Oral Medications in Diabetes Flashcards

1
Q

T/F all glucose lowering agents are only used for t2d

A

T

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2
Q

T/F all glucose lowering agents are contraindicated in pregnancy

A

F –> all except sulfonylurea and metformin

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3
Q

T/F all glucose lowering agents can be used in any combination

A

F –> any combination except sulfonylurea and meglitinides should not be mixed

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4
Q

T2D first drug of choice

A

metformin

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5
Q

Metformin/diguanide action and mechanism

A

activation of ampk –>

  1. increase muscle glucose tranport
  2. reduces hepatic glucose production
  3. sensitizes insulin (via reduced ACC and SREBP expression and consequent reduced hepatic FA production)

–>improves pre meal glucose and modestly affects post-prandial glucose

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6
Q

Thiazolidinendiones (TZD)/PPARgamma agonists MOA/Action

A

binds nuclear ppar gamma receptor –> increases GLUT4 transporter–> decreases peripheral insulin resistance in skeletal muscle, adipose, liver –> lowers premeal/post meal glucose

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7
Q

Insulin secretagogues

A

Induce beta cell secretion of insulin (short and long acting) –> suflonylureas and meglitinides

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8
Q

alpha glucosidase inhibitors MOA/action

A

competitively inhibit enzymes in brush border to breakdown carbohydrates –> delay carbohydrate absorption in gut –> reduce post prandial glucose only

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9
Q

GLP1 agonist

A

slows gut motility, induces satiety, increased insulin/lower glucagon

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10
Q

Incretin enhancers (DPP-4 inhibitors)

A

increase duration of action of GLP1 via 80% inhibition of DPP4 –> mostly on post-meal glucose

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11
Q

Advantageous characteristics of a good drug for t2d

A

weight loss/neutral, no hypoglycemia, oral, frequency of delivery

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12
Q

Disadvantageous characteristics of a good drug for t2d

A

weight gain (reversal of osmotic diuresis, reversal of relative starvation/normalization, fluid retention), hypoglycemia, frequency of delivery, injectable

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13
Q

T/F metformin is weight neutral and can induce weight loss

A

T

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14
Q

T/F metformin is metabolized at the liver

A

F –> renally excreted unexchanged and can accumulate if pt has renal insufficiency

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15
Q

Adverse effects of metformin

A

anorexia, nausea, diarrhea, lactic acidosis

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16
Q

T/F metformin does not cause hypoglycemia

A

T

17
Q

Contraindications of metformin

A

prone to metabolic acidosis, hypoxic states, renal failure, t1d, cardiac ischemia

18
Q

T/F metformin requires presence of insulin for its action

A

T

19
Q

Sulfonylurea action and MOA

A

binds to sulfonyl receptor in beta cell –> depolarization of ATP K channels –> pancreatic insulin secretion for 12-24 hours –> mostly premeal glucose effect

20
Q

T/F Sulfonylurea does not get metabolised

A

F –> hepatic and excreted in kidney

21
Q

Contraindications of sulfonylurea

A

T1d, DKA, sulfa allergy

22
Q

Adverse effects of sulfonylurea

A

hypoglycemia, weight gain, hunger

23
Q

K+ channel in the beta cell

A

induces calcium current which causes insulin release –> sulfonylurea and meglitinide binding sites

24
Q

Meglitinide action/MOA

A

stimualtes K+ channel on beta cells –> pancreatic insulin for 3-4 hours

25
Q

T/F Meglitinide is fast onset

A

T

26
Q

Adverse effects of meglitinide

A

low glucose after meal, weight gain

27
Q

Contraindications of meglitinide

A

T1d, liver failure, DKA, sulfa allergy

28
Q

T/F meglitinide is metabolized in the kidney

A

F –> in liver by p450 –> excreted mostly in GI tract

29
Q

Adverse effects of TZD

A

weight gain, hepatocellular injury

30
Q

Contraindications of TZD

A

active liver disease, heart failure, renal insufficiency

31
Q

T/F TZD has slow onset of action

A

T

32
Q

T/F TZD can induce low blood glucose

A

F –> no insulin secretory effect

33
Q

Adverse effects of alpha glucosidase inhibitors

A

flatulence, abdominal bloating

34
Q

T/F alpha glucosidase inhibitors are metabolized in the liver

A

F–> renally excreted unchanged

35
Q

T/F alpha glucosidase inhibitors can cause low glucose

A

F

36
Q

Metabolism of GLP agonists

A

rapidly degraded by DPP4 in blood

37
Q

SGLT2

A

major transporter of glucose in kidney, low affinity/high capacity- -> 90 % of renal glucose reabsorption in proximal tubule

38
Q

SGLT2 inhibitors

A

inhibit reabsorption of glucose –> excretion by kidney