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Liver disease 1 Flashcards

1
Q

List the different liver function tests

A
  • Bilirubin
  • Alkaline phosphatase
  • Alanine Transaminase
  • Gamma GT
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2
Q

What is hepatitis

A
  • Inflammation of the liver
  • Raised Transaminases
  • Raised ALT, AST( released when the liver is damaged)
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3
Q

What does ALT stand for

A

Alanine transaminase

  • An enzyme found mostly in the liver
  • Released by liver cells when they are damaged
  • An ALT test measures how much ALT is in the blood
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4
Q

What does AST stand for?

A
  • Aspartate aminotransferase
  • An enzyme that is normally present in liver & heart cells.
  • Released into the blood when the liver or heart is damaged
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5
Q

What is Cholestasis?

A
  • Obstructive
  • Reduction or stoppage of bile flow
  • Raised alkaline phosphatase
  • Raised GGT
  • To determine whether the patient has cholestasis or hepatitis, need to look at the ALT,AST &GGT
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6
Q

What is GGT?

A
  • Gamma-glutamyl transferase
  • Elevated levels may be due to liver diseases, such as hepatitis or cirrhosis, but they may also be due to other conditions eg congestive heart failure, diabetes or pancreatitis
  • A low/normal GGT test result indicates that it’s unlikely that the person has liver disease or has consumed any alcohol
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7
Q

Outline what biliary disorders are and list them

A
  • Diseases affecting bile ducts from small interlobular ducts down to common bile duct outlet in duodenum
    1. ) Large duct obstruction-generally referred to extrahepatic BD
    2. ) Primary sclerosing cholangitis -large and/or small BD
    3. ) Primary biliary cirrhosis- small interlobular BD
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8
Q

Outline the various causes of abnormal liver enzymes

A
  • Alcohol
  • Medications
  • NAFLD
  • Viral hepatitis( chronic hep B& C)
  • Haemochromatosis

Rarer causes=

  • autoimmune hepatitis
  • Primary biliary cirrhosis
  • Alpha-1-antitrypsin deficiency
  • Wilson’s disease
  • Coeliac disease
  • Sero-negative hepatitis
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9
Q

What investigations may be carried out when determining if a patient has liver disease?

A
  • FBC
  • INR
  • U&E/LFTs
  • Lipids
  • Imaging( ultrasound& dopplers) on the hepatic& portal veins
  • Immunology: autoantibodies, immunoglobulins
  • Virology: hepatitis B surface antigen; hep C Ab
  • Chemistry: ferritin; copper/caeruloplasmin
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10
Q

Which autoantibodies may be looked for when investigating liver disease?

A
  • Antinuclear antibodies, smooth muscle antibodies
  • Anti-mitochondrial abs
  • Anti-endomyseal abs
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11
Q

List the possible causes of cirrhosis

A
  • Alcohol
  • Chronic viral hepatitis (hep B& hep C)
  • Haemochromatosis
  • Non-alcoholic steatohepatitiis
  • Primary biliary cirrhosis
  • Autoimmune hepatitis
  • Primary sclerosing cholangitis
  • Alpha-1-antitrypsin deficiency
  • Wilson’s disease
  • Drug induced
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12
Q

List the different types of viral hepatitis

A

Hepatitis..

A,B,C,D,E

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13
Q

Outline the characteristics of Hep A

A

-Faeco-oral route
-Self limiting in 99%
-No chronicity
-Hep A IgM= acute Hep A
-Hep A IgG= previous exposure
-Vaccination available
common in travel

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14
Q

Outline the serology of Hep B

A
  • Hepatitis B surface antigen (HBsAg)= patient has hep B= refer patient!
  • Hepatitis B surface antibody(HBsAb)= patient is immune to Hep B
  • Hepatitis B core IgM= patient has acute Hep B
  • Hepatitis B core IgG= patient has been exposed to Hep B (particularly in people undergoing chemo or immunosuppression)
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15
Q

Outline the immunoglobulins from greatest to least in number within our body

A

GAMED( IgG, IgA, IgM,IgE,IgD)

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16
Q

What immunoglobulin is produced when your body first starts fighting off an infection?

A

-Body first produces IgM to fight off the infection, until it starts producing IgGs which stay in the body for years

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17
Q

What i the relationship between the quantity of HBsAg in your blood and your symptoms

A

-The greater the quantity of HBsAg in your blood, the more likely it is for you to develop symptoms

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18
Q

what is the HBeAg a marker of?

A

viral replication

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19
Q

what does HBsAg indicate

A

infection

-(regardless of whether it is acute or chronic)

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20
Q

What does IgG-HBsAg indicate?

A

immunity (cure or vaccine)

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21
Q

Describe the window period that exists during the course of the infection

A

The time period when the IgM-HBcAg is fighting off the virus so well that the virus particles become so few that they aren’t detected on serology

  • However the person still has Hep B infection as the body still hasn’t produced enough IGsAg
  • Infected despite a negative HBsAg
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22
Q

How do you tell the difference between immunity via cure and immunity via vaccination in an IgG-HBsAg positive patient?

A

If the person was once infected then they would have antibodies against core antigen.

  • Hep B virus vacicnation contains HBsAg only, so the body only produces antibodies against HBsAg and not HBcAg
  • The exception is the window period i.e infected despite a negative HBsAg
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23
Q

How can you tell the difference between an acute and chronic Hep B infection using the serology indicating the antibodies against HBcAg

A

-If the abs against HBcAg are IgM, that means acute infection. If they’re IgG, that means chronic infection

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24
Q

State the disease manifestation of the immune tolerant phase (phase I) of chronic HBV infection

A

minimal inflammation as the body’s immune system fails to respond to the infection

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25
State the management that should be followed for the following... HBeAg +Ve HBV DNA( copies mL) = <10^5 ALT normal
Follow, no treatment
26
State the management that should be followed for the following... HBeAg +Ve HBV DNA( copies mL) = >/= 10^5 ALT normal
Consider biopsy. | treat if diseased
27
State the management that should be followed for the following... HBeAg +Ve HBV DNA( copies mL) = <10^5 ALT elevated
TREAT
28
State the management that should be followed for the following... HBeAg -Ve HBV DNA( copies mL) = <10^4 ALT normal
Follow, no treatment
29
State the management that should be followed for the following... HBeAg -Ve HBV DNA( copies mL) = >/= 10^4 ALT normal
Consider biopsy. | Treat if diseased
30
State the management that should be followed for the following... HBeAg -Ve HBV DNA( copies mL) = >/= 10^4 ALT elevated
TREAT
31
What is HARVONI?
The first and only single-tablet regimen for the majority of HCV GT1 adult patients(excluding those who with decompensated cirrhosis or who are pre- or post liver transplant)
32
Outline the characteristics of Haemochromatosis
- Iron overload - Autosomal recessive - HFE gene - Homozygote gene frequency~ 1 in 150 - Phenotypic frequency~4 in 100
33
What are the clinical features of Haemochromatosis?
- Cirrhosis - Skin pigmentation - Diabetes - Cardiomyopathy - Arthritis - Pituitary failure
34
Explain how we diagnose haemochromatosis
- Raised ferritin - Difficult to differentiate from alcoholic haemosiderosis - HFE gene - Liver biopsy& hepatic iron estimation - Hepatic iron index= micromol iron per g dry weight/age - HII>1.9 (diagnostic of haemochromatosis, reliably differentiates from alcoholic iron overload)
35
Outline the characteristics of primary biliary cholangitis
- different from primary biliary cirrhosis - Middle aged female - Itching,tiredness - Cholestatic LFTs - Not necessarily 'cirrhotic' - Raised IgM, psoitive anti-mitochondrial ab - Liver biopsy( bile duct damage, granulomatous cholangitis) - Treatment: Ursodeoxycholic acid, Obeticholic acid
36
Outline the progression of the changes toward cirrhosis in primary biliary cirrhosis
- Portal tract expansion with radiating septa& absence of bile duct( ductopaenia) - Biliary interface activity with characteristic 'halo' - Cirrhosis with portal-portal pattern of bridging fibrous septa
37
Outline the characteristics of autoimmune hepatitis
Diagnosis: - Raised IgG - Positive anti-nuclear ab - Positive smooth muscle ab - Positive liver-kidney - Liver biopsy: interface hepatitis; plasma cell infiltrates - Treatment: prednisolone, azathioprine
38
Outline the characterstics of alpha-1-antitrypsin deficiency
``` -Associated with COPD Diagnosis: -alpha-1- antitrypsin level<25% -alpha-1-antitrypsin phenotype -Liver biopsy-PAS positive globules ```
39
Outline the characteristics of Wilson's disease
-Autosomal recessive -disorder of copper metabolism( Caeruloplasmin synthesis defective; reduced biliary copper excretion) -Young adults/children Clinical features= -Liver cirrhosis -Acute liver failure -Neuropsychiatric disorders -Kayser-Fleischer rings
40
How is Wilson's disease diagnosed
- Low serum caeruloplasmin - Reduced serum copper - High urinary copper excretion - Kayser-Fleischer rings - Liver biopsy(liver copper>250micrograms/g liver dry weight) - Treatment: penicillamine; transplantation
41
State the different chronicity stages of chronic HBV infection and link them to their disease state
Phase 1=immune tolerant phase;Minimal inflammation Phase 2=Immune active;chronic active hepatitis Phase 3=Non-replicative;cirrhosis/HCC Resolved=Normal to cirrhosis/HCC
42
Describe the serology according to the different chronicity stages of HBV
Phase 1= HBsAg; HBeAg Phase 2=continuation of phase 1 serology Phase 3=Anti-HBe Phase 4=Anti-HBs
43
Describe the changes in ALT level as a pt progresses through chronic HBV infection
Phase 1=stays low/o Phase 2=increases and peaks in the middle of phase Phase 3=stays at 0/low
44
Describe the changes in HBV DNA as a pt progresses through chronic HBV infection
Phase 1=very high i.e high viral load Phase 2=gradually decreases Phase 3=0
45
What does it mean when someone is HBeAg negative with a high viral load?
- Someone becomes HBeAg -ve when they ahve been infected/exposed during the perinatal period and remain infected unto above their 40s - overtime the virus mutates to evade the immune system - even when they lose HBeAg the mutated virus can carry on replicating; they may even have HBeAb - The mutated virus can put people at higher risk of liver damage
46
What are the treatment options for Hep B
Antivirals: - entecavir - tenofovir - lamivudine - adefovir - telbivudine
47
What are the treatment options for chronic hep C
-Harvoni= the first & only single tablet regimen for most HCV G1 adults - Ledipasvir - Sofosbuvir
48
When CAN'T harvoni be used for HCV G1 adults
-those pts with decompensated cirrhosis or who are pre or post liver transplant
49
What is the treatment for primary biliary cholangitis?
- Ursodeoxycholic acid | - Obeticholic acid
50
Outline the treatment in autoimmune hepatitis
- Prednisolone | - Azathioprine
51
What is primary sclerosing cholangitis(PSC) ?
- A long-term progressive disease of the liver and gallbladder characterized by inflammation and scarring of the bile ducts which normally allow bile to drain from the gallbladder. - Ulcers - Periductal fibrosis & epithelial atrophy - Bile ducts replaced by fibrosis cords
52
How can we diagnose PSC?
- Liver biopsy ('onion skin' fibrosis) | - ERCP/MRCP
53
How is Wilson's disease diagnosed
- Low serum caeruloplasmin - Reduced serum copper - High urinary copper excretion - Kayser-Fleischer rings - Liver biopsy( liver copper>250ug/g liver dry weight) - Treatment (penicillamine; transplantation)
54
How can we treat Wilson's disease
- penicillamine | - transplantation
55
Is there any association between Wilson's disease and diabetes
There's a strong association
56
Describe the course of NAFLD leading to liver failure
NAFLD--->NASH--->CIRRHOSIS--->LIVER FAILURE
57
What are the advantages of taking a liver biopsy
- Cannot differentiate between NASH and simple steatosis otherwise - Diagnosis of NASH important prognostically - Cirrhotic patients need to be screened for HCC - Future therapies will be available
58
Outline the non-invasive markers of cirrhosis
``` Physical: -Tissue elastography eg fibroscan (to see if the liver is stiff) Biochemical: -enhanced liver fibrosis score (ELF) -NAFLD fibrosis score -Fibrotest -AST to platelet ratio (APRI) ```
59
State the steps of progression in non-alcoholic liver disease
1. ) Steatosis 2. )Steatohepatitis 3. ) Fibrosis 4. )Cirrhosis
60
What are key differences in the liver enzymes during progression of non-alcoholic liver disease compared to alcoholic liver disease ?
Non-alcoholic: increases ALT and sometimes AST | -Alcoholic: increases AST and ALT to a lesser degree ; AST:ALT ratio increases in alcoholic

Inflammation block (27 decks)

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