Unit 1 Endocrine

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1 - Endocrine Outline NUR 207

Unit 1: Endocrine

A and P review: Complete before class - this will not be reviewed, all information is in text

The endocrine system releases_______________________ into the blood system to assist in ___________________ organfunction with the nervous system. Under normal condition this by a mechanism called ___________________ whichmonitor hormone concentrations in the blood stream, when concentrations _______________ to appropriate levels

production is _______________, and when concentrations decrease the rate of ___________________ increases. The_____________________ gland controls the "master gland" of the endocrine system or the _______________ gland. Thisgland is called the "master gland" because influences other endocrine glands to ___________ hormones based on anegative feedback loop.

Endocrine structures and Hormones we will focus on: (For the hormones listed below identify thesource/structure its major action

Hormone: Source/Structures: Major Action:Adrenalcorticotropic hormone(ACTH)

Pituitary gland(ANTERIOR)

Stimulates corticosteroid and androgensynthesis and release from

adrenocortical cells

Thyroid stimulating hormone(TSH)

Pituitary gland(ANTERIOR)

Stimulates thyroxine (T4) andtriodothyronine (T3) from throid glandStimulates iodine by t. gland

Antidiuretic Hormone (ADH) orvassopressin

Pituitary gland(POSTERIOR)

Increases water permeability in thedistal convoluted tubes and collectingducts of nephrons, promoting waterreabsorption, increasing blood volume

Triiodothyronin (T3) andThyroxine (T4) (follicular cells)

Pituitary gland(POSTERIOR)

Parathyroid hormone 1) Increases bone resorptiona) Pulling Ca out of bonesb) Quick

2) Ca resorption in kidneys, innephronsa) Pulled out of tubules into blood

supply3) Increases absorption of Ca from GI

system (intestines)


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Hormone: Source/Structures: Major Action:

1,25-Dihydroxyvitamin D

Mineralocorticosteriods(aldosterone)

Adrenal Cortex 1) Primary is Aldosterone: functionis to help regulate fluid volume

2) Primary control of release is theRenin-Angiotensin-Aldosteronesystem

Gluccorticoids (cortisol) Adrenal Cortex 1) Functions is CHO, protein and fat metabolism, emotional stability,stress response, immune fuctiona) Direct control by ACTH from the

pituitary gland2) Immunosuppressant effect

a) Ex. Organ transplant b) Higher doses increase

susceptibility to illness orsuppressed virus (e.g. Herpes,Shingles)

3) Anti-inflammatory effect a)

Calcitonin Pituitary(INTERMEDIATE)

Reduces serum Ca levelsIncreases Ca levels = Decreases bone

resorption ( into vascular space frombone) = Inhibits Ca release from boneHypercalcemia triggers release

The Pituitary glands: (identify where they are and what they do) small, pea size, inferior aspect of brain.

Anterior pituitary: Secretes the following hormones

1. Growth hormone2. Procactin

3. Gonadotrophins LH and FSH4. Stimulating hormones and trophic hormonesa. ACTHb. TSHc. MS


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Posterior Pituitary: Stores and releases

(1) Oxytocin(2) ADH/Vasopressin

The Thyroid gland: (identify where it is and what it does)

Parathyroid glands: (identify where they are and what they do)

Location: Anterior neck lateral to the trachea

Function: Produces the thyroid hormones by the thyroid follicles

1. Tri-iodothyronine or T32. Tetra-iodothyronine or thytoxine T4

Adrenal glands: (identify where they are) one attached to upper portion of each kidney

Adrenal medulla: (identify what it does)

Location:

Function: Secrets Adrenergic Hormones (essentially a part of the SYMPATHETIC autonomicsystem)

1. Epinephrine2. Nor-epinephrine

Adrenal cortex: (identify what it does)

Location:Function: Secretes three types of STERIOD hormones

1. Glucocorticoids like Cortisol, cortisone and corticosterone2. Mineralocorticoids like Aldosterone3. Sex hormones- like estrogen and testosterone


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Class Outline: There are no PowerPoint handouts; instead you will be able to utilize thisoutline for taking notes in class and as you study. We will be working in small groups to fill inmost of the sections below. If you fill in the sections when you read pre class you will find it easier to augment in class.

Gerontologic considerations related to the endocrine system:

1.

2. 3. 4. 5. 6. 7. 8.

Health assessment and the Endocrine system:

Subjective:

Objective:

Disorders of the Pituitary (DI and SIADH):A. Diabetes Insipidus (DI):

1. Define:


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2. Causes:

3. Clinical presentation:

4. Diagnostics:

5. Medical management:

5. Nursing Management:(include problem and


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interventions)

B. SIADH:1. Define:

2. Causes:


4. Diagnostics:


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5. Nursing Management:(include problem andinterventions)

Disorders of the thyroid (Hypo-, hyper-, thyrotoxicosis):A. Thyroid Lab Tests: For each Identify Normal range, why monitored, what results indicate regarding thyroidfunction and any related nursing concerns.

1. TSH - Thyroid stimulating hormone

2. T3 - Triiodithyronine

3. Total T4 - Thyroxine


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4. T3 Resin uptake

5. Free T4

6. TBG (thyroxine-binding globulin)

B. Hypothyroidsim:1. Define and identify for primary, Secondary, tertiary where the problem is:

Hypothyroid state is characterized by decreases secretion of T3 and T4

Primary problem

2. Causes:

1. Hashimotos Disease is the leading causeA. Autoimmune problem in which antibodies are formed that trigger lymphocytes to get

into the thyroid gland and destroy the thyroid tissue (cells that produce dT3 and T4)

2. Tumor and radiation therapy

3. Latrogenic ( something we did to them)


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4. Pituitary Gland ProblemA. Not producing TSH or enough TSH

B. Hypopituitarism

C. Hypophysectomy

5. Infections

6. Iodine Deciciency

7. Iodiopathic

8. Amiodarone and Lithium both cause hypothyroidism; D/C or cover with Levothyroxine


1. Slow onset, may be undiagnosed for a long time

2. Increased weight

3. Fatigue

4. Goiter

5. Difficulty swallowing due to goiter

6. Cold intolerance

7. Constipation

8. Dry skin

9. Menstrual changes

10. Memory problems

11. Slow speech

12. Difficulty problem solving


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13. Lethargy

14. Sluggish reflexes

15. Bradycardia

16. Respiratory depression

4. Diagnostics:

1. Serum T3 and T4 = reveals normal or below normal

2. Thyroid Scan = reveals enlarged thyroid gland

3. Serum Thyroid Stimulating Hormone (TSH) = increased (confirmatory diagnostic test)


1. No cure for Hashimotos; treat with HRT

2. Drugs:

a. Prototype = LevothyroxineI. Therapeutic classification: Thyroid Hormone

II. Pharmacologic Classification: Thyroid Hormone Replacement III. Synthetic form of T4IV. OralV. Takes 4-6 weeks for full effect

VI. IV form for Myxedema Coma

VII. Adverse Effects1. Rare at normal doses2. High doses: tachycardia, increased temperature, chest pain, signs that

you would expect to see with hyperthyroidism

VIII. Contraindications:1. MI due to potential for increased workload of heart due to increase in

metabolism


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6. Nursing Management:(include problem and interventions)

1. Monitor strictly vital signs and intake and output to determine presence of Myxedema

Coma

2. Force fluids

3. Administer isotonic fluid solution as ordered

4. Administer medications as ordered

5. Provide dietary intake that is low in calories due to weight gain

6. Provide comfortable and warm environment due to cold intolerance

7. Provide meticulous skin care

8. Provide client health teaching and discharge planning concerning

a. Avoid precipitating factors leading to myxedema coma

o Stresso Infectiono Cold intoleranceo Use of anesthetics, narcotics, and sedativeso Prevent Complications (myxedema coma, hypovolemic shock)o Hormonal replacement therapy for lifetimeo Importance of follow up care

7. Myxedema Coma: What is it

Myxedema Coma is a complication of hypothyroidism and an emergency case a severe formof hypothyroidism is characterized by severe hypotension, bradycardia, bradypnea,hypoventilation, hyponatremia, hypoglycemia, hypothermia leading to progressive stupor andcoma.


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C. Hyperthyroidism:1. Define:

Excess secretion of TH from the thyroid glands, causing a person to have high metabolism1. Elevations in Co

2. Elevations in peripheral blood flow

3. Elevations in body temperature

4. Elevations in O2 demand and consumption

2. Causes:

1) Most common cause is Graves diseasea. Most likely autoimmuneb. Antibodies are produced and they bing to the TSH receptors in the thyroid gland,and then act like TSHc. Increases production and secretion of T3 and T4

2) Problem with Pituitary Glanda. Producing too much TSH = increases TH releaseb. Thyroiditis (inflammation of the Thyroid Gland)c. Tumor

3. Clinical presentation: (use Graves disease as exemplar)

1. Gradual in onset

2. Expect to see signs that relate to increase metabolism

3. Tachycardia

4. HTN


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5. Palpitations

6. Increase appetite with weight loss

7. Frequent bowel movements

8. Heat intolerance

9. Insomnia, poor sleep quality, frequent waking during the night

10. Diaphoresis

11. Visual changes; double vision

12. Exophthalmos: protruding of eyes

13. Goiter; enlargement of Thyroid Gland

14. Hyperactive reflexes (Deep Tendon Reflexes DTRs)

15. Emotional lability, irritability

16. Hyperactive, manic-type manner

17. Exercise intolerance

4. Diagnostics:

1. TSH levels are low

2. Free T4 level (Thyroid Function Test) is elevated

3. Thyroid Scan: radioactive iodide uptake


1. Prototype = PTU (Propothyuricil)

2. Radioactive Iodine Uptake (Sodium- Iodide 131) Iodortope

3. Potassium Iodide, Sodium Iodide, SSKI (Saturated Solution of Potassium Iodide)4. Inderal (Beta Blocker)


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1. Monitor V/S, esp. BP, Pulse and Temperature

2. Patient might complain of chest pain, palpitations

3. Encourage rest and quiet environment

4. Frequent linen and clothing changes

5. Daily weights

6. Assess mental status

7. Safety issues

8. Frequent meals due to hypermetabolism

7. Thyroid storm Define and list and associated care

1. Acute exacerbation of signs, can be life-threatening

2. Generally patients with long-term untreated or undertreated hyperthyroidism, or

3. Patients that experience a stressor such as infection or illness

4. S&Sx: same as hyperthyroidism but more acute and happen more quickly

5. Need immediate treatment a. Monitor airway

b. Start on PTUc. Might give iodide in addition to PTUd. If temperature elevated, might be treated with acetaminophene. Beta blockers (e.g. Inderal) may be given to decrease heart rate and increasestrength of contraction (decreasing work load of heart) and because it blocksthe conversion of T4 to T3f. Small doses of insulin may be given to control hyperglycemiag. IV fluids: prevent vascular collapse but caution due to risk of heart failureh. Oxygen


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i. Cooling blanket j. Monitor heart rate (cardiac monitor) and rhythmK. Patient may become hypothyroid, which would necessitate hormonereplacement e.g. Synthroid

Disorders of the adrenal glands:

A. Adrenal insufficiency:

1. Define: Addisons disease and Secondary Adrenal insufficiency

Hypofunction of the adrenal cortex leads to insufficient production of Aldosterone and Cortisol

2. Causes:

1. Autoimmune problem

2. Tuberculosis

3. Sepsis

4. Adrenalectomy (medications are prescribed by physician to prevent when bilateraladrenalectomies are performed)

5. High doses of glucocorticoids that are abruptly discontinued; must wean off other wisethe normal negative feedback system does not kick in and as levels fall off the body doesnot worry about it; body needs time to recognize the decrease so that it can excrete ACTHto maintain normal circulating glucocorticoid


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1. Hyperpigmentation of the skin: caused by high levels of ACTH, which can arise withAddisons because the body doesnt know that the adrenal glands cant produce cortisol soit keeps secreting more from the pituitary gland

2. Weight loss and anorexia

3. Lethargy

4. Depression

5. Muscle weakness

6. Salt craving (hyponatremia)

7. Low cortisol levels

8. Low glucose levels (hypoglycemia)

9. Elevated serum K levels (hyperkalemia)

10. ACTH stimulating test: inject ACTH, will lead to no response in Cortisol levels withAddisons

4. Addisonian crisis: Define and list presentationResults from acute exacerbation of addisons disease characterized by

1. Severe hypotension2. Hypovolemic shock 3. Hyponatremia leading to progressive stupor and coma

5. Diagnostics:

1. Plasma cortisol is decreased

2. Serum sodium is decrease3. Serum potassium in increased


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1. Prototype: Hydrocortisone

2. Prototype: Florinef


1. Monitor I & O

2. Monitor daily weights

3. Encourage fluids

4. Increase sodium in diet

5. Safety related to mental changes and depression: simple directions, safe environment (slipand trip hazards)

B. Cushings Disease

1. Define:

1. Hyperfunction of the Adrenal Cortex2. Elevated levels of serum cortisol or too much ACTH, which increases cortisol levels3. Affect CHO metabolism and mineral metabolism and some potentially life-threatening

problems in term

2. Causes:

1. Typically tumor or adrenal cortex, which is causing too much cortisol to be released2. Secondary is caused by a problem in the Pituitary Gland or Hypothalamus, which is causing


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too much ACTH to be released3. Tumor in the lungs, GI tract or pancreas because they can produce an ACTH-like substance

(same physiologic actions)4. Exogenous glucocorticoids being used to treat asthma or autoimmune problems, or

patients that have received organ transplants: higher doses for longer periods of time


1. Muscle wasting, weakness

2. Bruise easily

3. Fragile skin

4. Mood swings

5. Poor wound healing

6. Susceptibility to infection

7. Osteoporosis

8. Abnormal fat depositsa. Moon face b. Truncal obesityc. Bufffalo hump: fat pad on back of neck

9. Impotence in males, amenorrhea in females

4. Diagnostics:

1. Serum cortisol: expect elevation

2. Na elevation

3. Elevated glucose

4. ACTH level may be drawn: can be decreased (high doses of glucocorticoid meds) orelevated (problem with pituitary gland or hypothalamus)


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1. Identify cause if possible and manage that causea. Tumor removal or chemo

b. Prescribed medication adjust dose

2. Drugs: Nizoral Blocks synthesis of glucocorticoids

3. Surgerya. Hypophysectomy: removal of pituitary glandb. Adrenalectomy: removal of one or both adremal gladsc. Both require physiological replacement


1. Monitor F & E, daily weight 2. I&O, daily weight 3. Safety issues due to susceptibility to fractures due to Ca resorption from bone:

environment safety4. Pace activities to prevent fatigue5. Risk for infection

C. Pheochromocytoma:

1. Define and causes

Define: Increased secretion of epinephrine and nor-epinephrine by the adrenal medulla

Causes: Presence of tumor at adrenal medulla


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1. Hypertension

2. Severe headache

3. Palpitations

4. Tachycardia

5. Profuse sweating and Flushing

6. Weight loss, tremors

7. Hyperglycemia and glycosuria

4. Diagnostics:


Surgery: Adrenalectomy (treatment of choice)Anti-hypertensive agents like alpha-adrenergic blockers phenoxybenzamineIV nitroglycerin for HypertensionMetryosine (Demsar)


1. Monitor VS especially BP2. Monitor for hypertensive crisis3. Avoid stimulation that can cause increased BP4. Administer Anti-hypertensive agents like alpha-adrenergic blockers

Phenoxybenzamine


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5. Monitor glucose and urine glucose6. Promote adequate rest and sleep periods7. Provide high calorie foods and vitamins/mineral supplements8. Prepare patient for possible surgery

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Unit 1 Endocrine