wk 6 6 Aetiologies and Pathophysiology of chronic liver disease Flashcards

(42 cards)

1
Q

t/f chronic liver disease is of a duration greater than 3 months

A

false 6 months

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2
Q

t/f chronic liver disease can present acutely q

A

true
duration (6mnths) may be sub clinical
signs/symptoms dependent on underlying disease/features of cirrhosis

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3
Q

describe the pathology of chronic liver disease

A

recurrent inflammation and repair with fibrosis and regeneration

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4
Q

fibrosis of the liver is due to the activation of hepatic stellate cells, how does this occur

A

quiescent HSC is activated through hepatocyte Kupffer inflammatory cells

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5
Q

TIMP is what turns the activated HSC into an apoptic HSC, what does it do

A

TIMP - Tissue Inhibitor of Metalloprotinease, determines the degradation of cells through MMP (matrix metalloprotineases)

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6
Q

other than alcohol, autoimmune disease and hepatitis, what else can cause Chronic liver disease

A

NAFLD (non-alcoholic fatty liver disease)
Primary Biliary/sclerosing Cholangitis
Haemochromatosis (iron overload)
WIlsons Disease (copper overload)
Alpha 1 anti-trypsin (pancreatic enzyme)
Budd-Chairi (hepatic portal occlusion)
Methotrexate

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7
Q

2 examples of chronic diseases that affect the liver (but arent chronic liver disease)

A
amyloid 
rotor syndrome (hyperbilirubinaemia)
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8
Q

what is the commonest disease in the world

A

NAFLD (simple steatosis)

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9
Q

NAFLD vs NASH

A

NASH is a type of NALFD

there is Non-alcoholic steatohepatitis, or simple steatosis

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10
Q

NALFD initiates due to excess fat accumulation, what does this cause 3

A

inrtrahepatic oxidative stress
lipid peroxidation
TNF-alpha/cytokine cascade

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11
Q

t/f progression to NASH can occur with/without increased expression of ARE-genes

A

true
with - large inc in ROS leads to greater expresssion
without - multiple factors (Fatty acids) instead cause

both lead to activation of NF–kB

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12
Q

how is a simple steatosis diagnosed

A

ultrasound

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13
Q

simple steasosis increases the risk of

A

cardiovascular disease

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14
Q

treatment for simple steatosis

A

weight loss

exercise

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15
Q

in NASH, there is a risk of progression to

A

cirrhosis

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16
Q

difference between primary biliary and primary sclerosing choangitis

A

primary biliary - interlobular bile ducts affected by granulomatous immune cells, leading to cholangitits

primary sclerosing - progressive inflammation of bile ducts leading to strictures

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17
Q

how does PBC present?

A
middle aged woman 
usually asymptomatic but may feel 
- fatigue
-itch and no rash 
- xanthesalma and xanthomas
18
Q

what antibodies are produced in PBC which allow it to be diagnosed

A

Antimitochondrial Antibodies (AMAs)

19
Q

other thn AMAs, give 2 ways PBC may be diagnosed

A

Cholestatic LFTs

Liver Biopsy

20
Q

treatment of PBC

A

urseo deoxycholic acid

21
Q

t/f auto-immune hepatitis affects woman more than men

22
Q

auto-immune hepatitis can be subtyped into Type 1 and 2, which one occurs in children/young adults? which is diagnosed through AMA alone? which will see IgG present?

A

type 2
type 2
type 1

23
Q

clinical presentation of type 1

A

patient: <40 yrs
hepatosplenomegaly
jaundice
stigmata of chronic liver disease
Elevated AST, ALT, PT (aspartate/alanine aminotransferase) (prothrombin time)
non specific - malaise,nausea,ab pain, anorexia

24
Q

how is type 1 diagnosed

A

elevated AST,ALT,IgG
rule out wilsons, antitrypsin, vira hep, drug induced liver disease, NASH, PBC/PSC
presence of autoimmune antibodies
liver biopsy

25
what is the hallmark finding of type 1 autoimmune hepatitis histologically
interface hepatitis also have chronic hepatitis with marked necrosis and lobular involvement with numerous plasma cells
26
which drugs can trigger autoimmune hepatitis
``` methyldopa diclofenac statins minocycline oxyphenistatin nitrofurantoin ```
27
treatment of autoimmune hepatitis
prednisone (coritcosteroid) + azathioprine (immunosuppressant)
28
what worsens the prognosis in AIH
if present with ascites or hepatic encephalopathy (brain damage due to irremoval of toxins in liver)
29
recurrent cholangitis is most likely
primary sclerosing Cholangitis
30
2 cancers which need to be monitored for in PSC
cholangiocarcinoma | colo-rectal carcinoma
31
how is PSC diagnosed
imaging of biliary tree
32
which inflammatory disease is PSC most typically seen inb
Ulcerative Colitis
33
haemochromatosis is ..... | and is treated using
iron overload | maintenance venesection for life, diets reducing iron
34
wilsons disease is due to the poor regulation of deposition of which metal? how is it treated?
copper copper chelation drugs
35
alpha 1 anti-trypsin defiency causes what
deregulation of neutrophil elastase (leading to emphysema)
36
Budd-chiari is the
thrombosis of hepatic veins
37
3 defiencies which lead to budd-chairi
thrombotic defiency protein C protein S
38
acute budd-chairi presents as jaundice and tender hepatomegaly, when woulld it be considered chronci
ascite formation
39
how is budd-chairi diagnosed
Ultrasound of hepatic veins
40
treatment for budd-chairi
recanalisation or TIPS (transjugular Intrahepatic Portosystemic Shunt)
41
methotrexate is used to treat Rheumatoid arthritis and proriasis (skin condition) what can it cause
cirrhosis | treatment - stop drug
42
cardiac cirrhosis is secondaruy to high right heart pressures (incompetent valves, congenital, rheumatic, pericarditis) how does it present and how is it treared
heart failure with ascites/liver impairment treat underlying cardiac condition