GI: Liver disease Flashcards Preview

Year 3 Medicine Block > GI: Liver disease > Flashcards

Flashcards in GI: Liver disease Deck (137)
Loading flashcards...
1
Q

Alcoholic liver disease has 3 stages of liver damage. What are they?

A
  1. Fatty liver (steatosis)
  2. Alcoholic hepatitis (inflammation and necrosis)
  3. Alcoholic liver cirrhosis
2
Q

What risk factors may be present in a patient attending your clinic with alcoholic liver disease?

A

Prolonged heavy alcohol consumption
Hep C
Female

3
Q

How may a patient with alcoholic liver disease present? (as if you were taking a Hx)

(Question made after talking to Reg in ward round about common presentations)

A

PC: Right upper quadrant abdominal pain. Sudden onset (as asymptomatic to start) Nauseous. Loss of appetite. Jaundice in eyes and skin. Haematemesis, jaundice.
PMH: previous admissions with alcohol related problem. Hepatitis C.
DH: previous use of diazepam, lorazepam, disulfiram, use of thiamine.
FH: alcohol misuse in family is a potential RF. Hepatitis in family.
SH: alcohol binging, live alone, smoker (occasionally).

4
Q

What may you find on examination of a patient with alcoholic liver disease?

A

Hepatomegaly.
Obvious distension to abdomen - ascites.
Discomfort in RUQ.
Engorged para-umbilical veins
Splenomegaly
Jaundice of sclera and skin
Palmar erythema
Spider naevi i.e Cutaneous telangiectasia (trunk, face, UL)
Asterixis - i.e. liver flap
Caput medusae
Signs of malnutrition - wasting and anorexia
Confusion

5
Q

What are functions of the liver?

A

Stores glycogen, releases glucose, absorbs fats, fat soluble vitamins and iron, makes cholesterol.

Bile salts dissolve dietary fats
Haemaglobin breakdown into bilirubin.
Produces most clotting factors
Has Kupfer cells to engulff antigens
Excretes drugs and breaks down alcohol
Produces important proteins - albumin and binding proteins

Nutrition/metabolic Bile salts
Protein synthesis
Clotting factors
Bilirubin
Detoxification
Immune function

6
Q

How does acute liver disease contrast to chronic liver disease?

A

Acute = no pre-existing liver disease. Chronic = starts with acute liver disease which may be asymptomatic.

Acute = resolves in 6 months. Chronic = Ongoing beyond 6 months.

7
Q

Which conditions can cause acute liver disease?

A

Hepatits A, E, cytomegalovirus, Epstein-Barr virus, Drug induced liver injury

if present - then need to look for acute liver failure

8
Q

Which conditions can lead to chronic liver disease?

A

Most common: Alcoholic liver disease, non-alcoholic steatohepatitis, viral hepatitis (B+C)

Less common but important:
- in women = AI hepatitis, PBC
- in men = PSC associated to IBD
- younger men = haemochromatosis
- adolescents and young adults = Wilson’s disease and anti-LKM AI hepatitis

9
Q

Which 3 conditions are part of autoimmune liver disease?

A

Primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis.

10
Q

What are some causes of liver cirrhosis?

A

Alcohol.
Non-alcoholic fatty liver/non-alcoholic steatohepatitis
Hep B, Hep C
Alpha-1-antitrypsin deficiency,
Methotrexate use
Haemachromatosis
Wilson’s disease
PBC
PSC

Z2F said to remember common 4:
Alcoholic liver disease, NAFLD, Hep B, Hep C

11
Q

How does liver cirrhosis present?

A

Asymptomatic with abnormal LFTs
Tiredness,
Itching
Arthralgia
Jaundice
Ascites
Upper GI bleed
Confusion or drowsy

12
Q

What are RF for liver cirrhosis/disease?

A

Blood transfusion before 1990.
IVDU
Operations or vaccines with non-sterile equipment
Sexual exposure
Medications
Fix of liver disease
Obesity, metabolic syndrome
Alcohol
Foreign travel

13
Q

Name 4 visible characteristics of chronic liver disease

A

Any from:

Spider nave, leukonychia, clubbing, Dupuytren’s contracture, parotid swelling, testicular atrophy, cachexia, para-umbilical vein engorgement, mild splenomegaly.

14
Q

What are complications of liver cirrhosis?

A

Portal HTN
Splenomegaly
Oedema,
Ascites with shifting dullness,
R sided pleural effusion, hepatic flap aka asterisks, jaundice
Hepatorenal syndrome

15
Q

A patient has liver cirrhosis. Over the phone, the radiologist says they have a R sided pleural effusion over 500ml. On their CXR, what typical sign may you see with this volume of effusion?

A

Hepatic hydrothorax

16
Q

What is NAFLD, and how does this differ to NASH?

A

NAFLD = non-alcoholic fatty liver disease. This is where you get deposition of fat in the liver.

NASH = is where you have deposition of fat in the liver (aka accumulation of triglycerides in the hepatocytes) AND have inflammation present as a result of this = non-alcoholic steatohepatitis.

17
Q

Risk factors of Non Alcoholic fatty liver disease?

A

DM, Obesity, Metabolic syndrome, Familial hyperlipidaemia

18
Q

What may you prescribe to a patient at risk of non alcoholic liver disease?

A

Oral hypoglycaemic agents e.g. Pioglitazone
social prescription - walking, lifestyle modifications.

19
Q

You are a foundation doctor working in a Gastroenterology rotation. A medical student presents the following history:

A 39-year-old man presents for the third time in 2 years with an intermittent productive cough and increasing dyspnoea on exertion. He has a 15 pack-year smoking history, reports thick, yellow phlegm at times. His medical history reveals mild intermittent asthma controlled with a salbutamol inhaler. His symptoms have persisted despite stopping smoking, with some attacks being unresponsive to salbutamol. Physical examination reveals a generally healthy-looking male apart from fatigue. He has hepatomegaly and ascites. Spirometry shows FEV1 of 40% of predicted value. I

What are your differentials and give reasoning why? Maximum of 3 so be selective !

A

Top differential = Alpha-1 antitrypsin deficiency - productive cough, cigarette smoker, hepatomegaly, ascites. A-1-antitrypsin= inherited, causes lung and liver problems. (Why is this relevant? Can cause inflammation and cirrhosis of liver!)

COPD - long period of smoking. Spirometry results.

Bronchiectasis - daily sputum.

20
Q

Where can varices form as a result of portal hypertension?

A

Oesophageal
Anorectal
Umbilical

21
Q

Describe the pathophysiology of hepatorenal syndrome. (Clue: this is the development of AKI in presence of cirrhosis - from GI module with Hannah Bonfield)

A
  1. Get portal hypertension
  2. This causes arterial vasodilation (splanchnic)
  3. This activates RAAS
  4. So get renal artery vasoconstriction = reduced blood flow to the kidney
22
Q

Define decompensated liver disease

A

Liver disease = damage to the liver which affects structure. Structure becomes distorted and get nodules and fibrosis. Synthetic, metabolic and excretory functions are affected.

Decompensated = Liver damage is so advanced that organ can not function, and clinical complications (e.g. jaundice and ascites) are present that can not be overcome.

23
Q

What does the Child-Pugh score assess?

A

Assess prognosis/severity of cirrhosis

24
Q

What features are included in Child-Pugh score?

A

Bilirubin, albumin, INR, ascites, encephalopathy - see pg76 Z2F

25
Q

What is the MELD score used for?

A

Used every 6months in pts with compensated cirrhosis.. Helps guide referral for liver transplant and percentage estimated 3 month mortality.

26
Q

Why may AST and ALT levels be normal in patient with liver cirrhosis?

A

Not enough healthy tissue to release elevated quantities of these enzymes, so appear normal

27
Q

What is hepatitis?

A

Inflammation of the liver

28
Q

What are causes of hepatitis?

A

Alcoholic hepatitis - alcohol
NAFLD
Viral hepatitis - viruses, CMV, EBV
Autoimmune
Drug induced

29
Q

What things is it important to ask when taking a history from a patient with suspected liver disease?

A

Did they have any blood transfusions in the UK before 1990?
IVDU?
Operations and vaccinations, any with dubious sterility
Sexual exposure
Medications
Fhx of liver disease, diabetes, IBD
Obesity/other features of metabolic syndrome
Alchohol (?dependency)
Foreign travel

30
Q

Acute vs Chronic liver disease

A

Acute:
Resolves within 6 months
Hep A,E, CMV, EBV
Drug induced liver injury

Chronic:
Usually starts as acute- usually asymptomatic
Still effects after 6 months
Can lead to cirrhosis
Alcohol
Hep C
Non-alcoholic steatohepatitis
Autoimmune

31
Q

What is the significance of ALT and ALP

A

ALT- released from hepatocytes
ALP- released from the ducts

32
Q

A patient has an ALT between 100-200, what are your differentials?

A

Non-alcoholic hepatitis
Chronic viral hepatitis
Autoimmune hepatitis
Drug induced liver injury

33
Q

A patient has an ALT>500, what are your ddx?

A

Viral
Ischaemia
Toxic- any drug but most commonly paracetamol
Autoimmune

34
Q

What are your ddx in patients with a higher ALP than ALT?

A

Cholestatic- dilated ducts:
Gallstone
Malignancy

Non-dilated ducts:
Alcoholic hep
Cirrhosis due to PSC, PBC or Alcohol
Drug induced liver injury e.g. antibiotics

35
Q

What is the stepwise progression of alcoholic liver disease?

A

1) Alcohol relate fatty liver- reversible
2) Alcoholic hepatitis- if mild may be reversible
3) Alcoholic cirrhosis- where normal tissue replaced with scar tissue- not reversible, but can slow progression if stop drinking, however poor prognosis if keep drinking

36
Q

What are some complications from alcohol consumption?

A

Increased risk of cancer
Pancreatitis
Alcoholic cirrhosis and complications from that
Hepatocellular carcinoma
Dependence and withdrawal
Alcoholic liver cirrhosis

37
Q

What are the causes for pancreatitis?

A

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps/malignancy
Autoimmune
Scorpion stings
Hypertriglyridaemia/hypercalcaemia
ERCP
Drugs e.g. thiazides

38
Q

What are the signs of liver disease?

A

Jaundice
Sceleral icterus
Bruising
Ascites
Palmar erythema
Spider naevi
Gynacomastia
Hepatomegaly
Caput medusa
Flapping tremor (in decompensated)

39
Q

What blood tests would you in a patient with suspected liver disease?

A

FBC- Increased MCV
LFTs- Increased ALT and AST, increased ALP in cirrhosis, Increased bilirubin in cirrhosis, decreased albumin
Coagulation Screening- Prothrombin time is increase
U&Es to check for hepatorenal syndrome

40
Q

What is hepatorenal syndrome?

A

Happens in cirrhosis
Portal hypertension leads to back pressure of blood, leading to vasodilators being released
This leads to arterial vasodilation which leads to a drop in pressure
This leads to RAAS being activated and so you get vasoconstriction of the renal arteries, leading to reduced blood flow to the kidneys

41
Q

What imaging would you use in a patient with liver disease?

A

USS- to detect any fatty changes and detect any changes related to cirrhosis
Fibroscan- elasticity of the liver and measures the degree of cirrhosis
CT/MRI- check for fatty infiltration, hepatocellular carcinoma, hepatosplenomegaly

42
Q

When would a biopsy be indicated in a patient with liver disease?

A

When considering starting steroids

43
Q

What is the general management in a patient with alcoholic liver disease?

A
  • Alcohol abstinence + withdrawl treatment: IV diazepam 10mg (long acting), use short acting in older pts/ hepatic dysfunction
  • Weight reduction + smoking cessation
  • Thiamine (to prevent W-K) and high protein diet ( be aware of refeeding syndrome)
  • Influenza and pneummococcal vaccines
  • Treat complications of cirrhosis
  • Consider prophylatic abx in some pts to prevent SBP
  • Steroids- short term (1 month) in severe alcoholic hepatitis
  • Liver transplant, but patient has to be sober for 3-6 months
44
Q

How does alcohol withdrawal present?

A

6-12hrs- craving, anxiety, sweats, headache
12-24hrs- hallucinations
24-48hrs-seizures- usually at 36hrs
48-72hrs- delirium tremens

45
Q

What is the pathophysiology of delirium tremens?

A

In alcohol dependency GABA receptors gets upregulated and glutamate receptors gets down regulated, so when you stop, you have under functioning of GABA and over functioning of Glutamate leading to increased excitability, causing delirium tremens

46
Q

What are the symptoms of delirium tremens?

A

Severe agitation
Confusion
Delirium and hallucinations
Tachycardia
hypertension
hyperthermia
Ataxia

47
Q

How you manage alcohol withdrawal?

A

Chlordiazepoxide (benzo)- reducing regime 10-40mg, 1-4hrs depending on patients needs
Pabrinex- high dose IV B vitamins and then followed by thiamine (oral)
Lactulose- to remove ammonia

48
Q

Why is thiamine so important to replace in alcohol dependency?

A

To prevent Wernicke-Korsakoff syndrome

49
Q

What is Wernicke Korsakoff Syndrome?

A

Made up of Wernicke encephalopathy which comes first- confusion, oculomotor disturbances, ataxia- medical emergency

Korsakoffs syndrome- comes after
Anterograde and retrograde memory loss
Behaviour changes
Irreversible and patient needs to be institutional care

50
Q

Characteristic findings in alcoholic hepatitis ?

A

AST/ALT ratio is 2:1 in alcoholic hepatitis
e.g. AST - 790
ALT- 375

+ Macrocytic anaemia (raised MCV)
+ Raised GGT

Present: RUQ pain, jaundice, and signs of liver failure

51
Q

What is liver cirrhosis?

A

Result of chronic inflammation of the liver–> scar tissue and nodules. Causes resistance in the vessels going to the liver, resulting in back pressure

52
Q

What are the most common causes of liver cirrhosis?

A

Alcoholic liver disease
Non-alcoholic liver disease
Hep B
Hep C

53
Q

What are the less common causes of liver cirrhosis?

A

Autoimmune hepatits
Primary biliary cirrhosis
Haemochromatosis
Wilsons disease
Alpha-1-antitrypsin deficiency
CF
Drugs e.g. amiodarone, methotrexate and sodium valproate

54
Q

What are the signs of liver cirrhosis?

A

Jaundice- due to high bilirubin
Hepatomegaly - however may be smaller the more cirrhotic it gets
Splenomegaly- due to portal hypertension
Spider naevi
Palmar erythema- caused by hyper dynamic circulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising- due to abnormal clotting
Ascites
Caput medusa-due to portal hypertension
Flapping tremor

55
Q

What investigations would you do for liver cirrhosis?

A

LFTs- often normal but in decompensated cirrhosis, they’re often deranged

Albumin- drop
Prothrombin time- increases
Both useful for synthetic function of the liver

Hyponatraemia- fluid retention in severe disease

Urea and creatinine become deranged in hepatorenal syndrome

Further bloods can help establish the cause
Alpha-fetoprotein- tumour marker for hepatocellular carcinoma, can be checked every 6 months in patients with cirrhosis as a screening tool

56
Q

How do you interpret the results of the Enhanced liver fibrosis blood test?

A

<7.7 -none to mild fibrosis
> or equal to7.7-9.8- moderate fibrosis
> or equal to 9.8- severe fibrosis

57
Q

What would an USS show in a pt with liver cirrhosis?

A

Nodularity of liver surface
Corkscrew appearance to hepatic arteries
Enlarged portal vein with reduced blood flow
Ascites
Splenomegaly

58
Q

What does fibroscan measure?

A

Liver elasticity, therefore helps assess degree of cirrhosis
Done every 2 years in high risk pts:
Hep C
Heavy alcohol drinkers
Diagnosed alcoholic liver disease

59
Q

What is the general management of liver cirrhosis?

A

USS and alpha-fetoprotein every 6 months to screen for heptocellular carcinoma
Endoscopy every 3 years for pt with known varices
High protein, low sodium diet
MELD score every 6 months
Consider liver transplant
Manage complications

60
Q

Why does liver cirrhosis relate to malnutrition

A

Increase use of muscle tissue as fuel and reduces amount of protein available in body for muscle growth .
Disrupts ability of liver to store glucose as glycogen and release it when required
= body using muscle tissue as fuel–> muscle wasting and weight loss

61
Q

Management of malnutrition secondary to cirrhosis?

A

Meals every 2-3 hours
Low Na diet–>minimise fluid retention
High protein and high calorie diet
Avoid alcohol

62
Q

Sites of varices?

A

Gastro-oesophageal junction
Ileocaecal junction
Rectum
Ant abdo wall via umbilical vein (caput medusa)

63
Q

Treatment of stable varices?

A

Propranolol reduces protein hypertension by acting as a non-selective B blocker
Elastic band ligation of varices
Injection of sclerosant (less effective than band ligation)

64
Q

What is TIPS?

A

Trans intra-hepatic portalsystemic shunt

X-ray guided wire into jugular vein–>vena cava–>liver via hepatic vein.
Connection between hepatic vein and portal vein and place stent–> relieves pressure in portal system

When other treatments fail or bleeding cannot be controlled

65
Q

What is ascites?

A

Fluid in peritoneal cavity
Increased pressure in portal system forces fluid out into peritoneal cavity–> drop circulating volume–> reduced BP–> RAAS activated–> aldosterone leads to increased fluid and sodium reabsorption–> fluid and sodium overload

66
Q

Management of ascites?

A

Anti-aldosterone diuretics–> Spironolactone
Paracentesis if tense
Low Na diet
Prophylactic antibiotics agains SBP–> ciprofloxacin or norfloxacin in pts with less than 15g/L of protein
Consider TIPS in refractory ascites
Consider liver transplant in refractory ascites

67
Q

Prophylatic antibiotic in liver cirrhosis against SBP?

A

ciprofloxacin or norfloxacin

68
Q

Presentation of SBP?

A

Can be asymptomatic
Fever
Abdo pain
Raised WCC, CRP, creatinine or metabolic acidosis
Ileus
hypotension

69
Q

Most common organisms in SBP?

A

Escherichia Coli
Klebsiella pneumoniae
Gram positive cocci- staphylococcus or enterococcus

70
Q

Management of SBP?

A

Ascitic culture before giving antibiotics
IV cephalosporin e.g. cefotaxime

71
Q

What is hepatic encephalopathy?

A

Build up of toxins that affect the brain e.g. ammonia

72
Q

Why do you get build up of ammonia in liver cirrhosis?

A

Builds up due to liver unable to metabolise the ammonia and collateral vessels between portal and systemic circulation mean that the ammonia bypasses liver all together

73
Q

Precipitating factors of hepatic encephalopathy?

A

Constipation
Electrolyte disturbances
Infection
GI bleeding
high protein diet
Medications

74
Q

Presentation of hepatic encephalopathy?

A

Reduced consciousness and confusion
Chronically–> personality changes, memory and mood

75
Q

Management of hepatic encephalopathy?

A

Laxatives e.g. lactulose, dose appropriately so patient has 2-3 motions a day

Rifaximin- antibiotic–> reduces ammonia producing bacteria

Nurtrional support

76
Q

Investigations fo NAFLD?

A

1st line-Enhanced liver fibrosis blood test
2nd line- NAFLD fibrosis score
3rd line- Fibroscan

77
Q

Management for NAFLD?

A

Weight loss
Exercise
Stop smoking
Control of diabetes, BP and cholesterol
Avoid alcohol

78
Q

Presentation of hepatitis?

A

Asymptomatic or vague symptoms
Abdominal pain
Fatigue
Pruritis
Muscle and joint aches
Nausea and vomitting
Jaundice
Fever (viral hepatits)

79
Q

Epidemiology of Hep A?

A

Most common hep worldwide but relatively rare in UK

80
Q

Transmission of Hep A?

A

Faecal oral route usually in contaminated water?

81
Q

What type of virus is Hep A?

A

RNA

82
Q

Presentation of Hep A?

A

Nausea, vomitting, jaundice and anorexia
Cholestasis- dark urine and pale stools
Moderate hepatomegaly

83
Q

Management of Hep A?

A

Basic analgesia
Resolves without treatment 1-3 months

84
Q

Prevention of Hep A?

A

Vaccination and it is a notifiable disease

85
Q

What type of virus is Hep B?

A

DNA

86
Q

Transmission of Hep B?

A

Direct contact with blood or bodily fluids, sharing household items e.g. toothbrush
Vertical transmission

87
Q

Prognosis of Hep B?

A

Most people fully recover in 1-2 months
10-15% become chronic hepatitis B carriers–> virus DNA integrated into their own DNA

88
Q

Viral markers and their relevance in Hep B?

A

Surface antigen (HBsAg)- active infection
E Antigen (HBeAg)- marker of replication–> high infectivity
Core antibodies (HBcAb)- past or current infection
Surface antibody (HBsAb)- vaccination or past or correct infection
Hep B virus DNA(HBV DNA)- direct count of viral load

89
Q

How can Core antibodies in hep B determine past or current infection?

A

Look at IgM or IgG.
IgM–> high in acute infection and low in chronic infection
IgG–> past infection where HBsAg is negative

90
Q

Outline the Hep B vaccine?

A

Inject HBsAg
3 doses at different intervals
Check of HBsAb
Included as past of UK routine

91
Q

Management of Hep B?

A

Low threshold for screening at risk patients
Screen for other blood borne viruses and other sexual transmitted disease
Reder to GI/hepatology or infectious disease for specialist management
Notify public health England
Stop smoking and alcohol
Education- transmission and at risk contacts
Test for complications
Antiviral medication to slow disease progression and reduce infectivity
Liver transplant for end stage liver disease

92
Q

What type of virus is Hep C?

A

RNA

93
Q

Transmission of Hep C?

A

Blood and bodily fluids

94
Q

Disease course of Hep C?

A

1 in 4–> full recovery
3 in 4–> chronic

95
Q

Complications of Hep C?

A

Liver cirrhosis
Hepatocellular carcinoma

96
Q

How do you test for Hep C?

A

Hep C antibody screening test
Hep C RNA testing used to confirm the diagnosis of Hep C, calculate viral load and assess for the individual genotype

97
Q

Management of Hep C?

A

direct acting antivirals- tailored to specific genotype–> successful in over 90% patients, take 8-12 weeks
Low threshold for screening at risk patients
Screen for other blood borne viruses and other sexual transmitted disease
Reder to GI/hepatology or infectious disease for specialist management
Notify public health England
Stop smoking and alcohol
Education- transmission and at risk contacts
Test for complications
Liver transplant for end stage

98
Q

What are the two types of Autoimmune hepatitis?

A

Type 1: occurs in adults
Type 2: occurs in children

99
Q

How does type 1 autoimmune hepatitis present? Who does it often affect?

A

Women around 40s-50s or around the menopause with fatigue and features of disease on examination

100
Q

How does type 2 autoimmune hepatitis present?

A

Teenage years or early 20s with high transaminases and jaundice

101
Q

Type 1 autoimmune hep antibodies?

A

Anti nuclease antibodies- ANA
Anti- smooth muscle antibodies- Anti- actin
Anti-soluble liver antigen- anti-SLA/LP

102
Q

Type 2 autoimmune hep antibodies?

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (Anti-LC1)

103
Q

Parameters in MELD score?

A

A patient’s bilirubin, creatinine, and the international normalized ratio (INR) to predict survival.

104
Q

Define acute liver failure

A

Rapid onset of hepatocellular dysfunction. Leads to a variety of systemic complications.

105
Q

Common causes of acute liver failure

A

Paracetamol overdose
Alcohol
Viral hepatitis - usually Hep A or Hep B
Acute fatty liver of pregnanvy

106
Q

Features of acute liver failure?

A

Jaundice
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure is common - hepatorenal syndrome

107
Q

Investigations for acute liver failure (ALF) and why?

A

1) LFTs: would be raised:

Bilirubin = Jaundice is a defining feature of acute liver failure - so look for hyperbilirubinaemia

AST and ALT = high in paracetamol hepatotoxicity

2) INR = coagulopathy is a defining feature of ALF

3) U+Es = renal failure common in ALF

4) FBC - high WCC for infection.Thrombocytopenia common. Anaemia common

5) Cross match and G+S = may need blood transfusion

6) ABG = metabolic acidosis in paracetamol overdose

108
Q

Immediate management for acute liver failure?

A
  • Intensive care management - if hepatic encephalopathy is present

plus the following if required:
- liver transplant assessment
- neurological status monitoring
- blood glucose (every 1-2hrs), electrolytes (2x a day) and cultures monitoring. Correct if needed.
- acetylcysteine if paracetamol overdose

109
Q

Compare AST : ALT liver enzyme results in:
1. NAFLD
2. Alcoholic liver disease
3 Acute alcoholic hepatitis
4. Liver cirrhosis

A
  1. NAFLD : ALT will be higher than AST
  2. ALD: AST >2 x higher than ALT
  3. Acute alcoholic hepatitis: AST>3 x higher than ALT
  4. Cirrhosis: AST > 2.5 x higher than ALT

In chronic hepatitis, you would expect AST to be 10x raised.

110
Q

What are the parameters of the Child-Pugh Score ? the 5 things it look at ?

A

Bilirubin
Albumin
INR
Ascites
Hepatic Encephalopathy?

111
Q

What are some risk factors for variceal haemorrhage?

A

High portal pressures (>12mmHg)
Large varices
Abnormal variceal wall at endoscopy (eg haematocystic spots)
High Child-Pugh score

112
Q

What are some complications of liver biopsy?

A

Shoulder tip pain
Bowel perforation
Renal laceration
pnuemothorax
billiary peritonitis

113
Q

In what groups of people might liver biopsy be contraindicated and why?

A

High risk of bleeding in pts with:

Large ascites
Disordered platelets / clotting
Not co-operative
Severe cirrhosis

WIth these ppl can do transjugular or laparoscopic routes

114
Q

Treatment of chronic liver disease?

A

Remove underlying aetiology - e.g. stop drinking (if alcohol related), weight loss (if non-alcoholic liver steatohepatitis), antivirals (if hep B or hep C), venesection (if haemochromatosis)

115
Q

Why is it important to treat chronic liver disease?

A

Prevent further liver damage and prevent progression to cirrhosis

116
Q

Benefits of using a fibroscan for liver cirrhosis over other imaging?

A

Quicker
More specific
Can be performed in clinic room

117
Q

What complications should you screen for in patients with liver cirrhosis? How would you screen for these?

A
  • DEXA scan = screen for osteoporosis
  • USS of liver and AFP = screen for hepatocellular carcinoma
118
Q

Pt has ascites. What investigation should be done for all pts with ascites?

A

Diagnostic ascitic tap (cell count and MC&S) - look for SBP.

119
Q

Initial blood tests to do for cirrhosis and reasoning?

A

1) LFTs - albumin, bilirubin, liver enzymes = assess liver function

2) FBC - WCC look for infective cause, thrombocytopenia = chronic liver disease, Hb for anaemia = normocytic in Wilson’s disease, oesophageal bleed or macrocytic if folate/b12 deficiency in alcohol excess

3)Urea and electrolytes to establish baseline renal function and to look for hepato-renal syndrome or any electrolyte abnormalities

4) INR - for coagulpathy

5) Others - autoantibodies - for AI hepatitis, alpha 1 antitrypsin, iron studies in haemochromatosis etc

120
Q

What is the primary mechanism causing gynecomastia in liver cirrhosis?

A

Disordered metabolism of sex steroids, which leads to excess levels of oestrogen

121
Q

What are the cardinal features of decompensation in liver disease?

A

Jaundice
Ascites
Hepatic flap
Altered mental status

122
Q

If a pt drinks around 2 litres of cider (ABV 5%) a day. How many units is that a week?

A

Alcohol units = volume (ml) * ABV / 1,000

2000 ml x 5% = 10,000

Divide this figure by 1,000 to get the number of units = 10,000/1,000 = 10 units/day

10 units/day x 7 days = 70 units

123
Q

What LFT results would you expect in a patient with autoimmune hepatitis?

A

Raised ALT and bilirubin

Normal/mildly raised ALP.

May be IgG predominant hypergammaglobulinemia.

124
Q

What are the drug causes of pancreatitis?

A

Azathioprine
Sulfasalazine
Valproate
Statins
ACE inhibitors
Oral contraceptives

125
Q

What is ischaemic hepatitis?

A

diffuse hepatic injury resulting from acute hypoperfusion (sometimes known as ‘shock liver’). It is not an inflammatory process. It is diagnosed in the presence of an inciting event (e.g. a cardiac arrest) and marked increases in aminotransferase levels (exceeding 1000 international unit/L or 50 times the upper limit of normal).

126
Q

When to suspect ischaemic hepatitis?

A
  • if the ALT is high: exceeding 1000 international unit/L or 50 times the upper limit of normal).AND
  • the pt just had a cardiac arrest
  • low BP
  • Any acute hypoperfusion
  • Often, it will occur in conjunction with acute kidney injury (tubular necrosis) or other end-organ dysfunction.
127
Q

How does alcoholic liver disease MOST COMMONLY present?

A
  • Asymptomatic elevation of aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) in a person consuming alcohol in excess
128
Q

What is important to remember in alchoholic liver disease when it comes to presentation?

A
  • symptoms do not reflect severity
129
Q
A
130
Q

What is the CAGE questionnaire?

A
  • screening tool for alcohol misuse and dependency
  • C-Have you ever felt you needed to CUT down on your drinking?
  • A: Have people ANNOYED you by criticising your drinking?
  • G: Have you ever felt GUILTY about drinking?
  • E: Have you ever felt you needed a drink first thing in the morning (EYE-OPENER) to steady your nerves or get rid of a hangover?
131
Q

What signs may a person with early stage ALD present with?

A

Ascites
Splenomegaly
Venous collateral circulations.

132
Q

Complications of ascites?

A
  • spontaneous infection of the fluid
  • development of abdominal hernias
  • difficulty in breathing
  • decreased food intake
  • progressive malnutrition
  • decreased physical activity with loss of muscular mass.
133
Q

What are some physical problems people with alcohol dependency face?

A

may co-exist with ALD because of chronic alcohol use.
* Poor nutritional status
* muscle wasting
* peripheral neuropathy
* dementia
* cardiomyopathy

134
Q

In bloods:

What are markers of alcohol induced liver injury?

A

AST and ALT
* AST and ALT can be normal in the absence of significant liver inflammation (a reassuring sign) or in advanced cirrhosis
* the AST level is almost always elevated (usually above the ALT level). The classic ratio of AST/ALT >2 is seen in about 70% of cases
* gamma-GT is frequently elevated in heavy drinking, but is not specific for alcohol use. It is helpful in identifying patterns of alcohol misuse.

135
Q

Blood results in ALD?

A
  • Anaemia: multiple causes, including iron deficiency, gastrointestinal bleeding, folate deficiency, haemolysis, and hypersplenism.
  • Leukocytosis may be from an alcoholic hepatitis-related leukemoid reaction or an associated infection.
  • Thrombocytopenia may be secondary to alcohol-induced bone marrow suppression, folate deficiency, or hypersplenism.
  • A high MCV may also indicate liver disease.
  • Hyponatraemia is usually present in patients with advanced liver cirrhosis.
  • Hypokalaemia and hypophosphataemia are common causes of muscle weakness in ALD.
  • Hypomagnesaemia can cause persistent hypokalaemia and may predispose patients to seizures during alcohol withdrawal.
  • Hyperphosphataemia predicts poor recovery in advanced liver disease.
  • Prolonged prothrombin time (PT) and international normalised ratio (INR) indicate diminished hepatic synthetic function in advanced liver disease with cirrhosis or liver failure in patients with ALD.
  • high AST and ALT
136
Q

A pt presents with ?ALD what tests do you need to do to rule things out?

A
  • Viral hepatitis serological panel (for hepatitis A, hepatitis B, hepatitis C)
  • Iron studies (for haemochromatosis) and copper studies (for Wilson’s disease)
  • Anti-mitochondrial antibody (AMA) is used to test for co-existent primary biliary cirrhosis.
  • ANA (anti-nuclear antibody) and ASMA (anti-smooth muscle antibody) are used to rule out the presence of associated autoimmune hepatitis.
  • Alpha-1 antitrypsin
137
Q

A pt with ?ALD presents, what imaging would you do?

A
  • Ultrasound should be performed among patients with harmful alcohol use, as it helps diagnose alcoholic fatty liver disease in patients with hepatic steatosis
  • Fibroscan for degree of cirhossis
  • CT/MRI: search for a tumour in patients with an elevated alpha-fetoprotein and high clinical suspicion of HCC whose ultrasound is negative.

Decks in Year 3 Medicine Block Class (56):