Liver disease CPC Flashcards Preview

DPD 2020 > Liver disease CPC > Flashcards

Flashcards in Liver disease CPC Deck (50)
Loading flashcards...
1
Q

Medical student

Incidentally find abnormal LFTs

Bilirubin: 32 [5-17]

ALT, ALP, AST, GGT: normal

Repeat fasting LFTs-> Bilirubin- 45, all other LFTs still normal

FBC

Hb- 14. 7 [normal]

WCC- normal

Platelets- normal

Doesn’t drink alcohol

No PMH

FH: cousin had an episode of jaundice once

What is the diagnosis?

A

Gilbert’s syndrome

Not haemolytic- b/c normal FBC and blood film

Not post hepatic -b/c normal ALP

2
Q

What does a high GGT indicate?

A

Alcohol abuse

3
Q

What is ALT?

A

Alanine aminotransferase Product of gluconeogenesis Should only be inside liver, pathogenic when in blood

4
Q

What does this liver biopsy show?

A

NORMAL LIVER

First pic on right: hepatic vein [white circle] surrounded by hepatocytes

Second pic: Portal tract on left hand side- [from portal vein from small intestine] draining into central vein which takes blood back to heart [on the right hand side]

5
Q

How does hepatic blood flow work?

What is the space of disse?

A

In via portal vein down sinusoid into central vein Space of disse = space between sinusoid and endothelial cells/hepatocytes- allows blood to go all the way up to the hepatocytes- increases metabolic efficiency

6
Q

How do hepatocytes and the blood supply to hepatocytes change going from the portal vein to the central vein?

A

Oxygen supply is best next to hepatic portal vein, then decreases along the way to central vein, where pO2 is low

  • This is fine for normal people
  • But dangerous if alcoholic liver disease

Hepatocytes are different colour around portal vein [on left hand side of pic] because they are newly generated here and therefore most metabolic here [all drug metabolism is happening here], then as you go along to central vein, they get older and die

7
Q

What does a liver lobule look like?

A
8
Q

What does this biopsy show?

Hint: it shows the portal triad

A
9
Q

What happens to liver architecture in liver damage?

A

The lobules are destroyed and lose their hexagonal structure when they regrow

10
Q

How do you investigate suspected Gilbert’s syndrome?

LFTs have been done:

All but bilirubin are normal, bilirubin is high

Patient is asymptomatic

What is the next most appropriate step?

A

FBC- low Hb, look for signs of haemolytic anaemia- pre hepatic

Repeat bilirubin - fasting- fasting makes bilirubin higher in Gilbert’s syndrome

Viral serology- hepatitis- hepatic jaundice

Repeat bilirubin - fasting- fasting makes bilirubin higher in Gilbert’s syndrome

Used to give phenobarbitone- induces enzyme that is faulty in Gilbert’s syndrome [UDP glucuronyl transferase] and reduces bilirubin- not done anymore because unethica

If ALP abnormal, consider:

US abdo- Might see physical obstruction of biliary duct/bile duct dilation [cancer of pancreas, gallstones, cholangiocarcinoma]- post hepatic

  • but not needed if normal ALP + no other symptoms

Not liver biopsy= dangerous [though absolute diagnostic]

Not CT- because extra radiation- and unnecessary at this stage

11
Q

What are the causes of high bilirubin, and how do you investigate them?

A

Pre hepatic = haemolysis

  • FBC, blood film

Hepatic = hepatitis

  • Repeat LFTs, viral serology

Post hepatic= cancer, gallstones

  • Imaging- US abdo
12
Q

How can you tell if bilirubin is conjugated or unconjugated?

In which group of people is this especially important?

A

Can use the van der Bergh reaction

Direct reaction= conjugated bilirubin

Adding methanol= total bilirubin- so unconjugated bilirubin can be worked out

Neonates

13
Q

Why does jaundice happen in neonates?

What type of bilirubin should they have if this is the case?

How can you treat the jaundice?

What alternative diagnoses should you consider if jaundice persists?

A

Underdeveloped liver, fall

Unconjugated

Light- phototherapy- breaks down bilirubin so it doesn’t need to be conjugated for excretion

Hypothyroidism, haemolytic anaemia [including Coombes/DAT for autoimmune]

14
Q

How common is Gilbert’s syndrome?

A

Common

6% of population

15
Q

How is Gilbert’s syndrome inherited- pattern of inheritance?

A

Autosomal recessive

50% of people are carriers

16
Q

Pathophysiology of Gilbert’s syndrome?

A

Enzyme- UDP glucuronyl transferase- in liver- does not function

Activity of enzyme reduced to 30%

17
Q

Why does pre hepatic jaundice not affect urine colour?

A

Unconjugated bilirubin doesn’t go into urine

Because it is tightly bound to albumin

18
Q

Which LFT is most representative of liver function?

A

Synthetic factors

So:

PT [prothrombin time]/Clotting factors

Also useful: [but not the best tests, because change more slowly]

  • Albumin
  • Bilirubin

If PT rises by more than one sec per hour= need liver transplant

Other liver tests look at enzymes, which is not truly a test of liver function

19
Q

35 year old patient

Chronic alcohol intake

Frequently presents drunk at A and E

Nausea, abdo pain, jaundice

Abnormal LFTs

Bilirubin: 90 [v high]

ALP: 200 [<130]

AST: 1500 [<50]

ALT: 750 [<50]

What is the most likely diagnosis?

What is the treatment?

A

Hepatitis [probably alcoholic, could also be viral, possible but unlikely to be autoimmune]

More inflammation of liver than obstruction= hepatic

AST:ALT- 2:1

Treatment

Supportive:

  • alcohol cessation
  • nutrition
  • vitamins- thiamine and B1/Pabrinex

Sometimes steroids occasionally

20
Q

How long does Hepatitis A take to present with jaundice after infection?

How does the antibody reponse/serology work?

Can you be a carrier for Hep A?

A

Four weeks

Cannot be a carrier- immune after one exposure

21
Q

How does Hep B serology work if:

  • Currently infectious?
  • Cleared infection?
  • Carrier for infection?

How long are carriers infectious for?

Which antibody is formed through vaccination?

When does patient present with jaundice?

A

Antigens

HBs Ag= currently infectious

HBe Ag= currently highly infectious

Antibodies

If cleared infection:

Anti-HBc antibodies get rid of HBe antigen

Anti-HBs= indicates immunity [natural or vaccine]

Anti-HBe= indicates natural immunity [no vaccine]

If carrier:

Illness subclinical- may or may not have jaundice

Secrete active virus for ten-twenty years after infection

HBs Ag

HBe Ag

Have antibodies against:

Anti-HBe

Anti- HBc

[but NO Anti-HBs]

  • HBs antigen used in vaccine
  • Present with jaundice three or four months after infection
22
Q

What changes can be seen on biopsy in alcoholic liver disease?

A

Fatty liver disease

Hepatitis - inflammation and scarring

Cirrhosis- fibrotic tissue

23
Q

What does this biopsy show?

What does the left hand arrow point to?

A

Large droplet fatty liver disease + alcoholic hepatitis

Left arrow: Mallory-Denk bodies- pink dots= cytoskeleton clumping due to acetaldehyde from alcohol metabolism linking to lysine residues

Right arrow: Neutrophils + ballooning cells- indicates hepatitis [inflammation]

Also accumulation of bile in bile canaliculi- cholestasis [can be seen better on close up below]

24
Q

What are some of the causes of fatty liver disease?

A

Alcohol

Drugs

Diabetes + insulin deficiency

25
Q

Features of alcoholic hepatitis/NASH on biopsy?

  • Defining
  • Associated
A

Defining:

  • Liver cell damage- ballooning
  • Inflammation
  • Fibrosis- scarring

Associated:

  • Fatty change [can stay or come and go- related to acute alcohol consumption]
  • Megamitochondria
26
Q

What is the most common cause of NASH [non alcoholic steatohepatitis]?

A

Insulin resistance- type two diabetes

27
Q

Which disease is caused by thiamine deficiency?

A. Rickets

B. Scurvy

C. Pernicious anaemia

D. Beri-beri

E. Pellagra

F. Neural tube defects

A

D. Beri-beri

28
Q

What vitamin deficiency causes Pellagra?

A

B3- niacin

[Probs extra knowledge tbh- was just a throwaway comment from Meeran]

29
Q

Signs of chronic stable liver disease

A

Palmar erythema

Spider naevi- blanches, refills from middle outwards

Dupuytren’s contracture

Gynaecomastia

Usually presents around two years after acute alcoholic hepatitis presentation

30
Q

What causes portal hypertension?

What are the clinical signs?

A

Cirhhosis- Lobules of liver destroyed structurally due to damage and remodelling, causing first micronodular cirrhosis, and macronodular cirrhosis

Causes poor flow of blood through sinusoids from portal to central vein + back pressure onto portal veins- causing hypertension

Clinical signs

  • Visible veins- varices at portosystemic anastomoses [oesophageal varices, caput medusae, haemorrhoids]
  • Ascites
  • Splenomegaly
31
Q

How to manage haematemesis in someone with portal hypertension + oesophageal varices?

A

Terlipressin [works a bit-veins don’t have much muscle- so not much constriction] + antibiotics

Then - Sengstaken Blakemore tube- NG tube with balloon- dilation

Then endoscopy

High mortality rate

32
Q

What liver pathology does flapping tremor indicate?

A

Liver failure [decompensated]- hepatic encephalopathy

33
Q

What are the main things compromised in liver failure?

A

Failed clotting factors and albumin - synthetic function

Failed clearance of ammonia [encephalopathy]

Failed clearance of bilirubin

34
Q

What does this show?

A

Micronodular cirrhosis

  • Nodules [of regenerating hepatocytes] separated by scar tissue [collagen]
  • Pallor- fat deposited everywhere
  • Involves whole liver- diffuse
35
Q

What is intrahepatic shunting?

What type of liver disease does it indicate + what does it indicate about progression of disease?

A

Fibrosis between portal vein and central vein

Blood goes down these fibrous scars, misses hepatocytes

Toxins can no longer be cleared- increased risk of encephalopathy

Indicates cirrhosis

First sign of irreversible disease

36
Q

What usually causes micronodular cirrhosis?

A

Alcohol

37
Q

What usually causes macronodular cirrhosis?

A

Viral hepatitis

38
Q

What is the progression of alcoholic liver disease?

A

Fatty liver

Alcoholic hepatitis

Chronic stable liver failure

Portal hypertension

Cirrhosis

Liver failure + hepatic encephalopathy- decompensated

39
Q

What are the sites of porto systemic anastomoses?

A

Caput medusae- umbilical

Oesophageal varices

Rectal varices - haemorrhoids

Spleno-renal shunt

40
Q

How can you permanently reduce portal hypertension?

What are the adverse results of this?

A

TIPS
Trans jugular intra hepatic portal shunt

Hole from portal vein to central vein

Toxins go straight into the IVC centrally- encephalopathy- if hole too big

41
Q

What is the definitive treatment for hepatic encephalopathy?

A

Liver transplant

42
Q

Seventy-one year old man

Presents with jaundice

No PMH

Weight loss

O/E

Jaundice- severe

Cachetic

Palpable gall bladder

Excoriations

Investigations

Bilirubin 340

ALP 1750

AST 50

ALT 45

What is the most likely diagnosis?

A

Cancer of the head of the pancreas

43
Q

What causes pruritus?

A

Bile salts entering circulation

44
Q

What does this liver biopsy show?

A

Tumour- adenocarcinoma- forming glands

Primary colon cancer- has metastasised to liver

Normal liver has no glands

45
Q

What does this liver biopsy show?

A

Melanoma- pigmented

46
Q

What does this liver biopsy show?

A

Poorly differentiated melanoma metastasised to liver

47
Q

What is Courvoisier’s Law?

Why is it true?

A

Palpable gallbladder + jaundice = cancer, not gallstones

Gallstones make gallbladder small and fibrotic so not palpable

48
Q

What investigations do you do for obstructive jaundice?

A

US abdo

  • look for dilated bile ducts
49
Q

What are the most common causes of obstructive jaundice?

A

Pancreatic cancer

Gallstones

  • Can differentiate using Courvoisier’s Law
50
Q

What do these post mortems show?

A

Liver mets

Decks in DPD 2020 Class (48):