Urogenital Flashcards

1
Q

Describe spermatogenesis

A
  1. Mitotic proliferation - Creates large number of identical, diploid spertogonia from gonocyte
  2. Meiotic division - Creates genetic diversity formind haploid spermatocytes and spermatids. 2 stages.
  3. Cytodifferentiation (spermiogenesis) - genes packed for delivery and spermatozoa elongated
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2
Q

What are the role of sertoli and leydig cells, where are they found and what hormones stimulate them ?

A

Sertoli cells

  • Found in the seminefrous tubules
  • Attached to sperm via gap junctions, mediating androgen hormone action and convert testosterone into dihydrotesttestorone
  • FSH stimulates them to increase receptors for androgens

Leydig cells

  • Convert choleterol in prognenolone which then forms testosterone
  • Testosterone passed into blood of sertoli cell to be converted. Dihydrotestosterone most potent androgen, stimulates spermatogenesis

GnRH released from Hypothalamus stimulates release of LH/FSH from Anterior pituitary. Negative feedback loop

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3
Q

Describe the changes undergone by spermatozoa during epididymal maturation

A
  • loss of surplus cytoplasm
  • addition of glycoproteins (decapacitation facters)
  • condensation of nuclear chromatin
  • depression of metabolic activity (prolong life)
  • increased dependance on external fructose
  • cAMP content in tail increased allowing Motility!
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4
Q

Describe the contents of seminal plasma and what accessory glands produce it

A

Produced in Ampulla, seminal vesicles and prostate

  • Glycoproteins
  • Fructose
  • Citric acid
  • Acsorbic acid (stop sperm being oxidated)
  • Buffers
  • Prostaglandins
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5
Q

Describe folliculogenesis

A

Primordial follicle - Fixed number at birth!

  • 1 primary oocyte and 1 layer of granulosa cells

Primary follicle

  • Increased oocyte size
  • 1 layer of cuboidal granulosa cells seperated from oocyte by zona pellucida (have GnRH receptors but no blood supply)

Secondary follicle

  • Multiple layes of granulosa
  • Theca cells for and differentiate to form interna & externa
  • Vascularisation of theca layer allowing LH/FSH into follicles

Tertiary follicle

  • Granulosa secrete fluid froming antrum
  • Pituitary LH causes theca cells to become steriodogenic producing Androstendione, the substrate for oestrogen synthesis by granulosa cells
  • Pituitary FSH stimulate granulosa proliferation

Graafian follicle

  • thought to be selected due to competition for FSH
  • Remaining tertiary follicles undergo atresia
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6
Q

Describe positive feedback loop involving eostrogen, LH and FSH

A
  • Oestrogen stimulates pituitary release of LH & FSH
  • FSH causes granulosa cells to proliferate
  • LH stimulates theca cells to produce androgens (Androstendione)
  • Androstendione converted into oestrogen by granulosa cells
  • More oestrogen = more LH/FSH!
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7
Q

How is ovulation induced?

A
  • High levels of eostrogen cause a LH surge
  • LH surge induces release of proteolytic enzymes that weaken follicular wall
  • LH also increase blood flow to follicle, causing an increase in pressure leading to rupture of the wall
  • stigma
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8
Q

What are the funtions of oestrogen and progesterone in the female

A

Oestrogen

  • prepare uterus for sperm transport
  • stimulate the growth of mammary glands and endometirum
  • regulate secretions of gonadotropins

Progesterone

  • Maintain uterus during pregnancy
  • Stimulate growth of mammary glands but suppress secretion of milk
  • regulate secretions of gonadotropins
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9
Q

Describe oestrus cycle

A
  1. Pro-oestrus - Immediately before onset of behaviour (Follicular phase, E2 dominant)
  2. Oestrus - Mating behaviour (follicular phase, E2 dominant)
  3. Metoestrus - Transition period
  4. Dioestrus - CL formed, length dependent on life of corpus luteum (Luteal phase, Progesterone dominant)
  5. Anoestrus - quiescent period
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10
Q

Describe sperm changes that occur in the female tract

A

Capacitation - uterus

  • Progressive destabilisation of the plasma membrane and removal of gylcoproteins exposing ZP3
  • Surface charge altered (attract to oocyte?)
  • membrane fluidity increased, aiding in breakdown of acrosome and influx of calcium ions

Hyperactivation - oviducts

  • Increased intracellular calcium leads to elevated cAMP levels
  • Increased force required to swim through viscous environment of oviduct

Acrosome reaction - at fertilisation

  • Sperm binds to oocyte via ZP3
  • Fusion of sperms plasma membrane and oute acrosomal membrane
  • Enzymes hyaluronidase/acrosin digest through zona pellucida and sperm moves into pervitelline space
  • Equatorial segment fuses with plasma membrane of oocyte and sperm engulfed
  • Cortical granules released by oocyte into pervitelline space to prevent polyspermy
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11
Q

Whats the difference between passive and active luteolysis

A

Passive Luteolysis

  • Occurs in primates
  • A decrease in LH during the luteal phase leads to regression of the corpus luteum
  • Blastocyst secretes LH like substance (hCG) to prolong CL life

Active Luteolysis

  • Oxytocin binding leads to the release of PGF2a
  • Release of Interferon Tau from trophoblast prevents production of PGF2a
    *
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12
Q

Describe the structure of a placentome

A
  • maternal curuncle
  • Foetal cotyledon
  • Six layers of seperation between foetal and mother blood, minimally invasive placenta. Good for prey species, reduction in blood loss when placenta is expelled
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13
Q

Describe how Parturition is induced by foetal stress

A
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14
Q

What are the roles of oxytocin, prostaglandins and oestroegn during parturition

A

Oestrogen

  • Cause hypertrophy of myometrial smooth muscle
  • Liberate phospholipase A2 from lysosomes, allow convertion on arachidonic acid to prostaglandin

Oxytocin

  • release from posterior pituitary in response to cervical stimulation by foetus
  • Lowers excitation threshold of muscles

Prostaglandins

  • Stimulate liberation of calicum ions from intracellular stores
  • facilitate softening of cervix by increasing collage breakdown, increasing proteoglycan matrix fibres and stimulating uterine activity
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15
Q

What is primary and secondary inertia and what are their causes

A

Primary inertia

  • Failure to initiate contractions
  • Lack of oxytocin or oxytocin receptors
  • obesity
  • small foetus

Secondary inertia

  • good initial uterine contractions then a sudden stop
  • Uterus can become fatigued and over stretched
  • Litter size is large
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16
Q

What is ring womb and how is it caused and treated

A

Ring womb is where there are normal uterine contractions but a failure of the cervix to soften. Caused by lack of prostaglandins/receptors, selenium defiency and genetics. Treated by prostaglandin gel on cervix or caesarean section.