Physiology lec#20
Date: 13,3,2011
Hey all,
Last time we discussed briefly the COPD’s ( Chronic Obstructive
Pulmonary Diseases) and it’s going to be continued throughout this
lecture.
Proteases are enzymes which digest proteins. Walls of alveoli are
membranes that consist of proteins that are susceptible to destruction by
these proteases therefore, they’re protected by anti-proteases.
Ex. Trypsin is inhibited by antitrypsin.
If antitrypsin is absent (most probably due to smoking) there’s nothing
to inhibit the trypsin from digesting the walls of the alveoli.
Emphysema: destruction of the walls of the alveoli leading to three main
problems:1) Obstruction  airway problems
2) Decreased surface area for diffusion of gases causing:
High arterial pCO2 and low pO2
But, the O2 is going to be affected before the CO2 because diffusion of
CO2 is easier.
Usually as surface area decreases, oxygen diffusion decreases too
ending in decreased arterial PO2 causing hypoxemia in the systemic
vascular bed which is a strong vasodilator. But, at the vascular bed of
the pulmonary system, when PO2 decreases the response is
vasoconstriction as to shift the blood to a more ventilated area.
(Hypoxemiavasoconstriction of pulmonary artery causing increased
resistance leading to increased pressure to guarantee the same flow(Q))
3) Vascular problem which is manifested by destruction and decrease of
the capillary beds causing:[Q= P/R(pulmonary vascular resistance)]
-
decreased surface area
increased resistance
As a result, P in the pulmonary arteries has to increase by the same
proportion as resistance to keep Q constant .
But, this will cause the right ventricle to increase the force of contraction
to overcome the high pressure and cause:1) Dilatation
2) Failure
As a conclusion, smoking clearly leads to emphysema and therefore right
heart failure.
NOTE: Emphysema increases vascular resistance due to:
1) Hypoxemia
2) Destruction of the capillary bed
Both reasons increased the load on the heart causing a condition called
Cor pulmonale which is right heart dilatation and sometimes failure due
to lung disease that either increases pulmonary vascular resistance or
decreases PO2.
NOTE: Destruction of the alveolar wall (Emphysema) is irreversible in
smoking since some alveolar cells can’t repair themselves.
People who live in high altitude areas where there is a decrease in PO2
It means they have hypoxia due to decreased arterial O2 ,but for a long
time with more decrease of O2 this will lead to Cor pulmonale.
Another COPD is [Chronic Bronchitis]
-Too much mucus secreted from bronchioles which is an ideal medium
for the growth of bacteria causing continuous infection
- Epithelium becomes very thick
- Obstruction
-Productive cough (cough with mucus)
So, if a smoker starts coughing every single day for three months in the
winter time for two successive years this is chronic bronchitis and is
irreversible. Anyone is able to make this diagnosis based on the previous
information.
Any patient with Emphysema has some aspects of Chronic bronchitis and
vice versa.
Both these COPD’s are mainly caused by alpha 1 deficiency that is
acquired for example due to smoking and is very rare at birth.
Bronchial Asthma
a) Extrinsic asthma gotten from outside the body.
b) Intrinsic asthma gotten from inside the body.
Both these types are induced by physical exercise.
What happens is:An inhaled irritant causes bronchoconstriction (contraction of the
muscles of the bronchus) followed by mucus secretion from goblet cells.
The water in the mucus is reabsorbed forming a solid and causing an
asthma attack.
The first line of treatment is a bronchodilator which uses beta 2
sympathetic agonist specific for the lungs or adrenaline for emergencies
which is given subcutaneously and causing bronchodilatation.
OR
-mucolytic degrades mucus
-antiinflammatory (cortisol which is an inhaler that decreases swelling)
-antibiotic to kill the bacteria in the mucus
NOTE: never give a cough suppressant
[Back to emphysema]
When the walls of the alveoli were destructed the elastic fibres were also
destroyed which means active expiration. This is going to decrease the
collapsing tendency of the lung meanwhile the expanding tendency of
the thorax remains the same so the system is not at equilibrium.
The solution would be to increase the FRC increasing the collapsing
tendency of the lung and decreasing expanding tendency of the thorax
reaching a new equilibrium point where the collapsing tendency is equal
to the expanding tendency.
[Testing for emphysema during expiration]
The first quarter of air is expired quickly, the middle 50 percent is
moderately quick and the last quarter is expired at a slower pace.
1) Fill the lungs to full capacity
2) Expire the Forced Vital Capacity (FVC) which is quick exhalation
3) Within 4 seconds for normal people the vital capacity is exhaled. But for
a person with an obstruction it takes more time.
4) We check the Forced expiratory volume(FEV) ( volume expired in 1
second)
5) Ex. Normal FEV/FVC= 4/5*100 %  80%
Abnormal FEV/FVC=3.5/5*100%  70%
The problem with this method is that it doesn’t really indicate the extent
of the obstruction therefore, the first and last quarters are going to be
deleted since they dilute the result.
This is called the MMEF( Mid Mean Expiratory Flow)
Ex. Normal 3.5/1*100%
Abnormal 1.5/1*100%
We can now say that more than 50% of the lung is destroyed making
the MMEF a more sensitive test.
Your colleague: Hala Salamin
Hope I conveyed the message =) Good luck all!