Difference between revisions of "Parathyroid glands"
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See: [http://instruction.cvhs.okstate.edu/Histology/HistologyReference/imagesco/parathyroid2F.jpg Parathyroid image (okstate.edu)]. | See: [http://instruction.cvhs.okstate.edu/Histology/HistologyReference/imagesco/parathyroid2F.jpg Parathyroid image (okstate.edu)]. | ||
====Parathyroid versus lymphoid tissue==== *Parathyroid: | ====Parathyroid versus lymphoid tissue==== | ||
*Parathyroid: | |||
**No germinal centres. | **No germinal centres. | ||
**Gland-like/follicular-like arrangement -- much smaller than normal follicles of | **Gland-like/follicular-like arrangement -- much smaller than normal follicles of | ||
Revision as of 19:47, 11 April 2013
The parathyroid glands are an endocrine organ that is important in calcium regulation. They often make an appearance in the context of thyroid surgery.
They produce parathyroid hormone (PTH). PTH acts to increase serum calcium and is important in the regulation of the calcium balance.
Clinical
Hyperparathyroidism
- Definition: increased secretion of parathyroid hormone (PTH).[1]
What PTH does:[1]
- Increase serum calcium.
- Decrease serum phosphate.
Classification
- Primary.
- Secondary.
- Tertiary.
Overview in a table
| Type | PTH | Calcium | Common causes |
|---|---|---|---|
| Primary hyperparathyroidism | high | high | parathyroid adenoma (~85-90% of cases), parathyroid hyperplasia (~10-15% of cases) |
| Secondary hyperparathyroidism | high | low or normal | chronic renal failure, vitamin D deficiency[2] |
| Tertiary hyperparathyroidism | high | high | persistent hyperparathyroidism after renal transplant[3] |
Hypercalcemia DDx
Mnemonic GRIMED:[4]
- Granulomatous disease (tuberculosis, sarcoidosis).
- Renal disease.
- Immobility.
- Malignancy (esp. squamous cell carcinoma, plasmacytoma).
- Endocrine (primary hyperparathyroidism, tertiary hyperparathyroidism, familial hypocalciuric hypercalcemia (FHH)).
- Drugs (thiazides ... others).
Note:
- Hyperparathyroidism and FHH are assoc. with an increased PTH.[5]
- Other causes are assoc. with a decreased PTH.
Primary hyperparathyroidism
Cause:[6]
- Parathyroid adenoma ~90%.
- Parathyroid hyperplasia ~10%.
- Parathyroid carcinoma ~1%.
Familial causes of primary hyperparathyroidism:
- MEN 1.
- MEN 2A.
- Familial hypocalciuric hypercalcemia.
- Autosomal dominant.
- CASR (calcium sensing receptor) gene defect.[7]
Classic manifestations moans, stones, bones, (abdominal) groans, psychiatric overtones.[8][9]
- Moans = bone pain.
- Stones = nephrolithiasis (kidney stones).
- Bones = bone pathology, e.g. osteitis fibrosa cystica.[10]
- Groans = constipation.
- Psychiatric overtones = CNS pathology.
- Can include: lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma.
Hypoparathyroidism
- Rare vis-à-vis hyperparathyroidism.
- Classically iatrogenic, i.e. the surgeon removing 'em.[5]
Other causes:[11]
- Autoimmune hypoparathyroidism.
- Autosomal dominat hypoparathyroidism.
- Familial isolated hypoparathyroidism.
- Congenital absence (DiGeorge syndrome).
Normal parathyroid glands
General
- Identification of normal can be tricky.
Gross
- No distinctive features - surgeons thus send 'em to pathologists.
Microscopic
Features:[12]
- Low power:
- May vaguely resemble lymphoid tissue - may have hyperchromatic cytoplasm.
- Does not have follicular centres like a lymph node.
- May form gland-like structure and vaguely resemble the thyroid at low power.
- Cytoplasm may be clear[13] - key feature.
- Surrounded by a thin fibrous capsule.
- May vaguely resemble lymphoid tissue - may have hyperchromatic cytoplasm.
- High power:
Images:
Parathyroid cell types
| Name | Staining (cytoplasm) | Quantity of cells | Cytoplasm (quantity) | Function |
| (parathyroid) chief cells | intense hyperchromatic to eosinophilic (see note) | abundant | moderate | manufacture parathyroid hormone (PTH) |
| oxyphil cells | moderate/light hyperchromatic to eosinophilic | rare | abundant | ? |
Notes - table:
- Cytoplasmic staining varies considerably on H&E preparations - it may vary from hyperchromatic[16] to clear to eosinophilic[17].
- Chief cells tend to stain more intensely than oxyphil cells.
Thyroid versus parathyroid
- Parathyroid cytoplasm:
- Hyperchromatic.
See: Parathyroid image (okstate.edu).
Parathyroid versus lymphoid tissue
- Parathyroid:
- No germinal centres.
- Gland-like/follicular-like arrangement -- much smaller than normal follicles of
- Occasional cell with rim of clear cytoplasm (oxyphil?).
- Nuclei are different:
- Slightly larger than in lymphocytes (1.2-1.5x the size)
- Stippled chromatin (unlike lymphocytes).
See: Parathyroid image (deltagen.com).
Specific entities
Parathyroid hyperplasia
General
- Chief cell hyperplasia - associated with MEN 1, MEN 2A.[18]
- Parathyroid hyperplasia - classically assoc. with renal failure.
Gross
- Classically all parathyroid glands are involved; however, some may be spared making it difficult to differentiate this from parathyroid adenoma.[19]
Microscopic
Features:[19]
- Classically have abundant adipose tissue.
- +/-Water-clear cells ("water-clear cell hyperplasia").
Note:
- Generally, it is impossible to discern between parathyroid adenomas and parathyroid hyperplasias by histology alone.[20]
- One requires information of the size of the other glands to make the diagnosis.
DDx:
- Parathyroid adenoma - classically have a rim of normal parathyroid gland around it.
Parathyroid adenoma
General
MEN 1:
- Parathyroid adenoma.
- Pancreatic neuroendocrine tumour.
- Pituitary adenoma.
MEN 2A:
- Parathyroid adenoma.
- Medullary thyroid carcinoma.
- Pheochromocytoma.
Subtypes
- Chief cell parathyroid adenoma.
- Common.
- Oxyphil parathyroid adenoma.
- Uncommon.[21]
Microscopic
Features - general:
- Classically have a rim of normal parathyroid gland around it.[20]
Note:
- Generally, it is impossible to discern between parathyroid adenomas and parathyroid hyperplasias by histology alone.[20]
- One requires information of the size of the other glands to make the diagnosis.
Chief cell parathyroid adenoma
Features:[6]
- Chief cells - key feature:
- Small central nucleus.
- Round with stippled chromatin - important.
- Moderate cytoplasm.
- Small central nucleus.
- +/-Scattered oxyphil cells:
- Large cells.
- Abundant cytoplasm.
- Architecture:
- Nests.
- Circular formations - often around capillaries (perivascular pseudorosettes).
Images:
Oxyphil parathyroid adenoma
Features:[6]
- Oxyphil cells:
- Large cells.
- Abundant cytoplasm.
DDx:
- Hürthle cell adenoma of the thyroid gland.
Image:
Sign out
PARATHRYOID GLAND, EXCISION: - CHIEF CELL PARATHYROID ADENOMA.
Note:
- One should not say "negative for malignancy".
Parathyroid carcinoma
General
- Extremely rare.
Microscopic
Features:[23]
- Histologically normal parathyroid cells.
- Cytologic features not reliable for diagnosis.
- Fibrous capsule.
- Invasion of surrounding tissue - key feature.
- +/-Metastasis - diagnostic feature.
Note:
- Diagnosis of parathyroid carcinoma is like that of malignant pheochromocytoma - cytology useless, tissue invasion and metastases are the key features.
Image:
See also
References
- ↑ 1.0 1.1 URL: http://emedicine.medscape.com/article/127351-overview. Accessed on: 24 January 2013.
- ↑ URL: http://emedicine.medscape.com/article/127351-overview#aw2aab6b5. Accessed on: 24 January 2013.
- ↑ URL: http://emedicine.medscape.com/article/127351-overview#aw2aab6b6. Accessed on: 24 January 2013.
- ↑ Shiau, Carolyn; Toren, Andrew (2006). Toronto Notes 2006: Comprehensive Medical Reference (Review for MCCQE 1 and USMLE Step 2) (22nd edition (2006) ed.). Toronto Notes for Medical Students, Inc.. pp. Emerg.. ISBN 978-0968592861.
- ↑ 5.0 5.1 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1129. ISBN 978-1416031215.
Cite error: Invalid
<ref>tag; name "Ref_PBoD8_1129" defined multiple times with different content - ↑ 6.0 6.1 6.2 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1127. ISBN 978-1416031215.
- ↑ Online 'Mendelian Inheritance in Man' (OMIM) 601199
- ↑ Lienert, D.; Rege, S. (Feb 2008). "Moans, stones, groans, bones and psychiatric overtones: lithium-induced hyperparathyroidism.". Aust N Z J Psychiatry 42 (2): 171-3. PMID 18350681.
- ↑ URL: http://www.usmleforum.com/files/forum/2010/1/505388.php. Accessed on: 4 December 2011.
- ↑ França, TC.; Griz, L.; Pinho, J.; Diniz, ET.; Andrade, LD.; Lucena, CS.; Beserra, SR.; Asano, NM. et al. (Apr 2011). "Bisphosphonates can reduce bone hunger after parathyroidectomy in patients with primary hyperparathyroidism and osteitis fibrosa cystica.". Rev Bras Reumatol 51 (2): 131-7. PMID 21584419.
- ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1130. ISBN 978-1416031215.
- ↑ http://www.medicalhistology.us/twiki/pub/Main/ChapterFourteenSlides/b56b_parathyroid_40x_he_labeled.jpg
- ↑ http://pathology.mc.duke.edu/research/Histo_course/parathyroid2.jpg
- ↑ http://www.bu.edu/histology/p/15002loa.htm
- ↑ http://dictionary.reference.com/search?q=oxyphil%20cell
- ↑ http://www.deltagen.com/target/histologyatlas/atlas_files/endocrine/parathyroid_and_thyroid_glands_20x.jpg
- ↑ http://instruction.cvhs.okstate.edu/Histology/HistologyReference/hrendo.htm
- ↑ URL: http://www.pathconsultddx.com/pathCon/diagnosis?pii=S1559-8675%2806%2970475-2. Accessed on: 29 July 2010.
- ↑ 19.0 19.1 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1128. ISBN 978-1416031215.
- ↑ 20.0 20.1 20.2 Taxy, J.; Husain, A; Montag, A. (2009). Biopsy Interpretation: The Frozen Section (1st ed.). Lippincott Williams & Wilkins. pp. 191. ISBN 978-0781767798.
- ↑ Fleischer, J.; Becker, C.; Hamele-Bena, D.; Breen, TL.; Silverberg, SJ. (Dec 2004). "Oxyphil parathyroid adenoma: a malignant presentation of a benign disease.". J Clin Endocrinol Metab 89 (12): 5948-51. doi:10.1210/jc.2004-1597. PMID 15579742.
- ↑ URL: http://library.med.utah.edu/WebPath/EXAM/IMGQUIZ/enfrm.html. Accessed on: 6 December 2010.
- ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1128. ISBN 978-1416031215.
