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Biochemistry topics

Ashutosh Kumar Chemical pathology Englisch 14 Karten

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  1. 1Errors in the testing cycle:Errors in the testing cycle:
    Most errors occur in the preanalytical phase.
  2. 2Specimen artifacts:Specimen artifacts:
    Haemolysis
    High Potassium; release of potassium from hemolyzed red blood cells.
    Unreliable troponin.
    Lipaemia
    Pseudohyponatremia: caused by lipids taking up volume, resulting in less water and therefore sodium (which is only dissolved in the water component of the blood sample). A similar phenomenon occurs in multiple myeloma where there are an excess of immunoglobulins.
    Haematopathology
    High WBC activity diminishes the glucose in the blood sample, resulting in insufficient glucose to maintain the structural integrity of the membranes of RBCs. As a consequence, potassium leaks out of the RBCs increasing serum potassium; pseudohyperkalemia.
    EDTA contamination
    EDTA binds calcium and other divalent cations ( e.g magnesium) which is need for alkaline phosphatase activity. In addition, EDTA is a potassium salt. Thus, samples contaminated with EDTA exhibit falsely, low levels of ALP and high potassium.
  3. 3Biochemistry tests-what you want to know:Biochemistry tests-what you want to know:
    Has this result changed significantly? (for monitoring)
    Is this result abnormal? (for diagnosis)
  4. 4Change in a test result may be due to:Change in a test result may be due to:
    Change in the patient’s state
    Change in the accuracy of the method
    Analytical variability- CVA
    Biological variability- CVI
    The values for the CVA and CVI are known
    The lab knows if there has been a change in accuracy
    Therefore, the likelihood of a real change can be determined.
  5. 5Reference intervals:Reference intervals:
    Statistical construct defining “normality”.
    Requires large numbers of screened individuals.
    Establish mean and S.D for distribution of values.
    Reference interval is mean +/- 2SD and describes 95% of the “normal” population.
    Caution: Non-gaussian analytes (e.g bilirubin), inter- and intra- individual variation, population selection (age, sex and ethnicity).
  6. 6Factors affecting reference intervals:Age
    ALP
    Gender
    Creatinine
    Fasting
    Glucose
    Pregnancy
    ALP
    Menstrual cycle
    Gonadotrophins
    Time of day
    Cortisol
    Time of year
    Vit D
  7. 7Other types of “reference intervals”:Other types of “reference intervals”:
    Action limits:
    Cholesterol
    Paracetamol, bilirubin in neonates
    Therapeutic ranges-for drugs
    Lithium
    Digoxin
  8. 8now how to calculate: Prevalence Sensitivity Specificity PPV NPV Test efficiencynow how to calculate:
    Prevalence
    Sensitivity
    Specificity
    PPV
    NPV
    Test efficiency
  9. 9Arguments for and against HBA1C to diagnose DM:HBA1C: preferred test to diagnose DM.
    For:
    No need for fasting.
    Easy to measure.
    Less biological variation.
    Less analytical variation.
    Against:
    Expensive compared with GTT.
    Not universally available.
    Haemoglobinopathies/ red cell defects.
  10. 10Criteria for DM:Criteria for DM:
    HBA1c ≥ 50 mmol/mol diabetes confirmed
    41-49= ‘pre-diabetes’. Check in 6-12 months.
    ≤40= normal. Check at next CVD review.
  11. 11Secondary hyperlipidaemia in DM:Secondary hyperlipidaemia in DM:
    Relative or absolute lack of insulin causes reduced TG clearance, increased release of FFA from adipose tissue increasing serum TG.
    Usual pattern is high TG and low HDL.
    LDL may be normal but particles are often smaller and denser= more easily incorporated and oxidized into vessel walls= more arthrogenic.
    Glycation of apolipoproteins.
    Therapy: Statins.
  12. 12Primary hyperlipidaemia:Primary hyperlipidaemia:
    Familial hypercholesterolaemia.
    Premature CVD.
    Extensor and achilles tendon xanthoma.
    Worst if homozygote.
    Defects in LDL receptor, ApoB100 or PCSK9- removes LDL receptor in gain of function mutation resulting in less internalization of LDL and more circulating LDL.
  13. 13Diagnosis of PCOS:Diagnosis of PCOS:
    Requires two out of three:
    Oligo- or anovulation.
    Clinical and/or biochemical signs of hyperandrogenism.
    Polycystic ovaries.
    And exclusion of other etiologies (CAH, androgen secreting tumours, Cushing’s).
    Other tests to assess associated co-morbidities:
    Lipids.
    HbA1c.
    Other tests where diagnosis is not clear:
    17-OH progesterone (CAH).
    DHEAS (adrenal androgen).
    Androstenedione (ovarian androgen).
  14. 14Causes, identification and treatment of: Primary hypothyroidism: Subclinical hypothyroidism: Grave’s disease:Primary hypothyroidism:
    E.g Hashimoto’s disease; lymphocytic infiltration of the gland; may initially present as thyrotoxicosis.
    Titrate thyroxine into lower end of RI, care in elderly and CAD, increase requirements in pregnancy.
    Subclinical hypothyroidism:
    Symptoms often vague and nonspecific.
    Can develop overt hypothyroidism or normalize.
    No clear benefit from thyroxine replacement.
    Grave’s disease:
    Key symptoms include exophthalmos and pretibial myxoedema.
    High T4 and T3, low TSH.
    Uniform increased uptake of radioactive iodine.
    Treatment: Carbimazole +/- Bblocker (radioiodine and surgery also options).

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Chemical pathology Karteikarten am Biochemistry topics, erstellt von Ashutosh Kumar am 25/02/2017.
Erstellt von
Ashutosh Kumar
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