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Semester 2 (3rd year) > Case 15: Jaundice (My liver tests are abnormal) > Flashcards

Case 15: Jaundice (My liver tests are abnormal) Flashcards

1
Q

which types of hepatitis are transmitted via faecal oral route

A

A and E

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2
Q

which types of hepatitis are transmitted via blood and bodily fluids route

A

B, C,D

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3
Q

what types of hepatitis are acute

A

A

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4
Q

what types of hepatitis are acute and chronic

A

B,C,D

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5
Q

what types of hepatitis are chronic

A

E

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6
Q

what is hepatitis D associated with

A

only people with hepatitis B can be infected with hepatitis D

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7
Q

what is hepatitis E associated with

A

it is rare and associated with immunosuppression

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8
Q

what are the 4 essential functions of the liver

A

produces clothing factors for clotting cascade

stores excess glucose as glycogen

stores/detoxifies harmful endogenous and exogenous substances (cellular debris, bacteria, drugs)

metabolism of carbohydrates, fats and proteins

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9
Q

3 most common causes of liver cirrhosis in the western world

A

non-alcoholic fatty liver disease

alcohol-related liver disease

chronic viral hepatitis

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10
Q

hepatitis B serology interpretation

A

Hepatitis B core antibody IgM (anti-HBc IgM) - appears within weeks of acute infection and remains detectable for 4-8 months

Hepatitis B core antibody IgG (anti-HBc IgG) - detectable in virtually all patients exposed to hepatitis B. Can be positive in both acute and chronic infection

Hepatitis B surface antigen (HBsAg) - first serological marker to become positive in a new, acute Hepatitis B infection. Detected on average 4 weeks after exposure to the virus. Usually becomes undetectable after 4-6 months. Detection after 6 months implies chronic hepatitis B infection

Hepatitis B surface antibody (HBsAb or Anti-HBs) - detected in the blood after person is able to clear Hepatitis B surface antigen. The presence of Hepatitis B surface antibody following acute infection suggests complete resolution of infection. It is also detectable in those immunised against hepatitis B

Hepatitis B e-antigen (HBeAg) - present in new acute infection and associated with high Hepatitis B virus DNA levels (HBV DNA)

Hepatitis B DNA - patients with high Hepatitis B DNA levels are more infectious

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11
Q

questions to ask about an overdose

A

number of tablets taken and the dose

was it taken once or staggered over time

timing- delay presentation may indicate a greater degree of liver toxicity

any other medication/drugs taken alongside

any medical conditions (including history of alcohol abuse)

what regular medications do they take (over counter, prescribed and herbal)- these may increase hepatotoxicity

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12
Q

what features may make you think a person is at serous risk of self harm

A

background of mental health problems

was the overdose planned- suicide note, changes to will, measures in place to prevent rescue

triggers- physical health problems, unemployment, bereavement, changes in relationship, social isolation, domestic violence

young/middle-aged men are at higher risk

how did they present to social services- was it them/someone else found them

how do they feel now- do they regret it/wish it was successful

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13
Q

what features on examination may indicate hepatotoxicity

A

confusion due to hepatic encephalopathy

liver asterixis (flapping tremor)

jaundice- skin/sclera

bruising of skin/bleeding gums/bleeding from anywhere- due to clotting derangement

tenderness in RUQ- liver inflammation

hepatomegaly

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14
Q

which herbal medication can increase risk of liver toxicity

A

St. Johns wart

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15
Q

what is a drug which can cause liver fibrosis

A

methotrexate

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16
Q

what are ALT and AST

A

they are enzymes found in hepatocytes which leak out and are found in large amounts when there is significant hepatic parenchymal damage

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17
Q

aside from liver injury, what may also increase ALT and AST levels

A

MI (they are found in the heart too)
rnhabdomylosis (they are found in skeletal muscle too)
haemolysis (they are found in RBCs too)

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18
Q

where is ALP found

A

liver, bone and placenta

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19
Q

what can increased ALP indicate

A

biliary obstruction

boney disease (Padgets)

fractures

metastatic disease

osteoperosis and myeloma typically don’t raise ALP unless associated with fractures

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20
Q

how to distinguish whether raise in ALP is due to liver or boney disease

A

look at GGT as well (it is raised in liver disease but not in boney)

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21
Q

what stages in life causes ALP to rise

A

during periods of growth (adolescence and pregnancy)

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22
Q

where is GGT found

A

liver
renal tubules
pancreas
intestine

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23
Q

aside from liver disease what can cause a raise in GGT

A

enzyme induction- for example prolonged exposure to hazardous alcohol and to some drugs (rifampicin, phenobarbitone, griseofulvin)

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24
Q

what is albumin and where is it made

A

is the predominant blood protein and is largely made by the liver

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25
Q

why might albumin levels be low

A

poor underlying liver systemic function

any illness can cause decreased albumin

extreme malnutrition

nephrotic syndrome (losing protein from kidneys)

protein losing enteropathy (losing protein from the intestines)

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26
Q

what is bilirubin

A

a waste product produced by the catabolism of haemoglobin

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27
Q

the liver and bilirubin

A

the liver is involved in the breakdown of Hb and conjugating bilirubin to make it water soluble for the its excretion in bile

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28
Q

what may cause raised bilirubin

A

pre-hepatic jaundice (increased red cell breakdown)

hepatic jaundice (reduced liver function)

post-hepatic jaundice biliary obstruction

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29
Q

what is Gilberts syndrome

A

there is low levels of conjugating enzymes which causes raised levels of unconjugated bilirubin in the presence of otherwise normal LFTs

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30
Q

what % of the population have Gilberts syndrome

A

5%

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31
Q

what markers are used to monitor chronic liver disease

A

serial measurement of albumin and bilirubin over long periods of time

those with chronic liver disease (cirrhosis) may have completely normal or only slightly raised LFTs

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32
Q

what is the most common cause of hepatic failure in the UK

A

paracetamol overdose

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33
Q

initial non-specific symptoms of paracetamol overdose

A

nausea/vomiting
abdominal pain

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34
Q

signs and symptoms of paracetamol overdose to be concerned about

A

acute confusion (encephalopathy)
reduced urine output
hypoglycaemia
reduced GCS

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35
Q

what treatment is given in paracetamol overdose

A

N-acetylcysteine (works as a glutathione donor, preventing the toxic build-up of NAQPI)

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36
Q

when should you commence acetylcysteine treatment

A

those with a high plasma-paracetamol concentration (on graph)

those presenting within 8-24hrs after ingesting more than 150mg/kg of paracetamol regardless of plasma-paracetamol concentration

those who present after 24hrs in they are- jaundiced, hepatic tenderness, elevated ALT above their normal, INR greater than 1.3 or paracetamol concentration is detectable

possibly give if they present within 24hrs with normal plasma-paracetamol, but have acute liver injury on biochemical testing

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37
Q

what dosage of paracetamol indicates high toxicity risk

A

above 150mg/kg in 24hr period

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38
Q

when should you be admitted to hospital for paracetamol overdose

A

if symptomatic

ingested more than licensed dose and more than or equal to 75mg/kg in any 24hr period

ingested more than the licensed dose but less than 75mg/kg per 24hrs on each of the preceding 2 or more days

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39
Q

what is a staggered overdose

A

ingestion of potentially toxic dose of paracetamol over more than one hour with the possible potential of wanting to cause self harm

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40
Q

management of staggered overdose

A

hospital admission
treated with acetlycystiene without delay

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41
Q

if you are unsure about a patients risk of liver toxicity following paracetamol overdose, where should you get advice

A

national poisons information service

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42
Q

what are the indications for liver transplant following paracetamol induced acute liver failure

A

arterial pH less than 7.3 or arterial lactate over 3 after adequate fluid resuscitation or if the 3 below happen within a 24hr period

creatinine over 300micromol/L
PT over 100 seconds (INR over 6.5)
grade III/IV encephalopathy

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43
Q

what is the most common reason for liver transplant and acute liver injury in UK

A

paracetamol overdose

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44
Q

when does toxicity peak after paracetamol overdose ingestion

A

48-72hrs after ingestion

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45
Q

liver toxicity is increased in people with what physiology

A

toxicity is from paracetamol metabolites therefore it is increased in people who have more highly induced cytochrome P450 physiology

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46
Q

what can be seen on ABGs in acute liver failure

A

acidosis

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47
Q

what is the best early indication of severity of liver failure

A

prothrombin

48
Q

what type of glucose concentration can be seen in hepatic necrosis

A

hypoglycaemia

49
Q

when should paracetamol levels be taken

A

4 hrs post ingestion

ASAP if staggered

ASAP if dose was more than 4 hrs ago

50
Q

definition of acute liver failure

A

liver failure with the presence of hepatic encephalopathy in a patient without pre-existing liver disease

51
Q

management of acute liver injury with coagulopathy

A

catheterisation and hourly monitoring of urine output

hourly capillary blood glucose recordings

10mg of vitamin K IV

repeat coagulation panel in 6 hrs

52
Q

what clinical signs would you look for as an indication the patient is developing liver failure

A

spontaneous bruising/bleeding at venipuncture sights (coagulopathy sign)

reduced urine output (AKI)

hypoglycaemia (hepatic necrosis)

metabolic acidosis despite hydration

hypotension despite hydration

encephalopathy (agitation, confusion and aggression rather than drowsiness seen in chronic liver disease)

53
Q

other causes of acute liver failure

A

severe acute viral hepatitis (especially E in pregnancy but also A and B)

acute vascular injury to liver (Budd Chiari syndrome)

autoimmune hepatitis

direct exposure to toxins (amanita mushroom poisoning)

54
Q

mental health management of overdose patients upon discharge

A

mental health liaison service for review

follow-up by mental health home treatment team in the community

GP follow-up on discharge

55
Q

what may cause raised ALT (with otherwise normal LFTs)

A

indicates liver inflammation (hepatitis), this could be due to:
fatty liver related to alcohol
viral infection
non-alcoholic related fatty liver disease
autoimmune disease

rarer-
alpha1 antitrypsin deficiency
Wilsons (presents at younger age)

56
Q

what blood transfusions may increase your hepatitis risk

A

those before 1991

57
Q

what may a mild raised MCV suggest

A

liver cirrhosis

58
Q

what may a largely raised MCV suggest (over 110fl)

A

hazardous alcohol consumption

59
Q

what antibodies to look for in autoimmune liver disease

A

antinuclear
anti smooth muscle
antimitochondrial

60
Q

what timeframe is considered chronic hepatitis

A

over 6 months

61
Q

what is cirrhosis

A

prolonged fibrosis and scarring of the liver
there must be nodules for it to be cirrhosis

62
Q

what other viruses can cause hepatitis

A

herpes (EBV epstein barr, HSV, CMV)
adenoviruses
coronaviruses

63
Q

what can the 3 results of acute hepatitis be

A
  1. recovery
  2. chronic hepatitis (over 6 months)- there is inflammation, increasing fibrosis and then cirrhosis
  3. fulminant hepatitis- requires transplant and can cause death
64
Q

acute hepatitis symptoms

A

generally unwell

jaundice

RUQ ache

stool/urine discolouration

if severe- confusion/drowsiness, hypoglycaemia, coagulopathy

65
Q

blood results in acute hepatitis

A

raised ALT/AST- over 1000
raised bilirubin

if severe- acidosis, increased lactate, coagulopathy, renal impairment

66
Q

chronic hepatitis symptoms

A

often none
fatigue
typically presents with cirrhosis

67
Q

bloods with chronic hepatitis

A

abnormal LFTs (mild elevation in ALT)

68
Q

what is fulminant hepatitis

A

acute hepatitis with liver failure
there is encephalopathy within 28 days of jaundice (in those without pre-existing liver disease)

69
Q

abnormal results in fulminant hepatitis

A

acidosis
coagulopathy
hypoglycaemia

70
Q

what can cirrhosis cause

A

loss of function:
jaundice
coagulopathy
decreased drug metabolism
decreased hormone metabolism
increased sepsis

portal hypertension:
varices
piles
ascites
encephalopathy
renal failure

71
Q

what is the transmission of hep A associated with

A

poor sanitation
food preparation
travel
is an endemic for children in low income countries

72
Q

is there a vaccine for hep A

A

yes (active and passive)
those with cirrhosis should be vaccinated

73
Q

99% if people with hep A what

A

recover (it is acute)

74
Q

clinical presentation of hep A

A

jaundice within 2 weeks

75
Q

when are you infectious with hep A

A

week 1-5

76
Q

in hep A and E what do IgM and IgG mean

A

IgM= acute infection

IgG= immune

77
Q

treatment of hep A

A

supportive as they will get better on their own after a few weeks

78
Q

what is hep E transmission associated with

A

poor sanitation
food preparation (pork)
travel
childhood endemic in south asia and north africa

79
Q

is there a vaccine for hep E

A

no

80
Q

hepatitis E can develop into chronic in which group of people

A

immunosupressed

81
Q

hepatitis E can develop into fulminant in which group of people

A

in pregnant women in 2nd/3rd trimester

82
Q

treatment of hep E

A

supportive

if chronic- reduce immunosuppression, ribavirin

83
Q

what group of people mainly get hepatitis C in UK

A

intravenous drug users

84
Q

what group of people mainly get hepatitis C in the rest of the world

A

medially due to poorly sanitised equipment

85
Q

is there a vaccine for hep C

A

no

86
Q

is sexual transmission common for hep C

A

no it is rare (more common in men who have sex with men however)

87
Q

do the majority with hep C have an acute or chronic infection

A

80% go on to develop chronic

88
Q

does hepatitis C cause symptoms

A

rarely

89
Q

who is screened for hep C

A

donors
IVDUs
those with abnormal LFTs

90
Q

testing for hep C

A

antibodies
PCR (genotype and viral load)

91
Q

treatment of hep C

A

direct acting antivirals (DAAs)

92
Q

how are DAAs used for hep C

A

used for 8-12 wks

93
Q

advantages of DAAs

A

side effect free
over 95% cure rate

94
Q

disadvantages of DAAs

A

they are expensive however
reinfection may occur

95
Q

which is the only hepatitis virus which is DNA

A

hep B

96
Q

most common transmission of hep B worldwide

A

vertical (from mother to child)

97
Q

after tobacco what is the worlds second biggest carcinogen

A

hep B (meaning it causes cancer)

98
Q

is there a vaccine for hep B

A

yes using surface ag

99
Q

are the majority of hep B infections chronic or acute

A

in adults, majority acute
in babies, majority chronic

100
Q

what is used to determine the progression of fibrosis in the liver

A

elastography

101
Q

when are people with hep B infectious

A

at 12-28 wks

102
Q

treatment of hep B

A

acute:
usually not necessary
nucleoside analogues if severe

chronic:
nucleoside analogues
interferon

103
Q

what does hepatitis delta need from hep B

A

needs its surface ag

104
Q

what does hep delta do to hep B prognosis

A

it worsens it

105
Q

treatment for hep delta

A

interferon (1-2 years and may have limited effectiveness)

106
Q

what % of population have non-alcoholic fatty liver disease

A

20%

107
Q

what % of those with diabetes have non-alcoholic fatty liver disease

A

70%

108
Q

stages of non-alcoholic fatty liver disease

A

first is hepatitis steatosis (fat content over 5% of liver volume)

progresses to non-alcoholic fatty liver disease when inflammation begins

109
Q

patients with non-alcoholic fatty liver disease are at a higher risk of what

A

progression to fibrosis, cirrhosis and hepatocellular carcinoma

110
Q

lifestyle advice for non-alcoholic fatty liver disease

A

weight loss
reduce alcohol intake

111
Q

Wilsons disease and liver

A

hepatic involvement typically presents with chronic hepatitis, cirrhosis or acute liver failure

112
Q

other symptoms of Wilsons

A

tremor
behavioural problems
depression

113
Q

what indicates Wilsons

A

low serum caeruboplasmin

114
Q

treatment of Wilsons

A

copper chelation agents

115
Q

lifestyle advice for hep C

A

vertical and sexual risk (don’t need to encourage condom use but possibly with men who have sex with men) is low but partners and children can be screened is they wish-

avoid blood borne contact (toothbrushes and razors)

reduce alcohol intake to reduce risk of fibrosis

doesn’t need to disclose the infection to anyone

116
Q

screening those with hep C

A

ultrasound screening for detection of hepatoma
offer endoscopic screening for varices

117
Q

complications of hep C

A

liver cirrhosis
skin complications (prophyria cutanea tarda)
sjogrens syndrome
hepatocellular carcinoma

Semester 2 (3rd year) (12 decks)

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