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GI > Session 6 > Flashcards

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
Q

Risk factors for gallstones

A

Diet, female, forties, pregnancy

26
Q

Feature of renal stones

A

Calcium so seen on X ray

27
Q

4 types of gallstones

A

Biliary colic
Acute cholecystitis
Ascending cholangitis
Acute pancreatitis

28
Q

biliary colic features

A

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
Q

Acute cholecystitis features

A

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
Q

Features of ascending cholengitis

A

Charcot’s triad: RUQ pain, inflammation, jaundice

Infection behind stone: antibiotics, fluids, surgery

31
Q

Comparable features of biliary colic, acute cholecystitis, ascending cholangitis

A
32
Q

Features of acute pancreatitis

A

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
Q

Other causes of pancreatitis

A

Steroids, alcohol, trauma, autoimmune

34
Q

What is jaundice

A

Clinical observation due to raised billirubin leading to yellow sclera/skin

35
Q

How does jaundice occur

A

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
Q

What should happen to billirubin

A

Enter duodenum (Stercobilin) makes poo brown

enter kidney (urobilinogen) make urine brown

Enter hepatic circulation as bile

37
Q

3 different types of jaundice

A

Pre hepatic, hepatic, post hepatic

38
Q

Features of pre hepatic jaundice

A

too much for liver to cope with

39
Q

Features of hepatic jaundice

A

Reduced conjugating ability
Enlarged liver and spleen may be seen if chronic liver disease

40
Q

Features of post-hepatic jaundice

A

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
Q

Features of intra hepatic obstruction

A

Inflammation/oedema
Tumour (compression locally)
Cirrhosis

conjugated billirubin cannot leave the liver

42
Q

Indications for LFT

A

Healthy for baseline (e.g. starting meds that could be harmful)

Liver conditions that need monitoring

Suspecting pathology of liver

43
Q

What does Albumin tell us

A

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
Q

What does ALT and AST tell us

A

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
Q

Other causes of raised AST

A

Skeletal muscle (also have increased creatine kinase)
Cardiac muscles (also have increased Troponin)
Red blood cells (do FBC)

46
Q

What does ALP show

A

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
Q

What does bilirubin tell us

A

Conjugated vs unconjugated

Important in newborns as unconjugated billirubin can cross BBB and harm brain development

48
Q

What does this LFT show

A

Liver function normal
Bile ducts normal
Bilirubin level raised of unconjugated

Pre-hepatic jaundice/haemolytic anaemia

49
Q

What does this LFT show

A

Hepatocellular damage

50
Q

What do these LFTs show

A

Post-hepatic jaundice, obstructive pattern, acute pancreatitis

51
Q

What does this LFT show

A

Hepatic and post-hepatic jaundice

Obstruction and hepatocellular damage

Potentially metastasis causing hepatocellular damage and bile obstruction = malignancy

52
Q

Haemochromatosis results in

A

XS deposition of iron within the liver and other organs

Can result in cirrhosis

Treatment includes venesection

53
Q

Cirrhosis is a common cause of

A

Portal hypertension

54
Q

What are normally unused connections between the portal venous system and the systemic system called

A

Porto-systemic anastomoses

55
Q

Gallstones tend to cause problems when

A

They move from the gallbladder into the biliary tree

Usually asymptomatic before this

56
Q

What happens if gallstones become impacted in the distal biliary tree

A

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
Q

Jaundice definition

A

Clinical manifestation of raised plasma bilirubin (hyperbilirubinanemia)

GI (22 decks)

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