Download Methodological Instruction to Practical Lesson № 11

MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
Approval on methodological meeting
of the department of pathophisiology
Protocol №
Chief of department of the pathophysiology,
professor
Yu.Ye.Rohovyy
“___” ___________ 2008 year.
Methodological Instruction
to Practical Lesson
Мodule 2 : PATHOPHYSIOLOGY OF THE ORGANS AND SYSTEMS.
Contenting module 5. Pathophysiology of blood circulation
and respiratory system.
Theme 11: Pathophysiology of the respiratory system-2
Chernivtsi – 2008
1.Actuality of the theme. Respiration insufficiency is a pathologic
process developing due to the disturbance of the external respiration. In respiration
in sufficiency the maintenance of gas contents adequate to organism requirements
isn't ensured. Even at rest respiration insufficiency may lead to hypoxia and
gaseous acidosis or limit the organism abilities as fulfill physical work. The main
mechanisms of respiration insufficiency development consist in disturbances of
ventilation, perfusion, diffusion as well as their quantitative ratio.
2.Length of the employment – 2 hours.
3.Aim:
To khow: Characterize obstructive pulmonary diseases.
To be able: to analyse the mechanisms of the obstructive pulmonary
diseases.
To perform practical work: to analyse the mechanisms of the pulmonary
defenses.
4. Basic level.
The name of the previous
disciplines
1.
histology
2.
biochemistry
3.
physiology
The receiving of the skills
Lung defense mechanisms.
The non-respiratory function of the lungs.
The structure of a normal bronchiole.
The normal structures of the acinus.
Microscopic structure of the alveolar wall.
5. The advices for students.
1. Pulmonary defenses
The respiratory tract has several protective metabolisms that dispatch most
organisms deposited in the respiratory tract before they can set up an infection. The
trachea and bronchi are coated with a layer of mucus produced by the goblet cells
of the bronchial mucosa and the glands in the lamina propria.
This layer provides a physical barrier to organisms deposited in the airways and
is swept upward to the oropharynx by ciliary action removing deposited microbes.
The mucus contains specific antibody, mainly Ig A, produced in the bronchus as
well as other antibacterial substances such as lysozyme and lactoferrin produced in
the serous cells of the glands. Most organisms that reach the alveoli are engulfed
by macrophages and killed long before they are physically cleared from the lung.
2. What is the main cause of damage of the pulmonary defenses?
Clinically important factors that have been shown to depress macrophage
function include starvation, ethanol ingestion, hypoxia, uremia, air pollutants,
cigarette smoke, and antecedent viral infection.
The alveolar lining layer contains some antibody (mainly Ig G) as well as
complement components. The alveolar macrophages when stimulated can also
produce a variety of chemotactic substances that recruit neutrophils and more
mononuclear phagocytes.
With lymphoid nodules located at the branch points of small airways and in the
pleura and with complete lymph nodes in the hila, the lungs are also one of the
major lymphoid organs of the body.
3. What is lung collapse and pneumothorax?
The expansion of the lung is maintained by the pressure difference between the
alveoli, which are normally in free communication with the atmosphere, and the
subatmospheric pressure of the pleural space.The lung collapses when compressed
by pleural effusions, tumors, other space occupying intrathoracic lesions, or
elevation of the diaphragm. In pneumothorax the lung collapses because air gains
access to the pleural space, permitting the negative pleural pressure to rise.
After collapse there is a progressive rise in pulmonary vascular resistance in the
involved better-ventilated tissue. Several mechanisms are probably involved,
including hypoxia, tortuosity and distortion of the vascular bed, and reflex
vasoconstriction.
4. Characterize obstructive pulmonary diseases
Diagram II.
Comparison of Obstructive Pulmonary Diseases
Etiology Asthma
Emphysema
Chronic Bronchitis
Cause of airway obstruction
Precipitating causes
Manifestations
Treatment
Thick mucous, mucosal edema, smooth muscle spasm
Extrinsic:
Environmental antigens or allergens, IgE-mast cell complex releases inflammatory
mediators, cytokines activate and recruit Eosinophils and T cells into airway
Intrinsic:
Respiratory infections, drugs, air pollutants, cold and dry air, exercise and
emotional stress damage epithelium, (parasympathetic dominance causes
bronchospasm)
Dyspnea, wheezing, nonproductive cough early but later mucoid, prolonged
expiration, tachycardia, tachipnea
Eliminate cause, antiinflammatory agents, bronchodilators
Enlargement and destruction of alveoli, loss of elasticity, trapping of air
Alpha-1-antitrypsin deficiency, cigarette smoke causes neutrophils to release
proteolytic enzymes
Marked dyspnea, no cough early but later, tachypnea with prolonged expiration,
uses accessory muscles for ventilation, barrel chest, normal or elevated hematocrit,
late cor pulmonale
Prophylactic antibiotics, relief of dyspnea
Inflammation and thickening of mucous membrane, ciliary impairment,
accumulation of mucus and pus, metaplasia Cigarette smoke, air pollutants,
infections
Exercise intolerance, late dyspnea, wheezing, productive cough, marked
hypoxemia leading to polycythemia and cyanosis, early cor pulmonale, CHF
Bronchodilators, expectorants, postural drainage, percussion, antiinflammatory
agents
Obstructive pulmonary disease is characterized by difficult expiration. More
force or the use of accessory muscles of expiration is required to expire a given
volume of air. The most common obstructive diseases are asthma, chronic
bronchitis, and emphysema. Because many individuals have both chronic
bronchitis and emphysema, these diseases are grouped together and are called
chronic obstructive pulmonary disease (COPD). Asthma is more acute and
intermittent than COPD, but it also can be chronic.
5. Define pneumonia and describe its causes and manifestations
Pneumonia is an acute infection of the lung caused by bacteria, bacteria-like
microbes, or viruses. See the box below for the most common causal microbes.
Diagram III
Gram-Positive Bacteria
Gram-Negative Bacteria Nonbacterial Organisms
Streptococcus pneumoniae
Staphylococcus aureus
Streptococcus pyogenes
Escherichia coli
Pseudomonas aeruginosa
Klebsiella pneumoniae
Proteus species
Bacteroides species
Haemophilus species
Legionella species
Pneumocystis carinii
Mycoplasma pneumoniae
Fungi
Streptococcus pneumoniae organisms cause most bacterial pneumonias. In this
bacterial infection, the involved lobe undergoes consolidation or solidification of
the tissue as it fills with exudate. A stage of red hepatization follows in which
alveoli fill with blood cells, fibrin, edematous fluid, and pneumococci. This gives
the lung tissue a red appearance. Next is a stage of gray hepatization in which
affected tissues become gray because of fibrin deposition over the pleural surfaces
and the presence of fibrin and leukocytes in the consolidated alveoli. Infection is
usually limited to one or two lobes; thus the term lobar pneumonia is used.
Viral pneumonia is usually mild and self-limiting, but it can set the stage for a
secondary bacterial infection by providing an ideal environment for bacterial
growth and by damaging ciliated epithelial cells. Viral pneumonia can be a primary
infection or a complication of another viral illness such as chickenpox or measles.
Viral pneumonia is usually caused by influenza viruses. Most cases of pneumonia
are preceded by an upper respiratory viral infection. Individuals then develop
fever, chills, productive or dry cough, malaise, pleural pain, and sometimes
dyspnea and hemoptysis. The white blood count is usually elevated, but it may be
low if the individual is debilitated. Chest radiographs reveal infiltrates that may
involve a single lobe of the lung (lobar pneumonia) or may be more diffuse
(bronchopneumonia). Purulent sputum is expectorated by individuals with bacterial
pneumonia, while viral pneumonia and pneumonia caused by Mycoplasma
pneumoniae characteristically show scant sputum production.
Antibiotics are used to treat bacterial and mycoplasmal pneumonia. Viral
pneumonia is treated with supportive therapy unless secondary bacterial infection
is present.
6. Characterize pulmonary embolism, pulmonary hypertension, and cor
pulmonale.
Blood flow through the lungs can be disrupted by a number of disorders that
occlude the vessels, increase pulmonary vascular resistance, or destroy the vascular
bed. Major disruptive disorders include pulmonary embolism, pulmonary
hypertension, and cor pulmonale.
5.1. Content of the theme. Pulmonary defenses. What is the main cause
of damage of the pulmonary defenses? What is lung collapse and pneumothorax?
Characterize obstructive pulmonary diseases. Define pneumonia and describe its
causes and manifestations. Characterize pulmonary embolism, pulmonary
hypertension, and cor pulmonale.
5.2. Control questions of the theme:
1. Pulmonary defenses.
2. What is the main cause of damage of the pulmonary defenses?
3. What is lung collapse and pneumothorax?
4. Characterize obstructive pulmonary diseases.
5. Define pneumonia and describe its causes and manifestations.
6. Characterize pulmonary embolism, pulmonary hypertension, and cor
pulmonale.
5.3. Practice Examination.
Task 1. In the tourists, which rised at height 3000 m, the breath has become often
and deep. These changes are a consequence of stimullating
А. Chemoreceptors of a carotid zone В. Mechanical receptors of
pulmonary alveoles С. Baroreceptors of arc aorta
D. Neurons of cortex brain Е. Myocytes of respiratory muscles
Task 2. In the patient is diagnosed croupous pneumonia. For this disease is
characterized
А. Often deep breath В. Often surface breath С. Infrequent deep breath
D. Cheyne-Stokes’ breath Е. Kussmaul’s breath
Task 3.
In the member of high-mountainous expedition at the height of 6 km has
arisen vertige, the sharp weakness has appeared. The climber lost
consciousness, the breath has stoped. These disorders have arisen in
consequence
А. Insufficient entrance of О2 in an organism
В. Insufficient utilization О2 by tissues
С. Insufficient release of О2 oxyhemoglobin
D. Excessive washout СО2 from an organism
Е. Insufficient produce of СО2 in tissues
Task 4. In the patient wich bronchial asthma after walk in park has arisen an attack
of dispnea. The disorders of breath are conditioned by primary disorder of
А. Excitability of respiratory centre В. Function of respiratory muscles
С. Mobility of chest D. Perfusion of pulmonary tissue
Е. Ventilating ability of the alveoles
Task 5. In the child suffering bronchial asthma after transferred pneumonia has
arisen heavy asthmatical attack, that has resulted in development of acute
respiratory insufficiency. This complication is conditioned by
А. Change for the worse of blood supply pulmonary tissue В. Decrease
of volume alveolar ventilation С. Difficulty of diffusion of gases in lung
D. Increasing of dead space of lungs Е. Mixing of arterial and venous
blood
Real-life situations to be solved:
Task 1
In one of the members of high-mountainous expedition the erose increasing
and deepening of breath has occured which was replaced by a sudden oppression it
and loss of consciousness.
1. Explain the mechanism of increasing and deepening of breath for rising at
height.
2. Why stimulation of breath was replaced it by an oppression?
3. How acid-base balance victim was changed which has suffered?
4. What for him is better - inhalation of pure oxygen or carbogen?
Task 2
In the patient, which was on surgical table under narcosis, the sharp oppression of
breath has occured. The pulse has become rare and weak. Has appeared cyanosis.
The emergency measures accepted by the anaesthesiologist, liquidated these
disorders.
1. What can be connected the oppression of breath with ?
2. How in yours opinion, the contents of oxygen and carbonic acid in
arterial of blood was changed in the patient?
3. Explain appearance of the cyanosis.
4. How are you evaluate changes of the pulse in this case?
Literature:
1. Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and clinical
pathophysiology/ Workbook for medical students and practitioners.-Odessa, 2001.P.194-202.
2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study
guide for medical students and practitioners.-Odessa, 2003.- P.224-232.
3. Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar,
Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.P. 697-753.