Difference between revisions of "Parathyroid glands"

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**CASR (calcium sensing receptor) gene defect.<ref name=omim601199>{{OMIM|601199}}</ref>
**CASR (calcium sensing receptor) gene defect.<ref name=omim601199>{{OMIM|601199}}</ref>


==Hypercalcemia DDx==
=Hypercalcemia DDx=
Mnemonic ''GRIMED'':<ref>TN06 Emerg.</ref>
Mnemonic ''GRIMED'':<ref>TN06 Emerg.</ref>
*Granulomatous disease (tuberculosis, [[sarcoidosis]]).
*Granulomatous disease (tuberculosis, [[sarcoidosis]]).
Line 27: Line 27:
*Immobility.
*Immobility.
*Malignancy (esp. squamous cell carcinoma, [[plasmacytoma]]).
*Malignancy (esp. squamous cell carcinoma, [[plasmacytoma]]).
*Endocrine (primary hyperparathyroidism - leads to [[brown tumour]]).
*Endocrine (primary hyperparathyroidism, tertiary hyperparathyroidism, familial hypocalciuric hypercalcemia (FHH)).
*Drugs (thiazides ... others).
*Drugs (thiazides ... others).
Note:
*Hyperparathyroidism and FHH are assoc. with an increased PTH.<ref name=Ref_PBoD8_1129>{{ref PBoD8|1129}}</ref>
**Other causes are assoc. with a decreased PTH.


=Normal parathyroid glands=
=Normal parathyroid glands=

Revision as of 15:37, 24 November 2011

The parathyroid glands are an endocrine organ that is important in calcium regulation. They often make an appearance in the context of thyroid surgery.

Clinical

Overview - hyperparathyroidism

Classification

  • Primary.
  • Secondary.
  • Tertiary.

Primary hyperparathyroidism

Cause:[1]

Familial causes of primary hyperparathyroidism:

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

Hypercalcemia DDx

Mnemonic GRIMED:[3]

  • 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.[4]
    • Other causes are assoc. with a decreased PTH.

Normal parathyroid glands

General

  • Identification of normal can be tricky.

Gross

  • No distinctive features - surgeons thus send 'em to pathologists.

Microscopic

Features:[5]

  • 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[6] - key feature.
    • Surrounded by a thin fibrous capsule.
  • High power:
    • Mixed cell population:[7]
      • Chief cells - predominant cell type, small, cytoplasm has variable staining (hyperchromatic-clear-eosinophilic).
      • Oxyphil cells (acid staining cells[8]) - 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 PTH
oxyphil cells moderate/light hyperchromatic to eosinophilic rare abundant ?

Notes:

  • Cytoplasmic staining varies considerably on H&E preparations - it may vary from hyperchromatic[9] to clear to eosinophilic[10].
  • 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.[11]
  • 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.[12]

Microscopic

Features:[12]

  • 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 I and MEN IIa/b (II/III).

MEN I:

MEN IIa/IIb (II/III):

Image: Parathyroid adenoma (med.utah.edu).[13]

Microscopic

Chief cell adenoma

Features:[1]

  • Chief cells:
    • Small central nucleus.
    • Moderate cytoplasm.
  • +/-Scattered oxyphil cells:
    • Large cells.
    • Abundant cytoplasm.

Image:

Oxyphil adenoma

Features:[1]

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

DDx:

Parathyroid carcinoma

General

  • Extremely rare.

Microscopic

Features:[14]

  • 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. ↑ 1.0 1.1 1.2 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.
  2. ↑ Online 'Mendelian Inheritance in Man' (OMIM) 601199
  3. ↑ TN06 Emerg.
  4. ↑ 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.
  5. ↑ http://www.medicalhistology.us/twiki/pub/Main/ChapterFourteenSlides/b56b_parathyroid_40x_he_labeled.jpg
  6. ↑ http://pathology.mc.duke.edu/research/Histo_course/parathyroid2.jpg
  7. ↑ http://www.bu.edu/histology/p/15002loa.htm
  8. ↑ http://dictionary.reference.com/search?q=oxyphil%20cell
  9. ↑ http://www.deltagen.com/target/histologyatlas/atlas_files/endocrine/parathyroid_and_thyroid_glands_20x.jpg
  10. ↑ http://instruction.cvhs.okstate.edu/Histology/HistologyReference/hrendo.htm
  11. ↑ URL: http://www.pathconsultddx.com/pathCon/diagnosis?pii=S1559-8675%2806%2970475-2. Accessed on: 29 July 2010.
  12. ↑ 12.0 12.1 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.
  13. ↑ URL: http://library.med.utah.edu/WebPath/EXAM/IMGQUIZ/enfrm.html. Accessed on: 6 December 2010.
  14. ↑ 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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