Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
87 Cards in this Set
- Front
- Back
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
|