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,...

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…