2nd Test - Endocrine Flashcards
TSH axis
…
How is TSH axis retroalimented
mostly T4 RAN
secondary to deficiency of thyroid hormones we can have what disorders
hypo/hyperthyroidism
thyroid cx
found in anterior neck
2 lobules and one isthmo
measurements of thyroid lobules
variable by px
2-4-5cm vertical
1-1.5cm transverese and AP
pyrimidal lobule
can have a third abnormal
increased function
30%
weight of thyroid gland
10-20gr
80gr at hypertrophy
irrigation of thyroid
superior and inferior thyroid artries directly from carotid
some have ima artery = accesory
not all px will have it (not pathological not to have)
inferior is from the subclavian
super medial thyroid veins –> IYV
inferior –> braquicefalia
2 cell types in thyroid
folicular (tirocitos) - structuiral functional cells of thyroid - make viscous cells that make glucoprotein tiroglobulin (cuboid in direct contact with colloid, basolateral memebrane directed with vessels)
otther cells 0.1% are parafoliculars –> produce calcitonin (minteral bone calcium metabolism) = C cells
thyroid follicle
pool of colloid surrouned by its cellsq in contact with basolateral memebrane and apical side in contact with colloid
functional unit of thyoid
monolayer of follicular cells
a million follicles per gland
colloid
viscous gell pool of thyroglobulin (glucoprotein 660kDa constitutes 75% of gland weight)
110-140 residuss of tyrosine
synthesisi of thyroid hormones
primary material = iodine (126) - absorbed from diet –> absorbed and converted to yduro in small intestine cells –> passes to circulation as inorganic yoduro –> travels through BVs to follicles
follicle traps inorganic yoduro (does its thing) = process of making thyroid hormones begins
tyrocyte: = follicular cell
1. IY has to enter BL (contact with BVs) membrane; FC traps it with NIS tranporter (sodium) (active transport) w/ Na+ - enter cell (synporter) (energy provided from ATPase K+, Na)
- inorganic yoduro in cell now - first step finally = OXIDATION
TPO enzyme, (with H202)
inorganic yoduro residues are converted to reactive iodine species (free radicals, iodinion ion, hypoyodito) - we think they are this, but not sure - ORGANIFICATION= 2nd step - union of 1 or 2 reactive yodantes with tyrosine residues
at apical membrane have Pendrin transporters which allow reactive yodant species to pass to colloid
1 tyrosine residue with 1 Reactive species = monoyodo
2 + 1 = diyodo
- ACOPLAMINETO = union of 1,2 or more molecules to form a bigger molecule
monoyodo + diyodo = T3
diyodo + diyodo = T4
now we have preformed thyroid hormones ready to be sent to circulation back thru follicular cell
lisosomes liberate proteolytic enzymes and proteosomes and decrade colloid droplet??
T3 and T4 are free in cell
(iodotyrosines…
attacked by dehalogenated, T4 can become T3 - run away from degradation
some free ydod that was dehalogenated renters cycle to get oxidaized again (recycable)
TSH union allows liberation of T3 T4 to BVs
2 steps of thyroid synthesis that occur in colloid
ORGANIFICAITON
ACOPLAMIENTO
Desyodasas
works in specific points
type I @ liver, kidney, muscle, thyroid –> desyodoacion of T4 to T3 in ciruclation of these organs
type II @ hyporthalamus and hypofisis
type III @ skin, brain, placenta
TSH functions
stiulate synthesis and all phases of metabolism of iodine and tyroid hormone synthesis
increase mRNA of tyorglobulin and tyroid peroxidase
increase 5’desyodasa type I activity
stimulationes glucose captation, oxygen consumption, CO2 production
stimulates: atrapment of iodione by folil cells TPO oxidation yodacion of tyrosine residues acomplamietno synthesis of TPO and troglobulin liberation of hormones and growth and bascularity of tyroid
Autoregulation
@ low iodine ingest
(low materia prima)
the gland will autoregulate and increase T3 (5’ desodasa I abailality increases) to avoid hypothyroidism
@ too much ingestion
blocks NIS
Wolf-Chaikoff block
less thyroid hormone synthesis
activity of T3 vs T4
T3 is 10x more active than T4
thyroid hormone metabolism
tyroid produces 80-90mcg of T4 per day and 3-6mcg of t3
most at expense of T4
tyroids make rT3 in 10% (desyodosa III @ T4)
T3 only made in 10%
the rest 90% T4 - from 5’DI..
T4 metabolic routes
20% conjuagetd in liver or deamidases a TETRAC or excreted thru urine and feces
35% converted to T3 thru 5’DII
45% converted to rT3
T3 metabolic routes
at liver in TRIAC
peripheral bockers of T4 T3 conversion
meds ( ptu, BB, contrast, glucocorticoides)
acute disease (qx, IAM)
chronic diseases
caloric malnutrion (IR, IH,)
selenium deficiency
burns
qx
hormonal circulation of T4
99.97% unite with proteins
75% to TBG
20% TBPA
5% to albumin
how much T4 free in circulation
0.03% - is the one that exerts most actiion
this is the one measuresd
half life of T4
7-8d