Respiratory p2 Flashcards
Where does tuberculosis infection tend to affect?
lung, lymph nodes and gut
What is Primary TB?
syndrome produced by M.Tuberculosis in those not previously affected
Describe the onset/location of primary tb
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
What is the primary complex?
infective focus + lymph node involvement
What is the ghon focus?
the infective focus in the lung
What happens 1-2 weeks after infection with M.Tuberculosis ?
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
What is the presentation of the patient at caseating granuloma stage?
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
Describe the methods by which primary TB can become symptomatic
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)
What is post-primary (secondary) TB?
M.Tuberculosis re-infection in tuberculin-sensitive individuals
How does secondary tb occur?
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
What are the outcomes of secondary TB?
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
What are the symptoms of TB?
non-specific: malaise, night sweats, anorexia, weight loss
When do specific symptoms of TB occur?
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
How can TB be coughed out?
release of tubercle bacilli into the main bronchus
Who are the high risk patients for TB?
endemic areas previously treated for TB close contact with TB immunosuppressive co-morbidities / drug tx live in overcrowded conditions alcohol/drug users
What are the investigations of active pulmonary TB?
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
What are the investigations for latent TB?
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)
What does a positive test for latent TB lead to?
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
What is the management of ACTIVE TB?
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
What are the risk factors for MDR TB?
previous tb treatment from endemic areas contacts with MDR-TB poor adherence to current treatment aged 25-45 HIV co-infection assess with PCR
How are household members managed if positive TB?
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)
What is the management of MDR-TB?
continue infection control measures until pulmonary / laryngeal disease has been excluded
treat with at least 6 drugs to which it is sensitive
What is the management of latent TB?
treat with 3 months of rifampicin and isoniazid (with pyridoxine)
What are the drug side effects of the TB treatment drugs?
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
What symptoms are caused when TB bacilli settle and cause later disease?
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
How does TB affect the world?
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
What is he presentation of pneumothorax?
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
How does tension pneumothorax present?
Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
Tachycardia
Hypotension
What are the classifications of pneumothorax?
Spontaneous: primary or secondary
traumatic: penetrating trauma, rib fractures
iatrogenic pneumothorax: lung biopsy, endoscopy, subclavian cancelation, positive pressure ventilation
How are primary / secondary pneumothoraces caused?
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
What investigations are done for pneumothorax?
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
What is a tension pnuemothorax?
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
how is tension pneumothorax differentiated?
respiratory distress, pallor, haemodynamic compromise, distended neck veins, tracheal deviation
What is the treatment of TENSION pneumothorax?
100% oxygen
Insert a large bore cannula into the second intercostal space in the midclavicular line
CXR
Insert chest drain
What is the management for pneumothorax?
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
Management if pneumothorax <2cm
discharge
avoid strenuous exercise
Interval CXR every 2 weeks until resolution
quit smoking
Management if pneumothorax >2cm
attempt aspiration and admit for at least 24 hours
if this fails - chest drain
How is aspiration of pneumothorax done?
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
How Is a chest drain inserted?
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
how should a patient be counselled following pneumothorax?
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)
What are the causes of pleural effusion?
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
What is the difference between transudate and exudate?
Transudate: occur due to increased hydrostatic pressure or decreased oncotic pressure (fluid shifting)
Exudates due to increased capillary permeability (Inflammation)
What are the causes of TRANSUDATIVE effusion?
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
What are the causes of EXUDATIVE effusion?
infections: bacterial pneumonia, TB
neoplasm: lung primary or secondary, mesothelioma
pulmonary infarction: PE
Autoimmune infection: RA / SLE
Abdominal disease: pancreatitis, subphrenic abscess
What are the symptoms of pleural effusion?
asymptomatic, dyspnoea and pleuritic pain
What are the examination findings of pleural effusion?
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)
What is the cause of empyema?
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)
What is the clinical presentation of empyema?
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
How are effusions investigated?
Unilateral, more likely to be exudative - bilateral more likely transudative
CXR - seen >300ml
USS - guide aspiration
Aspiration and LIGHTS CRITERIA
How are transudates / exudates differentiated?
exudates have a protein level >30g/L, transudates are <30g/L
If between 25-35, one positive element of LIGHTS = exudate
What is light’s criteria?
- pleural fluid protein divided by serum protein is >0.5
- pleural fluid LDH divided by serum LDH >0.6
- pleural fluid LDH more than two-thirds the upper limits of norma serum LDH
What is the management of pleural effusion?
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
What is the peak age of onset of lung cancer?
65 years of age
M:F 3:1
What is the most common risk factor for lung cancer?
SMOKING
stopping smoking decreases the risk by one half in 5 years
other rf: passive smoking, urban living, occupational exposure
How are lung cancers classified?
small cell disease (20%) and non-small cell disease (80%)
What are non small cell lung cancers?
SCC - 50%
Adenocarcinoma - 20%
Large cell anapaestic tumours (10%)
Where do SCCs arise from?
squamous metaplasia of the normally pseudo stratified ciliated columnar epithelium, in response to cigarette exposure
Where are SCCs usually found?
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
How are SCCs diagnosed?
sputum cytology
relatively slow growing
What is the aetiology of adenocarcinoma?
equal gender incidence, less related to smoking
Where do adenocarcinomas typically arise?
peripheral locations, potentially in areas of previous lung scarring
Where is small cell anaplastic carcinoma found?
centrally located
usually originate from the bronchial epithelium but
what effects on the endocrine system do small cell cancers have?
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
What is eaton Lambert syndrome?
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.
What are the clinical features of lung cancer?
persistent cough - distal infection haemoptysis - ulceration of tumour dyspnoea - local extension chest pain - pleural / chest wall involvement b symptoms clubbing
What are the examination findings of lung cancer?
clubbing cachexia signs of anaemia hypertrophic pulmonary osteoarthropathy chest signs of collapse signs of mets
What are the investigations for lung cancer?
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
What are the paraneoplastic manifestations of lung cancer?
Hypertrophic pulmonary osteoarthropathy, Lambert-eaton (myasthenia gravis type symptoms)
SIADH, secondary Cushing’s, HyperPTH
What are the consequences of local invasion of lung cancer?
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
What is the management of non-small cell cancer?
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
What is the management of small cell lung cancer?
nearly always disseminated at presentation - may respond to chemotherapy +/- radiotherapy
may have prophylactic cranial radiotherapy
What is the palliative management for lung cancer?
radiotherapy for obstructive symptoms or bone pain
SVC stenting
pleural drainage / pleurodesis for symptomatic effusions
What is interstitium?
The tissues that lies between the alveoli and pulmonary capillaries
What is interstitial lung disease?
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
Describe the aetiology of ILD
secondary to exogenous stimuli: occupational, drugs, hypersensitivity, infection
secondary to endogenous stimuli: sarcoidosis, RA, connective tissue disease
Idiopathic
What are the classical features of ILD?
dyspnoea on exertion and non-productive dry cough
What are the examination findings of ILD?
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
What is the most common form of ILD?
idiopathic
When does idiopathic ILD tend to present?
late 60s, more common in males
What is the presentation of idiopathic ILD?
dry cough, exertion dyspnoea, malaise, weight loss, arthralgia
history should attempt to exclude occupational exposure / connective tissue disease
What are the complications of idiopathic ild?
t2RF
pulmonary HTN
increased risk of lung cancer
What investigations should be done for ?ILD
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
What is the management of ILD?
?prednisolone - tapered down
lung transplant?
What is extrinsic allergic alveolitis?
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
Describe the aetiology of EAA?
Farmer’s lung: micropolyspora
bird fancier’s lung: proteins in bird droppings
Malt worker’s lung: aspergillus
What are the clinical features of acute exposure?
fevers, rigors, myalgia
dry cough and dyspnoea with possible wheeze
What is the managemnet of acute EAA?
oxygen
avoid precipitating thing
oral prednisolone
What are the investigations for EAA?
FBC: neutrophilia
Serum precipitant levels
CXR / CT / lung function tests
broncheoalveolar lavage
What is the treatment for EAA?
Aim for prevention, with no expire
long term prednisolone
established fibrosis not amenable to treatment
What is pneumoconiosis?
Disease of the lungs caused by inhalation of dusts, generally used to refer to pathology caused by coal dust
How does pneumoconiosis occur?
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
What are the main dusts causing industrial PF?
salicylates
What is simple coalworker’s pneumoconiosis
presence of small nodules (2-5mm) on CXR, not associated with any clinically significant impairment of respiratory function
What is progressive massive fibrosis?
Presence of large nodules (>10mm) on CXR, and the disease progresses –> mixed obstructive and restrictive pattern
COPD + and black sputum
What patients get affected with asbestos?
50+
worked in building/shipyards
latent period of up to 50 years
What do asbestos bodies show?
Marker of asbestos exposure
can only be seen histologically
When do pleural plaques occur?
light exposure
What changes are associated with pleural plaques, effusion and thickening?
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
How does mesothelioma form?
light exposure - interval of 20-40 years between exposure to disease onset
What are the symptoms of mesothelioma?
pleuritic chest pain, increasing dyspnoea, unilateral pleural effusion on XCR
How does asbestosis occur?
HEAVY exposure, with interval of 5-10 years
How does asbestosis present?
progressive dyspnoea , diffuse bilateral streaky strikes on CXR with honeycombing
outcome = poor
What is OSA?
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
What are the correctable OSA risk factors?
resp depressants
nasal obstruction
obesity
What are the presenting complaints of OSA?
loud snoring during sleep daytime sleepiness morning headache decreased libido nocturnal choking apnoeic episodes
What are the complications of OSA?
pulmonary HTN and cor pulmonale
T2RF
HTN and increased cardiac risk
What are the Ix for OSA?
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
How is diagnosis of OSA made?
> 15 episodes of apnoea/hypopnoea during 1hr of sleep
What is the management of OSA?
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
What is T1RF?
PaO2 low
PaCo2 normal
What is T2RD?
PaO2 low
PaCo2 high
When does T1RF occur?
diseases of the lung parenchyma
pulmonary oedema, pneumonia, PE, COPD, ARDS
When does T2RF occur?
when ventilation not enough to get rid of CO2
SEVERE pulmonary disease
reduced resp drive: drugs, CNS pathology
thoracic wall disease
neuromuscular disease
What is pectus excavatum?
concave chest
displaces heart
What are the clinical features of hypoxia?
dyspnoea, agitation, confusion, central cyanosis
What are the clinical features of hypercapnia?
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
What is the treatment for acute ventilatory failure?
Ix to determine underlying cause: Bloods - FBC, U+E, CRP ABG - in anyone with unexpected deterioration CXR Sputum/blood cultures
What is the management of T1RF?
Treat underling cause
Oxygen
Assisted ventilation if PaO2 remains <8kpa despite 60% O2.
e.g. BiPAP (NIV)
What is the management of T2RF?
Resp centre may be reliant on hypoxic drive, so oxygen therapy should be given with care (28% and rechecking ABG after 20 mins)
Describe the steps of ABG interpretation
- pH: <7.35 = acidemic and >7.35 = alkalotic
- PaCO2: if academic, is PaCo2 >6? (resp)
if alkalemic, Is PaCo2 <4.7? (resp cause) - if academic, is HCO3 <22? (metabolic cause)
if all, is HCO3 >26? (metabolic cause)
Compensation?
How do you assess compensation?
BASE EXCESS
+2 to -2
negative in met acidosis
positive in met alkalosis
What should lactate be?
<1 can go up to 2 in stressed patient
high is suggestive of shock
What is the cause of respiratory acidosis?
any type of type II resp failure
What is the cause of metabolic acidosis?
loss of bicarbonate: renal tubular acidosis diarrhoea drugs- ACETAZOLAMINE pancreatic / interstitial fistula
lactic acidosis
ketosis
urate
drugs
what is the cause of respiratory alkalosis?
Hyperventilation (blowing off Co2) anxiety pain altitude increased metabolic demands: fever, sepsis, pregnancy drugs
What is the cause of metabolic alkalosis?
ingestion of a base (antacids) Loss of acid: vomiting hypokalaemia burns hyperaldosteronism
What are the indications for lobectomy?
lung cancer
bronchiectasis
chronic lung abscess / TB
fungal infections
Describe the examination of lobectomy
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
What is sarcoidosis?
Systemic, non-caseating granulomatous disease most commonly affecting the lungs, mediastinal lymph nodes and skin
Who does sarcoidosis affect?
females: aged 20-40, presenting as a subactute illness, with non-specific features of malaise, arthralgia etc
What are the manifestations of sarcoidosis?
fibrosis
erythema nodosum
glomerulonephritis, cardiomyopathy, arthritis and cranial nerve lesions
What is the management of sarcoidosis?
simple analgesia and NSAIDS, occasional corticosteroid courses if there is progressive lung fibrosis
What is asperillus?
fungus commonly found in mould and soil
how does aspergillus affect the lungs?
5 ways:
- asthma: Type 1 hypersensitivity reaction to spores
- EAA
- allergic bronchopulmonary aspergillosis - more common in asthmatics and CF patients
- Aspergilloma: fungal ball formation within pre-existing lung cavities
- invasive aspergillosis - affects immunocompromised
What are the causes of clubbing?
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
What is supparative lung disease?
leads to chronic productive cough
suppuration = pus formation
What is Allergic bronchopulmonary aspergillosis
results from an allergy to Aspergillus spores.
often give a history of bronchiectasis and eosinophilia
What is the mx of allergic bronchopulmonary aspergillosis?
Oral steroids
