Resp Diseases Flashcards
types of pneumothorax?
Spontaneous- primary (no lung disease) and secondary (lung disease)-e.g. bronchiectasis, CF, emphysema, asthma
Traumatic
TENSION
Iatrogenic e.g. post central line or pacemaker insertion
RFs for pneumothorax?
smoking/cannabis diving pre-existing lung disease trauma/chest procedure height assoc. with other conditions e.g. Marfan syndrome- autosomal dominant condition assoc. with a mutation in the fibrillin-1 gene causing an increase in the protein transforming growth factor beta (TGF-beta) which causes CT problems- cardioresp include spontaneous pneumothorax, aortic dissection and aortic regurgitation.
Pneumothorax management as per BTS guidelines?
spontaneous primary- if symptomatic and rim of air more than 2cm on CXR (between lung margin and chest wall)=large pneumothorax, give O2 and needle aspirate. if unsuccessful, consider re-aspiration or intercostal drain (small bore). remove drain after full re-expansion/cessation of air leak. if small (so rim 2cm or less) and not significantly breathless, just OBSERVE. if no breathlessness, consider for discharge and early OP r.v, and advise to return if worsening breathlessness.
secondary- as above, but lower threshold for IC drain- if air rim more than 2cm and pt well, do IC drain as 1st line. should receive supplemental oxygen. if unfit for chest drain, consider medical pleurodesis or ambulatory management with a heimlich valve.
TENSION: emergency needle decompression with large bore cannula e.g. grey 16G into corresponding 2nd IC space anter. MCL before proceeding to chest drain.
if persistent air leak more than 5 days (bronchopleural fistula) refer to thoracic surgeons. may do open thoracotomy and pleurectomy if difficult or recurrent pneumothoraces.
emphasis on smoking cessation to minimise risk of recurrence
discharge advice- no flying or diving until resolved. diving should be permanently avoided.
if querying PE, what RFs should be identified in the history that may suggest risk of predisposing DVT/high risk of PE?
previous proven DVT/PE obese OCP malignancy lower limb fracture, varicose veins recent long haul flight, economy class-recent immobility immobilisation clotting disorder e.g. thrombophilia e.g. antiphospholipid syndrome* post-partum, C section
if the protein fluid of a pleural effusion is borderline, what criteria can be used to determine if the effusion is an exudate (pleural protein more than 30g/L)?
Light’s criteria: exudate if 1 or more of the following:
pleural fluid protein/serum protein more than 0.5
pleural fluid LDH/serum LDH more than 0.6
pleural fluid LDH more than 2/3 of the upper limit of normal serum lab value.
absolute contraindications to thrombolysis in PE patient?
haemorrhagic stroke or ischaemic stroke less than 6mnths ago CNS neoplasia recent trauma or surgery GI bleed less than 1 mnth ago bleeding disorder aortic dissection
relative contraindications to thrombolysis?
warfarin
pregnancy
advanced liver disease
infective endocarditis
complications of thrombolysis?
bleeding hypotension intracranial haemorrhage/stroke reperfusion arrhythmias systemic embolisation of thrombus allergic reaction
wells’ criteria for DVT, used to calculate DVT risk?
active cancer, treatment or palliation within 6 mnths
calf swelling more than 3cm compared to other leg
entire leg swollen
previous documented DVT
paralysis, paresis or recent plaster immobilisation of lower extremity
bedridden recently for 3 or more days, or major surgery within last 12 wks
pitting oedema confined to symtpmatic leg
localised tenderness along deep venous system
collateral (nonvaricose) superficial veins present, measured 10cm below tibial tuberosity
alternative diagnosis at least as likely
all score 1 point, apart from last which scores -2
implication of wells’ DVT risk score of 3 or more?
DVT likely, pt should receive diagnostic USS, pretest prob. 17-53%
implication of wells’ DVT risk score 1-2?
moderate risk, pretest prob. of 17%
should proceed to high sensitivity d-dimer testing
implication of wells’ DVT risk score of 0 or less?
DVT unlikely, prevalence 5%
proceed to d-dimer testing, where negative high or moderate sensitivity requires no further imaging, and positive d-dimer should proceed to USS.
wells’ criteria for PE?
previous VTE = 1.5
immobilisation or major surgery in previous 4wks = 1.5
cancer = 1
haemoptysis = 1
signs of DVT = 3
HR more than 100 = 1.5
alternative diagnosis less likely than PE = 3
max score=12.5
low risk= 0-1
moderate risk= 2-6
high risk= 7 or more
if pt deemed high risk of PE with wells’ criteria, how should management proceed?
consider CT pulmonary angiogram
d-dimer testing NOT recommended
if low risk, consider d-dimer testing.
causes of PE other than DVT?
RV thrombus post-MI septic emboli (R sided endocarditis) fat, air or amniotic fluid embolism thrombus formation after central venous access neoplastic cells parasites
define thrombophilia
an inherited or acquired coagulopathy predisposing to thrombosis, usually VTE.
conditions which increase thrombosis risk?
arterial=HTN, hyperlipidaemia, DM
venous= malignancy, thrombophilia, HF, IBD, nephrotic syndrome-lose proteins responsible for inhibiting clotting factors e.g. protein C-inactivates clotting factors Va and VIIIa, and antithrombin III-inactivates thrombin (II) and Xa, and paroxysmal nocturnal haemoglobinuria.
causes of inherited thrombophilia?
activated protein C (APC) resistance/factor V Leiden
Protein C and protein S deficiency
Antithrombin deficiency
Prothrombin gene mutation
what is antiphospholipid syndrome?
acquired coagulopathy. usually occurs as a primary disease, but be associated with SLE. antiphospholipid antibodies (anti-cardiolipin and lupus anticoagulant) cause CLOTS:
coagulation defect
livedo reticularis-pink-blue mottling caused by capillary dilatation and stasis in skin venules
obstetric (recurrent miscarriage)
thrombocytopenia
treament= low dose aspirin, or warfarin if recurrent thromboses
PE symptoms?
acute breathlessness
sudden onset pleuritic chest pain- sharp an worse with inspiration
sudden breathlessness and pleuritic chest pain most common
haemoptysis
low CO followed by collapse if massive PE-haemodynamic compromise and R heart strain, dizziness, syncope
PE signs?
pyrexia tachycardia tachypnoea cyanosis hypotension raised JVP pleural rub pleural effusion signs of a cause e.g. DVT- swollen calf, leg pitting oedema, tenderness, entire leg swollen
what might ABG show in PE?
type 1 RF:
PaO2 less than 8kPa
PaCO2 reduced as ventilation/perfusion mismatch with inadequate oxygen available in well perfused alveoli for Hb binding, so pt may hyperventilate.
therefore, may cause a respiratory alkalosis
what might a CXR in presence of PE show?
wedge shaped opacities or cavitation small pleural effusion- homogeneous white opacification, meniscus sign linear atelectasis* dilated PA oligaemia of affected segment*
what might an ECG show in PE?
normal
sinus tachycardia
RBBB, RAD
RV strain (inverted T in V1 to V4 and dominant R wave V1-V2, RAD, may be similar changes in II, III AND aVF, and may be deep S waves in I, path Q waves in III, and inverted T waves in III)
why can a massive PE cause haemodynamic compromise?
if a large clot obstructs more than 50% of the pulmonary vascular bed, pulmonary arterial pressure and RV pressure rise (R heart strain)-may be loud S2 and split S2, or gallop rhythm, reducing R heart filling pressure and CO, causing BP drop.
massive PE=haemodynamic compromise, presentation either peri-arrest or cardiac arrest usually.
define submassive PE
embolus at bifurcation of PA, with no haemodynamic compromise but presence of R heart strain.
what blds may indicate R heart strain and worse prognosis in PE?
raised troponin and BNP
importance of Us and Es in pt suspected high risk of having PE?
need CTPA for diagnosis, which requires use of contrast
must discuss with radiology if eGFR less than 60ml/min
alternative scan in looking for PE in pts unsuitable for CTPA e.g. poor renal function?
V/Q scan
but this is difficult to interpret in presence of abnormal CXR or pre-existing lung disease as looks for ventilation-perfusion mismatch.
acute massive PE mortality?
20%
how to deal with contraindications to thrombolysis in massive PE?
active bleeding or hamorrhagic stroke within 3 mnths= contraindications
all others are relative
if risks of thrombolysis exceed benefit in massive PE, what other management should be considered?
surgical/catheter embolectomy/fragmentation
discuss with consultant on call
tment of massive PE?
O2 via facemask, aiming for 100% sats
large bore cannulae, send blds including clotting, troponin/BNP
250ml boluses of IV crystalloid/colloid up to 1L to correct hypotension
urgent ECG if not already done
ECHO or urgent CTPA to confirm diagnosis
IV alteplase 10mg, then 90mg IV infusion over 2 hrs, followed by IV heparin infusion
observe and monitor in CDU/HDU/ICU
manage submassive PE similarly, but without thrombolysis with alteplase.
give IV heparin bolus, or SC LMWH
other PEs= SC dalteparin (LMWH) tment whilst confirming diagnosis
then start oral anticoagulation (warfarin), ensuring LMWH given for at least 5 days with 2 days overlap with warfarin once INR more than 2.
define bronchiectasis
characterised by irreversible dilatation of 1 or more bronchi with inflammation, sputum production, airflow obstruction and recurrent infection.
bronchial walls thickened, inflamed and irreversibly damaged. Impaired mucociliary transport mechanism predisposing to frequent bacterial infection.
important qns in taking a history from a suspected infective exacerbation of bronchiectasis?
previous CT confirming bronchiectasis?
underlying causes e.g. previous TB, childhood pneumonia, whooping cough, immunodeficiency, asthma-ABPA
length of time current infective symptoms been present
exercise tolerance, sputum colour and volume, use of beta-agonist, both now and usually?
already taken Abx?
how many courses of Abx/steroids in previous yr?
infections requir IV Abx or hospitilisation?
complications e.g. type 2 RF, cor pulmonale, major haemoptysis, empyema, pneumothorax or surgery.
investigations in order of priority when pt presents with acute asthma attack?
peak flow on arrival- record as % of best or predicted ( if no record of best within last 2 yrs)
SpO2, RR and pulse on arrival
ABG- if pt has signs of life-threatening features e.g. exhaustion, cyanosis, silent chest, or SpO2 less than 92% on room air.
post-nebulised salbutamol peak flows- after arrival for salbutamol, and within 90mins of arival if IV Mg sulfate indicated.
CXR-rule out pneumothorax and co-existing pathology e.g. lobar pneuonia. In asthma, likely CXR will show hyperinflated lungs, diagnosis is questionable if not.
Blds-FBC, ? blood eosinophilia. d-dimers should not be routinely done in wheezy pts where PE is not suspected clinically.
BTS definition of moderate asthma?
PEFR of more than 50 to 75% of best or predicted
increasing symptoms
no features of acute severe
BTS definition of acute severe asthma?
any 1 of: PEFR 33-50% of best or predicted inability to complete sentences in 1 breath RR 25 breaths/min or more HR 110 beats/min or more
BTS definition of life-threatening asthma?
ANY 1 of the following in pt with acute severe asthma PEFR less than 33% of best or that predicted SpO2 less than 92% PaO2 less than 8.0 kPa (type 1 RF) normal PaCO2 exhaustion cyanosis silent chest (no wheeze) poor resp effort low BP arrhythmia altered conscious level
BTS definition of mild asthma exacerbation?
PEFR more than 75% of best or predicted
no features of severe asthma
BTS definition of near fatal asthma?
raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures in pt with life-threatening asthma
(type 2 RF)
management guide for pt presenting to hospital with asthma attack?
A to E assessment, peak flow, SpO2, RR and pulse, ABG if spO2 less than 92% or other features of life-threatening asthma, portable CXR.
O2- humidified O2 via venturi-standard face mask to all with acute severe asthma to maintain SpO2 94-98%. CONTROLLED therapy- so being monitored with regular SpO2 checking, fixed- venturi e.g. yellow-35% 8L/min.
Nebulised bronchodilators (driven by O2) e.g. salbutamol 2.5mg-5.0mg as required. check response with PEFR measurement after each neb. continuous up to 10mg/hr (back to back every 15 mins) may be required if initial response is poor. with features of acute severe or life-threat/near fatal, can add 500mcg ipratropium bromide 6hrly (4 times a day max). IV salbutamol only if features of life-threat/near fatal and silent chest, and only after discussion with consultant on call.
steroids- oral prednisolone 40-50mg on arrival (STAT dose), IV of no additional benefit. takes 6 hrs to work. continue for at least 5 days or until recovery (usually need 10-14 days). Tapering doses only likely to be of benefit in pts on maintenance oral steroids.
IV Mg sulfate 1.2-2g over 20 mins may be considered in acute severe asthma if not responded to initial bronchodilator or in those with life-threat/near fatal. DON’T GIVE RPT boluses as hypermagnesaemia may cause resp muscle wkness.
IV aminophylline- in acute severe if not responded to inital nebs, or if life-threat/near fatal features. Dose according to ideal body weight, no loading dose if on oral theophylline, must check levels on admission and rpt daily if on oral theophylline, and put pt on cardiac monitor.
Abx usually not needed as most exacerbations related to viral infection.
indications for admission to ITU in asthma attack?
worsening hypoxaemia, hypercapnia, exhaustion, acidosis, deteriorating PEFR and altered conscious level.
co-morbidities assoc. with COPD?
IHD HTN Cancer HF DM
define COPD
a disease characterised by airflow obstruction which is progressive and not fully reversible. Encompasses chronic bronchitis and emphysema, and the airflow limitation is associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
In terms of COPD, why does stopping smoking prevent patients from experiencing the symptomatic breathlessness of COPD?
the initial inflammation of the small airways which can be brought about by smoking is reversible, so accounts for improvement in airway function if smoking is stopped early.
pathological findings in COPD?
goblet cell hyperplasia in the bronchial mucosa
loss of cilliated columnar epithelium, squamous cell metaplasia
mucus hypersecretion
SM mucous gland hypertrophy
lymphocytic infiltrate, predominantly CD8+
bronchial wall fibrosis following inflammation
abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles.
type of emphysema alpha 1 antitrypsin deficiency is assoc. with?
pan-acinar emphysema= distension and destruction affecting the whole acinus, lung may just be a collection of bullae* these can rupture, causing a pneumothorax.
3 classifications of emphysema?
centri-acinar- damage concentrated around resp bronchioles
pan-acinar
irregular- scarring and damage affecting lung parencyhma patchily independent of acinar structure.
features of emphysema?
destruction of the elastic tissue of the alveolar walls, reducing lung elastic recoil, increasing TLC, and causing premature airway closure during expiration as loss of elastic support.
reduced capacity for gas transfer as loss of alveoli, reducing SA available for GE and hence reducing diffusion rate.
pulmonary capillary bed destruction, causing pulmonary HTN, RHF and cor pulmonale.
Give 3 overall ways in which small airway airflow limitation occurs in COPD, and what this causes.
inflammation and scarring causes loss of normal small airway calibre, causing narrowing.
mucus hypersecretion as a result of goblet cell hyperplasia and SM mucous land hypertropy, plus loss of muco-ciliary clearance mechanism with squamous metaplasia blocks the airways.
reduced lung elastic recoil, and premature closure of the airways during expiration due to loss of elastic support in emphysema causes airway collapse and air trapping.
Small airway narrowing and airflow trapping causes lung hyperinflation, V/Q mismatch, increased work of breathing and dyspnoea.
classification of severity of airflow limitation in COPD?
mild- FEV1.0/FVC less than 70%, FEV1.0 80% or more of that predicted
moderate- ratio less than 70%, FEV1.0 between 50 and 79% of that predicted
severe-ratio less than 70%, FEV1.0 between 30 and 49% of that predicted.
very severe-ratio less than 70%, FEV1.0 less than 30% of that predicted.
MRC dyspnoea scale?
1-5
1= breathless only on strenuous exercise
2=SOB when hurrying on the level, or walking up a slight hill.
3=walks slower than most people on the level, has to stop for breath after 1 mile or so, or after 15mins walking at own pace.
4= stops for breath after walking 100 yards/100m?, or after a few mins on level ground.
5= too breathless to leave the house, or breathless when dressing/undressing.
what is the WHO scale of performance status and why is it used?
gives an idea of how fit someone is for tment, what is their prognosis? so can decide if fit for aggressive therapy, or more palliative treatment.
0-4, 5=dead
0=normal- fully active without restriction
1= restricted in physically strenuous activity, but ambulatory and able to carry out light work e.g. light house and office work.
2=up and about for more than 50% of waking hrs, ambulatory and capable of all self-care but unable to carry out work activities.
3= resting in bed or chair more than 50% of waking hrs, capable of only limited self-care.
4=completely disabled, cannot self-care, totally confined to bed or chair.
why are high dose inhaled corticosteroids NOT recommended in COPD tment?
increase rate of resp infections
By what mechanisms might COPD patients experience nocturnal hypoxia via alveolar hypoventilation?
shallow breathing in REM sleep, which reduces ventilation
inhibition of intercostal and accessory muscles in REM sleep
increase in upper airway resistance due to muscle tone reduction
why do most deaths in COPD pts occur at night?
possibly from cardiac arrhythmias associated with nocturnal hypoxaemia.
Tment of nocturnal hypoxia in COPD patients?
nocturnal O2 and ventilatory support- non invasive +ve pressure ventialtion with tightly fitting nasal mask and BiPAP- inspiratory to provide inspir assistances and exp to prevent alveolar closure.
most common resp cause of hospital admission?
acute exacerbation of COPD
define what a nebuliser is.
a machine to deliver medication by turning it into a mist to be inhaled through a face mask or mouthpiece.
history in acute exacerbation of COPD?
SOB-current and usual exercise tolerance
sputum- increased frequency or purulence suggest bacterial infection.
other symptoms-chest pain, haemoptysis, orthopnoea, oedema.
home O2 or nebulisers?
previous admissions/ course of steroids or Abx in last yr?
baseline function-MRC
social support network
smoking history
investigations in acute exacerbation of COPD?
FBC: HB- could SOB be due to anaemia, is there indication of polycythaemia from chronic hypoxia, is WBC raised indicating infective exacerbation? D-dimer only if clinical suspicion of PE.
CRP
CXR- ?pneumonia, pneumothorax, pulmonary oedema- bats wing hilar shadowing, fluid in fissures, kerley B lines.
ABG- type 1 o 2 resp failure?
ECG- signs of RHF?- tall R wave V1, V2, RBBB, R axis deviation.
points to note on examination of pt in acute exacerbation of COPD?
SOB at rest or on minimal exertion? use of accessory muscles?
hyper-resonant chest, loss of cardiac and liver dullness
reduced breath sounds, crackles, wheeze
raised JVP, ankle oedema
sputum pot
mechanism of ankle oedema in COPD?**
cor pulmonale- fluid retention and RHF as result of chronic lung disease.
Renal hypoxia as result of chronic lung disease leads to fluid retention as inability of the kidneys to excrete Na+ and water.
Hypoxic pulmonary vasoconstriction causes pulmonary HTN and RHR
describe the use of corticosteroids in COPD patients?
steroid trial in pts with symptomatic moderate/severe COPD always indicated. Pred 30mg daily for 2 wks. If FEV1.0 rises by more than 15% then COPD steroid responsive, so benefit may be had in using LT inhaled corticosteroids.
UHL advice on O2 in COPD exacerbation?
use controlled FiO2-venturi mask= fixed performance device. O2 delivered through injector of mask at a given flow rate. Fixed amount of air entrapped so no matter pt’s ventilation rate, inspired O2 can be predicted accurately. Can deliver 24% (blue), 28% and 35% O2.
In pts who retain CO2, aim for 88-92% sats, and 94-98% in those who don’t retain CO2.
rpt ABG 30-45mins after any change in O2 therapy in acute setting in hypercapnic pts, or if change in clinical condition e.g. reduced consciousness level.
IF hypoxic and hypercapnic, need ventilatory support, NOT reduced FiO2.
indications for LTOT?
-Pts with chronic hypoxaemia whose PaO2 is consistently at or below 7.3kPa when breathing air during a period of clinical stability- absence of exacerbation of chronic lung condition in last 5 wks.
-also if PaO2 between 7.3 and 8.0 in clinically stable pt, with 1 of either secondary polycythaemia or clinical or ECHO evidenced pulmonary HTN, or peripheral oedema (cor pulmonale features).
Pts should be non-smokers and not retain high levels of CO2.
what is ambulatory O2?**
O2 for short periods of the day during exercise e.g. walking about. AIm to allow pt to leave their home to improve their QOL, but studies shown that although activity can be enhanced, the actual amount of activity may not be increased.
should only be given if evidence of exercise desaturation and improvement in exercise capacity.
bronchodilators and steroids in exacerbations of COPD?
nebulised salbutamol 2.5mg qds, may need to give back to back initially, then PRN once stable
atrovent (ipratropium bromide-SA anti-muscarinic) nebuliser 500mcg qds- make sure to withhold ipratropium or tiotropium inhalers temporarily.
aminophylline infusion in severe cases- LD of 5mg/kg in 100ml normal saline over 1hr, skip if on oral theophylline, then continue 500mg diluted in 500ml normal saline, given at 0.5ml/kg/hr. Check theophylline levels at 6hr.
prednisolone 30mg OD in the morning for 5-7 days, but stat dose on presentation. Can give 1st dose as IV hydrocortisone 200mg if severe or unable to take oral meds. No need to tailor off unless given for more than 14 days or rpted courses in recent mnths.
appearance of pt with lung Ca causing SVC obstruction?
venous distension in neck and dilated superficial veins over the chest
swollen face
swollen arms
tment of SVC obstruction?
stent
radiotherapy
Lung Ca with familial assoc?
adenocarcinoma- type of non-small cell lung Ca
ABx in COPD exacerbations?
doxyclycline 200mg OD for 5 days if infective and no pneumonia
add amoxicillin po or iv only if CXR shows pneumonia, local guidelines if pen allergic.
indications for non invasive ventilation in acute exacerbations of COPD?
Pt must be able to breathe for themselves to use NIV
BiPAP ( 2 different strengths of CPAP, bilevel positive airway pressure) in type 2 RF with pH less than 7.35
CXR 1st to rule out pneumothorax
unless in extremis, give pt 30-45mins intensive therapy, then rpt ABG before NIV starting
NIV: start with IPAP 12 cmH2O and EPAP 4, with as much O2 as needed to maintain 88-92% sat., then increase IPAP as tolerated, e.g. up to 20.
aim for 88-92% sats, better to increase IPAP than O2 flow if possible. But caution with IPAP more than 24, increased pneumothorax risk and other complications.
always make a plan for ceiling treatment when starting NIV.
relative CIs to use of NIV?
pH less than 7.25, however often successful in practice, senior input required regarding appropriateness of ICU involvement. undrained pneumothorax life threatening hypoxaemia inability to protect airway haemodynamic instability inability to clear secretions impaired consciousness or agitation
BTS scoring of PE risk?
high risk= presence of major RF and absence of another cause for symptoms
moderate= presence of either of above
low= presence of neither of above
major RFs for PE?
previous VTE
immobility including long distance travel, care home, hospitilisation
malignancy
recent major/hip/knee surgery/post op ICU admission
up to 6 wks post partum
late pregnancy
commonly prescribed drugs known to cause pleural effusions?
MTX amiodarone beta blockers nitrofurantoin phenytoin
investigation of choice in moderate to large exudative pleural effusions where diagnostic pleural aspiration inconclusive and malignancy suspected?
thoracoscopy
how does talc pleurodesis work in treatment of malignant pleural effusion?*
talc= best sclerosant for pleurodesis in malignant effusion, and results in obliteration of pleural cavity as the 2 pleural become adhered to 1 another.
how can pulmonary HTN cause a hoarse voice?
enlarge PA compressing L recurrent laryngeal nerve
RFs for lung Ca?
SMOKING- large no. pack yrs airflow obstruction e.g. COPD increasing age FH-adenocarcinoma* previous carcinogen exposure- asbestos- ?plumbing, construction, boiler makers, radon gas, radiation therapy e.g. previous breast Ca, lymphoma as a child?
common sites lung Ca metastasises to?*
bone pleura liver adrenals CNS
what signs are you looking for o/e of pt with suspected lung Ca to rule in your diagnosis?
general appearance: muscle wasting
hands: clubbing, tar staining
swollen arms and face
enlarged LNs
Horner’s syndrome
distended neck veins and superficial vein dilation across chest
fixed elevation of JVP
Pindications of metastatic disease- hepatomegaly (liver), addison’s- pigmented palmar creases and buccal mucosa, postural hypotension, lean, pleura- pleural effusion- reduced air entry, reduced chest expansion, stony dull to percussion, reduced vocal resonance, CNS- confusion?
paraneoplastic- hypercalcaemia with squamous cell Ca-confusion?, anaemia- pale palmar creases and conjunctivae, SIADH- ?confusion, Cushing’s syndrome with small cell Ca- moon shaped face, central obesity, thin limbs, purple striae, dorsal fat pad/buffalo hump.
signs of TE disease- unilateral painful and swollen calf?, Lambert-Eaton myasthenic syndrome- proximal muscle wkness, waddling gait, reduced or loss of deep tendon reflexes, ptosis and diplopia, may be difficulty with chewing, speech or swallowing.
voice hoarseness- L recurrent laryngeal nerve compression, change in voice may also be noted if SVC obstruction- dilated vein compressing nerve
concerns if a pt with known lung Ca presents to emergency department confused?
infection- been on immunosuppressive chemotherapy
brain metastases
hypercalcaemia- PTHrP from squamous cell Ca
hyponatraemia- SIADH
why is malignancy a major RF for TE disease?
cancer= increased inflammatory cells, increases blood viscosity (Virchow’s triad- blood vessel wall, blood flow and blood components*)
define immunotherapy
also known as biologic therapy
involves use of materials made by the body or in a lab to mimic those inside the body, to boost body’s own IS to restore its function and allow it to fight a cancer.
what disorder of neuromuscular transmission is associated with small cell (oat cell) cancer of the lung?
Lambert-Eaton myasthenic syndrome (LEMS):
impaired presynaptic release of ACh at NMJ due to AI attack of VGCCs on presynaptic motor nerve terminal.
As these channels found in high numbers in tumour cells from SCLC assoc with the syndrome, its thought Abs prod. against tumour calcium channels, which then act against normal cells.
present with proximal muscle wkness e.g. thighs, with effect on gait, muscle tenderness/aching, may have autonomic features- postural hypotension, dry mouth and impotence in males.
mainstay tment for lambert-eaton myasthenic syndrome?
amifampridine- ACh release enhancer
if a pt with suspected lung Ca is found o/e to have reduced air entry, reduced vocal resonance and stony dull percussion note to his L lung, what can we say about his prognosis?
signs suggestive of pleural effusion, which indicates lung Ca has metastasised to the pleura, so prognosis poor- median survival 3 mnths*
diagnostic tests for lung Ca?
FBC- anaemia- metastasis to bone, cause of SOB, WCC_ infection differentials
INR- ?biopsy
US and Es- check renal function before IV contrast use in high-resolution staging CT and planning drug tment, indications of paraneoplastic syndromes e.g. low Na+ and K+-SIADH, metastases- high K+-addison’s
Ca2+- raised if PTHrP release, or bone met
LFTs- liver met
CXR
high res staging CT- chest/abdo/pelvis
histology: bronchoscopy and biopsy if endobronchial tumour, EBUS if mediastinal lymphadenopathy
US guided neck node FNA for cytology if lymphadenopathy
CT biospy- for parenchymal tumours- worry of needle causing pneumothorax risk. Thoracoscopy if pleural effusion present.
PET scan-radioactivity accumulates in highly metabolic active areas, helps detect small metastases not seen on staging CT, MDT decision if pt surgical candidate and initial CT suggestive of low stage.
importance of determining histological classification of lung Ca?
important for guiding tment
small cell- very aggressive, metastasises early on so unlikely can do surgery and poorer prognosis but very sensitive to chemo
causes of a lung nodule on CXR?
lung malignancy- primary or secondary carcinoid tumour abscess rheumatoid nodule granuloma hamartoma-rare benign tumour, may appear lobulated with calcification encysted effusion e.g. fluid,blood, pus AV malformation cyst FB skin tumour e.g. seborrhoeic wart
difference between radical and palliative radiotherapy?
radical- moreaggressive- more doses, aim is curative
palliative- aiming for symptom relief
SEs of radiotherapy?
N and V
chest burns
increased risk of other Cas
types of non small cell lung Ca?
squamous
adenocarcinoma
large cell
bronchoalveolar Ca
lung Ca other than small or non small cell?
carcinoid
bronchial gland Ca
Lung Ca tment stage 1/2 disease?
curative surgery if fit for surgery
Lung Ca tment stage 3/4 disease?
3a= surgery and adjuvant chemo clinical trial
tage 3/4 and PS 0-2, consider chemo
radiotherapy- curative (CHART- continuous hyperfractionated accelerated radiotherapy) for people not fit for surgery OR palliative.
palliative care
do nothing/watch and wait
what to do if lung nodule more than 2cm?
remove nodule
then CT surveillence every 2 yrs
tment for brain mets in lung Ca?
IV dexamethasone
cause of confusion if brain mets in lung Ca?
cerebral oedema causing compression and confusion
may also be headaches and N and V
hypercalcaemia tment?
aggressive fluid therapy- IV 0.9% sodium chloride
loop diuretics e.g. furosemide
bisphosphonates e.g. alendronate
SIADH tment?
fluid restriction
ADH receptor antagonsit e.g. demeclocycline
tment for SCLC other than chemo?
palliative radiotherapy
untreated- median survival 4-12wks
combination chemo- median survival 6-15 mnths
NSCLC 5 yr survival?
all= 10-13% stage 1 following surgical resection= 60-75% 2 following resection- 30-55% 3- 7% 4-1%
clinical definition of OSA?
upper airway narrowing, provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness.
pathophysiology of OSA?
pharyngeal muscles relax during sleep
excessive narrowing of upper airway may occur with normal degree of muscle relaxation during sleep when already small pharyngeal size
OR excessive narrowing may occur with relaxation during sleep.
causes of small pharyngeal size?
fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
large tonsils
craniofacial abnormalities
extra SM tissue e.g. myxoedema-hypothyroidism
what may cause excessive narrowing of the airway during sleep?
obesity may enhance residual muscle dilator action
NMD e.g. MND, stroke, myotonic dystrophy, with pharyngeal involvement may lead to greater loss of dilator muscle tone.
muscle relaxants e.g. sedatives, alcohol
increasing age
clinical effects of OSA?
if severe, leads to rpt upper airway collapse, with arousal necessary to re-activate pharyngeal dilators, may be assoc. hypoxia and hypercapnia, corrected during inter-apnoeic hyperventilatory period.
recurrent arousals cause highly fragmented and unrefreshing sleep- partner may witness snoring and apnoea attacks
excessive daytime sleepiness- epworth sleepiness scale score more than 9.
every arousal causes a rise in BP, often over 50mmHg, may damage CVS? also a rise in daytime BP.
nocturia
less common- nocturnal sweating, reduced libido, oesophageal reflux.
describe the epworth sleepiness scale
points for chance of dozing with particular activities, 0=would never doze, 1=slight chance, 2= moderate chance, 3=high chance. sitting and reading watching TV sitting in a public place passenger in car for 1hr lying down to rest in afternoon sitting and talking sitting quietly after lunch without alcohol in a car, while stopped in traffic
causes of transudate pleural effusions?
(pleural protein less than 30g/L) heart failure liver cirrhosis nephrotic syndrome or peritoneal dialysis, causing hypoalbuminaemia hypothyroidism PE mitral stenosis constrictive pericarditis SVC obstruction as occurs in lung Ca Meig's syndrome
3 cardinal features of meig’s syndrome?
benign ovarian tumour ascites pleural effusion (transudate)
causes of exudate pleural effusion?
(pleural fluid protein more than 30g/L)
malignancy
infections- parapneumonic, TB, HIV (kaposi’s)
inflammatory- RA, pancreatitis, benign asbestos effusion, Dressler’s, PE, lymphatic disorders, CT disease
yellow nail syndrome
fungal infections
drugs
how is OSA diagnosed?
overnight oximetry alone
limited sleep study- oximetry, snoring, body movement, chest/abdo movement, HR, oronasal flow, leg movements-usual study of choice.
full polysomnography- limited study plus EEG and EMG
management of OSA?
weight loss, sleep lying down rather than supine, avoid/reduce even alcohol intake
snores and mild OSA: mandibular advancement devices, pharyngeal surgery as last resort
significant OSA: nasal CPAP, consider gastroplasty/bypass, and rarely tracheostomy
severe OSA and CO2 retention: may require NIV period before CPAP if acidotic, but compensated CO2 may reverse with CPAP alone.
what must OSA pts be advised in terms of driving?
should notify DVLA of diagnosis
must NOT drive while sleepy, stop and have a nap
dr can advise drivers to stop all toether
how do CPAP and BiPAP compare in tment of OSA?
CPAP- usually via nasal mask, upper airways kept opem with approx. 10cmH2O pressure to prevent collapse, sleep fragmentation, and daytime sleepiness, also opens collapsed alveoli and improves V/Q matching.
CPAP= constant +ve pressure during I and E, so NOT a form of ventilatory support. Can help oxygenation in some pts with ARF e.g. pulm oedema.
NIV= does provide ventilatory support with 2 levels of positive pressure. Can be set up with back up rates so machine operates when RR drops below a fixed level.
where is cannula inserted to treat a pneumothorax?**
2nd IC space, MCL
key defining features of sarcoidosis?
non-caseating granulomas- need to BIOPSY
2 or more organ systems affected e.g. lungs- ILD, skin-erythema nodosum, eyes.
epidemiology of sarcoidosis?
more common in women
adults 20-40yrs of age
afrocaribbeans affected more commonly and more severly, part. by extra thoracic disease
assoc. with HLA-DRB1 and DQB1 alleles
stages of sarcoidosis according to CXR?
0=normal
1= bilateral hilar lymphadenopathy
2= BHL and peripheral pulmonary infiltrates
3= peripheral pulmonary infiltrates alone
4= progressive pulmonary fibrosis (irreversible, and causes a restrictive lung defect- FEV1.0 and FVC markedly reduced, so ratio more than 70%, TLC likely reduced, and TLCO reduced as lengthened diffusion pathway. also bulla formation (honeycombing) and pleural involvement.
this is helpful in prognosis
differentials for bilateral hilar lymphadenopathy?
TB lung Ca, metastases lymphoma sarcoidosis organic dust disease-silicosis, berylliosis
which ILD might cause a raised Ca2+ in the serum and 24hr urine?
sarcoidosis
presentation of acute sarcoidosis?
*Lofgrens syndrome- triad of erythema nodosum, bilateral hilar lymphadenoapthy and polyarthralgia/arthritis.
erythema nodosum
polyarthralgia
usually resolves spontaneously
outcome of PFTs in sarcoidosis?
restrictive defect if fibrosis (stage 3 disease on CXR- pulmonary infiltration, may be restrictive?)- FEV1.0/FVC ratio more than 70%, both markedly reduced.
reduced TLCO
normal if EP disease, or only bilateral hilar lymphadenopathy on CXR.
non pulmonary manifestations of sarcoidosis?
erythema nodosum-sarcoidosis is the most common cause uveitis- pt may complain of light hurting their eyes (increased lught sensitivity), floating specks, blurred vision, or eye redness and irritation. lymphadenopathy hepatomegaly splenomegaly terminal phalangeal bone cysts lacrimal and parotid gland enlargement brainstem and spinal syndromes arrhythmias, conduction defects and cardiomyopathy with CCF hypercalcaemia hypercalciuria renal stones pituitary dysfunction
causes of extrinsic allergic alveolitis/hypersensitivity pneumonitis?
birds fanciers lung- feathers
farmers lung- fungal spores in mouldy hay
paint- isocyante which hardens paint
investigations you would want to do for sarcoidosis?
bloods: normochromic noromocytic anaemia? raised ESR, lymphopenia- presumably as result of lung sequestration of lymphocytes, LFTs raised-sarcoid can affect liver?, serum ACE raised- more useful on monitoring response to tment, as ACE also raised with pulm TB, asbestosis, silicosis and lymphoma, with titres reducing with tment, raised Ca2+, raised immunoglobulins-hypergammaglobulinaemia.
24hr urine- Ca2+ raised
CXR- abnormal in 90%
transbronchial biospy- diagnostic- NC granuloma
bronchoalveolar lavage- raised lymphocytes in active disease, and neutrophils in pulmonary fibrosis
bone x-rays- punched out lesions in terminal phalanges
CT/MRI- espec. if pres. with headache, want to rule out neurosarcoidosis, can also assess severity of pulm disease.
cardiac MRI= gold standard for sarcoidosis affecting the heart
management of sarcoidosis?
50% spontaneous remission
acute- bed rest and NSAIDs
corticosteroids- indicated in parenchymal lung disase, uveitis, hypercalcaemia, neurol or cardiac involvement.
may try other immunosuppressants if steroids unsuccessful e.g. MTX, hydroxychloroquine
anti TNF alpha in refractory cases, or lung transplantation
differentials for granulomatous diseases?
TB, leprosy, syphillis, schistosomiasis PBC Crohn's sarcoidosis de quervain's thyroiditis silicosis wegener's granulomatosis giant cell arteritis extrinsic allergic alveolitis
5 defining characteristics of asthma?
reversibility chronic inflammatory process susceptibility airways hyper-responsiveness widespread, variable airflow obstruction
by what mechanism is aspirin thought to be implicated in asthma onset?
inhibit of COX used in PG synthesis, so arachidonic acid metabolism shifted towards the lipoxygenase pathway and production of leukotriene C4 and D4-inflammatory mediators.
causes of occupational asthma?
industrial
welders, soldering
farmers
bakers
what is intrinsic asthma?
that which is not the result of an allergic response with IgE development to specific allergens, generally appears in adults.
why does asthma produce a polyphonic wheeze?*
wheeze is the result of airway wall vibration in areas of narrowing, and asthma comprises widespread, variable airflow obstruction.
components to examining a pt with asthma?
inspection: bedside- inhalers, O2, nebulisers, sputum pot, obs charts
chest- hyperinflation, scars, deformities
general health- eczema, hayfever, lethargy, can they talk?
percussion-hyper-resonant?
auscultation- polyphonic wheeze?
what does allergy testing in asthma involve?
skin prick test
normal saline used as -ve, allergens then used- put onto the skin and pricked so small amount can enter the blood to see if pt develops an allergic response, and this is compared with that to histamine.
include cat, dog, grass, tree, HDM, and different type of mould. looking for wheal development around prick site- more than 3mm.
5 causes of airway narrowing in asthma?
bronchospasm- smooth muscle contraction
bronchia wall thickening as inflammtory cell infiltration
mucosal oedema as vascular leak
mucus over prod. thick and slow-moving, may plug the airways
shed epithelium from eosinophil mediated damage is incorporated into the thick mucus.
why might steroid tablets not provide much relief of symptoms for an asthmatic pt?
if non-allergic asthma (intrinsic asthma)- IgE independent- don’t have the eosinophilia that accompanies allergic asthma, and its eosinophils which are very sensitive to steroid therapy?*
pts likely to benefit from antileukotriene therapy in asthma e.g. montelukast?
aspirin-sensitive asthma
severe asthmatics taking steroids
exercise induced
allergic asthma
importance of good asthma control in terms of airflow obstruction reversibility?
in LT and poorly controlled asthma, airway remodelling occurs with smooth muscle hypertrophy and hyperplasia, mucus gland hypertrophy and BM thickening- some of which may not be reversible.
important investigations in 1st presentation of pt suspected of having asthma?
blds- ?WCC-infection?, eosinophilia?- asthma, ABPA, eczema
sputum pot- infection?
ECG- other causes of acute SOB e.g. PE- sinus tachy, S1, Q3, T3 pattern
CXR- lung hyperinflation?infection?
PEFR- compare to predicted if never done a peak flow before, or known best of the pt
PFTs- spirometry- obstructive defect? post-bronchodilator reversibility- can be used to distinguish between reversible and non reversible airways obstruction, and determine if asthma control is effective- if significant improvement achieved in FEV1.0 post bronchodilator, this implies best control of pt’s asthma isn’t currently being achieved.
skin allergen testing- determine if allergic asthma, any specific allergens pt can avoid?
2 overall types of inhaler?
metered dose inhaler
dry powder inhaler e.g. spiriva-tiotropium bromide- slow and deep breath, but at rate sufficient to hear/feel the capsule vibrate.
major asthma symptoms?
dry nocturnal cough, wakes pt, may sleep on their side
SOB-morning, exercise, cold air, allergens
recurrent wheeze
chest tightness
all associated with precipitating factors
which pts in acute asthma presentation require ABG as part of ABCDE assessment (B)?
those with SpO2 found to be less than 92% on pulse oximetry, or those found to have other features of life threatening asthma e.g. PEFR less than 33% of that predicted, cyanosis, silent chest, poor resp effort, arrhythmia, hypotension, exhaustion and altered consciousness level.
if resp effort failing, concern over type 2 resp failure- low PaO2 and high PaCO2 . Acidosis- enzyme denaturation.
specific triggers in asthma?
HDM faeces
pollen
animal fur
pathogenesis of extrinsic allergic alveolitis/hypersensitivity pneumonitis?
pt inhales antigen to which they have already been sensitised
initial airway infiltration with neutrophils, followed by T cells and macrophages, resulting in production of non-caseating granulomas.
clinical presentation of extrinsic allergic alveolitis?
ACUTE: 4-8 hrs post exposure, symptoms of dyspnoea, dry cough, fever and malaise, usually reversible- spontaneously settle 1-3 days, can recur.
CHRONIC: chronic exposure (mnths-yrs), less reversible, LT architectural lung damage, interstitial fibrosis.
tment of extrinsic allergic alveolitis?
remove cause! avoid particular exposure e.g. birds, farming, isocyanate paints.
steroids when needed-oral pred.
results of investigations in EAA?
blds: increased neutrophils in acute cases, precipitating antibodies in serum
CXR: diffuse micro-nodular infiltrate, denser towards hila, streaky shadows particularly in upper zones. fine reticuar/nodular shadowing, fuzzy heart borders, tracheal shift towards side of fiborosis. Honeycomb in very advanced. Chronic- may appear normal, but may progress to pulm fibrosis affecting upper zones.
CT- ground glass opacification
PFTs- reduced TLCO, restrictive defect- FEV1.0/FVC ratio more than 70%.
how can the ILD idiopathic pulmonary fibrosis (IPF/CFA/UIP) be distinguished from the other ILDs?
certain radiological features- reticular abnormality and volume loss, honeycombing, traction bronchiectasis- airway splayed open with restriction around it due to elastic recoil loss, focal ground glass opacification. CT distribution is peripheral, basal and subpleural.
criteria for safe hosp discharge of pt post asthma attack?
PEFR more than 75% of their best or predicted
off theophylline, blood levels checked
free of nebulised tment for a day before going home
must be seen by asthma nurses as IP for r/v to reassess inhaler technique and adherence
written asthma action plan and peak flow meter provided
at least 5 days oral pred
GP F/U within 2 working days
Resp clinic follow up within 4 wks
for severe or worse, consider psychosocial factors
examination and investigations in suspected infective exacerbation of bronchiectasis?
ABC approach
crepitations?-biphasic coarse? do they change on coughing?
?signs of decompensation- ankle oedema (cor pulmonale) and drowsiness (type 2 RF)
blds: FBC- ?WCC, Us and Es, LFTs, CRP
ABG if SpO2 less than 94%
CXR- look for new areas of consolidation- compare to previous films
sputum microscopy, culture and sensitivity- send for mycobacterial culutre if frequent exacerbations or failure to respond
if prev diagnosis of ABPA, r/v eosinophil count and send total IgE and aspergillus specific IgE
causes of bronchiectasis?
post infective: TB
whooping cough
immune deficiency: hypogammaglobulinaemia
genetic/mucociliary clearance defects:cystic fibrosis- most common cause in developed countries?
primary ciliary dyskinesia
young’s syndrome
kartagener syndrome
obstruction: FB, tumour, extrinsic LN
toxic insult: gastric aspiration part. post lung transplant, toxic chemicals/gases
ABPA
sec immune deficiency e.g. HIV, malignancy
RA
assoc- IBD, yellow nail syndrome
causes of an unresolving pneumonia? **
CHAOS:
complication- empyema, lung abscess
host- immunocompromised
antibiotic- inadequate dose, poor oral absorption
organism- resistant or unexpected
second diagnosis- PE, Ca, organising pneumonia
importance of chest physio in bronchiectasis management?**
clear mucus from distal airways to ease SOB and improve ET
? reduce risk of recurrent infections?
bronchiectasis common organisms?
H influenzae Pseudomonas aeruginosa- highly resistant moraxella catarrhalis stenotrophomonas maltophilia fungi-aspergillus, candida non TB mycobacteria S.aureus- think about CF*
bronchiectasis management?
ABCDE approach
treat underlying cause?
Abx- give LT if 5 or more exacerbations in 1 year
steroids
LMWH
CHEST PHYSIO
bronchodilators and influenza vaccination-supportive
paracetamol
senior input
pulmonary rehabilitation if MRC dyspnoea score of 3 or more- so pt at least has to stop for breath when walking at own pace on level ground or can’t keep up with others on the flat because of breathlessness.
can do lung transplant, if so must be bilateral as risk of cross infection.
differentials for eosinophilia?
asthma eczema ABPA parasitic infections hayfever/allergies drugs e.g. antibiotics churg-strauss/vasculitis eosinophilic pneumonia lymphoma SLE hypereosinophilic syndrome-when no other cause can be found
possible contributing factors to IPF(UIP)/ fibrosing alveolitis?
cigarette smoking chronic aspiration anti-depressants wood, metal dust infections-EBV
why is making the diagnosis of IPF accurately so important?**
now specific drug tment for this= pirfenidone- increases survival and preserves lung function
signs o/e of pt with IPF?
clubbing
central cyanosis
reducrd chest expansion
bilateral fine end-inspiratory crackles basally/axillary
features of pulmonary HTN- cor pulmonale e.g. ankle oedema
beading in the fissure on HRCT?
occurs in pulmonary sarcoidosis as lots of white circles due to granulomas
results of investigations in IPF?
blds: WBC- querying infection, eosinophilia- occurs in acute phase of EAA
Us and Es- contrast use in HRCT
Ca2+- raised with sarcoidosis
CRP/ESR- querying CTD
LFTs
CXR-small lungs, micro-nodular shadowing mainly in lower zones, ragged heart borders, ground glass appearance, CT- fibrosis, honeycombing peripherally, basally and subpleurally.
PFTs: reduced TLCO, FEV1.0/FVC ratio more than 70%.
describe the different venturi masks- a fixed performance device for controlled O2 therapy- aiming to achieve a particular SpO2, in terms of the %O2 delivered and the L of O2 required.
blue venturi- 24% O2- 2L/min
white venturi- 28%- 4L/min
yellow venturi- 35%- 8L/min
red venturi- 40%- 10 L/min
body systems that can be affected by CF and examples of the problems this causes?**
pancreas-DM, malabsorption- steatorrhoea
genital tract- infertility
symptoms of bronchiectasis?
persistent cough
copious purulent sputum
intermittent haemoptysis- may be blood stained sputum or massive haemorrhage
can be breathlessness from airflow limitation
if mild, may only produce green or yellow sputum after an infection
worsening condition- persistent halitosis, recurrent febrile episodes with malaise and episodes of pneumonia.
severe-continous prod of foul smelling thick khaki coloured sputum
signs of bronchiectasis?
finger clubbing
coarse inspiratory (and expiratory) crepitations so biphasic- often bilateral and throughout the lungs- heard over infected areas- often lung bases.
wheeze- asthma, COPD, ABPA, acute bronchitis, FB, anaphylaxis, cardiac wheeze-HF
CXR findings in bronchiectasis?
cystic shadows
thickened bronchial walls- tramline and ring shadows
may be fine reticular shadowing suggestive of ILD
bronchiectasis complications?
pneumonia pleural effusion pneumothorax haemoptysis-part. in CF pts, can be life-threatening, massive haemoptysis due to high-pressure systemic bronchial arteries, must allow bed rest and Abx, blood transfusion if required, bronchoscopy occasionally and bronchial artery embolisation cerebral abscess amyloidosis respiratory failure or cor pulmonale
results of investigations in bronchiectasis?
bloods*- serum Igs- up to 10% of adults with condition have antibody class or subclass deficiency-mainly IgA
sputum culture- e.g. h.influenzae, moraxella catarrhalis, pseudomonas aeruginosa
CXR
HRCT chest- thickened, dilated bronchi, and cysts at end of bronchioles, bronchi larger than their accompanying pulmonary artery branch-signet ring apperance
spirometry- obstructive pattern
bronchoscopy- can locate site of haemoptysis or exclude obstruction
CF sweat electrolyte test
aspergillus precipitans or skin-prick test
bronchiectasis management?
postural drainage- 3 imes daily for 10-20mins so affected lobes are uppermost
chest physio
ABx- prescribe according to bacterial sensitivities, consider LT antibiotics depending on number of exacerbations in previous year-5 or more
bronchodilators- neb salbutamol may be useful in those with asthma, COPD, CF, ABPA, or demonstrated airflow limitation
corticosteroids for ABPA, and to decrease rate of progression
surgery in localised disease or to control severe haemoptysis
how should a pt be taught to use the symbicort turboinhaler (formoterol and budesonide)?
deep breath in as hard as they can with mouthpiece placed gently between their teeth, and advise not to chew or bite on the mouthpiece.
Symptoms of IPF?
Dry cough, exertional dyspnoea, malaise, weight loss, arthralgia.
Resp diseases that may cause hypercalcaemia?
lung malignancy- squamous cell carcinoma secreting PTHrP
sarcoidosis
drugs causative of ILD (diffuse parenchymal lung disorders DPLD)?
methotrexate
amiodarone
nitrofurantoin e.g. pts on LT tment for recurrent UTIs.
what is a granuloma and why do they form?
a group of epithelioid histiocytes (modified macrophages forming multinuclear giant cells) formed as a chronic inflammtory response to an insoluble or slowly soluble irritant or antigen.
Form in response to macrophage difficulty phagocytosing the irritant.
how can the differentials for bilateral hilar lymphadenopathy be distinguished between via 1 test?
BIOPSY
define hypopnoea
a reduction in air flow by 50%
gold standard for diagnosing neurosarcoid disease?
head MRI
why might hypercalcaemia occur in sarcoidosis?
due to increase in circulating calcitriol- the active form of Vit D, with 1 alpha-hydroxylation occurring in sarcoid macrophages in the lung in addition to that taking place in the kidney.
when should tment be started in sarcoidosis?
if abnormal PFTs, pt unlikely to improve without corticosteroids
if disease not improving spontanously 6mnths after diagnosis, should stat pred 30mg for 6 wks, reducing to alternate-day tment with pred 15mg for 6-12mnths.
eye involvement or persistent hypercalcaemia indicate mandatory steroids.
most useful way of monitoring sarcoidosis progression?
lung volumes and gas transfer
when might talc pleurodesis be used as a tment?
malignant pleural effusion
SpO2 which necessitates performing an ABG in pt with no known respiratory failure?
92% or less
common differentials for CXR consolidation?
pneumonoa TB (usually upper lobe) malignancy lung Ca haemorrhage e.g. trauma lobar collapse (bronchi blocked)
how should pt clinically suspected of having pulmonary TB prior to results of sputum cultures be treated in hospital?
if unclear diagnosis, treat as pneumonia- give antibiotics as per CURB-65 score
if critically unwell and high likelihood of TB then start anti-TB therapy after sputum cultures sent
TB tment often started before culture confirmed diagnosis as can take 6-8wks for TB culture to come back.
most common cause of failed improved consolidation on CXR?
lung Ca
define the CURB-65
predictor of 30 day mortality
confusion, AMT 2 or more points worse (8 or less)
urea more than 7 mmol/L
respiratory rate 30 breaths per min or more
systolic BP less than 90mmHg and/or diastolic of 60 or less
age 65 or above
each scores 1 point
2= need hosp treatment
3 or more- consider contacting ITU
how can pneumonia be differentiated from an infective exacerbation of COPD?
CXR- consolidation MUST be present for pneumonia diagnosis
if high CURB-65 score, what other tests should be considered?
atypical pneumonia screen- serum mycoplasma and urine legionella
pneumonia investigations?
blds: FBC- ?raised WCC, raised CRP, Us and Es and LFTs- ?sepsis, blood culture if febrile
ABG if sats 92% or less
sputum culture
CXR
atypical pneumonia screen if CURB-65 high
pneumonia follow up?
once clinically stable, consider: HIV test immunoglobulins pneumococcal IgG serotypes H.influenzae b IgG F/U in clinic in 6 wks with rpt CXR to ensure resolution
non-resp TB clinical features?
erythema nodosum lymphadenopathy bone/joint abdo CNS (meningitis)- headache, photophobia, neck stiffness genitourinary miliary (disseminated) pericardial effusion (cardiac)
haemoptysis differential diagnoses?
infection: TB, pneumonia, bronchiectasis/CF, cavitating lung lesion (often fungal)
malignancy- lung Ca, metastases
haemorrhage: vasculitis- good pasture’s syndrome, bronchial artery erosion, coagulopathy
PE
test for latent TB?
quantiferon blood test (interferon gamma)
management principles for resp TB?
ABCDE
admit to side room and start infection control measures e.g. masks and -ve pressure room
if prod. cough then 3X sputum samples for acid fast bacillus staining and TB culture and establish sensitivity, ideally early morning samples.
consider bronchoscopy with BAL if no prod cough and suspect pulm TB in order to obtain sample to culture
routine blds: FBC, Us and Es, LFTs especially-deranged liver enzymes in miliary TB- disseminated TB through haematogenous spread, HIV, Vit D
blood culture in miliary TB
CT chest if pulm TB suspected but clinical features/CXR not typical
MRI brain/spine if miliary TB with CNS involvement suspected followed by lumbar puncture-CSF protein very high, glucose less than half of blood glucose, lymphocytosis.
notify case to TB nurse specialists- support pt in investigation, during tment, public health issues, and initiate contact tracing.
if pt critically unwell and high likelihood of TB, than start anti-TB therapy AFTER sputum samples sent.
why is Vit D often found to be low in TB patients?
Vit D used by macrophages to fight infection
idiopathic pulmonary fibrosis represents what type of ILD and is diagnosed on the basis of what pathological pattern?
IPF is a type of idiopathic interstitial pneumonia
it has the pathological pattern of usual interstitial pneumonia
can be diagnosed from HRCT alone if typical pattern of usual interstitial pneumonia, if not require biopsy.
BTS guidelines for CAP drug tment?
severity based on CURB-65 which determines tment as predictor of 30 day mortality, BUT should base drug prescribing on clinical picture of pt, not just score.
CURB 65 of 2 suggests need for short stay inpt hosp tment or hosp supervised OP tment.
relieve pleuritic pain with simple analgesia-paracetamol
tment in community= PO amoxicillin 500mg TDS, doxyclycline or clarithromycin in pen allergic, also use if in hosp for other co-morbidity and curb-65 0-1, amoxicillin 500mg IV TDS if PO not possible.
moderate severity-CURB-65 2, PO amoxicillin 500mg-1.0g TDS PLUS oral clarithromycin 500mg BD, IV amox or IV benzylpen and clarithro if can’t do oral route.
if score 3-5, give IV co-amoxiclav 1.2g TDS and oral doxycycline or clarithromycin 500mg BD IV
common cause of type 1 resp failure in post-op patients?
atelectasis
which resp disease do we treat with ethambutol and what are its ADRs?
TB optic neuritis (retrobulbar) and loss of visual acuity, possible complete blindness, and colour blindness.
when would we consider an ABG in a pneumonia pt?
if SpO2 92% or less and pt not known to have RF
what might a pt taking pyrazinamide for TB complain of?
arthralgia
also risk of hepatitis, rashes and vomiting
how can complience with TB tment be met in certain high risk individuals?
DOT- seen by nurse 3X a week to take their med.
how can malabsorption be investigated in CF patient?
faecal elastase in stool sample
A pt with known CF presents with a palpable RIF mass and is complaining of abdo pain, what is the likely diagnosis?
distal intestinal obstruction syndrome- faeces thick and dehydrated, wedge between SB and LB-obstruction is in ileocaecum vs whole bowel with constipation
bowel can be rehydrated with gastrograffin.
why is a signet ring sign seen on HRCT in bronchiectasis?**
dilated bronchus seen next to its accompanying pulmonary artery branch
reasons why a pt may have ‘unresponsive’ asthma?
asthma NOT the diagnosis e.g. may be ABPA, bronchiectasis
non-compliance with therapy/poor inhaler technique
steroid abs. problems?
tment of ABPA?**
oral corticosteroids
? oral anti-fungal
differentials for the presentation of a wheeze?
acute asthma exacerbation acute bronchitis anaphylaxis FB VC desynchronisation PE GORD pulmonary oedema
how is a pneumothorax diagnosed?
standard erect CXR in inspiration
CT scan for uncertain or complex cases
features of TENSION pneumothorax?
haemodynamic compromise- hypotension and tachycardia
trachea or mediastinal displacement away from affected side
severe breathlessness
distended neck veins
CXR NOT required
call for senior assistance IMMEDIATELY
RFs for TB?
immunocompromised-on corticosteroid or immunosuppressive therapy e.g. chemo, co-existing HIV, Vit D deficiency, DM, CKD, malnutrition
high risk travel e.g. sub-saharan africa
high risk contact
drug/alcohol misuse, homelessness/hostels/overcrowding
how does latent TB compare to active disease?
Latent: bacilli present in Ghon focus, sputum smear and culture -ve, tuberculin skin test usually +ve, normal CXR, small calcified ghon focus frequently visible, asymptomatic, not infectious to others.
Active TB: bacilli in tisues/secretions, sputum culture commonly +ve as is tuberculin test, CXR-consolidation signs-opacification, cavitation or effusion
night sweats, fever, weight loss, cough, infectious if bacilli detectable in sputum.
what is a Ghon complex/primary complex?
a Ghon focus= granulomas-caseating and TB bacilli, and the associated draining hilar LNS.
name of TB focus which can develop within the regional draining LN?
primary complex of Ranke
indications for treating latent TB with antibiotic therapy??
once active TB has been ruled out by CXR and examination consider in those identified through screening who are:
35 or younger ( as increasing risk of hepatotoxicity with age)
any age with HIV
any age and a healthcare worker
AND are either
Mantoux +ve without prior BCG OR
strongly Mantoux +ve, IF-gamma (quantiferon) +ve and with prior BCG vaccination
basics of anti-TB therapy?
standard regimen= 2 months of rifampicin, isoniazid, pyrazinamide and ethambutol, followed by 4 months on rifampicin and isoniazid.
tment for min 6mnths in total
weight important as dose of anti-TB antibiotics is weight dependent
check baseline LFTs and monitor closely
check visual acuity BEFORE giving ethambutol- can cause optic neuritis and visual acuity loss
DOT
leaflets on tment and ensure pt aware of common and serious ADRs
pyridoxine alongside isoniazid to prevent peripheral neuropathy
corticosteroids possibly if TB meningitis-headache, neck stiffness and photophobia
how is risk of peripheral neuropathy from isoniazid tment in TB tment reduced?
also give pyridoxine ( a form of Vit B6) which isoniazid causes a deficiency of to cause peripheral neuropathy
major ADRs of rifampicin?
liver toxicity-hepatitis
turn secretions red/orange- NB contact lenses
rashes
febrile reaction
many drug interactions as CYP450 inducer, including warfarin and OCP- metabolism increased so may be increased risk of clotting (warfarin) and pregnancy (pill)- must advise pts to use alternative forms of contraception e.g. barrier method
ADRs of isoniazid?
peripheral neuropathy due to vit B6 deficiency
rashes
hepatitis
psychosis
treatment regimen for latent TB?
6 months of isoniazid or 3 months of rifampicin and isoniazid or people aged 16–35 not known to have HIV
either 6 months of isoniazid or 3 months of rifampicin and isoniazid for people older than 35 in whom treatment for latent TB infection is recommended and who are NOT known to have HIV
6 months of isoniazid for people of any age who have HIV
6 months of rifampicin for contacts, aged 35 or younger, of people with isoniazid-resistant TB
staining for mycobacterium TB?
ziehl-neelsen staining for acid fast bacilli- high lipid content of cell wall means relatively impermeable and stain weakly with gram stain.
pulmonary TB symptoms in active disease?
productive cough
haemoptysis
weight loss
fevers
night sweats- drenching of clothes and bed sheets
pleuritic chest pain- sharp and worse on deep inspiration
inheritence pattern of CF?
autosomal recessive
mutation responsible for CF?
3bp deletion on the long arm of chromosome 7, resulting in loss of codon for phenylalanine at position 508, altering the secondary and tertiary structure of the CFTR channel protein so fails to open in response to increased cAMP in epithelial cells.
*CFTR= cystic fibrosis transmembrane conductance regulator
why is the mucus produced at epithelial surfaces in CF of increased viscosity and tenacity e.g. airway secretions?
CFTR protein channel on the surface of epithelial cells fails to open to move Cl- out of the cell, resulting in decreased excretion of Cl- and increased reabsorption on Na+ into epithelial cells to maintain electroneutrality. As less Na+ is excreted, less water is moved out of the epithelial cells via osmosis so secretions are more viscous e.g. airway secretions.
why is there are a high Na+ content of sweat in CF patients?
CFTR independent mechanism of Cl- secretion in sweat gland with an impaired reabsorption of sodium chloride in distal end of the duct.
gold standard for diagnosing CF?
sweat test-sweat chloride concentration of more than 60mmol/L
also now newborn screening- heel prick test at 1 week
what features of an infant may suggest the presence of CF?
failure to thrive
meconium ileus at birth
recurrent chest infections
process of diagnosing CF?
1 or more of characteristic phenotypic features e.g. failure to thrive, recurrent chest infections, OR a history of CF in a sibling, OR a positive newborn screeening test result
AND
an increased sweat Cl- concentration-more than 60mmol/L
or identifying 2 CF mutations-genotyping
or demonstrating abnormal nasal epithelial ion transport- nasal potential difference.
A pt presents with presumed pneumonia and 2 features of SIRS: temperature is 38.9 degrees and RR is 22, how should they be managed?
A to E approach, and start sepsis 6 pathway:
give empirical antibiotics 1st!, and consider paracetamol to reduce pyrexia
IV fluids
controlled O2 therapy, aiming for 94-98% sats if no a known retainer of CO2
measure blood lactate
do blood culture
put in urinary catheter to measure fluid output
SIRS criteria?
temp less than 36 or more than 38
RR more than 20 of PaCO2 less than 32 mmol/l
HR more than 90
WCC less than 4 or more than 12 X 10^9/L
2 or more=SIRS
define sepsis
SIRS plus suspected or present source of infection
define severe sepsis
organ dysfunction, hypotension or hypoperfusion:
lactic acidosis, SBP less than 90 or SBP drop of 40mmHg or more of normal
septic shock criteria?
severe sepsis and hypotension not responding to fluid resuscitation
respiratory presentations of CF?
recurrent chest infections (bronchopulmonary)
sinusitis
breathlessness and haemoptysis
in later stages as airflow obstruction and bronchiectasis develop
spontaenous pneumothorax
resp failure and cor pulmonale
what transport system is impaired in broncheictasis pts predisposing them to frequent bacterial infections?
mucociliary clearance
GI effects of CF?
steatorrhoea- enzymes from exocrine pancreas stagnated in thick viscous secretions in pancreatic ducts so unable to reach their site of action in the small bowel to allow fat absorption so undigested fat appears in the faeces.
children-meconium ileus at birth- sings of intestinal obstruction soon after birth with bilious vomiting, abd distension and delay passing meconium.
malabsorption- usually due to pancreatic exocrine insufficiency- can test for with faecal elastase test in stools-less than 100 micrograms/g indicates insufficiency.
poor nutrition- comb of malabsorption and maldigestion- increases risk of pulmonary sepsis.
cholesterol gallstones
liver cirrhosis
increased incidence of GI malignancy and peptic ulceration
CF features other than resp and GI effects?
delayed growth-puberty and skeletal maturity
infertility- males almost always as failure of vas deferens and epididymis development
females often develop secondary amenorrhoea, and fertilisation harder with thick cervical mucus
arthropathy and DM common
nasal polyps
osteoporosis
finger clubbing
CF lifestyle advice?
no smoking/smoking cessation
annual influenza and pneumococcal vaccines
pulmonary rehabilitation
avoid other CF patients- as chronic colonisation means risk of cross-infection and antibiotic resistance
sodium chloride tablets in hot weather/vigorous exercise
avoid jacuzzis-pseudomonas
clean and dry nebuklisers thoroughly
avoid stables, compost or rotting vegetation-risk of aspergillus fumigatus immunisation
CF treatments?
O2 therapy
Abx for resp infections-aggressive therapy plus physio, often proph antibiotics to maintain health
nebulised anti-pseudomonal antibiotic therapy to improve lung function and decrease riskk of infective exacerbations and hospitilisation
beta 2 agonsits and inhaled corticosteroids may provide symptomatic relief
inhalation of recombinant DNAse may improve FEV1.0
NIV in chronic resp failure
nutritional support and enzyme replacement e.g. creon, high calorie intake, may need NGT or PEG
transplant-can be chronic rejection-bronchiolitis obliterans syndrome
what is distal intestinal obstruction syndrome in CF pts most commonly due to?
insufficent prescription of pancreatic enzymes or non-compliance
also salt deficiency/hot weather
preferred initial test to assess presence and severity of airflow obstruction in asthma?
spirometry
non-pharmacological secondary prevenetion strategies in asthma?
smoking cessation
losing weight
breathing exercise programmes
define complete control of asthma
no daytime symptoms no night time awakening due to asthma no need for rescue med no asthma attacks no exacerbations no limitations on activity including exercise normal lung function-FEV1.0 and/PEFR more than 80% of predicted or best minimal side effects from med.
usefulness of combination inhalers in asthma tment?*
no known improved efficacy compared to long acting beta 2 agonist and inhaled corticosteroid used alone, but does improve adherence and ensures long acting beta 2 agonist isn’t taken alone.
principles for BTS stepwise management guidelines of chronic asthma in adults?
start pt on tment at step most appropriate to inital severity
achieve early control
maintain control by stepping up therapy as necessary and down when good control.
ensure checking of adherence, inhaler technique and eliminate trigger factors before stepping up therapy with new drug
when stepping down, need regular r/v, and must consider asthma severity, duration of current tment dose and its side effects, beneficial effects acheived and pt preference.
maintain pts on lowest possible dose of inhaled corticosteroid, and reduce dose slowly as pts deteriorate at different rates, consider reductions every 3mnths by approx 25-50% each time.
define brittle asthma
type 1=wide PEF variability (more than 40% diurnal variation for more than 50% of the time over a period of more than 150days) despite intense therapy
type 2=sudden severe attacks on background of apparently well controlled asthma
ADRs of salbutamol?
tremor
palpitations, tachycardia
hypokalaemia
what is the metacholine airways challenge?
give pt increasing dose of methacholina muscarinic agonist, and look for 20% reduction in FEV1.0 for asthma diagnosis.
what muscle problem can LT steroids cause?
proximal myopathy
management of COPD requires what type of approach?
a MDT approach- consultant resp, GP, pulmonary rehab nurses, physio, dietician, pharmacist etc.
ensure care bundle when d/c from hospital
pulmonary rehab-break the cycle of deconditioning where avoidance of exercise due to SOB reduces muscle strength and QOL further, lung function continues to decline and SOB worsens.
how does BiPAP (a form of NIV) improve CO2 elimination in COPD pts with type 2 RF?
alternating pressure between inspiration and expiration improves alveolar gas exchange
NIV follows tment with neb salbutamol and oral prednisolone-30mg
caution with use of ipratropium and tiotropium in which patients?
those with angle-closure glaucoma and BPH
aminophylline mechanism of action in bronchospasm?
inhibit phosphodiesterases so reduced cAMP breakdown, causing bronchodilation
ADRs of xanthines?
tachycardia headache GI upset gastric reflux dizziness palpitations
toxic effects-hypotension, seizures, N and V and serious arrhythmias, therapeutic window= plasma level 10-20mg/L.
common side effects of inhaled glucocorticoids?
cough
oral thrush (candidiasis)
unpleasant taste
hoarseness
what might be chosen to be given to a pt alongside steroid therapy?
PPI-gastric protection, reduce GORD
bisphosphonates-bone protection
steroid card to prevent adrenal crisis during acute emergency hospital admission
investigations you might like to perform and why if a patients presents with a large pleural effusion as already diagnosed on CXR?
Bloods: FBC-Hb-anaemia assoc with malignancy-mild normocytic anaemia, OR malignancy with bleeding-microcytic hypochromic anaemia assoc. with Fe deficiency?, WCC-raised with infection e.g. pneumonia or TB, clotting studies-check prior to biospy-thoracoscopy, Us and Es-baseline, check prior to contrast with staging CT scan, Ca2+ raised with lung Ca, also low Na+ and K+-SIADH, LFTs-malignancy, liver cirrhosis and transudate, CRP-raised with infection, malignancy.
US guided pleural fluid aspiration
thoracoscopy
staging CT scan chest, abdo, pelvis querying lung Ca
ECHO-querying transudate assoc. with left sided HF
PET-lung Ca metastases identify to plan approp. tment based on prognosis.
airway pathophysiological changes assoc. with asthma?
epithelial damage-epithelial shedding and subepithelial fibrosis, BM thickening
inflammatory reaction characterised by eosinophils, T helper 2 cells and mast cells-histamine release. also LKTs and PGs released. bronchial wall swelling with mucosal oedema mediated by increased capillary permeability e.g. IL-1, and inflammatory cell infiltration leads to widening.
cytokines amplify inflammatory response
increased numbers of mucus secreting goblet cells, and smooth muscle hyperplasia and hypertrophy. excessive bronchoconstriction with smooth muscle cell contraction.
mucus plugging in fatal and severe asthma.
management of anaphylaxis and angioedema?
GET HELP! remove trigger, maintain airway, give 100% oxygen IM adrenaline 0.5mg-rpt every 5 mins as needed to support CVS IV hydrocortisone 200mg IV chlorphenamine 10mg if hypotensive lie flat and resuscitate treat bronchospasm-NEB salbutamol laryngeal oedema-NEB adrenaline
define massive hamoptysis
more than 240mls in 24 hrs
OR
more than 100 mls/day over consecutive days
management of massive hamoptysis?
ABCDE approach
lie pt on side of suspected lesion if known
oral tranexamic acid for 5 days or IV
stop NSAIDs/aspirin/anticoags
antibiotics if evidence of any RTI
consider Vit K
CT aortogram-bronchial artery embolisation may be undertaken by interventional radiologist
Common causes of false positive sweat test?
adrenal insufficiency
hypothyroidism
anorexia nervosa
coeliac disease
symptoms and signs associated with type 2 respiratory failure?
exertional dyspnoea
fatigue
excessive daytime sleepiness-epworth score 10 or more
rapid shallow breathing-NM disease
impaired concentration
morning headache
symptoms of co-existing OSA_loud snoring, short apnoeic episodes
signs: pulmonary HTN-L parasternal heave (RV heave), pulsatile liver, raised JVP, pedal oedema-in absence of L sided HF, loud S2 (P2), tricuspid regurge-pansystolic murmur hear loudest over 4th L ICS during inspiration
plethoric-polycythaemia
obesity, muscle wasting/fasciculation, kyphosis/scoliosis, wheeze/COPD signs e.g. central cyanosis, hyperinflated chest with loss of cardiac and liver dullness and displaced apex beat.
causes of acute type II resp failure?
Decompensation of existing respiratory disease-exacerbation of COPD, near fatal asthma attack
First presentation of chronic respiratory failure
Depressed central respiratory drive-BZDs, opioids
Trauma
Severe hypothermia-J wave ECG
Mechanical/acute neurological defect in chest wall/diaphragm-Flail chest-rib detachment, acute neuropathy or myopathy e.g. Guillain-Barre
what is obesity hypoventilation syndrome?
a cause of chronic type 2 resp failure defined as obesity + daytime hypercapnia OSA co-exists in 90% cases Prevalence depends on BMI Treatment is initially nocturnal NIV May only require CPAP if able to correct hypercapnia in long-term (particulary if OSA is predominant)
what are we trying to improve with use of NIV in patients with type 2 respiratory failure?
trying to reduce PaCO2 by improving ventilation as alveolar hypoventilation is the principal cause of hypercapnia
bear in mind minute ventilation=tidal volume X RR
if we increase IPAP with NIV, we increase tidal volume (vol of air moving into and out of lungs in 1 breath) to increase minute volume and decrease PaCO2.
IPAP has little effect on hypoxia
EPAP splints open the alveoli so improves oxygenation
death from what type of metastases is common in patients with small cell lung Ca?
cerebral metastases-cerebral oedema
histological characteristics of different lung Ca types under light microscopy?
small cell Ca-oat cells, small nuclei, nuclear moulding, apoptotic bodies, often necrosis and lots of abnormla mitoses, very cellular.
squamous cell-keratin pearls, central tumours, intercellular bridges-prickles, eosinophilic cytoplasm
adenocarcinoma-peripheral, columnar/cuboidal cells, form glands, some produce mucin.
large cell-poorly differentiated
COPD risk factors?
smoking
environmental pollutant exposure
coal mining
smoke from cooking fires in developing countries
alpha 1 antitrypsin deficiency-onset in patient under age of 40, largely emphysema in lung bases.
most common clinical sign of a PE?
increased RR other signs: sinus tachycardia crackles fever
