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NURS 1064 - Pharm > Chapter 49 (Learning Outcomes) > Flashcards

Chapter 49 (Learning Outcomes) Flashcards

1
Q

What are some chronic complications of unmanaged diabetes (7)?

A
  • cardiovascular disease (HTN, heart disease, stroke)
  • kidney failure
  • blindness
  • nervous system disease
  • extremity amputations
  • dental diseases
  • pregnancy complication
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2
Q

What is the prototype of Sulfonylurea?

A

Glyburide

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3
Q

What is the prototype of Non-sulfonylurea?

A

Metformin

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4
Q

What are the three body systems that are involved in the regulation and use of glucose in the body?

A
  1. Liver
  2. Pancreas
  3. Skeletal muscle
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5
Q

What tissue is unable to store glucose for future use?

A

Brain!

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6
Q

What is the exocrine function of the pancreas?

A

Produce digestive enzymes

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7
Q

What is the endocrine function of the pancreas?

A

Synthesize and secrete peptide hormones

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8
Q

What 3 peptide hormones does the pancreas secrete?

A
  1. Insulin
  2. Glucagon
  3. Somatostatin
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9
Q

What do Beta cells do (in the pancreas)?

A

Secrete the HYPOglycemic hormone insulin

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10
Q

What do Alpha cells do (in the pancreas)?

A

Secrete the HYPERglycemic hormone glucagon

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11
Q

What do Delta cells do (in the pancreas)?

A

Release somatostatin

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12
Q

What is the role of somatostatin?

A

A hormone that inhibits both glucagon and insulin secretions

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13
Q

What is insulin secretion most commonly triggered by?

A

High blood glucose levels

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14
Q

What is the main function of insulin?

A

Regulates carbohydrate metabolism

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15
Q

How does insulin regulate carbohydrate metabolism?

A

Lowers blood glucose levels by stimulating peripheral glucose uptake (especially by skeletal muscles and fat)

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16
Q

What effect does insulin have on the liver (4)?

A
  • Promotes the uptake and storage of glucose in the form of glucagon
  • Promotes the conversion of excess glucose into fat
  • Suppresses heptaic gluconeogenesis (production of glucose)
  • Suppresses hepatic glycogenolysis (breakdown of glycogen to glucose)
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17
Q

Which tissues do NOT require insulin in order for glucose to enter their cells (7) ?

A
  • Brain
  • Nerves
  • Intestine
  • Liver
  • Retina
  • Erythrocytes
  • Renal tubules
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18
Q

Other than insulin, what other factors can affect blood glucose levels (6) ?

A
  • Stress
  • Illness
  • Secretion of insulin-antagonistic hormones (cortisol, E, growth hormone, glucagon, and somatostatin)
  • number of cellular insulin receptors
  • Use of glucose by cells
  • Rates of hepatic synthesis of glucose
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19
Q

What happens when blood glucose get too low?

A

Alpha cells (in the pancreas) release glucagon

  • stimulates release of glycogen from hepatic storage sites
  • prevents blood glucose from getting too low
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20
Q

How quickly after a meal are hepatic glycogen stores depleted?

A

Within 6 hours after a meal

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21
Q

If blood glucose levels are low, and the hepatic reserves are empty - where else can the body pull glucose from?

A
  • Muscles release amino acids (converted into glucose)

- Lipolysis occurs in adipose tissue

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22
Q

How are free fatty acids used as energy?

A

Used for energy by muscle and liver cells

- conserving glucose for use by the brain

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23
Q

What triggers the release of glucagon (5)?

A
  • low blood glucose levels
  • sympathetic nerve impulses
  • exercise
  • infection
  • trauma
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24
Q

What are the three types of diabetes?

A
  1. Type 1
  2. Type 2
  3. Gestational
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25
Q

What is the defining characteristic of Type 1 diabetes?

A

Destruction of insulin-secreting beta cells

  • absolute insulin deficiency
  • auto-immune disease
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26
Q

What is hyperglycemia?

A

Abnormally high blood glucose

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27
Q

What happens if the body’s reserve of insulin is depleted?

A

Hyperglycemia

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28
Q

Explain how ketoacidosis occurs.

A
  • Type 1 diabetes
  • Hyperglycemic state (cells cannot access available glucose)
  • Body starts to break down proteins and lipids for energy
  • Increase in lipid metabolism leads to an increase in ketoacids - causing ketoacidosis
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29
Q

True or False:

Insulin therapy isn’t always indicated for Type 1 diabetes

A

False!

  • Type 1 diabetes always requires insulin
  • Beta cells have been destroyed
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30
Q

What does Type 2 diabetes result from?

A

Insulin resistance by the tissues

- also usually a decrease in insulin production

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31
Q

Why are plasma levels of insulin in Type 2 diabetes essentially normal (or increased)?

A

Pancreas tried to overcome the resistance by producing more insulin
- problem is that the insulin does not ENTER the cells but stays in the bloodstream

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32
Q

What is the age of onset of Type 1 diabetes? Type 2?

A

Type 1 = Usually before 20

Type 2 = Usually after 40

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33
Q

What is the incidence of Type 1 diabetes? Type 2?

A

Type 1 = 5 - 10%

Type 2 = 90 - 95%

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34
Q

What is the typical body weight of a person with Type 1 diabetes? Type 2?

A

Type 1 = Thin, underweight

Type 2 = Overweight, obese

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35
Q

What are the clinical S/S of Type 1 diabetes?

A
  • Hyperglycemia
  • Polyphagia
  • Polydipsia
  • Polyuria
  • Weight loss
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36
Q

What are the clinical S/S of Type 2 diabetes?

A
  • Hyperglycemia
  • Fatigue
  • Mild Polyphagia/Polydipsia/Polyuria
  • Fungal infections
  • Blurred vision
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37
Q

What is the clinical management of Type 1 diabetes?

A
  • Insulin injections
  • Dietary controls
  • Exercise regimen
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38
Q

What is the clinical management of Type 2 diabetes?

A
  • Weight reduction
  • Dietary controls
  • Exercise regimen
  • Oral drug therapy
  • Insulin
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39
Q

What are the classic signs of hyperglycemia (6)?

A
  • Excessive urination (polyuria)
  • Excessive thirst (polydipsia)
  • Fatigue
  • Dry or itchy skin
  • Poor wound healing
  • Vision changes
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40
Q

What happens during the dawn phenomenon?

A

Blood glucose levels are at their highest between 5am and 6am

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41
Q

What is the believed to be the cause behind dawn phenomenon?

A

The release of growth hormone overnight

- increases blood glucose levels

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42
Q

How is dawn phenomenon treated?

A

By providing larger doses of intermediate-acting insulin at bedtime
- to prevent early morning elevations of glucose

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43
Q

What is the Somogyi effect?

A

Produces early morning hyperglycemia

  • but precipitating factor is actually a HYPOglycemic event after midnight
  • body compensates
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44
Q

What are the two main classifications of chronic complications of diabetes?

A
  1. Microvascular

2. Macrovascular

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45
Q

What are some examples of macrovascular complications (3)?

A
  • Atherosclerotic vascular disease
  • Myocardial infarction
  • Cerebrovascular accident
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46
Q

What are some example of microvascular complications (6)?

A
  • Cataracts
  • Glaucoma
  • Blindness from retinopathy
  • Lower extremity infections and gangrene
  • Foot ulcers
  • Renal failure
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47
Q

What is the lab value that measures chronic glucose levels?

A

Hemoglobin A1C

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48
Q

What happens if you lower Hemoglobin A1C levels?

A

Reduction of microvascular and neuropathic complications of diabetes
- may also lower macrovascular complications

49
Q

What is the danger of keeping a tight control of blood glucose levels?

A

Hypoglycemia

50
Q

What can severe hypoglycemia result in?

A

Altered consciousness or coma

51
Q

What are the two regimens that are used for the treatment of Type 1 diabetes?

A
  1. Non-physiologic regimen

2. Physiologic regimen

52
Q

Describe the non-physiologic regimen. When is it useful?

A

1-2 daily injections of long-acting insulin
- Ideal for those newly diagnosed (those who can still produce SOME endogenous insulin and have not progressed to complete beta cell failure)

53
Q

Describe the physiologic regimen. When is it useful?

A

Consists of BASAL and PRANDIAL insulin

- for patients in complete beta cell failure

54
Q

Define Basal Insulin

A

The continuous secretion that maintains glucose homeostasis

- the body’s baseline of insulin

55
Q

Define Prandial Insulin

A

Insulin secretion stimulated in response to meals

56
Q

What is the main goal of Type 1 insulin therapy?

A

Avoid hypoglycemic episodes

- improve hemoglobin A1C levels yet maintain a simple regimen to which the patient can adhere

57
Q

How can a hospitalized Type 1 diabetic patient, that is not eating regularly receive nutrition?

A
  • IV fluids with dextrose
  • Total parenteral nutrition
  • Partial parenteral nutrition
  • Tube feedings
58
Q

Define Correctional (or supplemental) insulin dose.

A

Dose to correct any elevations in blood glucose

- goal is to keep blood glucose as close to normal as possible

59
Q

What kind of insulin are given with correctional (or supplemental) insulin doses?

A

Short-acting or long-acting in addition to their prandial dose

60
Q

What is the first line of treatment for patients diagnosed with Type 2 diabetes?

A

Oral antidiabetic agents

61
Q

What kind of insulin is typically used for Type 2 diabetes (if it is used)?

A

Bedtime long-acting basal insulin

- while continuing with 1 or 2 daytime oral antidiabetic medications

62
Q

What are the names of the rapid acting insulin?

A
  1. Aspart
  2. Lispro
  3. Glulisine
63
Q

What speeds are insulin available at?

A
  • Rapid
  • Short
  • Intermediate
  • Long
64
Q

What is the prototype for short-acting regular insulin?

A

Insulin

65
Q

When is regular insulin used?

A

Used only to correct a current glucose elevation or an expected rise after eating
- not used to correct all day levels

66
Q

Why is regular insulin indicated for patients with hyperkalemia?

A

An infusion of glucose and insulin produces a shift of potassium into cells and lowers serum potassium levels

67
Q

What is the onset and duration of Regular insulin (Humulin R, Novolin R)?

A

Onset: 30 min - 1 hour
Dur: 8 - 12 hours

68
Q

What is the onset and duration of Lispro (Humalog)?

A

Onset = 15 mins

Dur: 6 - 8 hours

69
Q

What is the onset and duration of Aspart (Novolog)?

A

Onset = 5 - 10 mins

Dur: 3 - 5 hours

70
Q

What is the onset and duration of Isophane insulin suspension (Humulin N, NPH)

A 
Onset = 1 - 1.5 hours
Dur = 18 - 24 hours
71
Q

What is the onset and duration of Glargine (Lantus)?

A 
Onset = 1 hour
Dur = 24 hours
72
Q

What is the onset and duration of Glyburide?

A

Onset = 1 - 2 hours

Dur: 16 - 24 hours

73
Q

What is the onset and duration of Metformin?

A

Onset = 2 - 2.5 hours

Dur: 10 - 16 hours

74
Q

What is the fastest site of absorption of insulin subcutaneously?

A

Abdominal SC layer

  • then back of arm
  • then thigh
  • lastly, buttocks
75
Q

What happens when insulin is delivered by IV infusion?

A

Between 20 - 30% is absorbed by the plastic tubing

76
Q

How long is insulin stable for at room temperature?

A 
1 month
(for longer storage, place in the fridge)
77
Q

Where in the body is insulin filtered and reabsorbed?

A
  • Filtered in glomerulus

- Reabsorbed in proximal renal tubule

78
Q

What is the most common adverse effect of insulin therapy?

A

Hypoglycemia

79
Q

What are the signs of hypoglycemia?

A
  • Fatigue and malaise
  • Trembling
  • Irritability
  • Headache
  • Nausea
  • Numbness
  • Paresthesias
  • Muscle weakness
80
Q

How can hypoglycemia manifest?

A

Hunger, tachycardia, sweating, and nervousness

81
Q

What is lipodystrophy?

A

An adverse effect from repetitive SC injections into the same INJECTION site
- cause disturbances in fat metabolism

82
Q

How can lipodystrophy present?

A
  1. Lipoatrophy - SC fat breaks down

2. Lipohypertrophy - additional lipid deposits at a particular site

83
Q

How does alcohol affect the impact of insulin?

A

Alcohol potentiates the hypoglycemic effect of insulin

84
Q

Why is INTRA-SITE rotation used with insulin therapy?

A

Promotes regular absorption

- different sites have different absorption speeds

85
Q

What can result in a falsely higher glucose reading than it should be (4)?

A
  1. Low hematocrit
  2. Hypoxia
  3. Hyperbilirubinemia
  4. Tylenol overdose
86
Q

What can result in a falsely lower glucose reading than it should be (5)?

A
  1. High hematocrit
  2. Shock and dehydration
  3. Hypoxia
  4. Sodium fluriode
  5. Tylenol overdose
87
Q

How can we (as nurses) minimize adverse effects when administering insulin?

A
  • avoid administering cold insulin (lipodystrophy)

- assess blood glucose levels

88
Q

What are 4 ways we can treat hypoglycemic episodes?

A
  1. 4 oz of juice (or soda)
  2. 4 oz of water with 4 sugar packets
  3. 8 oz low fat milk
  4. 50% IV dextrose or glucagon if patient is not able to swallow
89
Q

When drawing up insulin, what do you always have to do?

A

Have another nurse check the dose - to prevent accidental overdose

90
Q

When referring to insulins, do we use generic names or trade names?

A

GENERIC!

91
Q

What 4 things do people with diabetes need to understand?

A
  1. What diabetes is and what treatment is necessary
  2. How to administer and store insulin
  3. How and when to test their blood glucose
  4. How and when to take oral medications if they have type 2 diabetes
92
Q

What are the two types of insulin that cannot be mixed with any other types of insulin?

A
  1. Glargine

2. Detemir

93
Q

What are the three rapid-acting drug related to Regular Insulin?

A
  1. Aspart (Novolog)
  2. Lispro (Humalog)
  3. Glulisine (Apidra)
94
Q

When can rapid-acting insulin be used?

A

Type 1 or Type 2 diabetes

95
Q

What happens when Protamine is added to Aspart or Lispro?

A

Provides some rapid action as well as prolonged action

  • longer component is always listed FIRST
  • Ex: NovoLog Mix 70/30
96
Q

Is NPH cloudy or clear?

A

Cloudy!

- only insulin that is NOT clear

97
Q

What is the most widely used intermediate acting insulin?

A

NPH

98
Q

What is the name of a long-acting insulin?

When is it used?

A

Detemir

- used in Type 1 and Type 2

99
Q

What are the two groups of oral antidiabetic medications used?

A
  1. Sulfonylureas

2. Non-sulfonylureas

100
Q

What is the prototype of sulfonylurea drugs?

A

Glyburide

101
Q

When is Glyburide used?

A

Type 2 patients that cannot control hyperglycemia with diet and exercise alone

102
Q

What is the BIDS system?

A 
Bedtime Insulin = NPH
Daytime Sulfonylurea (morning)
... BIDS
103
Q

How is Glyburide administered?

A

Orally

104
Q

Describe the hypoglycemic action of Glycuride.

A

Results from the stimulation of pancreatic beta cells, leading to increased insulin secretion
- reduces the glucose output from the liver (decreasing liver glycogenolysis and gluconeogenesis)

105
Q

Why is Glycuride ineffective on Type 1 diabetes?

A

B/c endogenous release of insulin is not possible from beta cells (they are destroyed)

106
Q

When is Glycuride contraindicated?

A

Sulfa allergy

- or hepatic or renal failure

107
Q

What are the most common adverse effects of Glyburide?

A
  • Nausea
  • Epigastric fullness
  • Heartburn
108
Q

What are the three different classes of non-sulfonylurea antidiabetics?

A
  1. Biguanides
  2. Thiazolidinediones
  3. Alpha-glucosidase inhibitors
109
Q

What class does Metformin fit into?

A

Biguanide (Non-sulfonylureas)

110
Q

When is Metformin used?

A

Type 2 diabetes

  • does not stimulate insulin secretion
  • rather it is an antihyperglycemic or “insulin sensitizer” agent
111
Q

What is the main action of Metformin?

A

Reduced insulin resistance

- suppresses hepatic glucose production and enhances insulin sensitivity

112
Q

Why does Metformin rarely cause hypoglycemia (by itself)?

A

Because it does not stimulate the release of insulin

113
Q

What are some adverse effects of Metformin?

A
  • Gi disturbances (anorexia, N/V, weight loss, abdominal discomfort, dyspepsia, flatulence, diarrhea)
114
Q

What are the two major contraindications for Metformin?

A

Serious renal or hepatic function impairment

115
Q

What are the drugs closely related to Metformin?

A

Thiazolidinediones (Rosiglitazone and Pioglitazone)

116
Q

What does glucagon do?

A

Opposite effect of insulin

- body’s mechanism to protect against hypoglycemia

117
Q

When is glucagon typically used?

A

On unconscious patients with diabetes ti reverse severe hypoglycemia
- RESULTING FROM INSULIN OVERDOSAGE

118
Q

When is glucagon ONLY effective?

A

Only when liver glycogen is available

119
Q

How do you minimize adverse effects when using Glucagon?

A

Administer supplemental carbohydrates as soon as possible (pt is awake) to restore liver glycogen

NURS 1064 - Pharm (9 decks)

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