Diabetes Flashcards

1
Q

COMPLICATIONS OF DIABETES

A

LEADING CAUSE OF:
Adult blindness
ESRD (including dialysis and transplantation)
Non-traumatic limb amputations
Other risk factors:
Death from heart disease 2-4x higher
Stroke 2-4x higher
>50% have HTN and hyperlipidemia

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2
Q

NORMAL GLUCOSE AND INSULIN METABOLISM - where is glucose transported to?

A

Insulin is produced in the β cells of the islets of Langerhans of the pancreas
Function is to regulate blood glucose
When BG is high, insulin promotes transport of glucose into tissues (skeletal muscles and adipose tissue). Excess is stored as glycogen in liver
Released in small increments throughout the day and increased with food intake

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3
Q

DIABETES MELLITUS - what happens to the cells?

A

YOUR BODY HAS TROUBLE MOVING GLUCOSE FROM BLOOD INTO THE CELL
THIS LEADS TO HIGH LEVEL GLUCOSE IN THE BLOOD AND NOT ENOUGH IN THE CELL
CELL NEEDS GLUCOSE TO PRODUCE ENERGY
NOT LETTING GLUCOSE ENTER THE CELL LEADS THE CELLS TO STAVE FOR ENERGY

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4
Q

what ARE CONSIDERED INSULIN-DEPENDENT TISSUES?

A

INSULIN
PROMOTES GLUCOSE TRANSPORT FROM THE BLOODSTREAM ACROSS THE CELL MEMBRANE TO THE CYTOPLASM OF THE CELL

CELLS BREAK DOWN GLUCOSE TO MAKE ENERGY
LIVER AND MUSCLE CELLS STORE EXCESS GLUCOSE AS GLYCOGEN
SKELETAL MUSCLE AND ADIPOSE TISSUE ARE CONSIDERED INSULIN-DEPENDENT TISSUES

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5
Q

CLASSIFICATIONS OF DIABETES: TYPE I

A

TYPE 1 DIABETES: BODY DOES NOT MAKE ENOUGH INSULIN
Formerly known as juvenile-onset diabetes or insulin dependent diabetes
5-10% of diabetics
Generally in people under 40 but can occur at any age
Absence of endogenous insulin
Autoimmune disorder
Exposure to virus
80-90% of β cell destruction before symptom onset

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6
Q

DM I SYMPTOMS (the Ps and one other)

A

POLYPHAGIA: GLUCOSE CANNOT GET INTO CELL, CELL STARVES FOR ENERGY, WEIGHT LOSS
GLYCOSURIA: BLOOD GETS FILTERED TO THE KIDNEY, GLUCOSE IN THE URINE
POLYURIA: WATER FOLLOWS GLUCOSE
POLYDIPSIA: DEHYDRATION AND THIRST FROM POLYURIA

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7
Q

CLASSIFICATIONS OF DIABETES: TYPE 2 - what ethnic groups?

A

TYPE 2 DIABETES
Formerly known as Non-insulin dependent diabetes or adult-onset diabetes
Endogenous insulin produced but inadequate amounts, tissue resistance or overproduction of glucose by the liver
90-95% of diabetics
Less frequently in children but incidents rising due to childhood obesity
Contributing risk factors that lead to insulin resistance:
Family hx, obesity, increasing age, certain ethnic groups (Hispanics, Pacific Islanders, Native Americans, African Americans, Asian Americans)

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8
Q

TYPE 2 DIABETES MELLITUS
ONSET OF DISEASE - is it fast or slow?

A

GRADUAL ONSET
HYPERGLYCEMIA MAY GO MANY YEARS WITHOUT BEING DETECTED
OFTEN DISCOVERED WITH ROUTINE LABORATORY TESTING
AT TIME OF DIAGNOSIS
ABOUT 50% TO 80% OF Β CELLS ARE NO LONGER SECRETING INSULIN
AVERAGE PERSON HAS HAD DIABETES FOR 6.5 YEARS

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9
Q

CLASSIFICATION OF DM: PREDIABETES- # for fasting and after oral glucose test

A

Individuals who are at an ↑ risk for developing diabetes
They have impaired glucose tolerance (IGT), impaired fasting glucose (IFG) or both
Impaired glucose tolerance – 140-200 mg/dL 2 hours after an oral glucose tolerance test (OGTT). Normal is <140
Impaired fasting glucose – 100-125 mg/dL (normal < 100)
Individuals should have BG and HbA1C checked regularly
Watch for symptoms of diabetes (fatigue, frequent infections, non-healing wounds)
Advise to lose weight, exercise and make healthy food choices to prevent diabetes

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10
Q

DIABETES: DIAGNOSIS AND MONITORING - how does Hba1c measure glucose?

A

FBG >126 mg/dL
OGTT >200 mg/dL
HbA1c >6.5
In 2010, the ADA recommended the use of *HbA1c for diagnosing diabetes. Advantages: fasting is not required. More accurate picture of glucose control over time (normal Hba1c < 6.55)
Classic Sx of hyperglycemia + random plasma glucose => 200 mg/dl
Hyperglycemia with 3 Ps (polyuria, polydipsia, polyphagia) & a FBG > 126, confirmed by repeat testing x1 = usually no more tests are needed

  • Hba1c (glycohemoglobin) measures the % of hg on a RBC that is coated with glucose. Measures the average BG over the past 2 to 3 months. The higher the number, the poorer the BG control
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11
Q

GOOD GLUCOSE CONTROL - what should BG and HbA1c be?

A

Euglycemia can delay the onset and slow the progression of retinopathy, nephropathy, neuropathy.

Maintain a mean BG of 155 and a HbA1c of <7.0 will reduce risk of developing micro and macrovascular diseases

For every % point ↓ in Hba1c, there was a 35% reduction in risk for kidney and eye complications, but not cardiac

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12
Q

METABOLIC SYNDROME

A

A collection of risk factors that increases an individual’s chance of developing HTN, cardiovascular disease, stroke and diabetes.

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13
Q

EDUCATION ON NUTRITION

A

Can use the food pyramid but new method is “myplate” introduced by Michelle Obama
For every Kg lost, a diabetic gains 3 months of life.
Avoid alcohol
high in calories and no nutritional value
leads to hypertriglyceridemia
liver damage
Etoh consumption during fasting state:
Inhibits gluconeogenesis
Altered CNS further contributes to hypoglycemia unawareness
Delayed recovery from hypoglycemia in DMI
Lifestyle change – Difficult to make changes after years old habits
Drug therapy

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14
Q

TYPES OF INSULIN - Rapid acting - ex (a rapid lisp is novel)

A

Rapid acting
Aspart (Novolog), Lispro (Humalog)

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15
Q

INSULIN FACTOIDS

A

Regular insulin and ..logs = always clear solution
NPH and protamine containing insulins are cloudy; preparations have additives of zinc, protamine and acetate buffer
Premixed insulin (short/rapid acting with intermediate acting) What are the benefits vs drawbacks?

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16
Q

MIXING AND ADMINISTERING - clear before cloudy

A

Mixing
Which do you draw up first and why?
Rapid or short-acting first (clear solution) then intermediate (cloudy) or long-acting
This is to prevent contamination of intermediate/long acting from contaminating short acting
Administering
Sites – Rotate injection sites within a particular area ½ to 1” apart. Fastest absorption is from the FAT in the abdomen (not muscle), then arm, then thigh and last buttock.

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17
Q

INSULIN REGIMEN: THINKING LIKE A PANCREAS- Basal-bolus regime (just rapid at meals and long acting all day)

A

Basal-bolus regimen
Regimen that closely mimics endogenous insulin production
Uses rapid or short acting (bolus dose) insulin at meal time and intermediate or long acting (basal dose)

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18
Q

CONSIDERATIONS - TSA

A

If exercising, do NOT inject in the thigh
Assess insulin administration barriers:
Neuropathies
Visual and motor deficits
When injecting prefilled insulin syringe, gently roll in palm 10-20x to warm insulin and resuspend particles
Alcohol swabs – not necessary at home
What about traveling with insulin?
***on test - According to TSA website, notify TSA officer that you have diabetes and are carrying insulin. Insulin pumps and supplies must be accompanied with insulin, and must be clearly labeled.

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19
Q

INSULIN STORAGE - temp, and how long?

A

Insulin vials and pens may be kept at room temperature up to 4 weeks as long as it’s not < 0 degrees or >86F degrees

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20
Q

INSULIN

A

ADMINISTRATION OF INSULIN
ABSORPTION IS FASTEST FROM ABDOMEN, FOLLOWED BY ARM, THIGH, AND BUTTOCK
ABDOMEN IS OFTEN PREFERRED SITE
DO NOT INJECT IN SITE TO BE EXERCISED
ROTATE INJECTIONS WITHIN AND BETWEEN SITES

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21
Q

PROBLEMS WITH INSULIN THERAPY - what about fat?

A

HYPOGLYCEMIA
ALLERGIC REACTION
LIPODYSTROPHY

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22
Q

INSULIN COMPLICATION: SOMOGYI EFFECT

A

A unique combination of hypoglycemia early morning (2am to 4am) and rebound hyperglycemia upon waking up
Due to too much evening insulin causing counterregulatory hormones (epinephrine, GH, cortisol, glucagon) release which stimulate lipolysis, gluconeogenesis, glycogenolysis → hyperglycemia

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23
Q

DAWN PHENOMENON - and what hormones cause it?

(dawn grows)

A

Hyperglycemia also present upon awakening
Due to 2 counterregulatory hormones (growth hormone and cortisol). GH & cortisol oppose insulin causing glucose to rise

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24
Q

DRUG THERAPY: ORAL AGENTS - Sulfonylureas - what do they do? (cooking)

(sulfur pancakes)

A

Know major classifications, where they work and timing of the oral agents
Sulfonylureas – stimulates pancreas to produce more insulin

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25
Q

ORAL AGENTS - Meglitinides- fast or slow? (mega lit, mega fast)

A

Rapid and short lived release of insulin from the pancreas.

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26
Q

Biguanides - how do they work?

(big liver)

A

Biguanides – Work at the liver to inhibit glucose release, enhances insulin sensitivity and glucose transport to tissues, esp muscles

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27
Q

⍺-Glucosidase inhibitors - how do they work?

(a gluc is blocking my starch)

A

(starch blockers) delays the absorption of carbs from the small intestine

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28
Q

Thiazolidinediones (TZDS) - how does it work?

(Thia is sensitive)

A

“insulin sensitizers”
Work at the muscle cells to ↑ insulin sensitivity and glucose transport and ↓ endogenous glucose production

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29
Q

DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITORS - how does it work?

dip into creatin to release insulin)

A

Enhances incretin activity (inhibits the enzyme that inactivates incretin)
Result
↑ insulin release from pancreatic β-cells when BG is normal or high esp in response to a meal

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30
Q

COMBINATION THERAPY

A

Combination therapy: combination of OAS classes to target different sites for optimal blood glucose control
Refer to Lewis, p 1131, table 48-7. There are more now than are listed there.

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31
Q

NON INSULIN INJECTABLES = peptide-1- what is it made from?

(1 peptide is a monster)

A

***Glucagon like peptide-1 (GLP-1) receptor agonists
Made from synthetic Gila monster saliva

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32
Q

BYETTA - side effects (bye headache)

A

Sides effects:
Mild to moderate nausea in 44% of the people. Dose-dependent and ↓ over time but some can’t tolerate this.
Headache, diarrhea, hypoglycemia (Risk of hypoglycemia increases with adjunct therapy such as sulfonylureas)
Acute pancreatitis and kidney problems are associated with this drug

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33
Q

GOAL IS EUGLYCEMIA

A

Goal is to aggressively control blood sugar and minimize side effects
Patient should have an endocrinologist in charge for the best and update to date interventions. 85% of diabetics in this country are managed by their PCP. Most generalists are not experts in Diabetes and are not current on the latest therapies

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34
Q

EXERCISE - how often?

A

Regular exercise decreases insulin resistance
which lowers BG, contributes to weight loss
and may reduce the need for medication

ADA recommends moderate aerobic exercise 30min 5x/wk with resistance training when cleared by PCP

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35
Q

MONITORING

A

Makes sure your client knows how to check BG properly
Keep log of BG levels when starting or optimizing treatment

Assess knowledge by return demonstration

Assess patient for barriers to learning

Teach patient S&S of hypo and hyperglycemia

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36
Q

FOOT CARE - water temp?

A

Instruct patient to:
Wash feet in warm water every
day, ensuring water is not too hot
Do not soak feet
Dry feet well. Especially between toes
Apply lotion on feet after washing and drying
File corns and calluses gently with emery board or pumice stone; do not cut

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37
Q

TEACHING - what to do if you can’t eat?

A

Meds
Insulin storage
Self care, foot care & hygiene
Medical identification
Sick day management
Continue to take insulin and oral agents
Check BG more frequently (every 3-4 hrs)
Notify care provider
Drink fluids if cannot eat
Traveling: travelling across time zones be sure to have more than adequate supplies.
Meds with carry-on or store with check in luggage?
Follow-up care (assess for barriers)

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38
Q

is hypoglycemai fast or slow? (fast and low)

A

There is usually a gradual onset of symptoms in hyperglycemia, but a rapid onset with hypoglycemia.

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39
Q

GESTATIONAL DIABETES - how to give birth?

A

DEVELOPS DURING PREGNANCY
INCREASES RISK OF NEED FOR CESAREAN DELIVERY AND OF PERINATAL COMPLICATIONS

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40
Q

OTHER SPECIFIC TYPES OF DIABETES (just injury to b-cells)

A

RESULTS FROM INJURY TO, INTERFERENCE WITH, OR DESTRUCTION OF Β-CELL FUNCTION IN THE PANCREAS
FROM MEDICAL CONDITIONS AND/OR MEDICATIONS
RESOLVES WHEN UNDERLYING CONDITION IS TREATED OR MEDICATION IS DISCONTINUED

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41
Q

HDL

A

good - H for happy

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42
Q

how many drinks per week for women?

A

3

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43
Q

synthetic insulin is made from

A

ecoli or yeast

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44
Q

we usually only give IV insulin if

A

the pt has hypercalcemia

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45
Q

need to know

A

slide 35

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46
Q

wont test us on

A

slide 39

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47
Q

if someone’s sugar is in the 200s

A

ask the pt about their lifestyle and check insulin

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48
Q

dont inject insulin

A

in thigh, because you exercise and lose the insulin, become hypoglycemic

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49
Q

insulin needle

A

prime w/ 2 needles

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50
Q

slide 54

A

some will drop sugar, some will not.

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51
Q

Exenatide (Byetta) on test -
what is it?

(bi creatures are high)

A

An incretin mimetic that enhances insulin secretion when BG is high

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52
Q

slide 65 on test

A

don’t need to know the time, just whether nyou take it before or after

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53
Q

normal glucose range (higher than you think)

A

Normal glucose range 70 -110 mg/dL
40-50 Units secreted/day or 0.6 U/kg

54
Q

metabolic syndrome (Serina)

A

insulin resistance related to excessive visceral fat
1 in 3 adults of metabolic syndrome

55
Q

metabolic syndrome - waist circumference (waist at 35)

A

Dx when 3 or more of the following are present:
Waist circumference: => 40 in men and > 35 in female

56
Q

metabolic syndrome - Triglyceride (tri for 150)

A

Triglyceride: > 150 mg/dl or current treatment

57
Q

metabolic syndrome - HDL (hiddle at 50)

A

HDL : < 40 in men and < 50 in women or treatment for low HDL

58
Q

metabolic syndrome - BP (just high)

A

BP : =>130 SBP or =>85 DBP, or treatment for high BP

59
Q

metabolic syndrome - FBG (same as pre-diabetes)

A

FBG: => 110 mg/dl or treatment for high BG

60
Q

Short acting insulin - ex (short is regular)

A

Short acting
Regular (Humulin R, Novolin R)

61
Q

intermediate acting insulin ex.

(to be human and NPH is intermediate)

A

Intermediate acting
NPH (Humulin N, Novolin N) , Lente

62
Q

Long-acting insulin - ex

(detremental glargle long time)

A

Long-acting
Ultralente (rarely used now)
Glargin (Lantus) - once or 2x/day
Detemir (Levemir) - once or twice a day

63
Q

combo insulin

A

Combination therapy (premixed)
NPH/regular 70/30 (Humulin 70/30
Lispro protamine/lispro 75/25 (Humalog mix 70/30)

64
Q

insulin storage - sunlight? and syringe in what position?

A

Avoid direct sun exposure
Store insulin syringes tip up to prevent clumping at tip

65
Q

how long are Prefilled combination insulin syringes good for? (prefilled is not great)

A

Prefilled combination insulin syringes stable only up to 1 week when stored in the refrigerator (note some prefilled combo insulins not recommended)

66
Q

risk w/ somogyi effect

A

Risk: physician may ↑ insulin dose based on morning hyperglycemia leading to worsening early morning hypoglycemia

67
Q

Somogyi effect - symptoms (somogyi has nightmares)

A

Suspect Somogyi effect if patient c/o headache, night sweats, or nightmares upon wakening. Check BG at 2am/4AM for hypoglycemia

68
Q

Somogyi effect - treatment

(somogyi needs a snack)

A

Treatment: Evening snack, reduce insulin dose in evening or both

69
Q

dawn phenonenon - who does it affect most?

(dawn is young)

A

Affects most diabetics but most severe with adolescence and young adults

70
Q

dawn phenomenon - how to tell if it’s dawn or somgyi? (symogi doesn’t get low early in the am)

A

Check early morning BG to determine if Dawn phenomenon vs Somogyi effect
NO hypoglycemia in early morning as seen in Somogyi effect

71
Q

dawn phenomenon - treatment (dawn needs more insulin)

A

Treatment: Increase insulin dose or adjust administration time from dinner to before bedtime. Could switch meds to include long acting insulin.

72
Q

Sulfonylureas - side effects

(sulfa is fat)

A

Side effects: weight gain and hypoglycemia
Loses effectiveness over time.

73
Q

Sulfonylureas - when to give?

(sulfa needs 30 min)

A

Give 30 minutes before breakfast or with breakfast and dinner.

74
Q

Sulfonylureas - ex

(sulfas ride or die)

A

1st generation: Chlorpropamide (Diabinase), Tolbutamide (Orinase)
2nd generation: Glimepiride (Amaryl), Glyburide (Diabeta or Micronase), Glipizide(GlucotrolandGlucotrolXL)

75
Q

meglitinides - when to give?

(mega lit before meals)

A

Give 15-30 minutes before or right before meal

76
Q

meglitinides - side effects

(mega lit is fat and low)

A

Side effects: Weight gain and hypoglycemia (but less so than Sulfonylureas if given with meal)

77
Q

meglitinides - ex. (megalit ends in glenides)

A

Nateglinide (Starlix)
Repaglinide (Prandin)

78
Q

biguanides - best for which patients? (the big 2)

A

Usually, 1st choice for patients with DM2 and useful for prediabetes who are overweight or obese

79
Q

biguanides - do they cause hypoglycemia?

A

Generally does not cause hypoglycemia since it works only when glucose is high

80
Q

biguanides - when to give? (big meal)

A

Give with meals

81
Q

biguanides - side effects (big lactic)

A

Side effects: Diarrhea, lactic acidosis, weight loss

82
Q

biguanides - be careful of what?

(big contrast)

A

Considerations:
Must be held 1-2 days before IV contrast and 2 days after
Do not give to pts with kidney failure; exacerbates lactic acidosis
Do not use in people who drink large amounts of alcohol

83
Q

biguanides - ex. (big metformin)

A

Metformin (Glucophage, Riomet, Fortamet, Glumetza)

84
Q

⍺-Glucosidase inhibitors - give when?

(a gluck at first bite)

A

Give with first bite of food

85
Q

⍺-Glucosidase inhibitors - what are they best at?

(gluck came after food)

A

Most effective in controlling postprandial (after dinner or lunch) blood sugar

86
Q

⍺-Glucosidase inhibitors - side effects (gluck has gas)

A

Side effects: gas, abd pain, bloating & diarrhea

87
Q

⍺-Glucosidase inhibitors - ex.

A

Acarbose (Precose)
Miglitol (Glyset)

88
Q

⍺-Glucosidase inhibitors - consideration (gluck can’t have table sugar)

A

Consideration: Cannot use table sugar to treat hypoglycemia (only use glucose and lactose sugars such as glucose tabs or milk)

89
Q

Thiazolidinediones (TZDS) - works best for who?

(thia is a resistent person)

A

Works best in people with insulin resistance

90
Q

Thiazolidinediones (TZDS) - give when? (thia can eat whenever)

A

Give PO daily with or without food unless given in combination with another OAS. Then give with meals.

91
Q

Thiazolidinediones (TZDS) - weight?

(thia is fat)

A

Side effects: weight gain, edema

92
Q

Thiazolidinediones (TZDS) - ex. (thia zone)

A

Pioglitazone (Actos)
Rosiglitazone (Avandia)

93
Q

Pioglitazone (Actos) (Piaget bladder)

A

may increase risk for bladder CA and exacerbate heart failure

94
Q

Rosiglitazone (Avandia) - (roz had a brain accident)

A

may increase risk of CVA (cerebral vascular accident) and recent research indicate may increase risk of diabetic macular edema after > 6 months of use; reversible; dose dependent.

95
Q

DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITORS - liver?

(dip into the liver)

A

DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITORS:
Enhances incretin activity (inhibits the enzyme that inactivates incretin)
Result
↑ insulin release from pancreatic β-cells when BG is normal or high esp in response to a meal
Decrease hepatic glucose production

96
Q

DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITORS - side effects (dip into the pancreas)

A

Side effects: pancreatitis, allergic reactions
No weight gain

97
Q

DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITORS - ex. (dip into liptin)

A

Sitagliptin (Januvia)
Now Janumet available (Januvia with Metformin)
Saxagliptin (Onglyza)
Vildagliptin (Galvus)

98
Q

non-insulin injectables - Incretin mimetics

A

may ↑ insulin sensitivity, delaying need for insulin therapy

99
Q

non-insulin injectables - Exenatide (Byetta) - what is it?

A

An incretin mimetic that enhances insulin secretion when BG is high
Suppresses glucagon

100
Q

xenatide (Byetta) - appetite? (Bye appetite)

A

May decrease appetite & slows stomach emptying, increases satiety

101
Q

xenatide (Byetta) - weight loss? (bye fat)

A

Weight loss: on average those on Byetta lost 5.1 lbs.; Those on insulin gained 4 lbs.

102
Q

xenatide (Byetta) - B-cells?

A

Byetta also stimulates β-cell replication, neogenesis and increases β-cell mass

103
Q

byetta - who can use it? and when to give it (in general)?

A

Currently only used for DM2
Given SQ before breakfast and dinner

104
Q

byetta - ex (bye victoria)

A

Newer: Liraglutide (Victoza) given SQ.

105
Q

byetta - who can’t use it? (mom can’t say bye)

A

Do not use if there is a family hx of thyroid CA

106
Q

byetta - give when? (say bye an hour before)

A

**Give PO meds 1 hr before these injectables d/t delayed gastric emptying effect that may alter drug absorption!

107
Q

ALL patients with DM in the hospital need

A

before meal and bedtime glucose checks no matter what type they are.

108
Q

for pts on oral agents, send them home checking BG how often?

A

once a day before one meal because the cost is prohibitive for some.

109
Q

how often to check glucose at home if pt is on insulin?

A

It’s recommended to only do home glucose checks 4 times per day for those on insulin

110
Q

exercise - what BG is not ok to excercise with?

A

Teach patient not to exercise if BG < 80 or > 250 mg/dL
Worsens hypoglycemia when BG low
Worsens hyperglycemia and ketone acidosis when BG high

111
Q

what to do before exercising?

A

Have a carbohydrate snack before exercise if more than 1 hour since a meal
Carry a simple sugar in case of hypoglycemia
Wear medic-identification

112
Q

gestational diabetes - when to screen pts?

A

SCREEN HIGH-RISK PATIENTS FIRST VISIT; OTHERS AT 24 TO 28 WEEKS OF GESTATION

113
Q

gestational diabetes - when is glucose normal again after birth?

A

USUALLY GLUCOSE LEVELS NORMAL 
6 WEEKS POST PARTUM

114
Q

rapid acting - onset

A

15 min

115
Q

rapid acting- peak

(rapid peak in 60)

A

60-90 min

116
Q

rapid acting - duration

A

3-4 hours

117
Q

short acting - onset

A

1/2 - 1 hr

118
Q

short acting - peak

A

2-3 hrs

119
Q

short acting - duration (short at 36)

A

3-6 hours

120
Q

intermediate acting - onset

(intermediate 2s)

A

2-4 hrs

121
Q

intermediate acting - peak

A

4-10 hrs

122
Q

intermediate acting - duration (10 is intermediate)

A

10-16 hrs

123
Q

long acting - onset

A

1/2 hr

124
Q

long acting - peak

A

none

125
Q

long acting - duration

A

24 hrs.

126
Q

byetta - glucagon? (bye glucagon)

A

Suppresses glucagon

127
Q

which is the only insulin that can be given IV?

A

only Regular insulin can be give IV

128
Q

onset

A

15 min
1/2 to 1 hr
2 - 4 hours
1/2 hr

129
Q

peak (peak at 60)

A

60 - 90
2-3 hrs
4 - 10 hours
none

130
Q

duration

(your duration starts at 3)

A

3 - 4 hours
3 - 6 hours
10 -16 hours
24