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General Gynaecology > Endometriosis and adenomyosis > Flashcards

Endometriosis and adenomyosis Flashcards

1
Q

What is the prevalence of endometriosis?

A

11.4% or 1/9 women have a suspected or confirmed diagnosis of endometriosis by the age of 44 in Australia (RANZCOG Australian Endometriosis Guideline DRAFT 2020)

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2
Q

What is the definition of endometriosis and adenomyosis?

A

An inflammatory condition with endometrial-like glands and stroma deposited at sites outside of the endometrial cavity.
Endometrial-like glands and stroma within the myometrium of the uterus.

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3
Q

What is the pathophysiology of endometriosis and endometriomas?

A

Retrograde menstruation leads to deposits of endometrial-like tissue within the abdominopelvic cavity. An abnormality in immune response stops the body from clearing these deposits. >55% cases demonstrate heritability and there is likely underlying epigenetic causes for endometriosis.
Endometriomas form when endometrial depositors become invaginated in the ovarian cortex, possibly due to cortex disruption during routine ovulation.

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4
Q

How does endometriosis affect fertility?

A

The answer is not certain. Theories include:

  • disruption of tubal/peritoneal anatomy
  • Chronic low grade inflammation (Peritoneal fluid from women with endometriosis has been found to contain increased numbers of immune cells, including macrophages, and mast, natural killer and T cells, as well as elevated levels of growth factors, chemokines and cytokines.)
  • Reduced receptivity of the endometrium
  • reduction in ovarian reserve, particularly with endometriomas, reduces effectiveness of gnRH analogues during assisted reproductive techniques (ART)
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5
Q

What is the cost of endometriosis on a national level?

A

Endometriosis cost $9.3 billion in Australia in 2017; mostly due to its impact on women’s function and productivity.
Endometriosis is associated with significant psychological and socioeconomic issues.

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6
Q

What are the medical options for treating endometriosis?

A
  • Analgesics (NSAIDs, paracetamol, neuromodulatory meds; try to avoid opiates)
  • COCP
  • Progesterone oral/implant (but can have significant premenstual sx)
  • Mirena levonorgestrel IUS
  • Danazol (complex action: weak androgen and progesterone, with anti-estogenic effects: it is an anabolic steroid)
  • Gestrinone (complex action: weak androgen and progesterone with anti-progestognenic and ant-estrogenic effects; it is an anabolic steroid)
  • GnRH analogues (for 3 months prior to surgery for DIE) or off-license can be taken for up to 6 months with add-back HRT
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7
Q

What are the surgical options for endometriosis?

A
  • Ablation or excision of endometriosis (similarly effective at reducing pain)
  • There is no evidence that hysterectomy reduces pain related endometriosis
  • Endometrioma excision with removal of cyst wall is preferable to I&D due to better success for reduction in recurrence
  • If family is complete counsel about hysterectomy with bilateral oophorectomy. Add back HRT should be considered until age of menopause; this should be a continuous combined regime to suppress any residual endometriosis.
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8
Q

Counsel a woman on the effects of endometriosis/endometrioma surgery on fertility?

A

Benefits:

  • Improving sx of pain
  • Can assess tubal patency at same time
  • Can confirm diagnosis of endometriosis
  • Excision of endometrioma can exclude malignancy diagnosis
  • Excision of endometrioma (particularly if >3cm) can improve spontaneous pregnancy rates
  • Removal of endometriomas >3cm can improve ovarian responsiveness to IVF and number of oocytes retrieved; though no significant difference in pregnancy, live birth rate, miscarriage has been noted

Risks:

  • Surgery can cause further adhesions
  • Ovarian surgery can compromise ovarian reserve
  • Risks of surgery can be significant, especially if has DIE
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9
Q

What is the prevalence of endometriosis in

  • the aussie population
  • patients attending pain clinic
  • patients attending fertility clinic
A
  • the general population = 11.4%
  • patients attending pain clinic = 65%
  • patients attending fertility clinic = 50-70%
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10
Q

What are the three “types” of endometriosis?

A
  1. Superficial endometriosis or peritoneal disease <5mm
  2. Ovarian endometriosis / endometriomas (superficial)
  3. Deep endometriosis - Foci of endometrial tissue >5mm in depth, affecting retrocervix, parametric, Rectovaginal septum, digestive tract, ureter, extra-abdominal
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11
Q

What is Sampson’s Theory? Explain the pathogenesis.

A

Retrograde menstruation
Flow of endometrial content in pelvis allowing implantation of endometrial lesions

Menstrual blood contains endometrial mesenchymal stem cells (eMSCs). As a result of retrograde menstruation, epithelial progenitor cells may make their way outside of the uterus to attach to the mesothelium. As clonogenic cells, they may initiate ectopic lesion growth. A similar process has been found in retrograde neonatal uterine bleeding where these cells remain dormant in the mesothelium until estrogen levels increase at menarche.

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12
Q

What is the theory of coelomic metaplasia?

A

Transformation of peritoneal tissue / cells into endometrial tissue through hormonal and/or immunological factors

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13
Q

What is the hormone theory of endometriosis?

A

Estrogen-driven proliferation of endometrial lesions.
Resistance to progesterone-mediated control of endometrial proliferation

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14
Q

What is the theory of immune dysfunction in endometriosis?

A

Failure of immune mechanism to destroy ectopic tissue and abnormal differentiation of endometriotic tissue

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15
Q

What is the sensitivity and specificity of laparoscopic histological diagnosis of endometriosis?

A 
Sensitivity = 94%
Specificity = 97%

In the absence of histology, the false-positive rate with laparoscopic visualisation alone may approach 50% especially in the mild-moderate endometriosis

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16
Q

How is the inflammatory state of endometriosis thought to impact fertility?

A
  • Toxic effect on gametes, embryos
  • Impaired tubal cilia motility
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17
Q

Describe the changes in the eutopic endometrial receptivity

A
  • Increased formation of antibodies to endometrial antigens
  • Resistance to progesterone
  • Decreased expression of integrity and genes regulating implantation
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18
Q

What ovarian cancers is ovarian endometriosis associated with?

A

Clear cell - 3 fold increase

Low-grade serous and Endometrioid - 2 fold increase

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19
Q

How do progestins help in the management of endometriosis?

A

Inhibit growth of lesions by inducing decidualisation followed by atrophy of uterine-type tissues.
Best hormonal tx for halting disease progression.

No effect on endometrioma recurrence.

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20
Q

What are the adverse effects of progestins?

A

Weight gain
Fluid retention
Depression
Breakthrough bleeding

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21
Q

How does the COCP help to manage endometriosis?

A

Relieves dysmenorrhea through ovulation suppression and continuous progestin administration suppressing endometrial growth.

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22
Q

How do GnRH agonists help manage endometriosis?

A

Produces hypogonadotrophic hypogonadal state through down regulation of hypothalamus, causing anovulation and suppression of endometrial like deposits.

Use for 6 months max, due to effect on BMD

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23
Q

What are the disadvantages of GnRH agonist use in endometriosis?

A

Cost
Implant
BMD loss
Hypo-oestrogenic side effects

Can minimise side-effects with add back HRT which does not affect efficacy of GnRH agonist

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24
Q

What is the definition of Adenomyosis?

A

Presence of endometrial like glands and stroma in the myometrium

Associated with heavy menstrual bleeding, pain and/or infertility

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25
Q

What is the aetiology of Adenomyosis?

A

1.Direct invasion of endometrial basalis layer into myometrium –weakness secondary to prior pregnancy or surgery

2.De Novo from embryologic -misplaced Mullerian Remnants (rests)
– Rectovaginal septum

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26
Q

What USS features are consistent with adenomyosis?

What is the sensitivity and specificity of USS diagnosis of adenomyosis?

A
  • Bulky, globular uterus
  • Heterogeneous myometrium
  • Venetian blind effect: linear striations radiating from endometrium.
  • Asymmetrical wall thickness (posterior wall thicker).
  • Myometrial cysts
  • Loss of clear endomyometrial border
  • Sensitivity 50-90%
  • Specificity 50-99%
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27
Q

What was the finding of the Cochrane Review Overview regarding Endometriosis
- options effective at alleviating pain?
2014

A
  • GnRH analogues
  • LNG-IUD
  • Danazol
  • Progestagens
  • Anti-progestagens
  • Laparoscopic surgical interventions
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28
Q

What was the finding of the Cochrane Review Overview regarding Endometriosis
- for women undergoing ART?
2014

A
  • 3 months GnRH agonist improved pregnancy rates
  • excisional surgery improved spontaneous pregnancy rates in the 9-12 months after surgery compared to ablative surgery
  • laparoscopic surgery improved live birth and pregnancy rates compared to diagnostic laparoscopy alone
  • no evidence that medical treatment improved clinical pregnancy rates
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29
Q

What is the definition of chronic pelvic pain?

A

Pelvic pain on most days lasting 3 months or longer.

Used interchangeably with persistent pelvic pain.

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30
Q

What is the aetiology of chronic pain?

A

Major changes in both afferent and efferent nerve pathways in the central and peripheral nervous system.

Local factors such as TNF-alpha and chemokines may change peripheral nerve function and/or stimulate normally quiescent fibres, resulting in altered sensation over a wider area than originally affected.

  • Persistent barrage of pain –> CNS changes –> magnifies signal.
  • Visceral hyperalgesia: pain perception and visceral function modified by previous experience and current circumstances.
  • Neuropathic pain

Frequently more than one factor contributing to chronic pelvic pain

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31
Q

What is the embolisation theory of endometriosis development?

A

Endometrial cells may spread via lymph of blood vessels to ectopic sites.

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32
Q

What are the most common sites of endometriosis (from most to least common)?

A

Ovaries, anterior and posterior cul-de-sac, posterior broad ligaments, uterosacral ligaments, uterus, fallopian tubes, sigmoid colon and appendix, and round ligaments.

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33
Q

How do endometriomas cause infertility?

A
  • Inflammatory
  • Distorted anatomy
  • Destruction of ovarian cortex
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34
Q

What are risk factors for endometriosis?

A

– A first-degree female relative (mother or sister) with endometriosis
– Shorter-than-normal menstrual cycle (< 27 days) Longer-than-normal menstruaaon (>
five days) Low body-mass index
– Early menarche
– Nulliparity
– Müllerian anomalies – anomalies that arise during the formaaon of parts of the
female reproducave organs
– Outflow obstructions, e.g. cervical stenosis, a transverse vaginal septum or an imperforate hymen

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35
Q

What factors decrease risk of endometriosis?

A
  • Multiple births
  • Extended periods of lactation
  • Late menarche
  • Increased consumption of long-chain omega-3 fatty acids
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36
Q

What non-hormonal medication options are available for endometriosis treatment?

A
  • Analgesics: paracetamol, NSAIDs, others.

Neuromodulators:

  • TCA, SNRI
  • Gabapentin, pregabalin
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37
Q

What are the indications for laparoscopic surgery for endometriosis?

A
  • Pain persistent despite medical therapy.
  • Severe symptoms limiting function
  • To restore distorted anatomy
  • Infertility

Note: NOT for diagnostic purposes only - should be done with aim of treatment at same time, therefore should only done if you have skills to excise/ablate endometriosis.

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38
Q

What is recommended following all endometriosis surgery (except for fertility)?

A

Hormonal treatment e.g. Mirena, COCP for secondary prevention of endometriosis-related pain and endometriomas

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39
Q

What negative outcomes/effects does endometriosis have on pregnancy?

A

Increased risk of:

  • Miscarriage
  • Ectopics
  • APH
  • Placenta praevia
  • Abruption
  • Preeclampsia
  • CS
  • MROP
  • NND
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40
Q

Outline the parameters measured in the ENZIAN system for endometriosis staging.

A

Three compartments:

  • A = posterior cul de sac
  • B = uterosacrals, cardinals, pelvic side wall, external ureter
  • C = rectum

Three levels of severity of lesion (listed for each A, B, C compartment):

  • 1 = <1 cm
  • 2 = 1-3 cm
  • 3 = >3 cm

F= other areas affected by endometriosis including deep endo:

  • Adenomyosis
  • Bladder
  • Ureter intrinsic
  • Bowel except rectum
  • Lung, diaphragm, inguinal region etc
41
Q

List the findings on the rASRM classification system that would correlate with stage IV (Severe) endometriosis:

A

Score >40:

  • Many dense adhesions
  • Complete obliteration of the posterior cul-de-sac
  • Large endometriomas one/both ovaries
  • Deep implants
42
Q

List the findings on the rASRM classification system that would correlate with stage I (minimal) endometriosis:

A

Score 1-5:

  • Superficial Peritoneal or Ovarian implants
  • Filmy adhesions
43
Q

Describe the appearance of focal adenomyosis (adenomyoma)

A

Resembles a fibroid but without the pseudocapsule.

44
Q

Describe the macroscopic and microscopic appearance of diffuse adenomyosis

A

Macroscopic:

  • Thickened myometrial wall
  • Islands of endometrial bleeding: small haemorrhagic or chocolate coloured areas.

Microscopic:

  • Non-neoplastic endometrial gland and stroma in myometrium.
  • Surroundingmyometrium is hyperplastic and hypertrophied
  • Junctional zone (inner myometrium) invasion 2.5 - 8 mm
45
Q

What is the incidence of adenomyosis

What age group is most affected?

A

20-30% on hysterectomy histology

Women in their 50s

46
Q

What is the pathophysiology of HMB in adenomyosis?

A
  • Increased endometrial surface area.
  • Overexpression of inflammatory mediators
47
Q

What are the risk factors for adenomyosis?

A
  • High parity
  • Vigorous curettage of uterus
48
Q

What additional findings do you get with MRI pelvis diagnosis of adenomyosis?

What are the advantages and disadvantages cf. pelvic USS?

A

Junctional zone (inner myometrium) >12 mm thick.

  • MRI has slightly better sensitivity and specificity for diagnosis of adenomyosis
    • Sensitivity 77% vs 72%
    • Specificity 89% vs 81%
  • MRI is better at defining malignant uterine neoplasia
  • MRI is better at differentiating focal adenomyosis from fibroids
  • MRI is more expensive and may be more difficult to access
  • Some patients may have contraindications for MRI, but can still have ultrasound
  • Some patients may not consent to TV US scanning, which further reduces sensitivity/specificity
49
Q

Management of adenomyosis:

What are the surgical options?

What are the medical options?

A

Surgical:

  • Hysterectomy
  • Uterus sparing
  • resection of adenomyoma
  • novasure ablation
  • Uterine artery embolisation

Medical:

  • Hormonal
  • NSAIDs
  • Tranexamic acid
50
Q

Compare and contrast the surgical options for management of adenomyosis

A

Hysterectomy
Advantages: definitive surgery.
Disadvantages:
- Unable to bear children
- Surgical and anaesthetic risks

Uterus sparing resection
Advantages:
- Fertility sparing
Disadvantages:
- Risk of uterine rupture 4%
- Risk of placenta acreta
- CS recommended

Uterine artery embolisation
Advantages:
- Less invasive than hysterectomy
- For patients who are not good surgical candidates
Disadvantages:
- High risk of loss of fertility / premature ovarian insufficiency 3%
- Failure of treatment 1.5%

51
Q

Compare and contrast the medical options for management of adenomyosis

A

Hormonal e.g. Mirena, COCP, progestogen, GnRH agonist
Advantages:
- Fertility sparing
- Reduces pain and bleeding
Disadvantages:
- Contraceptive effect/can’t get pregnant while on it
- Recurrence within 6 months of stopping
- Side-effects of hormones
- GnRH agonist: reduced BMD, menopausal sx

NSAIDS and TXA:
Advantages:
- Avoids risks of surgery
- May reduce bleeding

52
Q

What is the difference between primary and secondary dysmenorrhoea?

A

Primary: pain related to periods in absence of demonstrable disease.

Secondary: same but has a disorder that could account for symptoms.

53
Q

Outline causes of secondary dysmenorrhoea

A

Gynae:

  • Endometriosis / adenomyosis
  • Fibroids
  • Ovarian cysts
  • Adhesions
  • Chronic PID
  • Obstructive endometrial polyps
  • Congenital obstructive Müllerian defects
  • Cervical stenosis
  • IUD
  • Pelvic congestion syndrome
  • Hematometra

Non-gynae:

  • Inflammatory bowel disease
  • IBS
  • Psychogenic
54
Q

What is the pathophysiology of primary dysmenorrhoea?

A
  • Excessive endometrial PGF2.
  • Increased PGF2 to PGE2 ratio
  • Dysrhythmic uterine contractions, hypercontractility, increased muscle tone and uterine ischaemia
55
Q

What are risk factors for primary dysmenorrhoea?

What are protective factors for primary dysmenorrhoea?

A

Risk factors:

  • Young age
  • Smoking
  • Stress

Protective factors:

  • Young age at first childbirth
  • Multiparity
  • Use of hormone contraception
56
Q

Chronic pelvic pain assessment:

What is the utility of identifying soft marker on pelvic USS i.e. probe tenderness or poor ovarian mobility?

A

The presence of soft markers improve pre-laparoscopy probability of identifying relevant pathology from 58 to 73%.

Absence of soft markers reduces probability to 20%

57
Q

What are the principles of surgical management of endometriosis?

A
  • Laparoscopy preferred over open.
  • Aim to excise / biopsy all suspicious looking lesions.
  • Excision more effective than ablation.
  • Aim to restore normal pelvic anatomy where possible.
  • Endometriomas: cystectomy over I&D
  • Post-op hormonal treatment to achieve relief from dysmenorrhoea and prevent secondary recurrence.
58
Q

How does endometriosis affect a woman’s quality of life?

A

Main 2: pain and fertility

Also:

  • diminished quality of life,
  • increased incidence of depression,
  • adverse effects on intimate relationships,
  • limitations on participation in daily activities,
  • reduced social activity,
  • loss of productivity and associated income,
  • increased risk of chronic disease,
  • significant direct and indirect healthcare costs
  • greater risk of obstetric and neonatal complications
59
Q

Average delay from symptom onset to diagnosis for endo?

A

7 years in aussie

60
Q

Consequences for patient of delayed diagnosis of endo?

A

persistent symptoms
detrimental impact on quality of life,
erosion of the patient physician relationship
development of central sensitization

Evidence is limited but failure of timely diagnosis and
adequate endometriosis management may foster disease progression and adhesion formation that may compromise fertility and increase the risk of
central sensitization and chronic pelvic pain

61
Q

Definition central sensitisation?

A

Central sensitisation is defined as an increased responsiveness of nociceptors in the central nervous system to either normal or sub-threshold afferent input[1] resulting in:

  1. Hypersensitivity to stimuli.[2]
  2. Responsiveness to non-noxious stimuli.[3]
  3. Increased pain response evoked by stimuli outside the area of injury, an expanded receptive field.[4].
62
Q

Sx of endometriosis

A

dysmenorrhea,
pelvic pain,
heavy menstrual bleeding,
dyspareunia,
fatigue,
infertility

63
Q

What are the main theories to explain the pathogenesis of endometriosis? (9)

A
  1. Retrograde menstruation
  2. Metaplasia
  3. Hormones
  4. Oxidative stress and inflammation
  5. Immune dysfunction
  6. Apoptosis suppression
  7. Genetic
  8. Embryonic remnants
  9. Stem cells
64
Q

What is Retrograde menstruation theory?

A

Flow of menstrual fluid/debris including endometrial cells via the fallopian tubes into the peritoneal cavity during menstruation.

Retrograde menstruation may be one of the initiating steps for endometrial glands and stroma to reach the peritoneal cavity but other factors such as genetics, hormones, and immune dysfunction may be required to create a favourable environment in order to favour cell survival and promote endometriotic implant formation, proliferation and development

65
Q

What is Metaplasia theory?

A

Transformation of normal peritoneal tissue to ectopic endometrial tissue.

66
Q

What is Hormone theory of endo?

A

Oestrogen-driven proliferation of endometrial lesions. Resistance to progesterone-mediated control of endometrial proliferation.

67
Q

What is Oxidative stress and inflammation theory?

A

Chronic inflammatory changes in the peritoneal and eutopic endometrial environment result in immunological changes that promote the growth of endometrial lesions.

68
Q

What is Immune dysfunction theory?

A

Prevention of the elimination of menstrual debris and promotion of implantation and growth of endometrial lesions.

69
Q

What is Apoptosis suppression theory?

A

Promotion of the survival of endometrial cells and downregulation of apoptotic pathways

70
Q

What is Genetic theory?

A

A heritable genetic alteration that favours implantation of endometrial cells.

71
Q

What is Embryonic remnants theory?

A

Residual cells of embryonic origin which retain the capacity to develop into endometriotic lesions under the influence of oestrogen beginning at puberty, or oestrogen mimetics.

72
Q

What is Stem cells theory?

A

Initiation of endometriotic deposits by retrograde shedding and regeneration of undifferentiated cells in the pelvic cavity.

73
Q

Familial link with endometriosis?

A

10x increased risk if 1st degree relative has endo

74
Q

Risk factors for endometriosis?

A
  • FHX
  • Shorter or longer than normal menstrual cycle
  • Low BMI
  • Early menarche
  • Mullerian abnormalities
  • Outflow obstruction
75
Q

What is the systematic approach suggested for USS of endometriosis by the IDEA group? (7)

A

Uterosacral nodules
Posterior compartment
Endometrioma
Bladder
Rectovaginal disease
Rectal infiltration (size, depth, multifocal?)
Alan masters pockets

76
Q

USS appearance of endometrioma?

A

The classical example is a unilocular cyst with acoustic enhancement with diffuse homogeneous ground-glass echoes as a result of the haemorrhagic debris

77
Q

MRI T1 appearance of endometriomas?

A

typically, lesions appear hyperintense while acute haemorrhage occasionally appears hypointense
endometriomas with high T1 signal characteristically do not show loss of signal on T1 fat suppressed sequence, which is important for differentiating it from mature cystic teratoma of the ovary

78
Q

MRI T2 appearance of endometriomas?

A

typically hypointense owing to the presence of deoxyhaemoglobin and methaemoglobin (shading sign), which is very suggestive of endometrioma.
T2 dark spot sign is specific for chronic haemorrhage and is helpful in diagnosing endometriomas 9
old haemorrhage occasionally appears hyperintense

79
Q

What is stage 2 endo?

A

Mild disease
6-15 points
Superficial lesions,
Some deep (>5mm below peritoneal surface)
Small endometriomas

80
Q

What is stage 3 endo?

A

Moderate disease
16-40 points
deep implants
dense adhesions
partial obliteration cul de sac endometriomas

81
Q

If patients have bilateral endometriomas, they have an 80% chance of ____ involvement?

A

rectovaginal/bowel

82
Q

What % of patients have stage 1-2 disease?

A

80%

83
Q

What % of patients have stage 3-4 disease?

A

20%

84
Q

What tool can be used to calculate fertility with endometriosis?

A

Endometriosis fertility index calculator
- an online tool where operative findings can be entered to estimate chances of spontaneous conception

85
Q

Initial management of endo:

A
  • Validation of sx
  • Education (verbal/written/online)
  • Medical - hormonal and analgesia
  • Surgical
  • Alternative
  • Physio (pelvic floor)
  • MDT
  • Pain psychologist
  • Pain specialist
  • Patient information
86
Q

Medical management of endo- pain

A
  • Step wise approach
  • Start with simple analgesia
  • Avoid opioid derivatives
  • Conservative: heat packs, TENS, stretches/exercises, dietary change FODMAP
  • Avoid constipation
  • hormonal ovulation suppression - aiming for amenorrhea
87
Q

Surgical management of endo

A
  • Aim should be to diagnose AND treat endo - moving away from diagnostic laparoscopy
  • Preop workup with USS +/- MRI and MDT
  • Discuss risks, risk of further pain and/or further surgery, treatment goals
  • Discuss ovarian function if endometrioma surgery
  • If laparoscopy done and disease worse than anticipated- should stop operating and arrange with advanced laparoscopic surgeon. Don’t do partial surgery.
88
Q

Role of hysterectomy

A
  • Hysterectomy doesn’t cure endo and no evidence it improves pain symptoms
  • Hysterectomy can manage HMB
  • All other endo should be removed
  • If ovaries left behind, endo can recur
  • If oophorectomy performed will require add-back HRT to minimise complications of early surgical menopause
89
Q

Surgical mx of endo and fertility

A
  • stage 1-2: excision improves spontaneous conception and ART
  • Stage 3-4: no clear evidence (absence of evidence not evidence of absence) and balanced against risks of extensive surgery for ovarian resrerve
  • Endometrioma: excision of capsule improve spontaneous pregnancy rates but can decrease ovarian reserve. No evidence for improvement in ART
90
Q

Chronic pain- factors involved

A
  • Mood: fear/anxiety
  • Cognitive set: hypervigilance, attention, distraction, catastrophising
  • Context: pain beliefs, fear, expectation, placebo
  • Chemical and structure: neurodegeneration, metabolic, maladaptive plasticity
  • Injury: peripheral and central sensitisation
91
Q

What is viscero-visceral cross sensitisation?

A

Normal pain pathway:
- Pain stimulus in organ, travels to spinal cord then to brain

viscero-visceral cross sensitisation:

  • Connection between different organs- ie pain experienced in uterus transmits pain signals to bowel so bloating pain occurs
92
Q

Sx of obturator internus pain?

A
  • Stabbing pain in ovaries/pelvis
  • Radiates to back/anterior thigh
  • Pain when walking/prolonged standing
  • Relieved fetal position
  • Exacerbated by core exercises
93
Q

What is central sensitisation?

A

Pain experienced that is persistant, then causes:

  • Allodynia (reduction in pain threshold)
  • Hyperalgesia ( increased response to painful stimuli)
  • Increased duration of response after stimulus ends

Neurotransmitters for central sensitisation and depression are very similar and centres for control of each are located closely to each other in the brain

94
Q

Mx of persistant pelvic pain

A
  • MDT approach
  • Medication: amitryptilline, gabapentin etc
  • PV lidocaine gel
  • Physio - stretches
  • Diet - FODMAP
  • Mx of urinary sx e.g. drink 1.5L water a day
  • Psychology/relaxation/mindfulness
  • Pelvic floor botox for refractory cases
  • Sleep hygiene
  • CBT
95
Q

Symptoms suggestive of endometriosis?

A

1 or more of:

  • Dysmenorrhoea affecting QoL/work/social activities
  • Persistent pelvic pain
  • Deep dyspareunia
  • Period related or cyclical gastrointestinal or urinary sx
  • Infertility with 1 of above
96
Q

What may you find on vaginal examination in a patient with endometriosis?

A
  • Hypertonic pelvic floor
  • Tenderness
  • Tethering of the pelvic floor resulting in reduced mobility
  • Palpable plaques/nodules or areas of thickening (particularly posteriorly and over uterosacrals)
  • Fixed, enlarged ovarian masses
  • Visible vaginal lesions on speculum
97
Q

Summary on complementary medications for the treatment of endo

A
  • Accupuncture: insufficient evidence and pts have to pay
  • Melatonin: low quality evidence, high dose of melatonin, may have imrpoved pain but adverse outcomes weren’t reported
  • PEA: poor quality evidence with high risk of bias. May have potential for harm.

Summary:

  • Complementary medicine could be considered as an adjunct but not replacement for standard therapy
  • Consider impact of herbal/naturopath medication if trying to fall pregnant
  • No good quality data to support use
98
Q

What is the theory of mullerianosis?

A

– defects of embryogenesis
– aberrant differentiation or migration of the Müllerian
ducts causing spreading of cells or tracts of cells in the migratory pathway of foetal organogenesis
- leaving endometrial like glands/stroma outside uterus

General Gynaecology (16 decks)

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