NOTES

NOTES
ADRENAL HYPERFUNCTION

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES DIAGNOSIS
▪ Overproduction of ≥ one adrenal hormones DIAGNOSTIC IMAGING
→ complex systemic disorders
CT scan/MRI
▪ Image tumors
CAUSES
▪ Pituitary/adrenal endocrine tumors
LAB RESULTS
▪ Idiopathic, iatrogenic
▪ Blood/urine tests; measure hormone levels
▪ Increased aldosterone →
hyperaldosteronism
▪ Increased cortisol → Cushing syndrome TREATMENT
▪ See individual disorders
SIGNS & SYMPTOMS
▪ Diffuse systemic symptoms due to systemic
endocrine effects

CONN'S SYNDROME
osms.it/conns-syndrome

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

▪ Type of primary hyperaldosteronism
CAUSES
▪ Adrenal glands produce too much
aldosterone due to benign tumor (adrenal
adenoma)
▫ Forms in zona glomerulosa in adrenal
gland
▪ Headache, facial flushing (due to
hypertension)
▪ Constipation, muscle weakness,
arrhythmias (if severe, due to hypokalemia)
▫ Low potassium, high blood pressure
(BP); unresponsive to treatment

RISK FACTORS
▪ Individuals who are biologically female,
20–60 years old, with family history

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DIAGNOSIS
DIAGNOSTIC IMAGING
CT scan
▪ Abdominal CT scan to differentiate tumor
from idiopathic hyperaldosteronism

LAB RESULTS
▪ Adrenal vein sampling (CT scans do not
detect lesions < 1cm/0.39in)

TREATMENT
Figure 11.1 The gross pathological
SURGERY appearance of an adrenal cortical adenoma in
▪ Unilateral adrenalectomy an individual with Conn’s syndrome.

CUSHING'S SYNDROME
osms.it/cushings-syndrome
▫ Glucocorticoid steroid medications
PATHOLOGY & CAUSES to treat inflammatory, autoimmune
disorders (e.g. asthma, rheumatoid
▪ Endocrine disorder caused by increased arthritis, eczema, immunosuppression);
cortisol most common
▪ Can be endogenous (caused by cortisol ▪ Pituitary adenoma (benign)
production inside body)/exogenous ▫ Leads to excess adrenocorticotropic
(iatrogenic) hormone (ACTH), adrenal cortisol
▪ Pseudo Cushing’s syndrome: estrogen- secretion
containing oral contraceptive pills → ▪ Adrenal Cushing’s disease
increased cortisol-binding globulin →
▫ Adrenal gland tumors/hyperplastic
increased total cortisol
adrenal glands/nodular adrenal
▫ Active hormone total free cortisol levels hyperplasia of adrenal glands produce
found in a 24-hour urine sample normal excess cortisol
▪ Ectopic ACTH
CAUSES ▫ Increased ACTH secreted from benign
bronchial carcinoid tumors/malignant
Primary
oat-cell carcinoma
▪ Tumor in zona fasciculata of adrenal gland
secretes cortisol
▪ Adenoma (benign)/adenocarcinoma COMPLICATIONS
(malignant) ▪ Metabolic syndrome, diabetes, infection due
to immunosuppression, fragility fractures
Secondary due to osteoporosis
▪ Iatrogenic

OSMOSIS.ORG 69
 SIGNS & SYMPTOMS DIAGNOSIS
▪ Fat redistribution due to glucose release → DIAGNOSTIC IMAGING
insulin release
CT scan
▪ Muscle, bone, skin breakdown due to
protein breakdown ▪ Adrenal glands (primary Cushing’s)
▪ Hypertension due to corticosteroids cross- ▪ Chest, abdomen, pelvis (ectopic ACTH
reacting with mineralocorticoid receptors production)
▪ High cortisol → feedback inhibition of MRI
GH-releasing hormone (GRH) → disrupts
▪ Pituitary gland (Cushing’s disease)
ovarian, testicular function

LAB RESULTS
▪ ↑ free cortisol in 24-hour urine sample
▪ Cortisol blood/saliva test: ↑ cortisol
▫ Performed in evening when cortisol
levels are normally low

OTHER DIAGNOSTICS
Dexamethasone suppression test
▪ Differentiates endogenous, exogenous
Cushing’s syndrome
▪ Measure cortisol change after
Figure 11.2 Abdominal striae in an individual dexamethasone (exogenous steroid)
with Cushing’s syndrome. ▪ Endogenous Cushing’s syndrome: cortisol
unchanged, negative feedback cycle
broken by autonomous endocrine tumor in
MNEMONIC: pituitary, adrenal, etc. (ectopic ACTH)
BAM CUSHINGOID ▪ Positive dexamethasone test
Signs & symptoms of ▫ High ACTH: ACTH-producing tumor
Cushing’s syndrome ▫ Low ACTH: adrenal tumor, causing
Buffalo hump: fat redistribution pituitary ACTH suppression
Amenorrhea
Long dexamethasone suppression test
Moon face: fat redistribution
▪ If high ACTH
Psychosis/agitation: previously,
Crazed ▪ Differentiates ACTH-producing pituitary
tumor, ectopic ACTH-producing tumor (e.g.
Ulcers
small cell lung cancer)
Skin changes: acne, purple
▫ Cushing’s disease (pituitary adenoma):
striae/stretch marks
cells partly responsive to negative
Hypertension feedback → cortisol decrease
Infection: due to ▫ Ectopic ACTH-producing tumor:
immunosuppression no negative feedback → cortisol
Necrosis of femoral head unchanged
Glaucoma
Osteoporosis: causing fragility
fractures
Immunosuppression
Diabetes

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TREATMENT
MEDICATIONS
▪ Cortisol inhibitors
▫ Esp. if surgery ruled out by ectopic
ACTH production/metastatic adrenal
carcinoma
▪ Wean steroid medications
▫ For Iatrogenic Cushing’s
▫ Sudden withdrawal → adrenal crisis
Figure 11.3 A large fat deposit at the
SURGERY upper back in an individual with Cushing’s
▪ Transphenoidal resection of pituitary gland syndrome.
▫ For Cushing disease
▪ Surgical resection
▫ For adrenal adenoma

HYPERALDOSTERONISM
osms.it/hyperaldosteronism
angiotensin-aldosterone axis activation →
PATHOLOGY & CAUSES hyperaldosteronism
▪ Decreased blood flow to kidneys (e.g. renal
▪ Adrenal gland produces excess aldosterone stenosis)
→ hypertension (high blood pressure),
▪ Renal-secreting neoplasms
hypokalemia (decreased blood potassium)
▪ Increased aldosterone → sodium, water
retention → increased blood volume → COMPLICATIONS
hypertension ▪ Hypertension, hypokalemia
▫ Heart disease (ischemic heart disease,
TYPES arrhythmias), vascular disease, renal
disease, stroke, alkalosis (due to
Primary increased hydrogen ion excretion)
▪ Idiopathic (2/3 of cases): overproduction
from both adrenal glands
▪ Conn’s syndrome (1/3 of cases): benign
SIGNS & SYMPTOMS
adrenal tumor → excess aldosterone
▪ Headache, facial flushing (due to
▪ Familial hyperaldosteronism: rare genetic
hypertension)
condition, adrenocorticotropic hormone
(ACTH) → adrenal aldosterone, renin ▪ Constipation, muscle weakness,
secretion arrhythmias (if severe, due to hypokalemia)

Secondary
▪ Hypotension (e.g. congestive heart failure,
cor pulmonale, hypoalbuminemia, cirrhosis,
ascites, coarctation of aorta) → renin-

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 DIAGNOSIS TREATMENT
LAB RESULTS ▪ Goal: prevent complications of
▪ Renin, aldosterone levels in blood and urine hyperaldosteronism on organs (e.g.
▪ Primary ventricular hypertrophy, heart failure,
stroke, myocardial infarction, atrial
▫ Increased aldosterone, decreased renin;
fibrillation, metabolic syndrome)
potassium decreased/normal
▫ Metabolic acidosis secondary to
hypokalemia MEDICATIONS
▪ Secondary ▪ Potassium-sparing diuretic/aldosterone
▫ Increased renin, aldosterone in blood antagonist
▫ Spironolactone
▪ Additionally
OTHER DIAGNOSTICS
▫ Thiazide diuretics, angiotensin
▪ Increased blood pressure
converting enzyme inhibitors (ACE)
inhibitors, calcium channel antagonists,
angiotensin II blockers

OTHER INTERVENTIONS
▪ Control BP via lifestyle
▫ Sodium restriction, weight management,
regular exercise
▪ Second-line
▫ Thiazide diuretics, ACE inhibitors,
calcium channel antagonists,
angiotensin II blockers

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