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Gastro YR3 > Liver Tutorial > Flashcards

Liver Tutorial Flashcards

1
Q

How does hepatitis often present?

A
  • raised ALT compared to ALP
  • Moderate jaundice
  • Smooth, tender hepatomegally
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2
Q

How does hepatitis A present?

A

Flu like illness - anorexia, myalgia, nausea and headaches
Last 2 days felt better but now jaundice

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3
Q

Causes of hepatitis

A
  • Serology - Hep A,B,C (hep C often subclinical)
  • Autoimmune
  • EBV
  • Meds eg NSAIDs
  • Paracetamol overdose
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4
Q

How does cholangiocarcinoma present?

A
  • Painless jaundice - months
  • Aypyrexial
  • Very high ALP compared with ALT

Could also be pancreatic malignancy

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5
Q

How to tell between pancreatic maliganncy and biliary malignancy?

A

ERCP - stent if stricture present, get brushings to do histological testing on

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6
Q

Presentation of ascending cholangitis

A
  • RUQ pain
  • Fever
  • Jaundice
  • History of gallstones/biliary colic
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7
Q

Differential for ascending cholangitis triad

A

Liver abscess - USS scan to see if dilated bile ducts (AC) or holes in liver with fluid levels (abscess)

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8
Q

Abx for ascending cholangitis

A

Tazocin IV (Piperacillin and Tazobactam - beta lactamase inhibitor)

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9
Q

What is presentation of primary biliary cholangitis?

A
  • Pruritus
  • Mild jaundice
  • Antimitochondrial antibody positive
  • Liver US normal
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10
Q

What is primary biliary cholangitis?

A

Autoimmune destruction of small bile ducts within liver
Parenchymal damage
Leads to cirrhosis

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11
Q

Primary biliary cholangitis vs primary sclerosing cholangitis

A
  • PBC - affects small ducts, more common, antimitochondiral ab +ve
  • PSC - affects ANY duct, no antibody - use ERCP and MRCP to diagnose
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12
Q

Treatment for primary biliary cholangitis

A

Ursodeoxycholic acid - bile acid replacement, decreases damage to liver

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13
Q

How to tell cause of ascites?

A
  • Do SAAG - serum ascitic albumin gradient
  • This shows the portal pressure
  • Serum albumin minus ascitic albumin
  • If more than 11g/L this shows portal HTN = cirrhosis
  • If less, must be no cirrhosis so other cause of ascites inc cancer? TB? Nephrotic syndrome?
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14
Q

What are those with cirrhosis at risk of that can present as general unwellness?

A
  • Spontaenous bacterial peritonitis
  • Translocation of gut microbes into ascitic fluid = multiplication
  • Treat with antibiotics
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15
Q

Which are more at risk of peritonitis if bowel ruptured cirrhotic patients or malignancy?

A
  • Cirrhotic patients as their ascitic fluid is just water and sugar as fluid build up is due to increased hydrostatic pressure
  • In malignancy the vessels become more permeable = leakage of proteins inc immunoglobulins which can kill microbes
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16
Q

Which conditions which cause ascites cause a high SAAG?

A
  • Heart failure
  • Cirrhosis
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17
Q

What can be a post hepatitis C complication that can present years later with fatigue?

A
  • Hep C associated hepatocellular carcinoma
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18
Q

Tumour marker for hepatitis C associated hepatocellular carcinoma

A

AFP - alpha feto protein

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19
Q

Treatment for hepatocellular carcinoma

A

If less than 3cm - offer liver transplant
If 5cm or more - offer embolisation and chemotherapy - block blood supply

20
Q

What value of HCV RNA PCR suggests no detectable infection?

A

Less than 15 copies / ml means virus is undetectable

21
Q

Meaning of HBsAg?

A
  • Hepatitis Surface Antigen
  • If present shows that infection of heptatits B is present
22
Q

What is HBcAb IgM?

A
  • Hepatitis B core antibody IgM / aka IgM anticore
  • If positive shows infection is acute, if not infection is chronic
23
Q

What is HBeAg?

A
  • Hepatitis B e antigen
  • If positive shows virus is rapidly multiplying
24
Q

What is HBeAb?

A
  • Hepatitis B e antibody
  • If present shows body is having immune response to hepatitis B
25
Q

When do we treat hepatitis B?

A
  • If pregnant - within last 3 months of pregnancy to decrease viral load and decrease chance of passing onto baby via vaginal canal
  • If signs of liver damage
  • When no immune response and signs of liver damage
26
Q

When do we not treat hepatitis B?

A
  • When no signs of liver damage
  • When no immune response but no signs of damage

This is because 95% of people with mature immune systems will clear infection

27
Q

What can present with previous flu, now jaundice with normal LFTs, FBC and urine sample?

A
  • Gilberts syndrome - autosomal recessive disease
  • Triggered by stress, alcohol, infection, lack of sleep
  • When RBC are haemolysed, liver conjugates bilirubin to become soluble. People with Gilberts syndrome are slower at this
28
Q

What can cause jaundice and pruiritis post cellulitis treatment, normal USS and no autoantibodies?

A
  • Cholestasis - will have obstructive picture ie high ALP but USS will be normal
  • Cholestasis caused by antibiotic treatment eg Co-amoxciclav (clavulanic acid portion) or Flucloxacillin
29
Q

How would primary sclerosing cholangitis present?

A
  • Similar scenario to cholestasis caused by abx
  • No signs on USS and no positive autoantibodies
  • Diagnose via MRCP
30
Q

Treatment for Hep C - active infection but no fibrosis

A
  • 12 weeks antiviral drugs - then no follow up
31
Q

Treatment for Hep C active infection with fibrosis

A
  • 12 weeks antivirals
  • Then monitor via US and AFP for hepatocellular carcinoma as at increased risk every 6/12
32
Q

What to do if previous Hep C infection (HCV ab positive but RNA low) and no fibrosis?

A

Resolved - do nothing

33
Q

Iron studies in haemochromatosis

A
  • High ferritin
  • High serum iron
  • Low TIBC
34
Q

Why is TIBC low in iron overload?

A
  • There is no transferrin free to bind to iron
  • As there are high iron levels in the blood
  • So all of it is bound
  • So transferrin does not have capacity to bind to anymore iron
35
Q

What must you do to monitor haemochromatosis?

A

MRI to check iron load of liver and cardiac effects

36
Q

Treatment for iron overload haemochromatosis

A

500ml blood venesection weekly

37
Q

Haematinics for alcholic

A
  • High ferritin - acute phase protein, high in chronic liver disease
  • High MCV
  • Low folate
  • High GGT
38
Q

Haematinics for malnutrition from coeliac

A
  • Low ferritin
  • Low serum iron
  • High MCV
  • Low folate
  • But normal B12
  • Low calcium
39
Q

Why is B12 normal in coeliac?

A
  • Absorbed in terminal ileum
  • Folate is low as it is absorbed by proximal bowel ie duodenum
  • This is where we take biopsy via endoscopy from to diagnose coeliac (2nd part duodenum)
40
Q

Main causes malnutrition UK

A
  • Coeliac
  • Crohns
  • Chronic pancreatitis

Chrons and pancreatitis painful

41
Q

What tests prove autoimmune hepatitis?

A
  • ANA positive
  • Anti smooth muscle antibody positive
  • Then biopsy liver
42
Q

Anaemia of chronic disease haematinics

A
  • Iron low
  • TIBC low
  • Ferritin high - inflammation
43
Q

What regulates ferritin levels?

A
  • Hepcidin - more hepcidin = higher ferritin levels = more iron stored and less available in plasma
  • Bodys defence to infection, reduce iron availability of bacteria
44
Q

How is fatty liver disease diagnosed?

A

USS liver and kidney in same field
If liver is brighter than kindey = fatty liver

45
Q

Follow up for diagnosis of fatty liver

A
  • Enhanced liver fibrosis screen
  • Fibroscan –> if no fibrosis then no risk of cirrhosis
  • If yes there is risk
  • Weight loss needed in fatty liver disease with potential Vitamin E
46
Q
A

Gastro YR3 (10 decks)

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