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ORTHO > 2nd Test - Endocrine > Flashcards

2nd Test - Endocrine Flashcards

1
Q

TSH axis

A

…

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2
Q

How is TSH axis retroalimented

A

mostly T4 RAN

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3
Q

secondary to deficiency of thyroid hormones we can have what disorders

A

hypo/hyperthyroidism

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4
Q

thyroid cx

A

found in anterior neck

2 lobules and one isthmo

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5
Q

measurements of thyroid lobules

A

variable by px
2-4-5cm vertical
1-1.5cm transverese and AP

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6
Q

pyrimidal lobule

A

can have a third abnormal
increased function

30%

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7
Q

weight of thyroid gland

A

10-20gr

80gr at hypertrophy

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8
Q

irrigation of thyroid

A

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

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9
Q

2 cell types in thyroid

A

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

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10
Q

thyroid follicle

A

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

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11
Q

colloid

A

viscous gell pool of thyroglobulin (glucoprotein 660kDa constitutes 75% of gland weight)

110-140 residuss of tyrosine

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12
Q

synthesisi of thyroid hormones

A

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)

  1. 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
  2. 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

  1. 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

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13
Q

2 steps of thyroid synthesis that occur in colloid

A

ORGANIFICAITON

ACOPLAMIENTO

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14
Q

Desyodasas

A

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

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15
Q

TSH functions

A

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
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16
Q

Autoregulation

A

@ 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

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17
Q

activity of T3 vs T4

A

T3 is 10x more active than T4

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18
Q

thyroid hormone metabolism

A

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..

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19
Q

T4 metabolic routes

A

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

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20
Q

T3 metabolic routes

A

at liver in TRIAC

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21
Q

peripheral bockers of T4 T3 conversion

A

meds ( ptu, BB, contrast, glucocorticoides)

acute disease (qx, IAM)

chronic diseases

caloric malnutrion (IR, IH,)

selenium deficiency

burns

qx

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22
Q

hormonal circulation of T4

A

99.97% unite with proteins
75% to TBG
20% TBPA
5% to albumin

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23
Q

how much T4 free in circulation

A

0.03% - is the one that exerts most actiion

this is the one measuresd

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24
Q

half life of T4

A

7-8d

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25
Q

hormonal circulation of T3

A

99.7% united to proteins
75% to TBG
25% to albumin

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26
Q

half life T3

A

6-8hr

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27
Q

how much T3 ffree in circulation

A

0.3% free

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28
Q

@ high TBG

A

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
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29
Q

@ low TBG

A

more T3 and T4 total increase

low TSH

congenital from

glucocorticoid drugs

nefrotic syndrome

enteropathy losoing proteins

cirrosis

proteic malnutrion

acromegalia

hyperthyroidism

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30
Q

hormonal despalcement

A

salicilates

acido mefanmico
fenclofenac
mitotane
fenilbutazone
fenitoin
diazepam
furosemide

NO AINES! (more free homrmones)

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31
Q

effects of T3, T4

A

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

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32
Q

TSH N levels

A
  1. 4-4

3. 5 is low in pregnant woman

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33
Q

Goiter

A

any icrease in thyroid galnd size DOESNT MATTER THE CAUSE

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34
Q

prevalence of goiter

A

5%/10%

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35
Q

types of goiter

A

diffuse
nodular

multinodular

nodules are afnctional

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36
Q

causes of goiter

A

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)

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37
Q

ingest recommended of iodine

A

150-300ug/d

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38
Q

how to know of iodiene deficiencny dx

A

(it will cause urinary excretion < 50ug/d) = yoduria

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39
Q

primary cause of hyperthyrodisism

A

hashimoto thyroiditis

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40
Q

main types of dishormonogenesis

A

plasma thyrocyte transport

TPO deficiency

attered acoplamiento

desyodasas deficiency

excess yodoproteina

(resistance to hormones,
RT, neoplasia, fisiological) - pregnancy, lactancy , pubety increase gland size

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41
Q

MC of goiter

A

gland compression on surrounding structures - larynxtraquea

snoring, disfonia, , disnea at laying back, disfagia

pemberton sign

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42
Q

pemberton sign

A

reddened face and anterior thorax after raising arms

gland compresses vascular neck structures decreasing drainage

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43
Q

labs for goiter

A

thyroid hormones (TSH, T3, T4 free) (Ac TG, Ac TPO - autommune up in hashimotos)

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44
Q

images for goiter

A

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

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45
Q

tx of goiter

A

symptomatic observation

tyroidectomy depends on size/compression

levotiroxine = NOT INDICATED ANYMORE –> hyperthyroidism

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46
Q

extra ocular muscles

A

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

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47
Q

origin of superior recus

A

Anillo de Zinn, en el ápex orbitario.

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48
Q

insertion of superior rectus

A

Superior, a 7mm del limbo corneal.

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49
Q

innervation of supereior rectus

A

Rama superior del NC III.

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50
Q

irrigation of superior recus

A

Rama muscular superior de la arteria oftálmica.

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51
Q

size of superior rectus

A

41.8mm de longitud. o Tendón: 5.8mm de longitud o Ancho: 10.6mm

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52
Q

functions of superior rectus

A

Primaria: Elevación o Secundaria: Aducción o Terciaria: Intorsión

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53
Q

origin of rectus medio

A

Anillo de Zinn (Tendón superior) 

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54
Q

insertion of rectos medio

A

: Medial, 5.5mm del limbo.

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55
Q

innervation of rectus medio

A

: Rama inferior del NC III.

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56
Q

irrigation of rectos medio

A

Rama muscular inferior de la arteria oftálmica.

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57
Q

size of rectus medio

A

Longitud: 40.8mm o Tendón: 3.7mm o Ancho: 10.3mm

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58
Q

function of rectus meido

A

Aducción

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59
Q

neurooftalmogia in charge of what

A 
headaches
oculomotor and eyelid disorders
puilar defects
loss of vision
secuelas of CV events
secuelas of IC tumors and orbatry

fiacial paralysis

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60
Q

origin of inferior rectus

A

: Tendón inferior del anillo de Zinn.

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61
Q

insertion of inferior rectus

A

: Inferior, 6.5mm del limbo.

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62
Q

innervation of inferior rectus

A

Rama inferior del NC III.

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63
Q

irrigation of inferior rectus

A

Rama muscular inferior de la arteria oftálmica e infraorbitaria.

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64
Q

size of inferior rectus

A

Longitud: 40mm o Tendón: 5.5mm o Ancho: 9.8mm

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65
Q

function of inferior rectus

A

Primaria: Depresión o Secundaria: Aducción o Terciaria: Extorsión

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66
Q

origin of rectus lateral

A

Tendón superior del anillo de Zinn.

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67
Q

insertion of recto lateral

A

Tendón superior del anillo de Zinn.

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68
Q

innervation of rectus lateral

A

NC VI.

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69
Q

irrigation of rectus lateral

A

Arteria lacrimal

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70
Q

size of rectus lateral

A

ongitud: 40.6mm o Tendón: 8mm o Ancho: 9.2mm

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71
Q

function of rectus lateral

A

Abducción

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72
Q

origin of superior oblique

A

Superior y medial al foramen óptico, entre el anillo de Zinn y periórbita. 

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73
Q

insertion of superior oblique

A

7.7mm del limbo.

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74
Q

innervtion of superior oblique

A

NC IV 

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75
Q

trajectoru of superior oblique

A

Anterior a tróclea, como tendón atrás-abajo-detrás de recto superior.

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76
Q

irrigation of superior oblique

A

Rama muscular superior de arteria oftálmica.

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77
Q

size of superior of oblique

A

Longitud: 40mm o Tendón: 20mm o Ancho: 10.8mm

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78
Q

function of superior oblique

A

Primaria: Intorsión. o Secundaria: Depresor. o Terciaria: Abductor.

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79
Q

troclea

A

Polea cartilaginosa en forma de U, corresponde al cuadrante nasal superior de la órbita y está unida al musculo oblicuo superior por tejido conectivo.

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80
Q

incomplete vs complete III aparalysis

A

communic post aneurysism if midriasiss

miosis - horner

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81
Q

ptosis

A

some congenital some neurological

MS
marcus aGunn
Guillan Barre

pupillary fibers outside of III

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82
Q

paralysis of VI

A

Abd

inkid needs dilaion and fondus exam

only nerve suelto en senocavernoso

increased IC pressure in kid this is the first sign

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83
Q

origen of inrerior oblique

A

Nasal de la pared orbitaria, detrás de borde inferior orbitario y lateral a conducto nasolagrimal.

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84
Q

trajectory of inferior oblique

A

: pasa por debajo del recto inferior y recto lateral. 

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85
Q

innervation of inferior oblique

A

: rama inferior del NC III.

86
Q

irrigation of inferior oblique

A

Rama inferior de arteria oftálmica y arteria infraorbitaria

87
Q

size of inferior oblique

A

Longitud: 37mm o Tendón: no tiene o Ancho: 9.6mm

88
Q

function of inferio oblique

A

Primaria: extorsión. o Secundaria: elevación. o Terciaria: abducción.

89
Q

IV paralisis

A

px depresses menton and as they look

dipolopia

=

90
Q

what is strabism

A

Consiste en un trastorno que provoca desalineación de un ojo con respecto al otro al enfocar.

91
Q

PPM

A

Punto primario de la mirada (PPM): la posición normal de los ojos. 

92
Q

kappa angle

A

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).

93
Q

what to do at a paralysis of eye - any

A

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

94
Q

Existen dos tipos de movimientos oculares:

A

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

95
Q

Dentro de las versiones tenemos:

A

Dextroversión: mirada hacia la derecha. o Levoversión: mirada hacia la izquierda.

96
Q

vVergencias

A

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.

97
Q

classifcation of strabism

A

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)

98
Q

congenital esotropia

A

Aparece antes de los 6 meses de edad  Asociada a hipermetropía  Relacionado a nistagmos  Produce alteración de la binocularidad

99
Q

tx strabism? congential esotropia?

A

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

100
Q

consideratiosn at paraplysis of eye

A

pupil size
action of other craneal nerves
changing ptosis
proptosis enoftalmo

aparicion of regeeneration aberrant signs

Neuro MC

head compensatory positions

101
Q

primary exoptrpy

A

congenital

aquired

102
Q

secondary exotropy

A

Sindrome de Duane o Paresia de 3er nervio craneal o Anomalías craneofaciales

103
Q

Carajito que tenga esotropia con limitación hacia afuera hay que hacerle

A

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).

104
Q

intermittent exotropy

A

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

105
Q

A synrome

A

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».

106
Q

hyperthyroidism

A

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

107
Q

thyrotoxicosos vs hypetthyroidism

A

thyro - MC of too much hormone INDEPENDENT of cause

hypertheyroidism is thyrotoxicosis?q

108
Q

causes of hyper T

A

normal or elevated captation

<1% captation (elimianted)

low captation

(in gammagraphy)

109
Q

normal or high captation

A

autoimmune diseases

hyper T from autononmia of follicular cells

mediated by TSH

mediated by HCG

110
Q

<1%

A

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??)

111
Q

low captation 3-5%

A

amiodarone (200mg of this has approx 5mg of yodo - materia prima - increases synthesis)

medios de contraste yodados

too much iodine in diet

vaginal douches

112
Q

principal autoimmune cause of hyperT

A

Graves-basedow

113
Q

Graves-basedow cx

A

too much thyroid homrones in blood from too much synthesis of them

autoimmune (+ antibodies in plasma)

biopsy shows thyroid galdn full of autoimmune cells

114
Q

5 classic MC of GB

A

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

115
Q

Hashitoxicosis

A

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

116
Q

wben is there autonomy of follicular cells

A

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

117
Q

thyroid adenoma

A

benign
hyperfuncitoning
depends on size (qx - cheaper, could recurr)

somatic mutation

1-5% of hyper Ts

118
Q

toxic multinodular bocio

A

2 or more nodules

somatic mutations causing hyperfunction
5-15%

1-2 nodules cold or hypocaptating

usually qx

119
Q

non autoimmune hereditary hyperthyroidis

A

AD
inicio
germinal mutaion

thyroidectomy needed

from neonatal life

120
Q

Albright mcunne Syndrome

A

causes hyperfuncioning gland

hypercromic non pruriginou notn delimiated liesonform early age

mutation

121
Q

Marinne Lenhart syndrome

A

Grave

cold nodules

25-30%

toxic adeoma

like gravies and ultinodular bocio

more than one hot or hypercaptivating

not exclusive

122
Q

TSH mediated hyperthyroidism

A

only one iwth high TSH

tirotropoma

deficiency of desyodosasa

resistance of caction of thyroid hormones

hyperfuncitoning

123
Q

tyrotoxicosis from destruction of follicles

A

low TSH

inflamamtion

hypocaptation

124
Q

hypocaptation gammagraphy with bocio think of

A

throditis, ectop`c

125
Q

exogenous tirotoxicosis

A

iatrogenic
facticia
hamburgers

126
Q

ectopic hyper T

A

ovarian struma
mets functional ca folciular a(metastasis - cpatation at lung)
bocio lingual funcionante (captates)

127
Q

hyperT induced from iodine

A

walff-chaikoff

altered regulation

low TSH

find cause

128
Q

amiodarone thyrotoxicosis

A

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

129
Q

MC of hyper T

A

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

130
Q

dx hyper T

A

algorithm px

131
Q

nonspecific alterations in hper T

A

not pathognomotinc

hyperbillirubinemia

high tranaminases
high FA
hypercalcemia and calcuria
anemia
linfocytosis
granulocytosis
hypomagneemia
less B1 and B6 vtamin in plasma
132
Q

MISSED SLIDE

A

jamie

133
Q

tionamides

A

slide

dont respond if somatic
dont use ATT, BMN, HHNA - these px go to qx tiroidectomy

134
Q

radioactive yodo

A

administraation

eutyroidism in 6 months 50% of cases

dosis and exppetions

adverse affects

135
Q

yodo 123

A

for dx

131 for tx - emits ionizing beta particles that lyse tyroid tissue

136
Q

thyroidectomy

A

large bocio

potentially malignant nodule

pregs allergic or resistent to tx (ptu first trimestr)

px allergic

< 18-20yrs)

preference of px

(compressive MC)

137
Q

adjuvant tx

A

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..

138
Q

special cases

A

tyroid adenoma

non autoimmune hypertirodism

others

139
Q

hypothyroidism

A

deficiency of thyroid hormones

T3 and T4

more in women

(TSH is high, low in hyperthyrdoisim)

140
Q

Etiolgy of hypothyroidism

A

primary - @ thyroid gland

secondary - alteration in hypophysary axis

terciarry - hypothalamus

prolactiniemia causes a terciarty hypogonadism (inhibits GnrH)

141
Q

thyroiditis

A

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

142
Q

primary cause of hypothyroidsim

A

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

143
Q

classification of thyroiditis

A

etiology
pain?
evolution

144
Q

etiology thyroditis

A

autoimmune (linfocititca subaguda - sporadic or postpartum or…. linfocitica cronica = hashimoto, granulomatous)

infectious (viral bacterial

destructive (by radiation or trauma)

drug induced (amiodarone, cytokines)

145
Q

pain classification thyroii=tsis

A

pain - granulomatous subaguda

suparative or acute

radiation

trauma

the nonpainful
hashimoto, subacutere, drug induced, Riedel

146
Q

principal cause of hyperthyroidism

A

graves

147
Q

primary cause of painful inflammation of thyroid

A 
subacute thyroididtis (De Quervain) - ruptures follicles and liberation of preformed hormones - acute - 
increase of these horones with transitry hyperthyroidism --> eu --> hypo
148
Q

classification by evolution of thyroidisits

A

acute
subacute
chronic (autimmune , hashimoto)

149
Q

normal yodo consumption

A

150-300micrograms

150
Q

thyroid phases of evolution

A

normal function –> follicles rupture (liberates preformed hormones increasing peripherla presence of thyroid hormones) –> hyperthyroid (usually insidious MC, subclinical)–> eythyroid –> hypothyroidism –> normal function

151
Q

acute thyroiditis

A

aka supurative, bacterial, pyogena

152
Q

causes of central hypothyroidism

A

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

153
Q

MC of hypothyroidism

A

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

154
Q

cause of acute thyroiditis

A

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%
155
Q

normal TSH in preg

A

< 2.5

low , enough for her and baby??

156
Q

MC of acute thyroiditis

A

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

157
Q

thyroid protective factors

A

capsule and muscles

blood and drainage

iodine

(but adjacent structures, from linfatic or hematogenous spread, or penetrating truama can still cause its infection)

158
Q

labs at acute thyroiditis

A

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)

159
Q

complications of actue thyroiditis

A 
sepsis thromboembolism septic
abcess rupture
obstruction of airway
larynx edema
traqual estenosis
tirotoxicosis
160
Q

tx acute thyroiditis

A

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

161
Q

subacute de quervain thyroiditis

A

autolimited viral infalmation

with genetic prediposition HLA-35, B27 in summer and fall

more in women between 30-50yrs

eneterovirus incidence coorelates

162
Q

non specific signs of quervain

A

myalgia
atralgia
fatique low grade fever

163
Q

specific sign of quervain

A

thyroid pain
exquisto ini palapation

irradiates to mandible and ear

164
Q

phases of thyoridis quervain

A

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

165
Q

querviain lab

A 
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)

166
Q

dx quervain

A

thyroid pain
high ERS and TG
USG and gamma

167
Q

PAAF in quervain

A

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

168
Q

MC of hypothyroidism

A

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

169
Q

tx for hipothyrodisism ALL

A

levotiroxina (not only primary)

170
Q

tx quervain

A

AINES
glucocorticoids start with 30mg of prednisone and go decreasing by .2
betablockers (propanolol)
levotyroxine

171
Q

other subacteute thyroidistis

A

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)

172
Q

meds thyroiditism

A

cytotocixc effect on follicles

litio lesioins cells

cytokines - interferon a tx and IL2

amiodarone causes lesion type I (increases synthessi) or II (rupture)

173
Q

tx thyroitidis

A

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

174
Q

meds thyroiditism

A

cytotocixc effect on follicles

litio lesioins cells

cytokines - interferon a tx and IL2

amiodarone causes lesion type I (increases synthessi) or II (rupture)

175
Q

tx thyroitidis

A

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

176
Q

hashimoto thyroditis presentation

A

ddifuse bocio , symmetrical, firm, atrophic in 10%

177
Q

why gynecological changes in hypothyroidism

A

no retroalim
lactrotrope cells stimulated
prolactine up
inhibits GnRH

178
Q

hashimoto function

A

normal or elevated
RF of hypothyrodism

no genetic direct associttion (we think tho)

179
Q

hashimoto asoociated

A

other autoimmune pathologies (Grave, AAddison, premature ovarian failure)

180
Q

hashimoto linfoma

A

fast growing nodules in px with hashimoto

infiltration, encapsulate and form linfoma

181
Q

riedal thyroiditis

A

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

182
Q

dx reidal

A

low captation
ERS and thyroid profile normal or altered
PAAF necessary - fibroinflmmation (disscart tumor)

183
Q

hypothyroidism precipitating factors

A

infections (resp)
qx
CVD
metabolic alterations (dilipdiema, hipercalcemia/glucemia)

184
Q

riedel tx

A

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

185
Q

types of thyroid CA

A 
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

186
Q

epi of thyroid ca

A

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

187
Q

papilar CPT

A

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

188
Q

follicular CFT

A

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

189
Q

tx ca

A

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 ……………

190
Q

differentiated thyoi ca

A

papilar and follicular

agressive cariants

columnar cells
diffuse sclerosante
insular

191
Q

bethesda

A

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

192
Q

medular CA

A

from parafolicular cells

sporadic 75-80%
hereditary 25-20%

3-4% of all thyroid neoplasias

secrete CT and CEA

seen in MENs

193
Q

sporadic medular

A 
66-75%
RET gene somatic
more unicentric
alone nodule
LN metastasis 80%
also to liver, skeleton, lung with calcitonin > 5000pg/mL
194
Q

hereditary medualr

A

RET
part of MEN2
lesion in hyperplasia of cel C, diffuse or nodular
multifocal
any age
metastasis to local ganglio, higdao pulnon, hueso

195
Q

cant operate

A

hypothyroidsm px - low metabolism affects response to anesthesia

196
Q

MEN 2a

A

80% MTC hereditary multicentric
feocromocitoma 50% bilateral or unilateral
hyperparathyroidism primary…..pic

197
Q

Men 2b

A

pic

198
Q

dx CMT

A

history PE
anatopathological exploration
immunohistoquimica
tumor markters

199
Q

sublicinal hypothyroism

A

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

200
Q

tx CMT

A

1st group - localized sisease, < 500 calctonin can cure

2nd group - neck metastasis - possible to cure

3rd - mestastssis to distance - deadman

201
Q

1st grou p tx

A

tiroidectom total
dissection of LNs
25% cure

202
Q

2nd gorup tx

A

total tiredoicotmy and GL dissection

203
Q

3rd group

A

same as second ,

resecar identified disease

204
Q

when to tx subclinical hypothyroidism ( with levo?(

A

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)

205
Q

hypothyroidism dx

A

MC , px history

US of gland

hormonal profile

206
Q

TSH and T4 normal

A

healthy - euthyroid px

207
Q

high TSH, T4 free normal

A

sublincical hypothyroidsism

in eje tsh is changed first then after come MC

208
Q

high TSH, T4 low1f

A

frank primary hypothyroidsism

209
Q

TSH low, T4 low

A

hipothyroidism central

210
Q

complementary dx for hypothyrodissm

A

CPK-mm - muscle, skeletal

transminases up
LDH
mioglobina?
proteinuria

lipid profile altered - total cholerstarol, VDLD, LDL, IDL, triglicerides,

a chica protein

211
Q

tx hypothyroidism

A

levotirxoina

hormone substitution

weight dependent

1.6-1.8 xkg

old 0.5-1mg/kg

4microg/kg in kids - high metabolism

ORTHO (9 decks)

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