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Acutely Ill Patient > Jaundice > Flashcards

Jaundice Flashcards

1
Q

At what level of bilirubin does jaundice become noticeable to a patient?

A

> 50umol/L

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2
Q

Important points in the history of a jaundiced patient…

A
  • Pruritus (normally only seen in post-hepatic jaundice)
  • Pain - painful jaundice may be due to gallstones, painless is a red flag
  • Flu-like illness - may indicate Gilbert’s syndrome or viral hepatitis
  • Foreign travel - risk of Hep A, B
  • Alcohol consumption - alcoholic liver disease
  • Drug abuse - acute liver failure
  • Previous blood transfusions - haemolytic transfusion reaction (pre-hepatic jaundice)
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3
Q

Painless jaundice is a red flag for…

A

Ca Pancreas

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4
Q

What are the pre-hepatic causes of jaundice?

A
  • Haemolysis - accquired (drug-induced, or autoimmune haemolytic anaemia) and congenital (G6PD deficiency)
  • Defective bilirubin conjugation - Gilbert’s Syndrome
  • Neonatal jaundice
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5
Q

What are the intra-hepatic causes of jaundice ?

A
  • Alcoholic/ non-alcoholic fatty disease
  • Drug toxicity
  • Viral hepatitis
  • Malignancy
  • Rare causes e.g. Wilson’s disease, Budd-Chiari
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6
Q

What are the extra-hepatic causes of jaundice?

A
  • Intraluminal= gallstones
  • Transmural= PBC, PSC, strictures
  • Extraluminal= pancreatic tumour
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7
Q

What medications can cause jaundice?

A
  • Antibiotics e.g. flucloxacillin, co-amoxiclav
  • OCP
  • Antidepressants
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8
Q

Raised ALP and GGT suggests…

A

Obstructive jaundice or biliary pathology

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9
Q

AST>ALT suggests…

A

Cirrhosis

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10
Q

ALT>AST suggests…

A

Hepatocellular damage

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11
Q

What is included in a liver screen?

A
  • Viral serology
  • Autoimmune/vasculitic screen: ANA,AMA,SMA, LKM, IgG, IgM
  • Caeruloplasmin levels and urinary copper
  • Ferritin and total iron binding capacity (TBIC)
  • Alpha-1 antitrypsin deficiency
  • Paracetamol level and toxicology screen
  • AFP levels
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12
Q

What are the management principles of acute liver failure?

A
  • Distributive shock: haemodynamic vasodilation - important to catheterise and monitor hourly urine output, CVP and MAP should be monitored. Fluid resuscitation and inotropic support
  • Low albumin - give 20% human albumin solution (HAS) to maintain intravascular volume
  • Vit K 10mg/kg/day IV 3 days- to increase PT/ INR
  • Infection should be prevented - give prophylactic IV fluconazole / cefuroxime
  • Ulcer prophylaxis: IV H2 antagonists , IV/oral PPI
  • Hepatic encephalopathy: Lactulose/ Neomycin (reduces ammonia gut absorption)
  • AKI treatment is with haemodialysis
  • Transplantation may be required in the rare cases
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13
Q

What are the KCH criteria for transplant listing?

A
  • INR> 6.5 with encephalopathy

- Encephalopathy plus three of: age >40, jaundice to encephalopathy in <7d, bilirubin> 300umol/L, INR>3.5

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14
Q

What is the maximum therapeutic dose of paracetamol?

A

4g per day i.e. 8 x 500mg tablets

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15
Q

What is the pathophysiology of paracetamol OD?

A

Depletion of glutathione (which normally binds to toxic NAPQI metabolite allowing it to be safely excreted) –> leads to build up of NAPQI

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16
Q

Risk factors for paracetamol toxicity…

A
  • Alcoholics
  • Patients on drugs which induce hepatic enzymes (anticonvulsants. rifampicin, St.John’s Wort)
  • Malnutrition
  • Cachexia
  • HIV
  • Cystic fibrosis
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17
Q

Clinical features of paracetamol OD…

A
  • Within first few hours: nausea, vomiting, abdominal pain
  • Within 24 hours: vomiting continues and pain and tenderness over liver
  • 2-4 days: jaundice
  • 1-3 days: hypoglycaemia –> may lead to coma
  • 3-5 days: hepatic encephalopathy
  • Renal failure may occur: loin pain, haematuria, proteinuria
  • Bleeding abnormalities from coagulation abnormalities and hyperventilation from metabolic acidosis
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18
Q

When is clinically significant toxicity considered unlikely?

A
  • Asymptomatic

- Undetectable paracetamol levels, normal LFTs/INR >24hrs after last dose

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19
Q

When can paracetamol levels be accurately measured?

A

> 4hrs after ingestion of paracetamol

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20
Q

When should NAC be given?

A
  • Plasma paracetamol level above treatment line on plasma concentration/time graph
    Can only be given 4 hrs after ingestion (when levels can be checked) - when plasma paracetamol >100mg/kg
  • Patients presenting >8 hrs after overdose - need to establish if ingested >150mg/kg, then give NAC
  • In a staggered overdose - better to give NAC straight away, before plasma paracetamol levels return
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21
Q

What is the NAC regime for paracetamol OD?

A
  • BAG 1 : 150mg/kg NAC in 200ml 5% glucose - delivered over 1 hr
  • BAG 2 : 50mg/kg NAC in 500ml 5% glucose - delivered over 4 hrs
  • BAG 3 : 100mg/kg NAC in 1L 5% glucose - delivered over 16 hrs
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22
Q

What antihistamine is normally given for a hypersensitivity reaction from NAC?

A

Chlorphenamine 4mg every 4-6 hrs

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23
Q

What are the KCH criteria for transplant listing in paracetamol OD patients?

A 
- pH<7.25 after 24 hrs 
OR all of...
- INR > 6.5
- Creatinine >300umol/L
- High grade encephalopathy
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24
Q

What is the clinical presentation of Hep A?

A
  • Jaundice
  • Tender hepatomegaly
  • Infective prodrome of around 6 weeks (malaise, joint pain, fever)
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25
Q

What is the treatment for Hep A?

A
  • No specific treatment

- High dose steroids if there is prolonged cholestasis

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26
Q

What three markers are important for diagnosis of Hep B?

A
  • HbsAg = active infection due to presence of surface antigens
  • HbeAg= envelope antigen
  • anti-HBc IgM = acute infection
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27
Q

What is the treatment for fulminant hep B?

A

Lamivudine (anti-viral)

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28
Q

What is seronegative hepatitis?

A

Considered a common cause of acute liver failure that is usually a diagnosis of exclusion.
May be related to autoimmune/ viral/ medication/ toxin damage

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29
Q

What is Wilson’s disease?

A

Autosomal recessive inherited disorder of copper excretion –> there is impaired incorporation of copper into caeruloplasmin (major copper conjugating protein in blood)–> means that copper builds up in the tissues as it is not excreted in the bile.

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30
Q

What happens in Wilson’s disease?

A
  • Liver: ALF, cirrhosis, portal HTN, acute hepatitis
  • Brain: parkinsonism, behavioural changes, cognitive impairment, dysarthria, dyskinesia
  • Blood: Coombs neg, haemolytic anemia is common
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31
Q

Wilson’s disease diagnosis…

A
  • Kayser-Fleischer rings (copper rings aorund iris)
  • 24 hr urine copper excretion (>100 micrograms/24 hrs)
  • Low caeruloplasmin (<200mg/L)
  • Low serum copper (<11umol/L)
  • Positive liver histology
  • Genetic analysis
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32
Q

Management of Wilson’s disease…

A
  • Diet: avoid foods with high copper content
  • Drugs: lifelong penicillamine (500mg/ 6-8h PO for 1 yr) - promotes urinary excretion of copper
  • Liver transplantation
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33
Q

What is Budd Chiari Syndrome?

A

Occurs when there is obstruction of hepatic veins by thrombus formation or tumour.

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34
Q

Clinical features of Budd Chiari?

A
  • Abdominal pain
  • Hepatomegaly
  • Ascites
  • Increased ALT
  • Portal hypertension
35
Q

Causes of Budd Chiari ?

A
  • Hypercoaguable states e.g. combined OCP, pregnancy, polycythaemia, thrombophilia
36
Q

Diagnosis of Budd Chiari?

A
  • Doppler USS
  • CT with contrast
  • Venography
37
Q

Management of Budd Chiari?

A
  • Thrombolysis and anticoagulation is required if thrombus formation present - may need to be lifelong
  • Liver transplantation may be required
  • TIPSS is effective in reducing portal HTN
38
Q

What is the progression of chronic liver failure?

A

Steatosis–>inflammation leading to fibrosis –> cirrhosis

39
Q

What is the hallmark sign of cirrhosis?

A

Scar tissue replacing normal healthy liver parenchyma

40
Q

Presentation of chronic liver failure…

A

This is dependent on the potential systems and processes affected:

  • Sx caused by liver failure: palmar erythema, jaundice, spider naevi, gynaecomastia, hepatomegaly, ascites
  • Sx caused by portal hypertension: splenomegaly, oesophageal varices, caput medusa (dilated periumbillical collateral veins)
  • Sx of unknown cause: clubbing, duppurteyne’s contracture,
  • Sx of advanced disease: bruising and bleeding, hepatic encephalopathy, AKI, cachexia
41
Q

What is the best imaging modality for chronic liver failure?

A

Abdominal USS - can image the liver, biliary tree and vessels

42
Q

What is the Child-Pugh score?

A

Method of assessing the prognosis of chronic liver disease - mainly cirrhosis.
Categorised into A, B and C : points are assigned to different parameters - encephalopathy, ascites, bilirubin, albumin and PT
A= least severe liver disease –> C= most severe liver disease

43
Q

What is hepatorenal syndrome?

A

When cirrhosis leads to splanchnic and systemic vasodilation –> hypovolaemia occurs–> RAAS activated to increase CO and BP –>renal vasoconstriction occurs–> causes renal injury.
There is also involvement of inflammatory cytokines in the renal vasoconstriction.

44
Q

Routine outpatient follow up for chronic liver disease pts…

A
  • HCC screening –> 6-monthly abdominal USS and AFP

- Variceal screening –> gastroscopy every 1-3 years

45
Q

What is acute alcoholic hepatitis?

A

Acute hepatitis commonly seen after a few weeks of alcohol abstinence. Concomitant cirrhosis seen in 50-60% of patients.
Presents with jaundice,RUQ pain, fever, deranged LFTs

46
Q

What can be given for pruritus associated with jaundice?

A

Cholestyramine - bile acid sequestrant which prevents reabsorption in the GIT.

47
Q

What is the hepatic venous pressure gradient?

A

Difference in pressure between portal vein and IVC - used to determine severity of portal hypertension.

48
Q

What is the clinical measure of portal hypertension?

A

HVPG >5mmHg : increase >5mmHg in portal venous pressure.

49
Q

Anatomical function of portal vein…

A

Portal vein is responsible for transporting blood from the GIT, gallbladder, pancreas and spleen to the liver.
Around 75% of blood flow to the liver is from the portal vein - other 25% coming from hepatic artery.
Is the conduit of the superior mesenteric vein (GIT blood) and splenic vein (splenic blood).
Not a true vein as it delivers blood to the CAPILLARY BEDS instead of the HEART…

50
Q

Causes of portal hypertension…

A

Pre-hepatic: portal vein thrombosis, splenic vein thrombosis
Intra-hepatic: cirrhosis (increase in intra-hepatic resistance), schistosomiasis, hepatitis
Post-hepatic: Budd-Chiari, cardiac failure (RHF)

51
Q

Complications from portal hypertension…

A
  • Varices due to porto-systemic shunting at; oesophagus (gastro-oesophageal varices), umbilicus (caput medusae), rectum (haemorrhoids)
  • Ascites - due to splanchnic vasodilation leading to salt and water retention
  • Renal failure
52
Q

Management of varices…

A

Grade 2 or above: long-term beta blocker therapy (propranolol 40mg or carvedilol)
Secondary prophylaxis after variceal bleed = variceal banding or TIPSS

53
Q

Treatment of hepatocellular carcinoma …

A
  • Surgical resection
  • Transarterial chemoablation / radiofrequency ablation used in patietns that cannot tolerate surgery
  • Hepatic transplantation for 3 or less small tumours
54
Q

Management of chronic hep B infection?

A
  • Raised ALT = antivirals e.g. lamivudine, tenofovir

- Normal ALT = ALT, HBV DNA, and HCC screening (USS and AFP) every 6 months

55
Q

Management of chronic hep C infection?

A
  • Genotype 1 Hep C = 48 weeks of peg-interferon alpha and ribavarin
  • All other phenotypes = 24 weeks of peg-interferon alpha and ribavarin
56
Q

What is autoimmune hepatitis?

A

Inflammation of the liver caused by abnormal T cell function and autoantibodies directed against hepatocyte surface antigens.

57
Q

Presentation of AIH…

A
  • 40% present with: acute hepatitis and signs of autoimmune disease e.g. fever, malaise, polyarthralgia, pleurisy
  • 60% present with: jaundice or asymptomatic
58
Q

Diagnosis of AIH…

A
  • Bilirubin, AST, ALT, ALP raised
  • Raised IgG
  • Autoantibody tests : AMA, ANA , LKM (different types of AIH dependent on autoantibodies present)
59
Q

Different types of AIH…

A

Type 1: 80% of patients - ASMA, ANA, IgG positive

Type 2: LKM positive, ASMA and ANA negative

60
Q

Treatment of AIH…

A

Immunosuppression with Prednisolone 30mg/d PO for one month –> decreasing by 5mg per month to maintenance dose of 5-10mg/d PO
Azathioprine 50-100mg/d PO can be added to maintain remission

61
Q

Pathophysiology of PBC…

A

Destruction of interlobular bile ducts by autoimmune granulomatous inflammation –>progresses to intrahepatic cholestasis–> liver damage

62
Q

Diagnosis of PBC…

A
  • Raised IgM and AMA +ve = hallmark ,

- Liver biopsy may reveal granuloma formation but this will not be uniform across the whole liver

63
Q

Presentation of PBC…

A
  • Lethargy
  • Pruritis
  • Usually in middle-aged women
64
Q

Management of PBC…

A
  • Ursodeoxycholic acid 15mg/kg/day - reduces likelihood of transplantation and death
  • Immunosuppression can be used (to dampen autoimmune activity)
  • Pruritis eased with cholestyramine
  • Fatigue is managed with modafinil
65
Q

Pathophysiology of PSC…

A

Stricture and fibrosis of the intra and extra hepatic ducts which lead to obstruction of bile flow –> back up of bile into the liver –> intrahepatic cholestasis–>fibrosis-> cirrhosis

66
Q

What condition is PSC strongly associated with?

A

Ulcerative colitis - thought to have similar autoimmune pathology

67
Q

Diagnosis of PSC…

A
  • MRCP
  • Cholestatic LFTs (raised ALP and GGT)
  • -ve AMA
  • +ve ANA, SMA and pANCA
  • Liver biopsy used to stage disease (fibrosis and strictures seen)
68
Q

Management of PSC…

A
  • Liver transplantation is the only definitive treatment - PSC can recur after transplantation
  • Symptomatic relief available e.g. cholestyramine for pruritis
  • Ursodeoxycholic acid may improve LFTs but no proven benefit to survival
69
Q

Complications of PSC…

A
  • Cholangiocarcinoma
  • Gallbladder, liver and colon cancers are also more common
  • Need yearly USS and colonoscopy screening
70
Q

What is the progression of alcoholic liver disease?

A

Steatosis–> alcoholic hepatitis –>alcoholic cirrhosis –> liver failure

71
Q

What happens in alcoholic steatosis?

A

Steatosis is the first response to large doses of alcohol leading to fatty liver changes
It is normally an asymptomatic phase that can resolve entirely and rapidly with alcohol abstinence

72
Q

Spectrum of NAFLD…

A

Normal liver –>steatosis–>inflammation and fibrosis (non-alcoholic steatohepatitis=NASH) –> cirrhosis
NASH spectrum= no fibrosis –>NASH with increasing fibrosis –> NASH with cirrhosis
*NAFLD = increased fat in hepatocytes

73
Q

Risk factors for NAFLD…

A

METABOLIC SYNDROME - 3 out of 5 of:

  • Diabetes
  • Hypertension
  • Hyperlipidaemia
  • Hypertriglyceridaemia
  • Obesity (visceral fat levels = biggest RF)
74
Q

Diagnosis of NAFLD…

A
  • USS will show fatty changes in the liver
  • Raised LFTs (normally ALT>AST) seen with inflammatory changes
  • Liver biopsy or fibroscanning may be required for staging of the disease
75
Q

Management of NAFLD…

A
  • Lifestyle modifications e.g. weight loss
  • Liver directed medical management e.g. thiazolidinediones, GLP -1 agonist (anti-diabetic medication)
  • Bariatric surgery -gastric banding
76
Q

What are the two types of haemochromatosis?

A
  • Primary = hereditary condition - C28Y mutation of HFE gene leading to increased intestinal uptake of iron
  • Secondary = repeated blood transfusion, excess iron intake
77
Q

Presentation of haemochromatosis…

A 
Early = tiredness, arthralgia 
Later= slate-grey skin pigmentation, hepatomegaly, cirrhosis, cardiomyopathy
78
Q

Diagnosis of haemochromatosis…

A
  • Raised serum ferritin and transferrin saturation

- Liver biopsy =gold standard

79
Q

Management of haemochromatosis…

A
  • Regular venesection - about 1 unit of blood every 1-3 weeks until ferritin <50 mcg/L, and Hb low end of normal range (maintenance venesection required for life as iron will continue to accumulate in hereditary type)
  • Desferrioxamine infusions 3 times weekly - used when venesection not tolerated
80
Q

What is the pathophysiology of alpha-1 antitrypsin?

A

Alpha-1 antitrypsin = glycoprotein made in the liver that controls inflammatory cascades
Deficiency of this protease inhibitor leads to increasing levels of neutrophil elastase in the tissues, causing liver and lung damage
*Main cause of liver disease in children

81
Q

Presentation of alpha-1 antitrypsin deficiency…

A
  • COPD like symptoms (dyspnoea) and chronic liver disease (cirrhosis and jaundice)
82
Q

Diagnosis of alpha-1 antitrypsin deficiency…

A
  • Alpha-1 antitrypsin <11umol/L
  • Lung function tests will show reduced FEV1
  • Liver biopsy may show signs
83
Q

Management of alpha-1 antitrypsin deficiency…

A
  • Smoking cessation (preventing further lung insult)
  • Alcohol abstinence (preventing further liver insult)
  • Vaccine prohpylaxis for lung infections
  • Liver and lung transplantation may be required for treatment of advanced disease
  • Screening for HCC - affects 25% of patients >50 y/o

Acutely Ill Patient (16 decks)

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