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NURS 2514 > Week 2 - Diabetes Meds > Flashcards

Week 2 - Diabetes Meds Flashcards

1
Q

what is the MOA of alpha-glucosidase inhibitors

A
  • delay absorption of carbs in the intestine = reduces the rise in BG after a meal
  • does this by blocking the anzyme alpha-glucosidase which is responsible for breaking down carbs
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2
Q

what are the 5 categories of insulin?

A
  • rapid acting
  • short acting
  • intermediate acting
  • long-acting
  • combination insulin
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3
Q

what are incretin mimetics also known as?

A
  • glucagon-like peptide 1 receptor agonists
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4
Q

what is the treatment for type 2 diabetes? (3)

A
  • lifestyle changes
  • oral drug theraoy
  • insulin when the above no longer provide glycemic control
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5
Q

list the effects of incretin hormones (4)

A
  • slow gastric emptying (digestion)
  • stimulate glucose-dependent pancreatic release of insulin
  • inhibit post prandial release of glucagon
  • decreases appetite
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6
Q

describe the duration, onset of action, and peak of long-acting insulin

A
  • duration = up to 24 hrs
  • onset = 1-3 hr
  • no peak
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7
Q

what is the prototype of sulfonylureas

A
  • glyburide (diabeta)
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8
Q

what type of insulin cannot be combined with other insulins?

A

long acting

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9
Q

when is rapid-acting insulin given? why?

A
  • given with meals –> either with, immediately before, during, or immediately after
  • purpose: to counteract postprandial BG spike
  • also, rapid acting is very intense, so the food will avoid hypoglycemia as well
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10
Q

what is the purpose of rapid acting insulin?

A
  • they are administered in associated with meals to control the postprandial rise in BG
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11
Q

describe the duration for rapid-acting insulin

A
  • shorter duration
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12
Q

when is long acting insulin given?

A
  • at the same time each day
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13
Q

how do DPP-4 inhibitors and incretin mimetics differ?

A

both incretin agents but…

  • DPP-4 inhibitors = boost the effects of incretin hormones by slowing their degradation by the enzyme DPP-4
  • incretin mimetics = boost the effects of incretin hormones by activating receptors for GLP-1
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14
Q

what is the prototype of apha-glucosidase inhibitors

A
  • acarbose (glucobay)
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15
Q

what are incretin hormones

A
  • endogneous compounds that stimulate the glucose-dependent release of inulin & suppress release of glucagon
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16
Q

allergic cross sensitivity may occur with sulfonylureas & _____ (2)

A
  • loop diuretics

- sulfonamide antibiotics

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17
Q

what are 2 types of long acting insulin

A
  1. glargine (lantus)

2. detemir (levemir)

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18
Q

SGLT-2 inhibitors are _____ and _____ protective

A

-renal & cardio

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19
Q

should long acting insulin be given with food?

A
  • it can be given without food
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20
Q

can long-acting insulin be administered IV?

A
  • no, it is chemically modified
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21
Q

why does weight loss occur with SGLT-2 inhibitors?

A
  • bc loss of calories in urine
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22
Q

list 3 examples of rapid acting insulin

A
  • insulin lispro (humalog)
  • insulin aspart (novolog)
  • insulin glulisine (apidra)
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23
Q

list 3 things that may reduce hypoglycemic effects

A
  1. corticosteroids
  2. adrenergics
  3. thiazides`
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24
Q

what types of insulins can be mixed?

A
  • short-acting

- NPH (intermediate)

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25
Q

typically, how long does it take for BG to increase after meals

A
  • 15min - 1 hr
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26
Q

what can sulfonylureas negatively interact with? what does this cause?

A
  • beta blockers

= unawareness of SNS symptoms like tachycardia if the pt becomes hypoglycemic

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27
Q

why is there side effects of gential yeast infections & UTIs with SGLT-2 inhibitors?

A
  • increased conc of glucose in the urine
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28
Q

what is a prototype of glinides

A
  • repaglinide (prandin)
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29
Q

what is the MOA of incretin mimetics?

A
  • activate receptors for GLP-1 = cause the same effects of incretin hormones
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30
Q

what is the treatment for type 1 diabetes?

A
  • insulin therapy
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31
Q

what are 2 types of DPP-4 inhibitors

A
  1. stigaliptin

2. alogliptin

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32
Q

what is a prototype of glitazones/thiazolidinediones

A
  • rosiglitazone (Avandia)
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33
Q

ignore this card

A

ignore

34
Q

describe the administration of short-acting insulin

A
  • only insulin product that can be given by IV bolus, IV infusion (bc it is unmodified)
  • can be given IM and subcut as well
35
Q

list 2 side effects associated with GLP-1 receptor agonists

A
  • weight loss

- nausea (goes away w time)

36
Q

what are the primary adverse effects of metformin (5)

A

primarly affects the GI tract:

  • abdominal bloating
  • cramping
  • nausea
  • diarrhea
  • feeling of fullness
37
Q

what do biguanides NOT do? what does this cause?

A
  • does not increase insulin secretion from the pancreas

- therefore, biguanides do not have a risk of hypoglycemia

38
Q

what is the MOA of glinides/meglitinides

A
  • same mechanism of sulfonylureas –> stimulation of pancreatic insulin release
  • except shorting acting & non-sulfa
39
Q

why cant rapid acting insulin be given via IV

A
  • it is chemically modified which means it will irritate the veins
40
Q

what is the MOA of dipeptidyl peptidase 4 (DPP-4) inhibitors

A
  • enhances the actions of incretin hormones

- does so by inhibiting DPP-4, an enzyme that inactivates incretin hormones

41
Q

why are TZDs unpopular? (4)

A
  • can cause weight gain (due to increased fat storage)
  • fluid retention
  • CV risk
  • fractures
42
Q

list the 8 families of oral antidiabetic drugs

A
  1. biguanides
  2. sulfonylureas
  3. meglitinides/glinides
  4. thiazolidinediones/glitazones
  5. alpha-glucosidase inhibitors
  6. sodium-glucose cotransporter 2 inhibitors
  7. dipeptidyl peptidase 4 (DPP-4) inhibitors
  8. incretin mimetics
43
Q

what is the onset and peak for rapid-acting insulin

A
  • onset = 10-15 min

- peak = 30-90 min

44
Q

what is long-acting insulin also referred to as? why?

A
  • basal insulin

- bc it gives the body a steady, low level insulin to maintain BG

45
Q

describe the onset, duration, and peak of isophane insulin (humulin N)

A
  • onset = 1-3 hr
  • more prolonged in duration than endogenous insulin
  • peak = 4-8 hr
46
Q

what is the first line of oral antidiabetic drugs?

A
  • biguanides
47
Q

since sulfonylureas work by stimulating insulin secretion, what must be present for sulfonylureas to be effective?

A
  • beta cells must be present –> will not work in patients with type 1
48
Q

what is the goal of insulin therapy?

A
  • tight glucose control

- to reduce incidence of long-term complications

49
Q

list 3 other adverse effects of metformin

A
  • may cause metallic taste
  • reduced B12 & folic acid absorption
  • hepatic induced lactic acidosis –> rare but lethal
50
Q

what must meglitinides be taken with? why?

A
  • must be taken with meals

- because they are shorter actin =more intense effect

51
Q

when should you use caution when giving metformin

A
  • use caution with renal dysfunction –> metformin is excreted unchanged by the kidneys = can build up toxic levels if kidney impairment
52
Q

what is the main side effect of alpha-glucosidase inhibitors

A

GI upset:

  • flatuelnce
  • cramos
  • abdominal distension
  • diarrhea
53
Q

describe the appearance of long-acting insulin

A
  • clear, colorless solution
54
Q

what 2 types of insulin should always be given in conjuction w caloric intake?

A
  • rapid & short acting
55
Q

what is a type of intermediate-acting insulin

A
  • isophane insulin suspension (NPH or humunlin-N)
56
Q

how do sulfonylureas promote insulin release?

A
  • they bind with ATP-sensitive K+ channels in the cell membrane
  • this causes the membrane to depolarize, causing an influx of Ca++, causing insulin release
57
Q

describe the administration of rapid acting insulin

A

may be given :

  • SC
  • via continuous SC infusion pump
  • NOT iv
58
Q

what is insulin derived from?

A
  • human-derived using recombinsnt DNA tech
59
Q

list 2 examples of combined insulin

A
  1. NPH 70% and regular insulin 30% = Novulin 30/70

2. NPH 50% and regular insulin 50% = Humulin 50/50

60
Q

what should you be cautious about when giving sulfonylureas?

A
  • caution in sulfa allergy
61
Q

what is the MOA of thiazolidinedione (glitazones) (2)

A
  1. increases cellular response (sensitized tissue)

2. partly decreases liver production of glucose

62
Q

what are 2 major side effects of sulfonylureas

A
  • hypoglycemia

- weight gain

63
Q

what are glinides a good alternative for?

A
  • good for patients who cannot take sulfonylureas
64
Q

how many families of oral antidiabetic drugs are there?

A

8

65
Q

what is a type of short-acting insulin

A
  • regular insulin (Humulin R)
66
Q

what is the prototype of biguanides?

A
  • metformin (glucophage)
67
Q

when is short-acting insulin given?

A
  • ~20-30 min before or with meal
68
Q

what is the MOA of biguanides (3)

A
  1. inhibits glucose production by the liver
  2. sensitizes insulin receptors in tissues –> increased uptake of glucose
  3. slightly reduces glucose absorption in the gut
69
Q

what is the MOA of sulfonylureas

A
  • stimulate insulin secretion from the beta cells of the pancreas = increased insulin levels
70
Q

list 5 side effects of SGLT-2 inhibitors

A
  1. gential yeast infections
  2. UTIs
  3. weight loss
  4. increased urination
  5. low bp
71
Q

sulfonylureas have an increased hypoglycemic effect with… (3)

A
  • alcohol
  • anabolic steroids
  • & other drugs
72
Q

why cant insulin be given orally?

A
  • due to its peptide structure, it would be inactivated by the digestive system
73
Q

what is the action of insulin lispro

A
  • similar action to endogenous insulin
74
Q

if an episode of hypoglycemia occurs while taking alpha-glucosidase inhibtors, what cant you do? why not?

A
  • cannot take simple sugar bc the acarbose will delay the absorption
75
Q

describe the appearance of isophane insulin (humulin N)

A
  • cloudy appearance
76
Q

is there a risk of hypoglycemia with GLP-1 receptor agonists? why or why not?

A
  • low risk

- bc insulin secretion is glucose dependent

77
Q

what is a prototype of SGLT-2 inhibitors?

A
  • canagliflozin (invocana)
78
Q

what is the onset of action, duration, and peak for short-acting insulin

A
  • onset = 30-60 min
  • short duration
  • peak = 2-3 hr
79
Q

what is the MOA of sodium-glucose co-transporter 2 inhibitors?

A
  • inhibits the sodium-glucose co-transporter 2 in the kidney = prevents reabsorption of glucose = increase urinar excretion of glucose
80
Q

when is intermediate insulin given? why?

A
  • early am or at HS

- to cover in the background over the course of day or overnight

81
Q

what is an example of incretin mimetics (GLP1 receptor agonists)

A

liraglutide (saxenda)

NURS 2514 (75 decks)

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