H&N- Thyroid/Parathyroid Flashcards
Ectopic thyroid tissue: most common place?
Lingual
Lingual thyroid tissue:
Gender predominance?
Mos common clinical affection?
Other clinical manifestation?
Associations?
Other locations?
Best method of diagnosis
How does it look in CT
Female predominance.
25% of patients suffers from congenital hypothyroidism
Goiter
Associations: other developmental lesions such as thyroglossal duct cyst
Other locations: sublingual, prelaryngeal, other
Best Dx: nuclear medicine (TC-99 or radioiodine scan)’
Other: CT hyperdense in NECT. Homogenous enhancement post Contrast.
Physiopath of ectopic thyroid tissue
Faillure or normal migration of thyroid tissue between 3rd and 7th week of gestation.
Complications of a thyroglossal duct remnant?
Infection (fat stranding)
Malignant transformation 1% (papillary Ca) (Solid, cystic, Ca+)
Locations of thyroglossal remnant cyst?
Midline cystic structure.
-Hyoides 50% base of tongue
-Suprahyoides 25%
-Infrahyoides 25% (claw sign)
Physiopath of thyroglossal remnant
failure of involution of thyroglossal duct, which continues to produce secretion, which develops into a cyst.
Graves disease: physiopath
Explain graves ophthalmopaty and dermopathy
Resulting Lab profile
-Presence of thyroid stimulating autoantibodies directed against TSH receptors .
-Opthalmopathy: orbital preadipocytes express TSH receptors, succeptible for autoantibodies. Also, connective tissue and EOM suffers from mononuclear infiltration, inflammatory oedema and swelling, incrased extracellular matrix, deposits of GAG and increased number of adipocytes.
-Dermopathy: lymphoid hyperplasia , lymphocyte infiltration and GAG accumulation.
Results into: increased T3, T4, suppressed TSH.
Associations and complications of Graves disease
Associations: 10 times increase risk for other autoimmune disease (RA, LES, celiac, Addison, pernicious anemia..)
Complications:
-cardiac complications (faillure, arrhythmia)
-osteoporosis
-thyrotoxic crisis
Graves disease: epidemiology (age, gender, what is it most frequent of)
20-40yo.
Female (10 times more frequent)
Most frequent endogenous hyperthyroidism
Clinical tiad of Graves disease
Hyperthyroidism
Thyroid ophthalmopathy
Dermopathy
Diagnosis of Graves disease
Treatment?
-Normally it is a clinical diagnosis.
-US when failure of medical treatment or to exclude other reasons for goiter.
Diffusely increased in size (>90ml), hypoechoic , heterogeneous, hypervascular.
-NM TC-99m or I-123 (increaseD radioactive iodine uptake.
Treatment:
-betablocker
-reduce thyroid hormone synthesis (medical, radioiodine ablation, thyroidectomy)
Quervain: Definition
Epidemio
Self limiting autoimmune (T cell mediated) granulomatous subacute painful thyroiditis secondary to upper respiratory viral infection. (most common painful goiter)
Female. 5th decade.
Seasonal.
Quervain: Clinical phases
Prognosis
Clinically 4 phases (lasts 6-12 months if all 4 phases happen)
-Initial thyrotoxic phase (last 2 weeks) due to release of thyroid hormone.( T3, T4, TSH and radioactive iodine uptake due to failure of Iodine trapping)
-Brief euthyroid phase (last 1-3w)
-Hypothyroid phase (last weeks-months) failure to trap iodine by destroyed thyroid gland (50% of patients)
-Recovery phase (euthyroid)
Self-limiting
Quervain: complications
20% permanent hypothyroidism
2% recurrence within the first year.
Imaging diagnosis
Ultrasound:
-Acute phase: Focal, ill-defined, nodular, hypoechoic, avascular/hypovascular area in subcapsular region.
-Subacute phase: Diffuse enlargement of 1 lobe or entire thyroid gland with multifocal, patchy/confluent, ill-defined, hypoechoic, avascular/hypovascular areas
CT: NECT shows diffusely enlarged thyroid with low attenuation (~ 45 HU); CECT shows moderate enhancement indicating inflammatory process
MR: during acute phase, MR shows enlarged thyroid with irregular margins and higher than normal signal intensity on both T1W and T2W sequences
Hashimoto: definition
Autoimmune thyroiditis due to breackdown of self tolerance, which leads to progressive destruction of thyroid cells and hypothyroidism
Hashimoto, physiopath
-Breakdown in self-tolerance to thyroid autoantigens results in progressive autoimmune destruction of thyroid cells by a) infiltrating cytotoxic T cells, b) locally released cytokines due to thyrocyte injury, c)antibody dependent cytotoxicity.
-Presence of anti-thyroid antibodies: Anti-thyroblobulin ~70% , Anti-perosidase ~95%, Anti-mitochondrial, anti TSH receptor.
-Progresively there is thyroid epithelium depletion, mononuclear cell infiltrate and fibrosis.
-Familiar predisposition: ≤ 50% 1st-degree relatives have elevated thyroid autoantibodies
-Macro: firm, symmetrically enlarged, yellow parenchyma.
-Micro: Atrophic follicles, Hürthle cell metaplasia, fibrosis, lymphocyte & plasma cell infiltration, germinal centers and variable degree of fibrosis.
Hashimoto: associations
-Increased risk for other autoimmune disease (LES, Type 1 DM, Sjogren, miastenia gravis)
-> 90% of patients with primary thyroid non-Hodgkin lymphoma have CLT
-T21, Turner syndrome
Hashimoto, complications
-increased risk of primary B-cell non-Hodgkin lymphoma (~80%)
-Other malignant transformation (controversial, papillary thyroid Ca)
Diagnosis for hashimoto
Best modality ultrasound
US: - Early stage shows enlarged, capsule intact, lobulated thyroid with hypoechoic micronodules & marked Hypervascularity
- Late stage shows small, echogenic fibrosed gland with absent flow signals
CT: Diffuse, moderately, low-density thyroid without calcifications, cysts, or necrosis
Radioactive iodine:
Early stage: increased uptake
Late stage: single or multiple areas of reduced uptake.
Main features of Reidel
Definition, clinical presentation, path, dx.
Autoimmune thyroiditis characterized by extensive fibrosis involving thyroid and contiguous neck structures. May extend to retroperitoneum. Thought to be IgG4-mediated.
Clinically painless, hard and fixed thyroid mass, simulates carcinoma
Path: replacement of thyroid gland with fibrotic tissue that extend s to the surrounding tissues.
Associations: Other IgG4 mediated sclerosing disease: retroperitoneal fibrosis, sclerosing cholangitis, orbital pseudotumor, fibrosing mediastinitis.
Dx: US: hypoechoic, poor definition of gland borders. Enlarged thyroid gland.
CT: compression of local structures by enlarged thyroid gland.
MR: T1 and T2.
Thyroid adenoma:
Epidemiology
Age/gender
Most common incidental finding in the thyroid.
>95% benign
>95% non functioning (small % functional)
Clinical: mass/ mass effect
Any age. Female predominance
Thyroid adenoma:
types?
Ultrasound findings
2 types
-True adenoma: well defined encapsulated nodule compresses adjacent gland.
Degenerative changes common.
Spoke-wheel pattern of peripheral blood vessels
-Adenomatous nodule: Less distinct lesion contours; multiple lesions often present
More diffuse pattern of vascularity.
Thyroid adenoma: physiopath
Benign neoplasm of the thyroid epithelium with fibrous encapsulation.
2 types: true adenoma vs adenomatous hyperplasia.
-Somatic mutation resulting in gain of function of TSH receptor signaling causing autonomus proliferation.
-RAS mutation (oncogenic mutation) occurs in 20% non functioning adenomas.
Tyroid adenoma: When biopsy?
Scintigraphy with TC-99 or I-123:
Cold nodules <10% are malignant, biopsy (RAS mutation (oncogenic mutation) occurs in 20% non functioning adenomas)
Which are the well differentiated thyroid carcinomas?
Frequency?
Papillary >85%
Follicular ~15%
Papillary and follicular Ca: path
Both: Epithelial derived malignancies associated with gain-of function of mitogen activated protein (MAP) which leads to consitutive cell activation without TSH ligand binding.
Papillary: also RET mutation.
Follicular: RAS mutation.
Papillary and follicular Ca: age gender profile
Papillary: female, 20-50yo
Follicular: female 40-60yo
Papillary and follicular Ca: epidemiology
Papillary:
-Majority: sporadic.
-History of thyroid Ca associated with previous radiation exposure.
Follicular:
Increased prevalence in areas with dietary iodine deficiency.
Classification of hyperthytoidism
Primary: Autonomus overproduction of PTH
Secondary: compensatory hypersecretion of PTH in response to prolonged Ca+.
Tertiary: autonomous secretion of PTH (even after cause if hypoCa+ is corrected)
Difference between parathyroid adenoma and parathyroid hyperplasia?
Adenoma 95%
Solitary.
Well defined. With fibrous capsule.
Mostly sporadic (95%)
-40%: Cyclin D1 overexpression (50% of them due to Ch11 relocation)
-~30%: MEN 1 (tumour suppressor gene) somatic mutation leading to inactivation
Familial syndromes (5%)
-MEN 1 germline mutation.
-MEN2: activation mutation of RET tyrosine kinase receptor.
-Familiar hypocalciuric hypercalcemia (AD)
-Predominantly chief cell. Foci of oxyphil cells (packed with mitochondria) may be present.
-Uncommonly adenomas can be composed entirely of oxyphil cells (oxyphil adenomas)
-Rim of fibrous capsule.
Primary Hyperplasia ~10%
Diffused or nodular (but asymmetric).
Classically all 4 glands are involved but frequently asymmetric with sparing of one or two glands.
Sporadic
Part of MEN syndrome.
-Chief cell hyperplasia involving glands in diffuse or multinodular pattern.
-Less commonly water-clear cell hyperplasia (constituent cells contain abundant glycogen)
-many cases, there are island of oxyphils.
Symptoms of hyperparathyroidism
Symptomatic: “painfull bones, renal stones, abdominal goans, physic moans”
Skeletal:
-Osteoporosis: decreased bone mass by increased osteoclast activity.
Affects more cortical bone (subperiosteal and endosteal surphaces)
less in medullary bone (osteoclasts tunnel centrally along the traveculae railroad tracks, dissecting osteitis. Marrow replaced by fibrovascular tissue.
Preferential phalanges, vertebrae, proximal femour.
-Brown tumor: reactive tissue secondary to microfracture, haemorrhage, influx of macrophages, repair with fibrous tissue.
-Osteitis fibrosa cystica (Von Recklinghausen): osteoclast activity + peritrabecular fibrosis + brown tumors (hallmark of severe hyperPTH.
Renal: nephrolithiasis, nephrocalcinosis.
Other: intestinal (constipation, gallstone, pancreatitis), CNS (lethargy, depression, seizures), MSK (weekness, fatigue), Cardiac (valve calcification)
Main characteristic of secondary hyperparathyroidism
most commonly caused by renal failure: compensatory hypersecretion of PTH in response to prolonged Ca+.
Other causes: inadequate dietary intake of Ca, steatorrhea, vit D deficiency.
Mechanism:
Renal failure, drecreased phosphatete exretion, depressed serum Ca+ levels.
Other: loss or renal substance reduced availability of alfa-1 hydroxylase, inactivation of Vit D:
-Reduced intestinal absorption of Ca.
-Deficiency in suppression of parathyroid growth and secretion.
Clinically: not as severe as primary.
