Acute and chronic liver diseases Flashcards by Ryan Kane

what is acute liver failure?

a rapid decline in hepatic function characterised by jaundice, coagulopathy and hepatic encephalopathy in patients with no evidence of prior liver disease

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what are the causes of acute liver failure?

Paracetamol OD 
Infections e.g viral hep, yellow fever, leptospirosis 
Primary bilary cirrhosis 
Haemachromatosis and Wilsons 
HELLP syndrome from pre-eclampsia

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what is the classification of acute liver failure?

Hyperacute if < 7 days
Acute if 8-28 days
Subacute if 29 days to 12 weeks

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what are the S&S of acute liver failure?

Jaundice 
hepatic encephalopathy 
abdo pain 
N&V
malaise 
hepatomegaly (viral infection) 
fetor hepaticus

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what investigations should be done in acute liver failure?

LFTs

Hyperbilirubinaemia
Elevated liver enzymes (in 1000s for paracetamol OD)

Coag screen + G&S

prolonged clotting
increased INR

U&E’s

elevated urea and creatinine (RF common complication)
metabolic derrangements

FBC

anaemia and thrombocytopenia
leucocytosis in infection

ABG and lactate

metabolic acidosis in paracetamol OD
elevated lactate

Paracetamol level

Urine toxicology

Liver screen

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what is the treatment of acute liver failure?

ICU management

mandatory when encephalopathy present
20 degree head up tilt
intubate, NG, IV fluids, catheter

Liver transplant assessment

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what is the treatment for paracetamol induced acute liver failure?

acetylcystiene 140mg/kg orally as loading dose then 70mg/kg every 4 hours after

150mg/kg IV over 60 mins then 12.5mg/kg/hr after

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how should autoimmune hepatitis induced acute liver failure be treated?

methylprednisolone

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what are the complications of acute liver failure?

Cerebral oedema - 20 degree head tilt

Ascites

Renal failure

coagulopathy and bleeding

encephalopathy

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what receptors does alcohol work on?

GABA type A leading to downregulation

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alcohol withdrawal typically occurs 6-12 hours after cessation of alcohol consumption. What are the S&S?

agitation 
sweating 
tremor 
delirium 
seizures 
hallucinations 
N&V

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what type of seizures are seen in alcohol withdrawal?

Generalised tonic clonic

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what investigations should be carried out in suspected alcohol withdrawal?

Calculate GMAWS
- looks at tremor, sweating, hallucination, agitation and orientation (TASHO)

VBG

can see respiratory alkalosis in DT
metabolic acidosis with hypochloraemia may occur because of vomiting
MA with high anion Gap can also occur if alcoholic ketoacidosis present

FBC

increased MCV in chronic alcohol use
thrombocytopenia

U&E’s
- low in any electrolytes due to poor nutrition

LFTs

elevated enzymes
AST:ALT of >2:1 in alcoholic liver disease
GGT >10x norm

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what is the treatment of alcohol withdrawal?

Manage in quiet room with low lighting and minimal stimulation

Rehydrate

Correct electrolyte abnormalities

Benzodiazepine, usually diazepam 10-20mg

thiamine replacement usually via pabrinex

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What are the three stages of alcoholic liver disease?

steatosis
alcoholic hepatitis
alcoholic liver cirrhosis

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what the S&S of alcoholic liver disease?

RUQ pain 
hepatomegaly 
palmar erythema 
jaundice 
splenomegaly 
caput medusae

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what are the investigations and findings for ALD?

LFTs and liver tests

AST:ALT >2:1
alk phos may be elevated
GGT elevated
bilirubin elevated
albumin low

FBC
- anaemia, thrombocytopenia, high MCV and possible leucocytosis

U&E’s and coag

electrolyte deficiencies
increased clotting time

Hepatic US
- hepatomegaly, fatty liver, cirrohosis, liver mass, evidence of portal HTN

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What are the treatment options for ALD?

alcohol abstinence and withdrawal management

weight reduction and smoking cessation

Nutritional supplementation and multivitamins

Immunisation

Sodium restriction and diuretics if ascites developing

Corticosteroids for severe ALD

What is the aetiology of NAFLD?

Obesity 
DM 
Dyslipidaemia 
Wilson's disease 
Paraenteral feeding 
drugs e.g amiodarone, MTX, tetracycline

what are the S&S of NAFLD?

Presence of RFs 
no significant alcohol intake 
fatigue and malaise 
RUQ pain 
hepatomegaly 
truncal obesity 
jaundice 
signs of liver dysfunction

What investigations are done in NAFLD and what do they show?

LFTs and liver synthetic test

AST:ALT of <1 (opposite of ALD)
elevated bilirubin
elevated alk phos
GGT may be slightly raised but no where near ALD levels
low albumin
increased coag time

FBC
- anaemia and thrombocytopenia

lipid panel

Increased TC, LDL or triglycerides
reduced HDL

Fasting insulin
- elevated in insulin resistance

Liver US and biopsy

what might liver imaging and biopsy show in NAFLD?

diffuse hyperechogenic echotexture

increased liver echotexture compared to kidneys

Vascular blurring

deep attenuation

biopsy shows steatosis, fibrosis or cirrhosis

what are the treatment options for NAFLD?

lifestyle modifications

Vitamin E - alpha tocopherol

Weight loss - orlistat is pharmacological option

Gastric bypass

Metformin

statins

TIPS or transplant

What is the definition of cirrhosis?

A diffuse pathological process characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules

what are some causes of cirrhosis?

``` ALD NAFLD chronic viral hepatitis PBC and PSC haemachromatosis Wilson's disease ```

what happens in the pathophysiology of cirrhosis?

hepatic stellate cells become activated and deposit collagen in the hepatic parenchyma and space of disse hepatic sinusoids lose their fenestration altering exchange between hepatocytes and plasma perturbed bloodflow in the liver leads to increased pressure in the portal venous system causing portal HTN and varices

what are the clinical signs of cirrhosis?

``` ascites jaundice leuconychia terry's nails (white prox but distal 1/3 red) clubbing palmar erythema spider naevi hepatosplenomegaly Dupuytrens contracture encephalopathy hepatic fetor parotid enlargement ```

what would investigations of cirrhosis find?

LFT's and liver synthetic function - increased AST and ALT - increased alk phos in cholestasis - increased bilirubin - increased GGT - albumin low - coag prolonged Liver US and biopsy - liver surface nodularity - architectural distortion U&E's - hyponatraemia common

what investigation can be used to elucidate the underlying cause of cirrhosis?

hepatitis virology - hep B and C TIBC, transferrin and ferritin - haemachromatosis Antinuclear antibody and anti smooth muscle antibody - AIHA Anti mitochondrial antibody - PBC serum ceruloplasmin - decreased in Wilson's disease

How is cirrhosis managed?

treat underlying cause Lifestyle changes Avoid alcohol, NSAIDS, paracetamol and hepatotoxic drugs Monitor for complications - endoscopy for varices and CT for HCC Sodium restriction and spiro in ascites liver transplant

what are the complications of cirrhosis?

ascites portal HTN and varices HCC hepatorenal syndrome

how is cirrhosis graded?

the Child's-Pugh score Takes into account bilirubin, albumin, prothrombin time, ascites and encephalopathy - grade A = 5-6 - Grade B = 7-9 - Grade C >10

how is ascites diagnosed and treated?

serum ascites albumin gradient (SAAG) of >11g/l with low ascitic fluid total protein ``` Restrict salt intake diuretics - spironolactone (can add furosemide if response poor) Large volume paracentesis Albumin replacement TIPS ```

what are the S&S of SBP?

abdo pain, fever, vomiting, confusion and GI bleed

how is SBP diagnosed?

ascitic tap - cloudy appearance with neutrophils >250cells/mm3 culture bacteria?

what is the treatment of SBP?

IV amox and temo

what are the usual organisms in SBP?

E.coli, klebsiella or streps

what is hepatorenal syndrome and how is it treated?

stage 2/3 AKI with ascitic cirrhosis, no shock and no underlying renal pathology - Broad Abx e.g cefotaxime - Fluids - Terlipressin - Ocreotide, midodrine and albumin

what is Korsakoff syndrome?

Korsakoff syndrome is an amnestic disorder caused by thiamine (vitamin B1) deficiency typically associated with prolonged use of alcohol.

what are the S&S of Korsakoff syndrome? How is it treated?

retrograde and anterograde amnesia confabulation lack of insight treated with thiamine infusion, nutritional and fluid support

what is Wernickes encephalopathy?

Wernicke's encephalopathy is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1).

what are the features of Wernickes encephalopathy?

classical triad of ophthalmoplegia (eye movement disorders), ataxia and confusion treated with thiamine

what are the features of acute hepatitis?

Fever, malaise, anorexia, nausea, arthralgia—then: jaundice (rare in children) hepatosplenomegaly, and adenopathy.

what are the immunological and LFT markers for the major viral hepatitis'

A = V. high AST and ALT. IgM peaks at 6 weeks then falls, IgG remains high for life B = • sAg - Surface antigen – marker of infection • sAb – Surface antibody – marker of immunity • cAb – Core antibody * eAg – e antigen – suggests high infectivity * eAb – e antibody – suggests low infectivity • HBV DNA HBV infection is diagnosed if sAg or DNA are detectable C = Anti HCV IgG positive = chronic infection or cleared infection PCR or Antigen positive = current infection / viraemia