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(C) CM 1A: Heme/Onc/Endo > Lecture 26: DM Management Part 2 > Flashcards

Lecture 26: DM Management Part 2 Flashcards

1
Q

When is insulin indicated?

A
  • T1DM
  • Longstanding or refractory T2DM
  • Hyperglycemic crises
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2
Q

What two characteristics are insulin classified by?

A
  • Time to onset
  • Duration of action
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3
Q

What are the common SE of insulin?

A
  • HYPOGLYCEMIA
  • Wt gain
  • Injection-site reactions (lipohypertrophy, lipoatrophy)
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4
Q

Why does insulin cause weight gain?

A

Increased intake of excess glucose will be converted to fat.

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5
Q

What is the standard STRENGTH of insulin?

A

100 units/1mL

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6
Q

What is meant by basal and bolus insulin?

A
  • Basal: background/long-acting (50%)
  • Bolus: postprandial, short-acting (50%)
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7
Q

How much insulin does someone usually need?

A

0.5 Units/kg

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8
Q

What is the longest acting insulin?

A

Insulin degludec (Tresiba)

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9
Q

What are the concerns with inhaled insulin?

A
  • Cough
  • Increased risk of lung cancer (periodic PFT’s)
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10
Q

What are the concerns with mixed insulin preparations?

A
  • Difficult to adjust dosage.
  • NPH is often used, which has an unpredictable pattern.
  • Expensive for aspart/degludec combo.

NPH has a significant peak and trough.

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11
Q

What gauge are insulin pens and needles?

A

Ultrafine, 31g-33g

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12
Q

What is the dawn phenomenon?

A
  • Low insulin in the morning, resulting in hyperglycemia
  • Often a result of nocturnal release of glucagon.
  • Treated by taking more insulin at night.

Down insulin

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13
Q

What is the somogyi effect?

A
  • Hyperglycemia in the morning as a result of excess exogenous insulin at night.
  • Often a result of hypoglycemia at night, which is regulated and then converted to rebound hyperglycemia in the morning.
  • Treated by decreasing insulin at night.

So much insulin

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14
Q

How can you differentiate dawn phenomenon vs somogyi effect?

A
  • 3AM checks of BG
  • Decreasing bedtime insulin and seeing morning glucose levels.

Always test by decreasing insulin, NOT BY INCREASING

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15
Q

What is the physiologic dosing regimen for insulin?

A
  • 4 inj/day (3 short, 1 long)
  • 3-4 BG checks/day
  • 50/50 dosing or carb counting
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16
Q

What insulin is preferred for bolus dosing?

A

Rapid-acting > regular/short-acting

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17
Q

What is the premixed insulin dosing regimen?

A
  • BID
  • 2-3 BG checks/day
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18
Q

What is the sliding scale insulin?

A
  • Regular insulin, primarily IP settings.
  • Reactive approach, but causer wider swings.
  • May require a basal insulin.
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19
Q

What drug class is metformin and its MOA?

A

Metformin is a biguanide.
MOA: Inhibits hepatic gluconeogenesis.
Minor decrease in intestinal absorption of glucose.
Slightly improves insulin sensitivity.

Lowers A1C about 1-2% usually.

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20
Q

What is the first-line therapy for T2DM?

A

Metformin!

Unless a specific CI is present.

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21
Q

What secondary benefits does metformin have besides lowering BG?

A
  • Weight loss
  • Improving lipid TGs
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22
Q

What are the concerns regarding metformin?

A
  • GI SE: especially Diarrhea
  • B12 deficiency
  • BBW: Lactic acidosis (rare)
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23
Q

When is lactic acidosis more likely to occur with metformin use?

A
  • CKD
  • Liver Failure
  • Excess ETOH intake
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24
Q

What are the CIs to metformin?

A
  • Allergy
  • Acidosis
  • CKD
  • CHF, hospitalization, radiocontrast
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25
Q

What are the two thiazolidinediones (TZDs)?

A
  • Rosiglitazone
  • Pioglitazone
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26
Q

What is the MOA of a TZD?

A
  • Unlock muscle and fat cells to help them utilize glucose.
  • Improves insulin sensitivity.
  • Decreased gluconeogenesis
  • Increased adipogenesis
  • Binds to PPAR-gamma to carry out above effects.
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27
Q

What are both TZDs and metformin specifically NOT associated with?

A

Hypoglycemia.

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28
Q

What is the secondary beneficial effect of pioglitazone?

A

Improving HDL and TG

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29
Q

What are the concerns with TZDs?

A
  • Wt gain
  • Edema
  • Bladder cancer (pioglitazone risk)
  • lipids (rosiglitazone increases LDL, TG, and minor benefit of HDL.)
  • BBW: CHF, rosi also causes MI.
  • Fx risk
  • Anemia
  • Mnemonic: You get a PIzza and calZONE (pioglitazone) at a PPAR-lar, and the word is a mouthful (wtgain)
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30
Q

What are the CIs to TZDs?

A
  • Allergy
  • CHF (class 3/4)
31
Q

How do both sulfonylureas and meglitinides work?

A
  • Increased production of insulin by the pancreas.
  • Bind to ATP-sensitive K+ channel, depolarizing cell and opening Ca channels to release more insulin from beta cells.
  • Insulin secretagogue
32
Q

What are the sulfonylureas?

A
  • Glimepiride
  • Glipizide
  • Glyburide
  • Mnemonic: Sulfas smell like Gas
33
Q

What are the concerns with sulfonylureas/meglitinides?

A
  • HYPOGLYCEMIA
  • Wt gain
  • TID dosing for megs
  • Chronic liver or kidney disease makes for a poor candidate.
34
Q

What are the CIs to sulfonylureas/meglitinides?

A
  • Allergy to rx OR sulfa allergy
  • DKA
35
Q

What is the MOA of an alpha-glucosidase inhibitor?

A
  • Inhibits the breakdown of starch in the intestine.
  • Delayed carbohydrate absorption.
36
Q

What are the two alpha-glucosidase inhibitors?

A
  • Acarbose
  • Miglitol
37
Q

What are the main concerns with alpha-glucosidase inhibitors?

A
  • GI: Flatulence
  • Increased hypoglycemia risk if given with sulfonylureas or insulin
  • TID dosing
38
Q

What are the CIs to alpha-glucosidase inhibitors?

A
  • Allergy
  • DKA
  • Cirrhosis
  • Chronic GI disease (IBD, colon ulcers, obstruction, etc)
39
Q

What is the MOA of a SGLT2 inhibitor?

A
  • Inhibit renal glucose absorption
  • Increased renal glucose excretion via inhibition of protein.
  • Acts on proximal tubule.
40
Q

What are the 4 SGLT2 inhibitors?

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
  • Ertugliflozin
  • Mnemonic: GLucose FLOwing out
41
Q

Why are SGLT2 inhibitors used?

A
  • Wt loss
  • Insulin-independent
  • Lowers BP
  • Can improve CKD even in non-DM pts)
42
Q

What are the main concerns with SGLT2 inhibitors?

A
  • Incidence of GU infections
  • Genital mycotic infections
  • Dehydration
  • Can worsen GFR if it is low.

Sugar near the genitals = food for microbes.

43
Q

What are the CIs to SGLT2 inhibitors?

A
  • Allergy
  • Moderate-severe CKD (Doesn’t work once GFR is low)
44
Q

How do GLP-1 receptor agonists work?

A
  • Mimics incretin GLP-1
  • Increased insulin release
  • Decreased glucagon release
  • Decreased gastric emptying
  • Increased satiety
  • Increased beta cell proliferation
45
Q

What are the GLP-1 agonists?

A
  • Exenatide
  • Liraglutide
  • Lixisenatide
  • Dulaglutide
  • Semaglutide
  • Tirzepatide
46
Q

What is the main secondary benefit for a GLP-1 agonist?

A

Weight loss

47
Q

What are the concerns/disadvantages of GLP-1 agonists?

A
  • SC injection (except rybelsus)
  • Hypoglycemia if taking insulin secretagogues
  • BBW: Thyroid cancer
48
Q

What are the CIs to GLP-1 receptor agonists?

A
  • Allergy
  • PMHx or FMHx of medullary thyroid carcinoma or MEN2

Caution in someone using decreased GI motility drugs.

49
Q

How do DPP-4 inhibitors work?

A
  • Inhibits the enzyme that degrades GLP-1.
  • Exact same effects as GLP-1 receptor agonists.
50
Q

What are the DPP-4 inhibitors?

A
  • Sitagliptin
  • Saxagliptin
  • Linagliptin
  • Alogliptin
51
Q

What is the primary reason GLP-1 receptor agonists are preferred over DPP-4 inhibitors?

A

Higher efficacy.

52
Q

What is the CI to a DPP-4 inhibitor?

A
  • Allergy

Less SE than a GLP-1 receptor agonist as well.

53
Q

How do amylin analogs work?

A
  • Mimics amylin.
  • Decreases glucagon release
  • Decreased gastric emptying
  • Increased satiety
54
Q

Why are amylin analogs good?

A
  • Useful in both T1 and T2DM.
  • Wt loss.
  • Improves FBG and PPBG.
55
Q

What is the BBW of an amylin analog?

A

Hypoglycemia if used with insulin.

56
Q

What are the CIs to amylin analogs?

A
  • Allergy
  • Gastroparesis
  • Unawareness of hypoglycemia
57
Q

What is the amylin analog?

A

Pramlintide

58
Q

What are the two add-on drugs for DM?

A
  • Colesevelam (bile acid sequestrant)
  • Bromocriptine (Dopamine receptor antagonist)
59
Q

What medication can be combined with long-acting insulin?

A
  • GLP-1 agonists
  • Given as a single daily dose.
60
Q

What is the ideal target A1C for a diabetic?

A

< 7%

61
Q

What is the primary tx for T1DM? Regimen?

A

Insulin, ideally basal-bolus or pump.

Pramlintide can be adjunct.

62
Q

What drugs are not indicated for T1DM?

A
  • Metformin
  • GLP-1
  • DPP-4
  • SGLT2 inhibitor
63
Q

What is the preferred insulin type for T1DM?

A

Analog insulin (rapid-acting/long-acting) is more preferable than human insulin.

64
Q

How do we treat an unconscious, hypoglycemia patient?

A
  • Inj/Nasal Glucagon kit
  • IV Dextrose (D50W)
65
Q

What is the preferred treatment for prediabetes?

A
  • Behavioral interventions.
  • Metformin is recommended only if BMI> 35, Age < 60, or hx of gestational diabetes.
66
Q

How should we manage a newly diagnosed T2DM patient?

A
  • Metformin + diet + exercise
67
Q

When should insulin be considered as therapy for a newly diagnosed T2DM patient?

A
  • A1c > 9%
  • Significant hyperglycemia S/S
68
Q

How do we manage a T2DM pt not at goal within 3 months?

A
  • Add another agent
  • Add 2 more agents
  • Add insulin
69
Q

What T2DM meds are associated with hypoglycemia?

A
  • Sulfonylureas
  • Meglitinides
  • Pramlintide
  • Insulin
70
Q

Which T2DM drugs cause weight loss?

A
  • GLP-1 agonist
  • SGLT2 inhibitor
  • Pramlintide
  • Metformin
71
Q

Which T2DM drugs cause weight gain?

A
  • Sulfonylureas/meglitinides
  • TZDs
  • Insulin
72
Q

Glycemic control drug algorithm

A
73
Q

What are the rapid acting insulins?

A
  • Lispro
  • Aspart
  • Glulisine
74
Q

What are the long-acting insulins?

A
  • Determir
  • Glargine
  • Degludec

(C) CM 1A: Heme/Onc/Endo (28 decks)

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