Pathophysiology of Hypoglycemia, Pneumonia and Congestive Heart Failure - Term Paper Example

Pathophysiology of Hypoglycemia, Pneumonia and Congestive Heart Failure Hypoglycemia  Hypoglycemia, also known as low blood sugaror insulin shock, refers to a clinical situation marked by a decrease in the concentration of plasma glucose to a level that may induce such symptoms as the stimulation of sympathetic nervous system and/or mental status alteration. Generally, hypoglycemia results from anomalies in the methods used in glucose homeostasis (Hamdy, 2012). Pathophysiology Hypoglycemia is very common in patients suffering from type 1 diabetes as well as those suffering from advanced type 2 diabetes. Drugs used in the treatment of these types of diabetes are known to cause hypoglycemia (The McGraw-Hill Companies, 2012). The McGraw-Hill Companies (2012) further explains that individuals trying to attain better glycemic control experience a number of incidents of mild to moderate hypoglycemia. Although there are debates regarding plasma glucose level that indicates hypoglycemia, in a physiological context, it is best described as plasma glucose of less than 70 mg/dl (less than 60 mg/dl whole blood). This is owing to the fact that the glycemic threshold required for the initiation of the anti-insulin neuro-endocrine counter-regulatory response takes place when the plasma glucose is 70 mg/dl. In addition, counter-regulatory reactions to successive hypoglycemia have been known to be reduced by antecedent hypoglycemia of 70 mg/dl (Briscoe & Davis, 2006).  Hypoglycemia brings a marked impact on metabolism because brain tissue relies on glucose as its most important fuel. Brain function alterations are accountable for the characteristic symptoms of hypoglycemia. Signs and symptoms may appear with a fall in glucose levels. A further fall in the levels of glucose may lead to the impairment of cerebration, resulting in aberrant behavior, confusion, abnormal decision-making processes, and overt hostility, among others, as discussed later (The McGraw-Hill Companies, 2012). If there is a gradual fall in blood glucose, as happens with diabetic patients receiving long-acting insulin, there may be absence of prodromal syndrome and the patient is thereby not aware of any problem and may instead directly progress into confusion followed by unconsciousness (ODonnell & Ahuja, 2005). The symptoms of hypoglycemia can be classified into neurogenic (autonomic) and neuroglycopenic symptoms. Neurogenic/autonomic symptoms are the outcome of the physiologic changes’ perception brought about by the hypoglycemia-triggered sympathoadrenal discharge (Briscoe & Davis, 2006). They consist of such adrenergic and cholinergic symptoms, whose manifestations can include fatigue, difficulty with paying attention, behavioral changes, hallucinations, irritability, seizure (uncommon), focal impairments (for example hemiplegia), confusion, loss of consciousness (uncommon), and, eventually, coma and death in the event of severe hypoglycemia (The McGraw-Hill Companies, 2012). Sympatho-adrenal nervous system’s stimulation brings about hunger, paresthesias, anxiety, pallor (face becomes pale), irritability, tingling lips, accelerated heart rate, sweating, tremulousness and palpitations (Kronenberg, 2008 and Nordqvist, 2009). These symptoms have to do with sympathetic activation as well as dysfunction of the brain secondary to reduced glucose levels. Neuroglycopenia has to do with a decrease in the availability of cerebral glucose – neuroglycopenic symptoms directly result from the deficiency of the Central Nervous System’s neuronal glucose. Often, the adrenergic symptoms come earlier than the neuroglycopenic symptoms, thereby, presenting the patient with an early cautionary system (Cohen, 2007). Research indicates that the main stimulus for catecholamines release is the absolute plasma glucose level; glucose reduction rate is not as important. Earlier levels of blood sugar can affect the response of a person to a specific blood sugar level (Hamdy, 2012). Nevertheless, it is significant to take note of the fact that in a patient who experiences recurring hypoglycemia, there can be almost no warning signs. This is known as hypoglycemic unawareness. With recurrent hypoglycemia incidents, the threshold at which an individual experiences the symptoms of hypoglycemia reduces (Briscoe & Davis, 2006). Congestive heart failure Congestive heart failure (CHF) refers to an intricate clinical syndrome that can be brought about by any structural or functional cardiac illness that damages the ability of the right and/or left ventricles to eject or fill with blood (Nursingcrib.com, 2009). In the US, this syndrome is very frequent particularly in aged patients. Owing to the fact that heart failure has no definitive diagnostic test, the condition is still a clinical diagnosis founded mainly on a cautious history as well as physical examination and backed by such ancillary tests as electrocardiogram, echocardiography and chest radiograph (Figueroa & Peters, 2006). Pathophysiology During the last several years, researchers gathered additional information regarding the congestive heart failures pathophysiology. The primary cardiac abnormality has to do with a reduction in myocardiums intrinsic contractility, which usually arises due to prolonged volume or pressure overload. A number of associated biochemical transformations have been explained, but scholars have not been able to determine clear cause-and-effect connection. Various neurohumoral transformations that raise systemic vascular resistance take place and this augmented resistance leads to a further reduction in cardiac output. In fact, a number of such initially beneficial compensatory mechanisms may overshoot producing deleterious hemodynamic aftermaths (Parmley, 2004). For instance, with cardiac output reduction, there is a reflex systemic vascular resistance augment to facilitate the maintenance of perfusion pressure. Nevertheless, this resistance increase operates as a left ventricle load and decreases cardiac output further. The best proof for the prevalent of this cruel cycle is the positive hemodynamics change produced by vasodilators, inotropic drugs, ACE inhibitors and diuretics. These drugs are often invaluable in correcting overshooting compensatory mechanisms. Therefore, the comprehension of the pathophysiology of this condition allows rational therapy selection (Nursingcrib.com, 2009). Dumitru (2012) explains that the general pathophysiologic state responsible for the heart failure progression is very intricate, irrespective of the precipitating episode. Every organization level (from sub-cellular through organ-to-organ interactions) has compensatory mechanisms, and heart failure arises only when this adaptations network becomes devastated. It is important to note that congestive heart failure results from an anomaly in cardiac function, structure, conduction, or rhythm. The majorities of cases in developed countries arise from ventricular dysfunction and mostly result from hypertension (systolic and diastolic dysfunction), myocardial infarction (systolic dysfunction) or both in many cases (Figueroa & Peters, 2006). Parmley (2004) explains that the most frequent heart failure syndrome is systolic dysfunction with a decreased ejection fraction. He however explains that up to forty percent of patients may experience a comparatively conserved ejection fraction along with diastolic dysfunction. Several compensatory systems, which include the Frank-Starling mechanism, increased catecholamines, increased heart beat, atrial natriuretic peptides’ release and the renin-angiotensin system’s activation are stimulated as the heart begins failing. Figueroa and Peters (2006) pint out that other chief causes of heart failure include idiopathic cardiomyopathy, alcoholic cardiomyopathy and degenerative valve disease. Heart failure is most common occurs among elderly patients with such multiple comorbid conditions as chronic lung disease, diabetes, hypertension, and angina. While such common comorbidities as renal dysfunction are multifactorial (volume diminution from overdiuresis or reduced perfusion), others such as cachexia, anemia, breathing disorders, and depression) are understood poorly. Congestive heart failure indicates not only the heart’s lack of ability to sustain adequate delivery of oxygen; but it is also a systemic response trying to pay off for the insufficiency. Stroke volume and heart rate are the cardiac output determinants. Contractility, preload (volume that gets into the left ventricle), and afterload (the impedance of the gush from the left ventricle) further determine the stroke volume. In understanding heart failure’s pathophysiologic consequences as well as the possible treatments, these variables are imperative (Figueroa & Peters, 2006). Toth and Cannon (2010) explain that as heart failure syndrome take place, a patient experiences such symptoms as dyspnea, fatigue, chest pain, increased weight, paroxysmal nocturnal dyspnea, and orthopnea. A reduction in the function of the left ventricle raises the danger of sudden cardiac death, pump failure and arrhythmias. Pneumonia Pneumonia is a disease that affects a person’s lungs, characterized by fluid filling the lungs of a person. It is mostly is caused by viral, bacterial or fungal infections in a person’s lungs. Other minor causes of pneumonia are injuries to the lungs and bites from fleas. It is a common disease that affects people of all ages and sex with about one percent of the world’s population having been affected every year (Madara, 2008). Pneumonia is divided in to two main categories: the community acquired pneumonia and the hospital acquired pneumonia. The community-acquired pneumonia is further divided in to the mycoplasma and pneumococcal pneumonia (Dugdale, 2012). For people with low immunity, community pneumonia is witnessed after an influenza bout. Hospital acquired pneumonia infections are more pronounced and serious, as the human body has no mechanism to cope with the disease. The infectious agents of pneumonia enter the body through the respiratory system of the human being and proceeds to lungs. However, some causative agents of pneumonia like the gram negative bacilli and the staphylococcus gains entry through the circulation of the blood (Criner, 2012). Pathphysiology The condition has serious pathphysiology for children, the elderly and for people with weak immunity. It causes a person to be experience chest pains, rapid breathing, fever and body chills. At times, it causes the affected person to cough and producing green or yellow mucus (Dugdale, 2012). The rapid breathing is caused by low oxygen levels in the affected persons. The low oxygen levels is a result the human body trying to respond to the foreign matters by producing immune system in the body, this requires a lot of oxygen. The alveoli is filled with fluid as a result of the production of mucus, this also causes the rapid breathing as its in the alveoli that gases exchange takes place in the human lungs (Hui, 2011). As the effects of pneumonia continue, the affected individual’s count of white blood cells rises. As they continue to rise, the fragments they leave contribute to the filling of the alveoli, which is associated with the life threatening effects of pneumonia if it is not treated in time. Damageng toxins are released as the infection by the foreign organisms continues (Marrie, 2001). Viral pneumonia in excess causes the damaging of ciliated epithelial cells. When the virus reaches the lungs, it begins to invade the cells linings and the alveoli which causes death of the cells either directly or indirectly through apoptosis, which is a self-destruction process controlled by the cells. The response to the invasion causes more damage to the lungs as the fluid produced leaks in to the alveoli. This makes the lungs more prone to other bacterial infections (Hui, 2011). In children, pneumonia’s pathophysiology is seen in four distinct stages – the congestion stage (common during the first 24 hours following birth) where the lung experiences alveolar edema and vascular congestion. Medical examination at this stage shows few neutrophils and many bacteria. There is also the red hepatization stage where the fibrin and the red blood cells enter the alveoli. This leads to difficulty in breathing (Faix, 2011). Next is the grey hepatization stage where the dying white and red blood cells accumulate in the alveolar spaces. At this stage, the available area for gases exchange in the lungs is reduced and the last stage which is the resolution stage. It is in the resolution stage of pneumonia in children that inflammation is apparent. The white blood cells continue to fight off foreign organisms that may result to the child coughing up the remains as the yellow or green mucus (Porth, 2011). References Briscoe, V. J. and Davis, S. N. (2006). Hypoglycemia in Type 1 and Type 2 Diabetes: Physiology, pathophysiology, and Management. Retrieved from http://clinical.diabetesjournals.org/content/24/3/115.full Cohen, J. (2007). Hypoglycemia - Causes, Symptoms and Treatment Methods. Retrieved from http://www.articlesbase.com/diseases-and-conditions-articles/hypoglycemia-causes-symptoms-and-treatment-methods-210600.html Criner, G. (2012). Textbook of clinical pediatrics. Berlin: Springer. Dugdale, D. C. (2012). Pneumonia Classification. Retrieved from http://www.nlm.nih.gov/medlineplus/ency/article/000146.htm Dumitru, I. (2012). Heart Failure. Retrieved from http://emedicine.medscape.com/article/163062-overview#a0104 Faix, R. G. (2011). Congenital Pneumonia. Retrieved from http://emedicine.medscape.com/article/978865-overview Figueroa, M. S and Peters, J. I. (2006). Congestive Heart Failure: Diagnosis, Pathophysiology, Therapy, and Implications for Respiratory Care. Retrieved from http://www.rtjournalonline.com/chf.pdf Hamdy, O. (2012). Hypoglycemia. Retrieved from http://emedicine.medscape.com/article/122122-overview Hui, D. (2011). Approach to internal medicine a resource book for clinical practice. New York: Kronenberg, H. M. (2008). Williams Textbook of Endocrinology. Philadelphia: Saunders. Madara, B. (2008). Pathophysiology. Sudbury, Mass: Jones and Bartlett Publisher Marrie, J. (2001). Community-acquired pneumonia. New York: Kluwer Academic/Plenum Publishers. Nordqvist, C. (2009).What is Hypoglycemia? What Causes Hypoglycemia? Retrieved from http://www.medicalnewstoday.com/articles/166815.php Nursingcrib.com. (2009). Pathophysiology of Congestive Heart Failure. Retrieved from http://nursingcrib.com/pathophysiology/pathophysiology-of-congestive-heart-failure/ ODonnell, J. & Gopi. D. A. (2005). Drug Injury: Liability, Analysis, and Prevention. Tucson, Arizona: Lawyers & Judges Publishing Company. Parmley,W. W. (2004). Pathophysiology of congestive heart failure. Retrieved from http://www.sciencedirect.com/science/article/pii/0002914985907908 Porth, C. (2011). Essentials of pathophysiology : concepts of altered health states. Philadelphia: Springer. The McGraw-Hill Companies, (2012). Hypoglycemia: Introduction. Retrieved from http://akramania.byethost11.com/Harrison/Book/Part%2015.%20Endocrinology%20and%20Metabolism/Section%201.%20Endocrinology/339.htm Toth, P. P. and Cannon, C. P. (2010). Comprehensive Cardiovascular Medicine in the Primary Care Setting. New York: Springer. Read More