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
hormonal circulation of T3
99.7% united to proteins
75% to TBG
25% to albumin
half life T3
6-8hr
how much T3 ffree in circulation
0.3% free
@ high TBG
decreases T3-T4 (fraction) totales
increases TSH
doesnt affect free fractioend active ones
(subclinical hypothyroidsim)
congenital form, preg, neonates, drugs (ACO/estrogen/heroine) acute and chronic hepatitis hepatocel CA HIV hypothyroidism
@ low TBG
more T3 and T4 total increase
low TSH
congenital from
glucocorticoid drugs
nefrotic syndrome
enteropathy losoing proteins
cirrosis
proteic malnutrion
acromegalia
hyperthyroidism
hormonal despalcement
salicilates
acido mefanmico fenclofenac mitotane fenilbutazone fenitoin diazepam furosemide
NO AINES! (more free homrmones)
effects of T3, T4
develoment and maturation of CNS –> cretinism
increase of secretion and action of GH and IGF-1
increases gluconeogenesis and glucogenolisis of liver
increase in liver lypogenesis (cold intolerance)
increase LDL in liver
increase lypolysis in adipose tissue
increase in glucose captation
increase in contraction belocity and misuclar relaxation (myalgia)
increase O2 consumption and termogenesis (intolrance to T)\
increase eritropoyesis (anemia)
increase cardiac contractibility and beta-adrenergic rec\ (taki)
increase in intestinal motility and intestinal glucose absorption
TSH N levels
- 4-4
3. 5 is low in pregnant woman
Goiter
any icrease in thyroid galnd size DOESNT MATTER THE CAUSE
prevalence of goiter
5%/10%
types of goiter
diffuse
nodular
multinodular
nodules are afnctional
causes of goiter
iodine deficiency(TSH stimulates growth of thyroid due to deficiency causing hypertrophy of the gland)
biociogenos in diet (contain sustancias yodades - goitrina, and cglucosidos cianogenos)
drugs ( give yodo and interfere in synthesis ) beta blocker amiodarione
tyroiditis (hashimoto, de de quervain,acute)
dishormogenesis - genetic deficiency in enzymes of synthesis (complete or not)
ingest recommended of iodine
150-300ug/d
how to know of iodiene deficiencny dx
(it will cause urinary excretion < 50ug/d) = yoduria
primary cause of hyperthyrodisism
hashimoto thyroiditis
main types of dishormonogenesis
plasma thyrocyte transport
TPO deficiency
attered acoplamiento
desyodasas deficiency
excess yodoproteina
(resistance to hormones,
RT, neoplasia, fisiological) - pregnancy, lactancy , pubety increase gland size
MC of goiter
gland compression on surrounding structures - larynxtraquea
snoring, disfonia, , disnea at laying back, disfagia
pemberton sign
pemberton sign
reddened face and anterior thorax after raising arms
gland compresses vascular neck structures decreasing drainage
labs for goiter
thyroid hormones (TSH, T3, T4 free) (Ac TG, Ac TPO - autommune up in hashimotos)
images for goiter
used to do CTbut new gold standard is US
6-16cm3 = Normal range - total volume of gland
gammagram with isotopes before to a=capture contrast medium - not anymore
tx of goiter
symptomatic observation
tyroidectomy depends on size/compression
levotiroxine = NOT INDICATED ANYMORE –> hyperthyroidism
extra ocular muscles
Rectos: o Recto Medio o Lateral o Superior o Inferior Oblicuos o Superior (Inciclotorsión – abajo y afuera) o Inferior (Exciclotorsión – hacia arriba y hacia afuera) Elevador del parpado superior
origin of superior recus
Anillo de Zinn, en el ápex orbitario.
insertion of superior rectus
Superior, a 7mm del limbo corneal.
innervation of supereior rectus
Rama superior del NC III.
irrigation of superior recus
Rama muscular superior de la arteria oftálmica.
size of superior rectus
41.8mm de longitud. o Tendón: 5.8mm de longitud o Ancho: 10.6mm
functions of superior rectus
Primaria: Elevación o Secundaria: Aducción o Terciaria: Intorsión
origin of rectus medio
Anillo de Zinn (Tendón superior)
insertion of rectos medio
: Medial, 5.5mm del limbo.
innervation of rectus medio
: Rama inferior del NC III.
irrigation of rectos medio
Rama muscular inferior de la arteria oftálmica.
size of rectus medio
Longitud: 40.8mm o Tendón: 3.7mm o Ancho: 10.3mm
function of rectus meido
Aducción
neurooftalmogia in charge of what
headaches oculomotor and eyelid disorders puilar defects loss of vision secuelas of CV events secuelas of IC tumors and orbatry
fiacial paralysis
origin of inferior rectus
: Tendón inferior del anillo de Zinn.
insertion of inferior rectus
: Inferior, 6.5mm del limbo.
innervation of inferior rectus
Rama inferior del NC III.
irrigation of inferior rectus
Rama muscular inferior de la arteria oftálmica e infraorbitaria.
size of inferior rectus
Longitud: 40mm o Tendón: 5.5mm o Ancho: 9.8mm
function of inferior rectus
Primaria: Depresión o Secundaria: Aducción o Terciaria: Extorsión
origin of rectus lateral
Tendón superior del anillo de Zinn.
insertion of recto lateral
Tendón superior del anillo de Zinn.
innervation of rectus lateral
NC VI.
irrigation of rectus lateral
Arteria lacrimal
size of rectus lateral
ongitud: 40.6mm o Tendón: 8mm o Ancho: 9.2mm
function of rectus lateral
Abducción
origin of superior oblique
Superior y medial al foramen óptico, entre el anillo de Zinn y periórbita.
insertion of superior oblique
7.7mm del limbo.
innervtion of superior oblique
NC IV
trajectoru of superior oblique
Anterior a tróclea, como tendón atrás-abajo-detrás de recto superior.
irrigation of superior oblique
Rama muscular superior de arteria oftálmica.
size of superior of oblique
Longitud: 40mm o Tendón: 20mm o Ancho: 10.8mm
function of superior oblique
Primaria: Intorsión. o Secundaria: Depresor. o Terciaria: Abductor.
troclea
Polea cartilaginosa en forma de U, corresponde al cuadrante nasal superior de la órbita y está unida al musculo oblicuo superior por tejido conectivo.
incomplete vs complete III aparalysis
communic post aneurysism if midriasiss
miosis - horner
ptosis
some congenital some neurological
MS
marcus aGunn
Guillan Barre
pupillary fibers outside of III
paralysis of VI
Abd
inkid needs dilaion and fondus exam
only nerve suelto en senocavernoso
increased IC pressure in kid this is the first sign
origen of inrerior oblique
Nasal de la pared orbitaria, detrás de borde inferior orbitario y lateral a conducto nasolagrimal.
trajectory of inferior oblique
: pasa por debajo del recto inferior y recto lateral.
innervation of inferior oblique
: rama inferior del NC III.
irrigation of inferior oblique
Rama inferior de arteria oftálmica y arteria infraorbitaria
size of inferior oblique
Longitud: 37mm o Tendón: no tiene o Ancho: 9.6mm
function of inferio oblique
Primaria: extorsión. o Secundaria: elevación. o Terciaria: abducción.
IV paralisis
px depresses menton and as they look
dipolopia
=
what is strabism
Consiste en un trastorno que provoca desalineación de un ojo con respecto al otro al enfocar.
PPM
Punto primario de la mirada (PPM): la posición normal de los ojos.
kappa angle
Angulo de kappa: es el ángulo entre el eje visual y la línea pupilar central
(Entre el estímulo de luz y el grado de alteración).
what to do at a paralysis of eye - any
exam medical and neuro
TC with and without contrast
cerebral MRI
lumbar puncture
cerebral arteriograph
angiotomograph
angioresonance
other tests: BP
eoftalmotery
prueba del hielo
medicion de distancia
fptps fa,o;oar
test daccion forzada
Existen dos tipos de movimientos oculares:
Ducciones: movimientos monoculares que consisten en aducción, abducción, elevación y depresión. Versiones: Movimientos monoculares en que ambos ojos se mueven simétrica y sincrónicamente (mirada conjugada
Dentro de las versiones tenemos:
Dextroversión: mirada hacia la derecha. o Levoversión: mirada hacia la izquierda.
vVergencias
Movimientos binoculares en que ambos ojos se mueven sincrónicamente en direcciones opuestas. o Convergencia: capacidad de ambos ojos de mirar hacia adentro o Divergencia: capacidad de ambos ojos de mirar hacia afuera desde una posición de convergencia.
classifcation of strabism
Esotropia (Es lo mismo que una endotropia; si en vez de una S tuviera una X fuera para afuera)
o No parético
Infantil
Adquirido ( Acomodativo Parcialmente acomodativo o)
Parético (causado por paresia o parálisis de uno o ambos músculos extraoculares)
congenital esotropia
Aparece antes de los 6 meses de edad Asociada a hipermetropía Relacionado a nistagmos Produce alteración de la binocularidad
tx strabism? congential esotropia?
Gafas Prismas: lente especial doblado hacia el lado de la desviación. Parchado: estas obligando que el ojo bueno que esta parchado que funcione, para que el ojo que esta malo empiece a funcionar. Cirugía
consideratiosn at paraplysis of eye
pupil size
action of other craneal nerves
changing ptosis
proptosis enoftalmo
aparicion of regeeneration aberrant signs
Neuro MC
head compensatory positions
primary exoptrpy
congenital
aquired
secondary exotropy
Sindrome de Duane o Paresia de 3er nervio craneal o Anomalías craneofaciales
Carajito que tenga esotropia con limitación hacia afuera hay que hacerle
un fondo ojo, porque las hipertensiones endocraneanas en niños suelen cursar con parálisis del 6to, porque se comprime a nivel del seno cavernoso (Es más fácil encontrar una hidrocefalia por esto que por la hidrocefalia perse).
intermittent exotropy
Componente hereditaria Aparece de 1-3 años Se descompensan con fatiga o enfermedad Producen ambliopía entre el 9-13% Tratamiento de prismas Cirugía después de los 4 años
*Atropia = Todo el tiempo; *Folea = Es intermitente
A synrome
Estrabismo convergente: es el más común y se divide en parético (debida a paresia o parálisis de uno más músculos extraoculares) y no parético, que puede ser acomodativo y no acomodativo. o
Infantil: Inicia a los 6 meses.
*Foto: Estrabismo divergente intermitente. A: Con hiperacción de los oblicuos inferiores con síndrome «V». B: Con hiperacción de los oblicuos superiores con síndrome «A».
hyperthyroidism
frequent
more in women
exacerbation of MC of too much thyroid hormones
biochemical clinical syndrome with excessive exposure to thyroid hormones (secondary to increase in their synthesis)
2% women
0.5% men
thyrotoxicosos vs hypetthyroidism
thyro - MC of too much hormone INDEPENDENT of cause
hypertheyroidism is thyrotoxicosis?q
causes of hyper T
normal or elevated captation
<1% captation (elimianted)
low captation
(in gammagraphy)
normal or high captation
autoimmune diseases
hyper T from autononmia of follicular cells
mediated by TSH
mediated by HCG
<1%
thyroiditis from destruction of follicules
exogenous tirotoxicosis ( in px using levothyroxine, hamburgers with cow thyroid hormones, girls faking)
ectopic hyperthyroidism (thyroid tissue outside of gland, teratoma, esturma ovarico, intestinal??)
low captation 3-5%
amiodarone (200mg of this has approx 5mg of yodo - materia prima - increases synthesis)
medios de contraste yodados
too much iodine in diet
vaginal douches
principal autoimmune cause of hyperT
Graves-basedow
Graves-basedow cx
too much thyroid homrones in blood from too much synthesis of them
autoimmune (+ antibodies in plasma)
biopsy shows thyroid galdn full of autoimmune cells
5 classic MC of GB
diffuse bocio (can have nodules)
hypertheyroidism with MC
oftalmopathy (25-50%) - unilateral
dermatopathy ( 0.5-1% of cases) - mixedema, same as hypothyroidism
acropaquia in <1% - dedos en palillo de tambor
Hashitoxicosis
preformed follicles with hormones start to get inflammaed and get destroyed they break and liberate preformed hormones
px will have subclinical/frank hyperthyroidism
so this is a thyrotoxicosis (liberation)
px finishes in hypothyroidism thru euthyroidism
tissue then fibrosis , scar tissue that dont produce anymore horones
NO levotiroxina
wben is there autonomy of follicular cells
hyperfunciton: independent of TSH
circunscritp to one space of gland
the rest maintains hormonal production
the part that changed, memanicapted, produces regardless of TSH
7 trnasmembrane rec with 3 dominionss: Gs, GDP-GTP
changes that allow uion to adenilciclase
ATP-AMPc
PKA (is then liberated) -TSH acctions
why only this area seen as hypercaptating at hyperthyroidism - not inhibiting TSH, rest of gland seem hypofunctioning
thyroid adenoma
benign
hyperfuncitoning
depends on size (qx - cheaper, could recurr)
somatic mutation
1-5% of hyper Ts
toxic multinodular bocio
2 or more nodules
somatic mutations causing hyperfunction
5-15%
1-2 nodules cold or hypocaptating
usually qx
non autoimmune hereditary hyperthyroidis
AD
inicio
germinal mutaion
thyroidectomy needed
from neonatal life
Albright mcunne Syndrome
causes hyperfuncioning gland
hypercromic non pruriginou notn delimiated liesonform early age
mutation
Marinne Lenhart syndrome
Grave
cold nodules
25-30%
toxic adeoma
like gravies and ultinodular bocio
more than one hot or hypercaptivating
not exclusive
TSH mediated hyperthyroidism
only one iwth high TSH
tirotropoma
deficiency of desyodosasa
resistance of caction of thyroid hormones
hyperfuncitoning
tyrotoxicosis from destruction of follicles
low TSH
inflamamtion
hypocaptation
hypocaptation gammagraphy with bocio think of
throditis, ectop`c
exogenous tirotoxicosis
iatrogenic
facticia
hamburgers
ectopic hyper T
ovarian struma
mets functional ca folciular a(metastasis - cpatation at lung)
bocio lingual funcionante (captates)
hyperT induced from iodine
walff-chaikoff
altered regulation
low TSH
find cause
amiodarone thyrotoxicosis
TABLE
37.5g de yodo per pill
can cause lesino and rupture of folllicles= type II
@ inflammation no flujo nor capatation
tye pa# 1 increaesed synthsis (hy[erthyroidism) - more vascularized at sonography
MC of hyper T
excess hormones: hyperfagia
weight loss
increase TMB
termogenesisi onicolisis
B-adernergic activity: tyaki, palpitation, tremblor, anxiety, nerviosismo, hyperactivity, irritability
autommine - oftalmopatju
dermopathy
thyroid acorpathy
diffuse bocion
dx hyper T
algorithm px
nonspecific alterations in hper T
not pathognomotinc
hyperbillirubinemia
high tranaminases high FA hypercalcemia and calcuria anemia linfocytosis granulocytosis hypomagneemia less B1 and B6 vtamin in plasma
MISSED SLIDE
jamie
tionamides
slide
dont respond if somatic
dont use ATT, BMN, HHNA - these px go to qx tiroidectomy
radioactive yodo
administraation
eutyroidism in 6 months 50% of cases
dosis and exppetions
adverse affects
yodo 123
for dx
131 for tx - emits ionizing beta particles that lyse tyroid tissue
thyroidectomy
large bocio
potentially malignant nodule
pregs allergic or resistent to tx (ptu first trimestr)
px allergic
< 18-20yrs)
preference of px
(compressive MC)
adjuvant tx
beta blockers - propanolol dosis (block synthesis mechanisms and?)
liberation inhibitors - yoduro
ipodato
lopanoic acid
conversion inhibitors - PTU, glucocorticoides
volestiramine - enterohepatic decrease
litio decreases liberation, synthesis
recording..
special cases
tyroid adenoma
non autoimmune hypertirodism
others
hypothyroidism
deficiency of thyroid hormones
T3 and T4
more in women
(TSH is high, low in hyperthyrdoisim)
Etiolgy of hypothyroidism
primary - @ thyroid gland
secondary - alteration in hypophysary axis
terciarry - hypothalamus
prolactiniemia causes a terciarty hypogonadism (inhibits GnrH)
thyroiditis
not that common
hyperthyroid –> ey –> hypo –> total recuperation
heterogenous group of thyroid MC with in commun = inflammation even with diff etiology, MC, dx, tx
most are benign
some autolimited and others cause thyroid insuff that can be transitory or definitive
primary cause of hypothyroidsim
hashimoto thyroidisis = linfocitica cronica
autoimmune mechanisms cause infiltration of NK cells, linfocites, plasma cells to thyroid –> secuestro –> cause transitoory destruction of the gland
one of the primary causes of bocio as well (not repaired?)
ANOTHER cause is graves basedow (standard for hyperthyroidsism, hypo in late phase) - immunologibulins inhibit TSH to rec - gland isnt stimulated - hay bocio
Another cause after tiroidectomy,
ablative tx (131 iodine superindice)
infiltrative diseases (also in pituitary, but here in thyrdoi)
CA metastasic (lung, mama, colon, kidney)
subacute thyroididtis (De Quervain) -
trauma
RT
cell lesion - amiodarone, cytokines
blocki MIS no entrapment, decrase peripheral conversion no active hormone (litio, perclorato, estabudina, estonamidas, yodo, , amiodarone , etionamida, fenibutasona, aminoglutatinina, talidomida) - cause hypothyrdoisim maintaine
idiopathic
deficiency in yodo
congenital (should start around 6th gland) - here is afunctional - depends on moms thyroid levels
classification of thyroiditis
etiology
pain?
evolution
etiology thyroditis
autoimmune (linfocititca subaguda - sporadic or postpartum or…. linfocitica cronica = hashimoto, granulomatous)
infectious (viral bacterial
destructive (by radiation or trauma)
drug induced (amiodarone, cytokines)
pain classification thyroii=tsis
pain - granulomatous subaguda
suparative or acute
radiation
trauma
the nonpainful
hashimoto, subacutere, drug induced, Riedel
principal cause of hyperthyroidism
graves
primary cause of painful inflammation of thyroid
subacute thyroididtis (De Quervain) - ruptures follicles and liberation of preformed hormones - acute - increase of these horones with transitry hyperthyroidism --> eu --> hypo
classification by evolution of thyroidisits
acute
subacute
chronic (autimmune , hashimoto)
normal yodo consumption
150-300micrograms
thyroid phases of evolution
normal function –> follicles rupture (liberates preformed hormones increasing peripherla presence of thyroid hormones) –> hyperthyroid (usually insidious MC, subclinical)–> eythyroid –> hypothyroidism –> normal function
acute thyroiditis
aka supurative, bacterial, pyogena
causes of central hypothyroidism
all that alters eje hypophysiary (secondary and terciarty)
same causes of hipopituitarism
tumor invasion
infarct of pisary
infiltration/infection
lesion
iatrogenic
immunoloigcal
idiopathic
isolated deficiency of TSH
8 Is 1 A
MC of hypothyroidism
not evident at birth right away
unless so marked they have congenital MC
marked face, macroglossia, edemi periparto oral?, presentation in vientre
alteered development - llantp ronvp
histerical
dehyrdated
dry skin
fontanella anterior abombada
slow osteotendinous reflexes
psychomotor alterations -
retraso
cretinismo
affects CNS (T hormones are primordial for CNS development)
SCREEN these kids
cause of acute thyroiditis
hurt
due to inflammatory process from microbian agent
associated agents in adults - strep pyogenes and staph auresu
kids - strep alfa and beta hemolitico and anaerobes
circulation form distant infectious foci (GI, skin, resp traact), embryonic infeccted restos (cyst of tiroglose conduct, fistula of seno piriforme)
extension of neighboring infections like abscess mastoiditis otitis etc
unsual siutations from bad technique and accidental inoculation , bad fine needle aspiration or centra catheter, truama, esophageal rupture
main cause in kids seno piriform left infection infected from resp infection
68% bacteria 15% fungal mycobact %9 parasite 5% sifilitic 2%
normal TSH in preg
< 2.5
low , enough for her and baby??
MC of acute thyroiditis
after an high resp infection cuadro
can have presexisiting disease, fisutla seno piriforme, persistent ting, PAAF biopsy
100% neck pain, dysphagia 91%, disfonia 80%, pain at palaption, fever 92%, erithema of skin 80%, concomitant faringits
thyroid protective factors
capsule and muscles
blood and drainage
iodine
(but adjacent structures, from linfatic or hematogenous spread, or penetrating truama can still cause its infection)
labs at acute thyroiditis
leucocytosis > 20-25000
high ERS
tyroid hormones usually normal (depends on phsase)
normal captation at gammagrpahy (if full inflammaed it will be low )
USG can see abcess or edema in area - encapsulation suggesting infection
+ hemoculture (90% + of dx) with MC (aggressive so give these px ATBs right away before waiting on culture)
complications of actue thyroiditis
sepsis thromboembolism septic abcess rupture obstruction of airway larynx edema traqual estenosis tirotoxicosis
tx acute thyroiditis
EV antibiotics, hospitalize and drain lesion
(CS1gen, and aminoglycoside
pen anti st with aminoglycoside
amoxi with clavulinic acid or ampi and sulbactam
quinolones or C3g
drain lesion
subacute de quervain thyroiditis
autolimited viral infalmation
with genetic prediposition HLA-35, B27 in summer and fall
more in women between 30-50yrs
eneterovirus incidence coorelates
non specific signs of quervain
myalgia
atralgia
fatique low grade fever
specific sign of quervain
thyroid pain
exquisto ini palapation
irradiates to mandible and ear
phases of thyoridis quervain
pain predominates , manifestation s of tirotoxicosis 50%
pain irradiates retro acular
3-6wk
MC of infallmamtion and hyperthyroidism remit for 6-12months
px can be euthyroid
finally can or not have hypothyroidism
5-15% permanent
querviain lab
ERS high 50-100mm/h elevated tiroglobulin high PCR high thyroid hormones low iodine captation anti TPO and anti TG normal
USG - hipoecogenic areas without mass formation and without vascular flow (CUZ OF INFLAMMATION IOU CANT SEE CIRCULATION)
dx quervain
thyroid pain
high ERS and TG
USG and gamma
PAAF in quervain
not alaways
can have varies depends on stage of process
beginning inflammation and disorganzied folicular arquitecture
infiltration of PMN and lymphcytes and macrophages
most cx accumualtion f giant cells and with granoulomous image
coloid ceenter of granulomas
coloidophageia
formation of microabcesses
follicular disrption
MC of hypothyroidism
low metabolic rate and processes
affect all thyroid hormone functions
intolerance to cold (affects regulation)
initlally non specific - lethargo
CV - bradycardia, less contraction, less relexation phase of ventricle, less relaxation of SM regulated by NO, HTN, edema, congenital heart failure, prolonged AP cardiac, retention of liquid
causes disfunction
IDL, VDL, increase triglycerides - (hormones maintain rec liver LDL and increase plasm tranport of these to liver) - dislipidemia - correct cause
resp - should maintina balance of CO2 and O2 - disnea, intolerance to excercise, hyperventilation when body sees CO2 accumulating
diaphragmatic disfunction
neuropathy
resrtictive lung function - less muscle contraction, air entrapment
apnea sleep
edema glotisi, altered cornetes, compressed traquea
cutaneous - mixedema - seen more pretibial - hard edema similar to secondary to linfatic - no dent at pressure - icnrease of mucoplolyscarades and less degradation of acido iauronico - hydrofilic particles that attract water
facial changes - perioribital edema
loss of third distal of cejas signo de la renaja?? - also in sifilis and hepatopathous px (cirrosis, hepatitis b c)
dry skin, hard skinfine breaking hair, libedos in limbsreticular , palida macroglosiaa, cirrosis?, autimmune (more than onegland sindrome poliglandular/malechore - herpetiforme, vetiligo, dermatitis, pciartata, …vulgar )disease, periorbital edema
neuro - all downregulateed
bradilalia, bad memory, bradilasia, less vental function, bradikinesia, carpal tunnel syndrome (accumulation of liquid, mucopolysacardi depostions entrap nerves), dementia, ataxia, entumecimiento
psychosis mfranka (pura mixa edematousa), pseudodementia (altered mental state but gone after correcting), apatia change in mood, depression,
otorrino - rinitus, hear less, disfonia (accumulation of secretions in larynx affect vocal cords, macroglosia, bocio)
systemic -
GI - less transit - constipation, noausea, anorexia, ascitis, less filtrate golmerular, less free water
less relaxation contraction - mialgia, atralgia
amenorrea, metrorragia, altered ovulation and fertilty
eritropoyesis altered (micro_ , loss hierro, less GI absrption (micro) altered menstraution (normo), pernicious (macro)- anemia - micro, macro, normo -
coag panel changed - more thrombi
coma miximedatoso- emergency - 60-80% mortality - rare now with screenings - altered conciousness , not really coma, more in women, > 60yr, qx infection can precipitate it - exacerbation of all other MC
tx for hipothyrodisism ALL
levotiroxina (not only primary)
tx quervain
AINES
glucocorticoids start with 30mg of prednisone and go decreasing by .2
betablockers (propanolol)
levotyroxine
other subacteute thyroidistis
sporadic silent thyroiditis (autimmune with infiltraiotn more in iodine deficient women, with small painless bocoi in 50% inflmamatory so transitory
5-20% have h=thyoroid rofile altered
anti TPO + 50% low cpatation
evolution occurs in less than a year
10% of recurrence
pos partum
same as sporadic = autommune
can be 1yr postpartum
5-10% of px 30-50yr
HLA DR3/DR4/DR5
clinca: similar to sporadic and postpartum
doest hurt
25-30% can have permanent hypothyroidism
give propanolol to tx symptoms, most thyrodisits are tranistory
phases of hyperthyroidism (TSH supprsed and high T3, T4) tiroglobulin can be up, positive antibodies, captation low)
meds thyroiditism
cytotocixc effect on follicles
litio lesioins cells
cytokines - interferon a tx and IL2
amiodarone causes lesion type I (increases synthessi) or II (rupture)
tx thyroitidis
betablockers of MC of tirotoxicosis and tx hipotyroidism/TSH > 20mU/L (in pure thyroiditis, but if subclinical > 10 treat as well, could be hashimoto or thyroid has been taken out - other wise wait till 20 because transitory)
DONT tx sublicinical hypothyrodisim except (preg ladies and px with other coomorbilities that will also improve - recent infraction, cardiac insuff III,IV - oldies)
amiodarone - only suspend in type I
manage with glucocorticoides 0.5-1.25 mg/kg 3-6wk
meds thyroiditism
cytotocixc effect on follicles
litio lesioins cells
cytokines - interferon a tx and IL2
amiodarone causes lesion type I (increases synthessi) or II (rupture)
tx thyroitidis
betablockers of MC of tirotoxicosis and tx hipotyroidism/TSH > 20mU/L (in pure thyroiditis, but if subclinical > 10 treat as well, could be hashimoto or thyroid has been taken out - other wise wait till 20 because transitory)
DONT tx sublicinical hypothyrodisim except (preg ladies and px with other coomorbilities that will also improve - recent infraction, cardiac insuff III,IV - oldies)
amiodarone (used to tx arrytmia) - only suspend in type I
manage with glucocorticoides 0.5-1.25 mg/kg 3-6wk
at type II dont necessarily suspend but manage with above
hashimoto thyroditis presentation
ddifuse bocio , symmetrical, firm, atrophic in 10%
why gynecological changes in hypothyroidism
no retroalim
lactrotrope cells stimulated
prolactine up
inhibits GnRH
hashimoto function
normal or elevated
RF of hypothyrodism
no genetic direct associttion (we think tho)
hashimoto asoociated
other autoimmune pathologies (Grave, AAddison, premature ovarian failure)
hashimoto linfoma
fast growing nodules in px with hashimoto
infiltration, encapsulate and form linfoma
riedal thyroiditis
painless hard lenoso o petreo, unilateral slow growing bocio
lots of compressive MC disphagia, disfonia, disnea, estridor
ERS normal or high, AC poitive, or normal thyroid function
can invade other neighboring strcutures
dx reidal
low captation
ERS and thyroid profile normal or altered
PAAF necessary - fibroinflmmation (disscart tumor)
hypothyroidism precipitating factors
infections (resp)
qx
CVD
metabolic alterations (dilipdiema, hipercalcemia/glucemia)
riedel tx
elminante cpmreession with resection
steroids for inflmmation
replace with levothyroxinve
TABLE flow chart
elminante cpmreession with resection
steroids for inflmmation
replace with levothyroxinve
TABLE flow chart
types of thyroid CA
papilar - 80-85% folicular ca - 10% (hurthe) medular ca - 5% anaplasic ca - 3% miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)
papilar - 80-85%
folicular ca - 10% (hurthe) - good but most metsastaiss
medular ca - 5%
anaplasic ca - 3%
miscelaneous 1% ( linfoma, fibrosarcoma, hemangioendotelioma maligo, teratoma)
can be follicular or parafolicular (type C which make calcitonin - medular from this one :() cells and tis is how they are differentiated
epi of thyroid ca
PCT in women betwen 30-50yrs
folicular CA more common in women between 40-60yrs
differentiated carcinomas have 100% survical at 5yrs if detected on time
papilar CPT
firm cold on gammagraphy solid in US nodule
7% microcalcinomas
in BMN dominating nodules is usually carcinoma
in kids usually in 20-50% linfatic
usually intraglandular extension
slwo growth can delay dx
follicular CFT
small follicles and poor presence of coloid formation
diff from adenomas of follicles because present invation of vessels and capsular
metastasize to LNs anf through hematogenous reaching lung and bone more than CPT
secrete Tg
tx ca
TABLES
after total thryoid ablation tx with L,4 (2.5 mcg/kg/d)
at 3 motnshs during tx with L4 mesure TSH and Tg (glucoprotein with receidos de tirosina if + something in there is producing)
at 6-12hr conretirada of L4 measure TSH and Tg and do a RCT with 2-5mCi of I 131
RCT negative measure Tg ……………
differentiated thyoi ca
papilar and follicular
agressive cariants
columnar cells
diffuse sclerosante
insular
bethesda
I - …….repeat FNA - no dx , unsatisfactory
II - benign 0-3% risk of malignancy - follow clinic
III - atypucal of uncertain significanse, follicular lesion incertain - 5-15% - repeat FNA
IV - follicular neoplasia 15-30% - lobcomy/tiroidectomy
V - suspect malignity 6-75% - almost total thyroidectomy or lobectomy
VI - malignant 97-99% - total thyroidectomy
TABLe
medular CA
from parafolicular cells
sporadic 75-80%
hereditary 25-20%
3-4% of all thyroid neoplasias
secrete CT and CEA
seen in MENs
sporadic medular
66-75% RET gene somatic more unicentric alone nodule LN metastasis 80% also to liver, skeleton, lung with calcitonin > 5000pg/mL
hereditary medualr
RET
part of MEN2
lesion in hyperplasia of cel C, diffuse or nodular
multifocal
any age
metastasis to local ganglio, higdao pulnon, hueso
cant operate
hypothyroidsm px - low metabolism affects response to anesthesia
MEN 2a
80% MTC hereditary multicentric
feocromocitoma 50% bilateral or unilateral
hyperparathyroidism primary…..pic
Men 2b
pic
dx CMT
history PE
anatopathological exploration
immunohistoquimica
tumor markters
sublicinal hypothyroism
free T4 is normal
TSH elevated
no MC or very subtle
3-15% of cases
should rpt test in 6wks, do antibodies, and lipid profile
tx CMT
1st group - localized sisease, < 500 calctonin can cure
2nd group - neck metastasis - possible to cure
3rd - mestastssis to distance - deadman
1st grou p tx
tiroidectom total
dissection of LNs
25% cure
2nd gorup tx
total tiredoicotmy and GL dissection
3rd group
same as second ,
resecar identified disease
when to tx subclinical hypothyroidism ( with levo?(
if you lower coomorbilities of other MC (cardiopathy, bocio, hiperhemocisteinemia - RF for dislipidmia)
if TSH > 10mu/L
preg, postivie antbodies - autoimmne - will get a franco - (anti tpo, anti tg)
hypothyroidism dx
MC , px history
US of gland
hormonal profile
TSH and T4 normal
healthy - euthyroid px
high TSH, T4 free normal
sublincical hypothyroidsism
in eje tsh is changed first then after come MC
high TSH, T4 low1f
frank primary hypothyroidsism
TSH low, T4 low
hipothyroidism central
complementary dx for hypothyrodissm
CPK-mm - muscle, skeletal
transminases up
LDH
mioglobina?
proteinuria
lipid profile altered - total cholerstarol, VDLD, LDL, IDL, triglicerides,
a chica protein
tx hypothyroidism
levotirxoina
hormone substitution
weight dependent
1.6-1.8 xkg
old 0.5-1mg/kg
4microg/kg in kids - high metabolism
