1
Q
What are complications of DM?
A
Lower-extremity amputations Heart disease Stroke Neuropathy Diabetic eye disease (retinopathy) ESRD
7th leading cause of death!
DKA (DM1 >DM2)
2
Q
What are the types of DM?
A
Type 1: autoimmune disease, beta cell destruction, typically younger patients
Type 2: progressive insulin secretory defect
Gestational (GDM): occurs during 3rd trimester, increases your risk of type 2 in future
Others:
Genetic defects in beta cell function, insulin action
Diseases of exocrine pancreas
Drug- or chemical-induced
3
Q
Progressive Nature of Type 2 DM
A
Prediabetes and associated defects can go on for 10-15 years before diagnosis (often involve obesity, IFG, and impaired glucose tolerance)
By the time of diagnosis, typically about 50% of beta cells have already failed
4
Q
How does DM impact a person’s glucagon and insulin dynamics post meals?
A
Glucose: increased and prolonged endogenous release
Insulin: very little released from defective beta cells
Glucagon: continued release of glucagon even after a meal (this is abnormal)
5
Q
Who should you test for DM?
A
Adults who are overweight (BMI >25…or >23 in Asians) and who have 1 or more of the following:
- First-degree relative with DM
- AA, Latino, Native American, Asian, Pacific Islander (high risk races/ethnicities)
- Women who had GDM
- Hx of CVD
- HTN (<140/90 or on anti-HTN)
- HDL <35 and/or Trig >250
- Women with polycystic ovary syndrome (insulin sensitivity issues)
- Physical inactivity
- Other conditions associated with insulin resistance (sever obesity, acanthosis nigricans, metabolic syndrome)
ALL patients over the age of 45
6
Q
How frequently should you test for DM?
A
If tests are normal, testing should be repeated at least every 3 years
If pt has prediabetes, re-test yearly
7
Q
When can you diagnose DM?
A
- A1C >6.5% OR
- FPG >126 (no caloric intake for at least 8hrs) OR
- 2-h plasma glucose >200 during OGTT
In absence of unequivocal hyperglycemia, the above must be confirmed by repeat testing
OR
4. Patient with classic sx of hyperglycemia/hyperglycemic crisis and a random plasma glucose >200
8
Q
What are microvascular complications of DM? (Ask about these in ROS)
A
Retinopathy
Nephropathy
Neuropathy: sensory – foot lesions 2/2 LOPS (loss of peripheral sensation); autonomic – sexual dysfunction and gastroparesis
9
Q
What are macrovascular complications of DM? (Ask about these in ROS)
A
CHD
cerebrovascular disease
PAD
10
Q
What are screening components of a comprehensive DM evaluation?
A
Psychosocial: depression (PHQ2), anxiety, eating disorder (24hr food diary)
Cognitive impairment: dictates tx complexity
DSMES (self management education and support with DM educator/dietitian and group sessions. At least one 30-min visit covered by Medicare for new dx, if just started insulin, or major life change/event)
Hypoglycemia
Pregnancy planning
11
Q
What are physical exam components for a DM evaluation?
A
- Height, weight, BMI; growth and pubertal development (children and adolescents)
- BP, including orthostatic measurements when indicated
- Fundoscopic examination
- Thyroid palpation
- Skin examination (for acanthosis nigricans or infusion set insertion sites)
- Foot exam: inspection, screen for PAD (pedal pulses), and determine temperature, vibration/pinprick, and 10-g monofilament sensation
12
Q
What is acanthosis nigricans?
A
Velvety, hyperpigmented plaques on the skin often on neck or axillae
Most often associated with obesity and DM (associated with insulin resistance)
Benign and asymptomatic, but cosmetic concerns
Treatment of underlying cause (increased blood glucose) is preferred, but can be treated with topical steroids
13
Q
What is lipohypetrophy?
A
Rubbery spots on the skin from prolonged injection in the same site
Must rotate sites to prevent the formation of fat deposits, which decreases insulin absorption at these sites
14
Q
What are risk factors for developing foot ulcers?
A
Previous amputation Past foot ulcer history Peripheral neuropathy Foot deformity Peripheral vascular disease Visual impairment Diabetic nephropathy (esp pts on dialysis) Poor glycemic control Cigarette smoking
15
Q
What labs should you order when evaluating a patient with suspected DM?
A
-HgbA1c if results not available within the past 3 months (repeat every 3-6 months)
Order the following if no results within past year:
-Fasting lipid profile
-LFTs
-Urinalysis: urine albumin excretion with spot urine albumin-to-creatinine ratio
-Serum Creat and calculated GFR
-TSH in DM1, dyslipidemia, or women >50
-B12 if on metformin (when indicated) (can cause deficiency because of decreased absorption)
-Serum potassium in pts on ACE, ARB, or diuretics
16
Q
What is involved in the care coordination of DM? (Referrals, etc.)
A
- Eye care: needs annual dilated eye exam
- Family planning for women of reproductive age
- Registered dietitian for MNT (medical nutrition therapy)
- Diabetes self-management education/support (DSMES)
- Dentist for comprehensive periodontal exam
- Mental health professional (if needed)
17
Q
What are the immunization recommendations for patients with DM?
A
- Same as for general population according to age
- PPSV23 for anyone 2-64; PCV13 for <2; PCV and an additional PPSV23 for >65
- 3-dose series of HBV to unvaccinated between 19-59; and consider 3-dose HBV to unvaccinated >60
18
Q
How do you assess the effectiveness of management on glycemic control?
A
- Patient self-monitoring of blood glucose (SMBG)
- Continuous glucose monitoring (CGM) (covered by Medicare in older adults)
- A1c
SMBG may help guide treatment decisions and/or self-management for pts using less frequent insulin injections
Patients need glucometer, strips, lancets, alcohol swabs and should monitor BG when concerning sx
19
Q
When should patients on multiple-dose insulin (MDI) or insulin pump therapy be performing SMBG?
A
- Prior to meals and snacks
- Occasionally postprandial (good figure to look at if the preprandial BGs look good, but the A1C is bad)
- At bedtime
- Prior to exercise (if <80, eat a snack before; if >200, do not participate because of ketosis risk)
- When they suspect low blood glucose
- After treating blood glucose until they are normoglycemic
- Prior to critical tasks, such as driving (for high risk patients)
20
Q
What is important about good glycemic control?
A
It delays the progression of morbidity and mortality:
Decreased rates of microvascular and neuropathic complications
Reduced risk of CVD
21
Q
What are the ABCs of DM?
A
Target goals
A1C
BP
Cholesterol
22
Q
What are the recommendations for monitoring A1C?
A
- At least 2x/year in patients meeting treatment goals with stable glycemic control
- 4x/year in patients whose therapy has changed or for those not meeting goals
- Point of care testing for A1C provides opportunity for more timely treatment changes
23
Q
What are A1C goals in adults?
A
Non-pregnant adult: <7%
For selected pts (short duration of DM, type 2 treated w/ lifestyle or metformin only, long life expectancy, or no significant CV disease): <6.5%
Pts with history of sever hypoglycemia, limited life expectancy, advanced complications, extensive comorbidities, longstanding DM w/ difficulty achieving goal: <8%
24
Q
What are the glycemic recommendations for nonpregnant adults with DM?
A
A1C: <7.0%
Preprandial: 80-130
Peak postprandial (2hrs post): <180
25
What are the ADA recommendations regarding hypoglycemia?
- Ask about sx at each encounter for pts at increased risk
- For conscious pts with BG <70, treat with 15-20g glucose
- Glucagon Rx for pts at increased risk of clinically significant hypoglycemia (<54) so that it is available if needed and caregiver knows how to use it
- Re-evaluate pt in instances of hypoglycemia unawareness or episodes of severe hypoglycemia
26
What are s/sx associated with progressive hypoglycemia?
```
Shakiness
Irritability
Confusion
Restlessness
Weakness
Tachycardia
Hunger
Sleepiness
Paleness
Blurry vision
```
Blood glucose levels and sx:
80 - decreased insulin secretion
70 - increased glucagon, epinephrine, adrenocorticotropic hormone, cortisol, and growth hormone
50 - palpitations, sweating
40 - decreased cognition, aberrant behavior, seizures, coma
10-20 - neuronal cell death
27
How do you teach patients to treat their hypoglycemia?
Use fast acting carbohydrate (CHO) and try to avoid protein because that decreased gastric absorption
Good options: 4 oz fruit juice, 3-4 15g glucose tablets, 1 tube glucose gel, 4-6 small hard candies, 1-2 tbsp honey, 6oz regular soda (1/2 a can), 3 tsp table sugar, 1/2 tub of cake mate
Use the Rule of 15
After BS back in normal range, eat a meal
If meal is delayed, follow with a snack
If person is unable to swallow, administer 1 mg (1 unit) of glucagon with 1 mL of diluting solution
28
What is the Rule of 15 for treating hypoglycemia?
Eat 15 grams of CHO
Re-check BG in 15 minutes
Repeat this 3x, and if still low, seek help
29
What is glucagon?
Increases blood glucose concentration and is used in the treatment of hypoglycemia
Acts only on liver glycogen and converts it to glucose
30
What are the indications for the use of glucagon?
-Treatment of severe hypoglycemia
Consider that in patients with type 1 they may have less of an increase in blood glucose levels, so supplement with CHO as soon as possible
31
What are contraindications to using glucagon?
Contraindicated in patients with known hypersensitivity to it or patients with known pheochromocytoma
32
What are BP treatment goals in patients with DM?
<130/80 in individuals with high risk of CVD
An ACEi or ARB, used at the maximum tolerated dose, is recommended 1st-line treatment of HTN in patients with DM with a urinary albumin-to-creatinine ratio >300 (albuminuria)
33
What are the dyslipidemia screening and monitoring recommendations for patients with DM?
Screen with a fasting lipid panel:
At first diagnosis
At the initial medical evaluation
Every 5 years if <40 and more frequently if indicated
Continue monitoring:
4-12 weeks after initiating statin
4-12 weeks after changing statin dose
Annually thereafter to monitor response to therapy
34
What are lipid management goals in patients with DM?
- Lifestyle modifications should focus on weight loss (#1 modification), diet, reduced saturated and trans fat and decreased cholesterol, increased n-3 fatty acids, viscous fiber, and plant sterols, and increased physical activity (at least 150 min/week)
- Intensify lifestyle therapy and optimize glycemic control in pts with TGs >150 and/or HDL<50 (men) or HDL<40 (women)
- For ALL patients with DM and ASCVD, high intensity statin therapy
35
What are the anti-platelet recommendations in patients with DM?
- ASA 75-162 mg/day as secondary prevention strategy if hx of ASCVD
- In pts with ASCVD and ASA allergy, use Clopidogrel (Plavix) 75 mg/day
- Dual anti-PLT therapy (low dose ASA and Plavix/equivalent) is reasonable for 1 year after ACS
- ASA as primary prevention in those at increased risk of CV disease (>50 and family hx of ASCVD, HTN, smoking, HLD, or albuminuria)
If high risk of CVD, refer to cardiologist
36
What are CVD-specific recommendations in patients with DM?
- In patients with prior MI, beta blockers should be used for at least 2 years after
- In patients with stable HF, metformin can be used if GFR remains >30
DO NOT use metformin in unstable or hospitalized patients with HF
37
What are the nephropathy screening recommendations for patients with DM?
At least once a year, assess urinary albumin (spot UACR=spot urinary albumin-to-creatinine ratio) and estimated GFR
(In all patients with T2D and in patients with T1D for >5years)
38
How do you treat nephropathy in patients with DM?
Optimize glucose and BP control
ACEi or ARB is recommended for nonpregant pts with high urinary albumin excretion or GFR <60
Monitor serum Creat and K for increased Creat or changes in K when ACEs, ARBs, or diuretics are used
ACE or ARB NOT recommended for PRIMARY prevention of kidney disease in pts with normal BP and normal UACR (<30 mg/g) and normal eGFR
39
What are the screening recommendations for retinopathy in patients with DM?
To reduce the risk for progression, optimize glycemic control and BP control
Screen with an initial dilated/comprehensive eye exam w/in 5 yrs of T1D dx or at the time of T2D dx
If NO evidence of retinopathy for 1+ annual exams and glycemia is well controlled, exams can be 1-2 years
40
What are the screening recommendations for neuropathy in patients with DM?
Screen all patients for diabetic peripheral neuropathy at the time of T2D diagnosis or after 5 years of T1D.
41
How do you assess for distal symmetric polyneuropathy?
Careful history
Temperature or pinprick (small-fiber function)
Vibration sensation using 128-Hz tuning fork (large-fiber function)
10-g monofilament testing (annually) to identify feet at risk for ulcers and amputation
42
How do you treat diabetic neuropathy?
Optimize glycemic control to prevent/delay
Pregabalin (Lyrica) or duloxetine (Cymbalta) are initial treatments of neuropathic pain
Cymbalta (SNRI) can also help if pt has depression
43
What are recommendations for older adults with DM?
- If otherwise healthy and few chronic illnesses, glycemic goal should be <7.5%, while pts with multiple chronic conditions or functional dependence should have less stringent goals of <8-8.5%
- Be aware: increased risk of hypoglycemia (and less able to recognize sx), so use medication classes with lower risks (consult Beers)
- When palliative care is needed, can lessen BP and lipid management goals
- Primary goals at end of life: overall comfort, prevention of distressing sx, preserved QOL, dignity
44
What are physical factors that complicate the treatment of DM in older adults?
Decreased physical activity
Difficulty preparing food: arthritis, tremor (also difficulty with injections)
Alterations in taste, vision, smell
Difficulty consuming food: poor digestion, dry mouth
Altered renal and hepatic function
Coexisting diseases: infections
Interactions with multiple medications
45
What are psychosocial factors that complicate the treatment of DM in older adults?
```
Cognitive impairment
Social isolation
Poverty
Psych: depression, anxiety
Lack of access to medical care or community resources
```
46
Why are plant-based whole foods diets important?
Pathology: lower inflammation and some powerful anti-cancer effects of micronutrients
Nutrition: nutrient dense, vitamins and minerals providing micronutrients, high fiber increases satiety and improves gut microbiome
Environment: reduced carbon emissions, increased ability to feed world population
47
What are suggestions for physical activity?
150+ minutes of moderate-vigorous activity/week (no 2 consecutive days w/o activity)
Engage in 2-3 sessions/week of resistance exercise
Reduce sedentary behavior (interrupt sitting every 30 minutes)
Flexibility training and balance training 2-3x/week for older adults (yoga, tai chi)
48
What are suggestions for smoking?
All patients should not use cigarettes or other tobacco products
Routine component of diabetes care: smoking cessation counseling
49
What are factors to consider when deciding on medication for DM management?
```
Current A1C
Duration of DM
BMI
Age
Co-morbidities
Cost
Convenience
```
50
What are T1DM recommendations?
- Multiple daily injections (3-4/day of basal and prandial insulin) or continuous SC insulin infusion (CSII)
- Rapid acting insulin analogs to reduce hypoglycemia risk
- Educate about matching prandial insulin to CHO intake, premeal blood glucose, and anticipated activity
- If successfully using CSII, should have continued access to this therapy after turning 65
51
Metformin
- Biguanide (glucophage, glucophage XR)
- Generally first choice
- Reduces hepatic glucose output
- Positives: extensive experience (very safe), NO hypoglycemia, decreased CVD events (UKPDS), decreased weight, can use in prediabetes
- Negatives: GI SE, B12 deficiency (screen for this), lactic acidosis risk (rare)
- Contraindications: CKD (GFR <30), acidosis, hypoxia, dehydration
- Cost: low! (30-day supply of metformin ~$10)
- Decreases A1C by 1-2%
- Start: 500 or 875 mg QD; titrate up to 1,500 mg QD
- Max dosing: 2,000 to 2,500 mg BID to TID; XR QD
52
Sulfonylureas
- Glyburide (Diabeta, Gynase, Micronase), Glipizide (Glucotrol), Glimepiride (Amaryl)
- 2nd generation safer than 1st
- Increase insulin secretion from beta cells (close potassium channels on beta cells)
- Positives: extensive experience, decreased microvascular risks (UKPDS)
- Negatives: HIGHEST RISK of hypoglycemia (don't give to older adults), increased weight, high risk of tx "failure", renal metabolism and excretion, Sulfa allergies
- Cost: low (30-day supply less than $10)
- Decreases A1C by 1-2%
- Start dose: 2.5 mg QD and increase at 2-week intervals
- Max dosing: glyburide 20 mg (doses >10 mg divided BID); glipizide IR 40 mg/XR 20 mg; glimepiride 8 mg
53
Meglitinides (Glinides)
- Repaglinide (Prandin), Nateglinide (Starlix)
- Administered BEFORE meal and act by binding to alternate sites of SU receptor, increase beta cell insulin secretion
- Positives: decreased postprandial glucose excretion
- Negatives: hypoglycemia, increased weight, frequent dosing schedule, also consider if pt will be able to do before meal dosing
- Cost: moderate (30-day: $75-$120)
- Decreases A1C by 1-2%
- Start dose: 0.5 mg/meal and don't take med if skipping meal
- Max dose: Repaglinide 16 mg, divided TID; nateglinide 360 mg, divided TID
54
Thiazolidinediones (TZDs)
-Pioglitazone (Actos) now first (only?) choice; rosiglitazone (Avandia)
-Increase insulin sensitivity (mostly directly on fat and liver cells, enhances insulin action everywhere by activating nuclear transcription factor)
-Positives: low risk of hypoglycemia as monotherapy, increased HDL, decreased TGs, decreased CVD events
-Negatives: 3-6 weeks for glycemic effects, increased weight, edema/HF, bone fractures, ?increased MI (maybe for rosiglitazone)
-Monitor ALT at start, then monthly for 1 year, then q3 months
Cost: pioglitazone 30-day only $14; rosiglitazone $325
Max dosing: pioglitazone 45 mg; rosiglitazone 8 mg
Decreases A1C by 0.5-1%
55
Alpha-Glucosidase Inhibitors
- Acarbose (precose) and Miglitol (Glyset)
- Take before CHO-rich meals and they act by slowing intestinal carb digestion/absorption by inhibiting intestinal enzymes
- Positives: NO hypoglycemia, decreased postprandial glucose
- Negatives: GI side effects (flatulence, diarrhea), modest glycemic benefit, frequent doses
- Cost: low to moderate (30-day Acarbose $45; Miglitol $200)
- Start: 25 mg TID and increase every 4 weeks
- Max dose: 300 mg, divided TID
- Decreases A1C by 0.5-1%
56
Bile Acid Sequestrants
- Closevelam (Welchol)
- Binds bile acids in intestinal tract, increases hepatic bile acid production, ?decreased hepatic glucose production, ?increased incretins
- Positives: rare hypoglycemia, decreased LDL
- Negatives: GI SE (constipation, bloating), modest glycemic benefit, increased TGs, may decrease absorption of other meds
- Cost: high (30-day $600)
- Max dose: 3.75 gm, QD or divided BID
- Decreases A1C by 0.5% when taken with other glucose lowering agent
57
Dopamine-2-Agonists
Bromocriptine (Cycloset)
- Activates dopaminergic receptors, modulates hypothalamic metabolism regulation, increases insulin sensitivity
- Positives: rare hypoglycemia, ?decreased CVD events
- Negatives: SE: drowsiness, N/V, HA, fatigue, rhinitis, dizziness; modest glycemic benefit, increased TGs, may decrease absorption of other meds (CYP3A4 interactions)
- Cost: High (30-day $650)
- Max dose: 4.8 mg
- Decreases A1C 0.5% (when added to metformin and a sulfonylurea, adjuvant to diet and exercise)
58
Glucose Filtration in Kidneys
180 mg/day
59
Renal Reuptake of Glucose
In type 2 diabetes, enhanced renal glucose reabsorption contributes to hyperglycemia
The glucose transporter SGLT2 is responsible for 90% of this glucose reabsorption
Inhibition of SGLT2: 1) decreases glucose reabsorption and 2) increases urinary glucose excretion
Observe weight loss and reduction in blood pressure
60
SGLT2 Inhibitors
- Canagliflozin (Inovkana), Dapagliflozin (Fraxiga, Empagliflozin (Jardiance)
- Blocks glucose reabsorption by kidneys by inhibiting SGLT2 in proximal nephron, increases glucose excreted in urine --> higher osmolality of urine --> pee more
- Positives: NO hypoglycemia, decreased weight, decreased BP, associated with lower CVD event rate and mortality in pts with CVD
- Negatives: GU infections (sugar in pee, UTIs and yeast), angioedema/urticaria and other immune-mediated dermatological effects, increased LDL, increased Creat, DKA, ?acute pancreatitis, ?increased HF hospitalizations
- Cost: High (30-day $430)
- Max dose: Canagliflozin 300 mg; Dapagliflozin 10 mg; Empagliflozin 25 mg
- Decreases A1C 1%
61
What is the incretin effect in normal patients?
Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels.
In normal patients, incretins are released after eating and increase secretion of insulin from beta cells
62
What is the incretin effect like in patients with DM?
Incretin effect is severely reduced
Insulinotropic effects of GIP are basically absent
Insulinotropic effects of GLP-1 are at least partially preserved, but endogenous GLP-1 mediated insulin secretion doesn't compensate for the loss of GIP activity
Defective glucagon suppression produces hyperglucagonemia (fasting and post-nutrient state)
OVERALL, defective incretin-mediated stimulation contributes to defective insulin secretion
63
What does GLP-1 do in the body? (Incretin)
GLP-1 is secreted upon ingestion of food
Sites of action:
Brain - increases satiety and reduces appetite
Alpha cells - decreases postprandial glucagon secretion
Beta cells - enhances glucose-dependent insulin secretion
Liver - decreases glucagon release and decreases hepatic glucose output
Stomach - helps regulate gastric emptying
A natural enzyme (DPP-IV) breaks down incretins
64
GLP-1 Receptor Agonist
INJECTED: Exenatide (Byetta) BID before meals; Liraglutide (Victoza) daily; Exenatide weekly (Bydureon), Albiglutide (Tanzeum), Lixisenatide (Adlyxin), Dulaglutide (Trulicity)
-Incretin mimetic GLP-1 analog that is not recognized by DPPIV (not broken down); increases insulin secretion, decreases glucagon secretion, slows gastric emtpying, increases satiety
-Positives: rare hypoglycemia, decreased weight, decreased postprandial glucose, decreases some CV risk factors, associated with lower CVD events/mortality
-Negatives: injectable (SC), GI SE (N/V/D), increased HR, ?acute prostatitis
-Cost: HIGH
-Decreases A1C by 0.5-1.6%
Good adjuvant for increased weight loss
65
Amylin Mimetics
Pramlintide (Symlin)
- Activates amylin receptors, decrease glucagon secretion, slow gastric emptying, increase satiety
- Positives: decreased postprandial glucose excursions, decreased weight
- Negatives: injectable, GI SE (N/V), angioedema/urticarea and other immune-mediated dermatological effects, ?acute pancreatitis, ?increased HF hospitalizations
- Cost: HIGH (30-day $2,000)
- Max dose: 120 mcg/dose (usually 360 mg/day; divided prior to major meals)
- Decreases A1C by 0.36% when added to insulin with or without metformin and/or SU
- BBW for hypoglycemia
66
What is unique about degludec insulin?
It can last up to 42 hours, so can be good for patients who are forgetful
67
Why did we need newer basal insulins?
NPH can vary up to 50% in absorption
Glargine and detemir still have slight peak with some variability, may need BID injections, and can cause hypoglycemia
We need smoother, flatter, and more constant profiles with lower intra-patient variability, increased adherence, less hypoglycemia, and less weight gain
68
What is the deal with glargine (Toujeo) 300 U/mL?
Dose is given ONCE a day, but can be administered within a 3-hour window either way
69
What is the deal with degludec (Tresiba) 100 U/mL and 200 U/mL?
If a dose is missed, it can be given the next day as long as there is 8 hours before the next dose is due
70
What must you be aware of when using NPH?
- More people have to switch to NPH due to cost (cost effective)
- If switching from NPH, go down in dose until glycemic control is established
- Pt needs to demonstrate how to use vial and syringe, understanding the rolling technique for mixing (no shaking)
- Patients need to be aware of activity levels, meals/snacks, and possibly greater nighttime hypoglycemia
71
Dosing of Glargine
Start with 10 unites once daily and adjust weekly:
Self monitored FPG from preceding 7 days with no episodes of sever hypo or prandial glucose <72:
If FPG 100-120, titrate insulin 2 units
If FPG 120-140, titrate 4 units
If FPG 140-180, titrate 6 units
If FPG >180, titrate 8 units
72
What are the options for insulin intensification?
- Basal (glargine or lantus) plus one bolus (aspart) prandial insulin after largest meal
- Basal/bolus (2-3 prandial doses)
- Switch to insulin pre-mix BID (70/30, 50/50)
- Add GLP-1 RA once daily
73
Why might you combine GLP-1 RA with basal insulin?
This is not done frequently
- Improved A1C (comparable to adding prandial insulin)
- Added lowering of FPG
- Beneficial effects of PPG
- Lowers risk of hypoglycemia compared to increase basal insulin alone or adding prandial insulin
- Less weight gain
74
How do you add GLP-1 RA to Basal Insulin? And vice versa?
- Titrate basal insulin downward to reduce the risk of hypoglycemia and weight gain
- If adding basal insulin to GLP-1 RA, that obviates the need for downward titration of insulin
- Both provide safer and easier way to achieve control
75
Continuous Glucose Monitoring (CGM)
- Measure glucose in interstitial fluid rather than capillary blood
- CGM devices consist of 3 components: glucose sensor, transmitter, receiver (or type of monitor and/or compatible mobile device)
- Covered by Medicare: Dexcom G5, FreeStyle Libre
- NOT meant for longterm use, just gives assessment for like 2 weeks
76
What are some medication considerations for older adults?
- Consult Beers Criteria:
- Avoid insulin sliding scales and SUs
- Consider cost
- Metformin should be avoided in advanced renal insufficiency or HF
- Use TZDs very cautiously in HF or for those at risk for falls/fractures
- Consider incretin-based therapies (DPP-IV inhibitors and GLP-1 agonists)
- For insulin therapy, must have good visual and motor skills and cognitive ability
- Keys: achieve glycemic control while avoiding hypoglycemia, start low and go slow
646 Test 2
flashcards
Decks in class (8)
# Cards
