CHAPTER 449 HEAVY METAL POISONING Flashcards
LEAD METABOLISM
interferes with the mitochondrial oxidative phosphorylation and enhances the oxidation and cell apoptosi
HOW LEAD IS ABSORBED?
thru inhalation and ingestion
half life of lead in soft tissues and bone
soft tissue- 30 days
bone- >20 years
LEAD IS EXCRETED THRU?
URINE BUT SOME CAN BE FOUND IN THE BREASTMILK
ACUTE EXPOSURE OF LEAD
> 60 TO 80 mg
impair neurotransmission and neuronal cell death
impair hematopoiesis
renal tubular dysfunction
HIGHER LEAD EXPOSURE
> 80-120
Acute encephalopathy with convulsions
coma
death
SUBACUTE EXPOSURE IN CHILDREN OF LEAD
25-60 mg
anemia
mental retardation
deficits in language, motor function, language, hearing, balance, behavior and school performance
SUBACUTE EXPOSURE IN ADULTS OF LEAD
>40mg risk for anemia demyelinating peripheral neuropathy impairment of reaction time and hearing decline in recognition risk for cardiovascular disease death renal failure diminished sperm count spontaneous abortions
DIAGNOSIS OF LEAD EXPOSURE IN CHILDREN
abdominal pain irritability lethargy anorexia anemia fanconi syndrome pyuria azotemia epiphyseal plate lead lines in long bone xray
coma happens at what level of blood lead
> 120 mg
diagnosis of lead toxicity in adult
headaches myalgias depression memory loss loss of libido lead line at the gingiva pallor wrist drop
lab test in lead toxicity
normocytic normochromic anemia
basophilic strippling
elevated blood protoporphyrin level
motor delays in conduction
TREATMENT OF LEAD TOXICITY
chelation with oral DMSA (succimer)
acutely exposed treatment of lead
hospitalization with IM or IV chelation with CaEDTA addition with dimercaprol
what is the use of addition of dimercaprol in lead toxicity treatment
to avoid worsening of encephalopathy
weak but natural chelating agent of lead toxicity
vitamin c
shown to lower lead levels in pregnant woman
calcium supplementation (1200 mg at bedtime)