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48 Cards in this Set

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What substances are secreted in the thyroid gland and by which cells?
Thyroid Hormone is secreted by the follicular cells. C cells secrete calcitonin and somatostatin. Calcitonin=tones down the calcium in the blood serum by inhibiting osteoclasts from breaking down. The thyroid gland will synthesize thyroid hormone when stimulated by the pituitary thyroid-stimulating hormone (TSH), or when drugs interfere with the thyroid's uptake of iodide from the blood, or low serum iodide levels will also stimulate the thyroid gland to produce TH.
Explain the iodide gradient between the blood and the thyroid gland.
The gradient is between 30:1-40:1 so the iodide is moved through active transport into the thryroid gland. The iodide is then oxidized into iodine, which is then facilitated by the enzyme thyroidal peroxidase inside the follicular cells.
Explain the progressional steps in synthesizing TH.
Thyroglobulin (TG) a large glycoprotein synthesized within the follicular cell, is the precursor of thyroid hormones. Soooo TG is released into>>>>colloid>>>iodine combes with tyrosine in the TG>>>>forms iodotyrosines: triiodothyronine (T3) and thyroxine (T4). Thyroxine is converted to T3 which is actually what acts on the cell. There is 90% T4 and 10% T3. Most of thyroxine is bound into TBG or thyroxine-binding globulin or albumin, and the other small amounts are considered biologically free.
Why is the regulation of thyroid secretion considered a complex feedback system?
Because it involves feed back between several components: the hypothalamus, anterior pituitary, and the thyroid gland. It involves a series of negative feedback loops to shut things down get things going.
Identify each of these components and their source: TRH, TH TSH Calcitonin, T4, and T3 and Iodide, Iodine, TG, and TBG.
TRH=Thyroid releasing hormone comes from the hypothalamus, which initiates starts the whole feedback system of the thyroid gland; TH is thyroid hormone which is produced in the follicular cells; TSH is Thyroid stimulating hormone is a glycoprotein stored in the anterior pituitary gland that is triggered by TRH. Calcitonin is produced by parafollicular or Ccells found in the thyroid gland and lowers blood calcium by inhibiting osteoclasts from breaking down; T4 is called thyroxine, one of the hormones made by follicular cells; T3 is called triiodothyronine also made in the colloid of the follicular cells and Iodide=is the precursor to iodine that is moved by active transport from extracellular fluid to the thryoid follicular cells. Iodine is the product of iodide that has been oxidated. TG = Thyroglobulin a large glycoprotein that is also synthesized in the follicular cells that has tyrosine and the tyrosine will combine with the iodine to form the thyroid hormones t3 and t3; TBG= is the carrier of most of thyroid hormone so that most of it is bound and not biologically freely available.
What increases when our bodies are exposed to cold stress and decreased levels of T4 or thyroxine?
TRH or thyroid releasing hormone found in the hypothalamus increases when exposed to these instabilities. Makes sense since our hypothalamus is our thermostat.
What is the function of TH?
Thyroid hormone increased the rate of protein , fat and glucose metabolism and as a result increases heat production and body temperature. Normal linear growth requires TH as does the central and autonomic nervous systems.
Why is the thyroid gland so important?
Necessary for proper functioning of all other hormones, normal maturation of the nervous system, normal G & D
What is the necessary component for synthesis of thyroid hormone, t3 and t4?
Requires iodine
T₄ has 4 iodine atoms & T₃ has 3 iodine atoms
Thyroid cannot make sufficient amount of T₃ & T₄ with iodine deficient diet
Why does a goiter happen in hyperthyroidism?
Well, when there is lack of iodine in the diet there won't be enough t3 and t4 or thyroid hormones made, and when there aren't enough circulating in the blood to feedback and shut off TSH, then TSH will keep coming and stimulating the thyroid gland, this overstimulation causes the growth of a goiter due to the lack of the normal negative feedback that would normally shut off TSH.
What are the things to consider about the thyroid gland in pregnant women?
Pregnancy is a euthyroid state
Slight enlargement of thyroid may be noted by US d/t the action of hCG: human chorionic gonadotropin
Early & sustained  in renal clearance of iodine
Thyroid compensates by enlarging & ↑ plasma clearance of iodine to produce sufficient TH
↑ thyroid stimulation 2° hCG
Normal iodine intake 200 mcg/day encouraged
What are the gerentological considerations for the thryoid gland in the elderly population?
Rate of TH production & degradation ↓’s w/age
Atrophy, fibrosis & nodularity occurs
Hair growth ↓’s
Nails become thick, brittle & yellow
Facial skin sags, bones are more prominent
↓ DTRs; response to ?’s may be slower
What are the pediatric considerations regarding the thyroid gland?
Endocrine system of the newborn is supplemented by maternal hormones via the placenta
Endocrine system less developed at birth than any other body system
Hormonal control of many body functions is lacking until 12-18 months of age
Infants may manifest imbalances in concentration of fluids, electrolytes, amino acids, glucose & trace substances quicker than adult.
Hormonal disturbances during childhood may cause disrupted growth patterns and mental retardation
Congenital hypothyroidism may occur as a result of an absent, or nonfunctioning thyroid gland
What is PTU drug and what does it do?
Propylthiouracil (PTU) is used to manage hyperthyroidism which is due to an overactive thyroid gland. It is considered an anti-thyroid agent, like methimazole (Tapazole).

Grave's disease is the most common cause of hyperthyroidism. It is an autoimmune disease where an individual's own antibodies attach to thyroid stimulating hormone receptors within cells of the thyroid gland and then trigger overproduction of thyroid hormone. The two thyroid hormones manufactured by the thyroid gland, thyroxine (T4 ) and triiodothyronine (T3), are formed by combining iodine and a protein called thyroglobulin with the assistance of an enzyme called peroxidase. PTU inhibits iodine and peroxidase from their normal interactions with thyroglobulin to form T4 and T3. This action decreases thyroid hormone production. (PTU also interferes with the conversion of T4 to T3, and, since T3 is more potent than T4, this also reduces the activity of thyroid hormones.)
Describe thyroid nodules and tumors, causes and diagnostics.
Thyroid nodules are palpable nodes; that may be benign or malignant.Thyroid cancer is identified as a hard, painless nodule or nodules on an enlarged thyroid gland. If you have ↓ radioactive iodine uptake → > you have an increased risk for malignancy. An ↑ calcitonin level is possible as well.
Diagnostics: US (Urine studies), CT Computed Tomography, MRI, US-guided needle asp.
What are the various things that cause thyroiditis or inflammation of the thyroid?
There are several causes of thyroiditis: Viral infection: called deQuervain’s; Acute thyroiditis r/t bacterial & fungal infection;
Autoimmune version is called: Hashimoto’s; Silent, painless thyroiditis: ia a variable onset autoimmune dysfunction from lymphocytic infiltration of the thyroid. This version occurs in ♀ in postpartum period, may resolve in 3-12 months. People who get this version of thyroiditis might have early Hashimoto’s.
What is the difference between Grave's diseas and hyperthyroidism?
Grave's disease is the most common form of hyperthyroidism, but there are several types of hyperthyroidism a person could have. Grave's disease is an autoimmune form of hyperthyroidim, where antibodies attach to the TSH receptors found in thyroid hormone producing cells. These antibodies over stimlate the release and production of TH. Grave's disease can cause goiter, opthalmos, loss of weight, insomnia, irritability....
What are toxic nodule goiters?
A Nodule secreting TH, that is independent of TSH level is considered a toxic nodule.
Toxic if S/S of hyperthyroidism are present. These nodules > 3cm may result in clinical disease of hyperthyroidism.
How would you explain a thyrotoxic storm?
Thyrotoxic crisis or thyroid storm is an acute, rare condition where all hyperthyroid manifestations are heightened. It is considered a medical emergency, but death is rare if treated early and vigorously. The physiologic factors are unknown. The cause is thought to be stressors like infections, trauma and surgery in a person with preexisting hyperthyroidism (whether diagnosed or not). Manifestations include severe tachycardia, heart failure, shock, and hyperthermia, restlessness, agitation, seizures, abdominal pain, nausea, vomiting diarrhea, dellirium and coma.
What are the signs and symptoms of hyperthyroidism?
CardioV: VS: ↑HR, palpitations, ↑BP, ↑RR
GI: ↑ appetite,↑ peristalsis, ↑ BS, weight loss
Skin: warm, moist, diaphoresis, brittle nails, pretibial myxedema (orange peel appearance)
MS: Fatigue, weakness, proximal muscle wasting, dependent edema, osteoporosis
CNS: Nervous, tremor, insomnia, labile mood, agitation, exhaustion, ↓concentration, stupor
Repro: Menstrual Δ’s, ↓fertility, ↓ libido, gynecomastia in men
What are the nursing interventions for thyroid storm?
Treatment:
Immediate cooling measures & ↓HR
Hemodynamic monitoring
Maintain fluid & electrolyte balance
Promote rest
Administer antithyroid meds, iodine
Teach patients importance of compliance with treatment
What are the nursing interventions for thyroid storm?
Treatment:Immediate cooling measures & ↓HRHemodynamic monitoring Maintain fluid & electrolyte balancePromote rest
Administer antithyroid meds, iodine
Teach patients importance of compliance with treatment; Acute thyrotoxicosis is a systemic syndrome that requires aggressive treatment, often in an intensive care unit. The nurse needs to administer medications (previously discussed) that block thyroid hormone production. Nursing management also includes provisions for supportive therapy. Having an understanding of the major organ response to the hypermetabolic state is a critical aspect of nursing management. Supportive therapy includes monitoring for cardiac dysrhythmias and decompensation, ensuring adequate oxygenation, and administering IV fluids to replace fluid and electrolyte losses. This is especially important in the patient who develops vomiting and diarrhea.
Drug Therapy would include: antithyroid meds, iodine (which is given to rapidly inhibit synthesis of t3/t4 and blocks the release of these hormones into circulation. Iodine also decreases the vascularity of the thyroid gland to make surgery safer and easier. These changes can take 1-2 weeks. Iodine therapy is not a long term use. I comes as potassium iodine (SSKI) and Lugol's solution. There are also other treatments B-adrenergic blockers, RAI therapy (radioactive iodine therapy, the treatment of choice for most nonpregnant adults. Can make a person go to hypothyroid- ism.; Surgery; Nutrition: May have to eat as many as 4000-5000 cal a for high metabolism.
Explain goiters, goitrogens, excess or ineffcient effects of iodine in relation to goiters.
There are several types of hypertrophied (not to be confused with hyperthyroidism) goiters and they are named in relation to what is happening with nutrient iodide. Iodide is a trace element that everyone gets from their diet unless they live in a very mountainous, volcanic areas in other countries...These are called endemic goiters because they are attained due to the environment's lack of this nutrient. Iodide (iodine in its oxidized form) is necessary to make thyroid hormone. This type of goiter is called a colloid nodular goiter that forms because TSH is being constantly stimlated due to lack of TH that would feedback and shut it down. This goiter is caused by hypothyroidism, or underactive thyroid or inefficient TH. Other goiters are called toxic nodular goiters. This case is the opposite, in which there is too much iodine and there is an excess of Thyroid hormone, in which the nodules produce excess thyroid hormones causing thyrotoxicosis. Some of these toxic nodules can be caused independent of TSH stimulation, they are usually benign. But in another instance, called Grave's disease (an autoimmune disease), our own antibodies can attach to the TH receptors (something that TSH normally would do), but these antibodies (Igs) will do TSH's job and will stimulate secretion of TH that can cause thyroiditis, or excess TH, and cause these toxic nodules goiters to form.
Explain the extremes from hypothyroidism all the way to hyperthyroidism what you would expect in progression of stages and diseases.
On the hypo and hyper you can have goiters. On the severe end of hypothyroidism you have myxedema coma >then a little less severe is hashimoto's thyroiditis >then a little less severe is cretinism to the middle you have EUTHYROID > then starting to move toward hyperthyroidism you have can have thyrotoxicosis then >>Graves>>then thyroid storm (acute). On this side you would have toxic nodular goiter.
What is the mosst common cause of goiterous hypothyroidism?
It is Hashimoto's thyroiditis (also called chronic autoimmune thyroiditis), that starts with thyoid tissue is replaced by lymphoctes and fibrous tissue. Leading to a disfunctional thyroid gland resulting in hypothyroidism.Thyroid hormone levels are usually low in chronic Hashimoto's thyroiditis, and TSH is high, and antithyroid antibodies are present in Hashimoto's thyroiditis.
What is silent painless thyroiditis?
It is a form of lymphoctic thyroiditis with a variable onset. In women, this condition may occur in the postpartum period and usually resolves within 3-12 months. It is believed to be a possible precursor to eventual hashimotos's thyroiditis.
What are the 4 types of causes of thyroiditis (inflammation of the thyroid)?
Inflammation of thyroid gland
1) Viral infection: deQuervain’s
2) Acute thyroiditis r/t bacterial & fungal infection. 3) Autoimmune: Hashimoto’s 4) Silent, painless thyroiditis – variable onset autoimmune dysfunction from lymphocytic infiltration of the thyroid
Occurs in ♀ in postpartum period, may resolve in 3-12 months
May be early Hashimoto’s.
What is important to differentiate between the terms: thyrotoxicosis and hyperthryoidism.
First: Thyrotoxicosis is the physiologic effects or clinical syndrome of hypermetabolism that results from excess circulating levels of t4 and t3 or both. Second: Hyperthyroidism is the hyperactivity of the thyroid gland with sustained increase in synthesis and release of thyroid hormones. Usually these two will go hand in hand like in Graves disease, but not always, you can have thyrotoxicosis or a hypermetabolism effect without having hyperthyroidism. pg. 1299 lewis.
How do S/S Graves’ differ from hyperthyroidism?
Graves disease accounts for 75% of the cases of hyperthyroidism, but there are other causes like toxic nodular goiter, thyroiditis, exogenous iodine excess, pituitary tumors, and thyroid cancer. Graves is an autoimmune disease.
Describe the drug therapy for hyperthyoridism Part 1 and Part 2 cards.
The purpose of antithyroid drugs is to reduce the excessive secretion of thyroid hormones (T4 and T3) by inhibiting thyroid secretion. The use of surgery (subtotal thyroidectomy) and radioiodine therapy frequently leads to hypothyroidism. Thiourea derivatives (thioamides) are the drugs of choice used to decrease thyroid hormone production. This drug group interferes with synthesis of thyroid hormone. Thiourea derivatives do not destroy thyroid tissue, but rather block thyroid hormone action. Propylthiouracil (PTU) and methimazole (Tapazole) are effective thioamide antithyroid drugs. They are useful for treating thyrotoxic crisis and in preparation for subtotal thyroidectomy. Methimazole does not inhibit peripheral conversion of T4 to T3 as does PTU; however, it is 10 times more potent and it has a longer half-life than PTU. Prolonged use of thioamides may cause a goiter because of the increased TSH secretion and inhibited T4 and T3 synthesis. Minimal doses of thioamides should be given when indicated to avoid goiter formation.
In which instances would you use thyroid replacement and what are a few example names and prototyes for each>
Levothyroxine sodium (Levothroid, Synthroid) is the drug of choice for replacement therapy for the treatment of hypothyroidism. It increases the levels of T3 and T4. Levothyroxine is also used to treat simple goiter and chronic lymphocytic (Hashimoto) thyroiditis.
Liothyronine (Cytomel) is a synthetic T3 that has a short half-life and duration of action; it is not recom-mended for maintenance therapy. Liothyronine is better absorbed from the GI tract than levothyroxine, and because of its rapid onset of action and short half-life, it is frequently used as initial therapy for treating myxedema. Liotrix (Euthroid, Thyrolar) is a mixture of levothyroxine sodium and liothyronine sodium in a 4:1 ratio. For treating hypothyroidism, there is no significant advantage to using liotrix over levothyroxine sodium alone, because levothyroxine converts T4 to T3 in the peripheral tissues. Thyroid hormone
Trade names: T4, Synthroid, Levothroid; Eltroxin, Pregnancy Category: A: PO: Initially: 25–50 mcg/d (0.025-0.05 mg/d); maint: 50–200 mcg/d (0.05-0.2 mg/d)
IV: 0.2-0.5 mg initial dose; 0.1-0.2 mg/d until stable and then PO
C: >3 y: PO: 5–6 mcg/kg/d or 50–100 mcg/d.
What should a nurse be aware of when giving thyroid replacement drugs?

Part 1 Part 2 card
Should determine a baseline vital signs for comparison; Check serum T3 and T4 and thyroid stiulating hormone levels; Obtain a history of drugs the client currently takes because thryoid drugs enhance the action of many drugs such as; anitcoagulants, sympathomimetics, and anitdepresants and decrease action of insulin, oral hypoglycemics adn digitalis peraparation. Phenytoin and aspirin can enhance the action of thyroid hormone.The n dx for hypo or hyper are the following:
-Ineffective health maintenance related to inability to maintain drug regimen.; ▪Ineffective tissue perfusion related to hyposecretion of thyroid hormone;▪Activity intolerance related to generalized weakness
What are the nursing implications for those taking antithyroid medications?
Part 1 Card/Look at Part 2
•Assess for signs and symptoms of a thyroid crisis (thyroid storm), including tachycardia, cardiac dysrhythmias, fever, heart failure, flushed skin, apathy, confusion, behavioral changes, and later hypotension and vascular collapse. Thyroid crisis can result from a thyroidectomy (excess thyroid hormones released), abrupt with- drawal of antithyroid drug, excess ingestion of thyroid hormone, or failure to give antithyroid medication before thyroid surgery. NDX:
▪Ineffective health maintenance related to inability to maintain drug regimen ▪Ineffective tissue perfusion related to hyposecretion of thyroid hormone.▪Activity intolerance related to generalized weakness; Nurse Planning: ▪Client's signs and symptoms of hyperthyroidism will be alleviated in 1 to 3 weeks with the prescribed antithyroid drug. With hyperthyroidism, tachycardia and palpitations usually occur. Instruct client to take the drug with meals to decrease gastrointestinal symptoms; •Advise client about the effects of iodine and its presence in iodized salt, shellfish, and OTC cough medicines.•Emphasize the importance of drug compliance; abruptly stopping the antithyroid drug could bring on thyroid crisis.
•Teach client the signs and symptoms of hypothyroidism: lethargy, puffy eyelids and face, thick tongue, slow speech with hoarseness, lack of perspiration, and slow pulse. Hypothyroidism can result from treatment of hyper- thyroidism.;•
What are some collaborative pharmacological drugs that support the main therapy meds?
Beta-Blockers: propranolol (Inderal) to rapidly ↓cardiovascular symptoms that are common in hyperthyroidism
Strong Iodine solutions (Lugol’s solution), K+ Iodide (SSKI, Thyro-Block, Pima); Used Short-term tx to inhibit T₃& T₄ synthesis & release. Helps to ↓ vascularity of thyroid gland prior to surgery: to avoid bleeding. Hastens ability of anti-thyroid drugs to ↓natural hormone output. The Iodine Solution,called: SSKI saturated solution of iodide has a Bitter taste so may require dilution in water or OJ.Monitor for increased bleeding if taking warfarin has a synergistic effect. Maximal effect of Iodine 10-15 days; Not effective for long term control of hyperthyroidism
There is also Radioactive Iodine Therapy, the Treatment of choice (for nonpregnant adult).Response delayed up to 2-3 months
Antithyroid drug & propranolol prescribed together during the 1st 3 months after RAI initiation; There is also ↑ incidence of hypothyroidism following tx.
Explain thyroidectomy, its implications, and post-op care.

Part 1/Part 2 Card
A Subtotal thyroidectomy is for clients unresponsive to antithyroid Rx, or large goiters causing tracheal compression, a thyroid malignancy, In instances where t3 and t4 need to be removed more rapidly, surgery is the preferred choice over RAI therapy. Surgery will remove 90% of thyroid tissue; Post-op care:Prepare for possibility of an ETT (emergency tracheotomy) post-op; Head positioning – slight flexion; Reduce strain on incision, Relieve pain & throat discomfort. Assess for bleeding, Monitor CV status, VS, CBC, Assess for S/S of laryngeal edema or tracheal compression, which would exhibit Stridor, Hoarse- ness Emergency tracheostomy at bedside; O₂ & suction set-up ready
What would be the Nanda NDX for Hyperthyroidism?
Activity Intolerance r/t fatigue, exhaustion, heat intolerance
Sleep Disturbance: have insomnia.
Disturbed Sensory Perception: Visual
Imbalanced Nutrition< Body Req
Risk for ↓CO: the heart is beating fast and working hard!!
What are the symptoms and statistics of hypothyroidism?
Common among >65 y.o. ♀ > ♂
Insufficient circulating TH
Destruction of TH or defective TH synthesis
2* pituitary disease w/↓TSH, or
2* hypothalamic TRH dysfunction w/↓TRH secretion
Other causes: thyroiditis, inadequate thyroid HRT
What are the signs and statistics with congenital hypothyroidism?
More common disorder in infants & young children
May be congenital or acquired
Gland may be absent or not functioning
S/S may not be apparent for several months
Newborn metabolic screening done prior to DC
If untreated →
Irreversible mental retardation
Physical disabilities
Umbilical hernia
Explain juvenile hypothyroidism
Acquired: may be caused by a number of conditions
Most common cause is lymphocytic thyroiditis:
Often appears during periods of rapid growth
Mental retardation and neurological complications are not often seen in older child because brain growth is nearly complete by 3 yrs of age
Explain myxedema coma and the signs and symptoms.
Severe: Life-threateningcomplication of long-term, untreated hypothyroidism
Usually triggered by stressors: illness, infection, social stressors
Severe metabolic disorders of ↓Na⁺,
↓ ABG’s, lactic acidosis; Hypothermia, CV collapse, impaired mentation, coma; Occurs older ♀ in winter months with chronic hypothyroidism & elderly with co-morbidities; May result in multi-organ failure d/t resp. failure
Monitor cardiorespiratory status
Maintain O₂, fluids/electrolytes, acid-base balance, hemodynamics
Monitor for signs of multi-organ failure from poor tissue perfusion
Treat causal factors & manifestation
IV TH replacement & other meds - why? Correct hyponatremia (causes seizueres and confusion) with hypertonic saline (3% Saline) until Na⁺ ≥130; Manage hypothermia-
Maintain CV status
What are the diagnostics used to test for hypothyroidism?
TSH sensitive assay & Free T4
Correlate S/S with lab results
↑TSH after TRH injection → hypothalamic dysfunction; change suggests anterior pituitary problem
↑ cholesterol/triglycerides, anemia
↑’d creatine kinase
What is the collaborative care and drug therapy used for hypothyroidism?
Low-calorie diet to ↑weight loss
Lifelong thyroid HRT
Levothyroxine (Synthroid) “drug of choice” for hypothyroidism
Liotrix – synthetic combination of T4 and T3 in a 4:1 combination
Liotrix: faster onset of action; peaks @ 2-3 days Levothyroxine peaks @ 1-3 weeks; Monitor S/S of hyperthyroidism r/t excessive dosing
Random TSH levels Q 6 months or annually; Must be taken in AM on an empty stomach.
Compare the following clinical manifestations distinguishing between hypothyroidism and hyperthyroidism.
Serum levels of T3, T4 & TSH
Metabolic rate
Body weight
Presence of goiter
Skin appearance
Temperature tolerance
Eye appearance
Cardiovascular effects
Nervous system effects
what are goitrogens? and thyroid medications?
When someone has thyrotoxcity you could give goitrogens (foods or drugs that contain thyroid-inhibiting substances), (which you wouldn't give with hypothyroidism, only hyperthyroidism), in order to inhibit the thyroid hormone secretion. To find out whether the goiter is due hypo or hyper-thyroidism, you would measure TSH and T4 levels or Thyroid antibodies. Then you would know how to treat, either with more hormone or by inhibiting the hormone. The following are goitrogens that would inhibit the TH secretion: propylthiouracil PTU, or methimazole (Tapazole), or Iodine (in large doses). Others include: sulfonamides, salicylates, p-Amnosalicylic acid, phynylbutazone (Butazoladin) lithium, or amiodarone (Cordarone).
Part 2 of Nursing Implications
Advise client to avoid antithyroid drugs if pregnant or breastfeeding. Antithyroid drugs taken during pregnancy can cause hypothyroidism in the fetus or infant.
Self-Administration; •Demonstrate to client how to take a pulse rate. Instruct client to monitor the pulse rate and report increases or marked decreases in pulse rate.Side Effects:
•Teach client the side effects of antithyroid drugs: skin rash, hives, nausea, alopecia, loss of hair pigment, petechiae or ecchymoses, and weakness.; •Advise client to contact the health care provider if a sore throat and fever occur while taking antithyroid drugs. A serious adverse reaction of antithyroid drugs is agranulocytosis (loss of white blood cells). A complete blood count should be monitored for leukopenia.
Evaluate the effectiveness of the antithyroid drug in decreasing signs and symptoms of hyperthyroidism. If signs and symptoms persist after 2 to 3 weeks of therapy, other methods for correcting hyperthyroid- ism may be necessary.
Part 2 of Thyroid treatments
Strong iodide preparations such as Lugol's solution have been used to suppress thyroid function for clients who have undergone subtotal thyroidectomy as a result of Graves disease. Sodium iodide
administered IV is useful for the management of thyrotoxic crisis. Table 50-2 gives the drug data for antithyroid drugs used to treat hyperthyroidism. pg. 778 in Key.Antithyroid drugs. Administer @ same time Q day with meals
Watch for unusual bleeding, swelling, nausea, loss of appetite, epigastric pain. Watch for S/S of hypothyroidism w/ lithium (because of lithium’s reaction with hyper-thyroid medication) May take up to 12 wks before full effectexperienced. Do not d/c med; take regularly as scheduled: can’t be stopped suddenly. PTU 3x daily; Methimazole daily dosing.
Part 2 What should a nurse be aware of when giving thyroid replacement drugs?
(Kee, p780). The Nurse Plan for Hypothyroidism should be: Client's signs and symptoms of hypothyroid- ism will be alleviated within 2 to 4 weeks with prescribed thyroid drug replacement, and the client will not experience side effects.Nursing Interventions/implications: Record vital signs. With hypothyroidism, the temperature, heart rate, and blood pressure are usually decreased. Monitor client's weight. Weight gain commonly occurs in clients with hypothyroidism;Client Teaching: Encourage client to take drug at the same time each day, preferably before breakfast. Food will hamper absorption rate.•Teach client to check warnings on OTC drug labels. Avoid OTC drugs that caution against use by persons with heart or thyroid disease.•Direct client to report symptoms of hyperthyroidism (tachycardia, chest pain, palpitations, excess sweating) caused by drug accumulation or overdosing. •Suggest that client carry a MedicAlert card, tag, or bracelet with the health condition and thyroid drug used. Diet: Hypothyroidism •Caution client to avoid foods that can inhibit thyroid secretion (strawberries, peaches, pears, cabbage, turnips, spinach, kale, Brussels sprouts, cauliflower, radishes, and peas).
Post op implications continued

Part 2:
Post-op positioning: ↑ HOB to reduce post-op swelling; Prevent hyperextension or flexion; Soft, high protein diet; Assess for S/S of hypocalcemia from accidental parathyroid excision or injury; If parathyroid glands are affected, plasma Ca+ level ↓’s , Nerves irritable & fire → muscle contraction or tetany: TX: IV calcium gluconate @BS; Produced by parafollicular C-cells of the thyroid; Parathormone (PTH): Key to maintaining serum Ca+ level (9-11mg/dl); Calcitonin responds when Ca+ is high;
Controls Ca+ level by inhibiting resorption ↑Ca+ storage in bone
↑ renal excretion of Ca+ to ↓serum levels. Anxiety & mental depression - earliest indication of ↓PTH
Paresthesis & ↑neuromuscular excitability; Chvostek’s sign is
+ → facial twitching;Trousseau’s sign
+ → carpal spasm; Tetany: Other S/S
Stridor, dysphagia, Paresthesia (numbness and tingling)@ mouth,
extremities; Risk for seizures, EKG Δ’s.