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Rep Flashcards

1
Q

Describe the internal and external genitalia of the male
•

A
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2
Q

Describe and identify the main anatomical structures of the
male reproductive system
•

A
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3
Q

Relate male reproductive tract anatomy to common clinical
problems •

A
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4
Q

Identify in prosected specimens and anatomical models the
following structures:

A
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5
Q

Describe the histological features of the penis, testis, prostate
gland

A
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6
Q

Histological features of female reproductive

A

Uterus
External smooth muscle called myometrium
Internal endometrium

Ovaries
Covered by tunica albuginea
Covered by simple squamous mesothelium

Vagina
Non- keratinised stratified squamous
Then lamina propria without glands
Then inner circular and outer longitudinal smooth muscle
Then adventitia

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7
Q

Female

A

Ovaries
Uterus
In between bladder and rectum
Has fundus, body and cervix
Uterine cavity with endometrium
Uterine tube have fimbriae
Has infundibulum
Ampulla where fertilisation happens
Has cilia and peg cells to help sperm
Vesicouterine pouch - between bladder and uterus
Rectouterine pouch
Ovary and uterus connected by ovarian ligament from gubernaculum
Round ligament of uterus connects uterus to abdominal wall - goes through inguinal rings. Also from gubernaculum
Suspensory ligament where blood vessels tent up peritoneum
Broad ligament is how blood vessels get to uterus
Ureter under uterine artery
Internal iliac artery supplies

Cervix
Has cervical os
Cervical ectropian- due to hormones

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8
Q

Female 2

A

Angle of anteversion
Angle between long axis of vagina and cervix
Angle of anteflexion
Cervix + uterus
Round ligament keeps position

Vagina
Epithelium has large granules of glycogen which feeds lactobaccili to maintain acidic ph
Bacterial vaginosis- overgrowth of unwanted bacteria

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9
Q

Embryological Development
• Explain the development of the male and female gonads
•

A
  1. Primordial germ cells (precursors of gametes) arise from endoderm of yolk sac and develop after gastrulation.
  2. migrate along the retroperitoneum to the genital ridge.
    epithelium of the genital ridges proliferates and penetrates the intermediate mesoderm (in posterior abdominal wall) to form the primitive sex cords.
    The combination of germ cells and primitive sex cords forms the indifferent gonad.
  3. Karyotype of the primordial germ cells determines what gonad differentiates into.
  4. The Y chromosome contains a SRY gene.
    The SRY protein is the testis-determining factor -high amounts.
    This leads to the formation of medullary cords(becomes semineferous tubules), sertoli cells, leydig cells(8th week produce testosterone).
    primordial germ cells remain, and will begin gametogenesis at puberty.
  5. Without those genes, the gonad will differentiate into an ovary.
    Epithelium of gonad proliferates and produces cortical cords. Surround primordial germ cells to form primordial follicles which develop into oocytes at puberty.
  6. Gonad connected to scrotum or labia by gubernaculum.
    Peritoneum pinches off (processus vaginalis) then gubernaculum and testis follow to scrotum. Processus vaginalis closes.
  7. The same for ovary but it stays in pelvis due to barrier of uterus. Gubernaculum remains as round ligament.
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10
Q

Explain the development of male and female internal genitalia and its control by the gonads

A
  1. Both male and female embryos have a pair of ducts that are used in the development of the urinary system. These are called the mesonephric ducts and paramesonephric ducts
  2. Testes produce testosterone which develops duct system in men (epididymis and vas deferens) by maintaining the mesonephric duct (‘Wolffian duct’).

Also produce ‘Mullerian Inhibitory Substance to prevent it developing.

fuse with the testes so it is continuous and not open in the peritoneum.

  1. Without male androgens, the mesonephric duct degenerates.

Paramesonephric duct (‘Mullerian duct’) remains - needs no stimulation.

is separate to the gonad - no direct connection - gap in communication within the abdominal cavity.

The absence of testes will cause formation of the female internal genitalia; namely the uterus, fallopian tubes and part of the vagina.

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11
Q

Gametogenesis
• Describe the process of spermatogenesis and oogenesis

A

Spermatogenisis In seminiferous tubules:
Spermatogonia (germ cells) reside in basal compartment.
Divide by mitosis to give 2 types. Ad spermatogonium is reserve stock.
Ap spermatogonium is active. Primary spermatocyte.

Primary undergoes meiosis l to produce 2 secondary spermatocytes.
These undergo meiosis ll to produce 2 spermatids each. So 4 in total.

Spermiogenesis:
Spermatids released into lumen of tubules.
Non-motile (transport via Sertoli cell secretions assisted by peristaltic contraction).
Remodel as they pass through rete testis and ductuli efferentes and into the epididymis
now are spermatozoa and motile.

Oogenesis
Germ cells settle in ovary to form oogonia
Divide via mitosis
Cell death until 7th month
All surviving primary oocytes are now in meiosis 1 and stop at prophase 1
Primary oocytes - surrounded by follicular cells = primordial follicles before birth.
After birth no. again degenerates by atresia.

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12
Q

Distinguish the spermatogenic cycle and spermatogenic wave

A

Spermatids are at different levels of maturation at different sections of the seminiferous tubules.

The spermatogenic cycle refers to the length of time it takes for spermatids at the same stage in the cycle to ‘show up’ again when looking at a specific point along the seminiferous tubules.

The spermatogenic wave refers to the distance between groups of spermatids at the same level of maturation.

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13
Q

• Describe the ovarian cycle, including the stages of development of follicles and the corpus luteum

A

Puberty 15 - 20 oocytes:

Preantral phase:
Follicular cells of primordial follicles proliferate to form granulosa cells (go from cuboidal to stratified) which secrete glycoprotein called zona pellucida. Primary follicle.

Antral phase
Fluid filled spaces between granulosa cells called antrum. Outer fibrous layer develops into theca interna and externa.
Secondary follicle.

Pre-ovulatory phase
LH surge.
Completes meiosis 1. Produces 2 haploid cells.
Only one matures fully (other one is polar body with little cytoplasm) - Graafian follicle (FSH and LH needed for growth).
Enters meiosis 2 at ovulation (in oviduct) but only finishes at fertilisation.

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14
Q

Explain the development of male and female external genitalia and its control by the gonads

A

Undifferentiated external genitalia are the genital tubercle, the genital folds, and the genital swellings.

Testes produces dihydrotestosterone.
Genital Tubercle (GT) elongates to form the glans
Elongation and fusion of the genital folds = spongy urethra/ shaft penis
Fusion of the genital swellings into scrotum.

Female = no fusion as no testes
Genital folds become the labia minora
Genital swellings enlarge to become the labia majora
Genital tubercle = clitoris
Urethra opens into vestibule

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15
Q

Describe the common abnormalities of genital tract development

A

Imperforate hymen

Turner - ovaries degenerate, oocytes absent, female internal and external genitalia - 46XO

Kleinfelters - 47XXY - lack of secondary sexual characteristics and small testes, delayed pubertal development

CAH - excess androgens that masculinise so external genitalia ambiguous. I’m most case just Müllerian ducts but sometimes both.

Complete androgen insensitivity syndrome - in 46 XY -neither ducts - phenotypically female. Lack of androgen receptors or failure of tissues to respond. No male genitalia or uterus.

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16
Q

Describe the roles of the rete testis, the epididymis, vas deferens, seminal vesicles, prostate and bulbourethral glands finish

A

Semen - sperm delivery

Seminal vesicle secretions (~70%) Amino acids, citrate, fructose, prostaglandins

Secretions of Prostate (~25%) Proteolytic enzymes, zinc

Sperm (via vas deferens) (2-5%)

Bulbourethral gland secretions
Mucoproteins help lubricate and neutralise acidic urine in distal urethra.

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17
Q

Describe the processes and control of ovulation

A

Ovulation
LH surge inc collagenase activity.
Prostaglandins cause muscular contractions of ovary wall.
Oocyte breaks free from ovary and caught by fimbriae of fallopian tube.
Carried into tube by sweeping movements and by motion of cilia and peristaltic muscular contractions.

Granulosa and theca interna become vascularised and become corpus luteum which secretes oestrogen and progesterone.
Stimulates uterine mucosa to enter secretory stage in preparation for embryo implantation

If fertilised
Oocyte reaches uterine lumen in 3-4 days
2nd polar body produced and discarded and single ovum at end.
Implanted embryo releases β-hCG, which maintains the corpus luteum until the placenta can take over production of progesterone at approximately 20 weeks.

If no fertilisation
After 14 days corpus luteum degrades and becomes corpus albicans - scar tissue.
Progesterone production dec precipitating menstrual bleeding.

Summary of hormonal control:
Hypothalamus releases GnRH
Anterior pituitary releases FSH +LH
Folic,es stimulated to grow by FSH and mature by FAH + LH
Ovulation due to LH surge
LH promotes development of CL

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18
Q

Sperm capacitation

A

Sperm capacitation:
In female reproductive tract remove top layer of glycoproteins and cholesterol from membrane
activation of signalling pathways,
allow sperm to bind to zona pellucida and initiate acrosome reaction.
For in vitro mist first be incubated in capacitation media.

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19
Q

Puberty
• Explain the sequence of physiological and anatomical changes that occur in the male and female at puberty

A

Boys: Age 9-14 years
Tanner scale
1 = Prepubertal
II Scrotum and testes have enlarged. Sparse downy pubic hair at base penis
III Penis grown in length. Testes and scrotum growing. Hair darker and coarser.
IV Penis enlarged in length and breadth. Glans develops. Testes and scrotal enlargement and scrotal pigmentation darkening. Hair adult in appearance but smaller surface.
V Genitalia adult size and shape. Testicular length >5cm. Hair adult in appearance and quantity.

Girls - 8-13yrs
1 = prepubertal
2= Thelarche- breast bud, sparse growth of pubic hair - adrenarche
3= Further enlargement of the breasts and areola. Darker coarser hair
4= Areola and papilla project to form secondary mound above level of breast.
Hair adult in appearance but smaller area
V Mature stage. Projection only of papilla because of recession of areola to general contour of breast. Adult hair in appearance and quantity, spread to medial thighs.

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20
Q

Secondary sexual characteristics in puberty

A

-Increased and thickened hair on trunk, pubis, axillae and face
-Increased laryngeal size (Adams apple)
-Deepening of voice
-Increased bone mass
-Increased muscle mass and strength

-Pubic and axillary hair -Enlargement of labia minora and majora
-Keratinisation of vaginal mucosa
-Uterine enlargement -Increased fat in hips/ thighs

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21
Q

Explain the mechanisms underlying such changes at puberty

A

GnRH produced by hypothalamus
Release of LH and FSH from gonadotrophs in AP
Stimulate ovaries or testes to release androgens and oestrogen
Changes in puberty

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22
Q

Puberty disorders

A

Precocious puberty
Central - Elevated GnRH levels
Cause:
Idiopathic
CNS lesions
Pituitary gonadotropin-secreting tumors (rare)
Systemic conditions - tuberous
sclerosis, neurofibromatos
Obesity
Diagnosis:
Inc Basal LH and FSH
GnRH stimulation test
Early breast/testicular development

Peripheral
Causes
↑ Androgen production, e.g.: Ovarian cyst (most common cause)
Congenital adrenal hyperplasia
↑ oestrogen production, e.g.: HCG-secreting germ cell tumors (e.g., granulosa cell tumor)
↑ β-HCG production:e.g. Hepatoblastoma
Primary hypothyroidism
Not normal pattern - adrenarche appears first

Delayed puberty
No changes or failure of progression over 2 years.
Causes:
Constitutional delay
Hypothalamic suppression
Chromosomal abnormalities
Hypogonadotrophic hypogonadism

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23
Q

Describe the actions of the hormones involved in reproduction
which are produced by the hypothalamus, the anterior and posterior pituitary glands and the gonads

A

GnRH from hypothalamus stimulates anterior pituitary gland to secrete two gonadotropic hormones:
• follicle-stimulating hormone (FSH)
• luteinizing hormone (LH)

Male gonads
Seminiferous tubules - location for spermatogenesis - contain Sertoli cells
FSH stimulates Sertoli cells - spermatogenesis - then inhibin released - negative feedback on FSH on anterior pituitary.
Interstitial tissue: LH stimulates Leydig cells - Testosterone released. Negative feedback on hypothalamus and anterior pituitary

Female gonad:
FSH stimulates granulosa cells -Follicular development
LH stimulates theca interna cells: Releases androgens

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24
Q

Explain the control of gonadotrophin secretion by the hypothalamus

A

Triggers the start of puberty, and it is thought that leptin causes initial stimulation of hypothalamus to release GnRH.

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25
Q

Explain the action of gonadotrophins on the testes and ovaries

A

Ovaries
FSH - follicular development from 1st day of menstruation in order to nurture and sustain the development of the gamete. The follicles also produce oestrogen and inhibin.

LH - ovulation

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26
Q

List the actions of the gonadal steroids in the female and male

A

Female
Oestrogen
The effect of oestrogen on the reproductive tract is intended to promote fertilisation:
• Proliferation of endometrium
• Proliferation of myometrium
• Fallopian tube motility
• Thin, alkaline cervical mucus

Progesterone
The effect of progesterone on the reproductive tract is intended to sustain a viable pregnancy
• Secretory function of endometrium
• Reduction of motility of myometrium (assumes fertilisation has occurred)
• Thick, acidic cervical mucus to prevent further entry of sperm

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27
Q

Explain the changes occurring in the ovary during the ovarian
cycle and describe the changes in the endometrium
Look at slide for histology

A

Ovarain cycle
Follicular phase
Day 0-5
Granulosa cell secrete activin which inc FSH production.
Inc follicle growth, theca interna appears, inc oestrogen.
Then switch to inhibin (from activin)-dec FSH and inc oestrogen
Days 5-14
Oestrogen Inc LH receptors on granulosa cells
Day 14
LH surge - oestrogen rises
Ovulation- Mature oocyte (meiosis 2 not completed) travels through the capsule of the ovary into the fallopian tube
14-28
LH stimulates the remaining follicle (granulosa and theca cells) to develop into the corpus luteum.
Secretes oestrogen and progesterone in large quantities.
Set lifespan of 14 days.
After this, it regresses so levels of oestrogen, progesterone, and inhibin drop, allowing the cycle to start again.

Endometrium = epithelium + stroma
• Functional layer responsive to hormones, shed in menstruation

Early proliferative - Sparse glands, straight
Late proliferative - Thicker functional layer, glands coiled. In response to oestrogen produced by the ovary.
After ovulation
Secretory - Endometrial thickness at maximum, very coiled glands. Coiled arterioles.
Under the influence of progesterone.

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28
Q

Describe the phases of the menstrual cycle

A
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29
Q

Explain the processes involved in the control of ovulation

A
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30
Q

Explain the pattern of secretion of gonadotrophins and gonadal
steroids over the normal menstrual cycle

A
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31
Q

• Explain the hypothalamic and pituitary mechanisms underlying
cyclical gonadotrophin secretion and the interactions between
the ovaries and hypothalamus/pituitary

A
  1. FSH and LH from granulosa and theca interna cells
  2. LH means oestrogen produced. Oestrogen sends signal to stop FSH at low levels.
  3. Oestrogen inc to high levels and sends signal to release surge of FSH and LH
  4. Oocyte breaks off
  5. Menstruation - drop in inhibin, progesterone and oestrogen. Less neg feedback so rising FSH.
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32
Q

• Explain the actions of oestrogen and progesterone in the non-
pregnant woman

A
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33
Q

• Describe common menstrual disorders and explain the
pathophysiology of these conditions
Amenorrhoea
o Primary o Secondary
• Oligomenorrhoea • Menorrhagia • Dysmenorrhoea

A

Amenorrhoea
an absence of menstruation.

Primary - the failure to establish
menstruation by 15 years of age in girls with normal
secondary sexual characteristics or by 13 years of age in girls with no secondary sexual characteristics.
Secondary - The cessation of menstruation for 3–6 months in women with previously normal menses, or for 6–12 months in women with previous oligomenorrhoea.

Oligomenorrhoea
Infrequent menstruation defined by a cycle length between 6 weeks and 6 months.

Menorrhagia
heavy menstrual bleeding, either by objective volume >80ml and/or the subjective opinion of the patient that periods have become heavier or that she is passing clots. More than 7 days. Affects quality of life.

Dysmenorrhoea
This is defined as painful periods, to the point where it is interfering with quality of life.
It often leads to chronic pelvic pain.
Primary - absence of any identifiable underlying pelvic pathology.
• 6–12 months after the menarche
• production of uterine
prostaglandins during menstruation

Secondary:
• often starts after several years of painless periods
• caused by an underlying pelvic
pathology

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34
Q

Important features in the
history
.

A

Amenorrhoea - primary/secondary
Sexual history- pregnancy
Age - menopause or pre-pubertal
Weight loss,/anxiety/stress
1st - Look for other secondary sexual characteristics, if present then blockage of outflow tract
2nd - if none look at FSH/LH and GnRH
3rd - if low then hypo-gonadotropin hypogonadism
If high then hyper-gonadotropin hypogonadism - then karyotype analysis

Menorrhagia - quantity of blood loss, anaemia, Medication history (anticoagulants)

Dysmenorrhea -Location and timing of pain e.g. pelvic, cyclical, during intercourse?

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35
Q

3 things to assess

A

Hormonal - HPG axis
Defect in hypothalamus release of GnRH. Defect in pituitary release of FSH and LH. Or problem with ovary’s response.

Structural - structural problem of uterus or vagina. Investigated by USS, MRI or other imaging.

System review - thyroid disorders can cause menorrhagia or oligomenorrhoea so it is important to consider thyroid function tests.

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36
Q

Describe and explain the hormonal changes which lead to the features of the menopause

Describe the phases of the menstrual cycle

A

Menopause = Age = 45-55

Pre-menopause- oestrogen levels fall so -ve feedback removed and LH+FSH rise.
FSH rises more as inhibin removed.
Menstrual cycle shortens, ovulation is either early or absent so problems with fertility.

Peri-menopause - transition phase, greater infrequency of menstruation.

Menopause - complete cessation of menstrual periods for 12 months.

Post-menopause - women who have experienced the changes above are now deemed as post-menopausal. No primary follicles left so no reproduction.

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37
Q

Describe some of the symptoms experienced in peri-
menopause + post

A

Peri
hot flushes and sweating. insomnia and mood swings or depression.

Intermediate
further decreasing levels of oestrogen, so affects tissues reliant on oestrogen - vaginal atrophy leading to dyspareunia. Tissues lining the urethra and bladder, which can lead to increased frequency of UTIs and stress incontinence.

Ovaries will atrophy, thinning of the uterus, loss of vaginal rugae, reduction of pubic hair due to testosterone decline later in menopause, breast tissue reduce in size.

skin elasticity, fat storage

bloating, related to reduced motor activity of the GI activity and can also cause constipation.
and fracture healing

Post
Dec oestrogen = inc osteoclast activity = osteoporosis
NOF fractures after a fall
Dec height due to dec bone mass

Low oestrogen + progesterone = inc circulating lipid levels = inc risk of atherosclerosis = inc risk of MI + stroke.

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38
Q

• List the advantages and disadvantages of hormone
replacement therapy in the post- menopausal woman

A

Non-hormonal management
General lifestyle advice eg light weight clothing, avoid triggers
Dietary advice to reduce weight gain and cardiovascular risk.

Hormonal management
Vasomotor or mood disorders
Offer HRT with oestrogen and progesterone (p protects the endometrium from
hyperplasia)
Urogenital - vaginal oestrogen
Also dec risk of osteoporosis and colorectal cancer and muscle mass
Risk = DVT (oral), breast cancer(l with pro), CHD and stroke(over 60 and tablets), endometrial cancer (only o).

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39
Q

Conditions affecting menstruation/menopause

A

Polycystic ovarian syndrome- Triad = hyperandrogenism, menstrual irregularity, obesity (insulin resistance).
Diagnosis due to inc androgens + polycystic ovaries (ovaries become enlarged and contain many follicles that are unable to release an egg) on ultrasound.
Symptoms- secondary amenorrhoea, infertility, hirsutism and obesity.
Management = lifestyle, type 2 diabetes, cyclical progesterone

Fibroids
benign tumours of smooth muscle occurring in the myometrium. Can lead to very heavy menstrual bleeding. Risk factors - increasing age (until the menopause) -early menarche -older age at first pregnancy -black and Asian ethnicity -family history

Endometrial carcinoma - bleeding in menopause. in menopause ovulation is not occurring so no corpus luteum so no progesterone so unopposed oestrogen.

Ovarian cancer - present with symptoms as vague as bloating, so an important differential in post-menopausal women.

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40
Q

Explain the pattern of secretion of gonadotrophins and gonadal
steroids over the normal menstrual cycle

A
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41
Q

Causes of menstrual disorders

A

Amenorrhoea causes = hormonal disorders
or structural disorders:
Imperforate Hymen - thin layer of connective tissue (hymen) covers the vaginal entrance, and this has not perforated at the onset of menstruation. This can lead to a collection of blood behind the hymen, and progress to an infection.
Cervical Stenosis – where the os of the cervix is not open meaning blood cannot flow from the uterus into the vaginal canal.
Vaginal Septae – where a wall of tissue forms during the development of the vagina, separating the upper vagina into two parts, one of which forms a pouch where blood can collect.
Agenesis or Hypoplasia of the Genital Tract
Asherman’s Syndrome – an acquired condition where scar tissue forms in the uterus, often following IUS insertion or surgical termination, blocking the flow of blood.
Uterine Fibroids – can cause the blockage of blood in the uterus.
Physiological- pregnancy, menopause in older women
Other - weight loss, stress

Menhoragia Causes
Uterine/ovarian problems = endometrial cancer, fibroids, adenomyosis, polyps
Systemic = clotting disorders, Hypothyroidism, bleeding tendency
Iatrogenic = anticoagulation therapy, intrauterine contraceptive

Oligomenorrhoea cause - PCOS (irregular ovulation so to irregular periods), PID, Hyperthyroidism, High levels of prolactin

Dysmenorrhoea Cause = endometriosis- ectopic endometrial tissue that responds in the same way to hormonal stimulation as the endometrial lining of the uterus.
This can irritate the peritoneum leading to chronic pain, intra-abdominal adhesions, infertility, bowel obstruction. Test is laparoscopy. Risk - early menarche, white, late menopause.
Adenomyosis: endometrial tissue found deep within myometrium
➢ Fibroids, endometrial polyps can obstruct menses.
➢ pelvic inflammatory disease ➢ Intrauterine device (IUD) insertion.

Inter-menstrual bleeding- STIs/PID
Cervical ectropion – the evolution of the cells of the internal cervical canal to the outer surface of the cervix which can cause them to bleed.
Cervical cancer
Endometrial polyps or cancer
Ovarian cysts

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42
Q

describe the source and functions of the main constituents of
semen

A

Seminal vesicles - clotting factors

Prostate - proteolytic enzymes that break down coagulation

Coppers glands - alkaline fluid, a mucous that lubricates the end of the penis and urethral lining, (pre ejaculate)

Semen acts as nutrition source for the spermatozoa, transport medium and neutralises the acidic environment of the vagina.

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43
Q

explain the autonomic control of sexual function

A

Erection:
1. Stimulants - Psychogenic, tactile(sensory afferent of penis and perineum)
2. Spinal reflex
3. Efferent - activation of pelvic nerve (PNS)
4. Post-ganglionic fibres release ACh
5. Ach binds to M3 receptor on endothelial cells
6.. A rise in [Ca2+] , activation of NOS and formation of NO
7. NO causes vasodilation

Ejaculation - sympathetic
Emission - semen is moved into prostatic urethra which requires smooth muscle contraction from the prostate, vas deferens and seminal vesicles.
Expulsion - contraction of glands, ducts and internal sphincter(prevent retrograde). Also contraction of pelvic floor.

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44
Q

describe the processes of capacitation of sperm and the acrosome reaction

A

Capacitation (6-8hrs) - sperm is deposited at cervix - The sperm cell membrane changes to allow fusion with oocyte cell surface, and the tail movement changes - fully mature.

Acrosome - enzymes in the acrosome are released to remove the outer granulosa cells that surround ovum as the corona radiata.
sperm then interacts with the zona pellucida and digests it.

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45
Q

explain the mechanisms involved in fertilisation of the ovum

A

Ampulla of uterine tube
One sperm head fuses with membrane
A cortical reaction happens in the oocyte which prevents further sperm from entering.
Triggers meiosis II to finish - Pronuclei move together. Mitotic spindle forms leading to cleavage.

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46
Q

describe the physiological changes in the female which facilitate coitus

A

The character of cervical mucus changes over the course of the menstrual cycle
• Oestrogen - Thin, stretchy
• Oestrogen and progesterone - Thick, sticky - forms a plug

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47
Q

describe the process involved in sperm transport through the cervix and uterus

A
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48
Q

ASSISTED REPRODUCTIVE TECHNOLOGY (ART)

A

Oocytes are fertilised in vitro and allowed to divide to the 4- or 8-cell stage
• The morula is then transferred into the uterus
• Pre-implantation Genetic Diagnosis (PGD)

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49
Q

FERTILE WINDOW

A

sperm deposition up to 3 days prior to ovulation or day of ovulation.
Sperm - 72hr
Oocyte - 24hr

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50
Q

Describe the epidemiology of sexually transmitted infections (STIs) and other infections of the genital tract

A
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51
Q

• List the most common sexually transmitted infections, identifying the infecting organism in each case

A

CHLAMYDIA TRACHOMATIS - Obligate intracellular bacterium. Unique cell wall, inhibits
phagolysosome fusion (virulence factor).

NEISSERIA GONORRHOEAE - Gram -ve Diplococci, unencapsulated + pilated

TRICHOMONIASIS - Protozoa

Herpes - HSV-1 (oral and genital warts + cold sores) & HSV- 2 (genital warts + more likely to have HIV) - DNA virus (enveloped)

SYPHILIS - TREPONEMA PALLIDUM - Spirochete bacteria

Anogenital warts - HPV 6 and 11 - DNA virus (non-enveloped)
16 and 18 have the highest association with
cervical cancer

52
Q

• Provide a differential diagnosis for the common clinical syndromes notion

A

GENITAL LESIONS
Syphillis
Herpes
Anogenital warts - HPV

PELV I C / L OW E R A B D O M I N A L PA I N :
Ectopic pregnancy
Appendicitis
Endometriosis
Ovarian cyst
UTI
PID

Discharge:
Chlamydia +Gonorrhoea - normal but with pelvic pain, bleeding
Trichomoniasis - fishy, yellow, frothy, irritating to the vulva
BV - thin, grey, smell
Candidiasis - thick, white, non-offensive, irritating to the vulva

53
Q

• Describe recent trends in the incidence of sexually transmitted infections

A
54
Q

• Describe the clinical presentation, diagnosis and management of:
chlamydial infections
• gonorrhoea

A

Chlamydia
Female - typically asymptomatic, inc or purulent vaginal discharge, bleeding, dyspareunia, dysuria

Endocervical or vulvovaginal swab

Male - Urethral discharge, Dysuria, Epididymitis

NAATs - most sensitive and specific

Both treatment - doxycycline (or azithromycin), except in pregnancy/allergy where erythromycin is used.

Gonorrhoea
Men - 90% symptomatic, Causes thick, yellow discharge, dysuria, epididymo-orchitis

Women - 50% asymptomatic, Dysuria, inc or altered discharge, Lower abdominal pain, Dyspareunia, PID

Both treatment - ceftriaxone and azithromycin to ‘boost’ the effect, reduce the risk of resistance, treat chlamydia as a common co-infection.

55
Q

• List and describe, briefly, other STIs

A

SYPHILIS - can be co-infected with HIV
Primary - Typically painless ulcers
Secondary syphilis - 4 to 10 weeks after initial infection, rash, symptoms disappear, can enter a latent phase
Tertiary - reactivated eg in pregnancy
Swabs can be taken, and blood tests to confirm the infection.

Trichomonas - due to inc pH
Symptoms- copious, yellow, odourous discharge, Vulval itching/ soreness or ulceration
Treatment - Metronidazole

NON-GONOCOCCAL URETHRITIS IN MEN - Inflammation of the urethra with associated discharge, other STIs

56
Q

• Pelvic Inflammatory Disease (PID)
Definition
What does it cause
Symptoms
Signs
Complications
Management

A

PID - A general term for infection of the upper genital tract - almost always a STI

Ascending infection from the endocervix causing:
• Endometritis.
• Salpingitis.
• Parametritis.
• Oophoritis
• Tubo-ovarian abscess.
• Pelvic peritonitis

Symptoms - Pelvic pain/ lower abdominal pain, discharge, bleeding, Fever, Dyspareunia, secondary dysmenorrhea

Signs - Lower abdominal tenderness, cervical motion tenderness, or uterine tenderness (on bimanual vaginal examination), discharge, Fever >38°C

Complications- Early - Sepsis, Peritonitis
Late - • Chronic pelvic pain, Pelvic abscess, infertility, Ectopic pregnancy, Fitz-Hugh Curtis Syndrome (peri-hepatitis so RUQ pain)

Management - admit if signs of peritonitis, fever etc.
• Start empirical antibiotics eg Oral ofloxacin plus oral metronidazole
• Screen for other STIs
• Contact tracing
• ADVISE- complete course, potential complications, barrier contraceptive

57
Q

Describe the clinical presentation, diagnosis and management of:
• male and female genital tract infections that are not sexually transmitted

A

Bacterial Vaginosis (BV) - Gardnerella vaginalis - anaerobe

Gram staining- clue cells,
Vaginal pH >4.5

Risk factors - washing the vagina, smoking, Receiving oral sex

Symptoms: fishy-smelling, thin, grey discharge

Candidiasis
Candida albicans - yeast normal vaginal flora

Risk factors - Activated in immunocompromised states, diabetes or post antibiotics.
Favours high oestrogen (can be associated with
COCP)

Symptoms- Vulval or vaginal itching
• Vulval or vaginal soreness and irritation.
• Vaginal discharge (usually white, ‘cheese-like’, and
non-malodorous).
• Superficial dyspareunia.
• Dysuria

58
Q

Genital herpes and genital warts

A

Genital herpes
Initial then recurrent infection
with painful ulcers, dysuria or discharge, or asymptomatic.
Swabs - PCR/NAATs
Management - Antivirals e.g. aciclovir

Genital warts - painless genital warts on the penis, vulva, vagina, cervix and perianal skin. Warts typically regress without treatment, although topical treatments are available.
PCR to identify high risk types (biopsy/swab), vaccination

59
Q

STI diagnosing caveats

A

Female - urinanalysis only to rule out UTIs
Men - • ‘First catch’ urine for gonorrhoea/chlamydia
• ‘Mid-stream’ urine for culture & sensitivities
rectal and pharyngeal sampling for men who have sex with men

60
Q

X

A
61
Q

✓ describe the main methods of contraception
✓ explain their mechanisms of action
✓ explain their advantages and disadvantages

A

Abstinence

Withdrawal method
This is where ‘withdrawal’ occurs before ejaculation. Not reliable. Some sperm can be released in the pre-ejaculate, no protection against STIs.

Fertility awareness method -
This includes monitoring basal body temperature, avoiding intercourse around the time of ovulation, and monitoring of cervical mucus. This can be unreliable, requires a lot of education, no preventing STIs.

Lactational amenorrhoea
Lactation delays onset of ovulation, hypothalamus lowers release of GnRH due to high prolactin due to the suckling response. However, only effective for about 6 months, and is reliant upon exclusive breastfeeding. Unreliable and no STI cover.

Barrier contraception
Barrier to sperm entering the cervix. Male condoms, female condoms and diaphragm/caps can also be used.
Preventing STIs. Requires interruption of intercourse.

Hormonal contraception
This method of contraception can be broken down into short acting and long acting reversible hormonal contraception.

Sterilisation

62
Q

Short and long acting reversible contraception preventing ovulation

A

Short acting:
Progesterone only pill (POP) - effect on the cervical mucus, take every day
Does not inhibit ovulation
Does not control periods
Higher risk of ectopic pregnancy due to effect on cilia.

Combined Oral Contraceptive Pill (COCP):
containing oestrogen and progesterone - main aim to prevent ovulation by ‘tricking’ the hypothalamus into thinking it is in the luteal phase.

Secondary aims include reducing the endometrial receptivity to prevent implantation, and also thickening of cervical mucus.

Advantages - Also used to alleviate symptoms such as menorrhagia, irregular periods and dysmenorrhea. It is taken every day, with a break to allow bleeding to occur.
Reducing ovulation can reduce
risk of ovarian cancer, and preventing proliferation of endometrium can reduce risk of endometrial cancer.

Disadvantages - interaction with other medication via CYP450
Contraindicated in those who are at higher risk of stroke and MI as oestrogen is thromboembolic.
It therefore also needs to be stopped prior to surgery.
Increased risk of breast cancer because of effect of oestrogen on breast tissue.

Longer:
Progesterone injection
Intramuscular injection of high dose progesterone - prevent ovulation, thicken cervical mucus and thin the lining of the endometrium.
Injections taken every 12 weeks.
Can be used where COCP is contra- indicated.
Injection may be unpleasant, and there can be a delay in fertility returning.

Progesterone implant
Small subcutaneous tube inserted in the arm, releasing high dose progesterone
Same function and benefits as the injection.
Up to three years, and fertility can return much quicker than the injection.
It can cause amenorrhoea, irregularity of bleeding/spotting, or cause heavy periods.

63
Q

long acting reversible contraception preventing implantation

A

Coil
There are two types of intrauterine coil contraception.

The intrauterine system (IUS):
This coil contains progesterone, which is released locally but not into the systemic circulation.
It provides a physical barrier to implantation as well as thinning of the endometrial lining.
This is useful for those with menorrhagia.

The intrauterine device (IUD)
This coil is made of copper - provides a physical barrier
Toxic to sperm and ova.
No effect on reducing the endometrial lining.

These devices can be technically difficult to insert, they can displace or cause perforation, and no protection for STIs.

64
Q

Sterilisation
Emergency contraception

A

Vasectomy
Clips the vas deferens to prevent entry of sperm into the ejaculate.
High success rate
Samples must be provided afterwards to ensure it has been effective.

Tubal ligation
Aims to clip the fallopian tubes to prevent the ovum entering the uterus.
It requires general or local anesthetic and can have a slightly higher failure rate than vasectomy.

Emergency Contraception -
IUD up to five days after the event or ovulation
or hormonal pills
Levonorgestrel- high dose progesterone - 72hrs
Ulipristal acetate (EllaOne) – selective progesterone receptor modulator:
• inhibits ovulation.
• Upto 120 hours post

65
Q

✓ define subfertility, primary infertility and secondary infertility

A

Infertility - a couple who are having regular, unprotected sex (approximately every 2-3 days), who have been unable to conceive within 1 or 2 years.

Subfertility- generally describes any form of reduced fertility that results in a prolonged duration of unwanted lack of conception

Primary infertility = never been pregnant
Secondary infertility = have been pregnant in the past (including ectopic pregnancy and termination of pregnancy) and are struggling to conceive again.

Causes of Infertility
In about 25% of cases, no cause is identified.
It is important to ask a full sexual history, including menstrual history, and past medical history.

66
Q

✓ relate some common causes of subfertility back to the relevant anatomical and hormonal principles in men and women
Men

A

Factors affecting men

  1. Pre-testicular
    Hypogonadotropic hypogonadism
    Thyroid disorders
  2. Testicular
    a. Chromosomal or congenital abnormalities meaning that sperm production is decreased - Klinefelter syndrome (XXY), Cryptorchidism
    b. STIs, Mumps
    c. Vascular - testicular torsion, Varicocele
    d. Drugs such as chemotherapy
  3. Post-testicular
    Congenital – CBAVD (absent vas) Acquired – Infective, Vasectomy
    Coital Problems - Sexual Dysfunction, Hypospadias
67
Q

Women infertility

A

Factors affecting women

  1. Ovulatory disorders
    It can be divided into:

a. Failure of GnRH to act on the pituitary (hypothalamic- pituitary failure)
b. Failure of the axis to respond appropriately to stimulation (hypothalamic-pituitary-ovarian dysfunction). Eg: PCOS, and high levels of prolactin.
c. Failure of the ovary to respond appropriately (ovarian failure) eg: Turner’s syndrome, or early menopause.

  1. Uterine and peritoneal disorders - physical reasons why implantation is not possible.

a. Uterine fibroids

b. Conditions where scarring/adhesions have occurred
i. PID
ii. Asherman’s syndrome
iii. Endometriosis
iv. Abdominal surgery

c. Abnormal structure of the uterus from issues of the Mullerian duct developing incorrectly e.g. septate or bicornate uterus

  1. Tubal damage - disruption of transport of the ovum from the
    ovary to uterus.
    a. Endometriosis
    b. Iatrogenic from pelvic surgery
    c. Infection e.g. chlamydia
    d. Ectopic pregnancy
68
Q

Investigation and management of infertility

A

History - Past medical history, Social history- smoking, alcohol, occupation, Past pregnancies, Sexual health, Sexual dysfunction

In men:
1. Semen analysis - Sperm count, motility, liquification studies
2. Hormone levels - LH, FSH, testosterone
3. Ultrasound scan of testes, Examine Penis for structural abnormalities, Scrotal exam, Secondary sexual characteristics
5. Karyotyping

In women:
1. Hormone levels to assess whether ovulation is occurring; these have to be timed
a. LH, FSH (day 2)
b. Progesterone (day 21)
c. Androgens
2. Systemic blood tests - Prolactin, Thyroid function
3. Pelvic USS, Hysterosalpingogram, Laparoscopy
4. BMI, Secondary sexual characteristics, Hirsutism, Acne, Pelvic /abdominal exam and swabs

Management
• Smoking cessation, dec Alcohol intake
• Lifestyle changes – dec stress, weight loss
• Regular intercourse

Consider referral if normal in both partners, and not conceived after 1 year. Consider early if Woman is >35 Or
Known cause.

Medical Treatment – ovulation induction e.g. Clomifene
Surgical Treatment – to dec tubal occlusions e.g. laparoscopy
Assisted Reproductive Technology (ART) = e.g. intrauterine insemination, IVF etc.

69
Q

• Describe the processes of implantation of the conceptus into the endometrium

A

Implantation begins at day 6 - trophoblast cells interact with the endometrial lining once it has ‘hatched’ and lost the zona pellucida.
The blastocyst then embedded within the endometrium, to interact with vasculature and secretory glands of the endometrium.

70
Q

• Describe the structure of the placenta and explain its adaptation for the exchange of materials between fetal and maternal blood

A

The placenta begins to develop in the second week of the pregnancy.
placenta develops from trophoblast cells.
amniotic membrane fuses with the chorionic membrane to produce a single amniotic cavity.
Projections around the outer surface of the membrane are concentrated into a single disc-like space, which goes on to become the placenta.

initial unit of exchange- villi

71
Q

• Describe the arrangement of fetal blood vessels within the placenta
Structure of villi

A

Days 13-15
Primary
Cytotrophoblast sends off projections through the syncytiotrophoblasts. Forms a cytotrophoblastic shell
Intervillus spaces

Days 16-21
Extra Embryonic mesoderm (somatic layer) invades into the primary villi = secondary villus (3 layers)

Days 17-22
Chorionic vessels grow up into the villus - Branches of umbilical vein and artery - waste products to the villi through the umbilical arteries (paired), oxygen and nutrients to the fetus via the umbilical vein (singular).

Maternal blood vessels then surround villi - endometrial arteries and veins

Barrier becomes progressively less by reducing the number of cytotrophoblast cells so more optimised for transport.

4-5th month
Decidua form septae which separate tertiary villi into groups called cotyledons.

72
Q

• Explain the factors influencing the passive diffusion of substances across the placenta

• Identify the major substances which are actively transported across the placenta

A

Transport:
1. Simple diffusion across a concentration gradient
e.g. water, electrolytes, gases
Rate of gas exchange is flow limited, not diffusion limited. Therefore adequate uteroplacental circulation is required.

  1. Facilitated diffusion
    e.g. glucose
  2. Active transport - specific “transporters” expressed by the syncytiotrophoblast
    e.g. amino acids, iron, vitamins
73
Q

• Explain the function of the placenta as a provider of passive maternal immunity to the neonate

A

The immune system of the fetus is very immature.
Antibodies transported across the placenta into the fetal circulation so at birth the fetus has some defence against infection.
Only certain immunoglobulins can cross placenta - IgG.

74
Q

• Describe the role of the placenta as an endocrine organ supporting pregnancy
• Explain the hormonal basis of testing for pregnancy

A

Endocrine function
The placenta produces protein hormones - human chorionic gonadotrophin (hCG) - first 2 months
Produced by syncytiotrophoblasts and is therefore pregnancy specific and excreted in maternal urine.
Supports the secretory function of corpus luteum.

Human placental lactogen (hPL) causes insulin resistance, inc the glucose availability to the fetus.

Placental growth hormone (PGH)
Corticotropin-releasing hormone (CRH)

Steroid hormones - allows placenta to take on the role of the corpus luteum after first trimester.
Also, oestrogen and progesterone keep the HPG axis in a ‘pregnant state’.

Progesterone promotes an increase in appetite so increased fat deposition to support fetus and breastfeeding.

75
Q

Implantation - how deep and defects notion

A

Decidua - endometrium cells that become specialized to modulate degree of invasion of conceptus.
Balanced by factors that promote and inhibit decidualisation.
If implantation in a location with no decidua or suboptimal decidual reaction then get defects.

Defects:
Incorrect site:
– Ectopic pregnancy
– Placenta praevia

Incorrect depth:
Too shallow:
– placental insufficiency
– pre-eclampsia
Too Deep:
– Placenta accrete
– Placenta increta
– Placenta percreta

76
Q

PATHOPHYSIOLOGY OF PLACENTAL TRANSPORT

A

Transfer across the placenta can also lead to harmful substances (‘teratogens’) being transferred.

Blood group incompatibilities can also occur - Rhesus disease of the new-born - maternal antigens cross into the fetal circulation and attack fetal blood cells.

Teratogens have greatest effect in embryonic stage (3-8 weeks) - body system development. Also pre-embryonic can have lethal effects.

Harmful substances:
• thalidomide – Limb defects
• Alcohol – FAS and ARND
• therapeutic drugs – Anti-epileptic drugs, Warfarin, ACE inhibitors
• drugs of abuse – Dependency in the fetus and newborn
• maternal smoking

INFECTION IN PREGNANCY
T O R C H
Toxoplasmosis
Other- syphillus, HIV, varicella Rubella
Cytomegalovirus (CMV)
Herpes Simplex (HSV)

77
Q

• Explain oxygen transport in fetal blood

A

Oxygen transport in fetal blood:
The fetal blood has lower partial pressure of oxygen to allow gradient of transfer from mother to fetus.
Progesterone causes maternal hyperventilation which causes inc pH which inc Hb affinity and dec CO2
To dec affinity maternal 2,3-BPG produced
Release of O2 to foetus
HbF - week 12 - alpha and 2 gamma subunits - greater affinity as it does not bind 2,3-BPG.

Double Bohr effect
During exchange in placenta CO2 passes into intervillous blood so pH dec so dec affinity in mother.
Foetus give up CO2 down gradient so inc pH so inc affinity

Double haldane effect
Mother - gives up O2 so Hb accept more CO2
Foetus- gives up CO2 so accepts more O2

78
Q

Define the fetal period

A

longest period of development, from 9 weeks to term.
Prepares for independent life after birth.

79
Q

• Describe the pattern of increase of fetal size, weight and body
proportion during pregnancy

A

Size

Weight gain
in the early fetal period, the tissue contributing to the weight is protein e.g. due to muscle development. Later on during the fetal period, adipose tissue is developed for metabolic purposes and for regulation of heat.

Proportion of growth
Initially, the head forms approximately 50% of the length of the fetus
Then limbs and trunk elongate, so that the head is approximately ¼ of the overall length.
Assessment - Symphysis-fundal height - assess growth by measuring the length from the pubic symphysis to the top of the fundus of the uterus. 20 weeks = umbilicus
12 week and 20 week ultrasound scan to measure fetal growth.

80
Q

• Describe the important events in the development of each of the major body systems - notion for resp and nervous systems

A

Resp system
Embryonic - lungs outpocuhing of foregut to create bronchopulmonary tree.
Fetal - Budding and branching of the bronchioles starts in week 8-16; the pseudoglandular stage.
Canalicular stage - Further branching to form respiratory bronchioles in weeks 16-26. Differentiation of cuboidal cells to pneumocytes.
Saccular stage - The terminal sacs develop at week 26 to term. Type 1 and 2 pneumocytes develop to produce surfactant.
Alveolar stage - 36 weeks+

The Cardiovascular System
average fetal heart rate is between 110-160 beats per minute - fetal bradycardia is a sign of fetal distress.

The Urinary System
Starts producing urine - removal by placenta
Fetal kidney function begins in week 10. Fetal urine forms most of amniotic fluid from 20 weeks.

The Nervous System
No movement until the 8th week. Then “practising” for post- natal life e.g. suckling, breathing.
4th month = corticospinal tract for co-ordinated movements, myelination incomplete until after 1 year.
Myelination of brain starts at 9th month.

81
Q

• Describe the factors which influence the viability of the pre-
term neonate

A

Viability is only a possibility once the lungs have entered the terminal sac stage - 24 weeks
RESPIRATORY DISTRESS SYNDROME - Due to insufficient surfactant production
Management:
Antenatal - Glucocorticoid
Neonate - Nasal continuous positive airway pressure (nCPAP)
• Surfactant replacement therapy
• Mechanical ventilation

Infants born preterm are at high risk for neurodevelopmental disorders, cerebral palsy, Interventricular haemorrhage (blood vessels not well developed).
Magnesium sulphate for neuro protection when between 24-29 weeks.

82
Q

• Explain the techniques used to assess fetal development

A

MEASURING GROWTH AND WELLBEING
LMP- last menstrual period

Mother senses Fetal movements - quickening’ from approximately 17 weeks.

Symphysis-fundal height (20weeks = umbilicus)

Ultrasound scan - 12 week Scan (dating Scan), rule out ectopic (if it is done transvaginally), identify multiple pregnancy, screening for chromosomal abnormalities (Nuchal Translucency scan)
20 week to detect foetal abnormalities - most structures developed and big enough to be seen on USS.

Crown Rump Length - length of the fetus; i.e. from ‘head to tail’. Only early on at 7-13 weeks.
Biparietal diameter - The distance between the parietal bones of the fetal skull. date pregnancies in 2nd and 3rd trimesters

ABDOMINAL CIRCUMFERENCE & FEMUR LENGTH - Used in combination for dating and growth monitoring in 2nd and 3rd trimesters

83
Q

Birth weight and growth restriction

A

•low birth weight: <2.5 kg
•very low birth weight:
1.0 -1.5 kg
•extremely low birth weight, <1.0 kg
• Macrosomia > 4kg

Reasons
Premature, small or growth restriction, maternal malnutrition
2 types
Symmetrical - abdominal circumference, biparietal diameter and fetal length all proportionally reduced. Genetic and TORCH infections

Asymmetrical- abdominal circumference smaller. biparietal diameter and femur length normal. Placental insufficiency.

84
Q

• Explain the processes involved in the control of amniotic fluid
volume and composition
• Describe the function of the fetal kidneys

A

Amniotic fluid volume
8 weeks - 10ml
38 weeks - 1l
offers an element of mechanical protection but also contains substances that are critical for lung development.

Production - urine production by 9 weeks. Kidney function is to produce urine for amniotic fluid. Excretion by placenta.

Recycling - inhaling amniotic fluid by the fetus ‘practicing’ breathing movements. This helps with production of the lung - surfactant.
fetus swallowing the fluid, and so it enters the fetal GI tract.

Composition - 98% water, and electrolytes, bile, hormones, fetal skin etc.
AMNIOCENTESIS - Sampling of amniotic fluid, collects foetal cells, diagnostic test eg karyotyping. 1% Risk of miscarriage

Oligohydramnios-too little
• Placental insufficiency
• fetal renal impairment
• Premature rupture of membranes
• Pre-eclampsia

• Polyhydramnios- too much
indicate an issue in the recycling of amniotic fluid. Issues co-ordinating the swallowing movement (i.e. CNS defect) or congenital abnormalities (e.g. trachea-oesophageal fistula)
• Gestational diabetes
• Fetal anaemia
• Multiple pregnancy

85
Q

• Explain the effects on the fetus of poor nutrition during early
and late pregnancy
• Explain the fetal circulation and the changes which occur at
birth

A

Maternal malnutrition can cause symmetrical or asymmetrical growth restriction.

Gas exchange through placenta not lungs so oxy blood shunted away.

Summary:
Placenta
Umbilical vein
Liver - small amount
Ductus venosus shunts so from umbilical vein to IVC
Liver and IVC drain into RA
Foramen ovale so mostly LA
Left ventricle and some into right
Aorta and some into pulmonary trunk
Ductus arteriosus shunts from pulmonary trunk to aorta
Body

At birth - shunts close and lungs for gas exchange

86
Q

Fetus distress / response to hypoxia

A

meconium stained liquor - meconium released prematurely from GI tract. Can lead to meconium aspiration.
Can happen in pregnancies longer than 40 weeks.

Chronic Hypoxaemia:
• Growth restriction • Reduced fetal movement

Hypoxia - Fetal chemoreceptors detect dec pO2 or inc pCO2 - Bradycardia by vagal stimulation (unlike adults) - dec oxygen demand of heart
• HbF and increased [Hb]
• Redistribution of flow to protect supply to heart and brain

87
Q

Clinical implications for intrapartum monitoring - finish

A
88
Q

Explain the maternal physiological adaptations to pregnancy

A

Glucose Metabolism
• reduction in maternal blood glucose and amino acid concentrations
• maternal insulin resistance in the 2nd half of pregnancy - by Human Placental Lactogen (hPL) and prolactin. Oestrogen inc prolactin
• increase in maternal free fatty acid, ketone and triglyceride levels - progesterone inc appetite in 1st half of pregnancy and diverts glucose into fat synthesis.
• increased insulin release in response to a normal meal

Cardiovascular Changes
maternal vascular-neogenesis
Dec systemic vascular resistance by oestrogen and progesterone - activation of RAAS (can cause peripheral oedema)- inc cardiac output by 40%.
Inc plasma vol - can cause dilutional anaemia.

Haematological changes - prepare for blood loss
during delivery
Clotting - inc procoagulants, dec anticoagulants and dec fibrinolysis. Can lead to thromboembolic disease.

Renal
Inc vasodilation = inc GFR by 55%
Dec serum urea and creatinine
Dec PCT absorption so glucosuria
Smooth muscle relaxation + obstruction so inc size of kidney and dec speed of urine passage
Inc risk of infection

89
Q

Explain the maternal physiological adaptations to pregnancy - notion for skin changes

A

GI
Gravid uterus so displaces bowel - mechanical obstruction
Progesterone:
Dec LES tone so GORD
Dec small + large bowel motility - dec mineral + water absorption
Dec gallbladder contractility - gallstones
Smooth muscle relaxation so slow gastric emptying - nausea, constipation

Endocrine:
Euthyroid state
Oestrogen inc liver production of TBG
Inc in TSH And thyroxine
So same free levels for mother
More Ca and phosphate absorption as inc calcitriol by kidneys but also inc phosphate excretion

Resp
Progesterone - tidal volume and oxygen uptake increase
PCO2 dec - compensated resp alkalosis. ERV and TLC dec.

Changes in MSK and skin
Change in center of gravity → Increased lordosis and kyphosis → Forward flexion of neck

Stretching of abdominal muscles → Impede posture → Strain paraspinal muscles
This causes back+shoulder pain and tension headaches

Increased mobility of sacroiliac joints and pubic symphysis, anterior tilt of pelvis
This causes pelvic pain

Fluid retention can compress structures such as median nerve -carpal tunnel

Chloasma
More melanin - linea nigra- pigmentation of where rectus muscles join
Palmar erythema
Vascular spiders

90
Q

• Outline the type of maternal problems that may develop in
gestational diabetes and anaemia in pregnancy
pregnancy.

A

Iron deficiency anaemia is common. Complications are inc morbidity, preterm delivery, maternal fatigue and infant IDA

Gestational Diabetes - glucose intolerance first recognised in pregnancy but does not persist after delivery.
diagnosed using oral glucose tolerance test
Associated with macrosomia, congenital defects, hypoxia and sudden death in baby.
In neonate - hypoglycaemia (high insulin as adaptation but sugar suddenly gone), resp distress, jaundice.
In mother - pre-eclampsia, polyhydraminos, premature, shoulder dystocia
Risk factors. BMI above 30, previous macrosomia baby or gestational diabetes,
family history of diabetes and ethnicity associated with diabetes.

91
Q

• Describe the hallmark clinical features of pre-eclampsia,

A

pregnancy-induced hypertension, with proteinuria +/- maternal organ dysfunction after 20 weeks
Severe - severe hypertension and does not respond to treatment

Risk Factors:
•40 years or older
•Nulliparity
•pregnancy interval of more than 10 years
•family history/previous history
•BMI
•vascular disease eg hypertension
renal disease
multiple pregnancy

Pathogensis:
Impaired invasion of
trophoblast so shallow invasion of spiral arteries - high resistance - dec blood flow
• Leads to hypoperfusion
and ischemia

Symptoms:
• Headache • Vision disturbance
• Epigastric pain
• Swelling of hands, feet, face
• Vomiting
• SOB

Complications maternal:
• Seizure
• Cerebral hemorrhage
• Renal failure
• Pulmonary oedema
• HELLP syndrome: Haemolysis, Elevated Liver enzymes, Low Platelets
• DIC

Fetal:
• Growth restriction •Oligohydramnios
• Placental infarct or abruption • Fetal distress
• Premature
delivery • Stillbirth

92
Q

• Explain the aetiology of the major complications of pregnancy
pregnancy and their hormonal basis

A

Dyspnea of Pregnancy - Increase in wakefulness
drive
Could be:
• Anemia
• DVT/PE
• Pneumonia/ARDS
• Pulmonary oedema

93
Q

• Define the stages of labour

A

Labour (parturition)
process by which fetus and supporting placenta and membranes pass from the
uterus to the outside world.

1st stage = regular uterine contractions and cervical dilatation till 10cm
2nd = from full dilatation until the fetus is born.
3rd = from the birth of the fetus until delivery of the placenta and membranes.

94
Q

• Describe the processes necessary to create a birth canal and its
clinical assessment

A
  1. Softening of the pelvic
    ligaments may allow some
    expansion to occur.
  2. Increase in myometrial activity- contractions
  3. Cervical dilatation and effacement:
95
Q

• Describe the function and mechanisms of cervical ripening

A

Triggered by prostaglandins:
• Marked reduction in
collagen and increase in
glycosaminoglycans (GAGs)
• Decreases the aggregation of
collagen fibres.
•collagen bundles ‘loosen’.
• Influx of inflammatory cells,
and an increase in nitric oxide
output.

96
Q

• Describe the properties of uterine smooth muscle which
facilitate labour

A

During pregnancy, the myometrium gets much thicker due primarily to increased cell size and glycogen deposition.

Early pregnancy: contractions may occur every 30 minutes or so, but are of low amplitude

Braxton-Hicks’ contractions
Noticeable contractions later -
reduced frequency but increased amplitude - no effect on cervix.

Prostaglandins - enhance release of calcium from intracellular stores

Oxytocin:
• Peptide hormone secreted from posterior pituitary gland (under control of neurons in
the hypothalamus) - lower threshold for triggering action potentials.

97
Q

• Describe the normal physiological processes which initiate
labour
• Describe the processes which normally limit maternal blood
loss after birth

A

Cervical dilatation and effacement

Umbilical cord stop pulsating and then cut and then passive delivery of placenta. Oxytocin or ergometrine injection can be give to cause contraction of uterus.

98
Q

Factors affecting labour

• Describe in outline the most common fetal presentations

A

Passage:
The birth canal diameter cannot extend beyond pelvis diameter - 11cm

Passenger:
Molding: -The changes in fetal head shape from external compressive forces. -Reduces diameter
Fetal lie - longitudinal, transverse, oblique
Fetal presentation- cephalic, breech
Determine fetal position by Obstetric abdominal examination, Vaginal examination to feel sutures of baby’s head

99
Q

Shoulder dystocia

A

Shoulder dystocia - vaginal cephalic delivery that requires additional obstetric manoeuvres to deliver the fetus after the head has delivered and gentle traction has failed.
Occurs when either the anterior, or less commonly the posterior, fetal shoulder impacts on the maternal symphysis, or sacral promontory, respectively.

Pre-labour risk factors
Previous SD
Macrosomia
Diabetes mellitus
Greater than 30 BMI
Induction of labour
Intrapartum:
Prolonged 1st or 2nd stage of labour
Assisted vaginal delivery

Complications:
• Brachial plexus injury-
Erb’s palsy
• Neurological dysfunction/ disability
• Neonatal mortality
• PPH (post-partum haemorrhage)
• Tears

100
Q

• Describe how the physiological state of the fetus may be
monitored during labour

A

Intermittent monitoring:
• Doppler/ pinard stethoscope
• Every 15minutes in 1st stage and 5 minutes in 2nd stage

Continuous electronic fetal monitoring:
• CTG (Cardiotocography)
• Fetal scalp electrode

Fetal blood sampling- to check pH

101
Q

• Describe the principles of inducing labour

A

Membrane sweep- 39+
weeks
• Prostaglandins (prostin
vaginally) - starts contractions
• IV Oxytocin -regular contractions
• Artificial rupture of
membranes (ARM)

102
Q

• Describe, in principle, how delivery may be facilitated by
intervention

A

Assisted delivery - forceps, suction cup
Indicatons:
Fully dilated cervix - 2nd stage
• Failure to progress - in 2nd stage baby should be delivered within 2hrs
• Maternal exhaustion
• Maternal conditions (ie heart
disease)
• Fetal compromise in 2nd stage - HR drop etc

Caesarean section - can do in 1st stage
Indications:
• Malpresentation
• Macrosomia
• Failure to progress
• Fetal compromise
• Fetal malformations
• Previous caesarean

103
Q

Foetal distress

A

Lack of acceleration on CTG
Meconium
Lack of movements
Ante partum haemorrhage

NORMAL = deceleration of heart rate due to pressure on brainstem during labour

104
Q

The pathological features, epidemiology, aetiology, presentation
and spread of tumours of the vulva
Notability for histology

A

Commonly squamous cell carcinomas.

Clinical Features - Lumps Ulceration Skin changes

Epidemiology - older women - 80+

In older women - associated with longstanding inflammatory conditions (e.g. lichen sclerosus)

In women in their 60s associated with HPV 16

Can have precursor to squamous cell carcinoma which is vulval intraepithelial neoplasia - atypical cells but no invasion of basement membrane

Spread:
Direct extension - Anus Vagina Bladder
Lymph Nodes - Inguinal, Iliac, Para-aortic
Distant Metastases - Lungs Liver

Definitive surgery would include removing the primary tumour and nodes.

105
Q

• how cervical cancer develops, who it affects, cause, presentation and what is CIN.
Notability for histology + figo staging

A

The inner part of the cervix (endocervix) is made of simple columnar epilthelium.
Outer part (ectocervix) is covered by squamous epithelium.
Oestrogen everts cervix
Simple columnar in contact with acidic environment of vagina - becomes irritated - ectropion
Metaplasia occurs to change it to squamous in the transformation zone but inc risk of dysplasia.

Cause - HPV 16 & 18 - Infect transformation zone. Produce viral proteins E6 & E7.
Inactivate tumour suppressor genes p53 & Rb. Uncontrolled cellular proliferation of squamous cells in transformation zone.

Leads to CIN - dysplasia Confined to Cervical epithelium - divided into CIN 1 / 2 / 3.
1 = bottom 1/3 of epithelial cells are abnormal. 2=2/3. 3=full length.
SCC = when CIN invades basement membrane.

Risk factors:
• Sexual partner with HPV • Multiple partners
• Early age of first intercourse
• Early first pregnancy
• Multiple births
• Smoking
• Immunosuppression

Invasive Cervical Cancer (includes SCC and adenocarcinoma of endocervical glands) Presentation
Bleeding (Post coital, Inter menstrual, Post menopausal)
Abdominal Mass
Local spread can involve the ureters, bladder, rectum and is extremely distressing with pain and fistula formation.

Treatment:
CIN1
• Often regresses spontaneously
• Follow up cervical smear in 1 year

CIN 2 & 3
• Needs treatment:
• Colposcopy +/- • Large Loop Excision of Transformation zone (LLETZ)

Invasive Cervical Cancer
Hysterectomy and Lymph Node Dissection (iliac and aortic)
+/- Chemoradiotherapy

106
Q

• The principles of vaccination against human papilloma virus (HPV)
and screening for CIN

A

Cervical Cancer Screening - detect pre-invasive lesion and to excise area completely before invasive malignancy develop -

Brush used to scrape cells from transformation zone. Detects cells with abnormally enlarged nuclei possessing abnormal chromatin (dyskaryotic cells).

Tested for HPV If positive – cells looked at under microscope

Then referral for colposcopy where abnormal areas are excised by diathermy (loop biopsy).

• Aged 25 – 49 = every 3 years
• Aged 50 – 64 = every 5 years
• Over 65 – only if recent abnormality

Vaccination against HPV
• Gardasil • Recombinant • Against HPV (6/11/16/18)
• Protects from cervical, vulval, oral, anal cancers
• Given aged 12-13

107
Q

• The pathological features, epidemiology, aetiology, presentation
and prognosis of endometrial adenocarcinoma
Notability for pansomma bodies and histology

A

Endometrial cancer Presentation - Inter-menstrual/post- menopausal bleeding, mass
60-70yrs
Can get endometriod (from endometrial hyperplasia and look like normal glands) or serous adenocarcinoma (more aggressive, abnormal glands).
Endometriod spread by direct invasion - cervix (stage 2), vagina, ovaries (3), bladder, bowel (4).
Serous - Exfoliates, Travels through Fallopian tubes, Deposits on peritoneal surface
( Transcoelomic spread)
Associated with collections of calcium (Psammoma bodies)

Treatment:
Hysterectomy
Bilateral salpingo- oophorectomy
+/- lymph node dissection
+/- chemo radiotherapy

Risk factor = endometrial hyperplasia which is caused by excessive oestrogen
Endogenous
- Obesity (androgens -> oestrogens)
- Early menarche/late menopause
- Oestrogen secreting tumours
Irregular cycle - Polycystic Ovary Syndrome
Exogenous
- Unopposed oestrogen hormone replacement therapy for menopause
- Tamoxifen - for breast cancer - blocks oestrogen receptors in breast but stimulates in endometrium

HNPCC

Endometrial hyperplasia diagnosis - Thickened endometrium >7mm detected by ultrasound. Then biopsy taken and shows increased gland:stroma ratio

108
Q

• The pathological features, epidemiology, presentation and
prognosis of tumours of the myometrium

A

Fibroids are benign tumours of uterine smooth muscle - leiomyomas
Pale, homogenous, well circumscribed mass
oestrogen dependant so regresses after menopause.

Presentation
Pelvic pain
Heavy periods - menorrhagia
infertility.
Urinary frequency (bladder compression)
Uterine enlargement

Histology - Whorled, intersecting fascicles of benign smooth muscle cells

Malignant -leiomyosarcoma
Atypical cells
Doesn’t arise from a leiomyoma
similar symptoms
infiltrate locally with metastasis by the blood stream to the lungs

109
Q

• The pathological features, epidemiology, presentation,
classification and prognosis of ovarian tumours
Epithelium +germ

A

Tumours of the ovary may arise from the surface epithelium, germ cells or sex cord-stromal elements.

Presentation:

Later symptoms due to tumour mass
Abdominal pain, distension, ascites, intestinal obstruction
Urinary symptoms
Gastrointestinal symptoms
Hormonal disturbances

Diagnosis:
Ca -125 - Serum marker – diagnosis/monitoring recurrence - then do scan
BRCA1/2 - Tumour suppressor genes - familial ovarian epithelial carcinoma - high grade serous cancers - Prophylactic salpingo-oophrectomy

Epithelial Tumours - majority serous, mucinous or endometrioid - present as cystic masses
Further classified as benign, borderline or malignant depending on histological appearance.
Malignant epithelial tumours present late and prognosis poor

Ovarian Serous Adenocarcinoma - Often show Psammoma Bodies, Often spreads to peritoneal surface by exfoliates.

Ovarian Mucinous Adenocarcinoma - epithelial cells Secreting mucin

Ovarian Endometrioid Adenocarcinoma - Glands resembling endometrium,
May arise in endometriosis, May have synchronous endometrial endometrioid adenocarcinoma

Germ Cell - most common is teratoma - mature (benign), immature or monodermal.
Mature can have any of the 3 germ layers so skin, hair, teeth, bone, muscle, cartilage, neural tissue and epithelia.
Presence of immature tissue such as primitive neuroepithelium indicates malignancy, a risk for intra-abdominal spread and can cause death.

Other malignant germ cell tumours include yolk sac tumour, choriocarcinoma and embryonal carcinomas. All malignant.

Tumour markers - alpha-fetoprotein (AFP) and beta-human chorionic gonadotropin (hCG).

110
Q

Sex-cord stromal and metastases

A

Sex-cord Stromal Tumours - derived from the ovarian stroma, which is derived from the sex cords of the embryonic gonad.

  1. Granulosa/theca cell tumours - resemble cells lining the ovarian follicle. Produce oestrogens and may be responsible for endometrial hyperplasia and breast cancer or precocious puberty.
  2. Sertoli-Leydig cell tumours - sex-cord stromal tumours
    that produce androgens and cause masculinisation, amenorrhoea and infertility,
    Hirsuitism, Breast atrophy.

Metastases to the ovary:
tumours derived from Müllerian epithelium, i.e., from the uterus, Fallopian tubes, contralateral ovary or pelvic peritoneum. Also gi and breast carcinomas.

111
Q

• The classification of testicular tumours

A

Tumours of the testis are commonest in men aged 15-34.
Presentation- Painless testicular mass.
Classified as germ cell tumours and sex cord- stromal tumours.

Non-Germ Cell Tumours
Eg Sertoli or Leydig cell tumours - benign.
Lymphoma common.

Germ Cell Tumours -(precursor = intratubular germ cell neoplasia)
In postpubertal, 95% of tumours arise from germ cell tumours - malignant.
2 groups: seminomas and nonseminomatous (NSGCTs).

Seminomas
The peak age is 40-50 years.
Confined to the testis for long periods of time.
Metastasise by the lymphatics, most commonly to the iliac and paraortic lymph nodes. Further spread is rare.

NSGCT - Many are mixed tumours - at least 2.
1. Yolk sac tumours occur in young children, good prognosis. Produce alpha fetoprotein (AFP).
2.Choriocarcinomas (elevated serum conc of beta- hCG) - occur in young adults.
3. Teratomas occur in men of all ages.
Prepubertal men = benign,
postpubertal men = malignant.

NSGCTs tend to metastasise early via lymphatics and blood vessels. Can present with metastases and primary testicular tumour being non-palpable.

Risk factor for both:
Familial predisposition
Cancer in one testis so inc risk of cancer in other testis
3-5x inc risk in cryptorchidism (failure of testicular descent into the scrotum). Orchiopexy (surgical placement of the undescended testis into the scrotum) before puberty decreases this risk of cancer.

Management:
Testicular tumours are treated by radical orchiectomy.
Seminomas are radiosensitive so radiotherapy gives best prognosis.
After surgery, NSGCTS are treated with aggressive chemotherapy.

112
Q

Describe and define the post-partum period.

A

period from the delivery of the placenta to six weeks after this.

During this time the body returns to a pre-pregnancy state - Low oestrogen levels so:

Lower genital tract - Reduction in size of vulva, vagina and cervix — Poor lubrication of the vagina — Transformation zone of the cervix withdraws into
the endocervix —
Internal os is closed

haematological - Bleeding- initial heavy flow (lochia rubra) Changes from red-brown/red-pink-heavy white (lochia
alba). Passage of clots not normal.
Menstruation returns (new endometrium by week 3 and menses by week 6) unless nursing

cardiovascular function - reversal of pregnancy changes

skeletal - ligament laxity resolves

113
Q

• Describe common problems that may be encountered during the post-partum period

A

Haemorrhage (>500ml)
o Primary (up to 24hrs after birth). Postpartum H (PPH) if inadequate uterine contraction after delivery.
o Secondary (24h – 6 weeks later). Prolonged or excessive bleeding once mother is at home.
Causes of PPH:
Tone (atony)
Tissue (Retained placental tissue)
Thrombin (clotting disorder) Trauma

Uterine inversion
o The uterus turns inside out – occurs when delivering the
placenta. emergency.

Perineal trauma
o Bruises/tears
o Sequelae (e.g. involving perineal body and anal
sphincter)

• Maternal collapse/cardiac arrest
o Amniotic fluid embolism
o Hypoglycaemia
o Hypotension/hypovolemia

Thromboembolic disease - can lead to PE
Managed by assessing risk factors, taking preventative measures and then prompt
diagnosis.
Treatment is with anti coagulation - heparin,
warfarin, new anti-coagulants

• Pyrexia/sepsis focus in - Genital tract, urinary tract or lactation ducts. Am,e sure to examine.

114
Q

Post-partum mental health problems

A

Postnatal blues - more tearful or anxious - normal up to 2 weeks - reassurance

Post-partum depression- within 4 weeks - if greater than 1 month then pharmacological treatment

Puerperal psychosis - within 4 weeks - anxiety, mania, paranoid thoughts, delusions - esp in mothers with pre-existing mental health conditions- suicide and infanticide risk - pharmacological.

PTSD- psychological therapies.

115
Q

Describe the hormonal control of the growth and development of mammary tissues

•

A

During pregnancy high levels of these hormones cause full development of breasts:
oestradiol + progesterone
prolactin (PRL) + human placental lactogen (hPL)

116
Q

Describe the hormonal control of milk production • Describe the control of milk let down

A

Hormones which affect the breast are:

• Mammogenic (promote proliferation of alveolar & duct cells)

• Lactogenic (promote milk production) - PRL - Released when suckling which stimulates neurons from the spinal cord to inhibit dopamine release which maintains milk production.

• Galactokinetic (promote contraction of myoepithelial cells) - oxytocin - Neurons from the spinal cord stimulate oxytocin release, which causes myoepithelial cells to contract and eject milk – the “let-down” reflex.

• Galactopoietic (maintain milk production).

117
Q

Describe the mechanisms which produce cessation of lactation

A

Once lactation ceases, milk accumulates in the alveoli of the breast causing distention and atrophy of the glandular epithelium.

mechanical factors suppress milk secretion, not hormonal changes.

Dopamine agonists e.g. bromocriptine can be given to artificially supress lactation

118
Q

Puerperal mastitis

A

milk accumulation in the in the lactiferous ducts of the breast can lead to inflammation, with or without infection.
Typically occurs if the mother does not breastfeed with both breasts so one unused.
Staph aureus
Can lead to abscess
Continue feeding and inc frequency on affected side. Antibiotics.

119
Q

Describe the structure of the normal breast, including its
topography

A

The breast consists of a series of secretory lobules, which empty into ductules. These ductules from 15 to 20 lobules combine into a duct, which widens at the ampulla—a small reservoir. The lactiferous duct carries the secretions to the outside.

120
Q

pelvic floor functions

A

support of the pelvic organs, namely the vagina, uterus, ovaries, bladder and rectum.

  1. Suspension- strong vertical support. cardinal ligaments (holding the cervix and upper
    vagina in place) & the uterosacral ligaments (holding the back of the
    cervix and upper vagina laterally) and round ligament ( maintain the anteverted position
    of the uterus).
  2. Attachment - Arcus tendinosus fascia pelvis (ATFP) (“white line” —) Endopelvic fascia- stretches from the white line laterally to the vaginal wall medially.
    Urethra lies anterior and above it so gets compressed against it during inc intra-abdo pressure. Maintains urinary continence
  3. Fusion - involves urogenital diaphragm and the perineal body.
    Lower half of the vagina is supported by fusion of
    the vaginal endopelvic fascia to the perineal body
    posteriorly, the levator ani laterally and the urethra
    anteriorly.

Continence

Maintain high Intra-abdominal pressure

Childbirth - contributes to the birth canal

121
Q

Composition of the Pelvic floor

A

Deep muscles
pelvic floor is made up predominantly by the levator ani muscles:
Pubococcygeus
Puborectalis
Iliococcygeus
midpoint of these attachments is the perineal body - central point between the vagina and the rectum.

U-shaped
encircle the urethra, vagina, and rectum

Superficial muscles:
Bulbospongiosus
Ischiocavernosus
Superficial transverse perineal
1 and 3 can undergo
iatrogenic damage during medio-lateral episiotomy which is done to prevent 2nd or 3rd degree tear. Complications = infection, haemorrhage,
dyspareunia, and damage to the anal sphincter.

Urogenital diaphragm
sheet of dense fibrous tissue that spans the anterior half of the pelvic floor.
Arises from the inferior ischiopubic ramus. Attaches medially to the urethra, vagina and perineal body.

122
Q

Pelvic Floor Dysfunction

A

Pelvic Organ Prolapse
Loss of support so prolapse of structures into vagina.
Anterior compartment
bladder and/or urethra:
o Cystocele = bladder
Urethrocele = urethra
o Cystourethrocele = both

Middle
Uterus into vagina
Vault’ (apex of vagina) prolapse can occur after hysterectomy as the supportive ligaments have to be cut when removing the uterus.

Posterior
bowel or surrounding structures:
Rectocele = rectum
Enterocele = loops of bowel involved entering the
rectouterine pouch (Pouch of Douglas)

Urinary Incontinence - stress
increased abdominal pressure causes ‘leaks’ of urine, as the support to the urethral sphincter (via the pelvic floor) is inadequate.

Vulval problems
related to tension of the levator ani muscles.

Posterior Compartment Pelvic Floor Dysfunction - constipation/incomplete evacuation and anal incontinence due to anal sphincter injury - attached to levator ani muscles.

123
Q

Causes and risk factors
History and examination
Management

A

age, vaginal delivery, oestrogen deficiency e.g. post-menopausal, chronic increased abdominal pressure, connective tissue or neurological disorders.

Prolapse
lump down below, or something ‘coming down’. symptoms relating to where the prolapse is occurring, e.g. constipation.
Then do examination

For stress incontinence - passing urine on coughing, laughing, or other activities that increase abdominal pressure.
Not much to see on examination, other than
obvious injury to the pelvic floor.
Urodynamic studies

Management
1. Non-surgical options
Use of pessaries e.g. ring pessaries as additional support
2. Surgical options
many, depending on type of prolapse.
might involve hysterectomy or using ‘mesh’ support in a vault prolapse.

For stress incontinence - pelvic floor muscle training.
Surgical intervention to create ‘slings’ to support the urethral sphincter.

124
Q

Breast milk

A

Breast milk protects the baby from infection in a variety of ways:
1. Lactoferrin - binds iron, preventing the proliferation of E.coli
2. Populates neonatal gut with non-pathogenic flora
3. Presence of bacteriocidal enzymes
4. Contains specific immunoglobulins
5. Contains lymphocytes (mainly T-cells) and granulocytes that
play a role in cell-mediated immunity.

125
Q

Contraception post-partum

A

family planning following childbirth helps reduce both maternal and typically occurs if the mother does not breastfeed with both infant deaths, reduces the risk of pre-term birth, low birthweight and breasts, and therefore milk can build up in the lactiferous ducts small-for-gestational age babies.

126
Q

understanding of female genital mutilation by understanding the normal anatomy of the — vulva —

Demonstrate an understanding of the consequences of female — genital mutilation

legal requirements for recording — and reporting FGM for health professionals

A

Female Genital Mutilation
practice of damaging the female external genitalia. severe pain, potential sepsis,
or haemorrhage. complications include psychological effects, sexual dysfunction, and difficulty conceiving, as well as chronic pain and menstrual disorders.

127
Q

B lood supply, innervation, venous and lymphatic drainage
Of pelvic floor

A

Blood supply – — the internal and the external pudendal arteries and drains through corresponding veins.

Lymphatic drainage- — via the inguinal lymph nodes.

Nerve supply- — branches of the pudendal nerve, which derives its fibres from the ventral branches of the second, third
and fourth sacral nerve

Sem 3 (5 decks)

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