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HR MVST 1b > Puberty and Coition > Flashcards

Puberty and Coition Flashcards

1
Q

What are the stages of life?

A 
Embryonic and fetal existence
Infancy and childhood
Puberty and adolescence
Early and middle adulthood
Late adulthood and old age
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2
Q

Define puberty

A

The transition phase that takes a person from being a sexually immature child to a sexually mature, reproductively fertile adult

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3
Q

Define pubescence

A

The state of the child between onset of pubertal changes and the completion of sexual maturation

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4
Q

What is the definitive sign of puberty beginning? Do these represent fertility?

A

Menarche females
First ejaculation males (often nocternal)
No - first menstrual period often anovulatory, first ejaculate small quantities of seminal plasma and no spermatozoa

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5
Q

What is gonadarche?

A

Steroid hormones beginning to be secreted from the gonads

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6
Q

What is adrenarche?

A

Steroid hormones beginning to be secreted from the adrenal gland

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7
Q

Why are boys taller than girls?

A

Boys begin the adolescent growth spurt 2 years later, and so are taller at the point of take-off
Height gain during the spurt is similar for both boys and girls
10cm difference in average height thus due to difference at the point of take-off

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8
Q

What are the phases of the adolescent growth spurt?

A
  1. Time of minimum growth
  2. Time of peak height velocity
  3. Time of decreased growth velocity
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9
Q

What is the growth spurt dependent on?

A

Sex hormones and growth hormone from ant pit

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10
Q

Compare the body composition changes at puberty of men and women

A

Adult men 1.5x lean body mass of women
Women 2x as much body fat
Skeletal mass adult men 1.5x women
Men (due to more androgens) greater number muscle cells

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11
Q

How long after menarche is first ovulation?

A

Months to two years

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12
Q

Describe the changes of females at puberty

A

9 Growth spurt
10 Secondary sexual characteristics
- Growth and widening of pelvis
- Appearance of pubic hair
- Breasts grow and mature
Metabolic rate, BP and HR increase
11 Ovaries/oviducts/uterus/vagina grow and mature
12 Filling in of breasts, appearance of axillary hair, menarche
13 First ovulation, sketal growth declines,
- Sweat and sebaceous glands become more active
14
- Slight lowering of voice
15
- Adult stature reached

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13
Q

Describe the changes of males at puberty

A

9 Initial stages of spermatogenesis. Leydig cells appear and begin androgen secretion.
10 Growth and maturation of testes/
11 vas deferens/seminal vesicles/prostate gland
Growth scrotum and penis
Spontaneous erections more frequent (response to stressful or emotionally-charged stimuli)
Secondary sexual characteristics
- Pubic and axillary hair,
Growth spurt begins
12
Nocturnal emissions during sleep or after waking
- More pubic hair
13
- Hair in axilla
- Sweat glands in axilla
- Nipple pigmented and areola darkens and widens
- Vocal cords in larynx lengthen, voice deepens/breaks such that the pitch of the adult male voice is an octave lower than that of females
14 First fertile ejaculation, slight breast enlargement in some individuals
15 Adult hair pattern,
- Hair on face/chest/extremities
- Sebaceous glands active in skin of scrotum/face/back/chest with some acne
16 Broadening of shoulders, muscle growth
17 Adult stature reached

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14
Q

What are the Tanner stages for females?

A
  1. Prepubertal pubic hair and breasts
  2. Sparse lightly pigmented pubic hair on medial border labia. Breast and nipple elevated as small mound, areolar diameter increased
  3. Darker, beginning to curl, more pubic hair. Breast and areola enlarged, no contour separation
  4. Coarse, curly, abundant (less than adult) pubic hair. Areola and papilla form secondary mound.
  5. Adult feminine triangle spread to medial thigh pubic hair. Mature nipple projects, areola part of general breast contour.
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15
Q

Describe the Tanner stages for males

A
  1. Prepubertal pubic hair/penis/testes
  2. Scanty long slightly pigmented hair, slight penis enlargement, scrotum enlarged texture altered
  3. Darker begins to curl small amount hair, penis longer, testes larger
  4. Resembles adult type but less in quantity, coarse and curly. Larger, glans breadth increased penis. Larger testes.
  5. Adult distribution pubic hear, spread to medial surface thighs. Adult penis and testes.
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16
Q

What do ovarian oestrogens drive?

A

Growth of breast and female genitalia

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17
Q

What do testicular androgens drive?

A

Development of male genitalia and body hair. Enlarging larynx and laryngeal muscles.

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18
Q

What do ovarian and adrenal androgens drive?

A

Growth of female pubic and axillary hair.

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19
Q

Describe the gonadal changes of the ovaries

A

Newborn 2cm, 500K follicles
None ovulate in childhood but many cystic or atresic
Puberty 83K follicles remain
Ovaries of pubescent females weigh more than those of a child because some remaining follicles have enlarged

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20
Q

Describe the gonadal changes of the testes

A

Testes descend from abdominal cavity during 7-8th month of fetal life under control of MIS and testosterone via gubernaculum
Newborn - seminiferous tubules contain spermatogonia and Sertoli cells. Some Leydig cells present at birth but are invisible by 6 months.
9 years - spermatogenesis begins, Leydig cells visible.
14-15 years - mature spermatozoa produced, testes increase in size 24 fold due to enlarged diameter of seminiferous tubules (tubules fill with testicular fluid).

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21
Q

What is cryptorchid testes?

A

Failure of testes to descend
Overheat
Damage of all except Sertoli and Leydig cells - damage is caused by the spermatogenesis itself

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22
Q

How much cooler does spermatogenesis require than the abdominal cavity?

A

3.1 degrees

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23
Q

How do you treat cryptorchidism?

A

Surgery or treatment with gonadotrophins or GnRH to cause descent

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24
Q

How do plasma levels of hormones in neonates change?

A

First 20 weeks - LH and FSH high when plasma levels are at the adult level
Then secretion ceases and levels are low or undetectable through childhood and juvenile stages
First change is rise in FSH, following by increasingly pulsatile LH
Changes occur whether or not testosterone is present

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25
Q

What releases oestradiol or oestrone?

A 
Oestradiol = large growing follicles in ovary
Oestrone = body fat
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26
Q

What is the first hormonal change of puberty? What causes it?

A

BOTH SEXES
Adrenarche
Rise in DHEA
Weak androgens released in large quantities from adrenal gland

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27
Q

What secretes oestrogens in males?

A

Sertoli cells

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28
Q

What is the name of a slight growth of mammary cells in males?

A

Gynaecomastia

Normally goes away within 2 years

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29
Q

What determines secondary sexual characteristics?

A

Balance of androgens v oestrogens

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30
Q

How do you treat acne?

A

Antibiotics, salicylic acid, benzoyl peroxide, female hormones/androgen antagonists

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31
Q

GH
Source
Effect
Pathology

A

Ant pit near to puberty
Growth of long bones and tissues (along with androgens)
Protein synthesis and glucose homeostasis
GH deficiency –> short stature, delayed sexual maturation

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32
Q

Thyroid hormones
Source
Effect
Pathology

A

Thyroid gland secondary to TSH from ant pit
Rise in metabolic rate for both sexes
Essential for body growth

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33
Q

How do gonads, pituitary and hypothalamus change in puberty?

A

No obvious maturation
Gonads gain ability to respond to gonadotropins very early in life - follicular growth and atresia can occur in fetal and neonate ovary.
Fetal pit can secrete gonadotropins in response to GnRH stim, (but does become more sensitive)
Hypothalamus starts secretion of GnRH during second trimester of fetal development

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34
Q

Define sexual dimorphism

A

Differences in body composition between males and females

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35
Q

What is lean body mass?

A

Skeletal and muscle mass (+ extra water mass makes males heavier)

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36
Q

How do children suppress sexual maturation? + evidence

A
  1. Brain gonadostat - Steroids in children negative feedback on GnRH. Hypothalamus v sensitive to steroidal inhibition during childhood (6-15 times more than in adults). Evidence - smaller amount of oestrogen required to lower LH/FSH levels in girls than adult women.
  2. LECTURER THINKS IS THIS
    Central inhibition of GnRH pulse power: GnRH pulse generator inhibited by other brain areas during childhood. Evidence - specific lesions in rat brain cause early puberty + children born without gonads (no steroids for negative feedback) still have low LH/FSH levels through childhood and GnRH release occurs at normal age.
  3. ONLY GIRLS: Oestrogens can exert positive feedback on gonadotropin secretion but not in younger females. May result from maturation of hypothalamic GnRH surge centre or ability of pituitary to synthesise and store adequate gonadotropins.
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37
Q

What is the model of sexual response called?

A

EPOR
Desire
Excitement: response to psychogenic stimuli (visual or memory) or somatogenic stimuli ((touching, friction) resulting in increased arousal or sexual tension
Plateau: arousal is maintained and intensified causing increased pelvic haemodynamics
Orgasm: if level of arousal is adequate, a few seconds of involuntary climax relieves sexual tension by a wave of intense pleasure. Associated with ejaculation
Resolution: arousal dissipated and pelvic haemodynamics returned to the unstimulated state

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38
Q

What is the absolute refractory period? What does it depend on?

A

eIn men, time when sexual re-arousal and orgasm impossible
Duration depends on age and situational factors (novelty of partner, context)
Women don’t undergo same period

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39
Q

How do penises get erect?

A

Hameodynamic changes

  1. Flaccidity
  2. Tumescence
  3. Erection
  4. Detumescence
40
Q

What is the fibrous capsule around the corpora cavernosa called?

A

Tunica albuginea

41
Q

Why is the increase in pressure lower in the corpus spongiosum?

A

Prevent compression of urethra, ultimately to allow ejaculation

42
Q

Discuss the flaccid state

A
  1. Flaccidity - myogenic tone of smooth muscle of cavernous trabeculae and arteries maintained by sympathetic outflow of hypogastric nerve. Arterial input to corpus cavernosum hindered by contraction of mounds of smooth muscle near the tunica albuginea. Intercavernous space low-volume, low pressure.
43
Q

Describe tumescence

A

After 20-30s
Para symp by S234 pelvic nerve using prostacyclins and VIP leads to: reduced myogenic tone in the arterial smooth muscle, leading to arterial dilation and increased blood flow into corpora cavernosa, and also reduction in tone of cavernous trabecular muscle which decreases intracavernous resistance and expands the cavernous volume.
Arteriovenous shunts which bypass the sinuses of the corpora cavernosa when the penis is flaccid now direct blood into them.
Sub-tunical venous plexus compressed so venous outflow reduced. Flaps of smooth muscle occlude venular outflow from sinusoids.
Intracavernous space now high volume and high pressure.

44
Q

Describe the erect state

A

Penis in a fully rigid state so that in- and out- flow of blood nearly absent. High pressure v low flow. Rela

45
Q

Describe detumescence

A

Pressure reduction. Sympathetic lumbar outflow T12-L3 hypogastric nerves contract arterial smooth muscle to cause arterial flow to decrease. Increase in venous outflow returns the penis to the flaccid state.

46
Q

What is priapism?

A

Prolonged erection endangering the oxygenated blood supply to the penis as little blood flows in or out in the most rigid state. Can be relieved pharmacologically.

47
Q

Which nerve mediates flaccidity?

A

Sympathetic lumbar hypogastric nerve T12-L3

48
Q

Which nerve mediates tumescence?

A

Pelvic Nerve, para S234

49
Q

Which nerve mediates detumescence?

A

Sympathetic lumbar hypogastric T12-L3

50
Q

Which muscles increase penis rigidity and stabilise erection?

A

Ischiocavernosus (crus of penis)
Bulbospongiosus (surrounds bulb of penis)
Contract to compress proximal corpus cavernosum

51
Q

Which nerve mediates ejaculation?

A

NA sympathetic

Hypogastric (Lumbar splanchnics)

52
Q

Which nerve mediates pelvic floor contraction?

A

Pudendal S234

53
Q

How does erection occur molecularly?

A

Initiation
Pelvic nerve –>neuronal nNOS release –> NO –> GC –> cGMP –> vasodil
Maintenance
Endothelial eNOS –> NOS in corpus cavernosa

54
Q

How does detumescence occur molecularly? How is it affected?

A

cGMP –>5’GMP by PDE5

Viagra blocks PDE5

55
Q

Which nerve mediates bulbospongiosus and ischiocavernosus?

A

Pudendal S234

56
Q

Explain the bulbospongiosus reflex. What is it used for?

A

Test state of spinal cord injury. Squeeze glans of penis or clitoris, assess contraction of anal sphincter

57
Q

Define erectile dysfunction

A

Consistent and recurrent inability to attain and/or maintain a penile erection sufficient for sexual activity

58
Q

What causes erectile dysfunction?

A

Psychogenic factors
Organic factors:
1. Neurogenic - nerve damage physically/MS/diabetes (impaired nNOS release)/pelvic surgery/disc lesion
2. Arteriogenic - hypertension, diabetes (impaired eNOS release)/hyperlipidaemia/tears in fibrous capsule of corpora cavernosa/vessel obstruction supplying the penis
3. Endocrine - low testosterone, high prolactin
4. Drug use/abuse - anti-hypertensives, anti-depressants, smoking, alcohol, drugs that antagonise NTs that mediate tumescence

59
Q

What are the treatments for erectile dysfunction?

A

Sex therapy
Hormone replacement
Intercavernosal injection or intraurethral injection of smooth muscle relaxants i.e. synthetic prostanoid prostaglandin E1
Viagra - inhibits PDE5. Can lead to priapism.

60
Q

What is semen?

A

Spermatozoa + seminal plasma

61
Q

What is the pathway of sperm movement?

A 
Testes
Rete testes
Vasa efferentia 
Epididymis (muscle contractions)
Vas deferens - site of vasectomy
62
Q

What happens during sperm maturation in the epididymis?

A

Loss of cytoplasmic droplet
Increased spermatocrit 100x by absorption in vas efferentia and epididymis
Nuclear condensation (histamines –> protamines) and acrosomal remodelling
Metabolic changes including selective metabolism of cholesterol and phospholipids and increased dependence on external fructose for glycolytic energy production
Motility due to increase cAMP in flagellum, which becomes more rigid due to more disulphide bonds
Membrane surface coated with glycoproteins that will aid in sperm-oocyte interactions

63
Q

From where do sperm have the potential to be motile and fertilise oocytes?

A

Cauda epididymis

64
Q

How much seminal fluid is released?

A

3-5mL

65
Q

Where is seminal fluid released from?

A

Major accessory sex glands (seminal vesicle, prostate gland, Cowper’s gland)
V small contribution from epididymis

66
Q

What is the Cowper’s gland?

A

Bulbourethral gland

Secretes lubricant in pre-ejaculate and ejaculate

67
Q

Which hormone mediates activity of accessory glands? How do we know?

A

Androgens
5-DHT
Castration and hypophysectomy inhibit normal function of the prostate and seminal vesicle.

68
Q

What is the function and composition of seminal plasma?

A

Vehicle for transport
Nutritional factors e.g fructose
Buffering agent (pH 7.2-7.8) to counteract acidic pH vaginal fluids
Anti-oxidants e.g. ascorbate, hypoteurine
Prostaglandins (may stimulate vaginal muscle contractions)
NB may contain potentially infectious agents e.g. hep B or C, HIV, HPV
Leukocytes

69
Q

What can high levels of leucocytes in the seminal plasma indicate?

A

UTI or infertility

70
Q

When ejaculation approaches, which changes happen?

A
  1. Rhythmic contraction ischiocavernosus and bulbocavernous –> penis turgor increases and coronal ridge glans penis increases
  2. Testes increase in volume 50% and drawn reflexively towards perineum
71
Q

Define ejaculation

A

Semen expelled from posterior urethra by contraction of the smooth muscles of the urethra and striated muscles of the bulbocavernous and ischiocavernosus.
Contractions of pelvic floor.

72
Q

What is retrograde ejaculation and how is it prevented?

A

Contraction of vesicular urethral sphincter

Ejaculate entering the bladder

73
Q

What is a dry orgasm?

A

Abnormalities in or interference with alpha-adrenergic system such that an erection is not impaired but emission is

74
Q

How does ejaculate composition vary?

A

Sequential nature of contractions and relative lack of mixing of various components within urethra
Early fraction (30%) - rich in acid phosphatase from prostate
Mid-fraction (10%) - rich in spermatozoa from vas deferens
Late-fraction (60%) - rich in fructose from seminal vesicles.
In vagina mix together and coagulate
Liquefies again within 20-60 mins

75
Q

What is the normal sperm content in men?

A

1x10^8 - 7x10^8 sperm (50-150x10^6/ml)

76
Q

What proportion of sperm in an ejaculate are abnormal?

A

Less than 30%

77
Q

What is the criteria to be a subfertile man?

A

<1ml
Less than 5x10^7 sperm/ <2x10^6/ml
More than 60% sperm abnormal
Viscosity after liquefaction remains high
Large number of debris leucocytes and immature sperm cells present

78
Q

Average length of coitus in Western world?

A

4 mins

79
Q

What is the G spot?

A

The Grafenberg spot
In vagina
May be part of female prostate or Skene gland

80
Q

How is the vagina lubricated?

A

Transudation of fluid from Bartholin’s duct through the vaginal wall

81
Q

How does the female genitalia alter with sexual arousal?

A

Vaginal lubrication
Labia majora engorged with blood
Width and length of vagina increase
Uterus elevates upwards into false pelvis, lifting cervical os ‘tenting effect

82
Q

What proportion of women orgasm from coitus?

A

30-50%

Suggested not reflexive but learnt

83
Q

How do you treat sexual arousal in women?

A

Same as men (PDE5 inhibitors sildenafil/Viagra) but unsure how this works mechanistically

84
Q

Describe insemination

A 
350 million sperm
Most lost in flowback
35% remain after 30 min
Semen coagulates to become gelatinous
Liquefaction within 20-60mins by activation of a seminal proenzyme derived from the prostate
85
Q

How fast do sperm get to the cervix? How many make it? How do they get there?

A

Within a minute, sperm found in cervix or uterus
Less than 1% - after 2 hours 0.2%, after 12 0.6%
Own propulsion
With the help of ciliated cells of the cervical os

86
Q

What acts as a sperm reservoir?

A

Cervical walls contain longitudinal folds that form cervical crypts

87
Q

What does progress from the cervix to the uterus depend on?

A

Mucus consistency

Ciliated uterine and oviductal cells

88
Q

How does the cervix change during the ovarian cycle?

A

Oestrogen in follicular phase –> muscles of cervix relax, open cervical os, watery mucus easy passage of sperm, secretion highly elastic,
Progesterone in luteal phase –> cervix firmer, closed os, mucus thick, prevents passage of sperm and pathogens, low spinnbarkeit.

89
Q

What does the elasticity of mucus demonstrate?

A

Spinnbarkeit, stretchier indicates fibres are in a parallel orientation
Allows easier passage of sperm through cervix

90
Q

When does basal body temperature increase?

A

Several days after ovulation

91
Q

How long can viable spermatozoa survive?

A

24-48h

92
Q

What is the name of the pain experienced at ovulation? What is it caused by?

A

Mittelschmerz pain
20% women
Bleeding into peritoneal cavity caused by ovulation

93
Q

What stimulates oocytic movement to uterus?

A

Cumulus secretes oestrogen, stim ciliated oviductal cells of oviduct

94
Q

What is the transient sperm reservoir?

A

At isthmus where oviduct meets uterus, sperm briefly immobile and bind to oviductal epithelial cells. Only at ovulation do sperm re-acquire motility. Might depend on release of chemoattractants by both oocyte and cumulus mass to cause hyperactive flagellar beating.

95
Q

Where does fertilisation take place?

A

Ampullary region oviduct.

HR MVST 1b (6 decks)

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