Diabetes Flashcards

1
Q

Rapid Acting drugs

A

Insulin lispro (HUMALOG®), Insulin aspart (NOVOLOG®), Insulin glulisine (APIDRA®)

Very rapid onset (4-15 minutes), peak (30 - 90 min), short duration (3-5 hr).
These preparations are taken immediately before a meal and are used in continuous subcutaneous insulin infusion (CSII) devices.

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

Short/Fast acting drugs

A

“normal” insulin (Humalin R®, Novolin R®)

Rapid onset (30-45 minutes), peak 2-3 hr, short duration (4-6 hr).
Only insulin preparation used I.V.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Intermediate acting drug

A

NPH (neutral protamine Hagedon or insulin isophane)

Onset 2-5 hrs, duration 4-12 hr

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

Intermediate acting drug MOA:

A

After s.c. injection, proteases in tissues degrade protamine and release insulin.

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

Intermediate acting drug SE

A

hypoglycemia

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

Long acting drugs

A
Insulin glargine (LANTUS®)
Insulin detemir (LEVEMIR®)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Insulin glargine

A

Onset – 1-1.5 hr, duration 11-24 hr. It can be injected once or twice a day.

MOA: Insulin glargine is soluble at acid pH, and it aggregates at physiological pH after injection. It slowly dissolves from injection site.

*long acting drugs

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

Insulin detemir

A

Onset 1-2 hr, duration > 12 hr. Very reproducible kinetics.

MOA: The myristic acid residue promotes self aggregation at physiological pH and binding to albumin, this lengthens the onset and duration of action.

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

Ultra-long acting

A

Insulin degludec (Tresiba®)

Onset 30-90 min. 25 hr. half-life, > 24 hr. duration.

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

3 routes of administration

A

1) subcutaneous
2) IM
3) IV

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

What are the 5 insulin analogs?

A

1) Rapid Acting
2) Fast acting
3) Intermediate acting
4) long acting
5) insulin degludec

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

SE of Insulin analogs

A

1) hypoglycemia
2) immunopathology
3) lipodystrophy at injection site

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

What are the 6 drug class of oral antidiabetic agents?

A

1) Biguanindes
2) Sulfonylureas
3) Meglitinides
4) D-Phenylalanine derivative
5) Thiazolidinediones
6) Alpha-Glucosidase inhibitors

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

Metformin

A

MOA: decreases hepatic glucose production. Metformin decreases both fasting hyperglycemia and postprandial hyperglycemia

Metformin is the first line pharmacotherapy for T2DM

SE: Dose related GI distress (anorexia, nausea, vomiting, diarrhea). High doses may produce lactic acidosis

Contraindication: patients with renal disease, alcoholism, hepatic disease, pulmonary disease and uncompensated heart failure due to increased risk of lactic acidosis. Long-term therapy with metformin may cause a reduction in absorption of vitamin B12.

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

Sulfonylureas MOA

A

MOA: inhibit ATP-sensitive K channels & release insulin

- also decrease glucagon secretion

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

1st generation Sulfonylureas

A

Tolbutamide
SE: hypoglycemia
Chlorpropmide
SE: hypoglycemia

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

2nd generation Sulfonylureas

A

shorter half life than 1st generation agents and have less risk for hypoglycemia

1) Glyburide (don’t use)
2) Glipizide
3) Glimepiride

SE: hypoglycemia

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

Meglitinides

A

MOA: Inhibition of the ATP-sensitive K channels in the pancreatic β-cells, similar to sulfonylureas

  • Repaglinide
19
Q

Repaglinide

A
  • Meglitinides class

Very fast onset of action with peak effect within 1 hour and duration 4-7 hours. Used for postprandial glucose control and should be take just before a meal.

20
Q

D-Phenylalanine Derivatives

A

MOA: Inhibition of the ATP-sensitive K channels in the pancreatic β-cells similar to sulfonylureas.

  • Nateglinide
21
Q

Nateglinide

A
  • D-Phenylalanine Derivatives( (class)

Rapid onset and peak effects occur within an hour of oral administration. Nateglinide stimulates insulin secretion under a glucose load, but not during normoglycemia. Thus, it has the lowest incidence of hypoglycemia of the secretagogue drugs.

22
Q

Insulin sensitizers- Thiazolidinediones

“-litazone”

A

MOA: Increase sensitivity to insulin. (insulin sensitizers) Agonists for the peroxisome proliferation-activated receptor-gamma (PPAR-γ)

  • Pioglitazone
  • Rosiglitazone
23
Q

Thiazolidinediones effects on carbohydrate metabolism:

A
  • Increase insulin-stimulated uptake of glucose
  • Increase hepatic glucose uptake
  • Reduce hepatic gluconeogenesis
24
Q

Thiazolidinediones effects on lipid metabolism

A
  • Reduce plasma fatty acid by increasing clearance and reducing lipolyis
  • Increases differentiation of adipocytes
  • Shifts fat deposits from visceral stores to subcutaneous deposits
  • Increases weight**
25
Q

Thiazolidinediones onset and side effects

A

onset: action of these drugs is weeks to months

SE:

  • Weight gain (2-4 kg) due to increased adiposity
  • Edema (up to 10% of patients)
  • Increased risk of heart failure - contraindicated for use in patients with heart failure
  • Demineralization of bone and increased risk of bone fractures in women
26
Q

Pioglitazone

A

MOA: same as thiazolidinediones + reduces plasma triglycerides and raises HDL-cholesterol levels

27
Q

Rosiglitazone

A

Blackbox –> increase risk for cardiovascular events

28
Q

Glucagon-like peptide-1 agonists:

“-tide”

A

MOA: GLP-1 potentiates the glucose-stimulated release of insulin from the pancreas.

  • suppresses glucagon release, slows gastric emptying and decreases appetite
  • GLP-1 is rapidly degraded by dipeptidyl peptidase-4 (DPP-4)
  • Exenatide
  • Liraglutide
  • Dulaglutide
29
Q

Exenatide

A
  • GLP-1 agonist
  • analog of GLP-1 that is insensitive to degradation by DPP-4
  • Used as monotherapy or in combination with oral hypoglycemic agents (metformin, sulfonylurea, thiazolidinediones)
    SE: nausea, vomiting, diarrhea
30
Q

Liraglutide

A
  • Long acting GLP-1 agonists
    Approved for use with metformin and sulfonylureas. Not used as a monotherapy or with insulin. Administered daily S.C.

SE: nausea, vomiting, diarrhea, pancreatitis

31
Q

Dulaglutide

A
  • GLP-1 agonist

Blackbox for patients with family hx of medullary cancer or multiple endocrine neoplasia type 2

32
Q

Dipeptidyl peptidase-4 (DPP-4) Inhibitors

A

MOA: Inhibits degradation of GLP-1 and GIP and increases circulating levels of these hormones.

  • Sitagliptin
  • Saxagliptin
  • Linaglipton
33
Q

Sitagliptin (JANUVIA)

A
  • Dipeptidyl peptidase-4 (DPP-4) Inhibitors

SE: Nasopharyngitis, upper respiratory infections, headaches

34
Q

Saxagliptin

A
  • Dipeptidyl peptidase-4 (DPP-4) Inhibitors

SE: upper respiratory and urinary infections

35
Q

Linaglipton (TRADJENTA)

A
  • DPP-4
  • similar to sitagliptin and saxagliptin. Eliminated via entrohepatic system, so can use with patients with renal disease.
36
Q

Amylin Agonists

A

MOA: Amylin decreases glucagon release, slows gastric emptying and increases satiety

  • Pramlintide
37
Q

Pramlintide (SYMLIN)

A
  • Amylin agonists
  • Administered s.c. prior to meals. Pramlintide action is dependent on insulin and is given as an adjunct to insulin therapy in both T1DM and T2DM.

SE: nausea and hypotension

38
Q

Sodium-Dependent Glucose Linked Transporter-2 (SGLT-2) Inhibitors
“-flozin”

A

MOA: SGLT-2 inhibitors lower plasma glucose levels and decrease HbA1c.

-Canagliflozin 
(SE: UTI)
- Dapagliflozin 
(SE: genital mycotic infections)
- Empagliflozin  
(SE: increased urination, ketoacidosis)
39
Q

Alpha- glucosidase inhibitors

A

MOA: inhibits intestinal digestion of starch and polysaccharides

SE: flatulence, diarrhea, abdominal bloating and pain due to metabolism of undigested carbohydrates by bacterial in colon

  • Acarbose
  • Miglitol
40
Q

Bile Acid Sequestrants

A

MOA: unknown

  • Colesevelam
41
Q

Colesevelam

A
  • Bile Acid Sequestrants

Lowers HbA1c by 0.5% and LDL cholesterol by 15%. It is also used to treat hyperlipidemia

SE: GI (diarrhea, flatulence, abdominal pain). May also impair absorption of fat soluble vitamins, glyburide, levothyroxine and oral contraceptives.

42
Q

Hypoglycemic Agents

A

Glucagon

Diazoxide

43
Q

Glucagon

A

MOA: increases hepatic gluconeogensis

  • Glucagon is used for emergency treatment of hypoglycemia
  • Glucagon can be used to reverse an overdose of beta-adrenergic blocking drugs
44
Q

Diazoxide

A

MOA: stimulates ATP sensitive channels & inhibits insulin secretion