Hyperthyroidism
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Author:
Mikael Häggström [note 1]

Fixation
Generally 10% neutral buffered formalin. Fix all thyroids at least overnight to avoid artifactual nuclear atypia.[2]
See also: General notes on fixation
Gross processing
As per standard for thyroid.
Microscopic evaluation
The most common cause of hyperthyroidism is Grave's disease (50-80% worldwide). Its typical features are:[3]
- Hyperplastic thyroid follicles with papillary infoldings.
- Diffuse hyperplasia and hypertrophy of follicular cells with retention of lobular architecture.
- Prominent vascular congestion.
- Tall follicular cells with papillae that usually lack fibrovascular cores.
- Nuclei are round, often basally located, and rarely overlap.
- Typically decreased colloid amount, and when present it typically has peripheral scalloping.
- Variable patchy lymphoid stromal infiltrate.
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Graves' disease - low magnification: exuberant papillary hyperplasia.
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Graves' disease - medium magnification: cells with round nuclei and even chromatin pattern lining the papillae.
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Toxic multinodular goiter, whose typical findings are:
- Variably dilated follicles with flattened hyperplastic epithelium.[4]
- Nodules may be present[4] (but lack thick capsule in contrast to adenomas).
- Potentially focal fresh or old hemorrhages, rupture of follicles with granulomatous inflammation, fibrosis, calcification and even osseous metaplasia.[4]
- Also potentially papillary projections (Sanderson polsters) that may mimic papillary carcinoma, but they lack malignant nuclear features.[4] -
Amiodarone associated follicular cell damage - high magnification: large thyroid follicles filled with colloid and numerous histiocytes
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Amiodarone associated follicular cell damage - low magnification: large thyroid follicles filled with colloid and numerous histiocytes (arrow heads)
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Papillary hyperplastic nodule - high magnification: oncocytic cells lining the papillary structures (arrow)
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Papillary hyperplastic nodule - low magnification: cystic nodule with papillary architecture (arrow)
Notes
- ↑ For a full list of contributors, see article history. Creators of images are attributed at the image description pages, seen by clicking on the images. See Patholines:Authorship for details.
Main page
References
- ↑ Carlé, Allan; Pedersen, Inge Bülow; Knudsen, Nils; Perrild, Hans; Ovesen, Lars; Rasmussen, Lone Banke; Laurberg, Peter (2011). "Epidemiology of subtypes of hyperthyroidism in Denmark: a population-based study ". European Journal of Endocrinology 164 (5): 801–809. doi:. ISSN 0804-4643. PMID 21357288.
- ↑ . Gross Pathology Manual By The University of Chicago Department of Pathology. Updated 2-14-19 NAC.
- ↑ F. Zahra Aly, M.D., Ph.D., Swati Satturwar, M.B.B.S.. Thyroid gland - Hyperplasia / goiter - Graves disease. PathologyOutlines. Topic Completed: 1 November 2017, Minor changes: 14 March 2019
- ↑ 4.0 4.1 4.2 4.3 Swati Satturwar, M.B.B.S., F. Zahra Aly, M.D., Ph.D.. Thyroid gland - Hyperplasia / goiter - Multinodular goiter. PathologyOutlines. Topic Completed: 1 February 2018. Minor changes: 14 December 2019
Image sources
![Toxic multinodular goiter, whose typical findings are: - Variably dilated follicles with flattened hyperplastic epithelium.[4] - Nodules may be present[4] (but lack thick capsule in contrast to adenomas). - Potentially focal fresh or old hemorrhages, rupture of follicles with granulomatous inflammation, fibrosis, calcification and even osseous metaplasia.[4] - Also potentially papillary projections (Sanderson polsters) that may mimic papillary carcinoma, but they lack malignant nuclear features.[4]](https://upload.wikimedia.org/wikipedia/commons/c/c0/Histopathology_of_multinodular_toxic_goiter.jpg)