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MD3002 > Week 9 > Flashcards

Week 9 Flashcards

1
Q

What does WHO say about infertility as a disease?

A

“A disease of the reproductive system defined by failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse”

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2
Q

What are the main things the Wilkinson & Williams 2016 paper says about infertility as a disease?

A

If perceived as a disease, public funding for its treatment is construed as justified & what remains to be determined is its prioritization in relation to other required treatments competing for limited resources…if not, funding it may not be justified from the outset

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3
Q

Who is the legal father and mother in surrogacy?

A
  • Legal mother= person who gave birth (legal change through parental orders/adoption)
  • Legal father= genetic father
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4
Q

What does the Warnock & Brazier reports say about surrogacy?

A
  • Brazier (1997) stated that agreements should continue to remain unenforceable
  • Warnock (1984): “inconsistent with human dignity that a woman should use her uterus for financial profit”
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5
Q

What according to NHS Scotland (2013) are prenatal screening tests?

A
  • Offered to all pregnant women to assess chance of baby having a particular health problem/disability
  • Do NOT provide definitive diagnosis
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6
Q

What according to NHS Scotland (2013) are prenatal diagnostic tests?

A
  • Follow-on tests carried out to find whether baby does have a particular condition
  • Offered to “Higher-chance” result from screening
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7
Q

What are 5 reasons why you would carry out screening & testing?

A
  1. Reassure parents
  2. Inform & prepare parents for birth of an affected infant
  3. Allow in utero treatment, or delivery at a specialist centre for immediate postnatal treatment
  4. Allow termination of affected foetus
  5. Provide information so that parents may choose between 2,3,4. issue= choice
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8
Q

What are the 3 different types of screening & diagnostic testing for natural conception?

A
  1. Non-invasive ie. ultrasound, serum test, questionnaire
  2. Invasive prenatal dianostic (PND) testing ie. chorionic villus sampling, amniocentesis (increased chance of miscarriage)
  3. NIPT/ NIPD
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9
Q

What is the screening & diagnostic test for in vitro fertilisation (IVF)?

A
  • Preimplantation genetic diagnosis (PGD)

- (CRISPR if it was used)

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10
Q

What, when, why is ultrasound screening?

A
  • WHAT: sound waves, painless, no risk
  • WHEN: dating scan 12 weeks, anomaly scan 20 weeks
  • WHY: anomaly, physical abnormalities ie. spina bifida
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11
Q

What is the ethical issues arising from ultrasound screening?

A

Everyone is offered anomaly scan, not everyone chooses to take it

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12
Q

What, when, why is a Down’s Syndrome screen?

A
  • WHAT: combination of ultrasound & serum test
  • WHEN: 10-13 weeks
  • WHY: measures chance of DS, not a diagnostic test (can also detect Edward’s Syndrome T18)
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13
Q

What is the ethical issues arising from Down’s Syndrome screen?

A
  • Risk (low v high)

- If greater than 1:150 then option to take diagnostic test (amniocentesis or CVS)

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14
Q

What does a serum test analyse?

A
  • Markers in blood including:
  • Pregnancy associated plasma protein-A (PAPP-A)
  • Free beta-human chorionic gonadotrophin (free beta-hCG)
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15
Q

How good is the “combined” screening test for Down’s Syndrome?

A
  • False positives (2.2%): test abnormal, foetus not affected

- False negatives (16%): test normal, foetus affected

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16
Q

What is the Quadruple test for Down’s Syndrome?

A
  • Used if women presents later (14 weeks 2days +)
  • Blood test: alpha-fetoprotein (AFP), total human chorionic gonadotrophin (hCG), unconjugated oestriol, inhibin-A
  • FN: 20%, FP 3.5%
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17
Q

What, when, why is the amniocentesis diagnostic test?

A
  • WHAT: needle inserted through abdomen & into amniotic fluid
  • WHEN: 15+ weeks
  • WHY: previous pregnancy with fetal problems, family history, >35yrs, antenatal screening result suggests a problem
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18
Q

What 4 things is Amniocentesis used to test for?

A
  • Down’s syndrome
  • Other Chromosomal disorders
  • Blood disorders (sickle cell)
  • Genetic disorders (sex)
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19
Q

What are the ethical issues arising from amniocentesis?

A
  • 0.5-1% risk of miscarriage (also, delay in getting results)
  • Infection
  • Injury
  • FP 0.1-0.6%
  • FN 0.6%
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20
Q

What, when, why is Chorionic villus sampling?

A
  • WHAT: fine needle inserted through abdomen & into uterus, through cervix & small piece of developing placenta removed
  • WHEN: 11 weeks
  • WHY: tests inherited disorders (cystic fibrosis, sickle cell, thalassemias, muscular dystrophy) & chromosomal disorders (sex).
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21
Q

What are the ethical issues arising from chorionic villus sampling?

A
  • 1-2% risk of miscarriage (delay in getting results)
  • Infection
  • Heavy bleeding
  • FP 1-2%
  • FN 2%
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22
Q

Give 6 examples of diseases for which DNA tests are available?

A
  1. Cystic fibrosis
  2. Phenylketonuria
  3. Tay-Sachs
  4. Duchenne muscular dystrophy
  5. Huntington’s disease
  6. Inherited breast & ovarian cancers
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23
Q

What is the recent development of non-invasive prenatal genetic testing (NIPT)?

A
  • Cell-free foetal DNA (DNA from placenta, v similar to DNA from foetus)
  • Early use 9-10weeks
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24
Q

What are the positives of cell-free foetal DNA (NIPT)?

A
  • Risk of chromosomal abnormalities with more accuracy than other non-invasive methods (invasive still required for definitive results)
  • Definitive diagnosis of some conditions (cystic fibrosis, achrondroplasia)
  • Determine gender
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25
Q

What report discusses the use of NIPT?

A

Nuffield Report, March 2017

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26
Q

Describe preimplantation genetic diagnosis?

A
  • Offered to couples at risk of passing on genetic disorder
  • Removing 1 cell from early embryo (4-8 cell embryo)
  • PGD not common & expensive
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27
Q

What are the types of disorders acceptable for preimplantation genetic diagnosis (HFE Act 2008)?

A
  • Disorder that may affect capacity for live birth
  • Risk of child being born with/developing serious disability (genetic, chromosomal, mitochondrial)
  • Gender-related disorder, can use to select gender
  • 100+ conditions on HFEA site
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28
Q

According to Code of Practice, how serious is a “serious” disability?

A
  • Take into consider the views of those seeking treatment
  • Likely degree of suffering
  • Availability of effective treatment
  • Speed of degeneration
  • Extent of intellectual impairment
  • Social support available
  • Family circumstances
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29
Q

Describe Huntington’s Disease?

A
  • Inherited, late onset, degenrative condition
  • Manifests ~30-50yrs
  • 50/50 chance of inheriting it from affected parent
  • Non sex linked dominant inheritance pattern
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30
Q

What case talks about the preference for disabled embryos?

A
  • Tomato Lichy & Paula Garfield

- They did NOT want to positively select but it opened the debate

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31
Q

What is Saviour siblings?

A
  • Create embryo (PGD) that will be tissue match (Human leukocyte antigen (HLA)) for existing child who has a condition that requires ie. bone marrow transplant
  • 2001 this was approved for removal of cord blood cells & embryo had to be at risk of inheriting same disorder
  • 2004 both of these conditions were removed, hence bone marrow transplant now possible
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32
Q

What are 3 examples of saviour siblings?

A
  1. Hashmi family (2002)- beta-thalassaemia inherited, UK (HFEA) granted permission
  2. Whittaker family (2002)- diamond Blackfan anaemia, no inherited, UK (HFEA) refused, US granted
  3. Fletcher family (2004)- diamond Blackfan anaemia, not inherited, UK (HFEA) granted approval
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33
Q

Is saviour siblings ethical?

A
  • Savious sibling being “used” as a means to help other child than an end in themselves?… but people have children for all kinds of reasons
  • What is psychological effect on saviour sibling (& existing child) & resultant relationship?… what impact of bereavement on a family
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34
Q

What is CRISPR?

A

Gene editing technology at embryo stage (IVF) & post-birth

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35
Q

Where do the female reproductive organs lie within the pelvic cavity?

A
  • Above pelvic floor

- Vagina & urethra pass through pelvic floor & urogenital triangle

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36
Q

Where does the obturator nerve lie?

A

Lateral wall of pelvis (ovary lies just medial to it)

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37
Q

Describe the ovary?

A
  • Almond-shaped
  • Lateral pelvic wall in ovarian fossa
  • Between internal & external iliac vessels
  • Medial to obturator nerve & thin wall of acetabulum
  • Produces ovum monthly in response to FSH & LH
  • Also produces oestrogen & progesterone
  • Truly intraperitoneal
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38
Q

What is a possible clinical problem with the ovary being near the acetabulum?

A

Central dislocation of the hip may injure the ovary

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39
Q

What ligaments support the ovary?

A

Hangs off posterior aspect of broad ligament on mesovarium & supported by ovarian ligament & suspensory ligament

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40
Q

Describe the round ligament of the ovary?

A
  • Continuation of ligament of ovary (both remnants of gubernaculum)
  • Passes from uterus through inguinal canal to labia
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41
Q

What is at risk during surgery to the ovary?

A

Ureter as it lies posteriorly to ovary

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42
Q

Where does referred pain go to in ovarian disease?

A

Medial thigh due to obturator nerve lying laterally

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43
Q

What is the arterial supply of the ovary?

A

Ovarian artery from aorta at L1/2

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44
Q

What is the nerve supply of the ovary?

Where is the referred pain?

A
  • Pre-aortic sympathetic nerves from T10/11

- Referred pain peri-umbilical region

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45
Q

What is the venous supply of the ovary?

A
  • Ovarian vein forms plexus
  • Left drains to left renal vein
  • Right ovarian vein drains to IVC
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46
Q

What is the lymph drainage of the ovary?

A

Para-aortic nodes (lateral)

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47
Q

What forms the suspensory ligament?

A

Ovarian vessels about to enter the broad ligament

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48
Q

Describe the uterine tube?

A
  • Ostium surrounded by fimbriae within peritoneal cavity
  • Infundibulum, Ampulla (fertilisation occurs), Isthmus, Intramural part through uterine wall
  • Lies upper, free edge of broad ligament
  • Blood supply from anastomosis between ovarian & uterine arteries
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49
Q

Where does pain from uterine tube go?

A

Lower abdominal

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50
Q

Describe the uterus?

A
  • Pear-shaped
  • Thick, muscular walled
  • Narrow cavity
  • Implantation of fertilised ovum & growth of foetus & placenta
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51
Q

What supports the uterus?

A
  • Levator ani
  • Perineal body
  • Perineal membrane
  • Fascial thickenings on pelvic floor passing from uterus & cervic to sacrum, pubis & lateral pelvic walls
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52
Q

What forms the Tendinous Arch of Pelvic Fascia?

A

Visceral & parietal fasciae meeting & fusing as the organs pierce the pelvic floor

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53
Q

What are the different supportive uterine ligaments?

A
  • Transerve cervical/cardinal ligament with uterine artery
  • Pubocervical
  • Lateral ligament of bladder
  • Uterosacral
  • Paracolpium
  • Tendinous Arch of Pelvic fascia
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54
Q

Describe the peritoneum of the pelvis in relation to the female reproductive system?

A

Sheet over uterus, uterine tubes & ovarian ligaments to form broad ligament from uterus to lateral pelvic wall

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55
Q

What hold the uterus in an anteverted (entry to vagina) & anteflexed (between cervix & body) position over the bladder?

A

Broad & Round ligaments

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56
Q

What does the cervix of the uterus form?

A

Posterior & anterior fornices at the vagina

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57
Q

What is the clinical problem with vaginal fornices?

A
  • They are distensible & foreign bodies may get “lost”

- Peritoneal cavity may be accessed via the posterior fornix

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58
Q

Describe the female cervix?

A
  • Isthmus of uterus leads to internal ostium

- Vaginal part opens into vagina as external ostium & has vaginal fornices around it

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59
Q

The ureter lies ______ to the uterine vessels?

A

BELOW

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60
Q

What can retroversion &/or retroflexion of the uterus cause?

A

Back-ache & difficulty in conception

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61
Q

What is related to posterior vaginal fornix?

A

Recto-uterine pouch of Douglas

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62
Q

What is the blood supply of the uterus & vagina?

A

Anastomosing uterine & vaginal arteries (+ superior vesical artery)

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63
Q

Describe the vagina?

A
  • Angled upwards & backwards
  • Passing from cervix to vestibule
  • Between labia minora
  • Anterior & posterior walls in contact
  • Passes through levator ani into perineum where its surrounded by urethral/urethrovaginal sphincter
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64
Q

What arteries supply the urethra?

A

Vaginal & Internal pudendal

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65
Q

Describe the female urethra?

A
  • Many small mucous glands & lacunae
  • Para-urethral glands & ducts near orifice
  • Passes through deep perineal pouch with external sphincter & perineal membrane
  • External sphincter signet ring
  • Other longitudinal muscle to make urethra shorter, wider during micturition
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66
Q

What is the epithelial of the female urethra?

A

Urinary but quickly becomes stratified squamous

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67
Q

What is the lymph drainage of the bladder & urethra?

A

External & internal iliac nodes

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68
Q

What is the lymph drainage of the uterus & proximal vagina?

A

Internal iliac nodes

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69
Q

What is the lymph drainage of the uterine tube?

A

Para-aortic but may also pass superficial inguinal nodes

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70
Q

What is the lymph supply of the distal vagina & urethra?

A

Deep & superficial inguinal nodes

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71
Q

What is the nerve supply of the female pelvis?

A
  • Sympathetic pre-aortic plexus (T10-L2), continues as superior hypogastric plexus –> left & right pelvic plexuses (T12-L2)
  • Parasympathetic to pelvic plexuses (S2,3,4)
  • Somatic pudendal (S2,3,4)
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72
Q

Where does pain from the uterine body & proximal uterine tube go?

A

Via branches of pelvic plexus with sympathies mainly from T12 & L1 = suprapubic

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73
Q

Where does pain from the uterine cervix & proximal vagina go?

A

“Pain line” via the parasympathetic pelvic splanchnics & pelvic plexuses therefore felt deeply in the pelvis

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74
Q

What is the nerve supply of the distal vagina?

A

Somatic pudendal

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75
Q

Where does the diamond-shaped perineum lie?

A

Inferior to pelvic outlet & pelvic floor

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76
Q

Describe the location of the urogenital triangle of perineum?

A

Between pubic symphysis & ischiopubic rami, anterior to ischial tuberosities

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77
Q

What passes through the lesser sciatic foramen?

A

Pudendal nerve with internal pudendal vessels recurving into perineum, inferior to pelvic floor

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78
Q

What does the perineal membrane (between the ischiopubic rami) divide the urogenital triangle into?

A

Superficial, deep pouch & inferior, superficial pouch

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79
Q

What does the anterior aperture of the perineal membrane allow the passage of?

A

Nerves & vessels to penis/clitoris

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80
Q

Describe the inferior & superior boundary of the deep pouch in a male?

A
  • INFERIOR: thick perineal membrane

- SUPERIOR: thinner fascia covering superior surface

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81
Q

What does the deep pouch contain in the male?

A
  • External urethral sphincter
  • Deep transverse perineal muscles
  • Urethra
  • Bulbo-urethral glands
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82
Q

What does the superficial pouch contain?

A
  • Penis/Clitoris
  • Labia minora & majora
  • Vulva & vaginal vestibule
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83
Q

What are the comparable features of the penis & clitoris?

A
  • 2 crura, attached to ischiopubic rami become corpora cavernosa that fill with blood in erection
  • 1 central bulb split in female as bulb of vestibule, in male becomes corpus spongiosum housing urethra to prevent its compression during erection
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84
Q

What 2 things form the root?

A

Crura & bulb

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85
Q

What are the 3 corpora on the body of the penis?

A
  • 2 dorsal cavernosa

- 1 ventral spongiosum

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86
Q

Describe the skin of the penis?

A
  • Dark, loose, no fat
  • Superficial, dartos fascia surrounds whole penis
  • “Doubles back on itself” to form prepuce/foreskin continuous with glans at corona
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87
Q

Describe the corpora cavernosa of the penis?

A
  • Divided by septum that is complete proximally, but pectiniform distally (to even out pressure & stay straight)
  • Each surrounded by thick tunica albuginea & deep fascia (Buck’s) surrounds them all
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88
Q

Describe the corpus spongiosum of the penis?

A
  • Transmits urethra

- Forms glands as a cap over corpora cavernosa

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89
Q

Describe the 2 muscles which support the penis & contribute to erection?

A
  1. Ischiocavernosus surrounds each crus

2. Bulbospongiosis surrounds bulb & also compresses urethra during ejaculation/ to expel urine

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90
Q

What are the 2 supportive ligaments of the penis?

A
  1. Fundiform

2. Triangular (suspensory) from lines alba & pubic symphysis

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91
Q

Describe the foreskin of a penis?

A
  • Fold of skin, continuous with glans & also mucous membrane of urethra
  • Small frenulum, ventrally between foreskin & glans with increased sensation
  • Sebaceous glands form smegma
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92
Q

Describe the membranous part of the urethra in the male?

A
  • Narrowest part except for external orifice
  • Fibro-elastic tube & smooth muscle, within striated external sphincter & pubo-urethral/puboprostatic part of levator ani to resist surges of raised intra-abdominal pressure
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93
Q

Describe the external sphincter in the membranous urethra in the male?

A
  • Inverted pear shape
  • Base on perineal membrane
  • Apex pushing into prostatic urethra
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94
Q

Describe the spongy/anterior/bulbar/penile urethra in the male?

A
  • Narrowest part at external orifice
  • Bulbo-urethral glands
  • Many scattered glands esp. in navicular fossa (lacuna magna)
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95
Q

What must be straightened when passing a urethral catheter?

A
  • Right angle bend between membranous & bulbar urethra

- Right angle bend between spongy urethra as it becomes pendulous

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96
Q

Describe the different types of epithelium in the urethra in male?

A
  • Urothelium until ejaculatory ducts
  • Pseudostratified columnar
  • Stratified squamous in distal urethra
  • Keratinised at external orifice
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97
Q

What may glandular fossae (urethral lacunae) contain in elderly?

A

Concretions

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98
Q

What does navicular fossa, like vagina, produce?

A

Defensive lactobacilli

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99
Q

Describe the female external genitalia (vulva)?

A
  • Labium majus laterally, then labium minus, vagina & urethra opening in vestibule
  • Labia minora divide into medial & lateral folds to form prepuce of clitorus
  • Labia majora meet anteriorly = mons pubis, meet posteriorly = commissure/fourchette
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100
Q

How must episiotomy be performed & why?

A

Backwards & angled laterally, usually to right, to avoid cutting the anal sphincter

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101
Q

Describe the female clitoris?

A
  • Body is 2 crura
  • Bulb contributes minimally as a little cap over highly sensitive glans
    (urethra opens inferiorly to it, NOT in the clitoris)
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102
Q

What can occur at the greater vestibular or Bartholin’s glands in the female genitalia?

A

Site of painful cyst or abscess formation

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103
Q

What arteries does the internal pudendal artery give off?

A
  • Supplies perineum
  • Urethra
  • Posterior 2/3 of scrotum & labia
  • Cavernous tissue of penis/clitoris
  • Skin of shaft & glans of penis/clitoris
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104
Q

What supplies the anterior 1/3 of the scrotum & labia?

A

External pudendal artery from femoral artery

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105
Q

What is the venous drainage of the penile skin & foreskin?

A

Superficial dorsal veins to external pudendals

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106
Q

What is the venous drainage of the glans & shaft of penis?

A

Deep dorsal vein to prostatic plexus & then internal iliac

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107
Q

What is the venous drainage of the corpora cavernosa of the penis?

A

Deep arteries accompanied by veins draining to internal pudendal

108
Q

What is the lymph drainage of the corpora cavernosa, corpus spongiosum, bulb of penis & vesibule, proximal vagina & urethra (deep structures)?

A

Internal iliac nodes

109
Q

What is the lymph drainage of the superficial penis, scrotum & labia?

A

Superficial inguinal nodes

110
Q

What is the lymph drainage of the glans penis & clitoris?

A

Deep inguinal (Cloquet) & external iliac nodes

111
Q

Describe the branches that the pudendal nerve (S2,3,4 somatic motor & sensory) gives off?

A
  • Muscular brnahces to bulbospongiosum, Ischiocavernosus, external urethral sphincter
  • Dorsal nerve of penis/clitoris, sensory as far as glans
  • Perineal nerve giving posterior scrotal/labial nerves
112
Q

Describe the passage of cavernous nerves?

A

Directly to prostate & urethra, corpus spongiosum & erectile tissue of corpora cavernosa, penis & clitoris

113
Q

What is the different autonomic nerve supply of erection & ejaculation?

A
  • Erection: parasympathetic

- Ejaculation: sympathetic

114
Q

Describe the shape of the rectum?

A
  • Follows sacral curve

- Lateral curvatures/concavities that form left, right, left rectal folds or valves internally

115
Q

Describe the peritoneum on the rectum?

A
  • Upper 1/3: front & sides
  • Middle 1/3: front only
  • Lower 1/3: none
116
Q

What does the mesorectum, posterior to rectum, contain?

A
  • Superior rectal artery & vein

- Lymph nodes & nerves

117
Q

What nerves are at risk during rectal surgery?

A
  • Urogenital nerves & vessels

- Pelvic plexus

118
Q

Where is the recto-anal junction?

A

Pelvic floor, puborectalis & behind the perineal body

119
Q

What is special about the pectinate line in anal canal?

A

Embryological & afferent nerve supply changes: sensitive to pain below line

120
Q

Describe the changes in epithelium of the anal canal?

A

Columnar –> stratified squamous –> skin

121
Q

Describe the internal sphincter of the anal canal?

A
  • Smooth muscle
  • Autonomic
  • Derived from circular muscle layer
  • Ends at intersphincteric groove
122
Q

Describe the external sphincter of the anal canal?

A
  • Striated muscle
  • Deep, superficial & subcutaneous parts
  • One functional unit
  • Fuses with puborectalis, transverse perineal muscles, anococcygeal ligament & perineal body in female but not male
123
Q

Describe the puborectalis muscle?

A
  • Part of levator ani
  • Sling around anorectal junction, drawing it anteriorly to make more acute angle
  • Recto-anal continence
124
Q

Describe the anococcygeal ligament?

A
  • Formed by fused levator ani

- Attached the anal canal to coccyx

125
Q

Describe the internal features of the anal canal?

A
  • Anal columns
  • Valves
  • Pectinate line
  • Anal cushions
  • Anal sinuses
  • Glands§
126
Q

Describe the mucous membrane & submucosa of the anal canal?

A
  • Loose, mobile & distensible to allow expansion for defecation
  • Rich underlying vasculature (haemorrhoids/piles)
127
Q

What is the function of anal cushions & internal sphincter?

A

Maintain anal closure when there is no pressure or content from the rectum

128
Q

Describe the 4 recto-anal arteries?

A
  • Superior rectal: from inferior mesenteric
  • Middle rectal: from internal iliac (highly variable/absent)
  • Inferior rectal: from internal pudendal
  • Median sacral (may cause bleeding during surgery)
129
Q

Describe the recto-anal veins?

A
  • Superior rectal veins to inferior mesenteric to portal vein
  • Middle & inferior rectal veins to internal iliac veins, systemic
130
Q

What do the recto-anal veins form?

A

External & internal (submucosal) venous plexuses: porto-systemic anastomosis

131
Q

Describe the recto-anal lymph drainage (initially to nodes adjacent to rectum and then…)?

A
  • Inferior mesenteric nodes for superior rectum, possibly via sacral nodes
  • Internal iliac nodes for lower rectum & proximal anal canal
  • Superficial inguinal nodes for distal anal canal
132
Q

Describe the recto-anal nerve supply?

A
  • Parasympathetic, pelvic splanchnics (S2,3,4) to pelvic plexus
  • Pelvic plexuses carry sensation & control internal sphincter
  • Internal pudendal nerve (somatic) from S2,3,4 giving inferior rectal branches to supply external anal sphincter, adjacent pelvic floor muscles (puborectalis) & sensation to distal anal canal
133
Q

Describe the process of defecation?

A
  • Abdominal pressure flattens anterior wall of lower rectum over upper anal canal
  • Anal cushions close canal
  • Rectum can partially fill without increase in pressure
  • Sensation can allow cortex to distinguish between gas, fluid, solid
  • Stretch receptors in levator ani & anal canal tissue
134
Q

What prevents defecation?

A
  • Prevented by learned, cortical inhibition
  • Only gas may be allowed to escape
  • External sphincter forces faeces up into the rectum
135
Q

When is defecation allowed?

A
  • Puborectalis relaxes, allowing recto-anal angle to straighten
  • External sphincter relaxes (S2,3,4)
  • Lower colon & rectum contract, internal sphincter relaxes (parasympathetic pelvic splanchnics S2,3,4) via pelvic plexus
136
Q

When can recto-anal incontinence occur?

A
  • Following cortical/cord lesions above S2,3,4
  • Damage to external sphincter during obstetric or perineal procedures
  • Entrapment of pudendal nerve
137
Q

What are the arteries, veins, nerves and lymph above the pectinate line?

A
  • Autonomic (visceral) innervation
  • Inferior mesenteric artery
  • Veins to portal circulation
  • Lymph to internal iliac nodes
138
Q

What are the arteries, veins, nerves & lymph below the pectinate line?

A
  • Somatic innervation (sensitive to pain)
  • Inferior rectal artery & vein: systemic
  • Lymph to superficial inguinal nodes
139
Q

Where does the anal triangle lie between?

A

Ischial tuberosities, sacrotuberous ligaments & coccyx

140
Q

Describe the ischio-anal fossa?

A
  • Fat-filled pyramid region
  • Below levator ani
  • Either side of anal canal
  • Allows distension of anus during defecation
141
Q

Can the 2 ischio-anal fossae communicate with eachother?

A

YES- behind the anal canal

142
Q

The ischio-anal fossa has a small anterior extension above what?

A

Deep perineal pouch (urogenital diaphragm)

143
Q

Where does the pudendal neuromuscular bundle lie?

A

Laterally in Alcock’s canal (obturator fascia)

144
Q

Where is a site of infection and absecesses that may require surgical intervention?

A

Inferior rectal neuromuscular bundle passing across the apex to supply external sphincter & anal canal sensation

145
Q

What are the 2 common clinical conditions occurring in the anal-canal & ischia-anal fossa?

A
  • Dilatation of venous plexuses giving haemorrhoids/piles

- Ischio-anal abscess caused by sinus from anal canal

146
Q

Describe the 5 stages of pubertal maturation of male genitalia?

A
  • STAGE 1: no pubic hair or enlargement of penis/testes
  • STAGE 2: testicular enlargement to >2.5cm, start of pubic hair
  • STAGE 3: penal enlargement, enlarging testicles, more pubic hair
  • STAGE 4: further enlargement of scrotum & testes, darkening of pubic hair
  • STAGE 5: adult genital appearance
147
Q

What is the average age for puberty in boys and girls?

A
  • BOYS: 14yrs

- GIRLS: 13yrs

148
Q

What are the 3 possible causes for hypogonadism in phenotypic males?

A
  1. Temporary delay of puberty
  2. Hypogonadotrophic hypogonadism
  3. Hypergonadotrophic hypogonadism
149
Q

Give examples of things which would cause Temporary delay of puberty in male?

A
  • Constitutional delay of puberty (familial, sporadic)
  • Chronic illness (malabsorption, malnutrition, malignancy)
  • Hormonal disturbance (GH deficiency, hypothyroidism)
150
Q

Give examples of things which would cause Hypogonadotrophic hypogonadism?

A
  • Kallman’s syndrome (with anosmia)

- Hypopituitarism (tumour, trauma)

151
Q

Give examples of things which would cause hypergonadotrophic hypogonadism?

A
  • Klinefelter’s syndrome (XXY)
  • Anorchia
  • Orchitis (mumps)
  • Radiation treatment &/or cytotoxic chemotherapy (leukaemia)
  • Surgical/traumatic castration
152
Q

What can cause arrest in puberty in females?

A

Anorexia nervosa

153
Q

What are the symptoms/consequences of male hypogonadism?

A
  • Sexual dysfunction
  • Fatigue
  • Depressed mood
  • Osteoporosis
  • Decrease in muscle mass & strength
  • Loss of facial & body hair
154
Q

What is the treatment for Constitutional delay in puberty resulting in hypogonadism?

A

Short-term low does sex steroid treatment (testosterone 100mg monthly for 3 months)

155
Q

What is the treatment for Hypergonadotrophic hypogonadism?

A
  • Sex steroid replacement (testosterone)
  • Bisphosphonates & calcium
  • Reduction mammoplasty (for reducing possible gynaecomastia)
156
Q

What is the treatment for hypogonadotrophic hypogonadism?

A
  • Sex steroid replacement (testosterone)

- Exogenous GnRH administration to promote spermatogenesis

157
Q

Describe the current therapies for testosterone replacement?

A
  • Intramuscular injection: every 2-3weeks
  • Oral : 3-4 times daily
  • Subcutaneous pellets: every 4-6 months
  • Transdermal
  • Buccal
158
Q

What tests would be done to investigate a patients hypogonadism?

A
  1. FSH, LH & testosterone

2. Chromosome analysis

159
Q

What is Craniopharyngioma?

A

Brain tumor derived from pituitary gland embryonic tissue, can suppress puberty from occurring resulting in hypogonadotrophic hypogonadism

160
Q

What sexual health problems can blood test screen for?

A
  • HIV 1+2 antibodies & p24 antigen
  • Hepatitis B antigen
  • Syphilis
161
Q

What is Chlamydia (common STD)?

A
  • Bacterium Chlamydia trachomatis
  • Can damage woman’s reproductive organs
  • Symptoms mild/absent
  • Potential for irreversible damage including infertility
162
Q

What is the incidence of Chlamydia in Europe?

A

10 million new cases per year

163
Q

How do people catch Chlamydia?

A
  • During vaginal, anal or oral sex

- Passed from infected mother to baby during vaginal childbirth

164
Q

Why are teenage & young girls at a higher risk of catching Chlamydia?

A

Cervix is not fully matured

165
Q

What are the possible symptoms of the “silent” Chlamydia STD in women?

A
  • Abnormal vaginal discharge/ burning when urinating
  • Spread to fallopain tubes some women have no signs/symptoms
  • Lower abdominal pain, low back pain, nausea, fever, pain during intercourse, bleeding between menstrual periods
166
Q

What are the possible symptoms of the “silent” Chlamydia STD in men?

A
  • Discharge from penis/ burning when urinating
  • Burning & itching around opening of penis
  • Pain & swelling in testicles
167
Q

What is Pelvic Inflammatory disease (PID) and how can this occur in females?

A
  • Due to untreated chlamydial infection spread into uterus/fallopian tubes
  • 40% of women
  • Causing permanent damage leading to chronic pelvic pain, infertility & fatal ectopic pregnancy outside uterus
168
Q

What is the risk of women infected with chlamydia catching HIV?

A

5x more likely if exposed

169
Q

What serious complication (rare) can occur in untreated chlamydia in males?

A

Spread to epididymis causing pain, fever & rarely sterility

170
Q

What are the tests used to detect Chlamydia?

A
  • Traditional method: physical examination for collection of samples from urethra
  • Urine testing using immunoassays (home testing kits)
171
Q

Describe the Outreach Study regarding Chlamydia screening?

A
  • Aarchus county
  • All 21-23yr olds were offered home sampling test
  • RESULTS: 0.8% females, 0.4% males took up offer
172
Q

What was the conclusion for the BMJ Randomised controlled trial for Chlamydia trachomatis screening to prevent PID?

A
  • Effectiveness of single chlamydia tests in preventing PID might have been overestimated
  • Focus on more frequent testing of women at higher risk
173
Q

What are 3 approaches to behaviour change?

A
  1. Motivational interviewing
  2. Problem-focused conselling
  3. Modelling & rehearsal of change
174
Q

What is the correlation of patient change talk?

A

Change Talk –> Clinician listen + Clinician reframe

175
Q

What is the correlation of patient resistance?

A

Clinician confront –> Patient argue. Patient interrupt. Patient negative. Patient off-task

176
Q

Describe the Randomised controlled trial to test women at risk for HIV (carey et al 1997)?

A
  • US
  • 102 women from community
  • MI is4 group MET sessions
  • Comparison was waiting list group
  • Followed up after 3months
177
Q

What did the Carey et al 1997 show regarding MI vs waiting list control group?

A
  • MI group showed greater: HIV knowledge, preception of risk, intention to protect, communication with partner
  • MI group had significantly lower rates of: unprotected sex, substance abuse before sex
178
Q

What are the social aspects of screening?

A
  • Screening healthy individuals is ethically different from everyday practice
  • Individual attributes of health imply a message of dependency on experts & technology
  • Health aspects as belonging, competence, mastering & well-being disregarded & social emphasis on health determinants disappear
179
Q

What should health promotion & life style advice become so to be ethically defensible?

A
  • Alter natural history of diseases

- Be approved by patients

180
Q

What is the backlash from the public regarding screening?

A

Organisers of screening programmes seen to be paternalistic

181
Q

What can be done to reduce backlash from patients of screening programs?

A
  • Give people information to make an informed choice
  • Provide pros & cons
  • Effects of decisional aids are unknown & controversial
182
Q

Where is estrogen synthesised?

A
  • Ovary
  • Placenta
  • Small amounts in adrenal cortex & testis
183
Q

What is the most potent estrogen (3 main estrogens)?

A

Estradiol

184
Q

What is the effect of pharmacological estrogen at different sexual maturities?

A
  • Before puberty: stimulate secondary sexual characteristics
  • Cyclically in female adult to induce menstrual cycle/ contraception
  • At/after menopause to prevent symptoms & protect against osteoporosis
185
Q

What are the different therapeutic uses of estrogens?

A
  • Replacement therapy in primary ovarian failure (Turners syndrome)
  • Replacement therapy for menopausal symptoms
  • Contraception, used in combo with progestins
  • Prostate & breast cancer
  • Given to males cause feminisation
186
Q

What are the 2 natural estrogens?

A
  • Estradiol

- Estriol

187
Q

What are the 3 synthetic estrogens?

A
  • Mestranol
  • Ethinylestradiol
  • Diethylstilbestrol
188
Q

What are estrogens bound to in blood?

A

Albumin & sex hormone-binding globulin

189
Q

What can changes in the levels of binding proteins do to estrogen?

A

Active estrogens are in unbound state

190
Q

What does SERMs stand for?

A

Selective Estrogen Receptor Modulators

191
Q

What are SERMs?

A

Competitive antagonists or partial agonists of estrogens depending on the tissue

192
Q

Describe the use of Clomiphene (SERM)?

A

Estrogen antagonist in hypothalamus & anterior pituitary to inhibit negative feedback effect to induce ovulation

193
Q

Describe the use of Tamoxifen (SERM)?

A

Estrogen-dependent breast cancer as its has an anti-estrogenic on mammary tissue

194
Q

Describe the use of Raloxifene (SERM)?

A

Treat & prevent osteoporosis due to its estrogenic action on bone

195
Q

Where is the natural progestational hormone (progesterone) secreted?

A

Corpus luteum late in the menstrual phase & by placenta during pregnancy

196
Q

Estrogen ______ synthesis of Progesterone receptor (PR) & progesterone ______ synthesis of estrogen receptors?

A
  • Stimulates

- Inhibits

197
Q

Why is progesterone NOT given therapeutically?

A

Rapid clearance by liver

198
Q

What are the 3 common synthetic derivatives of progesterone (called progestins)?

A
  1. Medroxyprogesterone
  2. Hydroxyprogesterone
  3. Norethisterone (weak androgen)
199
Q

What are the therapeutic uses of progestogens?

A
  • Main: oral contraceptive pill alone or combo with estrogen
  • Progesterone only injectable/implantable contraception or part of an intrauterine contraceptive
  • Combine with estrogen for estrogen replacement therapy
200
Q

What 3 things does estrogen replacement therapy prevent in a women with an intact uterus?

A
  1. Endometrial hyperplasia
  2. Carcinoma
  3. Endometriosis
201
Q

What is Danazol?

A

Modified progestogen used to treat sex- hormone dependent conditions (endometriosis, breast dysplasia & gynaecomastia)

202
Q

How does Danazol work?

A
  • Acts via the progesterone receptor to inhibit gonadotrophin production
  • Reduces estrogen synthesis in women & androgen synthesis in men
  • Androgenic activity so virilizing when given to women
203
Q

What are the unwanted side effects associated with Danazol?

A
  • GI disturbances
  • Weight gain
  • Fluid retention
  • Dizziness
  • Headaches
  • Menopausal symptoms
204
Q

What are the adverse effects of progestins?

A
  • Acne
  • Fluid retention
  • Weight gain
  • Depression
  • Change in libido
  • Breast discomfort
  • Menstrual cycle irregularity
  • Increased risk of thromboembolism
205
Q

What is the anti-progestogen, Mifepristone, in combo with prostaglandin analogues used for?

A

Chemical abortion up to 9 weeks

206
Q

Describe the different forms of estrogen & progestogen in the combined contraceptive pill?

A
  • Estrogen is: ethinyloestradiol or mestranol

- Progestogen is: norethisterone, levonorgestrel, ethynodiol, desogestrel or gestodene

207
Q

How much estrogen is in the combined contraceptive pill?

A

20 – 50 ug

208
Q

How is most combined pills taken?

A
  • 21 consecutive days followed by 7 days pill free to allow a withdrawal bleed
  • Menstrual cycles return quickly after discontinuation
209
Q

What is the mode of action of the combined contraceptive pill?

A
  • Estrogen inhibits FSH via negative feedback on anterior pituitary & suppresses ovarian follicle development
  • Progestin inhibits LH & prevents ovulation.
  • Estrogen & progestin alter the endometrium to discourage implantation
  • Interfere with the coordinated contractions of the cervix, uterus & fallopian tubes
210
Q

What are the adverse effects of the combined contraceptive pill?

A
  • Mild nausea, flushing, dizziness, and bloating.
  • Weight gain, skin changes, depression or irritability.
  • Amenorrhea (variable duration) after stop taking the pill
  • Small number of women develop reversible hypertension
  • Small increase in risk of thromboembolism
211
Q

What do the progestin only contraceptive pills include?

A

Norethisterone, levonorgestrel or ethynodiol diacetate

212
Q

How is the progestin only contraceptive pill taken?

A

Daily without interruption

213
Q

What is the mode of action of the progestin only contraceptive pill?

A
  • Cervical mucous made inhospitable to sperm

- Hinders implantation through effects on the endometrium & motility & secretions of fallopian tubes

214
Q

Describe post-coital (emergeny) contraception?

A

Oral levonogestrel alone or in combo with estrogen is effective if taken within 72hrs & repeated 12hrs later

215
Q

Describe long-acting progestogen only contraception?

A
  • Medroxyprogesterone acetate intramuscularly
    as a contraceptive (effective & safe)
  • Levonorgestrel implanted subcutaneously. The capsules release progestogen slowly over 5yrs
216
Q

How long can a levonorgestrel impregnated intrauterine device can last for?

A

35yrs

217
Q

What are the symptoms of menopause?

A
  • Headaches & hot flushes
  • Teeth loosen & gums recede
  • Risk of cardiovascular disease
  • Backaches
  • Body & pubic hair becomes thicker & darker
  • Boens lose mass
  • Vaginal dryness, itching , shrinking
  • Stress/urge incontinence
  • Skin & mucous membranes become drier, rougher
  • Nipples smaller & flatten
  • Breasts droop
  • Hair thinning
218
Q

Describe Postmenopausal hormone replacement therapy?

A
  • Involves cyclic or continuous administration of low dose estrogens (estradiol, estriol) with/without progestogens
  • Improves symptoms cause by reduced estrogen
  • Prevents and treats osteoporosis.
219
Q

What are the drawbacks with using hormone replacement therapy?

A
  • Withdrawal bleeding
  • Increased risk of breast cancer & endometrial cancer
  • Increased risk of thromboembolism
220
Q

What are the influences of testosterone?

A
  • Hair growth
  • Synthesis of serum proteins in liver
  • Penile growth
  • Spermatogenesis
  • Prostate growth
  • Libido
  • Aggression
  • Increased strength & volume of muscle
  • Stimulation of erythropoietin in kidney
  • Stimulation of bone marrow stem cells
  • Accelerated linear growth closure of epiphyseal plates
221
Q

What are intramuscular depot injections/patches of testosterone esters used for?

A
  • Replacement therapy in male hypogonadism

- Female hypo sexuality following ovariectomy

222
Q

Give 2 examples of Antiandrogens?

A
  • Flutamide

- Cyproterone

223
Q

What can anti androgens be used for?

A

Part of treatment of prostatic cancer

224
Q

What can Dihydrotestosterone synthesis inhibitors (finasteride) be used to treat?

A

Benign prostatic hypertrophy

225
Q

How/why can androgens be modified?

A
  • Alter balance of anabolic & other effects

- Nandrolone, for example, increase protein synthesis & muscle development

226
Q

What are anabolic steroids used for?

A
  • Aplastic anaemia

- Abused by athletes

227
Q

What are the potential side effects of anabolic steroids?

A
  • Infertility
  • Salt & water retention
  • Coronary heart disease
  • Liver disease
228
Q

What is Gonadotrophin-releasing hormone & what are analogs of it used for?

A
  • Decapeptide

- Analogs used to manipulate reproductive axis

229
Q

Give 2 examples of Gonadotrophin-releasing hormone analogs?

A
  • Gonadorelin

- Nafarelin (more potent)

230
Q

What are the 2 different mode of action & uses of GnRH analogues?

A
  • Pulsatile fashion will stimulate gonadotrophins (FSH and LH) & induce ovulation, used in the treatment of infertility
  • Continuous regimen will induce gonadal suppression, used in sex hormone-dependent conditions (e.g. prostate and breast cancers, endometriosis & large uterine fibroids)
231
Q

What are gonadotropins (FSH & LH) used to treat?

A

Infertility in both male & female

232
Q

How are gonadotropins made?

A
  • Recombinant DNA technology

- Extracted from urine of pregnant or post-menopausal women

233
Q

What does puberty involve?

A
  • Growth in stature
  • Change in body composition
  • Development of secondary sexual characteristics
  • Achievement of fertility
234
Q

What are primary sexual characteristics?

A
  • Reproductive organs

- Present at birth

235
Q

What are secondary sexual characteristics?

A
  • Develop during puberty

- Not directly part of reproductive system

236
Q

What is Adrenarche?

A
  • Hypothalamic-pituitary-adrenal axis
  • Maturational increase in adrenal androgen (DHEA-S) production
  • Around 6yrs in boys & girls
  • Occurs in conjunction with gonadal maturation
237
Q

What is the primary stimulus of adrenarche?

A

Enhanced adrenal sensitivity to ACTH

238
Q

What are increased androgen levels responsible for?

A
  • Development of pubic & axillary hair (pubarche)
  • Development of pilosebaceous unit in skin (acne)
  • Increases cortical bone density
239
Q

Describe puberty in females (lasting 4.5yrs in total)?

A
  • 1st sign: breast development (8.5-12.5yrs)
  • Pubic hair growth & rapid height spurt
  • Menarche (~13yrs, 2.5yrs after start of puberty, signals end of growth)
240
Q

What is the normal amount of height gain remaining after female menarche?

A

5cm remaining

241
Q

What is Thelarche?

A

Female breast budding during puberty

242
Q

What is underlying the external female secondary sexual characteristic developments?

A

Endocrine axis controlling increased adrenal androgen production (adrenarche) & increased gonadal steroid production (gonadarche)

243
Q

Describe the 5 Tanner stages for female puberty?

A
  • Stage I: prepubertal
  • Stage II: breast & papilla elevated as small mound, areolar diameter increase. Sparse, light pubic hair
  • Stage III: further enlargement of breast bud. Darker, beginning to curl pubic hair
  • Stage IV: areola & papilla form secondary mound. Increased coarse, curly pubic hair
  • Stage V: mature areola. Adult feminine triangle pubic hair with spread to medial thigh
244
Q

When does menarche occur in females?

A

Ovaries mature becoming more sensitive to gonadotropin & release more steroid hormones exerting negative feedback on gonadotropin secretion = cycle will develop & menarche

245
Q

Describe what happens at male puberty?

A
  • 1st sign: Testicular enlargement (>4mls vol) at 10-15yrs
  • Pubic hair growth & penile growth
  • Spermarche (sperm in seminal fluid) mean age 13.4
  • Growth spurt when testicular vol 12-15mls
246
Q

Why are males, on average, taller than females?

A

Male growth spurt is later & of greater magnitude (they achieve more growth before peak velocity)

247
Q

What is the normal time interval between onset of pubic hair & axillary & facial hair?

A

2yr

248
Q

What are androgen-dependent secondary sexual characteristics?

A
  • Facial, underarm, pubic hair
  • Deepening of voice (growth of larynx)
  • Thick secretion of skin oil glands
  • Masculine pattern of fat
  • Bone growth via GH secretion then termination via closure of epiphyseal plates
  • Stimulating of muscle protein synthesis
  • Erythropoietin stimulations giving higher haematocrit
249
Q

What initiates puberty?

A

Gonadotropin (FSH/LH) release by hypothalamic-pituitary-gonadal axis

250
Q

What suppresses gonadotropin (FSH/LH) release?

A

Continuous infusion of GnRH

251
Q

When are pulses of GnRH most detectible?

A

Childhood yrs during sleep & low frequency & amplitude therefore don’t stimulate gonadotropin release

252
Q

What are the 4 phases of human growth?

A
  1. Fetal- uterine environment, fastest, 30% of eventual height determined
  2. Infantile- nutrition, happiness & thyroid (birth-18months), rapid but decreasing, 15%
  3. Childhood- thyroid hormones, GH, health & happiness, genetics. Slow
  4. Pubertal- sex hormones (testosterone/oestrogen), GH & insulin-like growth factor
253
Q

What is the peak height velocity in boys & girls?

A
  • BOYS: 10cm/yr (13.5 mean age)

- GIRLS: 9cm/yr (11.5 mean age)

254
Q

How does puberty limit adult height?

A

Gonadal steroids lead to epiphyseal closure of long bones

255
Q

When do changes in body composition begin in males & females?

A
  • MALE: ~9yrs

- FEMALE: ~6yrs

256
Q

What are factors contributing to earlier puberty?

A
  • Genetics (mother & sister)
  • Lower social class = obesity = earlier menarche
  • Close to equator, lower altitudes, urban setting
  • Endocrine disrupting chemicals ie. plastics, agriculture, fuels
  • Afro-carribean & African-american earlier
257
Q

How much can nutritional status in childhood explain puberty timing?

A

25% of variation in timing of puberty

258
Q

What is the relationship between increase in body fat & time of puberty onset?

A
  • Increase body fat may play critical role in turning on adrenal androgen secretion & adrenarche
  • Leptin may be link between adipose tissue, energy homeostasis centres in hypothalamus & reproductive system
259
Q

What is the relationship between reduced body fat & puberty onset?

A
  • Athletes often have delayed maturation & menarche

- Malnutrition/anorexia cause delay

260
Q

What is “critical fat mass”?

A

Girls will reach menarche as they reach body weight of ~47kg (55kg in boys)

261
Q

How much is FSH & LH increased in menopause due to lack of negative feedback?

A
  • FSH= 10-20x (excreted in urine)

- LH = 3x

262
Q

What are the consequences/symptoms of menopause?

A
  • Vascular instability
  • Atrophy of all oestrogen dependant tissues
  • Rise in adrenal androgens may lead to hirsutism
  • Loss of libido
  • Depression, anxiety, mental confusion
263
Q

What does vascular instability in menopause cause?

A
  • Night sweats

- Hot flushes

264
Q

What are the oestrogen dependant tissues which become atrophied in menopause?

A
  • Breast, uterus, vagina, urethra
  • Skin collagen loss
  • Bone catabolism with loss of Ca2+ leads to osteoporosis
  • LDL rises increasing risk of coronary thrombosis
265
Q

What does hormone replacement therapy replace when used for menopause?

A
  • Steroids
  • Maintains oestrogen dependent tissues
  • Delays osteoporosis

MD3002 (15 decks)

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