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Med Surg > Exam 3: Diabetes > Flashcards

Exam 3: Diabetes Flashcards

1
Q

Percentage of the US population affected by diabetes

A

8.3% (25.8 million people

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2
Q

Risk factors for getting DM (8)

A
  • Parent, brother, sister with diabetes
  • Race
  • Gestational diabetes / gave birth to baby with high birth weight
  • Pre-diabetes (FBC of 100-126)
  • Overweight
  • Inactivity
  • High BP
  • Abnormal Cholesterol levels
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3
Q

Abnormal cholesterol levels that put a person at risk for DM (3)

  • LDL
  • HDL
  • Triglyceride
A

LDL > 100

HDL 250

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4
Q

Function of the pancreas as an exocrine gland

A

Releases digestive enzymes

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5
Q

Function of the pancreas as an endocrine gland

A

Beta cells secrete insulin

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6
Q

How does glucose enter the bloodstream? (3 ways)

A
  • Intestinal absorption
  • Glycogenolysis in the liver
  • Gluconeogenesis (Protein catabolism)
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7
Q

What is glucose used for… in tissues?

A

Oxidation

• CO2 + H20 + E

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8
Q

What is glucose used for… in the liver?

A

Glycogenesis (glycogen formed)

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9
Q

What is glucose used for… in energy storage? (2)

A
  • Converted to fat

- Stored as glycogen in muscles

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10
Q

When is glucose excreted in urine?

A

BS level exceeds 200

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11
Q

Roles of insulin (5)

A

o Transports and metabolizes glucose for energy
o Stimulates the storage of glucose in the liver (Glycogenesis)
o Enhances the storage of fat in adipose tissue
o Transports amino acids and glucose into the cells
o Inhibits the breakdown of stored glucose, protein and fat

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12
Q

Constant level of blood sugars occurs in fasting state due to what two factors?

A
  • Pancreas releases insulin

* Pancreas releases small amounts of glucagon (Glycogenolysis)

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13
Q

When does glyconeogenesis occur?

A

After 8-12 hours without food

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14
Q

Pathophysiology of DM Type 1

  • MAIN THING
  • Three physiological results
  • MAIN RESULT
A
  • MAIN THING: Destruction of Beta cells

1) Means that glucose is not stored as glycogen
2) Glycogenolysis and gluconeogenesis occur unrestrained
3) Fat breakdown occurs

  • MAIN RESULT: Hyperglycemia
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15
Q

Pathophysiology of DM Type 2

  • Main thing (2)
  • Main result
A
  • MAIN THING: Insulin resistance and / or decreased production of insulin
  • MAIN RESULT: Hyperglycemia
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16
Q

Usually a DM2 patient would be started on lifestyle changes before any medication is introduced.

What patient would have lifestyle changes AND medication started right away?

A

A patient who also has cardiac problems

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17
Q

Length of onset: DM1 vs DM2

A

DM1: Rapid onset
DM2: Slow onset

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18
Q

What does “insulin resistance” mean?

A
  • Insulin resistance: Cells are not responsive to stimulating glucose uptake
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19
Q

What is the body’s initial response to insulin resistance?

What eventually occurs?

A

Insulin levels will rise to compensate

Eventually, body can’t produce enough insulin: Glucose rises.

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20
Q

DM Diagnosis: Fasting Blood Glucose #

A

126mg/dL or higher

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21
Q

DM Diagnosis: Random glucose level #

A

200 mg/dL or higher on more than one occasion

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22
Q

DM Diagnosis: Hemoglobin A1C #

A

> 6.5 or 7

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23
Q

Cause of hyperglycemia (4)

A
  • Too much food
  • Too little insulin or DM med
  • Illness
  • Stress
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24
Q

Onset of hyperglycemia

A
  • Gradual

- May progress to diabetic coma

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25
Q

Sxs of hyperglycemia

A
  • Extreme thirst
  • Frequent urination
  • Hunger
  • Dry skin
  • Frequent urination
  • Blurred vision
  • Drowsiness
  • Decreased healing
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26
Q

Why does a hyperglycemic patient experience hunger?

A

Becasue not enough glucose actually gets into cells - extreme hunger

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27
Q

How often should you check blood sugar for Type 1 DM?

A

2-4x per day

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28
Q

How often should you check blood sugar for Type 2 DM?

A

2-3x per week, with one two hours post prandial

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29
Q

What type of insulin is used for fractionals

A

Regular insulin always

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30
Q

What type of fluids should you use with hyperglycemic patients?

A

Hypotonic or Isotonic

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31
Q

CHO - PROTEIN - FAT

percentages for diabetic patients

A

CHO 50%
FAT 25%
Protein 25%

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32
Q

Why would you advise a DM patient to increase fibers?

A

Soluble fibers help control glucose because they slow absorption between the intestines

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33
Q

Oral meds for type 2 DM: For insulin resistance (general category)

A

ANTIHYPERGLYCEMIC AGENTS

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34
Q

Oral meds for type 2 DM: For decreased insulin production

general category

A

HYPOGLYCEMIC AGENTS

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35
Q

Examples of antihyperglycemic agents (5)

A 
Glucophage
Precose
Glycet
Actos
Ayandia
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36
Q

Examples of hypoglycemic agents (4)

A

Diabinase
Glucotrol
Micronase
Prandin

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37
Q

Goals of DM drug therapy - insulins

A
  • Blood sugar at 70-110
  • Px complications
  • Px hypoglycemia
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38
Q

Contraindication of Insulin

A

Hypoglycemia

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39
Q

Humalog

  • TIME
  • ONSET
  • PEAK
  • DURATION
A
  • TIME: Rapid acting (clear)
  • ONSET: 10-15 minutes
  • PEAK: 1 hour
  • DURATION: 3 hours
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40
Q

Regular (R) Insulin

  • TIME
  • ONSET
  • PEAK
  • DURATION
A
  • TIME: Immediate acting (cloudy)
  • ONSET: half hour to hour
  • PEAK: 2-3 hours
  • DURATION: 4-6 hours
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41
Q

NPH

(Humulin “N” or “L” (Lente))

  • TIME
  • ONSET
  • PEAK
  • DURATION
A
  • TIME: Intermediate acting
  • ONSET: 3-4 hours
  • PEAK: 4-12 hours
  • DURATION: 16-20 hours
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42
Q

Glargine (Lantus)

  • TIME
  • ONSET
  • PEAK
  • DURATION
A
  • TIME: Long-acting (clear)
  • ONSET: 1 hour
  • PEAK No peak
  • DURATION: 24 hours
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43
Q

Humalog: Indication

A

Rapid reduction of blood sugar

44
Q

R Insulin indication

A

Works on the immediate meal: Administer 20-30 minutes before a meal

45
Q

NPH Indication

A

Give after meals helps replace basal insulin

46
Q

Ultralente Indication

A

Controls FPG (Fasting Plasma Glucose)

47
Q

Ultralente (UL)

  • TIME:
  • ONSET
  • PEAK
  • DURATION
A
  • TIME: Long acting (cloudy)
  • ONSET 6-8 hours
  • PEAK: 12-16 hours
  • DURATION: 20-30 hours
48
Q

Glargine indication

A

Enables LT baseline insulin levels; still need to add insulin at mealtimes with separate needle.

49
Q

Which insulin should you NOT mix with other insulins?

A

GLARGINE (Lantus)

50
Q

Insulin percentage breakdown

A

70/30 insuiln: 70% NPH and 30% regular

51
Q

What type of insulin can be given IV?

A

ONLY regular insulin

52
Q

How is most of the insulin administered?

A

SUB Q

53
Q

Why should you rotate sites with subQ insulin injections

A

Lipo-atrophy can develop (gets hard, doesn’t absorb well)

54
Q

Mixing types of insulin:

A

Clear to cloudy

Regular first, then NPH in syringe

55
Q

Cause of hypoglycemia (3)

A
  • Too little food
  • Too much insulin or DM meds
  • Extra activity
56
Q

Onset of hypoglycemia

A
  • Sudden; may progress to insulin shock
57
Q

Sxs of hypoglycemia (10)

A

**MOSTLY NERVOUS SYSTEM

  • Shaking
  • Fast heartbeat
  • Sweating
  • Dizziness
  • Anxiety
  • Hunger
  • Imapired vision
  • Weakness / fatigue
  • Headache
  • Irritability
58
Q

Old saying for DM - hyper vs hypoglycemia

A

Cold and clammy, you need candy

Hot and dry, blood sugar is high

59
Q

If your DM pt is comatose, what is your priority?

A

To maintain an airway

60
Q

If you can’t tell if a pt is hypo- or hyperglycemic…

A

ERR ON THE SIDE OF HYPOGLYCEMIC

61
Q

Clinical picture of a patient with mild hypoglycemia (6)

A 
Conscious
Hungry
Sweaty
Tremors
Anxiety or drowsiness
Weakness
62
Q

Clinical picture of a patient with moderate hypoglycemia (6)

A 
Conscious
Headache
Behavioral change
Blurred, impaired or double vision
Irritation / confusion
Difficulty talking
63
Q

Clinical picture of a patient with severe hypoglycemia (4)

A

Unconscious
Unresponsive
Unable to take oral feeding
Seizure activity

64
Q

What do you give a hypoglycemic patient

A

15 grams of CHO

65
Q

DIabetic ketoacidosis is secondary to…

A

Inadequate insulin

66
Q

Clinical picture of diabetic ketoacidosis

A
  • Hyperglycemia
  • FVD
  • Acidosis
  • Hypokalemia
67
Q

Why is a ketoacidosis patient at risk for hypokalemia

A
  • K+ can move from intracellular to extracellular to compensate for acidity
  • Can get worse as treatment progresses
68
Q

Blood sugar of a ketoacidotic patient

A

300-800

69
Q

Respirations of a ketoacidotic patient

A

Rapid, deep

70
Q

Fluid and electrolytes in a ketoacidotic patient

A

Loss of both

71
Q

Medical management of DKA

A
  • Insulin IV

- NS or 0.45 NS for dehydration (as much as 500-1000mL over an hour)

72
Q

Mortality rate from ketoacidosis

A

5-30%

73
Q

Clinical picture of HHNS (4)

A
  • Hyperglycemia
  • FVD
  • Tachycardia
  • Altered senses, decreasd LOC
74
Q

What does HHNS stand for?

A

Hyperglycemic Hyperosmolar Nonketotic Syndrome

75
Q

Cause of HHNS

A

Usually non-compliance with treatment

76
Q

Nursing assessment of HHNS: Blood sugar

A

> 1000

77
Q

Nursing assessment of HHNS: RR, pH, ketones

A

All WNL

78
Q

How do you prevent HHNS?

A

Sick Day Rules

79
Q

Six Sick Day Rules

A
  1. Take insulin / oral medications as usual
  2. Test your blood sugar q 3-4 hours (if more than 200, test for ketones)
  3. Report a blood sugar reading greater than 300
  4. Eat small, frequent meals
  5. If you are vomiting or have diarrhea, have a half of a can of cola, juice or broth every half hour
  6. Report nausea, vomiting or diarrhea to your health care provider.
80
Q

DM Complications (7)

A

1) Complications with insulin therapy
2) DKA
3) HHNS
4) Macrovascular issues
5) Microvascular issues
6) Neuropathies

81
Q

Macrovascular issues with DM (3)

A
  • CAD
  • CVD
  • PVD
82
Q

What is unique with CAD in DM patients?

A

Typical ischemic symptoms (early warning sxs) might be absent, because these patients develop an autonomic neuropathy

83
Q

MIs and DM patients

A

Higher incidence / more complications / higher mortality with diabetic patients

84
Q

Correlation of HTN and DM

A

60% od DM patients have high BP

85
Q

DM patients and CVD

A

Higher incidence of strokes, CVAs

3x more likely to have a stroke than a non-DM patient

86
Q

PVD and DM: Amputations

A

600,000 amputations with DM patients

87
Q

Prophylactic meds for Macrovascular issues in DM patients (5)

A

o An aspirin a day
o beta blocker
o ACE inhibitor or Ca channel blocker
o and a statin

88
Q

Microvascular issues with DM (2)

A

o Retinopathy

o Nephropathy

89
Q

What can retinopathy lead to?

A

Blindness

90
Q

Who is at risk for neuropathies?

A

Patients with longstanding DM (25+ years)

91
Q

What is a big risk with neuropathies?

A

Peripheral sensorimotor nephropathy – affects distal portions of the nerves in the lower extremities

92
Q

Autonomic neuropathy: Systems affected (4)

A

o CV
o GI
o Urinary
o Adrenal

93
Q

DKA versus HHNK: Caused by which type of diabetes?

A

DKA: Type 1
HHNK: Type 2

94
Q

DKA versus HHNK: Serum glucose

A

DKA: 300-800
HHNK: Often >1,000

95
Q

DKA versus HHNK: Arterial pH

A

DKA: Acidic
HHNK: Normal

96
Q

DKA versus HHNK: Serum and urine ketones

A

DKA: Positive for both
HHNK: Negative for both

97
Q

DKA versus HHNK: Onset

A

DKA: Quick
HHNK: Slow

98
Q

DKA versus HHNK: Cause

A

DKA: Lack of insulin –> Breakdown of fats
HHNK: Inadequate insulin, but enough to prevent the breakdown of fats

99
Q

DKA AND HHNK: Clinical assessment

A
  • Dry skin and mucous membranes
  • Decreased skin turgor
  • Tachycardia
  • Hypotension
  • Altered LOC
100
Q

DKA versus HHNK: Breathing

A

DKA: Kussmaul’s respirations
HHNK: Regular and shallow

101
Q

DKA versus HHNK: Mortality

A

DKA: 5-30%
HHNK: Near 50%

102
Q

Diabetes insipidis is caused by a disorder of the ______

A

Pituitary gland

103
Q

What causes diabetes insipidus?

A

Head trauma or neurosurgery – damage to insipidus

104
Q

Sxs of Diabetes insipidus

A

Polyuria, Polydipsia

Can urinate 4-16 L per day

105
Q

Treatment for Diabetes Insipidus (3)

A

o Replace fluids
o Is & Os
o Diet: High sodium, high potassium

106
Q

Cluster of risk factors involved with syndrome X

A
  • High triglycerides (>150)
  • Low HDLs (130/85)
  • Insulin-resistance Blood sugar 110-125
  • Waist >35” (females) or 40” (males)

Med Surg (13 decks)

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