Liver Flashcards

Acute liver failure Chronic liver disease and cirrhosis

1
Q

Which condition is associated with SBP (spontaneous bacterial peritonitis)

A

Common in ascites caused by hepatic cirrhosis

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2
Q

Someone has poor liver function. Name two liver function tests and what changes will occur in disease

A

Increased PT

Decreased albumin

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3
Q

Which cells release ALT and AST

A

hepatocytes

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4
Q

Which cells release GGT and ALP

A

bile ductal cells

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5
Q

Name five causes of cirrhosis/chronic liver disease

A
  1. alcohol
  2. Hep B/C
  3. NAFLD
  4. autoimmune hepatitis
  5. haemochromatosis
  6. wilson’s disease
  7. PBC
  8. PSC
  9. alpha1 antitrypsin
  10. Drugs
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6
Q

How can alcoholic causes of cirrhosis be diagnosed?

A

thorough history + increased AST and ALT, ratio 2:1 (approx)

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7
Q

Which cause of cirrhosis is the only one associated with a higher AST to ALT ratio

A

alcohol induced

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8
Q

Which cells are damaged as a result of alcohol excess

A

hepatocytes, therefore incr ALT and AST

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9
Q

What are the risk factors for Hep B and C?

A

blood exposure e.g. needles, tattoos, IV drugs, blood transfusion
sexual
vertical
geography

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10
Q

Which cell is does hep B/C target in the liver? Which biomarkers are raised?

A

hepatocytes, raised ALT ++ raised AST +

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11
Q

Name three risk factors for NAFLD

A

central obesity, diabetes, hyperlipidaemia

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12
Q

Which LFTs are raised in NAFLD?

A

AST + ALT ++

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13
Q

What are the components of autoimmune hepatitis screen?

A

ANA/ASA, IgG

+liver biopsy

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14
Q

In which organs can ferritin be deposited in haemorchromatosis?

A

liver, pancreas, heart, skin, joints, gonads

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15
Q

What are the complications of ferritin storage in the affected organs?

A

pancreas- diabetes, heart- cardiomyopathy, skin- bronzing, joints- arthritis, gonads- infertility

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16
Q

What is the treatment for haemochromatosis?

A

venesection

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17
Q

A 23 year old patient presents with a tremor. Which liver related disease could be causing this?

A

wilson’s disease. copper can deposit and sequester in basal ganglia, resulting in tremor

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18
Q

Ceruloplasmin test is a diagnostic test for which disease?

A

Wilson’s disease

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19
Q

Which liver cells does PBC affect? What are the affected LFTs?

A

SMALL ductal cells. Incr GGT and ALP.

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20
Q

What is the pathophysiology of PBC?

A

Autoimmune destruction of small bile ducts due to granulomas, obstructing flow of bile

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21
Q

What is the treatment for PBC?

A

liver transplant

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22
Q

How does PSC compare to PBC?

A

PSC affects both small and large bile ducts. PBC is autoimmune while PSC is not.

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23
Q

Which LFTs are raised in PSC?

A

GGT and ALP

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24
Q

In alpha1 antitrypsin deficiency, are the lungs or liver affected first?

A

lungs

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25
Q

Which drugs can cause cirrhosis?

A

methotrexate and isoniazid

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26
Q

What are the categories of causes of jaundice?

A

Pre-hepatic, intrahepatic (failure to conjugate bilirubin in a damaged/inflamed liver or excrete it into bile ducts), and post-hepatic

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27
Q

Causes of pre-hepatic jaundice?

A

hereditary spherocytosis, DIC, G6PD, autoimmune, infection (malaria)

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28
Q

Causes of intrahepatic jaundie?

A

decompensated liver disease/cirrhosis (NAFLD, alcohol, viral)
Acute liver injury (viral)
Drugs
Gilbert’s

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29
Q

Causes of post-hepatic jaundice?

A

obstruction of large bile ducts: cholangitis, chlangiocarcinoma, pancreatic mass, cancer

drug or pregnancy induced cholestasis

autoimmune disease (PBC, PSC)

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30
Q

Jaundice and breathlessness. Which cause of jaundice are they likely to have?

A

pre-hepatic (symptoms of anaemia)

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31
Q

Pale stools, dark urine. Which cause of jaundice?

A

post-hepatic

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32
Q

Painless jaundice in elderly patient with weight loss. What is the likely cause?

A

pancreatic malignancy

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33
Q

Will bilirubin be positive in dipstick of biliary obstruction, hepatic disease, and haemolytic disease?

A

positive in obstruction and hepatic disease but not haemolytic disease

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34
Q

Which clinical findings on examination would be indicative of decompensated liver disease?

A

jaundice, shifting dullness/ascites, confusion, asterexis, GI bleeding

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35
Q

Why would you look at U&Es when investigating decompensated liver disease?

A

risk of hepatorenal syndrome, acute renal failure can complicated hepatic function

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36
Q

Why would you check CRP in decompensated liver disease?

A

infection can often trigger decompensation

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37
Q

Which investigations form part of a liver screen?

A
  1. Alpha fetoprotein
  2. Hepatitis screen
  3. ANA
  4. alpha 1 antitrypsin
  5. ceruloplasmin
  6. iron studies
  7. coeliac disease
  8. TFTs
  9. HIV screen
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38
Q

Why would you conduct alpha fetoprotein blood test?

A

liver tumour marker

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39
Q

Why would you test for ceruloplasmin?

A

wilson’s disease

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40
Q

Why would you do iron studies in jaundiced patient?

A

to rule out haemochromatosis

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41
Q

Why would you do an asicitic tap?

A

to ID spontaneous bacterial sponitinits

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42
Q

Name three causes of hepatic encephalopathy?

A

sepsis, constipation, medications, dehydration, bleeding

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43
Q

Which antibiotic to reduce the risk of recurrent hepatic encephalopathy?

A

rifaximin

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44
Q

What is SAAG?

A

serum-ascites albumin gradient

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45
Q

If SAAG> 11g/L, what will the likely cause of ascites be?

A

portal hypertension

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46
Q

Why do liver disease patients have low platelets?

A

portal hypertension results in splenomegaly and platelet sequestration

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47
Q

Name three reasons why liver disease patients at high risk of bleeding?

A

prolonged INR due to failing synthetic liver function
Low platelets
Oesophageal and gastric varices

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48
Q

What is the management of bleeding in liver disease patient?

A
vit K
withhold anticoag/NSAIDs
Endoscopy?
HDU?
Abx- reduces mortality
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49
Q

Which two scores stratify the risk of bleeding?

A

glasgow blatchford and rockall score

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50
Q

Patient with IgM and mitcochondrial antibody (AMA). Which condition do they have?

A

primary biliary cholangitis

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51
Q

Patient ANCA positive + jaundice. Which condition is likely causing this?

A

primary sclerosing cholangitis

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52
Q

ANA, ASMA positive, raised IgG. Which condition is causing their jaundice?

A

autoimmune hepatitis

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53
Q

What is the mode of inheritance of haemochromatosis?

A

autosomal recessive

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54
Q

Where can iron be deposited in haemochromatosis?

A

liver, pancreas, heart, joints, skin, pituitary

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55
Q

Which extraheaptic clinical manifestations of haemochromatosis are reversible?

A

skin discolouration
cardiomyopathy
hepatomegaly

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56
Q

Which extrahepatic clinical manifestations of haemochromatosis are irreversible?

A
hepatocellular carcinoma 
arthropathy
hypopituitarism
diabetes
cirrhosis
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57
Q

Patient with ascites. Which abx should you commence?

A

coamoxiclav

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58
Q

What are the signs of de-compensated liver cirrhosis?

A

asicites, encephalopathy, jaundice, coagulopathy, hypotensive

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59
Q

Which diuretics are used in the management of ascites?

A

furosemide and spironolactone

60
Q

What are three complications of ascites?

A
  1. SBP
  2. Malignancy (AFP/HCC)
  3. Portal vein thrombus
61
Q

Which guidelines can help with the management of decompensated cirrhosis?

A

BASL bundle care pathway

62
Q

What are the anatomical sites to perform paracentesis?

A

2/3 down from umbilicus to ASIS

63
Q

When should you be cautious about performing paracentesis?

A

if patient has prolonged PT + APTT

64
Q

What is pabrinex?

A

Vitamin B and C complexes= bright yellow

65
Q

Is Wernicke or Korsakoff irreversible?

A

Korsakoff is irreversible

66
Q

Can you still have cirrhosis if you have normal LFTs?

A

Yes!!!!

67
Q

What can be given as adjunct when offering fluids to patients with ascites?

A

albumin, promotes fluid accumulation in vascular space

68
Q

Give three causes for precipitating hepatic encephalopathy and provide treatment for each

A
UGIB- transfusions and resus
Constipation- laxatives
Infection- appropriate antibiotics
Electrolyte imbalance- replace
Increased alcoholic intake
69
Q

Give three management options for treating ascites

A

aspiration/drain
diuretics- spironolactone and furosemide
fluid restriction, low salt diet

70
Q

List two causes of asterexis

A

CO2 retention

uraemia

71
Q

Describe bilurbin metabolism

A
  1. Hb → unconjugated bilirubin by splenic macrophages
  2. Unconjugated bilirubin bound to albumin is converted to conjugated bilirubin in liver glucoronyl transferase
  3. In colon, colonic bacteria convert cBR to urobilinogen (colourless). 80% of urobilonogen is further oxidised to stercobilinogen. Some urobilinogen is reabsorbed and diverted to liver and re-excreted in bile, the rest is excreted in the urine
72
Q

What is Gilbert’s syndrome?

A

Auto dom partial UDP-GT deficiency

Jaundice occurs during intercurrent illness

73
Q

What are the results of LFTs of someone who has gilbert’s?

A

normal LFTs

74
Q

How is gilbert’s diagnosed?

A

increased unconjugated bilirubin whilst fasting

75
Q

List three drugs that can cause jaundice

A

Haemolysis- Antimalarials (e.g. dapsone)

Hepatitis: paracetamol OD, statins

Cholestasis: Sulfonylureas, oral contraceptive pills, fluclox

76
Q

Pre-hepatic jaundice. What would be detected in urine?

A

no bilirubin

increased urobilinogen

77
Q

Hepatic jaundice. Urine results?

A

increased bilirubin

increased urobilinogen

78
Q

Post hepatic jaundice. Urine?

A

incr bilirubin

no urobilinogen

79
Q

LFTs of pre-hepatic?

A

Incr LDH, AST, unconju-bilurbin

80
Q

LFTs of hepatic jaundice?

A
cBR incre
AST:ALT incr
GGT incr
ALP incr
decreased albumin, increased PT
81
Q

LFTs post hepatic jaundice?

A

Incr cBR
Incr ALT AST
Incr ALP
Incr GGT

82
Q

List three causes of acute liver failure

A

 Infection: Hep A/B, CMV, EBV, leptospirosis
 Toxin: EtOH, paracetamol, isoniazid, halothane
 Vasc: Budd-Chiari
 Other: Wilson’s, AIH
 Obs: eclampsia, acute fatty liver of pregnancy

83
Q

State three signs of liver failure

A
jaundice
oedema +ascites
bruising
encephalopathy- asterixis 
Foetor hepaticus
Signs of liver disease
84
Q

Name a complication of advanced liver failure

A

hepatorenal syndrome

85
Q

Why is it important to test for glucose in liver disease/failure?

A

liver is responsible for gluconeogensis and glycogen storage, therefore hypoglycaemia can ensue if liver function is impaired

86
Q

Describe three complications of liver failure

A
bleeding
sepsis
ascited
hypoglycaemia
encephalopathy
seizures
cerebreal oedema
87
Q

What is the management of sepsis in patient with liver failure?

A

tazocin (avoid gent due to nephrotoxicity)

88
Q

Management of ascites?

A

fluid and salt restrict, spiro, fruse, tap, daily weight

89
Q

Name two drugs that should be avoided in liver failure?

A

opioids (exacerbation of encephalopathy), oral hypoglyacaemics, warfarin effects, paracetamol, isoniazid

90
Q

List three hepatotoxic drugs

A

paracetamol
methotrexate
isoniazid
tetracycline

91
Q

Two signs of cirrhosis in hands?

A
  Clubbing (± periostitis) 
  Leuconychia (↓ albumin) 
  Terry’s nails (white proximally, red distally) 
  Palmer erythema 
  Dupuytron’s contracture
92
Q

Two signs of cirrhosis in face?

A

 Pallor: ACD

 Xanthelasma: PBC

93
Q

Two signs of cirrhosis in chest?

A

 Spider naevi (>5, fill from centre)
 Gynaecomastia
 Loss of secondary sexual hair

94
Q

Two signs of cirrhosis in abdomen?

A

 Striae
 Hepatomegaly (may be small in late disease)
 Splenomegaly
 Dilated superficial veins (Caput medusa)
 Testicular atrophy

95
Q

List three complications of cirrhosis

A
  1. Decompensation- hepatic failure
  2. SBP
  3. Portal hypertension
  4. Increased risk HCC
96
Q

Three signs of decompensated liver cirrhosis

A
jaundice
encephalopathy
ascited +oedema (hypoalbuminaemia)
coagulopathy
hypoglycaemia
97
Q

Three signs of portal hypertension?

A
SAVE
splenomegaly
ascites
varices
encephalopathy
98
Q

Which blood test in a liver screen indicates HCC?

A

alpha-fetoprotein

99
Q

Two signs of cirrhosis on ultrasound?

A

small/large liver
focal lesions
ascites

100
Q

SBP is infection of what?

A

ascitic fluid

101
Q

What is the pathophysiology of encephalopathy?

A

1.↓ hepatic metabolic function
2. Diversion of toxins from liver directly into systemic system.
3. Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine
4. ↑ glutamine → osmotic imbalance → cerebral oedema.

102
Q

Two symptoms of encephalopathy?

A

asterexis
confusion
seizures
dysarthria (motor speech disorder)

103
Q

List three precipitants of hepatic encphalopathy

A
HEPATICS
  Haemorrhage: e.g. varices 
  Electrolytes: ↓K, ↓Na 
  Poisons: diuretics, sedatives, anaesthetics 
  Alcohol 
  Tumour: HCC 
  Infection: SBP, pneumonia, UTI, HDV 
  Constipation (commonest cause) 
  Sugar (glucose) ↓: e.g. low calorie diet
104
Q

What are two agents that cause SBP?

A

e.coli, klebsiella, strep

105
Q

Treatment of SBP?

A

tazosin

106
Q

Source of spread for hep B?

A

blood, body fluids, pergnancy (vertical)

107
Q

Transmission for hep c?

A

blood

108
Q

transmission hep A?

A

faecal-oral, seafood

109
Q

NAFLD is associated with which syndrome?

A

metabolic syndrome

110
Q

what are three features of metabolic syndrome

A

central obesity
high triglycerides
HTN
hyperglycaemia

111
Q

What is Budd-chiari syndrome?

A

Hepatic vein obstruction → ischaemia and hepatocyte damage → liver failure or insidious cirrhosis.

112
Q

What is a cause of budd chiari syndrome?

A
hypercoagulable state (myeloproliferative disorder)
Local tumour
113
Q

Describe three clinical features of hereditary haemochromatosis

A

features of iron deposition in different organs

Cardiomyopathy
Diabetes
Cirrhosis
Arthritis
Grey skin
114
Q

What is the first line treatment for haemochromatosis?

A

iron removal- routine venesection

115
Q

Blood results for haemochromatosis?

A

incr ferritin
incr Fe
reduced TIBC

116
Q

65 y/o patient with signs of wilson’s disease. Could they have this disease?

A

no, presents between childhood and 30 (never >56)

117
Q

Why is there reduced Cu in blood in wilson’s disease?

A

Mutation of Cu transporting ATPase
Impaired hepatocyte incorporation of Cu into
caeruloplasmin and excretion into bile
Cu accumulation in liver and other organs

118
Q

Name three clinical features of wilson’s disease

A
Kayser-Fleischer rings
Liver disease
Arhtritis
PARKINSONISM
Haemolytic anaemia
119
Q

Which neuro disorder is associated with wilson’s disease?

A

parkinson’s disease

120
Q

Which autoantibodies can be present in autoimmune hepatitis?

A

SMA, LKM, SLA, ANA

121
Q

Autoimmune hepatitis can be associated with which other diseases? Name two

A

thyroiditis
DM
pernicious anaemia
UC

122
Q

How does the pathology of PBC and PSC differ?

A

PBC= intrahepatic bile duct destruction by chronic granulomatous inflammation

PSC= Inflammation, fibrosis and strictures and intra- and
extra-hepatic ducts.

123
Q

Are most of liver cancer primary or secondary?

A

90% are secondary

124
Q

Which primary cancers metastasize to the liver?

A

breast, colon, stomach, lung, uterus

125
Q

State two benign tumours of the liver

A

cysts
adenomas
haemangiomas

126
Q

Aside from viral hepatitis, name two infections that can cause acute hepatitis

A

malaria, EBV, syphilis

127
Q

What is the significance of core antibody lab test? cAb

A

only positive in people exposed to WHOLE virus e.g. current or previous infection, not present in response to vaccinations as only part of the virus is presented

128
Q

Which Hep B marker is a marker for current infection?

A

sAg- surface antigen

129
Q

Which hep B marker is a marker for previous infection?

A

sAb- surface antibody

130
Q

Which two tests are required to diagnose current hep b infection?

A

sAg and DNA

131
Q

How does presence of eAg influence disease?

A

eAg positive- early disease, highly infectious, high viral load, high risk of liver disease and carcinoma, while if negative then lower risks

132
Q

Name two cancers of the liver

A

hepatocellular carcinoma, and cholangiocarcinoma

133
Q

What are the symptoms of liver disease?

A

jaundice- dark urine, light stool, itchy, ankle swelling, abdominal swelling, nausea, vomiting, fever

134
Q

What is the definition of cirrhosis?

A

!! 1. Diffuse process with 2. Fibrosis and 3. Nodule formation

135
Q

Which blood markers are most helpful to determine actual liver function?

A

albumin, bilirubin, PT

136
Q

Name three metabolic liver diseases that result in chronic liver injury

A
  1. Haemochromatosis 2. Wilson disease (copper) 3. Alpha1 antitrypsin deficiency
137
Q

What is the treatment for autoimmune hepatitis?

A

corticosteroids, azathioprine

138
Q

How can NAFLD and alcoholic liver disease be distinguished?

A

AST/ALT ration >1.5 in ALD

139
Q

What are two features of the glasgow alcoholic hepatitis score?

A

age, WCC, urea, PT, bilirubin

140
Q

Which liver disease is interface hepatitis a typical feature of?

A

autoimmune hepatitis

141
Q

List four biochemical signs that you would see in cirrhosis

A

Increased bilirubin, raised PT, decreased albumin, and low platelets

142
Q

What is the cause of ‘bronze diabetes’?

A

genetic haemochromatosis

143
Q

Name two tests most useful in monitoring response to haemochromatosis management (phlebotamy)

A

ferritin and transferrin saturation

ferritin= total iron stores

144
Q

Triad of symptoms for Budd-Chiari syndrome?

A

Budd-Chiari syndrome presents with the triad of sudden onset abdominal pain, ascites, and tender hepatomegaly

145
Q

What is SAAG?

A

The SAAG is used to determine if the ascites has been caused by portal hypertension or not. A raised SAAG (>11g/L) indicates that it is portal hypertension that has caused the ascites. Budd-Chiari syndrome (hepatic vein thrombosis) is the only option that causes portal hypertension.

All the other options do not cause portal hypertension and would therefore result in a SAAG < 11g/L.