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Reproduction > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Describe the follicular phase of menstruation

A

FSH stimulates ovarian follicle to develop and the granulosa cells produce oestrogen. Rising oestrogen levels then subsequently inhibit FSH production.
Declining FSH levels cause atresia in all but one dominant follicle.

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2
Q

Describe ovulation

A

Luteinising hormone surge just before ovulation.

Dominant follicle ruptures releasing oocyte.

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3
Q

Describe the luteal phase of menstruation

A

Formation of corpus luteum

Progesterone production

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4
Q

Describe the endometrial lining in the proliferative phase of menstruation?

A

Oestrogen induced growth of endometrial glands and stroma.

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5
Q

Describe the endometrial lining in the luteal phase of menstruation?

A

Progesterone induced glandular secretory activity.
Decidualisation (changes in the endometrial lining in preparation for pregnancy).
Endometrial apoptosis and subsequent menstruation

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6
Q

Describe the endometrium during menstruation?

A

Arteriolar construction and shredding of the functional endometrial layer.
Fibrinolysis inhibits scar tissue formation.

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7
Q

At what day in the cycle does 1- ovulation and 2-menstruation occur?

A

1- 14 days

2- day 1-6.

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8
Q

How long is a normal menstrual cycle?

A

28 days +/- 7 days

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9
Q

Menorrhagia

A

Heavy periods (prolonged and increased menstrual flow)

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10
Q

Metrorrhagia

A

Regular intermenstrual bleeding

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11
Q

Polymenorrhoea

A

Periods occur at less than a 21 day interval

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12
Q

Polymenorrhagia

A

Increased bleeding and frequent cycle

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13
Q

Menometrorrhagia

A

Prolonged periods and intermenstrual bleeding

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14
Q

Amenorrhoea

A

Absence of menstruation >6 months.

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15
Q

Oligomenorrhoea

A

Periods at intervals of greater than 35 days.

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16
Q

What are the causes of menorrhagia?

A

Can be organic- caused by pathology

Or non-organic- absence of pathology

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17
Q

What is non-organic menorrhagia also known as?

A

Dysfunctional uterine bleeding.

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18
Q

What local disorders can cause organic menorrhagia?

A 
Fibroids
Adenomyosis
Endocervical or endometrial polyp
Cervical eversion
Intrauterine contraceptive device
Pelvic inflammatory disease
Endometriosis
Malignancy of the cervix or uterus
Hormone producing tumours 
Trauma
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19
Q

What are fibroids?
Why are they associated with heavy periods?
Do they cause symptoms?

A

Benign tumour of the myometrium. Usually results in the uterus being much larger than normal.
Associated with heavy periods because the surface endometrium is also enlarged.
Non- painful unless they are so enlarged they cause pressure symptoms.

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20
Q

What is adenomyosis?

Does it cause symptoms?

A

Lining of the uterus (endometrium) is present in the myometrium (muscle layer). Meaning blood can’t escape.
Can be quite painful.

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21
Q

What is cervical eversion?

Why does it cause bleeding?

A

Cervical epithelium of the cervical canal is pouched out into the uterus. The columnar epithelium tends to be more vascular so causes more bleeding.

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22
Q

Why do intrauterine contraceptive devices cause menorrhagia?

A

If its copper it causes bleeding.

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23
Q

What systemic disorders can cause menorrhagia?

A

Endocrine disorders- hyper/hypothyroidism
Diabetes
Adrenal disease
Prolactin disorders

Disorders of haemostasis- Von willebrands disease
ITP
Liver disorders
Renal disease
Drugs- anticoagulants.
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24
Q

How would you diagnose dysfunctional uterine bleeding?

A

Diagnosis made by exclusion.

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25
Q

How can dysfunctional uterine bleeding be subdivided? Describe each.

A

Anovolutary- 85%. Occurs at the extremes of reproductive life. Irregular cycle. More common in obese women
Ovulatory -15%. Regular heavy periods. Due to inadequate progesterone productive by corpus luteum. More common in women age 35-45.

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26
Q

What investigations would you do into dysfunctional uterine bleeding?

A 
FBC- measure haemoglobin to exclude anaemia
Cervical smear
TSH
Coagulation screen
Renal/liver function tests

Important ones

  • Transvaginal ultrasound- measure endometrial thickness. The thicker the endometrium the more likely you are to have endometrial carcinoma.
  • Endometrial sampling-pipelle biopsies. Uses a hysteroscope- an endoscope through the cervix however needs general aneasthetic
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27
Q

What is the general rule for treatment of DUB?

A

If irregular cycle- treat with hormonal manipulation e.g. progestogens and combined OCP
If regular cycle- treat with drugs.
Combination of heavy periods and shortened cycle- use both.

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28
Q

What medical options are there for treatment of DUB?

A 
Progestogens 
Combined oral contraceptive pill
Danazol- dated now
GnRH analogues 
NSAIDs
Anti-fibrinolytics 
Capillary wall stabilisers

Also-
Mirena coil

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29
Q

What surgical management can be offered for DUB?

A

Endometrial resection/ablation

Hysterectomy

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30
Q

Describe the pro’s and cons of treatment of DUB using surgical and medical management

A

Medical treatment

  • cheaper
  • No waiting list
  • No anaesthetic risks
  • Side effects temporary
  • Fertility retained
  • may not be effective

Surgical treatment

  • more expensive
  • Waiting list
  • Anaesthetic risks
  • Fertility lost
  • completely effective.
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31
Q

Compare endometrial ablation and hysterectomy for treatment of DUB

A

Endometrial ablation-

  • day case
  • shorter operating time
  • shorter recovery
  • fewer complications
  • requires cervical smears and HRT therapy

Hysterectomy

  • Major operation
  • longer operating time
  • longer recovery time
  • more complications
  • No cervical smears
  • Oestrogen only HRT
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32
Q

What are the roles of the ovary?

A

Produce gametes

Produce steroids- mainly oestrogen and progesterone

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33
Q

Describe the structure of the ovary?

A

Has a medulla and cortex.

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34
Q

Describe the medulla of the ovary?

A

Forms the core of the organ. Contains loose connective tissue, contorted arteries, veins and lymphatics. Its continuous with the hilum of the organ.

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35
Q

Describe the cortex of the ovary?

A

Has scattered ovarian follicles in a highly cellular connective tissue stroma. The outer layer of the cortex is a dense connective tissue layer called the tunica albuginea, which is covered by a single layer of cuboidal cells called the germinal epithelium.

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36
Q

Which layer of the ovary forms the white outer layer?

A

The tunica albuginea

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37
Q

Describe the maturation of the ovary from the primordial follicle to where it is released from the ovary?

A

Primordial follicle
Primary follicle
Secondary follicle
Mature graafian follicle

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38
Q

What is oogenesis?

A

Development of oocytes from oogonia.

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39
Q

What is folliculogenesis?

A

Growth of the follicle, which consists of the oocyte and any associated support cells.

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40
Q

Women lose oogonia and oocytes via what process?

A

Atresia.

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41
Q

Describe the development of follicles before birth

A

Before birth, the oocytes undergo meiosis but halt in prophase 1. They will then undergo further meiosis at puberty and will complete meiosis II if they are fertilised.

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42
Q

What will happen if an oocyte fails to associate itself with pregranulosa cells?

A

It dies.

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43
Q

What happens to the pregranulosa cells if the primary follicle enters the growth phase?

A

They are squamous before the growth phase, but become cuboidal after.

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44
Q

How can you distinguish between primary follicles and oocytes?

A

The presence of cuboidal granulosa cells- termed the zona granulosa.

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45
Q

Describe the cell arrangement around the primary follicle?

A

Squamous cells have proliferated to form a single layer of cuboidal cells. The cells adjacent to cuboidal cells, particularly closest to the follicle have started to develop. You can start to see the zona pellucida.

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46
Q

What is the theca interna and externa and how is it formed?

What is its function?

A

The theca interna is formed by differentiation of inner layers of stromal cells.
Goes on to secrete oestrogen precursors which are then converted to oestrogen by granulosa cells.
The theca externa remains fibroblast like.

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47
Q

What is the Antrum? What is it filled with? What layer does it form in?

A

As the follicle enlarges, a space called the Antrum develops.
Filled with Antrum fluid.
The granulosa layer.

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48
Q

When is it classed a Graafian follicle?

A

The largest of follicles has a large Antrum,

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49
Q

When does the oocyte complete meiosis I? What occurs after this?

A

One day before ovulation, the oocyte in the largest Graafian follicle will complete meiosis I. It doesn’t form two identical cells, it forms one large secondary follicle and one polar body.
The secondary oocyte then goes onto the second phase of meiosis but stops at metaphase II.

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50
Q

When will the secondary follicle complete meiosis II? What else is produced in this?

A

Only completes it if fertilised

A secondary polar body.

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51
Q

What is the follicular stigma?

A

The place where the follicle bulges against the side of the ovary.

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52
Q

What happens after ovulation in the ovary?

A

The follicle becomes the corpus luteum. It releases oestrogen and progesterone which help prepare the uterus for implantation.

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53
Q

What happens to the corpus luteum if no implantation occurs?

A

The corpus luteum becomes the corpus albicans.

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54
Q

What happens to the corpus luteum if implantation occurs?

A

The placenta secretes HCG which prevents degeneration of the corpus luteum for some time so progesterone levels can be maintained.

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55
Q

What are the projections of the Fallopian tubes called?

A

Fimbrae.

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56
Q

How does the egg get from the ovary to the uterus?

A

Ejected from the ovary. Collected by the fimbrae of the Fallopian tubes. Moves down the Fallopian tubes by gentle peristaltic movements and currents created by the ciliated epithelium.

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57
Q

Where does fertilisation usually occur?

A

In the ampulla of the Fallopian tubes.

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58
Q

What type of epithelium is present in the ampulla of the Fallopian tube?

A

Simple columnar epithelium with ciliated cells and secretory cells. This is surrounded by smooth muscle.

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59
Q

Describe the structure of the isthmus of the Fallopian tube?

A

Secretory epithelium with few ciliated cells. 3 layers of smooth muscle.

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60
Q

Describe the structure of the uterus?

A

Endometrium- inner secretory mucosal layer. Made up of tubular secretory glands embedded in a connective tissue stroma.
Myometrium- 3 layers of smooth muscle combined with collagen and elastic tissue.
Perimetrium- outer visceral layer of loose connective tissue covered by mesothelium.

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61
Q

How can the endometrium be divided? Describe each.

A

Stratum functionalis- undergoes monthly growth, degeneration and loss
Stratum basalis-reserve tissue that regenerates the functionalis.

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62
Q

What happens to the stratum basalis during the proliferative layer of menstruation?

A

The stratum basalis proliferates and glands, stroma and vasculature grow- increasing the thickness of the endometrium by reconstituting the stratum functionalis.

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63
Q

What happens to the layers of endometrium during the secretory phase of menstruation?

A

The glands become coiled with a corkscrew appearance and secrete glycogen.

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64
Q

What happens to the layers of the endometrium during the menstruation phase?

A

Arterioles in the stratum functionalis undergo constriction, depriving the tissue of blood and causing ischaemia, with resultant tissue breakdown and leakage of blood.

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65
Q

What tissues make up the cervix?

A

Mostly fibrous connective tissue covered with stratified squamous epithelium on its vaginal surface, transitioning to mucous secreting simple columnar epithelium.

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66
Q

What is the significance of the transition zone in the cervix?

A

Common site of dysplagia and neoplastic changes leading to cervical carcinoma being commonest in this area.

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67
Q

Describe the structure of the mucous secreting epithelium of the cervix?

A

Deeply furrowed so looks to form glands.

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68
Q

How are the majority of infections in the genital tract transmitted?

A

Through sex.

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69
Q

What are the common bacterial STI’s?

A

Chlamydia- chlamydia trachomitis
Gonorrhoea -Neisseria gonorrhoea
Syphilis- Treponema pallidum

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70
Q

What are the common viral STI’s?

A

HPV- genital warts
Herpes simplex- genital herpes
Hepatitis and HIV

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71
Q

What are the common parasitic STIs?

A

Trichomonas vaginalis
Phthirus pubis- pubic lice
Scabies

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72
Q

What sign will you see if gonococci infect the male urethra and explain why?
How would chlamydia differ?

A

Purulent discharge will occur- due to the high neutrophil infiltration. Also have pain on urination.

Chlamydia affects the same tissue but is likely to produce a watery discharge, mild symptoms or no symptoms at all.

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73
Q

What determines the efficacy of an STI?

A

Concentration and phenotype of the organism in the genital tract.
Susceptibility of the sexual partner
Resistance of the host.

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74
Q

Can you have a candida infection without symptoms?

A

Yes- 30% of woman have this.

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75
Q

Name some predisposing factors for candida infection?

A

Recent antibiotic therapy
High oestrogen levels e.g. pregnancy, certain types of contraceptive.
Poorly controlled diabetes.
Immunocompromised patients

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76
Q

How does symptomatic candida infection present?

A

Intensely itchy, white vaginal discharge.

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77
Q

How would you diagnose candida infection?

A

Clinical diagnosis

Can do a high vaginal swab for culture.

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78
Q

What is the most common cause of candida infection?

A

C. albicans

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79
Q

How would you treat candida infection?

A

Topical co-trimazole pessary or cream

Oral fluconazole

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80
Q

How would a gram film of candida infection look?

A

Budding yeasts and hyphae

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81
Q

How can prostatitis be classified?

A

Acute bacterial prostatitis
Chronic bacterial prostatitis
Chronic prostatitis/chronic pelvic pain syndrome

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82
Q

How does acute bacterial prostatitis present?

A

Symptoms of a UTI- pain on urination, may also have lower abdominal pain/back/perineal/penile pain and a tender prostate on examination

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83
Q

What are the likely causative organisms of acute bacterial prostatitis?

A

Check for UTI organisms e.g. E coli, coliforms etc

In men under 35- check for STI- gonorrhoea and chlamydia

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84
Q

Treatment of acute bacterial prostatitis?

A

Trimethoprim is the preferred treatment (28 days). Also used in high C diff risk. However if resistant give ciprofloxacin (28 days).

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85
Q

What is positive predictive value?

A

When a screening test comes back positive for the disease and the person actually is positive for the disease.

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86
Q

What is negative predictive value?

A

Subjects with a negative screening test actually are negative for the disease.

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87
Q

You are likely to be infected by a singular STI. True or false?

A

False- they tend to come in ‘packs’.

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88
Q

What test can be used to test for both gonorrhoea and chlamydia in the same sample?

A

Nucleic acid amplification tests.

Or PCR

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89
Q

On NAAT, how does gonorrhoea appear?

A

Gram negative intracellular diplococci.

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90
Q

What organisms are present on the normal vaginal flora?

A

Lactobacillus predominate
Strep viridans
Group B- beta haemolytic streptococci
Candida spp- in small numbers.

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91
Q

What do lactobacillus produce? What is their function?

A

Lactic acid and hydrogen peroxide

They suppress growth of other bacteria.

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92
Q

What is meant by the term bacterial vaginosis?

A

Overgrowth of bacteria in the vagina.

93
Q

Name specific species of lactobacilli that produce the lactic acid?

A

Lactobacillus crispatus

Lactobacillus jensenii

94
Q

What is the normal vaginal pH?

A

4-4.5.

95
Q

What occurs in bacterial vaginosis?

A

The normal vaginal flora is replaced with Gardrenella Vaginalis and many species of anaerobic bacteria.

96
Q

Describe the discharge of bacterial vaginosis?

A

Homogenous and may contain bubbles.

97
Q

What test can be done to confirm bacterial vaginosis- describe?

A

Whiff test- add potassium hydroxide to the discharge and it will produce a fishy odour.

98
Q

What is a wet mount?
What does it reveal?
What are clue cells?

A

A vaginal wet mount is where vaginal discharge is looked at under wet mount microscopy.
Reveals the absence of bacilli and replacement of them with coccobacilli.
Microscopy will show- lots of coccobacilli obscuring the edges- known as clue cells (clue to BV).

99
Q

What does a large number of leukocytes on a wet mount suggest?

A

Suggests an coincidental infection- possibly trichomoniasis or bacterial cervicitis

100
Q

What are some consequences of bacterial vaginosis?

A

Increased rate of upper tract infection.
Premature rupture of the membranes and preterm delivery
Increased risk of acquisition of HIV.

101
Q

What would you treat bacterial vaginosis with?

A

Metronidazole for 10 days.

102
Q

Which area of the body can chlamydia affect?

A 
Eyes
Rectum
Urethra
Throat
Also endocervix in females.
103
Q

What three serological groupings can chlamydia be divided into? What do they cause?

A

Serovars A-C- trachomatis- effects eyes (not an STI)
Serovars D-K- genital infection
Servers L1-L3- lymphogranuloma venereum. Long term chronic infection of the lymphatic system.

104
Q

Does chlamydia take up a gram stain? Explain why?

A

Nope.

The basis of gram stain is that you have to have peptidoglycan to retain it- chlamydia does not have this.

105
Q

How do you treat chlamydia?

A

Azithromycin 1g orally for uncomplicated.

Doxycycline BD 100mg for 7 days.

106
Q

Describe chlamydias infectious cycle?

A

Attaches and enters
Migrates to perinuclear area. EB to RB transition occurs.
Inclusion biogenesis and bacterial bioreplication
RB to EB transition and cell lysis (takes 48 hours to get to this stage).

107
Q

What samples are collected for testing for combined chlamydial and gonorrhoeal infection?

A

Male patients- first pass urine sample
Female patients- HVS or vulvo-vaginal swab. Or clinician taken endocervical swab.
Rectal and throat swabs can be taken
Eye swabs

108
Q

Describe the pathogenesis of gonococcal infection?

What do typical urethral infections result in?

A

Attaches to host epithelial cells and is endocytose into the cell to replicate, before being released into the tubepithelial space.
Result in prominent inflammation, release of toxic oligo-saccharide and peptidoglycan fragments as well as the release of chemotactic factors that attract neutrophilic leukocytes.
Some cause asymptomatic infection

109
Q

Where in the body can gonorrhoea affect?

A

Infects urethra, rectum, throat and eyes in men and females, and then the endocervix in just females.

110
Q

What shape is gonorrhoea under gram stain?

A

Gram negative diplococcus. Looks like two kidney beans facing one another. Often is intracellular on gram film due to it being phagocytosed.

111
Q

What other tests can you do for gonorrhoea?

A

Microscopy or urethral/endocervical swabs.

Culture on selective agar plates- not really done on vaginal swabs.

112
Q

Compare culture vs PCR/NAATs for testing for gonorrhoea?

A

NAATs- slight increase in sensitivity
NAATs- can also test urine and vaginal swabs
However can’t perform antimicrobial susceptibility testing. Or antibiotic resistance testing.
PCR- will be positive even if organism has died on the way to the lab
Takes hours not days

113
Q

How would you acquire pharyngeal gonorrhoeal infection?

How does it present?

A 
Orogenital exposure (oral sex). 
Generally an asymptomatic infection. Rare cases may cause an exudative pharyngitis with cervical lymphadenopathy.
114
Q

Why is it so important to treat pharyngeal gonococcal infection?

A

They may exchange genetic material with other bacteria to lead to gonococcal resistance.

115
Q

How would you treat gonorrhoea?

A

IM Cephalosporin plus azithromycin (used for resistant gonococcal infection and to treat chlamydia).

116
Q

What antibiotics are gonorrcoccus resistant too?

A

Penicillins, tetracyclines, quinolones and most oral cephalosporins.

117
Q

What is proctitis?

A

Inflammation of the lining of the rectum.

118
Q

How would you diagnose rectal gonorrhoeal infection?

A

NAAT.

119
Q

What is the differential diagnosis of rectal gonorrhoeal infection?

A

Other traditional STI’s, Ulcerative colitis, Crohns, anal fissure, rectal lacerations and proctocolitis.

120
Q

What organism causes syphilis?

A

Treponema pallidum

121
Q

Does syphillis gram stain? Can it be cultured? Which tests are used for diagnosis?

A

NOPE and nope

PCR is used.

122
Q

Describe the first stage of syphillis infection?

A

Primary lesion- chancre (painless ulcer). Organism multiplies at inoculation site, and enters the bloodstream. Chancre will heal with treatment.

123
Q

Describe the second stage of syphillis infection?

A

Large numbers of bacteria circulate in the bloodstream. with multiple manifestations at different sites (snail-track, mouth ulcers, generalised rash, flu-like symptoms)

124
Q

Describe the third stage of syphillis infection?

A

Latent stage- No symptoms but low level multiplication of spirochaete in intima of small blood vessels. Can be divided into early latent and late latent stages.

125
Q

What happens if the syphillis is left untreated?

A

Some patients will self cure.

Others will go on to develop neurological and cardiovascular complications.

126
Q

How would you diagnose syphillis?

A

Dark ground microscopy to look for spirochaetes in exudate from primary and secondary lesions.
Swab lesions for PCR
Blood tests- serology- tests for specific and non-specific antibodies to T palladium in the blood.

127
Q

What do non-specific tests in syphillis tell you?

A

The disease activity. Useful to monitor response to treatment.

128
Q

What non specific tests into syphillis are there?

A

VDRL- venereal diseases research laboratory
RPR-rapid plasma reagin

NOTE- they may be falsely positive e.g. in SLE, malaria and pregnancy.

129
Q

What specific serological tests can be used to diagnosis syphillis?

A

TPPA- T. Pallidum agglutination assay
TPHA- T. Pallidum haemaglutination assay
IgM and IgG Elisa- screening test.

130
Q

Which serological test in syphillis is not specific but remains positive for life?

A

TPHA- T. Pallidum haemaglutination assay

131
Q

If you test positive for IgM and IgG Elisa, what happens next?

A

Go on to have further tests performed on the blood
-VDRL test
TPPA test.

132
Q

What is the treatment for syphillis?

A

Injectable long acting penicillin.

133
Q

What causes genital herpes?

A

HSV type 1 (also causes cold sores) and type 2.

134
Q

How can you contract genital herpes?

A

Close contact with someone with herpes.

135
Q

Describe the pathogenesis of genital herpes?

A

Primary infection may be asymptomatic.
Virus replicates in dermis and epidermis.
Gets into nerve endings of sensory and autonomic nerves
Inflammation at nerve endings- very painful, multiple small vesicles which are easily deroofed.
Virus migrates to sacral root ganglion and hides from the immune system there.
Virus can reactivate from there causing recurrent genital herpes attacks.

136
Q

How would you diagnose genital herpes?

A

Swab in virus transport medium of the deroofed blisters for PCR.

137
Q

How would you treat genital herpes?

A

Aciclovir and pain relief.

138
Q

What is trichomonas vaginalis?

A

A single celled protozoal parasite.

139
Q

How is trichomonas vaginalis transmitted?

A

Sexual contact.

140
Q

What symptoms does trichomonas vaginalis cause?

A

Vaginal discharge and irritation in females.

Urethritis in men

141
Q

How would you treat trichomonas vaginalis?

A

Oral metronidazole

142
Q

What is pthirus pubis?

A

Pubic lice

143
Q

How can pubic lice be acquired?

What do the lice do?

A

Close genital skin contact.

The lice bite the skin and feed on blood causing itching in the pubic area.

144
Q

How would you treat pubic lice?

A

Malathion lotion.

145
Q

What is assisted conception treatment?

A

Any treatment which involves gametes outside of the body.

146
Q

Why is demand for assisted conception treatment increasing?

A 
Increasing parental age
Increasing chlamydia
Male factor infertility 
ACT more successful
Bigger range of ACT
147
Q

Other than parents struggling to have babies, when else may you use ACT?

A

Cancer patients- for preservation of eggs
Treatment to avoid transmission of blood borne viruses between patients
Treatment for single parents or same sex couples.

148
Q

What advice is given to couples before they undergo ACT?

A

Females are limited to 4 units a week of alcohol.
BMI must be between 19-29
Stop smoking
Give 0.4mg folic acid from preconception-12 weeks gestation
Check if female is immune to rubella- if not immunise
Check cervical smears are up to date
Occupational factors- exposure to hazards
Drugs- prescribed, over the counter and recreational.
Screen for blood borne viruses
Assess ovarian reserve
Counselling

149
Q

What ACT treatments are available?

A 
Donor insemination
Intra-uterine insemination
In-vitro fertilisation 
Intra-cytoplasmic sperm injection
Fertility preservation
Surrogacy
150
Q

What indications are there for intrauterine insemination?

A

Sexual problems, unexplained infertility, mild or moderate endometriosis, mild male factor infertility

151
Q

Describe the process of intrauterine insemination?

A

The sperm is inserted into the uterine cavity around the time of ovulation.

152
Q

What indications are there for in-vitro fertilisation?

A 
Unexplained infertility (> 2 years)
Pelvic disease (endometriosis, tubal disease, fibroids)
Anovulatory infertility (after failed ovulatory induction)
Male factor infertility (if greater than 1 x10^6 motile sperm present)
153
Q

Describe the down regulation stage in IVF?

A

Give a synthetic GnRH analogue or agonist. This reduces cancellation from ovulation and improves success rates. Allows precise timing of oocyte recover by using a HCG trigger.
A scan is also performed.

154
Q

What side effects can be experienced in the down regulation stage of IVF?

A

Hot flushes and mood swings
Nasal irritation
Headaches

155
Q

Describe the ovarian stimulation stage of IVF?

A

This occurs once you are happy the patient is down-regulated.
Then injections of gonadotrophins (FSH or LH) are given. Can be self-administered as a subcut injection.
This causes follicular development.

156
Q

What is the mans semen assessed for in IVF treatment?

A

Volume
Density- numbers of sperm
Motility- what proportion of the sperm are moving
Progression- how well they move

157
Q

What risks are there with oocyte collection in theatre?

A

Bleeding
Pelvic infection
Failure to collect oocytes

158
Q

How do you select an egg in IVF?

A

In the embryological lab- they go through follicular fluid and identify eggs and the surrounding mass of cells. They collect them and incubate them.

159
Q

How many eggs fertilise normally in IVF?

A

Approximately 60%.

160
Q

Describe the hormones, egg release and development of the normal human embryo?

A

Normal LH surge
Egg is released 36 hours later
Fertilisation occurs in the ampulla normally.
By day 4 the morula is formed. By day 5 they differentiate into a blastocyst.

161
Q

At what day does transfer and cryopreservation (cooling to low temps) occur?

A

Day 5.

162
Q

When does implantation of the embryo into the uteral cavity occur in IVF?

A

Day 7.

163
Q

How many embryos are usually transferred in IVF?

A

Usually 1- but a maximum of 3 in exceptional circumstances.

164
Q

What support do you need to give patients once the fertilised eggs have been transferred?

A

Progesterone depositories for 2 weeks.

Pregnancy test 16days after oocyte extraction.

165
Q

What are the indications for intra-cytoplasmic sperm injection?

A

Severe male factor infertility
Previous failed fertilisation with IVF
Preimplantation genetic diagnosis.

166
Q

What do you do if the man has azoospermia in ICSI?

A

Surgical sperm aspiration- can be withdrawn from epidydimus if obstructive or testicular tissue if non-obstructive.

167
Q

Describe the process of intra-cytoplasmic sperm injection

A

The egg is stripped
The sperm is demobilised
The sperm is injected into the egg.
Incubated

168
Q

What complications are associated with ART?

A

Ovarian hyperstimulation syndrome

169
Q

What is ovarian hyper stimulation syndrome?

A

Enlarged ovaries- due to excess follicles

170
Q

What symptoms are associated with ovarian hyper stimulation syndrome?

A

Abdominal pain/bloating
Nausea/diarrhoea
Breathless

171
Q

What treatment can be offered if ovarian hyper stimulation syndrome occurs before embryo transfer?

A

Electric freeze- freeze the embryos and wait 2-3 months to transfer them then.
Single embryo transfer

172
Q

What treatment can be offered if ovarian hyper stimulation syndrome occurs after embryo transfer?

A

Monitoring with scans and bloods
Reduce risk of thrombosis- fluids, TED stockings, fragmin
Analgesia
Hospital admission if IV fluids are required.

173
Q

What other issues are there with ART?

A

No eggs retrieved (however very uncommon)
Surgical risks of oocyte retrieval
Surgical risks of surgical sperm aspiration
Failed fertilisation
Problems in early pregnancy e.g. ectopic pregnancy
Increased risk in on-going pregnancy
Psychological problems

174
Q

What determines our gender?

A

The presence/absence of a Y chromosome.

Even if you have one X, you are still a girl.

175
Q

Describe the development of the internal reproductive tract?

A

The Y chromosome has the sex-determining region, causing the development of testis from the biopotential gonad.
Fetal testes secrete testosterone and mullerian inhibiting factors.

176
Q

What are the two primitive genital tracts called?

A

Mullerian- produce female genital system

Wolffian- produce male genital system

177
Q

If you are going to be female, what primitive tracts will be suppressed and which will be left?

A

Wolffian will be supressed

Mullerian will be allowed.

178
Q

If you are going to be male, what primitive tracts will be suppressed and which will be left?

A

Mullerian will be surpressed

Wolffian will be allowed.

179
Q

At what stage can you determine whether a baby will be a boy or a girl?

A

16 weeks gestation.

180
Q

What is testicular feminisation?

A

Someone is born looking like a female but when they hit puberty they don’t develop breasts. They actually have a male chromosome but female genitalia.

181
Q

What causes testicular feminisation?

A

Congenital insensitivity to androgens.
X linked recessive disorder
Androgen induction of Wolffian duct does not occur however Mullarian suppression does. Causes them to be born phenotypically female with external genitalia female, absent uterus and ovaries and a short vagina.

182
Q

When does testicular feminisation commonly present?

A

At puberty with lack of pubic hair and amenorrhoea.

183
Q

Why is it important that the testes descend?

A

Lower temp outside the body to facilitate spermatogenesis.

184
Q

What muscle controls where the testis sit in the scrotal sac?

A

Dartos muscle.

185
Q

What is the medical term for undescended testis?

A

Cryptorchidism- the individual has reached adulthood but the testis are not yet descended.

186
Q

What is the implications on fertility in cryptorchidism?

A

If unilateral they are usually still fertile however it reduces the sperm count.

187
Q

Do you treat cryptorchidism?

A

Orchidoplexy should be performed if they are below 14 years to minimise the risk of testicular germ cell cancer..
If an adult- consider orchidectomy

188
Q

What are the erectile tissues in the penis?

A

Corpus cavernosum

Corpus spongiosum

189
Q

What is the function of the testes?

A

Spermatogenesis (occurs in the seminiferous tubules)

Production of testosterone.

190
Q

What cells in the testes produce testosterone?

A

Leydig cells.

191
Q

What is the role of Sertoli cells?

A

Form a blood-testis barrier- this protects the sperm from antibody attack. Provides a suitable fluid composition which allows later development of sperm
Provide nutrients
Phagocytosis- destroy defective cells and removes surplus cytoplasm
Secrete seminiferous tubule fluid
Secrete androgen binding globulin
Secrete inhibin and activin hormones

192
Q

What is the function of androgen binding globulin?

A

Keeps the concentration of testosterone high (by binding to it) in the lumen

193
Q

What is the role of inhibin and activin hormones?

A

Regulates FSH secretion and controls spermatogenesis.

194
Q

What is the role of seminiferous tubule fluid?

A

Carries the sperm to the epididymis.

195
Q

What hormone stimulates the production of testosterone?

A

LH.

196
Q

What does gonadotrophin releasing hormone do?

Which hormone controls this by negative feedback?

A

Stimulates the anterior pituitary to release FSH and LH.

Testosterone causes less GnRH to be released by negative feedback.

197
Q

What does lutinising hormone do on the male reproductive tract?

A

Stimulates the leydig cells to produce testosterone.

198
Q

What does follicle stimulating hormone do to the male reproductive tract?
Which hormone regulates FSH?

A

Acts on Sertoli cells to enhance spermatogenesis.

Regulates by negative feedback from inhibin

199
Q

Where is testosterone secreted into?

A

The blood and seminiferous tubules.

200
Q

What are the effects of testosterone before birth?

A

Masculinises the male reproductive tract and promotes descent of testis.

201
Q

What are the effects of testosterone at puberty?

A

Promotes puberty and male characteristics

202
Q

What are the effects of testosterone in an adult?

A

Controls spermatogenesis

Secondary male characteristics (male body shape, deepens voice, thickens skin, libido)

203
Q

What cell secretes inhibin and activin? What is their function?

A

Sertoli cells

Inhibin inhibits FSH. Activin stimulates FSH.

204
Q

What occurs to spermatozoa after ejaculation?

A

They become liquified (by enzymes in the prostate gland)
Capacitation- a series of biochemical and electrical events occurring before fertilisation
Chemoattraction to oocyte and bind to zona pellucida of oocyte.
Acrosome reaction
Hyperactive motility
Penetration and fusion with oocyte membrane
Zonal reaction.

205
Q

Which area of the Fallopian tube does fertilisation occur?

A

Ampulla

206
Q

What is the function of the epididymis and vas deferens?

A

Exit route from testes to urethra, concentrate and store sperm, site for sperm maturation.

207
Q

What is the function of the seminal vesicles?

A 
Produce semen into ejaculatory duct. 
Supply fructose
Secrete prostaglandins (stimulates motility)
Secrete fibrinogen (clot precursor)
208
Q

What is the function of the prostate gland?

A

Produces alkaline fluid (neutralises vaginal acidity)

Produces clotting enzymes to clot semen inside female.

209
Q

What is the function of the bulbourethral gland?

A

Secrete mucus to act as a lubricant

210
Q

What is the definition of male infertility?

A

Failure of the sperm to normally fertilise the egg.

211
Q

What can cause of male infertility?

A

Idiopathic
Obstructive
Non-obstructive

212
Q

What is the most common cause of male infertility?

A

Idiopathic

213
Q

Name some examples of obstructive pathologies causing male infertility?

A

Cystic fibrosis
Vasectomy
Infection

214
Q

Name some examples of non-obstructive pathologies causing male infertility?

A 
Congenital- crytorchidism 
Infection- mumps, 
Iatrogenic- chemotherapy/radiotherapy
Pathological- testicular tumour 
Genetic- chromosonal e.g. Kleinfelters syndrome
Specific semen abnormality- azoospermia, 
Systemic disorder 
Endocrine disorder
215
Q

What are the common endocrine causes of male infertility?

A

Pituitary tumours- hyperprolactinaemia (decreases LH, FSH and testosterone), acromegaly, cushings
Hypothalmic cause-
Thyroid disorders
Diabetes
Steroid abuse (decrease LH, FSH and testosterone)
Androgen insensitivity (normal or raised LH and testosterone)

216
Q

What examinations would you do in male infertility?

A

General examination- including secondary male characteristics
Genital examination- testicular volume, presence of vas deferens and epididymus, penis (urethral orifice), presence of variceal or swelling.

217
Q

What is the normal testicular volume for adults?

In prepubertal boys?

A

12-25mls.

1-3mls

218
Q

What testicular volume are you likely to be infertile if you are below?

A

5mls.

219
Q

What do they analyse the semen for?

A 
Volume
Density- number of sperm
Motility- what proportion are moving
Progression- how well they move?
Morphology
220
Q

What does an obstructive male infertility show like on examination?

A

Normal testicular volume
Normal secondary sexual characteristics
Vas deferens may be absent

Endocrine- normal LH, FSH, testosterone

221
Q

What does a non-obstructive male infertility show like on examination?

A

Low testicular volume
Reduced secondary sexual characteristics
Present vas deferens

Endocrine- High FSH and LH, low testosterone

222
Q

What life style factors can be changed to help maximise fertility in the male?

A 
Frequent sexual intercourse
Less than 4 units a day of alcohol
Stop smoking
BMI less than 30
Avoid tight fitting underwear and long hot baths
Certain occupations
223
Q

When is intra-uterine insemination indicated?

A

Mildly reduced sperm count

224
Q

When is intra-cytoplasmic sperm injection indicated?

A

Very low sperm count

225
Q

When is surgical sperm aspiration indicated?

A

Azoospermia

226
Q

When is donor sperm insemination indicated?

A

Azoospermia or very low sperm count
Genetic conditions
Infectious

227
Q

What does oligoasthenospermia mean?

A

Low sperm count and motility

228
Q

What does teratoasthenospermia mean?

A

Low motility and abnormal forms

Reproduction (34 decks)

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