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Year 5 Chemical Pathology > 4s: Liver CPC > Flashcards

4s: Liver CPC Flashcards

1
Q

Causes of high BR (3)

A

Pre-hepatic (unconjugated) = haemolysis (e.g. drug induced aka rifampicin, hereditary, DIC)

Hepatic

  • hepatitis (viral, AI)
  • liver failure (drugs like ethanol/paracetamol/halothane/methyldopa/barbiturates, ALD)
  • gallstones
  • cirrhosis

Post-hepatic (obstruction)

  • cholecystitis
  • pancreatic cancer
  • cholangiocarcinoma, PSC, PBC
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2
Q

Sinusoid anatomy

A

Space of Disse = space between hepatocytes and discountuous endothelium of the sinusoids where blood comes into contact with all the liver enzymes

zones:

  • Zone 1 (periportal): closest to the portal tract and it has the highest oxygen concentration, directly hepatic substances, damage makes ALP rise more due to close proximity to bile ducts
  • Zone 3 (centrilobular): most susceptible to hypoxia
  • The cells in zone 3 are the most metabolically active cells in the liver, metabolised hepatotoxic substances
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3
Q

ix for high BR

A

Pre-hepatic (unconjugated) e.g. haemolysis (-> do a FBC and blood film)

Hepatic: repeat the LFTs

Post-Hepatic: obstructive jaundice

  • Liver is fine, but something is blocking the bile duct (e.g. gallstone, cancer)
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4
Q

Measuring fractions of BR

A

This is done using the van den Bergh reaction

The van den Bergh reaction measures serum bilirubin via fractionation

A direct reaction measures conjugated bilirubin

The addition of methanol causes a complete reaction, which measures total bilirubin (conjugated plus unconjugated); the difference measures unconjugated bilirubin (an indirect reaction)

Unconjugated bilirubin is highly albumin bound and does not enter the urine

Conjugated means the liver is working, and the problem is post-hepatic

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5
Q

Paediatric jaundice

A

usually normal

unconjugated hyperbilirunaemia as liver immature

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6
Q

What should we look for if paediatric jaundice does not resolve

A

hypothyroidism, causes of haemolysis → do ix:

  • TFT
  • Coombes terst/DAT for haemolytic anaemia
  • BR fractions
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7
Q

How do we manage paediatric jaundice

A

light (phototherapy); the skin can help to conjugate some of the bilirubin.

  • Phototherapy converts bilirubin into two other compounds: lumirubin and photobilirubin
  • These are isomers that do NOT need conjugation for excretion
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8
Q

Gilbert’s syndrome

A

benign and common

normal LFTs

Autosomal recessive

worsened on fasting (more yellow more BR)

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9
Q

Gilbert’s syndrome pathophysiology

A

UDP glucuronyl transferase enzyme activity is reduced to 30% - causes slight jaundice

Unconjugated bilirubin is tightly albumin bound and does not enter the urine

So, they do not have bilirubinuria (unconjugated BR does not enter the urine)

Urobilinogen is always present in the urine of normal people

  • This comes from the enterohepatic circulation

The bilirubin you make goes through the biliary tree and into the bowel (if GI tract is healthy)

Here, bacteria convert some of the bilirubin to stercobilinogen and urobilinogen

This is then reabsorbed into the circulation and you pee it out

So, the presence of urobilinogen in the urine tells you that the enterohepatic circulation is intact

Negative urobilinogen is suggestive of biliary obstruction

GILBERT’S URINE: THERE IS NO BILIRUBIN (UNCONJUGATED), BUT THERE IS UROBILINOGEN

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10
Q

What drug can reduce BR levels in Gilber’s syndrome

A

Phenobarbital = UDPGT enzyme inducer

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11
Q

Liver function

  • What is most representative marker of liver function (why not albumin)
  • paracetamol overdose
  • which other markers
  • are enzymes markers
A

PT (12-14 seconds) as liver makes all clotting factors

  • albumin good (represents synthetic function) but PT better

if PT is higher than number of hours since paracetamol overdose -> transfer patient to liver unit for liver transplant

other markers = albumin, clotting factors (PT,PTTK), BR

enzymes not true test of liver function = tells us that there is some liver damage

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12
Q

liver enzymes

A

ALP <130

AST <50

ALT <50

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13
Q

Hepatitis A serology

A

exposure to virus required (travel hx)

faeco-oral (food, MSM, contaminated water e.g. recent shellfish consumption)

asymptomatic but infectious for long time (incubation period)

after IgG made -> cured and immune (NO RECURRENCE)

Havrix vaccine = antigens of hep A

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14
Q

Hepatitis B serology: acute infection

A

hep B can be acute/chronic

we often measure HBs Ag and HBe Ag

When your immune response mounts and you produce antibodies, the HBeAg titre decreases

Once HBeAg levels go all the way down, you will be able to detect anti-HBe antibodies

Similarly, when HBsAg reaches the bottom, anti-HBs antibodies become detectable

In the end, you will have three antibodies and no antigens

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15
Q

What does anti-HBc tell us?

A

you have been exposed to hep B in the past but we don’t have the capability to measure this

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16
Q

What does the Hep B vaccine contain?

A

HBsAg (virulent) so you will not have HBeAg or Anti-HBe or Anti-HBc

If you see a patient who has HBsAb present and nothing else, this is consistent with a health worker who has been vaccinated. If you can measure both antibodies, this is consistent with someone who has had the infection.

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17
Q

Hepatitis B serology: chronic carrier

A

this patient never clears the virus

Although the HBeAg declines (and hence infectivity declines), the HBsAg remains for years

Some of these people never become jaundiced and so do not realise that they have the virus

These people are actively antigenic and can spread the virus

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18
Q

histology of hepatitis (2)

A

lots of cells containing fat

  • swollen/balloon cells containing Mallory’s hyaline
  • inflammatory cells (neutrophil polymorphs)
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19
Q

fatty liver disease

A

If anyone drinks too much alcohol, they get fat deposits in their liver. This is due to metabolic overload. However, these fatty deposits will go away if the patient stops drinking alcohol.

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20
Q

alcoholic hepatitis

A
  • associated histological feature = iif alcohol abuse persist neutrophils infiltrate liver and balloon cells (with Mallory-Den bodies seen)
  • megamitochondria
  • fatty change

Liver cell damage, inflammation, fibrosis

damage may not be reversible

21
Q

cirrhosis

A

end stage of all liver isease

bile accumulation in liver

hepatocytes swollen and full of Mallory hyaline blocking the flow of bile through the liver

bile levels mirrored by raised BR in blood

collagen fibres surrounding individual liver cells

22
Q

what does this show?

A

blue is staining collagen

collagen fibres around individual cells characteristic of alcohol abuse

this scarring is typical of cirrhosis

23
Q

FLD -> Alcoholic hepatitis -> cirrhosis

A

FLD = fat deposits

AH = neutrophils, balloon cells w/ Mallory hyaline, fat deposits, megamitochondria

cirrhosis = all of the above with bile, raised BR, and collagen fibres surrounding indiviual liver cells (scarring)

24
Q

DDx for FLD

A

Non-alcoholic steatohepatitis (NASH)

  • This looks exactly like alcoholic hepatitis (history is important)
  • It is the most common cause of liver disease in the Western world

Alcoholic hepatitis

Malnourishment (Kwashiorkor)

25
Q

tx for a patient with alcoholic hepatitis

how regeneration leads to portal hypertension

A

fluids

stop alcohol intake

  • regeneration -> little nodules -> portal hypertension

nutrition (B1 thiamine aka pabrinex)

occasionally steroids (controversial)

26
Q

B1, B2, B3 vitamins names and deficiency names

A

B1 (thiamine, pabrinex) + B2 riboflavin = dark yellow urine

  • B1 deficiency = Beri-Beri

B3 (niacin) deficiency = Pellagra

B12 (cobalamin) → B12 deficiency/SCD

27
Q

Chronic Stable Liver Disease (features)

are they unwell?

what can you develop?

A
  • Palmar erythema
  • Spider naevi (>5)
  • Gynaecomastia: due to failure of the liver to break down oestradiol
  • Dupuytren’s contracture

These patients are not necessarily unwell. If they stop drinking, they will be absolutely fine.

develop portal hypertension (caused by cirrhosis)

  • caput medusae (visible veins)
  • splenomegaly
  • shifting dullness (ascites)
  • scrotal oedema
28
Q

features of liver failure

A

Failed synthetic function

Failed clotting factor and albumin production (easy brusing and bleeding)

Failed clearance of bilirubin (hyperbilirubinaemia)

Failed clearance of ammonia (leads to encephalopathy)

  • flapping tremor (asterixis) = manifestation of hepatic encephalopathy
29
Q

mx of liver failure

A

This is managed by minimising the work done by the liver (difficult to do this).

  • Avoid protein intake
  • Avoid GI bleeding
  • Provide supportive care

Only true cure is a liver transplant.

30
Q

features of nodules (fatty liver)

A

You can see around the nodules very clearly because they have a cuff of fibrous tissue

Alcoholic livers tend to have small nodules (micronodular cirrhosis)

31
Q

intrahepatic shunting (fatty liver)

A

In this condition you get scarring between the portal tracts and the central veins

This bridge of fibrosis means that blood doesn’t get in close contact with the hepatocytes

Hence, the blood does not get filtered

This is i_ntrahepatic shunting of the blood_

32
Q

alcohol abuse pathway

A

Alcoholic hepatitis

Chronic stable liver disease

Resultant portal hypertension

Liver failure (asterixis)

33
Q

Portosystemic Anastomoses: importance

A

Places where the portal blood meets the systemic circulation. These occur in many places; if you have high portal pressure in the stomach, this can result in varices. Varices have very thin walls (have no muscle in the vessel); if they tear, this can lead to death:

  • Oesophageal varices
  • Rectal varices
  • Umbilical vein recanalising
  • spleno-renal shunt
34
Q

TIPSS: Transjugular intrahepatic portosystemic shunt

A

Done through the jugular vein by a radiologist. From SVC to IVC. Go through JVP to hepatic vein. Hole drilled from portal vein to hepatic vein. Prevents death but causes jaundice and liver failure

35
Q

what makes you itchy

A

obstructive jaundice (gallstones, pancreatic cancer)

  • Gallstones or cancer of the pancreatic head can block the bile duct
  • Bile is made up of bilirubin and bile salts (which emulsify fats and are reabsorbed)
  • Bile salts/acids only appear in the blood stream when the bile duct is physically blocked
  • Both bile salts and bile acids cause itchiness
36
Q

What is Courvoisier’s Law

A

if the gallbladder is palpable in a jaundiced patient, the cause is unlikely to be gallstones (i.e. it is more likely to be pancreatic cancer).

This is because a gall bladder with stones is usually small and fibrotic and incapable of being large.

37
Q

where does pancreatic cancer typically metastaise to

what ix result would you see in this metastasis

A

liver because the portal vein transports blood from the cancer to the liver

high ALP

USS = dilated bile ducts (means metastasis)

38
Q

pancreatic carcinoma

A

Formation of ducts in pancreas

Liver cells form units

Sarcoma are muscle cells

Melanoma will have pigment

Each met grows in round nodules

39
Q

What is normal BR?

A

5-17 mmol/L

40
Q

How do we treat Hep B

A

Acute = supportive

Chronic = anti-viral therapy

41
Q

Hep C (RNA virus)

A

60-80% go chronic = asymptomatic presentation leading to chronic infection

Associated with HCC (hepatocellular carcinoma) = “Hx of jaundice, hepatomegaly, weight loss” “RAISED AFP”

Blood product spread = Hx of thalassaemia (recurrent blood transfusions)

42
Q

Hep D

A
  • REQUIRES CO-INFECTION WITH HEPATITIS B, HDV needs HBV surface antigen to invade liver cells
43
Q

Hep E

A
  • Faeco-oral (food, MSM, shellfish, uncooked pork)
  • Acute = asymptomatic or N+D+V, fever, jaundice, RUQ pain

Increased risk in: expectant. Others, immunocompromised patients

44
Q

Give 3 features of portal HTN (usually caused by cirrhosis)

A

Visible veins

Ascites

Splenomegaly

45
Q

Acute vs Chronic hepatitis

A
  • Acute hepatitis → spotty necrosis
  • Chronic hepatitis → piecemeal necrosis, hepatocyte necrosis, fibrosis, nodules of regenerating hepatocytes
    • Portal Inflammation
    • Interface hepatitis (PIECEMEAL NECROSIS) – cannot see the border between the portal tract and parenchyma
    • Lobular inflammation
    • Bridging from the portal vein to central vein (critical stage in the evolution of hepatitis to cirrhosis)
46
Q

Micronodular vs marconodular hepatitis

A
  • Micronodular = alcoholic hepatitis, biliary tract disease
  • Macronodular = viral hepatitis, Wilson’s disease, A1AT
47
Q

Causes of chronic hepatitis

A
47
Q

Causes of chronic hepatitis

A
48
Q

How do score the prognosis in liver cirrhosis?

A

Modified Child-Pugh Score

Year 5 Chemical Pathology (18 decks)

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