week 6 7 - clinical syndromes of cirrhosis Flashcards
4 collateral pathways involved in portal venous system
(portocaval anastomosis)
eosophageal and gastric venous plexus
umbilical vin - left protal vein to the epigastric venous system
retroperitoneal collateral vessels
haemorrhoidal venous plexus
what may happen to the collateral pathways in portal hypertension
they may become engorged,dilated, varicosed and rupture
define portal hypertenson
> 8 mmHg (5-8 normal range)
a pressure gradient between portal vein and hepatic vein greater than 5mmHg
2 factors leading to portal hypertension
increased resistance to portal flow (r) and increased portal venous inflow (q)
P = QR
portal hypertension can be classified as prehepatic or intrahepatic , outline each
pre- blockage before liver (portalvein thrombosis, occlusion secondary to congenital portal venous abnormalities)
intra - distortion of liver architecture, either
- presinusoidal (schistomiasis, parasite infectioin - non-cirrhotic portal hypertension)
- postsinusoidal (cirrhosis, alcoholic, fibrosis, steatohepatitis)
hepatic carcinogenesis is
recurrent hepatocyte death (and regeneratioN)
difference in compensated and decompenated cirrhossis
compensated - clinical normal, lab test/imaging abnormalities, Portal HT may be present
decompensated - liver failure, acute-on-chronic, end stage liver disease
associated signs of compensated cirrhosis
spider naevi palmar erythema clubbing gynaecomastia hepatomegaly/splenomagly (maybe) or none
associated signs of decompensated cirrhosis
jaundice
ascites
enceophalopathy
bruising
recommended nutrition intake for decompensated cirrhosis
energy - 35-40 kcal/kg
protein - 1.2-1.5g/kg
small frequent meals/snacks to reduce fasting gluconeogenesis/muscle catabolism
vitB supplements may be necessary (esp if alcoholic)
1000mg Calcium 20uq Vit D
refeediing syndrome
which patients more at risk
malnourished overnourished (holocaust) alcoholics
how does ascites happen
cirrhosis/portal hypertension causes peripheral arteriolar vasodilation - reduced resitance and reduced arteriolar blood volume
this activates vasoconstriction
- increases portal presure/co/hr/plasma and blood volumes (na retention)/vascular resistance
fluids pished out
how is ascites diagnosed on examination
which imaging can also be used to confirm
shifting dullness
ultrasound
how is ascites treated
improve underlying liver disease
treat infection if there
if Na overload - reduce salt intake, maintain nutrition and no NSAIDS
spinolactone first
surgery - paracentesis/TIPSS/transplantation
in new ascites it is appropriate to increase sprinolactone (water diuretic) however if recurrent what is also given
loop diuretic (furosemide)
when is paracentesis carried out on an ascites patient 3
if at risk of infection
signs of encephalopathy
hypovolaemia
define spontaneous bacterial peritonitis
translocated bacterial infection of ascites
treatment for SBP
mild - co-trimoxazole
severe - piperacilin/tazobactam
if vascular instability - terlipressi
diagnosis of SBP
ascites tap
if neutrophil count ?250 cells/mm3
liver flap is seen in
encephalopathy
ammonia is the cause of encephalopathy, as is distrubs the neurotransmitters in the brain. This does not occur in skeletal muscle, why
skeletal able to metabolise ammonia to glutamine
drug given for encephalopathy
rifaximin (also used to treat travellers diarrhoea, IBS)
transplantation for liver disease is considered on events, LFT and quality og liife, give examples of when each may lead to consideration
event
- ascites - resistant/SBP
- variceal bleed
LFT
-bilirubin,albumin,PT high after therapy
quality - if persistant symptoms of
- itch
- lethargy
- spontaneous encephalopathy
patients requir a UKELD score of …. to be listed for elective liver transplant unless they have 2
> /=49
unless Variant syndrome (diuretic resistant ascites, hepatopulmonary/ chronic hepatic enceophalopathy intractable pruritis/ polycistic liver, familial amyloidosis/ primary hyperlipidaemia) Hepatocellular carcinoma
