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4TH YEAR - CSIM2 > Abnormal Liver Function (week 5) > Flashcards

Abnormal Liver Function (week 5) Flashcards

1
Q

What is the most common cause of liver disease?

A

NAFLD (20-30% of population)

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2
Q

What is the most common cause of liver death?

A

Alcoholic liver disease (84%)

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3
Q

How does cirrhosis develop from normal liver tissue?

A

Normal –> initial insult to liver (fat or alcohol) = inflammation Steatosis Steatohepatitis Fibrosis –> Cirrhosis (last stage isn’t reversible)

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4
Q

What are the complications of liver cirrhosis?

A 
Ascites
Liver failure
Liver cancer
Portal HTN (& associated complications)
etc.
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5
Q

How can cirrhosis present?

A 
Incidental findings - Abnormal LFTs, hepatosplenomegaly, raised MCV/abnormal clotting/low platelets
Non-specific symptoms - Anorexia, weight loss, lethargy
Specific symptoms (usually late stage) - Jaundice, pruritus (itchy skin due to cholestasis), bleeding varices, ascites/oedema, hepatic encephalopathy
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6
Q

What does raised alkaline phosphatase and raised gamma GGT indicate?

A

Indicates Cholestasis, malignancy or alcohol abuse

Alcohol will have raised MCV

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7
Q

What does increased ALT/AST (the transaminases) indicate?

A

Indicate hepatocellular damage
1.5-3x the upper limit of normal in ALD/NAFLD
> 3x uppler limit of normal in viral, drug induced (paracetamol) and AI hepatitis

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8
Q

At what level of bilirubin do you get clinical jaundice?

A

> 30 µmol/L

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9
Q

When do you get unconjugated bilirubin?

A

Gilberts, haemolysis, newborn babies (physiological)

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10
Q

Which clotting factor(s) are tested in Prothrombin Time (PTT) & therfore, which clotting pathway is being measured?

A

Factor VII.

Extrinsic pathway

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11
Q

Why is PTT relevant in liver screening?

A

Liver makes clotting factors II, VII, IX & X. This is disrupted in acute liver failure/damage, which causes the PTT to increase (this happens very quickly).

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12
Q

Which autoantibodies do we test for in liver studies? What do they indicate?

A

ANA (antinuclear Ab) & anti SMA (anti smooth muscle Ab) in AI hepatitis.
AMA (anti mitochondrial Ab) in PBC (95%).
(P Billy Connolly is a lAMA)
pANCA in PSC (50%)
(Private Steve Clark is a P wANCA)

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13
Q

Which immunoglobulins are measured in liver studies? What do they indicate?

A

Increased IgG - AI hepatitis
Increased IgM - PBC
Increased IgA - Alcoholic liver disease/NAFLD

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14
Q

Which tumour markers are relevant to the hepatobiliary system?

A

Alpha fetoprotein - HCC

CA19-9 - Cholangiocarcinoma

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15
Q

What is the first line imaging in Hepatobiliary disease? Which others may be helpful?

A

USS - 1st line

CT, MRI, ERCP

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16
Q

What are the benefits and limitations of USS in hepatobiliary disease?

A

Good to show obstruction of bile ducts, liver tumour or mass lesion, gallstones and can assess blood flow using doppler function.
Cant assess pancreas well.

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17
Q

What are the benefits and limitations of CT in hepatobiliary disease?

A

More sensitive than USS. Excellent investigation for focal liver lesions, varices and evidence of portal hypertension (hypervascularisation)
Needs IV contrast - caution in renal impairment

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18
Q

What is the main use of ERCP?

A

To remove stones or to place stents

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19
Q

What are the indications for liver biopsy?

A 
Chronic liver disease - Diagnosis or staging
Focal lesions (guided)
Post transplant (rejection)
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20
Q

What is the “gold standard” for liver disease staging?

A

Liver biopsy

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21
Q

Name 2 scoring systems that can non-invasively assess liver disease

A

FIB-4 score (Age, ALT, AST and platelet count)

NAFLD fibrosis score

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22
Q

What is the classical findings in primary biliary cirrhosis (PBC)?

A

AMA +ve

Raised ALP

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23
Q

What is PBC are what are the symptoms?

A

Granulomatous inflammation around the small intrahepatic bile ducts

Asymptomatic (incidental finding)
Fatigue, itch, dry eyes and mouth
If severe - symptoms of advanced liver disease

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24
Q

What is the diagnostic criteria of PBC?

A

Abnormal LFTs (cholestatic) = Raised ALP
Positive AMA
Compatible Hx
(2 of above = PBC probable, all 3 = definite PBC)

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25
Q

What is the treatment for PBC and what is the therapeutic aim?

A

Ursodeoxycholic acid (UDCA) (S/E = weight gain, hair thinning and diarrhoea)
Fibrates
Transplantation
Treat itch - Cholestyramine, Rifampicin or Naltrexone

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26
Q

What is the classical finding in AI hepatitis?

A

Raised ALT
ANA/ASMA +ve
Raised IgG

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27
Q

What are the main types of AI hepatitis? Which autoantibodies do you find for each?

A

Type 1 (75% of cases & can affect all ages)
ANA/AMSA
Type 2 (<10% of cases & affects young adults)
LKM-1 or LC

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28
Q

Is AI hepatitis more common in males or females?

A

Type 1 - F:M = 3:1

Type 2 - F:M = 10:1

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29
Q

How can AI hepatitis present?

A

Asymptomatic (incidental finding)
Fatigue, anorexia, nausea, joint pains
Acute hepatitis
Complications of cirrhosis

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30
Q

What is the treatment for AI hepatitis? What is the treatment aim/goal?

A

Immunosuppression - steroids (1st line short term), Azathioprine (1st line long term), Tacrolimus (2nd line)
Transplantation
Aim for normalisation of ALT and IgG

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31
Q

What is the classical findings in primary sclerosing cholangitis (PSC)?

A

Raised ALP
ANCA +ve
(Private Steve Clark is a wANCA)

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32
Q

What is PSC and what associated diseases does it have?

A

Inflammation and fibrosis of intra and extra hepatic bile ducts, causing multifocal strictures
60-80% patients have IBD
(Private Steve Clark is a wANCA and a Incredibly Boring Dude)

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33
Q

How does PSC present?

A

Asymptomatic (incidental finding)
Fatigue, itch, RUQ pain, weight loss
Cholangitis (often not at presentation)
Jaundice and complications of cirrhosis

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34
Q

What is the LFT pattern in PSC?

A

Shows Cholestasis

  • -> Increased bilirubin
  • -> Increased ALP (indicated obstruction)
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35
Q

Apart from blood tests, what investigations are useful in PSC? What would they show?

A

USS - often normal
MRCP - Multi-focal, short annular strictures alternating with normal or dilated segments (beading)
Liver biopsy - early (often non specific), later = ‘Onion skin’ fibrosis

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36
Q

How do you manage PSC?

A

Look and test for IBD
If strictures causing symptoms (cholangitis, jaundice, pruritus) - ERCP (insert balloons/stents)
Itch - Cholestyramine, Rifampicin or Naltrexone
Screen for malignancy - Cholangiocarcinoma

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37
Q

Summarise PBC - Type of patient, Hallmark LFT/autoantibodies, Symptoms and treatment.

A

Typical patient - Middle aged women
LFT/Autoantibodies - Raised ALP + AMA +ve
Symptoms - Fatigue, itch, dry eyes & mouth
Treatment - Ursodeoxycholic Acid (UDCA)

P Billy Connolly is a lAMA

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38
Q

Summarise AI hepatitis - Type of patient, Hallmark LFT/autoantibodies, Symptoms and treatment.

A

Typical patient - Any age or sex
LFT/Autoantibodies - Raised ALT + ANA + ASMA
Symptoms - often asymptomatic
Treatment - Immunosuppression

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39
Q

Summarise PSC - Type of patient, Hallmark LFT/autoantibodies, Symptoms and Management.

A

Typical patient - Men
LFT/Autoantibodies - Raised ALP + ANCA +ve
Symptoms - Fatigue, itch, RUQ pain, weight loss
Associated with IBD
Management - Screen for cholangiocarcinoma and bowel cancer

Private Steve Clark is a wANCA and an Incredibly Boring Dude

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40
Q

What is AMA associated with?

A

PBC

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41
Q

What is ANA + ASMA associated with?

A

AI hepatitis

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42
Q

What is ANCA associated with?

A

PSC

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43
Q

What is IgA associated with?

A

Alcohol, NAFLD

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44
Q

What is IgM associated with?

A

PBC

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45
Q

What is IgG associated with?

A

AI hepatitis

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46
Q

What are the 2 blood supplies of the liver?

A

Hepatic artery - Arterial blood from aorta

Portal Vein - Venous blood from the bowel (2/3)

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47
Q

How can we aid prevention of HCC (hepatocellular Carcinoma)?

A

Primary prevention - HBV vaccine & avoid carcinogens

Secondary prevention - Reduce alcohol and calorie intake, Reduce exposure to Hep C (increase education)

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48
Q

Who do we screen for HCC, how do we do it and how often?

A

Screen cirrhotic patients
AFP (upper normal limit is 10)
USS - every 6 months - look for liver nodules
If nodule <1cm - scan again in 3 months
If nodule 1-2cm - FNAB looking for HCC
If nodule >2cm - AFP > 400 = HCC (do CT/MRI angiography to stage and confirm HCC)

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49
Q

What are the 4 stages of CT or MRI scan for HCC?

A

Normal scan
Add contrast - Arterial blood supply (aorta/blood seen in white - white areas in liver = HCC) most important stage
Venous stage
Late venous stage

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50
Q

Which scoring system do we use to assess liver function? what are the 5 parameters?

A

Child-Pugh score (5 best function - 15 worst)- looks at fitness to undergo a surgical procedure
Encephalopathy, Ascites, Bilirubin, Albumin, PTT

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51
Q

What are the signs of chronic liver disease?

A

Dupuytrens contracture, palmar erythema, spider naevi (SVC distribution)
Bad signs - Jaundice, ascites, caput medusa, asterixis (liver flap - low level encephalopathy allowing toxins into the blood)

52
Q

What is the most common management of HCC?

A

TACE (TransArterial ChemoEmbolism)
(blocks off arterial blood supply to tumour - stops growth)
Often precedes the ultimate management is transplant

Also be aware of:

  • Single nodule - RESECT
  • Advanced with portal invasion - SORAFENIB
53
Q

How does simple steatosis present on biopsy?

A

Large white adipose cells

54
Q

How do you calculate HVPG (hepatic venous pressure gradient) and what value defines clinically significant portal HTN?

A

Gradient between Wedged hepatic venous pressure (WHVP) and the free hepatic venous pressure.
It gives an estimate of pressure between the portal vein and IVC.
HVPG >10 defines clinically significant portal HTN

55
Q

What is the formal diagnostic criteria for Acute (fulminant) liver failure (ALF)?

A

An Increase in PT by 4-6 seconds (INR>1.5)
+ Development of hepatic encephalopathy (HE) = Jaundice

In a patient without preexisting cirrhosis + illness < 6 months

56
Q

What is the most common cause of ALF?

What are some other causes?

A

Paracetamol OD (toxic = >150mg/kg)

Drug reaction
Viral hepatitis
Ischaemic hepatitis
AI hepatitis
Wilsons
Budd Chiari
57
Q

What is the mechanism of paracetamol poisoning?

A

Major route of Paracetamol metabolism:
P metabolised into sulphate and glucuronide (non-toxic) conjugates. This route is easily saturable.
When saturated, minor route of metabolism is used:
P metabolised into NAPQI causing cell death

58
Q

What is the antidote for paracetamol OD? Who do we treat?

A

Antidote = NAC (N-acetylcysteine)
Treat anyone with paracetamol levels over the “100 line” (100mg/L) - 4 hours after ingestion. (if under, no need treating) Best results within 8 hours.

59
Q

Apart from the antidote, is there any other treatment we can offer?

A

Activated charcoal (give asap)

60
Q

What is the most apparent LFT in paracetamol OD?

A

Massive ALT

61
Q

What are the differential diagnoses for massively raised ALT?

A

Vascular - hypotension, congestion
Viral - Hep A-E, CMV, EBV, HSV, PMV
Drugs/toxins - PARACETAMOL, halothane, Abx, antivirals etc.

62
Q

What are the best prognostic markers in ALF?

A

Bilirubin and PTT

ALT is a bad prognostic marker. If massively raised (1000’s) and now falling, this is likely due to significant cell death, therefore not enough functioning cells to release ALT

63
Q

When is the most common viral hepatitis causing ALF?

A

Hep E

64
Q

When is Hep E particularly dangerous?

A

In pregnancEEEEEEEEE

65
Q

What are the most dangerous risks/complications of ALF?

A 
Cerebral oedema (causing raised ICP, particularly if concurrent renal failure or patient under 35))
Infection - in ALF, WCC drops (especially neutrophils), therefore susceptible to infection. (Give prophylactic antibiotics)
66
Q

How does increased ammonia effect the brain?

A

Cause cerebral oedema
Brain acts as the alternative detoxification pathway, astrocytes convert ammonia –> glutamine. Excess glutamine has an osmotic effect and water is drawn into astrocytes (they swell), increasing water in the brain.

67
Q

What is the treatment of cerebral oedema?

A

Bolus IV hypertonic saline
Aim to keep serum Na < 150 mmol/L
Cool patient

68
Q

What is the definitive treatment for severe ALF?

A

Liver transplant

69
Q

What is the difference between compensated and decompensated cirrhosis?

A

Compensated - no clinical signs/symptoms
Decompensated - Clinically evident complications
- Liver cell failure –> Coagulopathy, hyperproteinaemia, jaundice
- Portal HTN

70
Q

Describe the process of cirrhosis formation (compensated)?

A

Stiff and scarred liver → increases intrahepatic vascular resistance →
In time develops an adaptive response with arterial vasodilatation in the Splanchnic circulation and an effective lower arterial blood volume →
Subsequent circulatory changes that initially can be regulated and compensated for.

71
Q

Describe the process of cirrhosis formation (decompensated)?

A

Stiff and scarred liver → increases intrahepatic vascular resistance →
Develops an adaptive response with arterial vasodilatation in the Splanchnic circulation and an effective lower arterial blood volume →
As things become more severe, disease develops and portal pressure increases
Arterial vasodilatation in the splanchnic circulation becomes much more severe →
Arterial blood volume becomes greatly reduced → Changes in cardiac and renal circulation, due to secondary neurohumoral changes →
Develop sodium and water retention → ascites → hepato-renal failure.

72
Q

What is decompensated cirrhosis? What can cause compensated cirrhosis to decompensate?

A 
Deterioration in liver function in cirrhosis, that can manifest with the following:
•	Jaundice, 
•	Increasing ascites, 
•	Hepatic encephalopathy, 
•	Renal impairment/hypovolaemia, 
•	Signs of sepsis

Decompensating events:

  • Infection
  • Constipation
  • Increased alcohol
  • Medication (opiates/NSAIDS)
  • Dehydration
73
Q

What is the natural history of cirrhosis, clinically?

A

Compensated cirrhosis → decompensating event → decompensated cirrhosis → If we can’t reverse it then it can lead to hepato-renal failure, death and/or the requirement for liver transplant.

74
Q

Why does cirrhosis increase cancer risk?

A

The cirrhosis cells are abnormal and therefore there is a greater risk of developing HCC (hepatocellular cancer).

75
Q

What is the most common complication of cirrhosis?

A

Ascites

76
Q

How does Ascites present?

A

Can often be found radiologically before clinically (USS)
Abdomen distension
Shifting dullness

77
Q

What is the pathogenesis of ascites?

A

Cirrhosis (Scarred and stiff liver) → Increased intrahepatic vascular resistance & increased portal blood flow → portal hypertension → RAAS activation + ADH secretion → Na retention → Water retention →t Ascites

78
Q

Why do we do ascitic fluid analysis?

A

1) measure neutrophil count to assess infection status.
- Neutrophil count > 250 cells/µL = SBP
2) measure SAAG (Serum ascites albumin gradient)
- SAAG = Albumin (serum) - Albumin (ascites)
- If >1.1g/L ascites due to portal HTN + cirrhosis (aka transudate, and not a rarer cause)

79
Q

What is SAAG? What is its significance?

A

SAAG (Serum ascites albumin gradient)

  • SAAG = Albumin (serum) - Albumin (ascites)
  • If >1.1g/L ascites due to portal HTN + cirrhosis (& not a rarer cause)
80
Q

What is the only definitive treatment for severe cirrhosis?

A

Liver transplant

81
Q

What is SBP? How does it present (clinically and in lab tests)?

A

Spontaneous Bacterial Peritonitis
- Infection of the ascitic fluid in the absence of a secondary cause
Patients can present with fever and abdo pain
Ascitic analysis -
- Neutrophil count > 250 cells/µL = SBP

82
Q

How do you treat SBP?

A

Abx ASAP –> IV co-amoxiclav or ciprofloxacin (oral)

83
Q

What is Hepatorenal syndrome and how is it caused?

A

Large sodium retention leading to functional renal failure.
Occurs exclusively on the background of ascites (and usually hyponatraemia)
Due to marked hormonal and haemodynamic changes that occur in advanced portal hypertension

84
Q

What are the 2 types of Hepatorenal syndrome?

A

Type 1 (acute) - secondary to precipitant
- Usually SBP, paracentesis, sepsis or GI bleed
- Rapidly progressive if untreated
Type 2 (chronic) - develops spontaneously
- usually in pts with diuretic resistance
- slower onset/progression
- median survival of 6 months without transplant

85
Q

What is the treatment of Hepatorenal syndrome?

A

Terlipressin and albumin - combat spanchnic vasodilation
Stop nephrotoxic drugs - (NSAID, diuretics, etc.)
Liver transplant always gold standard

86
Q

What are varices?

A

Essentially they are varicose veins that occur particularly in the oesophagus and the stomach.

87
Q

What causes varices?

A
  • Portal hypertension and vascular resistance lead to blood from the gut struggling to get through the liver and back to the heart and therefore it tries to find other routes.
  • There are embryonic channels and areas of portal systemic anastomoses, particularly around the left/short gastric vein.
  • Blood takes this route, collaterals develop, angiogenesis occurs and you develop these marked veins.
88
Q

What is the risks of varices?

A

As pressure is high, it can cause spontaneous variceal bleeds.

89
Q

How do we treat a patient with identified varices?

A

Primary prophylaxis

  • Beta blockers (reduce BP)
  • Nitrates
90
Q

How do we treat acute variceal bleeds?

A

ABCDE (may need transfusion)
Endoscopic treatment.
- Tamponade with balloon
- Do every 2-4wks after until eradication

91
Q

What secondary prophylaxis can we offer for recurrent variceal bleeds?

A

Telipressin (vasopressin analogue) currently best pharmalogical treatment.
Endoscopically tie off varies
TIPSS (artificial shunt to treat portal hypertension by allowing blood to bypass the liver)

92
Q

What is Hepatic Encephalopathy (HE)?

A

Spectrum of neuropsychiatric abnormalities observed in patients with liver failure, due to an increase in gut-derived toxins in the blood

NB - in contrast to the HE from acute liver failure, cerebral oedema is a rare feature

93
Q

What are the main causes of Hepatic Encephalopathy (HE)?

A 
Infection
GI bleeding
Electrolyte disturbance
Constipation – This is a massive cause. Therefore make them poo loads.
Sedative drugs
94
Q

What are the treatments of Hepatic Encephalopathy (HE)?

A

Treat underlying cause
Oral lactulose – aiming to prevent constipation, (2-3 stools/day) and decrease ammonia levels
Phosphate enemas
Rifaximin for persistent HE or >1 admission with HE

95
Q

What are the clinical features of decompensated liver disease?

A 
Jaundice – especially in the eyes
Finger clubbing
Gynacomastia 
Spider naevi in SVC distribution
Hepatomegaly
96
Q

Which blood tests indicate liver cell damage?

A

Increased ALT/AST indicate hepatocellular damage

97
Q

Which tests indicate haemochromatosis?

A

Raised Ferritin & Transferrin saturation

98
Q

Which tests indicate Wilson’s disease?

A

Low caeruloplasmin & increased urinary copper

99
Q

What type of virus if Hepatitis E and how is it transmitted?

A

RNA virus

Faecal-oral transmission

100
Q

When is hep E not self limiting and/or dangerous?

A

Dangerous in pregnancEEEEEEE (3rd trim)
Can cause chronic infection in immunocompromised pts
Can cause acute decompensation in cirrhotic patients

101
Q

What extra-hepatic manifestations can hep e cause?

A

Neurological – (HEV found in CSF) – neuropathy & brachial neuritis (winged scapula), encephalitis, Guillain-Barre syndrome
Renal – Glomerulonephritis
Rheumatological – Arthralgia, myalgia, cryoglobulinaemia.

102
Q

What are the zoonoses for Hep E? What is the implication of this?

A

Hep E strains found in pigs, deer and rodents.

Therefore undercooked meat can spread disease.

103
Q

What is the treatment of HEP E in immunocompromised patients?

A

Ribavirin

also use if patient has fulminant hepatitis secondary to viral infection

104
Q

How is Hepatitis B transmitted?

A

Blood bourne virus

  • Perinatal (from mother to baby at birth)
  • Unsafe injections and transfusions
  • Sexual contact
  • Child to child transmission
105
Q

What type of virus if Hepatitis B?

A

The hepatitis B virus is a DNA virus belonging to the Hepadnaviridae family

106
Q

Hep B serology.

What does HBsAg positive indicate?

A

HBV infection

107
Q

Hep B serology.

What does HBV DNA levels indicate?

A

level of virus in the blood

108
Q

Hep B serology.

What does HBeAg positive indicate?

A

high level of HBV replication – usually high HBV DNA

very infectious

109
Q

Hep B serology.

What does Anti-HBc IgM indicate?

A

suggests acute HBV

110
Q

Hep B serology.

What does Anti-HBc IgG indicate?

A

past or current HBV

111
Q

Hep B serology.

What does Anti-HBs Ab indicate?

A

vaccination or past infection

112
Q

Hep B serology.

What does Anti-HBe Ab indicate?

A

present in inactive HBV or the reactivation phase

113
Q

What anti-viral’s are available for the treatment of HEP B? What effects do they have on the liver?

A

Pegylated interferon Alpha2a
Entecavir - oral antiviral – Nucleotide/side analogues and stop viral replication
Tenofovir – oral antiviral - Nucleotide/side analogues and stop viral replication

Drugs dramatically reduce inflammation and can reverse liver fibrosis.

114
Q

What is the aim of HBV therapies?

A

Stop progression of liver disease to prevent cirrhosis or HCC

HBsAg/Ab seroconversion = closest thing we have to a cure
Reduced HBsAg levels
Undetectable HBV DNA (although never completely cleared)
Normalisation of ALT
Histology – reduced inflammation and fibrosis

115
Q

What type of virus if Hepatitis C?

A

Single-stranded RNA virus of the family Flaviviridae

116
Q

How is Hepatitis C transmitted?

A

IV drug use (80% UK cases)

Rarely - sexual contact

117
Q

Who do we screen for HCV?

A

Any hx of injecting or intranasal drug use
ALT elevation
HIV or HBV infection, test for them all – you may as well.
Born in a highly endemic country
Long term dialysis

118
Q

What are the new/best pharmalogical treatments of HCV?

A 
DAAs – Direct Acting Antivirals - inhibit HCV viral replication
Protease inhibitors
•	Telaprevir
•	Boceprevir
•	Simeprevir
•	Parataprevir
Polymerase inhibitors (NS5B)
•	Sofosbuvir
•	Dasabuvir
NS5A inhibitor
•	Ledipasvir
•	Daclatasvir
•	ombitasvir
119
Q

Which drugs commonly cause liver injury?

A

Flucloxacillin, Clopidogrel and Co-amoxiclav both cause cholestatic patterns of liver injury

Paracetamol causes hepatocellular injury → Acute liver failure
HAART, NSAIDS and omeprazole also cause hepatocellular injury

Amitriptyline, phenytoin and trimethoprim cause a mixed picture

120
Q

What is Budd-Chiari syndrome?

A

Occlusion of hepatic veins that drain the liver, which may cause acute liver failure

121
Q

How is ascites treated?

A

Paracentesis - however this does not treat the underlying portal hypertension

122
Q

What are the risk factors of TIPSS for varices?

A

Increased risk of hypoxic liver and transfer of toxins through the BBB

123
Q

What cells are key in hepatic fibrosis pathogenesis?

A

Hepatic stellate cells - once activated they take up vitamin A and become myofibroblasts.

124
Q

Which neurotransmitter has found to be involved in the fibrosis process (both regeneration and fibrosis?

A

Serotonin
5HT-2BR receptor - involved in fibrosis
5HT-2AR receptor - involved in regeneration

Therapies can antagonise the first receptor and agonise the second

125
Q

What are the 4 ways in which liver responds to injury?

A
  1. Resolution
  2. Overwhelming injury, inadequate regeneration and massive necrosis
  3. Suppuration and abscess formation
  4. Progression to chronic inflammation and fibrosis
126
Q

What are the two types of NAFLD?

A
  1. Simple steatosis - fat without inflammation/injury

2. Non alcoholic steatohepatitis - fat with inflammation and cell injury

4TH YEAR - CSIM2 (20 decks)

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