Endocrine - Thyroid gland
*Thyroiditis Differentials:
HYPO - THYROIDISM in adults --> 2 groups
--> Inflammatory Granuloma formatiion enlarged thyroid
--> Autoimmune Hashimoto enlarged thyroid
- Thyroiditis type 1 = Inflammatory Granuloma formatiion enlarged thyroid
--> presents as PAINFUL enlarged thyroid
--> POST VIRAL thyroiditis
--> HYPER thyroid dominant symptoms dominate at first
--> HYPO thyroid dominant symptoms dominate second - Thyroiditis type 2 = Autoimmune Hashimoto enlarged thyroid
--> PAINLESS enlarged thyroid
--> NO illness or preceding event
--> HYPO thyroid dominant symptoms
HYPER - THYROIDISM in adults --> 2 groups
HYPOTHYROIDISM in adults --> 2 groups
- Thyroiditis type 1 = Inflammatory Granuloma formatiion enlarged thyroid
--> presents as PAINFUL enlarged thyroid
--> POST VIRAL thyroiditis
--> HYPER thyroid dominant symptoms dominate at first
--> HYPO thyroid dominant symptoms dominate second - Thyroiditis type 2 = Autoimmune GRAVES disease enlarged thyroid
*HYPO thyroidism
*Riedel Fibrosing Thyroiditis
- Riedell Canal is HARD ice, painless when you fall though
- this is the differential for young people P/C with very hard thyroiditis that is non painful (benign)
--> in elderly though this exact same presentation is usually poorly diffferentiated thyroid CA
Congenital = cretinism hypothyroidism
- seen in kids once their maternal T4 levels are gone
--> and they can't produce their own - Congenital hypothyroidism = HYPROthyroidism
- protruding 6 Ps
Clinical Cases
Clinical Case
Notes:
- note that
Clinical Case
Primary vs Secondary Hypothyroidism
- primary organ = thyroid gland
--> classic low T4 high TSH - secondary hypothyroidism = Hypothal or Pituitary
--> low levels of TRH, and all other downstream hormones
Primary Hypothyroidism
- primary organ = thyroid gland
- classic low T4 high TSH
Clinical Cases
Clinical Case
Notes:
- note that
Clinical Case
Secondary = CENTRAL Hypothyroidism
- secondary hypothyroidism = Hypothal or Pituitary
--> low levels of both t4 and TRH
--> also all other downstream hormones - main other hormones affected = ACTH
--> this is key and can give alopecia since ACTH is a derivative of POMC that effects melanocytes - also low levels of sex hormones like DHEA from the ant pit can give
--> alopecia = hair loss
*Hashimoto HYPO thyroidism:
- Thyroiditis type 2 = Autoimmune Hashimoto
--> enlarged thyroid
--> PAINLESS enlarged thyroid
--> NO illness or preceding event
--> HYPO thyroid dominant symptoms
*Inflammatory Granuloma POST VIRAL thyroidism:
- POST VIRAL Thyroiditis = Inflammatory Granuloma formatiion enlarged thyroid
--> presents as PAINFUL enlarged thyroid
--> following a Viral illness
--> HYPER thyroid dominant symptoms
Thyroid *Storm
THYROID STORM GOD wrecking havoc on all the people down below and how they DEFEATED HIM
-
*Anatomy of Thyroid
- arteries and nerves to the thyroid gland
- recurrent laryngeal loop around and enter the thyroid area from below
--> it then goes into the thyroid and arytenoid cartilage to supply all the laryngeal muscles of the vocal cords etc.
*Blood vessels and nerve of the Thyroid
- arteries and nerves to the thyroid gland
- recurrent laryngeal loop around and enter the thyroid area from below
--> it then goes into the thyroid and arytenoid cartilage to supply all the laryngeal muscles of the vocal cords etc.
--> note ONLY the cricothyroid is supplied by the ? - inferior thyroid artery runs right by the recurrent laryngeal
*T3 and T4 - Thyroid Hormones production
- thyroglobulin is a protein that gathers BOTH iodine and tyrosine
--> binds tyrosine to iodine
--> makes both DIT = diiodotyrosine + MIT = monoiodotyrosine - T3 = MIT + DIT
- T4 = DIT + DIT
*Hashimotos Disease presntation
-
HASH TAG MOTO with THIGHS THIGH DROID is battling the other THIGH DROIDs in the MOTO ARENA
other THIGH DROIDS in the battle are
- ANTI TPO THIGH DROID who uses H2O2 GUNS to kill the other THIGH DROIDS
- then there is ANTI THIGH DROID GOBLIN who is a sneaky GOBLIN driver
in the STANDS watching the HASHTAG MOTO THIGH DROIDS battle are the NUNTENDER LARGE THYROID NUN
- NUNTENDER LARGE THYROID NUN is crazy and loves watching HASH TAG MOTO THIGH DROIDS battle each other
- NUNTENDER LARGE THYROID NUN sits on her NUN HODGE KING with LIME FOAM
--> increase NUN HODGE KING LIME FOAM cancer in HASTAG MOTO - NUNTENDER LARGE THYROID NUN is also HIGH FIVING a HULA HOOPING HIGH 5 DR
--> HLA DR5 in HASH TAG MOTO
*Hashimotos Disease tx
-
Diffuse lymphocytic infiltration of thyroid with WELL developed GERM CENTRES
- seen in autoimmune Hashimoto HYPO thyroidism
*Hypercholesteremia in HYPOthyroid
- there is a decrease in LDL receptors in HYPOthyroid
- think in HYPO thyroid everything gets BIGGER, SLOWER, and KEPT IN the body
--> weight gain
--> constipation
--> tired and fatigued - the 2 exceptions though are:
--> menorrhagia in women (blood leaves the body)
--> get lower LDL receptors leading to HYPERcholesterol
*HYPER thyroidism
- there is an increase in LDL receptors in HYPER thyroid
- think in HYPER thyroid everything gets SKINNIER, FASTER, and LEAVES the body
- HYPERthyroiodism = EVERYTHING a WOMAN WANTS...
--> weight loss
--> HOT all the time
--> diarrhea
--> anxiety - the 2 exceptions though are:
--> amennorhea in women (blood leaves the body)
--> get higher LDL receptors leading to HYPOcholesterol
*Graves Disease
- most common cause of hyperthyroidism
*Drugs for Hyperthyroidism and synthesis of t3/t4
-
*thyroid Peroxidase
- does the 3 main steps of t3/t4 production
- oxidation of iodide
--> from I- to I2 - organification of I2 into Thyroglobulin
- coupling of MIT and DIT to make either
--> t3 = 1 MIT and 1 DIT
--> t4 = 2 DIT - thyroid peroxidase is blocked by thioamides =
--> propylthiouracil = PTU
*PTU = propylthiouracil
- thyroid peroxidase is blocked by thioamides =
--> propylthiouracil = PTU
Graves Disease Tx
GRAVES TREATMENT leads to a GRAVES DISEASE FRANKENSTEIN that has gotten out of HAND
- he STEPS on the TSH lab BOTTLE
- T3 and T4 FORK JUMP UP HIGH to try and escape the GRAVES DISEASE FRANKENSTEIN
RADIOACTIVE GUYS get called in to clear up the situation with GRAVES DISEASE FRANKENSTEIN
- RADIOACTIVE IODINE GUYS diagnose GRAVES FRANKENSTEIN first
--> see if he ABSORBS the IODONE they spray at him
--> he ABSORBS the RADIOACTIVE IODINE and they confirm he is a GRAVES DISEASE FRANKNSTEIN - RADIOACTIVE IODINE GUYS then KILL GRAVES FRANKENSTEIN by spraying him with RADIOACTIVE IODINE
Propanolol in GRAVES for symptomatic treatmnt form high T3 and T4
- t3 t4 cause high BP
-->> BEta blockers lower BP
Graves Disease presentation
GRAVES DISEASE FUNERAL with the young women who PAY the GRAVE DISEASE a 20 to keep CRYING while they drink their 40s at the GRAVES DISEASE FUNERAL
- CRYING with their OPTHALMO and EXTRUDING X EYES
--> opthalmopathy
--> exopthalmos- they want TISSUE and grab the GRAVE FUNERAL ANTI TSH TISSUE BOX receptor who is trying to leave the GRAVE FUNERAL
- the GRAVE FUNERAL 2 CRYING SISTERS get so DRUNK that they try and bury the THYROOIDS bet GOITRE GOAT with him ALIVE
meanwhile in the corner of the GRAVES FUNERAL there is a PRAYING TIBETAN MIXER MONK praying for the GRAVE FUNERAL HYPERTHYROID
- PRAYING TIBETAN MIXER MONK at the GRAVES DISEASE THYROID FUNERAL
--> pretibial mixodema
*Exopthalmos and pretibial myxedema
- note the exopthalmos and the pretibial myxedema are from the excess activity of fibroblasts fromt he IgG stimulating the TSH receptors there
- it is NOT from the excess Thyroid hormone
- the increase in the TSH receptors behind the eyes and in front of the shins = pretibial area
--> these increase the activity of fibroblasts
--> fibroblasts relese glycosaminoglycans
--> this is the main driving factor and causes inflammation and swelling
--> leads to BOTH exopthalmos and pretibial myxedema
*HYPO cholesteremia in HYPER thyroid
- there is an increase in LDL receptors in HYPER thyroid
- think in HYPER thyroid everything gets SKINNIER, FASTER, and LEAVES the body
--> weight loss
--> HOT all the time
--> diarrhea
--> anxiety - the 2 exceptions though are:
--> amennorhea in women (blood leaves the body)
--> get higher LDL receptors leading to HYPOcholesterol
*Exogenous Hyperthyroidism
- you must always consider exogenous hyper thyroid in patients who are anorexic or bulemic or just want to lose weight
- important to know if a close family member has thyroxine tablets that they may steal and use
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
*POMC and ACTH in hypothyroidism
- ACTH is a derivative of POMC
--> this is key and can give alopecia since ACTH is a derivative of POMC that effects melanocytes
*Levothyroxine tx for HYPO thyroid
- levothyroxine = T4 analogue
--> this is important that it is T4 and not T3
--> since T4 to t3 conversion in peripheral tissues is done by the body so it maintains the proer dose - note that levothyroxine levels are monitored by the response of TSH to it
--> so if someone has a hypothyroid and they are on levothyroxine
--> if their TSH gets way too low, this indicates that you have to lower the t3 levo dose
High Dose levothyroxine
- note that levothyroxine levels are monitored by the response of TSH to it
--> so if someone has a hypothyroid and they are on levothyroxine
--> if their TSH gets way too low, this indicates that you have to lower the t3 levo dose - puts at risk of all the hyperthyroid dangers
--> atrial fibrillation is the most common and most dangerous one
Peripheral t4 to t3 conversion
- inhibited by PTU = propylthiouracil
Clinical Cases
Clinical Case
Clinical Case
Notes:
- note that
*T4, t3 TBPs
- t4 is the main transported form of thyroid hormone
- t3 is the active form of thyroid hormone
- TBG = thyroid binding proteins
--> these make up 70% of the binding - rest is done by albumin and other proteins int he blood
*TBG = thyroid binding proteins
- these make up 70% of the binding
- rest is done by albumin and other proteins int he blood
*Estrogen increases TBG = thyroid binding proteins
- this is the reason for hyperthyroidism during pregnancy
- most women just get an increase in PBGs and
--> get a slight reduction in free t4
--> the posterior pit releases more TSH to make more t4 and t3
--> the extra t4 and t3 saturate the newly made TBPs
--> free thyroid returns to nromal = euthyroid
--> then TSH also returns to normal levels
*Investogation and Dx of Thyroid Problems
- always measure TSH levels first before t4 and t3
- small changes in T4 lead to big changes in TSH
--> thus it is a more sensitive test for BOTH hyper and hypothyroidism
*Hyperthyroidism presentation
-
TSH?
High/Normal TSH
Low TSH
*Hypothyroidism presentation
-
TSH?
High TSH
Low / Normal TSH
Primary Hypothyroidism
- high TSH
- low T4 and T3
Secondary Hypothyroidism
- Normal TSH
- low T4 and T3
--> test for
**?
High TSH
Low / Normal TSH
*Reverse T3
- note that most T4 is converted to triiodo t3 = active form
- there is also an INACTIVE for of t3 = REVERSE T3
--> this cannot be made in the thyroid
--> it can ONLY be made from t4 in the periphery