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Emily: Pharm 2 > Quiz 8: Glucose Control > Flashcards

Quiz 8: Glucose Control Flashcards

1
Q

T/F: The use of oral diabetic medication in DM Type 1 is acceptable.

A

FALSE

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2
Q

What are the characteristic of DM 1:

A
  • Before age 30 (Child)
  • Abrupt Onset
  • Requires exogenous insulin to treat
  • Ketoacidosis prone
  • Wide fluctuations in BG concentration
  • Thin body habitus
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3
Q

What genetically predisposes people to DM 1:

A
  • Altered Human Lymphocyte
  • Defect causes “insulinitis
  • Auto antibodies may be detected at the time of diagnosis but maybe absent years later
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4
Q

What are the S/S when diagnosed with DM 1:

A
  • Hyperglycemia
  • Ketoacidosis (1/3)
  • 3 P’s
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5
Q

What are the characteristics of DM Type 2:

A
  • Adult onset
  • Appear after age 35
  • Occasionally requires exogenous insulin
  • NOT ketoacidosis prone
  • Relatively stable BG concentration
  • Obese body habitus
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6
Q

T/F: To be prone to ketoacidosis is to be diabetes mellitus type II.

A

FALSE (…is to be diabetes mellitus type I.)

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7
Q

What are the S/S of DM 2:

A

-3 P’s

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8
Q

What are the four medication the induce hyperglycemia:

A
  • Glucorticoids
  • Antipsychotics
  • HIV medication
  • Octreotide
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9
Q

What are the three stress situations that induce hyperglycemia:

A
  • Pregnancy
  • illness
  • Trauma
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10
Q

Diagnosis of diabetes mellitus of a fasting blood sugar is:

A

126 mg/dL or greater

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11
Q

Diagnosis of diabetes mellitus of a random blood sugar is:

A

greater than 200 mg/dL

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12
Q

What are the three main treatments for diabetes mellitus:

A
  • Diet
  • Oral hypoglycemic agents
  • Insulin
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13
Q

Insulin binds to plasma membrane insulin receptors.

A

TRUE

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14
Q

How does insulin affect the plasma membrane after it binds:

A
  • Phosphorylated receptor substrates then activate or inactivate numerous enzymes and other mediating molecules
  • Translocation of glucose transporters to plasma membranes
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15
Q

Insulin activates glucose transporters how:

A
  • moves glucose into the cell
  • change glucose into glycogen (glycogenesis)
  • Increase uptake of amino acids,phosphate, potassium and magnesium
  • Stimulate protein synthesis and inhibit proteolysis
  • Regulate gene expression via insulin regulatory elements in target DNA
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16
Q

What occurs during insulin resistance:

A
  • Less stimulation for insulin transportors to move to the outside of the cell to bring in the glucose
  • Hyperinsulinemia occurs to overcome this resistence
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17
Q

T/F: Insulin receptor saturation occurs with high circulating concentrations of insulin.

A

FALSE (… saturation occurs with LOW circulating …)

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18
Q

Insulin receptor numbers are _____ related to the plasma concentration of insulin.

A

-Inversely

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19
Q

Can insulin regulate the population of receptors.

A

YES

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20
Q

What is the elimination t1/2 of IV insulin (regular):

A

5-10 minutes

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21
Q

How much of insulin is metabolized through first pass through the liver.

A

50%

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22
Q

Which prolongs insulin half life more liver disease of renal disease:

A

Renal

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23
Q

Name the long acting insulin type(s):

A

Glargine (Lantus)

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24
Q

Name the intermediate acting insulin type(s):

A
  • NPH

- Detemir (Levemir)

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25
Q

Name the short acting insulin type(s):

A

-Regular

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26
Q

Name the rapid acting insulin type(s):

A
  • Novolog (aspart)
  • Humalog (lispro)
  • Glulisine (apidra)
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27
Q

What insulin may only be administered IV:

A

regular

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28
Q

What are the five side effect of insulin:

A
  • Hypoglycemia
  • Allergic reaction
  • Insulin resistance
  • Lipodystrophy
  • Drug interaction
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29
Q

What are the causes and effects of hypoglycemia:

A
  • Most SERIOUS side effect
  • Patient has NO carbo load to counteract insulin
  • Hard to detect under GA

-

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30
Q

What are the S/S of hypoglycemia:

A
  • Diaphoresis
  • Tachycardia
  • Hypertension
  • Mental confusion which leads to coma
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31
Q

How is hypoglycemia treated:

A
  • 50% dextrose 50-100cc IV

- Glucagon 0.5 to 1 mg IV

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32
Q

Chronic use of NPH may lead to antibody formation of what drug:

A

Protamine

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33
Q

Lipodystrophy is ______ of fat at the sites of SQ injection and is minimized by _______ the site of injection.

A
  • atrophy

- Rotating

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34
Q

Insulin resistance is associated with patients requiring how much insulin per day:

A

> 100 units/day

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35
Q

What three acute events causes insulin resistance:

A
  • Surgery
  • Infection
  • Trauma
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36
Q

Why was insulin switched from animal insulin to human insulin:

A

-immunoresistance

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37
Q

What is Somogyi Effect:

A

Rebound hyperglycemia caused by sympathetic nervous system activity in response to hypoglycemia that may mask the correct diagnosis

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38
Q

What increases glucose and counters hypoglycemic effects of insulin:

A
  • ACTH or glucocorticoid steroids
  • Estrogen
  • Glucagon
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39
Q

Epinephrine does what to insulin:

A
  • Inhibits the secretion of insulin

- Stimulate glycogenolysis

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40
Q

What is a HgA1C:

A

-measure of the percent of Hgb that has been non-enzymatically glycosylated by glucose on the Beta chain.

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41
Q

HgA1C gives the degree of BG levels over what time frame:

A

-1 to 3 months

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42
Q

Urinary ketones are used by diabetic patients under what condition(s):

A
  • cold
  • flu
  • vomiting
  • abdominal pain
  • polyuria
  • unexpectedly high glucose level
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43
Q

What percent (basal rate) of administration may be required of the diabetic at bedtime for a intermediate or long acting dose of insulin:

A

70%

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44
Q

What insulin medication are available through multidose pens:

A
  • Aspart (Novalog)
  • Lispro (Humalog)
  • NPH
  • FIxed mixture of regular or rapid acting analog and NPH
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45
Q

An insulin pump site needs to be changed every:

A

2-4 days

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46
Q

What insulin may be used with a insulin pump:

A
  • Regular

- Lispro

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47
Q

What is the basal rate of an insulin pump:

A

-0.5 to 1 unit/hour

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48
Q

Basal bolus administration total daily requirements with __% long acting and __% divided to AC and HS.

A
  • 70

- 30

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49
Q

An insulin sliding scale should _____ be used along and uses rapid acting insulin which would need some sort of _____ glucose _____.

A
  • never
  • basal
  • control
50
Q

What are the long term complication of diabetes mellitus:

A
  • Retinopathy
  • Atherosclerosis
  • Neuropathy
  • Nephropathy
51
Q

What are the risks of hyperglycemia:

A
  • Microangiopathy
  • Impaired leukocyte function
  • Cerebral edema
  • Impaired wound healing
  • Postoperative sepsis
52
Q

Which is better to have during general anesthesia high or low blood glucose levels and why?

A
  • HIGH

- Hypoglycemia can be masked during general anesthesia

53
Q

What are the blood glucose parameters during surgery:

A
  • Optimal BG 80-180 mg/dL

- < 80 mg/dL start glucose infusion

54
Q

How long would you monitor BG level after surgery:

A

24 - 72 hours

55
Q

A diabetic patient should have how much of their basal rate the day of surgery:

A

-1/4 to 1/2

56
Q

A patient on steroid therapy should have a insulin gtt at what blood glucose level:

A

-100

57
Q

What would the infusion rate be for a 70kg diabetic on D5W:

A

50 cc/hour

58
Q

How many unit(s) of rapid/short acting in insulin should be used per 50-60 mg/dL of BG:

A

1 unit regular insulin

59
Q

List the oral hypoglycemics:

A
  • Biguanides
  • Alpha-Glucodsidase Inhibitors
  • DPP-IV inhibitors
-SLGTS inhibitors
Meglitanides
-Incretin mimetics
-Thiazolidinediones
-Sulfonylureas
60
Q

What is the mechanism of action for sulfonylureas:

A

-act at pancreatic beta cells to stimulate release of insulin

61
Q

Sulfanylureas have a high first time failure rate of __% and each year after and __-__% failure.

A
  • 20
  • 10
  • 15
62
Q

How is Sulfonylureas metabolized and excreted in the body:

A
  • Metabolized by the liver

- Excreted by the kidneys

63
Q

What type of patient would be especially at risk for hypoglycemia using sulfonylureas:

A

-Renal failure patient

64
Q

Do sulfonylureas cross the placenta:

A

YES

65
Q

Which sulfonylureas have the longest t1/2 life (up to seven days):

A
  • glyburide

- chlorpropamide

66
Q

What are the side effect of sulfonylureas:

A
  • weight gain
  • N/V
  • Abnormal Liver function Test
  • Cholestasis
67
Q

Which sulfonylureas is safe to use in the patient with liver disease:

A

-Acetohexamide

68
Q

What are the contraindication for sulfonylureas:

A
  • Hypersensitivity to sulfonamides
  • Patients with hypoglycemic unawareness
  • Poor renal function
69
Q

List the 2nd generation sulfonylureas:

A
  • Glyburide
  • glipizide
  • glimepiride
70
Q

What is the dose for glyburide and the time it takes to be cleared from the plasma.

A
  • single dose for 24 hour effect

- cleared after 36 hours

71
Q

How long does glipizide stimulate insulin secretions:

A

-up to 12 hours, but has had effects persist for up to 3 years without evidence of tolerence

72
Q

What are 1st generation sulfonylureas:

A
  • Tolbutamide
  • Acetohexamide
  • Chlorpropamide
73
Q

Tolbutamide are the ______ acting and ____ potent.

A
  • shortest

- least

74
Q

Tolbutamide lever metabolite are:

A

much less potent compounds

75
Q

T/F: tolbutamide have the most side effects out of the 1st generation of sulfonylureas.

A

FALSE (… have the least side effects…)

76
Q

The main point about acetohexamide is:

A
  • most of the hypoglycemic action is due to its principle metabolite
  • kidneys excrete the metabolite
  • Uricosuric (excrete uric acid)
77
Q

Which hypoglycemic medication is uricosuric:

A

acetohexamide

78
Q

How long does chlorpropamide last:

A

72 hours

79
Q

What hypoglycemic drug could be used to cause a acute sensitivity to alcohol:

A

chlorpropamide

80
Q

How is chlorpropamide exreted:

A
  • 20% unchanged through the kidney

- Can cause HYPONATREMIA

81
Q

Are sulfonylureas bolus medications or basal medications for diabetes:

A

-bolus medications

82
Q

List the alpha glucosidase inhibitors:

A
  • Acarbose

- miglitol

83
Q

What is the method of action for alpha glucosidase inhibitors:

A

-decrease intestinal hydrolysis of complex carbohydrates

84
Q

What are the side effect of alpha glucosidease inhibitors:

A
  • GI upset

- Increase LFTs

85
Q

What would be the contraindication for alpha glucosidase inhibitors:

A
  • inflammatory bowel disease

- obstructions

86
Q

List the meglitinides:

A
  • Repaglinide

- Nateglinide

87
Q

What is the method of action for meglitinides:

A

-Increase insulin secretion from islet cells like the sulfonylurease

88
Q

What is the onset and duration of meglitinides:

A
  • 1 hour onset

- 4 hour duration

89
Q

T/F: It is important to continue taking meglitinides during fasting periods due to withdrawals symptoms.

A

FALSE…Meglitinides should NEVER be taken during fasting periods.

90
Q

What are the adverse effects of meglitinides:

A
  • hypoglycemia
  • weight gain
  • URI
91
Q

Which is more prevalent to cause hypoglycemia meglitinides or sulfonylureas:

A

meglitinides

92
Q

Name all the biguanides:

A

Metformin (glucophage)

93
Q

What are the benefits of metformin:

A
  • decrease BG concentration with only a very low risk of hypoglycemia
  • positive effect on lipid concentrations
  • lead to mild weight reduction in obese patients
94
Q

What is the mechanism of action for metformin:

A
  • decrease hepatic glucose production
  • reduces glucose absorption from the intestine
  • increases insulin sensitivity
95
Q

Metformin produces satisfactory resutls in __% of the sulfonylurea failures.

A

50

96
Q

What are the side effect of metformine:

A
  • anorexia
  • Nausea
  • diarrhea
  • Lactic acidosis
97
Q

What will the S/S be for lactic acidosis if on metformin:

A
  • Nausea/VOMITING
  • increase respiration
  • increase heart rate
  • abdominal pain
  • shock
98
Q

How long before surgery should metformin be stopped before surgery:

A

48 hours

99
Q

What would be monitored during surgery if on metformin:

A
  • ABG
  • pH
  • serum lactate
  • Renal function
100
Q

What should be avoided with patients on metformin:

A
  • dehydration
  • hypovolemia
  • hypoxemia
  • IV contrast
101
Q

What will IV contrast do to the patient on metformin:

A

-increase nephrotoxicity

102
Q

What are the contraindication/precautions for metformin:

A
  • Renal impairment
  • age > 80 years
  • hepatic impairment
  • CHF
103
Q

What is the contraindicated serum creatinine levels for both males and females:

A
  • male > 1.5

- female > 1.4

104
Q

List the thiazolidinediones:

A
  • rosiglitazone

- pioglitazone

105
Q

What is the method of action for thiazolidinediones:

A
  • Decrease insulin resistance

- decrease hepatic glucose output

106
Q

What does thiazolidinediones require to work:

A

-presence of insulin

107
Q

What are the side effect of thiazolidinediones:

A
  • weight gain
  • hepatotoxicity
  • peripheral edema
  • CHF exacerbations
  • risk of bone fractures
108
Q

Thiazolidinediones may increase the risk of __ and __ death with avandia.

A
  • MI

- CV

109
Q

List the DPP-4 Inhibitors:

A
  • Sitagliptin
  • Saxagliptin
  • Linagliptin
110
Q

What is the mechanism of action of DPP-4 inhibitors:

A
  • increases pancreatic insulin secretion
  • Limits glucagon secretion
  • Slows gastric emptying
  • promotes satiety
111
Q

What are the side effects of DDP-4 inhibitors:

A
  • URI and UTI
  • HA
  • Weight neutral
  • Lower risk of hypoglycemia
  • Post marketing pancreatitis
  • angioedema
  • stevens johnson
  • anaphylaxis
112
Q

List the incretin mimetics:

A
  • exanatide (GLP-1)
  • Liraglutide (GLP-1)
  • ?pramlinide (AMYLIN)?
113
Q

What is the Mechanism of action for Exaniatide and liraglutide:

A

-GLP 1 analog which prolong gastric emptying reduce postprandial glucagonsecretion

114
Q

What is the mechanism of action for pramlinide:

A

-increase insulin
-slows gastric emptying
increases beta cell GROWTH
-central appetite suppression

115
Q

What are the GLP-1 side effects:

A
  • N/V/D
  • pancreatitis
  • ARF
  • Weight loss
116
Q

What patient would you avoid exanatide in:

A

renal failure

117
Q

What patient would you avoid liragluted in:

A

-thyroid carcinoma

118
Q

What is the amylin side effects:

A
  • (BLACK BOX) hypoglycemia
  • N/V
  • anorexia
  • HA
  • Gatroparesis
119
Q

List the SLGT2 inhibitor:

A

-Canagliflozin

120
Q

What is the mechanism of action for SLGT2 inhibitor:

A

-increased URINARY glucose excretion

121
Q

What is the contraindication for SLGT2:

A
  • CrCl < 30 cc/
  • ESRD
  • HD (Hemodyalisis??)

Emily: Pharm 2 (11 decks)

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