臨床生化 trace elements,tdm, clinical toxicology 賴滄海 教授 12-30-2008
TRANSCRIPT
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臨床生化Trace Elements ,TDM, Clinical Toxicology
賴滄海 教授12-30-2008
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Biochemical Functions of Elements• Ion: Hemoglobin, Myoglobin ,Cytochromes, Peroxidase, Catalase, Thyroperoxidase • Copper: Ceruloplasmin, cytochrome, c oxidase, superoxide dismutase, dopamine-β- hydroxylase, tyrosinase, ascorbate oxidase • Zine: Essential for more than 300 enzymesi : alkaline phosphatase, alcohol dehydrogenase, carbonic anhydrase, DNA,RNA polymerase • Cobat: Constitute of Vit B12
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Biochemical Functions of Elements• Chromium: Essential activator of insulin• Fluoride: prevent dental caries, enhance bone formation• Manganese: Arginase, pyruvate carboxylase, superoxide dismutase • Molybdenum: Xanthine dehydrogenase/ xanthine oxidase, aldehyde oxidase, sulfite oxidase• Selenium: Cofactor in glutathione peroxidase, iodothyronine diodinase, Has antioxidant property
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Reasons for Therapeutic Drug Monitoring
• Serious consequences for Overdose
• Small therapeutic index (LD50/ED50)
• Poor correlation between dose and circulation concentration and therapeutic or toxic effects
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• There is a change of patient’s physiological states that may affect circulating drug concentration
• Drug interaction may be occurring
• TDM helps in monitoring patient compliance.
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Digoxin :
• Absorption of orally administered digoxin is variable. 25 % protein bound. Sequestered in muscle cells ( 15 - 30 times greater than plasma ) . T1/2
is 38 hours.
• Range : 0.8 to 2.0 ng/mL
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Digoxin :
• Toxicity : Nausea, vomiting, visual disturbance, premature, ventricular contraction ( PVC ) and AV node blockage.
• Interference : Low potassium, Magnesium, Hypothyroidism potentiate digoxin action.
• Elimination : Kidney, liver .• Determined by immunoassay. DLIS cause false p
ositive result.
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Lidocaine :• Administered IV. 70 protein bound.﹪• Range : 1.5 to 4.0μg/mL• Toxicity : CNS depression, Seizure, severe decr
ease in blood pressure and cardiac output.• Elimination : Metabolized in Liver ( first pas
s ) to MonoEthylXylidide ( MEGX ) , which is toxic but without therapeutic activity.
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Quinidine :
• Absorption of orally administered quinidine sulfate is complete. Quinidine gluconate is a slow releasing formulation. 70 protein bound.﹪
• Range : 2 to 5 μg/mL• Toxicity : Nausea, vomiting, abdominal discom
fort, premature, ventricular contraction ( PVC ) and AV node blockage.
• Elimination : Liver
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Procanamide :
• Absorption of orally administered drug is complete. 20 protein bound.﹪
• Range : 4 to 8 μg/mL • Toxicity : Myocardial depression and arrhythmi
a.• Elimination : Liver metabolism to N-Acetyl pro
canamide ( active metabolite ) and Kidney filtration.
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Disopyramide :
• Absorption of orally administered drug is complete. Protein binding is highly variable.
• Range : 3 to 5 μg/mL• Toxicity : Dry mouth, constipation ( 4.5
μg/mL ) . Bradicardia, AV node blockage(> 10 μg/mL )
• Elimination : Kidney, liver.
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Aminoglycosides : Amikacin, Gentamicin,
Kanamycin, Tobramycin.
• Administered IV or IM. Effective against gram-negative bacteria.
• Toxicity : Orotoxic, disruption of inner ear cochlear and vestibular membranes.
• Nephrotoxic, impair the function of proximal tubules of the kidney.
• Elimination : Kidney.
Antibiotics
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Vacomycin :
• Administered IV. Protein binding is highly variable. Effective against gram-positive cocci and bacilli.
• Range : 5 to 10 μg/mL
• Toxicity : Red-man syndrome, nephrotoxicity and orotoxicity.
• Elimination : Kidney.
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Antiepileptic drugs :
Phenobarbital, primidone• Absorption of orally administered drug is slow an
d complete. Protein binding is 50 . Long half-lif﹪e.
• Range : 15 to 40 μg/mL• Toxicity : Drowsiness, fatigue, reduced mental
capacity.• Elimination : Liver ( inducer of MFO ) and
kidney.
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Phenytoin, Fosphenytoin
• Absorption of orally administered drug is variable and incomplete. Protein binding is 87﹪to 97 .﹪
• Range : 10 to 20 μg/mL• Toxicity : Initiation of seizure. • Hirsutism, gingival hyperplasia, vitamine D
and folate deficiency.• Elimination : Kidney ( zero order kinetic
s )
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Valproic Acid :
• Absorption of orally administered drug is complete. Protein binding is 93 .﹪
• Range : 50 to 120 μg/mL
• Toxicity : Nausea, lethargy, weigh gain, pancreatitis, hyperammonemia and hallucinations.
• Elimination : Liver metabolism.
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Carbamazepine :
• Absorption of orally administered drug is variable. Protein binding is 70 to 80 .﹪ ﹪
• Range : 4 to 12 μg/mL
• Toxicity : rash, leucopenia, nausea, vertigo, febrile reactions, aplastic anemia.
• Elimination : Liver ( inducer of enzyme )
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Psychoactive drugs
Lithium• Absorption of orally administered drug is complete.• Range : 0.8 to 1.2 μg/mL• Toxicity : Apathy, lethargy, speech difficulties and
muscle weakness ( 1.2 to 2.0 mmole/L ) . Muscle rigidity, seizure and coma (> 2 mmole/L )
• Elimination : Kidney.• Analyzed with ISE, Flame emission photometry or A
AS.
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Tricyclic antidepressants
Impiramine, amitriptyline and active
metabolites, doxepin.• Absorption of orally administered drug is variabl
e. Protein binding is 85 to 95 .﹪ ﹪• Toxicity : Drowsiness, constipation, blurred vis
ion, memory loss ( 2X upper limit ) . Seizure, cardiac arrhythmia and unconsciousness.
• Elimination : Liver.
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Bronchodilators
Theophylline• Absorption of orally administered drug is v
ariable. Protein binding is 50 .﹪• Range : 10 to 20 μg/mL• Toxicity : Nausea, vomiting and diarrhea.
Cardiac arrhythmia, seizure (> 30 μg/mL )
• Elimination : Kidney and liver.
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Immunosuppressive drugs
Cyclosporine• Absorption of orally administered drug is variabl
e ( 5 to 50﹪ ﹪) . Sequestered in cells.• Range : 100-300 ng/mL• Toxicity : Renal tubular and glomerular dysfun
ction, hypertension.• Elimination : Liver.• Determined with immunoassays. Whole blood is
the specimen of choice.
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The categories with the largest number of deaths are as follows:
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Salicylate• Aspirin (Acetylsalicylic acid) has analgesic, antipyretic and antiinflammatory
properties.
Therapeutic concentration: analgesic-antipyretic (lower than 60 mg/L) anti-inflammatory (150 to 300 mg/L)
Aspirin interferes with platelet aggregation and thus prolongs bleeding times.
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Pharmacologic effect of salicylates
• Stimulate central respiratory center
• Uncoupling of oxidative phosphorylation
• Enhance anaerobic glycolysis, Inhibite Kreb’s cycle and transaminase enzyme.
• Respiratory alkalosis predominates in children over age 4 and in adults.
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• Respiratory alkalosis (19 % )
• Metabolic acidosis (15 % )
• Combined (61 % )
motality was associated with acidemia
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Fig.25-13. Nomogram for estimating the severity of acute salicylate intoxication.(From Done, A.K.:salicylate intoxication: Significance of measurements of salicylate in blood in cases of acute ingestion. Pediatrics, 26:800, 1960. Reproduced by permission of Pediatrics.)
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Symptoms of salicylate intoxication
• Tinnitus (耳鳴)• Diaphoresis (出汗)• Hyperthermia• Hyperventilation• Nausea, vomiting• Acid-base disturbances• CNS effects lethargy, disorientation, coma and seizures.
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Treatment
• Ipecac to induce vomiting
• Correction of acid-base and electrolyte imbalance, activated charcoal to prevent absorption
• Hemodialysis
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Screening Assay for Acetaminophen and Salicylate
• Acetaminophen After acid hydrolysis, the sample was reacted with
o-cresol in basic solution to show blue color.
• Salicylate Salicylates reacted with Ferric chloride solution to
produce a violet color reaction.
(Interferant: Diflunisal, labetalol, keto acids)
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Methemoglobin
• Less than 1.5 % of total hemoglobin in normal blood
• Caused by methhemoglobin reductase deficiency or ingestion of nitrites, nitrates, phenacetin, phenazopyridine, sulfonamides, sulfones, aniline dyes.
• Determined spectrophotometrically at
630 nm
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Alcohols
• Ethanol
• Methanol
• Ethyleneglycol
• Isopropylalcohol
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Effects of Ethanol
• Cardiovascular system—Increase high-density lipoprotein
• Central nervous system-CNS depression (Respiratory center, coma, death)
• Gastrointestinal tract-Stimulate the production of gastric juices
• Kidney-Diuretics ( Inhibit the secretion of ADH)• Liver-Fatty liver,Cirrhosis • Fetal alcohol syndrome
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Determination of Ethanols
1. Enzymatic
2. Headspace-GC
3. Breath-testing device (amount of ethanol in 1mL of blood equals to 2100mL of breath air)
Henry’s law
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Ethyleneglycol
資料來源: 2007 年 5月 7日自由時報
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Carbon Monoxide
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• Lithium Use to treat manic-depressive illness. It enhances reuptake of neurotransmitters, thus
produces sedating effect on the CNS
• Toxicity apathy, sluggishness, drowsiness, lethargy, speech
difficulties, irregular tremors, muscle weakness, ataxia, epileptic seizures.
Determined with ISE or Atomic Absorption
Spectrometry, Flame emission photometry
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Lead• Toxicity Inhibits amino levulinic acid dehydratase (causes accu
mulation of protoporphyrin in RBC)
Forms covalent bonds with the-SH group of cysteine in proteins (Nerve cells are particular susceptible)
• Determination whole blood was analyzed with atomic absorption spe
ctrometry
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•Fig.25-27. Effects of inorganic lead on children and adults (lowest observable adverse effect levels). (From Royce, S.E., Needleman, H. L., Eds.: Case Studies in Environmental Medicine: Lead Toxicity. U.S. Public Health Service, ATSDR, 1990.)
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Iron
• Toxicity Severe irritation of the epithelial lining of the GI tract a
nd results in hemosiderosis, which may develop into hepatic cirrhosis.
• Hemosiderosis A term used to imply iron overload without associated t
issue injury Determined spectrophotometrically after reaction with
Bathophenanthroline or Ferrozine
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