Diabetes Medication – Type 2 diabetes. This course covers the definition, symptoms, risk factors, diet, pathophysiology, treatment, medications, and more of type 2 diabetes.
The lessons and graphics below were written by guest author Charlotte Watson, and the medical commentary was created and provided by EZmed.
Diabetes Medication
Diabetes is a metabolic disease in which the body’s ability to produce insulin or respond to insulin is impaired, resulting in elevated blood glucose levels.
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Diabetes comes from the Greek word “diabetes” meaning to pass and the Latin word “melitus” meaning sweet.
Type 2 diabetes is a metabolic disorder in which the body’s response to insulin decreases, a condition known as insulin resistance.
However, over time, insulin production declines, leading to insufficient insulin levels.
Type 2 diabetes usually occurs in older age groups (over 45) when it is diagnosed in the 60s.
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Definition of type 2 diabetes. Type 2 diabetes is a metabolic disorder in which the body’s response to insulin decreases (insulin resistance), insulin levels in the pancreas decrease, and blood glucose levels increase.
Type 2 diabetes. This course covers the definition, symptoms, causes, risk factors, pathophysiology, diagnosis, treatment, and more of type 2 diabetes.
Type 2 diabetes is characterized by high blood glucose levels and low insulin levels associated with insulin resistance.
High blood glucose levels and the inability of cells to take up glucose can cause a number of symptoms.
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Type 2 diabetes usually develops more slowly than type 1 diabetes, with symptoms lasting from months to years (type 1 symptoms last from days to weeks).
Symptoms of type 2 diabetes. Symptoms of type 2 diabetes include increased thirst (polydipsia), increased hunger (polyphagia), unexplained weight loss, fatigue, increased urination (polyuria), blurred vision, and dizziness.
Many of the risk factors listed above contribute to insulin resistance; See “Causes of Type 2 Diabetes.”
A child with either parent has a 40% chance of developing type 2 diabetes.
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Risk factors for type 2 diabetes. Risk factors for type 2 diabetes include obesity, lack of exercise, unbalanced diet, pre-diabetes, family history, age, race, and gestational diabetes.
To better understand the etiology and pathophysiology of type 2 diabetes, let’s briefly review the anatomy and function of the pancreas and insulin.
The transpyloric plane is an imaginary line between the upper border of the pubic symphysis and the supraglottic notch, approximately at the level of the L1 vertebra.
The head of the pancreas is located in the curved part of the duodenum, and the tail is located in the spleen.
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Anatomy of the pancreas. location and labeled diagram of the pancreas and its parts, including head, inferior process, neck, body, and tail.
Beta cells are important in this lesson because they are responsible for the synthesis and release of insulin into the bloodstream.
Pancreatic function. digestive (exocrine) and hormonal (endocrine) functions of the pancreas, including the secretion of glucagon (alpha cells), insulin (beta cells), and somatostatin (delta cells).
Insulin is responsible for regulating blood glucose levels by allowing blood glucose to enter cells.
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Insulin is continuously secreted at low levels throughout the day by the beta cells of the pancreas (see above), which:
After the beta cells of the pancreas secrete insulin into the bloodstream, the insulin binds to insulin receptors on the surface of the body’s cells.
As a result of this cascade, the glucose transporter GLUT4 translocates from intracellular storage vesicles to the cell’s plasma membrane.
GLUT4 is the main transporter responsible for the uptake of blood glucose into cells.
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How does insulin work? Insulin receptor signaling pathway. Insulin binds to insulin receptors, which increases the recruitment of GLUT4 glucose transporters to the plasma membrane. GLUT4 allows glucose to be absorbed into cells.
Type 2 diabetes occurs when the beta cells of the pancreas produce less insulin than the body needs (insulin deficiency), and the body’s cells stop responding to insulin (insulin resistance).
This means that glucose cannot be transported from the blood to the cells. See function of insulin above.
Simply put, the blood is full of sugar (glucose), but due to reduced insulin action and a general lack of insulin, the sugar cannot enter the cells.
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To compensate for insulin resistance and maintain normal glucose levels, pancreatic beta cells first increase insulin synthesis and release.
Increasing insulin production and increasing fluid intake is a temporary solution to overcoming insulin sensitivity and allowing the body’s cells to absorb glucose.
However, increased insulin production and secretion can accelerate beta cell turnover and/or damage.
When the amount of insulin produced by the beta cells is insufficient to compensate for the sensitivity of the insulin receptors, the patient begins to develop symptoms of diabetes.
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Pathophysiology of type 2 diabetes. Type 2 diabetes is characterized by insulin resistance, insufficient insulin production by pancreatic beta cells, and hyperglycemia.
The combination of insulin resistance and inadequate insulin secretion further increases blood glucose levels in the liver.
Because the insulin receptors in the liver do not recognize insulin, the liver cannot store glucose in the blood.
This causes the liver to respond inappropriately to low blood sugar (when it is actually high), increasing gluconeogenesis and glycogenolysis.
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Gluconeogenesis = production of glucose in the liver; Glycogenolysis = Glycogen stored in the liver is broken down and released into the blood as glucose.
Pathophysiology of type 2 diabetes. Insulin resistance in liver cells and a decrease in insulin production by the pancreas cause the liver to “think” that the level of glucose in the blood is low, which leads to gluconeogenesis, glycogenolysis, and, consequently, an increase in blood glucose.
A patient with symptoms of diabetes needs only 1 biochemical test to confirm that they have type 2 diabetes.
Prediabetes = blood sugar levels that are higher than normal, but not high enough to be diagnosed as type 2 diabetes.
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Screening for type 2 diabetes (US). Graphs showing normal, pre-diabetic and pre-diabetic blood glucose levels using hemoglobin A1C, fasting blood glucose, oral glucose tolerance test, and random blood glucose testing.
Type 2 diabetes screening (UK, Canada, Australia). Normal, pre-diabetic and diabetic blood glucose level chart using hemoglobin A1C, fasting blood glucose test, oral glucose tolerance test and random blood glucose test.
Hemoglobin A1C (HbA1c) is a simple blood test that measures a patient’s average blood sugar levels over the past 2-3 months (8-12 weeks).
It measures the amount of glucose attached to hemoglobin (the protein that carries oxygen in red blood cells).
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Because HbA1c affects circulating red blood cells, it should not be tested in patients with conditions that affect these cells, such as hemoglobinopathy, hemolysis, persistent iron deficiency anemia, or HIV.
Research tip: Although a high HbA1c can be diagnostic of type 2 diabetes, it is important to remember that a low HbA1c cannot be ruled out.
A fasting blood glucose test (also known as self-plasma glucose or FPG) is a blood test that monitors your blood sugar levels without eating or drinking (except water) for at least 8 hours before the test.
Patients usually start fasting at midnight and have a blood test in the morning before breakfast.
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Glucose tolerance test (OGTT) first calculates fasting blood sugar, and then the patient drinks a 75-gram glucose drink.
In order to analyze how the level of glucose in the blood has changed, the sugar level is measured again 2 hours after drinking.
A random blood glucose test (also called a random plasma glucose test) is a blood test that randomly checks your blood sugar regardless of when you last ate.
When diagnosed with type 2 diabetes, the patient should have a lipid profile and a urinalysis for protein (protein in the urine) and ketones.
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Because of the potential complications of diabetes, patients are seen by many specialists including general practitioners, ophthalmologists, diabetes nurses, health care assistants, paediatricians and nutritionists.
Treatment of type 2 diabetes. Treatment for type 2 diabetes includes diet, exercise, medication, insulin, and glucose monitoring with HbA1c and fingerprinting.
As mentioned earlier, type 2 diabetes is caused by metabolic syndrome, which often improves with obesity, poor diet, lack of exercise, etc. (see causes above).
First-line treatment for patients with prediabetes and type 2 diabetes is conservative lifestyle management and dietary changes to lower blood sugar levels before starting any medication.
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If the patient is overweight, primary care staff may encourage the patient to lose 5-10% of their body weight.
Losing this much weight can reduce cardiovascular risk, improve glycemic control, and prevent complications from diabetes.
Patients are invited to an educational program to develop their diabetes self-management skills, knowledge and confidence.
If diet, exercise, and lifestyle changes are not enough to treat type 2 diabetes and maintain target glucose levels.
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