Thyroid disorders Flashcards
Congenital thyroid disorders
Thyroglossal duct cyst
THyroid ectopia
Thyroglossal duct cyst
cystic dilatation of persistent thyroglossal duct
Presentation: asymptomatic mass at level of hyoid or lower
Pathology: squamous, cuboidal, columnar (ciliated); lymphocytes, histiocytes, and PMNs. LIned by respiratory or squamous epithelium which may be replaced with granulation tissue if it has been infected, thyroid tissue in the walls
Complications: 1-2% chance of papillary carcinoma
Thyroid ectopia
Presence of thyroid tissue anywhere other than its usual location (between base of tongue, and thyroid, mediastinum, heart, GI)
Lingual thyroid:
- presentation: difficulty swallowing, breathing
- increased demand for thyroid hormone leads to increased TSH and enlargement of thyroid gland
-complications: rarely develop carcinoma
Accute suppurative thyroiditis
Acute inflammation due to infectino, most often bacterial (S aureus) or rarely fungal, parasitic
Neutrophil infiltration with follicle destruction
Elevated ESR, leukocytosis, normal thyroid function
Presentation: acutely ill with high fever, tachycardia, anterior neck pain, dysphagia, dysphonia, erythema, tender thyroid mass
Painful subacute thyroiditis (de Quervain)
inflammatory with unknown etiology characterized by pain and tenderness of thyroid and granulomatous inflammation
Pathogenesis: destruction of thyroid follicles, release of TG –> bound T4/T3 released –> transient hyperthyroidism followed by decreased thyroid function –> destroyed follicles unable to respond adequately to TSH stimulation
Presentation: prodrome of generalized myalgias,fatigue, fever, and pharyngitis –> fever with neck pain/swelling , 50% have hyperthyroid symptoms –> hypothyroid for weeks to months –> recover in 95%
See granulomatous inflammation, patchy infiltrate of lymphocytes and plasma cells, destruction of follicles
Hashimoto’s thyroiditis pathogenesis
autoimmune
Induction of B cells to make anti-TPO and anti-TG
TPO antibodies are complement fixing and cytotoxic to follicular cells
Cell death involving Fas receptor may play a role
Hashimoto’s thyroiditis presentation
bumpy, symmetric enlargement of thyroid gland
sometimes nodular
Hashimoto’s thyroiditis pathology
intense diffuse infiltrate of lymphocytes and plasma cells
germinal centre formation
oncocytic changes in follicular cells (cells have abundant eosinophilic granular cytosol filled with mitochondria - Hurthle cells)
Follicular destruction and disruption
with or without fibrosis
Hashimoto’s thyroiditis complications
much higher risk of non-Hodgkin’s lymphoma as compared to general population, minor increased risk of papillary carcinoma
Nodular goiter pathogenesis
not enough iodine/T3/T4 –> excessive TSH stimulation, ultimately leads to asymmetrical growth of follicles –> ruptuer or hemorrhage
Nodular goiter presentation
asymptomatic neck swelling
my compress esophagus –> dysphagia, airway obstruction
asymmetrical growht of follicles - individual follicular cells have different responses to TSH
DIffuse toxic goiter pathogenesis
Grave’s
antibodies to TSHreceptor with possible cross-reactivity between abs to thyroid antigens and CT antigens
leads to ophthalmopathy and dermopathy
can manifest wiht an initial hypothyroid phase because of thyroid inhibiting antibodies
Graves’ disease pathology
thyroid: diffuse symmetric enlargement, pale staining colloid, follicles of varying size/shape, thyroid lined by tall columnar cells, papillary projection into the follicular lumen, variable lymphocyte infiltration
ORbit: inflammation of orbital soft tissues and extraocular muscles with lymphocytes and plasma cells –> deposition of CT mucin
Skin: deposition of CT mucin
Follicular adenoma (thyroid) pathogenesis
etiology unknown
chronic overstiulation of cAMP - proliferation of thyroid epithelial cells
Follicular adenoma presentation
asymptomatic nodule discovered on PE or imaging
Follicular adenoma pathology
solitary nodules
well circumscribed
encapsulated
1-10 cm
follicles of varying size (micro/macro)
compresses surrounding thyroid parenchyma
unable to differentiate follicular adenoma from carcinoma on FNA
presence of multiple nodules - usually indicates nodular goiter than follicular adenoma
Follicular carcinoma presentation
asymptomatic nodule discovered on PE
Follicular carcinoma pathology
well circumscribed
thick capsule
invasion through capsule into blood vessels
biopsy with FNA
Follicular carcinoma complications
Hematogenous spread to lung and bone
Follicular carcinoma tx
total thyroidectomy followed by radioactive iodine therapy to eliminate microdisease
good prognosis
Papillary carcinoma
most common thyroid malignancy (80%)
associated with FAP, previous radiation exposure, RET oncogene
good prognosis
Poorly circumscribed, unencapsulated tumour, grow as papillae with fibrovascular cores
Optically clear nuclei with grooves and nuclear hole
Calcification
Some are purely follicular but have the clear nuclei (follicular variant of papillary carcinoma)
Spreads via lymphatics but spread to cervical LN has no effect on survival
Medullary carcinoma
Parafollicular differentiation
Can be associated with MEN or familial medullary carcinoma
Presents with an asymptomatic mass
Serum calcitonin often high but no functional problem
See polygonal/spindle cells, abundant amyloid (pink) made partly of calcitonin
Terrible prognosis if residual disease
Anaplastic carcinoma
Highly malignant thyroid carcinoma with no evidence of differentiation
See high grade spindle cell (resembling sarcoma) or squamoid malignancy
5 year survival <10%, one of worst tumours known!!!!!
Hypothyroidism S&S
cold intolerance fatigue, lethargy depression dry skin constipation hoarseness menstrual disturbances weight gain
Signs: bradycardia, diastolic HTN
myxedema
delayed relaxation phase of reflexes
Primary hypothyroidism lab values
high TSH
low T4/T3
Secondary hypothyroidism lab values
low TSH
low T4/T3
Hypothyroidism management
Levothyroxine (T4)
significant increase seen in 1-2 weeks, near-peak in 3-4 weeks, but may not experience full symptomatic relief until 3-6 months
Adjust dose based on TSH, which will not stabilize until around 2-3 months
Followup TSH
Investigations of thyroid cancers
nodules common, vast majority benign (95%)
Serum factors: TSH, calcitonin (suggest MCT)
Imaging: thyroid scan (hot nodules almost never malignant, 5-10% cold nodules are malignnat)
FNAB (fine needle aspiration): principal test to distinguish benign from malignant
DIffernetiated primary thyroid cancers
papillary
follicular
Undiffernetiated primary thyroid cancers
medullary
anaplastic
Hyperthyroidism symptoms
nervousness sweating heat sensitivity palpitations fatigue dyspnea increased appetite eye irritation swelling in legs increased frequency of bowel movement/diarrhea oligomenorrhea, amenorrhea
Hyperthyroidism signs
tachycardia goiter warm, moist skin tremor/hyperreflexia bruit over thyroid tenderness of thyroid gland eye signs (erythema, lid retraction, stare) exophthalmos (Graves') fever weight loss (or weight gain due to increased appetite) splenomegaly gynecomastia thyroid acropachy (Graves')
elderly: CHF, a fib, proximal muscle weakness, unexplained weight loss
Children: accelerated linear growth ,eye signs more common
Common causes of hyperthyroidism
Graves’ (mostcommon)
Toxic multinodular goiter - independent of TSH
TOxic uninodular goiter: independent of TSH
Subacute thyroiditis: usually idiopathic, but can be a result of autoimmune/virally-mediated inflammation
Amiodarone-induced: Type A is iodine-induced, B is a type of thyroiditis
Rare causes of hyperthyroidism
TSH-secreting tumours FUnctioning trophoblastic tumours Iodine-induced hyperthyroidism (when iodine given to iodine-deficient patients) Metastatic follicular thyroid cancer Struma ovarii interferon-induced
Thyroid imaging
US best, CT/MRI
US: overlap between characteristics of benign and malignant nodules
Benign: pure cysts
Malignant: lesions with punctuate calcified mural nodules
- poorly defined borders
- solid + hypoechoic
CT more useful in followup of selected thyroid cancer patients, look for LN involvement
MRI can see invasion through capsule or enlarged LN in cancer
Thyroid functional imaging
Nuclear medicine I-123 etc
most thyroid nodules are cold
limited role in euthyroid patient
can be used to find ectopic thyroid tissue, e.g. sublingual
Hyperthyroidism can be detected with I-123 - Graves’ (diffuse), toxic multinodular goiter (high in nodules)
Can also detect thyroid carcinoma
Parathyroid gland structural imaging
US, CT best
MRI
Functional imaging of parathyroid gland
nuclear medicine (Tc-99 MIBI)
ectopic PT location
PTH effect on skeleton with DEXA
Adrenal functional evaluation
nuclear imaging-MIBG
Islet cell tumour imaging
CT/US for structural
In 111-ctreotide nuclear med, MIBG
Graves’ disease treatment
1) Thyroid suppressants: propylthiouracil (PTU0 or methimazole
- 12-18 months, then consider radiotherapy
- can also give beta blockers for symptoms
2) radioactive I-131 ablation
3) subtotal thyroidectomy
- consider for patients with significant ophthalmopathy
Radioiodine can exacerbate Graves’ ophthalmopathy
PTU MOA
central: inhibits TPO
peripheral: blocks 5’-deiodinase, prevents conversion of T4 –> T3
Methimazole MOA
central: inhibits TPO
