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RANZCOG 2024 - maternal medical conditions > Gastro-Hepatic conditions > Flashcards

Gastro-Hepatic conditions Flashcards

1
Q

Discuss appendicitis in pregnancy
-Incidence (1)
-Complications (4)
-Obstetric complications (4)
-Management (2)

A
  1. Incidence 1:1000
  2. Complications
    -Sepsis, perforation, abscess, peritonitis
  3. Obstetric complications
    -Fetal loss 1% if simple appendicitis, 36% if ruptured
    -Miscarriage 33% in first trimester
    -PTL 14% in second trimester
  4. Management
    -Surgery - laparoscopic until 34 weeks
    -Open with site of incision depending on gestation
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2
Q

Discuss bilary colic in pregnancy
-Incidence of Gallstones in pregnancy
-Cause of gallstones in pregnancy
-Presentation in pregnancy
-Management

A
  1. Incidence
    -Gallstones present in approx 20% of pregnant women
    -33% of pregnant women have gallbladder sludge
  2. Cause of gallstones in pregnancy
    -Oestrogen increases gallstone formation
    -Progesterone reduces gallbladder contractility
  3. Presentation in pregnancy
    -Similar to outside of pregnancy
  4. Management
    -Aim for conservative management
    -Consider surgery if frequent attacks to reduce maternal morbidity
    -Increased risk of gallstone pancreatitis in pregnancy with high fetal mortality
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3
Q

Discuss acute fatty liver of pregnancy
-Incidence
-Risk factors (4)

A
  1. Incidence
    -1:7000 to 1:20000
  2. Risk factors
    -Multiple pregnancy
    -Male fetus
    -Nulliparity
    -Obesity
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4
Q

What is the pathophysiology of acute fatty liver of pregnancy

A

Thought to be due to an autosomal recessive disorder in the fetus where by it lacks LCHAD enzyme (Long chain 3-hydroxy acyl-CoA dehydrogenase).
This leads to a build up of medium to long chain fatty acids which enter the maternal circulation and accumulate in the maternal liver.
The gene affected most commonly is E474Q

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5
Q

Discuss acute fatty liver of pregnancy
-Clinical features (7)
-Investigations (9)
-Distinctive features (3)

A
  1. Clinical features
    -Onset in third trimester after 30/40 or postnatal (20%)
    -Gradual onset of malaise, nausea, anorexia
    -Severe vomiting and abdo pain in 60%
    -Pruritis or jaundice
    -Polyuria or ploydipsia secondary to impaired liver being unable to metabolise vasopressin = ADH (Diabetes insipidis)
    -DIC
    -Hepatic encephalopathy
  2. Investigations
    -LFTs deranged 3-10x. Bilirubin can be raised
    -FBC - neutrophillia
    -Creatinine - raised
    -Uric acid often raised more than in PET
    -Coagulopathy seen in 90% - low IR, low fibrinogen, prolonged PT
    -Hypoglycemia in 70%
    -Blood gases - lactic acidosis
    -Liver USS for fatty infiltrate
    -Liver Bx for definitive diagnosis but coagulopathy may preclude this. Shows microvascular fatty infiltration
  3. Distinctive features
    -Hypoglycemia - 70%
    -Hyperuricemia - 90%
    -Coagulopathy in absence of thrombocytopenia - 90%
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6
Q

What features distinguish HELLP from AFLP

A
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7
Q

How should AFLP be managed (8 points)

A
  1. MDT with obstetric, anaesthetics, haematology, gastro / hepatologist
  2. Expedite delivery once maternal condition stabilised
  3. Correct hypoglycemia - 10% or 50% IV glucose
  4. Correct coags - FFP, Vit K
  5. Consider NAC if LFTs severely deranged
  6. Fluid balance and if increased polyuria consider desmopressin
  7. Significant sepsis risk - consider Abx
  8. Screen baby for LCHAD deficiency
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8
Q

What are the risks associated with AFLP

A
  1. Maternal mortality - was 10-20% now improved to 2%
  2. Fetal mortality - was 20-30% now 11%
  3. Most women if they survive make a full recovery
  4. Recurrence risk - 25%
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9
Q

Discuss GORD in pregnancy
-Incidence
-Causes (3)
-Management (7)

A
  1. Incidence - 60%
  2. Causes
    -Decreased lower oesophageal sphincter pressures
    -Decreased gastric emptying and peristalsis
    -Enlarging uterus
  3. Management
    -Upright position after meals
    -Eat small meals
    -Avoid irritants
    -Gaviscon or mylanta - first line
    -Omeprazole - 2nd line
    -Consider metocloprimide for gastric emptying
    -Avoid ranitidine - cancer link
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10
Q

Discus HELLP disease
-Epidemiology (1)
-Definition
-Risk factors (2)

A
  1. Affects 20% of women with severe PET
  2. Definition
    -Complication of severe PET including haemolysis, elevated liver enzymes, low platelets
  3. Risk factors
    -Increased risk with increasing age and parity
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11
Q

Discuss HELLP disease
-Clinical features
-Onset
-Severe complications
-Rates of maternal and fetal mortality

A
  1. Clinical features
    -Epigastric pain most common
    -Headache, nausea, vomiting, oedema, haematuria
    -Jaundice, HTN
    -Diabetes insipidis (Liver unable to metabolise ADH
  2. Onset
    -15% second trimester, 50% third trimester, 35% postpartum
  3. Severe complications
    -Renal failure
    -DIC
    -Abruption
    -Pulmonary oedema
    -Liver capsule haematoma and rupture
  4. Mortality rates
    -Maternal mortality - 1-10%
    -Fetal mortality 8-60%
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12
Q

Discuss investigations for HELLP
1. Bloods
2. Urine
3. USS

A
  1. Bloods
    -FBC - anemia, thrombocytopenia
    -Bloods film - fragmented red cells
    -Haemolysis screen - LDH, reticulocyte count, bilirubin
    -LFTs - derranged
    -Coags - DIC present in 20%
  2. Urine - protienuria
  3. Liver USS to assess for subcapsular haematoma
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13
Q

Discuss management for HELLP

A
  1. Management same as for severe PET
  2. Stabilise mother and expidite delivery
  3. Control BP
  4. Careful fluid balance
  5. Seizure prophylaxis - MgSO4
  6. Steroids for fetal prematurity (Can also improve thrombocytopenia)
  7. Correct haematology
  8. If platelets <20 consider platelet transfusion
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14
Q

What is the risk of recurrence for HELLP

A

Risk of recurrence for HELLP is low 3-27% compared to PET which is high at 42%

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15
Q

What is the effect of pregnancy on inflammatory bowel disease (5)

A

-Chron’s disease - not change in risk of flare
-Ulcerative colitis - double the risk of relapse in pregnancy (35%). 6 times the risk of PP flare
-Malabsorption of fat, fat soluble vitamins and B12
-Obstruction of ileostomy as pregnancy progresses
-Peristomal cracking and bleeding due to abdominal wall stretching

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16
Q

What is the effect of inflammatory bowel disease on pregnancy (4)

A

-Reduced fertility if IBD active
-Increased miscarriage rate if active disease at time of conception
-Increased risk of PTD in active disease
-Most women have normal pregnancies

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17
Q

How should a pregnancy be managed for a woman with inflammatory bowel disease
-Pre-conception
-Antenatally
-Intrapartum
-Post natally

A
  1. Pre conception
    -Encourage conception during times of remission
    -5mg folate per day if on sulfasalazine
    -Review medications and stop those contra-indicated in pregnancy (Methotrexate)
  2. Antenatal
    -Monitor fetal growth
    -If on anti-TNF agents stop in third trimester to allow fetus to clear prior to delivery
  3. Intrapartum
    -Avoid vaginal birth and episiotomy in severe perianal disease
    -Prepare for surgical issues in previous abdominal surgery
  4. Postpartum
    -Monitor for UC flare
    -Avoid live vaccines in babies exposed to anti-TNF agents for 6/12
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18
Q

Discus the safety of IBD medications in pregnancy and breast feeding
-Mesalazine
-Sulfasalazine
-Corticosteriods
-Thiopurines (Azathioprine, mercaptopurine)
-Anti TNF agents (Infliximab, adalumamab
-Methotrexate

A
  1. Meselazine - low risk in both
  2. Sulfasalzine - low risk in both
  3. Corticosteriods - Low risk in both
  4. Thiopurines - low risk in both
  5. Anti TNF agents. Low risk in pregnancy. Stop in third trimester or earlier if in remission. Limited data for breastfeeding. Likely low risk
  6. Methotrexate - contra-indicated in both
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19
Q

Discuss intrahepatic obstetric cholestasis
-Incidence (2)
-Risk factors

A
  1. Incidence
    -0.7% in multiethnic populations
    -1.2-1.5% of South Asian women
  2. Risk factors (5)
    -Ethnicity
    -Family Hx (>30% have affected siblings, OR 12)
    -Multiple pregnancy (RR 5)
    -Hep C
    -Gallstones
    -Genetics
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20
Q

Discuss the clinical presentation of intrahepatic obstetric cholestasis (7)

A

-Pruritis - typically trunk and limbs but esp. palms and souls of feet. Worse at night. NB 25% of women have pruritis in pregnancy
-Absence of skin rash
-Jaundice, dark urine, steatorrhoea, pale stools = rare
-Raised bile salts >18
-LFT derangement
-Liver failure sx - prolonged PT or hypoglycemia = very rare in IOC
-More common in 3rd trimester. 5% in 1st T

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21
Q

What are the ranges for intrahepatic obstetric cholestasis
-General pruritis
-Mild IOC
-Moderate IOC
-Severe IOC

A
  1. General pruritis - itching with peak bile salts <18
  2. Mild IOC - itching with peak bile salts 19-39
  3. Moderate IOC - itching and peak bile salts 40-99
  4. Severe IOC - itching and peak bile salts >=100

Peak bile salts means the highest bile salt concentration recorded during pregnancy.

22
Q

Discuss the diagnosis of intrahepatic obstetric cholestasis (9)

A
  1. In women with itch and normal skin test for bile salts and LFT derangement
  2. Consider other causes of itch/bile salt and LFT derangement with careful Hx and exam
  3. Where women have normal bile salts and LFTs ongoing testing 1-2 weekly/as clinically indicated should be undertaken as IOC can develop up to 15 weeks post onset of itch
  4. Resolution of itch or normalisation of LFTs and bile salt derangement during pregnancy is unlikely to be IOC
  5. Resolution of itch and normalisation of LFT/Bile salts at least 4 weeks postnatally support diagnosis
  6. Testing to rule out other causes for clinical presentation (viral and autoimmune tests, liver USS) are no longer recommended in RCOG. SOMANZ recommends viral serology, USS but not immune screen or Bx
  7. Coag studies not routinely required
  8. Do Hx (RF for viruses, medications, Family Hx of liver disorders)
  9. Do Examination
23
Q

What is the impact of intrahepatic obstetric cholestasis for the woman? (5)

A
  1. Itch - can be generalised/focal. Mild to unbearable (poor correlation between itch severity and bile salt concentration)
  2. Poor sleep and poor mental wellbeing secondary to itch
  3. Increased risk of developing PET (OR 10)
  4. Increased risk of developing GDM (OR 3)
  5. Increased risk of developing autoimmune diseases later in life
24
Q

Discuss the impact of intrahepatic obstetric cholestasis for the fetus (6)

A
  1. Risk of still birth. Determined by bile salt concentration. Only increases once peak bile salts >100. RR 30
  2. Iatrogenic preterm delivery
  3. Risk of still birth in twins with IOC
  4. Increased risk of meconium at birth if BS >40
  5. Increased chance of neonatal care requirement
  6. PTB - BS acting on myometrial oxytocin
25
Q

Discuss timing of delivery for women affected by intrahepatic obstetric cholestasis. (4)

A

-IOL if peak bile salts >100 36/40 (30 times higher) 3.4% risk after 35/40
-IOL if peak bile salts 40-99 38/40 (10 times higher)
-IOL if peak bile salt <39 - Consider IOL at 40/40. Risk same as background risk
-If comorbidities (PET/GDM) increased risk of still birth and individualised timing of IOL

26
Q

Discuss the management of intrahepatic obstetric cholestasis in pregnancy
-Antenatal monitoring (4)
-Antenatal treatment (7 points, 5 treatments)

A
  1. Antenatal monitoring
    -MDT approach - MW, GP, Obs, Obs physician
    -Monitor bile salts weekly as peak bile salt can change and result in a change of severity and change in management. Fortnightly if mild, weekly if severe (>40)
    -Once BS >100 can stop testing as Rx won’t change
    -USS or CTG doesn’t predict or prevent still birth in IOC.
    -Fetal movement monitoring by the mother is recommended
    -IOC not associated with IUGR so no need for GS
    -Test coags in severe ICP >40 BS
    -OGTT given increased risk of GDM
    -PET monitoring given increased risk
  2. Treatment
    -No treatment improves pregnancy outcomes
    -Treatments to improve itch are of limited benefit
    -Consider topical emollients +/- menthol for itch
    -Sedative antihistamine for itch and sleep (Chlorphenamine)
    -Ursodeoxycholic acid doesn’t impact perinatal outcomes and should not be routinely offered. It has poor evidence to show improvement in itch.
    SOMANZ recommends use if remote from term.
    -Dose 500mg OD if mild, 1500mg OD if severe max dose 2000mg/OD
    -Rifampicin not recommended. No evidence of benefit.
    -Consider vit K if evidence of reduced fat absorption (steatorrhoea) or prolonged prothrombin time. APTT >40 or INR >1.4 treat with 10mg Vit K IV
27
Q

Discuss management of intrahepatic obstetric cholestasis:
-Labour and delivery (3)
-Postpartum FU (4)

A
  1. Labour and delivery
    -Aim VB unless other reasons to consider CS
    -Continuous fetal monitoring if bile salts >100 (if IOL have continuous monitoring anyway)
    -Active third stage. Increase in PPH
  2. Postpartum
    -4 week follow up to confirm resolution of IOC
    -Advise against estrogen containing contraception
    -IOC is not a contraindication for HRT
    -Risk of recurrence 90%
    -Do baseline LFTs and bile salts with booking bloods at subsequent pregnancies
    -Vit K for neonates
    -Long term FU for liver disease - at increased risk of chronic liver disease
28
Q

What are the proposed mechanisms of IUFD in women with intrahepatic obstetric cholestasis (2)

A
  1. Increased bile salts in amniotic fluid results in vasoconstriction of placenta chorionic veins leading to fetal asphyxia
  2. Increased bile salts cause fetal arrythmias due to bile salts action on myocytes
29
Q

Discuss hyperemesis in pregnancy
-Incidence (3)
-Definition
-What is the risk of recurrence for NVP and HG

A
  1. Incidence
    -Nausea and vomiting in pregnancy - 50-80%
    -Hyperemesis gravidarum - 0.3-3%
    -Resolution b y 20/40 75%. Ongoing until term 10%
  2. Definition
    -Nausea and vomiting caused by pregnancy leading to: significant reduction in oral intake, weight loss at least 5% of pre-pregnancy weight, +/- dehydration +/- electrolyte abnormalities
  3. Recurrence
    -83% NVP
    -15-26%HG
30
Q

How is nausea and vomiting in pregnancy classified

A
  1. Classification by the PUQE-24 score
  2. Score from 1-5 based on:
    -time of nauseas in hours
    -number of times vomited in previous 24hrs
    -number of times dry retched in 24 hrs
  3. Management is based on score.
    -<12 doesn’t need investigation
    ->12 needs investigation
    >=13 considered severe
31
Q

Discuss investigations for hyperemesis gravidarum

A
  1. Investigating N&V in pregnancy depends on PUQE-24 score
    -<12 = don’t investigate, >12 = investigate
  2. Bloods
    -U&Es, bicarbonate
    -TSH (usually biochemical). Only measure if refractory to Rx
    -LFTs
    -FBC - haematocrit
  3. MSU
    -Ketones
    -Rule out infection
  4. USS
    -look for molar and multiple pregnancy
32
Q

What is the pathogenesis of hyperemesis gravidarum (7)

A
  1. Direct correlation between HCG and hyperemesis
  2. Related to levels of TSH (supressed by HCG) and increased T4
  3. Progesterone driven gastric emptying and low oesophageal sphincter pressure worsens
  4. Other factors: genetics, female fetus elemental deficiencies
  5. Asociated with genetic predisoposition - calcium channel function
  6. 73% association with FHx
  7. Multifactorial
33
Q

What are the maternal complications of hyperemesis (8)

A
  1. Wernicke’s encephalopathy
    -due to thiamine deficiency
  2. Hyponatraemia
  3. Arrythmias and seizures
    -If severe electrolyte abnormalities
  4. Vitamin deficiencies
    -B6 and B12
  5. Malnutrition
    -Weight loss, muscle wasting
  6. Mallory Weiss tears
  7. Psychological complications
  8. Thrombosis
    -Secondary to dehydration and immobility
34
Q

What are the obstetric complications associated with hyperemesis gravidarum (5)

A
  1. SGA
  2. PTB
  3. PET
  4. Abruption
  5. GDM from steroids
35
Q

Discuss the management of hyperemesis gravidarum in mild to moderate hyperemesis gravidarum (PUQE <13) (13)

A
  1. Assess with Hx and examination and r/o other causes
  2. Assess dehydration and weight loss
  3. Assess PUQE score
  4. If PUGE-24 score <13 HG is considered mild/moderate
    -Assess weight and hydration
    -Don’t do any investigations
    -Assess mental health
    -Out-patient management by GP, MW etc
    -Diet as tolerated
    -Cease multivitamins apart from folate and iodine
    -Oral antiemetics (one first line med or Ondansetron)
    -Gastric acid suppressors
    -Laxatives
    -Dietician review if prolonged poor intake
36
Q

Discuss the management of hyperemesis gravidarum in severe cases (PUQE >13) (18)

A
  1. Assess with Hx and examination and r/o other causes
  2. Assess dehydration and weight loss
  3. Assess PUQE score
  4. If PUGE-24 score >13 HG - is considered severe
    -Assess weight and hydration
    -Undertake investigations (bloods, MSU, USS)
    -Mental health assessment
    -Consider IP management if:
    -T1DM, requiring essential medication, severe electrolyte disturbances, failed OP management
    -Cease multivitamins except folic acid and iodine
    -Given oral or parenteral antiemetics (Ondansetron + first line overnight)
    -Consider steroids
    -Gastric acid suppression PPI
    -Laxatives
    -IVF (avoid dextrose. Increased Wenickes)
    -Thiamine
    -Diet as tolerated
    -Dietician review if prolonged reduced intake
    -Replace electrolytes
37
Q

Discuss antiemetic use in hyperemesis gravidarum
-Principles of medication (2)
-Treatment in:
Mild
Moderate/severe
Refractory cases

A
  1. Principles of medication
    -If medication is not working discontinue
    -Max out one medication before switching to another
  2. Treatment in mild cases
    -B6 +/- ginger
    -PO antihistimine or dopamine antagonist
  3. Treatment in moderate to severe cases
    -Antihistamine and dopamine antagonist
    -IV/PO serotonin antagonist
    -Acid suppression
  4. Treatment in refractory cases
    -Consider prednisolone along side other antiemetics
    -Intensify acid suppression
38
Q

Discuss the use of steroids to manage hyperemesis gravidarum
-Mode of action
-Dose
-When to use
-How to use
-Possible complications

A
  1. Mode of action
    -antiemetic effect on chemoreceptor tigger zone
  2. Dose
    Prednisolone 40-50mg PO OD in divided doses
  3. When to use
    -For those who fail conventional treatment
  4. How to use
    -If no response within 48hrs discontinue (20-30%) won’t respond
    -Continue 7-10 days or until sx resolve
  5. Possible complications
    -HTN, Cushings syndrome, hyperglycemia
    -Prednisolone crosses placenta in small amounts increased risk cleft palate if used >10 weeks
39
Q

Discuss periodontitis in pregnancy
-Pathophysiologiy
-Impact on pregnancy
-Management

A
  1. Destructive inflammation of periodontium from bacterial infiltration and release of toxins producing chronic inflammation and release of PGE2
  2. Impact on pregnancy
    -PTL from inflammation cascade
    -LBW from release of PGE2 resulting in restriction of placental blood flow
  3. Management
    -Deep root scaling
    -Chlorhexidine rises
40
Q

Discuss Hepatitis A in pregnancy
-Mode of transmission
-Time when fetus most at risk
-Management

A
  1. Mode of transmission
    -Faecal oral route
    -Vertical transmission very rare
  2. Time of maximum risk
    -Near delivery
  3. If maternal infection around time of delivery given immunoglobulin
41
Q

Discuss hepatitis B in pregnancy
-Incidence (2)
-Mode of transmission (3)
-Risk of transmission (5)
-Treatment outside of pregnancy

A
  1. Incidence
    -<1% in NZ/Aus
    ->10% in Subsaharan africa/SEA/ PI
  2. Mode of transmission
    -Blood
    -Sexual transmission
    -Vertical transmission
  3. Risk of transmission
    -95% occurs at time of delivery
    -5% transplacental
    -35% of exposed fetuses become infected
    -HbeAg positive risk of transmission70-90%
    -Greatest predictor of transmission is viral load
    -90% of perinatal infection leads to chronic carriage
  4. Treatment outside pregnancy
    -Treat if transaminases double or if HBV DNA >20,000
    -Treat with interferon. tenofovir
42
Q

Discuss the antenatal management of women infected with HBV

A
  1. Universally screen all women with antenatal bloods regardless of previous testing or vaccination
  2. Screening is with HBsAg (surface antigen) shows acute or chronic infection
    -If HBsAg is positive refer to hepatitis service
    -If HBsAg positive test HBeAg / HBV DNA (Viral load)/LFTs/PT/Liver USS
    -Test all household contacts and sexual partners
    -If no evidence of vaccination offer vaccination to HH contacts.
    -Hep B vaccination safe in pregnancy
    -Consider repeat screening in those with RF (IVDU)
  3. Counsel regarding invasive procedures and transmission (Avoid if possible)- Amnio/CVS. NIPT may be a second tier test. Amnio safer than CVS
  4. Offer treatment with Tenofovir if:
    -active disease/cirrhosis/high viral load >200,000
    -Commence treatment in third trimester
    -Continue treatment up to 12 weeks PP
    -Good evidence it reduces perinatal transmission
43
Q

Discuss intrapartum and neonatal postpartum cares for women with HBV infection
-Intrapartum considerations
-Postpartum neonatal cares

A
  1. Intrapartum considerations
    -Avoid FSE and FBS
    -Mode of delivery aim VB
  2. Postpartum cares
    -HBV vaccination at 2 months, 4 months and 6 months
    -HBIG + HBV Vaccination within 12 hrs of birth
    -Infant serology testing at 9-12 months
    -Baby bath prior to any IM injections
    -Notify MOH
    -Breastfeeding ok if had immunoprophylaxis. Also OK if on tenofovir
44
Q

Discuss HCV in pregnancy
-Mode of transmission
-Incidence in women of child bearing age
-Markers of chronic infection
-Markers of infectivity

A
  1. Mode of transmission
    -Blood, IV drug use,
    -Vertical transmission uncommon (5% in RNA +)
  2. Incidence = 1%
  3. Marker of chronic infection = HCV antibodies
  4. Marker of infectivity = HCV RNA
45
Q

Discuss management of pregnant women with HCV
-Antenatal
-Intrapartum
-Postpartum

A
  1. Antenatal
    -RANZCOG recommends routine screening of all pregnant women to decrease perinatal infection and allow treatment before subsequent pregnancies - HCV-Ag check
    -Check LFTs and HCV RNA if HCV-Ag+ (Guides risk of perinatal transmission)
    -Check for HIV as can co-incide
    -Pregnancy doesn’t worsen HCV
    -Monitor for obstetric cholestasis - increased risk
    -Check RNA status before invasive procedures such as amnio or CVS and consider NIPT as a second tier test if appropriate
  2. Intrapartum care
    -Avoid FBS and FSE
    -Aim VB
  3. Postpartum
    -Bath baby prior to IM injections
    -Breast feeding not contra-indicated unless nipple trauma then pump and dump
    -Monitor infant for vertical transmission - HCV RNA in infant serum or anti HCV antibodies after 18months of age
    -Consider treatment for mother after breast feeding complete
    -Discuss need for contraception until 6months after treatment completion. Also includes if partners are on treatment
46
Q

Discuss mode of action of anti-emetics
1. Ginger and B6
2. Cyclizine/Promethazine
3. Prochlopromazine
4. Ondansetron
5. Metocloprimide
6. Corticosteriods

A
  1. B6 or ginger
    - equally effective.
    -Decreases nausea but not vomiting
    -Improves gastroinstestinal motility
  2. Cyclizine / Promethazine
    -Histamine antagonist
    -Indirectly acts on vestibular system
    -Decrease stimulation of vomit centre
  3. Prochlorperazine
    -Dopamine antagonists
  4. Ondansetron
    -Central and peripheral serotonin receptor blockers
    -Concern for small increased risk in cleft palate (1:1000 - > 1.4: 1000) and cardiac defects. Not seen in recent RCT 2019
  5. Metocloprimide
    -Dopamine and serotonin receptor antagonists
    -Stimulates GI motility
    -Acts on CNS vomiting centre
    -Equal to ondansetron for nausea but worse for vomiting
  6. Corticosteriods
    -Effects chemoreceptor trigger zine in brainstem
    -Increases appetite and sense of wellbeing
    -Possible increase in oral cleft malformations before 10/40 gestation
47
Q

Discuss the PITCHES trial
-Aim (1)
-Study design (3)
-Primary outcomes (1)
-Secondary outcomes ()

A
  1. Aim
    -To determine whether Urso reduces adverse perinatal outcomes in IOC
  2. Methods
    -Double blinded multicentre RCT
    -Included women with IOC 20-40/40
    -Randomised to Urso or placebo
  3. Primary outcome
    -Composite measure of perinatal death, PTD, NICU admission
  4. Secondary outcomes
    -Maternal LFTs and Bile salts concentrations
    -Maternal itch score
    -MOD
48
Q

Discuss the PITCHES trial
-Number included in the study
-Results from primary outcome
-Results from secondary outcomes

A
  1. Number included in the study
    -605
  2. Results from primary outcomes
    -No difference in composite outcome between groups 23% vs 27%
  3. Results from secondary outcomes
    -Urso group had significantly less itch (SS) But not clinically meaningful
    -Urso group had higher Bile salt conc but lower ALT (SS)
49
Q

What are the severe maternal complications of HG (10)

A
  1. Werneke’s encephalopathy
  2. Bleeding diathesis
  3. Splenic avulsion
  4. Mortality (Now rare)
  5. Oesophageal rupture
  6. Pneumomediastinum
  7. Radbomyositis
  8. Depression and psychosocial PTSD
  9. Dysrrythmias\10. AKI
50
Q

Outline how ursodeoxycholic acid works (9, 5 mechanisms, 4 recommendations)

A
  1. Improves billary flow
  2. Enhances the protective bicarbonate environment on the surface of cholangiocytes
  3. Reduces bile acid induced apoptosis
  4. Replaces more toxic hydrophilic bile acids in circulating blood
  5. May protect cardiomyocytes from damage by BS
  6. Cochrane review shows little impact on PTL or SB over all aOR 0.6)
  7. Cochrane did show reduction in SB and PTB <37/40 if only looked at RCT
  8. RCOG says don’t use routinely
  9. SOMANZ recommends if remote from term

RANZCOG 2024 - maternal medical conditions (14 decks)

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