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1. GI > Causes of Chronic Liver Disease > Flashcards

Causes of Chronic Liver Disease Flashcards

1
Q

What defines chronic liver disease?

A

Duration greater than 6 months

- can present after the 6 months

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2
Q

What is the pathology of chronic liver disease?

A

recurrent inflammation and repair with fibrosis and regeneration

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3
Q

What cells initiate the inflammatory response in the liver in response to damage?

A

Hepatic Stellate Cells

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4
Q

What do Hepatic Stellate Cells turn into before turning into fibrosis?

A

Hepatic Myofibroblast

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5
Q

What is the progression of Hepatic Stellate Cells producing fibrosis?

A

QUIESCENT HSC
ACTIVATED HSC
APOPTOTIC HSC

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6
Q

What are the causes of chronic liver disease?

A 
Alcohol
NAFLD
Hepatitis C 
Primary Biliary Cholangitis
Autoimmune Hepatitis
Hepatitis B
Haemochromatosis
Primary Sclerosing Cholangitis
Wilsons Disease
alpha 1anti-trypsin
Budd-Chiari
Methotrexate
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7
Q

What is Non Alcoholic Fatty Liver Disease (NAFLD)?

A

Fatty Liver or steato-hepatitis in absence of other cause

In obese = 60% have it

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8
Q

What is the pathogenesis of NAFLD?

A

“2 Hit” Paradigm
“First hit” – Excess fat accumulation
“Second hit” – Intrahepatic oxidative stress
Lipid peroxidation
TNF-alpha, cytokine cascade
Ischeamia reperfusion injury

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9
Q

What can generate TNFa?

A

Hepatocytes

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10
Q

What is the treatment for simple steatosis?

A

weight loss and exercise

increased CVS risk

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11
Q

What is the diagnosis and treatment for NASH?

A

Diagnosis = liver biopsy
Weight loss & exercise
Other treatments experimental

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12
Q

What is a risk of NASH?

A

progression to cirrhosis

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13
Q

Name some Autoimmune liver diseases?

A 
Primary Biliary Cholangitis (Cirrhosis)
Auto-immune Hepatitis
Primary Sclerosing Cholangitis
Alcohol related liver disease
Drug Reactions
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14
Q

What causes Primary Biliary Cirrhosis (PBC)?

A

Autoimmune component 1960s,1970s-1980s AMAs M1-M9

1980s target M2-E2 E3 subunits of PDC-E2 n inner leaflet of mitochondrial membrane
T-cell mediated, CD4 cells reactive to M2 target, why loss of tolerance

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15
Q

What are the symptoms of PBC?

A

Fatigue
Itch without rash
Xanthesalma and xanthomas - hypercholesterolemia
Normally middle aged women

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16
Q

How is PBC diagnosed?

A

2 of 3:
Positive AMA
Cholestatic LFTs
Liver Biopsy

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17
Q

How is PBC treated?

A

Urseo deoxycholic acid

18
Q

What are the consequences of PBC?

A

Most will not develop symptoms in their life time
The majority with PBC symptoms do not develop liver failure
- Itch can be particularly problematic.
Many developing liver failure will be unfit for transplant

19
Q

Describe auto-immune hepatitis?

A

Affects women more than men (3.6:1)
If untreated approximately 40% die within 6 months
40% develop cirrhosis

20
Q

Describe type 2 auto-immune hepatitis?

A

Children & young adults
LKM-1
Exclusive
AMA

21
Q

Describe type 1 auto-immune hepatitis?

A

Adult (teenagers + above)
ANA
ASMA - anti smooth muscle antibody
SLA severity

IgG –positive
AMA –positive
pANCA –positive

22
Q

What extrahepatic manifestations are associated with Type 2 auto-immune hepatitis?

A

Autoimmune thyroiditis, graves disease, chronic UC

Less commonly with RA, pernicious anemia, systemic sclerosis, ITP, SLE

23
Q

What is the clinical presentation of auto-immune hepatitis?

A 
Hepatomegaly
Jaundice
Stigmata of chronic liver disease
Splenomegaly
Elevated AST and ALT
Elevated PT
Non-specific symptoms: malaise, fatigue, lethargy, nausea, abdominal pain, anorexia
24
Q

How is auto-immune hepatitis?

A

Elevated AST and ALT
Elevated IgG
Presence of autoimmune antibodies
Liver biopsy – confirms diagnosis

25
Q

What is the pathology of auto-immune hepatitis?

A

Chronic hepatitis with marked piecemeal necrosis and lobular involvement
Numerous plasma cells
Interface hepatitis: hallmark finding

26
Q

What are the genetic predisposing factors of auto-immune hepatitis?

A

HLA-DR3: early onset, severe form
HLA-DR4: caucasian, late onset, better response to steroids, higher incidence of extrahepatic manifestations
IgG: part of the IgG molecule (mainly the heavy chain)
T-Cell receptors

27
Q

What drugs can cause auto-immune hepatitis?

A 
Oxyphenisatin
Methyldopa
Nitrofurantoin
Diclofenac
Minocycline
statins
28
Q

What is the treatment of auto-immune hepatitis?

A 
Corticosteroids
Azathioprine
Children: azathioprine or 6MP
Combination Therapy
Prednisone + Azathioprine
Prednisone: start at 30mg daily and taper down to 15mg at week 4, then maintain on 10mg daily until therapy endpoint
Azathioprine 50-100mg daily
MUST GIVE STEROIDS OR THEY WILL DIE
29
Q

What are the typical consequences of auto-immune hepatitis?

A

40% of all pts with AIH develop cirrhosis
54% develop esophageal varices within 2 years
Poor prognosis if has presence of ascites or hepatic encephalopathy
13-20% of patients can have spontaneous resolution
Of patients who survive the most early and active stage of disease, approximately 41% of them develop inactive cirrhosis.

30
Q

Describe Primary Sclerosing Cholangitis?

A

Autoimmune destructive disease of large and medium sized bile ducts.
M:F 4:1, 40% also have Colitis (mainly UC)
Commonest liver disease in Scandinavia.
Clinical: recurrent cholangitis
Diagnosis: imaging of biliary tree
Treatment: maintain bile flow, monitor for cholangiocarcinoma and colo-rectal cancer

31
Q

What are the three features of the “bronzed diabetic”?

A

Cirrhosis
cardiomyopathy
Pancreatic failure

32
Q

Describe Haemochromotosis?

A

Genetic Iron overload syndrome
Mono-genetic autosomal recessive disease of Iron over load, C282Y or H63D, mutations in HFE gene.
Gene carrier frequency 10%, genetic haemochromatosis 1 in 200 but partial penetrance.
Cirrhosis, cardiomyopathy, Pancreatic failure
Treatment: Venesection

33
Q

Describe Wilsons Disease?

A

Lenticulo-hepatic degenerationMono-genetic autosomal recessive disease.
loss of function or loss of protein mutations in caeruloplasmin
Causes massive brain and liver damage

34
Q

What is the clinical presentation of Wilsons Disease?

A

Neurological- chorea-atheitoid movements
Hepatic – cirrhosis or sub-fulminant liver failure
Kaiser Fleisher rings

35
Q

What is the treatment of Wilsons Disease?

A

copper chelation drugs

36
Q

Describe Alpha 1 anti-trypsin deficiency?

A

Genetic, Mutations in the A1AT genes, multiple sites, causes variable phenotype
Protein Function lost meaning excess tryptic activity
Trypsin destroys lung membrane and causes liver damage

37
Q

What are the clinical features and treatment of Alpha 1 anti-trypsin deficiency?

A

Lung emphyesma
Liver deposition of mutant protein, cell damage

Treatment is supportive

38
Q

Describe Budd-Chiari?

A 
Thrombosis of the hepatic veins
Congenital webs
Thrombotic tendency, protein C or S deficiency
Clinical:
- Acute- Jaundice, tender hepatomegaly
- Chronic- Ascites 
Diagnosis: U/S visualisation of hepatic veins
Treatment: recanalization or TIPS
39
Q

What can the drug Methotrexate do to the liver?

A

cause progressive fibrosis

40
Q

Describe cardiac cirrhosis?

A 
Secondary to High right heart pressures
Incompetent tricuspid valve
Congenital malformation
Rheumatic fever
Constrictive pericarditis
Clinical: CCF, with too much ascites and or liver impairment
Treatment: Treat the cardiac condition

1. GI (61 decks)

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