Anemia lead poisoning

Basophils Irradiation Pernicious anemia Parasitism Lead poisoning ... 

Vitamin Bg deficiency, iron deficiency, and lead poisoning all can cause anemia. These three conditions are summarized and compared in Ihble 1-17-6. 

Lead poisoning produces a microcytic anemia that arises from the abiiity of iead to biock erythro-poiesis by inhibiting heme synthesis in the bone marrow at two steps. 

The answer is C. The patient s symptoms represent a composite of neurologic and gastrointestinal dysfunction, which are consistent with the anemia that is due to lead poisoning. Testing for lead would be appropriate for the patient, the other members of the household, and the house itself. Inorganic lead produces the microcytic anemia by inhibition of heme synthesis in erythropoietic cells of the bone marrow. All the other options represent enzymes of heme synthesis or degradation, but none of them are affected by lead. 

Measuring the child s blood lead level will be very useful in assessing the possibility of lead poisoning. There is evidence that at blood lead levels of about 10 Jig/dL, children are at risk for developmental impairment. Other tests that may be useful include examination for microcytic anemia and erythrocyte stippling and radiographic examination of the long bones for lead lines. 

Drug may produce same signs of renal damage as severe acute lead poisoning (proteinuria, microscopic hematuria). Transient anemia/bone marrow depression, hypercalcemia (constipation, drowsiness, dry mouth, metallic taste) occurs occasionally. 

Acute inorganic lead poisoning is uncommon today. It usually results from industrial inhalation of large quantities of lead oxide fumes or, in small children, from ingestion of a large oral dose of lead in the form of lead-based paint chips small objects, eg, toys coated or fabricated from lead or contaminated food or drink. The onset of severe symptoms usually requires several days or weeks of recurrent exposure and manifests as signs and symptoms of encephalopathy or colic. Evidence of hemolytic anemia (or anemia with basophilic stippling if exposure has been subacute), and elevated hepatic aminotransferases may be present. 

Biochemical changes such as increased aminolaevulinate excretion and inhibition of amino-laevulinate dehydrase may be detected in urine and blood, respectively, at blood lead levels of 0.4 to 0.6 mg mL-1. Anemia is a late feature, however. Neurotoxicity may be detectable at blood lead levels of 0.8 to 1.0 mg mL-1. At blood lead levels greater than 1.2 mg mL-1, encephalopathy occurs. Peripheral nerve palsies are rare, and the foot and wrist drop, which were once characteristic of occupational lead poisoning, only occur after excessive exposure and are now rarely seen. Similarly, seizures and impaired consciousness may result from involvement of the CNS. Bone changes are usually seen in children and are detected as bands at the growing ends of the bones and a change in bone shape. 

Formation of porphobilinogen The dehydration of two molecules of ALA to form porphobilinogen by 8-aminolevulinic acid dehydrase is extremely sensitive to inhibition by heavy metal ions (see Figure 21.3, and p. 279). This inhibition is, in part, responsible for the elevation in ALA and the anemia seen in lead poisoning. 

Very toxic to most plants cumulative poison in mammals. Inhibits 6-aimnolevulinate dehydra se and thus hemoglobin synthesis in mammals (see Al). One of the symptoms of lead poisoning is anemia. Toxic to central nervous system. 

Lead adversely affects a number of systems in the body. The inhibition of the synthesis of hemoglobin by lead has just been noted. This effect, plus a shortening of the life span of erythrocytes, results in anemia, a major manifestation of lead poisoning. 

The lead (II) ion also is toxic to fishes and plants. In a recent report on lead poisoning, an adult was hospitalized due to severe anemia and other health-related problems. A high lead-blood concentration was found in all the family members. Subsequently, it was discovered that the family was eating flour contaminated with a high level of lead (38.7 mg/g). 

The Roman aristocracy had greater access to lead vessels and cosmetics containing lead compounds. It is believed that their life expectancy may have been as low as 25 years because of lead poisoning. In the body, lead accumulates in bones and the central nervous system. The production of hemoglobin is inhibited by lead because it binds to the enzymes that catalyze the reaction. High levels of lead cause anemia, kidney disfunction, and brain damage to occur, and the accumulation of lead interferes with proper development of the brain in children. Because of their toxicity, lead and its compounds are used much less today as paints or glazes than they were in earlier times. 

B-7) (B-7) Pyrimidine S -nucleotidase deficiency. RNA, in this condition, can not be completely degrad in maturing red blood cells. The nucleotides of uridine and cytidine accumulate. This is associated with a hemolytic anemia. In lead poisoning, lead inhibits 5 -nucleotidase and a1.< o mav result in an atieojia. In both... 

Chronic lead nephropathy from moonshine came to medical attention because of the dramatic symptoms of acute lead poisoning. Lead colic and anemia were... 

Exposure to lead in adults has been associated with hypertension, nephropathy, decreased hearing acuity, anemia, peripheral neuropathy, and encephalopathy. Onset of symptoms may be slow with chronic exposure. Anemia, common in chronically exposed adults and children, tends to be more severe in children. The life span of red blood cells decreases when lead concentrations in blood increase. In the past, the morphology of various blood cells was used to diagnose lead poisoning. Zero content is allowed in food (Food and Drug Administration). 

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