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Path: Liver 2 - Failure (ii) (HE (Pathogenesis (precipitants in known…
Path: Liver 2 - Failure (ii)
HE
spectrum of neuropsych abnormalities a/w liver dysfunction +/or portosystemic shunting
functional disturbance of brain, potentially reversible
if severe: cerebral oedema + hypoperfusion
classification
type A: ALF
type B: portosystemic shunting with normal liver
type C: cirrhosis (= decompensation)
can be episodic (may be recurrent/precipitated/not) or persistent
spectrum of effects on consciousness, behaviour, intellectual function, neuromuscular function, mood, sleep
stages
1: confusion
2: drowsiness
3: somnolence
4: coma
minimal HE may be revealed/suggested by psychometric testing
affects social function, work life, behaviour, fitness to drive
covert: can be minimal or stage 1
overt: stages 2-4
Pathogenesis
reduced endogenous + exogenous detoxification (incl from gut) due to reduced liver function
unprocessed portal blood shunted through/past liver
no definite single cause
ammonia accumulation (nitrogenous compounds)
altered neurotransmission (GABA, glutamate) + glial function
precipitants in known cirrhosis
infection
bleeding + other causes of hypoperfusion
dehydration
diuretics
paracentesis
vomiting
diarrhoea
drugs (sedatives - opiates, BZD)
alcohol
constipation
TIPSS/surgical shunt
Tx
identify + correct precipitating factors
reduce ammonia production (mostly in gut) + absorption
lactulose - moves gut contents faster - decreases absorption
non-absorbable antibiotic (rifaximin)
protein restriction abandoned (worsens muscle wasting, increases risk of HE)
Investigation of Liver + Biliary tract disease
presentation
asymp - screening
vague/non-specific symptoms
known possible risk factors
clinically obvious signs
Hx
sexual
migration
country of origin
IVDU
exam
LFTs
as screening or to establish cause
ALT, AST, ALP, gGT, bilirubin, albumin, coag function (PT/INR)
transaminases related to hepatocellular damage
ALP, gGT, bilirubin a/w cholestasis (bile obstructed)
bilirubin + albumin related to liver function
bilirubin abnormality not liver or biliary tract specific (normal < 18 mol/l)
low albumin
chronic liver damage
rises again after acute liver damage
malnutrition
kidney protein loss
cachexia
normal INR - 1-1.1 - coag factor levels drop within a day (short T1/2 can detect acute damage)
sent in coagulation tube to haematology lab
liver imaging
fibroscan (modified US, non-invasive assessment of hep fibrosis)
liver bx
Transaminases
alanine + aspartate transaminase
leak from damaged hepatocytes
ALT sensitive + specific marker of hepatocellular damage
AST less specific (also in muscle, myocardium, kidney)
level of rise has poor correlation with severity/prognosis
v high in acute hepatocellular damage
may be normal/only mildy elevated in chronic liver disease
AST:ALT ratio should be < 1, if > 2 suggests alcohol-related damage
ALP
situated on hepatocyte border of bile canaliculi
leaks when hepatocytes react to bile flow obstruction
other sources
bone (fractures, growth)
placenta (pregnancy)
gGT
gamma-glutamyl transferase
detects bile flow obstruction
good for correlating with elevated ALP to demonstrate liver origin
isolated increase: alcohol, drugs - not usually investigated
v sensitive but not specific
albumin
long T1/2 - therefore when low reflects chronic liver injury
v non-specific but useful in context
Additional liver blood tests
to detect cause
viral serology
Hep A,B,C
sometimes CMV, EBV, Hep E
iron storage status
transferrin saturation
% sat of total iron binding capacity
ferritin
immunological injuries/reactions
auto-Abs (ANA, SMA, anti-LKM, AMA, ANCA)
IgG + IgM
copper metabolism
for Wilson's (v rare)
caeruloplasmin
A1AT levels (deficiency v rare)