Sex And Reproduction 💘 Flashcards
Stages of sex- arousal/ excitement
Raised bp pulse respiratory rate flushing nipple erect ion genital and pelvic vascular engorgement
Vagina lubrication vasocongestion of vaginal walls erection of clitoris and labia
Scrotum thickens and testes rise
Plateau
Period of excitement prior to orgasm
Increased hr bp muscle tension etc
Sense of impending orgasm can last up to three minutes
Females orgasmic platform, bartholin secretions
Makes urethral sphincter contracts to prevent urine mixing with Semen and retrograde ejaculation pre ejaculatory fluid (cowpers gland)
Orgasm
Conclusion of plateau release of sexual tension and endorphins quick cycles of muscle contractions euphoric sensation
Peak pr bp reap flush etc
Females 5-12 muscle contractions and increased vaginal secretions
Male ejaculate 3-6 contractions of muscles
Resolution
Relaxation make have compulsory refractory period
Pr bp falls drowsiness
Females blood vessels dilate pelvic organs drain cervix opens sand drops into vagina
Makes everything relaxes and testes drop
Effects of aging
Delayed erections less firm longer excitement stage more stimulation needed less ejaculation with less semen
Females reduced lubrications and muscle tension and libido may need hrt
Hypoactive
Sexual desire
Lifelong generalized is never having desire
Situational is no sexual interest in ur partner but want sexual stimulation
Acquired generalized is previously having sexual interest but not don’t
Vaginismus
Can’t achieve penetration due to muscle spasm
May be due to abuse anxiety pain and phobia
Need vagina trainers
Female anorgasmia
Delay/ abscence of orgasm
Unmet needs poor technique can be normal for them
Premature ejaculation
Performance anxiety
Usually younger men
Psychological and drug treatment
Erectile dysfunction
Due to drugs alcohol hiv etc
Treated with injections pellets prostheses pumps psychological pherapy
Make orgasmic disorder
Delay/ abscence of ejaculation sexual trauma hostility lack of trust
Psychological management
Gene that gives male characteristics
SRY box/gene
Gonad formation
Form from potential primordia and form either side of dorsal aorta Form from somatic tissue genital ridge primordia
These cells produce chemoattractant primordial germ cells from the allontois
PGCs migrate along hindgut and populate femoral ridge by week 6
Two mesenchymal knots at either side of aorta
Most pgcs at developing kidney region by day 30
Coelemic epithelia migrate as columns- primitive sex cords
Gonad differentiation
I’m males pgcs colonize medulla in females the cortex
So medulla develops into a testis and cortex degenerates in males
and in females the cortex develops into an ovary and medulla degenerates
Male and female cell differences
Males form leydig cells vascular tissue and myoid cells from which tubule of rete blastema and rete testis
Females form theca cells and vascular tissue
None of the cells in both sexes express sry
Mesonephric primordia
Pgcs in the sexes
Males : pgcs encase in sex cords and cease mitosis
Females : surrounded by granulosa and enter meiosis forming oocytes
Amh and androgen essential for male development
The ducts
Males wolffian duct develops into epididymis vas deferens and c and Müllerian ducts degenerate
In female Müllerian ducts develop into oviducts and uterus and wolffian duct degenerates
Turners syndrome
Unpaired X chromosome
has ovaries but infertile
Woman
Klinfelters syndrome
Extra sec chromosome
Xxy
Has testes but infertile
Man
Androgen insensitivity syndrome
Androgen secrets but no androgen receptors
Xy but phenotypically female and infertile
No internal genitalia testes present testosterone produced
However some become phenotypically male at puberty
Clitoris expands into penis and testes descend so function as normal males
As sometimes rising androgen levels can overcome tissue insensitivity
Congenital adrenal hyperplasia
Xx fetal adrenals hyperactive yo overcome low production of corticosteroids
Both sec ducts retained so external male genitalia
Sry chain
SRY SOX9 inhibits fox12 PGD2->FGF9 AMH SOX 9 is a transcription factor absence results in person having both ovaries and testes ovotestis
FOX12 becomes
Wnt4
Granulosa cell
First mitotic stage of oogenesis
Diplotene into germinal vesicles
They then reside as primary oocytes in the primary follicle and are surrounded by granulosa cells
Folliculogenesis
Starts with primordial follicle which is a primary oocyte surrounded by single layer of granulosa cells and has supporting mesenchymal cells and surrounded by membrane propria
Takes 70+ days to become primary follicle and wiki have zona pellucida
Then preantral with multiple layers of granulosa
Then early Antral which has antral cavity
The mature follicle
Follivulogenesis order
Primordial follicle Primary follicle Preantral follicle Early antral follicle Nature follicle
Gnrh lh fsh action
Hypothalamus releases gnrh causing Anterior pituitary gland to release FSH and
LH acts on theca interna which has LH receptors causing androgens to be made
FSH acts on granulosa cells and androgen aromatase is made
Androgens get converted into
Androgen aromatase which converts into oestrogen
Increase in plasma estrogen inhibits hypothalamus and anterior pituitary secreting further
Androgen also produces amh to increase growth of granulosa cells
Increase estrogen levels causes granulosa cells to also express lh receptors and anterior pituitary secretion increased so lh levels increase and acts on both cells to trigger ovulation
At lh surge
Oocytes resume meiosis and go through a division called nuclear maturation
Secondary meiosis begins and oocytes arrest at metaphase
Cytoplasmic maturation
Cytoplasm reorganized
Mitochondria and cortical granules relocate to periphery
Associated granulosa cells called cumulus go under expansion
Ovulation
Day 14
Outer walls swell rapidly stigma forms viscous fluid oozes
Stigma ruptures viscous fluid envaginates carrying ovum and mass of granulosa cells
Lh acts on granulosa and theca converting them to produce progesterone
Estrogen secretion begins to fall prior to ovulation whilst progesterone secretion rises
Uterine cycle stages
Menstrual phase -shedding of uterine lining
Proliferative phase- endometrium and myometrium regrow and prepare for possible pregnancy
Secretory phase- blood supply remodeled cervical secretions change. Supported by progesterone.
Secretory phase
blood supply remodeled cervical secretions change.
Supported by progesterone.
Estrogen and progesterone produced by corpus luteum estrogen reduces proliferation progesterone causes swelling and secretion.
Ready for implantation
Menopausal symptoms
Hot flushes Mebstrual irregularity Mood swings Fatigue Dry skin
Hormone replacement therapy
Can he given as pills patches creams
Oestrogen alone can cause endometrial hyperplasia and carcinoma so usually prescribes with progesterone
Risks and benefits of hormone treatment
Benefits are relief of symptoms osteoporosis prevention protection against colon cancer and cardiac disease(younger)
Risks include thrombosis uterine cancer breast cancer Alzheimer’s and cardiac disease (older)
Adrenal he
Adrenal development towards puberty
Thelarche
Breast development in puberty
Pubarche
Pubic hair development in puberty
Menarche
First menstrual period
The higher ur weight the quicker u get it
Menopause
Last menstrual bleed
Perimenopause
12 months before and after menopause
Postmenopause
Life after menopause
Climacteric
Life leading up to the last menstrual bleed
Precocious puberty
Getting period below age of nine
Result of cerebral tumors congenital adrenal hyperplasia ovarian tumors or drugs
Delayed puberty
Getting period above age of 16
Can be due to athleticness congenital abnormalities or chromosome abnormalities
Which part of the penis fills with blood during an erection
Corpus cavernosum
Layers of uterine lining
Endometrium
Myometrium
Perimetrium
Most common site of carcinoma in prostate
Peripheral zone
Which hormone causes musculation of embryo
Anti Müllerian hormone causes regression of Müllerian ducts
First stage of spermatogenesis
5 mitotic divisions
Spermatogonium type a1 becomes a2 a2 divides into a3 then into a4 then into intermediate spermatogonium then into type b then the testing primary spermatocyte
After sperm mitosis
Then undergoes meiosis after entering that adluminal compartment primary spermatocyte produces secondary spermatocytes in meiosis one, then undergoes meiosis to producing early spermatids
Spermiogenesis
Early spermatids> late spermatids> spermatozoa
Spermatids change from round to elongated.
Golgi apparatus gives rise to granules which form the acrosome vesical which grows over the nuclear surface like a cap .
The centrioles lie at the opposite end
The centrioles lie at apposite end then what
Pole of spermatid and form the distal centriole and microtubule flagellum forms. Proximal centriole forms neck which joins to tail and head. Nucleus and acrosome Move to membrane causing elongation and the chromatin condenses. Superfluous nuclear membrane and nucleoplasm is lost. The mitochondria is moved to surround the mid-piece of the flagellum and as sperm is hatched excess cytoplasm is pinched off
Oligozoospermia
Low sperm count
Aspermia
Complete absence of sperm retrograde ejaculation
Azoospermia
No sperm due to genetic, chemo, or dysfunction of hypothalamic pituitary gonadal axis
Asthenozoospermia
Low motility
Teratospermia
Abnormal morphology
Eg globospermia- rounded heads- no acrosome
Male endocrinology
LH stimulates leydig cells which produce testosterone.
Testosterone the negatively feedbacks on the hypothalamus reducing LH.
FSH binds to receptors on Sertoli cells.
Testosterone then rapidly enters the blood and lymph and is converted into dihydrotestosterone in sertoli cells and binds to androgen receptors which is essential for Sertoli cell function
Semen
Contains sperm fructose citric acid and inositosol prostaglandins and more
Enlarged prostate
Due to a benign prostate hyperplasia or prostate cancer. Can be treated with GNRH antagonist e.g. gaserelin in androgen receptor antagonist e.g. bicalutamide reductase inhibitor e.g. finasteride
Erection
Sensory stimulation occurs which causes nitrogen oxide to be converted into SGC which is a catalyst for the conversion of GTP to see GMP this causes vasodilation PDE5 makes it flaccid again by inhibiting CGMP which causes vasoconstriction . Too much PD5 can cause erectile dysfunction
Erectile dysfunction treatments
Phosphodiesterase inhibitors e.g. sildenafil E1 agonists e.g. alprostadil, dopamine receptor agonist e.g. apomorphine
