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Endocrine > Diabetes Medications > Flashcards

Diabetes Medications Flashcards

1
Q

Thiazolidienediones Tzdx MOA

A

Peroxisome proliferator-activated receptor-gama (PPAR-Gamma receptor ligand

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2
Q

PPAR-gamma receptors actions

A

Nuclear hormone receptor
Transcription factor
Glucose and lipid metabolism gene regulation

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3
Q

PPAR-gamma endogenous ligand

A

oxidized fatty acids

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4
Q

Current available Tzds

A

Rosiglitazone (Avandia)

Pioglitazone (Actos)

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5
Q

Tissue with largest ppar-gamma receptor

A

Adipose

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6
Q

activation of ppar-gamma in adipose

A

Decreased release of FFA –> reduced insulin resistance
Decreased TNF-alpha
–> reduced inflammatin
–> reduced TNFalpha dependant insulin resistance

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7
Q

Secondary actions of Tzds

A

Increased insulin dependant glucose uptake in muscle (skeletal)
Due to decreased FFA

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8
Q

Tzd adverse effects (Chronic Use)

A

**Heart failure (increased blood volume)
PPAR-gamma –>increased renal fluid retention
Contraindicated with patients at risk for heart failure

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9
Q

Pioglitazone (Actos) Addition effects

A
  • Slight reduction in plasma triglycerides and increase in HDL-cholesterol levels
  • -> Dual effect on PPAR-alpha and gamma
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10
Q

Rosiglitazone (Avandia) and triglycerides/HDL levels

A

No such effect shown. Not ppar-alpha

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11
Q

Metformin (Glucophage) Mechanism of Action

A

Increase AMPK activity

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12
Q

What does AMPK activity do?

A

Reduces Gluconeogenesis
Stimulates glucose uptake in skeletalmuscle
–>Increased glut4 transporters on membrane
–>Increases insulin sensitivity
Reduces Intestinal glucose absorption

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13
Q

Metformin and normal glycemia

A

Decreased effect

At low insulin levels, glut4 moves from cell membrane to intracellular vesicles

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14
Q

Metformin and insulin release

A

no effect

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15
Q

First line T2DM

A

Metformin

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16
Q

Metformin advantages

A 
No increase in plasma insulin
--> low hypoglycemia risk
Persistent efficacy (2-5 years)
Positive lipid profile
--> decreased TGs, LDL, and increased HDL
-->lower risk of CVD
Unlikely to gain weight
Delays DM progression
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17
Q

Metformin Adverse Effects

A

GI NVD, decreases w/ food
Lactic acidosis BBW

Renal failure (sub 50ml/min) –> Metformin overdose –> lactic acidosis

Contraindicated with tissue anoxia

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18
Q

Metformin counseling point

A

Take with food

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19
Q

Metformin DDI

A 
No plasma protein binding
excreted unchanged in the urine
renal tubular secretion
OCT 2
Cationic drugs compete for transport
**Dose adjustment recommended with concurrent cationic meds: Cimetidine, furosemide, nifeedipine
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20
Q

Sulfonylureas: Insulin Secretagogue MOA

A

Bind and inhibit K-ATP

  • -> cell membrane depolarization
  • -> voltage-gated CA2+ channels open
  • -> release of preformed insulin

**No increase in insulin production

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21
Q

Sulfonylureas Prolonged administration

A

Reduced hepatic glucose production
Enhansed insulin sensitivity
–> increased insulin receptor expression
–> increased insulin receptor signaling

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22
Q

1st generation Sulfonylureas (Drugs)

Rarely used

A

Tolbutamide (Orinase)
Tolazamide (Tolinase)
Chloropropamide (Diabinese)

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23
Q

1st gen sulfonylurea duration and primary side effect

A

Long acting

High incidence of hypoglycemia (particularly at night)

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24
Q

2nd gen sulfonylureas

Selling points

A

More Potent, fewer adverse effects

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25
Q

2nd gen sulfonylureas

PK/PD & interactions

A

High plasma protein binding; effective dose

Elimination: Major elimination by hepatic metabolism, minor renal excretion

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26
Q

2nd gen sulfonylureas

Dosing

A

Same time every day, with breakfast
Start with low dose
Increase 1-2.5 mg/day every 1-2 weeks based on BG

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27
Q

2nd gen sulfonylureas

Drugs

A

Glyburide (Micronase, Diabeta)
Micronized glyburide tablets (Glynase PresTab)
Glipizide (Glucotrol)
Glimepiride (Amaryl)

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28
Q 
Glyburide (Micronase, Diabeta)
Duration
Doseing
Bioavailability
Elimination
A

~24 h
QD or BID
Poor and variable bioavailability
Eliminated by liver, partially liver

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29
Q

Micronize glyburide tablets (Glynase PresTab)
Tpeak compared
Bioavailability
Bioequivalent, result?

A

Quicker Tpeak
improved and consistent bioavailability
Not bioequivalent, must re-titrate dose

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30
Q 
Glipizide (Glucotrol)
Half life
Duration of action, result
Tabsoprtion/bioavailability
Elimination
A

~3 h t1/2, shortest
~12 h duration, less hypoglycemia
rapid absorption, consistent bioavailability
Primarily Liver, minor renal

31
Q

Glucotrol XL

A

Extended-release glipizide, more hypoglycemia

32
Q 
Glimepiride (Amaryl)
Half-life
Duration
Dosing
Elimination
A

10 h t1/2
24 h duration
Once daily dosing
Primarily liver, partly renal clearance

33
Q

Glimepiride (Amaryl) compared to Glyburide (Micronase, Diabeta)

A

Equivalent in controlling hyperglycemia
Lower plasma insulin and C-peptide values
Increased glucose uptake

34
Q

Temporal changes in plasma insulin levels with sulfonylurea treatment

A

Initial: increased fasting and respons insulin levels
Chronic (>1yr): Insulin levels decrease below original levels; downregulation of sulfonylurea cell surface receptors

**Reduction of plasma glucose levels are maintained

35
Q

Sulfonylurea long term effectiveness

A

Develop hyperglycemia >1yr

Results from progressive beta cell failure

36
Q

Sulfonylurea contraindications

A

T1DM, pregnancy, severe hepatic or renal dysfunction

37
Q

Sulfonylurea Adverse Effects

A

Late postprandial or fasting hypoglycemia
Most common with longer-acting in class
Caution in Hepatic impairment –> dose adjustment
Caution in Renal impairment

Weight Gain

38
Q

Sulfonylurea DDIs

A

Ethanol increases action
Plasma protein binding displaced by other drugs
Nonselective beta-blockers mask symptoms of hypoglycemia
Hyperglycemia inducing drugs: lower effectivenes (Diuretics, HTCZ and beta blockers propanolol)

39
Q

Meglitinide names

Secretagogues

A

Repaglinide (Prandin)

Nateglinide (Starlix)

40
Q

Repaglinide and Nateglinide MOA

A

Selectively blocks beta cell Katp

41
Q

Repaglinide and Nateglinide PK

A 
Rapid onset ~30 min
Peak ~1h
t0.5 ~1h
Take 5 min pre meal
restores insulin release
Less effect in normal glycemia
42
Q

Thiazolidinedione PK

A

Well absorbed from GI, No food effect

Metabolized by liver (Cyp2C8)

43
Q

Thiazolidinedione Adverse Effects and Contraindications

A

Fluid retention
Weight Gain

Heart Failure

44
Q

Which Drug Class(es) are useful in pt with renal insufficiency

A 
Thiazolidinediones
Metformin (down to 50 ml/min)
45
Q

Incretin Effect

A

Control:
Larger increase in insulin secretion with Glc PO compared to IV
- In T2DM, small increase

46
Q

GLP-1 and GIP

MOA

A

Increase AC –> inPKAcrease cAPM –> Amplified Glucose effect and insulin secretion (requires some level of Glc to be effective)

47
Q

Why didn’t GIP work as therapy?

A

Increased glucagon release = negated effect

48
Q

Effects of GLP1

A
  • Increased proinsulin transcription
  • Increased insulin biosynthesis
  • Direct stimulation of secretion
  • promotes satiety

*Inhibition of Glucagon secretion

49
Q

Effect of GLP1 decreased GI motility

A

Lowers post prandial glucose spike

50
Q

GLP-1 Given IV

A

Normalizes Fasting and post prandial insulin secretion

51
Q

How is GLP-1 deactivated in blood?

A

dipeptidyl peptidase IV (DPP-4)

52
Q

Exenatide (Byetta)

Structure and function

A

53% homology to GLP1, but not metabolized by DPP-4

  • Glucose-dependent insulin secretion
  • Delayed GI, Reduced Glucagon, satiety
53
Q 
Exenatide PK
Clearance
Half life
Dosing interval
Extended release
A

-Entirely renal (No use

54
Q

Exenatide immune reaction

A

Antibody development in 6-12%

55
Q

Liraglutide (victoza)

Structure

A

97% homology to GLP1

AA subs, with fatty acid to bind albumin
–>extends t1/2 and prevents peptidase breakdown

56
Q

albiglutide (Tanzeum)

Structure

A

Recombinant protein: 2 copies of human GLP-1, covelantly fused to human albumin

AA subs –> DPP-4 resistant,
Albumin–> 5 days (1/week dosing

57
Q

Liraglutide (Victoza) Dosing

A

SC QD independent of meals

58
Q

Dulaglutide (Dulaglutide)

Structure

A

2 Recombinant, disulfide linked chains of GLP-1 analog fused to h-IgG

AA subs –> dpp4 resistant
IgG ~5d (1/week dose)

59
Q

DPP-4 inhibitors

MOA (direct)

A

complete and long-lasting inhibition of dpp-4

60
Q

DPP-4 inhibitor MOA downstream

A

Increase conc. GIP and GLP-1

  • > increased insulin secretion
  • > Reduced glucagon levels
  • > Improvements in both fasting and postprandial hyperglycemia
61
Q

DPP-4 inhibitor adverse effect

A

Rare

62
Q

DPP-4 inhibitor Eg,

A

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

63
Q

DPP-4 inhibitor administration

A

QD PO without regard to meals

64
Q

DPP-4 inhibitor interactions

A

Additive effect with metformin, thazolidinediones, sulfonylureas, or insulin

65
Q

What do DPP-4 inhibitors lack that GLP-1 analogs have?

A
  • Delayed Gastric Emptying
  • Decreased food intake
  • Decreased weight
  • N/V side effects
66
Q

Alpha-glucosidase inhibitor examples

A

Acarbose (precose)

Miglitol (Glyset)

67
Q

Alpha glucosidase inhibitor MOA

A

inhibits metabolism of sucrose to Glc and Fru –> delays absorption of monosaccharides –> blunts rate post prandial glucose spike

68
Q

Alpha-glucosidase approved use

A

T2DM as monotherapy and in combo with Sulfonylureas

69
Q

AGluI counseling point

A

Diarrhea

Treat hypoglycemia with glucose, not sucrose

70
Q

Pramlintide (SymlinPen)

A

Synthetic analog of amylin

71
Q

Pramlinitide

MOA

A

Binds amylin receptors in brain:

  • > reduces glucagon release
  • > Delays GI emptying
  • > Produces satiety
72
Q

Pramlintide

Use and Admin

A

T1 and T2 DM

  • Immediatly before eating
  • adjunct to insulin –>retitrate insulin
73
Q

Pramlintide ADR

A

Hypoglycemia when used with insulin; particularily with T1DM

Endocrine (6 decks)

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