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phase 2a > liver > Flashcards

liver Flashcards

1
Q

ACUTE liver failure is liver failure without _______, with _________pathy and _______ _______pathy, within ___ weeks of onset

A

without chronic liver dis, coagulopathy, hepatic encephalopathy, 28

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2
Q

what is the most common cause of acute liver injury?

A

drugs eg alcohol, paracetamol, antidepressants, cocaine, ecstasy

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3
Q

4 infective causes of acute liver injury?

A

hep a, hep b, cmv, ebv, malaria, yellow fever

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4
Q

why is there systemic multi-organ failure in acute liver failure?

A

The hepatocytes die by necrosis. This means that the liver cannot clear the toxins anymore, so there is an inflammatory response around the body.The systemic inflammatory response causes vasodilation and hypo perfusion, which injures the rest of the organs through ischaemia

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5
Q

some symptoms of acute liver failure?

A

asterixis, flapping tremour, fatigue, jaundice, malaise, bleeding, bruising, haptatic encephalopathy, ruq pain, hypoglycaemia, pear drops smell (fetor hepaticus)

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6
Q

what would high ALT mean?

A

hepatocyte damage

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7
Q

what would high AST mean?

A

alcohol

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8
Q

what would high ALP mean?

A

bile duct pathology - if GGT is also raised

bone pathology - if everything else is normal

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9
Q

what would high GGT mean?

A

bile duct, obstruction, alcohol, phenytoin

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10
Q

what would the clottting profile look like in acute liver failure?

A

low albumin
high inr
high prothrombin time

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11
Q

what

what imaging would you use in liver failure?

A

ultrasound to see liver size

doppler to see hepatic and portal veins

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12
Q

two supplements you would want to give in acute liver failure?

A

thiamine and folate

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13
Q

what can you give for seizures in acute liver failure

A

phenytoin

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14
Q

5 aetiologies of chronic liver dis?

A 
alcohol
inf (hep b/c)
alpha 1 antitrypsin def
wilsons 
autoimmune 
cholangitis 
ischaemia 
drug
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15
Q

5 pathophysiological/histological features of chronic liver disease?

A 
steatosis
bands of cirrhosis/fibrosis
regenerative nodulues
hepatitis
balooned hepatocytes
irreversible remodelling
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16
Q

5 signs of chronic liver dis?

A 
sarcopenia
coagulopathy
ascites
hepatomegaly
jaundice
caput medusa 
spider naevi
palmar erythema
asterixis
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17
Q

5 symptoms of chronic liver failure?

A 
haematemesis
fatigue 
itching 
bruising 
anorexia 
confusion
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18
Q

what abnormal lfts are typical of chronic liver failure?

A

high bilirubin
low albumin
high pt

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19
Q

how do you assess the amount of fibrosis in the liver?

A

transient elastography

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20
Q

what is gold standard for chronic liver disease?

A 
liver biopsy 
(but is rarely done cos spenny)
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21
Q

what does fbc in chronic liver dis show?

A

thrombocytopenia

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22
Q

how to treat hepatic encephalopathy?

A

laxatives

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23
Q

how to treat ascites?

A

aldosterone antagonist or paracentesis

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24
Q

how to treat spontaneous bacterial peritonitis?

A

abx

albumin solution

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25
Q

cholecystitis vs cholangitis?

A 
cholecystitis = inflam of the gallbladder (usually because it is blocked at the neck by a stone)
cholangitis = inflam of the billiary tree tubes  - gallstones, ercp, cholangiosarcoma
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26
Q

3 aetiologies of gall stones?

A

too much cholesterol
poor bladder emptying
rbc turnover

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27
Q

simply, what’s in a gallstone?

A

cholesterol and bile salts

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28
Q

what is billiary colic?

A

intermittent pain caused by temporary obstruction

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29
Q

what is acalculous cholecystitis?

A

inflammation of the gallbladder not caused by a stone

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30
Q

where is the pain in gallbladder pathology?

A

ruq

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31
Q

symptoms of biliary colic?

A

intermittent ruq/epigastric pain
worse after eating
nausea

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32
Q

symptoms of acute cholecystitis?

A

severe constant ruq pain
worse on inspiration
referred to shoulder c3,4, 5 if severe
murphys sign

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33
Q

symptoms of ascending cholangitis?

A

ruq pain
jaundice, dark urine, itching, coagulopathy
rigors
fever

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34
Q

how can you treat cholecystitis?

A

ercp to remove stones
remove the gallbladder if stones are reoccuring
drain the gallbladder

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35
Q

4 pathophysiological effects of alcohol on the liver?

A

uses up NAD and creates NADH
NADH decreases gluconeogenesis and increases fatty acid oxidation
free radicals produced
activates kupffer ells which release TNFa and ROS
oxidative stress leads to more inflammation
end result of all the inflammation is fibrosis

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36
Q

3 stages of alcoholic liver disease and are they reversible?

A
  1. alcohol related fatty liver - reverses in 2 weeks
  2. alcoholic hepatitis - reverses in 2 months
  3. cirrhosis - not reversible
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37
Q

presentation of alcoholic fatty liver?

A

vague or no symptoms

hepatomegaly

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38
Q

5 clinical presentations of hepatitis/cirrhosis?

A 
hepatomegaly
jaundice
spider naevi
caput medusa 
asterixis 
clubbing 
oedema 
ascites 
bruising 
high temp 
palmar erythema 
gynaecomastia
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39
Q

what do you see on an fbc in alcoholic liver dis?

A

increased cell volume (macrocytic anaemia)

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40
Q

what do you see in alcoholic liver disease, on LFT?

A

raised AST
slightly raised ALT (AST>ALT)
raised GGT
if severe: low albumin, high PT, high bilirubin

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41
Q

3 changes you see on ultrasound, in alcoholic liver dis?

A

fatty
cirrhosis
ascites
changes in blood vessels

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42
Q

why might you do an endoscopy in liver dis?

A

to look for oesophageal varices

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43
Q

two screening question systems for alcoholism?

A

CAGE

AUDIT

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44
Q

management of alcoholic liver disease?

A

drinking cessation [supported]
high thymine, high protein diet
short period of steroids
transplant

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45
Q

aetiology of pancreatitis? (5)

A 
i - iatrogenic - ERCP is most common iatrogenic cause 
g - gallstones - most common
e - ethanol
t - trauma 
s - scorpion bite
m - measles/mumps/mycoplasma
a - autoimmune
s - steroids
h - hypercalcaemia 
e - ERCP
d - drugs eg valproate
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46
Q

aetiology of chronic pancreatitis? (3)

A

repeated acute
alcohol
CF
tumours

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47
Q

3 enzymes secreted by the pancreas?

A

amylase, lipase, trypsin

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48
Q

2 pathophysiological effects of pancreatitis?

A

hyperglycaemia

malabsorption

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49
Q

what is the pain like in pancreatitis?

A 
severe
generalised or upper abdo 
radiating to the back 
worse after eating 
relieved by sitting forward
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50
Q

clinical presentations of pancreatitis?

A 
cullens/fox sign
grey-turner syndrome 
abdo distention 
steatorrhoea 
nausea/vom 
diabetes-like/hyperglycaemia
weight loss 
jaundice
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51
Q

some blood tests you might do in pancreatitis?

A 
serum amylase (not specific but 1st line)
serum lipase 
hba1c (esp if chronic)
igG4 - if autoimmune suspected 
LFT - AST suggests alcohol is a cause
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52
Q

what imaging for pancreatitis?

A

USS

MRCP to look for gallstones

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53
Q

an example of a pancreatic enzyme replacement? what could you give it with?

A

creon

a PPI

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54
Q

What U&E disturbance is there in cirrhosis?

A

hyponatraemia

high urea and creatinine

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55
Q

on an USS what would you see in cirrhosis?

A 
nodules
corkscrew arteries 
large portal vein 
ascites 
splenomegaly
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56
Q

3 complications of cirrhosis

A

portal hypertension
varices
ascites

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57
Q

where does the portal vein drain from?

A

superior mesenteric and splenic veins

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58
Q

3 common places for varices to form?

A

varices form where the portal circulation meets the systemic circulation, eg:

  • gastro oesophageal junction
  • ileo caecal junction
  • rectum
  • umbilical vein (forms caput medusae)
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59
Q

management of stable varices?

A
  • propanolol
  • elastic band ligation
  • TIPSS: shunt blood from portal –> systemic circ , if refractory to other treatments
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60
Q

management of bleeding varices?

A

fluids
elastic band ligation/schlerotherapy/blakemore tube
-vasopressin analgue eg terlepressin to vasoconstrict
clotting factors and vit K
abx for peritonitis

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61
Q

what is ascites?

A

accumulation of fluid in the peritoneal cavity

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62
Q

non liver causes of ascites? (3)

A

peritonitis
water retention
cardiac failure

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63
Q

in portal hypertension, _____ is low, so the ________ releases _______ which worsens ascites

A

renal perfusion / kidney/ renin

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64
Q

transudative vs exudative ascites & some causes of each?

A

transudative: low protein in the exudate (below 25); caused by portal htn, malnutrition, fluid retention
exudative: high protein - malignancy and pregnancy

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65
Q

what does the SAAG (serum albumin ascites gradient) tell you?

A

if it is more than 11, it is transudative ascites, eg caused by portal hypertension

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66
Q

what hormone increases gallbladder contraction?

A

CCK in response to fatty food

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67
Q

what LFT result is the best indicator of liver function in chronic disease?

A

albumin

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68
Q

what is gilbert’s syndrome?

A

gGT deficiency, high bilirubin, jaundice, other LFTs normal, autosomal recessive

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69
Q

raised bilirubin and jaundice but normal LFTs suggests..

A

gilbert’s

haemolytic anaemia

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70
Q

if the urine is dark and the stools are pale the cause is most likely..

A

post hepatic obstruction

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71
Q

how does haemolytic anaemia affect jaundice/stools/urine?

A

there is yellow skin but the pathology is not with the production of bile (so stools not pale) or excretion of it, so the stools and urine are normal

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72
Q

in biliary obstruction, are there high levels of conjugated or unconjugated bilirubin?

A

conjugated bilirubin is high

unconj and hb are normal

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73
Q

which bacteria is associated with bloody diarrhoea, haemolysis, uraemia and anaemia?

A

ecoli 0157 h7

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74
Q

which bacteria is associated with RLQ pain and pork?

A

yersinia

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75
Q

some signs/symptoms of acute hepatitis?

A 
malaise
lethargy
myalgia
gi upset
jaundice
pale stools, dark urine 
tender hepatomegaly
76
Q

what hepatitis cannot be chronic?

A

A

77
Q

who gets hep D?

A

only when infected with hep B

78
Q

mode of transmission of hep A?

A

faecal oral

79
Q

what is significant about hep B?

A

bad if neonates get it, they develop a chronic infection
it is the only DNA virus, all the others are RNA
presents with jaundice

80
Q

which hepatitis causes neurological symptoms?

A

E

81
Q

which hepatitis has 2 phases of mild symptoms? what are those symptoms?

A

hep A
1 - mild - malaise/abdo pain
2 - jaundice

82
Q

3 causes of dysentery?

A 
dysentery = watery diarrhoea 
cholera 
e coli
clostridium perfringens
staph aureus 
giardia 
crypto 
bacillus cereus
83
Q

what blood test results would you see in c diff infection?

A

high crp
high wbc
low albumin

84
Q

5 reasons why you would culture diarrhoea?

A 
hypovolaemia 
dehydration 
for more than a week 
blood or mucus 
over 70
preg 
immunocomp 
ibd 
public health
85
Q

What is haaemachromotosis?

A

too much iron in the body, due to mutations in HFE protein, iron is deposited around the body resulting in organ damage

86
Q

how is haemachromotosis inherited?

A

autosomal recessive

87
Q

clinical presentation of haemachromotosis? (5)

A 
bronze patches on skin 
tiredness 
arthritis 
hair loss 
erectile dysfunction 
amenorrhoea 
poor cognition/mood
88
Q

haematinics in haemachromotosis?

A 
ferritin raised (not v specific)
transferrin raised (this is more specific)
89
Q

what do you use to see iron in heart and liver in haemachromotosis?

A

mri

90
Q

treatment for haemachromotosis?

A

venesection weakly, to remove the iron

91
Q

3 complications of haemachromotosis?

A 
t1 diabetes 
cirrhosis
hypothyroidism 
hypogonadism 
cardiomyopathy
chondrocalcinosis
92
Q

what is wilsons disease?

A

too much copper

due to a mutation in the copper binding protein ATP7B (which removes copper from the liver)

93
Q

how is wilsons disease inherited?

A

autosomal recessive

94
Q

5 complications/presentations of wilsons disease?

A 
liver cirrhosis
neuro problems eg concentration, dystonia, incoordination, parkinsonism
haemolytic anaemia
kidney dysfunction / acidosis
osteopenia
rings in eyes
95
Q

where is copper deposited in the brain to cause parkinsonism, how does the presentation differ to parkinsons?

A

basal ganglia

wilsons = symmetrical (parkinsons is not)

96
Q

what protein carries copper in serum, how specific is the test? what could you also test?

A 
caeruloplasmin 
not specific, low in cancer and inflam
24hr urine copper 
serum copper - low. free serum copper - high 
gold standard = liver biopsy
97
Q

management of wilsons disease?

A

copper chelation with penicillamine or trientene

98
Q

how is alpha 1 antitrypsin deficiency inherited?

A

autosomal recessive

99
Q

what two organs does alpha 1 antitrypsin affect?

A

lung (emphysaema) and liver (cirrhosis)

100
Q

what is the pathophysiological effect of alpha 1 antitrypsin deficiency?

A

alpha 1 antitrypsin breaks down neutrophil elastase
without it neutrophil elastase is overractive
damage to connective tissue
–> fibrosis

101
Q

clinical presentations of liver alpha 1 antitrypsin deficiency?

A

liver cirrhosis

the emphysaema develops first so they will already have COPD/barrel chested with cough and dyspnoea

102
Q

what is the test for alpha 1 antitrypsin deficiency?

A 
serum alpha 1 antitrypsin levels
liver biopsy - acid schiff pos 
ct chest
genetic testing 
deranged LFT `
103
Q

primary vs secondary peritonitis?

A 
primary = spontaneous bacterial peritonitis (e.coli, chlamydia, neisseria)
secondary = bile, barium, trauma
104
Q

what is spotaneous bacterial peritonitis?

A

infection of the peritoneal fluid

105
Q

two conditions where transmural bacterial peritonitis could happen?

A

pancreatitis, ischaemic bowel

106
Q

what is the pain like in peritonitis?

A

severe
generalised at first, may be localised if it affects the parietal peritoneum (to shoulder if diaphragm affected)
guarding
relieved by putting hands on abdo, and stretching out
worsened by moving

107
Q

when bowel sounds cease in peritonitis, what has happened?

A

paralytic ileus - bowel movements inhibited by pain

108
Q

what is a late presentation of peritonitis?

A 
circulatory collapse
hippocratic face 
thready pulse, cold peripheries 
paralytic ileus 
still in pain
109
Q

what investigations to diagnose peritonitis?

A

supine x ray - see dilated bowel
erect x ray - see subdiaphragmatic gas
ascitic tap
blood culture

110
Q

what differentials should you exclude in peritonitis and how?

A

preg -hcg
pancreatitis - aylase
mi - ecg / troponin
lactate, crp and wcc will also be raised

111
Q

Management of peritonitis?

A

abx
fluid
peritoneal lavage
analgaesia

112
Q

what are the two most common primary liver cancers?

A
  1. hepatocellular carcinoma

2. cholangiocarcinoma (of the bile duct)

113
Q

what are liver hemangiomas?

A

benign, asymptomatic tumours of blood vessels/birthmark

114
Q

what is focal nodular hyperplasia & some important features?

A

nodule of scar tissue in liver
benign, no malignant potential
more in women, associated with oestrogen

115
Q

a major risk factor for hepatocellular carcinoma?

A

cirrhosis

which may have been caused by hep B/C, alcohol, faty liver dis, HBV ..

116
Q

3 risk factors for cholangiosarcoma?

A

primary sclerosing cholangitis
IBD
Hep B
parasites

117
Q

what is the presentation of cholangiosarcoma?

A

painless jaundice

118
Q

some presentations of hepatocellular carcinoma?

A 
generally late / asymptomatic 
weight loss 
ruq pain 
enlarged, irregular liver 
n/v
jaundice 
bruit over liver
119
Q

a tumour marker for hepatocellular carcinoma?

A

alpha fetoprotein

120
Q

a tumour marker for cholangiocarcinoma?

A

CA19-9

121
Q

best imaging / investigation for cholangiosarcoma?

A

ERCP

122
Q

A drug that can be used in late stage liver cancers?

A

kinase inhibitors eg sorafenib

123
Q

what type of cancer is pancreatic cancer?

A

adenocarcinoma

124
Q

where is the most common location in the pancreas for pancreatic cancer to develop?

A

in the head of the pancreas

125
Q

what kind of jaundice does pancreatic cancer cause & why? what are the symptoms of this?

A

obstructive jaundice, because as the tumour grows it blocks the pancreatic duct
painless
pale stools and dark urine

126
Q

4 presentations of pancreatic cancer?

A

obstructive painless jaundice with pale urine and dark stools
itching
weight loss
upper abdo/back pain
mass
new or worsening diabetes
n/v
courveissers - painless obstructive jaundice + palpable gallbladder means gallstones are unlikely
troussea sign – migratory thrombophlebitis - blood clots that make lumps under the skin = pancreatic malignancy

127
Q

what investigations could you do in ?pancreatic cancer?

A

CA19-9 - raised but not specific
CT T.A.P
M/ERCP - to stent the bile duct and also take a biopsy

128
Q

Surgery for pancreatic cancer?

A

pancreatectomy
whipples
ercp for symptomatic management

129
Q

ERCP vs MRCP?

A

ERCP = endoscopic retrograde cholangiopancreatography
MRCP = magnetic resonance cholangiopancreatography
ERCP is more invasive but better diagnostically

130
Q

what does a hernia feel like (to the patient)?

A

soft lump
aching
pulling/dragging sensation

131
Q

what is an incarcerated hernia? what can happen as a result?

A

becomes irreducible and a portion of bowel is stuck through the hole
obstruction –> vomiting, pain, constipation
strangulation –> necrosis

132
Q

what sort of hernias do not need to be managed?

A

those with a wide neck - there is a lower risk of strangulation/herniation

133
Q

what are the two kinds of inguinal hernias?

A

direct - through the posterior wall of the inguinal canal. caused by heavy lifting. do not reduce when you press the inguinal ring. wide neck, usually unproblematic

indirect - through the deep inguinal ring into the inguinal canal. congenital. can strangulate. reduce when you press the inguinal ring

134
Q

where is a femoral hernia?

A

at the top of the thigh
abdominal contents move through the femoral ring into the femoral canal
small neck - complications

135
Q

who gets umbilical hernias?

A

neonates and old people
in neonates they resolve by themselves
in old people is because of weakening of the abs

136
Q

where is a spigelian hernia?

A

between the rectus abdominus and linear semilunaris

137
Q

who gets obturator hernias?

A

old women – due to pelvic floor damage

formed by herniation through the obturator foramen at the base of the pelvis

138
Q

what hernias can present as dyspepsia/nausea?

A

hiatus hernias – due to herniation of stomach into diaphragm

139
Q

what hernias present with lower groin or thigh pain and a positive howship-rhomberg sign on internal rotation of the hip?

A

obturator hernias

140
Q

what hernias present with non specific abdo pain and commonly cause complications?

A

spigelian hernias (between the rectus abdominus and linear semilunaris)

141
Q

how do you get hepatitic encephalopathy?

A

ammonia - usually metabolised by liver
if liver not working ammonia crosses BBB
ammonia –> glutamate
also draws water in –> cerebral oedema

142
Q

why do you get gynaecomastia in liver dis?

A

the liver is involved in oestrogen regulation

143
Q

what is leukonychia?

A

white nails
due to low protein (albumin)
which can indicate liveer failure

144
Q

two examples of autoimmune liver conditions?

A

primary biliary cholangitis - esp females

primary scherosing cholangitis

145
Q

if someone with liver failure was actively bleeding what blood product would you give them?

A

fresh frozen plasma

146
Q

what is the treatment for hep C?

A

ribavirin

147
Q

what is the treatment for hep b?

A

first line is pegylated interferon alpha 2a

second line is tenofovir

148
Q

what happens in paracetamol overdose?

A

glucoronidation and sulphation pathways are overwhelmed –> produce NAPQI by a CYP
NAPQI is fine if it is added to glutathione, then it can be excreted
in overdose you run out of glutathione –> NAPQI is toxic

149
Q

presentation of paracetamol overdose?

A

n/v
ruq pain
anorexia

150
Q

treatment of paracetamol overdose?

A

n-acetylcysteine

activated charcoal, if presents within an hour

151
Q

what is steatosis?

A

harmless build up of fat in the liver cells

can go on to develop steatohepatitis, which is what can cause fibrosis/cirrhosis

152
Q

what is wernicke-korsakoff encephalopathy?

A

liver associated
ataxia, confusion, nystagmus, memory impairment
treat with iv thymine / vit b1

153
Q

what is budd-chiari syndrome and what does it cause?

A

occlusion of liver veins –> portal hypertension

154
Q

what does TIPSS stand for?

A

transjugular intrahepatic portal systemic shunt

155
Q

what is the most common bacteria in spontaneous bacterial peritonitis & what would be the treatment?

A

e.coli

cefotaxime

156
Q

where is the ampulla of vater?

A

between the pancreatic duct and the common bile duct

157
Q

what is the pathophysiology of primary sclerosing cholangitis?

A

fibrosis and strictures of the bile ducts
= reduced flow of bile
= bile backs up into liver – hepatitis – cirrhosis

158
Q

what is the epidemiology of primary sclerosing cholangitis?

A

male
30-40
strong association with ulcerative colitis

159
Q

presentation of PSC?

A 
jaundice 
chronic RUQ pain
fatigue
itching
hepatomegaly
signs of cirrhosis
160
Q

investigations for PSC? 3

A

LFT - ALP high, bilirubin may be high, others increase as condition progresses
autoantibodies eg ANA, pANCA, anti-cardiolipin - don’t confirm anything but suggest autoimmune cause
MRCP - gold standard

161
Q

in gilberts syndrome, what are the urine and stools like?

A

even though there is jaundice, the urine and stools are normal, as this is prehepatic jaundice

162
Q

in pre hepatic jaundice, the urine is _____ and the stools are _____

A

normal

normal

163
Q

in intrahepatic jaundice, the urine is ____ and the stools are ____

A 
urine = dark
stools = normal
164
Q

in post hepatic jaundice, the urine is ____ and the stools are _____

A

dark urine

pale stools

165
Q

what is the pathophysiology of primary billiary cirrhosis?

A

autoimmune attack of bile ducts
= build up of bile, cholesterol and bilirubin as they cannot get to intestines
– put into blood instead

166
Q

what is the epidemiology of primary biliary cirrhosis?

A

women
autoimmune esp coeliac, hypothyroid
rheum eg RA, Sjogrens

167
Q

what is the presentation of PBC?

A 
itch
jaundice
pale stool
abdo pain 
fatigue
xanthoma/xanthelasma (cholesterol deposits)
168
Q

what is the test for PBC?

A 
LFT - ALP raised first
anti-mitochondrial antibodies 
ANA - not sensitive or specific 
ESR
IgM raised
169
Q

what is the treatment for PBC and PSC?

A

Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
Colestyramine is a bile acid sequestrate
liver transplant
consider immunosupression

170
Q

what is the best investigation to confirm ascending cholangitis?

A

contrast enhanced dynamic CT

171
Q

what is the treatment for autoimmune hepatitis?

A

prednisolone - 1st line

+ azathiopurine

172
Q

what is first line treatment for alcohol withdrawal?

A

chlordiazepoxide

173
Q

what is the most common cause of liver cirrhosis?

A

alcohol

174
Q

what is the name of the rings in the eyes in wilsons disease?

A

kayser-fletcher rings

175
Q

which 2 hepatitises have faecal-oral transmission?

A

A and E

176
Q

what is Murphys sign and what does it show?

A

pain on inspiration when you palpate the right subcostal area
= cholecystitis

177
Q

cullens and grey turners signs indicate ____

A

acute pancreatitis

178
Q

what is Charcot’s (liver) triad?

A

fever + rigors
jaundice
RUQ pain

typical of ascending cholangitis

179
Q

marker for testicular seminoma?

A

ALP

180
Q

Marker for choriocarcinoma?

A

hCG

choriocarcinoma = cells left behind from pregnancy become cancerous v rare
or a v rare type of testicular cancer

181
Q

what is testicular teratoma like at biopsy?

A

lots of different cells

182
Q

mallory bodies are associated with?

A

alcoholic liver damage

183
Q

if the serum ascites-albumin gradient is low what is the cause?

A

low gradient = exudative

eg inflam, infection

184
Q

what is the difference between the transmission of hep B and hep C?

A

B = sex

C = needles

185
Q

why is there decreased immunity in chronic liver disease?

A

liver does protein synthesis so poor liver function = decreased clotting factors, complement, opsonisation etc
bowel wall may be more permeable
liver regulates immune response

phase 2a (10 decks)

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