Hepatic Disease Flashcards
Define acute liver failure
development of hepatocellular dysfunction associated with coagulopathy and encephalopathy in patients without prior known liver disease
How is ALF classified?
According to time between jaundice and onset of encephalopathy
How is ALF classified according to time line of symptoms?
Hyperacute
Acute
Subacute
What are the causes of acute liver failure?
- Infective: hep B 12%
- Drug induced: acetaminophen 39%, phenitoin, halothane.
- Autoimmune disease
- Vascular :Budd chiari Syndrome
- Pregnancy : HELLP, acute fatty liver of pregnancy.
Define Chronic hepatic disease in
Chronic hepatitis is any hepatitis lasting >6months. Inflammation can lead to hepatic fibrosis, and, in some patients, there is progression to cirrhosis, characterized by nodular regeneration and disruption of the architecture of the liver, which can lead to portal hypertension.
What is decompansated liver cirrhosis
Developof portal hypertension ascites, varicella haemorrhage or liver insufficiency as marked by coagulopathy,jaundiceand encephalopathy
Schematic of decompensated liver dysfunction
Management strategy cirrhosis
Management
Management
Effects on cvs
Increased production or reduced excretion of vasodilators resulting in increased splamchnic vessels capacity which stimulated retention of na should h20, this leased to portal hypotension and further increase in capacitance e by formation of potosystemic shunts. These changes lead to hyperdynamic circulation with hypotension and tachycardia and blunted b adrenalin stimulation leading to cardiomyopathy
what are the ECG changes?
QT prolonged
BP
Coronary artery disease due to commodities
Pathogenesis portopulmonary hypertension
Not completely understood but histology also changes include midealhypertro0hy, intimate proliferation, thrombosis, and fubrosis
Diagnosis
Mean pulmonary pressure >25 /PVR > 240DYNES/s3c/m3
MODERATE portopulmonary hyp
MPP > 35-45/ PVR >250
Mortality rates associated with liver transplant in moderate ph
> 50%
Severe portal hypertension
map > 50/
Mortality rates associated with liver transplant in severe ph
100%
Pulmonary effect
Pleural effusion hydrothorax
Atelectasis diaphragm displacement ascites
aspiration pneumonia
Poto pulmonary hpt
Hepatopupmonary sx
Pathogenesis of hepatic pulmonary
Due 5o vasod8oatation 5here is increased blood flow with no matched increase in ventilation leading to vq mismatch. HPV is blunted due to blunting of vasoconstriction
Diagnostic criteria for hps
Clinical features
Exertional dyspnoea Fatigue Clubbing Spider angiomata Platypnia Orthodeoxia
GIT effects; portal hypertension
Increased gradient between portal and hepatic vein by > 5mmhg secondary to 8ncreased vascular resistance from fibrosis and flow this inturn increase splanchnic blood flow which exacerbates pulmonary hpt
Complications of portal hpt
Ascites
Increase in hydrostatic pressure and translation of fluid
Reduced oncotoc pressure
Management of ascites
Dietary salt restrictio
Diuretic
Paracentasis
transjugular intrahepatic potosystemic shunt
Varicella haemorrhage incidence
60%
Management
A- protect from aspiration
B-
C- fluid, blood, POC guided haemostatic resus, vit k
D-
Endoscopic ligation banding or sclerotheraphy
Balloon tampinade sengstaken blakemore
TIPSS
Secondary prevention
Propranolol
Ocreotide
Spontaneous bacterial peritonitis
Asymptomatic
Tap neutrophils cout> 200
Rx antibiotics
Prophylactic cotrimox or quinolone
Mortality rates of sbp
70% at 2y
Renal
Hypovolaemia
ATN
DRUG induced
Hepatorenal syndrome
Pathophysiology of hepatic renal syndrom
Sympathetic and RASS activation 2nd to splachnic vasodilatation withrofound vasoconstriction
Diagnosis of hrs
Cirrhosis with ascites, doubling Serum creatinine >1,5mg/dlnot reduced to < 1,5mg/dl with Albumin administration at dise 1g/kg and after min 2 day with no diuretic
Type 1hrs
Acute Doubling Serum creatinine > 2,5g/dl Or 221mcmol/l in less than 2 weeks
Type 2
Less aggressive course than type 1 Chara terized by asci
Management
Vasoconstriction
Albumin
RRT
Coagulation haemorrhage risk
Reduced vitamin dependent factor
Thrombocytopenia hyperspenism 9r uterine
Dysfibrinigenea
High tpa
Coagulation thrombosis risk
Low protein c s
Low antithrombin, plaeminogen, heparin cofactor 2, alpha2 macroglobulin
Increased procogulant factor vii,vWT
Overall coagulation
Assessment of coagulation
Pharmacokinetic
Decreased: hepatic metabolism, renal excretion, protein synthesis
Increased : total body water
Volatile
Avoid enflurane and halothane
Iso reduced hepatic clearance by o,2% improves hepatic blood flow
sevoflurane 2_5 % biotransformation
Des 0.02%
Benzos
Prolonged duration policy action
Worsen encephalopathy
Loran,9xaz,Texas undergoing glucoronide conjugation and less affected by liver dysfunction
Opioids
Neuromuscular blockers
Slow onset
Cisco independent of liver function
Induction
Protocol no change
Risk stratification child Pugh score
Meld
Modified king college
W3at haven score