Exam 2 Flashcards

1
Q

Role of hypothalamus

A

Release and stimulate hormones
No direct effect on the body

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2
Q

Releasing hormones

A

Adrenocortiocotropic hormone
Thyroid stimulating hormone

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3
Q

What releases parathormone (parathyroid hormone)

A

Parathyroid gland

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4
Q

What does parathormone do

A

Pulls calcium out of bones to increase serum calcium
Decreases phosphorus levels

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5
Q

What is the effect of hyperfunction of parathyroid

A

Hypercalcemia

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6
Q

What is the effect of hypofunction of the parathyroid

A

Hypocalcemia

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7
Q

Hyperparathyroidism

A

Increase in serum calcium
Bones turn to swiss cheese

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8
Q

Hyperparathyroidism risk factors

A

2-4x more in women, 60-70 yrs old

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9
Q

Hyperparathyroidism s/sx

A

Apathy, fatigue, muscle weakness
Loss of appetite
Constipation
Hypertension, cardiac dysrhythmias

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10
Q

Hyperparathyroidism complications

A

Osteoporosis
Skeletal pain and pathologic fractures
Kidney stones

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11
Q

How to dx hyperparathyroidism

A

Elevated calcium and increase parathormone levels
Pathologic bone changes on x-ray

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12
Q

Treatment for hyperparathyroidism

A

Laparoscopic removal of parathyroid gland
- For asymptomatic pts under 50, unlikely to follow up, calcium over 11, high urine calcium, or low bone density

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13
Q

Medications for hyperparathyroid

A

Calcitonin and corticosteroids
- Reduces serum calcium and increases calcium deposit in bones

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14
Q

Education/management of hyperparathyroidism

A

Hydration - 2+L/day
Encourage mobility (bone density)
Maintain dietary intake of calcium
Stool softeners

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15
Q

What to monitor post-op parathyroidectomy

A

Monitor Chvostek and Trousseau’s sign
- Looking for rebound hypocalcemia

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16
Q

Serious complication of hyperparathyroid

A

Hypercalcemic crisis

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17
Q

Hypercalcemic crisis s/sx

A

Neurologic, cardiovascular, and kidney symptoms
- Can be life threatening

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18
Q

Hypercalcemia crisis or hyperparathyroid tx

A

Rapid rehydration with large volumes of IV isotonic saline fluids
Calcitonin + corticosteroids to reduce serum calcium by increasing calcium deposition in bone

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19
Q

Causes for hypoparathyroid

A

Abnormal parathyroid development
Destruction of parathyroid gland (surgical or autoimmune)
Vit D deficiency

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20
Q

Hypoparathyroid s/sx

A

Tetany, numbness, tingling in extremities, stiffness of hands and feet
Bronchospasm, laryngeal spasm, carpopedal spasm
Anxiety, irritability, depression, delirium
ECG changes

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21
Q

Tx goal for hypoparathyroid

A

Increase serum calcium to 9-10 mg/dL

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22
Q

Tx for hypoparathyroid

A

Calcium gluconate IV - acute episodes
Pentobarbital - decreases neuromuscular irritability and tetany
Vitamin D

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23
Q

Hypoparathyroidism nursing education/considerations

A

Maintain cardiac monitoring
Monitor respiratory status
Quiet environment, soft lights
High calcium, low phosphorus diet

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24
Q

What hormones do the thyroid gland secrete

A

T3 and T4

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25
Q

What does T3 and T4 do

A

Regulates metabolism
Controls cell growth
Regulates basal metabolic rate, oxygen consumption, and glucose consumption

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26
Q

What stimulates hormones release from the thyroid

A

Pituitary gland releases thyroid stimulating hormone

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27
Q

What does TSH (thyroid stimulating hormone) do

A

Releases T3
Synthesis of T4 in liver

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28
Q

What do thyroid hormones require to be made

A

Iodine is needed for synthesis

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29
Q

Purpose of T3

A

Regulates metabolism

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30
Q

Purpose of T4

A

Steady state metabolism
Organ function, BMR, cholesterol, thermoregulation

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31
Q

Goiter

A

Enlarged thyroid
Caused by low iodine

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32
Q

What can a goiter lead to

A

Hypo or hyperthyroidism

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33
Q

Dx tests for thyroid

A

Primary screening of TSH
Serum T3/T4
Thyroid antibodies
Iodine uptake test
Thyroid biopsy
Thyroid scan

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34
Q

What leads to thyroid hyposecretion

A

Elevated TSH + decreased T3/T4

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35
Q

What leads to thyroid hypersecretion

A

Decreased TSH + increased T3/T4

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36
Q

Thyroiditis

A

Inflammation of thyroid gland

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37
Q

What is the effect of thyroiditis on thyroid hormones

A

Increased TSH and decreased T3/T4
Decreased function of thyroid gland

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38
Q

Is hypo or hyperthyroidism more common

A

95% of cases are d/t primary thyroid dysfunction

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39
Q

Cretinism

A

Congenital hypothyroid

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40
Q

Hasimotos Thyroiditis

A

Immune system (autoimmune) attacks thyroid
Leads to hypothyroidism

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41
Q

Most common population for Hashimotos Thyroiditis

A

Women 40-70

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42
Q

Hypothyroid s/sx

A

Extreme fatigue
Hair loss, brittle nails, dry skin
Numbness of fingers
Weight gain
Personality changes

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43
Q

What V/S changes can happen with severe hypothyroidism

A

Decreased pulse
Temperature changes

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44
Q

Myxedema coma s/sx

A

Depression, lethargy, somnolence, coma, hypoventilation, CO2 retention, hypoglycemia, bradycardia, hypothermia

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45
Q

Hypothyroidism tx

A

Synthroid - replaces thyroid hormones (long term)

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46
Q

Synthroid AE

A

Cardiac side effects

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47
Q

What medication is used for hypothyroidism crisis

A

IV T3/T4

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48
Q

What to monitor after synthroid administration (nursing consideration)

A

Monitor for angina and dysrhythmias

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49
Q

Common nursing dx for hypothyroidism

A

Activity intolerance - decreased metabolic activity
Impaired memory - reorient
Constipation - mobility, fluids, stool softeners

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50
Q

How long do patients have to take hypothyroidism medications

A

Lifelong (education)

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51
Q

Nursing considerations for myxedema coma

A

Maintain stable body temperature
Monitor gastric motility
Skin integrity
Reduced metabolism = hypoventilation
- Pulmonary toilet

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52
Q

Causes of hyperthyroidism

A

Graves disease (75% of cases)
Pituitary tumor - increases TSH
Too much thyroid hormone replacement
Hashimoto’s Thyroiditis

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53
Q

Thyrotoxicosis

A

Hypermetabolism d/t thyroid stimulation

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54
Q

S/sx of hyperthyroidism

A

Increase metabolic activity
- Tachycardia, HTN, tachypnea, hyperthermia, palpitations, bounding pulses
- Diarrhea, weight loss with increased appetite
- Irritability and mood swings, nervousness, twitching, insomnia
- Amenorrhea
- Thinned hair and skin with flushed appearance

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55
Q

Exopthalmos

A

Protruding eyes
Common in Grave’s disease or hyperthyroidism

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56
Q

Hyperthyroidism manifestations

A

Goiter - do not palpate
Pulse/thrill over thyroid
Decreased TSH, increased T4
Elevated iodine

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57
Q

Hyperthyroidism tx

A

Antithyroids - block hormone synthesis (Propylthiouracil [PTU] and methemazole)
Radioactive iodine - through straw
Beta blockers for tachycardia
Bedrest for acute hyperthyroid episodes

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58
Q

Radioactive iodine therapy

A

Tx of choice for nonpregnant pts
Removes sections of thyroid to decrease function
Takes up to 3 months for full effect

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59
Q

Hyperthyroidism surgical tx

A

Throidectomy
Requires long term thyroid hormone replacement

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60
Q

Hyperthyroidism nursing management

A

Increase calories
Extra fluids
Daily weight and calorie count
Ineffective coping - hypermetabolism puts pts on edge
- Low stress environment, dim lights, soft noises
Ice packs, cool room (hyperthermia r/t hypermetabolism)
Monitor for dysrhythmias d/t hypermetabolism - beta blockers, stress free environment, avoid stimulants/caffeine

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61
Q

Hyperthyroidism patient education

A

Avoid stimulants
High carb, high calorie, high protein diet
Cool room and loose clothes
Eye care - drops, lubricants, steroid drops
Long term hormone replacement after thyroidectomy

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62
Q

Thyroid storm

A

Acute episode of excessive thyroid production
Increase metabolism leads to diarrhea, weight loss, altered mental status

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63
Q

Thyroid storm dx

A

Fever >38.5
Tachy >130

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64
Q

Thyroid storm tx

A

IV glucose
Humidified O2
Iodine infusion
Beta blockers - for tachycardia and hypertension

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65
Q

What is the main concern for thyroid storm

A

Increased BP and tachycardia can lead to heart damage

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66
Q

Thyroid cancer

A

Malignancies on thyroid lead to increased secretion of thyroid hormones

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67
Q

Thyroid cancer common population

A

75% of cases are women, ⅔ are under age of 55

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68
Q

Thyroid cancer dx

A

Signs of hyperthyroidism
Hard, fixed, palpable lesions on thyroid
Biopsy confirms diagnosis

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69
Q

Thyroid cancer tx

A

Thyroidectomy and neck dissection
Radiation if possible

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70
Q

Thyroidectomy indications

A

Pregnancy
Pts with goiter
Thyroid med allergy

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71
Q

What procedure is done alongside thyroidectomy

A

Neck dissection - removal of lymph nodes from neck

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72
Q

Pre-op thyroidectomy nursing considerations

A

Reduce stress/anxiety to avoid thyroid storm
Decrease caffeine, stimulants
High carb, high protein diet
Vitamin supplements

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73
Q

Post op thyroidectomy nursing considerations

A

Monitor airway
Monitor for hemorrhage
Monitor voice changes
Supplement thyroid hormone
Monitor for hypocalcemia

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74
Q

What is normal for thyroid hormone levels post thryoidectomy

A

A surge of thyroid hormone can temporarily occur

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75
Q

Complications of thyroidectomy

A

Hemorrhage and hematoma
Edema in airway
Changes in calcium metabolism d/t manipulation of parathyroid

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76
Q

DM is the leading cause of

A

Adult blindness
End-stage renal disease
Lower limb amputations (nontraumatic)

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77
Q

DM is a major contributing factor of

A

Heart disease
Stroke
HTN
High cholesterol

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78
Q

What factors may cause DM

A

Genetic
Autoimmune
Environmental
Virus

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79
Q

Where is insulin produced

A

Beta cells in islet of Langerhans

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80
Q

Daily amount of insulin secreted by adult

A

40-50 U

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81
Q

Insulin function

A

Promote glucose transport from bloodstream across cell membrane to the cytoplasm of the cell

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82
Q

Where is excess glucose stored

A

Liver and muscle cells store glucose as glycogen

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83
Q

What does increased insulin do

A

Inhibits gluconeogenesis
Enhances fat deposition
Increases protein synthesis

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84
Q

What does decreased insulin do

A

Release glucose from liver
Release protein from muscle
Release fat from adipose tissue

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85
Q

What hormones are couterregulatory (opposite effect) to insulin

A

Glucagon
Epinephrine
Growth hormone
Cortisol

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86
Q

T2DM risk factors

A

Overweight/obese
Advanced age
Family hx

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87
Q

T2DM pathophysiology

A

Pancreas produces some endogenous insulin, but not enough produced
Body does not use insulin efficiently

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88
Q

T1DM pathophysiology

A

Absence of endogenous insulin d/t body developing antibodies against insulin and/or pancreatic beta cells

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89
Q

Metabolic syndrome

A

Increases the risk for T2DM
- Increased glucose levels
- Abdominal obesity
- High BP
- High level of triglycerides
- Decreased levels of HDLs
3 of 5 components = metabolic syndrome

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90
Q

Normal impaired glucose tolerance range for prediabetes

A

140-199 mg/dL

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91
Q

Normal fasting glucose for prediabetes

A

100-125 mg/dL

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92
Q

When does gestational diabetes resolve

A

6 wks postpartum

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93
Q

Gestational diabetes risks

A

Increased risk for C section and perinatal/neonatal complications

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94
Q

When is gestational diabetes dx during pregnancy

A

24-28 wks

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95
Q

What does gestational diabetes put you at risk for later in life

A

63% change of getting T2DM within 16 years

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96
Q

Other types of DM

A

Injury/destructino of beta cell function in pancreas
Medical conditions/drugs
- Resolves when underlying condition is treated

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97
Q

Symptoms of T1DM

A

Polyuria
Polydipsia
Polyphagia
Weight loss
Weakness
Fatigue
Ketoacidosis

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98
Q

Symptoms of T2DM

A

Nonspecific symptoms:
Fatigue
Recurrent infection
Recurrent vaginal yeast or candida infection
Prolonged wound healing
Visual problems

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99
Q

Rapid acting insulin

A

lispro (Humalog)
aspart (Novolog)
glulisine (Apidra)

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100
Q

Short acting insulins

A

Regular (Humulin R, Novolin R)

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101
Q

Intermediate acting

A

NPH (Humulin N, Novolin N)

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102
Q

Long acting

A

glargine (Lantus)
detemir (Levemir)
1-2x/day
Do not mix with other insulin

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103
Q

Inhaled insulin

A

Afrezza

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104
Q

When to use bolus of insulin

A

Rapid acting or short acting before meals

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105
Q

When to give basal dose of insulin

A

Intermediate or long-acting insulin 1-2x/day

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106
Q

Insulin storage

A

Extreme temps make insulin less effective
Can be left at room temp for 4 wks
Refrigerate extra unopened insulin
Avoid direct sunlight

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107
Q

Why is insulin given SQ

A

IM injection can cause hypoglycemia

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108
Q

Why can insulin not be given PO

A

Inactivated by gastric fluid

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109
Q

Regular insulin route

A

Can be given IV

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110
Q

How often to change insulin pump

A

Every 2-3 days

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111
Q

How often to check BG throughout day with insulin pump

A

4-8x/day

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112
Q

Nursing considerations for insulin pumps

A

Infection risk at insertion site
Risk for DKA
Costs
Being attached to a device

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113
Q

AE of insulin

A

Hypoglycemia
Allergic reactions
Lipodystrophy - loss of fatty tissue, atrophy
Hypertropy of SQ tissue - overuse of site

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114
Q

Somogyi effect

A

High dose of insulin causes glucose to drop at night
Counterregulatory hormones cause rebound hyperglycemia

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115
Q

Dawn phenomenon

A

Morning hyperglycemia
May be due to release of counterregulatory hormones in predawn hours (growth hormone and cortisol)

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116
Q

Afrezza

A

Rapid acting inhaled insulin
Used in combo with long-acting insulin

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117
Q

AE of Afrezza

A

Hypoglycemia
Cough
Throat pain
Irritation

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118
Q

Contraindications for Afrezza

A

Tx of DKA
Smokers
Asthma/COPD - risk of bronchospasm

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119
Q

Metformin uses

A

Most effective 1st line tx for T2DM
Used for prevention of T2DM

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120
Q

Metformin (glucophage) routes

A

Immediate release
Extended release
Liquid

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121
Q

Metformin (glucophage) MOA

A

Reduces glucose production by liver
- Enhances insulin sensitivity
- Improves glucose transport
- May cause weight loss

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122
Q

Metformin (glucophage) alerts

A

Withhold for surgery/radiologic procedure

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123
Q

Metformin (glucophage) contraindications

A

Renal, liver, cardiac disease; lactic acidosis
Iodine based contrast medium can cause AKI
Excessive alcohol intake

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124
Q

Metformin (glucophage) nursing considerations/education

A

Take with good to minimize GI side effects

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125
Q

Sulfonylureas MOA

A

Increases insulin production from pancreas

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126
Q

Sulfonylureas SE

A

Hypoglycemia

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127
Q

Sulfonylureas examples

A

Glipizide (Glucotrol)
Glyburide (Glynase)
Glimepiride (Amaryl)

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128
Q

Meglitinides MOA

A

Increases insulin production from pancreas

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129
Q

What is the benefit of Meglitinides having a rapid onset

A

Decreases risk of hypoglycemia

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130
Q

Meglitinide pt education

A

Take 30 minutes to just before each meal to mimic normal response to eating
Do not take if skip a meal

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131
Q

Meglitinide examples

A

Repaglinide (Prandin)
Nateglinide (Starlix)

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132
Q

α-Glucosidase Inhibitors MOA

A

“Starch blockers”
Slow down absorption of carbohydrate in small intestine

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133
Q

α-Glucosidase Inhibitors patient education

A

Take with first bite of each meal

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134
Q

α-Glucosidase Inhibitors nursing consideration/education

A

Check 2 hour postprandial glucose to determine effectiveness

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135
Q

α-Glucosidase Inhibitors examples

A

Acarbose (Precose)
Miglitol (Glyset)

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136
Q

Thiazolidinediones MOA

A

Improve insulin sensitivity, transport, and utilization at target tissues

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137
Q

Thiazolidinediones examples

A

Pioglitazone (Actos)
Rosiglitazone (Avandia)

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138
Q

Thiazolidinediones uses

A

Most effective in those with insulin resistance
Rarely used because of adverse effects

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139
Q

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors MOA

A

Block reabsorption of glucose by kidney
Increase urinary glucose excretion

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140
Q

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors examples

A

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)

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141
Q

What lifestyle modification can improve insulin sensitivity in T2DM

A

Wt loss of 5-7%

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142
Q

How to monitor effectiveness of therapy for T2DM

A

Blood glucose levels
A1C
Lipids
BP

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143
Q

Effect of alcohol on insulin/DM

A

Inhibits gluconeogenesis by liver
- Severe hypoglycemia
- Eat carbs when drinking

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144
Q

Recommended alcohol intake for DM

A

1 drink/day for women
2 drink/day for men

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145
Q

Risk during exercise (DM)

A

Hypoglycemia

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146
Q

When to delay activity for T1DM

A

If glucose is below 250 and ketones present in urine

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147
Q

When to self-test blood glucose

A

Before meals
Two hours after first bite
When hypoglycemia is suspected
Every 4 hours during illness
Before and after exercise

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148
Q

How often should diabetics check BG during illness

A

Every 4 hours

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149
Q

When and how often should diabetics check for ketones during illness

A

If glucose is over 240 check ketones every 3-4 hours

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150
Q

When should diabetic call HCP

A

If two consecutive BG are over 400 or if they have mod-high urine ketone levels

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151
Q

What is the risk for T1DM during illness

A

DKA d/t increased BG levels

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152
Q

What is the risk for all diabetic pts during illness

A

Risk of infection
Reduced healing

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153
Q

Nursing consideration for unconscious diabetic pt

A

Frequently monitor BG
Monitor for hypoglycemia: sweating, tachycardia, tremors

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154
Q

What condition may require pancreatic transplant

A

T1DM with ESRD and kidney transplant

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155
Q

Criteria for pancreas transplant

A

If no renal failure:
- Hx of acute/severe metabolic complications
- Incapacitating clinical/emotional problems with exogenous insulin
- Failure of insulin management

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156
Q

Islet cell transplantation

A

Donor islet cells infused into portal vein to liver

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157
Q

Effect of stress on glucose

A

Increases glucose secondary to counterregulatory hormones

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158
Q

Hypoglycemia Manifestations

A

Blood glucose < 70 mg/dL
Cold, clammy skin
Numbness fingers, toes, mouth
Tachycardia
Emotional changes
Headache
Nervousness, tremors
Faintness, dizziness
Unsteady gait, slurred speech
Hunger
Vision changes
Seizures, coma

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159
Q

Hypoglycemia causes

A

Alcohol intake without food
Too little food
Too much diabetes meds
Too much exercise without food
Diabetes med or food at wrong time
Loss of weight without med adjustment
Use of -adrenergic blockers interfering with symptoms

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160
Q

Hypoglycemia at home tx

A

Eat or drink 15 g of rapid-acting carbohydrates
Wait 15 minutes, check glucose
If less than 70 mg/dL, eat or drink another 15 grams of carbohydrates
If stable and meal more than 1 hour away or involved inn activity; give carbohydrate and protein

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161
Q

When hypoglycemic pt should call HCP/EMS

A

If glucose remains low after 2-3 times

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162
Q

Tx for acute care or unresponsive hypoglycemic pt

A

IV D50
IM glucagon

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163
Q

Hyperglycemia Manifestations

A

Elevated blood glucose
Increased urination
Increased appetite followed by lack of appetite
Weakness, fatigue
Blurred vision
Headache
Glycosuria
Nausea and vomiting
Abdominal cramps
Progression to DKA or HHS
Mood swings

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164
Q

Hyperglycemia causes

A

Illness, infection
Corticosteroids
Too much food
Too little or no diabetes meds
Inactivity
Emotional or physical stress
Poor absorption of insulin

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165
Q

Diabetic Ketoacidosis (DKA) cause

A

Profound deficiency of insulin

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166
Q

Most likely population for DKA

A

T1DM

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167
Q

DKA Precipitating factors

A

Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1 diabetes
Lack of education, understanding, or resources
Neglect

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168
Q

DKA pathophysiology

A

Body burns fat as fuel
By-product of fat metabolism—acidic ketones alter pH (metabolic acidosis)
Ketones excreted in urine along with electrolytes
Impairs protein synthesis, causes protein degradation resulting in nitrogen loss from tissues

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169
Q

DKA complications

A

Hypovolemia followed by shock may cause renal failure, causing retention of ketones and glucose and further acidosis
Dehydration, electrolyte imbalance, and acidosis causes coma and if not treated, death

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170
Q

DKA manifestations

A

Dehydration
- Poor skin turgor
- Dry mucous membranes
- Tachycardia
- Orthostatic hypotension

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171
Q

DKA early signs

A

Lethargy and weakness

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172
Q

DKA manifestations as it progresses

A

Skin dry and loose; eyes soft and sunken
Abdominal pain, anorexia, nausea/vomiting
Kussmaul respirations
Sweet, fruity breath odor (acetone)
Blood glucose level of greater than or equal to 250 mg/dL
Blood pH lower than 7.30
Serum bicarbonate level less than 16 mEq/L
Moderate to high ketone levels in urine or serum

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173
Q

DKA tx

A

Replace potassium before starting insulin (insulin drives K into cells = hypokalemia)
IV regular insulin to correct hyperglycemia and ketosis

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174
Q

Long term complications of diabetes

A

Stroke
Retinopathy, cataracts, glaucoma, blindness
HTN
Dermopathy
CAD
Gastroparesis
Atherosclerosis
Islet cell loss
Nephropathy
Erectile dysfunction
Neurogenic bladder
Peripheral neuropathy
Peripheral vascular atherosclerosis
Gangrene
Infections

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175
Q

Angiopathy

A

Chronic complication of DM
Damage to blood vessels secondary to chronic hyperglycemia
Leading cause of diabetes-related death

176
Q

Two categories of angiopathy

A

Macrovascular
Microvascular

177
Q

Annual exams for diabetics

A

Retinopathy
Nephropathy
Neuropathy (comprehensive foot exam)
Cardiovascular risk factor assessment

178
Q

As needed or every visit to HCP exams for diabetics

A

Foot and lower extremity exam
Exercise stress testing

179
Q

Daily exam for diabetic pts

A

Self foot exam

180
Q

Leading cause of end-stage renal disease in U.S.

A

Nephropathy d/t diabetes
- 20% to 40% of people with diabetes have it

181
Q

Nephropathy risk factors

A

Hypertension
Genetics
Smoking
Chronic hyperglycemia

182
Q

Monitoring for nephropathy

A

Annual screening for albuminuria and albumin-to-creatinine ratio

183
Q

Drugs for albuminuria from nephropathy

A

ACE inhibitors
or
Angiotensin II receptor antagonists

184
Q

When to screen T2 diabetic for neuropathy

A

At time of diagnosis

185
Q

When to screen T1 diabetic for neuropathy

A

5 years after diagnosis

186
Q

Distal symmetric polyneuropathy

A

Most common form
Both hands or feet are affected

187
Q

Paresthesias

A

tingling, burning, itching
“walking on pillows” or numb feet

188
Q

Sensory Neuropathy

A

Manage BG
Drugs:
Topical creams
TCA’s
SSRI’s and NRI’s
Antiseizure meds
pregabalin (Lyrica)

189
Q

Autonomic neuropathy complications

A

Bowel incontinence
Urinary retention - neurogenic bladder
Gastroparesis - N/V, anorexia, GERD
CV - postural hypotension, resting tachycardia, painless MI
ED, decreased libido, vaginal infections

190
Q

Urinary retention/neurogenic bladder d/t diabetes tx

A

Credé’s maneuver - manual pressure to abd
Cholinergic agonists
Self-catheterization

191
Q

Thrombocytopenia common nursing dx

A

Risk for bleeding

192
Q

Causes of thrombocytopenia

A

Blood disorders - dyscrasias
Chemotherapy

193
Q

Manifestations at different platelet levels

A

Symptoms present when under 50,000
Under 20,000 = spontaneous bleed
Under 5,000 = CNS/GI bleed

194
Q

Thrombocytopenia nursing interventions

A

Platelet transfusion
Reduce blood loss - needles, gums, invasive procedures
Fall precautions

195
Q

Thrombocytopenia complications

A

Hemorrhagic stroke
Shock
GI Bleed
Joint bleeds

196
Q

Hemophila patho

A

Deficiency in a coagulation factor

197
Q

Von Willebrand patho

A

Disorder of coagulation proteins

198
Q

Hemophila & Von Willebrand assessment findings

A

Prolonged bleeds after:
Dental procedures
Minor trauma
Nosebleed
GI ulcers
SubQ hematomas

199
Q

How to dx Hemophila & Von Willebrand

A

Deficient clotting factors on coagulation studies

200
Q

Causes of Hemophila & Von Willebrand

A

Genetic link

201
Q

Hemophila & Von Willebrand tx

A

Prevent bleeding
Genetic counseling
DDAVP - Desmopressin
Antifibrolynics

202
Q

Hemophila & Von Willebrand pt education

A

Bleeds monitored for 72 hours
Notify surgeon before procedures
Prophylactic coagulation factor replacement
Immobilize bleeding joints

203
Q

Disseminated Intravascular Coagulation patho

A

Not a disease but a sign of an underlying disorder
Increase in clotting combined with an increase in bleeding

204
Q

Disseminated Intravascular Coagulation causes

A

Sepsis
Trauma
Shock
Cancer
Abruptio placentae
Toxins
Allergic reactions

205
Q

Disseminated Intravascular Coagulation assessment findings

A

Bruising, hemoptysis, tachycardia & hypotension, bloody stools, hematuria

206
Q

Manifestations of clotting - DIC

A

Tissue necrosis
Diminished pulses
Pulmonary embolism
Abdominal pain, diminished bowel sounds

207
Q

DIC nursing interventions

A

Continuous cardiac monitor
Two large bore IV
Continuous O2 and BP monitoring
Platelet transfusion - for severe blleds
Cryoprecipitate or FFP
Heparin

208
Q

Myeloid cells become

A

Granulocytes: Neutrophils, Eosinophils, Basophils
RBC
Platelets

209
Q

Lymphoid cells become

A

Agranulocytes:
Lymphocytes - T cells, B cells, and Monocytes
Natural killer cell

210
Q

Leukemia patho

A

Abnormal growth of WBC’s
Normal during infections, abnormal if no infection is present

211
Q

What does leukemia cause

A

Leukocytosis

212
Q

Lymphoma

A

Neoplasms of lymphoid tissue, usually derived from B lymphocyte

213
Q

Multiple myeloma

A

Malignancy of plasma cell

214
Q

Leukemia cause

A

Many causes
Disease traced back to one type of stem cell

215
Q

Types of leukemias

A

Acute myeloid leukemia
Chronic myeloid leukemia
Acute lymphocytic leukemia
Chronic lymphocytic leukemia

216
Q

Acute leukemia is more common for

A

Children and young adults
- More fatal

217
Q

Chronic leukemia is more common for

A

25-60

218
Q

Dx for leukemia

A

CT scan - shows enlarged lymph nodes
PET scan - metabolic activity

219
Q

Abnormal WBC symptoms

A

Frequent, severe infections
Leukocytes under 15,000
Enlarged liver and spleen

220
Q

Symptoms of reduced RBC and/or platelets

A

Weakness, pallor, weight loss
Fatigue, lethargy, hypoxia
Bruising and hemorrhage

221
Q

General s/sx of WBC imbalance in later stages

A

CNS changes
Renal failure

222
Q

Leukemia dx

A

Bone marrow biopsy
Blood smears
CBC diff showing leukocytosis

223
Q

Acute Lymphocytic Leukemia complication

A

Severe neurological symptoms

224
Q

Chronic Myelogeous Leukemia

A

Occurs in stages:
Chronic stage can be controlled with meds
Blastic phase - acute drop in all cell counts

225
Q

Cause of Chronic Myelogeous Leukemia

A

Philadelphia chromosome

226
Q

Chronic Lymphocytic Leukemia s/sx

A

Can be asymptomatic
Lymph nodes enlarged
Chronic fatigue
Liver/spleen enlargement
B symptoms: fevers, drenching sweats (especially at night), and unintentional weight loss

227
Q

Leukocyte tx options

A

Chemotherapy
Total body radiation
Stem cell transplant
Palliative

228
Q

Induction therapy

A

Hard core chemo that destroys all abnormal leukemia cells
Similar to stem cell transplant
- Focus on neutropenia, thrombocytopenia and anemia

229
Q

What to expect after induction chemotherapy

A

Intensification
Consolidation
Maintenance low doses to maintain leukemia-free cells

230
Q

Cause of stomatitis and oral irritation

A

Gingival hyperplasia and chemo
- Frequent oral care
- Monitor for bleeding

231
Q

When to implement neutropenic precautions

A

ANC (absolute neutrophil count) under 1,000

232
Q

Neutropenic precautions

A

“Reverse isolation” keep pt from outside
No raw meats, fresh fruit, plants, vegetables
Avoid crowds
Handwashing
Minimize invasive devices - foleys
Avoid vaccinations and recently vaccinated people
Oral hygiene, avoid dental procedures

233
Q

Cause of fatigue and activity intolerance in neutropenic precaution

A

Anemia, chronic infections, and chemotherapy
- Iron supplements

234
Q

Pharmacological tx for chemotherapy/neutropenia

A

Filgrastim - for decreased ANC
Erythropoietin - for decreased RBC
Prophylactic antibiotics and antifungal

235
Q

Most common type of lymphoma

A

Non-Hodgkin’s

236
Q

Hodgkin’s lymphoma

A

Rare malignancy, high cure rate
Reed-Sternberg cells: abnormal cells found in lymph nodes (B-cell origin)

237
Q

Cause of Hodgkin’s lymphoma

A

Virus

238
Q

Hodgkin’s lymphoma manifestations

A

Painless lymph node enlargement
Pruritus
B symptoms: fever, night sweats, weight loss
Pain on ETOH ingestion

239
Q

Nursing management and tx of Hodgkin’s lymphoma

A

ABVD regimen of chemo
Radiation therapy for localized lymph node disease
Secondary malignancies common
Address fertility issues

240
Q

Non-Hodgkin’s lymphoma patho

A

Lymphoid tissues become infiltrated with malignant cells
Spread is unpredictable and localized disease is rare
Can originate outside of lymph nodes

241
Q

Non-Hodgkin’s common population

A

Increases with age
Average age is 66 years old

242
Q

Non-Hodgkin’s s/sx

A

Symptoms may depend on where lymph node masses spread
- Hepatomegaly
- Splenomegaly
- Renal failure

243
Q

Non-Hodgkin’s dx

A

Bone marrow biopsy
Lumbar puncture
Organ biopsy

244
Q

Non-Hodgkin tumor responses to tx

A

More aggressive tumors are more likely to respond to tx
T cells lymphomas are more difficult to tx

245
Q

Non-Hodgkin’s tx

A

Manage symptoms
- Pain, bleeding, infection
- Monitor for bowel perforations
- Care for radiation sites

246
Q

Multiple Myeloma patho

A

Plasma cells destroy the bone marrow
These create monoclonal B-cells that cannot fight infection
Cytokines engage in abnormal bone destruction

247
Q

Multiple Myeloma s/sx

A

Bone pain in pelvis, spine and ribs
Osteoporosis and fractures related to bone destruction
- Hypercalcemia
Hyperviscosity syndrome

248
Q

Multiple Myeloma dx

A

M proteins in blood
Bence-Jones proteins in urine
Decreased bone density on imaging

249
Q

Multiple Myeloma tx

A

Corticosteroids, chemo, immune therapy and targeted therapy

250
Q

Multiple Myeloma nursing interventions

A

Treatment for bone density:
- Ambulation and weight bearing exercise
- Monitoring for complications of hypercalcemia
- Hydration to improve renal function
Target UOP
Pain management: Peripheral neuropathy
High dose chemotherapy followed by HSCT

251
Q

Essential thrombocytopenia patho

A

AKA primary thrombocythermia
Stem cell disorder within the bone marrow

252
Q

Essential thrombocytopenia cause

A

Unknown

253
Q

Essential thrombocytopenia population

A

Affects women more than men
Median age 65 to 70 years old

254
Q

Essential thrombocytopenia symptoms

A

Vascular occlusion
Headaches
Enlarged spleen
Hemorrhage

255
Q

Essential thrombocytopenia nursing consideration

A

Risk for developing thrombosis or hemorrhage

256
Q

Primary Myelofibrosis patho

A

Chronic myeloproliferative disorder within the stem cell

257
Q

Primary Myelofibrosis population

A

Disease of older adults 65 to 70 years; survival rate 2 to 10 years

258
Q

Primary Myelofibrosis symptoms

A

Enlarged spleen
Fatigue
Pruritus
Bone pain
Weight loss
Infection
Bleeding
Cachexia
Pancytopenia common

259
Q

Primary Myelofibrosis tx

A

Decrease symptoms and splenomegaly
Improve blood count
Splenectomy for significant problems

260
Q

Types of genes (r/t cancer)

A

Protooncognes: Normal cell genes, important regulators in cell process, promotes growth
Tumor suppressor genes: Prevent tumor formation

261
Q

Onco-genes

A

Mutants of protoncognes that create malignant cells

262
Q

How are these genes changed during cancer

A

Onco-genes are turned ON
Tumor suppressor genes are turned OFF

263
Q

CAUTION warning signs of cancer

A

Change in bowel and bladder habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in tissue
Indigestion or difficulty swallowing
Obvious change in wart or mole
Nagging cough or hoarseness

264
Q

Breast cancer screening guidelines

A

Begin screening when you choose
Yearly mammograms by age 45
Every other year mammograms at 55

265
Q

Colon cancer screening guidelines

A

Over 50
African American - greater risk
Family hx

266
Q

Prostate cancer dx

A

PSA - Prostate specific antigen
Protein produced by the prostate gland
Increased = prostate cancer/condition
Prostate biopsy

267
Q

Types of biopsy

A

Fine needle
Surgical
Endoscopic

268
Q

TNM classification

A

Tumor size
Lymph node status
Metastasis

269
Q

Radiation uses

A

Isolated tumors
Reduction in tumor size
Instill radiation in body cavities

270
Q

Types of radiation

A

Electromagnetic
Particulate
High energy x-ray

271
Q

Different uses for low and high energy beams (radiation)

A

Low energy beams for external or superficial tumors
High energy beam for internal tumors

272
Q

External radiation pt teaching

A

Irritation at radiation 1-24 hours after treatment
- Frequent skin assessment
Unscented, mild soaps
- No lotion/deodorant
Avoid sunlight, temperature extremes
Avoid rough washcloths and tape

273
Q

Brachytherapy

A

Radiation “seeds” are implanted at the cancer site
Sealed sources of radiation placed near the tumor

274
Q

Unsealed radiation

A

Type of internal radiation
Ingested or instilled in body cavity

275
Q

ALARA

A

As low as reasonably achievable
- Reduce radiation

276
Q

Radiation nursing considerations/safety

A

Stay in room for no longer than 30 mins
Door closed
Visitors 6 ft
Private room
Disposable trays
Keep linen in room
Radiation warning sign
Avoid pregnant nurses
Dosimeters can be worn with lead apron

277
Q

Implanted brachytherapy seed nursing consideration

A

Bedrest while implant in place
Ensure location of implant
Body fluids are not radioactive

278
Q

Methods of chemo administration

A

Intra-arterial
Intraperitoneal
Intrathecal - bypasses blood brain barrier
Intravesical bladder chemo

279
Q

Chemo side effects

A

Hair, skin and nails
GI mucosa
Bone marrow cells: RBC, WBC, Platelets
- D/t destruction of all rapidly growing cells
Anaphylaxis, extravasation
Organ toxicity

280
Q

Stomatitis nursing interventions

A

Frequent oral care
Soft bristled toothbrush
Baking soda + saline after meals
Avoid acidic or spicy food
Avoid extremes in temperature

281
Q

Chemo nutrition considerations

A

Small, frequent meals - high protein, high calorie
Cachexia: muscle wasting
Monitor wt and nutrition labs - albumin, prealbumin
Monitor I&O’s for dehydration

282
Q

Chemo skin potential reactions

A

Erythema: redness of affected area
Wet desquamation: Exposure of underlying dermis
Hand-foot syndrome: redness/swelling
Extravasation: Many chemos are irritants or vesicants

283
Q

Nursing considerations/interventions for extravasation (during chemo)

A

Use central lines for chemo
Extravasation kit at bedside - warm/cold compress, antidote meds
Stop infusion and notify HCP for pain, redness, swelling

284
Q

SE of chemo/radiation

A
  • Bone marrow suppression
    Neutropenia
    Thrombocytopenia
    Anemia
285
Q

Priority intervention for chemo/radiation

A

Infection

286
Q

All blood cell types can be transfused except for

A

WBC

287
Q

What level indicates neutropenia

A

ANC (absolute neutrophil count) under 1500mm3
Certain infection when ANC under 100mm3

288
Q

What lab shows need for neutropenia isolation

A

WBC under 1000

289
Q

Neutropenia tx

A

Depends on cause:
Remove offending meds
Tx bone marrow cancer
Hospital admission with cultures and CXR for suspected infection

290
Q

Platelet labs levels and what they indicate

A

Below 150,000 = thrombocytopenia
Below 50,000 = increased risk of bleeding
Below 20,000 = spontaneous bleed

291
Q

When is the typical onset of anemia after chemo

A

3-4 months after chemo is started

292
Q

Anemia tx

A

erythropoetin (EPO) to stimulate RBC growth
RBC transfusion - last resort

293
Q

Fatigue tx (chemo)

A

Treat anemia
Correct electrolyte imbalances
Cluster care
Establish a sleep/wake cycle
Maintain light daily activity as tolerated

294
Q

Late effects of chemotherapy

A
  • months or years after
    In liver, kidneys, bone, heart muscle
    Cataracts
    Cardiac toxicity
    Osteoporosis
    Secondary malignancies
295
Q

Immunotherapy for cancer (prototypes)

A

Interleuken-2 (IL2)
Rifuximab

296
Q

Types of immunotherapy

A

Cytokines
Vaccines
Monoclonal antibodies (drugs ending in –mab)

297
Q

Immunotherapy SE’s

A

Flu-like symptoms
- Tylenol or IV Demerol

298
Q

Infusion related symptoms

A

Fever
Chills
Urticaria
Muscosal congestion
N/D

299
Q

What is the tx for cancer that fails to respond to chemo

A

Hematopoietic stem cell transplant or
Bone marrow transplant

300
Q

Myelosuppression

A

Performed on transplant recipients
Eliminates existing stem cells - similar effect as chemo

301
Q

Graft-vs-Host Disease

A

Major cause of morbidity and mortality in the allogeneic transplant population
Donor lymphocytes initiate immune response against the recipient’s tissues (skin, gastrointestinal tract, liver) during the beginning of engraftment

302
Q

Preventions of graft-vs-host disease

A

Immunosuppressant drugs - such as cyclosporine

303
Q

Acute vs chronic graft-vs-host disease

A

Acute: within 100 days
Chronic: after 100 days

304
Q

Superior vena cava syndrome

A

Obstruction of superior vena cava. Common causes are lung cancer, non-Hodgkin lymphoma

305
Q

Hypoproliferative anemia

A

Abnormal RBC’s are produced then destroyed

306
Q

Hemolytic anemia

A

Destruction of RBC’s
RBC’s appear normal
Increase in byproducts of RBC breakdown - bilirubin
Increase in immature RBC’s

307
Q

Iron deficiency anemia patho

A

Inadequate dietary iron
Inadequate iron absorption
Blood loss
RBC destruction

308
Q

Iron deficiency anemia specific assessment

A

Pallor
Inflammation of the tongue
Inflammation of the lips
Burning of tongue
Paresthesias

309
Q

Iron deficiency anemia dx

A

Hgb, Hct, RBC below normal
Serum iron
Serum ferritin
RBC smears
Stool exam

310
Q

Iron deficiency anemia causes

A

History of GI bleeds, heavy menses, peptic ulcers iron loss

311
Q

What foods are good/bad for anemia

A

ETOH - blocks iron absorption
Red meat, leafy greens - good sources of iron

312
Q

Iron deficiency anemia tx

A

Iron supplementation
Iron pill + calcium + stool softener
IM or IV iron

313
Q

Thalassemia patho

A

Abnormal hemoglobin production causes decreased O2 delivery
Abnormal cells are destroyed in spleen

314
Q

Thalassemia specific assessment

A

Pallor, deficits in growth and development
Jaundice
Bone marrow hyperplasia

315
Q

Thalassemia dx

A

Small, pale RBCs
Hgb < 10 = transfusion
Bone marrow biopsy

316
Q

Thalassemia cause

A

Genetic link – Mediterranean, north African, southeast Asian

317
Q

Thalassemia tx

A

Frequent blood transfusion
Chelation therapy for iron overload
Monitor for DVT, s/s heart failure
Splenectomy

318
Q

Megaloblastic Anemia patho

A

Lack of B vitamins leads to abnormally large RBCs that are destroyed in circulation

319
Q

Megaloblastic Anemia specific patho

A

Sore, red, beefy tongue
Nausea and vomiting, abd pain
Paresthesias
Neuro changes
Pernicious = potentially fatal

320
Q

Megaloblastic Anemia dx

A

Large RBCs on smear
Folate levels
Anti-IF antibodies

321
Q

Megaloblastic Anemia causes

A

Dietary intake of folate
Scandinavian or African American
Family history
GI s/s and food diary

322
Q

Megaloblastic Anemia tx

A

Pernicious anemia: IM B12 injections 2x week

B vitamin supplementation for inadequate dietary intake

323
Q

Chronic anemia patho

A

Chronic infection, inflammation, disease leads to decreased RBC production

324
Q

Chronic anemia specific assessment

A

Presence of 1 or more chronic diseases

325
Q

Chronic anemia dx

A

Decreased RBC production with no other distinct cause of anemia

Iron levels normal
IF present
B vitamin levels normal (same as aplastic anemia)

326
Q

Chronic anemia causes

A

1-2 month history of disease
Kidney disease

327
Q

Chronic anemia tx

A

Correct underlying disorder

328
Q

Anemia d/t renal disease patho

A

Decreased erythropoietin production
EPO stimulates RBC production

329
Q

Aplastic Anemia patho

A

Bone marrow disorder causes decreased production of all cells

330
Q

Aplastic Anemia specific assessment

A

Presence of 1 or more chronic diseases

331
Q

Aplastic Anemia causes

A

Frequent bleeding
Frequent infection
Underlying disorders

332
Q

Aplastic Anemia dx

A

Decreased RBC production with no other distinct cause of anemia

Iron levels normal
IF present
B vitamin levels normal (same as chronic anemia)

333
Q

Aplastic Anemia tx

A

Correct underlyingdisorder
Bone marrow transplant

334
Q

Anemia d/t acute blood loss patho

A

Trauma, surgery, esophageal varices causes acute anemia

335
Q

Anemia d/t acute blood loss specific assessment

A

Sudden blood loss of 30% of Hgb can cause s/s of shock

336
Q

Anemia d/t acute blood loss causes

A

Recent bleed

337
Q

Anemia d/t acute blood loss tx

A

PIV x2 and resuscitation fluids
Blood transfusion
Correct underlying bleed
Albumin or Dextran
Platelet or plasma transfusion
Continuous cardiac monitor and frequent VS

338
Q

Anemia d/t chronic blood loss patho

A

Slow GI bleed, menstrual bleeding, similar to iron deficient
Meds, ETOH

339
Q

Anemia d/t chronic blood loss specific assessment

A

Gradual blood loss of up to 50% blood volume may only cause mild s/s

340
Q

Anemia d/t chronic blood loss dx

A

S/s specific diagnostic tests

341
Q

Anemia d/t chronic blood loss tx

A

Identify and treat cause of bleed
May lead to iron deficient anemia

342
Q

Where does RBC breakdown happen

A

Spleen and liver

343
Q

What does an excess of RBC’s cause

A

Hepatomegaly
Splenomegaly

344
Q

Sickle Cell Disease cause

A

Genetic - primarily affects African descent
Abnormal genes make RBCs that “sickle” when O2 concentrations get low

345
Q

Sickle cell crisis

A

Severe clots and reduced circulations leads to tissue death

346
Q

Things that affect sickled cells

A

Infection
High altitude
Heavy exercise
Stress
Surgery
Dehydration

347
Q

Sickle cell disease s/sx

A

Chest pain, tachycardia
Pulmonary embolism, tachypnea - supplement with O2
Enlarged liver, gallstones
Damaged kidney - increased BUN/creat, decreased UOP
Grey skin, jaundice

348
Q

Sickle cell disease dx

A

(+) Hgb-S
Sickled cells on smear
Chronic anemia
Bone and joint deformities

349
Q

Primary concern for sickle cell disease

A

Respiratory failure

350
Q

Hospital interventions during acute sickle cell disease episodes

A

IV abx
Continuous O2 - lung assessments
Rest
Anticoagulants
IV fluids - hydration
Monitor renal labs
Folic acid supplements

351
Q

Sickle cell disease complications

A

Avascular necrosis – death of femoral head
Venous stasis ulcers
Iron overload
Changes in vision
Priapism

352
Q

Sickle cell disease tx

A

Stem cell transplant
Hydroxyurea promotes normal Hgb growth

353
Q

Acquired Hemolytic Anemia patho

A

Destruction of RBC from outside factors

354
Q

Acquired Hemolytic Anemia tx

A

Immunosuppression
Folate replacement
Remove cause if possible

355
Q

Acquired Hemolytic Anemia dx

A

Elevated bilirubin and decreased RBC

356
Q

Acquired Hemolytic Anemia specific assessment

A

Jaundice

357
Q

Acquired Hemolytic Anemia causes

A

Dialysis
Radiation
Poisoning
Heart valves - ask about hx
Antibodies

358
Q

Hemachromatosis patho

A

Iron overload
Can be secondary to blood transfusion
*likely don’t need to know this condition, skip over

359
Q

Hemachromatosis specific assessment

A

Fatigue, joint pain, weight loss, cirrhosis
Bronze skin

360
Q

Hemachromatosis dx

A

Iron levels > 6g and up to 50g

361
Q

Hemachromatosis causes

A

Genetic link
History of anemic disorders with transfusion

362
Q

Hemachromatosis tx

A

Therapeutic phlebotomy
Chelating agents

363
Q

Polycythemia patho

A

Excess RBC production leads to sludgy blood

Secondary – excess RBC production d/t chronic hypoxia

364
Q

Polycythemia specific assessment

A

Headache, dizziness, tinntus, vision changes
Itching and flushing
Chest pain and heart failure
DVT formation

365
Q

Polycythemia dx

A

Elevated RBC and Hgb
Microcytosis
Low EPO levels

366
Q

Polycythemia tx

A

Phlebotomy to target Hct < 45-42
Hydration

367
Q

Polycythemia causes

A

Genetic link
History of anemic disorders with transfusion

368
Q

Where are blood cells formed

A

Bone marrow

369
Q

Where does the breakdown of RBC’s occur

A

Spleen and liver

370
Q

Where are immune cells formed

A

Lymph system

371
Q

RBC’s are also called

A

Erythrocytes

372
Q

What controls RBC production

A

Erythropoietin
Released by kidneys

373
Q

Normal hct

A

35-50%

374
Q

Normal hgb

A

11-17

375
Q

Normal RBC

A

4.5-5.7

376
Q

Normal MCV

A

80-100
Mean corpuscular volume
- Size of RBC

377
Q

Types of lymphocytes

A

B cells
T cells
Natural killer (NK)

378
Q

Normal neutrophil count

A

4,500 - 7,000
Low = risk of infection

379
Q

Normal platelet count

A

150,000 - 400,000

380
Q

Normal aPTT

A

25-35 sec

381
Q

Normal PT

A

11-16 sec

382
Q

Normal INR

A

Below 1.1
2-3 in anticoagulated pts (warfarin)

383
Q

What level of Hgb diagnosis each severity of anemia

A

Mild anemia = Hgb 10-11
Moderate anemia = Hgb 7-10
Severe anemia = Hbg under 7 (transfusion)

384
Q

What does adrenal medulla release

A

Catecholamines - dopamine, norepinephrine, and epinephrine (adrenaline)
Sympathetic NS stimulation

385
Q

What does the adrenal cortex release

A

Steroid hormones - Glucocorticoids, mineralocorticoids, progestins, androgens, and estrogens

386
Q

What do glucocorticoids/corticosteroids do

A

Inhibit inflammation
Controls metabolism and stress response

387
Q

What does too little glucocorticoids/corticosteroids do

A

Causes an inability to respond to stress

388
Q

What does too much glucocorticoids/corticosteroids do

A

Suppress the immune response

389
Q

What do mineralcorticoids do

A

AKA aldosterone
Regulates Na, K, and water

390
Q

What does too much mineralcorticoids do

A

Increased Na, increased BV, decreased K

391
Q

What does too little mineralcorticoids do

A

Decreased Na, decreased BV, increased K

392
Q

Pheochromocytoma

A

Benign tumor in the adrenal medulla

393
Q

Pheochromocytoma s/sx

A

5H:
Hypertension
Headache
Hyperhidrosis
Hypermetabolism
Hyperglycemia

394
Q

Pheochromocytoma dx

A

Elevated urine and plasma catelcholamines
- Measured with 24 hr urine collection
Clonidine suppression test

395
Q

Pheochromocytoma nursing interventions

A

Bed rest
Raise HOB

396
Q

Pheochromocytoma med tx and what to monitor for after administering

A

Alpha and beta blockers
- Monitor for orthostasis, nasal drainage, fatigue

397
Q

Pheochromocytoma surgical tx

A

Removal of adrenal glands

398
Q

Adrenalectomy nursing considerations

A

Pre-op: Hydration to control HTN
Calcium channel blockers to supplement Beta-blockers
10-14 days of BP control before adrenalectomy

399
Q

What is the endocrine process that stimulates the adrenal glands

A

Hypothalamus secretes corticotropin-releasing hormone (CRH)
CRH stimualtes the pituitary gland to release adrenocorticotropic hormone (ACTH)
ACTH stimulates adrenal glands to release hormones

400
Q

Addison’s Disease

A

Decrease in glucocorticoid production - inability to generate stress response
Decrease in aldosterone - dehydration

401
Q

Addison’s Disease s/sx

A

Low glucocorticoids
- Decreased BG
- Fatigue, muscle weakness, depression
- Frequent infections
Low mineralcorticoids
- Decreased Na, dehydration
- Orthostatic hypotension
- Weak pulses
- Weight loss
Bronze mucous membranes

402
Q

Addison’s Disease dx

A

ACTH stimulation test
→ACTH given IV, then blood is drawn to see if cortisol levels increase
-Decreased Na, increased K
-Increased BUN

403
Q

Addison’s Disease tx

A

Lifelong hormone therapy
-Hydrocortisone is drug of choice
- “stress dosing”
Avoid high-stress activities

404
Q

Addison’s Disease risk factors

A

Adrenal tumor, hemorrhage, tuberculosis
Long term corticosteroid use
Critically ill
Adrenal/renal hemorrhage
(anything that damages the adrenal gland)

405
Q

Secondary Addison’s Disease cause

A

Damage to the pituitary gland causes decreased ACTH

406
Q

Addison’s Disease diet

A

High sodium
Low potassium
Increase fluids

407
Q

Adrenal Crisis patho

A

An acute drop in hormone production

408
Q

Adrenal Crisis causes

A

Stressor during Addison’s disease
-Critical illness

409
Q

Adrenal Crisis s/sx

A

Severe fatigue and weakness
Decrease in BP leading to shock
Hypoglycemia

410
Q

Adrenal Crisis tx

A

IV dextrose and hydrocortisone replacement

411
Q

Adrenal Crisis nursing interventions

A

V/S
Strict I/O’s
Daily wt
Prevent stress

412
Q

Adrenal Gland Removal postop meds

A

Continuous corticosteroid replacement with solumedrol or prednisone
- Avoids rebound Addison’s disease

413
Q

Cushing’s Disease patho

A

Excessive steroid hormone activity
-Increase in gluco- and mineral-corticoids

414
Q

Cushing’s Disease causes

A

Adrenal hyperplasia
Excessive steroid administration
Pituitary tumor

415
Q

Cushing’s Disease s/sx

A

Central obesity, “buffalo hump”, thin extremities
Fragile, thin skin, ecchymosis, striae
Weakness, personality/mood changes
Osteoporosis, muscle wasting, HTN
Moon-face, acne, infection, slow healing
Virilization in women, loss of libido
Increased Na, decreased K

416
Q

Cushing’s Disease dx

A

Serum and urine cortisols, dexamethasone (decadron) suppression test
-Decadron test given overnight to measure cortisol release
-Urine cortisol is 24 h collection

417
Q

Cushing’s Disease tx

A

Pituitary removal or adrenalectomy

418
Q

Cushing’s Disease nursing interventions

A

Monitor VS, daily weight, blood glucose
Close monitoring for early signs and symptoms of infection
Emotional support for body changes

419
Q

Cushing’s post-op tx

A

Supplemental steroid hormones
Monitor for rebound Addisonian crisis - extreme hypovolemia leading to shock

420
Q

Organs that pituitary gland stimulates

A

Adrenal glands
Thyroid gland
Ovaries/Testes
Bone and soft tissues

421
Q

Anterior pituitary hormones

A

Adrenocorticotrophic hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Luteinising hormone (LH)
Follicle-stimulating hormone (FSH)
Prolactin (PRL)
Growth hormone (GH)
Melanocyte-stimulating hormone (MSH)

422
Q

Posterior pituitary hormones

A

Vasopressin - antidiuretic hormone (ADH)
Oxytocin

423
Q

Panhypopituitarism

A

Decrease in all hormones of the pituitary gland, including all releasing and stimulating hormones

424
Q

What is the difference between anterior and posterior pituitary gland disorders

A

Anterior: Chronic, long term management
Posterior: Acute, hospitalization

425
Q

Acromegaly

A

Oversecretion of GH from anterior pituitary

426
Q

Dwarfism

A

Decrease in GH

427
Q

Diabetes insipidus dx

A

Plasm and urine specific gravities
Fluid deprivation test: water held for 8-12 hours
- DI will have large urine volumes

428
Q

Diabetes insipidus tx

A

Correct fluid imbalance
Long term: DDVAP - synthetic ADH, nasal spray

429
Q

SIADH (Syndrome of inappropriate ADH)

A

Unable to dilute urine
Concentrated urine, diluted blood, third spacing

430
Q

SIADH causes

A

Medications
Head injury
Brain surgery
Tumor

431
Q

SIADH s/sx

A

Fluid retention, hyponatremia, concentrated urine
Weight gain, severe edema, pulmonary edema

432
Q

Severe hyponatremia

A

Under 120
Neuro symptoms - seizures
N/V, cramps, muscle twitching

433
Q

Pituitary tumor dx

A

CT
MRI
Serum hormone levels

434
Q

Pituitary tumor tx

A

(Transsphenoidal) Hypophysectomy: removal of tumor through nasal passage
Hormone replacement

435
Q

(Transsphenoidal) Hypophysectomy nursing considerations

A

Used for either hypo or hyper pituitarism
Removal of gland always leads to panhypopituitarism
- Lifelong hormone replacement