B96 Thyroiditis, hypo and hyperfunction of the thyroid gland. Flashcards
What are the clinical types of thyroiditis and their causes?
Inflammation of the thyroid gland, with two clinical types.
1) With acute illness and severe thyroid pain, resulting from infection. Is uncommon.
* De Quervain Subacute granulomatous thyroiditis.
2) Main type: low level inflammation, no pain, and the manifestations are thyroid dysfunction.
- Hashimoto thyroiditis (aka chronic lymphocytic thyroiditis)
- Subacute lymphocytic thyroiditis (seen often as postpartum thyroiditis)
3) Rare forms of thyroiditis
- Riedel thyroiditis
- Palpitation thyroiditis
Describe the symptoms and presentation of Hashimoto Thyroiditis
- aka Chronic Lymphocytic Thyroiditis
- Strong lymphocytic infiltration, with germinal center formation in the thyroid.
- Most common cause of hypothyroidism in developed world
- has Anti-Thyroperoxidase antibodies (Graves disease does not)
- is painless
- 20:1 female to male ratio
- Hypothyroidism develops gradually and may be preceeded by hyperthyroidism
- There is compensatory indreased TSH levels once hypothyroidism occurs
- Presents most often in women ages between age 45 and 65
What is the histology of the itssue in Hashimoto thyroiditis?
lymphocyte infiltration and germinal center formation
Thyroid follicles are decreased in number, size, and atrophic.
Hurthle cell change, aka Oncocytic change aka Oxyphil cells with the epithelial cells having abundant pink cytoplasm from excess mitochondria. The epitheilail cells normally have a very pale/clear slightly basophilic cytoplasm.
There is increased connective tissue.
What is the pathogenesis of De Quervain Thyroiditis?
aka Subacute Granulomatous Thyroiditis
- Caused by viral infection or postinfection inflammation, often preceeded by upper resp infection.
- Acute onset of pain, fever, malaise
- May** or **may not present with thyroid enlargement
-
Transient hyperthyroidism followed by Transient hypothyroidism
- caused by inflammation and hyperactivity and subsequent gland destruction/dysfunction, both that self resolve in a few weeks.
- serologic evidence of inflammation, leukocytosis elevated ESR.
- Spontaneous recovery in 6-8 weeks.
What is the gross morphology of Hashimoto thyroiditis
Diffuse symmetric enlargement of the thyroid
In less common cases of the fibrosing variant, the thyroid is small and atrophic from extensive fibrosis and little inflammation/infiltration.
Gray/tan, firm on cut surface.
What is the etiology of DeQuervain thyroiditis?
It is rare, seen in women more often, occurs usually between 30 and 50 years.
What is the presentation, pathogenesis, and course of Subacute Lymphocytic Thyroiditis?
aka silent or painless thyroiditis
most likely autoimmune, and there are circulating antithyroid antibodies, in some patients presents after pregnancy as postpartum thyroiditis
causes a painless neck mass and transient thyrotoxicosis and then a abation of symptoms and retrun to normal.
it may cause mild symmetric thyroid enlargement, but often not.
There is lymphocytic infiltration and germinal center formation, but the whole disease is transient and resolves.
Thyrotoxicosis: hyperthyroidism due not to overproduction of T3 or T4, but from dsestruction and leakage of the hormones from the follicles.
nervousness, palpitations, rapid pulse, fatigability, muscular weakness, weight loss with good appetite, diarrhea, heat intolerance, warm skin, excessive perspiration, emotional lability, menstrual changes, a fine tremor of the hand (particularly when outstretched), eye changes, and variable enlargement of the thyroid gland.
Describe Riedel thyroiditis
Rare disorder with unkown etiology
Extensive fibrosis of the thyroid and surrounding neck structures
Presents as a hard, fixed thyroid mass, seemingly like a thyroid carcinoma, but importantly, Riedel’s Fibrosing Thyroiditis occurs in young women, childbearing aged women, and thyroid carcinomas occur in the elderly.
Associated with idiopathic fibrosis in other body parts
Antithyroid antibodies are present
Riedel thyroiditis(RT) is generally a self-limited disease with a favorable prognosis. Death due to airway compromise is very rare in treated patients. Occasionally, spontaneous remission has been reported. Patients can also relapse.
In RT, morbidity is most frequently related to local compressive symptoms, such as dysphagia, dyspnea, hoarseness, and cough. Hypothyroidism is present in 30% of cases. Fibrotic invasion of adjacent anatomic structures may infrequently result in symptoms related to recurrent laryngeal nerve paralysis or hypoparathyroidism
Describe palpation thyroiditis
Caused by heavy handed doctors vigorously palpating the thyroid gland.
Causes rupture/damage to thyroid follicles.
Inflammatory cell infiltrate with occasional giant cell formation.
Usually an incidental finding that does not cause clinical symptoms.
What are the causes of hypothyroidism?
- Iodine deficiency #1 worldwide
- Hashimoto thyroiditis #1 in US and Eur, aka Autoimmune thyroiditis, aka chronic lymphocytic thyroiditis
- Panhypopituitarism from pit adenoma
- End stage Graves disease
- Iatrogenic
- Radiation
- Chemo
- Thyroidectomy
- Long term use of TSH secretion inhibitors and T3/T4 substitution, and sudden withdrawal.
- Interferons, lithium
- Congenital agenesis or failure to descend (rare)
- Congenital lack or mutation of TPO (rare)
- Inflitrative destructive lesions
- amyloidosis
- lymphoma
- scleroderma
What is the clinical presentation of hypothyroidism?
Infants: cretinism
- severly stunted growth and mental retardation
- facial abnormalities, protruding tongue
- umbilical hernia
- used to be common in endemic iodine deficient areas
- now is more rare, and associated with enzyme defeiciencies of TPO and other enzymes.
- Iodine deficient cretinism mental retardation, is due to maternal deficiency, as her thyroid hormones cross the placental barrier and are critical for embryonic CNS development.
Adolescents and Adults:
- Myxedema
- Fatigue, apathy, and mental slowing are the main features.
- Droopy, tired face and periorbital edema
- Slurred speech
- Cold intolerance
- Weight gain
- cold, sweatless, pale skin
- bradycardia and low cardiac output
- Pericardial effusions are common and may cause heart failure.
- Constipation
- hyperlipidemia, hypercholesterolemia
- Non-pitting edema of the whole body, prominent in the periorbital region. From lots of ECM GAG deposition
- Macroglossia, same reason
- Hyperprolactinemia, elevated PRL secretion because TRH levels are high, (in attempt to stimulate T3 T4 secretion) and TRH weakly stimulate PRL release.
How is hypothyroidism diagnosed?
Must measure both the T4 hormone itself, and TSH.
Elevated TSH occurs in primary hypothyroidism, hashimoto thyroiditis
Normal/Decreased TSH in people with hypothalamic disease or hypopituitarism
Serum T4 is always decreased and is by definition hypothyroidism.
What are the causes of hyperthyroidism?
Diffuse toxic hyperplasia – Graves disease (most common)
Hyperfunctioning multinodular goiter
Hyperfunctioning adenoma
TSH‐secreting pituitary adenoma (rare)
transient acute stage of hashimoto thyroiditis
transient thyrotoxicosis in De Quervain subacute granulomatous thyroiditis
transient thyrotoxicosis in Subacute lymphocytic throiditis/postpartum thyroiditis
Describe clinical presentation of Graves disease
aka Basedow disease
Most common hyperthyroidism
triad:
- Thyrotoxicosis, with a diffusely enlarged hyperfunctional thyroid. Is always present.
-
Infiltrative ophthalmopathy causing swelling around the eyes and exopthalmos, protrusion of the orbits in 40% (not all!)
- Has prominent lymphocytic infiltration and inflammatory edema of the perioribital region and extra-ocular muscles
- there is also adipocyte infiltration of the periorbital redgion.
- the inflammatory infiltration and edema of extra ocular muscles causes exopthalmos
- Infiltrative dermopathy, aka pretibial myxedema seen in 1-5% of patients. Discoloration, inflammation, and lumpy swelling of the lower shins.
- it is important to note, the Infiltrative Opthalmopathy and the Infiltrative dermopathy are not due to T3 or T4 hyperthyroidism. Thats why these symptoms are not seen in general types of thyrotoxicosis. They are caused directly by the actions of TSH receptor stimulatin immunoglobulins stimulating TSH receptors on fibroblasts around the eye and in the pretibial region.
