Chronic Liver Disease Flashcards
(159 cards)
1
Q
What are three infectious causes of chronic hepatitis listed on page 4?
A
HBV (Hepatitis B Virus), HCV (Hepatitis C Virus), HDV (Hepatitis D Virus)
2
Q
According to the chart on page 4, what are two types of autoimmune chronic hepatitis?
A
Type 1 and Type 2
3
Q
Page 4 lists Alcohol as a common example of what category of causes for chronic hepatitis?
A
Drugs & Toxins
4
Q
Name two inherited metabolic causes of chronic hepatitis from the chart on page 4.
A
Hemochromatosis, Wilson disease, Alpha 1 antitrypsin deficiency (Any two)
5
Q
What is an example of an acquired metabolic cause of chronic hepatitis shown on page 4?
A
Non-alcoholic fatty liver disease (NAFLD)
6
Q
In the diagram on page 6 comparing acute and chronic hepatitis, what is a key feature of the portal tract in CHRONIC hepatitis?
A
Dense mononuclear infiltrate (also: Portal fibrosis, Interface hepatitis, Ductular reaction)
7
Q
What type of necrosis is depicted as characteristic of CHRONIC hepatitis in the diagram on page 6?
A
Bridging necrosis
8
Q
According to the page 6 diagram, ‘Ground-glass cells’ are a morphological feature associated with which type of viral hepatitis in its chronic form?
A
Hepatitis B
9
Q
The diagram on page 6 indicates ‘Fatty change’ as a morphological feature in chronic hepatitis associated with which virus?
A
Hepatitis C
10
Q
What are two forms of cell death or their sequelae visible in the CHRONIC hepatitis diagram on page 6?
A
Apoptosis, Macrophage aggregate (indicating necrosis)
11
Q
In the liver acinus model shown on page 8, which zone is closest to the portal triad (PV, HA, BD)?
A
Zone 1
12
Q
According to the liver acinus diagram on page 8, which zone is closest to the central vein (CV)?
A
Zone 3
13
Q
What is another term for ‘interface hepatitis’ as indicated on page 8 and 9?
A
Piecemeal necrosis
14
Q
Page 8 illustrates that interface hepatitis describes inflammation occurring at the junction of what two liver structures?
A
Portal tract and hepatic parenchyma (lobule)
15
Q
What three structures typically form a portal triad, as labeled on page 8?
A
Portal Vein (PV), Hepatic Artery (HA), Bile Duct (BD)
16
Q
According to the ‘Double Hit theory’ for NAFLD pathogenesis shown on page 20, what is considered the first ‘hit’?
A
Insulin resistance
17
Q
In the NAFLD ‘Double Hit theory’ on page 20, what does insulin resistance primarily lead to?
A
Hepatic steatosis (which then leads to inflammation and hepatocyte apoptosis)
18
Q
What is the second ‘hit’ in the ‘Double Hit theory’ for NAFLD pathogenesis as per the diagram on page 20?
A
Hepatocellular oxidative injury
19
Q
According to the diagram on page 20, what is the direct consequence of hepatocellular oxidative injury in NAFLD?
A
Lipid peroxidation of hepatocyte membranes (leading to liver cell necrosis)
20
Q
What are the two main damaging outcomes for hepatocytes resulting from the ‘Double Hit theory’ in NAFLD as shown on page 20?
A
Hepatocyte apoptosis (from first hit) and Liver cell necrosis (from second hit)
21
Q
The detailed NAFLD pathogenesis diagram on page 21 shows that increased fat supply, decreased fat export (VLDL), decreased FFA β-oxidation, and increased de novo lipogenesis all contribute to what condition?
A
Hepatic steatosis
22
Q
According to the diagram on page 21, what role do cytokines like TNF-α and IL-6 play in NAFLD pathogenesis?
A
They contribute to inflammation and can exacerbate insulin resistance.
23
Q
In NAFLD pathogenesis (page 21), what does ‘Lipotoxicity / Inflammation’ lead to?
A
Hepatic steatohepatitis
24
Q
As shown on page 21, activation of which two cell types follows hepatocyte apoptosis/necrosis in NAFLD, driving inflammation and fibrosis?
A
Kupffer cells and Hepatic stellate cells
25
What is the ultimate stage depicted in the NAFLD pathogenesis diagram on page 21, following inflammation and fibrosis?
Cirrhosis
26
The chart on page 24 (NAFLD: MICROSCOPY) states that steatosis involves fat deposition in what percentage of hepatocytes?
5-90% of hepatocytes
27
In steatohepatitis (NASH), what type of inflammatory cell is mainly seen in parenchymal inflammation, according to page 24?
Mainly neutrophils
28
What are two forms of hepatocyte death mentioned in the microscopy of steatohepatitis (NASH) on page 24?
Ballooning degeneration and apoptosis
29
What are Mallory bodies, a feature of steatohepatitis (NASH) described on page 24?
Eosinophilic degenerated material (within hepatocytes)
30
What type of fibrosis is mentioned in the microscopic features of NAFLD/NASH on page 24?
Sinusoidal fibrosis +/-
31
According to the chart on page 33, what is the primary defect in genetic (primary) hemochromatosis that leads to excessive iron absorption?
Decreased hepcidin synthesis
32
The HFE gene mutation, commonly implicated in primary hemochromatosis (page 33), is located on which chromosome?
Chromosome 6 (at 6p21.3)
33
In primary/genetic hemochromatosis, where is iron predominantly deposited initially, as per page 33?
Hepatocytes
34
List two causes of secondary/acquired hemochromatosis from the chart on page 33.
Blood transfusion dependent diseases, Ineffective erythropoiesis (e.g., Thalassaemia), Excess dietary iron, Chronic liver disease (e.g., alcohol) (Any two)
35
In secondary/acquired hemochromatosis, where is iron often deposited initially before involving hepatocytes, according to page 33?
Kupffer cells
36
The pathogenesis diagram for primary hemochromatosis on page 36 shows that decreased hepcidin leads to increased activity of which iron export protein?
Ferroportin
37
According to the diagram on page 36, increased iron absorption from the intestine in primary hemochromatosis leads to iron overload in which organs?
Liver, Heart, Pancreas, Skin, Brain (Any three mentioned)
38
The diagram on page 36 illustrates that genetic defects (like HFE mutation) in primary hemochromatosis cause a reduction in which key iron-regulating hormone?
Hepcidin
39
In primary hemochromatosis pathogenesis (page 36), increased ferroportin activity occurs on which two cell types, leading to increased iron release into circulation?
Enterocytes (intestinal absorptive cells) and Macrophages
40
Name three organs, besides the liver, commonly affected by iron deposition in primary hemochromatosis as shown on the diagram on page 36.
Heart, Pancreas, Skin, Brain, Endocrine organs (Any three)
41
The hemochromatosis pathogenesis diagram on page 38 shows that increased absorption of dietary iron leads to its deposition in which zone of hepatocytes?
Periportal (zone 1) hepatocytes
42
According to page 38, what are three pathological pathways triggered by iron deposition in hepatocytes in hemochromatosis?
Direct toxicity, ROS Generation (leading to lipid peroxidation), DNA damage
43
How does ROS (Reactive Oxygen Species) generation contribute to liver damage in hemochromatosis, as per page 38?
It causes lipid peroxidation, leading to hepatocyte necrosis.
44
Activation of which cells contributes to fibrosis in hemochromatosis following hepatocyte necrosis, according to the diagram on page 38?
Stellate cells
45
Besides cirrhosis, what other major liver complication can arise directly from the DNA damage pathway in hemochromatosis, as shown on page 38?
Hepatocellular carcinoma
46
The chart on page 40 (Primary/Genetic Haemochromatosis Clinical effects) states that iron accumulation in the liver leads to what condition?
Cirrhosis
47
According to page 40, iron accumulation in the pancreas in hemochromatosis results in what clinical condition?
Diabetes Mellitus
48
What is the characteristic skin change seen in hemochromatosis due to iron accumulation, as per page 40?
Hyperpigmentation
49
How can iron accumulation affect the heart in hemochromatosis, according to the chart on page 40?
Arrhythmias (or cardiomyopathy)
50
What is a common endocrine manifestation of hemochromatosis listed on page 40?
Hypogonadism
51
What is the mode of inheritance for Wilson Disease, as stated on page 46?
Autosomal recessive
52
The mutation causing Wilson Disease is in the ATP7B gene. According to page 46, what is the function of the protein encoded by this gene?
It is a copper-transporting ATPase in the hepatocyte bile canalicular membrane (essential for copper excretion into bile).
53
As per page 46, the ATP7B gene mutation in Wilson Disease results in what two primary defects in copper metabolism?
Impaired copper excretion into bile AND Failure to incorporate copper into ceruloplasmin
54
How is copper normally transported in the blood, according to the information on page 46?
Combined with ceruloplasmin
55
What is the approximate normal total body copper content mentioned on page 46?
Approximately 50-150mg
56
The pathogenesis diagram for Wilson Disease on page 47 shows that low excretion of copper into bile directly leads to what?
Accumulation of Cu in liver
57
According to the diagram on page 47, failure to incorporate copper into ceruloplasmin contributes to what state, which then causes hepatotoxicity?
High serum copper level (referring to non-ceruloplasmin bound copper)
58
In Wilson Disease, accumulation of copper in the liver leads to what primary pathological effect, as per page 47?
Hepatotoxicity
59
The diagram on page 47 indicates two main inputs leading to hepatotoxicity in Wilson's disease. What are they?
Accumulation of Cu in liver AND High serum copper level
60
The inability to excrete copper into bile is a key step in the pathogenesis of which inherited metabolic liver disease discussed on page 47?
Wilson Disease
61
According to the chart on page 53, what are the main effects of copper accumulation in the liver in Wilson Disease?
Chronic liver disease, cirrhosis
62
Name two neurological manifestations of copper accumulation in the brain in Wilson Disease, as listed on page 53.
Tremor, chorea, psychosis (Any two)
63
What are Kayser-Fleischer rings, a clinical sign in Wilson Disease mentioned on page 53?
Copper deposition in Descemet's membrane of the cornea
64
How can copper accumulation affect the blood in Wilson Disease, according to page 53?
It can cause haemolytic anaemia.
65
Copper accumulation in which three primary sites leads to the main clinical effects of Wilson's Disease as per page 53?
Liver, Brain, Eye
66
The detailed diagram of Wilson's Disease clinical effects on page 55 shows involvement beyond Liver/Brain/Eye. Name two other systems/organs that can be affected.
Renal system, Cardiac system, Bones (Any two)
67
List two specific CNS manifestations of Wilson's Disease shown in the diagram on page 55, beyond general tremor/chorea.
Deterioration in school performance, Behavioural Changes, Dystonia, Incoordination, Dysarthria, Dysphagia (Any two)
68
According to the diagram on page 55, how can Wilson's Disease affect the renal system?
Proximal renal tubular dysfunction, Aminoaciduria
69
What is a potential cardiac manifestation of Wilson's Disease shown on page 55?
Cardiomyopathy
70
What is a potential skeletal (bone) manifestation of Wilson's Disease mentioned in the diagram on page 55?
Arthritis, Rickets
71
According to the chart on page 56, what is considered the most specific *screening* test for Wilson Disease?
Increased urinary copper (Urinary Cu ↑)
72
What is the typical finding for serum ceruloplasmin levels in Wilson Disease, as per page 56?
Decreased serum ceruloplasmin (Serum Ceruloplasmin ↓)
73
Name one special stain mentioned on page 56 used to demonstrate copper in a liver biopsy for Wilson Disease.
Rubeonic acid stain OR Rhodanine stain
74
What is considered the most sensitive and accurate test for diagnosing Wilson Disease, according to page 56?
Increased hepatic copper content (Hepatic Cu content ↑) from a liver biopsy
75
A liver biopsy in Wilson Disease is used for demonstrating copper and also for what quantitative measurement (page 56)?
Measuring hepatic copper content
76
What are two defining characteristics of Autoimmune Hepatitis (AIH) that align it with autoimmune diseases, as per page 58?
Genetic predisposition AND Presence of autoantibodies (OR Association with other autoimmune diseases OR Therapeutic response to immunosuppression)
77
What type of therapeutic response is characteristic of AIH, according to page 58?
Therapeutic response to immunosuppression
78
The presence of what serological markers is a key feature of AIH, as stated on page 58?
Autoantibodies
79
Is AIH typically an acute or chronic condition, based on the description on page 58?
Chronic, progressive
80
Name two autoimmune diseases listed on page 59 that can be associated with Autoimmune Hepatitis (AIH).
Coeliac disease, Systemic lupus erythematosus, Rheumatoid arthritis, Thyroiditis, Sjögren syndrome, Ulcerative colitis (Any two)
81
Which inflammatory bowel disease is commonly associated with Autoimmune Hepatitis (AIH), according to page 59?
Ulcerative colitis
82
Sjögren syndrome, an autoimmune condition affecting glands, can be associated with which type of hepatitis (page 59)?
Autoimmune Hepatitis (AIH)
83
Can thyroiditis be associated with Autoimmune Hepatitis (AIH), as per the list on page 59?
Yes
84
Rheumatoid arthritis is an autoimmune joint disease that can be associated with which liver condition, according to page 59?
Autoimmune Hepatitis (AIH)
85
List two potential triggers for Autoimmune Hepatitis (AIH) pathogenesis, according to the diagram on page 60.
Genetic predisposition, Viral infections, Drugs, Herbal products (Any two)
86
What type of immune cells are central to the pathogenesis of Autoimmune Hepatitis (AIH), as shown on page 60?
T cells (specifically CD4+ and CD8+ T cells)
87
According to the diagram on page 60, how do CD4+ T cells contribute to hepatocyte damage in AIH?
They release IFNγ (Interferon-gamma), which leads to hepatocyte damage.
88
What is the mechanism by which CD8+ T cells cause hepatocyte damage in AIH, as depicted on page 60?
Direct cytotoxicity
89
The pathogenesis of AIH (page 60) involves an immune response primarily mediated by which arm of the adaptive immune system?
T Cell mediated immunity
90
What are the two main clinical presentations (courses) of Autoimmune Hepatitis (AIH), as per page 61?
Indolent course OR Severe form (e.g., fulminant hepatitis, submassive or massive liver cell necrosis)
91
Which demographic group is most commonly affected by Autoimmune Hepatitis (AIH), according to page 61?
Females, particularly young and perimenopausal women (78% of cases)
92
In the clinical diagnosis of AIH (page 61), what is the expected finding for serologic markers of viral infection?
Absent
93
What is a characteristic finding regarding serum IgG and γ-globulin levels in AIH, as stated on page 61?
Elevated (typically 1.2 to 3.0 times normal)
94
What is expected for serum autoantibody titers in AIH, according to the clinical diagnosis criteria on page 61?
High
95
Which type of Autoimmune Hepatitis (AIH) is more common and typically affects middle-aged women, as per page 62?
Type 1 AIH
96
What are the characteristic autoantibodies found in Type 1 AIH, according to the chart on page 62?
Antinuclear antibodies (ANA) and Anti-smooth muscle antibodies (ASMA)
97
Which demographic group is most commonly affected by Type 2 AIH, as stated on page 62?
Children
98
What are the characteristic autoantibodies found in Type 2 AIH, according to page 62?
Anti-liver kidney microsome-1 (ALKM-1) antibodies and Anti-liver cytosol-1 (ACL-1) antibodies
99
The presence of Anti-smooth muscle antibodies (ASMA) is associated with which type of Autoimmune Hepatitis (page 62)?
Type 1 AIH
100
What is a characteristic microscopic feature of AIH regarding the location and extent of inflammation, as per page 63?
Extensive inflammation and hepatocellular injury at the interface (portal-parenchymal junction) as well as within the hepatic parenchyma.
101
The presence of numerous clusters of which inflammatory cell type is typical in the microscopy of AIH (page 63)?
Plasma cells
102
What is emperipolesis, a feature sometimes seen in AIH microscopy, as mentioned on page 63?
The presence of one cell (e.g., lymphocyte) within the cytoplasm of another cell (e.g., hepatocyte) without phagocytosis.
103
What types of necrosis can be observed in the microscopy of AIH, according to page 63?
Confluent, panacinar, or bridging necrosis
104
What is a common finding regarding the portal-parenchymal junction in AIH microscopy, as per page 63?
Interface hepatitis
105
What is Budd-Chiari Disease, as defined on page 68?
Obstruction of two or more major hepatic veins.
106
What are three classic symptoms/signs of Budd-Chiari Disease listed on page 68?
Liver enlargement, pain, and ascites.
107
Name two conditions associated with thrombosis leading to Budd-Chiari Disease, from the list on page 68.
Myeloproliferative Disease, Thrombophlebitis migrans, Pregnancy, Use of Oral Contraceptive Pills, Hepatocellular carcinoma (Any two)
108
Can pregnancy be a risk factor for Budd-Chiari Disease, according to page 68?
Yes
109
What type of medication is mentioned on page 68 as a risk factor for thrombosis in Budd-Chiari Disease?
Oral Contraceptive Pills (OCP)
110
What is the typical gross appearance of the liver in Budd-Chiari Disease regarding color and size, as per page 69?
Swollen and red-purple
111
How is the liver capsule often described in Budd-Chiari Disease on gross examination (page 69)?
Tense
112
What contrasting areas can be seen on the cut surface of the liver in Budd-Chiari Disease macroscopically, according to page 69?
Areas of haemorrhagic collapse and areas of preserved/regenerating parenchyma
113
The macroscopic image on page 69 of a swollen, red-purple liver with a tense capsule is characteristic of what vascular liver disorder?
Budd-Chiari Disease
114
In Budd-Chiari Disease, severe congestion primarily affects which part of the liver lobule, as per the diagram on page 70?
Centrilobular region (around the central vein)
115
What is the immediate consequence of severe centrilobular congestion in Budd-Chiari Disease, according to page 70?
Necrosis (of hepatocytes in the centrilobular zone)
116
If Budd-Chiari Disease becomes chronic, what type of fibrosis develops as a result of centrilobular necrosis (page 70)?
Centrilobular fibrosis
117
What is the suspected cause of Primary Biliary Cholangitis (PBC), according to page 73?
Autoimmune
118
What is the typical gender predominance in Primary Biliary Cholangitis (PBC), as stated on page 73?
Female to male ratio is 6:1
119
Which autoantibody is most characteristically associated with Primary Biliary Cholangitis (PBC), according to page 73?
Antimitochondrial antibodies (AMA)
120
Name one other autoimmune disease commonly associated with Primary Biliary Cholangitis (PBC), from page 73.
Sjögren syndrome or Hashimoto thyroiditis
121
What is the key laboratory finding for diagnosing Primary Biliary Cholangitis (PBC), as per page 73?
Increased serum antimitochondrial antibodies (AMA)
122
What is the 'florid duct lesion' characteristic of Primary Biliary Cholangitis (PBC) microscopy, as described on page 74?
Lymphocytic and/or granulomatous bile duct destruction
123
What is 'ductopenia' as seen in the progression of Primary Biliary Cholangitis (PBC), according to page 74?
Loss of small intrahepatic bile ducts
124
What is 'feathery degeneration' of periportal hepatocytes in PBC indicative of, as per page 74?
Cholate stasis (bile salt accumulation)
125
What is the end-stage morphological outcome of untreated Primary Biliary Cholangitis (PBC), according to page 74?
Cirrhosis
126
The destruction of which structures is central to the pathology of Primary Biliary Cholangitis, as per page 74?
Small intrahepatic bile ducts
127
What are the key pathological features of Primary Sclerosing Cholangitis (PSC), as described on page 75?
Inflammation and obliterative fibrosis of large intrahepatic and extrahepatic bile ducts, with dilation of preserved segments.
128
What is the suspected cause of Primary Sclerosing Cholangitis (PSC), according to page 75?
Unknown, possibly autoimmune
129
Primary Sclerosing Cholangitis (PSC) is strongly associated with which other group of diseases, as per page 75?
Inflammatory bowel disease (especially ulcerative colitis, ~50-70% association)
130
What is the typical gender predominance in Primary Sclerosing Cholangitis (PSC), according to page 75?
Female to male ratio is 1:2 (i.e., more common in males)
131
PSC affects which parts of the biliary tree, as stated on page 75?
Large intrahepatic and extrahepatic bile ducts
132
What is the characteristic 'onion skin' fibrosis seen in Primary Sclerosing Cholangitis (PSC) microscopy (page 76)?
Concentric layers of fibrous tissue around the large bile ducts.
133
What is the typical appearance of bile ducts on imaging (e.g., ERCP/MRCP) in Primary Sclerosing Cholangitis (PSC), shown on page 76?
'Beaded' appearance (due to multiple strictures and dilatations)
134
Are small bile ducts typically directly involved by the primary inflammatory process in PSC when seen on biopsy, according to page 76?
No, they are usually not directly involved by inflammation but may show secondary changes (mild injury, ductular reaction) due to cholestasis.
135
What is the common long-term outcome of Primary Sclerosing Cholangitis (PSC) in terms of liver architecture, as per page 76?
Biliary cirrhosis
136
What does 'ductular reaction' signify when seen in liver biopsies of PSC patients, according to the notes on page 76?
It is a compensatory response where the liver attempts to repair itself by forming new ductules, often due to cholestasis and injury to larger ducts.
137
What is a major malignant complication of Primary Sclerosing Cholangitis (PSC) with a significant lifetime risk, as per page 77?
Cholangiocarcinoma (lifetime risk of around 20%)
138
Besides cirrhosis and cholangiocarcinoma, name one other complication associated with Primary Sclerosing Cholangitis (PSC) from page 77.
Chronic pancreatitis OR Chronic cholecystitis
139
The development of which type of cancer is a serious concern in patients with long-standing Primary Sclerosing Cholangitis (page 77)?
Cholangiocarcinoma
140
Can Primary Sclerosing Cholangitis (PSC) lead to chronic pancreatitis, according to the complications listed on page 77?
Yes
141
What is the most common ultimate liver-related structural complication of PSC, as listed on page 77?
Cirrhosis
142
Elevation of which two serum aminotransferases indicates compromised hepatocyte integrity, according to the lab evaluation chart on page 82?
Serum aspartate aminotransferase (AST) and Serum alanine aminotransferase (ALT)
143
What does an elevated serum bilirubin indicate about liver function, as per page 82?
Impaired biliary excretory function
144
Jaundice and pruritus can result from the elevation of what substance normally secreted in bile (page 82)?
Bilirubin (and bile acids for pruritus)
145
Elevation of which two plasma membrane enzymes suggests damage to the bile canaliculus or cholestasis, according to page 82?
Serum alkaline phosphatase (ALP) and Serum γ-glutamyl transpeptidase (GGT)
146
If total serum bilirubin is elevated, what does the 'direct' bilirubin measure, as per page 82?
Conjugated bilirubin
147
A decrease in which serum protein, synthesized by the liver, can lead to ascites, according to the chart on page 83?
Serum albumin (↓)
148
Impaired synthesis of coagulation factors by the liver leads to what clinical problem and what change in Prothrombin Time (PT), as per page 83?
Coagulopathy; Prolonged (increased) PT
149
Elevation of which substance in the blood, due to impaired hepatocyte metabolism, can lead to encephalopathy (page 83)?
Serum ammonia (↑)
150
What does a prolonged Prothrombin Time (PT) indicate about hepatocyte synthetic function, according to page 83?
Decreased synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X) and factor V.
151
The aminopyrine breath test, as mentioned on page 83, assesses which aspect of hepatocyte function?
Hepatocyte metabolic capacity (specifically demethylation), which would be decreased (↓).
152
In cirrhosis, impaired metabolism of which hormone can lead to various clinical signs, as per page 84?
Oestrogen (estrogen levels effectively increase ↑)
153
What are spider angiomas, a clinical sign seen in cirrhosis related to altered estrogen metabolism (page 84)?
Cutaneous vascular lesions consisting of a central arteriole with radiating small vessels.
154
What is palmar erythema, as seen in cirrhosis and mentioned on page 84?
Reddening of the palms, particularly the thenar and hypothenar eminences, due to local vasodilatation.
155
What is gynecomastia, and how is it related to cirrhosis, according to page 84?
Development of breast tissue in males, due to hormonal imbalance (e.g., increased estrogen effect) in cirrhosis.
156
Name two clinical signs of impaired estrogen metabolism in cirrhosis from the list on page 84.
Palmar erythema, Spider angiomas, Hypogonadism, Gynecomastia (Any two)
157
Kayser-Fleischer rings, copper deposition in the cornea, are a characteristic eye finding in which disease, as per the summary on page 85?
Wilson Disease
158
The presence of Antimitochondrial Antibodies (AMA) is a key diagnostic marker for which autoimmune biliary disease, according to page 85?
Primary Biliary Cholangitis (PBC)
159
'Onion skin' periductal fibrosis is a histological hallmark of which biliary disease, often associated with Inflammatory Bowel Disease, as summarized on page 85?
Primary Sclerosing Cholangitis (PSC)
