Liver CPC

Question 1

describe this liver histology

Answer 1

hepatocytes arranged in trabeculae

sinusoids

blood drain through central vein

Question 2

describe this liver histology

Answer 2

have central vein on L and portal triad on R (artery, vein and bile duct)

blood goes from R to L to central vein
Bile goes from hepatocytes to the bile duct in portal triad -> duodenum

Question 3

summarise flow through the liver

Answer 3

Dual blood supply from hepatic artery and portal vein travel down the sinusoid lined with endothelium
drain through central vein

endothelium are discontinuous (space of disse)

Question 4

summarise zones in the liver

Answer 4

zone 1 - around the portal tract - have best oxygen
zone 2
zone 3 - least oxygen. Most metobolically active cells

Question 5

histology of portal tract of liver

Answer 5

Question 6

what do you do with high BR in 20y/o

Answer 6

pre-hepatic:
* haemolysis (FBC and film)

Hepatic:
* repeat LFTs (GGT, AlkPhos etc)

Post-hepatic:
* obstructive jaundice - gallstones/pancreatic ca

Question 6

causes of high bilirubin

Answer 6

pre-hepatic:
* haemolysis (FBC and film)

Hepatic:
* repeat LFTs (GGT, AlkPhos etc)

Post-hepatic:
* obstructive jaundice - gallstones/pancreatic ca

Question 7

summarise the van den Bergh reaction

Answer 7

measures serum bilirubin via fractionation
direct reaction measures conjugated BR
addition of methanol causes complete reaction - measures total bilirubin (conjugated plus unconjugated)

the difference = unconjugated bilirubin (an indirect reaction)

Question 8

will pre-hepatic jaundice have high conjugated or unconjugated bilirubin

Answer 8

high conjugated - the liver is working fine and will conjugate the bilirubin

Question 9

summarise possible causes of paediatric jaundice

Answer 9

usually normal - unconjugated when liver is immature - give UV (skin can conjugate BR)

if it doesnt settle - look for hypothyroidism, other causes of haemolysis (including Coombs test or DAT), and unconjugated BR

Question 10

phototherapy for neonatal jaundice

Answer 10

converts BR into lumirubin and photobilirubin - dont need conjugation for excretion

Question 11

marker for obstructive jaundice

Answer 11

alk phos

Question 12

how is Gilberts inherited

Answer 12

recessive

Question 13

how do you diagnose Gilberts

Answer 13

High BR
rest of the liver tests are normal - including alkphos, ggt, ast, alt

tells you the liver cells are functioning well - if cells are damaged then some will leak into blood

Question 14

how common is Gilberts

Answer 14

50% carry the gene

Question 15

what percentage of people have the full gilbert’s syndrome

Answer 15

6% - very common
so dont Ix if jaundice and all other LFTs are normal

Question 16

what happens with fasting in gilberts

Answer 16

BR is worsened

Question 17

pathology of gilberts

Answer 17

UDP glucuronyl transferase activity reduced to 30% -> slight jaundice

unconjugated BR

when dip urine - no bilirubinuria. But there is urobilinogen

Question 18

summarise how urobilinogen ends up in urine, and the effects of an obstruction

Answer 18

Urobilinogen is present in normal people, comes from enterohepatic circulation.

Bilirubin goes into bowel (brown stool) -> stercobilinogen -> reabsorbed -> urobilinogen.

If block biliary tree (physical obstructioN) - bacteria dont see BR -> pale stools, and no urobilinogen in urine

Question 19

what is the most representative of liver function

Answer 19

prothrombin time (because liver makes all of the clotting factors)

Question 20

what happens in paracetamol OD to liver

Answer 20

enzymes go up as hepatocytes die - can deal with this give N-acetylcyteine

the problem is when the prothrombin time goes up

if PT is higher in seconds than the hr from OD - then need to transfer for liver transplant

Question 21

what are measures of liver function

Answer 21

albumin
clotting factors (PT PTTK)
bilirubin

Question 22

causes of hepatic jaundice

Answer 22

viral hepatitis
alcholic hepatitis
cirrhosis - end stage of damage to the liver

Question 23

does this suggest pre post or hepatic jaundice

Answer 23

hepatic
AST and ALT tell you that the liver itself is damaged

alk phos marginal - this excludes obstructive jaundice

Question 24

sequalae of hep A

Answer 24

virus replicates -> incubation period virus excreted -> infectious -> IgM -> Jaundice and unwell -> IgG **Then cured and immune** there is a vaccine

Question 25

sequalae of hep B

Answer 25

2 mo after pick it up - unwell and jaundice rise e Ag and surface Ag Then start to make Ab and Ag titre goes down then have Ab against the 3 probably wont get it again - dont know if going to be a carrier Anti-HBc - is an Ab agaisnt e ag. Tells you also been infected. **if vaccinated only have anti-HBs**

Question 26

serology for hep B carrier

Answer 26

never clears the virus even though e antigen decline **s antigen remains for years** infectious to people often subclinical

Question 27

Describe this liver pathology

Answer 27

swollen cells at arrow1 neutrophil polymorph - arrow 2 fat cells if any body who drinks - get fatty liver - this is reversible

Question 28

stages of alcoholic liver disease

Answer 28

fatty liver alcholoic hepatitis - neutrophilic inflammation, balloon cells. Not reversible Cirrhosis

Question 29

describe this liver histology

Answer 29

bile accumulate in liver because hepatocytes are swollen, damaged with mallory hyaline - blocking the bile flow

Question 30

describe this liver histopathology

Answer 30

histochemical stain - stain collagen blue collagen fibre around individual cells - characteristic of alcohol swelling of cells with mallory hyaline in scarring with fibrosis - high risk of cirrhosis

Question 31

histology of alcoholic hepatitis

Answer 31

defining histological features * liver cell damage * inflammation * fibrosis associated histological features * fatty change * megamitochondria - alcohol damage the mt -> giant mitochondria

Question 32

commonest cause of liver disease in west

Answer 32

**NASH** associated with BMI and DM. But can be in normal BMI

Question 33

how do you differentiate between NASH and alcoholic hepatitis

Answer 33

history

Question 34

treatment of hepatitis

Answer 34

stop drinking supportive nutrition vitamins (esp B1, thiamine) Pabrinex occasionally steroids if inflammation dont need new liver - liver will regenerate, but wont be well organised - blood has difficulty getting from portal triad to portal vein -> portal hypertension

Question 35

why do we use pabrinex for alcohol hepatitis

Answer 35

for thiamine - use it all up in alcoholism it contains other vitamins - dont need them

Question 36

what is caused by B1deficiency

Answer 36

Beri-Beri

Question 37

what is the consequence of vit 3 (naicin) deficiency

Answer 37

Pellagra

Question 38

Answer 38

palmar erythema

Question 39

Answer 39

spina naevi - shows liver disease

Question 40

mechanism of gynaecomastia

Answer 40

too much oestrogen because the liver breaks down oestradiol

Question 41

what do the signs: multiple spider naevi, dupuytren's contracture, palmar erythma, gynaecomastia suggest

Answer 41

chronic stable liver disease

Question 42

what is this and what does it signify

Answer 42

(visible veins on abdominal wall) caput medusae portal hypertension if have portal HTN (from cirrhosis, inflammation death and recovery) - portal triads squished into corner, + portal pressure goes up - blood cant go into liver - back down portal vein - back down to umbilicus -> pressure on the umbilical vein goes up -> might bleed

Question 43

other than caput medusae, what can you find on the abdomen in portal HTN

Answer 43

splenomegaly portal vein made of splenic vein and superior mesenteric vein -> spleen bigger

Question 44

what does shifting dullness suggest

Answer 44

ascites

Question 45

what is non-shifting dullness

Answer 45

dullness in flank that doesnt move when pt does it is a normal finding

Question 46

what does **visible veins, splenomegaly and ascites** suggest

Answer 46

portal HTN

Question 47

pathology of portal HTN

Answer 47

hepatocytes die -> nodules -> blood harder to get out of triad scarring between triads and central vein - so bridge of fibrosis -> blood bypasses hepatocytes - intrahepatic shunting of blood. pressure builds up and up

Question 48

what does a flapping tremor suggest

Answer 48

liver failure tells you brain has been poisened by toxins

Question 49

what does liver fail to do in liver failyre

Answer 49

synthetci function clotting factor and albumin clearance of bilirubin clearance of ammonia

Question 50

mx of liver failure

Answer 50

need to minimise work done by the liver - limit protein intake - prevent GI bleed - huge protein load wait and hope recover transplant

Question 51

describe this liver

Answer 51

pale because fatty nodules - regenerating hepatocytes cuff of fibrous tissue around the nodules alcoholic serous - micronudular cirrhosis

Question 52

describe this histology - alcoholic liver disease

Answer 52

nodule fibrous cuff around fatty change

Question 53

porto systemic anastomoses

Answer 53

where portal blood reaches systemic circ oesophagus. high portal pressure in stomach -> bv grow into systemic circ, down the veins -> varicies very thin wall -> bleed to death rectal umbilical vein spleen

Question 54

problem with spleno-renal shunt

Answer 54

shunt blood from portal circ to systemic circ, to reduce the pressure end up with liver failure because all toxins bypass liver

Question 55

what do scratch marks (itching) in context of jaundice suggest and why

Answer 55

**obstruction** of the bile ducts **bile salts/acids** - secreted into gut, then reabsorbed later downstream = enterohepatic circulation

Question 56

what is courvoisier's law

Answer 56

a palpable gall bladder in the presence of jaundice - is pancreatic ca (not gallstones because stones make gallbladder small and fibrotic - cant palpate)

Question 57

pathology of this spleen

Answer 57

irregular, firm, white tumour lymph nodes - metastased to intrahepatic lymph nodes

Question 58

is this primary or secondary malignanct

Answer 58

likely secondary - multiple deposits

Question 59

histology of this pancreatic carcinoma

Answer 59

adenocarcinoma - glands, mucus

Question 60

why does pancreatic ca met to liver

Answer 60

portal vein takes cancer to liver