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Med 3 > Male And Female Infertility > Flashcards

Male And Female Infertility Flashcards

1
Q

What are the 6 main reproductive hormones

A

Gonadotropin releasing hormone: hypothalamus ; decapeptide

Follicle stimulating hormone - anterior pituitary

Lutenizing hormone - anterior pituitary

Oestradiol - ovary (oestrogens, oestradiol, oestrone)

Progesterone - ovary

Testosterone - testes, adrenal glands, ovary

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2
Q

What happens in menstrual cycle days 0-14 (follicular phase)

A

Surge in gonadotropin releasing hormone

Stimulates FSH and LH (pituitary)

FSH acts on follicle causing oestradiol to be produced by granulosal cells

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3
Q

Why do oestradiol levels rise when FSH and LH levels have dropped

A

Oestrogens bind to receptors in granulosa cells

This stimulates proliferation of granulosa cells and more oestrogen receptors so more oestrogen produced

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4
Q

What is the corpus luteum

A

Formed from the collapsed follicle
Maintained by LH
Secretes progesterone
Oestradiol levels begin to drop (progesterone inhibits oestradiol synthesis)

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5
Q

Death of corpus luteum

A 
Corpus luteum degenerates 
Decrease in progesterone and oestradiol levels 
Increase in FSH and LH levels 
Allows new follicles to mature 
Onset of ovulation
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6
Q

What happens in females 2-4 years prior to menarche

A

Increase in steroid hormones from ovary and adrenal glands

Ovarian oestrogens regulate growth of breast and female genitalia
Androgens from ovary and adrenal control growth of pubic and axillary hair

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7
Q

What happens in puberty in males

A

Increase in steroid hormones from gonads and adrenal glands

Testicular androgens control development of genitalia and body hair as well as enlargement of larynx and laryngeal muscles

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8
Q

What is the effect of FSH and LH in days 0-14

A

FSH acts on granulosal cells of the follicles to increase synthesis of oestradiol

LH acts on thecal cells of the follicles to produce androgens

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9
Q

What is the role of cholesterol

A

Used to produce the androgens and eostrogens but also the glucocorticoids and mineralocorticoids in the adrenal cortex

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10
Q

How is androstendione produced

A

LH binds to its receptor in thecal cells and causes cholesterol to produce androstenidione. Only the thecal cells contain receptors to LH and granulosa cells to FSH in early stages

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11
Q

Synthesis of oestradiol

A

Granulosa cells do not have enzymes to produce androstenedione. Aromatase activity in granulosa cells allows androstenedione to form estradiol when FSH binds

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12
Q

Why do oestradiol levels rise when FSH and LH levels have dropped

A

Oestradiol increases proliferation of granulosal cells - more oestradiol produced

Oestrogen bind to receptors in granulosa cells

They are stimulated to proliferate and produce more oestrogen receptors

Positive feedback: where oestrogen stimulates further oestrogen output and a surge in circulating oestrogens

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13
Q

What does the production of oestradiol allow

A

Allows the new follicle to develop and grow into the Graafian follicle

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14
Q

What happens to the negative feedback loop mid cycle

A

Becomes positive allowing a short surge of LH to be released due to the high oestradiol levels (late follicular phase) acting on the pituitary

High oestradiol together with FSH cause change in action of LH

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15
Q

What happens after the action of LH is changed at ovulation

A

The appearance of LH receptors on granulosal cells is stimulated which increases progesterone synthesis
Oocyte is released
Recruitment of 5-9 new follicles

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16
Q

What is the corpus luteum

A

Formed from the collapsed follicle
Maintained by LH
Secretes progesterone

Oestradiol levels begin to drop (progesterone inhibits oestradiol synthesis)

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17
Q

Role of progesterone in latter half of menstrual cycle

A

Progesterone causes a decrease in gonadotropin secretion (suppresses GnRH secretion)
FSH and LH levels are low so no new follicles develop

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18
Q

Order of events in menstrual cycle

A

Menstruation

Release of recruited follicles. One to develop

Proliferation of granulosal cells, development of Graafian follicle

Proliferation of endometrium and myometrium

Ovulation (5-9 follicles recruited)

Growth of corpus luteum

Endometrium secretory

Inhibition of developing follicles

Death of corpus luteum

Final contraction of spiral arteries in endometrium

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19
Q

How does hormonal contraception work

A

Suppresses ovulation by negative feedback of progesterone on the pituitary and hypothalamus

Decrease in GnRH secretion resulting in low FSH and LH levels - no new follicles develop

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20
Q

How does the combined oral contraceptive work

A

Contains oestrogen and progesterone
Monocyclic
21 days on (output of GnRH, FSH, LH suppressed)
7 days off (endometrium breaks stimulating menstruation)
Estrogen: progesterone vary in different pills

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21
Q

How does the progesterone only contraception work

A

Needs to be taken continuously
Oral pill - compliance is essential
Injectable forms 8-12 weeks

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22
Q

Why does menstrual cycle not occur during pregnancy

A

No menstrual cycle occurs as high levels of progesterone are present
Inhibits secretion of pituitary gonadotropins

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23
Q

What happens at menopause

A

At around 50 years the menstrual cycle becomes less regular as ovaries lose the ability to respond to FSH and LH
Low oestradiol levels

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24
Q

What causes the onset of puberty

A

Activation of GnRH pulses to anterior pituitary (maturation within CNS)
Increase in LH and FSH
Increase in oestradiol and androgen synthesis

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25
Q

What occurs prior to puberty in males

A

Increase in steroid hormones from gonads and adrenal glands

Testicular androgens control development of genitalia and body hair as well as enlargement of larynx and laryngeal muscles

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26
Q

Function of the testes

A

Production and temporary storage of spermatozoa

Synthesis and secretion of testosterone, oestrogen, activin, inhibin, oxytocin

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27
Q

Role of ductal system in male genitals

A

Carriage of spermatozoa to the exterior ; maturation of spermatozoa

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28
Q

Role of secretory glands in the male genital system

A

Secrete seminal fluids and nutrients to support and nourish spermatozoa

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29
Q

Where does testes descend from

A

Posterior abdominal wall to scrotum outside the body at 7th month gestation. Keeps gametes to 2-3c below core body temperature; essential for spermatogenesis. Highly vascular

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30
Q

Describe the testes

A

4-5cm long, 11-17g weight
Right slightly larger and heavier
Fibrous septa from TA divides the testis into 250-350 lobules. Each lobule contains 1-4 coiled seminiferous tubules. Each 80cm long, 150 micron diameter
Closed loops, both ends open into rete testis

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31
Q

Role of Sertoli cells

A

Interconnect with each other to create the blood testes barrier. Results in a basal, adlumenal and lumenal compartment

They put out baso-lateral cytoplasmic extensions to each other which make tight junctions with each other. Thus there is a meshwork created (blood testis barrier)
This forms

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32
Q

What are the ablumenal and lumenal compartments

A

Ablumenal: this is where, upon release of spermatogonium, spermatocytes undergo spermatogenesis
Lumenal: spermatids are found on the lumenal surface. Fully formed spermatozoa are found in the lumen of the seminiferous tubules

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33
Q

What is the importance of the blood-testis barrier

A

Tight junctions cause complete apposition of adjacent plasma membranes forbidding movement of solutes from the basal to the adlumenal compartment and vice versa

Isolates the adlumenal from the basal compartment. Interstitial fluid cannot get in
Only unidirectional movement of germ cells are allowed through the tight junctions
TJs open transiently and allow spermatogonia to enter the adlumenal compartment

34
Q

Consequences of the blood testis barrier

A

Body cannot elicit an immune reaction and create antibodies against sperm antigens revealed during spermatogenesis

Protects the developing spermatocytes from pathogens and mutagens

35
Q

What is spermatogenesis

A

Mitotic proliferation - produces large number of cells
Meiotic division - generates genetic diversity and halves the chromosome number

Spermiogenesis- packaging of chromosomes for effective delivery to the oocyte. Formation of head, neck and tail, loss of cytoplasm

Production rate: 300-600 spermatozoa per gram of testis per second

36
Q

How is sperm production continuous not cyclical

A

Spermatogonia divide in sequence every 16 days
Before one set have completed maturation, a new entry into spermatogenesis by other cells start (staggered entry) this ensures continuous release of spermatozoa
It takes 64 days to develop a mature spermatozoan

37
Q

Endocrine support of spermatogenesis

A

LH stimulates leydig cells to produce testosterone which binds to receptors on Sertoli cells
Testosterone induces receptors for FSH on Sertoli cells
FSH from pituitary now stimulates Sertoli cells to produce androgen binding protein which binds and carries testosterone in testicular fluid to the entire ductal system

Sertoli cells also produce inhibin which is part of a negative feedback loop. It inhibits FSH production by the pituitary gland

38
Q

Importance of the spermatic cord

A

Site for sperm storage
Epididymis connects to the vas deferens which runs through the spermatic cord. The testicular artery runs along with it
The veins in this system form an unusual plexus around the testicular artery. The spermatic cord is encased in cremaster muscle

39
Q

Vascular supply of the spermatic cord

A

Pampiniform veins form a complex interconnecting plexus around the testicular artery. Excellent for heat exchange, protects contents of vas deferens from overheating. These veins are difficult to distinguish from arteries as they have muscular walls

40
Q

What are seminal vesicles

A

Mucosal folds create vast surface area
Secretes seminal fluid
60% of semen volume is seminal fluids
Contraction of seminal vesicle propels secretion into ejaculatory ducts which open into the prostatic urethra

41
Q

What is the prostate gland

A

Collection of concentric secreting glands which open into the urethra. Secretes citric acid, proteolytic enzymes, clotting enzymes, prostate specific antigen

42
Q

What are bulbourethral glands

A

Opens into the membranous urethra
Produces watery fluid rich in galactose and sialic acid
Acts as lubricant and neutralises acidic urine in urethra and vaginal fluids
Precedes semen during emission

43
Q

What is the erectile tissue of the penis made of

A

2 dorsal cylinders (corpora cavernosa) highly vascular

1 ventral cylinder (corpus spongiosum) which contains the penile urethra

44
Q

Erectile physiology (flaccid state)

A

Sinusoidal smooth muscle fibres remain contracted and blood flows from the internal pudenal arteries via central deep artery and helicine arteries to vascular cavernous spaces and out through the open emissary veins. Low volume low pressure

45
Q

Erectile physiology erect state

A

Closure of arteriovenous shunts - more blood flow into helicine arteries which straighten and dilate, smooth muscles of sinusoids relax, blood flows into the enlarged lacunar spaces. The resultant pressure compresses the emissary veins reducing venous outflow. Large volume high pressure

46
Q

What is the EDRF

A

Endothelium derived relaxant factor
Was identified as nitric oxide
Produced by blood vessels

47
Q

How do endothelial cells produce NO

A

Metabolise aa L -arginine by nitric oxide synthase to produce NO which then fizzes out of the endothelium and acts on vascular smooth muscle to active enzyme Guanlyl Cyclase which causes vasorelaxation

48
Q

Mode of action of sildenafil (viagra)

A

Increases levels of cyclic GMP and leads to vasodilation

Originally for angina but patients complained of penile erection as a side effect

49
Q

Side effects of viagra

A

Headache

Visual disturbances

50
Q

Causes of erectile dysfunction

A

Cardiovascular disease (damage to blood vessels and nerves in penis)
Smoking
Diabetes
Psychogenic
Drugs: thiazides, prazosin, antidepressants, antipsychotics

51
Q

Function of prostate gland

A

Accessory sex gland

Adds nutrients and enzymes to seminal fluid

52
Q

Notable contents of seminal fluid

A 
PSA 
Prostaglandins 
Fructose 
Zinc 
Citrate
53
Q

Lower urinary tract voiding symptoms

A

Slow to start = hesitancy
Slow to go = poor stream
Slow to finish = post micturition dribble
(Obstruction)

54
Q

Lower urinary tract storage symptoms

A 
Frequency 
Urgency 
Incontinence 
Nocturia 
(Bladder dysfunction)
55
Q

Define menopause

A

The permanent cessation of mensruation
Caused by loss of ovarian function / follicular activity
Average age in uk is 51
Associated with physical / psychological and social changes

56
Q

Other causes of menopause

A 
Surgical menopause 
Hysterectomy or removal of ovaries 
Chemotherapy / radiotherapy 
Premature ovarian insufficiency 
Genetic causes -Turner syndrome
57
Q

What is perimenopause

A

Can have symptoms of menopause but still having periods (can be more irregular)

58
Q

What is post menopause

A

When you have gone a year with no periods

59
Q

Symptoms of menopause

A 
Difficulty sleeping 
Memory loss 
Reduced muscle mass 
Hot flushes 
Vaginal dryness and pain 
Mood changes 
Palpitations 
Changing periods 
Headaches 
Joint stiffness, aches and pains 
Night sweats 
Recurrent UTIs
60
Q

Diseases associated with menopause

A

Breast cancer (HRT)
Ischaemic heart disease
Stroke
Osteoporosis

61
Q

Menopause treatment

A

Conservative management / education
Diet / exercise
Supplements-oil of evening primrose / black cohosh / agnus castus
Hormone replacement therapy

62
Q

What is sequential combined cyclical HRT

A

Estrogen daily plus progesterone / progesterone for 10-14 days every 28-30 days cycle

63
Q

What is sequential long cycle HRT

A

Estrogen daily for 12 weeks plus progesterone added in the last 14 days

64
Q

What is continuous combined HRT

A

Estrogen plus progesterone administered together continuously

65
Q

How does HRT help Osteoporosis

A

Trial data suggests there are 23 fewer fragility fractures per 1000 in post menopausal HRT users
Benefit might continue in women taking HRT for longer and the protection stops when HRT stops

66
Q

Summary of effects of HRT

A

Reduces vasomotor symptoms but effect is temporary

Reduces vaginal dryness symptoms but local therapy is better

Prevents osteoporosis

Increases breast cancer and stroke

No effect on myocardial infarction, memory or quality of life

67
Q

Current advice for HRT

A

Use only for debilitating symptoms in the lowest dose for the shortest time possible

Individualise the care
Discuss lifestyle issues
Refer to a specialist clinic and seek a second opinion

68
Q

What does obstruction of bladder lead to

A

Painful distension of bladder, hydronephorsis, irritated bladder = urgency, frequency, nocturia
Residual urine in bladder = infection
Acute urinary retention :
- one of the most common surgical emergencies however risk is low
Palpable bladder

69
Q

What is prostatits

A

Acute infection with E. coli or other gram -ve rods
Neutrophilic infiltrate, oedema, within glands initially, then stroma
Chronic: either same bacteria as acute or diagnosed by increased leucocytes in prostatic secretions but no bacteria found

Symptoms: dysuria, frequency, lower back pain, pelvic pain and enlarged tender prostate

70
Q

What is benign prostatic hyperplasia

A

Proliferation of both stroma and epithelial elements (initially in the central zone)
An imbalance between proliferation and apoptosis
Very common. Affects 90% of men over 70
Androgens have a role may be a consequence of age related oestrogen increase

Symptoms: lower UT obstruction, hesitancy, interruption of flow. Smooth and enlarged by DRE

71
Q

Describe prostate cancer

A

2nd highest cause of cancer death in men
Increases with age. Rare below 60 very common over 80
Adenocarcinoma
Occurs initially often in peripheral zones
Often found as clinically silent on biopsy for suspected hyperplasia
Symptoms: similar to BPH, hard, craggy, fixed prostate can spread to bone (back pain), lung, liver, brain and rarely kidney

72
Q

How to diagnose a prostate tumour

A

Trans rectal ultrasound and biopsy (tube inserted into rectum)
Antibiotics usually given prior
Complications: septicaemia and bleeding

73
Q

Treatment options for prostate cancer

A

Active monitoring - no treatment

Surgery (lots of complications)

Radiotherapy

New modalities eg bracytherapy (radioactive beads into prostate that release local radiation - less side effects)

Palliative: hormone manipulation to slow thing, radiotherapy for bones, pain relief, deal with obstructive renal failure

74
Q

Consequences of radiotherapy, bracytherapy and surgery (prostate cancer)

A 
Impotence
Incontinence 
Stricture 
Death 
Failure
75
Q

How can PSA (prostate specific antigen) be used as a way of screening for prostate cancer

A

Produced normally by prostate
4.0ng/ml is upper limit of normal
More than 10mg/ml is more than likely to be cancer
Is not always elevated in cancer but is elevated in hyperplasia and infection due to disruption of normal glandular architecture

76
Q

Types of disorders of ovulation

A

1) hypothalamic pituitary failure: failure to produce required amount of LH and FSH resulting in anovulation
2) hypothalamic pituitary ovulation dysfunction: the result of PCOS (the most common cause of female infertility)
3) ovarian failure: normal hypothalamic and pituitary function but insuffiecnet numbers of follicles within th ovary so less oestrogen produced and follicles do not develop fully. Results in anovulatory cycles

77
Q

What is sheehans syndrome

A

Hypopituitarism caused by ischaemic necrosis of the pituitary. Occurs as the result of severe hypotension or haemorrhagic shock secondary to massive post partum haemorrhage

78
Q

Tubal causes of infertility

A

Delicate structure of Fallopian tubes makes them more susceptible to damage. Most common cause is pelvic inflammatory disease which is usually secondary to chlamydia or gonorrhoea

Others:
Previous sterilisation
Endometriosis
Previous pelvic surgery

79
Q

Uterine / peritoneal causes of infertility

A

Endometriosis which causes inflammation and adhesions in the pelvis that can distort pelvic anatomy

  • cervical mucus dysfunction or defect
  • previous pelvic or cervical surgery
  • uterine fibroids
  • ashermans syndrome
  • previous abdominal infections which have resulted in adhesions
  • congenital abnormalities
80
Q

What are the 3 types of male infertility

A

Obstructive infertility - a problem with sperm delivery
Non obstructive infertility - a problem with sperm production
Coital infertility - infertility secondary to sexual dysfunction

81
Q

What fertility investigations may be done in males

A

Semen analysis - assesses sperm count, motility, morphology, vitality, concentration and volume
Chlamydia screen

Med 3 (10 decks)

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