Drugs Used in Diabetes Flashcards

1
Q

Pathology behind Type 1 DM?

A

loss of pancreatic B cells > absolute dependence on insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathology behind Type 2 diabetes?

A

decreased response to insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which type of diabetes is ketoacidosis prone?

A

Type 1 DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name some basal insulin forms.

A

glargine, determir, degludac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name some meal time insulin medications.

A

lispro, regular, aspart, glulisine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some factors/drugs that can increase insulin release?

A

increased by glucose, sulfonylureas, M-agonists, B2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some factors that can decrease insulin release?

A

a2 agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the symptoms associated with diabetic ketoacidosis?

A

polyuria, polydipsia, nausea, fatigue, dehydration, Kussmaul breathing, “fruity” breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the best treatment for diabetic ketoacidosis?

A

regular insulin IV, fluid and electrolyte replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Do most basal forms of insulin have a peak?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA of glargine.

A

insulin binds to the transmembrane receptors which activate tyrosine kinase to phosphorylate tissue-specific substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the DOC for Type II diabetes?

A

metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Does metformin cause hypoglycemia or weight gain?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MOA metformin.

A

may involve inc. tissue sensitivity to insulin and/or dec hepatic gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Indications for metformin.

A

mono therapy or combinations for treatment of Type II DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

S/E metformin use?

A

possible lactic acidosis, GI distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name a drug class that metformin has synergistic activity with?

A

sulfonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acarbose MOA.

A

inhibits a-glucosidase in brush borders of SI > dec formation of absorbable carbs > dec postprandial glucose > dec demand for insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the S/E of acarbose?

A

GI discomfort, flatulence, diarrhea; recent concern over potential hepatotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a way to tell if diabetic medication has potential to cause hypoglycemia vs if it doesn’t?

A

If the target in the diabetes medication is glucose > there is not a risk of hypoglycemia;

If the target in the diabetes medication is insulin; then it has potential to cause hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the MOA of sulfonylureas? How do they affect glucagon release?

A
  • Normally K+ efflux in pancreatic B cells maintains hyper-polarization of membranes; insulin is release only when depolarization occurs
  • Acute action of sulfonylureas is to block K+ channels> depolarization > insulin release
  • dec glucagon release
  • inc. insulin receptor sensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Glucagon is released from what pancreatic cells?

A

alpha cells

23
Q

How does glucose act as an insulinogen?

A

glucose increases intracellular ATP > closure of K+ channels > membrane depolarization> inc Ca2+ influx > insulin release

24
Q

Repaglinide MOA?

A

stimulates insulin release from pancreatic beta cells

25
Q

Indications for repaglinide.

A

adjunctive use in Type 2 diabetes - administer just before meals due to short half-life

26
Q

Which GLUT type usually bring glucose into the Beta pancreatic cell?

A

GLUT 2

27
Q

Indications for 1st generation sulfonylureas?

A

they were discontinued because had long t1/2 which increased the risk for hypoglycemia

28
Q

What are the second generation sulfonylureas?

A

glipizide, glyburide

29
Q

Would you decrease doses of glipizide in hepatic or renal dysfunction? (Which one would you decrease it in?)

A

hepatic dysfujnction

30
Q

Would you decrease the dose of glyburide in hepatic or renal dysfunction?

A

dec dose in renal dysfunction

31
Q

S/E of sulfonylurea use?

A

Hypoglycemia
weight gain

32
Q

What are some important adverse drug interactions to consider when using sulfonylureas?

A

inc. hypoglycemia with use of cimetidine, insulin, salicylates, sulfonamides, have A/E with first generation sulfonylureas.

33
Q

Symptoms of hypoglycemia.

A

lip/tongue tingling, lethargy, confusion, sweats, tremors, tachycardia, coma, seizures

34
Q

What is the best treatment for hypoglycemia?

A

oral glucose (or eat some candy), IV dextrose if unconscious, or glucagon (IM or inhalation)

35
Q

What is the MOA of the thiazolidinediones?

A
  • bind to nuclear peroxisome proliferator activating receptors (PPARy) involved in transcription of genes responsible for insulin regulation
  • sensitization of tissue to insulin,
  • plus dec hepatic gluconeogenesis and triglycerides
  • and inc. insulin receptor numbers
36
Q

Name the TZD drugs? What is the suffix to remember them?

A

“glitazones”
pioglitazone
rosiglitazone

37
Q

Is PPARy also implicated in the MOA for fibrates?

A

PPARa

so alpha type is the difference

38
Q

S/E of using TZDs?

A

less hypoglycemia than sulfonylureas, but weight gain and edema have been reported

39
Q

Be able to reproduce a table on the modes of action of drugs covered in this chapter and the organs implicated in their MOA?

A
40
Q

MOA Exenatide?

A

GLP1 is an incretin released from the SI. It augments glucose-dependent insulin secretion.

This drug is a long acting GLP-1 receptor full agonist

41
Q

Indications for Exenatide.

A

used in combination with other agents in Type 2 diabetes

42
Q

S/E of exenatide?

A

nausea, hypoglycemia when used with oral sulfonylureas

43
Q

MOA of the gliptins? Name a drug in this group?

A

sitagliptin

MOA: inhibits dipetidyl peptidase (DPP-4) thereby inhibiting inactivation of GLP-1

44
Q

Pramlintide MOA.

A

a synthetic version of amylin that slows rate at which food is absorbed from intestines.

Decrease glucose production and decreases appetite

45
Q

Indication for pramlintide?

A

type 1 and type 2 diabetes

46
Q

What is the suffix for the SGLT -2 inhibtors? Name a drug in this class.

A

“gliflozins”

canagliflozin

47
Q

GLP-1 agonist common suffix and drug names in this class?

A

“glutides”

liraglutide, exenatide

48
Q

MOA canagliflozin.

A

blocks SGLT-2 in the proximal tubule, increasing glucose excretion

49
Q

S/E of the SGLT-2 inhibitors?

A

UTIs

50
Q

SGLT-2 stands for what?

A

sodium-glucose cotransporter 2

51
Q

Drugs to think of when thinking of diabetic nephropathy treatment?

A

ACE, ARBs

52
Q

Drugs to think of when thinking of treating diabetic neuropathy symptoms?

A

TCAs (to a lesser degree), gabapentin

53
Q

Drugs to think of when thinking of gastroparesis related to diabetes?

A

metoclopramide, erythromycin (macrolide; macrolides stimulate motilin receptors)