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Semester 3 Unit 3-Endocrine > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the only type of insulin you can give IV?

A

Regular which is Humulin R and Novolin R

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2
Q

Rapid acting insulins act how quickly?

A

Onset of 10—30 min
Peak at 30min—-3 hours
Last 3—5hours

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3
Q

Short acting insulins act how quickly?

A

Onset of 30—–60 min
Peak in 2—-5 hours
Last 5—8 hours

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4
Q

Short and rapid acting insulins will look like what?

A

Clear

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5
Q

What will intermediate and long acting insulins look like?

A

Cloudy

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6
Q

What are the intermediate acting insulins? And what should we never do with them?

A

Humulin N
Novolin N
Also called isophane NPH
Never give it IV

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7
Q

Intermediate acting insulins work how fast?

A

Onset-1.5—4 hours
Peak-4—12 hours
Duration 12—-18 hours

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8
Q

What are the long acting insulins?

A

Glargine (Lantis)
Detemir (Levemir)
Degludec (Tresiba)

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9
Q

Long acting insulins work how fast?

A

Onset: 1 hour
Peak: Don’t have one
Duration: 24 hours

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10
Q

When will long acting insulins be given?

A

Bedtime

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11
Q

Where is glucose stored in body?
What is the stored form of glucose called?

A

Liver and muscle cells
It is called glycogen

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12
Q

How often do the beta cells release insulin in healthy person?

A

Continuous in small amounts

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13
Q

What does insulin in body do?

A

The key that unlocks the cell to allow entry of glucose

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14
Q

What is the three hallmark signs of DM1?

A

Polyuria
Polyphagia
Polydipsia
—can also have unexplained sudden weight loss, fatigue–

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15
Q

What type of diabetes will be the cause of DKA?

A

Type 1
–This emergency situation is usually when the patient becomes aware of problem–

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16
Q

What is cause of DM1?

A

Autoimmune
Pt will have islet cell ABx
Beta cells destroyed=no insulin production

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17
Q

What is difference in onset in DM1 vs DM2?

A

DM1= acute, rapid
DM2=gradual, usually undiagnosed for years

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18
Q

What is difference in average age of onset in DM1 vs DM2?

A

DM1=<40 yo (usually)
DM2=Usually older adult (but can occur in obese children, young adults)

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19
Q

What are the common s/sx of DM2?

A

Insidious. Patient will many times have no s/sx.
—Can have fatigue, recurrent infections, yeast overgrowth, vision problems, prolonged wound healing–
They CAN also have polydipsia, polyphagia, polyuria but many dont

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20
Q

Risk factors for DM2

A

Native American, Hispanic, Black
Older
Obese
Family Hx
Lack of exercise

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21
Q

What is happening with endogenous insulin in DM2?

A

Pancreas is tired from overwork
so not producing enough insulin.
In addition, insulin resistance has developed. So insulin can’t unlock cell.

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22
Q

What is insulin resistance?

A

Insulin receptors unresponsive, insufficient in number or both.

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23
Q

What is the major distinction between DM1 and DM2?

A

The presence or absence of endogenous insulin
1=absence
2=presence

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24
Q

What are the 5 factors of metabolic syndrome? How many do you need to have diagnosis?

A
  1. Hyperglycemia
  2. Abdominal obesity
  3. HTN
  4. High triglycerides
  5. Decreased HDL
    —3/5 of these means metabolic syndrome–
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25
Q

What is pre diabetes?

A

Intermediate stage
Glucose is higher than normal but not high enough to have DM2

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26
Q

What is gestational diabetes?

A

Hyperglycemia during pregnancy
These pts will usually be obese, have family hx of diabetes, be older moms.
Usually will develop DM2 later.

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27
Q

What are the metabolic changes that pave the way for DM2?
Four total

A
  1. Insulin resistance
  2. Pancreas gets tired and slows production of insulin
  3. Liver starts converting glycogen to glucose when it shouldn’t
  4. Adipose tissue produces hormones and cytokines. This affects glucose and fat metabolism and increases inflammation.
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28
Q

What are the ABC’s of diabetes management?

A

A=A1C
B=Blood pressure
C=Cholesterol
–This is something to help teach patient–

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29
Q

What are the short acting insulins?

A

Regular or Humulin R or Novolin R

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30
Q

What are the rapid acting insulins?

A

lispro (HumaLOG)
aspart (NovaLOG)
glulisine (Apidra)

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31
Q

DM1 patients usually use what insulin regimen?

A

A pump will infuse continuous rapid acting insulin (the –LOGs)—This is called the basal rate–
This can be controlled by the patient who can give more/less insulin as needed.
Then a long acting insulin will be given usually at bedtime.

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32
Q

What is the basal-bolus insulin plan?

A

Most closely mimics pancreas.
Multiple daily injections of rapid or short acting insulins before meals plus a long or intermediate acting background insulin once or twice daily.

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33
Q

What is meant by postprandial glucose level?

A

After a meal. Glucose will spike and needs insulin on board.

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34
Q

Which insulins must never be mixed with anything?

A

Long acting ones

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35
Q

What must you do with cloudy insulins before admin?

A

Roll in hand gently

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36
Q

How should insulin be stored?

A

Never at extremes of temp or direct sunlight.

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37
Q

How long can opened insulin be at room temp?

A

4 weeks

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38
Q

Where should you store unopened insulin?

A

Fridge

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39
Q

Where is the fastest SQ site for absorption?

A

Abdomen
Then arms
Then thighs
Then butt

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40
Q

How many units is 1 ml of insulin?

A

100 units

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41
Q

What are the needle lengths of insulin needles?

A

3/16
5/16
1/2

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42
Q

What are the needle gauges of insulin needles?

A

28—-31

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43
Q

At what angle should an insulin shot be given?

A

90 degrees (unless person has no fat, then at 45 degrees)

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44
Q

What are some common problems with insulin therapy?

A

Allergic reactions
Lipodystrophy (injections make SQ fat hypertrophy and thicken)
Somogyi effect
Dawn phenomenon

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45
Q

What is the Somogyi effect?

A

Overnight hypoglycemia leads to rebound hyperglycemia in morning. (This is because hypoglycemia overnight, which is the biggest difference between that and dawn phenomenon)

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46
Q

How do you differentiate between Somogyi effect and dawn phenomenon?

A

CBG between 2–4 AM
If Low=Somogyi
If High/normal=Dawn phenomenon

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47
Q

What may be some clues that our patients blood glucose is dropping too low at night (and point to Somogyi)?

A

Night sweats
Night terrors
Headache on awakening

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48
Q

What can we do to prevent Somogyi effect?

A

Either reduce bedtime insulin or give
bedtime snack (or both)

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49
Q

What is the dawn phenomenon? How is it different than Somogyi effect?

A

Hyperglycemia in morning. This is natural rise in blood glucose.
Dawn phenomenon will NOT experience hypoglycemia through the night.

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50
Q

What is treatment for dawn phenomenon?

A

Increase insulin

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51
Q

What are some factors that falsely increase blood glucose labs?

A

Keto diets
Acute illness
Meds like contraceptives and corticosteroids
Bed rest

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52
Q

What is a funduscopic exam and why is it important for a diabetic?

A

Dilated eye exam
This is important because the number 1 cause of blindness in US is diabetes.

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53
Q

How soon should patient eat after taking Humalog (lispro) or Novalog (aspart) or Apidra (glulisine)?

A

15 min

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54
Q

How do you draw up insulins in same syringe when one is clear and one is cloudy?

A

Air in cloudy
Air in clear
Draw up clear
Draw up cloudy

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55
Q

What are the 4 different methods of testing for diabetes?

A
  1. A1C >6.5 OR
  2. Fasting plasma glucose (after 8 hours of fasting) of >126 OR
  3. 2 hour plasma glucose level of >200 in an OGGT OR
  4. Classic s/sx AND random glucose of >200
    —The first 3 will need repeat testing to confirm, the last will not–
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56
Q

What is goal value of A1C in diabetic patient?

A

<7.0

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57
Q

What is goal blood glucose levels in diabetic patients?

A

80—-130 before meals

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58
Q

What is a normal blood glucose level in a NON diabetic patient?

A

70—110

59
Q

Which type of insulins have most risk of hypoglycemia?

A

Short acting (Regular like Humulin R and Novolin R)

60
Q

Which types of insulins do NOT have a peak?

A

Long acting
Lantis
Levemir
degludec (Tresiba)

61
Q

What should you NEVER do with long acting insulins?

A

Mix with other insulins or dilute

62
Q

What is the disadvantage of intermediate acting insulin (NPH)?

A

It has a peak of 4—12 hours.
This means your patient could bottom out in that time.

63
Q

How long are prefilled insulin syringes stable when mixed with 2 insulins?

A

One week in fridge

64
Q

How long are prefilled insulin syringes stable when only one type of insulin?

A

1 month in fridge

65
Q

How should prefilled insulin syringes be stored?

A

Sitting vertically so particles don’t clog needle

66
Q

What should we teach patient about insulin sites and exercise?

A

Don’t use a site that is about to be exercised. This increased blood flow means increased insulin absorption and could lead to hypoglycemia.

67
Q

Who should be the only one to ever recap an insulin needle?

A

The patient when self admin. As the nurse we NEVER recap needles

68
Q

What is lipodystrophy and what do we do about it?

A

Overuse of injection site causes SQ tissue to hypertrophy and harden. Reduces absorption there. Must rest the site for 6 month. Rotation of sites prevents this.

69
Q

What type of medication is metformin?
How does it work?

A

Biguanide (Bye-Gwan-ide)
THE FIRST LINE DRUG FOR DM2
Reduces glucose production by liver
Enhances insulin sensitivity
Improves glucose transport into cell

70
Q

What is necessary when pt on Metformin needs contrast medium for procedure?

A

Stop metformin 24 hours prior to contrast and 48 hours after.
Prevents CIN (contrast induced nephropathy)

71
Q

What organs does Metformin stress out?

A

Liver (Metformin contraindicated in heavy drinkers or liver disease)
Kidneys (metformin contraindicated in kidney disease and when contrast media on board)
Heart (HF patients=contraindication)

72
Q

What is a rare side effect of Metformin?

A

Lactic acidosis

73
Q

What are some drugs classed as sulfonylureas?
Sul-Fun-i-ureas

A

glimiperide
glipizide
glyburide

74
Q

How do sulfonylureas work?
What is the major side effect?

A

Kick pancreas to make more insulin
Major side effect is hypoglycemia
These are never given to DM2 patients

75
Q

What are the meglitinides?
Muh-glit-inides

A

nateglinide
repaglinide

76
Q

How do meglitinides work?
What are the advantages over sulfonylureas?

A

They work by kicking the pancreas to produce more insulin.
They are less likely to cause hypoglycemia because short half life.

77
Q

How should meglitinides be taken?

A

Between 30 min before the meal up to beginning of meal
Don’t eat?=Don’t take!

78
Q

What are some GLP-1 Receptor agonists? (these are injectables)

A

dulaglutide (Trulicity)
exenatide (Byetta)
liraglutide (Victoza)

79
Q

How do GLP-1 Receptor agonists work?

A

Increase insulin release
Decrease glucagon secretion
Slow gastric emptying
Increase satiety

80
Q

What is the drug alert for Byetta (exenatide) GLP-1 receptor agonist?

A

Can cause pancreatitis
and kidney problems

81
Q

What is the drug alert for Victoza (liraglutide) and Trulicity (dulaglutide)?

A

Can cause pancreatitis
Contraindicated in family history of thyroid cancer

82
Q

What is recommended limit of daily cholesterol in diabetic patient?

A

<200 mg/daily

83
Q

What is recommended daily limit of alcohol in diabetic patient?

A

Men=2 drinks
Women=1 drink
And consume alcohol with food

84
Q

What should we teach diabetic patients about exercise while taking any meds that can cause hypoglycemia (meds like sulfonylureas or meglitinides) or insulin?
How should they combat this?

A

Be careful. Moderate exercise, NOT rigorous
Exercise + glucose lowering meds can =hypoglycemia
Don’t exercise at meds peak action time. Exercise 1 hour after eating. Have a 10–15 mg carb snack 30 min before exercising. Have emergency candy. Check CBGs before and after exercise.

85
Q

When should a diabetic NOT exercise?

A

When glucose levels are over 250 AND ketones are in urine.
If ketones are NOT present, exercise is ok.

86
Q

How often should diabetics check glucose levels during illness?

A

At least every 4 hours or if they suspect hypoglycemia

87
Q

Why is it especially important for a DM1 patient to carefully monitor blood glucose levels (especially when exercising, during illness or stress)?

A

Insulin demand wil be higher during these periods
Because their body has NO backup plan. They are dependent on insulin or they will go into DKA and die.
They need to be aware of any unusual circumstances that alter blood glucose levels and monitor changes that require extra insulin.

88
Q

What should we teach patients about how to do finger sticks?

A

Wash and dry hands. No alcohol prep necessary. Use side of finger, not the pad of finger. Record results.

89
Q

Why are diabetic patients prone to UTIs?

A

Increased glucose in urine + warm, dark environment is perfect for bacteria to grow.

90
Q

At what age should we begin routine screening for diabetes in pts with no other risk factors? If those results come back normal, how frequently should screening be repeated?

A

45 years old
Every 3 years

91
Q

The American Diabetes Association recommends screening for DM2 in who?

A

Anyone with BMI >25 and have one additional risk factor.
Risk factors are:
1. First degree relative with DM
2. Inactive
3. High risk ethnicity
4. Women who had gestational diabetes or delivered babies >9 lb
5. Hypertensive
6. HDL <35 or triglyceride >250
7. Polycystic ovarian syndrome
8. A1C >5.7
9. Signs of insulin resistance like acanthosis nigricans

92
Q

What is recommended amount of exercise weekly for preventing DM?

A

150 min/weekly of moderate activity

93
Q

What should we teach DM1 patients about times of illness?

A

If glucose is >240, check for ketones in urine every 3-4 hours.

94
Q

When should a diabetic patient contact their HCP in times of illness?

A

If they cannot keep down food/water.
If they have a glucose >300 twice in row.
If they have ketones in urine.

95
Q

What are some carb containing fluids we can recommend to diabetic patients in times of illness?

A

Low sodium soups
Juices
Regular sugar sweetened decaf soft drinks (Sprite)

96
Q

Should diabetic patients stop eating during times of illness?
Should they stop taking their medications when sick and they are not able to eat?

A

No!
They should try to continue in their regular diet and get lots of sugar free fluids.
They should NOT stop taking their medication, even if they aren’t able to eat. Instead get some carb containing liquids on board.

97
Q

If a sick non insulin dependent diabetic patient needs insulin during illness, what should we teach them?

A

This does NOT mean their diabetes has gotten worse or they will need to continue on insulin. A temporary measure while sick. Illness raises glucose.

98
Q

What should we do if a new insulin user does not have the cognitive ability to manage his diabetes?

A

Teach family or a responsible person what they need to know.

99
Q

What should we stress in our teaching about food choices and medication?

A

Stress the importance of following their meal and activity plans.
Teach them not to take “extra” pills if they have overeaten.
Stress that managing diabetes takes ALL of these efforts (diet, exercise, medication) to hold ground.

100
Q

What should we teach diabetic patients about personal hygiene?

A

Oral care is essential
Regular bathing with attention to feet
Inspect feet daily

101
Q

If a diabetic patient has a minor injury to foot, what should they do?

A

Wash it and apply an antiseptic. Cover with dry, sterile pad. Notify HCP if doesn’t begin to heal in 24 hours or see signs of infection.

102
Q

How should diabetics care for their feet?

A

Inspect daily
Protect by:
Don’t go barefoot
Don’t wear flip flops or sandals that slide between toes.
Wear comfortable supportive shoes that fit.
Keep skin on feet moisturized but NOT in between toes.
Keep between toes dry and clean.
Don’t apply cold/heat to feet.
Cut toenails straight across.
Wear clean cotton or wool socks
Avoid prolonged sitting, standing, or crossing of legs
Mild foot powder is appropriate for sweaty feet.
Use elbow to test water temp.

103
Q

What should we teach diabetic patients about diet and alcohol?

A

No fad diets. Just regular healthy diet.
Low fat. Limit fried foods. Limit soda and fruit juice.
Limit alcohol. Eat at regular times.

104
Q

What should be included in annual checkups for diabetics?

A

Routine eye examination by ophthalmologist
Annual urine test for protein (indicates kidney disease)
Yearly flu shots and appropriate vaccines
Routine blood pressure checks

105
Q

How often should diabetics do an A1C?

A

Every 3—6 months

106
Q

What is pathophysiology of DKA?

A

–PROFOUND insulin deficiency–
Process happens as follows:
1. Insulin insufficient
2. Body breaks down fat/muscle as food source to raise already high glucose levels
3. Acidic ketones are byproduct
4. Ketosis»Metabolic Acidosis
5. Urine output greatly increases to off load ketones
6. Offload of ketones takes electrolytes with it (this is called osmotic diuresis)
7. Hypovolemia»shock»renal failure»coma»death

107
Q

What are clinical manifestations of DKA?

A

Dehydration S/Sx: (early signs)
Dry mucous membranes and mouth
Poor skin turgor
Delayed cap refill
Tachycardia and weak pulse
Orthostatic hypotension
Lethargy/weakness
Restless/confusion
Fever
Urinary frequency

Progresses to: (Late signs)
Sunken eyes
Abdominal pain
Anorexia
N/V
Acetone breath (fruity, sweet)
Kussmauls respirations

108
Q

What is first goal of therapy in treating DKA? In HHS? How are these same/different?

A

Establish large bore IV access and begin fluid/electrolyte replacement
–This is done HARD and FAST in DKA-
–This is done SLOWLY and CAREFULLY in HHS–

109
Q

What is typical fluid used for fluid replacement in DKA? How do we know when aggressive fluid replacement therapy can be slowed?

A

0.45% NS
0.9% NS
When BP starts to rise and kidneys start producing 30-60 ml of urine an hour.

110
Q

What must we always obtain before starting insulin in a patient in DKA? (besides blood glucose level) Why?

A

Potassium
When you shift the glucose from blood into cell with insulin, it WILL take potassium with it. This will drop potassium serum levels significantly. Baseline potassium level is needed.

111
Q

Why is it essential to lower blood glucose levels SLOWLY in DKA and HHS?

A

To prevent an overwhelming shift in potassium, fluid, glucose that could all lead to CEREBRAL EDEMA.

112
Q

When reducing glucose levels in DKA and HHS approaching the 250 mark frequently requires what?

A

Addition of D5 or D10 to fluid replacement to prevent too rapid of fluid shift»CEREBRAL EDEMA

113
Q

What is the biggest difference between DKA and HHS (hyperosmolar hyperglycemia syndrome)?

A

DKA has ketonuria
HHS does not have ketonuria

114
Q

What is pathophysiology in HHS?
(Hyperosmolar Hyperglycemia syndrome)

A

Usually happens in DM2 over 60 yo
Patient makes some insulin
Doesn’t make enough to prevent hyperglycemia. But doesn’t go into ketosis.
Leads to osmotic diuresis and fluid depletion.
Usually happens around stressful event that makes glucose climb or impaired cognition that impairs thirst.

115
Q

What are clinical manifestations of HHS?

A

Usually more neuro than DKA:
Somnolence
Coma
Seizures
Hemiparesis
Aphasia
–CAN LOOK LIKE A CVA–

116
Q

What is treatment for HHS?

A

Large volume fluid replacement (0.9 or 0.45% NS) Done SLOWLY AND CAREFULLY
Add dextrose to fluids when approach 250 blood glucose
Immediate IV admin of insulin
Watch for fluid overload and EKG changes
(these will usually be older patients who may have CHF, ESRD, must balance fluid replacement carefully)

117
Q

What is normal rate of insulin replacement in DKA?

A

Regular insulin infused at 0.1 U/kg/hour

118
Q

What are first 5 steps in DKA treatment?

A
  1. Establish IV with large bore
  2. Fluids at 1L/hour until BP rises and urine output starts
  3. Continuous IV drip of regular insulin at 0.1 U/kg/hour
  4. O2 therapy
  5. Potassium drip
119
Q

What are s/sx of hyperglycemia?
BAM HF

A

Hot and dry=glucose too high
Polyuria
Polydipsia=hungry
Polyphagia=thirsty
Fatigue/weakness
Blurred vision
N/V
Abdominal cramps
Mood swings
Headache

120
Q

What are s/sx of hypoglycemia?
Early: TNN
Late:

A

Early: (this is from epi dump)
Cold and clammy=need some candy
Sweating/pallor
Numbness of fingers, mouth, toes
Tachycardia/Palpitations
Nervousness/Tremors

Late: (brain isn’t getting fuel)
Faintness, dizziness
Slurred speech/stupor/confusion
Changes in vision
–Can look like drunk-called neuroglycopenia

121
Q

What number is considered HYPOglycemia?

A

<70

122
Q

When does hypoglycemia most frequently occur in diabetic patients?

A

When insulin or med is at its peak of action.

123
Q

What is the “Rule of 15” in hypoglycemia?

A

Glucose <70?
1. Give pt 15 g simple carb
2. Wait 15 min
–Glucose still <70?
3. Give pt another 15 g simple carb
4. Wait 15 min
–Glucose still <70?
Can try one more time or call HCP

124
Q

After treating patient for hypoglycemia and have stabilized CBG >70, what should we do?

A

Give them a complex carb snack to maintain glucose level.
This can be PB crackers, cheese and crackers, etc.

125
Q

What would be an example of a simple carb of 15 grams we give in hypoglycemia?

A

4 oz of sprite or juice
5-8 Lifesavers
1 Tablespoon honey
4 tsp jelly

126
Q

Why do we NOT give a carb that is high in fat to a pt in hypoglycemia?

A

Fat slows absorption

127
Q

What is treatment for an unconscious patient with no IV access in hypoglycemia? What is precaution?
What about it have IV access but can’t swallow?

A

Glucagon injection
IM or SQ in deltoid
1 mg
Precaution is it will make them nauseated and vomit. If unconscious, turn them to left side so don’t aspirate.
If have IV, can give 20-50 ml of 50% glucose.

128
Q

What are the two types of angiopathy? What’s difference?

A

Macrovascular-occurs in larger vessels in brain, heart, peripheral vessels.
Microvascular-occurs in smaller vessels in eyes, kidneys, nerves.

129
Q

What are long term complications of DM?

A
  1. CVA
  2. HTN
  3. Dermopathy
  4. Atherosclerosis
  5. Nephropathy
  6. Peripheral neuropathy
  7. Neurogenic bladder
  8. CAD
  9. Gastroparesis
  10. Erectile dysfunction
  11. Retinopathy
  12. Glaucoma
  13. Cataracts
  14. Peripheral vascular atherosclerosis>infections>gangrene
130
Q

What are modifiable risk factors for angiopathy in DM?

A

Obesity
Smoking
HTN
High fat diet
Sedentary lifestyle

131
Q

What is the number one way to prevent complications with DM? Number 2 and 3?

A

Tight control of blood glucose
Control BP
Control cholesterol

132
Q

What is a target BP for patient with DM?

A

< 140/90

133
Q

What is number one cause of ESRD? Blindness?

A

DM

134
Q

What meds will most patients with DM need? (in addition to OA’s or insulin)

A

Blood pressure (usually an ACE inhibitor, lisinopril) These help slow nephropathy.
Statin meds

135
Q

What is diabetes related retinopathy? What two classes are there? Which one is worse?

A

Microvascular damage to retina because of hyperglycemia, hypertension, nephropathy. Two classes are proliferative and non proliferative. Proliferative is worse and can lead to blindness.

136
Q

How often should pts with DM have eye exam?

A

Annually

137
Q

How often should pts with DM be screened for nephropathy?

A

Annually

138
Q

What is the only treatment for DM related neuropathy?

A

Glucose management

139
Q

What is autonomic neuropathy? What organs does it involve?

A

Neuropathy that affects all body systems. Usually seen in gastroparesis, orthostatic hypotension, resting tachycardia, bowel incontinence, urinary retention, neurogenic bladder, ED.

140
Q

What is neurogenic bladder?

A

Neuropathy of bladder. Don’t realize full. Urinary retention and stasis. Leads to UTIs

141
Q

What are signs of PAD? What does PAD do in DM patients?

A

Intermittent claudication (pain, weakness when walking)
Pain at rest
Cold feet
Hair loss on lower legs
Delayed cap refill
Dependent discoloration of limbs

Decreased blood flow to feet plus decreased sensation from peripheral neuropathy leads to damage, slow healing, increases risk for infection.

142
Q

What is DM related dermopathy?

A

Round, reddish brown skin lesions
Usually on shins but can be anywhere

143
Q

What is acanthosis nigracans a sign of?

A

Insulin resistance

144
Q

Should DM patients receive flu and other vaccines?

A

YES!!

Semester 3 Unit 3-Endocrine (3 decks)

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