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Year 2 > Liver Disease Symposium: Introduction to Liver disease > Flashcards

Liver Disease Symposium: Introduction to Liver disease Flashcards

1
Q

4 roles of the liver

A
  1. Glucose + Fat metabolism
  2. Detoxification + excretion
  3. Protein synthesis
  4. Defence against infection
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2
Q

What excretion takes place in the liver

A
  1. Bilirubin
  2. Ammonia
  3. Drugs/hormones/pollutants
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3
Q

Through what vessel does blood enter the liver

A

Portal vein + hepatic artery

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4
Q

What epithelium lines the hepatic artery, portal vein and bile duct

A

CUBOIDAL EPITHELIUM

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5
Q

Result of chronic liver damage

A

Fibrosis

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6
Q

What is severe fibrosis of the liver called

A

Cirrhosis

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7
Q

Presentation of liver injury

A
  1. Malaise
  2. Nausea
  3. Anorexia
  4. Jaundice

RARER:

  1. Confusion
  2. Bleeding
  3. Liver pain
  4. Hypoglycaemia
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8
Q

What would liver pain indicate

A

Obstruction

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9
Q

Presentation of chronic liver injury

A
  1. Ascites
  2. Oedema
  3. Haematemesis
  4. Malaise
  5. Anorexia
  6. Wasting
  7. Itching
  8. Hepatomegaly
  9. Abnormal LFTs
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10
Q

How do we test for liver function

A
  1. Serum bilirubin
  2. Albumin
  3. PTT
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11
Q

What cholestatic enzymes are looked at in blood tests

A
  1. Alkaline phosphatase

2. Gamma-GT

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12
Q

What hepatocellular enzymes are looked at in blood tests

A

Transaminases

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13
Q

Does looking at serum enzyme give an indication of liver function

A

No

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14
Q

What causes pre-hepatic jaundice

A

Haemolysis

Gilberts

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15
Q

What causes cholestatic jaundice (conjugated)

A

Liver disease

Bile duct obstruction

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16
Q

Why is PTT a good indicator of acute and chronic liver disease

A

Sue to its short half-life

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17
Q

What can cause a prolonged prothrombin time

A

Vit K deficiency in biliary obstruction - low conc. of bile salts causes poor absorption of vit K

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18
Q

In what disease is alkaline phosphatase levels raised

A

Intrahepatic and extra hepatic cholestatic disease - increased synthesis

Cirrhosis

Hepatic infiltration

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19
Q

How do bile pigments form

A

From harm when old/damaged erythrocytes are broken down in the spleen and liver

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20
Q

What is the most predominant bile pigment

A

Bilirubin

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21
Q

Where is bilirubin extracted

A

Hepatocytes

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22
Q

What colour is bilirubin

A

Yellow

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23
Q

What is haemoglobin broken down into

A

Haem + global

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24
Q

What is global broken down into

A

Amino acids - used to make new erythrocytes

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25
Q

What happens to harm

A

Broken down in bilirubin and Fe2+

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26
Q

What happens to biliverdin

A

Reduced to unconjugated bilirubin

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27
Q

Property of bilirubin

A

Lipid-soluble and insoluble in blood so must be bound to ALBUM

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28
Q

Where does bilirubin go

A

Glucuronidation in the liver

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29
Q

Describe the production of conjugated bilirubin

A

Action of UDP glucuronyl transferase

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30
Q

Why does Gilbert’s result in pre-hepatic jaundice

A

Lack of UDP glururonyl transferase

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31
Q

Where does the conjugated bilirubin go

A

Travels to ileum where it is reduced by bacteria into urobilinogen

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32
Q

What happens to urobilinogen

A

Some is absorbed into the blood + bound to albumin

Some is oxidised to form stercobilin

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33
Q

What give urine its yellow colour

A

Urobilinogen

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34
Q

What can cause post-hepatic jaundice

A
  1. Gall-stones

2. Mirizzi syndrome

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35
Q

What is mirizzi syndrome

A

Stone in gallbladder/cystic duct presses on common bile duct)

36
Q

What questions should i ask as a doctor if suspected jaundice

A
  1. Dark urine, pale stool + itching
  2. Biliary pain (radiates to shoulder)
  3. Rigors
  4. Abdomen swelling
  5. Weight loss

past history
Drug history
Social history

37
Q

Test for jaundice

A
  1. High AST/ALT suggests liver disease

Dilated intrahepatic bile ducts on ULTRASOUND - shows bile obstruction

38
Q

What is biliary colic

A

Term used for pain associated with temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder

39
Q

How to detect stone-induced ductular obstruction

A

Sudden onset, severe but constant and has crescendo characteristic

40
Q

What is cholecystitis

A

Gallbladder inflammation

41
Q

What doe bile consist of

A

Cholesterol
Bile Pigments
Phospholipids

42
Q

What gender do gallstones commonly effect

A

Females

43
Q

What ethnicity do gallstones generally effect

A

Scandinavians
SA
NA

44
Q

Symptoms of gall stones

A

Usually asymptomatic

45
Q

Main causes of gallstones

A
  1. Obesity + rapid weight loss
  2. Diet high in animal fat + low in fibre
  3. Diabetes mellitus
  4. Contraceptive pill
  5. Liver cirrhosis
46
Q

Risk factors of gallstones

A
  1. Female
  2. Fat
  3. Fertile = increased risk of gallstones
  4. Smoking
47
Q

What is the most common type of gallstone

A

Cholesterol gallstones

48
Q

Main causes of cholesterol gallstones

A

Female
Age
Obesity

49
Q

How do cholesterol gallstones form

A
  1. Cholesterol crystallisation in bile
  2. Cholesterol held in solution by bile salts and phospholipids which form micelles and vesicles
  3. Cholesterol gallstones form in EXCESS cholesterol
50
Q

How does an excess cholesterol arise

A

TOO little bile salts + phospholipids

Excess of cholesterol

51
Q

Why will many people with supersaturated bile never develop stones

A

Balance between cholesterol crystallising and solubilising factors that determines whether cholesterol with crystallise out of solution

52
Q

What other factors contribute to gallstone formation

A
  1. Reduced gallbladder motility and stasis

2. Crystalline promoting factors in bile

53
Q

Main cause of bile pigment stones

A

Haemolysis

54
Q

How do BLACK pigment gallstones from

A

Calcium bilirubinate and network of mucin glycoproteins that interlace with salts

55
Q

In what diseases are black pigment gallstones seen in

A

Haemolytic anaemia
Spherocytosis
Sickle cell
Thalassaemia

56
Q

What are brown pigment stones made of

A

composed of calcium salts

57
Q

When do brown pigment stones form

A

Presence of bile stasis and/or biliary infection

58
Q

What is the most common cause of brown pigment stones

A

Recurrent bile duct stones following cholecystectomy

59
Q

What is the problem if gallstones become symptomatic

A

Start to become recurrent

60
Q

Do gallstones cause dyspepsia, fat intolerance, flatulance

A

No

61
Q

Define gallstone colic

A

Pain associated with temporary obstruction of the cystic or common bile duct by a stone migrating out of the gallbladder

62
Q

When do symptoms for gallstone colics com in

A

Mid-evening + last till early hours of morning

63
Q

Initially where are gallstone colics felt

A

Pain in epigastrium and radiates to upper right quadrant component (right shoulder + right sub scapular region)

64
Q

Symptoms of gallstone colics

A

Nausea and committing

65
Q

What is the consequence of acute cholecystitis

A

Obstruction of gallbladder tempting

66
Q

What is acute cholecystitis caused by

A

Gallstones

67
Q

Pathophysiology of acute cholecystitis

A
  1. Obstruction = increased gall bladder glandular secretion leading to progressive distension that may compromise vascular supply to gall bladder
68
Q

How do we distinguish from cute cholecystitis from biliary colic

A

Inflammatory response in acute cholecystitis

69
Q

Where is pain felt in acute cholecystitis

A

Epigastrium

70
Q

What happens to the pain in acute cholecystitis over time

A

Localises in right upper abdominal quadrant corresponding to parietal peritoneal involvement (inflammation begins to irritate parietal peritoneum)

71
Q

NON-SPECFIC symptoms of acute cholecystitis

A

VOMITING
FEVER
LOCAL PERITONITIS

72
Q

What may happen if a stone from acute cholecystitis moves into the common bile duct

A

Cholangitis and JAUNDICE

73
Q

Differential diagnosis of Biliary colics

A
  1. IBS
  2. Carcinoma on right side of colon
  3. Pancreatitis
74
Q

Differential diagnosis of acute cholecystitis

A

Acute episodes of pancreatitis

Peptic ulceration

Basal pneumonia

Intrahepatic abscess

75
Q

How is biliary colic diagnosed

A

Abdominal ultrasound

76
Q

Blood tests when diagnosing acute cholecystitis

A
  1. RAISED WBC (due to inflammation) and C-reactive protein

2. Raised serum bilirubin, alkaline phosphatase and aminotransferase levels

77
Q

Abdominal ultrasound in acute cholecystitis

A
  1. Thick-walled, shrunken gallbladder
  2. Pericholecystic fluid
  3. Stones
78
Q

Clinical examination of acute cholecystitis

A

Right upper quadrant tenderness

Murphy’s signs

79
Q

What is murphy’s sign

A

Pain on taking a deep breath when examiner places two fingers on right upper quadrant

80
Q

How is acute cholecystitis and biliary colics treated surgically

A

Laparoscopic cholecystectomy (gallbladder removal)

81
Q

When is surgical intervention for acute cholecystitis and biliary colics needed

A

symptomatic

82
Q

How is acute cholecystitis non-surgically treated

A
  1. Nil by mouth
  2. IV fluid
  3. OPIATE ANALGESIA
  4. IV antibiotic - CEFUROXIME or CEFTRIAXONE
83
Q

What bacteria are associated with cholecystitis

A
  1. Klebsiella
  2. Enterococcus
  3. E.coli
84
Q

How are gallstones dissolved

A
  1. Increasing bile salt content

ORAL URSODEOCYCHOLIC ACID

SIMVASTATIN (lowers hcolesterol

85
Q

Why is shock-wave lithotripsy done in acute cholecystitis

A
  1. Shock wave directed on gallbladder stones to turn them into fragments
86
Q

When can shock wave lithotripsy be done

A

When cystic duct is patent - allows fragments to pass

Year 2 (155 decks)

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