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ILE I > ILE I U2 PO > Flashcards

ILE I U2 PO Flashcards

1
Q

glipizide, glyburide and glimepiride are what types of drugs? Which generations are these?

A

Sulfonylureas, 2nd and 3rd gen

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2
Q

Sulfonylurea MoA on pancreas

A

Inhibit efflux of K from beta cells through SUR receptor, which causes Ca channels to open, releasing Ca, which binds to calmodulin, and releases granules containing insulin

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3
Q

Name of the K-ATP channel in beta cells

A

Kir6.2

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4
Q

Glipizide in excretion

A

85% renal - patients MUST have renal function!

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5
Q

Glyburide in excretion

A

50:50 renal:fecal

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6
Q

When should you use a sulfonylurea?

A

Patients >40, duration of disease <5 years, no prior treatment with insulin

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7
Q

Combination sulfonylurea therapy

A

Okay with other anti diabetics, but cannot be used with meglitinides

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8
Q

Rosiglitazone/Glimepiride brand

A

Avandaryl

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9
Q

Pioglitazone/Glimepiride brand

A

Duetact

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10
Q

Glyburide/Metformin brand

A

Glucovance

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11
Q

Glipizide/Metformin brand

A

Metaglip

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12
Q

Sulfonylurea ADRs

A
  1. Weight GAIN

2. Hypoglycemia

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13
Q

Sulfonylurea considerations

A
  1. Cannot use with meglitinides
  2. Cannot use with gestational diabetes
  3. Cannot use with renal failure patients
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14
Q

Glipizide brand

A

Glucotrol

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15
Q

Glyburide brand

A

Glycron, Diabeta

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16
Q

Sulfonylurea advantages over other drugs

A

Extensive experience, decreases microvascular risk

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17
Q

Beta blockers and sulfonylureas

A

these drugs block the counter-regulatory response that prevents a dangerous hypo or–if it cannot prevent the hypo–at least gives the victim some warning that one is coming by causing shakes and pounding pulse.

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18
Q

Repaglinide and nateglinide are what kinds of drugs?

A

Meglitinides

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19
Q

Repaglinide brand

A

Prandin

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20
Q

Nateglinide brand

A

Starlix

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21
Q

Meglitinide MoA

A

Similar to sulfonylurea MoA, but different site. Block ATP-K channels, Ca influx induces insulin secretion.
Stimulate pancreatic insulin secretion: decrease glucose rise after a meal, however insulin is glucose dependent and thus diminishes at low blood glucose concentrations.

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22
Q

Meglitinide MoA is dependent on

A

functional pancreatic islet cells

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23
Q

Meglitinide vs suflonylurea: which has a faster “on/off” effect, and is more tissue selective?

A

Meglitinides. Therefore, these are less effective at a lower state of hypoglycemia

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24
Q

Meglitinide ADRs

A
  1. hypoglycemia (less than 8% A1C), less than SU due to glucose sensitive release of insulin
  2. slight weight GAIN
  3. Headache.
  4. GI disturbances.
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25
Q

Meglitinide excretion

A
  1. Renal

2. Bile

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26
Q

When to use meglitinides

A

patients that have postpranadial hyperglycemia and are close to glycemic goals.

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27
Q

Meglitinide combination therapies:

A
  1. Effective with metformin
  2. Can be used with other drugs
  3. Can NOT be used with SUs
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28
Q

Replaglinide/Metformin brand

A

PrandiMet

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29
Q

Additional meglitinide considerations

A
  1. Must be taken 30 min before meal
  2. Causes hypoglycemia in patients less than 8% A1C
  3. More flexible dosing and less weight gain than SU
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30
Q

Repaglinide and erythromycin

A

Causes increased serum concentrations

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31
Q

Drugs that ____ decrease effect of repaglinide

A

induce the CYP 3A4 (i.e. rifampin, phenytoin, barbiturates, carbamazepine)

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32
Q

Rosiglitazone and pioglitazone are what type of drugs?

A

TZDs (Thiazolidinediones)

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33
Q

Rosiglitazone brand

A

Avandia

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34
Q

Pioglitazone brand

A

Actos

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35
Q

TZD onset

36
Q

TZD target tissues

A

adipose, some skeletal/liver

37
Q

TZD MoA

A

By acting on PPAR-gamma (which regulates insulin responsive genes), they increase glucose and fatty acid uptake into adipose tissue and act on liver to decrease hepatic glucose production.
IMPROVED INSULIN SENSITIVITY

38
Q

TZDs lower A1C by

39
Q

Rosiglitazone/Metformin brand

40
Q

Pioglitazone/Metformin brand

A

Actoplus Met

41
Q

Rosiglitazone/Glimepiride brand

42
Q

Pioglitazone/Glimepiride brand

43
Q

TZD compatibility with other drugs

A

Can be used with all other antidiabetic drugs!

44
Q

TZD ADRs

A
  1. Can cause MI in patients with preexisting cardiovascular conditions
45
Q

Advantages of TZDs

A
  1. Less hypoglycemia
  2. durable
  3. Can be used with other anti diabetic meds
  4. decreases triglycerides
  5. Positive effect on lipid profiles!
46
Q

Disadvantages of TZDs

A
  1. Expensive
  2. Weight gain
  3. Edema
  4. Bone fractures
  5. Increased LDL
  6. MI possibility (rosi)
  7. Bladder cancer (pio)
47
Q

Which TZD was removed from the market? Why?

A

Rosiglitazone, because it causes MI in patients with a history of CVD.

48
Q

What kind of drugs are metformin, phenformin and buformin?

49
Q

metformin brand

A

glucophage

50
Q

Why was phenformin removed from the market?

A

it caused lactic acidosis

51
Q

GIP synthesized from

A

K cells small intestines

52
Q

GLP-1 synthesized from

A

L cells of bowel/colon

53
Q

GLP-1 function

A

increased insulin secretion
increase uptake of glucose
decreased gastric emptying
increased satiety

54
Q

GIP function

A

induces insulin secretion

55
Q

limitation of GIP and GLP-1

A

quick degradation by DPP4

56
Q

DPP4 function

A

degrades GIP and GLP4

57
Q

GIP degradation time

58
Q

GLP-4 degradation time

59
Q

Exenatide found in

A

Gila monster saliva

60
Q

Exenatide MoA

A

Exenatide enhances insulin secretion in aglucose-dependent manner, suppressing inappropriately high postprandial glucagon secretion resulting in decreased hepatic glucose production. It increases satiety, slows gastric emptying, and promotes weight loss.

61
Q

GLP-1 agonists are dependent on

A

the presence of elevated circulating glucose levels.

62
Q

GLP-1 vs exenatide; which is more potent?

63
Q

exenatide with metformin

64
Q

exenatide with SU

A

reduce the SU dose to reduce risk of hypoglycemia

65
Q

Liraglutide is a

66
Q

Exenatide is

67
Q

How does dosing a GLP-1 A differ from dosing a SU?

A

Give SU after, give GLP-1 A before meals

68
Q

Why give GLP-1 A before a meal?

A

Dependent on increase of glucose to work

69
Q

victoza

A

liraglutide

70
Q

advantage of victoza

A

plasma protein bound, lasts longer

71
Q

Problems with GLP-1 A

A 
GI upset,
injectable, 
anti-exenatide antibodies,
ACUTE PANCREATITIS
THYROID TUMORS
72
Q

DDP-4 inhibitor MoA

A

inhibits the enzyme that breaks apart GLP-1 and GIP,

73
Q

DDP4 inhibitor drug

A

sitagliptin

74
Q

Sitagliptin should be decreased when treating with another drug in combination

75
Q

GLP-1 A examples

A 
EXENATIDE (Bydureon, Byetta) 
LIRAGLUTIDE (Victoza) 
Albiglutide (Tanzeum)
Dulaglutide (Trulicity)
Lixisenatide(Adlyxin)
76
Q

DDP4 examples

A 
LINAGLIPTIN (Tradjenta)
Saxagliptin (Onglyza)
SINAGLIPTIN (Januvia)
Alogliptin (Nesina)
Vildagliptin(dialiptin, equa, galvus)
77
Q

Problems with DD4 inhibitors

A

Urticaria/angioedema, heart problems, PANCREATITIS

78
Q

Advantages of GLP-1A

A

weight loss, no hypoglycemia, CVD reduction

79
Q

Advantages of DD4 inhibitors

A

well tolerated, no hypoglycemia

80
Q

Antidiabetics that cause weight gain

A

Glinides
Insulin
Sulfonylureas
Thiazolidinediones

81
Q

Antidiabetics that cause weight loss

A 
α-Glucosidase inhibitors
DPP-4 inhibitors
GLP-1 receptor agonists
Metformin
SLGT2 inhibitors
82
Q

Which drugs most likely to cause hypoglycemia

A

SU, some meglitinides, rarely glitazones (TZDs)

83
Q

Which drugs will NOT cause hypoglycemia?

A

metformin, acarbose

84
Q

How much glucose is filtered each day?

A

180 g (SLGT2 90%, SLGT1 10%)

85
Q

SLGT2 inhibitor advantages

A

Weight loss, decreased BP, all stages of T2D

86
Q

SLGT2 inhibitor disadvantages

A

GI INFECTIONS,
polyuria,
LDL-C increase
hypotension

87
Q

SLGT2 inhibitor examples

A

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin(Jardiance)

ILE I (18 decks)

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