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IC > Treatment of diabetes > Flashcards

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
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
26
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
27
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
28
Q

alogliptin

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
29
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
30
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
31
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
32
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
33
Q

EMPAGLIFLOZIN

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
34
Q

PRAMLINTIDE

A
  • 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
Q

COVESEVALAM

A
  • 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
Q

bromocriptine

A
  • 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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