48. Cough/sputum/wheeze/sneezing Flashcards
1
Q
what are the atopic conditions
A
asthma, eczema, hay fever and food allergies
2
Q
presentation asthma
A
Episodic
Diurnal variability
Typical symptoms are:
Shortness of breath
Chest tightness
Dry cough
Wheeze
3
Q
o/e asthma
A
normal when well
widespread “polyphonic” expiratory wheeze
4
Q
what is key about the wheeze suggetsing asthma
A
WIDESPREAD
and polyphonic
5
Q
differentials for localised monophonic wheeze
A
inhaled foreign body, tumour or a thick sticky mucus plug obstructing an airway
A chest x-ray is the next step.
6
Q
triggers asthma
A
Infection
Nighttime or early morning
Exercise
Animals
Cold, damp or dusty air
Strong emotions
7
Q
common drugs that can exacerbate/trigger asthma
A
beta blockers
nsaids
8
Q
tests for making an asthma diagnosis
A
- Spirometry with bronchodilator reversibility
- Fractional exhaled nitric oxide (FeNO)
Where there is diagnostic uncertainty after initial investigations, the next step is testing the peak flow variability.
9
Q
results of spirometry with reversibility testing that suggest asthma
A
reversibility = greater than 12% increase in FEV1 on reversibility testing supports a diagnosis of asthma.
10
Q
what does FeNO test involve
A
The test involves a steady exhale for around 10 seconds into a device that measures FeNO.
11
Q
what may impact the result of FeNO
A
Smoking can lower the FeNO, making the results unreliable.
12
Q
FeNO positive result?
A
a level above 40 ppb is a positive test result
13
Q
what is peak flow varibaility? what is a positive result
A
Peak flow variability is measured by keeping a peak flow diary with readings at least twice daily over 2 to 4 weeks.
NICE says a peak flow variability of more than 20% is a positive test result, supporting a diagnosis.
14
Q
aim of treatment asthma
A
complete control of symptoms and normal lung function
No daytime symptoms.
No night-time waking due to asthma.
No need for rescue medication.
No asthma attacks.
No limitations on activity including exercise.
15
Q
principles of asthma management
A
Start at the most appropriate step for the severity of the symptoms
Review at regular intervals based on severity (e.g., 4-8 weeks after adjusting treatment)
Add additional treatments as required to control symptoms completely
Aim to achieve no symptoms or exacerbations on the lowest dose and number of treatments
Always check inhaler technique and adherence when reviewing medications
16
Q
what are the steps of asthma management in adults
A
- SABA
- ICS
- LTRA (e.g., montelukast)
- LABA +/- LTRA
- MART inc low dose ICS
- MART inc moderate dose ICS
- Consider high-dose inhaled corticosteroid or additional drugs (e.g., LAMA or theophylline)
- Specialist management (e.g., oral corticosteroids)
17
Q
when should you prescribe ICS for adults asthma
A
- using SABA 3/7
- symptoms 3/7
- woken at night 1/7
18
Q
if on SABA and ICS asthma, what should you do?
A
add Leukotriene receptor antagonist (e.g., montelukast)
19
Q
what is COPD
A
Long-term, progressive condition involving airway obstruction, chronic bronchitis and emphysema. It is almost always the result of smoking and is largely preventable
20
Q
what is chronic bronchitis
A
Chronic bronchitis refers to long-term symptoms of a cough and sputum production due to inflammation in the bronchi.
21
Q
what is emphysema
A
damage and dilatation of the alveolar sacs and alveoli, decreasing the surface area for gas exchange.
22
Q
presentation copd
A
A typical presentation of COPD is a long-term smoker with persistent symptoms of:
Shortness of breath
Cough
Sputum production
Wheeze
Recurrent respiratory infections, particularly in winter
23
Q
what does copd not cause
A
clubbing
haemoptysis
chest pain
These symptoms should be investigated for a different cause, such as lung cancer, pulmonary fibrosis or heart failure.
24
Q
what are the grades of the mrc dyspnoea scale
A
Grade 1: Breathless on strenuous exercise
Grade 2: Breathless on walking uphill
Grade 3: Breathlessness that slows walking on the flat
Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
Grade 5: Unable to leave the house due to breathlessness
25
what invetsigations should you do copd
spirometry with bronchodialtor reversibility testing
CXR
FBC
BMI
26
what tests do you need for a diagnosis of copd
clinical presentation and spirometry results
Spirometry will show an obstructive picture with a FEV1:FVC ratio of less than 70%. There is little or no response to reversibility testing with beta-2 agonists (e.g., salbutamol). Reversible obstruction is more suggestive of asthma.
27
why get a cxr ?copd
will show hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
28
why get fbc copd
exclude secondary polycythaemia
29
why get bmi copd
(weight loss occurs in severe disease)
30
further tests copd
ECG and echocardiogram to assess for heart failure and cor pulmonale
CT thorax for alternative diagnoses such as fibrosis, cancer or bronchiectasis
Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency
31
non-pharmacological management points copd
smoking cessation
pneumococcal and annual flu vaccine
Pulmonary rehabilitation
32
1st step pharmacological copd management
SABA or SAMA
33
copd pt is on saba or sama but still uncontrolled, next step?
Do they have asthmatic features/features suggesting steroid responsiveness?
Yes: Long-acting beta agonist (LABA) and Inhaled corticosteroid (ICS) (+SABA/SAMA as required)
No: LABA and LAMA. if taking SAMA, switch to SABA
34
management copd
1. SABA (e.g. salbutamol) or SAMA (e.g. ipratropium bromide)
2. Do they have asthmatic features/features suggesting steroid responsiveness?
Yes: Long-acting beta agonist (LABA) and Inhaled corticosteroid (ICS) (+SABA/SAMA as required)
No: LABA and LAMA. if taking SAMA, switch to SABA
3. Triple therapy: LABA + LAMA + ICS (+ SABA as required)
4. Specialist guided
35
3rd line treatment copd
Triple therapy LABA + LAMA + ICS (+ SABA as required)
36
if tried triple therapy, next step copd management
Specialist guided
eg theophylline
37
what criteria determines whether a pt has asthmatic/steroid resposnsive features?
any previous, secure diagnosis of asthma or of atopy
a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)
38
LABA and LAMA combination inhalers - examples
Anoro Ellipta, Ultibro Breezhaler and DuaKlir Genuair
39
LABA and ICS combination inhalers - examples?
Fostair, Symbicort and Seretide
40
LABA, LAMA and ICS combination inhalers - examples
Trimbow, Trelegy Ellipta and Trixeo Aerosphere
triple therpay - some begin with T
41
indication LTOT COPD
chronic hypoxia (sats < 92%),
cyanosis, polycythaemia,
cor pulmonale
42
factors which may improve survival copd
smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients
43
what is cor pulmonale
right-sided heart failure caused by respiratory disease
44
causes cor pulmoanle
COPD (the most common cause)
Pulmonary embolism
Interstitial lung disease
Cystic fibrosis
Primary pulmonary hypertension
45
symptoms cor pulmonale
Often patients with early cor pulmonale are asymptomatic. Symptoms of cor pulmonale include:
Shortness of breath
Peripheral oedema
Breathlessness of exertion
Syncope (dizziness and fainting)
Chest pain
46
signs of cor pulmonale o/e
Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Parasternal heave
Loud second heart sound
Murmurs (e.g., pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)
47
management cor pulmonale
loop diuretic
LTOT
48
high yield things to remember bronchiectasis
finger clubbing
Pseudomonas colonisation
diagnosis by HRCT
Extended courses of 7-14 days of antibiotics for exacerbations
49
what is bronchiectasis
permanent dilation of the bronchi, the large airways that transport air to the lungs. Sputum collects and organisms grow in the wide tubes, resulting in a chronic cough, continuous sputum production and recurrent infections.
50
causes of bronchiectasis
Idiopathic (no apparent cause)
Postinfectious:
Pneumonia
Whooping cough (pertussis)
Tuberculosis
Alpha-1-antitrypsin deficiency
Connective tissue disorders (e.g., rheumatoid arthritis)
Cystic fibrosis
Yellow nail syndrome
51
what is triad of yellow nail syndrome
Yellow fingernails, bronchiectasis and lymphoedema
52
presenting symptoms bronchiectasis
Shortness of breath
Chronic productive cough
Recurrent chest infections
Weight loss
52
signs of bronchiectasis o/e
Sputum pot by the bedside
Oxygen therapy (if needed)
Weight loss (cachexia)
Finger clubbing
Signs of cor pulmonale (e.g., raised JVP and peripheral oedema)
Scattered crackles throughout the chest that change or clear with coughing
Scattered wheezes and squeaks
53
most common infective organisms bronchiectasis
Haemophilus influenza is most common !!!!
Pseudomonas aeruginosa
54
xr findinfs bronchiectasis
Tram-track opacities (parallel markings of a side-view of the dilated airway)
Ring shadows (dilated airways seen end-on)
55
what investigation is test of choice for diagnosing bronchiectasis
High-resolution CT (HRCT)
56
management infective exacerbation bronchiectasis
Sputum culture (before antibiotics)
Extended courses of antibiotics, usually 7–14 days
Ciprofloxacin is the usual choice for exacerbations caused by Pseudomonas aeruginosa
57
general management for bronchiectasis
general:
Vaccines (e.g., pneumococcal and influenza)
Respiratory physiotherapy to help clear sputum
Pulmonary rehabilitation
pharma:
long term abx for freq infections
Inhaled colistin for Pseudomonas aeruginosa colonisation
Long-acting bronchodilators may be considered for breathlessness
Long-term oxygen therapy in patients with reduced oxygen saturation
Surgical:
Surgical lung resection may be considered for specific areas of disease
Lung transplant is an option for end-stage disease
58
when may a pt be on long term abx for bronchiectasis? what is the abx of choice
azithromycin) for frequent exacerbations (e.g., 3 or more per year)
59
management of pseudomonas colonisation bronchiectasis
Inhaled colistin
60
what is interstitial lung disease? what is fibrosis?
Interstitial lung disease includes many conditions that cause inflammation and fibrosis of the lung parenchyma (lung tissue). Fibrosis involves the replacement of elastic and functional lung tissue with non-functional scar tissue.
61
causes interstitial lung disease
Idiopathic pulmonary fibrosis (the most important to remember)
Secondary pulmonary fibrosis: drugs/other conditions
Hypersensitivity pneumonitis
Cryptogenic organising pneumonia
Asbestosis
62
key symptoms interstitial lung disease (ILD)
Shortness of breath on exertion
Dry cough
Fatigue
63
examiantion findings idiopathic pulmoanry fibrosis
Bibasal fine end-inspiratory crackles
Finger clubbing
64
what does HRCT show ILD
ground glass apperance
honeycombing
65
investigation of choice ILD
high-resolution CT scan (HRCT)
66
spirometry ILD
restrictive pattern
67
when there is diagnostic uncertainty interstitial lung disease, what invetsigations might you do
Lung biopsy
Bronchoalveolar lavage
68
general management interstitial lung disease
Remove or treat the underlying cause
Home oxygen where there is hypoxia
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine
Advanced care planning and palliative care where appropriate
Lung transplant is an option, but the risks and benefits need careful consideration
69
what is idiopathic pulmoanry fibrosis
Idiopathic pulmonary fibrosis features progressive pulmonary fibrosis with no apparent cause.
70
presentation idiopathic pulmonary firbosis
It presents with an insidious onset of shortness of breath and dry cough over more than 3 months. It usually affects adults over 50 years old.
71
prognosis idiopathic pulmonary fibrosis
The prognosis is poor, with a 2-5 years life expectancy from diagnosis.
72
drugs for idiopathic pulmoanry fibrosis
Pirfenidone reduces fibrosis and inflammation through various mechanisms
Nintedanib reduces fibrosis and inflammation by inhibiting tyrosine kinase
73
causes of drug induced pulmaonry fibrosis
Amiodarone (also causes grey/blue skin)
Cyclophosphamide
Methotrexate
Nitrofurantoin
74
causes of secondary pulmoanry fibrosis (Secondary to other conditions)
Alpha-1 antitrypsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis
Sarcoidosis
75
what is Hypersensitivity pneumonitis/Extrinsic allergic alveolitis
involves type III and type IV hypersensitivity reaction to an environmental allergens
Inhalation of allergens in patients sensitised to that allergen causes an immune response, leading to inflammation and damage to the lung tissue.
76
main invetsigation and results which suggest hypersensitivity penumonotis
bronchoalveolar lavage
- Raised lymphocytes (lymphocytosis)
77
what is bronchoalveolar lavage
Bronchoalveolar lavage is performed during a bronchoscopy procedure. The airways are washed with sterile saline to gather cells, after which the fluid is collected and analysed.
Raised lymphocytes (lymphocytosis) are suggestive of hypersensitivity pneumonitis.
78
specific types of hypersensitivity pneumonitis
Bird-fancier’s lung is a reaction to bird droppings
Farmer’s lung is a reaction to mouldy spores in hay
Mushroom worker’s lung is a reaction to specific mushroom antigens
Malt worker’s lung is a reaction to mould on barley
79
presentation hypersensitivity pneumonitis
acute (occurs 4-8 hrs after exposure)
dyspnoea
dry cough
fever
chronic (occurs weeks-months after exposure)
lethargy
dyspnoea
productive cough
anorexia and weight loss
80
management hypersensitivity pneumonitis
avoid precipitating factors
oral glucocorticoids
Oxygen if req
81
investigation findings hypersensitivity pneumonitis
imaging: upper/mid-zone fibrosis
bronchoalveolar lavage: lymphocytosis
serologic assays for specific IgG antibodies
blood: NO eosinophilia
82
what is cryptogenic organising pneumonia? - presentation, invetsigation, management
focal area of inflammation lung tissue - can be idiopathic or triggered by infection, drugs and inflamamtory disorders
presentation: same as pneumonia, cxr same as pneumonia
invetsigation: lung biopsy
management: systemic corticosteroids
83
what is asbestosis
Asbestosis refers to lung fibrosis related to asbestos exposure.
84
what lung problems can asbestos cause
Lung fibrosis (asbestosis)
Adenocarcinoma
Mesothelioma (Pleural thickening)
Pleural plaques and pleural thickening w/o the more serious diseases ^
85
what is allergic rhinitis
inflammatory disorder of the nose where the nose become sensitized to allergens such as house dust mites and grass, tree and weed pollens.
86
classifications of allergic rhinitis
seasonal
perennial
occupation
87
features allergic rhinitis
sneezing
bilateral nasal obstruction
clear nasal discharge
post-nasal drip
nasal pruritus
88
Management allergic rhinitis
allergen avoidance
mild/mod:
- oral or intranasal antihistamines
mod/sev:
intranasal corticosteroids
a short course of oral corticosteroids are occasionally needed to cover important life events
89
why should you not used decongestents for extended periods of time
there may be a role for short courses of topical nasal decongestants (e.g. oxymetazoline).
They should not be used for prolonged periods as increasing doses are required to achieve the same effect (tachyphylaxis) and rebound hypertrophy of the nasal mucosa (rhinitis medicamentosa) may occur upon withdrawal
90
what is alpha-1 antitrypsin deficiency
genetic condition caused by low levels of alpha-1 antitrypsin.
Two main organs are affected by alpha-1 antitrypsin deficiency:
- lungs: COPD/bronchiectasis (typically after 30 years old)
- liver Dysfunction, fibrosis and cirrhosis of the liver (depending on the specific genotype)
91
inheritance alpha-1 antitrypsin deficiency
autosomal co-dominant pattern
Co-dominant refers to when both gene copies are expressed and contribute to the outcome (neither is dominant or recessive over the other). The disease severity results from the combination of both copies of the gene.
92
what is alpha-1 antitrypsin
Alpha-1 antitrypsin is a protease inhibitor.
Proteases therefore have free attack of tissues such as the lungs
93
how does alpha-1 antitrypsin deficiency cause liver damage
Alpha-1 antitrypsin is produced in the liver.
in specific genotypes, alpha-1 antitrypsin gets trapped in the liver and is toxic to hepatocytes --> inflamamtion - fibrosis, cirrhosis and potentially hepatocellular carcinoma.
94
diagnosis of alpha-1 antitrypsin
Low serum alpha-1 antitrypsin (the screening test)
Genetic testing
95
how is lung damage assessed aloha 1 antitrypsin
Chest x-ray
High-resolution CT thorax
Pulmonary function tests
96
management of alpha 1 antitrypsin
Non-pharmacological:
Stop smoking
Monitoring for complications (e.g., hepatocellular carcinoma)
Screening of family members
Pharmacological:
Symptomatic management (e.g., standard treatment of COPD)
Surgical:
Organ transplant for end-stage liver or lung disease
97
liver biopsy alpha-1 antitrypsin deficiency
Liver biopsy shows periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment. These represent a buildup of the mutant proteins.
98
epidemiology klebsiella
more common in diabetics and patients with a history of alcohol excess. It is also frequently caused by aspiration.
99
where in lungs does klebsiella affect
upper lobes of the lungs.
100
pneumonia in alcohol excess, aspiration or diabetes
klebsiella
101
risk factors for lung abscess
most commonly forms secondary to aspiration pneumonia
poor dental hygiene, previous stroke and reduced consciousness are some of the risk factors for this
102
features lung abscess
symptoms may develop over weeks
systemic features such as night sweats and weight loss may be seen
fever
productive cough
often foul-smelling sputum
haemoptysis in a minority of patients
chest pain
dyspnoea
signs
dull percussion and bronchial breathing
clubbing may be seen
103
CXR lung abscess
fluid-filled space within an area of consolidation
an air-fluid level is typically seen
104
management lung abscess
intravenous antibiotics
if not resolving percutaneous drainage may be required and in very rare cases surgical resection
105
pulmonary fucntuon test sarcoidosis
restrictive
106
what is sarcoidosis
Sarcoidosis is a chronic granulomatous disorder.
Granulomas are inflammatory nodules full of macrophages. The cause of these granulomas is unknown.
It is usually associated with respiratory symptoms but has many extra-pulmonary manifestations, such as erythema nodosum and lymphadenopathy.
107
acute vs insidious sarcoidosis
acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia, purple lesions (lupus pernio)
insidious: dyspnoea, non-productive cough, malaise, weight loss
108
what skin changes do you get sarcoidosis
lupus pernio
- Lupus pernio is specific to sarcoidosis and presents with raised purple skin lesions, often on the cheeks and nose.
Erythema nodosum
- Erythema nodosum is characterised by nodules of inflamed subcutaneous fat on the shins.
109
risk factors sarcoidosis
Aged 20-39 or around 60
Women
Black ethnic origin
110
what lung changes do you get sarcoidosis
Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules
111
what is lofgrens syndrome?
Lofgren’s syndrome refers to a specific presentation of sarcoidosis with a classic triad of symptoms:
Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)
112
investigations sarcoidosis
Bloods:
Raised angiotensin-converting enzyme (ACE) (often used as a screening test)
Raised calcium (hypercalcaemia)
Imaging:
Chest x-ray may show hilar lymphadenopathy
High-resolution CT scanning may show hilar lymphadenopathy and pulmonary nodules
MRI can show central nervous system involvement
PET scan can show active inflammation in affected areas
Histology:
helps establish the diagnosis, often by bronchoscopy with an ultrasound-guided biopsy of mediastinal lymph nodes. Histology characteristically shows non-caseating granulomas with epithelioid cells.
ACE levels have a sensitivity of 60% and specificity of 70% and are therefore not reliable in the diagnosis of sarcoidosis although they may have a role in monitoring disease activity.
113
why do you get kidney stones in sarcoidosis
hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
hypercalcaemia
114
main CXR finding sarcoidosis
bilateral hilar lymphadenopathy
115
management sarcoidosis
Conservative management is considered in patients with no or mild symptoms.
Oral steroids (for 6-24 months) are usually first-line where treatment is required.
Bisphosphonates protect against osteoporosis whilst on long-term steroids.
Methotrexate is a second-line option.
Lung transplant is rarely required in severe pulmonary disease.
116
indications steroids sarcoidosis
stage 2 or 3 disease + symptomatic.
hypercalcaemia
eye, heart or neuro involvement
117
stages x-ray sarcoidosis
A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis
118
prognosis sarcoidosis
Sarcoidosis spontaneously resolves in around half of patients, usually within two years.
In some patients, it progresses to pulmonary fibrosis and pulmonary hypertension. Overall mortality is less than 10%.
119
histology sarcoidosis
non-caseating granulomas with epithelioid cells.
120
how to obtain sample for histology sarcoidosis
bronchoscopy with an ultrasound-guided biopsy of mediastinal lymph nodes.
121
cause bibasal altelectasis
common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.
122
management post-op bialteral altelectasis
positioning the patient upright
chest physiotherapy: breathing exercises
