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
Name the short acting insulin type(s):
-Regular
26
Name the rapid acting insulin type(s):
- Novolog (aspart) - Humalog (lispro) - Glulisine (apidra)
27
What insulin may only be administered IV:
regular
28
What are the five side effect of insulin:
- Hypoglycemia - Allergic reaction - Insulin resistance - Lipodystrophy - Drug interaction
29
What are the causes and effects of hypoglycemia:
- Most SERIOUS side effect - Patient has NO carbo load to counteract insulin - Hard to detect under GA -
30
What are the S/S of hypoglycemia:
- Diaphoresis - Tachycardia - Hypertension - Mental confusion which leads to coma
31
How is hypoglycemia treated:
- 50% dextrose 50-100cc IV | - Glucagon 0.5 to 1 mg IV
32
Chronic use of NPH may lead to antibody formation of what drug:
Protamine
33
Lipodystrophy is ______ of fat at the sites of SQ injection and is minimized by _______ the site of injection.
- atrophy | - Rotating
34
Insulin resistance is associated with patients requiring how much insulin per day:
> 100 units/day
35
What three acute events causes insulin resistance:
- Surgery - Infection - Trauma
36
Why was insulin switched from animal insulin to human insulin:
-immunoresistance
37
What is Somogyi Effect:
Rebound hyperglycemia caused by sympathetic nervous system activity in response to hypoglycemia that may mask the correct diagnosis
38
What increases glucose and counters hypoglycemic effects of insulin:
- ACTH or glucocorticoid steroids - Estrogen - Glucagon
39
Epinephrine does what to insulin:
- Inhibits the secretion of insulin | - Stimulate glycogenolysis
40
What is a HgA1C:
-measure of the percent of Hgb that has been non-enzymatically glycosylated by glucose on the Beta chain.
41
HgA1C gives the degree of BG levels over what time frame:
-1 to 3 months
42
Urinary ketones are used by diabetic patients under what condition(s):
- cold - flu - vomiting - abdominal pain - polyuria - unexpectedly high glucose level
43
What percent (basal rate) of administration may be required of the diabetic at bedtime for a intermediate or long acting dose of insulin:
70%
44
What insulin medication are available through multidose pens:
- Aspart (Novalog) - Lispro (Humalog) - NPH - FIxed mixture of regular or rapid acting analog and NPH
45
An insulin pump site needs to be changed every:
2-4 days
46
What insulin may be used with a insulin pump:
- Regular | - Lispro
47
What is the basal rate of an insulin pump:
-0.5 to 1 unit/hour
48
Basal bolus administration total daily requirements with __% long acting and __% divided to AC and HS.
- 70 | - 30
49
An insulin sliding scale should _____ be used along and uses rapid acting insulin which would need some sort of _____ glucose _____.
- never - basal - control
50
What are the long term complication of diabetes mellitus:
- Retinopathy - Atherosclerosis - Neuropathy - Nephropathy
51
What are the risks of hyperglycemia:
- Microangiopathy - Impaired leukocyte function - Cerebral edema - Impaired wound healing - Postoperative sepsis
52
Which is better to have during general anesthesia high or low blood glucose levels and why?
- HIGH | - Hypoglycemia can be masked during general anesthesia
53
What are the blood glucose parameters during surgery:
- Optimal BG 80-180 mg/dL | - < 80 mg/dL start glucose infusion
54
How long would you monitor BG level after surgery:
24 - 72 hours
55
A diabetic patient should have how much of their basal rate the day of surgery:
-1/4 to 1/2
56
A patient on steroid therapy should have a insulin gtt at what blood glucose level:
-100
57
What would the infusion rate be for a 70kg diabetic on D5W:
50 cc/hour
58
How many unit(s) of rapid/short acting in insulin should be used per 50-60 mg/dL of BG:
1 unit regular insulin
59
List the oral hypoglycemics:
- Biguanides - Alpha-Glucodsidase Inhibitors - DPP-IV inhibitors ``` -SLGTS inhibitors Meglitanides -Incretin mimetics -Thiazolidinediones -Sulfonylureas ```
60
What is the mechanism of action for sulfonylureas:
-act at pancreatic beta cells to stimulate release of insulin
61
Sulfanylureas have a high first time failure rate of __% and each year after and __-__% failure.
- 20 - 10 - 15
62
How is Sulfonylureas metabolized and excreted in the body:
- Metabolized by the liver | - Excreted by the kidneys
63
What type of patient would be especially at risk for hypoglycemia using sulfonylureas:
-Renal failure patient
64
Do sulfonylureas cross the placenta:
YES
65
Which sulfonylureas have the longest t1/2 life (up to seven days):
- glyburide | - chlorpropamide
66
What are the side effect of sulfonylureas:
- weight gain - N/V - Abnormal Liver function Test - Cholestasis
67
Which sulfonylureas is safe to use in the patient with liver disease:
-Acetohexamide
68
What are the contraindication for sulfonylureas:
- Hypersensitivity to sulfonamides - Patients with hypoglycemic unawareness - Poor renal function
69
List the 2nd generation sulfonylureas:
- Glyburide - glipizide - glimepiride
70
What is the dose for glyburide and the time it takes to be cleared from the plasma.
- single dose for 24 hour effect | - cleared after 36 hours
71
How long does glipizide stimulate insulin secretions:
-up to 12 hours, but has had effects persist for up to 3 years without evidence of tolerence
72
What are 1st generation sulfonylureas:
- Tolbutamide - Acetohexamide - Chlorpropamide
73
Tolbutamide are the ______ acting and ____ potent.
- shortest | - least
74
Tolbutamide lever metabolite are:
much less potent compounds
75
T/F: tolbutamide have the most side effects out of the 1st generation of sulfonylureas.
FALSE (... have the least side effects...)
76
The main point about acetohexamide is:
- most of the hypoglycemic action is due to its principle metabolite - kidneys excrete the metabolite - Uricosuric (excrete uric acid)
77
Which hypoglycemic medication is uricosuric:
acetohexamide
78
How long does chlorpropamide last:
72 hours
79
What hypoglycemic drug could be used to cause a acute sensitivity to alcohol:
chlorpropamide
80
How is chlorpropamide exreted:
- 20% unchanged through the kidney | - Can cause HYPONATREMIA
81
Are sulfonylureas bolus medications or basal medications for diabetes:
-bolus medications
82
List the alpha glucosidase inhibitors:
- Acarbose | - miglitol
83
What is the method of action for alpha glucosidase inhibitors:
-decrease intestinal hydrolysis of complex carbohydrates
84
What are the side effect of alpha glucosidease inhibitors:
- GI upset | - Increase LFTs
85
What would be the contraindication for alpha glucosidase inhibitors:
- inflammatory bowel disease | - obstructions
86
List the meglitinides:
- Repaglinide | - Nateglinide
87
What is the method of action for meglitinides:
-Increase insulin secretion from islet cells like the sulfonylurease
88
What is the onset and duration of meglitinides:
- 1 hour onset | - 4 hour duration
89
T/F: It is important to continue taking meglitinides during fasting periods due to withdrawals symptoms.
FALSE...Meglitinides should NEVER be taken during fasting periods.
90
What are the adverse effects of meglitinides:
- hypoglycemia - weight gain - URI
91
Which is more prevalent to cause hypoglycemia meglitinides or sulfonylureas:
meglitinides
92
Name all the biguanides:
Metformin (glucophage)
93
What are the benefits of metformin:
- 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
What is the mechanism of action for metformin:
- decrease hepatic glucose production - reduces glucose absorption from the intestine - increases insulin sensitivity
95
Metformin produces satisfactory resutls in __% of the sulfonylurea failures.
50
96
What are the side effect of metformine:
- anorexia - Nausea - diarrhea - Lactic acidosis
97
What will the S/S be for lactic acidosis if on metformin:
- Nausea/VOMITING - increase respiration - increase heart rate - abdominal pain - shock
98
How long before surgery should metformin be stopped before surgery:
48 hours
99
What would be monitored during surgery if on metformin:
- ABG - pH - serum lactate - Renal function
100
What should be avoided with patients on metformin:
- dehydration - hypovolemia - hypoxemia - IV contrast
101
What will IV contrast do to the patient on metformin:
-increase nephrotoxicity
102
What are the contraindication/precautions for metformin:
- Renal impairment - age > 80 years - hepatic impairment - CHF
103
What is the contraindicated serum creatinine levels for both males and females:
- male > 1.5 | - female > 1.4
104
List the thiazolidinediones:
- rosiglitazone | - pioglitazone
105
What is the method of action for thiazolidinediones:
- Decrease insulin resistance | - decrease hepatic glucose output
106
What does thiazolidinediones require to work:
-presence of insulin
107
What are the side effect of thiazolidinediones:
- weight gain - hepatotoxicity - peripheral edema - CHF exacerbations - risk of bone fractures
108
Thiazolidinediones may increase the risk of __ and __ death with avandia.
- MI | - CV
109
List the DPP-4 Inhibitors:
- Sitagliptin - Saxagliptin - Linagliptin
110
What is the mechanism of action of DPP-4 inhibitors:
- increases pancreatic insulin secretion - Limits glucagon secretion - Slows gastric emptying - promotes satiety
111
What are the side effects of DDP-4 inhibitors:
- URI and UTI - HA - Weight neutral - Lower risk of hypoglycemia - Post marketing pancreatitis - angioedema - stevens johnson - anaphylaxis
112
List the incretin mimetics:
- exanatide (GLP-1) - Liraglutide (GLP-1) - ?pramlinide (AMYLIN)?
113
What is the Mechanism of action for Exaniatide and liraglutide:
-GLP 1 analog which prolong gastric emptying reduce postprandial glucagonsecretion
114
What is the mechanism of action for pramlinide:
-increase insulin -slows gastric emptying increases beta cell GROWTH -central appetite suppression
115
What are the GLP-1 side effects:
- N/V/D - pancreatitis - ARF - Weight loss
116
What patient would you avoid exanatide in:
renal failure
117
What patient would you avoid liragluted in:
-thyroid carcinoma
118
What is the amylin side effects:
- (BLACK BOX) hypoglycemia - N/V - anorexia - HA - Gatroparesis
119
List the SLGT2 inhibitor:
-Canagliflozin
120
What is the mechanism of action for SLGT2 inhibitor:
-increased URINARY glucose excretion
121
What is the contraindication for SLGT2:
- CrCl < 30 cc/ - ESRD - HD (Hemodyalisis??)