Diabetes

Question 1

Dx of DMII with random blood glucose value

Answer 1

1x Random BG >200 + symptoms = DMII

Question 2

Dx of DMII with fasting blood glucose value

Answer 2

2x Fasting BG >125 = DMII

2x Fasting BG 100-125 reflexes to 2hr OGTT:

• > 200 = DMII
• <140 = WNL
• 140-200 = Pre-diabetes

2x Fasting BG <100 = WNL

Question 3

Dx of DMII with hgbA1c

Answer 3

>6.5 = DM
<5.7 = WNL

5. 7-6.5 = prediabetes
   * Not appropriate in people with hemoglobinopathies or in cases of acute insulin sensitivity changes (gestational diabetes)

Question 4

Confirmation Dx of DM I?

Answer 4

Test for antibodies: GAD or IA2

Question 5

Discuss the OP treatment algorithm for DM

Answer 5

1. Start with lifestyle mods + metformin, recheck in 3 mo
   * *Metformin CIx w/ CKD, CHF, liver disease 2/2 potential for lactic acidosis
2. If not at goal (hgbA1c =7%), add second oral agent, recheck in 3 mo
3. If not at goal, add insulin

**Go straight to insulin if initial HgbA1c is 9%+

Question 6

Name some sulfonylureas and describe their MOA and AEs

Answer 6

Ex: Glyburide, glipizide, tolbutamide, tolazamide

MOA: increases secretion of insulin by binding/closing K+ channels, depolarizing B-pancreatic cells, opening volt-gated Ca++ cells (releasing insulin)

AEs: hypoglycemia, weight gain, GI effects, HA

Question 7

Name some thiazolidinediones and describe their MOA and AEs

Answer 7

“-glitazone”s: ciglitazone, darglitazone, rivoglitazone, etc

MOA: Activate PPARs, decreasing fatty acids in circulation, causing cells to rely more heavily on carbs and increasing insulin sensitivity.

AEs: Weight gain, water retention/edema, CHF.

*Some evidence these may increase chance of serious Covid infection via increased expression of ACEII

Question 8

Name some DPP-4 inhibitor drugs and describe their MOA and AEs

Answer 8

“-gliptin”s: sitagliptin (Januvia), linaliptin (Tradjenta), etc

MOA: block dipeptidyl-peptidase-4 enzyme from breaking down incretins (GLP-1 and GIP), raising their levels, and inhibiting glucagon release, increasing insulin secretion.

AEs: HA, nausea, joint pain

*Weight neutral

Question 9

Name some GLP-1 agonist drugs and describe their MOA and AEs

Answer 9

“-utide”s: dulaglutide (Trulicity), exenatide, liraglutide (Saxenda)

These directly agonize GLP-1 receptors, inhibiting glucagon release and increasing insulin secretion.

AEs: Weight loss; possible pancreatitis?

Question 10

Pt on psych meds with very low urine specific gravity & osmolality, high plasma osmolality and serum sodium: pathophys, ass’d drugs, and treatment?

Answer 10

Nephrogenic DI is ass’d with lithium use (among others; lithium MC)

The kidneys stop responding to ADH:

• • ADH is normally secreted when vascular resistance falls
• • Inserts aquaporin channels to reabsorb water

When this doesn’t happen, the urine becomes dilute and the patient becomes hypernatremic

Question 11

Principles of management of patient in DKA

Answer 11

– IVF is most important – these patients are severely volume depleted (glucose in urine is osmotically pulling water out of them)

• • They need insulin to close the AG but they are also going to be hypokalemic (insulin moves K+ into cells and they are insulin deficient)
• –> giving insulin will make them more hypokalemic
• If K+ is <3.5, hold insulin
• If K+ is WNL, give insulin WITH K+ and maintain K+ 4-5

*Serum K+ levels will be artificially high

Give IV insulin until AG closes
– If they become hypoglycemic before this happens, give with D5W and maintain BSG <250

Transition to subQ
- Use first subQ as bolus pre-meal, continue IV for 2-3 more hours to overlap as basal coverage

Question 12

What kind of incontinence is MC with DM patients?

Answer 12

Neuropathy –> neurogenic bladder –> retention and overflow incontinence