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Primary Care Exam 2 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the general trend over time of incidence of diabetes in the US?

A

Incidence is growing

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2
Q

What races/ethnicities have the greatest prevalence of DM?

A
  1. American Indian/Native American
  2. Black, non-hispanic
  3. Hispanic
  4. Asian
  5. White
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3
Q

What epidemic is causing the current incidence of diabetes?

A

Obesity

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4
Q

What are some diabetes-related complications?

A
  • Lower extremity amputation
  • Heart disease
  • Stroke
  • Neuropathy
  • Diabetic eye disease
  • End-stage renal disease (ESRD)
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5
Q

What causes type 1 diabetes?

A

Beta cell destruction

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6
Q

What causes type 2 diabetes?

A

Progressive insulin secretory defect

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7
Q

What are some other types/causes of diabetes?

A
  • Gestational diabetes (GDM)
  • Genetic defects in beta cell function, insulin action
  • Diseases of the exocrine pancreas
  • Drug- or chemical-induced
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8
Q

When do macrovascular changes occur? When do microvascular changes occur?

A
  • Macrovascular changes occur first, even 15 years before onset of diabetes due to obesity, impaired fasting glucose, and impaired glucose tolerance
  • Microvascular changes occur second, about 5 years before onset of diabetes
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9
Q

What are the criteria for testing for DM or pre-DM in asymptomatic adults?

A
  1. Adults of any age who are overweight AND have 1+ additional risk factors:
    - 1st degree relative w/ DM
    - High-risk race (AA, latino, AI/NA, Asian, Pacific Islander)
    - Women who had GDM
    - Hx CVD
    - HTN (>140/90)
    - Low HDL (<35) and/or high trigs (>250)
    - Women with POS (polycystic ovary syndrome)
    - Physical inactivity
    - Other clinical conditions associated w/ insulin resistance (severe obesity, acanthosis nigricans)
  2. For all pts, testing should begin at age 45

If tests are normal, repeats testing at minimum q3yr. Those w/ pre-DM should be tested yearly

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10
Q

What are normal results of DM testing?

A
  • FPG < 100 mg/dL
  • 2hr PG < 140 mg/dL
  • A1c < 5.7%
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11
Q

What are the criteria for diagnosing pre-DM?

A
  • FPG 100-125 mg/dL
  • IGT
  • 2hr PG 140-199 mg/dL
  • A1c 5.7-6.4%
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12
Q

What are the criteria for diagnosing DM?

A
  • FPG >126 mg/dL
  • 2hr PG > 200 mg/dL
  • Random PG > 200 mg/dL + symptoms
  • A1c > 6.5%
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13
Q

What are some components of the comprehensive diabetes evaluation?

A
  1. PMH and FH
    - DM hx
    - FH
    - Personal history of complications and common comorbidities
  2. SH: assess lifestyle and behavior patterns
  3. Medications and vaccinations
  4. Technology use
  5. History of diabetes-related complications
    - Microvascular: retinopathy, nephropathy, neuropathy (sensory neuropathy, including hx foot lesions, & autonomic neuropathy, including sexual dysfunction and gastroparesis)
    - Macrovascular: CHD, cerebrovascular disease, PAD
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14
Q

What is some screening we should be doing in diabetics?

A
  • Psychosocial (depression, anxiety, eating disorder)
  • Cognitive impairment
  • DSMES
  • Hypoglycemia
  • Pregnancy planning
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15
Q

What should the physical exam involve when assessing someone with DM?

A
  • Ht, Wt, BMI
  • BP, including orthostatics when indicated
  • Fundoscopic exam
  • Thyroid palpation
  • Skin exam (for acanthosis nigricans and insulin injection/infusion set insertion points
  • Foot exam
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16
Q

What is acanthosis nigricans?

A
  • Common condition characterized by velvety, hyperpigmented plaques on the skin
  • Associated with conditions causing insulin resistance, most commonly obesity & DM
  • Benign, asymptomatic, cosmetic concerns are typically primary concern for tx
  • Tx of underlying cause is preferred method of managmeent
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17
Q

What is diabetic dermopathy?

A
  • Most common skin lesion in DM
  • Trauma + atrophy + chronic inflammation + poorly vascularized skin
  • High correlation with retino-vascular disease and sensory neuropathy
  • Asymptomatic
  • Irregular, round, oval, shallow, depressed, atrophic, hyper-pigmented lesions
  • Very few/many, present in crops, resolve slowly over 12-18 months
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18
Q

What causes lipohypertrophy?

A

Using same sites for insulin injection

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19
Q

What does a comprehensive DM foot exam look like?

A
  • Inspection
  • Screen for PAD (pedal pulses)
  • Determination of temperature, vibration, or pinprick sensation, and a 10g monofilament sensation
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20
Q

What are some risk factors for foot ulcers?

A
  • Previous amputation
  • Past foot ulcer hx
  • Peripheral neuropathy
  • Foot deformity
  • Peripheral vascular disease
  • Visual impairment
  • Diabetic nephropathy (esp. pts on dialysis)
  • Poor glycemic control
  • Cigarette smoking
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21
Q

What are some diagnostics tests to check in patients with diabetes?

A

A1c, if results not available in past 3 months

If not performed/available within past year

  • Fasting lipid profile (total, LDL, HDL, TGs)
  • LFTs
  • Urine albumin excretion/urine-to-creatinine ratio
  • Serum creatinine and calculated GFR
  • TSH in type 1 DM, dyslipidemia, or women over the age of 50 years
  • Vitamin B12 if on metformin
  • Serum potassium in pts on ACE, ARB, or diuretics
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22
Q

What are some refers to make for patients with diabetes?

A
  • Ophthalmologist for annual dilated eye exam
  • Family planning for women of reproductive age
  • Registered dietician for MNT
  • Diabetes self-management education/support
  • Dentist for comprehensive periodontal exam
  • Mental health professional if needed
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23
Q

How does DSME compare to metformin?

A
  • Both are highly effective, have low hypoglycemia risk, neutral wt/wt loss
  • DSME does not have the side effects or cost of metformin, while it can be potentially cost saving and have high psychosocial benefit
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24
Q

When are the 4 critical times to prescribe DSME for adults with type 2 DM?

A
  1. At diagnosis
  2. Annual assessment of educational, nutritional, and emotional needs
  3. When new complicating factors influence self-management
  4. When transitions of care occur
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25
Q

What is the recommended immunization schedule for diabetics?

A
  • Routinely recommended vaccines for general population
  • Pneumococcal (13-valent and 23-valent) vaccines
  • Hepatitis B 3 shot series
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26
Q

What are some techniques available for health providers and patients to assess effectiveness ofmanagement plan on glycemic control?

A
  • Patient self-monitoring of blood glucose (SMBG)
  • Continuous glucose monitoring (CGM)
  • A1c
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27
Q

Who should perform self-monitoring of blood glucose (SMBG)?

A
  • Patients using intensive insulin therapies
  • Patients using less frequent insulin injections or non-insulin therapies
  • Patients on multiple-dose insulin (MDI) or insulin pump therapy
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28
Q

When should patients perform self-monitoring of blood glucose (SMBG)?

A
  • Prior to meals and snacks
  • Occasionally postpradial
  • At bedtime
  • Prior to exercise
  • When they suspect low blood glucose
  • After treating blood glucose until they are normoglycemic
  • Prior critical tasks such as driving
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29
Q

What are the benefits of good glycemic control?

A
  • Delayed progression of disease and associated morbidity/mortality
  • Decreased rates of microvascular and neuropathic complications
  • Risk reduction for cardiovascular disease
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30
Q

What are the ABCs of DM?

A
  • A1c
  • BP
  • Cholesterol
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31
Q

What are the recommendations for WHEN patients should have A1c testing?

A
  • Twice a year for patients meeting treatment goals
  • Quarterly in patients whose therapy has changed or who are not meeting glycemic goals

Point-of-care for A1c provides opportunity for more timely tx changes

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32
Q

For which patients should we set a more stringent A1c goal of < 6.5%?

A

< 6.5% =

  • Patients with short duration of diabetes
  • Type 2 DM tx with lifestyle or metformin only
  • Long life expectancy
  • No significant CVD
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33
Q

For which patients should we set a reasonable A1c goal of < 7%?

A

Nonpregnant adults

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34
Q

For which patients should we set a less stringent A1c goal of < 8%?

A
  • Hx severe hypoglycemia
  • Limited life expectancy
  • Advanced microvascular/macrovascular complications
  • Extensive comorbid conditions
  • Longstanding DM in whom goals are difficult to achieve
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35
Q

What are the general glycemic recommendations for nonpregnant adults with diabetes?

A
  • A1c < 7%
  • Preprandial capillary plasma glucose 80-130 mg/dL
  • Peak postprandial capillary plasma glucose <180 mg/dL
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36
Q

What is the preferred treatment for conscious individual with blood glucose < 70 mg/dL?

A

15-20g glucose

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37
Q

How do you define clinically significant hypoglycemia, and what preventative measures should you take as a provider?

A
  • Blood glucose < 54 mg/dL

- Prescribe glucagon

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38
Q

What are the signs and symptoms of hypoglycemia?

A
  • Shakiness
  • Irritability
  • Confusion
  • Restlessness
  • Weakness
  • Tachycardia
  • Hunger
  • Sleepiness
  • Paleness
  • Blurry vision
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39
Q

What does the body do at a blood sugar of 80?

A

Decreases insulin secretion

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40
Q

What does the body do at a blood sugar of 70?

A

Increases glucagon, epinephrine, ACTH (adrenocorticotrophic hormone), cortisol, and GH (growth hormone)

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41
Q

What does the body do at a blood sugar of 50?

A

Palpitations, sweating

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42
Q

What does the body do at a blood sugar of 40?

A

Decreased cognition, aberrant behavior, seizures, coma,

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43
Q

What does the body do a blood sugar of 20-10?

A

Neuronal cell death

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44
Q

What is the rule of 15, and what are some examples?

A

15 g of fast acting carbohydrates used to treat hypoglycemia

  • 4 oz of fruit juice
  • 15 g glucose tablets (3-4 tablets)
  • 1 tube of glucose gel
  • 4-6 small hard candies
  • 1-2 tablespoons of honey
  • 6 oz regular (not diet) soda (about half a can)
  • 3 tsp table sugar
  • 1/2 tube of cake mate
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45
Q

What is the next step after administering fast acting carbohydrates for hypoglycemia?

A

Follow with a meal or a snack

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46
Q

What do you do if a person is hypoglycemic and unable to swallow?

A

Administer glucagon

47
Q

Describe the clinical pharmacology glucagon

A
  • Increases blood glucose concentration and is used in the treatment of hypoglycemia
  • Acts only on liver glycogen, converting it to glucose
48
Q

Describe the indications and usage for glucagon

A

Because patients with type 1 diabetes may have less of an increase in blood glucose levels compared with a stable type 2 patient, supplementary carbohydrate should be given as soon as possible, especially to pediatric patients

49
Q

Describe the contraindications of glucagon

A
  • Known hypersensitivity

- Pheochromocytoma

50
Q

When should patients with diabetes be treated for hypertension?

A

> 140/90 mmHg

130/80 mmHg may be appropriate for people with high risk of CVD

51
Q

What are first-line pharmacological therapies for patients with diabetes and hypertension?

A

ACE or ARB (then thiazide-type diuretic and CCB)

  • For BP > 140/90 mmHg but < 160/100 mmHg, 1 medication
  • For BP > 160/100 mmHg, 2 medications
52
Q

When is it appropriate to screen lipid profile in adults with diabetes?

A
  • At first diagnosis
  • At the initial medical evaluation
  • Every 5 years if under age 40, or more frequently if indicated
53
Q

When should you reassess a diabetic after initiating a statin or other lipid-lowering therapy, or after changing statin dose?

A

4-12 weeks after

Annually thereafter to monitor response to therapy

54
Q

In regards to lipid management of diabetics, when should you intensify lifestyle therapy and optimize glycemic control?

A
  • Elevated TGs > 150 mg/dL

- Low HDL < 40 mg/dL (men) or < 50 mg/dL (women)

55
Q

In high intensity statin treatment of diabetics, if LDL > 70 mg/dL despite max tolerated statin dose, what should you consider adding to their medication regimen?

A

LDL-lowering therapy (ezetimbe or PCSK9 inhibitor)

56
Q

What are two examples of high intensity statin therapies?

A
  • Atorvastatin 40-80 mg

- Rosuvastatin 20-40 mg

57
Q

When should aspirin therapy be used in diabetic patients?

A
  • As secondary prevention in those with DM and history of ASCVD
  • As primary prevention in those with type I or type II DM with increased risk for CVD
58
Q

What medication should be used in patients with an aspirin allergy?

A

Clopidogrel

59
Q

What is reasonable pharmacological therapy for diabetics a year after ACS?

A

Aspirin + P2Y12 inhibitor

60
Q

What are some risk factors for CVD in diabetics?

A
  • Family history of ASCVD
  • Hypertension
  • Smoking
  • Dyslipidemia
  • Albuminurea
61
Q

What medication should be used in diabetic patients with prior MI?

A

Beta blockers for at least two years after the event

62
Q

When can metformin be used in patients with stable heart failure?

A

If estimated GFR > 30 mL/min but should be avoided in unstable or hospitalized patients with heart failure

63
Q

When should diabetics be screened for nephropathy?

A

At least once a year in type 1 DM duration > 5 years and all type 2 DM

64
Q

How do you screen diabetics for nephropathy?

A
  • Urinary albumin (spot urinary albumin-to-creatinine ratio, UACR)
  • Estimated GFR
65
Q

What is the treatment for diabetic nephropathy?

A
  • Optimize glucose and BP control

- ACE or ARB when elevated urinary albumin excretion > 300 mg/day or GFR < 60 mL/min

66
Q

What labs should be periodically minored when using ACEs, ARBs, or diuretics?

A
  • Creatinine

- Potassium

67
Q

Should diabetics be placed on ACE or ARB for primary prevention of kidney disease in patients with

  • Normal BP
  • Normal UACR
  • Normal estimated GFR?
A

It is not recommended

68
Q

What is the best way to reduce the risk or slow the progression of retinopathy in diabetics?

A

Optimize glycemic and BP control

69
Q

When should diabetics have dilated and comprehensive eye exams by an ophthalmologist or optometrist?

A
  • Adults with type I DM = Within five years of DM onset
  • Patients with type II DM = At time of diagnosis of DM
  • If is no evidence of retinopathy for 1+ annual eye exams and glycemia is well controlled, then exams every 1 to 2 years may be considered
  • If any level of retinopathy Is present, then seen at least annually
70
Q

Who should be screened for diabetic peripheral neuropathy and when?

A

All diabetic patients

  • Diagnosis of type 2 DM and 5 years after diagnosis of type 1 DM, then annually
  • All patients should have annual 10g monofilament testing to identify feet at risk for ulcers and amputation
71
Q

What does the assessment for distal symmetric polyneuropathy involve?

A
  • Inspection every visit
  • Neurological assessment: temperature or 10g monofilament pinprick (small-fiber function) and vibration sensation (large-fiber function)
  • Vascular assessment: pulses in legs and feet

Symptoms of claudication or decreased/absent pedal pulses should be referred for further vascular assessment

72
Q

What is the treatment for diabetic neuropathy?

A
  • Optimize glycemic control to prevent or delay development of neuropathy
  • Pregabalin (Lyrica) or duloxetine (Cymbalta) are recommended as initial pharmacological treatment for neuropathic pain in diabetes
73
Q

What do A1c goals look like in the elderly?

A

< 7.5% = Otherwise healthy with few existing chronic illnesses and intact cognitive functioning
< 8-8.5% = MCI or CI or functional dependence

74
Q

What is a big risk associated with older adults with diabetes?

A

Increased risk of hypoglycemia => Use medication classes with low risk hypoglycemia

75
Q

What are the primary goals for diabetes management at the end of life?

A
  • Palliative care: strict BP control and intense lipid management may not be necessary
  • End of life: overall comfort, prevention of distressing symptoms, and preservation of quality of life and dignity
76
Q

What are some physical factors that complicate the management of DM in older adults?

A
  • Decreased physical activity
  • Difficulty in preparing food: arthritis, tremor
  • Alterations in sense: vision, taste, smell
  • Difficulty in consuming food: poor digestion, dry mouth
  • Altered renal and hepatic function
  • Coexisting diseases: infections
  • Interactions with multiple medications
77
Q

What are some psychosocial factors that complicate the management of DM in older adults?

A
  • Cognitive impairment
  • Social isolation
  • Poverty
  • Psychiatric problems: depression, anxiety
  • Lack of access to medical care or community resources
78
Q

What type of language should we use in diabetes education?

A

Language that is:

  • Neutral, nonjudgmental, and based on facts, actions, or physiology/biology
  • Free from stigma
  • Strengths based, respectful, inclusive, and imparts hope
  • Person-centered
79
Q

What is the most important Rx you can provide patients with DM?

A

Diabetes self-management education/support

80
Q

What self-care behaviors do DM educators help?

A
  • Healthy eating
  • Being active
  • Monitoring
  • Taking medication
  • Problem-solving
  • Healthy coping
  • Reducing risks
81
Q

Why is a plant-based whole foods dietary pattern recommended for diabetics?

A
  1. Pathology
    - Lower inflammation
    - Some micronutrients have powerful anti-cancer effects
  2. Nutrition: caloric density => nutrient density
    - Higher in variety (spectrum of colors)
    - Only complete source of micronutrients (vitamins and minerals)
    - High amount of fiber (increased satiety) => improved gut microbiome
  3. Environment
    - Significantly reduced carbon emissions (~20% estimated by UN and WHO)
    - Increased ability to feed growing world population
82
Q

What are the physical activity guidelines for DM?

A
  • 150 min/week moderate-to-vigorous physical activity
  • No consecutive 2 days without activity
  • 75 min/week vigorous physical activity
  • 2-3 sessions/week resistance exercise
  • Interrupt prolonged sitting q30min
  • Flexibility training and balance 2-3x/week
83
Q

What are the recommendations for smoking cessation in DM?

A
  • Advise all pts not to use cigarettes & other tobacco products or e-cigs
  • Include smoking cessation counseling & other forms of tx as routine components of DM care
84
Q

What are some factors to consider when choosing a pharmacological agent for DM?

A
  • Current A1c
  • Duration of diabetes
  • BMI
  • Age of pt
  • Comorbidities
  • Cost of medication
  • Convenience
85
Q

What are the pharmacological recommendations for therapy for type 1 DM?

A
  • Multiple daily injections (3-4 of basal and prandial insulin) or continuous SC insulin infusion
  • Use rapid-acting analogs to reduce hypoglycemia risk
  • Educate pts on how to match prandial insulin dose to carb intake, premeal glucose, and anticipated activity
  • Pts who have been successfully using continuous subcutaneous insulin infusion should have continued access to this therapy after they turn 65 years old
86
Q

What is important about potency of oral DM medications?

A

All oral agents require presence of some endogenous beta-cell function, as they work by either increasing insulin sensitivity of augmenting beta-cell insulin release

87
Q

What are some of the noninsulin agents available for T2DM?

A
  • Alpha-glucosidase inhibitors
  • Amylin analogues
  • Biguanides
  • Bile acid sequestrants
  • DPP-4 inhibitors
  • Dopamine-2 agonists
  • Glinides
  • GLP-1 receptor agonists
  • SGLT2 inhibitors
  • Sulfonylureas
  • Thiazolidinediones
88
Q

What is the class, MOA, advantages/disadvantages, cost, and max dosing of metformin?

A
  • Class: biguanides (glucophage IR/XR)
  • Action: reduces hepatic glucose output (HGO)
  • Advantages: extensive experience, NO hypoglycemia, reduced CVD events, weight reduction
  • Disadvantages: GI side effects, vit b12 deficiency, contraindicated in CKD (GFR <30), acidosis, hypoxia, dehydration, lactic acidosis risk (rare)
  • Cost: low ($10/mo)
  • Max Dosing: 2000-2500 mg
  • Decreases A1c 1-2%
  • acidic and kidney dependent - these things go along with most metformin considerations*
89
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of sulfonylureas?

A
  • used to be 1st choice med, 2nd gen safer than 1st gen*
  • Drugs: glyburide (diabeta, gynase, micronase), glipizide (glucotrol), glimeperide (amaryl)
  • Action: increase insulin secretion from beta cells by closing K-atp channels on beta-cell plasma membrane
  • Advantages: extensive experience, reduced microvascular risk
  • Disadvantages: HIGHEST risk of hypoglycemia, weight gain, high risk tx failure, renal metabolism/excretion, sulfa allergies
  • Cost: low ($10/mo)
  • Max Dosing: glyburide 20mg, glipizide IR 40mg/XR 20mg, glimeperide 8mg
  • Decreases A1c 1-2%
90
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of meglitinides (glinides)?

A
  • Drugs: Repaglinide (prandin), nateglinide (starlix) (before meal dosing)
  • Action: rapid acting, binds to alternative sites of SU receptor, closes K-atp channels on beta-cell plasma membranes to increase insulin secretion
  • Advantages: reduced postprandial glucose excursions
  • Disadvantages: hypoglycemia, weight gain,, frequent dosing schedule
  • Cost: mod (repaglinide $75/mo, nateglinide $120/mo)
  • Max Dosing: repaglinide 16mg, nateglinide 360mg
  • Decreases A1c 1-2%
91
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of thiazolidinediones (TZDs)?

A
  • Drugs: pioglitazone (actos) 1st choice, rosiglitazone (avandia)
  • Action: increases insulin sensitivity, enhances insulin action everywhere (activates nucluar transcription factor PPAR-gamma)
  • Advantages: low risk hypoglycemia as monotherapy, increases HDL, decreases TGs & CVD events
  • Disadvantages: 3-6wks for glycemic effects, weight gain, edema/HF, bone fractures, increased risk MI
  • Monitor ALT at tx start, q1mo x 12mo, then q3mo
  • Cost: low/high (pioglitazone $14/mo, rosiglitazone $325/mo)
  • Max Dosing: pioglitazone 45mg, rosiglitazone 8mg
  • Decreases A1c 0.5-1%
92
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of alpha-glucosidase inhibitors?

A
  • Drugs: acarbose (precose), miglitol (glyset) (take before CHO rich meals)
  • Action: slows intestinal CHO digestions/absorption by intestinal enzyme inhibition
  • Advantages: NO hypoglycemia, reduced post prandial glucose excursions
  • Disadvantages: GI side effects (flatulence, diarrhea), modest glycemic benefit, frequent dosing schedule
  • Cost: low-mod (acarbose $45/mo, miglitol $200/mo)
  • Max Dosing: 300mg
  • Decreases A1c 0.5-1%
93
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of

A
  • Drugs:
  • Action:
  • Advantages:
  • Disadvantages:
  • Cost:
  • Max Dosing:
94
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of bile acid sequestrants?

A
  • Drugs: colesevelam (welchol)
  • Action: binds bile acids in intestinal tract, increasing hepatic bile acid production, decreases HGP, increases incretin levels
  • Advantages: rare hypoglycemia, reduces LDL
  • Disadvantages: GI side effects (constipation, bloating), mod glycemic benefit, increases TGs, may reduce absorption of other meds
  • Cost: high ($600/mo)
  • Max Dosing: 3.75g
  • Decreases A1c 0.5% (when taken w/ other glucose-lowering agents)
95
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of dopamine-2 agonists?

A
  • Drugs: bromocriptine (cycloset)
  • Action: activates dopaminergic receptors, modulates hypothalamic regulation of metabolism, increases insulin sensitivity
  • Advantages: rare hypoglycemia, reduced cardiovascular events
  • Disadvantages: side effects of drowsiness, N/V, HA, rhinitis, dizziness; mod glycemic effect, increases TGs, may reduced absorption of other meds (CYP3A4 interactions)
  • Cost: high ($650/mo)
  • Max Dosing: 4.8mg
  • Decreases A1c 0.5% (when added to metformin & sulfonylurea)
96
Q

What are some patterns?

A

Drugs that increase insulin sensitivity reduce CVD events

97
Q

What are the role of SGLT transporters in the nephron?

A
  • SGLTs are located in proximal tubule of nephron, right after Bowman’s capsule
  • SGLT1s are at the S3 seg of proximal tubule, where they account for 10% of glucose reabsorbtion
  • SGLT2s are at the S1 seg of proximal tubule, where they account for 90% of glucose reabsorption
  • A total of 180g glucose is reabsorbed at the site of the proximal tubule/day by SGLT transporters
98
Q

How can SGLTs be targeted by pharmaceuticals to help manage diabetes?

A
  • In T2DM, enhanced rena; glucose reabsorption contributes to hyperglycemia
  • Glucose transporter SGLT2 is responsible for 90% of glucose reabsorption
  • Inhibition of SGLT2: decreases glucose reabsorption, increases urinary glucose excretion
  • Observe weight loss and reduction in blood pressure
99
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of SGLT2 inhibitors?

A
  • Drugs: canagliflozin (invokana), dapagliflozin (farxiga), empagliflozin (jardiance)
  • Action: blocks glucose reabsorption by kidney, increasing glucosuria, inhibits SGLT2 in the proximal nephron
  • Advantages: NO hypoglycemia, weight loss, BP reduction, lower CVD rate & mortality in pts w/ CVD
  • Disadvantages: GU infections, angioedema/urticaria & other immune-mediated dermatological effects, increased LDL, increased creatinine, DKA, ?acute pancreatitis, ?increase HF hospitalizations
  • Cost: high ($430/mo)
  • Max Dosing: canagliflozin 300mg, dapagliflozin 10mg, empagliflozin 25mg
  • Decreases A1c 1%
100
Q

What is the incretin effect and how does it related to diabetics?

A

In pts w/ T2DM:

  1. The incretin effect severely reduced
    - Insulinotropic effects of GIP are virtually absent
    - Insulinotropic effects of GLP-1 are at least partially preserved
    (endogenous GLP-1-mediated insulin secretion does not compensate for loss of insulinotropic activity of GIP)
    - Defective glucagon suppression produces hyperglucagonemia (fasting and post-nutrient state)
  2. Defective incretin-mediated stimulation contributes to defective insulin secretion
101
Q

Name the functions of GLP-1 in the human

A

GLP-1 is secreted upon the ingestions of food (broken down by DPP-IV)

  • Promotes satiety and reduces appetite
  • Work on alpha cells to reduce postprandial glucagon secretion => reduced glucagon reduces hepatic glucose output
  • Work on beta cells to enhance glucose-dependent insulin secretion
  • Work on stomach to help regulate gastric emptying
102
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of GLP-1 agonists?

A
  • Drugs: INJECTED exenatide (byetta qd, bydureon q1wk), liraglutide (victoza), albiglutide (tanzeum), lixisenatide (adlyxin), dulaglutide (trulicity)
  • Action: incretin memtic GLP-1 analog, not recognized by DPP-IV, activates GLP-1 receptors to increase insulin secretion, reduced glucagon secretion, slow gastric emptying, and increase satiety
  • Advantages: rare hypoglycemia, weight loss, reduced postprandial glucose, decreases some CV risk factors, associated w/ lower CVD event & mortality
  • Disadvantages: injectable, GI side effects (N/V/D), increased HR, ?acute pancreatitis
  • Cost: high
  • Max Dosing: ?
  • Decreases A1c 0.5-1.6%
103
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of DPP-IV inhibitors?

A
  • Drugs: sitagliptin (januvia), saxagliptin (onglyza), linaliptin (tradjenta), alogliptin (nesina)
  • Action: increases insulin secretion & reduces glucagon secretion (glucose dependent), inhibits DPP-IV activity increasing postprandial active incretin (GLP-1, GIP concentrations)
  • Advantages: rare hypoglycemia, well tolerated
  • Disadvantages: angioedema/urticaria & other immune-mediated dermatological effects, ?acute pancreatitis, ?increase HF hospitalizations
  • Cost: high (sitagliptin $380/mo, saxa $385/mo, lina $380/mo, alo $195/mo)
  • Max Dosing: sitagliptin 100mg, saxa 5mg, lina 5mg alo 25mg
  • Decreases A1c 0.6-0.9%
104
Q

What is the MOA, example drugs, advantages/disadvantages, cost, and max dosing of amylin mimetics?

A
  • Drugs: pramlintide (symlin)
  • Action: activates amylin receptors, reduces glucagon secretion, slows gastric emptying, increases satiety
  • Advantages: reduces postprandial glucose excursion, weight loss
  • Disadvantages: injectable, GI side effects (N/V), angioedema/urticaria & other immune-mediated dermatological effects, ?acute pancreatitis, ?HF hospitalizations
  • Cost: high ($2,000/mo)
  • Max Dosing: 120mcg/dose (360mg/day)
  • Decreases A1c ~0.36% when added to insulin w/wo metformin and/or sulfonylurea
105
Q

Algorithm for adding or intensifying insulin…

A
  1. Start basal insulin
    - If A1c < 8%, TDD 0.1-0.2u/kg
    - If A1c > 8%, TDD 0.2-0.3u/kg
  2. Insulin titration q2-3days to reach glycemic goal
    - Fixed regimen: increase TDD by 2 u
    - Adjustable regimen:
    ~ FBG > 180: add 20% of TDD
    ~ FBG 140-180: add 10% of TDD
    ~ FBG 110-139: add 1 u
    - If hypoglycemia, reduce TDD by:
    ~ BG < 70: 10-20%
    ~ BG <40: 20-40%
    *Consider d/c or reducing sulfonylurea after starting basal insulin
    *Glucemic goal:
    - <7% for most pts, fasting & premeal BG < 110, absense of hypoglycemia
    - A1c & FBG targets adjustd based on age, duration of DM, presence of comorbidities, & hypoglycemia risk
    *If glycemic goal not met with basal insulin, add GLP-1 RA, DPP-4I, or SGLT-2I, or intensify w/ prandial control
  3. Add prandial insulin
    - Basal plus 1 before biggest meal, if not met plus 2, if not met plus 3 - start 10% of basal dose or 5 u
    - Basal bolus: begin prandial insulin before each meal, 50% basal, 50% prandial, TDD 0.3-0.5u/kg - start 50% of TDD in 3 doses before meals
  4. Insulin titration q2-3days to reach glycemic goal
    - Increase prandial dose by 10% of 1-2u if 2h PPG of premeal glucose > 140
    - If hypoglycemia, reduce TDD basal &/ prandial insulin by:
    ~ BG consistently < 70: 10-20%
    ~ Severe hypoglycemia (requiring assistance from another person) of BG < 40: 20-40%
106
Q

Why is there a need for newer insulins?

A
  1. NPH, in the same dose by the same person in the same site at the same time of the day under the same conditions can vary up to 50% absorption
  2. Glargine & Detemir
    - Still slight peak
    - Hypoglycemia
    - Some variability
    - In some cases BID injections
    - More injections = less adherence
  3. Smoother, flatter, more constant profiles needed
    - Lower intra-patient variability
    - Increased adherence
    - Less hypoglycemia
    - Less wt gain
  4. Newer insulins have greater adherence
    - Glargine 300: dose is given qd but has 3hr window it can be given
    - Degludec: if dose missed can give next day if 8 hr window before next dose
107
Q

What are the different types of insulins?

A 
Basal:
- NPH - biggest spike of them all
- Glargine (also Glargine 300)
- Detemir
- Degludec
Basal-prandial: Regular U-500
Prandial:
- Aspart
- Glulisine
- Lispro
- Inhaled insulin
108
Q

What are some thing sto keep in mind with NPH?

A
  • More ppl ahve to swtich to NPH due to cost
  • Be prepared if switching from NPH to go down in dose until glycemic control established
  • Pt demonstrates how to use vial and syringe
  • Pt understands mixing (rolling technique)
  • Help pts be more aware of activity levels, meals/snacks, & possibility of greater nighttime hypoglycemia
109
Q

Titration for glargine

A

Start w/ 10 u & adjust weekly

  • 100-120: add 2u
  • 120-140: add 4u
  • 140-160: add 6u
  • > 180: add 8u
110
Q

Why add GLP-1 RA w basal insulin?

A
  • 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
111
Q

What are the rules for GLP-1 RA + basal insulin and vice versa?

A
  • If adding GLP-1 RA to basal insulin, downward titration of basal insulin in suggested => reduction of basal insulin dose reduces risk of hypoglycemia and weight gain
  • Adding basal insulin to GLP-1 obviates the need for downward titration of basal insulin
  • Both provide safer and easier way to achieving control
112
Q

When should you start insulin?

A
  1. FPG > 250
  2. A1c > 10%
  3. Random plasma glucose > 300
  4. Not meeting glycemic goals with oral hypoglycemics
  5. Oral hypoglycemics are contraindicated
  6. Hyperglycemia + ketonuria OR metabolic acidosis OR sx DM w/ polyuria, polydipsia, wt loss
113
Q

Framework for treating hyperglycemia in older adults

A
  1. Healthy
    - A1c < 7.5%
    - FPG 90-130
    - Bedtime glucose 90-150
  2. Complex (multiple comorbidities, 2+ IADL impairments, MCI)
    - A1c < 8%
    - FPG 90-150
    - Bedtime glucose 100-180
  3. Very complex (end stage, 2+ ADL impairments, mod-sev CI)
    - A1c < 8.5%
    - FPG 100-180
    - Bedtime glucose 110-200

Primary Care Exam 2 (2 decks)

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