Disorders of Adrenal Cortex and Adrenal Medulla Flashcards
Adrenal Medulla
makes epinephrine and norepinephrine
Adrenal Cortex
makes corticosteroids: Glucocorticoids, mineral corticoids, androgens
Glucocorticoids
Cortisol
Regulates metabolsim, Increased BS, Regulates body’s stress response
Mineralcorticoids
Aldosterone
Regulate Fluid and Electrolyte balance
excess amounts = low K, elevated BP, fluid retention
Androgens
Sex Hormones: estrogen, testosterone, andosterone
regulate growth and development in both genders, regulate sexual activity in women
Hormones of Adrenal Cortex: ACTH
Anterior Pituitary releases ACTH, ACTH fosters growth of adrenal cortex, stimulates secretion of corticosteroids
Once appropriate levels are reaches, ACTH stops corticosteroids from being released
Cushing Syndrome
Most common cause: Administration of exogenous corticosteroids
Too much corticosteroids; no specific etiology
other causes: adrenal tumors and actinic ACTH production by a tumor outside of hypothalamic-pituitary-adrenal axis
Exogenous corticosteroids
an outside source; too many steroids for too long
Endogenous corticosteroids
ACTH secreting pituitary tumor (Cushing’s Disease)
Cushing Syndrome Clinical Manifestations
Primarily r/t excess glucocorticoids; excess androgens and mineralcorticoids may be present:
Truncal Obesity, “Moon Face”, “Buffalo Hump”, purple striae on abdomen, breasts, buttock; acne, hirsutism and menstrual irregularities in women
Lack of muscle tone/bone breakdown
HTN, unexplained hypokalemia, hyperglycemia
Prolonged healing time of wounds (suppressed inflammation which is needed for healing)
Cushing Syndrome: Dx studies
24hr urine collection for free cortisol (needs to be started after the first urination in the morning)
Dexamethasone suppression test Plasma cortisol levels CT/MRI of pituitary and adrenal glands Plasma ACTH Serum Electrolytes (BS, K, Na)
*Cortisol levels are highest in the morning but vary during the day depending on time and whats going on (stress)
Cushing Syndrome Collaborative Care
Goal: return hormone levels to w/in normal limits!
tx depends on underlying cause
Pituitary Adenoma collaborative care
Transsphenoidal approach hypophysectomy
- meningitis concern, do not brush teeth (suture line in gums), cannot sneeze, cough b/c of ICP
Radiation Therapy
Ectopic ACTH - secreting tumor collaborative care
Treat primary neoplasm
Treat cancer!
Adrenal Tumors collaborative Care
Adrenalectomy (complex procedure)
- May need to perform bilaterally
- Laparoscopic procedure unless tumor is malignant
Pharmacologic Therapy - Medical Adrenalectomy (treat w/ meds)
- Ketaconazole “Azole”
- Aminoglutethimide
- May be used in addition to surgery or if surgery is contraindicated
Azoles for Adrenal Tumors
High does of antifungals can cause adrenal cortex injury
Prolonged exogenous corticosteroids collaborative care
discontinue by tapering dose (b/c the adrenal cortex will need to start producing it’s own steroids again)
reduce dose
convert to alternating day regimen (every other day)
Cushing Syndrome nursing dx
Risk for infection
Disturbed self-image
Impaired skin integrity (risk for wounds)
Risk for imbalanced fluid volume
Cushing Syndrome Nursing Management
monitor CV function, manage DM, closely monitor s/s of infection (fever and inflammation will be masked - look for pain and change in mentation)
- d/c care varies depending on client
- educate to wear MEDICAL ALERT BRACELET
- avoid temp. extremes, infections, emotional stress
Reassure client physical changes will resolve once hormone levels return to normal
Open and Laparoscopic Adrenalectomy Nursing Management
- high risk of hemorrhage
- manipulation may release large amounts of hormones
- carefully monitor BP, F&E status post op
- IV corticosteroids post-op (to replace everything that was taken away)
- fall risk post-op if hypotension develops from hypocorticolism
- morning urine cortisol levels evaluate surgery effectiveness
Adrenocortical Insufficiency
Primary Cause: Addison’s Disease; usually from autoimmune response
Secondary Cause: Lack of ACTH secretion by pituitary; may be from pituitary disease or result of exogenous administration of corticosteroids
Adrenocortical Insufficiency Clinical Manifestations
Generally 90% of adrenal cortex destroyed before symptoms present; significantly delays dx, insidious onset, manifestations for primary and secondary similar
Weakness, fatigue weightless, anorexia, skin hyper pigmentation (primary only)
Orthostatic hypotension, hyponatremia, hyperkalemia
N/V/D, irritability and depression, hypoglycemia
Acute Adrenal Insufficiency
Addisonian Crisis
life-threatening emergency; insufficient corticosteroid or rapid decrease in corticosteroids
- Stress related (infection, surgery, trauma, psychological stress)
- sudden withdrawal of exogenous corticosteroid therapy
Addisonian Crisis Manifestations
hypotension, tachycardia, dehydration, GI symptoms (N/V/D), hyponatremia
hyperkalemia
Hypoglycemia
Shock
Circulatory collapse usually unresponsive to fluid replacement and vasopressors
Need to give Steroids!!
Adrenocortical Insufficiency Dx Studies
ACHT stimulation test (normal response to this test: cortisol levels should go up, but if they have Addison’s disease -nothing will happen)
CT/MRI Serum Electrolytes (need to watch)
Adrenocortical Insufficiency Collaborative Care
treat underlying cause
Corticosteroid replacement therapy: Hydrocortisone
Hydrocortisone
Drug of choice:
has glucocorticoid and mineral corticoid properties
Doses INCREASED in times of STRESS!!
- moderate stress (test) - double dose
- severe stress (death) - triple dose
Fludrocortisone acetate (Florinef)
mineralcorticoid replacement therapy for adrenocortical insufficiency
increased salt in diet during periods of heat/humidity
replaces aldosterone
Addisonian Crisis Collaborative Care
manage shock
High dose IV hydrocortisone replacement
Large volume boluses of IV 0.9% NSS and D5%
Adrenocortical Insufficiency Nursing Dx
risk for imbalanced fluid volume
ineffective tissue perfusion
ineffective therapeutic regimen management
Adrenocortical Insufficiency Nursing Management
carefully monitor CV status, fluid and electrolyte status
protect from noise, light, environmental temp. extremes
Pharmacologic management:
- glucocorticoids: daily dose divided: 2/3 morning, 1/3 afternoon - mineralcorticoids: once daily in morning
Adrenocortical Insufficiency Teaching
importance of maintaining daily corticosteroid replacement therapy
appropriately increasing dose during stress
s/s of corticosteroid deficiency and excess
medical alert bracelet
Home BP monitoring
Emergency IM hydrocortisone kit for acute insufficiency state
early sign of Addisonial Crisis
Nausea and Vomiting
Pheochromocytoma
Rare condition caused by adrenal medulla tumor causing excess release of catecholamines (epinephrine and norepinephrine)
occurs in both genders and at any age
Usually benign
bilateral tumors occasional
Untreated: may cause DM, cardiomyopathy and death
Happens in Waves! secondary HTN
Pheochromocytoma Clinical Manifestations
severe, pounding headache tachycardia palpitations diaphoresis chest/abdominal pain anxiety
provoked by meds:
antihypertensives, opioids, radiologic contrast media, TCA’s
Pheochromocytoma Dx Studies
Secondary cause of HTN
Should be considered in clients that don’t respond to antihypertensive agents
-urine fractionated metanephrines
- urine fractionated catecholamines and creatinine
- plasma catecholamines
-CT/MRI
Pheochromocytoma Collaborative Care
Surgery: open or laparoscopic
(Adrenalectomy)
Preop: alpha adrenergic blockers and beta adrenergic blockers
Monitor BS
Avoid smoking, Caffeine
Do Not palpate abdomen
HTN usually resolves w/ tumor removal
HTN may persist after removal
- treat HTN w/ routine hypertensive meds
Med: Metyrosine
Adrenalectomy Collaborative Care
life-long steroid replacement, falls precaution
