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Flashcards in ADRENALS Deck (5)
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Functioning tumours

  1. Conn’s adenoma—accounts for 70% of Conn’s syndrome. Usually
    small, homogeneous, relatively low density due to cholesterol
    content. 30% of Conn’s syndrome is due to bilateral hyperplasia,
    which can occasionally be nodular and mimic an adenoma. Note
    that functioning and nonfunctioning adenomas are essentially
    indistinguishable on imaging, although functioning adenomas tend
    to be smaller and are more likely to be lipid-rich.
  2. Phaeochromocytoma—usually large (>5 cm) with avid contrast
    enhancement ± central necrosis/haemorrhage (NB: it is safe to
    administer IV iodinated CT contrast). Often markedly T2
    hyperintense on MRI. Rule of tens: 10% malignant, 10% bilateral,
    10% ectopic—of these 50% are located around the kidney,
    particularly the renal hilum (if not seen on CT, MIBG isotope scan
    may be helpful). 10% show calcification. 10% are multiple and
    usually part of MEN 2A/B syndrome, NF1, tuberous sclerosis or
  3. Cushing’s adenoma—accounts for 10% of Cushing’s syndrome.
    Usually >2 cm. 80% of Cushing’s syndrome is due to excess ACTH
    from a pituitary adenoma (Cushing’s disease) or ectopic source
    (small cell carcinoma, carcinoid, pancreatic NET,
    phaeochromocytoma, medullary thyroid carcinoma) with resultant
    adrenal hyperplasia. 10% of Cushing’s syndrome is due to adrenal
    carcinoma. The differentials for an adrenal mass in Cushing’s
    syndrome are:
    (a) Functioning adenoma/carcinoma—atrophy of the contralateral
    adrenal is suggestive.
    (b) Coincidental nonfunctioning adenoma—both adrenals may be
    hyperplastic (due to excess ACTH).
    (c) Metastasis from small cell primary.
    (d) Bilateral nodular hyperplasia—see Section 9.2.
  4. Adrenal carcinoma—rare, usually large (>5 cm). Functioning
    tumours (<50%) may present with Cushing’s, virilization,
    feminization or rarely Conn’s, and are more common in

Malignant tumours


. Metastases—often bilateral, usually >2 cm, irregular outline with
patchy contrast enhancement. Common sources include lung,
breast, renal and GI tract. Metastases from melanoma and RCC are
usually hypervascular and may mimic phaeochromocytoma. Recent
haemorrhage into a vascular metastasis can produce patchy high Adrenals, urinary tract, testes and prostate 229
attenuation on unenhanced CT. In patients without a known
extraadrenal primary tumour, the vast majority of adrenal masses
are benign; in the presence of a known primary malignancy
26-36% of adrenal lesions are metastatic.
2. Carcinoma—rare, aggressive. Typically a large (>5 cm), irregular,
heterogeneously enhancing mass with central necrosis/
haemorrhage ± foci of calcification and nodal, metastatic and/or
intravenous spread. May invade the adjacent kidney, making it
difficult to distinguish from an advanced RCC. Nonfunctioning
tumours (>50%) are more common in men and present at a larger
size than functioning tumours.
3. Lymphoma*—usually secondary in the presence of retroperitoneal
nodal disease. Unilateral or bilateral adrenal masses/diffuse
enlargement + mild homogeneous enhancement.
4. Neuroblastoma—very rare in adults. Usually large (>5 cm),
ill-defined and heterogeneous + calcification. Commonly surrounds
and displaces vessels (e.g. aorta and IVC) without causing
significant narrowing. Metastases are common at presentation.
5. Sarcoma—e.g. angiosarcoma, leiomyosarcoma. Very rare.
Nonspecific appearances: aggressive, irregular, heterogeneously
enhancing mass.



  1. Nonfunctioning adenoma—very common. Usually small (50%
    <2 cm), homogeneous and well-defined. If lipid-rich, will have
    unenhanced CT attenuation <10 HU and will drop signal on
    out-of-phase T1-weighted MRI.
  2. Myelolipoma—benign tumour composed of fat and haemopoietic
    tissue. Characteristic appearance on CT: discrete mass containing
    soft tissue and macroscopic fat (L), but can also occur in vascular
    masses (e.g. phaeochromocytoma, metastases), coagulopathies
    and severe stress (e.g. surgery, sepsis, burns, pregnancy,
    hypotension—often bilateral).
  3. Cyst—round, well-defined, water density, nonenhancing. May
    contain thin septa ± mural calcification. Pseudocysts due to
    previous haemorrhage > true cysts. Beware of cystic tumours (e.g.
    some phaeochromocytomas)—look for nodular wall thickening. If
    multiloculated, consider lymphangioma and hydatid cyst in the
  4. Granulomatous disease—e.g. TB, histoplasmosis. More commonly
    bilateral, see Section 9.2.
  5. Haemangioma—rare. Often contains phleboliths. Typically
    demonstrates peripheral nodular enhancement ± partial infilling on
    delayed phase. Central fibrotic scar usually does not enhance.
    Peripheral nonfibrotic component is usually markedly T2
    hyperintense. May mimic phaeochromocytoma.
  6. Ganglioneuroma—rare, occurs in children or young adults.
    Benign counterpart of neuroblastoma, arises from sympathetic
    ganglia. Well-defined, often shows heterogeneous delayed
    enhancement. Heterogeneously T2 hyperintense on MRI ± whorled
    appearance. Calcification is common.
  7. Other very rare lesions—adrenal lipoma, teratoma and
    angiomyolipoma can mimic myelolipoma due to macroscopic fat
    content (a fat–fluid level suggests teratoma). Schwannomas may
    be cystic ± calcification. Solitary fibrous tumours, leiomyomas,
    oncocytomas and inflammatory pseudotumours have also been
    rarely reported in the adrenals
    and present as a nonspecific solid heterogeneously enhancing
  8. Pseudolesions—e.g. exophytic renal/hepatic/pancreatic mass,
    gastric diverticulum, splenunculus, retroperitoneal varices. These
    can occasionally mimic an adrenal mass but IV/oral contrast and
    coronal reconstructions will nearly always clarify the diagnosis



  1. Metastases—bilateral in 15%. Usually do not affect adrenal
    function; may cause adrenal insufficiency if extensive (replacing
    >80% of adrenal gland).
  2. Phaeochromocytoma—bilateral in 10%. Suggests an underlying
    hereditary cause, e.g. MEN 2A/B, NF1, tuberous sclerosis or vHL.
  3. Adenomas—due to the prevalence of adenomas, they can
    occasionally be bilateral.
  4. Hyperplasia—congenital adrenal hyperplasia results in
    symmetrically enlarged and thickened adrenal glands in children.
    In adults, adrenal hyperplasia has several causes:
    (a) ACTH-dependent hyperplasia—more commonly due to ectopic
    ACTH secretion, but can occur in Cushing’s disease. Adrenals
    are usually mildly and diffusely enlarged but may be nodular
    in morphology.
    (b) ACTH-independent macronodular adrenocortical hyperplasia
    (AIMAH)—rare. Multiple bilateral large adrenal adenomas,
    each typically >1 cm and lipid-rich.
    (c) Primary pigmented nodular adrenocortical disease (PPNAD)—
    rare, autosomal dominant, typically presents in young females.
    Multiple bilateral adrenal micronodules, each usually <5 mm.
    Strongly associated with Carney complex.
  5. Adrenal haemorrhage—often bilateral in cases due to severe
    haemodynamic stress.
  6. Granulomatous disease—histoplasmosis/TB. Bilateral adrenal
    masses/enlargement ± central necrosis ± adrenal insufficiency in
    the acute setting. Results in adrenal atrophy and calcification in the
    chronic setting.
  7. Lymphoma*—primary adrenal lymphoma is rare; typically presents
    with bilateral large homogeneous adrenal masses/diffuse
    enlargement, often with adrenal insufficiency. Secondary adrenal
    involvement is more common, usually without adrenal


  1. Previous haemorrhage—unilateral or bilateral depending on
    aetiology. Old haemorrhage within a mass lesion (e.g. a large
    adenoma, myelolipoma or hypervascular metastasis) can also lead
    to calcification.232 Aids to Radiological Differential Diagnosis
  2. Cystic disease—curvilinear calcification within the cyst wall/septa.
    More common in pseudocysts than true cysts. Can also be seen in
    chronic hydatid cysts.
  3. Chronic TB*/histoplasmosis—atrophic calcified adrenals (often
  4. Calcification within a tumour—e.g. adrenal carcinoma (irregular
    punctate calcifications in 30%), phaeochromocytoma (10%),
    neuroblastoma (up to 90%, coarse/amorphous pattern),
    ganglioneuroma (fine/speckled pattern), haemangioma
    (phleboliths), teratoma and certain metastases (e.g. from mucinous
    adenocarcinoma, osteosarcoma).
  5. Addison’s disease—calcification is rare in primary autoimmune
    disease, and suggests a secondary cause, e.g. previous
    haemorrhage, TB or histoplasmosis.
  6. Wolman disease—rare autosomal recessive lysosomal acid lipase
    deficiency resulting in accumulation of cholesterol and triglycerides
    in organs. Presents in early infancy with failure to thrive.
    Pathognomonic appearance of enlarged densely calcified adrenals
    on AXR, US or CT. Fatty infiltration and enlargement of the liver,
    spleen and lymph nodes also occurs