected respiratory failure be investigated?
```
Routine bloods
ABD
CXR
Sputum and blood culture if febrile
Spirometry
```
45
How should type 1 respiratory failure be managed?
Type 1 – treat cause, give oxygen by facemask – 24-60%, and assisted ventilation if PaO2 < 8kPa despite 60% oxygen.
46
How should type 2 respiratory failure be managed?
Type 2 – be aware as the respiratory drive could be relying on oxygen. Treat underlying cause, controlled oxygen therapy starting at 24%. Repeat ABG in 20 minutes if CO2 is steady or lower then increase oxygen concentration. If CO2 has risen by >1.5kPa consider ventilatory support i.e. NIPPV or intubation and ventilation
47
What is acute respiratory distress syndrome? (ARDS)
Definition – acute lung injury characterised by severe hypoxaemia without a cardiac cause. The disease is self-perpetuating as more alveoli are damaged the swelling causes more trauma to more alveoli.
48
What causes ARDS?
Inflammatory damage to the alveoli causing pulmonary oedema, respiratory compromise, and consequently acute respiratory failure.
49
Describe the direct and indirect causes of ARDS?
```
Direct
Pneumonia
Smoke inhalation
Aspiration
Fat embolus
```
```
Indirect
Sepsis
Acute Pancreatitis
Polytrauma
Transfusion reaction
Head injury – sympathetic stimulation leading to pulmonary hypertension
```
50
Describe the clinical features of someone with ARDS?
```
Can start hours to days after the event
Dyspnoea
Cyanosis and hypoxia
Inspiratory crackles on auscultation
Multiorgan failure
Rising ventilatory pressures
```
In early stages – exudative phase with injury due to oedema
Later stage – fibroproliferative changes leading to scarring and poor lung function
51
How should someone with ARDS be investigated?
Routine bloods including amylase, clotting, CRP and blood cultures
Blood cultures
Arterial blood gas
CXR which usually shows bilateral pulmonary infiltrates
Pulmonary artery catheter to measures pulmonary capillary wedge pressure
52
What are the diagnostic criteria for ARDS?
Diagnostic criteria
• Acute onset
• CXR showing bilateral infiltrates
• PCWP < 19 or lack of clinical congestive cardiac failure
• Refractory hypoxaemia with PsO2:FiO2 <200
53
How should ARDS be managed?
Treat underlying cause e.g. antibiotics if signs of sepsis
Negative fluid balance with diuretics
Circulatory support – inotropes such as dobutamine, vasodilators and blood transfusions
Prone ventilation and use of PEEP
Mechanical ventilation using low tidal volumes to avoid pneumothorax
54
What is a pneumothroax?
Definition – Air in the pleural space
55
What are the risk factors for pneumothorax?
```
Tall, young, thin and male
Marijuana smoking
COPD
Interstitial lung disease
Cystic fibrosis
Sub pleural blebs
HIV leading to PCP
Marfan’s or rheumatoid arthritis
NIPPV
```
56
What can causes a pneumothroax?
Traumatic
Iatrogenic - chest drain, biopsy, subclavian line, ventilation in ITU etc.
Spontaneous – usually due to small blebs that burst on the lung surface.
57
What is the difference between a primary and secondary pneumothorax?
Pneumothorax in normal lung = primary pneumothorax
| Pneumothorax in diseased lung = secondary pneumothorax
58
What are the clinical features of a pneumothorax?
Pleuritic chest pain especially on inspiration
| Breathlessness and low saturation
59
How should someone with a suspected pneumothorax be investigated?
Investigated by X-ray on inspiration and if greater than 2cm from edge of rib cage then it equals a large pneumothorax as lung is 50% collapsed.
CT scan allows us to differentiate between pneumothorax and complex hollows lung disease, also of emphysema obscuring chest X-ray and finally if there is suspicion of aberrant drain position.
60
How are pneumothoraxes managed?
ABCDE and management of symptoms i.e. pain, SOB and blood sats.
Definitive management by aspiration or chest drain acutely or surgery – pleurectomy, fixing the bleb or pleuradhesis
Primary
Small – discharge home unless breathless in which case aspirate
Large – aspirate if this fails then chest drain
Secondary
If >50yrs, and large and/or patient is short of breath then a chest drain should be used
If 1-2cm attempt aspiration, if this fails (pneumothorax still greater than 1cm) then chest drain. Patient should be admitted for at least 24 hours.
If <1cm then give oxygen and admit for 24 hours
61
Are there any restriction after having a pneumothorax?
After a pneumothorax scuba diving should be permanently avoided unless the patient has undergone bilateral pleurectomy and has normal lung function and chest CT scan postoperatively.
62
Where are chest drains inserted?
Insertion of chest drain – triangle of safety in the mid axillary line, 5th intercostal space. This is bordered by the anterior edge of latissimus Dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple and the apex below the axilla.
There is another triangle situation behind the scapula. Bounded by the trapezius above, latissimus dorse below and laterally by the vertebral border of the scapula.
63
What are the relative contraindications of a chest drain?
```
Relative Contraindications
• INR > 1.3
• Platelet count < 75
• Pulmonary bullae
• Pleural adhesions
```
64
What is a tension pneumothorax?
This is where a flap has been created in the lungs and the pleural space fills up with more air with each breath. This places pressure on the mediastinum and will cause a tracheal deviation.
65
How are tension pneumothoraxes managed?
This is an emergency and must be immediately decompressed with a chest tube insertion – usually a wide bore cannula in the 2nd intercostal space on the affected side.
66
What is a pulmonary embolism?
Definition – Any embolus that becomes lodged in the pulmonary arterial system. 15% of all cases of sudden death are due to massive PE.
67
What are the risk factors for a PE?
```
Clotting disorders i.e. factor V Leiden or antiphospholipid syndrome
DVT
Varicose veins
Smoking
Prolonged immobility
Pregnancy
Surgery
Cancer
COCP
```
68
What are the clinical features of a pulmonary embolism?
```
Breathlessness
Pleuritic chest pain
Haemoptysis
Haemodynamic instability
Cough.
```
```
Rarely a pleural effusion
Left parasternal heave
Raised JVP
Crackly chest
ECG – large S waves in lead 1, a large Q wave in lead 3 and an inverted T wave in lead 3. May also noticed a RBBB and right axis deviation.
```
69
How should a pulmonary embolism be investigated?
CXR to exclude other pathology (very rarely a clot is visible)
PERC (pulmonary embolism rule-out criteria)
To rule out PE all criteria must be negative – Age >50, HR > 100, O2 sats on air <95%, unilateral leg swelling, haemoptysis, recent surgery or trauma, prior PE/DVT and hormones.
70
What scoring system is used if PE is suspected?
If PE is suspected a Wells Score should be performed.
• Clinical features of deep vein thrombosis (minimum of leg swelling and pain with palpation of the deep veins) — 3 points.
• An alternative diagnosis is less likely than pulmonary embolism — 3 points.
• Heart rate greater than 100 beats per minute — 1.5 points.
• Immobilisation for more than 3 days or surgery in the previous 4 weeks — 1.5 points.
• Previous deep vein thrombosis or pulmonary embolism — 1.5 points.
• Haemoptysis — 1 point.
• Cancer (receiving treatment, treated in the last 6 months, or palliative) — 1 point.
Score > 4 = PE likely
Score =/< 4 = PE unlikely
71
What is a done if the Well's score indicates a PE is likely vs unlikely?
PE likely
1. CTPA
2. Give immediate DOAC such as apixaban or rivaroxaban
PE unlikely
1. D-Dimer
2. If positive admit for CTPA and give DOAC if scan delayed
3. Otherwise consider alternative diagnosis.
If allergic to contrast or renal impairment then a V/Q scan should be used instead.
72
How are PEs managed?
Once PE is confirmed assess whether patient is haemodynamically stable if so then they must be started on anticoagulant therapy.
Heparin if pregnant and until the end of pregnancy
Heparin if due to cancer and continue until they have been considered cured for 6 months
DOAC for everyone else for at least 3 months, stop at 3 months if provoked PE, if unprovoked then continues for up to another 3 months (i.e. total 6 months) depending on bleeding risk, can use HAS-BLED score to assess this.
If haemodynamically unstable, then thrombolysis or embolectomy should be considered.
For recurrent PE can consider IVC filters
73
What is bronchiectasis?
Definition – permanent enlargement of the airways as a result of chronic inflammation
74
What can cause bronchiectasis?
Post-infective – TB, measles, pertussis, and pneumonia
Cystic fibrosis
Bronchial obstruction due to cancer or foreign body
Immuno-deficiency
Allergic bronchopulmonary aspergillosis (classically bronchiectasis with eosinophilia)
Ciliary dyskinetic syndromes
75
Which organisms often infect patients with bronchiectasis?
```
Most common organisms
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella
Streptococcus pneumoniae
Staph aureus
```
76
What are the clinical features of someone with bronchiectasis?
```
Persistent cough with copious sputum
Haemoptysis
Halitosis
Coarse crackles
Nail clubbing
```
77
How is suspected bronchiectasis investigated?
CXR – tramlines (thickened bronchial walls), cystic shadows
CT– signet rings Sputum cultures
Spirometry – shows an obstructive patters
Bronchoscopy – locate site of haemoptysis, exclude obstruction and obtain samples
78
How can bronchiectasis be managed?
Physical training e.g. inspiratory muscle training and airway clearing e.g. postural drainage
Antibiotics for exacerbation and long-term rotating antibiotics in severe cases
Immunisations
Control infections or other cause
Mucolytics
Long term steroids and itraconazole for allergic bronchopulmonary aspergillosis (ABPA)
Bronchodilators in selected cases – asthma, COPD, CF and ABPA
Surgery in selected patients
79
What is asthma?
Definition – chronic inflammatory disorder of the airways resulting in reversible airway obstruction as a result of inflammation, bronchoconstriction and mucus build up.
80
What are the risk factors for asthma?
```
Personal or family history of atopy
Maternal smoking, viral infection during pregnancy especially RSV
Low birth weight
Not being breastfed
Exposure to lots of allergens
Air pollution
Hygiene hypothesis
```
81
What are the signs and symptoms of asthma?
```
Wheeze
Breathlessness (especially in cold air, when exercising or at night)
Tight chest
Cough (rare)
Sensitivity to aspirin and nasal polyps
```
82
How should asthma be investigated?
Test peak flow volume – asthma usually different between morning and afternoon.
Spirometry – measures FVC (typically normal) and FEV1 (significantly reduced). From this we geta FEV1% which in asthma is usually <70%. Should be done with bronchodilator reversibility (BDR). In adults a positive is an improvement of 12% or more and an increase in volume of 200ml of more.
FeNO – fractional exhaled nitric oxide – increases in inflammatory cells. Should always be tested if their BDR test is negative or spirometry is normal. >40ppb is +ve, <35ppb is -ve.
Consider CXR
83
What should you look out for on examination of someone you suspect of having asthma?
```
Examination
Inspection – for eczema
Palpation – lung expansion is the same both side
Percussion – for resonance
Auscultation – listen for crackles etc.
```
84
If someone asthma is worse at work what should you do?
If though to be worse during work, then could be occupational asthma in which case a referral to a specialist should be arranged.
85
Describe the steps involved in managing chronic asthma?
BTS guidelines suggest considering stepping down treatment every3 months. If reducing steroid dose do this by 25-30% at a time.
1. SABA – short acting beta agonists – salbutamol
2. SABA + ICS – low dose inhaled corticosteroid – budesonide, beclomethasone dipropionate or fluticasone propionate
3. SABA + ICS + LTRA – leukotriene receptor antagonist – montelukast (oral drug)
4. SABA + ICS +/-LTRA + LABA – long acting beta agonist – salmeterol (continue LTRA if response was good)
5. SABA +/- LTRA + MART – maintenance and reliever therapy, this includes low dose ICS and a LABA with a short acting component –
6. SABA +/- LTRA + MART with medium dose ICS
7. SABA +/- LTRA + one of the following
• Increase ICS dose to high as part of a MART
• Add a trial of additional drug e.g. LAMA – long acting muscarinic antagonist or theophylline
• Seek advice from asthma specialist
86
Describe the features of a moderate acute asthma attack?
```
PEFR: 50-75% best or predicted
Saturations: >92%
Speech: Normal
RR: < 25
HR: < 110
ABG: Low pCO2
```
87
Describe the features of a severe acute asthma attack?
```
PEFR: 33-50% best or predicted
Saturations: > 92%
Speech: Cannot complete sentences
RR: > 25
HR: > 110
ABG: Low pCO2
```
88
Describe the features of a life-threatening acute asthma attack?
```
PEFR: < 33% best or predicted
Saturations: < 92%
Speech: None
RR: Feeble respiratory effort
HR: Bradycardic and hypotensive
ABG: Normal pCO2
Others: Silent chest, cyanosis, exhaustion, confusion or coma
```
89
What is a near fatal asthma attack?
Near fatal asthma is a 4th category characterised by raised pCO2 and/or requiring mechanical ventilation with raised inflation pressures.
90
How should an acute asthma exacerbation be managed?
Admit anyone with life threatening asthma, severe asthma that fails to respond to initial treatment, anyone with a previous near-fatal attack, anyone who is pregnant, already using oral corticosteroid or presentation at night.
1. High flow oxygen via non rebreathe mask
2. Prednisolone oral or IM continued for at least 5 days or until recovery
3. Salbutamol nebulised with oxygen if life-threatening otherwise via normal inhaler
4. Ipratropium bromide if severe or life threatening or in those who do not respond to SABA
5. Magnesium sulphate IV
6. IV aminophylline after consultation with senior
7. Intubate (insert tube) and ITU admission +/- ECMO
8. IV fluids
91
What are the criteria for discharging someone with an asthma attack?
Criteria for discharge
• Been stable on discharge medication for 12-24 hours
• Inhaler technique checked and recorded
• PEFR >75% best or predicted
92
What is interstitial lung disease?
Definition – general term for disease affecting the lung parenchymal in a diffuse pattern. These are characterised by chronic inflammation and progressive interstitial fibrosis.
93
What can cause fibrotic changes in the upper zones of the lungs?
Upper zones
Hypersensitivity pneumonitis
Coal workers pneumoconiosis/progressive massive fibrosis/beryliosis
Silicosis (silica is toxic to macrophages so silicosis is a risk factor for TB)
Sarcoidosis
Ankylosing spondylitis – HLA B27 induced spondyloarthropathy
Histiocytosis
Tuberculosis
94
What can cause fibrotic changes in the lower zones of the lungs?
Lower Zones
Idiopathic pulmonary fibrosis
Most connective tissue disorders except ankylosing spondylitis e.g. SLE, RA
Drug induced – amiodarone, bleomycin, and methotrexate
Asbestosis
95
What is idiopathic pulmonary fibrosis?
Idiopathic interstitial lung disease (most common), typically seen in 50-70yr old men
96
What are the clinical features of idiopathic pulmonary fibrosis?
```
Clinical Features
Dyspnoea on exertion
Non-productive paroxysmal cough
Abnormal breath sounds
Restrictive pulmonary spirometry
Malaise
Weight loss
```
Cyanosis
Finger clubbing
Bi-basal, fine, end-respiratory crepitations
97
How should someone you suspect of having interstitial lung disease be investigated?
Routine bloods
Spirometry – showing a restrictive pattern, FEV1 normal/decreased, FVC decreased and FEV1:FVC increased
CXR – bilateral interstitial shadowing (ground glass) that progresses to honeycombing
CT – gold standard investigation required to make a diagnosis
ANA +ve in 30%, rheumatoid factor +ve in 10% but does not necessarily link the fibrosis to a connective tissue disease.
98
How is idiopathic pulmonary fibrosis managed?
Supportive care and pulmonary rehabilitation
Pirfenidone (antifibrotic agent) may be useful in select patients
Steroids only if the diagnosis of IPF is in doubt
Supplementary oxygen
Lung Transplantation
Average life expectancy is around 3-4 years from diagnosis
99
What is sarcoidosis?
Sarcoidosis is a multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent
100
What are the clinical features of sarcoidosis?
Clinical Features
• Acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
• Insidious: dyspnoea, non-productive cough, malaise, weight loss
• Skin: lupus pernio
• Hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
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What is heerfodt's syndrome?
Heerfordt's syndrome (uveoparotid fever) there is parotid enlargement, fever, and uveitis secondary to sarcoidosis
102
What is Lofgren's syndrome?
Lofgren's syndrome is an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis
103
How should someone you suspect of having sarcoidosis be investigated?
Routine bloods looking for hypercalcaemia
CXR findings and staging
• stage 0 = normal
• stage 1 = bilateral hilar lymphadenopathy (BHL)
• stage 2 = BHL + interstitial infiltrates
• stage 3 = diffuse interstitial infiltrates only
• stage 4 = diffuse fibrosis
Spirometry: may show a restrictive defect
Tissue biopsy: non-caseating granulomas
104
How is sarcoidosis managed?
Indications for steroids
• Patients with chest x-ray stage 2 or 3 disease who are symptomatic.
• Hypercalcaemia
• Eye, heart, or neuro involvement
105
What is tuberculosis
Definition – infection by mycobacterium tuberculosis usually in the lungs but can become systemic. More common in migrants and the homeless between ages 20-44.
106
What organisms cause TB?
Caused by mycobacterium tuberculosis complex. There are 7 closely related species the most common being: M. Tuberculosis, M.Bovis and M.Africanum. Spread by respiratory droplets from coughing.
107
What is primary TB
Primary TB – Infects and resists killing from macrophages due to waxy cell wall. 5% progress to active disease then rest become latent carriers (Ghoun focus primary lesion) which can then turn active when stimulated i.e. when immunocompromised.
108
What is secondary TB or post primary?
Secondary Tuberculosis (post-primary) – reactivation generally happen in the apex of the lungs and can spread locally. Can also spread to distant sites i.e. CNS, vertebral bodies, cervical lymph nodes, renal and GI.
109
What are the clinical features of an acute TB episode?
Cough and SOB
Haemoptysis
Consolidation in upper lobes of lung (TB likes aerobic areas)
Tuberculous Granuloma with caseous necrosis and Giant cell langerhans type
Night sweats
Weight loss and anorexia
Tiredness and malaise
Pleural effusion
Cavitation and fibrosis in extensive pulmonary spread
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How can an acute TB infection be diagnosed?
* CXR – upper lobe cavitation and bilateral hilar lymphadenopathy
* Sputum smear – 3 early morning sputum samples minimum 5ml – stained for presence of acid-fast bacilli (Ziehl-Neelsen stain)
* Sputum cultures take many days but are gold standard, more sensitive and can assess drug sensitivities
* Nucleic acid amplification test (NAAT) – allows rapid diagnosis within 24-48 hours more sensitive that smear but less sensitive that the culture
111
How can a latent TB be diagnosed?
* Matoux test/Tuberculin sensitivity test – injection of purified protein derivative read result 2-3 days later. False positives with BCG and false negatives with HIV, miliary TB, sarcoidosis, lymphoma or very young.
* Interferon Gamma Releasing Assays – used if the Mantoux test is positive or equivocal or when the Mantoux may be falsely negative as above.
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What are the 4 drugs used to treat TB and what are their relevant SE?
Rifampicin – hepatitis, potent liver enzyme inducer, flu like symptoms and orange secretions
Isoniazid – peripheral neuropathy, hepatitis, agranulocytosis, and enzyme inducer
Pyrazinamide – hepatitis, hyperuricaemia causing gout, arthralgia and myalgia
Ethambutol – optic neuritis (check visual acuity before and during treatment)
113
What regimen should be used to treat acute TB?
Must treat with all 4 TB antibiotics for 2 months in active disease and then Isoniazid and Rifampicin for 4 more months.
114
What is the treatment regimen for CNS TB?
If central nervous system has become involved Isoniazid and rifampicin should be continued for 10 months with the addition of steroids.
115
What is the treatment regimen for latent TB?
Latent disease should be treated for 3 months with isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid with pyridoxine.
116
What is the DECAF score and what is it used for?
DECAF Score – scores patients based on prognostic factors and can help guide where and what management should take place for a patient with an infective exacerbation of COPD.
• MRC dyspnoea score – (1-4 = 0, 5a = 1 and 5b – 2)
• Eosinopenia = 1
• Consolidation on CXR = 1
• Acidaemia (pH < 7.3) = 1
• Atrial fibrillation on echo or history of paroxysmal AF = 1
Low risk = 0-1 – suitable for standard treatment and consideration of early discharge
Intermediate risk = 2 – utilise clinical judgement
High risk = >3 – high and quick mortality consider early escalation and high levels of monitoring
117
What 4 pathologies can asbestos cause in the lungs?
* Pleural plaques – benign, do not undergo malignant change and occur after a latent period of 20-40 years.
* Pleural thickening – asbestos exposure can cause diffuse pleural thickening similar to emphysema and haemothorax
* Asbestosis – severity related to length of exposure in contrast to mesothelioma. Latent period typically 15-30 years and causes lower lobe fibrosis
* Mesothelioma – malignancy of the pleura, managed with palliative chemotherapy
118
What is coal workers pneumoconiosis?
Coal dust overwhelms the mucociliary escalator causing macrophage accumulation in the alveoli and consequent immune response. Usually a 10-15 year lag
There are two possible presentations
Simple coal pneumoconiosis is the most common and patients are often asymptomatic, but its presence increases the risks of lung disease such as COPD and it may lead to Progressive massive fibrosis (PMF). Staging is based on X-ray appearance
Progressive massive fibrosis occurs as coal dust causes fibrotic masses several cm in size, most commonly in the upper lobes and patients are often symptomatic with breathlessness, exertion, cough and sometimes black sputum. Spirometry shows mixed obstructive/restrictive pattern.
119
How is coal worker's pneumoconiosis managed?
Avoid exposure and other irritants such as smoking
| Manage symptoms of chronic bronchitis
120
What is alpha 1 antitrypsin deficiency?
Lack of protease inhibitor that is normally produced in the liver. It normally protects cells from enzymes such as neutrophil elastase. Located on chromosome 14, inherited in autosomal recessive fashion/Co-dominant.
121
What are the clinical features of alpha 1 antitrypsin deficiency?
Emphysema in young non-smoking patients especially lower lobes
Liver – cirrhosis and hepatocellular carcinoma in adults and cholestasis in children
122
How should suspected alpha 1 antitrypsin deficiency be investigated?
Spirometry showing an obstructive picture
LFTs and clotting
Liver USS
A1AT concentrations
123
How is alpha 1 antitrypsin deficiency managed?
DO NOT smoke
Supportive with bronchodilators and physiotherapy
IV A1AT protein concentrates
Surgery – lung volume reduction and transplant
124
What organisms most commonly cause aspiration pneumonia and whihc lobes do they most commonly affect?
Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
Most commonly affects the right middle and lower lung lobes
125
What is Psittacosis and what causes it?
Psittacosis is infection caused by Chlamydia psittaci. The most common presentation is as a cause of atypical pneumonia.
Cause
Chlamydia psittaci is an obligate intracellular bacterium. Transmission is typically from birds or bird secretions including urine and faeces, typically occurring after cleaning bird cages
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What are the clinical features of psittacosis?
It is more common in young adults
Subacute onset of Flu-like symptoms (fever, headache and myalgia)
Typical respiratory symptoms dyspnoea, dry cough and chest pain
Unilateral crepitations and vesicular breathing
Pleural effusion
Hepatomegaly and splenomegaly (rare)
127
How should suspected psittacosis be investigated?
Routine bloods
Chest X-ray
Confirmation with serology (usually as part of atypical pneumonia screening)
128
What are the 1st and 2nd line management options for psittacosis?
1st-line: tetracyclines e.g. doxycycline
| 2nd-line: macrolides e.g. erythromycin
129
What is re-expansion pulmonary oedema?
Presents with cough and/or shortness of breath. If suspected the chest drain should be clamped and an urgent chest x-ray should be obtained. To avoid re-expansion pulmonary oedema, it is 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).
130
What are the requirements for removal of a chest drain?
Removal of the chest drain is dependent upon the indication for insertion:
• In cases of fluid drainage from the pleural cavity, the drain should be removed when there has been no output for > 24 hours and imaging show resolution
• In cases of pneumothorax, the drain should be removed when it is no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution of the pneumothorax.
• Drains inserted in cases of penetrating chest injury should be reviewed by the specialist to confirm an appropriate time for removal.
131
What is obstructive sleep apnoea?
Full or partial obstruction to the airway whilst asleep causing hypoxia, snoring and sudden waking.
132
What are the risk factors for obstructive sleep apnoea?
Obesity
Macroglossia – acromegaly, hypothyroidism, and amyloidosis
Large tonsils
Marfan’s syndrome
133
What are the clinical features of obstructive sleep apnoea?
Partner complains of excessive snoring and even period of apnoea
Day time somnolence
Compensated respiratory acidosis
Hypertension
134
How should suspected obstructive sleep apnoea be investigated?
Epworth Sleepiness scale – completed by patient and/or partner
Multiple sleep latency test – measure time to fall asleep in a dark room using EEG criteria
Diagnosis via sleep studies (polysomnography) ranging from pulse oximetry to full polysomnography
135
What is the management of obstructive sleep apnoea?
Weight loss
CPAP is first line for moderate to severe
Intra oral devices (mandibular advancement)
DVLA should be informed if this is causing excessive daytime sleepiness
136
What are the common indications for non-invasive ventilation?
* COPD with respiratory acidosis pH 7.25-7.35
* Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
* Cardiogenic pulmonary oedema unresponsive to CPAP
* Weaning from tracheal intubation
137
What are the recommended initial setting for non-invasive ventilation?
Recommended initial settings for bi-level pressure support in COPD
• Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
• Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O
• Back up rate: 15 breaths/min
• Back up inspiration: expiration ratio: 1:3
138
What are the guideline about prescribing drugs to help people stop smoking?
* Patients should be offered nicotine replacement therapy (NRT), varenicline or bupropion - NICE state that clinicians should not favour one medication over another
* NRT, varenicline or bupropion should normally be prescribed as part of a commitment to stop smoking on or before a particular date (target stop date)
* Prescription of NRT, varenicline or bupropion should be sufficient to last only until 2 weeks after the target stop date. Normally, this will be after 2 weeks of NRT therapy, and 3-4 weeks for varenicline and bupropion, to allow for the different methods of administration and mode of action. Further prescriptions should be given only to people who have demonstrated that their quit attempt is continuing
* If unsuccessful using NRT, varenicline or bupropion, do not offer a repeat prescription within 6 months unless special circumstances have intervened
* Do not offer NRT, varenicline or bupropion in any combination
139
What are the adverse effects of NRT?
Nausea & vomiting
Headaches
Flu-like symptoms
140
What should you offer alongside NRT to people with a high level of depenance on nicotine?
Offer a combination of nicotine patches and another form of NRT (such as gum, inhalator, lozenge or nasal spray) to people who show a high level of dependence on nicotine or who have found single forms of NRT inadequate in the past.
141
What is Varenicline?
This is a nicotinic receptor partial agonist and should be started 1 week before the patients target date to stop. The recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking). Has been shown in studies to be more effective than bupropion
142
What are the adverse effects of Varenicline?
Nausea is the most common
Headache
Insomnia
Abnormal dreams
143
Who should Varenicline not be used in?
Varenicline should be used with caution in patients with a history of depression or self-harm. Contraindicated in pregnancy and breast feeding
144
What is Bupropion?
A norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist. Should be started 1 to 2 weeks before the patients target date to stop.
145
What is the most important adverse effect to warn patient about when prescribing Bupropion?
Small risk of seizures (1 in 1,000)
146
Who should Bupropion not be used in?
Contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication
147
Why and how should we test pregnant women for smoking status?
All pregnant women should be tested for smoking using carbon monoxide detectors, partly because 'some women find it difficult to say that they smoke because the pressure not to smoke during pregnancy is so intense.'. All women who smoke, or have stopped smoking within the last 2 weeks, or those with a CO reading of 7 ppm or above should be referred to NHS Stop Smoking Services.
148
How should smoking in pregnancy be managed?
The first-line interventions in pregnancy should be cognitive behaviour therapy, motivational interviewing or structured self-help and support from NHS Stop Smoking Services
The evidence for the use of NRT in pregnancy is mixed but it is often used if the above measures failure. There is no evidence that it affects the child's birthweight.
Pregnant women should remove the patches before going to bed
149
How are pleural effusions classified and what are the different causes?
Pleural effusions may be classified as being either a transudate or exudate according to the protein concentration.
Transudate (< 30g/L protein)
• Heart failure (most common transudate cause)
• Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
• Hypothyroidism
• Meigs' syndrome
Exudate (> 30g/L protein)
• Infection: pneumonia (most common exudate cause), TB, subphrenic abscess
• Connective tissue disease: RA, SLE
• Neoplasia: lung cancer, mesothelioma, metastases
• Pancreatitis
• Pulmonary embolism
150
What are the clinical features of a pleural effusion?
```
Dyspnoea
Non-productive cough
Chest pain
Dullness to percussion
Reduced breath sounds
Reduced chest expansion
```
151
How should a pleural effusion be investigated?
* CXR
* Pleural aspiration using a 21G needle and 50ml syringe, fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
* Ultrasound to increase the likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septations
* Contrast CT to investigate the underlying cause, particularly for exudative effusions
152
What are light's criteria?
Helps distinguish between a transudate and an exudate. The BTS recommend using the criteria for borderline cases. Exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L, if the protein level is between 25-35 g/L, Light's criteria should be applied.
An exudate is likely if at least one of the following criteria are met:
Pleural fluid protein divided by serum protein >0.5
Pleural fluid LDH divided by serum LDH >0.6
Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
Other characteristic pleural fluid findings
Low glucose: rheumatoid arthritis, tuberculosis
Raised amylase: pancreatitis, oesophageal perforation
Heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis
153
How should suspected infected pleural effusion be managed based on their aspirates opacity?
If the fluid is purulent or turbid/cloudy a chest drain 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 drain should be inserted.
154
What is infectious mononucleosis?
Infectious mononucleosis (glandular fever) (EBV, also known as human herpesvirus 4, HHV-4) in 90% of cases. Less frequent causes include cytomegalovirus and HHV-6. It is most common in adolescents and young adults.
155
What are the clinical features of an infectious mononucleosis infection?
Triad of sore throat, pyrexia and lymphadenopathy
Lymphadenopathy may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically results in upper anterior cervical chain
Malaise, anorexia, headache
Palatal petechiae
Splenomegaly – occurs in around 50% of patients and may rarely predispose to splenic rupture
Hepatitis, transient rise in ALT
Lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
Haemolytic anaemia secondary to cold agglutins (IgM)
Maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
Symptoms typically resolve after 2-4 weeks.
156
How should infectious mononucleosis be investigated?
Heterophil antibody test (Monospot test) – NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.
157
How is infectious mononucleosis managed?
Supportive
Rest during the early stages, drink plenty of fluid, avoid alcohol
Simple analgesia for any aches or pains
Avoid contact sports for 8 weeks after having glandular fever to reduce risk of splenic rupture even in the absence of clinically palpable splenomegaly
158
What is acute bronchitis?
Acute bronchitis is a type of chest infection as a result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum. Viral infection is the leading cause and around 80% of episodes occur in autumn or winter.
159
What are the clinical features of acute bronchitis?
```
Usually self-limiting
Cough: may or may not be productive
Sore throat
Rhinorrhoea
Wheeze
Low grade fever
Normal chest examination and CXR
Low-grade fever
Wheeze
```
160
How is acute bronchitis investigated?
Acute bronchitis is typically a clinical diagnosis
| CRP testing is available this may be used to guide whether antibiotic therapy is indicated
161
How is acute bronchitis managed?
Analgesia
Good hydration
Consider antibiotic therapy if patients:
• Are systemically very unwell
• Have pre-existing co-morbidities
• Have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
Doxycycline or in children or pregnant ladies amoxicillin
