Thyroid disorders

Question 1

Congenital thyroid disorders

Answer 1

Thyroglossal duct cyst

THyroid ectopia

Question 2

Thyroglossal duct cyst

Answer 2

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

Question 3

Thyroid ectopia

Answer 3

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

Question 4

Accute suppurative thyroiditis

Answer 4

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

Question 5

Painful subacute thyroiditis (de Quervain)

Answer 5

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

Question 6

Hashimoto’s thyroiditis pathogenesis

Answer 6

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

Question 7

Hashimoto’s thyroiditis presentation

Answer 7

bumpy, symmetric enlargement of thyroid gland

sometimes nodular

Question 8

Hashimoto’s thyroiditis pathology

Answer 8

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

Question 9

Hashimoto’s thyroiditis complications

Answer 9

much higher risk of non-Hodgkin’s lymphoma as compared to general population, minor increased risk of papillary carcinoma

Question 10

Nodular goiter pathogenesis

Answer 10

not enough iodine/T3/T4 –> excessive TSH stimulation, ultimately leads to asymmetrical growth of follicles –> ruptuer or hemorrhage

Question 11

Nodular goiter presentation

Answer 11

asymptomatic neck swelling
my compress esophagus –> dysphagia, airway obstruction
asymmetrical growht of follicles - individual follicular cells have different responses to TSH

Question 12

DIffuse toxic goiter pathogenesis

Answer 12

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

Question 13

Graves’ disease pathology

Answer 13

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

Question 14

Follicular adenoma (thyroid) pathogenesis

Answer 14

etiology unknown

chronic overstiulation of cAMP - proliferation of thyroid epithelial cells

Question 15

Follicular adenoma presentation

Answer 15

asymptomatic nodule discovered on PE or imaging

Question 16

Follicular adenoma pathology

Answer 16

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

Question 17

Follicular carcinoma presentation

Answer 17

asymptomatic nodule discovered on PE

Question 18

Follicular carcinoma pathology

Answer 18

well circumscribed
thick capsule
invasion through capsule into blood vessels
biopsy with FNA

Question 19

Follicular carcinoma complications

Answer 19

Hematogenous spread to lung and bone

Question 20

Follicular carcinoma tx

Answer 20

total thyroidectomy followed by radioactive iodine therapy to eliminate microdisease
good prognosis

Question 21

Papillary carcinoma

Answer 21

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

Question 22

Medullary carcinoma

Answer 22

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

Question 23

Anaplastic carcinoma

Answer 23

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!!!!!

Question 24

Hypothyroidism S&S

Answer 24

cold intolerance
fatigue, lethargy
depression
dry skin
constipation
hoarseness
menstrual disturbances
weight gain

Signs: bradycardia, diastolic HTN
myxedema
delayed relaxation phase of reflexes

Question 25

Primary hypothyroidism lab values

Answer 25

high TSH

low T4/T3

Question 26

Secondary hypothyroidism lab values

Answer 26

low TSH

low T4/T3

Question 27

Hypothyroidism management

Answer 27

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

Question 28

Investigations of thyroid cancers

Answer 28

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

Question 29

DIffernetiated primary thyroid cancers

Answer 29

papillary

follicular

Question 30

Undiffernetiated primary thyroid cancers

Answer 30

medullary

anaplastic

Question 31

Hyperthyroidism symptoms

Answer 31

nervousness
sweating
heat sensitivity
palpitations
fatigue
dyspnea
increased appetite
eye irritation
swelling in legs
increased frequency of bowel movement/diarrhea
oligomenorrhea, amenorrhea

Question 32

Hyperthyroidism signs

Answer 32

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

Question 33

Common causes of hyperthyroidism

Answer 33

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

Question 34

Rare causes of hyperthyroidism

Answer 34

TSH-secreting tumours
FUnctioning trophoblastic tumours
Iodine-induced hyperthyroidism (when iodine given to iodine-deficient patients)
Metastatic follicular thyroid cancer
Struma ovarii
interferon-induced

Question 35

Thyroid imaging

Answer 35

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

Question 36

Thyroid functional imaging

Answer 36

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

Question 37

Parathyroid gland structural imaging

Answer 37

US, CT best

MRI

Question 38

Functional imaging of parathyroid gland

Answer 38

nuclear medicine (Tc-99 MIBI)
ectopic PT location
PTH effect on skeleton with DEXA

Question 39

Adrenal functional evaluation

Answer 39

nuclear imaging-MIBG

Question 40

Islet cell tumour imaging

Answer 40

CT/US for structural

In 111-ctreotide nuclear med, MIBG

Question 41

Graves’ disease treatment

Answer 41

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

Question 42

PTU MOA

Answer 42

central: inhibits TPO
peripheral: blocks 5’-deiodinase, prevents conversion of T4 –> T3

Question 43

Methimazole MOA

Answer 43

central: inhibits TPO