Organo phisporous poising diagnosis depend on

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organophosphate poisoning diagnosis cholinesterase clinical diagnosis guideline

Diagnosis of organophosphorus poisoning depends mainly on:
  1. History of exposure
    Recent ingestion, inhalation, or skin exposure to pesticide/insecticide, often in farming or pesticide work.
  2. Typical cholinergic toxidrome
    • Salivation, sweating, lacrimation
    • Miosis (pinpoint pupils), blurred vision
    • Bronchorrhea/bronchospasm, wheeze, respiratory distress
    • Bradycardia
    • Vomiting, diarrhea, abdominal cramps, urination
    • Muscle fasciculations, weakness, paralysis
    • Confusion, seizures, coma in severe poisoning
  3. Laboratory confirmation
    • Low red blood cell acetylcholinesterase (RBC AChE): more specific for significant organophosphate exposure
    • Low plasma pseudocholinesterase (butyrylcholinesterase): supportive but less specific
So, the standard answer is:
Diagnosis depends on a history of recent exposure, clinical features of diffuse cholinergic stimulation, and reduced erythrocyte acetylcholinesterase and plasma pseudocholinesterase activity.
Treatment should not be delayed while waiting for cholinesterase results if the clinical picture suggests poisoning. The ATSDR clinical guidance also stresses exposure history and recognition of the cholinergic syndrome. Textbook source: Henry's Clinical Diagnosis and Management by Laboratory Methods, organophosphates and carbamates section.
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organophosphate poisoning diagnosis

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organophosphate poisoning diagnosis cholinesterase ATSDR

Answers:
  1. A. Rf value
    Ratio of distance travelled by solute to distance travelled by solvent front in chromatography.
  2. C. HRE (Hormone Response Elements)
    Hormone-receptor complexes bind specific DNA hormone-response elements.
  3. D. Hydroxymethylbilane synthase
    Also called porphobilinogen deaminase. Deficient in acute intermittent porphyria.
  4. D. Single-stranded binding proteins
    Replication protein A, replication factor C, and PCNA are eukaryotic replication proteins. Generic SSB proteins are classically associated with prokaryotic DNA replication.
  5. A. Pribnow box
    The bacterial promoter region at about -10 bp.
  6. A. Estimation of cholinesterase
    Organophosphorus poisoning is supported by decreased cholinesterase activity, especially RBC acetylcholinesterase.
  7. A. Synthesized by hepatocytes
    Gamma globulins are immunoglobulins, produced by plasma cells derived from B lymphocytes, not hepatocytes.
  8. B. DNase I
    DNase I produces single-strand nicks in DNA.
  9. D. Cysteine is essential for individuals consuming a diet deficient in methionine
    Cysteine is normally nonessential but becomes conditionally essential when methionine is deficient.
  10. B. ALT and AST
    These are markers of hepatocellular injury. ALP and GGT mainly indicate cholestasis.
  11. A. Melatonin - Tryptophan
    Tryptophan → serotonin → melatonin.
  12. C. Fumarate
    Fumarate produced in the urea cycle enters the TCA cycle through the aspartate-argininosuccinate shunt.
  13. D. Dihydrofolate reductase - methotrexate
    Methotrexate inhibits dihydrofolate reductase.

Uga code for what is mitochondria

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mitochondrial genetic code UGA tryptophan

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human mitochondrial genetic code UGA tryptophan

In the human mitochondrial genetic code, UGA codes for tryptophan (Trp, W).
  • In the usual nuclear genetic code, UGA is a stop codon.
  • In mitochondria, it is reassigned to tryptophan.
Also remember: mitochondrial AUA codes for methionine, and AGA/AGG are stop codons. Basic Medical Biochemistry - A Clinical Approach, mitochondrial mRNA section.
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