Liver Disease Flashcards
Why does ascites start to develop in liver disease?
Portal hypertension and low albumin resulting in blood being pushed out
What drugs should you be careful of in liver disease?
Drugs that are highly metabolised as if the liver is damaged there will be less metabolism so can reach toxic levels. General clue: is the oral dose considerably higher than the IV dose?
Circulation changes in liver disease:
Low ___1____ will result in low plasma levels so the kidneys will produce more renin.
However, aldosterone cannot be metabolised by the damaged liver so will get _____2_______
This results in really low _______ as aldosterone pushes out potassium as it reabsorbs sodium (check this)
Will also get an increase in other hormones such as __________4____________ as these cannot be metabolised
There is also more __5__ produced due to low plasma volume.
Ultimately __________6_____________________
1) Albumin
2) secondary aldosteronism
3) potassium
4) endothelin and oestrogen and other sex hormones
5) ADH
6) there is sodium and water retention and potassium loss as well as lots of vasoconstriction in the kidneys.
What does albumin do?
What are consequences of a low albumin?
It is a plasma protein involved in maintaining oncotic pressure (ie its presence draws in fluid from the capillaries). It also binds many substances to it.
If there is low albumin will get low plasma levels. As many things travel bound to albumin these will also be free in the blood.
What are spider naevi? Why do you get them in liver disease?
Swollen blood vessels beneath the skins surface. They are caused by increased oestrogen, this happens in liver disease as the damaged liver cannot metabolise the oestrogen resulting in an increase.
In practice which drugs can and cannot be prescribed for liver disease?
• Paracetamol 1g twice daily – ‘Lesser of all evils’ – Do not exceed 3 g daily, avoid prolonged use • Codeine 30mg three times daily – Watch out for sedation • Avoid NSAIDs
Why can’t you give NSAIDs?
Renal PGE synthesis is decreased so: – Worsen renal impairment – Further sodium retention – Risk of hepato-renal syndrome – Worsening of CHF
(prostaglandins in the kidney usually cause vasodilation)
Why can’t you give opiates?
Act on brain- with liver disease have a hypersensitive brain
When paracetamol is metabolised the highly reactive intermediate reacts with ____1____. However, glutathione is finite and if you run out of stores ________2____________
1) glutathione
2) you’ll start to damage your liver.
Paracetamol overdose is treated with
Methionine
Most common drug induced hepatitis are caused by?
Amoxicillin and Clavulanic Acid
What is the best diuretic for those with liver disease? Why ?
Spironolactone as this is an aldosterone antagonist
Loop and Thiazide diuretics would increase hypokaelamia. Loop also causes reduced intra-vascular volume.
What drugs can be used for sedation in liver disease?
• Phase II metabolised benzodiazepines
– Lorazepam
– Oxazepam
– Lormetazepam
Antibiotics that may need to be avoided in liver disease?
- Aminoglycosides are nephrotic
- Quinolones are epileptogenic (could cause an epileptic attack)
- Metronidazole reduced metabolism
When is jaundice detectable clinically?
When serum bilirubin is more than 50 micro mol/l
What is the outcome of chronic liver disease?
Cirrhosis. There are liver diseases that affect the liver chronically but if they don’t lead to cirrhosis they are not classed as chronic liver disease.
What is NAFLD?
Non-alcoholic fatty liver disease- a fatty liver/ steatohepatitis in the absence of another cause
Risk factors for NAFLD?
Obesity, hypertension, type 2 diabetes and hyperlipidaemia
Presentation of NAFLD?
Often asymptomatic unless present late with liver fibrosis and failure
Diagnosis of NAFLD and NASH?
NAFLD by ultrasound and NASH by liver biopsy
Main treatment of NAFLD and NASH?
Weight loss and exercise
What is primary biliary cholangitis (cirrhosis)?
An auto-immune disorder that leads to progressive destruction of the small bile ducts leading to cirrhosis
Who classically gets primary biliary cholangitis?
Middle aged women
What antibodies will those is PBC have?
anti-mitochondrial antibodies (AMA)
Presentation of PBC?
May be asymptomatic. Symptoms include fatigue, itch without rash and xanthelasma and xanthoma
Treatment of PBC?
In early disease can give ursodeoxycholic acid or Obeticholic acid. Also may want to give symptomatic control for the itch. Advanced disease is an indication for liver transplant.
What is autoimmune hepatitis?
Progressive inflammatory autoimmune condition thought to be T cell mediated.
Who commonly gets autoimmune hepatitis?
More common in females and is associated with other autoimmune conditions
Presentation of autoimmune hepatitis?
In post menopausal groups it may be asymptomatic. In early teens and twenties it often presents acutely:
Hepatomegaly, splenomegaly, elevated ast and alt, elevated pt, malaise, fatigue, leathery, nausea, abdominal pain and anorexia.
What will biopsy of auto immune hepatitis show?
Marked piecemeal necrosis
Treatment of autoimmune hepatitis?
Prednisolone and Azathioprine
Liver transplant may be needed but there is a risk the disease recurs in the transplant
What is primary sclerosing cholangitis?
Autoimmune chronic liver disease characterised by fibrosing inflammatory destruction of both intra and extra hepatic bile ducts
Who commonly gets primary sclerosing cholangitis?
More common in men and there is a strong correlation with ulcerative colitis and IBD
Presentation of primary sclerosing cholangitis?
Usually detected at asymptomatic stage due to increased screening of those with IBD- abnormal LFTs usually a raised ALP
Symptomatic presentation is with a fluctuating pruritus, jaundice and cholangitis
Diagnosis of Primary sclerosing cholangitis?
Can be identified on MRCP and histopathology shows inflammation of the intrahepatic biliary radicles with associated scar tissue “onion skin” appearance.
Treatment for primary sclerosing cholangitis?
Only proven treatment is a liver transplantation. Also need to screen for cholangiocarcinoma as those affected are at increased risk.
Clinical manifestations of haemochromatosis? Who are they more common in?
Liver disease
Very late on bronzed skin, hepatomegaly and diabetes
More common in men as have no physiological blood loss
Haemochromatosis is
iron storage disorder resulting in deposition in several organs
Wilsons disease is
copper metabolism error resulting in copper deposition in organs
Symptoms of Wilsons disease
twitching. kaiser fleisher ins in eyes (gold rings) and hepatic issues
Management of haemochromatosis
Venesection weekly
Management of wilsons disease
lifelong copper chelating drugs e.g. penicillamine
AAT deficiency is
deficiency in alpha 1 antitrypsin an anti protease meaning that you get uncontrolled protease activity resulting in damage to lung and liver tissue. Emphysema and liver problems.
Is there a treatment for AAT
no
What is Budd-Chiari Syndrome?
Condition where there is obstruction to the venous outflow of the liver owing to the occlusion of the hepatic vein
Causes of Budd-Chiari Syndrome?
Congenital webs, thrombotic tendency, protein C or S deficiency
Presentation of Budd-Chiari Syndrome?
Acute presentation is with jaundice and tender hepatomegaly
chronic presentation is usually ascites
In Budd-Chiari syndrome what lobe is usually spared?
Caudate lobe
Treatment of Budd-Chiari Syndrome?
In acute situation thrombotic therapy can be given. Ascites should be treated as well as any underlying cause. Congenital webs treated radiologically or resected surgically. TIPs treatment. Liver transplantation for chronic disease. Life long anti-coagulation is mandatory following TIPs and transplantation.
Two drugs that can be given in variceal rupture?
Terlipressin or somatostatin (this is given if can’t give terlipressin usually)
Management of acute variceal bleed?
Resuscitation
Urgent endoscopy where will try to band or ablate etc and will also give terlipressin and somatostatin
Balloon tamponade is done if endoscopy fails or there is exsanguinating haemorrhage
If there is an acute rebleed may need to do a TIPs procedure where you make a shunt between the portal and systemic system
Emergency surgery is last resort
What is cirrhosis?
End stage of many liver diseases defined as: A diffuse process characterised by fibrosis and conversion of the liver architecture into abnormal nodules
Presentation of compensated cirrhosis
Liver is scarred but still able to perform most of its basic functions. Often an incidental finding, portal hypertension may be presents. Signs include spider naevi, palmar erythema, clubbing, gynaecomastia, hepatomegaly, splenomegaly. HOWEVER there may be no signs at all.
Presentation of decompensated cirrhosis?
This is end stage liver disease, signs include jaundice, ascites, encephalopathy and bruising.
Complications of cirrhosis?
Portal hypertension Ascites Encephalopathy Hepatorenal syndrome Hepatopulmonary syndrome Primary hepatocellular carcinoma
What is normal portal pressure?
5-8mmHg
3 things that cause ascites?
Sodium and water retention, portal hypertension and low serum albumin
How is the presence of fluid in ascites proven?
Shifting dullness
Treatment of ascites?
Need to restrict sodium in the diet
Spironolactone given
May need to do paracentesis
Explain why hepatic encephalopathy occurs?
In cirrhosis the blood bypasses the liver via collaterals and toxic metabolites pass directly to the brain, ammonia is the main cause.
How may patient present with hepatic encephalopathy?
May have disorder of personality, mood and intellect with reversal of normal sleep rhythm. Disorientated with slurred speech. May be vomiting or have nausea.
Signs of hepatic encephalopathy?
Fetor hepaticus (sweet smelling breath), liver flap constructional apraxia (e.g. can’t copy a drawing) and decreased mental function.
Treatment of cirrhosis?
Manage complications Screen for HCC Treat underlying cause (particularly in young people check for metabolic disorders) Manage dietary salts May get a transplant
