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Pathophysiology

Pathophysiology Case Study

Pathophysiology of Presenting Features

Dyspnea

Dyspnea is also referred as shortness of breath. It is characterized by unpleasant breathing sensation. Dyspnea is also associated with a feeling of inadequate ventilation hence labored breathing (Chang, 2009). Mr. John presents with breathing difficulties especially during the exercise episodes. Moreover, the condition is said to have progressed, and now John experiences dyspnea even at rest. Various factors can explain the pathophysiology behind John's dyspnea. The main causes are increased stimulation of chemoreceptor centers particularly those located in the carotid and aorta arteries. Due to decreased oxygen partial pressure in the blood, and increased carbon dioxide, the chemoreceptors stimulate the brain to increase ventilation efforts. These involve increased activity of respiratory muscles. However, the respiratory muscles in John are weakened due to old age combined with the long duration of smoking. As a result, the patient ends up struggling to breathe to compensate the presenting hypoxemia (Chang, 2009). John is also unable to raise cardiac output that would increase the supply of oxygen in the body. As a result, various stimulatory impulses from the brain tend to increase breathing efforts by stimulating centers that can increase ventilation and reduce the hypoxia.

Dyspnea tends to occur during exercise due to the increased oxygen demand for metabolism during energy breakdown. During exercise, there is need to increase the amount of oxygen and reduce the accumulating carbon dioxide from catabolism of carbohydrates. Currently, dyspnea presents during rest indicating progressive weakening of the respiratory muscles. The progression of the diseases can be explained by reduced elasticity, increased collagen, malformation of cells due to old age and effects of heavy and prolonged period of cigarettes smoking. (Porth, 2007) The progression can also be explained by continued narrowing of airways, loss of alveoli and their associated blood capillaries. With time, there is also worsening of the cardiovascular system hence reducing cardiac output further. Mr. John stopped his regular walk due to the exacerbation of his symptoms especially due to age and lack of early management. Dyspnea and exacerbation of respiratory symptoms are characteristics of chronic illness such as COPD (Chronic obstructive pulmonary disorder), asthma, CHF (congestive heart failure), pneumonia and myocardial infarction (Porth, 2007).

Mr. John is said to have added about nine kilograms in weight. Additionally weight also tends to worsen respiratory and cardiovascular diseases due to increase deposition of fats in the blood vessels and breathing airways.

Fatigue

Fatigue is defined as exhaustion, especially from exercise, or decreased level of energy due to various pathophysiological mechanisms (Bleske, 2000). John’s loss of energy could be linked to the inadequate cardiac output. Low blood oxygen known as hypoxemia besides results in consistency productive cough. Hypoxemia due breathing difficulties leads to low oxygen partial pressure in the blood. Consequently, there is a low amount of oxygen in critical tissues such as brain, liver, and muscles. As a result respiration that depends on oxygen to produce energy is compromised. Another factor that complicate the hypoxemia is reduced the reduced blood circulation due to inability to pump adequate amount of blood from the heart. Accumulation of blood in neck vessels and extremities indicates right-sided heart failure (Bleske, 2000). Therefore, there is pooling of blood in capacitance veins. Moreover, John spends a lot of time and energy coughing which tends to be weary and exhaustive overtime. Fatigue is a characteristic of numerous diseases, including: asthma, COPD, congestive heart failure and many others.
Chronic Cough

Mr. John is said to have a productive cough for the last fifteen years. The cough is productive with gray, yellow or green sputum. The changes in the color of the sputum indicate progressing exacerbation of the symptoms. The pathophysiology of increased cough can be explained with active immune system chemicals that lead to inflammation and increased secretion (Lilly, 2011). The fact that John was as both an active and heavy smoker means that the chemical in the cigarettes caused permanent changes in the airways and lung parenchyma. These changes include increased fibrin tissue, collagen and modification of airway system. The impulses from the sensory nerves in the respiratory stimulate the coughing centers epithelium and cells of the airway. The inflammation occurs as a result of increased cytokines, neutrophils, macrophages, lymphocytes and associated factors such as histamine and bradykinin (Lilly, 2011).

The immune system leads to inflammation and increased mucus secretion that in turn irritate the larynx and in the brain. The result is activation of cough reflex leading to increased efforts to clear the airway. The worsening of the cough leading to yellow, green and grey cough may be indicative of bacterial infection. The bacteria infection may have occurred when Mr. John used to work as an electrician due to the associated damp environment. John is said to have noticed blood stains in his sputum. The probable pathophysiology behind the sign is ruptured capillaries in the bronchioles as a result of the progressive immune attack and wearing out of the epithelium leading to exposed blood vessels (Dhalla, 2004). Cough is a characteristic of respiratory disorders such as COPD, asthma, bronchiectasis, among others. Fever tends to occur due to stimulation of thermoregulatory centers in the brain by various pyrogens.

Vital Signs and Physical Examination

Temperature and Blood Pressure

John’s body temperature was found to be 37 oC. The value is relatively normal for normal human beings and does not necessarily indicate any fever at the time of measurement. However, his blood pressure that is 115/65 is indicative of underlying heart condition (Dhalla, 2004). Although single measurement is not reliable, the current value shows the presence of hypotension due to reduced cardiac output. The values show low systolic and diastolic pressure respectively. The condition is present in a condition such as congestive heart failure.

Respiratory Rate (RR)

John’s respiratory is 28 breaths per minute. The value is above the normal reference value that is about 16 breaths per minute and implies tachypnea (Hosenpud & Greenberg, 2000). Tachypnea occurs as a result of a feedback mechanism to balance ventilation-perfusion mismatch. The patient experiences dyspnea which means his blood carries less amount of oxygen to the tissues. These changes in blood oxygen and carbon dioxide levels stimulate the vagal nerve, carotid and aortic bodies (Hosenpud & Greenberg, 2000). The stimulation activates various brain centers for instance apnea center, pneumotaxic center, and medulla oblongata. The result is increased motor outflow increasing the rate of relaxation and contraction of respiratory muscles.

Pulse Rate

Mr. John presents with a pulse rate of 110 beats per minute. The value is far higher than the normal reference. Therefore, 110 beats/min shows tachycardia. Tachycardia is increased heart rate that occurs in attempt to increase cardiac output and supply the body with enough oxygen (Yontz, 1994). The condition is characteristic of congestive heart failure, myocardial infarction among others.

Bilateral Extension of Neck Veins and Pitting Edema

On physical examination, John was found to have distended jugular veins. The most probable explanation of the distension is a failure of the right heart. Right heart failure can occur due to the inability of right ventricle to blood to the lungs. This occurs as a result of pulmonary hypertension secondary to COPD (Yontz, 1994). The vasoconstriction of pulmonary vessels blocks the flow of blood to the lungs and from the lungs to the right auricle. The results are pooling of blood in veins such as jugular veins and vena cava. The blood accumulates in the tissues in the peripheral, for example, lower limbs resulting in pitting edema. The failure of blood to flow in veins is known as venous stasis and associated with congestive heart failure and secondary pulmonary hypertension. Veinous stasis also explains abdomen distension. Congestive heart failure is the main cause of hepatomegaly, altered heart beats and wheezing. Hepatomegaly occurs due raised central nervous pressure, accumulation of bilirubin, and elevation of liver enzymes (Lainščak, von Haehling, Springer, & Anker, 2007).

The symptoms are partly ascribed to inability to handle the metabolic process as consequences of decreased perfusion. Decreased perfusion in John is evident from the lowered cardiac output. CHF tends to cause irregular heartbeats and loud sounds to as measure to increase cardiac output. The bluish extremities show a condition that is characterized by low blood oxygen and high carbon dioxide hence inadequate oxygen in tissues. The condition is known as cyanosis and presents due to breathing difficulties that results in hypoventilation. Decreased cardiac output combined with hypoxemia causes hypoxia that manifests as bluish tissues (Lainščak et al., 2007). Dyspnea and shortness of breath are the major causes of hypoxia and are mostly common in COPD, asthma, bronchiectasis, heart failure and myocardial infarction.

 

Blood Test Results

A blood test is one of the vital tests that to every disease that affects people. The test is significant as it direct the doctor to know what could be probably wrong. They can also help to identify any concurrent illnesses. Moreover, depending on the results, the doctor what other tests are significant to be carried out.

Erythrocyte Count (RCC)

Mr. John RCC was found to be 6.8 * 1012. The maximum normal value for RCC is 84 * 109 (Musser, 2003). Therefore, the results clearly indicate that Mr. John has excess red blood cells, a condition known as erythrocytosis. However, evaluation of hematocrit value shows 58% implying increased erythrocyte mass. The maximum value of RBC mass is 52% in male (Blann, 2007). Therefore, chances are that erythrocytosis is secondary to the increased RBC mass (Musser, 2003). There is increased production of RBC so that to counteract the ensuing hypoxia as a result of lung and cardiovascular system failure. Erythrocytosis is most likely to occur in COPD patients due to compromised airway function. The condition can also be present in asthmatic patients as a result of reduced ventilation. Other conditions that can present with erythrocytosis are CHF, myocardial infarction, and pulmonary hypertension. All these are characterized by reduced cardiac output and reduced tissue perfusion.

Hemoglobin

Mr. John blood test shows that his hemoglobin amount is 200 g/L. The normal range for hemoglobin amount in males is 140-174 g/L (Risley, 2005). Therefore, John has an excess amount of hemoglobin. Since RBC carries hemoglobin, the increase can be attributed to the increase in RCC and RBC mass. The sole reason for the increased HB is to compensate the reduced blood and tissue oxygen. Raised amount of HB occurs together with erythrocytosis. As a result, the diseases mentioned in erythrocytosis above are likely to cause increased amount of HB as well (Booth, 2009).

Normal WCC is 4-10 * 109 /L. Mr. John WCC is 8 * 109 /L. Therefore, his WCC I normal and indicates minimal chances of infection or absence of foreign antigens.

Normal MCH is 27-33 pg while normal MCHC is 33-36 g/dL. Consequently, John’s values for MCH and MCHC are 29.4 pg and 340g/l respectively. These indicate that MCH is within the normal range while MCHC is too elevated. Mean cell Volume for John is 84 fL while the normal range is 77-95 fL (Booth, 2009). John’s value is within normal range as well. The increased MCHC is a body’s mechanism to control low blood oxygen by facilitating transportation of the available oxygen efficiently. MCV, MCH, and MCHC are good indicators of anemia to show the bodies efforts to control hypoxia. In John’s case, the reason for elevated MCHC is ascribed to conditions that interfere with cardiac output such MI, HF, and PH (pulmonary hypertension) (Blann, 2007). John’s reticulocyte is slightly elevated to compensate for the persistence hypoxia. Mr. John has C - reactive protein value of 5.5 mg/L. This shows that John is suffering from cardiovascular diseases or is at high risk of developing heart diseases.

Differential Diagnosis

Mr. John’s symptoms are show probability of various diseases. Some of the most likely diseases that John would be suffering from are discussed below.

Chronic Obstructive Pulmonary Disorder (COPD)

COPD is described as a chronic lung disorder that is characterized by progressive worsening of symptoms such as increased phlegm secretion, shortness of breath and narrowing of airways. The condition is irreversible and is mainly characterized by bronchitis and emphysema. John presents with various symptoms and risk factors that suggest he might be suffering from COPD. These symptoms include persistence and worsening cough with productive cough. The hallmark of COPD is progressive worsening of respiratory symptoms (Lopez-Sendon, MuÞoz, Palomo, & Garcia Robles, 2006). The other symptoms are shortness of breath, colored sputum and wheezing. Risk factors include cigarette smoking, old age and environment factors (Lopez-Sendon et al., 2006). John is described to have been smoking an average of 35 cigarettes per day. He is also aged 60 years and used to work in the damp environment.

Congestive Heart Failure (CHF)

CHF is also known as heart failure and present as the inability of the heart to pump blood effectively (Francis GS, 2001). CHF is characterized by symptoms such as tachycardia, hepatomegaly, irregular heart murmurs, distention of neck veins, and dyspnea (Lainščak et al., 2007). Mr. John suffers from all these symptoms hence CHF is a differential diagnosis. Risk factors for old age are smoking, being male and old age.

Asthma

Asthma is respiratory disorder presenting with reversible inflammation and narrowing of the airways. Asthma also present with similar clinical manifestations. These symptoms include dyspnea, shortness of breath on exertion, productive cough, wheezing, rales, tachycardia, and tachypnea.

Bronchiectasis

John suffers some symptoms that indicate the probability of bronchiectasis. These include cough accompanied by a lot of sputum, fatigue, wheezing, shortness of breath on exertion, and sometimes patient produces blood-stained phlegm (Phelan, 2012).

 

Pneumonia

Pneumonia is defined as lung infection that may cause inflammation in one or both lungs. The affected lung is then filled with fluid. John presents with several symptoms that suggest the probability of pneumonia. These include chronic pain with or without a productive cough. Difficulties in breathing, shortness of breath and fast respiratory rate are characteristics of pneumonia (Edmundson & Harris, 2001). The patient may also experience fever, malaise, and tachycardia.

Acute Myocardial Infarction

Myocardial infarction is also commonly known as heart attack. It is described as the blockage of heart vessels hence preventing blood flow to some areas of the heart (Lainščak et al., 2007). John suffers a few symptoms that may suggest a heart attack. However, the likelihood of the disease is minimal. Some of John’s symptoms that may indicate MI are fatigue, tachycardia, and dyspnea.

Further Diagnostic Tests

John needs to undergo other diagnostic tests to rule out some of the differential diagnosis. Additional tests will assist in identifying John’s disease.

To rule out CHF, the doctor needs to perform transthoracic echocardiogram test (TET). The test works best if done together with B-type natriuretic peptide blood test (Feinstein, 2003). In case of systolic failure, the echocardiogram will indicate either depressed left or right ventricle. Sometimes, the test can show that both left and right ventricle are depressed. Systolic heart failure is also shown to be accompanied by a low ejection fraction. However, in diastolic heart failure, echocardiogram shows normal ejection fraction along with altered diastolic filling sequence. TET can also be used to check other diseases such as MI (Feinstein, 2003). In MI, the test will show blocked coronary arteries and areas of the heart that have no blood supply. Therefore, this test can confirm or eliminate CHF and MI as a differential diagnosis.

Other diseases such as COPD, asthma, and bronchiectasis can be assessed by detailed by comprehensive patient history. However other tests for instance spirometry, x-ray, and CT scan (Risley, 2005). Spirometry tests the extent of lung functionality while X-ray and CT scan are imaging tools that detect damaged alveolus in COPD. Asthma can also be tested by use spirometry where the test shows compromised lung functionality. Another test for asthma is exhaled nitric oxide test. High levels NO levels in breath indicates inflamed lungs which is a characteristic of asthma. Nonetheless, imaging tests and comprehensive patient medical history are sufficient to rule out either asthma or COPD in John. X-ray can also be used to rule out the possibility of pneumonia in John.

Depending on the presented symptoms and risk factors the most probable disease affecting John is Heart failure secondary to COPD. However comprehensive and confirmatory tests are necessary.

 

 

References

Blann, A. D. (2007). Routine blood results explained. Keswick, Cumbria: M & K Pub.

Bleske, B. E. (2000). Evolution and Pathophysiology of Chronic Systolic Heart Failure. PHAR Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 20(11P2), 349S–358S.

Booth, P., (2009). Haemoglobin concentrations, packed cell volume and reticulocyte count of cord blood in Papuans. Papua and New Guinea Medical Journal, 10(1), 13–14.

Chang, A. B. (2009). Common respiratory symptoms and illnesses: a graded evidence-based approach. Philadelphia, Pa.: Saunders.

Dhalla, N. S. (Ed.). (2004). Pathophysiology of heart failure. Boston: Kluwer Academic Publishers.

Edmundson, W. C., & Harris, S. A. (2001). Management of pneumonia in India and Indonesia. Social Science & Medicine : A Multi-Disciplinary Journal Covering: Medical Sociology, Medical Geography, Medical Anthropology, Medical Psychology, Health Economics, Medical & Social Ethics, Health Policy Social Science and Medicine, 29(8), 975–982.

Feinstein, A. R. (2003). Physical Examination in Health and Disease. JAMA JAMA, 190(6).

Francis GS. (2001). Pathophysiology of chronic heart failure. The American Journal of Medicine, 110.

Hosenpud, J. D., & Greenberg, B. H. (2000). Congestive heart failure: pathophysiology, diagnosis, and comprehensive approach to management. Philadelphia: Lippincott Williams & Wilkins.

Lainščak, M., von Haehling, S., Springer, J., & Anker, S. D. (2007). Biomarkers for chronic heart failure. Heart Failure Monitor, (5), 77–82.

Lilly, L. S. (2011). Pathophysiology of heart disease: a collaborative project of medical students and faculty. Baltimore, MD: Wolters Kluwer/Lippincott Williams & Wilkins.

Lopez-Sendon, J., MuÞoz, R., Palomo, J., & Garcia Robles, J. A. (2006). Pathophysiology of chronic congestive heart failure. REVISTA LATINA DE CARDIOLOGIA EUROAMERICANA, 16(6), 208–210.

Musser. (2003). Reticulocyte count. The Journal of the Indiana State Medical Association, 55(6), 57–8.

Phelan, P. . (2012). Asthma. Baillière’s Clinical Paediatrics, 1995, 247–448.

Porth, C. (2007). Essentials of pathophysiology: concepts of altered health states. Philadelphia: Lippincott Williams & Wilkins.

Risley, W. B. (2005). Quick information on test results: blood chemistry, urinalysis, hematology. Phoenix, Ariz.: Labdata Service.

Yontz, L. L. (1994). Congestive Heart Failure: Early Recognition of Congestive Heart Failure in the Primary Care Setting. JAAN Journal of the American Academy of Nurse Practitioners, 6(6), 273–279.            

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