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MandyStroyerTeacher
Terms in this set (6)
- Type 1 DM: absolute insulin deficiency typically due to autoimmune destruction of pancreatic beta cells; 5-10% of all cases
- Type 2 DM: varying degrees of beta cell dysfunction coupled with insulin
resistance; 90-95% of cases; most commonly in Native Americans, African
Americans, Latino/Hispanic Americans, Asian Americans and Pacific Islanders
- Type 2 DM: varying degrees of beta cell dysfunction coupled with insulin
resistance; 90-95% of cases; most commonly in Native Americans, African
Americans, Latino/Hispanic Americans, Asian Americans and Pacific Islanders
- diagnosis for DM requires the use of glycemic cut points that differentiate between normal BG and impaired BG and diabetes
Criteria (any of these):
- FPG ≥126 mg/dL (7.0 mmol/L); fasting is defined as no caloric intake for at least 8 hours
- 2h PG ≥200 mg/dL (11.1 mmol/L) during OGTT
- A1C ≥6.5% (48 mmol/mol)
- in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L)
Criteria (any of these):
- FPG ≥126 mg/dL (7.0 mmol/L); fasting is defined as no caloric intake for at least 8 hours
- 2h PG ≥200 mg/dL (11.1 mmol/L) during OGTT
- A1C ≥6.5% (48 mmol/mol)
- in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L)
- age ≥45 years old
- family history of T2DM
- high-risk race or ethnicity
- overweight/obese
- sedentary lifestyle
- history of impaired glucose tolerance, impaired fasting glucose, or elevated HbA1C
- hypertension
- dyslipidemia
- history of GDM or delivery of a baby weighing more than 9 pounds
- presence of acanthosis nigiricans
- PCOS
- family history of T2DM
- high-risk race or ethnicity
- overweight/obese
- sedentary lifestyle
- history of impaired glucose tolerance, impaired fasting glucose, or elevated HbA1C
- hypertension
- dyslipidemia
- history of GDM or delivery of a baby weighing more than 9 pounds
- presence of acanthosis nigiricans
- PCOS
Biguanides (e.g., metformin):
- decreases hepatic glucose production and enhances insulin sensitivity in peripheral (muscle and adipose) tissues
Sulfonylureas (e.g., glyburide, glipizide, glimepiride):
- enhances insulin secretion by binding to a specific sulfonylurea receptor (SUR1) on pancreatic β-cells
Thiazolidinediones (e.g., pioglitazone, rosiglitazone):
- binds to the peroxisome proliferator activator receptor-g (PPAR-g) leading to activation of PPAR-g which alters the transcription of genes involved in glucose and lipid metabolism and energy balance
- this leads to enhanced insulin sensitivity at muscle, fat, and liver tissues
GLP-1 Receptor Antagonists (e.g., exenatide, lixisenatide, dulaglutide, semaglutide):
- mimic GLP-1
- stimulate insulin secretion from the β-cells in a glucose-dependent manner
- reduce inappropriately elevated levels of glucagon which results in reduced hepatic glucose output during hyperglycemia
- slow gastric emptying, thus reducing meal-related glucose spikes
- penetrate the blood-brain barrier, leading to increased satiety
DPP-4 Inhibitors (e.g., sitagliptin, saxagliptin, linagliptin):
- inhibit the DPP-4 enzyme which is responsible for degradation of GLP-1 and GIP, thus prolonging the half-life of these endogenous incretin hormones
- block nearly 100% of the DPP-4 enzyme for at least 12 hours
SGLT2 Inhibitors (e.g., canagliflozin, dapagliflozin, empagliflozine):
- blocks glucose reabsorption in kidney and increases glucosuria by inhibiting SGLT2 in the proximal nephron
⍺-Glucosidase Inhibitors (e.g., acarbose, miglitol):
- competitively inhibit maltase, isomaltase, sucrase, and glucoamylase in the small intestine, thus delaying the breakdown of sucrose and complex carbohydreate.
- primarily reduce PPG levels
Meglitinides (e.g., nateglinide, rapaglinide):
- stimulate insulin secretion from the β-cells
Bile Acid Sequestrants (e.g., colesevelam):
- glucose lowering mechanism is poorly understood
Dopamine Agonists (e.g., bromocriptine):
- unknown, but may improve insulin sensitivity and reduce hepatic glucose output
Amylin Analogs (e.g., pramlintide):
- mimics amylin and regulates glucose by reducing glucagon secretion,
slowing gastric emptying, and increasing satiety
- decreases hepatic glucose production and enhances insulin sensitivity in peripheral (muscle and adipose) tissues
Sulfonylureas (e.g., glyburide, glipizide, glimepiride):
- enhances insulin secretion by binding to a specific sulfonylurea receptor (SUR1) on pancreatic β-cells
Thiazolidinediones (e.g., pioglitazone, rosiglitazone):
- binds to the peroxisome proliferator activator receptor-g (PPAR-g) leading to activation of PPAR-g which alters the transcription of genes involved in glucose and lipid metabolism and energy balance
- this leads to enhanced insulin sensitivity at muscle, fat, and liver tissues
GLP-1 Receptor Antagonists (e.g., exenatide, lixisenatide, dulaglutide, semaglutide):
- mimic GLP-1
- stimulate insulin secretion from the β-cells in a glucose-dependent manner
- reduce inappropriately elevated levels of glucagon which results in reduced hepatic glucose output during hyperglycemia
- slow gastric emptying, thus reducing meal-related glucose spikes
- penetrate the blood-brain barrier, leading to increased satiety
DPP-4 Inhibitors (e.g., sitagliptin, saxagliptin, linagliptin):
- inhibit the DPP-4 enzyme which is responsible for degradation of GLP-1 and GIP, thus prolonging the half-life of these endogenous incretin hormones
- block nearly 100% of the DPP-4 enzyme for at least 12 hours
SGLT2 Inhibitors (e.g., canagliflozin, dapagliflozin, empagliflozine):
- blocks glucose reabsorption in kidney and increases glucosuria by inhibiting SGLT2 in the proximal nephron
⍺-Glucosidase Inhibitors (e.g., acarbose, miglitol):
- competitively inhibit maltase, isomaltase, sucrase, and glucoamylase in the small intestine, thus delaying the breakdown of sucrose and complex carbohydreate.
- primarily reduce PPG levels
Meglitinides (e.g., nateglinide, rapaglinide):
- stimulate insulin secretion from the β-cells
Bile Acid Sequestrants (e.g., colesevelam):
- glucose lowering mechanism is poorly understood
Dopamine Agonists (e.g., bromocriptine):
- unknown, but may improve insulin sensitivity and reduce hepatic glucose output
Amylin Analogs (e.g., pramlintide):
- mimics amylin and regulates glucose by reducing glucagon secretion,
slowing gastric emptying, and increasing satiety
Basal:
- "background" insulin
- refers to intermediate and longer-acting insulins that help to regulate BG between meals by suppressing glucose production and maintaining near normal glycemic states
- options include insulin NPH, detemir, glargine, and degludec
- most basal insulins do not have a peak level, last for approximately 24 hours or longer, and may be dosed once daily
- NPH has a distinct peak and duration is less than 24 hours (requires twice daily dosing)
Bolus:
- prandial insulin
- refers to short- or rapid-acting insulins that cover meals
- bolus insulins are also used to cover glycemic excursions as a correction dose
- options include regular insulin, insulin aspart, lispro, and glulisine, and ultra-rapid inhaled human insulin
- onset and duration of these options are shorter and rapid acting
- most closely mimics prandial endogenous insulin release
- rapid acting insulins have a slightly lower risk of hypoglycemia compared to regular insulin
**U-500 regular insulin is reserved for patients with extreme insulin resistance and is given 2-3 times daily
**pre-mixed insulins contain both basal and prandial components (helpful for simpler regimens with fewer injections; dosing modifications are less flexible)
- "background" insulin
- refers to intermediate and longer-acting insulins that help to regulate BG between meals by suppressing glucose production and maintaining near normal glycemic states
- options include insulin NPH, detemir, glargine, and degludec
- most basal insulins do not have a peak level, last for approximately 24 hours or longer, and may be dosed once daily
- NPH has a distinct peak and duration is less than 24 hours (requires twice daily dosing)
Bolus:
- prandial insulin
- refers to short- or rapid-acting insulins that cover meals
- bolus insulins are also used to cover glycemic excursions as a correction dose
- options include regular insulin, insulin aspart, lispro, and glulisine, and ultra-rapid inhaled human insulin
- onset and duration of these options are shorter and rapid acting
- most closely mimics prandial endogenous insulin release
- rapid acting insulins have a slightly lower risk of hypoglycemia compared to regular insulin
**U-500 regular insulin is reserved for patients with extreme insulin resistance and is given 2-3 times daily
**pre-mixed insulins contain both basal and prandial components (helpful for simpler regimens with fewer injections; dosing modifications are less flexible)
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