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DCES exam 2021 > Pharmacotherapy for glucose management-2 > Flashcards

Pharmacotherapy for glucose management-2 Flashcards

1
Q

What do SGLT inhibitors increase the risk of?

A

euglycemic ketoacidosis (DKA with BG <300 mg/dl)

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2
Q

Canagliflozin may cause what in pt’s with DM and decreased kidney function?

A

Hyperkalemia

Also may cause increased risk of bone fracture and/or lower limb amputation

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3
Q

what are the contraindications for taking SGLT inhibitors?

A

Persons with DM with severe kidney disease (<30 mL/min) or on HD should not use these agents

hypotension, mycotic infection, UTIs, and renal insufficiency

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4
Q

What should be monitored for patients on SGLT inhibitors?

A

Routine A1c monitoring in addition to K+ and LDL-C monitoring. BP and symptoms of mycotic infection should also be checked

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5
Q

What medication is a bile acid sequestrant?

A

Colesvelam

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6
Q

What is the mechanism of action for Colesevelam?

A

In regards to glucose control, mechanism of action is poorly understood; binds to bile acids in intestine, thus impeding their reabsorption

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7
Q

In which patient’s should colesevelam be contraindicated?

A

In persons with DM with TG > 500 mg/dL, PMH of pancreatitis due to elevated TG levels or bile obstruction

May also cause constipation, use in caution in pt’s with gastroparesis or motility disorders

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8
Q

What should be monitored throughout therapy for a patient on colesevelam?

A

Triglycerides

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9
Q

What is a drug interaction to consider for pt’s on colesevelam?

A

Fat soluble vitamins; should take at least 4 hours apart. May also decrease absorption of warfarin, phenytoin, levothyroxine, and birth control pills

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10
Q

What time frame should a pt with DM expect to see some glycemic lowering while taking colesevelam?

A

4-6 weeks, with max effect seen in 12-18 weeks

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11
Q

How to GLP-1 receptor agonists affect plasma glucose?

A
  1. promotion of satiety
  2. decreased/slowed gastric emptying rate
  3. increased glucose dependent insulin release from beta cells
  4. decreased glucagon relase from pancreatic alpha cells
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12
Q

Glucagon like peptide-1 receptor agonists are used as glycemic lowering agents in ppl with DM2 as well as used for ____ benefits based on recent evidence

A

CVD

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13
Q

What is the mechanism of action for a GLP-1 agonist?

A

These agents bind to and activate GLP-1 receptors, resulting in drop in fasting an postprandial glucose concentrations

Improve glycemic control through several mechanisms: increased insulin synthesis and secretion in the presence of elevated glucose concentrations, improvement of first phase insulin response, reduced glucagon concentration during hyperglycemic swings, slowed gastric emptying and reduced food intake

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14
Q

Which of GLP one agonists is NOT approved for the management of DM (approved for weight reduction only)

A

Liraglutide; this agent is only approved for weight reduction

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15
Q

Which GLP-1 agonists are dosed daily?

A

liraglutide, lixisenatide, and exenatide

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16
Q

Which of the three GLP-1 agonists is dosed weekly?

A

exenatide ER, dulaglutide, and semaglutide

weekly agents are dosed without regards to meals

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17
Q

Which GLP agonists is a synthetic form of a protein found in the saliva of the Gila monster?

A

Exenatide

18
Q

True or false: concurrent use of insulin, metformin, SU or a combo with GLP-1 is NOT recommended

A

False

19
Q

How are all GLP-1 RA administred?

A

By subq infection in the thigh, upper arm, or abd

20
Q

When should GLP-1 RA be administred?

A

With the exception of exanatide IR and lixisenatide, all agents can be administered any time of day, w/o regard to meals

Exenatide IR should be administered anytime w/in the 60 mins before morning and evening meals and should not be given after meal. Lixisenatide should be administered w/in 1 hour before the fist meal of the day

21
Q

GLP-1 RAs have been shown to increase risk of what?

A

Acute pancreatitis; alternate agents should be considered for a pt with DM and /ho pancreatitis

exenatide and lixisenatide should be avoided in persons with severe renal impairment or ESRD

22
Q

What are the drug interactions associated with GLP-1 RAs?

A

D/t ability of GLP-1 RA to slow gastric emptying, extent and absorption rate of orally administered drugs should be considered; drugs with narrow therapeutic indices should be carefully monitored (warfarin, digoxin, oral contraceptives, statins)

Consider taking med at least 1 hr before injection, esp with exenatide IR and lixisenatide

23
Q

What are the contraindications for GLP-1 RAs?

A

DM2, ketoacidosis, personal or family h/o medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, pancreatitis

24
Q

What are the side effects associated with GLP-1 RA?

A

N/V/C, dyspepsia, HA

Nausea more common w/ shorter acting agents, severity may decrease as treatment continues

25
Q

What should be monitored for pt’s on GLP-1 RAs?

A

Antibody formation (may reduce effectiveness of drug)

S/s of pancreatitis should also be monitored

Risk of thyroid tumors should be discussed

26
Q

What is the mechanism of action for DPP-4 inhibitors?

A

by competitive inhibition of the enzyme responsible for GLP-1 inactivation, thus prolonging the effects of endogenous GLP-1

Increased insulin synthesis and secretion, reduced glucagon concentration, slows gastric emptying, reduces food intake

27
Q

What is the main advantage of GPP-4 inhibitors compared to GLP-1 RA?

A

Oral formulation; however, DPP-4i produce less weight loss and less glycemic lowering than GLP-1 RAs

28
Q

How are DPP-4i dosed in regards to meals?

A

Once daily, with or without food

With the exception of linagliptin, doses of these agents should be reduced in the presence of renal dysfunction

29
Q

What medical conditions should use precaution w/ DPP-4i?

A

Pancreatitis, hypersensitivity reactions, CHF (alogliptin, saxagliptin), joint pain that can be disabling

30
Q

What are the side effects associated with DPP-4i?

A

Upper resp tract infection and HA, UTI infections (saxagliptin), occurrence of peripheral edema (saxagliptin)

31
Q

What should be monitored for pt’s taking GPP4-i?

A

kidney function (creatinine), s/s of pancreatitis, baseline liver function

32
Q

What medication is an Amylin analog?

A

Pramlintide (symlin)

33
Q

What is the mechanism of action for Pramlintide?

A

Slows gastric emptying, surpasses glucagon secretion and reduces total caloric intake

34
Q

True or false: Parmlintide can be used for both type 1 and type 2 DM

A

True

35
Q

How is Pramlintide administer?

A

Subq just before major meals (at least 250 kcals and 30 g CHO)

36
Q

What are the contraindications to pramlintide?

A

Gastroparesis, pt’s taking drugs for antimotility disorders. Can slow absorption of orally administered meds

37
Q

True or false: Pramlinitide can be mixed with insulin

A

False; pramlintide and insulin should be administered separately

38
Q

When taking Pramlinitde, it is recommended to reduce mealtime insulin by how much to avoid hypoglycemia?

A

~50% (depending on pt’s overall glucose control)

39
Q

What are the side effects associated w/ Pramlintide?

A

Nausea (most common), anorexia, vomiting, fatigue, and HA

40
Q

When taking Pramlintide, meds that demand prompt/rapid onset of action should be taken __ hour(s) before or ___ hour(s) after pramlintide dose?

A

1 hour before; 2 hours after

41
Q

How should Pramlintide be stored?

A

Can be refrigerated or vial in use can be stored at room temp of <77 . Opened vials must be used w/in 28 days.

42
Q

Where should Pramlintide be administered in the body?

A

Subq into abd or thigh sites distinctly different from concomitatn insulin injections. Should NOT be administered in upper arm d/t variable absorption

DCES exam 2021 (35 decks)

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