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PathologicalPresentationIntroduction to COPD:Chronic Obstructive PulmonaryDisorder (COPD) is an insidious disorder of the lungs due to an impediment ofairflow that hinders normal breathing (1).

It is an umbrella term for a groupof long-term respiratory conditions that are made distinctive by lung lesionsas a result of ongoing tissue deterioration and obstruction of the airways. Thedisorders included are emphysema, chronic bronchitis, and chronic asthma. Eachof these conditions differ and overlap in some way. For example, the aetiologyfor emphysema is due to smoking and/or genetics, whereas air pollution isconsidered a contributing cause for the onset of chronic bronchitis (2). Although,there are similarities between these conditions, there is debate that suggestsasthma should not be included under the COPD group. As emphasised by Cukic etal. (3) who states that Asthma is a respiratory inflammatory disease withhyperresponsiveness that generates the presentation of symptoms.

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Asthmaticepisodes are reoccurring but not persistent, and the condition can bereversible or treated and managed. Whereas, COPD is a degenerative disease characterizedby airflow restriction and is a debilitating disease that impacts on functionin everyday living. It is said to be the fourth leading cause of death in theworld. Once the damage is done it is completely irreversible. Emphysema willpresent itself via three cardinal symptoms: 1) Dyspnea 2) Chronic cough 3)Sputum production (4).

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:Thelungs are a vital organ therefore, they are protected by the sturdy structureof the rib cage.

Breathing, or pulmonary ventilation, is a mechanical processthat occurs when volume and pressure changes in the lungs and the diaphragmcontracts and moves downwards, which creates chest expansion, allowing thelungs to inflate. Also, “The intercostal muscles between the ribs help enlargethe chest cavity. They contract to pull the rib cage both upward and outwardwhen you inhale” (5, 6). This allows for a breath of oxygen (O?) to be inhaled through the nose. Ittravels down the upper respiratory tract into the lungs, reaching the alveoli.These small air sacs are positioned next to capillaries, which are supplied bythe 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.

RBCsare biconcave in shape, anucleate and largely haemoglobin with very feworganelles. It is the haemoglobin that transports much of the oxygen (HbO?) carried in blood and only binds with asmall 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) Theopposite happens during exhalation, carbon dioxide diffuses from the red bloodcells to the alveoli and back up the pathway to exit the body via the nose ormouth. Meanwhile, the diaphragm relaxes and moves upwards which reduces thespace 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 naturalelasticity” (5).

Alveoliare positioned on the ends of the bronchioles deep inside the lungs. Their mainfunction is to increase surface area in order to sustain sufficient gasexchange 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 atotal average surface area of around 75 square metres” (8).

The alveoli arelocated next to a cobweb-like network of capillaries, held together bymembranes and elastic fibres, known as the respiratory membrane (5). The maincell covering the alveoli is simple squamous epithelial therefore, aiding withthe diffusion process, making it a rapid one. The pulmonary arteriole allowsdeoxygenated blood to travel to the alveoli and the pulmonary venule allowsoxygenated blood to travel away from the alveoli to organs, tissues, cells etcthat need it (9).

Inside a single alveolus is an alveolarmacrophage, it’s function is to keep the internal environment clear frominfection. If an infection does occur, it will fight against it. Also, thealveoli will release antiproteases which are enzymes that defend againstprotease activity. Protease is destructive therefore, having the secretion ofantiprotease balances the enzyme activity keeping an equilibrium (4).

Unhealthy respiratory system:Emphysemais caused by the imbalance of protease and antiprotease. For somebody sufferingwith this condition, the surface area provided by the alveoli is significantlydecreased due to the alveolar wall and elastic fibres being obliterated by theprotease enzymes. The reduction of surface area means that the diffusion of gascannot happen as efficiently. Alveoli are extremely unique and well adapted,they are the only site of respiratory gas exchange within the respiratorysystem therefore, once they are destroyed they will not function and thiscannot be reversed (2). This means that somebody suffering with emphysema willstruggle with taking deep breaths in and exhaling long breaths out. When thelungs fill with air they do so within the rib cage which constricts the smallbronchi, thus increasing the demand on the lungs.

“This is especially evident during expiration, when contraction of themuscles of the chest wall and abdomen increase intrathoracic pressure andfurther 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 thattravels around in the circulatory system. A1AT is an antiprotease enzyme thatis present in both the lungs and the liver. Its function is to protect theseorgans by keeping an optimum enzyme balance. This avoids damage to normaltissues therefore, people with this deficiency are more susceptible toEmphysema and/ or Cirrhosis, a liver disease (2, 11, 12). This is usually thecause of emphysema found in non-smokers and young people.

Tests for thisinclude “A1AT blood test, chest x-ray, genetic testing, and lung function test”(12). Smoking:Smoking is a key cause ofemphysema because it contains oxidative toxins which destroys importantfeatures in the lungs causing malfunction of expiration which can lead totrapped air, and reduction of elastic fibres which results in the inability of lungrecoil during inhalation and exhalation of gases. (4) “Cigarette smokingincreases both the number of neutrophils in the alveoli and the release andactivity of elastase, but decreases the effect of Alpha-1 Antitrypsin, thusgreatly contributing to the breaking down of the alveolar structures” (2). Whenthe reactive oxidative toxins are inhaled via smoking, the lungs will producean inflammatory response which will amplify inflammation.

The macrophages willbegin to release chemicals such as elastase which destroys the elastic fibresand protease which damages the surrounding tissues “through alveolar septalcell apoptosis and destruction of the extracellular matrix (ECM)” (13). Therefore, emphysema causes anoverwhelming imbalance of protease (4).A variety of processes takeplace in the lungs for alveolar maintenance, but when the lung environment isfilled with cigarette smoke it is hard for these processes to protect thealveoli because the smoke is recognised as danger, via a sensor molecule calledRapamycin (mTOR).

This is because the smoke triggers an inflammatory andanti-oxidative stress response in the lungs which disrupts the maintenance ofthe alveoli. This form of Emphysema is referred to as ‘panacinar’ because itoccurs at the distal alveolar (2). These statistics from theMedscape risk factor list (14) suggest that what and how much is being smoked aday can affect the onset of emphysema.

“15-20% of 1 pack-per-day smokers and25% 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 thatsmoking damages the lungs however, it can also cause many other complicationsand conditions as well. One of which being Osteoporosis (17). Introduction to Osteoporosis:Osteoporosis is anasymptomatic condition that involves the loss of bone density and bone strength,often causing bone to gradually become more fragile and brittle which increasesthe risk of fracture. It can be described as a clinically silent conditionbecause one can be completely unaware of having osteoporosis until it presentsitself 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 berelated to the post-menopausal stage in a female’s life because low oestrogenlevels can lead to bone density being lowered up to 20%.

Secondly, senileosteoporosis which is linked to old age. Moreover, secondary osteoporosis (ortype 2) can occur due to other factors for example, diseases, hormones, medication(16). Osteoporosis seems to be more prevalent in women, specifically women aged50 and over, but in recent times it is now becoming more apparent in men. It isestimated 1 in 8 men also lose bone mass (2).

The NHS (17) says sometimes evena cough, or a sneeze can cause an osteoporotic-related fracture of a rib or avertebral body in the spine, this could cause kyphosis, which would furtherimpair lung function in a COPD patient. The condition isn’t painful until afracture occurs and if serious, can leave the sufferer with long-term chronicpain. Healthy bone structure:”The skeleton makes up 15% ofthe body’s weight. The bones are comprised of half water and half solid matterand 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 thereis a lot more cartilage present. This is to allow for growth. Thetransformation of cartilage to bone should be complete after adolescence. Boneand cartilage are both forms of connective tissue but consist of very differentstructures. Cartilage is stiff yet flexible with hardly any blood supply. It iscomprised of specialized cells, and examples of cartilage include: hyaline andfibrocartilage. Again, these cell structures would differ. On the other hand,bone has lots of blood vessels supplying it therefore, it is extremely capablerepairing itself.

Bone cells are positioned within a mineralized matrix,creating a durable tissue (9). “Bone is three times stronger than the samequantity of reinforced concrete” (18). Bone is comprised of compact bone whichis a strong, solid surface on the outer border, followed by spongy bone whichis 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 andbone mass naturally decrease in bone which could result in Osteoporosis. Reasonswhy people could be prone to developing Osteoporosis are as follows: genetics,White or Asian ethnicity, female, diet that is low in nutrition, vitamins, andminerals, certain medications, lack of weight baring, smoking, and consumingtoo much alcohol (19). Heany (20) says, an injury can stem from a combinationof factors, these include: the way a fall occurs (for example, falling to theside), bad posture and reduced soft tissue that can no longer protect the bonesfrom force.

Bone fragility itself develops from deteriorated quality of thebone material. “This is primarilythe result of accumulated fatigue damage, but reduced collagen cross-links andother intrinsic material defects may play a role as well”. Bones have cells calledosteoclasts and osteoblasts and they both have very opposite functions.

Osteoclastsdestroy bone and osteoblasts rebuild the bone tissue via essential minerals carriedin blood, e.g. calcium (19). “In adults, bone maintenance involves dailyremoval of small amounts of bone mineral, a process called resorption, whichmust be balanced by an equal deposition of new mineral if bone strength is tobe preserved.

If this process becomes unbalances, it’ll result in excessiveresorption, leading to bones weaken (osteopenia) and over time can become proneto fracture (osteoporosis). (21). There are many ways to maintain bone strengththroughout life, such as exercise. Also, having adequate levels of oestrogenand testosterone keep the level of osteoblasts higher than osteoclasts. Peakbone mass is reached in the 4th decade (19).

Introduction to GERD:Gastroesophageal RefluxDisease (GERD) is a disease that allows acidic stomach content to regurgitate,causing it to travel back up the oesophagus. This condition presents itselfthrough symptoms such as heartburn, nausea, chronic cough, and it can benoticeable by acid erosion on the teeth (22).The stomach is protected bymany mechanisms, one of which being the lower oesophageal sphincter (LES),which is a valve at the junction of the oesophagus and the stomach that providespressure by usually being taut.

This is to stop any bolus or acid flowing backup the oesophagus, but to continue the route of the digestive system. Duringnormal digestion, bolus will travel down the oesophagus which will reducepressure at the LES just enough to allow the bolus to pass through via the aidof smooth muscle mobility (peristaltic waves), then into the stomach. Smoothmuscle lines the hollow oesophagus which allows for peristalsis which is aninvoluntary movement. Smooth muscle is visceral and non-striated (5). Anotherstructure 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 anycontents beneath the oesophagus. Therefore, both the LES and the diaphragm workto protect the stomach by making it a one-way pathway which prevents acidiccontent 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 stomachis positioned with the oesophagus creates a steep angle, termed the Angle ofHis, which makes the gastroesophageal junction longer. With reference toPoiseuille’s Law, this increases the pressure or resistance on thegastroesophageal junction creating a tight seal (24).

Many people who haveadvanced COPD also develop GERD and GERD worsens COPD. The exact cause of GERDand the relationship between it and COPD is unknown however, lots ofmedications that are used to manage the symptoms of COPD weaken the LES. “Also, many COPD sufferers have airtrapped in their lungs, which pushes upwards on the abdomen, which causes acidreflux” (25). Mannino (26) says the acidic content that gets refluxed into the oesophaguscan irritate the lungs, and cause a COPD sufferer to cough frequently andexperience difficulty breathing which could potentially cause the acidiccontent to get into the lungs. Conclusion:With reference to the linkedcase study (Appendix), this patient is suffering from numerous complications, alsoknown as comorbidities, not just one problem. It is common for COPD patients (colloquiallyknown as ‘pink puffers’) to experience exacerbations and/or comorbidities dueto this primary disease. Hillas says “COPD is a leading cause of morbidity andmortality worldwide” (27). There are many potential coexisting diseases thatcould present themselves along side COPD, but this case study focuses specificallyon Osteoporosis and GERD.

Furthermore, Hillas suggests that “GERD is present in60% of COPD patients” (27). Numerous resources have made it clear that otherconditions and complications can develop alongside or as a result of COPD, butwhat can COPD lead to? The Mayo Clinic (28) states that COPD sufferers are moresusceptible to respiratory infections and even at high risk of developing lungcancer due to the destructive nature of the disease. Moreover, high bloodpressure in arteries can result in blood in the lungs which is known aspulmonary hypertension, and for unknown reasons COPD can heighten the risk of heartproblems. Finally, depression is a key complication that can occur in peoplewith COPD. This is because COPD can be physically debilitating and prevent thesufferer from doing everyday routines and/or enjoyable activities and hobbieswhich they used to be able to do and this is saddening to the patient. To conclude, Emphysema is apathophysiology that clinically presents itself as alveoli enlargement anddestruction, and the lungs lose elasticity. Associated dysfunction includesgreat difficulty to exhale as COPD patients will need to use a lot more energythan a healthy person to do so. This will cause breathlessness, fatigue andexhaustion.

This can overinflate the lungs which will lead to a barrel chest(5). The main contributing factors are smoking but some may develop emphysemathrough A1AT Deficiency. Referencing list:1.

   World Health Organisation. Chronic Respiratory Diseases: COPD: Definition. Available at: Accessedon 17th November 2017.

2.   Gould B, Dyer R. Respiratory Disorders, In: Pathophysiology for the Health Professions.4th ed.

Canada: Saunders Elsevier; 2011. P.330-354 Accessed on 15thNovember 2017. 3.   Cukic V, Lovre V, Dragisic D, Ustamujic A.Asthma and Chronic Obstructive Pulmonary Disease (COPD) Differences andSimilarities. Mater Sociomed.

2012;24(2): 100-105. Available at: on 29th November 2017. 4.

   Hasudungan A. Emphysema- Pathophysiology (COPD) video file 2014. Available at: https://www. on 3rd January 2018. 5.   Marieb E. The Respiratory System, In: Essentials of Human Anatomy &Physiology. 11th ed. England: Pearson Education Limited; 2015.P.

143-479 Accessed on 12th January 2018. 6.   National Heart, Lung and Blood Institute. How the lungs work. Available at: https://www.nhlbi.nih.

gov/health-topics/how-lungs-workAccessed on 28th December 2017. 7.   Health Direct. Respiratory System. Available at: https://www. on 28th December 2017.

8.   Kenhub. Alveoli.Available at: https://www. on 28th December 2017. 9.   Professor Roberts A. Anatomy, In: The Complete Human Body. The DefinitiveVisual Guide.

2nd ed. London: Dorling Kindersley Limited; 2016.P. 152-160 Accessed on 29th December 2017.

10. Hansen-FlaschenJ. Emphysema Medical Disorder.Available at: https://www.britannica.

com/science/emphysemaAccessed on 7th January 2018.11. WebMD.What is Emphysema, and what causes it?Available at: https://www. on 17th December 2017.12. MedlinePlus. Alpha-1 Antitrypsin Deficiency.

Available at: on 18th December 2017. 13.

GoldklangM, Stockley R. Pathophysiology of Emphysema and Implications. Journal of the COPD Foundation. 2016;3 (1): 454-458. Available at: Accessedon 2nd January 2018.

14. BokaK. Medscape Emphysema. Available at: on 28th November 2017. 15. InternationalOsteoporosis Foundation.

What isOsteoporosis? Available at: on 2nd January 2018. 16. HasundunganA.

Osteoporosis (Part 1) video file2011. Available at: on 5th January 2018. 17. NHS.

Osteoporosis. Available at: on 2nd January 2018. 18. BielA.

Navigating the Body, In: Trail Guideof the Body. 5th ed. Canada: Books of Discovery; 2014. P. 32Accessed on 28th December 2017.19. NucleusMedical Media.

Osteoporosis: NucleusHealth video file 2014. Available at: on 5th January 2018.20. HeanyRP.

Pathophysiology of Osteoporosis. NationalCentre of Biotechnological Information. 1998; 27 (2): 255-265 Accessed on3rd January 2018.21. InternationalOsteoporosis Foundation: Pathophysiology:Biological causes of Osteoporosis. Available at: Accessedon 5th January 2018.

22. MarksJ. GERD (Acid reflux, Heartburn).Available at: on 2nd January 2018.23.

DoctorSecrets. GERD Gastroesophageal RefluxDisease Explained video file 2013. Available at: on 7th January 2018.

24. WolfA. Pathophysiology of GastroesophagealReflux Disease (GERD) video file 2012. Available at: on 5th January 2018. 25.

LungInstitute. COPD and Acid Reflux.Available at: https://lunginstitute.

com/blog/copd-and-acid-reflux/Accessed on 7th January 2018. 26. RodriguezD. COPD and GERD: The connection betweenyour symptoms. Available at: https://www. on 7th January 2018. 27. HillasG. Managing comorbidities in COPD. NationalCentre of Biotechnological Information. 2015; (10): 95-109 Accessed on 11thJanuary 2018. 28.

MayoClinic. COPD. Available at: on 11th January 2018. 

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