6 Medicine Respiratory System

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Respiratory System

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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 :
adequate provision of fresh air to the alveoli (ventilation),
adequate circulation of blood through the pulmonary vasculature
(perfusion),
adequate movement of gas between alveoli & pulmonary
capillaries (diffusion),
appropriate contact of alveolar gas and pulmonary capillary blood
(ventilation-perfusion matching).

1.
2.

3.

4.

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 <200 ml/day.
Massive hemoptysis is variably defined as the expectoration of :
>500 mL over a 24-h period,
or >150ml/hr,
or >100ml for continous 3 days, or requiring transfusion.
Although the patient’s estimation of the amount of blood is
notoriously unreliable.

Physical signs












Pulse to Respiratory rate ratio : 1:4
Clubbing
Tracheal Shift : Traile’s sign.
Pull of trachea – Fibrosis, Collapse.
Push of trachea – Consolidation, hyperinflation, pleural
effusion, hemothorax and malignancy.
No change in – Bronchiectasis, ILD
Tracheal tug – Olliver’s sign – Aortic arch aneurysym,
Mediastinal tumour attached to aortic arch
Traube’s 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), a mass (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
Wegener’s 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 time—i.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 FEF25–75%, 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 patient’s age and height in the appropriate
regression equation; different equations are used
depending on the patient’s 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 FEF25–75% 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.
(C)
FEV1/FVC is high. (D)

8.

(B)
FEV1 is high
All of the above

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)
2L
(B)
(C)
4.5 L
(D)

12.

4L
7L

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.

Steps

Symptoms

Step 1 :
Intermittent

<1 /week

Nocturnal
symptoms
< 2/month

>80% of
predicted but
normal in
between
attacks
>1/week but > 2/month > 80% never
< 1 /day
normal even
during
asymptomatic
period.
> 1/week
Daily
>60% <80% of
attacks.
predicted with
variability > 30%
Functional
impairment

Treatment

Step 2 : Mild
persistent

Step 3 :
Moderate
persistent

Step 4 :
Severe
persistent

PEFR

Continuous
Limited
activity

Frequent

Short-term
Long-term
relief
prevention
none
Inhaled B2
agonist – short
acting.
Inhaled B2
Inhaled
agonist – short corticosterio
d
acting.
SOS
Inhaled B2
agonist –
shortacting.
not to exceed
3-4/day

Inhaled
corticosteroi
d
LABA

< 60% of
Inhaled B2
predicted with
agonist –
variability > 30% 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


Kartagener’s 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

PREDOMINANEMPHYSEMA

PREDOMINANT
BRONCHITIS

AGE OF ONSET

6TH DECADE

5TH DECADE

COUGH
SPUTUM

AFTER
BREATHLESSNESS
SCANTY

INFECTIONS

LESS COMMON

BEFORE
BREATHLESSNESS
COPIOUS,
PURULENT
COMMON

RESPIRATORY DISTRESS

OFTEN TERMINAL

EPISODIC

CXR

HYPERINFLATION

INCREASED BVM

CYANOSIS

TERMINAL

COMMON

PULMONARY
HYPERTENSION
COR PULMONALE

MILD

MODERATE/SEVER
E
EARLY

LATE

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 (Hoover’s 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 CommunityAcquired 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)
(B)
(C)

They contain heparin proteoglycan
Their number is increased in patients with bronchial asthma.
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
(C)
Eosinophils

(B)
(D)

Monocytes
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 lung—the
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 <200
Pulmonary capillary wedge pressure < 18 (by Swan Ganz catheter)
Incidence is 20 cases per 1,00,000 population.
ARDS is caused by direct lung injury in response to a pathophysiologic stimuli.
Direct lung injury
Pneumonia
Gastric aspiration
Pulmonary contusion
Fat embolism
Drowning
Toxic inhalation

Indirect lung injury
Sepsis
Trauma
Shock
Transfusion
Pancreatitis
Drugs




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-worker’s disease.

Hypersensitivity pneumonitis
Disease









Antigen

Source of Antigen

Bagassosis --- Thermophilic actinomycetesa --- “Moldy”
bagasse (sugar cane)
Bird fancier’s lung----Parakeet, pigeon, chicken---Avian
droppings
Coffee worker’s lung --- Coffee bean dust----Coffee beans
Compost lung --- Aspergillus --- Compost
Detergent worker’s --- Bacillus subtilis enzymes---Detergent
Familial HP --- Bacillus subtilis ---Contaminated wood dust
in walls
Farmer’s 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

: Loeffler’s 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 Horner’s
syndrome and arm/shoulder pain due to brachial plexus
involvement.
 Horner’s 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, Trosseau’s 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 Horner’s 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., endexpiratory 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 <3 years
after diagnosis.
 Death from RV failure or arrhythmia,.
 Secondary

pulmonary hypertension :
 depends on underlying disease.

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
 Acute

DIAGNOSIS :

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
• An alternative diagnosis is less likely than PE
• Heart rate _100 beats/min
• Immobilization or surgery in the previous 4 weeks
• Previous DVT/PE
• Hemoptysis
• Malignancy (on treatment, treated in the past 6 months)

3.0
3.0
1.5
1.5
1.5
1.0
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 (Westermark’s sign),
A peripheral wedged-shaped density above the diaphragm (Hampton’s
hump),
or an enlarged right descending pulmonary artery (Palla’s 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)
(B)
(C)
(D)

30.

Cryptostroma corticale
Asperigullus
Thermophilic actinomycetes
Grain dust

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)
(C)

Pseudomonas
Klebsiella

(B)
(D)

Staphylococcus
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)
(C)
INH
(D)

56.

Fluroscopy is useful in....
(A)
Valvular calcification
(B)
Diaphragmatic palsy
(C)
LV. function
(D)
Coronary wall carcinoma

Vitamin B12
Steroids

TEST 3
57..

Commonest symptoms of pulmonary embolism....
(A)
Chest pain
(B)
Dyspnoea
(C)
Haemoptysis
(D)
Cough

58.
is.....

In acute pulmonary embolism, the most frequent ECG finding

(A)
(B)
(C)
(D)
59.

S1Q3T3 pattern
P. pulmonale
Sinus tachycardia
Right axis deviation

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)
(C)

Malignancy
Oesophageal rupture

(B)
(D)

Pancreatitis
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

THANK YOU

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