Week 5 Liver In More Detail Flashcards

1
Q

Which segments of the liver are suitable for living transplant? e.g. will grow back in doner and grow into a new one in receiver

A
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2
Q

Based on your knowledge of liver function tests, which if these markers within the hepatacycte is which?

A

ALP - Choleostasis
AST/ ALT - Hepatocyte damage
GGT - Both

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3
Q

Complete this liver cell table

A
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4
Q

Complete this liver cell table

A
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5
Q

How to remember difference between glycogen and glucagon?

A

GlycoGEN - is generated when there is plenty of glucose

GlucaGON - is released when glucose is gone from the bloodstream

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6
Q

Describe the livers role in lipid metabolism

A
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7
Q

What is an enterocyte?

A

Absorption cell in small and lerge intestine

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8
Q

Functions of liver in proteine metabolism

A
  • Catabolism of circulating protein/peptides
  • Interconversion of amino acids
  • Deamination of amino-acids allowing gluconeogenesis
  • Synthesis of non-essential amino acids
  • Catabolism of hepatic (stored) proteins in fasted state
  • Protein synthesis
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9
Q

Proteins that are synthesised by the liver

A
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10
Q

What is the liver’s role in ammonia metabolism?

A

Ammonia is absorbed in the gut

It is then turned into urea by the liver thus detoxifying it

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11
Q

What are the three phases of liver drug metabolism?

Which parts are involved?

A
  1. endoplasmic reticulum
  2. cytoplasm
  3. bile side of cell
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12
Q

What role does the liver play in immune regulation, why is this important?

A

‘firewall’ filtering all blood from gut
Kupffer cells phagocytose pathogens from gut
Supply of important chemokines/cytokines
Interleukins
Tumour necrosis factor
Priming T cell responses

Takeaway is that you can recover from acute liver failure but then catch a severe infection due to immunosurpression

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13
Q

What is the gold standard for diagnosing liver cirrhosis?

Two other methods as well

A
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14
Q

What is Hepatic Encephalopathy

A

This is where toxins absorbed by the gut that normally get detoxified on first pass don’t get detoxified due to portal hypertension and shunting.

They therefore make it to the brain causing brain toxicity

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15
Q

What are the serum markers of liver function?

A
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16
Q

Fill these signs in

A
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17
Q

What are the causes of ALF that we will actually get asked about in 2nd year?

A

Paracetamol and viral hepatitis

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18
Q

 23 female
 Nausea and abdominal pain
 Intentional overdose of paracetamol (64 tablets) 2
days before
 2 previous overdoses
 Drinks ½ bottle wine and 4-5 vodkas/night at
weekends

 No stigmata of cirrhosis
 ALT 4500 (< 50)
 Bilirubin 110 (< 21)
 PT 23 (< 13)
 Albumin 38 (>36) (Albumin normal rules out chronic liver damage)
 Lactate 6 (< 2)
 Ultrasound normal

What would you do?

A

 Started on N-acetyl cysteine infusion
 Given vitamin K

Moniter

If doesn’t get better refer for liver transplant

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19
Q

Why is albumin only raised in chronic liver failure and not acute liver failure?

A

Albumin half life is about 20 days so in acute liver damage there often isn’t enough time for albumin to fall

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20
Q

Why would you give vitamin K in chronic liver failure?

A

It’s not actually to fix coagulation.

If the liver if damaged giving vitamin K won’t help PT as the liver can’t make clotting factors in response to vitamin K.

So it is to rule out raised PT through vit K deficiency, if it rises with vit K then liver ok.

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21
Q

What is prothrombin time?

A

It is the time it takes for blood to coagulate.

With regards to liver a raised PT is a sign of liver damage as the liver is required for the production of clotting factors

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22
Q

In paracetamol induced ALF, considering PT, anuria, creatinine and encephalopathy. At what point is spontaineous recovery extremely unlikely (transplant required)

A

 PT>100 AND
 Anuric / creatinine >300 AND
 Grade 3-4 encephalopathy (stupor/coma)

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23
Q

What is Hepatorenal Syndrome (HRS)?

A

This is where portal hypertension leads to portal system dialating and releasing NO in order to vasodialate.

This systemically dialates the vessels particularly the splanchic vessels resulting in reduced renal perfusion.

RAAS fails to compensate through Na/H2O retention as it mostly leaks into abdomen through ascites.

Result is percieved renel failure when actually the kidneys are functioning just fine.

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24
Q

Why might you get percieved kedney failure such as anuria and raised serum creatinine in ALF when in ALF you don’t get portal hypertension?

A

ALF causes release of inflammatory cytokines, nitric oxide, and other mediators still leading to widespread systemic vasodialation and perceived hypovolaemia

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25
What is seronegative hepatitis?
Seronegative hepatitis refers to acute or chronic hepatitis (liver inflammation) where no standard viral markers (like Hep A, B, C, E, CMV, EBV, etc.) are found on blood tests.
26
When it comes to non-paracetamol ALF what conditions need to be filled for spontaineous recovery to be unlikely?
 Age (< 10 or >40 worse)  Aetiology (drug/seronegative worse than viral)  PT > 50 or INR > 3.5  Bilirubin > 300  Time from jaundice to encephalopathy < 7d
27
In non-paracetamol ALF which out of drug/seronegative or viral has a worse prognosis?
Drug/seronegative is a worse prognosis than viral.
28
What is the difference in progression between paracetamol ALF and other causes?
Paracetamol causes hyperacute liver failure. Usually encephalopathy in less than 1 week  Other causes usually more gradual onset  Progression over several weeks
29
ALF treatment?
Identify and treat underlying cause:  NAC for paracetamol  Antivirals for hepatitis B  Steroids for autoimmune hepatitis For all:  Supportive care  Close monitoring (especially paracetamol)  Liver transplantation if appropriate
30
How should you treat oesophageal varices?
Mild: Beta blockers to reduce pressure and risk of bleeding Severe: Band ligation
31
How should you assist with alcohol withdrawal?
Diazepam
32
What suppliments does someone need after chronic liver failure due to alchohol?
Thiamine
33
How do you manage ascites in chronic liver failure?
Low salt diet and diuretics
34
What is the difference between liver cirrhosis and chronic liver failure?
Chronic liver failure can be considered as decompensated liver cirrhosis
35
36
Does autoimmune hepatitis, hepatitis B/C cause ALF or CLF?
All can cause both
37
What are the common clinical symptoms of viral hepatitis?
Jaundice, dark urine, clay-colored stool, nausea, vomiting, loss of appetite, fever, abdominal pain, weakness
38
What serological markers are used to diagnose viral hepatitis?
Viral antigens, anti-viral antibodies (EIA), viral load, genotype (PCR)
39
What type of virus is HAV?
Non-enveloped, ss+RNA, picornavirus
40
How is HAV transmitted?
Fecal-oral route
41
Can HAV become chronic?
No, resolves spontaneously with lifelong immunity
42
What serological markers indicate recent and past HAV infection?
IgM (recent); IgG (past or vaccinated)
43
Is there a vaccine for HAV?
Yes, inactivated virus vaccine
44
What type of virus is HBV?
Enveloped, partially dsDNA, hepadnavirus
45
How is HBV transmitted?
Parenteral, sexual, vertical
46
What percentage of neonates progress to chronic HBV?
>95%
47
Who is hepatitis B primarily found in?
Primarily babies and young adults
48
Which HBV antigen indicates active infection?
HBsAg
49
Which antibody indicates immunity from vaccination or past infection?
Anti-HBs
50
Which marker indicates recent HBV infection?
Anti-HBc IgM
51
Is there a vaccine for HBV?
es, recombinant HBsAg vaccine
52
Is HBV associated with cancer?
Development into chronic hep B can lead to hepatocellular cancer
53
Hep B treatment for chronic infection
Treatment (for chronic infection): Interferon alpha OR antivirals
54
What type of virus is HCV?
Enveloped, ss+RNA, flavivirus
55
How is HCV transmitted?
Parenteral (possibly sexual)
56
Does HCV often cause chronic infection?
Yes, 70–90% develop chronic infection
57
Is there a vaccine for HCV?
No
58
What treatments are available for HCV?
Direct-acting antivirals (DAAs), interferon + ribavirin
59
What type of virus is HDV?
Defective circular ss–RNA virus; needs HBV to replicate
60
What are the infection types in HDV?
Co-infection with HBV (severe acute, low risk of chronicity) Superinfection on chronic HBV (severe chronic, high risk of severe chronic liver disease)
61
How can HDV be prevented?
HBV vaccination (indirect protection) as need a hep B infection in order to replicate
62
What type of virus is HEV?
Non-enveloped ss+RNA, hepevirus
63
How is HEV transmitted?
Fecal-oral route
64
Can HEV become chronic?
Only in immunocompromised patients
65
Why is HEV dangerous in pregnancy?
High fatality (15–25%) with genotype 1
66
Is there a vaccine for HEV?
Yes, but only available in China (genotype 1)
67
Where is HBV most prevelent?
South-east Asia, Parts of China, Sub-Saharan Africa
68
Name some non-A to E viral causes of hepatitis
EBV, CMV, HSV-1/2, Rubella, Enteroviruses, Yellow fever