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Alimentary system > liver failure and jaundice > Flashcards

liver failure and jaundice Flashcards

1
Q

why do we produce bile?

A

Cholesterol homeostasis

Dietary lipid / vitamin absorption

Removal of xenobiotics/ drugs/ endogenous waste products

e. g. 
- cholesterol metabolites
- adrenocortical 
- other steroid hormones
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2
Q

other substances excreted into bile

A

adrenocortical and other steroid hormones
drugs/xenobiotics
cholesterol
alkaline phosphatase (ALP)

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3
Q

bile production- how much produced?

What’s the colour?

where is most of the bile secreted from?

A

500ml produced/secreted daily

Green/yellow colour

60% bile secreted by hepatocytes (liver cells) and up to 40% secreted by cholangiocytes (biliary epithelial cells)

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4
Q

pathway of the bile (which organs does it go through?)

A

bile duct from:
liver
bile ducts
duodenum at duodenal papilla

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5
Q

bile production: role of biliary tree

A

alters pH, fluidity and modifies bile as it flows through
Water drawn into bile
luminal glucose and some organic acids also reabsorbed
HCO3- and Cl- actively secreted into bile by CFTR mechanism
Cholangiocytes contribute IgA by exocytosis

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6
Q

bile flow is closely related to?

A

concn of bile acids and salts in blood

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7
Q

biliary excretion of bile salts and toxin performed by

A

transporters on apical surface of hepatocytes and cholangiocytes

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8
Q

the biliary transporters also

A

govern rate of bile flow

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9
Q

Dysfunction of the transporters is a cause of

A

cholestasis

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10
Q

Main transporters

A

Main transporters include the:

Bile Salt Excretory Pump (BSEP)

MDR related proteins (MRP1 & MRP3)

products of the familial intrahepatic cholestasis gene (FIC1) and multidrug resistance genes (MDR1 & MDR3).

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11
Q

What does BSEP (ABCB11 gene) do?

A

BSEP (ABCB11 gene): active transport of bile acids across hepatocyte canalicular membranes into bile, and secretion of bile acids is a major determinant of bile flow

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12
Q

what does MDR1 do?

A

MDR1: mediates canalicular excretion of xenobiotics, cytotoxins

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13
Q

What does MDR 3 do?

A

MDR 3: encodes a phospholipid transporter protein that translocates phosphatidylcholine from inner to outer leaflet of canalicular membrane

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14
Q

Na and K salts of bile acids are conjugated into what and where?

what is the basis of bile acid?

A

Na and K salts of bile acids (conjugated in liver) to glycine and taurine (cysteine derivative)

Bile acids synthesised from cholesterol

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15
Q

Four bile acids in humans:

A

2 primary
Cholic acid and chenodeoxycholic acid

these can be converted by colonic bacteria into secondary acids
deoxycholic acid and lithocholic acid respectively

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16
Q

bile salt functions

A

Reduce surface tension of fats

Emulsify fat preparatory to its digestion/absorption

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17
Q

bile salts form micelles and are amphipathic- what does this mean?

A

One surface has hydrophilic domains, facing OUT
2nd has hydrophobic domains, facing IN
free Fatty Acids and Cholesterol INSIDE
thus transported to GIT epithelial cells for absorption

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18
Q

anatomy of the biliary system

A

Each hepatocyte is apposed to several bile canaliculi

these drain:

  • intralobular bile ducts, coalesce
  • interlobular ducts
  • right/left hepatic ducts
  • join outside liver to form common hepatic duct

Cystic Duct drains the gall bladder

Cystic Duct unites with Common Hepatic Duct to form COMMON BILE DUCT (CBD)

CBD joined by Pancreatic Duct prior to entering duodenal papilla

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19
Q

what is the ampulla of bile duct controlled by?

A

Ampulla of bile duct; controlled by Sphincter of Oddi

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20
Q

what occurs between meals and during eating?

A

Between meals duodenal orifice closed, therefore bile diverted into gall bladder for storage

Eating causes sphincter of Oddi to relax

21
Q

how is cholecystokinin released?

what does cholecystokinin do?

A

Gastric contents (F.As, A.As > CHOs) enter duodenum causing release of cholecystikinin, CCK (Gut mucosal hormone)

Cholecystikinin causes gall bladder to contract

22
Q

enterohepatic circulation

A

liver to the bile, followed by entry into the small intestine, absorption by the enterocyte and transport back to the liver

Liver cells transfer various substances, including drugs, from plasma to bile
Many hydrophilic drug conjugates (esp. glucoronide) are concentrated in bile

23
Q

where is majority of bile ducts absorbed? and by what?

A

95% bile salts absorbed from small (terminal) ileum by Na+/bile salt co-transport Na+-K+ ATPase system

24
Q

5% converted to? and how?

A

secondary bile acids in the colon:

  • deoxycholate absorbed
  • lithocholate 99% excreted in stool
    absorbed
  • B.salts back to liver and then re-excreted in bile
25
enterohepatic circulation of bile salts | - how much pools?
3g bile salt pool re-cycles repeatedly in enterohepatic circulation (2x/meal; 6 – 8x/day)
26
what occurs in terminal resection/disease?
Terminal Ileal Resection/Disease: bile salt reabsorption and stool [fat] (because enterohepatic circulation interrupted and liver can’t increase rate of bile salt production enough to make it up)
27
what happens if bile stopped from entering gut?
If bile stopped from entering Gut: Up to 50% ingested fat appears in faeces malabsorption fat soluble vitamins (A,D,E,K)
28
Functions of gall bladder
Stores bile (50ml), released after meal for fat digestion Acidifies bile Concentrates bile by H20 diffusion following net absorption of Na+, Cl-, Ca2+, HCO3 ( intra-cystic pH) Gall bladder can reduce volume of its stored bile by 80 – 90%
29
Functions of Gall Bladder:Effects of Cholecystectomy (removal of gall bladder)
Periodic discharge of bile from GB aids digestion BUT is NOT ESSENTIAL Normal health and nutrition exist with continuous slow bile discharge into duodenum Avoid foods with high fat content
30
Bilirubin (BR) Metabolism & Excretion Where does the bilirubin come from? 3 places
BR = H2O-INSOLUBLE, yellow pigment 75% BR from Hb breakdown 22% from catabolism of other haem proteins 3% from ineffective bone marrow erythropoiesis
31
BR is bound to? Most dissociates in? Free BR enters? And binds to? What does it conjugate to? and what does it lead to?
BR bound to albumin, then most dissociates in liver Free BR enters hepatocyte, binds cytoplasmic proteins conjugated to glucoronic acid (UDPGT from smooth ER) LEADS TO diglucoronide-BR (more soluble > free BR) transported ACROSS concentration gradient into bile canaliculi LEADS INTO GIT
32
TOTAL BR:
FREE BR + CONJUGATED BR
33
Urobilinogens =
Urobilinogens = H2O-SOLUBLE, colourless derivatives of BR formed by action of GIT bacteria urobilinogen is formed mainly in the intestines by bacterial action on bilirubin. About half of the urobilinogen formed is reabsorbed and taken up via the portal vein to the liver, enters circulation and is excreted by the kidney.
34
GIT mucosa is Impermeable to?
GIT mucosa (relatively) IMpermeable to CONJUGATED BR but is PERMEABLE to UNCONJUGATED BR and Urobilinogens Therefore some UNCONJUGATED BR enters enterohepatic circulation; and some forms urobilinogens
35
Some urobilinogens passed in stool as?
20% urobilinogens reabsorbed into gen.circulation urine excretn Some urobilinogens passed in stool as Stercobilinogen
36
Why Faeces is Brown?
Why Faeces is Brown: | Oxidation of stercobilinogen to stercobilin
37
Jaundice?
Cholestasis: slow/cessation of bile flow Jaundice: Excess BR in blood (> 34 – 50microM/L) (yellow tinge to skin, sclerae, mucous membranes) Cholestasis normally results in jaundice Jaundice does not necessarily mean there is cholestasis
38
causes of jaundice?
Excess bilirubin (BR) in blood (> 34 – 50uM/L)
39
causes of prehepatic
``` Increased quantity of BR: Haemolysis Massive Transfusion Haematoma resorption Ineffective erythropoiesis ```
40
Causes of Jaundice: Hepatic/Hepatocellular
Defective uptake Defective conjugation Defective BR excretion Liver Failure: Acute/Fulminant Acute on Chronic Viral hepatitis, EtOH, Autoimmune disease etc. Intrahepatic cholestasis: sepsis, TPN, Drugs
41
Post-hepatic/Obstructive
Post-hepatic/Obstructive Defective Transport of BR by Biliary duct system e.g. common bile duct stones, HepPancBil malignancy, local LNpathy Look out for sepsis (cholangitis) Dilated bile ducts on scans
42
gilbert's syndrome
Commonest hereditary cause of increased bilirubin Up to 5% of the population Autosomal recessive inheritance Elevated unconjugated bilirubin in bloodstream Cause: 70%-80% reduction in glucuronidation activity of the enzyme Uridine-diphosphate-glucuronosyltransferase isoform 1A1 (UDPGT-1A1). No serious consequences Mild jaundice may appear under: exertion, stress, fasting, infections otherwise usually asymptomatic
43
liver failure- pathophysiology
“… when rate of hepatocyte death > regeneration …various aetiologies …combination of apoptosis &/or necrosis” Apoptosis (e.g. Acetaminophen=Paracetamol): Necrosis (Ischaemia): Clinical result = catastrophic illness…can rapidly lead to coma/death due to multi-organ failure
44
Fulminant hepatic failure =
Fulminant hepatic failure = rapid development (< 8wks) of severe acute liver injury with impaired synthetic function (INR/PT, albumin) + encephalopathy in person with previously normal liver or well-compensated liver disease "Sub-fulminant" = < 6 months
45
causes of chronic liver failure
``` Causes: Viral hepatitis (B, C) Alcohol Excess Fatty Liver Autoimmune Disease Genetic: Wilson’s, Haemachromatosis Drug induced e.g. methotrexate ```
46
what is acute liver failure
Relatively uncommon (< 500 deaths/yr) < 15% of liver transplants/yr (< 100 transplants/yr) As in USA, over past 30y, Paracetamol (Acetaminophen, ACM) is commonest cause
47
normal functions of liver
``` detoxification glycogen storage production of clotting factors immunological function and globulin production maintenance of homeostasis ```
48
consequences of hepatocyte failure
``` encephalopathy and cerebral oedema hypoglycaemia coagulopathy and bleeding increases susceptibility to infection circulatory collapse, renal failure ```

Alimentary system (9 decks)

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