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Pathology by week > W2 - Liver CPC > Flashcards

W2 - Liver CPC Flashcards

1
Q

Describe the movement of blood along the hepatocytes in the liver

A

There is a portal triad consisting of the hepatic artery, portal vein, and bile duct. The portal vein and hepatic artery supply mix and travel down the sinusoid towards the central vein. The flow in the bile duct is the opposite direction.
The endothelial cells lining the sinusoid are fenestrated (discontinuous), so the blood can go into the space (space of disse) and come into DIRECT contact with the hepatocytes

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2
Q

What is the space between the endothelial cells of the sinusoids and the hepatocytes?

A

Space of Disse

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3
Q

What is the nature of the lining of the hepatic sinusoids

A

Discontinuous endothelial cells

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4
Q

How many zones are there between the portal triad and central vein? Which zone has the best oxygenated blood

A

3
Zone 1 - most oxygen

zone 3 - least oxygen as it is utilised by the hepatocytes in zone 1 and 2

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5
Q

What is the hepatic unit arrangement like?

A

hexagon arrangement

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6
Q

Describe what (3 things) should have happened to the blood entering the central vein in a HEALTHY liver

A
  1. all toxins should be removed
  2. extra glucose should be removed
  3. 1st pass metabolism has occurred so active metabolites
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7
Q

What are some causes of high bilirubin?

A
  1. Pre-hepatic (unconjugated) = liver is okay but something beforehand is increasing the through-put of bilirubin
    - Haemolysis
    - Gilberts
  2. Hepatic disease (viral hepatitis, alcoholic hepatitis, cirrhosis)
  3. Post-hepatic (obstructive jaundice) gallstones and cancer of the pancreas
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8
Q

What investigations would you do if pt had high bilirubin?

A
  1. FBC + film (i.e. check for haemolytic anaemia)
  2. Repeat LFTs (check for hepatic causes)
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9
Q

Describe the conjugated vs unconjugated bilirubin

A

If liver working = conjugated bilirubin = DIRECT
if liver NOT working = unconjugated bilirubin = TOTAL - DIRECT

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10
Q

What is total and what is direct bilirubin?

A

Direct = conjugated

Total = conjugated + unconjugated

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11
Q

What is the most common cause of paediatric jaundice? What sort of bilirubin rise is expected? How to treat it?

A

usually due to liver immaturity coupled with a fall in the Hb early in life

  • HIGH unconjugated bilirubin
  • Phototherapy - converts bilirubin into 2 other compounds which do NOT need conjugation for excretion
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12
Q

What are rarer causes of paediatric jaundice?

A
  • hypothyroidism,
  • other causes of haemolysis (including a Coombes test to check for AHA)
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13
Q

Which LFT result is a good marker for obstructive jaundice?

A

RAISED ALP

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14
Q

Describe inheritance of Gilbert’s disease? % of population that are carriers? % affected

A

recessive
50% carriers
6% affected

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15
Q

What act causes worsening of bilirubin in Gilbert’s disease?

A

FASTING

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16
Q

What is the pathophysiology of Gilberts?

A

UDP glucuronyl transferase activity reduced to 30%

unconjugated bilirubin binds tightly to albumin and does NOT enter urine
* pt will have urobilinogen - which is normal as everyone has it

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17
Q

Which is the most representative of liver function?

  • Prothrombin time
  • Albumin
  • Bilirubin
  • Alanine Amino Transferase (ALT)
  • Aspartate Amino - Transferase (AST)
  • Alkaline phosphatase
  • Gamma GT
A

A - PT time as the clotting cascade components are made by the liver

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18
Q

Normal PT time

A

12-14 seconds

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19
Q

Function of liver is measured by… (3)

A
  • albumin
  • clotting factors (PT)
  • Bilirubin
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20
Q

Aged 35
Chronic alcohol intake
Often appeared drunk to A + E
Nausea, abdo pain and jaundice.

LFTs abnormal: Bilirubin 90
Alk Phos 200 (NR <130)
AST 1500 (<50); ALT 750 (<50)

Pre-hepatic/hepatic/post-hepatic?
What is excluded?
Give top 2 ddx

A

ALT and AST very raised - suggests HEPATIC

Obstructive jaundice excluded as ALP only marginally raised

ALCOHOLIC or VIRAL hepatitis

21
Q

Describe serology changes following hepatitis A infection?

A

shed virus in faeces for initial 5 weeks

anti-hepatitis A IgM between 2-12 weeks

anti-hepatitis A IgG starting from 5 weeks

22
Q

How is hepatitis A transmitted?

A

faeco-oral route

23
Q

What is the serology of someone who has cleared hepatitis A?

A

anti-hep A IgG +

24
Q

what are the 2 antigens measured in hepatitis B?
What does each mean?

A

E antigen = soluble viral peptide that flows freely in serum = means person is HIGHLY CONTAGIOUS

S antigen = surface antigen = = can be elevated in both acute and chronic phases of hepatitis B

25
Q

what happens post hepatitis B exposure?

A

2 months post exposure, HBs Ag and HBe Ag begin to increase.
Following this, an immune response builds and antigen titres go down

once cleared, 3 antibodies remain = anti-HBs, anti-HBe, and anti-HBc

26
Q

Serology wise, what is the difference between someone who has cleared hepatitis B and someone vaccinated for it?

A

Vaccinated = anti-HBs +

Cleared naturally = anti-HBs+, anti-HBe +, anti-HBc +

27
Q

Hepatitis B carrier:

  • Describe their clearance of the virus
  • Are they contagious?
  • How to identify carriers?
A

Never clear virus - antigen levels DROP but never go to zero

they are ALWAYS contagious

problem is they’re often SUBCLINICAL hence they do not become jaundiced.

28
Q

Describe histological features of alcoholic hepatitis?

A
  1. liver cell damage:
    - ballooning degeneration +/-
    - Mallory-Denk Bodies
  2. inflammation (i..e, neutrophilic infiltration)
  3. fibrosis (increased collagen)
  4. Pericellular fibrosis

*mainly seen in zone 3!!

29
Q

Describe associated histological features of alcoholic hepatitis?

A
  • fatty change
  • megamitochondria
  • bile accumulation (cholestasis) due to damaged/swollen bile ducts
30
Q

What is the commonest cause of liver hepatitis?

what is it correlated with?

A

Non-alcoolic fatty liver disease (NAFLD) including NASH - non-alcoholic steatohepatitis

BMI

31
Q

What does NASH look like histologically?

A

exactly like alcoholic hepatitis - ballooning, cellular damage, fibrosis

32
Q

Treatment for alcoholic hepatitis?

A
  • Supportive.
  • Stop alcohol.
  • Nutrition:
  • Vitamins (esp B1, thiamine – pabrinex)
  • Occasionally steroids.
33
Q

If hepatocytes can regenerate, why can hepatitis lead to more severe complications or diseases?

A

new hepatocytes will not grow in nicely organized hexagons – so they won’t be nicely organized

Inflammation > cell death > cell regeneration

As a result of this poorly organized regeneration, the blood will not flow through the liver well enough, and you get portal hypertension in these patients with chronic liver damage

34
Q

What deficiency causes each disorder?

Rickets
Scurvy
Pernicious anaemia
Beri-Beri -
Pellagra
Neural tube defects

A

Rickets - vit D
Scurvy - vit C
Pernicious anaemia - vit B12
Beri-Beri - vit B1
Pellagra - vit B3 (niacin)
Neural tube defects - folate

35
Q

what are some clinical features of chronic stable liver disease?

A

Multiple spider naevi
Dupuytren’s contracture
Palmar erythema
Gynaecomastia

HINT: these are the people you see in PACEs

36
Q

What are some common complications of portal hypertension?

A
  1. Variceal veins - portal hypertension causes pressure to go down portal vein and cause varices, such as in the umbilical vein, oesophageal varices, etc.
  2. Splenomegaly - due to increased pressure in the portal vein, which is made of the splenic vein and superior mesenteric vein
  3. Ascites
37
Q

Visible veins
Splenomegaly
Ascites (shifting dullness.)

What has happened?
Jaundice
Hepatitis
Chronic stable liver disease
Portal hypertension.
Liver failure
Obstruction of the bile ducts

A

Portal hypertension

38
Q

What is portal hypertension caused by?

A

cirrhosis

39
Q

A patient is admitted to drain ascites, but developed a flap shortly afterwards.
Jaundice
Hepatitis
Chronic stable liver disease
Portal hypertension.
Liver failure
Obstruction of the bile ducts

A

Liver failure
This means the brain is being poisoned by the toxins that the liver cannot get rid of – encephalopathy

We think the toxin is ammonia but we’re not too sure. The concept is the same as the CO2 flap – where CO2 intoxicates the CNS

40
Q

What does the liver FAIL (4) to do in liver failure?

A
  1. Failed synthetic function
  2. Failed clotting factor and albumin
  3. Failed clearance of bilirubin
  4. Failed clearance of ammonia
    (encephalopathy)
41
Q

what types of nodules is seen in alcoholic cirrhosis?

A

Micronodules

42
Q

List 4 sites of porto-systemic anastomoses

A
  1. Oesophageal varices
  2. Rectal varices
  3. Umbilical vein
  4. recanalising
    Spleno-renal shunt
43
Q
  • Severely jaundiced
  • Cachectic
  • Palpable gall bladder
  • Multiple scratch marks on skin

What do scratch marks suggest?

A

The cause of jaundice is OBSTRUCTION OF THE BILE DUCTS

44
Q

71 year old man presents with jaundice

  • cachectic
  • palpable gallbladder
  • multiple scratch marks
  • No previous history at all
  • Weight loss

Give some ddx

A

Seems post-hepatic jaundice (obstructive) –> gallstones, pancreatic cancer

45
Q

Bilirubin 340
Alk Phos: 1750
AST 50 ALT 45
What do these results suggest?

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

A

Obstruction of the bile ducts

46
Q

In obstructive jaundice, what causes the itching?
Bilirubin
Urobilinogen
Bile salts
Bile acids
Stercobilinogen

A

bile salts and bile acids (technically the same thing)

47
Q

Courvoisier’s law - what is it?

A

If GB is PALPABLE in a jaundiced patient, cause is UNLIKELY to be gallstones

(b/c GB with stones is usually SMALL and FIBROTIC)

cause is more likely to be pancreatic or biliary cancer

48
Q

Obstructive jaundice is commonly caused by ________ ______ or _________, which can be distinguished clinically by which examination?

A

pancreatic cancer
gallstones

Palpable/unpalpable GB

Pathology by week (70 decks)

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