2017
SYSTEMATIC &
CELLULAR PATHOLOGY
NOTES
RESPIRATORY SYSTEM
,PULMONARY SYSTEM INTRODUCTION
Vast area – epithelial surface is the size of a tennis court
Tracheobronchial tree is divided into conducting airways and the respiratory airways
o Conducting zone:
o The conduction zone conducts air breathed in that is filtered, warmed, and moistened,
into the lungs.
o Characterizes with low resistance pathway for airflow
o Contains cartilage as far as the bronchioles
o Gas exchange DOES NOT OCCUR
o Respiratory zone:
o Contains alveoli and gas exchange occurs
o The respiratory zone includes the respiratory bronchioles, alveolar ducts and alveoli, and
is the site of oxygen and carbon dioxide exchange with the blood.
Basic anatomical structures:
The epithelium of the upper airways is made of pseudostratified columnar cells with cilia and
goblet cells (secreting mucus cells)
The mucus is responsible for trapping dust particles
Cilia are responsible for wafting (to pass) the mucus with dust particles to mouth and nasal
cavities.
Another mechanism of protection lungs from foreign particles are the macrophages. They
protect the base of lungs by engulfing dust, smoke, bacteria
, Gas exchange occurs at alveolar walls which contain capillaries
There are about 300 million alveoli
There are four types of layers that separate blood from alveolar air:
o Type I alveolar cells
o Epithelial basement membrane
o Capillary basement membrane
o Capillary endothelial cells
Oxygen enters blood capillary by simple diffusion:
CO2 leaves the blood by simple diffusion as well
CO2 controls:
o pH of the blood (may cause acidosis)
o lowering of pH evokes contraction of airways
o widespread changes in pH alter all cellular activities
o Low CO2 causes bronchoconstriction
o Decreases pH impedes (delays) ciliary action and increases mucus viscosity
MOST COMMON LUNG DISEASE:
o Acute respiratory distress syndrome
o Asbestosis
o Asthma
o Chronic bronchitis
o Cystic fibrosis
o Emphysema
o Farmer’s lung (mold disease)
Can be divided into OBSTRUCTIVE AND RESTRICTIVE
OBSTRUCTIVE LUNG DISEASE
Upper respiratory inflammation produces increased mucous and serous fluid secretion by the
mucous membranes that line the nasal fossae and pharynx. Usually this is in response to viral
infection, but inhaled irritants are also involved.
Lung airway obstruction usually produces hypoventilation, essentially due to reduced expiration,
which is indicated by smaller FEV1 values. Outflow is restricted by reduced airways size, the
presence of excess secretion, or by a reduction of the lung’s elastic coil that reduces expiration
pressure.
, ηL
Poiseuille’s equation for flow in a tube: Rα = 4 (R – vessel resistance/ r -radius / η – viscosity and L
r
-length of the tube.) Half the radius gives 1/16 th of the flow.
Mechanisms of obstruction:
o Excessive secretion
o Chronic bronchitis (COPD)
o Pulmonary oedema
o Reduced airway diameter
o Asthma
o Inflammation
o Loss of radical traction
o Reduction in parenchymal (functional tissue of an organ) support of the airways due
to loss of lung elastic recoil
Chronic bronchitis:
Most common obstructive chronic obstructive disease in the Western World. To distinguish from
recurrent acute inflammation, it is usually diagnosed on the basis of two consecutive years in which
a productive cough is present for three months. The cough is an attempt to clear sputum formed in
response to chronic irritation of the respiratory mucous membranes.
1) Diagnosis is based on presence of productive cough
2) Excessive mucus sufficient to cause excessive expectoration (cough sputum)
3) Principal etiologic factor is inhalation of irritants: cigarette smoke, pollutants
4) Symptoms: cough, dyspnoea (shortness of breath), respiratory infections
Effects: Pathogenesis in chronic bronchitis reflects the mucous membrane response to long-term
irritant exposure. Inflammatory hyperaemia (excess blood in the vessel) and exudate cause
thickening of the mucosa, as does hypertrophy and hyperplasia of its mucous secreting glands.
a) inflammation and oedema of bronchial mucosa
b) hyperplasia and hypertrophy of submucosal glands
c) hyperplasia and hypertrophy of smooth muscle
d) reduction in cilia
e) squamous metaplasia
Metaplasia of the bronchial epithelium also develops. This results in loss of cilia which favours mucus
accumulation and reduced clearance of particles and microorganisms. This factor, coupled with
increased mucus secretion that can plug smaller airways, contributes to an increased incidence of
acute respiratory infections that complicate the underlying chronic bronchitis.
SYSTEMATIC &
CELLULAR PATHOLOGY
NOTES
RESPIRATORY SYSTEM
,PULMONARY SYSTEM INTRODUCTION
Vast area – epithelial surface is the size of a tennis court
Tracheobronchial tree is divided into conducting airways and the respiratory airways
o Conducting zone:
o The conduction zone conducts air breathed in that is filtered, warmed, and moistened,
into the lungs.
o Characterizes with low resistance pathway for airflow
o Contains cartilage as far as the bronchioles
o Gas exchange DOES NOT OCCUR
o Respiratory zone:
o Contains alveoli and gas exchange occurs
o The respiratory zone includes the respiratory bronchioles, alveolar ducts and alveoli, and
is the site of oxygen and carbon dioxide exchange with the blood.
Basic anatomical structures:
The epithelium of the upper airways is made of pseudostratified columnar cells with cilia and
goblet cells (secreting mucus cells)
The mucus is responsible for trapping dust particles
Cilia are responsible for wafting (to pass) the mucus with dust particles to mouth and nasal
cavities.
Another mechanism of protection lungs from foreign particles are the macrophages. They
protect the base of lungs by engulfing dust, smoke, bacteria
, Gas exchange occurs at alveolar walls which contain capillaries
There are about 300 million alveoli
There are four types of layers that separate blood from alveolar air:
o Type I alveolar cells
o Epithelial basement membrane
o Capillary basement membrane
o Capillary endothelial cells
Oxygen enters blood capillary by simple diffusion:
CO2 leaves the blood by simple diffusion as well
CO2 controls:
o pH of the blood (may cause acidosis)
o lowering of pH evokes contraction of airways
o widespread changes in pH alter all cellular activities
o Low CO2 causes bronchoconstriction
o Decreases pH impedes (delays) ciliary action and increases mucus viscosity
MOST COMMON LUNG DISEASE:
o Acute respiratory distress syndrome
o Asbestosis
o Asthma
o Chronic bronchitis
o Cystic fibrosis
o Emphysema
o Farmer’s lung (mold disease)
Can be divided into OBSTRUCTIVE AND RESTRICTIVE
OBSTRUCTIVE LUNG DISEASE
Upper respiratory inflammation produces increased mucous and serous fluid secretion by the
mucous membranes that line the nasal fossae and pharynx. Usually this is in response to viral
infection, but inhaled irritants are also involved.
Lung airway obstruction usually produces hypoventilation, essentially due to reduced expiration,
which is indicated by smaller FEV1 values. Outflow is restricted by reduced airways size, the
presence of excess secretion, or by a reduction of the lung’s elastic coil that reduces expiration
pressure.
, ηL
Poiseuille’s equation for flow in a tube: Rα = 4 (R – vessel resistance/ r -radius / η – viscosity and L
r
-length of the tube.) Half the radius gives 1/16 th of the flow.
Mechanisms of obstruction:
o Excessive secretion
o Chronic bronchitis (COPD)
o Pulmonary oedema
o Reduced airway diameter
o Asthma
o Inflammation
o Loss of radical traction
o Reduction in parenchymal (functional tissue of an organ) support of the airways due
to loss of lung elastic recoil
Chronic bronchitis:
Most common obstructive chronic obstructive disease in the Western World. To distinguish from
recurrent acute inflammation, it is usually diagnosed on the basis of two consecutive years in which
a productive cough is present for three months. The cough is an attempt to clear sputum formed in
response to chronic irritation of the respiratory mucous membranes.
1) Diagnosis is based on presence of productive cough
2) Excessive mucus sufficient to cause excessive expectoration (cough sputum)
3) Principal etiologic factor is inhalation of irritants: cigarette smoke, pollutants
4) Symptoms: cough, dyspnoea (shortness of breath), respiratory infections
Effects: Pathogenesis in chronic bronchitis reflects the mucous membrane response to long-term
irritant exposure. Inflammatory hyperaemia (excess blood in the vessel) and exudate cause
thickening of the mucosa, as does hypertrophy and hyperplasia of its mucous secreting glands.
a) inflammation and oedema of bronchial mucosa
b) hyperplasia and hypertrophy of submucosal glands
c) hyperplasia and hypertrophy of smooth muscle
d) reduction in cilia
e) squamous metaplasia
Metaplasia of the bronchial epithelium also develops. This results in loss of cilia which favours mucus
accumulation and reduced clearance of particles and microorganisms. This factor, coupled with
increased mucus secretion that can plug smaller airways, contributes to an increased incidence of
acute respiratory infections that complicate the underlying chronic bronchitis.
