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GI/Liver > Clinical Aspects of Liver Disease > Flashcards

Clinical Aspects of Liver Disease Flashcards

1
Q

What are the standard liver function tests?

A 
Bilirubin
AST
ALT
GGT
ALP
Albumin
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2
Q

What tests indicate liver function? (not just liver inflammation etc.)

A

Albumin
Bilirubin
PT time

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3
Q

What is the problem with LFTs?

A

Around 20% of the population have abnormal LFTs
Might not be liver in origin
- ALP elevation could be bone
- AST might be muscle
- isolate bilirubin might be haemolysis
Advanced cirrhosis might have normal LFTs

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4
Q

What investigations into chronic liver disease can you perform?

A 
US
Chronic viral hepatitis 
- HBV, HCV
Autoimmune liver disease
- ANA/SMA/LKM (AIH); AMA (PBC; Igs (raised IgG)
Metabolic liver disease
- ferritin (haemochromatosis) 
- caeruloplasmin (Wilson's disease)
- alpha-1 antitrypsin deficiency
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5
Q

What investigations into acute liver disease can you perform?

A 
US
Acute viral hepatitis 
- HAV, HBV, (HCV), HEV and CMV
Autoimmune liver disease
- ANA/SMA/LKM (AIH); immunoglobulins (raised IgM)
Paracetamol levels
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6
Q

What are the most common causes of abnormal liver blood tests?

A 
Fatty liver
- alcoholic liver disease
- NAFLD
Chronic viral hepatitis
- chronic Hep C
Autoimmune liver disease
- primary biliary cirrhosis 
- autoimmune hepatitis
Haemochromatosis
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7
Q

Describe how steatosis can progress to cirrhosis?

A

Macrovesicular stastosis with lipid vacuole filling the hepatocyte cytoplasm
Staetohepatitis
- neutrophils and lymphocytes surround the hepatocytes with Mallory hyaline
Pericellular fibrosis as well as bands of fibrous tracts between the portal tracts (fatty liver disease cirrhosis)

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8
Q

What risk factors increase the risk of getting NAFLD?

A

Obesity
Hypertension
Type 2 Diabetes
Hypertension and T2DM

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9
Q

What is the main way to tell the difference between alcohol fatty liver disease and NAFLD?

A 
ALD
- AST>AST
- ratio >1.5
NAFLD
- ratio <0.8
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10
Q

Why are rates of ALD increasing?

A

Alcohol is becoming more available and affordable

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11
Q

Describe the biochemical patterns of ALD.

A 
Raised AST:ALT ratio
- preferential AST elevation as mitochondrial disease and pyridoxine deficiency 
AST doesnt normallt go above 500
ALT isn't normally less than 300
May appear cholestatic
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12
Q

What are the clinical features of alcoholic hepatitis?

A 
Recent alcohol excess
Bilirubin >80mol/l
AST:ALT ratio >1.5
Hepatomeagly
Fever
Leucocytosis 
Hepatic bruit
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13
Q

Describe the Glasgow Alcoholic Hepatitis Score.

A 
1 point for each 
- age: <50
- WCC: <15 109/l
- urea: <5mmol/l
- PT ratio/INR: <1.5
- bilirubin: <125mol/l
2 points for each
- age: >50
- WCC: >15 109/l
- urea: >5mmol/l
- PT ratio/INR: 1.5-2.0
- bilirubin: 125-250mol/l
3 points for each
- PT ratio INR: >2.0
- bilirubin: >250mol/l
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14
Q

What accelerates the progression of fibrosis in Hep C infections?

A 
Male sex
Age >40 at time of acquisition 
Alcohol >50g/week
HIV
Hep B
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15
Q

What is the natural history of a chronic Hep C infection?

A

Slow, intermediate or rapid fibrosis progression
Cirrhosis
- leads to decompensated liver disease or hepatocellular carcinoma
Death

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16
Q

What are the risk factors for getting a HCV infection?

A 
IVDU; bloos transfusions
Sexual transmission
- increased prevalence with multiple partners 
Vertical transmission
Needle-stick transmission
No risk factors in some patients
17
Q

What are the signs and symptoms of chronic liver disease?

A 
Stigmata
- spider nevi
- foetor
- encephalpathy
Synthetic dysfunction
- PTT
- hypoalbuminaemia
18
Q

What are the signs and symptoms of portal hypertension?

A 
Caput medusa
- recanulisation of the umbilical veins
Hypersplenism
Ascites
Thrombocytopenia (pancytopenia)
19
Q

What grades are associated with severity of liver injury?

A

Childs-Turcotte-Pugh Score

  • Grade A (score 5-6) - mild
  • Grade B (score 7-9)
  • Grade C (score 10-15) - decompensated
20
Q

What is portal hypertension?

A

Increased resistance to flow in the portal venous system and sustained increase in portal venous pressure

21
Q

Describe the pathophysiology of portal hypertension.

A

Pre-hepatic, hepatic and post-hepatic obstructions occur to block the portal venous system
- raised portal pressure occurs, which causes hypersplenism and porto-systemic shunting
Porto-systemic shunting means blood that should be in the liver is being forced into the system (encephalopathy)
- oesophago-gastric varices also form
The opening of new vessels causes NO release, which again increases the BP of the portal system
- splanchnic vasodilation
- reduced effective circulating volume leads to release of compensatory vasopressors (RAAS)
This causes sodium retention and renal vasoconstriction
- ascites
- hepato-renal syndrome

22
Q

Name a pre-hepatic, hepatic and post-hepatic cause of portal hypertension.

A 
Pre-hepatic
- portal vein thrombosis
Hepatic
- cirrhosis
Post-hepatic
- Budd Chiari
23
Q

How is a diagnostic tap of ascites assessed?

A

Cell count
- >500 WBC/cm3 and >250 neutrophils/cm3 suggest spontaneous bacterial peritonitis
Albumin
- serum ascites albumin gradient = serum albumin minus ascitic albumin
- SAAG>11g/l = portal hypertension

24
Q

How is ascites treated?

A 
Low salt diet (if sodium retention is a problem)
Diuretics
- spironolactone
- frusemide
Paracentesis
25
Q

What is hepatorenal syndrome?

A

Rapid deterioration in kidney function in people with terminal liver failure and ascites

26
Q

What are the two types of hepatorenal syndrome?

A 
Type 1
- rapid decline in function, often triggered by spontaneous bacterial peritonitits
- almost 100% mortality in 10 weeks
Type 2
- moderate, stable decline
- 3-6 months survival
27
Q

Describe the Conn Score for Grading Mental State in Hepatic Encephalopathy.

A 
Grade 0
- no personality of behavioural abnormality detected
Grade 1
- lack of awareness
- euphoria or anxiety
- shortened attention span
- impaired performance of addition
Grade 2
- lethargy or apathy
- minimal disorientation for time or place
- subtle personality changes
- inappropriate behaviour
- impaired performance of subtraction
Grade 3
- somnolence to semi-stupor, response to verbal
- confusion
- gross deterioration
Grade 4
- coma
28
Q

What are the precipitating factors for Hepatic Encephalopathy?

A 
GI bleeding
Infections
Constipation
Electrolyte imbalance 
Excess dietary protein
29
Q

How is hepatic encephalopathy treated?

A 
Don't make it worse
- avoid regular sedation
- caution with opiates
- avoid hyponatraemia 
Laxatives
- lactulose/phosphate enemas
Non-absorbable antibiotics

GI/Liver (12 decks)

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