FRACP Part I Exam
Respiratory Teaching Session
Past Papers Review
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Options:
Excessive PTHrP Secretion
Increased Bone Resorpsion
Increased 1,25 (OH) Vitamin D
Reduced Renal Clearance
Minerolocorticoid Deficiency
Hypercalcemia in Sarcoidosis
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Hyperabsorpsion of dietary Ca occurs in 30-50% of Sarcoidosis patients
Excessive Ca is initially excreted in urine leading to hypercalciuria
30-50% Sarcoid patients have Hypercalciuria
– potentially can lead to nephrocalcinosis – in 50% of renal patients with renal
insufficiency
– Nephrolithiasis – 1-14%. Initial presenting sx in 4-14% of Sarcoid patients.
– Granulomatous interstitial nephritis – most patients have systemic active sarcoid.
Renal biopsy shos noncaseating granulomas, mononuclear cells, intersitital
fibrosis
– Polyuria – nephrogenic or central diabetes insipidis (Pituitary Sarcoid)
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10-20% have hyperalcemia – aggravated by sunlight exposure
Etiology
– Increased 1,25 dihydroxyvitamin D production by Monocytes (mainly
Macrophages) in lungs and lymph nodes
• Mainly due to increased intestinal Ca absorpsion
• Increased Bone Resorpsion
– Excessive PTHrP also contributes
• PTHrP is found in 85% of biopsies of granulomatous tissue
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Which intervention is least likely to
improve this gentleman’s
problems?
A. Thiazide
B. Avoidance of Sunlight
C. Restriction of Dietary Calcium
D. Prednisone
E. Reduce Dietary Oxalate
Treatment of Hypercalcemia in
Sarcoidosis
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Treatment Aim:
– Reduces intestinal absorption of Ca and
– reduce Calcitiol Synthesis
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Restriction of Ca intake (Aim dietary Ca of < 400mg/day)
Reduce Oxalate intake
– – to prevent marked increase in Oxalate absorption and hyperoxaluria which increases the
risk of nephrocalcinosis
Eliminate Vit D supplement
Avoidance of sun exposure
Thiazide diuretic is CONTRAINDICATED in Sarcoidosis
– Thiazide is usually used to inhibit hypercalciuria related renal stones
– Contraindicated in Sarcoidosis – inhibition of hypercalciuria leads to aggravates underlying
hypercalcemia
Low-dose Glucocorticoid therapy
– inhibition of mononuclear cells and inhibition of Ca absoroption
– 10-30mg prenisone is usually adequate in sarcoidsosi
– Treatment response: Serum Ca falls within 2 days.
– Full hypocalcemic response takes up to 7-10 days
Second Line Treatment:
– Bisphosphone Choroquine/Hydroxycholorquine to reduce inflammatory activity of the
disease
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Asbestosis
• Interstitial lung disease secondary to Asbestos
exposure
• Severity is directly proportionate the amount of
asbestos bodies deposited in lung tissue
• CT evidence of interlobular thickening.
Subpleural based band like densities.
• Basilar and Dorsal lung parenchymal interstitial
changes – interlobular/ intralobular
Asbestos bodies
Asbestosis on CT
Diagnosis of Pleural TB
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Pleural Biopsy – Most sensitive test
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Pleural Fluid Culture: 42% sensitive
Mantoux test – high false negative rate: up to 31% - due to suppression of sensitised T-cells
Sputum culture : More likely to be positive in Parenchymal disease
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Sensitivities: 78-95%
Useful as an aid to differential diagnosis – in high pretest probability, lymphocytic pleural effusion with
negative microbiology on culture and histology
Specificity: 95%
Interferon- Gamma:
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Sensitivity: 20-50%
Sensitivity in Patients with Parenchymal disease: 90%
Sensitivity in those without parenchymal disease:11 %
Adenosine deaminase:
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Combination of histological exam + Tissue culture – Sensitivity > 90%
Plerual biopsy culture is 60% sensitive
Histological examination – Granulomatous tissue – 70% sensitive. > 6 samples – sensitivity 80%
Sensitivity: 89%, Specificity 97%,
Positive likelihood ratio: 23.
Useful in differentiating TB pleurisy from other lymphocytic pleural effusions.
TB PCR: Sensitivity ranges between 41% to 80%. Expensive.
2003 Respiratory Questions
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Benefits of pulmonary rehabilitation in
COPD
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Improves exercise capacity (Evidence A)
Reduces the perceived intensity of breathlessness (Evidence A)
Can improve health-related quality of life (Evidence A)
Reduces the number of hospitalizations and days in the hospital (Evidence
A)
Reduces anxiety and depression associated with COPD (Evidence A)
Strength and endurance training of the upper limbs improves arm function
(Evidence B)
Benefits extend well beyond the immediate period of training (Evidence B)
Improves survival (Evidence B)
Respiratory muscle training is beneficial, especially when combined with
general exercise training (Evidence C)
Psychosocial intervention is helpful (Evidence C)
» Global Initiative for Chronic Obstructive Pulmonary Disease, based on an April1998
meeting of the National Heart, Lung, and Blood Institute and the World Health
Organization.
LVRS
• Feasible in a small subset of severe
COPD patients
– Highly selective
– Upper lobe predominant Emphysema +
Poor exercise tolerance
– DLCO & FEV1 have to be > 20%
• Mortality signicifantly increased in the group with
DLCO & FEV1 < 20%
• Non upper lobe dominant emphysema has higher
mortality rate compared to Placebo group
• Severe COPD with good functional status again
has increased mortality
Inhaled Corticosteroids in COPD
4 Major studies
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ISOLDE
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Lung Health Study
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N=290
FEV1 86% predicted
1200mcg Budesonide/d for 6 months then 800mcg Budesonide/d for 30 months
No Treatment effect on frequency of exacerbation or lung function decline
Euroscope Study
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N=1116. Moderately severe COPD. (FEV1 64% predicted)
1200mcg Inhaled Triamcinolone
1. Less outpatient visits for respiratory complaints
2. Less Respiratory Symptoms
3. Reduction in frequency of severe exacerbations
Copenhagen City Lung Study
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N= 751. 1000mcg Fluticasone/d for 6 months
No significant difference in FEV1 decline. Small reductionin frequency of exacerbtions and
slower rate of decline in health status
N=912
FEV1 77% predicted
Budesonide 800mcg / day – significantly more dysphonia/ bruising
Prolonged therapy with high dose ICS required to achieve modest effects
No beneficial effect on disease progression
Tiatropium Bromide in COPD
• Anticholinergic - M1/ M3 Muscarinic receptor
antagonist. Does not block M2 receptor like
Iprotropium (M2 facilitates bronchodilatation.)
– more symptomatic relief
– Fewer exacerbations
– Delay in first presentation to hospital with
exacerbations when compared with LABA
• More bronchodilatation and better symptomatic
relief than regular Ipratropium
Varenicline
• New therapy in smoking cessation
• Partial Nicotine Acetylcholine receptor agonist
• Patients treated with Varenicline are more likely
to achieve both short term and sustained
smoking cessation (up to 1 year) when
compared with Buproprion or Placebo
• OR of Smoking Cessation: Varnicline: 3.2,
Buproprion 1.7
Indications for long-term oxygen therapy
• General indications
– PaO2 55 mmHg or SaO2 88%
• In the presence of cor pulmonale
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PaO2 59 mmHg or SaO2 89%
EKG evidence of P pulmonale
Hematocrit >55%
Clinical evidence of right heart failure
• Specific situations
– PaO2 60 mmHg or SaO2 90% with lung disease and other
clinical needs such as sleep apnea with nocturnal desaturation
not corrected by CPAP.
– If the patient meets criteria at rest, O2 should also be prescribed
during sleep and exercise, and appropriately titrated.If the
patient is normoxemic at rest but desaturates during exercise or
sleep (PaO2 55 mmHg),
– Consideration of nasal continuous positive airway pressure
(CPAP) or bilevel noninvasive nocturnal ventilation is warranted
in patients with desaturation during sleep.
Fertility in CF
CF Male:
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95% have defects in sperm transport
Absence of Vas deferens
CF Females
20% infertile
Due to Thick Cervical Mucus secretions
Secondary Amenorrhea
Exercise Physiology
• VO2 (Oxygen Uptake)
VO2 = Cardiac Output x (A-V Oxygen content)
VO2 Max
• Definition:
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the maximum capacity of the cardiovascular
system to deliver oxygen to the exercising muscles
and the ability of the exercising muscles to
consume oxygen at maximum exercise capacity.
• VO2 Max is limited by Maximum Cardiac output
during exercise
• Maximal HR decreases as a function of age:
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Maximal HR = 208- 0.7 x age (years)
Determination of VO2 Max:
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Alveolar Volume (VA) x kCO = DLCO
VA= number of contributing alveolar units
kCO – efficiency of individual units
DLCO: Gas exchange capacity of lung as
a whole
SVC Obstruction
Lung Cancer – Commonest cause for SVC obstruction
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2-5% of lung Cancer patients
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20% SCC develop SVC obstruction due to central airways involvement
Marker for poor prognosis in NSCLCA – median survival 5 months
Management:
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Lymphoma
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Non Hodgkins Lymphoma
Mediastinal metastasis
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Tissue diagnosis,
Chemo/Radiotherapy,
Endovascular stent – in refractory disease or rapid symptomatic progression
Germ Cell Cancer
Metastastic Breast Cancer
Thymoma
Non Malignant Causes
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Mediastinal Fibrosis – Endovascular stent, SVC bypass surgery
Thrombosis of indwelling catheter devices e.g. Pacemaker
Etiology of Pancoast’s syndrome
• NSCLCA – Commonest – Squamous
Cell CA
• Lyphoma
• TB
• Primary Chest wall tumors
• Typically T3/T4 on presentation
(Involvement of surrounding solid organs)
• Investigation: Transthoracic FNA
Pancoast tumor
• Right Shoulder Pain
– Commonest first symptom
(44-96%)
– invasion into brachial plexus,
1st or 2nd ribs, Vertebral
bodies, parietal pleura, chest
wall
• Horner’s Syndrome
– 14-50%.
– Paravertebral sympathetic
chain and inferior stellate
ganglion
• Neurological complication of
the upper limbs
– C8/T1 Nerve root involvement
• 10% profound weight loss
• 10% have Recurrent
laryngeal nerve palsy
• Lung Cancer + Pleural Effusion + Liver
Mets
• T4 (pleural effusion)
• * Refer to Lung Cancer Staging Table on
UTD
CT+PET Scan Is superior to CT
alone in Lung Cancer Staging
• Useful in assessing mediastinal disease –
If there is no mediastinal
lymphadenopathy, in the absence of
metastasis – stage IIIA, if there is
mediastinal disease Stage IIIB – surgical
treatment is inappropriate