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Gastrointestinal > Lecture 11- Liver function and pathology > Flashcards

Lecture 11- Liver function and pathology Flashcards

1
Q

function of the liver

A

storage

synthetic

metabolic

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2
Q

storage function

A
  1. Glycogen
  2. Vitamins
  3. Iron
  4. Copper
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3
Q

synthetic function

A
  1. Glucose
  2. Lipids/cholesterol
  3. Bile
  4. Proteins
    1. Clotting factors
    2. Albumin
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4
Q

Metabolic function

A
  1. Bilirubin
  2. Ammonia
  3. Drugs
  4. Alcohol
  5. Carbohydrates
  6. Lipid metabolism
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5
Q

symptoms of luver disease

A
  • jaundice
  • oedema/ascites
  • bleeding
  • confusion
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6
Q

jaundice

A
  • Increase in bilirubin
  • Impaired ability of liver to metabolise bilirubin
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7
Q

oedema/ascites

A
  • Albumin- maintain colloid osmotic pressure
  • portal hypertension
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8
Q
  • Bleeding
A

Reduced clotting factor production

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9
Q

Confusion

A

Impaired metabolic function of the liver esp build up of ammonia

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10
Q

Decompensated liver disease-

A

when there are all four of these symptoms

- jaundice

-oedema/ascites

- bleeding

- confusion

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11
Q

Acute liver disease

A

sudden onset of these symptoms- no previous history

  • Alcohol
  • Paracetamol
  • Viral
  • Medications e.g. aspirin in children
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12
Q

all liver disease leads to

A

cirrhosis

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13
Q

cirrhosis​

A

Permanent irreversible damage to the liver, impairment of liver function and distortion to the architecture of the liver. In response to chronic inflammation

  • Inflammation –> fibrosis and hepatocyte necrosis –> bands of fibrous tissue form which causes nodules to form (think of her balloon analogy)
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14
Q

causes of inflammation in the liver

A

drugs, infection, depsition disease, autoimmune disorders

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15
Q

drugs which cause inflammation

A
  • can be iatrogenic
  • alcohol
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16
Q

alcoholic liver disease

A
  • Most common cause of chronic liver disease
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17
Q

changes causes by excessive alcohol intake

A
  • Fatty change –> excessive amount of sugar converted to triglycerides and can cause build-up of fatty deposits in the liver within weeks of exposure to alcohol
    • Hepatomegaly
    • Usually reversible
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18
Q
  • Alcoholic hepatitis
A
  • Years of exposure (initially reversible)
  • Presence of inflammatory cells alongside fatty changes
  • More serve symptoms
    • RUQ pain
    • Jaundice
    • Oedema
    • Ascites
  • Leads to cirrhosis
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19
Q

infections which can cause liver inflammation

A

hep B and hep c

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20
Q
  • Hepatitis B
A
  • Vaccine
  • No cure
  • Symptoms during acute infection
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21
Q
  • Hepatitis C
A
  • No vaccine
  • Cure
  • Asymptomatic
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22
Q

hepatitis increases

A

risk of malignancy due to chronic inflmmation

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23
Q

Deposition disease which cause inflammation can be caused by

A

fat, iron, copper

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24
Q

fat deposition in the liver

A

Non-alcoholic fatty liver disease (NAFLD)

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25
Q

Non-alcoholic fatty liver disease (NAFLD)

A
  • Insulin resistance
  • Accumulation of TAG and other lipids within hepatocytes
    • Specific to inflammation present= NASH- Non-alcoholic steatohepatitis- inflammation
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26
Q

iron deposition i.e.

A

hereditary haemochromatosis

27
Q
A
28
Q

hereditary haemochromatosis

A
  • Increased absorption of iron
  • Increased deposition of iron in the liver
  • Due to increased levels of ferrite
  • Recessive
  • Risk of hepatocellular carcinoma
  • Treatment: venesection- remove amount of iron in circulation
  • Can also affect pancreas
29
Q

copper deposition in the liver called

A

wilsons disease

30
Q

wilsons disease

A
  • Reduced secretion of copper from the biliary system into circulation to be removed
  • Therefore accumulation in the tissue
  • Low levels of caeruloplasmin ( a ferroxidase enzyme that in humans is encoded by the CP gene)
  • Therefore accumulates in liver- site of storage
  • Usually in young people
  • Symptoms
    • CNS
      • Seizures
      • Memory problems
  • Treatment- will need liver transplant
31
Q

Autoimmune disorders which cause inflammation

A

Autoimmune hepatitis

Primary biliary cirrhois

Primary sclerosing cholangitis

32
Q

*

A
  • Autoantibodies which attach liver cells e.g.
    • Hepatocytes ASMA, ANA
33
Q

autoimmune heptitis

A

autoantibodies which attach liver cellls e.g. hepatocytes ASMA, ANA

34
Q

Primary biliary cirrhois

A

anti-mitochondrial antibodies

35
Q

Primary sclerosing cholangitis

A
  • No anti-mitochondrial antibodies
  • Can be linked to UC
36
Q

Other causes of cirrhosis

A
  • Alpha- antitrypsin
  • Glycogen storage
  • Budd- chiari
37
Q

Portal circulation-

A

the network of veins that drains via the liver into the inferior vena cava

38
Q
  • Three main veins that comprise the portal system:
A
    • Inferior mesenteric vein
      * Drains the descending colon
      • Superior mesenteric vein
        • Drains the ascending colon and other midgut structures
      • Splenic vein
        • Inferior mesenteric vein drains into splenic vein and join with the superior mesenteric vein to form the portal vein
  • Portal vein enters the liver and drains it, then forms the hepatic veins which drain into the inferior vena cava
39
Q

portal hypertension

A
  • Build up of blood within the portal venous system
40
Q

why does portal hypertension occur

A
  • Due to cirrhosis
  • Too much fibrotic tissue
  • Not very expansive – needs to be because it drains the whole GI tract
    • If its not very expansive veins entering the liver (from portal venous system) will be compressed
    • Increase hydrostatic pressure within portal venous system
41
Q
  • Portal hypertension can cause
A
  • ascites
  • build-up of pressure in splenic circulation
  • blood can shunt from portal system to systemic circulation- varcices
  • hepatorenal syndrome
42
Q
  • Ascites- fluid leakage into abdomen
    *
A
  • High hydrostatic pressure forcing water out
  • Low albumin would also help this
43
Q
  • Build-up of pressure in splenic circulation causes
A

splenomegaly (need to feel for spleen and liver on exam)

44
Q
  • Blood can shunt from portal system to systemic circulation
A
    • In normal life there are anastomoses between p. and s. system- not usually used
      • If increase in venous pressure in portal system- blood shunts the other way
        • Distention at site of anastomoses–> varices
45
Q

varices can occur in the

A
  • Oesophagus
  • Anal-rectal
  • Umbilical
46
Q

oesophageal varices

A
  • Upper 2/3 drains into oesophageal veins- goes through the azygous drains into the superior vena cava
  • Distal portion drains into the left gastric vein- drains into the portal vein
    • At the junction where there are veins draining into the main systemic circulation (SVC) is where the pressure builds up.
    • Veins are superficial- therefore become dilatedà easy to rupture
    • Significant Haematemesis
47
Q
  • Anal-rectal varices
A
  • Between superior (which drain into the mesenteric vein) and middle and inferior rectal vein (internal iliac vein–> drains into IVC)
  • Very rarely cause pain or bleed–> patients don’t usually present with these
48
Q
  • Umbilical varices
A
  • Ligamentum teres in adults- usually non functioning in adults
  • Can become enlarged
  • Caput medusae sign
49
Q

The biliary system

A
  • Key function of the liver is creating bile which is stored in the gall bladder
  • Need a way to get the bile into the gall bladder from the liver and from the gall bladder into the duodenum
50
Q

outline the route of the biliary system

A
  • Right and left hepatic duct join together to form the common hepatic duct
  • Duct from the gall bladder (cystic duct) joins to the CHD–> this forms the common bile duct
    • How bile is released into the duodenum
  • Pancreas releases enzymes via the pancreatic duct into the common bile duct
  • Both bile and pancreatic enzymes leave the common bile duct via the ampulla of vater which is controlled by the sphincter of Oddi into the second part of the duodenum
51
Q

Both bile and pancreatic enzymes leave the common bile duct via the

A

ampulla of vater which is controlled by the sphincter of Oddi into the second part of the duodenum

52
Q

common pathology of the biliary system

A

gall stones

53
Q

gall stone are made up of

A
  • Cholesterol
  • Bile pigments
  • Mixed (cant find on x-ray- usually need ultrasound)
54
Q
  • Risk factors for gallstones
A
  • Diet- high cholesterol
  • Women
  • Older
  • Pregnancies
55
Q
  • Complications of gall stones
A
  • Biliary colic
  • acute cholecystitis
  • ascending cholangitis
  • acute pancreatitis
56
Q

Biliary colic

A
  • Gall stones happily sitting within gall bladder, but can cause sudden onset of RUQ pain typically a few hours after eating a fatty meal
    • Due to cholecystokinin (CCK) release after meal, which causes the gall bladder contract and push a gallstone up against the neck of the gall bladder- temporary obstruction of biliary duct
    • Constant pain- can last for a long time and then ease for a while
  • Treatment- pain relief and removal
57
Q
  • Acute cholecystitis
A
  • RUQ pain- caused by full impaction of stone in cystic duct
  • Inflammatory features
  • Positive Murphy sign place a hand on right side of the patients stomach and ask them to take a deep breathe in- will push gall bladder down and cause them to take a sharp breathe in pain (wont happen on left hand side)
  • Treatment- pain relief and Ab, will need to be removed
58
Q
  • Ascending cholangitis
A
  • Statis due to blockage of Common Bile Duct by stone
  • Infection of biliary tree
  • Charcots triad
59
Q

charcots triad

A
  • Inflammation, RUQ pain, jaundice (when stone reaches common bile duct)
60
Q
  • Positive Murphy sign
A

place a hand on right side of the patients stomach and ask them to take a deep breathe in- will push gall bladder down and cause them to take a sharp breathe in pain (wont happen on left hand side)

61
Q

Acute pancreatitis

A
  • Stone in common bile duct after the point when the pancreatic duct has joined the common bile duct
  • Autodigestion of pancreas- due to enzyme not being able to be released into duodenum
62
Q

symptoms and signs of acute pancreatitis

A
  • Epigastric (back) pain
  • Vomiting
  • Cullen’s and Grey Turners sign
  • Look for raised levels of amylase and lipase in the blood
  • CT scan
63
Q

management of acute pancreatitis

A
  • Management
    • Lots of fluids
    • Antibiotics
    • Pain relief

Gastrointestinal (35 decks)

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