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Clinical Biochemistry > Lab Investigation of Cardiac Disease > Flashcards

Lab Investigation of Cardiac Disease Flashcards

1
Q

What are the roles of biochemical tests in clinical medicine?

A
  • Screening (subclinical conditions)
    can assess if at risk of heart disease using cholesterol
    (HDL,LDL)
  • Diagnosis (normal vs abnormal values)
  • Monitoring (course of disease)
  • Clinical management (treatment/ response)
  • Prognosis (Risk stratification)
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2
Q

Describe the analytical characteristics of ideal markers

A
  • Measurable by cost-effective method
  • Simple to perform
  • Rapid turnaround time - quick results
  • Sufficient precision & accuracy
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3
Q

What are the clinical characteristics of ideal markers

A
  • 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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4
Q

What is cardiovascular disease?

A

Umbrella term for a number of linked pathologies including:

  • Coronary heart disease (CHD)
  • Cerebrovascular disease
  • Peripheral arterial disease
  • Rheumatic + congenital heart diseases
  • Venous thromboembolism
  • Lymphatic disease
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5
Q

What is the clinical significance of Coronary heart disease?

A

CHD causes the most deaths in men and women from CVD especially through:

  • Myocardial Infarction
  • Heart Failure
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6
Q

How does an MI originate?

A

MI starts off as a coronary vessel disorder where atherosclerosis and plaque has developed

Long process over decades

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7
Q

Describe the process of developing myocardial infarction

A
  1. Initial lesions (endothelial cell dysfunction)
  2. Fatty streaks from cholesterol and fat build up which
    calcifies
  3. Extensive lipid accumulation and deposition
  4. Fibroatheroma - lipid core capped and fibrotic
  5. Fibroatheroma breaks through endothelium to become
    a complicated lesion into vessel lumen

→ initiates thrombosis and coagulation = occlusion of vessel

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8
Q

Describe the epidemiology of MI occurrence depending on age

A

<20 y ~ 20% already have significant coronary atherosclerosis and lesions

20-29 y ~ 50%

30-39 y it’s up to 65%

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9
Q

What is atherosclerosis?

A

A complex inflammatory disease where plaque builds up inside your arteries

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10
Q

Outline the initiation of atherosclerosis

A
  1. Endothelial activation
  2. LDL penetrates endothelium
  3. LDL retained in intima, where it undergoes oxidative modification
  4. Proinflammatory lipids released from LDL
  5. Stimulates endothelial cells to express adhesion molecules
  6. Circulating monocytes adhere to endothelial cells expressing adhesion molecules e.g. VCAM-1
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11
Q

In atherosclerosis, What is the purpose of monocytes sticking to endothelial cells expressing adhesion molecules?

A

This enables them to migrate into intima due to increased permeability between endothelial cells (dysfunction)

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12
Q

What happens to monocytes once in the intima?

A

Monocytes differentiate into macrophages once migrated to the intima

Signalling molecules upregulate receptors on macrophage surfaces causing higher LDL uptake

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13
Q

Outline how calcification occurs in the intima

A

Foam cells accumulate from macrophages and are calcified

Proinflammatory response within vasculature from macrophages release cytokines, interleukins and interferons to exacerbate the response (T cell influx as well)`

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14
Q

How does coronary thrombosis occur?

A

Occlusion in a vessel due to deposition of cholesterol leads to atheroma formation that initiates thrombosis

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15
Q

What are the consequences of coronary thrombosis?

A

Ischemia → necrosis → myocardial infarction

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16
Q

Why does ischaemia occur in the heart?

A

Significant ischaemia occurs due to lack of oxygen to a part of the heart (necrosis)

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17
Q

How does ischaemia and necrosis lead to a myocardial infarction?

A

Insufficient fibrinolysis enables a myocardial infarction to ensue due to lack of perfusion
(necrosis of myocardial tissue)

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18
Q

How can atherosclerosis lead to Myocardial infarction?

A

Plaque rupture can lead to myocardial infarction

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19
Q

Describe the process of chest pain to heart attack

A

Angina → acute coronary syndromes → heart attack

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20
Q

What causes angina?

A

Angina: atherosclerosis present but sufficient flow to compensate

Chest pain but no cardiomyocyte necrosis

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21
Q

Why is it important to distinguish between types of IHD?

A

It’s important to define the type of Ischemic Heart Disease for:

Stable angina vs. acute myocardial infarction

  • Treatment
  • Prognosis
  • Management
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22
Q

Outline the various causes of chest pain

A
  • Broken rib
  • Collapsed lung
  • Nerve infection (shingles)
  • “Pulled” muscle
  • Infection
  • Heartburn (hernia)
  • Blood clot in the lungs (PE)
  • Pericarditis
  • Angina
  • Myocardial infarction
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23
Q

Why do we need to identify cause of chest pain?

A

Need to be able to differentiate between conditions as they all present with similar symptoms but can be the difference between life and death

24
Q

How do we assess IHD?

A
  1. Medical history
  2. Risk factors
  3. Presenting signs and symptoms
  4. ECG
  5. Biomarkers
  6. Imaging/scans
25
Q

What is the significance of cardiac biomarkers?

A

Biochemical markers of cardiac dysfunction/damage can contribute to:

  • Rule in/out an acute MI
  • Confirm an old MI
  • Help to define therapy
  • Monitor success of therapy
  • Diagnosis of heart failure
  • Risk stratification of death
26
Q

How long does a myocardial injury require to become irreversible?

A

Irreversible injury typically requires 30 minutes of ischaemia

High risk: 80% cardiac cells die within 3 hours and almost 100% by 6 hours

27
Q

Describe what occurs in myocardial injury

A

Cellular content leak out through membrane dependent on size and solubility

ions released first and then larger macromolecules later

Can use to identify when MI occurred

28
Q

How does the concentration gradient effect ability to detect myocardial damage?

A

Concentration gradient from inside to outside important (high gradient improves detection of early damage)

29
Q

Describe the markers seen in myocardial damage post MI

A

7-36 h peak after MI

  1. Troponin-T and troponin-I: Heart muscle specific
    markers
  2. Creatine kinase ↑ 90% MIs
    Less specific: also released from skeletal muscle
    Heart specific creatine phosphokinase isoform: CPK-
    MB
  3. Myoglobin raised early but less specific for heart
    damage
30
Q

What are troponins?

A

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

31
Q

What are the different troponin types?

A

There are three types of troponins:

  • Troponin T (tropomyosin binding)
  • Troponin I (inhibits actomyosin ATPase)
  • Troponin C (calcium binding)
32
Q

Describe the structure of the troponins

A

The troponins are three different proteins structurally unrelated with each other

33
Q

How does cardiac troponin differ from other troponins?

A

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

34
Q

What are the advantages of using cardiac troponin as a marker?

A
  • An index of cardiac damage
  • Blood levels related to severity of cardiac damage
  • Predicts major adverse cardiac events such as MI
35
Q

How do troponin levels change during MI?

A

Acute myocardial infarction causes increased levels of troponin release

36
Q

Describe troponin levels in a minor myocardial infarction

A

Minor myocardial infarction shows a smaller increase in troponin release

37
Q

How do troponin levels change in myocarditis?

A

No elevation seen in troponin levels

38
Q

What test is used to detect troponin levels?

A

Troponin (protein) levels measured using ELISA test = enzyme linked immunosorbent assay

39
Q

Outline how an ELISA test detects troponin levels

A

2 antibodies, second antibody with marker detects presence of troponin
Rapid detection

40
Q

What is heart failure?

A

Complex clinical syndrome resulting from any structural / functional cardiac disorder impairing ability of ventricles to fill or eject blood

41
Q

Outline the incidence of heart failure in the UK

A

Incidence: 920,000 people living with Heart failure in the UK

Prevalence: 1- 2 % of men and women

Poor prognosis: 1 year survival ~ 50%

42
Q

What are the major causes of heart failure?

A 
Coronary Artery Disease 
Chronic Hypertension 
Cardiomyopathy 
Heart Valve Disease 
Arrhythmias- AF,VT 
Infective endocarditis 
Pulmonary Hypertension- PE, COPD 
Alcohol and Drugs (eg cocaine)
43
Q

What marker is used to diagnose heart failure?

A

v. acute signs and symptoms so require natriuretic peptides (A,B,C) as markers of cardiac overload - gold standard of cardiac stretch markers

44
Q

What are the signs and symptoms of heart failure?

A
  • Shortness of breath
  • Swelling of feet and legs
  • Chronic lack of energy
  • Difficulty sleeping due to breathing problems
  • Swollen / tender abdomen with loss of appetite
  • Cough with frothy sputum
  • Increased urination at night
  • Confusion and/or impaired memory
45
Q

What is the use of natriuretic peptides in heart failure?

A
  1. Initial evaluation of heart failure
  2. Screening for cardiac dysfunction
  3. Guiding management of heart failure
  4. Assessment of prognosis and survival
46
Q

What are the different types of natriuretic peptides?

A

(a) Atrial
(b) brain
(c) C-type

47
Q

Describe the structure of natriuretic peptides

A

V. small structures found in different areas of cardiovascular structures (atrium, ventricle and endothelial cells) released as high mw precursor forms with active components

48
Q

Describe the main functions of ANP and BNP

A
  • natriuretic
  • vasorelaxant
  • RAAS Inhibition
49
Q

What are the effects of CNP in the body?

A
  • vasorelaxant

- CNS effects

50
Q

What stimulates secretion of ANP?

A

Atrial stretch

51
Q

What stimulates secretion of BNP?

A

Ventricular dilatation

52
Q

How does heart failure induce natriuretic peptide secretion?

A

Heart failure; oedema, trying to remove excess volume as kidneys aren’t filtering well → AV receptor stimulation causes release of ANP, BNP

53
Q

How do we measure plasma natriuretic peptides?

A

Assays available for the active peptides and the N-terminal precursor forms of BNP (and ANP)

54
Q

What are the advantages of measuring N-terminal precursor forms of the natriuretic peptides?

A

Advantages of N-terminal precursor forms of BNP

  • Longer half-life
  • Higher plasma concentrations
  • Less sensitive to rapid fluctuations
55
Q

Under what conditions is plasma BNP measured?

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
56
Q

How do we determine probability of developing Heart failure?

A

Concentration dependent manner - probability of heart failure by measuring [N-terminal pro BNP]

57
Q

Outline the varying [BNP] for the likelihoods of developing HF

A

Low probability:

  • BNP > 100pg/ml
  • NT-proBNP < 300pg/ml

Intermediate probability:

  • 100-400 pg/ml
  • NT-proBNP 300-1800 pg/ml

High probability:

  • BNP > 500 pg/ml
  • NT-proBNP > 1800 pg/ml

Clinical Biochemistry (7 decks)

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