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Clinical biochem. > Hepatobiliary disease > Flashcards

Hepatobiliary disease Flashcards

1
Q

Function of the liver

A
  • Performs 500+ chemical processes
  • Produces 160+ different proteins
  • Makes clotting factors for the blood
  • Stores & releases sugar from glycogen
  • Metabolism, detoxification, synthesis
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2
Q

6 Types of liver disease

A
  1. Autoimmune hepatitis
  2. Cirrhosis due to alcoholism, hepatitis, obstruction
  3. Genetic
  4. Hepatitis
  5. Infections
  6. Obstruction of bile ducts
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3
Q

markers for hepatocellular damage (liver damage)

A

ALT, AST, ALP, gammaGT

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4
Q

markers for determining liver excretory function

A

Bilirubin

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5
Q

markers for determining liver synthesis function

A

Albumin, PTT

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6
Q

What is de-ritis ratio & purpose? & significance of results

A

a) AST ÷ ALT ratio
> differentiate between causes of hepatocellular damage or hepatotoxicity (e.g. alcoholic)
b) >2.0 (& inc GGT) = alcoholic liver disease

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7
Q

which is more specific indicator for inflammation in liver? AST or ALT? How does this affect ALT/AST

A

ALT.

AST follows ALT (i.e. it will inc./dec. w/ it)

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8
Q

Define cholestasis. & marker for cholestasis

A

decrease in bile duct/f;low due to obstruction

marker inc. GGT, ALP (normal AST & ALT)

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9
Q

ALP is mainly high in the (organ)

A

placenta in pregnancy

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10
Q

An ALT result of >2 or 3:1 means

A

alcoholic liver disease

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11
Q

marker for cholestasis is __ as it [inc. / dec.] with _ or _ _

A

a. liver ALP

b. increases with obstruction or infiltrative disease (stones/tumour)

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12
Q

cholestasis is a condition where….

A

there is a dec. in bile flow (blocked fully/partially) from liver to duodenum

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13
Q

substrate, product, activator, pH for testing ALP (alkaline phosphatase)

A

Substrate: p-nitrophenyl phosphate
Product: p-nitrophenol
Activator: Magnesium sulfate
pH: ~10

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14
Q

Reason for rise GGT & ALP

A

cholestasis

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15
Q

Reason for rise GGT, ALT, AST (& normal ALP)

A

hepatodisease

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16
Q

Reason for rise GGT (& normal ALP, AST, ALT)

A

alcoholism/drug

17
Q

Reason for rise ALP (& normal GGT)

A

skeletal bone disease

18
Q

5’ nucleotidase (5’NTD) is a test that can substitute _ , to determine if inc ALP is due to biliary / extra-biliary origin

A

GGT (if not available in clinical settings)

19
Q

people w/ cirrhotic liver can end up being _ because liver cells are dead ≠ can’t store _

A

a. hyoglycemic b/w meals

b. glycogen

20
Q

_ is broken down to _ which is [water in/soluble] & converted by _ into _ which is [water in/soluble]

A

a. Haem (from RBC)
b. indrirect/uncojugated bilirubin - insoluble
c. UDP-glucuronosyl-transferase
d. direct/conjugate bilirubin - soluble

21
Q

Gilbert’s syndrome cause _ due to reduced activity of (enzyme)

A

a. Unconjugated hyperbilirubinemia

b. UDP-glucuronosyl-transferase

22
Q

describe the normal excretion of biliruben * (look back on slide 16)

A
  1. RBC broken down in spleen & bone haem => indirect biliruben
  2. indirect biliruben travel in blood w/ Alb to liver
  3. indirect converted to direct biliruben
  4. direct goes to kidney & intestine to be excreted => normal colour pee & poo
23
Q

Reasons that you may get hyperbilirubinaemia = jaundice

A
  • Increased haemolysis
  • Gilbert’s syndrome due to lack of gulcuronyltransferase, which conjugates bilirubin
  • Cholestasis
  • Obstruction of bile duct
24
Q

Describe the process of retention jaundice? slide 19

A
  1. excess haemolysis of RBC => heme => excess unconj./indirect bilirubin
  2. liver work @ full capacity to convert indirect bilirubin to direct, but still indirect > direct = jaundice
  3. Hi [ ] of direct bilirubin -> intestine & converted by a bacteria => stercobilinogen
  4. excess stercobilinogen
    => dark poo bc stercocilin
    => dark urine bc stercobilinogen
25
Q

Describe the process of regurgitative jaundice? slide 22

A
  1. excess haemolysis of RBC => heme => excess unconj./indirect bilirubin
  2. liver work @ full capacity to convert indirect bilirubin to direct via UDP, but still indirect > direct = jaundice
  3. obstruction/cholestasis in intra-/ post- hepatic ≠> intestine = low stercobilinogen formed = pale poo & urine
  4. direct bilirubin reabsorbed back in blood excreted via urine (water soluble)
26
Q

Cause of Hepatic comma “Encephalopathy” & resulting to

A

a) inc. ammonia due to severe liver disease bc liver can’t convert ammonia to urea
b) => loss of brain function

27
Q

describe haemochromatosis & treatment

A
  • inc. intestinal absorption of Fe => deposit in spleen & liver
  • men more vulnerable bc women can remove Fe in menstruation
  • treatment: phlebotomy (preferred); chelation of excess iron
28
Q

Describe Wilson’s disease

A
  • excess Cu in tissues due to lack of ceruloplasmin
29
Q

describe Alpha-1-Antitrypsin Deficiency

A

low Alpha-1-Antitrypsin ≠ inhibit proteases = proteins break down

30
Q

The stages of Hepatitis and liver damage are:

A

Fat accumulation – Fibrosis – Cirrhosis

31
Q

a) Cirrhosis is caused by

b) & characterized by …

A

a) Alcohol, heart failure, problems in biliary (gall bladder, bile duct), post necrotic/viral (hepatitis)
b) jaundice, liver enlargement and ascites..

32
Q

Which condition has the highest ASL & ALT b/w Chronic & acute hepatitis

A

Acute > chronic

33
Q

Steatohepatitis vs Non-alcoholic steatohepatitis

A
  • steatohepatitis: fat deposit in the liver & inflammation due to alcohol
  • Non-alcoholic steatohepatitis: fat deposit not due to alcohol
34
Q

primary causes of Non-alcoholic steatohepatitis

A
  • diabetes mellitus (type 2)
  • obesity
  • hyperlipidemia
  • inc. insulin resistance
35
Q

describe hepatoma & 3 specific markers for hepatoma

A

a) most common type of liver cancer. (malignant)

b) Des-gamma carboxyprothrombin (DCP), Hepatic ultrasound and Alpha fetoprotein (AFP)

36
Q

Non-alcoholic steatohepatitis (NASH) is the most common cause of _ _

A

cryptogenic cirrhosis

37
Q

Vitamin _ is fat soluble and it needs the bile salts for its absorption by the blood.

A

vitamin K

38
Q

A decrease in prothrombin could be seen in case of __ jaundice due to lack in bile salt.

A

obstructive

Clinical biochem. (12 decks)

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