Tri-7 Sunday - Thyroid Talk

holding at Wk12, Day 444

I'm not sure how to count these last couple days. The powers that be decided it would be a good idea to hold our Monday classes on a Saturday - I'm not sure who thinks of these things but it's not like our weekends are free - Clinic is open from 9 to 12 and post graduate classes for both Acupuncture and the Internal Health Specialist (IHS) programs were also held this weekend. The IHS program has been fantastic and I'd love to go over some of the stuff learned in this blog but I have to keep my gears and direction shifted into the Thyroid ....

Amazingly complex at this level but, I'm going to try and hit just the high points in this blog. This may not be the most readable blog but I'll be sharing this info w/ a classmate (that's what I have in mind anyway) also kind of a way to take notes

page 1699 -

T4 is 100ugm - T3 is 5umg / day

T4 is 90% of what's secreted by the thyroid - ppt

T3 is 8x more powerful than T4 per book

T3 is 4x more powerful than T4 per Dr Sanders ppt ...

80% of T3 comes from T4

T3 burns brighter and dies faster - (shorter half life)

3 types of deiodinase convert T4 to T3

Type 1 is found in the liver and kidneys

Type 2 is present in the pituitary gland and brain - can you say pi-TWO-itary?

Type 3 is present in the glial cells of the CNS

TBG - Thyroxine-binding globulin is synthesized by the liver and functions as the main trasport protein for thyroid hormones.

Thyroid Hormone Action

thyroid hormone binds receptors that are members of the nuclear receptor superfamily, regulating expressioni of thyroid hormone-responsive genes.

Isoforms of the thyroid hormone receptors (alpha1, beta1 and beta2) bind to a specific hexameric oligonucleotide sequence in the transcrptional regulatory regionof the thyroid hormone-responsive genes.

Thyroid hormone increases oxygen consumption, thermogenesis and expression of the low-density lipoprotein (LDL) receptor, resulting in accelerated LDL cholesterol degradation.

In myocardium, T3, increases myocyte contractility and relaxation by altering myosin heavy chain and sarcoplasmic reticulum adenosine triphosphatease (ATPase).

In cardiac conducting system, T3, increases the heart rate by altering sinoatrial node depolarization and repolarization.

Other physiologic effects of thyroid hormone include increased mental alertness, ventilatory drive, gastrointestinal motility and bone turnover -

from ppt - increases # of mitochondria within target cells and increases rate of intestinal glucose absorption

page 1699

DIAGNOSIS -

Physical Examination -

inspection of lower anterior portion of the neck to check for diffuse or asymmetrical gland enlargement, tracheal deviation, lymphadenopathy and jubular venous distention.

Laboratory Findings -

log linear neagative relationships btw levels of T4+T3 and TSH makes it a sensitive indicator of primary thyroid gland dysfunction.

ppt - GD is no longer thought of as an idiopathic disease but rather as an autoimmune disorder in which B lymphocytes produce immunoglobulins, some of which bind to and activate the TSH receptor, stimulating excess thyroid growth and hormone secretion.

Cecil goes with hyperthyroidism, ophthalmopathy and dermopathy

m/c onset for Graves is with women btw ages of 30-60

Pathobiology of Graves

The proximate cause of hyperthyroidism is production of thyroid stimulating immunoglobulins that bind to and activate the TSH receptors, promoting thyroid hormone secretion and growth of the thyroid gland.

Other thyroid autoantibodies also commonly identified in the setting of Graves dz include antithyroid peroxidase antibodies, antithyroglobulin antibodies and anti-TSH receptor antibodies that block TSH binding.

The fundamental pathogenesis of Graves dz remains unknown. A genetic predsposition is implicated by a higher incidence in monozygotic twins and first degree relatives of affected individuals.

Environmental factors implicated in triggering the onset of Graves dz include exposure to cigarette smoke, high dietary iodine intake, stressful life events and certain antecedent infections.

Clinical Manifestations

Affected individuals usually present with thyrotoxicosis and a thyroid gland that is diffusely enlarged with a rubbery consistency, smooth contour, definable pyramidal lobe and audible bruit or palpable thrill due to increased blood flow.

When it is clinically evident, thyroid eye disease usually presents within a few months of the onset of jyperthyroidism. In rare cases, it may develop long before, long after or without any biochemical confirmation of hhyperthyroidism.

Prognosis -

The hyperthyroidism associated withthis condition often follows a persistent and progressive course but approximately 1/4th of pts w/ Graves dz demonstrate spontaneous dz remission.

TSI - Thyroid Stimulating Immunoglobulins - THS receptor binding antibodies

Other antibodies occur in Graves and other autoimmune dz such as Hashimoto's dz. These antibodies bind to the TSH receptor but stimulate only thyroid growth without increasing thyroid hormone secretion.

GD - occur in 1.7 to 1.9% of females and 0.2 to 0.3% of males

Peak incidence of onset is 30 to 40 years old w/ strong familial component.

I've had enough thyroid for one night ....heading to the gym :)