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Medicine Phase 2a GI > Liver general > Flashcards

Liver general Flashcards

1
Q

Functions of the liver

A

Glucose and fat metabolism
Detoxification and excretion
Protein synthesis
Defence against infection (reticulo-endothelial system)

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2
Q

Give examples of chemicals in the body which are detoxified and excreted

A

Biilirubin
Ammonia
Drugs/hormones/pollutants

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3
Q

Example of proteins synthesised by the liver

A

Albumin

Clotting factors

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4
Q

Types of liver injury

A

Acute

Chronic

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5
Q

What can result from acute liver injury

A

Recovery

Liver failure

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6
Q

Acute causes of liver failure

A 
Viral (A, B, EBV)
Drugs, Alcohol
Vascular
Obstruction
Congestion
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7
Q

Chronic causes of liver failure

A

Recovery
Cirrhosis
Liver failure (varies, hepatoma)

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8
Q

Presentation of acute liver injury

A

Malaise, nausea, anorexia
Occasionally jaundice (doesn’t occur with everyone)
Rare:
-Confusion (encephalopathy)
-Bleeding
-Liver pain
-Hypoglycaemia (since liver breaks down glycogen to glucose, also the liver is the bodies major glucose store)

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9
Q

Presentation of chronic liver injury

A 
Ascites
Oedema (varices)
Malaise
Anorexia
Wasting
Easy bruising (since the liver produces clotting factors)
Itching
Hepatomegaly
Abnormal LFTs
Rare = Jaundice, Confusion
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10
Q

What are ascites?

A

Fluid accumulation in the peritoneal cavity

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11
Q

Examples of Liver Function Tests (LFTs)

A

Serum albumin
Bilirubin
Prothrombin time

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12
Q

Examples of liver biochemistry tests - is this a types of liver function test?

A

Liver biochemistry tests give NO index of liver function:
Aminotransferases
Alkaline Phosphate

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13
Q

In acute liver disease, what is expected from initial albumin levels?

A

May be normal

Low albumin is a bad prognostic sign

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14
Q

In LFTs, is bilirubin normally all conjugated or unconjugated?

A

All unconjugated

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15
Q

What can cause prolonged prothrombin time and what can it be a marker of?

A

Marker of synthetic function.
Sensitive indicator due to its short half-life for both acute and chronic liver disease.
Longer P time can result from vitamin K deficiency.

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16
Q

What is effect of biliary obstruction on Prothrombin time?

A

Biliary obstruction leads to low concentration of bile salts
Results in poor absorption of vitamin K and thus deficiency in vitamin K means reduced coagulation and longer prothrombin time

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17
Q

Give examples of amino-transferases that can be measured to assess liver biochemistry
Where are amino-transferases found?

A 
Enzymes are found in hepatocytes and leak into blood with liver cell damage.
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
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18
Q

Which aminotransferase is more specific to the liver?

A

ALT - Alanine Aminotransferase
Rise only occurs in liver disease
AST also present in heart, muscle, kidney and brain

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19
Q

In what other cases are Aspartate aminotransferases high, other than liver damage?

A

Hepatic necrosis
Myocardial infarction
Muscle injury
Congestive cardiac failure

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20
Q

What colour is bilirubin?

A

Yellow (contributes to colour of bile)

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21
Q

What are bile pigments formed from

A

Haem portion of Hb when old/damaged erythrocytes are broken down in the spleen and liver

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22
Q

What is the predominant bile pigment?

A

Bilirubin

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23
Q

What cells break down old or damaged erythrocytes and where are these cell found?

A

Macrophages

Spleen, bone marrow, liver (Kupffer cells here)

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24
Q

When erythrocytes are ingested by macrophages, what are they initially broken into?

A

Haem and globin

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25
Q

What is globin broken down into

A

Amino acids which can be used to generate new erythrocytes in the bone marrow

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26
Q

What is haem broken down into

A

Biliverdin
Fe2+ (transported to bone marrow to be implemented into new erythrocytes by transporter transferrin)
CO

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27
Q

What happens to biliverdin from haem breakdown?

A

Biliverdin is reduced by biliverdin reductase into UNCONJUGATED BILIRUBIN (toxic and must be secreted)

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28
Q

Why is unconjugated bilirubin bound to albumin in the blood

A

Lipid soluble and thus insoluble in blood

Must be transported bound to albumin to the liver

29
Q

What happens to unconjugated bilirubin when it reaches the liver

A

GLUCURONIDATION
In liver, unconjugated bilirubin undergoes the addition of a glucuronic acid to make it soluble to be excreted under the action of UDP Glucuronyl Transferase, which converts it to CONJUGATED bilirubin

30
Q

What enzyme converts unconjugated bilirubin to conjugated bilirubin

A

UDP Glucuronyl Transferase

31
Q

In what condition do you have a deficiency in UDP Glucuronyl transferase and what is the result of this?

A

Gilbert’s syndrome

Raised unconjugated bilirubin

32
Q

What happened to conjugated bilirubin once it enters the small intestine

A

Travels until it reaches the Ileum or beginning of colon, where it is reduced under the action of intestinal bacteria to form Urobilinogen

33
Q

How is Urobilinogen formed

A

Conjugated bilirubin undergoes hydrolysis reaction under the action of intestinal bacteria, reducing it to form urobilinogen
(glucuronic acid group is removed)

34
Q

What happens to urobilinogen once formed

A

10% is reabsorbed into the blood and bound to albumin (as is lipid soluble) and transported back to the liver.
90% remaining is oxidised by a different type of intestinal bacteria to form stercobilin

35
Q

What happens to the 10% of urobilinogen that is transported back to the liver

A

Urobilinogen oxidised to urobilin
Here it is either recycled into bile or transported into the kidneys where it is excreted in urine - responsible for yellowish colour of urine

36
Q

What happens to stercobilin

A

Excreted into faeces - responsible for the brownish colour

37
Q

Types of jaundice

A

Unconjugated aka Pre-hepatic

Conjugated (Hepatic and Post-hepatic) aka Cholestatic

38
Q

What causes the yellow discolouration of the skin in jaundice

A

Raised serum bilirubin

39
Q

Give examples of Unconjugated or pre-hepatic causes of jaundice

A 
Gilberts syndrome (deficiency in UDP Glucuronyl transferase)
Haemolysis
40
Q

Give examples of causes of (Conjugated/Cholestatic) Hepatic jaundice

A 
Liver disease:
Hepatitis
-Viral (A, B, C, EBV)
-Drug
-Immune
-Alcohol
Ischaemia
Neoplasm
Congestion (congestive heart failure)
41
Q

What is EBV

A

Epstein–Barr virus

Herpes simplex virus

42
Q

Causes of post-hepatic jaundice

A 
Bile duct obstruction due to:
Gall-stone in Bile Duct
Gall-stone in gallbladder/cystic duct pressing on the Common Bile) - Mirizzi syndrome
Stricture
Blocked stent
43
Q

Describe presentation of Pre-hepatic jaundice

A

Urine = Normal
Stools = Normal
Itching = No
Liver tests = normal

44
Q

Describe presentation of Cholestatic (hepatic or post-hepatic) jaundice

A

Urine = dark
Stools = may be pale
Itching = maybe
Liver tests = Abnormal

45
Q

Useful questions for diagnosis jaundice

A 
Dark urine, pale stool, itching?
(if yes then likely cholestatic, not pre-hepatic)
Symptoms?
Past History?
Drug Hx
Social Hx
46
Q

Jaundice: What symptoms would you ask about?

A

Biliary pain (right upper abdomen that radiates to shoulder)
Rigors
Abdomen swelling
Weight loss

47
Q

Jaundice: What past history topics would you ask about?

A 
Biliary disease/intervention?
Malignancy?
Heart failure?
Blood products?
Autoimmune disease?
48
Q

What topics of social history would you ask in jaundice/liver disease

A 
Alcohol?
Potential Hepatitis contact:
-Irregular sex?
-IV drug use?
-Exotic travel?
49
Q

Diagnostic tests of liver

A

Liver enzymes - very high AST/ALT suggests liver disease

Biliary obstruction - 90% have dilated intrahepatic bile ducts on ultrasound

50
Q

What is a hepatocellular carcinoma

A

cancer of the hepatocyte

51
Q

Hepatocellular carcinoma clinical presentation

A

Fever, malaise, weight loss
Right upper quadrant pain, jaundice (late)
Hepatomegaly, ascites

52
Q

Hepatocellular carcinoma aetiology

A

Hep B and C, Aflatoxin, alcohol, haemochromotosis, cirrhosis and anabolic steroids

53
Q

Hepatocellular carcinoma epidemiology

A

90% of primary liver cancers (however 90% of cancer in the liver is a result of metastasis)

54
Q

Hepatocellular carcinoma diagnosis

A

CT and biopsy

55
Q

Hepatocellular carcinoma treatment

A

Surgery to resect individual tumours.

Liver transplant if multiple

56
Q

Define liver failure

A

Loss of the livers ability to regenerate or repair

57
Q

Types of liver failure

A

Fulminant hepatic failure
Late-onset hepatic failure
Chronic decompensated hepatic failure

58
Q

Liver failure clinical presentation

A 
Hepatic encephalopathy
Abnormal bleeding
Ascites
Jaundice
Mental state shows drowsiness and confusion, due to cerebral oedema
59
Q

What are the differences between the types of liver failure

A

Time of liver failure relative to illness:
Fulminant hepatic failure = within 8 weeks of onset of underlying illness
Late-onset hepatic failure = 8-26 wks since onset of underlying illness
Chronic decompensated hepatic failure = latent period >6 months

60
Q

Liver failure pathophysiology

A

Depends on aetiology.
Generally:
the destruction of hepatocytes,
the development of fibrosis in response to chronic inflammation,
the destruction of the architecture of the nodules of the liver removes the ability of the liver to adequately perform functions, repair and regenerate

61
Q

Liver failure aetiology

A 
Various:
Toxins
Infections
Neoplastic e.g. Hepatocellular carcinoma
Metabolic
Others e.g. Acute fatty liver of pregnancy, ischaemia, autoimmune liver disease
62
Q

Liver failure aetiology examples of toxins

A

Alcohol

Paracetamol poisoning

63
Q

Liver failure aetiology examples of infections

A

Viral hepatitis
Epstein-Barr virus
CMV

64
Q

Liver failure aetiology examples of Metabolic causes

A

Wilsons
A1AT deficiency
Haemochromatosis

65
Q

Liver failure epidemiology

A

1/100,000

Paracetamol poisoning most common cause in acute liver failure

66
Q

Liver failure diagnosis

A 
Raised bilirubin
Glucose low (no gluconeogenesis)
67
Q

Liver failure treatment in more severe cases

A

Transplant

68
Q

Complications of liver failure

A

Infection
Haemorrhage
(Hypoglycaemia)

Medicine Phase 2a GI (35 decks)

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