wk 6 6 Aetiologies and Pathophysiology of chronic liver disease Flashcards Preview

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Flashcards in wk 6 6 Aetiologies and Pathophysiology of chronic liver disease Deck (42)
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1
Q

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

A

false 6 months

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

3
Q

describe the pathology of chronic liver disease

A

recurrent inflammation and repair with fibrosis and regeneration

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

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)

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

7
Q

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

A
amyloid 
rotor syndrome (hyperbilirubinaemia)
8
Q

what is the commonest disease in the world

A

NAFLD (simple steatosis)

9
Q

NAFLD vs NASH

A

NASH is a type of NALFD

there is Non-alcoholic steatohepatitis, or simple steatosis

10
Q

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

A

inrtrahepatic oxidative stress
lipid peroxidation
TNF-alpha/cytokine cascade

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

12
Q

how is a simple steatosis diagnosed

A

ultrasound

13
Q

simple steasosis increases the risk of

A

cardiovascular disease

14
Q

treatment for simple steatosis

A

weight loss

exercise

15
Q

in NASH, there is a risk of progression to

A

cirrhosis

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

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

A

true

3:1`

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
Q

what is the hallmark finding of type 1 autoimmune hepatitis histologically

A

interface hepatitis

also have chronic hepatitis with marked necrosis and lobular involvement with numerous plasma cells

26
Q

which drugs can trigger autoimmune hepatitis

A
methyldopa 
diclofenac
statins 
minocycline
oxyphenistatin 
nitrofurantoin
27
Q

treatment of autoimmune hepatitis

A

prednisone (coritcosteroid) + azathioprine (immunosuppressant)

28
Q

what worsens the prognosis in AIH

A

if present with ascites or hepatic encephalopathy (brain damage due to irremoval of toxins in liver)

29
Q

recurrent cholangitis is most likely

A

primary sclerosing Cholangitis

30
Q

2 cancers which need to be monitored for in PSC

A

cholangiocarcinoma

colo-rectal carcinoma

31
Q

how is PSC diagnosed

A

imaging of biliary tree

32
Q

which inflammatory disease is PSC most typically seen inb

A

Ulcerative Colitis

33
Q

haemochromatosis is …..

and is treated using

A

iron overload

maintenance venesection for life, diets reducing iron

34
Q

wilsons disease is due to the poor regulation of deposition of which metal? how is it treated?

A

copper

copper chelation drugs

35
Q

alpha 1 anti-trypsin defiency causes what

A

deregulation of neutrophil elastase (leading to emphysema)

36
Q

Budd-chiari is the

A

thrombosis of hepatic veins

37
Q

3 defiencies which lead to budd-chairi

A

thrombotic defiency
protein C
protein S

38
Q

acute budd-chairi presents as jaundice and tender hepatomegaly, when woulld it be considered chronci

A

ascite formation

39
Q

how is budd-chairi diagnosed

A

Ultrasound of hepatic veins

40
Q

treatment for budd-chairi

A

recanalisation or TIPS (transjugular Intrahepatic Portosystemic Shunt)

41
Q

methotrexate is used to treat Rheumatoid arthritis and proriasis (skin condition) what can it cause

A

cirrhosis

treatment - stop drug

42
Q

cardiac cirrhosis is secondaruy to high right heart pressures (incompetent valves, congenital, rheumatic, pericarditis) how does it present and how is it treared

A

heart failure with ascites/liver impairment

treat underlying cardiac condition

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