Interrelatedness of Diseases Grim Causes,

Interrelatedness of Diseases

GRIM CAUSES, GRIM CONSEQUENCES

Type-2 Diabetes

Also called adult-onset or non-insulin-dependent diabetes, this is a chronic condition in the body's metabolism of sugar or glucose (Mayo Clinic Staff 2009). The body resists the effects or insulin or does not produce enough of it to maintain a normal glucose level. Glucose is the body's main source of fuel or energy. The consequences can be fatal if the condition remains untreated (Mayo Clinic Staff).

Symptoms -- These can develop very slowly for years and some may not even know it (Mayo Clinic Staff 2009). Main symptoms are increased thirst and frequent urination, increased hunger, weight loss, fatigue, blurred vision, slow healing of sores or frequent infections and darkened skin. (Mayo Clinic Staff).

Causes and Risks - The condition occurs when the body becomes resistant to insulin or the pancreas stops producing sufficient insulin (Mayo Clinic Staff 2009). The precise mechanism that causes this is still unknown. However, excess weight and physical inactivity are considered important factors. The hormone insulin is produced by the pancreas, a gland found just behind the stomach. When food is ingested, the pancreas secretes insulin into the bloodstream. When it circulates with the blood, it starts the mechanism whereby sugar may enter the body cells. It then lowers the amount of sugar in the bloodstream. Insulin secretion decreases when the blood sugar level goes down. Glucose or sugar is needed by body cells for energy. It comes from food consumed and the liver. After food is digested and absorbed, sugar goes to the bloodstream and then enters the cells with the help of insulin. Liver, on the other hand, stores and manufactures glucose. When insulin levels go down, it metabolizes stored glycogen into glucose to maintain a normal insulin level (Mayo Clinic Staff).

This normal process is disturbed in type-2 diabetes (Mayo Clinic Staff 2009). Instead of going to the cells, sugar or glucose remains and builds up in the bloodstream. This is because either the body cells resist the action of insulin or the pancreas does not produce enough insulin. While the direct cause of the disorder is not yet known, certain factors appear to increase the risk. These are weight, inactivity, family history, race, age and the conditions of pre-diabetes and gestational diabetes. . Overweight is a primary factor. The more fatty tissues in the body, the more resistant the cells become to insulin. Physical activity uses up more glucose as energy and increases body cells' sensitiveness to insulin. The risk increases if a parent or sibling has type-2 diabetes. Certain races appear to develop the disorder more than other races. These races include Blacks, Hispanics, American Indians and Asian-Americans. The risk seems to increase with age, especially after age 45. At this age, people tend to exercise less, lose muscle mass and gain weight. The disorder has, however, been recently observed to increase among children, adolescents and younger adult. A pre-diabetic condition often progresses to type-2 diabetes if left untreated. In the pre-diabetic condition, the blood sugar level is higher than normal but not high enough for a type-2 diabetes diagnosis. Gestational diabetes is one more risk factor. A woman with gestational diabetes has an increased risk of developing type-2 diabetes at a later time or if the baby weighs more than 9 pounds at birth (Mayo Clinic Staff).

Complications - Type-2 diabetes affects major organs, such as the heart, blood vessels, nerves, eyes and kidneys, in the long-term (Mayo Clinic Staff 2009). It can lead to various cardiovascular diseases and disorders, such as coronary artery disease with chest pain or angina, heart attack, stroke, atherosclerosis, and hypertension. It can also damage the kidneys' filtering system and lead to kidney failure. An irreversible end-stage kidney disease requires dialysis or a transplant (Mayo Clinic Staff).

The complications of type-2 diabetes are not immediately apparent in the patient when first diagnosed with COPD. But because type-2 diabetes affects the heart, blood vessels, nerves, eyes and kidney, the complications eventually manifest themselves in the succeeding diagnoses.

Chronic Obstructive Pulmonary Disease or COPD

This is primarily a combination of two related diseases, chronic bronchitis and emphysema (Schiffman, 2009). Both involve chronic obstruction of airflow through the airways and out of the lungs. The obstruction is generally permanent and progressive. The major cause of COPD is smoking at 90%. Although not all cigarette smokers develop COPD, statistics said 15% will. Smokers with COPD have higher death rates than non-smokers with the disorder. They also suffer from frequent respiratory symptoms and deteriorating lung function more than non-smokers (Schiffman).

Complications

The main complication is lung damage, which is beyond repair (WebMD, 2009). The rate at which breathing becomes harder can only be slowed down and if the condition is still mild to moderate. Other complications include flare-ups or exacerbations in coughing and shortness of breath; more frequent lung infections like pneumonia; increased risk of osteoporosis; depression or anxiety; weight problems; heart failure on the right side of the heart; collapsed lung or pneumothorax; and sleep problems because of insufficient oxygen in the lungs (Schiffman).

COPD already compromised the patient's respiratory health and exposed him to lung damage; frequent lung infections, such as pneumonia; and insufficient oxygen in the lungs. These would eventually become evident. He also became vulnerable to heart failure.

High Blood Pressure or Hypertension

This condition means high pressure or tension in the arteries (Cunha 2009). Normal blood pressure is less than 120/80. Blood pressure between 120/80 and 139/89 is "pre-hypertension," and 140/90 or above is high. The number on top is the systolic blood pressure is the measurement of pressure in the arteries as the heart contracts and pumps blood into the arteries. The number below is the diastolic blood pressure, the measurement when the heart relaxes between contractions. An increase in these numbers exposes the person to health risks. The two forms of hypertension are essential and secondary. Essential hypertension accounts for 95% of all cases and secondary hypertension for 5% (Cunha).

Causes

The causes of high blood pressure are still unknown but certain factors are associated with it (Cunha, 2009). Advancing age, high salt intake, the African-American race, obesity, genetics, susceptibility and renal insufficiency are factors associated with essential hypertension. Kidney, adrenal and aortic artery abnormalities are associated with secondary hypertension (Cunha).

Complications

Elevation in blood pressure also increases the risk of cardiac or heart disease, kidney or renal disease, hardening of the arteries or atherosclerosis, eye damage and stroke or brain damage (Cunha, 2009). These complications are also called end-organ damage in that they are the result of chronic high blood pressure. According to the American Heart Association, one in three adults in the United States suffers from high blood pressure. This means 73 million people. Chronic or long-standing hypertension often leads to enlarged heart, kidney failure, damage in the brain or nerves, and changes on the retina (Cunha). Hypertension and hart attack are two of the complications of type-2 diabetes. Both hypertension and type-2 diabetes increase the risk of heart disease. Coronary artery disease, heart attacks, and chronic hypertension are among the causes of congestive heart failure.

Congestive Heart Failure or CHF

In congestive heart failure, the pumping capacity of the heart becomes inadequate to meet the body's need for oxygen (Kulick, 2009). The body regularly needs oxygen-rich blood in order to function. Diseases that weaken or make the heart muscle stiff or exert demand for oxygen beyond the capacity of the heart can cause CHF. Heart attacks or infections can weaken the muscles of the ventricles. Hemochromatosis or amyloidosis can stiffen the heart muscle and disturb the capacity of the ventricles to relax. Chronic hypertension is the most common cause. In other cases, disorders like hyperthyroidism can strain the heart and lead to high-output heart failure (Kulick).

Causes and Complications

Besides chronic hypertension, the other common causes of CHF are coronary artery disease, chronic alcoholism and disorder of the heart valves (Kulick, 2009). It can affect many organs and their functions. The weakened heart muscle may fail to supply sufficient blood to the kidneys. The kidneys lose the normal ability to eliminate salt and water. . They begin to retain more fluid. The lungs become congested with fluid, a condition called pulmonary edema. The person finds exercising difficult. Fluid may also accumulate in the liver and this disturbs or destroys its ability to eliminate toxins from the body and produce needed protein. The intestines are less able to efficiently absorb nutrients and medicines. Without treatment, CHF will gradually affect and damage all the other organs of the body (Kulick).

Chronic hypertension, the most common cause of CHF, is one of the causes of Myocardial Infarction or MI. The patient has earlier been diagnosed with diabetes mellitus, another cause of MI, and with COPD, of which smoking is the major cause. Smoking is another cause of MI.

Myocardial Infarction or MI

Incidence

MI is the irreversible necrosis of the heart muscle on account of prolonged ischemia

(Garas & Zafari, 2009). An imbalance between oxygen supply and demand is oftentimes the cause. The presence of cardiac enzymes in the blood often indicates myocardial necrosis. Medical experts generally view MI as one among acute coronary syndromes. Unstable angina and non-ST-elevation MI are among the syndromes. Statistics said that approximately 1.5 million cases come up each year. MI is a cardiovascular condition. About 12 million deaths worldwide each year are attributed to cardiovascular diseases as cause, according to the World Health Organization. These diseases are blamed for half of all deaths in many developed countries and one of the causes of death in many developing countries. On the whole, they are the major cause of adult deaths everywhere in the world (Garas and Zafari).

Mortality, Morbidity, Risk Factors

Cardiovascular disease is the number-one cause of death in the United States with approximately 500,000-700,000 of these relating to coronary artery every year (Garas & Zafari, 2009). More specifically, ischemic heart disease is the leading cause of death in the world. The prevalence of coronary artery disease has been increasing in non-industrialized countries. It is the leading cause of death and sickness among African-American, Hispanic and White populations in the United States. Sufferers are predominantly male up to age 70 but the rate is comparable between the genders after this age. Premenopausal women seem protected from atherosclerosis, likely because of the effects of the hormone estrogen. Age appears to be a factor: the risk increases with age, as most of those who develop acute MI are over 60 years old. Age, gender and family history are non-modifiable risk factors. Sickness and death rates are also higher among those older than 60 who develop MI (Garas & Zafari).

Causes

These are atherosclerosis with occlusive or partially occlusive thrombus formation, the non-modifiable risk factors earlier mentioned, modifiable risk factors for atherosclerosis, new and other risk factors and those unrelated with atherosclerosis (Garas & Zafari, 2009). The modifiable risk factors for atherosclerosis are smoking, diabetes mellitus, hypertension, dyslipidemia, and obesity. New and other risk factors include raised homocysteine levels, male baldness, sedentary lifestyle or lack of exercise, psychosocial stress, peripheral vascular disease and poor oral hygiene. Causes unrelated to atherosclerosis are vasculitis; coronary emboli; congenital coronary disorders; coronary trauma; coronary spasm; cocaine use; factors requiring increase of oxygen like intense activity, fever and hyperthyroidism; and factors reducing oxygen delivery, such as hypoxemia of severe anemia (Garas & Zafari).

Complications

These include benign-to-fatal arrhythmias, which are a major cause of both death and illness (Garas & Zafari, 2009). The close monitoring and immediate treatment are the single and most important parts of the treatment within the first 48 hours. Electrolyte disturbances, hypoxemia, drugs and acidosis should be watched and immediately treated. Ventricular fibrillation and/or ventricular tachycardia may occur within the first 48 hours on account of ischemia. Other complications are supraventricular arrhythmias, conduction abnormalities on account of ischemia, necrosis or chronotropic drugs; recurrent ischemia, congenital heart failure, cardiogenic shock, acute mitral regurgitation and ventricular rupture. Ventricular rupture accounts for more than 90% of all deaths from MI. Other complications include pericarditis, ventricular aneurysms, mural thrombi, and hypertension. The earlier these are recognized and the sooner the treatment, the greater the chances of survival (Garas & Zafari).

Prognosis

Mortality rate is 30% of deaths occurring before reaching the hospital and 5-10% of patients succumb to MI within the first year (Garas & Zafari, 2009). On the whole, changes or survival are quite variable and largely depends on the extent of the infarct, the residual LV function and if the patient had undergone revascularization (Garas & Zafari).

Hypertension is a complication of MI and a direct cause of acute renal failure. Diabetes is an existing condition in the patient of which atherosclerosis is a complication.

Acute Renal Failure

Also called acute kidney injury or AKI, this is the abrupt or swift decline in renal filtration function (Agraharkar et al., 2009). It is characterized by a rise in serum creatinine or blood urea nitrogen concentration. Medications, which inhibit the kidney's tubular secretion can raise the creatinine level. GI or mucosal bleeding, use of steroids, or protein loading can raise the blood urea nitrogen level. AKI is classified into pre-renal, intrinsic, and post-renal. Pre-renal AKI is the most common form of kidney injury and progresses to intrinsic AKI if not promptly corrected. It can be the result of decreased renal perfusion in heart failure or shock or certain medications. These medications include angiotensin-converting enzyme inhibitors or ACEIs and angiotensin receptor blockers or ARBs. They are prescribed for chronic kidney diseases and are otherwise safely tolerated. Pre-renal AKI can also develop from hypercalcemic states through the use of radiocontrast agents, non-steroidal anti-inflammatory drugs, amphotericin, calcineurin inhibitors, norepinephrine and other pressure medications. Intrinsic AKI involves structural injury in the kidney, mostly as acute ischemic or cytotoxic tubular injury. Frank necrosis is not prominent in most cases. And in post-renal AKI, there is mechanical obstruction of the urinary collecting system, which includes the renal pelvis, ureters, bladder or urethra. Causes of the obstruction include stone disease, stricture, and intraluminal, extraluminal or intramural tumors. Bilateral obstruction often results from prostate enlargement or tumor in men and urologic or gynecologic tumors in women (Agraharkar et al.).

Frequency, Morbidity and Mortality, Complications

Recent U.S. statistics said that approximately 1% of all hospital in-patients have AKI at the time of admission (Agraharkar et al., 2009). It rises to 2-5% during hospitalization: 1% of all general surgery cases within 30 days after surgery and up to 67% of intensive care unit cases. About 95% of all consultations with nephrologists involves AKI in approximately 70 cases per million. On the whole, 25-90% of all AKI patients die from the disease. Of this number, 40-50% die in the hospital and 70-80 die in intensive care settings. Those who survive require long-term treatment and follow-ups of 1-10 years. About 12.5% of survivors are dependent on dialysis from 1-64% and 19-31% and develop chronic kidney disease. On physical examination, a patient with AKI is usually found to suffer from hypotension, volume contraction, congestive heart failure, nephrotoxic drug ingestion, a history of trauma or un-accustomed exertion, blood loss or transfusion, connective tissue or autoimmune disease, and exposure to toxic substances and vapors. Persons stand a higher risk of developing AKI if they already suffer from hypertension, congestive cardiac failure, diabetes, multiple myeloma, chronic infection or a myelo-proliferative disorder (Agraharkar et al.).

Prognosis

The likelihood of either survival or death directly related to the cause and the duration of renal failure before treatment (Agraharkar et al., 2009). A sudden increase in serum creatinine of 0.5-1 mg/dL has a 30-60% mortality rate. It goes up to 50-90% if the patient is on or needs dialysis therapy. Mortality rate is 31% in those with normal urine sediment test result and 74% with abnormal urine sediment test result. Survival is almost 0% in those who score more than 40 in the Acute Physiology and Chronic Health Evaluation II and 40% to those who score 10-19. Chances of survival also depend on age, the presence of multiple organ failure, oliguria, hypotension, vasopressor support, number of transfusions, and non-cavitary surgery (Agraharkar et al.).

Chronic kidney disease is a complication, which is one of the causes of encephalopathy. The lack of oxygen is another cause in common with COPD and a complication of congestive heart failure. Kidney failure is one of the complications of untreated diabetes, a chronic condition in the patient. Renal insufficiency is also a complication of hypertension.

Encephalopathy

This refers to brain disease, damage or malfunction (Davis, 2009). It presents in a wide variety of symptoms from mild to severe. These range from memory loss or subtle changes in personality to dementia, seizure, coma and death. It has broad meanings, depending on the reason, cause or special conditions, which lead to brain malfunction (Davis).

Causes, Categories of Causes

Potential causes of encephalopathy include infection from bacteria, viruses, parasites or prions; anoxia or lack of oxygen in the brain; alcohol consumption; liver failure; kidney failure; metabolic diseases; brain tumors; toxic chemicals, alterations in pressure in the brain; and poor nutrition (Davis, 2009). Many cases suggest several major categories of the disorder. These are infection, liver damage, anoxia and kidney failure (Davis).

Symptoms, Diagnosis, Treatment

These include subtle and slowly developing altered mental state, lethargy, dementia, seizures, tremors, muscle twitching, and coma (Davis, 2009). Mental status tests, memory tests and coordination tests reveal an altered mental state. This mental state is usually accompanied by another or other primary diagnoses of chronic liver disease, kidney failure, or anoxia. Most physicians see encephalopathy as a complication from primary and underlying health problems for which exhaustive must be conducted. Treatment is directed at the primary cause of the symptoms. It is as varied as the causes. It can be short-term or long-term, depending on the primary cause. Static encephalopathy is the one type, which is difficult or impossible to treat. It involves an altered mental state or permanent brain damage. The best management to it is to prevent more damage and rehabilitation so as to help the person reach the highest functional level (Davis).

Complications and Prognosis

These depend on the underlying primary health problem or diagnosis (Davis, 2009). But collectively, encephalopathy can lead to profound mental disorders, which lead to death. Hepatic encephalopathy can progress to brain swelling with herniation, coma and death; metabolic encephalopathy can produce irritability, lethargy, tremors, occasionally lead to coma or death; anoxic encephalopathy can bring on personality changes, severe brain damage and, in the long-term, to death; uremic encephalopathy can produce lethargy, hallucinations, stupor, muscle twitching, seizures and death; Hashumoto's encephalopathy can result in confusion, intolerance to heat and dementia; Wernicke's encephalopathy can lead to mental confusion, loss of memory and decreased ability for eye movement; Bovine spongiform encephalopathy or "Mad Cow's Disease can produce ataxia, dementia and un-rhythmical muscle twitching; Shigella encephalopsthy can produce headache, stiff neck, delirium, seizures and coma; and infectious pediatric encephalopathy can produce irritability or result in poor feeding, hypotonia or floppy baby syndrome, seizures and death. Prospects of improvement or recovery depend on the initial causes and the length of time involved in reversing or inhibiting these causes. A poor prognosis often leads to permanent brain damage or death (Davis).