Pathophysiology Paper

Patient Data Mr. F. is a seventy-three year old Caucasian male who is twice divorced and lives alone in Sweetwater, Texas. He has two children living, and two deceased children. Both of his parents are deceased; his father died at the age of sixty-nine of prostate cancer, his mother at the age of seventy-two of a stroke. He is self-employed, owning a local dirt contracting company for about thirty years now. Mr. F. tands five-foot and nine inches tall and weighs two hundred sixty pounds, exhibiting moderate obesity and has been for the past twenty-five years. He has a longstanding history of hypertension; approximately twenty years as well as a history of diabetes mellitus type two for twelve years, never having been insulin dependant. He has a smoking history of about fifty years smoking two packs per day and has been diagnosed a few years ago with chronic obstructive pulmonary disease, making him oxygen-dependant for two years. He claims to only drink alcohol on a social basis.

Prior to his current admission, he stated that he has not been compliant with his diabetic diet, that he does not check his blood glucose regularly nor has he been following his medication regimen as he should. His last doctors appointment was two years ago. On July 6, 2008, Emergency Medical Services was called to Mr. F. ’s residence by a friend who found him in bed, conscious, but speaking incoherently. He had a nasal canula in place at three liters per minute. His glucometer done by emergency personnel showed a blood sugar of thirty-six.

He was then given a bolus of dextrose fifty percent; he then returned to consciousness, but complained of some right arm and leg weakness. He had 3+ pitting edema bilaterally to lower extremities as well as 1+ presacral edema. He was then transported to Rolling Plains Memorial Hospital emergency room. Upon arrival to the hospital, his vital signs were as follows; blood pressure- 200/103, heart rate- 80, respirations- 18, and oxygen saturation at 95% on oxygen via nasal canula at 3 liters per minute. His right sided weakness seemed to resolve per patient.

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He denied headache, vertigo and tinnitus. Diagnostics done at the emergency room showed a white blood cell count of 7. 8, hemoglobin of 12. 4, hematocrit of 37. 2, MCV of 95, and the platelet count along with coagulation studies showed to be normal. His renal function was abnormal at a BUN of 68 and a creatinine of 6. 1. His potassium level was 5. 4 and CO2 was 22. 3. His sodium level was 133, phosphorus levels were elevated at 6. 1, globulins were elevated at 4. 3, troponin level was slightly elevated at 0. 14 and CPK was normal. His BNP NT-Type was extremely elevated at 9674. along with his hemoglobin A1C was at 5. 8. Thyroid studies were Integrated Pathophysiology 3 found to be normal. The total cholesterol was 127, with HDL only at 24, LDL at 79 and triglycerides at 136. A further diagnostic study revealed by way of chest x-ray has shown cardiomegaly with mild venous congestion. The EKG shows poor R wave progression and nonspecific ST wave changes from previous. The echocardiogram showed 2+ mitral valve regurgitation with mild aortic stenosis and also an ejection fraction of over 50%. A renal sonogram shows diffuse cystic changes.

A CT scan of his head revealed mild white matter changes but no other abnormalities. The 24 hour urine shows a urinary creatinine of 1449 and a urinary protein of 190. 3. The patient denied problems with urination such as frequency, urgency, dysuria, recurrent urinary tract infections or renal stones. Home medications included; Potassium chloride 10 mEq t. i. d. daily, Metformin 500 mg daily, Nifedipine 90 mg daily, Ramipril 10 mg b. i. d. for a total of 20 mg daily, Albuterol inhaler, Furosemide 80 mg in the am and 40 mg in the pm. Mr. F. was admitted into the intensive care unit from the emergency room.

Diseases/Pathophysiology

Mr. F. ’s current disease processes are long-standing hypertension, obesity, COPD, Diabetes mellitus, chronic renal failure, and congestive heart failure. Hypertension is defined as a blood pressure greater than 140/90 mm Hg (Ignatavicius & Workman, 2006). It is caused by increases in cardiac output, total peripheral resistance, or both. The cardiac output is the volume of blood that is ejected by the heart each minute. Peripheral resistance is a resistance to the flow of blood out side of the heart. It can be considered either primary or secondary.

Primary hypertension has no known causative factors other than relation to genetic predisposition, obesity, stress, increased alcohol intake, diabetes, and or sodium and water retention in which all increase the total workload of the heart and increase fluid volume with in the vascular space (Zerwekh, Claborn & Gaglione, 2006). Secondary hypertension is elevated blood pressure with an identifiable cause that may include but not limited to; renal stenosis, congenital heart defects, Cushing’s syndrome, pheochromocytoma, untreated sleep apnea, MAOIs, chemical stimulants such as cocaine, methamphetamines etc. or pregnancy induced (Zerwekh, Claborn & Gaglione, 2006).

Obesity is a disease within many diseases with many varying causes. According to Ignatavicius and Workman (2006), an obese person weighs at least 20% above the upper limit of the normal range for ideal body weight and refers to an excessive amount of body fat in which can be distributed differently and cause an array of problems according to the distribution, Integrated Pathophysiology 4 especially android obesity with excess fat at the waist and abdomen; this pattern carries the greatest health risk.

Chronic Obstructive Pulmonary Disease is a progressive and irreversible condition characterized by diminished inspiratory and expiratory capacity of the lungs (Mosby’s, 2002). Emphysema along with chronic bronchitis is complications that lead to COPD. The etiology is more often than not, a long history of smoking cigarettes or other forms of smoking tobacco. The lungs lose elasticity and tend to cause hyperinflation due to the alveoli in the lung losing its elastin, in which then narrows and produces a surface area that decreases and is no longer functioning properly for adequate gas exchange.

The accumulated air that is unable to be absorbed properly becomes trapped and causes the collapse of the smaller airways called bronchioles. With the lungs hyperinflated, this flattens the diaphragm, thus causing the individual to utilize accessory muscles to breath, increasing the respiratory rate to compensate. Patients with COPD have bouts with chronic bronchitis which is an inflammation of the bronchi and bronchioles triggered usually by tobacco smoke.

The irritants from the smoke cause inflammation, with vasodilation, mucosal edema, and bronchospasms; the increased inflammation increases the size of the mucosal glands and produce large amounts of thick mucus, causing the bronchial walls to thicken and impair airflow (Ignatavicius & Workman, 2006). Diabetes Mellitus comes in many forms; the main characteristic is elevated blood glucose due to complications in the insulin secretion or action or both (Ignatavicius & Workman, 2006).

When diagnosed with diabetes other than type one, the beta cells in the islets of Langerhans that produce insulin and the alpha cells that produce glucagon, which counteract one another, either decrease in production of these hormones or can possibly produce at a normal balance. If there is normal production of these hormones, mainly insulin (the hormone that transports glucose into the cells), it is usually cellular resistance to insulin that is causing the diabetes.

When the cells are not receiving the necessary glucose needed for cellular function and metabolism, the body is unable to utilize the glucose, store carbohydrates, fats and proteins; therefore the unused glucose remains in the blood causing hyperglycemia and regulatory mechanisms in the body tend to cause the release of more glucagon which cause the release of stored glucose in the liver into the bloodstream as well, therefore increasing the blood glucose level even more.

Homeostasis is Integrated Pathophysiology 5 nterrupted, systemically causing damage. The etiology of type two diabetes can be a combination of many factors; however the well known contributor is obesity. Chronic renal failure is a progressive, irreversible kidney injury, and kidney function does not recover (Ignatavicius & Workman, 2006). The kidneys are in charge of filtering the metabolic wastes in the bloodstream that comes from cellular metabolism throughout the body as well as reabsorption of necessary electrolytes.

When long-term damage is sustained in the cells of the kidneys (nephrons) by factors such as longstanding hypertension, function is progressively altered exhibited by the inability to excrete the nitrogenous wastes; therefore they accumulate in the kidneys and blood stream. Altered glomerular filtration rate, abnormal urine production, poor water excretion, electrolyte imbalances, and metabolic abnormalities occur as a result of renal failure. The body’s ability to dilute urine is decreased; therefore urine output decreases causing fluid overload.

The failure occurs in stages with the last being end-stage renal disease in which all renal function eventually ceases. Congestive heart failure also known as left-sided heart failure may result from hypertensive coronary artery and valvular diseases arising particularly from the mitral and aortic valves. When CHF occurs from any etiology such as systemic hypertension and structural changes, the ventricles of the heart are unable to contract and or relax properly causing blood to congest around the heart.

As a result of this congestion in and around the heart, tissue perfusion diminishes and blood accumulates in the pulmonary vessels. Cardiac output eventually decreases and compensatory mechanisms such as sympathetic nervous system stimulation, the renin-angiotensin system activation in the kidneys (RAS), other neurohumoral responses and myocardial hypertrophy will occur (Ignatavicius & Workman, 2006).

The hypoxic state of the tissues stimulate the nervous system which increases the heart rate and blood pressure due to vasoconstriction and this stimulation increases venous blood return to the heart, which in turn stretches the myocardial fibers causing dilation and eventually thickening of the walls of the heart and chambers within it, consequently causing enlargement (cardiomegaly). The heart then tries to contract harder and eventually exhausts and reduces the force of the contractions; therefore decreasing cardiac output.

The vasoconstriction of the arteries increases the afterload which is the resistance that the heart must pump. This low output causes a decrease in blood flow to the kidney’s which results in the activation of the RAS in turn causes sodium and water retention. Cardiac preload and afterload increase causing contractile dysfunction. Integrated Pathophysiology 6 Integration Mr. F. reported that he has been obese for approximately twenty-five years. A few years after the significant weight gain, he was diagnosed with hypertension.

At his own admission, his lifestyle of high fat, cholesterol, salt and sugar intake as well as a long history of smoking cigarettes left little to be desired and have contributed significantly to his current condition. Several years after having been diagnosed with hypertension, he was told he had diabetes and COPD. Upon his recent hypoglycemic episode, he was diagnosed then as having chronic renal failure with congestive heart failure. All of these diagnoses tie well in together, starting with obesity. When a person is obese, the excess weight, especially around the waist and abdomen as seen in Mr.

F. causes the workload on the heart to increase due to the excess adipose tissue surrounding the visceral organs and weight in general. Being obese puts one at high risk factors for developing hypertension and heart disease as Mr. F. has. Obesity also places one at high risk for developing diabetes type two due to the fact that adipose tissue and cells that accumulate have a high tendency to become insulin resistant as well as the surrounding cells and tissue; therefore the body can not utilize the glucose and hyperglycemia occurs.

A prolonged period of insulin resistance eventually leads to the beta cell failure causing decreased insulin production. The same high fat, cholesterol, and sodium diet that contributed to the patient’s obesity in the first place, causing his heart to have to work harder, more than likely caused him to develop hypertension. The fact of his non-compliance with his medication regimen for hypertension and diabetes, 100 pack per year smoking habit as well as noncompliance with prescribed diabetic diet, lead to his further complications of renal failure and lastly CHF.

With prolonged hypertension and particularly uncontrolled diabetes mellitus, diabetic nephropathy changes the kidneys in a way that reduces kidney function and eventually, renal failure. Chronic high blood glucose levels cause hypertension in kidney blood vessels and excess kidney perfusion (Ignavicius &Workman, 2006). This increase in pressure within the kidneys cause the blood vessels to leak out that allows large particles such as albumins and proteins to form deposits in the kidneys and their blood supply.

This narrows the vessels and decreases oxygenation to surrounding kidney tissue; therefore causing hypoxia and eventually irreversible cell death. As this progresses, scarred tissue forms and the ability to filter urine from the blood ceases causing renal failure. Once in renal failure, the patient’s kidneys were not able to regulate the fluid volume by adequate excretion, therefore the excess fluid was pooled back into the vascular Integrated Pathophysiology 7 space. This fluid volume overload caused an increased cardiac workload which eventually leads to congestive heart failure.

Mr. F. ’s smoking history was the primary cause of his COPD; however it is exacerbated by the collection of fluid in his vascular space due to renal failure, the loss of elasticity of vascular system and congestive heart failure. The medication prescribed for Mr. F. ’s diabetes was Metformin 500 mg daily. This medication primary action was to decrease hepatic glucose production. The excess insulin in the blood triggers production of glucagon in which signals the liver to release stored glucose, in turn hyperglycemia results. This medication was changed due to Mr. F. s elevated BUN and creatinine which is where this medication is metabolized and excreted as well as his state of CHF. Continuing this medication could cause toxicity. The new medication he was placed on was a low dose of Actos which is metabolized in the liver and does not cause hypoglycemia as Metformin may. To treat his hypertension, Nifedipine was prescribed and it acts to lower blood pressure by inhibiting calcium transport into myocardial cells and smooth muscle cells within the vascular space resulting in vasodilation counteracting the vasoconstriction caused by hypertension.

In addition to Nifedipine, the patient is prescribed an ACE inhibitor named Ramipril. This ACE inhibitor works on the renin-angiotensinogen system ultimately causing systemic vasodilation. This medication not only decreases the blood pressure, it decreases cardiac afterload in patients with CHF. Ramipril is metabolized in the liver, therefore indicated for patients at risk or in renal failure. Furosemide is a loop diuretic that is especially helpful in patients with edema due to hypertension, renal disease as well as CHF.

Furosemide increases the renal excretion of water as well as sodium and other electrolytes, thus reduces the fluid volume in the vascular space. It also has a vasodilating effects that are beneficial in this patients regimen; however a potassium supplement must be given due to the potassium wasting caused by this loop diuretic. This patient’s dose of Furosemide was significantly increased due to the necessity of ridding his body of the accumulating fluid and stabilizing his blood pressure which in turn will prevent further damage to his kidney’s. Potassium is necessary for proper contractility of the heart.

Mr. F. is on Potassium chloride 10 mEq t. i. d. to make up for the loss due to the loop diuretic effects. The Albuterol inhaler is used to dilate the bronchi thus increasing surface area of the air ways to enable oxygen and CO2 exchange. This inhaler can exacerbate hypertension, palpitations and have a negative cardiac effect as well as cause hyperglycemia; therefore must be used cautiously. Integrated Pathophysiology 8 Prediction of Outcomes Although Mr. F. ’s acute condition was stabilized, his prognosis appears poor at this point due to his history of noncompliance.

Even though he has decreased his cigarette habit to one pack per day, his condition will probably deteriorate unless he could totally abstain from smoking. While speaking with the patient, he assures that this has got his attention and he will remain compliant from here on out. The damage at this point is irreversible; therefore maintaining remaining function as it is now becomes a new priority, meaning that compliance is necessary at this point for this patient as continuing to be noncompliant will definitely lead to his demise.

Aggressive diabetic counseling as well as reinforcement of adhering to his current medication regimen is crucial for this patient’s survival. Other disciplines that should be involved to ensure a better prognosis for Mr. F. are ones such as a dietician to help with meal and snack planning per diabetic protocol, continuing respiratory therapy to aid in oxygenation and supplies, physical therapy to build the patients strength and prevent venous stasis hence blood clots, and maybe even occupational therapy to assist him with maintaining independent activities of daily living.

Routine follow up appointments with his physician as well as specialist for cardiac and pulmonary function are essential to his outcome. A diabetic support group would be ideal for this patient as he appears to be a person in need of a support team. Lifestyles are hard to modify, but when one gets backed into a corner, it can be done, even in the most noncompliant patients otherwise death is imminent. Integrated Pathophysiology 9

References

1. Deglin, J. H. & Vallerand, A. H. (2007). Davis’s Drug Guide, Tenth Edition. Philadelphia: F. A. Davis Company.
2. Ignatavicius, D. D. & Workman, M. L. (2006). Medical Surgical Nursing, Critical Thinking for Collaborative Care. St. Louis: Elsevier Saunders. Mosby’s Medical, Nursing, & Allied Health Dictionary (6th ed. ). St. Louis: Mosby, Inc.
3. Zerwekh, J. , Claborn, J. C. & Gaglione, T. (2006). Mosby’s Pathophysiology Memory Notecards, Visual, Mnemonic, and Memory Aids for Nurses. St. Louis: Mosby, Inc.

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