Respiratory Flashcards

1
Q

what are the two types of lung cancer?

A

non small cell (majority) - adenocarcinoma, squamous cell carcinoma, large cell carcinoma, other
small cell - contain neurosecretory granules that can release neuroendocrine hormones..paraneoplastic syndromes

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2
Q

what are the signs and sx 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

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3
Q

which investigations are required for lung cancer?

A

chest x ray - hilar enlargement, peripheral opacity (lesion), pleural effusion (usually unilateral), collapse
staging CT TAP with contrast
PET-CT for metastatic spread
bronchoscopy with endobronchial USS - detailed assessment of the tumour
histological diagnosis - types of cells in cancer

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4
Q

what are the tx options for lung cancer?

A

MDT
surgery for non small cell such as lobectomy, segmentectomy
radiotherapy for non small cell
chemo - adjuvant or palliative for non small cell
chemo + radio - small cell
endobronchial tx with stents or debulking - small cell

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5
Q

what are the extrapulmonary manifestations of lung cancer?

A

recurrent laryngeal nerve palsy - hoarse voice, compresses as passes through mediastinum
phrenic nerve palsy - diaphragm weakness - SOB
SVC obstruction - facial swelling, difficult breathing, distended veins..pemberton’s sign (raising the hands over head causes facial congestion and cyanosis)
horner’s syndrome - partial ptosis, anhydrosis, miosis caused by pancoast tumour pressing on sympathetic ganglion
SIADH - by ectopic ADH by small cell, hyponatraemia
Cushing’s - ectopic ACTH from small cell
hypercalcaemia - ectopic PTH from squamous cell
limbic encephalitis - small cell causes immune system to make antibdoies to tissues in brain, esp limbic sx…memory impairment, hallucinations, confusion, seizures…anti-Hu antibodies
Lambert-eaton myasthenic syndrome

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6
Q

define labert-eaton myasthenic syndrome

A

result of antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones - weakness, in the proximal muscles also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

The tendon reflexes become temporarily normal for a short period following a period of strong muscle contraction. For example, the patient can maximally contract the quadriceps muscle for a period, then have their reflexes tested immediately afterwards, and display an improvement in the response. This is called post-tetanic potentiation.

In older smokers with symptoms of Lambert-Eaton syndrome consider small cell lung cancer.

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7
Q

define mesothelioma

A

lung malignancy affecting mesothelial cells of the pleura
linked to asbestos but latent period between exposure and sx (45 yrs)
prognosis poor, chemo can help

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8
Q

define pneumonia

A

inflammation of the lung tissue and sputum filling the airways and alveoli

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9
Q

how does pneumonia present?

A

Shortness of breath
Cough productive of sputum
Fever
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Sepsis

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10
Q

what are the signs of pneumonia?

A

Tachypnoea (raised respiratory rate)
Tachycardia (raised heart rate)
Hypoxia (low oxygen)
Hypotension (shock)
Fever
Confusion
possibly septic
bronchial breath sounds - harsh breath sounds equally loud on inspiration and expiration
focal coarse crackles - like a straw blowing into a drink
dullness to percussion due to tissue collapse/consolidation

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11
Q

how is the severity of pneumonia measured?

A

in hospital - CURB 65
out of - no urea measured

C – Confusion (new disorientation in person, place or time)
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65

Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment

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12
Q

what are the common causes of pneumonia?

A

step pneu
haemoph influe

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13
Q

what are the other causes of pneumonia and their associations?

A

Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease
Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
Staphylococcus aureus in patients with cystic fibrosis

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14
Q

define atypical pneumonia and the possible causes

A

pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain. They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).
- legionella pneumophila - infected water supplies/air conditioning units -> hyponatraemia from SIADH
- mycoplasma pneumonia - erythema multiforme rash with pink rings and pale centres, neurological sx in young patients
- chlamydiophila pneumonia - school aged child, chronic pneumonia and wheeze
- coxiella burnetii - Q fever - linked to animals and bodily fluids like farmers
- chalmydia psittaci - infected birds like parrot owners

“Legions of psittaci MCQs”

M – mycoplasma pneumoniae
C – chlamydydophila pneumoniae
Qs – Q fever (coxiella burnetii)

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15
Q

what is fungal pneumonia, the risk factors and treatment?

A

immunocompromised
poorly controlled or new HIV with low CD4
dry cough, SOB on exertion and night sweats
tx with co-trimoxazole, prophylactic for HIV to protect against PCP

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16
Q

which investigations are required for pneumonia?

A

Chest xray
FBC (raised white cells)
U&Es (for urea)
CRP (raised in inflammation and infection) - can see abx working but VRP delayed and WCC is faster picture, if immunocompromised may not be raised at all

Patients with moderate or severe cases should also have:
Sputum cultures
Blood cultures
Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing)

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17
Q

which abx are used to treat pneumonia?

A

Mild CAP: 5 day course of oral antibiotics (amoxicillin or macrolide)
Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin and macrolide)
—per local guidlines and resistance patterns

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18
Q

what are the complications of pneumonia?

A

Sepsis
Pleural effusion
Empyema
Lung abscess
Death

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19
Q

define FEV1 and how it is affected

A

forced expiratory volume in 1 second…reduced in obstruction

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20
Q

define FVC and how it is affected

A

forced vital capacity…reduced in restriction

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21
Q

what is the FEV1:FVC ratio in obstructive disease?

A

<75%

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22
Q

give 2 examples of obstructive disease and how these can be differentiated

A

asthma - reversible >12% with bronchodilator
COPD -> irreversible, <12%

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23
Q

what is the FEV1:FVC ratio in restrictive disease?

A

FEV1 and FVC are equally reduced, >75%

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24
Q

what are the causes of restrictive disease?

A

ILD
neurological - MND
scoliosis
obesity

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25
Q

how can the severity of an asthma exacerbation and how well the asthma is controlled be estimated?

A

peak flow meter - measured peak expiratory flow rate
- stand tall, takes deep breath in, make good seal around device, blow as fast and hard as possible
- take 3 attempts and record best one
- varies on size and age of patient - so recorded as percentage of predicted based on sex, height and age

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26
Q

how can the severity of an asthma exacerbation and how well the asthma is controlled be estimated?

A

peak flow meter - measured peak expiratory flow rate
- stand tall, takes deep breath in, make good seal around device, blow as fast and hard as possible
- take 3 attempts and record best one
- varies on size and age of patient - so recorded as percentage of predicted based on sex, height and age

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27
Q

define asthma

A

chronic inflammatory condition of the airways where bronchocontriction cocurs

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28
Q

what triggers asthma?

A

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

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29
Q

what is the typical presentation of a patient who is likely to have asthma?

A

Episodic symptoms
Diurnal variability. Typically worse at night.
Dry cough with wheeze and shortness of breath
A history of other atopic conditions such as eczema, hayfever and food allergies
Family history
Bilateral widespread “polyphonic” wheeze

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30
Q

what kind of presentation indicated 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. This suggests a focal lesion or infection.

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31
Q

what are the NICE guidlines of the diagnosis of asthma?

A

not based on clinical diagnosis, requires testing
first line - Fractional exhaled nitric oxide
- Spirometry with bronchodilator reversibility
If there is diagnostic uncertainty after first line investigations these can be followed up with further testing:
Peak flow variability measured by keeping a diary of peak flow measurements several times per day for 2 to 4 weeks
Direct bronchial challenge test with histamine or methacholine

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32
Q

how is asthma managed long term?

A

SABA - salbutamol acts as reliever in exacerbation
ICS - beclometasone acts as preventer
LABA - salmeterol - longer action
LAMA - tiotropium
leukotriene receptor antag - montelukast
theophylline - relax smooth muscle (narrow therapeutic window and can be toxic in excess)
maintenance and reliever therapy - combination of ICS and LABA…preventor and reliever

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33
Q

what is the BTS/SIGN stepwise ladder?

A

Add short-acting beta 2 agonist inhaler (e.g. salbutamol) as required for infrequent wheezy episodes.
Add a regular low dose corticosteroid inhaler.
Add LABA inhaler (e.g. salmeterol). Continue the LABA only if the patient has a good response.
Consider a trial of an oral leukotriene receptor antagonist (i.e. montelukast), oral beta 2 agonist (i.e. oral salbutamol), oral theophylline or an inhaled LAMA (i.e. tiotropium).
Titrate inhaled corticosteroid up to “high dose”. Combine additional treatments from step 4. Refer to specialist.
Add oral steroids at the lowest dose possible to achieve good control.

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34
Q

what are the NICE guidlines stepwise ladder for asthma?

A

Add short-acting beta 2 agonist inhaler (e.g. salbutamol) as required for infrequent wheezy episodes.
Add a regular low dose inhaled corticosteroid.
Add an oral leukotriene receptor antagonist (i.e. montelukast).
Add LABA inhaler (e.g. salmeterol). Continue the LABA only if the patient has a good response.
Consider changing to a maintenance and reliever therapy (MART) regime.
Increase the inhaled corticosteroid to a “moderate dose”.
Consider increasing the inhaled corticosteroid dose to “high dose” or oral theophylline or an inhaled LAMA (e.g. tiotropium).
Refer to a specialist.

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35
Q

which additional management as well as inhalers are used for 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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36
Q

how can an acute asthma exacerbation present?

A

Progressively worsening shortness of breath
Use of accessory muscles
Fast respiratory rate (tachypnoea)
Symmetrical expiratory wheeze on auscultation
The chest can sound “tight” on auscultation with reduced air entry

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37
Q

how is acute asthma graded?

A

Moderate - PEFR 50 – 75% predicted
Severe -
PEFR 33-50% predicted
Resp rate >25
Heart rate >110
Unable to complete sentences
Life-threatening -
PEFR <33%
Sats <92%
Becoming tired
No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
Haemodynamic instability (i.e. shock)

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38
Q

how is acute asthma treated?

A

Moderate:
Nebulised beta-2 agonists
Nebulised ipratropium bromide
Steroids. Oral prednisolone or IV hydrocortisone. These are continued for 5 days
Abx if have infection
Severe:
Oxygen if required to maintain sats 94-98%
Aminophylline infusion
Consider IV salbutamol
Life threatening:
IV magnesium sulphate infusion
Admission to HDU / ICU
Intubation in worst cases – however this decision should be made early because it is very difficult to intubate with severe bronchoconstriction

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39
Q

what will the results of an ABG in asthma?

A

tachypnoea - drop in CO2 - respiratory alkalosis
if normal CO2 or hypoxia - life threatening
if high CO2 - very bad

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40
Q

what is the main side effects of salbutamol?

A

hypokalaemia
tachycardia

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41
Q

how must patients with asthma be admitted?

A

asthma action plan
rescue pack or steroids

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42
Q

how does COPD present?

A

long term smoker
chronic SOB, cough, sputum, recurrent resp tract infections, haemoptysis, chest pain, NOT CLUBBING

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43
Q

what are the grades used for assessing the impact of breathlessness?

A

MRC dysponea scale
Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

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44
Q

how is COPD diagnosed?

A

clinical presentation
spirometry - obstructive and not reversible

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45
Q

how can the severity of airway obstruction be measured?

A

FEV1 -
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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46
Q

what other investigations are useful in diagnosing COPD?

A

chest x ray - lung cancer
FBC - polycythaemia, anaemia
BMI - weight loss - cancer, COPD and weight gain - steroids
sputum culture - pseudomonas
ECG and echo - heart
CT thorax - fibrosis, cancer, bronchiectasis
serum alpha 1 antitrypsin - early onset COPD
TLCO - decreased in COPD

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47
Q

what is the long term management of COPD?

A

smoking cessation
pneumococcal and flu vaccine
step 1 - SABA or SAMA
step 2 - combined LABA + LAMA if no asthma/steroid responsive features, if they do have those features - LABA + ICS such as symbicort and add in LAMA
if severe - nebulisers, oral theophylline, oral mucolytics, long term prophylactix abx, long term o2

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48
Q

when might 02 therapy be used?

A

if COPD is causing chronic hypoxia, polycythaemia, cyanosis, HF secondary to cor pulmonale
…not if smoke as risk of fire

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49
Q

how are exacerbations of COPD investigated?

A

ABG - low pH with raised CO2 - acutely retaining - resp acidosis
if raised HCO3 they chronically retain CO2
distinguish type of resp failure
Chest xray to look for pneumonia or other pathology
ECG to look for arrhythmia or evidence of heart strain (heart failure)
FBC to look for infection (raised white cells)
U&E to check electrolytes which can be affected by infection and medications
Sputum culture if significant infection is present
Blood cultures if septic

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50
Q

why might you be cautious of oxygen therapy in COPD?

A

Too much oxygen in someone that is prone to retaining CO2 can depress their respiratory drive. This slows down their breathing rate and effort and leads to them retaining more CO2. Therefore in someone who retains CO2 the amount of oxygen that is given needs to be carefully balanced to optimise their pO2 whilst not increasing their pCO2. This is guided by oxygen saturations and repeat ABGs.
-venturi mask are used - so some ox leaks out and normal air to be inhaled along with o2 so percentage of inahled o2 can be carefully controlled

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51
Q

what are the target oxygen saturations in COPD?

A

If retaining CO2 aim for oxygen saturations of 88-92% titrated by venturi mask
If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations > 94%

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52
Q

what is the medical tx of an exacerbation of COPD?

A

Typical treatment if they are well enough to remain at home:
Prednisolone
Regular inhalers or home nebulisers
Antibiotics if there is evidence of infection
In hospital:
Nebulised bronchodilators (e.g. salbutamol 5mg/4h and ipratropium 500mcg/6h)
Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)
Antibiotics if evidence of infection
Physiotherapy can help clear sputum
Options in severe cases not responding to first line treatment:
IV aminophylline
Non-invasive ventilation (NIV)
Intubation and ventilation with admission to intensive care
Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate

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53
Q

define non invasive ventilation and when it is used

A

an alternative to full intubation and ventilation to support the lungs in respiratory failure due to obstructive lung disease
using full face mask or tight fitting nasal mask
either by BiPAP or CPAP

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54
Q

define BiPAP and when it is used

A

bilevel positive airway pressure
- cycle of low and high pressure to correspond to patients inspiration (IPAP) and expiration (EPAP)
used in type 2 resp failure when resp acidosis <7.35 and co2 >6 despite medical tx
monitor with ABG

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55
Q

what are the main contraindications of BiPAP?

A

untreated pneumothorax or any structural abnormality affecting face, airway or GI tract

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56
Q

define CPAP and its indications

A

continuous positive airway pressure - continuous air so keeps airways expanded
- obstructive sleep apnoea
- congestive HF
- acute pulmonary oedema

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57
Q

define ILD

A

inflammation and fibrosis of lung parenchyma
replacement of normal elastric and functioning lung tissue with scar tissue

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58
Q

how is ILD diagnosed?

A

high resolution CT of thorax - ground glass appearance
lung biopsy if required

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59
Q

how is ILD managed?

A

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 where appropriate
Lung transplant

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60
Q

define idiopathic pulmonary fibrosis

A

progressive pulmonary fibrosis with no clear cause
SOB, dry cough >3 mths
>50 yr olds
bibasal fine inspiratory crackle and finger clubbing
poor prognosis

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61
Q

how is idiopathic pulmonary fibrosis medically treated?

A

only slows progression of disease-
Pirfenidone is an antifibrotic and anti-inflammatory
Nintedanib is a monoclonal antibody targeting tyrosine kinase

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62
Q

which drugs are responsible for causing pulmonary fibrosis?

A

‘drug induced’
Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

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63
Q

which conditions cause pulmonary fibrosis?

A

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

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64
Q

define hypersensitivity pneumonitis

A

aka extrinsic allergic alveolitis
type 3 - parenchymal inflammation and destruction due to allergen

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65
Q

how is hypersensitivity pneumonitis diagnosed?

A

Bronchoalveolar lavage involves collecting cells from the airways during bronchoscopy by washing the airways with fluid then collecting that fluid for testing. This shows raised lymphocytes and mast cells in hypersensitivity pneumonitis.

66
Q

how is hypersensitivity pneumonitis managed?

A

removing the allergen, giving oxygen and steroids.

67
Q

what are some examples of specific causes of hypersensitivity pneumonitis?

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

68
Q

define cryptogenic organising pneumonia

A

bronchiolitis obliterans organising pneumonia - a focal area of inflammation of the lung tissue
can be idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.

69
Q

how does cryptogenic organising pneumonia present?

A

similar to pneumonia
- SOB, cough, fever, lethargy
focal consolidation

70
Q

how is cryptogenic organising pneumonia diagnosed and treated?

A

lung biopsy
systemic steroids

71
Q

what substance can cause lung fibrosis?

A

asbestos
can be oncogenic but takes several years to develop

72
Q

what other conditions are caused by asbestos?

A

Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma

73
Q

what are the exudative causes of pleural effusion?

A

all related to inflammation - protein leaking out to pleural space
Lung cancer
Pneumonia
Rheumatoid arthritis
Tuberculosis

74
Q

what are the transudative causes of pleural effusion?

A

fluid moving across into pleural space
Congestive cardiac failure
Hypoalbuminaemia
Hypothroidism
Meig’s syndrome (right sided pleural effusion with ovarian malignancy)

75
Q

how does pleural effusion present?

A

Shortness of breath
Dullness to percussion over the effusion
Reduced breath sounds
Tracheal deviation away from the effusion if it is massive

76
Q

which investigations are required to diagnose pleural effusion?

A

chest x ray -
Blunting of the costophrenic angle
Fluid in the lung fissures
Larger effusions will have a meniscus. This is a curving upwards where it meets the chest wall and mediastinum.
Tracheal and mediastinal deviation if it is a massive effusion
sample of pleural fluid by aspiration or chest drain - protein, cell count, pH, glucose, LDH, microbiology

77
Q

how is pleural effusion treated?

A

conservative - if small
pleural aspiration
chest drain

78
Q

define empyema

A

infected pleural effusion
suspect with improving pneumonia but new fever
pus in aspiration, with pH <7.2, low glucose, high LDH
treated by chest drain and abx

79
Q

define pneumothorax

A

air into pleural space separating lung from chest wall

80
Q

what are the causes of pneumothorax?

A

Spontaneous
Trauma
Iatrogenic such as due to lung biopsy, mechanical ventilation or central line insertion
Lung pathology such as infection, asthma or COPD

81
Q

which investigation sif the first line choice for a simple pneumothorax?

A

erect chest x ray - an area between the lung tissue and the chest wall where there are no lung markings. There will be a line demarcating the edge of the lung where the lung markings ends and the pneumothorax begins
can measured size -> measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum
if too small - use CT thorax

82
Q

how is pneumothorax managed?

A

If no SOB and there is a < 2cm rim of air on the chest xray then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.
If SOB and/or there is a > 2cm rim of air on the chest xray then it will require aspiration and reassessment.
If aspiration fails twice it will require a chest drain.
Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.

83
Q

define tension pneumothorax and what it is caused by

A

trauma to the chest wall creates a one way valve that lets air in but not out of pleural space…air is trapped and more air is drawn in with each breath
pushes mediastinum across, kinks big vessels and causes cardiorespiratory arrest

84
Q

what are the signs of a tension pneumothorax?

A

Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
Tachycardia
Hypotension

85
Q

how is a tension pneumothorax managed?

A

“Insert a large bore cannula into the second intercostal space in the midclavicular line.”
then requires chest drain for definitive management

86
Q

what is the location for a chest drain to be fixed?

A

The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)
just above the rib to avoid neurovascular bundle below

87
Q

why are PE’s dangerous?

A

Once they are in the pulmonary arteries they block the blood flow to the lung tissue and create strain on the right side of the heart. DVTs

88
Q

what are the risk factors for PE?

A

Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia
…make sure to ask in hx

89
Q

what is used as VTE prophylaxis and what is contraindicated?

A

LMWH - enoxaparin:
active bleeding, existing warfarin or NOAC use
anti embolic stockings:
peripheral arterial disease

90
Q

how does PE present?

A

Shortness of breath
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Hypoxia
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability causing hypotension
signs of DVT - unilateral leg swelling and tenderness

91
Q

what score predicts the risk of DVT/PE?

A

Well’s score - recent surgery, tachycardia, haemopytsis

92
Q

how is a PE diagnosed?

A

history, exam
chest x ray
well’s score - if likely perform CT pulmonary angiogram, if not d dimer and if postiive CTPA
can use VQ scan (when CTPA is unsuitable like in renal impairment)

93
Q

what will a PE present as on an ABG?

A

resp alkalosis - the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic.
Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.

94
Q

how is PE managed?

A

supportive - admission, oxygen, analgesia, monitor
initial - apixaban or rivaroxaban - if suspected, immediate
long term - warfarin, DOAC, LMWH(pregnancy or cancer) for warfa- target INR for warfarin is 2-3. When switching to warfarin continue LMWH for 5 days or the INR is 2-3 for 24 hours on warfarin (whichever is longer).
continue for 3 months if obvious reversible cause, beyond 3 months if irreversible or unclear, and 6 months in active cancer

95
Q

what is a tx option for a massive PE with haemodynamic compromise?

A

thrombolysis but huge risk of bleeding so benefits must outweigh risks
- streptokinase, atelplase either via peripheral cannula or into central catheter into pulmonary arteries

96
Q

define pulmonary hypertension

A

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

97
Q

what are the causes of pulmonary hypertension?

A

Group 1 – Primary pulmonary hypertension or connective tissue disease such as systemic lupus erythematous (SLE)
Group 2 – Left heart failure usually due to myocardial infarction or systemic hypertension
Group 3 – Chronic lung disease such as COPD
Group 4 – Pulmonary vascular disease such as pulmonary embolism
Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders

98
Q

what are the signs and sx of pulmonary hypertension?

A

SOB
Syncope
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema.

99
Q

which investigations are required to diagnose pulmonary hypertension?

A

ECG - right ventricular hypertophy - larger R waves on R side chest leads (V1-3), and S waves on left side (V4-6)
- right axial deviation
- right bundle branch block
chest x ray -
dilated pulmonary arteries and R ventricular hypertrophy
other - A raised NT-proBNP blood test result indicates right ventricular failure
Echo can be used to estimate pulmonary artery pressure

100
Q

how is pulmonary hypertension managed?

A

primary - IV prostanoids, endothelin receptor antagonist, phosphodiesterase-5-inhibitors
secondary - treat underlying cause
supportive - resp failure, arrythmias, HF

101
Q

what is the prognosis of pulmonary hypertension?

A

poor - 30-40% survival

102
Q

define sarcoidosis

A

granulomatous inflammatory condition (lots of macrophages)
cause is unknown
affects young adult and around 60
women and black people

103
Q

what are the sx of sarcoidosis?

A

most common to least
chest sx - dry cough, SOB, lungs - mediastinal lymphadenopathy, pulmonary fibrosis, pulmonary nodules
systemic sx - fever, weight loss, fatigue
liver - nodules, cirrhosis, cholestasis
eyes - uevitis, conjuncitivits, optic neuritis
skin - erythema nodusum - nodules on shins, lupus pernio (purple lesions on cheek and nose), granulomas in scar tissue
heart - bundle branch block, heart block,
kidneys - stones, nephrocalcinosis, interstitial nephritis
CNS - nodules, diabetes inspidius, encephalopathy
PNS - facial nerve palsy, mononeuritis multiplex
bones - arthralgia, arthritis, myopathy

104
Q

define lofgren’s syndrome and the triad of sx

A

specific presentation of sarcoidosis
triad of Erythema nodosum, Bilateral hilar lymphadenopathy, Polyarthralgia (joint pain in multiple joints)

105
Q

what are the ddx of lofgren’s syndrome?

A

Tuberculosis
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis

106
Q

which blood tests are used to diagnose lofgren’s syndrome?

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

107
Q

which imaging is used to diagnose lofgren’s syndrome?

A

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

108
Q

what is the gold standard for confirming sarcoidosis?

A

histology from biopsy usually bronchoscoy with USS guided biopsy of mediastinal lymph nodes
…shows non caseating granulomas with epithelioid cells

109
Q

what tests are used to diagnose sarcoidosis from extra pulmonary involvement?

A

U&Es - kidney involvement
Urine dipstick or urine albumin-creatinine ratio to look for proteinuria indicating nephritis
LFTs - liver involvement
Ophthalmology review - eye involvement
ECG and echocardiogram for heart involvement
Ultrasound abdomen - liver and kidney involvement

110
Q

how is sarcoidosis treated?

A

if mild or no sx - no treatment, resolves spontaneously
first line - oral steroids for 6-24 months, and bisphosphonates to protein against osteoporosis
second line - methotrexate, azathioprine
lung transplant for severe pulmonary disease

111
Q

what is the prognosis of sarcoidosis?

A

spontaneously resolves witin 6 months in around 60% of patients
can progress with pulmonary fibrosis and hypertension…so require lung transplant
death caused by arrythmias or CNS

112
Q

define obstructive sleep apnoea

A

collapse of pharyngeal airway during sleep
stop breathing periodically for up to a few mins
usually reported by partner

113
Q

what are the risk factors of obstructive sleep apnoea?

A

Middle age
Male
Obesity
Alcohol
Smoking

114
Q

what are the fx 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

115
Q

what can severe cases of sleep apnoea cause?

A

hypertension
HF
MI

116
Q

what scale is used to determine the severity of obstructive sleep apnoea?

A

epworth sleepiness scale - assess sx of sleepiness

117
Q

what is important when in a consultation for obstructive sleep apnoea?

A

ask about daytime sleepiness and their occupation as may require urgent referral if occupation is dangerous

118
Q

how is obstructive sleep apnoea managed?

A

referral to ENT specialist or specialist sleep clinic - sleep studies - monitor oxugen sats, HR, RR and breathign when asleep
- correct reversible risk fx - stop alcohol, smoke, lose weight
- CPAP which provided continuous pressure to maintain patency of airway
- surgery - uvulopalatopharngoplasty (UPPP)

119
Q

what are the absolute contraindications of performing spirometry?

A

Myocardial infarction 4 weeks
Unstable angina
Ascending aortic aneurysm
Pneumothorax
Pulmonary embolism

120
Q

what are the types of flow volume loops?

A

Identify upper airway obstruction, which can be undetectable with standard expiratory measurements

A characteristic limitation of flow (plateau) during forced inhalation suggests variable extra-thoracic obstruction

Limitation of flow during forced exhalation suggests variable intrathoracic obstruction

Fixed upper airway obstruction causes flow limitation during both forced inhalation and forced exhalation

121
Q

what is a normal lung volume?

A

normal: 80-120%
>120% - hyperinflation
<80% - restriction

122
Q

what is DLCO and how can it be affected?

A

1)DLCO assesses gas exchange

2) A decreased DLCO accompanied by restrictive disease suggests intrinsic
lung disease

3) Normal DLCO accompanied by restrictive disease suggests a non-
pulmonary cause of restriction

4) Decreased DLCO accompanied by obstructive airways disease suggests
emphysema

5) A reduced DLCO with normal lung volumes suggests possible pulmonary
vascular disease

                           80-120% predicted: Normal
                           < 80% Reduced
123
Q

spirometry

A

see notability notes and flow vol loops

124
Q

how are exacerbations of copd managed?

A

Oxygen
Salbutamol
Hydrocortisone/prednisolone
Ipratropium bromide
Triotropium bromide

125
Q

how to prescribe oxygen in copd?

A

1 and 2
1- not co2 retainer on ABG - aim for 96% sats
2 - co2 retainer on abg - aim for 88-92%

126
Q

aspiration pneumonia

A

This man has likely aspirated following nasogastric tube insertion. Nasogastric tube insertion is a risk factor for aspiration pneumonia. Aspiration pneumonia is when contents from the stomach or oropharyngeal secretions enter the airway and then the lungs. This leads to inflammation and pneumonia.

Due to the anatomy of the airway the right bronchus is more straight and vertically orientated than the left side meaning aspiration is most likely to affect the lungs on the right hand side.

127
Q

squamou cell

A

Squamous cell carcinoma is associated with hypertrophic pulmonary osteoarthropathy (HPOA)

128
Q

asbestosis

A

Asbestosis causes pulmonary fibrosis predominantly affecting the lower zones

129
Q

mesothelioma

A

pleural thickening indicative of mesothelioma on the right, almost certainly due to asbestos exposure during his shipbuilding or construction work.

130
Q

severity of copd

A

FEV1
>80% = MILD
50-79 = MOD
30-49 = SEVERE
<30 = V SEVERE

131
Q

azathioprine in coopd

A

According to NICE 2018, consider azithromycin (usually 250 mg 3 times a week) for people with COPD if they:

do not smoke and
have optimised non-pharmacological management and inhaled therapies, relevant vaccinations and (if appropriate) have been referred for pulmonary rehabilitation and continue to have 1 or more of the following, particularly if they have significant daily sputum production:

132
Q

sucultation of bronchiectasis

A

The auscultation findings of coarse crackles and high-pitched inspiratory squeaks are typical of bronchiectasis

133
Q

copd ltot

A

LTOT if 2 measurements of pO2 < 7.3 kPa

134
Q

cap in community

A

NICE have provided guidance on what advice patients should be given in terms of response to treatment and recovery, by:
week 1: fever should resolve
week 4: chest pain and sputum should have significantly reduced
week 6: cough and shortness of breath should have significantly reduced
month 3: most symptoms should have resolved, except for tiredness
month 6: should be returned to nor

135
Q

normal or rised TLCO

A

NICE have provided guidance on what advice patients should be given in terms of response to treatment and recovery, by:
week 1: fever should resolve
week 4: chest pain and sputum should have significantly reduced
week 6: cough and shortness of breath should have significantly reduced
month 3: most symptoms should have resolved, except for tiredness
month 6: should be returned to nor

136
Q

diffuclty walking

A

Difficulty walking and muscle tenderness are features of Lambert-Eaton myasthenic syndrome, which is one of many paraneoplastic syndromes associated with small cell lung cancer

137
Q

chrug strauss syndrome

A

Churg-Strauss disease is associated with pANCA.

There are three stages to the presentation of Churg-Strauss disease.

The initial phase is characterised by allergy with many patients having a history of asthma or allergic rhinitis. This inflammation of the nasal passages can lead to the development of nasal polyps.

The second phase is eosinophilia

The third stage is the vasculitis itself which affects small and medium-sized blood vessels and therefore resulting in damage to many organs. Given this patient’s kidney failure, it appears to be affecting his renal blood supply.

138
Q

ARDS

A

Acute pancreatitis is known to precipitate ARDS. ARDS is characterised by bilateral pulmonary infiltrates and hypoxaemia. Note that pulmonary oedema is excluded by his normal pulmonary capillary wedge pressure.

139
Q

copd exacerb

A

Oral prednisolone is recommended for 5 days in acute exacerbations of COPD

140
Q

inhaler technique

A

When using an inhaler, for a second dose you should wait for approximately 30 seconds before repeating

141
Q

bronchiectasis organism

A

Bronchiectasis: most common organism = Haemophilus influenzae

142
Q

contraindication for chest drain

A

An INR >1.3 is a relative contraindication for chest drain insertion

143
Q

copd abx criteris

A

Azithromycin prophylaxis is recommended in COPD patients who meet certain criteria and who continue to have exacerbations

144
Q

meig’s syndrome

A

Meig’s syndrome: Benign ovarian tumour, ascites, and pleural effusion.

145
Q

mulitple round lesions on cxr

A

lung mets

146
Q

copd + asthma

A

COPD - still breathless despite using SABA/SAMA and asthma/steroid responsive features → add a LABA + ICS

147
Q

tb part of lung

A

Tuberculosis typically causes upper zone pulmonary fibrosis

148
Q

mimic pneumothorax

A

Large bullae in COPD can mimic a pneumothorax

149
Q

lung abscess

A

Percutaneous drainage should be considered if a lung abscess is not improving with intravenous antibiotics

150
Q

tension v simple

A

tension = hypotension

151
Q

hypovent

A

high 02 low co2

152
Q

exacerbation of copds

A

5 day course of pred
NICE only recommend giving oral antibiotics in an acute exacerbation of COPD in the presence of purulent sputum or clinical signs of pneumonia

153
Q

Legionella pneumophilia

A

Legionella pneumophilia is best diagnosed by the urinary antigen test

154
Q

bilateral hilar lymphadenopathy ddx

A

bilateral hilar lymphadenopathy are sarcoidosis and tuberculosis.

155
Q

rash from sarcoidosis

A

lupus pernio, which describes dark indurated plaques that can involve the face and extremities.

156
Q

asx sarcoidosis with cxr features

A

no treatment

157
Q

pleural effusion exudate

A

If a pleural effusion fluid protein/serum protein ratio is >0.5, the effusion is an exudate

158
Q

obstructive sleep apnoea investigation

A

Polysomnography is diagnostic for obstructive sleep apnoea

159
Q

kartageners syndrome

A

The combination of bronchiectasis and dextrocardia is highly suggestive of Kartagener’s syndrome

160
Q

extrinsic allergic alveolitis tx

A

The treatment of extrinsic allergic alveolitis is mainly avoidance of triggers

161
Q

normal pco2 asthma

A

A normal pCO2 in a patient with acute severe asthma is an indicator that the attack may classified be life-threatening