DKA and stuff

Diabetic ketoacidosis (DKA) is: a severe and life-threatening complication of diabetes

DKA is characterized by: uncontrolled hyperglycemia, metabolic acidosis, and increased production of ketones.

DKA typically occurs in individuals: with type 1 diabetes when insulin levels are insufficient.

Without insulin, the body cannot use glucose for energy and begins: breaking down fat, producing ketones as a by-product.

Accumulation of ketones causes: the blood to become acidic.

Symptoms of DKA include: polyuria, polydipsia, polyphagia, dehydration, abdominal pain, vomiting, fruity-smelling breath, confusion, and rapid deep breathing known as Kussmaul respirations.

Treatment for DKA includes: administration of intravenous fluids, insulin therapy, and correction of electrolyte imbalances

Effective diabetes management requires: maintaining a consistent daily routine involving diet, exercise, medications, and blood glucose monitoring.

Nutrition therapy focuses on: maintaining stable blood glucose levels through consistent carbohydrate intake.

 Carbohydrate counting is commonly used: as a meal planning strategy.

One carbohydrate serving equals approximately: fifteen grams of carbohydrates.

 Most meals contain approximately: forty-five to sixty grams of carbohydrates.

Exercise is an important component of diabetes management because: it increases insulin sensitivity, lowers blood glucose levels, and helps maintain a healthy weight.

However, exercise can also: increase the risk of hypoglycemia

Exercise can increase the risk of hypoglycemia particularly: if the patient is using insulin or medications that increase insulin secretion.

Patients should monitor their blood glucose levels: before, during, and after exercise.

Patients may need to consume a carbohydrate snack: before physical activity.

Blood glucose monitoring allows individuals with diabetes to track: fluctuations in blood sugar throughout the day.

Some patients monitor blood glucose: before meals and at bedtime.

Proper technique for monitoring blood glucose includes: washing the hands, using the side of the finger pad to obtain a drop of blood, and recording the results.

Continuous glucose monitoring systems are also available.

Insulin therapy is required for: all individuals with type 1 diabetes and may be necessary for some individuals with type 2 diabetes.

 Insulin is: a protein hormone and cannot be taken orally because it would be destroyed by digestive enzymes.

insulin is typically administered through: subcutaneous injection.

Common injection sites include: the abdomen, upper arms, thighs, and buttocks.

Regarding SubQ injections, the abdomen is often preferred: because insulin is absorbed more rapidly from this area.

Injection sites should be: rotated within the same area to maintain consistent absorption and prevent tissue damage.

Insulin types are classified according to their: onset, peak, and duration of action.

Rapid-acting insulin begins working: within approximately fifteen minutes, peaks within one to three hours, and lasts about three to five hours.

Short-acting insulin begins working within: about thirty minutes and lasts approximately eight hours.

Intermediate-acting insulin begins working: within one to two hours, peaks around six hours, and can last up to twenty-four hours.

Long-acting insulin begins working: within three to four hours and provides steady insulin levels for approximately twenty-four hours without a pronounced peak.

Several oral medications: are used to treat type 2 diabetes.

Biguanides such as metformin: reduce glucose production in the liver, decrease glucose absorption in the gastrointestinal tract, and improve insulin sensitivity.

Sulfonylureas: increase insulin production from the pancreas but may cause hypoglycemia.

Alpha-glucosidase inhibitors: slow carbohydrate digestion and absorption in the intestines.

DPP-4 inhibitors: increase insulin release and decrease glucagon secretion.

GLP-1 agonists: mimic natural gut hormones to stimulate insulin production and reduce appetite.

Sodium-glucose cotransporter inhibitors promote: glucose excretion through the urine by reducing glucose reabsorption in the kidneys.