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Reproductive System > Complications in Pregnancy > Flashcards

Complications in Pregnancy Flashcards

1
Q

difference between abortion and miscarriage

A
  1. miscarriage: spontaneous loss of pregnancy < 24 wks

2. abortion: voluntary termination of pregnancy

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2
Q

6 types of miscarriages

A
  1. threatened: vaginal bleeding +/- pain, viable, closed cervix
  2. inevitable: vaginal bleeding +/- clots, dilated cervix
  3. incomplete: vaginal bleeding, partial expulsion of retained tissue, dialted cervix
  4. complete: vaginal bleeding, complete expulsion of retained tissue, dilated cervix
  5. missed: gestational sac present but no fetus, or fetal ole present but no heartbeat, not viable
  6. septic: infection usually from incomplete pregnancy, but can precede it as well
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3
Q

what are the 2 potential outcomes of threatened miscarriage, and what is the management for each?

A
  1. stops bleeding spontaneously - conservative management

2. progresses to inevitable miscarriage - progesterone enhance the endometrium 7 delay contractions

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4
Q

management for each kind of miscarriage:

A
  1. threatened: conservative, progesterone
  2. inevitable: evacuation of uterus
  3. missed: conservative, evacuation of uterus (prostaglandin misoprostol, surgical suction)
  4. septic: abx + evacuation of uterus
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5
Q

what is the most common location of ectopics? How common is ectopic pregnancy?

A

95 - 97% = ampulla of fallopian tube

1:90 pregnancies (~1%)

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6
Q

presentation of ectopic pregnancy

A
  1. vaginal bleeding
  2. pain in the abdomen
  3. GI or urinary symptoms
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7
Q

2 methods of investigation for ectopic

A
  1. USS
    • no gestational sac +/- adnexal mass
    • fluid in rectouterine pouch
  2. serial serum BhCG: normal pregnancy should +66% in 48 hrs, ectopic pregnancy will increase less or -50%
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8
Q

management of ectopic pregnancy (3)

A
  1. conservative - watch BhCG
  2. medication: methotrexate - watch BhCG
  3. surgery: laparoscopy, salpingectomy, salpingotomy
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9
Q

what are the 4 medications given in PPH?

A
  1. oxytocin - uterine contraction
  2. ergometrine - uterine contraction
  3. carboprost - synthetic prostaglandin analogue with oxytoxic properties
  4. tranexamic acid - inhibits fibrinolysis, treats haemorrhage
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10
Q

what are the mechanical (1) and surgical treatments (3) for PPH?

A

mechanical - balloon tamponade

surgical - B lynch suture, ligation of uterine/iliac vessels, hysterectomy

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11
Q

causes of APH (4)

A
  • placenta previa/vasa previa (rare)
  • placental abruption
  • idiopathic
  • local lesions (polyps, cervical cancer, erosions, infections - thrush, trachminos)
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12
Q

definition of APH (in weeks)

A

vaginal bleeding from 24 weeks - delivery

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13
Q

what is the difference between placenta and vasa previa in terms of bleeding?

A

vasa previa has less bleeding because the haemorrhage is coming from fetal circulation within the fetal membrane, more risk for fetus than mom

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14
Q

classification of placenta previa: 1. RCOG classification, 2. old classification

A
  1. RCOG classification:
    • low lying (<20 mm away from os)
    • placenta previa (covering the os)
  2. old classification:
    • Grade I (enroaching the os)
    • Grade II (reaching the os)
    • Grade III (partially covering the os)
    • Grade IV (centrally/completely covering the os)
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15
Q

risk factors for placenta previa (3)

A
  1. multiple pregnancies
  2. multiparous
  3. previous C section
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16
Q

presentation of placenta previa (4)

A
  1. PAINLESS vaginal bleeding
  2. soft nontender uterus
  3. malpresentation of fetus (transverse lie)
  4. incidental detection
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17
Q

GOLD standard investigation for placenta previa - what is contraindicated?

A

USS: to locate placental site, might need transvaginal USS for posterior placenta previa
- vaginal examination contraindicated

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18
Q

management of placenta previa (2)

A
  1. C section (GOLD standard), but prolong the pregnancy if little bleeding and < 36 wks
  2. Hysterectomy
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19
Q

what is the lie of fetus in placeta previa vs placental abruption

A

previa - malpresentation transverse lie

abruption - longitudinal lie

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20
Q

definition of placental abruption

A

hemorrhage from premature separation of placenta before delivery, associated with reptrouterine clot .
0.6% of all pregnancies

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21
Q

risks of placental abruption (8)

A
  1. increasing maternal age
  2. parity
  3. smoking
  4. pre-eclampsia/chronic hypertension
  5. previous abruptions
  6. multiple pregnancy
  7. polyhydraminos
  8. cocaine use
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22
Q

classification of placental abruption (3)

A
  1. revealed: externally visible haemorrhage
  2. concealed: haemorrhage not visible because bleeding occurs between uterine wall and placenta.
  3. mixed
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23
Q

presentation of placental abruption (6)

A
  1. APH of varying amount
  2. abdominal pain
  3. increased uterine activity/tone - may experience contractions
  4. couvelaire uterus/uteroplacental apoplexy (bruised appearance from blood seeping through myometrium)
  5. longitudinal fetal lie (unlike placental previa)
  6. increased uterine volume and larger fundal height than gestation.
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24
Q

management of placental abruption

A

conservative, vaginal delivery, C section, depending on:

  • gestation
  • amount of bleeding
  • condition of mom and baby
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25
Q

complications (mom + baby) of placental abruptions (5)

A
  1. maternal shock/collapse
  2. fetal distress/death
  3. maternal DIC (disseminated intravascular coagulation), renal failure
  4. PPH
  5. Couvelaire uterus
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26
Q

classification of preterm labor

A

mildly preterm: 32-36 weeks
very preterm: 28-32 weeks
extremely preterm: 24-28 weeks
poor prognosis if 24-26 wks

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27
Q

risks/etiology of preterm delivery (7)

A
  1. idiopathic - MAIN
  2. multiple pregnancies
  3. polyhydraminos
  4. pre-eclampsia
  5. APH
  6. infection (UTI)
  7. PROM
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28
Q

what are the signs to look for when examining for preterm delivery?

A
  • contractions

- cervical changes

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29
Q

what is the blood test done to predict preterm delivery?

A

fetal fibronectin - predicts preterm labor

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30
Q

management of preterm delivery (4)

A
  1. tocolysis
    - delay delivery until steroids take effect
    - delay delivery until mom is transferred
  2. steroids
  3. transfer to hospitals with NICU
  4. aim for vaginal delivery
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31
Q

fetal complications of preterm delivery (8)

A
  1. RDS
  2. intraventricular haemorrhage
  3. cerebral palsy
  4. nutrition
  5. tempereature control
  6. infections
  7. jaundice
  8. visual impairment + hearing loss
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32
Q

at what week gestation would you need to give steroids to help mature the lungs?

A

< 36 weeks

33
Q

classification of chronic/essential hypertension

A

mild: 140/90-149/99
moderate: 150/100-159/109
severe: >=160/110

34
Q

what is the difference between essential HT and gestational HT?

A

chronic/essential HT: bp > 140/90 which starts <20 wks BEFORE pregnancy
gestational HT/pregnancy induced HT (PIH): bp > 140/90 which starts >20 weeks gestation

35
Q

management of chronic hypertension (before and during pregnancy)

A 
before pregnancy (teratogenic prophylaxis): 
   - ACEI (ramipril,l enalapril)
   - ARB (losartan, candesartan)
   - antidiuretics 
during pregnancy (safe, aim for bp < 150/100): 
   - BB (labetolol)
   - CCB (nifedipine)
   - alpha blocker (methyldopa)
monitor: 
   - preeclampsia 
   - fetal growth
36
Q

define preeclampsia (PET), when is it considered mild or moderate?

A

preeclampsia: new HT > 140/90 starting > 20 wks gestation + significant proteinuria
- mild: mild HT > 4 hrs apart on 2 separate occasions
- moderate: moderate/severe HT

37
Q

during which period of pregnancy is PET most common? Give percentages

A

44% - postpartum
38% - antepartum
18% - intrapartum

38
Q

when is proteinuria considered significant in PET? what are the 3 tests you can do to determine this?

A
  1. urinalysis (reagent strip) > 1+
  2. spot urinary protein: creatinine ratio > 30 mg/mmol
  3. 24 hrs urine protein collection > 300 mg/day
39
Q

presentation of PET (9)

A
  1. headache, blurring of vision
  2. epigastric pain, below the ribs –> vomiting
  3. sudden swelling or hands, face, legs, papilloedema
  4. severe HT, proteinuria > 3+
  5. DIC features
  6. clonus, brisk reflexes
  7. decrease urine output
  8. eclampsia
  9. HELLP syndrome
40
Q

define HELLP syndrome

A
  • heamolysis
  • elevated hepatic enzymes
  • low platelets
41
Q

investigation for PET

A
  1. bloods:
    • FBC: - platelets, - Hb
    • LFTs: + enzymes, + bilirubin
    • renal function tests: + urea, + creatinine, + urate
  2. frequent bp monitoring
  3. urinalysis
  4. examination: headache, visual disturbances, epigastric pain, hyper reflexia, etc.
  5. fetal monitoring
    • growth scan
    • CTG
42
Q

potential pathophysiological causes of PET (3)

A
  1. immunological
  2. genetic disposition
    • secondary invasion of trophoblasts into spiral vessels –> decreased placental perfusion
    • increased uterine arterial resistance –> increased sensitivity to vasoconstrictors –> chronic placental ischemia –> IUGR/fetal death
    • imbalance of maternal vasodilator (prostacyclin).vasoconstrictors (thomboxane) in pregnancy
    • inhibition of nitric oxide pathway –> prevents embryo implantation
  3. endothelial dysfunction
    • hepatic endothelium –> HELLP
    • cerebral endothelium –> neurological disorders and preeclampsia
43
Q

risks of PET (8)

A
  • increased maternal age
  • first pregnancy
  • multiple pregnancy
  • pregnancy interval > 10 yrs
  • BMI > 35
  • previous PET (esp with preterm delivery < 34 wks, severe PET, IUGR baby, IIUD, abruption)
  • FH of PET
  • underlying medical conditions like chronic HT, renal disease, DM, autoimmune disorders (SLE, antiphospholips antibodies)
44
Q

management of PET (6)

A
  1. the ONLY cure - deliver the baby + placenta
  2. conservative: aim for fetal maturity
    • close observation
    • safe antihypertensives: labetalol, nifedipine, methyldopa
    • steroids if < 36 wks
  3. prepare induction of labor/CS
  4. monitoring continues PN, most PET postpartum
  5. treatment of seizures/eclampsia
  6. prophylaxis PET treatment for subsequent pregnancies
45
Q

what are the medications given to treat seizures or impending eclampsia? (3)

A
  1. Magnesium sulfate bolus + IV
  2. bp control if > 160/110 (severe) with labtetalol, hydralazine (vasodilator)
  3. avoid fluid overload: aim for 80mL/hr intake
46
Q

what is the medication given as a prophylaxis to prevent future PET with subsequent pregnancies?

A

low dose aspirin - from 12 weeks till delivery

47
Q

complications of PET? (8)

A
  1. eclampsia + seizures
  2. DIC
  3. HELLP
  4. cerebral haemorrhage, storke
  5. renal failure
  6. pulmonary edema, heart failure
  7. increased HT risk later in life
  8. impaired placental/fetal perfusion:
    • IUGR
    • fetal distress
    • premature birth
    • increased PN death
48
Q

what is the difference between gestational DM and pre-existing DM?

A

preexisting has a more severe impact on maternal and fetal morbidity.
GDM:
- carbohydrate intolerance that happens/detected in pregnancy
- abnormal GTT that reverts back to normal PN

49
Q

complications of pre-existing DM in pregnancy? divide into maternal (4) and fetal (9)

A

maternal:

  • increased PET risk
  • reduced hypoglycemia awareness
    - increased neuropathy/ retinopathy
    - infections
    fetal:
  • fetal hyperinsulinemia –> macrosmia
  • PN hypoglycemia
  • risk of congenital abnormalities (cardiac, sacral agenesis)
  • miscarriage
  • polyhydraminos
  • shoulder dystocia –> CS/operative delivery
  • malformations - 1st trimester
  • increased still birth and PN mortality - 3rd trimester
  • jaundice
  • RDS
50
Q

management of pre-existing DM, divided into preconception, conception, and intrapartum

A

preconception:
- better glycemic control
- folic acid 5 mg
- dietary advice
- retinal/renal assessment
conception:
- increase insulin regimen
- optimase gluc control (can continue metformin)
- avoid hypos: glucagon injects/glucose solution
- repeat retinal assessment at 28 and 34 weeks
- monitor for ketonuria/infection
- monitor fetal growth
intrapartum:
- labor induced at 38-40 wks, but can be earlier in DM
- consider CS if macrosmia
- dextrose insulin infusion (prevent hypos)
- CTG monitoring
- early baby feeding to prevent hypos

51
Q

what is the target glycemix control for those with DM before getting pregnant?

A

4-7 mmol/L bg

< 6.5% HbA1c (< 48mmol/mol)

52
Q

why do you need to increase insulin regimen in pregnancy before returning to normal PN?

A

human placental lactogen, progesterone, HCG, cortisol from the placenta all have anti-insulin actions

53
Q

optimal bg during pregnancy at different times of the day

A

fasting: < 5.3 mmol/L
before bed: < 6
1 hr postprandiol (after eating): < 7.8
2 hrs postprandiol: < 6.4

54
Q

risks of GDM (7)

A
  1. BMI > 30
  2. previous microsmia > 4.5 kg
  3. current microsmia or polyhydraminos
  4. previous GDM
  5. FH of DM
  6. high risk ethnic group for DM - southeast asian
  7. recurrent glycosuria in current pregnancy
55
Q

investigation for GDM (if high risk)

A
  1. HbA1c offered at booking if high risk > 6% (43 mmol/mol)

2. OGTT - if normal repeat at 24-28 weeks 75mg/dL

56
Q

management of GDM

A
  • control bg through diet, proceed to metformin/insulin if not working
  • check OGTT 6-8 weeks PN
  • annual HbA1c checks afterwards (increased overt DM risk)
57
Q

presentation of venous thromboembolism

A
  1. virchow’s triad
    • hypercoagulibility
    • venous stasis
    • venous wall damage
  2. pain in calf, muscle tenderness
  3. unlilateral swelling
  4. PE - pain on breathing, SOB, cough, tachycardia, hypoxia, pleural rubs
58
Q

what are the markers that increase or decrease during pregnancy that makes it a natural hypercoagulable state?

A
  • increased fibronogen, factor VII, VW factor, platelets
  • decreased natural anticoagulants (antithrombin III)
  • decreased fibrinolysis
59
Q

what are the things that happens in pregnancy that further exacerbates the veirchow’s triad?

A
  1. venous stasis: progesterone (enlarge uterus)
  2. vessel wall injury: damage can happen during operative delivery/CS
  3. hypercoagulability: natural state during pregnancy
60
Q

risks of VTE in pregnancy

A
  • increasing age
  • increased parity
  • smoker
  • high BMI
  • IVDU
  • PET
  • dehydration - hyperemesis (prolonged vomiting in pregnancy)
  • infections
  • operative delivery, prolonged labor
  • haemorrhage, blood loss > 2L
  • previous VTE, thrombophilia, FH
  • sickle cell disease
61
Q

investigation for VTE

A
  • doppler
  • ECG
  • blood gas
  • VQ scan (for PE)
  • CTPA (CT pulmonary angiogram)
62
Q

management

A
  • TED stockings
  • increase mobility and hydration
  • anticoagulants until 6 wks PN (indicated if >= 3 risk factors)
63
Q

causes of miscarriage (5)

A
  1. abnormal conception (fetal issues) - 50% spontaneous miscarriage
    • chromosomal abnormality
  2. uterine/cervix abnormality
    • congenital: mullerian ducts not fusing
    • uterine incompetence
    • fibroids
    • cervical weakness: primary/secondary - trauma, iatrogenic, hormonal imbalances (decreased progesterone), etc.
  3. maternal problem
    • increased age, DM, SLE, thyroid
    • infection
    • drugs
  4. placental/cord/membranes problem (infection)
  5. unknown
64
Q

why do human contractions only last in bouts of 1 minute?

A

to prevent hypoxia of the baby during delivery (brain damage after 3 minutes)

65
Q

different between intrauterine death and still birth?

A

IUD - death inside the uterine

stillbirth - when IUD baby is delivered

66
Q

why does cocaine cause placental abruption?

A

it is a vasoconstrictor

- also causes CA constriction in baby

67
Q

physiological explanation of molar pregnancy

A

egg –> baby
sperm –> placental development
if 2x sperms fertilize with 1 empty ovum (no chromosome and therefore no baby formation) –> overgrowth of placenta and trophoblasts –> molar pregnancy

68
Q

presentation of molar pregnancy

A

presents like a miscarriage, but large grape like vesicles formed from chorionic villi might be seen.

69
Q

what malignant disease is molar pregnancy a precursor of?

A

choriocarcinoma (malignant cancer of trophoblast cells)

70
Q

management of molar pregnancy (escalating steps)

A
  1. scraping of endometrium, followed by BhCG check
    • repeat again if BhCG still high
  2. 1 dose methotrexate if still high after 2 scrapings - very little amount and therefore no risk for future pregnancy, followed by BhCG check
71
Q

why does BhCG work as a marker for pregnancy? What is it specific to?

A

BhCG is produced by trophoblast cells, which only appear on the outer surface of a fertilized egg.

72
Q

what are the 2 complications for pregnancy in which methotrexate can be used for?

A
  1. ectopic pregnancy

2. molar pregnancy

73
Q

what is the legal gestation age for TOPFA?

A

< 24 weeks
- later than this still possible for certain abnormalities, but less legally complicated if done before fetus is considered a ‘baby’

74
Q

what are the organisms to watch out for in ascending infection?

A

normal commensals

  1. E coli
  2. Strep B
75
Q

fetal complications in ascending infection

A

(mother can be ill or well)

  • IUD
  • ill in the first few days and get better
  • cerebral palsy later in life even if well at birth
76
Q

Ascending infection is one of the biggest causes of cerebral palsy, how does this happen?

A

neutrophils invade the placenta, umbilical cord, amniotic sac –> causes cytokine storm in the brain –> further damaged if hypoxic during delivery

77
Q

why is a vaginal swab not a good investigation for ascending infection or chorioamnionitis?

A

because even if an organism is found, you can’t tell if it stopped at the vagina or involved amniotic fluid.

78
Q

will the baby be born safely if the mother is a drug addict? what precautions must be made to prepare for the delivery of this baby?

A
  • baby will be born safely unless the drug was teratogenic

- however, it will experience withdrawal symptoms and delivery must happen in a hospital with large neonatal unit.

79
Q

what injections are given to the baby to help withdraw from opiates, and how long is it normally given?

A

phenobarbital > 5 days, slowly tapering

Reproductive System (7 decks)

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