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Dannys Medicine Finals > Hepatology > Flashcards

Hepatology Flashcards

1
Q

What are the functions of the liver

A 
PUSHDoG
Protein Synthesis
Urea Production (bile) 
Storage (ADEK, B12, Minerals) 
Hormone synthesis
Detoxification
Glucose and fat metabolism
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2
Q

ALCOHOLIC LIVER DISEASE

what is the stepwise progression?

A

Fatty Liver (Steotosis)
Hepatitis (Inflammation)
Cirrhosis (scarred - irreversible)

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3
Q

Signs of Liver Disease?

A 
Caput Medusa (engorged epigastric superficial veins)
Hepatomegaly
Asterixis 
Ascites
Palmar erythema
Spider Naevi (increased oestrogen)

Gynaecomastia (increased oestrogen)
Bruising (decreased clotting factors)
Jaundice

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4
Q

What is the Child Pugh Score and what are the 5 measurements?

A

Used assess the prognosis of chronic liver disease

1) Encephalopathy
2) Ascites
3) Bilirubin
4) Albumin
5) Prothrombin time prolonged by

Can get either 1,2,3 for each measurement

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5
Q

The AST/ALT ratio can be used to determine the likely cause of LFT derangement

What can the ratio tell us?

A

ALT > AST is associated with chronic liver disease

AST > ALT is associated with cirrhosis and acute alcoholic hepatitis

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6
Q

Common causes of chronic hepatocellular injury include:

A

Alcoholic fatty liver disease
Non-alcoholic fatty liver disease
Chronic infection (Hepatitis B or C)
Primary biliary cirrhosis

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7
Q

Less common causes of chronic hepatocellular injury include:

A

Alpha-1 antitrypsin deficiency
Wilson’s disease
Haemochromatosis

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8
Q

Causes of an isolated rise in bilirubin include:

A

Gilbert’s syndrome: the most common cause.

Haemolysis

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9
Q

Causes of an isolated rise in ALP include:

A

Bony metastases or primary bone tumours (e.g. sarcoma)
Vitamin D deficiency
Recent bone fractures
Renal osteodystrophy

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10
Q

The combination of the colour of urine and stools can give an indication as to the cause of jaundice:

What are they?

A

Normal urine + normal stools = pre-hepatic cause

Dark urine + normal stools = hepatic cause

Dark urine + pale stools = post-hepatic cause (obstructive)

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11
Q

Causes of unconjugated hyperbilirubinaemia include:

A

Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (e.g. Gilbert’s syndrome)

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12
Q

Causes of conjugated hyperbilirubinaemia include:

A

Hepatocellular injury

Cholestasis

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13
Q

ALCOHOLIC LIVER DISEASE

Signs shown on blood investigations?

A

FBC - increased MCV

LFT - increased ALT, AST and particularly gGT
AST/ALT ratio >2

Decreased Albumin
Increased Bilirubin
Increased Prothrombin time

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14
Q

ALCOHOLIC LIVER DISEASE

Acute Management?

A 
Steroids 
Vitamin Replenishment (Thiamine)
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15
Q

Gold standard Imaging for diagnosing cirrhosis?

A

Liver biopsy

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16
Q

Signs of Alcohol withdrawal after:

6-12hrs?
12-24hrs?
24-48hrs?
72hrs?

A

6-12hrs - sweating, anxiety, tremor
12-24hrs- hallucinations
24-48hrs- seizures
72hrs- delirium tremens

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17
Q

Treatment of alcohol withdrawal?

A

Chlordiazepoxide

IV Pabrinex

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18
Q

Wernickes Encephalopathy triad?

A

Opthalmaparesis + Nystagmus
Confusion
Ataxia

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19
Q

Korsakoffs syndrome triad?

A

Psychosis
Confabulation
Amnesia (anterograde/ retrograde)

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20
Q

ACUTE LIVER FAILURE

Signs?

A

Coagulopathy INR >1.5

Hepatic encephalopathy

Transaminitis (deranged LFTs) + Hyperbilirubinaemia

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21
Q

ACUTE LIVER FAILURE

Main causes in europe and worldwide?

A

Europe - drug induced

Worldwide - Viral (Hep A,B,E)

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22
Q

ACUTE LIVER FAILURE

first line imaging?

A

Ultrasound

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23
Q

ACUTE LIVER FAILURE

What does hyperammonaemia increase the risk of?

A

Cerebral Oedema

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24
Q

What is difference between ALF and ALI?

A

ALI has no hepatic encephalopathy

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25
Q

ACUTE LIVER FAILURE

Who should receive emergency liver transplant?

A

Primary causes of ALF only

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26
Q

ACUTE LIVER FAILURE

What features should be investigated for?

A

Features of chronic liver disease as it could be first presentation of decompensated cirrhosis

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27
Q

How is HE tested?

A

normally clinical, however arterial ammonia and EEG can be completed

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28
Q

Treatment of HE?

A

1st - Lactulose (excretion of ammonia)

+ Rifaximin (reduce no of bacteria in gut producing ammonia)

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29
Q

What is normal ICP?

A

7-15mmHg

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30
Q

Ascites Treatment?

A 
Aldosterone antagonists  and loop diuretics 
Reduce salt intake 
Drain if tense (paracentesis) 
Prophylactic Abx (ciprofloxacin or norfloxacin)
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31
Q

What prophylactic Abx can be given for Ascites?

A

Ciprofloxacin/ Norfloxacin

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32
Q

Treatment of raised ICP?

A

Head elevation to 30 degrees

MANNITOL and Hypertonic SALINE

Removal of CSF

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33
Q

Features of raised ICP?

A 
Headache.
Blurred vision.
Confusion.
High blood pressure.
Shallow breathing.
Vomiting.
Changes in your behaviour.
Weakness or problems with moving or talking.
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34
Q

What is Cushings Reflex?

A

The Cushing reflex is a physiological nervous system response to acute elevations of intracranial pressure (ICP)

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35
Q

What is Cushings Triad?

A

Bradycardia

Widening pulse pressure (Increasing systolic and decreasing diastolic)

Irregular breathing

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36
Q

How does Fibrosis cause portal hypertension?

A

Fibrosis causes increased resistance in vessels leading into the liver = portal hypertension (portal vein)

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37
Q

Most common causes of liver cirrhosis?

A

ALD
NAFLD
Hep B
Hep C

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38
Q

Markers of synthetic function of the liver?

A
  • Prothrombin time
  • Albumin

Bilirubin
blood glucose

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39
Q

What should be measured every 6 months for people with liver cirrhosis?

A

Alpha fetoprotein tumour marker for Hepatocellular carcinoma + ULTRASOUND!

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40
Q

First line investigation in NAFLD/ Cirrhosis

A

Enhanced Liver Fibrosis (blood test)

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41
Q

What does enhanced liver fibrosis blood test involve?

A

Measures 3 direct biomarkers of fibrosis

1) HA
2) PIIINP
3) TIMP

and then combines them to produce a result

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42
Q

What are the possible results from ELF test?

A

<7.7 mild/ no fibrosis

> 7.7 -9.8 = moderate fibrosis

> 9.9 = severe fibrosis

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43
Q

What may be found on US in a cirrhotic liver?

A

1) Nodules
2) Corkscrew appearance to arteries due to increased blood flow

3) Enlarged portal vein with reduced flow
4) Ascites
5) splenomegaly

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44
Q

what is transient elastography?

A

Fibroscan - measures stiffness of the liver

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45
Q

who should be screened for using Fibroscan?

A

people with hepatitis C virus infection

men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week and have done so for several months

people diagnosed with alcohol-related liver disease

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46
Q

What should be carried out for patients with a new diagnosis of cirrhosis

A

upper endoscopy to check for varices

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47
Q

How should a cirrhotic patient change their diet

A

Low sodium
high protein
meals every 2/3 hours - high calorie

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48
Q

What is MELD score?

A

Uses a combination of a patient’s bilirubin, creatinine, and (INR) to predict survival in patients with cirrhosis

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49
Q

Treatment of stable varices?

A

Beta blockers (propanolol)

endoscopic variceal band ligation performed at two-weekly intervals until all varices have been eradicated. for medium to large varices

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50
Q

What is given alongside endoscopic variceal band ligation?

A

Proton pump inhibitor cover is given to prevent EVL-induced ulceration

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51
Q

What is the treatment of a bleeding variceal

A

1) Vasopressin analogues (Terlipressin)
2) Correct clotting (Vit K and FFP)
3) Prophylactic Abx (Quinolones - ciprofloxacin)
4) ENDOSCOPY - elastic band ligation or previously sclerotherapy

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52
Q

Last line treatment of variceal haemorrhage

A

TIPS - make connection between hepatic and portal vein to relieve pressure on portal system

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53
Q

Complication of TIPS?

A

Exacerbation of hepatic encephalopathy

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54
Q

Likely causative organisms for Spontaneous Bacterial Peritonitis and the treatment?

A

E.coli Klebsiella

IV Cefotaxime

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55
Q

What is Hepatorenal syndrome and how is it caused?

A

1) Portal hypertension causing dilation of portal vessels and blood pooling
2) This causes hypotension in kidneys which activates RAAS
3) Vasoconstriction due to RAAS and low circulatory volume results in lack of blood to kidneys
4) lack of blood to kidneys results in rapidly deteriorating kidney function

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56
Q

Common associations with NAFLD?

A

OBESITY

type 2 diabetes

Sudden weight loss/ starvation

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57
Q

Stepwise development of NAFLD?

A

1) Steatosis
2) Steatohepatitis (NASH)
3) Fibrosis
4) Cirrhosis

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58
Q

Features of NAFLD?

A

usually asymptomatic

hepatomegaly

ALT is typically greater than AST

increased echogenicity on ultrasound

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59
Q

Investigations of NAFLD?

A

1st - ELF test

2nd - NAFLD fibrosis score

3rd - Fibroscan

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60
Q

What will NAFLD with advanced fibrosis be recommended

A

Liver biopsy to stage disease

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61
Q

What is PBC?

A

Primary Biliary Cholangitis which is the autoimmune inflammation of small bile ducts

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62
Q

Which ducts are inflamed in PBC?

A

Intralobular ducts / Canals of Hering

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63
Q

Clinical features of PBC

A

PRURITIS
FATIGUE

Jaundice - pale stools 
Hyperpigmentation 
RUQ pain (10%)
Clubbing / Hepatosplenomegaly 
XANTHOMA/ XANTHELASMA (increased cholesterol)
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64
Q

What do PBC patients have a high risk of

A

HCC - 20 fold increase in risk

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65
Q

Treatment of Pruritis?

A

Cholestyramine

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66
Q

What age and gender is typical of PBC

A

middle aged females

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67
Q

Diagnostic investigations of PBC?

A

1) Anti - mitochondrial antibodies (AMA) found in 98% of patients
2) Increased serum IgM / ESR
3) Liver biopsy to stage

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68
Q

Management of PBC?

A

Ursodeoxycholic acid

Replenish Fat soluble vitamins

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69
Q

What is involved in ongoing research for treatment of NAFLD?

A

gastric banding and insulin-sensitising drugs (e.g. metformin, pioglitazone)

70
Q

process of cirrhosis to varices?

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage

71
Q

when should liver transplant in PBC be considered

A

If bilirubin over 100

72
Q

how do bile acids, cholesterol and bilirubin end up in the blood

A

They are normally excreted via bile ducts into intestines.

Obstruction to this outflow means chemicals build up in the blood

73
Q

What symptoms/signs do bile acids, cholesterol and bilirubin cause

A

Bile acids - itching

Cholesterol - Xanthoma, Xanthelasma, CV disease

Bilirubin - jaundice

74
Q

How do you get Steatorrhoea from biliary obstruction

A

less bile acids in gut so more fat malabsorption

75
Q

How do you get pale stools from biliary obstruction

A

Less bilirubin reached the gut which darkens stools

76
Q

PRIMARY SCLEROSING CHOLANGITIS

What is it?

A

when intra and extra hepatic ducts become strictured and fibrotic

77
Q

PRIMARY SCLEROSING CHOLANGITIS

Risk factors?

A

Ulcerative colitis (70 of PSC pts have both)

male

aged 30-40

78
Q

PRIMARY SCLEROSING CHOLANGITIS

Likely autoantibodies?

A

pANCA (94%)
ANA (70%)
aCL (63%)

79
Q

PRIMARY SCLEROSING CHOLANGITIS

Presentation?

A 
Jaundice
RUQ pain
Pruritis 
Fatigue 
Hepatomegaly
80
Q

PRIMARY SCLEROSING CHOLANGITIS

Associations?

A 
Cholangiocarcinoma (20%)
Colorectal cancer
Acute bacterial cholangitis 
Bone disease 
Vit ADEK deficiencies
81
Q

PRIMARY SCLEROSING CHOLANGITIS

LFT picture?

A

Cholestatic

^^ALP
^ Bilirubin
^ ALT and AST if hepatitis

82
Q

PRIMARY SCLEROSING CHOLANGITIS

Diagnosis?

A

MRCP shows biliary stricturing

MRI bile ducts, liber, pancreas

83
Q

PRIMARY SCLEROSING CHOLANGITIS

Management?

A

Liver transplant

ERCP to stent and dilate strictures

84
Q

PRIMARY SCLEROSING CHOLANGITIS

treatment of pruritis?

What can slow progression of the disease?

A

Cholestyramine

Ursodeoxycholic acid

85
Q

PRIMARY SCLEROSING CHOLANGITIS

What should be monitored for?

A

Cirrhosis and associated cancers (CCA)

86
Q

what is charcots triad?

A

Fever Jaundice RUQ pain

87
Q

What LFTs show hepatic/ cholestatic picture?

A

Hepatic = ^^ AST/ALT

Cholestatic = ^^ ALP/gGT

88
Q

What does ERCP increase the risk of

A

Pancreatitis and Cholangitis

89
Q

What is the tumour marker of CCA?

A

Ca 19.9

90
Q

How are cholangiocarcinomas diagnosed?

A

Gold standard is ERCP

91
Q

Who typically gets autoimmune hepatitis type 1

A

Female menopause age characterised by fatigue and liver features

92
Q

Autoantibodies found in Type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

93
Q

Autoantibodies found in Type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomes-1 (anti-LKM1)

Anti-liver cytosol antigen type 1 (anti-LC1)

94
Q

Diagnosis of autoimmune hepatitis?

A

Liver biopsy

95
Q

Who typically gets autoimmune hepatitis type 2

A

patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

96
Q

Most common types of primary liver cancer?

A

HCC (80%)

CCA (20%)

97
Q

Risk factors of:

HCC?

A

Hepatitis B
Alcohol
NAFLD
Cirrhosis!!!!

98
Q

Risk factors of:

CCA?

A

PSC

99
Q

Symptoms of liver cancer

A

Non specific liver signs + weight loss + Anorexia

CCA -possible jaundice

100
Q

Tumour markers for:

HCC

CCA

A

HCC - alpha fetoprotein

CCA - Tumour marker Ca 19.9

101
Q

how are HCC and CCA diagnosed

A

HCC - CT/MRI

CCA - ERCP

102
Q

Treatment of liver cancer?

A

Extremely poor prognosis, possible surgical resection/ ablation

Sorafenib - multi kinase inhibitors

103
Q

Treatment of Autoimmune Hepatitis

A

Prednisolone + Azathioprine

104
Q

Symptoms of biliary colic?

A

Abrupt RUQ pain after eating + Nausea/ vomiting

105
Q

Who is typical patient of biliary colic

A

Fat fair fertile females in forties

106
Q

Acute Cholecystitis symptoms?

A

Persistent RUQ pain that radiates to back/shoulder

pyrexia/ fever

Murphys sign!

107
Q

Why does biliary colic happen?

A

occur due to ↑ cholesterol, ↓ bile salts and biliary stasis

the pain occurs due to the gallbladder contracting against a stone lodged in the cystic duct

108
Q

Investigations and treatment of biliary colic?

A

Ultrasound

Elective laparoscopic cholecystectomy

109
Q

How may jaundice occur after cholecysectomy

A

Gall stones in common bile duct in 15% therefore would present with obstructive jaundice

110
Q

Notable risk factors of biliary colic?

A

Crohns
Diabetes
COCP
rapid weight loss (weight reduction surgery)

111
Q

what does Acute Cholecystitis occur secondary to

A

Gallstones in 90% of cases

112
Q

How would LFTs show in Acute Cholecystitis

A

Usually Normal

113
Q

Signs of Acute Cholecystitis

A

RUQ pain (radiate to right shoulder)
fever
N/V
Murphys Sign

114
Q

Acute Cholecystitis investigation choice?

A

Ultrasound 1st line

cholescintigraphy (HIDA scan) if dx still unsure

115
Q

Treatment of Acute Cholecystitis?

A

IV Abx and Elective Laparoscopic Cholecystectomy within 1 week

116
Q

What is ascending cholangitis

A

bacterial infection (typically E. coli) of the biliary tree.

The most common predisposing factor is gallstones.

117
Q

Ascending Cholangitis management?

A

intravenous antibiotics

endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction

118
Q

Ascending Cholangitis Features?

A

Charcot’s Triad
Fever 90%
RUQ pain 70%
Jaundice 60%

AND

Hypotension
Confusion

(the additional 2 factors in addition to the 3 above make Reynolds’ pentad)

119
Q

What is Reynolds Pentad

A

Fever
RUQ pain
Jaundice

HYPOTENSION
CONFUSION

Diagnosis of Septic Ascending Cholangitis

120
Q

What is Courvoisier sign

A

Palpable mass in RUQ

121
Q

HAEMOCHROMATOSIS

What is it?

A

Autosomal recessive iron storage disorder resulting in widespread iron deposits in tissues

122
Q

HAEMOCHROMATOSIS

what gene is affected?

A

HFE protein on chromosome 6

123
Q

HAEMOCHROMATOSIS

at what age does it typically present

A

After 40 and later in females due to menstruation

124
Q

HAEMOCHROMATOSIS

Symptomatic presentation?

A

Cognitive problems (memory/ mood)
Hair loss
ED
Fatigue

joint pain
bronze discolouration

125
Q

HAEMOCHROMATOSIS

How is it diagnosed?

A

1) Transferrin saturation and Serum Ferritin

2) genetic testing

126
Q

HAEMOCHROMATOSIS

How did it used to be diagnosed

A

Used to be diagnosed using Perls Stain + liver biopsy

127
Q

HAEMOCHROMATOSIS

potential complications (by organ)

A

Pancreas - T1DM

Liver - Cirrhosis (can lead to HCC)

Pituitary/ Gonads (hypotrophic hypogonadism/ infertility)

Heart - Cardiomyopathy

Hypothyroid

Joints - Chondrocalcinosis (pseudogout)

128
Q

HAEMOCHROMATOSIS

how is it managed?

A

Venesection (weekly blood removal)

2nd - Desferrioxamine

129
Q

WILSON’S DISEASE

What is it?

A

Autosomal recessive condition causing excess copper deposits in tissues

130
Q

WILSON’S DISEASE

Defective gene?

A

ATP7B geen on chromosome 13

131
Q

WILSON’S DISEASE

Features?

A

HEPATIC (40%) - chronic hepatitis - cirrhosis

NEUROLOGICAL (50%) - spectrum of subtle to dysarthria

PSYCHIATRIC (10%) - depression / psychosis

KAYSER - FLEISCHER RINGS

ASTERIXIS

132
Q

What are Kayser- Fleischer Rings?

A

green/brown ring in Descemets Corneal Membrane due to copper deposits

133
Q

What happens if copper deposits get into basal ganglia?

A

Parkinsonism (symmetrical unlike parkinsons)

134
Q

WILSON’S DISEASE

Diagnosis?

A

Decrease in serum Caeruloplasmin / total body copper

Increase in 24hr urinary copper excretion

135
Q

How to assess for Kayser Fleischer rings?

A

Slit lamp exam

136
Q

WILSON’S DISEASE

Management?

A

Copper Chelation

1) Penicillamine
2) Trientine

137
Q

What is A1AT?

A

Alpha 1 antitrypsin is a protease inhibitor - inhibiting neutrophil elastase which breaks down tissue - therefore a deficiency results in tissue breakdown

138
Q

What happens as a result of Neutrophil elastase levels being high?

A

Lung - emphysema, COPD, bronchiectasis

Liver - cirrhosis

139
Q

What is the defective chromosome in A1AT deficiency?

A

Chromosome 14

140
Q

Diagnosis of A1AT deficiency?

A

low serum A1AT
liver biopsy
CT thorax and spirometry for emphysema and COPD

141
Q

Management of A1AT deficiency?

A
  • Smoking cessation
  • Symptomatic (COPD e.g. bronchodilators)
  • End stage liver transplant
  • Monitor for hepatocellular carcinoma
142
Q

Name of RNA in Hepatitis A?

route of transmission?

A

RNA Picornavirus

Faeco-oral

143
Q

Is there a vaccine for Hep A?

A

Yes - for high risk such as MSM, travellers of prevalent countries

144
Q

Features of Hep A?

A 
Flu like prodrome 
RUQ pain
tender hepatomegaly 
Jaundice , N+V
Cholestatic LFTs
145
Q

Management of Hep A -

A

resolves in 1-3 months + Analgesia

146
Q

HEPATITIS B

Route of transmission?

A

Infected bodily fluids + vertical transmission from mother to baby

147
Q

HEPATITIS B

name of virus?

A

DNA Hepadnavirus

148
Q

HEPATITIS B

Is there a vaccine?

A

Immunised at 2,3,4 months old + booster for high risk groups e.g healthcare

149
Q

HEPATITIS B

Signs?

A

Fever
Jaundice
Elevated transaminases (AST/ALT)

150
Q

HEPATITIS B

What % are likely to be chronic infection carriers?

A

10%

151
Q

HEPATITIS B

What viral marker implies active infection?

A

HbsAg surface antigen

152
Q

HEPATITIS B

What viral marker implies highly infective?

A

E antigen HbeAg is a marker of viral replication (acute phase)

153
Q

HEPATITIS B

How to test for past / current infection?

A

HbcAb (antibody)

154
Q

HEPATITIS B

What does it mean if HbeAg negative but HbeAb positive?

A

Virus stopped replicating (out of acute phase)

155
Q

HEPATITIS B

HbcAb can be measured using IgM and IgG

what does IgM HbcAb imply?

What does IgG imply?

A

IgM is acute phase so virus active

IgG HbcAb implies past infection of HbsAg is -ve.

156
Q

HEPATITIS B

Management?

A

Antivirals - Pegylated interferon alpha

testing for liver cirrhosis / HCC

157
Q

What is name of Hepatitis C virus and is there a vaccine

How is it normally transmitted

A

RNA flavivirus and no vaccine

Infected blood

158
Q

What percentage of Hep C patients become chronic f

A

75%

159
Q

What % of Hep C patients are symptomatic and what are the symptoms

A

30% get:

transient rise in aminotransferases + jaundice
Fatigue
Arthralgia

160
Q

Management of Hep C?

A

Direct acting antivirals based on viral genotype

Usually combination of Sofasbuvir + Daclatasvir/ Simeprevir (PROTEASE INHIBITORS)

successful in 90% of cases

161
Q

How is Hep C screened?

A

Hep C Antibodies

Hep C RNA testing confirms diagnosis and calculates viral load

162
Q

What is Hepatitis D?

How is it transmitted?

A

Single stranded RNA only survives if also infected with Hep B - attaches to Hep B surface antigen

Bodily fluids similarly to Hep B

163
Q

Hep E virus and route of transmission?

A

RNA hepevirus

Faeco-oral

164
Q

Hep E normally clears with no treatment after a month but when is it dangerous?

A

Pregnancy (20% mortality)

165
Q

What is the risk if someone has Hep B and D superinfection

A

Fulminant hepatitis, cirrhosis

166
Q

What can be found on blood test in pernicious anaemia?

A

antibodies to intrinsic factor +/- gastric parietal cells

Macrocytic anaemia

167
Q

What cancer is there an increased risk of in pernicious anaemia

tx of pernicious anaemia?

A

gastric cancer

IM B12 replacement (hydroxocobalamin)

168
Q

What are Sister Mary joseph nodes?

A

Periumbilical lymphadenopathy

169
Q

Where is Virchows Node?

A

Left supraclavicular

170
Q

Potential signs on examination in Cholangiocarcinoma?

A

A palpable mass in the right upper quadrant (Courvoisier sign),
periumbilical lymphadenopathy (Sister Mary Joseph nodes)
left supraclavicular adenopathy (Virchow node)

171
Q

Budd-Chiari Syndrome (Hepatic Vein Thrombosis) Features?

Ix of choice?

A

Triad of:

1) sudden onset abdominal pain
2) Ascites
3) tender hepatomegaly

Ultrasound with Doppler flow studies

Dannys Medicine Finals (9 decks)

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