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Gastroenterology > Acute and chronic liver diseases > Flashcards

Acute and chronic liver diseases Flashcards

1
Q

what is acute liver failure?

A

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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2
Q

what are the causes of acute liver failure?

A 
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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3
Q

what is the classification of acute liver failure?

A

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

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4
Q

what are the S&S of acute liver failure?

A 
Jaundice 
hepatic encephalopathy 
abdo pain 
N&V
malaise 
hepatomegaly (viral infection) 
fetor hepaticus
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5
Q

what investigations should be done in acute liver failure?

A

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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6
Q

what is the treatment of acute liver failure?

A

ICU management

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

Liver transplant assessment

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7
Q

what is the treatment for paracetamol induced acute liver failure?

A

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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8
Q

how should autoimmune hepatitis induced acute liver failure be treated?

A

methylprednisolone

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9
Q

what are the complications of acute liver failure?

A

Cerebral oedema - 20 degree head tilt

Ascites

Renal failure

coagulopathy and bleeding

encephalopathy

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10
Q

what receptors does alcohol work on?

A

GABA type A leading to downregulation

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11
Q

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

A 
agitation 
sweating 
tremor 
delirium 
seizures 
hallucinations 
N&V
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12
Q

what type of seizures are seen in alcohol withdrawal?

A

Generalised tonic clonic

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13
Q

what investigations should be carried out in suspected alcohol withdrawal?

A

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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14
Q

what is the treatment of alcohol withdrawal?

A

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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15
Q

What are the three stages of alcoholic liver disease?

A

steatosis
alcoholic hepatitis
alcoholic liver cirrhosis

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16
Q

what the S&S of alcoholic liver disease?

A 
RUQ pain 
hepatomegaly 
palmar erythema 
jaundice 
splenomegaly 
caput medusae
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17
Q

what are the investigations and findings for ALD?

A

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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18
Q

What are the treatment options for ALD?

A

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

19
Q

What is the aetiology of NAFLD?

A 
Obesity 
DM 
Dyslipidaemia 
Wilson's disease 
Paraenteral feeding 
drugs e.g amiodarone, MTX, tetracycline
20
Q

what are the S&S of NAFLD?

A 
Presence of RFs 
no significant alcohol intake 
fatigue and malaise 
RUQ pain 
hepatomegaly 
truncal obesity 
jaundice 
signs of liver dysfunction
21
Q

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

A

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

22
Q

what might liver imaging and biopsy show in NAFLD?

A

diffuse hyperechogenic echotexture

increased liver echotexture compared to kidneys

Vascular blurring

deep attenuation

biopsy shows steatosis, fibrosis or cirrhosis

23
Q

what are the treatment options for NAFLD?

A

lifestyle modifications

Vitamin E - alpha tocopherol

Weight loss - orlistat is pharmacological option

Gastric bypass

Metformin

statins

TIPS or transplant

24
Q

What is the definition of cirrhosis?

A

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

25
Q

what are some causes of cirrhosis?

A 
ALD 
NAFLD 
chronic viral hepatitis 
PBC and PSC 
haemachromatosis 
Wilson's disease
26
Q

what happens in the pathophysiology of cirrhosis?

A

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

27
Q

what are the clinical signs of cirrhosis?

A 
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
28
Q

what would investigations of cirrhosis find?

A

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

29
Q

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

A

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

30
Q

How is cirrhosis managed?

A

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

31
Q

what are the complications of cirrhosis?

A

ascites
portal HTN and varices
HCC
hepatorenal syndrome

32
Q

how is cirrhosis graded?

A

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
33
Q

how is ascites diagnosed and treated?

A

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
34
Q

what are the S&S of SBP?

A

abdo pain, fever, vomiting, confusion and GI bleed

35
Q

how is SBP diagnosed?

A

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

culture bacteria?

36
Q

what is the treatment of SBP?

A

IV amox and temo

37
Q

what are the usual organisms in SBP?

A

E.coli, klebsiella or streps

38
Q

what is hepatorenal syndrome and how is it treated?

A

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
39
Q

what is Korsakoff syndrome?

A

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

40
Q

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

A

retrograde and anterograde amnesia
confabulation
lack of insight

treated with thiamine infusion, nutritional and fluid support

41
Q

what is Wernickes encephalopathy?

A

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).

42
Q

what are the features of Wernickes encephalopathy?

A

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

treated with thiamine

43
Q

what are the features of acute hepatitis?

A

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

44
Q

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

A

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

Gastroenterology (5 decks)

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