thyroid evaluation and disorders Flashcards
active T3
free T3
total T3
active and inactive T3 (inactive T3 bound to thyroid binding globulin, albumin and transthyretin)
TSH test
the most sensitive test
thyroid stimulating immunoglobulin
causes autoimmune Grave’s hyperthyroidism- excessive thyroid hormone production and thyroid enlargment
*** produces all the effects og TSH
Anti-thyroid peroxidase (TPO) Abs, a.k.a. anti-microsomal Abs
Anti-thyroglobulin Abs
elvated in?
Hashimoto’s
radiocative iodine
- uptake
- scan
- why is it used?
- Uptake = How much radioactive iodine is taken up into the gland (low, normal, high)?
- Scan = Where is the radioactive iodine being taken up?
- Single best test to determine etiology of hyperthyroidism
radioactive scan in graves
high uptake and diffuse pattern
radioactive scan in subacute thyroiditis
low uptake
Fine Needle Aspiration (FNA) Biopsy purpose
distinguish a benign from a malignant nodule
what happens if we do a thyroid nodule evaluation and it turns up HOT?
Don’t biopsy. Hot nodules are almost never malignant
The volume of both the extraocular muscles and retroocular tissue is increased seen in Graves, due to (3)
fibroblast proliferation, inflammation, and the accumulation of glycosaminoglycans, secreted by fibroblasts
radioactive iodine ablation
use I-131
which drug inhibits the thyroid leading to hypothyroidism
lithium
A hyperplastic process stimulated by autoantibodies leading to diffuse hyperplasia of follicular cells
grave’s disease
A destructive process mediated mostly by cytotoxic lymphocytes leading to shriveled, damaged follicular cells
Hashimoto’s disease
what do we see on hist o with graves?
increase in height of cells to form tall columnar cells forming pseudopillary buds
- irregular follicles with a scalloped appearance
is lymphocytic infiltration common in graves?
yes but it is more in Hashimoto’s
histo for hashimoto’s
hurthle cells and fibrosis
Gland symmetrically or asymmetrically enlarged and tan or gray tan due to inflammatory cell infiltrate
what are hurthle cells?
it is where follicular cells accumulate mito and become oxyphilic
seen in hypo
what happens to the thyroid parenchyma in hypo?
it is replaced by intense infiltration by lymphocytes and plasma cells
de Quervain’s thyroiditis
Subacute granulomatous thyroiditis
“silent” or “painless”thyroiditis
Subacute lymphocytic thyroiditis
Riedel’s thyroiditis
IgG4 disease
thyroiditis:
usually presents as a painful neck mass in middle-aged women often preceded by URI/viral etiology leading to thryoid tissue destruction.
_ we see a neutrophilic followed by lymphoplasmacytic infiltrate, with foreign body granulomatous response to colloid from disrupted follicles
- remits within a few months but sometimes progresses to hypo
Subacute Granulomatous Thyroiditis (de Quervain’s thyroiditis)
Incidental asymptomatic finding in up to 20% of adult autopsies. Most common in elderly women.
Focal Lymphocytic Thyroiditis
Incidental asymptomatic finding most common at institutions with lots of residents!
Scattered lymphohistiocytic aggregates and occasional giant cells formed in response to damage of follicles by palpation
Palpation Thyroiditis
painless goiter where the thyroid shows dense fibrosis and mild inflammatory process involving thyroid and it extends into adjacent neck strucutres. It might present with sclerosing in other locations
riedel’s thyroiditis
Enlarged thyroid gland, which can be due to a number of etiologies.
aka “thyromegaly”
goiter
goiter can compress the (3)
- trachea
- esophagus
- blood vessels- pemberton’s sign–> you get red with raised arm
what happens if the goiter if there are compressive symptoms?
surgery to remove it
the most common type of goiter
adenomatous goiter- irregularly enlarged thyroid with multiple soft large nodules
Histo presentation of goiter:
Many nodules with absent or
incomplete capsules,
Irregular, variable size follicles
No compression of surrounding follicles
adenomatous goiter
histo presentation of goiter:
Solitary Complete capsule No invasion through capsule Follicles uniform Compression of surrounding tissue Often different morphology
adenoma
differentiating goiters
fine needle aspiration biopsy
allele that can be present with family history of thyroid cancer
MEN2
most aggressive type of thyroid cancer
anaplastic
histo of thyroid cancer:
Complex branching fronds with fibrovascular core and epithelial covering (Latin, papilla, nipple)
Calcificatons with concentric lamination: psammoma bodies Greek, psammos, sand)
Little colloid
Distinctive nuclei
papillary thryoid carcinoma
artefact from formalin fixation of FINELY DISPERSED CHROMATIN
orphan annie eyes (vesicular/optically clear)
seen in follicular variant PTC
histo of thyroid cancer:
Partially or non-encapsulated
Prominent capsular and/or vascular invasion
Frequently metastatic, often distant spread
Up to 20% have distant mets at presentation
May grossly resemble adenoma or may be widely invasive
May histologically resemble normal thyroid or may be more cellular
BUT DO NOT HAVE ORPHAN ANNIE EYE NUCLEI
follicular carcinoma
besides in hypo, where else can you see hurthle cells?
in adenoma/carcinoma
thyroid cancer:
Mainly elderly, >60 yrs, F/M ~ 1.5:1
OFTEN ARISES FROM A PRE-EXISTING PTC OR FTC
Rapidly growing, hard, fixed irregular mass, frequently invasive with distant metastases
Solid growth pattern with giant, spindle and squamoid cells, necrosis, numerous and atypical mitoses. NO RESEMBLANCE TO NORMAL THYROID
Does not take up radioactive iodine
anaplastic thyroid carcinoma
cancer that is derived from C-cells and not follicular epithelium there is some family hx associated with MEN2A/B
medullary thryoid CA
C cells
neuroendocrine cells that produce calcitonin
thyroid cancer physical description:
Firm, white gray, sometimes fleshier than other thyroid CA
medullary carcinoma
In medullary carcinoma the definitive marker is calcitonin but it also produces other neuroendocrine substances. We can often see _____ stroma due to it being derived from calcitonin precuros
amyloid
________________ prior to carcinoma formation in familial MTC
Multifocal with C cell hyperplasia
Disease states or drugs may affect thyroid binding proteins and metabolism which can change TFTs. Oral estrogens and acute hepatitis may ________ binding proteins. Malnutrition, cirrhosis and nephrotic syndrome may __________ binding proteins.
Disease states or drugs may affect thyroid binding proteins and metabolism which can change TFTs. Oral estrogens and acute hepatitis may increase binding proteins. Malnutrition, cirrhosis and nephrotic syndrome may decrease binding proteins.
Thyroglobulin is made in the thyroid and is most commonly used as a
tumor marker for differentiated thyroid cancers.
In primary hypothyroidism, TSH is _____ while T4 and free T4 are_______. T3 levels may not be ____ due to an increase in deiodinase converting T4 to T3. Thus, T3 is less useful for biochemical diagnosis of hypothyroidism.
In primary hypothyroidism, TSH is elevated while T4 and free T4 are low normal or low. T3 levels may not be low due to an increase in deiodinase converting T4 to T3. Thus, T3 is less useful for biochemical diagnosis of hypothyroidism.
is a state of decompensated hypothyroidism requiring intravenous thyroid hormone and other supportive therapy
Myxedema coma
why is it important to check T3 if hyperhtyroidism is suspected?
In mild cases, T4 and free T4 might be at the upper end of the normal range while T3 is elevated.
why are beta blockers used un treatment of hyperhtyroidism?
help control symptoms
thyroid storm treatment
corticosteroids and cold iodine
Propylthiouracil (PTU) and methimazole (mostly methimazole) are the antithyroid medications used for treatment in the United States. They both interfere with thyroid hormone synthesis at multiple steps. what is the other effect that PTU has that methimazole does not?
PTU also blocks T4 to T3 conversion (methimazole does not)
____________ is a destructive process mediated mostly by cytotoxic T-lymphocytes. Glands show dense lymphocytic infiltrate, follicular destruction, Hürthle cell metaplasia of residual follicular epithelium.
Hashimoto’s thyroiditis
____________ is a hyperplastic process caused by agonist antibodies against TSH receptor. Tissue infiltration by lymphocytes is variable and less dense than in Hashimoto’s.
Graves’ disease
is the most common type of thyroid cancer and has a very good prognosis in the vast majority of patients.
Papillary thyroid carcinoma
______________ is mostly used as a tumor marker for differentiated thyroid cancer. Calcitonin is a tumor marker for ______________
Serum thyroglobulin is mostly used as a tumor marker for differentiated thyroid cancer. Calcitonin is a tumor marker for medullary thyroid cancer
__________ are encapsulated, often look different from adjacent thyroid, do not have “Orphan Annie” nuclei, are not invasive. Entire capsule must be sampled to distinguish from follicular carcinoma. which can be diagnosed only by capsular invasion.
Adenomas
in benign multinodular (adenomatous) goiter have absent or incomplete capsules, variable size and morphology, often look like adjacent thyroid, do not have “Orphan Annie” nuclei.
“Adenomatous nodules”
PTC and FTC are distinguished from each other by _______________, not follicular architecture. “Follicular variant” of PTC has ________________ (FTC does not), behaves mostly like classic PTC (lymphatic vs hematogenous spread).
PTC and FTC are distinguished from each other by nuclear morphology, not follicular architecture. “Follicular variant” of PTC has Orphan Annie nuclei (FTC does not), behaves mostly like classic PTC (lymphatic vs hematogenous spread).
PTC and FTC are considered “well differentiated”. ______________ is by definition undifferentiated, does not resemble anything in normal thyroid morphologically or immunohistochemically (no thyroglobulin, no RAI uptake).
Anaplastic carcinoma
Abnormal genes in thyroid cancers include BRAF and RET/PTC in______________________, RAS and PAX8-PPARγ1 in_____________________ and p53 in _____________________
Abnormal genes in thyroid cancers include BRAF and RET/PTC in papillary thyroid carcinomas, RAS and PAX8-PPARγ1 in follicular carcinomas and p53 in anaplastic thyroid carcinoma
___________________ are developmentally distinct from thyroid follicular cells, synthesize calcitonin and give rise to medullary thyroid carcinoma
C-cells (C stands for calcitonin)
