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Bioregulatory systems 4 > Liver failure > Flashcards

Liver failure Flashcards

1
Q

What causes jaundice?

A

BILIRUBIN:

  • more than 30 micromoles/L=yellow sclera and mucous membranes(eyes)
  • more than 34 micromoles/L =yellow skin

CHOLESTASIS:

-slow/cessation of bile flow=retention of contents of bile including bilirubin

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2
Q

What are the 3 types of jaundice?

A

Pre-hepatic Jaundice

Intrahepatic Jaundice

Post-hepatic Jaundice

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3
Q

What are the 4 main cause of Pre-hepatic jaundice?

A

1) Haemolysis(as when RBCs breakdown they release bilirubin):
- Haemolytic anaemia
- toxins
2) Massive transfusion -where the transfused erythrocytes are short lived
3) Large Haemotoma reabsorption- this is broken down and this leads to high bilibrubin
4) Ineffective erythropoiesis

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4
Q

What are the causes of post hepatic jaundice?

A

(also called obstructive jaundice)

interruption to drainage of bile containing conjugated bilirubin caused by:

  • GALLSTONES blocking the common bile duct
  • CANCER in the head of the oancreas
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5
Q

What are causes of Intra-hepatic Jaundice?

A

Autosomal recessive disorders in the liver:

  • GILBERTS SYNDROME-decreased bilirubin uptake into liver =more unconjugated bilirubin in blood (5%)
  • CRIGLER-NAJAR SYNDROME-decreased conjugation of Bilirubin=gets into blood stream=can cross blood brain barrier(can happen in infants)
  • DUBIN JOHNSON +ROTOR SYNDROME-decreased Bilirubin secretion into bilary canaliculi

Intrahepatic Cholestasis:

  • decreased bilirubin output
  • sepsis, TPN , drugs

Liver Failure

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6
Q

What is the differnece between conjugated and non-conjugated bilirubin

A

Conjugated is not toxin

-conjugated is made in the liver when unconjugated bilirubin binds to gucoronic acid

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7
Q

What si the pathophysiology of liver failure?

A
  • When rate of hepatocyte death> regeneration
  • combination of apoptosis and necrosis
  • can lead to death and coma
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8
Q

What are the twon types of liver failure?

A

ACUTE LIVER FAILURE:

  • fuliment hepatic failure=rapid development (less than 8 weeks)
  • impaired synthetic function
  • encephalopathy
  • previously normal liver of well compensated liver disease

CHRONIC LIVER DISEASE:

  • over years
  • cirrhosis
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9
Q

What are the common causes of acute liver failure in the west and east?

A

In the West:Toxins

  • too much paracetomal
  • Amanita Phalloides(mushrooms)
  • Bacillus cereus(bacteria)

In the east:inflammation

  • Exacerbation of chronic Hepatitis B(hong kong)
  • Hepatitis E(India)
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10
Q

What are other rare causes of acute liver disease?

A

Diseases of Pregnancy:

-AFLP, HELLP syndrome, hepatic infarction, HEV, Budd-Chiari

Idiosyncratic drug reactions:

  • Single agent-isoniazid, NSAIDS, valproate
  • Drug combinations- amoxicillion/ clavulonic acid, trimethoprim/sulphamethoxazole, rifampicin/isoniazid

Vascular disease:

  • ischaemic hepatitis
  • post-OLTx
  • hepatic artery thrombosis
  • post arrest
  • VOD

Metabolic causes:

  • Wilsons diseases(deposition of too much copper)
  • Reye’s syndrome(if kids take aspirin after flu or chickenpox)
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11
Q

What are the causes of chronic liver failure(Cirrosis)?

A

INFLAMMATION:

-chronic persistant viral hepititis

Alcohol abuse

SIDE EFFECTS OF DRUGS:

  • folic acid antagonists
  • phenylbutazone

CARDIOVASCULAR CAUSES:

-decreased venous return=right heart failure = knok on effect on liver

INHERITED DISEASES:

  • glycogn storage diseases
  • wilsons disease
  • Galactosaemia
  • Haemochromatosis
  • alpha 1 antitrypsin defficiency

NON-ALCOHOLIC STEATOHEPATITIS(NASH):

-fatty liver

AUTOMIMMUNE HEPATITIS:

-PBC, PSC

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12
Q

Describe the development of chronic liver disease?

A

1) Necrosis of hepatocyte
2) enzymes release that kick of cytokines
3) cytokines and cell debri activates Kupiffer cells that realease growth factors
4) This stimulates Ito fat cell(hepatic stellate cell)=production of myofibroblasts= increased deposition of cellular matrix
5) at the same time ctokines and cell debri both cause chemotaxis of inflammatory cells(monocytes-> macrophages) and macrophages = fibroblast proliferation=increased deposition of matrix
6) increased matrix =FIBROSIS= CIRRHOSIS
7) Cirrhosis= metabolic failure, cholestasis and portal hyper tension

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13
Q

What are normal liver functions and the consequences of Hepatocyte/liver failure whcih stop these functions?

A

Production of clotting factors-coagulation and bleeding

Protein synthesis-Ascites(decreased albumin), decreases clotting factors

Detoxification- encephalopathy and cerebral odeoma

glycogen storage-hypoglycaemia

immunological function and globin production-increased susceptibility to infection

Maintainence of homeostasis-circulatory collapse and renal failure

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14
Q

What is the funtion of albumin?

What does decreased albumin lead to?

A
  • Albumin keeps fluid in your blood stream so it doesnt leak into other tissues
  • less albumin production = fluid leak out of capillaries=plasma volume decrease=secondary hyperaldosteronism, hypokalaemia(decreased k+), alkolosis(excess alkaline in body fluids and tissue which can cause cramp and musle weakness)

less albumin=ASCITES(build upn of fluid in the abdominal cavity)

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15
Q

Which clotting factors do hepatocytes synthesis?

A

all except-von willebrand factor and factor VIIIC

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16
Q

What are the problems caused by cholestasis?

A

aggravates bleeding tendencies:

-decreases in bile salts=decrease in micelles and vit K absorption, decrease in y-carboxlation of VIT K DEPENDENT CLOOTING FACTORS(prothrombin(II), VII, IX, X)

17
Q

What are the 5 mechanisms of Cholestasis?

A
  • bilary canalicular dilation(bilary obstruction)
  • decreased cell membrane fluidy due to increase in cholestrol=deformed brush borders
  • Bilary transporters in the wrong place(basplateral side instread apical side where it should be pumping things into bile)
  • tight juction permeability is increased
  • mitochondrial ATP production decreased
18
Q

What are the consequences of cholestasis?

A

ICTURUS- another name for jaundice

PRURITUS-itching often due to bile salts being deposited under skin

CHOLESTROL DEPOSITION

MALABSORPTION-due to bile defficiency

CHOLANGITIS

19
Q

What can liver failure lead to?

A

Cholestasis

Portal hypertension

hypoalbuminia-less albumin

20
Q

What is portal hypertension?

What problems does it cause?

A

Blood is supposed to go from portal vein to liver, but if it cant use this route it uses other vessels which are MUCH smaller =bad

Problems:

  • Blood coming from the spleen cant enter liver=back pressure =SPLENOMEGALY(enlarged spleen)=THROMBOCYTOPENIA(reduction in platelets(thombocytes)
  • OESOPHAGEAL VARICES
  • combination of decreased clotting factors in liver failure, thrombocytopenia, varices, and small vessels carrying too much blood(ruptue) = SEVERE BLEEDING
  • EXUDATIVE ENTEROPATHY-loss of albumin from the blood into large bowel=feeds bacteria =produces ammonia (toxic to the brain
21
Q

What are the causes of portal hypertension?

A

Prehepatic:

-Portal vein thrombosis

Post-hepatic:

  • right heart failure
  • constrictive pericarditis

Intrahepatic:

-Presinousoidal-chronic hepatitis, PBC, granulomas(TB)

  • sinusoidal-acute hepatitus, alcohol, fatty liver, toxins, amyloidosis
  • Post sinosoidal- venous occulsive disease of venules and small veins, Budd-chiari syndrome
22
Q

What are the consequences of portal hypertension?

A

increased portal vein pressure:

MALABSORPTION-as blood cant enter the liver

SPLENOMEGALY

VASODILLATORS-decrease blood pressure but this mean cardiac output increases to make up for this= HYPERPERFUSION(increased blood pressure ) in abdo organs= increased varices(enlarged swollen veins) as blood travels thorugh small alternative pathways

ENCEPHALOPATHY-toxins (ffa, biogenic amines, NH3) form intestines that are normally extracted from blood in portal vein by hepatocytes crossing the blood brain barrier

VARICES- thinwalled collateral vessels =bleeding

23
Q

What are the causes for hepatic Encephalopathy?

A

Encephalopathy-brain disease/damage/malfunction

HYPERAMMONEAMIA-GI bleeding =increased protein in bowel=feeds bacteria = produces nitogen/ammonia

HYPERKALAEMIA-intracellular acidosis=activates ammonium formation in proximal tubes=systemic alkolosis OR hyperventilation of lungs=alkalosis

TOXINS(amines, phenyl, ffa)-bypass liver =not extracted from blood=go to brain=encephalopathy

FALSE TRANSMITTERS- toxins can cause production in serotonin and others from aromatic amino acids in the brain=increased liver failure=encephalopathy

24
Q

What organs blood goes toward the portal vein which goes to the liver?

A

GI Tract, pancreas, spleen

everything else should be ging to the systemic venous system

25
Q

What happens when organs that send blood to the liver via the portal vein cant do it via this vein?

A

there are some places where the portal blood supply anastomoses with the systemic venous supply- blood can go through these pathways and htis froms VARICES

26
Q

What are the common portal-system anastomoses that form varices?

A
  • eosophageal tributaries of the left gastric vein (from portal vein) connect to the tributaries of the azygous vein(conneceted to vena cava). This forms eosphageal VARICES(common place of bleeding)
  • middle and inferior rectal veins anastomose with vena cave
  • paraumbilial vein(normally closed) opens up and connects with superficial veins of anterior abdominal wall
27
Q

What is hepatorenal syndrome?

A

kidney failure seen in people with severe liver damage

28
Q

What causes hepatorenal syndrome?

A

liver disease=portal hypertension and decrease cardiac output=splenic artery vasodialation=decreased vascular resistance=acivation of vsoconstriction factors=renal vasoconstriction=renal failure

29
Q

How do work out the severity of liver failure?

A

CHILD PUGH SCORE:

assesses 5 parameter and then gives it a score

30
Q

What is a clinical sign of liver failure?

A

ASTERIXIS-tremour of the hand when wrist is extended

-known as ‘liver flap’

31
Q

What is the treatment for each of the problems involved in liver failure?

A

ENCEPHALOPATHY:

  • Reduce protein intake
  • give phosphate enemas/lactulose (clear bacteria)
  • no sedation

HYPERGLYCAEMIA:

-IV glucose(10-50% dextrose)

HYPOCALCAEMIA:

10ml of 10% calcium gluconate

RENAL FAILURE:

-haemofiltration

RESPIRATORY FAILURE:

-ventilation

HYPOTENSION:

  • albumin
  • vasoconstrictors

INFECTION:

-frequent blood tests

BLEEDING:

  • vit K
  • FFP (fresh prozen plasma)
  • Platelets
32
Q

What are causes of death fron people with liver falure?

A
  • Bacterial and fungal infections
  • circulatory instability
  • cerebral odema
  • renal failure
  • respiratory failure
  • acid-base and electrolyte ditubance
  • coagulopathy
33
Q

What are alternative treatments if the normal treament doesnt work?

A
  • Artificial albumin exchange system(MARS)-removal of albumin from the blood based on albumin bound toxins
  • Bioartificial-diffusing blood through hepatocyte cultures

Hepatocyte(liver ) transplant

34
Q

What are the indications you need a liver transplant?

A

Cirrosis-58%

cancer-14%

cholestatic disease-10%

acute liver failure -8%

Metabolic disease-6%

others(buud chiari, beneign liver tumours, polycystic liver disease)-4%

35
Q

In a liver transplant which vessels do you have to cut?

A
  • divide inferior vena cave under the liver as is goes in and above the liver as it leaves
  • portal vein
  • hepatic duct
  • cystic duct
  • common hepatic duct

and then you replace the liver and rejoin the vessels

36
Q
A
37
Q

What is the survival rate if you have a liver transplant?

What is the chance of disease reoccuring?

A

5 years(60-80%)

no recurrence but pateint will require lifelong immuno-supressants

Bioregulatory systems 4 (11 decks)

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