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DCES exam 2021 > Pharmacotherapy for glucose management > Flashcards

Pharmacotherapy for glucose management Flashcards

1
Q

Drug therapy (in combo with lifestyle modifications) may be considered for all persons with DM with a BMI greater than what?

A

27; bariatric surgery should be considered for persons with DM and BMI > 35

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2
Q

How many classes of orally administered agents are currently FDA approved for obesity management?

A

8 available meds, 3 are considered for short term use (over several weeks) and 5 are considered for long term use

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3
Q

In patients with DM, which medications used to treat obesity are associated with a greater degree of weight loss

A

Phentermine/topiramate and liraglutide (45-70% of pt’s achieve 5% weight loss and 20-50% achieve 10% weight loss)

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4
Q

What is the one GLP-1 inhibitor that is FDA approved for weight loss?

A

Liraglutide, brand name Saxenda

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5
Q

Per the 2020 AACE guidelines, for pt with A1c <7.5%, what are some reasonable alternatives to Metformin?

A

GLP-1 agonists, SGLT inhibitors, DPP-4 inhibitors, and alpha glucosidase inhibitors

Caution with TZDs, SU, or meglitinides

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6
Q

What is a new pharmacologic recommendation added to the AADE algorithim for 2020?`

A

Rec to add a GLP-1 agonist or SGLT2 inhibitor for ppl w/ established ASCVD or at risk risk, CKD, or HFrEF regardless of glycemic control

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7
Q

What pharmacological intervention is rec’d for pt’s with A1c>7.5%

A

Dual or triple drug therapy with Metformin as the base

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8
Q

For pt’s with A1c > 9.0% (plus symptoms), what is the pharmacological intervention?

A

Rec’d to start insulin in addition to other agents

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9
Q

Per the ADA 2020 guideline recommendations, what pharmacological agent should be recommended for a patient with DM in whom ASCVD predominates?

A
  1. Rec a GLP-1 inhibitor

2. Rec a SGLT2 inhibitor (2nd step)

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10
Q

How many classes of oral agents are currently used to treat DM2, and what are they?

A

Sulfonylurea, meglitinides, biguanides, TZDs, alpha glucosidase inhibitors, Dopamine receptor agonists, sodium glucose co transporter 2 inhibitors, Dipeptidyl peptidase inhibitor, bile acid sequestrants

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11
Q

Generally, monotherapy with any of the oral agents used to treat DM1 will decrease A1c by how much?

A

0.5-2.0%. When combo therapy is used (2 or more oral agents or an oral agent combined with insulin), an additive effect is observed

**fixed dose combo products are available, may improve compliance

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12
Q

What is considered first line therapy for a pregnant woman with DM or GDM?

A

Insulin; howeer, metformin or glyburide may also be considered in women unable/unwilling to use insulin

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13
Q

Which oral DM mediations are approved for use in children with DM2 > 10? Which injectable meds are approvide?

A

metformin

liraglutide
insulin

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14
Q

Which medications are Sulfonylureas?

A

Glimeperide, Glipizie, and Glyburide

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15
Q

Why will some pt’s not respond to sulfonylureas?

A

2/2 to disease progression and mechanism of action that puts increased workload on the beta cells

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16
Q

What is the mechanism of action for sulfonylureas?

A

They increase the release of insulin from the pancreas, esp. at the onset of therapy

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17
Q

In which disease(s) should caution be exercised when using a SU?

A

liver disease or renal failure

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18
Q

What are the side effects of SU?

A

Hypoglycemia, weight gain, blurry vision and skin rashes (usually resolve and SU can be cont’d, and mild GI disturbance)

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19
Q

What labs should be monitored prior to starting a SU?

A

Baseline renal and hepatic function; blood glucose should also be self monitored daily, usually preprandial and/or at bedtime (determine by goals of therapy and concomitant meds)

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20
Q

When should SUs be taken?

A

~30 mins before a meal

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21
Q

Which medications are Meglitinides?

A

Nateglinide and Rapaglinide

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22
Q

What is the mechanism of action for Meglitinides?

A

They increase insulin secretion from the pancreas; similar to SUs although there duration of action is very short. Often used in combo w/ other oral agents

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23
Q

True or false: adding Meglitinides to concurrent SU therapy offers no benefit

A

True; Meglitinides should not be used in pt’s with DM who previously experienced primary or secondary failure w/ SU

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24
Q

What are the side effects associated with Meglitinides?

A

Hypoglycemia (both repaglinide and nateglinide, though mild in nateglinide) upper respiratory infection (repaglinide) congestion problems (repaglinide), and back pain (repaglinide)

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25
Q

When should blood glucose monitoring be rec’d for to assess the effectiveness of a meglitinide?

A

pre and post meal

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26
Q

SU may enhance sensitivity to what?

A

Sunlight

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27
Q

True or false: Biguanides are considered hypoglycemic agents

A

False;, their major pharmacologic action does not increase insulin secretions and thus does not increase risk of hypoglycemia

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28
Q

Why is metformin considered a first line agent for patient’s with DM2?

A

Due to its efficacy, CVD benefit, and relatively low cost

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29
Q

What is Metformin’s mechanism of action?

A

Decreases hepatic glucose production through reduced gluconeogenesis and decreased intestinal absorption of glucose–> improves insulin sensitivy in skeletal muscle

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30
Q

True or false: Food decreases the bioavailability of Metformin

A

True

31
Q

When should patients with DM be instructed to take Metformin?

A

Just prior to a meal

32
Q

What is the max dose for Metformin for adults?

A

2550 mg/day, but the max effective dose is achieved w/ 2000 mg/day

33
Q

When should Metformin be held?

A

In acute illness or any situation that would predispose pt to acute renal dysfunction or tissue hypoperfusion (MI, CHF, use of iodinated contrast media, and major surgical procedures)

34
Q

When is Metformin contraindicated?

A

In GFR <30 mL/min and not recommended for those with GFR between 30-45 mL/min (Metformin is excreted by the kidneys)

35
Q

The presence of hepatic dysfunction can predispose a pt with DM to what?

A

Lactic acidosis (b/c lactate metabolism is carried out by the liver). Pt’s with h/o severe or decompensated hypoxic conditions are also not good candidates d/t potential for lactate accumulation, also contraindicated in alcoholism/binge drinking

36
Q

What are some positive “side effects” of Metformin?

A

Slight wt loss (2-5 kg), reduced TG (16%), reduced LDL-C (8%), and total cholesterol (5%). Also increases HDL-C by 2%.

37
Q

What are some “negative” side effects of Metformin and how are they minimized?

A

GI effects (nausea, bloating, cramping, fullness, diarrhea), metallic taste in mouth. To minimize side effects, pts with DM should start at low dose and slowly titrate upward. May also consider taking w/ food or switching from IR to ER formulation

38
Q

What deficiency is associated with Metformin?

A

Vit B12 (may contribute to anemia or neuropathic symptoms)

39
Q

What should be checked prior to initiation of metformin?

A

GFR (prior and periodically during therapy), esp for those w/ renal function or > 80 years

40
Q

How should a person with DM be instructed to take Metformin?

A

With meals to reduce GI side effects. Should be informed a metallic taste may be present but will subside in time

41
Q

What is the mechanism of action for TZDs?

A

Results in improved insulin sensitivity of peripheral muscle, adipose, and hepatic cells

42
Q

True or false: TZDs should be taken with food

A

False; TZDs may be taken with or without food

43
Q

How much time is needed to assess the full effect of TZDs?

A

8-12 weeks

44
Q

In which cases are TZDs contraindicated?

A

Persons w/ DM with NYHA class III and IV HF and active liver disease

45
Q

What risks are associated with TZDs?

A

Increased risk of fracture in women, macular edema, and bladder CA (pioglitazone).

TZDs should also be used w/ caution in ppl with hepatic dysfunction

46
Q

True or false: Rosiglitazone increases the risk of MI by 30-40%

A

False; the FDA eliminated the REMS program for rosiglitazone in 2015 suggesting no increased CV risk of rosiglizaone compared with metformin or SU

47
Q

What should be monitored for patients on TZDs?

A

Serum transaminase levels should be monitored prior to starting therapy and periodically thereafter per the clinical judgement of the healthcare provider

48
Q

Both rosiglitazone and pioglitazone retain FDA approved labeling for what?

A

Monotherapy or in combo with other agents to treat DM2

49
Q

Alpha glucosidase inhibitors are most effective at lowering what?

A

Post prandial hyperglycemia

50
Q

What is the mechanism of action for Alpha glucosidase inhibitors?

A

Inhibit alpha glucosidase enzymes in the brush border of the small intestine and pancreatic alpha amylase, leading to reduction in CHO mediated post prandial blood glucose elevation

51
Q

How should alpha glucosidase inhibitors be taken?

A

With the first bite of a meal

52
Q

How should hypoglycemia be managed for a person taking alpha glucosidase inhibitors?

A

with oral glucose or IV glucose or glucagon; alpha glucosidase inhibitors blunt the digestion & conversion of complex sugars to glucose

53
Q

What should be monitored for a patient taking alpha glucosidase inhibitors?

A

serum transaminases (esp for those on acarbose)

54
Q

What are the contraindications to taking alpha glucosidase inibitors?

A

Pt’s with DM and IBD, colonic ulceration, obstructive bowel disorders, or chronic intestinal disorders of digestion or absorption

55
Q

What are the side effects of alpha glucosidase inhibitors?

A

Abd pain, diarrhea, and gas (occur primarily at the beginning of therapy; can be minimized by starting w/ a low dose and titrating upwards slowly)

56
Q

When should BG be monitored for a patient using an alpha glucosidase inhibitor to see if it is effective?

A

2 hour post prandial glucose measurement

57
Q

How should a pt with DM be instructed to take acarbose?

A

With the first bite of a meal or large snack; should be encouraged to maintain physical movement after eating to limit buildup of gas from fermenting CHO, as drug limits CHO absorption

58
Q

What medication is a dopamine receptor agonist?

A

Bromocriptine mesylate

59
Q

What is the mechanism of action for a dopamine receptor agonist?

A

Unkown; following morning administration of bromocriptine mesylate, postprandial glucose levels improve without increasing plasma insulin concentrations

60
Q

What are the contraindications to a dopamine receptor agonist?

A

DM1, DKA, syncopal migraines, psychotic disorders , concomitatn use w/ other dopamine receptor agonists (for treatment of Parkinsons, RLS, acromeagly, etc)

61
Q

What are the side effects associated with bromocriptine?

A

Somnolence, nausea, fatigue, dizziness, vomiting, and HA

62
Q

When should blood glucose moniotring be done for pt’s on bromocriptine?

A

pre and postmeal readings to assess the effectiveness

63
Q

How should a pt with DM be instructed to take bromocriptine?

A

2 hours after waking with the first meal of the day

64
Q

When are SGLT2 inhibitors typically used?

A

As glycemic lowering agents for DM patients as well as used for CV protection and renal protection based on recent evidence

65
Q

What is the mechanism of action for SGLT2 inhibitors?

A

Result in increased excretion of glucose in the urine resulting in lower plasma glucose and potentially less kcals for fat accumulation

66
Q

In which case does the 2020 ADA standards of care recommend SGLT2 inhibitors?

A

For persons with DM, especially if HF or CKD predominates

67
Q

True or false: If injectable therapy is needed to reduce A1c, consider GLP1 RA in most patient prior to starting insulin

A

True

68
Q

When adding basal insulin if glucose is above target for pt with DM2, what are the recommended guidelines?

A

Initiation: Start 10 U/day or 0.1- 0.2 u/kg/day

Choose evidence based titration algorithim (i.e. increase by 2 units every 3 days to reach target w/o hypo)

69
Q

when titrating basal insulin, if hypoglycemia w/out clear reason, by how much should basal insulin be reduced?

A

10-20%

70
Q

When should overbasalization be suspected in DM2?

A

when basal dose >0.5 units/kg, elevated bedtime-morning and/or post-preprandial differential, hypoglycemia (aware or unaware), high variability

71
Q

For pt’s with DM1 who are metabolically stable, what may be used as a typical starting dose to determine TDD?

A

0.5 units/kg/day (50% given as basal, 50% given as prandial)

Typical doses range from 0.4-1.0 g/kg/day, with higher amounts required during pregnancy, puberty, and/or medical illenss

72
Q

After basal therapy has been maximized, if A1c still above target, what type of insulin should be considered?

A

Prandial; usually one dose w/ largest meal

Initiate at 4 units/day or 10% basal dose If A1c <8%, consider lowering basal dose by 4 IU/day or 10%)

Titrate by increase dose by 1-2 units or 10-15% twice weekly

For hypo w/ no clear reason lower corresponding dose by 10-20%

73
Q

After ____ months if A1c target is not achieved, Metformin can (and should) be combined with another treatment option

A

three months

DCES exam 2021 (35 decks)

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