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12- REPRO > Physiology > Flashcards

Physiology Flashcards

1
Q

2 functions of gonads

A
  1. endocrine

2. gametogenic

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2
Q

Role of SRY in males

A

SRY > SOX9 > Other genes > sertoli cells > leydig cells/testes > hormones > male ducts and genitals

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3
Q

What is the biopotential gonad?

A

Embyro - bipotential genital ridge has both Wolffian and Mullerian ducts

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4
Q

What happens to the Wolffian and Mullerian ducts in males and females?

A

Male:
• Mullerian ducts regress (apoptosis)
• Wolffian ducts differentiate epididymis + vas deferens

Female:
• Wolffian ducts regress – apoptosis
Mullerian ducts differentiate oviducts, fallopian tubes, uterus, cervix and upper vagina

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5
Q

At what point in parturition are the reproductive axes differentiable?

A

7 weeks
7-8 weeks: primitive gonad cortex development = SRY activation

Males: SRY controls early testes differentiation and stimulates sertoli and leydig cells to secrete Testosterone and AMH

Females: primitive gonad cortex develops into ovary (medulla regresses) and the embryonic ovary does not secrete hormones

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6
Q

How is puberty regulated by the HPG axis?

A

Brain stimulates the hypothalamus > increase GnRH Ant pit. > increase LH + FSH > gonads to produce sex hormones > ovaries produce estrogens and testis produce testosterone

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7
Q

Pulsatile secretion of GnRH

A
  • Onset of GnRH pulses typically occurs at night, due I part to gradual decrease in nocturnal melatonin secretion from pineal gland
  • Also influenced by nutritional status of body and growth rate (Leptin/ghrelin, GH + IGF-1)
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8
Q

What converts testosterone to DHT in target cells?

A

5 alpha reductase

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9
Q

What complexes are required for male external genitalia?

A

DHT-R complexes

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10
Q

Testosterone feedback control

A
  • Systemic T powerfully inhibits GnRH +LH secretion ( reduced testosterone)
  • Blood testis barrier – sertoli
  • Leydig cells secrete T bathes seminiferous epithelium, provides 100x increase in local androgen
  • Sertoli cells also secrete ABP

**IV testosterone does not raise testes androgen level much so = reduced sperm count

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11
Q

Temperature difference and regulation between body and testes

A
  • Temperature in testes is 2-3’C lower than body temperature
  • Scrotum > sweat glands, pampiniform plexus, cremaster + dartos muscle (increase temp cremaster m dartos relaxes > testes descend > cool)
  • Pampiniform plexus CCX
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12
Q

Spermatogenesis steps

A
  1. primordial germ cells (embryonic) migrate become spermatogonia
  2. @puberty, spermatogonia mature, proliferate and differentiate&raquo_space; 1° spermatocyte
  3. Meiosis I&raquo_space; 2x 2 spermatocytes
  4. Meiosis II&raquo_space; 4x spermatids
  5. Differentiate into mature spermatozoa
  6. 1 spermatogonium can&raquo_space; ~512 sperm, takes ~74 days
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13
Q

4 functions of sertoli cells

A
  1. Envelope/create niche/nourish germs cells (lose
    contact = die) – contain lipid, glycogen
  2. Secretory: AMH, inhibins/activins, ABP, oestradiol
  3. Create blood-testis barrier (apical sp. movement reqs constant reforming of gap junctions)
  4. Modify seminiferous tubule fluid (↑ local [steroid], [nutrients])
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14
Q

Contents of head and tail of spermatozoa

A

Head
¥ Contain haploid genome – X or Y
¥ Acrosome: large quantities of hyaluronidase and proteolytic enzymes to facilitate ovum penetration
¥ Minimal cytoplasm

Tail
¥ Mitochondria-packed&raquo_space; power
¥ Motile microtubules flagellate – propels sperm @ 1-3mm/min

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15
Q

Sperm maturation

A

Achieved at distal corpus or caudal (6-8 days)

  1. Acquire progressive motility
  2. Biochemical changes
    o ↑ capacity for glycolysis

o ↑ phospholipid & phospholipid-like fatty acid content

o Activation of CatSper (Ca2+-R reqd for acrosome rxn)

o Olfactory Rs&raquo_space; chemotaxis (lily of the valley)

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16
Q

Vascular event of erection

A

Parasympathetic
Vasodilation: increased arterial blood flow to corpora cavernosa turgor compresses veins = limits loss of blood erection

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17
Q

Ejaculation

A

Sympathetic - 2 part spinal reflex
Emission
o Movement of semen through urethra
o Vas deferens sm. Muscle contraction move sperm forward
o Prostate, seminal vesicle sm muscle contraction move prostatic + seminal fluid forward
Ejaculation
o Propulsion, expulsion
o Rhythmical contraction of bulbospongiosus

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18
Q

Capacitation

A

PSA degrades semenogelin&raquo_space; increase motility, alkaline uterine/fallopian fluid alters membrane (reduces chol, increases Ca2+ perm)

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19
Q

Acrosome reaction

A
  • Hyaluronidase and proteolytic enzymes digest proteins in ovum ECM
  • Sperm reaches zona pellucida&raquo_space; sperm membrane binds receptor proteins (ZP3), entire acrosome rapidly dissolves enzyme release
  • Open penetrating pathway for passage of the sperm head through the zona pellucida&raquo_space; inside ovum.
  • Sperm head + oocyte membranes fuse (cortical rxn) &raquo_space;deliver sperm genome
20
Q

Endocrine function of the ovaries

A

Oestrogens (potency: beta-estradiol > oestrone > oestriol)
o Granulosa cells - also corpus luteum
o Require aromatase activity
o Regulated by LH and FSH

Progesterone
o Corpus luteum – tiny amount from follicular theca cells
o Regulated by LH (via Camp)

Inhibin B (inhB)
o	Secreted CL granulosa cells granulosa cells – inhibit anterior pituitary FSH secretion
21
Q

Effects of estrogens

A
  • Facilitate growth of ovarian follicles + uterine tube motility
  • Cyclical changes in endometrium
  • Increased blood flow + smooth muscle contractility of uterus
  • Oestrogen dominated uterus is more sensitive to oxytocin
  • Increases breast duct growth
22
Q

Feedback of oestrogen’s

A
  • Inhibits FSH

* LH – complex, either increase or decrease

23
Q

Progesterone effects

A

Uterus – progestational changes in endometrium, cervix and vagina

Antioestrogenic effects – prevents uterine contraction
o Reduces excitability, oxytocin response, number of ERs

Breast – stimulates lobule + alveoli devt, supports lactation

Brain – stimulates thermogenesis and respiration

24
Q

Feedback of progesterone

A

Inhibits LH - prevent ovulation

25
Q

Follicular changes in the follicular phase of the ovarian cycle

A
  • Several follicles enlarge, cavity forms around ovum (antrum) filled with follicular fluid
  • 10-15 days before ovulation – dominant follicle starts to grow rapidly, others regress (apoptosis – atretic follicles)
  • estrogen is now produced from ovary granulosa cells (via theca interna cells)
  • oocyte increases zone pelucida (glycoprotein shell)
26
Q

When are ALL oocytes formed by?

A

7 months gestation

27
Q

What inhibits other primordial cells from entering the primary follicle transition>

A

Granulose cell aMH or pre-astral follicles

28
Q

The luteal phase

A
  1. After ovulation (d14), ruptured follicle fills with blood corpus haemoragicum
  2. Granulosa/theca cells proliferate corpus luteum (lipid-filled)
    a. CL secretes megadoses of progesterone + oestrogen

b. plus lots of VEGFa + Fgf2 vasculogenic
c. CL growth

29
Q

2 things the LH surge causes

A
  1. Theca externa releases proteolytic enzymes (collagenase) dissolve follicular capsule wall degeneration of the preovulatory opening (stigma).
  2. Prostaglandins follicular tissue smooth muscle contraction of the follicle ovum expulsion
30
Q

What causes the LH surge?

A

¥ GnRH LH+FS Prog, inhB (-ve fbk), + oest

¥ Oestrogen has 2 opposing effects on ant. pit. LH secretion:
Moderate, constant oestrogens suppress GnRH + LH secetion
Aberrantly elevated oestrogens increase GnRH + LH secretion

31
Q

When does the fertilised oocyte become a blastocyst and implant?

A

Blastocyst: by day 4
Implantation: 6-9 days post conception

32
Q

Endocrine changes post conception

A

¥ CL fails to regress enlarges secretes oest, prog, relaxin (inhibits myometrial contraction maintains pregnancy)

¥ Implanting syncytiotrophoblasts form placenta
o Mother’s endometrial tissue also contributes to placenta

¥ Placenta becomes a hormone-secreting factory!

33
Q

Primary and secondary ageing

A

1°aging: intrinsic changes occurring with age, unrelated to disease or environmental influences
2°aging: changes caused by the interaction of primary aging with environmental influences or disease processes

34
Q

Evolutionary mechanisms of ageing

A

Mutation accumulation - Any mutations that result in a post-reproductive reduction in fitness will not be removed by natural selection
¥ GBA, LRRK2, SNCA (PD), Huntingtin, et al.

Antagonistic pleiotropy – a gene that exerts a small pre-/reproductive benefit and a large post- reproductive cost will still be selected for
¥ P53 activating mutations (anti-tumour, ↓ lifespan)

35
Q

Programmed theories of ageing

A

Programmed theories:
¥ Neuroendocrine: biological clock and endocrine control
¥ Immune: immune system is a pacemaker of ageing
¥ Finite cell division: cells stop dividing after finite number of divisions

36
Q

Wear and tear theories of ageing

A

¥ Free radicals: FR damage accumulates ageing
¥ DNA damage: DNA damage accumulates ageing
¥ Aggregation: proteins become aggregated, not cleared
¥ Recycling failure: old/dysfunctional proteins not cleared

37
Q

Cellular and molecular processes that cause ageing

A
  1. Damage caused by oxidative stress
  2. Inadequate repair of damage
  3. Dysregulation of cell number
38
Q

How cells respond to damage/replicaiton

A

Ð Arresting growth of old/damaged/dysfunctional cells (anti-cancer)
Ð Beneficial early in life; may contribute to aging later - altered secretion of proteases, cytokines and growth factors

39
Q

Senescence effect on skeletal cells

A

¥ Late 30s ↓1-2% mass/year, >75 yo accelerates
• ↓myofibre size + number
¥ Myogenic or neurogenic? ↓ activity + MNloss

40
Q

Senescence effect on bone remodelling

A

– Starting in middle age, resorption>formation progressive mass loss
– Menopause accelerates loss

41
Q

Senescence effects on synovial joints

A

– joint flexibility declines, articular cartilage thins, and↓tensile
stiffness, fatigue resistance, and strength.

– ↑glycosylation & collagen cross-linking, loss of proteoglycans.

– Loss of elasticity, tendency towards osteoarthritis

42
Q

Senescence effects on CNS

A
  • Atrophy 0.1% per year 20 to 60, then 0.5% after 70
  • Diffuse uniform increase in cortex and hippocampus, ventricles expand
  • Aggregate accumulation
  • Reduced neurotransmission
43
Q

Senescence effects on pNS

A
  • Reduced regenerative response
  • Demyelination/axonal atrophy/electrophysiology slowed conduction
  • Damped signal transduction
  • Reduced beta adrenergic and muscarinic responsiveness
  • Reduced response to beta blockers
44
Q

Sensory effects from senescence

A
  • Touch, vibration, spatial distinction, proprioception, vestibular function
  • Hearing loss (esp. high-frequency)
  • Vision deteriorates
  • Central processing deficit  difficulty distinguishing spoken words from background noise
  • Taste & olfaction modality qualities deteriorate
45
Q

Effects of senescence on motor functions

A
  • Slowing of central processing

* Reduction in simple response, greater reduction in complex ones

46
Q

Pulmonary function in senescence

A
  1. reduced respiratory muscle strength and endurance – atrophy of type 2a myofibres
  2. lung volumes (static and forced) reduced gradually
    a. reduced vital lung capacity, RV, FEV1
  3. Lung elasticity (compliance)
    a. Collagen and elastin degenerate
    b. Small airways collapse (atelectasis)
    c. Results in impaired ventilation, increased V/Q mismatch and lowers resting PaO2

12- REPRO (7 decks)

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