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Pharmacology > Drugs for Diabetes > Flashcards

Drugs for Diabetes Flashcards

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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
what is an example of an intermediate acting insulin preparation?
humulin N (Lilly)
26
what is found in intermediate acting insulin preparation?
protamine | suspension is at neutral pH in phosphate buffer
27
what is the peak level and DoA for intermediate acting insulin preparation?
``` duration = 10-20h peak = 4-8h ```
28
what are three examples of long acting insulin preparation? what is the downside to one of the preparations?
``` insulin glargine (LantusR) insulin detemir (LevemirR) - requires BID dosing rather than OD dosing with LantusR Novolin 70/30%(NPH) ```
29
what is long acting insulin preparation?
insulin with 3 altered AAs in B chain (Asparagine replaces glycine, 2 arginines added at C-terminus)
30
what is the benefit to using long acting insulin preparations?
useful for providing basal insulin concentration overnight
31
what is the DoA for long acting insulin preparations?
22-24h
32
what are some SE's related to insulin preparation use?
``` hypoglycemia (with insulin overdose) - sweating, tachycardia, trembling, confusion, unconsciousness, coma local reactions at injection site (rare) allergic reactions (Rare) ```
33
what is an insulin pump? | what is a downside to using the insulin pump?
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
what are two drug classes of insulin releasing agents?
sulfonyureas | meglitinide analogs
35
what are some examples of sulfonylureas?
glimepiride glipizide glyburide
36
what is the MoA for sulfonylureas?
1) stimulate pancreatic insulin secretion and sensitize beta cells to glucose 2) increase insulin sensitivity of target tissues
37
what causes insulin secretion?
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
briefly describe the PK for sulfonylureas?
absorbed from GI tract | considerable protein binding
39
what are some potential SE's of sulfonylureas?
hypoglycemia (overdose) - worst with those taking glyburide weight gain aggravation of myocardial ischemia
40
when is sulfonylurea use contraindicated?
in patients with CV disease or liver/kidney insufficiencies
41
what are the indications of sulfonylureas?
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
what are some examples of meglitinide analogs?
repaglinide | nateglinide
43
what is the MoA for meglitinide analogs?
increases insulin secretion by binding to the ATP-sensitive K+ channels
44
briefly describe the PK for meglitinide analogs
rapidly absorbed with short half life and fast onset | must be taken 15-30 min prior to meals
45
what is a side effect of meglitinide analogs?
may cause weight gain
46
what is a drug class of weight reducing agents?
biguanides
47
what is the first line treatment for T2DM?
metformin
48
give an example of a biguanide
metformin
49
what is the MoA for biguanides?
activates AMP-activated protein kinase (AMPK), triggering decreased gluconeogenesis in liver/skeletal muscle and increased peripheral insulin response. Does not effect insulin secretion
50
briefly describe the PK for biguanides
not metabolized or protein bound no drug interactions renal impairment reduces excretion
51
what is a major concern of using biguanides?
increased risk of fatal lactic acidosis | note: risk of this with metformin is reduced compared to other biguanides
52
what is a benefit to using metformin?
associated with mild weight loss | lowers parandial glucose but does not produce hypoglycemia
53
what is a drug class for insulin sensitivity enhancers?
thiazolidinedione derivates
54
what are two examples of thiazolidinedione derivates?
rosiglitazone | pioglitazone
55
what is the MoA of thiazolidinedione derivates?
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
what is the difference between rosiglitazone and pioglitazone?
rosiglitazone does not interfere with CYP3A4 activity, so there is less chance for side effects
57
what are some side effects to using pioglitazone?
``` edema macula edema loss of bone density weight gain concerns with bladder cancer ```
58
what are two examples of alpha-glucosidase inhibitors?
acarbose | miglitol
59
what is the MoA of alpha-glucosidase inhibitors? what is one benefit of this drug class?
slows the break down and absorption of starch and complex carbohydrates pro: does not cause hypoglycemia
60
what is the indication for alpha-glucosidase inhibitors?
type 2 diabetes
61
what is a side effect to alpha-glucosidase inhibitors?
abdominal discomfort
62
when is the use of alpha-glucosidase inhibitors contraindicated?
chronic intestinal diseases
63
what are two classes of drugs under incretins?
DPP-4 inhibitors | GLP-1 analogs
64
what are two examples of DPP-4 inhibitors?
sitagliptin-PO4 (Januvia) | saxagliptin (Onglyza)
65
what is the MoA of DPP-4 inhibitors?
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
name two examples of GLP-1 analogs. what is the difference between the two?
exenatide (Byetta) - BID SC injection | liraglutide (Victoza) - OD SC injection
67
what is a benefit to using GLP-1 analogs?
reduced weight and blood glucose
68
what is an example of an amylin?
pramlintide (Symlin)
69
what is the MoA of pramlintide?
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
what is the indication of pramlintide?
type 1 and type 2 diabetes
71
what can cause complications of diabetes?
periods of less severe hyperglycemia result in glycosylation of various proteins and accumulation of sorbitol in non-insulin dependent cells
72
what are some complications of diabetes?
``` micro: neuropathy nephropathy retinopathy macro: CV disease ```

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