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CVD markers

Amber Jade Lewis 8 preguntas

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Preguntas del test (8)

  1. 1Aspartate [blank_start]aminotransferase[blank_end] is an [blank_start]enzyme[blank_end] present in highest concentrations in cardiac/ [blank_start]liver[blank_end] muscle, but is also present in [blank_start]pancreas[blank_end] and kidney in low concentrations. AST rises after [blank_start]6-8[blank_end] hours, peaking as [blank_start]24[blank_end] hours and normalising after [blank_start]5[blank_end] days. It is measured by breakdown of [blank_start]NAD+[blank_end] which is automated.
    1. Aaminotransferase
    2. Benzyme
    3. Cliver
    4. Dpancreas
    5. E6-8
    6. F24
    7. G5
    8. HNAD+
  2. 2Creatine [blank_start]Kinase[blank_end] exists as a dimer in three different isoforms, [blank_start]CK-MM[blank_end] which is found in heart and skeletal muscle; common in MI, muscular dystrophy, and [blank_start]physical activity[blank_end]. [blank_start]CK-MB[blank_end] also found in heart and skeletal; common in MI, ischaemia, angina, [blank_start]CO poisoning[blank_end]. [blank_start]CK-BB[blank_end] is common in the lung, bladder, brain, prostate, [blank_start]uterus[blank_end] and colon. CK-MM is the major isoform found in healthy individuals, a rise is either due to skeletal or [blank_start]cardiac injury[blank_end]. CK-MB is a cardiac only source and is much more specific, if over [blank_start]6%[blank_end] is detected then a MI is indiciated. It rises after [blank_start]4-8[blank_end] hours, peaks at [blank_start]12-24[blank_end]hrs and falls [blank_start]48-72[blank_end] hours.
    1. AKinase
    2. BCK-MM
    3. Cphysical activity
    4. DCK-MB
    5. ECO poisoning
    6. FCK-BB
    7. Guterus
    8. Hcardiac injury
    9. I6%
    10. J4-8
    11. K12-24
    12. L48-72
  3. 3Myoglobin is found in [blank_start]straited[blank_end]/ cardiac muscle, on damage [blank_start]myoglobin[blank_end] is released rapidly rises within [blank_start]1-3[blank_end]hrs; peaking at [blank_start]5-12[blank_end] and normalising [blank_start]18-30[blank_end]hrs after. It is an [blank_start]early[blank_end] and sensitive marker for cardiac damage, however it can also be raised in [blank_start]crushing injuries[blank_end], renal failure, after vigorous excerise and fractures.
    1. Astraited
    2. Bmyoglobin
    3. C1-3
    4. D5-12
    5. E18-30
    6. Fearly
    7. Gcrushing injuries
  4. 4Troponin is a complex made up of 3 proteins, Troponin T, Troponin I and Troponin [blank_start]C[blank_end] (related to mysoin binding to actin filaments during [blank_start]muscle contraction[blank_end]). TnT is coded for by three genes in cardiac/ fast and slow [blank_start]skeletal[blank_end] muscle. TnC doesn't have a [blank_start]cardiac[blank_end] specific form. TnT levels rise after [blank_start]3-4[blank_end] hrs, peak at [blank_start]10-14[blank_end] and persist for around [blank_start]10-14[blank_end] days. The cardiac form has a generally high sensitivity and specificity which is independent of age, [blank_start]hypertension[blank_end], anti-angial drugs, [blank_start]ECG[blank_end] changes. The immunoassay has been widely produces, however false positives do arise in [blank_start]renal failure[blank_end]. TnI is also very sensitive as it is not normal seen in the [blank_start]circulation[blank_end]. It is [blank_start]13x[blank_end] more abundant in the myocardium than [blank_start]CK-MB[blank_end]. It rises after [blank_start]3-6[blank_end]hrs, peaks [blank_start]14-20[blank_end] and normalises [blank_start]5-10[blank_end]days. It is usually associated with a [blank_start]poorer prognosis[blank_end].
    1. AC
    2. Bmuscle contraction
    3. Cskeletal
    4. Dcardiac
    5. E3-4
    6. F10-14
    7. G10-14
    8. Hhypertension
    9. IECG
    10. Jrenal failure
    11. Kcirculation
    12. L13x
    13. MCK-MB
    14. N3-6
    15. O14-20
    16. P5-10
    17. Qpoorer prognosis
  5. 5Natriuretic peptides (BNP) are secreted when [blank_start]expanded fluid volume[blank_end] occurs (in either [blank_start]renal[blank_end] or heart failure). It is normally detected in the [blank_start]atria[blank_end] but can be synthesized in the [blank_start]ventricles[blank_end] during disease. Cleavage of a pro-BNP is stimulated by [blank_start]arterial stretch[blank_end] and has [blank_start]vasodilating[blank_end] properties and stimulates [blank_start]sodium secretion[blank_end]. It is degraded by endopeptidase a CNP agonist. A [blank_start]negative[blank_end] BNP can rule out [blank_start]HF[blank_end] however elevation isn't [blank_start]specific[blank_end].
    1. Aexpanded fluid volume
    2. Brenal
    3. Catria
    4. Dventricles
    5. Earterial stretch
    6. Fvasodilating
    7. Gsodium secretion
    8. Hnegative
    9. IHF
    10. Jspecific
  6. 6C-reactive protein is a established marker of [blank_start]inflammatory[blank_end] processes, produced by the [blank_start]liver[blank_end] in response to [blank_start]IL-6[blank_end]. It increases in response to injury or [blank_start]infection[blank_end]. In healthy individuals it is not present in large amounts, in cardiac disease a small increase is seen which can be detected by high-sensitivity [blank_start]CRP assays[blank_end]. Baseline hs-CRP correlates with increased [blank_start]future risk[blank_end] of CVD. Allows early detection of [blank_start]heart failure[blank_end].
    1. Ainflammatory
    2. Bliver
    3. CIL-6
    4. Dinfection
    5. ECRP assays
    6. Ffuture risk
    7. Gheart failure
  7. 7Heart fatty acid binding protein (H-FABP) is involved in [blank_start]fatty acid metabolism[blank_end] in skeletal and cardiac muscle. It rises after [blank_start]2-4[blank_end]hours, peaks [blank_start]5-10[blank_end] and normalises within [blank_start]24-36[blank_end] hours. It is a good prognostic indicator of death within [blank_start]1 year[blank_end].
    1. Afatty acid metabolism
    2. B2-4
    3. C5-10
    4. D24-36
    5. E1 year
  8. 8Ischaemia modified albumin has the ability to bind to [blank_start]transition metals[blank_end] such as cobalt and [blank_start]copper[blank_end] via [blank_start]N-terminals[blank_end]. Albumin exposed to [blank_start]ischaemic[blank_end] tissue has a modified N-terminus structure so that binding [blank_start]no[blank_end] longer occurs. This is a continual processes during ischaemia, which rises after [blank_start]2-3[blank_end]hrs. However its [blank_start]specificity[blank_end] needs to be established.
    1. Atransition metals
    2. Bcopper
    3. CN-terminals
    4. Dischaemic
    5. Eno
    6. F2-3
    7. Gspecificity

Información

Descripción
6 (Blood Science) Flashcards Test sobre CVD markers, creado por Amber Jade Lewis el 09/01/2016.
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