LFTs Flashcards
1
Q
Raised ALT meaning
A
hepatocellular injury
2
Q
Raised AST
A
Hepatocellular injury
3
Q
raised ALP
A
Cholestatic (vit D deficiency, bone fracturew, bony mets/tumours if raised on own)
4
Q
raised GGT
A
cholestasis (raised with ALP)
Alcoholic
5
Q
Raised bilirubin alone
A
Gilberts or haemolysis
6
Q
decreased albumin
A
can indicate hepatocellular injury
7
Q
increased prothrombin time
A
hepatocellular injury (clotting factors are not being produced)
8
Q
ALT>AST
A
chronic liver disease
9
Q
AST>ALT
A
acute liver disease (e.g. cirrhosis or alcoholic hepatitis)
10
Q
how do hepatocellular pathologies usually effect stool and urine
A
will cause intrahepatic jaundice so will have dark urine but normal stool
11
Q
Cause of alcoholic liver disease
A
excessive alcohol consumption over a long time
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
13
Q
Features of alcoholic liver disease
A
Abdo pain, typically RUQ
Hepatomegaly
Ascites maybe
14
Q
What is this: raised ALT and AST AST>ALT hyperbilirubinaemia GGT raised
A
Alcoholic liver disease
15
Q
investigations for alcoholic liver disease
A
LFTs, FBC, PT - indicate if advanced liver cirrhosis or liver failure is present
US
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
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)
18
Q
risk factors for NAFLD
A
obese, diabetes, hypertension, medication (tamoxifen (most common, oestrogen blocking breast cancer drug) corticosteroids, antidepressants, antipsychotics.
19
Q
features of NAFLD
A
no signs of alcohol abuse fatigue malaise hepatosplenomegaly abdominal obesity RUQ discomfort
20
Q
What is this: ELevated ALT and AST ALP mildly elevated Bilirubin elevated ALT>AST
A
NAFLD
21
Q
Investigations for NAFLD
A
LFTs
FBC (may see anaemia or thrombocytopenia - low platelets)
PT - normally raised
serum albumin - normally reduced
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
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
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)
25
What is this?
ALT and AST significantly raised
elevated bilirubin levels
elevated ALP (but not as much as AST and ALT)
Hep A
NOTE: similar AST and ALT
cant really have chronic hep A so ALT and AST always significantly raised as an acute infection
26
Investigations for Hep A
LFTs (AST and ALT)
serum creatinine
PT time
IgM anti-HAV (accepted marker for accute hep A infection)
27
management for hep A
ABCDE
| supportive management from home
28
Causes of Hep B
spread through bodily fluids (high risk sexual activity or sharing needles)
passed from mother to child
29
features of hep B
Most people are asymptomatic (70%)
30
```
What is this?
Raised AST and ALT
raised (could be >10x or <10x) bilirubin
slightly raised ALP
low albumin
```
hep B
| NOTE: if acute then over x10 raised, chronic then <10
31
Investigations for hep B
```
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
```
32
Explain how the different Hep B antigens can figure out if someone is infected, has been infected, or had the vaccine
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
33
Management of Hep B
if acute: ABCDE
Supportive care
some patients may require antiviral therapy
If chronic: antiviral therapy, assess need for liver transplant
34
Causes of Hep C
spread via blood exposure - sharing needles, unsafe medical procedures less common to be spread sexually
35
Presentation of Hep C
asymptomatic
| rarely: jaundice, ascites
36
how does Hep C effect LFTs
ALT may be raised
37
Investigations for hep C
Hepatitis C virus antibody enzyme immunoassay
Hep C PCR
LFTs
38
Management of Hep C
Antivirals (DAA) for 8-12 weeks
39
causes of autoimmune hepatitis
Chronic inflammatory hepatic disease with no known cause
40
Types of autoimmune hepatitis
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
Features of autoimmune hepatitis
```
Females
fatigue and malaise
Anorexia
Abdo discomfort
Hepatomegaly
Jaundice (maybe normal stools, dark urine)
Pruritus
Spider naevi
```
42
how does autoimmune hepatitis effect LFTs
Raised ALT and AST (<10% increase as chronic)
bilirubin/GGT/ALP may be increased
prolounged PT
43
Investigation for autoimmune hepatitis
LFTs
US
Antibodies
44
Management of autoimmune hepatitis
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
causes of wilsons disease
excessive copper accumulating in the body leading to toxicity (copper stored in the liver, hence causing hepatitis)
autosomal recessive
46
Features of wilsons disease
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
how does wilsons disease present on LFTs
ALT and AST may be raised due to hepatitis
48
Investigations for wilsons disease
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
management of wilsons disease
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
haemochromatosis
Excessive iron in the body
autosomal recessive transmission which causes a haemochromatosis gene (HFE) mutation, which would normally regulate iron stores
51
Features of haemochromatosis
```
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
How does haemachromatosis present on the LFT
AST and ALT raised chronically
53
investigations for haemochromatosis
```
LFTs
serum transferrin saturation of >45% measures a protein which regulates absorption of iron into the blood
serum ferritin (high)
```
54
management of haemochromatosis
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
what is ascending cholangitis
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
features of ascending cholangitis
RUQ pain
fever
jaundice (charcots triad)
pale stools and dark urine
57
How does ascending cholangitis present on a LFT
Hyperbilirubinaemia
| raised ALP
58
Investigations for ascending cholangitis
```
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
management of ascending cholangitis
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
biliary tree
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
What is acute cholecystitis
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
Features of acute cholecystitis
```
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
how does acute cholecystitis present
Elevated ALP and GGT
| also elevated ALT but ALP more
64
Investigations of acute cholecystitis
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
Management of acute cholecystitis
```
ABCDE
Pain relief
Fluids
Antibiotics if sepsis indicated
Cholecystectomy within a week of diagnosis
```
66
biliary colic
gall stone blocking the bile duct, causes pain
67
what are gall stones made from and why do they form
cholesterol (high in fatty foods), normally formed due to hypomotility of the gallbladder and high cholesterol levels
68
Features of biliary colic
constant epigastric or RUQ pain lasting <3hrs (THIS IS HOW IT DIFFERS FROM ACUTE CHOLECYSTITIS)
pain after eating (particularly fatty food)
Jaundice maybe
69
Risk factors for biliary colic
fertile, fat, female, 40
70
how does biliary colic present on LFTs
Raised ALP, raised bilirubin
71
investigations for biliary colic
LFTs
FBC - usually normal
Serum amylase or lipase - to test for acute pancreatitis
Abdominal ultrasound
72
Management of biliary colic
Diet advice and pain relief
| cholecystectomy or ERCP
73
what is Primary biliary cholangitis
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
Features of primary biliary cholangitis/cirrhosis
```
age 45-60
female
hx of autoimmune conditions
high cholesterol
pruritus due to cholestasis
fatigue
hepatomegaly
dry eyes and mouth
```
75
how does primary biliary cirrhosis/cholangitis effect LFTs
raised ALP, raised GGT
raised bilirubin
maybe raised ALT if hepatic fibrosis is present
decreased albumin
76
Investigations for primary biliary cirrhosis/cholangitis
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
Management of Primary biliary cirrhosis/cholangitis
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
Primary sclerosing cholangitis
inflammation and damage to the bile ducts causing obstruction and can lead to fibrosis and strictures (cause not well understood)
79
Features of primary sclerosing cholangitis
```
males
40
IBD
RUQ or epigastric pain
Pruritus
Fatigue
jaundice
```
80
how does primary sclerosing cholangitis effect LFTs
```
ALP >3x
elevated GGT
mild-moderate ALT raise if hepatocellular injury
bilirubin maybe elevated
PT may be prolounged
```
81
Investigations for primary sclerosing cholangitis
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
Management of Primary sclerosing cholangitis
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
Causes of vit D deficiency
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
features of vit D deficiency
```
fatigue and tiredness
aches and pains
excessive sweating
children - rickets/failure to thrive
bone discomfort due to osteomalacia
proximal muscle weakness
malaise
```
85
how does vit D deficiency present on LFTs
Raised ALP - NOT RAISED GGT
86
investigations for vit D deficiency
LFTs
serum 25-hydroxyvitamin D - low
Xray of knees and wrists
87
Management of vit D deficiency
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
types of bone cancer
osteosarcoma
Ewing's sarcoma
chondrosarcoma etc
89
Which cancers are most likely to metastasise to the bone
breast, prostate thyroid, lung and kidney (myeloma)
90
features of bone cancer/mets
constant bone pain
swelling
increased fractures
unintentional weight loss
91
How does bone cancer/mets present on LFTs
raised ALP but NOT GGT
92
investigations for bone cancer/mets
FBC
LFTs
CT/MRI/Xray
Biopsy - to grade tumour and determine if benign or malignant
93
Management of bone cancer and mets
depends on the type, options are surgery, chemo, radiotherapy, cryotherapy and targeted therapy
94
what could isolated hyperbilirubinaemia mean, and what tests should you subsequently ask for
gilberts
| haemolysis (ask for FBC, blood film, reticulocyte count, coombs, LDH, haptoglobin)
95
Cause of gilberts syndrome
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
features of gilberts syndrome
Jaundice (usually after stress or sport)
| Positive FH
97
Investigations for gilberts syndrome
unconjugated bilirubin test - positive as elevated
Direct coombs for haemolysis - should be normal
LFTs - rest should be normal
98
management of gilberts syndrome
No treatment
| patient education is vital so that the patient understands their condition and why there is no need for treatment
