Gastroenterology Flashcards

Interpreting Hep B serology, Autoimmune hepatitis (66 cards)

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
What can cause abdominal distension 5 F's
``` Flatus Fat Fluid Faeces Fetus ```
26
What are differential of ascites? [6]
``` Malignancy Infection - TB Decreased albumin CCF Pancreatitis / cancer Portal hypertension - cirrhosis / IVC / portal vein thrombosis ```
27
How do you investigate differentials for ascites [7]
``` FBC + film U+E, LFT, CRP Ca tumour marker - Ca19-19 (pancreas) TB USS CT, MRI ```
28
What are RF for jaundice [7]
BBV - Blood transfusion, IVDA, Piercing / tattoo, STI, Foreign travel Alcohol FH Drugs
29
What causes mass in RIF [8]
``` Appendicitis Caecal cancer Crohn's disease Intussception TB Kidney malformation / transplant Undescended testis ```
30
What can obstructive jaundice be further classified into [2]
Calcular | Malignant
31
Calcular causes of obstructive jaundice features [4]
F>M Biliary colic No weight loss Fluctuates
32
Malignant causes of obstructive jaundice features [4]
M>F Painless Weight loss Progressive
33
Ascitic fluid investigations, biochemistry [7]
Tap: MC&S and AFB, cytology, albumin, LDH, glucose, protein
34
Ascitic fluid investigations: SAAG | What does it mean if SAAG >1.1g/dL and what does it mean if <1.1 [4]
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
Management of ascites [4]
``` 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
Spontaneous bacterial peritonitis Ax [4] Symptoms [3] Ix [2]
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
Spontaneous bacterial peritonitis Mx Cx Prevention
Mx: IV CEFOTAXIME Cx: hepatorenal syndrome 30% Pre: prophylactic CIPROFLOXACIN if ascites and protein <15g/L
38
What is PBC
Chronic autoimmune granulomatous attack on bile duct INSIDE liver Leads to cholestasis Cirrhosis / portal hypertension
39
What causes PBC
Autoimmune Genetic Environment M rule - Middle age - IgM - Anti mitochondrial Ab
40
What are the symptoms of PBC
``` None Incidental raised ALP Fatigue *Tiredness & Pruritus = classic Jaundice RUQ pain Bone and joint pain Dry eyes and mouth Hyperpigmentation HSM Clubbing Xanthesomata ```
41
Who is at risk of PBC
``` Women Smoking Autoimmune Pregnancy UTI Nail polish FH ```
42
What is associated with PBC
Sjogren Systemic sclerosis RA Thyroid
43
How do you Dx PBC
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
How do you treat PBC
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
How do you monitor PBC
Regular LFT | USS and AFP 6 monthly
46
What are the complications of PBC
``` Cirrhosis Decompensated liver Vitamin deficiency due to fat malabsorption - ADEK -Osteomalacia -OSteoporosis -Coagulopathy HCC ```
47
What is PSC
Chronic autoimmune inflammation and scarring of intra and extra hepatic ducts Cholestasis
48
What causes PSC
Unknown | 80% = UC
49
Who is at risk of PSC
Male Young adult pANCA ANA +ve AMA -ve Autoimmue hepatitis UC > Crohns HIV
50
What are the symptoms of PSC
``` Fatigue CHolestasis = jaundice / pruritus Abdo pain RUQ Fever Ascending cholangitis if advanced Cirrhosis Hepatic failure ```
51
How do you Dx PSC
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
How do you treat PSC
``` URODEOXYCHOLIC ACID Treat itch - rifampicin Liver transplant = main stay Endoscopic treatment of bile duct / stent Ax if infection ```
53
When do you transplant
Chronic and poor QOL Carcinoma Genetic MELD score
54
What do you give before transplant
Anti-rejection Immunosuppresion Steroid Ax
55
What are the complications of PSC
Cirrhosis Intrahepatic obstruction Cholangiocarcinoma
56
What is advised in patients with PSC
Annual colonoscopy especially if UC
57
What is cholangiocarcinoma
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
What are the symptoms of cholangiocarcinoma
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
What tumour markers are elevated
Ca-125 - ovarian Ca19-19 - pancreas CEA - bowel
60
What are the RF for cholangiocarcinoma
Age Liver fluke Choledochal cysts Chronic liver inflammation
61
How do you Dx cholangiocarcinoma
``` Raised bilirubin and ALP Coag and INR may be affected USS = 1st line may show dilatation EUS Staging = CT / MRI / MRCP ```
62
How do you treat cholangiocarcinoma
Surgery = only option but only 30% operable | Adjuvant chemo / RT
63
What is palliative Rx for cholangiocarcinoma
Surgical bypass ECRP / PTC to stent Chemo or RT
64
What are post-op complications
Liver failure Bile leak Bleeding
65
What is Ddx
Stone Cholecystitis Benign stricture
66
What is ampulla cancer
Cancer of ampulla Adenocarcinoma Rx = endoscopic excision or pancreaticoduodectomy