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Dr Ibraheem Bashayreh
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Location of the major endocrine glands.
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 Chemical messengers of the body
 Act on specific target cells
 Regulated by negative feedback
 Too much hormone, then hormone release reduced
 Too little hormone, then hormone release increased
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 Hypothalamus
 Posterior Pituitary
 Anterior Pituitary
 Thyroid
 Parathyroids
 Adrenals
 Pancreatic islets
 Ovaries and testes
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 Sits between the cerebrum and brainstem
 Houses the pituitary gland and hypothalamus
 Regulates:
 Temperature
 Fluid volume
 Growth
 Pain and pleasure response
 Hunger and thirst
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 Releasing and inhibiting hormones
 Corticotropin-releasing hormone
 Thyrotropin-releasing hormone
 Growth hormone-releasing hormone
 Gonadotropin-releasing hormone
 Somatostatin-=-inhibits GH and TSH
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Sits beneath the hypothalamus
Termed the “master gland”
 Divided into:
 Anterior Pituitary Gland
 Posterior Pituitary Gland
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 Promotes growth
 Stimulates the secretion of six hormones
 Controls pigmentation of the skin
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 Growth Hormone--
 Adrenocorticotropic hormone
 Thyroid stimulating hormone
 Follicle stimulating hormone—ovary in female, sperm in males
 Luteinizing hormone—corpus luteum in females, secretion of testosterone in males
 Prolactin—prepares female breasts for lactation
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Actions of the major hormones of the anterior pituitary.
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 Stimulates the secretion of two hormones
 Promotes water retention
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 Antidiuretic Hormone
 Oxytocin—contraction of uterus, milk ejection from breasts
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 Mineralocorticoid—aldosterone. Affects sodium absorption, loss of potassium by kidney
 Glucocorticoids—cortisol. Affects metabolism, regulates blood sugar levels, affects growth, antiinflammatory action, decreases effects of stress
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 Adrenal androgens—dehydroepiandrosterone and androstenedione. Converted to testosterone in the periphery.
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 Epinephrine and norepinephrine serve as neurotransmitters for sympathetic system
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 Butterfly shaped
 Sits on either side of the trachea
 Has two lobes connected with an isthmus
 Functions in the presence of iodine
 Stimulates the secretion of three hormones
 Involved with metabolic rate management and serum calcium levels
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 Follicular cells—excretion of triiodothyronine (T3) and thyroxine (T4)—Increase BMR, increase bone and calcium turnover, increase response to catecholamines, need for fetal G&D
 Thyroid C cells—calcitonin. Lowers blood calcium and phosphate levels
 BMR: Basal Metabolic Rate
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 Embedded within the posterior lobes of the thyroid gland
 Secretion of one hormone
 Maintenance of serum calcium levels
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 Located behind the stomach between the spleen and duodenum
 Has two major functions
 Digestive enzymes
 Releases two hormones: insulin and glucagon
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Insulin
Glucagon
—stimulates glycogenolysis and glyconeogenesis
Somatostatin
—decreases intestinal absorption of glucose
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 Produced by the Beta cells in the islets of
Langerhans
 Regulates blood glucose levels
 Mechanisms
 Eases the active transport of glucose into muscle and fat cells
 Facilitates fat formation
 Inhibits the breakdown and movement of stored fat
 Helps with protein synthesis
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Action of insulin and glucagon on blood glucose levels. (A) High blood glucose is lowered by insulin release.
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( continued) Action of insulin and glucagon on blood glucose levels. (B) Low blood glucose is raised by glucagon release.
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 Produced by the alpha cells in the islets of Langerhans
 Glucagon released when blood glucose falls below 70 mg/dL
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 Prevents blood glucose from decreasing below a certain level
 Functions:
 Makes new glucose
 Converts glycogen into glucose in the liver and muscles
 Prevents excess glucose breakdown
 Decreases glucose oxidation and increases blood glucose
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 1, 25 dihydroxyvitamin D—stimulates calcium absorption from the intestine
 Renin—activates the RAS
 Erythropoietin—Increases red blood cell production
 RAS: Renin-Angiotensin System
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 Pyramid-shaped organs that sit on top of the kidneys
 Each has two parts:
 Outer Cortex
 Inner Medulla
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 Secretion of two hormones
 Glucocorticoids: cortisol
 Mineralocortocoids: aldosterone
 Involved with blood glucose level, antiinflammatory response, blood volume, and electrolyte maintenance
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 Secretion of two hormones
 Epinephrine
 Norepinephrine
 Involved with the stress response
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 Estrogen
 Progesterone—inportant in menstrual cycle,*maintains pregnancy ,
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 Androgens, testosterone—secondary sexual characteristics, sperm production
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 Releases thymosin and thymopoietin
 Affects maturation of T lymphocetes
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 Melatonin
 Affects sleep, fertility and aging
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 Work locally
 Released by plasma cells
 Affect fertility, blood clotting, body temperature
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 Hormone replacement therapy
 Surgeries, chemotherapy, radiation
 Family history: diabetes mellitus, diabetes insipidus, goiter, obesity, Addison’s disease, infertility
 Sexual history: changes, characteristics, menstruation, menopause
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 General appearance
 Vital signs, height, weight
 Integumentary
 Skin color, temperature, texture, moisture
 Bruising, lesions, wound healing
 Hair and nail texture, hair growth
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 Face
 Shape, symmetry
 Eyes, visual acuity
 Neck
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Palpating the thyroid gland from behind the client. (Source: Lester V.
Bergman/Corbis)
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 Extremities
 Hand and feet size
 Trunk
 Muscle strength, deep tendon reflexes
 Sensation to hot and cold, vibration
 Thorax
 Lung and heart sounds
 Extremity edema
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 Relationship unclear
 Aging causes fibrosis of thyroid gland
 Reduces metabolic rate
 Contributes to weight gain
 Cortisol level unchanged in aging
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 Ask the client:
 Energy level
 Fatigue
 Maintenance of ADL
 Sensitivity to heat or cold
 Weight level
 Bowel habits
 Level of appetite
 Urination, thirst, salt craving
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 Ask the client:
 Cardiovascular status: blood pressure, heart rate, palpitations, SOB
 Vision: changes, tearing, eye edema
 Neurologic: numbness/tingling lips or extremities, nervousness, hand tremors, mood changes, memory changes, sleep patterns
 Integumentary: hair changes, skin changes, nails, bruising, wound healing
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 Thyroid abnormalities
 Diabetes mellitus
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 GH: fasting, well rested, not physically stressed
 Water deprivation: fasting for 12 hours, no fluids/smoking after midnight
 T3/T4: no specific preparation
 Serum calcium/phosphate: fasting may or may not be required
 Collection that needs to be iced or refrigerated
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 Cortisol/aldosterone level: two blood samples, client to be up for at least 2 hours before test is drawn
 Urine 17-ketosteroids: 24-hour urine collection that needs to be iced or refrigerated
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 FBS: fast before the test
 HbA1c: No fasting required
 2-hour OGTT: drink 75 g of glucose and do not eat anything until blood is drawn
 Urine glucose/ketones: fresh urine specimen
 Urine microalbumin: fresh urine specimen
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 MRI: metallic implants, lie motionless during test; remove all metal objects
 CT scan: assess for allergies to iodine and seafood; lie immobile during the test
 Thyroid scan: allergies to iodine and seafood; hold thyroid drugs containing iodine for weeks before the study
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 RAI: fast for 8 hours before; can eat 1 hour after radioiodine capsule/liquid taken; hold thyroid drugs with iodine for weeks before the study
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1The gland as seen from the front is more nearly the shape of a butterfly.
2composed of 2 encapsulated lobes, one on either side of the trachea, connected by a thin isthmus.
3The thyroid extending from the level of the fifth cervical vertebra down to the first thoracic. The gland varies from an H to a U shape, overlying the second to fourth tracheal rings.
4The pyramidal lobe is a narrow projection of thyroid tissue extending upward from the isthmus and lying on the surface of the thyroid cartilage.
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5The thyroid is enveloped by a thin, fibrous, nonstripping capsule that sends septa into the gland substance to produce an irregular, incomplete lobulation. No true lobulation exists.
6The weight of the thyroid of the normal nongoitrous adult is: 10-20 g depending on body size and iodine supply.
7The width and length of the isthmus average; 20 mm, and its thickness is ; 2-6 mm .
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8The lateral lobes from superior to inferior poles usually measure 4 cm . and their thickness is 20-39 mm.
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1-Anterolaterally:
* The sternothyroid
* The superior belly of the omohyoid
* The sternohyoid
* The anterior border of the sternocleidomastoid
2-Medially:
* The larynx & the trachea.
* The pharynx & the oesophagus.
* Associated with these structures are the cricothyroid muscle & its nerve supply, the external laryngeal nerve.
* In the groove between the esophagus and the trachea is the recurrent laryngeal nerve.
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3-Posterolaterally:
The carotid sheath with: The common carotid artery, the internal jugular vein, and the vagus nerve.
Relations of the Isthmus
1-Anteriorly:
The sternothyroids
The sternohyoids
The anterior jugular veins
Fascia & skin.
2-Posteriorly:
The second, third, & fourth rings of the trachea.
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1-The superior thyroid vein: ascends along the superior thyroid artery and becomes a tributary of the internal jugular vein.
2- The middle thyroid vein: follows a direct course laterally to the internal jugular vein.
3- The inferior thyroid veins : follow different paths on each side. The right passes anterior to the innominate artery to the right brachiocephalic vein or anterior to the trachea to the left brachiocephalic vein. On the left side, drainage is to the left brachiocephalic vein.
Occasionally, both inferior veins form a common trunk called the thyroid ima vein, which empties into the left brachiocephalic vein.
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The thyroid follicles secretes tri-iodothyronine(T3)and thyroxin(T4)synthesis involves combination of iodine with tyrosine group to form mono and di-iodotyrosine which are coupled to form T3 andT4.
The hormones are stored in follicles bound to thyrogobulin .
When hormones released in the blood they are bound to plasma proteins and small amount remain free in the plasma .
The metabolic effect of thyroid hormones are due to free (unbound)T3 and T4.
90%of secreted hormones is T4 but T3is the active hormone so, T4is converted to T3 peripherally.
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Synthesis and libration of T3 and T4 is controlled by thyroid stimulating hormone(TSH)secreted by anterior pituitary gland.
TSH release is in turn controlled by thyrotropin releasing hormone (TRH)from hypothalamus .
Circulating T3and T4 exert –ve feedback mechanism on hypothalamus and anterior pituitary gland .
So, in hyperthyroidism where hormone level in blood is high ,TSH production is suppressed and vice versa.
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Hormone
Function Stimulated by
T3/T4 h metabolic rate h protein synthesis h energy production
Most important hormone in day today regulation of metabolic rate i metabolic rate i
T3/T4 h
TSH
Calcitonin i blood calcium concentration i the reabsorption of Ca and Ph from bones to blood
Calcitonin “tones” down serum
Ca levels h blood Ca levels
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Hypothyroidism is the disease state in humans and animals caused by insufficient production of thyroid hormone by the thyroid gland .
•
•
INCEDENCE
30-60 yrs of age
Mostly women
 Clinical Manifestations:
1. Goiter.
2. Fatigue.
3. Constipation.
4. Weight gain.
5. Memory and mental impairment and decreased concentration.
6. Depression.
7. Menstrual irregularities and loss of libido.
8. Coarseness or loss of hair.
9. Dry skin and cold intolerance.
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10. Irregular or heavy menses.
11. Infertility.
12. Hoarseness.
13. Myalgias.
14. Hyperlipidemia.
15. Reflex delay.
16. Bradycardia, elevated diastolic BP.
17. Hypothermia.
18. Ataxia.
19. Decreased serum T4,T3 levels.
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T3
T4
TSH
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LIFELONG THYROID HORMONE REPLACEMENT
 levothyroxine sodium (Synthroid, T4, Eltroxin)
 IMPORTANT: start at low does, to avoid hypertension, heart failure and MI
 Teach about S&S of hyperthyroidism with replacement therapy
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Rare serious complication of untreated hypothyroidism
Decreased metabolism causes the heart muscle to become flabby
Leads to decreased cardiac output
Leads to decreased perfusion to brain and other vital organs
Leads to tissue and organ failure
LIFE THREATENING EMERGENCY WITH HIGH
MORTALITY RATE
With low metabolism metabolites build up inside the cells which increases mucous and water leading to cellular edema
Edema changes client’s appearance
Nonpitting edema appears everywhere especially around the eyes, hands, feet, between shoulder blades
Tongue thickens, edema forms in larynx, voice husky
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 Coma
 Respiratory failure
 Hypotension
 Hyponatremia
 Hypothermia
 hypoglycemia
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 Patent airway
 Replace fluids with IV.
 Give levothyroxine sodium IV
 Give glucose IV
 Give corticosteroids
 Check temp, BP hourly
 Monitor changes LOC hourly
 Aspiration precautions, keep warm
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Hyperthyroidism is a condition caused by the effects of too much thyroid hormone on tissues of the body. Although there are several different causes of hyperthyroidism, most of the symptoms that patients experience are the same regardless of the cause.
Clinical Manifestations:
1. Heat intolerance.
2. Palpitations, elevated systolic BP.
3. Weight changes.
4. Menstrual irregularities and decreased libido.
5. Increased serum T4, T3.
6. Exophthalmos (bulging eyes)
7. Goiter.
8. Insomnia.
9. Muscle weakness.
10. Heat intolerance.
11. Diarrhea.
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THYROIDITIS:
Thyroiditis is an inflammation (not an infection) of the thyroid gland. Several types of thyroiditis exist .
1-Hashimoto's Thyroiditis. Hashimoto's Thyroiditis (also called autoimmune or chronic
lymphocytic thyroiditis) is the most common type of thyroiditis.
Fatigue-Depression-Modest weight gain--Cold intolerance-Excessive sleepiness-Dry, coarse hair-Constipation-Dry skin-Muscle cramps-Increased cholesterol levels-Decreased concentration-Vague aches and pains-Swelling of the legs
2-De Quervain's Thyroiditis. (also called subacute or granulomatous thyroiditis). The thyroid gland generally swells rapidly and is very painful and tender.]
Patients will experience a hyperthyroid period as the cellular lining of colloid spaces fails, allowing abundant colloid into the circulation, with neck pain and fever. Patients typically then become hypothyroid as the pituitary reduces TSH production and the inappropriately released colloid is depleted before resolving to euthyroid. The symptoms are those of hyperthyroidism and hypothyroidism. In addition, patients may suffer from painful dysphagia. There are multi-nucleated giant cells on histology.Thyroid antibodies can be present in some cases.There is decreased uptake on isotope scan.
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3-Silent Thyroiditis. Silent Thyroiditis is the third and least common type of thyroiditis ..
Silent thyroiditis features a small goiter without tenderness and, like the other types of resolving thyroiditis, tends to have a phase of hyperthyroidism followed by a phase of hypothyroidism then a return to euthyroidism. The time span of each phase is not concrete, but the hypo- phase usually lasts 2-3 months.
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Dysphagia. breathlesness & orthopnoea.
Hoarseness.
Facial congestion.
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Enlargement of thyroid gland.
Classification:
Simple (non-toxic) goitre.
Toxic goitre.
Neoplastic goitre.
Inflammatory goitre.
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include: simple hyperplastic goitre (colloid goiter)
Cause: -physiological in pregnancy, puberty
-iodine definiecy.
Appearance: Large, smooth firm, non-tendern goitre
Effect: euythyroid & pressure effect.
Multinodular goitre.
Cause: presence of areas of hyperplasia & areas of hypoplasia in gland.
Appearance: Large, irregular, nodular goiter
Effect: euythyroid & pressure effect.
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Grave’s disease
Cause: Autoimmune disease characterizeby presence of antibodies stimulate TSH receptors in gland.
Appearance: Diffuce, nodular, hyperemic gland.
Effect: hyperthyroidism.
Toxic Multinodular goiter (plummer’s disease)
Cause: Toxic effect of MNG
Appearance: Large, irregular, nodular goiter.
Effect: hyperthyroidism
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Include :
benign : adenoma
malignant : papillary, follicular, anaplastic, medullary and lymphoma
Cause: -complication of MNG.
-radiation
Appearance: Enlarged goiter associated with lymphadenopathy
Effect: -pressure effect.
-euthyroid.
-invasive effect
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Rediel’s thyroditis
Cause: Fibrosis of thyroid
Appearance: Enlarged stony hard thyroid
Effect: Pressure effect
De quervain’s thyroiditis
Cause: Viral infection
Appearance: Diffuse, firm, tender swelling
Effect: Mild hyperthyroidism
Hashimoto’s thyroiditis
Cause: Autoantibody against thyroid gland.
Appearance: Diffuse, enlarged, non-tender goitre
Effect: Hypothyroidism
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Laboratory investigation:
-serum T3, T4.
-serum TSH.
-serum LATS: ( Long Acting Thyroid Stimulator) in grave’s disease
-thyroid antibodies: in hashimoto’s disease.
-serum cholesterol increase cholesterol level in hypothyroidism
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IN HYPERTHYROIDISM:
 T3
 T4
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TSH in Graves disease
Radioactive Thyroid Scan
 Ultrasonography: used to determine goiter or nodules
 EKG: note tachycardia
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-chest and neck x-ray:
Show descend of thyroid gland to thorax and mediastanal shifting in retrosternal goitre.
-iodine isotopes
By i.v injection of I131. Then, use gama rays to show hot and cold nodules.
-CT scan
Show thyroid size and if there is compression to trachea
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Endoscopic investigation:
-bronchoscopy: show compression and infiltration of trachea by tumer
Biopsy :
-fine needle aspiration biopsy.
-true-cut biopsy.
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 Antithyroid drugs:
 Thioamides : blocks thyroid hormone production; takes time
 propylthiouracil (PTU)
 methimazole (Tapazole)
 carbimazole (Neo-Mercazole)
 Need to control cardiac manifestations (tachycardia, palpitations, diaphoresis, anxiety) until hormone production reduced: use Beta-adrenergic blocking drugs : propranolol
(Inderal, Detensol)
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Iodine preparations :
 Lugol’s Solution
 SSKI (saturated solution of potassium iodide)
 Potassium iodide tablets, solution, and syrup
ACTION:
 decreases blood flow through the thyroid gland
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This reduces the production and release of thyroid hormone
Takes about 2 wks for improvement
 Leads to hypothyroidism
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 Lithium Carbonate
 ACTION: inhibits thyroid hormone release
 NOT USED OFTEN BECAUSE OF SIDE EFFECTS: depressions, diabetes insipidus, tremors, N&V
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RADIOACTIVE IODINE THERAPY:
 Receives RAI in form of oral iodine
 Takes 6-8 Weeks for symptomatic relief
 Additional drug therapy used during this type of treatment
 Not used on pregnant women
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Why use surgery?
 Used to remove large goiter causing tracheal or esophageal compression
 Used for pts who do not have good response to antithyroid drugs
TWO TYPES OF SURGERIES :
1.
2.
Total thyroidectomy (must take lifelong thyroid hormone replacement)
Subtotal thyroidectomy
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Patient should become euthyroid before surgery to prevent thyroid crisis.
Assessmment vocal cord condition
Low weight:
 Hi protein, hi CHO diet for days/weeks before surgery
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1.
2.
3.
Antithyroid drugs to suppress function of the thyroid
Iodine prep (Lugols or K iodide solution) to decrease size and vascularity of gland to minimize risk of hemorrhage, reduces risk of thyroid storm during surgery
Tachycardia, BP, dysrhythmias must be controlled preop
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 Teach C&DB
 Teach support neck when C&DB
 Support neck when moving reduces strain on suture line
 Expect hoarseness for few days (endotracheal tube)
 C&DB: cough & deep breathing
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1.
2.
3.
4.
5.
6.
7.
8.
9.
VS, I&O, IV
Semifowlers
Support head
Avoid tension on sutures
Pain meds, analgesic lozengers
Humidified oxygen, suction
First fluids: cold/ice, tolerated best, then soft diet
Limited talking , hoarseness common
Assess for voice changes: injury to the recurrent laryngeal nerve
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CHECK FOR
HEMORRHAGE 1st 24 hrs:
Look behind neck and sides of neck
Check for c/o pressure or fullness at incision site
Check drain
REPORT TO MD
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CHECK FOR
RESPIRATORY DISTRESS
Laryngeal stridor (harsh hi pitched resp sounds)
Result of edema of glottis, hematoma,or tetany
Trach set/airway/ O2, suction
CALL MD for extreme hoarseness
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Hemorrhage
Recurrent laryngeal nerve damage.
Superior laryngeal nerve damage
Hypoparathyrodism
Hypothyroidism
Septesis
Postoperative infection
Hypertrofic scaring (keloid)
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