Diabetes (Slide Deck 4) Flashcards

1
Q

What does metformin do?

A
  • ↓’s hepatic glucose production
  • Can also enhance sensitivity to insulin
  • Increases glucose utilization via action in the gut
  • Has effects on the gut microbiome which may explain some anti- inflammatory effects
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2
Q

What is the typical dose of metformin?

A

Start at 250-500 then work to 850-1000mg (Titrating dose decreases the side effect profile)

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3
Q

By how much does the A1C decrease typically decrease on Metformin?

A

1-1.5%

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4
Q

What is a common AE with metformin?

A

Diarrhea and GI discomfort

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5
Q

How can the side effects of metformin be avoided?

A

Titrating doses, Take with food, Extended release version

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6
Q

What are the precautions when taking metformin?

A

Lactic Acidosis which decreases arterial PH and accumulation of serum lactate

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7
Q

What ClCr is used for metformin decrease

A

Less then 60ml/min

45-59=1500mg/day
30-44 1000mg/day

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8
Q

What happens if someoen has a ClCr of <30ml/min and is on metformin

A

Can continue 500mg OD but should not start but can continue the dose

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9
Q

What is the MOA of Sulfonylureas

A

Enhance insulin secretion by binding to Su receptors on beta cells of the pancreas

This leads to K+ closing and opening of CC stimulating insulin secretion

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10
Q

What are the three 2nd generation sulfonylureas?

A

glyburide, gliclazide, glimepiride

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11
Q

How much A1C decrease do we see with Sulfonylureas usage?

A

1-1.5%

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12
Q

What are the adverse effects of Sulfonylureas usage?

A

Hypoglycemia and weight gain

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13
Q

Which of the sulfonylureas can you use during pregnancy?

A

glyburide

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14
Q

Which contraindications are present for sulfonylureas?

A

CI in hepatic and renal impairment
Hold in acute ilness

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15
Q

What are some common DI with sulfonylureas?

A

Sulfonamides
Alcohol

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16
Q

What is the MOA of Meglitinides?

A

Binds to a site adjacent to the SU receptor, resulting in stimulation of the secretion of insulin from the pancreas

Similar to SUs but have a faster onset and shorter D of A * Peak levels within 1 hour and half-life is 1 hour

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17
Q

What is the medication that falls under meglitinides?

A

Repaglinide

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18
Q

How much A1C decrease does repaglinide cause?

A

1 to 1.5

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19
Q

What adverse effects are associated with repaglinide?

A

Hypoglycemia and weight gain

20
Q

What precautions must be taken when on repaglinide?

A

Cyp 3A4 inhibitors (Increases concentration) grapefruit juice is the biggest one

21
Q

Alpha-Glucosidase Inhibitors MOA?

A
  • α-Glucosidase enzymes in the small intestine are responsible for the breakdown of polysaccharides into absorbable glucose
  • Acarbose inhibits these enzymes, hence there is a delay in the rate of digestion of CHO’s and glucose absorption

Net effect is reduction in PPG levels

22
Q

What level of A1C decreasing doe we see on Alpha-Glucosidase Inhibitors?

A

0.5%-0.8%

23
Q

What is a common Alpha-Glucosidase Inhibitors

A

Acarbose

24
Q

What are some adverse effects of Acarbose?

A

GI Flatulence and diarrhea

25
Q

What is cautioned with taking acarbose?

A

IBD and Gi conditions

eGFR <25ml/min and severe liver disease

26
Q

What is a common Alpha-Glucosidase Inhibitors?

A

Acarbose

27
Q

What is a common Alpha-Glucosidase Inhibitors?

A

Acarbose

28
Q

What are the thiazolidinediones drugs

A

Rosiglitazone and Pioglitazone

29
Q

What are the MOA thiazolidinediones drugs

A

Bind to PPAR-γ receptors which are primarily found in adipose tissue. Activation alters genes that influence glucose and lipid metabolism.

Which enhances insulin sensitivity at muscle liver and fat tissues

30
Q

What are the clinical effects of Thiazolidiendiones

A

Enhance insulin sensitivity at muscle, liver, and fat tissues.

Decrease insulin resistance

Decrease hepatic glucose production

31
Q

What is the typical decrease in A1C level when on Thiazolidinediones?

A

1-1.5%

32
Q

What are the adverse effects of Thiazolidinediones

A

Peripheral edema (~5%); combined with insulin (~15%)

Weight gain

New onset of worsening of HF

Increase in distal fractures in postmenopausal women

33
Q

What is the concern with TZDs and what did it cause?

A

Cardiovascular Effects,

Hence all new Diabetes drugs require cardiovascular trials to back it up

34
Q

What are the Incretin Based therapies targets?

A

GLP-1 DPP4 and GIP

35
Q

What are the GLP-1 receptor agonists drugs

A
  • Exenatide (Byetta®)
  • Liraglutide (Victoza®) ®
  • Dulaglutide (Trulicity®)
  • Exenatide weekly (Bydureon®)
  • Lixisenatide (Adlyxine®)
  • Semaglutide (Ozempic® SC), and Rybelsus® oral)
36
Q

What are the DPP-4 inhibitors?

A
  • Linagliptin (Trajenta®)
  • Sitagliptin (Januvia®)
  • Saxagliptin (Onglyza®)
  • Alogliptin (Nesina®)
37
Q

What are the effects of activating GLP-1

A

Increase insulin secretion, decrease glucagon, slow gastric emptying and increase satiety

38
Q

What does DPP-4i do?

A

Inhibits DPP-4 which stops the cleaving GLP-1

39
Q

How much does DPP4 inhibitors decrease A1C?

A

0.7, but typically less then 1

40
Q

What are some adverse effects and precautions of taking DPP4I

A

headaches Nasopharyngitis and URTI

41
Q

Are DPP5 inhibitors CV safe?

A

yes! but not proven or shown to be cardioprotective

42
Q

What are DPP4i typically good for?

A

Elderly and for individuals who do not have large A1C lowering targets

43
Q

What is the GLP1RA MOA?

A

Stimulates insulin secretion in a glucose-dependent manner, decreases glucagon, slows gastric emptying, increases satiety

44
Q

What is the GLP1RAs A1C lowering abilities

A

1-1.5%

45
Q

What are the general AE of GLP1RA?

A

N/V/D, but will resolve in 4-8 weeks

Weight loss due to medication not N/V/D

46
Q

What are the drug interactions of GLP1RA

A

Oral Contraceptives
Antibiotics
Narrow TI drugs
Levothyroxine

47
Q

What renal measurement should Repaglinide be cautioned with?

A

<30ml/min