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Cardio > Biochemistry Enzymes and Biomarkers > Flashcards

Biochemistry Enzymes and Biomarkers Flashcards

1
Q

Enzymes are:

A
  1. Intracellular catalysts

2. Measured by activity (U/L) or concentration (ng/L)

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2
Q

Serum enzyme activity is a marker of

A

Tissue function or dysfunction

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3
Q

Isoenzymes:

A

Enzymes of similar catalytic activity but structural differences, pattern may be helpful to localize origin, e.g. CK, ALP

e.g. alkaline phosphatase isoenzymes

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4
Q

Clinical important enzymes:

A
  • Liver enzymes
  • Creatine kinase (CK)
  • Amylase
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5
Q

LFT looks at

A 
Bilirubin
ALk Phosphatase (cholestasis measurement)
ALT – hepatocullar function
Total Protein
Albumin
Globulin
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6
Q

Tranaminases types

A

ALT and AST (intracellular enzymes)

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7
Q

ALT location

A

Largely confined to hepatic cytoplasm

Use routinely to test liver function

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8
Q

AST location**

A

o Hepatic cytoplasm and mitochondria
o Skeletal and cardiac muscle (will rise post MI)
o Red blood cells (haemolysis causes increased0

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9
Q

Causes of increased transaminase

>10 x ULN (>400 U/L)

A
  • Acute hepatitis and liver necrosis
  • Paracetamol poisoning
  • Major crush injuries (AST)
  • Severe hypoxia
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10
Q

Increased Transaminase

5-10 x ULN (200-400 U/L)

A
  • Chronic hepatitis
  • Following surgery or liver trauma
  • Myocardial infarction (AST)
  • Skeletal muscle disease (AST)
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11
Q

Increased Transaminase Usually <5x ULN (40-200 U/L) – upper limit of normal

A
  • Other liver disease (e.g. drug induced)
  • Pancreatitis
  • Haemolysis (in vivo and in vitro) (AST)
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12
Q

Haemolysis can cause

A

increased in AST

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13
Q

Necrosis of the liver cells e.g. fatty liver disease LF shows

A

– AST rises more than ALT

• Non-alcohol fatty liver disease

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14
Q

Tests of cholestasis:

A

Alkaline Bone phosphatase (ALP)
• Bone (osteoblasts) – can be seen in late childhood with finishing growing
• Liver (biliary tree and cell surface)

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15
Q

Minor Sources of ALP

A
  • Intestine (some patients, postprandial)
  • Placenta (third trimester, variable)
  • Rare cancers (e.g. germ cell)
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16
Q

Causes of increased alkaline phosphatase

Physiological

A
  • Pregnancy (third trimester) – usually use bile acids as test of choice for cholestasis
  • Childhood – germ cell tumours
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17
Q

Causes of increased alkaline phosphatase:
Pathological
Often >5 x ULN

A
  • Cholestasis (intra – and extra hepatic)
  • Cirrhosis
  • Paget’s disease of bone (metabolic)
  • Osteomalacia, rickets
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18
Q

ALP - Usually <5 x ULN

Seen in

A
  • Hepatitis
  • Infiltrative liver disease
  • IBD – ascending cholangitis
  • Hepatic space-occupying lesions –obstruction drainage
  • Bone tumours (primary and secondary) – Mets very common
  • Renal bone disease (RARE)
  • Primary hyperparathyroidism (longstanding)
  • Healing fractures
  • Osteomyelitis
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19
Q

Pregnancy (late) disease:

A
  • HeLLPs syndrome

* Obstetric Cholestasis

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20
Q

Tests of cholestasis:

A

Not in liver function tests as very sensitive e.g. ptients with autumn virus (subclinical disease will cause a rise in γGT.

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21
Q

Gamma glytamyl trnasferase (γGT)

Source – very sensitive

A

Liver
Kidney
Pancreas
Seminal vesicles

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22
Q

γGT increased in

A

Cholestasis and hepatocellular damage

Also due to enzyme induction – alcohol, phenobarbitone, phenytoin, oestrogen

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23
Q

γGT clinical uses

A

Detection of alcohol – via hyper-lipid detection – not extremely specific
Identification of the source of ALP (.e. Liver or Bone) – of γGT is normal then ALP likely to be coming from bone.

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24
Q

γGT in alcohol abuse elevation due to

A

Enzyme induction

Structural damage – cholestasis e.g. alcoholic cirrhosis

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25
Q

γGT is elevated in

A

50-66% of subjects consuming >80g/day

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26
Q

γGT sensitivity in alcoholics

A

54-85%

27
Q

Predictive value of a positive test for the diagnosis of alcoholism is approximately

A

20% (if prevalence is 1%)

28
Q

AST/ALT elevated and normal alkaline phosphatase means that

A

Approx. 90% have hepatitis

29
Q

AST/ALT normal and elevated alkaline phosphatase means that

A

Approx. 90% have obstructive jaundice

30
Q

CK structurally

A

Two subunits: M and B

Three isoforms: MM, MB and BB

31
Q

CK skeletal muscle Often >10 x URL

A

Polymyositis
Rhabdomyolysis (trauma, drugs etc)
Duchemme muscular dystrophy

32
Q

CK skeletal muscle 5-10 x URL

A 
Following surgery
Physical trauma
grand -mal convulsions
Myositis
Duchenne carriers
33
Q

CK skeletal muscle Usually <5 x URL

A

Physiological (Afro-Caribbeans
Hypothyroidism
Drugs (e.g. statins)

34
Q

Myocardium:

CK

A

Myocardial infarction
Cardiac Myopathy
Myocarditis

35
Q

MI Diagnosis methods

A

Cardiac Troponins (TnT, Tnl, TnC*) – 100% cardiac specific

36
Q

cTnl and cTnT

A
  • Highly sensitivity for myocardial injury (different structurally form skeletal muscle)
  • Not released until 4-6 hours after MI – not for acute
  • 100% diagnostic sensitivity not achieved until 12 h - confirmatory
  • Remain elevated for up to one week
37
Q

Amylase description

A

Exocrine pancreatic and salivary enzyme

38
Q

Amylase used in

A

Diagnosis of acute pancreatitis

39
Q

Amylase: Minor elevations are

A

Not specific *

40
Q

Amylase: Results are

A

Highly method dependent

41
Q

Amylase clearance

A

Kidney

42
Q 
raised serum amylase activity:
Marked increase (>5x upper reference limit)
A
  • Acute pancreatitis
  • Severe diabetic ketoacidosis
  • Severe renal glomerular failure (clearance)
  • Perforated peptic ulcer
43
Q

raised serum amylase activity:

Moderate increase

A
  • Other intra-abdominal disorders
  • Renal dysfunction
  • Salivary disorders
  • Morphine
  • Macromylasaemia
44
Q

Tumour Markers

A

Substance measured in body fluids in order to diagnose or stage malignancy, or monitor response to therapy:

45
Q

Tumour Marker types

A

Structural proteins
Enzymes
Secretion products

46
Q

Structural proteins

A
  1. CEA, Mucins (CA125, 153, 199) – carbohydrate antigen (CA(
47
Q

Enzymes

A
  1. PSA
48
Q

Secretion products

A
  1. Thyroglobulin (medullary carcinoma of thyroid)
  2. AFP (foetal life – then switches to albumin )- hepatocellular carcinoma indication.
  3. BJP (benns johns proteins (myeloma etc. –B cell)
49
Q

Potential uses of Tumour Markers

A
  1. To screen for early disease (useless)
  2. To aid diagnosis (useless)
  3. To stage disease and or assess prognosis
  4. To monitor patients with disease
    a. Assess response to Rx
    b. Detect early relapse
50
Q

Practical use of tumour marker sin diagnosis:

A
  1. To rule out disease in an anxious patient (selective screening)
  2. To make a diagnosis when disease is strongly suspected
  3. To identify primary in patients with signs of metastatic disease
51
Q

Sensitivity

A

The percentage of those with disease who test positive

52
Q

Specificity

A

The percentage of those without disease who test negative

53
Q

Higher cut off means

A

More specific but less sensitive

54
Q

Lower cut off means

A

More Sensitive but less Specific

55
Q

Positive predictive Value

A

% of those with a positive test result who have disease

56
Q

Negative Predictive Value

A

% with a negative test result who are free of disease

57
Q

Depend on

A

Sensitivity, specificity and prevalence

58
Q

PPV problems

A

Falls dramatically at low prevalence

59
Q

CA125

A

Screening high risk individuals (with ultrasound)
Diagnosis of ovarian mass
Monitoring RX

60
Q

CA153

A

Monitoring response of breast cancer to treatment

61
Q

AFP/HCG

A

Staging prior to orchidectomy

62
Q

CEA

A

Pre-op
Postop (but only if liver mets would be resected)
Monitoring treatment response (chemo)

63
Q

PSA

A

Diagnosis if used with DRE 9+/-)

Monitoring RX

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