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Chronic Liver Disease Flashcards

1
Q

what is the outcome of chronic liver disease

A

cirrhosis

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2
Q

when does liver disease become chronic

A

when duration is longer than 6 months- duration may be subclinical

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3
Q

what is the difference between compensated and decompensated chronic liver disease

A

compensated- patients do not have symptoms relating to their cirrhosis

decompensated- symptomatic complications related to cirrhosis

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4
Q

what are symptomatic complications relating to cirrhosis

A

jaundice, ascites, variceal haemorrhage, hepatic encephalopathy

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5
Q

why are sinusoidal capillaries leaky

A

to allow the movement of protein etc

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6
Q

what cells initiate fibrosis and how

A

hepatocyte kupffer cells/ inflammatory cells cause quiescent hepatic stellate cells to turn into activated HSC which are pro inflammatory and then turn into apoptotic HSC

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7
Q

what are the causes of chronic liver disease (cirrhosis) in order of most common

(the ddx for cirrhosis)

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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8
Q

what other disease can chronic affect the liver as a bystander

A

amyloid,
rotor syndrome,
sarcoid

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9
Q

what is NAFLD

A

fatty liver or steato-hepatits in absence of other cause

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10
Q

what is seen microscopically in NASH

A

fat globlets, black dots- neutrophils infiltration, collagen/ fibrosis

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11
Q

what is the ‘2 hit; pathogenesis of NASH

A

1st= excess fat accumulation

2nd= intrahepatic oxidative stress, lipid peroxidation, TNF-alpha; pro inflammatory cytokine cascade, lipopolysaccharide, ischaemia- reperfusion injury

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12
Q

what causes oxidative stress and lipid peroxidation

A

MCD diets (methionine-choline deficient)

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13
Q

what does the ‘second hit’ activate and lead to

A

activates NF-kB and the progression of NASH with increased ARE gene expression

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14
Q

what metabolic syndrome factors are associated with NASH/NAFLD

A

type II diabetes, obesity, HDL cholesterol, hypertension, triglycerides

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15
Q

when NASH is in conjunction with metabolic syndrome what depends what you present with

A

your genes

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16
Q

what is the treatment for a simple steatosis

A

weight loss and exercise

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17
Q

what are the risks of simple steatosis

A

increased cardiovascular risks

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18
Q

what is the treatment for NASH

A

weight loss and exercise (some experimental treatments)

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19
Q

what is the risk of NASH

A

progression to cirrhosis

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20
Q

what are the types of auto immune liver disease

A

primary biliary cholangitis,

auto-immune hepatitis,

primary sclerosing cholangitis,

alcoholic related liver disease (has autoimmune components),

drug reactions

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21
Q

what causes primary biliary cholangitis

A

autoantibodies (AMA- antimitochondrial antibodies) against mitochondrial antigens (M2-E2 E3 subunits of PGC-E2) in the inner leaflet of the mitochondrian

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22
Q

what mediates PBC

A

T cell mediates- CD4 cells reactive to M2 target

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23
Q

who is PBC most commonly seen in

A

women 10;1

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24
Q

what is the presentation of PBC

A

usually symptomatic/ incidental

symptoms;

  • fatigue
  • itch without rash
  • xanthesalma (around eyelids) and xanthomas
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25
Q

what is a xanthoma

A

an irregular yellow patch or nodule on the skin, caused by deposition of lipids.

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26
Q

how is PBC diagnosed

A

2 of 3;

  • positive AMA,
  • cholestatic LFT’s
  • liver biopsy
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27
Q

how is PBC treated

A

urseo deoxycholic acid

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28
Q

what are the outcomes of PBC

A

most will not develop symptoms of if they do majority of symptomatic will not develop liver failure

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29
Q

who does auto-immune hepatitis affect more

A

women 3.6:1

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30
Q

who gets type 2 auto immune hepatitis and what is involved in it

A

Children & young adults

  • LKM-1 (Liver kidney microsomal type 1 antibody)
  • AMA
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31
Q

who gets type 1 auto immune hepatitis and what is involved in it

A

adults

  • ANA (anti-nuclear antibodies)
  • ASMA (anti smooth muscle antigen (actin))
  • SLA severity (anti soluble liver antigen)
  • IgG
  • AMA
  • pANCA (Perinuclear Anti-Neutrophil Cytoplasmic Antibodies)
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32
Q

how can type 1 auto immune hepatitis present

A

with acute onset of symptoms similar to toxic hepatitis or acute viral hepatitis

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33
Q

what extra hepatic manifestations are associated with type 1 auto immune hepatitis

A 
autoimmune thyroiditis, 
graves disease,
chronic UC,
less commonly with RA (rheumatoid arthritis),
pernicious anaemia,
systemic sclerosis,
ITP,
SLE
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34
Q

what is the clincal presentation of auto immune hepatitis

A 
hepatomegaly,
jaundice,
stigmata of chronic liver disease,
splenomegaly,
elevated AST and ALT (show liver damage),
elevated PT,

malaise, fatigue, lethargy, nausea, abdo pain, anorexia

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35
Q

how is autoimmune hepatitis diagnosed

A

elevated AST, ALT and IgG,
presence of autoimmune antibodies,
liver biopsy

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36
Q

what is the histology of autoimmune hepatitis

A

piecemeal necrosis and nodular involvement,

numerous plasma cells,

interface hepatitis

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37
Q

what causes autoimmune hepatitis

A

when a genetically predisposed patient is exposed to triggering environmental triggers

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38
Q

what are the environmental triggers of auto immune hepatitis

A 
viruses, toxins, drugs (Oxyphenisatin
Methyldopa
Nitrofurantoin
Diclofenac
Minocycline
statins)
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39
Q

how is autoimmune hepatitis

A

corticosteriods (combo of prednisone and azathioprine)

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40
Q

how many of autoimmune hepatitis patients will develop cirrhosis

41
Q

what is primary sclerosing cholangitis

A

autoimmune destructive disease of large and small bile ducts- dilatation and stricturing seen on imaging (how its diagnosed)

42
Q

what is the treatment for primary sclerosing cholangitis

A

maintain bile flow and monitor for colo-rectal cancer and cholangiocarcinoma

43
Q

what is haemochromatosis

A

genetic iron overload syndrome- autosomal recessive mutation in HFE gene (C282Y or H63D)

44
Q

what are the clinical features of haemochromatosis

A

cirrhosis, cardiomyopathy, pancreatic failure, ‘the bronzed diabetic’

45
Q

how is haemochromatosis treated

A

venesection- letting out blood, iron offloading

46
Q

what is wilsons disease

A

leniculo-hepatic degeneration- mono genetic autosomal recessive disease- loss of function or loss of protein mutations in caeruloplasmin

caeruloplasmin= copper binding protein, loss of copper regulation= massive tissue deposition of copper

47
Q

how is wilsons disease treated

A

copper chelation drugs, low copper diet

48
Q

what is anti 1 anti0trypsin deficiency

A

when mutation on A1AT gene causes protein function loss and excess tryptic activity

49
Q

what is the clinical presentation and treatment of alpha 1 anti-trypsin deficiency

A

lung emphysema,

liver deposition of mutant protein, cell damage, accumulation of protein

treatment= supportive management

50
Q

what is budd chiari

A

thrombosis of the hepatic veins

51
Q

what is the clinical presentation of budd chiari

A

acute- jaundice, tender hepatomegaly

chronic- ascites

52
Q

how is budd chiari diagnosed and treated

A

diagnosed by U/S visualisation of hepatic veins

treatment= recanalization or TIPS

53
Q

what is TIPS

A

Transjugular intrahepatic portosystemic shunt

54
Q

what is methotrexate

A

drug used to treat rheumatoid arthritis and psoriasis

55
Q

why is methotrexate bad

A

liver toxin causing progressive fibrosis

56
Q

what is cardiac cirrhosis

A

secondary to high right heart pressure

57
Q

what causes high right heart pressures

A

incompetent tricuspid valve, congenital, rheumatic fever, constrictive pericarditis

58
Q

what is the presentation of cardiac cirrhosis

A

congestive heart failure- too much ascites and/or liver impairment

59
Q

what effects does cirrhosis of the liver that lead to dysfunction

A

disruption of vasculature and generation of abnormal signalling

60
Q

what makes up the portal vein

A

Superior mesenteric + Splenic vein+ gastric + part from inferior mesentric

61
Q

what organs does the portal vein carry outflow from

A

spleen, oesophagus, stomach, pancreas, small and large intestine

62
Q

where does blood from the livers dual blood supply )hepatic artery and portal vein) go after that

A 
liver sinusoids 
central vein 
hepatic vein
IVC
RA of heart
63
Q

what is the pressure in the portal vein

A

very low 5-8 mmHg

64
Q

what are the collateral (4) pathways of the portal venous system (portocaval anastomosis with systemic venous system)

A

Esophageal and gastric venous plexus

umbilical vein from the left portal vein to the epigastric venous system

retroperitoneal collateral vessels

the hemorrhoidal venous plexus

65
Q

what happens the portal vein collaterals in portal hypertension

A

anastamoses may become engorged, dilated, varicosed and subsequently rupture

66
Q

what defines portal hypertension

A

Portal vein pressure above the normal range of 5 to 8 mm Hg

Portal vein - Hepatic vein pressure gradient greater than 5 mm Hg

67
Q

what does portal hypertension result from

A

increased resistance to portal flow

increased portal venous inflow

68
Q

what can increase resistance to portal flow

A

increased intra-hepatic resistance

collateral resistance increased

69
Q

how does cirrhosis cause hyperdynamic circulation and ascites

A

cirrhosis

impaired liver function + sinusoidal hypertension and portal systemic shunting
=
endogenous vasodilators
=
splanchnic + peripheral vascular resistance
=
pooling of blood
= decreased effective arterial blood volume
=
hyperdynamic circulation
=
increased renin angiotension + symp stim + arginine vasopressin
=
increased renal vascular resistance + tubular reabsoprtion of sodium
=
ascites

70
Q

what are the pre-hepatic causes of portal hypertension

A

blockage of the portal vein before the liver- portal vein thrombosis or occlusion due to congenital abnormalities

71
Q

what are the intrahepatic causes of portal hypertension

A

distortion of the liver architecture pre (schistosomiasis) or post sinusoidal
(cirrhosis, alcoholic hepatitis, congenital hepatic fibrosis)

72
Q

whats happening to the prevelence of chronic liver disease in scotland

A

increasing

73
Q

describe compensated cirrhosis

A

Clinical normal

Incidental finding

Lab test or imaging abnormalities

Portal Hypertension may be present

74
Q

describe decompensated cirrhosis

A

liver failure

  • chronic
  • acute on chronic (infection, insult, SIRS-sepsis)
  • end stage liver disease (insufficient hepatocytes)
75
Q

what are the sings of compensated cirrhosis

A

Spider naevi

Plamar erythema

clubbing

gynaecomastia

Hepatomegaly (most wont have this)

Spleenomegaly

NONE

76
Q

what are the clinical signs of decompensated cirrhosis

A

Jaundice
Ascites
Encephalopathy
Easy bruising

77
Q

what are the complications of cirrhosis

A

ascites
encaphalopathy
variceal bleeding
liver failure

78
Q

how is decompensated cirrhosis treated

A

treat underlying cause

treat infection (common decompensator)

treat for: NaCl retention, and low threshold to switch to gluconeogensis and lipolysis and catabolism (small frequent meals 35-40 kcal/kg)

79
Q

what supplement is mandatory in cirrhosis due to excessive alcohol intake

A

vit B supplementation thiamine

80
Q

what complications arise from poor calcium intake and absorption, poor vit d synthesis, malnutrition and steroid use

A

osteoporosis and osteomalacia

81
Q

retention of what causes ascites

A

sodium and water

82
Q

how is ascites treated

A

Reduce salt intake, maintain nutrition

Diuretics- spironolactone first

Paracentsis

TIPSS

Transplantation

treat liver function, treat any infection, no NSAIDS

83
Q

how is the treatment of heart failure the opposite of ascites

A

refers to diuretics

-start with spironalactone and then go onto loop

84
Q

what does TIPSS connect

A

portal and hepatic veins

85
Q

what is SBP

A

spontaneous bacterial peritonitis

-translocated bacterial infection of ascites

86
Q

what is the treatment of SBP

A

Urgent

Antibiotics and Alba

Vascular instability-terlipressin

Maintain renal perfusion

HRS (hepatorenal syndrome) development very poor prognosis

87
Q

how is encephalopathy diagnosed

A

flap
confusion
any neurology
alcohol withdrawal

88
Q 
what causes hepatic Urgent
Antibiotics and Alba
Vascular instability-terlipressin
Maintain renal perfusion
HRS development very poor prognosis
encepthalopathy
A

Ammonia generated in the intestines from nitrogenous compounds in the diet is taken directly into the systemic circulation rather than being metabolized in the liver. This causes disturbances in neurotransmitter trafficking.

89
Q

what is ammonia metabolised into in the liver

90
Q

how is encephalopathy treated

A

treat cause-infection, metabolic, drugs, liver failure

Lactulose to clear gut/ reduce transit time
Rifaxamin
Maintain nutritional status with small, frequent meal/snack pattern and bedtime CHO

consider transplant if spontaneous

91
Q

where can you get varices

A

oesophagus, gastric, rectal, ectopic

92
Q

what is the pathophysiology of variceal bleeding

A

increased intrahepatic resistance and portal blood flow

increase varicus vein size and decreased wall thickness

increased variceal wall tension

93
Q

how are variceal bleeds prevented- prophylaxis

A

beta blockers (non selective): propranolol, carvideolol

variceal ligation

94
Q

what is the treatment for acute variceal bleeds

A

resus

drugs

TIPSS and transection/ shunt therapy

95
Q

what is endoscopic therapy used to do to treat varices

A

ligation, banding, sclerotherapy

96
Q

when should a balloon tamponade be used

A

in emergency as gateway to other therapy for acute variceal bleed

97
Q

why do patients with cirrhosis have increased pro thrombin time

A

as are deficient in both pro and anti thrombotic factors, coagulation balance disrupted, risk of both bleeding and clotting, give heparin unless having variceal bleed

98
Q

when do people become eligible for transplant

A

when they are more likely to die from the disease than the operation

UKELD score of >= 49 to be listed

UNLESS

  • variant syndrome
  • small HCC
99
Q

what are the variant syndromes of cirrhosis

A

Diuretic resistant ascites

Hepatopulmonary syndrome

Chronic hepatic encephalopathy

Intractable pruritus
Polycystic liver disease

Familial amyloidosis

Primary hyperlipidaemia

GI (64 decks)

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