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Phase 2a > Liver > Flashcards

Liver Flashcards

1
Q

What are the functions of the liver and what can go wrong?

A

-Oestrogen level regulation - spider navei, palmer erythema
-Albumin - ascites + oedema
-Clotting factors - bleeding disorders
-Storage of vits/Fe/Cu/fat -Wilsons, haemachromatosis
-Metabolism of carbs
-Immunity (Kupffer)-SBP
-Detoxification -hepatic encephalopathy
-Billirubin metabolism- jaundice

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2
Q

What are the markers of liver function that indicate liver damage?

A

Bilirubin- Conj/unconj =High
Albumin =Low
Prothrombin time =High

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3
Q

What enzymes are increased tat would suggest liver damage?

A

-ALT =Alanine transaminase
-AST =Aspartate aminotransferase
Both found in liver, heart, kidney and lungs
-GGT=Gamma glutamyl transferase
-ALP= Alkaline phosphate

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4
Q

What would AST:ALT typically suggest?

A

> 2:1. - ALD
4.5:1 -Wilosns or hyperthyroid
<0.9:1 - Suggest NAFLD

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5
Q

What would high GGT suggest?

A

High in ALD + helps differentiate high ALP as a hepatic or bony cause

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6
Q

What would high ALP suggest?

A

High in billiary tree specific damage + bony pathology

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7
Q

What is liver failure?

A

Liver loses its ability to repair and regenerate leading to decompensation

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8
Q

What is decompensation?

A

Characterised by abnormal bleeding, ascites, hepatic encephalopathy and jaundice

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9
Q

What is acute liver failure?

A

Liver injury accompanied with hectic encephalopathy, jaundice and coagulopathy(>1.5INR), and ascites in a patient with a previously normal liver

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10
Q

What is fulminant liver failure?

A

rare syndrome of massive hepatocyte necrosis (histologically = multiacinar necrosis)
- hyper acute (HE within 7 days of jaundice)
-acute (8-28 days HE within jaundice)
-Subacute (5-26 weeks)

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11
Q

What is the most common cause of fulminant liver failure?

A

Paracetamol overdose (50%case sin the UK)

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12
Q

What is acute on chronic liver failure?

A

Abrupt decline in patient with chronic liver Sx

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13
Q

What is Chronic liver failure?

A

Patient with progressive Hx of liver disease;
Hepatitis -> fibrosis-> compensated cirrhosis-> decompensated cirrhosis (ESLF)

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14
Q

What are the causes of acute liver failure?

A

-Viral = HEP A,B,E ; CMV;EBV
-Autoimmune hep
-Drugs - paracetamol, alcohol, ecstasy
-HCC
-Metabolic - Wilkinsons, haemochromatosis, A1ATD
-Budd Chiari

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15
Q

What is the presentation of acute liver failure?

A

Acute Px of Jaundice, coagulopathy, HE:
-spider naevi
-fetor hepaticus -breath
-caput medusae - distended abdo BVs
Dupuytren’s contracture - abnormal thickening of skin on palms of hands

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16
Q

What is West haven criteria grades 1-4?

A
  • Severity of encephalopathy (HE)
    1. altered mood, sleep issues
    2. lethargy, mild confusion, asterixis
    3.marked confusion
    4. comatose
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17
Q

What is the diagnosis of acute liver failure?

A

Bloods: LFTs (high bilirubin, low albumin, Hugh PT/INR)
High serum AST/ALT, high ammonia, low glucose

Imaging - EEG- grade HE
USS abdo to check Budd chiari
Microbiology to rule out infections - blood culture, urine culture, ascitic tap

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18
Q

What is Budd Chiari?

A

an uncommon disorder characterized by obstruction of hepatic venous outflow.

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19
Q

What is the treatment for acute liver failure?

A

Acutely - ABCDE, fluid, analgesia
Tx underlying cause + complications

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20
Q

What are the complications and treatments of acute liver failure?

A

Increased ICP = IV Mannitol
HE= Lactulose (increase ammonia excretion)
Ascites = diuretics
Haemorrhage = Vit K
Sepsis = sepsis 6

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21
Q

What is chronic liver failure?

A

Progressive liver disease over 6+ months due to repeated liver insults

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22
Q

What are the causes of chronic liver failure?

A

ALD - mc
NALD
Viral - hep BC
+ metabolic, Budd chiari, drugs, autoimmune, PBC, PSC

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23
Q

What is the pathology of chronic liver failure?

A

Hepatitis/ Cholestasis –> fibrosis(reversible damage) –> cirrhosis (irreversible) -> either compensated or decompensated (ESLF)

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24
Q

What is the Child Pugh score?

A

Assessing prognosis and extent of Tx required for chronic liver failure; essentially decompensated cirrhosis
-Classes scores ABC

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25
Q

What consists of the child Pugh score?

A
  • billirubin
    -ascites presence
    -serum albumin
    -PT/INR
    -Hepatic encephalopathy
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26
Q

What are the ABC Child Pugh class system?

A

A = 100% 1year survival
B=80% 1 year survival
C=45% 1 year survival

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27
Q

What is Meld score?

A

Model for end stage liver disease, stratifies severity of ESLD for transplant planning

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28
Q

What is a risk factor for developing HCC?

A

ESLF - decompensated cirrhosis

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29
Q

What is the presentation of decompensated ESLF?

A
  • jaundice
    -HE
    -Coagulopathy
    -Ascites
    -Portal HTn +oesophageal varices
    -low serum albumin
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30
Q

What are the patient symptoms of chronic liver failure?

A
  • jaundiced
    -Ascites
    -HE
    -Portal HTN+ oesophageal varices
    -Caput medusae
    -Spider nave
    -Palmar erythema
    -clubbing
    -fetor hepaticus
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31
Q

What is the diagnosis of chronic liver failure?

A

Liver biopsy - GS - needed to determine extend of CLD (fibrosis vs cirrhosis)
-LFT,Imaging,USS, ascitic tap culture

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32
Q

What is the treatment of chronic liver disease?

A

-Prevent progression - lifestyle modifying (low alcohol, low BMI, avoid drugs)
-Consider liver transplant (if decompensated liver)
-Manage complications
HE- lactulose
Ascites- diuretics
Oesophageal varices rupture

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33
Q

What is alcoholic liver disease?

A

Liver disease caused by excessive alcohol intake - most common cause of liver failure

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34
Q

What are the risk factors of alcoholic liver disease?

A

-chronic alcohol
-obesity
-smoking

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35
Q

What is the pathology of alcoholic liver disease?

A

Steatosis (fatty liver, undamaged) -> alcoholic hepatitis (with mallory bodies) -> Alcoholic cirrhosis (micro nodular)

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36
Q

What is the presentation of alcoholic liver disease?

A

-Early stages may show very little symptoms/ signs
-Later more severe stages = chronic liver failure Sx + alcohol dependency
- Jaundice, hepatomegaly, palmar erythema, Dupuytren contracture , ascites, HE, spider naevi, caput medusae, easy bruising

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37
Q

What does an alcohol dependency questionnaire include ?

A

CAGE and audit
- 10 questions alcohol use disorder test
-2 or more = dependent

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38
Q

What is the diagnosis of alcoholic liver disease?

A

Bloods - LFT= high bilirubin, low albumin, high PT, high GGT(AST:ALT >2)
-FBC = macrocytic non megaloblastic anemia
Biopsy needed confirm extent of cirrhosis
- inflammation, necrosis, mallory cytoplasmic inclusion bodies

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39
Q

What is the conservative treatment of alcoholic liver disease?

A

Conservative = stop alcohol - give diazepam for delirium tremors + with drawl Sx

-healthy diet, low BMI

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40
Q

What are the withdrawal Sx of alcohol?

A

Tremors
Agitation
ataxia
Disorientation

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41
Q

What is the pharmacological treatment for alcoholic liver disease?

A

Steroids short term
B1 + folate supplements
Maddrey’s discriminant - severity of ALD + treatment requirements

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42
Q

What is the surgical treatment for ALD?

A

Liver transplant for ESLF cases- abstain for 3+ months from alcohol before consideration

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43
Q

What are the complications and treatments for ALD?

A

Pancreatitis = IgE smashed
HE - lactulose
Ascites- diuretics
HCC- chemo/surgery
Mallory weiss tear
Wernicke Korsakoff syndrome

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44
Q

What is Wernicke Korsakoff syndrome?

A

Combined B1 deficiency (alcohol causes B1 deficiency ) and alcohol withdrawal Sx - ataxia, nystagmus, encephalopathy

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45
Q

What is the treatment for wernicke Korsakoff syndrome?

A

IV Thiamine

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46
Q

What is non alcoholic liver disease?

A

Chronic liver disease not due to alcoholism, results from fat deposition

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47
Q

What are the risk factors of NAFLD?

A

obesity
HTN
Hyperlipidemia
T2DM
FHx
Endocrine disorders
Drugs - NSAIDs/amiodarone

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48
Q

What is the pathology of NAFLD?

A

Hepatosteatosis (NAFLD) -> non alcoholic steatohepatitis -> fibrosis -> cirrhosis

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49
Q

What is the presentation of NAFLD?

A

typically aSx; any findings are incidental initially
- if very severe present with signs of liver failure

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50
Q

What is the diagnosis of NAFLD?

A

Bloods -deranged LFTs
(high PT/INR, low albumin, high bilirubin)
FBC - thrombocytopenia, hyperglycaemia
Imaging- 1st line for suspected NAFLD = USS abdomen
Assess risk of fibrosis with non invasive scoring system therefore avoid invasive biopsy

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51
Q

What is the treatment for NAFLD?

A

Lose weight (low BMI) and control risk factors :
-statins
-metformin
-ACEi
VITAMIN E - improves steatotic/ fibrotic liver appearance

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52
Q

What are the complications of NAFLD?

A
  • HE
    -Ascites
    -Portal HTN
    -Oesophageal varices
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53
Q

What is viral hepatitis?

A

Inflammation of the liver as a result of viral replication within the hepatocytes

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54
Q

What is hepatitis A?

A

-Acute, mild, positive strand RNA
-Faeco-oral spread
-Picornavirus
-associated with travel, endemic in Africa
-notifiable disease

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55
Q

What are the risk factors of HEP A?

A
  • overcrowding
    -poor saturation
    -shellfish
    -travel
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56
Q

What is the pathology of HepA?

A

incubation for 2 week - replicated in liver and excreted in bile
- then self limiting within 6 weeks

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57
Q

What is the presentation of hep A?

A
  • prodomal phase (1-2weeks)- malaise, n+v, fever
    -Then jaundice, dark urine, pale stools, hepatosplenomegaly
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58
Q

What is the diagnosis of hep A?

A

Bloods = raised ESR + leukopenia
LFT= raised bilirubin when icteric
HAV serology = HAV IgM = acutely infected

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59
Q

What is the treatment for HepA?

A

Supportive - travellers vaccine available

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60
Q

What is a complication of hep A?

A

Fulminant liver failure

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61
Q

What is HEP E?

A

-Acute, ssRNA
-faecal-oral spread
-calcivirus

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62
Q

What is the epidemiology of HEP E?

A
  • commoner than HAV in UK
  • associated with undercooked pork
    -common in inso-china
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63
Q

what is the presentation of of hep E?

A

usually aSx
Self limiting

64
Q

What are the complications of HEP E?

A
  • can cause chronic disease in immunosuppressed
    -can cause fulminant liver failure
    -normal mortality 1-2%
    -in pregnant ladies 10-20%
65
Q

What is the diagnosis of HEPE?

A

HEV IgM- acutely infected

66
Q

What is the treatment for hep E?

A

supportive
self limiting
vaccine only in china

67
Q

What is HEP D?

A

Acute + chronic , SSRNA
Blood Bourne - sex/IVDU

68
Q

What is the pathology of hep D?

A

unable to replicate on its own, requires HBV for assembly
- manifests as a co-infection

69
Q

What is the diagnosis of hep D?

A

serology = IgM HDV +IgM HBV

70
Q

What is the treatment for Hep D?

A

Same as Hep B

71
Q

What is Hep B?

A

-Acute + chronic
-dsDNA
-bloodbourne
-hepadnavirus

72
Q

What is the epidemiology of Hep B?

A

-presents worldwide

73
Q

what is the transmission of Hep b?

A

needles
sexual
vertical - mother to child
horizontal - between children

HBV found in semen and saliva

74
Q

What are the risk factors for hep B?

A

IVDU
MSM
Dialysis patients
Healthcare workers

75
Q

What is the presentation of hep B?

A

1-2 week prodome
- jaundice, dark urine , pale stools, hepatosplenomegaly , urticaria, arthralgia
-incubation 1-6months

76
Q

What is the diagnosis of hep B?

A

serology = HBV DNA - direct count of viral blood
- HBVsAg = present for 1-6 months of infection
-HBsAB= present after 6 months -denotes immunity
HBcAg= exposed to hep B at some point
HBcIgM = acute infection
HBCIgG = chronic infection/carrier
HBeAg = marker of patient infectiousness - acutely infected
HBeAb= in all ironically affected patients or if they have cleared
AntiHBsAg = cleared/ vaccine

77
Q

What are the complications of hep B?

A
  • 5-10% cases will progress to chronic liver failure +HCC risk

-90% cases in children become chronic decompensated = poor prognosis and need a transplant

78
Q

What is the treatment for Hep B?

A

SC Pegylated interferon alpha 2a -stimulates immune response
Antiviral treatment - tenofovir

79
Q

What is HEP C?

A
  • acute + chronic
    -ssRNA
    Blood bourne -IVDU
  • flavivirus
80
Q

What are the risk factors of hep c?

A
  • association with IVDU limited vertical + sexual transmission
81
Q

What is the presentation of hep C?

A

often acutely aSX
- can be influenza like symptoms
- present later with chronic liver signs + hepatosplenomegaly

82
Q

What is the diagnosis of hep C?

A

Serology:
HCVRNA =current infection
HCVAB =presents within 4-6 weeks of infection

83
Q

What is the treatment for hep C?

A

Direct acting antivirals (DAA)
- oral ribavirin + NS5A/B inhibitors - needed for viral replication

84
Q

What is the complication with Hep c?

A

30% cases progress to chronic liver failure - cirrhosis + HCC risk

85
Q

What is autoimmune hepatitis ?

A
  • aka lupus hepatitis
    -rare
    -causes lupus like rash
    -adaptive immunity mounts autoimmune response vs hepatocytes
86
Q

What are the risk factors of autoimmune hepatitis?

A
  • females
    -other autoimmune diseases
    -viral hepatitis
    -HLADR3/4
87
Q

What is type 1 autoimmune hepatitis?

A

Type 1= Adult females 80% cases :
- ANA (anti nuclear antibody - found in other autoimmune diseases)
-ASMA( anti smooth muscle Ab)

88
Q

What is type 2 autoimmune hepatitis?

A

Type 2 =young females - rare
-ALC-1 (anti liver cytosol)
-ALKM-1 (anti liver-kidney microsomal)

89
Q

What is the presentation of autoimmune hepatitis?

A

-25
-aSx
-many = jaundice, fever, hepatosplenomegaly

90
Q

What is the diagnosis of autoimmune hepatitis?

A

Serology (ANA,ASMA +/- ALC-1/ALKM-1)

91
Q

What is the treatment for autoimmune hepatitis?

A

Corticosteroids (prednisolone) + azathioprine
-Hep A/B vaccination
- transplant = last resort

92
Q

What is jaundice?

A

AKA icterus - yellowing of skin, eyes due to accumulation of conj/unconj bilirubin. Sign of liver dysfunction.

93
Q

What are the causes of jaundice?

A

Pre hepatic
Intrahepatic
Post hepatic

94
Q

what is pre hepatic jaundice?

A
  • unconjugated hyperbilirubinemia due to increase in RBC breakdown;

Haemolytic anemias:
-sickle cell
-G6PDH def
-Autoimmune haemolytic anemia
-Thalassemia
-MAlaria

95
Q

What is intra hepatic jaundice?

A

conjugated/ unconjugated hyperbilirubinemia, may be mixed
Parenchymal disease( failure of hepatocytes to take up metabolise or excrete bilirubin):
-HCC
-ALD/NAFLD
-Hepatitis
-Hepatotoxic drugs
-Gilbert syndrome
-crigler nijjar syndrome

96
Q

What is Gilbert syndrome?

A

-Auto recessive mutation of UGT1A1 gene; low UGT enzyme therefore low conj billirubin and high unconj so sometimes classed as pre hepatic
Typical patient = young male with painless jaundice, sudden onset
-Okay without treatment

97
Q

What is crippler nijjar syndrome?

A

Auto recessive absence of UGT, more rare than Gilberts
More severe - Jaundice with N+V
Can die from kernicterus - accumulation of bilirubin in basal ganglia causing neurological deficits
Tx= phototherapy - breaks down unconj bilirubin

98
Q

What is post hepatic jaundice?

A

Conjugated hyperbilirubinemia due to biliary obstruction :
Biliary tree pathology:
-Choledocholithiasis (stone stuck in cBD)
-pancraetic cancer
-cholangiocarcinoma
-PBC/PSC

Pale stool + dark urine

99
Q

Why is there pale stools and dark urine in obstructive?

A

As conjugated bilirubin affects stool and urine
- conj -hyperbilirubinamia high in blood and low in intestine therefore less effect on stool -stercobilin
pee - urobilin

100
Q

What is Courvoisier sign?

A

painless jaundice + palpable gall bladder
- most likely in pancreatic cancer

101
Q

What is charcot’s triad?

A

Fever
RUQ pain
Jaundice

102
Q

What is Reynold pentad?

A

present in ascending cholangitis
-Fever, RUQ pain, Jaundice, confusion , hypotension

103
Q

What is Murphy signs?

A

RUQ tenderness, ask patient to take a breath in while pressing on RUQ; will see them whince - cholecystitis

104
Q

What is the diagnosis for jaundice?

A

Imaging USS - 1st line
Bloods + LFTs = bilirubin, albumin, PT/INR,AST,ALT,GGT,ALP

Urine bilirubin =normally negative , positive (dark urine)in obstruction /hepatic disease

Urine urobillinogen = normally positive - high in haemolysis/pre, low in intra/post hepatic

105
Q

What is pancreatic cancer?

A

Adenocarcinoma of exocrine pancreas of ductal origin typically affecting head

106
Q

What is the epidemiology of pancreatic cancer?

A
  • males, 60+
    -head -60%
    -body-25%
    -tail -15%
107
Q

What are the risk factors of pancreatic cancer?

A

smoking
alcohol
DM
FHx
Chronic pancreatitis
Genetic predisposition - PRSS-1 gene mutation

108
Q

What is the pathology of pancreatic cancer?

A

Head= courvoiser sign (painless jaundice, palpable GB) with pale stool and dark urine

Body +tail. =epigastric pain radiating to back, relieved by sitting forward

May show trousseau sign of malignancy - episodes of vessel inflammation + clots in parts of body

109
Q

What is the diagnosis of pancreatic cancer?

A

suspected pancreatic cancer = pancreatic CT - GS/diagnostic
1st line abdo USS
CA19-9 tumour marker positive = monitor disease progression

110
Q

What is the treatment of pancreas cancer?

A

-poor prognosis - 5y survival - 3%
- surgery+post op chemo if no mets
-otherwise palliative

111
Q

What are the types of liver cancers?

A

primary - least common. :
- hepatocellular carcinoma
-cholangiocarcinoma
-benign

Secondary - most common:
-GIT, breast, bronchial

112
Q

What is hepatocellular carcinoma?

A
  • arise from liver parenchyma
    -90% all primary liver cancers
    -males
113
Q

What are the risk factors of hepatocellular carcinoma ?

A

-chronic hepatitis virus c+b
-cirrhosis from ALD/NAFLD/haemochromatosis

114
Q

What is the pathology of HCC?

A
  • metastases to lymph nodes, bones, lungs via haematogenous spread (hepatic/portal vein)
115
Q

What is the presentation of HCC?

A
  • signs of decompensated liver failure. - jaundice, ascites, HE and cancer signs - weight loss, fatigue
    -irregular hepatomegaly
116
Q

What is the diagnosis of liver HCC?

A

may show high serum AFP
Imaging. = 1st line USS
GS CT
biopsy avoided prevent seeding of tumour

117
Q

What is the treatment of HCC?

A

surgical resection of tumour
When develop cirrhosis/ decompensated = liver transplant
Prevention - HBV vaccination

118
Q

What is cholangiocarcinoma?

A

arises from biliary tree, typically adenocarcinomas
- 10% of all liver cancers

119
Q

What are the risk factors of cholangiocarcinoma?

A

parasitic fluke worms , biliary cysts, IBD, PSC

120
Q

What is the presentation of cholangiocarcinoma?

A
  • abdopain , jaundice , weight loss, pruritus, fevers, may be courvoiser sign
    Late constellation of Sx as slow growing tumour
121
Q

What is the diagnosis of cholangiocarcinoma?

A

1st line imaging - abdo USS +CT
GS = ERCP (imaging of biliary tree) - obtain sample for biopsy/ diagnostic
can also stent strictures present in biliary tree
-High CEa/ high CA19-9
-LFT = high bilirubin, high ALP

122
Q

What is the treatment for cholangiocarcinoma?

A

Majority of cases unrepairable as patients present very late

123
Q

What are primary benign liver tumours?

A

Haemangioma (mc seen in infants as ‘strawberry mark on skin”
Hepatic adenoma

124
Q

What are the secondary liver tumours?

A
  • more common than primary tumours
  • from GIT,Lungs, breast so Px variable depending on site of primary tumour
125
Q

What is the diagnosis of secondary tumour ?

A

High serum ALP
Imaging - 1st line USS
GS CT/MRI for staging and primary tumour

126
Q

What is the treatment of secondary lung tumours?

A

surgical resection if possible , chemo

127
Q

What are the biliary tract diseases?

A
  • gallstones
    -cholecystitis
    -ascending cholangitis
128
Q

What are the risk factors of biliary tract disease?

A

fat, female, forty, fertile , FHx,, T2DM, NAFLD

129
Q

What are gallstones?

A

stones made from supersaturation of bile made of cholesterol, pigment or both

130
Q

What is the presentation of gallstones?

A

-RUQ ‘biliary colic’(constant severe episodes of pain 30+ minutes)
-worse after a fatty meal

131
Q

What is the diagnosis of gall stones?

A

1st line - Abdo USS - iD gallstones

132
Q

What is the treatment for gall stones?

A
  • elective laparoscopic cholecystectomy if symptomatic
  • until then - NSAIDs/ IM diclofenac
    -lifestyle change , reduce fats
133
Q

What is cholecystitis?

A

inflammation of the gall bladder

134
Q

What is the presentation of cholecystitis?

A

-RUQ pain + fever , tender gall bladder
- may have referred pain to tip of right shoulder ; phrenic
-murphy sign positive ; press on GB and ask patient to inhale = whince

135
Q

What is the diagnosis of cholecystitis?

A

FBC - leukocytosis + neutophilia
LFT- normal
Abdo USS shows thickened GB wall >3mm

136
Q

What is the treatment for cholecystitis?

A
  • surgery within one week - typically done within 72hr
    -laproscopic cholecystectomy

Until then = IV fluid, analgesia, Abx if needed

137
Q

What is ascending cholangitis?

A

Inflammation of the bile duct system - bile isn’t flushing out due to blockage so bacteria can climb up the ducts

138
Q

What is the presentation of ascending cholangitis?

A

RUQ pain ,Fever, jaundice - charcot’s triad
- dark urine + pale stool
Reynolds pentad - confusion , altered mental state , hypotension

139
Q

What is the diagnosis of ascending cholangitis?

A

FBC - leukocytosis + neutrophilia
LFT = high conjugated hyperbilirubinemia
Abdo USS - 1st line= CBD dilation +gall stones
MRCP - GS= diagnostic and best pre intervention management

140
Q

What is the treatment fir ascending cholangitis?

A

ERCP (bile duct clearance) then laparoscopic cholecystectomy once stable
- consider risk of sepsis - biliary obstruction , E.coli from intestines can climb up through AOV and colonise biliary tree

141
Q

What is MRCP?

A

magnetic resonance cholangio pancreatography

142
Q

What is ERCP?

A

Endoscopic retrograde cholangio - pancreatography

143
Q

What is Primary biliary Cholangitis/ Cirrhosis? (PBC)

A

Intrahepatic autoimmune jaundice affecting interlobular bile ducts
Women , typical autoimmune

144
Q

What are the risk factors of PBC?

A

Female
40-50 year old
Other autoimmune disease -SLE, Sjorgens
Smoking
- more common than PSC

145
Q

What is the pathology of PBC?

A

Autoantibodies cause interlobular bile duct damage ; chronic autoimmune granulomatosis inflammation
Resulting in cholestasis -> fibrosis, cirrhosis, portal HTN, infection

146
Q

What is the presentation of PBC?

A

initially often aSx, routine test shows high AMA (anti mitochondrial Ab’s)
- pruritus + fatigue earliest , then jaundice , then hepatomegaly, Xanthelasma

147
Q

What is the diagnosis of PBC?

A

USS - 1st line to exclude extrahepatic cholestasis
LFT = high ALP, high Conj bile, low albumin
Serology = AMA
Liver biopsy - granulomatosis/ portal tract infiltrate, portal tract fibrosis

148
Q

What is the treatment for PBC?

A

1st line - improves Sx- ursdeoxycholic acid lifelong (bile acid analogue, dampens immune response and decreases cholestasis)

For pruritus - colestyramine

Vit ADEK supplements

149
Q

What are the complications of PBC?

A

cirrhosis, malabs of fats +ADEK therefore stearrhoea , osteomalacia , coagulopathy

150
Q

What is pruritus?

A

excess conj bilirubin excess concentration so can leak out + cause skin to itch

151
Q

What is Primary sclerosing cholangitis? (PSC)

A

Autoimmune destruction of intra and extra lobular hepatic duct
- men (atypical)

152
Q

What are the risk factors of PSC?

A

male, 40-50, strong link to IBD (UC)

153
Q

What is the pathology of PSC?

A

Same as PBC but affects more ducts..
Autoantibodies cause extra/ interlobular hepatic duct damage ; chronic autoimmune granulomatosis inflammation
Resulting in cholestasis -> fibrosis, cirrhosis, portal HTN, infection

154
Q

What is the presentation of PSC?

A

initially aSx, then pruritus, fatigue, jaundice , Charcot triad (if CBD involved ), hepatosplenomegaly , IBD

155
Q

What is the diagnosis of PSC?

A

LFT
Serology : AMA neg - coeliac neg
pANCA positive
GS imaging - MRCP

156
Q

What is the treatment for PSC?

A

Conservative Sx management
- Colestyramine for pruritis
-Fat soluble ADEK
-consider liver transplant

Phase 2a (9 decks)

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