Reproduction

Infertility in male
1 Hypogonadism
 Too little or almost no testosterone
 Spermatogenesis do not take place
 Less sperm produce

2 Cryptorchidism
 Testes fail to descend
 One or both testis in abdominal cavity
 ↑ temp (heat), not suitable for spermatogenesis, irreversible damage
 Risk to testicular tumor
 Testes in the scrotal ; countercurrent exchange system between arteries and veins, large
surface area of scrotum, muscle control scrotal position

*when there is no spermatogenesis, ↓ normal sperm count (normal 60-100 x 100⁶ per ml), lead to
oligospermia, num of sperm< 20 x 10⁶ per ml, infertility

Function testosterone (T)

1 Prenatal / fetus
 Sexual differentiation
 Descend of testis from abdomen
 Development of prostate and seminal vesicle
 No testosterone → female genitalia form

2 Infancy
 Brain, testosterone →E2 by aromatase
 Responsible for masculinization of the brain in male

3 Pubertal
 2ᵒ sex characteristic
 Sebaceous gland enlargement, cause acne
 Phallic enlargement
 ↑ libido & frequency of erection
 Hair growth; facial, axillary, pubic, chest, leg
 Deepening of voice
 Growth of spematogenic tissue in testicle
 Remodeling of facial bone, shoulder become broader,↑ linear growth of bone (limited,
early closing o
 Spermatogenesis; spermatogonia → spermatozoa, including FSH, LH from ant pit

4 Adult
 Normal sperm development, activate gene in Sertoli cell.
 Action; T and DHT bind to ABD (androgen binding protein), concentrate this hormone in
seminiferous tubule (ST), ↑ level enable spermatogenesis in ST, maturation in
epididymis
  Mental and physical energy; ↑protein synthesis and tissue growth muscle size ↑
 Stimulate erythropoiesis, regulates population of thromboxane A₂; platelets aggregation

Anabolic steroid
 T : LH ratio
 Normally LH ↑,
 If T ↑↑, -ve feedback to ant pit & hypoT
 Side effect: ↓ spermatogenesis, ↓ sperm production

Ovarian cycle, uterine cycle & menstruation cycle

 Ovarian cycle + Uterine cycle = Menstruation cycle
 Ovarian cycle, occur at ovary
 Uterine cycle, occur at uterus
 Ovarian cycle; follicular phase, luteal phase (14 days)
 Uterine cycle; proliferative phase, secretory phase, menstruation
 Relation btwn uterine cycle & ovarian cycle
o 1st day of menstruation indicates 1st day of ovarian cycle
o Growth of follicle release E2, promotes thickening of endometrium
o Small follicles very dependent on FSH, large follicle less dependent on FSH → that why
there is a dominant follicle
o Continuation of high level of E2, give +ve feedback to ant pit & hypoT to ↑ GnRH, ↑LH
causing LH surge
o LH surge → completion 1st meiotic division, ovulation
o Follicle cell → CL, release Pg, vascularised endometrium, ready for implantation
o CL maintain; Pg, E2 give –ve feedback keeps FSH, LH levels low but CL very sensitive to
LH
o CL degenerate; no fertilization, CL sensitivity to LH ↓, low levels LH insufficient to keep
CL going, menstruation.
*low Pg at follicular phase, secretion of Pg does not release into blood
*Luteal phase exactly 14 days, calculate follicular phase if the menstruation cycle is 33 days
33 – 14 = 19 days

Pregnancy test
 Measure the hCG (human Chorionic Gonadotrophin)
 hCG secreted by the placenta
 +ve after 35 days of LMP

Gestational Diabetes Mellitus (GDM)

 Due to placental hormone; hPL, hGH
 Anti insulinic effect, insulin resistance to the maternal by increasing maternal blood glucose
 Causing hyperglycemia by providing glucose to the fetus

Physiology changes during pregnancy

1 Lower limb edema during late pregnancy
 Fetal growth compress the IVC
 Causing ↑HP, ↓ OP
 Estrogen causing H₂O retention

2 Reduction in Hct is seen despite increase in RBC mass

  Haemodilution, estrogen causing compensatory Na⁺ & H₂O retention
 ↑plasma volume
 ↑ RBS mass; to optimize O2 transport to fetus
 20 % ↑ in total number & volume of RBC, 50 % ↑ plasma volume
 Despite an ↑ in RBC volume, there is ↑↑ plasma volume
 Causing < in Hct

3 Constipation and gastritis

 Pg causing relaxation of muscle,
 ↓ small bowel activity, ↓motilin activity, ↑ H2O reabsorption, constipation
 Fetal growth exert pressure to stomach, contain of stomach might efflux, over flamed the
lower part of esophagus due to acidity, gastritis

4 Hyperventilation can occur during late pregnancy

 Pg stimulate respiratory center by ↑ sensitivity to CO2
 ↑ BMR , total amount of O2 used > than normal, ↑ CO2 formed

5 No increase in free T4 despite an overall increase in total thyroid hormone during pregnancy
 E2 stimulate production of TBG
 T3 , T4 stimulate TSH, ↑thyroid hormone production
 More bind to TBG

6 GDM is more common twin pregnancy

 Large size of placenta, ↑ placental hormone, anti insulin effect, > insulin resistance
 Placental hormone; hPL, hCC

7 Maternal hyperglycemia, result in fetal hyperinsulinemia

 Fetal receive high blood glucose from the mother
 Compensate by ↑ insulin production
 After parturition, causing hypoglycemia
 Insulin level takes time to decrease, take up glucose within the body
 As no more receive high blood glucose from mother

8 Maternal MAP lowest in mid pregnancy

 Pg causing vasodilation at the uterine bed
 ↓ TPR to a > degree than the CO ↑
 Leading to a drop in arterial P

9 Pregnant women feel thirsty easily

 ADH threshold secretion ↓, causing ↑ in ADH secretion stimulate thirst centre
 Pg also weak antagonism to aldosterone action
 More fluid excrete from the body