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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
What are the fetal risks/ considerations with obstetric cholestasis?
``` Intrapartum fetal distress Passage meconium Spontaneous or iatrogenic preterm delivery IUFD Fetal intracranial haemorrhage ``` Magnitude difficult to determine
26
In obstetric cholestasis, the risk of stillbirth is related to the
Serum concentration of maternal bile acids
27
In obstetric cholestasis, where have high concentrations of bile acids been found?
Maternal serum Amniotic fluid Fetal circulation
28
How can we predict fetal compromise in obstetric cholestasis?
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
What is the management of obstetric cholestasis?
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
How does URSO work in obstetric cholestasis?
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
What are the benefits of URSO in Obstetric Cholestasis?
Relief of pruritis Reduction of total bile acid and liver enzyme levels in 80-90% patients Protection of hepatocytes
32
For a woman who has had Obstetric Cholestasis, what is the risk of her developing it in a future pregnancy?
90%
33
What should women with obstetric cholestasis avoid in the future?
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
What risk factors is Acute Fatty Liver of Pregnancy associated with?
primigravida Male foetuses 3:1 Multiple pregnancy 20%
35
What is the maternal and perinatal mortality rate in Acute Fatty Liver of Pregnancy?
Maternal: 10-20% Perinatal: 20-30%
36
How does Acute Fatty Liver of Pregnancy present?
- 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
What are the abnormal blood test results seen in Acute Fatty Liver of Pregnancy?
``` LFT derangement: transaminases and raised ALP Coaguloapathy due to DIC AKI Lactic acidosis Raised ammonia Hypoglycaemia ```
38
What are the complications of Acute Fatty Liver of Pregnancy?
``` Fulminant liver failure Hepatic encephalopathy Diabetes insipidus DIC AKI ``` Maternal and fetal death
39
A subgroup of women with AFLP and HELLP have been reported to be heterozygous for...
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
What are three distinctive features of AFLP that help in its distinction from HELLP syndrome
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
What is the gold standard for diagnosis of Acute Fatty Liver of Pregnancy?
Liver biopsy With stains for fatty change or electron microscopy Characteristic histopathological lesion: microvesicular fatty infiltration (steatosis) of hepatocytes
42
What it the management of AFLP?
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
Of patients with HELLP, what percentage will present with placental abruption?
16%
44
How is HELLP diagnosed?
Haemolysis - elevated LDH, bilirubin (unconjugated) - low grade haemolysis evident on peripheral blood smear Elevated liver enzymes - transaminases Low platelets - <100
45
What are the histopathological findings in the liver in HELLP syndrome?
Fibrin deposition in the periportal regions and along the hepatic sinusoids, and periportal haemorrhage Hepatic cell necrosis Subcapsular haemorrhages
46
Is profound thrombocytopenia more common in HELLP or TTP-HUS?
TTP-HUS
47
In HELLP, what are complications that are contribute to maternal morbidity and mortality?
``` Abruption Subcapsular liver haematoma AKI Massive hepatic necrosis Liver rupture ```
48
What is an unintended benefit of corticosteroids in HELLP?
Improvement in haematological and hepatic abnormalities
49
What are the postnatal risks for a woman with HELLP?
Pulmonary oedema AKI (VTE)
50
What is the risk of recurrent HELLP syndrome?
3-5%
51
What is NASH compared to NAFLD. What is the prevalence of the two conditions?
NAFLD: hepatic steatosis, 20% NASH: the association of liver inflammation and hepatocyte damage with NALFD, 3-5%
52
What is NAFLD associated with?
Obesity Hyperlipidaemia Insulin resistance / T2DM
53
What are the risks of NAFLD?
Progression to T2DM Liver fibrosis, cirrhosis Hepatocellular carcinoma
54
What is the treatment of NAFLD?
Weight loss Increased exercise Healthy diet Avoidance of alcohol
55
What blood test results are associated with Autoimmune Chronic Active Hepatitis?
Anti-smooth muscle antibodies | Raised IgG levels
56
How is Autoimmune Chronic Active Hepatitis managed?
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
How does primary biliary cirrhosis present?
Pruritis Bloods: Raised ALP and GGT Anti-mitochondrial antibodies
58
How does primary biliary cirrhosis affect pregnancy and vice versa?
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
What is sclerosing cholangitis? How does it present What is there a significant risk of? (2)
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
What is the management of women with portal hypertension from cirrhosis in pregnancy?
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
What are the obstetric risks for a woman after liver transplantation?
PRB Reduced birth weight NICU admission
62
What is the prevalence of acute cholecystis in pregnancy?
0.1%
63
What is the pathogenesis of gallbladder disease in pregnancy?
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
Why does RANZCOG recommend universal screening for Hep C ?
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
Regarding neonate in Maternal hep c
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
Describe the postnatal care for mother after HepB
- 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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