Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR 230 > M4 L3: Insulin and Anti-diabetic Agents > Flashcards

M4 L3: Insulin and Anti-diabetic Agents Flashcards

1
Q

treatment of diabetes

A

diet control, antidiabetic agents, treatment of complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are 2 types of antidiabetic agents

A
  1. insulin
  2. oral hypoglycemic agents (T2D)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

indications of insulin therapy

A
  1. type 1 diabetes
  2. type 2 diabetes
  3. gestational diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when can you not take oral hypoglycemic agents

A

during pregnancy, gestational diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

administration of insulin

A

injection: IV, IM, SC
alternative methods: pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

onset peak and duration of fast (rapid) insulin

A

onset: 5-15 min
peak: 3/4-1 hr
duration: 2-4 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

onset peak and duration of short insulin

A

onset: 0.5-1 hr
peak: 2-3 hr
duration: 5-8 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

onset peak and duration of intermediate insulin

A

onset: 1-2 hr
peak: 4-12 hr
duration: 10-20 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

onset peak and duration of long insulin

A

onset: 1-2 hr
peak: minimal
duration: 18-24 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

onset peak and duration of ultra long insulin

A

onset: 1-2 hr
peak: minimal
duration: >24 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

insulin preparations for fast-acting

A

lispro-aspart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

insulin preparations for short-acting

A

regular (crystalline) insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

insulin preparations for intermediate-acting

A

NPH (neutral protamine hagedorn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

insulin preparations for long-acting

A

detemir-glargine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

insulin preparations for ultra-long

A

degludec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

insulin preparations for mixed types

A

(combinations)

rapid onset + prolonged duration
ex: NPH/regular 70/30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is conventional therapy for insulin regimens

A
  • 1-2 injections/day
  • daily self monitoring of glucose
  • lower risk of hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is intensive therapy for insulin regimens

A
  • multiple daily injections
  • daily self monitoring of glucose and dose adjustment
  • reduction in retinopathy, nephropathy, and neuropathy
  • higher risk of hypoglycemia (3- fold more than conventional)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does a daily insulin schedule for fast/short type 1 diabetes

A
  • injection time before breakfast (BF)
  • major affect BF->lunch
  • end effect before lunch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does a daily insulin schedule for fast/short type 1 diabetes

A
  • injection time before breakfast
  • major effect lunch -> dinner
  • end effect before dinner
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does a daily insulin schedule for fast/short type 2 diabetes

A
  • injection time before dinner
  • major effect dinner -> bed snack
  • end effect before bed snack
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does a daily insulin schedule for NPH/long type 2 diabetes

A
  • injection time before dinner
  • major effect overnight
  • end of effect before breakfast the next day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

absorption of SC insulin

A
  • highly variable: inter (diff from one person to another based on their metabolism and so on)/intraindividual (some conditions will be associated with high rate of absorption.

factors affecting absorption:
- site of injection
- blood flow to site of injection
- depth of injection
- exercise increases absorption
- massage of the area increases absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are alternatives to insulin injections?

A
  • insulin pumps, insulin pens (most common)
  • transdermal: jet injection, patches
  • inhaled insulin (afrezza)
  • oral formulas (under investigation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

systemic complications of insulin therapy

A
  • hypoglycemia -> most dangerous
  • insulin allergy -> rare w human insulin
  • insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are local complications of insulin therapy

A
  • lipoatrophy
  • hypertrophy
    (change the site of injection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ex of oral hypoglycemic agents

A
  • sulfonylureas (insulin secretagogues)
  • meglitinides (insulin secretagogues)
  • biguanides
  • thiazolidinediones (TZDs, glitazones)
  • alpha-glucosidase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how is insulin stimulated by beta cell (inulin secretagogues)

A

they inhibit potassium on the beta-cell, which causes depolarization, resulting in increased calcium entry, and increased insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what causes increased receptor sensitivity for insulin (sulfonylureas)

A

potentiate insulin action in different tissues
- they require functional beta-cells to work, and are only useful for type 2 NOT type 1 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

alpha cells secrete…

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

beta cells secrete…

A

insulin

32
Q

what are endocrine glands

A
  • form clusters called pancreatic islets
  • secrete hormones
33
Q

what are the effects of insulin

A
  1. accelerates glucose uptake and utilization
  2. stim glycogen formation
  3. stim triglyceride formation in adipose tissue
  4. stim amino acid absorption and protein synthesis
34
Q

sulfonylureas pharmacokinetics

A
  • bind to plasma proteins
  • metabolized in the liver
  • excreted through kidneys
  • exaggerated effects in elderly and renal or liver disease
  • cross the placenta -> teratogenic effect

contraindicated during pregnancy**

35
Q

what are sulfonylureas drugs that increase hypoglycemic effects

A
  • NSAIDs, warfarin, MAO inhibitors, alcohol, some antibacterials (ex: sulfonamides)
  • microsomal enzyme inhibitors
36
Q

what are sulfonylureas drugs that decrease hypoglycemic effects

A
  • microsomal enzyme inducers (ex: rifampicin)
  • phenytoin (inhibits insulin release)
37
Q

what sulfonylureas drugs mask the symptoms of hypoglycemia

A

beta blockers

38
Q

sulfonylureas preparations for 1st gen examples

A

tolbutamide, chlorpropamide

39
Q

sulfonylureas preparations for 2nd gen examples

A

glipizide, glibenclamide, gliclazide

40
Q

sulfonylureas preparations for 3rd gen examples

A

glimepiride

41
Q

duration of tolbutamide & glipizide (sulfonylurea agents)

A

6-10 hrs
dose frequency: BID-TID

42
Q

duration of glibenclamide & gliclazide (sulfonylurea agents)

A

12-16 hrs
dose frequency: OD-BID

43
Q

duration of glimepiride & chlorpropamide (sulfonylurea agents)

A

24-72 hrs
dose frequency: OD

44
Q

sulfonylureas adverse effects

A
  • hypoglycemia
  • GI disturbances
  • hepatic toxicity
  • allergic skin reactions
45
Q

biguanides mech of action

A
  • decreased gluconeogenesis in liver
  • increased glucose uptake by skeletal muscles
46
Q

biguanides indications

A
  • 1st choice for obese patients with type 2
  • can be combined with sulfonylurea or insulin
47
Q

what is the advantage of biguanides

A
  • do not cause hypoglycemia as they do not alter insulin levels
48
Q

biguanides side effects

A
  • anorexia
  • nausea, diarrhea, metallic taste
  • lactic acidosis
49
Q

what is metformin

A

(only available biguanide on the market so far)
- 2 tablet forms: glucophage, glucophage XR

50
Q

what are meglitinides

A
  • short acting insulin secretagogues
  • action is similar to sulfonylureas
  • short acting, half life is 1hr
51
Q

indications of meglitinides

A

type 2 DM
- can be combined w metformin

52
Q

adverse effects of meglitinides

A

hypoglycemia (rare)

53
Q

examples of meglitinides

A

repaglinide, nateglinide

54
Q

mech of action for thiazolidinediones (TZDs)

A
  • activate a transcription regulator PPARy
  • this improved glucose uptake in skeletal muscles
  • decreased hepatic glucose production
  • modulate lipogenesis in adipocytes
  • reverse insulin resistance
55
Q

what are the indications of thiazolidinediones

A
  • T2D
  • alone or combined w metformin, sulfonylurea
56
Q

thiazolidinedione adverse effects

A

congestive heart failure and myocardial ischemia
- may cause hepatic injury (monitor liver function)

57
Q

what are ex. of thiazolidinediones

A

rosiglitazone, pioglitazone

58
Q

what are alpha-glucosidase inhibitors

A
  • inhibits alpha-glucosidases in intestine -> reduces absorption of carbs
  • not absorbed from intestine
  • control post-prandial glucose levels not adequately controlled by diet and sulfonylureas
59
Q

side effects of alpha-glucosidase inhibitors

A

GI upset and flatulence

60
Q

name an example of a alpha-glucosidase inhibitor

A

acarbose

61
Q

recent antidiabetic agents

A
  • glucagon-like peptide-1 (GLP-1) agonists
  • DPP-4 inhibitors (gliptins)
  • amylin analogues
  • gliflozins
62
Q

what are glucagon-like peptide-1 (GLP-1) agonists

A
  • group of GIT hormones called “incretins”
  • adjunct treatment in T2D
  • SC injection
63
Q

example of glucagon-like peptide-1 (GLP-1) agonists

A

exenatide

64
Q

what are incretins

A

GIT hormones stim insulin release and inhibit glucagon. Includes GLP-1 and GIP (gastric inhibitory peptide)

65
Q

mech of action for glucagon-like peptide-1 (GLP-1) agonists

A
  • increase insulin release (insulin secretagogues)
  • decrease glucagon release
66
Q

mech of action for DPP-4 inhibitors (gliptins)

A
  • decreased DPP-4 enzyme -> increased incretins
  • is the adjunct treatment in type 2
  • take them orally
67
Q

what are the adverse effects of DPP-4 inhibitors (gliptins)

A
  • joint pain
  • HF
  • pancreatitis
  • ? pancreatic cancer
68
Q

ex of DPP-4 inhibitors (gliptins)

A

sitagliptin, saxagliptin

69
Q

what is amylin

A
  • a hormone made by the beta cells of the pancreas (not just insulin!)

made in a 99:1 ratio (larger being insulin)

70
Q

mech of action for amylin analogues

A
  • slows gastric emptying
  • decrease postprandial glucagon release
71
Q

what is amylin analogues for, how is it administered

A
  • adjunct treatment for T1D, and T2D
  • SC injection
72
Q

what is an example of amylin analogues

A

pramlintide (only product available)

73
Q

what do glifolzins do

A

decrease SGLT-2 (sodium-glucose cotransporter 2) -> decrease renal glucose reabsorption -> glycosuria

74
Q

what is gliflozins used for and how is it administered

A
  • T2D (alone or in combo)
  • orally
75
Q

adverse effects of gliflozins

A
  • hypoglycemia
  • ketoacidosis
  • UTI
76
Q

gliflozins example

A

canagliflozin

PHAR 230 (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions