Difference between revisions of "Parathyroid glands"

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=Clinical=
=Clinical=
==Hyperparathyroidism==
==Hyperparathyroidism==
Increased secretion of PTH.<ref>URL: [http://emedicine.medscape.com/article/127351-overview http://emedicine.medscape.com/article/127351-overview]. Accessed on: 24 January 2013.</ref>
===Classification===
===Classification===
*Primary.
*Primary.

Revision as of 12:26, 24 January 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

Increased secretion of PTH.[1]

Classification

  • Primary.
  • Secondary.
  • Tertiary.

Overview in a table

Type PTH Calcium Common causes
Primary high high parathyroid adenoma (~90% of cases)
Secondary high low or normal chronic renal failure
Tertiary high low [citation needed] chronic renal failure

Hypercalcemia DDx

Mnemonic GRIMED:[2]

  • 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.[3]
    • Other causes are assoc. with a decreased PTH.

Primary hyperparathyroidism

Cause:[4]

Familial causes of primary hyperparathyroidism:

  • MEN 1.
  • MEN 2A.
  • Familial hypocalciuric hypercalcemia.
    • Autosomal dominant.
    • CASR (calcium sensing receptor) gene defect.[5]

Classic manifestations moans, stones, bones, (abdominal) groans, psychiatric overtones.[6][7]

  • Moans = bone pain.
  • Stones = nephrolithiasis (kidney stones).
  • Bones = bone pathology, e.g. osteitis fibrosa cystica.[8]
  • 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.[3]

Other causes:[9]

  • 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:[10]

  • 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[11] - key feature.
    • Surrounded by a thin fibrous capsule.
  • High power:
    • Mixed cell population:[12]
      • Chief cells - predominant cell type, small, cytoplasm has variable staining (hyperchromatic-clear-eosinophilic).
      • Oxyphil cells (acid staining cells[13]) - abundant cytoplasm.
      • Adipocytes - increased with age, may be used to help differentiate from thyroid - key feature.


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:

  • Cytoplasmic staining varies considerably on H&E preparations - it may vary from hyperchromatic[14] to clear to eosinophilic[15].
  • Chief cells tend to stain more intensely than oxyphil cells.

Thyroid vs. parathyroid (see: parathyroid image):

  • Parathyroid cytoplasm:
    • Hyperchromatic.

Parathyroid vs. lymphoid tissue (see parathyroid image):

  • Parathyroid:
    • No germinal centres.
    • Gland-like/follicular-like arrangement -- much smaller than normal follicles of
    • Occasional cell with rim of clear cytoplasm (oxyphil?).

Images:

Specific entities

Parathyroid hyperplasia

General

  • Chief cell hyperplasia - associated with MEN 1, MEN 2A.[16]
  • Parathyroid hyperplasia - classically assoc. with renal failure.
  • Classically all parathyroid glands are involved; however, some may be spared making it difficult to differentiate this from parathyroid adenoma.[17]

Microscopic

Features:[17]

  • Similar to parathyroid adenoma.
  • +/-Water-clear cells ("water-clear cell hyperplasia").

Parathyroid adenoma

General

  • One parathyroid is big... the others are small.
  • Associated with MEN 1 and MEN 2A.

MEN 1:

MEN 2A:

Subtypes

  1. Chief cell parathyroid adenoma.
    • Common.
  2. Oxyphil parathyroid adenoma.

Microscopic

Chief cell parathyroid adenoma

Features:[4]

  • Chief cells - key feature:
    • Small central nucleus.
    • Moderate cytoplasm.
  • +/-Scattered oxyphil cells:
    • Large cells.
    • Abundant cytoplasm.
  • Architecture:
    • Nests.
    • Circular formations - often around capillaries (perivascular pseudorosettes).

Images:

Oxyphil parathyroid adenoma

Features:[4]

  • Oxyphil cells:
    • Large cells.
    • Abundant cytoplasm.

DDx:

Image:

Sign out

PARATHRYOID GLAND, EXCISION:
	- CHIEF CELL PARATHYROID ADENOMA.

Parathyroid carcinoma

General

  • Extremely rare.

Microscopic

Features:[20]

  • 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. ↑ URL: http://emedicine.medscape.com/article/127351-overview. Accessed on: 24 January 2013.
  2. ↑ 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.
  3. ↑ 3.0 3.1 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
  4. ↑ 4.0 4.1 4.2 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.
  5. ↑ Online 'Mendelian Inheritance in Man' (OMIM) 601199
  6. ↑ 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.
  7. ↑ URL: http://www.usmleforum.com/files/forum/2010/1/505388.php. Accessed on: 4 December 2011.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ http://www.medicalhistology.us/twiki/pub/Main/ChapterFourteenSlides/b56b_parathyroid_40x_he_labeled.jpg
  11. ↑ http://pathology.mc.duke.edu/research/Histo_course/parathyroid2.jpg
  12. ↑ http://www.bu.edu/histology/p/15002loa.htm
  13. ↑ http://dictionary.reference.com/search?q=oxyphil%20cell
  14. ↑ http://www.deltagen.com/target/histologyatlas/atlas_files/endocrine/parathyroid_and_thyroid_glands_20x.jpg
  15. ↑ http://instruction.cvhs.okstate.edu/Histology/HistologyReference/hrendo.htm
  16. ↑ URL: http://www.pathconsultddx.com/pathCon/diagnosis?pii=S1559-8675%2806%2970475-2. Accessed on: 29 July 2010.
  17. ↑ 17.0 17.1 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.
  18. ↑ 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.
  19. ↑ URL: http://library.med.utah.edu/WebPath/EXAM/IMGQUIZ/enfrm.html. Accessed on: 6 December 2010.
  20. ↑ 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.
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