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Delta Med - Gastroenterology > Gastroenterology 3 - Liver Disease > Flashcards

Gastroenterology 3 - Liver Disease Flashcards

1
Q

What are basic features of HCV infection?

A

RNA virus
HCV AB detectable 4-24 weeks post infection
May decline in long term after recovery
70% become chronic carriers
30% clear spontaneously (all will be HCV Ab +ve, hence must measure HCV RNA)

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2
Q

What is the relationship between SVR and clinical outcomes?

A

Patients achieving SVR have lower mortality, lower liver related mortality, liver transplantation, HCC and liver failure

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3
Q

What are extra-hepatic manifestations of HCV infection?

A 
40-70% of individuals
Mixed cryoglobulinaemia (vasculitis, skin, kidney, nerves)
Lymphoproliferative disorders - NHL, MALT
Porphyria cutanea tarda
Lichen planus
Thyroid dysfunction
Diabetes
Sjogren syndrome
Polarthritis
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4
Q

What are predictors of SVR?

A
  1. IL28B CC (not relevant now)
  2. HCV RNA high
  3. Non-black
  4. Hispanic
  5. Lower grades fibrosis
  6. fasting glucose +/-5.6
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5
Q

What are examples of NS3/4 protease inhibitors?

A

Inhibit serine protease NS3/4A

Simeprevir
Partaprevir
Teleprevir
Boceprevir

-evir E for NS-thrEE/four

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6
Q

What are examples of NS5A inhibitors?

A

Block replication complex formation and assembly

Daclatasvir
Ledipasvir
Ombitasvir

-avir A for NS5A

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7
Q

What are examples of NS5B inhibitors?

A

Inhibit NS5B polymerase, preventing the production of viral RNA

sofosbuvir
dasabuvir

-buvir - B for NS5B

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8
Q

What patients are at high risk of death if treated with Peg interferon, ribavarin and a protease inhibitor?

A

Albumin

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9
Q

Which cirrhotics should be treated for HCV?

A

ESLD - treatment is C/I
Child pugh B - very high risk/contraindicated
Compensated with portal hypertension - high risk, treat with caution
Well compensated cirrhosis - treatment candidates

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10
Q

What is the effect of adding boceprevir to Peg and Ribavarin?

A

improves SVR in G1 patients.

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11
Q

What is the relationship between Q80K positivity and Simeprevir?

A

No improvement with imeprevir if Q80K positive

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12
Q

What is the rate of SVR12 in patients treated with Sofosbuvir and Ledipasvir?

A

G1 patients who are treatment Naive have a 99% SVR rate at 12 weeks with LDV-SOF

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13
Q

What are response rates seen in Ombritasvir/paritprevir/ritonavir tablets + dasabuvir + RBV in G1, treatment experienced, non-cirrhotic patients?

A

95-100%

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14
Q

What are current recommended regimes for the treatment of genotype 1 HCV in non-cirrhotics?

A

Sofosbuvir + Ledipasvir w/o Ribavarin
Sofosbuvir + Daclatasvir w/o RBV
Sofosbuvir + simeprevir w/o RBV

duration 12 weeks

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15
Q

What are current recommended regimes for genotype 2 HCV in non-cirrhotics?

A

12 weeks of sofosbuvir + RBV OR

12 weeks of sofosbuvir and daclatasvir

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16
Q

What are recommended treatment types for genotype 3 HCV in non-cirrhotics?

A

24 weeks of sofosbuvir and ribavarin OR

12 weeks of sofosbuvir + daclatasvir w/o ribavarin

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17
Q

What are recommended treatment options for genotype 4 HCV in non-cirrhotics?

A

12 weeks of sofosbuvir and daclatasvir
12 weeks of sofosbuvir and simeprevir
12 weeks of sofosbuvir and ledipasvir

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18
Q

What are recommended treatment options for genotype 5 HCV in non-cirrhotics?

A

12 weeks of sofosbuvir and ledipasvir or sofosbuvir plus daclatasvir

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19
Q

What are AEs associated with boceprevir, teleprevir, simeprevir?

A

BOC - anaemia, neutropenia, dysgeusia
TEL - rash, anaemia, anorectal events, GI events
SIM - rash, photosensitivity, increased bili

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20
Q

What is the current PBS approved treatment for G1 HCV?

A

PEG-IFN + RBV + PI (BOC, SIM, TPV) RGT or 48 weeks

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21
Q

What is the current PBS approved treatment for G2/3 HCV?

A

PEG-IFN + RBV for 24 weeks

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22
Q

What is the current PBS approved treatment for G4, 5, 6 HCV?

A

PEG IFN + RBV for 48 weeks

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23
Q

What are the phases of HBV infection?

A
  1. immune tolerance
  2. immune clearance
  3. immune control
  4. immune escape
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24
Q

What are characteristics of the immune tolerance phase of HBV infection?

A 
>6 months HBsAg +ve
HBeAg -ve
-ve anti HBe
ALT normal
HBV DNA >20,000
Normal or mild hepatitis on histo
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25
Q

What are characteristics of the immune clearance phase of HBV?

A

HBsAg +ve >6 months
HBeAg +ve
Anti-HBe - spont seroconversion may occur
ALT perisistent/intermittent elevation
HBV DNA >=20,000
Liver-histology - Moderate/severe hepatitis or cirrhosis

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26
Q

What are characteristics of the immune control phase of HBV?

A 
>6 months HBsAg +ve
HBeAg -ve
Anti-HBe +ve
Persistently normal ALT
HBV dna
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27
Q

What are characteristics of the immune escape phase of HBV infection?

A

HBsAg >6 months
HBeAg -
Anti-HBe +ve
Persistently or intermittently elevated ALT
HBV DNA >=2000
Liver histology - moderate severe hepatitis - cirrhosis

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28
Q

What are high risk groups for HBV?

A 
Persons born in endemic areas
Indigenous
IVDU
Household contacts of +ve Dx
HIV
Inmates
MSM
HCV
Dialysis
Chemo/immunosuppression
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29
Q

What factors are associated with more rapid HBV progression?

A 
Older age
Alcohol
HCV/HDV, HIV
Carcinogens - alfatoxin, tobacco
Male
FHx HCC
Hx of reversion from anti-HBe to HBeAg
Presence of cirrhosis
HBV genotype C
Core promoter mutation
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30
Q

What are treatment options in Patients HB-eAg+ve with HBV DNA >=20,000?

A

If in immune tolerance phase with normal ALT - consider Bx if age >40, only treat if inflammation or fibrosis on Bx

If ALT >2x ULN and High DNA (immune clearance phase) - observe for 3-6 months for spontaneous seroconversion, liver Bx prior to treatment.

If treating, TDF, ETV, pegIFN are appropriate
monitor virological response
long term Rx may be required.
continue NA therapy after seroconversion for at least 6-12/12

monitor for relapse post therapy

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31
Q

What is treatment of HBV in patients with HBV DNA

A 
If HBeAg (-) and normal ALT patients are in immune control phase
- observe only, consider treatment in patients only if significant inflammation or fibrosis on Bx, even if low level replication or ALT is normal
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32
Q

What is treatment of patients who are HBeAg -ve and HBV DNA >2000?

A

If elevated ALT >1-2xULN - Immune escape

  • review alternate cause of ALT elevation
  • consider Bx if clinical suspicion of sig liver Dz
  • Treat if mod-severe inflammation or fibrosis on Bx

TDF, ETG or peg IFN preferred
Monitor virological response
Continue treatment until HBsAg clearance is achieved

If immune escape with ALT >2 x ULN, treat, consider Bx, long term NA treatment is required

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33
Q

What is the management of patients with compensated cirrrhosis and HBV?

A

either HBeAg status - if HBV 2000, treat with TDF, ETV, ADV

Long term treatment is required

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34
Q

What is the management of decompensated cirrhosis?

A

Treat at any detectable level of HBV DNA with TDF/ADV AND LAM/ETV, lifelong, no PEGIFN, screen for HCC - USS and AFP every q6-12

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35
Q

What are recommendations in pregnancy and HBV?

A

All pregnant women should be screened for HBV
All HBsAG should have all contacts screened/treated/vaccinated
All newborn infants should recieve a monovalent HBV at birth, and 3 doses of combo vaccine at 2, 4 and 6 months.
HBsAg +ve mothers - children should have passive HBIG at birth
Consider HBV Tx in 3rd trimester if highly viraemic (>106-7) in mothers who carry a >10% risk of vertical HBV transmission despite HBIg and vaccination
Breastfeeding in HBs-Ag +ve mothers is ok

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36
Q

What are lost in fanconi syndrome?

A 
urinary loss of amino acides
glucose
uric acid
phosphorous
bicarbonate
low molecular weight proteins
37
Q

What are features of HDV?

A

small defective RNA virus, requires HBsAG for transmission and packaging
HBV/HDV acquisition at exposure - more severe acute hepatitis and higher mortality
HBV DNA usually low or negative in chronic HDV infection, as HDV suppresses HBV replication
pegIFNa for at least 48 weeks

38
Q

What are features of HEV?

A

RNA virus, 5 different genotypes
Diagnosis - HEV antibodies
may be negative in immunocomproised, recommend RNA
May cause chronic infections in immunocompromised patients, can be associated with extrahepatic symptoms
Genotype 3 most common, 4 mostly foodborne.
PIG MEAT

39
Q

What histology is seen in autoimmune hepatitis?

A

INterface hepatitis - hypercellular

Note NASH has white holes (where fat was lost in fixing process)

40
Q

What drugs are commonly associated with hepatitis?

A 
minocycline
nitrofurantoin
isoniazid
PTU
methyldopa
41
Q

What are Ab associated with AIH-1?

A

ANA (AIH-1 70-80%)
Anti-SMA (80%)
Anti-ASGPR (AIH in general)
pANCA (65-95%)

42
Q

What are Ab associated with AIH2?

A

Anti-LKM1 (99%)
Anti-LKM3 (10%)
Anti LC1 (30-50%)
Anti-ASGPR (AIH in general)

43
Q

What is the general treatment methodology in AIH?

A

Treat with Prednisone 40mg/day
Add AZA with reduction in ALTs
If ongoing disease - can add MMF or Calcineurin inhibitors

44
Q

What are features of PBC?

A

? autoimmune
present w fatigue and pruritis
? other AI phenomenon
increased IgM, Lipids and AMA (95%), ANA (30%)
AMA -ve PBC may have +ve anti-GP210 or anti SP100
Treat with urso
Cholestyramine, antihistamines, rifampin for pruritis
can consider tranplantation

45
Q

what are complications of PBC?

A

OP
ADEK deficiency
lipid issues
thryoid and other AI issues

46
Q

What are features of histology in PBC?

A

granulomas with bile duct damage

47
Q

What are features of sclerosing cholangitis?

A

unknown aetiology
strongly associated with IBD (75% - UC > CD)
Assess activity with LFTs
pANCA +Ve
Ursodeoxycholic acid - no effect on prognosis
? transplant
MRCP for Dx

48
Q

What are features of histology in PSC?

A

PSC bile duct inflammation with fibrosis - onion skinning

49
Q

What is the most important factor in the management of NAFLD?

A

Weight loss!
Patients who achieve weight loss of 7% go on to have significant improvements in steatosis, parenchymal inflammation, ballooning injury and overall NAS

50
Q

What are effects of the mediterranean diet in NAFLD?

A

Decreases intrahepatic lipid
Increase in glucose infusion rate
Decrease in serum insulin

51
Q

What is the algorithm for Dx of HCC?

A

If identified nodule is 1cm, perform 4 phase MDCT/dynamic contrast enhanced MRI

if arterial hypervascularity and venous or delayed phase washout - HCC

IF not, perform other contrast study, if meets criteria above, HCC. Alternative to further imaging is Bx

52
Q

What is the interval of surveillance for patients who are at risk of HCC?

A

6 months recommended USS

53
Q

What are preferred treatment options for HCC?

A
  1. surgery
  2. transplant
  3. RFI
  4. tace
  5. sorafinib
54
Q

What are prognostic factors in HCC?

A

CP A/B/C
Performance status
Disease burden

55
Q

What are significant AEs associated with sorafenib therapy?

A

VEGFR PDGFR and RAF inhibitor (C>B), cKIT, RET, RET/PTC
Diarrhoea
Hand food syndrome
Fatigue

Used in CP-A cirrhosis, 3 month prolongation of survival in HCC

56
Q

What is the significance of PNPLA3 in alcoholic liver disease?

A

Mutations in PNPLA3 on chromosome 12 leads to higher rates of fibrosis in alcoholic liver disease

57
Q

What is the natural history of chronic alcohol misuse?

A

90-95% develop steatosis
10-20% progress to fibrosis - 40-50% develop steatohepatitis
8-20% of fiborsis develop cirrhosis
3-10% develop HCC

58
Q

What genetic and environmental factors predispose to cirrhosis in alcohol abuse?

A 
Female gender
SNPs
Haemochromatosis
Binge drinking
viral hepatitis
HIV
obesity and insulin resistance
Cigarette smoking
59
Q

What are features of mallory hyaline?

A

Sign of alcohol related liver damage

consist of aggregates of intermediate filaments in cytoplasm, resulting from hepatocyte injury

60
Q

What histological changes are seen in alcoholic hepatitis?

A 
Mallory's hyaline
neutrophils
necrosis of hepatocytes
collagen deposition
fatty change
61
Q

What is the mechanism of hepatocyte injury in alcoholic liver disease?

A

Alcohol increases LPS, acetaldehyde - activate stellate cells (LPS activates TLR4, and in Kuppfer cells too, which release CKs, chemokines, and other mediators)
Ethanol metabolism and innate immunity leads to hepatocyte apoptosis/necrosis - ROS, DNA, apoptotic bodies and necrotic debris activate stellate cells.
Stellate cells produce more ECM, and liver fibrosis

EtOH also inhibits viral hepatitis IFNa therapy, which blocks inhibition of Stellate cells by NK cell activation and TRAIL, IFN-gamma

62
Q

What are two proven therapies in alcoholic hepatitis?

A

Corticosteroids - reduce short term mortality in severe alcoholic hepatitis
Pentoxyfylline - improves in hospital survival in patients with severe alcoholic hepatitis - fewer instances of hepatorenal syndrome

63
Q

What is the management of alcoholic steatohepatitis?

A

Perform prognostic assessment (Maddrey’s DF, Glasgow Score)

If low risk - optimise nutrition and treat complications

If high risk - confirm diagnosis with TJLBx
Exclude sepsis, biliary obstruction, HBV, HCV status and renal dysfunction pre commencement of prednisone (consider pentoxifylline if pred CI)

Proceed then to Pred and NAC - response at 7 days

if lille score

64
Q

What are components of maddrey DF?

A

bili, PT, and PT control/reference level

> =32 is high risk

65
Q

What are components of the glasgow score?

A 
Age
WCC
BUN
Bilirubin
PT
PT reference

> =9 is high risk

66
Q

What are components of the lille score

A 
Age
albumin
Bilirubin index
Bilirubin d7
creatinine
PT
67
Q

What are causes of ALT >1000?

A

ischaemic hepatitis
acute viral hepatitis
drug induced hepatitis

68
Q

What is the metabolism of paracetamol?

A

90% metabolised to inactive sulphate and glucuronide conjugates, excreted in urine
CYP450 2E1 and 3A4
NAPQI is hepatotoxic, usually conjugated by intracellular glutathione, excreted in urine. If depleted, shunts to toxic NAPQI

69
Q

What are general principles of paracetamol overdose management?

A

IF 8 hours, commence infusion immediately, measure serum paracetamol and ALT. Plot level on nomogram - if under nomogram, OR 24 hours post OD and ALT is normal, can stop NAC.

IF over treatment line, continue NAC, or if ALT is abnormal.

Continue NAC until ALT normalises and INR is normal

70
Q

What are king’s college indications for liver transplantation in paracetamol OD?

A

Arterial ph 100
AND
Serum creat >301

71
Q

What are king’s college indications for liver transplantation in other causes of acute liver failure?

A 
PT >100
OR
Any 3 of:
Age 40
non A/B hep, halothane hep, idiosyncratic drug Rxn
>7 days of jaundice pre encephalopathy
PT >50
Bili >18
72
Q

What drugs are frequently associated with drug induced cholestasis?

A 
Anti androgens (flutamine, CPA) 2-4%
Others include:
chlorpromazine
estrogen induced cholestasis
ketoconazole
flucloxacillin
amoxicillin/clavulanate, terbinafine, dicloxacillin
newer psychotropics, NSAIDs
73
Q

When should statins be considered as a cause of hepatotoxicity?

A

when 3x ULN of ALT, should consider statin as possible cause of hepatic injury.
do cause mild increase in ALT in 10% of recipients.
Note that lovastatin was not shown to produce higher rates of 3x ULN ALT vs placebo
statins are OK in patients with liver disease

74
Q

What are nutritional considerations in the Mx of CLD patients?

A

1-1.5g/kg of protein intake/day

promotion of a balanced diet

75
Q

What are coagulopathy considerations in the Mx of CLD patients?

A 
Vitamin K supplementation
FFP transfusion
IV cryoprecipitate
IV administration of Recombinant factor VIIa
Platelet transfusions
76
Q

What are considerations in the Mx of ascites?

A

Paracentesis with analysis for infection

Dietary sodium restriction (

77
Q

What are considerations in the management of renal dysfunction in CLD?

A

avoidance of nephrotoxic insults

albumin infusion with paracentesis volumes >5L

78
Q

What are considerations in the management of portosystemic encephalopathy?

A

correction of reversible metabolic factors
Avoidance of sedatives or opiod narcotics as much as possible
oral lactulose - 3-4 BM/day
admin of nonabsorbable antibiotics
decreased protein intake

79
Q

Which patients with small varices should be treated?

A 
patients with red whale marks or child C class cirrhosis should be treated with NSBB
patients with small varices without signs of increased risk should be treated with NSBB to prevent progression of varices and bleeding
surveillance with q1y endoscopy
80
Q

Which patients with medium-large varices should be treated?

A

Either NSBB or endoscopic band is recommended foor the prevention of first variceal bleeding in medium or large varices.
Shunt therapy, sclerothearpy or ISMN should not be used as prophylaxis in first bleeding
Insufficient data to recommend the use of NSBB in combination with ISMN or spironolactone or EBL as primary prophylaxis

81
Q

What are recommendations for secondary prophylaxis in variceal bleeds?

A

Commence secondary prophylaxis on day 6 of index event.
combination of BB and band ligation is preferred therapy, has lower re-bleeding rates compared to either therapy alone.
Haemodynaic response to drug therapy provides information re: re-bleeding risk
Addition of ISMN to b-blockers may improve in those who do not respond, and can be considered in those unwilling to undergo EBL
EBL is preferred therapy in those where BB are C/I
Failure of EBL and pharmacological therapy should be considered for TIPS, with surgical shunt in CP A/B if tips is unavailable
Transplantation should be considered in appropriate candidates

82
Q

What is the primary indication for liver transplantation in Australia?

A

HCV

83
Q

What is the effect of rifaximin in hepatic encephalopathy?

A

reduces the risk of hospitalisation

recommended as add on therapy to lactulose in patients to prevent recurrent episodes of OHE

84
Q

What are features of severe pre-eclampsia and eclampsia?

A

After week 22
prevalence increases with increased gestation
high BP, proteinuria, oedema, renal failure, seizure, pulmonary oedema
plts >70, u prot >5g/24h and abnormal liver enzymes
BP control - b-blockers, methyldopa, masulf, delivery
1% maternal death rate

85
Q

What are features of HELLP syndrome?

A

late T2 to early post partum
0.1%
abdo pain, NV, overlap with PET findings
low plts, haemolysis, elevated liver enzymes, PT time may be normal, normal fibrinogen
Prompt delivery, 5% maternal death, 1% hepatic rupture
1-30% foetal death

86
Q

What are features of Acute fatty liver of pregnancy?

A

Third trimester
Increases in male foetus, multiple gestations, primiparous
Abdo pain NV, jaundice, hypoglycaemia and hepatic failure
Plt

87
Q

What are features of haemochromatosis?

A

require C282Y and H63D mutations
screening test = transferrin saturation >45%
do genetic screening in 1st degree relatives
- siblings of pt with HFE mutations should undergo HFE genotyping - 25% chance of being affected
If normal LFTs and HC then recommend regular blood donation
cirrhosis is unusual if ferritin

88
Q

What are features of wilson’s Dz?

A

AR
Copper overload
low ceruloplasmin, increased urinary copper, decreased serum coppper
if high index of suspicion require liver Bx
screen 1st degree relatives with caeruloplasmin and ur Cp, and LFTs
neuropsychiatric, dystonia, choreoathetiod, parkinsonian features
early liver disease, late neuro disease
Rx - zinc, pnicillamine, tirentine

Delta Med - Gastroenterology (3 decks)

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