Happy New Year !

Hi Everyone ...

HAPPY NEW YEAR !!!

Thesis -New PGs in particular

Update your Thesis.
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CONGRATULATIONS !!!

My heartfelt Congratulations !!! to firstly Dr.Rajkumar, for having won the FIRST Prize ,in the South India Respiratory Medicine Quiz contest ,at Calicut.

Congrats yet again !!! to Dr. Bimal and Dr. Sakthivel for getting first place, and Dr. Supraja and Dr. Padmavathi ,for getting third place; in the ACCP Conference conducted in Chennai on last Sunday.

It is good that these are signs of Good Academic Standards in our Department.  It gives a feel-good-factor and gives us motivation to still do better.

I wish you to study harder and be more SMART.  Remember :You are here to pass your exams and your main focus should be academics and the Academic schedule and clear your DNB exams in the first shot.

The quiz competitions have proved the following –

1. That you ARE capable of doing great things.
2. Other departments in India are not upto standards.
3. It also means that we have to set our own standards for excellence.  

clubbing-mechanism of

Digital clubbing is one of the oldest, yet poorly

understood, signs in clinical medicine.

Hypertrophic osteoarthropathy is a clinical

syndrome characterised by clubbing of digits,

periosteal bone formation and arthritis. Clubbing

is an invariable feature of HOA but can also occur

as an isolated manifestation. It is now believed

that isolated clubbing represents either an early

stage or one element in the spectrum of HOA4.

The clinical significance of isolated clubbing is the

same as that of HOA.

The bulbous deformity of the digits results from

oedema and excessive collagen deposition. The

small blood vessels in the digits are dilated and

have thickened walls. The number of arteriovenous

anastomoses is also increased. The

pathogenesis of HOA is not known. Two theories

traditionally put forward to explain HOA are:

(a) Neurogenic theory

(b) Humoral theory

The neurogenic theory proposes that a neural

reflex initiated by vagal stimulation from the site

of disease leads to vasodilatation and other

features of HOA. This is supported by the fact that

the disorders associated with HOA involve sites

innervated by the vagus nerve. Also, vagotomy

may result in resolution of symptoms5. The

humoral theory6 postulates that mediators

responsible for HOA are humoral and normally

present in the venous circulation. These are

ordinarily inactivated by the lung. In conditions

like cyanotic congenital heart disease these

mediators escape filtration/inactivation by the

lungs. A strong argument in favour of the humoral

theory is afforded by causes of congenital cyanotic

heart disease in which bone abnormalities are

limited to cyanotic limbs. Even in conditions like

lung cancer, intestinal polyposis, and

hepatopulmonary syndrome of liver cirrhosis,

lesser degrees of right to left shunt are evident.

However, recent studies suggest that platelets play

an important role in the development of HOA.

The circulating megakaryocytes and large platelet

particles present in the venous circulation normally

break up in the pulmonary vascular bed. In

patients with right to left shunt, macrothrombocytes

reach distal extremity sites where they interact with

endothelial cells resulting in release of platelet

derived growth factor (PDGF) and fibroblast

growth factor(s) thus inducing acropachy7.

Stimulation of fibroblasts by PDGF and

transforming growth factor beta results in cell

growth and collagen synthesis. The finding of

elevated levels of von Willebrand factor antigen

in patients with cardiogenic hypertrophic

osteoarthopathy as well as those with primary

HOA lends further support to this hypothesis8.

Other putative mediators include prostaglandins,

estrogen, growth hormone, etc. In idiopathic cases

a genetically determined overproduction of bone

remodelling substance may be culprit6.

The clinical features of HOA include asymptomatic

deformity of digits. The digital clubbing may

precede the clinical features of underlying illness.

HOA occurs in 5-10% of patients with intrathoracic

Journal, Indian Academy of Clinical Medicine Vol. 2, No. 1 and 2 January-June 2001 37

malignancy. Some patients complain of burning

sensation in finger tips and and deep seated bone

pains in distal extremities. These may be more in

the lower extremities due to limb dependency.

Bone thickening may be evident in some patients.

Joint effusions without synovial hypertrophy may

also be seen. Wrists, matacarpophalangeal, ankle,

knee, and the metatarsophalangeal joints may be

affected. Arthrocentesis yields non-inflammatory

fluid (cells typically less than 1000/mm3). It is

believed that the joint effusion is not due to synovial

disease but more of a sympathetic reaction to the

adjacent periostitis9. Plain X-rays of the extremities

may reveal new perisosteal bone. Radionuclide

bone scan is a sensitive method for demonstrating

this phenomenon. It reveals pericortical linear

uptake along the cortical margins of long bones.

Periostosis is symmetrical in distribution and

evolves in a centripetal fashion. Bone changes

occur in toes first. Radiographic evidence of

periostitis coupled with preservation of joint space

and absence of erosions/periarticular osteopenia

help one to exclude inflammatory arthritis.

Primary hypertrophic osteoarthropathy is less

common than secondary HOA. It is also known

as pachydermoperiostitis or Touraine-Solente-

Gole syndrome. This has a high male to female

ratio (9:1). It is inherited as an autosomal

dominant trait with variable expression. Skin

changes may be very prominent in primary

HOA9,10. This takes the form of cutaneous

hypertrophy and glandular dysfunction. The skin

hypertrophy roughens facial features. The

furrowed forehead, deep nasolabial folds and

corrugated scalp give rise to a leonine

appearance. The extreme skin hyprtrophy is

termed ‘cutis verticis gyrata’9. Glandular

dysfunction of skin results in hyperhidrosis,

seborrhoea, or acne. Acrolysis of terminal

phalanges has been reported. In contrast,

excessive sweating, oily skin, and thickening of

facial features are uncommon in secondary HOA.

Some of the variants of HOA include thyroid

acropachy seen in Graves’ disease. Here clubbing

and periostititis commonly co-exist with

exophthalmos and pretibial myxoedema.

Unilateral clubbing has been reported in

association with aneurysms of the aorta,

subclavian or innominate artery and with

arteriovenous fistlula of brachial vessels4. Clubbing

of toes without finger involvement is seen in

infected abdominal aortic aneurysm. Trauma,

sarcoidosis, and tophaceous gout may give rise

to single digit clubbing4.

Hypertrophic osteoarthropathy is usually

asymptomatic and does not require any treatment.

Joint and bone pains, if present, are treated with

NSAIDs or analgesics. Elevation of the affected

limb may afford pain relief. The treatment of

secondary HOA is to treat the underlying cause.

Removal of lung cancer, correction of cardiac

malformation, and successful treatment of

bacterial endocarditis may lead to a reversal of

the clinical features.

In conclusion, HOA is a syndrome characterised

by abnormal proliferation of skin and osseous

tissue at the distal extremities. The presence of

bone pains with joint pains in a patient with

clubbing should alert a clinician to the possibility

of HOA. Treatment is directed towards removal

of underlying cause, if any, and symptom relief.

7 Habits of Highly Successful People

STEPHEN COVEY
7 Habits of Highly Successful People
Are U??

The First Three Habits surround moving from
Dependence to Independence

(Self Mastery)

1: Be Proactive
2: Begin with the End in Mind
3: Put First Things First
The First thing is the keep the First thing always the First thing!

The Next Three are to do with
Interdependence

4: Think Win/Win
5: Understand, to be Understood
6: Synergize

The Last habit relates to
Self-Rejuvenation

7: Sharpening the Saw

Chest physiotherapy

The purpose of chest physiotherapy, also called chest physiotherapy, is to help patients breathe more freely and to get more oxygen into the body. Chest physiotherapy includes postural drainage, chest percussion, and chest vibration, turning, deep breathing exercises, and coughing. It is usually done in conjunction with other treatments to rid the airways of secretions. These other treatments include suctioning, nebulizer treatments, and the administration of expectorant drugs.

Chest physiotherapy can be used with newborns, infants, children, and adults. People who benefit from chest physiotherapy exhibit a wide range of problems that make it difficult to clear secretions from their lungs. Some people who may receive chest physiotherapy include people with cystic fibrosis or neuromuscular diseases like Guillain-Barré syndrome, progressive muscle weakness (myasthenia gravis), or tetanus. People with lung diseases such as bronchitis, pneumonia, or chronic obstructive pulmonary disease (COPD) also benefit from chest physiotherapy. People who are likely to aspirate their mucous secretions because of diseases such as cerebral palsy or muscular dystrophy also receive chest physiotherapy, as do some people who are bedridden, confined to a wheelchair, or who cannot breathe deeply because of postoperative pain.

Precautions

Chest physiotherapy should not be performed on people with

• bleeding from the lungs
• neck or head injuries
• fractured ribs
• collapsed lungs
• damaged chest walls
• tuberculosis
• acute asthma
• recent heart attack
• pulmonary embolism
• lung abscess
• active haemorrhage
• some spine injuries
• recent surgery, open wounds, or burns

Description

Chest physiotherapy can be performed in a variety of settings including critical care units, hospitals, nursing homes, outpatient clinics, and at the patient's home. Depending on the circumstances, chest physiotherapy may be performed by anyone from a respiratory care therapist to a trained member of the patient's family. Different patient conditions warrant different levels of training.

Chest physiotherapy consists of a variety of procedures that are applied depending on the patient's health and condition. Hospitalised patients are revaluated frequently to establish which procedures are most effective and best tolerated. Patients receiving long term chest physiotherapy are revaluated about every three months.

Turning

Turning from side to side permits lung expansion. Patients may turn themselves or be turned by a caregiver. The head of the bed is also elevated to promote drainage if the patient can tolerate this position. Critically ill patients and those dependent on mechanical respiration are turned once every one to two hours around the clock.

Coughing

Coughing helps break up secretions in the lungs so that the mucus can be suctioned out or expectorated. Patients sit upright and inhale deeply through the nose. They then exhale in short puffs or coughs. Coughing is repeated several times a day.

Deep breathing

Deep breathing helps expand the lungs and forces better distribution of the air into all sections of the lung. The patient either sits in a chair or sits upright in bed and inhales, pushing the abdomen out to force maximum amounts of air into the lung. The abdomen is then contracted, and the patient exhales. Deep breathing exercises are done several times each day for short periods.

Postural drainage

Postural drainage uses the force of gravity to assist in effectively draining secretions from the lungs and into the central airway where they can either be coughed up or suctioned out. The patient is placed in a head or chest down position and is kept in this position for up to 15 minutes. Critical care patients and those depending on mechanical ventilation receive postural drainage therapy four to six times daily. Percussion and vibration may be performed in conjunction with postural drainage.

Percussion

Percussion is rhythmically striking the chest wall with cupped hands. It is also called cupping, clapping, or tapotement. The purpose of percussion is to break up thick secretions in the lungs so that they can be more easily removed. Percussion is performed on each lung segment for one to two minutes at a time.

Vibration

As with percussion, the purpose of vibration is to help break up lung secretions. Vibration can be either mechanical or manual. It is performed as the patient breathes deeply. When done manually, the person performing the vibration places his or her hands against the patient's chest and creates vibrations by quickly contracting and relaxing arm and shoulder muscles while the patient exhales. The procedure is repeated several times each day for about five exhalations.

Preparation

The only preparation needed for chest physiotherapy is an evaluation of the patient's condition and determination of which chest physiotherapy techniques would be most beneficial.

Aftercare

Patients practice oral hygiene procedures to lessen the bad taste or odour of the secretions they spit out.

Risks

Risks and complications associated with chest physiotherapy depend on the health of the patient. Although chest physiotherapy usually poses few problems, in some patients it may cause

• oxygen deficiency if the head is kept lowered for drainage
• increased intracranial pressure
• temporary low blood pressure
bleeding in the lungs
• pain or injury to the ribs, muscles, or spine
• vomiting
inhaling secretions into the lungs
• heart irregularities
• Normal results

The patient is considered to be responding positively to chest physiotherapy if some, but not necessarily all, of these changes occur:

• increased volume of sputum secretions
• changes in breath sounds
• improved vital signs
• improved chest x ray
• increased oxygen in the blood as measured by arterial blood gas values
• patient reports of eased breathing

LAB DIAGNOSIS OF TB

DNB questions

SYMPTOMS AND SIGNS IN RESPIRATORY DISEASE

1. Pulmonary Hypertrophic osteoarthropathy
2. Approach to a patient with chronic cough and normal CXR
3. Hemoptysis management
4. Massive hemoptysis – management
5. DD of chest pain
6. Intractable hemoptysis in different age groups with normal CXR
7. Pathogenesis of hemoptysis
8. Seasonal variations of lung diseases
9. Causes of pulsus paradoxus
10. Assessment of nutritional status
11. Predisposing factors for pulmonary aspiration
12. Evaluation of 50-yr-old male with SOB on exertion
13. Causes of chest pain an a diabetic
14.Evaluation &Management of 18yr.old lean thin boy with recurrent pnuemothorax
15.Systematic approach to evaluation of a patient with breathlessness.

EPIDEMIOLOGY

1. Relative risk, odds ratio
2. Primary prevention
3. Cumulative incidence
4. Population attributable risk
5. Audiovisuals in health education about respiratory system
6. Define sensitivity, specificity, predictive value of a diagnostic test
7. Attack rate
8. Impact of population growth on smoking related lung disorders
9. Epidemiological risk factors for COPD
10. Tuberculin test with specific reference to its epidemiological significance.

INVESTIGATIONS OF RESPIRATORY SYSTEM

1. DD of bihilar lymphadenopathy
2. Risks of diagnostic bronchoscopy
3. Bronchoalveolar lavage
4. Sputum induction techniques
5. Recent radiographic advances in chest disease assessment
6. Role of mini peak flow meters in asthma
7. DD of unilateral hypolucency of lung
8. Virtual bronchoscopy
9. Maximum inspiratory and expiratory pressures – clinical application
10. Cardiopulmonary exercise testing
11. Flow-volume loop
12. Ultrasound in lung diseases
13. Serum ACE
14. Digital subtraction angiography
15. Bronchial provocation test
16. Pulse oximetry
17. DD of radio opaque hemithorax
18. CT and MRI in diagnosis of mediastinal tumors
19. PCR
20. Luciferase
21. ANCA
22. Test for small airway disease
23. Virtual bronchoscopy
24. Medical thoracoscopy
25. Diagnostic approach to a non-resolving consolidation RLL
26. Bronchial artery embolisation
27. Endo bronchial ultrasonography (EBUS)
28. Capnometry – definition and clinical utility
29. Laboratory approach to diagnosis of ILD.
30. Diagnosis of sequestration of lung.
31. Evaluation and management of 18 yrs old lean thin boy with recurrent pneumothorax.
32. Therapetic bronchoscopy current status.
33. Role of spirometry in assessment of obstruction.
34. Role of USG in respiratory diseases.
35. Clinical applications of spirometry.
36. Indications,contraindications,complications of medical thoracoscopy.
ANATOMY/PHYSIOLOGY/PATHOLOGY

1. Surfactant – role in physiology, clinical utility
2. Pulmonary sequestration
3. IgE - role in pulmonary disorders
4. Blood supply of lung.
5. Lymphatic drainage of lung
6. Mediastinal compartments – tumors in each compartment
7. Ventilatory response in hypoxia
8. Fate of an inhaled particle in lung
9. Compensation of respiratory acidosis
10. Anatomy of respiratory bronchiole
11. Developmental lung abnormalities
12. Alveolar macrophage
13. Diffusion coefficient
14. Mucociliary clearance
15. Non ventilatory function of lungs
16. Pulmonary defense mechanisms
17. Eosinophil
18. Abnormalities of gas exchange, methods of evaluation
19. Lipo oxygenase pathway
20. Structure of interstitium
21. Erythropoietin
22. Compensation in metabolic acid-base disorders
23. Respiratory acidosis
24. Lactic acidosis
25. Anion gap in acid-base disorders
26. Oxidant-antioxidant role in respiratory disease
27. Structure of cilia
28. Wide A-a gradient
29. Metabolic functions of lung
30. Ultra structure of acinus
31. Pressure-volume relationship of the lung
32. Metabolic alkalosis
33. Oxygen transport
34. Pulmonary gas exchange
35. Congenital abnormalities of diaphragm
36. Arachidonic acid pathway
37. Respiratory center
38. Alpha-1 antitrypsin
39. Nerve supply of lung
40. J receptors
41. Inspiratory capacity
42. Flow volume loops in diagnosis of upper airway obstruction and airway disease.
43. Factors affecting oxygen dissociation curve
44. Discuss anatomy of mediastinal lymph nodes
45. Control of breathing
46. Vocal cord dysfunction.
47. Effect of pregnancy on pulmonary functions.
48. Concept of physiological dead space &alveolar ventilation& clinical utility.
49. Anatomical & Physiological changes in pregnancy.
50. What is surfactant? Discuss it’s clinical utility.


DISORDERS OF PULMONARY CIRCULATION

1. Fat embolism.
2. Hepatopulmonary syndromes.
3. Prophylaxis of venous thromboembolism.
4. Ventilation-perfusion defects in massive pulmonary infarction.
5. Arteriovenous shunts in lungs and effect on acid-base balance.
6. Goodpasture’s syndrome.
7. Prevalence of pulmonary thromboembolism.
8. Pulmonary vasculitis.
9. Heparin in PTE.
10. Wegener’s granulomatosis.
11. Etiopathogenesis and management of Pulmonary hypertension.
12. Advances in pharmacotherapy of pulmonary arterial hypertension.
13. Treatment of pulmonary infarction.
14. Drug treatment of PHA.
15. ANCA associated vasculitis.Discuss in brief .

ALVEOLAR DISEASES

1. Alveolar hemorrhage syndromes
2. Neurogenic pulmonary edema
3. Diagnosis of intrapulmonary hemorrhage
4. Diffuse alveolar haemarrhage.
5. DDS of pulmonary alveolar haemorrhage.

PHARMACOLOGY/THERAPY

1. Pharmacokinetics, drug interactions of theophylline
2. Tiotropium
3. Mechanism of action of theophylline
4. Drugs causing bronchospasm
5. Leukotriene receptor antagonists, antileukotrienes in asthma
6. Gene therapy
7. Effect of ATT on blood sugars
8. Steven-Johnson’s syndrome
9. Cyclosporin A
10. Beta lactamase inhibitors
11. Pharmacokinetics, metabolism of Rifampicin, INH, PZA. Describe postulated theory of toxic hepatitis
12. Antibiotic MIC
13. Neurological side effects of ATT
14. Stem cell concepts
15. Newer macrolides
16. New ATT
17. Inhaled steroids
18. Antihistamines
19. Clofazamine
20. LASER in lung diseases
21. Radio sensitizers
22. Salbutamol
23. Drug interactions of rifampicin
24. Heliox
25. Bronchial artery embolisation
26. Advances in pharmacology of PAH.




OBSTRUCTIVE LUNG DISEASES

1. Risk factors for COPD
2. Asthma education
3. Nicotine replacement therapy
4. Pulmonary rehabilitation in patients with COPD
5. Alpha-1 antitrypsin deficiency
6. Non-pharmacological & complementary interventions in asthma management
7. Pathogenesis, lab diagnosis of bronchial hypersensitivity
8. Topical steroids in asthma
9. Drug-induced asthma
10. Epidemiology of asthma in india.
11. Smoking cessation clinics
12. COPD and nutrition
13. Smoking, cadmium and emphysema
14. Primary prevention of asthma/allergy
15. Gene therapy of cystic fibrosis
16. Mechanism of airflow obstruction in emphysema
17. Prevention of COPD and complications
18. Steroids in COPD
19. Aerosol therapy – mechanism
20. Hypoxia during sleep in COPD
21. Genetic link in asthma
22. Dyskinetic cilia syndrome
23. Nicotine addiction – remedial measures
24. Steroid resistant asthma
25. Acute on chronic respiratory failure in COPD
26. Acute severe asthma
27. Pathology of emphysema
28. Pathology of bronchiectasis
29. DNAse in cystic fibrosis
30. New drugs in asthma
31. Elastase-antielastase in emphysema
32. Genetic basis of CF
33. Post mortem histology in acute severe asthma
34. Management of episodic asthma
35. Macleod’s syndrome
36. Indicators of severe airflow obstruction in asthma
37. Ventilatory parameters in small airways dysfunction
38. Flail chest
39. Predisposing factors for bronchiectasis
40. Susceptible smokers and the Dutch hypothesis
41. Middle lobe syndrome
42. Nocturnal asthma
43. Epidemiology of COPD
44. Management of acute hypercapneic failure in a patient of COPD
45. Reactive airway dysfunction syndrome
46. Bullous lung disease
47. Asthma mortality
48. Enumerate different approaches for smoking cessation. Pharmacological management strategies
49. Relationship/associations between tobacco smoking and asthma
50. Assessment and monitoring of severity of COPD
51. Heliox.
52. Reactive airway disease diagnostic criteria & management.
53. What are the aerosols?discuss the properties of aerosols that are important inhalational therapy.
54. Immunology:Current status in management of asthma.
55. Determinants of aerosol therapy.
56. Enumerate the common mimics of Asthma & their features which are important in differential diagnosis.


RESPIRATORY SYSTEM AND OTHER SYSTEMS

1. Pulmonary manifestations of SLE
2. Lung in rheumatoid arthritis
3. Respiratory system and diabetes
4. Thyroid disorders and respiratory system
5. Pleuropulmonary complications in acute pancreatitis
6. Pulmonary changes in CCF
7. Prevention of Postoperative pulmonary complications
8. Causes of cor pulmonale
9. Lung and inborn errors of metabolism
10. SIADH
11. Diseases affecting kidneys and lungs
12. Pulmonary complications of malaria
13. Marfan’s syndrome
14. Idiopathic kyphoscoliosis
15. Pulmonary complications of obesity
16. Myxedema coma
17. Lung in neurocutaneous syndromes
18. Diastolic heart failure
19. Pathogenesis and clinical features of rheumatoid lung
20. Uremic lung.
21. Hepato pulmonary syndrome.

TUBERCULOSIS/HIV/INFECTIONS

1. Pneumococcal vaccination
2. Invasive aspergillosis of lungs
3. TB in immunocompromised host
4. Advances in immunological and microbiological methods in diagnosis of TB
5. Chemoprophylaxis in TB
6. Pool of TB infection in community
7. Respiratory infections / disorders in AIDS
8. Candidemia
9. Effect of MDR-TB on RNTCP
10. Role of persisters in TB
11. Risk factors in hospital-acquired infections
12. Pneumonia in elderly
13. Plan sample survey for TB
14. Western Blot in HIV
15. Mucormycosis of lungs
16. Mechanisms of drug resistance in TB
17. Bacterial adhesions/adherence
18. Poncet’s disease
19. Tuberculoma – diagnosis and clinical features
20. Impact of HAART in HIV/TB
21. Management of Addisonian crisis in TB
22. Radiological presentation of hydatid of lung
23. Anaerobic pleuropulmoanry infections of lungs
24. Vaccines to prevent respiratory diseases/Vaccinations against pulm infections
25. Ranke’s complex
26. Treatment and diagnosis of lung abscess
27. Histoplasmosis
28. Legionellosis
29. Steroids in TB
30. Pathogenesis/pathology of TB in AIDS
31. Voluntary testing and counseling centers
32. Sentinel surveillance in HIV
33. Public and private mix in TB
34. DOTS issues
35. Newer diagnostic techniques in TB
36. Pulmonary Nocardiosis
37. Antibacterial rotation and VAP
38. Medical treatment of lung hydatid
39. AIDS vaccine
40. Transmission of TB and prevention
41. Molecular biology and diagnosis of TB
42. Secondary Chemoprophylaxis of TB
43. PCR in TB
44. Humidifier fever
45. Hantavirus infection
46. Constraints of DOTS
47. MDR TB
48. Serologic diagnosis of TB
49. Penicillin resistant Pneumococci
50. Rapid diagnosis of Rifampicin resistance
51. Natural history of HIV
52. VAP – diagnosis
53. Window period of HIV
54. HAP, nosocomial pneumonia
55. Antifungal agents in ABPA
56. Causes of immunosupression and respiratory infections in ICH and prevention
57. Chronic granulomatous disease
58. Role and limitations of penicillins in CAP
59. ABPA
60. Bacterial adherence
61. Uses of BCG other than in TB prevention
62. Nonspecific tuberculin sensitivity
63. Pathogenesis of Staphylococcal pneumonia
64. Pleuropulmonary amebiasis
65. Prevention of influenza
66. Cryptococcal infection of lung
67. Culture methods in TB
68. Lab diagnosis of respiratory viral infections
69. Life cycle of Echinococcus
70. MOTT
71. Lung in helminthic diseases
72. PCP
73. Principles of antibiotic use and selection of empiric therapy for pneumonia
74. HIV and tuberculosis: Management issues
75. Emerging Respiratory infections
76. Avian flu
77. What is TB control? Describe briefly its epidemiological indices
78. XDR TB
79. Antibacterial rotation and VAP.
80. Diagnosis prevention & treatment of H1N1 influenza.
81. Measures of tuberculosis infection.
82. DOT PLUS programme.
83. Predisposing factors & clinical manifestations of lung abscess.
84. Diagnostic criteria &management of ABPA.
85. Diagnostic & therapeutic modalities in pulmonary hydatid.

NEOPLASMS

1. Screening of lung cancer
2. Management of stage III lung cancer
3. Diagnostic approach to a 45-yr-old male with solitary pulmonary nodule
4. Serum/tumor markers in lung cancer
5. Free radical damage of DNA and cancer
6. Radioisotopes in lung cancer
7. Trends in chemotherapy in lung cancer
8. Adjuvant treatment in lung cancer
9. Non-metastatic complications in lung cancer
10. Role of bronchoscopy in SPN
11. Non-metastatic neuromuscular syndromes in lung cancer
12. Tumor-suppressor genes
13. Classification and staging oh Hodgkin’s disease
14. Staging, management of lung cancer
15. Choriocarcinoma
16. Ectopic hormone production
17. Etiology of lung cancer
18. What is quality of life, Scales used to measure QOL in cancer.
19. Chemotherapy for NSCLC
20. Staging of Non Small Cell Lung Cancer.
21. Non tobacco risk factors for lung cancer.

SURGERY AND RESPIRATORY SYSTEM

1. Pre operative pulmonary complication
2. Post operative pulmonary complications
3. Complications of lung resection
4. Pulmonary complications of abdominal surgery
5. Lung resection candidates/indications
6. LVRS
7. Post operative and long-term management in transplant recipients
8. Surgical management of bronchiectasis
9. Surgery in MDR TB
10. (Single) Lung transplantation
11. Heller’s operation
12. Preop eval for lung resection surgery
13. Surgery in TB
14. Thoracoplasty
15. Criteria for deciding operability in a 60 yrs old man for Ca lung having COPD.
16. Surgical interventions for management of advanced COPD.

MECHANICAL VENTILATION, CRITICAL CARE, OXYGEN

1. Optimum, Intrinsic PEEP
2. Severity scoring systems in ICU – rationale for use
3. Severe sepsis
4. Decision to forego life-sustaining treatment in ICU
5. Sepsis syndrome
6. Evaluation of hypoxia
7. Management of myasthenic crisis
8. Metabolic causes of respiratory muscle weakness
9. Weaning from ventilation, indicators and strategies for successful weaning
10. Cardiac output in ICU
11. Mechanism of invasive ventilation
12. Mechanism of non-invasive ventilation
13. Complications of mechanical ventilation and prevention
14. Hypoventilation syndromes
15. Different parameters in mechanical ventilation
16. Management of hemodynamic instability
17. CVP monitoring
18. Transfusion associated lung injury
19. Oxygen toxicity
20. Oxygen concentrators
21. Oxygen therapy – modes, equipment
22. Risk factors for ARDS
23. DIC
24. Management of cobra bite
25. Management of GBS
26. Modes of artificial ventilation
27. Complications, hemodynamics, pathogenesis of septic shock
28. BiPAP
29. CO poisoning
30. End-of-life issues
31. Respiratory stimulants
32. LTOT
33. OP poisoning
34. MODS
35. Infectious control measures in the ICU
36. Management of sepsis with multiple organ dysfunction
37. NIV-indications and contraindications in acute repiratory failure
38. Low tidal volume ventilation in ARDS
39. Palliative care in terminally ill patients with respiratory diseases
40. Non-cardiogenic pulmonary edema
41. Septic shock
42. Idiopathic resp. distress syndrome of the newborn HMD pathophysiology & management.
43. Ventilater management strategies in ARDS.
44. O2 uptake transport & utilization in critically ill patients.
45. C/I to use of NIPPV.

DRUG-INDUCED LUNG DISEASES

1. Drug-induced lung diseases
2. Effect of cardiovascular drugs on lungs
3. Radiation pneumonitis.
4. Clinical manifestations of various drug induced lung diseases.

SLEEP

1. Syndrome Z
2. Effect of sleep on breathing
3. Sleep-disordered breathing
4. Sleep apnea syndrome
5. Consequences and management of OSA
6. Polysomnography.
7. Insulin resistance & OSA
8. What is metabolic syndrome? Discuss its association with OSA
9. Positive pressure therapy in Rx of OSA efficacy & complications.
10. Epidemiology of OSA.




OCCUPATIONAL/ENVIRONMENTAL LUNG DISEASES

1. Bioterrorism
2. Indoor/Outdoor Air pollution
3. Risk from passive smoking
4. Classify,enumerate environmental pollutants & diseases caused by them
5. CFCs
6. Byssinosis
7. Air travel
8. Classification of occupational lung diseases
9. Impact of population growth in smoking related lung diseases
10. Future perspective in pneumoconiosis
11. Occupational asthma
12. Asbestos related lung diseases
13. Pulmonary adaptation and clinical disorders caused at high altitude
14. Pulmonary barotraumas in sea divers
15. Carcinogens in tobacco smoke
16. Caplan’s syndrome
17. Inhaling environmental tobacco smoke
18. Complicated pneumoconiosis
19. HAPE
20. Non malignant resp disorders in agriculture industry
21. Complications of silicosis
22. Bagassosis
23. Sick Building syndrome
24. Decompression Sickness
25. Environmental Tobacco smoke (ETS)
26. Global warming
27. Respiratory ailments & fitness to fly
28. Coal workers pneumoconiosis
29. Jet lag
30. Enumerate important causes of indoor air pollution & discuss in brief their effects on lung health.

INTERSTITIAL/INFLAMMATORY LUNG DISEASES

1. Classification and diagnosis of IIPs
2. Hypersensitivity pneumonitis-pathogenesis,
3. Farmers’ lung
4. Lung function abnormalities in ILD,Function derangements in IPF.
5. Churg-Strauss syndrome
6. Sarcoidosis in India
7. Assessment of activity of alveolitis in ILD
8. Chronic eosinophilic pneumonia
9. BOOP
10. Lymphangioleiomyomatosis
11. Value of HRCT in ILD
12. Eosinophilic syndromes
13. Recent advances in management of IPF
14. Amyloidosis of lower respiratory tract
15. Pathologic changes in ILD
16. Histiocytosis X
17. Lung in systemic sclerosis
18. Bronchiolitis obliterans
19. Sjogren’s syndrome
20. Recent advances in mgt of sarcoidosis
21. Diagnostic approach to ILD
22. Diagnostic approach to 70 yrs old man with ILD.
23. Drug treatment of sarcoidosis
24. Tropical pulmonary eosinophilia. Etiology, clinical features & management.

PLEURAL DISEASES

1. Differences between transudative and exudative effusions
2. Pleural calcification
3. Bronchopleural fistula - management
4. Pleurodesis
5. Pleuropulmonary endometriosis
6. Meig’s syndrome
7. Hydrothorax
8. Parapneumonic effusion/Synpneumonic effusion
9. Pneumothorax
10. Management of malignant pleural effusion.
11. Management of hepatic hydrothorax .
12. Causes & DD’s of non malignant pleural effusion.

MISCELLANEOUS

1. Pulmonary disability assessment
2. Biologicals in resp diseases
3. High altitude pulmonary edema.
4. Transfusion related lung injury.
5. Cardio pulmonary exercise testing indication & utility.
6. Cardio pulmonary resuscitation.
7. Diagnosis & treatment of metabolic alkalosis.

Respiratory System clinical examination

Respiratory System - History and Exam

Competence in history and examination should be acquired by the aspiring clinician.

An hour is often the allocated time for history, examination, management formulation and suitable explanation to the patient in medical training. In UK general practice patients are usually given 10 minute appointments. Hence it is necessary to be efficient in acquiring important information without taking too many shortcuts and missing the diagnosis.

Basic principles of a history

"Listen to the patient. He is telling you the diagnosis," comes the wisdom of ages.

· To do this efficiently questions should be open-ended and allow for patients to speak freely.

· Be selective with direct questioning. The patient may gloss over something that demands deeper inquiry.

· Try not to interrupt unnecessarily (but there are times when it is essential to hone in on detail).

· Avoid irrelevant detail. Some patients can meander aimlessly with irrelevant anecdotes and these need to be gently curtailed.

· Avoid leading questions.

· Let the patient speak freely in his own words.

History of presenting complaint

Following the principles above ask:

· What is the principle complaint? Examples include dyspnoea, wheezing or cough as below.

· Are there subsidiary complaints?

· What is the time scale of the complaint?

· Is the disease progressive or static?

· Is the problem constant or paroxysmal? If it is variable, are the good times symptom free or less severe?

· Are there any aggravating or relieving factors?

· How severely does it affect the patient's life?

Dyspnoea and wheeze

The questions may apply to both dyspnoea and wheezing.

· When do symptoms occur?

· Is there shortness of breath on exertion? How much exertion?

· Is it getting worse?

· Do symptoms occur at rest?

· Does anything else precipitate it? This can include cold air, pollution and lying flat.

· What does the patient do when it happens? He may stop for breath, he may seek fresh air, he may sit up.

· Are there any undue problems with a cold? Asthma and COPD are often aggravated by a cold.

Remember that respiratory symptoms may be caused by disease of other systems:

· Congestive heart failure may cause dyspnoea at night. The patient sits up and throws open the windows.

· Severe anaemia causes shortness of breath on exertion.

· Neuromuscular disease can cause dyspnoea.

· Dyspnoea can be psychogenic (with features of the hyperventilation syndrome).

· Only moderate asthmatics wheeze. In severe asthma there may be no wheeze and a silent chest.

· It is important to distinguish wheeze from stridor.

Cough

Questions to ask about cough include:

· Does anything bring it on? Think of the same precipitants as asthma.

· When does it tend to happen? A nocturnal cough could be heart failure, a postnasal drip or gastro-oesophageal reflux.

· Is it dry or productive? "Do you bring anything up?" is the question to ask the patient.

· If the cough is productive, what colour is the sputum? Green or yellow suggests infection.

· "Do you ever cough up blood?" You should have a mental differential diagnosis for haemoptysis.

Remember that mild asthma can present with cough. Paroxysmal nocturnal coughing can be from heart failure. ACE inhibitors may cause cough.

Previous diagnosis and treatment

Between the history of the presenting complaint and past medical history, it is worth asking if there has been any previous consultation about the problem, a previous diagnosis and any previous treatment? This may seem a little like cheating in finals but in real life it is very important. Has there been previous investigation and a diagnosis? It may be right or it may be wrong but it is important to know about it. Has there been any previous attempt at treatment? If so, with what and how successful was it?
Blessed is he who sees the patient last.

Past medical history

It is often the past history that gives the clue to the aetiology. Ask about:

· Childhood asthma, wheezing or 'bronchitis'.

· Malignant disease (pulmonary metastases). Remember busulphan can cause pulmonary fibrosis.

· Infections including pneumonia, tuberculosis and whooping cough.

· Chest trauma and operations.

· Thromboembolic disease, specifically deep vein thromboses and pulmonary embolus.

Drug history

Specifically:

· Use of inhalers (assess compliance and technique).

· Use of steroids (some measure of severity in asthma).

· Other drugs which may have relevance in respiratory disease (such as busulphan, ACE inhibitors,aspirin, NSAIDs).

Allergies

Ask about all allergies including for example food, inhaled allergens and drugs.

Family history

Diseases can have a genetic component or aetiology such as asthma and cystic fibrosis. Ask also about:

· Infectious diseases such as tuberculosis (remember high risk groups).

· Atopic diseases such as hay fever and eczema.

· Emphysema (alpha-1-antitrypsin deficiency).

Social history

· An occupational history may be very important in respiratory disease. This is highlighted with conditions such as asbestosis where there may have been exposure in the building industry for example. It is important to ask about past occupations too. Remember an electrician, a carpenter and a sailor in the merchant navy may all have been exposed to asbestos.

· Hobbies and pets may also be responsible for respiratory disease.

· Lifestyle and alcohol consumption are also very relevant to respiratory diseases. Ask about illicit drugs. They may be smoked or inhaled.

· Smoking history should detail for example the type and number of cigarettes smoked currently and in the past. Remember that some children start to smoke very early in life. Ask about passive smoking.

· Sexual history may be relevant to risk of HIV and AIDS.

Systematic inquiry

It is important to ask about other body systems. There may be undiagnosed illnesses in other systems which are relevant to the respiratory symptoms.

· Loss of appetite is a common feature whenever people are unwell. It suggests that the disease is having a significant effect on wellbeing.

· Significant loss of weight may well be indicative of serious illness. Remember malignancy and tuberculosis.

· Ask about urinary symptoms. Middle-aged and older women, in particular, may be less concerned about the cough than the associated stress incontinence. Ask about it as they are often too embarrassed to complain directly.

· Heart disease may cause respiratory symptoms. Are there for example symptoms of heart failure,angina or ankle swelling?

· Rheumatoid arthritis and other connective tissue diseases may cause respiratory symptoms.

· Neuromuscular diseases may cause respiratory symptoms, particularly dyspnoea.

Examination

Before examination likely diagnoses and what to expect on examination will usually have been formulated. Examination should be performed in a competent manner to confirm the diagnosis and possibly to direct further investigations. In medical exams, getting the right answer by the wrong method may result in failure but achieving the wrong answer with the correct technique can achieve a pass.

It is impossible to give an adequate description of sounds with words and the reader is recommended to use an audio aid to become familiar with breath sounds. What is normal in terms of percussion, tactile vocal fremitus, etc can only be assessed on the basis of experience. Hence it is important to examine patients with and without abnormalities. The various breath sounds available on mentor media audio are recommended. (Make sure you have speakers turned on).

Inspection

Observe the patient.

· Do his cheeks and temples look sunken as if he has lost much weight?

· Is he blue and bloated? Peripheral oedema may be noted.

· What is the general physique? Pneumothorax is most common in those who are tall and thin with a habitus rather similar to Marfan's syndrome.

· Do the lips look cyanosed?

· Is he breathing through pursed lips. This suggests premature airways closure as in COPD.

· Is he struggling to breath? Perhaps you can see that the accessory muscles of respiration are being used. The alae nasae may be in action. Such patients often look anxious too. The respiratory rate may be fast, especially in children.

· The face may have a Cushingoid appearance from current or frequent treatment withcorticosteroids.

· You may be able to hear a wheeze from across the room.

Hands

· Is there nicotine on the fingers?

· Is there clubbing of the fingers? You should have a mental list of causes of clubbing (pulmonary, cardiac and other causes). If it is present, ask the patient if his nails have always been that shape or if he has noticed a change.

· Do the nails look blue as in peripheral cyanosis? In anaemia they may look pale and with iron deficiency there may be koilonychia.

· You may notice a tremor, especially with carbon dioxide retention.

· Note the radial pulse too. Tachycardia suggests significant respiratory difficulty or marked overuse of a beta agonist. Lung cancer can cause atrial fibrillation. A large pneumothorax or atension pneumothorax can cause pulsus paradoxus.

Head and neck

The first part of the airways is the nose and mouth.

· Just briefly note if they look healthy?

· Does the tongue look cyanosed?

· Is there halitosis?

· Are there palpable lymph nodes in the neck? This may suggest lung cancer or tuberculosis.

· The jugular venous pulse may be raised in cor pulmonale.

· Eye examination may reveal Horner's syndrome or signs of sarcoidosis or tuberculosis (iridocyclitis). Papilloedema can be caused by carbon dioxide retention and cerebral metastases.

· Superior vena cava obstruction occurs with carcinoma of the bronchus and produces characteristic signs.

Chest wall

Ensure that the patient is adequately undressed and comfortable. Inspect the chest, front and back.

· Does it look normal? Pectus excavatum is very obvious but usually of no significance except that it may cause an innocent systolic murmur.

· Observe the pattern of breathing.

· Does it look hyperinflated?

· Does it move normally?

· In small children with airways obstruction, the chest is indrawn on inspiration. Children with respiratory trouble often have a very fast respiratory rate.

· Is there any asymmetry of movement?

· Sometimes a parasternal heave of right ventricular hypertrophy is visible.

· Are there any scars? Confirm what they indicate. There may have been resection of a lung or drainage of an empyema.

· Does the spine look normal. There may be kyphosis or scoliosis. If there is any doubt, run your finger along the spine. It is often easier to feel than to see an abnormal curve.

Tactile examination and percussion

· The patient may feel hot if he is pyrexial (acute infection).

· You have already inspected for asymmetry of movement but grasp both sides of the chest and ask the patient to take a big breath right in then right out. It is often easier to feel asymmetry than to see it.

· If the chest seems overinflated and does not move much, pass a tape measure around the chest. This should be at nipple level in a man but it may be easier to pass under the breasts in a women. Ask for a deep breath in and then right out. The difference in chest circumference should be at least 5cm. Expansion may also be limited in diseases such as ankylosing spondylitis.

· Use the index finger to feel the trachea. Does it feel central or is it deviated?

· Also feel for the apex beat of the heart. It will be displaced if the mediastinum is displaced or distorted.

· Now percuss the chest. It is usual to use the middle finger of the dominant hand to do this. The clavicle is percussed directly, usually about a third of the way between the sternum and the acromium. The rest of the chest is percussed by placing the non-dominant hand on the chest and using the dominant middle finger to tap the other middle finger over the middle phalanx. Percuss over all the lobes of the lung, front and back except that the middle lobe does not have surface anatomy on the back. Percuss over the heart. In hyperinflation there is loss of cardiac dullness.

· A very resonant sound suggests hyperinflation or a pneumothorax. A dull sound is easier to distinguish from normal. It may suggest collapse or consolidation. It may suggest fluid. It may be possible to tap out the margins of dullness. It is suggested that an effusion rises up into the axilla laterally whilst with collapse the dullness sinks down laterally. This is not a reliable sign.

· To assess tactile vocal fremitus, use the medial side of the hand, by the hypothenar eminence with the palms facing upwards. Place it at various levels over the back, each time asking the patient to say,"Ninety-nine". Note how the sound is transmitted to the hand.

Auscultation

It is now time to use the stethoscope placing the diaphragm lightly on the chest.

· Listen to the heart in the 4 standard places for the 4 valves as described in examination of the cardiovascular system. Severe lung disease may cause pulmonary hypertension and a loud P2. Agallop rhythm will suggest heart failure. This brief examination of the heart is to exclude cardiac disease as a cause of the respiratory symptoms. This is usually conducted quite briefly with the patient sitting up when attention is on the respiratory system, ignoring the full technique forauscultation of the heart, such as having the patient lying on his left side to hear the mitral valve and sitting forward in full expiration for the aortic valve.

· Place the stethoscope over each of the 5 lobes of the lungs in turn, on the front of the chest and ask the patient to take a deep breath in and out. Do the same over 4 lobes of the back and also over the bases of the lungs.

· If there are rales over the bases, ask the patient to cough or take a few deep breaths to see if they disappear. If they do, they can be dismissed as atelectasis from sitting still or lying down and it is of no consequence.

· Bronchial breathing is when sounds are harsh and poor in nature. Unlike normal vesicular breath sounds, there is a gap between the inspiratory and expiratory phase sounds.

· Some people test vocal fremitus with the stethoscope rather than the hand. Place the stethoscope at various levels over the back and ask the patient to whisper "ninety-nine" each time. Note how well the sound is transmitted.

· Another sign that is often overlooked in these days of ready access to imaging, is whispering pectoriloquy It is elicited as for vocal fremitus but ask the patient to whisper "one, two three."

Peak flow

It may be debated if peak flow measurement is part of examination or investigations but as most GPs carry a mini Wright's peak flow meter in their cases, it may be seen as a tool for examination, as is the ophthalmoscope, auriscope or stethoscope. A smaller, lower reading version may be required for children or adults with severe airways obstruction.

Take 3 readings and record the highest figure. If they are rising significantly each time then take a 4th as the patient is getting used to correct use of the instrument. Peak flow will be significantly reduced in asthma and COPD but may be remarkably normal in restrictive lung disease such as pulmonary fibrosis.

Normal values for peak flow are taken from a chart. They vary with height, age and sex of the patient.

Interpretation of physical signs

Eliciting the signs is of very limited value without being able to interpret them too.

Inspection

· Central cyanosis means that there is at least 5g of deoxygenated haemoglobin per 100 ml of blood. It tends to imply severe hypoxia but it occurs more readily with polycythaemia and is rare with anaemia.

· An overinflated chest implies COPD and premature airways closure. It may also occur in severe acute asthma. The patient breathes out through pursed lips to raise the pressure in the airways to reduce premature closure.

· If expansion is asymmetrical, the abnormality is on the side that moves less. This may be pneumothorax, collapse, consolidation or effusion.

· Clubbing tends to be particularly severe in lung cancer.

Tactile signs

· The trachea is deviated away from pneumothorax and effusion and towards collapse and consolidation.

· Dull percussion is heard over collapse, consolidation and effusion. It is hyper-resonant over a pneumothorax.

· Tactile vocal fremitus is increased over areas of consolidation and decreased or absent over areas of effusion or collapse.

Auscultation

· Normal breath sounds are called vesicular. They are sometimes described as quiet and gentle like the sound of a breeze rippling through the leaves of a tree.

· Rhonchi are wheezes. They are a musical sound heard on expiration. In severe cases they may be both inspiratory and expiratory. They imply narrowing of the airways so that turbulent flow occurs. Whether with air or with blood, laminar flow is silent but turbulent flow makes a sound. Turbulent flow is responsible for heart sounds, whether a murmur or the normal closure of a valve. If rhonchi are purely inspiratory and not expiratory, it may suggest that obstruction is outside the thoracic cavity. Perhaps there is a foreign body in the upper airways or disease of the larynx or vocal cords. The loudness of rhonchi gives no indication of the severity of the condition. Severe asthma is too tight to wheeze.

· Rales are sometimes called crackles. They probably represent opening of small airways and alveoli. As mentioned above, they may be normal at the lung bases if they clear on coughing or a few deep breaths. Basal rales are a classical feature of pulmonary congestion with left ventricular failure. They may be more diffuse in pulmonary fibrosis.

· Bronchial breathing suggests consolidation or fibrosis. The sounds of bronchial breathing are generated by turbulent air flow in large airways and similar sounds can be heard in healthy patients by listening over the trachea. The sounds are not normally conducted to the chest wall because they are attenuated by air filled alveoli and lung parenchyma. Consolidation or fibrosis permits the sound of air flow in the bronchi to be conducted more effectively to the chest.

· Whispering pectoriloquy is the increased quality and loudness of whispers that are heard with a stethoscope over an area of lung consolidation.

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Internet and further reading

· Introduction to the Symptoms and Signs of Clinical Medicine: A Hands-on Guide to Developing Core Skills. David Gray (Editor), Peter Toghill (Editor) Hodder Arnold 2000

· Chamberlain's Symptoms and Signs in Clinical Medicine: An Introduction to Medical Diagnosis. by E.Noble Chamberlain, Colin Ogilvie, Christopher C. Evans. Hodder Arnold 1997

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