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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.
Contrast sensitivity and specificity
- Sensitivity: ability of test to detect patients with disease (true positives)
- Specificity: ability of test to detect true negatives)
- 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
What is a more sensitive test to detect MI, creatinine kinase or troponins?
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?
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)
What is the equation for creatinine clearance?
Multiple above by 0.85 if woman
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
Which drugs can induce renal dysfunction?
- NSAIDs (alter kidney prostaglandins)
- DRI(aliskerin)aminoglycosides (digoxin)
Important drugs that need to be dose adjusted for renal dysfunction
Most beta-lactam antibiotics, digoxin, allopurinol
What are some properties of drugs likely to be renally cleared?
- low MR
- Low Vd
- low tissue/protein binding
- Water soluble
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
What should you consider if you suspect drug induced lab abnormalities?
- Consider causality
- Consider temporal relationship
- Consider d/c or rechallenge
- Consider clinical significance
- reflect hepatocyte destruction
- Caused by:
- acetaminphen, methotrexate, azole antifungals, statins, isoniazid
Bilirubin and alkaline phosphatase
- reflect cholestatic dysfunction
- drugs: macrolides, neuroleptics
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
Are phase 1 or phase 2 more affected by hepatic dysfunction?
phase 1; thus reduce dose/avoid phase 1 metabolized drugs
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
since albumin is decreased in chronic liver damage:
reduce dose of drug as there ill be an increase in free drug
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
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)
What is the cutoff for treatment for hypokalemia?
- >3.0mmol= only treat if symptomatic
- <2.7 mmol=risk of arrhythmias+ glucose intolerance, so treat!
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
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)
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
What is characteristic of normocytic/normochromic anemia?
Decreased HB, normal MCV
associated with chronic diseases
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
What does WBC signify?
- High: infection, leukemias
- drug induced: corticosteroids
- Low: immunocompromised (monitor fever-> seek medical attn)
- drug induced: chemotherapy or clozapine
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)
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)
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
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
Indications for TDM
- assess compliance/absorption
- ensure efficacy (provided good correlation between levels and effect)
- avoid/confirm toxicity
- assess for a drug interaction
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??