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liver Flashcards

1
Q

what divides the left and larger right lobe

A

falciform

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2
Q

fibrous protective lining

A

external Glisson’s capsule

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3
Q

metabolic function carbohydrate

A 
hormonally regulated 
glucogeogenesis 
glycolysis
glycogenesis
glycogenolysis
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4
Q

fat metabolism

A

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

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5
Q

protein metabolism

A

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

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6
Q

hormone metabolism

deactivates

A

insulin
glucagon
ADH
steroid hormones

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7
Q

hormone metabolism

activates

A

conversion T3 to T4

vitamin D to calcidiol

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8
Q

functions storage

A

vitamin ADEK - fat soluble
vitamin B12
iron, copper
glycogen

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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
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10
Q

functions protection

A

Kupfer cells

production immune factors

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11
Q

functions detoxification

A

endogenous substances - bilirubin

exogenous substances - drugs, ethanol

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12
Q

phases 1

A 
oxidation 
reduction 
hydrolysis
increases drug polarity 
new chemically reactive group permits conjugation 
cytochrome P450
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13
Q

phase 2

A 
conjugation 
further increases polarity 
adds endogenous products 
results in inactive products 
glucuronidation
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14
Q

drug metabolism excretion

A 
renal 
faeces - bile 
lungs
sweat/tears
milk, saliva
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15
Q

ALT

A 
alanine aminotransferase 
liver enzyme 
high conc. within hepatocytes 
increased levels in blood following hepatocellular injury 
marker for hepatocellular injury
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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

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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

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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

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19
Q

GGT and ALP elevated

A

biliary epithelial damage and bile flow obstruction

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20
Q

GGT and alcohol

A

elevated by large alcohol intake

may also be increased by drugs

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21
Q

AST

A

chronic liver disease

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22
Q

AST>ALT

A

cirrhosis and acute alcoholic hepatitis

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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

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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

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25
prothrombin time
time taken for blood to clot in absence of secondary causes, increased PT can indicate liver disease reduced production of clotting factors increases PT
26
bilirubin
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
27
pre-hepatic jaundice
excessive red cell breakdown overwhelms liver decreased conjugated, increased unconjugated normal urine normal stool
28
hepatocellular jaundice
``` liver looses conjugating ability cirrhosis compresses biliary tree can be mixed conjugated and unconjugated dark urine normal stool ```
29
post-hepatic jaundice
obstruction biliary drainage but bilirubin still conjugated in liver dark urine pale stool
30
Gilbert's syndrome
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
31
haemolytic anaemia
abnormal breakdown of red blood cells fatigue, SOB jaundice many causes
32
hepatocellular jaundice
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
33
obstrctive jaundice
gallstones strictures tumours congenital biliary atresia
34
chronic liver disease
> 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
35
decompensated cirrhosis
ascites jaundice variceal haemorrhage hepatic encephalopathy
36
liver injury
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
37
NAFLD
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
38
NAFLD history
fatigue LUQ pain alcohol, drugs, sexual activity obesity
39
NAFLD diagnosis
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
40
NAFL simple steatosis
``` 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 ```
41
NASH
``` non alcoholic steatohepatitis steatosis and inflammation and scarring diagnosed liver biopsy risk of progression to cirrhosis mallory bodies ballooning treatment - weight loss, exercise ```
42
alcohoilc liver disease
increased release and synthesis of fatty acids and TAGs in hepatocytes acetaldehyde responsible for damage involves pro-inflammatory cytokines, oxidative stress, lipid peroxidation
43
ALD history
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
44
ALD diagnosis
``` may be asymptomatic liver screen to rule out other causes LFTs USS, CT, MRI liver biopsy ```
45
ALD treatment
no alcohol corticosteroids may be used in acute inflammation transplant
46
ALD complications
``` acute liver failure cirrhosis hepatocellular carcinoma focal liver lesions hepatic encephalopathy oesophageal varices ascites thrombocytopenia malnutrition ```
47
cirrhosis
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
48
causes of cirrhosis
``` ALD NASH hep b and C autoimmune hepatitis cardiac cirrhosis ```
49
cirrhosis signs and symptoms
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
50
cirrhosis history
chronic alcohol abuse NAFLD chronic infection autoimmune or inherited disorders
51
cirrhosis diagnosis
liver biopsy - regenerating nodules of hepatocytes, fibrosis/connective tissue between these nodules liver screen to determine cause LFTs USS
52
compensated cirrhosis
asymptomatic stage LFTs show damage some back pressure signs may be visible to physician palmar erythema, clubbing, gynaecomastia, hepato/splenomegaly
53
decompensated cirrhosis
symptomatic - ascites, jaundice, variceal haemorrhage, easy bruising, hepatic encephalopathy
54
grading cirrhosis
``` child-pugh score A - well compensated B - functional compromise C - decompensated MELD ```
55
cirrhosis management
cannot be reversed healthy diet no alcohol increase calories - small frequent meals
56
cirrhosis symptom management
``` ascites - furosemide itch medication - colestyramine caution with paracetamol treat cause weight loss transplantation ```
57
liver transplant
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
ascites
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
ascites diagnosis
shifting dullness | USS
60
ascites treatment
``` treat underlying disease look for infection decrease salt intake no NSAIDs spironolactone first line loop diuretics paracentesis TIPSS or transplant ```
61
hepatorenal syndrome
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
spontaneous bacterial peritonitis
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
hepatic encephalopathy
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
hepatic encephalopathy symptoms
``` liver flap confusion non-coordination/shaking drowsiness/coma slurred speech siezures cerebral oedema ```
65
hepatic encephalopathy treatment
lactulose | antibiotics - neomycin, rifaximin
66
acute liver failure
any insult to liver causing damage in previously normal liver < 6 months causing encephalopathy and impaired protein synthesis
67
acute liver failure clinical features
``` non jaundice lethargy, arhtlargia N&V, anorexia RUQ pain itch ```
68
acute liver failure diagnosis
``` physical exam - jaundice, ascites history infections, alcohol, pregnancy mental changes coagulopathy abnormal LFTs ```
69
acute liver failure investigations
``` alcohol drugs - paracetamol, over the counter, herbal, supplements possible toxins LFTs USS virology investigation of chronic liver disease rarely biopsy ```
70
acute liver failure treatment
``` rest 3-6 months recovery fluids no alcohol increase calorie intake regular observation monitor and supplement K, PO4, Mg ```
71
acute liver failure causes
``` viral hep A-E, CMV, EBV, toxoplasmosis drugs - paracetamol chock liver cholangitis alcohol malignancy Budd Chiari acute fatty liver of pregnancy cholestasis pregnancy ```
72
NSAIDs
decrease renal PGE synthesis worsen renal impairment bu increasing renal vasoconstriction and sodium retention increase risk of hepatorenal syndrome
73
opiates
increased levels in blood due to decreased metabolism | increases risk of respiratory depression
74
diuretics
``` furosemide - decreases IV volume, hypokalaemia, hepatorenal syndrome #thiazide - same as furosemide spiralactone - combats secondary aldosteronism ```
75
hepatitis A
``` most common viral hepatitis transmission faecal oral associated with poor sanitation and overcrowding high risk - gay men, PWID acute infection ```
76
hepatitis A clinical presentation
systemic upset - nausea and anorexia jaundice, most infectious just before jaundice hepatic jaundice vomiting and altered mental state - hospital admission enlarged liver, splenomegaly
77
hepatitis A investigations
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
hepatitis A management
stop alcohol consumption when acutely unwell | supportive treatment
79
hepatitis E
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
hepatitis E clinical presentation
nausea and anorexia jaundice vomiting altered mental state enlarged liver, splenomegaly
81
hepatitis E investigations
``` viral RNA (HEV RNA) can be detected by PCR in the stool or serum ELISA for IgG/IgM HEV ```
82
hepatitis E management
stop alcohol consumption | supportive treatment
83
hepatitis B transmission
bone - sex baby blood if infected in infancy infection is more likely to become chronic
84
people with increased risk of hepatitis B
``` born in areas of high prevalence multiple sex partners men who have sex with men PWIDs children of infected mums ```
85
hepatitis B clinical presentation
``` 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
hepatitis B investigations
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
hepatitis B prognosis
self resolving most people full recovery chronic infection prognosis depends on age
88
hepatitis B management
symptomatic constant HBV marker monitoring antivirals - antecavir, tenofovir, suppress not cure
89
controlling hepatitis B
vaccination minimise exposure post exposure prophylaxis
90
hepatitis D
a parasite of a parasite only found in those with hepatitis B infection exacerbates a hep B infection
91
hepatitis C
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
hepatitis C investigations
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
hepatitis C management
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
chronic viral hepatitis
caused by HBV and HCV spontaneous cure in chronic HBV is not uncommon no spontaneous cure in chronic HCV
95
chronic hepatitis virus outcomes
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
when to treat chronic viral hepatitis
HBV - raised ALT and high HBV DNA | HCV - chronic hep C is always treated right away
97
management of chronic HBV
perginterferon alpha-2a first line tenofovir disoproxil second line entercavir can be second line instead
98
management of chronic HCV
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
autoimmune hepatitis
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
autoimmune hepatitis clincal features
hepatomegaly jaundice signs of chronic liver disease may present similar to acute on hepatitis
101
autoimmune hepatitis investigations
``` 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
autoimmune hepatitis management
corticosteroids and azathioprine combined gradually reducing steroids may eventually need a liver transplant
103
benign hepatic tumours
haemangioma focal nodular hyperplasia adenoma liver cysts
104
haemangioma
most common liver tumour hypervascular tumour small mass contained within a capsule with clear borders usually asymptomatic
105
haemangioma management
diagnosis US - echogenic spot which is well demarcated CT - venous enhancement from periphery to centre MRI - high intensity area no treatment
106
focal nodular hyperplasia
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
FNH investigations
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
hepatic adenoma
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
hepatic adenoma investigations
``` US - filling defect CT - diffuse arterial enhancement MRI - hypo/hyper intense lesion FNA - may be required cold on sulphur colloid scan ```
110
hepatic adenoma treatment
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
malignant hepatic tumours
primary tumours are rare - hepatocellular carcinoma, fibro-lamellar carcinoma secondary tumours are more common - multiple lesions, metastases - colon, pancreas, stomach, breast, lung
112
hepatocellular carcinoma
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
hepatocellular carcinoma pathology
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
clinical features of HCC
``` 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
investigating suspected HCC
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
HCC treatment
``` resection is the first choice liver transplant local ablation TACE - transarterial chemoembolisation systemic therapies - sorafenib, kinase inhibitor ```
117
fibro-lamellar carcinoma
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
cystic lesions
simple cyst hysatid polycystic liver disease pyogenic or amoebic abscesses
119
simple cyst
liquid collection lined by epithelium solitary - so no biliary tree usually asymptomatic - RUQ pain, fever
120
simple cyst investigation
USS fist line
121
simple cyst treatment
asymptomatic no treatment | symptomatic/uncertain diagnosis surgical intervention required
122
hydatid cyst
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
hydatid cyst investigation
AXR - mauy show cyst calcification US/CT check for anti-echinococcus antibodies
124
hydtid cyst management
surgery is most common albendazole - reduce size drained using PAIR
125
polycystic liver disease
caused by embryonic ductal plate malformation | three types - von meyenburg complexes, polycystic liver disease, AD polycystic kidney disease
126
von meyenburg complexes
benign cystic nodules throughout liver originate in the peripheral biliary tree asymptomatic
127
polycystic liver disease presentation
abdominal pain abdominal distention may be atypical symptoms may be signs of liver failure if there is severe disease
128
polycystic liver disease investigations
gene studies CT kidney function tests
129
polycystic liver disease treatment
aim to halt cyst growth surgical - aspiration and liver transplantation pharmacological therapy somatostatin analogues
130
liver abscess
can be pyogenic or caused by Protozoas
131
liver abscess presentation
``` high fever abdominal pain nausea and vomiting jaundice pleural rub in lower right chest malaise ```
132
liver abscess investigations
``` check for leucocytosis CXR - raised right hemi-diaphragm US CT echocardiogram ```
133
liver abscess management
initial empiric board spec antibiotics - amoxicillin, metronidazole, gentamicin IV aspiration/drainage operation if no clinical improvement
134
haemochromatosis
an inherited disease characterised by excess iron deposition in the liver as well as other organs autosomal recessive inheritance pattern symptomatic 20-40g
135
haemochromatosis clinical features
``` classic triad - bronze skin pigmentation, hepatomegaly, diabetes mellitus cardiac arrhythmias and heart failure liver fibrosis/failure joint pain hypogonadism ```
136
haemochromatosis investigations
serum iron elevated >30 in most cases LFTs often normal biopsy MRI
137
haemochromatosis management
venesection | avoid iron rich food
138
Wilson's disease
autosomal recessive disorder leading to reduced ceruloplasmin defect in copper transorting and excretion into bile
139
Wilson's disease symptoms
Kayser-fleisher rings signs of liver disease CNS issue - tremor, involuntary movements
140
Wilson's disease investigations
urinary copper increased | serum copper and ceruloplasmin usually reduced
141
Wilson's disease management
penicillamine | nausea, rash, haematuria

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