Respiratory medicine

1. 1

Respiratory Medicine
This guide is intended to be used as a resource alongside many other sources

Knowledge:
 Anatomy &Physiology
 Normal ranges
 Respiratory failure
 Pleural diseases
 Asthma
 COPD
 Bronchiectasis
 Cystic Fibrosis
 Pneumonia
 Tuberculosis
 Lung cancer
 Pulmonary Fibrosis
 Occupational
 Thromboembolism
 Sleep Medicine

2. 2

Anatomy & Physiology
The lungs are lined by visceral pleura which is continuous with the parietal pleura and facilitates
movement for breathing. Pleura lubricated by surfactactant produced by type II pneumocytes.
23 generations form bronchus to alveolar sacs, cartilage ends at generation 12 (bronchioles)

Trachea divides at carina @ T4
Right bronchus wider, shorter & more vertical

Left lung – 2 lobesseparated by oblique fissure
 upper (mainly anterior) – 4 bronchial subdivisions
 lower (mainly posterior)– 4 bronchial subdivisions
Surface contacts
1. Aortic arch
2. Common carotid
3. Thoracic duct
4. Vagus & phrenic nerves

Right Lung – 3 lobes. U & M separated by transverse fissure, L separated by oblique fissure
 upper (mainly anterior) - 4bronchial subdivisions
 middle (small and only anterior) - 2bronchial subdivisions
 lower (mainly posterior) - 5 bronchial subdivisions
Surface contacts
1. Oesophagus
2. IVC & SVC
3. Brachiocephalic &azygos veins
4. Vagus & phrenic nerves

Normal ABG Ranges



H
+
-35 -45nmol/l (pH 7.35 -7.45)
HCl
-
-22 -26 mmol/l
PaO
2->10kPa
PaCO
2-4.7 -6.1kPa
Base Excess --2 -+2 mmol/l

3. 3

Respiratory Failure
A ventilation/perfusion mismatch causes pulmonary gas exchange to fail to maintain normal oxygen
and carbon dioxide levels.

Type 1 – Hypoxia (PaO2<8 kPa)
Type 2 – Hypoxia & Hypercapnia (PaCO2>6.6 kPa)

Causes

Type 1 Type 2
Acute Chronic Acute Chronic
H
+
Normal/Raised Normal Raised Normal/Raised
HCl
-
Normal Normal Normal Raised
Causes Acute asthma Emphysema Severe asthma COPD
Pulm oedema Fibrosis COPD exacerbation Sleep Apnoea
Pneumonia Lymphangitis Airway obstruction Kyphoscoliosis
Pneumothorax Carconomatosa Acute paralysis Myopathies
PE Right-to-Left shunt Narcotics Ankylosing spondylitis
ARDS Brain-stem Lesion Prim alveolar hypovent

Investigations
ABG
CXR

Management
Oxygen (maximum unless severe COPD (24-28% with venture mask))
Treat underlying condition
If worsening/no improvement in ABG patient needs mechanical ventilation.

Long Term Oxygen Therapy (LTOT)
Indications (+smoking cessation)
-PaO2<7.3kPa & FEV1<1.5L
-7.3kPa < PaO2< 8kPa & Pulm Hypertension/Peripheral Oedema
Aim for PaO2> 8kPa without unacceptable rise in PaCO2

Therapy >15 hours/day

4. 4

Pleural Diseases
Pneumothorax–air in pleural space
Primary – occurs in absence of underlying lung disease (Male, 20s, tall, thin, smoker w/ apical blebs)
Secondary – occurs in presence of underlying lung disease (COPD & TB... others also)
Traumatic – caused by surgery, chest wall injury etc.

Clinical features
Symptoms
Sudden, unilateral pleuritic chest pain
Breathlessness
Cough

Signs
Decreased/absent breath sounds & vocal resonance
Hyper-resonant percussion
Reduced expansion
Tracheal deviation & mediastinal shift (Tension)
Investigations
CXR – complete translucency. Small <2cm Large >2cm (>2cm = 49% hemi-thorax)

Management
Tension & secondary = Intercostal tube drainage (ICD)
Primary &>50 years old =ICD
Primary &<50 years old = Percutaneous aspiration
Primary &<15 % hemithorax = Observation for 6 hours and follow up as outpatient
Video assisted thoracoscopic surgery (VATS) indicated when:
Failure for lung to re-expand (5 days)
1
st
contralateral PTX
2
nd
ipsilateral PTX
Spontaneous bilateral/haemothorax
Professions at risk
No flying for 6 weeks
No diving (unless pleurectomy performed)

Pleural effusion – fluid in pleural space
Fluid - effusion
Pus – empyema
Blood – haemothorax

Clinical features
SOB
Underlying disease

Signs
Reduced expansion/breath sounds & vocal resonance
Stony dull percussion
Investigation & Management
CXR - >200ml required before evident
USS – useful for aspiration
CT – distinguishes between benign & pleural disease

Aspiration
Microbiology - culture
Biochemistry – protein, glucose, LDH, pH
Pathology – cytology
Biopsy (Abram’s or VATS)
Histology
TB culture
Common causes
Pneumonia Ex
TB Ex
PE Ex (occasionally Trans)
Malignancy Ex
Cardiac failure Trans
Renal problemsTrans
Light’s Criteria
Pleural Fluid Protein:Serum protein ratio >0.5
Pleural Fluid LDH:Serum LDH ratio >0.6
Pleural Fluid LDH > 2/3 of normal upper limit serum LDH

Any positive = Exudative (infection/malig/inflamm/PE)

5. 5

Asthma
No universal definition. Paroxysmal airway obstruction caused by inflammation triggered by a
specific stimulus.
Airway narrowing due to bronchoconstriction & mucus plugging. Hypersensitive & increased inflame
cells. Chronic leads to permanent remodelling.

 Extrinsic – Specific allergen identified. 80%. IgE production esp to dust mites, pollen and pet
dander
 Intrinsic – Occurs in adults and does not improve
 Drug induced – NSAIDS (esp aspirin) inhibit COX = Leukotriene…think anti-leukotriene therapy
 Exercise induced –Hyperventilation = water loss = mediator production = asthma symptoms

Epidemiology – 8 million diagnosed (5.1 M on treatment). Prevalence increasing (300 M worldwide)
possibly due to central heating, pollution, processed foods & hygiene hypothesis. 1/6 occupational.

Onset – Any age, but commoner in early decades. (Worse prognosis in adult-onset)

Symptoms – Breathlessness, chest tightness, wheeze & cough
Think of variability, time of onset, provoking factors etc.

Diagnosis
Characteristic history
 Diurnal symptoms (worse in early morning & disturbing sleep)
 Cough lasting >10 days & difficult to clear
 Recurrent episodes of wheezing esp. when associated with a provoking factor
FEV1>15% following bronchodilator
>20% diurnal variation
FEV1>15% decrease following 6 mins of exercise

Management
Step 1 Step 2 Step 3 Step 4 Step 5
Education and environmental control
Β2 agonist (salbutamol)
Low dose ICS 200µg -
800µg (prednisolone)
High dose ICS 2000µg Glucocorticosteroid
Low dose
Long acting β-agonist
(salmeterol)
Leukotriene
antagonist/inhibitor
Anti-IgE treatment
Theophylline
Consider if >2
exacerbations on step
1

Step up to control symptoms. Bear in mind non-complianceif symptoms worsening.
If symptoms stable, step down therapy.

Acute exacerbations
Preceded by viral infections, moulds, pollen & pollution

Mild/Moderate–Generally worsening symptoms of PEF <60% of best
Doubling of ICS dose
Severe –PEF<50%

6. 6

Heart rate >110
Resp rate >25
Inability to complete sentences in 1 breath

Life threatening - PEF <33%
SpO2 <92%
Silent chest
Bradychardia
Cyanosis, exhaustion, confusion & coma

Near Fatal - Raised PaCO2 and/or requiring mechanical ventilation

Immediate treatment
ABG
Oxygen – High concentration as possible. If not above 92%, mechanically ventilate
Bronchodilators – High dose salbutamol. Ipratropium bromide in life threatening cases
Systemic Corticosteroids – O Prednisolone or IV hydrocortisone. Reduce inflame & hasten
resolution
Theophylline – monitor serum levels if giving regularly
IV fluids – No evidence to support, but usually necessary. Esp K, as serum K can be low

If PEF remains below 30%, IV magnesium, aminophyllines&leukotriene RAs.

PEF measured every 15-30 mins and then 4-6hrs.

Discharge 24hrs after PEF >75%

Indications for Mech ventilation
Coma, exhaustion, drowsiness
Resp arrest
ABG deterioration despite best therapy (PaO2<8kPa & falling or PaCO2>6kPa & rising)

Pregnancy
1/3 get better, 1/3 remain the same, 1/3 get worse. 90% no symptoms during labour
Biggest threat to foetus is exacerbation, most drugs fine.

Occupational
Symptoms improve at weekends/holidays.
Diagnosed by recording 2-hourly peak flows

Causative agents Occupations most at risk
Isocyanates Paint sprayers
Flour & grain Bakers
Animals Nurses
Aldehydes Chemical workers
Colophony & fluxes Animal workers
Latex Welders
Wood dust Food processing workers
Timber workers

7. 7

COPD
Airflow limitation that is not fully reversible. Characterized by chronic bronchitis (cough & sputum
for >3 consecutive months over 2 years) and/or emphysema (permanent enlargement of airspaces
distal to terminal bronchioles w/ wall destruction) which can be panlobular (Lower lobe.α1 ATD) or
centrilobular (Upper lobe. Smokers)

Preventable & treatable with significant extra-pulmonary effects (muscle weakness, per oedema,
weight loss, osteoporosis). Progressive with abnormal inflam response to noxious particles/gasses.

Epidemiology
Directly related to tobacco smoking (and use of biomass fuels in low/middle income countries).
30,000 deaths per year. 5% of all deaths
1/8 of all hospital admissions. 220,000 per year
80 M worldwide

Risk Factors
Tobacco (95% of cases in UK) & cannabis smoke
Biomass fuels
Occupation – Coal miners
Air pollution
Low birth weight – Lower maximal lung volume
Lung growth - Lower maximal lung volume (maternal smoking &
childhood infection)
Infections – Accelerate decline of lung function. HIV asx w/
emphysema
Genetic – α1-antiprotease deficiency. Other COPD genes likely to be
identified in future.

Clinical Features

Chronic bronchitis and/or breathlessness
Pulmonary oedema
RR >20
Accessory muscle use
Pursed lip breathing
Chest wall abnormalities – Horizontal ribs, barrel shaped chest, protruding abdomen, Intercostal in-
drawing, flattened hemi diaphragm, decreased cricosternal distance. (All hyperinflation)
Central cyanosis, signs of CO2 retention.
Peripheral oedema & weight/muscle loss

Investigations

X-ray – Eliminate other causes: heart failure, lung cancer & identify bullae
FBC – Eliminate anaemia & Document polycythaemia. Assay α1AT in young patients.
Spirometry – FEV/FVC <70%. Non reversible.
Transfer factor/diffusing capacity. Low gas exchange
Exercise testing
HRCT



α1-antiprotease deficiency

1/5000 live births
α1-AT aggregates in liver = liver
damage in some individuals
Emphysema <50 years old
Some individuals normal
Panlobar basal emphysema
Smoking cofactor

8. 8

Management
No COPD cure, but therapy can slow disease progression, ease symptoms and reduce exacerbations.
Smoking cessation critical & reduction in other possible RFs (e.g. pollution)
Β-agonist (better in asthma) & anticholinergics (better in COPD) improve symptoms & Spirometry.
Theophylline improves exercise testing& blood gases.



Pulmonary rehabilitation improves exercise tolerance and QoL. No impact on Lung function
Long term oxygen therapy decreases mortality (>15 hours/day). Criteria: COPD
PaO2<7.3kPa (when well)
Smoking is contraindication
Surgery: Bullectomy
Lung volume reduction surgery
Lung Transplantation

Exacerbations
Two of following three symptoms: Breathlessness
Lung volume
Change of sputum colour
Management
Optimise bronchodilators (β-agonist +/- Ach + Oral glucocorticoids)
Antibiotics (Think small, Amoxicillin 250mg/Doxycycline 500mg or Clarithromycin if penn aller or Co-
amox if β-lactam +ve)
Oxygen (Check ABG within 60 mins of Oxygen administration or any change)
Ventilation (Non-invasive better)

Factors asx w/ death in acute on chronic resp failure
Age
Acidosis (H
+
>55nmol/l
Hypotension
Uraemia






Breathelessness & exercise limitation
•SABA/SAACh
Exacerbation and/or persistant breathlessness
•FEV>50% -LAACh
•FEV<50% -LABA + ICS
Persistent exacerbations
•FEV>50% -LABA + ICS
•FEV<50% -LABA + LAMA + ICS

9. 9

Bronchiectasis
Abnormal dilation of the bronchi w/ progressive scarring & lung damage

Causes
 Congenital
 Cystic Fibrosis
 Ciliary Dysfunction Syndromes (primary ciliary dyskinesia & Kartanger’s)
 Primary Hypogabbaglobinaemia
 Acquired – Children
 Pneumonia (complicating whooping cough/measles)
 Primary TB
 Inhaled foreign body
 Acquired – Adult
 Supprative pneumonia (pneumonia w/ pus & perm lung damage, asx w/ abscess)
 Allergic broncho-pulmonary aspergillosis (complicating
asthma)
 Pulmonary TB
 Bronchial tumours

Clinical Features
Cough – Chronic and productive of copious purulent sputum. Worse in
mornings & on changing posture. Asx w/ halitosis
Haemoptysis – Slight or massive. Usually asx w/ sputum & purulence.
Can be only symptom (dry bronchiectasis)
Pneumonia & pleurisy – Inflammation causes fever & malaise as well
as a sharp pain upon breathing,
Poor general health – weight loss, anorexia & failure to thrive.

Signs
Finger clubbing
Coarse inspiratory crackles
Wheeze

Investigation
Sputum culture (Routine, fungal & TB)
Blood tests – FBC, U&Es, LFTs, Immunological
X-Ray – Not apparent unless severe
CT – May show Bronchial dilation & wall thickening
Ciliary dysfunction – Saccharin test

Management
Smoking cessation
Antibiotics 1
st
line Amox 500mg TDS
2
nd
line Clarithromycin 500mg bd
Vaccination (annual flu & 5yr pneumococcal)
Pulmonary rehabilitation (>2 times daily)
Pharmacology – SA-βA to improve function, then LA-βA if minimal improvement
ICS to reduce number of infections
LT-Abx if >3 exacerbations/year w/ Ps Aeruginosa
Surgery – Only consider in patients with no co-morbidities with localised, unresponsive & severe
bronchiectasis. (Emphysema is a CI)
Mild – CXR normal
Diagnosis by CT scan

Severe – CXR abnormal
-Cystic changes
-Tramlining
-Collapse
Mucus plugging
Diagnosis by CT scan

Bacterial colonisation
2/3 chronically colonised by
H. influenzae β-lactam +ve Co-amox 375mg TDS
β-lactam -ve Amoxicillin 500mg bd
S. Pneumonia Amoxicillin 500mg bd
M. catarrhalis Co-amox 375mg TDS
S. Aureus Flucoxicillin 250mg QDS
Ps. Aeruginosa See below
Sputum
Serous – frothy/clear. Pulmonary oedema
Rusty - pneumococcal (lobar) pneumonia.
Mucoid - clear, white or grey. Asthma,
chronic bronchitis and in acute viral
respiratory infections
Mucopurulent – yellow/green/brown.
Pulmonary infection. Darker = serious
Ps. Aeruginosa eradication
Step 1 Ciprofloxacin 750mg BD 2 weeks
Step 2 Anti-pseudomonal abx IV 2 weeks
Step 3 repeat ciproflox 4 weeks + nebulised
colomycin 2MU bd 3 months
Step 4nebulised colomycin 2MU bd 3 months

10. 10

Cystic Fibrosis
Mutation in CFTR (most common ΔF508) gene (on chromosome 7) resulting in abnormal
sodium/chloride movement and dehydration in airway epithelium increasing chances of chronic
infection, ciliary dysfunction & bronchiectasis.

Epidemiology
Most common fatal genetic disorder in Caucasians. Autosomal recessive. 1/25 carrier rate with
1/2500 live birth rate.

Clinical features
At birth, the lungs are macroscopically normal and lung function normal.

Respiratory
-Infective exacerbations of
bronchiectasis
-Spontaneous Pneumothorax
-Haemoptysis
-Nasal Polyps
-Resp failure
-Cor pulmoale
-Lobar Collapse

GI
-Meconium ileus (14%)
-Malabsorption
-Steatorrhea
-Distal intestinal obstruction
syndrome
-Biliary cirrhosis & portal
hypertension
-Gallstones
-Rectal prolapse

Other
-Diabetes (25%)
-Delayed puberty
-Male infertility (failure of vas
deferens to develop)
-Stress incontinence (due to
persistent forced cough)
-Osteoporosis
-Arthropathy

Investigations
Screening (detects ~50% of affected children)
Sweat test (increased sodium chloride in sweat)
Low elastase in stools

Management
Similar to severe bronchiectasis
Pulmonary physiotherapy
S. Aureus infections managed with oral abx
Ps. Aeruginosa therapy managed with IV abx (@home through S/C vascular port)
Regular nebulised abx therapy (colomycin/tobramycin) between exacerbations to suppress chronic
Ps A colonisation.
Many resistant strains develop & treatment becomes tailored to each patient
Home Oxygen & NIV treat resp failure in latter stages of disease.
Lung transplantation would be ideal, but limited by donors.

Non resp management
Malabsorption treated by oral pancreatic enzyme supplements & vitamins.
High calorie diet

Somatic gene therapy to replace faulty gene with a working one is under trial and is an exciting
research field.

11. 11

Pneumonia (Community Acquired)
A lower respiratory tract infection w/ new X-ray shadowing with no other cause.

Epidemiology
5-11/1000
Mortality <1% in community
6-12% in hospitalised patient
>35% in ITU

Clinical Features
Symptoms
Cough (92%)
Breathlessness (67%)
Pleuritic pain (62%)
New sputum production (54%)
Haemoptysis (15%)
Signs
Fevers, rigors, tachypnoea, tachycardia,
hypotension, rigors

Coarse crackles, reduced expansion, bronchial
breathing, pleural rub

Aetiology
Community Hospital
S. Pneumoniae 36% 39%
H. Influenzae 10% 5%
Legionella 0.4% 3.6%
Atypicals 2.6% 27%
Viruses 13% 13%
No cause 45% 31%

CURB65–used to predict 30 day mortality (poor for very sick, very young & very old)

Confusion
Urea >7
Resp Rate >30
BP <90/60 (either one)
>65 years old

1 point for each

0-1 Outpatient (mort <2%)
2 In-patient; short stay (mort ~10%)
>3 In-patient; consider ICU (mort 15-40%)
Investigations
CXR – usually confirms diagnosis. Opacity occurs within 12-18 hours of onset in the affected lobe.
(May take 6 weeks to clear)
ABG
FBC (WCC very high in severe but may be normal when caused by atypical organisms) U&Es & LFTs
CRP usually elevated
Microbiology:
CURB 0-1– not necessary in mild pneumonia
CURB 2 – Blood & Sputum culture
Pneumococcal urine antigen test
Pleural fluid (if present) aspirated for microscopy & culture
CURB >3 – As CURB 2
DIF for atypical pathogen (eg M. pneumonia, adenovirus)
Management
Oxygen (>35% humidified)&IV fluids
Physiotherapy
Pain control (beware opiates with poor resp funct)
Legionella suspected?
 Urine for legionella antigen
 Sputum sample for legionella culture
& Direct Immunofluorescence (DIF)

Abx 1
st
line therapy
Low severity O amoxicillin 500mg
Mod severity (within 4 hours) O amoxicillin 500mg +
clarithromycin 500mg
Very severe (asap) IV co-amoxiclav 1.2g + clarithromycin
500mg
If Legionella suspected, add in IV levofloxacin

12. 12

Tuberculosis
Infection caused predominantly by Mycobacterium tuberculosis (Mtb)
Epidemiology
~10/100,000 in UK. Mortality 10%
1/3 worldwide have latent Mtb infection with 2-3 million deaths /year

Risk Factors
TB contact
Very young/elderly
Ethnic minorities
Immunosuppressed (HIV/chemotherapy)
Health care worker
Silicosis

Clinical Features
Several weeks/months
Weight loss/anorexia
Night sweats
Cough +/-sputum +/- haemoptysis
General Malaise

Investigations
CXR – Upper lobes predominate (ΔΔ sarcoid, old infection & infection from other pathogen)
Consolidation, cavitation, military (<5mm nodules)
Blood tests - ESR, Hb, Na, serum albumin & deranged LFTs
Tuberculin test
Early morning urine
Sputum samples

Diagnosis
Sputum x3 (including an early morning sample)& blood culture
Bronchoscopy with washings (or BAL)
Gastric washing (used for children)

Management
RifampicinR 6 months
Isoniazid H 6 months
Pyrazinamide Z 2 months
Ethambutamol E 2 months
Pyridoxine B6 6 months

Different regimes available based on patient resistance.
Multi-Drug Resistant TB is resistant to Rifampicin & Isoniazid

Oral steroids to be used in extensive TB or with extensive extra-pulmonary features (2-3 months)

Control & prevention
Contact tracing to establish source


Tuberculin test 0-5mm –ve (or v severe)
5-15mm immune
>15mm active TB (or strong
reaction to BCG)
Only useful to differentiate Sarcoid from TB
Result read 48-72 hours after

Extra-pulmonary features
Lymphadenitis
GI – esp lower tract & acute abdomen
Pericardial – effusion & constrictive
CNS – meningeal disease (high mort rates)
Bone & joint – Lower spine, hip & knee
GU- renal symptoms for many years
Side effects
R H Z E
P450 inducer P450 inhibitor Rash Retrobulbar neuritis
Bodily fluids orange Rash Hepatitis Dose halved in CRF
Rash Hepatitis Arthralgia
Hepatitis Gout
Nausea & Vomiting

13. 13

Lung cancer
Malignant tumours more common than benign

Small cell lung cancer 20% (Many metastases)
Non-small cell lung cancer
Squamous 30-40%
Adenocarcinoma 20-30%
Large cell 10%
Undifferentiated 10%
Mixed/other <5%

Clinical Features
All 6
Hoarseness, Horner’s (apical tumour), arm pain, SVCO

Investigation
CT scan better than CXR, used for staging
PET scan (must be done with CT)

Staging
TNM
PET scan more sensitive than CT

Management
SCLC chemosensitive (80% responds)
Prolongs survival from 2 – 16 months

NSCLC surgery (only stage T1 &T2)

Radiotherapy can be good, but can be bad

Mesothelioma
Presents as pleural effusion w/ chest wall pain
40 years between asbestos exposure and diagnosis
CXR – Pleural thickening
Thoracotomy to diagnose
Chemotherapy may be useful
Survival 9-12 months
















CXR Nodule differentiation

Benign Malignant
Small Large
Smooth Spiculated
Calcified Non-calcified
Equal distribution Upper lobes & Right side
more common


TNM Staging
T1 Tumour <3cm
T2 Tumour >3cm &<7cm
T3 Tumour >7cm +/- invasion of diaphragm/chest wall
T4 Invasion of heart/great vessels/mediastinum/trachea

N0 No nodal involvement
N1 Ipsilateral but close
N2 Ipsilateral bit distant
N3 Contralateral

M0 No distant metastases
M1 Distant metastases

14. 14

Interstitial Lung Disease (ILD)(>200 types)

CXR shadowing Bi-basal -IPF
ILD asx w/ connective tissue disorder
Asbestosis
Bilateral mid-zone – Sarcoidosis
Bilateral upper – Sarcoidosis
Silicosis
Coal workers pneumoconiosis
Hypersensitivity pneumonitis
Peripheral bilateral – Eosinophilic pneumonia
Flitting shadows – Cryptogenic organising pneumonia (COP)

Idiopathic Pulmonary Fibrosis (IPF)
Clinical Features
Breathlessness
Cough (dry)

Signs
Clubbing
Fine bi-basal mid & late crackles
Dull Percussion & Decreased vocal resonance
Epidemiology
5-15/100,000. 4000-5000 new cases per year in UK (90 in Lothian)
Median age presentation – 68
M:F 2:1 Smokers:non-smokers

Investigations
Spirometry – Restrictive. Lung volume & gas transfer
HRCT – bi-basal sub-pleural honeycomb cysts
Lung biopsy – if HRCT not conclusive, biopsy shows distorted lung architecture w/ honeycomb cysts

Management
No good therapy. Usually join an RCT & palliate with oxygen, opiates etc.
Lung transplant if <65?
Median survival 3-4 years after presentation

Sarcoidosis
Systemic disease characterised by non-caseating granulomas (small inflame nodules). Cause unknown

Clinical features
SOB
Cough (dry)
Fatigue& Skin lesions
Hypercalcemia

Investigations
Spirometry – Normal stage 1. Restrictive. Reduced TLC& KCO
Blood tests generally normal. Serum ACE may monitor disease activity.
Tuberculin skin test – ΔTB
Biopsy – skin/lymph node/lung. Non caseating granuloma.

Management
Sarcoidosis is usually self-limiting. ICS possible & lung transplant is curative

Staging
1 – Bi-hilar lymphadenopathy (BHL). Asympt. 60-80%
spontaneously remit with 1 year. Erythema Nodosum
2 – BHL + infiltrates (=parenchymal disease) remits in 50-60%
3 – Infiltrates. remits in 20-30%
4 – Fibrosis. Occurs in 5-10%. Irreversible.

15. 15

Occupational lung disease

Pneumoconiosis
Reaction of lung to inhaled dust

Coal Workers Pneumoconiosis (CWP) –small rounded opacities in upper & middle zones
Progressive Massive Fibrosis (PMF) – Irregular opacities

Risk of developing increases with increasing exposure to dusts

Silicosis
A pneumoconiosis caused by inhalation of silica

Risk of developing increases with increasing exposure to silica

Progressive & irreversible

Can be complicated by pulm hypertension & cor-pulmonale
Appears 10 years after exposure

Asbestosis
Tiny blue fibres
Requires much asbestos exposure

15-30 years after exposure before symptoms appear.

16. 16

Venous Thromboembolism (VTE)
PE & DVT – Most PEs arise from lower limb.

Annual risk 0.1-0.3%
Mortality 1-2% (10% of hospital deaths)

Risk Factors
Major Surgery –major surgery
Obstetrics –late pregnancy, C section
Lower limb problem -fracture. Varicose veins
Malignancy
Immobility
Previous VTE
Minor Cardio – Hypertension, CHF
Oestrogen
Loads others

Thrombophilia (eg Factor V Leiden)
Found in 25-50% of VTE <50 years old.

Clinical Features
SOB
Pain
Cough
Haemoptysis

Signs
HS 4
Loud P2
Tachycardia

Investigations
ABG – Hypoxaemia&Hypocapnia
CXR – Normal/effusion/Westermarck’s/Hampton’s hump
ECG –S wave in lead I, Q wave and T wave inversion in lead III, and T wave inversion in leads V1 to
V4. More commonly, the ECG demonstrates minor non-specific ST segment or T wave changes
D-Dimer – Useful for exclusion (if –ve, PE unlikely)
Well’s PE probability score >6 = high chance
Ventilation/Perfusion scan
CTPA
Doppler USS
Echo – trans-oesophageal. Useful in massive PE

Management
LMW Heparin
Warfarin – 6 weeks to 6 months
Thrombolysis – tPA. Use if patient is shocked
IVC filter –if anticoagulation is contraindicated.

17. 17

Sleep Apnoea (Obstructive Sleep Apnoea/Hypo-apnoea Syndrome (OSAHS))
Sleep disruption due to breathing pauses

Clinical features
Sleepiness
Snoring/apnoeas
Unrefreshing sleep
Awake choking
Poor concentration
Depression
Nocturia
50% obese

Epidemiology
Affects 1-2% of western middle aged people
OSAHS commonest resp patient referral
90& cases undiagnosed

Obstruction arises from narrow pharynxwhich may be caused by: Retrognathia
Obesity
Alcohol

OSAHS is associated: Hypertension
Increased chance of having an RTA
Sudden nocturnal death (!)
Cardiovascular events
Diabetes
Liver damage
Acromegaly
Hypothyroidism

Investigations & Diagnosis
Epworth Sleepiness score (>11 =referral)
Overnight breathing study (>15 breathing pauses)

Management
Lifestyle –lose weight
Continuous Positive Airway Pressure (CPAP) therapy - 1
st
line. Improves symptoms & blood pressure
Mandibular splints – 2
nd
line
Other causes of sleepiness
Insufficient sleep
Shift work
Drugs
Psychiatric illness
Narcolepsy (autoimmune)