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Clinical Nutrition 3 > Glycemic Control in Diabetes > Flashcards

Glycemic Control in Diabetes Flashcards

1
Q

How is A1C formed? What is the rate of formation proportional to?

A
  • A series of stable, minor hmg components formed slowly and non-enzymatically from hmg and glucose
  • Proportional to glucose concentration
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2
Q

What does A1C provide and predict? How often should it be assessed?

A
  • Glycemic history of the previous 120 days, with the most accurate reflection of the previous 2-3 months of glycemic control
  • Predicts risk for complications
  • Assess every 3-6 months
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3
Q

What are other glycated proteins? Are they proven to be shown as an indicator of risk for complications?

A
  • Glycosylated serum albumin (GSA) and glycosylated total serum proteins (GSP)
  • Not yet shown, minimal clinical relevance
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4
Q

A1C target for adults with T2DM to reduce risk of CKD and retinopathy if at low risk of hypoglycemia?

A

= 6.5%

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5
Q

What is the A1C target of most adults with type I or Type II diabetes?

A

= 7.0%

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6
Q

A1C target for those who are functionally dependant?

A

7.1-8.0%

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7
Q

When is an A1C target of 7.1-8.5% recommended?

A
  • Recurrent severe hypoglycemia and/or hypoglycemia unawareness
  • Limited life expectancy
  • Frail elderly and/or with dementia
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8
Q

Why should A1C concentrations above 8.5% be avoided?

A

To minimize risk of symptomatic hypoglycemia and acute and chronic complications

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9
Q

A1C suggestion for end of life?

A

-A1C recommendations are not recommended, avoid symptomatic hyperglycemia and any hypoglycemia

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10
Q

What are the pre-prandial and 2 hour post-prandial glucose targets in most patients to reach an A1C of = 7.0%?

A
  • Pre-prandial: 4.0-7.0

- Post-prandial: 5.0-10.0

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11
Q

What are the pre-prandial and 2 hour post-prandial glucose targets if A1C = 7.0% despite previous targets?

A
  • Pre-prandial: 4.0-5.5

- Post-prandial: 5.0-8.0

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12
Q

(T/F) A1C values are identical to estimated mean glucose levels

A

False, but their are correlated

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13
Q

What can INCREASE A1C within the context of erythropoiesis?

A
  • B12/Fe deficiency

- Decreased erythropoiesis

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14
Q

What can DECREASE A1C within the context of erythropoiesis?

A
  • Use of EPO, Fe or B12
  • Reticulocytosis
  • Chronic Liver disease
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15
Q

What can change A1C variably within the context of altered hemoglobin?

A
  • Fetal hemoglobin
  • Hemoglobinopathies
  • Methemoglobin
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16
Q

What can INCREASE A1C within the context of altered glycation?

A
  • Chronic renal failure

- Decreased erythrocyte pH

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17
Q

What can DECREASE A1C within the context of altered glycation?

A
  • ASA, vitamin C/E
  • Hemoglobinopathies
  • Increase in erythrocytes pH
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18
Q

What can INCREASE A1C within the context of erythrocyte destruction?

A

-Splenectomy

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19
Q

What can DECREASE A1C within the context of erythrocyte destruction?

A
  • -Hemoglobinopathies
  • Chronic renal failure
  • Splenomegaly
  • Rheumatoid arthiritise
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20
Q

What may cause falsely elevated A1C? Falsely low?

A
  • Elevated in the context of hyperbilirubinemia

- Decreased in the context of hypertriglyceridemia

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21
Q

When are glycemic targets higher than the ret of the population?

A

Adolescent (<18 y/o)

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22
Q

A1C target for <18 y/o?

A

= 7.5%

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23
Q

FPG <18 y/o?

A

4.0-8.0

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24
Q

2hr PG <18 y/o?

A

5.0-10.0

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25
Q

How can we measure plasma glucose?

A
  • Blood glucose meter
  • Continuous glucose monitor
  • Flash glucose monitor
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26
Q

What are the advantages of the CGM and flash systems?

A

-We will not get a singular, random measurement but rather monitor our blood glucose over time and observe trends

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27
Q

Why are adolescents prone to having higher glycemia and A1C levels?

A
  • Could have difficulties managing their glycemic
  • Busy lifestyle
  • Social changes
  • High growth hormone
  • Changing from a paediatric to an adult clinic
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28
Q

If A1C is < 1.5% over target, what is the initial choice of therapy?

A

-Initiate healthy behaviour interventions and start metformin if not at target in 3 month

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29
Q

If A1C >/= 1.5% over target. what is the initial choice of therapy?

A

-Start metformin with healthy behaviour interventions AND consider second concurrent agent

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30
Q

what is the overarching intervention at diagnosis, and throughout treatment of Type II diabetes?

A

Healthy behaviour interventions (nutritional therapy, weight management, PA, with or without metformin)

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31
Q

What should be initiated if preliminary interventions have not achieved glycemic target and there is a risk of CVD risk?

A

Starts antihyperglycemic agent with demonstrated CVD benefit

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32
Q

What should be initiated if preliminary interventions have not achieved glycemic target and there is NO risk of CVD risk?

A
  • Provide an additional antihyperglycemic agent best suited to the individuals based on clinical considerations, such as
  • Avoidance of hypiG, weight gain
  • Reduced eGFR
  • Degree of hyperglycemia
  • Cost/coverage
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33
Q

Which medications have CVD benefits?

A
  • Empagliflozin
  • Liraglutide
  • Canagliflozin
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34
Q

What are the 4 key points in the pharmacotherapy in Type 2 Diabetes checklist?

A
  • Choose initial therapy based on glycemia
  • Start w/ metformin and +/- others
  • Individualize your therapy choice based on characteristics of the person w/ diabetes and the agent
  • Reach target within 3-6 months of diagnosis
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35
Q

Biguanides?

A

Metformin/glucophage

-Decrease hepatic glucoe production

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36
Q

a-glucosidase inhibitors?

A

Acarbose/Glucobay

-Delay intestinal glucose absorption

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37
Q

Insulin secretagogues (Meglitinide, sulfonylurea)?

A
  • LINIDE/RIDE
  • stimulate insulin secretion
  • Meg is short-acting (4-7h)
  • Sulf is long acting (once daily)
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38
Q

What are examples of incretin mimetics?

A
  • DPP-4 inhibitors

- GLP-1 receptor agonists

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39
Q

DPP-4 inhibitors?

A

SitaglipTIN

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40
Q

GLP-1 receptor agonist?

A

ExenaTIDE

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41
Q

What is the mechanism of incretin mimetics?

A

Stimulate insulin and reduce glucagon secretion, will delay gastric emptying

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42
Q

Thiazolidinediones?

A
  • ZONES

- Increase insulin sensitivity in the peripheral tissues and liver (decrease insulin resistance)

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43
Q

SGLT-2 Inhibitors?

A
  • OZIN

- Decrease glucose reabsorption, increase glucose excretion

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44
Q

What is the first line therapy?

A

Biguanides (Metformin)

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45
Q

Key benefits of metformin

A
  • 1 to 1.5% reduction in A1C
  • Negligible risk as monotherapy
  • No weight gain
  • May improve CV outcomes in overweight subjects
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46
Q

Key risks of metformin?

A
  • GI side effects
  • Creatinine clearance (Caution if <60 ml/min)
  • Lactic acidosis
  • B12 deficiency
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47
Q

When is metformin contraindicated?

A

When GFR <30 ml/min or in hepatic failure

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48
Q

(T/F) Metformin carries a risk of hypoglycemia

A

F

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49
Q

Key insulin secretagogue benefits?

A
  • 0.7 to 0.8% reduction in A1C
  • Rapid onset of responce
  • Decrease microvascular risk
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50
Q

When is postprandial glucose especially reduced?

A

Through use of meglitinides (insulin secretagogue, short-acting)

51
Q

Key insulin secretagogue risks?

A
  • **Hypoglycemia
  • Weight gain
  • May blunt myocardial ischemic preconditioning
  • Blood sugar control is lost earlier than with Metformin
52
Q

When should caution surrounding hypoG be exerted on IS?

A
  • Kidney disease
  • Liver problems
  • Elderly
53
Q

Which IS poses the highest risk to hypoG and weight gain?

A

-Glyburide (Sulfonylureas)

54
Q

Key benefits of alpha-glucosidase inhibitors (AGIs)?

A
  • 0.6% reduction in A1C
  • Negligible risk as monotherapy
  • Weight neutral
  • Beneficial in patients with IGT
55
Q

How are AGIs beneficial for patients with IGT?

A
  • 49% reduction in CV events

- Prevention if T2DM

56
Q

Key risks of AGIs?

A
  • GI side effects
  • TID dosing
  • NOT recommended as initial therapy in people w/ AIC >/= 8.5%
  • Ceratin contraindications
57
Q

GI side effects w/ AGIs?

A

-Delays the absorption of glucose, therefore causing more fermentation

58
Q

Significance of TID dosing of AGIs?

A

As they act on delaying glucose absorption, must be taken with meals

59
Q

Contraindications to AGIs?

A
  • Diabetic ketoacidosis

- IBD

60
Q

Key benefits to thiazolidinediones (TZDs)?

A
  • 0.8% risk reduction
  • Negligible risk as monotherapy
  • CVD benefits
61
Q

CVD benefits observed with TZDs?

A
  • Increase HDL-c
  • Decrease TGs (pioglitazone)
  • Decrease CVD events
62
Q

Which anti-hyperG agents demonstrates a longer duration of glycemic control w/ monotherapy vs, metformin o glyburide?

A

-TZDs

63
Q

Key risks of TZDs?

A
  • Weight gain
  • CVD
  • 6-12 weeks for full glycemic effects
  • Bladder cancer, macular edema (rare)
  • Contraindications
64
Q

CVD risks of TZDs?

A
  • May induce edema and/or CHF
  • May increase MI
  • Increase LDL-c (rosiglitazone)
65
Q

Contraindications to TZDs?

A
  • Serious liver dysfunction

- Known clinical heart failure or evidence of ventricular dysfunction

66
Q

Key benefits of DPP-4 inhibitors?

A
  • 0.7% reduction in A1C
  • Negligible risk as mono-therapy
  • Weight neutral
  • Neutral CV studies
  • Well tolerated
  • No risk of hypoglycemia
67
Q

How does DPP-4 inhibitors impact blood glucose?

A

-Reduction in postprandial glycemia in combination with metformin

68
Q

Key risks of DPP-4 inhibitors?

A
  • Rare cases of pancreatitis
  • Long-term safety unknown due to “new” drug
  • Cardiac insufficiency if Saxagliptin
69
Q

Discuss the action of GLP-1 Receptor agonists

A

An injection which will results in a higher level of GLP-1 being releases, and a large surge of insulin (beyond physiological levels)

70
Q

Discuss the action of DPP-4 inhibitors

A

An oral agent which will block the DPP-4 enzyme which inhibits the release of GLP-1, therefore the drug will elicit a “normal” or physiological response of insulin

71
Q

What are the impacts of DPP-4 inhibitors?

A
  • Increase insulin secretion

- Decrease glucagon secretion

72
Q

What are the impacts of GLP-1 receptor agonists?

A
  • Decrease gastric emptying
  • Increase satiety
  • Decrease energy intake
  • Increase nausea
  • Decrease weight
  • Increase insulin secretion
  • Decrease glucagon secretion
73
Q

Key benefits of GLP-1 receptor agonists?

A
  • 1.0% reduction in post-prandial glycemia
  • Negligible risk as mono-therapy
  • Significant weight loss
  • May decrease BP, CV events, mortality, kidney protection
  • Potential for improved B-cell mass function
74
Q

Risks of GLP-1 receptor agonists?

A
  • Gi side effects
  • Rare cases of pancreatitis
  • Parafollicular cell hyperplasia
  • Long-term safety unknown due to “new drug”
  • nausea
  • Injectable
75
Q

Is there a hypoglycemic risk in GLP-1 receptor agonists?

A

no

76
Q

Contraindication for GLP-1 receptor agonists?

A

-Personal/family history of medullary thyroid cancer or MEN2

77
Q

Required patient education for GLP-1 receptor agonist theory?

A
  • GI symptoms
  • If on insulin, monitor for hypoG
  • Delivered via pen (like insulin)
78
Q

Recommendations for administering meds by pen (insulin/GLP-1 receptor agonist)?

A
  • Refrigerate the pen prior to use

- hand wash, and inspect med for cloudiness/particulate matter

79
Q

Discuss SGLT-2 inhibitors

A
  • Both sodium and glucose co-transporters are blocked, inhibiting their reabsorption in the blood and are excreted
  • Ultimately decreases glucose renal reabsorption and increases its excretion (turning symptoms into therapy)
80
Q

Where is the SGTL2 channel found?

A

In the proximal tubule of the kidney

81
Q

What is the estimated amount of glucose excreted per day on SGLT2?

A

77–119 g/day or 308-476 kcals/day

82
Q

Discuss SGLT-2 effects on weight

A

-Can have significant weight-loss, however will plateau within 6-8 months (does not continue with expected weight-loss trajectory)

83
Q

Discuss SGLT-2 on A1C reduction

A

Will act very rapidly on reducing A1C - an then there is a steady regain over about 2 years close to baseline, but still overall lower

84
Q

What other impacts does SGLT2 have ?

A
  • Will have a marked reduction in blood pressure

- Can slow the progression of kidney disease (Empagliflozin) for those w/ T2DM and high CVD risk

85
Q

Empagliflozin impact on CVD death and heart failure?

A

-Reducing CVD death and heart failure over 4 years, where the reduction occurs quite rapidly and is relatively maintained.

86
Q

SGLT-2 inhibitors key benefits?

A
  • 0.7% A1C reduction
  • Negligible risk as monotherapy
  • Weight loss (~3kg)
  • Decreases BP, weight, mortality, CVD death, heart failure and kidney protection
87
Q

Is there hypoglycemic risk for SGLT-2 inhibitors?

A

No

88
Q

Key risks of SGLT-2 inhibitors?

A
  • Mycotic genital infection (most common)
  • Hypovolemia
  • Increased LDL-c
  • Euglycemic ketoacidosis
  • Long-term safety unknown
89
Q

(T/F) SGLT-2 inhibitors are appropriate for both T1DM andT2DM

A

F, T2DM only

90
Q

When should SGLT-2 be discontinued? Why?

Should insulin be stoped?

A
  • Stop before surgery and acute illness (~3 days)
  • The 1/2 life ranges from 11-13 hours, and their effects can persist for a few days after discontinuation
  • Do NOT stop insulin
91
Q

Which medications are not recommended to be used if eGFR is <45?

A

SGLT-2 and GLP-1 RA

92
Q

What is euglycemic ketoacidosis?

A

Where there is minimal insulin secretion, but their glucose is OK -ketone body production continues and pH will still change

93
Q

What are the two drugs which are not negligible risks as monotherapy?

A
  • Insulin and IS

- Due to hypoglycemia risk

94
Q

Which two drugs have the greatest potential fo weight gain?

A

-Insulin and TZDs

95
Q

Which GLP-1RA is superior in T2DM w/ clinical CVD?

A

Lira

96
Q

Which SGLT-2 inhibitor is superior in T2DM w/ clinical CVD?

A

-Cana and Empa

97
Q

Which medications have the greatest potential for A1C lowering when added to metformin?

A
  • Insulin
  • SGLT-2 Inhibitors
  • GLP-1RA
98
Q

How many types of insulin pumps are available in Canada?

A

5-types

99
Q

Which insulin pump does not have CGM available?

A
  • Omnipod

- Ypsomed

100
Q

What are the two kinds of insulins delivered in intensive insulin therapy?

A

-Bolus and Basal

101
Q

Sub-types of bolus insulins?

A

Rapid acting and short acting

102
Q

Rapid acting bolus insulin?

A
  • Glulisine
  • Lispro
  • Asapart
  • Faster acting asapart
103
Q

Glulisine onset, peak and duration?

A

10-15 min
1-1.5 hr
3.5-5 hr

104
Q

When should glulisine be injected?

A

0-15 mins before a meal

105
Q

Lispro onset, peak and duration?

A

10-15 min
1-2h
3-4.75 hr

106
Q

When should lispro be injected?

A

0-15 mins before meal

107
Q

Aspart onset, peak and duration?

A

9-20 min
1-1.5h
3-5h

108
Q

When should aspart be injected?

A

0-10 mins before the meal

109
Q

Faster acting Aspart onset, peak and duration?

A

4min
0.5-1.5 h
3-5h

110
Q

When should faster acting Aspart be injected?

A

0-2 mins before meal or can be administered up to 20 minutes after the start of the meal when necessary

111
Q

What are sub-types of short-acting insulins?

A
  • Insulin regular (Humulin)

- Insulin regular U-500

112
Q

Insulin regular (humulin) onset, peak and duration?

A

30 min
2-3 h
6.5 h

113
Q

When should insulin regular (humulin-R) be injected?

A

~30 mins before meal

114
Q

Insulin regular U-500 onset, peak and duration?

A

15 min
4-8 h
17-24 h

115
Q

When should insulin regular U-500 be injected?

A

~30 mins before meal

116
Q

Two types of basal insulin?

A
  • Intermediate acting

- Long-acting

117
Q

Intermediate acting insulin humulin-N onset, peak and duration?

A

13h
5-8h
Up to 18 h

118
Q

When should humulin-N be injected?

A

Morning and/or night

119
Q

When should long acting insulin such as glargine be injected? What is its onset, peak and duration?

A
  • Morning/Night and no less than 8h between 2 injections

- 90 min, NO PEAK and ranges from 16-42 hrs

120
Q

When should premixed regular insulins be ingected? (Humulin 30/70, Novolin 30/70)

A

-30 mins before meal

121
Q

When should premixed insulin analogues be injected? (Novomix, Humalog Mix 25)

A

0-10 mins before meal

0-15 mins before meal

122
Q

What should insulin be titrated to achieve? What if A1C not achieved? When is a higher FPG acceptable?

A
  • a target of fasting BG of 4.0-7.0 mmol/L
  • 4.0-4.4 mmol/L
  • When goal of avoiding hypoglycemia is more important
123
Q

Equation to estimate A1C based on given mean BG level?

A

A1C % = 0.625(Mean BG) + 1.7

Clinical Nutrition 3 (30 decks)

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