Respiratory Pathology Guide

CLINICAL PATHOLOGY
MODULE 1 CLINICAL PATHOLOGY I
Page 1 Carey Francis Okinda
By CAREY FRANCIS OKINDA,
October 2014
Unit 2: The Respiratory System
UNIT OBJECTIVES
1. Describe congenital anomalies of the respiratory tract
2. Describe the aetiology, pathophysiology, pathology, features and
complications of disorders of the respiratory system
3. Explain the investigations in respiratory disorders
UNIT OUTLINE
Topics Hours
1. Introduction – Anatomy, Physiology, Pathology and
Investigations
2
2. Paediatric Lung Diseases 1
3. Disorders of Upper Respiratory Tract 1
4. Respiratory Failure and Lung Collapse (Atelectasis) 1
5. Obstructive and Restrictive Lung Diseases 2
6. Pulmonary Infections 3
7. Pulmonary Vascular Disease and Acute Lung Disease 2
8. The Pleura 2
9. Tumours 1
TOTAL 15
Lesson 1: Introduction to Respiratory System Pathology
Learning Outcomes
At the end of the lesson, the leaner should be able to -
1. Review the anatomy and functions of organs of the respiratory tract
2. Outline conditions and diseases that affect the respiratory system
3. Discuss investigations in respiratory disease
1.0 INTRODUCTION
 Respiration is the process by which O2 is transported to and used by cells,
and CO2 produced is eliminated from the body which is a task effectively
carried out by the cooperative work of the respiratory system, red blood
cells and the circulatory system
 Oxygenation of blood and elimination of CO2 is called external respiration
while utilization of O2 by cells and production of CO2 by the cell is described
as internal respiration or cellular respiration
 Most cells in the human body require O2 for survival and to carry out their
functions thus during their normal processes of work they use up O2 and
produce CO2 as a waste product that must be eliminated from the body.

 The normal intake of air is 7 litres/min of which 5 litres is available for
alveolar ventilation.
 Factors that maintain adequate respiration include adequate intake of air,
rapid diffusion along the alveolar ducts and through alveolar walls and
adequate perfusion
 In chronic lung disease, ventilation, diffusion and perfusion disorders are
present in varying degrees
 Under normal circumstances, the upper area of the lung is better ventilated
than perfused while the base is better perfused than ventilated an imbalance
magnified in lung disease.
2.0 DIVISIONS AND ORGANIZATION
 Divided into upper and lower tracts or divisions with organs of the upper
respiratory tract are located outside the thorax or chest cavity whereas
those in the lower division are located almost entirely within the chest
 The upper respiratory tract comprises of nose, pharynx, nasopharynx,
oropharynx, laryngopharynx, larynx and trachea while the lower
respiratory tract has the bronchial tree and lungs (these are the passages)
 Comprises of lungs and respiratory passages (airways), which work in
intimate collaboration with the thoracic cage, respiratory muscles and the
pulmonary circulation. It uses highly effective convective systems of
ventilation and circulation for long distance transport of O2 and CO2 and
uses diffusion exclusively for short distance movements of O2 and CO2
 The main components of the respiratory system are: - the air pump,
mechanism for oxygen and carbon dioxide carrying, gas exchange surface,
circulatory system and regulatory mechanisms.
3.0 PHYSIOLOGY RESPIRATORY SYSTEM
 Respiratory physiology is a complex series of interacting and coordinated
processes that ensure adequate and prompt supply of oxygen and removal
of carbon dioxide in an effort to maintain the stability and consistency of the
internal environment
 It involves physiological control mechanisms such as acid-base, water and
electrolyte balance, circulation and metabolism. Lungs are structures where
gas exchange between blood and inspired air takes place whereas the
respiratory passages are structures along which air is conveyed to and from
the lungs
Functions
1. Provide oxygen to the blood stream and remove carbon dioxide
2. Enables sound production or vocalization as expired air passes over the
vocal cords
3. Assists in abdominal compression during micturition, defecation and
parturition (childbirth)
4. Lung Defence mechanism - protective and reflexive non-breathing air
movements e.g. coughing and sneezing to keep the air passageways clean.
5. Temperature regulation – loss of heat during expiration
6. Maintenance of water balance - small amounts of water are lost during
expiration

7. Regulation of acid-base balance
8. Anticoagulant function – lungs contain mast cells which secret heparin which
prevents intravascular clotting
9. Metabolic functions – manufacture surfactant for local use, fibrinolytic
system
10. Endocrine functions
a. Pulmonary capillary endothelial cells secrete angiotensin converting
enzyme (ACE) which activates angiotensin I into angiotensin II
b. Lung tissues synthesize prostaglandins, acetylcholine, bradykinin and
serotonin
4.0 INTRODUCTION TO PATHOLOGY OF THE RESPIRATORY SYSTEM
 The prime role of the respiratory system is oxygenation of blood and
removal of carbon dioxide CO2
 The function requires that air comes into close approximation with blood
through the anatomical arrangement of the alveoli and blood vessels.
1) Constant inward and outward flow of the enormous air exposes the
respiratory system to infection by both microbes present in inspired air and
by downward spread of bacteria that colonize the nose and throat
2) Inhalation of pollutants such as dust, fumes, smokes increase the incidence
of bronchitis, chronic lung disease and bronchial carcinoma
3) Vascular architecture of the lungs allows passage of blood into the lungs
during each cycle makes the lungs to be vulnerable to effects of
cardiovascular diseases. This is due to disturbance of pulmonary
haemodynamics e.g. pulmonary oedema and on the other hand, lung
diseases interfere with the pulmonary blood flow with noticeable effects on
the heart and systemic circulation because cardiac and pulmonary functions
are closely interdependent.
4) The lung is a frequent victim of malfunction elsewhere for example failure
of the left side of the heart results in pulmonary congestion and oedema,
systemic thrombosis on many occasions causes pulmonary embolism and
the lungs are a common site for secondary tumours.
 Main diseases of the airways and the lungs are caused by infection and
inflammation
 Environmental factors such as smoking and occupational exposure to dust
contributing to the morbidity and mortality resulting from respiratory
problems
 Tumours of the bronchial tree and lung are common and important, as
almost all of them are malignant. The key effect of respiratory problems is
poor oxygenation resulting in respiratory failure.

Carey Francis Okinda
5.0 INVESTIGATIONS
1) Chest X-ray
Use the ABCDEFGH mnemonic
Chest X-ray - Systematic Approach
 Reading a chest X-ray (CXR) requires a systematic approach.
The "right film for the right patient"
 Check that the film bears the patient's name, age or hospital number too
 The label may also tell features such as anteroposterior (AP) projection or
supine position
 Check the date of the film to ascertain which one you are viewing
Technical details
 Check the position of the side marker (left or right) against features such
as the apex of the heart and air bubble in the stomach. A misplaced marker
is more common than dextrocardia or situs inversus.
 Most films are a poster anterior (PA) projection. The usual indication for AP
is a patient who is confined to bed.
 AP vs PA Views
o Look at the relationship of the scapulae to the lung margins
o A PA view shows the scapulae clear of the lungs whilst in AP projection
they always overlap
o Vertebral endplates are more clearly visible in AP and laminae in PA. This
is important because the heart looks bigger on an AP view.
 Lateral films
o A lateral view may have been requested or performed on the initiative
of the radiographer or radiologist. As an X-ray is a two-dimensional

shadow, a lateral film helps to identify a lesion in 3 dimensions. The usual
indication is to confirm a lesion seen on a PA film.
o The heart lies in the anteroinferior field. Look at the area anterior and
superior to the heart; this should be black because it contains aerated
lung. Similarly, the area posterior to the heart should be black right
down to the hemidiaphragms. The degree of blackness in these two
areas should be similar, so compare one with the other. If the area
anterior and superior to the heart is opacified, it suggests disease in the
anterior mediastinum or upper lobes. If the area posterior to the heart is
opacified there is probably collapse or consolidation in the lower lobes.
 The normal posture for films is erect (supine is usually for patients confined
to bed). In an erect film, the gastric air bubble is clearly in the fundus with a
clear fluid level but, if supine, in the antrum. In a supine film, blood will flow
more to the apices of the lungs than when erect.
 Rotation should be minimal. This can be assessed by comparing the medial
ends of the clavicles to the margins of the vertebral body at the same level.
Oblique chest films are requested to look for achalasia of the cardia or
fractured ribs.
 CXR should be taken with the patient in full inspiration but some people
have difficulty holding full inspiration (except when seeking a small
pneumothorax as this will show best on full expiration) A CXR in full
inspiration should have the diaphragm at the level of the 6th rib anteriorly
and the liver pushes it up a little higher in the right than on the left.
 Penetration
o Is affected by both the duration of exposure and the power of the beam
o More kV gives a more penetrating beam
o A poorly penetrated film looks diffusely light (an x-ray is a negative) and
soft tissue structures are readily obscured, especially those behind the
heart
o An over-penetrated film looks diffusely dark and features such as lung
markings are poorly seen.
Airway
 Trace the lucency from the neck down towards the carina
 Should be midline and you should be able to see two bronchi splitting from
it
Bones and soft tissues
 Look at the shoulder joint and trace out each rib contour to check for
fractures or other abnormalities such as lytic lesions
 Are both breast shadows present
 Attention may be merited to apices, periphery of the lungs, under and
behind the hemidiaphragms and behind the heart
Cardiac
 Check the cardio-thoracic ratio (CTR)
o The width of the heart should be no more than half the width of the chest
o About a third of the heart should be to the right and two thirds to the left
of centre
o Note: the heart looks larger on an AP film and thus you cannot comment
on the presence or absence of cardiomegaly on an AP film.

Diaphragm (e.g. flat or elevated hemidiaphragm)
 Ascertain that the surface of the hemidiaphragms curves downwards, and
that the costophrenic and cardiophrenic angles are not blunted
 Blunting suggests an effusion
 Extensive effusion or collapse causes an upward curve
 Check for free air under the hemidiaphragm - this occurs with perforation
of the bowel but also after laparotomy or laparoscopy
Edges (borders) of the heart
 The left border of the heart consists of the left atrium above the left ventricle
 The right border is only the right atrium alone and above it is the border of
the superior vena cava. The right ventricle is anterior and so does not have
a border on the PA chest X ray film. It may be visible on a lateral view.
 To rule out lingular and left middle lobe pneumonia or infiltrates
Fields (The Lungs)
 The pulmonary arteries and veins are lighter and air is black, as it is
radiolucent.
 Check both lungs, starting at the apices and working down, comparing left
with right at the same level
 The lungs extend behind the heart, so try to look there too
 Note the periphery of the lungs - there should be few lung markings here
 Disease of the air spaces or interstitium increases opacity
 Look for a pneumothorax which shows as a sharp line of the edge of the lung
Gastric Bubble
 Check for a lucency in the left upper abdominal quadrant
Hilum
 Look at the mediastinal contours, first to the left and then to the right. The
trachea should be central. The aortic arch is the first structure on the left,
followed by the left pulmonary artery. The branches of the pulmonary artery
fan out through the lung.
Instrumentation
 Look for obvious unusual opacities such a chest drain, a pacemaker or a
foreign body. This is a two-dimensional picture and so a central opacity may
not be something that was swallowed and is now impacted in the
oesophagus. It might be a metal clip from a bra strap or a hair band on a
plait.

Interpretation
Abnormal opacities
 When observing an abnormal opacity, note:
 Size and shape
 Number and location
 Clarity of structures and their margins
 Homogeneity
 The common patterns of opacity are:
o Collapse
o Consolidation
o Heart and mediastinum
Collapse and consolidation
 Collapse, also called atelectasis, and consolidation are caused by the
presence of fluid instead of air in areas of the lung.
 An air bronchogram is where the airway is highlighted against denser
consolidation and vascular patterns become obscured.
 Confluent opacification of the hemithorax may be caused by consolidation,
pleural effusion, complete lobar collapse and after a pneumonectomy.
 To find consolidation, look for absence or blurring of the border of the heart
or Hemidiaphragm. The lung volume of the affected segment is usually
unaffected.
 Collapse of a lobe (atelectasis) may be difficult to see. Look for a shift of the
fissures, crowding of vessels and airways, and possible shadowing caused
by a proximal obstruction like a foreign body or carcinoma.
 A small pleural effusion will cause blunting of the costophrenic or
cardiophrenic angles. A larger one will produce an angle that is concave
upwards. A very large one will displace the heart and mediastinum away
from it, whilst collapse draws those structures towards it. Collapse may also
raise the hemidiaphragm

Heart and mediastinum
 The heart and mediastinum are deviated away from a pleural effusion or a
pneumothorax, especially if it is a tension pneumothorax and towards
collapse.
 If the heart is enlarged, look for signs of heart failure with an unusually
marked vascular pattern in the upper lobes, wide pulmonary veins and
possible Kerley B lines. These are tiny horizontal lines from the pleural edge
and are typical of fluid overload with fluid collecting in the interstitial space.
 If the hilum is enlarged, look for structures at the hilum such as pulmonary
artery, main bronchus and enlarged lymph nodes.
Chest X-ray in children
 Identification of the patient are still important
 A child, especially if small, is more likely to be unable to comply with
instructions such as keeping still, not rotating and holding deep inspiration

 Technical considerations such as rotation and under or over penetration of
the film still merit attention and they are more likely to be unsatisfactory
 A child is more likely to be laid down and have an AP film with the
radiographer trying to catch the picture at full inspiration
Assess lung volume
 Count down the anterior rib ends to the one that meets the middle of the
hemidiaphragm
 A good inspiratory film should have the anterior end of the 5th or 6th rib
meeting the middle of the diaphragm
 More than six anterior ribs shows hyperinflation
 Fewer than five indicates an expiratory film or underinflation.
Tachypnoea in infants causes trapping of air
 Expiration compresses the airways, increasing resistance and, especially
less than 18 months, air enters more easily than it leaves and is trapped,
causing hyperinflation.
 Bronchiolitis, heart failure and fluid overload are all causes
 With underinflation, the 3rd or 4th anterior rib crosses the diaphragm. This
makes normal lungs appear opaque and a normal heart appears enlarged.
Positioning
 Sick children, especially if small, may not be cooperative with being
positioned
 Check if the anterior ends of the ribs are equal distances from the spine
 Rotation to the right makes the heart appear central, and rotation to the left
makes the heart look large and can make the right heart border disappear.
Lung density
 Divide the lungs into upper, middle, and lower zones and compare the two
sides
 Infection can cause consolidation, as in an adult
 Collapse implies loss of volume and has various causes
 The lung is dense because the air has been lost
 In children, the cause is usually in the airway, such as an intraluminal
foreign body or a mucous plug
 Complete obstruction of the airway results in reabsorption of air in the
affected lobe or segment
 Collapse can also be due to extrinsic compression such as a mediastinal
mass or a pneumothorax.
 Differentiating between collapse and consolidation can be difficult or
impossible, as both are denser. Collapse may pull across the mediastinum
and deviate the trachea. This is important, as pneumonia is treated with
consolidation
antibiotics but collapse may require bronchoscopy to find and remove an
obstruction.
Pleural effusion
 In children, unilateral effusion usually indicates infection whilst bilateral
effusion occurs with hypoalbuminaemia as in nephrotic syndrome.
 Bronchial wall thickening is a common finding on children's X-rays
 Look for "tram track" parallel lines around the hilar

 The usual causes are viral infection or asthma but this is a common finding
with cystic fibrosis.
Heart and mediastinum
 The anterior mediastinum, in front of the heart, contains the thymus gland
 It appears largest at about 2 years old but it continues to grow into
adolescence. It grows less fast than the rest of the body and so becomes
relatively smaller
 The right lobe of the lung can rest on the horizontal fissure, which is often
called the sail sign.
 Assessment of the heart includes assessment of size, shape, position and
pulmonary circulation
 The cardiothoracic ratio is usually about 50% but can be more in the first
year of life and a large thymus can make assessment difficult, as will a film
in poor inspiration.
 As with adults, one third should be to the left of centre and two thirds to the
right. Assessment of pulmonary circulation can be important in congenital
heart disease but can be very difficult in practice.
2) Bronchoscopy
3) Blood Gas analysis
 This is analysis of the oxygen and carbon dioxide levels in the blood
4) Total Blood count
 Shows the various red blood cell indices, white blood cells (total and
differential count) and the platelets
5) Sputum Examination
 Refer to earlier class
discussions

6) Blood cultures
 Done to determine the microbes present and their sensitivity to various
drug agents (details in microbiology)
7) Peak Expiratory Flow
 The purpose is to measure lung function
 The patient inhales deeply and exhales hard into a plastic tube in order to
get a reading for how fast the patient is able to exhale successfully
 The result of this test is a peak flow number.
8) Spirometry
 Is a non-invasive method of lung function testing, which measures the
amount (volume) and/or speed (flow) of air that can be inhaled and
exhaled
 A spirometer is a device used
 Indications
i) To determine how well the lungs receive, hold, and utilize air
ii) To monitor a lung disease
iii) To monitor the effectiveness of treatment
iv) To determine the severity of a lung disease

v) To determine whether the lung disease is restrictive (decreased
airflow) or obstructive (disruption of airflow)
 After taking a deep breath, a person forcefully breathes out into the
spirometer as completely and forcefully as possible. The spirometer
measures both the amount of air expelled and how quickly the air was
expelled from the lungs. The measurements are recorded by the
spirometer
 The normal, healthy values measured by the spirometer for the amount of
air exhaled vary from person to person. The results are compared to the
average expected in someone of the same age, height, sex, and race,
 Values below 80 percent of the average, it may be a sign of lung disease or
other airflow obstruction.
9) ECG
10) Ultrasound
11) CT Scan
12) MRI
13) Biopsy
 What are the indications of a biopsy?

Lesson 2: Paediatric Lung Disease
Learning Outcomes
1. Discuss the developmental anomalies of the respiratory system
2. Describe the causes and effects of acute respiratory distress syndrome
(hyaline membrane disease)
Developmental Abnormalities
Developmental defects of the lungs include agenesis or hypoplasia of both
lungs, one lung or single lobe; tracheal and bronchial anomalies – atresia,
stenosis and tracheobronchial fistula; vascular anomalies; congenital lobar
over-inflation (emphysema), bronchogenic cysts; congenital airway
malformation and pulmonary sequestrations
1.0 PULMONARY HYPOPLASIA
 Incomplete development of both lungs resulting in reduced weight,
volume and acini compared to body weight and gestational age
 Lung smaller than normal
 Incidence 10% associated with other congenital abnormalities and lung
compression by abnormal masses and oligohydromnious
 Usually secondary to space occupying lesion in the uterus,
oligohydromnious or impaired foetal respiratory movements as seen in
congenital diaphragmatic hernia, renal cystic kidney, renal agenesis and
anencephaly.
2.0 BRONCHIAL ATRESIA
 Results in severe narrowing of the bronchus
3.0 BRONCHOGENIC SEQUESTRATION
 Cysts attached to the trachea
 Represent accessory bronchial buds
4.0 BRONCHOPULMONARY SEQUESTRATION
 Patients develop abnormal lung mass without any normal connection to the
airway or bronchial system
 There are two types of sequestration – extralobular and intralobular.
Extralobular sequestrations – external to the lungs and found elsewhere in
the thorax and mediastinum. Intralobular sequestrations – found in the lung
tissue and usually associated with recurrent localized infections or
bronchiectasis
Summary of Paediatric lung disease
-bronchial atresia
-pulmonary hypoplasia
-bronchogenic sequestration
-bronchopulmonary sequestration
-neonatal RDS /HMD

5.0 Neonatal Respiratory Distress Syndrome (Hyaline
Caesarean
Section
Maternal
Diabetes
Amniotic Fluid
aspiration
IMMATURE/DAMAGED TYPE II PNEUMOCYTES
FIBRIN/HYALINE Membrane
Endothelial Damage
Alveolar Lining
damage
Hypoxia Pulmonary Vasoconstriction
Membrane Disease)
Introduction
 Occurs due to deficiency of surfactant and primarily disease of premature
infants
 Seen in infants of diabetic mothers (excess insulin production by the foetus
suppresses surfactant production)
 Neonates born at the gestation 32 – 36 weeks have 20% mortality while those
at < 28 weeks have 60% mortality
 The risk factors include prematurity, diabetic mother, neonatal aspiration
and multiple births.
Pathogenesis
 Immature or damaged lung is unable to make enough surfactant (a lecithin-rich
surface-active lipid) that reduces surface tension in the alveoli and
keeps the alveoli open
Diagram 2.1: Pathogenesis of ARDS
RISK FACTORS
Prematurity (<
36 weeks)
Low Level surfactant
Lung Collapse
Multiple
Pregnancy
 ARDS results from widespread acute injury to the alveolar capillary
membrane, which produces high permeability oedema and inhibits
surfactant function (especially fibrin monomers)
 Epithelial injury also impairs new surfactant synthesis and inflammation may
exacerbate the injury because of release of oxidants and lysosomal
enzymes from activated leukocytes
 Lack of surfactant results in lung collapse with microatelectasis.
 Hypoxia causes damage to the alveolar lining cells and pulmonary arterial
constriction resulting in endothelial damage hence plasma leaks into the
alveoli where it is deposited as fibrin (bright pink-stained membrane) and
thus the name hyaline membrane disease. Fibrin reduces gas exchange
further worsening the hypoxic state.

 Lung compliance is decreased because many airspaces contain oedema
(and hence cannot accept air) and because abnormally high surface
tension counteracts the negative intrapleural pressure.
What are the differential
Pathology
The lungs: -
1. Have fibrous obliteration of bronchioles
2. Peribronchial fibrosis
3. Overdistended alveolar
Clinical Features
 Dyspnoea
 Tachypnoea (faster than 60 breaths a minute
 Makes a grunting sound when he breathes out
 Has respiratory distress (what are the features)
 Cyanosis
 Crepitations
Diagnosis
1) Blood culture - check for infection
2) Blood gas analysis - check amount of oxygen in blood
3) Chest X-ray
Differential Diagnosis
diagnoses?
Complications
1. Intracerebral bleed ( hypoxia related)
2. PDA (failure to close as normal closure is stimulated by oxygenation)
3. Necrotizing enterocolitis ( ischaemic/hypoxic damage of the gut)
4. Bronchopulmonary dysplasia (high pressure ventilation and oxygen toxicity
to alveolar lining cells)
RISK FACTORS OF ARDS
-premature (<36wks gestation)
-infants to diabetic mothers
-cs
-amniotic fluid aspiration
-multiple pg
-
COMPLICATIONS
-intracerebral bleed
-PDA
-necrotizing enterocolitis
-bronchopulmonary dysplasia

Lesson 3: Upper Respiratory Tract Disorders
Learning Outcomes
1. Discuss the pathology of conditions affecting organs of the upper
respiratory tract
A. EPISTAXIS
disorder
Epistaxis is common affecting 60% of the population of which only 6% seek
medical advice. The bleeding may be spontaneous or profuse and life
threatening. Bleeding may originate from anywhere within the nose, but
frequently from the Little’s area. The peak incidence is in children, young adults
and above the age of 55 years.
Causes
1. Nasal
a. Idiopathic (85%)
b. Trauma – nose pricking, fractures
c. Inflammation – rhinitis, sinusitis
d. Iatrogenic – nasal sprays, surgery
e. Hereditary – Hereditary haemorrhagic telangiectasis
f. Neoplasms – carcinoma, juvenile angiofibroma
2. Systemic
a. Anticoagulants – warfarin, NSAIDS
b. Hypertension
c. Blood dyscrasias – leukaemia
d. Hereditary coagulopathies – haemophilia
B. ACUTE INFLAMMATIONS
Infections of the nose, nasal sinuses, pharynx and larynx are common and
usually self-limiting illnesses often because of viral infection, which on many
occasions, is followed by bacterial super infection.
Viral Infections
Viral infections have characteristic features of acute inflammation such as
redness; oedema, nasal stuffiness, swelling of the nasal mucosa, duct
obstruction and abundant clear nasal discharge (mucous secretion) without
exudation of neutrophils.
Aetiology
1. Rhinovirus
2. Corona virus
3. Myxovirus e.g. Influenza
4. Paramyxovirus e.g. respiratory syncytial virus

Bacterial Phase
After the viral invasion, commensal bacteria present in the respiratory system
e.g. Streptococcus mutans and Haemophilus influenza can superinfect the
damaged tissue. This stage exhibits features of acute inflammation and
exudation of neutrophils with a mucopurulent discharge.
Pathogenesis
Viruses adhere to the cell surface proteins e.g. the cilia and enter the host cells
and replicate during which period the cells become damaged and readily
invaded by commmensal bacteria
1. Common Cold (Acute Coryza)
This is the commonest illustration of acute inflammations of the upper
respiratory tract. It involves the nose and adjacent structures such as the nasal
sinuses (maxillary, sphenoidal and frontal) where there occurs blocking of their
drainage by the swollen mucosa resulting in sinusitis. Acute coryza is spread
by droplet via sneezing.
2. Rhinitis
Rhinitis is inflammation of the mucous membranes of the nose.
Acute Rhinitis
The commonest causes of acute rhinitis are common cold (acute coryza) and
hay fever.
Allergic Rhinitis “Hay Fever”
Hay fever is an acute allergic or atopic rhinitis that occurs as a result of
hypersensitivity (type I) to pollen, house dust, animal dandruffs and other
antigens. Patients develop immediate symptoms of sneezing, itching and water
rhinorrhoea.
Chronic Rhinitis
Chronic rhinitis follows an acute inflammatory episode that fails to resolve.
Because of acute inflammation, there is inadequate draining of the nasal sinuses
due to nasal obstruction, polyps or enlargement of the adenoids leading to
chronic sinusitis and chronic nasopharyngitis.
3. Acute Sinusitis
Acute sinusitis occurs often as a complication of acute infection of the nose with
the responsible organs such as Strep. pyogenes, Strep. pneumoniae and Staph.
aureas.

C. THE PHARYNX
1. Acute Nasopharyngitis
Acute nasopharyngitis usually accompany acute rhinitis or acute tonsillitis. The
common organism implicated is Staphylococcus aureas.
The histopathology includes -
 Hyperaemia
 Oedema
 Hyperactive mucosal glands
 Increased mucosal secretions
 Neutrophil polymorphs – usually sparse in viral infections but increase with
secondary bacterial infections
 Superficial destruction of ciliated epithelium
 Swollen/enlarged/distended mucosal glands
2. Nasal Polyps
Nasal polyps usually form on the middle turbinate bones and within the
maxillary sinuses because of chronic recurrent inflammation of the nasal
mucosa particularly of allergic aetiology that result in polypoid thickening of
the mucosa. Polyps are rounded or elongated masses that are usually bilateral
with gelatinous consistency and smooth and shiny surface.
Diagram 3.1: Nasal Polyps
D. THE LARYNX AND TRACHEA
1. Acute Laryngitis and Tracheaitis
Acute laryngitis and tracheaitis are common occurrences
Aetiology
1. Viral - Adeno virus;Epstein Barr virus (EBV)
2. Bacteria - Strep. Pneumonia, Strep. Pyogenes, Neisseria catarrhalis,
Heamophilus influenzae and Corynebacterium diptheriae

Complicates acute febrile states such as measles, influenza and typhoid and
may spread to cause bronchitis resulting in laryngo-tracheo-bronchitis (LTB).
In situations where there is secondary infection with Strep. pyogenes, Strep.
pneumoniae and Staph. aureas leads to pseudomembranous inflammation.
Tonsillitis is common because of streptococcal infection while Heamophilus
influenza type B usually causes acute epiglottitis, which is a childhood illness.
Chronic Laryngitis
Frequently associated with excessive, smoking, repeated attacks of infection
and atmospheric pollution.
TB Laryngitis
Is usually secondary to pulmonary tuberculosis when the tubercle bacilli are
carried directly in the sputum to the larynx affecting the larynx and to a less
extend to the trachea. It causes thickening, caseation and ulceration of the
pharynx. The lesion is very painful and inflammatory swelling and oedema of
the glottis may supervene.
E. UPPER AIRWAY OBSTRUCTION
 Upper airway obstruction is one of the most serious emergencies faced by
clinicians
 Early diagnosis followed by restoration of airflow is essential to prevent
cardiac arrest or irreversible brain damage that occurs within minutes of
complete airway obstruction
 May be functional or anatomic and may develop acutely or subacutely
 Occurs at any level of the upper respiratory tract but laryngeal obstruction
has a particular importance because the larynx is the narrowest portion of
the upper airway.
Causes
1) Traumatic causes
 Laryngeal stenosis; airway burn; acute laryngeal injury; facial trauma
(mandibular or maxillary fractures); haemorrhage
2) Infections - suppurative parotitis; retropharyngeal abscess; tonsillar
hypertrophy; Ludwig’s angina; epiglottitis; laryngitis.;
Laryngotracheobronchitis (croup); Diphtheria
3) Iatrogenic causes
a) Tracheal stenosis post-tracheostomy
b) Tracheal stenosis post-intubation
c) Mucous ball from transtracheal catheter
4) Foreign bodies
5) Vocal cord paralysis
6) Tumours
a) Laryngeal tumours (benign or malignant)
b) Laryngeal papillomatosis
c) Tracheal stenosis (caused by intrinsic or extrinsic tumours)
7) Angioedema

a) Anaphylactic reactions
b) Angiotensin-converting enzyme inhibitors
Clinical Features
 Marked respiratory distress; altered voice; dysphagia; odynophagia; the
hand-to-the-throat choking sign; stridor; facial swelling; prominence of
neck veins; absence of air entry into the chest; tachycardia
 In an unconscious or sedated patient, the first sign of airway obstruction
may be inability to ventilate with a bag-valve mask after an attempt to
open the airway with a jaw-thrust maneuver
 Asphyxiation progresses; cyanosis; bradycardia; hypotension; irreversible
cardiovascular collapse
Investigations
1) Plain Chest and Neck Radiographs
2) Computed Tomography
3) Spirometry
4) Bronchoscopy
F. TUMOURS
Benign tumours
1. Polyps
2. Squamous papilloma
3. Lipomas
4. Angiomas
Malignant Tumours
1. Squamous cell carcinoma e.g. ca larynx.
Laryngitis
Laryngitis is inflammatory process/condition of the larynx due to various
causes.
Types
1. Simple laryngitis/acute laryngitis
2. Chronic laryngitis
3. Diphtheric laryngitis
4. Tuberculous laryngitis
5. Syphilitic laryngitis
Group Work – LTB
1. What are the causes?
2. Definition and predisposing factors
3. What is the pathophysiology and the pathology?
4. What are the features?
5. Diagnosis and differential diagnosis
6. What are the complications?
7. Management

Lesson 4: Respiratory Failure & Atelectasis (Lung Collapse)
Task: Using examples explain how the above factors cause respiratory failure.
Learning Outcomes
At the end of the lesson, the learner should be able to -
1. Describe the causes of lung collapse
2. Discuss the effects and features of lung collapse
3. Describe causes and effects of lung collapse
4. Discuss the pathophysiology and complications of lung collapse
5. Investigate a patient with lung collapse
Respiratory Failure
1.0 INTRODUCTION
 Normal respiratory function maintains blood gases within physiological
limits where the normal PaO2 is 10.7 kPa – 13.3 kPa (80 – 100 mmHg) and
PaCO2 is 4.7kPa – 6.0 kPa (35 – 45 mmHg)
 Respiratory failure is defined as when PaO2 falls below 8 kPa (60 mmHg).
 Respiratory failure is a syndrome of inadequate gas exchange due to
dysfunction of one or more essential components of the respiratory system
namely chest wall, airways, alveolar–c capillary units, pulmonary
circulation, nerves and CNS/brain Stem
2.0 MECHANISMS OF ARTERIAL HYPOXAEMIA
a) Low inspired partial pressure of O2 as a result of ambient air at high altitude
and reduced oxygen tension in inspired air
b) Mismatch of alveolar ventilation to perfusion
c) Alveolar hypoventilation
d) Increased shunt fraction of blood passing from the right heart to systemic
arterial circulation in right to left cardiac shunts without being oxygenated
e) Disease of the alveolar capillary membrane locking exchange of gases
3.0 PREDISPOSING FACTORS
1. Infection in the tracheobronchial tree, pneumonia, fever
2. Change in tracheobronchial secretions (increased volume and
viscosity)
3. Bronchospasms

4. Disturbance in ability to clear secretions
5. Drugs – sedatives, narcotics, anaesthetics
6. Oxygen therapy
7. Trauma
8. Cardiovascular disorders
9. Pneumothorax
4.0 CAUSES
1. Extrinsic Lung Disorders
a. Respiratory centre depression e.g. Drug overdose (sedatives,
narcotics); cerebral trauma or infarction; bulbar poliomyelitis and
encephalitis
b. Neuromuscular disorders - cervical cord injury; Guillain-Barre
Syndrome; myasthenia gravis and muscular dystrophy
c. Pleural and chest wall disorders e.g. chest injury (flail chest, rib
fracture); pneumothorax; pleural effusion; kyphoscoliosis (abnormal
lung) and obesity – Pickwickian syndrome
2. Intrinsic Lung Disorders
a. Diffuse obstructive disorders e.g. emphysema and chronic bronchitis
(COPD); asthma and status asthmaticus and cystic fibrosis
b. Diffuse restrictive disorders e.g. Interstitial fibrosis e.g. silica and coal;
pulmonary oedema (cardiogenic, non-cardiogenic e.g. ARDS);
atelectasis ; consolidated pneumonia
c. pulmonary vascular disorders e.g. pulmonary emboli and severe
emphysema
5.0 CLASSIFICATION
1. Type I – Failure of oxygen exchange (PaO2 <60)
2. Type II – Failure to exchange or remove carbon dioxide (PaCO2 >45)
1. Type III – Post operative respiratory failure (both oxygen and
ventilatory failure)
2. Type IV – Shock
5.1. Type I Respiratory Failure
 Is a state of hypoxaemia without CO2 retention (blood carbon dioxide
remains within the normal limits)
 Failure of oxygen exchange
 Pathophysiologic mechanisms of arterial hypoxaemia include
1) Decreased partial pressure of O2 in alveoli
a) Hypoventilation
b) Decreased partial pressure of O2 in the inspired air
c) Underventilated alveoli (areas of low ventilationperfusion)
2) Intrapulmonary shunt (areas of zero ventilation-perfusion)
3) Decreased mixed venous O2 content (low-haemoglobin saturation)
a) Increased metabolic rate
b) Decreased cardiac output
c) Decreased arterial O2 content

Causes
1. Adult respiratory distress syndrome (ARDS)
2. Asthma
3. Pulmonary oedema
4. Chronic obstructive pulmonary disease (COPD)
5. Interstitial fibrosis
6. Pneumonia
7. Pneumothorax
8. Atelectasis
Diagnosis
1. Arterial blood gases analysis – reduced PaCO2
2. Respiratory function tests – reduced FEVR and FEV1
5.2. Type II Respiratory Failure
 Failure to exchange or remove carbon dioxide
 A state of decreased PaO2 and increased PaCO2 (> 6.7 kPa/50 mmHg)
 Results from alveolar hypoventilation and is commonly from chronic
bronchitis and emphysema
Causes
1) Disorders affecting central ventilatory drive
a) Brain stem infarction or haemorrhage
b) Brain stem compression from supratentorial mass
c) Drug overdose, narcotics, benzodiazepines, anaesthetic agents etc.
2) Disorders affecting signal transmission to the respiratory muscles
a) Myasthenia Gravis
b) Gullain-Barrè syndrome
c) Spinal –Cord injury and Head injury
d) Multiple sclerosis
e) Residual paralysis (Muscle relaxants)
3) Disorders of respiratory muscles or chest-wall
a) Muscular dystrophy
b) Polymyositis
c) Flail Chest
d) Thoracic wall deformities
Mechanism
Reduced alveolar ventilation results in reduced ventilator effort and there is
inability of the alveolar to overcome increased resistance to ventilation.
5.3. Type III Respiratory Failure
 Perioperative respiratory failure
 Increased atelectasis due to low functional residual capacity (FRC) in the
setting of abnormal abdominal wall mechanics

 Often results in type I or type II respiratory failure and can be enhanced by
anaesthetic or operative technique, posture, incentive spirometry, post-operative
analgesia, attempts to lower intra- abdominal pressure
Causes
1. Inadequate post- operative analgesia, upper abdominal incision
2. Obesity, ascites
3. Pre- operative tobacco smoking
4. Excessive airway secretions
5. Adult ARDS
6. Asthma
7. Chronic obstructive pulmonary disease
5.4. Type IV Respiratory Failure
 Describes patients who are intubated and ventilated in the process of
resuscitation for shock
 Goal of ventilation is to stabilize gas exchange and to unload
Causes
1. Cardiogenic shock
2. Septic shock
3. Hypovolemic shock
6.0 EFFECTS ON CVS
 Chronic respiratory failure has major effects in the cardiovascular system
including pulmonary hypertension and polycythaemia.
Pulmonary Hypertension
 Pulmonary vasoconstriction results in increased pulmonary artery pressure
and increased work of the ventricles
 The effects are felt in pulmonary arteries resulting in intimal proliferation
and occlusion of the lamina.
Polycythaemia
 Hypoxia stimulates release of erythropoietin by the kidney, which is the
cause of increased viscosity of blood and the risk of thrombosis.
7.0 FEATURES OF RESPIRATORY FAILURE
 Tachycardia, tachypnoea, sweating, inability to speak
 Use of accessory muscles of respiration
 Pulsus paradoxical and paradoxical respiration (abdominal and thoracic
components move in opposite directions), asynchronous respiration
(discrepancy in the rate of movement of the abdominal and thoracic
components), respiratory alternans
8.0 INVESTIGATIONS
1) Chest x-ray
2) ECG
3) Echocardiogram

4) Pulmonary function tests
5) Bronchoscopy
6) Blood gas analysis
Collapse of Lung Tissue – Atelectasis
1.0 INTRODUCTION
 Lung collapse comprises of atelectasis and acquired collapse
 ‘Atelectasis’ is a Greek word for imperfect expansion
 Atelectasis refers to incomplete expansion of the lungs (neonatal
atelectasis) or the collapse of a previously inflated lung (acquired
atelectasis) encountered in adults.
 Atelectasis has important clinical consequences of disturbing the respiratory
function namely: -
1) Obstruction of an airway results in resorption of air from the lung distal to
the obstruction
2) Compression of the lung as seen when fluid or air accumulates in the
pleural cavity
3) Scarring of the lung resulting in contraction of parenchyma and collapse
4) Loss of normal surfactant (developmental or acquired) results in
generalized failure of lung expansion (microatelectasis).
Diagram 4.1: Lung Collapse
2.0 ATELECTASIS (Neonatal)
Atelectasis is incomplete expansion of neonatal lung (failure of lungs to expand
at birth).
Aetiology
1. Failure of the respiratory centre
2. Prematurity – lack of surfactant, immaturity of the respiratory centre
3. Hyaline membrane disease
4. Laryngeal dysfunction
5. Obstruction of airway passages
6. Idiopathic
7. Cerebral damage – depresses respiration

3.0 ACQUIRED LUNG COLLAPSE
Can occur because of resorption atelectasis, compression atelectasis and
contraction atelectasis
Resorption Atelectasis
 Occurs because of complete obstruction of an airway resulting in resorption
of oxygen trapped in independent alveoli without impairing blood flow
through the affected alveoli
 Lung volume is reduced and hence the mediastinum shifts to towards the
atelestatic lung
 Excessive secretions e.g. mucous plugs or exudates with smaller bronchi
may cause the obstruction
 Seen in bronchial asthma, chronic bronchitis, bronchiectasis, post-operative
states and aspiration of foreign bodies
 Secretions then replace the air and oedema fluid, which become infected
quite easily resulting suppuration and tissue destruction that results in
irreversible pulmonary fibrosis.
Diagram 3.2: Resorption
Compression Atelectasis
 Occurs when pleural cavity is partially or completely filled with fluid
exudates; tumours blood or air e.g. pneumothorax and tension
pneumothorax
 Commonly encountered in patients with cardiac failure who develop pleural
effusion and patients with neoplastic effusions within pleural cavities
 Pressure collapse results from compression of the lung tissue from without
due to pressure on the visceral pleura fluid or air
 The mediastinum shifts away from the affected lung

Diagram 4.3: Compression Atelectasis
Causes
1. Pleural effusion
2. Haemothorax
3. Empyema
4. Pneumothorax
5. Haemo-pneumothorax
Contraction Atelectasis
 Occurs when local or generalized fibrotic changes in the lungs/pleural
cavity prevent full expansion of the lung.
Diagram 4.4: Contraction Atelectasis
CLINICAL TASK
1. What are the clinical features of lung
collapse?
2. What investigations will be important?
3. What are the differentials?

Left Side Collapse
Upper Lobe Collapsed

Lesson 5: Bronchial Obstruction and Emphysema
Learning Outcomes
1. Describe causes and effects of bronchial obstruction and emphysema
2. Diagnose bronchial obstruction and emphysema
3. Investigate bronchial obstruction and emphysema
Obstructive Pulmonary Diseases
 The bronchi have ciliated mucous secreting cells that defend the airways
and lungs against bacteria and foreign bodies
 Chronic irritation of the bronchi leads to hyperplasia and hypertrophy of the
mucous secreting glands and goblet cells
 Obstructive pulmonary diseases affect the airways and are characterized by
increased resistance to airway flow due to partial or complete obstruction at
any level along the respiratory passages (trachea  respiratory
bronchioles)
 The main diffuse obstructive disorders are emphysema, chronic bronchitis,
bronchiectasis and asthma
 Patients with bronchial obstruction have limitations of maximal airflow rates
during forced expiration at 1 second (reduced FEV1).
 Emphysema and chronic bronchitis are grouped together as chronic
obstructive pulmonary diseases (C.O.P.D) or chronic obstructive airway
diseases (C.O.A.D)
 COPD refers to patients who have largely irreversible airways obstruction.
 Key aetiological factors in COPD are smoking (major risk), environmental
pollutants (e.g. occupation – mines, dust) andantitrypsin deficiency.
Table 1: Disorders of Airflow Obstruction
Clinical
Anatomic
Term
site
Major Pathologic
changes
Aetiology Signs/symptoms
Chronic
Bronchitis
Bronchus Mucous gland
hyperplasia and
hypersecretion
Tobacco smoke
and pollutants
Cough and
sputum
production
Bronchiectasis Bronchus Airway dilatation and
scarring
Persistent or
severe infections
Cough, purulent
sputum and fever
Asthma Bronchus Smooth muscle
hyperplasia, excess
mucous and
inflammation
Immunologic or
undefined causes
Episodic
wheezing, cough
and dyspnoea
Emphysema Acinus Airspace enlargement
and wall destruction
Tobacco smoke Dyspnoea
BRONCHIAL OBSTRUCTION
 Occurs in various degrees from partial obstruction to complete obstruction
affecting small and large bronchi
 The obstruction, which may be sudden or gradual, results in accumulation
of secretions with oedema formation leading to some degree of dilatation of
the bronchi

 Secondary bacterial infection ensues producing suppurative bronchitis and
by extension suppurative bronchopneumonia.
1.0 CAUSES
1. Tumours - Bronchial carcinoma and Bronchial adenoma
2. Enlarged tracheobronchial lymph nodes – malignancy, tuberculous
3. Inhaled foreign body (FB)
4. Bronchial casts or plugs consisting of inspissated mucous or blood clot
5. Collections of mucous or mucopus retained due to ineffective expectoration
6. Congenital bronchial atresia
7. Fibrous bronchial stricture (post TB)
8. Aortic aneurysm
9. Giant left atrium
10. Pericardial effusion
2.0 EFFECTS
1. Lung collapse - complete obstruction of the bronchioles leads to absorption
of the air in the alveoli with the alveolar spaces collapsing.
2. Emphysema (obstructive) - Results in a resonant note on percussion,
diminished breath sounds and a displaced mediastinum
3. Secondary infection/suppuration
4. Impaired pulmonary function – dyspnoea and hypoxaemia
5. Features related to obstruction
EMPHYSEMA
 Emphysema is abnormal permanent dilatation/enlargement of airspaces
distal to the terminal bronchiole accompanied by destruction of the
bronchiole walls without fibrosis
 It is a constituent of COPD/COAD
Diagram 5.1: Emphysema

Elactase normally inactivated by protease inhibitors (e.g.-1-antitrypsin)
.-1-antitrypsin deficiency leads to failure
of elastase inactivation
Elastases
destroy alveolar
wall
1.0 AETIOLOGY
The main factors are -
1. Smoking – major risk factor that is dose related
2. -antitrypsin deficiency – a protease inhibitor that prevents lung damage
especially in smokers
3. Occupation – dusty environments e.g. coal mines
2.0 PATHOGENESIS
 Is due to imbalance between protease and anti-protease activities in the
lung resulting in destruction of the alveolar walls (Anti-protease hypothesis)
o -antitrypsin protease inhibitor) is a glycoprotein constituent of
globulin in plasma is synthesised in the liver and is usually present in
serum and tissue fluids. Protease inhibits protelytic enzymes, which
degrade elastin or neutrophil derived elastase. Increased neutrophil
infiltration of the lung causes excessive production of elastase
o Deficiency of-antitrypsin occurs in homozygous states however in
smoking accelerates the damage in heterozygous situations
 Smoking
o Reduces anti-elastase and increases elastolytic protease in the lungs due
to oxidants in cigarette smoke which inhibit -antitrypsin and smokers
have increased phagocytes and neutrophils in the lungs
 After the damage the pressure inspired air expands the damaged portion
into an emphysematous space
 With continued enlargement more pressure is required to cause further
dilatation resulting in increased dilatation and damage
 Coughing in chronic bronchitis aggravates the situation
Diagram 5.2: Pathogenesis of Emphysema
Smoking
Neutrophils and
macrophages
release elastase
3.0 PATHOLOGY
Macroscopy
 Voluminous pale lungs with dilatation of air spaces
Microscopy
 Dilatation of air spaces
 Destruction of septal wall resulting in thin walls
 Compressed capillaries
 Rupture of walls producing honeycombs
Emphysema

4.0 CLASSIFICATION
Classification is based on anatomical distribution within the lobule.
a) Centrilobular/centriacinar
b) Panaacinar/panlobular
c) Paraseptal/distal acinar
d) Irregular
4.1. Centrilobular/Centriacinar
 Predominant in male smokers and chronic bronchitis
 Central or proximal parts of the acinar are involved
 Involves enlargement of terminal airspaces and the respiratory bronchioles
because of destruction and enlargement of the central or proximal parts of
the respiratory unit (the acinar).
 Distal acinar are spared
 Associated with cigarette smoking, chronic bronchitis and inflammation of
distal airways
4.2. Panacinar (Panlobular) Emphysema
 Affects all acinar which are uniformly enlarged from the level of the
respiratory bronchioles to the terminal blind alveoli
 Associated with 1-antitrypsin deficiency
4.3. Distal Cinar (Paraseptal) Emphysema
 Affects distal portion of the acinus
 Proximal portions of the acinus are spared
 Usually due to infections accompanied by inflammatory changes and
fibrosis
4.4. Irregular Emphysema
 Acinar irregularly affected
 Mainly associated with scarring
 Most common form of emphysema
5.0 CLINICAL FEATURES
Cough, expectoration; wheezing; slowly increasing severe exertional
dyspnoea; respiratory distress; chest – barrel shaped; hyper-resonant
percussion note; hyperventilation; tachycardia; patients are “pink puffers” –
they remain well oxygenated and have tachycardia; do not tolerate, hypoxia;
Weight loss
6.0 COMPLICATIONS
1) Cor pulmonale
2) Congestive Cardiac failure
3) Pulmonary hypertension
TASK
 Compare and contrast emphysema and
chronic bronchitis.
 State the important investigations

Lesson 6: Bronchiectasis, Bronchitis and Bronchiolitis
Learning Outcomes
1. Describe causes and effects of bronchiectasis, bronchitis and bronchiolitis
2. Diagnose bronchiectasis, bronchitis and bronchiolitis
3. Investigate bronchiectasis, bronchitis and bronchiolitis
Bronchiectasis
1.0 INTRODUCTION
 Bronchiectasis is localized or generalized permanent abnormal dilatation of
the bronchi or bronchioles (more than 2 mm in diameter) caused by
destruction of the muscle and elastic tissue, resulting from or associated with
chronic necrotizing infections
 Usually results from the weakening of the bronchial wall a sequel of
destruction of elastic and muscular components of the walls following
necrotizing infection of the bronchi and bronchioles.
Diagram 6.1: Bronchiectasis
2.0 AETIOLOGY
The main categories: -
1. Pulmonary infection
2. Bronchial obstruction

3. Associated factors
a. Congenital and hereditary conditions e.g. Cystic fibrosis; Intralobular
sequestration of the lung; Immunodeficiency states; Kartagener’s
syndrome (Bronchiectasis, sinusitis, displacement of viscera (heart) –
immobility of the cilia; Congenital bronchiectasis; atelectasis
b. Post infection conditions e.g. Necrotising pneumonia caused by bacteria
(Myocobacterium tuberculosis, Staphylococcus aureus, Haemophilus
influenza and Pseudomonas), viral (HIV, adenoviruses and influenzae),
fungal (Aspergillus)
c. Bronchial obstruction e.g. tumours, foreign bodies and mucous
impaction
d. Others e.g. Bronchiolitis and bronchopneumonia in childhood;
Rheumatoid arthritis; S.L.E; Inflammatory bowel syndrome; post-transplant
3.0 PATHOGENESIS
 The major factors in the pathogenesis of bronchiectasis are obstruction and
infection.
Diagram 6.2: Pathogenesis of Bronchiectasis
3.1. Obstruction
 Obstruction leads to accumulation and stagnation of secretions
 Secretion later become infected resulting in an inflammatory reaction that
leads to destruction and weakening of the bronchial walls facilitating
dilatation of the bronchi.
 Obstruction reduces mural clearing mechanisms resulting in pooling of
secretions distal to the point of obstruction and increases susceptibility to
infections.
 Necrotizing inflammation results in destruction of the bronchi and
bronchioles leading to formation of multiple large spaces or cavities. This
destruction tends to include the surrounding lung tissue, which heals by
fibrosis with resultant obliteration and destruction of smaller bronchi and
bronchioles.

 Cavities formed accommodate a lot of secretion within the bronchi, which
become infected becoming purulent
 Without treatment of the infection, the fluid trapped within cavities becomes
infected persistently by putrefying microorganisms resulting in formation of
purulent fluid that becomes decomposed producing foul smelling breath
and sputum. The organisms spread from this focus to the alveoli by air
passages or direct spread through the vein forming a septic embolus that
forms secondary abscesses (especially in the brain).
Diagram 6.3: Pathogenesis - Obstruction
 Destruction of the bronchi involves ulceration of the bronchial walls. The
respiratory passage may wholly or partly be lined by respiratory simple
columnar epithelium but later become squamous metaplasia
 Haemoptysis which may be little or massive occur as bleeding from thin
walled vessels in the dilated bronchi/bronchioles.
 Chronic bronchiectasis leads to haemodynamics changes due to alveolar
hypoxia and fibrous obliteration of the pulmonary arteries, which results in
enlargement, and development of bronchopulmonary vascular
anastomoses.
3.2 Infections
 Chronic necrotizing inflammation of the bronchial walls causes destruction
of the elastic and muscle tissues resulting in damage of the walls leading to
dilatation of the bronchi that allows accumulation and stagnation of the
secretions that easily become secondarily infected causing further damage
of the bronchial wall. Microorganisms associated with this phenomenon are
bacterial infection with
 Mycobacterium tuberculosis, Heamophilus influenzae, Staphylococcus and
fibrosing, suppurative pneumonias and corrosive chemicals. Infection may
be primary infection of secondary to local obstruction and impaired
systemic defence systems.
 Repeated infections results in increased damage to the airway walls with
destruction of the supporting smooth muscle and elastic tissues and
eventually fibrosis with further dilatation of the bronchi. The infection also
causes necrosis of the walls leading to healing with fibrosis hence dilatation
of the bronchi. small bronchi progressively become obliterated due to
fibrosis (bronchitis obliterans)

Diagram 6.4: Pathogenesis – Infections
4.0 PATHOLOGY
Macroscopy
1. Dilated bronchi with thickened walls
2. Lumen filled with mucous or muco-pus
3. Firbrotic surrounding lung
4. Dilatation
Microscopic
1. Epithelium - normal, ulcerated or squamous epithelium
2. Bronchial wall - infiltrated by acute and chronic inflammatory cells,
destruction of muscle and elastic tissues
3. Lung fibrosis
4. Adherent pleura
1. Severe , persistent/chronic cough
2. Sputum – haemoptysis, foul smelling, purulent
3. Recurrent pneumonia
4. Fever, weight loss, anaemia, weakness
5. Sinusitis
6. Digital clubbing
7. Metastatic abscess
8. Cyanosis
6.0 DIAGNOSIS
1. Bronchophony
2. Bronchoscopy
3. Sputum – colour, volume, cellular component, bacterial infection, Gram
stain, culture, white blood cells, bacteriological examination
4. Blood count
5. ECG
6. Urinalysis
7. Oxygen tension
8. Lung function tests
What is the relationship
between Bronchiectasis and
cystic fibrosis?

7.0 EFFECTS/COMPLICATIONS
1) Suppuration/empyema
2) Septic emboli (Brain abscess)
3) Pyaemia - brain abscess (metastatic) and meningitis – from involvement
of the pulmonary vein
4) Finger clubbing (Hypertrophic pulmonary osteodystrophy)
5) Pulmonary hypertension
6) Cor pulmonalae
7) Amyloidosis
8) COPD
9) Recurrent pneumonia
10) Respiratory failure
BRONCHITIS
1.0 Acute Bronchitis
This is inflammation of the large and medium bronchi.
1.1. Aetiology
1. Viral - respiratory syncytial virus; rhinovirus; echovirus; parainfluenza types
1, 2 3; Influenza, Herpes viruses, Coxsackie viruses, Corona viruses,
Adenoviruses and Measles
2. Mycoplasma - Candida albicans, Candida tropicalis, Histoplasma capsulatum
and Cryptococcus neoferans
3. Bacteria (secondary infection) - Strep pneumonia, H. Influeanzae, Strep
pyogenes (common in infants, ), Staph aureus (common in infants) and
Salmonella typhi
Diagram 6.5: Bronchitis

1.2. Pathogenesis
 Invasion by microbes leads to inflammatory reaction by the bronchial
epithelium
 There is activation of the mucous and serous glands leading to production
of mucous secretions that cause crackles on auscultation.
 Spread of the inflammatory reaction to involve bronchioles in debilitated
subjects’ results in bronchiolitis and bronchopneumonia, which is fatal.
 Because of inflammatory oedema, there is reduction in lumen size resulting
in wheezing and rhonchi.
1.3. Pathology
Macroscopy
 Congested, swollen/oedematous, hyperaemia and tenacious mucous
exudate, sputum – yellow/green
Microscopy
 Congested mucosa with infiltration by neutrophils
1.4. Clinical Features
 Cough – initially unproductive but later yellow/green sputum.
 Wheezes/rhonchi, crepitations
 Shortness of breath
 Fever
 Neutrophilia
2.0 Chronic Bronchitis
2.1. Introduction
 Chronic bronchitis is defined clinically as persistent cough with sputum
production on most days for at least 3 months in at least two consecutive
years
 It is not primarily an inflammatory condition but consists of metaplastic
changes as a result of chronic irritation of the bronchial epithelium.
2.2. Aetiology
1. Smoking - prolonged cigarette smoking impairs cilia movement, causes
hyperplasia and hypertrophy of mucous secreting glands, inhibits function
of alveolar macrophages and stimulates the vagus nerve causing
bronchoconstriction.
2. Atmospheric pollution - sulphur dioxide, nitrous oxide, toxic fumes and
particulate dust particles.
3. Occupational hazards - Cotton mills, Plastic factories
4. Infection- bacterial, viral and myocoplasmal infections occur as a result of
bronchitis and predispose to acute exacerbations of chronic bronchitis
5. Familial/genetic factors - poorly understood

Bronchiolar and Bronchial injury
2.3. Pathogenesis
 Chronic irritation of the bronchial epithelial cells causes hypertrophy and
hyperplasia of the mucous glands leading to excessive secretion of mucous
secretions(more goblet cells than ciliated cells)
 Excessive mucous production and destruction of cilia leads to accumulation
of the secretions and exudate in the bronchi and bronchioles causing
obstruction. This extends to involve the bronchioles hence bronchiolitis
ensues.
 Destruction of the epithelial causes some areas of ulceration, which heal by
fibrosis causing narrowing of the bronchial lumen.
 Invasion of secretions by bacteria mainly H. influenzae and Strep.
pneumoniae results in secondary infection leading to pus formation.
 Destruction of the epithelia occurs resulting in metaplasia where the
squamous epithelium is replaced by columnar epithelium.
Diagram 6.6: Evolution of Chronic Bronchitis
Bronchospasms
2.4. Pathophysiology
 Mucous hypersecretion is a physiological response to inhaled irritants
 Increased secretion impairs normal clearance
 Impaired cilia function and increased accumulation of mucous secretions
 Increased susceptibility to acute respiratory infections with bacterial -
suppuration.
2.5. Pathology
Macroscopy
 Hyperaemia and oedema of mucous membrane
 Mucous secretions and increased size of mucous glands
 Plugging of bronchi and bronchioles
 Fibrosis and inflammatory changes
Microscopy
 Venous congestion
 Metaplasia, hypertrophy and dysplasia
 Inflammatory cells
Infections
Hyper secretion
of mucous
Reversible obstruction in
bronchioles and small bronchi
Chronic Bronchitis
Continued and
repeated
infections
Continued and repeated
injury (e.g. smoking)

 Increased thickness of the mucosal gland layer (at post mortem, Reid index
which is the ratio of glandular layer to the whole thickness is significant if
the value is more than 1:2.)
2.6. Differential Diagnosis
1. Bronchial asthma
2. Emphysema
3. COPD
4. Bronchiectasis
5. Chronic pulmonary infections
6. Chronic sinusitis with post-nasal drip
2.7. Complications
1. Respiratory failure
2. Emphysema
BRONCHIOLITIS
1.0 INTRODUCTION
 Bronchiolitis is inflammation of small, intralobular bronchi and bronchioles
seen in children, old people and debilitated states.
 Bronchiolitis is a lower respiratory tract infection usually caused by a virus
and occurs in children younger than two years old
 It is fatal as organisms spread to adjacent acini resulting in
bronchopneumonia
 It is usually caused by a virus which causes inflammation of the small airways
(bronchioles) partially or completely blocking the airways resulting in
wheezing. Less oxygen enters the lungs, potentially causing a decrease in
the blood level of oxygen.
 Catarrhal bronchitis is characterized by excessive secretion of mucous and
increased inflammatory exudate. The mucoid sputum becomes
mucopurulet after invasion by bacteria such as Strep. pneumoiae, H.
influezae, Strep. pyogenes ad Staph. aureas. In severe cases, superficial
layers are sloughed off resulting in ulcer formation (ulcerative bronchitis).
 Breast-feeding is considered protective and should be encouraged. Breast
milk with colostrum rich has high levels of immunoglobulin A (IgA)
 Infants are affected most often because of their small airways, high closing
volumes, and insufficient collateral ventilation
2.0 CAUSES
 Respiratory syncytial virus (RSV) – most common cause
 Human metapneumovirus (hMPV) - second most common cause
 Adenovirus - occasionally causes a similar syndrome with a more virulent
course
 Parainfluenza virus
 Other less common causes include Mycoplasma pneumonia, Enterovirus,
Influenza virus, Rhinovirus, Chlamydophila pneumoniae

3.0 RISK FACTORS
1. Low birth weight, particularly premature infants
2. Gestational age (independently associated with hospital resource use
and outcome among infants hospitalized for RSV infection)
3. Lower socioeconomic group
4. Crowded living conditions, day-care, or both
5. Parental smoking
6. Chronic lung disease,
7. Severe congenital or acquired neurologic disease
8. Congenital heart disease (CHD) with pulmonary hypertension
9. Congenital or acquired immune deficiency diseases
10. Age less than 3 months
11. Airway anomalies
4.0 PATHOPHYSIOLOGY
 Bronchioles are small airways (< 2 mm in diameter), lack cartilage, and
submucosal glands. The terminal bronchiole, a 16th-generation airway, is
the final conducting airway that terminates in the respiratory bronchioles.
 The acinus (gas exchange unit) consists of respiratory bronchioles, the
alveolar duct, and alveoli
 The bronchiolar lining consists of surfactant-secreting clara cells and
neuroendocrine cells, which are the source of bioactive products such as
somatostatin, endothelin, and serotonin.
Mechanisms
1. Bronchiolar injury and the consequent interplay between inflammatory
and mesenchymal cells can lead to diverse pathologic and clinical
syndromes. Effects of bronchiolar injury include:
a. Increased mucus secretion
b. Bronchial obstruction and constriction
c. Alveolar cell death, mucus debris, viral invasion
d. Air trapping
e. Atelectasis
f. Reduced ventilation that leads to ventilation-perfusion mismatch
g. Laboured breathing
2. Complex immunologic mechanisms - Type 1 allergic reactions mediated
by immunoglobulin E (IgE) may account for some clinically significant
bronchiolitis.
3. Necrosis of the respiratory epithelium and epithelial regeneration with
non-ciliated cells impairs elimination of secretions.
4. Proliferation of goblet cells results in excessive mucus production
5. Cytokines and chemokines - released by infected respiratory epithelial
cells, amplify the immune response
6. Airway obstruction was due to epithelial and inflammatory cell debris
mixed with fibrin, mucus, and oedema fluid but not to bronchial smooth
muscle constriction

Symptoms
 Early symptoms are those of a viral URTI, including mild rhinorrhoea,
cough and fever. Fever >39°C
 Paroxysmal cough and dyspnoea develop within 1-2 days.
 Wheeze, cyanosis, vomiting, irritability and poor feeding
Signs
 Look for tachypnoea, tachycardia, fever, cyanosis and signs of
dehydration. It is unusual for a child to appear 'toxic' (suggested by
drowsiness, lethargy, pallor, mottled skin)
 Mild conjunctivitis, pharyngitis.
 Evidence of increased respiratory work: intercostal, subcostal and
supraclavicular recession, nasal flaring.
 Widespread fine inspiratory crackles, high-pitched expiratory wheezing
 Liver and spleen may be palpable due to hyperinflation of the lungs.
Diagram 6.7: Features of Bronchiolitis
6.0 PATHOLOGY
 Virus-induced inflammation of the bronchiolar epithelium, with
hypersecretion of mucus and oedema of the surrounding submucosa
 These changes result in formation of mucous plugs obstructing bronchioles
with consequent hyperinflation or collapse of the distal lung tissue
 Resistance in small air passages is increased during inspiration and
expiration, but because airway radius is smaller during expiration,
resultant ball valve respiratory obstruction leads to early air trapping and
overinflation
 Atelectasis may occur when obstruction becomes complete and trapped
air is absorbed

Diagnosis and Grading
Feature Mild Moderate Severe
Wheeze
None or end
expiratory
Entire expiration
Inspiratory & Expiratory
Feeding Normal
Less than usual. Frequently
stops feeding.
More than ½ normal feeds.
Not interested.
Gasping / coughing.
Less than ½ normal feeds
Oxygen No oxygen
requirement
May require oxygen Requires oxygen
In
drawing
No / mild
in drawing
Intercostal and / or
tracheosternal
Severe with nasal flaring
Behaviour Normal Some/intermittent irritability Irritability and/or lethargy
7.0 DIFFERENTIAL DIAGNOSIS
1. Asthma
2. Bronchitis
3. Pulmonary oedema
4. Foreign body inhalation
5. Pneumonia
6. Aspiration
7. Cystic fibrosis
8. Pneumothorax
8.0 INVESTIGATIONS
1. Pulse oximetry
2. Nasopharyngeal aspirate for viral cultures for RSV, influenza A and B,
parainfluenza and adenovirus
3. CXR
a. Children with a clear clinical diagnosis of bronchiolitis do not require a
chest x-ray.
b. Show signs of hyperinflation, peribronchial thickening, and often-patchy
areas of consolidation and collapse
4. Full Blood Count
5. Electrolytes and renal function
6. Blood and urine culture: consider if pyrexia >38.5°C or the child has a
'toxic' appearance.
7. Arterial blood gases: may be required in the severely ill patients,
especially in those who may need mechanical ventilation.
9.0 COMPLICATIONS
 Cyanosis
 Dehydration: when the normal water content of the body is reduced
 Fatigue: extreme tiredness and a lack of energy
 Severe respiratory failure: an inability to breathe unaided
 Pneumonia
 Atelectasis
 Pleural effusion

Lesson 7: Bronchial Asthma
Learning Outcomes
At the end of the lesson, the learner should be able to: -
1) Discuss the causes , pathogenesis and pathophysiology of asthma
2) Investigate a patient with asthma
3) Discuss complications of asthma
1.0 INTRODUCTION
 Bronchial asthma is a chronic relapsing inflammatory disorder
characterized by increased responsiveness of the tracheobronchial tree to
various stimuli resulting in widespread paroxysmal contraction of bronchial
airways due to muscular spasms and plugging by increased thick mucous
secretions from the mucosal glands
 The changes that occur result in a state whereby the respiratory tree is
drawn longer with a reduced diameter forming a physiological valve
mechanism that leads to easy or normal inspiration and difficult and
prolonged expiration
 The short inspiration and long expiration produces the characteristic
wheeze/rhonchi in bronchial asthma.
 Asthmatic attacks cause shortness of breath and wheezing respirations
because of restricted movement of air through tightly constricted air
passages
 Bronchial spasms exert great effect on expiration than inspiration because
the calibre of bronchioles varies with the phase of respiration.
Diagram 7.1: Anatomical Considerations in Asthma

2.0 AETIOLOGY
 Unclear but associations exist with genetic makeup, atopy or allergy and
increased responsiveness of the airways
 Precipitants include occupational sensitises, allergens, infections and non-specific
e.g. cold air, exercise, diet, atmospheric pollution/irritants, dust,
vapours, fumes, emotion, drugs e.g. NSAIDS
3.0 AETIOLOGICAL CLASSIFICATION
1. Extrinsic (atopic, allergic) asthma
2. Intrinsic (cryptogenic, non-atopic, idiosyncratic) asthma.
3. Exercise induced asthma
4. Drug induced
5. Occupational asthma
6. Asthma associated with COPD
Diagram 7.2: Progression in Asthma
Hypersensitivity
Hypersensitive airway disease
Bronchitis
Asthma (overt)
3.1. Extrinsic (Atopic, Allergic) Asthma
 Commonest type of asthma that has a definite cause associated with the
disease as it runs in families and individuals with history of allergy
 Individuals may have a history of diseases such as rhinitis, urticaria and
infantile eczema. Atopic or extrinsic asthma begins in childhood and early
adult life
 Subjects with extrinsic asthma have increased levels of IgE representing
type I hypersensitivity reaction mechanisms and they do show characteristic
wealing skin reactions to common allergens in the environment.
Pathogenesis
 Exposure of pre-sensitized IgE coated mast cells to allergens (antigens)
results in release of chemical mediators in a reaction that first takes place
on the mucosal surface and results in the opening of the intercellular tight
junctions thereby enhancing penetration of the mast cells by antigens to
reach the numerous submuocal mast cells.
 Direct stimulation of the subepithelial vagal (parasympathetic) receptors
provokes bronchoconstriction through both central and local reflexes.
 This is an acute or immediate response, which consists of
bronchoconstriction, oedema, mucous secretion and hypotension (in
severe cases).
 Mast cells release cytokines, which result in influx of leucocytes
(neutrophils, monocytes, lymphocytes, basophils and oesinophils)
which mediate the late phase reaction together with recruited chemotaxic
factors.

 Other sources of mediators of the late phase reaction include the vascular
endothelium and airway epithelial cells (produce cytokines in response to
infection, drugs and gases.
Diagram 7.3: Pathogenesis
3.2. Intrinsic Asthma (Non-atopic)
 Develops in adult life staring during the middle age and is commonly
associated with chronic bronchitis
 There is a negative family history of the disease as well as personal history
of allergy as these individuals fail to reveal a responsive allergen.
 However, there may be a history of respiratory symptoms compatible with
childhood asthma
 Individuals with intrinsic asthma tend to develop drug hypersensitivity
especially with aspirin and penicillin.
3.3. Drug Induced
 Drugs such as aspirin trigger asthma by inhibiting COX pathway of
arachidonic acid metabolism without affecting the lipoxygenase route thus
resulting in increased production of bronchoconstritive leukotrienes.
3.4. Exercise Induced
 Is a phenomenon that can occur in isolation or in association with any type
of asthma
 Many patients experience airway obstruction, 5 to 20 minutes after
completing the exercise or in the course of it, by a mechanism that seems to

include the cooling, the relative dryness of the airway secondary to
increased ventilation and loss heat the air.
 The precise pathophysiology remains unclear, but may involve heat and
water loss from the airway
 The osmotic hypothesis proposes that this water loss leads to dehydration
and hyperosmolarity of the airway surface liquid causing the release of
water from airway cells. This water loss results in cell shrinkage, vascular
leak and the release of mediators, which cause airway smooth muscle
contraction, edema, and bronchoconstriction. This shift in water from the
cells and the subsequent regulatory volume increase most likely involve
alterations in ion channels and signalling pathways
 The thermal hypothesis proposes that the rapid rewarming of the airway
following heat loss during exercise is associated with a reactive hyperemia
of the bronchial vasculature, which results in congestion of the vascular bed
and airway obstruction.
3.5. Occupational Asthma
Occupational asthma is stimulated by fumes (epoxy resin, plastics), organic
and chemical dusts (wood, cotton, platinum), gases (toluene), chemicals
(formaldehyde and penicillin products).
4.0 PATHOGENESIS AND PATHOPHYSIOLOGY
The pathogenesis of bronchial asthma pivots around: -airway hypersensitivity,
inflammation and airway obstruction
4.1. Airway Hypersensitivity (hyperesponsiveness)
 There is increased responsiveness of the respiratory airways of the lung to
allergens in the environment whose inhalation triggers an immediate acute
response initiated by IgE sensitised mast cells in the mucosal surface of the
respiratory tree
 Mast cells degranulate releasing mediators of inflammation such as
histamine, leukotrienes, prostaglandins and platelet aggregating factor
(PAF) and chemostatic factors for oesinophils and neutrophils
 The respiratory tree is hypersensitive to normal allergens, which can
trigger off reactions. These allergens include inhaled and non-inhaled ones.
The inhaled allergens include - aeroallergens (house dust mites, pollens,
animal dander and fungal spores) air pollution, extreme cold. The non-inhaled
are exercise and ingested substances.
4.2. Inflammation and oedema
 Following the hypersensitivity reaction and release of mediators of
inflammation, there ensues an inflammatory reaction that results in oedema
formation, bronchoconstriction and hypersecretion of mucous and
accumulation of oesinophils and neutrophils. There is infiltration of the
airways with inflammatory cells, Thelper lymphocytes, oesinophils and mast
cells, which is a common feature in asthma.

4.3. Airway Obstruction/bronchoconstriction
The pathologic basis of airway obstruction is: -
1. Constriction of the airway’s smooth muscles due to release of bioactive
mediators and neurotransmitters.
2. Thickening of the airway epithelium due to oedema formation
3. Presence of liquids and mucous secretions within the confines of the
bronchial lumen
4.4. Airway remodelling
 In some patients permanent structural changes can occur in the airway
 The changes are associated with a progressive loss of lung function that is
not prevented by or fully reversible by current therapy
 Airway remodelling involves an activation of many of the structural cells,
with consequent permanent changes in the airway that increase airflow
obstruction and airway responsiveness and render the patient less
responsive to therapy
 The changes can include thickening of the sub-basement membrane,
subepithelial fibrosis, airway smooth muscle hypertrophy and hyperplasia,
blood vessel proliferation and dilation, and mucous gland hyperplasia and
hyper secretion
4.5. Cells Involved
Mast Cells
 The number is increased in the respiratory epithelium and surface
secretions
 They cells generate and release powerful smooth muscle and vasoactive
mediators such as histamine, prostaglandin D2 (PD2) and leukotrienes C4
(LTC4) that cause the immediate asthmatic reaction. Note that 2
adrenoreceptor e.g. salbutamol inhibit release of mediators by the mast
cells.
The Epithelium
 Shed during exacerbations of asthma resulting in desquamations, which
increase permeability of the airway to inhaled allergens and exposure of
nerve fibre endings
 Desquamated materials from the columnar epithelium can be identified in
the sputum as twisted strips called Curschmann’s spirals
 Inflamed epithelium produces mediators such as cytokines, granulocytes
macrophage colony stimulating factor (GM-CSF) that prolong the life of
tissue oesinophils, TNF and interlukins that capture the inflammatory cells
within the epithelium.
Inflammatory Cells
i). Macrophages and Lymphocytes - are abundant in the mucous membranes
of the airways and alveoli.
ii). Oesinophils - are abundant in bronchial secretions and when activated they
release mediators such as PAF and LTC4, major basic protein (MBP) and

eosinophil cationic protein (ECP) which are toxic to epithelial cells.
Oedema, vascular congestion and infiltration by oesinophils produce the
Charcot Leyden crystals.
iii). Vascular Epithelium - exhibits congestion, leakage, increased permeability
and contraction. 2 agonists and theophylline can prevent the contraction.
4.6. Nerves
 Exposure of the nerve endings especially C-fibre afferent nerves leads to
release of neurotransmitters such as substance P, neurokinin (NK) A and
calcitonin gene-related peptide (CGRP) which are tachykinins that increase
the inflammatory response
 This usually contributes to bronchoconstriction, microvasculature leakage
and mucous secretion
 Vasoactive intestinal peptide (VIP) and nitric oxide are potent
neurotransmitters that are rapidly degraded in inflammation resulting in
bronchoconstriction
 and adrenergic systems of the autonomic nervous system are activated
resulting in increased release of mediators from the mast cells but the
cholinergic system, which is extensive in the smooth muscles of the
respiratory passages remains normal, is asthma.
5.0 PATHOLOGY
Macroscopy (at autopsy)
 Overinflated lungs that do not deflate when the thorax is opened
 Widespread plugging of airways with thick mucous
Diagram 7.4: Pathological Changes in Asthma
Microscopy
 Desquamation of the epithelium
 Hypertrophy of smooth muscle
 Thickening of the basement membrane
 Infiltration by oesinophils and inflammatory cells

 Hyperplasia of mucosal glands
 Goblet cell metaplasia
 Curschmann’s spirals – mucosal plugs containing normal or desquamated
epithelium forming twisted strips.
 Charcot Leyden crystals – sputum containing numerous oesinophils and
diamond shaped crystals derived from eosinophils.
Outline the clinical classification of asthma stating the main
clinical features
Clinical features of asthma vary with age, severity, duration of disease, amount
and nature of treatment and presence of complications.
 Main Features include – cough, headache, difficulty in breathing,
hyperventilation, wheezing and chest pain/tightness
 Severe asthma
o Inability to complete a sentence in one breath
o Respiratory rate > 25 breaths per minute
o Tachycardia > 110 (pulsus paradoxicus)
o PEFR< 50% of predicted normal best
 Life threatening asthma
o Silent chest, cyanosis or feeble respiratory effort
o Exhaustion, confusion or coma
o Bradycardia, hypotension
o PEFR< 30%
TASK
7.0 DIFFERENTIAL DIAGNOSIS
Common
1. Acute bronchiolitis (infections, chemical)
2. Aspiration (foreign body)
3. Bronchial stenosis
4. Cardiac failure
5. Chronic bronchitis
6. Cystic fibrosis
7. Eosinophilic pneumonia
Uncommon
1. Airway obstruction due to masses
a. External compression (thoracic, superior vena cava syndrome,
substernal thyroid)
b. Intrinsic airway – pulmonary lung cancer and metastatic breast cancer
2. Pulmonary emboli

8.0 INVESTIGATIONS
1. Lung Function tests – diagnosis of asthma is based on demonstration of a >
15% improvement I FEV1 or PEFR following inhalation of a bronchodilator.
 Peak flow charts – take PEFR on walking, middle of the day and before
bed. It shows reduced PEFR, MMEFR
 Reduced FEV1
Diagram 7.5: Lung Volumes
Diagram 7.6: FEV
Note: FEV1 is reduced in obstructive disease > in restrictive disease
FEV1 x 100/sec (the normal ratio is 80 – 97%)
FVC
 During an asthmatic attack FEV1 is greatly reduced while FVC is
increased hence, the ration is markedly reduced
2. Exercise tolerance
3. Analysis of arterial gases
 Check for the partial pressures of oxygen and carbon dioxide (normal -
oxygen PaO2 is over 12 kPa (90 mmHg) and PaCO2 is less than 6.0 kPa
(45 mmHg). This is reversed in asthma due to carbon dioxide retention
resulting from the physiological valve.

4. Haemogram - increased haemoglobin, normal WBC (only increase in the
presence of an infection), eosinophils> 0.4 x 109/L
5. Sputum Examination - Charcot Leyden spirals, Curschmann’s crystals,
White blood cells
6. Bronchial provocation test (is not done if the FEV1 is < 1.5 litres)
7. Chest X-ray - shows hyperinflation, depressed diaphragm and excludes
pneumothorax (a complication)
8. Skin test
9. Allergen provocation test
9.0 COMPLICATIONS
1. Pneumothorax
2. Pneumomediastinum
3. Respiratory failure
4. Heart failure/CCF/Cor Pulmonale
5. COPD
6. Pneumonia
7. Lung Collapse
What is the pathophysiology of these
complications?

Lesson 8: Restrictive Pulmonary Diseases
Alveolitis
Inflammatory destruction of pulmonary parenchyma
Leaning Outcomes
1) Classify restrictive diseases of the lungs
2) Describe the pathogenesis and pathology of restrictive lung diseases
3) Investigate patients with restrictive lung diseases
1.0 INTRODUCTION
 A group of lung diseases that cause reduced compliance of the lungs
resulting in difficult to expand with respiration usually because of
abnormalities of alveolar walls which are rigid due to oedema or fibrosis
 ARLD is characterized by oedema and exudation
 CRLD diseases present with inflammation and fibrosis and is characterized
by reduced expansion of the lung parenchyma with reduced total lung
capacity.
2.0 CLASSIFICATION
There are three types: -
1. Restriction due to chest wall disorders such as: - kyphosis, poliomyelitis and
severe obesity
2. Pleural diseases (see later in the unit)
3. Restriction due to interstitial and infiltrative diseases characterized by non-infectious
involvement of interstitial connective tissue of the lung
parenchyma
3.0 PATHOGENESIS
 Characterized by damage to the alveolar walls resulting in haemorrhage
and high protein exudation into the alveolar producing the hyaline
membrane disease; oedema and inflammation of interstitium and fibrosis
in the interstitial.
Diagram 8.1: Pathogenesis of Restrictive Lung Disease
Stimuli Inflammation
Increased accumulation of lymphocytes, macrophages, neutrophils, oesinophils
Widespread destruction - “HONEYCOMB” lung
Fibrosis

Find out the inorganic
(mineral dusts) and
organic (biologic) dusts
1) Dyspnoea
2) Tachycardia
3) End-inspiratory crackles
4) Cyanosis without wheezing or evidence of airway obstruction
5) CXR shows diffuse infiltration by small nodules, irregular lines and grand
glass shadows
6) Secondary pulmonary hypertension
7) Right heart failure/Cor pulmonale
8) Reduced CO diffusing capacity
9) Reduced lung volume
10) Reduced lung compliance
5.0 PNEUMOCONIOSIS
 Lung disease caused by inhalation of dust (dust diseases/occupational lung
disease)
 Type of disease produced varies according to the nature of the dust causing
the problem
 Extent of damage caused by inhaled gases is determined by -
1. Size and shape of the particles
2. Solubility and physiochemical composition
3. Amount of dust retained in the lungs
4. Additional effects of other irritants such as
tobacco.
5. Host factors – efficiency in clearing mechanisms and immune status
 Tissue response will include –
1. Fibrous nodules e.g. coal-workers pneumonitis and silicosis
2. Interstitial fibrosis e.g. asbestosis
3. Hypersensitivity reactions – e.g. in berylliosis
6.0 FIBROSING LUNG DISEASE (INTERSTITIAL LUNG DISEASE)
 Fibrosing lung disease is characterized by chronic inflammation in the walls
of the alveoli resulting in progressive diffuse fibrosis in the lung
parenchyma
 Presents with dyspnoea and dry cough
Cause of Chronic Interstitial Lung Disease
1) Idiopathic interstitial pneumonitis (interstitial pneumonia)
2) Connective tissue disease e.g. rheumatoid disease
3) Drug induced damage e.g. cytotoxics
4) Atypical pneumonia (Chlamydia, Mycoplasma)
5) Pneumonia
6) Extrinsic allergic alveolitis
7) Sarcoidosis
8) Radiation damage

7.0 SILICOSIS
 Caused by prolonged exposure to silicon dioxide (silica/quartz)
 Common in slate mining, metal foundries, stone masonry, tunnelling,
granite quarrying and coal mining
 Lung lesions slowly progress over many years
 Damages lung macrophages and if the exposure is chronic thus leads to
death of macrophages
 There is release of cytokines, which enhance fibrosis. A silicotic lung is
susceptible to tuberculosis
Clinical Features
 Dyspnoea
Complications
1. Obstructive pulmonary disease
2. pulmonary tuberculosis
3. rheumatoid arthritis (Caplan’s syndrome)
4. Cor pulmonale
8.0 ASBESTOSIS
 Causes lung and pleural diseases
 Produces pleural plaques, pleural effusions, visceral pleural fibrosis,
asbestosis (chronic progressive fibrosis of the lung), malignant
mesothelioma (a highly malignant lung tumour) and cancer of the lung
(bronchogenic carcinoma).
Clinical Features
 Insidious onset, dyspnoea, cough – dry or productive, pulmonary
hypertension, cor pulmonale and various forms of cancer
9.0 ADULT ACUTE RESPIRATORY DISTRESS SYNDROME
 ARDS is a manifestation of diffuse alveolar damage with widespread
systemic metabolic derangements
 Diagnosis depends on presence of precipitant ARDS, refractory
hypoxaemia (PaO2< 8.0 kPa in > 40% O2), radiological evidence of
evolving pulmonary shadowing and clinical signs of lungs being
abnormally rigid with low total compliance.
Causes
1) Major trauma especially associated with increased intracranial pressure
2) Septicaemia
3) Pulmonary aspiration of gastric contents
4) Major burns
5) Inhalation of toxic fumes or smoke
6) Near drowning
7) D.I.C

Progression to fibrosis of alveoli Restrictive lung disease
Hypoxia Respiratory failure
8) Massive blood transfusion
9) Acute pancreatitis
10) Radiation injury
Pathogenesis
Diagram 8.2: Pathogenesis of ARDS
10.0 IMMUNOLOGIC LUNG DISEASE
 Immunologic mechanisms play a crucial role in lung disease as outlined in
the table below
Table 1: Pathophysiology of Restrictive Lung Diseases
Disease Pathogenesis/pathology
Bronchial asthma Explain
Hypersensitivity
(allergic) pneumonitis
 Immune mediated inflammation of the lung
tissues - Examples – Farmer’s lung, Bird breeders
lung, Malt workers lung, Mushroom workers lung
Pulmonary Eosinophilia  Immunological meditated lung diseases
characterized by infiltration of the lungs and
elevated eosinophil counts e.g. Loeffler’s
syndrome
Good Pastures
Syndrome
 Necrotizing haemorrhagic interstitial pneumonitis
11.0 VASCULAR COLLAGEN DISEASE
Table 2: Pathogenesis of Restrictive Lung Disease in Vascular Collagen Disease
Disease Pathogenesis/pathology
Rheumatoid arthritis  Pleural effusion; Interstitial pneumonitis;
Rheumatoid pneumoconiosis
S.L.E  Pleurisy; Pleural effusion; Interstitial pneumonitis;
Pulmonary haemorrhage; Vasculitis
“Honeycomb” lung with numerous
cysts especially in the lower lobes
Right Ventricular Failure
Pulmonary
hypertension
Right ventricular hypertrophy
Compare and contrast obstructive and restrictive lung diseases

Lesson 9: Pulmonary Infections – Pneumonia
Learning Outcomes
1) Identify causes of pulmonary infections
2) Discus predisposing factors to pulmonary infections
3) Describe the pathology of different types of pneumonia
4) Investigate pneumonia
1.0 INTRODUCTION
 Respiratory tract infections are more frequent than any other infections.
 Majority URTIs are caused by viruses (common cold, pharyngitis) while
bacterial, viral, mycoplasmal and fungal infections of the lung (pneumonia)
 Acute and chronic pulmonary infections which are frequent causes of death
are common at all ages and occur when normal lung or systemic defence
mechanisms are impaired
 Impairment of the defence mechanisms includes -
1. Loss or decreased/suppression of cough reflex leading to aspiration
2. Injury to mucociliary apparatus by cigarette smoking and gaseous
inhalation, genetic disorders, inhalation of corrosive substances
3. Decreased phagocytic or bactericidal function of the alveolar
macrophages
4. Pulmonary oedema or congestion (congestive cardiac failure)
5. Accumulation of secretions e.g. Post-operative , cystic fibrosis and
bronchial obstruction
 Defective innate immunity (neutrophil and complement defects) and
humoral immunodeficiency) result in increased incidence of infections with
pyogenic bacteria
 Defects in cell mediated immunity lead to increased infections with
intracellular microbes e.g. mycobacterium and herpes viruses and
Pneumocystis jiroveci
2.0 DEFINITION
 Pneumonia is inflammation of the lung parenchyma distal to the terminal
bronchioles (respiratory bronchiole, alveolar ducts, alveolar sacs and
alveoli) characterized by vascular changes and exudation of fluid and cells
 Inflammation may reach the pleural surface causing irritation and
inflammation of the pleura and accumulation of fluid exudate (pleural
effusion).
 The process is influenced by the spongy character of the lung that allows
unimpeded spread of the inflammatory exudate filling the alveolar and
affected portions of the lung become relatively solid (consolidation).
3.0 PREDISPOSING FACTORS
 Viral infections, hospitalization, cigarette smoking, alcohol excess,
bronchiectasis, bronchial obstruction, immunosuppression, intravenous
drug use, inhalation, crowding, post operation
How would these factors predispose individuals to pulmonary infections?

4.0 ROUTES OF INFECTION
1. Inhalation of microbes present in the air
2. Aspiration – naso and oropharynx
3. Haematogenous spread from a distant foci of infection
4. Direct spread from an adjacent site of infection
5.0 PATHOGENESIS
 A number of defence mechanisms at different levels normally protects the
lung and failure of the defence mechanisms and presence of predisposing
factors results in development of pneumonia.
 Such situations include -
a) Altered consciousness - oropharyngeal contents can be aspirated into
the lungs in states of unconsciousness e.g. coma, cranial trauma,
seizures, cerebro-vascular accidents, drug overdose and alcoholism.
b) Depressed cough and gag reflexes - allows aspiration of gastric contents
e.g. in old age, pain from trauma, thoraco-abdominal surgery,
neuromuscular disease, malnutrition, kyphoscoliosis, severe obstructive
pulmonary disease, endotracheal intubation and tracheostomy
c) Impaired mucociliary transport - impairment or destruction of the
mucous-covered ciliated epithelium as in cigarette smoking, respiratory
viral infections, immotile cilia syndrome, inhalation of hot or corrosive
gases and old age.
d) Impaired alveolar macrophage function - cigarette smoking, hypoxia,
starvation, anaemia, pulmonary oedema and viral respiratory infections.
e) Endobronchial obstruction - interferes with effective clearance of the
bronchial tree
f) Leucocyte dysfunctions - congenital and acquired immunodeficiency,
HIV/AIDS and granulocyte abnormalities.

6.0 INVESTIGATIONS
1) Chest x-ray PA and lateral view
o Chest radiography may reveal a lobar consolidation (common in typical
pneumonia most commonly in the lower lobes; or it could show bilateral
diffuse interstitial infiltrates and cavitations.
o Used to evaluate for complications of pneumonia like empyema, lung
abscess, pneumothorax etc.
o Gives a clue for suspecting the aetiological agent.
 Multi lobar involvement (Bacteraemic pneumococcal)
 Pleural effusions (Bacteraemic pneumococcal)
 Lymphadenopathy (Mycoplasma infection)
 Multilobe involvement, cavitation, or spontaneous pneumothorax
(Staphylococus aureus).
 Upper lobe preponderance may denote klebsiella pneumonia.
2) Chest CT (computed tomography) can reveal pneumonia that is not seen
on chest x-ray
3) HIV serology
4) Lung Function Tests
5) Blood picture
o Show a high blood cell count, indicating the presence of bacterial
infection.
o Leucopenia may suggest viral pneumonia.
6) Sputum gram stain and culture
o The presence of > 25 white blood cells and, 10 squamous epithelial
cells per high power field suggests that the sputum is appropriate for
examination.
o Specialized cultures for Mycobacterium sp., Legionella sp., and endemic
fungi may be valuable in the appropriate clinical circumstance. If the
patient is not receiving antibiotics at the time of admission
7) Sputum culture and sensitivity results may be useful
8) Blood culture
9) Urea and electrolytes
10) Blood chemistry
a) Glucose
b) Electrolytes
c) Liver and renal function tests
11) Pulse oximetry
12) Arterial Blood Gases – If oxygen saturation < 90%
13) Serum antibodies - Detection of antibodies to Streptococcus pneumonia,
mycoplasma, chlamydia, adenovirus, influenza A and B viruses,
parainfluenza viruses 1, 2, and 3, and respiratory syncytial virus etc.
14) Polymerase Chain Reaction (PCR) - useful for identifying certain atypical
bacteria strains, including mycoplasma, Chlamydia pneumonia and
Haemophilus influenzae type b. One study found that using a real-time PCR

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