Thyroid Disorders Flashcards
Thyroid anatomy
the thyroid gland has two wings with an isthumus in the middle at the level just below the cricoid cartilage
the recurrent laryngeal nerve (a bracnh of vagus X) sits behind, and should be noted to avoid hoarseness as a resut if cut
Thyroid physiology
relationship to anterior pituitary
Thyroid Hormones include
TSH
T3
T4
and other imporant aspects
Thyroglobulin = a binding protein fro the T3 and T4 hormones (as they cannoy exist in the serum/circulation along or they would be readily degraded)
iodine is uptaken into thetyroid through the coupling action of the NA/I symporter
Iodine + thyroglobuin = MIT or DIT
MIT and DIT combined together (through the action of thyroxine peroxidase) creates T3
DIT and DIT together (through TPO) create T4
follicular cells - outside
colloid = fluid within the middle
T3 is the active form, T4 is not the active form, it is converted to T3
thus, T4 is more readily avalible in larger concentration in serum and made in larger amounts by thryoid – which is why we test for it
Anterior Pituitary
- produces TSH which stimulates the thyroid to product T3 and T4
- pituitary is stimulated by TRH from they hypothamlus
Thyroid Hormone levels and bindnig proteins
only a SMALL amount of free T3 and T4 are within the circulation (medabolically active)
otherwise, theyre bound to the following proteins
- Thyroxine binding globuin = 70% of the hormones are bound to this
- albumin
- transthyretin
- cahgnes in these serum protein levels can significantly impact the level of total T4 and total T3 – thus we dont like to check these
Role of Iodine and Thyroid
too much? not enough?
meds which can impact?
Iodine: majority is uptaken by the thyroid
but Excess iodine actually shuts down the thyroid hormone production
excess iodine = shut down = wolf-chaikoff effect
in this condition — if exacerbated in dividausl with underlying thyroid conditions can lead further to issues
Jod-Basedow Effect = hyperthyroidism with multi-nodular goiter, Graves (predisposed to hyperthyroid after this effect)
Wolf-Chaikoff Effect = hyothyroidism with hashimotos thyroiditis
amioderone and lithum also can induce hyper or hypothyroidism
Thyroid Labs
- TSH
- Total T4
- Total T3
- FT4
- FT3
- rT3
- TPO ab
- thyroglobuin ab
- TSHr ab
- TSI
TSH = lab test of choice for the first look at thyroid function
Total T4 = the amount of bound T4
Total T3 = the amount of bound T3
FT4 = free T4 (measure this)
FT3 = free T3 (measure this)
rT3 = reflex T3 (the inactive T3) rarely looked at
Antibodies
- TPO: hashimotos thyroiditis will have this antibody (anti-thyroxine peroxidase)
- TSI: Grave’s disease will have this thyroid STIULATING immunglobin
- Thyroglobulin ab (not crazy specifcic)
- TSHr ab (rarely checked)
Explain the Patho behind
- pirmary hypothyroid
- primary hyperthyroid
- secondary hypothyroid
- secondary hyperthyroid
Primary HypOthyroid
- LOW levels of T3 and T4
- HIGH levels of TSH
- they thyroid gland is the issue = primary
- the pituitary is trying to tell the thyroid to increase its production becuase its getting feedback that there isnt enough T3 and T4
Primary HyPERthyroid
- HIGH levels of T3 and T4
- LOW levels of TSH
- pirmary = thyroid issue
- thyroid is pumping out T3 and T4, whihc is signalling to the pituitary to turn off the TSH (low) but the thyroid isnt listening
Secondary HYPOthyroidism
- LOW T3 and T4
- LOW TSH
- secondary = pituitary issue
- even with low T3 and T4 trying to tell the pituitary to increase TSH to increase production, the TSH remains low
secondary HYPERthyroidism
- HIGH T3 T4
- HIGH TSH
- evern with T3 and T4 levels high, trying to tell pituitary to turn off the signal by decreasing TSH, it wont becuase hte pituitray is the issue
Hypothyroid
- what is it
- 3 classifications
- severe leads to
HypOthyroid = low amounts of thyroid hormones (T3/T4)
- this leads to a decrease in metabolic activites and processes within the body
in its most severe form it can lead to a myxedema coma
3 Classifications
Primary Hypothyroid
- an issue of the tyroid gland itself
- most commony primary hypothyroid disorder cause is Hasimotos thyroiditis (an autoimmune destruction of the thyroid)
- can be iatrogenic in cause: (from hyperthyroid treatment)
- Subacute hypothyroid: a high TSH but normal T3/T4 (not low yet)
- medications!!: Amioderone and Lithium (or anti-hyerthyroid meds)
- congenitial reasons
Secondary Hypothyroid
- a resut of the pituitary issue: a pituitary adenoma causing a decrease in the TSH produced, therefore a decrease in T3/T4
- or can be a result of pituitary ablation
Signs and Symptoms of Hypothyroidism
Symptoms
- fatigue
- cold intolerance
- weight gain
- constipation
- muslce cramping
- xeroderma
- lethargy
- menorrhagia
Signs
- thyromegaly (at first; autoimmune attack inflammation) leading to atrophy eventually
- bradycardia
- low voltage EKG
- increased cholesterol (because slow metabolism)
- hypercapnia, hypoxia
- constipation, decreased BS
- neurologic: HUNG reflexes: ones that are rapdi but SLOW recovery of the relaxation phase
How is Hypothyroidism Diagnosed
get TSH first
- if the TSH is abnormal = then get FT4 (not FT3)
- if the TSH is elevated = get antibodies to decided if there is Hasimoto’s
- TPO ab and Thyroglobuilin ab (these are not NEEDEd to make the dx. if they have other signs, but can help helpful)
High TSH, Low FT4 = overt hypothyroidism
High TSH, normal FT4 = subclinical hypothyroidism
Hypothyroidism: Hashimoto’s Thyroiditis
- population you will see with it
- history of what
HashimOto’s Thyroiditis (chronic lymphocytic throiditis)
- an autoimmune condition in which the body attackes the thyroid (specifically the TPO or thyroglobuin proteins) leading to low levels of thyroid hormones
- BY FAR most common cause of hypothyroidism
- common in older women
- can see a goiter, but not always
- if family history of it, or other auto-immune disease, or personal history of auto-immune diseases have high suspicion
- possible link to iodide deficiency in diet
- antibody testing = not necessary to make dx. (if have symptoms and labs)
- US not needed either: may falsely look like nodules beacuse the antibodies are breaking down different parts of the thyroid leaving some ares to look like nodes
those with hashimoto’s may develop post-partum dx. because their auto-immune ability increased post-partum
Subclinical Hypothyroidism
what is it
when do you treat
who do you NEVER treat
Subclincal hypothyroid = early hashiomtos (usually this) or early development of hypothyroid
on labs..
- elevated TSH
- but normal T3 T4 (not low yet)
Treat Subclinical when…
- they have symptoms
- they have a large goiter
- they have high cholesterol as a result
- TSH >10
- pregnant pt.
DO NOT TREAT
- eldely (risk of the med causing tachyarrythmias) & those with CAD (tachyarrythmia risk in med)
how does Amioarone, Lithium and hypothyroidism relate
how do you treat the issue
Amioderone and Lithuim can induce hypothyroidism (suprress thyroid function through different mechanisims)
- remove the offending agent (the drug, but check with other provider who rx. it)
- if it canny be removed (like amioderone) you need to treat them for hypothyroid and monitor thier labs closely!
What is Endemic Goiter
What is Congenital Hypothyroidism
most common cause of goiter worldwide is an iodine deficiency = but thats never the case in the US
Iodine Deficiency
- causes a goiter
- but you have have the goiter, check labs and have either a normal functioning thyroid, hypothyroid or hyper (maybe)
- check for deficiency with a urine iodine test
- and treat with iodized salt
Congential Hypothyroidism
- due to an embryologic defect in thyroid development
- can cause intellectual disabilities
- treat the overt hypothyroid and the subclinical ( if it is persistent)
Myxedema Coma
etiology
symptoms
labs
imaging
treatment
Etiology
- a severe form of long-standing hypothyroidism
- can occur as an acute event in someone who is poorly controlled (acute event = sepsis, infection, surgery, etc.) triggering this unregualted severe form og hypothyroid
Symptoms
- AMS, obtunded, lethargy
- mania
- hypothermia
- hypoventilation
- bradycardia
- NON-PITTING EDEMA of hands and face
- thickend nose
- swollen ips
- enlarged tongue
Labs
- could see hypoglycemia
- TSH = very high
- T4 = VERY LOW
- cortisol = could be variable to normal
Imagins
- pericardial effusion
- low voltage EKG
Treatmnet
- IV levothyroxine (T4) + Triiodothyronine = swap to PO when thhey can tolerate it
- hydrocortisone IV
- supportive care (rewarm, give fluids/pressors, treat any acute infections)
Treatment of Hypothyroidism
First-Line = Levothyroxine (a synthetic form of T4 to replete deficiency and allow body to convert it to active T3)
- if they skip a dose; this drug lingers (so they can just double the next)
Liothyronine (Armour Thyroid)
- studies indicate this shouls not be used: except in specific populations
- this is a T3 =thuse rapid onset = palpatations/anxiety
- aurmor = pig/cow thyroid hormones (variable and unpredictable)
Side Effects of these Meds
- accidental “overdose” into hyperthyroid ranges
- afib possible
- osteoporosis
(subclinical if treating = start with low dose, otherwise everone else is weight base dosing)
Patient Monitoring of Hypothyroid
- what labs
- how often to get them
- goals
labs
- TSH should be used to monitor
- FT4 only rarely
- NEVER FT3
frequency
- check 6-8 weeks
- pregnant women: should have repeat TSG, FT4 monthly
goals
- ideally: get the TSH to be about 2.0
- in pregnancy: also around 2
- in thyroid cancer pts. : want to keep TSH < 0.01 for the first year (to ensure reccurrance doesnt happen) ; then can let it go 0.1-0.5
Hyperthyroidism
- what is it
- 3 classifications
Hyperthyroidism : increase in the thyroid hormones (T3/T4) leading to hyper-metabolism
usually, hyperthyroid symptoms come and go in a phase-like pattern
3 Classifications
Primary Hyperthyroidism (meaning the problem is at the level of the thyroid)
- majority of primary is Grave’s Disease : autoimmune condition
- can be drug induced (amioderone, lithium , contrast)
- subactue presentation
- toxic multinodular goiter
- toxic adenoma
- “silent” thyroiditis
- post-partum thyroiditis
Secondary Hyperthyroidism
- a TSH-secreting adenoma
Additional Class
- facticious hyperthyroidism
- struma ovarii
- hydatidid form mole
Hyperthyroidism Signs and Symptoms
Symptoms
- weigh loss
- heat intolerance (sweating)
- proximal muslce weakness
- fatigue
- anxiety
- chest palpaitations
- oligomenorrhea
- diarrhea
Signs
- exopthalmos
- thyromegaly
- thyroid bruits
- thyroid nodules
- tachycardia
- arrythmias (A fib or sinus arrythmias)
- hyperactive bowel sounds
- hyperreflexia, tremor
- proximal weakness (because metabolic overdrive starts to breakdown muscles)
- warm mosit skin
- pretibial myedema (in graves)
Diagnosis of Hyperthyroidism
start by getting a TSH
TSH - LOW (trying to stop the production of the T3/T4)
- if TSH is abnormal: then follow up by getting FT4 and FT3
- can get the antibdoies of TPO, Thyroglobuin and TSI (TSI will be + in Grave’s)
unless CONFIDENT in your dx. of Grave’s – you need to get a radioactive iodine scan (RAI) to confirm (this will show where thye thyroid is taking up more idodine leading to hyperactivie)
Reasons for an RAI Scan
- what will it distinguish between
- what meds can pt. not be on
- who cannot get one
etiology of hyperthyroid unclear? get RAI
- CANNOT BE DONE ON PREGNANT PTS. obv, its radioactive
- CANNOT BE DONE if the pt. is currently on hypertyroid meds. (methimazole, PTU) it will interfer with scan
Distinguishes between…
- Graves Disease = will show DIFFUSE uptake
- Toxic Adenoma = one LARGE area of uptake
- Toxic MNG = uptake in multiple areas
- subacute, painless, and faticious = decreased uptake diffusely
Grave’s Disease
- etiology
Etiology: an auto-immune funtion which is the most common cause of hyperthyroidism
- seen in the younger women population
- think of this if family history, or personal/family history of auto-immune diseases in general
- has a varying presentation = depending on how much hyperthyroid activity is occuring
how is it autoimmune
- body makes TSI antibodies: (thyroid stimulating immunoglobulin) which go an attach to the TSH receptors: triggering an increased production of T3/T4 in the absence of TSH triggers
can also be due to
- tobacco
- infection
- stress
- iodine exposure (exposure then triggers this)
- can be developed post-partum
most pts. have diffuse non-tender (not painful) goiter
Grave’s Disease
- physical exam findings (key ones)
- Workup
- Treatment
Two big key PE findings
Exopthalmos = eye protrusion
- periorbital edema also, eye congestion, swelling of conjuctiva
- lid retraction due to adrenergis stimulation of the upper lid
- can use hertel exopthameter to measure
- can result in vision loss, diplopia, etc.
- if present with hyperthyroid + exopthalmous = enough to go ahead and dx. and treat (without RAI)
Pre-Tibial Myxedema
- a NON-PITTING EDEMA of the LE at the shins only
- discoloration
- rare
Workup
- if etiology unclear, can always do and should do the RAI
- check TSI (can check for TPO, Thyroglobuin if concerned for hasimotos or acute thyroiditis)
- also check TSH, FT4, FT3
Treatment
- Methimazole = first line in everyone NON-pregnant
- can use BB to help with palpataions symptoms
- pregnant = PTU
- preferred treatment = RAI: ablate the thyroid to stop they hyper symptoms then treat the hypothyroid with levothyroxine
- thryectomy if needed
Radioactive Iodine Thearpy for Hyperthyroid
- why its used
- how it works
- contraindications
for definitive treatment of hyperthyroid = this is the best option
ideal for young women who wish to become pregnant in the future= treat with this, become hypothyroid & treat with levo can wait 1 year then try to become pregnant (because levo is safer than PTU which must be used if pregnant)
(RAI does not cause infertility, birth defects or cancer in life) its SAFE!
Contraindications
- those with graves ++ SeVERE exopthalmous ( the RAI might make it worse, so pre-treat with steroids to reduce swelling first)
Hyperthyroidism
Treatment (specifically Graves)
details about each med and choice
acutely, treat with thioamides and BB for symptoms
Methimazole = most commonly used
- inhibits TPO: therefore decreases amount of T3/T4 being produced
- cannot be used in pregnancy 1st trimester
- side effects: rash, agranulocytosis & pancytopenia, cholestatic jaundice
Prophylthiouricail (PTU) = can be used in pregnancy 1st trimester
- inhibits TPO and decreases T3/T4 production
- Side Effects: cholestatic jaundice, agranulocytosis, rahs, hepatoellular toxicity & vasculititis
Beta Blockers (non-selective)
- Atenolol & Propranolol
- help with the sympathetic symtpoms
- at high doses: propranalol can help block conversion of T4 to T3
Toxic Multinodular Goiter
- Etiology
- Labs
- Symptoms
- Treatment
Etiology
- a large thyroid with multiple hyperfunctioning nodules show as “hot” on a RAI scan
- classically presenting in eldery pt.
Labs
- Low TSH
- FT4 COULD be elevated or normal, T3 is usually elevated
- could present as a subclinical hyperthyroids, (wiht low TSH and high T4 and T3)
Symptoms & Signs
- simialr to hyperthyroid symptoms
- weight loss, nervousness/anxiety
- goiter with irregular texture, nodules
on RAI
- see hyperfunctionig nodules multiple
Treatment
- typically: thioamides, low dose (methimazole, PTU)
- unable to control = RAI or thyroidectomy
Toxic Adenoma
etiology
Symptoms
labs/diagnosis
treatment
Etiology
- a functionig ademona which hypersecretes FT4 and FT3
- adenoma so large that it came compress the other parts of the thhyroid - leading to underactivity there
- typically in older patients
- will NOT have opthompathy
Symptoms and SIgns
- consistent with hyperthyroidism
Labs/Diagnosis
- RAI : mutliple “hot” nodes at first with suppression of the surroudning tissue
- TSH low, FT4 MAY be normal or elevated, FT3 WILL be elevated
- these are non-cancerous nodules!!!
Treatment
- initally, thioamides can be sed but long term treatment is RAI therapy
- surgery too can be considered
Non-Toxic Multinodular Goiter
Etiology
Symptoms
Diagnosis
Treatmetn
worldwide: iodine deficiency is the number one cause of non-toxic multinodular goiter
- a result of TSH stimulation (if hypothyroid related) OR can be genetic & have normal funcitoning thyroid (familial)
- rare in teh US ( because iodoin deficiency is not an issue)
- majority of pts. are euthyroid: no hormone abnormalities: just goiter
Symptoms
- thyromegaly
- dysphagia or SOB ( if substernal)
- facial flusing (+ pepberton sign)
- dystonia
- wont have the symptoms of hypothyroid (because slow growing)
Treatment
- in those without hashimotos thyroiditis, suppression of the thyroid function is NOT recommended
- monitor with US
- if high risk nodes: biopsy them
- RAI scan to guide biopsy: high risk cold nodes not the hot ones!
- surgery if substernal into thorax
Secondary Hyperthyroidism
etiologies
ademona
Struma Ovarii
hydatidiform mole
“Hamburger” thryotoxicosis
facticious
(remember: secondary means issues are at the level of the pituitary - not the thyroid)
Adenoma: TSH-producing adenoma increases the signal to the thyroid to produce T3 and T4
Struma Ovarii: teratoma of the ovary containing thyroid tissue (need RAI full body to make dx.)
Hydatdiform Mole: elevated B HCG gives TSH like activity inducing hyperthyroidism
Hamburger: neck trim of stap muscle in beef causes hyperthyroid - FDA prohibits this
FActicious: ingesting T4 for the weight loss effects
What is Thyroid Storm
etiology
symptoms
labs
treatment
Etiology
- a rare, LIFE THERATENING cause of hyperthyroidism
- usually a result of untreated hyperthyroidism
- often: precipitated by a cause: illness, infection, surgery
Symptoms
- tachycardia ( 140+)
- hypotension
- arrythmia
- cardiogenic shock
- hyperreflexia
- agitated/anxious
- psychosis
- stupor
Labs
- hyperglycemia (mild)
- hypercalcemia
- liver enzymes
- leukocytes high or low
Treament
- BB (propranolol) for symptoms
- PTU preferred (faster) and methimazole
- glucocorticoids
- iodine but only ONE HOUR after the thioamide
Subacute Thyroiditis
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- likely due to a viral infection (mumps, coxsackie, adenovirus)
- causes viral destruction of the thyroid (with recovery usually) because viral infection causes damange, leading to leakage of the T3/T4 initially (hyper) then it all leaks out and can be replenished (hypo)
Symptoms
- first: symptoms of hyperthyroidism (triggerd inflammation) & then, later: hypothyroid after its been attcked
- fever
- malaise
- tender anterior neck soreness
Diagnosis
- key: anterior neck tenderness, acute onset of symptoms
- have phases of hyperthyroid, to euthyroid, to hypothyroid back to euthyroid
- initially: TSH low, elevated T3, T4
- ESR elevated
- Thyroid antibodies will be negative: indicated its not autoimmune
- later on: TSH high, T3/T4 low/normal
- RAI: show significant decreased/no uptake because the thyroid is damange
Treament
- 90% of cases willrecover witout issues
- 10% go on to develop hypothryoidism
- pts. can have reccurence
- NSAIDS = help with inflammation
- if severe –> steroids (prednisone)
- BB for symptoms of hyperthyroid
- DO NOT GIVE THIOAMIDES: no need to block thyroid function: its damanged and needs time to recover
Pos-Partum Thyroiditis
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- a destructive auto-immune process within 6 months - 1 year post partum
- can present as ANy form of thyroid dysfunction: hypo or hyper
- majory will recover: some go on to have longer term hypothyroidism
Treament
- with mild abnromalities of thyroid = monitor, no treatmen t
- if they have Symptoms of hyper = give BB, DO NOT GIVE THIAMIDE!!!!
- if they have symptoms of hypo or the TSH > 10 = levothyroxine
Silent Thyroiditis
etiolgoy
symptoms
diagnosis
treatment
Etiology
- the start of lymphocytic infilteration = causes an acute thyroiditis picture
- differ from subacute thyroiditis = beause this is auto-immune mediated = not viral
Symptoms
- simialr to subacute thyroiditis BUT will not be tender at neck
Diagnosis
- positive thyroid antibodies
- on RAI: low or normal
Treatment
- NSAIDS (no prednilisilone)
- no thioamides
- as they progress: thye become hypothyroid and need to be treated (but not all)
- BB for they hyperthyroid symptoms (in beginning)
Infectious (suppurative) thyroiditits
Etiology
Symptoms
Diagnosis
Treatment
Etiology
- uncommon; acute bacterial infection, abscesses, bacteremia which seed into the thyroid; fistual from larynx, etc.
- MCC: fistual from piriform sinus to larynx causing this in kids
- step and staph = acute settings
- mycibacterial, funcal, pneumocysitis in chronic setting
Symptoms
- severe, acute neck pain
- fever chills
- fluctuant mass on exam
Treatment
- aspiration, darin and abx.
- admit, IV abx and OR if needed
Additional cuases of thyroiditis
- radiation
- trauma
- interferon alpha, interleukin
- amioderone/lithum
- kinase inhibitors
- check-point inhibitors in cancer treatment
Euthyroid Sick Syndrome
- etiology
- symptoms
- diagnosis
- treatment
Etiology
- a very COMMON cause of homorne abnormalities in the acute setting
- ICU, inpatients
- sepsis, schokc, Acute decomp. HF pts. can have this
- because the severe sepsis/shock cuases an inability to conver T4 into T3 in the peripheral tissue: abnormal thyroid labs
Diagnosis
- TSH can be 5-20 OR TSH can be 0.1-0.4 either end
- FT4 typically normal: can be overtly high or low
- FT3 Low !!
Treament
- if the TSH is 0.1-0.5 + normal FT4 = no treatment, follow up
- if the TSH is elevated + normal FT4 = no treatment, follow up
- TSH < 0.01 with HIGH FT4 = work up
- TSH 10 - 20 with LOW FT4 = ususally hypothyroidism and treat that
Thyroid Nodules
Etiology
best imaging
risk factors
Etiology
- lots of people have them, more common in women (4:1)
- 95% + are benign
- but need to identify the high risk ones
- best assessment is through an US»_space; CT!!!!
Risk Factors
LOW risk if…
- nodules are “hot” on RAI
- cystic looking
HIGH risk if…
- family history of thyroid CA (meduallry)
- history of head/neck radiation
- children, young adults or a man
- cold nodules on RAI
- solide or complex nodule
US findings of a Class 1 low Risk nodules
- cystic or cystic appearing
- isoechoic or spongiform looking
- very low risk of malignancy
US finding of a Class 2 Intermediate Nodules
- hypoechoic (solid-grey in color)
- oval/rounded shape
- ill-defined
- preipeheral or intranodular vascularization
- 5-10% risk of malignancy
US findings of a Class 3 HIGH risk Nodule
- hypoechoic (solid )
- spiculated or irregular margins
- microcalcifications
- central vascularization
- taller than it is wide
- extra-thyroidal growth seen
- 50-90% malignant
Workup of a Thyroid Nodule
always obtain TSH first
get a formal thyroid US
- if normal TSH + high/risk on US = biopsy
- high TSH + high risk US = probably hypothyroidism treatment and biopsy
- low TSH = RAI!!!!!!
autonomously function, toxic adenomas (making high T3/T4 with low TSH because tumor on the thyroid) have no risk of malignancy = do not biopsy!!!
Biopsy with FNA of thyroid nodules
what is it
who gets it
What is it
- a small needle passed thorugh the lesion multiple times to obtain cytology
- large core biopsy RARELY done
- used with US guidance of the nodules
Who gets one
- high risk US lesion > 1.0 cm
- intermediate risk US lesion > 2.0 cm
- low risk US lesion > 2.0 cm AND growing in size with high risk factors
- any sus. lymph nodes with thyroid nodules present
lesions 0.5-1.0 can be watch ed or biopsied depenidng on the setting and risk factors
inturpretation of teh FNA results
- benging in 55-75%!
- suspicious indetermine 10-15%
- then you get Afirma/genetic testing if you get this result
- negative afirma = < 6% risk of cancer
- positive = surgery recommended
- ## postive afirma + sus lesions = 40% risk of cancer
Thyroid Cancer
- types (4)
Papillary Cancer
- common
- a firm, cold nodule
- can have cervical nodes
- metastisis via glands near by and local LN = RARELY hematogenous
Follicular Cancer
- more aggressive than papillary, can spread local or can spread through blood to prostate, thyroid, bone, lung, kidney
Medullary Thyroid Cancer
- “C cell cancer”
- most agressive
- extends to LN and msucle, trachea too
- calcitonin= secreted from tehse tumors, so use this to follow
- 80% are sporadic
anaplastic thyroid cancer
- most aggressive, indifferentiated, rapid growht
- goiter in weeks/months
- dysphagia, dystonia
- death within 6-36 months due to invasion
- very poor prognosis
Management of Thyroid cancer
- determine if high risk or low risk
Low Risk
- under 45, lesion < 1-1.5 cm & no gland spreading
- totaly thyroidectomy
High Risk
- total thyroidectomy + neck dissection with LN involvement
- most will need to have radioactive iodine ablation
- follow them with thyroglobuin and calcitonin
thyroid replacement: shoot for TSH goald of 0.1-0.5
