Ow: Hepatitis, ALD, NAFLD + CASE 1 -cirrhosis Flashcards
LFT:
- GGT up alone
- GGT and ALP up
- AST and ALT up
LFT:
- GGT up alone = Usually indicates steatosis (fat deposit into liver cells)
- GGT and ALP up = Think cholestasis (obst. to biliary drainage)
- AST and ALT up = Hepatitic (hepatocellular damage)
Causes of steatosis?
- Alcohol
- NAFLD
- metabolic syndrome
- diabetes, dyslipidaemia, hypertension, increased BMI
Causes of hepatits?
- Viral hepatitis
- Alcohol hepatitis
- Non-alcoholic hepatitis
- Autoimmune
- Ischaemic
- Haemochromatosis
- drugs/herbal and natural supplements - (can give cholestasis and or hepatits and only way to really know is stop the drug)
Liver tumours can present with? Can be? risk factors?
Present with:
- Cholestasis
- Muixed pattern
- Primary/hepatocellular carcinoma
- secondary/metastatic
Risk Factors:
- HCC is rare outside of HepB with/without underlying liver cirrhosis
- Liver mets arise from other known cancer
Differentiation between alcoholic and NAFLD?
Compare results after abstaining from alcohol or you can get the patient to loose weight however, changes as a result of reversal of metabolic syndrome can take some time so not overly easy in many patients.
Presentation of ALD?
- Alcohol exposure causes fatty change and periventricular fibrosis
- Severe exposure can lead to hepatitis
- Repeated attacks of both of these leads to cirrhosis - fibrosis and hyperplastic nodules
NAFLD?
- Metabolic syndrome drives steatosis
- Intermittently causes hepatitis
- Drives fibrosis through recurrent attacks
ALD and NAFLD common pathophysiology?
- BOTH are related to excessive fat and inflammation
- BOTH are diagnosed using clinical parameters with history and LFTs and don’t use biopsy as diagnostic due to unnecessary risk
Viral Hepatits? - Transmission, Can give chronic?
A = Faecal-oral, No -(mostly subclinical)
B = Parenteral, Yes -(mostly spontaneously resolved)
C = Parenteral, Yes -(mostly chronic)
D = Parenteral, Yes (must be co-infected with B)
E = faecal-oral, No
EBV and CMV - All resolved causing infection mononucleosis - characteristic atypical nucleocytes on blood film.
Autoimmune Hepatitis?
- Chronic autoimmune disease
- Unknown aetiology
- Episodic, recurrent (look at history!)
- More common in females than males
- Biomodal age distribution
- Diagnosis: autoimmune screen or liver biopsy
Ischaemic hepatitis is? Caused by?
Results from severe haemodynamic compromise (ie. shock)
- Cardiogenic
- Severe dehydration/blood loss
- Severe sepsis
- Blood clot to hepatic artery
What is haemochromotosis? Diagnosis?
Hereditary, autosomal recessive mutation of the HFE gene
- Elevated ferratin (with high saturation - will be low or normal in inflammation)
- Gene analysis looking for mutation of genes - C282Y is most common
Seconday haemochromotosis:
- Blood disorders that require repeated blood transfusion
Drugs causing hepatitis?
- Paracetamol overdsose
- Many others: present with cholestasis, mixed but predomionantly hepatitis
- Causes of AST and ALT in the 1000s?
- AST and ALT in the 100s?
- AST > 2x ALT?
- Viral, ischaemic or paracetamol
- Can be anything….
- Usually suggests alcoholic hepatitis (AST/ALT ratio reversal)
What can we assess from the Bilirubin, Albumin, PR and CBC?
If bilirubin is elevated/ patient is jaundice it suggests they have severe inflammation or decompensated cirrhosis (rise in Bilirubin with only slight hepatitis is indicative of liver impairment)
Albumin looks at the synthetic function of the liver, low albumin suggests possible cirrhosis - normal PR suggests NO acute liver failure
Low platelet count in the context in CLD indicates portal hypertension leading to splenomegaly caused by cirrhosis
Investigations to follow Blood tests for suspected cirrhosis?
Ultrasound looking for gall stones and any obstruction of bile duct
Hepatitis Serology:
HAV IgM (current), IgG (past)
HBV sAg (current), sAb (immunised or past), cAb (past infection)
anti-HVC Ab (past or current) - send further for RNA
Iron studies
Autoantibodies
Diagnosis of Cirrhosis?
Using US NOT to lookm at the liver but rather using doppler to look at blood flow and also at the spleen for signs of splenomegaly
Fibroscan to measure the stiffness of the liver - used over biopsy
Cause of short history of abdominal distension in patient with previosly diagnosed cirrhosis? LFT show mildly elevated biliruubin, GGT and AST with low albumin and platelet count as well.
Portal hypertension due to Cirrhosis - The LFTs are not massively elevated as you need normal cells for this and his liver is massively fibrosed and so not producing these enzymes nor performing its syntheic function indicated by the low albumin.
Ascites and low platelet count are caused by portal hypertension
Treatment of portal hypertension?
- Diuretics for ascites (eg. spironolactone)
- Proteion supplements to improve nutrition and albumin
- Stop alcohol consumption
Complications of progressive liver failure? Acute illness - LFTs and bloods? Treatement?
Often even with no further insults to the liver, cirrhosis can worsen and with the introduction of a new illness like pneumonia they can decompensate and become actuely unwell.
- LFTs show elevated bilirubin, GGT, AST and ALT as well as low albumin
- Prothrombin ration is elevated indicating acute liver failure on top of chronic liver cirrhosis
- Neutrophils and up due to infection (eg. pneumonia) and platelts are low still due to portal hypertension
Treatment: IV antibiotics, IV fluids, Lactulose and fleet enema for HE, NG feeding
Over 5 days post treatment:
- Pnemonia is improving
- HE still present
- Liver function worsening withh higher Bili, GGT, AST, ALT and PR from 1.9→2.1
- Code red in the night as hi BP drops and HR raised to 140
- Peripheries cold
???
Further complications 3 days later - abd pain tender on palpation?
Variceal bleed due to portal hypertension
3 days later he has developed SBP - spontaneuos bacterial peritonitis = only develops in people who have ascites from liver failure (diagnosed from ascitic tap)
- start AB then get a culture
- Occurs due to an impaired gut barrier not from rupture or damage
