Reading...
Play button
Play button
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;
120 Cards in this Set
- Front
- Back
|
what is indicative on histo for hyperthyroidism
|
papillary infolding
scalloping coloid |
|
|
how is papillary carcinoma diagnosed?
|
nuclear features
cleared out nuclei open ring appearance psommoma bodies intranuclear inclusion with groove |
|
|
what is metastatic potential of papillary carcinoma?
|
50% spread to lymph nodes by the time you find it.
|
|
|
what is main metastaic potential in follicular carcinoma of thyroid?
|
like to metastasize to the blood.
|
|
|
what is characterized by pretibial myxedema?
|
graves disease only thing that has this
exopthalhma bulging eyes also indicitave of this |
|
|
myxedema is seen in what?
|
hypothyroidism
|
|
|
what is seen in radionuclides scans of thyroid?
|
darker the more iodide it takes up
multilobulated goiter-leads to both dark spots and light spots hyperthyroid- would show dark uniform hypothyroid would show light uniform |
|
|
hashimotos thyroiditis has slight increased risk of what?
|
lymphoma
|
|
|
what type of thryoidism is seen in hashimotos thyroiditis?
|
hypothyroidism
|
|
|
what throws off T4 levels measured?
|
oral contraceptives increase thyroid binding globulin and T4 measures only thyroid binding globulin bound T4
if a pt is hypothyroid you will need a free T4 test to see what their actual thyroid state is. |
|
|
what is another name for T3?
|
triiodothyronine
|
|
|
what is another name for T4?
|
thyroxine
|
|
|
what type of receptor is the TSH receptors of the thyroid and what does it do?
|
Gprotein receptor when activated converts GTP to GDP and creates cAMP.
|
|
|
how does T3 and T4 travel in the serum?
|
most is bound to thyroxine binding globulin,albumin, or transthyretin protiens
small amount travels in a free unbound state. |
|
|
what is the activity of T3 compared to T4?
|
T3 binds to nuclear receptors with 10 fold affinity compared to T4
|
|
|
what does T3 (and T4) bind to in the target tissue?
|
binds to a multiprotiene hormone receptor complex that binds thyroid homrone response elements(TREs) in target genes
|
|
|
what is the effect of TREs?
|
when activated they bind to target genes and upregulate transcription
|
|
|
what are the metabolic effects of thyroid hormone?
|
upreg of carbs and lipid catabolism
stim of protein synthesis net effect increases basal metabolic rate |
|
|
what is thyroid hormone effects on brain?
|
critical role in brain development absence fo thryoid hormone during fetal/neonatal development = profound intellectual stunting
|
|
|
what is thryoid effect on bone?
|
thyroid also produces calcitonin via the parafollicular cells(c cells)
promotes absorption of calcium by skeletal system inhibits resorption of bone by osteoclasts |
|
|
what is throtoxicosis?
|
hypermetabolic state brought on by hyperthyroidism
|
|
|
what are the causes of primary hyperthyroidism?
|
diffuse gland hyperplasia related to graves disease
hyperfunctional multinodular goiter hyperfunctional adenoma |
|
|
what is the most common cause of primary hyperthyroidism?
|
graves disease 85%
|
|
|
what are the causes of secondary hyperthyroidism?
|
pituitary adenoma
exogenous thyroid hormone intake inflammatory conditions |
|
|
what is thyroid storm?
|
abutp onset severe hyperthyroidism
|
|
|
what are the cardiac features of hyperthyroidism?
|
earliest and most consiten features
increased cardiac output b/c of increased contractility and peripheral oxygen needs tachycardia, palpitation, cardiomegaly, arrhythmias |
|
|
what are the ocular effects of hyperthryoidism
|
wide staring gaze with lid lag
graves Ds with exopthalmos |
|
|
what are the neuromuscular effects of hyperthyroidsm/
|
overactive sympthaetic nervous system
-tremors, hyperactivity, emotinoal lability, anxiety, inability to focus, insomnia |
|
|
what are the skin effects of hypethyroid?
|
vasodilated warm flushed moist trying to rid heat
graves disease with inlfitrative dermopathy |
|
|
what are the GI effects of hyperthyroidism?
|
hypermotility, malabsoprtion, diarrhea
|
|
|
what are the skeletal effects of hyperthyroidism?
|
osteoporosis
|
|
|
what is the earlist and most constistant symptom seen in hyperthyroid?
|
cardiac effects
|
|
|
what is the most useful test for hyperthyroid?
|
Serum TSH
will be low in primary will be elevated in secondary |
|
|
what labs will be elevated in hyperthryoidism?
|
TSH if secondary
Free T4 (used to confirm diagnosis) Free T3 sometimes increased radioactive iodine uptake |
|
|
what is the triad of graves disease?
|
hyperthyroidism due to hyperfunctional diffuse enlarged thryoid
infiltrative opthalmopathy with resulting exopthalmos infiltrative localized dermopathy-pretibial myxedema |
|
|
what is the difference btw exopthalmos and normal hyperthyroidism effects?
|
normal is just wide staring gaze and lid lag but in exopthalmos eyes are bulging out.
|
|
|
what is pretibial myxedema?
|
thickening of skin on anterior shins
|
|
|
what type of condition is graves disease?
|
autoimmune
|
|
|
what is the pathology behind graves disease?
|
autoantibodies to TSH receptors
they bind and stimulate |
|
|
who are the most likely people to get graves disease/
|
20-40yo women
|
|
|
what are some genes associated with graves disease?
|
PTPN22, CTLA-4, HLA-DR3
|
|
|
what is graves disease often associated with?
|
other autoimmune diseasese
such as lupus, type I DM, pernicious anmeia, Addisons disease |
|
|
what are the 4 causes of exopthalma in graves disease?
|
T cell infiltration of retro orbital space
inflammaroty edema/swellling of muscles extracellulary matrix compenets accumulate in space increased adipocytes in area all these things work together to increase pressure and take up space behind eye pushing it out |
|
|
what is gross and micro finding in graves disease?
|
gross-diffusely enlarged thyroid
histo-hypertrophy and hyperplasia of follicular epithelial cells crowding of colmnar follicular cells into irregular papillary folds decresed colloid due to excess size of follicle cells hyperplastic lymphoid tissue |
|
|
what is TSH level be in graves disease?
|
low
|
|
|
what are the causes of primary hypothyroidism?
|
intrinsic problem of thryoid
goitrous: Hashimotos, dietary iodine def, inborn errors of metabilism, medications small thryoid-surgury, radiation, infiltrative disroder, genetic |
|
|
what is the most common autoimmune cause of hypothyroidism?
|
Hashimotos
|
|
|
what is secondary hypothyroid?
|
probelm of pituitary, TSH defcit
|
|
|
what is Tertiary hypothyroid?
|
problem with hypothalmus, TRH deficiency
very rare |
|
|
what is TSH level in primary vs secondary hypothyroid?
|
primary-high
secondary-low |
|
|
what is cretinism?
|
hypothryoidism which develops during infancy or early childhood
|
|
|
what is the most common cuases of cretinism?
|
mainly caused by lack of dietary iodine
some cases result from inborn errors of metabolism or congenital developmental failure of the thryoid |
|
|
what are signs of cretinism?
|
impaired develpment of skeletal sytem and CNS
severe MR short coarse facial features wide set eyes large proturding tongue umbillical hernia |
|
|
what is Myxedema?
|
generalized hypothyroid state in the older child or adult
|
|
|
what are the signs of myxedema?
|
progressive over time slowing of mental an physcial activity
fatigue, cold intolerance, apathy periobital edema(NO EXOPTHALMIA) coarsening of skin/facial features cardiomegaly, pericardial effusion, fine hair/hair loss accumulation of MPS rich ground substanc with dermis of all tissue(specifically the myxedema) |
|
|
what is the difference btw mxyedema and pretibial myxedema
|
myxedema is due to hypothyroid and is generalized
pretibial edema is in graves disease and is only in the pretibial region. |
|
|
what is thyroiditis?
|
inflammation of the thyroid gland
|
|
|
what are signs of acute thyroiditis?
|
fever chills, pain in neck, malaise
caused by several differnt organisms |
|
|
what is hashimotos thyroiditis?
|
autoimmune disorder
that causes inflammation of the thyroid |
|
|
who gets hashimotos?
|
women 45-60
|
|
|
what is the most common cause of hypothyroidism in areas of sufficient dietary iodine?
|
hashimotos
|
|
|
is there a genetic compenent to hasimotos?
|
yes it clusters in families
|
|
|
what are the three pathways that can occur to bring on hashimotos?
|
T-cell mediated cytotox
CD4 cell activation of macophages causing damage anti-thyroid antibodies form that lead to antibody dependent cell mediated cytotox. |
|
|
what is gross appearance of hashimotos thyroid?
|
usually enlarged vaguely nodular, but pale
can be small if its the atrophic varient |
|
|
what is the histo look of hashimotso?
|
exuberant infiltrate of lymphocytes, plamsa cells, and macrophages with germinal center formation
HURTHLE CELLS/oncocytes- follicular cells with ample eosinophilc(pink) cytoplasm(pink and puffy) |
|
|
what is the clinical coarse of hashiomotos?
|
initial transient hyperthyroid with gradual deelopment of hypothyroid
painless enlargement of gland chronic will eventually lead to atrophy and gland fibrosis and shrinking |
|
|
what lab values do you expect in hashimotos?
|
suppression of TSH, decreased radioactive iodine uptake, elevated free T4,T3 seen in the begining during a transient thyrotoxicosis
expeceted that after that passes you will see T4 adn T3 levels fall with compensatory elevation in TSH. |
|
|
what is associated with hashimotos?
|
increased risk of autoimmune disorders
SLIGHTLY INCREASED RISK OF LYMPHOMA in thyroid |
|
|
what is subacute (granulomatous) thyroididis?
|
aka quervain thyroiditi
viral or postviral eiology |
|
|
what is the expected history of pt with subacute thyroiditis
|
history of URI, coxsuki, mumps, measles, adenovirus
|
|
|
what gene is associated with subacute granulomatous thryoiditis?
|
HLA-B35
|
|
|
what is the the gross picture of subacute granulomatosu thryditis
|
variable enlargment of gland irregular or symmetric
|
|
|
what is the histo picutre of subacute granumoatous thyroiditis?
|
neutrophilic infiltrat in early stages
lymphocytes, plamsa cells, macrophages in later stages MULTINUCLEATE GIANT CELLS surround pools of colloid |
|
|
what is clinical presentation of subacute granulomatous thyroididtis?
|
sudden or gradual presentaion
neck pain sometime radiating to jaw, throat, ears espeaically with swallowing fever, fatigue, malaise, anorexia, myalgia transient hyperthryoidism follwed by asymptomatic transient hypothyroidism complete recovery by itself |
|
|
what is the cause of subacute lymphocytic thryoiditis?
|
etiology unknown
|
|
|
In whom dos subacute lymphocytic thryoiditis occur?
|
post partum women
|
|
|
what is clinical coarse of subacute lymphocytic thyroditis?
|
most common is hyperthyroidism developing over 1-2 weeks and lastup to 8 weeks before subsiding
usually subclinical no symptoms noticed found on routine labs. non specific lypohid infilatrate of gland |
|
|
what is prognosis for subacute lymphocytic thryoiditis?
|
1/3 go on to develop hypothryoidisim(Hashimotos)
|
|
|
what is reidels thyroiditis?
|
rare disorder of unknown etiology
extensive fibrosis of gland and surrounding structures. atrophic shrunken thyroid |
|
|
what is the pathology of reidels thryoiditis?
|
extenseiv fibrosis that pentrates capusle and extends into the contiguous structures of the neck can mimik carcinoma
causes obstuctive symptoms, hypothryoidism associated with fibrosis at other sites as well. |
|
|
what is thyroglossal duct cyst?
|
congenital midline neck mass
cyst lined by cuboidal cells with follicles in the stroma. |
|
|
what is a goiter?
|
enlargment of the thryoid gland reflects imparied synthesis of thryoid homone most commonly do to iodine deficiency
|
|
|
what are the two types of goiter?
|
diffuse nontoxic
multinodular goiter |
|
|
what is functionality of diffuse nontoxic goiter?
|
typically euthyroid problems arise from mass effects
|
|
|
what is the cause of diffuse nontoxic goiter/
|
endemic form caused by lack of iodine leads to decreased syntheiss of thryoid hormone which leads to incrase in TSH with stims folliculars celsl to hypertrophy and hyperplasia
not common anymore do to iodine salt sporadic form -femals in young adulthood ingestoin of substance that interfere with thryoid hormoen syntheiss hereditary enzymetic defect. |
|
|
what are some foods that inhibit thyroid syntheiss?
|
cabage
calliflour |
|
|
what is the cause of multinodular goiter?
|
end point of stimuation and nvolutio episodes of a simple diffuse goiter
|
|
|
what are the risks invovled in multinodular goiter/
|
some induce thyrotoxicosis ie become true hyperthyroid state
can result in hemorrhage, fibrosis, calcification, and cystic changes. |
|
|
what is the clinical presentation of multinodular goiter?
|
most are euthryoid
radioiodine uptake is uneven different activty if different regions mass effect leds to cosmetic deformity , esophageal compression, tracheal compression, SVC obstuction hemorrhage may cause pain and add to enlargment |
|
|
what is plummer syndrome?
|
ocassionally hyperfuctioning nodules may lead to hyperthyroidism in multinodular goiter.
|
|
|
what is the epidemeology of solitary nodules of the thyroid?
|
incidence of 1-10% of adults in US
incidence increases as you age 4x more common in women most are benign |
|
|
WHAT ARE THE CLINCIAL CRITERIA FOR DETERMINING WHETHER A NODULE IS NEOPLASTIC?
|
solitary nodules more likely to be neoplastic than multiple nodules
nodules in younger under 40 more likely to be neoplastic nodules in males mroe liekly to be neoplastic history of prior radiation treatment to head and neck is increased risk for neoplasi hot nodule(take up radioacive iodine) more likely benign(most cold are benign as well but most neoplasia are cold) |
|
|
what is a good way to evaluate thyroid nodules
|
fine needle aspriation
|
|
|
what are the characteristic of thyroid adenoma?
|
derived from follicular epithelium
discrete solitary painless mass most are nonfunction(if functioning called toxic adenoma and causes thyrotoxicosis very rare) most are cold nodules not usually a precursor to malignancy |
|
|
what is important in evaluation of cold nodules?
|
10% are malignatn so pathologic eval is imperative
|
|
|
what is the pathogenesis involved in Toxic adenoma?
|
causes thyrotoxicosis
pathgenesis related to mutaion resulting in constitutive cAMP activation |
|
|
what are the histo characters of thyroid adenoma?
|
well defined fibrous capusule
may contain the hurthle cells(pink and swollen) that are found in hashimotos uniform appearing follciles with colloid, much more compressed look than normal tissue |
|
|
how do you differentiate thyroid adenoma from carcninoma?
|
integretiy of the capsule distinguishes adenoma from carcinoma ***********
|
|
|
what are the risk factors for thyroid carcinomas?
|
adult female
prio ionizing radiation especially in the first 2 decades of life |
|
|
what are the thyroid carincoma?
|
papillary
follicular medullary anaplastic |
|
|
what is the most common thyroid carcinoma?
|
papillary
|
|
|
what is the big risk factor for papillary carcinoma
|
prior radiation expose is a big factor here
|
|
|
what is papillary carcinoma metastatic risk?
|
very likely 50% of patient have regional node invovlement at time of diagnosis
high propensity for lymphnodes. |
|
|
what is the prognosis in papillary carcininoma?
|
95% survival rate at 10 years
only bad prog is age over 40 with distant mets . |
|
|
how does papillary carcinoma present?
|
usually asymptomatic single nodules often present due to mass in a node.
|
|
|
what are the genetic of papillary carcinoma?
|
mutation in genes encoding fro tyrosine receptors(RET/PTC, NTRK1) or activating mutation in BRAF
|
|
|
how is papillary carcinoma diagnosed?
|
papilary architechture often present but not always
DIAGNOSIS MADE BY NUCLEAR FEATURES empty nuclei devoid of nucleoli=orphan annie eyes nuclear grooves intranuclear inclusions psammoma bodies |
|
|
what is the second most common type of thyroid carcinoma?
|
follicular carcinoma
|
|
|
what is a predisposing factor for follicular carcinoma?
|
multinodular goiter
|
|
|
what is the metastatic risk of follicular carcinoma?
|
vasular invasion with hematogenous spread to bone, lungs and liver is most common.
80% present with widely invasive folicuar CA that develop mets. |
|
|
what is prognosis in follicualr carcinoma?
|
depends on exten of invasino at presentatino but with widly invasive ca and mets 50% 10 year survival.
minimally invasive has up to 90% 10 year survivial |
|
|
what is the medullary carcinoma?
|
derived from parafollicular cells- Ccells
neuroendorcine tumor secretes calcitonin |
|
|
what is presentation of meduallry carcinoma?
|
mass associated dysphagia, hoarsness, cough, rarely manifestion related to a secretiory product.
|
|
|
what are the types of medullary carcinoma?
|
sporadic(80%)
MEN II type A and B FMTC-familial. |
|
|
what gene is associated with all variation of medullary carcinoma?
|
RET proto oncogene
|
|
|
what is the prognosis of the different tyeps of medullary carcnina?
|
FMTC fairly indolent, MEN II A lesions intermediate, MEN II B lesions aggressive with high likley hood of hematogenous spread.
|
|
|
what is the distinguishing hist feature of medullary carcinoma?
|
presence of amyloid deposits in stroma
|
|
|
what are characters of anaplastic carcinoma?
|
very rare
EXTREMELY AGGRESSIVE mortality rate of nearly 100% affects mean age of 65 associated with multinodular goiter also associate with history of other thyroid tumors rapidly enlarging buliky mass in neck locally invasino and mets common at presentation mass effect causes dyspnea, dysphagia, hoarsness, and cough. |
|
|
what is histo appearance of anaplastic carcinoma?
|
highly pleomorphic tumro with giant cells, spindle cells, mixed or small cells. mitotic figures
|
|
|
what are the parathyroid gland derived from?
|
3rd and 4th pouches along with thymus
|
