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Biochemistry > Organ Function Tests - Heart > Flashcards

Organ Function Tests - Heart Flashcards

1
Q

What are the 4 reasons for changes in concentrations of some plasma proteins/peptides in organs? What are these changes known as? Why are they not always accurate?

A

Surgery, trauma, infection, tumour growth. ‘Markers’ to monitor a condition/treatment. Not necessarily related to organ function.

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2
Q

What does an organ function test measure to help diagnose disease/organ damage? Why are they not always accurate?

A

The measurement of the released enzymes. Not always accurate as the release of enzymes is only roughly proportional to damage.

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3
Q

What are symptoms from acute coronary syndrome due too?

A

Ischaemia caused by occlusion or partial occlusion of vessels supplying the heart.

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4
Q

What causes arterial narrowing?

A

Atheromatous plaque.

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5
Q

What is an atheromatous plaque?

A

Plaque core of cholesterol, oxidised cholesterol, and cells including macrophages.

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6
Q

What are the similarities and the main difference between unstable angina and MI?

A

Ischaemia caused by occlusion/partial occlusion in both. Difference is: no permanent damage to cardiac muscle cells in UA. But permanent damage to cardiac muscle cells in MI (necrosis).

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7
Q

What does angina mean and when does it occur?

A

Heart pain. Occurs during times of increased O2 requirement only (e.g. exercise) and stops soon after resting (this is why GPs ask people who come in complaining of chest pain if their chest felt tight during exercise, which will help them to reach an accurate diagnosis).

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8
Q

What is infarction define as?

A

Death or necrosis of cardiac muscle caused by ischaemia (loss of blood supply).

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9
Q

Why is a differential diagnosis of MI important?

A

As MI may require quick treatment to limit the area of infarction.

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10
Q

Why is it hard to come up with a differential diagnosis for MI? (ECG)

A

Only 30% of MI sufferers will show ECG changes characteristics of MI.

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11
Q

What can help determine whether patients with no ECG changes have MI or unstable angina?

A

Biochemical markers of cardiac necrosis can help to determine.

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12
Q

What 3 markers are used to detect myocardial necrosis in patients presenting with acute cardiac chest pain?

A

Troponin T and I and CKMB.

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13
Q

If there is no ST segment elevation and markers of MN are not elevated then what do patients have?

A

Unstable angina.

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14
Q

If there is no ST segment elevation and markers of MN ARE elevated then what do patients have? And what is usually absent.

A

Non-ST segment elevation MI (Q waves are usually absent).

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15
Q

If there IS ST segment elevation and markers of MN ARE elevated then what do patients have? And what is usually present?

A

ST segment elevation MI. Q waves usually present.

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16
Q

What is the 3rd Universal definition of MI?

A

Rise and/or fall of specific cardiac marker level (troponin or CKMB).

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17
Q

What else will show that a patient has a MI?

A

Specific ECG changes OR symptoms of ischaemia OR imaging evidence (MRI/echocardiography) of new myocardial loss OR angiographic evidence of thrombus.

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18
Q

What are specific ECG changes to show MI/unstable angina?

A

Development of pathological Q waves OR ST elevation/depression = ECG changes indicative of new ischaemia

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19
Q

In a normal ECG what is the ST segment like?

A

Straight.

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20
Q

What is a T wave inversion?

A

ST segment is straight, then where the T wave should be slightly elevated (like in a normal ECG) it inverts down.

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21
Q

What happens when myocardial cells die?

A

Release their contents into the blood.

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22
Q

What cardiac enzymes have been used to diagnose MI in the past as they increase (but all at different levels and times)?

A

CK, CKMB, aspartate transaminase, lactate dehydrogenase (especially LDH1/hydroxybutyrate), myoglobin.

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23
Q

What is myoglobin and after what event is it elevated?

A

Haem-containing protein that is often elevated after heart disease.

24
Q

How many afters after is myoglobin most sensitive for diagnosing MI? However what are the faults of using myoglobin as a biomarker for MI?

A

After 6 hours. Not specific to the heart. Levels also increase after crush injuries if there is any muscle damage.

25
Q

Which enzyme is used to diagnose MI but i also raised after liver damage so therefore lacks organ specificity?

A

Aspartate transaminase.

26
Q

Where is CK found? How many sub-units does it have and what are they?

A

Found in different tissues existing as isoenzymes. 2 sub-units, type B (brain) or M (muscle) - there is also a mitochondrial form.

27
Q

Where is CK-MM (the predominant form) found and what %?

A

Found primarily in skeletal muscle (98%) and cardiac muscle (70-80%).

28
Q

Where is CK-MB found (and what % in skeletal muscle)?

A

Found in cardiac muscle (20-30%), tongue, diaphragm, and 1-2% in skeletal muscle.

29
Q

Where is CK-BB found?

A

Found in the brain, smooth muscle, thyroid, lungs, and prostate.

30
Q

Which isoenzyme rises the earliest after an MI and how many hours post-event?

A

CKMB. 3-8 hours post event.

31
Q

What modern treatments provide a quicker response to test for CKMB levels in a patient? And why is this good?

A

Thrombolysis, angioplasty. To limit permanent damage to cardiac muscle.

32
Q

Which isoforms of which cardiac marker are specific to the MYOCARDIUM rather than skeletal muscle?

A

Isoforms of troponin, T and I.

33
Q

What is troponin and how many are there in muscle?

A

Proteins that regulate muscle contraction, 3.

34
Q

What does troponin T do?

A

Binds tropomyosin (to block myosin binding sites on actin).

35
Q

What does Troponin I do?

A

Inhibitory protein, binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. Because of it, myosin cannot bind actin in relaxed muscle.

36
Q

What does troponin C do?

A

Binds calcium.

37
Q

What levels should Troponins T and I be looked at to detect heart damage?

A

Increasing levels, above 99th percentile.

38
Q

How are troponins T and I useful for retrospective diagnosis?

A

Because they stay elevated for around 7-10 days.

39
Q

What are the usual units of cTn (cardiac troponin) since the introduction of ultra-high sensitivity assays when diagnosing acute coronary syndrome?

A

ng/mL.

40
Q

Why is problematic that 4th generation ultra high-sensitivity assays detect down to 3ng/L? And what is used to confirm a large increase in troponin levels to confirm MI?

A

It is less specific to MI. They will pick up levels which may appear slightly raised but may be naturally slightly higher in some patients for other reasons such as rena l issues (slows down clearance of troponin from the blood). Serial measurements.

41
Q

How are current clinical research on troponin finding rule-out algorithms?

A

By measuring plasma troponin concentrations at presentation (with acute coronary syndrome) using a high-sensitivity cardiac troponin I assay and evaluated the negative predictive value of a range of troponin concentrations for the primary outcome of: index myocardial infarction, subsequent myocardial infarction or cardiac death at 30 days. Implementation of this approach could substantially reduce hospital admissions and have major benefits for both patients and health-care providers.

42
Q

What is cMyC?

A

Cardiac-myosin-binding protein-C. Protein from cardiac sarcomere.

43
Q

Why is cMyC good to be used in the early diagnosis of AMI?

A

Concentrations rise more quickly in the blood than cTn does, better for early chest pain <3hrs rule out.

44
Q

What were the results of using cMyC to rule out AMI against other protein biomarkers?

A

Ruled out AMI in 9% more patients than hscTnT and 17% more than hscTnI.

45
Q

When is repercussion injury possible and what can the damage from it cause?

A

Following a period of ischaemia following MI, stroke, traumatic injury or other forms of O2 deprivation in an area of tissue. Damage caused can extend the area of necrosis.

46
Q

Why is there calcium ion overload after myocardial ischaemia?

A

Anaerobic respiration. Na/K ATPase pump stops working, leading to intracellular overload of sodium ions.

47
Q

Following an acute episode of sustained myocardial ischaemia what does the opening of the mitochondrial permeability transition pore (MPTP) cause?

A

Opening of MPTP in the first few minutes of reperfusion mediates cell death.

48
Q

What is thought to play a role in reperfusion injury?

A

Reactive oxygen species.

49
Q

What happens when the MPTP remains closed (due to acidic condition) during ischaemia?

A

Myofibrils can’t contract.

50
Q

When reperfusion occurs what is reactivated and what is produced? How does this lead to cell membrane and DNA damage?

A

Electron transport is reactivated and ROS are produced. Damage by oxidation.

51
Q

What is the treatment for reperfusion injury?*

A

No effective treatment currently, many attempts to find therapy.

52
Q

What is the current basis of treatment for reperfusion injury?

A

1) limit time of ischaemia as far as possible - treat MI quickly by thrombolytic drugs or angioplasty; consider when treating other causes of ischaemia. 2) general supportive therapy.

53
Q

What advances have there been in reperfusion research?

A

Accumulation of succinate during ischaemic period due to reverse reaction of fumarate to succinate (succinic dehydrogenase) detected, when perfusion is restored rapid conversion of large amounts of succinate to fumarate leads to production of reactive O2 species (ROS).

54
Q

79 y/o admitted with chest pain after working in garden. What tests should be carried out? Has troponin level changed? What diagnosis can be ruled out? What possible diagnoses are there?

A

ECG showed no specific sings of MI. Troponin T on admission: 5.4ng/L. Troponin T 6hrs post admission: 5.0ng/L.

55
Q

What are the reference ranges for a male and female for MI?

A

99th percentile males = 14.5 ng/L

Females = 10.0ng/L

Biochemistry (7 decks)

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