Zusammenfassung der Ressource
The lungs and lung disease
- Structure of human lungs
- Trachea
- Supported by rings of cartilage to
prevent collapse when breathing in
- Walls made up of
muscle and ciliated
epithelium
- Goblet cells produce mucus
that traps dirt/pathogens
- Bronchi
- 2 subdivisions of trachea
- Lined with cilia
- Supported by rings of cartilage, amount
reduces are bronchi get smaller
- Bronchioles
- Subdivisions of the bronchi
- Lined with muscle
- Allows them to constrict and control airflow
- Alveoli
- Air sacs at the end of bronchioles
- Contain collagen and elastin
- Fibrous proteins, collagen - high
tensile strength, elastin is elastic!
- Mixed to prevent elastin overstretch
- Squamous epithelium
- Thin cells - short diffusion pathway
- Large sa:v ratio
- Partially permeable
- Rich supply of capillaries
- Narrow so red blood cells are
flattened against them
- Shorter diffusion distance
- Slows rbc's allowing more time
for diffusion
- Endothelium is one cell thick
- Equations
- Pulmonary ventilation = tidal volume (dm^3)
x ventilation rate (min^-1)
- Fick's Law
- Diffusion is proportional to
- Surface area x conc. gradient / length of diffusion pathway
- Pulmonary Tuberculosis
- Caused by 2 species of rod-shaped bacteria
- Mycobacterium tuberculosis
- Mycobacterium bovis
- Symptoms
- Persistent cough
- Tiredness
- Loss of appetite
- Weightloss
- Development can lead to coughing up
blood and fever
- Transmission
- Airborne droplets
- Close contact over
long period of time
- Infected cows milk
- People with reduced immunity more
susceptible, eg:
- HIV/AIDS
- Very young and old
- Immunosuppressant drugs
- Course of infection
- 1. The bacteria grow and divide in
the upper regions of the lungs
- 2. The body's immune system
responds with white blood cells
accumulating in the area
- 3. This causes inflammation,
enlargement of lymph nodes -
PRIMARY INFECTION
- 4. Some bacteria remain in tubercules
surrounded by white blood cells with
the bacteria and infected phagocytes
in the middle
- 5. POST-PRIMARY INFECTION
can occur years later when
the immune system is
weakened
- 6. The bacteria reproduce quickly, destroying the
lungs and causing cavities
- Hence, sufferers cough up damaged tissue
and bacteria, and scar tissue develops
- 7. The bacteria may spread to
other regions if they reach blood
supply
- Pulmonary fibrosis
- Scar tissue on epithlium
- Irreversibly thickens the alveoli walls
- Longer diffusion pathway
- Less efficient gas exchange
- Smaller lung volume
- Reduces elasticity
- Lack of elastic recoil
- Makes breathing more difficult
- Difficult to maintain conc. gradient
- Effects
- Shortness of breath
- Chronic, dry cough
- Pain and discomfort in chest
- Weakness and fatigue
- Causes
- Microscopic injury (asbestosis)
- Unknown (idopathic)
- Damage to alveoli resulting in
overproduction of fibroblasts
- Asthma
- Causes
- Genetic predisposition
- Allergens
- Anxiety, cold air, exercise can
worsen or trigger asthma
- 1. Allergens cause white
blood cells on the
linings in the bronchi
and bronchioles to
produce histamine
- 2. Histamine causes the
following effects in the
airways
- Inflammation
- Increased mucus secretion
- Fluid leaving capillaries and entering airways
- Contraction of smooth muscle
surronding bronchioles
constricting airways
- Effects
- Greater resistance to the
flow of air
- Difficult to ventilate lungs and
maintain conc. gradient
- Difficulty breathing
- Wheezing
- Tigh-chest feeling
- Coughing
- Emphysema
- Usually a result of long term smoking
- Particles from smoke cause immune response,
over a long time of smoking the enzymes released
by white blood cells breaks down elastin
- Lack of elastic recoil
- Alveoli burst
- Reduced surface area
- Alpha-1 Antitrypsin Deficiency
- Mutation to the gene coding for the enzyme
alpha-1 antitrypsin,gets stuck in the liver
- Enzyme protects the lungs from
neutophil elastane which breaks
down elastin
- Often looks like emphysema
- Injection of alpha-1 antitrypsin and
gene therapy is promising