Greetings everyone. I am very busy with exams coming up in a few days, but I did want to share a recent slide - this one is related to lead poisoning.
Talk soon!
-Bob
Peripheral blood smear in a patient with lead poisoning
Organ Basis of ID
Blood. RBC’s.
Morphology
Red cell with basophilic stippling. (Indicates clustering of ribosomes).
Disease
Microcytic hypochromic anemia.
Etiology
Lead poisoning (aka Plumbism).
Pathogenic mechanism
Deficient HEME synthesis due to:
Inhibition of ALA dehydratase
Inhibition of Ferrochelase
Decreased incorporation of Iron into Heme.
Divalent lead “competition” with Calcium - systemically.
Other Structural changes seen
Possibly mild hemolytic anemia in CBC.
Other sites of involvement
Encephalopathy: Seizures, coma, violence. (PB, a divalent cation like Ca)
Kidneys: PCT Damage (Shows intra-nuclear inclusions (of Pb-Protein complexed.) Produces a FANCONI-Like syndrome as AA’s are lost in the urine – NO PCT re-absorption).
Gums: Show lines of hyperpigmentation that are blue/black.(lead sulfide deposition.)
Long Bones: Lead Lines, Pb deposited instead of Calcium.
Blood: Na/K ATPase Pump inhibited. Possible HEMOLYTIC anemia.
Other diseases w/ similar changes
Thalassemia.
Iron-deficiency.
Signs and Symptoms
Peripheral neuropathy in adults. (Wrist drop/ Foot drop).
Acute encephalopathy (CNS) in YOUNG children.
Older children show Behavior changes and developmental regression.
Constipation and colicky pain. (ANS involvement in GIT).
A chronic disease. Children present with a more abrupt onset of CNS problems. Adults present with headache, metallic taste, abdominal discomfort and personality changes.
Reversible disease in adults, not necessarily children.
Laboratory Investigations
Blood - for blood lead and erythrocyte protoporphyrin and Zn-protoporphyrin.
Urine – during chelation therapy for progress.
Screening questions and health department involvement.
Course of disease process
1.Lead ingestion via absorption, inhalation or consumption.
2.Pb’s high affinity for -SH (SULFHYDRYL GROUPS) inhibits Heme synthesis.
3.Iron won’t incorporate into Heme. - Protoporphyrin builds up. (Zn substitutes for Fe).
4.Ribsomes in RBC’s remain clustered – producing stippling.
5.Pb affects BBB permeability, complexes with proteins and incorporates where calcium normally acts.
6.Death is a possibility. The source must be removed.
Treat with EDTA/BAL chelation therapy combination.
3 important points
Protoporhpyrin accumulates – provides for testing
RBC’s become small with “little blue dots.”
Children at serious risk.
Clinical Vignette
A 19-month-old, previously healthy Hispanic child was found to have anemia during a routine screening examination; her hemoglobin level was 5.4 g per dL. The family lived in an older neighborhood and drank tap water from the city’s water supply which was recently chemically treated for contamination by Enteric bacteria.
The peripheral blood smear showed round, dark-blue granules within the red blood cells. During the workup, radiography of the child’s long bones was performed showing radiodensity in the epiphyses.
Which one of the following is the most likely diagnosis?
A. Beta-thalassemia
B. Carbon Monoxide Exposure
C. Lead toxicity
D. Sickle cell anemia
E. Gram-negative hemolysins.
