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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
When should blood glucose monitoring be rec'd for to assess the effectiveness of a meglitinide?
pre and post meal
26
SU may enhance sensitivity to what?
Sunlight
27
True or false: Biguanides are considered hypoglycemic agents
False;, their major pharmacologic action does not increase insulin secretions and thus does not increase risk of hypoglycemia
28
Why is metformin considered a first line agent for patient's with DM2?
Due to its efficacy, CVD benefit, and relatively low cost
29
What is Metformin's mechanism of action?
Decreases hepatic glucose production through reduced gluconeogenesis and decreased intestinal absorption of glucose--> improves insulin sensitivy in skeletal muscle
30
True or false: Food decreases the bioavailability of Metformin
True
31
When should patients with DM be instructed to take Metformin?
Just prior to a meal
32
What is the max dose for Metformin for adults?
2550 mg/day, but the max effective dose is achieved w/ 2000 mg/day
33
When should Metformin be held?
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
When is Metformin contraindicated?
In GFR <30 mL/min and not recommended for those with GFR between 30-45 mL/min (Metformin is excreted by the kidneys)
35
The presence of hepatic dysfunction can predispose a pt with DM to what?
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
What are some positive "side effects" of Metformin?
Slight wt loss (2-5 kg), reduced TG (16%), reduced LDL-C (8%), and total cholesterol (5%). Also increases HDL-C by 2%.
37
What are some "negative" side effects of Metformin and how are they minimized?
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
What deficiency is associated with Metformin?
Vit B12 (may contribute to anemia or neuropathic symptoms)
39
What should be checked prior to initiation of metformin?
GFR (prior and periodically during therapy), esp for those w/ renal function or > 80 years
40
How should a person with DM be instructed to take Metformin?
With meals to reduce GI side effects. Should be informed a metallic taste may be present but will subside in time
41
What is the mechanism of action for TZDs?
Results in improved insulin sensitivity of peripheral muscle, adipose, and hepatic cells
42
True or false: TZDs should be taken with food
False; TZDs may be taken with or without food
43
How much time is needed to assess the full effect of TZDs?
8-12 weeks
44
In which cases are TZDs contraindicated?
Persons w/ DM with NYHA class III and IV HF and active liver disease
45
What risks are associated with TZDs?
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
True or false: Rosiglitazone increases the risk of MI by 30-40%
False; the FDA eliminated the REMS program for rosiglitazone in 2015 suggesting no increased CV risk of rosiglizaone compared with metformin or SU
47
What should be monitored for patients on TZDs?
Serum transaminase levels should be monitored prior to starting therapy and periodically thereafter per the clinical judgement of the healthcare provider
48
Both rosiglitazone and pioglitazone retain FDA approved labeling for what?
Monotherapy or in combo with other agents to treat DM2
49
Alpha glucosidase inhibitors are most effective at lowering what?
Post prandial hyperglycemia
50
What is the mechanism of action for Alpha glucosidase inhibitors?
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
How should alpha glucosidase inhibitors be taken?
With the first bite of a meal
52
How should hypoglycemia be managed for a person taking alpha glucosidase inhibitors?
with oral glucose or IV glucose or glucagon; alpha glucosidase inhibitors blunt the digestion & conversion of complex sugars to glucose
53
What should be monitored for a patient taking alpha glucosidase inhibitors?
serum transaminases (esp for those on acarbose)
54
What are the contraindications to taking alpha glucosidase inibitors?
Pt's with DM and IBD, colonic ulceration, obstructive bowel disorders, or chronic intestinal disorders of digestion or absorption
55
What are the side effects of alpha glucosidase inhibitors?
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
When should BG be monitored for a patient using an alpha glucosidase inhibitor to see if it is effective?
2 hour post prandial glucose measurement
57
How should a pt with DM be instructed to take acarbose?
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
What medication is a dopamine receptor agonist?
Bromocriptine mesylate
59
What is the mechanism of action for a dopamine receptor agonist?
Unkown; following morning administration of bromocriptine mesylate, postprandial glucose levels improve without increasing plasma insulin concentrations
60
What are the contraindications to a dopamine receptor agonist?
DM1, DKA, syncopal migraines, psychotic disorders , concomitatn use w/ other dopamine receptor agonists (for treatment of Parkinsons, RLS, acromeagly, etc)
61
What are the side effects associated with bromocriptine?
Somnolence, nausea, fatigue, dizziness, vomiting, and HA
62
When should blood glucose moniotring be done for pt's on bromocriptine?
pre and postmeal readings to assess the effectiveness
63
How should a pt with DM be instructed to take bromocriptine?
2 hours after waking with the first meal of the day
64
When are SGLT2 inhibitors typically used?
As glycemic lowering agents for DM patients as well as used for CV protection and renal protection based on recent evidence
65
What is the mechanism of action for SGLT2 inhibitors?
Result in increased excretion of glucose in the urine resulting in lower plasma glucose and potentially less kcals for fat accumulation
66
In which case does the 2020 ADA standards of care recommend SGLT2 inhibitors?
For persons with DM, especially if HF or CKD predominates
67
True or false: If injectable therapy is needed to reduce A1c, consider GLP1 RA in most patient prior to starting insulin
True
68
When adding basal insulin if glucose is above target for pt with DM2, what are the recommended guidelines?
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
when titrating basal insulin, if hypoglycemia w/out clear reason, by how much should basal insulin be reduced?
10-20%
70
When should overbasalization be suspected in DM2?
when basal dose >0.5 units/kg, elevated bedtime-morning and/or post-preprandial differential, hypoglycemia (aware or unaware), high variability
71
For pt's with DM1 who are metabolically stable, what may be used as a typical starting dose to determine TDD?
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
After basal therapy has been maximized, if A1c still above target, what type of insulin should be considered?
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
After ____ months if A1c target is not achieved, Metformin can (and should) be combined with another treatment option
three months

DCES exam 2021 (35 decks)

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