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ailmentary > Jaundice and liver failure > Flashcards

Jaundice and liver failure Flashcards

1
Q

what is the function of bile

A

cholesterol homeostasis - increase/decrease conc
absorption and digestion - of lipids by emulsification and solubisation, and vitamins ADEK
toxin excretion - eliminated in faeces, endogenous/exogenous eg cholesterol metabolites, adrenocortical, steroid hormones

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2
Q

how much of bile is water

A

97%

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3
Q

substances that are secreted into bile

A

adrenocortical and other steroids
drugs/xenobiotics
cholesterol
alkaline phosphatase

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4
Q

where does bile come from

A

secret 1/2L/day
hepatocytes secrete primary bile - reflective of conc of blood in sinosoids - 60%
cholangiocyts - modify bile, reabsorb as required of sugar and acid, secretion of HCO3- and cl-, IgA exocytosed into bile -mmune func - 40%

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5
Q

describe the pathway of the biliary tree

A

starts in bile canaliculi exit to hepatocytes - prouce biule
drain into suctiles
drain into small bile ducts - intralobular
drain into interlobular bile ducts
merge to form L and R hepatic ducts
convege to common hepatic duct
connects to cystic duct
connects to gall bladder (not part of tree)
merge of common hepatic duct and cystic duct form common bile duct which extend to duodenum
at distal end pancreatic duct joins and vessel is called ampulla of Vater
opens to medial wall of duodenum at duodenal papilla

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6
Q

what happens to the bile as it goes through the biliary tree

A

alters pH
H2O drawn in to bile - osmosis paracellularly
luminal glucose and organic acids are reabsorbed
HCO3- and Cl- actively secreted into bile by CFTR
cholangiocytes contribute IgA by exocytosis into bile

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7
Q

what governs the rate of the bile flow

A

biliary transporters on apical surface of hepatocytes and cholangiocytes
they perform the excretion of bile salts and toxins
pump bile acid in and out of bile
change cl, H and pH -> make bile more fluid
genetic - dysfunction = cholestasis

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8
Q

what are the main bile transporters

A

bile salt excretory pump (BSEP)
MDR related proteins (MRP1, MRP3)
products of the familial intrahepatic cholestasis gene (F1C1) and multidrug resistant genes (MDR1 MDR3)

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9
Q

describe the bile salt excretory pump

A

controlled by ABCB1 gene
AT of bile acids into bile across canalicular membrane
secretion of acids

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10
Q

describe MDR1

A

mediate canalicular excretion of xenobiotics and cytotoxins

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11
Q

describe MDR3

A

encodes phospholipid transporter

that translocates phosphatidylcholine from inner to outer leaflet of canalicular membrane

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12
Q

what are bile salts

A

component of bile
cholic acid and chenodeoxycholic converted to deoxycholic acid and lithocolic acid (secondary acids) by colonic bacteria
amphipathic = hydophobic and philic region

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13
Q

function of gut bacteria on bile salts

A

convert primary bile salts to secondary
cholic - deoxycholic acid
chenodeoxyxholic - lithocolic acid

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14
Q

function of bile salts

A

reduce fat surface tension
emulsify fat for digestion/absorption
micelles = larger surface area

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15
Q

structure of micelles

A

amphiphilic
philic - out
phobic - in
FFA and chol - in

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16
Q

problem with bile salts

A

detergent like -> cytotoxic in high conc
= not reabsorbed = gut irritation = diarrhoea
OR intrahepatic cholestasis of pregnancy = damage foetus - cardiac

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17
Q

describe the actions of the sphincter of Oddi

A

when don’t eat - closed - bile goes to cystic duct to gall bladder
when eat - gastric contents entering duodenum trigger release of cholecystokinin - sphincter relax - gall bladder squeeze - bile inter duodenum

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18
Q

describe the enterohepatic circulation

A

from liver in bile -> gut -> intestine -> liver

substances cycle between gut and liver by cont reabsorption in gut - carriage in portal to liver and hepatic secetion inyo bile canaliculi
recycle bile salts - reabsorbed from the portal circulation into liver by active transport
drugs might get reabsorbed - increasing their half life

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19
Q

describe the enterohepatic circulation of bile salts

A

absorbed bile salts go to liver via portal vein -> liver -> re-excreted as bile
95% reabsorbed from terminal ileum
by Na/bile salt co-transport Na/K ATPase system
5% converted to secondary bile acids in colon - deoxycholate absorbed, 99% lithocholate excreted

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20
Q

comparison between gall bladder bile and hepatic duct bile

A

gall bladder bile - more acidic, higher % solids and conc of bile salts

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21
Q

importance of gall bladder

A

aids digestion but not essential

basal level anyway if have cholecystectomy

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22
Q

what is bilirubin, and what is it made of

A

water insoluble, yellow pigment

from Hb breakdown in blood
catabolism of other haem proteins
ineffective erythropoiesis

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23
Q

describe the excretion of bilirubin

A

BR bound to albumin -> dissociate in liver -> free BR enter hepatocyte -> bind to cytoplasmic proteins -> is conjugated to glucuronic acid by glucuronyl transverase -> BR-diglucuronide and UDP -> active transport into canaliculi -> GI tract

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24
Q

total BR =

A

unconjugated (free) BR + conjugated BR

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25
Q

why is bile conjugated

A

it is more soluble

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26
Q

describe urobilinogens

A

water soluble
derived from bile by GI bacteria
half reabsorbed -> liver -> kidney -> excretion
some urobilinogens passed as stool as stercobilinogeen

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27
Q

why is faeces brown

A

stercobilinogen from urobilinogen is oxidised to stercobilin - brown

28
Q

what is jaundice

A

yellow discolouration of sclerae and skin because of rasied bilrubin
detecatble when bilrubin is >40umol/L

29
Q

how does cholestasis cause jaundice

A

less bile enters intestine - flow is slowed/stopped
= less excreted
failure of bile secretion or bile duct obstruction
intrahepatic cholestasis - hepatocellular swelling/ abnormalities at cellular level
extrahpatic cholestasis - obstruction of bile flow distal to canaliculi

30
Q

describe pre-hepatic jaundice

A 
cause: increased quality of BR from: 
haemolysis
transfusion
haematoma resorption - road accident where cells die quickly 
ineffective erythropoiesis

problem: more BR than downstream path can cope with, increase urobilinogen

type of BR: problem before reach liver = unconjugated

31
Q

describe hepatic/hepatocellular jaundice

A

cause: defective uptake, defective conjugation, defective BR excretion - because of liver failure: acute/fulminant from paracetamol OD, acute on chronic from Hep B/C, alcohol, autoimmune disease

type of BR - unconjugated

32
Q

describe post hepatic/obstructive jaundice

A

problem: defective transport of BR by biliary duct system eg biliary duct stones, HepPancBil malignancy, local LNpathy
BR increase - it is not taken to the gut = less stercobilinogen = less stercobilin = pale faeces
some bilirubin diverted to kidney to try and get rid of it - dark urine

type of BR - conjugated
confirm with MRI scan - see blockage

33
Q

summarise Gilbert’s syndrome

A

commonest congenital
autosomal recessive #
2-7% population

34
Q

type of BR in Gilbert’s syndrome

A

unconjugated

35
Q

cause of Gilbert’s syndrome

A

mutation coding for UDP-glucuronsyltransferase isoform 1A, reduce glucuronidation activity, reduce conjugation

36
Q

consequence of Gilbert’s syndrome

A

benign
can cause jaundice under triggers:
dehydration, fasting, exertion and iral illnss

37
Q

consequence of liver disease

A

lead to coma/death - multiorgan failure

38
Q

what is fulminant hepatic failure

A 
rapid development <8wks 
acute injury 
impaired sympathetic function 
encephalopathy 
previously normal liver or well compensated liver disease
39
Q

time frame for sub-fulminant hepatic failure

A

<6months

40
Q

cause of chronic liver failure

A 
Hep B or C 
alcohol 
fatty liver 
autoimmune 
genetic - Wilson's, haemachromatosis 
drug - methotrexate
41
Q

cause of acute liver failure

A 
paracetamol OD 
amanita phalloides 
bacillus cereus 
acute fatty liver disease of pregnancy
hepatic infarction 
HEV 
Budd-chiari 
Single Agent: Isoniazid, NSAID’s, valproate
Drug combinations: Amoxicillin/clavulanic acid, trimethoprim/sulphamethoxazole, rifampicin/isoniazid
Vascular Diseases
Ischaemic hepatitis, post-OLT hepatic artery thrombosis, post-arrest, VOD
Metabolic causes
Wilson’s disease, Reye’s syndrome
42
Q

results of liver disease

A 
encephalopathy (astrocyte) and cerebral oedema
hypoglycaemia
coagulopathy and bleeding  
increased suseptibilty to infection 
circulatory collapse 
renal failure
43
Q

causes of death in ALF

A 
Bacterial and fungal infections
Circulatory instability
Cerebral Oedema
Renal failure
Respiratory failure
Acid-base and electrolyte disturbance
Coagulopathy
44
Q

liver transplant

A 
for ALF - only useful intervention 
timing crucial 
dangerous 
expensive
immunosuppression
45
Q

how does alcohol cause liver disease

A

hepatotoxin
fatty change, alc hepatitis, cirrhosis
genetic and immunological mech

46
Q

early stage symptoms - liver failure (LF)

A 
Lethargy
Right upper quadrant pain
Pruritus – itchy skin
Malaise
Anorexia
47
Q

later symptoms

A 
Peripheral swelling
Confusion and somnolence
Vomiting of blood
Bruising
Abdominal bloating
48
Q

signs of liver disease

A

jaundice
spider naevi - because unable to met oestrogen = telangiectases: central arteriole ith radiating small vessels - distribution of SVC
loss of body hair - unable to met oestrogen
gynaecomastia - unable to met oestrogen - enlargement of male breast
testicular atrophy - unable to met oestrogen
palmar erythema - unable to met oestrogen - liver palms, at thena and hypothemar eminences
xanthelasma - sharply demarcated yellowish deposit of cholesterol under skin around eyelids
finger clubbing
puritis - itchy skin
dupuytren’s contracture - sign of alcoholic liver disease
ascites and dilated veins of abdomen
hepatomegaly
hepoatosplenomegaly
caput medusa - portal hypertension, distended and engorged paraumbilical veins - radiate from umbilicus across abdomen to join systemic veins

49
Q

cirrhosis

A

necrosis of liver cells
followed b progressive fibrosis and nodle formation
imapirment of func
distortion of the liver = portal hypertension

50
Q

aetiology of cirrhosis

A

alcohol
hep B and C
in response to chronic liver injury
liver biopsy to confirm disease

51
Q

micronodular cirrhosis

A

uniform, small noules 3mm

ongoing alcohol damage/bilary tract disease

52
Q

macronodular cirrhosis

A

nodules of variable size

following viral hepatitis

53
Q

hyperacute liver failure

A

encephalopathy occurs within 7 days of jaundice

54
Q

acute liver failure - encephalopathy

A

after 8-28 days of jaundice.

55
Q

subacute liver failure

A

encephalopathy occurs 5-12 weeks after the onset of jaundice.

56
Q

clinical features of acute liver failure

A 
jaundice 
CNS complications 
coagulopathy 
renal failure 
sepsis 
CV complications
metabolic complications
57
Q

sepsis

A

bacterial infection in 90% cases, fungal in 32% cases
present within 3 days of hospital admission
fever and high white cell count absent

58
Q

way to reduce sepsis

A

prophylactic IV antibiotic therapy in acute hepatic failure

59
Q

CV

A

reduction in peripheral resistance
reflec increase in CO to maintain bp
cardiac failure and hypotesion

60
Q

metabolic effects of LF

A

Hypoglycaemia and Hypoxia

61
Q

CNS effects of LF

A

hepatic encephalopathy - inevitable

accumulation of toxins induces cerebral oedema and reduced consciousness -> coma

62
Q

renal

A

hepatorenal syndrome - unexplained failure when undergoing surgery for biliary tract obstruction or with liver disease
reduced renal flow because of cortical vasoconstriction - perhaps because of accumulation of endotoxin, normally cleared in liver
irreversible and fatal
only survive if have liver transplant

63
Q

coagulopathy

A

liver plays an important role:
synth of coagulation factors I, II, V, VII, IX, X.
vitamin K dependant factors - 2, 7, 9, 10
and factor V 1st affected
factor VII 1st to decline- short half life
factor I only affected in severe disease
inhibition of fibrinolysis/coagulation - liver responsible for synthesising anticoagulant proteins - protein C, S, antithrombin III
clearance of activated cogulation factors - fibrin and tissue plasminogen activator tPA are removed by livers reticuloendothelial system
absorption of vitamin K
impairment of any of this = bleeding

64
Q

suggestions of a coagulation defect

A

bleeding at any site
oozing at venepuncture sites
bruising

65
Q

function of gall bladder

A

store bile - released after a meal for fat absorption
acidify bile
concentrate bile by water diffusion followed by net absorption of Na/Cl/Ca/HCO3

reduce vol of stored bile by 80-90%

ailmentary (15 decks)

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