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Define vital capacity

Volume of air expired from the lungs from a maximal inspiration using a slow/relaxed manoeuvre


Define forced vital capacity

Volume of air that can be forcible expelled from the lungs from a position of maximal inspiration


Define forced expiratory volume

volume of air forcibly expelled from the lungs in the first second - following maximal inspiration


Pathophysiology of anaphylaxis

Sensitised individual exposed to specific antigen
Immunological response:
– IgE → antigen → mast cell & basophils ‡ → histamine ↑ → body response


Features of anaphylaxis

Uritus, urticaria & angioedema, hoarseness, progressing to stridor & bronchial obstruction, wheeze & chest tightness from bronchospasm


Management of anaphylaxis

• Remove trigger, maintain airway, 100% O2
• IM adrenaline 0.5 mg
(Repeat every 5 mins as needed to support CVS)
• IV hydrocortisone 200mg
• IV chlorpheniramine 10 mg
• If hypotensive: lie flat and fluid resuscitate
• Treat bronchospasm: NEB salbutamol
• Laryngeal oedema: NEB adrenaline

monitor for secondary deterioration; advice about epipens and wearing medic alert braclet
arrange f/u in clinic


Severity of asthma exacerbations

• No features of severe asthma
• PEFR >75%
• No features of severe asthma
• PEFR 50-75%
Severe (if any one of the following):
• PEFR 33 – 50% of best or predicted
• Cannot complete sentences in 1 breath (or unable to feed/talk in children)
• Respiratory Rate > 25/min (2y/o - >40; >5; >30)
• Heart Rate >110/min (2y/o - >140; >5; >125)
Life threatening (if any one of the following):
• PEFR < 33% of best or predicted
• Sats <92% or ABG pO2 < 8kPa
• Cyanosis, poor respiratory effort, near or fully silent
• Exhaustion, confusion, hypotension or arrhythmias
• Normal pCO2
Near Fatal:
• Raised pCO2


Acute asthma attack management

Oxygen - aim 94-98%
Salbutamol 5mg NEB (repeat after 15 min) - 2.5-5 if <11y/o
Hydrocortisone 100mg IV (or prednisolone 40mg PO)
(>2 = 20mg)
Ipratropium bromide 500mcg (250mcg in children) NEB
Theophyilline (IV amionophylline)
Magnesium sulphate
Escalate care - ITU

Consider IV salbutamol
Life threatening - portable CXR


Features of an infective COPD exacerbation

Change in sputum volume / colour
Raised WCC +/- CRP


Management of COPD exacerbation

Oxygen - 24-28% fixed performance face mask. AIm sats 88-92%
Antibiotics (if infective)
Salbutamol NEB
Ipratropium NEB
Steroids - prednisolone 30mg STAT and 7d

Consider IV aminophyline
Consider NIV if pH <7.35
ITU if pH <7.25


CURB -65

C Confusion, MMT 2 or more points worse
U Urea > 7.0
R >30/min
B < 90 mm Hg systolic or < 60 mm Hg diastolic 65 Age above 65 years


Treatment of pneumonia

If any features of sepsis – immediately treat using sepsis pathway – NO DELAY in initiating IV antibiotics and fluids
-ABx as per CURB-65 score, local pneumonia guidelines and awareness of any patient drug allergies
- analgiea; PT

CURB SCORE - amoxicillin <1 - home rx; 2 - hospital
- Co-Amoxiclav IV 1.2g tds and Doxycycline PO --> rx; 3 - itu or HAP


Features of pneumonia

Consolidation on CXR with fever +/- purulent sputum +/ raised WCC and / or CRP

- May have malaise; dyspnoea; cough; pleuritic pain

Signs - tachypnoea; tachycardia; cyanosis; confusion; consolidation\( reduced expansion; dull percussion; bronchial breathing; reduced air entry; crackles; pleural rub)


Classification of massive haemoptysis

>240mls in 24 hours OR >100mls / day over consecutive days


Management of massive haemoptysis

• Lie patient on side of suspected lesion (if known) • Oral Tranexamic Acid for 5 days or IV
• Stop NSAID’s / aspirin / anticoagulants
• Antibiotics if any evidence of respiratory tract
• Consider Vitamin K
• CT aortogram – interventional radiologist may be able to undertake bronchial artery embolisation


Features of pneumothorax +/- tension

- sudden onset dyspnoea, pleuritic chest pain which reduced chest expansion and breath sounds and resonant percussion
o hypotension
o tachycardia
o deviation of the trachea away from the side of
the pneumothorax
o Mediastinal shift away from pneumothorax


Management of tension pneumothorax

- ABCDE (no CXR)
- Large bore intravenous cannula into 2nd ICS MCL
- Chest drain into the affected side (0.9% saline-water seal)


Symptoms and signs of PE

– Chest pain (pleuritic)
– Syncope
– Haemoptysis
– Massive --> RHF - hypotension, raised JVP, loud P2, +/- cardiac arrest

- fever, cyanosis, tachycardia, tachypnoea, evidence of DVT


Risk factors for PE

Thrombopillia/ antiphospholipid syndrome
Recent travel
Obstetric - pregnancy/ OCP
Break lower limb/ varicose veins
Old age
Surgery / smoking
Sex (F)


Management of PE

A - sit up and 100% oxygen
B - CXR (exclude pleural effusion/ consolidation)
C - ECG, bloods (Trop, FBC, U+E, Clotting, D-Dimer), ABG
D -
E -

• Fluid resuscitation (if hypotensive), analgesia +/- anti-emetic
• Thrombolysis should be considered if a massive PE
is confirmed on Echo or CT scan ( IV Alteplase) --> senior!
• LMWH and Ted Stockings

Wells score
<4 --> if D-dimer -ve - exclude; if +ve --> CTPA
>4 --> CTPA
Ongoing - Graduated compression stockings for 2 years if sign of DVT; Start warfarin -3m if known cause; 6m if unknown

ECG --> T wave inversion, AF, RBBB, RAD --> ?S1Q3T3


Absolute thrombolysis contraindications

Haemorrhagic stroke or Ischaemic stroke < 6 months
CNS neoplasia
Recent trauma or surgery
GI bleed < 1 month
Bleeding disorder
Aortic Dissection


Relative thrombolysis contraindications

Advanced Liver Disease
Infective Endocarditis


Complications of thrombolysis

• Bleeding
• Hypotension
• Intracranial haemorrhage / stroke
• Reperfusion arrhythmias
• Systemic embolisation of thrombus
• Allergic reaction


Pathophysiology of asthma

Airway epithelial damage – shedding and subepithelial fibrosis, basement membrane thickening
• An inflammatory reaction characterised by eosinophils, T-lymphocytes (Th2) and mast cells. Inflammatory mediators released include histamine, leukotrienes, and prostaglandins
• Cytokines amplify inflammatory response
• Increased numbers of mucus secreting goblet cells
and smooth muscle hyperplasia and hypertrophy
• Mucus plugging in fatal and severe asthma


define asthma and features

• Asthma is a chronic inflammatory disease of the airways
• Airway obstruction that is reversible (but not completely so in some subjects), either spontaneously or with treatment
• Increased airway responsiveness (bronchoconstriction) to a variety of stimuli

sx- cough, wheeze (high pitched polyphonic), dyspnoea, diurnal variation, chest tightener
signs - increased RR and HR, widespread polyphonic wheeze, hyperinflated chetst, ? reduced air entery, tracheal tug/recession, nasal flaring/ accessory muscle use


Differentials of a wheeze

> Acute Asthma Exacerbation
• Bronchitis – viral or bacterial
Other causes of wheeze less likely:
• Pulmonary oedema
• PE
• Vocal cord dysfunction
• Gastro-oesophageal reflux
• Foreign body
• Allergy
• Hyperventilation / psychosocial
• Cardiac disease
• Vasculitides – Churg-Strauss syndrome, polyarteritis nodosa, Granulomatosis with Polyangiitis (Wegener’s granulomatosis)
• Carcinoid syndrome with hepatic metastases – release of HIAA


Criteria for safe asthma discharge after exacerbation

• PEFR >75%
• Stop regular nebulisers for 24 hours prior to discharge
• Inpatient asthma nurse review to reassess inhaler
technique and adherence
• Provide PEFR meter and written asthma action plan
• At least 5 days oral prednisolone
• GP follow up within 2 working days
• Respiratory Clinic follow up within 4 weeks
• For severe or worse, consider psychosocial factors


Differentials of eosinophilia

• Airways inflammation (asthma or COPD)
• Hayfever / allergies
• Allergic Bronchopulmonary Aspergillosis
• Drugs
• Churg-Strauss / vasculitis
• Eosinophilic Pneumonia
• Parasites
• Lymphoma
• Hypereosinophilic syndrome


Asthma trigger factors

• Smoking
• Upper respiratory tract infections – mainly viral
• Allergens – pollen, house dust mite, pets
• Exercise – also cold air
• Occupational irritants
• Pollution
• Drugs – aspirin, beta blockers (including eye drops)
• Food and drink – dairy produce, alcohol, orange
• Stress
• Severe asthma – consider inhaled heroin, pre-menstrual, psychosocial aspects


NICE definition of COPD

COPD is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.


Pathophysiology of COPD

COPD is an umbrella term which encompasses emphysema and chronic bronchitis:
• Mucous gland hyperplasia
• Loss of cilial function
• Emphysema – alveolar wall destruction causing
irreversible enlargement of air spaces distal to the
terminal bronchiole
• Chronic inflammation (macrophages and
neutrophils) and fibrosis of small airways


Causes of COPD

> Smoking
• Inherited α-1-antitrypsin deficiency
• Industrial exposure, e.g. soot


Members involved in MDT management of COPD

• Physicians
• G.P.’s
• Specialist nurses
• Physiotherapists
• Pharmacists
• Occupational therapists
• Dieticians


Outpatient COPD management

• ‘COPD Care Bundle’
• Pulmonary Rehabilitation
• Bronchodilators
• Antimuscarinics
• Steroids
• Mucolytics
• Diet
• LTOT if appropriate
• LUNG VOLUME REDUCTION if appropriate


Criteria for long term oxygen therapy in COPD

> pO2 consistently below 7.3 kPa, or below 8 kPa with cor pulmonale
• Patients must be non-smokers and not retain high levels of CO2


Reason for pulmonary rehabilitation in COPD

Many COPD patients with COPD avoid exercise and physical activity because of breathlessness
• This may lead to a vicious cycle of increasing social isolation and inactivity leading to worsening of symptoms
• Pulmonary Rehabilitation aims to break this cycle – an MDT 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease education


CXR consolidation differentials

TB (usually upper lobe)
Lung cancer
Lobar collapse (blockage of bronchi)


Investigations for pneumonia

Sputum culture - MC+S
Blood culture (if febrile)
Serology and urine legionella test (if high CURB65)


Pneumonia follow up

• HIV test
• Immunoglobulins
• Pneumococcal IgG serotypes
• Haemophilus influenzae b IgG
F/u in clinic in 6 weeks with a repeat CXR to
ensure resolution


Causes of non-resolving pneumonia and other complications

• Complication – empyema, lung abscess
• Host – immunocompromised
• Antibiotic – inadequate dose, poor oral absorption
• Organism – resistant or unexpected organism not
covered by empirical antibiotics
• Second diagnosis – PE, cancer, organising

Complications - respiratory failure; hypotension; AF; pleural effusion (exudate); sepsis; pericarditis; jaundice (sepsis/drugs)


Clinical features of TB

- fever
- nocturnal sweats
- Weight loss (weeks – months)
- Malaise
- Respiratory TB: cough ± purulent sputum/ haemoptysis, (+/-pleural effusion)
Non-Respiratory TB: Skin (erythema nodosum); Lymphadenopathy; Bone/joint; Abdominal; CNS (meningitis); Genitourinary; Miliary (disseminated); Cardiac (pericardial effusion)


Differentials of Haemoptysis

• Pneumonia
• Tuberculosis
• Bronchiectasis / CF
• Cavitating lung lesion (often fungal)
• Lung cancer
• Metastases
• Bronchial artery erosion
• Vasculitis
• Coagulopathy
• PE


Risk factors for TB

Past history of TB
Known history of TB contact
Born in a country with high TB incidence
Foreign travel to country with high incidence of TB
Evidence of immunosuppression–e.g. IVDU, HIV, solid organ transplant recipients, renal failure/ dialysis, malnutrition/ low BMI, DM, alcoholism


Management for respiratory TB

Admit to side room and start infection control
3 x early morning sputum samples (AAFB and TB culture)
FBC,LFT, UE, vit D levles
HIV test
CT chest if CXR not clear
MRI/Spine if milary
Abx for pneumonia if diagnosis not clear
If highly likley TB - start anti-TB therapy (after cultures)
Notify TB nurse specialist (initiate contact tracing - Mantoux test to those at risk; IFN gamma if had bcg); notify public health etc)
TB culture can take 6-8 weeks


Anti-TB therapy

4 antibiotics for 2 months
(Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) followed by 4 months on two antibiotics (Rifampicin, Isoniazid)
+ Pyridoxine as prophylaxis against peripheral neuropathy

-Dose is weight dependent
- check baseline LFT’s and monitor closely
- Check visual acuity

Compliance is crucial and Directly Observed Therapy (DOT) sometimes used for patients
Provide leaflets on treatment & ensure patient is aware of common and serious SE
Corticosteroids sometimes used, mainly seen in those with TB meningitis


Side effects of TB treatment

Rifampicin – Hepatitis, rashes, febrile reaction, orange/red secretions (N.B. contact lenses), many drug interactions including warfarin and OCP

Isoniazid – Hepatitis, rashes, peripheral neuropathy, psychosis

Pyrazinamide – Hepatitis, rashes, vomiting, arthralgia

Ethambutol – Retrobulbar neuritis


Definition of bronchiectasis

Chronic dilatation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection


Ix for bronchiectasis

- High Resolution CT (diagnositic) - dilated and thickened airways

- sputum culture; bloods; CXR? (tramlines and rings); spirometry (obstructive); ?bronchoscopy; ?CF sweat teast


Causes of bronchiectasis

• Post infective – whooping cough, TB, measles, bronchiolitis
• Immune deficiency – Hypogammaglobulinaemia
• Genetic / Mucociliary clearance defects – Cystic
fibrosis, primary ciliary dyskinesia, Young’s syndrome (triad of bronchiectasis, sinusitis, and reduced fertility), Kartagener syndrome (triad of bronchiectasis, sinusitits, and situs inversus)
• Obstruction – foreign body, tumour, extrinsic LN, Ca
• Toxic insult – gastric aspiration (particularly post lung transplant), inhalation of toxic chemicals/gases
• Allergic bronchopulmonary aspergillosis
• Secondary immune deficiency – HIV, malignancy
• Rheumatoid arthritis
• Associations – inflammatory bowel disease; yellow
nail syndrome


Common organisms that cause bronchiectasis

• Haemophilus influenzae
• Pseudomonas aeruginosa
• Moraxella catarrhalis
• Stenotrophomonas maltophilia
• Fungi – aspergillus, candida
• Non-tuberculous mycobacteria
• Less common - Staphylococcus aureus (think about


Management of bronchiectasis

• Treat underlying cause (CF - DNAase; ABPA - steroids; immune def - IVIg)
• PT – mucus clearance/ expectoration; drainage
• Abx according to sputum cultures /
sensitivities for acute exacerbations and often
chronic suppressive therapy
• Supportive – flu vaccine, bronchodilators if required
• Pulmonary Rehab – MRC Dyspnoea Score >3


Definition of CF

CF is an autosomal recessive disease leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). This can lead to a multisystem disease (most commonly affecting the respiratory and GI systems) characterised by thickened secretions - impairs mucociliary clearance.


Diagnostic criteria for CF

One or more of the characteristic phenotypic features -
• Or a history of CF in a sibling
• Or a positive newborn screening test result (increased immunoreactive trypsinogen)
• An increased sweat chloride concentration
(> 60 mmol/l) – SWEAT TEST
• Or identification of two CF mutations – genotyping
• Or demonstration of abnormal nasal epithelial ion
transport (nasal potential difference)


Presenting features of CF

- failure to thrive; meconium ilies; rectal prolapse

Children/ young adults
-chronic sinusitis
- nasal polyps (infancy/childhood)
- repeated LRTI (throughout life)
- bronchiectasis
- Liver disease; portal hypertension; gallstones
- Steatorrhoea
- Abnormal sweat secretions
- Pancreatic insufficiency (malabsorption/ steatorrhoea and DM)
- Finger clubbing
- Osteoporosis
- Male infertility (as teenager)
- Arthritis

Signs - clubbing; arthritis; cyanosis; bilateral creps

Meconium ileus - bowel is blocked by sticky secretions, Signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium. (+/- jaundice)


Common complications of CF

1.Respiratory Infections
- Needs aggressive therapy with PT and
Abx +/- prophylactic Abx
common organisms - p. aeruginosa (s.aurues in early life)
2.Low Body Weight
- needs careful monitoring
? pancreatic insufficiency--> Creon (pancreatic enzyme replacement therapy)
- high calorie intake and often extra supplements
- may need NG or PEGf eeding
- may need insulin
3.Distal Intestinal Obstruction Syndrome (DIOS)
- DIOS vs.constipation faecal obstruction in ileocaecum versus whole bowel
- Due to intestinal contents in the distal ileum and proximal colon (thick, dehydrated faeces)
-Often insufficient prescription of pancreatic
enzymes or non-compliance, also salt deficiency / hot weather
- Often presents with palpable RIF mass (faecal)
-Diagnosis: Symptoms; palpable RightIliacFossaMass,
AXR demonstrating faecal loading at junction of small
and large bowel
4. CF Related Diabetes


CF lifestyle advice advice

• No smoking
• Avoid other CF patients
• Avoid friends / relatives with colds / infections
• Avoid jacuzzis (pseudomonas)
• Clean and dry nebulisers thoroughly
• Avoid stables, compost or rotting vegetation – risk of
aspergillus fumigatus inhalation
• Annual influenza immunisation
• Sodium chloride tablets in hot weather / vigorous


Types of pneumothorax

i.Primary (no lung disease) ii.Secondary (lung disease) 2.Traumatic (penetrating)
3.TENSION: emergency
4.Iatrogenic (e.g. post central line or pacemaker insertion)


Risk factors for pneumothorax

- Pre-existing lung disease -COPD; pulmonary fibrosis
- Height
- Smoking/ Cannabis
- Diving
- Trauma/ Chest procedure
- Association with other conditions e.g. Marfan’s
syndrome/ Ehler's danlos


Ix and Management for pneumothorax

Ix - ABG and bloods; CXR (translucent, collapse, mediastinal shift +/- depressed hemidiaphragm; surgical emphysema)

Primary – If symptomatic and rim of air >2cm on
CXR give O2 and aspirate. If unsuccessful consider re-aspiration or intercostal drain. Remove drain after full re-expansion / cessation of air leak.

Secondary – if 1-2cm; >50 and SOB --> insert ICD; otherwise as above - admit for 24 hours

If persistent air leak >5 days (bronchopleural
fistula) refer to thoracic surgeons - chemical pleurosis/pleurectomy etc

Traumatic - ABCDE, analgesia, 3 sided wet dressing and ICD

Discharge advice – No flying or diving until


Investigations for pleural effusion

USS guided pleural aspiration
- biochemistry (protein, pH, LDH)
- Cytology
- Microbiology

•Bloods: FBC, U+E’s, LFT’s, CRP, Bone profile, LDH, clotting
•ECHO (if suspect heart failure)
•Staging CT (with contrast) if suspect exudative cause


Indications for urgent chest drain for new pleural effusion

underlying empyema (pH of pleural fluid <7.2 or visible pus on aspirate).


Causes of transudate effusion
- pleural protein <30g/L

" Heart failure
" Cirrhosis
" Hypoalbuminaemia (nephrotic syndrome or
peritoneal dialysis) Less common:
" Hypothyroidism, mitral stenosis, pulmonary embolism
" Constrictive pericarditis, superior vena cava
obstruction, Meig’s syndrome


Causes of Exudate effusions
- pleural protein >30 g/L

" Malignancy
" Infections – parapneumonic, TB, HIV (kaposi’s) Less common:
" Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease
" Yellow nail syndrome, fungal infections, drugs


Lights criteria - and when is it used

If pleural fluid protein level between 25 and 35 g/L (i.e. borderline) use Light’s criteria
– exudate if one or more of the following:
– Pleural fluid/Serum protein >0.5
– Pleural fluid/Serum LDH >0.6
– Pleural fluid LDH > 2/3 of the upper limit of normal


Management of pleural effusion

Often no diagnostic tap is required
• Treat the underlying cause
• If effusion resolves, stop or reduce treatment
• If effusion persists, then therapeutic
aspiration/drainage is required

- treat underlying cause
- if established diagnosis - drain/ ICD


Causes of interstitial lung disease and commonest type of pulmonary fibrosis

- asbestos, silicon, drugs (bleomycin, amiodarone, sulfasalasime, methotrexate), EAA, TB
- Assoc systemic disease - sacoid, RA, SLE, systemic sclerosis, UC, A.S.
- Usual Interstitial Pneumonia


Classical findings in UIP and other sx

Classical Findings:
• clubbing, reduced chest expansion
• Auscultation – fine inspiratory crepitations (like pulling Velcro slowly) – usually best heard basal / axillary areas
• Cardiovascular – may be features of pulmonary hypertension

Other sx -Dry cough, dyspnoea, malaise, wt loss, arthralgia, OSA, cyanosis


Cause and clinical presentation of extrinsic allergic alveolitis

Inhalation of organic Ag to which the individual has been sensitised

–ACUTE – short period from exposure, 4-8 hrs. Usually reversible: spontaneously settle 1-3 days. Can recur.
- Fevers, rigors, malaise, dry cough, dyspnoea, crackles

–CHRONIC – chronic exposure (months – years). Less reversible
- Increasing dyspnoea, weight loss, t1 resp failure, cor pulmonale


Define and presentation sarcoidosis

Multisystem inflammatory condition of unknown cause
• Non-caseating granulomas

Presentation - GRANULOMAS
- General - fever, reduced wt, fatigue, lyphadenopathy and HSM
- Resp - otitis/sinusitis; dry cough, SOB, Chest pain
- Arthraligia
- Neuro - peripheral and cranial polyneuropathy, headache
- Urine - hypercalciuria (stones, DI)
- Low hormones (amenorrhoea)
- Opthamology - uveitis, keratoconjunciticis, sjogrens
- Myocaridal - restrictive cardiomyopathy, effusion
- abdo - HSM
- Skin - erythema nodosum, lupus pernio


Investigations and management of sarcoidosis

• PFTs: (obstructive until) fibrosis
• CXR: 4 stages (BHL --> mid zone fibrosis)
• Bloods: renal function, ACE (increased) , Calcium
• Urinary Calcium
• Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid

- acute - bed rest and NSAIDS
- chronic - steroids +/- methotrexate/ ciclosporin
- stop smoking
- remove occupational exposure


Treatment for Interstitial lung disease

• Occupational exposure – remove
• Drug associated – avoid
• Stop smoking
• ? N-Acetylcysteine ? Immunosuppressant ? Pirfenidone
• Transplantation
• Treatment of infections (atypical)
• Oxygen
• Palliative care
? pul rehab


Clinical features of lung cancer

Asymptomatic, incidental finding
• Any respiratory symptom/systemic deterioration
- Chronic cough +/- haemoptysis (or chnage in smokers cough); chest pain; recurrent chest infection; hoarse voice; stridor; malaise; weight loss; SOB
• Horner’s syndrome
• Metastatic disease – liver, adrenals (Addison’s),
bone, pleural, CNS
• Paraneoplastic – clubbing, hypercalcaemia,
anaemia, SIADH, Cushing’s syndrome, Lambert- Eaton myasthenic syndrome, thrombo-embolic disease


Risk factors for lung cancer

• Large number of smoking pack years
• Airflow obstruction
• Increasing age
• Family history of lung cancer
• Exposure to other carcinogens, e.g. asbestos


WHO performance status

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 work, office work

2 Ambulatory and capable of all self-care but
unable to carry out any work activities. Up and
about more than 50% of waking hours

3 Capable of only limited self-care, confined to
bed or chair more than 50% of waking hours

4 Completely disabled. Cannot self-care. Totally
confined to bed or chair

5 Dead


Investigations of lung cancer

Bloods – FBC, U+E, Calcium, LFT’s, INR
•CXR (? hilar enlargement; consolidation; collapse; effusion; bony secondaries)
• Staging CT – Spiral CT Thorax and Upper Abdo –
helps to stratify TNM stage
•PET (detect small mets)

• US guided neck node FNA for cytology if
• Bronchoscopy – endobronchial, transbronchial,
endobronchial USS (if mediastinal
lymphadenopathy) + biopsy
• CT Biopsy
• Thoracoscopy if pleural effusion present

Lung function test and WHO performance status


Treatment for NCSLC

• Curative surgery for stages I+II – assuming fit for surgery
• Surgery + adjuvant chemotherapy clinical trial for stage IIIa – assuming fit for surgery + chemo
• Chemotherapy – consider in patients with stage III/IV disease and PS 0-2
• Radiotherapy – curative (CHART = continuous hyperfractionated accelerated radiotherapy) for people not fit for surgery OR palliative
• Palliative Care (SVCO stent; analgesia; pleural drainage etc)
• Do nothing / watch & wait


Prognosis for SCLC

Rapid growth rate and almost always too extensive for surgery at time of diagnosis
• Mainstay of treatment is chemotherapy
• Also palliative radiotherapy (for bronchial obstruction, haemoptysis, bone or CNS mets)
• Untreated – median survival is 4-12 weeks
• Combination chemotherapy – median survival 6- 15 months


Define Obstructive Sleep Apnoea

upper airway narrowing,
provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness


Pathophysiology of OSA

- Upper airway patency depends on dilator muscle activity. All muscles relax during sleep (including pharyngeal dilators).
- Some narrowing of the upper airway is normal
- Excessive narrowing can be due to either an
already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occurring with relaxation during sleep


Risk factors for OSA

- Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
- Large tonsils
- Craniofacial abnormalities
- Extra submucosal tissue, e.g. myxoedema
- NMD - greater loss of dilator muscle tone, e.g. stroke, MND, myotonic dystrophy
- Muscle relaxants – sedatives, alcohol
- Increasing age


Clinical effects for OSA

- repetitive upper airway collapse, with arousal required to re-activate the pharyngeal dilators.
- associated hypoxia and hypercapnia -->corrected during the inter-apnoeic hyperventilatory period.
- Recurrent arousals lead to highly fragmented and unrefreshing sleep – snoring and apnoea attacks often witnessed by partner
- Excessive daytime sleepiness results (Epworth Sleepiness Scale score >9)
- With every arousal there is a rise in BP, often over 50 mmHg. It is not clear if this damages the CVS. There is also a rise in daytime BP.
- Nocturia
- Less common - Nocturnal sweating, reduced
libido, oesophageal reflux


Epworth sleepiness scale

Points for following:
0=would never doze,
1=slight chance,
2=moderate chance,
3=high chance

-Sitting and reading
- Watching TV
- Sitting in a public place, e.g. theatre
- Passenger in a car for an hour
- Lying down to rest in the afternoon
- Sitting and talking
- Sitting quietly after lunch without alcohol
- In a car, while stopped in traffic


Diagnosis of OSA

- Overnight oximetry alone
- Limited sleep study – oximetry, snoring, body
movement, heart rate, oronasal flow, chest/abdominal movements, leg movements – usual study of choice
- Full polysomnography – limited study plus EEG, EMG


Management of OSA

Given based on symptoms/quality of life – NOT on severity seen on sleep study

- Weight loss
- sleep decubitus rather than supine
- avoid/reduce evening alcohol intake

- Mandibular advancement devices, consider
pharyngeal surgery as last resort
- Nasal CPAP (upper airway splinted open with 10cm H20 This prevents airways collapse, sleep fragmentation, and ultimately daytime somnelence)
- consider gastroplasty/bypass, and rarely tracheostomy
- May require a period of NIV prior to CPAP if
acidotic, but compensated CO2 may reverse with CPAP alone


Driving advice for OSA

- Tell all patients with OSA to NOT drive while sleepy; stop and have a nap. On diagnosis the patient should notify the DVLA
- The doctor can advise drivers to stop altogether (e.g. HGV drivers)


Action of salbutamol, salmeterol

ß2-selective adrenergic agonists
Increase cAMP in SMC’s resulting in relaxation and thus bronchodilation


SE of salbutamol, salmeterol

Tremor, headache, GI upset, palpitations, tachycardia, hypokalaemia


Action of Ipratropium/ Tiotropium

Muscarinic antagonist Decreases cGMP which affects intracellular calcium resulting in decreased SMC contractility


SE Ipratropium/ Tiotropium

Dry mouth, constipation, cough, headache


CI of Ipratropium/ Tiotropium

angle- closure glaucoma +Benign Prostatic Hypertrophy


Action of aminophylline

Block phosphodiesterases resulting in decreased cAMP breakdown causing bronchodilation

Positive chronotropic and inotropic effects, diuretic action


SE and toxic effects aminophylline

Headache, GI upset, reflux, palpitations, dizziness
TOXIC - serious arrhythmias, seizures, N+V, hypotension


Action of inhaled steroids e.g. beclomethasone

Increase airway calibre by decreasing bronchial inflammation +/- modifying allergic reactions


SE of inhaled steroids e.g. beclomethasone

Cough, oral thrush, unpleasant taste, hoarseness


Advice after use inhaled steroids

good oral hygiene


Examples of corticosteroids

Prednisolone (PO), Hydrocortisone (IV/IM), Dexamethasone (PO/IV), Triamcinolone (IM)


Actions of corticosteoids

Supress inflammation, allergy + immune responses by altering gene transcription


SE of corticosteroids

Adrenal suppression (especially courses > 3 weeks), hyperglycaemia, psychosis, insomnia, indigestion, mood swings

Other Side Effects

Diabetes, cataracts, glaucoma, peptic ulceration, susceptibility to infections, osteoporosis, muscle wasting, skin thinning, Cushingoid appearance


Additional medication to prescribe with long-term steroids and patient information

May need PPI (reduce GORD), Bisphosphonates (bone protection) and steroid card.


MRC Dyspnoea Score

1 Not troubled by breathlessness except on strenuous exercise
2 Short of breath when hurrying or walking up a slight hill
3 Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace
4 Stops for breath after walking about 100m or after a few minutes on level ground
5 Too breathless to leave the house, or breathless when dressing or undressing


Management of chronic asthma - BTS guidelines

Assess symptoms, measure lung function, check inhaler technique and adherence, adjust dose, update self-management plan. Use spacer in children.
Short acting β2 agonists as required – consider moving up if using three doses a week or more

1) Low-dose ICS (V. low in kids) - <5y/o - LTRA
2) + inhaled LABA (<5 y/o - LTRA +v. low ICS)
3) - No response to LABA – stop LABA and consider
increased dose of ICS
- If benefit from LABA but control still inadequate- continue LABA and increase ICS to med dose (low in kids)
- If benefit from LABA but control still inadequate
- continue LABA and ICS and consider trial of other therapy - LTRA (adults - also SR theophylline, LAMA)
4) Increasing ICS up to high dose (med - kids)
- Addition of a fourth drug, eg SR theophylline (or LTRA, beta agonist tablet, LAMA in adults)
- Refer to specialist care
5) Use daily steroid tablet and Maintain high-dose ICS (med - kids)

Advice - avoid triggers and personal asthma action plan for emergencies


Management of chronic COPD - stable management

- smoking cessation advice
- annual influenza vaccination
- one-off pneumococcal vaccination
FEV1 --> Mild = >80%; mod 50-79%; severe <50%

2) FEV1 > 50% - LABA or LAMA e.g. tiotropium
- FEV1 < 50% - LABA + ICS or: LAMA
3) Then LABA +ICS
- + LAMA

- Mucolytics = productive cough


Management of pulmonary oedema

 Sit up and give high-flow O2
 Morphine 2.5mg IV (± metoclopramide 10mg IV)
 Frusemide 120-250mg IV over 1h
 GTN spray ± ISMN IVI (unless SBP <90)
 If no response consider:
 Haemofiltration / haemodialysis ± venesection


Causes of clubbing

L - lung - Abscess; Bronchiectasis; CF; Disease (IL) Empyema/ TB
U - UC/ CD
B - baby coming - pregnancy
B - Biliary cirrhosis
I - IE; idiopathic; familial
N - Neoplasm - Bronchial/ mesothelioma
G - GI lymphoma/graves


Stages of clubbing

1) fluctuant nail bed
2) loss of nail angle
3) curvature of nail
4) broadening of distal phalnx


Organisms causing pneumonia

o Streptococcus pneumoniae
o Haemophilus influenza
o Moraxella cattarrhalis

o Gram –‘ve enteric bacteria - 10%
o Staphylococcus aureus

- Above +
- PCP; TB; fungi; CMV/HSV


Causes, features, ix and mx of lung abscess

- Aspiration
- bronchial obstruction (ca/FB)
- septic emboli
- pulmonary infarction
- hepatic disease

- swinging fever
- cough, foul purulent sputum, haemoptysis
- malaise, wt loss
- pleuritic pain
- clubbing
- empyema

Ix - bloods; sputum; CXR; ?CT/bronchoscopy

Mx - Abx, aspiration/ surgical excision


Features of Bronchiectasis

- persistent cough and purulent sputum
- haemoptysis
- fever, wt loss
- clubbing
- coarse inspiratory crackles
- wheeze
- ?situs inversus (kartageners)/ splenomegaly (immune def)


Complications of bronchiectasis

- pneumonia
- pleural effusion
- pneumothorax
- pulmonary HTN
- massive haemoptysis
- Cerebral abscess
- Amyloidosis


Allergic Bronchopulmonary Aspergillosis
- features, ix and rx

hypersensitivity to aspergillus
sx - wheeze; productive cough; dyspnoea +/- recurrent pneumonia
Ix - CXR (bronchiectasis); aspergillus in sputum; high IgE/Eosinophils
Rx - steroids +/- bronchodilators


Features of COPD

Sx - cough + sputum; SOB; wheeze; wt loss
signs - increased RR, prolonged expiratory phase, hyperinflation and hyperesonant (air trapping), wheeze, ?early inspir crackles, cyanosis, cor pulmonale, signs of steroid use, accessory muscles


COPD complications

- acute exacerbation
- pneumothorax
- cor pulmonale
- polycythaemia
- lung ca


Ix for COPD

- spirometry (obstructive pattern)
- CXR - hyperinflation, flat hemi-diaphragm, decreased lung markings, bulla, prominent hila


Sx and signs of pleural effusion

- asymptomatic; dyspnoea; pleuritic chest pain

- tracheal deviation away; reduced expansion; stony dull percussion; reduced air entry; bronchial breathing just above effusion
- Of associated disease e.g. Ca, CLD, Cardiac failure


Causes of cavity in lungs

C: cancer --> SCC/ mets
A: AI; granulomas - granulomatosis with polyangiitis, RA
V: vascular (both bland and septic pulmonary emboli)
I: infection (bacterial/fungal); abscess; TB
T: trauma - pneumatoceles
Y: youth --> CPAM (congenital pulmonary airway malformation); pulmonary sequestration; bronchogenic cyst


Cause of ILD on location

Upper zone
- Aspergillus, coal, silica, EAA, TB, A.S, radiation

Lower zone
- Sarcoid(mid), toxins, asbestos, UIP, rheum


Features and Ix for pulmonary fibrosis

- SOB (progressive); dry cough; clubbing, sx of disease e.g. RA/SLE
Signs - dyspnoea, reduced expansion and fine end-inspiratory crepitations

- High-resolution CT (honeycombing and ground glass changes)
- Spirometry (restrictive +/- reduced transfer factor)
- blood tests for cause
- lung biopsy
- ?BAL


Ix and Mx of EAA

- bloods (neutrophiia, raised inflam markers)
- CXR - honeycomb lung
- spirometry (restrictive)
- BAL - increased lymphocytes and mast cells

- steroids
- avoid exposure