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NURS 320 > Exam #3: Study Guide Part 2 > Flashcards

Exam #3: Study Guide Part 2 Flashcards

1
Q

Thyroid Gland

A

Gland responsible for secretion of hormones that regulate metabolism.

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2
Q

What is the function of the thyroid gland?

A
  • Works through negative feedback (TRH from hypothalamus -> TSH from anterior pituitary -> T3 & T4 immediately released)
  • Communicates with parathyroid glands.
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3
Q

What are the hormones that are secreted by the thyroid gland?

A
  1. Thyroxine (T4)
  2. Triiodothyronine (T3)
  3. Calcitonin

These hormone regulate metabolism.

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4
Q

Parathyroid gland

A

Produces parathyroid hormone (PTH)

Most important factor in increasing serum calcium and decreasing serum phosphate

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5
Q

What is the function of PTH?

A
  • Decreased serum-ionized calcium stimulates PTH secretion acting directly on bone to release calcium.
  • PTH also acts on kidney to increase calcium reabsorption and to decrease phosphate reabsorption.
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6
Q

What hormones are released by the parathyroid gland?

A

PTH

*Not sure if there’s more

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7
Q

What hormones are released by the anterior pituitary gland?

A 
TSH
ACTH
LH
FSH
Prolactin
Growth Hormone
Melanocyte Stimulating Hormone
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8
Q

Anterior Pituitary Gland

A

..

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9
Q

Posterior Pituitary Gland

A

..

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10
Q

What hormones are released by the posterior pituitary gland?

A

ADH

Oxytocin

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11
Q

Adrenocorticotropic Hormone (ACTH)

A

Stimulates production and release of cortisol.

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12
Q

What is the pathophysiology of diabetes insipidus?

A

Insufficiency of ADH activity.
Caused by:
1. Neurogenic (lesions, brain injury, aneurysm)
Hypothalamus doesn’t make enough ADH OR posterior pituitary doesn’t release ADH
2. Nephrogenic: kidney abnormalities affect the way ADH is processed.
3. Unknown (30%)

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13
Q

What are the signs and symptoms of diabetes insipidus?

A
  • Polydipsia
  • Polyuria
  • Dehydration (dry skin, dry mucous membranes, poor Skin turgor, fever, tachycardia, sunken appearance of eyes, unintentional weight loss)
  • Electrolyte imbalance (fatigue, lethargy, headache, irritability, and muscle pains)
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14
Q

How do you treat diabetes insipidus?

A 
ADH replacement (Vasopressin)
Fluid replacement
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15
Q

What is the mechanism of action for Vasopressin (Pitressin)?

A

Causes renal collecting tubules to increase permeability to water.
Enhances water reabsorption.

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16
Q

What are the adverse effects of Vasopressin (Pitressin)?

A
  • Hypertension
  • Can precipitate angina episodes and MI in clients with CAD.
  • Excessive fluid retention can cause water intoxication.
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17
Q

Hypothyroidism

A

Congenital:
Lack of thyroid gland
Cretinism (severely stunted physical and mental growth)

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18
Q

How can hypothyroidism be acquired?

A
  • hashimoto or autoimmune thyroiditis (most common)
  • irradiation or removal of thyroid
  • iodine deficiency
  • Goitrogenic foods (Brussels sprouts, broccoli, cauliflower, cabbage..etc)
  • Drugs such as lithium
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19
Q

What are complications of hypothyroidism?

A

MYXEDEMA - occurs when the body’s level of thyroid hormones become severely low.
SYMPTOMS - below normal temperature, decreased breathing, BP and Blood Sugar, unresponsiveness

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20
Q

How is hypothyroidism treated?

A

Levothyroxine (Synthroid)

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21
Q

What is the mechanism of action for Levothyroxine (Synthroid)?

A
  • Synthetic form of thyroxine (T4).
  • MOA: Same as endogenous thyroid hormone.
  • Leads to weight loss, improved tolerance to environmental temperature, increased activity and pulse rate.
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22
Q

What are the adverse effects of Levothyroxine or Synthroid?

A

Symptoms of Hyperthyroidism:

  • Palpitations
  • Dysrhythmias
  • Anxiety, insomnia, weight loss, heat intolerance
  • Menstrual irregularities and osteoporosis in women (long term treatment)
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23
Q

What are the drug interactions for Levothyroxine for Synthroid?

A 
Questran
Aluminum containing antacids (Maalox)
Iron and calcium supplements 
Warfarin
Dilantin
Zoloft
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24
Q

Hyperthyroidism

A
  • An autoimmune disorder of unknown origin with a genetic component.
  • A syndrome initiated by excessive production of thyroid hormones -> multiple system abnormalities.
  • Graves’ disease is the most common type.
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25
Q

What is the pathophysiology of hyperthyroidism?

A

..

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26
Q

What are the signs and symptoms of hypothyroidism?

A 
Cold intolerance
Unintentional weight gain
Depression
Dry, brittle hair
Fatigue
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27
Q

What are the signs and symptoms of hyperthyroidism?

A 
Diarrhea
Flushing
Increased appetite
Muscle weakness
Fatigue
Palpitations
Irritability
Nervousness
Sleep disorders
Heat intolerance
Altered menstrual flow
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28
Q

What are the complications of hyperthyroidism?

A
  • Cardiac insufficiency: tachycardia, a-fib, CHF
  • Generalized muscle wasting
  • Corneal ulcers
  • Osteoporosis
  • Impaired fertility
  • Thyroid Storm (thyroxic Crisis)
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29
Q

What is the primary goal of treatment for hyperthyroidism?

A

Purpose is to control over-activity of thyroid gland.

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30
Q

How is hyperthyroidism treated?

A
  1. Beta-blockers (Propranolol): treats symptoms of tachycardia, swearing, tremors and palpitations.
  2. Administer antithyroid agents (propylthiouracil)
  3. Radioactive Iodide
  4. Surgery: Thyroidectomy
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31
Q

What is the mechanism of action for propylthiouracil (PTU)?

A

Interfere with synthesis of T3 and T4 in thyroid gland.

Also prevents conversion of T4 to T3 in target tissues.

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32
Q

What are the adverse effects of propylthiouracil (PTU)?

A

Symptoms of hypothyroidism:
Rash and transient leukopenia (most frequent)
Small percentage experience agranulocytosis

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33
Q

How does radioactive iodine therapy treat hyperthyroidism?

A

Destroys active thyroid gland with ionizing radiation.

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34
Q

Cushing’s Disease vs Cushing’s Syndrome

A

Cushing’s Disease: excessive anterior pituitary secretion of ACTH -> too much cortisol

Cushing’s Syndrome: excessive level of cortisol, regardless of cause.

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35
Q

Addison’s Disease

A

Characterized by the hyposecretion of adrenal cortex hormones (glucocorticoids (cortisol) and mineralcorticoids (aldosterone)) from the adrenal gland, resulting in deficiency of the corticosteroid hormones.

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36
Q

Signs and Symptoms of Cushing’s Disease

A
  • Truncal obesity*
  • Moon face*
  • Buffalo hump on the back*
  • Easy bruising
  • Purple Striae*
  • HTN
  • Edema
  • Weakness
  • Osteoporosis
  • Hirsutism*
  • Acne
  • Mood/affect changes to psychosis
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37
Q

Signs and Symptoms of Addison’s Disease

A
  • Begins with weakness and easy fatigability progressing to N/V/D
  • Skin changes (hyperpigmentation and vitiligo)
  • Hyponatremia, hyperkalmeia and salt cravings
  • Hypotension (can progress to vascular collapse and shock)
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38
Q

What is the treatment for Cushing’s Disease/Syndrome?

A
  • Surgical removal of tumor
  • Radiation of tumor
  • Tapering of the glucocorticoid therapy
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39
Q

What is the treatment for Addison’s Disease?

A

-Replace both cortisol and aldosterone

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40
Q

Glucocorticoids

A

Used as replacement therapy for clients with adrenocrotical insufficiency.
Dampen inflammatory and immune responses.

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41
Q

What is the mechanism of action of glucocorticoids?

A

..

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42
Q

What are the adverse effects of glucocorticoids?

A

..

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43
Q

Glucocorticoids include

A

Hydrocortisone

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44
Q

Hydrocortisone (Cortef)

A

Glucocorticoids used as a drug of choice in treating adrenocortical insufficiency.

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45
Q

What is the mechanism of action for hydrocortisone (Cortef)?

A

Acts as synthetic corticosteroid.

46
Q

What are the adverse effects of hydrocortisone?

A
  • Sodium and Fluid Retention.
  • CNS effects: insomnia, anxiety, headache, vertigo, confusion and depression.
  • HTN, tachycardia, PUD, Cushing’s Syndrome
47
Q

What are adverse effects of long-term glucocorticoid therapy?

A
  • Increased susceptibility to infection
  • PUD increased risk when combined with NSAIDs
  • Osteoporosis
  • Behavioral changes: nervousness or moodiness; hallucinations or increased suicidal thoughts.
  • Eye changes: cataracts and open-angle glaucoma
  • Metabolic changes: raises serum glucose -> glucose intolerance or diabetes; hyperlipidemia and abnormal fat deposits; electrolyte changes (hypocalcemia, hypokalmeia, hypernatremia)
  • Myopathy: muscle wasting -> weakness and fatigue
  • Fluid Retention, weight gain, HTN, edema common
48
Q

What is the role of PTH in calcium balance?

A
  • Stimulates osteoclasts
  • Accelerates bone resorption
  • Causes breakdown of bone
  • Consequently increases calcium in blood.
49
Q

What is the role of calcitonin in calcium balance?

A
  • Calcitonin stimulates bone deposition.
  • This removes calcium from the blood.
  • Works with PTH to control calcium homeostasis.
50
Q

What is the role of Vitamin D in calcium balance?

A

Vitamin D is necessary for effective absorption of calcium

More info on PP, not sure if need to know?

51
Q

What are the concerns with low calcium levels?

A

Cause cell membranes to become hyper-excitable.

Convulsions or muscle spasms.

52
Q

What are the concerns with high calcium levels?

A

Decreases sodium permeability across cell membranes - a dangerous state.

53
Q

What is the mechanism of action of Vitamin D supplements (i.e calcitriol)?

A

Acts as an active form of Vitamin D:

  • promotes intestinal absorption of calcium.
  • reduces bone resorption
  • elevates serum levels of calcium
54
Q

What are the adverse effects of Vitamin D supplements (Calcitriol)?

A 
May cause symptom of hypercalcemia including:
Headache*
Lethargy*
Confusion*
Palpitations*
Dysrhythmias*
55
Q

What are the nursing implications of Vitamin D supplements?

A
  • Assess for symptoms of hypercalcemia (palpitations, dysrhythmias, blurred vision, photophobia, lethargy and confusion)
  • Obtain a thorough history of current medications including intake of fat-soluble vitamins (ADEK)
  • Monitor lab studies
56
Q

What are the causes of osteomalacia?

A
  • Bone requires adequate concentration of Ca and Phosphate.
  • Vitamin D enhances the absorption of calcium from the intestines.
    - Low serum Ca levels stimulate PTH
    - PTH raises serum Ca levels but decreases phosphate levels.
    - Without phosphate bone mineralization can’t occur.
57
Q

What are the signs and symptoms of osteomalacia?

A
  • Muscular and Skeletal Pain: Hip most common
  • Muscle Weakness
  • Hypocalcemia
  • Fragility and fractures may occur
  • Bowlegs and pigeon chest (in Rickets)
58
Q

What is the pathophysiology of osteoporosis?

A
  • Bone resorption and bone formation cycle is disrupted

- Osteoclasts are disrupted

59
Q

What are the signs and symptoms of osteoporosis?

A
  • Pain and bone deformity (secondary to fracture)

- Vertebral collapse - kyphosis (hunchback)

60
Q

What are the risk factors for osteoporosis?

A
  • Most common: onset of menopause
  • High alcohol or caffeine consumption
  • Anorexia Nervosa
  • Tobacco use
  • Physical inactivity
  • Testosterone deficiency
  • Hyperthyroidism
  • Lack of Vitamin D or calcium
  • Drugs that lower calcium in the blood (corticosteroids, anticonvulsants, immunosuppressants)
61
Q

Osteomalacia

A

Characterized by softening of bones due to demineralization.

62
Q

Osteoporosis

A

Related to bone deterioration (Bone resorption outpaces bone deposition):

  • Lack of dietary calcium and Vitamin D
  • Disrupted bone homeostasis
63
Q

What is the treatment used to treat osteoporosis?

A

Bisophophonates

Raloxifene (Selective Estrogen Receptor Modulators aka SERMs) - Second line drug

64
Q

What is the mechanism of action of bisphosphonates (i.e alendronate or Fosamax)?

A

Becomes incorporated into skeletal tissue.

Blocks bone reabsorption by inhibiting osteoclast activity.

65
Q

What are the adverse effects of bisphosphonates (i.e alendronate or Fosamax)?

A 
GI disturbances (abdominal pain, flatulence, dyspepsia, N/V/D)
*TAKE ON EMPTY STOMACH
66
Q

What is the mechanism of action for SERMs (i.e raloxifene or Evista)?

A
  • Decreases bone resorption.
  • Increases bone density.
  • Binds to estrogen receptors (may be estrogen agonists or antagonists - depends on drug or tissue involved)
67
Q

What are the adverse effects of SERMs (i.e raloxifene or Evista)?

A

Most common:

  • Hot flashes
  • Migraine headache
  • Leg cramps
  • Weight gain
  • Flu-like symptoms
68
Q

Osteoarthritis

A
  • Degenerative, age-onset disease

- Affects the entire joint - characterized by wearing away of cartilage at articulate joint surfaces.

69
Q

What is the pathophysiology of osteoarthritis?

A
  • Failure of chondrocytes to maintain balance between degradation and synthesis of collagen.
  • Biochemical, biomechanical, inflammatory and immunologic factors contribute to cartilage loss
70
Q

What are the signs and symptoms of osteoarthritis?

A

Muscle spasms
Localized pain and stiffness
Joint and bone enlargement

71
Q

What is the treatment for osteoarthritis?

A

Analgesics
NSAIDs (Ibuprofen)
Corticosteroid Injection

72
Q

How do NSAIDs (Ibuprofen or Naproxen) treat osteoarthritis?

A

Goal of osteoarthritis treatment is to reduce pain and inflammation.
NSAIDs are analgesics and anti-inflammatory agent.

73
Q

Rheumatoid Arthritis

A
  • Systemic autoimmune damage to connective tissue, primarily in joints (synovial membrane)
  • Autoantibodies (rheumatoid factors) activate inflammatory response in joints symmetrically
74
Q

What is the pathophysiology of Rheumatoid Arthritis?

A
  • An insult (infection, smoking, trauma) precipitates an autoimmune reaction.
  • Anti-body activation results in endothelial activation (synovial hypertrophy, joint inflammation)
  • Systemic disorder:
    • abnormal B- and T-cell interactions
    • overproduction of cytokines
75
Q

What are the signs and symptoms of Rheumatoid Arthritis?

A
  • Painful, tender and stiff joints (usually affects both sides equally): hands, wrist and feet joints are most common
  • Stiffness usually lasts for about 1 hour after rising in morning (synovitis).
  • Reduced ROM, difficulties with ADLs
76
Q

What is used to treat Rheumatoid Arthritis?

A
  • DMARD Therapy
  • NSAIDs (naproxen or ibuprofen)
  • Prednisone (if not responding to NSAIDs)
77
Q

What is the mechanism of action of DMARDs (i.e hydroxychloroquine sulfate or Planequil)?

A

Relieves severe inflammation of arthritis and lupus.

MOA is unknown.

78
Q

What are the adverse effects of Disease Modifying Anti-Rheumatic Drugs (DMARDs)?

A 
Anorexia
Aplastic Anemia
Agranulocytosis
Seizures
Retinopathy
Headache
Mood and mental changes
79
Q

Gout

A

Characterized by buildup of uric acid in blood or joint cavities.
Triggered by diet (high purine), injury or other stress.
Attacks often occur at night.

80
Q

What is the pathophysiology of gout?

A

Overproduction or underexcretion of uric acid.

Leads to inflammation and pain in joints: Often in big toes, ankles, fingers, wrists, knees, elbows

81
Q

What are the sings and symptoms of gout?

A
  • Monoarticular arthritis
  • Tophi (helix of ear, arm or leg)
  • Renal Disease
  • Renal Calculi
  • Abrupt attacks (red swollen tissue; peripheral joint)
  • Pain several hours to several weeks
82
Q

How do you treat an acute exacerbation of gout?

A

Glucocorticoids(used for short-term relief; injected into joint)
NSAIDs (for pain and inflammation)

83
Q

How is colchicine or colycrys treat gout?

A
  • Terminates acute attacks of gout by reducing inflammation.
  • Does so by inhibiting the synthesis of microtubules (subcellular structures responsible for helping WBCs infiltrate area)
84
Q

What is anti-gout prophylaxis (i.e allopurinol or Zyloprim)?

A
  • Prevents future attacks of gout.
  • Indicated for hyperuricemia.
  • Does so by inhibiting xanthine oxidase (which prevents uric acid production).
85
Q

Osteomyelitis

A

Most often caused by an infection.

86
Q

What is the pathophysiology of osteomyelitis?

A
  • Similar to body tissue
  • Invading pathogen revokes Inflammatory response
  • Suppurative infection of bone with edema and vascular compromise
  • Can occur as a result of:
    • Bacteria transported through blood
    • Spread of infection through contact
    • Direct inoculation into intact bone (trauma or surgery)
87
Q

What are the signs and symptoms of osteomyelitis?

A
  • Varies
  • Abrupt onset of inflammation (acute)
  • Fever, chills, lethargy (in children)
  • Lymphadenopathy
  • Chronic - necrotic bone
88
Q

What is used to treat osteomyelitis?

A

Antibiotics
Debridement
Surgical removal of exudates
Hyperbaric oxygen therapy

89
Q

What class of drugs increases the risk for peptic ulcers?

A

..

90
Q

What class of drugs increases the risk of decreased wound healing?

A

..

91
Q

What class of drugs increases the risk of capillary fragility?

A

..

92
Q

Adequate levels of calcium in the body are necessary to:

A
  • Transmit nerve impulse
  • Prevent muscle spasms
  • Provide stability and movement

-Also important for blood coagulation and myocardial activity.

93
Q

Calcium balance in th body is regulated by

A

The parathyroid hormone

94
Q

What is the recommended daily allowance of calcium for adults?

A

800 to 1,200 mg/day

*Increased amounts are needed for pregnant women, growing children and menopausal women

95
Q

What is the normal serum calcium range?

A

4.5 - 5.5 mEqL

OR 8.5 - 10 mg/dL

96
Q

What three organs does calcitonin and PTH target?

A

Bones
Kidneys
GI Tract

97
Q

What is the mechanism of action for alendronate (bisophosphonate)?

A

Lowers serum alkaline phosphatase (enzyme associated with bone turnover)

98
Q

What is the most frequent cause of osteomalacia?

A

Deficiency of vitamin D and calcium in the diet.

99
Q

What is the etiology of osteoarthritis?

A

Etiology is poorly understood.

Thought to be d/t excessive wear of weight-bearing joints (hip, knee and spine)

100
Q

What can trigger gout?

A

Diet (high purine)
Injury
Other stress

101
Q

Look at negative feedback of thyroid gland

A

MIGHT BE IMPORTANT

102
Q

Primary Hypothyroidism

A

Direct dysfunction of the thyroid.

Thyroid can’t produce amount of hormones the pituitary gland calls for.

103
Q

Secondary Hypothyroidism

A 
Defects in TSH production such as:
Head trauma
Brain infections
Brain neoplasm
Neurosurgery
Cranial irradiation
104
Q

Early Symptoms of Hypothyroidism include

A

General Weakness
Muscle Cramps
Dry Skin

105
Q

More severe symptoms of hypothyroidism include

A 
Lethargy
Poor memory
Decreased appetite
Slurred speech
Bradycardia
Weight gain
Constipation
Decreased sense of taste and smell
Intolerance to cold environments
Facial edema (periorbital)
Goiter
106
Q

Thyroid Storm (Thyrotoxic Crisis)

A

Life-threatening form of hyperthyroidism.

107
Q

Symptom of Thyroid Storm

A 
High fever
Cardiovascular effects (tachycardia, CHF, angina, MI)
CNS effects (agitation, restlessness, delirium, progressing to coma)
Hepatic dysfunction
Severe diarrhea (may lead to electrolyte imbalance and dehydration)
108
Q

Cushing’s disease is caused by

A

A tumor or excess growth (hyperplasia) of the pituitary gland.

109
Q

Cortisol

A

Normally released during stressful situations.
Controls the body’s use of carbs, fats and proteins.
Also reduces the immune system’s response to swelling (inflammation).

110
Q

What is the role of calcium in maintaining homeostasis?

A

-Critical to proper function of the nervous, muscular and cardiovascular systems.

NURS 320 (28 decks)

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