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CHAPTER10 Respiratorymedicine
Idiopathic pulmonary brosis (IPF) 6000 people are diagnosed
every year in the UK. ♂ > ♀. Incidence i with age. ~85% diagnoses made
in people >70y. Progressive condition of unknown cause with insidious
onset. Can only be diagnosed if other causes of interstitial lung disease
have been excluded and symptoms present >3mo.
Riskfactors
• Smoking
• Environmental exposure, e.g.
metals dusts, animal dusts
Presentation
• Progressive exertional dyspnoea
• Dry cough
• Clubbing (>50%)
• Fine ‘Velcro- like’ crepitations
Investigations
• CXR Diuse shadowing (although may be normal)
• Lung function tests Restrictive picture
Dierentialdiagnosis
• LVF
• COPD
• Other causes of lung brosis— dust exposure (coal, asbestos, silica,
farmer’s lung, bird fancier’s lung)
Management Refer to a respiratory physician for diagnosis and advice
on management. Treatment, where appropriate, is with oral steroids +
azathioprine. Pulmonary rehabilitation may be helpful. Lung transplant is
a last option. Most patients have poor prognosis with median survival 3y.
Asubgroup with brotic non- specic interstitial pneumonia (NSIP) has substantially better prognosis with >50% surviving 5y.
0 Patients with IPF have a 10× i risk of lung cancer. This risk is multiplicative with that from smoking. Patients with IPF who smoke 20 cigarettes a
day may have a 200× i risk of lung cancer compared with non- smokers
without IPF.
• Chronic viral infection, e.g. EBV,
hepatitis C
• GORD
• Malaise
• Weight d
• Central cyanosis and right heart
failure (advanced cases)
• Inhalant exposure (O2, NO2)
• Radiation
Sarcoidosis Multisystem inammatory disease of unknown cause
characterized by non- caseating granuloma. Annual incidence in the UK is
7/ 100,000. Typically presents with lung granuloma in a young adult. ♀ > ♂.
Non- respiratory manifestations ofsarcoidosis
• Fever and malaise
• Erythema nodosum
• Lupus pernio (blue- red nodules
on the nose, face, and/ or hands)
• Scar inltration
• Enlarged lacrimal glands
• Hypopyon
• Uveitis
• Arthralgia
• Hepatosplenomegaly
• Arrhythmias
• Heart failure
• Pericardial eusion
• Cranial and/ or peripheral nerve
palsies
• Seizures
• Hypercalcaemia
• Renal stones
• Lymphadenopathy
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INTERSTITIAL LUNGDISEASE
Acute sarcoidosis (Löfgren’s syndrome)
• Polyarthralgia
• Swinging fever
Insidious onset CXR shows hilar lymphadenopathy— incidental nding in
30– 50%. If symptomatic, usually presents with tiredness, malaise, weight d,
and/ or arthralgia. 15% have lung symptoms with gradual onset of progressive exertional dyspnoea and dry cough.
Management Refer any patient with bilateral hilar lymphadenopathy for further investigation. For patients with conrmed sarcoidosis, specialist management is needed. Steroids are the rst- line treatment, but should only
be used if:
• Progressive disease (on imaging or lung function testing)
• Signicant symptoms
• Extra- pulmonary disease requiring treatment
Rarely, if steroids are not controlling disease progression or symptoms,
methotrexate will be added. Inhaled steroids may be helpful to control
cough, but do not inuence disease progression. For patients with severe
symptoms, pulmonary rehabilitation may be helpful. Lung transplant may be
considered for patients with end- stage pulmonary sarcoidosis.
Prognosis Variable natural history, so predicting the course of disease and
prognosis is dicult. Spontaneous remission occurs in 55– 90% of patients
with stage Iradiological disease, 40– 70% with stage II disease, and 10– 20%
with stage III disease. Most remissions occur in the rst 6mo. Mortality
ranges from 1– 5%, due to pulmonary, myocardial, or CNS involvement.
• Erythema nodosum
• Bilateral hilar lymphadenopathy on CXR
Occupational lung disease Ep. 306
Further information
British Thoracic Society Interstitial lung disease guideline. Thorax
63:v1– v58. M https:// www.brit- thoracic.org.uk/ document- li-
brary/ clinical- information/ interstitial- lung- disease/ ild- guidelines/
bts- interstitial- lung- disease- guideline/
NICE (2013, updated 2017)Idiopathic pulmonary brosis in adults:diagnosis and management. M www.nice.org.uk/ guidance/ cg163
Patient support
British Lung Foundation F 03000 030 555 M www.blf.org.uk
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CHAPTER10 Respiratorymedicine
Occupational lungdisease
Exposure to gases, vapours, and dusts at work can lead to lung disease.
Coal- worker’s pneumoconiosis 90% of all compensated industrial
lung disease in the UK. ‘Pneumoconiosis’ means accumulation of dust in the
lungs and tissue reaction to its presence. Incidence is related to total dust
exposure. Divides into:
• Simple pneumoconiosis Deposition of coal dust in the lung. Graded
on CXR appearance. Grading determines whether disability benet is
payable in the UK. Eect on lung function is debated. Predisposes to
progressive massive brosis
• Progressive massive brosis Round brotic masses several cm diameter
form in the upper lobes. Presents with exertional dyspnoea, cough,
black sputum, and eventually respiratory failure. Symptoms progress
(or even start) after exposure to coal dust has ceased. Lung function
tests show a mixed restrictive and obstructive picture with loss of lung
volume, irreversible airow limitation, and d gas transfer
Asbestosis Before legislation banning its use, exposure was widespread
and occurred particularly in naval shipyards and power stations. Eects of
asbestos exposure— Table 10.14. Consider diagnosis in relatives who came
into contact with asbestos while washing clothes etc. too— they can claim
compensation if aected.
Silicosis Uncommon. Aects stonemasons, pottery workers, workers
exposed to sand- blasting, and fettlers (remove sand from metal casts).
Caused by inhalation of silica. CXR appearance is distinctive. Presents with
exertional dyspnoea ± cough.
Lung function tests as for progressive massive brosis. Associated with i
risk of lung cancer and TB.
Byssinosis Aects cotton mill workers. Symptoms (tightness in the chest,
cough, and breathlessness) start on the 1st day back at work after a break
(Monday sickness) with improvement as the week progresses. CXR is
normal.
Berylliosis Rare. Long latent period. Aects workers in the aerospace,
nuclear power, and electrical industries and their close relatives. Presents
similarly to sarcoidosis (E p. 304).
Iron (siderosis), barium (baritosis) and tin (stannosis) dust
inhalation Result in dramatic dense nodular shadowing on the CXR, but
eects on lung function and symptoms are often minimal.
Occupational asthma >200 industrial materials cause occupational
asthma. Accounts for 17% of all adult asthma cases. Important causes are
recognized occupational diseases in the UK— patients may be eligible for
statutory compensation if they apply <10y after leaving the occupation in
which asthma developed. Suspect if a patient has symptoms which improve
on days away from work/ holiday.
Hypersensitivity pneumonitis (‘farmer’s lung’) E p. 302
Management In all cases refer to a respiratory physician for con-
rmation of diagnosis (essential if seeking compensation) and advice on
management.
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OCCUPATIONAL LUNGDISEASE
Table10.14 Conditions caused byasbestos exposure
Condition Asbestos exposure Features/ management
Benign pleural
eusion
Bilateral
diuse pleural
thickening*
Asbestosis* Follows heavy
Mesothelioma* Can follow even
Asbestosisrelated lung
cancer*
* Eligible for industrial injuries benet in the UK.
Usually occurs
<20y after
exposure
Follows light or
moderate exposure
to asbestos.
May progress even
in the absence of
further exposure
exposure after a
5– 10y interval
light exposure to
asbestos.
20– 40y time lag
between exposure
and appearance of
disease
Patients exposed to asbestos who have evidence of that
exposure (pleural plaques, bilateral pleural thickening, or
asbestosis) have an i risk of bronchial carcinoma— usuall y
adenocarcinoma. Smokers exposed to asbestos have a 5× i risk
compared to non- smokers exposed to asbestos
Manage as for lung cancer— E p. 290
Increasing dyspnoea ± pleuritic pain
Refer for drainage of eusion.
May be recurrent and require pleurodesis
Dened as pleural thickening >5mm thick
covering >¼ of the chest wall
Symptoms: exertional dyspnoea
Lung function tests: restrictive picture
Treatment is symptomatic
Presents with progressive dyspnoea, nger
clubbing, and basal end- expiratory crackles
CXR: ‘honeycomb lung’— di use streaky
shadowing
Lung function tests: severe restrictive
defect and d gas transfer
Treatment is symptomatic
Presents with i shortness of breath
±pleuritic pain.
Examination and CXR reveal unilateral
(rarely bilateral) eusion
There is no eective active treatment.
Palliative care— E p. 1011
Median survival is 2y from diagnosis
307
Benets E p. 91
Notication and compensation E p. 90
Further information
European Lung White Book M www.erswhitebook.org
Patient support
British Lung Foundation F 03000 030 555 M www.blf.org.uk
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CHAPTER10 Respiratorymedicine
Snoring and obstructive sleepapnoea
Snoring During sleep, the pharyngeal airway narrows due to d dilator
muscle tone. Snoring is vibratory noise generated from the pharynx and
soft palate as the air passes through this narrowed space. Further narrowing
produces louder snoring, laboured inspiration, and eventually apnoeic episodes. Social consequences are the usual reason for the patient to seek
help. They can be distressing:banishment from the bedroom, marital disharmony, no holidays, fear of travelling or falling asleep in a public place, etc.
0 Snoring may be used by the spouse as an excuse to leave the marital bed
and may actually be trivial/ absent. If suspected, ask the patient to bring a
recording of the oending noise.
Obstructive sleep apnoea Occurs when the pharyngeal airway com-
pletely closes during sleep resulting in apnoeic episodes. i inspiratory eort
is sensed by the brain and a transient arousal provoked. Afew of these
arousals do not matter, but many (sometimes hundreds) per night l fragmented sleep and consequent daytime sleepiness. Aects 4% ♂ and 2%
♀ in the UK.
Clinicalfeatures
• Dominant features Excessive daytime sleepiness (not tiredness—
Epworth Sleepiness Scale is a useful assessment tool), impaired
concentration, snoring
• Other features Unrefreshing sleep, choking episodes during sleep,
witnessed apnoeic episodes, restless sleep, irritability/ personality
change, nocturia, d libido
Causes ofsnoring and sleep apnoea Overweight (neck circumfer-
ence >43cm), nasal congestion, evening alcohol/ sedatives, large tonsils, receding lower jaw, smoking, hypothyroidism, menopause.
Management
Snoring withoutsleepapnoea
• Initial approaches Suggest changing sleeping position (discourage from
sleeping on back); elevate head of the bed (e.g. prop up on bricks— can
d nasal congestion); limit number of pillows to 1 thick/ 2 thin pillows
to maximize pharyngeal size; d weight if obese; d or stop evening
alcohol/ sleeping tablets; suggest partner tries ear plugs (purchase from
chemist— takes several nights to get used to wearing them)
• If clinically indicated
• Nasal congestion— start beclometasone nasal spray (applied head
downwards) 2 pus bd ± ipratropium bromide nasal spray 2
pus nocte
• Check TFTs to exclude hypothyroidism
• If simple measures fail Refer to:
• Dentist or ENT for a mandibular advancement device
• ENT for surgery— septal straightening, polypectomy, turbinate
reduction, tonsillectomy or uvulopalatopharyngoplasty
Sleepapnoea
• Advise patients to:d weight if obese; d or stop evening alcohol/
sleeping tablets and
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SNORING AND OBSTRUCTIVE SLEEPAPNOEA
• Refer to a sleep unit or physician with a special interest in sleep
problems. If diagnosis is proven and causing signicant daytime
sleepiness, usual treatment is with CPAP therapy at night. Mandibular
advancement devices are alternatives for patients who cannot tolerate
CPAP or have very mild symptoms with no daytime sleepiness.
Occasionally, if large tonsils, referral to ENT for surgery is warranted
• Complications:i BP, DM, i risk of stroke and road trac accidents
The Epworth Sleepiness Scale How likely are you to doze o or fall
asleep in the following situations, in contrast to feeling just tired?
This refers to your usual way of life in recent times. Even if you have not
done some of these things recently, try to work out how they would have
aected you.
Situation Chance of dozing
Sitting and reading
Watching TV
Sitting inactive in a public place (e.g. a theatre or a
meeting)
As a passenger in a car for an hour without a break
Lying down to rest in the afternoon when
circumstances permit
Sitting and talking to someone
Sitting quietly after a lunch without alcohol
In a car, while stopped for a few minutes in trac
0=no chance of dozing
1=slight chance of dozing
If score >10— consider sleep apnoea.
Murray W.Johns. ANew Method for Measuring Daytime Sleepiness:The Epworth Sleepiness
Scale. Sleep (1991) 14 (6):540– 545, doi:10.1093/ sleep/ 14.6.540. Translated and reproduced by
permission of Oxf ord University Press on behalf of the Sleep Research Society.
2=moderate chance of dozing
3=high chance of dozing
□
□
□
□
□
□
□
□
309
• Driving Warn patients NOT to drive if sleepy. Once diagnosis is con-
rmed, must inform DVLA and insurance company (E p. 98).
Sleep apnoea inchildren Common in children aged 2– 7y
in association with tonsil enlargement during URTI. Sleep disruption can cause daytime sleepiness, hyperactivity, poor attention span and bad behaviour.
If tonsils are big enough to produce sleep apnoea in the absence of current infection, refer to ENT for consideration of
tonsillectomy.
Patient support
The Sleep Apnoea Trust (SATA) M www.sleep- apnoea- trust.org
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Chapter11
Endocrinology
Symptoms of endocrine disease 312
Diabetes mellitus 314
Organization and monitoring of care 316
Management of diabetes:education 318
Treatment of type 2 diabetes 320
Insulin 322
Hypoglycaemia and diabetic renal disease 324
Diabetic complications:cardiovascular and skin 326
Diabetic complications:eye and nerve 328
The diabetic foot 330
Lumps in the thyroid gland and goitres 332
Thyroid disease 334
Hyper- and hypocalcaemia 336
Adrenal disorders 338
Pituitary problems 340
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CHAPTER11 Endocrinology
Symptoms ofendocrinedisease
Hormones secreted by the endocrine system perform a wide range of
functions. Therefore, clinical presentation of dierent endocrine disorders
varies widely from non- specic symptoms such as tiredness, to very specic
signs such as delayed puberty. Specic features depend on the gland and
hormones involved.
Polydipsia Over- frequent drinking of uid— often associated for logical
reasons with polyuria. Ask if associated with thirst. Take a history of uid intake.
If no history of excess uid intake and capillary blood glucose/ fasting blood
glucose/ HbA1c is normal, investigate further with U&E, Cr, eGFR, and Ca2+.
Commoncauses
• Change in lifestyle:diet/ activity/ exercise level— may be associated with
polyuria but no other symptoms. No history of thirst
• DM— usually accompanied by a history of thirst
Other causes Diarrhoea, diabetes insipidus (E p. 341), i Ca2+ (E p. 336),
compulsive water drinking (may be a feature of psychotic illness), phosphorus poisoning.
Polyuria Passage of excessive urine. Check the patient does not mean
frequency of urination. It can be dicult to distinguish the two. Causes are
similar to those of polydipsia and the 2 symptoms are related. Take a history of uid intake. If no history of excess uid intake and capillary blood
glucose/ fasting blood glucose/ HbA1c is normal, investigate further with
MSU (for M,C&S), U&E, Cr, eGFR, and Ca2+.
Consider
• DM
• Diabetes insipidus
• Hypercalcaemia
• Excessive intake— due to change in lifestyle or psychiatric conditions,
e.g. schizophrenia
• Chronic renal failure
• Drugs— diuretics, caeine, alcohol
Glycosuria Often detected incidentally on urine dipstick. Causes:
• DM
• Pregnancy
In all cases check HbA1c/ fasting blood glucose (+ glucose tolerance test
if pregnant). Check immediate capillary blood glucose if other symptoms
suggestive of DM.
Hirsutism Aects 10% of ♀. Excess hair in androgenic distribution.
Causes:
• Most cases are idiopathic; there may be a family history
• Drugs— phenytoin; corticosteroids; ciclosporin; androgenic oral
contraception; anabolic steroids; minoxidil; diazoxide
• Polycystic ovarian syndrome (PCOS)
• Late- onset congenital adrenal hyperplasia (rare)
• Sepsis
• Renal tubular damage
• Low renal threshold
• Cushing’s syndrome
• Ovarian tumours (rare)
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SYMPTOMS OFENDOCRINEDISEASE
Assessment
• History Long- standing or recent onset, family history, ethnic origin
(more common if of Mediterranean origin), menstrual history
• Examination Distribution of excess hair
Investigation Women with longstanding hirsutism (since puberty) and
regular periods need no further investigation, unless abnormal signs.
Otherwise: blood— testosterone (i in PCOS, androgen- secreting tu-
mour, late- onset congenital adrenal hyperplasia); LH/ FSH ratio (>3:1
suggests PCOS).
Refer to gynaecologist or endocrinologist if Recent onset, abnormal blood
tests, virilism, galactorrhoea, menstrual disturbance, infertility, and/ or
pelvic mass.
Treatment ofidiopathichirsutism
• Cosmetic— bleaching, shaving, waxing, depilatory creams, electrolysis
• Weight d in obese individuals
• Psychological support
• Topical eornithine d growth of unwanted facial hair. Continuous use
for >8wk is required before benet is seen. Must be used indenitely to
prevent regrowth. Discontinue if no improvement in 4mo
• Oral medication— all must be taken for ≥6mo to take eect and none
abolish the problem. In all cases continue treatment until acceptable
level of hair growth then stop. Relapse usually follows withdrawal and
repeat courses are then required. Drugs used:COC pill containing
desogestrel or co- cyprindiol; spironolactone
Sweating E p. 575 Facial ushing E p. 568
Delayed or precocious puberty E p. 871
Obesity E p. 152
Metabolic syndrome (syndrome X; insulin resistance syndrome) Impaired glucose tolerance or DM, insulin resistance (in patients
on insulin, suggested by insulin doses >1 unit/ kg/ d) + other risk factors for
CVD including:
• Truncal obesity— waist circumference >0.9m (♀); >1.0m (♂)—
subtract 0.1m from these gures for people of South Asian extraction
• i BP >135/ 80mmHg
• Dyslipidaemia— serum HDL <1.2.mmol/ L (♀) or <1.0 (♂); fasting
serum triglycerides >1.8mmol/ L
Associated with high risk of CVD. Treat risk factors aggressively.
Tiredness and lethargy E p. 502
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