SlideShare a Scribd company logo
1 of 52
LIPID PROFILE TEST
Lipid Panel; Coronary Risk Panel
RAJENDRA DEV BHATT, PhD Scholar
Asst. Professor
Clinical Biochemistry and Laboratory Medicine
Fellow: Translational Research (2018-2022) in CVD in Nepal, NHLBI & NIH, USA
What is a lipid profile Test ?
• The lipid profile is a group of tests that have
been shown to be good indicators of whether
someone is likely to have a Coronary disease
or heart attack or stroke caused by blockage of
blood vessels or hardening of the arteries
(atherosclerois).
What is a lipid profile?
• The lipid profile typically includes:
– Total cholesterol
– High density lipoprotein cholesterol (HDL-C) — often called good cholesterol
– Low density lipoprotein cholesterol (LDL-C) —often called bad cholesterol
– Triacylglycerol
– An extended profile may also include:
• Very low density lipoprotein cholesterol (VLDL-C)
• Non-HDL-C
• Lipoprotien ( a)-LPa
• Sometimes the report will include additional calculated values
such as the Cholesterol/HDL ratio etc
Lipid Profile panel Test
• Serum
– Total Cholesterol (TC)
– HDL-Cholesterol (HDL-C)
– Triacylglycerol
– LDL-Cholesterol
– Calculated VLDL
– Non-HDL Cholestrol
– TC/HDL-C ratio
– TAG/HDL ratio
– LDL-C/HDL ratio
How is the sample collected for testing?
• Subject need to fast for 9-12 hours before blood is drawn; only
water is permitted.
• Total and HDL-C levels are similar when fasting or non-fasting, but
TAG should be measured after 12 to 14 hours of fasting.
• Serum TC and HDL-C can be done in random sample.
• TAG levels are inversely related to HDL-C levels.
• Diurnal variation causes TAG to be lowest in the morning and
highest around noon.
CARDIAC BIOMARKERS
“A biomarker is a substance used as an
indicator of a biological state”.
Morrow and De Lomos suggested three criteria for
biomarkers
• Accurate repeated measurements at reasonable cost
• Must provide additional information
• Should aid treatment
An indicator used for objective
measurement and evaluation of
Response to
therapeutic
intervention
Pathogenic process
Normal biological
process
Characteristics of an ideal biomarker
• Standardized
• High Sensitivity and Specificity
• Accurate
• Reproducible
• Easy to interpret
• Consistent and Cost effective
• Has an impact on clinical/risk
management
• Rule out an acute MI
• Confirm an old MI (several days)
• Monitor the success of thrombolytic therapy
• Risk stratification of patients with unstable angina pectoris
Risk stratification in apparently healthy persons is not
done with cardiac markers, but by measurement and
assessment of cardiac risk factors
QUESTIONS MAYANSWEREDBY CARDIAC MARKERS
History of Cardiac Biomarkers
 1954 - SGOT (AST)
 1955 - LDH
 1960 - CPK
 1972 - CPK isoforms by Electrophoresis
 1975 - CK - MB by immunoinhibition
 1975 - Myoglobin
 1985 - CK - MB Mass immunoassay
 1989 - Troponin T
 1992 - Troponin I
Cardiac biomarkers
• Cardiac biomarkers were first developed for assisting the
cardiac events, especially acute myocardial infarction.
• Better understanding of cardiac disease process and
advancement in detection technology has pushed the application
of cardiac biomarkers beyond the diagnosis boundaries.
• Cardiac biomarkers are now used for staging of cardiac disease,
timing of cardiac events and prognostification.
• Markers of cardiac tissue damage
• Markers of myocardial function
• Cardiovascular risk factor markers
• Genetic analysis for candidate genes or
risk factors
CLASSIFICATION OF LABORATORY TESTS IN CARDIAC
DISEASE
High sensitivity C-Reactive Protein (hs-CRP) &
Homocysteine
Marker of Inflammation
• CRP is Pentameric structure consisting of five identical
subunits of 23-kDa.
• Its plasma levels can increase rapidly to 10,000x levels.
• It is the most extensively studied marker of inflammation. Despite
some controversy regarding its clinical use, it appears to be the most
promising to date.
• Although considered to be a general nonspecific marker of
inflammation, elevated baseline levels of hsCRP are correlated with
higher risk of future CV morbidity and mortality among those with
or without clinical evidence ofCVD.
High-Sensitivity
C-Reactive Protein
Clinical Uses
– Screening for cardiovascular risk in otherwise “healthy”
individuals
– Predictive value of CRP levels for disease severity in pre- existing
Coronary artery disease
Elevated levels are predictive of
• Long-term risk of first MI
• Ischemic stroke
High-Sensitivity
C-Reactive Protein
• Low specificity
• No evidence that lowering CRP levels decreases CV risk
Industry and FDA staff guidelines 2005 had given clinical cut off
value as less than 1 mg/l as safe levels with hs-CRP tests
CRP
Less than 1.0 mg/L
1.0-2.9 mg/L
Greater than 3.0 mg/L
Risk for CVD
Low
Intermediate
High
Limitations of CRP
• Intermediary amino acid formed by the conversion of methionine
to cysteine
• Moderate hyperhomocysteinemia occurs in 5-7% of the population
• Recognized as an independent risk factor for the development of
atherosclerotic vascular disease and venous thrombosis
• Can result from genetic defects, drugs, vitamin deficiencies
Homocysteine
• Homocysteine is implicated directly in vascular injury including:
– Intimal thickening
– Disruption of elastic lamina
– Smooth muscle hypertrophy
– Platelet aggregation
• Proposed mechanisms by which it induces vascular injury are
leukocyte recruitment, foam cell formation, and inhibition of NO
synthesis.
• Normal levels : 3.7 – 13.9 µmol/L
Homocysteine
• Elevated levels of homocysteine appear to be an
independent risk factor, though less important than
the classic CV risk factors.
• Treatment includes supplementation with folate, B6
and B12.
Homocysteine
Marker of Mocardial Ischemia
Ischemia Modified Albumin (IMA) and
Heart type-fatty Acid Binding Protein (H-
FABP)
• Ischemia modified albumin is a marker formed after
damage in the N terminal region of the albumin in
ischemic conditions.
• This structural change leads to loss of its ability to bind with
transitional metals (cu/co).
• Endothelial or extracellular hypoxia, acidosis and free
oxygen radicals causes increase in IMA.
• IMA rises within minutes from onset of ischemia and remains
elevated for several hours after cessation of ischemia.
Ischemia
Modified Albumin
It is used as diagnostic criteria for myocardial necrosis
that develops after Coronary artery bypass graft
surgery (CABG).
It is a non specific marker, since it is also reported to be
elevated in pulmonary infarction, critical limb ischemia
and cerebrovascular disorders.
Basically, it is used to rule out ischemia rather than
diagnosing the occurrence of ischemia. Which is helpful in
differentiating pain of Angina from Myocardial ischemia.
Clinical uses of IMA :
• Heart type fatty acid binding protein is a very stable low
molecular weight (14-15kDa) in the cytoplasm of myocardial
cells.
• FABPs are involved in active fatty acid metabolism where it
transports fatty acid from cell membrane to mitochondria for
oxidation.
• Small size of H-FABP facilitates rapid diffusion through interstitial
space, appearing as early as 1-3 hrs after onset and peaking within
6hrs. It return to normal levels with in 12-24hrs.
• Normal levels : 1.6 – 19 ng/ml
H-FABP
• H-FABP is 20 times more specific to cardiac muscle than myoglobin
• H-FABP is recommended to be measured with troponin to identify MI
and ACS in patient presenting with chest pain.
• In addition to its diagnostic potential H-FABP also has prognostic
value. The risk associated with ↑ H-FABP is dependent upon its
concentration. Patients who were cTnI normal but H-FABP high have
more risk of morbidity and mortality after 1 year follow up than
those with cTnI high but HFABP normal.
H-FABP
Marker for cardiac necrosis
cTn
CK-MB
Myoglobin
• Troponin is a complex of three regulatory proteins
(Troponin C, Troponin I and Troponin T) that is
associated with muscle contraction in skeletal and
cardiac muscle.
• Cardiac troponin is slightly different from skeletal
troponin structurally hence serve as a potent and
specific marker for cardiac disease.
Cardiac Troponins
THE TROPONIN
REGULATORY COMPLEX
Individual subunits serve different functions:
• Troponin C binds to calcium ions to produce a
conformational change in TnI
• Troponin T binds to tropomyosin, interlocking them to
form a troponin-tropomyosin complex
• Troponin I binds to actin in thin myofilaments to hold
the troponin-tropomyosin complex in place
• Usually, Troponin is not detectable in healthy
individual.
Cardiac Troponins
• It is extremely useful in patients who do not seek
attention in the 2 to 3 days window when CK-MB is
elevated.
• Rise : with in few hours after onset of chest pain Peak
: 2 days returns normal : 7-10 days
• cTnT may show a biphasic release in some patients
with a first peak occurring during first 24 hr of onset
of symptom and second peak on appx. 4th day after
admission.
• TnT has cardiac as well as skeletal muscle source.
cTnT :
• It is cardiac specific because it has additional amino acid
residue on its N-terminal that are non existent in skeletal
muscle.
Rise : b/w 4-6 hr after onset of pain
Peaks : 12-18 hrs
Returns normal : 6 days
• Its measurement is advantageous over CK-MB as it is not
found in detectable amount in serum of patients with
multiple injuries, renal disease and in those with acute
and chronic skeletal muscle disorders.
cTnI :
• Creatine kinase (CK) is a cytosolic enzyme involved with the
transfer of energy in muscle metabolism. It catalyses the
conversion of creatine to phospho-creatine degrading ATP to
ADP.
• CK is a dimer composed of two subunits B (brain type) and
M (muscle type), resulting in three isoenzyme:
CK-BB (CK1) : is of brain origin, found in blood only when
BBB is damaged.
CK-MB (CK2) : it is relatively specific for myocardial origin
CK-MM (CK3) : it is found primarily in skeletal muscle
CREATINE KINASE: CK-MB
CREATINE KINASE: CK-MB
• CK-MB is the most cardiac-specific CK isoenzyme
• Proportion of CK-MB varies in skeletal & cardiac
muscle
• In normal population CK-MB < 6% Tot CK
• Sensitive marker with rapid rise & fall
• More specific than Tot CK but has limitations
• “Gold standard” biochemical marker for past few
decades
It is a valuable tool for the diagnosis of MI because of its
relative high specificity for myocardial damage.
Rise : 4-6 hrs after onset of symptoms
Peak : 12 hrs
Return to normal : 24-36 hrs
Can be used to indicate early re-infarction if level
normalizes and then increases again.
CK-MB :
• Small-size heme protein found in all tissues mainly assists in oxygen
transport
• It is released from all damaged tissues
• Its level rises more rapidly than cTn and CK-MB.
• Released from damaged tissue within 1 hour
• Normal value: 17.4-105.7 ng/ml
• Timing:
– Earliest Rise:
– Peak
– Return to normal:
1-4 hrs
6-9 hrs
12 hrs
Myoglobin
• Acute myocardial infarction
• Skeletal muscle damage, muscular dystrophy,
inflammatory myopathies
• Renal failure, severe uremia
• Shock and trauma
CONDITIONS FOR
MYOGLOBIN INCREASE :
*if myoglobin concentration remains within the reference range 8 hours
after the onset of chest pain, AMI can be ruled out essentially.
*because of its rapid clearance by the kidney, a persistently normal
Mb concentration will rule out reinfarction in patient with recurrent
chest pain afterAMI
*Rapid monitor of success of thrombolytic
therapy DRAWBACKS
• Due to poor specificity, myoglobin levels do not always predict
myocardial injury
Clinical usefulness of
myoglobin :
NEW GENERATION
CARDIAC MARKERS
• Myoglobin
– Currently earliest marker
– Like total CK it is by no means cardio-
specific
• Troponins
– Kinetics comparable with total CK and
CK-MB
– Cardio-specific
Sensitivity
Specificity
2
3
4
5
7
6
myoglobin
CK-MB
cTnT
cTnI
Comparison of cTn, CK-MB , Mb
1
0
0 4 8 12 16 20 24 28 32 36 40 44 48
Time after onset of AMI (hours)
Χ
upper
limit
of
reference
interval
Marker for haemodynamic stress
natriuretic peptides
• The natriuretic peptides (NP) are a group of structurally similar but
genetically distinct peptide hormone.
It includes : ANP : atrial natriuretic peptide (28 a.a.) N-terminal proANP
(98 a.a.)
BNP : brain natriuretic peptide (32 a.a.) N-terminal proBNP (76 a.a.)
CNP : C-type natriuretic peptide (22 and 53 a.a.)
DNP : D- type natriuretic peptide
The NPs play important role in regulation of salt and water balance(CV
homeostasis)
Natriuretic peptides
• ANP is released primarily in response to atrial wall
stretching and intravascular volume expansion.
• BNP is mainly secreted by the ventricles
• CNP is found predominantly in the brain and also
synthesized by vascular endothelial cells
natriuretic peptides
• Circulating levels of BNP are raised in patients
with cardiovascular or renal disease
• BNP is More important than ANP in heart failure
• Greatest proportion of circulating BNP is thought
to come from the ventricles (left)
BRAIN NATRIURETIC PEPTIDE (BNP)
• BNP and the terminal fragment of its prohormone (NT-proBNP) are
released on ventricular stretch or stress to the myocyte in the absence
of the necrosis.
• Therefore, BNP is increased in diseases characterised by an
expanded fluid volume (e.g. CHF, renal failure,hepatic cirrhosis etc.)
• BNP has circulating T₁/₂ of 20 minutes, so it is indicative of snapshot
of myocardial function, while NT-proBNP has T₁/₂ of 90 minutes
giving a longer view of myocyte .
BRAIN
NATRIURETIC
PEPTIDE (BNP)
SUMMARY
• “Cardiac Enzymes” are obsolete
• Medical & laboratory progress has required a redefinition of
Cardiac Events
• Cardiac Troponins & Myoglobin now play a pivotal role in the
diagnosis of AMI
• Cardiac Troponins play an important role in the risk stratification
of ACS patients
• Elevated Troponin levels in patients without ECG changes & with
normal CK-MB levels may identify patients at increased risk of
cardiac events
1. What is the earliest cardiac marker that can be
detected?
a. Myoglobin
b. CK-MB
c. Cardiac Troponin I
d. Cardiac Troponin T
2. A biomarker is substance used as
an……………. Of a biological state
a. Inhibitor
b. Indicator
c. Cofactor
d. None of these
3. How many hours do troponin begin to rise?
a. 1 hour
b. 2 hours
c. 4 hours
d. 8 hours
4. What is the most sensitive and specific marker
available today for AMI?
a. CKMB
b. Myoglobin
c. CKBB
d. Troponin
5. What is a marker for heart failure?
a. Myoglobin
b. Troponin
c. BNP
d. CKMB

More Related Content

What's hot

Lect 6. (digestion and absorption in git)
Lect 6. (digestion and absorption in git)Lect 6. (digestion and absorption in git)
Lect 6. (digestion and absorption in git)
Ayub Abdi
 

What's hot (20)

Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptx
Cholesterol Biosynthesis  and catabolism for MBBS, Lab. MEd. BDS.pptxCholesterol Biosynthesis  and catabolism for MBBS, Lab. MEd. BDS.pptx
Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptx
 
KETONE BODIES METABOLISM
KETONE BODIES METABOLISMKETONE BODIES METABOLISM
KETONE BODIES METABOLISM
 
Local control of blood flow
Local control of blood flow Local control of blood flow
Local control of blood flow
 
Chemistry of nucleotides
Chemistry of nucleotidesChemistry of nucleotides
Chemistry of nucleotides
 
GANDHAM RAJEEV-BIOCHEMISTRY IMPORTANT QUESTIONS-RGUHS-2017
GANDHAM RAJEEV-BIOCHEMISTRY IMPORTANT QUESTIONS-RGUHS-2017GANDHAM RAJEEV-BIOCHEMISTRY IMPORTANT QUESTIONS-RGUHS-2017
GANDHAM RAJEEV-BIOCHEMISTRY IMPORTANT QUESTIONS-RGUHS-2017
 
Beta Oxidation of Fatty Acids
Beta  Oxidation of Fatty Acids Beta  Oxidation of Fatty Acids
Beta Oxidation of Fatty Acids
 
9. integration of metabolism
9. integration of metabolism9. integration of metabolism
9. integration of metabolism
 
Posterior pituitary gland (The Guyton and Hall physiology)
Posterior pituitary gland (The Guyton and Hall physiology)Posterior pituitary gland (The Guyton and Hall physiology)
Posterior pituitary gland (The Guyton and Hall physiology)
 
Arterial blood pressure
Arterial blood pressureArterial blood pressure
Arterial blood pressure
 
Extra Cellular Matrix (ECM)
Extra Cellular Matrix (ECM)Extra Cellular Matrix (ECM)
Extra Cellular Matrix (ECM)
 
regulation of cholesterol synthesis
regulation of cholesterol synthesisregulation of cholesterol synthesis
regulation of cholesterol synthesis
 
isoenzymes and clinical enzymology
 isoenzymes and clinical enzymology isoenzymes and clinical enzymology
isoenzymes and clinical enzymology
 
Lect 6. (digestion and absorption in git)
Lect 6. (digestion and absorption in git)Lect 6. (digestion and absorption in git)
Lect 6. (digestion and absorption in git)
 
Lipid metabolism
Lipid metabolismLipid metabolism
Lipid metabolism
 
0. physiology of the gastrointestinal tract
0. physiology of the gastrointestinal tract0. physiology of the gastrointestinal tract
0. physiology of the gastrointestinal tract
 
Metabolism , Metabolic Fate& disorders of cholesterol.pptx
Metabolism , Metabolic Fate& disorders of cholesterol.pptxMetabolism , Metabolic Fate& disorders of cholesterol.pptx
Metabolism , Metabolic Fate& disorders of cholesterol.pptx
 
Transport across cell membranes
Transport across cell membranesTransport across cell membranes
Transport across cell membranes
 
Reverse cholesterol metabolism
Reverse cholesterol metabolismReverse cholesterol metabolism
Reverse cholesterol metabolism
 
De Novo synthesis of fatty acids
De Novo synthesis of fatty acidsDe Novo synthesis of fatty acids
De Novo synthesis of fatty acids
 
Hematopoiesis
HematopoiesisHematopoiesis
Hematopoiesis
 

Similar to Lipid Profile test & Cardiac Markers for MBBS, Lab. Med. and Nursing.pptx

CARDIAC MARKERS new powerpoint for mbbs students
CARDIAC MARKERS new powerpoint for mbbs studentsCARDIAC MARKERS new powerpoint for mbbs students
CARDIAC MARKERS new powerpoint for mbbs students
dinesh kumar
 
cardiac troponin assay utility in early detection of acute coronary syndrome
 cardiac troponin assay utility in early detection of acute coronary syndrome cardiac troponin assay utility in early detection of acute coronary syndrome
cardiac troponin assay utility in early detection of acute coronary syndrome
anaonline
 

Similar to Lipid Profile test & Cardiac Markers for MBBS, Lab. Med. and Nursing.pptx (20)

cardiac markers ppt.pptx
cardiac markers ppt.pptxcardiac markers ppt.pptx
cardiac markers ppt.pptx
 
cardiac injury markers.pdfhfcfhxcfhchfcjfhcjhc
cardiac injury markers.pdfhfcfhxcfhchfcjfhcjhccardiac injury markers.pdfhfcfhxcfhchfcjfhcjhc
cardiac injury markers.pdfhfcfhxcfhchfcjfhcjhc
 
CARDIAC MARKERS new powerpoint for mbbs students
CARDIAC MARKERS new powerpoint for mbbs studentsCARDIAC MARKERS new powerpoint for mbbs students
CARDIAC MARKERS new powerpoint for mbbs students
 
Cardiac Markers (Recap and Update)
Cardiac Markers (Recap and Update)Cardiac Markers (Recap and Update)
Cardiac Markers (Recap and Update)
 
Cardiac bio markers
Cardiac bio markersCardiac bio markers
Cardiac bio markers
 
Novel Cardiac biomarkers in Ischemic heart disease
Novel Cardiac biomarkers in Ischemic heart diseaseNovel Cardiac biomarkers in Ischemic heart disease
Novel Cardiac biomarkers in Ischemic heart disease
 
Cardiac biomarkers
Cardiac biomarkersCardiac biomarkers
Cardiac biomarkers
 
Cardiac Biomarker past, today and future by Dr. Anurag Yadav
Cardiac Biomarker past, today and future by Dr. Anurag YadavCardiac Biomarker past, today and future by Dr. Anurag Yadav
Cardiac Biomarker past, today and future by Dr. Anurag Yadav
 
Cardiac Injury Marker.pptx
Cardiac Injury Marker.pptxCardiac Injury Marker.pptx
Cardiac Injury Marker.pptx
 
Cardiac biomarkers(1)
Cardiac biomarkers(1)Cardiac biomarkers(1)
Cardiac biomarkers(1)
 
Cardiac biomarkers - I
Cardiac biomarkers  - ICardiac biomarkers  - I
Cardiac biomarkers - I
 
Cardiac Biomarkers by sandip
Cardiac Biomarkers by sandipCardiac Biomarkers by sandip
Cardiac Biomarkers by sandip
 
CARDIAC BIOMARKERS.pptx
CARDIAC BIOMARKERS.pptxCARDIAC BIOMARKERS.pptx
CARDIAC BIOMARKERS.pptx
 
Serum markers of cardiac damage
Serum markers of cardiac damageSerum markers of cardiac damage
Serum markers of cardiac damage
 
cardiac troponin assay utility in early detection of acute coronary syndrome
 cardiac troponin assay utility in early detection of acute coronary syndrome cardiac troponin assay utility in early detection of acute coronary syndrome
cardiac troponin assay utility in early detection of acute coronary syndrome
 
Acs biomark final
Acs biomark finalAcs biomark final
Acs biomark final
 
Bio-Markers of Heart Failure (Dr.LIKHIT T)
Bio-Markers of Heart Failure (Dr.LIKHIT T)Bio-Markers of Heart Failure (Dr.LIKHIT T)
Bio-Markers of Heart Failure (Dr.LIKHIT T)
 
C reactive protein
C  reactive proteinC  reactive protein
C reactive protein
 
Cardiac biomarkers - II
Cardiac biomarkers  - IICardiac biomarkers  - II
Cardiac biomarkers - II
 
Cardiac Profile Biochemistry Test - Presentation.pptx
Cardiac Profile Biochemistry Test - Presentation.pptxCardiac Profile Biochemistry Test - Presentation.pptx
Cardiac Profile Biochemistry Test - Presentation.pptx
 

More from Rajendra Dev Bhatt

More from Rajendra Dev Bhatt (20)

Plasma proteins and their functions for Nursing .pptx
Plasma proteins and their functions for Nursing .pptxPlasma proteins and their functions for Nursing .pptx
Plasma proteins and their functions for Nursing .pptx
 
Heme synthesis for medical And Nursing studentspptx
Heme synthesis for medical And Nursing studentspptxHeme synthesis for medical And Nursing studentspptx
Heme synthesis for medical And Nursing studentspptx
 
EICOSONOIDS METABOLISM FOR MBBS, LAB. MED.BDS.pptx
EICOSONOIDS METABOLISM FOR MBBS, LAB. MED.BDS.pptxEICOSONOIDS METABOLISM FOR MBBS, LAB. MED.BDS.pptx
EICOSONOIDS METABOLISM FOR MBBS, LAB. MED.BDS.pptx
 
PTH & Calcitonin for MBBS, BDS, Lab. Med..pptx
PTH & Calcitonin for MBBS, BDS, Lab. Med..pptxPTH & Calcitonin for MBBS, BDS, Lab. Med..pptx
PTH & Calcitonin for MBBS, BDS, Lab. Med..pptx
 
Thyroid function tests for MBBS, LAB. MED & BDS.pptx
Thyroid function tests for MBBS, LAB. MED & BDS.pptxThyroid function tests for MBBS, LAB. MED & BDS.pptx
Thyroid function tests for MBBS, LAB. MED & BDS.pptx
 
Amino Acid Metabolism for MBBS, Laboratory Medicine.pptx
Amino Acid Metabolism for MBBS, Laboratory Medicine.pptxAmino Acid Metabolism for MBBS, Laboratory Medicine.pptx
Amino Acid Metabolism for MBBS, Laboratory Medicine.pptx
 
Cell :Structure & Functions for Medical and Health allied Students
Cell :Structure & Functions for Medical and Health allied StudentsCell :Structure & Functions for Medical and Health allied Students
Cell :Structure & Functions for Medical and Health allied Students
 
Biochemistry of Carbohydrates for MBBS, BDS, Lab Med 2024.pptx
Biochemistry of Carbohydrates for MBBS, BDS, Lab Med 2024.pptxBiochemistry of Carbohydrates for MBBS, BDS, Lab Med 2024.pptx
Biochemistry of Carbohydrates for MBBS, BDS, Lab Med 2024.pptx
 
5. Renal Function Tests.pptx
5. Renal Function Tests.pptx5. Renal Function Tests.pptx
5. Renal Function Tests.pptx
 
4. Renal Block-Acid Base Balance-for Medical students.pptx
4. Renal Block-Acid Base Balance-for Medical students.pptx4. Renal Block-Acid Base Balance-for Medical students.pptx
4. Renal Block-Acid Base Balance-for Medical students.pptx
 
3. Renal Block-Water and Electrolyte Balance-MBBS-2024.pptx
3. Renal Block-Water and Electrolyte Balance-MBBS-2024.pptx3. Renal Block-Water and Electrolyte Balance-MBBS-2024.pptx
3. Renal Block-Water and Electrolyte Balance-MBBS-2024.pptx
 
2. Automationa & AI in Clinical Laboratory.pptx
2. Automationa & AI in Clinical Laboratory.pptx2. Automationa & AI in Clinical Laboratory.pptx
2. Automationa & AI in Clinical Laboratory.pptx
 
Basic Instruments-Equipment; Application and Management.pptx
Basic Instruments-Equipment; Application and Management.pptxBasic Instruments-Equipment; Application and Management.pptx
Basic Instruments-Equipment; Application and Management.pptx
 
What is Research.pptx
What is Research.pptxWhat is Research.pptx
What is Research.pptx
 
2.Mysthenia & Parkinson_BDS.ppt
2.Mysthenia & Parkinson_BDS.ppt2.Mysthenia & Parkinson_BDS.ppt
2.Mysthenia & Parkinson_BDS.ppt
 
1. Neurotransmitter-4-BDS.pptx
1. Neurotransmitter-4-BDS.pptx1. Neurotransmitter-4-BDS.pptx
1. Neurotransmitter-4-BDS.pptx
 
Biochemistry of Cell Membrane.pptx
Biochemistry of Cell Membrane.pptxBiochemistry of Cell Membrane.pptx
Biochemistry of Cell Membrane.pptx
 
CSF FOR all.pptx
CSF FOR all.pptxCSF FOR all.pptx
CSF FOR all.pptx
 
VITAMIN A_MBBS_II.pptx
VITAMIN A_MBBS_II.pptxVITAMIN A_MBBS_II.pptx
VITAMIN A_MBBS_II.pptx
 
Biochemistry of Lipids_MBBS_BDS-Lab.Med.pptx
Biochemistry of Lipids_MBBS_BDS-Lab.Med.pptxBiochemistry of Lipids_MBBS_BDS-Lab.Med.pptx
Biochemistry of Lipids_MBBS_BDS-Lab.Med.pptx
 

Recently uploaded

Tortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdf
Tortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdfTortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdf
Tortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdf
Dr. Afreen Nasir
 
Top 20 Famous Indian Female Pornstars Name List 2024
Top 20 Famous Indian Female Pornstars Name List 2024Top 20 Famous Indian Female Pornstars Name List 2024
Top 20 Famous Indian Female Pornstars Name List 2024
minkseocompany
 
تقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdf
تقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdfتقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdf
تقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdf
د حاتم البيطار
 
100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @
100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @
100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @
Abortion pills in Kuwait Cytotec pills in Kuwait
 
Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...
Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...
Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...
Levi Shapiro
 
Spauldings classification ppt by Dr C P PRINCE
Spauldings classification ppt by Dr C P PRINCESpauldings classification ppt by Dr C P PRINCE
Spauldings classification ppt by Dr C P PRINCE
DR.PRINCE C P
 
obat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragen
obat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragenobat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragen
obat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragen
siskavia171
 
Abortion pills in Qatar (+919707208804) Get Cytotec Pills IN Doha
Abortion pills in Qatar (+919707208804) Get Cytotec Pills IN DohaAbortion pills in Qatar (+919707208804) Get Cytotec Pills IN Doha
Abortion pills in Qatar (+919707208804) Get Cytotec Pills IN Doha
Abortion pills in Kuwait Cytotec pills in Kuwait
 

Recently uploaded (20)

Tortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdf
Tortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdfTortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdf
Tortora PRINCIPLES OF ANATOMY AND PHYSIOLOGY - Tortora - 14th Ed.pdf
 
Personnel and Equipment - Code and Rapid Response Workshop
Personnel and Equipment - Code and Rapid Response WorkshopPersonnel and Equipment - Code and Rapid Response Workshop
Personnel and Equipment - Code and Rapid Response Workshop
 
Top 20 Famous Indian Female Pornstars Name List 2024
Top 20 Famous Indian Female Pornstars Name List 2024Top 20 Famous Indian Female Pornstars Name List 2024
Top 20 Famous Indian Female Pornstars Name List 2024
 
Technology transfer documentation and strategies
Technology transfer documentation and strategiesTechnology transfer documentation and strategies
Technology transfer documentation and strategies
 
تقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdf
تقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdfتقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdf
تقرير منظمة الصحة العالمية الخاص بالغذاء د حاتم البيطار.pdf
 
Session-17-KANGAROO-MOTHER-CARE_final-blue.pptx
Session-17-KANGAROO-MOTHER-CARE_final-blue.pptxSession-17-KANGAROO-MOTHER-CARE_final-blue.pptx
Session-17-KANGAROO-MOTHER-CARE_final-blue.pptx
 
100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @
100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @
100%Safe& effective {+918133066128} Abortion Pills for sale Kuwait all areas @
 
Organisation and Management of Eye Care Programme Service Delivery Models
Organisation and Management of Eye Care Programme Service Delivery ModelsOrganisation and Management of Eye Care Programme Service Delivery Models
Organisation and Management of Eye Care Programme Service Delivery Models
 
Famous Indian Vedic Astrologer | Best Astrological Solutions UK
Famous Indian Vedic Astrologer | Best Astrological Solutions UKFamous Indian Vedic Astrologer | Best Astrological Solutions UK
Famous Indian Vedic Astrologer | Best Astrological Solutions UK
 
POSHAN ABHIYAAN-Poshan 2.0 will concentrate on Maternal Nutrition, Infant and...
POSHAN ABHIYAAN-Poshan 2.0 will concentrate on Maternal Nutrition, Infant and...POSHAN ABHIYAAN-Poshan 2.0 will concentrate on Maternal Nutrition, Infant and...
POSHAN ABHIYAAN-Poshan 2.0 will concentrate on Maternal Nutrition, Infant and...
 
I urgently need a love spell caster to bring back my ex. +27834335081 How can...
I urgently need a love spell caster to bring back my ex. +27834335081 How can...I urgently need a love spell caster to bring back my ex. +27834335081 How can...
I urgently need a love spell caster to bring back my ex. +27834335081 How can...
 
Communication disorder and it's management
Communication disorder and it's managementCommunication disorder and it's management
Communication disorder and it's management
 
Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...
Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...
Healthcare Market Overview, May 2024: Funding, Financing and M&A, from Oppenh...
 
Spauldings classification ppt by Dr C P PRINCE
Spauldings classification ppt by Dr C P PRINCESpauldings classification ppt by Dr C P PRINCE
Spauldings classification ppt by Dr C P PRINCE
 
obat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragen
obat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragenobat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragen
obat aborsi Sragen wa 082223595321 jual obat aborsi cytotec asli di Sragen
 
The Power of Technology and Collaboration in Research - Rheumatology Research...
The Power of Technology and Collaboration in Research - Rheumatology Research...The Power of Technology and Collaboration in Research - Rheumatology Research...
The Power of Technology and Collaboration in Research - Rheumatology Research...
 
Lactation Mraining Management Session-2-Comm-Building-Conf.ppt
Lactation Mraining Management  Session-2-Comm-Building-Conf.pptLactation Mraining Management  Session-2-Comm-Building-Conf.ppt
Lactation Mraining Management Session-2-Comm-Building-Conf.ppt
 
Navigating Conflict in PE Using Strengths-Based Approaches
Navigating Conflict in PE Using Strengths-Based ApproachesNavigating Conflict in PE Using Strengths-Based Approaches
Navigating Conflict in PE Using Strengths-Based Approaches
 
Abortion pills in Qatar (+919707208804) Get Cytotec Pills IN Doha
Abortion pills in Qatar (+919707208804) Get Cytotec Pills IN DohaAbortion pills in Qatar (+919707208804) Get Cytotec Pills IN Doha
Abortion pills in Qatar (+919707208804) Get Cytotec Pills IN Doha
 
Session-3-Promoting-Breastfeeding-During-Pregnancy.ppt
Session-3-Promoting-Breastfeeding-During-Pregnancy.pptSession-3-Promoting-Breastfeeding-During-Pregnancy.ppt
Session-3-Promoting-Breastfeeding-During-Pregnancy.ppt
 

Lipid Profile test & Cardiac Markers for MBBS, Lab. Med. and Nursing.pptx

  • 1. LIPID PROFILE TEST Lipid Panel; Coronary Risk Panel RAJENDRA DEV BHATT, PhD Scholar Asst. Professor Clinical Biochemistry and Laboratory Medicine Fellow: Translational Research (2018-2022) in CVD in Nepal, NHLBI & NIH, USA
  • 2. What is a lipid profile Test ? • The lipid profile is a group of tests that have been shown to be good indicators of whether someone is likely to have a Coronary disease or heart attack or stroke caused by blockage of blood vessels or hardening of the arteries (atherosclerois).
  • 3. What is a lipid profile? • The lipid profile typically includes: – Total cholesterol – High density lipoprotein cholesterol (HDL-C) — often called good cholesterol – Low density lipoprotein cholesterol (LDL-C) —often called bad cholesterol – Triacylglycerol – An extended profile may also include: • Very low density lipoprotein cholesterol (VLDL-C) • Non-HDL-C • Lipoprotien ( a)-LPa • Sometimes the report will include additional calculated values such as the Cholesterol/HDL ratio etc
  • 4.
  • 5. Lipid Profile panel Test • Serum – Total Cholesterol (TC) – HDL-Cholesterol (HDL-C) – Triacylglycerol – LDL-Cholesterol – Calculated VLDL – Non-HDL Cholestrol – TC/HDL-C ratio – TAG/HDL ratio – LDL-C/HDL ratio
  • 6. How is the sample collected for testing? • Subject need to fast for 9-12 hours before blood is drawn; only water is permitted. • Total and HDL-C levels are similar when fasting or non-fasting, but TAG should be measured after 12 to 14 hours of fasting. • Serum TC and HDL-C can be done in random sample. • TAG levels are inversely related to HDL-C levels. • Diurnal variation causes TAG to be lowest in the morning and highest around noon.
  • 7.
  • 9. “A biomarker is a substance used as an indicator of a biological state”. Morrow and De Lomos suggested three criteria for biomarkers • Accurate repeated measurements at reasonable cost • Must provide additional information • Should aid treatment
  • 10. An indicator used for objective measurement and evaluation of Response to therapeutic intervention Pathogenic process Normal biological process
  • 11. Characteristics of an ideal biomarker • Standardized • High Sensitivity and Specificity • Accurate • Reproducible • Easy to interpret • Consistent and Cost effective • Has an impact on clinical/risk management
  • 12. • Rule out an acute MI • Confirm an old MI (several days) • Monitor the success of thrombolytic therapy • Risk stratification of patients with unstable angina pectoris Risk stratification in apparently healthy persons is not done with cardiac markers, but by measurement and assessment of cardiac risk factors QUESTIONS MAYANSWEREDBY CARDIAC MARKERS
  • 13. History of Cardiac Biomarkers  1954 - SGOT (AST)  1955 - LDH  1960 - CPK  1972 - CPK isoforms by Electrophoresis  1975 - CK - MB by immunoinhibition  1975 - Myoglobin  1985 - CK - MB Mass immunoassay  1989 - Troponin T  1992 - Troponin I
  • 14. Cardiac biomarkers • Cardiac biomarkers were first developed for assisting the cardiac events, especially acute myocardial infarction. • Better understanding of cardiac disease process and advancement in detection technology has pushed the application of cardiac biomarkers beyond the diagnosis boundaries. • Cardiac biomarkers are now used for staging of cardiac disease, timing of cardiac events and prognostification.
  • 15. • Markers of cardiac tissue damage • Markers of myocardial function • Cardiovascular risk factor markers • Genetic analysis for candidate genes or risk factors CLASSIFICATION OF LABORATORY TESTS IN CARDIAC DISEASE
  • 16. High sensitivity C-Reactive Protein (hs-CRP) & Homocysteine Marker of Inflammation
  • 17. • CRP is Pentameric structure consisting of five identical subunits of 23-kDa. • Its plasma levels can increase rapidly to 10,000x levels. • It is the most extensively studied marker of inflammation. Despite some controversy regarding its clinical use, it appears to be the most promising to date. • Although considered to be a general nonspecific marker of inflammation, elevated baseline levels of hsCRP are correlated with higher risk of future CV morbidity and mortality among those with or without clinical evidence ofCVD. High-Sensitivity C-Reactive Protein
  • 18. Clinical Uses – Screening for cardiovascular risk in otherwise “healthy” individuals – Predictive value of CRP levels for disease severity in pre- existing Coronary artery disease Elevated levels are predictive of • Long-term risk of first MI • Ischemic stroke High-Sensitivity C-Reactive Protein
  • 19. • Low specificity • No evidence that lowering CRP levels decreases CV risk Industry and FDA staff guidelines 2005 had given clinical cut off value as less than 1 mg/l as safe levels with hs-CRP tests CRP Less than 1.0 mg/L 1.0-2.9 mg/L Greater than 3.0 mg/L Risk for CVD Low Intermediate High Limitations of CRP
  • 20. • Intermediary amino acid formed by the conversion of methionine to cysteine • Moderate hyperhomocysteinemia occurs in 5-7% of the population • Recognized as an independent risk factor for the development of atherosclerotic vascular disease and venous thrombosis • Can result from genetic defects, drugs, vitamin deficiencies Homocysteine
  • 21. • Homocysteine is implicated directly in vascular injury including: – Intimal thickening – Disruption of elastic lamina – Smooth muscle hypertrophy – Platelet aggregation • Proposed mechanisms by which it induces vascular injury are leukocyte recruitment, foam cell formation, and inhibition of NO synthesis. • Normal levels : 3.7 – 13.9 µmol/L Homocysteine
  • 22. • Elevated levels of homocysteine appear to be an independent risk factor, though less important than the classic CV risk factors. • Treatment includes supplementation with folate, B6 and B12. Homocysteine
  • 23. Marker of Mocardial Ischemia Ischemia Modified Albumin (IMA) and Heart type-fatty Acid Binding Protein (H- FABP)
  • 24. • Ischemia modified albumin is a marker formed after damage in the N terminal region of the albumin in ischemic conditions. • This structural change leads to loss of its ability to bind with transitional metals (cu/co). • Endothelial or extracellular hypoxia, acidosis and free oxygen radicals causes increase in IMA. • IMA rises within minutes from onset of ischemia and remains elevated for several hours after cessation of ischemia. Ischemia Modified Albumin
  • 25. It is used as diagnostic criteria for myocardial necrosis that develops after Coronary artery bypass graft surgery (CABG). It is a non specific marker, since it is also reported to be elevated in pulmonary infarction, critical limb ischemia and cerebrovascular disorders. Basically, it is used to rule out ischemia rather than diagnosing the occurrence of ischemia. Which is helpful in differentiating pain of Angina from Myocardial ischemia. Clinical uses of IMA :
  • 26. • Heart type fatty acid binding protein is a very stable low molecular weight (14-15kDa) in the cytoplasm of myocardial cells. • FABPs are involved in active fatty acid metabolism where it transports fatty acid from cell membrane to mitochondria for oxidation. • Small size of H-FABP facilitates rapid diffusion through interstitial space, appearing as early as 1-3 hrs after onset and peaking within 6hrs. It return to normal levels with in 12-24hrs. • Normal levels : 1.6 – 19 ng/ml H-FABP
  • 27. • H-FABP is 20 times more specific to cardiac muscle than myoglobin • H-FABP is recommended to be measured with troponin to identify MI and ACS in patient presenting with chest pain. • In addition to its diagnostic potential H-FABP also has prognostic value. The risk associated with ↑ H-FABP is dependent upon its concentration. Patients who were cTnI normal but H-FABP high have more risk of morbidity and mortality after 1 year follow up than those with cTnI high but HFABP normal. H-FABP
  • 28. Marker for cardiac necrosis cTn CK-MB Myoglobin
  • 29. • Troponin is a complex of three regulatory proteins (Troponin C, Troponin I and Troponin T) that is associated with muscle contraction in skeletal and cardiac muscle. • Cardiac troponin is slightly different from skeletal troponin structurally hence serve as a potent and specific marker for cardiac disease. Cardiac Troponins
  • 31. Individual subunits serve different functions: • Troponin C binds to calcium ions to produce a conformational change in TnI • Troponin T binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex • Troponin I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place • Usually, Troponin is not detectable in healthy individual. Cardiac Troponins
  • 32. • It is extremely useful in patients who do not seek attention in the 2 to 3 days window when CK-MB is elevated. • Rise : with in few hours after onset of chest pain Peak : 2 days returns normal : 7-10 days • cTnT may show a biphasic release in some patients with a first peak occurring during first 24 hr of onset of symptom and second peak on appx. 4th day after admission. • TnT has cardiac as well as skeletal muscle source. cTnT :
  • 33. • It is cardiac specific because it has additional amino acid residue on its N-terminal that are non existent in skeletal muscle. Rise : b/w 4-6 hr after onset of pain Peaks : 12-18 hrs Returns normal : 6 days • Its measurement is advantageous over CK-MB as it is not found in detectable amount in serum of patients with multiple injuries, renal disease and in those with acute and chronic skeletal muscle disorders. cTnI :
  • 34. • Creatine kinase (CK) is a cytosolic enzyme involved with the transfer of energy in muscle metabolism. It catalyses the conversion of creatine to phospho-creatine degrading ATP to ADP. • CK is a dimer composed of two subunits B (brain type) and M (muscle type), resulting in three isoenzyme: CK-BB (CK1) : is of brain origin, found in blood only when BBB is damaged. CK-MB (CK2) : it is relatively specific for myocardial origin CK-MM (CK3) : it is found primarily in skeletal muscle CREATINE KINASE: CK-MB
  • 35. CREATINE KINASE: CK-MB • CK-MB is the most cardiac-specific CK isoenzyme • Proportion of CK-MB varies in skeletal & cardiac muscle • In normal population CK-MB < 6% Tot CK • Sensitive marker with rapid rise & fall • More specific than Tot CK but has limitations • “Gold standard” biochemical marker for past few decades
  • 36. It is a valuable tool for the diagnosis of MI because of its relative high specificity for myocardial damage. Rise : 4-6 hrs after onset of symptoms Peak : 12 hrs Return to normal : 24-36 hrs Can be used to indicate early re-infarction if level normalizes and then increases again. CK-MB :
  • 37. • Small-size heme protein found in all tissues mainly assists in oxygen transport • It is released from all damaged tissues • Its level rises more rapidly than cTn and CK-MB. • Released from damaged tissue within 1 hour • Normal value: 17.4-105.7 ng/ml • Timing: – Earliest Rise: – Peak – Return to normal: 1-4 hrs 6-9 hrs 12 hrs Myoglobin
  • 38. • Acute myocardial infarction • Skeletal muscle damage, muscular dystrophy, inflammatory myopathies • Renal failure, severe uremia • Shock and trauma CONDITIONS FOR MYOGLOBIN INCREASE :
  • 39. *if myoglobin concentration remains within the reference range 8 hours after the onset of chest pain, AMI can be ruled out essentially. *because of its rapid clearance by the kidney, a persistently normal Mb concentration will rule out reinfarction in patient with recurrent chest pain afterAMI *Rapid monitor of success of thrombolytic therapy DRAWBACKS • Due to poor specificity, myoglobin levels do not always predict myocardial injury Clinical usefulness of myoglobin :
  • 40. NEW GENERATION CARDIAC MARKERS • Myoglobin – Currently earliest marker – Like total CK it is by no means cardio- specific • Troponins – Kinetics comparable with total CK and CK-MB – Cardio-specific Sensitivity Specificity
  • 41. 2 3 4 5 7 6 myoglobin CK-MB cTnT cTnI Comparison of cTn, CK-MB , Mb 1 0 0 4 8 12 16 20 24 28 32 36 40 44 48 Time after onset of AMI (hours) Χ upper limit of reference interval
  • 42. Marker for haemodynamic stress natriuretic peptides
  • 43. • The natriuretic peptides (NP) are a group of structurally similar but genetically distinct peptide hormone. It includes : ANP : atrial natriuretic peptide (28 a.a.) N-terminal proANP (98 a.a.) BNP : brain natriuretic peptide (32 a.a.) N-terminal proBNP (76 a.a.) CNP : C-type natriuretic peptide (22 and 53 a.a.) DNP : D- type natriuretic peptide The NPs play important role in regulation of salt and water balance(CV homeostasis) Natriuretic peptides
  • 44. • ANP is released primarily in response to atrial wall stretching and intravascular volume expansion. • BNP is mainly secreted by the ventricles • CNP is found predominantly in the brain and also synthesized by vascular endothelial cells natriuretic peptides
  • 45. • Circulating levels of BNP are raised in patients with cardiovascular or renal disease • BNP is More important than ANP in heart failure • Greatest proportion of circulating BNP is thought to come from the ventricles (left) BRAIN NATRIURETIC PEPTIDE (BNP)
  • 46. • BNP and the terminal fragment of its prohormone (NT-proBNP) are released on ventricular stretch or stress to the myocyte in the absence of the necrosis. • Therefore, BNP is increased in diseases characterised by an expanded fluid volume (e.g. CHF, renal failure,hepatic cirrhosis etc.) • BNP has circulating T₁/₂ of 20 minutes, so it is indicative of snapshot of myocardial function, while NT-proBNP has T₁/₂ of 90 minutes giving a longer view of myocyte . BRAIN NATRIURETIC PEPTIDE (BNP)
  • 47. SUMMARY • “Cardiac Enzymes” are obsolete • Medical & laboratory progress has required a redefinition of Cardiac Events • Cardiac Troponins & Myoglobin now play a pivotal role in the diagnosis of AMI • Cardiac Troponins play an important role in the risk stratification of ACS patients • Elevated Troponin levels in patients without ECG changes & with normal CK-MB levels may identify patients at increased risk of cardiac events
  • 48. 1. What is the earliest cardiac marker that can be detected? a. Myoglobin b. CK-MB c. Cardiac Troponin I d. Cardiac Troponin T
  • 49. 2. A biomarker is substance used as an……………. Of a biological state a. Inhibitor b. Indicator c. Cofactor d. None of these
  • 50. 3. How many hours do troponin begin to rise? a. 1 hour b. 2 hours c. 4 hours d. 8 hours
  • 51. 4. What is the most sensitive and specific marker available today for AMI? a. CKMB b. Myoglobin c. CKBB d. Troponin
  • 52. 5. What is a marker for heart failure? a. Myoglobin b. Troponin c. BNP d. CKMB

Editor's Notes

  1. a
  2. b
  3. c
  4. d