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xB15W2 > PBL 1 > Flashcards

PBL 1 Flashcards

1
Q

whats the blood supply to the liver>

A
  • arterial blood from right and left hepatic arteries (branches of coeliac trunk) - 10%
  • venous blood from hepatic portal vein which drains the GIT, gallbladder, pancreas and spleen - 90%
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2
Q

why is the liver much less affected by vascular disease than other organs?

A

because it has a dual blood supply

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3
Q

what are the cells in the liver?

A

hepatocytes, kupffer cells, hepatic stellate cells (aka Ito cells) and liver sinusoidal endothelial cells.

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4
Q

what are hepatocytes?

A

major parenchymal cells and they have a pivotal role in metabolism, detoxification and protein synthesis.

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5
Q

what are kupffer cells?

A

resident liver macrophages that phagocytose and defend the liver against pathogens

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6
Q

what are hepatic stellate cells?

A

mesenchymal cells located in the space of Disse and are the main place of vitamin A storage in characteristic lipid droplets.

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7
Q

Outline the movement of bile from hepatocytes>

A

bile is excreted into tiny canaliculae. It is propelled towards the portal tracts (the opposite direction to sinusoidal blood flow). It is carried via canals of Hering and ductules into the small interlobular bil ducts in the portal tracts. From this it drains into the right and left hepatic ducts at the porta hepatis.

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8
Q

what is the portal triad?

A

bile duct, hepatic artery, portal vein

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9
Q

what does it mean to say liver cells are classified as stable?

A

they normally replicate only very infrequently but when the liver is injured nearly all hepatocytes enter the cell cycle and rapidly replace destroyed tissue

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10
Q

what are the common symptoms of acute liver injury?

A

malaise and jaundice

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11
Q

what is cirrhosis

A

end stage liver disease

defined anatomically by the presence of fibrous septa throughout the liver that subdivide the parenchyma into nodules.

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12
Q

what are some causes of liver disease?

A 
viruses
drugs
autoimmune
idiopathic
non-alcoholic steatohepatitis
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13
Q

what is acute hepatitis?

A

hepatocyte injury with cell death, inflammation and regeneration without structural change to the liver

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14
Q

what are the potential outcomes for acute hepatitis?

A

This may resolve on its own, become acute liver failure or chonic hepatitis.

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15
Q

what is liver failure?

A

when liver can no longer function sufficiently to maintain the bodys homeostasis

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16
Q

what are the 2 main causes of chronic hepatitis?

A

viral

autoimmune

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17
Q

outline the pathophysiology of viral hepatitis?

A

Viruses enter the blood stream and spread to the liver. They infect the hepatocytes and multiply. Infected cells present the virus on its surface via MHC1 where a CD8+ T cell recognises it and initiates cytotoxic killing and cell apoptosis

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18
Q

what viruses can the liver be infected with othwe than hepatotrophic viruses?

A

epstein barr
herpes simplex
cytomegalovirus

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19
Q

how is HAV spread?

A

faecal oral

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20
Q

how is HBV spread?

A

blood

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21
Q

how is HCV spread?

A

blood

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22
Q

how is HEV spread?

A

water borne

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23
Q

how is HDV spread?

A

blood

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24
Q

which hepatotrophic viruses cause acute hepatitis?

A

HAV, HEV

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25
Q

which hepatotrophic viruses cause chronic hepatitis?

A

blood borne ones i.e. HBV, HCV and HDV

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26
Q

whats the most common type of viral hepatitis in the UK?

A

HCV

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27
Q

what is special about HDV?

A

its an incomplete RNA virus that can only infect hepatocytes in the presence of HBV
It just aggrevates the consequences of HBV infection

28
Q

outline the pathophysiology of alcoholic hepatitis, the steatosis stage?

A

Alcohol enters hepatocytes and can be converted to acetaldehyde by 1 of 3 pathways: cytochrome P450 2E1, catalase in peroxisomes or alcohol dehydrogenase. As alcohol dehydrogenase is used to convert alcohol to acetaldehyde, it converts NAD+ to NADH; as NADH levels increase, the cell starts to produce more fatty acids and lower NAD+ levels result in less fatty acid oxidation. Both of these lead to more fat production in the liver (fatty change / steatosis). This tends to be asymptomatic at this point and is reversible at this stage.

29
Q

outline the pathophysiology of alcoholic hepatitis, the steatohepatitis stage?

A

Reactive oxygen species are produced in the conversion of alcohol to acetaldehyde. These react with different components of the hepatocyte, causing serious damage
Acetaldhyde can also bind to parts of the hepatocyte, inhibiting it = acetaldehyde adducts. The immune system recognises these as foreign so neutrophils destroy hepatocytes
As cells become inflamed and damaged, it is now referred to as steatohepatitis. On histology, bundles of proteins called mallory bodies can be seen now in hepatocytes. At this point the patient may have hepatomegaly that is painful, neutrophil leukocytosis, raised ALT/AST levels (AST levels raised more than ALT), ALP and GGT will also be elevated, thrombocytopenia, hypoglycaemia

30
Q

whats the treatment for alcoholic hepatitis?

A

Treatment is stopping drinking alcohol and sometimes corticosteroids to suppress the immune system.

31
Q

outline the pathophysiology of non-alcoholic fatty liver disease?

A

Excess calorie intake and little exercise results in insulin resistance, raised levels of insulin/glucose in the blood and eventually type 2 diabetes where pancreatic islets fail to keep pace with the increasing requirements for insulin.

32
Q

in which patients do we mostly see non-alcoholic fatty liver disease?

A

those with metabolic syndrome

33
Q

what are the 3 chronic liver diseases with an autoimmune basis?

A

autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis.

34
Q

what is primary biliary cirrhosis?

A

chronic disease in which the bile ducts in your liver are slowly destroyed

35
Q

what is primary sclerosing cholangitis?

A

an uncommon chronic liver disease in which the bile ducts inside and outside the liver progressively decrease in size due to inflammation and scarring (fibrosis)

36
Q

outline the prevalence of autoimmune hepatitis in females: males

A

much more common in females 4:1

37
Q

outline the pathophysiology of cirrhosis?

A

Activated hepatic stellate cells transform into myofibrosblast-like cells to promote fibrosis in response to liver injury/inflammation; myofibroblast-like cells are capable of producing collagen, pro-inflamamtory cytokines and transforming growth factor 1. Collagen builds up, compressing the central vein and the sinusoids so intrasinusoidal pressure starts to build up, leading to the development of portal hypertension

38
Q

what are the effects if portal hypertension?

A
  • Portal hypertension pushes fluids to the tissues in the peritoneal cavity, leading to the development of ascites. Blood flows back and becomes engorged in the spleen causing congestive splenomegaly. The circulatory system starts to shunt and divert blood from the liver, leading to portal systemic shunt following the path of least resistance. Blood will start flowing back to the stomach and oesophagus causing oesophageal varices.
  • Increased resistance to renal blood flow due to renal vasoconstriction causes low filtration = hepatorenal failure
  • Reduced detoxification function of the liver leads to accumulation of toxins in the body and the brain = hepatic encephalopathy and asterisix (ammonia)
  • Increased oestrogen levels leads to the development of gynaecomastia, spider angiomata and palmar erythema
  • Excessive accumulation of unconjugated bilirubin = jaundice
  • Liver cant secrete albumin = hypoalbuminemia
  • Liver cant synthesise clotting factors = coagulopathies
  • Development of hepatic pulmonary syndrome can occur
39
Q

what is hepatopulmonary syndrome?

A

a rare lung complication of liver disease.
When the liver is not functioning properly, blood vessels in the lungs may dilate. If this is severe enough, the lungs can lose their ability to effectively transfer oxygen to the body.

40
Q

what are the most common causes of cirrhosis?

A

alcohol
non alcoholic steatohepatitis
HCV
HBV

41
Q

what are the major complications of cirrhosis?

A

liver failure, infection, liver cell carcinoma and portal hypertension

42
Q

what is the commonest cause of portal hypertension?

A

cirrhosis

43
Q

what is pre-sinusoidal portal hypertension?

A

obstruction to the portal vein blood flow before the blood enters the sinusoids

44
Q

what is post-sinusoidal portal hypertension?

A

obstruction to the blood leaving the liver or beyond the liver.

45
Q

what are oesophageal varices?

A

enlarged and swollen veins caused by the increased portal hypertension which causes increased pressure in veins so they expland

46
Q

whats the mortality rate from variceal haemorrhage?

A

15%

47
Q

what are normal bilirubin levels?

A

0.2 - 1.2mg/dL

48
Q

why is the earliest sign of jaundice the yellowing of the sclera?

A

the scleral tissue is high in elastin which has a particularly high affinity to bilirubin

49
Q

what are some causes of prehepatic jaundice?

A

haemolytic anaemia
gilberts sundrome
crigler Najjar syndrome

50
Q

what are some intrahepatic causes of jaundice?

A 
◦ alcoholic liver disease
	◦ viral hepatitis
	◦ inatrogenic medication
	◦ hereditary haemochromatosis
	◦ autoimmune hepatitis
	◦ primary biliary/sclerosing cholangitis
	◦ hepatocellular carcinoma
51
Q

what are some post hepatic causes of jaundice?

A 
◦ intraluminal causes e.g. gallstones
	◦ cholangiocarcinoma
	◦ structures
	◦ drug induced cholestasis
	◦ pancreatic cancer
	◦ abdominal masses
52
Q

what are some causes of jaundice that cause unconjugated hyperbilirubinaemia?

A 
extravascular haemolytic anaemias
ineffective haumatopoeisis
physiologic jaundice of the newborn
gilberts sundrome
crigler najjar syndrome
breast milk jaundice
breast feeding failure jaundice
53
Q

what are some causes of jaundice that cause conjugated hyperbilirubinaemia?

A 
dubin johnson syndrome
rotor syndrome
primary sclerosing cholangitis
primary biliary cholangitis
obstructive jaundice
biliary atresia
54
Q

what are some causes of jaundice that cause mixed hyperbilirubinaemia?

A

viral hepaitis

cirrhosis

55
Q

why does haemolytic anaemia cause jaundice?

A

RBCs are broken down causing high levels of UCB. Hepatocytes get overwhelmed and cannot conjugate the bilirubin fast enough; this causes increased serum UCB but also increased CB in the bile which is a risk for gallstones. This increase in CB leads to increased urobilinogen and therefor increase urobilin = darker urine

56
Q

outline the pathophysiology of physiologic jaundice of the newborn?

A

newborn livers have a lower level of UGT to convert UCB to CB and after birth UCB levels are high due to the natural process of macrophages destroying RBCs. Hepatocytes cant keep up with these normal levels and we get jaundice.

57
Q

whats a consequence of UCB collecing in the basal ganglia?

A

kernicteus - causes brain damage and even death

58
Q

why can gilberts syndrome cause jaundice?

A

• Gilberts syndrome is a genetic defect where UGT enzyme activity is low. If something comes along that increases haemolysis e.g. stress or infection, the UCB load will icnrease and easily overwhelm the hepatocytes and cause buildup of UCB in the blood

59
Q

why does crigler najjar syndrome cause jaundice?

A

• Crigler najjar syndrome is a genetic defect where there is pretty much no UGT enzyme so no ability to conjugate the UCB. This leads to super high levels of UCB in the blood and likely will lead to kernicterus. This is usually fatal.

60
Q

what is breast milk jaundice?

A

babies gut flora isnt established until 1-2 years after birth so they dont have enough bacteria to convert CB to UBG or stercobilin. High levels of glucuronidase in breast milk actyally deconjugates conjugated intestinal bilirubin.

61
Q

what is breast feeding failure jaundice?

A

decreased/poor intake of breastmilk so babies have inadequate stooling and so decreased elimination of bilirubin by stool. This leads to increased enterohepatic circulation causing unconjugated hyperbilirubinemia

62
Q

why does dubin johnson syndrome cause jaundice?

A

autosomal recessive disorder where theres a deficiency in the protein MRP2 that helps move CB from the hepatocytes to the bile ducts. This causes upregulation of MRP3 which moves the CB into the blood instead of the bile ducts so we get increased CB serum levels which gets excreted in the urine causing it to be a darker colour

63
Q

why does rotor syndrome cause jaundice?

A

defects in proteins that enable normal hepatic uptake and excretion of bilirubin leading to high levels of CB.

64
Q

outline the pathophsyology of obstructive jaundice?

A

blockage to the flow of bile (stones, tumours etc) = increased pressure in the bile ducts = leakage of bile between hepatocytes. Bile salts, bile acids, cholesterol also get into the blood which can cause pruritis if they reach the skin, hypercholesterolemia and xanthomas. Because the CB enters the blood, its excreted by the kidneys causing darker urine. Also, because you lose bile, you will have increased fat excretion (steatorrhoea) and decreased fat soluble vitamin absorption.

65
Q

why can viral hepatitis cause jaundice?

A

infected hepatocytes start to die off so they lose their ability to conjugate UCB leading to excess UCB in the blood. These cells line the bile ducts so when they die they let bile leak into the blood causing an increase in blood CB as well = darker urine.

xB15W2 (8 decks)

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