Endo Repro Koulton Flashcards
Fhs lh tsh hcg
Alpha subunit
Follicular phase
Onset menstration to preovulatory LH surge
Estradiol
Lumen
Tart with LH surge to start menstration
Theca
LH cholesterol to androstenedione and testosterone
Granulosa
FSH aromaiation a and t to estradiol
FHS LH
High follicular down luteeal from high progesterone
Corpus luteum to albicans
FSH up and estradiol positive feedback later LH surge
What day try and conceive
14
If cycle 114 days when have intercourse
Day 100…first half can be off but once ovulate bleed 14 days later ***
GnRH
Decapeptide from arcuate nucleus cause secretion of gonadotrops (LH and FSH)
LH FSH forms
Release and storage
As estradiol goes get get wht
Positive feedback and surge
Gonadotrops on GnRH
Decrease
Why get progesterone follicular
Prior to ovulation the unruptured luteinizing Graafian follicle begins to produce increasing amounts of progesterone
When secretion of progesterone by CL reaches max
5-7 days after ovulation and returns before menstration
Primordial follicles
Undergo sequential development, differentiation and maturation until mature
Rupture follicle
Release egg ovum
Luteinization of ruptured follicle
Makes cl
When do oocytes become surrounded by precursor granulosa cells
8-10 weeks
Called a primordial follicle
In ADULT ovary, graffiti follicle form
Inner most 3-4 layers of multiplying granulosa cells become cuboidal and adherent to the ovum thi is called cumulus oophorus
A fluid filled antrum forms among the granulosa cells
Antrum enlarges and the centrally located primary oocyte migrates t the wall of the follic;e
The innermost layer of the granulosa cells of the cumulus become elongated and for the corona radiata
Corona radiata
Released with the oocyte at ovulation
Innermost layer of granulosa cells of the cumulus becomes elongated and rorm it
LH surge
Ovulation
After ovulation
Granulosa undergoes luteinization
Corpus luteum
Lutenized granulosa cells, theca cells, capillaries and CT from corpus luteum
-make progesterone
Lifespan CL
9-10 days
Pregnancy not occur what is fate of CL
Gradually replaced by an avascular scar called corpus albicans
How does pituitary respond decreasing p and e
Increase LH and FSH
Diagnose menopause
FSH high from no neg feedback
2 zones of endometrium
Basalis and functionalis
Functionalis
Outer potion
Cyclic changes during menstrual cycle and sloughed off
Spiralis
Basalis
Remains relatively unchanged
Basal arteries
Provides stem cells
Cyclic changes
Menstrual phase
Proliferative
Secretory phase
Cycle day 1
1st day menstruation
When reach maximal thickness
Secretory phase
Proliferative 4-8 mm
Secretory 8-14. Ml
Conception not by day 23
CL regress, decrease p and e, endometrial involution
Menstration cycle
Terminal event of process for uterus to get baby
Intact coagulation pathways important
Healed with normal hemostasis
Need platelets and clotting factors
Warfarin
Heavy enstruation
Girls with HEAVY period at 12 years old. What have
Von williebrands disease.
Age menarche
12.43
2-3 years of thelarche at tanner IV
Primary amenorrhea
No menstration by 13 without secondary characteristics
By 15 with sex characteristics
Excessive flow
Greater than 80 cc (30 cc normal) associated with anemia
-changing pat q1-2 hours and considered excessive if >7 days
Puberty and factors
10-16
Geographic location, genetic, nutritional status
20 week in uteru
Have 6-7 million oocytes
HPO suppressed when
4-10 years
Function of low level gonadotropins and sx steroids during prepubertal period
Gonadostat sensitivity to the negative feedback of low circulating estradiol
Intrinsic central nervous system inhibiton of the hypothalmic GnRH secretion
8-11
Increase serum DHEA and DHEaS
Initial endocrine changes associated with puberty
Adrenal androgen production and differentiation by zone reticularis of the adrenal cortex
Rise in adrenal androgens
Growth of axillary and pubic hair
11
Loss of sensitivity by gonadostat to the negative feedback of sex steroids. In combination with the intrinsic loss of central nervous system inhibiton of GnRH
Sleep associated GnRH secretion occur and gradually shift into adult type secretory patterns
Increase GnRH 11
Promotes ovarian follicular maturation and sex steroid production, which leads to the development of secondary sex characteristics
Mid to late puberty
Positive feedback mechanism of estradiol on LH release from anterior pituitary is complete and osculatory cycles are established
Thelarche requires ___
Estrogen
Pubarche/adrenarche requires ___
Androgens
Maximal growth or peak height velocity when
2 years earlier in girls and 1 year before menses
Menarche
Require pulsatilla GnRH from hypothalamus, FHS< and LH from the pituitary, estrogen and progesterone from the ovaries, normal outflow tract
Thelarche race
African American and Hispanic go through before caucasion
Tanne 1
Preadolesence, elevate pilla
2
Breast bud
3
Enlarge breast aerola
4
Projection secondary mound
5
Projection papilla recession aerola
1
No pubes
2
Slight pigment and down
3
Coarser hair pubes
4
Adult hair not medial thighs
5
Medial thighs and inverted triangle
Precocious puberty
Secondary sexual characteristics prior to 2.5 SD expected
8 year old girl 9 boys
Rare
What do
Thorough evaluation to rule out serious disease and stop premature fusion of long bones so as adults short
Tall when prsent then close then short
Emotionally hard for girls and icnreased risk sexual abuse
Heterosexual precocious puberty
Dev of secondary sex characteristics opposite expect
Virilizing neoplasma
CAH
Exogenous androgen exposure
Isosexual precocious puberty
Premature sexual maturation that is appropriate for the phenotype of the affected individual
Constitutional and organic brain disease
-tumors, trauma, infectious process
Heterosexual precocity androgen secreting neoplasms
Rare
Usually in ovaries
Diagnosed PE and radiological exam and treated with surgical
CAH heterosexual
Most commonly 21 hydroxylase
Classical-birth of females with ambiguous genetalia-if untreated virilization and short
Nonclassical-resemble POCS premature pubarche
Isosexual precocity true
Arises from premature activation of the normal process of pubertal development involving the HPA
Isosexual precocity pseudosexual precocity
Exposure of estrogens independent of HPO axis
Estrogen producing tumors
Diagnose true
Idiopathic most common
Give GnRH see rise in LH
CNS disorder
-willl have neurological symptoms before sexual dev
MRI head
Treat true
Gnrh agonsit (leuprolide acetate) -decrease gonadotropins to prepubertal
Not treater true
Will not attain 5 foot adult height
Pseudo
Without activation of HPO
Ovarian tumor, exogenous estrogenic, mccune Albright and peutz=jeghers
Mccune Albright
Somatic mutation during embryogenesis which causes them to function independent of their normal stimulating hormones
5%
Multiple cystic bone defects, cafe au last spots
Adrenal hypercortisolism
Peutz jeghers
Associated with a sex cord tumor that secretes estrogen
GI polyposis and mucocutaneous pigmentation
Delayed puberty
Secondary sex not by 13 or thelarche not by 14
No menses 15 or 16
Menses not 5 years after thelarche
Cause
Hypergonadotropic hypogonasism
-turner/gonadal dysgenesis
FSH>30
Hypogonadotropic hypogonasism (FSH LH <10) Kallman, anorexia, pituitary tumors, hyperprolactinemia, drug use
Anatomic causes
-mullerian agenesis, imperforate hymen, transverse vaginal septum
Amenorrhea primary
No spontaneous uterine bleeding by 13 without secondary sex characteristics
No menstruation by 15 years with secondary sexual development
Amenorrhea secondary
Patient with prior menses has absent at least 6 months
If primary amenorrhea
Does she have secondary sex
Low-look FSH LH
Primary with absence of secondary sex
FSH LH<5
Hypogonadotropic hypogonadism
MRI
Causes hypogonadotropic hypogonadism
Lesions/tumors HPA Anorexia/exercise Hyperprolactinemia Kallman Constitutional delay -most common, hereditary factors may play role 20%
Most common delayed puberty
Constitutional
Hypogonadotropic hypogonadism kallman
Mutation KAL gene on X chromosome that prevents the migration of GnRH neurons into hypothalamus
Have anosmia or hyposmia
Hypergonadotropic hypogonadism (chromosomal or injury to ovaries by surgery, chemo, radiaiton
Ok
Treat to evaluate delayed puberty
MRI, FSH, karyotype, progesterone, prolactin
What is karyotype comes back with Y chromosome
Gonadectomy is recommended to prevent malignant neoplastic transformation
Primary amenorrhea with absence of secondary sexual characteristics
FSH>20 L LH >40
Hypergonadotropic hypogonadism
Karyotype to rule out Y chromosome
Cause hypergonadotropic hypogonadism
Gonadal agenesis/dysgenesis of the presence of an abnormally developed gonad due to chromosomal defects (TURNER 45 XO)
Turner
MOst common female gonadal dysgenesis
No signs of secondary sexual characteristics
Mosaicism in 25% may have normal phnenotype with spontaneous onset of puberty and menarche
Signs turner
Broad flat chest wide neck
Streak ovaries
No puberty
Coarctation aorta
Primary amenorrhea with secondary sexual characteristics US show no uterus
Do karyotype
Androgen insensitivity syndrome
46XY
Male levels of testosterone
Defect in androgen receptor
Testes in abdominal wall
-secrete antimullerian hormone so no uterus
-external female genetalia with no pubic hair
Breast development with small aerola/nipples
-caused by estrogen secretion in testes and conversion of androgens to estrogen int he liver
Mullerian dysgenesis/agenesis
Primary amenorrhea, normal breast dev, levels of testosterone with females
-mullerian defects that cause obstruction of vaginal canal
—imperforate hymen or a transverse septum
-absence of normal uterus is known as mullerian agenesis
-failure of Müllerian ducts to defuse distally and to form the upper GI tract will have a vaginal dimple
-absent uterus but may have a unilateral or bilateral rudimentary uterine tissue, tubes and ovaries
-associated with renal abnormalities
-IV pyelogram should be ordered to assess urinary system
Abnormal shaped uterus…
Order IV pyelogram to assess urinary system or CT to see ureters
Get IVP
Androgen insensitivity
Normal breasts no sexual hair
Normal looking female external genetalia
Absent uterus and upper vagina
Karyotype 46 XY
Male range T level
Test with gonadectomy
Mayer rokitansky kuster hauler
Normal secondary dev and external female genetalia Normal female range testosterone Absent uterus and upper vagina Normal ovaries 46 XX Renal abnormalities get IVP
Most common cause or primary amenorrhea in women with normal breast dev.
Primary amenorrhea with secondary with urterus : outflow obstruction
Normal uterus
Imperforate hymen or transverse vaginal septum
Imperforate hymen
Present complaining monthly dysmenorrhea without vaginal bleeding
Vaginal bulge and midline cystic mass
US confirm normal uterus
Do hymenectomy
Transverse vaginal septum
Simila symptoms but no vaginal bulge
Diagnosed with MRI
Correct with surgery
Secondary ameonrrhea
Absence for 6 months after having it
Causes secondary amenorrhea
Pregnancy! Get pregnancy test
What do if present with secondary amenorrhea
Look for weight change, preg test, exercise, diet, ill, abnormal facial hair, galactorrhea, dyspareunia, hot flashes or night sweats
Uring HcG, TSH prolactin, FSH
Secondary amenorrhea: hypothyroidism porlactinoma
Normal TSH
Galactorrhea is most common symptom of hyperprolactinemia
Really high >100
-MRI for empty sella, pituitary adenoma
High prolactin<100
-if MRI negative consider other causes
Secondary amenorrhea hypothyroidism
Normal prolactin
Abnormal TSH
Mild hypothyroidism-hypermenorrhea or oligomenorrhea,
Treat-restore menes
Abnormal micro vs macroadenomas
<10 mm on MRI-slow growing, manage , bromocriptine
> 1 cm-bromocriptine, resection or craniotomy
What causes prolactin <100
Ectopic production
Breast feeding and stimulation
Exercise
Head trauma
Hypothyroidism
Liver renal failure
Meds
Cause proacting >100
Pituitary adenoma
Empty sella
Secondary amenorrhea did tsh prolactin and negative
Progesterone challenge test
-give provers for several days then stop it. Positive bleed usually POCS
Negative-no bleeding-inadequate estrogen or abnormal outflow tract
Negative progesterone channelge
Estrogen/progesterone challenge
Negative-outflow tract of
Positive-abnormalities with HPA or ovaries
—-
Positive e/p test elevated fsh and lh
Hypergonadotropic hypogonasism
Ovarian abnormalities
Positive e/p test and normal or low FSH LH
Pituitary or hypothalmic abnormality
Get MRI
-no tumor then a hypothalmic cause of amenorrhea diagnosis
Anatomic causes
Asherman
Cervical stenosis
Asherman
Incomplete abortion but had normal periods
DNC was done…can be scarring so menstruation come out
As age sometimes opening of cervical os narrow
Secondary amenorrhea normogonadotropin hypogonadism
Adrenal disorders, ovarian, other
Adrenal nonclassical
CAH increase 17 hydroxyprogesterone
-no genital abnormalities
But have hirsutism, acne and menstrual irregular near puberty
Cushing
Central obesity, moon like faces, buffalo hump, HTN, striae, hirsutism, acne and irregular menses
High cortisol
Adrenal androgen secreting tumor
DHEAS>700
Ovarian disorders
POCS
Ovarian androgen secreting tumor
-sertoli leydig tumros (T>200)
Other
Exogenous androgens
POCS
10%
Leading cause of female anovulatory infertility
Insulin sensitivity
-decrease insulin hypersecrtion
Elevated insulin and androgen levels reduce the hepatic production of sex hormone binding globulins
-increased T
Diagnose POCS
Oligomenorrhea and amenorrhea
Biochemical or clincial signs or hyperandrogenism
-LH to FSH 2:1
US revealing multiple small cysts beneath the cortex of the ovary
Lab POCS
Increase LH decrease FHS
Extraglandular armoatization, chronic anovulation, decreased follicular maturation, stim of stroma and theca
Androgen excess
POCS stuck in ___ phase
Follicular
Increase stroma stimulation increase LH
Chronic anovulation
Features POCS
Anovulation T LH up Acyclic estrogen production Fat Acanthosis nigricans Lipid abnormalities DM CVD Anovulation -increase chance endometrial hyperplasia and cancer
Treat POSC
Weight loss
OC
-suppress FSH and LH
-allow regression of T and androstenedione of ovary
Estrogen stimulates the sex hormone binding globulin
Clomiphene citrate
-can induce ovulation
Ovarian diathermy/laser
Spironolactone and or electrolysis
-competes for testosterone binding sites thereby exerting. Direct antiandrogenic effect at target organ and also interferes with steroid enzymes and decreases testosterone production
Insulin sensitizing agents-biguanides (metformin)
Secondary amenorrhea hypergonadotropic hypogonadism
Pct neg, e p positive, check fsh lh
FSH>20 LH>04
-hypergonadotropic hypogonadism
Postmenopausal ovarian failure-average age of menopause is 51
Premature ovarian failure before 40
Cause-ovarian injury from surgery, pelvic radiation, chemo, carrier status of fragile syndrome, autoimmune, mumps
FSH LH<5
MIR for pituitary tumor
Normal=hypogonadotropic hypogonadism
-anorexia, bulimia
-chronic renal dinsuffiency< DM, IBD
Radiation, exercise, malnutrition, HPA destruction
History hyperandrogenism
PCOS and late onset CAH
Neoplastic disorders
PE-hirsutism, acne, alopecia document, cushing, acanthosis nigricans, bimanual exam for ovarian enlargement
Acanthosis nigricans
Dark velvety skin
Hirsutism
Excess terminal hair in male pattern baldness
Represents exposure of hair t androgen excess
Virilization
Masculinization of a females associated with marked increase in circulating T
Enlargement of clit, temporal balding, deep voice, decreased breast, loss sof female body fat distribution, and hirsutism
Fast rapid onset
Ferrima galloway scale
For hirsutism
Labs hyperandrogenism
17 hydroxyprog
24 hr urinary cortisol and overnight dexameth suppression test
Prolactin and tsh
Glucose and lipid
Testosterone and DHEA-S
(If DHEEAS over 7000 suspect adrenal androgen producing tumor and if T over 200 suspect ovarian androgen producing tumor)
Polymenorrhea
<21 days
Menorrhagia
Prolonged bleeding at normal intervals
Menorrhagia
Irregular episodes bleed
Menometorrhagia
Heavy and irregular
Intermenstrual bleeding
Scant bleeding at ovulation for 1 to 2 days
Oligomenorrhea
Menstrual cyclets occurring>35 days but less then 6 months
Dysfunctional uterine bleeding
Abnormal from HPA and bimodal first start and menopause
PALM-COEIN
Palp structural
Polyp, adenomyosis, leimyoma, malignancy