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Pharmacology Exam 5 > Oral Anti-diabetic agents > Flashcards

Oral Anti-diabetic agents Flashcards

1
Q

MOA: enhances secretion of insulin by beta cells, decreases glucagon production, and increases tissue sensitivity to insulinGlimepiride (sulfonylurea)

A

Glimepiride (sulfonylurea)

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2
Q

How does glimepiride increase the secretion of insulin from beta cells?

A

By blocking the same ATP-sensitive K+ channels that are blocked by ATP when endogenous glucose is high

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3
Q

Administered once-daily with ER formulation or 30 minutes before meals
Metabolized by liver AND kidneys
Contraindication in patients with liver or kidney disease

A

Glimepiride (sulfonyurea)

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4
Q

AEs: hypoglycemia, esp. when given with insulin (not as bad as earlier formulations)
Weight gain
GI/skin/liver/blood abnormalities

A

Glimepiride (sulfonylurea)

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5
Q

Similar mechanism as for SUs, but lower effect
Faster, but shorter action than SUs
Perhaps safer in kidney disease

A

Meglitinides

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6
Q

MOA: targets AMP kinase, a critical regulator of glucose metabolism

A

Metformin (biguanide, additional liver enzyme targets are being identified or implicated)

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7
Q

MOA: effects primarily in the LIVER, decreases glucose production, increases glucose uptake, so makes insulin work better

A

Metformin (biguanide)

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8
Q

T/F: Metformin cannot be used with sulfonylureas, due to the risk of hypoglycemia

A

False. Different MOAs and metformin does not cause hypoglycemia

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9
Q

Administered once-daily with ER formulation or 2-4 times per day after meals
Renal excretion without metabolism (concerns with moderate-severe kidney disease)

A

Metformin (biguanide)

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10
Q 
AEs: does not cause hypoglycemia or weight gain
Lactic acidosis
GI effects (metallic taste, diarrhea, nausea, vomiting, anorexia)
A

Metformin (biguanide)

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11
Q

This potentially serious side effect from this drug is more common in patients with impaired renal function, excessive alcohol intake, and/or increased hypoxemic conditions.

A

What is lactic acidosis from metformin (biguanide)?

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12
Q

Microbial sugars that inhibit sugar metabolizing enzymes, like a-glucosidase and amylase, in the gut

A

Acarbose

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13
Q

MOA: slow formation and absorption of glucose in the gut, by inhibiting hydrolysis of disaccharides and complex carbohydrates

A

Acarbose

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14
Q

Poorly absorbed, remains in the gut

Not a powerful drug. Mainly used in mild disease or with other agents.

A

Acarbose (decrease glucose formation in the gut)

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15
Q

Do not cause hypoglycemia ON THEIR OWN, but with insulin or other oral agents, can increase hypoglycemia risk

A

Acarbose

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16
Q

What do you give someone on acarbose who is hypoglycemic?

A

Glucose (NOT SUCROSE, or other di+saccharides)

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17
Q

AEs: flatulence, cramps, diarrhea that diminish with time and are additive with another agent with similar side effects
Limited use in the US because of all the farting

A

Acarbose (additive with metformin)

18
Q

MOA: binds and activates peroxisome proliferator-activated receptor-y (PPAR-y), a nuclear transcription factor receptor that enhances transcription of insulin-responsive genes

A

Pioglitazone, rosiglitazone (thiazolidinediones, TZDs)

19
Q

Effects: decreases gluconeogenesis, glucose output, and triglyceride synthesis is LIVER
Increases glucose uptake and utilization in MUSCLE
Increases glucose uptake and decreases fatty acid production in ADIPOCYTES

A

Pioglitazone, rosiglitazone (TZDs)

20
Q

Used for Type 2 insulin resistance
Best taken with food one time daily
Metabolized in liver (safe with renal disease)

A

Pioglitazone, rosiglitazone

21
Q

AEs: hepatotoxicity and fatal liver disease
CVD/death risk
May increase bladder cancer risk
Increase fracture risk

A

Pioglitazone, rosiglitazone

22
Q

AEs: dose-dependent edema, increase in CHF, myocardial ischemia, angina, and myocardial infarction
Similar for all agents in this class

A

Pioglitazone, rosiglitazone (had a BBW for over a year, but was removed)

23
Q 
Metformin + sulfonylureas
A. Decreased uptake + increased insulin effects
B. Proven efficacy, different mechanisms
C. Effects not well documented
D. Additive GI side effects
A

B. Proven efficacy, different mechanisms

24
Q

Metformin + meglitinides
A. Decreased uptake + increased insulin effects
B. Proven efficacy, different mechanisms
C. Effects not well documented
D. For fasting hyperglycemia + for post-prandial sugar

A

D. For fasting hyperglycemia + for post-prandial sugar

25
Q

Metformin + thiazolidinediones
A. Decreased uptake + increased insulin effects
B. Useful synergy for reducing insulin resistance
C. Effects not well documented
D. Additive GI side effects

A

B. Useful synergy for reducing insulin resistance

26
Q

Acarbose + SUs
A. Decreased uptake + increased insulin effects
B. Useful synergy for reducing insulin resistance
C. Effects not well documented
D. Additive GI side effects

A

A. Decreased uptake + increased insulin effects

27
Q

Thiazolidinediones + SUs or meglitinides
A. Decreased uptake + increased insulin effects
B. Useful synergy for reducing insulin resistance
C. Effects not well documented
D. Additive GI side effects

A

C. Effects not well documented

28
Q

Analog of gut peptide glucagon-like peptide-1, an “incretin” release in response to food

A

Exenatide (GLP-1 agonists, Bydureon)

29
Q

Effects:

Potentiates insulin SECRETION, decreases glucagon, slows gastric emptying, promotes satiety

A

Exenatide (GLP-1 agonists, Bydureon)

30
Q

Induces moderate reductions in fasting glucose but marked reductions in post-prandial glucose
Does not cause weight gain…often causes weight loss!

A

Exenatide (GLP-1 agonists, Bydureon)

31
Q

Exenatide (GLP-1 agonists, Bydureon)

A

Exenatide (GLP-1 agonists, Bydureon)

32
Q

Exenatide cousin approved for weight loss

A

Liraglutide (Victoza)

33
Q

ADEs: nausea
Increased risk of hypoglycemia, esp. with SUs
Avoid in renal failure

A

Exenatide (GLP-1 agonists)

34
Q

ADEs: alters absorption of some antibiotics and contraceptives, take 1 hour before
Thyroid tumors
Pancreatitis

A

Exenatide (GLP-1 agonists)

35
Q

MOA: inhibits dipeptidyl-peptidase IV, the enzyme that degrades endogenous incretins (like GLP-1)

A

Sitagliptin (Januvia, DDP-IV inhibitors)

36
Q

Effects- through increasing ENDOGENOUS incretins

Potentiates insulin SECRETION, decreases glucagon, no obvious weight gain or loss

A

Sitagliptin (Januvia, DPP-IV inhibitors)

37
Q

Orally effective in once per day monotherapy or in combination
Risk of severe joint pain
Heart failure risk, but only with certain drugs in the class

A

Sitagliptan (Januvia, DPP-IV inhibitors)

38
Q

ADEs: increased hypoglycemia risk when used in combo
Increased risk of respiratory tract infections
Renal elimination is a concern in some patients

A

Sitagliptin (Januvia, DPP-IV inhibitors)

39
Q

MOA: inhibits sodium-glucose co-transporter 2 (SGLT2), the enzyme that mediates glucose re-absorption in the kidney
Increases urinary glucose excretion

A

Canagliflozin (Invokana)

40
Q

Orally effectives, one time daily dosing, usually in the AM
No effects directly on insulin
Concerns about renal injury (with at least some agents)

A

Cangliflozin (Invokana, SLGT2 inhibitors)

41
Q

ADEs: increased risk of genital and urinary tract infections
Diuretic effect can cause dehydration, hypovolemia, hypotension (esp. in elderly and those on diuretics)
Fracture risk warning

A

Cangliflozin (Invokana, SLGT2 inhibitors)

Pharmacology Exam 5 (8 decks)

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