NUR 146 - Week 5 - Adrenal Cortex Flashcards
What types of hormones are produced by the adrenal medulla and adrenal cortex?
Medulla:
Catecholamine hormones = epinephrine, norepinephrine
Cortex:
- Glucocorticoids (cortisol is a glucocorticoid)
- Mineralocorticoid
- Androgens
What are the general effects of catecholamines (epinephrine + norepinephrine)
Released in “fight or flight” response
- increases blood flow to heart and skeletal muscle
- Results in increased HR, increased BP, dilated pupils
- Reduces blood flow to GI tract
- Promotes catabolism of stored fuels to release energy
What are the specific effects of epinephrine?
Increases alertness
Dilates pupils
Increased rate and depth of respirations
Increases rate and force of cardiac contraction (increased cardiac output and BP)
Increased glycogenolysis
Inhibits insulin secretion
Increases energy production and consumption
What are the specific effects of norepinephrine
Vasoconstriction → increased cardiac output and BP
Not as potent as epinephrine
Pheochromocytoma:
What is it?
Incidence?
Etiology?
Tumor of adrenal medulla
- Usually benign
- Highly vascular
Incidence:
- Peak incidence at 40-50 years
- Men and women equally
Etiology:
- Genetic link
- Parathyroid tumor
Pheochromocytoma:
Pathphysiology
How does it present?
Excess catecholamine released by adrenal medulla
s/s presentation:
- Headache
- Diaphoresis
- Palpitations
- Tremors
- Flushing
- Anxiety
- Hyperglycemia
Pheochromocytoma:
Clinical manifestations / s&s
Acute paroxysmal attacks
Severe hypertension (life threatening)
- BP as high as 250/150
- Vertigo
- Blurred vision
- Tinnitus
- N/V/D
- Feeling of impending doom
Pheochromocytoma:
Diagnostic Tests
Education prior to testing
- Serum & urine metanephrine
- 24-hour urine collection
- Urine studies immediately following an attack
- Imaging studies (“looking for the tumor”)
Education:
- Avoid: coffee, tea, tobacco, vanilla, chocolate, aspirin & unnecessary prior to lab testing
Pheochromocytoma:
Treatment
Management
Preferred treatment = surgical removal aka adrenalectomy
- If patient gets bilateral adrenalectomy, pt requires hormone replacement for adrenal hormones
- control HTN whil pre-op (use alpha blockers)
What is the priority nursing intervention pre-op for a adrenalectomy?
Monitor blood pressure and administer anti-hypertensives as orders
Pheochromocytoma:
Nursing care
- Emotional support
- Bedrest with HOB >45 to prevent orthostatic hypotension
- Decrease stimulating foods
Pheochromocytoma:
Adrenalectomy Post-Op Care
“Patient’s body is used to having high levels of epinephrine, to now being dropped. Can go from HTN –> low bp.”
- ICU until stable
- Monitor BP, and for hemorrhage
Glucocorticoids:
Name them?
When are they secreted?
What do they do?
1) Cortisol, cortisone, corticosterone
2) Secreted in response to ACTH from Anterior pituitary
3) Regulates carb, protein and fat metabolism; promotes gluconeogenesis; maintains immune system function
Mineralocorticoids:
Name them?
When are they secreted?
1) Aldosterone
2) Released in angiotensin II or hyperkalemia; minimally affected by ACTH
3) sodium reabsorption, hydrogen/potassium losses, vasoconstriction
Renin-Angiotensin-Aldosterone System
Hypotension detected by kidneys –> kidneys release renin
Renin turns Angiotensin into Angiotensin 2 & causes
Angiotensin causes vasoconstriction & activates Aldosterone
Adrenocortical insufficiency
Primary & Secondary
Primary: Local problem to adrenal gland
Addison’s disease
Cause: dysfunction of hypothalamus pituitary gland feedback loop; can be autoimmune
Result: insufficient steroid production by adrenal glands
leads to high levels of ACTH
Secondary: Pituitary gland doesn’t stimulate adrenals enough
- Iatrogenic withdrawal of cortisone too rapidly
- Result of hypophysectomy
- Manifested by low levels of ACTH
Addison’s disease:
Clinical manifestations
Deficiency of mineralocorticoid
- Low Na+, High K+
- Muscle weakness
Deficiency of glucocorticoid
- GI symptoms, N/V, anorexia, weight loss, hypoglycemia
Decreased sex hormones
- Sparse pubic, axillary hair
Increased ACTH levels = hyperpigmentation of skin
Addison’s disease:
diagnostics
Tests:
- ACTH stimulation test (most reliable) “Normal patient’s adrenals should release cortisol in response to ACTH. Addison’s patient won’t react.”
- Plasma cortisol levels <15 mg/dl in morning
- ACTH levels
- 24 hour urine for urine cortisol levels
Addisonian crisis:
What is it?
Cause?
Life threatening complication of addison’s disease
Cause: stress (emotional, dehydration)
Addisonian Crisis:
s/s?
Lack of aldosterone = lack of fluid + sodium reabsorption
- Severe hypotension
- Dehydration
- Hypoglycemia
- Hyponatremia
- Hyperkalemia
- Cyanosis
- Fever
- N/V
- Abdominal/back pain
- Shock
- Confusion
- Hypovolemic shock –> cardiac arrest
Addison’s disease:
Management
- Lifelong Hormone replacement therapy
- Prevent Addisonian Crisis
Crisis management: - Fluid volume replacement
- Patient in recumbent position with legs elevated
- Hydrocortisone IV
Addison’s Disease:
Nursing care
Assessment:
- Vital signs; check for orthostatic hypotension
Cushing’s Syndrome:
What is it?
Causes?
Excessive production of glucocorticoid by adrenal cortex
Causes:
- Use of corticosteroid medications
- Excessive production d/t adrenocortical hyperplasia
- Pituitary tumor = excess ACTH
Cushing’s Syndrome:
Clinical Manifestations / s&s
Alteration in metabolism:
- Hyperglycemia with insulin resistance, gluconeogenesis, central obesity with thin extremities, buffalo hump aka fat in back of neck
Muscle weakness, fatigue:
- Osteoporosis, pathologic fractures
Skin changes:
- Thin, fragile skin, ecchymosis, Striae, poorly healing skin
Androgens:
- Decreased libido, acne, mood changes
- Opposite sex changes
Mineralocorticoid effects:
- Decreased potassium
- Increased sodium
- Fluid retention
Other:
- HTN, insomnia
