PB

Adrenal Glands

Anatomy and location

  • Adrenal glands located above each kidney: right adrenal gland, left adrenal gland.

  • Anatomy noted: two adrenal glands sit atop the kidneys (Right adrenal gland, Left adrenal gland).

  • Relationship: adjacent to the kidneys; right and left glands have distinct anatomies but share core functions.

  • Adrenal Medulla- MANE – Epinephrine & norepinephrine

    Adrenal cortex- sugar, sex, and salt – glucocorticoid, mineralocorticoid, androgens

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Adrenal glands overview

  • Two endocrine glands: Adrenal Medulla and Adrenal Cortex.

  • Functions regulated by the hypothalamic-pituitary-adrenal (HPA) axis.

Adrenal Medulla (Medullary function and hormones)

  • Part of the autonomic nervous system (ANS).

  • Secretes catecholamines: Epinephrine and Norepinephrine.

  • Epinephrine is the predominant catecholamine, comprising about 90\% of catecholamine release.

  • Primary role: mediates rapid "fight-or-flight" responses to stress (e.g., increased heart rate, bronchodilation, glucose mobilization).

  • Summary: Epinephrine (~90\%) and norepinephrine are key mediators of acute autonomic responses.

Adrenal Cortex (Cortical hormones and functions)

  • Secretes three main classes of hormones:

  • Glucocorticoids: cortisol (hydrocortisone) – regulated by ACTH from the pituitary; ACTH is stimulated by CRH from the hypothalamus.

  • Mineralocorticoids: aldosterone – principal hormone for long-term regulation of sodium balance.

  • Adrenal sex hormones (androgens) – mainly regulated by ACTH.

Glucocorticoid functions:

  • Glucose production and metabolism (carbs, proteins, fats).

  • Critical role in the stress response.

  • Immune modulation: suppresses immune response.

  • Mineralocorticoids functions:

  • Regulation of sodium and potassium balance; maintenance of blood pressure and extracellular fluid volume.

  • Gonadal and adrenal androgen production contributes to secondary sexual characteristics; regulated by ACTH.

Hormonal axis and regulation details

  • Hypothalamus releases CRH in response to stress and circadian cues.

  • CRH stimulates pituitary to release ACTH.

  • ACTH stimulates adrenal cortex to produce glucocorticoids and mineralocorticoids (androgens to a lesser extent).

  • Cortisol exerts negative feedback on both hypothalamus (CRH) and pituitary (ACTH) to modulate axis activity.

  • Diurnal pattern: cortisol typically shows a daily rhythm (higher in the morning, lower in the evening).

Addison’s Disease (Adrenocortical Insufficiency)

Definition

  • Addison’s disease = adrenocortical insufficiency; inadequate production glucocorticoids and mineralocorticoids

  • Primary manifestation: insufficient glucocorticoid and mineralocorticoid output.

  • Glucocorticoids are important for glucose control, immune suppression, and stress response; mineralocorticoids regulate Na+ and K+ balance.

Causes

Primary Adrenal Insufficiency

  • Autoimmune destruction/atrophy of the adrenal cortex.

  • Atrophy or surgical removal of adrenal tissue.

  • Infections affecting adrenal glands.

Secondary Adrenal Insufficiency (problem in pituitary/hypothalamus):

  • Steroid withdrawal after prolonged therapy.

  • Pituitary or hypothalamic dysfunction leading to reduced ACTH.

  • NEVER ABURPTLY STOP STEROIDS!!!!

Clinical manifestations (common presentations)

  • muscle weakness, fatigue, anorexia, weight loss, n/v

  • Hyperpigmentation (especially knees, elbows, mucous membranes) due to ACTH precursor effects in primary disease.

  • Hypotension orthostatic

  • depression, apathy, confusion.

Laboratory findings (typical profile)

  • Morning cortisol (AM cortisol): low.

  • ACTH levels: variable; if primary adrenal failure, ACTH is high; if secondary cause (pituitary/hypothalamic), ACTH is low.

  • Glucose: low.

  • Sodium (Na+): low.

  • Potassium (K+): high.

  • White blood cell count (WBC): elevated in some cases.

  • We stimulate the pituitary to see where problem is, if the adernal is not stimulated, thats the problem

Pharmacologic interventions

  • Glucocorticoids replaced w/hydrocortisone (cortef), prednisone, cortisone acetate

  • Mineralocorticoids replaced w/ fludrocortisonelorinef}$$

Nursing interventions

  • Assess: vital signs, daily weight, I/Os, signs of infection, fluid/electrolytes, patient’s stress level, diet.

  • Prevent Addisonian crisis: recognize early signs and trigger management.

  • Plan for lifelong hormone replacement; monitor adherence and response.

Home care education and patient empowerment

  • Lifelong adrenal cortex hormone replacement; never abruptly stop therapy.

  • Teach how to adjust medication during illness, hot weather (increase salt intake), or times of stress (sick-day rules)

  • Diet: maintain fluid and electrolyte balance.

  • Have injectable corticosteroid available for emergencies.

  • Wear a MedicAlert bracelet

Addisonian crisis

  • Triggered by sudden drop in circulating adrenal hormones

  • Causes: overexertion, cold exposure, infection, surgery stress, or dehydration from testing.

  • Circulatory shock: cyanosis, anxiety, rapid weak pulse, rapid respirations, hypotension.

Management goals for Addisonian crisis

  • 1) fluids, appropriate positioning, vasopressors

  • Administer high-dose steroids IV

  • Identify and treat underlying cause (infection, illness, or stressor).

  • Correct electrolyte abnormalities (e.g., potassium, sodium) and maintain glucose levels.

  • Monitor and manage cardiac rhythm; glucose supplementation as needed (e.g., D50, glucagon).

  • Continual assessment and patient education during and after crisis.

Glucocorticosteroid therapy

Hydrocortisone (IV), Prednisone (PO)

  • Decreases Inflammatory response

  • Steroid replacement

  • Side Effects: HTN, Hyperglycemia, Weight gain, masked infection-WBC, fever

  • Assess:     

    • Monitor BP & glucose

    • Never stop abruptly, taper

    • Long term use- Monitor weight, glucose, and BP

Cushing’s Syndrome

  • Cushing’s syndrome = excessive adrenal cortex secretion

  • Women > men 20-40 years

Causes

  • Hyperplasia of adrenal cortex.

  • Use of steroids

  • Pituitary tumors producing ACTH

  • Production of ACTH by malignant tumors

  • Loss of normal diurnal cortisol feedback regulation.

  • Diurnal cortisol pattern is disrupted

Clinical manifestations

  • Integumentary: thin or oily skin, acne, easy bruising, striae, petechiae.

  • Metabolic: buffalo hump, moon face, truncal obesity, irregular menses, hirsutism, potential erectile changes

  • hypertension, potential heart failure.

  • pancreatitis, peptic ulcers.

  • Immunologic: impaired wound healing, increased infections.

  • sleep disturbances, muscle wasting, osteoporosis, mood changes.

Diagnostics and interpretation

TWO/THREE MUST be abnormal

  • Serum cortisol: loses diurnal variation; cortisol remains high throughout the day in Cushing’s syndrome.

  • Urinary cortisol (24-hour collection): elevated (often three times the upper limit of normal).

  • Dexamethasone suppression test: cortisol does not suppress to less than 5

  • Glucose and potassium abnormalities: glucose tends to be high; potassium may be low.

Management strategies

  • Identify the underlying cause (pituitary vs adrenal source).

  • Surgical: pituitary tumor resection, adrenalectomy, chemo and radiation

  • Meds that interfere:

    • Lysodren (mitotane)

    • Aminoglutethimide

    • Metyrapone

    • Ketoconazole

  • Careful assessment of corticosteroid use with tapering and consideration of alternate-day therapy

Nursing and patient-care considerations

  • Monitor for HTN

  • Subtle signs of infection or inflammation

  • Encourage hand washing

  • Prevent falls and trauma

Nursing problems commonly associated with corticosteroid disorders

  • Injury risk and infection risk due to immunosuppression.

  • Inability to care for self and impaired skin integrity due to skin fragility and edema.

  • Body image