Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Core Conditions - Abdominal > Cirrhosis & its Consequences > Flashcards

Cirrhosis & its Consequences Flashcards

1
Q

What is cirrhosis?

What is the end result of this process?

A

it is a diffuse process that results from liver cell necrosis** followed by **fibrosis** and **nodule formation

the end result is impairment of liver cell function and gross distortion of the liver architecture, leading to portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the most common cause of cirrhosis?

A
  • alcohol is the most common cause in the western world
  • viral hepatitis is the most common cause worldwide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 most common causes of cirrhosis and what are non-invasive markers of aetiology?

A

Alcohol:

  • history of excess alcohol consumption

Chronic hepatitis B:

  • HBsAg +/- HBeAg/DNA in serum

Chronic hepatitis C:

  • HCV antibodies and HCV RNA in serum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 4 other conditions that are commonly seen in clinical practice that can cause cirrhosis?

What are non-invasive markers of aetiology?

A

Haemochromatosis:

  • family history
  • raised serum ferritin + transferrin saturation

Non-alcoholic fatty liver disease:

  • features of the metabolic syndrome
  • hyperechoic liver on ultrasound

Primary biliary cirrhosis:

  • presence of serum antimitochondrial antibodies

Sclerosing cholangitis (primary & secondary):

  • most patients have IBD and serum pANCA
  • multifocal stricturing and dilatation of bile ducts on cholangiography (MRCP or ERCP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are non-invasive markers of aetiology for autoimmune hepatitis and cystic fibrosis, which can cause cirrhosis?

A

Autoimmune hepatitis:

  • circulating autoantibodies
  • hypergammaglobulinaemia

Cystic fibrosis:

  • presence of extrahepatic manifestations of CF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What non-invasive markers of aetiology are present in Budd-Chiari syndrome, causing cirrhosis?

A
  • presence of known risk factors
  • caudate lobe hypertrophy
  • abnormal flow in major hepatic veins on USS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What non-invasive markers of aetiology are present in Wilson’s disease, leading to cirrhosis?

A
  • young age
  • reduced serum caeruloplasmin and total copper
  • increased 24-hour urinary copper excretion
  • Kayser-Fleisher rings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are non-invasive markers of aetiology in a1-antitrypsin (AAT) deficiency, leading to cirrhosis?

A
  • young age
  • associated emphysema
  • reduced serum AAT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 2 different types of cirrhosis histologically?

A
  • micronodular cirrhosis
  • macronodular cirrhosis
  • there is a mixed picture, with both small and large nodules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is micronodular cirrhosis and when is this often seen?

A
  • characterised by uniform, small nodules up to 3mm in diameter
  • this is often caused by alcohol damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is macronodular cirrhosis and what is this associated with?

A
  • this involves large nodules that are up to several centimetres in diameter
  • this often occurs following hepatitis B infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the clinical features of cirrhosis a result of?

A

clinical features are secondary to portal hypertension and liver cell failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the difference between compensated and uncompensated cirrhosis?

A

Uncompensated cirrhosis:

  • cirrhosis with the complications of encephalopathy, ascites or variceal haemorrhage

Compensated cirrhosis:

  • cirrhosis without any of these complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why are investigations carried out in cirrhosis?

A
  • to assess the severity of the liver disease
  • to identify the aetiology
  • to screen for complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do liver biochemistry and liver function tests usually show in cirrhosis?

A

Liver biochemistry:

  • may be normal
  • in most people there is at least a slight elevation in serum alkaline phosphatase (ALP) and aminotransferase

Liver function:

  • serum albumin is reduced
  • prothrombin time is prolonged
  • these reflect reduced hepatic synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What will serum electrolytes show in cirrhosis?

A
  • low sodium concentration indicates severe liver disease secondary to either impaired free water clearance or excess diuretic therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is serum a-fetoprotein (AFP) and why is this test performed?

A
  • usually undetectable after foetal life, but raised levels may occur in chronic liver disease
  • measured to screen for complications of hepatocellular carcinoma (HCC)
  • normal range is 10-20 ng/mL
  • a level > 400 ng/mL is regarded as diagnostic of HCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is the aetiology of cirrhosis confirmed?

A

the cause is determined by the history combined with laboratory investigations

a liver biopsy is performed to confirm the severity and type of liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What further investigations may be carried out in cirrhosis?

A
  • oesophageal varices are sought with endoscopy
  • USS is useful for detection of hepatocellular carcinoma (HCC)
  • USS is used to assess the patency of the portal and hepatic veins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is involved in the management of cirrhosis?

How are the underlying causes commonly corrected?

A
  • cirrhosis is irreversible, so treatment is aimed at treating the complications seen in decompensated cirrhosis as they arise
  • venesection is used to correct haemochromatosis
  • abstinence from alcohol is used to correct alcoholic hepatitis
  • correcting the underlying cause may halt the progression of liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What 5 variables are used to grade the severity and prognosis of liver disease?

What is 5-year survival like?

A
  • encephalopathy
  • ascites
  • prothrombin time
  • serum bilirubin
  • serum albumin
  • overall the 5-year survival rate without transplantation is 50%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the 7 most common complications of cirrhosis?

A
  • portal hypertension and variceal haemorrhage
  • ascites
    • this can become infected ascites (spontaneous bacterial peritonitis)
  • portosystemic encephalopathy
  • acute renal failure (hepatorenal syndrome)
  • hepatocellular carcinoma (HCC)
  • malnutrition
  • osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the role of the portal vein?

A
  • it carries blood from the gut and the spleen to the liver
  • it accounts for 75% of hepatic vascular inflow
    • the other 25% comes from the hepatic artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does blood enter and leave the liver?

A
  • blood enters the liver via the hepatic artery and the portal vein
  • these blood vessels enter the liver via the hilum (porta hepatis)
  • blood passes into the hepatic sinusoids via the portal tracts
  • blood leaves the liver via the hepatic veins, which join the inferior vena cava
  • the vena cava returns blood to the right side of the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is normal portal pressure?

What happens in portal hypertension?

A
  • normal portal pressure is 8 - 10 mmHg
  • portal hypertension occurs when there is an increase in pressure within the portal vein and its branches
  • these are draining blood from the intestines, stomach, pancreas etc. to the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens when the inflow of portal blood to the liver is obstructed?

What site is the most significant for collateral formation?

A
  • the inflow of portal blood to the liver can be partially or completely obstructed at a number of sites
  • this leads to high blood pressure proximal to the obstruction and the diversion of blood into portosystemic collaterals
  • the most important site for collateral formation is at the gastro-oesophageal junction (varices)
  • here the collaterals are superficial and liable to rupture, causing massive gastrointestinal haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 3 main sites of obstruction to the inflow of portal blood to the liver?

A

Prehepatic:

  • obstruction of the portal vein before it reaches the liver

Intrahepatic:

  • this results from distortion of the liver architecture

Posthepatic:

  • this results from obstruction of the hepatic veins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the main prehepatic cause of portal hypertension?

A

portal vein thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the main causes of intrahepatic portal hypertension?

A
  • cirrhosis
  • alcoholic hepatitis
  • idiopathic non-cirrhotic portal hypertension
  • schistosomiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the post-hepatic causes of portal hypertension?

A
  • Budd-Chiari syndrome
  • veno-occlusive disease
  • right heart failure (this is rare)
  • constrictive pericarditis
32
Q

What are the 3 characteristic clinical manifestations of portal hypertension?

A
  • gastrointestinal bleeding from oesophageal or gastric (less common) varices
  • ascites
  • hepatic encephalopathy
33
Q

How common is variceal haemorrhage?

What is the mortality like?

A
  • 30% of patients with varices will actually bleed from them
  • bleeding is most common in patients with large varices
  • bleeding is often massive with high mortality of 50%
34
Q

What is the management of acute bleeding from variceal haemorrhage?

A

patients should be resuscitated and undergo urgent gastroscopy to confirm the diagnosis and exclude bleeding from other sites

endoscopic therapy is the treatment of choice for active variceal haemorrhage

35
Q

What are the 2 forms of endoscopic treatment to stop bleeding from oesophageal varices?

A

Sclerotherapy:

  • this involves injection of a sclerosant solution (e.g. ethanolamine) into the varices

Variceal band ligation:

  • similar to haemorrhoidal banding and involves placing small elastic bands around the varices
36
Q

When is pharmacological treatment used for the treatment of oesophageal varices?

A
  • this is used for emergency control of bleeding whilst waiting for endoscopy and in combination with endoscopic techniques
  • this usually involves terlipressin or octreotide
37
Q

What does terlipressin do?

What dose is given and when is it contraindicated?

A
  • terlipressin is a synthetic analogue of vasopressin
  • it restricts portal inflow by splanchnic arterial constriction
  • it is given by intravenous bolus injection - 2mg every 6 hourly
  • it is contraindicated in patients with ischaemic heart disease
38
Q

What is octreotide and how does it work?

What dose should be given?

A
  • it is a somatostatin analogue
  • it lowers portal pressure by a similar mechanism to terlipressin but it is less effective
  • 50ug IV stat is given followed by 50ug hourly by intravenous infusion
39
Q

What is used to treat acute bleeding from oesophageal varices if endoscopy and pharmacological treatment don’t work?

What are the risks associated with this and how are they managed?

A
  • balloon tamponade with a Sengstaken-Blakemore tube is used if bleeding continues
  • It can have serious complications, such as:
    • aspiration pneumonia
    • oesophageal rupture
    • mucosal ulceration
  • to reduce complications the airway should be protected and the tube left in situ for no longer than 12 hours
40
Q

What method is used if there is a second rebleed after treatment for variceal haemorrhage?

What does this involve?

A

transjugular intrahepatic portosystemic shunting (TIPS)

  • a metal stent is passed over a guidewire in the internal jugular vein
  • the stent is pushed into the liver substance, under radiological guidance, to form a shunt between the portal and hepatic veins
  • this lowers portal pressure
41
Q

What additional antibiotics and medication are given to cirrhosis patients following treatment for variceal haemorrhage?

A
  • bacterial infection is common after upper GI bleeding in cirrhosis patients

all patient should have antibiotic prophylaxis with ciprofloxacin

this is 500mg twice daily for 7 days

  • lactulose should be given to prevent portosystemic encephalopathy
  • sucralfate should be given to reduce oesophageal ulceration, which is a complication of endoscopic therapy
42
Q

What type of prophylaxis is given after an episode of variceal bleeding and why?

A
  • there is a high risk of recurrence (60-80% over a 2-year period)
  • treatment is given to prevent further bleeds
  • this is secondary prophylaxis
43
Q

What drug is given as secondary prophylaxis for variceal bleeding?

A

oral propanolol

  • this decreases portal pressure
  • some patients are intolerant of treatment due to side effects
  • it is also given as primary prophylaxis for patients who have never bled
44
Q

If oral propanolol does not work or is not tolerated, what secondary prophylaxis may be given for variceal bleeding?

A
  • repeated courses of variceal banding at 2-weekly intervals until the varices are obliterated
  • TIPS or a surgical portosystemic shunt (portal vein to vena cava)

this is done if endoscopic or medical therapy fails

45
Q

What is ascites?

A

it is the presence of fluid in the peritoneal cavity

it is a common complication of cirrhosis of the liver

46
Q

Why does ascites occur?

A
  • in cirrhosis, there is peripheral arterial vasodilation that is mediated by vasodilators including nitric oxide
  • this leads to a reduction in effective blood volume
  • there is activation of the renin-angiotensin system
  • this promotes renal salt and water retention
  • the formation of oedema is encouraged by hypoalbuminaemia and is localised to the peritoneal cavity as a result of portal hypertension
    • increased pressure can force fluid into the abdominal cavity
47
Q

What are the clinical features of ascites?

A
  • there is fullness in the flanks, with shifting dullness
  • tense ascites is uncomfortable and may produce respiratory distress
  • a pleural effusion (usually right-sided) and peripheral oedema may be present
48
Q

What investigations are carried out when ascites is present?

A

a diagnostic aspiration (paracentesis) of 10-20ml of fluid is carried out in all patients and the following performed:

  • cell count
  • Gram stain and culture for bacteria and acid-fast bacilli
  • protein
  • cytology for malignant cells
  • amylase to exclude pancreatic ascites
49
Q

Why is a cell count performed in patients with ascites?

A

a neutrophil count > 250 cells / mm3 indicates underlying (usually spontaneous) bacterial peritonitis

50
Q

Why is ascitic fluid tested for protein?

A
  • an ascitic protein level of 11 g/L or more below the serum albumin level suggests a transudate
  • a ascitic protein level of < 11 g/L below the serum albumin level suggests an exudate
51
Q

What is the difference between a transudate and an exudate?

A

Transudate:

  • an ultrafiltrate of plasma that contains very few cells
  • it does NOT contain large plasma proteins
  • results from increased hydrostatic or reduced oncotic pressure

Exudate:

  • this is a sign of inflammation that contains many inflammatory cells
  • a consequence of increased vascular permeability
52
Q

What are the causes of transudate ascites?

A
  • cirrhosis
  • constrictive pericarditis
  • cardiac failure
  • hypoalbuminaemia (e.g. nephrotic syndrome)
  • Meig’s syndrome
    • a combination of an ovarian tumour, ascites and a hydrothorax
53
Q

What are the causes of exudate ascites?

A
  • malignancy
  • infection
  • pancreatitis
  • Budd-Chiari syndrome
  • myxodema
  • lymphatic obstruction
54
Q

What is the first stage in the management of ascites resulting from cirrhosis (portal hypertension)?

A
  • management is a stepwise approach
  • it starts with dietary sodium restriction (60 mmol/day)
  • and oral spironolactone (100mg daily) is also given
    • this is a potassium sparing diuretic
  • this is increased gradually up to 400 mg daily if necessary
55
Q

What medication is added if the response to spironolactone is poor in ascites caused by portal hypertension?

A
  • furosemide 20 - 40 mg daily is added
  • this is increased up to 160 mg if necessary
56
Q

By how much does diuretic therapy aim to reduce fluid by daily in ascites?

How is this best measured?

A
  • the rate of fluid loss is best assessed through changes in bodyweight
  • the aim is to produce weight loss of around 0.5kg per day
  • this is because the maximum rate of transfer of fluid from the ascitic to the vascular compartment is only about 700 mL / day
57
Q

What can happen if diuresis of ascitic fluid occurs too rapidly?

A
  • it can cause volume depletion and hypokalaemia
  • it also precipitates encephalopathy
58
Q

What treatment approach is used in patients with tense ascites or those who are resistant to standard therapy with diuretics?

A

paracentesis

  • this involves a needle / drain being inserted into the peritoneal cavity
  • all of the ascites is removed over several hours
  • this provides rapid symptoms relief and reduced hospital stay compared with treatment with diuretics
59
Q

What is the major danger associated with paracentesis to treat ascites and how is this overcome?

A
  • the major danger of this approach is the production of hypovolaemia
  • this is because the ascites reaccumulates at the expense of the circulating volume
  • this is overcome by administering an intravenous infusion of albumin (8g per litre removed) immediately after paracentesis
60
Q

What is the most common complication associated with ascites?

How does this tend to present?

A

spontaneous bacterial peritonitis (SBP)

  • the most common infecting organism is E. coli
  • clinical features are minimal, but include abdominal pain and fever
61
Q

How is spontaneous bacterial peritonitis diagnosed?

What is the treatment?

A
  • diagnosis is made based on the ascitic fluid white cell count, Gram stain and culture
  • empirical therapy is started in all patients with an ascitic fluid neutrophil count >/= 250 cells/mm3 rather than waiting for the results of the culture
  • this usually involves IV cefotaxime 2g every 8 hourly
62
Q

What antibiotic can be given for prophylaxis following SBP?

A
  • SBP recurrence is common
  • oral norfloxacin can be given for prophylaxis
63
Q

What is portosystemic encephalopathy?

A

it refers to a chronic neuropsychiatric syndrome which occurs with advanced hepatocellular disease

this is either chronic (cirrhosis) or acute (fulminant hepatic failure)

64
Q

What is involved in the pathophysiology of portosystemic encephalopathy?

A
  • the mechanisms are unknown but are believed to involve “toxic” substances, normally detoxified by the liver, bypassing the liver via the collaterals and gaining access to the brain
  • a putative toxin is ammonia, produced from the breakdown of dietary protein by gut bacteria
65
Q

What are the early and later clinical features of portosystemic encephalopathy?

A

Earliest features:

  • lethargy
  • mild confusion
  • anorexia
  • reversal of the sleep pattern
    • the patient sleeps during the day and is restless at night

Later features:

  • disorientation
  • decreased conscious level
  • eventually this leads to coma
66
Q

What are the 4 main clinical features associated with portosystemic encephalopathy?

A
  • fetor hepaticus - this is a sweet smell to the breath
  • asterixis - flapping tremor of the outstretched hand
  • constructional apraxia - the inability to draw a five-pointed star
  • prolonged trail-making test - the ability to join numbers and letters within a certain time
67
Q

What investigations are involved in portosystemic encephalopathy?

A
  • the diagnosis is clinical
  • an EEG showing delta waves and visual evoked potentials may aid diagnosis in difficult cases
68
Q

What are the factors known to precipitate portosystemic encephalopathy?

A
  • gastrointestinal haemorrhage (i.e. a high protein load)
  • infection
  • fluid and electrolyte disturbance (spontaneous or diuretic induced)
  • sedative drugs
    • e.g. opiates, diazepam
  • development of a hepatoma (HCC)
  • portosystemic shunt operations and TIPS
  • constipation
  • high dietary protein
69
Q

What are the aims of management for portosystemic encephalopathy?

A

the aims of management are to identify and treat any precipitating factors

and to minimize the absorption of nitrogenous material, particularly ammonia, from the gut

70
Q

What is the main medication given for the treatment of portosystemic encephalopathy?

A

laxatives

  • oral lactulose (10 - 30 ml three times daily)
  • this is an osmotic purgative that reduces colonic pH and increases transit
  • it is given via a nasogastric tube if the patient is comatose
  • the dose should be titrated to result in 2-4 soft stools daily
71
Q

What antibiotics are given in the management of portosystemic encephalopathy and why?

A
  • antibiotics are given to reduce the number of bowel organisms and hence production of ammonia
  • rifaximin is mainly unabsorbed and well tolerated
  • oral metronidazole (200 mg four times daily) is also used
72
Q

What supportive treatment is given in portosystemic encephalopathy?

A

maintenance of nutrition with adequate calories

protein is initially restricted but increased after 48 hours as encephalopathy improves

73
Q

What is hepatorenal syndrome?

A

this is the development of acute renal failure in a patient who usually has advanced liver disease

this is either cirrhosis or alcoholic hepatitis

74
Q

Why does hepatorenal syndrome occur?

A
  • splanchnic vasodilation (vessels that supply the intestines) results in a fall in systemic vascular resistance
  • and severe vasoconstriction of the renal circulation with markedly reduced renal perfusion
75
Q

How is hepatorenal syndrome diagnosed?

A
  • oliguria
  • a rising serum creatinine (over days to weeks)
  • a low urine sodium (<10 mmol/L)
  • absence of other causes of renal failure
  • lack of improvement after volume expansion (if needed) and withdrawal of diuretics
76
Q

What is the prognosis like in hepatorenal syndrome and what treatments are available?

A
  • the prognosis is poor and renal failure will often only respond to an improvement in liver function
  • albumin infusion and terlipressin have been used with some success

Core Conditions - Abdominal (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions