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Chornic respiratory conditions Flashcards

1
Q

what is IdiopathicPulmonary fibrosis

A

Rare lung condition where scar tissue forms in the lungs and gets progressively worse over several year

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2
Q

Key risk factors for Idiopathic pulmonary fibrosis

A
  • men
  • FH
  • advancing age
  • cigarette smoking
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3
Q

What are the key features of Idiopathic pulmonary fibrosis

A
  • dyspnoea
  • dry cough
  • weight loss
  • fatigue/malaise
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4
Q

What are the key signs of Idiopathic pulmonaru fibrosis

A
  • End expiratory basilar crackles
    (If asymptomatic, may have fine inspiratory crackles)
  • clubbing 25-50%
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5
Q

What might you see on CT in IPF

A
  • honeycombing
  • bronchiectasis
  • increased reticulation
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6
Q

What might you see in CXR in IPF

A

Likely to be abnormal at time of presentation but need CT

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7
Q

What PFTs would you find in IPF

A

Restrictive: reduced forced vital capacity, reduced total lung capacity.

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8
Q

What is asthma

A
  • chronic inflammatory condition
  • exacerbations of bronchoconstriction. Bronchoconstriction is where the smooth muscles of the airways (the bronchi) contract causing a reduction in the diameter of the airways. Narrowing of the airways causes an obstruction to airflow going in and out of the lungs.
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9
Q

What is bronhoconstriction

A

Bronchoconstriction is where the smooth muscles of the airways (the bronchi) contract causing a reduction in the diameter of the airways causing obstruction

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10
Q

Typical asthma triggers

A 
Infection
Night time or early morning
Exercise
Animals
Cold/damp
Dust
Strong emotions
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11
Q

Presentation that suggests asthma

A

Episodic symptoms
Diurnal variability. Typically worse at night.
Dry cough with wheeze and shortness of breath
Atopy/FH
Bilateral widespread “polyphonic” wheeze heard by a healthcare professional

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12
Q

What features may suggest a diagnosis other than asthma

A

Wheeze related to coughs and colds more suggestive of viral induced wheeze
Isolated or productive cough
Normal investigations
No response to treatment
Unilateral wheeze: focal lesion or infection.

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13
Q

According to NICE, what is the first investigations you should consider in ? asthma

A
  • Fractional exhaled nitric oxide
  • Spirometry with bronchodilator reversibility
    Further investigations:
  • Peak flow diary 2 to 4 weeks
  • Direct bronchial challenge test with histamine or methacholine
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14
Q

Explain Short acting beta 2 adrenergic receptor agonists,

A
  • Work quickly
  • effect lasts 1-2 hours
    . Adrenalin acts on the smooth muscles of the airways to cause relaxation
  • dilatation of the bronchioles
  • “reliever” or “rescue” medication during acute exacerbations of asthma when the airways are constricting.
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15
Q

Explain Long-acting muscarinic antagonists (LAMA),

A
  • tiotropium.
  • block the acetylcholine receptors which prevents the parasympathetic nervous system to cause contraction of bronchial smooth muscle
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16
Q

Explain Leukotriene receptor antagonists

A
  • montelukast.
  • Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways.
  • blocking the effects of leukotrienes.
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17
Q

How does theophylline work

A
  • relaxing bronchial smooth muscle and reducing inflammation.
  • narrow therapeutic window and can be toxic in excess
  • plasma monitoring 5 days after starting treatment and 3 days after each dose changes.
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18
Q

What advise should you give to everyone with asthma

A

Each patient should have an individual asthma self-management programme
Yearly flu jab
Yearly asthma review
Advise exercise and avoid smoking

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19
Q

What is COPD

A
  • Non-reversible, long term deterioration in air flow through the lungs
  • damage due to smoking.
  • The damage to the lung tissues causes an obstruction to the flow of air through the airways making it more difficult to ventilate the lungs and making them prone to developing infections.

Unlike asthma, this obstruction is not significantly reversible with bronchodilators such as salbutamol

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20
Q

Features of COPD

A
  • chronic shortness of breath
  • cough
  • sputum production
  • wheeze
  • Recurrent respiratory infections, particularly in winter.
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21
Q

Does COPD cause clubbing

A

NO

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22
Q

What investigations should be done to diagnose COPD

A
  • Chest xrayr.
  • Full blood count
  • Body mass index (BMI)
  • Sputum culture: chronic infections e.g. pseudomonas.
  • ECG and ech
  • CT thorax: fibrosis, cancer or bronchiectasis.
  • Serum alpha-1 antitrypin: Deficiency leads to early onset and more severe disease.s
  • Transfer factor for carbon monoxide (TLCO)
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23
Q

What type of spirometry does COPD show

A
  • Obstructive picture
  • FEV1/FVC radio <0.7
  • No dramatic response of obstructive picture to bronchodilators
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24
Q

What are the stages of severity of COPD

A

Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted

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25
Q

What investigation may you consider if a person presents young with a severe onset of disease

A

alpha-1-anti-trypsin deficiency

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26
Q

What may you see on FBC in a patient with COPD

A

polycythaemia or anaemia. Polycythaemia (raised haemoglobin) is a response to chronic hypoxia

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27
Q

What is the long term management of COPD

A
  • STOP SMOKING
  • Inhaled treatment
  • Annual flu and pneumococcal vaccine
  • Oral mucolytic therapy to break down sputum (e.g. carbocisteine)
  • Long term prophylactic antibiotics (e.g. azithromycin)
  • Long term oxygen therapy at home
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28
Q

What are the steps of Inhaled treatment in long term management of COPD

A
  1. SABA
  2. a. FEV1 >50% (Non- asthmatic features): LABA + LAMA
    b. FEV1 <50% (Asthmatic features): LABA + ICS (or LAMA)
  3. SABA + LABA+ICS + LAMA
  4. Theophylline
  5. Home O2
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29
Q

Who get’s long term oxygen therapy

A
  • chronic hypoxia
  • polycythaemia
  • cyanosis
  • heart failure secondary to pulmonary hypertension (cor pulmonale)
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30
Q

What does oxygen therapy in a chronic retainer lead to

A
  • Depress their respiratory drive

- slows down their breathing rate and effort and leads to them retaining more CO2

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31
Q

What is the general rule about target saturations in patients with COPD

A
  • If retaining CO2 aim for oxygen saturations of 88-92% titrated by venturi mask (raised bicarbonate)
  • If not retaining CO2 and their bicarbonate is normal then give oxygen to aim for oxygen saturations > 94%
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32
Q

What type of oxygen mask should you use in a patient with COPD

A
  • Venturi mask: deliver a specific % of oxygen. They allow some of the oxygen to leak out of the side of the mask and normal air to be inhaled along with oxygen.
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33
Q

What various venturi masks deliver what % of O2

A
  • 24% (blue)
  • 28% (white)
  • 31% (orange)
  • 35% (yellow)
  • 40% (red)
  • 60% (green)
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34
Q

What is Obstructive sleep Apnoea

A
  • collapse of the pharyngeal airway during sleep
  • characterised by apnoea episodes during sleep where the person will stop breathing periodically for up to a few minutes
  • usually reported by the partner as the patient is unaware
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35
Q

What are the risk factors of obstructive sleep apnoea

A 
Middle age
Male
Obesity
Alcohol
Smoking
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36
Q

What are the features of obstructive sleep apnoea

A
  • Apnoea episodes during sleep (reported by partner)
  • Snoring
  • Morning headache
  • Waking up unrefreshed from sleep
  • Daytime sleepiness
  • Concentration problems
  • Reduced oxygen saturation during sleep
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37
Q

In a patient you suspect with obstructive sleep apnoea, what must you always ask

A
  • daytime sleepiness + occupation

- If e.g. Heavy goods driver needs urgent referral and ammended duties until referral if severe

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38
Q

In severe cases of sleep apnoea what can it lead to

A
  • hypertension
  • heart failure
  • increase the risk of MI and stroke.
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39
Q

What is the management of Obstructive sleep apnoea

A
  • ENT referral or specialist sleep clinic (sleep studies)
  • Correct reversible factors e.g. alcohol, weight, smoking
  • continuous positive airway pressure (CPAP) (maintain airway)
  • Surgery: restructuring of the soft palate and jaw.
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40
Q

What do the sleep studies used to diagnose obstructive sleep apnoea look at

A
  • oxygen saturations
  • heart rate
  • respiratory rate
  • breathing: any apnoea episodes and the extent of their snoring.
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41
Q

What is pulmonary hypertension

A
  • increased resistance and pressure of blood in the pulmonary arteries
  • causes strain on the right side of the heart trying to pump blood through the lungs
  • causes a back pressure of blood into the systemic venous system.
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42
Q

Signs of symptoms of Pulmonary hypertension

A
  • SOB
  • Syncope
  • Tachycardia
  • Raised JVP
  • Hepatomegaly
  • Peripheral oedema.
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43
Q

Causes of pulmonary hypertension in group 1

A

Primary pulmonary hypertension

connective tissue disease such as systemic lupus erythematous (SLE)

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44
Q

Causes of pulmonary hypertension in group 2

A

Left heart failure usually due to myocardial infarction or systemic hypertension

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45
Q

Causes of pulmonary hypertension in group 3

A

Chronic lung disease such as COPD

46
Q

Causes of pulmonary hypertension in group 4

A

Pulmonary vascular disease such as pulmonary embolism

47
Q

Causes of pulmonary hypertension in group 5

A

Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders

48
Q

What investigations should be done if suspected pulmonary HTN

A
  • ECG
  • CXR
  • Raised NT-proBNF: indicates right ventricular failure
  • Echo: estimate pulmonary artery pressure
49
Q

What ECG changes might you see in someone with pulmonary HTN

A

Right sided heart strain:

  • Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)
  • Right axis deviation
  • Right bundle branch block
50
Q

What might you see on CXR in a patiet with pulmonary HTN

A

Dilated pulmonary arteries

Right ventricular hypertrophy

51
Q

What is the management of patients with primary pulmonary HTN

A 
IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)
52
Q

What is the management of pulmonary HTN

A
  • treat underlying cause

- Supportive treatment for things like HF, arrythmias, resp failure

53
Q

What is the prognosis in a patient with pulmonary HTN

A
  • poor with a 30-40% 5 year survival from diagnosis

- can increase to 60-70% where specific treatment is possible

54
Q

What are the 3 most common cancers in the UK

A
  • Breast
  • prostate
  • Lung: 80% thought to be preventable
55
Q

What are the key histologies of lung cancer

A

Non-small cell lung cancer:
- Squamous cell carcinoma (35%)
- Adenocarcinoma (25%)
Small Cell Lung Cancer (SCLC) (20%)

56
Q

What can small cell lung cancer cause

A

Small cell lung cancer cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.

57
Q

What are the signs and symptoms of lung cancer

A 
Shortness of breath
Cough
Haemoptysis (coughing up blood)
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
58
Q

What might you see on CXR in a patient with lung cancer

A

Hilar enlargement
“Peripheral opacity” – a visible lesion in the lung field
Pleural effusion – usually unilateral in cancer
Collapse

59
Q

What investigations should be done to rule out lung cancer

A
  • CXR
  • Contrast enhanced Staging CT scan
  • PET-CT (positron emission tomography)
  • Bronchoscopy + biopsy
  • histological diagnosis
60
Q

What is PET-CT (positron emission tomography)

A
  • injecting a radioactive tracer (usually attached to glucose molecules) and taking images using a combination of a CT scanner and a gamma ray detector to visualise how metabolically active various tissues are.
  • useful in identifying areas that the cancer has spread to by showing areas of increased metabolic activity suggestive of cancer.
61
Q

What is the treatment of small cell lung cancer

A
  • Discussion at an MDT
  • Surgery: disease isolated to a single area with intention to cure
  • Radiotherapy
  • Chemotherapy
62
Q

What is the treatment of non small cell lung cancer

A
  • Chemotherapy and radiotherapy

- prognosis in generally worse

63
Q

What palliative treatments are available to those with lugn cancer

A
  • Endobronchial treatment with stents or debulking can be used as part of palliative treatment to relieve bronchial obstruction caused by lung cancer.
  • Radiotherapy
64
Q

What is Recurrent laryngeal nerve palsy

A

presents with a hoarse voice. It is caused by the cancer pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.

65
Q

What is phrenic nerve palsy

A

due to nerve compression causes diaphragm weakness and presents as shortness of breath.

66
Q

What is superior vena cava obstruction

A
  • caused by direct compression of the tumour on the superior vena cava
  • presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest. “Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.
67
Q

What is Recurrent laryngeal nerve palsy

A

presents with a hoarse voice. It is caused by the cancer pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.

68
Q

What is phrenic nerve palsy

A

due to nerve compression causes diaphragm weakness and presents as shortness of breath.

69
Q

What is superior vena cava obstruction

A
  • caused by direct compression of the tumour on the superior vena cava
  • presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest. “Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.
70
Q

What is Horner’s Syndrome

A

triad of partial ptosis, anhidrosis and miosis. It is caused by a Pancoast’s tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.

71
Q

What is SIADH

A

caused by ectopic ADH secretion by a small cell lung cancer and presents with hyponatraemia.

72
Q

what is `Cushing’s syndrome

A

can be caused by ectopic ACTH secretion by a small cell lung cancer.

73
Q

What causes hypercalcaemia in lung cancer

A

caused by ectopic parathyroid hormone from a squamous cell carcinoma.

74
Q

What is limbic encephalitis

A
  • paraneoplastic syndrome
  • small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation
  • It is associated with anti-Hu antibodies.
75
Q

What symptoms may you see in limbic encephalitis

A
  • short term memory impairment
  • hallucinations
  • confusion
  • seizures
76
Q

What extrapulmonary manifestations are there with lung cancer

A
  • Lambert-Eaton myasthenic syndrome.
  • SVC obstruction
  • Horners syndrome
  • SIADH
  • Cushings syndrome
  • Hypercalcaemia
  • recurrent laryngeal and phrenic nerve palsy
77
Q

What is mesothelioma

A
  • lung malignancy affecting the mesothelial cells of the pleura
  • strongly linked to asbestos inhalation.
  • huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years
  • Poor prognosis
  • Chemotherapy can improve survival but it is palliative.
78
Q

What is the presentation of sarcoidosis

A
  • Cough
  • SOB
  • Chronic fatigue
  • arthralgia
  • Wheeze/Rhonci
  • fever
  • weight loss
  • Uveitis: red, painful eye with photophobia
79
Q

What is the epidemiology of sarcoidosis

A
  • 2 spikes in young adulthood and the over 60
  • Woman > men
  • More common in black ethnic group
80
Q

What lung symptoms are seen in sarcoidosis

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules
( over 90%)

81
Q

What is the presentation of sarcoidosis

A
  • Cough
  • SOB
  • Chronic fatigue
  • arthralgia
  • Wheeze/Rhonci
  • Uveitis: red, painful eye with photophobia
82
Q

Shat skin symptoms may you see in sarcoidosis

A
  • Erythema nodosum
  • Lupus pernio
  • Granulomas develop in scar tissue
83
Q

Whta is lupus pernio

A

raised, purple skin lesions commonly on cheeks and nose

84
Q

What is erythema nodosum

A

tender, red nodules on the shins caused by inflammation of the subcutaneous fat

85
Q

What liver symptoms can you get in sarcoidosis

A

Liver nodules
Cirrhosis
Cholestasis
(20%)

86
Q

What is Lofgren’s Syndrome

A

This is a specific presentation of sarcoidosis:

  • Erythema nodosum
  • Bilateral hilar lymphadenopathy
  • Polyarthralgia (joint pain in multiple joints)
87
Q

What are the differentials for sarcoidosis

A 
Tuberculosis
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis
88
Q

What blood tests should you do for suspected sarcoidosis

A

Raised serum ACE. This is often used as a screening test.
Hypercalcaemia (rasied calcium) is a key finding.
Raised serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins

89
Q

What imaging should be done for suspected sarcoidosis

A

Chest xray shows hilar lymphadenopathy
High resolution CT thorax shows hilar lymphadenopathy and pulmonary nodules
MRI can show CNS involvement
PET scan can show active inflammation in affected areas

90
Q

What do you see on histology of sarcoidosis

A
  • Biopsy and histology is gold standard: usually mediastinal lymph node
  • non-caseating granulomas with epithelioid cells.
91
Q

If suspecting other organ involvement what other investigations should you complete for sarcoidosis

A
  • U&Es
  • Urinalysis or urine albumin-creatinine ratio: proteinurea
  • LFTs
  • Ophthalmology review
  • ECG and echocardiogram
  • Ultrasound abdomen for liver and kidney involvement
92
Q

What is the treatment of sarcoidosis

A
  • No treatment if no or mild symptoms: often resolves spontaneously.
  • Oral steroids: first line when symptom (6 & 24 mo)
  • Bisphosphonates to protect against osteoporosis whilst on such long term steroids.
  • Second line options are methotrexate or azathioprine
  • Lung transplant is rarely required in severe pulmonary disease
93
Q

What is the prognosis of sarcoidosis

A
  • 60% resolves spontaneously in about 6 months
  • Small number progresses with pulmonary fibrosis and pulmonary hypertension
  • Death usually only occurs when ti affects the heart and CNS
94
Q

What is Interstitial lung disease

A
  • umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis.
95
Q

What is fibrosis

A

Fibrosis involves the replacement of the normal elastic and functional lung tissue with scar tissue that is stiff and does not function effectively.

96
Q

How do you diagnose interstitial lung disease

A
  • High resolution CT showing ‘ground glass’ affect

- Lung biopsy if unsure of cause to look at histology

97
Q

What is the management of interstitial lung disease

A
  • Limited, mostly supportive
  • Remove or treat the underlying cause
  • Home oxygen where they are hypoxic at rest
  • Stop smoking
  • Physiotherapy and pulmonary rehabilitation
  • Pneumococcal and flu vaccine
  • Advanced care planning and palliative care
  • Lung transplant is an option but the risks and benefits need careful consideration
98
Q

What medications are licensed to slow the progression of Idiopathic pulmonary fibrosis

A
  • Pirfenidone is an antifibrotic and anti-inflammatory

- Nintedanib is a monoclonal antibody targeting tyrosine kinase

99
Q

What drugs can induce pulmonary fibrosis

A

Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

100
Q

Pulmonary fibrosis can occur secondary to which conditions?

A

Alpha-1 antitripsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis

101
Q

What is Hypersensitivity Pneumonitis (AKA Extrinsic Allergic Alveolitis)

A

type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction

102
Q

How do we investigate for Hypersensitivity Pneumonitis (AKA Extrinsic Allergic Alveolitis)

A
  • Bronchoalveolar lavage: collecting cells from the airways during bronchoscopy by washing the airways with fluid then collecting that fluid for testing
  • shows raised lymphocytes and mast cells
103
Q

Examples of Hypersensitivity Pneumonitis (AKA Extrinsic Allergic Alveolitis)

A

Bird-fanciers lung is a reaction to bird droppings
Farmers lung is a reaction to mouldy spores in hay
Mushroom workers’ lung is a reaction to specific mushroom antigens
Malt workers lung is a reaction to mould on barley

104
Q

What is the management of Hypersensitivity Pneumonitis (AKA Extrinsic Allergic Alveolitis)

A
  • removing the allergen,
  • giving oxygen where necessary
  • steroids.
105
Q

What is Asbestosis

A
  • lung fibrosis related to the inhalation of asbestos

- effects of asbestos usually take several decades to develop

106
Q

What problems can asbestosis inhalation cause

A

Lung fibrosis
Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma

107
Q

What is Cryptogenic organising pneumonia

A
  • AKA. bronchiolitis obliterans organising pneumonia

- Focal area of inflammation of the lung tissue

108
Q

What causes Cryptogenic organising pneumonia

A 
Idiopathic
Triggered by:
- infection
-inflammatory disorders
-medications
- radiation 
- environmental toxins 
- allergens.
109
Q

What is the presentation of Cryptogenic organising pneumonia

A
  • Similar to infectious pneumonia
  • Shortness of breath
  • cough
  • fever
  • lethargy.
110
Q

How do you diagnose Cryptogenic organising pneumonia

A
  • Focal consolidation on CXR
  • Delayed diagnosis due to similarities to infective pneumonia
  • Lung biopsy is the definitive diagnosis
111
Q

How do you treat Cryptogenic organising pneumonia

A

corticosteroids

Respiratory (3 decks)

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