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Treatment of diabetes Flashcards

1
Q

insulin lispro

A

rapid acting insulin

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2
Q

insulin aspart

A

rapid acting insulin

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3
Q

insulin glulisine

A

rapid acting insulin

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4
Q

regular novolin

A

short acting insulin

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5
Q

regular humulin

A

short acting insulin

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6
Q

NPH humulin N

A

intermediate acting insulin

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7
Q

NPH novolin N

A
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8
Q

insulin detemir

A

long acting insulin

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9
Q

insulin glargine

A

long acting insulin

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10
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
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11
Q

tolazamide

A

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
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12
Q

chlorpropamide

A

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
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13
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
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14
Q

glipizide

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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15
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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16
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
17
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
18
Q

METFORMIN

A

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
19
Q

rosiglitazone

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
20
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
21
Q

exenatide

A

incretin - GLP-1 analogues

22
Q

liraglutide

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
23
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
24
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
25
sitagliptin
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
26
saxagliptin
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
27
inagliptin
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
28
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
29
acarbose
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
30
miglitol
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
31
canagliflozin
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
32
DAPAGLIFLOZIN
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
33
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
34
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
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
bromocriptine
* MOA: we don’t know why this lowers glucose * AE * Nausea, fatigue, dizziness, vomiting and headache * not very effective

IC (32 decks)

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