Respiratory p2 Flashcards

1
Q

Where does tuberculosis infection tend to affect?

A

lung, lymph nodes and gut

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2
Q

What is Primary TB?

A

syndrome produced by M.Tuberculosis in those not previously affected

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3
Q

Describe the onset/location of primary tb

A

common sites: sub-pleural in the mid-zones of the lungs, in the pharynx or terminal ileum

mild inflammatory response at the site of infection followed by spread to regional lymph nodes
infection then spreads to hilarity, cervical or mesenteric nodes respectively

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4
Q

What is the primary complex?

A

infective focus + lymph node involvement

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5
Q

What is the ghon focus?

A

the infective focus in the lung

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6
Q

What happens 1-2 weeks after infection with M.Tuberculosis ?

A

Onset of immune sensitivity - tissue reaction at both sites of the primary complex changes to form caseating granuloma

In the majority of cases, these heal with fibrosis, and frequently calcify without therapy

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7
Q

What is the presentation of the patient at caseating granuloma stage?

A

asymptomatic or have a single enlarged LN that may be palpable if cervical

Viable bacteria may remain within walled off in the primary complex, giving latent TB

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8
Q

Describe the methods by which primary TB can become symptomatic

A

Ghon focus erodes through the visceral pleura to discharge organisms and cause TB pleurisy / pleural effusion

Enlarged hilar LNs can cause bronchial obstruction and collapse

The hilar lymph nodes can erode into bronchus and rupture (bronchopneumonia)

The enlarging nodes can erode into vessels, giving miliary dissemination to the lung or systemic dissemination (pulmonary vein)

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9
Q

What is post-primary (secondary) TB?

A

M.Tuberculosis re-infection in tuberculin-sensitive individuals

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10
Q

How does secondary tb occur?

A

infection can be from exogenous sources, or more commonly ‘reactivation’ from a healed primary complex

Immediate granulomatous response to the disease, thus regional lymph involvement is not common

in the lung, this creates a classical apical lesion termed an Assman focus, with destruction of lung parenchyma leading to cavitation

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11
Q

What are the outcomes of secondary TB?

A

Lesion may heal with fibrosis and calcification if the immune system is strong, or will progressively enlarge in those with poor immune systems

This has greater risks of eroding into vessels/airways and causing complications

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12
Q

What are the symptoms of TB?

A

non-specific: malaise, night sweats, anorexia, weight loss

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13
Q

When do specific symptoms of TB occur?

A

Late, in established disease:
productive mucoid cough
repeated small haemoptysis
pleural pain

Can present with pneumonia or pleural effusion. on examination there may only be a fever and apical crepitations, with late signs of consolidation or pleural effusion

patients may be clubbed in advanced disease

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14
Q

How can TB be coughed out?

A

release of tubercle bacilli into the main bronchus

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15
Q

Who are the high risk patients for TB?

A
endemic areas
previously treated for TB
close contact with TB
immunosuppressive co-morbidities / drug tx
live in overcrowded conditions 
alcohol/drug users
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16
Q

What are the investigations of active pulmonary TB?

A

SPUTUM sample: 3 x (1 in morning)
Microscopy(24h) + PCR + Culture (takes 6 weeks)

sputum grows acid-fast bacilli that stain red with Zeihl-Neelsen staining. This is mycobacterium tuberculosis and the diagnosis is TB.

If sputum = negative, bronchoscopy with biopsy or broncho-alveolar lavage may be useful

CXR: upper lobe cavitation, pleural effusions, lymphadenopathy
Ix for extra pulmonary disease as clinically indicated

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17
Q

What are the investigations for latent TB?

A

Mantoux test: TB antigen injected, size of wheal reaction monitored

>5mm = +VE in immunosuppressed, prior TB or recent contacts
>10mm = +ve in those with risk factors for TB
>15mm = +ve in any individual 

Interferon gamma release assay: IGRA blood test also required to diagnose latent TB in immunocompromised individuals (can have false -ves in skin test)

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18
Q

What does a positive test for latent TB lead to?

A

Assessment for active TB
if no evidence, treat for latent TB

FBC, U+E, LFT to rule out other causes
screening for HIV, HEP B/C

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19
Q

What is the management of ACTIVE TB?

A

Admit - negative pressure side room OR
TB service within 2 weeks. do not delay referral

Assess risk factors for drug resistant TB

RIPE: Rifampicin + isoniazid 6 months with Pyraziname and ethambutol for first 2 months

If CNS involvement, R+I continued for 12 months

If poor adherence - given under key worker supervision

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20
Q

What are the risk factors for MDR TB?

A
previous tb treatment
from endemic areas
contacts with MDR-TB
poor adherence to current treatment aged 25-45 
HIV co-infection 
assess with PCR
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21
Q

How are household members managed if positive TB?

A

Notifiable disease:
All household members and close contacts should be traced and assessed for latent TB

Casual contact (work) should be traced only if the person with TB is particularly infectious (10% or more of close contacts develop TB) or if casual contacts are at increased risk of infection (healthcare workers/people with HIV)

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22
Q

What is the management of MDR-TB?

A

continue infection control measures until pulmonary / laryngeal disease has been excluded

treat with at least 6 drugs to which it is sensitive

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23
Q

What is the management of latent TB?

A

treat with 3 months of rifampicin and isoniazid (with pyridoxine)

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24
Q

What are the drug side effects of the TB treatment drugs?

A

Rifampicin: abnormal LFTs, pink urine (red-and-orange-pissin). Also a cytochrome P450 inducer

Isoniazid: peripheral neuropathy / encephalopathy. very rare when prophylactic pyridoxine co-prescribed (I’m-so-numb-azid)

Pyrazinamide: hepatotoxic

Ethambutol: optic neuritis, assess with colour vision testing (eye-tham-butol)

R, I and P all associated with hepatotoxicity

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25
Q

What symptoms are caused when TB bacilli settle and cause later disease?

A
Painless lymphadenopathy: lymphatic TB
mono arthritis: joint/spinal TB
sterile pyuria: renal TB
Meningitic syndrome: TB meningitis 
Erythema nodosum / lupus vulgaris: cutaneous TB
Chest pain: TB pericarditis
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26
Q

How does TB affect the world?

A

kills 2 million people/year worldwide
with 350 deaths/year in the UK

Most common cause of death in people with HIV
Most common drug resistance in UK = isolated isoniazid resistance
rifampicin = marker for multi-drug resistant TB

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27
Q

What is he presentation of pneumothorax?

A

May be asymptomatic in young patients or present with sudden onset of unilateral pleuritic pain, with progressive breathlessness

reduced expansion
increase resonance to percussion
decreased breath sounds and reduced vocal resonance

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28
Q

How does tension pneumothorax present?

A

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

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29
Q

What are the classifications of pneumothorax?

A

Spontaneous: primary or secondary

traumatic: penetrating trauma, rib fractures
iatrogenic pneumothorax: lung biopsy, endoscopy, subclavian cancelation, positive pressure ventilation

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30
Q

How are primary / secondary pneumothoraces caused?

A

primary: lung parenchyma otherwise normal, caused by a rupture of the apical bleb, often in tall, thin young men
secondary: underlying lung disease / abnormality e.g. in COPD, pneumonia, CF, asthmatic, malignancy

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31
Q

What investigations are done for pneumothorax?

A

Expiratory CXR - trace the outline for areas devoid of lung markings and look for tracheal deviation

ABG: if signs of respiratory distress / chronic lung disease

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32
Q

What is a tension pnuemothorax?

A

air in the pleural space leading to cardiac compromise

a valvular mechanism allowing air entry to the pleural space during inspiration, but no air exit during expiration

Therefore more air keeps getting drawn into the pleural space with each breath and cannot escape

The intrapleural space is very high, deflating the lung and decreasing venous return to the heart

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33
Q

how is tension pneumothorax differentiated?

A

respiratory distress, pallor, haemodynamic compromise, distended neck veins, tracheal deviation

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34
Q

What is the treatment of TENSION pneumothorax?

A

100% oxygen

Insert a large bore cannula into the second intercostal space in the midclavicular line

CXR
Insert chest drain

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35
Q

What is the management for pneumothorax?

A

Primary:
if the rim of air is < 2cm and the patient is not short of breath - discharge
otherwise, aspiration should be attempted
if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted

secondary:
> 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.

otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) chest drain

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36
Q

Management if pneumothorax <2cm

A

discharge
avoid strenuous exercise
Interval CXR every 2 weeks until resolution
quit smoking

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37
Q

Management if pneumothorax >2cm

A

attempt aspiration and admit for at least 24 hours

if this fails - chest drain

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38
Q

How is aspiration of pneumothorax done?

A

Insert a 16G cannula under local anaesthetic into second intercostal space, mid-clavicular line and attach to 3-way tap and a 50ml syringe to aspirate

stop when resistance is felt, or if the patient coughs excessively

Check with X ray

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39
Q

How Is a chest drain inserted?

A

Triangle of safety: 5th ICS, mid-axillary line and anterior axillary line, and chest X-ray to check positioning

the drain should be attached via tubing to the underwater seal, which must be below the level of the patient

check the drain is swinging with respiration, bubbling and then check positioning with repeat CXR

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40
Q

how should a patient be counselled following pneumothorax?

A

flying should be avoided for 6 weeks and diving should be permanently avoided

if there is recurrent pneumothorax surgery may be indicated, pleurectomy if fit, talc pleurodesis if not (some risk of recurrence)

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41
Q

What are the causes of pleural effusion?

A

empyema / pylothorax - accumulation of pus, due to infection
chylothorax - accumulation of lymph due to thoracic duct leakage
haemothorax - accumulation of blood, due to trauma

fluid effusion: transudative / exudative

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42
Q

What is the difference between transudate and exudate?

A

Transudate: occur due to increased hydrostatic pressure or decreased oncotic pressure (fluid shifting)

Exudates due to increased capillary permeability (Inflammation)

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43
Q

What are the causes of TRANSUDATIVE effusion?

A

Cardiac failure: LHF leading to increased hydrostatic pressure

Hypoalbuminaemia: Liver failure - decreased protein production decreasing oncotic pressure

Renal failure: nephrotic syndrome decreasing oncotic pressure

Peritoneal dialysis

Rarely: hypothyroidism, ovarian tumours

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44
Q

What are the causes of EXUDATIVE effusion?

A

infections: bacterial pneumonia, TB
neoplasm: lung primary or secondary, mesothelioma

pulmonary infarction: PE

Autoimmune infection: RA / SLE

Abdominal disease: pancreatitis, subphrenic abscess

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45
Q

What are the symptoms of pleural effusion?

A

asymptomatic, dyspnoea and pleuritic pain

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46
Q

What are the examination findings of pleural effusion?

A

Decreased Chest expansion, tracheal deviation away if large.

Stony dull to percussion

Decreased breath sounds - can be bronchial breathing

Reduced vocal resonance

Mediastinal deviation (in massive effusion)

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47
Q

What is the cause of empyema?

A

Bacterial invasion of the pleural space, either spreading into an exudative effusion from adjacent pneumonia or from direct inoculation (e.g. poor aseptic technique in chest drain)

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48
Q

What is the clinical presentation of empyema?

A

fever + signs of pleural effusion
Aspirated fluid is yellow and turbid, with pH <7.2, low glucose, high LDH

Requires ABX IV and chest drain

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49
Q

How are effusions investigated?

A

Unilateral, more likely to be exudative - bilateral more likely transudative

CXR - seen >300ml
USS - guide aspiration
Aspiration and LIGHTS CRITERIA

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50
Q

How are transudates / exudates differentiated?

A

exudates have a protein level >30g/L, transudates are <30g/L

If between 25-35, one positive element of LIGHTS = exudate

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51
Q

What is light’s criteria?

A
  1. pleural fluid protein divided by serum protein is >0.5
  2. pleural fluid LDH divided by serum LDH >0.6
  3. pleural fluid LDH more than two-thirds the upper limits of norma serum LDH
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52
Q

What is the management of pleural effusion?

A

if aspirated fluid = purulent, place a chest drain and consider IV antibiotics (or if PH is <7.2, also suggest empyema)

drainage should also take place if symptomatic, either with aspiration as per the diagnostic tap, or using an intercostal drain

Manage underlying cause

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53
Q

What is the peak age of onset of lung cancer?

A

65 years of age

M:F 3:1

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54
Q

What is the most common risk factor for lung cancer?

A

SMOKING
stopping smoking decreases the risk by one half in 5 years

other rf: passive smoking, urban living, occupational exposure

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55
Q

How are lung cancers classified?

A

small cell disease (20%) and non-small cell disease (80%)

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56
Q

What are non small cell lung cancers?

A

SCC - 50%
Adenocarcinoma - 20%
Large cell anapaestic tumours (10%)

57
Q

Where do SCCs arise from?

A

squamous metaplasia of the normally pseudo stratified ciliated columnar epithelium, in response to cigarette exposure

58
Q

Where are SCCs usually found?

A

central, close to carina
frequently present with collapse/infection secondary to obstruction

Small cell lung cancer cells contain neurosecretory granules that can release neuroendocrine hormones

may secrete PTH

59
Q

How are SCCs diagnosed?

A

sputum cytology

relatively slow growing

60
Q

What is the aetiology of adenocarcinoma?

A

equal gender incidence, less related to smoking

61
Q

Where do adenocarcinomas typically arise?

A

peripheral locations, potentially in areas of previous lung scarring

62
Q

Where is small cell anaplastic carcinoma found?

A

centrally located

usually originate from the bronchial epithelium but

63
Q

what effects on the endocrine system do small cell cancers have?

A

differentiate into neuroendocrine cells to secrete active products;
ADH - dilution hyponatraemia due to retention of water but not solute, leading to muscle weakness, cheyne-stokes respiration and neurological signs

ACTH - Cushing’s syndrome

64
Q

What is eaton Lambert syndrome?

A

myasthenia gravis like symptoms from lung cancer,
weakness, particularly in the proximal muscles but can 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).

This weakness gets worse with prolonged used of the muscles.

65
Q

What are the clinical features of lung cancer?

A
persistent cough - distal infection
haemoptysis - ulceration of tumour 
dyspnoea - local extension 
chest pain - pleural / chest wall involvement 
b symptoms
clubbing
66
Q

What are the examination findings of lung cancer?

A
clubbing 
cachexia
signs of anaemia 
hypertrophic pulmonary osteoarthropathy 
chest signs of collapse
signs of mets
67
Q

What are the investigations for lung cancer?

A

FBC: anaemia, polycythaemia
LFTs: signs of liver mets
U&Es: hypercalcaemia, hyponatraemia
CXR: tumours visible if normal - ?central tumour

Sputum/ pleural fluid cytology
staging CT: head to pelvis
biopsy - CT guided
pulmonary function tests: useful if planning surgery

PET/radionucleotide - if suspected metastatic

68
Q

What are the paraneoplastic manifestations of lung cancer?

A

Hypertrophic pulmonary osteoarthropathy, Lambert-eaton (myasthenia gravis type symptoms)

SIADH, secondary Cushing’s, HyperPTH

69
Q

What are the consequences of local invasion of lung cancer?

A

Recurrent laryngeal nerve palsy
Phrenic nerve palsy
SVC obstruction - raised JVP, raised arm/BP swelling, facial swelling (usually due to local nodes)

Pancoast syndrome: Horner’s shoulder pain, atrophy, oedema

Pericarditis
AF

Distant mets - brain, bone, liver or adrenal gland

70
Q

What is the management of non-small cell cancer?

A

surgical excision if peripheral enough with no lymph node involvement + chemotherapy
Must be >2cm from carina

curative radiotherapy if poor respiratory reserve, with adjuvant chemotherapy
chemoradiotherapy for more advanced disease

71
Q

What is the management of small cell lung cancer?

A

nearly always disseminated at presentation - may respond to chemotherapy +/- radiotherapy

may have prophylactic cranial radiotherapy

72
Q

What is the palliative management for lung cancer?

A

radiotherapy for obstructive symptoms or bone pain
SVC stenting
pleural drainage / pleurodesis for symptomatic effusions

73
Q

What is interstitium?

A

The tissues that lies between the alveoli and pulmonary capillaries

74
Q

What is interstitial lung disease?

A

generic term used to describe a number of conditions that diffusely affect the lung parenchyma, sharing certain common features:

repeated exogenous/endogenous stimuli
chronic inflammation
fibrosis of the interstitium
restrictive lung disease

75
Q

Describe the aetiology of ILD

A

secondary to exogenous stimuli: occupational, drugs, hypersensitivity, infection

secondary to endogenous stimuli: sarcoidosis, RA, connective tissue disease

Idiopathic

76
Q

What are the classical features of ILD?

A

dyspnoea on exertion and non-productive dry cough

77
Q

What are the examination findings of ILD?

A

Inspection: signs of respiratory distress, clubbing
Palpation: reduced expansion
Percussion: normal unless secondary pathology
Auscultation: fine end insp crackles - sometimes wheeze

decompensation signs
restrictive spirometry with reduced DLCO

78
Q

What is the most common form of ILD?

A

idiopathic

79
Q

When does idiopathic ILD tend to present?

A

late 60s, more common in males

80
Q

What is the presentation of idiopathic ILD?

A

dry cough, exertion dyspnoea, malaise, weight loss, arthralgia
history should attempt to exclude occupational exposure / connective tissue disease

81
Q

What are the complications of idiopathic ild?

A

t2RF
pulmonary HTN
increased risk of lung cancer

82
Q

What investigations should be done for ?ILD

A

Bloods: FBC, ANA/RF
CXR: reduced lung volume, bilateral reticula-nodular shadowing
High resolution CT - honeycombing seen on CT

spirometry: restrictive

Broncheoalveolar lavage
lung biopsy if uncertain

83
Q

What is the management of ILD?

A

?prednisolone - tapered down

lung transplant?

84
Q

What is extrinsic allergic alveolitis?

A

Hypersensitivity pneumonitis - caused by immune reactivity in the lungs to inhaled antigens - type III hypersensitivity response with immune complex formation

repeated exposure - type IV

the chronic inflammation eventually results in interstitial fibrosis

85
Q

Describe the aetiology of EAA?

A

Farmer’s lung: micropolyspora
bird fancier’s lung: proteins in bird droppings
Malt worker’s lung: aspergillus

86
Q

What are the clinical features of acute exposure?

A

fevers, rigors, myalgia

dry cough and dyspnoea with possible wheeze

87
Q

What is the managemnet of acute EAA?

A

oxygen
avoid precipitating thing

oral prednisolone

88
Q

What are the investigations for EAA?

A

FBC: neutrophilia
Serum precipitant levels
CXR / CT / lung function tests
broncheoalveolar lavage

89
Q

What is the treatment for EAA?

A

Aim for prevention, with no expire
long term prednisolone
established fibrosis not amenable to treatment

90
Q

What is pneumoconiosis?

A

Disease of the lungs caused by inhalation of dusts, generally used to refer to pathology caused by coal dust

91
Q

How does pneumoconiosis occur?

A

Dust is toxic to macrophages (the normal defence for inhaled dust), thus there will be a local inflammatory response similar to that seen in COPD
If this becomes chronic, there will also be fibrosis leading to restrictive lung disease

92
Q

What are the main dusts causing industrial PF?

A

salicylates

93
Q

What is simple coalworker’s pneumoconiosis

A

presence of small nodules (2-5mm) on CXR, not associated with any clinically significant impairment of respiratory function

94
Q

What is progressive massive fibrosis?

A

Presence of large nodules (>10mm) on CXR, and the disease progresses –> mixed obstructive and restrictive pattern

COPD + and black sputum

95
Q

What patients get affected with asbestos?

A

50+
worked in building/shipyards
latent period of up to 50 years

96
Q

What do asbestos bodies show?

A

Marker of asbestos exposure

can only be seen histologically

97
Q

When do pleural plaques occur?

A

light exposure

98
Q

What changes are associated with pleural plaques, effusion and thickening?

A

mild restrictive deficit on spirometry, pleural thickening and calcification on CXR

more heavy exp - diffuse pleural thickening which will produce restrictive deficits, effort dyspnoea and can be progressive

99
Q

How does mesothelioma form?

A

light exposure - interval of 20-40 years between exposure to disease onset

100
Q

What are the symptoms of mesothelioma?

A

pleuritic chest pain, increasing dyspnoea, unilateral pleural effusion on XCR

101
Q

How does asbestosis occur?

A

HEAVY exposure, with interval of 5-10 years

102
Q

How does asbestosis present?

A

progressive dyspnoea , diffuse bilateral streaky strikes on CXR with honeycombing

outcome = poor

103
Q

What is OSA?

A

interrupted and repeated collapse of the upper airway during REM sleep - associated with hypopnea/apnoea and desaturations

hypoxia leads to increasing resp effort until they overcome resistance

the combination wakes the patient, leading to excessive daytime sleepiness

104
Q

What are the correctable OSA risk factors?

A

resp depressants
nasal obstruction
obesity

105
Q

What are the presenting complaints of OSA?

A
loud snoring during sleep
daytime sleepiness
morning headache
decreased libido 
nocturnal choking
apnoeic episodes
106
Q

What are the complications of OSA?

A

pulmonary HTN and cor pulmonale
T2RF
HTN and increased cardiac risk

107
Q

What are the Ix for OSA?

A

Epworth sleepiness scale - distinguish from simple snoring

Endoscopic exam by ENT of upper airway

Home pulse oximetry

Polysomnography - gold standard for diagnosis, with in-patient assessment of variable parameters

108
Q

How is diagnosis of OSA made?

A

> 15 episodes of apnoea/hypopnoea during 1hr of sleep

109
Q

What is the management of OSA?

A

behavioural changes - allow partner to sleep first, sleep on side
weight reduction
avoidance of alcohol + tobacco

CPAP via nasal mask
intra-oral devices

Daytime sleepiness = modafinol
Upper airway surgery

110
Q

What is T1RF?

A

PaO2 low

PaCo2 normal

111
Q

What is T2RD?

A

PaO2 low

PaCo2 high

112
Q

When does T1RF occur?

A

diseases of the lung parenchyma

pulmonary oedema, pneumonia, PE, COPD, ARDS

113
Q

When does T2RF occur?

A

when ventilation not enough to get rid of CO2
SEVERE pulmonary disease
reduced resp drive: drugs, CNS pathology
thoracic wall disease
neuromuscular disease

114
Q

What is pectus excavatum?

A

concave chest

displaces heart

115
Q

What are the clinical features of hypoxia?

A

dyspnoea, agitation, confusion, central cyanosis

116
Q

What are the clinical features of hypercapnia?

A

headache, tachycardia, bounding pulse, Co2 retention flap, acidosis ft…:
Kussmal respiration
CV dysfunction
K+ abnormalities
Cerebral dysfunciton
peripheral vasodilation and increased permeability leading to oedema

117
Q

What is the treatment for acute ventilatory failure?

A
Ix to determine underlying cause: 
Bloods - FBC, U+E, CRP 
ABG - in anyone with unexpected deterioration 
CXR
Sputum/blood cultures
118
Q

What is the management of T1RF?

A

Treat underling cause
Oxygen
Assisted ventilation if PaO2 remains <8kpa despite 60% O2.
e.g. BiPAP (NIV)

119
Q

What is the management of T2RF?

A

Resp centre may be reliant on hypoxic drive, so oxygen therapy should be given with care (28% and rechecking ABG after 20 mins)

120
Q

Describe the steps of ABG interpretation

A
  1. pH: <7.35 = acidemic and >7.35 = alkalotic
  2. PaCO2: if academic, is PaCo2 >6? (resp)
    if alkalemic, Is PaCo2 <4.7? (resp cause)
  3. if academic, is HCO3 <22? (metabolic cause)
    if all, is HCO3 >26? (metabolic cause)

Compensation?

121
Q

How do you assess compensation?

A

BASE EXCESS

+2 to -2

negative in met acidosis
positive in met alkalosis

122
Q

What should lactate be?

A

<1 can go up to 2 in stressed patient

high is suggestive of shock

123
Q

What is the cause of respiratory acidosis?

A

any type of type II resp failure

124
Q

What is the cause of metabolic acidosis?

A
loss of bicarbonate: 
renal tubular acidosis
diarrhoea
drugs- ACETAZOLAMINE 
pancreatic / interstitial fistula 

lactic acidosis
ketosis
urate
drugs

125
Q

what is the cause of respiratory alkalosis?

A
Hyperventilation (blowing off Co2)
anxiety 
pain
altitude
increased metabolic demands: fever, sepsis, pregnancy 
drugs
126
Q

What is the cause of metabolic alkalosis?

A
ingestion of a base (antacids)
Loss of acid: 
vomiting
hypokalaemia
burns
hyperaldosteronism
127
Q

What are the indications for lobectomy?

A

lung cancer
bronchiectasis
chronic lung abscess / TB
fungal infections

128
Q

Describe the examination of lobectomy

A

Inspection: thoracotomy scar - with chest wall flattening on side of surgery - ribs pulled in over surgical site

Palpation: tracheal displacement towards the surgical site. reduced expansion on that side

Percussion: hyper-resonant on the side of the lobectomy as the remaining lung expands to fill the cavity

Auscultation: reduced air entry over the site

129
Q

What is sarcoidosis?

A

Systemic, non-caseating granulomatous disease most commonly affecting the lungs, mediastinal lymph nodes and skin

130
Q

Who does sarcoidosis affect?

A

females: aged 20-40, presenting as a subactute illness, with non-specific features of malaise, arthralgia etc

131
Q

What are the manifestations of sarcoidosis?

A

fibrosis
erythema nodosum
glomerulonephritis, cardiomyopathy, arthritis and cranial nerve lesions

132
Q

What is the management of sarcoidosis?

A

simple analgesia and NSAIDS, occasional corticosteroid courses if there is progressive lung fibrosis

133
Q

What is asperillus?

A

fungus commonly found in mould and soil

134
Q

how does aspergillus affect the lungs?

A

5 ways:

  1. asthma: Type 1 hypersensitivity reaction to spores
  2. EAA
  3. allergic bronchopulmonary aspergillosis - more common in asthmatics and CF patients
  4. Aspergilloma: fungal ball formation within pre-existing lung cavities
  5. invasive aspergillosis - affects immunocompromised
135
Q

What are the causes of clubbing?

A

intrathoracic neoplasm: primary / secondary
suppurative lung disease: lung abscess, CF, bronchiectasis, fungal infection
CV disease: congenital, infective endocarditis, aortic aneurysm
GI disease: IBD, coeliac
Liver disease: chronic active hepatitis, cirrhosis
Thyroid acropathy

136
Q

What is supparative lung disease?

A

leads to chronic productive cough

suppuration = pus formation

137
Q

What is Allergic bronchopulmonary aspergillosis

A

results from an allergy to Aspergillus spores.

often give a history of bronchiectasis and eosinophilia

138
Q

What is the mx of allergic bronchopulmonary aspergillosis?

A

Oral steroids