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Liver disease Flashcards

1
Q

What happens in cirrhosis?

A
  • liver gets small and shrunken

- reduced liver blood flow, reduced metabolic function and reduced plasma proteins

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2
Q

What is happening if the oral dose of a drug is much higher than the IV dose?

A

first-pass metabolism in the liver

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3
Q

How is alcohol metbaolised?

A

by first-order until a set point then it is by zero order

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4
Q

What happens in liver disease with RAS?

A

there is an increase in renin

there is a decrease in the metabolism of aldosterone so there is secondary aldosteronism

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5
Q

What can happen to the kidneys in liver disease?

A
  • too much angiotensin 2 (vasoconstrictor), aldosterone, SNS and ADH
  • there is potassium loss, sodium retention and water retention
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6
Q

What are the consequences of moderate hepatic impairment?

A

gut oedema, liver and kidney congestion, gross oedema and ascites and CHF

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7
Q

Why are NSAIDs not used in liver disease?

A
  • get rid of renal prostaglandins
  • so harm kidneys and cause ulcers and bleeding
  • increase blood pressure
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8
Q

What must always be prescribed with an NSAID?

A

a PPI

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9
Q

What is the summary of drug metabolism?

A
  • phase 1 is P450 biotransformation

oxidation, reduction and hydrolysis

  • phase two is conjugation
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10
Q

How can paracetamol be dangerous?

A

can make a dangerous substance which is removed by out glutathione stores

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11
Q

What is the rule used to assess drug-induced liver disease severity?

A

Hy’s Rule

- uses ALT/AST and Bilirubin as parameters

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12
Q

What is the diuretic used in liver disease and how is this administered?

A
  • Spironolactone as it removes secondary aldosteronism

- 1kg/day weight loss of fluid is ideal

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13
Q

What is given to sedate patients with liver disease?

A

Phase 2 metabolised benzodiazepines eg Lorazepam

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14
Q

What are the features of Hep A?

A
  • faecal-oral spread
  • common in gay and IVDUs
  • acute not chronic
  • peak is in older children and young adults
  • confirmed by presence of IgM against Hep A
  • vaccine available
  • mild illness will usual full recovery
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15
Q

What are the features of Hep B?

A
  • sex, mother to child or by blood
  • chronic only if first exposure is in childhood
  • adults usually get acute
  • confirmed by presence of Hep B surface antigen (HBsAg)
  • carriers possible
  • antiviral therapy to those with liver inflammation and a high level of Hep B DNA
  • treat with vaccine, suppressive antivirals or peginterferon
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16
Q

What are the risk factors for Hep B?

A
  • people who live in affected areas
  • have multiple sexual partners
  • IVDUs
  • children of infected mothers
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17
Q

What are the features of Hep C?

A
  • no vaccine
  • transmission is blood or sex
  • test for antibody to virus then test for RNA by PCR
  • usually chronic
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18
Q

What are the features of Hep D?

A

only found with Hep B

makes acute or chronic Hep B worse

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19
Q

What are the features of Hep E?

A

Common in the tropics
Faecal-oral spread
More common than A
Caught from pigs
Genotypes in the tropics cause disease in pregnant women
No vaccine is available
Only chronic infection if there is an abnormal immune system

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20
Q

When is a viral infection classed as chronic?

A

over 6 months

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21
Q

Which Hep can spontaneously resolve?

A

Hep B not Hep C

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22
Q

What is the management of acute viral Hep?

A

monitoring for encephalopathy, resolution and vaccinate those at risk

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23
Q

What is the management of chronic viral Hep?

A

antivirals, vaccination, infection control, alcohol cessation and awareness and screening for hepatocellular carcinoma

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24
Q

Who is treated with antivirals?

A
  • chronic infection
  • inflammation is seen
  • if fit for treatment
  • HIV co-infection is difficult
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25
What are the common antiviral and their sideffects?
- infterferon alpha - peginterferon (flu symptoms) - ribavirin (anaemia) - sofosbuvir is active against all genotypes
26
What is compensated cirrhosis?
scarring in the liver without loss of normal functions such as metabolism and removal of toxins
27
When does liver disease become chronic?
6 months
28
What drug can cause cirrhosis?
methotrexate which is a treatment or rheumatoid arthritis and psoriasis
29
What is numerically classed as portal hypertension?
5-8mmHg
30
What are the clinical features of compensated cirrhosis?
normal from outside, found on imaging or labs, maybe portal hypertension, signs are spider naevi, clubbing, palmar erythema or none
31
What are the clinical features of decompensated cirrhosis?
liver failure present, end stage liver disease, signs are jaundice, ascites, encephalopathy or bruising
32
What are the complications of cirrhosis?
ascites, encephalopathy, variceal bleeding and liver failure
33
What is ascites caused by?
- increased number of vasodilators - enhanced sensitivity to these - resistance to vasoconstrictors
34
What is the diagnosis and management of ascites?
- diagnosis with shifting dullness - treat with spironolactone, paracentesis or TIPSS - stop drinking - sodium must be balanced
35
What is the diagnosis and treatment of encephalopathy?
- diagnosis is flap, neurology, ammonia | - treat with lactulose, Rifaxamin
36
What is the treatments for oesophageal varices?
- primary = beta blockers and ligation - acute = resuscitation, terlipressin, banding and TIPSS - emergency = balloon tamponade - secondary treatment = band ligation or beta blockers
37
What are the main benign liver lesions?
- haemangioma - focal nodular hyperplasia - hepatic adenoma - liver cysts - polycystic liver disease - abscess
38
What are the main malignant liver lesions?
- primary are hepatocellular carcinoma or cholangiocarcinoma | - metastases are common
39
What are the features of haemangioma?
``` common females single and small asymptomatic diagnosis is US, CTl, MRI no treatment ```
40
What are the features of focal nodular hyperplasia?
- benign nodule of normal liver tissue - central scar with artery radiating branches to periphery - young middle aged females - asymptomatic - diagnosis is US, CT, MRI or FNA - no treatment
41
What are the features of hepatic adenoma?
- proliferation of normal hepatocytes - females - associated with contraceptive hormones and anabolic steroids, - asymptomatic or RUQ pain - present with rupture or haemorrhage - diagnosis is US, CT, MRI, stop hormones - weight loss for treatment and remove in males as malignancy is more common
42
What are the types of liver cysts?
``` simple hydatid atypical polycystic lesion pyogenic/amoebic abscess ```
43
What are the types of polycystic liver disease?
-Von Meyenburg complexes (benign cystic nodules) -Polycystic liver disease -Autosomal dominant PK disease (treat with somatostatin)
44
What are the features of liver abscesses?
- high fever - leukocytosis - abdominal pain and complex liver lesion - treat with antibiotics, aspiration, echo then operation
45
What is the epidemiology, aetiology and presentation of hepatocellular carcinoma?
- men - most common primary cancer - risk factor is cirrhosis - presentation is abdo pain, RUQ, asymptomatic, worsening of chronic liver disease, cirrhosis signs, RUQ mass
46
Where do hepatocellular carcinoma metastases move to?
liver, portal vein, pymph, lung, bone and brain
47
What is the diagnosis and treatment of hepatocellular carcinoma?
- AFP is high - liver transplant, can use RF ablation or chemoembolization - sorafenib
48
What parts of the LFT are hepatocellular?
ALT and AST
49
What parts of the LFT are cholestatic?
ALP gGT Bilirubin
50
What does a raised ALT or AST say?
hepatocellular injury or hepatocellular necrosis
51
What would the LFTs be in cholestasis?
very raised ALP, gGT and Bilirubin | raised or normal ALT
52
What would the LFTs be in chronic hepatocellular damage?
normal or raised ALT, ALP, gGT and Bilirubin
53
What would the LFTs be in acute hepatocellular damage?
very raised ALT normal or raised ALP and gGT raised Bilirubin
54
What is acute liver disease?
- rapid development of liver disease without any previous liver damage which is less than 6 months - causing encephalopathy and prolonged coagulation
55
What are the true liver function tests?
- Bilirubin - Albumin - Prothrombin time
56
How does acute liver failure present?
jaundice, lethargy, nausea, anorexia, pain, itch, arthralgia and abnormal LFTs
57
What are some of the main causes of acute liver disease?
``` hepatitis drugs shock liver cholangitis alcohol malignancy chronic liver disease ```
58
What are some of the rarer causes of acute liver disease?
Budd Chiari, acute fatty liver of pregnancy or cholestasis of pregnancy
59
What are the main investigations for acute liver disease?
- HISTORY esp drug history - LFTs - prothrombin - examination - US including vascular - virology - investigations of chronic liver disease
60
What is the treatment for acute liver disease?
rest up to 3 months, fluids, no alcohol, increase calories, observe for FHF
61
What drugs can cause liver injury?
antibiotics (co-amox or fluclox), paracetamol, NSAIDs or statins
62
What is fulminate hepatic failure?
- a clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function - presents as an acute episode of severe liver dysfunction in a patient with a previous normal liver
63
What is FHF caused by?
paracetamol, fulminant viral, drugs, HBV or non A-E
64
What is the treatment for FHF?
supportive fluids renal replacement transplant

My Gastrointestinal (18 decks)

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