Gynaecological Conditions

Question 1

What is hyperemesis gravidarum? (HG)How does it come about?

Answer 1

1 in 750 women. Most: moderate NV of pregnancy- (NVP)
Xs N+ vomitting in early pregnancy so severe to cause & severe dehydration, wt loss or electrolyte distrurbances.
Aetio: asc w/ ⬆️ levels of hCG.
assc w/ ketosis

Question 2

RF for hyperemesis gravidarum?

How would u recognise it from the Hx and O/E?

Answer 2

Multiple /molar pregnancies, gestational trophoblastic disease, previous HG, ⬆️BMI, nulliparity, ⬇️maternal age, hyperthyroidism. UTI.
1% of women.
Hx: severe N+V, anorexia, wt loss.
O/E : general; signs of dehydration: dry mucous membranes, tachycardia, postural hypertension.

Question 3

How would u investihate HG,?

Answer 3

Urine: asses degree of ketosis, exclude UTI (RF)
Bloods: FBC(haemoconcentration) , U&Es, LFTs, TFTs
USS: exclude multiple pregnancy and gestational trophoblastic disease

Question 4

How would u manage HG?

Answer 4

Admit, rehydrade IV (normal saline) -dextrose contraindicated (Hartman’s) + antiemetics - cyclizine, prochlorperazine, metaclopramide.
Ondasteron + PO thiamine (to prevent neuro complications of vit depletion–> Werinkes Encephalopathy)
Consider thrombophylaxis.
Severe: steroids; prednisolone., total parenteral care-rare
Psychological support- emotional/ social probs.

Question 5

What are some complications of HG?

Answer 5

Mallory-Weiss Tear, Werinke’s Wncephalopathy (thiamine deficiency) , muscle wasting, VTE (dehydration) , electrolyte disturbance, renal impairment.

Prognosis: complications rare w/ appreciate treatment.

Question 6

Whats gestational trophoblastic disease?GTD.

Answer 6

Trophoblastic tissue( part of blastocyst that invades endometrium) –> more aggresive- HCG ⬆️⬆️, can also be choriocarcinoma.
O/E- uterus large, pre-eclampsia & hyperthyroidism.
Hx vajj bleeding + may be heavy. Hyperemesis
Routine USS- detected.
“Snowstorm appearance”. Diagnosis- histologically.

Question 7

How do u manage GTD?

Answer 7

Trophoblastic tissue suctioned out by suction curettage- ERPC + diagnosis confirmed histologically.

Question 8

What are some complications of GTD,??

Answer 8

Recurrence of molar pregnancies.

Question 9

What happens in diabetes in pregnancy? What are some associations/RFs?

Answer 9

Epidem: 2-5%, 90% of pregnancies.
Pre-existing or new onset diabetes- gestational.
Aetiology: pre-existing: type1: F of pancreas to produce insulin. Type2: relative insulin deficiency assc w/ ⬆️ peripheral insulin resistance.
Gestational DM: altered glucose tolerance in pregnancy.
Assc:
⬆️ maternal age, ethnicity: S. Asian, middle eastern, afro-Caribbean)
Obesity, smoking, PCOS( polycystic ovarian syndrome) , FHx, previous macrosomic baby.

Question 10

What findings are there on Hx and O/E?

for GDM?

Answer 10

Hx: pre-existing- known to mother
GDM: asymptomatic, detected on scan.
Abdo: fundal height (macrosomia/ polyhydraminos)

Question 11

Whats the pathophysiology of GDM?

Answer 11

Type1: autoimmune destruction of pancreatic islet cells
Type 2: genetic component + i fluence of age+ obesity on peripheral insulin resistance.
GDM: ⬆️ insulin resistance in pregnancy (⬆️ secretion of insulin antagonists, including HPL-human placental lactogen- glucagon + cortisol, altered carbs metabolism, Failure of normal pregnancy incease in insulin production.
Fetus: hyperglycemia in early pregnancy may affect development- cong. abn. Hyperglycemia causes fetal hyperinsulinaemia + macrosomia.
Neonatal: hypoglycaemia- withdrawal of maternal glucose while fetal insulin high- ⬆️⬆️ insulin secretion since maternal glucose passes through placenta- fetus tries to compensate and store the extra glucose.

Question 12

How would u investigate GDM?

Answer 12

Delivery: aim for delivery-38 weeks- sliding scale in labour
Pre-existing: detailed anomaly scan, fetal cardiac scan, opthalmic examination.
GDM: screening(universal or selective) Glucose tolerance test at 26-28/40 weeks.

Question 13

How would you manage diabetes in pregnancy?

Answer 13

Pre-existing: preconceptual: optimisation of glucose control.
Medical: optimise diet, consider converting oral hypoglycaemics to insulin. Likely to require incrasing doses of insulin.
Pregnancy: capillary blood glucose monitoring, monitor for pre-eclampsia, serial USS for fetal growth- macrosomia?
Delivery: sliding scale in labour
Postpartum: return to pre-pregnancy doses.

GDM:
Medical- diet control, persistent hyperglycemia may require insulin tx.
Pregnancy/delivery: as for pre-existing.
Postpartum: stop insulin after delivery. Fasting glucose 6/52 postpartum.

Question 14

What are some complications of Diabetes in pregnancy? Whats the prognosis?

Answer 14

Maternal: progression of pre-existing nephropathy/neuropathy/retinopathy, miscarriage, pre-eclampsia, operative delivery.
Fetus/neonate: congenital abn.(pre-existing only),fetal death, polyhydraminos, polycythaemia, macrosomia (+traumatic delivery) resp distress syndrome, neonatal hypoglycaemia, neonatal jaundice.

Prognosis:
Dependent on adequate control.
GDM: 70% occurance in further pregnancies.
⬆️40-60% risk for type 2 DM

Question 15

What happens in eclampsia?

Answer 15

Definition+ O/E :Grad-mal seizures on a backround of pre-eclampsia.
RF: pre-eclampsia
4.9 per10000 maternities. Postpartum more.
Hx: sx of impeding eclampsia: headache, epigastric tenderness, visual disturbance, oedema, hyperflexia, clonus.
Patho: unclear- cerebral vasospasm, hypertensive encephalopathy, tissue oedema, ischamia + Haemorrhage proposed.

Inv: as for pre-eclampsia: bloods: FBC, clotting, U&Es, urate, LFTs, G+S, consider ABG.
Urine: protrinuria??
Imaging: post-seizure: CT head, CXR if chest signs.

Question 16

How would u manage eclampsia? What are some complications?

Answer 16

ABC
Apply O2, maintain patency :NG tube? Ventilation
C: left tilt, large bore IV access, evaluate pulse and BP.
Drugs: IV MgSO4- monitor UO, patellar reflexes, resp rate.
Recurrent seizures: further magnesium sulphate, diazepam, IPPV- intermittent +ve pressure ventilation + muscle relaxation.
Post seizure: asses chest, control BP
Deliver baby when mum stabilised.

Compl: cardiac arrest, death, permanent CNS damage - cortical blindness, CVA- cerebrovascular accid, DIC- disseminated intravascular coagulopathy, renal F, ARDS.

Question 17

What happens in Pelvic Inflammatory disease ? (PID)

Answer 17

• inflammation and infex arising from endocervix leading to endometritie, salpingotis, oophoritis, pelvic peritonitis and tube-ovarian and pelvic abscesses.
  Chlamydia, gonococcoal infx common, bacterial vaginosis.
  Patho: infx ascends, fallopean tubes (FT) damaged. - inflm- destroys the cilia in FT- scarring of tubal lumen. - pocketing within lumen…- ectopic..
  Peritoneal inflammation: severe infx: mucopurulent discharge exudes through fibrial end of FT. –> scarring and adhesions b/w pelvic structures. –> omental adhesions..
  Perihepatic adhesions: fitz hugh curtis syndrome- violin string appearance at laparoscopy.

Question 18

What else could cause perihepatitis leading to adhesions b/w the liver and peritoneal structures?

Answer 18

Chlamydia and gonorrhoea

Question 19

SandS of PID

Answer 19

🔹Abdo, pelvic pain and dyspreunia,
🔹mucopurulent vajj discharge, pyrexia >38,
🔸heavy/ intermenstrual bleeding,
🔹pelvic tenderness and cervical excitation during examination,
🔹tender adnexal or palpable pelvic mass,
🔸generalised sepsis in severe + systemic infx,
🔹Tubal damage–> tubal occlusions, abscess and hydrosalpinx.

Question 20

How would u diagnose PID?

Answer 20

⬆️ WCC- neutrophilia- acute inflammatory D
⬇️ WCC- neutropenia- severe disease
⬆️ CRP/ESR
Adnexal mass on USs

Question 21

What is the gold standard for diagnosing PID?

Answer 21

Laparoscopy- mild cases might not be obvious-

Also exclude other causes of pain; appendicitis, endometriosis, ovarian cyst

Question 22

How would you treat PID?

When are people admitted?

Answer 22

Pregnancy test- ectopic !
Mild/ moderate- outpatient tx
1. Oral ofloxacin + metronidiazole
2. IM ceftriaxone(1) + oral doxacyclin + oral metronidiazole
3. Single IM caftriaxone + azithromycin.

Broader spec- PID+ chlamydia + gonorrhoea- triple Antibiotic therapy.
Hospitalisation + parenteralbtherapy
Admitted when:
Severe infx, adnexal mass suscpicious of abscess, generalised sepsis, poor respomse to tx,
Severevpelvic/ abdo pain requiring strong analgesics.

Question 23

Principles of tx of severe PID???

Answer 23

Supportive care, strict fluid balanace, parenteral Antibiotics:

1. Ceftiaxone IV/oral doxacyclin, + oral metronidiazole -24 hrs better–> switch to oral therapy for 14 days
2. Clinamycin IV 3 times a day+ gentamicin iv followed by clindamycin/ oral doxacyclin + oral metronidiazole for 14days.
3. Ofloxacin iv + metronidiazole iv 14 days.

In pregnancy: combo of cefotaxime + azithromycin + metronidiazole.

Surgical tx:
Ptx w/ pelcvic abscess / not responding to oral tx–> laparoscopy is warranted + used for exclusions.
Drainage of abscess + smts affected tube/ ovary might have to be removed.

Question 24

What antibiotics should be avoided in pregnancy? When PID?

Answer 24

Doxycyclin, gentamycin, oflaxicin,

Question 25

What should be included in pt counselling?

Answer 25

Partner + sexual contacts should be screened.
Risk of reinfx if partner not treated.
Barrier contraception used. ⬇️ risk of reinfx
Risk of tubal damage–> subfertility–> chronic pelvic pain, –> ⬆️ chances of ectopic.
Early + good tx will ⬇️ risk of subfertility.
If pregnant- early medical advice- might be ectopic

Question 26

What are bartholins cysts? What do the glands do?

Answer 26

Bartholins glands- resp for keeping vagina moist.
Blocked- abscess– can get infected.
If after 40, consider malignant cause.
Hx- rapid onset, days- hours. Labial oedema before swelling. If very painful- dyspareunia. If bursts- suddeen relief of pain.
O/E- wide gait, unilateral labial mass, if infected- inguinal nodes palpable,
Dx- swab from inside of cyst- usually commendals rather than pathogens.
Chlamydia, gonorrhoea, escheria coli(gut) + more than 1 organism.
DD- sebaceous cyst, >40Y vulval carcinoma, lipomata, STDs
Mx->40Y- excised- histology to exclude malignancy
Best- marsupialisation- local anaesthesia,
Ballon catheter can also be used.
If small and asymptomatic- conservative, no action
Antibiotics if culture not sterile, marsupialisation, last- remove gland.

Question 27

What could cause a vulval lump?

Answer 27

Local va icose veins, sebaceous cysts, 
Keratocanthomata(rare) 
Viral warts (condylomata, -vulval -acuminata-anal) 
Syphilis
Batholins cyst/abscess
Uterine prolapse/polyp
Inguinal hernia, 
Variocele, 
Carcinoma

Question 28

What are vulval warts? Could it be cancerous?

How are warts destroed?

Answer 28

Human paillopma virus (hpv) - usually - benign tumour- squamous cell papilloma-could be cause of cervical cancer
Spread by sex
Incubation: weeks- partner may not have obvious ones.
Types 16,18,33- vulval and cervicak intra-epithelial neoplasia–> needs annual cervical smears + vulva observation.
Warts may also cause anal carcinoma
Treat both partners, exclude other genital infx,
Mx- cryotherapy, diathermy or laser.
Vulval + anal– surgeries–> only a few warts at once- to avoid toxicity- 15% podophylin paint, washed off after 30mins (CI: pregnancy)
Podophyllotoxin cream- self applicable.

Question 29

Whats a urethral carnucle? How is it treated?

Answer 29

Small red swelling at urethral orfice.
Caused by meatal (foramen) prolapse
Tender + pain on micturition
Tx- excision or diathermy

Question 30

What happens in a bartholins cyst? What is it? How do u treat it?

Answer 30

Lie under labia minora
Secrete thin lubrication mucun during sexual excitation
Duct; blocked- painless cyst- if infected–> Extremely painful- cannot sit down- swollen red labia.
Tx- abscess is incised- permanent drainage ensured by marsupialization or ballon catheter
Tests- exclude gonococcus.

Question 31

How does marsupialization works?

Answer 31

Inner cyst wall is folded back and stiched to the skin

Question 32

What happens in vulvitis?

How do toI treat vulvitis?

Answer 32

Vulval inflammation due to candida, herpes simplex, chemicals (bubble baths, detergants, assc w/ vaginal discharge.

Management : depends on the cause
Antibiotics…

Question 33

What are some causes of vulval ulcers?

Answer 33

Always consider syphillis.
Xeroes simplex common in young.
Carcinoma
Chancroid
Lymphogranuloma,
Granuloma inguinale
TB
Bechet syndrome
Apthous ulcers
Crohns :(

Question 34

What happens in Hepres simplex?

Answer 34

Herpes 2 - sex aquired –> genital infx but type 1 transferred form cold sores- oral sex can be the cause.
Vulva is ulcerated and extremely painful
Urinary retention may occur
Tx: strong analgesia, lidocaine gel,
Salt baths & mictirating in bath
200mg aciclovir- ⬇️ symptoms and infectivity.

Question 35

Disease framework of the carcinoma of vulva

Answer 35

Refer unexplained vulval lumps urgently.
90% are squamous
Others: melanoma, basal cell carcinoma, or carcinoma of bartholins gland. Rare- elderly(70-80s)
Presentation: lump
Ulcer-unoticable unless painful or bleeding- so late.
Tx
If tumour1mm–> triple incision therapy- >15mm margin local excision, + ipsilateral inguinal node biopsy + if affected sample contralateral too.
More severe- radical vulvectomy- wide radical excision of the vulva + removal of ingunial nodes. Skin grafts may be needed.
Radiotherapy may be used pre op to shrink the tumours of sphincters may be affected.
Chemoradiation used if surgery unsuitable, to shrink large tumours preop, and for relapses.
5Y >80% with

Question 36

What epithelia make up the cervix? What part is usually affected by cancer?

Answer 36

Below internal os of uterus,
Endocervical canal- mucun columnal epithelium
Vaginal cervix- squamous epithelium
The squamo-columnar junction is predisposed to malignant change.

Question 37

Disease framework of cervical ectropion/erosion

Answer 37

Normal phenomenon
Red ring around os cz endocervical epithelim has exteneded its terriority over paler epithelium of ectocervix.
Ectropions extend temporarily under hormonal influence; puberty, combined bill, during pregnancy.
Columnar epithelium- soft and grandular- ectropuion soft to bleed, to Xs mucus production and infection.
Tx- cryoautery if nuisance - if bothering,

Question 38

What are the napothian cysts?

Answer 38

Mucus Retention cysts- harmless- cryocautery- instrument that destroys tissue by freezing.

Question 39

What are cervical polyps?

Answer 39

Penduculated benign tumours may cause mucus discharge and postcoital bleeding
Young- avulsed
OlderD D&C

Question 40

Why do we have cervical screening?

Answer 40

Carvical cancer has a pre- invaseve phase : cervicak intra-epithelial neoplasia (CIN)
Affects lower basal third of cervical epithelium
Assc with oncogenic HPV 6+11 commonly regresses (57%)
Papanicolaou smears- collect cervical cells for mocroscopy for dyskaryosis- abnormalities which reflect CIN
Smear identifies women who need cervical biopsy.- from squamous-columnar-transformation zone- special spatula- brush- junction
Degree of dysrkaryosis approx severity of CIN.
CIN III- 10Y.. Invasive carcinoma- faster in younger
1st-25 ,then every3Y till 49, 5Y from 50-64 .
Only screen after 65 if one of last 3 abnoramal.
HIV+ve annual smears.
Risk: older women, smoking, inner cities

Question 41

Uterine conditions:

Whats endometritis? What other parts can it infect? How does it present and how is it managed?

Answer 41

Uterine infx- uncommon unless barriers to ascending infx is broken break- acid vaginal pH + cervical mucus.
E.g after miscarriage, TOP, childbirth, IUCD insertion and surgery.
Can infect fallopean tubes and ovaries.
PC:
Lower abdo pain+ fever, uterine tenderness on bimanual palpation.
Low- grade infx usually due to chlamydia

Tests: cervical swabs and cultures
M: antibiotics: doxycycline w/ metronidiazole

Question 42

What happens and what stimulates endometrial proliferation?how does Dysfunctional uterine bleeding comes about?

Answer 42

Oestrogen stimulates endometrial proliferation in the first half of the menstrual cycle.
It is then influenced by progesterone and sheds away.
Exuberant proliferation- assc w/ HMB
Continuous high levels of oestrogen (anovulatory cycles) make endometrium hyperplastic- cystic grlandular hyperplasia after D&C. It eventually breaks down causeing irregular bleeding–> dysfuntional uterine bleeing (DUB)

Treatment: cyclical prog sterones

In older women- proliferation may contain foci of atypical cells which may lead to edometrial carcinoma

Question 43

Whats pyometra? How is it treated?

Answer 43

Uterus distended by pus assc w/ salpingitis or secondary to outflow blockage.
T: drain uterus, treat cause.

Question 44

Whats haematometra?

Answer 44

Uterus filled with blood due to outflow obstruction: rare.

Could be carcinoma, iatrogenic cervical stenosis eg after cone biopsy.

Question 45

How do we use the uterine ultrasound?

Answer 45

Transvaginal USS-better resolution than transabdominal.
Normal cycle thickness: 20mm, >5mm if post menopausal not on hormones.
Polyps should be

Question 46

What hapoens in vaginal carcinoma? How is it treated?

Answer 46

Squamous tumours, commonest in upper third of vagina.
Cervical carcinoma risk increasing x3
PC: bleeding
Spread is local and by lymphatics
Treatment:
Radiotherapy
Prognosis: 58%_ 5Y survival for squamous vaginal carcinoma.
34% for adenocarcinoma.

Question 47

What are uterine leiomyomata?

Answer 47

Fibrosus ds are benign smooth muscle tumours of the uterus (leiomyomas) .
Often multiple. They start as lumps on the uterine wall- and outgrow -bulge out of wall- lie under peritoneum( sunserosal, 20%) , or under the endometrium (submucosal, 5%) or become pendunculated.
Fibroids are common (20% ) of women and are increasing with age and in non-Caucasians.
Assc w/ renal cell cancer,
Natural history:
Fibroids are oestrogen-dependent, so they enlarge in pregnancy and on the combined pill and atrophy after menopause. They may degenerate gradually or suddently (red degeneration)
Occasionally they calcify- womb stones
Rarely they undearego saecomatous change- pain, malaises, bleeding, incrase in size in post menopausal women.

Question 48

How do fibroids present?

Answer 48

Many are asymptomatic.
🔹Menorrheagia- haevy and prolonged periods +- anaemia eg dysponea. They do not usually cause intermenstrual or post-menopausal bleeding.
🔹fertility probs- submucosal fibroids may interfere with implantation ‘natural IUCD’. Large or multiple tumours may cause a miscarry.
🔹Pain- due to torsion of penduculated fibroid -sx similar to that of torted ovarian cyst.’ Red degeneration following theombosis of the fibroid blood supply.
🔹Mass- large ones may he felt abdominally- if press on the bladder- frequency, or on the veins- causing oedematous legs and varicose veins.
Pelvic fbroids may cause obstruction of labour or cause retention of urine.

Question 49

How would you treat fibroids?

Answer 49

In many, no treatment needed.
🔸Menorrhagia - responds poorly to progesterons, anti-prostaglandins and danazol.
If uterus not too distoreted, a Mirena IUD may decreased their size.
If completed families- hysterectomy.
Younger ones- reversible menopausal state induced- LHRH- Lutenising hormome releasing hormone- goserelin, reduce fibroid bulk+ used pre-op.
Surgery- myomectomy- compl- torrential bleeding needing hysterectomy. Post-op adhesions.
Laparoscopic +- laser = patience.
Embolizing fibroids- interventional radiology) can shrink them, so resolving menorrhagia. Very painful.

Red degeneration- analgesia till sx settle.
Torsion- may present as an acute abdomen, requiring urgent surgery.

Question 50

Whats the treatment of choice in subfertility?

Answer 50

Myomectomy

Chance of succesful pregnancy better,

Question 51

Fibroids in pregnancy- what happens?

Answer 51

5-1000 Caucasians- commoner in Afro-Caribbean women.
May cause miscarriage, increase in size in pregnancy esp in 2nd trimester.
USS aids siagnosis.
Colour Doopler- distinguishes fibroids from myometrium.
Tx: of red degeneration
Bed rest, analgesia, expectant tx w/ resolution of 4-7 days.
If large: C/S
Obstruction of labour- aldo requires C/S.

Question 52

Whats red degeneration?

Answer 52

Is when thrombosis of capsular vessels is followed by venous engorgemend and inflammation causing abdo pain (+/- vomitting & low grade fever) and localised peritoneal tenderness- last half of pregnancybor pueperium.

Question 53

Whats endometriosis?
What causes it?
How does it present?

Answer 53

Foci of endothelial glandular tissue looking like burnt match, beyond the uterine cavity.
Eg on ovary- chocolate cyst- endometrioma, peritoneum, rectovaginal pouch, uterosacral ligaments, distand organs like lungs.
-10%?of women, 35-50% subfertility
Causes:
Cell rests,mretrofrade menstruation (sampsons theory- assc w/ age- typically 40-44Y), long duration of IUCD, tampon use
Neg assc w/ pregnancy and pill.
Genetic copmonents, environmental Nd autoimmune factors.
Endometriotic foci are under hormonal influence
Get smaller in pregnancy and not always in menopause.
Bleed during menstruation.
Free blood irritates , provoking fibrosis,adhesions and subfertility.

PC:
Asymptomatic or cyclical pelvic pains during periods.
Constant pain if adhesions
2o dyssmenhorroea and deep dyspareunia common.
May: thigh pain and defecation pain.
Or subfertility

Extra- pelvic endometriosis causes pain or bleeding at the time of menstruation at the side of pathology e.g. Haemothorax, haematuria.

Question 54

What hapoens if the focci are present in the myometrium?- uterine wall muscle.
Whats a typical presentation?

Answer 54

Adenomyosis

An enlarged boggy tender uterus is typical.

Question 55

What other differential diagnosis should we think of ALWAYS with endometriosis?

Answer 55

IBS

Question 56

How do you diagnose and treat endometriosis?

Answer 56

Per vaginum ; fixed retroverted uterus or uterosacral ligaments nodules and general tenderness.
💎 laparoscopy- differentiates it from chronic infx, reveals cysts, adhesions, peritoneal deposits.
Missed in adolescents.

Tx:
If asymptomatic don’t treat, join endometriosis society- tx long and difficult… (Mutual support helps)
Stress is a key exacerbating factors - key management.
If NSAIDS and analgesia fail try:
Hormonal therapy- supress menstruation 6-12 months till non GI lesions atrophy. ❌ if pregnant or lactating.
Combined pill helps some. If not worked/CI/SE, give :
progestogens–> oral: norethisterone
–> injected, or intrauterine (Mirena) - e.g if adenomyosis.
Danazol, or gonadorelin analogues- leuprorelin
Not for adolescents- ⬇️ bone density up to 13% loss
SE: premature menopause- flashings…
Give oestrogen back-up to protect bones.

Surgery/laparoscopy- excision, fulguration (destruction by electric current) or laser ablation or peritoneal endometrial implants. Endometrioma ans rectovaginal nodule removals reduce pain.
Alternative; total hysterectomy and bilateral salpingo-ooohrectomy (BSO) depending on lesion site+ fertility wishes.
Best if sx affect patients life
Relapses common, repeat surgery….

Question 57

What are some complications of endometriosis? Whats the prognosis?

Answer 57

Obstruction - GI, fallopean tubes, ureteric,
Assc with ovarian endometroid and clear cell cancers, Hodgkins lympoma and melanoma.
Prognosis:
Chronic or relapsing,
Being progressive in 50%
Surgery minimally helps fertility but is recommended by NICE….. So nice.

• encourage oprimism, discourage pssive dependancy, biofeedback
  ⬇️ endometriotic pain.

Question 58

What happens in a prolapse?

Answer 58

When weakness of the supporting structures allows the pelvic organs to sag within the vagina. Weakness may be congenital, but usually after stretching in childbirth.
Weakness exacerbated by coughing, straining and menopausal atrophy.
Distressing incontenece
No danger to health
Expect 3rd degree uterine prolapse with cytocele when ureteric obstruction may occur.

Question 59

What are the types of prolapses?

Answer 59

Cystocele- upper front wall of the vagina and the bladder attatched to it bulge. Residual urine within the cystocele may cause frequency amd dysuria.
Urethrocele- if lower anterior wall of vajj bulges, it will dispace the urethra- stress inconentence- does she leak when she laughs?
Rectocele- middle posterior wall- rectum- bulges through weak levator ani, often symptomless BUT 😔 may have to reduce herniation prior to defecation by putting a finger in the vagina or pressing the peritoneum.
Enterocele- bulges of the upper posterior wall of the vagina may contain loops of intesrime from the pouch of douglas.
Uterine prolapse-
1st degree- cervix stays in vagina
2nd degree- protruding from the introitus when standing or straining-
3rd degree- Procidentia- the uterine fundus lies outside the vagina . The vagina becomes keratinised and the cervix may ulcerate 😔

Question 60

What are some sx of prolapses?
How could one prevent that?
How would you treat a prolapse?

Answer 60

Dragging or something coming down is worse by day.
Cystitis, stress incontencne, pain on defectaion- dependent on type.
Examine vagina in left lateral position……with sims speculum
Tell pt to bear down to reveal prolapse
Do urodynamics studies to exclude detrusor overactivity and asses voiding.
Lower parity, better obstetric practises, pelvic floor exercises.

Tx:
Mild disease may improve with reduction in intra-abdominal pressure, somencourage her to lose weight, stop smokinh, and stop straining.
Muscle tone may improve with pgysiotheraoy or exercises.
If post-menopausal- topical estrogens eg estriol cream 0.1% twice weekly.
Estradiol vaginal tableys used weekly provide a less messy vaginal alternative.

Severe symptomatic prolapse- best treated surgically.
Incontinence- urodynamic studies
Repair operations excise reduntant tissue and strenghten support but reduce vaginal width- if sexually active- must compromise between reducing prolapse and maintaining a width.
Hysterectomy- marked uterine prolapse
Ring pessaries
Sacroplopexy- mesh- post hysterectomy vault prolapse.
Cystocele- transvaginal mesh repair- ✔️ but 1Y stress imcontinence and serious operative complications.

Question 61

What happens in subfertility? What might cause it?

What would the initial management be?

Answer 61

Devastating for both partners
84% young couples- regular intercourse conceive within a yesr, 92% within 2 years.
Offer inv if trying >1Y or earlier if female >35Y, amenorrhoea, oligomenorrhoea, past PID.
Arrange counselling
Fertiliy decreases with age
Is she producing ova?(anovulation-21%)
Enough healthy sperm? (Male fx -24% )
Are ova and sperm meeting?(tubal cause (14%, hostile mucus 3%, sexual dysfunction 6%) .Aim for intercourse 3 times a week
Is the embryo implanting?
Idiopathic27%,
Endometriosis-6%_ laparoscopy helps

Initiam Mx
Takes 2 to be infertile- see both partener, (F -67% causes) advice to stop smoking and lose wt if BMI >29. Take folic acid from now. Reduce stress amd boosting wellbeing helps. —> so diet might help
Ask HER about : menstrual hx, previous pregnancies, any miscarry, contraception, drugs, pelvic infx, abdo surgery.

Ask HIM: puberty, previous fatherhood, previous surgery- hernias, bladder neck surgery, illness- veneral, adult mumps, drugs, alcohol, job- is he home at ovulation? Erectile probs-seen in 4%

Ask BOTH: mood, feeling about subfertility, technique, frequemcy, timing of intercourse, parenthood, previous tests.,

Question 62

How would u examine and investigate subfertility?

Answer 62

Check F general health and sexual development and examen abdomen pelvis. If male sperm abnormal- endocrine and penile abnormalities, varioceles, confirm 2 testes, whats his BMI? 30nmol/L–> indicative of ovulation
Day 5- FSH >10nmol/L – indicative of poor ovulation..ovarian failure?
Day 5 LH- for polycystic ovarian syndrome- TFS if symptomatic
Blood prolactin- if anovulation or galactorrhoea- if high may be due to prolactinoma- MRI brain and pituitary gland.

Serum analyisis. - volume, morphology, infiection,

Question 63

Subfertility-

What are some tetts of tubal patency?

Answer 63

Donor imsemination- kids want to know their fathers and be proud of them…

Screen for chlamydia first !

1. Hysterosalpingogram(contrast x-ray)
2. Laparoscopy with dye- pelvic organs visualised.

Tx:
-Azospermia- uresponsive to sx. A low sperm count might be improved by decreasing tobacco and alcohol.
-Probs with sperm deposition- erectile dysfunction) artificial imsemination usuing partners sperm- EWW
- hyperprolactinaemia- remove cause- eg pituitary microadenoma, drugs, until blood prolactin normal-!SE- nausea
Tubal problems-
Surgery may sometimes help, proximal blocks- tubal catheterisation, hysteroscopic cannulation.
-endometriosis- if amenorrghagic with intrauterine adhesions , use hysteroscopic adhesiolysis.

Question 64

How would you treat anovulation?

Answer 64

WHO
Class 1- hypothalamic pituitary failure- GnRH &LHRH
Class 2- hypothalamoc pituitary dysfunction- usually polycystic ovarian syndrome (POS) - stimulate follicle development- with clofimene- SE- flushing, abdo pain, visual disturbance.
!! Warn risk bout mulriple pregnancy, excess risk of ovarian cancer,-
Monitor with luteal phasw progesterone. + USS
If still no ovulation try gonadotrophins.

Class 3- ovarian failure- tx is IVF using donated ova.