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>
<p>What are patient risk factors for the development of prediabetes/diabetes </p>
- impaired fasting glucose
- impaired glucose tolerance test
- A1c > 5.7-6.4%
- BMI > 30
- < 60 yo
- women w/ hx of gestational DM
<p>Place in therapy for metformin in the tx of T2D</p>
<p>if lifestyle changes fail to achieve glycemic goals and A1c is <7.5% then metformin is the drug of choice </p>
<p>expected clinical effect of metformin on the patient's blood glucose control </p>
<p>-lowers fasting plasma glucose concentrations by about 55 mg/dl
- reduces A1c by 1-2%
- no hypoglycemia
- no weight gain </p>
<p>contraindications to metformin</p>
<p>-renal function
- unstable CHF
- liver dz
- alcohol abuse
- pregnancy/lactation </p>
<p>renal function guidelines for metformin use</p>
<p>-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 </p>
<p>initial dose of metformin</p>
<p>500 mg once or twice daily (Letassy said she starts w/ once daily) </p>
<p>titration dose of metformin</p>
<p>-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 </p>
<p>ADRs of metformin</p>
<p>GI are MC
- early satiety and anorexia
- nausea w/ or w/o vomiting, anorexia, diarrhea, bloating, and abdominal discomfort</p>
<p>what needs to be monitored when taking metformin? </p>
<p>-B12 concentrations
| -some pts may beed replacement </p>
<p>what is the expected clinical effect of the sulfonylureas and meglitinides on the pts BG control? </p>
<p>-fasting BG to drop 60-70 mg/dl
-A1c reduction of 1-2%
</p>
<p>what is the expected clinical effect of pioglitozone on the pts BG control? </p>
<p>-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) </p>
<p>what is the expected clinical effect of the DPP-4 inhibitors on the pts BG control? </p>
<p>0.6-0.8% drop in A1c</p>
<p>what is the expected clinical effect of the SGLT2 inhibitors on the pts BG control? </p>
<p>-A1c decrease of about 1%
| -some weight loss d/t increased excretion of glucose </p>
<p>risk factors for euglycemia DKA d/t SGLT2 inhibitors</p>
<p>-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 </p>
<p>given a child w/ T2D, select the most appropriate therapy</p>
<p>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 </p>
<p>consequences of absolute or relative lack of insulin on the liver </p>
<p>-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 </p>
<p>consequences of absolute or relative lack of insulin on the muscle</p>
<p>-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 </p>
<p>consequences of absolute or relative lack of insulin on the adipose tissue</p>
<p>-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 </p>
Which insulin types are insulin analogues?
- Novolog
- Humalog
- Apidra
- Lantus
- Levemir
Given a patient with newly diagnosed type 1 diabetes:
-Explain the concept of intensive insulin therapy
Intensive insulin therapy tries to achieve a more physiologic replacement of insulin by giving long acting insulin that provides basal insulin and by giving a rapid acting or short acting insulin before meals to provide a bolus of insulin.
Given a patient with newly diagnosed type 1 diabetes:
-Select the best basal/bolus insulin regimen for that person (include the amounts provided by basal and bolus insulin—percent breakdown)
50 to 70% of the total daily dose should be a basal insulin
-Basal insulins are glargine (Lantus®), detemir (Levemir®) and NPH
30 to 50% of the total daily dose should be given in divided doses before a meal with rapid-acting or short-acting insulin (bolus)
-Bolus or Preprandial insulins are Novolog®, Humalog®, Apidra®
Given a patient with newly diagnosed type 1 diabetes:
-Explain the rule of 500 and how to use it to establish an insulin:carb ratio
•Establishing insulin to carbohydrate ratios for each meal
- Insulin:Carb ratios will vary throughout the day
- Rule of 500 is the carbohydrate coverage ratio
- 500 ÷ Total Daily Insulin Dose = 1-unit insulin covers so many grams of carbohydrate
Given a patient with newly diagnosed type 1 diabetes:
-Explain how the rule of 1800 is used to determine an insulin sensitivity factor
- use the “1800 rule” to calculate insulin sensitivity factor for people who use the rapid-acting insulin analogs lispro (brand name Humalog), aspart (NovoLog), and glulisine (Apidra)
- this is done by dividing 1800 by the total daily dose (TDD) of rapid-acting insulin
- if the total daily insulin dose is 40 units, the insulin sensitivity factor would be 1800 divided by 40 = 45
Given a patient with newly diagnosed type 1 diabetes:
-Explain how an insulin correction dose is used
- An insulin sensitivity factor is used to determine an insulin correction factor
- Insulin Correction factors are used to correct or adjust the premeal bolus insulin dose in order to cover the carbohydrate content in a meal plus “correct” a higher than desired blood preprandial blood glucose
Given a patient experiencing a hypoglycemic reaction:
-Identify common reasons for hypoglycemia
When the patient..
- skips a meal
- delays a meal
- eats less at a meal than usual and does not adjust insulin
- increases their activity
- commits a dosage error
Given a patient experiencing a hypoglycemic reaction:
-Identify symptoms commonly associated with hypoglycemia
- Headache
- Shaking
- Sweating
- Feeling tired
- Weakness
- Hunger
- *Rapid onset
Determine the severity of the hypoglycemia
-Mild hypoglycemia
- Usually manifested as adrenergic symptoms (mediated by epinephrine).
- These symptoms are anxiety, sweating, tremulousness, tachycardia, hunger.
- Clinically significant hypoglycemia is defined as a glucose <54 mg/dL.
Determine the severity of the hypoglycemia
-Moderate hypoglycemia
- Includes adrenergic symptoms plus neuroglycopenic symptoms including headache, mood change, irritability, confused thinking, and slurred speech.
- These reactions are usually longer lasting, and the patients usually require assistance in obtaining a glucose source.
- A second dose of 10 to 15 grams of a simple sugar is usually required.
Determine the severity of the hypoglycemia
-Severe hypoglycemia
- Characterized by unresponsiveness, unconsciousness or convulsions.
- These reactions require emergency care with an intravenous dextrose or IM glucagon injection.
Given a patient experiencing a hypoglycemic reaction:
-Determine the appropriate course of treatment and monitoring to bring blood glucose back to normal.
- For severe hypoglycemic reactions in children and adults - use GlucaGen Hypokit (glucagon injection)
- Use food sources that provide 10 gm of carbohydrate (apple juice, orange juice, sugar, lifesavers, B/D glucose tablets)
- Use commercial products (Instant glucose, Dex4, cake frosting gel, monojel)
- To stabilize blood glucose and decrease risk of hypoglycemia use Extendbar and NiteBite
Given a patient experiencing a hypoglycemic reaction:
-Select the most likely cause of their hypoglycemia.
Medical causes:
- Altered kidney or liver function
- Hormonal deficiencies (e.g., pituitary or adrenal)
- Rapid gastric emptying
- Hypoglycemic unawareness: MC
Given a patient experiencing a hypoglycemic reaction:
-Explain the rule of 15
Check blood sugar –> eat 15 gm of carbs –> wait 15 min –> blood glucose will go up.
Identify the glycemic goals for children.
- A1c goal of < 7.5%
- 90 to 130 mg/dL before meals
- 90 to 150 mg/dL bedtime and overnight
Identify the screening for other autoimmune diseases in people with T1DM.
-Thyroid disease
Test for antithyroid peroxidase (ANTI-TPO) and antithyroglobulin (ANTI-TG) antibodies soon after the diagnosis
•Measure TSH soon after diagnosis
•If values are normal, consider rechecking every 1-2 years or sooner if symptoms occur.
Identify the screening for other autoimmune diseases in people with T1DM.
-Celiac disease
Consider screening for celiac disease by measuring either tissue transglutaminase or deamidated gliadin antibodies with normal total serum IgA levels.
•Consider screening in children who have a first degree relative with celiac disease, growth failure or failure to gain weight, weight loss, signs of malabsorption, unexplained hypoglycemia or a loss of glycemic control.
•Children with biopsy-confirmed celiac disease should be placed on a gluten-free diet and consult with dietician to help manage both diabetes and celiac disease.
Identify the screening for other autoimmune diseases in people with T1DM.
-In children
**hypothyroidism.
•Screen for thyroid peroxidase (TPO) and thyroglobulin antibodies at diagnosis.
•Monitor TSH after metabolic control is established.
Given a patient with diabetes, identify the symptoms consistent with hyperglycemia.
- Increased thirst that is not normal
- Increased need to urinate especially at night
- Unintended weight loss
- Repeated vaginal yeast infections (2-3 or more in a 6-month period) or yeast/fungal infections on other parts of the body (otitis externa or in body folds)
- Fatigue
- Repeated urinary tract infections
- Sores that do not heal
- Erectile dysfunction in men
- Blurred vision
Given a patient with diabetes, select the diagnostic modality.
- Fasting plasma glucose (FPG) (this one is commonly done) OR
- 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT) (this one is not commonly done) OR
- A1c criteria (this one is commonly done in conjunction with FPG)
Select the diagnostic criteria (fasting blood glucose, A1c) for prediabetes.
- IFG (impaired fasting glucose) –fasting blood glucose > 100 mg/dl and <125 mg/dl OR
- IGT (impaired glucose tolerance) –2-hour plasma glucose 140 to 199 mg/dl OR
- A1c 5.7% to 6.4%
Select the diagnostic criteria (fasting blood glucose, A1c,) for diabetes.
- A1c > 6.5% OR
- Fasting plasma glucose > 126 mg/dl (fasting—no caloric intake for 8 hrs) OR
- A random (without regard to last food intake) plasma glucose level of >200 mg/dL plus clinical signs and symptoms of diabetes (polyuria, polyphagia, polydipsia, fatigue, weight loss or blurred vision and persistent hyperglycemia).
What is the renal threshold for glucose
180 mg/dL of glucose
- after this, glucose spills into urin
what’s the normal range for serum sodium?
135-145 mEq/L
What is the effect of DKA on serum sodium
- Hyponatremic
* Osmotic changes pull water out of cells, reducing plasma Na concentration
What is the effect of DKA on serum potassium
- DKA causes a potassium deficit, average 300-600 mEq.
- Factors that cause hypokalemia:
• Urinary losses
• Glucose osmotic diuresis
• Excretion of potassium ketoacid anion salts
Presentations of potassium when in DKA
- Hyperkalemic: shift of K out of cells but hasn’t been peed out yet
- Eukalemic: shift of K out of the cells but have peed enough out that the serum concentration appears normal. Person has lost sig amts of K
- Hypokalemic: shift of K out of the cell and have peed it out, this is worst case scenario
What is the effect of DKA on serum phosphate
- Hypophosphatemia
- Causes
• Decreased intake
• Acidosis-related shift into ECF
• Phosphaturia dt osmotic diuresis - Same as potassium, might present early with hyperphosphatemia or euphosphatemia
What is the effect of DKA on serum creatinine
- Acute elevations in serum Cr (and BUN)
* Reflects reduction in glomerular filtration dt hypovolemia
What is the effect of DKA on plasma osmolality
- Increased dt elevations in glucose
* Plasma osmolality = sodium + glucose + BUN (not full equation)
What is the effect of DKA on WBC count
Generally slightly elevated 12,000-13,000 (4,000-11,000 nl)
What is the effect of DKA on lipids
elevated TG
Given a blood glucose and a serum Na, determine the corrected sodium value
- Serum Na concentration will fall approx. 1.6 mEq/L (2) for every 100 mg/100mL increase in glucose concentration
Ex: If blood sugar is 550 and measured serum Na is 130
• 550-100 = 450, the amount of sugar above normal
• 450/100 = 4.5, conversion based on ratio
• (4.5)(2) = 9, amount serum Na is under reported
• 130 + 9 = actual serum sodium level
