Endocrine system
Adrenal Anatomy & Physiology
Anatomical Structure & Secretory Zones
● The adrenal glands are bilateral endocrine organs located superior to each kidney.
● The gland is divided into two distinct functional regions:
○ the outer adrenal cortex
○ the inner adrenal medulla
Hormonal Secretions & Target System Actions
● Glucocorticoids (Cortisol):
○ Secreted by the adrenal cortex
○ exerts widespread metabolic effects on proteins and carbohydrates
○ maintains vascular tone
○ regulates blood pressure
○ suppresses immune and inflammatory responses
○ mobilizes cellular fuel sources
○ promotes free water clearance
○ Cortisol is vital for maintaining homeostatic stress responses.
● Mineralocorticoids (Aldosterone):
○ Secreted by the adrenal cortex;
○ essential for maintaining fluid volume and sodium-potassium balance by
stimulating renal reabsorption of sodium and subsequent water retention
● Adrenal Androgens:
○ Secreted by the adrenal cortex;
○ contributes to secondary sex characteristics
■ facial hair and voice deepening in males
■ pubic/axillary hair and breast development in females
● Catecholamines (Epinephrine, Norepinephrine, Dopamine):
○ Secreted by the adrenal medulla in response to sympathetic nervous system
(SNS) stimulation.
○ Epinephrine activates all α and β adrenergic receptors.
○ Norepinephrine activates α1 and α2 receptors, causing potent vasoconstriction.
○ Dopamine serves as a catecholamine precursor.
Addison’s Disease (Primary Adrenal Insufficiency)
Pathophysiology & Etiology
● Characterized by inadequate production of adrenal steroid hormones (cortisol and
aldosterone) due to adrenal cortical destruction.
, ● Approximately 80% of primary cases stem from an autoimmune response destroying the
adrenal cortex.
● Exogenous glucocorticoid therapy suppresses the hypothalamic-pituitary-adrenal (HPA)
axis, rendering the glands incapable of immediate cortisol synthesis upon steroid
removal.
Expected Assessment Findings
● Subjective Symptoms:
○ Progressive fatigue
○ lassitude
○ malaise
○ generalized weakness
○ anorexia
○ nausea
○ abdominal pain
○ myalgias
○ arthralgias
○ postural dizziness
○ loss of libido
○ salt craving
● Objective Signs:
○ Weight loss
○ hypotension
○ orthostatic syncope
○ cutaneous hyperpigmentation ("bronze" skin tone)
○ vitiligo
○ thinning of axillary and pubic hair.
● Acute Adrenal Crisis (Addisonian Crisis):
○ Manifests as severe hypotension (unresponsive to fluid resuscitation and
vasopressors)
○ intractable vomiting
○ pallor
○ diaphoresis
○ severe hypoglycemia
○ altered mental status (confusion, lethargy, seizures)
○ cardiovascular collapse, and death.
Diagnostic Findings
● Laboratory Profile:
○ Hyponatremia (<135 mEq/L),
○ hyperkalemia (>5.0 mEq/L),
○ hypoglycemia,
○ hypercalcemia,
, ○ elevated Blood Urea Nitrogen (BUN)
○ metabolic acidosis
○ elevated Erythrocyte Sedimentation Rate (ESR)
○ neutropenia
○ eosinophilia
○ lymphocytosis
○ reduced morning plasma cortisol levels
● Diagnostic Procedures:
○ Abdominal CT
○ Head CT
○ C ACTH stimulation test (Cosyntropin stimulation)
■ primarily to see if your adrenal glands are working properly or if they are
"underactive."
● Normal result: Your adrenal glands are healthy and capable of
producing cortisol when triggered.
● Low response (below the cutoff): Your adrenal glands did not
respond adequately, confirming adrenal insufficiency.
Priority Interventions & Pharmacotherapy
● Acute Crisis Management:
○ Secure airway, breathing, and circulation (ABCs).
○ Immediately administer IV hydrocortisone to replace deficient glucocorticoids.
○ Rehydrate with IV 0.9% Normal Saline with 5% Dextrose (D5NS), adding 50%
Dextrose (D50) for refractory hypoglycemia.
● Maintenance Therapy:
○ Daily oral
■ glucocorticoid replacement (hydrocortisone)
■ mineralocorticoid replacement (fludrocortisone/Florinef)
● Supportive Measures:
○ Administer vasopressors for fluid-refractory hypotension
○ replace electrolytes
○ provide empiric antibiotic therapy if infection precipitated the crisis.
Clinical Contradiction/Pitfall: Abrupt Glucocorticoid Withdrawal
● Abruptly stopping chronic exogenous glucocorticoid therapy suppresses endogenous
ACTH and causes acute adrenal failure.
● Exogenous steroids must always be slowly tapered.
● During periods of acute physical stress, infection, trauma, or surgery, steroid dosages
must be doubled or tripled ("stress dosing") to prevent fatal adrenal collapse.
Cushing’s Syndrome
Pathophysiology & Etiology
Adrenal Anatomy & Physiology
Anatomical Structure & Secretory Zones
● The adrenal glands are bilateral endocrine organs located superior to each kidney.
● The gland is divided into two distinct functional regions:
○ the outer adrenal cortex
○ the inner adrenal medulla
Hormonal Secretions & Target System Actions
● Glucocorticoids (Cortisol):
○ Secreted by the adrenal cortex
○ exerts widespread metabolic effects on proteins and carbohydrates
○ maintains vascular tone
○ regulates blood pressure
○ suppresses immune and inflammatory responses
○ mobilizes cellular fuel sources
○ promotes free water clearance
○ Cortisol is vital for maintaining homeostatic stress responses.
● Mineralocorticoids (Aldosterone):
○ Secreted by the adrenal cortex;
○ essential for maintaining fluid volume and sodium-potassium balance by
stimulating renal reabsorption of sodium and subsequent water retention
● Adrenal Androgens:
○ Secreted by the adrenal cortex;
○ contributes to secondary sex characteristics
■ facial hair and voice deepening in males
■ pubic/axillary hair and breast development in females
● Catecholamines (Epinephrine, Norepinephrine, Dopamine):
○ Secreted by the adrenal medulla in response to sympathetic nervous system
(SNS) stimulation.
○ Epinephrine activates all α and β adrenergic receptors.
○ Norepinephrine activates α1 and α2 receptors, causing potent vasoconstriction.
○ Dopamine serves as a catecholamine precursor.
Addison’s Disease (Primary Adrenal Insufficiency)
Pathophysiology & Etiology
● Characterized by inadequate production of adrenal steroid hormones (cortisol and
aldosterone) due to adrenal cortical destruction.
, ● Approximately 80% of primary cases stem from an autoimmune response destroying the
adrenal cortex.
● Exogenous glucocorticoid therapy suppresses the hypothalamic-pituitary-adrenal (HPA)
axis, rendering the glands incapable of immediate cortisol synthesis upon steroid
removal.
Expected Assessment Findings
● Subjective Symptoms:
○ Progressive fatigue
○ lassitude
○ malaise
○ generalized weakness
○ anorexia
○ nausea
○ abdominal pain
○ myalgias
○ arthralgias
○ postural dizziness
○ loss of libido
○ salt craving
● Objective Signs:
○ Weight loss
○ hypotension
○ orthostatic syncope
○ cutaneous hyperpigmentation ("bronze" skin tone)
○ vitiligo
○ thinning of axillary and pubic hair.
● Acute Adrenal Crisis (Addisonian Crisis):
○ Manifests as severe hypotension (unresponsive to fluid resuscitation and
vasopressors)
○ intractable vomiting
○ pallor
○ diaphoresis
○ severe hypoglycemia
○ altered mental status (confusion, lethargy, seizures)
○ cardiovascular collapse, and death.
Diagnostic Findings
● Laboratory Profile:
○ Hyponatremia (<135 mEq/L),
○ hyperkalemia (>5.0 mEq/L),
○ hypoglycemia,
○ hypercalcemia,
, ○ elevated Blood Urea Nitrogen (BUN)
○ metabolic acidosis
○ elevated Erythrocyte Sedimentation Rate (ESR)
○ neutropenia
○ eosinophilia
○ lymphocytosis
○ reduced morning plasma cortisol levels
● Diagnostic Procedures:
○ Abdominal CT
○ Head CT
○ C ACTH stimulation test (Cosyntropin stimulation)
■ primarily to see if your adrenal glands are working properly or if they are
"underactive."
● Normal result: Your adrenal glands are healthy and capable of
producing cortisol when triggered.
● Low response (below the cutoff): Your adrenal glands did not
respond adequately, confirming adrenal insufficiency.
Priority Interventions & Pharmacotherapy
● Acute Crisis Management:
○ Secure airway, breathing, and circulation (ABCs).
○ Immediately administer IV hydrocortisone to replace deficient glucocorticoids.
○ Rehydrate with IV 0.9% Normal Saline with 5% Dextrose (D5NS), adding 50%
Dextrose (D50) for refractory hypoglycemia.
● Maintenance Therapy:
○ Daily oral
■ glucocorticoid replacement (hydrocortisone)
■ mineralocorticoid replacement (fludrocortisone/Florinef)
● Supportive Measures:
○ Administer vasopressors for fluid-refractory hypotension
○ replace electrolytes
○ provide empiric antibiotic therapy if infection precipitated the crisis.
Clinical Contradiction/Pitfall: Abrupt Glucocorticoid Withdrawal
● Abruptly stopping chronic exogenous glucocorticoid therapy suppresses endogenous
ACTH and causes acute adrenal failure.
● Exogenous steroids must always be slowly tapered.
● During periods of acute physical stress, infection, trauma, or surgery, steroid dosages
must be doubled or tripled ("stress dosing") to prevent fatal adrenal collapse.
Cushing’s Syndrome
Pathophysiology & Etiology
