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Endocrine > DM- Management Part 2 - Exam 4 > Flashcards

DM- Management Part 2 - Exam 4 Flashcards

1
Q

What is the MOA of insulin? How is it classified?

A

mimics the effect of regular insulin.

Classified by time of onset and duration of action

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2
Q

Which type of insulin is considered to have less ideal timing and is less expensive

A

Non-analog insulins (regular, NPH)

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3
Q

What are common SE of insulin? What is the major one?

A

hypoglycemia**- MC
weight gain
inflammation
fibrosis
pain
lipohypertrophy
lipoatrophy

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4
Q

How are insulin pens dosed? What effect does alcohol have?

A

dosed in units

Alcohol - often causes hypoglycemia in insulin-dependent patients!

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5
Q

What are the 3 rapid acting insulins?

A

Insulin lispro (Humalog) / Insulin lispro-aabc (Lyumjev) - U100, U200

Insulin aspart (Novolog) / Insulin faster aspart (Fiasp)

Insulin glulisine (Apidra)

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6
Q

What is the rapid acting inhaled insulin?

A

Technosphere insulin (Afrezza)

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7
Q

______ is the short acting insulin

A

Human regular (Humulin R, Novolin R) - U100, U500

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8
Q

_____ is the intermediate acting insulin

A

Human NPH (Humulin N, Novolin N)

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9
Q

What are the 4 long acting insulin? Which 2 are ultra long?

A

Insulin detemir (Levemir)
Insulin glargine U100 (Lantus)

Ultra long:
Insulin glargine U300 (Toujeo) - ultra-long
Insulin degludec (Tresiba) - U100, U200 - ultra-long

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10
Q

**When is inhaled insulin CI? What are the major SE? What are the monitor requirements?

A

not for use in smokers or pts with chronic lung conditions

cough; possible increased risk of lung cancer

requires periodic PFTs - baseline, 6 mo, then yearly

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11
Q

What is the major advantages of premixed insulin?

A

advantage: fewer injections

disadvantage: less ability to adjust dose. NPH insulin can be harder to predict

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12
Q

Where are some common insulin injections site? What is the pt education?

A

arms, abdomen and thighs

need to rotate within each site but need to keep it within the site due to how the body metabolizes it to keep the dose steady

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13
Q

If the pt is carb counting, what is the recommended carb intake for males and females? meals and snack

What is the insulin recommendation?

A

Males - 60 g per meal, 30 g per snack
Females - 45 g per meal, 15 g per snack

1 U per 15 g of carbohydrate, PLUS
1 U for every 50 mg/dL of BG at pre-meal screening above a set goal (i.e., 120 mg/dL)

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14
Q

What is the dawn phenomenon? How do you correct it?

A

hyperglycemia in the morning

Nocturnal release of counterregulatory hormones (glucagon, epinephrine, cortisol) leads to increased glucose levels

Inadequate levels of insulin to balance increased glucose leads to AM hyperglycemia

“Down Insulin” -> need to increase insulin

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15
Q

What is the Somogyi Effect? How do you correct it?

A

due to excess amounts of exogenous insulin with evening dose

pt becomes hypoglycemic while sleeping and the body releases counterregulatory hormones

increased glucose levels in the AM leads to rebound hyperglycemia

“so much insulin”-> need to decrease insulin

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16
Q

Which cause of hyperglycemia in the morning, leads to the sugar bottoming out in the middle of the night?

A

somogyi effect

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17
Q

How do you tell the difference between the dawn phenomenon and somogyi effect? What do you expect for each?

A

Have patient wake up a few nights in a row to check his/her sugar at 3 am

Low readings - Somogyi Effect
Medium-high readings - Dawn Phenomenon

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18
Q

What is the Professor Jensen way to tell the difference between dawn phenomenon and somogyi effect? What do you expect for each?

A

try decreasing evening/bedtime dose of insulin

Hyperglycemia improves - Somogyi Effect
Hyperglycemia persists or worsens - Dawn Phenomenon

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19
Q

**If you are unsure if its the dawn phenomenon and somogyi effect, what should you NOT do?

A

If you aren’t sure - don’t increase insulin dose!

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20
Q

What are the general guidelines for a T1DM insulin dosing schedule?

A

Starting calculation of 0.5 U/kg - divided into two portions
50% - basal (long-acting) insulin dose
50% - bolus (rapid-acting or short-acting) - divided into 3 equal parts

Requires 4 injections/day (3 rapid-acting or short-acting, 1 long-acting) should also check BS 3-4 times a day

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21
Q

What are the recommendations to adjust your bolus insulin?

A

If BS is under 80 need to subtract 2 units from the injection prior

80-130 keep insulin the same.

BS over 130, add to units to your previous insulin injection

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22
Q

Which is considered the better choice, long acting insulin or NPH? Why?

A

long acting is better because it has better predictable absorption and LESS hypoglycemia,

long acting is dosed QD

NPH is dosed BID

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23
Q

Is rapid acting or regular insulin preferred? Why?

A

rapid acting is preferred because it has more predictable absorption
Shorter duration of action - less “leftover” hypoglycemia

regular: has less predictable absorption
but can give IV
more hypoglycemia

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24
Q

How many injections is premix dosing? How many BS checks?

A

BID

2-3 BG check a day

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25
Q

How do you instruct a pt to start premix insulin?

A
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26
Q

When is sliding scale insulin commonly used? Why?

A

in pts setting

Reactive approach to hyper- and hypoglycemia
Often results in wide swings in glucose control

does not address basal insulin needs, can use basal insulin alongside

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27
Q

_____ is an TNF-alpha inhibitor
In animal trials, has shown improved β-cell function; may help both T1DM or T2DM

A

Infliximab (Remicade)
\

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28
Q

______ MAb that binds to receptors on CD4+ and CD8+. Approved for pts 8 y/o and up who are at high risk for T1DM. What does it do overall? What are the SE?

A

Teplizumab mzwv (Tzield)

Delays the onset of T1DM (2.5 yrs in clinical trials) and improves β-cell function

transient leukopenia and lymphocytopenia; rash; headache

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29
Q

When is a pancreas transplant often recommended for a T1DM? What are the drawbacks?

A

Often recommended for patients who are also receiving renal transplant

have to be on lifetime immunosuppression

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30
Q

______ “cellular therapy” rather than organ transplant
Deceased donor pancreatic islet cells infused via the hepatic portal vein
Allows for a less toxic immunosuppressive drug regimen

A

Donislecel-jujn (Lantidra)

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31
Q

What is the MOA of metformin? What is the drug class?

A

Inhibits hepatic gluconeogenesis

helps “fix a leaky liver”. Helps decrease intestinal absorption of glucose
Slightly improves insulin sensitivity
Increa

drug class: Biguanides

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32
Q

Is metformin associated with hypoglycemia? What is the major SE? What is the BBW? Need to avoid use in what type of pts?

A

NOT associated with hypoglycemia

GI SE: diarrhea

BBW: lactic acidosis,

Avoid in chronic renal failure (GFR <30mL), liver failure and excess alcohol intake

33
Q

What is the MOA of Pioglitazone (Actos)? What line are they? What drug class?

A

“Unlock” muscle and fat cells to help them utilize glucose.
-Improves insulin sensitivity
-decreases gluconeogenesis
- increases glucose uptake
- increases adipogenesis

2nd or 3rd line

Thiazolidinediones

34
Q

______ bind a nuclear receptor called PPAR-gamma, which affects the expression of several genes relevant to glucose metabolism!

A

Pioglitazone (Actos)

drug class: Thiazolidinediones

35
Q

Is Pioglitazone (Actos) associated with hypoglycemia? What are the SE? What is the BBW?

A

NOT associated

SE: weight gain, peripheral edema, BLADDER CANCER

BBW: CHF

36
Q

What DM med carries a increased risk for bladder cancer?

A

pioglitazone increases risk

thiazolidinediones

37
Q

Glimepiride (Amaryl)
Glipizide (Glucotrol)
Glyburide (DiaBeta, Micronase)

What drug class? What is the MOA?

A

Sulfonylureas

“Zap” the pancreas to stimulate increased production of insulin

38
Q

Repaglinide (Prandin)
Nateglinide (Starlix)

What drug class?
What is the MOA?

A

Meglitinides

Repaglinide (Prandin)
Nateglinide (Starlix)

39
Q

______ bind to a site on the ATP-sensitive K+ channel of beta cells, leading in turn to depolarization, opening of voltage dependent Ca channels, and release of insulin

A

both Sulfonylurea and Meglitinide

40
Q

Are Sulfonylurea/Meglitinide associated with hypoglycemia? What are the SE? Avoid use in what pt? Are they first line?

A

IS associated with hypoglycemia (but not as bad as insulin)

SE: weight gain

Patients with chronic liver disease
or chronic renal failure may be poor candidates

NOT first line

41
Q

Acarbose (Precose)
Miglitol (Glyset)

What drug class?
What is the basic MOA?

A

α-Glucosidase Inhibitors

“Block” the breakdown of starches in the intestine by inhibiting the enzymes that breaks down starch and sucrose

42
Q

Are α-Glucosidase Inhibitors associated with hypoglycemia? What are the SE? What are the CI?

A

NOT associated with hypoglycemia

GI: flatulence, elevated LFTs, bloating, belly pain due to undigested starches

CI: Diabetic ketoacidosis, Cirrhosis, Major chronic GI disease

43
Q

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)
Bexagliflozin (Brenzavvy)
Ertugliflozin (Steglatro)

What drug class?
What is the basic MOA? What part of the tubule?
Is it first line?

A

SGLT2 Inhibitors

“Halt” renal glucose reabsorption
↑ glucose excretion by inhibiting protein that accounts for about 90% of glucose reabsorption in the kidney aka they pee out glucose

Act on the proximal tubule

Alternative first line therapy

44
Q

_____ : blocks SGLT1 AND SGLT2; indicated for _____

A

Sotagliflozin (Inpefa)

heart failure

45
Q

Are SGLT2 inhibitors associated with hypoglycemia? **What are the SE? What are the CI? Are they used in T1DM?

A

NOT associated with hypoglycemia

**GU - ↑ incidence of UTIs, genital mycotic infections.
increases LDL, dehydration, may increase risk of DKA

CI: Moderate-severe CKD

NOT used in T1DM

46
Q

SGLT2 inhibitor that is associated with bladder cancer?

SGLT2 inhibitor that is associated with bone fractures and amputations?

A

bladder cancer: dapagliflozin

bone fractures, amputations: canagliflozin

47
Q

Exenatide (Byetta/Bydureon)
Liraglutide (Victoza, Saxenda)
Lixisenatide (Adlyxin)
Dulaglutide (Trulicity)
Semaglutide (Ozempic, Rybelsus)
Tirzepatide (Mounjaro)

What drug class?
What is the basis MOA?
Which one is available in oral form?
Which one also acts as a GIP agonist?

A

GLP-1 Receptor Agonists

mimic the incretin GLP-1

Semaglutide (Ozempic, Rybelsus*

Tirzepatide (Mounjaro)**

48
Q

What is the detailed MOA of GLP-1 Receptor Agonists?

A

↑ insulin release
↓ glucagon release
↓ gastric emptying
↑ satiety
May ↑ beta-cell proliferation

49
Q

______ may cause hypoglycemia if patient is also taking insulin secretagogues

A

GLP-1 Receptor Agonists

50
Q

Are GLP-1 receptor agonists associated with hypoglycemia? What kind of pt would these meds be of considerable benefit? **What are some SE? What are the BBW?

A

Not associated with hypoglycemia

NASH/NAFLD - May be helpful to reduce hepatic steatosis

SE: dose dependent N/V/D

BBW: thyroid cancer (especially medullary)

51
Q

Which GLP-1 receptor has the highest GI SE?

A

Moujaro

52
Q

Sitagliptin (Januvia)
Saxagliptin (Onglyza)
Linagliptin (Tradjenta)
Alogliptin (Nesina)

What drug class?
What is the basic MOA?
Is it first line?

A

DPP-4 Inhibitors

“Stretch” out the effects of endogenous incretin GLP-1 by inhibiting the enzyme that degrades it

good 2nd line drug!

53
Q

Are DPP-4 Inhibitors associated with hypoglycemia? SE? What medication should not be prescribed at the same time?

A

NOT associated with hypoglycemia

N/V/D - less than GLP-1 agonists, pancreatitis, increased risk of severe arthralgias

Not indicated for co-treatment with GLP-1 agents

54
Q

DPP-4 inhibitors: _____ and _____ have an alert for possible increased risk of heart failure

A

Alogliptin and Saxagliptin

55
Q

Pramlintide (Symlin)

What drug class?
What is the basic MOA?

A

Amylin Analogs

“Impersonate” the effects of amylin (synthetic amylin analog)

56
Q

**What other drug besides insulin can be used in T1DM? (can also be used in T2DM)

What form dose it come in?

A

Pramlintide (Symlin): Amylin Analogs

SC injection

57
Q

Does Amylin Analogs cause hypoglycemia? SE? What is the BBW?

A

SE: Nausea

BBW: may cause hypoglycemia when
used with insulin

NOT used frequently

58
Q

Lowers A1c 0.3-0.5%
Also helps reduce LDL
SE - constipation, dyspepsia, ↑ TG

What am I?
What is the recommendation?

A

Colesevelam (Welchol): Bile Acid Sequestrants

Due to significant SE and only moderate effects on glucose, these are not recommended for primary tx of DM.

59
Q

Lowers A1c 0.1-0.5%
SE - N/V, dizziness, HA

What am I?
What is the recommendation?

A

Bromocriptine (Parlodel, Cycloset): Dopamine Receptor Agonists

Due to significant SE and only moderate effects on glucose, these are not recommended for primary tx of DM

60
Q

What is Soliqua a combination of?

Xultophy?

What is their limitation?

A

Soliqua - Insulin glargine (Lantus) + lixisenatide (Adlyxin)

Xultophy - Insulin degludec (Tresiba) + liraglutide (Victoza)

Max doses due to GLP-1 agonist component
May not be enough insulin for poorly controlled diabetics

61
Q

What are the glycemic control guidelines for non-pregnant adult pt? How often should they get their A1C checked?

A

q3 months if NOT well controlled

q6 months if well controlled

62
Q

What are some adjunct therapy options for T1DM?

A

Teplizumab (Tzield) - consider for early or pre-DM cases with high risk of T1DM

Donislecel-jujn (Lantidra) - consider for refractory or severe T1DM

63
Q

**_____ consider for early or pre-DM cases with high risk of T1DM

A

Teplizumab (Tzield)

64
Q

_____ consider for refractory or severe T1DM

A

Donislecel-jujn (Lantidra)

65
Q

_____ mimics the effects of endogenous glucagon. What form is used the most often?

A

Glucagon

3 mg intranasal

66
Q

_____ provides body with monosaccharide fuel for metabolic processes. Cannot give if pt is allergic to _____

A

Dextrose

corn

67
Q

What is the management for preDM? What do you need to monitor for?

A

7% weight loss

at least 150 minutes of moderate physical activity per week

consider metformin (off-label use)
GLP-1 agonists are used to tx obesity

yearly visit to f/u on glycemic status
screen for obesity, HTN, HLD

68
Q

What is the management of T2DM?

A

weight loss, exercise, healthy eating

medications (see other notecard)

69
Q

What is the medication management guidelines for a T2DM pt?

A

At diagnosis - metformin + diet + exercise

If A1c not at goal in 3 mo - metformin + another agent + diet + exercise

If A1c not at goal in 3 mo - metformin + two other agents + diet + exercise

If A1c not at goal in 3 mo - metformin + insulin +/- other agents + diet + exercise

70
Q

When do you consider insulin as a rx treatment at diagnosis of T2DM?

A

Consider insulin therapy at onset if patient has a markedly elevated A1c (9.0% or higher) or if significant hyperglycemia s/s

71
Q

If pt has ASCVD and T2DM, what medications are considered 1st line?

A

ASCVD - GLP-1 or SGLT2

72
Q

If pt has heart failure and T2DM, what medications are considered 1st line?

A

HF - SGLT2

73
Q

If pt has CKD and T2DM, what medications are considered 1st line?

A

CKD - SGLT2 or GLP-1

74
Q

What 2 classes of DM meds are considered moderate efficacy? What are all the others considered?

A

moderate efficacy: DPP-4 and SGLT2

all others: high efficacy

75
Q

Which DM meds have a risk of hypoglycemia? (4)

A

risk with sulfonylureas, meglitinides, pramlintide, insulin

76
Q

Which 3 DM meds are associated with weight loss? weight neutral? weight gain?

A

loss: GLP-1 agonists and SGLT2 inhibitors, Pramlintide

neutral: Metformin, DPP-4 inhibitors

gain: Sulfonylureas, TZDs, insulins

77
Q

Which 3 DM meds are considered the most affordable?

A

metformin, sulfonylureas, and TZDs

78
Q

For a T2DM pt on insulin, how many units should their basal insulin be?

A

basal: 10 units

79
Q
A

Endocrine (14 decks)

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