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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 ]
[8] proper treatment usually results in full recovery, though death can result from inadequate or delayed treatment, or from complications (e.g., brain edema). [12] Preventing DKA is attainable by following some precautions. [16] While feeling unwell, Start with regular monitoring of blood glucose levels.
Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis.While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention.
Diabetic ketoacidosis (DKA), most typically seen in those with type 1 diabetes, is triggered by the build-up of chemicals called ketones. These are strongly acidic and a build-up can cause the blood to become acidic. [5] When these levels get too high it essentially poisons the body and causes DKA. [6]
Type 2 diabetes is different in that it is usually caused by insulin resistance in the body in older patients leading to beta cell burnout over time, and is not prone to DKA. KPD is a condition that involves DKA like type 1, but occurs later in life and can regain beta cell function like type 2 diabetes.
Even though people with diabetes aren’t able to produce their own insulin, they can still respond to insulin, so treatment involves lifelong insulin therapy to regulate their blood glucose levels and basically enable their cells to use glucose. One really serious complication with type 1 diabetes is called diabetic ketoacidosis, or DKA.
Commonly prescribed thyroid drug levothyroxine was linked with bone mass and bone density loss in a cohort of older adults in a recent study. Common thyroid drug levothyroxine linked to bone mass loss
The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant. Treatment of the low levels of potassium in the blood, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks.
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