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Pharmacology > Drugs for Diabetes > Flashcards

Drugs for Diabetes Flashcards

1
Q

what is diabetes mellitus?

A

insufficiency of insulin signalling relative to the requirements of the tissues for this hormone

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2
Q

what are some symptoms of DM?

A 
polyuria (sweet urine)
polydipsia (excessive thirst)
polyphagia (excessive hunger)
elevated fasting blood sugar
ketosis
weight loss
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3
Q

What are the normal fasting blood glucose levels?

A

4.4-6.1mmol/L

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4
Q

what fasting blood glucose level indicates DM?

A

7 mmol/L or over

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5
Q

what is type 1 DM? type 2 DM?

A

type 1 - autoimmune destruction of beta cells in pancreas

type 2 - insulin resistance; insulin secretion is present but inappropriate in requirement and timing

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6
Q

what are some differences between T1DM and T2DM?

A

1) T1DM onset primarily in childhood; T2DM onset primarily after 40y.o
2) T1DM are often normal weight; T2DM typically obese
3) T1DM prone to ketoacidosis, not T2DM
4) T1DM requires insulin admin, T2DM does not require it
5) T1DM tx = insulin; T2DM tx = healthy diet/exercise, hypoglycemic tabs, insulin

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7
Q

what is the relative prevalence of T1DM and T2DM?

A

1 - 10-20%

2 - 80%

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8
Q

what is preproinsulin?

A

a very large peptide that is cleaved to produce proinsulin?

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9
Q

what is proinsulin?

A

the precursor to insulin. it is cleaved to produce insulin and C-peptide

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10
Q

where is insulin secreted from?

A

pancreatic beta cells

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11
Q

what is the potential function of C peptide?

A

has a role in rate of endogenous insulin release

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12
Q

what does insulin consist of?

A 
A chain (21 AA)
B chain (30 AA)
these are attached in parallel by two disulfide links
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13
Q

what stimulates insulin secretion?

A

elevated blood glucose

also by physiological levels of AAs, FAs, and ketone bodies

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14
Q

what signals an increase in insulin secretion? decrease?

A

incr - parasym

decr - sym

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15
Q

what inhibits insulin/glucagon secretion?

A

somatostatin (product of pancreatic D cells)

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16
Q

describe the PK for insulin

A 
largely unbound
distributed in ECF volume
first pass metabolism
also degraded by kidney
t1/2 = 9min
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17
Q

what are some results of lack of insulin in the body?

A

1) hyperglycemia (underutilization of glucose by muslce and fat; overproduction of glc in liver)
2) reduced glycogen/protein synthesis
increased lipolysis

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18
Q

what is the difference between the different insulin preparations?

A

duration of action - depending on rate of absorption after SC injection

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19
Q

what are the four kinds of insulin preparations?

A

rapid acting
short acting
intermediate acting
long acting

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20
Q

what are some examples of a rapid acting insulin preparation?

A 
insulin Lispro (Humalog)
insulin aspart (Novolog)
insulin glulisine (Apidra)
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21
Q

what are rapid acting insulin preparations?

A

insulin where the 28th and 29th AA are reversed on the B chain, resulting in rapid absorption

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22
Q

what is the benefit of using rapid acting insulin preparations?

A

better post-prandial glucose control with reduced risk for hypoglycemia

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23
Q

what is an example of a short acting insulin preparation?

A

regular novolin R (Novo Nordisk)

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24
Q

what is a short acting insulin preparation?

A

has rapid onset and short duration

peak effect in 5h, duration up to 12h

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25
Q

what is an example of an intermediate acting insulin preparation?

A

humulin N (Lilly)

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26
Q

what is found in intermediate acting insulin preparation?

A

protamine

suspension is at neutral pH in phosphate buffer

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27
Q

what is the peak level and DoA for intermediate acting insulin preparation?

A 
duration = 10-20h
peak = 4-8h
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28
Q

what are three examples of long acting insulin preparation? what is the downside to one of the preparations?

A 
insulin glargine (LantusR)
insulin detemir (LevemirR) - requires BID dosing rather than OD dosing with LantusR
Novolin 70/30%(NPH)
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29
Q

what is long acting insulin preparation?

A

insulin with 3 altered AAs in B chain (Asparagine replaces glycine, 2 arginines added at C-terminus)

30
Q

what is the benefit to using long acting insulin preparations?

A

useful for providing basal insulin concentration overnight

31
Q

what is the DoA for long acting insulin preparations?

A

22-24h

32
Q

what are some SE’s related to insulin preparation use?

A 
hypoglycemia (with insulin overdose) - sweating, tachycardia, trembling, confusion, unconsciousness, coma
local reactions at injection site (rare)
allergic reactions (Rare)
33
Q

what is an insulin pump?

what is a downside to using the insulin pump?

A

delivers insulin at a constant slow rate, plus a bolus when desired (ex: before meals)
con: requires frequent self-monitoring of blood glucose and dosage adjustment

34
Q

what are two drug classes of insulin releasing agents?

A

sulfonyureas

meglitinide analogs

35
Q

what are some examples of sulfonylureas?

A

glimepiride
glipizide
glyburide

36
Q

what is the MoA for sulfonylureas?

A

1) stimulate pancreatic insulin secretion and sensitize beta cells to glucose
2) increase insulin sensitivity of target tissues

37
Q

what causes insulin secretion?

A

due to inhibition of ATP sensitive K+. High glc increases ATP, which inhibits K+ channels, leading to depolarization and opening of Ca2+ channels with influx of Ca2+

38
Q

briefly describe the PK for sulfonylureas?

A

absorbed from GI tract

considerable protein binding

39
Q

what are some potential SE’s of sulfonylureas?

A

hypoglycemia (overdose) - worst with those taking glyburide
weight gain
aggravation of myocardial ischemia

40
Q

when is sulfonylurea use contraindicated?

A

in patients with CV disease or liver/kidney insufficiencies

41
Q

what are the indications of sulfonylureas?

A

mild T2DM when diet alone is not sufficient and insulin injection is not practical
Not proven to be of benefit in preventing long-term complications of diabetes

42
Q

what are some examples of meglitinide analogs?

A

repaglinide

nateglinide

43
Q

what is the MoA for meglitinide analogs?

A

increases insulin secretion by binding to the ATP-sensitive K+ channels

44
Q

briefly describe the PK for meglitinide analogs

A

rapidly absorbed with short half life and fast onset

must be taken 15-30 min prior to meals

45
Q

what is a side effect of meglitinide analogs?

A

may cause weight gain

46
Q

what is a drug class of weight reducing agents?

A

biguanides

47
Q

what is the first line treatment for T2DM?

A

metformin

48
Q

give an example of a biguanide

A

metformin

49
Q

what is the MoA for biguanides?

A

activates AMP-activated protein kinase (AMPK), triggering decreased gluconeogenesis in liver/skeletal muscle and increased peripheral insulin response.
Does not effect insulin secretion

50
Q

briefly describe the PK for biguanides

A

not metabolized or protein bound
no drug interactions
renal impairment reduces excretion

51
Q

what is a major concern of using biguanides?

A

increased risk of fatal lactic acidosis

note: risk of this with metformin is reduced compared to other biguanides

52
Q

what is a benefit to using metformin?

A

associated with mild weight loss

lowers parandial glucose but does not produce hypoglycemia

53
Q

what is a drug class for insulin sensitivity enhancers?

A

thiazolidinedione derivates

54
Q

what are two examples of thiazolidinedione derivates?

A

rosiglitazone

pioglitazone

55
Q

what is the MoA of thiazolidinedione derivates?

A

decreases insulin resistance by binding to insulin-responsive genes
decreases gluconeogenesis and glucose output; increases glc uptake and utilization in skeletal muscle
decreases insulin requirement
no effect on insulin secretion

56
Q

what is the difference between rosiglitazone and pioglitazone?

A

rosiglitazone does not interfere with CYP3A4 activity, so there is less chance for side effects

57
Q

what are some side effects to using pioglitazone?

A 
edema
macula edema
loss of bone density
weight gain
concerns with bladder cancer
58
Q

what are two examples of alpha-glucosidase inhibitors?

A

acarbose

miglitol

59
Q

what is the MoA of alpha-glucosidase inhibitors? what is one benefit of this drug class?

A

slows the break down and absorption of starch and complex carbohydrates
pro: does not cause hypoglycemia

60
Q

what is the indication for alpha-glucosidase inhibitors?

A

type 2 diabetes

61
Q

what is a side effect to alpha-glucosidase inhibitors?

A

abdominal discomfort

62
Q

when is the use of alpha-glucosidase inhibitors contraindicated?

A

chronic intestinal diseases

63
Q

what are two classes of drugs under incretins?

A

DPP-4 inhibitors

GLP-1 analogs

64
Q

what are two examples of DPP-4 inhibitors?

A

sitagliptin-PO4 (Januvia)

saxagliptin (Onglyza)

65
Q

what is the MoA of DPP-4 inhibitors?

A

ingesting a meal leads to secretions of GLP-1 from gut, which is insulinotropic and are decreased in T2DM. DDP-4 inhibitors inhibit dipeptidyl peptidase-4, an enzyme that degrades GLP-1

increase insulin synthesis and release; decrease glucagon levels

66
Q

name two examples of GLP-1 analogs. what is the difference between the two?

A

exenatide (Byetta) - BID SC injection

liraglutide (Victoza) - OD SC injection

67
Q

what is a benefit to using GLP-1 analogs?

A

reduced weight and blood glucose

68
Q

what is an example of an amylin?

A

pramlintide (Symlin)

69
Q

what is the MoA of pramlintide?

A

amylin is a hormone co-secreted with insulin from beta cells in response to glc
Pramlintide is a synthetic analog of amylin, which is more soluble and does not readily aggregate like amyline
Decreaes glucagon secretion and glc absorption

70
Q

what is the indication of pramlintide?

A

type 1 and type 2 diabetes

71
Q

what can cause complications of diabetes?

A

periods of less severe hyperglycemia result in glycosylation of various proteins and accumulation of sorbitol in non-insulin dependent cells

72
Q

what are some complications of diabetes?

A 
micro:
neuropathy
nephropathy
retinopathy
macro:
CV disease

Pharmacology (9 decks)

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