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
