Obs and Gynae Flashcards
Abdo pain DDX in preggers and timing if known
Non Gyane
UTI Pyelonephritis Cholesystitis Appendicitis Pancreatitis Ligament strain Rectus sheath haematoma Gastroenteritis
Gynae
Miscarriage Pre Eclampsia Ovarian cyst rupture/ torsion Uterine torsion Uterine rupture T3 Fibroids T2 Abruption
Presentation of cholecystitis in preggers and management
Presentation Less likelly jaudice Pain, nausea and vomiting Diagnosis If appendicitis cannot be ruled out (presence of stone?) then lapaoroscopy Management Conserve Severe then lap chole - some risk of miscarriage/ pre term labour
Presentation, DDX adn Management of pyelonephritis in preggers
More common in congenital renal abnormalities, neuropathic bladder and stone Presentation Frequency Urgency May not have other symptoms May be severe with Tachy Vomiting Loin pain DDX Hyperemesis gravidarum Management Blood and urine culture IV cefuroxime (2nd) If septic - stat gentamicin
management of UTI in preggers
Management
Trimethaprim CI in T1
Nitrofluratoin CI in T3 (neonatal haemolytic anaemia)
Cefalexin (1st gen) first line
Argument for treasting asymptomatic bacteriuria due to risk of UTI
Follow up post cystiits with MSU to ensure resolution
Classical presentation of abruption adn complications
The triad Abdo pain Uterine rigidity Vaginal bleeding 1 in 200 preggers Comps DIC - high rate up to 50% PPH High fetal loss
Uterine perforation presentation
abdominal pain (may be vague) Tenderness (over scar) PV bleed (may be absent) Late T3/ Labour Signs Shock Maternal hypertension Cessation of contraction Dissapearence of presenting part of baby during labour Fetal distress (CTG) Post partum Failure of PPH to cease with well contracted uterus
Uterine perforation RFs
C section - scar pain
Obstruction
High foceps delivery - (CI above ischael spine)Internal version - manual turning via vagina
Obstructed in multiparous - especially if oxytocin used
Previous cervical/ uterine surgery
Breech extractaction
Management of uterine perforation
If in labour then cat 1 CS
High flow O2
Crossmatch 6 units and fast transfusion
Repair may be possible unless involves cervix or vagina in which case hysterectomy
Post op abx - cef and metro?
Uterine torsion patho
When it rotates >90 deg
Adrenax mass
Fibroids
Congential asymmetrical uterine anomalies
Uterine torsion presention
Mid to late preggers Abdo pain Shock Tenderness Urinary retention
Management of uterine torsion
Resus
Catheter ( may shows location of uterus)
Diagnostic lapaotomy
LSCS
Fibroids presentation in preggers
Abdo pain \+/- vomiting and low grade fever Localised peritoneal tenderness Last half of preggers or puerperium Large for dates
Fibroids pathophysiology and investigation in preg
RF Afro Carribean Increase in size during preggers/ T2 Investigation US Colour flow Doppler - Fibroids vs Myometrium Patho If pedunculated may become tort Red degendeation in 50% preggers= thrombosis of capsular vessels followed by venous enghorement and inflammation = pain
Fibroids management in preg
Bed rest and analgesia (resolution =4-7 days
Most in body so do not obstruct(tend to rise in preggers)
Obstructed = CS
OVarian torsio/ cyst rupture patho
x Uterine cysts are very common
>5cm troublesome unless symptomatic
Uterus growing raises and displaces ovaries
Venous return becoming oedematous eventually impeding arterial
Benign cyst presentation
Asymptomatic Chronic pain with full ache Irregular vaginal bleed Abdo swelling or mass (if malig then ascites) Unilateral iliac fossa pain
Presentation torsion/ rupture
Torsion = severe pain and vomiting
Improve over 24hr as ovary starts to due
Rupture = torsion symptoms with shock/ ?bleeding
Examination Adnexal mass Cervical excitation Bleeding/ discharge
Investigations of benign cysts
TVS Malignant (multilocaular cyst, wall projections, solid areas, mets, ascites, bilateral lesion Transabdo imagin ing if large >7cm then ?MRI Staging CT/ MRI
management of acute torsion/rupture
Acute pain
Urgent laparoscopy after TVS
Management of benign cysts
Pre menopausal Preserve fertility and exclude malig Nothing if <5 cm and non malig. Follow up Vs laparoscopy (avoid spilling) Post meno Risk of Malignancy Index Repeat TVS and CA125 to folow up every 4 months Bilater oophorectomy High risk = staging
Fibroids patho and natural history and RFs
Benign SM tumours, 20% of white and 50% of black women
Normally regress after menopause
RF
AfroCarribean
Age - response to puberty/ oestrogen
Fibroids Symptoms
may be asymptomatic
menorrhagia
lower abdominal pain: cramping pains, often during menstruation
bloating
urinary symptoms, e.g. frequency, may occur with larger fibroids
subfertility
Diagnosis fibroids
TV US
Management fibroids
Management
symptomatic management with a levonorgestrel-releasing intrauterine system is recommended by CKS first-line
other options include tranexamic acid, combined oral contraceptive pill etc
GnRH agonists may reduce the size of the fibroid but are typically useful for short-term treatment
Hot flushes
Osteoporosis
surgery is sometimes neede if >3cm/ distoring uterine cavity: myomectomy, hysterscopic endometrial ablation, hysterectomy
uterine artery embolization
GnRhH before surgery to shrink
Comps of fibroids
red degeneration - haemorrhage into tumour - commonly occurs during pregnancy
Presentaiton of endometrial hyperlasia
IMB
PMBMenorrhagia
Dysmenorrhea
Management of endometrial hyperplasia
Management Simple High dose prog every 3-4 months Levonorgestrel IUD Rebiopsy after 6-12months Atypia Hysterectomy with bilat salpingo oophorectomy (risk of malignant progression
Chronic pelvic pain cause
Physical: IBS, interstitial cystitis, Chronic infection e.g. PID, endometriosis/adenomyosis, Neuopathic pain form previous laproscopies.
Psychosexual: Depression, child abuse, Emotional problems, stress
Chronic pelivc pain management
Mnaagement
MDT
Consider GnRH analogie to supress ovaries if cylical, can predict outcome of hysterectomy
DDX Pelvic congestion/ migraines (treat with migrain treatment)
BIo Exploration of depressive symptoms - SSRI? Trial of GnRH anologue as pain is cyclical Psycho CBT Pain clinic referral Social Exercise Diet Cognitive methods e.g. meditation
If GnRH does not improve symptoms oophorectomy less likely to work. If not then could trial a neuropathic pain modifier e.g. amitryptilline before offering surgery
Pathology/ RF endometrial hyperplasia
Abnormal proliferation of endometrium in excess if norm
RF for endometrial cancer
Continuous ostrogen = RF
Obestity
Diagnosis of endometrial hyperplasia
Types - histology Simple Complex Simple atypical Foci of atypical that may lead to ca in older personsHR Complex atypical
Diagnosis Histological diagnosis
Miscarriage diagnoses
Threatened - bleeding and or pain and preggers
Likely to mischarriage
Closed cervix
Up to 24 weeks
Inevitable miscarriage
Open cervical Os even if viable preggers with fetal heart beat
POC may not be pased by inevitably will
Incomplete miscariage
Some POC have been passed
Tissues and blood clot remain within uterus
Cervix stays open
Complete miscarriage
Only say for fact if you have a scan prior showing a fetus
Cervix now closed
Resolution of symptoms
No strict USS diagnosis
CRL >7mm or gestational sac >25mm with no cardiac miscarriage is diagnostic of a miscarriage
Septic miscarriage
Infected
More likely if didnt present with miscarriage and incomplete occured with infection of POC
Rare if TOP is legal
Miscarriage US classoifed
Missed miscarriage/ early fetal demise#
(not recognised)
Failed preggers with no cardiac pulsitation on USS
Blighted ovum/ Anembryonic pregnancy
Failed preggers with empty gestation sac (previosly chorionic cavity identiyable at 3-5 weeks)
Incomplete miscarriage/ Retained products of conception
Echogenic mass of blood clot and tissue within the uterine cavity >20mm in AP diameter
Complete miscarriage
May be preggers of unknown location
Empty uterine cavity roughly <20mm AP
Must have seen IUP intrauterine preg or PUL preg unknow location
Causes of miscarriage
Chromosomal abnormality (most T1 = aneuploidy) Congenital abnormality Maternal disease (10% in T1) DM Acute illness Uterine anomalies Thrombophilia / APLS T2 =Cervical weakness, uterine abnormality or maternal disease, infection (CMV)
RFs miscarriage
Advancing maternal age 40 Previous miscarriage (3 = recurrent and threshold for investigation) Smoking Alchol (moderate to heavy) and drug use NSAIDs adn Aspirin Street drugs Folate def Consanguinity - cousins marrying DM
Conservative management missed Miscarriage
x Wait and watch
Usually POC pass over 2 weeks but can be longer
Step in after 2 weeks due to risk of infection
Must have 24hr access to gynae service
Adv
Avoid rsks
Can be at home
Disadv
Pain and bleeding can be unpredictable
Takes longer
May be unsuccessful
Unpredictable - may be sudden heavy bleeding
Medical management missed miscarriage
Day 1 :Mifepristone (antiprogesterone - like with CL causes shedding?).
Day 3: Misoprostol (prostaglandin) -
Adv
85% effective
Avoids surgery
Outpatient
Disadv
Pain and bleeding may be unpleasant and or severe
ADR drugs
Need for emergency surgical management (SERPC)
Moa Mifepristone
Blocks prog causing decidual degen (part of endometrium that forms placenta, cervical softening and dilation, release of prostglandings and increase sensitivity to contractile effect of prostaglandins. Decidual breakdown leads to trophoblack detachment, Decreased HCG and therefore Decrease progesterone from Corpus luteumx
MoA Misoprostol
causes contraction along with dilation and softening of cervix
Surgical management of miscarriage
Suction curette to empty uterus 5 minutes under GA Day case Physically normall after 24 hrs Bleeding 24 hrs... Disadv Harder to do after 12 weeks due to suction method Perforation, bowel bladder Damage to cervix Asherman's syndrome = severe pevic infection, adhesions which block menstruation, pain during ovulation/ menstruation Cervical weakness Anaesthetic risk
What is recurrent miscarriage
Loss of >=3 consecutive preggers with same partner
Causes of recurrent miscarriage and management brief
x Balanced (Robertsonian translocations)
Mother is phenotypically nomral btu 50-75% of games are unbalance
Refer to clinical geneticist
PIGD has LOWER rates of healthy pregnancy than natural conception
Uterine anomalies
E..g septum which can be removed
Increased risk of uterine rupture with hystroscopy
Antiphospholipid syndrome
Bacterial vaginosis and T2 loss
Thrombophilia e.g. Factor V Leiden mutation
Alloimmune causes (both parents have same HLA alleells so cant protect fetus)
Diagnosis of APLS
3 miscarraiges in 10 weeks
1 fetal loss >10 weeks
1 normal birth with severe PE or FGR
Management of APLS
x Give aspirin from day of prositive preggers test
Give LMWH from FHR seen
Monitor
Liver birth rate 80%
General management of recurrent miscarriage and investigation. outcome
Miscarriage clinic
Test for APLA
Thrombophilia screen
Pelvic US and consider further if abnormal
Karyotype fetal products in products of conception
75% achieve ongoing preggers with supportive care only
Diagnosis of PUL
No IU conception or ectopic on TVS but a positive preggers test
Cause of PUL
x Too small for TVS e.g. less skilled scanner
Complete miscarriage
Ectopic
Failing PUL (never seen but self resolveing)
Rare = HCG secreting tumour
Persistent PUL
Rare plateu of HCG without and trophoblastic seen on TVS or diagnostic laparoscopy or uterine currettage
Management PUL
HCG monitoring
>66% rise in 48hrs reassuring (should double). Rescan at HCG=1500 (predicted) or 2 weeks
<66% rise in 48hrs Monitor untill <15ui and contact senior
Flucuating HCG continue expectant management or offer methotrexate
Progesterone <20 suggests failing pregnancy, if asymptomatic repeat hCG in 7 days
Ectopic investigation
FBC, G&S (unless acute the cross match 6 units)
Urine PT
TVSbHCG
Serum progesterone
If not TVS then consider laparoscopy vs conservative
Location of most ectopics
Tubal (99) Ampullar (55) Fimbrial Less rare types e.g. Cornua Ovarian (0.5) Abdominal Cercival Uterine diverticulum, intramural, rudimentary horn - split off part due to Mallarian defect and bicornuate uterus (cornual)/ scar Heterotopic with IVF, ovuation induction. (ectopic and intrauterine together)
Risk factors for ectopic pregnancy
1/3 have no risk factors Previous ectopic Tubal surgery e.g. Sterilization or reversal Tubal pathology Previous PID/ endometrosis Preggers with Cu IUCD POP Tobacco smoking Previous ectopic
Presentation of ectopic preggers
Unilateral pain RIF/LIF Irregular PV spotting/ bleeding Fainting, dizziness (rupture) Shoulder tip pain GI symptoms N&V although usually not prominent with low bHCG
Management ectopics
Expectant - where HCG falling
Increasingly offered
24 hr access to gynae services
Medical
Criteria to meet
Methotrexate single dose
Follow up bHCG 25% need repeat MTX - 3 month contraception
Longer resolution and follow up, avoid preggers for 3-6/12 months
ADR: conjunctivitis, stomatitis, diarrhoea, abdo pain
Surgical
Laparoscopic/ laparotomy
Salpingectomy (removal)/ otomy (incision)
Ectomy If controlateral tube is patent
Salpingotomy more persistent trophoblast rates and subsequent ectopcs (if woman wants more and other tube damaged)
Follow up with HcG
Invasive tissues
If clinically unwell or patient unwell
Need to get all trophoblastc tissue to prevent re surgery
Criteria for conservative management and medical management
expectant management of an ectopic pregnancy can only be performed for
1) An unruptured embryo
2) <30mm in size
3) Have no heartbeat
4) Be asymptomatic
5) Have a B-hCG level of <200IU/L and declining
6) Understand risks and willing for regular follow up
Medical management of an ectopic pregnancy can only be performed for
1) An unruptured embryo
2) <30mm in size
3) Have no heartbeat
4) Be asymptomatic
5) Have a B-hCG level of <3000IU/L and declining
Understand risks and willing for regular follow up
What is gestational disease
A spectrum of disorders of trophoblastic development arising from abnormal fertilsation.
Types of mole
Potentially pre-malignant Hydratidiform Mole/ Molar pregnacy Complete mole - empty egg, 1sperm Benign Paritial mole (egg and 2 sperm) more common Triploid e.g. 69XXX Less malignant and slower growing
Maligant Invasive mole Choriocarcinoma
Mole features
Bleedingin in T1 or early T2 Exaggerated symptoms e.g. hyperemesis Uterus large for dates Very high hCG (mimic TSH) Hypertension and hyperthyroidism may be seen No pain/ Aysymptomatic
Management of a mole
SERPC
3 national GTD centres
Postal follow-up of serum and urine serial bHCG
Anti D
Contraception to avoid preggers in 12 months
Hyperemesis gravidum presentation (when)
Excessive nausea and vomiting in early pregnancy (although a very common in pregnancy and usually normal) Usually 6-12 weeks Dehydration Deranged bloods Ketosis Weight loss Nutritional deficiency Complications of all of above
Pathology of hyperemesis theories
Elevated HCG
More common in twin/molar preggers
Same alpha subunit TSH - linked to thyrotoxicosis
Elevated oestrogen/ progesterone
Helicobacter pylori - subclinical infection activitaed by altered immunity in preggers
Psychological
Difference in different pop and cultures
DIagnosis of hyperemesis
Hyperemesis gravidarum, diagnostic criteria triad:
5% pre-pregnancy weight loss
dehydration
electrolyte imbalance
DDX hyperemesis
Diagnosis of exlusion Normally no abso pain DDX infection UTI Gastroentertis Appendicitis Pancreatitis DDX metabolic Biochemical thyrotoxicosis Graves disease Addisons DKA Drugs Antibiotics, iron preps Tumours Hydratiform mole formation Choriocarcinoma Teratoma with elements of choriocarcinoma Germ cell tumours Islet cell tumour
Hyperemesis investigations
Urine PT Ketonria UTI Bloods FBC Haematocrit Ues K+ especially - Addisons and vomiting LFT and amylase TFT HCG USS exclude GTD/ multiple pregnacy
Hyperemesis complications
Wernicke’s encephalopathy
Mallory-Weiss tear
central pontine myelinolysis (Na? low)
Paralysis, dysphagia, dysarthria, neuro symptoms
acute tubular necrosis
fetal: small for gestational age, pre-term birth
Management hyperemesis
Rehydration - not with glucose as can precipitate Weernicke's, replace K Vitmains and nutrients Thiamine replacement and folic acid Vitamins B and C (Pabrinex) if Wernicke's enceph) Often cant tolerate oral Antiemetics Parenteral route initially Ranitidine Thromboprophylaxis Rarely Steroids - appetite stimulation TPN/ JEG Termination
Diagnosis of mole
Suspected on scan
Confirmed on histology only
6 week PV bleed history questions
Bleeding - how much and clots How many pads/ soaking etc Dizziness (from this) Spotting Gi symptoms Diarrhoea Rectal pressure (can get due to irritation from ectopic) Pain Shoulder tip pain
Preggers - may need to get parents or partner out LKMP Previous ectopic/miscarrage Planned unplanned unwanted PMHx - DM SH Consanguinous marriage Smoker Drugs
6 week PV bleed investigation
Bloods Coag clotting UE FBC Serum HCG Disrimminatory level >1500 Serial measurements- dobling time/rate of change Serum Prog >30 = likely viable or not Cautious on these predictions in early Blood group Rhesus status for surgey Imaging US scan Trans-abdominal (TA) Trans-vaginal (TV) Easier to see Free fluid = bleeding Urine Preggers test
Define abortion
Termination of pregnancy by the removal or expulsion from the uterus of a fetus or embryo prior to viability (24 weeks/20 weeks)
Complications of induced abortion public health worldwide
Comps worldwide Haemorrhage Infection DIC GA
Abortion law in UK
HSA 1 form must be signed by two doctors
Premises approved by secretary of state
Social abortion clause C & D - pregnancy <24 weeks unless fetal abnormality
Consent
16-18 can consent as young people
Less than 16 can consent to contraception/ including abortion
Competency as per Gillick case, can consent tomedicak treatment
Frasier allow medical practitioner to provide contraception advice <16. ensures confidentiality
Abortion proceedures <9 weeks
Early medical abortion (EMA) using mifepristone (antiprogesterone) + prostaglandin. Person signing is taking responsibility
Conventional suction TOP should be avoided (higher failure)
Earlier surgical abortion - manual vacuum aspiration (MVA), US guided/ checking falling HCG post abortion etc
Abortion proceedures 9-24 weeks
7-15 weeks
Early medical TOP (EMTOP) up to 9 preferred
Surgical preferred 9-15 via suction TOP
Cervical prep with prostaglandin is an option pror to surgery and routine for nulliparous women or >10 week with multiparous
Greater risk with high BMI
Medical abortion for 9-15 - may be pain/ bleeding for a few weeks but safe
>15/13 weeks
Surgical by D&E - dilation and excision receded by cervical prep
Beyond 18 is a 2 stage procedure
>21
Medical top with Urea and KCL prior
Induciton of labour with prostaglandins
Alternate medical methods
Cervagem (prostaglandin analogue) more expensive not used
Highly effective
Contra indications to medial abortion
Suspected ectopic prep Any risk of heavy bleeding Chronic renal failure Mifepristone -similar to aldosterone and electrolyte Hepatic falure (bleeding) Severe asthma or COAD CVD/ Prosthesis Long term steroids - electrolyte Allergy to Mifegyne (Mifepristone) Haemorrhagic disorders and treatment with anticoagulants
Complications of abortion
Low risk of haemorrhage, increases with weeks
4.5% get sepsis
Can give prophylactic abc
Uterine performation
Cervical tears
Dilated with prostagladin to prevent
And widened with dilator
Can tear wall causing bleeding or incontinence
Failure (<1%)
Post abortion Sepsis
Trauma during cervical dilatation and curettage
Fundal perforation with suction curette
Uterine perforation and suction of a loop of bowel
PReventions of complicaiton of abortion
Early referral within 5 weeks
Counselling for risk and options
Day care procedure if possible under LA
Patient info written and verban
Investigation: STI screenig, Rh factor, FBC, blood group, BBVs
US scan
Cervial priming for STOP with dilator - prostaglandin
Trained personal TOP
After care of surgical abortion
Anti D for Rh -ve
Abx propho - STI - metronidazole 1g rectally at time of abortion and doxy 100mg BD orally for 7 days or azythromycin 1g orally on day of abortion
Verbal and written info and comps and actions
No sex/ tampons for 2 weeks
Future contraceptive plans- prescribe where appropriate
Follow up 2 weeks
Contacts for physical and emotional help
Communication with appropriate health professionals
Describe rhythm method theory
Calender/ rhythm/ safe period 14 days fixed 7 days ovulation time Rhythm method (sperm survival of 7 days – ovulation on day 14-15) based on temp) Fertilie if sex between 8-19
Other “natural” contraceptions
Cervical mucus assessment BBT - temp Breast feeding 90% contraception in first 6 months Withdrawal Persona - LH surge Expensive and misleading
MoA COCP
1 ovulation suppression (primary)
2 penetration of Cx mucus
3 prevention of blastocyst implantation
Types of COCP
Phasic (fixed dose)
Biphasic
Triphasic
ED - 7 days of placebo pulls
CI COCP
Hypertension Migraine Smoker >35 History of Cerbro or CVD Breast cancer DM with retinopathy/ comp Severe cirrhosis Gallbladder disease History of OCP related cholestasis ? CYP modifiers
ADRs Oestrogen
Bloatedness, breast fullness leg cramps, headache, PV bleed, VTE, Migraines worse,
ADRs Progesteron
xIrritability, weight gain, hirtsuitism, irregular periods, premenstrual depression, low mood, low libido, breast tenderness
Beneftits of COCP
Less bleeding, regular, less anaemic, less dysmenorrhoea
Endometriosis - less pain, less dysperiunea
Premenstrual tension- less
PID - less risk
Fewer Ectopic pregers due to anovulation
Less benign breast disease
Less functional ovarian cyst
Ovarian, endometrial and colorectal Ca less
Long term health risks COCP
Increased risk of breast and cervical ca, VTE, stroke, IH
Other methods of oestrogen delivery as contraception
Patch Delay of 48hrs then barrier for 7 and consider emergency contraception NuvaRing (oestrogen ring) Lunelle injection monthly combined Lovelle vaginal combined pills
IUD time span, use and SE
Up to 10 yrs Above 40 can be longer and can leave Copper Licensed for emergency contraception and better Instant Primarily prevent fertilisation May also prevent implantation
Bleeding pattern change - heavier with copper Progesterone - risk of ovarian cysts increased Explosion PID Rare: uterine perforation
Nexplanon MoA, use, when is it effective
Releasing Etonogestron over 3 years
Ovulation suppression main
Takes 7 days
Effective imediately if <5 days inserted after period
Mirena use and when is it effective
Up to 5 yrs
20mg LNG / day
Not for emergency
Takes 7 days
MoA of oral levonorgestal emergency
Emergency Oral levonorgestrel 1.5mg stat
Anti ovulation
History regarding prenatal diangosis and why
Maternal age
Maternal disease
DM
First few weeks of control really important (6 weeks heart is formed)
Epilepsy
Medication esp in 1st trimester
Folic acid 5mg per day start from planning prior to birth
Previous obs history
Child with aneuploidy (abnormal number of chromo)
Genetic disorder
Structural abnormality
Consanguinity
Are you and your partner related?
Parent with known balanced translocation
Exposure in pregnancy-drug related malformations
Antiepileptics
Warfarin
Vit A - acne
Intrauterine infection
Rubella
CMV
Ask have you been unwell recently or travelled?
If seroconvert first time during pregnancy
Pass to embryo
May get long term sequelae (1-2%) e.g. Sensorineural defness or learning disability
Parvovirus
Zika
Recent travel
Maternal blood screen for prenatal dianosis
Haemoglobinopathy
Thalassaemia
Sickle cell disease
VDRL/ RPR screening - Venereal disease research laboratory
Syphilis
HIV, Hep B
AFP screening
Produced in fetal liver and small bowel
Raised level associated with open neural tube defect, gastroschisis (unlike exomphalos no peritoneum and not a herniation through umbilicus), cystic hygroma, congenital nephrosis, teratoma, fetal infection, oesophageal atresia, late preggers probs too
Maternal Rhesus antibody
Anti D at 28 and 32 offered for second pregges to prevent risk
Combined first trimester serum screening for Trisomy 21, 18 and 13
Look for free foetal DNA from blood system from October 2018
Describe Down’s screening - combined test
Combined test detects 75%, 3% FP
Uses NT, hCG and preg associated plasma protein a PAPA, woman’s age
11-13+6. Higher rates for trisomy 18 and 13
Other causes for raised nuchal lucency?
ystic hygroma (lymph sac in neck), cardiac malformations, thoracic compressive syndromes- congenital diaohragmatic hernia, congenital infections
Cut off for blood test for Down’s Screening
1 in 150 before further is offered
Dating scan purpose
ibilitity - HB
Accurate dating
Detection of fetal abnormalities
Anencephaly
Large anterior abdo wall defects
Cystic hygroma
Nuchal translucency
Twin determination and chorionicity
Cytocitiy
Zygocity - 2 completly split - monozygous same egg and sperm
2 sepearate egg and sperm then dizigous
Chorionicity = number of placentas
One egg and one sperm split, own membrane and own placenta
Dichorionic, diamniotic
monochorionic (one placenta) Diamniotic (2 sacs)
Most monozygotic twin preggers
Monochorionic, monoamniotic have high mortality due to cords getting twisted
Worst is when babies don’t separate = conjoined twins, higher mort
Can only tell chorionicity and amniocity on scan unless opposite sex or sharing placenta
Anomaly scan purpose
bility Measurements (growth) Liquor volume Fetal anatomy Placental location Previa - can cover internal os - life threatening bleed Assessment of normal variants/ soft markers for aneuploidy, renal-pelvic dilatation, choroid plexus cysts •nuchalfold •short femur •choroidplexus cysts •echogenic focus in heart •dilated renal pelvis •talipes equinovarus (club foot) Not perfect detection. CVD particularly low Normal shaped cerebellum 98% of spinal sbifida ruled out DM can have sacral probs Frontal bossing Absent nasal bone - downs Cleft lip Normal variants Nuchal fold >6mm Ventriculomegaly
When is amniocentesis performed? facts too
After 15 weeks gestation]
Under direct US
15-20ml using a 22G needle
Culture of amniocytes, harvesting and banding
Karyotyping p to 3 weeks
1% risk of miscarriage also preterm delivery and chronic liquor leak
Indications for amniocentesis
Assessment of fetal karyotupe if risk of Downs, USS findings, parental translocation, maternal request
Measurement of AFP and ACHE (being negative) - ?congenital nephrosis
Virology screen
PPROM (Preterm (<37week) prematuure rupture of membranes) to rule out chorioamnionitis
Loss of barrier so can get infected
OD 450 (amniotic bilirubin scan)-haemolytic disease
Use of Chorionic Villus Sampling, risks, when is it performed, how,
Results = 1 week, (can be 2 days) After 10 weeks ideally US guided TA or Tcervical 2 cell lines True mosaic or contamination
Risks of CVS
1% get mosaic result from placental mosacism Mum contamination (false positive) 1% risk of failure Transmission of BBV 1-2% Miscarriage
How to terminate >21
Painful
As part of procedure do KCl inject into heart
Distressing for parents if baby has signs of life
Induction of labour with prostaglandins preceded by fetocide after 22 weeks of gestation in many countries
PEG2 - Oxytocin after ROM
Explain PIGD
FISH analysis At 8 cell satage Indication Known parental translocation Increased age FH X linked recessive
Explain quadruple test
Quadruple test
16 weeks
Dating scan, AFP, unconjugated estriol, BHCG, inhibin A, womens age
15-20 weeks
Integrated test
Expensive
NT and PAPP-A in 1st then quaruple in 2nd
How long is a normal cycle
- Length 24-32 (not normal to be 28 every time over years)
* Regularity best between 20-40, longer after menarche, shorter pre-menopause
Normal cause for PCB and follow up
post coital bleed, normally cervix as lesions of vagina rare and epithelium thick. Check smears and lesion on cervix
Cause of menorrhagia
○ Abnormal clotting § Von Willebrands, thrombocytopenia, platelet disorders, coat disorder, leukaemia ○ Pathology § Fibroids (benign tumour of muscle § Adenomyosis/ endometriosis § IUCD - copper makes heavier § PID § Polyps -heavy ○ Metabolic/ Medical § Hypothyroid § Liver disease § SLE § Cancer Polyps/ pro contraception • DUB ○ 60% primary menorrhagia ○ Dysfunctional uterine bleeding ○ Diag by exclusion No recognisable pathology, preggers or general condition disorder
Risk factors for Menorrhagia
• Age 40_
• Correlation in twins - hereditary
• +Ve parity
Uterine pathology fibroid or endometrial abnormality, endometrial cancer in post menopausal
Brief history menorrhagia
History
How much
Clots Flooding
Subjective vs objective assessment
○ Only 50% with subjective menorrhagia have > normal loss
Only 60% of women with MBL >80ml consider their periods heavy
Investigations into menorrhagia
Hb TFTs and coag if needed Pregnancy test TVUS Investigations futher • Hysteroscopy +/- Biopsy • Cancer rare in menstruating but increases towards menopaus ○ Smear if due • Consider STI screen Subserous vs submucosal fibroid - more bleeding
Treatment of menorrhagia (with 1st 2nd and 3rd line)
- Tranexamic acid - antifibrinolytic (2nd or for baby)
- NSAID/ Fenamates (not in handbook)
○ Norethisterone (not in handbook)
○ Mirena-IUCD ○ Depot/ IM prog 3rd § Irreg bleeding ○ OCP 3rd • GnRH analogues
• Ulipristal acetate Surgical ○ Hysterectomy - dont need ovaries § Risks □ ○ Endometrial ablation § Resection § Roller ball § Laser - old § Cold coat § Microwave § Balloon- thermal current - common § Radio frequency (controlled thermal damage)- also common. 1-2mins
MoA and SE transexamic acid
x ○ Inhibit plasminogenhibition of tPA and uPA thus reduce fibronoylsis
○ Reduce 50% of MBL
○ Side effect nausea, dizziness, tinnitus, dont give to us of PE DVT etc
MoA and efficacy of NSAID/ Fenamate for menorrhagia
○ Inhibit PG and binding to PGE2
§ Reduce platelet aggregation
○ Reduce MBL by 20-44.5%
○ Pain killer too
Efficacy and ADR of Norethisterone for menorrhagia
§ No literal administration
§ 21/28 with a break reduce MBL
§ Nause, headache, bloated ness, weight weigh, skin rash, adverse on lipids, breast tenderness (think early prey symptoms/ last half)
Efficacy of Mirena IUCD for menorrhagia
1st line 80% reduction 3 months, 97% at 1 year) § 5 years § Major reduction in MBL § Some BTB (break through bleed( § Not increase ectopic or PID
GnRh analogue mOA and ADR
○ Large dose actually inhibits pit (after brief stimulation)
○ = menopause
○ Hot flushes, osteoporosis
○ Temporary?
Ulipristal acetate MoA and ADR
○ Prog antagonist
○ Help shrink fibroids and may help fibroids
○ Can grow back after
○ abdominal pain; acne; breast pain; dizziness; endometrial thickening; headache; hot flushes; hyperhidrosis; malaise; menstrual disturbances; myalgia; nausea; oedema; ovarian cyst (including rupture); pelvic pain; uterine haemorrhage
Risks of hysterectomy
Bleeding, Bowel, bladder, ureter damage, infection e.g. peritonitis, wound infection, Scarring, VTE, early menopause (with ovaries).
Effectiveness of endometrial ablation for menorrhagia
Expect 30% amen, 30% failure, 40% llight
Causes of amenorrhea
Pathological Brain - Pit/ hypothalmic □ Stress □ Psychoactive drugs ○ Cryptomenorrhea (hidden) e.g. imperforate hymen ○ Uterine/ endometrial/ Ovaries • Physiological ○ Prepubertal ○ Preg ○ Menopause
Cause/ pathology of PCOS
○ Heterogenous endocrine disorder with unknown aetiology
○ FAmilial clustering/ RF
○ 90% Amennorhea
○ US - string of pearls = diag
• Patho
○ Recruit follicles which get stuck and dont get to follicular ovulation stage
○ Each produce oestrogen and androgen
○ No prog so no ovulation and infertile
○ Ovarian theaca cell hyperplasia leading to enlargement with icing sugar coating
○ Tendency to DM due to insulin resistance
○ Characterised by
§ Hypersecretion of androgens
§ Increased pilsatile secretion of LH
§ Theca cell (follicle) hyperplasia leading to ovarian enlargement
§ Anovulation
Insulin resistance
Clinical features of PCOS
○ Oligo/ amen ○ Dysfunctional uterine bleeding ○ Obesity ○ Hurtsuitis ○ Acne ○ INfert String of pearls
Biochemical features PCOS
§ Increased LH/FSH
§ Decreased Sex Hormone Binding Blobulin (SHBG)
§ Raised free androgen index (FAI)
Increased serum insulin
DDX PCOS
○ Anovulatiory cycles ○ CAH - congenital adrenal hyperplasia ○ Androgen secreting tumours ○ Cushings’s syndromes (also oligo) ○ Hypothalamic dysfunction ○ Female athlete triad ○ Eating disorder ○ Hyperprolactineamia Thyroid disorders
Long term comps PCOS
○ MIscarriage ○ Gestational diabetes ○ NIDDM ○ Hypertension ○ CVD Endometrial hyperplasia/ carcinoma (oestrogen) Ovarian ca
Management PCOS
○ Weight adjustment ○ COCP ○ Cyproterone acetate d ○ Cyclical progestogen ○ Metform ○ Ovulation induction in fertility § Something citrate Ovarian drilling
What is cypropterone acetate and important ADR
§ Antiandrogen
§ Normal ones can cause meningioma
§ Some prog functions
§ With oestrogen
Causes of dysmennorhea
Primary dysmennorhea Often with anovulation after menarchy Excessive prostagladins = contractions and ischaemic pain Secondary Adenomyosis Endometriosis PID Fibroids Ovarian cancer (less likely endometrial)
Treatment dysmennorhea
Primary NSAIDs e.g. mefanamic acid Paracetamol If ovulatory cycle then COCP can help Hyoscine butylbromide (SM anti-spasmodics) unreliable Secondary Treat cause IUCDs can increase- levonogesterol may help
Absolute CI OCP
Migraine with aura Breastfeeding <6 weeks post-partum Age 35 or over smoking 15 or more cigarettes/day Systolic 160mmHg or diastolic 95mmHg Vascular disease History of VTE Current VTE (on anticoagulants) Major surgery with prolonged immobilisation Known thrombogenic mutations Current and history of ischaemic heart disease Stroke (including TIA) Complicated valvular and congenital heart disease Current breast cancer Nephropathy/retinopathy/neuropathy Other vascular disease Severe (decompensated) cirrhosis Hepatocellular adenoma Hepatoma Raynaud's disease with lupus anticoagulant Positive antiphospholipid antibodies
Define menopause and peri-menopause
Permanent cessation of menstruation due to the loss of ovarian follicular activity (12 months amen)
• Peri menopause- the period from the beginning of symptoms of approaching menopause and ending 12 months after the final menstrual period
Symptoms of menopause
○ Hot flush and sweats ○ Irritability ○ Lack of conc ○ depression ○ Loss of libido ○ INcrease bone loss ○ Increase CVD risk ○ Vaginal dryness ○ Dowager’s hump due to osteoporosis and spontaneous collapse § Resp function too
Diagnosis menopause
○ Age ○ Cessation of menstruation ○ Atophy ○ ? Role of hormone profile - NICE do not recommend ○ ? Role of ovarian biopsy DDX thyroid and psych
Management options menopause
○ Diet and exercise
○ ERT and prog if they have a uterus = HRT
§ Prog reduce the increased risk of endometrial hyperplasia and carcinoma with unopposed oestrogen in non-hysterectimized women
○ E.g. Stradiol or premarin and meedroxyprogesterone acetate, Duphaston (Provera),
○ Sequential or continuous
§ Retro gem cont with 12-14 of prog causing bleeding, less prog so possible less CVD risk
§ Continue less likely for period
○ COCP Monophasis or triphasic
Risks and beenfits of HRT
○ Risks of HRT § Unapposed oestrogen: □ Endometrial cancer □ Ovarian cancer? § Breast cancer § IHD ? § Gall blasser § Stroke § VTE § Uterine bleed § Lipid profile neg affected § Thrombophilia profile neg affected ○ Benefits Less vasomotor symptoms Improvement in urogenital and sexual function symptoms Osteoporotic fracture reduction (only if lifelong and sustained) Reduced Colorectal cacner by 1/3 ?alz ?CVD, Ovarian Alz
Cyclical vs combined HRT?
x Women should be prescribed cyclical combined HRT if their LMP was less than 1 year ago and continuous combined HRT if they have:
taken cyclical combined for at least 1 year or
it has been at least 1 year since their LMP or
it has been at least 2 years since their LMP, if they had premature menopause (menopause below the age of 40)
Route for HRT
○ Oral ○ Transdermal ○ Implant ○ Transvaginal ○ Nasal ○ Local ○ Patch Prog: Transderm, oral, IUS
Symptom specific treatment alternatives to HRT
• Prevention of osteoporosis ○ Bisphosphonates ○ Calcium and Vit D ○ Raloxifene § SERM § Increase hot flush and VTE § Less action on breast and uterine bleeding ○ Exercise • Vaginal dryness - lubricants or vaginal oestrogen transderm • Vasomotor symptoms ○ SSRI ○ Clonidine (less efficacy) - alpha 2 in brain stem cuasing less TPR ( Gabapentin
Contraception around menopause
x • Stop <50 years is amenorrhic 2 years
• Stop >50 if 1 year
Stop COCP in >50 after 2 years post amen or POP
Diagnosis of hypertension in preggers
> =140/90 on 2 occasions more than 4 hrs apart or a single reading of the diastolic BP >110
Korotkoff phase V should be used (when it stops as per normal)
What is significant proteinuria?
Next investigations?
• 2+ more of protein on urinanalysis is significant
• Protein:creatinine ratio is acceptable measure
○ <30mg/mol implies non-significant proteinuria
○ >30 prompt 24hr urine collection
• >300mg in 24hrs is abnormal
MSU and C&S but infection unlikely if absence of symptoms (more likely to be preeclampsia)
Classifcation of hypertensive disorders of preggers?
• Preeclampsia (only cause in T3)
• Gestation hypertension/ proteinuria (only one possible)
• Chronic hypertension
• Pre-eclampsia superimposed on chronic hypertension (15-25% of chronic hypertensive cases)
Differentiating this from gestational hyp can be difficult as pre eclamp can be without proteinuria
Normal variation of BP in preggers?
Drops MAP by -5mmHg from 0 to 21 weeks then returns to normal by 40
Risks, and urate in chronic hypertension in preggers?
• Risks are mainly related to superimposed PET (pre eclapmptic toxaemia
• Normal urate
• WIth proteinuria IUGR common
Abortion 1/50
BP target in chronic/ secondary hypertension in preggers?
xKeep BP in all women below 150/100 with urgent treatment
If BP >140/90 on 2 occasions then transfer to consultant led labour ward
Agitation and restlessness is sign of underlying problem in women with HYT
Define pre eclampsia
○ Miltisystem disorder
○ Usually recognised by new onset hypertension (140/90) and protein urea (>300mg) in the second half of preggers that resolves after delivery
Can occur with or without HYT or without or with/out proteinuria but will have other symptoms
Pathophysiology of pre eclampsia
○ Two stage placental disease concept
§ Abnormal trophoblastic invasion and adaptation of spiral arteries
□ Converts muscular layer to trophoblast cells (dilated) - Trophoblast fails to invade maternal spiral arterioles
□ If not then poor dilation and resistance to blood flow
□ Reduction of vasodilators PGI2 and NO in endothelium
□ Maternal plasma vol fails to expand
□ Placenta fails to be a low pressure supply system
§ Placental ischaemia affecting maternal and fetal circ e.g. HYT to compensate
Complications of pre eclampsia
• CNS ○ MAP >125 then intracranial haemorrhage/ cortical blindness risk ○ Cerebral oedema/ eclampsia • Renal ○ Renal tubular necrosis, renal cortical necrosis • Resp ○ Pulmonary oedema ○ ARDS • Liver ○ Haemorrhage beneath capsule ○ Hepatic rupture ○ Acute fatty liver of preggers ○ HELLP § Hemolysis § Elevated liver enzymes (EL) § Low platelet count (LP) • Thrombosis ○ High risk ○ Microangiopathic haemolysis/ DIC • PLacenta infarction/ placental abruption • Fetus ○ FGR - fetal growth restriciton ○ Preterm death Preterm labour
Risk factors for pre eclampsia
○ Socio-demograph § Age >40 § SESEthnicity § Smoking reduces risk? ○ Preggers § Nulliparous § Multiple preggs § Previous pre eclapsia § Hydrops (oedema/ fluid in fetal compartment e.g. rhesus disease), trophoblastic diseas ○ Medical Hx § PAst HYT (on pill too) § FHx Lupus or CKD or other systemic/ autoimmune
Clinical features of pre eclampsia and biochem
• Symptoms ○ Headache ○ Visual disturbance ○ Epigastric pain (not sure why) ○ Oedema, can be usual too, non dependent ie..e face and hands in pre eclampsia only ○ Vomiting • Signs ○ Hyper reflexia/clonus ○ Oedema Epigastric tenderness and RUQ
○ Abnormal blood results § Raised urea and creatinine § Raised urate § Low platelets Elavated ALT/AST
INvestigation (asessment of risk)
• Bedside ○ Blood pressure level § Diastolic for preeclampsia § Systolic for maternal morbidity ○ Proteinuria § Fetal risk § Protein:creatinine ratio • Bloods ○ FBC - anaemia, Platelet count ○ Ues Uric acid ○ LFTs ○ +/- coag screen - PT, APTT (DIC) • Fetal movements ○ Slowing of movements not good as non essential activity reduced • CTG ○ Cardiac topograph ○ Only if reduced movement • Umbilical Doppler ○ Notching • US ○ Fetal size - FGR ○ Liquor Volume • If baby well on admission Can prolong pregnancy if mother stable
Managment pre eclampsia
• Early intervention ○ IF BP >140/90 refer ○ Antenatal Day Assessment Units ○ Closer monitoring ○ Assess the need for therapy • Admit if ○ BP >170/110 ○ OR ○ BP >140/90 and Sig symptoms § Proteinuria 2+/300 § Sig symptoms • Meds ○ Acute then Oral Labetalol first line if >160/110 § Also hydralazine or nifidipine • Chronic meds ○ Labetalol ○ If not the methyldopa or nifidipine rolongation of preggers • If no convulsions • A few days allows use of steroids Ø A week may increase fetal survaval Ø However ○ Fetal signs of compromise, delivery is necessary ○ Better small and healthy than big and compromised Ø Deliver on labour ward
Prevention pre eclampisa
• Antenatal care appropriate
○ Appropriate RFs indentified in T1 (before onset)
○ After 20 weeks monthly visits or fortnightly after 34 in primigravida
○ Clear history
• Primary
○ Rest and exercise (not strong)
○ Ca shops but no effect on baby outcome
○ No benefit of Vt C and E
Low dose aspirin if high risk women
Fetal risks of severe hypertension in preggers
• Direct effect of disease ○ Intra-uterine growth restriction • From intervention ○ Premature delivery ○ Intervention ○ Cerebral haemorrhage ○ Pneumothorax • Related to both Cerebral palsy
MoA, use, ADR and CI methyldopa
§ Methyldopa
□ NOt if history of dep
□ Stop PN due to risk of PN dep
□ ADR tiredness/dry mouth/ GI/ dep
Mechanism - metabolised to methynoradrenaline and stimulates alpha adrenergic receptors
250mg BD increased over 2 days up to 3g
CI - history of depression, pheochromocytoma, acute porphyrias
