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AMENORREA

PRIMARIA Y SECUNDARIA


DEFINICIN
ES LA FALTA DE MENSTRUACION .

PRIMARIA (AUSENCIA DE MENARCA)
SIN CARACTERES SEXUALES DESARROLLADOS
DESDE LOS 14 ANOS
CON CARACTERES SEXUALES DESARROLLADOS
DESDE LOS 16 ANOS

SECUNDARIA : FALTA DE MENSTRUACION
POR EL PERIODO MAYOR DE 90 DIAS LUEGO DE
HABER TENIDO SU MENARCA

CORTEZA CEREBRAL-
SUPRAHIPOTALAMICO-SISTEMA
LIMBICO-EJE HIPOTALAMO-
GONADAL-EFECTOR

CORTEZA CEREBRAL
FEMENINA (RECEP. ESTROG.)
SISTEMA LIMBICO- NUCLEOS S.
OPT. Y PARAVENT. . ADRENAL (C.
R.H.)- HIPOTALAMO
(PROCESAMIENTO DE
INFORMACION) INHIBICION DE
PROCREAR.
HIPOFISIS-GONADA----------UTERO-
-----VIA GENITAL PERMEABLE
CAUSAS DE AMENORREAS
SECUNDARIAS
A) HIPOTALAMICA

B) HIPOFISARIAS

C) OVARICAS

D) UTERINAS

E) EXTRAGENITAL

ESTUDIO DE LA AMENORREA
SECUNDARIA
PRUEBA DE PROGESTERONA
PRUEBA DE ESTROGENOS
PRUEBA DEL GNRH
DIAGNOSTICAR SI LA FALLA ESTA
1)EN EN EJE HIPOTALAMO-
HIPOFISO-GONADAL
2)EN EL EFECTOR: UTERO Y
PERMEABILIDAD CERVICO-VAGINAL
PRUEBA DE PROGESTERONA
10 MG. DE MEDROXIPROGESTERONA
DURANTE 5 DIAS .DEPRIVACIN DE 2 A 10 DIAS
POSTERIORES A LA ULTIMA PASTILLA .
RESULTADO POSITIVO: ORIENTADOR DE
CICLOMONOFASICO
RESULTADO NEGATIVO: DESCARTAR
EMBARAZO , SE EFECTUA PRUEBA DE
ESTRGENO.
PEDIR TSH, PROLACTINA, ESTROGENO, FSH
LH , 17OH PROGESTERONA (3 A 5 DIA DE
MENSTRUACION)
PRUEBA DE ESTROGENO
0,625 DE ESTROGENO CONJUDADO
EQUINO DURANTE 21 DIAS.
SE ESPERA DEPRIVACION HASTA 10 DIAS
POSTERIOR A LA ULTIMA PASTILLA.
RESULTADO POSITIVO: INVESTIGAR
EJE HIPOTALAMO-HIPOFISARIO.
RESULTADO NEGATIVO: CAUSA
UTERINA



PRUEBA DE GNRH
ADMINISTRACION ENDOVENOSA DE
100 MICROGRAMOS DE GNRH
OBTENER MUESTRAS DE SANGRE A
LOS 30, 60 Y 90 MINUTOS
LA RESPUESTA NORMAL LA FSH
DUPLICA SU VALOR BASAL Y LA LH
LO TRIPLICA .
LA FALTA DE RESPUESTA INDICA
QUE LA CAUSA ESTA EN LA
HIPOFISIS
PRUEBA DE PROGESTERONA

POSITIVA : CICLO ANOVULATORIO
NEGATIVA : PRUEBA DE ESTROGENO

PRUEBA DE ESTROGENO

NEGATIVA: FALLA EL EFECTOR (UTERO)
POSITIVA: FSH,LH,ESTROGENO.PRUEBA DE GNRH

PRUEBA DE GNRH

NEGATIVA: CAUSA HIPOFISARIA
POSITIVA: CAUSA HIPOTALAMICA

ESTUDIO HORMONAL
FSH LH
TSH
CORTISOL
17 OH FSH
PROGESTERONA
PROLACTINA
ESTRADIOL
GLUCEMIA
INSULINA
3 A 5 DIA DEL CICLO

UN BUEN ALGORITMO ILUMINA
OTROS ESTUDIOS
PROGESTERONA 21
TESTOSTERONA
SHBG
DEHIDROEPIANDROSTERONA
SULFATO (DHEAS)
ESTUDIOS CROMOSOMICOS EN
AMENORREAS PRIMARIAS
ALGORITMO
Figure 1. Flow diagram f
CAUSAS DE AMENORREAS
1)HIPOTALAMICAS

POR STRESS
ANOREXIA
SOBREENTRENAMI
ENTO FISICO
AMENORREA MAS
TRATORNOS
OLFATORIOS
2)HIPOFISARIAS

ADENOMA
PROLACTINICO
CRANEOFARINGIO
MA
SINDROME DE
SHEEHAN
HIPOFISITIS
CAUSAS DE AMENORREA
3)OVARICAS

FALLA OVARICA
PRECOZ
POLIQUISTOSIS DE
OVARIO
DISGENESIAS
GONADALES
4) UTERINAS
SINEQUIAS UTERINAS
TUBERCULOSIS

5) EXTRAGONADALES
A) ENDOCRINAS
HIPOTIROIDISMO
INSUFICIENCIA
SUPRARRENAL .
HIPERPLASIA SUPRARENAL
CONGENITA
B) METABOLICAS
DIABETES.
OBESIDAD
INSUFICIENCIA HEPATICA

OTRA CLASIFICACION
1) CAUSA ANATOMICA
Anomalas de la va de eliminacin de la menstruacin
2) CAUSA FALLA OVARICA
Alteracin citogentica del cromosoma X
Mutacin especfica de gen
Defectos en las enzimas de la esteroideognesis
Defectos en la secrecin o accin de las gonadotrofinas
Disfuncin inmunolgica
Agresiones fsico-qumica
3) AMENORREA CRONICA
Hipotalmica
Hipofisaria
Falla en la retroalimentacin negativa
Otros desordenes endcrinos
4) Relacin con el hiperandrogenismo



1. Anatomic Causes
a. Pregnancy
b. Mllerian agenesis or dysgenesis
(uterine, cervical, or vaginal)
c. Imperforate hymen
d. Cervical stenosis
e. Various disorders of sexual
differentiation
f. Intrauterine adhesions
(Asherman syndrome

2. Tentative Classification of
Premature Ovarian Failure
A) Citogenetic Alterations of the X Chromosome

i. Absence of an X chromosome
ii. Trisomy X with or without mosaicism
iii. Structural abnormalities of the X chromosome
B) Mutations of Specific Genes
i. Premutation of FMRl gene (Fragile X; 6% of
cases)
ii. INHA (inhibin alpha)
iii. FOXL2 (a forkhead transcription factor associated with the
blepharophimosis/ptosis/epicanthus inverse syndrome)
iv. ELF2B (a family of genes associated with CNS leukodystrophy and
ovarian failure)
v. BMP15 (bone morphogenetic factor 15, involved with
folliculogenesis)
vi. PMM2 (phosphomannomutase)
vii. AIRE (autoimmune polyendocrinopathy-candidiasis-ectodermal
dystrophy syndrome))
producing androgens or estrogens
iv. Neoplasms producing hCG (including trophoblastic disease)
v. Liver and renal disease
vi. Obesity

2. Tentative Classification of
Premature Ovarian Failure
c) Enzymatic Defects
Steroidogenic enzyme defects
A. 17-Hydroxylase or 17,20-lyase deficiency
B. 20,22-Desmolase deficiency
C. c. Aromatase deficiency
ii. 2. Galactosemia
D) Defects in Gonadotropin Secretion or Action
i. Receptor and post-receptor defects
A. FSH receptor (FSHR) mutations
B. LH receptor (LHR) mutations
C. G-protein alterations
ii. Secretion of biologically inactive gonadotropin
iii. - or -Subunit defects
E) Immune Dysfunction
i. Association with other autoimmune disorders (15-20% of
cases, 4% with steroidogenic cell autoimmunity)
ii. Isolated
iii. In association with congenital thymic aplasia
F) Physical Insults
i. Chemotherapeutic (especially alkylating) agents
ii. Ionizing radiation
iii. Viral agents
iv. Surgical extirpation
g. Gonadotropin-Secreting Pituitary Tumors (Extremely Rare)
h. Idiopathic
3 Chronic anovulation
a) HIPOTALAMIC
Psychogenic, including pseudocyesis
ii Exercise-associated
iii. Eating disorders, nutritional
iv. 2 to systemic illness
v. Hypothalamic neoplasms
b. Pituitary
i. Isolated gonadotropin deficiency (including Kallmann
syndrome)
ii. Hypopituitarism
iii. Pituitary neoplasms, including mucroadenomas
c. With inappropriate steroid feedback
i. Functional androgen excess (PCOS)
ii. Adrenal Hypoplasia
iii. Neoplasms producing androgens or estrogens
iv. Neoplasms producing hCG (including trophoblastic disease)
v. Liver and renal disease
vi. Obesity
d.Other endocrine disorders
i. Thyroid dysfunction
ii. Adrenal hyperfunction
. Causes of Hyperandrogenism
Common
Polycystic Ovary Syndrome80%
Idiopathic Hirsutism15%UncommonLate-Onset
21-Hydroxylase Deficiency1-5%
Rare< 1%
Steroidogenic Enzyme Deficiencies3b-hydroxysteroid
dehydrogenase17-ketosteroid
reductasearomataseAndrogen
Secreting Tumors of Ovary or Adrenal-Ovarian
Hyperthecosis (a PCOS variant)
Other
Endocrine
Hyperprolactinemia Cushing syndrome
Defects in cortisol metabolism
Acromegaly
. Classification of Anovulation Associated with
the CNS Hypothalamic-Pituitary System
1) Functional Hypothalamic Anovulation
Exercise-related factors
Nutritional factors
Psychogenic or stress factors
2) Physiologic Anovulation
Prepubertal phase
Postpartum phase
Breastfeeding phase
3) Pharmacologic-Associated Anovulation
Opiate agonist
Dopaminergic agonist
4) Psychiatric-Associated Disorders
Pseudocyesis
Anorexia nervosa
Bulimia
5) Organic Defects of the Hypothalamic-Pituitary Unit
Kallmann syndrome
Isolated gonadotropin deficiency
Pituitary tumors
Sheehan syndrome
Pituitary apoplexy/aneurysm
Empty sella syndrome
Inappropriate prolactin secretion
Infection (human immunodeficiency virus, tuberculosis)
Post-radiation effects
Head trauma
Common Features of Women with
Psychogenic Hypothalamic Amenorrhea
Single marital status
Obsessive-compulsive habits
History of significant stressful life events
History of sexual abuse
History of prior irregular menstrual cycles
Normal or thin habitus
Tendency to use sedatives or hypnotic
drugs
Involved in professional occupations
High intelligence
Associated Neuroendocrine Abnormalities in
Hypothalamic Amenorrhea.
Increased daytime cortisol secretion
Increased amplitude and duration of
nocturnal melatonin secretion
Increased nocturnal secretion of GH
Elevated CRH levels in cerebral
spinal fluid
Blunted elevation of PRL, ACTH, and
cortisol during the noon meal
Common Features of Anorexia
Nervosa
Preoccupation with handling of food
Bulimic behavior
Calorie counting
Distortion of body self-image
Hyperactivity-Obsessive-compulsive personality
Increased incidence of past sexual abuse
Amenorrhea
Constipation
Coarse, dry skin
Soft, lanugo-type hair
Hypothermia with defective thermoregulation
Mild bradycardia
Cardiac arrhythmias
Hypotension
Hypokalemia secondary to diuretic or laxative abuse
Osteopenia
Increased serum beta-carotene levels
AnemiaLeukopenia
Elevated hepatic enzymes



Neuroendocrine Abnormalities
Associated with Anorexia Nervosa
Diminished GnRH-LH pulsatile frequency and
amplitude
Low blood LH and FSH levels
Impaired ACTH response to CRH stimulation
testing
Resistance to dexamethasone suppression
Increased ACTH levels
Increased 24 hour urinary free cortisol levels
Low prolactin levels
Low TSH levels High reverse T3 and low T3 levels
Elevated GH levels
Decreased IGF-1 levels
Diabetes insipidus
EXERCISE-INDUCED
HYPOTHALAMIC AMENORRHEA
Ballet (6-43%) and middle and long distance
running (24-26%). The incidence appears to be
less frequent in bicycling (12%) and swimming
(12%) .
Pulsatility is not disrupted by the stress of
exercise but rather LH pulsatility is disrupted
because of reduced energy availability .
It is important to emphasize that for so many of
these athletes the "female athlete triad" of
amenorrhea, osteoporosis, and eating
disorders coexist.


AMENORREA
PRIMARIA
DIFERENCIACION
SEXUAL
ESTUDIO
CROMOSOMICO
ESTUDIOS HORMONALES
Regulation of germ cell migration. A:
4-week embryo. Differentiation of
primordial germ cells (PGC) occurs
from epiblast-derived cells pressent
in the yolk sac near the base of the
allantois. PGcs express alkaline
phosphatase (AP), Oct4 and c-kit.
Stem cell proteins, like fibronectin
and laminin, are expressed along the
PGC pathway. B: 5-week embryo.
PGCs migrate along the dorsal
mesentery of the hind gut to the
gonadal ridges.
. Undifferentiated
reproductive tract.
Both Wolffian and
Mllerian ducts are
present. Mllerian ducts
open in the urogenital
sinus at the level of the
Mllerian tubercle
between the orifices of the
Wolffian duct.
\
. Diagrams representing five degrees of
virilization affecting the urogenital sinus and
external genitalia in females.
CON Y SIN TRATAMIENTO
AMENORREA PRIMARIA
1)SINDROME DE KALLMANN
2)SINDROME DE TURNER
3)INSENSIBILIDAD AL RECEPTOR
ANDROGENICO
4)AGENESIA UTERO-VAGINAL
5)HIPERPLASIA ADRENAL
CONGENITA
1)SINDROME DE KALLMANN_
AMENORREA ASOCIADA A ANOSMIA
RECESIVA LIGADA AL X
AUSENCIA DEL DESARROLO
PUBERAL
UTERO Y OVARIOS HIPOPLASICOS
QUE CONSERVAN FOLICULOS
PRIMORDIALES CON RESPUESTA AL
GNRH
TIENEN VELLO AXILAR Y PUBIANO
2)SINDROME DE TURNER

PATRON X0
FALTA DE DESARROLO CARACTERES SEXUALES
SECUNDARIOS
ESTATURA BAJA
INFANTILISMO
COARTACION DE AORTA
CINTILLAS OVARICAS : GONADOBLASTOMA
MOSAICISMOS

3) INSENSIBILIDAD AL
RECEPTOR ANDROGENICO

PATRON XY
INSENSIBILIDAD DE LOS RECEPTORES A LOS
ANDROGENOS
TESTICULOS ECTOPICOS: DESARROLLO DE LOS
CARACTERES SEXUALES SECUNDARIOS Y LA
POSIBILIDAD DE TRANSFORMARSE UN
SEMINOMA
FALTA DE VELLO AXILAR Y PUBIANO
VAGINA CORTA (PROCESO CLOACAL)
FALTA DE UTERO Y VAGINA
4)AGENESIA DE UTERO-
VAGINA
PATRON XX
VAGINA CORTA (PROCESO
CLOACAL)
PRESENCIA DE VELLO AXILAR Y
PUBIANO
DIAGNOSTICO DIFERENCIAL CON
TESTICULO FEMINIZANTE
5)HIPERPLASIA ADRENAL NO CLASICA

DEFECIT ENZIMATICO 17 ,3 Y 21
HIRSUTISMO
SIGNOS DE DEFIMINIZACION
VIRILIZACION

AMENORREA
PRIMARIA
DIFERENCIACION
SEXUAL
ESTUDIO
CROMOSOMICO
ESTUDIOS HORMONALES
AMENORREA SECUNDARIA

. P.PROG.(+)ANOVULACION: LABORATORIO
(- ) P. ESTROGENO: (-) EFECTOR (utero-canal)
(+) EJE HT-HF-GONADAL

TSH FSH LH PRL Gluc./Ins 17OHPRO
Hipotiroidismo Falla PCO Tumor HOMA HSC
ovarica

IMC CARIOTIPO HIPERANDROGENISMO
ANOREXIA X/0 X/Y TESTO DHEAS VIRILIZACION
ANOVULACION
HIPOTALAMICA
UN BUEN aDIAGNOSTICO QUE ILUMINE
UN BUEN ALGORITMO ILUMINA