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87 Cards in this Set

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How are the thyroidititis categorized?
Acute (painful) and subacute (painless, which involves lymphocytic infiltration and fibrosis rather than infections/granulomas)
How are infectious thyroiditities characterized?
acute or chronic
Thyroid infections in IC people?
the chronic thyroiditities: mycobacterial, fungal, PCP
Most common thyroiditis?
1) Hashimoto thyroiditis
2) subacute granulomatous thyroiditis
3) subacute lymphocytic thyroiditis
Presentation of infectious thyroiditis?
suddent onset of neck pain and tenderness, fever, chills, and other signs of infection
Residual effects of infectious thyroiditis?
usually self-limiting and resulve without problems except maybe a small foci of scarring
MCC of hypothyroidism in areas of the world where iodine levels are sufficient?
Hashimoto's thyroiditis.
What is struma lymphomatosa?
intense lymphocytic infiltration of the thyroid
Patient population of Hashimoto's
women between 45-65 but is a major cause of nonendemic goiter in children
Cases of Hashimoto thyroiditis linked to?
HLA-DR5, HLA DR3
Usual course of Hashimotos?
Early phase: folicular distruction causing hyperthyroidism,
then gradual loss of thyroid function
What other disorders usually accompany hashimotos?
Just like in Graves, the frequency of other AI disorders is increased in patients with Hashiomoto disease.
Pathogenesis of Hashimotos?
Primarily a defect in T cells, causing increased B cell activity (autoantibody secretion), and apoptosis via the Fas-FasL system
Why does it make sense that HLA-DR5 is implicated in Hashimotos?
Because improper antigen presentation by T cells and activation of B cells is the main destructive process
What T-cell dysfunctions are involved in Hashimotos?
the MHC molecules improperly recognize and process thyroid antigen. 1) Presentation to B Cells stimulate the secretion of a variety of antithyroid antibodies
2)formation of CD8+ cells that are cytotoxic to thyroid cells
Also diminished suppressor T Cells are implicated
What are Hashimoto's autoantibodies agains?
thyroglobulin, thyroid peroxidase,
TSH receptor (same as graves and is specific to these diseases)
sometimes iodine transporter
Hashimoto's autoantibodies that are not specific for the disorder and present in many thyroid disorders?
thyroglobulin and thyroid peroxidase and iodine transporter
Hashimotos vs Grave's?
In hashimoto's, the anti-TSH receptor Abs block the action of TSH causing hypothyroidism. In Grave's, the Ab stimulates the TSH receptor
Apoptosis of what is also implicated in Hashimotos?
Fas-FasL mediated apoptosis of thyroid epithelial cells.
Explain Fas-FasL mediated apoptosis of thyroid epithelial cells.
IL1B is expressed by Hashimoto glands which induces Fas expression. FasL is always expressed on epithelial cells and so the Fas-FasL interaction triggers apoptosis
Cut surface of hashimoto thyroid gland?
Like hashimoto: pale, gray, firm, somewhat nodular
Special cells seen histologically in Hashimotos
Hurthle cells: they are epithelial cells that line the follicules that have abundant eosinophilic cytoplasm
Parenchyma histology of hashimotos?
lymphocyte, plasma cells with developed germinal centers and Hurthle cells
Serum levels of hormones during transient thyrotoxicosis seen in Hashimotos?
High T3/T4, low TSH, low radioactive iodine uptake.
Clinical presentation of Hashimotos?
Middle aged woman with painless enlargement of the thyroid and hypothyroidism
Serum levels of hormones in Hashimoto patient?
low T3/T4 levels and increased TSH
Patients with Hashimotos have increased development of what?
B-Cell lymphomas. Makes sense, because of the hyper-activity
Pathogenesis of subacute granulomatous thyroiditis?
post-viral infection; HLA-B35 macrophages process viral antigen and form cytotoxic T cells that destroy follicular cells and release thyroid hormone
Genetic association with DeQuervain's thyroiditis?
HLA-B35
Cut section of DeQuervain's thyroid
firm yellow-white nodules amongst rubbery brown normal thyroid
histologic changes seen inDeQuervain's
1) neutrophilic microabcesses
2)lymphocytic/histiocytic/plasma cell infiltration with granulomas
3) fibrosis at foci of injury
Lesion stages seen in DeQuervain
Lesions are all of different stages, sugessting waves of destruction over time
Unilaterally or bilateral enlargement of throat area with pain in the neck which radiates to the upper neck, jaw, throat, post viral infection.
Subacute granulomatous (painful) thyroiditis
Time period of DeQuervain's?
2-6 weeks and recovery complete even without treatment
Serum levels during DeQuervains?
TRANSIENT hyperthyroidism with high T3/T4 and low TSH; IODINE UPTAKE IS LOW, then hypothyroidism.
Treatment of DeQuervain's thyroiditis?
Beta blockers and NSAIDS or corticosteroids
Increased thyroid and increased iodine uptake?
Grave's
HLA haplotypes associated with subacute lymphocytic thyroiditis?
HLA-DR3 and HLA-DR5, considered a variant of Hashimoto's thyroiditis, as they both have Abs to thyroid peroxidase and thyroglobulin
clinical manifestation of painless thyroiditis?
hyperthyroidism and mild symmetric enlargement of thyroid.
Histologic comparison of subacute lymphocytic thyroiditis vs hashimoto's?
both have multifocal inflammatory infiltrate with small lymphocytes but plasma cells and germinal centers are suggestive of Hashimoto's disease only.
Thyroid replaced by fibrous tissue?
Reidel's thyroiditis; hard, rock-like and painless goiter.
Pot-bellied, pal, puffy-faced child with protruding umbilicus and protuberant tongue
severe fetal hypothyroidism (cretinism)
What is endemic cretinism?
Common in China and where dietary iodine is lacking.
Most common cause of endemic hyperthyroidism?
Graves disease
Triad of clinical findings in Graves
Hyperthyroidism, Exopthalmos, pretibial myxedema
Patient population with Graves
women 20-40
Genetic association with Graves
HLA-B8 and HLA-DR3
What is LATS
Long acting thyroid stimulator which is IgG against TSH receptor that acts as a TSH agonist
Pathogenesis of Graves
1) autoantibodies to TSH receptor causing T3/T4 release
2)autoAbs to TSH receptor causing proliferation of parafollicular epithelial cells
What is Graaves dermopathy?
Pretibial myxedema - increased fibroblast GAG production causing dermal symptoms (peu d'orange)
Trigger for Graves autoimmunne reaction?
molecular mimicry to an agent yet to be determined, T-cell (MHC-B8) thyroid Ag processing that causes B-Cell anti-TSH receptor production
Histologic presentation of Graves?
hypercellularity with crowding of the follicles by small follicular papillae. B-cell follicles present.
Bruit in the neck area?
Seen in Graves, where diffuse thyroid enlargement is accompanied by increased blood flow, causing a bruit.
Opthalmopathy in Graves caused by?
increased sympathetic activity and deposition of matrix components behind the eyebal
Pretibial myxedma common where?
on shins, doi (pretibial!) seen in 1-4% of Graves patients and can look like orange peel
Lab findings of Graves?
Elevated T3/T4, depressed TSH, increased iodine uptake
Diffuse and multinodular goiters indicates what?
High TSH levels which causes hypertrophy and hyperplasia of thyroid follicular cells. High TSH due to impairment of thyroid hormoney and inhibition of negative feedback
MCC of diffuse and multinodular goiters?
iodine insufficiency
Causes of endemic goiter?
areas where iodine is low and people eat goiterogens like cavassa root
AR conditions of colloid goiter?
Iodide transport defect, organification defect, dehalogenase defect, iodotyrosine coupling defect.

IODIne utilization defects!
Phases of diffuse nontoxic goiter?
1) hyperplastic stage that looks like non-uniform Graves
2)colloid involution
What causes multinodular goiter?
recurrent episodes of hyperplasia and involution, which happens to virtually all longstanding simple goiters
Population of patients with multinodular goiter?
same as sporadic and endemic distributions but in older people because multinodularity is a late complication of simple goiter
What causes the multinodularity seen in a multinodular goiter?
monoclonal proliferation of follicular cells having different proliferative potentials in response to TSH.
Uneven follicular hyperplasia seen in multinodular goiter causes what?
tensions and stresses that lead to follicular and vessel rupture causing hemorrhage, scarring, calcifications
Dominant clinical feature of multinodular goiters?
They produce the most extreme goiter enlargements; clinical symptoms are mass effects.
uneven radioiodine uptake... what syndrome?
Plummer syndrome where a hyperfunctioning nodule develops within the goiter and hyperthyroidism results
Goiters mask what neoplasm?
thyroid neoplasms
Neoplastic nodules are commonly:
solitary, in males, in younger patients, patients with a history of radiation, and take up iodine poorly
Most thyroid nodules are what?
benigne lesions such as follicular adenomas or non-neoplastic conditions
Most thyroid neoplasms are what?
adenomas. Carcinomas are extremely rare.
What causes follicular adenomas?
somatic mutations of Gas subunit, causing chronic stimulation of the cAMP pathway and generating cells with a growth advantage.
macrofollicular adenoma
thyroid with large colloid-filled follicules lined by flattened epithelial cells
microfollicular adenoma
thyroid with numerous small, well-developed follicles lined by flattened epithelial cells
trbvecular or embryonal adenoma
thyroid composed of closely packed cells forming cords or tabeculae of cells
atypical thyroid adenoma
follicular adenoma demonstrating pleomorphism and variability in cell and nuclear size
Hurthle cell adenoma
with Hurthle cells, seen also in Hashimoto's
Papillary adenoma
papillary excrecences (can be large, branched) with large follicular or cystic space
iodine usage of thyroid adenoma?
most adenomas appear as cold nodules because they take up less radioactive iodine less avidly;

hyperactive nodules however, appear as hot also because extranodal tissues are quiescent and suppressed.
Female predominance of thyroid carcinoma in early and middle adult years due to?
estrogen receptor expression on neoplastic thyroid epithelium
Major thyroid carcinoma subtypes:
PFMA: please feed me apples
Papillary, Follicular, Medulary, Anaplastic carcinoma - in order of frequency
The major risk factor predisposing to thyroid cancer:
ionizing radiation during first 20 yrs of life.
Cytogenics of papillary and medullary thyroid carcinomas?
RET/PTC oncogene that expressed tyrosine kinase portion of the receptor at high levels in the malignant cells; constitutively activated gene provides thyroid cells with unregulated cell growth signal
What is MEN-2?
a heritable disorder that involves a triad of medullary thyroid carcinoma, pheochromocytoma, and hyerparathyroidism.
95% of families have what?
RET oncogene responsible for papillary and medullary thyroid carcinoma
Diagnosis of Papillary thyroid carcinoma?
based upon nuclei rather than papillary architecture: ground glass nuclei or Orphan Annie nuclei present and psammoma body (calcification)
types of papillary thyroid carcinomas?
Encapsulated, follicular, and tall cell variants