Lab Investigation of Cardiac Disease Flashcards

1
Q

What are the general biochemical tests in clinical medicine?

A
  • Screening (subclinical conditions)
  • Diagnosis (normal vs abnormal values)
  • Monitoring (course of disease)
  • Clinical management (treatment/ response)
  • Prognosis (Risk stratification)
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2
Q

What are the classifications of laboratory tests in cardiac disease?

A
  • Markers of risk factors for development of coronary artery disease
  • Genetic analysis for candidate genes of risk factors
  • Markers of cardiac tissue damage
  • Markers of myocardial function/overload
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3
Q

What are cardiac markers?

A

They are located in the myocardium, and are released in response to:

  • cardiac overload
  • cardiac injury.
  • cardiac failure

They can be measured in blood samples.

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4
Q

What can biochemical markers of cardiac dysfunction/damage contribute to?

A
  • can rule in/out an acute MI
  • can confirm an old MI
  • can help to define therapy
  • can monitor success of therapy
  • diagnosis of heart failure
  • risk stratification of death
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5
Q

What are the analytical and clinical characteristics of an ideal cardiac marker?

A
ANALYTICAL:
• Measurable by cost-effective method 
• Simple to perform 
• Rapid turnaround time 
• Sufficient precision & accuracy 
• Reasonable cost 
CLINICAL:
• Early detection of disease 
• Sensitivity vs specificity 
• Validated decision limits 
• Selection of therapy 
• Risk stratification 
• Prognostic value 
• Ability to improve patient outcome
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6
Q

Describe the development of an atheromatous plaque.

A

INITIAL LESION:

  • histologically ‘normal’
  • macrophage infiltration
  • isolated foam cells

FATTY STREAK:
- mainly intracellular lipid accumulation

INTERMEDIATE LESION:

  • intracellular lipid accumulation
  • small extracellular lipid pools

ATHEROMA:

  • intracelullar lipid accumulation
  • core of extracelullar lipid

FIBROATHEROMA:

  • single or multiple lipid cores
  • fibrotic/calcific layers

COMPLICATED LESION:

  • surface defect
  • haematoma-haemorrhage
  • thrombosis
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7
Q

What are the major consequences of coronary thrombosis?

A

The blockage can lead to ischaemia (restriction of the oxygen supply to the tissue), leading to necrosis (tissue death) and ultimately a myocardial infarction.

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8
Q

List some chronic ishcaemic heart diseases.

A
  • stable angina
  • variant angina
  • silent myocardial ischaemia
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9
Q

List some acute coronary syndromes.

A
  • unstable angina
  • ST-segment elevation MI
  • non ST-segment elevation MI
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10
Q

Why is it important to define the type of IHD?

A

This is because different heart diseases have/need different:

  • treatments
  • prognosis
  • management
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11
Q

What are some causes of chest pain?

A
  • broken rib
  • collapsed lung
  • nerve infection (shingles)
  • “pulled” muscle
  • infection
  • heart burn (hernia)
  • pericarditis
  • blood clot in the lungs (PE)
  • angina
  • myocardial infarction
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12
Q

How would you assess IHD?

A
  • medical history
  • risk factors
  • presenting signs and symptoms
  • ECG
  • biomarkers (cardiac troponin, cTn)
  • imaging/scans
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13
Q

Describe the prognosis of myocardial injury (i.e. relation between time and damage done).

A

An irreversible injury typically requires 30 minutes of ischaemia.
There’s a high risk that 80% of cardiac cells die within 3 hours and almost 100% by 6 hours.

Cellular contents leak out through membrane dependent on their size and solubility.
This concentration gradient from inside to outside is important (as a high gradient improves detection of early damage).

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14
Q

Which myocardial cell constituents are released first?

A

Ions (such as potassium or phosphate) are released first since they are the smallest, followed by metabolites (such as lactate or adenosine), and then finally, we have macromolecules (such as enzymes or proteins).

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15
Q

What are some markers of myocardial damage?

A

Most are release at the 7-36 hour peak after an MI.

There are heart muscle specific markers such as troponin-T and troponin-I.

Creatine kinase (found in more than 90% of MIs, but less specific as it’s also released from skeletal muscle).

There are heart specific isoforms of creatine phosphokinase (CPK-MB).

Myoglobin is raised early, but is less specific for heart damage.

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16
Q

Describe troponins.

A

The troponin complex is a component of the thin filaments in striated muscle complexed to actin.

There are three types of troponins:
• Troponin T (tropomyosin binding)
• Troponin I (inhibits actomyosin ATPase)
• Troponin C (calcium binding)

The troponins are three different proteins structurally unrelated with each other.

Cardiac troponin T and I differ significantly from troponin T and I found in skeletal muscle.

17
Q

What are the advantages of cardiac troponin?

A
  • it’s an index of cardiac damage
  • the blood levels are related to the severity of cardiac damage
  • it predicts major adverse cardiac events such as myocardial infarction
18
Q

How would you detect troponins in the blood?

A

You would do an ELISA (enzyme-linked immunosorbant assay) test.

19
Q

Briefly describe heart failure in the UK, and list some of the major causes of heart failure.

A

It is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

Incidence: 920,000 people living with heart failure in the UK.
Prevalence: 1- 2 % of men and women
Poor prognosis: 1 year survival ~50%

Some major causes of heart failure:

  • Coronary Artery Disease
  • Chronic Hypertension
  • Cardiomyopathy
  • Heart Valve Disease
  • Arrhythmias- AF,VT
  • Infective endocarditis
  • Pulmonary Hypertension- PE, COPD
  • Alcohol and Drugs (eg cocaine)
20
Q

What are some signs and symptoms of congestive heart failure?

A
  • shortness of breath
  • swelling of feet and legs
  • chronic lack of energy
  • difficulty sleeping at night due to breathing problems
  • swollen or tender abdomen with loss of appetite
  • cough with frothy sputum
  • increased urination at night
  • confusion and/or impaired memory
21
Q

What is the clinical utilisation of cardiac biomarker testing in heart failure?

A

They are used for:

  • initial evaluation of heart failure
  • screening for cardiac dysfunction
  • guiding management of heart failure
  • assessment of prognosis and survival
22
Q

For the three natriuretic peptides, list their source, main effects, secretion stimulus and function.

A
ANP
Source (main): atrium
Main effects: natriuretic, vasorelaxant, RAAS inhibition
Secretion stimulus: atrial stretch
Function: endocrine

BNP
Source (main): ventricle
Main effects: natriuretic, vasorelaxant, RAAS inhibition
Secretion stimulus: ventricular dilatation
Function: endocrine

CNP
Source (main): endothelial
Main effects: vasorelaxant, CNS effects
Secretion stimulus: -
Function: paracrine?
23
Q

How would you measure plasma natriuretic peptides?

A

There are assays available for the active peptides and the N-terminal precursor forms of BNP.
However, it was found that measuring the N-terminal precursor forms of the NPs were more clinically useful.

The advantages of measuring the precursor:

  • Longer half-life
  • Higher plasma concentrations
  • Less sensitive to rapid fluctuations
24
Q

What conditions can be investigated using BNP?

A
  • Assessment of severity of congestive heart failure
  • Screening for mild heart failure
  • Monitor response to treatment in congestive heart failure
  • Prognostic outcome/risk stratification