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DPD 2019 > Liver disease CPC > Flashcards

Liver disease CPC Flashcards

1
Q

How do you measure the difference between conjugated and unconjugated bilirubin

A

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).

DIRECT reaction measured conjugated

INDIRECT measures unconjugated

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2
Q

What is paediatric jaundice usually due to

A

It usually is normal, but the bilirubin should be unconjugated as the cause is usually liver immaturity coupled with a fall in the haemoglobin early in life.

If it doesn’t settle, other rare causes should be looked for including hypothyroidism, other causes of haemolysis (including a Coombes test or DAT), and the unconjugated bilirubin will be useful.

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3
Q

How is gilberts inherited

A

Recessive- 50% carry the gene so 6% of the population

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4
Q

What is the effect of fasting. What would be the effect of giving phenobarbitone

A

Worsened by fasting (so bili will increase)

Phenobarbitone induces the liver so bili should fall in this case

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5
Q

What happens in gilberts

A

UDP glucuronyl transferase activity reduced to 30%

Unconjugated bilirubin tightly albumin bound and does NOT enter urine.

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6
Q

What tests assess liver function

What will you measure in paracetemol overdose, what will you use to assess for liver transplant need.

What if the liver enzymes are really high with paracetemol overdose

A

Albumin (not a quick marker)
Clotting factors (PT, PTTK)
Bilirubin

Other tests are “enzymes”, not truly tests of liver function.

In paracetemol overdose, if the PT climbs by more than 1 second per hour then they may need to be transferred for a liver transplant.

If the enzymes are really high, it doesn’t tell you how well or badly they are doing. If the enzymes are high and the PT is not rising, thehn they are safe.

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7
Q

What is the treatment for paracetemol overdose

A

N-acety cysteine

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8
Q

What clotting test do you use to assess warfarin and heparin

A

Warfarin- PT

Heparin- PTT

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9
Q

What are the types of hepatitis and how would you check

A

Viral: check viral titres.
Autoimmune - do antibodies
Alcoholic ?

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10
Q

How do you get Hep A

A

Through water… can only get it once

You’re well for two weeks, jaundice after 4 weeks, IgM after 3 weeks and IgG after 5 weeks

One off infection… no such thing as a carrier, it either kills you or you make antibodies and it’s gone

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11
Q

How does Hep B work

A

You get it through IVDU/sex

3 months peak HBs Ag and HBe Ag.

You can tell if somebody has had hepatitis B because they will have anti-HBs and Anti-HBe.

In an immunisation they only give Anti-HBs

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12
Q

What if you’re a hep B carrier

A

You mae antibodies to HBe but not to HBs.

So they have high HBs for 10 years

They are infectious but subclinical

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13
Q

Causes of fatty liver disease other than alcohol

A

Drugs, diabetes and insulin resistance

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14
Q

Complication of alcoholic hepatitis on histology

A

Bile can actually be seen in the cannaliculi because for whatever reason the bile gets stuck in the ducts

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15
Q

Defining histological features of alcoholic hepatitus

vs

associated histological features of alcoholic hepatitis

A

-defining histological features:
liver cell damage
inflammation
fibrosis

-associated histological features:
fatty change
megamitochondria

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16
Q

What is non alcoolic steato hepatitis

A

NASH

-fatty hepatits can be caused by insulin reistance obesity

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17
Q

What treatment is needed for alcoholic hepatitis

A

Supportive.
Stop alcohol.
Nutrition:
Vitamins (esp B1, thiamine)

Occasionally steroids.

18
Q

What is caused by B1 deficiency

A

Beri-beri (–> wernickes)

19
Q

What do these things signify:

Multiple spider naevi
Dupuytren’s contracture
Palmar erythema
Gynaecomastia

out of: 
Jaundice
Hepatitis
Chronic stable liver disease 
Portal hypertension.
Liver failure
Obstruction of the bile ducts.
A

Chronic stable liver disease

20
Q

Which of these are you most likely to find on examination given a visible vein on anterior abdominal wall

Hepatomegaly
Splenomegaly
Bilateral palpable kidneys
A palpable bladder
An enlarged prostate gland on PR.
A

Splenomegaly

21
Q

these three things:

Visible veins
Splenomegaly
Ascites (shifting dullness.)

Mean you have what:

Jaundice
Hepatitis
Chronic stable liver disease 
Portal hypertension.
Liver failure
Obstruction of the bile ducts
A

Portal HTN

22
Q

Portal HTN is cuased by what

A

Portal HTN

23
Q

What clinical signs are associated with portal HTN

A

Visible veins, splenomegaly, ascites

24
Q

What would you do in the case of acute eosophageal rupture

A

A Sengstaken–Blakemore tube goes down into the stomach and you blow up a balloon. Then you pull it up into the stomach. This presses on the vein.

You give lots of blood as well

25
Q

Admitted to drain ascites, but developed a flap shortly afterwards.

What do they have:

Jaundice
Hepatitis
Chronic stable liver disease 
Portal hypertension.
Liver failure
Obstruction of the bile ducts
A

Liver failure

26
Q

What is liver failure

A 
Failed synthetic function
Failed clotting factor and albumin
Failed clearance of bilirubin
Failed clearance of ammonia
(encephalopathy)
27
Q

Hallmarks of cirrhosis

A

Pallor due to fat

Micronodules

Affects the whole liver, not localised

28
Q

What is the nodule composed of

A

Centrally regenerating hepatocytes, and they are surrounded by fibrous tissur collagen

29
Q

Differentiate cirrhosis caused by alcohol v viruses

A

Alcohol-micronodular

Viral-macronodular

30
Q

What is intrahepatic shunting

A

Now a scar will connect hte portal triad to the central vein.

So the blood doesn’t come into contact with the hepatocytes, it doesn’t get filtered

So this when you get hepatic encephalopathy

31
Q

What can you do to solve portal hypertension

A

TIPPS

This allows you to divert blood from the portal vein to the hepatic vein.

But they get very confused and jaundice!

32
Q

4 sites of Porto systemic anastomoses

A

….

33
Q

Q21: What do scratch marks suggest?

Jaundice
Hepatitis
Chronic stable liver disease 
Portal hypertension.
Liver failure
Obstruction of the bile ducts
A

Obstruction of the bile ducts.

It means that the jaundice is due to obstruction

34
Q

What is itching caused by

A

Colourless BILE SALTS/ACIDS (NOT bilirubin)…. they are blocked from getting into the gut so they get into the bloodstream and are irritants.

They make you itch!!!!!

35
Q

What is courvoisier’s law

‘gall bladder is palpable in a jaundiced patient…

The cause is gallstones
The cause is pancreatic Ca.

A

The cause is pancreatic cancer!

In the presence of jaundice, if the gall bladder is palpable, the cause is unlikely to be gall stones.

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

36
Q

What investations would you do for painless but itchy jaundice

A

Ultrasound abdomen
Dilated bile ducts

Probable metastatic disease

37
Q

What is obstructive jaundice usually caused by

A

Obstructive jaundice commonly caused by pancreatic cancer or gallstones

38
Q

Just to be clear, when do you know there’s cirrhosis, when do you know there’s failure

A

So you go from alcoholic hepatitis (jaundiced)

Chronic stable liver disease (spider naevi, gynaecomastia, palmar erythema, dupytrens contracture)

Then to cirrhosis (which is characterised by portal HTN, so distended abdo vein, splenomegaly and ascites)

Then liver failure is after all that, when you get hepatic flap and encephalopathy (liver fails to clear ammonia)

39
Q

Scratch marks indicates which kind of jaundice and why

A

It indicates OBSTRUCTIVE ONLY.

Because it’s caused by the bile salts.

If it is a hepatic picture, then bile salts will drain fine through the CBD (or might not even be produced at all).

The only cause that you get itching is if the bile salts are blocked from going into the GI tract

40
Q

What happens to urobilinogen in the urine if there is obstructive picture

A

It goes down.

Urobilinogen is only produced from the enterocytes, and is then reabsorbed in the gut.

But if no bilirubin can get into the GI tract due to obstruction, there is no urobilinogen produced.

Therefore, there is no uribilinogen in the urine.

Normally you would get at least some urobilinogen in the urine in normal people.

Instead, with obstructive disease, you just get bili in the urine, which makes the urine dark

DPD 2019 (30 decks)

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