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1st test endocrine Flashcards

1
Q

Wolfram Syndrome

A 
rare
progressive
degenerative 
transmited AR
DNA
central diabtes insipidus
DM
optic atrophy - blindness
neurosensorila deafness
neuro/psch alterations
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2
Q

neurohipofisis

A

post pituitary
connected to hypothalamus via axons
secretes vasopressin and oxytocin

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3
Q

Nephrogenic Diabetes Insipidis

A

ADH is okay but its afunctional

rec is messed up

poor response of renal tube cells

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4
Q

classification in NDI

A 
primary
familiar congenital (AD X linked)
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5
Q

secondary NDI

A

tubulointersticial nephroamties
polycystic kidney, distal tubular acidosis, cistinosis, idiopathic hypercalciuria, renal amyloidosis
secondary tubularintersiticail nefropathy

litio
demeclocicline

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6
Q

DIC

A

altered conservation of body water as a consequence of inadequate ADH
large V of water eliminated in urine

poliruia
compensatory [plidipsia

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7
Q

psycogenic polydipsia or primary polidipsi

A

increased ingestion of water more than necessary –> physiological suppression of ADH due to over hydration and hypotony –> polyuria (sudden 10-12L), nicturia, polydipsia

hipoosmotic polyuria

hypovolemia and hypotension

hypertonic dehydration

astenia with sleep disorder

hipernatremia

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8
Q

PP seen in

A

young women
psychiatric px
fenotiazide (dry mouth) takers
hypothalamic lesions alteraing thirst center

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9
Q

normal urine

A

50cc/hr

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10
Q

cause of primary DIC

A

immunolocial

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11
Q

secondary cause of DIC

A 
tumor
qx
trauma
IC tumor = 3rd cause
craneofaringeoma in kids
lung breast CA metastasis in adults
supraselar germinomas
intraselar GI tumors via metastasis
toxoplasmosis, herpes simplex, AIDS, 
qx
truma
Lawrence Moon Biedel Synrome

linfocitic hipofifis (infiltariotn)??

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12
Q

phases of DIC from head trauma

A

polyuria 4-5 days
secondary to transsphenoidal qx

2-3d after qx -> polyuria
this alters ADH liberation

oliguria 4-5d
(cell degeneration with liberation of preformed hormone into circulation)

polyuria and polydipsia (compensatory)
neurosecretory cell death causes Permanent ADH deficit

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13
Q

cx of Lawrence Moon Biedel syndrome

A

obesity, mental deficit, pigmental rhinitis…

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14
Q

dx DI

A

<1010 urine density
urine and serum electrolytes (one high one low)

hypernatremia

plasma osmolarity > 350 mOsm/L

urine osmolarity (lower)

prueba de depuracion aquosa - remove all diuretics, solutions, ingestion - (doesn’t have - oliguria - anuria) if they do will have polydipsia from IC liquid –> coma (2-4hr)

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15
Q

what is endocrinology

A
  • Branch of internal medicine that studies regulatory functions of hormones
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16
Q

anatomy of hypothalamus

A
  • Weight = 4gr

- 0.3-04cm

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17
Q

tx DI

A

desmopresin - agonist of ADH uniting with V2 rec of acuoporin –> tubular water reabsorption
VO/SC/Spray
1-2mg every 6hr, px responds within days
something about falcemics?

hydration

clorpropamid - increases ADH action - psychiatric use

carbamacepine - increases ADH liberation (high doses) > 1200mg/day

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18
Q

irrigation of hypothalamus?

A

?

- Primary capillary plexus Hypophysary arteries ant branches
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19
Q

limits of hypothalamus

A
  • optic chiasm (ant)
    • thalamus/3rd ventricle (sup)
    • mamillary bodies (post),
    • infundibulo tallo-hipofisario (int)
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20
Q

ADH is also produced where

A

adenohipofisis

periventricular nucleus

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21
Q

SSIADH

A

excessive persistend ADH secretion , not responding to inhibition -

retain water
low plasma osmolarity - dilution, high urine osmolality

edematized
oliguria

water retained

hyponatremia
nypoosmolarity

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22
Q

2 connections of hypothalamus hypofisis

A
  1. Sistema porta hipotalámico-hipofisario.
    • Originates in eminencia media.
    • retrógrado & anterógrado flow
    • parvocelulare hypothalamic neurons (parvo = small [short axón -magnocelulares]) secrete hormones that reach AP
  2. Neuronas hipotalámicas magnocelulares send axons to NP.
     ○ Porta-hipotalamo-hipofisario = anterior (circulatory)
     • Eminencia media is where portal system is formed
 ○ Neuronas neurohipofisarias magnocelularesPosterior from hypothalamic neuronal axonal connection
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23
Q

MC of SSIADH

A

change personality irritable confusion hallucinate nausea vomit, extrapyrimadial signs
convulsion crisis, altered consciousness

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24
Q

DX criteria of SIADH

A

TABLE… fundamental

complentary
uricemia < 4mg/dL
BUN < 10mg/dL
FENa > 1%

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25
Q

functions of hypothalamus can be

A

endocrine or non endocrine

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26
Q

tx of SIADH

A 
hydration - hypertonic saline
ADH blockers (carbonate litium) loop diuretic

vaptan (conivaptan, tolvaptan, relcovaptan)

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27
Q

endocrine function of hypothalamus

A 
1. parvocelular neurons secrete liberating facors or inhibitory that act at AP.
Magnocelular neurons (supraóptico &amp; paraventricular nuclei) send axons to NP, store these products
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28
Q

ADH does what

A

retains water

reabsorbs Na+

secretes K+

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29
Q

no endocrine function of hypothalmsu

A

Based in nuclei that regulate sleep, thirst, T, appetite, libido, weight.

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30
Q

hyperprolactinemia

A

incrased prolactin plasma levels > 20ng/mL in men
too much produced or liberated and systemic effects

> 25ng/mL in wommen

2 separate occations

amenorrea,/oligomenorrea galactrea

produced in lactotrope cells

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31
Q

What is hypothalamus?

A
  • The hypothalamus controls theanteriorand posterior pituitary’s release of hormones differently.
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32
Q

substances that stimulate prolactine/etiology of hiperprolactinemia

A 
TRH
striadol
GnRH
AVP
oxytocin
Serotonin
AcH
glutamate
physiological :
stimulation of pezon
sex
sleep
ovulation
pregnancy
neonatal life
ovulation
lactancy
ingesting AAs
exercise
emotional stress and physical
Trauma
qx
Hipoglucemia
IAM
Convulsiones del lóbulo temporal
Síncope
Venopunción
Deshidratación
Dolor

DRUGS

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33
Q

sub that inhibit prolactin

A 
dopamine
opoid
GABA
GAP 
somatostanina, 
.........
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34
Q

first cuase of non tumoral hipoerprolactinemia from drugs

EXAM

A

cause 25-100ng/dl
metoclopramida, risperidona, fenotiazina à >200ng/mL)

if MC change tx -
stop for 3 days , reread levels to see if secondary to drug

Si la medicación no puede ser descontinuada y el inicio de la hiperprolactinemia no coincide con el inicio de la terapia, se recomienda MRI de hipófisis en busca de prolactinoma.

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35
Q

increased prolactin due to hypothalamic damage

A 
tumors
granulomatouse and infiltrative diseases
cranial RT
vascular cause
seccion of tallo

also alterations of hypofisis

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36
Q

hyperprolactinemia from hypothyroidism

A

due to increased TRH –> secrete effect on lactotrope cells (more sensibile)

decrease sensibility of lactrotoope cells to dopamine

increased VIP

decrease in PRL wasting in circulation o aclaramiento renal (hipometabolic state lowers GFR) - more in plasma

hypofisiary hyperplasia (like puberty )

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37
Q

most cells in pituitary are…?

A

????

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38
Q

polyscystic ovary syndrome - PRL

A

hyperandrogen and estrogen –> lots of estradiol which stimulates prolactin liberation

increase number and size of lactotropes

decrease of dopamine hypothalamus

increased transcriptionfor PRL

resistence to dopamine acction

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39
Q

adrenal deisease PRL

A

increased transcription
increased lactotrophe cell differentiation
PRL increased secretion

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40
Q

liver disease PRL

A

cirrhosis decreased hepatic circulation of PRL

increases steroidogenesis - more estrogen/estradiol

decreased hypothalamic dopamine (dad)

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41
Q

Renal disease PRL

A

rests action nof dopamine

resists…..PRL

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42
Q

isiopathic hyperprolactimea

A

microprolactinomas?

20% of cases

MRI cortes

ateration /inactivation of dopamine rec

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43
Q

lesions of thorax wall PRL

A 
toractomy
masectom
trauma
mammoplasty
dermatitis
burns
herpes zoster
breast cyst
nipple piercing

any stimulation of 4,5,6 intercostal nerve increases neuronal afferent stimulation postsynaptic increased serotonin liberation with stimulates TRH –> PRL increase

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44
Q

ectopic production of PRL

A 
hypernefroma
renal adenoCA
bronchogenic CA
uterine fibroma
ovaric teratioma
gonadotroma
ovaric dermoid cyst
Hodgkin linfoma and T cell linfoma

macroprolactinoma and med form before??

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45
Q

MC of hiper PRL

A

increases hypothalamus of dopamine and beta-endorphins

rec of PRL in GnRH cells
down regulation of GnRH (hypogonadism, galactorrea, hirsutism)

decreasd ovarian secretion of estradiol and progesterone (no LH, FSH for steroidogenesis at ovary_

decreased testosterone

decreased 5alfa-reductase (converts dihydro..to testosterone)

  1. Galactorrea: 80% hiperprolactinémicas, 30% hiperprolactinémicos.
  2. Hipogonadismo hipogonadotrópico. Hay ↓FSH, ↓LH, debido a que:
    a. Neuronas de GnRH tienen receptores para PRLà ↓liberación de GnRH.
    b. ↑PRL à ↑DA + ↑β-endorfinas en hipotálamo à ↓liberación de GnRH.
women
Hipoestrogenismo à
¾ Amenorrea / oligomenorrea.
¾ ↓libido. 
¾ ↓lubricación vaginal à Dispareunia
¾ Osteopenia/osteoporosis: ↓densidad ósea (-25% lumbar), irreversible
¾ Irritabilidad
¾ Oleadas de calor.
Infertilidad.
men
Hipoandrogenismo: PRL à ↓actividad 5α-reductasa à ↓dihidrotestosterona. 
¾ Disfunción eréctil.
¾ ↓libido. 
¾ Oligospermia à infertilidad.
¾ ↓volumen eyaculado. 
¾ Ginecomastia.
¾ Osteopenia/osteoporosis.

la mujer.
¾ PRL à ↑producción ovárica de andrógenos y adrenal de DHEA-S (sulfato de dehidroepiandrosterona).
¾ PRL à ↓síntesis hepática de SHBG à ↑proporción de esteroides sexuales libres (biológicamente activos) en plasma.

Presentación clínica
2. Prolactinemia >200ng/mL.
3. Clínica: galactorrea, hipogonadismo hipogonadotrópico, hirsutismo, efecto de masa (neuroftálmicos, hipopituitarismo).

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46
Q

sampling in hiperPRL

A

2 separate occasions
1-2 hour after waking up
discart other causes (meds, liver, preg, renal failure, mammillary stimulation, sex)
macroprolactinemia in asymptomatic px (no galactorrea but elevated levels - sim hormones?)

drugs
1:100 dilution

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47
Q

dx evaluation of hiperprolactimea

A

hipofisary macroadeoma
measure PRL

below 200
1:100 dilution - discart hook effect if above ya tu sabe
if below 200 - pseudoprolactinoma (something else compressing, dopamine e obstructed)

more than 200 - macroprolatinoma1)
Tomar muestra adecuadamente:
¾ 2 muestras separadas por 20-40 minutos >1h después de haber despertado, sin tener sexo (coito, manipulación de mamas) o ejercicio.
¾ Diluir muestra 1:100 para evitar efecto hook.
¾ Excluir mediante historia clínica y examen físico: embarazo, uso de fármacos; mediante laboratorio: hipertiroidismo (T4 libre, TSH), IR (creatininemia), IH (transaminasas y fosfatasa alcalina).
Si nada de lo anterior es evidente o prolactinemia >100ng/mL:
2) MRI de hipófisis antes y después de administrar gadolinio.
¾ Si se confirma adenoma hipofisario à
û Evaluar función hipofisaria
û Campimetría visual computarizada (en particular si es un macroadenoma).
¾ Si no se confirma adenoma hipofisario à hiperprolactinemia idiopática.

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48
Q

tx of hiperprolactinmeia

A

dopamine agonsits
Tx de elección. Se unen a D2 en superficie de lactotropas normales y tumorales y producen inhibición de PRL, como lo haría la DA, restauran función gonadal y causan regresión tumoral en 80-90%. Se deben usar de por vida.
a) Bromocriptina. Aprobada por FDA.
b) Cabergolina. Aprobada por FDA. La más potente y se da 1-2x/semana.
c) Quinagolida.
d) Lisurida.
e) Pergolida.

qx - if px wont take drugs,
1. Tumorectomía transesfenoidal, indicada en:
¾ Intolerancia/resistencia a los agonistas de DA. ¾ No deseo de consumir agonistas DA por largo tiempo.
¾ Crecimiento de prolactinoma a pesar del uso de estos. ¾ Deseo de embarazo por parte de la paciente (aunque la mayoría no crece durante el embarazo: indicación relativa).
¾ Prolactinomas con componente quístico. ¾ Preferencia del paciente.
¾ No mejoría de los campos visuales tras 1-3 meses de agonistas DA

  1. Agonistas de DA. Tx de elección. Se unen a D2 en superficie de lactotropas normales y tumorales y producen inhibición de PRL, como lo haría la DA, restauran función gonadal y causan regresión tumoral en 80-90%. Se deben usar de por vida.
    a) Bromocriptina. Aprobada por FDA.
    b) Cabergolina. Aprobada por FDA. La más potente y se da 1-2x/semana.
    c) Quinagolida.
    d) Lisurida.
    e) Pergolida.
    Tumorectomía transesfenoidal,
  2. Radioterapia hipofisaria. Fallo en tx médico y quirúrgico. 150-200 rads/día, 5x/semana por 5 semanas. Dosis total: 4,500-5,000rads. Alta probabilidad de desarrollar hipopituitarismo.
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49
Q

tx if drugs and qx don’t work for hiperPRL

A
  1. Radioterapia hipofisaria. Fallo en tx médico y quirúrgico. 150-200 rads/día, 5x/semana por 5 semanas. Dosis total: 4,500-5,000rads. Alta probabilidad de desarrollar hipopituitarismo.
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50
Q

2 types of hypothalamic cells

A

hypofisiotropic hypothalamic (liberators and inhibitors)

vs

neurohipofisiary hypothalamic (oxytosin and AVP/ADH)

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51
Q

liberators do what?

A

induce hormonal secretion

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52
Q

hypothalamic liberating hormones

A

TRH –> TSH and prolactin

CRH –> ACTH/corticotropin secretion @ suprarenal gland and proopiomelanocortin peptides (MSH, beta-endorphin)

GnRH –> LH and FSH (gonadotropins) @ genitals and Prolactin

GHRH/somatocrinin –> GH/somatotropin in pulses @ all organs

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53
Q

GH secretion is increased by

A

exercise
starvation (hypoglycemia)
Sleep

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54
Q

relationship between dopamine prolactin and TRH

A

Prolactin is under tonal dopamine inhibition, andexcess TRH levels suppress dopamine. Thus, prolactin levels will increase as dopamine decreases.

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55
Q

hypothalamic nucleus/region for TRH

A

paraventricular (medial portion)

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56
Q

hypothalamic nucleus/region for CRH

A

paraventricular (anterior portion)

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57
Q

hypothalamic nucleus/region for GnRH

A

arcuate-preoptic (ant)

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58
Q

hypothalamic nucleus/region for GHRH

A

arcuate

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59
Q

Hypopfisis cell populations that produce for TSH

A

tirotrope cells

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60
Q

Hypopfisis cell populations that produce

Prolactin

A

lactotrope cells

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61
Q

Hypopfisis cell populations that produce

ACTH

A

corticotrope cells

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62
Q

Hypopfisis cell populations that produce

FSH and LH

A

gonadotrope cells

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63
Q

Hypopfisis cell populations that produce

GH

A

somatotrope cells

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64
Q

melanocyte inhibiting factor inhibits

A

release of MSH

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65
Q

which are the hypothalamic inhibiting hormones

A

dopamine (DA) - prolactin release inhibiting hormone - inhibits liberation of Prolactin and lactropes and TSH

somatostatin (SS) - inhibits liberation of PRL, TSH, GH

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66
Q

region/hypothalamic nucleus for dopamine

A

arcuate

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67
Q

region/hypothalamic nucleus for somatostatine

A

supraquiasmatic periventricular region (ant)

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68
Q

lactancy hormone that stimulates milk ejection

A

oxytocin

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69
Q

what do AVP/ADH do

A

stimulate reabsorption of water

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70
Q

non endocrine functions of the hypothalamus

A

○ Thirst, temperature, sexual desire, etc thorugh hypothalamic nuclei

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71
Q

anterior pituitary hormones are produced by what

A

parvocellular hypothalamic neurons

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72
Q

anterior pituitary hormones

A 
ACTH
LH, FSH
GH
TSH
Prolactin
MSH
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73
Q

weight of pituitary gland

A

0.5-0.9gr

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74
Q

blood flow of pituitary gland

A

very vascularized

0.8ml/gr/min

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75
Q

Situations in which Pituitary can double size:

A
  • Pregnancy
  • Puberty (especially girls)
  • Primary hypothyroidism
  • Primary hypogonadism
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76
Q

% gland of adeno vs neurohipofisis

A

75% adeno

25% neuro

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77
Q

embryological origin of adenohipofifis

A

Bolsa de Rathke (evaginación del techo de la orofaringe primitiva).

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78
Q

embryological origin of neurohipofisis

A

Evaginación del hipotálamo ventral y del piso del 3° ventrículo

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79
Q

irrigation of adenohipofisis

A

Arteria hipofisaria superior + sistema porta hipotalámico (0.8ml de sangre/g de tejido)

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80
Q

irrigation of neurohipofisis

A

Arteria hipofisaria media + Arteria hipofisaria inferior

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81
Q

Venous drainage of pituitary glland

A

cavernous senos –> sup and inf petrous senos –> yugular veins –> SVC –> RA

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82
Q

pituitary cell types

A
  • Nulas - don’t secrete hormones, do secrete NTs

* Secretory - classified in 5 types

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83
Q

cx of somatotropic cells

A

@ lateral portions
acidofiles
50%

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84
Q

function of somatotropic cells in skeletal muscle

A

increases muscle mass
increases AA capitation
decreases proteolysis
decreases glucose capitation (CONTRAREGULATOR) –> hyperglucemiant

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85
Q

function of somatotropic cells in adipose tissue

A 
decrease capitation of glucose
increase lipolysis (degradation of TGs/FAs) -increases activity of hormonosensible/GH lipase
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86
Q

function of somatotrpic cells in liver

A

increase protein synthesis
increases gluconeogenesis (formation of glucose from lactate, pyruvate, glycerol, AAs)
increases IGF-1 synthesis (somatomedine C) –> which in turn increases bone lineal growth , muscle and visveral growth

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87
Q

what is IGF-1

A

a cofactor that helps GH functions/efficacy = NECESSARY

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88
Q

cx of lactotrpic cells

A

acidofiles
posterior
10-25%

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89
Q

function of lactotropic cells

A

in mammary glands increase milk production during lactancy

decreases GnRH (FSH LH) –> amenorrea

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90
Q

cx of corticotropic cells

A

basophils

15-20%

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91
Q

function of corticotropic cells

A

@ adrenal cortex
increase growth, development, vascularization
increase LPL capitation which increases synthesis and adrenal secretion of glucocorticoids (cortisol) and sex steroids (androgens and estrogens)

increases melanin synthesis

stimulate mineralocorticoids, sex hormones

increase CyP450 : cholesterol –> pregnenolone

decrease GnRH and GH

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92
Q

cx of gonadotropic cells

A

basophiles
anterior
10-15%

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93
Q

function of LH in women

A

theca cells: make androgens - testosterone and androstenedione by theca cells in ovaries that by diffusion pass to granulouse cells (through aromatase converts androgens to estrogens)

ovaric follicle: rupture causing ovulation

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94
Q

function of LH in men

A

Leydig intersticial cells of testicle: synthesis and secretion of testosterone

decreases hypothalamic secretion of GnRH and pituitary secretion of FSH and LH by RAN

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95
Q

function of FSH in w0men

A

acitmates aromatase

androstenedione –> estrone (E1)in adipocytes

testosterone –> estradiol (E2)
growth and follicular development
dominant foliculo selection
production of inhibine by granous cells in ovaries which cause less secretion of FSH from pituitary

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96
Q

estrogen byexcellence

A

estradiol

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97
Q

function of FSH in men

A

proliferation of seminiferous tubes

principal determinant of testicular volume

spermatogenesis

production of inibine thru sertoli cells in the testicle –> decreases pituitary FSH secretion

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98
Q

cx of tirotropic cells

A

anterolateral
anteromedial
10%

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99
Q

function of tirotropic cells in thyroid

A

stimulate vascularity and thyroid growth

stimulate production of T3 and T4

morphological changes causing pseudopod formation increases iodine trapping and bone reabsorption
(that’s why hyperthyroidism causes early osteoporosis)

decreases colloid, fotitias of IC colloid

stimulates tiroglobulin hydrolysis

  1. Iodine metaoblism phases stimulation
  2. Increases mRNA of tiroglobulin and thyroid peroxidase
  3. Increases 5’ deyodase I (T4–>3 peripheral)
  4. Glucose captation, O2 consumption and CO2 production +
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100
Q

hormones that share alfa subunits

A

LH
FSH
TSH

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101
Q

80% of somatomelina C / IGF-1 produced where?

A

liver

but it acts in the muscle

=

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102
Q

how can IGF-1 lead to microsomal children

A

mothers pancrease stimulates insulin also stimulating IGF-1

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103
Q

which homones are glucoproteins

A

TSH
LH
FSH
share homology

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104
Q

which are somatotropins

A

PRL

GH

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105
Q

irrigation of hypothalamus

A

thru superior hypophyseal artery

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106
Q

TFs involved in development of adenohipofisary cells

A
  1. POU1F1 (Pit-1): lactotropas, somatotropas y tirotropas.
  2. Prop-1: gonadotropas. (promiscuous)
  3. T-pit: corticótropas.
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107
Q

TSH also stimulates

A

estrogen

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108
Q

ADH nucleus

A

is a nonapeptide that is synthesized predominately in thesupraoptic nucleusof the hypothalamus, and secreted from theposterior pituitaryupon stimulation of these cell bodies.

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109
Q

primary stimulus for ADH secretion

A 
The primary stimulus for antidiuretic hormone (ADH) secretion is anincrease in serum osmolarity. A loss of intracellular water from hypothalamic osmoreceptor neurons bathed by hyperosmolar blood will stimulate ADH release. Other factors thatincreaseADH secretion include:
	• Pain/stress
	• Hypoglycemia
	• Nausea
	• Volume contraction
	• Nicotine and opiates
	• Angiotensin II
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110
Q

2 primary functions of ADH

A
  • Regulate serum osmolarity
    • Maintain (increase)blood pressure
    Antidiuretic hormone alsoincreases the permeabilityof the inner medullary collecting duct to urea. This increases the osmotic gradientcreated by the countercurrent multiplier, facilitating the production ofconcentrated urine(i.e. increasing urine osmolarity).
    - Increases water reabsorption in renal colector tubules
    - Modualtes BP by increasing SM arterial tone
    Stimulates liberation of ACTH by hypofisary corticotrope cells
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111
Q

oxytocin nucleus

A

Oxytocin is a nonapeptide that is primarily produced by theparaventricular nucleiwithin thehypothalamus, and secreted from the posterior pituitary

112
Q

how does oxytocin travel to posterior pituitary

A

Like ADH, oxytocin travels to the posterior pituitary via carrier proteins calledneurophysins.

113
Q

stimulus for oxtocin secretion

A

The major stimulus for oxytocin secretion issuckling. Other positive stimuli includedilation of the cervixandorgasm, Bconfidence , memory, conection and empathy.

114
Q

effects of oxytocin

A

The primary effects of oxytocin aremilk ejection@ lactation anduterine contraction @ labor.

115
Q

adverse effects of oxytocin

A
  • Hyponatremia and seizures(due to anti-diuretic properties similar to antidiuretic hormone)
    • Subarachnoid hemorrhage
    • Uterine rupturein pregnant patients
116
Q

irrigation of hypothalamus

A

MCA of ICA

117
Q

function of thyroid hromones

A 
Thyroidhormones:
	• induce central nervous system maturation during growth
	• increase basal metabolic rate
	• increase cardiac output
	• promote bone growth
118
Q

what stimulates TRH

A

cold

119
Q

what inhibits TRH

A

stress

120
Q

what inhibits TSH

A

DA, SS, cortisol, GH, T3 y T4 thyroxine

121
Q

TSH does what

A

stimulates T3 and T4 secretion from thyroid and - neg feedback to decrease TRH and TSH

@ thyroid increase growth and vascularity, capitation of I- inorganic,
increases oxidation of Inorganic I- creating more reactive yodant species (EIRs)

4) ↑Incorporación de EIR en residuos tirosina de la tiroglobulina[4] à ↑formación de yodotirosinas: MIT[5] y DIT[6].

increases formation of thyroid peroxidase

6) ↑Acoplamiento de yodotirosinas: MIT + DIT = T3, DIT + DIT =T4.
7) ↑formación de la gota de coloide.
8) ↑Liberación de T3 y T4.

122
Q

what increases TSH

A

TRH and estradiol

123
Q

difference between types of hypothyroidism

A

a. Primary: damage to thyroid gland: ↑TSH + ↓T3 y T4.
b. Central: ↓TSH (o inapropiadamente normal) + ↓T3 y T4.

Secundary: damage/disfunción of tirotrpic cells that makeTSH.

Terciario: damage /disfunción to hypothalamic neuronas that produce TRH.
2° y 3° son bioquímicamente indistinguibles.

	- Pirmary = @ thyroid gland
		○ High tsh
		○ Low T4
	- Secondary
		○ Both low
	- Tertiary
		○ Both low
124
Q

90% of T3 in circulation comes from

A

T3 circulante (forma biológicamente activa) se deriva de la T4.

125
Q

feedback of increased cortisol

A

less hypothalamic secretion of CRH and hypofisary secretion of ACTH (por RAN)

126
Q

what increases ACTH

A

CRH and AVP

Stress, trauma , int. qx, infections, hypoglicemia (similar to GH contraregulatory hormones)–> ACTH and catecolamines @ adrenal gland

127
Q

cortisols effect on hormones

A

AVP, ↓CRH, ↓ACTH, ↓GnRH.

128
Q

what is cortols made from

A

cholesterol and needs cytochrome p450

129
Q

cx of cortisol

A
  • Catabolic - hyperglucemic
    • Anabolic only I liver –> + cytocrome p450
    • Antiinflammatory
    • Immunosuppressor
130
Q

different types of hypoadrenalism

A

c. Primary (Addisons disease): damage to adrenals ↑ACTH + ↓cortisol + hiperpigmentación of skin and mucus due to RAN deficit).
d. Central: ↓ACTH (o inapropiadamente normal) + ↓cortisol.

Secundary: damage/disfunción in corticotropas cells that produce ACTH

Terciary: damage/disfunción hipotalámic neurons that produce CRH.

Primary Adrenal Insuff

- ACTH up
- Low cortisol

Secondary @ corticotrope cell lesion
- Both down

Hypofisis trurmor of ACTH
- Both up

Adrenal tumor that secretes cortisol

- Low ACTH
- High cortisol
131
Q

circadian rhythm of cortisol secretion

A
  • Different quantitites @ different times
  • máxima @6:00-8:00am;
  • mínima @12:00am.
132
Q

how to know if there is a loss of cortisol circadian rythm

A
  • Para determinar si hay pérdida de este ritmo circadiano (propio del Síndrome de Cushing Endógeno) se mide cortisolemia @8:00am (5-25μg/dL) y @4:00pm (suele estar al 50% respecto a 8:00am, es decir, 2.5-12.5μg/dL)
133
Q

GnRH pulse

A

Hipotálamo produce GnRH en pulsos de 60/90-120 minutosà sistema porta va a gonadotropas adenohipofisarias à ↑FSH (end) y ↑LH. (beginning)

134
Q

different types of masculine hypogonadism

A

primary (hypergonadotropic) damage , testicular dysfunction - ↑FSH + ↑LH + ↓testosterona + ↓inhibina.

Central (hypogonadotropic) - ↓FSH + ↓LH + ↓testosterona + ↓inhibina
…secondary - damge corticotropes that produce FSH and LH
…tertiary - damage to hypothalamic neurons that produce GnRH

135
Q

aromatase

A
  • Testosterone to estradiol (E2) -↓hipotalámic secretion of GnRH and pituitary FSH y LH (por RAN),

when secreción is >200pg/mL during >40-50h will be ↑secreción hipotalámica of GnRH (por retroalimentación positiva [RAP]) à↑↑↑LH (pico de LH) à ovulación.
○ Estradiol negative feedback vs LH, FSH, GnRH

- Androstenediona à estrona (E1).  ¾ Also pulsatilie
- If > 200mg/dl > 40-50hr --> negative feedback - more than this time --> postiive feedback --> dominant follicular rupture --> primary oocyte = OVULATION ¾ Andrógenos à ↓secreción hipotalámica de GnRH e hipofisaria de FSH y LH (por RAN). ¾ Inhibina?
- Can only inhibit FSH - not LH
136
Q

feminine hypogonadism

A
  1. Primary (hipergonadotrópic): damage disfunción of ovary: ↑FSH + ↑LH + ↓estradiol + ↓inhibina.
  2. Central (hipogonadotrópico): ↓FSH + ↓LH + ↓testosterona + ↓inhibina

Secundario: damage/disfunción en corticotropas productoras de FSH y LH.

¾ Terciario: damage/disfunción de hipotalámic neurons that produce GnRH.

137
Q

where is the Kiss1 gene

A 
in hypothalamus (núcleos anteroventral periventricular [AVPV] y arcuato), placenta and oncocytes --> produces 145 AA protein that is cleabed into 4 peptides: (Kisspeptines - ligands of Kiss1-R (GPR54 linked to G protein expressed in productor neurons of GnRH)
		○ Discovered in philadelphia - hersheys kisses
- Kp54 (metastine), Kp14, Kp13, Kp10
138
Q

function of kisspeptins

A

Sex steroids increase Kiss1 gene expresion in AVPV nucleus and degrease it inn arcuate nucleus –> LH peak

Stimulate GnRH liveration

Initiate puberty
¾ Regulation of ovulation (neuroendocrine)
¾ Initiation, maintenance, and regulation of fertility

139
Q

3 circulation forms of prolactin

A
  1. native PRL (de 23.5 kDa). the one that is normally secreted in 6-14 pulsos during the day(60% while sleeping).
  2. Big-PRL (de 50kDa).co secreted in small quantities
  3. Big-Big-PRL (de 150kDa). also cosecreted in small quantities
140
Q

macroprolactina

A

all 3 PRL + 1 IgG

immunoreactive

low biological activity

141
Q

dx macroprlactinemia

A

measure prolactin precipitación inpolietilenglicol o cromatografía . gel

142
Q

when to suspect macroprolactinemia

A

Suspect macroprlactinemia? - fem, high prolactin, no drugs that stimualte , no galactorrea - at expense of macroprolactins, also inhibit GnrH

in asymptomatic px with hyperprolactinemia

143
Q

inhibitors of PRL secretion

A 
Dopamina[1][2]
Somatostatina
GABA (ácido γ-aminobutírico).
GAP (péptido asociado a GnRH)
Calcitonina.
144
Q

stimulators of PRL secretion

A 
Estradiol[3]
TRH
GnRH
AVP
Oxitocina
VIP
Serotonina
Bombesina
Galanina
Histamina
Neuropéptido Y
Sustancia P
Angiotensina II
Neurotensina
Péptido histidina-metionina
145
Q

Physiological factors that liberate PRL (date night)

A 
stimulación de las mamas
Coito, especialmente en mujeres
Sueño
Ovulación
Embarazo
Vida neonatal
Lactancia
Ingesta de aminoácidos
Ejercicio
146
Q

ACTH does what @ adrenals

A

increases growth and development of adrenal cortex

increases adrenal capture of lipoproteins (cholesterol is substrate for adrenal steroidogenesis)

increases activity for CyP450scc, enzyme that transforms (cutting lateral chain) cholesterol –> pregnenolone

increases stimulation of MSH alfa-R –> which increases synthesis of melanin by melanocytes

147
Q

action of kisspeptines in hypothalamus

A

increases secretion of GnRH to begin puberty
neuronendocrine control of ovulation

initiation, maintenance, metabolic regulation of fertility

148
Q

Prolactin function

A

stimulates production of maternal milk during latency

149
Q

differentiating types of hyperthyroidism

A 
Hyperthyroidism
	- Primary
		○ Low TSH
		○ High T4
	- With levated TSH and T4
150
Q

Hipergonadotropic Hipogonadism

A
  • High LH and FSH

- Low estradiol , low testosterone

151
Q

Hipogonadotropic Hipogonadism

A
  • Both low
152
Q

cx of hypofisary adenoma

A
  • Benign tumors of hypofisial gland
    • 10-15% of IC neuplasias
    • 3rd cause + Fc
    • 90% of hypofisial neoplasias
153
Q

% of hipofisary adenomas that are prolactinoma

A

45%

			□ Inhibit GnRH can call a combined syndrome
154
Q

epi cx of prolactinoma

A

○90% Micro in women, 60% macro in men
○ 3rd decade women
○ Men older

(Son 8 veces más frecuentes en mujeres y se suelen diagnosticar entre 20-40 años.

155
Q

MC of prolactinoma in men

A

disfunción eréctil, disminución volumen testicular y del eyaculado, oligospermia, ginecomastia., glactorrea, low libido, infertility, azoospermia

156
Q

what is prolactinoma

A

○ Tumor of lactotrope cell line mostly in adenohipofifsis ‘

	○ Cosecretion of hormones and PRL level  hyperprolactinemia --> decreased secretion GnRH --> decreased LH and FSH
157
Q

pseudoprolactinoma

A

effecto de tallo - too much prolactin from compression of tallo

macroadenomas even if they aren’t prolactinomas cause hyperprolactinemia < 200ng/mL due to effecto de tallo

158
Q

MC of prolactinoma in women

A

amenorrea, oligomenorrea, disminución lubricación vaginal, dispareunia, oleadas de calor, osteopenia/osteoporosis. Falla en menarquia, regular period with short lutea fase, infertility, low libidio, galactorrea
i. Inhhibition of GnRH

159
Q

MC of prolactinoma common to both sexses

A

decresed libido, infertlility e. Reduction of bone mass and osteoporosis

160
Q

mass effect MC of prolactinoma

A

i. Loss of vision
ii. Headache
iii. Convulsions
iv. Hydrocefaly
v. Unilateral exoftalmo
vi. Paralysis of craneal nerves

	○ Neurological/oftalmological
	○ Headache, IC HTN, convulsions, apoplejia, compression of quiasm
161
Q

Hook Effect - de cancho

A

results in elevated PRL levels which interfere with immunoradiometric ensayo and arrojan a abnormally low cifra (20-200ng/ml) what would lead one to believe its a nonsecreting macroadenoma

to aboid this sample should be diluted 1:100 if there is a pituitary macroadenoma and prolactinemia < 200

if its still in 20-200 range its a pseudo prolactinoma

i. >200ng/dl
ii. Interference with radioimmunoensayo
iii. Low PRL

162
Q

before samplimg for prolactinoma what is important to consider

A

i. Take prolacin 1-2hr at wake up to aboid false +
ii. 2 separate elvated tests
iii. Discard hyperprolactinemia (pregnancy meds 25-100ng/ml, hypothyroidism, renal insuff, or hepatic insuff)

163
Q

hipofisial adenoma 20%

A

somatotropoma
○ High GH
○ Gigantism , acromegaly

164
Q

hipofisial adenoma 10-12%

A

corticotropoma ○ High ACTH
○ Cushingnhibit GnRH
® So these we cause combined sydrome

165
Q

hipofisial adenoma 1-2%

A

tirotropoma ○ High TSH

○ Bocio and hyperthyroidism

166
Q

hipofisial adenoma 15%

A

gonadotropoma

	○ High FSH, LH
	○ No clinical syndrome
167
Q

hipofisial adenoma 5-10%

A

tumor of celulas nulas

168
Q

what is hypopituitarism

A

○ Low hormonal secretion (2 or more)
○ Can be total

Syndrome –> decrease/absence of 1 or more hormones of pit. Gland

169
Q

mechanisms for hypopituitarism

A 
§ Tumor compresses hypothalamus - decreasing
			§ Compressing pit. Gland
			§ Compression of THH
			§ Decrease of pit. Irrigation
			§ Necrosis of hipofisis
170
Q

what is combined syndrome

A
  • Combined syndrome of hypersecretion of 1 hormone associated to decrease in secretion of 1 o more adenohipofisial hormones
171
Q

microadenoma

A

< 10mm

172
Q

what is corticotropoma

A

hypersecretion of ACTH –> hyperproduction of adrenal cortisol –> decreased GnRH –> decreased LH, FSH, GH

173
Q

examples of microadenomas

A

prolactinoma

corticotropoma

174
Q

macroadenoma

A

> 10mm
○ More in adults

	○ Mechanical compression of hypothalamus, hypofisis, infundibulo, portal vessels --> focal pituitary necrosis
	○ (craniofaringioma in kids)
175
Q

neurological MC of hypopituitarism??

A
  1. Cefalea. 4. Epilepsia del lóbulo temporal. 7. Alteración de conciencia (somnolencia, estupor y coma).
  2. Parálisis de NC III, IV, VI (compresión senos cavernosos). 5. Rinorrea de LCR (si destruye piso de silla turca). 8. Defectos de campos visuales (hemianopsia bitemporal; por compresión del quiasma óptico).
  3. Hidrocefalia obstructiva (compresión 3° ventrículo). 6. Obstrucción vía aérea nasal. 9. Disminución agudeza visual y ceguera (compresión del nervio óptico y de las cintillas).
176
Q

hipofisial apoplejia

A

Spontaneous Infarto/hemorrage of hypophysary adenoma (10-15%) clinically in 66%.

177
Q

local consequences of hipofisial apoplejia

A

Signos de irritación meníngea: cefalea, Kernig, Brudzinski.
Parálisis ocular, diplopía, proptosis, defectos de campos visuales.
Alteración de la conciencia
Alteración de autorregulación simpática
Dolor facial
Hidrocefalia obstructiva

178
Q

systemic consequences of hipofisial apoplejia

A 
Hipopituitarismo:
1. Insuficiencia suprarrenal secundaria aguda: hipotensión y choque.
2. Hipotiroidismo central.
3. Hipogonadismo secundario.

Silla turca vacía
179
Q

wermer syndrome

A

(Múltiple Endocrine Neoplasia 1, las 3 P). HAD, coexistence of 2/3of the following:
1. Pituitary adenoma.
a. In 60% of NEM1, generally prolactinomas (60%), somatotropomas y corticotropomas, y generally are macroadenomas.
2. Primary Hiperparatiroidism (from hiperplasia or multiple adenomas).
a. Initial clínica-bioquímica presentation.
b. 60-90% of NEM1.
3. pancreáticos y duodenales neuroendocrinos tumors: insulinomas, glucagonomas, gastrinomas, VIPomas, somatostatinomas.

180
Q

gigantism vs acromegaly

A

excessive secretion of GH that if before closure of hipofisis is gigantism (prominent lineal growth of long bones)

if after closure = acromegaly (exaggerated growth of bland tissues, bones of hands, feet, mandible, internal viscera)

181
Q

etiology of gig/acro

A

somatotropoma 1. Somatotropoma productor de GH (99%). 65% son macrosomatotropomas.

  1. Secreción ectópica de GH: in pancreatic and lung cancer
3. excessive secretion of GHRH
Eutópica: gangliocitoma o hypothalamic coristoma 
. 
b. Ectópica: 
Tumores islotes pancreáticos.
	¾ Carcinoides bronquial, intestinal o tímico.
	¾ CA microcítico de pulmón.
	¾ CA medular de tiroides.
	¾ Feocromocitoma.
	¾ Adenoma adrenal.
182
Q

general MC of gig/acro

A 
Fatiga 
Intolerancia al calor
Ganancia de peso
Diaforesis
Hiperhidrosis palmoplantar
183
Q

osteomegalia in gig/acro

A

Prognatismo: aumento de espacios interdentales maloclusión.
Dedos engrosados y elongados (acropaquia)[1].
Rasgos faciales grotescos[2].
Crecimiento de manos y pies[3]
Tórax en tonel[4]

184
Q

Dermatolomegalia ig/acro

A

Engrosamiento cutáneo por depósito de glucosaminoglucanos.
Hipersecreción sebácea: piel oleosa, acné, quistes sebáceos.
Hipertricosis (50%). Cutis verticis gyrata[6]
Hiperpigmentación (40%) Papilomas
Acantosis nigricans[5] (10%) Moluscos fibrosos

185
Q

organomegalia acro/gig

A 
Laringomegalia y apnea del sueño
Parotidomegalia
Nefromegalia
Hepatomegalia
Macroorquidismo

Cardiomegalia (15%) asociada a ICC/ cardiomiopatía hipertrófica.
186
Q

endocrinological metabolopathies in acro/gig

A 
HTA (25%)
Intolerancia a glucosa (50%)
DM (25%)
Hiperfosfatemia[7]
Hipocalcemia por hipercalciuria[8]
Nefrolitiasis
Hipopituitarismo[9]
Hiperprolactinemia[10]
187
Q

neuropathy in acro/gig is due to

A

comprisive effect

188
Q

neuroatropathies in acro/gig

A

Neuropatía periférica por compresión de nervios periféricos por osteomegalia.
Compresión de médula espinal.
Síndrome del túnel carpiano
Artropatía.

189
Q

dx of gig/acro

A

Medir IGF-1 (somatomedina C, (+: >1ng/mL) o GH (+: >1ng/mL) en sangre a los 0, 30, 60, 90, 120 minutos.

2) MRI de hipófisis con gadolinio à
a. adenoma hipofisario: evaluación hormonal + campimetría visual computarizada
b. No adenoma hipofisario: GHRH en plasma, MRI de tórax, TAC de abdomen.

190
Q

tx of gig/acro

A

1) Extirpación transesfenoidal. Cura 70% de microadenomas y 50% de macroadenomas.
2) Análogos de la somatostatina: lanreótido, octreótido. Inhiben síntesis de GH hasta en un 90% por somatotropas y reducen tamaño tumoral.
3) Pegvisomant. Bloquea unión a GH-R.
4) Agonistas dopaminérgicos: bromocriptina, cabergolina, quinagolida, lisurida y pergolida a dosis mayores que las usadas para prolactinomas.
5) Radioterapia hipofisaria, con el riesgo de producir hipopituitarismo. Tx dura 6 meses a 20 años, pero normaliza los niveles en 90% de casos.

191
Q

Etiology of CUshing syndrome

A

deberse a:
¾ Exógeno. Forma más frecuente. Por el uso a dosis excesivas o prolongadas de glucocorticoides (estados inflamatorios crónicos).
Endógeno. Por tumor productor de ACTH,

192
Q

endogenous causes of Cushing are classified into

A

ACTH dependent (excess produced due to tumor which increases cortisol production by suprarenals)

and ACTH independent (excess cortisol produced by adrenal hyperplasia/tumor)
Cortisol causes RAN on ACTH

193
Q

ej of ACTH dependent causes

A

§ Corticotropoma hipofisario (“Enfermedad de Cushing”). 68% de casos de síndrome de Cushing endógeno en adultos.
Secreción ectópica de ACTH por tumor extrahipofisario. 12% de casos de síndrome de Cushing endógeno en adultos.

194
Q

acute presentation of ACTH dependent causes of cushing

A

CA de pulmón 75%.

195
Q

chronic presentation cushing (ACTH dependent)

A

v Carcinoides bronquial, intestinal o del timo.
v Tumores de células de los islotes pancreáticos, especialmente insulinomas.
v CA medular del tiroides.
v Feocromocitoma.
§ Síndrome de secreción ectópica de CRH por tumor extrahipotalámico. <1% de los casos de síndrome de Cushing endógenos en adultos.
v CA medular del tiroides.
v Carcinoide bronquial.
v CA de próstata metastásico.

196
Q

ej of ACTH independent causes of cushing

A

§ Adenoma/CA productor de cortisol.

§ Hiperplasia micronodular/macronodular.

197
Q

general MC of cushing

A

Obesidad centrípeta
Cefalea
Psicopatías
Miastenia proximal

198
Q

cutaneuous MC of cushing

A 
Estrías purpúricas >1cm de diámetro @ abdomen, flancos, MS, MI.
Adelgazamiento cutáneo.
Fragilidad capilar (equimosis o moretones espontáneos o por traumas mínimos)
Hiperpigmentación (en ACTH dependiente).
Cara redonda.
Acné.
Hirsutismo.
Plétora
Acantosis nigricans
Micosis
Pobre cicatrización
199
Q

endocrinological metabolic MC of cushing

A 
Alcalosis hipocalémica
Retraso de crecimiento óseo
Oligomenorrea/amenorrea.
Alteración libido/ disfunción eréctil.
HTA (80%)
Intolerancia a glucosa y DM
Hipercalciuria con Nefrolitiasis

Leucocitosis neutrofílica.
Osteopenia/osteoporosis.
Hiperlipidemia.
Poliuria.

200
Q

dx of cushing

A

confirm biochemically dx of cushing (confirm endogenous hiperorisolism)

distinguish between ACTH dependent vs independent

distinguish between corticotropoma vs ectopic secretion

201
Q

how to biochemically confirm cushing

A

a. Cortisol libre en orina de 24h 2-4x mayor del límite superior.
b. Prueba de Nugent: supresión con 1mg de dexametasona:
¾ 1° día de la prueba: 1mg VO de dexametasona a las 11pm.
¾ 2° día de la prueba: medir cortisolemia @ 8am y si es <1.8 μg/dL se excluye.
c. Medir cortisol salival a las 11pm: >145 ng/dL (>4nmol/L).
d. Cortisolemia >1.8 μg/dL @12nm con paciente dormido (no tiene aplicabilidad clínica).
e. Prueba de dexametasona-CRH.

202
Q

how to distinguish between ACTH dependent vs independent

A

Determinar ACTH en plasma:
a. ACTH bajo à ACTH independiente à hacer TAC de suprarrenales.
ACTH normal (10 pg/mL) /alto à ACTH dependiente

203
Q

how to distinguish between corticotropoma and ectopic secretion

A

MRI de hipófisis con gadolinio à (neg) à MRI de tórax + TAC de abdomen + perfil hormonal:
¾ Insulinemia à insulinoma.
¾ Catecolaminas en suero y orina de 24h + metanefrinas à feocromocitoma.
¾ Ácido 5-OH-indol-acético en orina de 24h à tumor carcinoides.
¾ Calcitonina à CA medular de tiroides.

204
Q

tx for cushing

A
  1. Extirpación transesfenoidal. Cura 80%, 10-30% tiene recurrencia à 30-50% no son curados.
  2. Radioterapia hipofisaria. 40% son curados (85% si son <18años). El 60% no es curado pero está protegido contra el síndrome de Nelson (crecimiento excesivo de un corticotropoma + defectos de campos visuales + hiperpigmentación cutánea [cuando tx inicial es adrenalectomía bilateral])
  3. Mitotane (adrenolítico: destructor de adrenales) + inhibidor de la síntesis adrenal de cortisol. 80% se cura.
  4. Inhibidores de enzimas adrenales de la síntesis del cortisol (ketoconazol, metirapona).
  5. Adrenalectomía bilateral total.
205
Q

10% of prolactinomas cosecrete

A

GH

206
Q

cx of macroprolactinoma in men

A

estos producen prolactinemia >200ng/mL).

207
Q

dx evaluation of prolactinoma

A

1) Tomar muestra adecuadamente:
¾ 2 muestras separadas por 20-40 minutos >1h después de haber despertado, sin tener sexo (coito, manipulación de mamas) o ejercicio.
¾ Diluir muestra 1:100 para evitar efecto hook.
¾ Excluir mediante historia clínica y examen físico: embarazo, uso de fármacos; mediante laboratorio: hipertiroidismo (T4 libre, TSH), IR (creatininemia), IH (transaminasas y fosfatasa alcalina).
Si nada de lo anterior es evidente o prolactinemia >100ng/mL:
2) MRI de hipófisis antes y después de administrar gadolinio.
¾ Si se confirma adenoma hipofisario à
û Evaluar función hipofisaria
û Campimetría visual computarizada (en particular si es un macroadenoma).
¾ Si no se confirma adenoma hipofisario à hiperprolactinemia idiopática.

208
Q

psychopharmacological drugs that cause hyperprolactinemia

A

drugs
psychodrugs - decrease tono hypothalamic of dopamine
Fenotiazinas (40-90%, clorpromazina y demás)
Butirofenonas (haloperidol y demás, 40-90%)
Risperidona (100%).
Antidepresivos (IMAO, tricíclicos, IRSS)
Benzodiacepinas
Sulpirida
Amoxapina

209
Q

antiHTN drugs that cause hyperprolactinemia

A 
Antihypertensives
Metildopa y reserpina (disminuyen producción DA)

Verapamilo
Clonidina
Labetalol
Atenolol
210
Q

antiemetics that cause hyperprolactinmia

A 
Antiemetics
Metoclopramida
Domperidona
Cisaprida 

Bloquean receptores D2 de DA en lactotropas
211
Q

hormonal prepared drugs that cause hyperprolactinemia

A 
hormonal preps
Estrógenos. Disminuyen tono dopaminérgico, aumentan # y tamaño de lactotropos y aumentan síntesis de PRL.
AO	GABA
Progesterona	Serotonina (5-HT)
Testosterona	Noradrenalina (NE)
Endorfinas	TRH
212
Q

toxic drugs that cause hyperprolactinemia

A 
narcoticsCocaína
Morfina y heroína
Anfetaminas
Metadona
Nicotina
Cerveza
Codeína
213
Q

antihistaminic H2 drugs that cause hyperprolactinemia

A

H2 histamine blockersCimetidina

Ranitidina

214
Q

Miscellanious drugs that cause hyperprolactimeia

A 
miscelanious
Inhibidores de proteasas (SIDA)
Fenitoína (anticonvulsivante)
Isoniazida (antituberculoso)
Piridostigmina (colinérgico)
Medroxalol (antiadrenérgico)
215
Q

causes of hyperprolactinemia that are related to damage of hypolathamus or infundible

A 
Tumores:
a. Craniofaringiomas.
b. Germinomas.
c. Meningiomas
d. Metástasis a hipotálamo.
e. Extensión supraselar de AH
Enfermedades granulomatosas
Enfermedades infiltrativas
Radioterapia craneal
Vasculopatías.
Sección infundibular
216
Q

causes of hypofisiopathy that are related to hipofiospathy

A

Prolactinomas (AH más frecuente). En mujeres suelen ser micro (90%, 100-200ng/mL) y en hombres macro (60%, >200ng/mL). 8x más frecuente en mujeres, edad de dx más frecuente: 20-40 años.

Macro-AH, por “efecto de tallo” (<200ng/mL).
Hipofisitis linfocítica.
Quiste intraselar.
Quiste de hendidura de Rathke.
Silla turca vacía
Acromegalia (50% de somatotropomas coproducen PRL

217
Q

causes of hyperprolactinemia associated with primary hipothyroidism

A

Produce híper-PRL en 10-40%. Se da por:

  1. ↑TRH hipotalámica à ↑PRL
  2. ↑sensibilidad a TRH de lactotropas
  3. ↑VIP à ↑PRL.
  4. ↓DA hipotalámica
  5. ↓metabolismo PRL à ↓eliminación PRL
218
Q

causes of hyperprolacinemia associated with polycystic ovary

A

Produce híper-PRL en 10-30%. Estado hiperandrogénico o hiperestrogénico (ver atrás)

219
Q

causes of hyperprolactinemia associated with organ failure

A

Suprarrenal: ↓cortisol à ↑expresión gen PRL.
Renal: produce híper-PRL en 20-75%. ↓depuración.
Hepática: Produce híper-PRL en 5-20%. ↓depuración hepática, acumulación de estradiol.

220
Q

causes of prolactinemia associated with thoracic wall , medular lesions

A

Toracotomía, mastectomía, traumatismo, mamoplastía, dermatitis, quemaduras, herpes zoster, brassiere ajustado, quiste mamario, mesotelioma, esofagitis, piercings en pezones, lesión, cirugía o tumor de médula espinal.
Por estimulación nervios costales 4°-6° produce galactorrea por estimulación del SNA.

221
Q

causes of prolactinemia associated with ectopic prodcution

A 
CA broncogénico (secreción VIP)
Hipernefroma
AdenoCA renal.
Teratoma ovárico
Gonadoblastoma
Leucemia mielógena aguda
Linfoma de Hodgkin y de células T
222
Q

causes of prolactinemia associated with - miscellanous

A 
Encefalitis
Neurofibromatosis
Pseudotumor cerebral
Seudociesis
Porfiria
223
Q

causes of prolactinemia associated with macroprolactienmia

A

Autoanticuerpos anti-“big-big” PRL. Sospechar ante hiperprolactinémicos asintomáticos, pues estas moléculas tienen muy poca actividad biológica.

Se presenta hasta en el 40% de las detecciones de híper-PRL.

224
Q

causes of prolactinemia associated with - idiopathic

A

20% de los hiperprolactinémicos. Puede ser por mínimas dimensiones. Se piensa en resistencia de lactotropos a la DA o poca actividad de sus receptores. Se normalizan espontáneamente en 30%.

225
Q

for hyperprolactinemia when is transesfenoidal tumorectomy ndicated

A

¾ Intolerancia/resistencia a los agonistas de DA. ¾ No deseo de consumir agonistas DA por largo tiempo.
¾ Crecimiento de prolactinoma a pesar del uso de estos. ¾ Deseo de embarazo por parte de la paciente (aunque la mayoría no crece durante el embarazo: indicación relativa).
¾ Prolactinomas con componente quístico. ¾ Preferencia del paciente.
¾ No mejoría de los campos visuales tras 1-3 meses de agonistas DA

226
Q

what are somatotropoma

A

tumor of somatotropes that secrete GH

227
Q

what is cosecreted in 20-25% in somatotropomas

A

PRL

228
Q

65-80% of somatotrpomas are

A

macroadeomas

229
Q

MC of somatotropomas

A

gigantism /acromegaly in 99%

mass effect

230
Q

mass effect in somatotropma

A

(hipopituitarismo, hiperprolactinemia y neurooftalmopatías

231
Q

< 1% of gigantism and acromegaly is due tu

A

ectopic secretion of GH

excessive secretion of GHRH

  1. Eutópica (hipotalámico): gangliocitoma o coristoma.
  2. Ectópica: tiroides (CA medular), timo (carcinoide), bronquio (carcinoide), pulmón (CA microcítico), intestino (carcinoide), páncreas (CA de islotes), adrenales (adenoma o feocromocitoma).
232
Q

Dx of somatotropoma

A
  1. Confirmación bioquímica:
    a. IGF-1 (somatomedina C) elevado.
    b. Prueba de sobrecarga oral de glucosa midiendo GH (SOG-GH). Medir GH en ayuna y cada 30mins durante 2h después de la sobrecarga con 75g glucosa VO. Confirmación: GH > 1ng/mL por lo menos en 1 de las muestras tomadas post-administración de glucosa.
  2. MRI de hipófisis con gadolinio …
    ¾ Positivo à
    a. Campimetría visual computarizada.
    b. Evaluación hipofisaria.
    ¾ Negativo à
    c. GHRH en plasma.
    d. TAC tórax y abdomen.
233
Q

what are corticotropomas

A

tumors of corticotropas that secrete ACTH producing CUSHINGS disease

234
Q

what is cushings diesase

A

a state of hypercortisolism due to hyperstimulation of adrenal gland

235
Q

cortico tropoma is responsible for what percent of endogenous cushing in adults

A

68%

90% are microadinomas

236
Q

biochemical confirmation of corticotropoma

A

a. Cortisol urinario libre de 24h. Positivo: 2-4x > límite superior.
b. Prueba de supresión con 1mg nocturno de dexametasona. Se administra 1mg de dexametasona @11pm del primer día y se mide cortisolemia a la mañana siguiente. Positivo: >1.8μg/dL.
c. Cortisol salival @11pm. Positivo: >145ng/dL

237
Q

least frequent AHs 1-2%

A

tirotropmas

238
Q

most invasice AHs

A

tirotropmas

239
Q

% of tirotropomas that are macroadenomas

A

85% are macroadenomas causeing mass effect ontop of hormonal effects (bocio, hiperhyroidism with increased TSH
¾ Cosecretan GH (16%), PRL (11%), LH/FSH (1.4%) y subunidad α[2].

240
Q

hpo vs pan

A

decreased or no of one or more pit hromes

pan is all > 90% of mass

241
Q

causes of hypopituitarism (one or more hormons)

8Is
A

A

direct or indirect

tumoral invasion (meningioma, glioma, )
pit infarct
infiltration of hipofisis
infection in this region
injury in this region - postqx, RT, trauma
iatrogenic
immunological
idiopathic
isolated - deficit of just one hormone
242
Q

types of tumors that cause hipopituitarism

A

hipofisiary adenoma
compression

hypothalamic tumor
cystic lesion (craneofaringoma, Rathke, aracnoidoceles)

metastasis

vascular lesions (necrosis) - no cells to produce hormenes

243
Q

adenomas and hipoputuitarism

A

compress hypothalamus and pituitary and THH (tallo)
decrease pit irrigation
increase intrasellar pressure

prolactinoma (PRL inhibits GnRH)

corticotropoma (ACTH inhibits GnRH)
so two hormones are down thru RAN

down FSH, LH, testerone men, estradiol women

244
Q

pituitary infart

A

apoplejia don’t know if hemorrhage or infart acute
both caus epituitary infarct (10-15% adenomas inernal hemorrhage??, autocorrection)

local MC:cefalea, meningeal irritation, visual signs, altered conscieness, facial pain
(due to increase in ICP - blood irritates calls cytokines and proinfalmmatory factors causing headache by VD)
altrered sympathetic regulation
obstructive hydrocefaly

systemic: hypopituitarism
empty silla turca syndrome

245
Q

pathogenesis of apoplejjia

A

adenoma of pituitary grows fast
mass compresses superior pit artery , less perfusion, necrosis

can also cause its own vascular anomalies

all 3 of these conditions cass perfusion insuff and causes isquemic necrosis –> death of pit cell death

246
Q

pituitary infract, Sheehan syndrome

A

@ post partum

blood loss in labor causes less blood flow up
which is already big (pit) due to preg

necrosis

failed lactancy, failed reinico of menstruation, massive labor hemorrhage (PRL inhibits GnRH - after nipple stimulation) cells dead anyway no PRL or GnRH

247
Q

infiltrations and infections for hipopituitarism

A 
infiltrative: amyloidosis
sarcoidosis
histocitiosis X
hemochromatosis
(destroynormal tissue that's there)
infection: micosis (coccido, crypto)
Tb
sifilis
AIDS
pituitary abcess

(hipofisisits linfocitica px ej?)

248
Q

cranial injury hipopituitarism

A

trauma can be direct to brain

indirect.....causes of pituitary infarct
cerebral edema (compresses)

hemorrhage or fracture of cranium (blood irritative ,and proinflammatory)

cerebral hypoxia

249
Q

iatrogenic causes of hipopituiraism

A

qx of pit gland due to hypothalamic lesion

cranial RT (gammaknife) - waves destroy the mass/lesion but its not selective just like the surgery

250
Q

hipofisitis –> hypopituitarism can be

A

primary or secondary

251
Q

primary hipofisitis

A

linfocitic (1A)
granulomatous
xantomarous

252
Q

secondary hipofisitis

A 
local lesion (germinoma)
systemic enf (saroidis)
253
Q

isolated hypopituitarism ca n have 3 MC cx

A

isolated FSH LH down (without corticotropoma, hiperPRL)
- kallman syndrome (anosmia –> hipogonadismo hippanotropica??)
FSH alone
hyperprolactimea

TSH down alone
(IRC, linfocitic hipofisitis, pseudohipoparatiroidism)

ACTH down alone
(hipofisitis linfocitic, Sheehan, cranial trauma, Tpit gene mutation)

254
Q

tpit gene

A

transcription for??

255
Q

empty silla turca cause

A

partial or toal

deficiency in sella diaphragm and LCR infiltrates

compresses pit gland

256
Q

clinical empty silla turca

A

oftalmologica (hemaniopsia bitemporal, blurry, blind, papilledema), neurological (cefalea, increased pressure, convulsions, paraplejias), endrological (hipo) 50%

257
Q

@ def GH

A

neonates: hipoglicemia, hiperbilirrubinemia, convulsions
(confused with kernicterus)

short stature - infantile, delayed denticion, facial mcizo hypoplasia, frente oprominente, small mouth, occipital prominence

258
Q

@ def ACTH

A

tired, less quality sleep, less muscular

dislipidemia

259
Q

def gonadotropins

A

no cx sexuals ni 1 or secondary

criptoquidia
micropene
delayed puberty
small testicles
little pubic hair
gynecomastia

adults: less libido less energy, less EPO, less testicle, heat waves, dyspareunia (SSAME AS MENOAPAUSE) amenorrea, dry vaginal, osteopenia

260
Q

TSH def

A 
HIPOTHYROIDISM MC
weak
dry skin
palpebral edema
adinamia, somnolencia
hair falls
cold skin
thin nails striated
bradipsiquia, bradilalia
attention deficit
memory loss
depression, psycosis
disfonia
261
Q

def ACTH

A 
depression
weight loss
postural hypotension (why)
epigastric pain
nausea vomit
hipoglicemia (no contrareg_
hipnatremia
anemia, linfocitosis
262
Q

def GH

A

hipoglicemia induced with insulin

GH < 10ng/ml in ALL samples

give insulin (0.05-0.15 unidades/kg) to induce hipoglicemia
take basal glicemia (84mg/dl ej) 0
measure glicemia, GH, cortisol

0, 15, 30, 45, 60, 90, 120

well done to dx if glicemia is < 40mg/dl or half of what px had a basal if (43 CANT USE)

GH should be increasing

> 10 is no deficit - GH

this test measures somatotrope and corticotrope RESRERVES

to say px has GH deficit has to be 9 and down (1 at 10 = healthy)

cortisol should go up and if not its a def in reserve of corticotrope cells (cut off is = 18, healthy below deficit) In all samples

263
Q

contraregulating hormones

A

cortisol
GH
glucagon
catecolamines

@ hypoglycemia these hormones go up

264
Q

masculine hypogonadism dx

A

infertile
measure serum testosterone at 8 and 11am (nadir times)

if < 300ng/dl = confirmation

primary or secondary

(gonadotripinas )
in primary will be one elevated??

secondary hipo hipo

265
Q

hipogonisms in women

A

amenorrea
measure LH, FSH, E2…. also prolactin

E2 down , LH, FSH up - primary (karyotype, precoz menopause, autoimmune ooforitis) = menopause if > 50

E2 down, LH, FSH down
secondary hypogonadism
MRI hipsifis, evaluate hipo function, central?

discart preg and hiperprolactinemia

266
Q

insuff suprarenal dx

A

measure cortisol 8am (5-25) and 4pm (half)

Cortisol in morning @ insuff should be < 3
if < 18 = falla adrenal
if > 18mcg/dl = sano
if 3-18 - short ACTH stimulation test - inject 250microg of ACTH or 0.25mg - cortisol up N, doesn’t if sick (<18 = ADRENAL FAILURE)

267
Q

hormone replacement tx GH

A

give GH in kids 0.035mg/kg/d SC

268
Q

hormone replacement tx ACTH

A

give hydrocortisone - 20-30mg/d VO
Prednisina 5-7.5mg/d VO
Cortisone 25-37.5 mg/d VO

269
Q

hormone replacement tx TSH

A

levoritoxine - 1.6-1.8mcg/kg/d VO

270
Q

LH FSH

A

men - testerone esters 250mg C/3wk
2.5-7.5mg/d
5-10 gel/24hr

women
estrogen 1-2mg/d
estrogen and progestogens 25-100ug/24hrs (combined birth control)

271
Q

craneofaringioma

A

tumors atht originate in remnants of cells from Rathke sac and can cause hipopit in kids

most common cause of hipopit in kids

2-3% of IC tumors

seen in 2 peaks of life
between 2-25yr or > 65yr

25% cause hypothalamic alterations
5% @ hypofisis
both @ 70%

25-30% mixed
15% solid
55-60% cystic

usually > 1cm = macroadenomas, mass effect –> hipopit

highly invasice with hypothalamic extension

272
Q

MC of craneofaringoam

A

neuro MC
- headache, visual camp deficit, hydrocephaly, convulsions

hipopituiartism (tumba ADH)
- 80%
deficit MC
delayed puberty
DI

hyperprolactinemia
- tallo effect
<100ng/dl

273
Q

dx of craneofaringeoma

A

MRI of hypofisis with gadolinio - fine, cortes, if small can catch it most are big (cant see calcifications which cystic lesions do become)

CT craneo (can see calcifications)

Xray (calcification, other lesion, silla turca issues)

campimetric deficits

altered III, IV, VI

less visual acuity

measure prolactin in plasma, FSH LH, estradiol,
FSH LH testosterone
RSH T4 free
GH, IGF1
Cortisol ACTH
hipoglicemia induced by insulin test (FOR LAS RESERVAS) -

274
Q

tx craniofaringioma

A

qx

hormone replacement therapy

275
Q

post qx complications for craneofaringioma

A

DI - 16-66%
adrenal insuff 40%
panhipopituitarism 23%
hipotiroidism 28%

ORTHO (9 decks)

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