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Pharm 2 Final > chapter 57: drugs for DM > Flashcards

chapter 57: drugs for DM Flashcards

1
Q

the overall metabolic disturbances seen with diabetes is caused by what two things?

A

the lack of insulin and cellular insulin resistance

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2
Q

what is the hallmark sign of DM?

A

hyperglycemia

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3
Q

what two things characterize sustained hyperglycemia

A

impaired glucose uptake by the cells and increased glucose production

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4
Q

what is insulin released from

A

beta cells in the pancreas

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5
Q

what does the reaction of insulin stimulate?

A

the transport of glucose into the cells to be used for energy

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6
Q

where does glucagon come from?

A

alpha cells of the pancreas

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7
Q

what is glucagon an antagonist to

A

insulin

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8
Q

what does glucagon maintain

A

adequate glucose levels between meals

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9
Q

what does type 1 DM result from

A

an autoimmune disorder that destroys pancreatic beta cells

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10
Q

what type of onset does type one DM have

A

sudden

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11
Q

how do the glucose levels vary in type one DM

A

they have wide fluctuations

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12
Q

what are the classic clinical manifestations of type one DM

A

polyuria, polydipsia, polyphagia, weight loss.

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13
Q

what type of insulin do type 1 diabetics receive?

A

exogenous insulin

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14
Q

what is type II DM characterized by?

A

impaired insulin secretion and insulin resistance (desensitization)

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15
Q

what type of onset doest type II DM have

A

gradual onset

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16
Q

which type of diabetes has a more stable glucose levels

A

type 2

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17
Q

what type of factors are involved in the cause of type 2 DM

A

genetic and environmental factors

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18
Q

the amount of insulin required for type II DM declines due to what

A

increased workload of beta cells

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19
Q

most patients with type II diabetes are frequently what

A

obese

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20
Q

how long should you be NPO for a FPG test

A

8 hours

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21
Q

what is the normal FPG level

A

< 100 mg/dl

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22
Q

what is a prediabetic FPG level

A

100-125 mg/dl

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23
Q

what is a diabetic FPG level

A

> or equal to 126 mg/dl

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24
Q

what does a hemoglobin A1C provide information on?

A

long-term glycemic control

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25
Q

what is the goal for hemoglobin A1C

A

less than or 7%

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26
Q

what hemoglobin A1C is considered diagnostic

A

> or 6.5%

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27
Q

what is the principle stimulus of the secretion of insulin

A

elevated blood glucose levels

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28
Q

most of the body’s cells require insulin for what

A

to facilitate glucose entry into the cells

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29
Q

what is the exception of cells that need glucose entry?

A

cerebral cells

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30
Q

metabolic actions of insulin are what

A

anabolic

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31
Q

what 3 things promote the synthesis of complex molecules

A

CHO, amino acids, and lipids

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32
Q

what do CHO increase

A

glycogen storage

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33
Q

what are amino acids synthesized into

A

proteins

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34
Q

lipids are fatty acids that are incorporated into what

A

triglycerides

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35
Q

lack of insulin causes what type of effects

A

catabolic effects

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36
Q

what contributes to the s/sx of DM

A

favors breaking down complex molecules into their simpler forms

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37
Q

what is glycogen converted into

A

glucose

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38
Q

proteins are degraded into what

A

amino acids

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39
Q

fats are reduced to what two things

A

glycerol and free fatty acids

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40
Q

lack of insulin promotes hyperglycemia via what 3 mechanisms?

A

increased glycogenolysis, increased gluconeogensis, reduced glucose utilization

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41
Q

exogenous insulin mimics effects as what

A

endogenous insulin

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42
Q

what is the only effective treatment for type I DM

A

insulin

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43
Q

when is insulin required for a person with type II DM

A

when the person is unable to control disease with lifestyle changes and oral agents of needed during times of stress

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44
Q

what is insulin used to prevent or treat?

A

hyperglycemia induced by TPN or other medications

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45
Q

what three medications could induce hyperglycemia

A

loops, thiazides, corticosteroids

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46
Q

what electrolyte imbalance can insulin treat

A

hyperkalemia

47
Q

why would you not want to give insulin orally

A

it is a protein and will be destroyed by gastric enzymes

48
Q

what type of insulin can be given IV and mixed with other insulins

A

short duration insulins

49
Q

what are examples of rapid acting, short duration insulins

A

lisper, aspart, glulisine

50
Q

what are examples of slower acting short duration insulins

A

regular?

51
Q

what is an example of an intermediate duration insulin

A

NPH

52
Q

what kind of appearance does NPH have

A

cloudy

53
Q

what is an example of a long duration insulin

A

Glargine U-100 and Deter

54
Q

what type of insulin has no defined peak effect

A

long duration

55
Q

what type of insulin is Glargine U-300 and Degludec

A

ultra long duration

56
Q

what temperature should insulin be administered at

A

room temperature

57
Q

what should you stress the importance of to people with DM

A

following a prescribed diet, exercise regimen and reducing stress levels

58
Q

what is crucial to correlate for type I DM

A

timing of meals and administration of insulin

59
Q

what is a loss of SQ fat and appears as slightly dimpling or pitting of SQ fat

A

atrophy?

60
Q

what is caused by administering insulin that is too cold

A

atrophy

61
Q

what is the accumulation of SQ fat at the injection site due to repeated used of the same insulin site

A

hypertrophy

62
Q

what develops at peak insulin times during the night

A

somogyi effect

63
Q

what is an early morning increase in BG levels

A

dawn phenomenon

64
Q

what is dawn phenomenon usually associated with

A

release of GH

65
Q

what will help differentiate between dawn and somogyi

A

monitoring 0200/0300 blood glucose levels

66
Q

what is a decrease in BG levels between 0200-0300 to hypoglycemic levels

A

somogyi effect

67
Q

what does the somogyi effect result in the release of

A

counter regulatory hormones (epi, cortisol)

68
Q

what does the release of counter regulatory hormones cause

A

elevated BG levels in the morning

69
Q

what is the blood glucose level for someone with hypoglycemia

A

< 70 mg/dL

70
Q

what does a rapid fall in BG levels cause

A

SNS activation (tachycardia and sweating)

71
Q

what does a gradual fall in BG levels cause

A

CNS organ (headache, confusion, drowsiness)

72
Q

rapid treatment of hypoglycemia is crucial why?

A

to prevent irreversible brain damage or death

73
Q

how can glucagon be administered

A

IV, SQ, or IM

74
Q

what does glucagon promote?

A

the breakdown of glycogen to glucose

75
Q

what does glucagon reduce?

A

the conversion of glucose to glycogen

76
Q

how much complex carb should you administer to a pt when regaining consciousness

A

15gm

77
Q

if patient is still hypoglycemic 15 minutes after administering 15gm of CHO what should you administer

A

another 15gm of complex CHO

78
Q

what is used to treat type II diabetes

A

oral anti diabetic agents

79
Q

what class is metformin

A

biguanides

80
Q

what agent could metformin be used as

A

weight-neutral agent. could be used for weight loss

81
Q

what is the MOA of metformin

A

sensitizes insulin receptors, decreases hepatic glucose production, and decreases intestinal glucose absorption

82
Q

who is metformin the drug of choice for

A

newly diagnosed patients

83
Q

biguianides rarely causes what

A

hypoglycemia

84
Q

what is the serious ADR biguanides

A

lactic acidosis

85
Q

what could metformin cause when given with contrast dye

A

renal failure

86
Q

when should you discontinue metformin before a test?

A

48 hours before

87
Q

what does metformin decrease the absorption of

A

vitamin B12 and folic acid

88
Q

what is the prototype for sulfonylureas

A

glipizide

89
Q

what is the MOA of glipizide

A

stimulates release of insulin from pancreas

90
Q

what is the ADR for for glipizede

A

hypoglycemia

91
Q

what type of reaction is produced when alcohol is consumed with glipizide

A

disulfiram like reaction (N/V, flushing)

92
Q

what does glipizde stimulate

A

the release of ADH

93
Q

what can the stimulate of ADH release

A

SIADH

94
Q

what class is repaglinide

A

meglitinides

95
Q

what is the MOA for repaglinide

A

stimulates the release of insulin from the pancreas

96
Q

when should you take repaglinide in regards to meals?

A

< or 30 meals before a meal with EACH meal

97
Q

what class is pioglitazone

A

Thiazolidinediones

98
Q

what is the MOA of pioglitazone

A

decreases insulin resistance by stimulating receptors on skeletal muscle and adipose tissues–> reduced production of glucose by the liver

99
Q

what are the ADRs for pioglitazone

A

renal retention of fluid, increased risk of pathological fractures, increases LDL, increases HDL, decreases triglycerides

100
Q

what drug inhibits enzymes in the small intestine that is responsible for breaking down complex carbs

A

acarbose

101
Q

what form does CHO have to be in to be absorbed

A

monosaccharide

102
Q

what should you teach the patinet about with acarbose

A

oral glucose tablets should be used if hypoglycemia symptoms are experienced

103
Q

what is the MOA of sitagliptin

A

enhances the actions of incretin hormones by preventing their enzymatic breakdown by DPP-4

104
Q

what are incretin hormones released in response to

A

glucose elevations that occur after a meal to maintain normal glucose levels

105
Q

what do incretin hormones suppress

A

post prandial release of glucagon

106
Q

what is the MOA for SGLT-2 inhibitors

A

blocks the SGLT-2 transport system

107
Q

what are ADRs of SLGT-2 inhibitors

A

UTI (glucose in urine) and increased diuresis (hypovolemia and dehydration)

108
Q

what is the prototype for amylin mimetic

A

pramlintide

109
Q

what is amylin co released with

A

insulin

110
Q

who is pramlintide used in

A

patients not able to achieve glucose control with insulin alone- acts synergistically with insulin

111
Q

how is pramlinitide administered

A

SQ

112
Q

when is pramlinitide administered

A

immediately before a major meal

113
Q

how many carbs must a meal contain to be able to receive pramlinitide

A

30g

Pharm 2 Final (3 decks)

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