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
