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MLAB 2401: Clinical Chemistry Keri Brophy-Martinez Cardiovascular Conditions and Assessment.

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Presentation on theme: "MLAB 2401: Clinical Chemistry Keri Brophy-Martinez Cardiovascular Conditions and Assessment."— Presentation transcript:

1 MLAB 2401: Clinical Chemistry Keri Brophy-Martinez Cardiovascular Conditions and Assessment

2 Functions of the Heart Pumps blood to the organs of the body Delivers oxygen and nutrients where they are needed Removes waste products from tissues

3 Symptoms of Heart Disease

4 Pathologic Conditions of the Heart Congenital Cardiovascular Defects – Abnormality arises from abnormal formation of heart or its major blood vessels – Present at birth All defects develop before the 10 th week of pregnancy – Origin unknown but appear to be based on genetic disposition and environmental influences

5 Congenital Cardiovascular Defects Symptoms – Cyanosis – Pulmonary hypertension – Embolism – Clubbed fingers – Reduced growth – Syncope Examples – Tetralogy of Fallot – Ventricular septal defects “hole in the heart”

6 Pathologic Conditions of the Heart Heart Failure or Congestive Heart Failure – Any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood – Result Excess fluid accumulates in the lungs producing edema Reduced output of blood to systemic circulation Retention of fluid by the kidneys

7 Heart Failure or Congestive Heart Failure Examples – Left ventricular dysfunction – Coronary artery disease – Cardiac arrhythmias See it:

8 Pathologic Conditions of the Heart Acute Coronary Syndromes – Term used to describe a series of events Angina Reversible tissue injury Unstable angina Myocardial infarction Extensive tissue necrosis

9 Acute Coronary Syndromes Clinical Symptoms – Chest pain – Referred pain – Nausea – Vomiting – Dyspnea – Diaphoresis – Light headedness

10 Acute Coronary Syndromes Causes – Atherosclerosis Inflammatory disorder Plaques deposit in artery walls Leads to ischemia

11 Stages of Atherosclerosis 1.Initial vascular injury caused by: 1.Hypertension, hyperlipidemia, hyperhomocysteinemia 2.Increased permeability to lipids especially LDL/VLDL 1.Results in inflammation 3.Monocytes & Leukocytes arrive to help! 4.Macrophages scavenge LDL/cholesterol-rich lipoproteins- become foam cells 5.Foam cells promote lesion progression 6.T and B lymphocytes are recruited by the plaque 7.Interactions between T/B lymphs and foam cells recruits smooth muscle cells into the lumen 8.Smooth muscle cells secrete collagen, elastin, and proteoglycans to fix the plaque to the vessel wall

12 Presentation of Coronary Heart Disease

13 Hypertension Persistent systolic BP of at least 140 mm HG and/or diastolic BP of at least 90 mm Hg Prevalence increases with age Contributing factors – Obesity – Physical inactivity – Unhealthy nutrition

14 Hypertensive Heart Disease Term used to describe heart disease caused by direct or indirect effects of increased BP Peripheral resistance determining factor in BP – Increases workload of left ventricle resulting in hypertrophy and dilation of mitral valve. This valve is affected and blood is regurgitated to the left atrium

15 Infective Heart Disease Heart disease caused by infectious agents Examples – Rheumatic Heart Disease Complication of rheumatic fever due to autoimmune response. Causative organism is Group A streptococcus Usually affects young adults and children – Infective Endocarditits Infection of endocardial surface of the heart Causative organism Group D streptococcus, but others also – Pericarditis Inflammation of the pericardium Causative agents include bacteria, fungi, viral, autoimmune, others

16 Diagnosing Heart Disease Myocardial Infarction – Diagnosis based on clinical symptoms, EKG changes and the rise/fall of biochemical markers – Samples collected at onset, 6-9 hours and hours if previous samples were negative – Preferred biomarkers are Troponin I and T. Specific and sensitive for myocardial necrosis Current guidelines suggest the use of 2 markers for diagnosis

17 Current Cardiac Panel – Myoglobin Released from damaged cardiac/skeletal muscle – Cardiac troponins See upcoming slide – CK – CK-MB – BNP Discussed later

18 Time Course Of Enzyme Activity in MI’s Historically CK, CK-MB, AST, LD/LDH isoenzymes used EnzymeOnset of Elevation (Hr) Peak activity (Hr) Duration of Elevation CK CK-MB AST LD LDH isoenzymes

19 Time Course Of Enzyme Activity in MI’s Troponin – Rises 4-10 hours after onset – Peak at hours – Elevated for 4-10 days Myoglobin – Released 1-4 hours after onset CK-MB – Rises within 4-6 hours after onset – Peaks at hours – Normal at 2-3 days

20 Troponin Consists of three proteins that bind to thin filament(actin) of cardiac and skeletal muscle – Troponin T (TnT) – Troponin I (TnI) – Troponin C (TnC) Function to bind Ca + and regulate muscle contraction Absent in the serum of healthy people

21 What’s So Special About Troponin? Specific for cardiac tissue High diagnostic specificity and sensitivity Early detection following MI Remain elevated for several days Undetected in healthy people Few interfering substances in detection

22 Markers of Inflammation High Sensitivity C-Reactive Protein (hsCRP) – Acute phase protein – Produced in the liver in response to injury, infection and inflammation – Increases in CRP correlate with the risk of coronary artery disease

23 Markers of Congestive Heart Failure Natriuretic peptide – Hormones that include atrial natriuretic peptide (ANP), B-type natriuretic peptide(BNP), C-type and D- type – Assist in regulation of cardiovascular homeostasis – BNP Released on ventricular stretch or stress to myocytes in the absence of necrosis Increased BNP indicates expanded fluid volume such as that seen in renal failure and CHF

24 Vascular Inflammation Plaque Destabilization Plaque Rupture Acute Phase Reactant (CRP) Ischemia Necrosis (Troponin) Myocardial Dysfunction (BNP, NT-proBNP)

25 References Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical Chemistry: Techniques, principles, Correlations. Baltimore: Wolters Kluwer Lippincott Williams & Wilkins. heart-failure.html heart-failure.html cular_disease/atherosclerosis.html cular_disease/atherosclerosis.html Sunheimer, R., & Graves, L. (2010). Clinical Laboratory Chemistry. Upper Saddle River: Pearson.


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