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Maternal Medicine > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

Why does ALP increase in pregnancy?

A

Placental production of ALP, which increases with successive trimesters.

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2
Q

In women who have hyperemesis severe enough to cause fluid, electrolyte and nutritional disturbance, what % are associated with abnormal LFTs?
What abnormalities are seen?

A

50%

Moderate rise in transaminases (50-200)
Slightly raised bilirubin

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3
Q

How is Hep B transmitted?

A

Blood borne

Sexual, vertical or via blood

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4
Q

For chronic carriers of Hep B, what is the risk of getting cirrhosis or hepatocellular cancer?
And chance of dying from it?

A

HCC - 40%

Death - 25%

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5
Q

For mothers with Hep B who are both HBsAg and HBeAG positive, what is the risk of vertical transmission?

A

70-90%

RANZCOG

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6
Q

When does mother to child transmission of Hep B occur?

A

Labour and Delivery (95%)

Antenatally (5%)
- TPTL
- Abruption
- Invasive procedures
increase the risk
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7
Q

For a neonate infected with Hep B at birth, what is the chance of becoming a chronic carrier?
Why?

A

> 90%

Young age at contracting virus correlates with risk of chronic hep B (adults <5% become chronic HBV carriers).
Perinatal transmission is leading cause of transmission in endemic countries.

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8
Q

For mothers with Hep B who are HBsAg positive but HBeAG negative, what is the risk of vertical transmission?

A

10-40%

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9
Q

For HepB, when is antiviral therapy indicated in pregnancy?

A

Active disease or cirrhosis

Third trimester in women with high viral loads >200,000 or >6 log copies, or HBeAg positive to reduce the risk of perinatal transmission at birth.

Tenofovir should be started ideally 30-32 weeks and continued till 6 weeks post partum, under the supervision of designated hepatology team.

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10
Q

For HepB in pregnancy, what is the preferred antiviral if required?
What is the evidence for its use?

A

Tenofovir

Reduced neonatal infection at 28 weeks from 18% in controls to 5% in women taking tenofovir.

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11
Q

All neonates born to women with acute or chronic HBV should be given…

A

HepB Immunoglobulin and HBV vaccine after birth, ideally within 12 hours of birth

Usual HPV vaccine as per the vaccination program - at 6wks, 3 month and 5 month.

Serology for HBV immunity or infection should be checked at 5 months.

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12
Q

What is the commonest risk factor for Hep C?

A

IVDU (75%)

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13
Q

In Hep C, what is the risk of chronic infection and progressive cirrhosis?

A

80% risk of chronic infection

30% develop slowly progressive cirrhosis

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14
Q

What is the preferred therapy for Hep C?

A

Interferon-alpha combined with ribavirin

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15
Q

Women with Hep C have an increased risk of what complication in pregnancy?

A

Obstetric cholestasis / Intrahepatic cholestasis of pregnancy

May present earlier than usual

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16
Q

In Hep C in pregnancy, what is the risk of vertical transmission?

A

<5%

Increased if HIV confection or viremia (positive HCV RNA)

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17
Q

In which type of hepatitis is there a dramatically increased mortality in pregnant women?

A

Hep E.
With acute Hep E infection
Mortality rate = 5%
Also increased risk of hepatic encephalopathy and fulminant hepatic failure (15-20%)
Particularly if the virus is acquired in the third trimester

Transmission by faeco-oral route.
Usually self-limiting similar to hep A in the immune competent host.

Also HSV hepatitis

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18
Q

Which type causes HSV Hepatitis?

A

Most are primary HSV Type 2 infections

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19
Q

What is the incidence of Obstetric Cholestasis?

A

0.5-1% in UK

Indian and Pakistani women at higher risk

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20
Q

What is the pathogenesis of Obstetric Cholestasis?

A

Genetic inheritance - familial clustering and evidence for genes for transmembrane transporters being implicated.

Elevated oestrogens are associated with significant impairment in sulphation capacity (sulphation of bile acids is important in attenuating their Cholestatic potential).

Progestogens may also play a role.

Reproductive hormones also affect the function of bile acid transports within the hepatocytes

Environmental - low vit D and selenium

Pre-exisitng liver disease (hep C and B)

Effect on fetus:
Bile acids, cause a dose-dependent vasoconstrictive effect on isolated human placental chorionic veins. An abrupt reduction of oxygenated blood flow at the placental chorionic surface leading to fetal asphyxia may be an explanation for fetal distress and demise

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21
Q

What is the genetics of obstetric cholestasis?

A

Positive family history may be found in about 35% patients and 12% parous sisters are affected

Family studies suggest either AD or sex-linked dominant inheritance

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22
Q

What are three steps to diagnosing Obstetric Cholestasis?

A
  1. Typical history of pruritis without rash
  2. Abnormal LFTs
  3. Exclusion of other causes of itching and abnormal liver function

It is a diagnosis of exclusion

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23
Q

When diagnosing Obstetric Cholestasis, what investigations should you do, given that it is a diagnosis of exclusion?

A
  1. Liver USS
  2. Viral serology: Hep B, C. If clinical features of acute hepatitis: HAV, HEV, EBV, CMV
  3. Liver autoantibodies: anti-smooth muscle antibodies, anti-mitochondrial antibodies
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24
Q

What are the maternal risks of Obstetric Cholestasis?

A

Vitamin K deficiency due to malabsorption of fat-soluble vitamins
Possible increased risk of PPH

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25
Q

What are the fetal risks/ considerations with obstetric cholestasis?

A 
Intrapartum fetal distress
Passage meconium
Spontaneous or iatrogenic preterm delivery
IUFD
Fetal intracranial haemorrhage

Magnitude difficult to determine

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26
Q

In obstetric cholestasis, the risk of stillbirth is related to the

A

Serum concentration of maternal bile acids

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27
Q

In obstetric cholestasis, where have high concentrations of bile acids been found?

A

Maternal serum
Amniotic fluid
Fetal circulation

28
Q

How can we predict fetal compromise in obstetric cholestasis?

A

Difficult.
Fetal death is sudden and unpredictable. It is not related to placenta insufficiency. As such USS growth, liquor or doppler studies do not predict fetal outcome. CTG is poor predictor.

High bile acid levels have been linked with fetal death, passage of meconium, abnormal cardiotocograph, prematurity and non-fatal asphyxial events.

Bile acids >100 have been suggested as cut-off for early induction.

29
Q

What is the management of obstetric cholestasis?

A

Weekly LFTs and bile acids until delivery
Prothrombin time - If prolonged, consider Vit K 10mg orally
No evidence for fetal scanning/CTG
Sedating antihistamines
Ursodeoxycholic acid
Consider delivery at 37-38/40
Continuous CTG in labour

30
Q

How does URSO work in obstetric cholestasis?

A

In obstetric cholestasis, the proposed mechanism of action of UDCA is displacement of more hydrophobic endogenous bile salts from the bile acid pool.This may protect the hepatocyte membrane from the damaging toxicity of bile salts, enhance bile acid clearance across the placenta from the fetus.

31
Q

What are the benefits of URSO in Obstetric Cholestasis?

A

Relief of pruritis
Reduction of total bile acid and liver enzyme levels in 80-90% patients
Protection of hepatocytes

32
Q

For a woman who has had Obstetric Cholestasis, what is the risk of her developing it in a future pregnancy?

A

90%

33
Q

What should women with obstetric cholestasis avoid in the future?

A

Oestrogen-containing oral contraceptives
If they are used, LFTs should be monitored

The risk of cholestasis with the POP is less, but it is prudent to monitor LFTs

34
Q

What risk factors is Acute Fatty Liver of Pregnancy associated with?

A

primigravida
Male foetuses 3:1
Multiple pregnancy 20%

35
Q

What is the maternal and perinatal mortality rate in Acute Fatty Liver of Pregnancy?

A

Maternal: 10-20%

Perinatal: 20-30%

36
Q

How does Acute Fatty Liver of Pregnancy present?

A
  • Onset after 30 weeks - usually near term
  • Gradual onset of nausea, anorexia, malaise
  • Severe, peristent vomiting
  • abdominal pain
  • Can have co-existing features of mild pre-eclampsia, but HTN and proteinuria are usually mild
  • Jaundice and ascites may be present
  • 3-10 fold increase in transaminases
  • AKI
  • Hypoglycemia
  • Polyuria and polydipsia: features of transient diabetes insipidus
  • signs of fulminant liver failure including coagulopathy
37
Q

What are the abnormal blood test results seen in Acute Fatty Liver of Pregnancy?

A 
LFT derangement: transaminases and raised ALP
Coaguloapathy due to DIC
AKI
Lactic acidosis
Raised ammonia
Hypoglycaemia
38
Q

What are the complications of Acute Fatty Liver of Pregnancy?

A 
Fulminant liver failure
Hepatic encephalopathy 
Diabetes insipidus
DIC
AKI

Maternal and fetal death

39
Q

A subgroup of women with AFLP and HELLP have been reported to be heterozygous for…

A

Long-chain 3-hydroxy-acyl-coenzyme A dehydrognase (LCHAD) deficiency
A disorder of mitochondrial fatty acid oxidation

These women may succumb to AFLP/ HELLP when the fetus is homozygous for beta-fatty acid oxidation disorders

40
Q

What are three distinctive features of AFLP that help in its distinction from HELLP syndrome

A
  1. Profound hypoglycamiea (70%)
  2. Marked hyperuricaemia (out of keeping with other features of pre-eclampsia)
  3. Coagulopathy (90%) in the absence of thrombocytopenia
41
Q

What is the gold standard for diagnosis of Acute Fatty Liver of Pregnancy?

A

Liver biopsy
With stains for fatty change or electron microscopy
Characteristic histopathological lesion: microvesicular fatty infiltration (steatosis) of hepatocytes

42
Q

What it the management of AFLP?

A

Expeditious delivery
MDT approach, with ICU support
Correction of coagulopathy (prior to delivery) - fibrinogen,FFP, Vit K
Hypoglycaemia should be aggressively treated before delivery
Antibiotics: low threshold for antibiotic therapy as AFLP arrives a significant risk of sepsis
Less evidence: N-acetylcysteine, Desmopressin,
Fulminant liver failure: referral to Liver Unit and consideration of Liver Transplantation

43
Q

Of patients with HELLP, what percentage will present with placental abruption?

A

16%

44
Q

How is HELLP diagnosed?

A

Haemolysis - elevated LDH, bilirubin (unconjugated)
- low grade haemolysis evident on peripheral blood smear
Elevated liver enzymes - transaminases
Low platelets - <100

45
Q

What are the histopathological findings in the liver in HELLP syndrome?

A

Fibrin deposition in the periportal regions and along the hepatic sinusoids, and periportal haemorrhage
Hepatic cell necrosis
Subcapsular haemorrhages

46
Q

Is profound thrombocytopenia more common in HELLP or TTP-HUS?

A

TTP-HUS

47
Q

In HELLP, what are complications that are contribute to maternal morbidity and mortality?

A 
Abruption
Subcapsular liver haematoma
AKI
Massive hepatic necrosis
Liver rupture
48
Q

What is an unintended benefit of corticosteroids in HELLP?

A

Improvement in haematological and hepatic abnormalities

49
Q

What are the postnatal risks for a woman with HELLP?

A

Pulmonary oedema
AKI

(VTE)

50
Q

What is the risk of recurrent HELLP syndrome?

A

3-5%

51
Q

What is NASH compared to NAFLD. What is the prevalence of the two conditions?

A

NAFLD: hepatic steatosis, 20%

NASH: the association of liver inflammation and hepatocyte damage with NALFD, 3-5%

52
Q

What is NAFLD associated with?

A

Obesity
Hyperlipidaemia
Insulin resistance / T2DM

53
Q

What are the risks of NAFLD?

A

Progression to T2DM
Liver fibrosis, cirrhosis
Hepatocellular carcinoma

54
Q

What is the treatment of NAFLD?

A

Weight loss
Increased exercise
Healthy diet
Avoidance of alcohol

55
Q

What blood test results are associated with Autoimmune Chronic Active Hepatitis?

A

Anti-smooth muscle antibodies

Raised IgG levels

56
Q

How is Autoimmune Chronic Active Hepatitis managed?

A

Immunosuppressive drug regimens
- should be continued in pregnancy to prevent relapse
Withdrawal of immunosuppressive is associated with a high risk of relapse

Poor disease control in the year prior to pregnancy and the absence of drug therapy are associated with poor outcomes in pregnancy

57
Q

How does primary biliary cirrhosis present?

A

Pruritis
Bloods:
Raised ALP and GGT
Anti-mitochondrial antibodies

58
Q

How does primary biliary cirrhosis affect pregnancy and vice versa?

A

Reported pregnancy outcomes variable. Stable disease unlikely to cause problems
Pruritis may worsen in pregnancy and UCDA can be continued or added
Majority of women remain stable LFTs during pregnancy
Postpartum biochemical exacerbation are common

59
Q

What is sclerosing cholangitis?
How does it present
What is there a significant risk of? (2)

A

Rare, chronic, fibrosis inflammatory disorder of unknown aetiology affecting the biliary tree

Obstructive jaundice
Characteristic findings at ERCP and MRI
Significant risk of cholangiocarcinoma
3x increased risk of PTB

60
Q

What is the management of women with portal hypertension from cirrhosis in pregnancy?

A

Continue b-blockers
Due to risk of bleeding from oesophageal varies

Those with documented portal HTN not already receiving therapy should commence b-blocker therapy in the second trimester

61
Q

What are the obstetric risks for a woman after liver transplantation?

A

PRB
Reduced birth weight
NICU admission

62
Q

What is the prevalence of acute cholecystis in pregnancy?

A

0.1%

63
Q

What is the pathogenesis of gallbladder disease in pregnancy?

A

Increasing concentrations of bile cholesterol leads to formation of cholesterol gallstones
Pregnancy (and OCP) increase cholesterol saturation of bile to chenoxycholic acid, which results in increase bile lithogenicity.
Pregnancy impairs gallbladder contractility, leading to stasis

64
Q

Why does RANZCOG recommend universal screening for Hep C ?

A

Risk stratification
Interventions to reduce perinatal transmission (avoidance of invasive procedures)
Minimise occupation exposure
Allow counselling for women eligible to treatment after pregnancy and breast feeding completed - 95% success after treatment
(NB. cannot be started during pregnancy)

65
Q

Regarding neonate in Maternal hep c

A

Bathe off secretions before IM anything (vit K)

Can breastfeed, but discard milk if cracked or bleeding nipples

Usually a symptomatic of contract at birth but at risk of long term liver disease

Can test baby
Either HCV RNA at 3 months, or HCV antibody at 18/12, if negative, not infected
If HCV positive, refer to paed gastro or paed ID

66
Q

Describe the postnatal care for mother after HepB

A
  • If on tenofovir - continue till 6 weeks post partum
  • Breast feeding is safe in HBV (present but no increased risk of transmission, so long as baby received appropriate HBIG and vaccination
  • Breast feeding is safe if taking tenofovir
  • Review under designated hepatology team
  • Monitor closely for several months postpartum as high risk for hepatitis flares as immune competence returns
  • Long-term follow-up should be arranged due to risk of cirrhosis and HCC.

Maternal Medicine (18 decks)

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