Coitus and Fertilisation Flashcards

1
Q

Describe the role of LH and FSH in males?

A

LH (anterior pituitary) → Leydig cells (testis) → testosterone → spermatogenesis
FSH → androgen binding protein (Sertoli cells) → formation of blood testis barrier (↑ testosterone concentration) → spermatogenesis

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2
Q

How can we artificially induce spermatogenesis in males without a pituitary gland?

A

If pituitary gland is removed, spermatogenesis can be initiated with FSH and testosterone alone.

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3
Q

What is the of role of oestrogen and inhibin in males?

A

Oestrogen from the Leydig cells increases sperm viability and just like in the female we have a -ve feedback loop inhibin from Sertoli cells selectively decreasing FSH.

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4
Q

What happens to the sperm in spermatogenesis

A

Nuclear condensation. Acrosome is formed from the Golgi apparatus that develops into a lysosome-like (hydrolytic enzymes) enabling sperm to penetrate ovum.
Midpiece: mitochondria packed around contractile filaments
Tail: flagellum produced by microtubules growing from centriole to form axoneme

Cytoplasm and organelles are stripped under influence of testosterone and the spermatozoa are now mature but lack motility (infertile).

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5
Q

How do the immature sperm get from the sertoli cells to the epididymis and where are they stored? What happens in sexual arousal?

A

They are released from Sertoli cells into lumen of seminiferous tubule (spermiation) and transported to epididymis in testicular fluid (produced by Sertoli cells) by peristaltic contraction. Here they gain motility and become ‘fertile’ in epididymis.

They can be stored in epididymis for several months with no loss of fertility. During sexual arousal → contraction of epididymal wall muscle expels spermatozoa into vas deferens. If not expelled, eventually phagocytosed by epididymal epithelial cells

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6
Q

What are the 4 phases of coitus?

A

Excitement Phase, plateau Phase, orgasmic Phase and resolution Phase

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7
Q

Describe the male excitement phase?

A

Sensory and psychological stimulation → limbic system, activation of sacral parasympathetic neurons and inhibition of thoracolumbar sympathetic neurons. This all results in ACh → M3 receptors on endothelial cells → ↑ Ca2+ → activation of eNOS → NO production. Arteriolar vasodilation in corpora cavernosa increased penile blood flow, penile filling (latency) and penile tumescence (erection). Scrotal skin thickens and tenses. Cowper’s gland secretions

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8
Q

Describe the male plateau phase?

A

Activation of sacrospinous reflex resulting in contraction of ischiocavernosus (compresses crus penis and impedes venous return) causing venous engorgement.
Rise in intracavernosus pressure results in decreased arterial inflow. There is stimulation of secretion from accessory glands: Cowper’s and Littre’s glands which lubricate distal urethra, neutralise acidic urine in urethra and accounts for 5% of ejaculate.

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9
Q

Describe the 2 parts to the male emission phase

A

Emission
Stimulation of thoracolumbar sympathetic reflex
Contraction of smooth muscle in ductus deferens, ampulla, seminal vesicle and prostate. Internal and external urethral sphincters contract and Semen is pooled in urethral bulb

Ejaculation 
Spinal reflex (with cortical control), sympathetic Nervous System (L1, L2), contraction of glands and ducts (smooth muscle), Internal urethral sphincter contracts, filling of the internal urethra stimulates pudendal nerve causing contractions of the genital organs - ischiocavernosus and bulbocavernosus muscles resulting in expulsion of semen. Note contraction of the anal sphincter too.
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10
Q

Describe the male resolution phase?

A

Activation of thoracolumbar sympathetic pathway causing contraction of arteriolar smooth muscle in corpora cavernosa and so increased venous return. Detumescence and flaccidity
Refractory period.

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11
Q

Describe the female excitement phase?

A

Same neuronal responses as male. Vaginal lubrication begins (due to vasocongestion), clitoris engorges with blood, uterus elevates and there is an increase in muscle tone, heart rate, and BP.

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12
Q

Describe the female plateau phase?

A

Further increase in muscle tone, heart rate and BP, Labia minora deepens in colour, clitoris withdraws under its hood and bartholin’s gland secretion lubricates vestibule for entry of penis. Orgasmic platform forms in lower 1/3rd of vagina and the uterus is fully elevated

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13
Q

Describe the female orgasm phase?

A
Orgasmic platform (outer 1/3 of vagina) contracts rhythmically 3-15 times. Uterus contracts, anal sphincter contracts and clitoris remains retracted under hood 
No refractory period - multiple orgasms possible.
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14
Q

Describe the female resolution phase?

A

Clitoris descends and engorgement subsides, labia returns to unaroused size and colour, Uterus descends to unaroused position and vagina shortens and narrows back to unaroused state.

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15
Q

Describe female breast changes during excitement and orgasm.

A

Nipple becomes errect and veins become more distinct, during plateau and orgasm the areolar increases in size and the breast may become flushed.

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16
Q

What is the G spot?

A

Area of erotic sensitivity located along the anterior wall of the vagina. Some women are able to experience orgasm and possibly ejaculation from G spot stimulation. G spot tissue is similar to male prostate; therefore, fluid may be similar to prostatic component of semen.

17
Q

What happens to the female sexual response as they age?

A

Some women report reduced desire, reduced vasocongestion response, causing reduced vaginal lubrication, vaginal and urethral tissue lose elasticity, length and width of vagina decrease; reduced expansible ability of inner vagina during arousal, number of orgasmic contractions is often reduced and there is more rapid resolution.

18
Q

What sexual dysfunctions are there involving desire?

A

Most common sexual dysfunction, increasing incidence. Can be hypoactive – little or no interest in sex (for age, etc.) which may present as aversion – revulsion or fear of one or all aspects of sex, often a result of abuse or assault.

Hyperactive
Nymphomaniac Klüver Bucci syndrome – Bilateral medial temporal lobe lesions – Hyperphagia (eating too much), hypersexuality, hyperorality (putting everything in their mouth), visual agnosia (inability to recognise sensations) and docility

19
Q

What sexual dysfunctions are there involving arousal?

A
Female = persistent, recurrent inability to attain or maintain lubrication-swelling response = lack of lubrication (especially in menopause) 
Male = impotence – Psychological (descending inhibition of spinal reflexes) – Tears in fibrous tissue of corpora cavernosa – Vascular: atherosclerosis, diabetes – Drugs: Alcohol, anti-hypertensives (β-blockers, diuretics). Viagra: Inhibits cGMP breakdown in corpus cavernosum → ↑ nitric oxide-stimulated vasodilatation → ↑ penile blood flow → erection
20
Q

What are the glandular components of semen

A
Bulbourethral glands (Cowper's glands): 5% volume, alkaline fluid and mucous lubricates the tip of the penis and urethral lining 
Seminal vesicles: 60% of volume, alkaline fluid (neutralizes the acid in male urethra and female reproductive tract) and Fructose (ATP production), prostaglandins (↑ sperm motility, ↑ female genital smooth muscle contraction), clotting factors (particularly semenogelin) 
Prostate: 25% volume, milky, slightly acidic fluid, proteolytic enzymes (e.g. PSA, pepsinogen: break down clotting factors from seminal vesicles, re-liquefying semen in in 10-20 minutes), citric acid (ATP production), acid phosphatase
21
Q

How does cervical mucus change through a woman’s menstrual cycle?

A

Days 7-14 – abundant clear non-viscous cervical mucus – this is when sperm can get in
Days 14-28 – thick sticky mucus plug to prevent infection.

22
Q

Describe oocyte maturation

A

Oocyte maturation: cytoplasmic maturation 1
Mitochondria – Dispersed throughout cytoplasm
Endoplasmic reticulum – Accumulates in oocyte cortex – Protein and lipid synthesis → cortical granules – Immature oocyte: Cortical granules displaced throughout cytoplasm (Fig. E) – Become cortical during maturation (Fig. G).

Oocyte maturation: cytoplasmic maturation 2
Lipid droplets provide energy (meiosis, maturation, fertilisation, and early embryo development) Cytoskeleton: Microfilaments migrate toward oocyte cortex

23
Q

When can fertilsation take place

A

Sperm survive for up to 5 days in female genital tract, Oocyte survives 6- 24 hours before phagocytosis. Fertile period: sperm deposition up to 3 days prior to ovulation or on day of ovulation. Oocyte takes 3-4 days to travel from ovary to body of uterus (cilia and Fallopian tube peristalsis) Fertilisation is in Fallopian tube.

24
Q

What processes does the sperm need to do to fertilise the egg?

A

Sperm needs to penetrate corona radiata (follicular cells) and zona pellucida (glycoprotein membrane).

Capacitation
Further maturation of sperm in female reproductive tract (6-8 hours). Sperm cell membrane changes to allow fusion with oocyte cell surface – Removal of protein coat of sperm – Acrosomal enzymes are exposed. Tail movement changes from beat to whip-like action (3mm/hour).

When sperm contacts corona radiata, it has an intact acrosome. The sperm pushes through granulosa cells of corona radiata and the proteins on sperm head bind to ZP3 proteins of zona pellucida (ZP). Binding triggers acrosome reaction – Key signalling mechanism involves intracellular Ca2+ – Acrosomal enzymes digest path through ZP – One sperm penetrates and fuses with plasma membrane of egg. Sperm moves into cytoplasm: oocyte and sperm → zygote – Polyspermy blocked (cortical reaction).

25
Q

How is the oocyte plasma membrane divided into two parts?

A

The oocyte plasma membrane can be divided into two major regions:
The part of the membrane that directly overlies the metaphase chromosomes has a smooth surface devoid of microvilli.
The remainder of the oocyte is rich in microvillar protrusions. This is the region of the oocyte where sperm bind and fuse.

26
Q

What are the two types of block for polyspermy?

A

Block to polyspermy: Fast block
Electrical change in oocyte membrane. Sodium channels open (Resting potential -75mV, fertilisation potential +20mV). Wave of depolarisation starts at the site of entry of sperm and propagates across cytoplasm.

Block to polyspermy: Slow block
Ca2+ released from ER, induces local exocytosis of cortical granules. Granules release enzymes to stimulate adjacent cortical granules to undergo exocytosis. Wave of exocytosis occurs around oocyte in 3 dimensions from original site of sperm entry.

27
Q

What is syngamy?

A

Oocyte completes meiosis II. Expels second polar body. Male and female pronuclei migrate toward each other (23 + 23 chromosomes). Union of male and female pronuclei to form diploid zygote (46 chromosomes) = syngamy.

28
Q

Describe the interesting nature of the first few divisions of the fertilised egg?

A

Increased number of cells (16 – 32 blastomeres) of decreasing size, without increase in size of fertilised ovum. Totipotency = each cell has capacity to develop into entire individual.
Monozygotic twins = in cleavage, totipotent cells become divided into 2 separate independent cell masses (25-35% of twins follow separation after 1st cleavage). Dizygotic/ non-identical twins = 2 eggs ovulate, 2 eggs are fertilised.

29
Q

Why is cleavage important?

A

Generation of many cells that can undergo differentiation and gastrulation to form organs.
Increase in the nuclear/cytoplasmic ratio – One nucleus cannot transcribe sufficient RNA to support the enormous cytoplasm of the zygote – No G1 (duplication of organelles and cytosol) or G2 (synthesis of enzymes and proteins) stages in cell cycle during cleavage. With each mitotic division during cleavage, the nuclear-cytoplasmic ratio increases. Cleavage is asynchronous (not all blastomeres divide at the same time).

30
Q

What occurs at the 8 cell stage?

A

At the 8 cell stage, blastomeres undergo polarisation and form tight junctions to create ‘inner embryo environment’. Morula - 16 blastomere stage, 3-4 days after fertilisation. Embryo passes from oviduct into uterus.

31
Q

What is ectopic pregnancy?

A

Presents with iliac fossa pain. Failure of transport of morula into uterus. Implantation in Fallopian tube, ovary or peritoneal cavity. Risk of maternal haemorrhage. Embryo is nonviable.

32
Q

What is hatching?

A

Local digestion of zona pellucida cells by enzyme produced in trophoblast cells this occurs opposite the inner cell mass (minimizes risk of enzymatic damage to the embryo). After escaping from the ZP, blastocyst begins process of implantation.