Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > liver > Flashcards

liver Flashcards

1
Q

what divides the left and larger right lobe

A

falciform

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

fibrous protective lining

A

external Glisson’s capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

metabolic function carbohydrate

A 
hormonally regulated 
glucogeogenesis 
glycolysis
glycogenesis
glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

fat metabolism

A

breakdown and synthesis
processing chlomicron remnants
lipoprotein HDL and cholesterol synthesis
ketogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

protein metabolism

A

synthesis plasma proteins - albumin
transamination/deamination amino acids
converts ammonia to urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hormone metabolism

deactivates

A

insulin
glucagon
ADH
steroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hormone metabolism

activates

A

conversion T3 to T4

vitamin D to calcidiol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

functions storage

A

vitamin ADEK - fat soluble
vitamin B12
iron, copper
glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

functions synthesis of proteins

A 
for liver and for export 
clotting factors (II, VII, IX, X)
proteins C and S 
albumin 
complement proteins 
apolipoproteins 
carrier proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

functions protection

A

Kupfer cells

production immune factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

functions detoxification

A

endogenous substances - bilirubin

exogenous substances - drugs, ethanol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

phases 1

A 
oxidation 
reduction 
hydrolysis
increases drug polarity 
new chemically reactive group permits conjugation 
cytochrome P450
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

phase 2

A 
conjugation 
further increases polarity 
adds endogenous products 
results in inactive products 
glucuronidation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

drug metabolism excretion

A 
renal 
faeces - bile 
lungs
sweat/tears
milk, saliva
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ALT

A 
alanine aminotransferase 
liver enzyme 
high conc. within hepatocytes 
increased levels in blood following hepatocellular injury 
marker for hepatocellular injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AST

A

aspartate aminotransferase
similar to ALT but less specific
enzyme in liver, heart, skeletal muscle, kidneys, brain, RBC
may be elevated in liver injury
may be elevated in MI, pancreatitis, haemolytic anaemia, renal or MSK disease
AST>ALT may suggest muscle source for enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ALP

A

alkaline phosphatase
enzyme present in liver, bile duct, bone, placenta
altered levels - biliary obstruction, liver disease, bony mets, primary tumours, bone fractures, oseomalacia, vitamin D deficiency, hepatitis, cirrhosis, hyperthyroidism, hyperparathyroidism, renal osteodystrophy, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

GGT

A

gamma glutamyltransferase
enzyme present in liver/bile duct, kidneys, pancreas, gallbladder, spleen, heart, brain
altered levels - biliary obstruction, liver and pancreas disease, CV disease, alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

GGT and ALP elevated

A

biliary epithelial damage and bile flow obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

GGT and alcohol

A

elevated by large alcohol intake

may also be increased by drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

AST

A

chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

AST>ALT

A

cirrhosis and acute alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

AST level increase

A

20x normal in viral hepatitis, muscle trauma, surgery, drug induced hepatic trauma
10-20x alcoholic cirrhosis or MI
5x chronic cirrhosis
mildly raised steatosis, liver mets and PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

albumin

A

synthesised in functioning liver
maintains IV osmotic pressure
levels may famm due to - cirrhosis, inflammation , albumin loss due to protein losing enterpathies, nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

prothrombin time

A

time taken for blood to clot
in absence of secondary causes, increased PT can indicate liver disease
reduced production of clotting factors increases PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

bilirubin

A

breakdown product of haemoglobin
conjugated when taken up in liver
jaundice >60mmol/l
unconjugated insoluble - no effect on urine
conjugated passes to liver causing darker urine
if bile and lipases can’t reach bowel from blockage, fat not absorbed and stools pale and bulky

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

pre-hepatic jaundice

A

excessive red cell breakdown overwhelms liver decreased conjugated, increased unconjugated
normal urine
normal stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

hepatocellular jaundice

A 
liver looses conjugating ability
cirrhosis compresses biliary tree
can be mixed conjugated and unconjugated 
dark urine 
normal stool
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

post-hepatic jaundice

A

obstruction biliary drainage but bilirubin still conjugated in liver
dark urine
pale stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Gilbert’s syndrome

A

mild disorder of bilirubin processing in liver
mutation decreases activity of liver enzyme that processes bilirubin
autosomal dominant or recessive
increased unconjugated bilirubin in blood with normal LFTs
usually asymptomatic
jaundice may appear due to illness, alcohol, stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

haemolytic anaemia

A

abnormal breakdown of red blood cells
fatigue, SOB
jaundice
many causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hepatocellular jaundice

A

acute - poisoning (paracetamol), infection (hepatitis), liver ischaemia
chronic - alcoholic fatty liver disease, NASH, cirrhosis, chronic infection, primary biliary cholangitis, pregnancy, autoimmune hepatitis, PSC, haemochromatosis, Wilson’s diease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

obstrctive jaundice

A

gallstones
strictures
tumours
congenital biliary atresia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

chronic liver disease

A

> 6 months
present acutely or subclinical
progress to cirrhosis
signs and symptoms depend on underlying disease
insult to hepatocytes - recurrent inflammation - process of fibrosis - compensated cirrhosis - decompensated cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

decompensated cirrhosis

A

ascites
jaundice
variceal haemorrhage
hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

liver injury

A

hepatic stellate cells (HSC) in space of disse activated by injury and cause fibrosis
normally exist in quiescent state
change to activated state when liver is damaged
secrete fibrogenic factors that encourage portal myofibroblasts to produce collagen and thus cause fibrosis
responsible for regression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

NAFLD

A

NAFL and NASH
first hit - excess lipid accumulation in liver
second hit - oxidation stress and lipid peroxidation, pro-inflammatory cytokine release, lipopolysaccharide, ischaemia-reperfusion injury
associated with metabolic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

NAFLD history

A

fatigue
LUQ pain
alcohol, drugs, sexual activity
obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

NAFLD diagnosis

A

usually detected incidentally
suspect if abnormal USS or LFT derangement for >3 months
biopsy
examine patient for signs of advanced liver disease
liver screen to rule out any other causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

NAFL simple steatosis

A 
steatosis - fatty acid build up in cells 
no inflammation or fibrosis 
most common 
diagnosed ultrasound 
no liver outcomes 
increased CV risk 
treatment - weight loss, exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

NASH

A 
non alcoholic steatohepatitis
steatosis and inflammation and scarring 
diagnosed liver biopsy 
risk of progression to cirrhosis
mallory bodies 
ballooning 
treatment - weight loss, exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

alcohoilc liver disease

A

increased release and synthesis of fatty acids and TAGs in hepatocytes
acetaldehyde responsible for damage
involves pro-inflammatory cytokines, oxidative stress, lipid peroxidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

ALD history

A

same questions as for NAFLD
there will be a clear history of alcohol excess
ensure you get an accurate picture of how much and how long
fever, N&V may be present in alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

ALD diagnosis

A 
may be asymptomatic 
liver screen to rule out other causes 
LFTs
USS, CT, MRI
liver biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

ALD treatment

A

no alcohol
corticosteroids may be used in acute inflammation
transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

ALD complications

A 
acute liver failure 
cirrhosis
hepatocellular carcinoma 
focal liver lesions 
hepatic encephalopathy
oesophageal varices 
ascites 
thrombocytopenia 
malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

cirrhosis

A

final common end point if liver disease
irreversible
bands of fibrosis separating regeneration nodules of hepatcytes
macronodular, micronodular ALD or mixed
pattern depends on what caused the cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

causes of cirrhosis

A 
ALD
NASH
hep b and C
autoimmune hepatitis 
cardiac cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

cirrhosis signs and symptoms

A

liver dysfunction - spider nevi, palmar erythema, gynecomastia, ascites, shrunken or enlarged liver, jaundice, abnormal bruising, intense itching, acute kidney injury, hypogonadism, encephalopathy
portal hypertension - splenomegaly, eosophageal varices, caput medusa, anorectal varices
unestablished cause - finger clubbing, Dupuytren’s contracture, weakness, fatigue, weight loss, anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

cirrhosis history

A

chronic alcohol abuse
NAFLD
chronic infection
autoimmune or inherited disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

cirrhosis diagnosis

A

liver biopsy - regenerating nodules of hepatocytes, fibrosis/connective tissue between these nodules
liver screen to determine cause
LFTs
USS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

compensated cirrhosis

A

asymptomatic stage
LFTs show damage
some back pressure signs may be visible to physician
palmar erythema, clubbing, gynaecomastia, hepato/splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

decompensated cirrhosis

A

symptomatic - ascites, jaundice, variceal haemorrhage, easy bruising, hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

grading cirrhosis

A 
child-pugh score 
A - well compensated 
B - functional compromise 
C - decompensated 
MELD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

cirrhosis management

A

cannot be reversed
healthy diet
no alcohol
increase calories - small frequent meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

cirrhosis symptom management

A 
ascites - furosemide 
itch medication - colestyramine 
caution with paracetamol 
treat cause 
weight loss
transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

liver transplant

A

event based
liver function based
quality of life
UKELD score
49 is minimum score to be considered to go on transplant waiting list
UKELD calculated using - INR, creatinine, bilirubin and sodium

58
Q

ascites

A

cirrhosis causes portosystemic shunting, increases capillary hydrostatic pressure in splanchnic vessels
results in release of vasodilators to decrease pressure
vasodilation causes decreased arterial blood volume
decreaed blood volume activates - RAAS, sympathetic system, ADH
leads to sodium and water retention by kidneys and renal vasoconstriction

59
Q

ascites diagnosis

A

shifting dullness

USS

60
Q

ascites treatment

A 
treat underlying disease 
look for infection 
decrease salt intake 
no NSAIDs
spironolactone first line 
loop diuretics 
paracentesis
TIPSS or transplant
61
Q

hepatorenal syndrome

A

kidney failure seen in those with severe liver damage
mechanism for ascites
can lead to kidney failure
look for altered liver function, abnormalities in circulation, kidney failure
treat - transplant and TIPSS

62
Q

spontaneous bacterial peritonitis

A

bacterial infection in the peritoneum, despite the abscenece of an obvious source of infection
diagnosis - neutrophils >250
mild - co-trimaxazole PO
severe - piperacillin/tazobactam IV then step down to co-trimoxazole
IV albumin sometimes given

63
Q

hepatic encephalopathy

A

urea cycle takes places in cytosol and mitochondrial matrix of liver cells
produces urea from ammonia, dissolved in blood, excreted via kidneys
liver failure causes hyperammonaemia - toxic to CNS
portosystemic shunting increases NH3 in blood

64
Q

hepatic encephalopathy symptoms

A 
liver flap
confusion 
non-coordination/shaking 
drowsiness/coma
slurred speech
siezures
cerebral oedema
65
Q

hepatic encephalopathy treatment

A

lactulose

antibiotics - neomycin, rifaximin

66
Q

acute liver failure

A

any insult to liver causing damage in previously normal liver
< 6 months
causing encephalopathy and impaired protein synthesis

67
Q

acute liver failure clinical features

A 
non 
jaundice 
lethargy, arhtlargia
N&amp;V, anorexia
RUQ pain 
itch
68
Q

acute liver failure diagnosis

A 
physical exam - jaundice, ascites
history 
infections, alcohol, pregnancy 
mental changes 
coagulopathy
abnormal LFTs
69
Q

acute liver failure investigations

A 
alcohol 
drugs - paracetamol, over the counter, herbal, supplements
possible toxins
LFTs
USS
virology 
investigation of chronic liver disease 
rarely biopsy
70
Q

acute liver failure treatment

A 
rest 3-6 months recovery 
fluids
no alcohol
increase calorie intake 
regular observation 
monitor and supplement K, PO4, Mg
71
Q

acute liver failure causes

A 
viral hep A-E, CMV, EBV, toxoplasmosis
drugs - paracetamol
chock liver
cholangitis
alcohol
malignancy 
Budd Chiari
acute fatty liver of pregnancy
cholestasis pregnancy
72
Q

NSAIDs

A

decrease renal PGE synthesis
worsen renal impairment bu increasing renal vasoconstriction and sodium retention
increase risk of hepatorenal syndrome

73
Q

opiates

A

increased levels in blood due to decreased metabolism

increases risk of respiratory depression

74
Q

diuretics

A 
furosemide - decreases IV volume, hypokalaemia, hepatorenal syndrome 
#thiazide - same as furosemide 
spiralactone - combats secondary aldosteronism
75
Q

hepatitis A

A 
most common viral hepatitis
transmission faecal oral
associated with poor sanitation and overcrowding 
high risk - gay men, PWID
acute infection
76
Q

hepatitis A clinical presentation

A

systemic upset - nausea and anorexia
jaundice, most infectious just before jaundice
hepatic jaundice
vomiting and altered mental state - hospital admission
enlarged liver, splenomegaly

77
Q

hepatitis A investigations

A

hepatitis A IgM (HAV IgM)- acute infection
IgG - HAV = vaccinated
LFTs
serum bilirubin reflects the level of jaundice
serum AST and ALT rise before jaundice

78
Q

hepatitis A management

A

stop alcohol consumption when acutely unwell

supportive treatment

79
Q

hepatitis E

A

similar presentation to hepatitis A
more common in tropical countries
faecal oral transmission
contaminated drinking water
pregnancy associated with severe disease
acute infection, chronic infection in immunocompromised patients

80
Q

hepatitis E clinical presentation

A

nausea and anorexia
jaundice
vomiting altered mental state
enlarged liver, splenomegaly

81
Q

hepatitis E investigations

A 
viral RNA (HEV RNA) can be detected by PCR in the stool or serum 
ELISA for IgG/IgM HEV
82
Q

hepatitis E management

A

stop alcohol consumption

supportive treatment

83
Q

hepatitis B transmission

A

bone - sex
baby
blood
if infected in infancy infection is more likely to become chronic

84
Q

people with increased risk of hepatitis B

A 
born in areas of high prevalence 
multiple sex partners 
men who have sex with men 
PWIDs
children of infected mums
85
Q

hepatitis B clinical presentation

A 
children are more likely to develop chronic infection 
adults more likely to develop an acute infection 
may be asymptomatic 
similar to HAV
illness may be more severe 
itchy rashes 
arthritis 
fever 
diarrhoea, abdo pain
86
Q

hepatitis B investigations

A

hep B surface antigen (HBsAg) - in all infectious individuals
hep B e antigen (HBeAg) - highly infectious individuals
hep B virus DNA (HBV DNA) - highly infectious individuals
hep B c IgM - high titre: acute, low titre: chronic infection
hep B IgG - past exposure usually vaccine
anti-HBs (hep B surface antibody - HBsAb) - recovery/immunity to HBV, seen in vaccinated

87
Q

hepatitis B prognosis

A

self resolving
most people full recovery
chronic infection prognosis depends on age

88
Q

hepatitis B management

A

symptomatic
constant HBV marker monitoring
antivirals - antecavir, tenofovir, suppress not cure

89
Q

controlling hepatitis B

A

vaccination
minimise exposure
post exposure prophylaxis

90
Q

hepatitis D

A

a parasite of a parasite
only found in those with hepatitis B infection
exacerbates a hep B infection

91
Q

hepatitis C

A

most common
bone -sex
baby
blood
no vaccine
acute infection - asymptomatic, mild flu and jaundice with raised amino transferases
chronic infection are more common - a result of asymptomatic acute infection

92
Q

hepatitis C investigations

A

initially test for antibody - anti-HCV
HCV-RNA test positive after 1-8 weeks infection
anti-HCV usually positive after 8 weeks of infection - past or current infection

93
Q

hepatitis C management

A

continually monitor HCV-RNA levels
almost half of those with acute HCV infection spontaneousy clear the virus within 6 months
if viral load falls treatment not required
viral load does not decrease - anti-viral therapy

94
Q

chronic viral hepatitis

A

caused by HBV and HCV
spontaneous cure in chronic HBV is not uncommon
no spontaneous cure in chronic HCV

95
Q

chronic hepatitis virus outcomes

A

20 years from initial infection to cirrhosis
30 years chronic infection hepatocellular carcinoma
a child with HBV infection acquired perinatally is far more likely to develop chronic infection

96
Q

when to treat chronic viral hepatitis

A

HBV - raised ALT and high HBV DNA

HCV - chronic hep C is always treated right away

97
Q

management of chronic HBV

A

perginterferon alpha-2a first line
tenofovir disoproxil second line
entercavir can be second line instead

98
Q

management of chronic HCV

A

aiming for undetectable HCV RNA 12 weeks after treatment completion
specific treatment depends on disease progression
antivirals
regular screening for hepatocellular carcinoma
no alcohol

99
Q

autoimmune hepatitis

A

755 cases occur in females - young females, oral contraceptives
T cells directed against hepatocyte surface antigen
type 1 - ages 10-20 and 45-70
type 2 - presents usually in young kids/adults

100
Q

autoimmune hepatitis clincal features

A

hepatomegaly
jaundice
signs of chronic liver disease
may present similar to acute on hepatitis

101
Q

autoimmune hepatitis investigations

A 
raised LFTs
antibodies 
type 1 - ASMA and ANA positive 
type 2 - LKM positive (ASMA and ANA negative)
Igg will be raised 
liver biopsy to confirm disease severity
102
Q

autoimmune hepatitis management

A

corticosteroids and azathioprine combined gradually reducing steroids
may eventually need a liver transplant

103
Q

benign hepatic tumours

A

haemangioma
focal nodular hyperplasia
adenoma
liver cysts

104
Q

haemangioma

A

most common liver tumour
hypervascular tumour
small mass contained within a capsule with clear borders
usually asymptomatic

105
Q

haemangioma management

A

diagnosis
US - echogenic spot which is well demarcated
CT - venous enhancement from periphery to centre
MRI - high intensity area
no treatment

106
Q

focal nodular hyperplasia

A

benign nodule formation on liver tissue - congenital vascular anomaly causing a hyperplastic response to abnormal arterial flow
classic description - central scar containing a large artery, radiating branches to the periphery
contains all liver ultra structure
most common in middle aged women
usually asymptomatic but may cause pain

107
Q

FNH investigations

A

Us - nodule with varying echogenicity
CT - hypervascular mass with central scar
MRI - iso/hypo intense
FNA - normal hepatocytes and Kupffer cells
no treatment
no malignancy potential
isointense on sulphur colloid scan

108
Q

hepatic adenoma

A

benign neoplasm composed of normal hepatocytes
more common in women, associated with contraceptive hormones, associated with anabolic steroids
usually asymptomatic, may be RUQ pain
can rupture causing haemorrhage
can undergo malignant transformation

109
Q

hepatic adenoma investigations

A 
US - filling defect 
CT - diffuse arterial enhancement 
MRI - hypo/hyper intense lesion 
FNA - may be required
cold on sulphur colloid scan
110
Q

hepatic adenoma treatment

A

stop taking contraceptives, hormone, anabolic steroids
males - surgical excision irrespective of size
females <5cm or reducing in size - annual MRI
females >5cm or increasing in size - sugical excision

111
Q

malignant hepatic tumours

A

primary tumours are rare - hepatocellular carcinoma, fibro-lamellar carcinoma
secondary tumours are more common - multiple lesions, metastases - colon, pancreas, stomach, breast, lung

112
Q

hepatocellular carcinoma

A

most common primary liver cancer
important risk factor is cirrhosis
carriers of HBV and HCV high risk of developing HCC
more common in males than females

113
Q

hepatocellular carcinoma pathology

A

usually a single nodule but can be multifocal in rarer cases
it consists of cells resembling hepatocytes
metastasis can spread to bones, lungs, lymph nodes

114
Q

clinical features of HCC

A 
weight loss, malaise, fever, anorexia 
ache in RUQ
worsening of pre-existing chronic liver disease 
ascites 
signs of cirrhosis 
hard enlarged RUQ mass
liver bruit
115
Q

investigating suspected HCC

A

serum alpha-fetoporotein may be raised but is normal in a third of cases
USS can show filling defects
CT to identify HCC
tumour biopsy is used less frequently

116
Q

HCC treatment

A 
resection is the first choice 
liver transplant 
local ablation
TACE - transarterial chemoembolisation 
systemic therapies - sorafenib, kinase inhibitor
117
Q

fibro-lamellar carcinoma

A

more common in younger patients
no correlation with cirrhosis
AFP isn’t raised
investigations - CT shows stellte scar with radial septa showing persistent enhancement
treatment - resection or transplant, TACE

118
Q

cystic lesions

A

simple cyst
hysatid
polycystic liver disease
pyogenic or amoebic abscesses

119
Q

simple cyst

A

liquid collection lined by epithelium
solitary - so no biliary tree
usually asymptomatic - RUQ pain, fever

120
Q

simple cyst investigation

A

USS fist line

121
Q

simple cyst treatment

A

asymptomatic no treatment

symptomatic/uncertain diagnosis surgical intervention required

122
Q

hydatid cyst

A

caused by tapeworm echinoccocus granulosus
more prevalent in farming communities
cysts can erode into adjacent structures and vessels
asymptomatic - dull ache and swelling in right hypocondrium

123
Q

hydatid cyst investigation

A

AXR - mauy show cyst calcification
US/CT
check for anti-echinococcus antibodies

124
Q

hydtid cyst management

A

surgery is most common
albendazole - reduce size
drained using PAIR

125
Q

polycystic liver disease

A

caused by embryonic ductal plate malformation

three types - von meyenburg complexes, polycystic liver disease, AD polycystic kidney disease

126
Q

von meyenburg complexes

A

benign cystic nodules throughout liver
originate in the peripheral biliary tree
asymptomatic

127
Q

polycystic liver disease presentation

A

abdominal pain
abdominal distention
may be atypical symptoms
may be signs of liver failure if there is severe disease

128
Q

polycystic liver disease investigations

A

gene studies
CT
kidney function tests

129
Q

polycystic liver disease treatment

A

aim to halt cyst growth
surgical - aspiration and liver transplantation
pharmacological therapy somatostatin analogues

130
Q

liver abscess

A

can be pyogenic or caused by Protozoas

131
Q

liver abscess presentation

A 
high fever 
abdominal pain
nausea and vomiting 
jaundice 
pleural rub in lower right chest 
malaise
132
Q

liver abscess investigations

A 
check for leucocytosis 
CXR - raised right hemi-diaphragm 
US
CT
echocardiogram
133
Q

liver abscess management

A

initial empiric board spec antibiotics - amoxicillin, metronidazole, gentamicin IV
aspiration/drainage
operation if no clinical improvement

134
Q

haemochromatosis

A

an inherited disease characterised by excess iron deposition in the liver as well as other organs
autosomal recessive inheritance pattern
symptomatic 20-40g

135
Q

haemochromatosis clinical features

A 
classic triad - bronze skin pigmentation, hepatomegaly, diabetes mellitus 
cardiac arrhythmias and heart failure 
liver fibrosis/failure 
joint pain
hypogonadism
136
Q

haemochromatosis investigations

A

serum iron elevated >30 in most cases
LFTs often normal
biopsy
MRI

137
Q

haemochromatosis management

A

venesection

avoid iron rich food

138
Q

Wilson’s disease

A

autosomal recessive disorder leading to reduced ceruloplasmin
defect in copper transorting and excretion into bile

139
Q

Wilson’s disease symptoms

A

Kayser-fleisher rings
signs of liver disease
CNS issue - tremor, involuntary movements

140
Q

Wilson’s disease investigations

A

urinary copper increased

serum copper and ceruloplasmin usually reduced

141
Q

Wilson’s disease management

A

penicillamine

nausea, rash, haematuria

GI (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions