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Pathology > C - Enzymes & Cardiac Biomarkers > Flashcards

C - Enzymes & Cardiac Biomarkers Flashcards

1
Q

define enzyme

A

substance (usually a protein that increases the rate of a chemical reaction without itself being changed in the process

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2
Q

what is Km (michaelis menten constant)

A

substrate concentration at which reaction velocity is 50% of maximum

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3
Q

what does having a high Km mean

A

weak binding

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4
Q

what does having a low Km mean

A

strong binding

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5
Q

when are intracellular enzymes released
- give examples of this

A

tissue / cellular injury
- infection, immune mediated, inflam, MI, inherited, trauma, toxins, tumour

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6
Q

where is ALP found

A

bone
biliary system
tumour marker - testicular etc
placenta
intestine

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7
Q

what does a lack of ALP cause

A

osteomalacia

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8
Q

when is ALP found in trimester

A

last trimester

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9
Q

when is ALP release from bone physiological

A

childhood as bones grow

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10
Q

raised ALP. Dx?

A

LFTs - gamma GGT or ALT
vitamin D

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11
Q

why check vit D with raised ALP

A

low vit D can cause raised ALP

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12
Q

why is ALP high in kids

A

bone growth releases ALP

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13
Q

where is ALT predominantly found

A

liver

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14
Q

where is AST predominantly found

A

heart, liver, muscle, kidney

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15
Q

why is AST not used for heart / kidney / muscle then but is used for liver?

A

heart - use trop
kidney - use creatinine or eGFR
muscle - use CK
liver - only AST and ALT are really useful

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16
Q

common causes of high ALT

A

hepatic - toxins, hepatitis, NAFLD, cancer, ischaemia
kidney issues
pancreatitis
MI

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17
Q

best biomarker for pancreatitis

A

amylase

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18
Q

when can you get hepatic ischaemia

A

post MI

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19
Q

upper limit of ALT

A

45

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20
Q

what happens to ALP when you fast

A

drops down low

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21
Q

where is gamma GGT released from

A

hepatobiliary system
pancreas
kidney

22
Q

is GGT useful at distinguishing between hepatic and biliary issues?

A

no - high in both

23
Q

what marker is useful in distinguishing between hepatic and biliary issues

A

ALT:ALP ratio

24
Q

when is high GGT released due to high levels intracellularly that get released during normal cell turnover

A

alcoholics

25
Q

what drugs induce enzymes to create high levels of GGT

A

rifampacin, phenytoin, phenobarbitone

26
Q

where is LDH found

A

WBCs
RBCs
placenta
skeletal muscle
liver
cardiac

27
Q

what diseases is LDH raised in

A

WBCs - lymphoma
RBCs - haemolysis
placenta - germ cell testicular Ca
skeletal muscle - myositis
hepatic disease
cardiac disease

28
Q

where in a tissue is LDH found

A

intracellular

29
Q

how is LDH used in lyphoma care

A

initially - high LDH = poor prognosis
subsequent - monitor treatment effectiveness

30
Q

where is amylase produced

A

pancreas
salivary gland

31
Q

what type of raised amylase is benign

A

macro amylase (large so not cleared by kidneys)

32
Q

number 1 pathology with high amylase

A

pancreatitis

33
Q

does high amylase = bad pancreatitis ?

A

no

34
Q

what organs make CK

A

skeletal muscle
cardiac muscle

35
Q

causes of raised CK

A

rhabdmyolysis
myositis / polymyositis / dermatomyositis
severe exercise
myopathy eg DMD
cardiac injury

36
Q

what is the problem with high CK

A

can cause acute tubular necrosis and AKI

37
Q

when is slightly high CK physiological

A

Afro Carribean

38
Q

where is tropinin I found

A

cardiac and skeletal myocytes

39
Q

causes of elevated troponin I

A

ACS
myocarditis
cardiomyopathy
aortic dissection

PE
infection
anaemia

40
Q

what factors affect troponin result

A

age
gender
AKI / CKD
number of myocytes injured
time of test

41
Q

when is troponin I raised after STEMI

A

rises within 2 hours, peaks at 12 hours, decreases steadily over 1 week

42
Q

how is troponin practically used in ED

A

repeat troponin after 1-3 hours to check its increasing / decreasing by 50% (indicates ACS)

43
Q

how is pathology of NSTEMI and STEMI different

A

NSTEMI is not full thickness ischaemia / occlusion, but STEMI is

44
Q

how does Ix results of unstable angina differ from STEMI

A

abnormal ECG + normal troponin (unstable angina)
abnormal ECG + troponin (STEMI)

45
Q

what chest pain is seen in stable angina

A

exertional cardiac chest pain

46
Q

can 2 negative troponins and a normal ECG rule out ACS?

A

yes

47
Q

why is BNP released

A

cardiac overload
cardiac myocytes stretch

48
Q

what does BNP causes

A

increased urination to offload the fluid

49
Q

why is BNP hard to measure in blood

A

short half life

50
Q

what is measured in blood instead of BNP and why is that okay

A

NT-proBNP (produced from the same molecule as BNP so made in the same quantity, but is not active so doesn’t degrade)

Pathology (87 decks)

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