RESP Flashcards

1
Q

Define COPD

A

Chronic, progressive lung disorder characterised by airflow obstruction, with the following:
Chronic Bronchitis & Emphysema

chronic bronchitis: Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years

emphysema: Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles

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2
Q

What is chronic bronchitis?

A
Narrowing of the airways resulting in bronchiole 
inflammation (bronchiolitis)  
Bronchial mucosal oedema   
Mucous hypersecretion   
Squamous metaplasia  

COPD criteria:
Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years

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3
Q

What is emphysema?

A

Destruction and enlargement of alveoli
Leads to loss of elasticity that keeps small airways open in expiration
Progressively larger spaces develop called bullae (diameter > 1 cm)

COPD criteria:
Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles

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4
Q

What are the PC of COPD?

A
Recognise the presenting symptoms of COPD  
Chronic cough  
Sputum production  
Breathlessness  
Wheeze  
Reduced exercise tolerance
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5
Q

Recognise the signs of COPD on physical examination on INSPECTION

A
Respiratory distress  
Use of accessory muscles   
Barrel-shaped over-inflated chest   
Decreased cricosternal distance   
Cyanosis
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6
Q

Recognise the signs of COPD on physical examination on PERCUSSION

A

Hyper-resonant chest

Loss of liver and cardiac dullness

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7
Q

Recognise the signs of COPD on physical examination on AUSCULTATION

A
Quiet breath sounds  
Prolonged expiration  
Wheeze  
Rhonchi 
Sometimes crepitations  

rhonchi= rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions

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8
Q

Recognise the signs of Co2 retention of COPD on physical examination

A

Bounding pulse
Warm peripheries
Asterixis

LATE STAGES: signs of right heart failure (cor pulmonale)
Right ventricular heave
Raised JVP
Ankle oedema

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9
Q

What is cor pulmonale?

A

Abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.

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10
Q

What are the results of spirometry and pulmonary function tests of a COPD pt?

A
Shows obstructive picture 
Reduced PEFR 
Reduced FEV1/FVC 
Increased lung volumes  
Decreased carbon monoxide gas transfer coefficient
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11
Q

What does a CXR of a COPD pt look like?

A

May appear NORMAL

Hyperinflation (> 6 anterior ribs, flattened diaphragm)
Reduced peripheral lung markings
Elongated cardiac silhouette

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12
Q

What would the FBC of a COPD pt show?

A

Increased Hb and haematocrit due to secondary polycythaemia

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13
Q

List the tests you would do for a COPD pt

A

Spirometry & Pulmonary Function Tests
FBC
CXR
ABG (may be hypoxic with raised paco2)
ECG and Echo (cor pulmonale)
Sputum and blood cultures (for infective exacerbations)
a1-antitrypsin deficiency if they are really young

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14
Q

Generate a management plan for COPD

A

STOP SMOKING

Bronchodilators

SABA(e.g. salbutamol)

Anticholinergics (e.g. ipratropium bromide)

LABA (if > 2 exacerbations per year)

Steroids

Inhaled beclamethasone - considered in all patients with FEV1 < 50% of predicted OR > 2 exacerbations per year Regular oral steroids should be avoided if possible

Pulmonary rehabilitation

OXYGEN THERAPY
Only for those who stop smoking
Indicated if: PaO2 < 7.3 kPa on air during a period of clinical stability
PaO2: 7.3-8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension

Prevention of infective exacerbations: pneumococcal and influenza vaccination

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15
Q

What is the mx of ACUTE COPD exacerbations?

A

24% O2 via Venturi mask *
Increase slowly if no hypercapnia and still hypoxic (do an ABG)
Corticosteroids
Start empirical antibiotic therapy if evidence of infection Respiratory physiotherapy to clear sputum
Non-invasive ventilation may be necessary in severe cases

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16
Q

Identify the possible complications of COPD

A
Acute respiratory failure  
Infections  
Pulmonary hypertension  
Right heart failure   
Pneumothorax (secondary to bullae rupture)   
Secondary polycythaemia
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17
Q

What is the normal FEV1/FVC?

A

80%

<80% = obstructive picture 
>80% = restrictive picture

reversible in asthma but not in COPD

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18
Q

CURB 65
Criteria for each
And interpretation of scores

A

Clinical prediction rule for COMMUNITY ACQUIRED PNEUMONIA

C - Confusion
U- Urea  = >7
R - RR > 30
B - BP <90/60mmHg
65 - >65years old

Score:
0-1 = outpatient <5% mortality
2-3 = hospitalise for a bit then outpatient <10% mortality
3-5 = severe pneumonia and hospitalisation possible escalate to ICU 15-30% mortality

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19
Q

How does a classic pneumonia pt present?

A

Pyrexia
Productive cough with green sputum

Rigors  
Sweating  
Malaise  
Cough  
Sputum 
Breathlessness  
Pleuritic chest pain  
Confusion (in severe cases or in the elderly)
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20
Q

Define pneumonia and its 4 categories.

A

Infection of distal lung parenchyma.

It can be categorised in many ways: 
Community-acquired  
Hospital-acquired/nosocomial  
Aspiration pneumonia  
Pneumonia in the immunocompromised  
Typical
Atypical
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21
Q

Which organisms cause atypical pneumonia?

A

Mycoplasma
Chlamydia
Legionella

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22
Q

What are common organisms for Community acquired pneumonia?

A

Streptococcus pneumoniae (70%) *
Haemophilus influenzae *
Moraxella catarrhalis (occurs in COPD patients) Chlamydia pneumonia
Chlamydia psittaci (causes psittacosis)
Mycoplasma pneumonia
Legionella (can occur anywhere with air conditioning) Staphylococcus aureus
Coxiella burnetii (causes Q fever)
TB

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23
Q

What are common organisms for Hospital acquired pneumonia?

A

Gram-negative enterobacteria (Pseudomonas, Klebsiella)

Anaerobes (due to aspiration pneumonia)

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24
Q

How does atypical pneumonia present?

A

Headache
Myalgia
Diarrhoea/abdominal pain
DRY cough

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25
Q

Recognise the signs of pneumonia on physical examination

A
Pyrexia 
Respiratory distress 
Tachypnoea (CURB RR>30)
Tachycardia 
Hypotension (CURB <90/60mmHg)
Cyanosis  
Decreased chest expansion  
Dull to percuss over affected area   
Increased tactile vocal fremitus over affected area   Bronchial breathing over affected area  
Coarse crepitations on affected side* 
Chronic suppurative lung disease (empyema, abscess) --> clubbing
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26
Q

Identify appropriate investigations for pneumonia

A
Bloods  
FBC - raised WCC *
U&amp;Es 
LFT 
Blood cultures  *
ABG (assess pulmonary function)   
Blood film - Mycoplasma causes red cell agglutination *

CXR
Lobar or patchy shadowing
Pleural effusion
NOTE: Klebsiella often affects upper lobes
May detect complications (e.g. lung abscess)
Sputum/Pleural Fluid - MC&S
Urine - Pneumococcus and Legionella antigens **
Atypical Viral Serology
Bronchoscopy and Bronchoalveolar Lavage - if Pneumocystis carinii pneumonia is suspected, or if pneumonia fails to resolve

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27
Q

Generate a management plan for pneumonia

A

Assess severity using the British Thoracic Society CURB 65
Guidelines

Start empirical antibiotics
Oral Amoxicillin (0 markers)
Oral or IV Amoxicillin + Erythromycin (1 marker)
IV Cefuroxime/Cefotaxime/Co-amoxiclav + Erythromycin (> 1 marker)

Add metronidazole if:
Aspiration
Lung abscess
Empyema

Switch to appropriate antibiotic based on sensitivity

Supportive treatment:
Oxygen
IV fluids
CPAP, BiPAP or ITU care for respiratory failure
Surgical drainage may be needed for lung abscesses and empyema

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28
Q

What is the Discharge planning for pneumonia?

A

If TWO OR MORE features of clinical instability are present (e.g. high temperature, tachycardia, tachypnoea, hypotension, low oxygen sats) there is a high risk of re- admission and mortality

Consider other causes if pneumonia is not resolving

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29
Q

Identify the possible complications of pneumonia

A

Pleural effusion
Empyema
Localised suppuration (e.g. abscess)

Symptoms of abscesses:
Swinging fever *
Persistent pneumonia
Copious/foul-smelling sputum

Septic shock  
ARDS 
Acute renal failure   
Extra complications of Mycoplasma pneumonia 
Erythema multiforme  
Myocarditis  
Haemolytic anaemia  
Meningoencephalitis   
Transverse myelitis   
Guillain-Barre syndrome
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30
Q

What tests do you do for the atypical community acquired pneumonias?

A

Legionella - urinary antigen

Mycoplasma & Chlamydia - serology

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31
Q

Type 1 respiratory failure - how does it present on ABG?

A

Low PaO2

Normal/Low PaCO2

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32
Q

Type 1 respiratory failure - causes

A

Ventilation perfusion mismatch V/Q mismatch.

eg:
Pneumonia
Pulmonary Oedema
Pulmonary Embolism
Asthma
Emphysema
Fibrosing alveolitis
ARDS
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33
Q

Type 2 respiratory failure - how does it present on ABG?

A

Low PaO2

High PaCO2

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34
Q

Type 2 respiratory failure - causes

A

Alveolar hypoventilation with or without v/q mismatch

CAUSES:

Respiratory diseases: 
Pneumonia
COPD
Asthma
Obstructive sleep apnoea

Reduced respiratory drive:
Sedative drugs
CNS tumour
Trauma

Neuromuscular disease:
Cervical cord lesion
Diaphragmatic paralysis
Myasthenia gravis
Guillain-Barre syndrome

Thoracic wall disease:
Flail chest
Kyphoscoliosis

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35
Q

54yo woman presents with weight loss, loss of apettite, SOB.
RR = 19, o2 sats = 93%
OE: reduced air entry and dullness to percussion on the lower to midzones of the right lung and reduced chest expansion on the right

What is this?
+ explanation

A

Pleural effusion

Explanation:
Stony dullness is classic for pleural effusion but no one can really distinguish so consider dullness as classic pleural effusion as well.
Dullness + reduced chest expansion = Pleural effusion

Its NOT cancer because = no cheeky history of smoking also she is quite young
Bronchial carcinoma would present with = BRONCHIAL breathing over affected are of lung (not reduced air entry and dullness)

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36
Q

How can pleural effusions be categorised into? And what are the criteria (and the name of the criteria) ?

A

Transudates & Exudates

LIGHTS CRITERIA
Transudates = protein content <30g/L low LDH
Exudates = High in protein >30g/L high LDH

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37
Q

What are common causes of TRANSUDATE pulmonary effusion?

A

TRANSUDATES

Increased venous pressure
eg: cardiac failure, restrictive pericarditis, fluid overload,

Hypoproteinaemia
eg: cirrhosis, nephrotic syndrome, malabsorbtion

Hypothyroidism

Meig’s shyndrome (right pleural effusion coupled with ovarian fibroma)

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38
Q

What are common causes of EXUDATE pulmonary effusion?

A

EXUDATES:

Increased capillary permeability secondary to infection
eg: pnemonia, TB

Inflammation
eg: pulmonary infarction, RhA, SLE

Malignancy
eg: bronhogenic carcinoma, seconary metastases, lymphoma, mesothelioma, lymphagitis carcinomatosis

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39
Q

45yo woman presents with weight loss, anorexia, SOB
OE: reduced air entry and dullness to percussion in the right lung
Pleural tap = protein content >30g/L

What is this?

A

Pleural effusion
Exudate pleural effusion because protein content is above 30
Adding this with a weight loss and anorexia history = bronchial carcinoma (malignancy is a cause for exudative pleural effusion)

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40
Q

What is the first line investigation for pulmonary embolism?

A

Ct-Pa (given wells is above 2 aka high risk)

It’s the most readily avaiable , sensitive and specific test for PE.
It can detect them down to the 5th order pulmonary arteries
It’s readily obtainable out of hospital hours

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41
Q

What are the steps of the british thoracic society approach to mx of chronic asthma

A

Step 1: SABA in mild intermittent asthma
Step 2: SABA + inhaled regular low dose corticosteroid (beclamethasone 400mcg/day) if pt uses SABA more than 3 times a week or has required oral CS the past 2 years then
Step 3: SABA + low dose inhaled CS + LABA
if the patient is still symptomatic
Step 4: SABA + HIGH dose inhaled CS + LABA + Leukotriene receptor antagonists
if there is still poor asthma control
Step 5: SABA + high dose inhaled CS + LABA + Leukotriene R antagonists + Oral CS

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42
Q

What would you expect to see on an ECG of a pulmonary embolism pt?

A

May be normal
May show tachycardia, right axis deviation or RBBB
May show S1Q3T3 pattern = which means: deep s waves in lead 1, deep q waves in lead 3 and inverted t waves in lead 3.

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43
Q

What would you expect the ABG of a COPD pt to look like?

A

low o2
high co2
normal pH
bicarbonate on the high side

AKA:
HYPOXIC
Respiratory acidosis = AKA type 2 respiratory failure
Normal Ph

COPD pts rely on hypoxic drive in order to drive respiration. The respiratory centre in the brain is relatively insensitive to co2 (this is also why o2 therapy must be used cautiously in COPD pts - giving too much o2 may cause a decrease in respiratory drive and hence pt deterioration)

ABG in COPD = type 2 resp failure caused by alveolar hyperventilation with or without v/q mismatch

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44
Q

Define bronchiectasis

A

Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections

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45
Q

Causes of bronchiectasis

A

Idiopathic (50%)
Post-infectious (e.g. pneumonia, whooping cough, TB) HostMdefence defects (e.g. Kartagener’s syndrome, cystic fibrosis)
Obstruction of bronchi (e.g. foreign body, enlarged lymph nodes)
GORD
Inflammatory disorders (e.g. rheumatoid arthritis)

NOT: left ventricular failure

46
Q

Common organisms in bronchiectasis - causing the chronic infection

A

H influenzae
S pneumoniae
S aureus
P aeruginosa

47
Q

How does bronchiectasis classically present?

A

Productive cough with purulent sputum*** or haemoptysis Breathlessness
Chest pain
Malaise
Fever
Weight loss
Symptoms usually begin after an acute respiratory illness

48
Q

Other things you should be thinking with respiratory presenting complains accompanied with weight loss besides cancer

A

Pulmonary Effusion
TB
Bronchiectasis

Chronic allergic alveolitis
Idiopathic pulmonary fibrosis

dry cough + FLAWS = TB
Weight loss + dullness to percussion + reduced air entry = Pulmonary Effussion
Bronchiectasis = mucopurulent cough* + wtvr

49
Q

What are the respiratory causes of clubbing

A
Respiratory causes:
Malignancy			
Interstitial lung disease
Empyema lung abscess		
Cystic fibrosis			

!!!!!!!!!NOT COPD!!!!!!!!!!!!!

50
Q

What are causes of clubbing?

A
RESP:
Malignancy			
Interstitial lung disease
Empyema lung abscess		
Cystic fibrosis			
**NOT COPD**
CVS:
Malignancy			
Infective (bacterial) Endocarditis		
Tetralogy of Fallot 
Congenital cyanotic heart disease	
Atrial myxoma
GI:
Malignancy			
Coeliac’s disease
IBD	 - UC, Crohn's
Cirrhosis
51
Q

What signs on the hands during examination do you expect to find with COPD pts?

A

Tremor - co2 retention tremor
Peripheral cyanosis
Tar staining - SNIFF the nails lol

52
Q

Recognise the presenting symptoms of lung cancer

A

May be ASYMPTOMATIC

Symptoms due to primary 
o  Cough 
o  Haemoptysis 
o  Chest pain 
o  Recurrent pneumonia 

Symptoms due to local invasion
o Brachial plexus invasion –> shoulder/arm pain
o Left recurrent laryngeal nerve invasion –> hoarse voice and bovine cough
o Dysphagia
o Arrhythmias
o Horner’s syndrome

Symptoms due to metastatic disease or paraneoplastic phenomenon  
o  Weight loss  
o  Fatigue 
o  Fractures   
o  Bone pain
53
Q

Recognise the signs of lung cancer on physical examination

A

• May be NO SIGNS
• Fixed monophonic wheeze (suggesting that there is a single obstruction)
• Signs of lobar collapse or pleural effusion
• Signs of metastases (e.g. supraclavicular lymphadenopathy or hepatomegaly)
- reduced air entry

54
Q

Identify appropriate investigations for lung cancer

A
•  Diagnosis  
o  CXR 
o  Sputum cytology 
o  Bronchoscopy with brushings or biopsy 
o  CT/US-guided percutaneous biopsy 
o  Lymph node biopsy  

• Staging - requires CT/MRI of head, chest and abdomen (to check for mets). PET scans may also be useful

•  Bloods 
o  FBC  
o  U&amp;Es  
o  Calcium** (hypercalcaemia is a common feature)  
o  ALP **(raised with bone metastases)  
o  LFTs 

• Pre-Op - ABG and pulmonary function tests

55
Q

What is the most common type of lung cancer in non smokers?

A

Adenocarcinoma

It’s the most common type in smokers as well.

56
Q

28yo man with no history of resp disease
Comes to a&e with acute onset pleuritic chest pain and SOB while playing football
o2 sats = 93%, rr = 20, temp = 37.1
OE: decreased expansion of the left side and hyper-resonant to percussion and recued air entry on the left

What is this?

A

Pneumothorax - classic

YOUNG MALE playing football = spontaneous pneumothorax
Sudden onset SOB + Pleuritic Chest pain - CLASSIC.

With no hint of trauma in the history (iatrogenic or otherwise)
No fever
No underlying respiratory disorders (COPD, asthma, TB)

57
Q

Explain the aetiology/risk factors of pneumothorax

A

Spontaneous
Occurs in people with typically normal lungs
Typically in tall, thin males “while playing football”
It is probably caused by the rupture of a subpleural bleb

Secondary
Occurs in patients with pre-existing lung disease (e.g. COPD, asthma, TB)

Traumatic
Caused by penetrating injury to the chest
Often iatrogenic (e.g. during jugular venous cannulation, thoracocentesis)

Risk Factors  
Collagen disorders (e.g. Marfan's syndrome, Ehlers-Danlos syndrome)
58
Q

Recognise the presenting symptoms of pneumothorax

A

May be ASYMPTOMATIC if the pneumothorax is small Sudden-onset breathlessness
Pleuritic chest pain

Distress with rapid shallow breathing in tension pneumothorax

59
Q

Recognise the signs of pneumothorax on physical examination

A

There may be NO signs if the pneumothorax is small Signs of respiratory distress
Reduced expansion **
Hyper-resonance to percussion **
Reduced breath sounds **

60
Q

Recognise the signs of TENSION pneumothorax on physical examination

A
Severe respiratory distress   
Tachycardia  
Hypotension  
Cyanosis  
Distended neck veins   
Tracheal deviation away from the side of the pneumothorax **
61
Q

Where does the trachea deviate in a tension pneumothorax?

A

AWAY from the side of the pneumothorax

Other causes of AWAY from affected side:
Pleural effusion
Large mass.

62
Q

Whats the first line investigation of pneumothorax?

A

CXR

small - small rim of air around the lung = dont require chest drain
large - lung collapsed half way towards heart border = require chest drain

63
Q

What is the first line treatment of PE?

A

Treatment dose SC LMWH
+ Loading with WARFARIN and aim for 2-3 INR

When INR is reached stop LMWH and continue warfarin for 3< months

64
Q

Which respiratory disease is horner’s syndrome highly associated with?

A

Pancoast’s tumour
Apical lung tumour
mostly non-small

65
Q

Horner’s syndrome signs/symptoms

A

o Ptosis
o Miosis
o Anhydrosis

o (and enophthalmos)

PC:
•  Inability to open the eye fully on the affected side  
•  Loss of sweating on affected side  
•  Facial flushing  
•  Orbital pain/headache  
•  Other symptoms based on CAUSE
66
Q

What is the cause of Horner’s syndrome?

A
•  It is caused by disruption of the sympathetic nerves   
eg: 
o  Strokes  
o  Multiple sclerosis  
o  Apical lung tumours  - pancoast's tumour
o  Lymphadenopathy  
o  Basal skull tumours  
o  Carotid artery dissection  
o  Neck trauma
67
Q

Which ethinicites are commonly affected in sarcoidosis?

A

Afro-Caribbean

68
Q

What does tissue biopsy show under histology for sarcoidosis?

A

Non-caesating granulomas

69
Q

What is erythema nodosum?

A

Panniculitis (inflammation of subcutaneous fat tissue) presenting as red or violet subcutaneous nodules

Tender red or violet tender nodules bilaterally on BOTH
shins

70
Q

What does a FBC show in sarcoidosis?

A

Increased ESR

Increased ACE

71
Q

What’s the pathogenesis of sarcoidosis?

A
An UNKNOWN antigen is presented on MHC class 2 complexes on macrophages  to CD4+ T-lymphocytes  
These accumulate and release cytokines   
This leads to the formation of non-caseating granulomas in organs
72
Q

How does cor pulmonale present?

A

RHF symptoms on a history of respiratory disease - chronic pulmonary hypertension.

PC: dyspnoea, fatigue/syncope,
OE: cyanosis, tachycardia, raised JVP, right ventricular heave, pansystolic murmur, early diastolic (graham steel murmur), hepatomegaly, oedema.

73
Q

What are common causes of cor pulmonale?

A

In Laz:
Pulmonary fibrosis
Pneumoconiosis
COPD

Lung disease:
COPD, bronchiectasis, pulmonary fibrosis, lung resection

Pulmonary vascular disease:
Pulmonary Emboli, Pulmonary vasculitis, Primary pulmonary hypertension, ARDS, sickle cell disease, parasite infestation.

Thoracic cage abnormality:
kyphosis, scoliosis, thorocoplasty.

Neuromuscular disease:
myasthenia gravis, poliomyelitis, motor neuron disease

Hypoventilation:
sleep apnoea, cerebrovascular disease.

NOT MS.

74
Q

Which disease has the classic finding of reticulo-nodular shadowing on CXR?

A

Pulmonary Fibrosis

and pneumoconiosis

75
Q

Define idiopathic pulmonary fibrosis

A

Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium.

76
Q

Pulmonary fibrosis symptoms/signs

A

Symptoms:
Gradual-onset, progressive dyspnoea on exertion
Dry irritating cough
NO wheeze
Symptoms may be preceded by a viral-type illness Fatigue and weight loss are common
IMPORTANT: take a full occupational and drug history

Signs:
Clubbing (50%)
Bibasal fine late inspiratory crackles
Signs of right heart failure in advanced stages of disease

77
Q

Which diseases show ground glass pattern on scans?

A

Aspergillus lung disease - invasive aspergillosis
Extrinsic allergic alveollitis
Idiopathic pulmonary fibrosis

Either on CT or CXR.

78
Q

Whats the pathophysiology behind fall in volume of peripheral pulse on inspiration during an asthma attack?

A

At high RR as the patient inspires in, there is a negative intrathoracic pressure (due to air flow compromise due to narrowing of airways) which causes dilatation of the pulmonary vasculature. This causes pooling of blood in the lungs which results in diminished pulmonary venous return to the left atrium - decreased left atrial filling - hence reducing stroke volume causing the BP to drop and hence the peripheral pulse falls in response.

79
Q

What is the first line mx in pneumonia with curb65=0

A

Oral amoxicillin
(covers S. pneumoniae aka the most common organism better than erythromycin which is better for atypical organisms. Also its broad-spectrum)

80
Q

Define empyema

A

Pus in the pleural space which can occur in patients with resolving pneumonia.

81
Q

How does a pt with empyema present?

A

PMH of pneumonia recently
Transient fever
SOB
Pleural effusion on the same side of the resolving pneumonia

82
Q

What is the mx of empyema?

A

US-guided chest drain insertion

AB therapy

83
Q

What is the appearance of empyema fluid from chest drain?

A

Turbid and yellow/straw in colour

84
Q

What is the content of empyema fluid?

A

HIGH >30g/L protein - because its an exudate
HIGH LDL - because its an exudate
LOW Pleural pH <7.2 with normal blood pH
LOW glucose level

85
Q

What is normal pleural pH

A

7.6

Normal body pH: 7.35-7.45

86
Q

What does asbestosis mainly cause?

A

Malignant mesothelioma

90% of malignant mesotheliomas have asbestosis exposure.

87
Q

Define mesothelioma

A

• Aggressive tumour of the mesothelial cells, which

usually occurs in the pleura (90%) but can also occur in other sites, such as the peritoneum, pericardium and testes.

88
Q

Define extrinsic allergic alveolitis

A

Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts.
Also known as hypersensitivity pneumonitis.

89
Q

What causes allergic alveolitis?

A

Inhalation of antigenic dusts induce a hypersensitivity response in susceptible individuals
Antigenic dusts include microbes and animal proteins
Examples:

Farmer’s Lung - caused by MOULDY HAY containing thermophilic actinomycetes

Pigeon Fancier’s Lung - caused by BLOOD ON FEATHERS and excreta

Maltworker’s Lung - caused by barley or maltlings containing Aspergillus clavatus

Mushroom picker’s lung

(not coal worker)

90
Q

What are the pc of ACUTE allergic alveolitis?

A
Present 4-12 hrs after exposure  
REVERSIBLE episodes of:  
Dry cough  
Dyspnoea  
Malaise   
Fever  
Myalgia 
Wheeze and productive cough may develop if repeat high-level exposure   

IMPORTANT: make sure you get a full occupational history and enquire about hobbies
and pet

91
Q

What are the pc of CHRONIC allergic alveolitis?

A

Slowly increasing breathlessness
Decreased exercise tolerance
Weight loss
Exposure is usually chronic, low-level and there may be no history of previous acute episodes

IMPORTANT: make sure you get a full occupational history and enquire about hobbies
and pet

92
Q

Recognise the signs of extrinsic allergic alveolitis on physical examination

A

ACUTE
Rapid shallow breathing
Pyrexia
Inspiratory crepitations

CHRONIC
Fine inspiratory crepitations
Clubbing (rare)

93
Q

Identify appropriate investigations for extrinsic allergic alveolitis

A

Bloods
FBC - neutrophilia, lymphopenia
ABG - reduced PO2 + PCO2

Serology
Test for IgG to fungal or avian antigens
NOTE: these are not diagnostic because you may find these in normal individuals

CXR
Often NORMAL in acute episodes
Fibrosis may be seen in chronic cases

High Resolution CT-Thorax
Detects early changes
May show patchy ‘ground glass’ shadowing and nodules

Pulmonary Function Tests
Restrictive defect (low FEV1, low FVC)
Preserved or increased FEV1/FVC ratio
Reduced total lung capacity

Bronchoalveolar Lavage
Increased cellularity
Lung biopsy can also be performed

94
Q

A known AF patient who is on amiodarone presents with respiratory complains over the past 4 months. Including SOB at rest and a dry cough.

What are you thinking

A

Pulmonary fibrosis secondary to amiodarone treatment

95
Q

Which long term use drugs are RF for pulmonary fibrosis?

A

Amiodarone (AF)
Methotrexate (immunosupressant)

Others:
bleomycin
Bulsufan
Nitrofurantoin
Sulfasalazine
96
Q

Whats the most common organism causing aspergillus lung disease

A

Aspergillus fumigatus

97
Q

Which are the 3 ways aspergillus presents?

A

ASPERGILLOMA
Growth of an A. fumigates mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess)

Allergic Bronchopulmonary Aspergillosis (ABPA)
Colonisation of the airways by Aspergillus leads to IgE and IgG-mediated immune responses
Usually occurs in asthmatics
The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage and central bronchiectasis

Invasive Aspergillosis
Invasion of Aspergillus into lung tissue and fungal dissemination
This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS)

98
Q

Whats the epidemiology of aspergillus?

A

Immunocompromised

Elderly

99
Q

78yo woman with hyponatraemia, weight loss and haemoptysis.
CT: mass lesion in lung

What’s the most likely diagnosis?

A

Small cell carcinoma

EXPLANATION: Small cell cancers are thought to originate from the NEUROENDOCRINE cells of the bronchus and express neuroendocrine markers which may lead to ectopic hormone profuction (ADH ACTH), resulting in the PARANEOPLASTIC SYNDROME - causing SIADH (hyponatraemia)

100
Q

What are the spirometry values for the different COPD severities?

A

Mild - fev1/fvc <0.7 FEV1 % predicted >80%
Moderate - fev1/fvc <0.7 FEV1 % predicted 50-79%
Severe - fev1/fvc <0.7 FEV1 % predicted 30-49%
Very severe - fev1/fvc <0.7 FEV1 % predicted <30%

101
Q

What are the spirometry values for the different COPD severities?

A

Mild - fev1/fvc <0.7 FEV1 % predicted >80%
Moderate - fev1/fvc <0.7 FEV1 % predicted 50-79%
Severe - fev1/fvc <0.7 FEV1 % predicted 30-49%
Very severe - fev1/fvc <0.7 FEV1 % predicted <30%

102
Q

COPD mx steps

A

STEP 1: mild (>80%) SABA or SAMA
STEP 2: moderate (50-79%) add LABA or LAMA
STEP 3: severe (30-49%) LABA + LAMA or LABA + ICS
STEP 4: Very severe (<30%) LAMA + LABA + ICS

103
Q

Which medication used in asthma mx causes hypokalaemia?

A

Salbutamol

104
Q

Whats ARDS?

A

Acute Respiratory Distress Syndrome

A syndrome of acute and persistent lung inflammation with increased vascular permeability.

105
Q

What is ARDS classically characterised by/ 4 criteria?

A
  1. Acute onset
  2. Bilateral infiltrates consistent with pulmonary oedema present on CXR
  3. Hypoxaemia - pao2:FiO2 <200
  4. No clinical evidence of increased left arterial pressure (pulmonary capillary wedge pressure <19mmHg)

ARDS is the severe end of the spectrum of acute lung injury

106
Q

Whats the pathophysiology behind ARDS?

A
  • Severe insults to the lungs and other organs leads to the release of inflammatory mediators
  • These lead to increased capillary permeability, NON CARDIOGENIC* pulmonary oedema, impaired gas exchange and reduced lung compliance
107
Q

What are the causes of ARDS?

A
o  Sepsis  
o  Aspiration  
o  Pneumonia  
o  Pancreatitis  
o  Trauma/burns 
o  Transfusion  
o  Transplantation (bone marrow and lung)   
o  Drug overdose/reaction  

Pulmonary: pneumonia, gastric aspiration, inhalation of smoke/soot, trauma, contusions, vasculitis

Extrapulmonary: septic/haemorrhagiv shock, multiple transfusions, DIC, pancreatitis.

108
Q

What are the THREE pathological stages of ARDS?

A

o Exudative
o Proliferative
o Fibrotic

109
Q

Recognise the presenting symptoms of ARDS

A
  • Rapid deterioration of respiratory function
  • Dyspnoea
  • Respiratory distress
  • Cough
  • Symptoms of CAUSE
110
Q

Signs of ARDS OE?

A
  • Cyanosis
  • Tachypnoea
  • Tachycardia
  • Widespread inspiratory crepitations - BILATERAL *
  • Hypoxia refractory to oxygen treatment
  • Signs are usually bilateral but may be asymmetrical in early stages

Peripheral vasodiltion

111
Q

Identify appropriate investigations for ARDS

A

• CXR - bilateral alveolar infiltrates* and interstitial shadowing
• Bloods - to figure out the cause (FBC, U&Es, LFTs, ESR/CRP, Amylase, ABG, Blood Culture)
o NOTE: plasma BNP < 100 pg/mL could distinguish ARDS from heart failure

• Echocardiography
o Check for severe aortic or mitral valve dysfunction
o Low left ventricular ejection fractions = haemodynamic oedema rather than ARDS

• Pulmonary Artery Catheterisation
o Check pulmonary capillary wedge pressure (PCWP)

• Bronchoscopy
o If the cause cannot be determined from the history