Adrenal Cortex Disorders Fall 2019 - lahc323325.weebly.comlahc323325.weebly.com/uploads/1/1/0/6/110686185/adrenal_cortex_disorders_handouts_fall...Adrenal Cortex Disorders Fall 2019.ppt

Fall 2019 -‐ Spring 2020

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Disorders of Adrenal Cortex

•  Cushing Syndrome

(Adrenocortical Hyperfunction)

•  Addison’s Disease (Adrenocortical Insufficiency)


Fluid & Electrolytes

Mobility

Perfusion

Stress & Coping

How will you know if your paBent has an adrenal gland disorder?

What nursing assessments are involved? 1

Changes in CorBsol RegulaBon Altera1on Descrip1on/Defini1on Manifesta1ons Interven1ons and

Therapies

Changes in corBsol regulaBon

Symptoms result from excess or deficient secreBon of corBsol from the adrenal glands. •  Cushing Syndrome •  Addison’s Disease

Excess corBsol results in Cushing syndrome, which is accompanied by a moon face and central obesity along with other symptoms. CorBsol deficiency results in Addison’s disease, which is accompanied by muscle weakness, faBgue, weight loss, and other symptoms.

Cushing syndrome is treated with either decreasing corBcosteroid dosage or surgery to remove a tumor, depending on the cause. Addison’s disease is treated with oral or injected corBcosteroids.

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ADRENAL CORTEX

•  GLUCOCORTICOIDS: Regulate metabolism, increase bood glucose levels, criBcal in physiological stress response

•  MINERALOCORTICOIDS: Regulate sodium & potassium balance (Aldosterone)

•  ANDROGENS: Growth & development, sexual development in women

Three classificaBons:

1.  GlucocorBcoids 2.  MineralocorBcoids 3.  Androgens

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GLAND: ADRENAL; HORMONE: CORTISOL

ETIOLOGY & PATHOPHYSIOLOGY: • Common causes: –  Iatrogenic administration of exogenous corticosteroids (prednisone)

– ACTH-‐secreting pituitary adenoma

– Adrenal tumors – Ectopic ACTH production by tumors

Cushing Syndrome – Clinical condiBon that results form chronic exposure to excess corBcosteroids, parBcularly glucocorBcoids

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Cushing Syndrome ñ Glucocorticoids •  Excess glucocorticoids

dominate: – Hyperglycemia related to glucose intolerance and ↑ gluconeogenesis

– Muscle wasting → weakness – Loss of bone matrix → osteoporosis and back pain

– Loss of collagen → thin skin, easily bruises

– Delay in wound healing

DIAGNOSTIC STUDIES: •  Confirmation of ↑ plasma

cortisol levels: (1) midnight or late night salivary cortisol, (2) low-‐dose dexamethasone suppression test, (3) 24-‐hour urine cortisol (Levels >80-‐120 mcg/24 hours)

•  Plasma ACTH levels: •  High or normal with

Cushing disease (pituitary etiology)

•  Low or undetectable with Cushing syndrome –adrenal/medication etiology

•  CT/MRI (brain/abdomen)

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Cushing Syndrome ñ Glucocorticoids

CLINICAL MANIFESTATIONS: General appearance: truncal obesity, moon face, fat deposits back of neck & shoulders (buffalo hump) Integumentary: thin, fragile skin, purplish/red striae, petechial hemorrhages, bruises, rosey cheeks, acne, poor wound healing Cardiovascular: hypervolemia, HTN, lower extremity edema Gastrointes1nal: épepsin and HCL acid secreBon, PUD, anorexia Renal/urinary: glycosuria, hypercalciuria, renal stones

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Cushing Syndrome ñ Glucocorticoids CLINICAL MANIFESTATIONS:

Musculoskeletal: extremity muscle wasBng, faBgue, osteoporosis, awkward gait, back pain, weakness, compression fx Immune: inhibited immune response, allergic response suppression Metabolic: hyperglycemia, negaBve nitrogen balance, dyslipidemia Emo1onal: euphoria, irritability, depression, insomnia, anxiety

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Cushing Syndrome ñMineralocorticoids

CLINICAL MANIFESTATIONS:

Cardiovascular: HTN, hypervolemia F&E: sodium & water retenBon, hypokalemia, edema, alkalosis

•  Mineralocorticoid excess: •  Hypokalemia •  Hypertension

•  Adrenal androgen excess → •  Severe acne •  Virilization in

women •  Feminization in

men

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Cushing Syndrome •  If cause is iatrogenic (e.g.

prednisone) –  Gradually discontinue therapy –  Decrease dose –  Convert to an alternate-‐day regimen

•  Dose must be tapered gradually to avoid adrenal crisis

•  Surgical Therapy: –  Pituitary adenoma –  Adrenalectomy

•  RadiaBon therapy for paBents who are not good surgical candidates

² Primary goal – normalize hormone secretion

² Treatment depends on cause

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Nursing Implementation

ACUTE INTERVENTIONS: •  Monitor VS, I&O, F&E, daily

weight, glucose + complicating conditions (e.g. CVD, DM, infection)

•  Assess for S&S of inflammation/infection (which may be minimal or absent), pain, loss of function, thromboembolism, pulmonary emboli

•  Provide emotional support –  Patient may feel unattractive or unwanted

–  Remain sensitive to patient’s feelings and be respectful

–  Reassure patient that physical changes and emotional lability will resolve when hormone levels return to normal

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Audience Response QuesBon An IV hydrocortisone infusion is started before a patient is taken to surgery for a bilateral adrenalectomy. Which explanation, if given by the nurse, is most appropriate? a.  “The medication prevents sodium and water retention after surgery.” b.  “The drug prevent clots from forming in the legs during your recovery from surgery.” c.  “This medicine is given to help your body respond to stress after removal of the adrenal glands.” d.  “This drug stimulates your immune system and promotes wound healing.”

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Interprofessional Care –Surgical Therapy Cushing Syndrome

•  Surgical removal of pituitary tumor using the transsphenoidal approach (see pg. 1158)

•  Adrenalectomy –if caused by adrenal tumors or hyperplasia

INDICATIONS:

•  Surgical removal or irradiation of pituitary adenoma

•  Adrenalectomy for adrenal tumors or hyperplasia

•  Removal of ACTH-‐secreting tumors

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Interprofessional Care Surgical Therapy Cushing Syndrome

•  Surgically opBmized – Cardiac clearance – F&E correcBons – Hyperglycemic control – NutriBonally adequate

SURGICAL THERAPY: Preoperative Care Ø  Surgical/

Anesthesia consent Ø  Pre-‐op labs Ø Medical clearance Ø  Pre/Post-‐op

teaching Ø NPO Fall 2019 -‐ Spring 2020 13

SURGICAL THERAPY ADRENALECTOMY: Unilateral/Bilateral

•  Laparoscopic •  Open ²  Compare & contrast

postop complicaBons between surgery of the adrenal vs. thyroid/parathyroid glands



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•  Monitor VS, ↑ Risk of hemorrhage •  Large release of hormones into

circulation → instabilities in BP, F&E •  Monitor for acute adrenal insufficiency:

–  Vomiting, increased weakness, dehydration, hypotension, painful joints, pruritus, peeling skin, severe emotional disturbances

•  Monitoring for subtle signs of infection

•  Meticulous care to prevent infection •  Increased risk for:

–  Problems with glycemic control –  Susceptibility to infection –  Delayed wound healing

SURGICAL THERAPY: Postoperative Care Ø  Surgical site Ø  IVF,I&O,F&E balance Ø  NGT, FC, JP drains Ø  Diet Ø  Activity Ø  VTE prophylaxis Ø  Pain management Ø  High doses of

corticosteroids are given IV during and several days after surgery



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Nursing Implementation

TEACHING NEEDS: (lack of endogenous corBcosteroids) •  Home health nurse •  Wear MedicAlert bracelet at all times •  Avoid exposure to extremes of temperature,

infection, and stress •  Teach patients about medication use and to monitor

for side effects •  Teach how to adjust medication and when to call

health care provider •  Lifetime corBcosteroid replacement therapy

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Patient Goals/Outcomes: •  Experience relief of

symptoms •  Experience no S&S infection •  Avoid serious complications •  Maintain positive self-‐image •  Verbalize acceptance of

appearance and actively participate in therapeutic plan

•  Maintain weight appropriate for height

•  Heal skin wounds and maintain intact skin

Nursing Diagnoses: •  Risk for

infection •  Risk for

overweight •  Disturbed body

image •  Impaired skin

integrity Fall 2019 -‐ Spring 2020 17

GLAND: ADRENAL; HORMONE: CORTISOL

ETIOLOGY & PATHOPHYSIOLOGY: •  Primary: caused by lack of

glucocorticoids, mineralocorticoids, and androgens

•  Secondary: lack of pituitary ACTH, lack of glucocorticoids and androgens, mineralcorticoids rarely deficient

Addison’s Disease – HypofuncBon of the adrenal cortex from a primary cause. All 3 classes of adrenal corBcosteroids are reduced

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Addison’s Disease êGLUCOCORTICOIDS •  Common causes:

–  Autoimmune, antibodies destroy adrenal cortex

–  Amyloidosis –  Fungal infections –  AIDS Metastatic cancer

•  Iatrogenic Addison’s disease –  Adrenal hemorrhage –  Chemotherapy –  Ketoconazole therapy for AIDS –  Bilateral adrenalectomy

DIAGNOSTIC STUDIES: •  ACTH SBmulaBon Test

•  Baseline levels of cortisol and ACTH, IV injection of synthetic ACTH

•  Levels rechecked after 30 and 60 minutes = ↑ Blood cortisol levels is normal

•  Little or no ↑ in cortisol levels in Addison’s disease

•  CRH SBmulaBon Test •  Abnormal ACTH test

response •  IV injection of synthetic CRH •  Blood drawn after 30 and 60

minutes = High ACTH levels with no cortisol indicates Addison’s disease

•  ↑ Potassium, ↑ BUN, ↓ Chloride, sodium, glucose

•  Anemia •  ECG changes •  CT scan, MRI

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CLINICAL MANIFESTATIONS: General appearance: weight loss, emaciaBon Integumentary: bronzed/smokey hyperpigmentaBon of face, neck, hands (creases), buccal membranes, nipples, genitalia, and scars (if pituitary funcBon normal), viBligo, alopecia Cardiovascular: hypotension, vasodilaBon Gastrointes1nal: anorexia, n/v, cramping, abd pain, diarrhea Musculoskeletal: faBgue Immune: tendency for coexisBng autoimmune diseases Metabolic: hyponatremia, insulin sensiBvity, fever Emo1onal: depression, exhausBon or irritability, confusions, delusion

•  Insidious onset •  Anorexia •  Nausea •  Progressive weakness •  Fatigue •  Weight loss

•  Disease often advanced before diagnosed


Addison’s Disease êGLUCOCORTICOIDS

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Addison’s Disease êMINERALOCORTICOIDS

CLINICAL MANIFESTATIONS: Cardiovascular: hypovolemia, tendency toward shock, decreased cardiac output F&E: sodium loss, decreased ECF volume, hyperkalemia, salt craving

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Addisonian Crisis MANIFESTATIONS OF GLUCOCORTICOID AND MINERALOCORTICOID DEFICIENCIES:

– Hypotension, tachycardia – Dehydration – ↓ Sodium, ↑ potassium, ↓ glucose

– Fever, weakness, confusion – Severe vomiting, diarrhea, pain

– Shock → circulatory collapse

•  Acute adrenal insufficiency •  Insufficient or

sudden, sharp decrease in hormones

•  Various triggers: •  stress (infection,

surgery, psychologic)

•  Sudden withdrawal corticosteroids

•  Adrenal surgery •  Sudden pituitary

gland destruction

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Addisonian Crisis •  Shock management •  High-‐dose

hydrocortisone replacement

•  0.9% saline solution and 5% dextrose

•  Correct fluid and electrolyte imbalance

•  Assess vital signs and neurologic status

•  Daily weight •  Accurate I&O (FC) •  Calm environment •  Watch for signs of

Cushing syndrome

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Audience Response QuesBon

The nurse administers corticosteroids to a patient with acute adrenal insufficiency. The nurse determines that treatment is effective if what is observed? a.  The patient is alert and oriented b.  The patient’s lung sounds are clear c.  The patient’s urinary output increases d.  The patient’s potassium level is 5.0 mEq/L

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Addison’s Disease Interprofessional Care

Patient teaching of dosing medications: •  Glucocorticoids in divided doses •  Mineralocorticoids once in the morning

–  Reflects normal circadian rhythm –  Decreases side effects of

corticosteroids •  Need to increase corticosteroids during

times of stress Pa1ent Teaching: •  Report signs and symptoms of

corticosteroid deficiency and excess to HCP

•  Carry identification and wear medical ID bracelet

•  Emergency kit •  How to administer IM hydrocortisone •  Written instructions

•  Manage underlying cause

•  Hormone therapy: •  Hydrocortisone •  Fludrocortisone

(Florinef)

•  Increase dietary salt intake

Fall 2019 -‐ Spring 2020 25

Corticosteroid Therapy •  Expected effects of

corticosteroid therapy – Antiinflammatory action –  Immunosuppression – Maintenance of normal BP

•  Effective in treating many diseases and disorders ² What are

examples?

•  Complications and side effects with long-‐term use

•  Potential benefits must be weighed against risks

Fall 2019 -‐ Spring 2020 26

Corticosteroid Therapy

Pa1ent Teaching: •  Dietary needs •  Rest and exercise* needs •  Sodium restriction if edema

occurs •  Need to monitor for

hyperglycemia * •  Notify health care provider if

epigastric pain develops * •  Need to prevent injury/

infection •  Inform all health care providers

Side effects: •  ↓ Potassium and calcium •  ↑ Glucose and BP •  Delayed healing •  Susceptibility to infection •  Suppressed immune

response •  Peptic ulcer disease •  Muscle atrophy/weakness •  Mood and behavior

changes •  Moon facies, truncal

obesity •  Protein depletion •  Risk for acute adrenal

crisis if therapy is stopped abruptly

Fall 2019 -‐ Spring 2020 27

Documents

Adrenal Cortex Disorders Fall 2019 - lahc323325.weebly.comlahc323325.weebly.com/uploads/1/1/0/6/110686185/adrenal_cortex_disorders_handouts_fall...Adrenal Cortex Disorders Fall 2019.ppt