Quiz #2 Flashcards
Oral agents Injectibles Tx of T1DM Chronic complications of DM
<p>What is the expected clinical effect of the GLP-1 agonists on blood glucose control</p>
<p>about 1% (0.9% to be exact)</p>
<p>Contraindications to GLP-1 agonists</p>
<p>- Type 1 DM
- Ketoacidosis
- Severe GI dz
- Hx of pancreatitis </p>
<p>Additional contraindication to Byetta (GLP-1)</p>
<p>ESRD or severe renal impairment (CrCl <30 ml/min)</p>
<p>Additional contraindication to Victoza (GLP-1)</p>
<p>Hx or fam hx of medullary thyroid cancer (MTC) or hx of multiple endocrine neoplasia syndrome type 2 (MEN 2)</p>
<p>GLP-1 Agonist
| - MoA</p>
<p>- Incretin analogue
- Activate GLP receptors on the cell surface of beta cells → insulin release in the presense of elevated blood glucose
- Decreases glucagon secretion in a glucose-dependent manner
- Lowers blood glucose by delaying gastric emptying</p>
<p>GLP-1 Agonist
| - ADR (5)</p>
<p>1. (MC) mild to moderate dose-dependent nausea
• frequency and severity decrease over time with continued use
2. HA
3. Diarrhea
4. Hemorrhage and necrotizing pancreatitis
• Early in therapy (w/in 4-6 weeks)
• Rare
5. Serious hypoglycemia
• Seen when use in combo with secretagogue (sulfonylurea or meglitinide)</p>
<p>Novolog
- speed of onset
- bolus or basal</p>
<p>- rapid acting
| - bolus</p>
<p>Humalog
- speed of onset
- bolus or basal</p>
<p>- rapid acting
| - bolus</p>
<p>Apidra
- speed of onset
- bolus or basal</p>
<p>- rapid acting
| - bolus</p>
<p>Lantus
- speed of onset
- bolus or basal</p>
<p>- long acting
| - basal</p>
<p>Levemir
- speed of onset
- bolus or basal</p>
<p>- long acting
| - basal</p>
<p>Regular
- name the two
- speed of onset
- bolus or basal</p>
<p>- Humulin R and Novolin R
- short acting
- bolus</p>
NPH
- name the two
- speed of onset
- bolus or basal
- Humulin N and Novolin N
- intermediate acting
- basal
<p>Which insulins are used as bolus</p>
<p>- Fiasp
- Humalog
- Novolog
- Apidra
- Regular</p>
<p>When should inject rapid acting insulin?</p>
<p>15 min before meal</p>
<p>When should inject short acting insulin?</p>
<p>30 min before meal</p>
<p>Which insulins are used as basal</p>
<p>- NPH
- Lantus
- Levemir
- Toujeo
- Basaglar
- Tresiba</p>
<p>What is the key to successful basal insulin injections?</p>
<p>inject at the same time every day without regard to meals</p>
<p>What does U-100, U-200, U-300 mean?</p>
<p>- U is the number of units of insulin per milliliter of fluid
- Ex: U-100 means there are 100 units of insulin per mL of fluid
- All vials are 10 mL (1,000 units of insulin per vial)</p>
<p>Choose the appropriate starting dose and monitoring parameters for a patient with T2DM starting insulin</p>
<p>- Start with 10 U of bedtime basal insulin (Lantus, Levemir, NPH)
- Monitor fasting am and pre-prandial glucose
Also:
- If A1C goal is not met within 2-3 months add bolus insulin
- Use A1C and pre-meal monitoring to guide
- If hypoglycemia occurs, reduce dose by 10%</p>
How to initiate a bolus insulin dose in a patient who is already using basal insulin
- Add a rapid acting insulin for post-prandial control
- Start with the time of day blood sugar is highest
- Start with 4 Units, 0.1 U/kg, or 10% of basal dose (Letassy says 5-10 units is fine)
- Adjust dose by 1-2 U or 10-15% once or twice weekly until reach target glucose levels
- Dosing is best based on CHO counting
<p>Given a pt at risk for DM, select the medication to reduce or prevent progression to DM based on the outcomes of the prevention studies</p>
<p>metformin</p>
<p>State the outcomes of the DCCT on the development or progression of microvascular diabetes complications</p>
<p>-this study proved normalizing blood glucose could prevent or delay progression of diabetic complications
- in the primary prevention group:
- 76% RRR in the development of retinopathy
- 34% reduction in nephropathy
- 60% reduction in neuropathy
- secondary prevention group:
- 54% RRR in retinopathy
- 43% reduction in nephropathy </p>
<p>glycemic goals of therapy for a nonpregnant adult with T2DM
- a1c
- preprandial blood glucose</p>
<p>-A1c: <7%
| -BG: 80-130 </p>
What are patient risk factors for the development of prediabetes/diabetes
Place in therapy for metformin in the tx of T2D
if lifestyle changes fail to achieve glycemic goals and A1c is <7.5% then metformin is the drug of choice
expected clinical effect of metformin on the patient's blood glucose control
-lowers fasting plasma glucose concentrations by about 55 mg/dl - reduces A1c by 1-2% - no hypoglycemia - no weight gain
contraindications to metformin
-renal function - unstable CHF - liver dz - alcohol abuse - pregnancy/lactation
renal function guidelines for metformin use
-DO NOT use in CKD stages 4 and 5 - do not initiate therapy at stage 3B but may continue use at 1000mg max dose - avoid initiating therapy at stage 3A if expected to become unstable but may continue use at 2000mg max - CKD stages 1 and 2: max dose 2550 mg
initial dose of metformin
500 mg once or twice daily (Letassy said she starts w/ once daily)
titration dose of metformin
-start at 500 mg daily - dose should be increased at the rate of 1 tab weekly - up to a max dose of 2500 mg per day *her example: 500mg daily x 1 week; increase to 500 mg BID x 1 month; then add 500 mg where needed
ADRs of metformin
GI are MC - early satiety and anorexia - nausea w/ or w/o vomiting, anorexia, diarrhea, bloating, and abdominal discomfort
what needs to be monitored when taking metformin?
-B12 concentrations | -some pts may beed replacement
what is the expected clinical effect of the sulfonylureas and meglitinides on the pts BG control?
-fasting BG to drop 60-70 mg/dl -A1c reduction of 1-2%
what is the expected clinical effect of pioglitozone on the pts BG control?
-average decrease in A1c is 1.5% (in pts w/ a baseline of 9%) and is seen after 12-14 weeks -average decrease in A1c when added to another agent: 0.8-1.3% (the numbers don't agree with this but the pack says it's more effected when used in combo)
what is the expected clinical effect of the DPP-4 inhibitors on the pts BG control?
0.6-0.8% drop in A1c
what is the expected clinical effect of the SGLT2 inhibitors on the pts BG control?
-A1c decrease of about 1% | -some weight loss d/t increased excretion of glucose
risk factors for euglycemia DKA d/t SGLT2 inhibitors
-major illness - reduced fluid and food intake - reduced insulin dose - type 2 DM **the packet doesn't specifically state the risk factors, this is just what I interpreted them as
given a child w/ T2D, select the most appropriate therapy
1. Insulin therapy indications: - ketosis or DKA - unclear if T1 or T2 - unusual cases like a random BG >250 or A1c >9% * all other cases: 1. lifestyle changes: nutrition interventions and physical activity 2. metformin - confirm T2 - start low (500mg) d/t GI side effects - monitor for glycemic deterioration - add insulin if needed 3. test A1c every 3 months - target = <7% - intensify tx if needed
consequences of absolute or relative lack of insulin on the liver
-glycogenolysis occurs to release glucose into the blood - amino acids are released from the muscle and taken up by the liver to produce new glucose - lipolysis occurs and releases free fatty acids into the blood which are taken up by the liver to produce ketones - glycerol is released from adipose and can be taken up by the liver for gluconeogenesis
consequences of absolute or relative lack of insulin on the muscle
-protein breakdown occurs as well as decreased amino acid uptake by muscle - protein breakdown occurs at a higher rate than protein synthesis and therefore there is a net loss of protein - possible decreased muscle mass
consequences of absolute or relative lack of insulin on the adipose tissue
-lipoprotein lipase doesn't work well in the absence of insulin - leads to increased lipolysis and decrease in triglyceride synthesis - net result: weight loss and decreased fat stores - liver converts free fatty acids to ketones which can lead to ketoacidosis
