ACUTE CORONARY SYNDROME Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary

arteries. The most common symptom prompting diagnosis of ACS is chest pain, often radiating of the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST elevation myocardial infarction (30%), non ST elevation myocardial infarction (25%), or unstable angina (38%).[1] These types are named according to the appearance of the electrocardiogram (ECG/EKG) as non-ST segment elevation myocardial infarction(NSTEMI) and ST segment elevation myocardial infarction (STEMI).[2] There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome.[3] ACS should be distinguished from stable angina, which develops during exertion and resolves at rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or with minimal exertion, or at lesser degrees of exertion than the individual's previous angina ("crescendo angina"). New onset angina is also considered unstable angina, since it suggests a new problem in a coronary artery. Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use.[4] Cardiac chest pain can also be precipitated by anemia, bradycardias (excessively slow heart rate) or tachycardias (excessively fast heart rate).

with diabetes). Some may report palpitations, anxiety or a sense of impending doom (angor animi) and a feeling of being acutely ill. The description of the chest discomfort as a pressure has little utility in aiding a diagnosis as it is not specific for ACS.

Prevention Acute coronary syndrome often reflects a degree of damage to the coronaries by atherosclerosis. Primary prevention of atherosclerosis is controlling the risk factors: healthy eating, exercise, treatment for hypertension and diabetes, avoiding smoking and controlling cholesterol levels; in patients with significant risk factors, aspirin has been shown to reduce the risk of cardiovascular events. Secondary prevention is discussed in myocardial infarction. After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17% reduction in hospital admissions for acute coronary syndrome. 67% of the decrease occurred in non-smokers.[11] Treatment People with presumed ACS are typically treated with aspirin, Clopidogrel, nitroglycerin, and if the chest discomfort persists morphine. Other analgesics such as nitrous oxide are of unknown benefit.

COMPLICATED UTI, BENIGN PROSTATIC HYPERPLASIA, HYPERTENSION II, DIABETES MELLITUS II UTI Predisposition to urinary tract infections (UTIs) in diabetes mellitus results from several factors. Susceptibility increases with longer duration and greater severity of diabetes. [1] High urine glucose content and defective host immune factors predispose to infection. Hyperglycemia causes neutrophil dysfunction by increasing intracellular calcium levels and interfering with actin and, thus, diapedesis and phagocytosis. Vaginal candidiasis and vascular disease also play a role in recurrent infections. SIGNS AND SYMPTOMS The cardinal sign of decreased blood flow to the heart is chest pain experienced as tightness around the chest and radiating to the left arm and the left angle of the jaw. This may be associated with diaphoresis (sweating), nausea and vomiting, as well as shortness of breath. In many cases, the sensation is "atypical", with pain experienced in different ways or even being completely absent (which is more likely in female patients and those Over time, patients with diabetes may develop cystopathy, nephropathy, and renal papillary necrosis, complications that predispose them to UTIs. Long-term effects of diabetic cystopathy include vesicourethral reflux and recurrent UTIs. In addition, as many as 30% of women with diabetes have some degree of cystocele, cystourethrocele, or rectocele. All of these may contribute to the frequency and severity of UTIs in female diabetics.

Complicated UTIs in patients who have diabetes include renal and perirenal abscess, emphysematous pyelonephritis, emphysematous cystitis, fungal infections, xanthogranulomatous pyelonephritis, and papillary necrosis. The current article focuses on emphysematous UTIs, with which diabetes is closely associated. Diabetes mellitus and obstruction of the urinary tract are the predominant risk factors for developing emphysematous UTIs. The exact mechanism for developing these distinctive infections is not well known. It appears that associated vascular thrombosis of the kidney produces a more fulminant infection because of necrosis and hemorrhagic infarction.[2] Upper tract emphysematous UTIs are divided into pyelonephritis and pyelitis. Emphysematous cystitis also occurs. Emphysematous infection can involve one or all 3 of these processes. Emphysematous pyelonephritis is necrotizing infection of the body of the kidney that may spread to the pararenal areas. Emphysematous pyelitis is limited to the collecting system and emphysematous cystitis to the bladder. The organisms involved most commonly are Escherichia coli, Klebsiella pneumoniae, and Candida. Emphysematous upper tract infections may be classified into 4 prognostic categories based on CT scan appearance. These range from gas that is isolated to the collecting system (class I ) to the appearance of gas that is limited to the body of the kidney (class 2) to extension of the gas or abscess to the perinephric space or to adjacent tissue (class 3A and class 3B, respectively). Class 4 denotes involvement of both kidneys. BPH The exact relationship of BPH to diabetes remains unclear. The specific pathway interfering in the development of both conditions is still poorly investigated. However, evidence suggests that an association between BPH and diabetes through a common pathogenic mechanism through male hormone activity alteration mediated by IGF is possible. The above potentially constitutes the key for the comprehension of the insulin effect and the abnormalities of glucose homeostasis in the development of BPH. HTN II Hypertension is an extremely common comorbidity in patients with type 2 diabetes mellitus. The coexistence of hypertension in patients with type 2 diabetes is particularly destructive because of the strong linkage of the two conditions with CVD, stroke, progression of renal disease, and diabetic nephropathy. The high BP associated with diabetic nephropathy is usually characterized by sodium and fluid retention and increased peripheral vascular resistance. Isolated systolic hypertension is considerably more common in diabetics, and supine hypertension with orthostatic hypotension is not uncommon in diabetic individuals with autonomic neuropathy.

Glucose appears in the urine (glycosuria) because the kidney excretes the excess glucose to make the blood glucose level normal. Glucose excreted in the urine acts as osmotic diuretic and causes excretion of increased amount of water, resulting in fluid volume deficit or polyuria. Nursing Diagnosis: Deficient Fluid Volume r/t intracellular DHN 2 the DM II 1. 2. 3. 4. 5. 6. 7. Establish rapport Take and record vital signs Monitor the temperature Assess skin turgor and mucous membranes for signs of dehydration Encourage the patient to increase fluid intake Administer IVF as ordered by the Doctor Administer anti-pyretic as prescribed by the Doctor.

The patient will have maintained fluid volume at a functional level as evidenced by individual good skin turgor, moist mucous membrane and stable vital signs Due to decrease of lack of insulin in the body, the glucose level continuously rises because glucose cannot be utilized without the presence of insulin. Glucose is the source of energy, while insulin is the vehicle to transport glucose to the body tissues. Because of decrease insulin level in the blood stream, the cells starved, leading to alteration of metabolism. The body needs glucose for metabolism; there will be a breakdown of energy reserved from adipose tissue, muscles and liver (glucagons). This will result to weight loss. But the energy breaks down, the glucose level continuously increase because there is less amount of insulin. The body tissues need to be fed, this will lead to polyphagia and polydipsia because the tissue are not being fed and need glucose for metabolism. NDx: Imbalanced Nutrition: less than body requirement r/t insulin deficiency 1. 2. 3. 4. 5. Establish rapport Ascertain understanding of individual nutritional needs Discuss eating habits and encourage diabetic diet as prescribed by the Doctor Document actual weight, do not estimate.Note total daily intake including patterns and time of eating. Consult dietician/physician for further assessment and recommendation regarding food preferences and nutritional support.

Diabetes Mellitus is a group of metabolic diseases characterized by increased levels of glucose in the blood resulting from defects in insulin secretion, insulin action, or both. In type 2 diabetes, people have decreased sensitivity to insulin and impaired beta cell functioning resulting in decreased insulin production. Glucose derived from food cannot be stored in the liver thereby remaining into the bloodstream. The beta cells of the islets of Langerhans release glucagon which stimulates the liver to release the stored glucose. After 8 12 hours, the liver forms glucose from the breakdown of noncarboghydrate substances, including amino acids resulting to muscle wasting which results to weakness.

DM DIAGNOSIS:

Nursing Diagnosis: Fatigue RT decreased muscular strength 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Assess response to activity Assess muscle strength of patient and functional level of activity. Discuss with patient the need for activity Alternate activity with periods of rest/ uninterrupted sleep. Monitor pulse, respiration rate and blood pressure before/after activity Perform activity slowly with frequent rest periods Promote energy conservation techniques by discussing ways of conserving energy while bathing, transferring and so on. Provide adequate ventilation Provide comfort and safety Instruct patient to perform deep breathing exercises Instruct client to increase Vitamins A, C and D and protein in her diet. Instruct also patient to increase iron in diet Administer oxygen as ordered

During surgery, the surgeon will attempt to remove the entire breast mass, along with the wire. To help ensure that the entire mass has been removed, the tissue is sent to the hospital laboratory to check the edges (margins) of the mass. If it's determined in the laboratory that cancer cells are present in the margins (positive margins), some cancer may still be in the breast and more tissue must be removed. If the margins are clear (negative margins), it's more likely that all the cancer has been removed. At the time of the breast biopsy, a tiny stainless steel marker or clip may be placed in your breast at the biopsy site. This is done so that your doctor or surgeon can easily find the area biopsied, for future monitoring or in the event that a follow-up procedure is needed to remove more tissue. Breast biopsy is necessary to confirm or rule out cancer. Needle biopsy or fine-needle biopsy can provide a core of tissue or a fluid aspirate, but needle biopsy should be restricted to fluid-filled cysts and advanced malignant lesions. Both methods have limited diagnostic value because of the small and perhaps unrepresentative specimens they provide. Open biopsy provides a complete tissue specimen, which can be sectioned to allow more accurate evaluation. A breast biopsy can usually be done on an outpatient basis under local anesthesia; however, an excisional open biopsy may require general anesthesia. In sufficient tissue is obtained and the mass is found to be a malignant tumor, specimens are sent for estrogen and progesterone receptor assays to assist in determining future therapy and the prognosis.

Hyperthermia related to the reaction iflamasi. Goal: body temperature back to normal. Expected outcomes: client reported no fever, no palpable heat, vital signs within normal limits. Intervention: 1. Assess any complaints or signs of increased body temperature changes. Rationale: Increased body temperature will shows a variety of symptoms such as red eyes and the body feels warm. 2. Observation of vital signs, especially temperature, as indicated. Rationale: To determine interventions. 3. Warm water compress on the forehead and both axilla. Rationale: To stimulate the hypothalamus to the temperature control center. 4. Collaboration of antipyretic drugs. Rationale: Controlling fever.

Nursing Interventions 1. If the patient has received a general or local anesthetic, monitor the patients vital signs regularly. If she has received a general anesthetic, check her vital signs every 15 minutes for 1 hour, every 30 minutes for 2 hours, every hour for the next 4 hours, and then every 4 hours. 2. 3. 4. 5. Administer analgesics for pain, as ordered, and provide ice bags for comfort. Instruct the patient to wear a support bra at all times until healing is complete. Observe for and report bleeding, tenderness, and redness at the biopsy site. Provide emotional support to the patient awaiting diagnosis.

S/P EXCISION BIOPSY OF BREAST MASS/ FROZEN SECTION MRM RIGHT (RIGHT ARM PREC.) Surgical biopsy. During a surgical biopsy, a portion of the breast mass is removed for examination (incisional biopsy), or the entire breast mass may be removed (excisional biopsy, wide local excision or lumpectomy). A surgical biopsy is usually done in an operating room, with sedation and a local anesthetic. If the breast mass can't be felt, your radiologist may use a technique called wire localization to map the route to the mass for the surgeon. During wire localization, the tip of a thin wire is positioned within the breast mass or just through it. This is usually done right before surgery.