ENDOCRINE IMAGING Flashcards
(35 cards)
: What is hyperparathyroidism?
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A: A condition of abnormally elevated parathyroid hormone (PTH) output, which increases blood calcium and leads to hypercalcemia and bone resorption, eventually causing bone diseases.
Q: What is PRIMARY hyperparathyroidism?
A: It is caused by hyperplasia or neoplasms in the parathyroid glands, such as adenomas or enlargement of all four glands, often due to familial syndromes like MEN I, MEN IIA, and isolated familial hyperparathyroidism. (Mutliple endocrine neoplasia)
Q: What is SECONDARY hyperparathyroidism?
A: Increased PTH secretion in response to hypocalcemia, typically due to chronic kidney disease.
Q: What is the main cause of increased PTH in primary hyperparathyroidism?
A: Usually due to an adenoma in one of the parathyroid glands (80%) or hyperplasia of multiple glands; rarely, it is due to malignancy.
Q: What are the MEN syndromes related to hyperparathyroidism?
A: MEN I (PPP - parathyroid, pancreatic, pituitary tumors), MEN IIA (MPP - medullary thyroid carcinoma, pheochromocytoma, parathyroid tumors), and MEN IIB (medullary thyroid carcinoma, pheochromocytoma, neuromas).
Q: What are the parathyroid-related causes of hypercalcemia?
A: Primary hyperparathyroidism (adenomas/MEN syndrome), lithium therapy, and familial hyperparathyroidism.
Q: What other conditions can cause hypercalcemia?
A: Malignancies (metastatic bone disease, paraneoplastic syndrome), vitamin D intoxication, sarcoidosis, hyperthyroidism, immobilization, thiazide diuretics, vitamin A intoxication, and renal failure-related conditions.
Q: What are the clinical symptoms of parathyroid hyperplasia and adenomas?
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A: Many patients are asymptomatic, but symptoms can include bone cysts, decalcification, kidney stones, muscle weakness, depression, constipation, and high blood pressure.
: How is hyperparathyroidism commonly diagnosed?
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A: Through routine serum calcium tests as part of biochemical testing, which often detects hypercalcemia early.
Q: What is the approach to elevated serum calcium levels?
A: Confirm hypercalcemia with elevated PTH levels, perform Sesta-MIBI to localize the affected gland(s), and remove the affected gland(s) with minimally invasive surgery. Repeat localization with at least two imaging modalities if disease recurs or persists (in 5% of cases).
Q: What is the principle behind the MIBI “washout” technique?
A: MIBI is washed out slower from pathological parathyroid glands than from normal parathyroid or thyroid glands, showing retention of activity in adenomas on late images.
Q: What is the role of Sestamibi in parathyroid imaging?
A: Sestamibi is used to identify pathological parathyroid glands by highlighting areas with retained radioactivity, such as adenomas.
: What factors influence the retention of MIBI in parathyroid adenomas?
A:
Biochemical properties of the tracer: Lipophilicity and cationic charge.
Local factors: Blood flow, trans-capillary exchange, and interstitial transport.
Intracellular characteristics: Negative charge of mitochondria and membranes.
:
A:
Biochemical properties of the tracer: Lipophilicity and cationic charge.
Local factors: Blood flow, trans-capillary exchange, and interstitial transport.
Intracellular characteristics: Negative charge of mitochondria and membranes.
Q: What does late imaging reveal in pathological parathyroid glands?
A: Retention of MIBI activity in adenomas, distinguishing them from normal glands.
Q: What are APUD cells?
A: Specialized cells that produce peptide hormones and amines from precursors, functioning as hormones or neurotransmitters.
What are APUDOMAS?
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A: Tumors arising from APUD cells.
Q: Where can APUDOMAS develop?
A: Pituitary gland, pancreas, adrenal medulla, thyroid, gastrointestinal system, paragangliomas, and lungs.
Q1: What type of tissue do catecholamine-secreting tumors arise from?
A1: Catecholamine-secreting tumors arise from sympathetic nervous tissue and the adrenal medulla.
Q3: Name the catecholamine-secreting tumors associated with the sympathetic nervous system and adrenal medulla.
Benign and malignant pheochromocytomas
Adrenal medulla hyperplasia
Carcinoids
Neuroblastomas
Medullary thyroid carcinoma
Paragangliomas
Q1: What are some radio-nuclide physiological imaging modalities used to detect catecholamine-secreting tumors?
→Technetium-labelled studies (e.g., bone scans with 99mTc-MDP)
→Iodine-labelled MIBG studies (e.g., 123I MIBG, 131I MIBG)
→Somatostatin receptor imaging (e.g., OctreoScan–111In, Ocreotide–123I)
FDG-PET
→ FDG-PET
medications that block MIBG
check slide 35
medication that can be used in MIBG
barbiturates, benzodiazepines,beta adrenergic blockers, diuretics, alpha methyldopa
Q1: What is the difference between 123-I MIBG and 131-I MIBG in imaging catecholamine-secreting tumors?
123-I MIBG: Better imaging agent, used for diagnostic purposes and possibly quantification.
131-I MIBG: Used for both diagnostic imaging and as a therapeutic agent.
Q2: What is the sensitivity of iodine-labelled MIBG studies for detecting pheochromocytomas?
A2: The sensitivity for detecting pheochromocytomas is 80-90%.
