Lead poisoning pathophysiology: Difference between revisions

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{{Lead poisoning}}
{{Lead poisoning}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} Aksiniya K. Stevasarova, MD
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.


OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==
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===Pathogenesis===
===Pathogenesis===


Lead has no known physiologically relevant role in the body. The toxicity of lead comes from its ability to mimic other biologically important [[metal]]s, most notably [[calcium]], [[iron]] and [[zinc]] which act as [[cofactor]]s in many enzymatic reactions. Lead is able to bind to and interact with many of the same [[enzyme]]s as these metals but, due to its differing chemistry, does not properly function as a cofactor, thus interfering with the enzyme's ability to catalyze its normal reaction(s).
*Lead has no known physiologically relevant role in the body.
 
*The toxicity of lead comes from its ability to mimic other biologically important [[metal]]s, most notably [[calcium]], [[iron]] and [[zinc]] which act as [[cofactor]]s in many enzymatic reactions.
Most lead poisoning symptoms are thought to occur by interfering with an essential [[enzyme]] [[Delta-aminolevulinic acid dehydratase]], or ALAD.  ALAD is a zinc-binding protein which is important in the biosynthesis of [[heme]], the cofactor found in[[hemoglobin]]. Lead poisoning also inhibits the enzyme [[ferrochelatase]] which catalyzes the joining of [[protoporphyrin IX]] and[[Fe]]2+ to form a [[Heme]].
*Following ingestion, lead is able to bind to and interact with many of the same [[enzymes]] as these are metal,s but due to its differing chemistry, does not properly function as a co-factor, thus interfering with the enzyme's ability to catalyze its normal reaction(s).
 
*[[Lead toxicity]] symptoms arise are thought to occur by interfering with an essential [[enzyme]] [[Delta-aminolevulinic acid dehydratase]], or ALAD.  ALAD is a zinc-binding protein which is important in the biosynthesis of [[heme]], the cofactor found in[[hemoglobin]]. Lead poisoning also inhibits the enzyme [[ferrochelatase]] which catalyzes the joining of [[protoporphyrin IX]] and[[Fe]]2+ to form a [[Heme]].
 
 
*The exact pathogenesis of [disease name] is not fully understood.
OR
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
*The development of [disease name] is the result of multiple genetic mutations.
 
==Associated Conditions==
 
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


==References==
==References==

Revision as of 14:14, 15 June 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya K. Stevasarova, MD

Overview

Pathophysiology

Pathogenesis

  • Lead has no known physiologically relevant role in the body.
  • The toxicity of lead comes from its ability to mimic other biologically important metals, most notably calcium, iron and zinc which act as cofactors in many enzymatic reactions.
  • Following ingestion, lead is able to bind to and interact with many of the same enzymes as these are metal,s but due to its differing chemistry, does not properly function as a co-factor, thus interfering with the enzyme's ability to catalyze its normal reaction(s).
  • Lead toxicity symptoms arise are thought to occur by interfering with an essential enzyme Delta-aminolevulinic acid dehydratase, or ALAD. ALAD is a zinc-binding protein which is important in the biosynthesis of heme, the cofactor found inhemoglobin. Lead poisoning also inhibits the enzyme ferrochelatase which catalyzes the joining of protoporphyrin IX andFe2+ to form a Heme.

References

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