1. Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by diffuse alveolar capillary damage and severe pulmonary edema, resulting in hypoxemia that is refractory to oxygen therapy. 2. ARDS is caused by direct or indirect injury to the lungs from sources such as sepsis, gastric aspiration, trauma, or smoke inhalation. This causes damage to the alveolar capillary endothelium and epithelium. 3. The damage leads to increased capillary permeability, leakage of fluid into the alveoli, and formation of hyaline membranes. This results in impaired gas exchange and respiratory failure.

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Why learn the disorders of respiratory system?
Respiratory symptoms most common cause of
presentation to family doctor.
Rhinitis = common cold
Sinusitis = inflammation of paranasal air
sinuses
Pneumonia , Asthma , Bronchitis
Bronchogenic carcinoma – MC cancer causing
death in men and women.
Lungs are the major site of opportunistic
infections in immuno-compromised individuals.
Tuberculosis

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Relevant normal anatomy and histology of
respiratory system.
The major manifestations of respiratory
diseases
The laboratory testing in respiratory
disorders (self study)
Review of ……..
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The respiratory system
Consists of
Lungs and
The airways
Functional divisions:
Conducting and
Respiratory portions
Clinical divisions:
Upper respiratory tract
Lower respiratory tract
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Structure of Respiratory System
Lungs:
Right lung:
3 lobes
Upper ,
middle and
lower lobes
Left lung:
2 lobes
Upper and
lower lobes.
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6. Spr 09
Trachea divides in to :
– Right and
– Left principal (main) bronchi.
Right main bronchus
shorter and more vertical*
Divides in to 3 lobar Bronchi
Left main bronchus
longer and more horizontal
Divides into 2 lobar bronchi.
Lobar bronchi divide to give rise to segmental
bronchi.
Each segmental bronchi passes to a broncho-
pulmonary segment
Lung airways
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Segmental bronchi
Bronchioles
Terminal bronchioles
Terminal respiratory
unit
= Acinus
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8. Spr 09
Acinus= the respiratory unit
Is the basic gas
exchange unit of lungs
Also Known As = The
respiratory unit
Composed of:
Respiratory bronchiole
Alveolar ducts
Alveolar sacs
Alveolus
Cluster of 3-5 terminal
bronchioles with acinus
k/a pulmonary lobule
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9. Spr 09
False Vocal cords : lined by stratified squamous
epithelium.
Larynx, trachea and bronchi : lined by pseudo-
stratified ciliated columnar epithelium.
Contain
Mucus secreting goblet cells.
Cartilage plates
Smooth muscles
Neuroendocrine cells.
Bronchioles: no mucus glands and no cartilage
Respiratory system: Histology
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Type II pneumocyte (EM)*
Lamellar bodies
Nucleus
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The alveolar wall= Alveolar septa
Blood to air:
Capillary endothelium
BM and interstitial tissue
Alveolar epithelium
2 cell types:
Type I pneumocytes
Type II pneumocytes
Secrete surfactant
Repair
Alveolar macrophage
Pores of Kohn
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Pulmonary vasculature
Dual blood supply:
Respiratory portion  by pulmonary
artery
Conducting airways  by bronchial
artery
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Pleurae
Two parts:
1. Parietal layer
2. Visceral layer
Both layers
separated from one
another by pleural
cavity.
Which contains
Pleural fluid
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Physical Examination of
respiratory system
1. Inspection
2. Palpation
3. Percussion
4. Auscultation
Then,
Perform general physical examination :
Look for :
Lymphadenopathy
Clubbing of fingers etc.
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Major manifestations of lung diseases
1. Dyspnea: Difficulty in breathing
2. Cough:
Due to stimulation of irritant receptors in
tracheobronchial tree by
1. Inflammation or distortion of bronchial wall.
3. Hemoptysis:
Coughing up blood or blood tinged sputum.
4. Chest pain:
Mainly due to pleural irritation (pleuritis).
Sharp inspiratory pain, increases with breathing.
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Physical diagnostic signs in respiratory
disease
1. Respiratory rate abnormalities:
Tachypnea : rapid shallow breathing (>18/min)
Hyperpnea: rapid deep breathing.
2. Cyanosis:
dusky blue appearance of skin or mucous
membrane
3. Abnormal breath sounds:
1. Stridor
2. Wheeze
3. Crackles (rales)
4. Gurgles (ronchi) 19

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Clubbing: Bulbous enlargement of the ends of
fingers or toes with
Loss of normal angle between the skin and
the nail.
(normal ≤ 160 0 ; abnormal ≥180 0)
Respiratory diseases associated with
clubbing:
Primary or metastatic lung cancer
Bronchiectasis
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Disorders of respiratory system
1. Atelectasis (collapse)
2. Acute lung injury
3. Vascular disorders
4. Obstructive and restrictive lung diseases
5. Pulmonary infections
6. Lung tumors
7. Pleural lesions
8. Lesions of the upper respiratory tract*

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Atelectasis (Collapse)
Refers to either :
incomplete expansion or to the collapse of
aerated lung.
Secondary to obstruction, compression of
lung tissue or loss of surfactant.
Consequences:
Gives rise to airless lung parenchyma.
Reduces oxygenation and predisposes to
infection.
MCC of fever 24 hrs after surgery**
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23. Atelectasis (Collapse)
 Four Types
1. Resorption atelectasis
2. Compression atelectasis
3. Contraction atelectasis
4. Micro-atelectasis (RDS of newborn)
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Resorption atelectasis
Results when airway obstruction
prevents air from reaching the
alveoli.
Cause of alveolar collapse: lack of air
and resorption of trapped air.
Causes of obstruction:
Mucous or mucous plug
Seen in Bronchial asthma, chr.
bronchitis, bronchiectasis, post
op. period.
Aspiration of foreign bodies
Tumors and enlarged lymphnodes.
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Resorption atelectasis
 Clinical findings:
1. Fever and dyspnea
• Both usually occur 24 to 36 hrs of
collapse
2. Absent breath sounds and vocal
vibratory sensation (tactile fremitus)
3. Dullness to percussion.

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Compression atelectasis
Air or fluid in the
pleural cavity
collapses small
airways under the
pleura.
Seen in:
1. Pleural effusion
2. Leakage of air
into pleural cavity
(= Pneumothorax)
Pneumothorax
Pleural
effusion
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Contraction atelectasis
Occurs when
Fibrotic changes in lungs or
pleura prevent full
expansion.
Note:
Atelectasis (except that
caused by contraction) is
potentially reversible.
Should be treated promptly
To prevent Hypoxemia
and infection.
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Respiratory distress syndrome of the
newborn (RDS)
Also k/a
Hyaline membrane disease (HMD)
Is primarily due to lack or deficiency of
surfactant.

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RDS of newborn
Surfactant:
Present in lamellar bodies of type II
pneumocytes.
Synthesis begins in 28th week of gestation
Maximal amount of surfactant by 35 weeks.
Phosphatidylcholine (lecithin) is the major
component.
Synthesis increased by cortisol and thyroxine.
Synthesis is decreased by insulin
Reduces surface tension in the small airways.
Prevents collapse on expiration, when
collapsing pressure is greatest.

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Causes of decreased surfactant in the
fetal lungs
1. Prematurity
• (gestational age <36 weeks)
2. Maternal diabetes:
• fetal hyperglycemia  ↑insulin release
 ↓surfactant synthesis
3. Cesarean section:
• no stress on baby  no release of
cortisol.

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RDS
Result of deficiency of surfactant:
Generalized loss of lung expansion causing
atelectasis.
Atelectasis  decreased oxygenation of
blood  hypoxemia.

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Pathogenesis

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Prematurity
Reduced surfactant synthesis, storage and release
Decreased alveolar surfactant
Increased alveolar surface tension
Atelectasis
Uneven perfusion Hypoventialtion
Hypoxemia + CO2 retention

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Acidosis
Pulmonary vasoconstriction
Pulmonary hypoperfusion
Endothelial damage Epithelial damage
Plasma leak into alveoli
Fibrin + necrotic cells
(Hyaline membrane)
Hypoxemia + CO2 retention

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RDS
Clinical findings:
Often normal at birth
Within few hours develop Respiratory
difficulty.
Tachypnea, nasal flaring, grunting and
Cyanosis
Gross:
Solid and airless lungs, sink in water
Microscopy:
Collapsed alveoli lined by Hyaline membrane
derived from proteins leaking from
pulmonary capillaries.

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Hyaline membrane disease

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Hyaline membrane disease
Thick pink membranes lining the alveolar spaces

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RDS
Labs:
Lecithin/sphingomyelin ratio <2
Treatment:
Surfactant replacement
Oxygen therapy
Positive pressure ventilation.
Prevention:
Delay labor till lungs mautre
Corticosteroids to mother

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Complications
Superoxide free radical damage from oxygen
therapy:
May result in blindness (retrolental
fibroplasia) and
permanent damage to small airways
(bronchopulmonary dysplasia)
Necrotizing enterocolitis
Intraventricular hemorrhage
Patent ductus arteriosus with machinery
murmur : due to persistent hypoxemia.

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Retinal detachment Scar tissue
Retinopathy of
prematurity
Intraventricular hemorrhage

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Disorders of respiratory system
 Atelectasis (collapse)
2. Acute lung injury
3. Vascular disorders
4. Obstructive and restrictive lung diseases
5. Pulmonary infections
6. Lung tumors
7. Pleural lesions
8. Lesions of the upper respiratory tract*

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Acute lung injury
1. Acute respiratory distress syndrome
(ARDS) aka Diffuse Alveolar Damage
(DAD)
2. Pulmonary edema

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Acute respiratory distress syndrome
(ARDS)
Noncardiogenic pulmonary edema resulting from
acute alveolar-capillary damage.
A clinical syndrome characterized by:
Diffuse alveolar capillary damage with
resultant
 Increased capillary permeability causing
leakage of protein rich fluid into alveoli and
severe pulmonary edema.
Marked by formation of intra-alveolar hyaline
membrane (composed of fibrin and cellular
debris)

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ARDS
Results in
severe impairment of gas exchange with
consequent hypoxia (respiratory failure )
refractory to oxygen therapy.
Patients present with:
severe acute dyspnea and hypoxemia.
Synonyms:
Shock lung, diffuse alveolar damage (DAD).

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Causes of ARDS
Due to direct or indirect injury to lungs.
Risk factors for ARDS:
Gram negative sepsis (40% of cases)***
Gastric aspiration (30% of cases)
Severe trauma with shock (10% of cases)
Pneumonia, Smoke inhalation, heroin,
bleomycin etc.

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Pathogenesis
Two factors responsible for ARDS:
1. Damage to alveolar capillary endothelium
and alveolar epithelium
2. Damage to type II pneumocytes.

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Pathogenesis
Damage mediated by neutrophils and alveolar
macrophages.
Alveolar macrophages release cytokines:
1. Cytokines are chemotactic to neutrophils
2. Neutrophils transmigrate into alveoli.
 Release proteases, O2 FR etc causing
 Capillary damage.
 Results in leakage of protein rich
exudate producing hyaline membranes &
pulmonary edema.
3. Neutrophils also damage type I and type II
pneumocytes.
 Decrease in surfactant causes atelectasis.

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Morphology
Gross: lungs are dark red, airless and firm
(liver-like)
Micro:
Early findings (exudative stage)
 Diffuse alveolar damage and necrosis
 Alveolar edema, collapsed alveoli
 Some alveoli lined by hyaline membrane.
Late findings (proliferative stage)
 Repair by type II pneumocytes
 Progressive interstitial fibrosis (restrictive
lung disease).

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Interstitial inflammationHyaline membrane

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Residual hyaline membranesThickened alveolar septa

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Clinical findings
Acute stage:
Dyspnea, with severe hypoxemia not
responsive to oxygen therapy
Respiratory acidosis.
Late stage:
Interstitial fibrosis compromises the lung
function.
Prognosis:
Poor, Mortality almost 60% even with
improved methods.

53. Pulmonary edema
Edema due to alterations in Starling’s pressure.
Increased HP in pulmonary capillaries
 Left sided heart failure, MS
Decreased oncotic pressure
 Nephrotic syndrome, cirrhosis
Edema due to microvascular or alveolar injury.
Infections (sepsis, pneumonia)
Aspiration (gastric contents)
Drugs (heroin), massive trauma, High altitude