RESPIRATORY

SYSTEM Dr.Srinath.Chandramani

RESPIRATORY SYSTEM : AN APPROACH

Respiratory system is one of the vital systems in the human body which has been extensively studied. The basic functions of the

system are :

Exchange of gases : oxygen and carbon-di-oxide,

Filtering of inhaled pathogens and pollutants.

Anatomy :

The respiratory system can be divided into following anatomical

levels :

Upper respiratory tract

Airway

Parenchyma

Interstitium

Pleura

Mediastinum

Pulmonary vasculature

Diagphragm

Anatomy Ctd Upper respiratory tract consists of Nose, Turbinates, Paranasal sinuses,

pharynx, Tonsils.

Their functions are : Filtering the inhaled air, adding timbre to voice,

first line Immunity.

Airway extends from the larynx to the terminal bronchiole.

It constitutes the anatomical dead space. (about 150ml)

Parenchyma Lung are divided into bronchopulmonary segments.

BPS are 10 on each side. Lingula split into Superior and Inferior.

While on right side the middle lobe is split into medial and lateral.

Interstitium consists of alveoli, alveoli membrane, fibrous connective

tissue & capillary network.

Pleura consists of the Parietal and the visceral pleura.

Anatomy Ctd Mediastinum is the region between the pleural sacs.

It is separated into three compartments.

The anterior mediastinum extends from the sternum anteriorly to the

pericardium and brachiocephalic vessels posteriorly. It contains the

thymus gland, the anterior mediastinal lymph nodes, and the internal

mammary arteries and veins.

The middle mediastinum lies between the anterior and posterior

mediastina and contains the heart; the ascending and transverse

arches of the aorta; the venae cavae; the brachiocephalic arteries

and veins; the phrenic nerves; the trachea, main bronchi, and their

contiguous lymph nodes; and the pulmonary arteries and veins.

The posterior mediastinum is bounded by the pericardium and

trachea anteriorly and the vertebral column posteriorly. It contains the

descending thoracic aorta, esophagus, thoracic duct, azygos and

hemiazygos veins, and the posterior group of mediastinal lymph

nodes.

Anatomy Ctd Lymphatic drainage :

Whole of right lung and left lower lobe to right supraclavicular

nodes.

Left upper lobe to the left supraclavicular nodes

Parietal pleura to the axillary lymph nodes.

Surface anatomy

The apices of both the lungs rise 2-3 cms above the clavicles

The margins of the lung are on 6th ICS in the MCL. 8th rib at the mid

axillary line.

10th rib at the scapular line and the paravertebral line at D10

vertebrae.

The pleural border is 2 spaces lower than corresponding lung margin

i.e. 8th space in MCL, 10th in Mid axillary line and D12 at the scapular

and vertebral line.

Physiology The primary functions of the respiratory system are to remove the

appropriate amount of CO2 from blood entering the pulmonary

circulation and to provide adequate O2 to blood leaving the

pulmonary circulation.

For these functions to be carried out properly, there must be :

1. adequate provision of fresh air to the alveoli (ventilation),

2. adequate circulation of blood through the pulmonary vasculature

(perfusion),

3. adequate movement of gas between alveoli & pulmonary

capillaries (diffusion),

4. appropriate contact of alveolar gas and pulmonary capillary blood

(ventilation-perfusion matching).

Symtomatology Cough : may indicate the presence of lung disease, but cough

per se is not useful for the differential diagnosis.

Types of cough :

1. Dry cough pleural, ILD and Mediastinal diseases

2. Productive cough Airway and Parenchymal disorders

3. Short cough URTI

4. Brassy cough external tracheal compression

5. Bovine cough Recurrent laryngeal n. palsy

6. Barking Epiglottic lesions/ hysteria.

Nocturnal cough :

PND,Post nasal drip, Chronic bronchitis, asthma, GERD,

Tropical Eosinophilia.

Drug Induced cough - ACEI

Sputum The presence of sputum accompanying the cough often

suggests airway disease and may be seen in asthma, chronic

bronchitis, or bronchiectasis.

Normal Bronchial secretion 60-100ml/day.

> 100ml is bronchorrhea .

Saliva contains Squamous cells. Sputum contains Epithelial cells.

Copious Sputum :

Bronchiectasis

Lung Abcess

Necrotising Pneumonia

Alveolar cell carcinoma ( large amount of colourless sputum)

Colour of Sputum

Green or Yellow Bacterial Myeloperoxidase

Black Coal miners pneumoconiosis

Rusty Pneumococcal pneumonia

Red currant jelly Klebsiella

Pink frothy Pulmonary edema

Blood stained Kochs

Anchovy sauce Amoebic liver abscess

Hemoptysis Hemoptysis : can originate from disease of the airways, the

pulmonary parenchyma, or the vasculature.

Frank hemoptysis only blood Bronchogenic carcinoma

Spurious hemoptysis above level of larynx.

Pseudo hemoptysis Coloured pigment Serratia marcescens gram negative bacteria

Endemic hemoptysis Paragonimus westermani infection (lung fluke )

Mild < 100ml /day. Moderate/severe 500 mL over a 24-h period,

or >150ml/hr,

or >100ml for continous 3 days, or requiring transfusion.

Although the patients estimation of the amount of blood is

notoriously unreliable.

Physical signs

Pulse to Respiratory rate ratio : 1:4

Clubbing

Tracheal Shift : Trailes sign.

Pull of trachea Fibrosis, Collapse.

Push of trachea Consolidation, hyperinflation, pleural effusion, hemothorax and malignancy.

No change in Bronchiectasis, ILD

Tracheal tug Ollivers sign Aortic arch aneurysym, Mediastinal tumour attached to aortic arch

Traubes Space Quadrilateral. Tympanic.

Normal chest expansion 5 cms.

Cracked pot resonance over large cavity.

CHEST RADIOGRAPHY Chest radiography is often the initial diagnostic study

performed to evaluate patients with respiratory symptoms,

but it can also provide the initial evidence of disease in

patients who are free of symptoms.

Steps in reading a chest x ray

AP vs PA view

Exposure and centralisation

Bony thorax

Cardio-pulmonary ratio

Cardiac shadow

Lung fields

Diagnostic possibilities based on

radiographic pattern.

A localized region of opacification involving the pulmonary

parenchyma can be described as a nodule (usually 3 cm in diameter), or an infiltrate.

Diffuse disease with increased opacification is usually characterized

as having an alveolar, an interstitial, or a nodular pattern.

In contrast, increased radiolucency can be localized, as seen with a

cyst or bulla, or generalized, as occurs with emphysema.

The chest radiograph is also particularly useful for the detection of

pleural disease, especially if manifested by the presence of air or liquid in the pleural space.

(Role of lateral Decubitus X-ray)

An abnormal appearance of the hila and/or the mediastinum can

suggest a mass or enlargement of lymph nodes.

SOLITARY PULMONARY NODULE

It is defined as a circumscribed nodular density within the lung

parenchyma < 3cm in size.

(anything bigger is called a Mass). It is asymptomatic by definition.

Often occurs as an incidental finding on X-ray or CT, may represent a

benign, asymptomatic process to a life threatening malignancy.

Differential diagnosis : Granuloma : TB, Histoplasma

Primary lung cancer

Metastatic lung cancer

Bronchial adenoma

Lymphoma

Benign hamartoma, Lipoma

Arterio-venous malformation

Wegeners disease

Rheumatoid nodule

Amyloidosis

Bronchogenic cyst

Pulmonary infarction.

Solitary Pulmonary nodule Prognosis : Malignant versus Benign

Age : Under 35 2% malignant

35-45 15-20% malignant

Over 45% - 50% malignant

Size : < 1cm 90% are benign

> 2cm 70% are malignant

Stability : Lesions unchanged for 2 years are likely benign.

Calcification : are more likely benign.

50% 5 year survival for cancers presenting as Solitary nodule.

PULMONARY FUNCTION TESTS

The two measurements of lung volume commonly used for

respiratory diagnosis are

(1) total lung capacity (TLC), the volume of gas contained in the

lungs after a maximal inspiration;

(2) residual volume (RV), the volume of gas remaining in the lungs

at the end of a maximal expiration.

The volume of gas that is exhaled from the lungs in going from TLC

to RV is the vital capacity.

Common clinical measurements of airflow are obtained from

maneuvers in which the subject inspires to TLC and then forcibly

exhales to RV.

Pulmonary Function test Three measurements are commonly made from a recording of

forced exhaled volume versus timei.e., a spirogram:

(1)the volume of gas exhaled during the first second of expiration

[forced expiratory volume (FEV)in 1 s, or FEV1],

(2)the total volume exhaled [forced vital capacity (FVC)], and

(3) the average expiratory flow rate during the middle 50% of the VC

[forced expiratory flow (FEF)between 25 and 75% of the VC,

or FEF2575%, also called the maximal midexpiratory flow rate (MMFR).

Lung volumes and capacity

Interpreting PFT Predicted values for a given patient can then be obtained

by using the patients age and height in the appropriate regression equation; different equations are used

depending on the patients race and sex. Because there is some variability among normal individuals, values

between 80 and 120% of the predicted value have

traditionally been considered normal.

The normal value for the ratio FEV1/FVC is approximately

0.75 to 0.80, although this value does fall somewhat with

advancing age. The FEF2575% is often considered a more sensitive measurement of early airflow obstruction, particularly in small airways.

Interpreting PFT Assessing the strength of respiratory muscles is an additional

part of the overall evaluation of some patients with

respiratory dysfunction.

When a patient exhales completely to RV and then tries to inspire maximally against an occluded airway, the pressure

that can be generated is called the maximal inspiratory

pressure (MIP). On the other hand, when a patient inhales to

TLC and then tries to expire maximally against an occluded airway, the pressure generated is called the maximal

expiratory pressure (MEP). In the proper clinical setting, these

studies may provide useful information regarding the cause

of abnormal lung volumes and the possibility that respiratory muscle weakness may be causally related to the lung

volume abnormalities.

Patterns of airway disease

Etiology

PFT - Conclusion

Reversibility is traditionally defined

as a 15% increase in FEV1 after two

puffs of a B-adrenergic agonist.

PEFR (Peak expiratory flow rate) is a

OPD test using a peak-flow meter.

Can be done at home also.

Good for follow-up cases to assess

improvement in lung function with

intervention.

Test 1 1. To qualify as a solitary pulmonary nodule in chest X-ray the size should not exceed....

(A) 3 cm (B) 6 cm

(C) 8 cm (D) 9 cm

2. Spirometry is useful to calculate all the except....

(A) Tidal volume

(B) FEV

(C) Residual volume

(D) Vital capacity

3. A 28-years old woman having limited capacity for the last 10 years complains of shortness of breath for last one month. Her pulmonary function tests are as follows :

PFT Observed Predicted

FVC 2.63 2.82

FEV1 88% 80%

What is the most likely diagnosis in this case

(A) Interstitial lung disease

(B) Pulmonary artery hypertension

(C) Congestive heart failure

(D) Bronchiectasis

Test 1 4. In COPD all are affected except....

(A) FEV

(B) Ratio of FEV to vital capacity

(C) FVC

(D) None

5. In chronic obstructive pulmonary disease all are seen

except....

(A) Low FEV1

(B) Increased FeV1/ VC ratio

(C) Smoking strongly associated

(D) Partially reversible by bronchodilator

therapy

Test 1 6. For diagnosis of obstructive airway disease which of the following

measurement is usual ?

(A) Vital capacity

(B) Timed vital capacity

(C) Tidal volume

(D) Blood gas analysis

7.. In restrictive lung disease....

(A) FVC is high. (B) FEV1 is high

(C) FEV1/FVC is high. (D) All of the above

8. Pulmonary wedge pressure correspond to

(A) Right Atrial pressure

(B) Right ventricular pressure

(C) Left atrial pressure

(D) Left ventricular pressure

Test 1 9. Swan-Ganz catheter is used to measure

(A) Right atrial flow

(B) Pulmonary capillary pressure

(C) Central venous pressure

(D) Right ventricular pressure

10. A patient presents with decreased vital capacity and total lung volume. What is most probable diagnosis?

(A) Bronchiectasis (B) Sarcoidosis

(C) Cystic fibrosis (D) Asthma

11. Total minute volume of normal lung is

(A) 2 L (B) 4 L

(C) 4.5 L (D) 7 L

12. Therapeutic oxygen therapy is not useful in

(A) TOF

(B) Interstitial lung disease

(C) Acute pulmonary edema

(D) Anaemia hypoxia

Test 1 13. The blood gas parameters: pH - 7.58, pCO2 23 mm Hg PO3 300

mm Hg and oxygen saturation 60% are most consistent with.....

(A) Carbon monoxide poisoning

(B) Ventilatory malfunction

(C) Voluntary hyperventilation

(D) Methyl alcohol poisoning

14. Alveolar arterial O2 gradient is increased in all except....

(A)nterstitial fibrosis

(B) Right to left shunt

(C) Cryptogenic fibrosing alveolitis

(D) Hypoventilation

Test 1 15. Best position to reveal small pleural

effusions on chest X-ray is.....

(A)APview

(B)PA view

(C) Lateral view

(D)Lateral decubitus view

16.. Best view to demonstrate right pleural

effusion in chest X-ray is....

(A) Right lateral decubitus

(B) Left lateral decubitus

(C)Prone

(D)Supine

Asthma and Airway disorders Introduction :

Asthma is defined as a chronic inflammatory disease of

airways that is characterized by increased responsiveness

of the tracheobronchial tree to a multiplicity of stimuli.

Epidemiology :

Bronchial asthma occurs at all ages but predominantly in

early life.

About one-half of cases develop before age 10, and

another third occur before age 40. Elderly onset is

unlikely.

In childhood, there is a 2:1 male/female preponderance,

but the sex ratio equalizes by age 30.

EOSINOPHILS

Eosinophils are metabolically very active.

Contain Toxic protein (Major Basic

Protein), Histaminases, etc. which

inactivate Mast cell products.

They are attracted by factors released by

T-cells, Mast cells and Basophils. They aid

in defences against worms, Schistosoma

and implicated in Asthma.

Mast cell series

They contain granules which are inflammatory

and chemotactic mediators.

All have receptors for IgE and are degranulated

when an allergen cross links to specific IgE

molecules bound to the surface of the cell.

Mast cells and Basophils are involved in Parasite

immunity, Allergic reactions and Delayed

Hypersensitivity reactions.

Special types Drug-induced asthma : Aspirin induced asthma is a triad of

asthma, nasal polyps and aspirin sensitivity. It is potentially life

threatening.

Exercise induced asthma : pathophysiology unexplained.

Increased vagal tone may contribute. Inhaled bronchodilators pre-exercise is the treatment.

Gastric-asthma : induced due to regurgitation of food.

Treatment is by anti-reflux therapy.

Nocturnal asthma : is defined as an overnight fall of more than 20% in theFEV1. It is presumed to be due to :

early morning fall in adrenaline/sympathetic tone.

Increased vagal; tone in the morning

Airway cooling at night

Circadian cortisol rhythm (fall in early morning)

Clinical presentation

Episodic presentation is most common

Exacerbations are commonly due to infection

(viral most common).

Status asthmaticus : is a medical emergency.

Patient is hypoxic and cyanosed due to severe

bronchospasm. It is characterized by :

Tachycardia - >120/min

Tachypnoea > 30/min

Pulsus paradoxus

Altered sensorium and

Inspiration to expiration ratio > 1:3 or 1:4.

Life threatening features

Patient unable to speak

Central cyanosis

Altered sensorium

Bradycardia

Silent chest

Unrecordable peak flow

Severe hypoxemia

High CO2 retention

Low pH.

Treatment

Steps Symptoms Nocturnal symptoms

PEFR Short-term relief

Long-term prevention

Step 1 : Intermittent

80% of predicted but

normal in

between attacks

Inhaled B2

agonist short acting.

none

Step 2 : Mild persistent

>1/week but < 1 /day

> 2/month > 80% never normal even

during

asymptomatic period.

Inhaled B2

agonist short acting. SOS

Inhaled

corticosteriod

Step 3 :

Moderate persistent

Daily

attacks.

Functional impairment

> 1/week >60% 30%

Inhaled B2

agonist shortacting.

not to exceed 3-4/day

Inhaled

corticosteroi

d LABA

Step 4 :

Severe persistent

Continuous

Limited activity

Frequent < 60% of predicted with variability > 30%

Inhaled B2

agonist shortacting.

not to exceed 3-4/day

Inhaled

corticosteroi

d

LABA Oral steriods

Drugs Short acting B2 agonists : Salbutamol. Terbutaline.

LABA : long acting B2 agonist : Salmeterol, Formeterol

Inhaled corticosteroid : Budesonide, Beclomethasone

Methyl-xanthines : Theophylline, Doxiphylline.

Mast-cell inhibitors : Sodium Chromoglycate

Anti-Leukotrienes : Montelukast

Indications for assisted ventilation :

Coma

Respiratory arrest

Exhaustion, Altered sensorium

Deterioration in ABG despite therapy.

BRONCHIECTASIS DEFINITION : Bronchiectasis is an abnormal and permanent

dilatation of bronchi. It may be either focal, involving airways

supplying a limited region of pulmonary parenchyma, or

diffuse, involving airways in a more widespread distribution.

PATHOLOGY The bronchial dilatation of bronchiectasis is

associated with destructive and inflammatory changes in the

walls of medium-sized airways, often at the level of segmental

or subsegmental bronchi. The normal structural components

of the wall, including cartilage, muscle, and elastic tissue, are

destroyed and may be replaced by fibrous tissue. The dilated

airways frequently contain pools of thick, purulent material,

while more peripheral airways are often occluded by

secretions or obliterated and replaced by fibrous tissue.

BRONCHIECTASIS CLASSIFICATION : Three different patterns of bronchiectasis

were described by Reid.

In cylindrical bronchiectasis the bronchi appear as uniformly

dilated tubes that end abruptly at the point that smaller airways are obstructed by secretions.

In varicose bronchiectasis the affected bronchi have an

irregular or beaded pattern of dilatation resembling varicose veins.

In saccular (cystic) bronchiectasis the bronchi have a

ballooned appearance at the periphery, ending in blind sacs without recognizable bronchial structures distal to the sacs.

BRONCHIECTASIS Kartageners syndrome, in which situs inversus

accompanies bronchiectasis and sinusitis.

In Cystic fibrosis the tenacious secretions in the bronchi

are associated with impaired bacterial clearance, resulting

in colonization and recurrent infection with a variety of organisms, particularly mucoid strains of P. aeruginosa but

also S. aureus, H.influenzae, Escherichia coli, and

Burkholderia cepacia.

Noninfectious Causes Some cases of bronchiectasis are

associated with exposure to a toxic substance that incites

a severe inflammatory response. Examples include

inhalation of a toxic gas such as ammonia or aspiration of acidic gastric contents, though the latter problem is often

also complicated by aspiration of bacteria.

BRONCHIECTASIS

An immune response in the airway may also

trigger inflammation, destructive changes, and

bronchial dilatation. This mechanism is

presumably important for bronchiectasis with

allergic bronchopulmonary aspergillosis (ABPA).

In the yellow nail syndrome, which is due to

hypoplastic lymphatics, the triad of

lymphedema, pleural effusion, and yellow

discoloration of the nails is accompanied by

bronchiectasis in approximately 40% of patients.

ABPA MAIN DIAGNOSTIC CRITERIA

Bronchial asthma

Pulmonary infiltrates

Peripheral eosinophilia (_>1000/_L)

Immediate wheal-and-flare response to A. fumigatus

Serum precipitins to A. fumigatus

Elevated serum IgE

Central bronchiectasis

OTHER DIAGNOSTIC FEATURES

History of brownish plugs in sputum

Culture of A. fumigatus from sputum

Elevated IgE (and IgG)class antibodies specific for A.

fumigatus

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) has been defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as

a disease state characterized by airflow limitation that is not fully

reversible.

COPD includes :

emphysema, an anatomically defined condition characterized by

irreversible destruction and enlargement of the lung alveoli;

chronic bronchitis, a clinically defined condition with chronic cough

with expectoration for most days for atleast 3 months a year for 2

consecutive years.

small airways disease, a condition in which small bronchioles are

narrowed.

COPD is present only if chronic airflow obstruction occurs; chronic

bronchitis without chronic airflow obstruction is not included within

COPD.

RISK FACTORS FOR DEVELOPMENT OF COPD ARE :

Cigarette Smoking

Airway Responsiveness

Respiratory Infections

Occupational Exposures

Ambient Air Pollution

Passive, or Second-Hand, Smoking Exposure

GENETIC : Alpha-1 Antitrypsin deficiency.

Pathophysiology : is mainly chronic airway inflammation, infections and repair based.

Proteases Anti-protease hypothesis explains the balance between the damage done by inflammatory markers and the repair of the tissue.

FEATURES PREDOMINAN-EMPHYSEMA

PREDOMINANT BRONCHITIS

AGE OF ONSET 6TH DECADE 5TH DECADE

COUGH AFTER BREATHLESSNESS

BEFORE BREATHLESSNESS

SPUTUM SCANTY COPIOUS, PURULENT

INFECTIONS LESS COMMON COMMON

RESPIRATORY DISTRESS OFTEN TERMINAL EPISODIC

CXR HYPERINFLATION INCREASED BVM

CYANOSIS TERMINAL COMMON

PULMONARY HYPERTENSION

MILD MODERATE/SEVERE

COR PULMONALE LATE EARLY

COPD Patients with predominant emphysema are classically

referred to as pink puffers, a reference to the lack of cyanosis, the use of accessory muscles, and pursed-lip

breathing. Such patients also have a dramatic decrease

in breath sounds throughout the chest.

Patients with a clinical syndrome of chronic bronchitis are

classically labeled blue bloaters, a reference to fluid retention and more marked cyanosis.

Advanced disease may be accompanied by systemic

wasting, with significant weight loss, bitemporal wasting,

and diffuse loss of subcutaneous adipose tissue. Such

wasting is an independent poor prognostic factor in

COPD.

COPD Ctd.. Some patients with advanced disease have

paradoxical inward movement of the rib cage with

inspiration (Hoovers sign), the result of alteration of the vector of diaphragmatic contraction on the rib cage as

a result of chronic hyperinflation.

Signs of overt right heart failure, termed cor pulmonale,

are relatively infrequent since the advent of

supplemental oxygen therapy.

Clubbing of the digits is not a sign of COPD, and its

presence should alert the clinician to initiate an

investigation for causes of clubbing viz malignancy.

Pneumonia Pneumonia can be broadly categorized as community-acquired or

hospital-acquired (nosocomial).

Based on pattern of lung involvement they are classified as : Lobar,

Broncho, Interstitial or Miliary.

Etiology of pneumonia :

For pneumonia to occur, a potential pathogen must reach the lower

respiratory tract in sufficient numbers or with sufficient virulence to

overwhelm host defenses.

Possible routes include gross aspiration, microaspiration, aerosolization,

hematogenous spread from a distant infected site, and direct spread

from a contiguous infected site.

By far the most common route for bacterial pneumonia is

microaspiration of oropharyngeal secretions colonized with pathogenic

microorganisms.

Etiological agent : Streptocoocus pyogenes.

Management Prognosis and clinical grading :

The single most useful clinical sign of the severity of pneumonia is a

respiratory rate of > 30/min in a person without underlying lung

disease.

British Thoracic Society Rule for Definition of Severe Community-Acquired Pneumonia ( CURB)

Confusion

Urea: _7 mmol/L

Respiratory rate: _30/min

Blood pressure: diastolic _60 mmHg or systolic _90 mmHg

If none of these features is present, the mortality rate is 2.4%; with one

feature, the mortality

rate is 8%; with two, 23%; with three, 33%; and with all four, 83%.

The mortality rate is highest (_50%)for pneumonia due to P.

aeruginosa, followed by the rates for Klebsiella spp., E. coli, S. aureus,

and Acinetobacter spp. (all 30 to 35%).

PULMONARY COMPLICATIONS OF PNEUMONIA

necrotizing pneumonia,

formation of abscesses,

vascular invasion with infarction,

cavitation, and

extension to the pleura with empyema or bronchopleural fistula.

Complications of mechanical ventilation and supplemental oxygen administration.

In patients with severe damage, tissue repair may lead to fibrosis with various anatomical distributions, such as organizing pneumonia, bronchiolitis obliterans, and pleural adhesions.

TEST 2 17. All of the following statements regarding mast cells are true except...

(A) They contain heparin proteoglycan

(B) Their number is increased in patients with bronchial asthma.

(C) Disodium cromoglycate brings about their degranulation.

(D) They have receptors for F portion of IgE.

18. True about asthma....

(A) Increasing incidence day by day.

(B) Allergic asthma common in older patient

(C) Increase in IgE in idiosyncratic asthma

(D) Bronchodilatation

19. Major basic protein is produced by

(A) Basophils (B) Monocytes

(C) Eosinophils (D) Mast cells

TEST 2 20. Charcot -Leyden crystals are derived from...

(A) Eosinophils

(B) Basophils

(C) Neutrophils

(D) Bronchial goblet cells

21. Exercise induced asthma is not precipitated by...

(A) High altitude climb and exercise

(B) Cycling in cold weather

(C) Swimming in hot water

(D) Swimming in cold water

22. Central cyanosis is not seen with A/E

(A) Below 5 gm/100 ml reduced haemoglobin

(B) Pulmonary aspergillosis

(C) Bronchial Asthma

(D) Congenital pulmonary stenosis

TEST 2 23. Which of the following durgs are used in

bronchial asthma?

(A) Isoprenaline (B) Salbutamol

(C) Aminophylline

(D) All of the above.

24. Which a2 agonist is not given for acute

bronchial asthma?

(A) Salbutamol (B) Terbutaline

(C) Salmeterol (D) Methyl xanthine

25. Drug of choice in asthma with heart disease is...

(A) Rimiterol

(B) Terbutaline (C) Ipratropium

(D) Cromolyn sodium

TEST 2 26. Zileuton is... (A) 5 lipo oxygenase inhibitor

(B) TX A2 inhibitor (C) Leukotriene receptor antagonist (D) Lymphocyte inhibitor 27. Use of disodium cromoglycate as a

preventive measure has been found to be of value in (A) Intrinsic asthma (B) Excercise induced asthma (C) Chronic bronchitis (D) Famer's lung

28. All of the following are useful for treating acute bronchial asthma in children except.... (A) 100% oxygen (B) Hydrocortisone infusion

(C) IV aminophylline (D) Sodium chromoglycate inhalation

Interstitial lung diseases The interstitial lung diseases (ILDs) represent a large number of conditions that involve the parenchyma of the lungthe

alveoli, the alveolar epithelium, the capillary endothelium, and the spaces between these structures, as well as the perivascular and lymphatic tissues.

Approach to classification is to separate the ILDs into two groups based on the major underlying histopathology:

those associated with predominant inflammation and fibrosis, and

those with a predominantly granulomatous reaction in interstitial or vascular areas.

Each of these groups is further subdivided according to whether the cause is known or unknown.

Sarcoidosis, idiopathic pulmonary fibrosis (IPF), and pulmonary

fibrosis associated with CTDs are the most common ILDs of unknown etiology.

ILD Among the ILDs of known cause, the largest group

comprises occupational and environmental

exposures, especially the inhalation of inorganic

dusts, organic dusts, and various fumes or gases.

PATHOGENESIS : The ILDs are nonmalignant

disorders and are not caused by identified

infectious agents. The precise pathway(s)

leading from injury to fibrosis is not known.

IDIOPATHIC PULMONARY FIBROSIS

IPF is the most common form of idiopathic interstitial pneumonia.

Clinical Manifestations Exertional dyspnea, a nonproductive cough, and inspiratory crackles with or without digital clubbing may be present on

physical examination.

The HRCT lung scans typically show patchy, predominantly basilar, subpleural reticular opacities, often associated with traction bronchiectasis and honeycombing.

Pulmonary function tests often reveal a restrictive pattern.

Lung biopsy is confirmatory.

TREATMENT : The clinical course is variable, with a 5-year survival rate of 20 to 40% after diagnosis. Treatment options include glucocorticoids, cytotoxic agents (e.g., azathioprine, cyclophosphamide), and antifibrotic

agents (e.g., colchicine, pirfenidone, or interferon gamma-1b), alone or in combination with glucocorticoids.

IPF has a distinctly poor response to therapy and prognosis.

Because of the poor prognosis in untreated patients, a therapeutic trial

may be tried.

Lung transplantation should be considered for those patients who experience progressive deterioration despite optimal medical management.

ACUTE INTERSTITIAL PNEUMONIA (HAMMAN-RICH SYNDROME)

AIP is a rare, fulminant form of lung injury characterized histologically by diffuse alveolar damage on lung biopsy. Most patients are older than 40 years.

The onset is abrupt in a previously healthy individual. A prodromal illness, is common.

Diffuse, bilateral, air-space opacification is present on chest radiograph.

HRCT scans show bilateral, patchy, symmetric areas of ground-glass attenuation.

The diagnosis of AIP requires the presence of a clinical syndrome of idiopathic ARDS and pathologic confirmation of organizing diffuse alveolar damage.

Therefore, lung biopsy is required to confirm.

Most patients have moderate to severe hypoxemia and develop respiratory failure.

Mechanical ventilation is often required.

The mortality rate is high (_60%), with most patients dying within 6 months of presentation. Recurrences have been reported. However, those who recover often have substantial improvement in lung function. The main treatment is supportive. Glucocorticoid therapy is of no proven value.

ACUTE RESPIRATORY DISTRESS SYNDROME

ARDS is the most severe form of lung injury. It is diagnosed by following criteria :

Bilateral diffuse alveolar infiltrates on chest X-ray.

PaO2/FiO2 ratio

ACUTE RESPIRATORY DISTRESS SYNDROME

Inciting agent

Generalised pulmonary inflammation

Increased pulmonary vascular permeability

Interstitial edema

Alveolar consolidation and atelectasis.

ARDS Clinical features :

Sudden onset pulmonary infiltrates with hypoxemia and extreme VQ

mismatch.

Tachypnoea, Dysnoea, Diffuse crackles/rhonchi

Rapid respiratory failure requiring ventilation.

Severe hypoxemia poorly responding to oxygen

High peak airway pressure.

Treatment ;

Mechanical ventilation is the mainstay of treatment.

High PEEP and low tidal volume (6ml/kg) is the ideal setting for ARDS

Supportive measures and treatment of underlying cause if any.

Prognosis : in best centres, mortality is 40-60%.

Hypersensitivity pneumonitis

Hypersensitivity pneumonitis (HP), or extrinsic allergic

alveolitis, is an inflammatory disorder of the lung,

involving alveolar walls and terminal airways, that is

induced by repeated inhalation of a variety of organic

agents by a susceptible host.

The diagnosis of HP requires a constellation of clinical,

radiographic, physiologic, pathologic, and immunologic

criteria, each of which is rarely pathognomonic alone,

and the preferred treatment is avoidance of the

causative antigen.

Monday Morning Heaviness is pathognomic sign of Cotton-workers disease.

Hypersensitivity pneumonitis

Disease Antigen Source of Antigen

Bagassosis --- Thermophilic actinomycetesa --- Moldy bagasse (sugar cane)

Bird fanciers lung----Parakeet, pigeon, chicken---Avian droppings

Coffee workers lung --- Coffee bean dust----Coffee beans

Compost lung --- Aspergillus --- Compost

Detergent workers --- Bacillus subtilis enzymes---Detergent

Familial HP --- Bacillus subtilis ---Contaminated wood dust

in walls

Farmers lung ---Thermophilic actinomycetes ---Moldy hay, grain, Silage

Cigarrete Factories --- Aspergillus species

Pulmonary infiltrates with Eosinpophilia

Known Etiology : Allergic bronchopulmonary

mycoses (ABPA), Parasitic infestations, Drug

reactions, Eosinophilia-myalgia syndrome.

Idiopathic : Loefflers syndrome, Acute eosinophilic pneumonia, Allergic granulomatosis of Churg and

Strauss, Hypereosinophilic syndrome.

ABPA : is an important differential for bronchial

asthma.

CYSTIC FIBROSIS Cystic fibrosis is an autosomal recessive genetic disorder. Incidence in whites >> blacks >> Asians

Etiology : Caused by a defect in the cystic fibrosis

transmembrane receptor (CFTR) protein which results in defective ion transport in the exocrine gland.

In the lungs, abnormal sodium and chloride transport causes

thick, poorly cleared mucous, resulting in chronic bacterial

colonization and recurrent infections.

Chronic inflammation impairs lung function, eventually resulting in respiratory failure.

Thickened secretion in the pancreas result in retention of

pancreatic enzymes with eventual destruction of the pancreas

and steatorrhea.

Cystic Fibrosis Clinical features :

1. Pulmonary : a. chronic cough b. purulent sputum c. wheezing

d. chronic sinusitis e. recurrent pneumonia

f. Pneumothorax g. clubbing h. Nasal polyps

i. hemoptysis

Commonest Infective agent is Pseudomonas followed by S.Pyogenes.

2. Gastrointestinal : a. pancreatic insufficiency (90%)

b. Protein/Fat malabsorption

c. Diabetes mellitus (10%)

d. Obstruction/Intususception

e. Biliary stasis

3. Reproductive : a. Sterility in males (95%) and 20% in females.

Cystic Fibrosis Chilhood presentation : Meconium ileus, recurrent LRTI, cachexia.

Adult presentation is chronic/recurrent sinusitis.

Diagnosis :

Clinical symptoms plus sweat chloride >80mEq in adults.

Treatment :

Antibiotics inhaled during exacerbation and chronic use.

Mobilisation of chest secretions : Physiotherapy, inhaled

bronchodilators.

Nutritional therapy : increased fat diet, vitamins.

Control of airway inflammation : vaccination and steroids

Gene therapy for definitive cure.

Lung transplant has relatively good results.

Prognosis :

Median survival >30 years. Respiratory failure is cause of death in most

cases.

LUNG CANCER Types :

Cancer of the respiratory epithelium (bronchogenic)

Non-Small cell lung cancer (NSCLC) : 70% of lung cancers, spreads to

regional lymph nodes.

Squamous (30%) : central mass in upper lobes, slow growth, late

metastasis

Adenocarcinoma (30%) : peripheral mass, slow growth, early

metastasis

Large cell (10%) : peripheral mass, early metastasis and early

cavitation.

Small-cell lung cancer (SCLC) : Rapid growth and very early,

widespread mets (70%)

Rare types : Carcinoid, Broncho-alveolar (in non-smokers)

Etiology :

Smoking 90%

Others : Asbestos, pollutants.

Lung Cancer Clinical features :

Pulmonary : cough, hemoptysis, dysnoea, post-obstructive pneumonia, effusion

SVC syndrome : Face and neck edema due to superior vena

cava obstruction

Pancoast tumour : Apical tumour leading to Horners syndrome and arm/shoulder pain due to brachial plexus

involvement.

Horners syndrome : Miosis, Ptosis and anhidrosis

Hoarseness : due to recurrent laryngeal nerve palsy

Extra-thorasic :Anorexia, cachexia, fever, adenopathy and

night sweats

Para-neoplastic syndrome(15%) : SIADH, Eaton-Lambert syndrome, Trosseaus syndrome (hypercoagulability), Ectopic PTH leading to hypercalcemia.

Lung Cancer

Diagnosis : Lung biopsy.

Treatment :

NSCLC : Resection + Chemotherapy. Radiation is

palliative.

SCLC : Responds well to chemotherapy. Radiation +/-

Smoking cessation reduces risk of recurrence.

Prognosis :

NSCLC : Resection effective at stage 1 and 2. But few

are diagnosed at this stage.

SCLC : 80-90% respond to chemotherapy. But problem is

of 90% relapse.

Pancoast Syndrome Pancoast syndrome is caused by either a superior

sulcus tumour (Pancoast tumour) or an infiltrative

disorder e.g. Tuberculosis.

The components of this syndrome are :

Compression of C8, T1,T2 nerve roots resulting in

shoulder and arm pain.

Compression of cervical sympthetic chain and

stellate ganglion producing Horners syndrome

Erosion of adjacent ribs and vertebrae producing

constant chest pain.

PNEUMOTHORAX Pneumothorax is the presence of gas in the pleural space.

Types :

A spontaneous pneumothorax is one that occurs without antecedent

trauma.

A primary spontaneous pneumothorax occurs in the absence of underlying lung disease,

a secondary spontaneous pneumothorax occurs in presence of underlying

disease.

Primary Spontaneous Pneumothorax Primary spontaneous pneumothoraces are usually due to rupture of apical pleural blebs, small cystic spaces that lie within or immediately under the visceral pleura. Primary spontaneous pneumothoraces occur almost exclusively in smokers, which suggests that

these patients have subclinical lung disease.

Approximately one-half of patients with an initial primary spontaneous pneumothorax will have a recurrence. The initial recommended treatment for primary spontaneous pneumothorax is simple aspiration. If the lung does

not expand with aspiration, or if the patient has a recurrent pneumothorax, thoracoscopy with stapling of blebs and pleural abrasion is indicated.

Thoracoscopy or thoracotomy with pleural abrasion is almost 100% successful in preventing recurrences.

PNEUMOTHORAX Secondary Spontaneous Pneumothorax Most secondary

spontaneous pneumothoraces are due to chronic

obstructive pulmonary disease, but pneumothoraces have been reported with virtually every lung disease.

Patients with secondary spontaneous pneumothoraces who

have a persistent air leak, an unexpanded lung after 3 days

of tube thoracostomy, or a recurrent pneumothorax should

be subjected to thoracoscopy with bleb resection and

pleural abrasion.

Traumatic Pneumothorax Traumatic pneumothoraces can

result from both penetrating and nonpenetrating chest

trauma. Traumatic pneumothoraces should be treated with

tube thoracostomy unless they are very small.

Pneumothorax Tension Pneumothorax This condition usually occurs during

mechanical ventilation or resuscitative efforts. The positive pleural

pressure is life threatening both because ventilation is severely

compromised and because the positive pressure is transmitted to

the mediastinum, which results in decreased venous return to the

heart and reduced cardiac output. Difficulty in ventilation during

resuscitation or high peak inspiratory pressures during mechanical

ventilation strongly suggests the diagnosis.

The diagnosis is made by the finding of an enlarged hemithorax with

no breath sounds and shift of the mediastinum to the contralateral

side.

Tension pneumothorax must be treated as a medical emergency. If

the tension in the pleural space is not relieved, the patient is likely to

die from inadequate cardiac output or marked hypoxemia.

A large-bore needle should be inserted into the pleural space

through the second anterior intercostal space. If large amounts of

gas escape from the needle after insertion, the diagnosis is

confirmed. The needle should be left in place until a thoracostomy

tube can be inserted.

VENTILATION DISORDERS Definition : Alveolar hypoventilation exists

by definition when arterial PCO (PaCO )

increases above the normal range of 37 to

43 mmHg, but in clinically important

hypoventilation syndromes PaCO is

generally in the range of 50 to 80 mmHg.

OBESITY-HYPOVENTILATION SYNDROME

Massive obesity represents a mechanical load to the

respiratory system because the added weight on the rib

cage and abdomen serves to reduce the compliance

of the chest wall.

As a result, the functional residual capacity (i.e., end-

expiratory lung volume) is reduced, particularly in the

recumbent posture.

In humans with obesity-hypoventilation syndrome, serum

leptin levels are elevated, suggesting that leptin

resistance may play a role in the pathogenesis of the

disorder.

Hypoventilation syndrome

SLEEP APNEA SYNDROME A syndrome of repetitive periods of apnea (>10sec without air flow)

or hypopnoea during sleep leading to frequent desaturation and

disturbed sleep.

Types :

Obstructive : upper airway soft tissue impedes airway.

Risk factors are : Obesity, Macroglossia, Alcohol, Sedatives,

hypothyroidism, smoking, vocal cord dysfunction and bulbar disease

Central : Absent signal from CNS respiratory centre to breathe.

Sleep apnea occurs in 2% women and 4% men. Most common in

middle aged obese men.

Obstructive sleep apnea (OSA) is more common than central type.

Snoring is often present for years before actual obstruction happens.

Hence snoring alone is not a reason for a full workup.

SLEEP APNEA SYNDROME Clinical features; Loud snoring, restlessness during sleep.

Breath cessation while sleeping

Obesity

Daytime fatigue. Somnolence ,morning sluggishness

Cognitive impairment

Headaches

Impotence

Personality changes

Diagnosis : Polysomnography is diagnostic : include

EEG,ECG,SpO2, airflow and respiratory effort. Positive test has

10 apneac spells per hour lasting at least 10seconds each.

Sleep Apnea Syndrome Treatment :

Avoid alcohol and sedatives

Lose weight

Oral dental prosthesis

Nasal septoplasty if DNS present

Uvulopalatopharyngoplasty

CPAP

Prognosis : Repitative apnea leads to cardiac arrhythmia, Pulmonary hypertension and cor pulmonale

Polycythemia and hyperviscosity syndrome.

Good response to therapy especially nasal CPAP.

Pulmonary Circulation PHYSIOLOGY OF PULMONARY CIRCULATION

The pulmonary vasculature handles the entire output of right

ventricle, i.e. 5 L/min

The normal mean pulmonary artery pressure is 15 mmHg, as

compared to 95 mmHg for the normal mean aortic pressure.

Regional blood flow in the lung is dependent on vascular geometry

and on hydrostatic forces. In an upright person, perfusion is least at

the apex of the lung and greatest at the base.

When cardiac output increases, as occurs during exercise, the

pulmonary vasculature is capable of recruiting previously

unperfused vessels and distending underperfused vessels, thus

responding to the increase in flow with a decrease in pulmonary

vascular resistance.

In consequence, the increase in mean pulmonary arterial pressure

(PAP), even with a three- to fourfold increase in cardiac output, is

small.

CLINICAL CORRELATIONS OF INCREASED PAP Hypoxemia : All diseases of the respiratory system causing hypoxemia are

potentially capable of increasing PVR, since alveolar hypoxia is a very potent

stimulus for pulmonary vasoconstriction. The more prolonged and intense the

hypoxic stimulus, the more likely it is that a significant increase in PVR

producing pulmonary hypertension will result.

Diseases affecting pulmonary vasculature : With diseases directly affecting the pulmonary vessels, a decrease in the cross-sectional area of the

pulmonary vascular bed is primarily responsible for increased PVR, while

hypoxemia generally plays a lesser role.

e.g.1. case of recurrent pulmonary emboli, parts of the pulmonary arterial

system are occluded by intraluminal thrombi originating in the systemic

venous system.

e.g.2. With primary pulmonary hypertension or with pulmonary vascular

disease secondary to scleroderma, the small pulmonary arteries and

arterioles are affected by a generalized obliterative process that narrows and

occludes these vessels. PVR increases, and significant pulmonary

hypertension often results.

PULMONARY HYPERTENSION Pulmonary hypertension is defined as mean artery pressure > 25mm Hg at rest.

Classification :

Primary pulmonary hypertension : No identifiable cause but patients may have increased systemic vasoconstrictors (endothelin-1, Thromboxane A2) and

decreased vasodilators.

Secondary pulmonary hypertension : due to increased pulmonary blood flow, increased vascular resistance ( PTE, Hypoxia), decreased pulmonary venous

drainage (CCF) and decreased cross-section (interstitial disease)

Clinical features :

Fatigue, Breathlessness, Chest pain (secondary to RV ischemia)

Hemoptysis (due to rupture of distended pulmonary vessels)

Hoarseness (recurrent laryngeal nerve compression due to enlarged pulm

artery)

Cor pulmonale.

PULMONARY HYPERTENSION Diagnosis :

Clinical : loud P2, Dull note in pulmonary area, Thrill

i9n pulmonary area.

ECG : RVH, P pulmonale.

2D-ECHO ; is diagnostic,

Treatment :

Treat underlying disorder.

Treatment of cor pulmonale as appropriate.

Vasodilators : Diltiazem, Sildenafil

Lung transplant.

PULMONARY HYPERTENSION Prognosis :

Primary pulmonary hypertension :

usually diagnosed late.

Poor prognosis. Mean survival

PULMONARY THROMBOEMBOLISM

Embolization of the pulmonary vasculature is defined as pulmonary thromboembolism.

Usually it is venous. Rarely it is arterial (paradoxical) through patent foramen ovale(PFO)

Nonthrombotic pulmonary embolism may be easily

overlooked. Possible etiologies include: a. fat embolism after blunt trauma and long bone fractures,

b. tumor embolism,

c. air embolism.

d. Intravenous drug users may inject themselves with a wide

array of substances, such as

hair, talc, or cotton.

e. Amniotic fluid embolism occurs when fetal membranes leak or tear at the placental margin.

PULMONARY THROMBOEMBOLISM

CLINICAL MANIFESTATIONS :

Dyspnea is the most frequent symptom of PE, and tachypnea is its most frequent sign. Whereas dyspnea, syncope, hypotension, or cyanosis indicates a massive PE, pleuritic pain, cough, or hemoptysis often suggests a small embolism located distally near the pleura.

On physical examination, young and previously healthy individuals may simply appear anxious but otherwise seem deceptively well, even with an anatomically large PE.

They may only have dyspnea with moderate exertion.

They often lack classic signs such as tachycardia, low-grade fever, neck vein distention, or an accentuated pulmonic component of the second heart sound.

In older patients who complain of vague chest discomfort, the diagnosis of PE may not be apparent unless signs of right heart failure are present.

PTE DIFFERENTIAL DIAGNOSIS :

Acute coronary syndrome, including unstable angina and acute myocardial infarction

Pneumonia, bronchitis, exacerbation of asthma or COPD

Congestive heart failure

Pericarditis

Pleurisy, including viral syndrome, costochondritis, other musculoskeletal discomfort

Rib fracture, pneumothorax

Primary pulmonary hypertension

Anxiety

PTE Wells Diagnostic Scoring System for Suspected PE

Clinical signs and symptoms of DVT 3.0 An alternative diagnosis is less likely than PE 3.0 Heart rate _100 beats/min 1.5 Immobilization or surgery in the previous 4 weeks 1.5 Previous DVT/PE 1.5 Hemoptysis 1.0 Malignancy (on treatment, treated in the past 6 months) 1.0

The Wells Scoring System has a maximum of 12.5 points. If the score is _ 4 points, the

likelihood of PE is only 8%.

COMPLICATIONS OF PTE : Right Ventricular Dysfunction

Progressive right heart failure is the usual cause of death from PE.

PTE DIAGNOSIS:

Clinical suspicion is of atmost importance.

Serology : D-dimer.

ECG : tachycardia, S1Q1T3 pattern.

CXR: A normal or near-normal chest x-ray in a dyspneic patient suggests PE.

Well-established abnormalities include focal oligemia (Westermarks sign),

A peripheral wedged-shaped density above the diaphragm (Hamptons hump),

or an enlarged right descending pulmonary artery (Pallas sign).

VQ scan

CT pulmonary angiography : is the gold standard of diagnosis.

2D-ECHO will reveal right ventricular dysfunction

Venous Doppler for DVT.

Treatment :

Patients with massive PE present with systemic arterial hypotension and

usually have anatomically widespread thromboembolism.

Primary therapy with thrombolysis or embolectomy offers the greatest

chance of survival.

PTE Those with moderate to large PE have right ventricular hypokinesis on

echocardiography but normal systemic arterial pressure. Optimal

management is controversial; such patients may benefit from

thrombolysis or embolectomy rather than anticoagulation alone.

Patients with small to moderate PE have both normal right heart

function and normal systemic arterial pressure. They have a good

prognosis with either adequate anticoagulation.

Thrombolysis : drug of choice for thrombolysis for PE is

tissue-plasminogen activator (tPa)

Dosage is 100mg over 1 hour.

Urokinase is alternative agent.

Anticoagulation : is done with either Heparin or Low-molecular

weight Heparin.

Warfarin is indicated for longterm anticoagulation.

PTE PREVENTION

Prophylaxis against PE is of paramount importance because

venous- thromboembolism is difficult to detect and poses an

excessive medical and economic burden.

Mechanical and pharmacologic measures often succeed in

preventing this complication. Patients at high risk can receive a combination of mechanical and pharmacologic modalities.

Graduated compression stockings and pneumatic

compression devices may complement mini-dose

unfractionated heparin (5000 units subcutaneously twice or preferably three times daily), low-molecular- weight heparin, a

pentasaccharide or warfarin administration.

Patients who have undergone total hip replacement, total

knee replacement, or cancer surgery will benefit from extended pharmacologic prophylaxis for a total of 4 to 6

weeks, especially with low-molecular-weight heparin.

TEST 3 29. Farmer's lung is caused by exposure to.....

(A) Cryptostroma corticale

(B) Asperigullus

(C) Thermophilic actinomycetes

(D) Grain dust

30. The typical feature of interstitial lung

disease is....

(A) End inspiratory rales

(B) Expiratory rales

(C) Inspiratory rhonchi

(D) Expiratory rhonchi

TEST 3 31. Which is not a feature of fibrosing alveolitis?

(A) Clubbing

(B) Tachypnea

(C) Basal rales

(D) Pulmonary osteoarthropathy

32. Parasite causing pulmonary eosinophilia syndrome

(A) Strongyloides

(B) Enterobiasis

(C) Hook worm

(D) Trichilnella

33. Allergic bronchopulmonary aspergilosis is related to sarcoidosis

involving the lung by which cell type?

(A) Macrophage

(B) Plasma cell

(C) Eosinophil

(D) Type-II pneumocyte

TEST 3 34. Pulmonary eosinophilia is not caused by.....

(A) Ascariasis

(B) Paragonimus

(C) Filariasis

(D) Babesia microti

35. Leoffler's syndrome is seen with all except

(A) Toxocara

(B) Strongyloides stercoralis

(C) L. tryptophan

(D) Giardiasis

36. True statement about asbestosis......

(A) Causes Lung Ca

(B) Pleural mesothelioma

(C) Peritoneal mesothelioma

(D) All

TEST 3 37. Asbestosis is usually related to.....

(A) Small cell carcinoma lung

(B) Large cell carcionoma lung

(C) Mesothelioma

(D) All

38. The following does not occur with

asbestosis....

(A) Methaemoglobinemia

(B) Pneumoconiosis

(C) Pleural mesothelioma

(D) Plueral calcification

39. Silicosis causes which of the following?

(A) Apical nodular fibrosis

(B) Coin shadow

(C) Hilar lymphadenopathy

(D) All

TEST 3 40. 'Monday chest tightness' is characteristic of...

(A) Asbestosis

(B) Coal worker's pneumoconiosis

(C) Byssinosis

(D) Berylliosis

41. The most common causative organism for lobar pneumonia is....

(A) Staphylococcus aureus

(B) Neisseria

(C) Streptococcus pheumoniae

(D) Haemophilus influenzae

42. The following modes of ventilation may be used for weaning off patients from

mechanical ventilation except.....

(A) Controlled Mechanical Ventilation (CMV)

(B) Synchronized Intermittent Mandatory Ventilation (SIMV)

(C) Pressure Support Ventilation (PSV)

(D) Assist Control Ventilation (ACV)

TEST 3 43. Foreign body aspiration is most common in..

(A) Left apical lobe

(B) Left lower lobe

(C) Right middle and inferior apical lobe

(D) Right apical lobe

44. Nosocomial pneumonia is caused most commonly by....

(A) Streptococci

(B) Mycoplasma

(C) Gram negative bacteria

(D) Viruses

45. True about kartagener's syndrome except:

(A) Dextrocardia

(B) Infertility

(C) Mental retardation

(D) Bronchiectasis

TEST 3 46. Cystic bronchiectasis occurs in.all except....

(A) Malignancy

(B) Sarcoidosis

(C) Tuberculosis

(D) Fungal infections

47. Ultra structural abnormalities reported in defectivedilia immotile cilia

syndrome are....

(A) Dynein in arm deficiency

(B) Absence of radial spokes

(C) Absence of central microtubule

(D) All of the above

48. Which of the following is not a feature of kartagener's syndrome?

(A) Bronchiectasis

(B) Pancreatic insufficiency

(C) Sinusitis

(D) Situs in versus

TEST 3 49. In cystic fibrosis the most common organism which causes infection is....

(A) Pseudomonas (B) Staphylococcus

(C) Klebsiella (D) Streptococcus

50. In cystic fibrosis, pseudomonas aeroginosa is most common organism.

The next

common is.....

(A) Streptococci

(B) Klebsiella

(C) Pneumococci

(D) Staphylococcus aureus

51. A mother kissing her baby finds that the baby's skin is salty, the

diagnosis is.....

(A) Fanconi syndrome

(B) Thalassemia

(C) Cystic fibrosis

(D) Niemann pick disease

TEST 3 52. Alpha-I antritrypsin deficiency which is true?

(A) Autosomal recessive

(B) Associated with emphysema

(C) All

(D) High protease activity is present.

53. The complication least likely to occur in a case of chronic

bronchitis is....

(A) Pulmonary hypertension

(B) Pneumothorax

(C) Emphysema

(D) Amyloidosis

TEST 3 54. Bronchoalveolar lavage is beneficial in the evaluation of....

(A) Interstitial lung diseases

(B) Acute bronchitis

(C) Bronchopleural fistula

(D) Pneumothorax

55. Haman-rich syndrome is treated with...

(A) Vitamin B6 (B) Vitamin B12

(C) INH (D) Steroids

56. Fluroscopy is useful in....

(A) Valvular calcification

(B) Diaphragmatic palsy

(C) LV. function

(D) Coronary wall carcinoma

TEST 3 57.. Commonest symptoms of pulmonary embolism....

(A) Chest pain (B) Dyspnoea

(C) Haemoptysis (D) Cough

58. In acute pulmonary embolism, the most frequent ECG finding

is.....

(A) S1Q3T3 pattern

(B) P. pulmonale

(C) Sinus tachycardia

(D) Right axis deviation

59. In pulm embolism, finding in perfusion scan is.....

(A) Perfusion segmental defect

(B) Perfusion defect with normal lung scan & radiography

(C) Tenting of diaphragm

(D) Normal chest scan

TEST 3

60. The most definitive method of diagnosing pulmonary

embolism is.....

(A) Pulmonary ateriography

(B) Radioisotope perfusion pulmonary

scintigraphy

(C) EKG

(D) Venography

61. IVC filter is used in following except.....

(A) Massive emboli

(B) Negligible size of emboli

(C) Repeated emboli

(D) None

TEST 3 62. Increased amylase levels in pleural fluid are seen in.....

(A) Malignancy (B) Pancreatitis

(C) Oesophageal rupture (D) All

63. Pleural fluid low in glucose is seen in....

(A) Rheumatoid arthritis

(B) Tuberculosis (C) Mesothelioma

(D) Empyema ( E) ALL

64. Tuberculous pleural effusion is characterised by all except....

(A) LDH in the fluid is more than 60 times

that of serum.

(B) High mesothelial counts

(C) Increased Adenosine deaminase levels

(D) Hemorrhagic effusion

TEST 3 65. A patient with spontaneous pneumothorax involving more than 50% of

hemithorax is best treated with....

(A) Needle aspiration

(B) Closed drainage by tube in underwater

seal

(C) Let spontaneous remission occurs

(D) Open thoracotomy

66 Commonest cause for mediastinitis is.....

(A) Esophageal perforation

(B) Cervical spondylitis

(C) Osteomyelitis of sternum

(D) Osteomyelitis of clavicle

67. Hypercapnea at rest is most indicative of....

(A) Hypoventilation

(B) Right to left shunt (C) Impaired diffusion

(D) CO poisoning

TEST 3 67.. Isobaric O2 is used for treatment of....

(A) Co poisoning

(B) Ventilation failure

(C) Gas gangrene

(D) Divers bends

68.. Main treatment for hypoventilation with

obesity is...

(A) Diresis

(B) Weight loss

(C) Oxygen mask

(D) Respiratory stimulants

69. Sleep apnea is defined as a temporary pause in breathing during

sleep at least....

(A) 40 seconds (B) 30 seconds

(C) 20 seconds (D) 10 seconds

TEST 3 70. Obstructive sleep apnoea syndrome....

(A) Associated with sudden cardiac death.

(B) Road traffic accidents

(C) Bulimia nervosa

(D) Anorexia nervosa

71. Blood gas analysis in type-I respiratory

failure shows....

(A) pCO2 pO2

(B) N.pCO2 pO2

(C) pCO2 pO2

(D) pCO2 pO2

(E) All are the false.

72.. In ARDS all are seen except....

(A) Dilated bronchioles

(B) Edema

(C) Fibrosis

(D) Alveolar damage

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