Introduction to COPD:

Chronic Obstructive Pulmonary
Disorder (COPD) is an insidious disorder of the lungs due to an impediment of
airflow that hinders normal breathing (1). It is an umbrella term for a group
of long-term respiratory conditions that are made distinctive by lung lesions
as a result of ongoing tissue deterioration and obstruction of the airways. The
disorders included are emphysema, chronic bronchitis, and chronic asthma. Each
of these conditions differ and overlap in some way. For example, the aetiology
for emphysema is due to smoking and/or genetics, whereas air pollution is
considered a contributing cause for the onset of chronic bronchitis (2). Although,
there are similarities between these conditions, there is debate that suggests
asthma should not be included under the COPD group. As emphasised by Cukic et
al. (3) who states that Asthma is a respiratory inflammatory disease with
hyperresponsiveness that generates the presentation of symptoms. Asthmatic
episodes are reoccurring but not persistent, and the condition can be
reversible or treated and managed. Whereas, COPD is a degenerative disease characterized
by airflow restriction and is a debilitating disease that impacts on function
in everyday living. It is said to be the fourth leading cause of death in the
world. Once the damage is done it is completely irreversible. Emphysema will
present itself via three cardinal symptoms: 1) Dyspnea 2) Chronic cough 3)
Sputum production (4).

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Table 1 (2)

Characteristics

Emphysema

Chronic
Bronchitis

Asthma

Aetiology
 

Smoking
Genetic

Smoking
Air
pollution

Hypersensitivity
type 1
Hyperresponsiveness

Environmental
allergens/ pollutants

Site

Alveoli

Bronchi

Bronchioles

Pathophysiology
Overview

Destruction
of alveolar walls
Loss
of elasticity
Impaired
expiration
Barrel
chest
Hyper-inflation

Increased
mucous glands and secretion
Inflammation

Infection

Obstruction

Inflammation
Broncho-constriction

Increased
mucous production
Obstruction

Repeat
attacks leading to damage

Symptoms

Some
coughing
Marked
Dyspnea (laboured breathing)
Little
bit of sputum
Some
infections
Potentially
cor pulmonale

Early,
constant cough, some Dyspnea
Large
amount of sputum
Bluish
discolouration of the skin due to poor circulation. Inadequate oxygenation of
the blood (cyanosis)
Frequent
infections
Common
cor pulmonale

Cough,
Dyspnea, wheezing
Thick
tenacious mucus
Cyanosis
if status asthmaticus
Some
infections
Rare
cor pulmonale

Typical
age
 

Approx.
40 but can be younger in genetic cases

Can
be all ages but predominantly 45+

Usually
as a child and young people but can have a late onset, approx. 65+

 

What happens internally?

Healthy respiratory system:

The
lungs are a vital organ therefore, they are protected by the sturdy structure
of the rib cage. Breathing, or pulmonary ventilation, is a mechanical process
that occurs when volume and pressure changes in the lungs and the diaphragm
contracts and moves downwards, which creates chest expansion, allowing the
lungs to inflate. Also, “The intercostal muscles between the ribs help enlarge
the chest cavity. They contract to pull the rib cage both upward and outward
when you inhale” (5, 6). This allows for a breath of oxygen (O?) to be inhaled through the nose. It
travels down the upper respiratory tract into the lungs, reaching the alveoli.
These small air sacs are positioned next to capillaries, which are supplied by
the pulmonary artery, in order to directly diffuse oxygen from the lungs,
through the plasma membrane, to the red blood cells (RBC) in the blood stream. RBCs
are biconcave in shape, anucleate and largely haemoglobin with very few
organelles. It is the haemoglobin that transports much of the oxygen (HbO?) carried in blood and only binds with a
small amount of carbon dioxide (CO?).
Elements of blood include: plasma which makes up 55% and Erythrocytes (RBC),
Leukocytes/ white blood cells (WBC) and platelets comprise 45%. (5)

The
opposite happens during exhalation, carbon dioxide diffuses from the red blood
cells to the alveoli and back up the pathway to exit the body via the nose or
mouth. Meanwhile, the diaphragm relaxes and moves upwards which reduces the
space in the chest cavity, this aids to force the carbon dioxide out (6, 7, 8).
“Exhalation is more of a passive process and depends more on the lungs natural
elasticity” (5).

Alveoli
are positioned on the ends of the bronchioles deep inside the lungs. Their main
function is to increase surface area in order to sustain sufficient gas
exchange to meet the demands of the large organism, the human body. “In the average adult lung, there is an average of 480 million alveoli with a
total average surface area of around 75 square metres” (8). The alveoli are
located next to a cobweb-like network of capillaries, held together by
membranes and elastic fibres, known as the respiratory membrane (5). The main
cell covering the alveoli is simple squamous epithelial therefore, aiding with
the diffusion process, making it a rapid one. The pulmonary arteriole allows
deoxygenated blood to travel to the alveoli and the pulmonary venule allows
oxygenated blood to travel away from the alveoli to organs, tissues, cells etc
that need it (9).

Inside a single alveolus is an alveolar
macrophage, it’s function is to keep the internal environment clear from
infection. If an infection does occur, it will fight against it. Also, the
alveoli will release antiproteases which are enzymes that defend against
protease activity. Protease is destructive therefore, having the secretion of
antiprotease balances the enzyme activity keeping an equilibrium (4).

Unhealthy respiratory system:

Emphysema
is caused by the imbalance of protease and antiprotease. For somebody suffering
with this condition, the surface area provided by the alveoli is significantly
decreased due to the alveolar wall and elastic fibres being obliterated by the
protease enzymes. The reduction of surface area means that the diffusion of gas
cannot happen as efficiently. Alveoli are extremely unique and well adapted,
they are the only site of respiratory gas exchange within the respiratory
system therefore, once they are destroyed they will not function and this
cannot be reversed (2). This means that somebody suffering with emphysema will
struggle with taking deep breaths in and exhaling long breaths out. When the
lungs fill with air they do so within the rib cage which constricts the small
bronchi, thus increasing the demand on the lungs. “This is especially evident during expiration, when contraction of the
muscles of the chest wall and abdomen increase intrathoracic pressure and
further reduce the passage of air through the small bronchi” (10).

Causes of COPD:

Genetics:

Alpha-1 Antitrypsin (A1AT)
Deficiency causes the body to not produce enough of this natural protein that
travels around in the circulatory system. A1AT is an antiprotease enzyme that
is present in both the lungs and the liver. Its function is to protect these
organs by keeping an optimum enzyme balance. This avoids damage to normal
tissues therefore, people with this deficiency are more susceptible to
Emphysema and/ or Cirrhosis, a liver disease (2, 11, 12). This is usually the
cause of emphysema found in non-smokers and young people. Tests for this
include “A1AT blood test, chest x-ray, genetic testing, and lung function test”
(12).

Smoking:

Smoking is a key cause of
emphysema because it contains oxidative toxins which destroys important
features in the lungs causing malfunction of expiration which can lead to
trapped air, and reduction of elastic fibres which results in the inability of lung
recoil during inhalation and exhalation of gases. (4) “Cigarette smoking
increases both the number of neutrophils in the alveoli and the release and
activity of elastase, but decreases the effect of Alpha-1 Antitrypsin, thus
greatly contributing to the breaking down of the alveolar structures” (2). When
the reactive oxidative toxins are inhaled via smoking, the lungs will produce
an inflammatory response which will amplify inflammation. The macrophages will
begin to release chemicals such as elastase which destroys the elastic fibres
and protease which damages the surrounding tissues “through alveolar septal
cell apoptosis and destruction of the extracellular matrix (ECM)” (13). Therefore, emphysema causes an
overwhelming imbalance of protease (4).

A variety of processes take
place in the lungs for alveolar maintenance, but when the lung environment is
filled with cigarette smoke it is hard for these processes to protect the
alveoli because the smoke is recognised as danger, via a sensor molecule called
Rapamycin (mTOR). This is because the smoke triggers an inflammatory and
anti-oxidative stress response in the lungs which disrupts the maintenance of
the alveoli. This form of Emphysema is referred to as ‘panacinar’ because it
occurs at the distal alveolar (2).

These statistics from the
Medscape risk factor list (14) suggest that what and how much is being smoked a
day can affect the onset of emphysema. “15-20% of 1 pack-per-day smokers and
25% of 2 pack-per-day smokers develop COPD. Next are cigars and pipe smoke,
followed by second-hand and third-hand smoke.” Today, it is well known that
smoking damages the lungs however, it can also cause many other complications
and conditions as well. One of which being Osteoporosis (17).

Introduction to Osteoporosis:

Osteoporosis is an
asymptomatic condition that involves the loss of bone density and bone strength,
often causing bone to gradually become more fragile and brittle which increases
the risk of fracture. It can be described as a clinically silent condition
because one can be completely unaware of having osteoporosis until it presents
itself with the first fracture (15). Osteoporosis can be divided in two types;
primary (or type 1) can be split into two subcategories. Firstly, it can be
related to the post-menopausal stage in a female’s life because low oestrogen
levels can lead to bone density being lowered up to 20%. Secondly, senile
osteoporosis which is linked to old age. Moreover, secondary osteoporosis (or
type 2) can occur due to other factors for example, diseases, hormones, medication
(16). Osteoporosis seems to be more prevalent in women, specifically women aged
50 and over, but in recent times it is now becoming more apparent in men. It is
estimated 1 in 8 men also lose bone mass (2). The NHS (17) says sometimes even
a cough, or a sneeze can cause an osteoporotic-related fracture of a rib or a
vertebral body in the spine, this could cause kyphosis, which would further
impair lung function in a COPD patient. The condition isn’t painful until a
fracture occurs and if serious, can leave the sufferer with long-term chronic
pain.

Healthy bone structure:

“The skeleton makes up 15% of
the body’s weight. The bones are comprised of half water and half solid matter
and contain nearly two pounds of calcium and more than a pound of phosphorus” (18).
Much of an adult skeleton is comprised of bone whereas during childhood there
is a lot more cartilage present. This is to allow for growth. The
transformation of cartilage to bone should be complete after adolescence. Bone
and cartilage are both forms of connective tissue but consist of very different
structures. Cartilage is stiff yet flexible with hardly any blood supply. It is
comprised of specialized cells, and examples of cartilage include: hyaline and
fibrocartilage. Again, these cell structures would differ. On the other hand,
bone has lots of blood vessels supplying it therefore, it is extremely capable
repairing itself. Bone cells are positioned within a mineralized matrix,
creating a durable tissue (9). “Bone is three times stronger than the same
quantity of reinforced concrete” (18). Bone is comprised of compact bone which
is a strong, solid surface on the outer border, followed by spongy bone which
is less dense than compact bone and does have the appearance of a holey sponge,
as the name suggests. This fills the inner area of bone (19). 

Osteoporotic bone structure:

With age, calcium levels and
bone mass naturally decrease in bone which could result in Osteoporosis. Reasons
why people could be prone to developing Osteoporosis are as follows: genetics,
White or Asian ethnicity, female, diet that is low in nutrition, vitamins, and
minerals, certain medications, lack of weight baring, smoking, and consuming
too much alcohol (19). Heany (20) says, an injury can stem from a combination
of factors, these include: the way a fall occurs (for example, falling to the
side), bad posture and reduced soft tissue that can no longer protect the bones
from force. Bone fragility itself develops from deteriorated quality of the
bone material. “This is primarily
the result of accumulated fatigue damage, but reduced collagen cross-links and
other intrinsic material defects may play a role as well”.

Bones have cells called
osteoclasts and osteoblasts and they both have very opposite functions. Osteoclasts
destroy bone and osteoblasts rebuild the bone tissue via essential minerals carried
in blood, e.g. calcium (19). “In adults, bone maintenance involves daily
removal of small amounts of bone mineral, a process called resorption, which
must be balanced by an equal deposition of new mineral if bone strength is to
be preserved. If this process becomes unbalances, it’ll result in excessive
resorption, leading to bones weaken (osteopenia) and over time can become prone
to fracture (osteoporosis). (21). There are many ways to maintain bone strength
throughout life, such as exercise. Also, having adequate levels of oestrogen
and testosterone keep the level of osteoblasts higher than osteoclasts. Peak
bone mass is reached in the 4th decade (19).

Introduction to GERD:

Gastroesophageal Reflux
Disease (GERD) is a disease that allows acidic stomach content to regurgitate,
causing it to travel back up the oesophagus. This condition presents itself
through symptoms such as heartburn, nausea, chronic cough, and it can be
noticeable by acid erosion on the teeth (22).

The stomach is protected by
many mechanisms, one of which being the lower oesophageal sphincter (LES),
which is a valve at the junction of the oesophagus and the stomach that provides
pressure by usually being taut. This is to stop any bolus or acid flowing back
up the oesophagus, but to continue the route of the digestive system. During
normal digestion, bolus will travel down the oesophagus which will reduce
pressure at the LES just enough to allow the bolus to pass through via the aid
of smooth muscle mobility (peristaltic waves), then into the stomach. Smooth
muscle lines the hollow oesophagus which allows for peristalsis which is an
involuntary movement. Smooth muscle is visceral and non-striated (5). Another
structure that provides protection to the stomach is the diaphragm. This thick,
strong band of muscle wraps around the neck of the stomach in order to keep any
contents beneath the oesophagus. Therefore, both the LES and the diaphragm work
to protect the stomach by making it a one-way pathway which prevents acidic
content refluxing. (23, 24). Therefore, GERD occurs when the LES malfunctions.
The Lung Institute (25) says the GERD will worsen the symptoms of COPD.

The way in which the stomach
is positioned with the oesophagus creates a steep angle, termed the Angle of
His, which makes the gastroesophageal junction longer. With reference to
Poiseuille’s Law, this increases the pressure or resistance on the
gastroesophageal junction creating a tight seal (24). Many people who have
advanced COPD also develop GERD and GERD worsens COPD. The exact cause of GERD
and the relationship between it and COPD is unknown however, lots of
medications that are used to manage the symptoms of COPD weaken the LES. “Also, many COPD sufferers have air
trapped in their lungs, which pushes upwards on the abdomen, which causes acid
reflux” (25). Mannino (26) says the acidic content that gets refluxed into the oesophagus
can irritate the lungs, and cause a COPD sufferer to cough frequently and
experience difficulty breathing which could potentially cause the acidic
content to get into the lungs.

Conclusion:

With reference to the linked
case study (Appendix), this patient is suffering from numerous complications, also
known as comorbidities, not just one problem. It is common for COPD patients (colloquially
known as ‘pink puffers’) to experience exacerbations and/or comorbidities due
to this primary disease. Hillas says “COPD is a leading cause of morbidity and
mortality worldwide” (27). There are many potential coexisting diseases that
could present themselves along side COPD, but this case study focuses specifically
on Osteoporosis and GERD. Furthermore, Hillas suggests that “GERD is present in
60% of COPD patients” (27). Numerous resources have made it clear that other
conditions and complications can develop alongside or as a result of COPD, but
what can COPD lead to? The Mayo Clinic (28) states that COPD sufferers are more
susceptible to respiratory infections and even at high risk of developing lung
cancer due to the destructive nature of the disease. Moreover, high blood
pressure in arteries can result in blood in the lungs which is known as
pulmonary hypertension, and for unknown reasons COPD can heighten the risk of heart
problems. Finally, depression is a key complication that can occur in people
with COPD. This is because COPD can be physically debilitating and prevent the
sufferer from doing everyday routines and/or enjoyable activities and hobbies
which they used to be able to do and this is saddening to the patient.

To conclude, Emphysema is a
pathophysiology that clinically presents itself as alveoli enlargement and
destruction, and the lungs lose elasticity. Associated dysfunction includes
great difficulty to exhale as COPD patients will need to use a lot more energy
than a healthy person to do so. This will cause breathlessness, fatigue and
exhaustion. This can overinflate the lungs which will lead to a barrel chest
(5). The main contributing factors are smoking but some may develop emphysema
through A1AT Deficiency. 

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