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Adult Health I Test II > Class Day I > Flashcards

Class Day I Flashcards

1
Q

What is Cushing’s?

A
  • Hypercortisolism
  • Caused by an over secretion of the hormones the adrenal cortex produces
  • Can be the result of a tumor in the pituitary gland resulting in release of the hormone ACTH
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2
Q

what hormones are made by the adrenal cortex?

A
  • Mineralocorticoids: aldosterone increases sodium reabsorption and causes potassium excretion in the kidney
  • Glucocorticoids: cortisol affects glucose, protein, and fat metabolism; the body’s response to stress; and the body’s immune function
  • Sex Hormone: androgens and estrogens
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3
Q

risk factors for Cushing’s

A
  • women ages 20-40 yo
  • endogenous causes of inc cortisol
    • adrenal hyperplasia
    • adrenocortical carcinoma
    • pituitary carcinoma secreting ACTH
  • exogenous causes of inc cortisol
    • organ transplant
    • chemo
    • autoimmune dz
    • asthma
    • allergies
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4
Q

Cushing’s: expected findings

A
  • weakness , fatigue, sleep disturbances
  • Back and joint pain
  • fluid retention: JVD, SOC, crackles, tachypnea, HTN, edema
  • Altered emotional state
  • Decreased libido
  • Evidence of decreased immune function and decreased inflammatory response
  • Thin, fragile skin
  • Bruising and petechiae
  • Hypertension
  • Tachycardia
  • Gastric ulcers due to over secretion of hydrochloric acid
  • Weight gain and increased appetite
  • Irregular menses
  • Dependent edema
  • Fractures (osteoporosis)
  • Bone pain and fractures with an increased risk for falls
  • Muscle wasting
  • Frequent infections, poor wound healing
  • Hirsutism
  • Acne
  • Red cheeks
  • Striae
  • Clitoral hypertrophy
  • Thinning, balding hair
  • Hyperglycemia
  • Emotional liability
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5
Q

Cushing’s: Lab Tests

A
  • Elevated plasma cortisol levels: in the absence of acute illness or stress indicate cushing’s dz. Urine contains elevated levels of free cortisol
  • Plasma ACTH levels: hypersecretion of ACTH by anterior pituitary, disorders of the adrenal cortex or medication therapy results in decreased ACTH levels
  • Salivary cortisol: elevations confirm the diagnosis of Cushings dz
  • Potassium and calcium: decreased
  • Glucose: increased
  • Sodium: increased
  • Lymphocytes: decreased
  • Dexamethasone suppression tests: usually done through 24 hr urine collection
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6
Q

Cushing’s: Diagnostic Procedures

A
  • X-ray, MRI, CT identify lesions of the pituitary, adrenal glands, lungs, GI tract, and pancreas
  • Radiological imaging determines the source of adrenal insufficiency
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7
Q

what occurs with potassium and calcium in Cushing’s? why?

A
  • decreased due to an increase in aldosterone which causes water and sodium retention and potassium excretion
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8
Q

what will we see with WBCs and RBCs in Cushing’s?

A
  • WBCs: inc (leukocytosis)
  • RBCs: inc (polycythemia)
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9
Q

what are the three medications used for Cushing’s?

A
  • Ketoconazole
  • Mitotane
  • Hydrocortisone
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10
Q

Ketoconazole for Cushing’s

A
  • Corticosteroid inhibition
  • Antifungal agent that inhibits adrenal corticosteroid synthesis in high doses
  • Supplements radiation or surgery
  • Monitor liver enzymes
  • Monitor fluids and electrolytes for clients who have gastric effects
  • Can cause N/V, dizziness
  • Only temporary relief - cannot stop taking meds
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11
Q

Mitotane for Cushing’s

A
  • Produces selective destruction of adrenocortical cells
  • Treats inoperable adrenal carcinoma
  • Monitor for indications of shock, renal damage, and hepatotoxicity and orthostatic hypotension
  • Purpose is to reduce the size of the tumor
  • Need lifelong replacement with glucocorticoids
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12
Q

Hydrocortisone for Cushing’s

A
  • For replacement therapy who have adrenocortical insufficiency
  • Monitor potassium and glucose
  • Measure daily weight
  • Monitor BP, HR, manifestations of infections
  • pt needs to carry emergency ID about corticosteroid use
  • Report black or tarry stools
  • Need diet high in calcium and vit D
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13
Q

what therapeutic procedures can be used to help with Cushing’s?

A
  • chemotherapy
  • radiation therapy
  • hypophysectomy
  • adrenalectomy
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14
Q

explain adrenalectomy for Cushing’s

A
  • Surgical removal of the adrenal gland (can be unilateral or bilateral)
  • Provide glucocorticoid and hormone replacement
    • will want to give IV hydrocortisone to prevent problems in surgery, then the pt will need lifelong replacement
  • Monitor for adrenal crisis
  • Monitor bleeding, fluids, electrolytes, bowel sounds
    • bleeding–>distention
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15
Q

what are the 4 complications possible with Cushing’s?

A
  • perforated viscera/ulceration
  • bone frxs due to hypocalcemia
  • infection due to immunosuppression
  • adrenal crisis
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16
Q

explain perforated viscera/ulceration as a complication of Cushing’s

A
  • Decreases production of protective mucus in the lining of the stomach due to an increase in cortisol
  • Monitor for evidence of GI bleed
  • Need antiulcer medications
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17
Q

explain bone frxs due to hypocalcemia as a complication of Cushing’s

A
  • Caution when moving pt
  • Provide assistance when the client is ambulating
  • Encourage diet high in calcium and vit D
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18
Q

explain infection as a complication of Cushing’s

A
  • Occur due to elevated glucocorticoid levels which often cause immunosuppression
  • Monitor subtle indications of infections
  • Minimize exposure to infectious organisms
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19
Q

explain adrenal crisis as a complication of Cushing’s

A
  • Sudden drop in corticosteroids is due to sudden tumor removal; stress of illness, trauma, surgery, or dehydration or abrupt withdrawal of steroids
  • Taper medication
  • Might need more medication for times of stress
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20
Q

discharge teaching for a client with Cushing’s

A
  • explain how to take glucocorticoid replacement medication: 2/3 in the morning and 1/3 in the afternoon (to mimic normal cortisol)
    • do not d/c abruptly
    • teach them that they will have to increase dosage when under stress
  • monitor for signs of immunosuppression
  • monitor weight
  • monitor glucose
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21
Q

What is Addison’s?

A
  • Adrenocortical insufficiency caused by damage or dysfunction of the adrenal cortex
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22
Q

Addison’s: Risk factors

A
  • Primary causes
    • Idiopathic autoimmune dysfunction
    • TB
    • Histoplasmosis
    • Adrenalectomy
    • Cancer
    • Radiation therapy of the abdomen
  • Secondary
    • Steroid withdrawal
    • Hypophysectomy
    • Pituitary neoplasm
    • High dose radiation of pituitary gland or entire brain
  • Acute insufficiency
    • Sepsis
    • Trauma
    • Stress: can be emotional or physical
    • Adrenal hemorrhage
    • Steroid withdrawal
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23
Q

Addison’s: expected findings

A
  • late sign: bronze are to arms, legs, and face
  • Weight loss
  • Craving for salt
  • Hyperpigmentation
  • Weakness and fatigue
  • Nausea and vomiting
  • Abdominal pain
  • Constipation or diarrhea
  • Dizziness with orthostatic hypotension: can occur if BP drops and/or pulse elevates
  • Severe hypotension
  • Dehydration
  • Hyponatremia
  • Hyperkalemia
  • Hypoglycemia
  • Hypercalcemia
  • Manifestations of chronic addison’s dz develop slowly
  • Manifestations of acute adrenal insufficiency develop rapidly
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24
Q

Addison’s: Lab Tests

A
  • Serum electrolytes: increased K, decreased Na, increase Ca
  • BUN and Cr: increase
  • Serum glucose: normal to decreased
  • Serum cortisol: decreased
  • ACTH stimulation test: plasma cortisol remain same or decrease
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25
Q

Addison’s: Diagnostic Procedures

A
  • ECG: assess for ECG changes or dysrhythmias assoc with electrolyte imbalance
  • Xray, CT, MRI: determine source of adrenal insufficiency such as a tumor or adrenal atrophy
26
Q

what are the medications used for Addison’s?

A
  • hydrocortisone/prednisone
  • fludrocortison
27
Q

explain hydrocortisone use for Addison’s

A
  • Adrenocortical replacement for adrenal insufficiency and as anti-inflammatory
    • this is a replacement for mineralocorticoids and glucocorticoids
  • Monitor BP, weights, electrolytes
  • Increase dose during stress
  • Do not abruptly stop
28
Q

explain fludrocortisone use for Addison’s

A
  • Replacement in adrenal insufficiency
  • Monitor weight, BP and electrolytes
  • HTN potential SE
29
Q

what are the complications of Addison’s?

A
  • acute adrenal insufficiency
  • hypoglycemia
  • hyperkalemia/hyponatremia
30
Q

explain acute adrenal insufficiency as a complication of Addison’s

A
  • When an acute drop in adrenocorticoids due to sudden discontinuation of glucocorticoid meds or when induced by severe trauma, infection, stress
  • Insulin and dextrose to move potassium into cells
  • Admin calcium to counteract the effects of hyperkalemia
  • Monitor electrolytes
31
Q

explain hypoglycemia as a complication of Addison’s

A
  • Insufficient glucocorticoid causes increase in insulin sensitivity, and decreased glycogen → hypoglycemia
  • Monitor glucose
  • Need to have carbohydrate snacks easily accessible
32
Q

explain hyperkalemia/hyponatremia as a complication of Addison’s

A
  • Decrease in aldosterone levels can cause an increased excretion of sodium and decreased excretion of potassium
  • Monitor electrolytes and ECG
  • Take meds as directed
33
Q

discharge teaching for Addison’s

A
  • explain how to take glucocorticoid replacement medication: 2/3 in the morning and 1/3 in the afternoon (to mimic normal cortisol)
    • do not d/c abruptly
    • teach them that they will have to increase dosage when under stress
  • monitor for signs of immunosuppression
  • monitor weight
  • monitor glucose
  • teach them S/S of Cushing’s which she could develop from the use of the glucocorticoids
  • should wear a medic alert ID
  • should carry an emergency kit with IM hydrocortisone
34
Q

what is hypothyroidism?

A

Inadequate amount of T3 and T4 causing a decrease in metabolic rate that affects all body systems

35
Q

Hypothyroidism: Risk Factors

A
  • F 30-60 y/o are affected 7-10 times more than M
  • Mild is usually undiagnosed
  • Use of certain meds - lithium and amiodarone
  • Inadequate intake of iodine
  • Radiation therapy to head or neck
36
Q

Hypothyroidism: expected findings

A
  • Usually vague and carried findings that develop slowly over time
  • fatigue/ lethargy
  • Irritability
  • Intolerance to cold
  • Constipation
  • Weight gain without an increase in caloric intake
  • Pale skin
  • Thick, brittle fingernails
  • Depression and apathy
  • Periorbital edema
  • Joint or muscle pain
  • Bradycardia, hypotension, dysrhythmias
  • Slow thought processes and speech
  • Hypoventilation, pleural effusion
  • Thickening of the skin
  • Thinning of hair on the eyebrows
  • Dry, flaky skin
  • Swelling in face, hands, and feet
  • Decreased acuity of taste and smell
  • Hoarse, raspy speech
  • Abnormal menstrual cycle
  • Decreased libido
  • goiter
37
Q

Hypothyroidism: Lab Tests

A
  • T3: decreased
  • Serum TSH: increased with primary hypothyroidism, decreased or within the expected reference range in secondary hypothyroidism
  • Free Thyroxine index and T4 levels: decreased
  • T3 resin uptake: decreased
  • Thyrotropin receptor antibodies: no response
  • Serum cholesterol: increased
38
Q

Hypothyroidism: Diagnostic Procedures

A
  • thyroid scan
  • Radioisotope scan and intake: clients who have hypothyroidism have a low uptake of the iodine preparation
  • ECG: sinus bradycardia, dysrhythmias
39
Q

how to treat hypothyroidism

A
  • Levothyroxine
    • Thyroid hormone replacement therapy
    • monitor HR before you give it to make sure it is not overly therapeutic
    • Increases effects of warfarin and can increase the need for insulin and digoxin
    • 4 hr apart from cimetidine, lansoprazole, Sucralfate, and colestipol
    • Meds can accelerate metabolism: phenytoin, carbamazepine, rifampin, sertraline, and phenobarbital
    • Dosage increase every 2-3 weeks
      • will need lab tests to monitor thyroid H levels
    • Do not stop taking the medication
40
Q

what is a complication of hypothyroidism?

A
  • Myxedema coma:
    • S/S: stuporous, non responsive, ventilatory support needed, bradycardia, hypothermia, dec O2 sats, hypoTN, dec Na and glucose
    • life threatening condition when hypothyroidism is untreated or when a stressor affects a client
    • ensure patent airway, continuous ECG, monitor ABGs
    • continuously monitor the pt’s temperature and I/O
    • will have to administer IV levothyroxine
41
Q

hypothyroidism: nursing considerations

A
  • monitor A&O status b/c if dec, it is a sign of myxedema
  • keep them warm
  • monitor V/S: HR, BP, temp
  • put them on telemetry to monitor HR
  • monitor edema, bowel sounds
  • inc fluids, movement, and fiber
42
Q

hypothyroidism: discharge teaching

A
  • take levothyroxine 30-40 min before eating, on an empty stomach
  • teach S/S of hypo and hyperthyroid
  • f/u is vital: need labs Q2-3 weeks to adjust meds
    • start low and slow with levothyroxine so you don’t cause hyperthyroid
43
Q

what are the hormones the thyroid produces?

A
  • Thyroid produces T3, T4 and calcitonin
  • T3 and T4 secreted from anterior pituitary through negative feedback
  • Calcitonin inhibits mobilization of calcium from bone and reduces blood calcium levels
44
Q

what is hyperthyroidism?

A
  • clinical syndrome caused by excessive circulating thyroid hormone. This exaggerates normal body functions and produces a hypermetabolic state
45
Q

hyperthyroidism: risk factors

A
  • Graves’ disease is the most common cause
  • Autoimmune antibodies result in hypersecretion of thyroid hormones
  • Autosomal recessive trait passed in females
  • Toxic nodular goiter, a less common form of hyperthyroidism is caused by overproduction of thyroid hormone due to nodules
  • Exogenous hyperthyroidism is caused by excessive dosages of thyroid hormones
46
Q

hyperthyroidism: expected findings

A
  • Nervousness, irritability, hyperactivity, emotional lability, decreased attention span, cries or laughs without cause, change in mental or emotional status
  • Weakness, easy fatigability, exercise intolerance
  • Muscle weakness
  • Heat intolerance
  • Weight change (usually loss) and increased appetite
  • Insomnia and interrupted sleep
  • Frequent stools and diarrhea
  • Menstrual irregularities and decreased fertility
  • Libido initially increased in both M and F, followed by a decrease as the condition progresses
  • Warm, sweaty, flushed skin with velvety-smooth texture
  • Hair thins, and develops a fine, soft, silky texture
  • tremor , hyperkinesia, Hyperreflexia
  • Exophthalmos (Graves only) due to edema in the extraocular muscles and increased fatty tissue behind the eye
  • Blurred or double vision and tiring of eyes due to pressure on the optic nerve
  • Photophobia
  • Excessive tearing and bloodshot appearance of eyes
  • Pretibial myxedema: dry, waxy smelling of frontal surfaces of lower legs that resembles benign tumors (graves only)
  • Vision changes
  • Hair thinning and loss
  • Goiter
  • Bruit over thyroid gland
  • Elevated systolic blood pressure and widened pulse pressure
  • Tachycardia, palpitations and dysrhythmias
  • Dyspnea
  • More subtle in older adults
47
Q

hyperthyroidism: lab tests

A
  • Serum TSH test: decreased in the presence of Graves dz → can be elevated in secondary and tertiary hyperthyroidism
  • Free T4 index, T4 (total) T3: elevated in the presence of disease
  • Thyroid - stimulating immunoglobulins: elevated in graves’ disease, normal in other hyperthyroidisms
  • Thyrotropin Receptor antibodies: elevation most indicative of Graves dz
48
Q

hyperthyroidism: diagnostic procedures

A
  • Ultrasound: used to produce images of the thyroid gland and surrounding tissue
  • Electrocardiogram: used to evaluate the effects of excessive thyroid hormone on the heart. ECG changes include Afib, and changes to the P and T waves
  • Radioactive iodine uptake
49
Q

radioactive iodine uptake test for hyperthyroidism

A
  • gold standard for diagnosing hyperthyroidism
  • clarifies size and function of gland
  • contraindicated in pregnant women
    • will have to give every female a pregnancy test
  • must assess iodine or shellfish allergy
  • elevated uptake is indicative of hyperthyroidism
50
Q

what are the classes of medications used for hyperthyroidism?

A
  • thionamides
  • beta adrenergic blockers
  • iodine solutions
51
Q

explain thionamides use in treating hyperthyroidism

A
  • Methimazole and propylthiouracil inhibit production of thyroid hormone
  • Used to treat graves’ dz as an adjunct to radioactive iodine therapy
  • take 1-2 weeks to become therapeutic
  • Monitor for manifestations of hypothyroidism
  • Monitor CBC for leukopenia or thrombocytopenia
  • Monitor for indications of hepatotoxicity
  • Take meds with meals
  • Report jaundice
52
Q

explain beta blockers use in treating hyperthyroidism

A
  • Propranolol, atenolol, and metoprolol treat sympathetic nervous system effects
  • Counteract the effects of increased thyroid hormones but do not alter levels
  • Monitor BP, HR, ECG
  • Monitor for hypoglycemia in clients who have DM
  • Pt needs to check pulse prior to taking the medication
53
Q

explain iodine solutions use in treating hyperthyroidism

A
  • Nonradioactive 5% elemental iodine in 10% potassium iodine that inhibits the release of thyroid hormone
    • will inhibit T3 and T4 release
  • often used to prepare someone for a thyroidectomy
  • Short term use only
  • 1hr after an antithyroid med
  • Contraindicated in pregnancy
54
Q

what are the therapeutic procedures used to treat hyperthyroidism?

A
  • radioactive iodine therapy
  • thyroidectomy
55
Q

explain radioactive iodine therapy as a tx for hyperthyroidism

A
  • tx of choice
  • Destroys some of the hormone producing cells
  • Degree of destruction varies
  • Contraindicated in pregnancy
    • must take a pregnancy test prior to procedure
  • Monitor for hypothyroidism manifestations
  • Effects may not be effective for 6-8 weeks
    • so will need to be on methimazole or PTU while waiting for it to become effective
  • Continue to take meds as directed
  • Stay away from pregnant women and children
56
Q

explain thyroidectomy as tx for hyperthyroidism

A
  • often performed when: thyroid storm emergency, thyroid cancer, large goiter causing airway obstruction
  • Surgical removal of part or all of thyroid gland
  • Incision in the neck with possible drainage
  • Received propylthiouracil or methimazole 4 to 6 weeks before surgery
  • High protein - high carbohydrate diet preop
  • Receives iodine for 10-14 days preop to reduce the glands size and prevent excessive bleeding
57
Q

what are postop considerations with a thyroidectomy?

A
  • Semi-fowlers
  • Monitor vital signs q15 until stable
  • Assist with deep breathing
  • Check surgical dressing for excessive bleeding
  • Monitor for parathyroid damage
    • risk for hypocalcemia
    • can lead to laryngospasm–monitor for stridor
      • would have to administer IV calcium gluconate to make up for low calcium
  • can cause a hoarse voice: if that lasts for more than 5-10 days, then look for laryngeal N damage
58
Q

what are possible complications of hyperthyroidism?

A
  • hemorrhage at incision site
  • thyroid storm
  • hypothyroidism
  • airway obstruction
  • nerve damage
  • hypocalcemia and tetany
59
Q

explain hemorrhage as a complication of hyperthyroidism/thyroidectomy

A
  • Due to loosened surgical tie or excessive coughing or movement
  • Avoid neck flexion and extension
  • Show client how to change position with support of the neck
60
Q

explain thyroid storm

A
  • Results from a sudden surge of large amounts of thyroid hormones into the bloodstream, causing an even greater increase in body metabolism
  • Medical emergency
  • may need to go in and do a thyroidectomy
  • Maintain airway
  • Aspirin is contraindicated
61
Q

explain airway obstruction as a complication of hyperthyroidism/thyroidectomy

A
  • Hemorrhage, tracheal collapse, tracheal mucus accumulation, laryngeal edema, and vocal cord paralysis can cause respiratory obstruction with sudden stridor and restlessness
  • Tracheostomy tray should be kept near pt
  • High fowlers

Adult Health I Test II (3 decks)

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