Laboratory Investigation of Cardiac Disease Flashcards Preview

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Flashcards in Laboratory Investigation of Cardiac Disease Deck (55)
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1

What are the 5 biochemical tests in clinical medicine?

➝ Screening (subclinical conditions)
➝ diagnosis (normal vs abnormal values)
➝ monitoring (course of disease)
➝ clinical management (treatment/response)
➝ prognosis (risk stratification)

2

What are the 4 analytical characteristics of ideal biomarkers?

➝ measurable by cost-effective method
➝ simple to perform
➝ rapid turnaround time
➝ sufficient precision & accuracy

3

What are the 6 clinical characteristics of ideal biomarkers?

➝ Early detection of disease
➝ sensitivity vs specificity
➝ validated decision limits
➝ selection of therapy
➝ risk stratification
➝ prognostic value
➝ ability to improve patient outcome

4

What 6 pathologies come under the umbrella of cardiovascular disease?

➝ Coronary heart disease
➝ cerebrovascular disease
➝ peripheral arterial disease
➝ rheumatic and congenital heart diseases
➝ venous thromboembolism
➝ lymphatic disease

5

How does development of atheromatous plaques occur and what can this lead to?

➝ Starts off with a development of atherosclerotic plaque
It is a long process that takes decades before patients show signs of disease
➝ First there is endothelial dysfunction, which leads to a fatty streak, more lipid gets deposited and the plaque will get calcified and fibrotic
➝ It can break through the endothelium and turn into a complicated lesion and initiate thrombosis which leads to occlusion of the vessel

6

What % of <20 year olds have significant coronary atherosclerosis?

➝ 20%

7

What % of 20-29 year old have significant atherosclerosis?

➝ 50%

8

What % of 30-39 year olds have significant atherosclerosis?

➝ 65%

9

Describe the mechanism of the formation of atheromatous plaques?

➝Inflammation is thought to initiate the onset of disease
➝This results in the endothelial cells lining the blood vessels to becoming activated
LDL can penetrate the intima and will undergo oxidation
➝It starts to release pro-inflammatory mediators that enhance the expression of adhesion molecules on the surface of endothelial cells
➝The rolling hypothesis suggests that circulating monocytes come into contact with the adhesion molecules and move through into the intima
➝Once the monocytes are in the intima they differentiate into macrophages and upregulate receptors and cause more uptake of LDL
➝You have foam cells that accumulate from macrophages
➝They build up and start to get calcified

10

How does coronary thrombosis lead to an MI?

Ischaemia ➝ necrosis ➝ myocardial infarction

11

What is angina caused by and why does this not cause heart attacks?

➝ a plaque with a fibrous cap blocking one of the coronary vessels
➝there is enough flow to compensate so there is no necrosis

12

How are acute coronary syndromes and heart attacks caused?

➝ plaque cap ruptures
➝ blood clot forms around the rupture which blocks the artery

13

Why is it important to define the types of ischemic heart disease?

➝ There is different treatment, prognosis and management of stable angina vs an acute myocardial infarction

14

What are the 10 possible causes of chest pain?

➝ Broken rib
➝ collapsed lung
➝ nerve infection 'shingles'
➝ pulled muscle
➝Infection
➝Heartburn
➝Pericarditis
➝Blood clot in the lungs (pulmonary embolism)
➝Angina
➝Myocardial infarction

15

What 6 assessments are done if a patient comes in with chest pain?

➝ Medical history
➝Risk factors
➝Presenting signs and symptoms
➝ECG
➝Biomarkers
➝imaging/scans

16

What 6 things can biochemical markers of cardiac dysfunction/damage contribute to?

➝ rule in or out an acute MI
➝ confirm an old MI
➝ help to define therapy
➝ monitor success of therapy
➝ diagnosis of heart failure
➝ risk stratification of death

17

How long does irreversible injury take to occur?

➝ 30 minutes of ischaemia

18

If there is irreversible ischemia what does this tell you about the death of cardiac cells?

➝ high risk that 80% of cardiac cells die within 3 hours and almost 100% by 6 hours

19

What happens to the cellular content during an MI?

➝ cellular content leaks out through membrane dependent on size and solubility (ions will be released first and then proteins and enzymes)

20

What is important when looking at cellular content from an MI and why?

➝ Concentration gradient from the inside to the outside
➝ a high gradient improves detection of early damage

21

What are the two heart muscle specific markers?

➝ Troponin T
➝ Troponin I

22

What is a less specific cardiac marker and why?

➝ Creatine kinase
➝ it is also released from skeletal muscle

23

When do myocardial damage markers peak?

➝ 7-36 hours after MI

24

In what % of MIs is creatine kinase raised?

➝ 90%

25

What MI marker is raised the first and why is this not used?

➝ myoglobin
➝ less specific for heart damage

26

When do Troponin I & T peak after an MI?

➝ 24-36 hours

27

What is the duration of elevation of CK, myoglobin, troponin T & I?

➝ Troponin T & I : depends on the extent of damage
➝ Myoglobin : 1 day
➝ CK : 3 days

28

What is the troponin complex?

➝ a component of the thin filaments in striated muscle complexed to actin

29

How many types of troponin are there?

➝ 3

30

What are the 3 types of troponin and what are their functions?

➝ Troponin T (tropomyosin binding)
➝ Troponin I (inhibits actomyosin ATPase)
➝ Troponin C (calcium binding)