Brainscape's Knowledge GenomeTM

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


See full index

Yr3 Medicine- Gastroenterology > Chronic Liver Disease > Flashcards

Chronic Liver Disease Flashcards

1
Q

Remind yourself of some functions of the liver

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

When taking a history from someone with liver disease it is important to ask about risk factors; state some risk factors you must ask about

A
  • Blood tranfusion prior to 1990 in UK
  • IVDU
  • Operations/vaccination with dubious sterile procedures
  • Sexual exposure
  • Medications (prescribed or over counter)
  • FH of liver disease, diabetes, IBD
  • Obesity and other features of metabolic syndrome
  • Alcohol
  • Foregin travel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is meant by chronic liver disease?

A

Progressive destruction of the liver parenchyma over a period greater than 6 months leading to fibrosis and cirrhosis (idea that damage to liver has built up over time)

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

State some causes of chronic liver disease- highlight which 4 are the most common

A
  • Alcoholic liver disease
  • Non-alcoholic fatty liver disease
  • Hepatitis B
  • Hepatitis C
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons disease
  • Alpha-1 antitrypsin deficiency
  • Cystic fibrosis
  • Drugs e.g. Amiodarone, methotrexate, sodium valporate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

For each of the following state whether it is more common in men or women:

  • Autoimmune hepatitis
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis
  • Haemochromatosis
A

Women

  • Autoimmune hepatitis
  • PBC

Men

  • PSC
  • Haemochromatosis occurs earlier in men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What cause of chronic liver disease is associated with IBD?

A

Primary sclerosing cholangitis (PSC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What two causes of chronic liver disease ONLY occur in adolescents & young adults

A
  • Wilson disease
  • Anti-LKM autoimmune hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Is chronic liver disease reversible?

A

???

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

State some of the symptoms of chronic liver disease

*NOTE: there are lots of potential symptoms so try to highligh most common

A

General Symptoms

  • Fatigue
  • Anorexia
  • Weight loss
  • Nausea & vomitting
  • Abdominal tenderness
  • Loss of sex drive

Build up of Toxins

  • Pruritis
  • Forgetfulness, confusion

Coagulation Disorder

  • Frequent nose bleeds
  • Bleeding gum
  • Easy bruising
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What might you find on clinical examinatino of someone with chronic liver disease

*HINT: to help you remember go through it like you would when actually doing a clinical examination on a pt

A

Hands

  • Asterixis/hepatic flap (increased urea)
  • Leuconychia
  • Terry’s nails
  • Clubbing
  • Palmar erythema
  • Dupuytren’s contracture

Face

  • Xanthelasma
  • Sleral icterus & yellow skin (jaundice)

Chest

  • Gynaeocmastia: excess oestrogen
  • Spider naevi: excess oestrogen

Abdomen

  • Ascites
  • Caput medusa
  • Bruising
  • Hepatomegaly

Legs

  • Peripheral pitting oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

If you suspect chronic liver disease, what bedside investigations may you want to do and why?

A
  • 24hr urinary excretion of copper (test for Wilson’s disease)i
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

If you suspect chronic liver disease, what blood tests should you do?

*Just state the tests, separate flashcards will ask you why you do each one.

A
  • FBCs
  • U&Es
  • LFTs
  • Coagulation tests
  • TFTs
  • Lipids
  • Glucose
  • Non-invasive liver screen:
    • Hep B & C serology
    • Autoantibodies
    • Ferritin, Trasnferrin saturation, TIBC
    • Alpha-feto protein
    • Caeruloplasmin, serum copper
    • Alpha-1 antitrypsin
    • Serum protein electrophoresis
    • Viral screen for EBC, CMV etc..
    • Coeliac serology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What might you find on FBC of someone with chronic liver disease?

A
  • Anaemia
  • Thrombocytopenia
    • Pooling of blood in enlarged spleen
    • Decreased thrombopoietin production
    • Increased use if bleeding
  • Decreased WCC
    • Pooling of blood in large spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What might you find on U&Es of someone with chronic liver disease?

A
  • Hyponatraemia: fluid retention in severe liver disease
  • Urea & creatinine deragned in heaptorenal syndrome:
    • Creatinine may be high due to pre-renal AKI
    • Urea could be low (due to decreased hepatic synthesis) or high due to GI bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why would you do TFTs in someone with suspected chronic liver disease?

What could the TFT results be of someone with chronic liver disease?

A

Liver abnormalities can cause thyroid dysfunction because:

  • Liver converts T4 into T3
  • Liver produces proteins that carry thyroid hormones around body e.g. thyroxine binding globulin

Hence in chronic liver disease may have

  • Low total T3
  • Low free T3
  • High reverse T3 (liver removed 3’ iodide instead of 5’ iodide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What might you find on the coaugulation tests of someone with chronic liver disease?

A
  • Increased prothrombin time
  • Increased INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why do you want to test for lipids and glucose as part of your blood tests for suspected chronic liver disease?

A

Risk factors for non-alcoholic fatty liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

For each of the blood tests in the non-invasive liver screen, state why you are doing them/what disease you are testing for

A

Non-invasive liver screen is about trying to identify cause of chronic liver disease:

  • Hep B & C serology: hep B or C
  • Autoantibodies:
    • ANA: autoimmune hepatitis
    • SMA: autoimmun hepatitis (70%)
    • ​AMA: primary biliary cholangitis (95%)
    • LKM1: autoimmune hepatitis
  • Ferritin, Trasnferrin saturation, TIBC: haemochromatosis
  • Alpha-feto protein: hepatocellular carcinoma
  • Caeruloplasmin, serum copper: Wilson’s disease
  • Alpha-1 antitrypsin: deficiency as 15% of adults with this deficiency develop cirrhosis
  • Serum protein electrophoresis: help confirm alpha-1 antitrypsin deficiency
  • Viral screen for EBC, CMV etc..: check for other viral cause
  • Coeliac serology: coeliac pts more likely to develop liver problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What might you find on LFTs of someone with chronic liver disease?

A
  • ALT: raised if hepatocellular damage
  • AST: raised if hepatocellular damage
  • ALP: raised if bile duct dammage
  • Gamma GT: raised if bile duct damage
  • Albumin: decreased
  • Prothrombin time: increased
  • INR: increased
  • Bilirubin: increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

For the following LFT results, state where it suggests the damage is occuring:

  • Raised ALT, AST
  • Raised ALP, gamma GT
A
  • Raised ALT, AST = hepatocellular damage
  • Raised ALP, gamma GT= bilde duct damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does each of the following LFT results suggest about the cause of damage:

  • ALT >10x upper limit
  • AST:ALT ratio >2
  • AST:ALT ratio <1
  • Gamma GT > ALP
A
  • ALT >10x upper limit: acute hepatitis
  • AST:ALT ratio >2: alcoholic liver disease
  • AST:ALT ratio <1: non-alcoholic liver disease
  • Gamma GT > ALP: acute ethanol intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

The differential diagnosis of abnormal liver tests depends on the pattern of LFT abnormality and the level of abnormality. If the LFTs suggest a cholestatic abnormality what should be the first test?

A

If LFTs suggest cholestatic abnormality the first test should be ultrasound to assess if ducts are dilated (obstructive jaundice) or not.

Ultrasound may also show findings that suggest cirrhosis e.g. coarse texture, nodularity, splenomegaly, ascites etc…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

A pts LFTs showed a raised ALP hence you did an ultrasound to assess if the ducts were dilated or undilated; state some causes for cholestasis with dilated ducts and some causes for cholestasis with non-dilated ducts

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

We have already said that the differnetial diagnosis of abnormal liver tests depends on the pattern of LFT abnormality and the level of abnormality. State some potential causes of:

  • ALT >500
  • ALT 100-200
A

*Remember, we said if ALT>10x upper limit suggests acute hepatitis. ALT upper limit 35-40 dependent on gender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

State 5 modes of imaging you may use to investigate chronic liver disease

A
  • Ultrasound
  • Fibroscan
  • Endoscopy
  • CT scan
  • MRI scan
26
Q

Describe what you might see on ultrasound of someone with cirrhosis due to chronic liver disease (5)

A
  • Nodularity on surface of liver
  • “Corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal vein with reduced flow
  • Ascites
  • Splenomegaly
27
Q

What is a fibroscan/how does it work?

A

Uses high frequency sound waves to check elasicity of liver; helps to assess degree of cirrhosis

28
Q

NICE recommends that a fibroscan should be offered to _______ every _____ years to test for cirrhosis

A

NICE reccomends a fibroscan should be offered to those at high risk of cirrhosis every 2 years; this includes:

  • Hepatitis C
  • Heavy alcohol drinkers
  • Diagnosed alcoholic liver disease
  • Non-alcoholic fatty liver disease
  • Chronic hepatitis B (the suggest yearly for hep B)
29
Q

Why would you do an endoscopy in someone with suspected chronic liver disease?

A

Check for oesophageal varices when portal hypertension suspected

30
Q

What are you looking for, in CT & MRI scans, of pts with chronic liver disease?

A
  • Hepatocellular carcinoma
  • Hepatosplenomegaly
  • Abnormal blood vessel changes
  • Ascites
31
Q

Liver biopsies can be done to confirm the diagnosis of cirrhosis; discuss whether these are done often

A

Rarely needed as by time cirrhosis has developed it is unlikley that biopsy will give you any clue as to the underlying aetiology.

32
Q

Cirrhosis is the end pathology of any chronic liver disease; who should you suspect cirrhosis in?

*HINT: two key things

A

Suspect cirrhosis in anyone who has chronic liver disease and has either:

  • Thrombocytopenia
  • Or clinical stigmata of chronic liver disease
33
Q

State 2 scoring systems used in liver cirrhosis and state what each scoring system is used for

A
  • Child-Pugh score: indicate severity and prognosis of cirrhosis
  • MELD (model for end stage liver disease) score: NICE reccommend this is used every 6 months in pts with compensated cirrhosis to estimate 3 month mortality & help guid referall for liver transplant
34
Q

What factors does the Child-Pugh score consider?

A
35
Q

What factors does the MELD score consider?

A
36
Q

Treatment of chronic liver disease is based around…..

A
  • Treating underlying cause to prevent further damange (and progression to cirrhosis if cirrhosis hasn’t occured)
37
Q

What is the end pathology of chronic liver disease?

A

Cirrhosis

38
Q

If you suspect cirrhosis, what imaging is usually preffered to check for this?

A

Fibroscan (quicker, more specific and can be done in clinic room)

39
Q

Discuss the general management of cirrhosis (5)

A
  • Managing complications
  • Ultrasound & alpha-fetoprotein every 6 months to check for hepatocellular carcinoma
  • Endoscopy every 3yrs to check for varices
  • High protein, low sodium diet
  • Avoid all alcohol
  • MELD score every 6 months to help consideration for liver transplant
  • DEXA scan
40
Q

Why should pts with cirrhosis have a DEXA scan?

A

Increased risk of osteoporosis

41
Q

State 6 potential complications of cirrhosis

A
  • Malnutrition
  • Portaly hypertension, varices & variceal bleeding
  • Ascites & spontaneous bacterial peritonitis
  • Hepato-renal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
42
Q

Briefly explain why malnutrition occurs as a consequence of liver cirrhosis

A
  • Cirrhosis affects metabolism of proteins in liver:
    • ​Liver would usually break amino acids into carbon skeleton and amino group to produce glucogenic & ketogenic amino acids which can be used as energy (see MEH). This is reduced in cirrhosis.
  • Cirrhosis affects livers ability to store glycogen
  • Cirrhosis affects livers ability to perform gluconeogenesis

This results in body using muscle tissue as fuel leading to muscle wasting & weight loss

43
Q

Discuss how we manage malnutirtion as a compliction of cirrhosis

A
  • Regular meals (every 2-3hrs)
  • High protein
  • High calorie (if underweight)
  • Avoid alcohol (further impair liver func and also can cause anorexia)
44
Q

Discuss how we treat stable varices

A
  • Propanolol (see next flashcard for mechanism)
  • Elastic band ligation
  • Injection of sclerosant (ligation more effective)
  • TIPs
45
Q

Explain how propanolol can be used to treat stable varices

A
  • Propanolol= non-selective beta blocker
  • Alpha-1 adrenoceptors in smooth muscle vasculature causes vasoconstriction. Beta-2 adrenoceptors in smooth muscle vaculature causes vasodilation
  • Non selective beta blocker works by:
    • B1- block heart beta-adrenoceptors to decrease cardiac output, decrease splanchnic flow
    • B2- block smooth muslce beta-2 adrenoceptors to prevent vasodilation/cause vasoconstriction to reduce portal flow
46
Q

Remind yourself briefly how to treat bleeding oesphageal varices (see upper GI bleed cards for more detail)

A
  • A-E
  • Bloods
  • Access (2 wide bore cannulas)
  • Resucitation
  • Transfuse
    • Bloods
    • Clotting factors
  • Endoscopy (within 24hrs)
  • Drugs
    • Stop drugs that cause bleediing e.g. warfarin, NSAIDs…
    • Consider prothrombin complex
    • FOR VARICES ONLY:
      • IV terlipressin 1-2mg/6hr
      • Empirical IV antibiotics
      • Ligation, Sengstaken-Blakemore tube, TIPS
47
Q

Causes of ascites can be grouped into those with serum-ascites albumin gradient <11g/L or SAAG >11g/L; state some potential causes of each

A
48
Q

Discuss how we manage ascites as a complication of chronic liver disease

A
  • Low sodium diet: try to reduce water retention
  • Fluid restriction
  • Anti-aldosterone diuretics e.g. Spironolactone
  • Other diuretics e.g. furosemide
  • Paracentesis
    • Diagnostic tap
    • Ascitic drain
  • Prophylactic antibiotics (ciprofloxacin) against spontaneous bacterial peritonitis in pts with following until the ascites has resolved:
    • patients who have had an episode of SBP
    • patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
  • Consider TIPS in refractory ascites
  • Consider transplant in refractory ascites
49
Q

What is mean by refractory ascites?

A

Ascites that cannot be removed by medical treatment e.g. low Na+ diet and diuretics

50
Q

Explain why spironolactone is used as diuretic in ascites

A
  • Cirrhotic liver compresses blood vessels in liver
  • Increases pressure in portal system
  • Fluid (transudate) leak out of capillaries in liver & bowel into peritoneal cavity
  • Fluid loss causes reduction in blood entering kidneys
  • Kidneys think this is because blood pressure is low so activates RAAS
  • Causes reabsorption of Na+ and water in kidneys
  • Increase circulating volume, increase pressure in portal system, worsen ascites
  • Spironolactone blocks aldosterone receptor and hence reduces impact of activated RAAS
51
Q

Spontaneous bacterial peritonitis occurs in around 10% of pts with ascites secondary to cirrhosis; describe the presentation of spontaneous bacterial peritonitis

A
  • Asymptomatic
  • Fever
  • Abdo pain
  • Hypotension
  • Ileus
  • Bloods show signs of infection
52
Q

Who should have a diagnostic tap of their ascites?

A

All pts with ascites who are admitted to hospital

53
Q

State some of the most common organisms causing spontaneous bacterial peritonitis in ascites secondary to cirrhosis

A
  • Escherichia coli
  • Klebsiella pneumoniae
  • Gram +ve cocci (e.g. staphylococcus and enterococcus)
54
Q

What is the management of spontaneous bacterial peritonitis secondary to cirrhosis?

A
  • Take ascitic culture prior to antibiotics
  • Treat IV antibiotics (see local guidelines- passmed says IV cefotaxime)
55
Q

What is hepatorenal syndrome?

A
  • Cirrhosis causes hypertension in portal system
  • This causes dilation of portal blood vessels and also causes fluid to leak out of circulation and form ascites
  • Both of the above decrease effective circulating volume that reaches the kidneys
  • Kidneys detect this as hypotension so active RAAS
  • This causes renal vasoconstriction
  • Renal vasoconstriction combined with low circulating volume leads to ischaemia of kidneys
  • Rapidly deteriotating kidney function (AKI) develops
56
Q

Describe the difference between hepatorenal syndrome 1 and hepatorenal syndrome 2

What is the treatmen for HRS?

A
  • HRS1= rapildy progressive- median survival untreated= 1-2 weeks
  • HRS2= more steady deterioration- median survival= 6 months

Treatment depends on severity. If HRS2 caught early may be able to do TIPS and kidneys recover to some extent. Liver transplant may be required. Liver & kidney transplant may be requred.

57
Q

What is hepatic encephalopathy (also known as portosystemic encephalopathy)

A

Hepatic encephalopathy (HE) is a brain dysfunction caused by liver insufficiency and/or portosystemic shunt. Due to build of toxins- key one to remember is ammonia. Ammonia is produced by intestinal bacteria when they break down proteins absorbed in the gut. There are two reasons ammonia builds up in pts with cirrhosis:

  • Liver cells are damanged and hence can’t metabolise ammonia into harmless waste products
  • Collateral vessels between portal and systemic circulation mean that ammonia bypasses liver and enters systemic circulation directly
58
Q

How does hepatic encephalopathy present acutely?

How does hepatic encephalopathy present chronically?

A

Acute

  • Reduced consciousness
  • Confusion

Chronic

  • Changes to mood, personality and memory
59
Q

State some factors that can precipate hepatic encephalopathy

A
  • infection e.g. spontaneous bacterial peritonitis
  • GI bleed
  • post transjugular intrahepatic portosystemic shunt
  • constipation
  • drugs: sedatives, diuretics
  • hypokalaemia
  • renal failure
  • increased dietary protein (uncommon)
60
Q

Describe the 4 different grades of hepatic encephalopathy

A

Grading of hepatic encephalopathy (PASSMED)

  • Grade I: Irritability
  • Grade II: Confusion, inappropriate behaviour
  • Grade III: Incoherent, restless
  • Grade IV: Coma
61
Q

Discuss the management of hepatic encephalopathy

A
  • Treat underlying precipitating cause
  • 1st line= lactulose to promote excretion of ammonia. *NOTE: aim is 2-3 soft stools per day. May need enamas intially
  • Plus antibiotics e.g. rifaximin which reduce the number of intestinal bacteria producing ammonia. *Rifaximin is useful as it is poorly absorbed so stays in GI tract
  • Nutritional support e.g. NG tube feeding

Yr3 Medicine- Gastroenterology (8 decks)

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