This is definitely not Reidel's thyroiditis. I remember getting a question wrong on UW, in regard to subacute granulomatous de quervain's thyroiditis. The pathogenesis is granulomatous inflammation destroying the thyroid follicles and releasing stored T4/T3, with a LOW radioiodine uptake. I think this line is super important to get the diagnosis right. Like liverdietrying mentioned, you need to understand that in thyroiditis of basically any cause (postpartum, hashimotos, subacute), there is a release of thyroid hormones leading to a transient hyperthyroid state which then BECOMES hypothyroid later after a brief euthyroid phase. Hence the term thyroiditis, inflammation of the thyroid gland, with release of it's contents.
This is a patient case of postpartum thyroiditis. Can arise up to a year after delivery and has lymphocytic infiltrate.
The explanation by liverdietrying plus the explanation in the article posted below (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/) are the best, just need to be combined :). The differential diagnosis table 1 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/table/OM-10-0041-SLTB1/?report=objectonly) specifically identifies the condition in this question as postpartum thyroiditis.
Ultimately, if you know that hypothyroidism has a transient hyperthyroidism phase (due to autoimmune destruction of the cells which already had preformed TH and so it was released upon destruction) before hypothyroidism (nonfunctioning cells so can't take up iodine) and that hypothyroidism is a lymphocytic infiltrating thyroiditis, you will know the answer. I had a hard time understanding this at first because we evaluate/diagnose based on the presence of anti-TPO Ab, but the underlying pathogenesis of the thyroid destruction is cell-mediated (type IV hypersensitivity) not Ab mediated (type II hpyersensitivity) like graves. Hashimoto's = lymphocytic infiltration wiht germinal centers (which can transform to B cell lymphoma) with hurthle cells (pinker cytoplasm cells).
Can someone explain the difference between C. (release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes) and D. (Release of thyroid hormone from a lymphomatous thyroid gland.
According to this paper, Postpartum Thyroiditis presents with anti-TPO antibodies. The answer choice uses lymphocytes. So this is a transient Hashimotos Hyperthyroidism. Good Luck with that one!
I think that since they're asking for an explanation of the patient's current SSx which shows that she's in the state of Transient Hyperthyroidism: which is due to C: Release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes
Subacute lymphocytic thyroiditis Subacute lymphocytic thyroiditis is characterized by damage to follicular cells with lymphocytic infiltration resembling Hashimoto's thyroiditis instead of granuloma formation. Drugs: α-interferon, lithium, amiodarone, interleukin-2, tyrosine kinase inhibitors Autoimmune disease Postpartum thyroiditis: affects 5% of women during the postpartum period and is 3 times more common among women with type 1 diabetes mellitus.
submitted by ∗liverdietrying(111)
This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).
So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.
I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.
Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire