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Session 6 Flashcards

1
Q

3 broad functions of liver

A

Storage
Synthetic
Metabolic

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2
Q

Liver stores

A

Glycogen, vitamins, iron, copper

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3
Q

Liver synthesises

A

Glucose, lipids, cholesterol, bile, clotting factors, albumin

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4
Q

Liver metabolises

A

Bilirubin, ammonia, drugs, alcohol, carbohydrates, lipids

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5
Q

Sudden onset of liver symptoms in a person with previous liver disease is called

A

Decompensated liver disease

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6
Q

Acute onset of liver failure symptoms name

A

Acute liver failure

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7
Q

4 liver failure symptoms

A

Jaundice (increased billirubin)
Oedema/ascites (reduced albumin secretion and oncotic pressure)
Bleeding (reduced clotting factors)
Confusion (build up of ammonia)

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8
Q

Acute causes of liver failure

A

Alcohol
Paracetamol
Viral e.g. EBV, hepatitis
Medications e.g. aspirin (especially in children)

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9
Q

Drug causes of cirrhosis

A
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10
Q

Infection causes of cirrhosis

A
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11
Q

Deposition causes of liver disease

A
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12
Q

Autoimmune causes of liver disease

A
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13
Q

Other causes of liver disease

A
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14
Q

Cirrhosis leads to

A

Fibrosis and hepatocyte necrosis

Nodules

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15
Q

What is systemic circulation

A

Any venous network that does not go through liver

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16
Q

What happens to the portal circulation in cirrhosis

A

Fibrotic = not v expensive
Compresses veins

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17
Q

What is portal hypertension caused by

A

Build up of blood in portal venous system

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18
Q

3 features of portal hypertension

A

Ascites (increased hydrostatic pressure)
Splenomegaly (bigger spleen)
Varices (distension of veins, blood shunts to systematic due to pressure increase)

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19
Q

3 places varices occur

A

Oesophagus (haemotemesis)

Ano-rectal (Superior rectal vein, middle and inferior rectal veins, painless as above pectinate)

Umbilical (not common, ligamentum teres,capule medusa)

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20
Q

Hepatorenal syndrome sequence of events

A

Arterial (splanchnic) vasodilation

Perceived decreased circulating volume

Activation of RAAS

Renal artery vasoconstriction (decreased perfusion)

Lowers kidney function

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21
Q

Hepatorenal syndrome outcomes

A

Correct liver pathology = kidneys function returns to normal

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22
Q

What does sphincter of Oddi do

A

Control rate of release of pancreatic and liver enzymes into duodenum

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23
Q

What are gallstones

A

cholesterol, bile pigments, or mixtures

24
Q

How can gallstones be seen

A

Usually not on X-ray, need ultrasound

25
Risk factors for gallstones
Diet, female, forties, pregnancy
26
Feature of renal stones
Calcium so seen on X ray
27
4 types of gallstones
Biliary colic Acute cholecystitis Ascending cholangitis Acute pancreatitis
28
biliary colic features
RUQ pain that is constant but worsens a few hours after a fatty meal as cholecystokinin causes GB contraction Neck of gallbladder No inflammation Treated with cholecysterectomy
29
Acute cholecystitis features
RUQ pain Impacted in cystic duct- pain always bad Stasis causes inflammation which you can see on ultrasound Leads to Murphy’s sign: hand on Right side, deep breath in, GB hits hand = pain
30
Features of ascending cholengitis
Charcot’s triad: RUQ pain, inflammation, jaundice Infection behind stone: antibiotics, fluids, surgery
31
Comparable features of biliary colic, acute cholecystitis, ascending cholangitis
32
Features of acute pancreatitis
Stone blocks pancreatic enzymes, leads to acinar cell injury and necrosis Autodigestion, epigastric pain radiating to back, vomiting, Cullens and Grey Turner’s (bruising around umbilicus and flanks), amylase and lipase levels increased Can be seen on CT or MRI
33
Other causes of pancreatitis
Steroids, alcohol, trauma, autoimmune
34
What is jaundice
Clinical observation due to raised billirubin leading to yellow sclera/skin
35
How does jaundice occur
RBC to spleen, broken down into globin (draws out amino acids) and Haem Haem broken down into biliverdin and bilirubin (bound to albumin as not water soluble) Liver conjugates to make water soluble- if this does not happen then levels of bilirubin increase
36
What should happen to billirubin
Enter duodenum (Stercobilin) makes poo brown enter kidney (urobilinogen) make urine brown Enter hepatic circulation as bile
37
3 different types of jaundice
Pre hepatic, hepatic, post hepatic
38
Features of pre hepatic jaundice
too much for liver to cope with
39
Features of hepatic jaundice
Reduced conjugating ability Enlarged liver and spleen may be seen if chronic liver disease
40
Features of post-hepatic jaundice
Conjugated bilirubin can’t get out due to obstruction Dark urine as can get to kidney to form urobilinogen but pale stool as cannot get to duodenum to form stercobilin
41
Features of intra hepatic obstruction
Inflammation/oedema Tumour (compression locally) Cirrhosis conjugated billirubin cannot leave the liver
42
Indications for LFT
Healthy for baseline (e.g. starting meds that could be harmful) Liver conditions that need monitoring Suspecting pathology of liver
43
What does Albumin tell us
Synthetic function Can have renal cause of low albumin though due to nephrotic syndrome if too much is secreted Decreased albumin can mean chronic liver disease
44
What does ALT and AST tell us
ALT- alanine transaminase is more specific to the liver AST- aspartate transaminase is less specific Increased ALT = acute, increased AST = chronic as cirrhosis and hepatitis
45
Other causes of raised AST
Skeletal muscle (also have increased creatine kinase) Cardiac muscles (also have increased Troponin) Red blood cells (do FBC)
46
What does ALP show
Alkaline phosphatase is an indicator of bile duct problems e.g. cholestasis Test for Gamma-GT to confirm Can also be high in kids or malignancy
47
What does bilirubin tell us
Conjugated vs unconjugated Important in newborns as unconjugated billirubin can cross BBB and harm brain development
48
What does this LFT show
Liver function normal Bile ducts normal Bilirubin level raised of unconjugated Pre-hepatic jaundice/haemolytic anaemia
49
What does this LFT show
Hepatocellular damage
50
What do these LFTs show
Post-hepatic jaundice, obstructive pattern, acute pancreatitis
51
What does this LFT show
Hepatic and post-hepatic jaundice Obstruction and hepatocellular damage Potentially metastasis causing hepatocellular damage and bile obstruction = malignancy
52
Haemochromatosis results in
XS deposition of iron within the liver and other organs Can result in cirrhosis Treatment includes venesection
53
Cirrhosis is a common cause of
Portal hypertension
54
What are normally unused connections between the portal venous system and the systemic system called
Porto-systemic anastomoses
55
Gallstones tend to cause problems when
They move from the gallbladder into the biliary tree Usually asymptomatic before this
56
What happens if gallstones become impacted in the distal biliary tree
Block secretions from pancreas Acute pancreatitis results Pro-enzymes that normally are only activated within the lumen of the gut become prematurely activated within the ductal system of the pancreas causing a varying degree of auto-digestion and inflammation
57
Jaundice definition
Clinical manifestation of raised plasma bilirubin (hyperbilirubinanemia)

GI (22 decks)

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