3. Evaluation of metabolic and
endocrine disorders
• Most metabolic and endocrine disorders are
characterized radiographically by
abnormalities in bone density
Increased Bone
Production
Increased
Bone
Resorption
Inadequate
Bone
Mineralization
6. Gigantism and acromegaly
• Growth hormone (GH), produced by the somatotropic
cells of the pituitary gland
• Regulated by -
GHRH - induces secretion
Somatostatin - inhibits release
• Two conditions –
• Hypersecretion prior to physeal fusion-
Gigantism
• Increased levels after skeletal maturity- Acromegaly
7. Causes
• Benign pituitary adenomas (90%)
• GH-secreting adenocarcinomas (rare)
• Hypothalamic adenomas resulting in excess GHRH
with secondary increase in GH
• Extra- pituitary hypersecretion of either GH (i.e.,
pancreatic islet cell tumors and carcinoid tumors) or
GHRH
8. Pathogenesis
• Prior to skeletal maturity,
endochondral bone formation still occurring at physis
excess GH results in exaggeration of normal process
increased longitudinal bone growth
• After physeal fusion,
normal endochondral bone formation has ceased
excess GH results in stimulation of cartilaginous growth factors
reactivation of endochondral bone formation
primarily at the chondroosseous junctions
new bone deposition
9. Clinical Features
• Insidious, with slow progression
• Physical features - malocclusion, prominent forehead;
thickened tongue; and broad, large hands.
• Bitemporal hemianopia, headache, and carpal tunnel
syndrome are common.
• Acromegalic patients are predisposed to degenerative
arthritis, especially of the spine and weight-bearing
joints.
10. Imaging Findings
• Gigantism - Increased longitudinal bone growth leading
to excessive height
• Acromegaly - Coarsened facial features with frontal
bossing and mandibular prognathism
- Spade-like terminal tufts and widened
phalanges
- Joint space widening early but
premature osteoarthritis
- Soft tissue hypertrophy, Including heel
pad thickening, median neuropathy, and
trigger finger
11.
12. Hypercortisolism
• Cortisol is a glucocorticoid produced by the zona fasciculata of adrenal gland
• Regulation is a complex process primarily mediated by the hypothalamic–
pituitary axis
• The hypothalamus secretes CRH
acts on the corticotroph cells of the anterior pituitary
to release adrenocortico - tropic hormone (ACTH)
which then stimulates the adrenal cortex
to secrete cortisol
acts as a negative feedback agent to the hypothalamus to limit its production.
The hypersecretion of cortisol leads to the clinical entity of Cushing syndrome
13. CAUSES
ACTH-dependent causes
ACTH - secreting pituitary adenomas (most common)
Ectopic production of ACTH, such as in small cell lung cancer
and carcinoid tumor
Ectopic CRH secretion
ACTH-independent causes
Adrenal adenoma
Adrenal cortical carcinoma
Adrenal hyperplasia
Most common cause of Cushing syndrome is
exogenous intake of glucocorticoids for medical uses
(e.g., treatment for asthma, rheumatoid arthritis, or immunosuppression following
organ transplantation).
14. Clinical Features
Cortisol involved in metabolism and glucose regulation
Suppresses the immune system and decreases bone formation
Prolonged increase results in muscle breakdown and osteoporosis.
o Truncal obesity
o Rounded (moon) facies
o Buffalo hump
o Striae
o Myopathy, fatigue, lethargy, bone pain
o Hirsuitism, acne, skin thinning, and easy bruising
15. Imaging Findings
• Osteopenia and osteoporosis with
insufficiency fractures
• Osteonecrosis
• Muscle wasting and increased fat
deposition
16. Thyroid disorders
• Thyroid hormone is synthesized and secreted by the follicular
cells within the thyroid gland in two forms: triiodothyronine
(T3) and thyroxine (T4)
• T4 is less metabolically active but is converted peripherally
into T3 by iodothyronine deiodinase.
• Thyroid hormone is regulated by the hypothalamic–pituitary
axis. The hypothalamus secretes thyroid-hormone-releasing
hormone, which then acts on the pituitary to secrete thyroid-
stimulating hormone (TSH). TSH in turn stimulates the thyroid
gland to produce T3 and T4 from thyroglobulin by complex
metabolic reactions in the follicular cells.
17. Hyperthyroidism
Causes
(a) Toxic multinodular goiter
(b) Graves disease
(c) Hyperfunctioning thyroid adenoma
• Other rare causes include
1) TSH-secreting pituitary adenoma
2) Metastatic thyroid carcinoma
3) Gestational trophoblastic disease and Struma ovarii
4) Iatrogenic due to patients taking too much
supplementation (exogenous or factitious hyperthyroidism)
18. Pathogenesis
•Thyroid hormone increases bone turnover by
increasing osteoclast-mediated bone resorption
•This results in decreased BMD, resulting in osteopenia
•The effects are more pronounced in cortical bone
than trabecular bone
19. Clinical Features
•Myopathy, most common manifestation, primarily
involving the proximal muscles of the extremities.
•Thyroid acropachy is uncommon, but it is
pathognomonic of hyperthyroidism.
•Thyroid ophthalmopathy (exophthalmos)
• Clubbing, swelling of digits, and joint pain
•Adhesive capsulitis
20. Imaging Findings
• Osteopenia and osteoporosis
with insufficiency fractures
• Myopathy with atrophy and
fatty infiltration
• Acropachy, pretibial
myxedema, and
ophthalmopathy
• Adhesive capsulitis
21. Hypothyroidism
Causes –
• In children,
- Anatomic defect in the gland
- Inborn error of thyroid metabolism,
- Iodine deficiency(mc)
- Congenital hypothyroidism aka cretinism.
• In adults,
-Medical or surgical treatment for hyperthyroidism, such as
medical thyroid gland suppression, surgical resection, or
radioiodine ablation
-Infiltrative disorders (e.g. lymphoma, amyloidosis)
-Hypopituitarism
-Thyroiditis
-Medication induced
22. Clinical Features
In children,
• Delayed skeletal maturation
• Brachycephaly
• Underdevelopment of the paranasal sinuses and mastoid air cells
• Delayed closure of fontanelle andfragmented epiphyses
• Occasional wormian bones
• Wedged thoracolumbar sail vertebra.
• Bilateral slipped capital femoral epiphysis (rare)
In adults,
• Proximal muscle myopathy
• Dupuytren contracture
• carpal tunnel syndrome
24. Parathyroid hormone
• Synthesized and secreted by the parathyroid glands
• Four glands, which are located posterior to the thyroid
gland
• PTH is involved in calcium, phosphate, and vitamin D
homeostasis through its complex actions on the bones,
kidneys, and the gastrointestinal tract
• It primarily acts to increase serum calcium, which it
accomplishes via several routes
• The regulation of PTH is primarily governed by the serum
calcium level through negative feedback
25. Hyperparathyroidism
• AKA Generalized Osteitis Fibrosa Cystica or
Recklinghausen disease of bone
• Hyperparathyroidism is the general term applied to
overactivity of the parathyroid gland
26. Types
• Primary hyperparathyroidism-
Most common cause of hypercalcemia
Due to a parathyroid adenoma , carcinoma, hyperplasia, or
ectopic tumors, producing a parathormone type
Elevated levels of parathormone, hypercalcemia, and hypophosphatemia.
• Secondary hyperparathyroidism-
Most common complications of chronic renal disease, allowing for
persistent loss of calcium and phosphorous and thus stimulating
parathormone release.
• Tertiary hyperparathyroidism-
In dialysis patients, the parathyroid gland may act independently
of serum calcium levels.
28. Clinical Features
30 to 50 years old female
Weakness, lethargy, polydipsia, and polyuria
Hypercalcemia - muscles will be hypotonic and formation of
renal calculi
Elevated Parathormone concentration
29. Radiological Findings
• Subperiosteal resorption including acroosteolysis
• “salt and pepper” skull
• “pseudowidening” of sacroiliac
• Brown tumors
• Tendon rupture
• Soft tissue calcifications, including chondrocalcinosis
32. अव्यक्तोऽयमचिन्त्योऽयमविकायोऽयमुच्यते |
तस्मादेिं विदद्िैनं नानुशोचितुमर्हसि || 25||
avyakto ’yam achintyo ’yam avikāryo ’yam
uchyate
tasmādevaṁ viditvainaṁ nānuśhochitum
arhasi
Meaning-The soul is spoken of as invisible,
inconceivable, and unchangeable. Knowing
this, you should not grieve for the body.
