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PATHOLOGY > Liver CPC > Flashcards

Liver CPC Flashcards

1
Q

describe this liver histology

A

hepatocytes arranged in trabeculae

sinusoids

blood drain through central vein

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2
Q

describe this liver histology

A

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

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3
Q

summarise flow through the liver

A

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)

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4
Q

summarise zones in the liver

A

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

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5
Q

histology of portal tract of liver

A
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6
Q

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

A

pre-hepatic:
* haemolysis (FBC and film)

Hepatic:
* repeat LFTs (GGT, AlkPhos etc)

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

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6
Q

causes of high bilirubin

A

pre-hepatic:
* haemolysis (FBC and film)

Hepatic:
* repeat LFTs (GGT, AlkPhos etc)

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

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7
Q

summarise the van den Bergh reaction

A

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)

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8
Q

will pre-hepatic jaundice have high conjugated or unconjugated bilirubin

A

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

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9
Q

summarise possible causes of paediatric jaundice

A

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

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10
Q

phototherapy for neonatal jaundice

A

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

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11
Q

marker for obstructive jaundice

A

alk phos

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12
Q

how is Gilberts inherited

A

recessive

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13
Q

how do you diagnose Gilberts

A

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

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14
Q

how common is Gilberts

A

50% carry the gene

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15
Q

what percentage of people have the full gilbert’s syndrome

A

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

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16
Q

what happens with fasting in gilberts

A

BR is worsened

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17
Q

pathology of gilberts

A

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

unconjugated BR

when dip urine - no bilirubinuria. But there is urobilinogen

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18
Q

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

A

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

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19
Q

what is the most representative of liver function

A

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

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20
Q

what happens in paracetamol OD to liver

A

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

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21
Q

what are measures of liver function

A

albumin
clotting factors (PT PTTK)
bilirubin

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22
Q

causes of hepatic jaundice

A

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

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23
Q

does this suggest pre post or hepatic jaundice

A

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

alk phos marginal - this excludes obstructive jaundice

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24
Q

sequalae of hep A

A

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

25
Q

sequalae of hep B

A

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

26
Q

serology for hep B carrier

A

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

27
Q

Describe this liver pathology

A

swollen cells at arrow1
neutrophil polymorph - arrow 2
fat cells

if any body who drinks - get fatty liver - this is reversible

28
Q

stages of alcoholic liver disease

A

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

29
Q

describe this liver histology

A

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

30
Q

describe this liver histopathology

A

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

31
Q

histology of alcoholic hepatitis

A

defining histological features
* liver cell damage
* inflammation
* fibrosis

associated histological features
* fatty change
* megamitochondria - alcohol damage the mt -> giant mitochondria

32
Q

commonest cause of liver disease in west

A

NASH

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

33
Q

how do you differentiate between NASH and alcoholic hepatitis

A

history

34
Q

treatment of hepatitis

A

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

35
Q

why do we use pabrinex for alcohol hepatitis

A

for thiamine - use it all up in alcoholism

it contains other vitamins - dont need them

36
Q

what is caused by B1deficiency

A

Beri-Beri

37
Q

what is the consequence of vit 3 (naicin) deficiency

A

Pellagra

38
Q
A

palmar erythema

39
Q
A

spina naevi - shows liver disease

40
Q

mechanism of gynaecomastia

A

too much oestrogen
because the liver breaks down oestradiol

41
Q

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

suggest

A

chronic stable liver disease

42
Q

what is this and what does it signify

A

(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

43
Q

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

A

splenomegaly

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

44
Q

what does shifting dullness suggest

A

ascites

45
Q

what is non-shifting dullness

A

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

46
Q

what does visible veins, splenomegaly and ascites suggest

A

portal HTN

47
Q

pathology of portal HTN

A

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

48
Q

what does a flapping tremor suggest

A

liver failure

tells you brain has been poisened by toxins

49
Q

what does liver fail to do in liver failyre

A

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

50
Q

mx of liver failure

A

need to minimise work done by the liver
- limit protein intake
- prevent GI bleed - huge protein load

wait and hope recover
transplant

51
Q

describe this liver

A

pale because fatty
nodules - regenerating hepatocytes
cuff of fibrous tissue around the nodules

alcoholic serous - micronudular cirrhosis

52
Q

describe this histology - alcoholic liver disease

A

nodule
fibrous cuff around
fatty change

53
Q

porto systemic anastomoses

A

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

54
Q

problem with spleno-renal shunt

A

shunt blood from portal circ to systemic circ, to reduce the pressure

end up with liver failure because all toxins bypass liver

55
Q

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

A

obstruction of the bile ducts

bile salts/acids - secreted into gut, then reabsorbed later downstream = enterohepatic circulation

56
Q

what is courvoisier’s law

A

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

57
Q

pathology of this spleen

A

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

58
Q

is this primary or secondary malignanct

A

likely secondary - multiple deposits

59
Q

histology of this pancreatic carcinoma

A

adenocarcinoma - glands, mucus

60
Q

why does pancreatic ca met to liver

A

portal vein takes cancer to liver

PATHOLOGY (94 decks)

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