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Year 2 > Stones in common bile duct + ascending acute cholangitis > Flashcards

Stones in common bile duct + ascending acute cholangitis Flashcards

1
Q

What is acute cholangitis

A

Infection of the biliary tree + most often occurs secondary to common bile duct obstruction by gallstones

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2
Q

What causes stones in common bile duct

A
  1. Benign biliary structures following biliary surgery
    2 .Cancer of the pancreatic head = bile duct obstruction
  2. In far east + mediterranean biliary parasites can cause blockage and ascending/acute cholengitis
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3
Q

Clinical presentation of acute cholangitis

A
  1. Biliary colic
  2. Fever (rigors), Jaundice (proceeded by abdominal pain), right upper quadrant pain - may not alway see present
  3. CHolestatic jaundice (dark urine, pale stools and skin may itch)
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4
Q

What should show in blood tests for acute cholangitis

A
  1. ELEVATED neutrophil count
  2. Raised ESR and CRP
  3. Raised serum bilirubin - bile duct obstruction if very high
  4. Raised serum alkaline phosphatase
  5. Aminotransferase levels are elevated (ALTs are higher than ASTs normally)
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5
Q

What would show up in a transabdominal ultrasound for cholangitis

A
  1. Initial imaging choice
  2. Dilatation of common bile duct
  3. Mar or may not show cause of obstruction
  4. Distal common bile duct stones are easily missed
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6
Q

What would a Magnetic Resonance Cholangiography show for cholangitis

A
  1. Shows biliary, common bile duct stones and dilated ducts
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7
Q

Why do we use a CT to check for cholangitis

A
  1. Excludes pancreatic carcinomas

2. Easy to spot pigmented stones

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8
Q

How is cholangitis treated

A 
IV antibiotics (CEFOTAXIMME, METRONIDAZOLE)
Urgent biliary drainage using ERCP or spincterectomy
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9
Q

What is sphincterectomy

A

Cutting off biliary sphincter
Remove stones
crushing stones
stent placement

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10
Q

How long do we give patients with cholangitis IV antibiotics for

A

Until symptoms resolved (after biliary drainage)

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11
Q

When is surgery done for cholangitis

A

Large stones

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12
Q

Gallstones in gallbladder vs bile duct

A
  1. Biliary pain in GB and BD
  2. Cholecystitis in GB not BD
  3. Obstructive Jaundice in GB and BD
  4. Cholangitis not in GB but in BD
  5. Pancreatitis not in gallbladder but is in bile duct
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13
Q

Gallstone Compications in gallbladder + cystic duct

A
  1. Biliary colics
  2. Acute cholecystitis
  3. Empyema
  4. Mirizzi’s syndrome
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14
Q

What is Empyema

A

Gallbladder fills with puss

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15
Q

What is hepatitis

A

Inflammation of the liver

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16
Q

What define acute hepatitis

A

Within 6 months onset

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17
Q

What defines chronic hepatitis

A

Hepatitis lasting longer than 6 months

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18
Q

Symptoms of acute hepatitis

A
  1. Malaise
  2. Myalgia (muscle pain)
  3. GI upset
  4. Abdominal pain - right upper quadrant
  5. With/without cholestatic jaundice
  6. Tender hepatomegaly

Raised bilirubin

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19
Q

What causes acute hepatitis

A
  1. Viral: Hep A + E
    Herpesvirus
  2. Non-viral (Leptospirosis, toxoplasmosis, coxiella)
  3. Alcohol
  4. Drugs
  5. Toxins
  6. Pregnancy
  7. Autoimmune
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20
Q

Is chronic hepatitis symptomatic

A

can be

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21
Q

Signs of chronic liver disease

A
  1. Clubbing
  2. Palmar erythema
  3. Dupuytren’s contracture
  4. Spider naevi
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22
Q

What is Dupuytren’s contracture

A

One or more fingers bending into palm of the hand

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23
Q

Level of LFTs in the blood in chronic liver disease

A

AST and ALT normal

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24
Q

Can liver function be maintained during cirrhosis

A

Yes

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25
Q

What happens if fibrosis is too severe

A 
Jaundice
Ascites
Low albumin
Coagulopathy
Encephalopathy
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26
Q

Complications of Chornic hepatitis

A

Hepatocellular carcinoma

Portal hypertension (varices + bleeding)

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27
Q

Causes of chronic hepatitis

A

Infection:
1. Hepatitis B/C

Non-Infective:

  1. Alcohol
  2. Drugs
  3. Autoimmune
  4. Hereditary metabolic
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28
Q

Where is Hep A most common

A

Africa and South A

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29
Q

What time of the year does Hep A commonly occur

A

Autumn and affects children + young adults

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30
Q

How does Hep A occur

A

Ingestion of contaminated food or water (shellfish)

Overcrowding or poor sanitation facilitate spread

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31
Q

How does Hep A spread

A

Faeco-Oral route

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32
Q

What virus causes Hep A

A

Picornavirus

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33
Q

Where does Picornavirus replicated

A

Liver

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34
Q

Where is Picornavirus excreted

A

Bile -> faeces about 2 weeks before onset of clinical ullness

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35
Q

When is Hep A maxmillay infectious

A

JUST BEFORE jaundice

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36
Q

Incubation period of Hep A

A

2-6 weeks

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37
Q

What does Hep A cause

A

Acute Hepatitis

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38
Q

How long is Hep A self-limiting for

A

3-6 weeks

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39
Q

Does acute hepatitis commonly cause fulminant hepatitis

A

No - RARE

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40
Q

What is fulminant hepatitis

A

Hepatitis that causes wick liver failure

100% immunity after infection n

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41
Q

Clinical presentation of Hep A

A
  1. Viraemia causes patients to feel unwell, nausea, fever, malaise
  2. Jaundice
  3. Hepatosplenomegaly
  4. Jaundice sessions after 6 weeks
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42
Q

How long does it take for patients to go jaundiced after have Hep A

A

1-2 weeks - symptoms often improve

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43
Q

Is Hep A jaundice common in children

A

No

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44
Q

How does jaundice effect symptoms seen in Hep A

A

Urine become darks

Stool becomes pale

Due to INTRAHEPATIC CHOLESTASIS

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45
Q

Differential diagnosis of Hep A

A
  1. Jaundice

2. Drug-induced hepatitis

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46
Q

How do we diagnose Hep A in the prodromal stage (Between initial symptoms + jaundice)

A
  1. Serum bilirubin normal
  2. Bilirubinuria + raised urinary urobilinogen
  3. Raised serum AST or ALT
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47
Q

How do we diagnose Hep A in the Icteric stage (once jaundice has presented)

A

Serum bilirubin levels

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48
Q

Blood test result in Hep A

A

Lecupenia (reduced WBC)

Raised ESR

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49
Q

Viral markers seen in hep A

A

HAV antibodies

Anti-HAV IgM

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50
Q

Prognosis of Hep A

A

Good

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51
Q

How is Hep A Treated

A

Avoid alcohol

Monitor liver function to spot fulminant hepatic failure

Manage close contacts by giving normal immunoglobulins for hep A

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52
Q

How is Hep A prevented

A
  1. . Good hygiene
  2. Resistant to chlorination but not boring water
  3. Active immunisation
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53
Q

What virus is Hep E

54
Q

What hepatitis does HEV cause

A

ACUTE only

55
Q

Where is Hep E common

56
Q

What people does Hep E effect

57
Q

When is mortality from Hep E high

58
Q

How does Hep E spread

A

Falco-Oral route of transmission

59
Q

What can acute hepatitis caused by Hep E resulting

A

Fulminant hepatitis

60
Q

Serology of Hep E

A

Similar to Hep A

61
Q

How is Hep E treated

A

Vaccines

HEV RNA to detect chronic infection

62
Q

How is Hep E prevented

A

Good sanitation

63
Q

How is Hep B caused

A
  1. Tattoos
  2. needles
  3. Sexual
  4. Blood products
  5. IV drug abusers
  6. Vertical transmission (mother to child
64
Q

Where is horizontal transmission common

A

Children through minor abrasions or close contact with other children

HBV can survive on household articles for prolonged time

65
Q

Where is HBV common

A

Far east, africa and mediterranean

66
Q

In what bodily fluids is HBV common in

A

Semen and Saliva

67
Q

What can HBV result in

A

Chronic Hepatitis

68
Q

Risk factors for HBV

A
  1. Healthcare personnel
  2. Emergency and rescue teams
  3. CKD/Dialysis patients
  4. Travellers
  5. Homosexual men
  6. IV drug users
69
Q

What virus is HBV

70
Q

How does HBV cause disease

A

HBsAg is produced in excess by infected hepatocytes

After penetrating into hepatocyte, virus loses its coat and core is transported to the nucleus without processing

71
Q

What percentage of patients will develop chronic Hep B

A

1-10% - can’t clear whole viral population

72
Q

Consequence of chronic Hep B

A

Cirrhosis and decompensated cirrhosis -> liver failure -> HEPATIC CARCINOMA

73
Q

Clinical Presentation of Hep B

A
  1. Viraemia causes patients to feel unwell, nausea, fever, malaise, anorexia and arthralgia
74
Q

What is arthralgia

A

Joint Pain

75
Q

Incubation period for Hep B

A

1-6 months

76
Q

When do patients become jaundiced in Hep B

A

1-2 weeks after

Jaundice depends when urine becomes dark and stool becomes pale due to intrahepatic cholestasis

77
Q

What follows jaundice in Hep B

A

Hepatosplenomegaly

78
Q

What is HBsAg

A

Hep B surface antigens

79
Q

In Chronic HBC, what can happen

A

Cirrhosis
Liver Failure
Hepatocellular Carcinoma

80
Q

How is Hep B diagnosed

A

HBsAG present 1-6 months after exposure

Anti-HBs

81
Q

What does HBsAg presence for more than 6 months imply

A

Carrier status

82
Q

How is ACUTE Hep B treated

A
  1. Supportive
  2. Avoid Alcohol
  3. Monitor Liver Function
  4. Manage close contacts by giving human normal immunoglobulin for Hep B and vaccination
  5. Monitor HBsAg at 6 months to ensure full clearance and no progression
83
Q

Primary prevention of Hep B

A

Vaccination

84
Q

treatment for chronic Hep B

A
  1. SC PEGYLATED INF-alpha 2a

2. Nucleotide analogues

85
Q

how is SC PEGYLATED INF-alpha 2a given

A

Weekly subcutaneous injection

86
Q

Side-effects of SC PEGYLATED INF-alpha 2a

A 
Flu-like illness
Fever
Lethargy 
Autoimmune disease
reduction in WBC and platelets
Anxiety
Mental Issues
87
Q

How do nucleotide analogues function

A
  1. Inhibit viral replication
  2. One tablet a day
  3. High barrier to resistance
  4. Minimal side-effects
88
Q

How often do we give nucleotide analogues for

A

Life-long (no immune response stimulated)

89
Q

Name a nucleotide analogue

A

ORAL TENOFOVIR and ENTECAVIR

90
Q

What extra thing do you need to do with ORAL TENOFOVIR

A

Renal monitoring

91
Q

What virus causes Hep D

A

INCOMPLETE RNA VIRUS

92
Q

Onset of Hep D

A

Chronic hepatitis

93
Q

What other virus does Hep D require for assembly

94
Q

Where is HDV common

A

Eastern Europe

95
Q

How does HDV spread

A

Blood-borne transmission

96
Q

Risk factors for HDV

A

IV drug users

97
Q

What is the Hep D virus structurally

A

Incomplete RNA enclosed in a shell of Hep B surface antigen

98
Q

How does Hep D co-infection occur

99
Q

What condition can co-infection of HBV and HBD be mistaken for

A

Acute icteric (jaundice) HBV infection

100
Q

What confirms co-infection

A

Serum IgM anti-HDV with IgM anti-HBV

101
Q

How does superinfection by HDV occur

A
  1. Chornic HBV (usually dormant) gets HBD
102
Q

Consequence of Superinfection

A

Secondary acute hepatitis and increased rate of liver fibrosis progression

103
Q

What risk is significantly increased by superinfection by HDV

A

Increased risk of fulminant hepatitis

104
Q

Diagnosis of superinfection

A

Rise serum AST or ALT

105
Q

How severe can superinfection become

A

Chronic hepatitis -> hepatocellular carcinoma

106
Q

Clinical presentation of HDV

A

Same as Hep B

107
Q

Diagnosis of HDV

A

Same as Hep B

108
Q

Treatment of HDV

A

SC PEGYLATED INF alpha-2a

109
Q

Where is HCV common

110
Q

How is HCV transmitted

A

Blood products

111
Q

What people are most at risk of HCV

A

Haemophilia
IV drug users
STD

112
Q

Is vertical transmission of HCV common

113
Q

What virus is HCV

A

RNA flavivirus

114
Q

How many genotypes does RNA flavivirus have

115
Q

Most common HCV genotypes that infect people

116
Q

Why is it hard to make a vaccine for HCV

A

Rapid mutations change envelope proteins

117
Q

What can HCV result in

A

Chronic hepatitis -> HEPATOCELLULAR CARCINOMA

118
Q

Symptoms of HCV

A

Most asymptomatic
10% have flu
Jaundice
Rise in serum aminotransferases (ALT and AST)

119
Q

Diagnosis of HCV

A

HCV antibody present in 4-6 weeks

HCV RNA - indicates current + diagnosis acute infection

120
Q

When would HCV antibody screening be negative

A

Immunosuppressed and acute infection (before 4 weeks)

121
Q

How is acute HCv treated

A

If VIRAL LOAD DOES NOT FALL:

SC PEGYLATED INF-alpha 2a/b + ORAL RIBAVIRIN

122
Q

When is HCV treatment not needed

A

When viral load is falling

123
Q

Side-effect of PEGYLATED INF-alpha 2a/b

A

Mental health side-effects

124
Q

Side-effect of oral Ribavirin

A

Haemolytic anaemia + anxiety

125
Q

Why are DAAs (direct acting antivirals) better than INF PEGYLATED

A

Because they don’t cause mental health effects

126
Q

How is DAA given

A

ORALLY + triple therapy

127
Q

Describe triple therapy of DAA

A
  1. NS5A inhibitor end in ASVIR (ritonasvir)
  2. NS5B inhibitors (end in BUVIR)
  3. ORAL RIBAVIRIN
128
Q

Role of NS5A

A

Initiates viral replication

129
Q

Role of NS5B

A

Needed or viral replication

130
Q

Cons of DAA

131
Q

How is Hep C prevented

A

Precaution (no immunity so can get re-infected and no vaccine)

Year 2 (155 decks)

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