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Hyperchloremia is an electrolyte disturbance in which there is an elevated level of chloride ions in the blood. [1] The normal serum range for chloride is 96 to 106 mEq/L, [2] therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. [3]
Ingestion of ammonium chloride, hydrochloric acid, or other acidifying salts; The treatment and recovery phases of diabetic ketoacidosis; Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3–4L can cause acidosis; Hyperalimentation (i.e., total parenteral nutrition)
[3] [4] [5] Some non-modifiable risk factors such as age at diabetes onset, type of diabetes, gender, and genetics may influence risk. Other health problems compound the chronic complications of diabetes such as smoking, obesity, high blood pressure, elevated cholesterol levels, and lack of regular exercise.
The normal level for fasting blood sugar in non-diabetic patients is 70 to 99 mg/dL (3.9 and 5.5 mmol/L). Another useful test that has usually done in a laboratory is the measurement of blood HbA1c (hemoglobin A1c) levels. In the blood, there is a molecule called hemoglobin which carries oxygen to the cells. Glucose can attach itself to this ...
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. [1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. [1]
Apples. The original source of sweetness for many of the early settlers in the United States, the sugar from an apple comes with a healthy dose of fiber.
Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate (HCO − 3), or alternatively a direct result of increased bicarbonate concentrations.
Chlortalidone (or other thiazide medication) is a key component of treatment of nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus occurs when the kidney is unable to concentrate urine because it has an inadequate response to vasopressin-dependent removal of free water from the renal tubular filtrate.