Vous êtes sur la page 1sur 83

LEARNING OUTCOME (A)

Students should be able to describe the structure of the human gas exchange system, including the microscopic structure of the walls of the trachea, bronchioles and alveoli with their associated blood vessels; Identify the structure of various tissue layers in the gaseous exchange system Connect the role of various layers of tissue in the gaseous exchange system Smooth muscle C-shaped cartilage Identfiy and draw structure of chondrocytes Cilliated epithelial layer Identify and draw cilliated cell Identify and draw goblet cells

TRACHEA

ciliated epithelium Goblet cells mucous glands C- shaped Cartilage rings

CILLIATED EPITHELIUM LAYER

LUNGS Protected by ribcage Rib cage includes ribs and intercostal muscles that help lungs expand and contract Lungs connected to atmosphere by trachea Trachea branches into 2 bronchi Each bronchi has many bronchioles Each bronchiole has many air sacs (alveoli)

BRONCHUS

SECTION OF A TRACHEA

CARTILAGE TISSUE

Chondrocyte Lacuna

BRONCHUS

BRONCHUS

BRONCHIOLE

RESPIRATORY BRONCHIOLE

TERMINAL BRONCHIOLE

THE ALVEOLI

LEARNING OUTCOME (B) AND (C)


Students should be able to describe the distribution of cartilage, ciliated epithelium, goblet cells and smooth muscle in the trachea, bronchi and bronchioles; Students should be able to describe the functions of cartilage, cilia, goblet cells, smooth muscle and elastic fibres in the gas exchange system; Connect the role of various layers of tissue in the gaseous exchange system Smooth muscle C-shaped cartilage Identfiy and draw structure of chondrocytes Cilliated epithelial layer Identify and draw cilliated cell Identify and draw goblet cells

CARTILAGE

Surrounds the trachea to provide structural support for the trachea and bronchus C-shaped/ horseshoe-shaped

Rigid

GOBLET CELLS

Glandular columnar cells Sole purpose to secrete mucus Found in trachea, bronchus and (larger) bronchioles Entraps particles and pathogens so that WBC can engulf them

CILLIATED EPITHELIUM CELLS


Thin layer of epithelial cells with hair-like organelles called cillia
Responsible for moving (wave-like manner) entrapped dirt and pathogen particles up to the pharynx At the pharynx dirt laden mucus enters the esophagus and into the stomach In the stomach pathogens are destroyed due to acidic conditions

SMOOTH MUSCLE
Capable of contraction Found in trachea, bronchi & bronchioles Its effect is in the bronchioles Bronchioles are not supported by cartilage Contraction of the rings of smooth muscles around them causes the bronchioles to constrict to control air flow

ELASTIC FIBERS
Allows alveoli to expand during inspiration and contract passively during expiration

ALVEOLUS

ALVEOLUS

no

no

Airway Trachea Bronchus Terminal bronchiole Respiratory bronchiole Alveolar duct Alveoli

No. 1 2 48 000 300000 9 x 106 3 x 109

Cartilage Yes Yes No No No No

Goblet cells Yes Yes No No No No

Smooth muscles Yes Yes Yes No No No

Cilia Yes Yes Yes Yes No No

gas exchange No No No Yes Yes Yes

LEARNING OUTCOME (D)


Students should be able to describe the process of gas exchange between air in the alveoli and the blood; Describe the movement of oxygen from alveolar space into the blood vessels Describe movement of carbon dioxide out of blood out of into alveolar space Able to understand the gradients involved Describe the manner in which the molecules move Features of the alveoli to increase efficiency of gas exchange

PROCESS OF GASEOUS EXCHANGE IN THE ALVEOLUS


Air enters alveoli

Oxygen dissolves into film of liquid


Oxygen diffuses into blood or carbon dioxide diffuses out down concentration gradient Gas passes through epithelium of alveolus and endothelium of capillary

Short distance between alveolus and capillary and thin wall of capillary allows efficient exchange of gas

ADAPTATIONS OF CAPILLARIES FOR GAS EXCHANGE


Thin cell wall (1 cell thick) approximately 0.5m (squamous epithelium)
short diffusion distance High amount of blood/capillaries quickly takes away CO2 and supplies O2 (alveoli provide) large surface area (when expanded) ;

thinner layer of mucus/ moist surface ;

EMPHYSEMA Healthy alveoli have elastin fibers around the alveoli Alveoli will expand when filled with air Elastin fibers will force the alveolus to return to their original shape

LEARNING OUTCOME (E)


Students should be able to describe the effects of tar and carcinogens in tobacco smoke on the gas exchange system Describe the effect of TAR on the cilliated epithelial layer Describe the sequence of events that lead to chronic bronchitis a form of COPD Describe the sequence of events that lead to the formation of cancer cells in the gaseous exchange system

EFFECT OF TAR ON GASEOUS EXCHANGE


Settle on the lining of the airways in the lungs It is an irritant that causes inflammation of the mucus membranes lining the trachea, bronchi, bronchioles (Bronchitis) As a response to tar deposition, goblet cells produce more mucus Cillia would be paralysed as mucus and tar accumulates So these cilia cannot remove the mucus secreted by the epithelial lining. Also components of tar (benzpyrene) are carcinogenic and can cause lung cancer

LEARNING OUTCOME (F)


Students should be able to describe the signs and symptoms of lung cancer and chronic obstructive pulmonary disease Identify how the sequence of events in developing lung cancer and COPD may result in symptoms Identify how symptoms may bot be absolute indications of the disease Identify how the diseases influence lung capacities and volumes

There are four volume subdivisions which:


do not overlap.

can not be further divided.


when added together equal total lung capacity.

Lung capacities and volumes


INSPIRITORY RESERVE VOLUME INSPIRATION CAPACITY
VITAL CAPACITY

TIDAL VOLUME

EXPIRATORY RESERVE VOLUME

EXPIRATION CAPACITY

FUNCTIONAL RESIDUAL TOTAL CAPACITY RESERVE CAPACITY VOLUME

DEFINITIONS
Tidal volume
Inspiratory reserve volume Expiratory reserve volume
Volume of air breathed in and then breathed out during a single breath
After a normal inspiration and continue to inhale or the amount of air that can be taken into lungs after normal expiration After a normal expiration and continue to exhale or the amount of air that can be exhaled after a normal inhalation Maximum volume of air that can be exchanged during one breath in and out (forced inspiration and expiration)

Vital capacity

Residual volume

The volume of air that is always left in the lungs. (Air remain in the lungs even after forced expiration) * Without the residual volume, the moist walls of the alveoli would stick together and it would be impossible to re-inflate the lungs Total volume of air that the lungs can hold

Total lung capacity

Total Lung Capacity (TLC). The volume of air contained in the lungs at the end of a maximal inspiration. Called a capacity because it is the sum of the 4 basic lung volumes. TLC=RV+IRV+TV+ERV Vital Capacity (VC). The maximum volume of air that can be forcefully expelled from the lungs following a maximal inspiration. Called a capacity because it is the sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume. VC=IRV+TV+ERV=TLC-RV Functional Residual Capacity (FRC). The volume of air remaining in the lung at the end of a normal expiration. Called a capacity because it equals residual volume plus expiratory reserve volume. FRC=RV+ERV Inspiratory Capacity (IC). Maximum volume of air that can be inspired from end expiratory position. Called a capacity because it is the sum of tidal volume and inspiratory reserve volume. This capacity is of less clinical significance than the other three. IC=TV+IRV

EMPHYSEMA Healthy alveoli have elastin fibers around the alveoli Alveoli will expand when filled with air Elastin fibers will force the alveolus to return to their original shape

EMPHYSEMA
A result of heavy smoking WBC will produce a type of enzyme (elastase) that breaks down elastin Normally a protein inhibitor will prevent this from happening In smokers chemicals in the cigarette smoke inactivate protein inhibitors. Increased Elastase activity and breakdown of Elastin

Breakdown of elastin results in alveoli unable to return to original size Very little exchange of gas occurs as air remains in the lungs

CHRONIC BRONCHITIS
Caused by an accumulation of irritants (such as tar, asbestos dust etc.) in trachea, bronchus and bronchioles Goblet cells respond by over-producing mucus thick mucus makes it difficult to remove all the dirt and pathogens Smooth muscle spasms Acumulation of dirt results in bacterial infection Bronchiole lining gets inflamed and narrows airways

Results in coughing (a reflex to get rid of excess mucus) Breathlessness (restricted air movement in the bronchioles)

LUNG CANCER

LEARNING OUTCOME (G)


Students should be able to describe the effects of nicotine and carbon monoxide on the cardiovascular system Recognize nicotine and carbon monoxide as components of cigarette smoke Recognize that nicotine and carbon monoxide will enter the blood circulatory system but not TAR

MAIN COMPONENTS OF CIGARETTE SMOKE


Tar Carbon monoxide Nicotine

EFFECT OF CARBON MONOXIDE ON GASEOUS EXCHANGE


Carbon monoxide readily diffuses through the walls of alveoli in the lung Hb has a higher affinity for carbon monoxide than it has for oxygen Binds with haem groups in Hb to form carboxyhaemglobin

Oxyhaemoglobin releases its oxygen BUT carboxyhaemoglobin not released Hb is not available to carry oxygen

EFFECT OF NICOTINE
Acts as a vasoconstrictor Increases heart rate and blood pressure Makes blood platlets more sticky Reduces bloodflow to extremities Damages endothelium of arteries

Less glucose/ oxygen supplied to the heart


Less waste removed Causes heart to contract less strongly

LEARNING OUTCOME (H)


Students should be able to explain the link between smoking and atherosclerosis, coronary heart disease and Recognize that nicotine and carbon monoxide will enter the blood circulatory system Identify the effects of nicotine and carbon monoxide on tissues in the circulatory system and how it initiates the beginning of certain chronic diseases

ATHEROSCLEROSIS
Damage to artery inner lining/ endothelium due to CO or nicotine Development of atheroma which consists of dead muscle, fibers and cholesterol. high amounts of LDL molecules will deposit cholesterol in damage sites deposition of fatty plaque and cholesterol will block the arteries. Blood will no longer be able to flow properly and will clot and form a thrombus.

Cholesterol Lipoprotein

Low density lipoprotein LDL

High density lipoprotein HDL

~ Transport cholesterol from the liver to the tissues ~ They tend to deposited their cholesterol at any damage site

~ Remove cholesterol from tissues and transport it to the liver ~ Helps to protect arteries against atherosclerosis

thrombus

Normal artery

CORONARY HEART DISEASE When atherosclerosis occurs in the heart arteries, it can starve the heart muscle of oxygen Angina pectoris-blockage of heart arteries. Heart starved of oxygen. Accumulation of lactic acid causes acute pain. Myocardial infarction- heart arteries blocked. Death of heart muscle. Heart faliure-heart weakened due to blockage. Long term effect.

LEARNING OUTCOME (I)


Students should be able to evaluate the epidemiological and experimental evidence linking cigarette smoking to disease and early death; Understand the differences between epidemiological and experimental evidence Use knowledge in identifying trends in data to support or oppose the idea that smoking and diseases are linked.

EPIDEMIOLOGICAL EVIDENCE OF SMOKING AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE


Epidemiological evidence of smoking and disease
50% smokers die due to smoking-related disease Smokers 3x more likely to die in middle age COPD incidences increase in smokers but is rare in non smokers

Emphysema -98% of emphysema patients are smokers; 20% of smokers are suffering from emphysema Chronic bronchitis
Lung cancer Risk of lung cancer increases when: Smokers inhale Start young No. of cigarettes smoked per day increased Smoke high tar cigarettes

HOWEVER. Epidemiological evidence provides no direct link to disease. Only shows a casual association Many other things can cause lung disease, eg. Air pollution, occupation, climate. Epidemiological evidence is highly dependant on data collection and interpretation. Eg. Were all the populations sampled, What other factors contribute to COPD?

PROVING THE LINKS BETWEEN SMOKING & CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
Experimental evidence shows a direct link between smoking and pulmonary diseases Experiment 1: 48 dogs were divided into 2 groups 1 group exposed to filtered cigarette smoke & did not develop cancer The other was exposed to unfiltered cigarette smoke & developed abnormalities similar in humans lung cancer patients The group with filtered cigarettes had some dogs develop precancerous lesions

Experiment 2: Lab mice painted with cigarette tar develops cancerous growths Proves the presence of carcinogenic chemicals in cigarette tar

There is no positive correlation AW e.g. no link/no direct connection,between increased cigarette consumption and number of deaths; use of comparative figures to support this; both no of cigarettes and deaths must be quoted (2 sets of figs needed) people die before COPD develops (sufficiently); only 20 countries;

cause of death may not be recorded accurately/maybe other cause(s) recorded on death certificate;
COPD contributed to death but not main cause; maybe other factors contribute to developing COPD eg. air pollution/occupation/ climate/population density; maybe other factors involved with smoking are more important e.g. number of years smoked/number of cigarettes smoked by smokers;

LEARNING OUTCOME (J)


Students should be able to discuss the difficulties in achieving a balance between preventions and cure with reference to coronary heart disease, coronary bypass surgery and heart transplant surgery; Understand the difference between coronary bypass and heart transplant Understand the differences and difficulties in preventing a chronic disease and curing a chronic disease

CORONARY BYPASS
Blockage in the coronary artery may be difficult to remove especially if extensive Ablood vessel from another part of the body is used to bypass the blocked section to allow blood to flow through

This allows the heart to continue to receive oxygen

HEART TRANSPLANT
Heart transplant patients require a donor heart to be provided and replace their own damaged heart Requires a suitable donor. Lack of a donor results in high mortality rates in heart disease patients

High chance of complications even with a suitable donor ie. rejection