1. DISORDERS OF THE THYROID AND PARATHYROID GLANDS

2. HYPERTHYROIDISM ETIOLOGY/PATHOPHYSIOLOGY
Also called Graves’ disease, or exophthalmic goiter, or thyrotoxicosis
DUE TO: Overproduction of the thyroid hormones T3 and T4  Exaggeration of metabolic processes
Collective term for a condition marked by increased thyroid activity and overproduction of thyroid hormones thyroxine (T4) and triiodothyronine (T3)
Thyroid gland itself may be enlarged
Variations are:
Graves disease (most common)
Parry’s disease
Thyrotoxicosis
Graves disease generally affects females more than males but tends to affect males more severely
Highest incidence in the 20- to 40-year-old group
Autoimmune disorder
TSIs bind with TSH receptors and abnormally stimulate thyroid functioning

3. HYPERTHYROIDISM ETIOLOGY/PATHOPHYSIOLOGY cont. Exact cause unknown
Possible genetic factors with precipitive factors of:
Infection, ↓ iodine, or extreme physical or emotional stress
Affects females more than males
May occur during adolesence or pregnancy

4. HYPERTHYROIDISM CLINICAL MANIFESTATIONS:
Edema of the anterior portion of the neck
Exophthalmos (bulging eyeballs)
SUBJECTIVE ASSESSMENT : Pt. C/o:
Inability to concentrate; memory loss
Dysphagia
Hoarseness
Increased appetite
Weight loss, insomnia
Nervousness, jittery, excitable
Manifestations include two obvious physical changes:
Thyroid may enlarge 3 to 4 times its normal size (goiter)
Accumulation of orbital fluid behind the eyeball forcing protrusion (exophthalmos)
Increased thyroid production leads to increased metabolic rate which leads to:
Weight loss despite increased appetite
Fatigue
Poor tolerance to heat
Profuse perspiration
Client is very nervous leading to:
Restlessness
Irritability
Difficulty concentrating
Emotional liability
Mood swings
Possible personality changes
Sleep disturbances
Client may have:
Fine tremors of the fingers and tongue
Shaky handwriting
Clumsiness
Trouble climbing stairs
Dyspnea on exertion and possibly at rest
Skin is warm and moist with a velvety texture; may be a characteristic salmon color
Hair is fine, soft, prematurely gray; increased hair loss
Nails appear fragile with onycholysis
May be general or local muscle atrophy and acropachy
There is tachycardia (160 beats/minute; down to 80 during sleep); pulse pressure is widened
May be muscular weakness and atrophy, osteoporosis, and paralysis
May be vitiligo (milky white patches on skin)
Decreased libido, impaired fertility, and gynecomastia (abnormal enlargement of one or both breasts in males)
Diagnostic tests generally include TSH, T3, T4, radioactive iodine uptake, thyroid scan
A major complication is thyrotoxic crisis, also called thyroid storm
Medical emergency that can lead to cardiac, hepatic, or renal failure
Can be precipitated by stressful situation such as surgery, infection, or trauma
Less common causes include cerebrovascular accident, myocardial infarction, etc.
Any of these events can lead to overproduction of thyroid hormone causing:
Increase in systemic adrenergic activity
Overproduction of epinephrine and severe hypermetabolsim leading to:
Rapid cardiac, gastrointestinal, and sympathetic nervous system decompensation
Severe and rapid manifestations exhibited
If nurse suspects thyrotoxic crisis, physician must be informed immediately
Client is transferred to ICU; monitored for:
Vital signs
EKG pattern
Cardiopulmonary status
Temperature
Antithyroid therapy begun immediately

5. EXOPTHALMUS
Internet picture

6. HYPERTHROIDISM

7. HYPERTHROIDISM CLINICAL MANIFESTATIONS OBJECTIVE ASSESSMENT
Tachycardia; hypertension; bruit over thyroid
Warm, flushed skin
Fine hair
Amenorrhea
Elevated temperature/heat intolerance
Diaphoresis
Hand tremors, clumsiness
Hyperactivity for some

8. HYPERTHYROIDISM DIAGNOSTIC TESTS Confirmed by: ↓ TSH and ↑ Free T4
RAIU – radioactive iodine uptake – uptake of 35-95% of the drug

9. HYPERTHYROIDISM Meds reduce symptoms in 6-8 wks.
MEDICAL MANAGEMENT
Medications – Block production of thyroid hormone
Propylthiouracil / PTU
Methimazole/ Tapazole
Meds reduce symptoms in 6-8 wks.
Goal is to decrease excessive thyroid production; can be a combination of treatment methods
First method is to administer antithyroid meds (usually a temporary solution)
Radiation therapy
Most accepted method is oral administration of radioactive iodine (liquid or capsule)
Most commonly used for women past reproductive years or who do not want children
If of reproductive age, consent needs to be signed as small amounts could lodge in gonads
Antithyroid meds should be stopped 4 to 7 days prior to treatment
Inform physician of amiodarone hydrochloride use as it contains large amounts of iodine
Oral 131I should not be given to client with severe vomiting or diarrhea
This method involves a single dose of 131I orally
Destroys some iodine concentrating cells that produce the thyroxine
Clinical manifestations decrease in about 3 weeks
Effected fully in about 3 months
Some may require a second or third dose
Safety: Radioactive Iodine
No pregnant nurse should care for client
Client should expectorate carefully for the first day since saliva is radioactive
Drink plenty of fluids for 2 days to help circulate and eliminate iodine
Toilet should be flushed at least twice after each use during hospitalization
Disposable eating utensils should be used
Close contact with children or pregnant women should be avoided for a week afterward
Women should avoid pregnancy for 6 months
Thyroid hormone antagonist usually resumed 3 to 5 days after 131I therapy until physician determines thyroid to be atrophic (decreased size)
Client may continue to take propranolol hydrochloride (Inderal) for tachycardia, tremor, diaphoresis
Client requires continued monitoring of thyroid hormone blood levels and physical condition
Most common complication is hypothyroidism
Occurs about 2 to 4 months after treatment
Client placed on thyroid replacement therapy, generally for life
Surgical
Generally just a portion of the thyroid gland is removed
Remaining tissue should provide adequate amounts of hormones
A total thyroidectomy may be performed
Most expensive option with most risks
May be done for respiratory obstruction by a goiter or cancer
Lifetime thyroid replacement therapy required
Pre-op, client should be given explanations concerning activities after surgery
Neck incision with drain
May experience sore throat, hoarseness
Medications given up to 6 weeks prior to surgery
Thyroid function tests and EKG as baseline information prior to surgery
Post-op, client placed in high-Fowler’s position to promote venous drainage
Client should support head with a hand when moving to prevent strain on incision
Respiratory problems may occur
Respiratory obstruction can be a result of:
Tracheal collapse
Tracheal mucous accumulation
Laryngeal or local tissue edema
Tracheotomy tray or tubes may be kept at bedside in case of emergency
Since thyroid so vascular, check drainage frequently
Expect about 50 cc of drainage first day
If no drainage, check for obstruction of tubing
Nurse should encourage voice rest for 48 hours
Check voice every 2 to 4 hours to make certain there’s no laryngeal nerve damage
Blood calcium levels must be monitored in case of accidental removal of parathyroid glands
Analgesics administered as needed
Complications of thyroidectomy are:
Respiratory distress and hemorrhage
Damage to laryngeal nerves affecting voice
Thyroid storm (rare)
Tetany can occur up to 10 days after surgery:
Sharp flexion of wrist and ankle joints
Muscle twitchings
Cramps (decreased blood calcium)
Pharmacological
Several drugs may be used for antithyroid therapy
Propylthiouracil (PTU) is used frequently, especially for thyroid storm
OTC meds must be checked for iodine
Avoid foods high in iodine (shellfish, iodized salt)
Drugs may be administered up to 2 years
May cause agranulocytosis (decreased number of granulocytes)
Methimazole (Tapazole) is another preparation; does not have as much consistency in effect
Iodine preparations may be given; take effect in 2 days
Inderal may be prescribed to counteract tachycardia and peripheral effects of hyperthyroidism
Clients should not smoke
Abrupt withdrawal can cause hypertension, myocardial ischemia, cardiac arrhythmias
Isotonic eye drops may be ordered for exophthalmos
Corticosteroids help reduce exophthalmos
Antithyroid drugs given during thyrotoxic crisis
Diet
May require 4,000 to 5,000 calories a day due to greatly increase metabolic rate
Need for increased proteins, vitamins, and minerals
In addition to 3 meals a day, additional meals or snacks needed
Encourage fluids; avoid caffeine
Nursing Management
Provide high-calorie diet & snacks throughout the day
Keep client’s skin dry & clean, change gown & linens as needed
Pre Op –
Teach client how to support his head while turning or sitting or standing position
Inform client that “voice rest” may be enforced for 48 hours and provide paper & pencil for writing notes
Post Op –
Keep bed in semi-Fowler’s position with head and shoulders supported by pillows
Keep suction equipment and tracheotomy tray in client’s room
Inspect dressing, sides and back of neck, and shoulders frequently for bleeding
Watch for signs of internal bleeding
Watch for signs of tetany and for signs of edema in the operative area

10. HYPERTHYROIDISM Radioactive iodine/ ablation therapy
MEDICAL MANAGEMENT
Medication may be followed by:
Radioactive iodine/ ablation therapy
Destroys some of the hypertrophied thyroid tissue
Low dose – no “radiation” precautions needed

11. HYPERTHYROIDISM MEDICAL MANAGEMENT cont.
Radioactive iodine/ Ablation therapy cont.
Outcome: in most pts.  hypothyroidism treat with Levothyroxine
Adequate medical supervision follow up is important!

12. HYPERTHYROIDISM MEDICAL MANAGEMENT cont.
Surgery: for pts. who cannot tolerate antithyroid drugs; are not good candidates for radiation tx.; have a poss. malignancy; or have large goiters causing tracheal compression
Most common surgery: Subtotal Thyroidectomy
Removal of 5/6ths of the thyroid gland
If too much thyroid tissue is removed  gland will not regenerate hypothyroidism

13. HYPERTHYROIDISM MEDICAL MANAGEMENT cont.
Surgery: usually delayed until pt in a normal thyroid state d/t the risk of bleeding during surgery and thyroid crisis (thyroid storm) post op.

15. HYPERTHYROIDISM NURSING ASSESSMENT AND INTERVENTIONS:
Post-operative Subtotal Thyroidectomy
Assess for s/sx internal or external bleeding
Assess for tetany:
Chovstek’s Sign: is + when abnormal spasm of facial muscles occurs when elicited by light tapping on facial nerve in the pt. with low calcium
Trousseau’s Sign: is + if there is carpal spasm in the hypocalcemic and hypomagnesemia pt. When BP cuff inflated above pt. normal systolic pressure and held there for 3 min.
(3 min 5 sec)
(9 min 49sec)

16. HYPERTHYROIDISM NURSING ASSESSMENT AND INTERVENTIONS:
Post-op Subtotal Thyroidectomy (cont.)
Assess for Thyroid Crisis/Storm
May occur as a result of manipulation of the thyroid gland during surgery releasing large amts of thyroid hormone  bloodstream
Occurs within the first 12 hrs.
S/SX: exaggerated s/sx of hyperthyroidism + n/v, severe tachycardia, severe HTN, severe hyperthermia (106F+), extreme restlessness, dysrhythmias, delirium, heart failure  death
min 38 sec)Thyroid Storm part 1
(5 min 47 sec) Thyroid Storm part 2

17. HYPERTHYROIDISM Thyroid Storm cont.: DIAGNOSTIC TESTS ↑FT4, ↓TSH
MEDICAL MANAGEMENT goals during thyroid storm:
1. induce a normal thyroid state
2. prevent cardio-vascular collapse
3. prevent ↑ hyperthermia

18. HYPERTHYROIDISM NURSING ASSESSMENT AND INTERVENTIONS:
Post-op Subtotal Thyroidectomy (cont.)
Voice rest x48 hrs – provide communication tool
Voice checks – q 2-4 hrs. “ahh”; note hoarseness or other changes
Bed – semifowler’s position; pillow support for head and shoulders

19. HYPERTHYROIDISM NURSING ASSESSMENT AND INTERVENTIONS:
Post-op Subtotal Thyroidectomy (cont.)
Avoid hyperextension of neck; support head during position change
Reinforce DB exercises; check with MD re: coughing
Tracheotomy tray at bedside and suction
Cool mist humidifier prn
Nutrition care – watch for dysphagia

20. HYPERTHYROIDISM NURSING DIAGNOSES: Pre-op
Risk for hyperthermia, related to increased metabolism
Imbalanced nutrition:less than body requirements r/t increased metabolism
Post-op
Impaired swallowing, r/t edema
Ineffective breathing,risk for, r/t post-op edema and pain

21. HYPERTHYROIDISM PATIENT EDUCATION
Post op:
follow up with medical supervision
Thyroid function tests
Care incision site
Diet: high calorie, CHO’s , and protein
PROGNOSIS: normal life with appropriate medical or surgical tx.
Expophthalmos may remain to lesser degree

22. HYPOTHYROIDISM Etiology/pathophysiology
Due to insufficient secretion of thyroid hormones
Decreased hormones cause slowing of all metabolic processes
R/T Failure of thyroid or insufficient secretion of thyroid-stimulating hormone from pituitary gland
Hashimoto talks: (Just to be funny-hehe)
Personal Story (5 minutes)
Metabolic processes decreased because of deficient thyroid hormone
Termed primary if solely a dysfunction of the thyroid
Secondary if gland not stimulated to produce normally or if target cells fail to respond
More common in females than males
Significant increase in incidence between 30 to 60
CRETINISM
Congenital condition due to lack of thyroid hormones
Causes defective physical development and retardation
Occurs in about 1 of 3,000 live births
Rare in the U.S. and tested by T4
MYXEDEMA
Severe hypothyroidism in adults
Variety of abnormalities lead to decreased hormone production including:
Surgery or irradiation
Hashimoto’s thyroiditis (chronic autoimmune)
Inflammatory conditions

23. HYPOTHYROIDISM Myxedema refers to severe hypothyroidism in adults
Will see edema in hand’s face, feet, and periorbital tissues
Inflammation and thickening of the skin
Cretinism – congenital hypothyroidism
Floppy infant
Thick,protruding tongue
Poor feeding
Choking episodes
Constipation
Prolonged jaundice
Short stature
Depression
Loss of hair
Rough voices
Swollen eyelids
 Hearing problem
Fatigue
Weight gain
Clinical manifestations are vague and varied
Develop slowly over a period of time; primarily related to reduced metabolic rate

25. HYPOTHYROIDISM Clinical Manifestations:
Because all metabolism processes slow 
Hypothermia; intolerance to cold
Weight gain
ASHD/CAD  ↓exercise tolerance + dyspnea on exertion

26. HYPOTHYROIDISM SUBJECTIVE ASSESSMENT:
Mental and emotional assessment may include:
Depression; paranoia
Impaired memory; slow thought process
Hearing/speech impairment
Lethargic, forgetful, irritable
Anorexia
Constipation
Cold intolerance
Decreased libido; reproductive difficulties

27. HYPOTHYROIDISM OBJECTIVE ASSESSMENT Menstrual irregularities
Thin hair, falls out
Skin thick and dry
Enlarged facial appearance
Low, hoarse voice
Bradycardia
Hypotension
Weakness, clumsiness, ataxia
Diagnostic tests generally include TSH, T3, T4, radioactive iodine uptake, thyroid scan
Complications effect almost every system including cardiovascular, gastrointestinal, sensorineural, psychiatric, etc.
Myxedema coma or hypothyroid crisis is a serious complication; life threatening; characterized by:
Severe metabolic disorders
Hypothermia
Cardiovascular collapse leading to coma
Gradual onset but triggered by severe stress (infection, exposure to cold, trauma)
Can be caused by withdrawal of thyroid meds or use of narcotics, sedatives, or anesthetics
Must be reported to physician immediately
Client moved to ICU and monitored closely
Often fatal

29. HYPOTHYROIDISM
Diagnostic tests : TSH, T3, T4, FT4 (low levels of these are the underlying stimuli for TSH)
For hypothyroidism: expect ↑TSH (compensatory); ↓T3, T4, and FT4
Thyroid replacement therapy lasts a lifetime
Thyroid (Armour Thyroid) is a natural form
Levothyroxine sodium (Levothroid, Sythroid) is synthetic
Thyroid hormone begins slowly with dosage increased every 2 to 3 weeks until desired response achieved
Given in the morning to prevent insomnia
Dosage adjusted for diabetics; blood sugar must be closely monitored
Anticoagulant therapy and digitalis preparations potentiated by thyroid hormone
Due to impaired metabolic rate, may be difficulty in metabolizing meds
Other drugs may impair synthesis of thyroid hormone
Diet
Avoid foods high in iodine or that interfere with treatment:
Dried kelp
Shellfish
Iodized salt
Saltwater fish
Cabbage
Turnips
Pears and peaches
High-fiber, high-protein, low-calorie diet is given
Decrease sodium to prevent fluid retention
Dietary consultation for meal planning and a list of foods to avoid should be provided to client
Nursing Management
Prevent client fatigue by providing rest periods between activities
Provide high-fiber diet, encourage intake of oral fluids
Administer stool softener, bulk laxative, or enema as ordered
HASHIMOTO’S THYROIDITIS
Autoimmune disease characterized by production of antiperoxidase antibodies which destroy an essential enzyme necessary for production of T3 and T4
Occurs more often in females, between 30 and 50
Shows a marked hereditary pattern
Increased incidence with Down and Turner syndromes
Clinical manifestations include:
Enlarged thyroid with lumpy surface
Goiter is asymptomatic but could cause dysphagia and feeling of local pressure
Thymus gland also enlarged
Other manifestations similar to hypothyroidism
Thyroid hormone replacement therapy is the treatment
Chronic disorder, incurable; lifetime therapy

30. HYPOTHYROIDISM MEDICAL MANAGEMENT
Medications: replacement therapy; titration needed
Synthroid
Levothyroid
Proloid
Cytomel
Symptomatic treatment

31. HYPOTHYROIDISM NURSING INTERVENTION/PT. TEACHING:
For the hospitalized pt. with severe hypothyroidism  focus on symptom relief
Watch for s/sx hyperthyroidism while adjusting doses of replacement medication
Watch for chest pain or dyspnea
Keep room 70-74⁰F
Avoid the pt. getting chilled
BM monitor/protocol

32. HYPOTHYROIDISM NURSING INTERVENTIONS/PT. TEACHING cont.
Diet : ↑protein, fiber, fluid
↓ calories
Adequate iodine intake
Instruct pt. to take med daily and not to stop without consulting his MD
Instruct pt./family – to anticipate clearing of mental slowness as pt. adjusts to dose of med

33. HYPOTHYROIDISM NURSING DIAGNOSES:
Decreased cardiac output r/t decreased metabolism
Constipation r/t decreased peristalsis
Risk for noncompliance r/t therapy
Risk for disturbed body image, r/t altered physical appearance (goiter)

34. HYPOTHYROIDISM
PROGNOSIS: Pt. will do well with medication and medical supervision.
In children, if the T4 replacement begins before the epiphyseal fusion, chance for normal growth is greatly improved
(Hypo/hyper/goiter symptoms & treatment 4 min 3 sec)

35. SIMPLE (COLLOID) GOITER
ETIOLOGY/PATHOPHYSIOLOGY
Enlarged thyroid due to low iodine levels or the gland’s inability to use the iodine properly
Enlargement is caused by the accumulation of colloid in the thyroid follicles
When blood level of T3 is too low to signal the pituitary gland to reduce TSH secretion, the thyroid gland responds by increased formation of thyroid globulin (colloid)  accumulates in the thyroid follicles  gland enlargement
Usually caused by insufficient dietary intake of iodine  overgrowth of thyroid tissue
Enlargement of thyroid unrelated to inflammation or neoplasm
Three types of goiter:
Diffuse toxic goiter found in hyperthyroidism
Can be moderate or massively enlarged
Varies from soft to firm and rubbery; generally feels smooth
Frequently associated with exophthalmos
Simple nontoxic goiter develops when thyroid is unable to utilize iodine properly or in response to a low iodine level in the blood
More common in females
Develop during times of great metabolic demands such as adolescence or pregnancy
Large goiter can compress the esophagus or trachea causing dysphagia
Dizziness and syncope may occur if goiter impairs venous return from head and neck
Diagnosis based on history, clinical manifestations, results of thyroid tests
Treatment concentrates on cause
Thyroid hormone replacement therapy
Iodine supplements
Surgery when respiration or swallowing impaired or for cosmetic effect
Third type is nodular goiter
Palpation reveals multiple nodules causing the enlargement
Frequent in females over 40
Usually asymptomatic
Treatment varies with age and manifestations

36. GOITER

37. SIMPLE (COLLOID) GOITER
CLINICAL MANIFESTATIONS/ASSESSMENT
Assessment based on physical manifestations:
SUBJECTIVE ASSESSMENT:
Enlargement of the thyroid gland
Pt. emotional response to the enlargement
Interview to determine pt. need for medication, diet, and medical follow up
May c/o: Dysphagia, Hoarseness. Dyspnea

38. SIMPLE (COLLOID) GOITER
CLINICAL MANIFESTATIONS/assessment
OBJECTIVE DATA:
Assess increase of goiter
Voice changes
Adequate food/fluid intake
MEDICAL MANAGEMENT
Potassium iodide
Diet high in iodine
Surgery—thyroidectomy

39. SIMPLE (COLLOID) GOITER
NURSING INTERVENTIONS/GOALS
Post Thyroidectomy: prevent complications such as bleeding, tetany, and thyroid crisis
Interventions: (discussed previously)
NSG. DIAGNOSES
Risk for non-compliance with therapeutic regimen
Risk for disturbed body image r/t physical appearance

40. Figure 51-10
Simple goiter.

41. Thyroid Cancer ETIOLOGY/PATHOPHYSIOLOGY CLINICAL MANIFESTATIONS
Malignancy of thyroid tissue; rare
About 75% are papillary well-differentiated adeno carcinoma- grows slowly, usually contained, doesn’t spread beyond adjacent lymph nodes; cure rates are excellent.
CLINICAL MANIFESTATIONS
Firm, fixed, small, rounded mass or nodule on thyroid
Benign thyroid cyst and adenoma are firm, encapsulated, noninvasive, slowly growing neoplasms of unknown etiology
Diagnosis done by needle biopsy
Growths do not affect thyroid function (non-functioning) so no treatment other than continued monitoring
Functioning adenoma is treated by radioactive iodine or surgery
CANCER OF THE THYROID
Rare and occurs in all age groups
Susceptible with radiation therapy to the neck
Four major types:
Papillary carcinoma is most common.
More common in females of childbearing age
Well-differentiated, grows slowly
Usually contained; does not spread beyond adjacent lymph nodes
Cure rate after thyroidectomy is excellent
Follicular carcinoma metastasizes to regional lymph nodes and spreads through blood vessels to:
Bone, liver, lungs
Very low cure rate
Medullary carcinoma is a solid carcinoma associated with pheochromocytoma
Curable if detected before signs and symptoms occur
Without treatment, metastasizes quickly to bones, liver, kidneys
Anaplastic or undifferentiated carcinoma resists radiation
Almost never curable by resection
Metastasizes rapidly
Generally causes death by invasion of the trachea and adjacent structures
Generally affects those over 60
Several risk factors:
Radiation exposure
Prolonged secretion of TSH from radiation or heredity
Familial disposition
Chronic goiter
First clinical manifestation is a painless lump
It enlarges destroying the thyroid leading to manifestations of hypothyroidism
Although rare, tumor could cause excessive thyroid hormone production
Thyroid scan shows “cold” nodule (decreased uptake of 131I) for papillary carcinoma
Follicular carcinoma and benign adenomas show a “hot” nodule
Thyroid function tests are usually normal
Needle biopsy may be done to confirm diagnosis
Medical-Surgical Management
Surgical
All carcinomas can be treated with surgery
Radioactive iodine or external radiation therapy may also be used
Response depends on early diagnosis and treatment
Treatment may be used individually or in combination
Client care is the same as for hyperthyroidism
Pharmacological
Exogenous thyroid hormone may suppress thyroid activity
To increase tolerance to surgery, simultaneous exogenous thyroid hormone and adrenergic blocker may be prescribed
With widespread metastasis, cancers will be treated with neoplastic chemotherapy
Nursing Management
Nurse will:
Monitor client’s level of anxiety
Encourage discussion of feelings about diagnosis and possible surgery
Assist in identifying previously successful coping methods
Teach new coping methods if needed

42. CANCER OF THYROID

43. Thyroid Cancer Assessment SUBJECTIVE ASSESSMENT OBJECTIVE ASSESSMENT
Pt. coping method and support system
Pt. understanding of importance of medical follow up
OBJECTIVE ASSESSMENT
Progressive enlargement of tumor area
Response to 131I tx.
Skin care post radiation

44. Thyroid Cancer DIAGNOSTIC TESTS: MEDICAL MANAGEMENT Thyroid scan
Thyroid function tests
Needle bx.
MEDICAL MANAGEMENT
Total thyroidectomy
Thyroid hormone replacement
If metastasis is present: radical neck dissection; radiation, chemotherapy, and radioactive iodine

45. CANCER OF THE THYROID

46. CANCER OF THE THYROID

47. Thyroid Cancer NURSING INTERVENTIONS/Pt. TEACHING
Per thyroidectomy (previously discusses)
Post op:
Risk for respiratory distress
Risk for laryngeal damage
Bleeding
S/sx hypothyroidism

48. Thyroid Cancer NURSING DX. Pt. Teaching:
Anxiety r/t situational crisis
Ineffective coping r/t personal vulnerability in a crisis
Pt. Teaching:
Proper medical follow up
Monitor thyroid replacement therapy
Proper care of surgical incision

49. PARATHYROID GLANDS
Website written information resource for students:

50. HYPERPARATHYROIDISM ETIOLOGY/PATHOPHYSIOLOGY
ETIOLOGY/PATHOPHYSIOLOGY
Overactivity of the parathyroid glands, with increased production of parathyroid hormone (PTH)
Hypertrophy of one or more of the parathyroid glands (usually in the form of an adenoma)
Also from: CRF, Pyelonephritis, glomerulonephritis
Overactivity of one or more of the parathyroid glands
Results in increased secretion of parathyroid hormone (PTH) causing calcium to leave bones and accumulate in blood
Occurs twice as often in postmenopausal females than males
Occurs frequently between ages of 35 and 65
Hypercalcemia may occur from excessive intake of thiazide diuretics, vitamin D, or calcium supplements
X-rays show skeletal decalcification
Blood PTH and alkaline phosphate levels increased
Serum calcium level elevated
Termed primary if enlargement of one or more glands increase secretion of PTH (increases blood calcium)
Most common cause is adenoma
Other causes include genetics or multiple endocrine neoplasms
Termed secondary if excess compensatory production of PTH
Stems from hypocalcemia-producing abnormality other than parathyroid gland including:
Rickets
Chronic renal failure
Vitamin D deficiency
Osteomalacia due to laxative abuse or phenytoin (Dilantin)
Many are asymptomatic; however there are several clinical manifestation:
Polyuria
Chronic low back pain
Bone tenderness
Renal calculi
May also experience nausea, vomiting, anorexia, constipation, lethargy, drowsiness
Changes in level of consciousness
Disorientation
Stupor
Coma
Personality changes
Loss of initiative and memory
Marked muscle weakness and atrophy, etc.
Without treatment there can be permanent damage to skeleton or kidneys
There can be bone and articular problems
Renal complications
Stone formations in various organs
Cardiac or vascular problems
CNS changes

52. HYPERPARATHYROIDISM CLINICAL MANIFESTATIONS
Hypercalcemia – primary clinical manifestation
Calcium leaves the bone  serum calcium increases
Bones become demineralized  formation of renal calculi, pathological fx.
Skeletal pain; pain on weight-bearing

53. HYPERPARATHYROIDISM SUBJECTIVE ASSESSMENT
As a result of neuromuscular dysfunction, pts. c/o:
Fatigue, drowsiness
nausea, anorexia;
severe skeletal pain, muscle weakness
constipation
personality changes, disorientation

54. HYPERPARATHYROIDISM OBJECTIVE ASSESSMENT Skilled observation for:
Skeletal deformity
Abnormal movement
Urine results
Vomiting, weight loss
HTN
Cardiac dysfunction
Bradycardia
↓ LOC

55. HYPERPARATHYROIDISM DIAGNOSTIC TESTS RADIOGRAPHS/XRAYS
PTH blood level (usually ↑)
Ca++ levels
Bone Density measurements
MRI, CT, and US to localize an adenoma

58. Hyperparathyroidism

59. HYPERPARATHYROIDISM MEDICAL MANAGEMENT
Removal of tumor
Removal of one or more parathyroid glands
Autotransplantation
NURSING INTERVENTIONS/Pt. TEACHING
Assess for hypercalcemia
Restore fluid and electrolyte imbalance
Diet: low in calcium
Medical
Management aimed at decreasing overactivity of parathyroid glands
Accomplished by med therapy or surgery
If severe renal involvement, dialysis may be required
Surgical
Primary type can be treated by surgical removal of three and one half of the four parathyroid glands
Can relieve bone pain but may not reverse renal damage
Pre-op care includes:
Explanations
Encouraging fluids
Limiting calcium intake
Administering meds to lower blood calcium
Post-op care involves administration of magnesium or phosphate
Client may receive calcium supplements for several days
Nursing care is similar to thyroidectomy
Major complication is airway obstruction
Pharmacological
Aimed toward correcting secondary hyperparathyroidism
Meds geared to decreasing calcium level in blood
Includes use of diuretics such as furosemide (Lasix) and ethacrynic acid (Edecrin)
Phosphate-based drugs lower calcium level
Nursing Management
Pre Op –
Encourage oral fluid intake
Strain urine for calculi
Offer cranberry juice to acidify the urine
Post Op –
Assess for signs of hypocalcemia
Teach client principles of good body mechanics
Reassure client that bone pain will gradually disappear
Encourage mild exercise as ordered

60. HYPERPARATHYROIDISM NURSING INTERVENTIONS/Pt. TEACHING cont.
Postoperatively, assess for hypocalcemia
Tetany, cardiac dysrhythmia, carpo-pedal spasms
Pain management – skeletal, renal stones
NURSING DIAGNOSES
Activity intolerance r/t neuromuscular dysfunction
Acute pain r/t skeletal – joint pain, renal colic

61. HYPERPARATHYROIDISM PATIENT TEACHING
Body mechanics to prevent pathological fx
Mild exercise
Urine checks for blood and stones
PROGNOSIS: can lead a normal life with proper med-surg tx. With cancer dx. – prognosis is poor

62. http://www.youtube.com/watch?v=E9QvAdxeap0 (2 min 42 sec)
HYPOPARATHYROIDISM
(2 min 42 sec)
Etiology/pathophysiology
Decreased parathyroid hormone  Decreased serum calcium levels
Most common causes:
Inadvertent removal or destruction of one or more parathyroid glands during thyroidectomy
Also, can be autoimmune or familial in origin
Results from a deficiency of parathyroid hormone (PTH) secretion by the parathyroids or the decreased action of peripheral PTH
Results in decreased serum calcium level
Can be acute or chronic
If idiopathic, may be result of autoimmune disorder or congenital absence of parathyroid glands
Acquired hypoparathyroidism is generally irreversible
Most common cause is accidental removal during thyroid or other neck surgery
Reversible types as well
Classic sign is tetany (muscle spasms and tremors caused by lack of calcium)
Some other clinical manifestations include:
Dry skin
Brittle hair; alopecia
Stained, cracked, decayed teeth (weak enamel)
Personality or EKG changes, etc.
Two diagnostic assessment tests:
Chvostek’s sign
Trousseau’s sign
Expected test results include:
Decreased serum calcium
Increased urinary calcium
Increased serum phosphorus
Decreased urinary phosphorus
Complications related to long-standing hypocalcemia
Leads to decreased heart contractility leading to cardiac failure
May be cataract formation, papillary edema, bone deformity

63. HYPOPARATHYROIDISM CLINICAL MANIFESTATIONS Lab results show:
↓serum Ca++ and ↑ serum phosphorus  Neuromuscular hyperexcitability
Involuntary and uncontrollable muscle spasms
Hypocalcemic tetany

64. HYPOPARATHYROIDISM CLINICAL MANIFESTATIONS cont. Severe hypocalcemia:
Laryngeal spasms
Stridor
Cyanosis/asphyxia
Parkinson-like syndrome
Chvostek’s and Trousseau’s signs

65. TROUSSEAU’S SIGN

66. HYPOPARATHYROIDISM ASSESSMENT
SUBJECTIVE DATA – evidence of and/or c/o:
Dysphagia
Numbness/tingling lips, fingertips
Increased muscle tension
Parasthesis and stiffness
c/o anxiety, irritability, depression
Headaches
nausea

67. HYPOPARATHYROIDISM ASSESSMENT OBJECTIVE DATA
+ Chvostek’s and Trousseau signs
Laryngeal spasm, stridor, cyanosis
Decreased cardiac output, dysrhythmias
Tetany

68. HYPOPARATHYROIDISM DIAGNOSTIC TESTS Serum PTH, Phosphorus, Calcium
Urinary calcium and phosphorus
 if + for hypoparathyroidism, results will be:
↓ PTH, and serum Ca++ and ↑ urinary Ca++, with
↑ serum phosphorus and ↓ urinary phosphorus

69. HYPOPARATHYROIDISM MEDICAL MANAGEMENT Blood tests r/t ca levels
Calcium gluconate or calcium chloride will be given IV for hypoparathyroid tetany
NURSING: if IV rate is too rapid  ↓ BP, serious cardiac dysrhythmias/ cardiac arrest
IV may be irritating to vessel wall; watch for s/sx extravasation
EKG monitoring
Vitamin D orally – improves GI absorption of Ca++
Calcium gluconate or calcium chloride may be given intravenously
Too rapid IV calcium infusion can cause cardiac arrest
May be given orally after initial IV dose
Unless reversible, lifelong calcium replacement required
Vitamin D may be given to assist in calcium absorption
Best sources of calcium are from the diet
Advise that calcium may cause digitalis toxicity
Diet
Foods high in calcium and low in phosphorus
Asparagus
Broccoli
Collards
Tomatoes
Fruits such as apricots, bananas, cantaloupe, many berries
Kidney and lima beans, brown sugar
Avoid high phosphorous foods: most legumes, nuts, cheeses, seafood
Nursing Management
Monitor for signs of hypercalcemia
Assess for respiratory distress
Provide diet high in calcium-containing foods
Emphasize importance of having blood level of calcium & phosphorus checked

70. HYPOPARATHYROIDISM NURSING INTERVENTIONS Monitor for hypercalcemia:
Vomiting, disorientation, anorexia, abdominal pain, weakness
Assess for:
Respiratory function
VS – bradycardia, syncope, hypotension
Renal involvement

71. HYPOPARATHYROIDISM NURSING INTERVENTIONS cont. Preferred medications:
Hytakerol
Calcitriol (Rocaltrol)
Diet: ↑ dairy, dark green leafy veg., soybeans, tofu, canned fish with bones

72. HYPOPARATHYROIDISM NURSING DIAGNOSES:
Risk for injury r/t postop hypocalcemia
Imbalanced nutrition, less than body requirements, r/t calcium intake
Nearly all interventions r/t ca levels