Biochemical Tests for Heart Disease Flashcards

1
Q

mechanism of acute coronary syndromes

A

rupture/erosion of the fibrous cap of coronary artery plaque with subsequent formation of platelet rich clot and vasoconstriction produced by platelet release of serotonin and thromboxane A2

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2
Q

how do NSTEMIs and unstable angina differ from each other?

A

NSTEMIs cause enough damage to cause an elevation in the serum markers of myocardial injury; unstable angina would not elevate the markers

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3
Q

which are the serum markers of myocardial injury?

A
  • troponin

- creatinine kinase

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4
Q

causes of chest pain

A
  • angina pectoris
  • MI
  • pericarditis
  • aortic dissection
  • reflux esophagitis
  • pulmonary infarct
  • pneumothorax
  • pneumonia
  • costochondritis
  • fractured rib
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5
Q

what type of pain do patients with angina pectoris present with?

A

crushing pain on exercise, relieved by rest. may radiate to the jaw or arms

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6
Q

what type of pain do patients with MI present with?

A

similar in character to angina but more severe, occurs at rest, lasts longer

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7
Q

what type of pain do patients with pericarditis present with?

A

sharp pain aggravated by movement, respiration and changes in posture

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8
Q

what type of pain do patients with aortic dissection present with?

A

severe tearing chest pain which radiates to back

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9
Q

what type of pain do patients with reflux oesophagitis present with?

A

pain may occur at night and when bending or lying down. Pain may radiate into the neck

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10
Q

what type of pain do patients with pulmonary disease present with?

A

sharp, well-localised pain aggravated by inspiration, coughing and movement (pleurisy)

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11
Q

what type of pain do patients with musculoskeletal problems present with?

A

sharp, well-localised pain with a tender area on palpation

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12
Q

what is the aim of investigating cardiac problems?

A
  • estimate the risk

- give a differential diagnosis of acute coronary syndrome

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13
Q

what are differentials of acute coronary syndromes

A
  • minor myocardial damage
  • unstable angina pectoris
  • stable angina pectoris
  • myocardial infarction
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14
Q

diagnosis of MI

A
  • history
  • initial and serial ECGs
  • serial enzyme/chemical changes
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15
Q

when do ECG changes start showing up?

A

1-2hrs after the onset of MI symptoms

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16
Q

what ECG changes are associated with MI?

A
  • ST elevation
  • T wave flattening/inversion
  • Pathological Q waves
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17
Q

what does the clinical presentation depend on?

A
  • plaque activity
  • plaque location
  • degree of stenosis
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18
Q

what are Troponins?

A
  • regulatory proteins
  • highly specific to myocardial damage
  • released early (within 8hrs) and persist for days
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19
Q

what are AST/ALT/LDH?

A
  • their levels remain elevated up to 10d after infarction

- LDH is also elevated with leukaemia, kidney damage, liver damage

20
Q

which other markers can be measured for myocardial damage?

A
  • cardiac enzymes - CK, LDH
  • cardiac iso-enzymes
  • contractile proteins
  • tissue isoforms
  • myoglobin
21
Q

characteristics of the ideal biomarker?

A
  • sensitive for early identification of MI
  • present in extremely low amounts of the marker of interest under basal conditions
  • rapidly released from the heart
  • present for some time from the event
  • specific to heart tissue
  • easy to analyse quickly
  • the reference range depends on physiology and on the time from the acute event
22
Q

what is the troponin complex?

A

component of the thin filament of striated muscle linked to actin; regulation of muscle contraction

23
Q

which type of troponin is the most cardiac-specific

A

Troponin I

24
Q

which other cardiac injuries can release TntI

A
  • AMI
  • non-Q wave AMI
  • reversible ischaemia
  • angina
  • unstable angina
  • cardiac cell necrosis
  • CHF
  • micro-infarcts
  • myocarditis
  • CABG
  • PTCA
  • myocardial contusion
25
Q

what is Troponin T?

A

tropomyosin-binding protein of the troponin regulatory complex located on the thin filament of the contractile apparatus

26
Q

what is Troponin I?

A

thin filament regulatory protein which inhibits the troponin-tropomyosin complex

27
Q

what does the unbound troponin fraction depend on?

A

perfusion of the infarct zone

28
Q

at what time intervals should you test troponins?

A
  • 2-4hrs
  • 6-9hrs
  • 12-24hrs
29
Q

in which coloured bottle should you collect blood for troponins?

A

yellow

30
Q

what is the abnormal value?

A

> 95% of the upper limit reference value

31
Q

what can give a false positive in troponins?

A
  • Heterophilic antibodies
  • Human anti-mouse antibodies
  • Autoantibodies
  • Fibrin clots
  • Rheumatoid factor
  • Microparticles in specimen
  • High alkaline phosphatase
  • Immunocomplex formation
  • Analyser malfunction
32
Q

which cardiac conditions can elevate troponins?

A
  • acute coronary syndrome
  • severe tachycardia
  • heart failure
  • myocarditis and myopericarditis
  • cardiomyopathy
  • heart injury
  • cardiac procedures
33
Q

which non-cardiac conditions can elevate troponin levels

A
  • Critical illness eg sepsis
  • Severe gastrointestinal bleeding
  • Chemotherapy agents
  • Several toxins and venoms
  • Some patients with dissection of the ascending aorta
  • Primary pulmonary hypertension
  • Pulmonary embolism
  • Acute exacerbations of Chronic Obstructive Pulmonary Disease (COPD)
34
Q

characterisitics of CK-MB

A
  • measurable at 6hrs of myocardial necrosis
  • levels peak at 19-24hrs from onset of chest pain declines thereafter
  • can also be found in the skeletal muscle and in the blood (after injury)
35
Q

causes of elevated CK-MB

A
  • muscle trauma
  • crash injuries
  • burns
  • electrical injuries
  • non-cardiac surgery
  • heavy exercise
  • grand mal seizures
  • myositis
  • various inflammatory and non-inflammatory myopathies
  • hypothyroidism
  • chronic alcoholism
  • hyperthermia and hypothermia
  • CK-MB producing tumours
  • decreased clearance
36
Q

characteristics of myoglobin

A
  • peak elevation: 6-9hrs and declines to baseline by 24-36hrs
  • exclude patients with concomitant skeletal muscle damage
  • also increases by severe shock, severe renal failure and multiple trauma
  • best for detections of re-infarctions and monitoring reperfusion therapy
37
Q

risk factors for CAD

A
Modifiable 
- Dyslipidaemia 
• Smoking 
• Hypertension 
• Diabetes mellitus 
• Physical inactivity 
• Abnormal LFTs 

Non-modifiable
• Age
• Male gender
• Family history

  • Lipoprotein (a)
  • Homocysteine
  • hs-CRP
  • Prothrombotic factors e.g. plasma fibrinogen, plasminogen activator inhibitor
  • Impaired glucose tolerance
  • Microalbuminuria
  • Subclinical atherosclerosis
38
Q

in which populations are coronary risk prediction charts not appropriate for?

A
  • major atherosclerotic disease,
  • Familial Hypercholesterolaemia & other inherited dyslipidaemias,
  • renal dysfunction
39
Q

who is at more risk of developing CHD?

A
  • family history of premature CHD which increases the risk by a factor of 1.5 - raised triglycerides - women with premature menopause
  • impaired glucose tolerance
  • type I diabetes
  • in people originating from the Indian subcontinent it is safest to assume that the CHD risk is higher than predicted from the charts (1.4-1.5x)
40
Q

what is ischaemia-modified albumin?

A
  • marker for ischaemia

- produced when circulating albumin comes into contact with ischaemic tissue in the heart or other organs

41
Q

limitations of ischaemia-modified albumin

A
  • can be elevated with stroke, ESRF, liver disease and some neoplasms
  • increased lactate levels appear to decrease IMA concentrations (in patients with sepsis and renal failure)
42
Q

what is elevated high sensitivity CRP associated with?

A
  • infarct expansion and coronary rupture after AMI
  • indicates a more inflammatory plaque
  • may worsen the prognosis
43
Q

what is hs-CRP associated with?

A
  • small dense LDL only

- features of metabolic syndrome

44
Q

which biochemical marker is used to check for heart failure?

A

brain-natriuretic peptide

45
Q

characteristics of BNP

A
  • Natriuretic peptides play an endocrine role in the regulation of cardiorenal homeostasis
  • Indicator of heart failure with significant left ventricular (LV) dysfunction
  • Unproven usefulness in MI
  • BNP indicates larger infarcts and signals poorer prognoses.