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My MRCP > Gastroenterology > Flashcards

Gastroenterology Flashcards

Interpreting Hep B serology, Autoimmune hepatitis

1
Q

Interpretating Hepatitis B serology
* HbsAg
* Anti-Hbs

A
  • HbSag surface antigen is the first marker to appear and causes the production of anti-HbS
  • if HBsAg is present for > 6 months then this implies chronic disease (i.e. Infective)
    Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease
    previous immunisation: anti-HBs positive, all others negative
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2
Q

Interpretating Hepatitis B serology

  • Explain Anti-HBc and what having IgM vs IgG means
A

Anti-HBc implies previous (or current) infection.
* IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months.
* IgG anti-HBc persists and positivity indicates past infection or reactivation

Will never appear in a vaccinated individual

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3
Q

Interpreting Hepatitis B serology

What would previous hepatitis B >6 months ago, NOT a carrier?
What would hepatitis B but now a carrier?

A
  1. previous hepatitis B (> 6 months ago), not a carrier: anti-HBc positive, HBsAg negative
  2. previous hepatitis B, now a carrier: anti-HBc positive, HBsAg positive
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4
Q

What is hepatitis B
Transmission
Incubation period
Features

A

Hepatitis B is a double-stranded DNA hepadnavirus
spread through exposure to infected blood or body fluids, including vertical transmission from mother to child.
The incubation period is 6-20 weeks.

The features of hepatitis B include fever, jaundice and elevated liver transaminases.

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5
Q

Complications of hepatitis B infection

A

chronic hepatitis (5-10%). ‘Ground-glass’ hepatocytes may be seen on light microscopy
fulminant liver failure (1%)
hepatocellular carcinoma
glomerulonephritis
polyarteritis nodosa
cryoglobulinaemia

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6
Q

National immunisation program Hep B

A
  • children born in the UK are now vaccinated as part of the routine immunisation schedule. This is given at 2, 3 and 4 months of age
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7
Q

How to interpret anti-Hbs levels
When do you test anti-Hbs

A
  • testing for anti-HBs is only recommended for those at risk of occupational exposure (i.e. Healthcare workers) and patients with chronic kidney disease. In these patients anti-HBs levels should be checked 1-4 months after primary immunisation
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8
Q

Management of hepatitis B

A
  • pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of chronic carriers.
  • A better response is predicted by being female, < 50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy
  • whilst NICE still advocate the use of pegylated interferon firstl-line other antiviral medications are increasingly used with an aim to suppress viral replication (not in a dissimilar way to treating HIV patients)
  • examples include tenofovir, entecavir and telbivudine (a synthetic thymidine nucleoside analogue)
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9
Q

Hepatitis C
Incubation period
Features

A

Incubation period 6-9 weeks
After exposure to the hepatitis C virus only around 30% of patients will develop features such as:
* a transient rise in serum aminotransferases / jaundice
* fatigue
* arthralgia

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10
Q

Hepatitis C
Investigations
Prognosis

A

Investigations
HCV RNA is the investigation of choice to diagnose acute infection
whilst patients will eventually develop anti-HCV antibodies it should be remembered that patients who spontaneously clear the virus will continue to have anti-HCV antibodies

Outcome
around 15-45% of patients will clear the virus after an acute infection (depending on their age and underlying health) and hence the majority (55-85%) will develop chronic hepatitis C

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11
Q

What is defined as chronic hepatitis C

What are the complications

A

Chronic hepatitis C may be defined as the persistence of HCV RNA in the blood for 6 months.

Potential complications of chronic hepatitis C
rheumatological problems: arthralgia, arthritis
eye problems: Sjogren’s syndrome
cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer
cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)
porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse
membranoproliferative glomerulonephritis

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12
Q

Hepatitis C - management

A
  • treatment depends on the viral genotype - this should be tested prior to treatment
  • the management of hepatitis C has advanced rapidly in recent years resulting in clearance rates of around 95%. Interferon based treatments are no longer recommended
  • the aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
  • currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
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13
Q

Ribavirin side effects

A

ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic

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14
Q

Interferon alpha side effects

A

interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia

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15
Q

Define hepatitis D co-infection vs superinfection

How to distinguish between the two

A

Hepatitis D terminology:
* Co-infection: Hepatitis B and Hepatitis D infection at the same time.
* Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.

Diagnosis is made via reverse polymerase chain reaction of hepatitis D RNA. Interferon is currently used as treatment, but with a poor evidence base.

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16
Q

What are causes of hepatomegaly

3 C’s and 3 I’s

A

C - cirrhosis (early)
C - cancer (craggy)
C - congestion (portal hypertension 2 to RHF or cirrhosis)

I - infection (HBV HCV / CMV / EBV / malaria)
I - immune - (hepatitis / PSC / PBC)
I - infiltration with amyloid / sarcoid / haem malignancy / haemochromatosis

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17
Q

What should you do if abnormal LFT and what is 1st line imaging / other imaging [4]

A

Liver screen
USS = 1st line to show duct dilatation / mets
MRCP - MRI
ERCP if removing i.e. cholangitis / pancreatitis

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18
Q

What is in a liver screen [8]

A 
Hep B,C,E
EBV, CMV, HIV
Auto-immune / Ab / Ig
Serum copper -  for Wilson disease 
Ferritin and transferrin - Haemochromatosis
A1-anti-trypsin 
Glucose
Lipids
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19
Q

How do you investigate hepatomegaly [6]

A

LFT’s
If abnormal = liver screen
FBC - liver disease cause BM suppression / MCV alcohol
U+E - hepatorenal syndrome / malnourishment
CLotting / albumin
CRP
Imaging

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20
Q

What is 1st line imaging

A

USS to show mets / stone / cirrhosis

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21
Q

What is hepatorenal syndrome

A

HRS is a form of functional renal failure without renal pathology that occurs in 10% of patients with advanced cirrhosis or acute liver failure
Arterial renal circulation disturbanced causing increased vascular resistance causing renal vasoconstriction
Type 1
Type 2
distinguished by chronicity - type 1 is acute occurring within 1-2 weeks while type 2 is a more chronic picture

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22
Q

What are causes of splenomegaly [7]

A

Infection - Lyme’s, meningitis, sepsis, Glandular fever, TB
DIC
Malignancy - lyphhoma / leukaemia / myeloma
Sjogren / SLE / RA / vasculitis/ Sarcoid
Portal hypertension
IE, Rheumatic fever
Amyloid

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23
Q

What are causes of massive splenomegaly [4]

A

Malaria
CML
Myelofibrosis
Leishmaniasis

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24
Q

What is important in history of splenomegaly [7]

A

Fever - infection / TB / malignancy / sarcoid
Lymphadenopathy - glandular / malignancy
Ascites - portal / malignancy
Arthritis / vasculitis/ RA / sjogre / SLE / lyme
Weight loss - malignancy / TB
Purpura - meningitis / DIC /sepsis
Murmur - IE / rheumatic

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25
Q

What can cause abdominal distension 5 F’s

A 
Flatus
Fat
Fluid
Faeces
Fetus
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26
Q

What are differential of ascites? [6]

A 
Malignancy
Infection - TB 
Decreased albumin
CCF
Pancreatitis / cancer
Portal hypertension - cirrhosis / IVC / portal vein thrombosis
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27
Q

How do you investigate differentials for ascites [7]

A 
FBC + film
U+E, LFT, CRP
Ca tumour marker - Ca19-19 (pancreas)
TB
USS
CT, MRI
28
Q

What are RF for jaundice [7]

A

BBV - Blood transfusion, IVDA, Piercing / tattoo, STI, Foreign travel
Alcohol
FH
Drugs

29
Q

What causes mass in RIF [8]

A 
Appendicitis
Caecal cancer
Crohn's disease
Intussception
TB
Kidney malformation / transplant
Undescended testis
30
Q

What can obstructive jaundice be further classified into [2]

A

Calcular

Malignant

31
Q

Calcular causes of obstructive jaundice features [4]

A

F>M
Biliary colic
No weight loss
Fluctuates

32
Q

Malignant causes of obstructive jaundice features [4]

A

M>F
Painless
Weight loss
Progressive

33
Q

Ascitic fluid investigations, biochemistry [7]

A

Tap: MC&S and AFB, cytology, albumin, LDH, glucose, protein

34
Q

Ascitic fluid investigations: SAAG

What does it mean if SAAG >1.1g/dL and what does it mean if <1.1 [4]

A

Serum ascites albumin gradient (SAAG): serum albumin – ascites albumin
o SAAG >1.1g/dL: portal HTN (transudates)
o SAAG <1.1g/dL: other causes (peritoneal or visceral neoplasia, inflammation (pancreatitis), nephrotic syndrome, TB peritonitis) (exudates)

35
Q

Management of ascites [4]

A 
daily weights (aim for <0.5kg/d) & restrict Na intake
fluid restriction (<1.5L/d)
therapeutic paracentesis (with 100mL 20% albumin per L drained to reduce post paracentesis circulatory dysfunction)
TIPSS transjugular intrahepatic portosystemic shunt
36
Q

Spontaneous bacterial peritonitis
Ax [4]
Symptoms [3]
Ix [2]

A

Ax: ascites becomes infected with E. coli, Klebsiella or strep
Sy/Si: ascites, abdo pain, fever
Ix: paracentesis (neutrophil count >250 cells/uL and MC&S tends to show E. coli)

37
Q

Spontaneous bacterial peritonitis
Mx
Cx
Prevention

A

Mx: IV CEFOTAXIME
Cx: hepatorenal syndrome 30%
Pre: prophylactic CIPROFLOXACIN if ascites and protein <15g/L

38
Q

What is PBC

A

Chronic autoimmune granulomatous attack on bile duct INSIDE liver
Leads to cholestasis
Cirrhosis / portal hypertension

39
Q

What causes PBC

A

Autoimmune
Genetic
Environment

M rule

  • Middle age
  • IgM
  • Anti mitochondrial Ab
40
Q

What are the symptoms of PBC

A 
None
Incidental raised ALP
Fatigue
*Tiredness &amp; Pruritus = classic
Jaundice
RUQ pain
Bone and joint pain
Dry eyes and mouth
Hyperpigmentation
HSM
Clubbing
Xanthesomata
41
Q

Who is at risk of PBC

A 
Women
Smoking
Autoimmune
Pregnancy
UTI
Nail polish
FH
42
Q

What is associated with PBC

A

Sjogren
Systemic sclerosis
RA
Thyroid

43
Q

How do you Dx PBC

A

Initial investigations
Blood - raised ALP, GGT
AMA + IGM = Dx
Increased bilirubin, INR, decreased platelet
Increased TSH?

Other imaging
USS to exclude extra-hepatic
Liver biopsy / cholangiogram not usually needed unless AMA negative which it can be in 10%

44
Q

How do you treat PBC

A

UDCA - doesnt cure but halts progression
Fat soluble vitamins
Bone protection like bisphosphonates
Treat dry eyes
Treat pruritus - cholestryalmine, plasma exchange
Liver transplant if severe

45
Q

How do you monitor PBC

A

Regular LFT

USS and AFP 6 monthly

46
Q

What are the complications of PBC

A 
Cirrhosis
Decompensated liver
Vitamin deficiency due to fat malabsorption - ADEK
-Osteomalacia 
-OSteoporosis 
-Coagulopathy 
HCC
47
Q

What is PSC

A

Chronic autoimmune inflammation and scarring of intra and extra hepatic ducts
Cholestasis

48
Q

What causes PSC

A

Unknown

80% = UC

49
Q

Who is at risk of PSC

A

Male
Young adult
pANCA
ANA +ve
AMA -ve
Autoimmue hepatitis
UC > Crohns
HIV

50
Q

What are the symptoms of PSC

A 
Fatigue
CHolestasis = jaundice / pruritus
Abdo pain RUQ
Fever
Ascending cholangitis if advanced
Cirrhosis
Hepatic failure
51
Q

How do you Dx PSC

A

Bloods - LFT / ANCA / IgG
USS - look for other cause e.g. gall stone
MRCP = diagnostic, beaded appearance
ERCP if going to do invasive Rx
Liver biopsyy / cholangiogram not usually needed

52
Q

How do you treat PSC

A 
URODEOXYCHOLIC ACID
Treat itch - rifampicin
Liver transplant = main stay
Endoscopic treatment of bile duct / stent
Ax if infection
53
Q

When do you transplant

A

Chronic and poor QOL
Carcinoma
Genetic
MELD score

54
Q

What do you give before transplant

A

Anti-rejection
Immunosuppresion
Steroid
Ax

55
Q

What are the complications of PSC

A

Cirrhosis
Intrahepatic obstruction
Cholangiocarcinoma

56
Q

What is advised in patients with PSC

A

Annual colonoscopy especially if UC

57
Q

What is cholangiocarcinoma

A

mucin-producing adenocarcinomas arising from the biliary tract with features of cholangiocyte differentiation
grouped by site of origin: intrahepatic, perihilar or peripheral
90% adenocarcinoma
Extrahepatic 80%

58
Q

What are the symptoms of cholangiocarcinoma

A

Obstructive painless jaundice - gradual onset
Weight loss
Pruritus

Signs
Mass in RUQ
LN (peri-umbilical) + Virchow
Ascites
Hypercalcaemia
Hypophosphate

Bloods
Ca-125, CEA, Ca 19-9

59
Q

What tumour markers are elevated

A

Ca-125 - ovarian
Ca19-19 - pancreas
CEA - bowel

60
Q

What are the RF for cholangiocarcinoma

A

Age
Liver fluke
Choledochal cysts
Chronic liver inflammation

61
Q

How do you Dx cholangiocarcinoma

A 
Raised bilirubin and ALP
Coag and INR may be affected
USS = 1st line may show dilatation
EUS
Staging = CT / MRI / MRCP
62
Q

How do you treat cholangiocarcinoma

A

Surgery = only option but only 30% operable

Adjuvant chemo / RT

63
Q

What is palliative Rx for cholangiocarcinoma

A

Surgical bypass
ECRP / PTC to stent
Chemo or RT

64
Q

What are post-op complications

A

Liver failure
Bile leak
Bleeding

65
Q

What is Ddx

A

Stone
Cholecystitis
Benign stricture

66
Q

What is ampulla cancer

A

Cancer of ampulla
Adenocarcinoma
Rx = endoscopic excision or pancreaticoduodectomy

My MRCP (43 decks)

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