n180 endocrine

8/6/2019 N180 Endocrine

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March 31, 2011

Endocrine System

y Function is to help maintain homeostasisy Plays a vital role in the bodys response to external and internal situations

o External Envt: temperature, stress, trauma, illnesso Internal Envt: shock, fluid & electrolyte changes (changes in osmolality/osmolarity)

System Review

y Consists of glands, includingo Thyroido Pituitaryo Adrenalso Hypothalamuso Gonadso Parathyroido Pancreas (little coverage since addressed in 182)

y Hormones produced are the primary mode of cmu between origin of hormones and other tissuey Amount of activity or impact depends on the hormoney Hormones have 4 types of action:

1. Maintain internal envt/homeostasis2. Regulate energy availability (particularly TH)3. Effect reproduction4. G & D

y Endocrine glands are ductless and most secrete their hormone into the blood and then the hormone isdelivered to the different body tissues via the bloodstream

y Exocrine glands have ducts and secrete their product through ducts into an organ or onto a surface ofthe body

The Endocrine System works with Neurologic System

1. Hypothalamus (part ofCNS andEndocrine system Input from CNS causes messages (hormones) to be sent to the pituitary gland, and pituitary gland

responds and affects other glands

2. Catecholamines (produced by Nervous System andEndocrine System) Ex. Epinephrine and Norepinephrine: fn in Nervous System is neurotransmission, produced in the

Adrenal Medulla in the Endocrine System

The Endocrine System also works with the Immune System

1. Cytokines (enzymes) Cause macrophages to release other hormones that have an effect on the hypothalamus to release

other hormones

Nottestablesubjectmatter, justknowendocrinesystemworkswithothersystemsModes ofCmu within Endocrine System

y Traditional thinking: hormones are released, travel to distant target tissuey Current thinking:

1. Paracrine cmu: hormones act on cells which neighbor the releasing cell


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o Ex. insulin: released from beta cells and transports glucose, but also acts on alpha cells(neighbors) to suppress glucagon release

2. Autocrine cmu: the hormone has an effect on the cell that releases ito Ex. GH: released and causes growth of tissue in periphery, but also has an effect on the releasing

cell itself

Hormone Regulation

y Negative Feedback System: primary mechanism of control in the Endocrine Systemo Glands do not produce hormone until existing, circulating hormone is depleted: depletion triggers

production

o Ex. release ofTH is regulated by TSH which is controlled by the amount ofTH which is circulating(negative feedback loop)

o Ex. Negative Feedback Loop:In the case of elevated circulating levels ofTH, suppression ofTSH hormoneoccurs, which inhibits TH release; eventually, circulating TH is metabolized and levels start to fall, which

causes the hypothalamus to release TRH, which has its effect on the pituitary gland, which releases TSH,

which causes the thyroid gland to release TH; TH levels come back up and the hypothalamus doesnt

release any more TRH, so TSH isnt released, and TH secretion stops until the TH is reduced

y Positive Feedback System: uncommono Ex. FSH is released, causing development of a follicle on an ovary, and the follicle releases estradiol (a

hormone), which causes the release of more FSH, which causes further development of the follicle,

leading to further release of estradiol; eventually the follicle necroses and then all the hormone levels

return to normal until the next cycle starts again

Regulation of Endocrine Function

y Primary control is the hypothalamic-pituitary complexy Hypothalamus receives input from the CNS and secretes releasing or inhibiting hormones, which make their way

to the pituitary gland

y Hypothalamus also has non-endocrine function1. Sleep2. Hunger3. Temperature Control

y Most hormones released from the hypothalamus travel via capillary connection to the pituitary glandy Other hormones are produced in the hypothalamus and travel to the pituitary gland following a neural pathway

1. ADH2. Oxytocin

y ADH and Oxytocin travel to the Posterior Pituitary gland, where they are stored until theyre neededy All other hormones travel through the vascular connection to the Anterior Pituitary gland

Adenohypophysis = Anterior Pituitary

Neurohypophysis = Posterior Pituitary

Adrenal Glands

1) Adrenal Cortexa) Produces 3 classifications of corticosteroid hormones

i) Glucocorticoids(1) Primary is Cortisol: function is CHO, protein and fat metabolism, emotional stability, stress response,

immune function

(a) Direct control by ACTH from the pituitary gland(2) Immunosuppressant effect


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(a) Ex. Organ transplant(b) Higher doses increase susceptibility to illness or suppressed virus (e.g. Herpes, Shingles)

(3) Anti-inflammatory effect(a) Ex. significant Asthma exacerbation treated with IV Solu-Medrol(b) Ex. Prednisone may be administered PO to wean off Solu-Medrol(c) Ex. Decadron, Dexamethasone, Declomethasone(d) Anti-inflammatory effect because it decreases the production of prostaglandins, which set up theinflammatory process

(4) Can be given as replacement hormones(a) Ex. Post-adrenalectomy(b) Lower doses because not given as therapeutic use

(5) Gluconeogenesis(a) Can lead to hyperglycemia at higher doses watch BG ifType I or II DM, pre-DM; may require

temporary insulin

(b) Poor wound healing(i) Hyperglycemia(ii) Immunosuppressive effect

(c) Muscle wasting(i) Weakness(ii) Fatigue disrupts ADLs

(6) Mood(a) Emotional lability

(7) Absorbs Ca from bone(a) Risk of osteoporosis(b) Risk of pathological Fx(c) Encourage Ca supplement, ample dairy consumption, Vitamin D

(8) Gastric acid secretion increases(a) Increases risk of gastric ulcers(b) Combined with decrease in prostaglandins in gut (which produce mucus); loss of protection against

ulcers(9) Increase plasma lipids and cholesterol

ii) Mineralcorticoids(1) Primary is Aldosterone: function is to help regulate fluid volume(2) Primary control of release is the Renin-Angiotensin-Aldosterone system

(a) Renin released from kidneys when poorly perfused. Renin causes the conversion ofAngiotensin I toAngiotensin II. Angiotensin II is a potent vasoconstrictor in the periphery.Kidney perfusion increases

as a result

(b) Renin also causes the release ofAldosterone, leading to retention of water and Na from the renaltubules (resorption of water and Na into intravascular space), which increases blood volume and

perfusion

(c) ACTH

has a small effect on the release ofA

ldosterone and is a short-lived effectiii) Sex Hormones(1) Small amounts ofAndrogens (Testosterone) and Estrogens secreted in males and females

(a) Impact sexual maturation and secondary sex characteristics(b) Most sex hormones are released by the gonads

2) Adrenal Medullaa) Primarily produces catecholamines (epinephrine, norepinephrine) in response to SNS stimulus (stress or trauma)

Thyroid Glands

y Regulated by hypothalamusy Secretes 3 hormones


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(1) T3: Triiodothyronine(2) T4: Thyroxine(3) Calcitonin

Thyroid Hormone: T3 and T4 can be lumped together

y Most of the hormone released is T4 (90%), but the more active hormone is T3 (10%)y T4 is converted to T3 in the liver and kidneyy Most TH bound by protein when its released (99%) and only 1% is actually active at a given time; more TH can

break away from protein if needed

y TH affects metabolism,O2 demand,O2 consumption, heat production; therefore, problems with thyroid glandcause systemic issues that affect many tissues

y Actions *see handouty Iodide is essential for TH synthesis

Calcitonin

y Reduces serum Ca levelsy Ca levelsqbone resorption (into vascular space from bone)y Hypercalcemia triggers release

ParathyroidGlands (4)

y PTH is released when serum Ca levels are lowFunction ofPTH

1. Increase bone resorptiona. Pulling Ca out of bonesb. Quick

2. Ca resorption in kidneys, in nephronsa. Pulled out of tubules into blood supply

3. Increases absorption ofCa from GI system (intestines)a. Requires activated Vitamin Db. Slower than bone resorption

Pancreas

y Insulin and GlucagonDisorders of the Anterior Pituitary

1. Hypopituitarisma. Deficiency of one or more hormones of the anterior pituitary gland or all of the hormones

(panhypopituitarism; rare)

b. Most important anterior pituitary hormones are ACTH and TSHc. Etiology

i. Tumors that compress the pituitary gland or destruction of pituitary glandii. Radiation therapy

iii. Trauma; increased intracranial pressureiv. Malnutritionv. Infarction

1. Most often post-delivery2. Blood supply increases, hemorrhage deprives pituitary gland tissue of blood


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3. Pituitary gland hypertrophies during pregnancy and requires larger blood supplyd. Assessment

i. Depend on hormone, gender and age of patientii. Visual changes/problems, possibly due to tumors

1. Peripheral vision2. Acuity

iii. Headachesiv. Cranial nerves II, III, IV, VIv. Labs

1. Serum hormone levels; more likely in clinic setting vs. hospitala. Testosterone in am

2. Stimulation testsa. Check pituitary reserves or a reserve of a particular endocrine glandb. Ex. TSH: Measure TSH level, administer TRH injection, after a period of time

draw another TSH level and note difference; TSH level would not change if

pituitary gland is not functioning, TSH level would go up if pituitary gland is

functioning

e. Deficiencies ofGonadotropinsi. Effects are different based on the gender of the patient

1. Males: Testicular failure (decreased sperm production, or absent) in post-pubertal,delayed onset of puberty or slow development of secondary sex characteristics

2. Females: Ovarian failure, loss of follicle stimulation, sterility, loss of ovulation,amenorrhea

ii. Assessment differs for adults and children1. Adult males: Loss of secondary sex characteristics, loss of facial hair, loss of body hair,

impotence, decreased libido, decreased sperm production, increased sub-cutaneous fat,

decreased muscle mass

2. Adult females: Amenorrhea, difficulty conceiving, breast atrophy, absence of pubic hair,absence of axillary hair

3. Pre-pubertal: delay in secondary sex characteristicsiii. Interventions

1. Drugsa. Prototype: Testosterone

i. Therapeutic Classification: Male sex hormoneii. Pharmacologic Classification:Androgen

iii. Buccal, transdermal, IM (typical), implantable pelletsiv. Onset of action 3-4 weeksv. Duration of action 2-4 weeksvi. Main use is to treat delayed puberty (development of secondary sex

characteristics) or to treat hypo-gonadism in males (causes maturation

of sex organs)vii. Adverse effects:1. Decreased or increased libido2. Water retention/weight gain3. May cause liver damage with prolonged use4. Acne5. Elevated cholesterol levels

viii. Prescribed to females, generally in cases of inoperable breast cancer1. Side Effects:

a. Ovulation suppressionb. Suppression of menstruation


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c. Deep voice, which may be irreversibled. Hirsutism (excessive hair growth)e. Male pattern baldnessf. Elevated cholesterol levels

ix. Contraindications:1. Prostatic hyperplasia2. Pregnancy3. Renal or hepatic dysfunction warrants caution4. Anti-coagulant use increases risk for bleeding

x. Nursing Considerations:1. Complete health history2. Impaired sexual function3. Complications4. Lab tests

a. LFTb. Cholesterol/lipid panelc. Testosterone baseline

xi. Patient Education1. Monitor weight (inform physician if of > 5lbs/wk)2. Preapism (prolonged or painful erection) > 4 hrs indicates notify

physician

a. Cold packsb. Intra-cavernous injection of alpha agonists that

constrict veins

c. Aspiration of blood from penis3. Therapeutic response is slow4. Men can develop breast cancer; usually occurs within 6 months5. Pre-pubertal patients may experience precocious sexual

development; warn patients to monitor

6. Pre-pubertal patients may experience premature closing ofepiphyses, leading to short stature

7. Injection instructions8. Dose starts low until needed effect is achieved, may be delayed

to prevent growth disruption

b. Prototype: Premarin (conjugated Estrogens)i. Therapeutic Classification:Hormone Medicationii. Pharmacological Classification: Estrogen

iii. Oraliv. Main use is female hypogonadismv. Adverse Effects:

1. H

eadache2. Bloating3. Cramps4. Breast tenderness5. More seriously:

a. Thromboembolic events (DVT, pulmonary embolus,stroke)

b. Pancreatitis6. Contraindications:

a. Breast cancer or history ofb. Cervical cancer


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vi. Nursing Responsibilities:1. Consider age of patient & whether or not theyve reached their

full growth potential, but premature closure of epiphyses can

occur and subsequent stature problems

2. History of cancers, HTN, MI, strokevii. Patient Education:

1. Take medication as prescribed2. S&Sx to report: calf pain, redness or swelling (DVT), chest painor dyspnea (pulmonary embolus)

3. Monitor BP, avoid or stop smoking (medication may not beprescribed to a patient who smokes): smoking increases risk of

adverse effects

f. Deficiencies ofGrowth Hormonei. Problems can be due to impaired synthesis, secretion, use of (tissue insensitivityii. Growth retardation is major effect

iii. Assessment1. Adults: no symptoms probably because full growth potential has been achieved2. Younger people might not meet growth expectations3. Infants may be normal size at birth, but fall off chart with age (5-6 months)

iv. Interventions1. Adults typically not treated because not needed to achieve growth2. Children, younger people (in whom epiphyses have not closed) might be treated with

exogenous GH

3. Drugsa. Prototype: Somatropin

i. Therapeutic Classification:Human Growth Hormoneii. Pharmacological Classification: Pituitary Hormone

iii. SubQ (typical) or IMiv. Produced by recombinant DNA techniquev. Expensive ($30-40K/yr)vi. Replacement therapy for young people that are not meeting their

growth potential

vii. Initial very rapid growth1. First year: 72. Second year: 3-53. Thereafter: more normal rate

viii. Growth of long bonesix. Follow patient closely by monitoring height and for growth plate closurex. Adverse Effects

1. Hyperglycemia due to insulin resistance2.

Edema3. Headache

4. HTN5. Joint or muscle pain due to hastened growth

xi. Contraindications1. Epiphysis closure2. Intracranial tumors may be enlarged3. Renal problems warrants caution

xii. Nursing Responsibilities1. Monitor for ephiphyseal closure


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2. Reconstitute fragile medication via agitation or rolling, notshaking

xiii. Patient Education1. Hip or knee pain should be reported2. Report limp to HC provider3. Discuss referral to dietician now that nutritional needs have

changed2. Hyperpituitarism

a. Etiologyi. Hormone-secreting tumor (commonly ACTH, GH, Prolactin)ii. Hypothalamus dysfunction, resulting in loss of communication between Hypothalamus and

Pituitary Gland

b. Assessmenti. Neuro S&Sx

1. Headache2. Visual disturbances3. Increased intracranial pressure ( headache)

c. Hypersecretion ofGHi. Giantism

1. Occurs when GH before epiphyses close2. Accelerated growth of long bones3. Tall stature develops

ii. Acromegaly1. Occurs when GH after the epiphyses close2. Physical changes:

a. Skeletal thicknessb. Skin hypertrophy (thickening)c. Enlarged visceral organs

iii. Assessment1. Changes in hat size, ring size, glove size2. Lethargy, fatigue3. Visual changes4. Physical changes

a. Lip & nose size with Acromegalyb. Increased size of supra-orbital ridge with Acromegalyc. Projection of jaw beyond facial features with Acromegalyd. Increased metabolism with bothe. Increased strength with bothf. Dentures that dont fit most likely with Acromegaly

iv. Drugs1.

Prototype: Sandostatina. Therapeutic Classification:Growth Hormone Antagonist

b. Pharmacological Classification: Somatostatinc. SubQ (better absorption) or IMd. Therapeutic effect: mimics action ofGH inhibiting hormone (Endogenous form is

from Hypothalamus)

e. Effective in children and adultsf. TID for Acromegaly; longer acting form can be given q 4wks via depotg. Adverse Effects

i. Hypo- or Hyperglycemiaii. N/V/D


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iii. Liver problems, monitor LFTiv. Edemav. Headachevi. Renal or liver failure warrant caution

h. Nursing Considerationsi. Height and weight monitoringii. Baseline EKGiii. Monitor heart rate: cardiac monitor in hospital or teach how to take

and log pulse; bradycardia indicates need to contact HC provider

iv. Monitor liver and biliary functionv. Monitor serum glucose levels for hypo- or hyperglycemia

i. Patient Educationi. Knowledge regarding injection of medicationii. Administer medication between meals

iii. Administer at bedtime to GI symptomsiv. RUQ pain, jaundice, N/V must be report to HC providerv. Fragile medication must be agitated or rolled (not shaken) upon

reconstitution

2. Parlodela. Has been effective in reducing size of tumors, which hopefully will cause

reductions in secretion ofGH

b. Not used very oftenc. Side effects:

i. GI Sx: N/V/D, upset stomach give w/meals to Sxii. Can cause hypotension; discuss precautions (stay in bed, go the

bathroom prior to administration)

iii. Hallucinations, nightmares, confusion, delusionsiv. Dont drive or operate heavy equipment until body gets accustomed to

medication

v. Headachesv. Hypophysectomy

1. Surgical removal of the pituitary gland2. Pre-op education is similar to other surgeries, but cough is not encouraged post-op

(deep breathing only), sneezing, lifting for fear ofCSF leakage

3. Post-op monitor for LOC; confusion, mental status changes, poor mentation because itis a CNS surgery, and CSF leakage (check for drainage in case of runny nose) on drip pad

a. Glucose strips can be used to test for CSF: + = glucoseb. Drips on pillow: + = dries with halo

4. Monitor for fluid balance due to impact of removal of pituitary gland on release of otherhormones that impact fluid balance

5. O

ral rinsesu

pon resu

mption of eating after day of NPO

/clear liqu

ids versu

s bru

shing toprotect surgical site

6. Prevent constipation in order to prevent straining (Valsava maneuver) which canpotentially lead to CSF leakage

7. Soft tissue changes might occur in feet, face and hands; Acromegaly changes probablywill not

3. Disorders of the Posterior Pituitarya. Diabetes Insipidus

i. Disorder of water metabolism: excess water loss caused by hyposecretion ofADH, or lack ofresponsiveness to ADH that is available (kidney problem)

1. Deficiency ofADH synthesis in Hypothalamus


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2. Deficiency ofADH secretion in Posterior Pituitary3. Decrease in use is a kidney problem

ii. Sx: similar to Diabetes Mellitus1. Polyuria:Large volumes of dilute urine

a. ADH ability of kidneys to concentrate urine2. Polydipsia: increased thirst and drinking due to urine loss3. Dehydration, especially in elderly due to impaired ability to ambulate to replace fluids4. Hypernatremia

iii. May be permanent of transient1. Ex. intracranial surgery leads to manipulation of pituitary gland, which shocks into

improper functioning

2. Ex. intracranial surgery leads to edema, which exerts pressure on pituitary glandiv. Classification

1. Central (CNS), or neurogenic Diabetes Insipidusa. Absent ADH or diminished ADH

i. Primary1. Problem in Pituitary Gland2. Could be familial or idiopathic

ii. Secondary1. Problem with Hypothalamus (not producing enough or any

ADH)

2. Surgical procedure3. Infection4. Trauma

2. Nephrogenica. Kidney problemb. Plenty ofADH available, but kidney is not receptive, able to recognize or

respond

c. Less commond. Not related to a in ADH, may actually be an in ADH because the body may

attempt to compensate for lack of functioning by tubules, lack of resorption of

water

e. Other medications may cause:i. Lithium may cause Diabetes Insipidusii. Declomycin may also cause DI

v. Assessment1. Polyuria: 4-30L ofurine/day2. Polydipsia: drinking lots of water to correct urine loss3. Dehydration in patients that cant adequately replace water4. Nocturia tiredness, lack of energy, lethargy5. Circulatory collapse: significant hypotension with tachycardia6. Hypernatremia lethargy, confusion, seizures

vi. Laboratory Findings1. Dilute urine: Specific Gravity < 1.005 (NL = 1.015-1.025)2. Osmolality ofurine can be 50-200 (NL = 300-1200)3. qurine Na, K4. Serum osmolality can be > 300 (NL = 280-295) because intravascular volume is due tourine elimination (hemoconcentration: solvent leads to solute, relatively)

5. serum Na, K6. Water deprivation test: demonstrates inability of kidneys to concentrate urine


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7. Draw ADH: ifCentral, primary DI expect ADH levels to be low; if Nephrogenic DI expectADH levels to be normal or elevated because the body is trying to fix the problem

8. Vasopressin test: give injection ofVasopressin (ADH), expect SG ofurine toADH ifCentral problem (not enough or no ADH), if Nephrogenic, no response because kidneys

arent receptive so more doesnt do any good

vii. Interventions1. I&O: rule of thumb, output > 200mL/hr for 2consecutive hrs, or > 500mL in any 2hrperiod needs to reported to physician2. Monitor daily weight: report weight loss3. Monitor lab work: urine SG , serum osmolality should be reported4. Encourage fluid intake >output (match or exceed output with next hours intake)5. Monitor S&Sx of dehydration6. Monitor V/S7. Monitor changes in LOC8. Oral intake preferred for fluid replacement, but IV may be needed; most likely solution

would be D5W, or NS (hypotonic)

9. Drugsa. Prototype: Desmopressin

i. Therapeutic Classification:ADH Replacementii. Pharmacological Classification: Pituitary Hormone

iii. Intra-nasal, SubQ, IV, PO (preferred)iv. Therapeutic Effects

1. Controls polyuria and polydipsia2. Effective for neurogenic (not nephrogenic) DI3. Increases permeability of collecting tubules resorption of

water in the kidneys

4. Vasoconstriction at higher dosesv. Adverse Effects

1. Water intoxicationa. Drowsinessb. Headachec. Convulsionsd. Comae. Facial flushingf. HTN

vi. Contraindications1. Nephrogenic

vii. Nursing Responsibilities1. Monitor BP2. Monitor I&O3.

Monitor weight4. Monitor for S&Sx of water intoxication (may lead to retention oftoo much fluid)

5. Monitor electrolytes6. May restrict fluids relatively7. Listen to lungs and monitoring for edema due to potential for

over-retention of fluids

8. Journal micturation frequency, I&O after discharge at homeb. Vasopression

i. Synthetic ADH (identical to ADH)ii. Immediate onset of action, given several times/day


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iii. Can cause HTN due to potent vasoconstrictive effectiv. Monitor for water intoxication due to fluid retention (I&O)

c. Diabinese (Chlorpropamide)i. First generation sulfonylureac agentii. CanADH secretion or improve its effect in the kidneys

iii. Unintendeduse (off-label)iv. May be used for patients with Nephrogenic DIb. SIADH: Syndrome ofInappropriateAnti-DiureticHormone

i. Opposite of Diabetes Insipidus (too much ADH)ii. Leads to water intoxication and Hyponatremia

iii. Feedback mechanisms that control ADH are not functioning or not functioning well enough, andADH continues to be released even though the serum osmolality is low

1. Serum osmolality goes because solute: volume ratio is too high, causing ADH to bereleased, which causes the kidneys to resorb more water, leading to osmolality

2. With SIADH, osmolality is OK, but for some reason ADH continues to be released, so theosmolality goes and ; intravascular volume as more fluids are retained

3. RAS system suppressed because kidneys are perfused renal excretion of Na, whichmay result in Hyponatremia

iv. Etiology1. Tumor, perhaps of the lung or pancreas, leukemia, Hodgkins Lymphoma

a. Tumors secrete an ADH-like substance with same physiologic action as ADH2. Head injury3. Meningitis4. Encephalitis5. Stroke6. Positive-pressure ventilation

a. Can increase intra-thoracic pressure, which can cause ADH secretion from theHypothalamus because the baroreceptor send messages to the Hypothalamus

to release ADH

7. Stress8. Pain

v. Assessment1. BP elevation2. Crackles due to fluid overload3. N/V4. Abdominal distention5. Headache6. Abdominal cramps7. Weight gain8. Altered LOC9.

Concentrated

urine (osmolality > 1200, S

G> 1.032)10.Decreased serum osmolality (


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a. Serum Na and osmolalityb. Urine osmolality and SG

4. Daily weights5. Changes in LOC and mentation6. Muscle twitching7. Seizures8. Hyponatremia may necessitate replacement with Na tablets or hypertonic IV solution(Ex. 3% NaCl, not D5W because its basically free water)9. Medications

a. Diureticsi. Caution because of potential for Na loss

b. Conivaptani. Vasopressin-receptor antagonistii. IV or PO

iii. Increases urine production ( excretion of free water)iv. plasma osmolality and serum Na but not excretion of Na

c. Declomycini. Off-label useii. Tetracycline antibiotic that happens to inhibit ADH

iii. Allowsurine production4. Disorders of the Adrenal Glands

a. Adrenal Insufficiency: Addisons Diseasei. Hypofunction of the adrenal cortex leads to insufficient production ofAldosterone and Cortisolii. Etiology

1. Autoimmune problem2. Tuberculosis3. Sepsis4. Adrenalectomy (medications are prescribed by physician to prevent when bilateral

adrenalectomies are performed)

5. High doses of glucocorticoids that are abruptly discontinued; must wean off otherwisethe normal negative feedback system doesnt kick in and as levels fall off the body

doesnt worry about it; body needs time to recognize the decrease so that it can excrete

ACTH to maintain normal circulating glucocorticoid

iii. Assessment1. V/S2. LOC and mentation3. Hyperpigmentation of the skin: caused by high levels ofACTH, which can arise with

Addisons because the body doesnt know that the adrenal glands cant produce cortisol

so it keeps secreting more and more from the pituitary gland

4. Weight loss and anorexia5.

Lethargy6. Depression

7. Muscle weakness8. Salt craving9. Low cortisol levels10.Low glucose levels11.Elevated serum K levels12.ACTH stimulation test: inject ACTH, will lead to no response in Cortisol levels with

Addisons

iv. Interventions1. Monitor I & O


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2. Monitor daily weight3. Encourage fluids4. Increase Na in diet5. Safety R/T mentation changes and depression: simple directions, safe envt (slip & trip

hazards)

6. Drugsa. Prototype: Hydrocortisonei. IV, PO, IM, SQ

ii. Decadron, Deltasone, Solu-Medroliii. Replacement hormone: physiologic (lower) dose versus therapeutic

dose

iv. Adverse Effects1. Careful with patients with DM due to risk of hyperglycemia2. Careful with patients with osteoporosis due to Ca loss from

bones

3. Less risk because physiologic dose is lowv. Nursing Considerations

1. Monitor blood sugar2. Monitor Ca, Na, K3. Monitor weight4. Back aches, bone pain might indicate fracture, especially with

higher doses over longer durations

5. Mood changes6. Assess for infection due to immunosuppressive action7. Monitor for S&Sx ofCushings Syndrome (opposite ofAddisons

disease): hyperfunction of the adrenal cortex

vi. Patient Education1. Awareness of potential for weight gain2. Report Sx of heart burn and indigestion due to risk for peptic

ulcers3. Watch wound healing4. Caution not to stop meds, must be weaned off

b. Prototype: Florinefi. Therapeutic Classification:HypoaldosteroneAgentii. Pharmacological Classification: Mineralcorticoid

iii. Replacement therapy for Addisons Diseaseiv. Adverse Effects due to Mineralcorticoid activity:

1. Na and fluid retention2. Edema3. Hypertension4.

Renal impairment, heart fail

u

re,HT

N requ

ire cau

tion5. Hypokalemiaa. Lethargy, weakness, confusion, disorientation

6. Monitor weight and I&Oa. Weight gain expected

v. Patient Education1. S&Sx of hypokalemia;K in diet2. Daily weight; report changes to HC provider

b. Hyperfunction of the Adrenal Cortex: Cushings Syndromei. Elevated levels of serum cortisol or too much ACTH, which increases cortisol levels


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ii. Affect CHO metabolism and mineral metabolism and some potentially life-threatening problemsin terms of physiologic and psychologic function

iii. Etiology:1. Typically tumor of 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 too much ACTH to be released

3. Tumor in the lungs, GI tract or pancreas because they can produce an ACTH-likesubstance (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

iv. Assessment:1. Muscle wasting, weakness2. Bruise easily3. Fragile skin4. Mood swings5. Poor wound healing6. Susceptibility to infection7. Osteoporosis8. Abnormal fat deposits

a. Moon faceb. Truncal obesityc. Buffalo hump: fat pad on back of neck

9. Impotence in males, amenorrhea in females10.Labs:

a. Serum cortisol: expect elevationb. Na elevationc. Elevated glucosed. ACTH level may be drawn: can be decreased (high doses of glucocorticoid meds)

or elevated (problem with pituitary gland or hypothalamus)

v. Interventions1. Monitor F&E2. I&O, daily weight3. Safety issues due to susceptibility to fractures due to Ca resorption from bone: envt

safety

4. Pace activities to prevent fatigue5. Risk for infection6. Therapeutic Management

a. Identify cause if possible and manage that causei. Tumor removal or chemoii. Prescribed medication adjust dose

b. Drugs: Nizorali. Blocks synthesis of glucocorticoidsii. Would not be given to patients prescribed glucocorticoids

iii. Patients pituitary gland compensates and may increase production ofACTH, which could reverse effect of medication

iv. LFT baseline due to potential for toxicity to liverc. Surgery

i. Hypophysectomy: removal of pituitary glandii. Adrenalectomy: removal of one or both adrenal glands

iii. Both require physiological replacement5. Thyroid Problems


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a. Hyperthyroidismi. Excess secretion ofTH from the thyroid glands, causing a person to have a high metabolism

1. Elevations in CO2. Elevations in peripheral blood flow3. Elevations in body temperature4. Elevations in O2 demand and consumption

ii. Etiology1. Most common cause is Graves disease (80%)a. Most likely autoimmuneb. Antibodies are produced and they bind to the TSH receptors in the thyroid

gland, and then act like TSH

c. Increases production and secretion ofT3 and T42. Problem with Pituitary Gland

a. Producing too much TSH increases TH releaseb. Thyroiditis (inflammation of the Thyroid Gland)c. Tumor

iii. S&Sx1. Gradual in onset2. Expect to see Sx that relate tometabolism3. Tachycardia4. HTN5. Palpitations My heart is pounding out of my chest6. Anxiety, nervousness7. appetite with weight loss8. Frequent bowel movements9. Heat intolerance10. Insomnia, poor sleep quality, frequent waking during the night11.Diaphoresis12.Visual changes; double vision13.Exophthalmos: protruding of eyes

a. Fluid accumulates in extraocular muscles and fat pads accumulate behindeyeballs

b. Tends to be irreversible even when hyperthyroidism corrected14.Goiter; enlargement ofThyroid Gland15.Hyperactive reflexes (Deep Tendon Reflexes DTRs)16.Emotional lability, irritability17.Hyperactive, manic-type manner18.Exercise intolerance

iv. Labs1. TSH levels are low: 0.4-4.0 = Normal2.

Free

T4 level (

Thyroid

Function

Test) is elevated3. Thyroid Scan: radioactive Iodide uptake

a. Graves: whole Thyroid Gland is activeb. Tumor: hot spot(s)c. Malignant tumor: cold spot(s)

v. Interventions1. Monitor V/S, esp. BP and P, T2. Patient might complain of chest pain, palpitations3. Encourage rest and quiet envt4. Frequent linen and clothing changes5. Daily weights


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6. Assess mental status7. Safety issues

a. Eye protection: Exophthalmos puts patient at risk for corneal abrasions andulcerations

8. Frequent meals due to hypermetabolisma. More caloriesb. More protein9. Medicationsa. Prototype = PTU (Propothyuricil)

i. Therapeutic Classification : Anti-Thyroid Agentii. Pharmacological Classification: ThyroidHormone Inhibitor

iii. POiv. Rapid absorptionv. Blocks the production ofTHvi. May give to a patient prior to Thyroidectomy to normalize levels ofTH

because surgical manipulation ofThyroidGland could lead to further

release ofTH (significant, i.e. Thyroid Storm)

vii. Blocks conversion ofT4 to T3 in the periphery (and T3 is the more activeform)

viii. Doesnt affect TH that is already synthesized; rapid absorption but notrapid reduction in Sx (takes several weeks or months to lower TH levels

sufficiently to reduce Sx)

ix. Usually administered for 12-18 months; about 50% of patientsexperience a relapse after completion of therapy

x. Adverse Effects:xi. Some patients can have leukopenia, so Sx of infection should be

reported to HC provider

xii. Contraindications:1. Caution with liver disease2. Typically not given to pregnant women, but might be used in

case of crisis; some can cross placenta may choose

Thyroidectomy instead

xiii. Nursing Responsibilities1. Continue to assess for Hyperthyroidism2. Watch HR via cardiac monitoring3. Lab results: Free T4 (Thyroid Function Test), TSH levels4. Once therapy starts, monitor Sx for response to therapy

a. Weight gainb. Decrease heart rate and temp

xiv. Patient Education1.

Monitor p

u

lse daily: report >100 (may need to dose), < 60(may need to dose)

2. Fever spike or rash should be reported due to risk ofleukopenia, agranulocytosis; may require antibiotics

b. Radioactive Iodine Uptake (Sodium-Iodide 131) Iodotropei. Preferred treatment by most endocrinologists

1. Effective2. Safe3. Cost-effective4. Administered orally


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ii. Thyroid Gland picks of Sodium Iodide (with radioactive element), and itstarts destroying the thyroid tissue, eventually lowering the TH levels

iii. Most likely patient will become Hypothyroid and will need to be placedon thyroid replacement (Synthroid)

iv. May see change in Sx in a month or sov. Usually radioactive precautions are not necessary, except with very high

doses1. life is 8 days2. Most is excreted (90% gone within 48 hours)3. Caution with household infants and children (holding); may

need to limit contact while on medication

4. Handwashing after voiding because it is excreted from thekidneys

c. Potassium Iodide, Sodium Iodide, SSKI (Saturated Solution ofPotassium Iodide)i. Used more in the past prior to PTU and Radioactive Iodideii. High concentrations ofIodide reduce Iodide uptake due to excess

(reduces synthesis ofTH)

iii. Side effects:1. Metallic taste in mouth2. Ulcers in mouth3. Ulcerations in GI system4. Discoloration of teeth (may require straw)

d. Inderali. Beta blockerii. Slows rapid heart rate to increase comfort

10.Thyroidectomya. Not treatment of choice, but can be used for patients that refuse or cant

tolerate other therapies

b. PostOp: monitor for respiratory distressi. Edema around larynx could compromise airway

c. Monitor vital signsd. Support head and necke. Wear ice collar to decrease edemaf. Humidified air or O2g. Trach set at bedside in case of airway problemsh. Encourage deep breathing exercisesi. Try to reduce coughing/dont encourage

j. Observe for complicationsi. Respiratory problemsii.

Bleeding: blood may not be on dressing over incision site, co

uld leakbehind neck

iii. Keep suction availableiv. Keep trach set availablev. Monitor for hypocalcemia

1. Numbness2. Tingling of the mouth or toes or fingers3. Muscle twitching4. Takes time to develop5. Occurs due to removal ofPT glands that are embedded in the

Thyroid


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6. Tests for hypocalcemiaa. Trousseaus sign: inflate BP cuff on arm to above SBP

and keep in place for 3 min + leads to carpal spasm

(pain in forearm)

b. Chvosteks sign: lightly tap facial nerve + leads tospasm of facial muscle

7. Laryngeal nerve damage; weak or hoarse voicea. Should passb. Voice rest after surgery perhaps

vi. Exophthalmos may require eye lubrication or dark glasses due toproblems with photophobia

vii. Thyroid Storm1. Acute exacerbation of Sx, can be life-threatening2. Mortality rate of > 50%3. Generally patients with long-term untreated or undertreated

hyperthyroidism, or patients that experience a stressor such as

infection or illness

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

5. Need immediate treatmenta. Monitor airwayb. Start on PTUc. Might give Iodide in addition to PTUd. If temperature elevated, might be treated with

acetaminophen

e. Beta blockers (e.g. Inderal) may be given to heartrate and strength of contraction (decreasing work

load of heart) and because it blocks the conversion ofT4to T3

f. Small doses of insulin may be given to controlhyperglycemia

g. IV fluids: prevent vascular collapse but caution due torisk of heart failure

h. Oxygeni. Cooling blanket

j. Monitor heart rate (cardiac monitor) and rhythmk. Patient may become hypothyroid, which would

necessitate hormone replacement e.g. Synthroid

b. Hypothyroidismi. Etiology

1. Hashimotos Disease is leading causea. Autoimmune problem in which antibodies are formed that trigger lymphocytesto get into the thyroid gland and destroy the thyroid tissue (cells that produce T3and T4)

2. Tumor and radiation therapy3. Iatrogenic (something we did to them)

a. Radioactive Iodide uptake therapyb. Thyroidectomy

4. Pituitary Gland Problema. Not producing TSH or enough TSHb. Hypopituitarism


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c. Hypophysectomy5. Infections6. Iodine Deficiency7. Idiopathic8. Amiodarone and Lithium both cause hypothyroidism; D/C or cover with Levothyroxine

temporarily

ii. Assessment1. Slow onset, may be undiagnosed for a long time2. Increased weight3. Fatigue4. Goiter5. Difficulty swallowing due to goiter6. Cold intolerance7. Constipation8. Dry skin9. Mentation changes10.Memory problems11.Slow speech12.Difficulty problem-solving13.Lethargy14.Sluggish reflexes15.Bradycardia16.Respiratory depression

iii. Labs & Diagnostics1. TSH levels are expected to be elevated with hypothyroidism unless Pituitary Gland

dysfunction

2. Free T4 (Thyroid Function Test) expected to be low with hypothyroidism3. May test for antibodies with Hashimotos4. Skull X-ray5. CT scan or MRI to see if problem lies in Pituitary Gland

iv. Interventions1. No cure for Hashimotos; treat with HRT2. Drugs:

a. Prototype = Levothyroxinei. Therapeutic Classification: Thyroid Hormoneii. Pharmacologic Classification: Thyroid Hormone Replacement

iii. Synthetic form ofT4iv. Oralv. Takes 4-6 weeks for full effectvi. IV form for Myxedema Coma

vii. A

dverse Effects:1. Rare at normal doses2. High doses: tachycardia,temperature, chest pain, Sx that you

would expect to see with hyperthyroidism

viii. Contraindications:1. MI due to potential for workload of heart due to in

metabolism

ix. Nursing Responsibilities1. Assess for S&Sx of hypothyroidism before treatment, but

monitor for S&Sx of hypo- and hyperthyroidism after onset of

therapy (may be getting to much TH)


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2. Monitor labs: T3, T4 (TSH) levels3. Cardiac monitor4. Monitor pulse: P > 100 hold and talk to physician

x. Patient Education1. Monitor for S&Sx of hyperthyroidism notify physician2. Check pulse daily, keep log and look for trends3. No external warming measures (e.g. electric blanket) becausevasodilation could lead to hypotension4. Stool softeners, higher bulk diet5. Monitor for lethargy6. Monitor for mental status changes7. Safety: more careful, frequent directions, reminders,

environment

xi. Myxedema Coma1. Equivalent to Thyroid Storm in a person who is hypothyroid, i.e.

an acute exacerbation of hypothyroidism

2. 50% mortality rate3. May develop due to stressor, chemotherapy, surgery, acute

illness

4. Decreased metabolism can affect the heart, as it can the othertissues, and if the hearts metabolism goes too low it can affect

the cardiac output which leads to hypotension, brain

perfusion and eventually organ and system failure

5. S&Sx (same as you would expect with hypothyroidism but moreacute and quicker onset)

a. Bradycardiab. Respiratory Depressionc. Hypothermia

6. Treatmenta. Monitor BP, P, CV systemb. IV perhaps, to maintain fluids/circulationc. Monitor airwayd. Thyroid Hormone quickly, e.g. IV Synthroide. Cont. to monitor I/O, V/S, cardiac collapsef. Monitor heart rhythm (may need a pace maker ifHR

too slow)

6. Disorders of the ParathyroidGlandsa. Hyperparathyroidism

i. Types1. Primary:Hyperplasia of one or more of 4 PTH glands, can be due to tumor(s)2.

Secondary:

PTHgland enlargement d

ue to chronic hypocalcemiaa. Hypertrophy

b. Can be caused by renal disease3. Tertiary: Loss of negative feedback control

a. PT gland cont. to make PTH even though Ca levels are adequateii. Actions ofPTH

1. Causes Ca to be removed from bone risk of osteoporosis2. Causes Ca to be resorbed from the renal tubules3. Causes Ca to be resorbed from the GI system

iii. Assessment1. Polyuria because kidneys try to reduce serum Ca by making more urine


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2. Kidney stones3. N/V, abdominal pain4. Bone pain, pathological fractures5. Weakness

iv. Labs1. Elevated serum Ca2. Elevated PTH levelsv. Interventions1. Patient safety r/t Ca being pulled out of bones: envt, slip and trip2. Straining the urine, flank pain kidney stones3. Daily weight4. Encourage progressive activity

vi. Therapeutic Management1. IV NS to serum Ca andintravascular volume so kidneys make more urine and

thereby eliminate more Ca

2. Diuretics3. Parathyroidectomy4. Calcitonin: function is to reduce serum Ca levels

b. Hypoparathyroidismi. Hypocalcemia that could lead to tetany due to increased (?) threshold for excitability of nerves

and muscles and causes them to be easily stimulated

ii. Generally iatrogenic (ex. Parathyroidectomy)iii. Assessment

1. Abdominal pain, N/V2. Anxiety3. Tremors4. Muscle spasm5. Difficulty swallowing6. Trousseaus and Chvosteks signs can be +

iv. Interventions: consider safety and comfort1. High Ca diet2. Medications:

a. Prototype = Calcium Saltsi. Therapeutic Classification:Calcium Supplementsii. Pharmacological Classification:Calcium Replacement

iii. Can be given IV or POiv. Ex. TUMSv. Can also be used to treat osteoporosisvi. Adverse Effects:

1. Rare2.

Hypercalcemia if high doses3. Kidney stones

vii. Nursing Responsibilities1. Assess for S&Sx of hypercalcemia

a. Drowsyb. Weakc. N/Vd. urine production

2. Assess for S&Sx of hypocalcemiaa. Chvosteks signb. Paresthesias


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c. Seizures3. Monitor Ca levels

viii. Patient Education1. Must take meds every day, with meals or within hr following

b. Calcitrioli. Therapeutic Classification:Vitamin Dii. Pharmacologic Classification: Bone Resorption Inhibitoriii. Adverse Effects:

1. Atypical2. Could become hypercalcemic: monitor

n180 endocrine

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