Respiratory Medicine Flashcards

(82 cards)

1
Q

What is Anaphylaxis?

A

SERIOUS allergic reaction
• Sensitised individual exposed to specific antigen

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2
Q

Causes of anaphylaxis and angio-oedema

A

insects bites/ stings, food, medications

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3
Q

Immunology of anaphylaxis

A

IgE → antigen → mast cell & basophils ‡ → histamine ↑ → body response

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4
Q

Anaphylaxis symptoms?

A

Pruritus, urticaria & angioedema

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5
Q

Anaphylaxis treatment

A

• Remove trigger, maintain airway, 100% O2
• Intramuscular 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

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6
Q

Asthma Severity?

A

Mild:
• No features of severe asthma
• PEFR >75%
Moderate:
• 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
• Respiratory Rate > 25/min
• Heart Rate >110/min
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
chest
• Exhaustion, confusion, hypotension or arrhythmias
• Normal pCO2
Near Fatal:
• Raised pCO2

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7
Q

Acute Asthma management

A

ABCDE

Aim for SpO2 94-98% with oxygen as needed, ABG if
sats <92%

5mg nebulised Salbutamol (can repeat after 15 mins)

40mg oral Prednisolone STAT (IV Hydrocortisone if
PO not possible)

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8
Q

Severe asthma treatment

A

Nebulised Ipratropium Bromide 500 micrograms
 Consider back to back Salbutamol

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9
Q

Life threatening or near fatal asthma

A

 Urgent ITU or anaesthetist assessment
 Urgent portable CXR
 IV Aminophylline
 Consider IV Salbutamol if nebulised route ineffective

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10
Q

What is Asthma?

A

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 (airway narrowing) to a variety of stimuli

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11
Q

Asthma pathophysiology

A

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

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12
Q

Asthma safe discharge criteria

A

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

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13
Q

Asthma Triggers

A

• 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
juice
• Stress
• Severe asthma – consider inhaled heroin, pre-menstrual, psychosocial aspects

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14
Q

Eosinophilia causes

A

Some patients with asthma have eosinophilic inflammation which typically responds to steroids. However, there are several differentials of eosinophilia:
• Airways inflammation (asthma or COPD)
• Hayfever / allergies
• Allergic Bronchopulmonary Aspergillosis
• Multiple courses of antibiotics for chronic infections
• Eosinophilic Granulomatosis with Polyangiiitis
• Eosinophilic Pneumonia
• Parasites e.g. Hookworm
• Lymphoma
• SLE
• Hypereosinophilic syndrome

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15
Q

What is COPD

A

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.

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16
Q

COPD Pathophysiology

A

COPD is an umbrella term which encompasses emphysema and chronic bronchitis.

Mucous gland hyperplasia
Loss of cilia function
Emphysema - alveolar wall destruction causing irreversible enlargement of air spaces distal to the terminal bronchiole.
Chronic inflammation and fibrosis of small airways.

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17
Q

COPD causes

A

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

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18
Q

Outpatient COPD management

A

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

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19
Q

COPD Long term oxygen therapy

A

Extended periods of hypoxia cause renal and cardiac damage – can be prevented by LTOT
• LTOT to be used at least 16 hours/day for a survival benefit
• LTOT offered if 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
• O2 needs should be balanced with loss of independence and reduced activity which may occur • Note: oxygen is not a treatment for breathlessness; it is a treatment to help prevent organ hypoxia.

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20
Q

Pulmonary rehabilitation

A

MDT 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease education

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21
Q

COPD exacerbation treatment

A

ABCDE approach

Oxygen:
- aim for target SaO2 94-98% but if any evidence of acute (raised pCO2 on ABG) or previous Type 2 Respiratory Failure, then target SaO2 88-92%
• NEBs – Salbutamol and Ipratropium
• Steroids – Prednisolone 30mg STAT and OD for 7
days
• Antibiotics if raised CRP / WCC or purulent sputum
• CXR
• Consider IV aminophylline
• Consider NIV if Type 2 respiratory failure and pH
7.25-7.35
• If pH <7.25 consider ITU referral

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22
Q

Community acquired pneumonia - typical causative organisms

A

streptococcus pneumonia; haemophilus influenza, moraxella catarrhalis

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23
Q

Community acquired pneumonia atypical organisms

A

legionella pneumphila, chlamydia pneumoniae, mycoplasma pneumoniae

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24
Q

Hospital acquired pneumonia causative organisms

A

organisms include e. coli, MRSA, pseudomonas

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25
Pneumonia management
Use CURB-65 score to direct antibiotic treatment in accordance with local trust guidance.
26
Pneumonia investigations
CXR FBC, U&E, CRP, Sputum Blood cultures if febrile High CURB-65 score; initiate atypical pneumonia screen,
27
Legionnaire’s disease
form of pneumonia, usually caused by Legionella pneumophila. Association with infected water in showers or hot tubs – ask your patient if there is a history of recent travel or stay in a hotel? Associated with higher CURB-65 scores.
28
Pneumonia follow up
• HIV test • Immunoglobulins • Pneumococcal IgG serotypes • Haemophilus influenzae b IgG • Follow up in clinic in 6 weeks with a repeat CXR to ensure resolution
29
Non-resolving pneumonia causes
CHAOS • 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 pneumonia
30
Haemoptysis differentials
Infection: • Pneumonia • Tuberculosis • Bronchiectasis / CF • Cavitating lung lesion (often fungal) Malignancy: • Lung cancer • Metastases Haemorrhage: • Bronchial artery erosion • Vasculitis • Coagulopathy Others: • PE
31
TB clinical features
Often fever and nocturnal sweats (typically drenching) Weight loss (weeks – months) Malaise Respiratory TB: cough ± purulent sputum/ haemoptysis, may also present with pleural effusion Non-Respiratory TB: Skin (erythema nodosum); Lymphadenopathy; Bone/joint; Abdominal; CNS (meningitis); Genitourinary; Miliary (disseminated); Cardiac (pericardial effusion)
32
TB risk factors
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
33
Management of TB part 1
ABCDE approach & aim to culture whenever possible • Admit to a side room& start infection control measures (e.g. masks & negative pressure room) • If productive cough: x3 sputum samples for AAFB (acid-alcohol fast bacilli – acid-fast stain also called Ziehl-Neelsen stain) &TB culture • (If no productive cough & pulmonary TB suspected consider bronchoscopy) • Routine bloods (especially LFTs) & include HIV test and vitamin D level
34
Management of TB part 2
Consider CT chest if pulmonary TB suspected but clinical features/ CXR not typical • If diagnosis between pneumonia and TB not clear: start antibiotics for pneumonia (as per CURB-65) whilst investigating possibility of TB. • If patient critically unwell and high likelihood of TB (no time to wait for sputum results) then start anti-TB therapy AFTER sputum samples sent. • Notify case to TB nurse specialists (support patient in investigation, during treatment, public health issues and initiate contact tracing) • TB culture can take 6-8 weeks. So, treatment is often started before a culture confirmed diagnosis can be made. A novel PCR test (Gene Xpert) is available in some centres which can give immediate information regarding drug sensitivities or resistance.
35
Anti TB therapy
Standard regimen is with 4 antibiotics for the first two months (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) followed by 4 months on two antibiotics (Rifampicin, Isoniazid) Treatment for a minimum of 6 months in total (can vary – see NICE/ BTS guidelines) Patient’s weight is important: dose of anti-TB antibiotics is weight dependent Check baseline LFT’s and monitor closely Check visual acuity before giving Ethambutol Compliance is crucial and Directly Observed Therapy (DOT) sometimes used for patients Provide leaflets on treatment & ensure patient is aware of common and serious side effects (see below) Pyridoxine also given (while on Isoniazid) as prophylaxis against peripheral neuropathy If CNS TB suspected MRI Brain is the test of choice, (more likely to identify tubercles than CT)
36
TB treatment side effects
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 Management Principles for Respiratory TB • ABCDE approach & aim to culture whenever possible • Admit to a side room& start infection control measures (e.g. masks & negative pressure room) • If productive cough: x3 sputum samples for AAFB (acid-alcohol fast bacilli – acid-fast stain also called Ziehl-Neelsen stain) &TB culture • (If no productive cough & pulmonary TB suspected consider bronchoscopy) • Routine bloods (especially LFTs) & include HIV test and vitamin D levels Leicester Medical School Phase II Respiratory Medicine Booklet 14 Therefore, MUST do a baseline visual acuity test and LFT’s which must be monitored closely
37
What is Bronchiectasis?
Chronic dilatation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection
38
Bronchiectasis gold standard investigation?
Gold standard diagnostic test = High Resolution CT
39
Bronchiectasis causes?
Post infective – whooping cough, TB  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 lymph node  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
40
Blood tests identify Bronchiectasis in newly diagnosed?
Immunoglobulin levels  Cystic Fibrosis Genotype  Aspergillus IgE / IgG and Total IgE  HIV test  Rheumatoid Factor  Auto Antibodies  Alpha-1-antitrypsin level
41
Bronchiectasis Common Organisms
Haemophilus influenzae • Pseudomonas aeruginosa • Moraxella catarrhalis • Stenotrophomonas maltophilia • Fungi – aspergillus, candida • Non-tuberculous mycobacteria • Less common - Staphylococcus aureus (think about CF)
42
Bronchiectasis Management
Treat underlying cause • Physiotherapy – mucus / airways clearance • Sputum for routine culture as well as nontuberculous mycobacteria • 10-14 days antibiotics according to sputum cultures / sensitivities for acute exacerbations (infections) Amoxicillin - Haemophilus Influenzae Ciprofloxacin - Pseudomonas aeruginosa Long-term (prophylactic) antibiotics for patients with recurrent infective exacerbations Supportive – flu / covid vaccines, bronchodilators if required Pulmonary Rehab – MRC Dyspnoea Score >3
43
Allergic Bronchopulmonary Aspergillosis
Caused by aspergillus fumigatus exposure • Aspergillus is a common fungus found indoors and outdoors • ABPA is a combination of types 1 and 3 hypersensitivity reactions following inhalation of fungal spores i.e. it is not a fungal infection • Repeated damage from these immunological reactions leads to bronchiectasis (often upper lobe) • ABPA is seen more in patients with Asthma, Bronchiectasis and Cystic Fibrosis • Diagnosis is made by a combination of symptoms (often dry cough and wheeze) along with positive blood tests (raised Aspergillus IgE level as well as a high Total IgE – these are often accompanied by a high eosinophil level too) • Treatment (steroids) may be required if ongoing symptoms and high total IgE level
44
What is Cystic Fibrosis
CF Definition CF is an autosomal recessive disease leading to mutations in theCysticFibrosisTransmembraneConductanceRegulator (CFTR). This can lead to a multisystem disease (most commonly affecting the respiratory and gastrointestinal systems but can affect any part of the body with CFTR) characterised by thickened secretions.
45
Diagnosing CF
One or more of the characteristic phenotypic features - • Or a history of CF in a sibling • Or a positive newborn screening test result And • 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)
46
Presentation of Cystic Fibrosis
1. Meconium ileus • In 15-20% of newborn CF infants the bowel is blocked by the sticky secretions. There are signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium. 2. Intestinal malabsorption • Over 90% of CF individuals have intestinal malabsorption. In most this is evident in infancy. The main cause is a severe deficiency of pancreatic enzymes. 3. Recurrent Chest infections 4. Newborn screening
47
Cystic Fibrosis complications
1.Respiratory Infections - Needs aggressive therapy with physio and antibiotics - Patientsoftenreceiveprophylacticantibioticstomaintain health 2.Low Body Weight - needs careful monitoring - may be consequence of pancreatic insufficiency (lack of pancreatic enzymes), therefore in those patients give pancreatic enzyme replacement therapy - highcalorieintakeandoftenextrasupplements - may need NG or PEG feeding 3.Distal Intestinal Obstruction Syndrome (DIOS) - DIOS vs. constipation – faecal obstruction in ileocaecum versus whole bowel - Duetointestinalcontentsinthedistalileumandproximal colon (thick, dehydrated faeces) - Mostoftenduetoinsufficientprescriptionofpancreatic enzymes or non-compliance, also salt deficiency / hot weather - Oftenpresentswithpalpablerightiliacfossamass (faecal) - Diagnosis:Symptoms,palpableRightIliacFossaMass, AXR demonstrating faecal loading at junction of small and large bowel - Treatment:POGastrografin–thisworksbydrawing water across the bowel wall by osmosis into the bowel lumen, aiming to rehydrate the dehydrated faecal mass and allow it to pass 4. CF Related Diabetes
48
Cystic Fibrosis lifestyle 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 exercise
49
Cystic Fibrosis management
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 exercise
50
Pneumothorax types
Air in pleural cavity 1.Spontaneous i.Primary (no lung disease) ii.Secondary (lung disease) 2.Traumatic 3.TENSION: emergency 4.Iatrogenic (e.g. post central line or pacemaker insertion)
51
Pneumothorax risk factors
- Pre-existing lung disease - Height - Smoking/ Cannabis - Diving - Trauma/ Chest procedure - Association with other conditions e.g. Marfan’s syndrome
52
Pneumothorax management
 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 – as above but lower threshold for ICD  If persistent air leak >5 days (bronchopleural fistula) refer to thoracic surgeons  Discharge advice – No flying or diving until resolved
53
Pleural effusion approach
•CXR •ECG •Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting •ECHO (if suspect heart failure) •StagingCT(withcontrast)ifsuspectexudativecause
54
Pleural Effusin Diagnosis
Ultrasound guided pleural aspiration - Biochemistry (protein, pH, LDH) - Cytology - Microbiology (including AAFB) N.B. Never insert a chest drain unless the diagnosis is well established (e.g. known metastatic lung cancer) otherwise draining all fluid off may hinder the opportunity to obtain pleural biopsies. Only indication for urgent chest drain insertion for a new effusion would be an underlying empyema (pH of pleural fluid <7.2 or visible pus on aspirate). Consider Thoracoscopy or CT Pleural Biopsy
55
Causes of Transudate effusions (pleural protein <30 g/L)
Common:  Heart failure  Cirrhosis  Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis) Less common:  Hypothyroidism, mitral stenosis, pulmonary embolism Rare:  Constrictive pericarditis, superior vena cava obstruction, Meig’s syndrome
56
Causes of Exudate effusions >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 Rare:  Yellow nail syndrome, fungal infections, drugs
57
Interstitial lung disease
Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner including:  Usual Interstitial Pneumonia (UIP)  Non-specific Interstitial Pneumonia (NSIP)  Extrinsic Allergic Alveolitis  Sarcoidosis  Several other conditions
58
On PFT for ILD?
Usually a restrictive pattern
59
Investigations for interstitial lung disease?
ANA – connective tissue disease OR SLE ENA – connective tissue disease Rh F – Rheumatoid Arthritis ANCA – Vasculitis Anti-GBM – Pulmonary Renal disease ACE – Sarcoidosis Ig G to serum precipitins e.g. pigeon, budgie – Extrinsic Allergic Alveolitis HIV
60
UIP?
Commonest type of Pulmonary Fibrosis Usually Idiopathic 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
61
Extrinsic Allergic Alveolitis?
Also known as Hypersensitivity Pneumonitis • Inhalation of organic antigen to which the individual has been sensitised Clinical Presentation: –ACUTE – short period from exposure, 4-8 hrs. Usually reversible: spontaneously settle 1-3 days. Can recur. –CHRONIC – chronic exposure (months – years). Less reversible. Common Drug causes:  Amiodarone  Bleomycin  Methotrexate  Nitrofurantoin  Penicillamine
62
Sarcoidosis?
• Multisystem inflammatory condition of unknown cause • Non-caseating granulomas (Histology important) • Immunological response • Commonly involves Resp system BUT can affect nearly all organs • 50% get spontaneous remission, others get progressive disease Investigations: • PFTs: (obstructive until) fibrosis • CXR: 4 stages • Bloods: renal function, ACE, Calcium • Urinary Calcium • Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid
63
Treatment for interstitial lung disease?
• Multisystem inflammatory condition of unknown cause • Non-caseating granulomas (Histology important) • Immunological response • Commonly involves Resp system BUT can affect nearly all organs • 50% get spontaneous remission, others get progressive disease Investigations: • PFTs: (obstructive until) fibrosis • CXR: 4 stages • Bloods: renal function, ACE, Calcium • Urinary Calcium • Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid
64
Lung cancer clinical features
Asymptomatic, incidental finding • Any respiratory symptom/systemic deterioration • Superior Vena Caval Obstruction • Horner’s syndrome • Metastatic disease – liver, adrenals (Addison’s), bone, pleural, CNS • Paraneoplastic – clubbing, hypercalcaemia, anaemia, SIADH, Cushing’s syndrome, Lambert- Eaton myasthenic syndrome • Increased risk of thrombo-embolic disease
65
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
66
Performance status lung cancer
WHO scale Gives an indication of patient’s level of fitness • 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
67
Lung cancer investigations
Bloods – FBC, U&E, Calcium, LFT’s, INR • CXR • Staging CT – Spiral CT Thorax and Upper Abdo helps to stratify TNM stage Histology options • US guided neck node FNA for cytology if lymphadenopathy • Bronchoscopy – endobronchial, transbronchial, endobronchial ultrasound (if mediastinal lymphadenopathy) • CT Biopsy • Thoracoscopy if pleural effusion present PET Scan • MDT Decision if patient is a surgical candidate and initial CT suggestive of low stage • Helps to detect small metastases not seen on staging CT
68
Lung cancer Histology
Classified primarily into two groups which account for about 95% of cases 1. Small cell (oat cell) lung cancer (SCLC) 2. Non-small cell lung cancer (NSCLC) - includes squamous cell, adenocarcinoma, and large cell carcinoma, bronchoalveolar cancer Others -, bronchial gland ca, carcinoid tumour
69
Lung cancer treatment
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 • Do nothing / watch & wait
70
Non-small cell lung cancer survival
All NSCLC – 15-23% • Stage 1 following surgical resection – 65-80% • Stage II following surgical resection – 50-60% • Stage III – 20% • Stage IV – 1-5%
71
Small cell lung cancer treatment and prognosis
Rapid growth rate and almost always too extensive for surgery at time of diagnosis • Mainstay of treatment is chemotherapy • Also palliative radiotherapy • Untreated – median survival is 8-16 weeks • Combination chemotherapy – median survival 7- 15 months
72
What is obstructive sleep apnoea?
Upper airway obstruction during sleep  Clinical definition = upper airway narrowing, provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness  Most patients with significant OSA are male, and tend to have a combination of upper body obesity (collar size >17 in), and a relatively undersized or set back mandible
73
Sleep Apnoea pathophysiology
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
74
Causes of small pharyngeal size in sleep apnoea?
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
75
Causes of excessive narrowing of the airway during sleep?
Obesity may enhance residual muscle dilator action  Neuromuscular disease with pharyngeal involvement may lead to greater loss of dilator muscle tone, e.g. stroke, MND, myotonic dystrophy  Muscle relaxants – sedatives, alcohol  Increasing age
76
Clinical effects of sleep apnoea
Severe OSA leads to repetitive upper airway collapse, with arousal required to re-activate the pharyngeal dilators. There may be associated hypoxia and hypercapnia which are 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
77
Epworth sleepiness scale?
Points for following:0=would never doze, 1=slight chance, 2=moderate chance, 3=high chance -Sitting & 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 & talking -Sitting quietly after lunch without alcohol -In a car, while stopped in traffic
78
Diagnosis of sleep apnoea?
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
79
Management of sleep apnoea?
Treatment is given based on symptoms/quality of life – NOT on severity seen on sleep study -Also consider livelihood, e.g. driving as occupation SIMPLE APPROACHES: -Weight loss, sleep decubitus rather than supine, avoid/reduce evening alcohol intake FOR SNORERS & MILD OSA: -Mandibular advancement devices, consider pharyngeal surgery as last resort FOR SIGNIFICANT OSA: -Nasal CPAP, consider gastroplasty/bypass, and rarely tracheostomy FOR SEVERE OSA & CO2 RETENTION: -May require a period of NIV prior to CPAP if acidotic, but compensated CO2 may reverse with CPAP alone
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Driving with sleep apnoea?
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)
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CPAP?
Usually given via nasal mask, but can use mouth/nose masks  Upper airways splinted open with approximately 10cm H2O pressure – this prevents airways collapse, sleep fragmentation, and ultimately daytime somnelence  Also opens collapsed alveoli and improves V/Q matching
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CPAP vs BIPAP (NIV)
CPAP supplies constant positive pressure during inspiration and expiration and is therefore not a form of ventilatory support. It can be used to treat OSA and helps oxygenation in some patients with acute respiratory failure, e.g. pulmonary oedema  Non-invasive ventilation (NIV) does provide ventilatory support with two levels of positive pressure (bilevel) – pressure support provided between selected inspiratory and expiratory positive pressures (IPAP & EPAP). They can also be set up with back up rates so the machine operates when the respiratory rate drops below a fixed level.