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Repro > Complicated pregnancy 6 > Flashcards

Complicated pregnancy 6 Flashcards

1
Q

Hyperemesis gravidarum
Ax
RF [5]

A 
Ax: raised beta-HCG levels
RF:
- Multiple pregnancies
- Trophoblastic disease
- Hyperthyroidism
- Nulliparity
- Obesity
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2
Q 
Hyperemesis gravidarum
Presentation
Onset, duration
Diagnostic triad
Systemic signs [5]
A

Extreme form of nausea and vomiting in pregnancy

  • usually 8-12w but can persist up to 20w
  • Diagnostic triad: 5% pre-pregnancy weight loss, dehydration, electrolyte imbalance
  • Dehydration, weight loss, hypokalemia, muscle weakness, tetany
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3
Q

Hyperemesis gravidarum
Investigations [4]
Management [4]

A 
Investigation:
•	Urinalysis: ketones
•	U&E and creatinine: hyponatraemia, hypokalaemia
•	Severity
•	USS: excl. hydratiform mole 
- TFTs

Mx:

  • Antihistamines promethazine or cyclizine
  • Admit for IV fluids if unable to tolerate oral or electrolyte imbalance
  • High dose folic acid and pabrinex
  • Avoid glucose as it precipitates Wernickes
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4
Q

How do u formally assess severity in hyperemesis gravidarum?

Complications of HG
Maternal [4]
Fetal [2]

A

Pregnancy Unique Quantification of Emesis (PUQE) score

Complications:
• Maternal: Wernicke’s encephalopathy, Mallory-Weiss tear, central pontine myelinolysis, acute tubular necrosis
• Fetal: SGA, pre-term birth

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5
Q

Why is there an increased risk for thromboembolic disease in HG patients?

A

The coincidence of pregnancy, dehydration [2] and associated immobility in a woman with hyperemesis increase the risk of venous thromboembolic events

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6
Q

Rationale for doing TFT in HG?

A

Excessive hCG secretion may cause hyperthyroidism in patients with hyperemesis gravidarum

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7
Q

Jaundice in pregnancy causes [2]

A

Intrahepatic cholestasis of pregnancy

Acute fatty liver of pregnancy

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8
Q 
Intrahepatic cholestasis of pregnancy
Ax
Symptoms [3]
Sign
Complications [3]
A

Ax: impaired release of bile causing bile to build up in the liver
Symptoms:
- Pruritus of palms, abdomen, soles but no rash
- Second half of pregnancy
- Worse at night
Signs: visible jaundice
Cx:
- premature birth, stillbirth, can recur with COCP or future pregnancies

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9
Q

Intrahepatic cholestasis of pregnancy
Ix [2]
Mx [4]
Prognosis

A

Ix:
- LFTs (mildly elevated AST and ALT with elevated bilirubin)
- clotting
Mx:
- induction of labour (IOL) at 37w (due to increased risk of stillbirth)
- URSODEOXYCHOLIC ACID (symptomatic relief)
- weekly LFTs
- VITAMIN K supplementation (to mum if abnormal clotting and to baby at delivery)

Prognosis: resolves within days of delivery

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10
Q

Acute fatty liver of pregnancy
Presentation [6]
Ix [5]

A

Sy/Si:

  • abdo pain, N&V
  • headache
  • jaundice
  • hypoglycaemia
  • pre-eclampsia
  • usually after 30w

Ix:

  • LFTs (high ALT, bilirubin)
  • U&Es (AKI)
  • Urate
  • Glucose (low)
  • Clotting
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11
Q

Acute fatty liver of pregnancy
Mx [3]
Complications [2]

A

Mx:

  • HDU or ITU mx with BP monitoring
  • Mx of liver and renal failure, low glc
  • Deliver once stabilized

Complications:

  • PPH
  • Neonatal hypoglycemia
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12
Q

VTE
Investigations [5]
Management
Prevention [3]

A
  1. Bloods: FBC, U&E, clotting, LFTs D dimer INACCURATE
  2. Suspected DVT: duplex USS
  3. Suspected PE: duplex USS (can presume PE if +ve and chest symptoms)
    - if -ve then CXR and V/Q scan if no abnormality on CXR
    - do ECG look for right heart strain

Mx:
- treatment dose LMWH for 3m

Pre:

  • prophylactic LMWH stat if previous VTE,
  • immediately if >4 RFs and from 28w
  • if 3 RFs continued until 6w post-natal
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13
Q

Small for gestational age
Define
Non-placental [4]
Placental classified into 2 mechanisms

A

Born with birth weight < 10th centile

Non-placental

  • Structural (gastroschisis)
  • Chromosomal
  • Inborn errors of metabolism
  • TORCH

Placental

  • Nutrient transfer
  • Implantation and vasculature
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14
Q

What are underlying causes for problems with nutrient transfer causing SGA? [3]

What are underlying causes for problems with IMPLANTATION AND VASCULATURE causing SGA? [3]

A
  • Nutrient transfer
    > Low pre-pregnancy weight, undernutrition
    > Cocaine, alcohol, smoking
    > Severe anemia
- Implantation and vasculature
 > Pre-eclampsia
 > Essential HTN
 > Thrombophilia
 > Autoimmune
 > Repeated APH
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15
Q

Define Low birth weight

Association between IUGR and SGA

A

<2.5kg

More likely in severe SGA where pathological growth restriction
- majority of SGA babies are actually appropriate for maternal height and ethnicity)

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16
Q

RF for SGA

Major [7]

A

Major:

  • > 40y/o, smoker >11/d
  • paternal SGA, previous SGA baby
  • cocaine, vigorous daily exercise
  • chronic HTN, DM with vascular disease, renal impairment
  • anti-phospholipid syndrome
  • low PAPP-A
  • fetal echogenic bowel
17
Q

RF for SGA

Minor [7]

A

Minor:

  • > 35y/o
  • IVF singleton, nulliparity
  • BMI <20 or 25-34.9
  • smoker 1-10/d
  • low fruit intake before pregnancy
  • previous pre-eclampsia
  • pregnancy interval <6m
18
Q

SGA presentation

Investigations that need to be done

A

SFH >3cm below number of weeks gestation or identified at anomaly scan

  • Always check BP and urine for pre-eclampsia
  • Serial growth scans from 26-28w (if any major RFs)
  • Umbilical artery doppler
  • Anomaly scan
  • Amniocentesis and karyotype
  • Toxoplasmosis and CMV serology
19
Q

SGA management

Surveillance protocol depends on Doppler scan [4]

A

Surveillance
o Normal Doppler: serial growth scans NOT indicated unless other cx
o Abnormal Doppler: serial growth scans from 26-28w every 2w and Doppler

20
Q

Labour & Delivery for SGA:

  • If <32w and abnormal Doppler
  • If >32w and abnormal Doppler
  • If >32w and normal Doppler
A

o <32w and abnormal Doppler: deliver <32w
o >32w and abnormal Doppler: deliver before 37w
o >32w and normal Doppler: deliver at 37w

21
Q 
LGA definition
Risk factor 
Presentation
Ix
Mx
Cx [4]
A 
Define: Weight at gestation >4.5kg
Risk factor: maternal DM, obesity
Presentation: picked up on USS
Ix: regular growth scans
Mx: deliver at 37w
Cx:
- CS, tears, PPH
- Fetal death
22
Q

Rhesus disease
Ax
Ix
Mx [2]

A

Ax: mother is Rh-ve and father is Rh +ve
Ix: screen at 8-12w for mothers rhesus status
Mx:
- No abs: give prophylactic anti-D IgG at 28 and 34w to prevent mother making own anti-D
- Antibodies present: monitor pregnancy for signs of fetal anemia

23
Q

Twin pregnancies
Incidence
Monozygotic
Dizygotic

A

1 in 105 pregnancies
• Monozygotic: identical; develop from single ovum which has divided to form 2 embryos
• Dizygotic (80%): non-identical; develop from 2 separate ova that are fertilised at the same time

24
Q

Risk factor for dizygotic twins [4]

A

RF:

  • induced ovulation, IVF
  • previous twins, FHx
  • increasing maternal age, multigravida
  • Afro-Caribbean ethnicity
25
Q

Dizygotic: dichorionic, diamniotic (DCDA) pathophysiology

Types of monozygotic [3]

A

DCDA: split days 1-3; usually dizygotic

  • Monochorionic diamniotic
  • Monochorionic monoamniotic
  • Conjoined twins
26
Q

Pathophysiology of:

  • Monochorionic diamniotic (MCDA)
  • Monochorionic monoamniotic (MCMA)
  • Conjoined twins
A
  • MCDA: split days 4-8, usually monozygotic
  • MCMA: split days 8-13, riskiest due to placental insufficiency and cord entanglement
  • Conjoined twins: split days 13-15
27
Q

What are specific associations with monozygotic? [5]

A

Increased risk of:

  • spontaneous miscarriage
  • perinatal mortality, IUGR
  • malformations
  • prematurity
  • twin to twin transfusion syndrome
28
Q

Diagnosis [2]

A

Confirmed by first ultrasound scan

Lamda sign if dichorionic

29
Q

Ante-natal care of twin pregnancies [4]

A

Rest
Monthly USS
Additional Fe, folate
Weekly antenatal care after 30w

30
Q

Timing of delivery for DCDA, MCDA, MCMA

Labour and delivery of twin pregnancies steps [7]

A

Timings:

  • DCDA at 37-38w
  • MCDA at 36-37w
  • MCMA at 32-34w
  • Requires 2 obstetricians present
  • In theatre
  • Continuous CTG
  • Cord clamping
  • 2nd scan to assess presentation of twin 2
  • Oxytocin
  • Vaginal assisted delivery or C-section
31
Q

Complications of twin pregnancies
Maternal [5]
Fetal [6]

A

Maternal

  • Pre-eclampsia, GDM
  • Polyhydramnios
  • APH, PPH
  • Placental abruption
  • Cord prolapse

Fetal

  • Preterm labour
  • Congenital malformations
  • IUGR
  • Placental insufficiency
  • Perinatal mortality x5 twins, x8 triplets
  • Twin to twin transfusion syndrome
32
Q

Twin to twin transfusion syndrome pathophysiology [4]

Mx [2]

A
  • Monochorionic twins share chorion
  • blood vessels anastomose so donor twin’s blood supply disproportionately goes to recipient twin
  • Donor > IUGR and oligohydramnios
  • Recipient > larger, polyhydramnios

Mx: serial amniocentesis, laser photocoagulation

Repro (34 decks)

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