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Treatment of diabetes COPY Flashcards

1
Q

albiglutide

A

incretin - GLP-1 analogues

  • Secretion
    • Etneroendocrine cells (L cells) in ileum encoded by proglucagone gene and derived from natrual proglucagon protein
  • GLP1 release stimulated by nutrient entering the gut
  • Physiological effects
    • Pancreas: increases insulin secretion but decreases glucagon secretion
    • Stomach: delays gastric emptying
    • Hypothalamus: decrease appetite
  • Analog
    • Exenatide, liraglutide, albiglutide, duraglutide
    • AE
      • Nausea, vomiting and diarrhea
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2
Q

acarbose

A

alpha glucosidase inhibitor

  • MOA
    • Competitive and reversible inhibitors of pancreatic a-amylase and intestinal a-glucosidase enzymes
      • Increased time required to absorb complex carbs
      • Reduces postprandial glucose peak
  • Acarbose and miglitol
    • Often used in combination with other hypoglycemic agents
    • No risk for hypoglycemia (you just arent absorbing as much)
  • AE
    • Flatulence, bloating, diahhea - not recommended for patienst with IBD or working around people
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3
Q

canagliflozin

A

SGLT2 inhibitor - inhibit glucose reupatake in the kidney

  • MOA: stops reabsorption of glucose from the tubules
    • Cuases glycosuria
  • Efficacy is reduced in kidney disease
  • Also promotes weight loss (you are loosing energy in the urine)
  • AE
    • Increased incidence of genital infections and UTIs
    • Osmotic diuresis - can also cuase Intravascular volume contraciton = hypotension
  • Drugs
    • Canagliflozin, dapagliflozin, empagliflozin
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4
Q

inagliptin

A

incretin - DDP4 inhibitor

  • MOA: increases the level of endogenous incretins
  • Drugs
    • Sitagliptin, saxagliptin, linagliptin, alogliptin
  • Use
    • Monotherapy or in combination with metformin or other agents
  • Not used in comb with GLP-1 analogs (these are less susceptible to DDP4 degredation
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5
Q

regular novolin

A

short acting insulin

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6
Q

regular humulin

A

short acting insulin

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7
Q

nateglinide

A

insulin secretagogues - meglitinide

more rapid onset of action

  • MOA
    • Similar to sulfonylureas by binding to SUR1 but at a different site to activation the K channel
  • Cleared by liver, don’t give to patients with hepatic insufficiency
  • Major adverse effect is hypoglycemia
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8
Q

glimepriride

A

insulin secretagogues - sulfonylurease - second generation

  • MOA: activate residual b cells to release insulin by binding and activating SUR1
    • SUR1 (sulfonylurea receptor 1) = subunit of K/ATP channel
      • Activates the channel = similar to feed state - they block the K channel that closes when there is glucose around = more insulin secretion (cell thinks there is a ton of glucose around)
    • May decrease hepatic clearance of insulin; decrease serum glucagon by stimulating somatostatin release
  • Contraindications
    • Type 1 DM - there are no cells to secrete insulin so this wont do anything
    • Preganancy
    • Lactation
    • Significant hepatic or renal insufficiency
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9
Q

insulin glargine

A

long acting insulin

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10
Q

duraglutide

A

incretin - GLP-1 analogues

  • Secretion
    • Etneroendocrine cells (L cells) in ileum encoded by proglucagone gene and derived from natrual proglucagon protein
  • GLP1 release stimulated by nutrient entering the gut
  • Physiological effects
    • Pancreas: increases insulin secretion but decreases glucagon secretion
    • Stomach: delays gastric emptying
    • Hypothalamus: decrease appetite
  • Analog
    • Exenatide, liraglutide, albiglutide, duraglutide
    • AE
      • Nausea, vomiting and diarrhea
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11
Q

NPH humulin N

A

intermediate acting insulin

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12
Q

DAPAGLIFLOZIN

A

SGLT2 inhibitor - inhibit glucose reupatake in the kidney

  • MOA: stops reabsorption of glucose from the tubules
    • Cuases glycosuria
  • Efficacy is reduced in kidney disease
  • Also promotes weight loss (you are loosing energy in the urine)
  • AE
    • Increased incidence of genital infections and UTIs
    • Osmotic diuresis - can also cuase Intravascular volume contraciton = hypotension
  • Drugs
    • Canagliflozin, dapagliflozin, empagliflozin
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13
Q

insulin lispro

A

rapid acting insulin

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14
Q

insulin glulisine

A

rapid acting insulin

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15
Q

NPH novolin N

A
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16
Q

insulin detemir

A

long acting insulin

17
Q

sitagliptin

A

incretin - DDP4 inhibitor

  • MOA: increases the level of endogenous incretins
  • Drugs
    • Sitagliptin, saxagliptin, linagliptin, alogliptin
  • Use
    • Monotherapy or in combination with metformin or other agents
  • Not used in comb with GLP-1 analogs (these are less susceptible to DDP4 degredation
18
Q

tolbutamide

A

insulin secretagogues - sulfonylurease - first generation

sulfa drug (all secretagogues are sulfas)

  • MOA: activate residual b cells to release insulin by binding and activating SUR1
    • SUR1 (sulfonylurea receptor 1) = subunit of K/ATP channel
      • Activates the channel = similar to feed state - they block the K channel that closes when there is glucose around = more insulin secretion (cell thinks there is a ton of glucose around)
    • May decrease hepatic clearance of insulin; decrease serum glucagon by stimulating somatostatin release
  • Contraindications
    • Type 1 DM - there are no cells to secrete insulin so this wont do anything
    • Preganancy
    • Lactation
    • Significant hepatic or renal insufficiency
19
Q

repaglinide

A

insulin secretagogues - meglitinide

  • MOA
    • Similar to sulfonylureas by binding to SUR1 but at a different site to activation the K channel
  • Cleared by liver, don’t give to patients with hepatic insufficiency
  • Major adverse effect is hypoglycemia
20
Q

miglitol

A

alpha glucosidase inhibitor

  • MOA
    • Competitive and reversible inhibitors of pancreatic a-amylase and intestinal a-glucosidase enzymes
      • Increased time required to absorb complex carbs
      • Reduces postprandial glucose peak
  • Acarbose and miglitol
    • Often used in combination with other hypoglycemic agents
    • No risk for hypoglycemia (you just arent absorbing as much)
  • AE
    • Flatulence, bloating, diahhea - not recommended for patienst with IBD or working around people
21
Q

insulin aspart

A

rapid acting insulin

22
Q

glyburide

A

insulin secretagogues - sulfonylurease - second generation

  • MOA: activate residual b cells to release insulin by binding and activating SUR1
    • SUR1 (sulfonylurea receptor 1) = subunit of K/ATP channel
      • Activates the channel = similar to feed state - they block the K channel that closes when there is glucose around = more insulin secretion (cell thinks there is a ton of glucose around)
    • May decrease hepatic clearance of insulin; decrease serum glucagon by stimulating somatostatin release
  • Contraindications
    • Type 1 DM - there are no cells to secrete insulin so this wont do anything
    • Preganancy
    • Lactation
    • Significant hepatic or renal insufficiency
23
Q

saxagliptin

A

incretin - DDP4 inhibitor

  • MOA: increases the level of endogenous incretins
  • Drugs
    • Sitagliptin, saxagliptin, linagliptin, alogliptin
  • Use
    • Monotherapy or in combination with metformin or other agents
  • Not used in comb with GLP-1 analogs (these are less susceptible to DDP4 degredation
24
Q

pioglitazone

A

insulin sensitizer - thiazolidinediones (TZDs)

  • PPAR gamma agonists with PPAR alpha agonist activity
    • Rosiglitazone ahs 10X PPAR gamma affinity than pioglitazone
    • Troglitazone was removed from the market due to hepatotox
  • MOA
    • In adepose tissue PPAR gamma activators promote transport of serum lipids to adipose tissue
    • May also activate PPAR gamma in other tissues to promote insulin sensitivity
      • Decrease hepatic gluconeo
      • Enhance uptake of glucose by skel muscle
  • Use
    • Effective in reducing glucose as well as triglycerides
  • Metabolized in liver
  • AE
    • Weight gain
    • Hepatic tox
    • Congestive heart failure
25
PRAMLINTIDE
* amylin analog - * Pancrease: increases insulin secretion and decrease glucagon secretion * Stomach: delays gastric emptying * Hypothalamus: decrease appetite * These effects are very similar to the incretins * Use * Adjunct to insulin - improves postprandial glucose control in type 1 and 2 * Renal met and excretion * AE * Hypoglycemia and GI symptoms (the incretins don’t have as big of a risk for tehse things - so they are probably better) * not very effective
26
glipizide
insulin secretagogues - sulfonylurease - second generation * MOA: activate residual b cells to release insulin by binding and activating SUR1 * SUR1 (sulfonylurea receptor 1) = subunit of K/ATP channel * Activates the channel = similar to feed state - they block the K channel that closes when there is glucose around = more insulin secretion (cell thinks there is a ton of glucose around) * May decrease hepatic clearance of insulin; decrease serum glucagon by stimulating somatostatin release * Contraindications * Type 1 DM - there are no cells to secrete insulin so this wont do anything * Preganancy * Lactation * Significant hepatic or renal insufficiency
27
bromocriptine
* MOA: we don’t know why this lowers glucose * AE * Nausea, fatigue, dizziness, vomiting and headache * not very effective
28
EMPAGLIFLOZIN
SGLT2 inhibitor - inhibit glucose reupatake in the kidney * MOA: stops reabsorption of glucose from the tubules * Cuases glycosuria * Efficacy is reduced in kidney disease * Also promotes weight loss (you are loosing energy in the urine) * AE * Increased incidence of genital infections and UTIs * Osmotic diuresis - can also cuase Intravascular volume contraciton = hypotension * Drugs * Canagliflozin, dapagliflozin, empagliflozin
29
rosiglitazone
insulin sensitizer - thiazolidinediones (TZDs) * PPAR gamma agonists with PPAR alpha agonist activity * Rosiglitazone ahs 10X PPAR gamma affinity than pioglitazone * Troglitazone was removed from the market due to hepatotox * MOA * In adepose tissue PPAR gamma activators promote transport of serum lipids to adipose tissue * May also activate PPAR gamma in other tissues to promote insulin sensitivity * Decrease hepatic gluconeo * Enhance uptake of glucose by skel muscle * Use * Effective in reducing glucose as well as triglycerides * Metabolized in liver * AE * Weight gain * Hepatic tox * Congestive heart failure
30
tolazamide
insulin secretagogues - sulfonylurease - first generation * MOA: activate residual b cells to release insulin by binding and activating SUR1 * SUR1 (sulfonylurea receptor 1) = subunit of K/ATP channel * Activates the channel = similar to feed state - they block the K channel that closes when there is glucose around = more insulin secretion (cell thinks there is a ton of glucose around) * May decrease hepatic clearance of insulin; decrease serum glucagon by stimulating somatostatin release * Contraindications * Type 1 DM - there are no cells to secrete insulin so this wont do anything * Preganancy * Lactation * Significant hepatic or renal insufficiency
31
liraglutide
incretin - GLP-1 analogues * Secretion * Etneroendocrine cells (L cells) in ileum encoded by proglucagone gene and derived from natrual proglucagon protein * GLP1 release stimulated by nutrient entering the gut * Physiological effects * Pancreas: increases insulin secretion but decreases glucagon secretion * Stomach: delays gastric emptying * Hypothalamus: decrease appetite * Analog * Exenatide, liraglutide, albiglutide, duraglutide * AE * Nausea, vomiting and diarrhea
32
chlorpropamide
insulin secretagogues - sulfonylurease - first generation * MOA: activate residual b cells to release insulin by binding and activating SUR1 * SUR1 (sulfonylurea receptor 1) = subunit of K/ATP channel * Activates the channel = similar to feed state - they block the K channel that closes when there is glucose around = more insulin secretion (cell thinks there is a ton of glucose around) * May decrease hepatic clearance of insulin; decrease serum glucagon by stimulating somatostatin release * Contraindications * Type 1 DM - there are no cells to secrete insulin so this wont do anything * Preganancy * Lactation * Significant hepatic or renal insufficiency
33
METFORMIN
insulin sensitizers - biguanide * Use * 1st line therapy for type 2 DM * Not bound to plasma protien, not metabolized, excreted by kidney as parent compound * Tox * Lactic acidosis (rare but life threatining) * By blocking gluconeogenesis, may impair hepatic metabolism of lactic acid * More common in patients with renal insufficnecy * Acute adverse effects * Mostly GI related: diarrhea, abdominal discomfort, nausea, metalic tase, and anorexia * Reduced vitamin B12 absortption
34
alogliptin
incretin - DDP4 inhibitor * MOA: increases the level of endogenous incretins * Drugs * Sitagliptin, saxagliptin, linagliptin, alogliptin * Use * Monotherapy or in combination with metformin or other agents * Not used in comb with GLP-1 analogs (these are less susceptible to DDP4 degredation
35
COVESEVALAM
* Bile acid sequesterant, cholesterol lowering drug * MOA: not fully understood * Decreases farnesoid X receptor (FXR) nuclear receptor activation * FXR has multiple effects on cholesterol, glucose and bile acid metabolism * May impair glucose absorption * AE * Can exacerbate hypertriglyceridemia (more common in type 2) * not very effective
36
exenatide
incretin - GLP-1 analogues

IC (32 decks)

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