Case 14 Flashcards

1
Q

What is the clinical relevance of the rectovesical pouch?

A

It is the most inferior portion of the pelvic cavity where fluid from trauma is most likely to collect in males.

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2
Q

Describe the rectovesical pouch in males

A

It is a reflection of the pelvic peritoneum which dips behind the urinary bladder and rectum, and lines the back of the seminal vesicle and prostate.

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3
Q

Describe the clinical relevance of the pouch of Douglas (rectouterine pouch)

A

In females it is where fluid is most likely to collect e.g. from trauma

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4
Q

Describe the pelvic peritoneum in females

A

It starts from the superior border of pubic symphysis and continues over the urinary bladder, dips down into the vesicouterine recess and is reflected back up onto the funds and portion of the body of the uterus. It continues down the surface of the uterus to the posterior fornix. the pelvic basin of the rectouterine pouch, back onto the rectum and to the abdominal wall.

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5
Q

Identify the 7 branches of the anterior division of the internal iliac artery

A
  1. Umbilical → Superior vesicle (bladder, urethra)
  2. Obturator → Towards obturator foramen
  3. Inferior vesicle (Male) / Vaginal (Female)
  4. Uterine → Uterus, cervix, vagina, uterine tubes
  5. Middle Rectal → Rectum
  6. Inferior Gluteal → Gluteal Region
  7. Internal Pudendal → Perineum (deep to levator ani)
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6
Q

What arch attaches to and divides the obturator internus in 2?

A

The tendinous arch

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7
Q

What is located in the urogenital hiatus in females?

A

Urethra and vagina

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8
Q

What muscles make up the pelvic diapragm and pelvic floor?

A

Pelvic Diaphragm
Levator ani (iliococcygeus, pubococcygeous, puborectalis)
Ischiococcygeous

Pelvic wall
Piriformis
Obturator internus

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9
Q

What is the puborectalis?

A

The puborectalis forms a sling around the rectal junction to create the anorectal junction, unless undergoing defecation.

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10
Q

Describe the false greater pelvis

A

The false greater pelvis occurs from the iliac crest to the pelvic inlet and contains abdominal viscera, not pelvic.

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11
Q

Describe the true lesser pelvis and pelvic inlet

A

The true lesser pelvis occurs from the pelvic inlet to the pelvic outlet and contains the true pelvic viscera.
The pelvic inlet is where the pelvic cavity begins.

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12
Q

Describe the male pelvic viscera

A

Sperm travels into the pelvis from the testes through the ductus deferens along the bladder, underneath and into the prostate gland where it unites with the urethra. The male reproductive and urinary tracts merge, however in females they are completely separate.
The seminal vesicles sit behind the bladder and provide fluid for the sperm to travel within.
Main content – Distal Urinary, reproductive and digestive tracts

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13
Q

Describe the female pelvic viscera

A

The fundus is in front of the uterine tube. The fallopian (uterine) tubes and the ovaries are not directly connected. Fimbriae (cilia) help to guide the eggs into the fallopian tube where fertilisation occurs, avoiding oocyte entry into the abdominal cavity.

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14
Q

Describe the position of the uterus

A

The vaginal canal slopes posteriorly towards the rectum whilst the cervix and uterus curve anteriorly to sit over the bladder. The junction between the vagina and cervix is known as the angle of anteversion.
The junction between the cervix and uterus is known as the angle of anteflexion.
The opposite to anteflexed is retroflexed and the opposite to anteverted is retroverted. There is increased risk of prolapse with retroversion or retroflexion. Prolapse is where one or more of the organs in the pelvis slip down from their normal position ad bulge into the vagina.

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15
Q

Describe the ligaments in females

A

Suspensory ligament - ovarian vessels to pelvic walls
ovarian ligament - ovary to uterus
Round ligament - passes through the inguinal canal and attaches to the external genitalia

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16
Q

Describe the anal and urogenital triangle

A

The anal triangle and urogenital triangle are divided by an imaginary line between the ischial tuberosities.

The anal triangle contains the anal canal and external anal sphincter. It also contains a fat filled space with pudendal neurovasculature known as the ischio-anal fossae. It lies lateral to the anal canal.
The sacrotuberous ligament attaches the sacrum and the ischial tuberosities.

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17
Q

Contents of the male deep pouch

A
Urethra
urethra sphincter
bulbourethral glands
deep transverse perineal muscle 
perineal neurovasculature
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18
Q

Contents of the female deep pouch

A
Urethra
urethral sphincter
vagina
deep transverse perineal muscle
perineal neurovasculature
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19
Q

Muscles in the male and female superficial pouch

A

Bulbospongiosis muscle covers the (corpus spongiosum)
Ischiocavernosus muscle covers the corpus cavernous
Superficial transverse perineum

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20
Q

Contents of the male superficial pouch

A

Penis - corpus spongiosusm contains the urethra
corpora cavernosa paired structures- crura attach to the ischiopbic rami

Scrotum containing the testes and spermatic cord (ductus deferens)

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21
Q

Contents of the female superficial pouch

A

Clitoris -
corpus spongiosum attached to the perineal membrane
Corpora cavernosa paired structures - crura attach to the ischiopubic rami

main pubis, labia major and minor

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22
Q

Describe the neurovasculature of the perineum

A

Pudendal nerve (S2-S4) - gives rise to the inferior rectal nerve and perineal nerve and its branches

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23
Q

Describe the blood supply of the perineum

A

Internal pudendal artery which is a branch of the anterior division of the internal iliac artery

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24
Q

Pelvic fistula and it’s causes

A

An abnormal connection via a tunnel-like hole between two epithelium-lined organs or vessels

Causes:
Obstructed/prolonged labour, severe inflammation due to infection, pelvic surgery, trauma

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25
Q

Prostate gland location and the 3 prostate glands

A

Superiorly - bladder
Inferiolaterally - levator ani
posteriorly - ampulla
anteriorly - pubic symphysis

  1. Inner periurethral glands (opens directly into urethra)
  2. Outer periurethral glands (ducts connect into urethra)
  3. Main prostatic/external glands

Pale columnar epithelium and as you move towards the urethra they become more cuboidal and transitional like the urethra

Gland Secretions - acid phosphatase, citric acid and amylase

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26
Q

Arterial supply and innervation of the prostate gland

A

Arterial supply:
Inferior vesicle artery
middle rectal artery
internal pudendal

Innervation:
Sympathetic fibres originating T12-L3
Parasympathetic fibres originating S2-S3

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27
Q

Functions of Sertoli cells

A

Located in the seminiferous tubules
Respond to FSH to cause spermatogenesis
1. Attachment and reattachment of sperm to cells - guide towards lumen
2. Provide nutrients
3. Tight junctions between cells - provide safe, immunological environment
4. Fluid secretions - flush immotile sperm
5. Phagocytosis of dead sperm and residual cytoplasm

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28
Q

Steroidogenesis

A

Testosterone precursors are covered to testosterone or DHT via 5a reductase. They either bind to peripheral targets (active - 2%) or SHBG/albumin to act as a reservoir (inactive - 98%).
Testosterone or testosterone pre cursors are converted to oestrogen via aromatase

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29
Q

HPT Axis

A

The hypothalamus secretes GnRH which acts on the anterior pituitary gland. This the secretes FSH to act on Sertoli cells and LH to act on leydig cells. Sertoli cells cause spermatogenesis and produce inhibin which inhibits FSH via negative feedback.
Leydig cells release testosterone to act on the seminiferous tubules and peripheral targets.

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30
Q

Describe spermatogenesis

A

Spermatocytogenesis
Meiotic divisions - 4 haploid spermatids
Spermiogenesis
1. Golgi coalesce to form the acrosome
2. Mitochondria align and form the mid piece of the tail
3. Sertoli cells remove residual cytoplasm to form immature immotile spermatozoa.

Maturation at the epididymis
Closure of acrosomal binding sites to prevent hyperactivity
Sperm becomes motile

Storage at ductus deferens (approx 2-3 months)

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31
Q

Describe the composition of semen

A

60% seminal vesicle - thick alkaline fluid
20% prostate - thin milky fluid (citrate, zinc, PSA)
10% Bulbourethral gland - mucus

Semen enters the ampulla and then travels through to the ejaculatory duct, through the penile urethra and then deposited into the vagina.

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32
Q

Clinical Reasoning of breast lump

A

Fibroadenoma (Breast Mouse)
Highly mobile, smooth, painless, benign lump
Common in early 20s

Fibrocystic Changes
Multiple, tender, painful, benign lumps
Due to hormonal changes in week before menstruation

Breast Cyst
Fluid filled, painful lump
Common in pre-menopausal women (30s-50s)

Breast Abscess
Fluid filled painful lump - clinically indistinguishable from cysts due to infective symptoms - hot, swollen

Fat necrosis
Painless lump, erythema/bruising due to trauma

Lipoma
Several benign lumps - well circumscribed, soft, smooth, lobulated non tender. Found in breasts, abdomen, neck commonly

Breast Cancer
Lump with skin changes - tethering, nipple discharge, eczematous changes.
Peau d’orange - indicates secondary metastatic spread

Benign (smooth, regular borders, mobile)
DCIS - ductal lump, nipple discharge
LCIS - Abnormal cells in lobule - asymptomatic

Malignant (hard, irregular, fixed, skin/nipple changes)
Inflammatory carcinoma - red, hot, swollen breasts
Paget’s disease - follicular, red, eczematous rash at nipple/areola with palpable nipple lump

Spread - direct to muscles, axillary spread, haematogenous

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33
Q

Breast Cancer modifiable and non-modifiable risk factors

A
Modifiable
Increasing age 
large gap between menarche and menopause
Female 
FH 
Radiation
Non modifiable 
Not breast feeding 
nulliparous/first child over 30
COCP/HRT
obesity 
sedentary lifestyle
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34
Q

Breast Cancer Triple Assessment

A

Specialist examination
Mammogram>40, ultrasound<40
Fine needle aspiration

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35
Q

Chemotherapy

A

2,3,4 weekly cycles combination drugs which target multiple signalling pathways to reduce resistance and attack heterogenous tumours
Adjuvant - after surgery to reduce relapse risk
Neo-adjuvant - before surgery to increase operability
Metastatic - palliative treatment only

Side effects:
Alopecia/rashes
GI disturbances - mucosal linings - diarrhoea/constipation/nausea
BM - reduced erythrocytes, platelet, leukocytes = reduced clotting = anaemia

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36
Q

Non-targeted anti cancer drugs

A

Alkylating agents - cyclophosphamide
cross link alkyl groups of guanine which stops DNA replication

Platinum agents - cisplatin
DNA inter and intra strand cross links stops DNA replication

Antimetabolites - methotrexate
inhibit DHFR enzyme - stops nucleotide synthesis

Anthracyclines - doxorubin
Inhibit topoisomerase II enzyme - stops DNA reannealing
inhibits DNA helicase
produces a reactive O2 radical species

Antimicrotubule agents
Vinca alkaloids - vincristine - stops mitotic spindle formation
Texans - docetaxel - inhibits mitotic spindle contraction

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37
Q

Targeted Cancer Drugs

A

Hormone antagonists - Tamoxifen (SERM)
Competitive inhibitor of ERs, forms a tamoxifen:ER dimer, binds to DNA - unstable complex

Protein Kinase Inhibitors - imatinib
Inhibit kinase domains which form the proliferative fusion protein that allows unregulated tumour division

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38
Q

Cancer Immunotherapy

A
  1. Monoclonal antibodies
  2. Cancer Vaccines - HPV
  3. Immune checkpoint inhibitors - PD-1 antagonists - deactivate PD-1 receptors on T cells which tumours bind to to evade immune system
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39
Q

Ectocervix, Endocervix and cervical stroma microanatomy

A

Endocervix - columnar epithelium which is mucus secreting (low viscosity to allow sperm passage and ovulation) - connects uterine and vaginal cavities

Ectocervix -stratified sqaumous epithelium covers the ectocervix and projects into vaginal canal to vaginal fornices

Cervical stroma
lots of smooth muscle which decreases as you move distally down the cervix
very collagenous body for strength - pregnancy sphincter

40
Q

Layers of the vagina

A
  1. Stratified squamous epithelial mucosa (pale appearance as high in glycogen)
  2. Lamina propria - elastic fibres and thin walled vessels
  3. Fibromuscular layer - inner = circular fibres, outer - longitudinal
  4. Adventita - fibrocollagenous tissue - thick elastic fibres, nerves and vessels
41
Q

Describe the transformation zone of the cervix and vagina

A

change that occurs at puberty onset and during 1st pregnancy
replacement of the endocervical columnar epithelium to stratified squamous epithelium in vagina = squamous metaplasia

Squamocolumnar junction is located in the distal cervix at birth but with this change extends distally

3 cell types present

  1. original squamous/columnar epithelium
  2. metaplastic squamous cells
  3. atypical epithelium - malignant potential (loss of regular stratified pattern/high nucleus to cytoplasmic ratio)
42
Q

Carcinoma of the Cervix

A

Cervical intraepithelial neoplasia (CIN) = no invasions to basement membrane but malignant
Invasive cervical carcinoma - CIN breaches basement membrane - spread via blood and lymph vessels

43
Q

Define Reproductive Cycle

A

The physiological changes that occur from conception to gestation through to partition

44
Q

Define menstrual cycle

A

the cyclical changes in the ovaries where the ovum develops for ovulation and the uterus prepares for implantation, which results in either pregnancy or menstruation.

45
Q

Define ovarian cycle

A

The cycle of follicle growth resulting in ovulation and corpus luteum formation.

46
Q

Oestrogen and Progesterone production and roles

A

LH binds to theca cell LH receptors causes the conversion of cholesterol to progesterone to testosterone.
Testosterone diffuses to granulosa cells and is converted to oestrogen via aromatase.

Oestrogen
Increases endometrial and follicular growth and increases fallopian tube transport
Inhibits milk let down
Causes breast duct growth
Development of secondary sexual characteristics (breast and external genitalia)

Progesterone
Reduces endometrial growth, follicular growth and fallopian tube motility
Increases breast alveolar/lobular growth and milk secreion
PMS (progesterone withdrawal)

47
Q

Follicular cycle of growth

A
  1. Low oestrogen stimulates the hypothalamus to release GnRH and the APG to release FSH
  2. Increased FSH causes follicular development
  3. Increased oestrogen for 48 hours causes the LH surge
  4. LH surge = ovulation - corpus luteum formation
  5. CL releases progesterone and oestrogen until placenta can produce enough
  6. If not pregnant, CL regresses and oestrogen and progesterone decreases
48
Q

HPO axis

A
  1. GnRh released by the hypothalamus
  2. Acts on APG to release FSH and LH
  3. Acts on the ovaries to release oestrogen or progesterone
49
Q

Menstrual Cycle Frequency disorders

A

Primary Amenorrhea - absence of menses and SSC at 14
OR absence of menses with SSC at 16
Secondary Amenorrhea - absence of menses for 3-6 consecutive months

Polyamenorrhea = less than 24 days
Regular - 24-32 days
Oligomenorrhea - over 32 days
Amenorrhea - absent

50
Q

Uterine Bleeding disorders

A

Menorrhagia - (>80ml) - measured by increased changing of tampons and pads
Metrorrhagia - Post-coital/intermenstrual/post menopausal bleeding

51
Q

Dysmenorrhea

A

Normal to have headaches, diarrhoea nausea, cramps (due to imbalance of prostaglandins and leukotrienes - SM contractions and vasoconstriction). (more common in younger women who recently started menses)

Primary = no pelvic pathology 
Secondary = underlying pelvic pathology
52
Q

Investigations of menstrual disorders

A
Prolactin (high = APT)
FSH (high = ovarian failure)
Testosterone (high = PCOS)
TFT 
Clotting factors (reduced = excess bleeding)

Further investigations - Ultrasound, Hysteroscopy, laparoscopy

53
Q

Hormonal Changes during menstrual cycle

A
  1. Menses (0-5) = Progesterone withdrawal
    Endometrial shedding of functional zone (Stratum Compactum and Spongiosium)
  2. Proliferative Phase (5-14) - Increase in oestrogen
    Increased functional zone regeneration via basal layer, thin watery electrolyte rich secretion with high spinbarkeit for sperm passage, increased embryo transport speed in FT
  3. Secretory Phase (14-28) = high in progesterone and oestrogen
    reduced differentiation of epithelium to prepare for decidualisation
    reduce endometrial growth
    reduce FT transport speed
    thick viscid secretions with low spinbarkeit to prevent sperm passage
54
Q

Eating disorders impact on reproductive hormones

A

Low BMI - anorexia
stops GnRH secretions which disrupts HPO axis , reduces FSH/LH, reduces oestrogen and progesterone and stops endometrial thickening = no menstruation

High BMI - obesity
Increased basal oestrogen levels - no oestrogen decrease for FSH increase = low oestrogen levels = no FSH increase and follicular development = no endometrial thickening

55
Q

PCOS impact on reproductive hormones

A

Increased LH on theca cells = increased testosterone levels, reduced FSH means no conversion to progesterone (reduced levels)

Diagnostic criteria:
1. Hyper-androgenism 
2. Cystic Ovaries (caused by low progesterone)
3.  Oligo/Anovulation 
Linked to obesity in 50% of cases
56
Q

Thyroid Disorders impact on reproductive hormones

A

Hyperthyroidism (High T3/4, low TSH)
Increased SHBG and LH - No significant LH surge - light, infrequent periods (oligo-ovulation)

Hypothyroidism (Low T3/$, high TSH)
ineffective blood clotting = irregular periods and menorrhagia

57
Q

MofA, Advantages and Disadvantages of Male condoms

A

Male Condoms
Barrier method to ejaculate or pre-ejaculate preventing sperm meeting the ovum.

Advantages:
Easy to use
Effective
No side effects (latex allergy)
Some STI Protection	

Disadvantages
Sensitivity loss
Interruption of Sex
Can break or slip off

58
Q

MofA, advantages and disadvantages of caps and diaphragms

A

(Barrier) Dome-shaped rubber ring which fits into vagina between posterior fornix and behind the pubic symphysis to cover cervix. Spermicide is applied and must be left in 6 hours after having sex.

Advantages 
Effective
No side effects
Direct control by women
Can be put in convenient time before sex	
Disadvantages 
Increase in UTI or cystitis rate
Not suitable if TSS history 
Must be used with spermicides 
Must be comfortable with self examination
59
Q

MofA, advantages and disadvantages of female condoms

A

(Barrier)Loose sheath with inner ring with closed end in the vagina. Ring sits on the vulva and acts as a barrier to sperm.

Advantages
Some STI protection
No side effects
No spermicide need
Direct control by women	

Disadvantages
Requires careful insertion
Can be noisy
Can interrupt sex

60
Q

MofA, advantages and disadvantages of withdrawal method

A

Withdrawing penis before ejaculation

Advantages
Slight reduced risk of fertilisation
Use of spermicide increases reliability

Disadvantages
Very unreliable as pre ejaculate contains some motile sperm

61
Q

MofA, advantages and disadvantages of spermicide

A

(Nonoxynol-9)
Inserted into the vagina prior to intercourse to alter vaginal pH and integrity of the sperm cell membranes.

Advantages 
No side effects
Easy and simple to use
Provides lubrication
Enhances efficacy of barrier methods	

Disadvantages
Increased risk of vaginal and urinary infections
Possible sensitivity, irritation, or allergy
Should not be used as sole contraceptive

62
Q

MofA, advantages and disadvantages of LAM (lactational amenorrheic method)

A

Suckling infant reduces the release of gonadotrophins, which suppress ovulation but as suckling reduces, ovulation returns.

Advantages
Over 98% effective if:
Less than six months postpartum.
Amenorrhoeic- no vaginal bleeding after the first 56 days postpartum.
Fully breast-feeding day (at least four-hourly feeds) and night (at least six-hourly feeds).

Disadvantages 
Less effective if:
Breast-feeding decreases e.g. fewer night feeds, use of formula
Menstruation resumes
More than six months postpartum.
63
Q

MofA, advantages and disadvantages of Female Sterilisation

A

Tying or removal of tubes, sealing using diathermy to prevent re-joining of cut tubes.
Laparoscopy = abdominal access
Hysterectomy = vaginal access

Advantages
Highly effective 
Permanent
No weight gain
No heavy periods – potential amenorrhea. 	
Disadvantages 
Irreversible 
Surgical procedure – local anaesthetic 
No STI protection
Potential complications
64
Q

MofA, advantages and disadvantages of Intra-uterine Devices

A

Prevents fertilisation primarily but also may prevent implantation and be spermicidal.

Nearly 100% effective

65
Q

Natural Family Planning as a non-hormonal contraception method

A

Women abstain from sexual intercourse during their ovulary period and fertile window (5 days) - but sperm can live in the cervix for up to 9 days.

Detection of ovulation:
Increase in basal temperature (0.2C)
Sensitive breasts
Mood changes
Change to cervical mucus 
Cycle length 
Mid cycle ovulation pain, discharge, and bleeding
66
Q

MofA, advanatages and disadvantages of Progesterone only hormonal contraceptives

A

(POP, Injectables, Implant)
Contains a third of progesterone as in COCP.
Affects ovulation via thickening of cervical mucus, thinning of endometrium and reducing fallopian motility.

Advantages
Very effective and safe - 12 hour window of protection
No oestrogen 
Decreased risk of endometrial cancer
May relieve dysmenorrhoea or menorrhagia
Suitable for:
-Older women (up to 55yo) 
-Smokers
-Diabetes / obesity
-Hypertension
-Migraine
Disadvantages 
12 hour window of protection  
Menstural disturbance
Breast tenderness
Worse acne
Mood changes
Headaches
Surgical procedure with implants
No STI Protection

Injectables:
Weight gain
Cant be removed
Delay to return to fertility (1 year)

67
Q

MofA, advantages and disadvantages of combined oral contraceptives

A

(COCP, Ring, Patch)
Prevents ovulation by suppressing GnRH release by hypothalamus and pituitary glands, inhibiting sperm transport, thickening cervical mucus, thinning endometrium lining and reducing fallopian motility.

Advantages
Reliable and reversible
Relives dysmenorrhea and menorrhagia by 60%
Improves acne
Reduces risk of cysts, ovaria and cervical cancers, PID
Treatment of endometriosis
Relieves PMS

Disadvantages
Not suitable if:
Migraine with aura
Breast cancer 
BMI >35 kg/m2
Hypertension
Multiple risk factors for CVD
Diabetes
No STI protection
68
Q

Describe the types, MofA, advantages and disadvantages of emergency contraception

A

Prevention or delay of ovulation for 5-7 days if taken prior to the LH surge. Progesterone only which can be use dafter UPSI

Levonorgestrel (LNG) eg Levonelle
Taken as a Single dose
Within 72 hours. Available with a prescription or to buy.

Ulipristal acetate eg EllaOne
-Single dose which can be taken up to 120 hours after unprotected sex, but is only available with a prescription

Advantages
97-99% effective

Disadvantages
Side effect - nausea, vomiting, irregular short term cycle

Contraindication if current or suspected pregnancy

All women should take a pregnancy test

69
Q

MofA, advantages and disadvantages of IU copper devices

A

Prevents implantation by thinning endometrium lining. Can be used as emergency contraception up to 5 days after UPSI.

Advantages
Almost 100% effective

Disadvantages
Contraindication in suspected pregnancy or acute pelvic infections.

70
Q

Describe a vasectomy and its advantages and disadvantages

A

A small incision is made along the midline of the scrotum to remove/cut/tie part of the vas deferens (cute tubes should be sealed by cautery to stop rejoining). This means no sperm will enter the ejaculate - semen only.
Vasectomy success should be confirmed by doing via some analysis for azoospermia.

Advantages:
Effective and permanent
Minor, easy operation done at GP
no increased risk of CVD, Testicular or prostate cancer

Disadvantages:
Not easily reversible 
Not immediately effective 
Surgical procedure - potential complications 
No STI protection
71
Q

Stages of Sexual Response in females and males

A

Male
Arousal - Plateau - Orgasm - Refractory period and resolution (can go on to have second orgasm after refractory period).

Female 
Less definitive sexual response
No refractory period 
Can have long plateau but no orgasm 
Can have multiple orgasms
Can have no plateau - straight to orgasm
72
Q

Female Sexual Dysfunction definition and causes

A

Subjective dissatisfaction with the level or nature of sexual activity, involving one or more of the following:
Sexual interest/arousal disorder
Orgasmic disorder
Genitopelvic pain/penetration disorder

Causes:
Dyspareunia
- Arousal pain
- Sensitive external genitalia 
- PID/Upper reproductive tract infection 
-Endometriosis
- Vaginismus (invol.contractions)

Reduced desire

  • psychological
  • hormonal* (reduced androgens = reduced libido)

Reduced arousal

  • vascular (reduced blood supply = clitoral erectile dysfunction)
  • CNS/PNS damage
  • Hormonal*
Additional:
medication
chronic pain/illness
pregnancy 
post partum
73
Q

Management of Female sexual dysfunction

A

Non-pharmacological:

  • CBT - physiological cause
  • Lifestyle changes - reducing obesity, alcohol and smoking
  • Pelvic floor exercises
  • Medical devices - vaginal dilators

Pharmacological:

  • Androgens
  • Oestrogen
  • Sildenafil (PDE-5 inhibitor)
74
Q

Penile Erection and Ejaculation physiology

A

Erection

  1. NO binds to guanyl cyclase (GTP to cGMP)
  2. increased cGMP = decreased intracellular Ca = SM relaxation
  3. Blood fills spaces - dialled pudendal arteries = increased BP of corpus cavernosum which causes veins to collapse = trapping of blood
  4. Blood trapping limits tunica expansion - increases SBP - erection

Ejaculation - sperm deposition (not the same as orgasm = rhythmic contractions, increased HR and RR associated with ejaculation)
1. Emission
Sperm flow from distal epididymis - ductus deferens - ejaculatory duct (seminal fluid secreted here)
Internal urinary sphincter closes at neck of bladder to prevent sperm entry

  1. Expulsion
    external urinary sphincter relaxes in deep perineal pouch
    striated muscles contract to expel ejaculate
    (innervation - somatic pudendal nerve S2-4)
75
Q

Male sexual dysfunction definition and causes

A

The persistent inability to initiate or sustain penile erection for sufficient sexual activity

Causes
- Psychogenic - young men with poor relationship/sexual experiences
- Vasculogenic - penile artery atherosclerosis
- Neuro - CNS/PNS damage, spinal cord injury
- endocrine - reduced testosterone = primary/secondary hypogonadism
increased prolactin = hyperprolactinaemia
- iatrogenic - antihypertensive drugs prevents increased BP for erection, recreational drugs (cannabis) reduce NO, alcohol/opiates reduce testosterone

76
Q

Male sexual dysfunction management

A

Non-pharmacological

  • CBT - psycho
  • Lifestyle changes (reduced alcohol, obesity, smoking, drug use)
  • Associated disease screening

Pharmacological
- Sildenafil - PDE-5 inhibitor (Viagra) - increases cGMP = increased SM relaxation
(NOT for use if CVD, diabetes or any nitrate meds)
- Prostaglandin E injection - increases SM relaxation
- Penile implant
- Vacuum erection device

77
Q

Transmission of Chlamydia Trachomatis, Neisseria gonorrhoea and treponema palladium

A

Unprotected sexual intercourse
Sharing sex toys
Mother to fetus

78
Q

Methods to reduce STI spread

A

regular HIV testing
increased education
Correct and regular condom use
Annual/new partner (<25) chlamydia testing

79
Q

Chlamydia trachomatis clinical features and treatment

A

Most prevalent = M -19-24, W = 16-19

Clinical Features:
Asymptomatic (50% Men, 70% women)
Penile/vaginal discharge (cottage cheese)
Dyspareunia 
Dysuria 
Metrorrhagia 
Testicular pain
Epididymitis/Proctitis/salpingitis/cervicitis 

Mother - fetus = neonatal opthalmia
Repeated infections can cause infertility and rarely in homosexual men lymphogranuloma venereum infection

Treatment
5-7 day course oral doxycycline

80
Q

Neisseria gonorrhoea clinical features and treatment

A

Most prevalent - 15-24yo

Clinical Features
Males - Urethritis (Penile discharge), dysuria
Females - Endocervical infection (Abnormal vaginal discharge), PID

Mother- fetus = neonatal opthalmia

Treatment
IM ceftriaxone and azithromycin

81
Q

Treponema Palladium clinical features and treatment

A

Primary Syphilis - lesion at inoculation site around 3 wks after exposure which heals within 2-6 weeks
Secondary Syphilis - 6 weeks later red, eczematous rash on rest of body
80% latency, 20% tertiary syphilis - dementia (irrational, wild proclamations), gummata - inflammatory nodules which are locally destructive around the body)

Treatment
IM benzathene benzylpenecillin

82
Q

Pappilomavirus infections

A

HPV - ds non-enveloped ds DNA virus, sexual transmission
HPV 6,11 responsible for anogenital warts (condylomata acumiate) in genital, perineal, perianal and anal regions.
HPV 16, 18 - responsible for genital, anal, mouth and throat cancers

Gardasil vaccine - HPV vaccine given to all 12-13 year olds to reduce incidence of anogenital warts and genital, anal, mouth and throat cancers

83
Q

Step by Step Process of Fertilisation including polyspermy blocks

A

1) Capacitation (when sperm enters the female reproductive tract)
Uterine wall secretions remove glycoproteins and sterol groups from membrane to cause sperm hyperactivity and increased flagella action
2) Penetration of corona radiata
3) Attachment to zona pellucida
4) Activation - Acrosome reaction
In oocyte vicinity, release of hydrolytic enzymes
Acrosome binds to zona pellucida allowing sperm to penetrate ovum
5) Plasma membrane binding and sperm entry
6) Polyspermy blocks
Block 1 = only 200-300 sperm make it to the ampulla of the uterine tubes out of the 1x10(9) sperm in the ejaculate

Fast block - 2-3 seconds after fertilisation
Na channel opening = depolarisation of membrane to prevent sperm binding

Slow block - 10-60 seconds after fertilisation
Cortical reaction - release of lysozyme from the cortical granules prevents sperm dining to plasma membrane
Zona reaction - structural changes make ovum impenetrable

84
Q

Results of fertilisation

A

1) First meiotic division occurs prior to fertilisation (one polar body)
2) second meiotic division occurs after fertilisation resulting in 3 polar bodies (one is reabsorbed)
3) Male and female pro nuclei form
4) Pronuclei dissolve releasing genetic material
5) First cleavage division

85
Q

Male and female causes of sub-fertility

A
Female 
Ovulatory disorders (25%) 
Tubal damage (20%) - non-latency, sterilisation
Uterine/peritoneal disorders (10%) - endometriosis, PID< fibroids

Male
Pre-testicular - HPT axis, genetics
Testicular = impaired spermatogenesis - congenital (undescended testes), acquired (variocoele)
Post testicular - Ejaculatory/Erectile dysfunction, obstructive azoospermia

86
Q

Sub-fertility Initial Investigations

A

Investigate any couple who are having regular UPSI (2-3 times a week) for one year and have failed to conceive
Investigate earlier if known underlying issues, or if women under 35 with amenorrhea

Female
Mid luteal phase progesterone to check ovulation
Measure weekly serum FSH and progesterone if irregular cycles
Measure TFT if indicative of thyroid issues
Measure prolactin if symptoms

Male
Semen analysis - repeated 3 months later

Both
Full medical examination
Full medical, social and sexual history
Chlamydia screening

87
Q

Sub fertility Secondary Investigations

A

Female
Tubal patency tests
Hysterosalpingography/hysterosalpingo-contrast ultrasonography

Male
Any sperm abnormalities do, testicular biopsy, sperm culture, urogenital imaging, endocrine tests, microbiological tests.

88
Q

Emotional issues of assisted conception

A

Guilt/blame - pushes couple apart
Shared trauma/hope - brings couple together
Depression
Social family and friend relationships breakdown - jealousy of children etc

89
Q

Ethical and legal issues of assisted reproduction and use of embryos

A

Sperm donation
Donors must be between 18 and 41
Samples must be kept fresh/frozen for 180 days before use
All donors must be screened for serious infectious diseases
Donors are not paid for their contribution, only given loss of earnings

Egg Donations
Donors must be between 18 and 35
Can only be given loss of earnings
Donors whose eggs have been used for research and surrogacy can receive discounted IVF

Surrogacy - have legal parentage of the child which can be changed through court or adoption.

Sex selection - prohibited unless it is to avoid a serious gender related condition

Embryo research - all embryos must not be kept past the primitive streak appearing, and researchmust be involved in:

a) finding more effective contraception
b) infertility treatment advances
c) congenital disease causes
d) miscarriage causes
e) detecting chromosomal abnormalities before embryo implantation

Ethical Issues
Playing god
Non-malificience - destroying life

90
Q

Define pre-embryo, embryo and fetus

A

pre-embryo = Conceptus prior to implantation into uterine wall (day 0-12)
embryo - conceptus after complete implantation - most susceptible to teratogens
fetus - growth period between week 9 to birth

91
Q

Pre implantation stages

A

Day 1-2 = Cleavage (2-8 totipotent cells)
Day 3 - Morulla - 16 pluripotent cells
Day 4 - Blastocyst formation - embryoblast, trophoblast, blastocoele
Day 5 - implantation

92
Q

Implantation process

A

Day 5-6 = attachment and invasion
Trophoblast differentiates into cyto- and synctiotrophoblast
Embryoblast differentiates into epi- (embryo) and hypoblast (supportive roles)

Day 7-8 = incomplete implantation
Pre-embryo sheds zona pellucida and begins attachment to endometrium of uterine wall

Day 9-10 = approaching complete implantation
decidual reaction - endometrium prepares for nutritional support and reducing immune attack

Day 11-12 = interstitial implantation
uterine lining repair, complete implantation and lacunae formation

93
Q

Abnormal implantation sites and ectopic pregnancy

A

Occurs in less than 1% of pregancies - Increased risk with pID, previous surgery, fertility treatment, increasing age, past ectopic surgery, PID
Tubal pregnancy - associated with PID, endometriosis
Ampullary-54%, Isthmic - 25%, Fimbrial - 17%, Ovarian - 0.5%
Interstitial - 2%, Cervical, 0.3%
Abdominal - intestinal, rectouterine pouch

94
Q

Describe intrauterine insemination

A

1) follicles are monitored by USS - ovulation is induced
2) Fresh/frozen sperm sample inserted directly into uterine activity

NICE Guidelines for usage
Requires patent tubes
1)Use of common donor (heterosexual relationships)
2)Vaginal intercourse difficulties 
3) Must have reasonable sperm quality
95
Q

Descrive IVF

A

2-3 month cycles costing £5-10,000 each

  1. Down regulation of the natural cycle occurs using a GnRH agonist or antagonist for 2-3 months
  2. Daily injections of an FSH analogue for 10-13 days cause super ovulation. This is monitored via USS and medication is taken to trigger maturation.
  3. The oocyte is retrieved using a US guided needle collection under sedation.
  4. If using IVF, thousands of prepared sperm are added to the oocyte, if using ICSI (IVF but injected sperm not in vitro) one motile sperm is added.
  5. Fertilisation takes around 18 hours to complete. The female is given hormones to prepare the uterus for implantation.
  6. The embryos develop with its growth carefully monitored.
  7. At day 5 the 2 best embryos are transferred (only 2 to reduce risk of multiple births). No sedation is required.
  8. After 2 weeks a pregnancy test is completed.