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BRS Bioregulatory Systems > Live Failure > Flashcards

Live Failure Flashcards

1
Q

What is normal plasma bilirubin

A

17 μmol/L

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2
Q

What happens if bilirubin increases to beyond 30 μmol/L?

A

Yellow sclera and mucous membranes

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3
Q

What happens if it increases beyond 34 μmol/L?

A

Skin turns yellow

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4
Q

Cholestasis

A

Cessation of/slow bile flow

Normally results in jaundice but jaundice doesn’t necessarily mean there’s cholestasis

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5
Q

3 types of jaundice

A

Pre hepatic
Intra hepatic
Post hepatic

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6
Q

Pre-hepatic → what is it and what causes it?

A
  • Problem with bilirubin before liver
  • Too much bilirubin is made in the spleen than downstream structures can cope which can be due to:
    • Haemolysis
    • Massive transfusion (transfused short-lived RBCs)
    • Ineffective erythropoiesis
    • large haematoma resorprtion- cells quickly die and BR released
  • Blood test shows mainly unconjugated BR as conjugation occurs in liver
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7
Q

Intra-Hepatic → what is it and what causes it (5)?

A
  • Normal BR levels arrive at liver but damaged hepatocytes lead to defective bilirubin uptake, conjugation and secretion of BR
  • Liver failure- (acute & chronic)
  • Intrahepatic cholestasis (sepsis, TPN, drugs)

Blood test shows mainly unconjugated BR but liver enzymes are abnormal (damaged hepatocytes)

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8
Q

basic terms when does liver failure happen?

A

When rate of hepatocyte death > regeneration

Normally due to combination of apoptosis (e.g. paracetamol) and/or necrosis (e.g. ischaemia)

Can rapidly lead to coma/death due to multi-organ failure

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9
Q

Acute liver failure types

A

Fulminant hepatic failure
Sub fulminant hepatic failure

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10
Q

What is fulminant hepatic failure?

A
  • Rapid development (<8 weeks) of severe acute liver injury, leads to;
  • Impaired synthetic function leads to e.g. reduced PT time (as liver produces clotting factors)
  • Encephalopathy
  • Previously normal liver or well-compensated liver disease (liver is scarred but still able to function
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11
Q

What is sub-fulminant hepatic failure?

A

Acute liver disease that develops in <6 months

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12
Q

Causes of acute liver failure

A
  • Inflammation (Eastern), give examples of it’s causes?Inflammation
    • Exacerbations of chronic Hep b (Hong Kong)
    • Hepatitis E (India)
  • Toxins (Western cause), such as?
    • Paracetamol
    • Amanita phalloides (Death cap)
    • Bacillus cereus
  • Vascular diseases- like?
    • Ischaemic hepatitis
    • post liver transplant hepatic artery thrombosis
    • post-arrest
    • VOD
  • Metabolic causes- like?
    • Wilson’s disease
    • Reye’s syndrome
  • Idiosyncratic drug reactions- like?
    • Single agent- isoniazid, NSAIDs, valproate
    • Drug combinations- amoxicillin/clavulonic acid, trimethoprim/sulphamethoxazole, rifampicin/isoniazid
  • Diseases of pregnancy- like?
    • AFLP- acute fatty liver of pregnancy
    • HELLP syndrome- Haemolysis, Elevated Liver enzymes, Low Platelets
    • Hepatic infarctions
    • Hep E
    • Budd-Chiari syndrome
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13
Q

Chronic liver failure

A

Over many years and cirrhosis is a big cause

  • Inflammation- usually chronic persistent viral hepatitis
  • Alcohol abuse
  • Side effects of drugs (folic acid antagonists e.g phenylbutazone)
  • Cardiovascular causes e.g. decreased venous return leads to right heart failure meaning back pressure on liver causes cirrhosis
  • Inherited diseases e.g. glycogen storage diseases, Wilson’s disease, galactosaemia, haemochromatosis, alpha1-antitrypsin deficiency
  • Non-alcoholic steatohepatitis (NASH)- increasing cause of cirrhosis and hepatocellular cancers
  • autoimmune hepatitis e.g. primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC)
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14
Q

Describe the process of developing cirrhosis/ the pathophysiology of cirrhosis

A

Noxious factors (alcohol, virus) cause necrosis of hepatocytes

2) This causes lysosomal enzyme leak

3) Causes cytokine release

4) This activates Kuppfer cells in the sinusoids and also activates granulocytes and lymphocytes

5) This releases more growth factors and cytokines

6) Hepatic stellate cells become activated into myofibroblasts. Cytokines also convert monocytes to macrophages which cause fibroblast proliferation along with cytokines

7) Increased collagen, proteoglycans and matrix glycoprotein deposition → Fibrosis of hepatic tissue which leads to cirrhosis

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15
Q

Consequences of liver failure

A
  • Production of clotting factorsThere will be less clotting factors since hepatocytes produce all coagulation proteins except VWF and factor VIIICLeads to coagulopathy and bleeding
  • Protein synthesis (+ explain how alkalosis occurs)
    • Decreased albumin means we can’t retain fluid in our vasculature leading to ascites (edema)
    • This decrease in plasma volume leads to secondary hyperaldosteronism → hypokalaemia → alkalosis (because H+ out and K+ in through H+/K+ATPase, potassium ion reabsorption, + increases ammonium formation (which is a base))
  • Detoxificationencephalopathy and cerebral oedema
  • Glycogen storagehypoglycaemia
  • Immunological function and globulin productionincreased susceptibility to infection
  • Maintenance of homeostasiscirculatory collapse, renal failure
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16
Q

Cholestasis

A
  • Intrahepatic cholestasis causes liver damage and decrease in bile salts -what does this lead to?
    • This means less micelle formation and less absorption of vit K -what does the latter lead to?
      • This means less gamma-carboxylation of vit-K dependent clotting factors (prothrombin (II), VII, IX, X)
        • This aggravates bleeding tendency, particularly increasing risk of GI bleeding
17
Q

What are the 6 mechanisms/pathophysiologies of cholestasis?

A
  • Canalicular dilation and bile can’t get out (bile canalicular contractility is a requirement for normal bile flow)
  • Decreased cell membrane fluidity (bile plugs form)
  • Deformed brush borders
  • Biliary transporters problem e.g. carriers inserted on wrong side
  • Increased tight junction permeability due to increased bile hanging around in duct → increasing amount of bile passing through sinusoidal space → reducing bile flow in canaliculi
  • Decreased mitochondrial ATP synthesis -reduces ability for active transport of bile salts
18
Q
  • What are the 5 consequences of cholestasis? JPMCC (like JPMorgan Chase & Co.)
A

Increased BR causes

  • Jaundice
  • Pruritis (itching)- main one
  • Malabsorption
  • Cholesterol deposition, particularly around eyes
  • Cholangitis (inflammation of bile duct system)
19
Q

Portal hypertension causes what S(T)OMEE VVs

A
  • Decreased lymphatic flow which worsens ascites (oedema)
  • Splenomegaly resulting in thrombocytopenia & anaemia
    Oesophageal varices all the above cause severe bleeding
  • Protein) Exudative enteropathy- what’s this? (+ explain how it can lead to encephalopathy)
    • Loss of albumin from plasma leads to increased ascites
    • This favours bacteria in large bowel being fed with proteins
    • Increases liberation of ammonium (toxic to brain) causing encephalopathy
  • Encephalopathy- toxins from intestine (NH3, biogenic amines, FFAs etc) normally extracted from portal blood by hepatocytes- cross BBB and cause problems to CNS
  • Malabsorption (because proteins are pushed out + high pressure so less nutrients get into liver)
  • Vasodilators (glucagon, VIP, substance P, prostacyclins, NO etc release)- decreases blood pressure- we get increased cardiac output to compensate- this causes hyperperfusion of abdominal organs and contributes to varices
  • Varices- what happens?since big arteries and veins are blocked e.g. superior mesenteric vein + portal vein, blood takes routes down other vessels that aren’t meant to take high volumes of blood- this dilates them and leads to thin walled collateral vessels prone to sudden rupture- this combined with thrombocytopenia and decreased clotting factors can lead to bad bleeding issue
20
Q

3 types of portal hypertension

A

Pre hepatic– Thrombus (blockage) outside liver
- Portal vein thrombosis

Posthepatic– Right heart failure (right ventricle weak/pumping little)
- Constrictive pericarditis- blood can’t get out so back pressure through liver occurs

Intra hepatic– Presinusoidal e.g. chronic hepatitis, PBC, granulomas (schistosomiasis, TB etc)
- Sinusoidal- acute hepatitis, alcohol, fatty liver, toxins, amyloidosis etc
- Postsinusoidal- venous occlusive disease of venules and small veins, Budd-Chiari syndrome (obstruction of large hepatic veins- right, middle and left ones)

21
Q

How does hepatic encephalopathy present?

A

Apathy, memory gaps, tremor, liver coma

  • Hyperammonaemia- GI bleeding increases colonic proteins, which are broken down and liver can’t convert NH3 and NH4+ into urea (they’re toxic i.e ammonia etc.)
  • Hypokalaemia- secondary hyperaldosteronism causes it- leads to intracellular acidosis which activates NH4+ formation in proximal tubules → systemic alkalosis

Caused by - Toxins (amines, phenols and FFAs) bypass liver and not extracted- contribute to encephalopathy
- ‘False transmitters’ (e.g. serotonin) from aromatic amino acids in brain- are increased in liver failure- contribute to encephalopathy

22
Q

Where are the locations of varices (portal-systemic anastomoses)?

A
  • Oesophageal varices (top right circle)- anastomoses open up between oesophageal tributaries of gastric vein and azygos veins
  • Between middle + inferior rectal veins and superior rectal veins (bottom circle)- can get torrential bleeds from rectal mucosa
  • Between paraumbilical veins and superficial veins of anterior abdominal wall
23
Q

How is severity of liver failure assessed?

A

Child-Pugh score → also a prognosticator for peri-op death

  • Class A → 5-6 points → expectancy of 15-20 years, 10% peri-operative mortality
  • Class B → 7-9 points → transplant candidates, may have 30% POM
  • Class C → 10-15 points → life expectancy 1-3 months, 82% POM
24
Q

What are the causes of death with liver failure? (7)

A
  • Bacteria and fungal infections
  • Circulatory instability
  • Cerebral oedema
  • Renal failure
  • Respiratory failure
  • Acid-base and electrolyte disturbance
  • Coagulopathy
25
Q

What are liver support devices?

A
  • Artificial (MARS) → is an albumin exchange system- based on selective removal of albumin-bound toxins from blood
  • Bioartificial hepatocytes in culture attempted to use to remove toxins- not v effective
  • Hepatocyte transplantation- none been really effective
26
Q

What are the indications for liver transplantation?

A

Liver transplant for hepatocellular cancer is effective since the cancer comes from a cirrhotic liver (and it originates in the liver and doesn’t metastasise)

Other causes are:

  • Budd-Chiari
  • Benign liver tumours
  • Polycystic liver disease
27
Q

What is the supportive treatment for the following issues?

A
  • Encephalopathy
    • reduce protein intake- reduce NH3 & NH4+
    • phosphate enema/lactulose- try to empty bowels
    • no sedation- will affect it
  • Hypoglycaemiainfusion 10-50% dextrose
  • Hypocalcaemia10ml 10% calcium gluconate
  • Renal failureHaemofiltration
  • Respiratory failureventilation
  • Hypotensionalbumin and vasoconstrictors
  • Infection
    • Frequent cultures
    • Antibiotics
  • Bleeding
    • Vit K
    • FFP
    • platelets
28
Q
  • Gilbert Syndrome- what is it?
A

Reduced uptake of BR into hepatocytes → increased serum unconjugated BR levels within sinusoidal space and systemic circulation

Also decreased activity of a liver enzyme ( bilirubin uridine diphosphate glucuronosyltransferase enzyme.) leads to less conjugation of bilirubin, so unconjugated bilirubin accumulates. (Non-lecture info)

29
Q
  • Crigler-Najjar Syndrome- what is it?
A

Decreased conjugation of BR in liver→ so high levels of unconjugated BR in blood which enters into systemic circulation and passes through BBB

30
Q

Dubin-Johnson syndrome and Rotor Syndrome -what is it?

A

Decreased BR secretion into biliary canaliculi → Black liver

31
Q

Post-hepatic/obstructive → what is it and what causes it (2), what will the faeces and urine look like & why?

A
  • Physical obstruction reducing the bile and thus reduced bilirubin flow into duodenum and colon
  • Less BR can be excreted and it builds up
  • Gallstones/CBD stones and tumours (e.g. pancreatic, biliary, hepatic)
  • Blood tests shows mainly conjugated BR, which is water soluble so excess bilirubin excreted from kidneys leading to dark urine
  • Less BR in colon → less stercobilinogen → less stercobilin → white pale faeces

BRS Bioregulatory Systems (54 decks)

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