Thyroid Handout Flashcards
Goiter is
2 morphologies
can be
Non toxic leads to
results in
diffuse endemic due to
TSH then
also caused by
diffuse sporadic, incidence
demographic
potential cause
enlarged gland
diffuse, multinodular
eu/hypo/hyper T
impaired ability to make T3/T4, inc TSH
hypertrophy/hyperplasia of follicular epithelium, normal production of T3/T4 (euthyroid)
Iodine def, dec T3/T4 production
inc, leading to enlargement
goitrogens (cabbage/cauliflower/cassava root)
Female, adolescence, early adult, less common
goitrogens/hereditary enzyme defect
Multinodular goiter arises from
leads to
Plummer syndrome
Dx
Toxic goiter
longstanding, diffuse nontoxic goiter
different response of follicular epithelial cells to inc TSH
nodule produces lots of T3/T4 (hyperT)
Neck mass
Compressive sx (dysphagia, stridor, hoarse)
HyperT (if plummer)
overproduce T3/T4 (hyperT)
HyperT due to
leads to
Cardiac NM GI Skin Skeletal sx
inc TH
Thyrotoxicosis, hypermetabolic
palpitations, tachycardia, arrh hyperreflex, tremor, anxiety inc GI motility, diarrhea, WL heat intoler, sweating, warm inc bone resorp, fracture/osteoporosis
HyperT causes
P
H
G, aka
presenting age, predominance
pathology
Clinical of graves
Optho
Pretibial myxedema
Plummer syndrome
Hyperfxn thyroid adenoma
Graves, diffuse toxic hyperplasia/goiter
20-40, Female
AI- AA (such as thyroid stimulating immunoglobulin) binds to TSH receptor, inc T3/T4 release
Diffuse, toxic goiter
Exophthalmos- infiltrated retroorbital soft tissues/EOM (edema, inflam/ECM/Fat)
Dermopathy over shins- skin is thick/indurated
HypoT due to, ___ state
Primary ____ or second ____
Primary cause
Secondary cause
Cretinism is hypoT in
presentation
Myxedema due to hypoT
age
sx
def of T3/T4, hypometabolic
thyroid do, do of pituitary/hypothalamus w dec TSH
thyroid hyoplasia/aplasia, removal, severe I defic, AI
TSH def
infancy/child
mental retard, short stature, coarse facial features, large tongue
older kids, adults
mental retard, fatigue, depression, slow speech, WG, cold intolerarnce, dec CO
Hashimoto Thyroiditis pop
presents w
may cause
patho
leads to
histology
atrophic follicles lined w
Pt may have
inc risk of
MA women
diffuse enlarged, painless thyroid (may have nodule)
hypoT
AI- IS fails to recognize thyroid antigens (thyroglobulin/TP) as self
apoptosis of thyroid epithelial cells, dec TH
lymphs/plasma cells, germinal centers
Hurthle cells (pink cells meaplastic from follicle epithelium)
other AI cx
B cell lymphoma from GC
Subacute Thyroiditis aka D, G
pop
____ play a role, such as
Presnetation
Histology
Course
DeQuervain/granulomatous thyroiditis
MA women
Viruses (influenze, coxsackie, mumps, measles, adeno)
enlarged, tender thyroid, pain to neck, fever, malaise
PMN w abscess, lymphs/PC, giant cells, granulomas, FB (colloid released by disrupted follicles)
Self limiting 6-8 wks
Subactue lymphocytic thyroiditis aka P, S
pop
etiollogy
Present
Histo
Damaged follicles release, resulting in
recovery
remainde
painless subacute/silent thyroiditis
MA women
AI- antithyroid perxidase ab/FH of AI dz, post partum
diffuse, enlarged, painless gland
lymphs, germinal center, disrupted follicles
T3/T4, transient hyperT
2-3 mnths for some (eu)
hypoT in 10 yrs
Reidel thyroiditis
pop
Etiology
Clinical
Tx
If extensive,
MA women
fibrosis of thyroid/exta areas in neck/retroperitoneum
assym enlarged thyroid, hard, painless nodule (woody), compression sx
surgical removal of nodule
hypoT
Neoplasms present as
Benign
arises from
appearance
histo
Potential ____, therefore
nodules
Follicular adenoma
follicular epithelium
well demarcated, thick fibrous capsule
benign, follicules
malignant transform, must be removed
Malignant
(MC) Papillary carcinoma
genetics
RF
Histology
metastasizes to
Clinical
Tx
25-50, Female
translocated RET/PTC gene, BRAF mutation
neck radiation
branching papillae w fibrovascular cores, nuclei are clear (orphan annie eye), Psammoma bodies (whorls of Ca)
regional LN
freely movable, painless
surgical removal of gland w radioiodine therapy
Malignant
Follicular carcinoma pop
Genetics
Clinical
Well circum/encap histo
widely invasive histo
metastasize by, to
Tx
Prognosis
old woman, iodine def areas
RAS oncogene PM, translocation of PAX8 and PPARG w fusion gene
slow growing, painless nodule
follicles make colloid, capsular invasion, no projections/annie eyes
solid growth w follicular areas
vascular invasion- Bone, lung, liver
total thyroidectomy w radioiodine, FU w serum thyroglobulin levels
WD= good
WI- not as much
Malignant
Medullary thyroid Carcinoma
Derived from
pt does not get
can secrete
Genetics
Histology
Metastasizes via, to
Parafollicular (C cells)- produce Calcitonin to excess
hypoCa
other hormones, 5HT3, ACTH,VIP
mutation in RET
amyloid deposit in stroma, procalcitonin, use H/E and congo red stain w polarizing light
blood, lung, liver, bone, LN
MTC sporadic type (MC)
pop
clinical
Paraneoplastic syndromes such as
familial type
FH
collectively called
pop
Clinical
Sx due to
such as
40-50, M and F
Nodule, compresion
Cushing (ACTH), diarrhea (VIP)
MTC or MTC plus other familial endocrine tumors
Multiple endocrine neoplasia (MEN)
Younger, children
Multiple nodules
endocrine abnorm
pheochromo w HTN, hyperPTH w inc Ca
MTC tx
better prog
worse prog
Family members of anyone w MTC should have
if abnormal, may indicate
tx
total thyroidectomy (no radioiodine)
women, low grade/stage
older, men
blood drawn for calcitonin/RET mutation
familial syndrome
prophylactic thyroidectomy
