Gen Med Midterm Lab Values

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  1. What is the framework for assessment of lab values?
    • Is the value abnormal?
    • Is it a a clinically significant change?
    • Is management necessary?

    Always analyze in context of the patient.
  2. Contrast sensitivity and specificity
    • Sensitivity: ability of test to detect patients with disease (true positives)
    • Specificity: ability of test to detect true negatives)
  3. Digoxin assays
    • Canrenoate(spironolactone metabolite) can interfere with digoxin assay
    • endogenous cardiac glycosides can interferere with digoxin assay (hepatic/renal failure)
    • Must wait 4-6 hours after administration to assay absorption/distribution
  4. What is a more sensitive test to detect MI, creatinine kinase or troponins?
  5. What are some considerations when deciding whether to treat somebody
    • What are the consequences of not treating?
    • Are there risk in unnecessary treatment?
    • Is there evidence that treatment is beneficial, or there is a certain threshold for treatment to be beneficial?
  6. What are some tests to assess renal function?
    • Urine oiuotput
    • serum creatinine
    • creatinine clearance-> GFR
    • metabolic consequences of renal dysfunction (hyperkalemia, metabolic acidosis, fluid overlad)
  7. What is the equation for creatinine clearance?
    (140-age)(IBR)/ (50*SCr)   

    Multiple above by 0.85 if woman
  8. Implications of renal dysfunction (i.e., what should u do if a person is renally impaired?)
    • limit intake of sodium, potassium, magnesium, phosphate (including drugs/dietary sources)
    • restrict fluid and protein
    • reduces doses of renally eliminated drugs (water soluble, low MW, low protein/tissue binding, small Vd)
    • ex. allopurinol, digoxin, cefazolin
  9. Which drugs can induce renal dysfunction?
    • NSAIDs (alter kidney prostaglandins)
    • ACE-I
    • ARB
    • DRI(aliskerin)
    • aminoglycosides (digoxin)
    • amphotericin
  10. Important drugs that need to be dose adjusted for renal dysfunction
    Most beta-lactam antibiotics, digoxin, allopurinol
  11. What are some properties of drugs likely to be renally cleared?
    • low MR
    • Low Vd
    • low tissue/protein binding
    • Water soluble
  12. What are the two types of drug induced renal toxicity?
    • Direct toxicity: amphotericin B (antifungal), aminoglycosides, cisplatin
    • often dose related, and may be irreversible

    • Indirect toxicity: anything that changes perfusion (thus dont start these drugs if already low GFR)
    • -interference with RAAS, or NSAIDs causing autoregulation dysfunction
    • reversible with early intervention
  13. What should you consider if you suspect drug induced lab abnormalities?
    • Consider causality
    • Consider temporal relationship
    • Consider d/c or rechallenge
    • Consider clinical significance
  14. AST/ALT
    • reflect hepatocyte destruction
    • Caused by:
    • virus/toxins
    • acetaminphen, methotrexate, azole antifungals, statins, isoniazid
  15. Bilirubin and alkaline phosphatase
    • reflect cholestatic dysfunction
    • causes:
    • gallstones
    • drugs: macrolides, neuroleptics
  16. Liver dysfunction scales
    • Child-Pugh Classification (cirrhosis): 
    • based on bilirubin, INR, Ascites, hepatic encephalopathy

    • MELD score:
    • for purposes of prognosis of transplantation
    • based on bili, INR, serum creatinine
  17. Are phase 1 or phase 2 more affected by hepatic dysfunction?
    phase 1; thus reduce dose/avoid phase 1 metabolized drugs
  18. High ER vs Low ER
    • high ER: limited by blood flow
    • reduce dose if perfusion decreased
    • ex. lidocaine, propranolol

    • low ER: limited by intrinsic clearance
    • reduce dose if hepatocytes damaged.
    • ex. theophylline, phenytoin
  19. Protein binding
    since albumin is decreased in chronic liver damage: 

    reduce dose of drug as there ill be an increase in free drug
  20. What is a general rule for K+ in body?
    What can cause intracellular/extracellular shifts?
    Decrease of 0.3mmol/L in serum K represents 100mmol of K+ lost in body

    • intracellular shift: B-agonist, insulin, alkalosis
    • extracellular shift: B-antagonist, a-agonist, acidosis
  21. Signs and causes of hypokalemia
    • CV-arrhythmias+hypotension+ ischemia
    • Muscular weakness
    • Metabolic: glucose intolerance, decreased Mg

    • usually too much loss from gut/kidney (diuretics or aldosterone)
    • intracellular shift (insulin, alkalosis, b-agonist)
  22. What is the cutoff for treatment for hypokalemia?
    • >3.0mmol= only treat if symptomatic
    • <2.7 mmol=risk of arrhythmias+ glucose intolerance, so treat!
  23. What are the risks of over-treating hypokalemia?

    What can you treat with?
    • QRS widening, asystole, ventricular fibrillation (if too much/too fast)
    • low risk of normal renal function, and regular bedside monitoring, and max dose/rate is established. 

    • Potassium chloride (better than concentrated potassium )
    • IV minibags (better than oral supplements) due to longer timecourse
  24. When should you monitor potassium (i.e. on which drugs)
    • Hypokalemia: patients with diarrhea, renal losses of K
    • patients receiving diuretics or digoxin 

    • Hyperkalemia: patients with renal dysfunction
    • patients receiving ACE-I, ARB, aldosterone antagonist, DRI (aliskiren)
  25. What's the difference between microcytic and macrocytic anemia?
    Microcytic: decreased HB, decreased MCV, iron deficiencey, hypochromic (treat with iron replacement)

    Macrocytic: decreased HB, increased MCV: folate, B12 defeciency
  26. What is characteristic of normocytic/normochromic anemia?
    Decreased HB, normal MCV

    associated with chronic diseases
  27. What are some causes of anemia?

    What is the lower threshold for treatment of anemia?
    • Lack of EPO (renal disease)
    • Iron deficiency
    • Bone marrow suppression from chronic disease or from chemotherapy (zidovudine)
    • Increased destruction: blood loss, hemolysis

    70g/L Hb
  28. What does WBC signify?
    • High: infection, leukemias
    • drug induced: corticosteroids

    • Low: immunocompromised (monitor fever-> seek medical attn)
    • drug induced: chemotherapy or clozapine
  29. What does increased Neutrophil, Lymphocytes, Eosinophils, Basohils or monocytes signify?
    • Neurophil- 50-70%: Absolute Neutrophil Count (ANC)<500; then you have neutropenia (increased risk of infection)
    • Lymphocytes (20-40%)- increased viral infections
    • Eosinophils(0-5%): increase in parasitic or allergic rxns
    • Basophils are useless
    • Monocytes (0-7%): increased atypical infections (TB)
  30. What does the platelet count signify?
    • Thrombocytopenia-> increased risk of bleeding due to decreased platelets
    • Decreased production-> chemotherapy
    • Increased destruction: heparin, autoimmune diseases, sepsis
    • spontaneous bleeds when count is less than 20

    ASA/NSAIDs/clopidogrel: predispose to bleeding but don't decreased platelet count (thus measure their effect with bleeding times)
  31. What are the requirements for TDM
    • readily available assay
    • correlation between serum drug levels and efficacy/toxicity (digoxin has significant overlap between efficacy and toxicity-> treat symptoms with digoxin)
    • correlation between concentration at site of action and sampled fluid
  32. Which kinds of drug are ideal for TDM?
    • difficult to measure therapeutic response (antibiotic, seizures, prophylaxis)
    • narrow therapeutic index (digoxin, theophyllin)
    • significant concentration-dependent toxicity
  33. Indications for TDM
    • assess compliance/absorption
    • ensure efficacy (provided good correlation between levels and effect)
    • avoid/confirm toxicity
    • assess for a drug interaction
  34. How should you interpret TDM levels/
    • timing of sample relative to dose
    • timing of sample relative to initiation of therapy
    • free vs total drug
    • drug interactions
    • correlation to symptoms??
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Gen Med Midterm Lab Values
Gen Med Midterm Lab Values
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