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Year 4 - Obs and Gynae > Gynae > Flashcards

Gynae Flashcards

1
Q

What are some causes of HMB?

A

PALM COIEIN

PALM: Structural causes

  • Polyp
  • Adenymyosis
  • Leimyosis (fibroid)
  • Malignancy + hyperplasia

COEIN

  • Coagulatopathy
  • Ovulatory dysfunction
  • Endometrial
  • Iatrogenic
  • Not yet classifed
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2
Q

What are some of the causes of HMB/ AUB?

A
  • Pathology: Fibroids, Adenomyosis / endometriosis, IUCD, PID, Polyps
  • Medical disorders: Hypothyroidism, Liver disease
  • Abnormal clotting: von Willebrand’s, thrombocytopenia, platelet disorders, coagulation disorders, leukaemia.
  • Other: Cancer/hyperplasia
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3
Q

How can HMB be managed?

A
  • Medical
    • Symptomatic: tranexamic acid, mefanamic acid
    • Fibroids: GnRH analogues e.g. goserelin, ulipristal acetate
    • Hormonal: POP, LARC: mirena IUS, implant, depo provera, COCP
  • Surgical
    • Polyps: hysterocopic removal of polyps (myosure), myomectomy, uterine a. embolisation, endometrial ablation, hysterectomy
  • short term control: norethisterone, GnRH analogues
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4
Q

What are some of the causes of 1o +2o amenorrhoea?

A

Primary: delayed puberty, obstructive issues: imperforate hymen, transverse septum, Müllerian a genesis (no uterus), Turner syndrome (gonadal dysgenesis), PCOS (less common in primary)

Secondary: Prolactinoma, Thyroid disease Cushing’s, Eating disorder, Exercise induced, Asherman Syndrome, Sheehan Syndrome

  • Physiological: prepubertal, pregnancy, menopause
  • Cryptomenorrhea:
    • Haematocolpos: vagina is pooled with menstrual blood due to multiple factors
    • Haematometra: retention of blood in the uterus. Causes: imperforate hymen or transverse vaginal septum
  • Uterine, ovarian failure, hypothalmic
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5
Q

What ix are used for 1o + 2o amenorrhea?

A

+ USS FOR PCOS

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6
Q

How do tranexemic acid + mefanamic acid work?

A

Tranexamic Acid: Antifibrinolytic

  • Inhibit plasminogen activation (inhibit tPA, and uPA), thus reduce fibrinoysis
  • Reduces MBL by 50%
  • Side effects: Nausea, dizziness, tinnitus, rash, abdominal cramp
  • Low incidence of thrombotic disorders

Mefanamic: NSAID

  • Inhibit the production of PG and inhibit the binding of PGE2 to its receptor
  • Reduces MBL by 20-44.5%
  • Side effects: gastrointestinal (50%) usually mild. Dizziness and headaches 20%, deranged liver function, asthma, renal disease.
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7
Q

How would u clinically examine/ investigate someone with HMB?

A
  • Examination: abdominal palpation, speculum and bimanual examination
    • Assess for: pallor, palpable uterus/ pelvic mass
    • Smooth or irregular uterus (fibroids)
    • Tender uterus/ cervical excitation – adenomyosis/ endometriosis
    • Inflamed cervix/ cervical polyp/ tumour
    • Vag tumour
  • Ix: FBC, coagulation disorders (vWB)
    • Hysteroscopy may be needed + biopsy (endometrial - >45 and failure of treatment)
    • Imaging: pelvic US, If a woman declines transvaginal US, consider transabdominal ultrasound or MRI
    • Other not routine: TFTs (hypothyroidism); hormones (PCOS)
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8
Q

What is 1o + 2o amenorrhoea?

A
  • Primary: No menarche by age 16
  • Secondary: absent period for 3/12 cycles if cycles previously regular. Absent periods for at least 6/12 if previously had oligomenrrhoa
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9
Q

What is oligomenorrhea + some of its causes?

A
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10
Q

What are the features of male vs female anovulation in terms of history, examination, investigations and mx?

A
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11
Q

What is PCOS?

A
  • Heterogenous endocrine disorder with unknown aetiology
  • Familial clustering
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12
Q

What are the features and sx of PCOS?

A
  • Features: hyperandrogenism: acne, hirsutism, obesity, chronic pelvic pain, depression, oligo/amenorrhoea
  • On examination: hirtuism, acne, acne, acanthosis nigricans (darkened skin, which occurs secondary to insulin resistance), male pattern hair-loss, obesity and/or hypertension.
    • Multiple ovarian follicles on USS (12 or more in one or both ovaries)
    • Increased ovarian volume > 10cm3
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13
Q

How is PCOS diagnosed (criteria)?

A

Diagnosis: Rotterdam criteria:two out of three features must be present

  1. Clinical or biochemical signs of hyperandrogenism
  2. Oligo amenorrhoea
  3. USS features of polycystic ovaries
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14
Q

What are the Ix for PCOS?

A
  • Ix: sex binding globulin (↓), total testosterone (↑), free androgen Index (FAI), FSH (normal), LH (↑), TFT prolactin, progesterone (↓),
    • Other: glucose tolerance test
    • Imaging: USS - peripheral ovarian follicles and ovarian volume >10cm
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15
Q

How is PCOS managed?

A
  • Conservative: weight loss, encourage healthy lifestyle; assess mental wellbeing and refer appropriately, fertility assessment and referrals
  • Medical – depends on needs
  • Wants regular periods: COCP + Cyclical progestogens (dydrogesterone)
  • Obesity: orlistat - (pancreatic lipase inhibitor)
  • Infertility: reduce BMI, folic acid, baseline fertility assessment and referral to fertility services, possible ovarian induction
    • 1st line: Clomifene +/- metformin – controversial – SE: increased risk of multiple pregnancies, ovarian hyperstimulation syndrome and ovarian cancer (so it is limited to use in 6 cycles).
    • Laparoscopic ovarian drilling: if BMI normal
  • Acne and Hirsutism: COCP
    • Anti-androgen medication such as cyproterone, spironolactone or finasteride.
    • Eflornithine is a topical cream that can also be used to help reduce the growth rate of facial hair.
    • Treatment for acne - retinoids, antibiotics etc as per dermatology
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16
Q

What are the complications of PCOS?

A
  • Metabolic disorders – impaired glucose tolerance and T2DM, CVS, obstructive sleep apnoea
  • Gynae: infertility, recurrent miscarriage, pregnancy complications (pre eclampsia and gestational diabetes
  • Endometrial cancer
  • Psychological disorders: anxiety + depression
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17
Q

What is the definition of oligomenorrhoea and its causes?

A
  • Infrequent periods
  • Cycle > 35 days but <6 months in length
    • Causes: constitutional, anovolution: PCOS, thyroid disease, prolactinoma,
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18
Q

What is the definition of secondary and primary amenorrhoea and its causes?

A
  • Primary: No menarche by age 16
    • ​​Causes: delayed puberty, obstructive issues: imperforate hymen, transverse septum, Müllerian a genesis (no uterus), Turner syndrome (gonadal dysgenesis), PCOS (less common in primary)
  • Secondary: absent period for 3/12 cycles if cycles previously regular.
    • Absent periods for at least 6/12 if previously had oligomenrrhoa
    • Causes: Prolactinoma, Thyroid disease Cushing’s, Eating disorder, Exercise induced, Asherman Syndrome, Sheehan Syndrome

Causes

  • Physiological: prepubertal, pregnancy, menopause
  • Cryptomenorrhea: menstruation occurs but is not visible due to obstruction of the outflow tract.
    • Haematocolpos: vagina is pooled with menstrual blood due to multiple factors
    • Haematometra: retention of blood in the uterus. Causes: imperforate hymen or transverse vaginal septum
  • Uterine, ovarian failure, hypothalmic
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19
Q

What is chronic pelvic pain?

A
  • Intermittent or constant pain in the lower abdomen or pelvis (sx and not a diagnosis)
  • At least 6 months in duration
  • Not occurring exclusively with menstruation or intercourse and not associated with pregnancy
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20
Q

What are some of the cause of Chronic Pelvic Pain

A
  • Causes: PID, adenomyosis, endometriosis, adhesions (residual ovary syndrome and trapped ovarian syndrome), IBS, interstitial cystitis
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21
Q

What is the pathophysiology of chronic pelvic pain?

A
  • Acute pain - resolve when tissue heals
  • Chronic pain - additional factors contribute hence pain persist longer
    • Local factors at the site of pain - chemokines and TNF ⍺ affect peripheral nerves
  • Central nervous system response - persistent pain lead to changes within the central nervous system which eventually magnify the original signal.
  • Visceral hyperalgesia - Alteration in visceral sensation and function
  • Pelvic pain can be multifactorial
    • IBS or endometriosis, adenomyosis MSK, PID, Interstitial cystitis, adhesions (intraabdo), social and psychological factors
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22
Q

What investigations are important for chronic pelvic pain?

A
  • History and examination
  • Bloods, CA125; STI screening: Chlamydia trachomatis and gonorrhoea, should be taken if there is any suspicion of pelvic inflammatory disease (PID).
  • Imaging: TVS, MRI. Gold standard: Diagnostic laparoscopy
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23
Q

What is endometriosis?

A
  • Presence of endometrial glands and stroma like lesions outside of the uterus
  • Predominantly found in the pelvis: can occur in the ovaries, pouch of Douglas, uterosacral ligaments, pelvic peritoneum, bladder, umbilicus and lungs.
  • Peritoneal lesions, superficial implants or cysts (chocolate cysts) on the ovary, or deep infiltrating
  • Responds to cyclical hormonal changes and bleeds at menstruation
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24
Q

What are some of the RFs for endometriosis?

A
  • Early menarche
  • FH of endometriosis
  • Short menstrual cycles
  • Long duration of menstrual bleeding
  • Heavy menstrual bleeding
  • Defects in the uterus or fallopian tubes
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25
Q

How does endometriosis present?

A
  • Painful periods (dysmenorrhea),
  • Painful intercourse (dyspareunia),
  • Painful defecation (dyschezia) and
  • Painful urination (dysuria)
  • HMB
  • Lower abdominal pain persistent
  • IMB and PCB
  • Epistaxes , rectal bleeding
  • Little correlation between symptom severity and disease severity
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26
Q

What are some of the clinical fx found on examination for endometriosis?

A
  • NAD
  • Thickened uterosacral ligaments
  • Adnexal masses
  • Fixed retroverted uterus
  • Uterine/ovarian enlargement
  • Forniceal tenderness
  • Uterine tenderness
  • Speculum: may show visible lesions in vagina or cervix (rare)
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27
Q
  • What are some of the visible features of endometriosis on laparoscopy?
A
  • Powder burn depsoits
  • Red flame hamorrhaghes
  • Scarring
  • Peritoneal defects
28
Q

What are some of the Ix used for endometriosis?

A
  • TVS – for ovarian cysts but useless for identifying other parameters of disease
    • Bowel involvement: MRI, CA125 (raised but not used as a screening tool)
    • Gold standard: laparoscopy with biopsy – important for diagnosis of infiltrating lesions and should be avoided within 3 months of hormonal therapy due to under diagnosis
29
Q

How is endometriosis managed?

A
  • Management: cure after treatment not guaranteed,
    • Treatment depends on: fertility issues, type and severity of symptoms, therapies tried and failed
    • 1st: NSAIDs + paracetemol
    • Medical: Hormonal medical therapies that suppress ovulation:
      • COCP, continuous progrestogen therapy MPA.
      • 3rd: GnRH analogues (nasal spray, implants) +/- HRT
      • Danazol, mefenamic acid/ tranexamic acid
    • 4th: Surgical: laparoscopic – diathermy, laser ablation, excision
      • TAH + BSO: risk of bladder, ureteric bowel injury, subtotal hysterectomy, role of HRT – either open or lap
30
Q

What is adenomyosis?

A
  • Presence of endometrial tissue within the myometrium of the uterus
  • Thought to occur when the endometrial stroma (connective/supporting tissue) is allowed to communicate with the underlying myometrium after uterine damage. Can occur in:
    • Pregnancy and childbirth, previous C section
    • Uterine surgery (e.g endometrial curettage)
    • Surgical management of miscarriage or termination of pregnancy
31
Q

What is the aetiology of adenomyosis?

A
  1. Retrograde menstruation (Sampson’s theory)
  2. Coelomic metaplasia (Meyer’s theory)
  3. Müllerian remnants
32
Q

What are some of the RFs for adenomyosis?

A
  • High parity
  • Uterine surgery
  • Previous C-section caesarean section
  • Hereditary
33
Q

What are the investigations for adenomyosis and what can be seen on examination?

A
  • Symmetrically enlarged tender uterus may be palpable.
  • Ix:
    • TVS:
      • Globular uterine configuration
      • Poor definition of the endometrial-myometrial interface
      • Myometrial anterior-posterior asymmetry
      • Intramyometrial cysts and a heterogeneous myometrial echo texture.
    • MRI – shows an ‘endo–myometrial junctional zone’
34
Q

By what aetiology are adenomyosis and endometriosis thought to arise?

A
  1. Mullerian remnants
  2. Retrograde menstruation - Sampson theory
  3. Coloemic metaplasia - Meyers theory
35
Q

What are some of the causes of pelvic pain adhesions?

How can these be managed

A
  • Vascular adhesions
  • Residual ovary syndrome – ovary or component of ovary which cannot be removed. E.g. hysterectomy but the ovary was left
  • Trapped ovary syndrome

Management

  • Medical: GnRH agonists
  • Surgery: division of vascular adhesions, removal of residual ovaries
36
Q

Another cause of chronic pelvic pain is IBS. What diagnostic criterias are required for IBS to be diagnosed?

A
  • ROME III CRITERIA-THE DIAGNOSIS OF IBS
  • Continuous or recurrent abdominal pain or discomfort on at least 3 days a month in the last 3 months
  • Onset at least 6 months previously
  • Associated with at least two of the following:
    • Improvement** with **defecation
    • Onset associated with a change in frequency of stool
    • Onset associated with a change in the form of stool.
37
Q

What is PID? How is it caused?

A
  • Infection of the upper genital tract. Many cases go undetected due to lack of symptoms so difficult to ascertain
  • Causes: ascending infection from endocervix: STI: chlamydia and gonorrhoea
    • Uterine instrumentation (e.g. hysteroscopy), IUCD insertion, TOP
    • Post partum
38
Q

What organisms commonly cause PID?

A
  • Chlamdydia: 14-35% of causes. 10-20% untreated infections -> PID
    • 10% of women with untreated chlamydia may develop PID within 12 months of infection
    • Risk increases with subsequent infections – hypersensitivity response
  • Gonorrhoea
    • 10-19% of infections -> PID
  • Gardnerella vaginalis/ anaerobes (prevotella, atopobium, leptotrichia) – more common in older women
  • Mycoplama genitalium/ mycoplasma hominis
39
Q

What are some of the long term complications of PID?

A
  • Ectopic pregnancy
  • Chronic pelvic pain (due to adhesions)
  • Tubo ovarian abscess (more common with NG)
    • Fitz hugh Curtis syndrome: RUQ, perihepatitis, more commonly associated with chlamydia PID
      • Violin string adhesions in peritoneal cavity and attach themselves to liver capsule inflammation with perihepatic adhesions
    • Subfertility from tubal blockage
40
Q

What are the RFs for PID?

A
  • young age <25
  • Previous PID
  • TOP/ miscarriage
  • STI: chlamydia, gonorrhoea
  • Coil insertion
  • Douching (increased risk of BV)
  • New sexual partner
  • Instrumentation of uterus
  • Hx of multiple partners
41
Q

What are some of the symptoms of PID?

A
  • Lower abdo pain (bilateral)
  • Deep dyspareunia
  • Abnormal PV discharge (purulent)
  • Abnormal vaginal bleeding: IMB or PCB.
    • Fever + chills – gonococcal
    • ASSYMPTOMATIC
42
Q

What are some of the signs of PID?

A
  • Lower abdo tenderness (bilateral)
  • Speculum: abnormal/ purulent vaginal disrhcage,
    • Cervical motion tenderness
    • Bilateral adnexal tenderness + mass (if tubo ovarian abscess)
    • Fever 38
    • When taking swabs: Contact bleeding from cervix (cervicitis)
43
Q

What are some of the differentials for PID and what is most important to rule out?

What Ix would you use to do this?

A
  • Ectopic pregnancy: pregnancy test
  • GI: IBD, IBS, appendicits
  • Endometriosis
  • UTI: cystitis
44
Q

How would you investigate PID?

A
  • Bloods: elevated WCC, CRP, ESR
  • STI screening: NG, CT, MG, BV
  • Gram stain microscopy
  • Imaging (limited use):
    • USS:hydrosalpinx/ free fluid/ abscess
    • MRI/ CT
    • Laparoscopy
45
Q

How is PID managed?

A
  • C: rest, analgesia
  • Admit if: if temp >38), admit + observe I severe disease, pregnant or suspected tubo ovarian abscess.
  • M: Broad spectrum abx: (OP regimen)
    • 500mg IM Ceftriaxone
    • 100mg Doxycyline BD PO 14 days
    • 400mg Metranidazole BD PO 14 days
  • IP regimen - cont’d till 24h post improvement then switch to oral
    • IV Ceftriazone 2g OD
    • IV doxycycline 100mg BD
  • Surg: lap draiange +/- division of adhesions
46
Q

What are fibroids?

A
  • Benign smooth muscle tumours arising from the uterus Their production is oestrogen dependent
  • They are the most common benign tumour in women of reproductive age (20-40%)
  • Risk of malignancy is v. low (<0.1%)
47
Q

What are the different types of fibroids?

A
  • Intramural - most common
  • Submucosal - develops immediately underneath the endometrium of the uterus, and protrudes into the uterine cavity.
  • Subserosal - protrudes into and distort the serosal (outer) surface of the uterus. They may be pedunculated (on a stalk).
48
Q

What are some of the RFs of fibroids?

A
  • Increasing age
  • Obesity
  • Early menarche
  • FH
  • Ethnicity - more common in african americans
49
Q

What are some of the symptoms of fibroids?

What are the features of examination?

A
  • Menorrhagia (>7 days) - PMB and IMB is rare
  • Dyspareunia
  • Lower abdominal pain
  • Acute pelvic pain - worse during menstruation
  • Feeling of abdominal fullness - distension, pressure sx
  • Subfertility
50
Q

What are the features of fibroids on examination and what investigations are used?

A
  • Examination: Non tender solid mass or enlarged uterus
  • Ix: hysteroscopy
  • USS
  • Pelvic MRI - rare. Usually used pre surgically only
51
Q

How are fibroids managed?

A
52
Q

What are some of the complications of fibroids?

A
  • HMB, iron deficiency anaemia
  • Reduced fertility
  • Pregnancy complications: miscarriages, premature labour and obstructive delivery
  • Constipation, Urinary outflow obstruction and UTIs
  • Red degeneration of the fibroid - ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply
  • Torsion of the fibroid, usually affecting pedunculated fibroids
  • Malignant change to a leiomyosarcoma is very rare (<1%)
53
Q

What is infertility?

A
  • Defined as the inability to conceive after 12 months of regular unprotected intercourse:
  • Prevalence is ~ 14% of couples
54
Q

What are some of the causes of infertility?

A
  • Tubal disease 20%
  • Male factors 30%
  • Ovulation defects 25%
  • Unexplained infertility 25%
  • Uterine factors
  • Endometriosis
55
Q

What are some of the primary causes of anovulation

A
  • Weight
  • PCOS
  • Hyperprolactinaemia
  • Ovarian failure
56
Q

What Ix are used for measuring incontinence?

A

Subjective

  • Diaries
  • Pad tests

Objective

  • Urinalysis
  • Ultrasound/IVP
  • Cystoscopy
  • Urodynamics
57
Q

What quantitative questionnaires are used for incontinence?

A

King’s Health Care

BFLUTs

IIQ & UDI

58
Q

What are some of the causes of incontinencne?

A

Urodynamic stress incontinence

Detrusor overactivity

Mixed incontinence

Other stuff

59
Q

Define urodynamic stress. incontinence and what is seen?

A
  • Incompetent urethral sphincter: childbirth, menopause, prolapse, chronic cough
  • Involuntary leakage of. urine on exertion, sneezing, coughing
  • Detrustor pressure > closing pressure of urethra
  • Positional displacement (most)
  • Intrinsic weakness (few)

Ix

  • Mobile bladder neck
  • May be prolapse: cystocoele, urethrocoele

Cystometry

  • Normal capacity bladder
  • leakage in absence of detrusor pressure rise
  • provoked by cough test
  • usually small to moderate loss
60
Q

Define what is seen in Detrusor overactivity?

A
  • Uncontrolled and unprovoked detrusor muscle activity - pressure generated exceeds sphincter tone
  • Often occurs in patients with a history of childhood UTIs
  • May occur as a new problem following incontinence surgery
  • Remember neurological disease

Findings: often little

  • may demonstrate leakage on coughing
  • Signs of NS involvement eg MS

Cystometry

  • reduced capacity bladder
  • leakage with detrusor pressure rise
  • often large loss
  • triggers include running water, washing hands
    *
61
Q

How is incontinence mxd?

A
62
Q

What needs to be offered before a TOP?

A
  • Offer counselling and support
  • Ultrasound – confirm gestation and identify non viable or ectopic pregnancies
  • Chlamydia + STI screening
  • Antibiotic prophylaxis- to reduce post op infection rate
    • Metronidazole 1g PR at TOP + azithromycin
  • Contraception – discuss – IUCD, sterilisation, pills
  • Bloods: Hb, ABO, Rh – d – anti D must be given, HIV, anti bodies, hep B+C, haemoglobinopathies
63
Q

What medications are used for TOP

A
64
Q

How is a TOP carried out?

A
  • <9 weeks: mifepristone (an anti-progestogen, often referred to as RU486) followed 48 hours later by prostaglandins (misoprostol) to stimulate uterine contractions
  • < 13 weeks: surgical dilation + suction of uterine contents
  • >15 weeks: surgical dilation + evacuation of uterine contents or late medical abortion (induces ‘mini-labour’)
65
Q

What is needed for TOP?

A
  • two registered medical practitioners must sign a legal document (in an emergency only one is needed)
  • only a registered medical practitioner can perform an abortion, which must be in a NHS hospital or licensed premise

Year 4 - Obs and Gynae (7 decks)

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