Early Pregnancy Flashcards

1
Q

what is the pathophysiology of ectopic pregnancy?

A

pregnancy which is implanted at a site outside of the uterine cavity

  • 97% tubal
  • 3% ovary, cervix or peritoneum

trophoblast invades the tubal wall, producing bleeding which may dislodge embryo

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2
Q

what are the possible consequences of an ectopic pregnancy?

A
  • tubal abortion
  • tubal absorption: if the tube does not rupture, the blood and embryo may be shed or converted into a tubal mole and absorbed
  • tubal rupture
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3
Q

what are some risk factors for an ectopic pregnancy?

A

*anything slowing the ovums passage to the uterus

  • damage to tubes: PID, surgery
  • previous ectopic
  • endometriosis
  • IUCD
  • POP - fallopian tube ciliary dysmotility
  • IVF - 3% of pregnancies are ectopic
  • iatrogenic - pelvic surgery, reversal of sterilisation, assisted reproduction ie. embryo transfer in IVF
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4
Q

how might an ectopic present?

A

*leading sx of ectopic pregnancy is pain → lower abdo/ pelvic pain, with or without vaginal bleeding with potential hx of amenorrhoea

shoulder tip pain - irritation of diaphragm by blood in peritoneal cavity
vaginal discharge - brown, prune juice colour

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5
Q

what might you see on examination in an ectopic pregnancy?

A
  • localised abdominal tenderness
  • vaginal examination revelas cervical excitation, adnexal tenderness
  • full pouch of Douglas
  • haemodynamic instability
  • peritonitis signs
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6
Q

what are some differentials for an ectopic?

A
  • Miscarriage
  • Ovarian cyst accident (this refers to cyst haemorrhage, torsion or rupture)
  • Acute pelvic inflammatory disease
  • Urinary tract infection
  • Appendicitis
  • Diverticulitis
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7
Q

how would you investigate an ectopic?

A
  • pregnancy test
  • B-HCG serum
  • pelvic USS
  • urinalysis
  • any swabs etc for differentials
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8
Q

how is an ectopic managed immediately?

A

A to E
medical for those who are stable, pain controlled, no visible heart beat
IM methotrexate - anti-folate cytotoxic agent that disrupts the folate dependent cell division

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9
Q

what are the advantages and disadvantages of medically managing an ectopic?

A
  • advantages: avoids the complications of surgery, pt can be at home
  • disadvantages: potential side effects methotrexate like abdo pain, myelosuppression, renal dysfunction, hepatitis, teratogenesis ((advice contraception for 3-6m after), if fails surgery needed
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10
Q

when would you offer surgical and discuss the advantages and disadvantages?

A

severe pain, serum B-HCG >5000, adenexal mass >34mm, foetal heart beat visible on scan

  • advantages: reassurance about definitive treatment, high success rate
  • disadvantages: GA risk, risk of damage to neighbouring structures like bladder, bowel, ureters, DVT, PE, haemorrhage, infection, wisk of tx failure with salpingotomy if some pregnancy remains
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11
Q

when would you offer a salpingostomy over a salpingectomy?

A
  • if damage to contralateral tube from infection, disease or surgery - salpingotomy (a cut in fallopian tube)
    • can be performed to remove ectopic and salvage the tube to preserve future fertility
    • HCG follow up is required until the level reaches <5iU (negative), to ensure there is no residual trophoblast
    • risk of recurrent ectopic pregnancy in the salvaged tube will be increased
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12
Q

what should you remember for someone who is having surgical mx of ectopic?

A

Anti-D prophylaxis → rhesus negative women who receive surgical mx

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13
Q

when would you manage an ectopic conservatively?

A

for stable pt where rupture is unlikely with well controlled pain, low basleine B-HCG, small unruptured ectopic on USS

  • Advantages:Avoid the risks of medical and surgical management, can be done at home.
  • Disadvantages:Failure or complications necessitating medical or surgical management (25% of patients), rupture of ectopic
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14
Q

what are some differentials for bleeding in first trimester?

A

Spontaneous abortion
Ectopic pregnancy
Hydatidiform mole

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15
Q

what are some differentials for bleeding in second trimester?

A

Spontaneous abortion
Hydatidiform mole
Placental abruption

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16
Q

what are some differentials for bleeding in third trimester?

A

Bloody show
Placental abruption
Placenta praevia
Vasa praevia

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17
Q

what is a spontaneous abortion?

A

loss of pregnancy at less than 24 weeks gestation

  • early (1st trimester) more common than late miscarriage
  • occurs in 20-25% pregnancies
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18
Q

what are the classifications for abortion?

A
  • threatened: mild bleeding, pain, cervix closed, pregnancy viable
  • inevitable: heavy bleeding, clots, pain, cervix open
  • missed: asymptomatic with no foetal heartbeat
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19
Q

compare incomplete vs complete pregnancy?

A

POC** partially expelled – Sx of missed miscarriage or bleeding/clots

Hx of bleeding, passing clots and POC and pain. Sx settling/settled now, no POC

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20
Q

how is a threatened miscarriage managed?

A

If heavy bleeding admit/observe, if not reassure and back to GP/Midwife
* If >12 weeks & Rhesus negative: Anti-D

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21
Q

how is an inevitable miscarriage managed?

A

If heavy bleeding admit/observe
* Offer conservative/medical/surgical options. Likely to proceed to incomplete/complete miscarriage
* If >12 weeks & rhesus negative: Anti-D

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22
Q

what is the management of a missed miscarriage?

A

May want to rescan and second person to confirm
* Manage conservatively (lower success rated), medically or surgically
* If >12 weeks & rhesus negative: Anti-D

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23
Q

what are some causes of

A
  • early - aneuploidy, abnormal foetal development
  • mechanical - cervical weakness
  • uterine abnormalities
  • chronic maternal disease - SLE, DM
  • infection - CMV
  • foetal cause
  • no cause
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24
Q

what are some risk factors of spontaneous abortion?

A
  • maternal age >30-35 (chromosomal abnormalities)
  • previous miscarriage
  • obesity
  • chromosomal abnormalities in parents
  • smoking
  • uterine abnormalities
    • fibroids
  • previous uterine surgery
  • anti-phospholipid syndrome
  • coagulopathies
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25
Q

what are some clinical features of a miscarriage?

A
  • vaginal bleeding - may include clots or POC
  • haemodynamic instability if bleeding excessive
  • suprapubic, cramping pain (similar to primary dysmenorrhoea)
26
Q

what features are seen on examination of miscarriage?

A
  • haemodynamic instability
  • abdo exam - distended, localised tenderness
  • speculum - assess diameter of cervical os, observe any POC in cervical canal, local bleeding
  • bimanual - assess uterine tenderness, adnexal masses or collection (ectopic)
27
Q

what are some ways of investigating miscarriage?

A

EPAU
imaging - transvaginal USS, doppler
bloods: serum b-HCG, FBC, blood groups, rhesus status, triple swabs

28
Q

evaluate conservative management of miscarriage?

A
  • advantages - can remain at home, no side effects, no anaesthetic risk
  • disadvantages - unpredictable timing, heavy bleeding, pain during passage of POC, chance of being unsuccessful
29
Q

what are some contraindications for conservative mx of miscarriage?

A

infection, high haemorrhage risk, coagulopathy or haemodynamic instability

30
Q

how is medical management done for miscarriage?

A

Mifepristone is a progesterone receptor antagonist → weakening of attachment to the endometrial wall + cervical softening and dilation + induction of uterine contractions

vaginal misoprostol (prostaglandin analogue) to stimulate cervical ripening and myometrial contractions

31
Q

evaluate medical management for miscarriage?

A
  • advantages - home if patient desires, avoid anesthetic risk
  • disadvantages - side effects of meds, D+V, heavy bleeding, pain during POC, chance of emergency surgical intervention
  • follow up - pregnancy test 3w later
32
Q

what is the surgical management for miscarriage?

A

manual vacuum aspiration with local if >12w, evacuation of retained POC (ERPC)

ERPC, the patient is under a general anaesthetic, a speculum is passed to visualise the cervix, it is dilated allowing suction tube to be passed and remove the products of conception

33
Q

evaluate the surgical management of a miscarriage?

A
  • advantages - planned, unaware during procedure GA
  • disadvantages - Anaesthetic risk, infection (endometeritis), uterine perforation, haemorrhage, Ashermen’s syndrome, bowel or bladder damage, retained products of conception
34
Q

what do you have to make sure to do after a miscarriage?

A
  • help with grief
  • offer follow up
  • respect wishes of dealing with foetal products
  • give in opaque container
35
Q

what are some causes of recurrent miscarriages?

A

endocrine: PCOS, thyroid, DM
infection: BV in first 3m
chromosomal, uterine abnormalities
thrombophilia - protein c/s
anti phospholipid syndrome

36
Q

how is recurrent miscarriages managed?

A
  • genetic clinic
  • cervical cerclage
    • Previous poor obstetric history (≥3x 2trimester losses)
    • Cervical length shortening on USS (<25mm before 24/40 and a previous 2trimester loss)
    • Symptomatic women with premature cervical dilatation and exposed fetal membranes in the vagina
  • low dose aspirin plus heparin for antiphospholipid
37
Q

what is a hydatidiform mole?

A
  • tumours consist of proliferating chorionic villi which have swollen and degenerated
  • derived from chorion and makes lots of hCG exaggerating pregnancy sx
38
Q

what are some risk factors for hydatidiform mole?

A
  • higher rates in latin american, asian and middle eastern women
  • past moles
  • extreme maternal age
  • FHx
39
Q

how would a mole pregnancy present?

A
  • exaggeration of normal pregnancy sx with extreme b-HCG
    • hyperemesis gravidarum
    • vaginal bleeding - prune juice discharge which accumulated in uterine cavity and oxidised
      • may look like frogspawn
    • pelvic discomfort - pain or pressure
40
Q

what signs are seen on examination of a mole?

A
  • uterus larger than expected
  • possible adenexal mass
  • possible grape like mass in vagina
41
Q

how is a mole investigated?

A
  • transvaginal USS
    • central heterogenous mass with numerous anechoic spaces
    • snowstorm, cluster of grapes, honeycomb appearance
  • b-HCG
  • bloods
42
Q

how is a mole managed?

A
  • tell anaesthetist as b-HCG can act like TSH and cause thyrotoxic storm at evacuation
  • gentle suction to remove molar tissue
    • histology
  • anti-D if Rh-ve
  • avoid pregnancy until b-HCG normal for 6m
  • oral contraceptives can be used if levels drop rapidly
43
Q

what are some molar pregnancy complications?

A
  • invasive moles metastasise - lung, vagina, brain, skin and liver
  • choriocarcinoma
  • hyperthyroidism
  • pre-eclampsia
  • RDS
44
Q

what is a bloody show?

A

small amount of blood and mucus released from the vagina as a result of cervix dilating and softening and effacing to dilate in preparation for labour

  • mucus plug blocks the opening of the cervix during pregnancy to protect the baby from bacteria
  • blood from your cervix is mixed in with the mucus plug, it is called a bloody show
45
Q

how does a bloody show present?

A
  • can be red, brown, pink and jelly or string-like
  • no more than a tablespoon or two of blood
  • triggers
    • sexual intercourse
    • membrane sweeping
    • trauma
  • symptoms
    • cramping
    • pelvic pressure
    • contractions
46
Q

how would a placental abruption present?

A
  • abdominal pain → posterior placental abruptions with back pain
  • vaginal bleeding
  • uterine contractions
  • dizziness and loss of consciousness
  • Clinical exam
    • woody, tense uterus
    • foetal heart may be absent or distressed
47
Q

how is placental abruption managed?

A
  • foetus alive → no signs of distress → observe closely is <36w→ induce and deliver vaginally is >36w
  • foetus alive → signs of distress → immediate C-section
  • foetus dead → induce vaginal delivery unless haemodynamically compromised → C-section
48
Q

how is placental praevia managed?

A
  • 16-20w → if identified rescan at 32w, and again at 36w
  • in still at 36w, delivery via C-section
    • risk of spontaneous labour, associated haemorrhage
49
Q

what is vasa praevia?

A

fetal blood vessels (the two umbilical arteries and single umbilical vein) arewithin the fetal membranesand run across theinternal cervical os and not protected within umbilical cord or placenta

50
Q

how is vasa praevia managed?

A
  • elective C- section at 34-36 w
  • corticosteroids from 32w to promote foetal lung maturity
  • APH → C-section required
51
Q

what is hyperemesis gravidarum?

A

persistent and severe vomiting during pregnancy, leading to weight loss, dehydration and electrolyte imbalances

52
Q

what is the physiology of hyperemesis?

A

normally startsbetween4 and 7 weeks’ gestation. It reaches a peak in the 9thweek, and settles by week 20

53
Q

what is the pathophysiology of hyperemesis?

A

increasing levels of b-HCG released by placenta which stimulate chemoreceptor trigger zone in brainstem feeding onto vomiting centre of brain

54
Q

what are some risk factors for hyperemesis?

A
  • First pregnancy
  • Previous history of hyperemesis gravidarum
  • Raised BMI
  • Multiple pregnancy
  • Hydatidiform mole
55
Q

which score is used in hyperemesis?

A

Pregnancy-Unique Quantification of Emesis(PUQE) score; a score of 6 correlates to mild NVP, 7-12 moderate and 13-15 severe

56
Q

what are some differentials for hyperemesis?

A

Infections: Gastroenteritis, urinary tract infection, hepatitis, and meningitis

Gastrointestinal problems: Appendicitis, cholecystitis, bowel obstruction

Metabolic conditions: Diabetic ketoacidosis, thyrotoxicosis
Drug toxicity

Molar pregnancy: Characterized by abnormally high levels of beta-hCG due to gestational trophoblastic disease, which can cause severe nausea and vomiting

57
Q

how is hyperemesis investigated?

A
  • electrolyte levels
  • bedside - weight, urine dip
  • lab - midstream urine, FBC, U&E, glucose
  • refractory cases
    • LFT to exclude liver disease
    • amylase - pancreatitis
    • thyroid function
    • ABG - monitor severity
  • imaging - USS to confirm gestation, viability, exclude honeycomb etc
58
Q

how is hyperemesis managed?

A
  • mild - community with oral antiemetics, oral hydration, dietary advice, reassurance
  • moderate - ambulatory daycare, IVF, parenteral antiemetics, thiamine, until ketonuria resolves
  • severe - inpatient
59
Q

how is hyperemesis managed as an inpatient?

A
  • IV hydration with 0.9% saline with potassium chloride as indicated
  • H2 receptor antagonist or PPI for reflux, oesophagitis, gastritis
  • thiamine - prolonged vomiting to prevent wernickes
  • thromboprophylaxis
60
Q

what antiemetics are given in hyperemesis?

A
  • first line: cyclizine, prochlorperazine
  • second: metoclopramide for 5 days max
  • third: hydrocortisone IV