Drugs for Diabetes Mellitus

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Drugs for Diabetes Mellitus by Mind Map: Drugs for Diabetes Mellitus

1. Meglitinides

1.1. Repaglinide

1.2. Nateglinide

1.3. MOA

1.3.1. Similar to Sulfonylreas

1.3.1.1. binds different site on the K channel

1.4. PK

1.4.1. Fast onset of action (15-30 min)

1.4.2. Short duration of action

1.4.2.1. Repa>Nate

1.4.3. Take before meal to control postprandial glycemia

1.5. Use

1.5.1. Type II DM

1.6. SE

1.6.1. Hypoglycemia

2. Sulfonylureas

2.1. Glimepiride

2.2. Glipizide

2.3. Glyburide

2.4. MOA

2.4.1. Antagonized K channel on pancreatic beta cell

2.4.1.1. Cause cell depolarization and allows efflux of Ca

2.4.1.1.1. Increased insulin release

2.4.2. Increases AMOUNT, not FREQUENCY of pulsatilue release of insulin

2.4.2.1. No effect on basal insulin levels!

2.4.3. Minor effect: Subsequently decreases glucagon release (b/c of increased insulin release)

2.4.3.1. Possibly enhance by increased release of SMSTN w/ insulin

2.5. Use

2.5.1. Type II DM

2.5.2. Take 1/day

2.6. SE

2.6.1. Hypoglycemia

2.6.1.1. Both basal and postprandial

2.6.2. Weight gain

2.6.2.1. d/t high insulin levels

2.6.3. NV

2.6.4. Allergic skin rxns

2.6.5. Cholestatic jaundice

2.6.6. TCP, leukopenia, hemolytic anemia

2.6.7. Hyponatremia and SIADH

3. Thiazolidinediones (TZDs)

3.1. Pioglitazone

3.2. Rosiglitazone

3.3. MOA

3.3.1. Stimulate PPAR-gamma (intracellular receptor that increases transcription of GLUT-4)

3.3.1.1. Found in fat and some muscle tissue

3.3.2. Increases glucose uptake in M and fat tissue

3.3.3. Decreased levels of free TGs

3.3.4. Inhibit GNG

3.4. Use

3.4.1. Type II D

3.4.2. Taken one/day, with food

3.4.2.1. Requires presence of insulin to work

3.4.2.1.1. GLUT-4 is an insulin sensitive receptor

3.5. SE

3.5.1. Weight gain

3.5.1.1. PPAR activation

3.5.1.1.1. collecting tubules

3.5.1.1.2. Differentiation of pre-adipocytes into mature adipose cells

3.5.2. Fluid retention

3.5.2.1. CI in pts with > Stage III CHF or acutely decompensated

3.5.3. Bone fracture

3.5.3.1. PPAR activated diverts stromal cells from osteoblasts to adipocyte lineage

3.5.3.1.1. fat deposition in bone

3.5.4. Anemia

3.5.5. Hepatotoxicity

3.5.6. Increased risk of CV events

4. Incretin (GLP-1) mimetics

4.1. GLP-1 agonist

4.1.1. Exanatide

4.1.2. Liraglutide

4.1.3. Admin - SQ injection

4.1.4. SE

4.1.4.1. Hypoglycemia

4.1.4.2. Pruritis, urtecaria, rash

4.1.4.3. Acute pancreatitis

4.1.4.4. Lira ONLY - risk of thyroid Ca

4.1.4.4.1. Black box warning!!!

4.2. DPP-IV inhibitors

4.2.1. Sitagliptin

4.2.2. Saxagliptin

4.2.3. Admin - oral

4.2.4. SE

4.2.4.1. Hypoglycemia

4.2.4.2. Allergic rxns

4.2.4.2.1. Stevens-Johnson Syndrome

4.2.4.2.2. angioedema

4.2.4.2.3. anaphyllaxis

4.3. MOA

4.3.1. GLP-1 is secreted by L-cells in ileum

4.3.1.1. Slows gastric emptying in stomach

4.3.1.1.1. Reduces postprandial spike in blood glucose levels

4.3.1.2. Promotes sense of satiety in brain

4.3.1.3. Increases glu-stimulated insulin and decreases glucagon secretion in pancreas

4.3.1.3.1. If target glu-stimulated insulin release, less chance of hypoglycemia

4.3.2. DPP-IV is the NZ that metabolizes GLP-1

4.3.2.1. GLP-1 1/2 life in circulation = 1-2 minutes

4.4. Use

4.4.1. Type II DM

5. Amylin analog

5.1. Primlintide

5.2. Use

5.2.1. Type I & II DM who inject insulin at meal times

5.2.2. SQ injection

5.3. MOA

5.3.1. Released w/ insulin from beta cells

5.3.1.1. Increases satiety

5.3.1.2. Delays gastric emptying

5.3.1.3. Inhibits glucagon release

5.3.2. Reduces postprandial glucose spike

5.4. SE

5.4.1. NVA

5.4.2. Headache

5.4.3. Hypoglycemia when combined w/ insulin

6. alpha-glucosidase inhibitors

6.1. Acarbose

6.2. Miglitol

6.3. MOA

6.3.1. Reversible inhibition of NZ on brush border that breaks down disaccharides into glucose

6.3.1.1. Slows absorption of glucose from gut

6.3.1.1.1. Reduces postprand insulin spike

6.3.1.1.2. No effect on fasting glucose levels

6.4. Use

6.4.1. Type II DM

6.4.2. Reduces risk of Type II DM in pts with impaired glucose tolerance

6.5. SE

6.5.1. Flatulence, bloating, abdominal discomfort

6.5.2. Diarrhea

6.5.3. Elevated liver NZs

7. Biguanides

7.1. Metformin

7.1.1. Use

7.1.1.1. Reduces insulin resistane in Type II

7.1.1.2. Decreases risk of Type II D in pts with insulin resistance

7.1.1.2.1. Not as effective as lifestyle changes!!!

7.1.2. Admin/PK

7.1.2.1. Ineffective in the absense of insulin

7.1.2.1.1. Must take with food

7.1.2.2. Excreted in urine

7.1.2.3. 1/2 life = 2 hrs

7.1.3. MOA

7.1.3.1. Improves glucose uptake in M and fat celss

7.1.3.2. Reduces hepatic glucose production - Major Action!!!

7.1.3.3. Ultimately decreases serum insulin and glucose levels

7.1.3.3.1. Decreases both fasting and postprandial hyperglycemia

7.1.4. SE

7.1.4.1. Positives

7.1.4.1.1. No risk of hypoglycemia

7.1.4.1.2. Weight loss or stabilization

7.1.4.1.3. Prevent macrovascular complications

7.1.4.1.4. Decreased TG, total and LDL-C

7.1.4.1.5. Cheap!!!

7.1.4.2. Negative

7.1.4.2.1. NVD (pretty common)

7.1.4.2.2. Metallic taste

7.1.4.2.3. Lactic acidosis (rare)

7.1.5. CI

7.1.5.1. Pt predisposed to lactic acidosis

7.1.5.1.1. Renal Dz, Hepatic Dz, or alcoholics

7.1.5.1.2. Hx of LA

7.1.5.1.3. Decreased tissue perfusion or hemodynamic instability

7.1.5.1.4. Discontinue prior to

8. Insulin

8.1. Rapid Acting (4 hrs activity)

8.1.1. Insulin Lispro

8.2. Short Acting

8.2.1. Regular Humulin R

8.3. Intermediate Acting

8.3.1. NPH Humulin N

8.4. Long Acting (24 hrs activity)

8.4.1. Insulin Glargine

8.5. Use

8.5.1. Pt often on > 1 type

8.5.1.1. Ex - 1 LA dose/day for basal levels + RA injection before every meal to handle addition carb load

8.5.2. Insulin pump

8.5.2.1. maintains basal raid + gives a meal bolus

8.5.2.2. Only use RA insulin

8.5.3. Injection

8.6. SE

8.6.1. Lipohypertrophy

8.6.1.1. Occurs when you give the injection in the same spot

8.6.2. Hypoglycemia

8.6.2.1. Sx of activated sympathetics

8.6.2.2. Sx of brain not getting enough glucose

9. Glucagon

9.1. Use

9.1.1. Tx hypoglycemia

9.2. MOA

9.2.1. Made by alpha cells in pancreas; stimulate liver into GNG and glycogenolysis

9.3. Admin

9.3.1. SQ injection

10. Type II Diabetes causes

10.1. Insulin resistance

10.1.1. Failure of liver to decrease glucose production

10.1.2. Impaired glucose uptake in muscle and fat cells

10.1.3. Drugs that work here:

10.1.3.1. Metformin

10.1.3.2. TZDs

10.2. reduced GLP-1

10.2.1. Drugs that work here:

10.2.1.1. Incretins

10.3. Pancreatic Beta cell dysfuntion

10.3.1. reduced insulin secretion

10.3.1.1. Drugs that work here:

10.3.1.1.1. Sulfonylureas

10.3.1.1.2. Meglitinides

10.3.2. Reduced amylin secretion

10.3.2.1. Drugs that work here:

10.3.2.1.1. Pramlintide