Med sure 2 quiz # 6 pituitary, adrenal, thyroid and parathyroid Flashcards Preview

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Flashcards in Med sure 2 quiz # 6 pituitary, adrenal, thyroid and parathyroid Deck (36)
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Blood studies for endocrine disorders

T3 and T4

  • test purpose- serum T3 (triidothyronine) and T4 (thyroxine)dectect abnormal levels of thyroid hormones.
  • Elevated T3 indicates possible graves, toxic adenoma, or toxic nodular goiter.
  • elevated T4 = hyperthyroididm or too much hormone replacement.
  • decreased T3 or T4 is hypothyroidism.
  • PT prep- nothing really maybe some meds need to be held.
  • after- pressure on site for a few minutes. 


Age related changes to the endocrine system

  • Diminished response ADH, older person less able to conspensatew for inadequate fluid intake ir excess fluid loss, at risk for dehydration.



  • occurs in early childhood and puberty when long bones are still growing. 
  • excessive growth occurs in the epiphysis or diaphysis before it epiphyseal  (growth plate) closes from excess GH. 
  • growth is ususally proportional
  • may grow 8 feet and over 300 lbs
  • multiple health problems and early adulthood death



  • rare but more common than gigantism
  • most also have pitiutary macroadenomasd that secrete excess GH.
  • appears in 40's/50's both men/women equally.
  • GH production occurs after epiphyseal closure
  • closed epiphyseal= thicker and wider bones
  • also affects the cardio, GI, nervous and genitourinary system. 



  • Diagnosis- physical assessment, radiographic studies and labs.
  • skull x rays may show large sella turcica and > bone density. 
  • Enhanced computer tomography (CT) and MRI may locate intra and extracellular lesions or tumor formation.
  • angiography= vascular abnormalities, aneurysms and anteriovenous malformations.
  • Labs- GH or prolactin produced in excess
  • anterior pitiuatary hormones levels measured
  • LH and FSH elevation ok in postmeoposal women
  • elevate GH and insulin growth factor 1 (IGF-1) suggest acronemaly.
  • GH suppression test is most definite 
  • nomaly GH falls in response to glucose but not in ppl with acromegaly
  • dexamethasone suppression to R/O adrenal function issues.


focused assessment for acromegaly and gigantism

  • Energy levels
  • HT and WT
  • vitals
  • face/skull contours
  • visual acuity
  • speech
  • voice quality
  • abdominal distention
  • if sx, what are the expectations of pt and knowledge.



  • S/S: depends on stage of life adn hormones involved
  • dwarfism: very short, (as low as 36in), porportional.
  • delayd or absent sexual maturation
  • > frequency of mental retardation
  • accelerated pattern of aging= shorter life span by 20 yrs
  • panhypopituitarism- simmonds cachexia syndrome present= muscle/organ wasting, disruption of digestion and metabolism., < muscle /organ size due to low GH
  • An absence of ACTH affects the persons ability to cope effectively with stress. This affects a persons ability to metabolize glucose and hypoglycemia may result. 
  • TSH depleted the thyroid is not stimulated to produce thyroid hormone resulting in hypothyroidism. 
  • People with hypothyroidism don't have normal metabolism or thermogenesis or heat production they are unable to maintain a normal basil metabolic rate or body temperature. 
  • In lack of melanocyte stimulating hormone MSH exist, decreased pigmentation of the skin occurs. Resulting in power. With the absence of gonadotrophins, gonads may be atrophy. Both men and women lose libido, decreased body hair, and sexual dysfunction may occur, and woman amenorrhea. 
  • General symptoms are fatigue, weakness, malaise, cold intolerance, and lethargic. If this is function is caused by a tumor the patient may have headaches, vision disturbances, seizures, and loss of sense of smell.  


Diabetes Insipidus

  • Characterized by excessive output of dilute urine.
  • Caused by a number of factors, it's classified as nephrogenic, neurogenic (central or hypothalmic), or dipsogenic (primary polydipsia). 


Nephrogenic DI


Neurogenic DI

  • defect in production or secretion of ADH


Dipsogenic DI

  • disorder of thirst stimulation
  • when PT ingest water, serum osmolality decreases, which cause vasopressin secretion
  • other factors: 
  • habitual excessive H2O intake
  • psychiatric conditions


DI focused assessment

  • complete Hx of symptoms, medical Hx, and drug Hx by RN
  • LVN can monitor for thirst, change in urine appearance or volume, dizziness, weakness, fainting and palpitations.
  • monitor hydration, skin turgor, mucous membranes, pulse rate and quality, BP, mental status, I and O, daily wt, urine specific gravity.


Innapropriate ADH syndrome

  • S/S: reflects dilutional hyponatremia and water retention
  • weakness
  • muscle cramps/twitching
  • anorexia
  • nausea
  • diarrhea
  • irritability
  • headache
  • wt gain w/o edema


Adrenal Hypofunction-addisons

  • primary or secondary
  • primary-results from destructive disease process affecting adrenal gland causing deficiencies in  cortisol and aldosterone-from idiopathic atrophy autoimmue process
  • other primary reasons from- tuberculosis, hemorrhage r/t anticoagulants, fungal infecvtions, AIDS, metastatic cance, gram neg sepsis, adrenalectomy, adrenal toxin, abrupt withdrawl od exogenous steroids.
  • secondary reasons- insufficiency of the hypthalamus or pituitary= androgen and cortisol production. pituitary tumors, postpartum necrosis of pituitary, hypophysectomy, radiation, pituitary/intracranial lkesions,m high dose long term glucocorticoids tx.


Addisons pathophysiology

  • insufficiensy of adrenocortical steroids causes defects associated with mineralcorticosteroids and glucocorticosteroids.
  • impaired secretions of cortisol results in decreased gluconeogenesis and decreased liver and muscle glycogen.
  • causes:
  • hypoglycemia
  • slows glomerular FR, and gastric acid productions
  • all this shit causes:
  • decreased urea nitro excretiomn
  • irritability
  • anorexia
  • wt loss
  • nausea
  • vomiting
  • diarrhea


Other manifestations of adrenal insufficiency 

  • Weakness, lethargic, unexplained abdominal pain, and malaise.
  • Skin hyperpigmentation, particularly in sun exposed areas, pressure points, joints and creases of the body, is another possible sign.
  • When levels are lowered there's a decrease or loss of body, axillary, and pubic hair.
  • And prepubescent people facial, pubic, and axillary hair may fail to grow entirely.


Acute adrenal crisis/addisonian crisis

  • Life-threatening emergency
  • Sudden decrease in adrenal hormones
  • Precipitating factors are adrenal surgery, pituitary destruction, abrupt withdrawal of steroid therapy, and stress.
  • Examples of stressors include infection, illness, trauma, and emotional or psychiatric disturbances.
  • Signs and symptoms hypotension, tachycardia, dehydration, confusion, hyponatremia, hypokalemia, hypercalcemia, and hypoglycemia. 
  • If not treated fluid and electrolyte in balance is lead to circuit Tory collapse, cardiac dysrhythmias, cardiac arrest, coma, and death.


Addison disease medical treatment 

  • Hormone replacement with glucocorticoid and mineralcorticoids.
  • Glucocorticoids peek in the early morning and our lowest level afternoon.
  • If patient has an acute illness, additional glucocorticoid or needed to prevent a life-threatening condition.
  • Addisonian crisis is treated with IV fluids, hydrocortisone, electrolytes, and dextrose to restore normal BP.


Adrenal hypersecretion


  • patho- clinical manifestations of Cushing's syndrome affects most body systems and I related to access levels of circulating cortical steroids. In some instances such as symptoms of mineral corticoid an adjunct in exes me up here; however, symptoms of glucocorticosteroid excess usually predominate. 
  • Hyperadrenalism produces changes in the personal appearance including obesity, facial redness,hirtuism, menstrual disorders, hypertension a verying degrees, muscle wasting of extremities.
  • Additional findings are delayed wound healing, insomnia, irrational behavior, mood disturbances, irritability, anxiety.
  • Hallmark findings; truncal obesity, protein wasting, facial fullness, purple stray an admin breath by text or thighs, osteoporosis, hypokalemia.




  • Also known as thyrotoxicosis 
  • Most common type is Graves' disease and multi nodular goiter. 
  • Graves' disease is autoimmune disorder triggered by genetic and or environmental factors.
  • Antibodies activate TSH receptors which intern stimulate thyroid enlargement and hormone secretion.
  • Graves is more often diagnosed in women.
  • Has periods of remission and exaggeration.
  • Eventually may develop into hypothyroidism.
  • Multinodular goiter occurs most and women in their sixth and seventh decade. Caused by thyroid nodules that secrete excess thyroid hormone without TSH stimulation. There may be multiple hyperfunvtioning small nodules or a single module called toxic adenoma.
  • Nodules may be benign or malignant. 
  • Symptoms are usually less severe with multi nodular goiter than with Graves' disease.


Signs and symptoms of hyperthyroidism


  • Weight loss
  • nervousness
  • restlessness irritability
  • sleep disturbances
  • emotional liability
  • personality changes
  • hair loss
  •  fatigue.
  • Poor tolerance of heat and excessive perspiration \
  • changes in the menstrual and bowel patterns
  • warm moist velvety skin
  • fine tremors of hands
  • swelling of neck
  •  exophthalmos



  • Some patients with Graves' disease develop skin changes that are manifested as itching and thickening on the anterior aspect of the shins. Occlusive wraps with topical glucocorticoids may limit the progression of dermopathy he but there is no definite cure.


Severe thyrotoxicosis

  • Referred to as thyrotoxic crisis or thyroid storm.
  • Medical emergency requiring intensive monitoring and treatment.
  • Excessive stimulation by elevated thyroid hormones produced dangerous tachycardia and hypothermia.
  • Risk of heart failure exists.
  • The patient is restless and agitated and may lapse into a coma.


Medical diagnosis of hyperthyroidism

  • Lab findings consistent with Graves' disease are decreased TSH and elevated serum T4.
  • TSH can be so low that it cannot be detected in the blood.
  • Measurement of thyroid stimulating and antibodies and results of an RAA uptake test are useful and specifically diagnosing Graves' disease


Treatment of hyperthyroidism

  • Drug therapy- anti-thyroid drugs and better adrenergic blockers. Thionamides and iodides are anti-thyroid drugs.
  • Drugs could be used for long-term treatment but are often used for temporary to lower the level of hormones before surgery or radiation the process reduces the risk of bleeding and lowers the dangers of releasing large amount of thyroid hormones into the blood stream during surgery. 
  • thionamides- propylthiouracil (PTU) and mathematical (tapazole) are currently in use. It can take up to eight weeks for a fax to be noticeable drug may be given for months or years. 
  • Rare but serious effects or hepatitis and agranulocytosis
  • iodides inhibit the synthesis of thyroid hormones. Most often used after a course of PTU to the press Harmons accretion before thyroidectomy. May also be used to treat thyrotoxicosis. SSKI saturated solution of potassium iodide can be given to people who have been exposed to radiation to prevent damage to the thyroid gland.
  • Most common iodides arm lugols solution which is 5% iodine and 10% SSA & SSKI. Relief within 24 hours but several weeks for Max effects affects does not last as long therefore not generally use as a sole treatment for hyper thyroidism. 
  • idodine solutions can cause discoloration of the teeth and gastric upset. Effects or minimize of the iodine is diluted with milk, fruit juice, or other beverage and sit through a straw. Signs of iodine toxicity include swelling and irritation of the mucous membranes and increased salavation. 
  • Radiation therapy
  • Surgery
  • In addition, better adrenergic blockers such as propranolol (inderal) may be given to relieve some of the cardiovascular symptoms associated with hyperthyroidism.


Thyroid surgery preop care


  • Ask the patient what they know about the surgery and what to expect before and after the procedure. 
  • Identify and address learning needs.
  • Notify the patient that there will be a surgical dressing in front of the neck.
  • Of the incision will depend the size of the incision will depend on the surgical approach use. 
  • Demonstrate how to avoid straining the neck incision by supporting the head one rising.
  • To evaluate the effectiveness of the teaching ask the patient to repeat the information presented. Ask patient to demonstrate activity such as deep breathing and supporting the head during position changes.


Postop care

  • Usually discharged home in one or two days
  • Serious complications are airway obstruction, recurrent laryngeal nerve damage, hemorrhage, and tetany. A sign of hypocalcemia associated with damage to the parathyroid.
  • Another complication is thyrotoxic crisis usually prevented by preop anti-thyroid drugs.
  • Important to monitor and document respiratory status, level of consciousness, wound drainage or bleeding, voice quality, comfort, and neuromuscular irritability muscle twitching spasms.


Nursing interventions

  • Potential for airway obstruction;
  • turning and deep breathing or recommended to prevent respiratory complications.
  • Patient may not be able to cough due to stress to the suture line.
  • Monitor and document the rate and ease of respiration. Respiratory distress can result from compression of the trachea or from a spasm of the larynx because of nerve damage or hypercalcemia.
  • Suction equipment, laryngoscope, and endotracheal tube, oxygen and an emergency tracheotomy tray must be available in the room.
  • Elevate the head of the bed to decrease edema.
  • Use pillows to prop and support the head to avoid stress on the suture line.
  • edema bleeding cause pressure on the trachea.
  • Signs and symptoms of poor oxygenation because of airway obstruction or blood loss include restlessness, increasing pulse and respiratory rates, dyspnea
  • Vocal cord paralysis me occure may cause spasms that close the airway called laryngospasms. Signs of laryngeal nerve damage or hoarseness and in ability to speak.
  • Muscle contractions begin as twiches around the mouth at eyes. The face, fingers, and toes begin to tingle. Painful cramps . The most serious signs of hypocalcemia spasm of the larynx. tetany treated with calcium salts given IV or orally.


decreased cardiac output

  • Frequently inspect the dressing to detect bleeding and take vital signs. Blood make flow under the dressing to the back of the neck check behind the patient's neck and upper back to detect this.


Thyroid crisis

  • Can develop with large amount of thyroid hormone enter the bloodstream during surgery or when patient with severe hypothyroidism develop a severe illness or infection.
  • Complication is rare because surgery is typically delayed until serum hormone levels are reduced.
  • Approximately 12 hours after surgery the patient and thyroid crisis show signs of severe hyper thyroidism:
  • Tachycardia, cardiac dysrhythmias, vomiting, fever, confusion.
  • Must be treated properly or patient with time as a result of heart failure.
  • Treatment consist of anti-thyroid drugs IV sodium iodide, corticosteroids, better adrenergic blockers, antipyretics, IV fluids, 02, and hypo thermia blanket or other measures to reduce body temperature.