Lab Investigation of Cardiac Disease Flashcards
1
Q
What are the biochemical tests in the treatment of medicine?
A
- Screening tests: subclinical conditions
- Diagnosis: normal vs abnormal values
- Monitoring: course of disease
- Clinical management: treatment/response
- Prognosis: risk stratification
2
Q
What are the two characteristics of ideal biomarkers?
A
- Analytical Characteristics
- Measurable by the cost-effective method
- Simple to perform
- Rapid turnaround time
- Sufficient precision and accuracy - Clinical Characteristics
- Early detection of the disease
- Sensitivity vs specificity
- Validated decision limits
- Selection of therapy
- Risk stratified
- Prognostic value
- Ability to improve patient outcome
3
Q
Example of Cardiovascular Disease
A
Umbrella term for a number of limited pathologies including:
- Coronary heart disease (CHD)
- Cerebrovascular disease
- Peripheral arterial disease
- Rheumatic and congenital heart disease
- Venous thromboembolism
- Lymphatic disease
4
Q
Development of an atheromatous plaque: How does an MI occur
A
- Start off as a disorder of the coronary vessel where is there is atherosclerosis. This is a long process that will take a long time to show disease.
- There is an initial lesion and then a build-up of fatty acids that get calcified.
- The atheroma can break in the end and form a complicated lesion and eventually occlusion of the vessel.
MI - is a significant disease in young adults
5
Q
How is atherosclerosis initiated?
A
- LDL penetrates the endothelium and is retained in the intima where it will undergo oxidation.
- It then starts to release pro-inflammatory mediators, which enhance the expression of the adhesion molecules on the surface of the endothelial cells.
- The circulating monocytes will then come in contact with adhesion molecules on the surface of endothelial cells such as VCAM-1.
- The monocytes will then be able to move and enter between the endothelial cells into the intima.
- They will start to differentiate into macrophages and acquire receptors on their surface so they can uptake more LDL.
- Eventually, foam cells will start to accumulate from macrophages.
- They will build up and start to get calcified.
- At the same time, there is a pro-inflammatory response occurring where the macrophages are releasing interferons and cytokines which will exacerbate the response.
This is why it is thought to be an inflammatory response modified by life factors such as smoking and drinking.
6
Q
Consequences of coronary thrombosis
A
- Ischaemia: not enough oxygen to this part of the heart
- Necrosis: The death of tissue in response to hypoxia
- Myocardial infarction: when the thrombosis does not dissolve
7
Q
What can plaque rupture cause?
A
Can lead to myocardial infarction
8
Q
How does a plaque rupture cause myocardial infarction?
A
- In angina, there is reduced blood flow due to the plaque build-up making the diameter of the vessel smaller.
- Therefore, there is reduced blood flow.
- Whereas, when the atheroma ruptures and a blood clot can form, this will lead to complete obstruction of the vessel.
- Therefore, no blood flow leading to heart attack and necrosis of tissue.
9
Q
Difference between Angina, Acute coronary syndromes and “Heart Attack - myocardial infarction”
A
Angina - Plaque with a fibrous cap
Acute coronary syndromes - Cap ruptures
Myocardial Infarction - Blood clot forms around the rupture, blocking the artery
10
Q
Causes of chest pain
A
- Range from non-serious effects such as broken ribs and collapsed lung to angina and myocardial infarction.
- It is important to detect which cause it is, in order to be able to treat it appropriately.
11
Q
Assessments of ischaemic heart disease (IHD)
A
- Take medical history
- Risk factors
- Presenting signs and symptoms
- ECG
- Biomarkers that help to rule in/out an acute MI; confirm an old MI; help to define therapy; monitor success of therapy; diagnosis of heart failure; and risk stratification of death.
- Imaging and scans
12
Q
Time-span of a myocardial infarction
A
- The irreversible injury typically requires 30 mins of ischaemia
- The high risk that 80% of cardiac cells die within 3 hours and almost 100% by 6 hours
- Cellular content leaks out through membrane dependent on size and solubility
- Concentration gradient from inside to outside important
- This is because high gradient improves detection of early damage.
13
Q
Markers of myocardial damage
A
- Troponins (Troponin T and Troponin I): most important markers for myocardial damage because they are specific to the heart and therefore helps rule of false results
- Creatinine kinase: Can be used as early detection, however, it is not specific to the heart, therefore any skeletal muscle damage will release creatinine kinase in the blood.
- Heart specific isoforms of creatinine phosphokinase can be used.
- Myoglobin can also be used as it is raised early but it is less specific for heart damage.
- There is a 7-36 hour peak after MI of the biomarkers
14
Q
What is the troponin complex?
A
A component of the thin filament in striated muscle complexed to actin.
15
Q
What are the three types of troponins?
A
- Troponin T: tropomyosin binding
- Troponin I: inhibits actomyosin ATPase
- Troponin C: calcium-binding
The troponins are 3 different proteins structurally unrelated to each other.
Cardiac troponins differ significantly from troponin I and T found in skeletal muscles
