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
Q

State the management that should be followed for the following…
HBeAg +Ve
HBV DNA( copies mL) = <10^5
ALT normal

A

Follow, no treatment

26
Q

State the management that should be followed for the following…
HBeAg +Ve
HBV DNA( copies mL) = >/= 10^5
ALT normal

A

Consider biopsy.

treat if diseased

27
Q

State the management that should be followed for the following…
HBeAg +Ve
HBV DNA( copies mL) = <10^5
ALT elevated

A

TREAT

28
Q

State the management that should be followed for the following…
HBeAg -Ve
HBV DNA( copies mL) = <10^4
ALT normal

A

Follow, no treatment

29
Q

State the management that should be followed for the following…
HBeAg -Ve
HBV DNA( copies mL) = >/= 10^4
ALT normal

A

Consider biopsy.

Treat if diseased

30
Q

State the management that should be followed for the following…
HBeAg -Ve
HBV DNA( copies mL) = >/= 10^4
ALT elevated

A

TREAT

31
Q

What is HARVONI?

A

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
Q

Outline the characteristics of Haemochromatosis

A
  • Iron overload
  • Autosomal recessive
  • HFE gene
  • Homozygote gene frequency~ 1 in 150
  • Phenotypic frequency~4 in 100
33
Q

What are the clinical features of Haemochromatosis?

A
  • Cirrhosis
  • Skin pigmentation
  • Diabetes
  • Cardiomyopathy
  • Arthritis
  • Pituitary failure
34
Q

Explain how we diagnose haemochromatosis

A
  • 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
Q

Outline the characteristics of primary biliary cholangitis

A
  • 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
Q

Outline the progression of the changes toward cirrhosis in primary biliary cirrhosis

A
  • 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
Q

Outline the characteristics of autoimmune hepatitis

A

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
Q

Outline the characterstics of alpha-1-antitrypsin deficiency

A
-Associated with COPD
Diagnosis:
-alpha-1- antitrypsin level<25%
-alpha-1-antitrypsin phenotype
-Liver biopsy-PAS positive globules
39
Q

Outline the characteristics of Wilson’s disease

A

-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
Q

How is Wilson’s disease diagnosed

A
  • 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
Q

State the different chronicity stages of chronic HBV infection and link them to their disease state

A

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
Q

Describe the serology according to the different chronicity stages of HBV

A

Phase 1= HBsAg; HBeAg
Phase 2=continuation of phase 1 serology
Phase 3=Anti-HBe
Phase 4=Anti-HBs

43
Q

Describe the changes in ALT level as a pt progresses through chronic HBV infection

A

Phase 1=stays low/o
Phase 2=increases and peaks in the middle of phase
Phase 3=stays at 0/low

44
Q

Describe the changes in HBV DNA as a pt progresses through chronic HBV infection

A

Phase 1=very high i.e high viral load
Phase 2=gradually decreases
Phase 3=0

45
Q

What does it mean when someone is HBeAg negative with a high viral load?

A
  • 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
Q

What are the treatment options for Hep B

A

Antivirals:

  • entecavir
  • tenofovir
  • lamivudine
  • adefovir
  • telbivudine
47
Q

What are the treatment options for chronic hep C

A

-Harvoni= the first & only single tablet regimen for most HCV G1 adults

  • Ledipasvir
  • Sofosbuvir
48
Q

When CAN’T harvoni be used for HCV G1 adults

A

-those pts with decompensated cirrhosis or who are pre or post liver transplant

49
Q

What is the treatment for primary biliary cholangitis?

A
  • Ursodeoxycholic acid

- Obeticholic acid

50
Q

Outline the treatment in autoimmune hepatitis

A
  • Prednisolone

- Azathioprine

51
Q

What is primary sclerosing cholangitis(PSC) ?

A
  • 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
Q

How can we diagnose PSC?

A
  • Liver biopsy (‘onion skin’ fibrosis)

- ERCP/MRCP

53
Q

How is Wilson’s disease diagnosed

A
  • 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
Q

How can we treat Wilson’s disease

A
  • penicillamine

- transplantation

55
Q

Is there any association between Wilson’s disease and diabetes

A

There’s a strong association

56
Q

Describe the course of NAFLD leading to liver failure

A

NAFLD—>NASH—>CIRRHOSIS—>LIVER FAILURE

57
Q

What are the advantages of taking a liver biopsy

A
  • 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
Q

Outline the non-invasive markers of cirrhosis

A
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
Q

State the steps of progression in non-alcoholic liver disease

A
  1. ) Steatosis
  2. )Steatohepatitis
  3. ) Fibrosis
  4. )Cirrhosis
60
Q

What are key differences in the liver enzymes during progression of non-alcoholic liver disease compared to alcoholic liver disease ?

A

Non-alcoholic: increases ALT and sometimes AST

-Alcoholic: increases AST and ALT to a lesser degree ; AST:ALT ratio increases in alcoholic