31. Placental Problems in Pregnancy Flashcards
List some problems of placentation?
What are the 3 stages of pregnancy?
What is hyperemesis gravidarum?
How is it managed?
Exaggerated symptoms of pregnancy, bleeding disorders, medical problems, multiple pregnancy.
Antepartum (early = <24w, later = >24w). Intrapartum (1st and 2nd stages of labour). Postpartum (foetus delivery -> 6w later).
Severe nausea and vomiting -> electrolyte imbalance, weight loss and hospital admission. Reasons for nausea: betaHCG stimulates CTZ in brain. TSH can be produced by placenta and shares terminal aa sequence with bHCG so also stimulates CTZ. ALSO placenta makes lots oestrogen -> hepatocytes swell and block hepatic sinusoids -> bilirubin passes out to gut and enters mum’s circulation -> nausea. ALSO delayed emptying of stomach caused by progesterone which relaxes SM.
Dietary advice, IV fluids, thiamine, antiemetics.
What is spontaneous miscarriage?
What are the 6 types of miscarriage?
Foetus dies/delivers dead <24w. More common in older women.
1) Threatened: light painless bleeding, foetus alive, uterus expected size, cervical os closed, 25% go on to miscarry.
2) Inevitable: bleeding heavier, foetus may be alive, os open, pelvic pain, miscarriage about to occur.
3) Incomplete: only some foetal parts passed, os open, bleeding continues.
4) Complete: all foetal tissues passed, bleeding stopped, uterus no longer enlarged, os closed.
5) Missed: foetus not developed/died in utero (only recognised later with USS/bleeding), uterus smaller than expected, os closed, abdo pain and bleeding minimal.
6) Septic: contents of uterus infected causing endometritis, vaginal loss offensive, tender uterus, +/- fever, may progress to pelvic infection -> abdo pain and peritonism.
SIC TIM
How would a spontaneous miscarriage be investigated?
How would it be managed?
What is recurrent miscarrage? What are the causes?
USS (location, viability, retained foetal tissue etc.), serum bHCG (normally increases by >66% in 48hr with viable pregnancy), bloods (FBC, Rhesus group).
Expectant (wait for spontaneous resolution), medical (remove foetal tissue - using prostaglandins - misoprostol), surgical (infection swabs and broad spectrum abx, anti D to rhesus -ve women). Support and counsel pt!
3 or more consecutive miscarriages, affects 1%. Causes: autoimmune disease e.g antiphospholipid syndrome (25%), chromosomal defects (4%), hormonal factors e.g. PCOS, LH hypersecretion, anatomical factors e.g. uterine septa, cervical incompetence, infection, others e.g. obesity, smoking, age, drugs.
What investigations would be done for recurrent miscarriage? How would it be managed?
What is cervical incompetence?
What is ectopic pregnancy?
What are some risk factors for ectopic pregnancy?
Autoimmune and thrombophilia screen. Karyotyping. Pelvic USS. Mx: anticoags e.g. heparin, genetic counselling, metformin for PCOS, cervical cerclage (cervical suture) etc.
Cervix fails to retain pregnancy.
Implantation of a fertilised ovum outside the endometrial cavity, commenest site = ampulla.
On the INCREASE due to STIs (tubal motility (i.e. ciliary function) lost for every exposure and can’t regain) /PID, Emergency contraception, assisted conception, pelvic surgery, IUCD in situ (copper coil), failed sterilisation, previous ectopic, congenital abnormalites of tube e.g. diverticulum. Also insufficient eggs and slow divisions of older women.
What is the clinical presentation of an ectopic pregnancy?
What might be found upon examination?
What investigations would you do?
How would you manage it?
Women of reproductive age, PV bleeding (scanty, dark), lower abdo pain, collapse (shoulder pain suggests intraperitoneal blood loss), amenorrhoea for 4-10w.
Tachycardia, abdo tenderness, cervical motion tenderness, adnexal tenderness on side with pathology, uterus smaller then expected, cervical os closed.
Urine bHCG (confirm pregnancy), transvaginal USS (locate foetus - if not either foetus too young/complete miscarriage/ectopic), quantitative serum bHCG (if uterus empty), diagostic laparoscopy.
Acute: admission, IV access, cross-match blood, anti D to R-ve. Subacute: surgical (laparoscopy/salpingectomy), medical (methotrexate - destroys placenta and serial bHCG levels), conservative (observe if small, unruptured with declining bHCG). Counselling and support!
What is a molar pregnancy?
What are the 3 different presentations?
Differentiate between a partial mole and a complete mole.
Gestational trophoblastic disease: trophoblast tissue that forms part of the blastocyst proliferates more agressively than normally.
1) Non-invasive - hydatiform mole. 2) Locally invasive - invasive mole. 3) Metastatic - choriocarcinoma.
Partial mole: 2 sperm fertilse egg (triplody), foetal tissue present. Malignant change is rare (prod of bCHG not as agressive).
Complete mole: 2 sperm fertilise egg and push out maternal DNA/1 sperm fertilises, divides into 2 and pushes out maternal DNA, entirely paternal in origin. No foetal tissue in histology, just swollen chorionic villi. 5-10% turn malignant.
What are the clinical features of gestational trophoblastic disease?
What would you find on examination?
What investigation would you do, and how would you manage it?
PV bleeding (light/lots), hyperemesis gravidarum (excess HCG prod), passage of vesicles per vaginum.
Large uterus, early pre-eclampsia and hyperthyroidism may occur.
USS - snowstorm appearance (lots of vesicles). Mx: ERPC and send tissue for histology diagnosis, serial bHCG levels (persistant/rising = malignancy?), pregnancy and COCP avoided until bHCG levels normal.
What is antepartum haemorrhage? What are the causes?
What are the risk factors and clinical features of placental abruption?
How would you investigate and manage?
Bleeding from genital tract >24 weeks of gestation but before delivery. Causes: Common - undetermined/placental abruption/placental praevia. Rarer - incidental genital tract pathology/uterine rupture/vasa praevia.
Risk Factors: multiparity, PIH, polyhydraminos, ECV, trauma, smoking, malnutrition, previous abruption, unknown. Clinical Features: intense constant abdo pain +/- vaginal bleeding, profound shock, DIC, tense tender uterus, foetal parts not easily felt and it’s heart weak/absent.
FBC, urea, creatinine, coag screen, cross-match blood, USS, CTG, catheterization with hourly urine output, CVP monitoring to assess blood loss. Mx: admit and resus, steroids if <34w, opiate analgesia, anti-D to R-ve.
A patient has placental abruption. What would you do in the following situations:
a) Foetal distress
b) No foetal distress + gestation 37w or more
c) Dead baby
What is placenta praevia? What is it associated with?
What are some complications of placenta praevia?
a) urgent C-section. b) induced labour with amniotomy. c) coagulopathy likely thus give blood products and induce labour. If no foetal distress, pre-term and minor abruption, give steroids and monitor on ward.
Placenta inserted into lower segment of uterus after 24w. Minor: doesn’t cover internal os. Major: covers internal os. Usually painless vaginal bleeding. Associated with: twin pregnancies, multiparous, older mums, scarring of uterus (previous c-section).
Obstructs engagement of head -> c-section, baby malpresentation, postpartum haemorrhage, preterm delivery, IUGR, placenta accreta (placenta implants in prev c-section scar).
How would you manage placenta praevia?
What is pre-eclampsia characterised by? What are some risk factors?
What are some predisposing factors to PE?
Hospital admission if bleeding, NO VAGINAL EXAM, IV, blood-match, anti-D if needed, if bleeding stops and <34w give steroids, deliver by c-section if heavy bleeding/foetal compromise/>37w.
Hypertension, proteinuria, oedema, weight gain and DIC. Due to abnormal maternal adaptation to trophoblast -> placenta secretes toxins which vasoconstrict mum’s circulation. Also tunica media in spiral arteries NOT replaced with trophoblasts so SM retained -> can vasoconstrict. Risk factors: primigravidity, genetic, multiple pregs, diabetes.
Primigravidity, hypertension, diabetes, multiple preg, molar preg.
How is pre-eclampsia managed?
Which one is due to genes? Monozygotic or dizygotic twinning?
What is a main complications of multiple pregnancy?
Rest and obs, BP every 4hrs, daily urinalysis, FBC, Us and Es, LFTs, Foetal CTG. Antihypertensives and anticonvulsants. Deliver baby ASAP.
Dizygotic + older women tend to hyperovulate. Monozygotic is a chance event. When cleavage occurs = determine whether di/monochorionic or di/monoamiotic.
Twin to Twin Transfusion syndrome (TTTS)- vascular communications within the placenta. Most miscarry 16-24w. Discrepant growth and oligo/polyhydraminos. Can be treated by laser now. Smaller twin does better as neonate but not older (Barker hypothesis).
