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

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*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

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Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

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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

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Clinical Cases

Clinical Case

Notes:

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Clinical Case

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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

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*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

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Thyroid *Storm

THYROID STORM GOD wrecking havoc on all the people down below and how they DEFEATED HIM


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*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

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*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

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*Hashimotos Disease presntation
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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

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*Hashimotos Disease tx
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Diffuse lymphocytic infiltration of thyroid with WELL developed GERM CENTRES

  • seen in autoimmune Hashimoto HYPO thyroidism

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*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

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*Graves Disease

  • most common cause of hyperthyroidism

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*Drugs for Hyperthyroidism and synthesis of t3/t4
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*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

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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

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Propanolol in GRAVES for symptomatic treatmnt form high T3 and T4

  • t3 t4 cause high BP
    -->> BEta blockers lower BP

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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

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*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

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*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

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*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

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Clinical Cases

Clinical Case

Clinical Case

Notes:

  • note that

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*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

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*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

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Clinical Cases

Clinical Case

Clinical Case

Notes:

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*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

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*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
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TSH?

High/Normal TSH

Low TSH

*Hypothyroidism presentation
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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

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*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

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