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Adult Clinical Medicine > Dyslipidemia and Type 2 Diabetes > Flashcards

Dyslipidemia and Type 2 Diabetes Flashcards

1
Q

indications of PCSK9 inhibitors

A

Indicated when more LDL-C lowering is needed despite maximally “tolerated” statin therapy:

  • Heterozygous Familial Hypercholesterolemia (FH)
  • Homozygous FH – Evolocumab only
  • Patients with known ASCVD (high risk patients
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2
Q

characteristic of plaque prone to rupture

A

-fibrous cap over lipid core (thin wall- prone to rupture)

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3
Q

how do the current guidelines use HDL

A

use HDL primarily as a risk marker and use statins as indicated

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4
Q

NCEP ATP III steps in management of dyslipidemia

A

evaluate
Set goals
Treat and educate

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5
Q

caveats to measuring lipoprotein profile

A
  • Biologic variation 4-12%
  • Seasonal variability 10% higher winter
  • Lab variability 5 – 7%

**Therefore, repeated measurements are recommended

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6
Q

risk factors used in ASCVD calculation

A 
- Sex
–  Age
–  Race (White, African American, other)
–  Total Cholesterol (untreated)
–  HDL
–  Systolic BP (current)
–  Treatment for HTN (Y/N)
–  Diabetes (Y/N)
–  Smoker (Y/N)

*theres an APP for this

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7
Q

if one experiences true myopathy with a statin what should you do

A

stop the statin and retry them on another one

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8
Q

biological roles of HDL

A
  • HDL “removes” cholesterol from periphery?

- HDL has antioxidant and anti-inflammatory effects

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9
Q

Low HDL levels are associated with ____

High HDL levels are associated with ____

A

increased risk for CVD

a protective effect against CVD

*Unclear whether HDL raising reduces CVD related events/death

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10
Q

Cholesterol lowering therapy especially with statin therapy is effective in preventing __

A

acute atherosclerotic events, both acutely and chronically

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11
Q

Heterozygous Familial Hypobetalipoproteinemia is associated with

A

LDL-C of ~20-30 and longevity

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12
Q

Calculate LDL using Friedewald formula:

A

In fasted state (TG less than 400): LDL = Total-C – HDL – TG/5 + VLDL

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13
Q

traditional Major CVD risk factors

A
  1. Cigarette smoking
  2. Hypertension
  3. Low HDL-C: less than 40 mg/dL*
  4. Family history of premature CHD (1st-degree): male relative age less than 55 years and female relative age less than 65 years
  5. Age (male less/equal to 45 years, female less/equal to 55 years)

*HDL-C greater/equal to 60 mg/dL is a negative risk factor.

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14
Q

benefits of statins

A
  • help reduce dementia
  • plaque regression
  • decrease circulating LDL
  • stabilize plaque
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15
Q

describe endogenous lipid metabolism

A

Liver secretes VLDL (TG rich)–> lipoprotein lipase break down TG into FFA–> used for energy–> remant (IDL)–> broken down by LPL again to LDL–> taken up by liver or recycled by HDLs

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16
Q

exam findings associated w/ severe hypertriglyceridemia

A
  • Lipemia retinalis
  • eruptive xanthomas (on weight baring areas-buttocks, shoulders, arms and legs but may occur all over the body)
  • Lipemic serum (doesnt cause MI but does cause pancreatitis
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17
Q

how often should you be tested for dyslipidemia

A
  • Adults 20 y/o and older should have a fasting lipid panel done at least every 5 years
  • kids screen 9-11y/o and then at teenage yrs too unless FHX screen earilier
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18
Q

In those whose 10-year risk is less than 7.5% (5-7.5%) or when the decision is unclear, other factors may be used to enhance the treatment decision making including:

A
  1. Family History of Premature ASCVD
  2. LDL-C greater than 160 mg/dl
  3. hsCRP greater/equal 2 mg/dl (inflammation)
  4. Coronary Calcium Scoregreater/equal 300 Agatston units or greater/equal 75th percentile for age, sex, ethnicity
  5. ABI less than 0.9
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19
Q

“other” life-habit Cardiac risk factors

A
  1. Obesity (central/abdominal)
  2. Insulin Resistance (IFG, IGT)
  3. Sedentary Lifestyle (lean and unfit is also unhealthy)
  4. Atherogenic Diet
  5. Pyschosocial Factors
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20
Q

if statin therapy does not achieve anticipated LDL Reduction consider:

A
  • Consider adherence issues

- Consider dose titration and/or combination therapy especially in high-risk individuals

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21
Q

what lab values should you obtain when checking lipids?

A
  • complete lipoprotein profile after 8-12 hr fast (no chylomircons)
  • Measure: Total Cholesterol, HDL, LDL** and Triglycerides
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22
Q

what is the physiological purpose of cholesterol

A
  • used for synthesis and repair of cell membranes and organelles
  • precursor of steroid hormones
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23
Q

moderate-intensity statin therapy effects and drug examples

A

-daily dose lowers LDL-C on avg by greater/equal 30-50%

Atorvastatin 10 (20) mg
Rosuvastatin (5) 10 mg
Simvastatin 20-40 mg
Pravastatin 40 (80) mg
Lovastatin 40 mg
Fluvastatin XL 80 mg
Fluvastatin 40 mg BID
Pitavastatin 2-4 mg
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24
Q

major recommendations for statin therapy for ASCVD prevention

A
  • heart healthy habits

- recalc. 10yr ASCVD risk every 4-6 yrs in individuals 40-75y w/o clinical ASCVD or diabetes and with LDL-C 70-189mg/dL

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25
Q

how do PCSK9 (Proprotein Convertase Subtilisin/Kexin type 9) inhibitors help lower cholesterol?

aka Evolocumab and Alirocumab

A
  • PCSK9 binds to LDL receptor and it no longer recycles the LDL receptors so less LDL receptors and more LDL
  • the antibodies recycle LDL receptor to it can bind to, endocytose, and breakdown more

*good in ppl w/ heterozygous familial hypercholesterolemia

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26
Q

4 major statin benefit groups

A
  1. those w/ known clinical ASCVD
  2. individuals w/ LDL grearer/equal 190mg/dl
  3. individuals w/ diabetes (over 40 and LDL over 70)
  4. individuals (over 40 and LDL over 70) w/o ASCVD or diabetes who have an estimated 10-yr ASCD risk greater/equal 7.5%
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27
Q

what should you do before initiating statin therapy

A
  1. initial eval
    - Fasting Lipid Panel
    - AST/ALT
    - CK only if indicated
    - Consider secondary causes (TSH, U/A, LFTs)
  2. Counsel on healthy lifestyle habits
  3. Start on HIGH or MODERATE intensity statin (if not contraindicated)
    - discuss potential SE
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28
Q

treatment of low HDL-C

A
  1. Intensify weight management and increase physical activity
  2. Consider higher mono- and poly-unsaturated fat diet
  3. Consider moderate alcohol intake?
  4. Consider niacin?
  5. New therapies on the way
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29
Q

secondary causes of hypertriglyceridemia

A
  1. Diet: very low-fat diets, high intake of refined carbohydrates, excessive alcohol intake
  2. Weight gain, Obesity, Lipodystrophies
  3. Hyperglycemia, uncontrolled diabetes
  4. Pregnancy (high estrogen)
  5. Hypothyroidism
  6. Nephrotic syndrome, chronic renal failure
  7. Drugs: oral estrogens, raloxifene, tamoxifen, glucocorticoids, bile acid sequestrants, beta blockers (not carvedilol), thiazides, protease inhibitors, retinoic acid, anabolic steroids, sirolimus,
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30
Q

what conditions raise LDL and HDL?

A

estrogen and EtOH

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31
Q

why do some say atherosclerosis is an inflammatory disease?

A

circulating oxidized LDL attracts monocytes and macrophages which are used in activating inflammatory response

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32
Q

marker of particle number

Useful in those with hypertriglyceridemia

A

ApoB

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33
Q

what meds are used to lower TG and by what mechanism?

A

Fibric Acid Derivatives (Fibrates)
ex. Gemfibrozil and fenofibrate

Mechanisms:

  • Activate lipoprotein lipase
  • inhibit VLDL production
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34
Q

lifestyle modifications to reduce blood cholesterol/reduce ASCVD risk in adults

A
  1. heart healthy diet
  2. exercise
  3. avoid tobacco
  4. maintain healthy weight
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35
Q

what does cholesterol lowering meds do to plaque?

A

stabilizes plaque and reduces CVD-related events

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36
Q

effects of Fibric Acid Derivatives (Fibrates)

A
  • decrease TG
  • raise HDL moderately (5-10%)
  • CAN raise LDL
  • SE: few-GI, cholelithasis

*proven reduction in CV events esp in obesity, diabetes

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37
Q

secondary causes of hypercholesterolemia

A
  1. Diet: saturated or trans fats, weight gain, anorexia
  2. Drugs: diuretics, cyclosporine, glucocorticoids, amiodarone
  3. Hypothyroidism
  4. Nephrotic syndrome
  5. Biliary Obstruction
  6. Pregnancy
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38
Q

when should you rechallenge a patient on another statin

A

after 1 month– give CK chance to go down and for sx to resolve

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39
Q

what is hypertriglyceridemia associated w/

A

severe: acute pancreatitis– unclear why

moderate:

  • “Risk factor” for ASCVD
  • Associated with insulin resistance, metabolic syndrome, type 2 diabetes
  • But unclear whether triglyceride lowering is beneficial
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40
Q

what are fish oils used for

A

-Primarily lowers triglycerides
-Need large doses to be effective
6-12 g daily!
2-6g daily with new preparations (Lovaza, Vascepa)

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41
Q

describe exogenous lipid metabolism

A

-dietary fat–> absorbed in intestine–>release chylomicrons (TG rich particles)–> lipoprotein lipase break down TG into FFA–> used for energy–> remnant taken up by liver

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42
Q

If TG greater/equal 500 mg/dL, primary goal is to prevent __-

A

pancreatitis:

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43
Q

pros and cons of NMR spectroscopy when assess dyslipidemia

A
  • LDL particle number, size/density, etc
  • Don’t have to be fasting but what do you do with all these measurements?
  • Expensive
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44
Q

treatment of MODERATE hypertriglyceridemia, If TG 200-499 mg/dL:

A
  1. Use elevated TG as a risk marker and treat LDL with statin therapy if indicated per guidelines
  2. Treat/Eliminate secondary causes of dyslipidemia
  3. Intensify weight management, physical activity
  4. Consider higher mono-, poly-unsaturated fat diet
  • Unclear if medical therapy targeting triglycerides (fibrates, fish oil) is beneficial in addition to statin therapy
  • Consider other markers of risk (apo B)?
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45
Q

clinical effects of Nicotinic acid (niacin)

A
  1. Raises HDL (15-35%)
  2. Modestly lowers LDL (5-25%) and TGs (20-50%)
    - Reduces VLDL production by liver?
  3. Proven reduction of clinical events (monotherapy)
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46
Q

what is the physiological purpose of triglyceridess

A

-fuel source for muscle use and adipose tissue storage

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47
Q

what is a heart healthy diet

A

-Aim for 5-6% saturated fat and low trans fat
-Healthy “dietary pattern”
-Mediterranean or DASH Diet patterns
-Emphasize fresh vegetables/fruits, whole grains, low-fat dairy, poultry, fish, legumes, nuts, vegetable oils
Aim for lower sodium intake esp in HTN

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48
Q

what do you do if your patient cannot tolerate statin therapy

A
  • Readdress lifestyle issues
  • Check CK if muscle symptoms
  • Decrease the dose of statin or try a different statin
  • Try all statins before calling patient “intolerant”–(goal is to get on biggest tolerable dose/slow titration)
  • Evaluate for other conditions that may cause muscle weakness (hypothyroidism)
  • Check vitamin D levels and replace as needed?
  • Consider CoQ10?
  • Consider non-statin therapy
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49
Q

what should your diet be if you have SEVERE hypertriglycermidemia vs MODERATE hypertriglycermidemia

A

SEVERE hyperTG: no fat, high carb
-no meat, no dairy–basically carb diet w/ VERY LOW FAT for a couple weeks

MODERATE hyperTG: lower carb, high fat
-high fat diet (mono- poly-unsaturated fat diet)

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50
Q

what are HDL composed of

A

40% protein
27% cholesterol
3% TGs
30% phosolipids

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51
Q

statin therapy follow up

A

Recheck in 6-12 weeks

  • Discuss medication and healthy lifestyle adherence
  • Look for side effects
  • Check for efficacy – Fasting Lipid Panel
  • Look for hepatotoxicity - check ALT/AST
  • Do not check CK unless symptomatic (check for true myopathy)
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52
Q

atherogenic lipoproteins and their importance

A

LDL, VLDL

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53
Q

types of lipoproteins

A

chylomicrons
LDL
HDL
VLDL

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54
Q

Most of us are born with LDL-C of

A

30-40

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55
Q

non-statin therapy

A
  • Ezetimibe
  • Bile Acid Seqestants (cholestryamine, colesevelam)
  • Niacin
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56
Q

Potential SE of statins

A
  1. myopathy

2. increase in liver enzymes

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57
Q

what is the net effect of lipid particles during lipid metabolism?

A
  • Reduction in TG content

- therefore, reduction in particle size

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58
Q

low-intensity statin therapy effects and drug examples

A

-daily dose lowers LDL-C on avg by less than 30%

Simvastatin 10 mg
Pravastatin 10-20 mg
Lovastatin 20 mg
Fluvastatin 20-40 mg
Pitavastatin 1 mg
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59
Q

what are chylomicrons composed of

A
  • mostly TGs (the most)

- Little protein and cholesterol

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60
Q

what are VLDLs composed of

A
  • 55% TGs
  • 20% cholesterol
  • least cholesterol
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61
Q

Why is elevated LDL bad?

A

LDL cholesterol leads to atherosclerosis–> increased risk of coronary heart disease

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62
Q

high-intensity statin therapy effects and drug examples

A

-daily dose lowers LDL-C on avg by greater/equal 50%

ex. Atorovastatin 40 (80) mg
Rosuvastatin 20 (40) mg
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63
Q

Side effects of fish oils

A
  • Safe to combine with statins/fibrates
  • Generally well tolerated
  • Slight increased risk of bleeding due to decreased platelet aggregation

-Benefits of “supplement” doses (500-1000mg) of fish oil are unclear based on newer RCTs

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64
Q

treatment of SEVERE hypertriglyceridemia:

If TG greater/equal 500 mg/dL, primary goal is to prevent pancreatitis:

A
  1. Treat/Eliminate Secondary Causes: hyperglycemia, estrogens, alcohol, etc
  2. Reduce “chylomicronemia” with a very low fat diet (less than 10% calories from fat)
  3. No alcohol
  4. Weight Management, Physical Activity
  5. Medical Therapy: Fibrates, Fish Oils
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65
Q

what are LDL composed of

A

50% cholesterol** (the most)

  • 22% protein
  • least TG
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66
Q

side effects of Nicotinic acid (niacin)

A
  1. flushing
  2. contraindicated in uncontrolled diabetes, peptic ulcer, liver disease,

*Niacin extended-release can be taken once daily with fewer side effects

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67
Q

other clinical markers that could possible be used to assess dyslipidemia

A
  1. ApoB
  2. Lp(a)
  3. NMR Spectroscopy
  4. Inflammatory Markers: hsCRP
  5. EB-CT Coronary Calcium scan
  6. Carotid US

*consider if it will change your management first

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68
Q

Use of PCSK9 inhibitors

A
  • lowers LDL-C by 50-60% (used in addition to maximally tolerated statin therapy)
  • Appear safe even with very low LDL-C levels
  • May reduce CVD events
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69
Q

how many people in theUS have diabetes and how many are T2DM and “pre-diabetic”

A 
~29 Million In US With Diabetes 
~10% of adult US population
7 million are still undiagnosed
90-95% are T2DM
~ 86 million with “pre-diabetes”
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70
Q

what is the incident rate of DM

A

-Increasing at a rate of 7% per year
-Type 2 occurring at younger age
-1 in 3 chance of diabetes for a child born in 2000
~7 years of life lost (primarily from CVD)

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71
Q

what is the annual cost for diabetes

A

$245 billion (2013)

-~2.3 x higher costs

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72
Q

what is diabetes?

A

-Diabetes: Greek: dia (through), bainein (to go)
to go through or “siphon”, ie excessive urination
-Mellitus: Latin: sweet like honey

*Diabetes Mellitus-Defined as “relative” hyperglycemia

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73
Q

what is the pathogenesis of type 2 diabetes?

A

Normal–> insulin resistance–> decreased insulin secretion–> DM2

  • environment and genetics also play a role at any of these phases
  • insulin resistance does NOT directly cause DM2
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74
Q

What are roles of normal insulin/ glucose physiology?

A

high glucose–> increased insulin:

  1. stimulates muscle cells to take up glucose
  2. stimulates liver to decrease glucose production, uptake glucose and store it as glycogen
  3. stimulates adipose to decrease lipolysis and increase fat storage
  4. high BG stimulates pancreas to decrease glucagon secretion (from alpha cells) which causes the liver to decrease glucose production
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75
Q

what stimulates the release of insulin

A

-high glucose stimulates pancreas (beta cells) to release insulin

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76
Q

what cells secrete insulin and glucagon

A

insulin: beta cells of pancreas
glucagon: alpha cells of pancreas

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77
Q

what are pancreatic islet

A

also called islets of Langerhans, are tiny clusters of cells scattered throughout the pancreas. Pancreatic islets contain several types of cells, including beta cells, that produce the hormone insulin. Insulin helps cells throughout the body absorb glucose from the bloodstream and use it for energy

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78
Q

where is glucose primarily made in the body?

A

liver

  • stimulated by glucagon
  • kept in check by insulin
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79
Q

how can genetics and the environment cause insulin resistance

A
  • there are increased glucagon levels and stimulates the liver to produce more glucose—insulin cannot signal the liver to stop synthesis
  • insulin cannot signal muscles to uptake glucose so there is decreased peripheral glucose uptake
  • The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The level of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed.
  • when the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level.
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80
Q

what is insulin deficiency and how is it caused by genetics and environment

A

It occurs when insulin-producing cells (beta cells) are damaged or destroyed and stop producing insulin and it continues to produce glucagon (liver produces glucose–> further increase BG levels)

Insulin is needed:

  • to move blood sugar into cells throughout the body.
  • signal liver to stop glucose production

*The resulting insulin deficiency leaves too much sugar in the blood and not enough in the cells for energy

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81
Q

what are the core defects of DM2

A
  1. islet cell dysfunction
  2. Insulin resistance in cells (ie. muscle cells)
  3. increased hepatic glucose output ( no signal from insulin to stop production–high glucagon tells it to keep going)

*pts can have one of these or a combination of these

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82
Q

describe the trend of insulin resistance, insulin secretion, postprandial glucose, and fasting glucose with pre-diabetes to diabetes

A
  • insulin resistance: increases w/ pre-DM, then levels off
  • insulin secretion: incrases w/ pre-DM, peaks then drops off w/ DM
  • postprandial glucose: slight increase w/ pre-DM, then spikes fast w/ diabetes
  • fasting glucose: fairly normal w/ pre-DM, then slowly increases w/ DM
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83
Q

who should we be screening for diabetes?

A
  1. Age 45 and older
  2. Overweight (BMI equal/greater 25 regardless of age)
  3. Fhx of DM
  4. Sedentary Behavior
  5. Race/ethnicity (hispanics)
  6. h/o IFG, IGT, GDM
  7. HTN
  8. Low HDL-C and/or elevated Triglycerides
  9. PCOS
  10. hx of vascular disease
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84
Q

what is metabolic syndrome

A

a cluster of conditions that occur together, increasing your risk of heart disease, stroke and diabetes:

  1. HTN
  2. high blood sugar
  3. excess body fat around the waist
  4. bnormal cholesterol or triglyceride levels

*2-3 increased risk for diabetes

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85
Q

how should we screen for diabetes?

A
  1. fasting plamsa glucose
  2. oral GTT (more sensitive than FPG)
  3. HbA1c**
  4. Random glucose? (not sensitive)
  5. insulin or c-peptide? (No, varies day to day)
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86
Q

why is screening diabetes with HbA1c preferred?

A
  • don’t need to be fasting

- can use to Dx and to follow

87
Q

what is the ADA criteria for the diagnosis of diabetes?

A
  • FBG: greater or equal to 126mg/dL
  • 2hr PG: greater or equal to 200mg/dL w/ OGTT
  • Random BG: greater or equal to 200 + Sx (polyuria, polydypsia, proteinuria)
  • HbA1c: greater or equal to 6.5%
  • repeat the test or do 2 of the tests to truly dx DM
  • Cannot test when the person is acutely ill
88
Q

what is the ADA criteria for the diagnosis of increased risk for diabetes (aka pre-diabetes)?

A
  • FBG: 100-125
  • 2hr PG: 149-199
  • Random BG: ?
  • HbA1c: 5.7-6.4
89
Q

what are the normal values for

  • FBG:
  • 2hr PG:
  • Random BG:
  • HbA1c:
A
  • FBG: less than 100
  • 2hr PG: less than 140
  • Random BG: ?
  • HbA1c: less than 5.7
90
Q

how can you manage metabolic syndrome?

A
  • weight loss*****
  • activity/exercise
  • pharacotherapy (Phentermine/Topiramate- weight loss drugs)
91
Q

what are your goals with someone who has metabolic syndrome and is at increased risk for DM

A
  • prevent diabetes
  • prevent CV disease

*Weight loss/life style changes is the best way

92
Q

____ is the biggest predictor for decreasing diabetes

A

weight loss

*diet and exercise had ~60% more than placebo with reducing DM

93
Q

what is the proposed clinical approach to managing DM

A
  1. ID at risk populations
  2. encourage lifestyle changes and ~5% weight loss
  3. if improvement (Body weight, glucose, lipids, etc)–> lifestyle changes
  4. if no improvement/worsening –> weight loss agents, metformin or other (bariatric surgery)
94
Q

how much weight does one need to lose inorder to significantly reduce their risk of DM

A

5%

95
Q

symptoms of diabetes

A
  • polyuria- due to elevated blood gluocse
  • polydyspia
  • generalized fatigue- starving because not enough insulin to get glucose into cells
  • blurred vision- water in eye and changes shape of lens
  • unintentional weight loss
  • acanthosis nigricans
96
Q

what is the natural progression TO diabetes if you don’t intervene w/ meds or lifestyle changes

A

11%/yr increased risk of getting DM

97
Q

what are goals for management of DM2?

A
  1. Acute- reverse acute sx of hyperglycemia (get below 200)
  2. Glycemic control- (prevent microvascular and macrovascular complications, and minimize hypoglycemia)
  3. BP control
  4. Tx metabolic dyslipidemia
  5. Other CFR: Smoking, ASA
98
Q

why is getting glycemic control important when managing DM2

A
  1. Prevent microvascular complications:
    - Neuropathy, Nephropathy, Retinopathy
  2. Prevent macrovascular complication (CVD- what ppl die from)
  3. Minimize hypoglycemia
99
Q

what should a goal BP be for someone w/ DM?

A

below 130/80 (some say 140/80)

100
Q

every 1 HbA1c you drop, you reduce your risk of microvascular complications by ___

A

35%

101
Q

Does Intensive Diabetes Treatment Reduce “Macrovascular” Disease?

A

most studies say yes!

Yes:
DCCT/EDIC (T1DM)
UKPDS (10-YEAR)
PROactive (pioglitazone)
EMPA REG (empagliflozin)
LEADER (liraglutide)

No:
ACCORD- only study showed it actually increases your risk for Macrovascular disease
ADVANCE
VADT

102
Q

what are the ADA recommendations for glycemic control goals?

A
  1. HbA1c: desirable less than 7%- individualize per pt and may get lower if attainable w/o sign. adverse effects like hypoglycemia
  2. Preprandial Plasma Glucose: 90-130 mg/dl
  3. Postprandial Plasma Glucose: less than 180 mg/dl

*individualize

103
Q

when might you set a patient with DM goal for HbA1c less than 7%?

A

-preconception

104
Q

when might you set a patient with DM goal for HbA1c higher than 7%?

A
  • they are having a hard time managing glucose levels- lots of hypoglycemic episodes w/ hospitalizations
  • goal would to keep patient out of hospital
105
Q

When creating a management plan for DM2 what do we need to consider

A
  1. pathophysiology
  2. Tx goals
  3. Tx options- in general and for pt population (insured vs uninsured)
  4. Costs and resources
  5. Pt and provider “buy in”

*remember there is not one right way– must individualize!

106
Q

stepwise management of DM2

A
  1. diet and exercise
  2. oral monotherapy
  3. oral combo tx or orals + injectables
  4. oral + insulin
  5. insulin
  • start w/ step 1 and go up if tx fails
  • general rule of thumb is that you add on therapy (occasionally you will swap drugs due to side effects or contraindications)
107
Q

what is the most important thing to do when managing someones DM

A

Educate!

108
Q

what lifestyle modifications can one make w/ DM or trying to prevent DM

A
  1. Diet- no DM diet! (find the right diet for that individual that helps them control their diabetes and lose weight)
  2. Physical Activity - Exercise (walk 10 min after eating)
  3. Work towards weight loss
109
Q

what are ways people can achieve weight loss?

A
  1. lifestyle modification
  2. medications
  3. bariatric surgery
110
Q

what is the number 1 effective therapy for DM2

A

bariatric surgery

*leave hospital w/o diabetes

111
Q

what are some oral agents used to manage DM

A
  1. Secretagogues: sulfonylureas, meglitinides
  2. Biguanides: metformin
  3. Thiazolidinediones
  4. alpha-Glucosidase Inhibitors
  5. DPP-4 Inhibitors
  6. SGLT2 Inhibitors
  7. “Others”: colesevelam, bromocriptine
112
Q

non-insulin injectable agents used to manage DM

A
  1. Incretin/GLP-1 Mimetics

2. Amylin analogs: pramlintide

113
Q

what are different pathophsyiology you can target to manage DM

A
  1. decrease glucose production
  2. decrease insulin resistance
  3. decrease glucose absorption
  4. increase incretin effects
  5. increase insulin secretion
  6. increase CNS effects
  7. increase glycosuria (urinary release of glucose)
114
Q

Example of pathophysiology based therapy of DM to target:

decreased glucose production

A

metformin

115
Q

Example of pathophysiology based therapy of DM to target:

increase insulin secretion

A
  • Sulfonylurea

- Meglitinide

116
Q

Example of pathophysiology based therapy of DM to target:

decreased glucose absorpotion

A
  • Bile Acid Resin

- Glucosidase Inhibitor

117
Q

Example of pathophysiology based therapy of DM to target:

increase CNS effects

A

-Bromocriptine

118
Q

Example of pathophysiology based therapy of DM to target:

decrease insulin resistance

A

Thiazolidinedione

119
Q

Example of pathophysiology based therapy of DM to target:

increase incretin effect

A

GLP-1 Analog

DPP4 Inhibitor

120
Q

Example of pathophysiology based therapy of DM to target:

increase glycosuria

A

SGLT-2 Inhibitor

121
Q

what is the mechanism of action for Secretagogues

A

enhance insulin secretion

122
Q

Pros and cons of sulfonylureas

A

Pros: they work, INEXPENSIVE

Cons: hypoglycemia, weight gain, hyperinsulinemia? (turns on insulin all the time), enhanced beta-cell destruction?

123
Q

examples of Secretagogues

A
  • Sulfonylureas: Glyburide, Glipizide, Glimepiride

- Meglitinides: Repaglinide, Nateglinide

124
Q

Pros and cons of Meglitinides

A

Pros: good for post-prandial hyperglycemia and in renal insufficiency, rapid acting insulin secretagogues

Cons: hypoglycemia, EXPENSIVE

*take w/ meals

125
Q

what is the mechanism of action for metformin

A
  • reduces hepatic glucose production
  • reduce insulin resistance (liver greater than muscle)
  • some direct effect on insulin sensitivity?
126
Q

pros and cons of metformin

A

Pros: effective, relatively inexpensive, no weight gain, no hypoglycemia (unless you use it with a sulfonylureas)

Cons: GI side effects (bloating, diarrhea), Lactic Acidosis

127
Q

contraindications for metformin

A
  • CRI: Cr greater than 1.5 or GFR less than 30-45,
  • significant cardiopulmonary - liver dz,
  • hypotension,
  • binge drinking
128
Q

how should metformin be dosed?

A

-Start low and go slow for better tolerability! *Discontinue for hospitalizations or procedures (bc of risk of getting acute renal injury)

129
Q

mechanism of action for Thiazolidinediones

A

“Insulin sensitizers”

*Remember: little clinical effect for ~6 weeks

130
Q

examples of Thiazolidinediones

A

Pioglitazone, Rosiglitazone

131
Q

pros and cons of Thiazolidinediones

A

Pros: effective, no hypoglycemia, CVD/endothelial benefits?, B cell protection?

Cons: expensive, weight gain, edema, CHF, fractures, bladder CA

132
Q

mechanism of action for DPP4 inhibitors

A

-Increased levels of “native” active GLP-1 (by preventing its breakdown), which results in enhance glucose dependent insulin secretion

  • Prevents Native GLP-1 Breakdown
  • Prolongs Duration of Native GLP-1 Action
133
Q

mechanism of action for GLP-1 analog/agonist

A

-Resistant to DPP4 Action

134
Q

examples of DPP-4 Inhibitors and how do you does DPP-4 inhibitors

A

Sitagliptin, Saxagliptin, Linagliptin, Alogliptin

-oral, once daily

135
Q

pros and cons of DPP-4 inhibitors

A

Pros: Effective, no hypoglycemia, no weight gain, OK in CKD, best for post-prandial hyperglycemia

Cons: Expensive, pancreatitis**, CHF risk?

136
Q

what drug can you not use if you have a hx of pancreatitis

A
  • DPP-4 inhibitors (Sitagliptin, Saxagliptin, Linagliptin, Alogliptin )
  • GLP-1 analongs (Exenatide, Liraglutide, Albiglutide, Dulaglutide)
137
Q

examples of GLP-1 analogs

A

Exenatide, Liraglutide, Albiglutide, Dulaglutide

*injectable therapies

138
Q

Increased GLP-1 “like” activity leads to:

A
  1. glucose dependent insulin secretion
  2. glucagon suppression
  3. reduced gastric emptying*– prevents glucose spikes
  4. reduced energy intake
139
Q

pros and cons of GLP-1 analogs

A

Pros: effective, no hypoglycemia, weight loss, best for post-prandial hyperglycemia

Cons: expensive, injections, nausea, pancreatitis**

140
Q

dosing for GLP-1 analogs

A

Exenatide: 5-10 mcg BID or 2 mg once weekly
Liraglutide: 0.6 mg to 1.2 mg to 1.8 mg daily
Albiglutide: 30-50 mg once weekly
Dulaglutide: 0.75-1.5 mg once weekly

141
Q

examples of SGLT2 inhibitors and dosing

A

Canagliflozin: 100-300 mg once daily
pagliflozin: 5-10 mg once daily
Empagliflozin: 10-25 mg once daily

142
Q

mechanism of action for SGLT2 inhbitiors

A

Blocks SGLT2 co-transporter reducing renal glucose reabsorption and thus increasing urinary glucose excretion (80-100 g/day)

143
Q

pros and cons of SGLT2 inhibitors

A

Pros: Effective, no hypoglycemia, some weight loss, decrease BP (diuretic)

Cons: Expensive, less clinical experience, genital mycotic and urinary tract infections, increase LDL, renal dosing (not effective with decrease GFR), DKA?, fractures?

144
Q

ADA recommends considering____ at

time of diagnosis of DM2 especially if HbA1c greater than 6.5% and no contraindications

A

Metformin

*Reasonable to consider lifestyle modification first especially if HbA1c less than 7.0%.

145
Q

when someone diagnosed with new onset DM2 what should they be screened for

A
  • diabetic eye (retinal exam annually)
  • kidney (microalbumin and Cr ratio)
  • nerve disease (monofilament testing)
  • dental
  • foot exams
146
Q

when do you add a second agent with DM management? And what are 1st line therapies added

A
  1. lifestyle intervention + metformin
  2. 3 months A1c still above goal add additional agent
  • first line additions:
  • GLP-1 analog- wt. loss, no hypo
  • DDP4 inhibitor-wt. neutral, no hypo
  • SGLT2 inhibitor-wt loss, no hypo
  • Basal insulin- most effective
  • TZD- no hypo
  • SU- low cost
147
Q

what DM2 med lowers LDL

A

bile acid resin

148
Q

2nd line therapies for DM

A
  1. Bile acid resin- LDL reduction
  2. Glucosidase inhibitor- no hypo
  3. bromocriptine- no hypo
  4. pramlintide- wt. loss, no hypo
  5. basal/bolus insulin- most effective
149
Q

ideally how should we choose the primary pharmacology therapy for pts?

A
  • primary pathophysiology
  • Severe insulin resistance?
  • Fasting or preprandial hyperglycemia?
  • Postprandial hyperglycemia or insulin secretory defect?

Real life:

  • formulary, what is covered
  • contraindications
  • pt and provider acceptance
150
Q

DM comorbidities

A 
Obesity
hypertension
hyperlipidemia
non-fatty liver disease
PVD
CAD
151
Q

when should you follow up with someone w/ poorly controlled DM

A
  • 4-6 weeks with home blood glucose monitoring (pre and post prandial BG’s, daily vs q 3-4 days)
  • 3 months w/ A1c

*individualize

152
Q

pts w/ DM often present with MI w/

A

atypical chest pain

*always ask about SOB and CP though

153
Q

when do you consider adding insulin?

A
  1. Poor control on oral agents
  2. Cannot take/tolerate oral agents
  3. Severe hyperglycemia
  4. Hyperosmolar State and/or Ketoacidosis
  5. Pregnancy
  6. when A1c is over 10 and they are on 2-3 therapies already

**consider whether this could be in face DM1

154
Q

what are 3rd line therapies for someone w/ A1c above goal after adding a 2nd line agent (“non-insulin agent”)

A

add after 3 more months after adding 2nd line

  • Non-insulin agent
  • basal insulin
  • basal/bolus insulin
155
Q

what insulin preparations have the fastest onset of action?

A

Glulisine (Apidra)
Aspart (Novolog)
Lispro (Humalog)

Onset of action: ~15 min.
Peak: 1 hr
Duration of action: 2-4 hrs

***Fast and short acting

156
Q

For Human regular insulin prep, what is the:
onset of action:
peak:
duration of action:

A

onset of action: 30-60 min
peak: 2-4 hrs
duration of action: 4-6 hrs

157
Q

For Human NPH insulin prep, what is the:
onset of action:
peak:
duration of action:

A

onset of action: 1-4 hrs
peak: 6-10 hrs
duration of action: 12-20 hrs

158
Q

For Detemir (Levemir) insulin prep, what is the:
onset of action:
peak:
duration of action:

A

onset of action: 1-2 hrs
peak: relatively flat
duration of action: 18-24 hrs

159
Q

For Glargine (Lantus, Toujeo) insulin prep, what is the:
onset of action:
peak:
duration of action:

A

onset of action: 1-2 hrs
peak: flat
duration of action: ~24 hrs

160
Q

For Degludec (tresiba) insulin prep, what is the:
onset of action:
peak:
duration of action:

A

onset of action: 1-2 hrs
peak: flat
duration of action: ~42 hrs

161
Q

Pre-mixed insulins

A

*take before meal (breakfast and dinner)

NPH/Reg 70/30
NPH/Aspart 70/30
NPH/Lispro 70/25 and 50/50
Degludec/Aspart 70/30 (Ryzodeg)

162
Q

concentrated insulins

A

Regular U-500
Lispro U-200 (Humalog U-200)
Glargine U-300 (Toujeo)

*5x concentrated – good for those on high doses of insulin

163
Q

inhaled technosphere insulin

A

Afrezza

*very fast acting

164
Q

how do you add/start basal insulin

A
  1. start w/ 10-15 units at bedtime (likely underdosing but want to avoid hypoglycemia)
  2. ask patient to monitor fasting and occasional bedtime blood glucose
  3. “self” titration vs at provider (increase 2-5 units every 3-7 days until reach FBG goals)

*add to current regimen

165
Q

what are basal insulin therapies you can add?

A

-NPH (bedtime/BID), Glargine, Detemir or Degludec

*Especially good for persistent fasting hyperglycemia
Usually add to current regimen

166
Q

how should you add mealtime or bolus insulin?

A
  • Add a fixed dose of a fast acting insulin before the largest meal of the day.
    1. Start with a dose that is 10-30% of the basal dose.
    2. check some pre and post (2hr) prandial BG
    3. Either increase dose at the single meal, add same dose to a second meal, or add a CF
    4. Continue to increase/add doses until patient is on “full basal/bolus insulin”
167
Q

what insulin should you use when adding mealtime or bolus insulin

A
  • Usually use a rapid-acting analog insulin (ie. Lispro)
  • Regular can also be used, when cost is an issue OR with patients with gastroparesis

*Consider premixed insulin preparations- don’t need drugs that increase insulin secretion anymore because you are replacing insulin

168
Q

what should you do for a patient who is severely insulin resistant?

A

-Consider U-500 insulin

  • 5 x concentrated Human Regular Insulin
  • Onset within 30 min, peak 2-4 hrs, lasts 6-10 hrs
  • Similar profile to NPH
169
Q

who is a good candidate for U-500

A

someone who is severely insulin resistant

more than 200 units/day or more than 2 units/kg/day

170
Q

how do you use concentrated insulin (ex U-500 insulin)

A
  1. Stop all other forms of insulin
  2. -If A1c less8 decrease dose 10-20%
    - If A1c greater than 10 increase dose 10-20%
  3. If TDD is 100-300 use BID - 60% BF, 40% D
  4. If TTDis 300-600 use TID - 40% BF, 30% L, 30% D
  5. Prescribe it in “syringe units”

*TTD- Thiazide-type diuretic
TDD- total daily dose

171
Q

describe the efficacy of insulin therapy

A
  • Efficacy is very high
  • Improves “glucose toxicity”
  • Indirectly improves insulin sensitivity and Beta-cell function
  • No maximum dose!
172
Q

how does insulin therapy help hypoglycemia

A
  • Don’t use basal insulin to cover meal-related needs!

- Less hypoglycemia with insulin analogs

173
Q

Tips for taking Bolus insulin

A
  • Consider starting bolus insulin with biggest meal

- Don’t take it if you don’t eat!

174
Q

how does insulin therapy affect weight

A

Insulin is an “anabolic” hormone so can lead to wt gain

*insulin–> get hypoglyemic–> eat more to help with high insulin but actually they should just be taking less insulin
helps increase glucose storage
*insulin does NOT make someone hungry

175
Q

Drugs that can cause hypoglycemia:

A
  • Sulfonylureas

- Meglitinides

176
Q

Drugs that DO NOT cause hypoglycemia:

A
  • metformin
  • Thiazolidinediones
  • DPP-4 inhibitor
  • GLP-1 analogs
  • SGLT2 inhibitor
  • Glucosidase inhibitor
  • Bromocriptine
  • Pramlintide
177
Q

Drugs that Cause weight gain:

A
  • Sulfonylureas

- Thiazolidinediones

178
Q

Drugs that DO NOT cause weight gain:

A
  • Metformin
  • DPP-4 inhibitors
  • *GLP-1 analogs– good for weight loss
  • SGLT2 inhibitors- good for weight loss
  • *Pramlintide- good for weight loss
179
Q

when can you not use regular insulin prep?

A

someone with gastroparesis

180
Q

what are microvascular complications of diabetes

A
  1. diabetic kidney disease
  2. diabetic retinopathy
  3. neuropathy
  4. foot care
181
Q

what is the single most common cause of ESRD (end stage renal disease)

A

diabetic kidney disease

25-40% patients develop it

182
Q

How do you screen for diabetic kidney disease?

A
  1. urinary micro albumin (spot urinary albumin-to-creatine ratio)
  2. estimated GFR
183
Q

when do you screen for diabetic kidney disease?

A

Start screening at:

  • diagnosis for DM2 (or DM1 with HTN)
  • 5 years for DM1

Screen AT LEAST 1x year

184
Q

what is the treatment for diabetic kidney disease?

A
  1. optimize glucose control
  2. optimize BP control
  3. ACE inhibitor/ARB
185
Q

when is an ACE inhibitor/ARB recommended for diabetic kidney disease?

A
  • Not recommended for primary prevention
  • 30-299 microalbumin: recommend
  • Over 300 microalbumin (aka proteinuria): Strongly recommend
  • microalbumin less than 30 is normal
  • *can hlep with the progression of DKD but not PRIMARY prevention
186
Q

when a patient is on ACE, ARB, diuretics, what are you suppose to monitor?

A

serum creatinine and potassium

187
Q

what is the leading cause of blindness for persons 20-74 yrs

A

retinopathy from diabetes

8000-12,000 new cases/yr

188
Q

if you have retinopathy, what are you chances of getting glaucoma and cataracts?

A

glaucoma- 40% more likely

cataracts- 60% more likely

189
Q

when and how should you screen for diabetic retinopathy/eye disease w/ DM?

A
  • comprehensive eye exam by othalmologist or optometrist
  • screen:
  • 5 yrs of onset w/ DM1
  • at diagnosis of DM2
  • before preg. or in first trimester then 1 yr post paratum (growth factors can change in eye)

*then every 1-2 yrs

190
Q

how do you treat diabetic retinopathy

A
  1. Optimize Glycemic Control
  2. Optimize Blood Pressure and Serum Lipids Control
  3. promptly refer to opthalmlogist (can do laser photocoagulation or intravitreal injections-block GFs)
191
Q

other terms for diabetic peripheral neuropathy

A
  1. distal symmetric polyneuropathy
  2. distal sensory loss first (feet then moves its way up)
  3. hyperesthesia (over sensitize to touch)
  4. dysesthesia (unpleasant, abnormal sense of touch)
192
Q

sx of diabetic peripheral neuropathy

A
  1. sensation of numbness, tingling, sharpness, or burning
  2. begins in the feet and spreads proximally
  3. pain typically involves the lower extremities, is usually present at rest,
    and worsens at night
193
Q

PE to diagnose diabetic peripheral neuropathy

A
  1. reveals sensory loss
  2. loss of ankle reflexes
  3. abnormal position sense.
194
Q

when and how do you screen for diabetic neuropathy?

A
  • careful hx and 10gm monofilament testings and:
  • pinprick, temp, or vibration sensation
  • also assess for sx and signs of autonomic neuropathy in pts w/ complications
  • screen at least 1x year
195
Q

types of autonomic neuropathy in patients with DM complications

A
  • Hypoglycemia unawareness
  • Cardiac Autonomic Neuropathy
  • Gastrointestinal Neuropathies-aka gastroparesis- stomach doesn’t empty well (slows it down), get full easily or if you eat too much you vomi
  • Genitourinary Neuropathy
196
Q

what 3 things lead to high risk of amputation

A

smoking, neuropathy, poor circulation

197
Q

tx of neuropathy

A
  1. Optimize Glucose Control
  2. Rule out other Non-Diabetic Neuropathies
  3. tx complications bc you cannot fix it (improving BG control can slightly improve sx)
  4. Gabapentin, Duloxetine, Tapentadol
  5. Off Label: Tricyclic, Venlafaxine, Carbamazepine, Tramadol,
    Topical Capsaicin
198
Q

complications associated w/ neuropathy (and how do you tx some of them)

A
  1. ED- PDE-5 Inhibitors, Prostaglandins, Vacumn
  2. gastroparesis- Metoclopromide, Gastric Pacer, Roux-En-Y
  3. GU distrubances
  4. orthostatic hypotension
199
Q

how do you screen for Foot complications w/ diabetes

A
  1. hx (ulcers, amputatin, charcot foot, angioplasty, smoking, retinopathy, renal disease, vascular disease)
    - may need foot exam at every visit
  2. PE (neuro, inspection, vascular)
200
Q

when should you screen for Foot complications w/ diabetes

A

at least 1x yr.

-may need foot exam at every visit if you have one of these in your history: ulcers, amputatin, charcot foot, angioplasty, smoking, retinopathy, renal disease, vascular disease

201
Q

tx of foot complications w/ diabetes

A

multi-disciplinary approach

  • Poor Pulse or Claudication- Refer to Vascular
  • Consider Podiatry for Positive History
202
Q

__ out of __ people w/ diabetes die from heart disease ands stroke

A

1 cause of death

2 out of 3

-treating complications has less an effect in preventing macrovascular diseases

203
Q

how do you screen for macrovascular disease from diabetes

A
  • HTN: BP at every visit (Goal less than 140/90)

- lipid management: at Dx and every 5 yrs or more

204
Q

when would you consider an anti-platelet for macrovascular disease w/ DM?

A
  • 10 yr risk is greater than 10%
  • multiple risk factors
  • secondary prevention

*use ASA 75-162mg or clopidogrel 75mg for ASA allergy

205
Q

___ is the preferred tx for someone w/ HTN and obese and FHx of diabetes

A

ACE

ex. lisinopril

206
Q

what labs do you check w/ someone you suspect has DM?

A
  1. BMP- look at BG level and kidney (K+)
  2. lipid profile
  3. A1c
207
Q

where do you typically see acanthosis nigrican

A
  • typically seen around neck and can see in ankles or armpits
  • seen w/ insulin resistance (don’t necessarily have to have DM)
  • –cells need sugar to work and insulin helps cell get the sugar it needs
  • insulin resistance- need more insulin to over come it
208
Q

what is a normal fasting PG?

A

less than 95mg/dL

209
Q
  • ___ americans have DM
  • ___ new case every ___ seconds
  • _____ new cases every yr
A
  • 29.1 Million Americans
  • 1 New Case Every 17 Seconds
  • 2,000,000 New Cases Every Year
210
Q

types of long-acting insulin

A
  1. Detemir (Levemir)
  2. Glargine (Lantus)
  3. Glargine U-300 (Trujeo)
  4. Degludec (Tresbia)
211
Q

what insulin is preferred w/ CO medicaid

A

Detemir (Levemir)

212
Q

intermediate acting insulin

A

NPH (humulin N)

213
Q

how much basal insulin should you increase with a fasting glucose level of:

  1. ) 141-160 mg/dL
  2. ) 161-180 mg/dL
  3. ) more than 180 mg/dL
A
  1. ) 141-160 mg/dL– 4 units
  2. ) 161-180 mg/dL– 6 units
  3. ) more than 180 mg/dL– 8 units

Adult Clinical Medicine (26 decks)

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