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Placement > LFTs > Flashcards

LFTs Flashcards

1
Q

Raised ALT meaning

A

hepatocellular injury

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2
Q

Raised AST

A

Hepatocellular injury

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3
Q

raised ALP

A

Cholestatic (vit D deficiency, bone fracturew, bony mets/tumours if raised on own)

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4
Q

raised GGT

A

cholestasis (raised with ALP)

Alcoholic

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5
Q

Raised bilirubin alone

A

Gilberts or haemolysis

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6
Q

decreased albumin

A

can indicate hepatocellular injury

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7
Q

increased prothrombin time

A

hepatocellular injury (clotting factors are not being produced)

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8
Q

ALT>AST

A

chronic liver disease

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9
Q

AST>ALT

A

acute liver disease (e.g. cirrhosis or alcoholic hepatitis)

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10
Q

how do hepatocellular pathologies usually effect stool and urine

A

will cause intrahepatic jaundice so will have dark urine but normal stool

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11
Q

Cause of alcoholic liver disease

A

excessive alcohol consumption over a long time

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12
Q

3 stages of liver damage caused by alcoholic liver disease

A

steatosis (fatty)
alcoholic hepatitis (steatohepatitis)
Alcoholic liver cirrhosis All these can lead to hepatocellular carcinoma

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13
Q

Features of alcoholic liver disease

A

Abdo pain, typically RUQ
Hepatomegaly
Ascites maybe

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14
Q 
What is this:
raised ALT and AST 
AST>ALT
hyperbilirubinaemia 
GGT raised
A

Alcoholic liver disease

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15
Q

investigations for alcoholic liver disease

A

LFTs, FBC, PT - indicate if advanced liver cirrhosis or liver failure is present
US

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16
Q

Management

A

lifestyle advice - stop drinking and loose weight if obese, stop smoking
Manage alcohol withdrawal symptoms - normally give benzodiazepines (diazepam or chlordiazepoxide)
If severe a liver transplant may be required

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17
Q

Causes of non-alcoholic fatty liver disease

A

not fully understood, possibility that if person is resistant to insulin they may develop hepatic steatosis (fatty liver)

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18
Q

risk factors for NAFLD

A

obese, diabetes, hypertension, medication (tamoxifen (most common, oestrogen blocking breast cancer drug) corticosteroids, antidepressants, antipsychotics.

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19
Q

features of NAFLD

A 
no signs of alcohol abuse 
fatigue
malaise
hepatosplenomegaly 
abdominal obesity 
RUQ discomfort
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20
Q 
What is this: 
ELevated ALT and AST 
ALP mildly elevated 
Bilirubin elevated
ALT>AST
A

NAFLD

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21
Q

Investigations for NAFLD

A

LFTs
FBC (may see anaemia or thrombocytopenia - low platelets)
PT - normally raised
serum albumin - normally reduced

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22
Q

Management of NAFLD

A

if end stage liver disease not present: lifestyle modification (weight loss, good diet, increased exercise)
Vitamin E (thought to improve liver function)
Gastric bypass
metformin aor thiazolidinediones may be given as they are insulin sensitizers
end stage liver disease present - liver transplant

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23
Q

Causes of hepatits A

A

transmitted via contaminated water or food, or being in close proximity with an infected individual
can be spread through sharing needles or having sex

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24
Q

features of Hep A

A 
Sudden onset fever
malaise 
N&V 
Jaundice 
Hepatomegaly 
RUQ pain 
pale stool and dark urine fatigue 
joint pain 
diarrhoea 
(can last up to 6 months)
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25
Q

What is this?
ALT and AST significantly raised
elevated bilirubin levels
elevated ALP (but not as much as AST and ALT)

A

Hep A
NOTE: similar AST and ALT
cant really have chronic hep A so ALT and AST always significantly raised as an acute infection

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26
Q

Investigations for Hep A

A

LFTs (AST and ALT)
serum creatinine
PT time
IgM anti-HAV (accepted marker for accute hep A infection)

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27
Q

management for hep A

A

ABCDE

supportive management from home

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28
Q

Causes of Hep B

A

spread through bodily fluids (high risk sexual activity or sharing needles)
passed from mother to child

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29
Q

features of hep B

A

Most people are asymptomatic (70%)

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30
Q 
What is this?
Raised AST and ALT 
raised (could be >10x or <10x) bilirubin 
slightly raised ALP
low albumin
A

hep B

NOTE: if acute then over x10 raised, chronic then <10

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31
Q

Investigations for hep B

A 
LFTs
FBC - may have microcytic anaemia
U&Es - may have hyponatraemia 
Serum hepatitis B surface antigen 
serum antibody to hepatitis B surface antigen  
Serum antibody to hepatitis B core antigen  
Serum hepatits B e antigen 
Serum antibody to hepatitis B e antigen
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32
Q

Explain how the different Hep B antigens can figure out if someone is infected, has been infected, or had the vaccine

A

Serum hepatitis B surface antigen will be positive if infection active
serum antibody to hepatitis B surface antigen indicates immunity (will be positive if person has had the infection or vaccination)
Serum antibody to hepatitis B core antigen - only present if previously infected

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33
Q

Management of Hep B

A

if acute: ABCDE
Supportive care
some patients may require antiviral therapy
If chronic: antiviral therapy, assess need for liver transplant

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34
Q

Causes of Hep C

A

spread via blood exposure - sharing needles, unsafe medical procedures less common to be spread sexually

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35
Q

Presentation of Hep C

A

asymptomatic

rarely: jaundice, ascites

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36
Q

how does Hep C effect LFTs

A

ALT may be raised

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37
Q

Investigations for hep C

A

Hepatitis C virus antibody enzyme immunoassay
Hep C PCR
LFTs

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38
Q

Management of Hep C

A

Antivirals (DAA) for 8-12 weeks

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39
Q

causes of autoimmune hepatitis

A

Chronic inflammatory hepatic disease with no known cause

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40
Q

Types of autoimmune hepatitis

A

Type 1 - 95% of the time, usually ANA and/or ASMA autoantibody positive
Very elevated IgG levels
45% progress to cirhosis
Most commonly effect 10 years plus
histology shows hepatitis with prominent plasma cells
Type 2
5% of the time
Anti-liver/kidney microsomal antibody (LKM t1)and anti-liver cytosol antibody (LC-1) positive
elevated IgG
Paeds (2-18)
80% progress to cirrhosis
Hepatitis with prominent plasma cells on hisology

41
Q

Features of autoimmune hepatitis

A 
Females 
fatigue and malaise 
Anorexia 
Abdo discomfort 
Hepatomegaly 
Jaundice (maybe normal stools, dark urine)
Pruritus 
Spider naevi
42
Q

how does autoimmune hepatitis effect LFTs

A

Raised ALT and AST (<10% increase as chronic)
bilirubin/GGT/ALP may be increased
prolounged PT

43
Q

Investigation for autoimmune hepatitis

A

LFTs
US
Antibodies

44
Q

Management of autoimmune hepatitis

A

asymptomatic, no fibrosis/inflammation: watch and wait
Symptomatic but not severe: observation and monitoring, corticosteroids (e.g. pred) for 6+ months
Severe: corticosteroids, immunosuppressant therapy such as azathioprine

45
Q

causes of wilsons disease

A

excessive copper accumulating in the body leading to toxicity (copper stored in the liver, hence causing hepatitis)
autosomal recessive

46
Q

Features of wilsons disease

A

Hx of hepatitis
hepatomegaly
cardiomyopathy
renal tubular dysfunction
arthritis
behavioural abnormalities
tremor
slurred speech
dystonia (uncontrollable contraction of muscles)
Lack of coordination Kayser-Fleischer rings in eyes
problems with eye movements such as diplopia

47
Q

how does wilsons disease present on LFTs

A

ALT and AST may be raised due to hepatitis

48
Q

Investigations for wilsons disease

A

LFTs
24hr urine copper
FBC - haemolytic anaemia
ceruloplasmin (will be decreased as no ATP7D (enzyme) to convert apoceruloplasmin to ceruloplasmin to the bind to the copper)

49
Q

management of wilsons disease

A

Asymptomatic - zinc maintenance therapy
shouldnt eat shellfish for the first 6 months
mold/moderate hepatic failure: trientine - helps to eliminate excess copper
zinc - helps block copper absoprion (no shellfish)
Severe hepatic failure: liver transplant

50
Q

haemochromatosis

A

Excessive iron in the body
autosomal recessive transmission which causes a haemochromatosis gene (HFE) mutation, which would normally regulate iron stores

51
Q

Features of haemochromatosis

A 
males 
fatigue 
weakness 
lethargy
arthralgia
hepatomegaly 
male impotence
erectile dysfunction 
loss of libido
bronze skin pigmentation
cirrhosis
hepatomegaly 
hepatocellular carcinoma
white/flat/spoon nails (koilonychia), 
osteoporosis 
melanoma 
dry skin
Diabetes
52
Q

How does haemachromatosis present on the LFT

A

AST and ALT raised chronically

53
Q

investigations for haemochromatosis

A 
LFTs
serum transferrin saturation of >45% measures a protein which regulates absorption of iron into the blood
serum ferritin (high)
54
Q

management of haemochromatosis

A

Stage 0: asymptomatic with normal ferritin and serum transferrin saturation (monitor every 3 years, avoid iron and vit c supplements)
Stage 1: asymptomatic with normal ferritin but increased transferrin saturation monitor yearly and avoid iron and vit C supplements
Stage 2, 3, 4:
phlebotomy - remove blood to stimulate new blood cells to be made usuing up the bodies own iron stores
avoid iron and vit C supplements
if phlebotomy contraindicated iron chelation therapy - e.g. desferrioxamine

55
Q

what is ascending cholangitis

A

aka acute cholangitis is an infection of the bile duct
commonly caused by gall stones (cholelithiasis) blocking the bile duct and causing biliary obstruction
can lead to sepsis

56
Q

features of ascending cholangitis

A

RUQ pain
fever
jaundice (charcots triad)
pale stools and dark urine

57
Q

How does ascending cholangitis present on a LFT

A

Hyperbilirubinaemia

raised ALP

58
Q

Investigations for ascending cholangitis

A 
FBC (high WCC and decreased platelets)
LFTs
serum urea and c reatinine - raised if disease is severe 
ABG
CRP
Blood culture 
Transabdominal US 
ERCP for diagnosis and possible treatment
59
Q

management of ascending cholangitis

A

ABCDE
IV broad spectrum antibiotics (e.g. pip taz or ceftriaxone + metronidazole)
if antibiotics dont work ERCP is conducted to either put in a stent in the biliary tree to allow for decompression or removing the gallstones
pain relief
fluids

60
Q

biliary tree

A

left and right hepatic duct make the common hepatic duct
+ the cystic duct to make the common bile duct
Pancreatic duct joins at the ampulla of vater

61
Q

What is acute cholecystitis

A

acute inflammation of the gall bladder, most commonly due to gall stones (gallstones cause irritation if trapped and impacted, which have the potential to cause infection)

62
Q

Features of acute cholecystitis

A 
RUQ pain lasting more than 3 hrs 
Murphys sign may be present! pain on plapation of the RUQ along the costal margin on inspiration
Fever 
palpable mass in the RUQ 
nausea
63
Q

how does acute cholecystitis present

A

Elevated ALP and GGT

also elevated ALT but ALP more

64
Q

Investigations of acute cholecystitis

A

Abdomen MRI or CT if sepsis is suspected, or abdo US if sepsis not suspected
FBC
CRP
LFTs
serum amylase or lipase - identify if acute pancreatitis is present

65
Q

Management of acute cholecystitis

A 
ABCDE 
Pain relief
Fluids 
Antibiotics if sepsis indicated 
Cholecystectomy within a week of diagnosis
66
Q

biliary colic

A

gall stone blocking the bile duct, causes pain

67
Q

what are gall stones made from and why do they form

A

cholesterol (high in fatty foods), normally formed due to hypomotility of the gallbladder and high cholesterol levels

68
Q

Features of biliary colic

A

constant epigastric or RUQ pain lasting <3hrs (THIS IS HOW IT DIFFERS FROM ACUTE CHOLECYSTITIS)
pain after eating (particularly fatty food)
Jaundice maybe

69
Q

Risk factors for biliary colic

A

fertile, fat, female, 40

70
Q

how does biliary colic present on LFTs

A

Raised ALP, raised bilirubin

71
Q

investigations for biliary colic

A

LFTs
FBC - usually normal
Serum amylase or lipase - to test for acute pancreatitis
Abdominal ultrasound

72
Q

Management of biliary colic

A

Diet advice and pain relief

cholecystectomy or ERCP

73
Q

what is Primary biliary cholangitis

A

aka primary biliary cirrhosis
chronic
autoimmune condition against the biliary epithelial cells of the bile ducts. progressive bile duct damage leads to hepatic fibrosis

74
Q

Features of primary biliary cholangitis/cirrhosis

A 
age 45-60
female 
hx of autoimmune conditions 
high cholesterol
pruritus due to cholestasis 
fatigue 
hepatomegaly 
dry eyes and mouth
75
Q

how does primary biliary cirrhosis/cholangitis effect LFTs

A

raised ALP, raised GGT
raised bilirubin
maybe raised ALT if hepatic fibrosis is present
decreased albumin

76
Q

Investigations for primary biliary cirrhosis/cholangitis

A

LFTs
Antimitochondrial antibody immunofluorescence will be present
Antinuclear antibody immunoferecence - antinuclear rim or nuclear dots may be present if positive
Antipyruvate dehydrogenase complex-E2 ELISA
abdominal ultrasound - to excluse obstructions
MRCP - to exclude obstructions (MRI scan that looks at liver, gall bladder, bile duct and pancreas)

77
Q

Management of Primary biliary cirrhosis/cholangitis

A

Bile acid therapy such as ursodeoxycholic acid
immunomodulatory therapy such as prednisolone if pruritus is present
antipurritis medications such as cholestyramine
end stage liver disease or chronic pruritis - liver transplant

78
Q

Primary sclerosing cholangitis

A

inflammation and damage to the bile ducts causing obstruction and can lead to fibrosis and strictures (cause not well understood)

79
Q

Features of primary sclerosing cholangitis

A 
males
40
IBD
RUQ or epigastric pain 
Pruritus 
Fatigue 
jaundice
80
Q

how does primary sclerosing cholangitis effect LFTs

A 
ALP >3x 
elevated GGT 
mild-moderate ALT raise if hepatocellular injury 
bilirubin maybe elevated 
PT may be prolounged
81
Q

Investigations for primary sclerosing cholangitis

A

LFTs
FBC
Antimitochondrial antibody - would be negative (wheres positive in PBC)
Abdo US
MRCP (magnetic resonance Cholangiopancreatography (MRCP)
Endoscopic retrograde cholangiopancreatography (ERCP) for diagnosis and treatment

82
Q

Management of Primary sclerosing cholangitis

A

asymptomatic - observation, lifestyle change (diet, weight, exercise, reduced alcohol)
pruritis - cholestyramine
Ca and vit D supplement
acutely ill - ERCP - to dilate stricture and/or remove gall stones
end stage liver disease - liver transplant

83
Q

Causes of vit D deficiency

A

lack of sun or increased skin pigmentation
malabsorption (chrons, coeliac)
lack of dietary vit D (oily fish, liver, milk, egg yolks, red meat, cereals, fortified foods)

84
Q

features of vit D deficiency

A 
fatigue and tiredness 
aches and pains 
excessive sweating 
children - rickets/failure to thrive 
bone discomfort due to osteomalacia 
proximal muscle weakness 
malaise
85
Q

how does vit D deficiency present on LFTs

A

Raised ALP - NOT RAISED GGT

86
Q

investigations for vit D deficiency

A

LFTs
serum 25-hydroxyvitamin D - low
Xray of knees and wrists

87
Q

Management of vit D deficiency

A

mild - vit D supplements (ergocalciferol)
sun exposure (to a safe extent)
Ca supplement
moderate - add 1,25-dihydroxyvitamin D3 such as calcitriol if there is a problem with vit D metabolism

88
Q

types of bone cancer

A

osteosarcoma
Ewing’s sarcoma
chondrosarcoma etc

89
Q

Which cancers are most likely to metastasise to the bone

A

breast, prostate thyroid, lung and kidney (myeloma)

90
Q

features of bone cancer/mets

A

constant bone pain
swelling
increased fractures
unintentional weight loss

91
Q

How does bone cancer/mets present on LFTs

A

raised ALP but NOT GGT

92
Q

investigations for bone cancer/mets

A

FBC
LFTs
CT/MRI/Xray
Biopsy - to grade tumour and determine if benign or malignant

93
Q

Management of bone cancer and mets

A

depends on the type, options are surgery, chemo, radiotherapy, cryotherapy and targeted therapy

94
Q

what could isolated hyperbilirubinaemia mean, and what tests should you subsequently ask for

A

gilberts

haemolysis (ask for FBC, blood film, reticulocyte count, coombs, LDH, haptoglobin)

95
Q

Cause of gilberts syndrome

A

mutation in the AGT1A1 gene (autosomal recessive) which results in decreased activity of the UDP GT enzyme (uridine diphosphate glucuronosyltransferase), which usually conjugates bilirubin

96
Q

features of gilberts syndrome

A

Jaundice (usually after stress or sport)

Positive FH

97
Q

Investigations for gilberts syndrome

A

unconjugated bilirubin test - positive as elevated
Direct coombs for haemolysis - should be normal
LFTs - rest should be normal

98
Q

management of gilberts syndrome

A

No treatment

patient education is vital so that the patient understands their condition and why there is no need for treatment

Placement (10 decks)

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