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Pathways

PathWhiz ID Pathway Meta Data

PW128225

Pw128225 View Pathway
drug action

Pyridostigmine Action Pathway

Homo sapiens
Pyridostigmine is a cholinesterase inhibitor used for the treatment of myasthenia gravis. It is usually administered intravenously and is very similar to neostigmine but with a less adverse effect profile and longer duration of action. The autoimmune disease known as myasthenia gravis is characterized defect of acetylcholine interacting at the neuromuscular junction. This results in muscle weakness, muscle loss and overall fatigue. Pyridostigmine inhibits the breakdown of acetylcholine allowing for an increase in activation and relieving the aforementioned symptoms. It specifically targets and inhibits acetylcholinesterase and cholinesterase, this increases extracellular levels of acetylcholine. Pyridostigmine is administered orally or intravenously, the latter having a better bioavailability. It is hydrolyzed in the blood by cholinesterases and in the liver by microsomal enzymes in the liver. Its main metabolite is 3-hydroxy-N-methyl-pyridinium and eliminated through the urine.

PW144663

Pw144663 View Pathway
drug action

Pyridostigmine Drug Metabolism Action Pathway

Homo sapiens

PW144262

Pw144262 View Pathway
drug action

Pyridoxal phosphate Drug Metabolism Action Pathway

Homo sapiens

PW000547

Pw000547 View Pathway
disease

Pyridoxine Dependency with Seizures

Homo sapiens
The condition pyridoxine dependent-epilepsy is a condition that sees seizures beginning in infancy. In some cases, the seizures begin before birth. The seizures involve status epilepticus, which are seizures that last several minutes. The symptoms specific to pyridoxine dependent seizures can include hypothermia, dystonia and irritability right before an episode. They also include loss of consciousness, convulsions, and muscle rigidity. Rarely does this condition manifest between 1 to 3 years of age, although it has occured. Traditional anticonvulsant medication has proven ineffective in patients with this condition; patients are instead treated with pyridoxine daily in large doses. This compound is a b-vitamin found in food. Encephalopathy can occur if this condition is not treated, which can result in permanent brain damage. Although this condition is treated with pyridoxine, it can still cause neurological issues, such as learning disorders or developmental delay, regardless of treatment.

PW121891

Pw121891 View Pathway
disease

Pyridoxine Dependency with Seizures

Mus musculus
The condition pyridoxine dependent-epilepsy is a condition that sees seizures beginning in infancy. In some cases, the seizures begin before birth. The seizures involve status epilepticus, which are seizures that last several minutes. The symptoms specific to pyridoxine dependent seizures can include hypothermia, dystonia and irritability right before an episode. They also include loss of consciousness, convulsions, and muscle rigidity. Rarely does this condition manifest between 1 to 3 years of age, although it has occured. Traditional anticonvulsant medication has proven ineffective in patients with this condition; patients are instead treated with pyridoxine daily in large doses. This compound is a b-vitamin found in food. Encephalopathy can occur if this condition is not treated, which can result in permanent brain damage. Although this condition is treated with pyridoxine, it can still cause neurological issues, such as learning disorders or developmental delay, regardless of treatment.

PW127267

Pw127267 View Pathway
disease

Pyridoxine Dependency with Seizures

Homo sapiens
The condition pyridoxine dependent-epilepsy is a condition that sees seizures beginning in infancy. In some cases, the seizures begin before birth. The seizures involve status epilepticus, which are seizures that last several minutes. The symptoms specific to pyridoxine dependent seizures can include hypothermia, dystonia and irritability right before an episode. They also include loss of consciousness, convulsions, and muscle rigidity. Rarely does this condition manifest between 1 to 3 years of age, although it has occured. Traditional anticonvulsant medication has proven ineffective in patients with this condition; patients are instead treated with pyridoxine daily in large doses. This compound is a b-vitamin found in food. Encephalopathy can occur if this condition is not treated, which can result in permanent brain damage. Although this condition is treated with pyridoxine, it can still cause neurological issues, such as learning disorders or developmental delay, regardless of treatment.

PW122115

Pw122115 View Pathway
disease

Pyridoxine Dependency with Seizures

Rattus norvegicus
The condition pyridoxine dependent-epilepsy is a condition that sees seizures beginning in infancy. In some cases, the seizures begin before birth. The seizures involve status epilepticus, which are seizures that last several minutes. The symptoms specific to pyridoxine dependent seizures can include hypothermia, dystonia and irritability right before an episode. They also include loss of consciousness, convulsions, and muscle rigidity. Rarely does this condition manifest between 1 to 3 years of age, although it has occured. Traditional anticonvulsant medication has proven ineffective in patients with this condition; patients are instead treated with pyridoxine daily in large doses. This compound is a b-vitamin found in food. Encephalopathy can occur if this condition is not treated, which can result in permanent brain damage. Although this condition is treated with pyridoxine, it can still cause neurological issues, such as learning disorders or developmental delay, regardless of treatment.

PW144300

Pw144300 View Pathway
drug action

Pyridoxine Drug Metabolism Action Pathway

Homo sapiens

PW144336

Pw144336 View Pathway
drug action

Pyrimethamine Drug Metabolism Action Pathway

Homo sapiens

PW002063

Pw002063 View Pathway
metabolic

Pyrimidine Deoxyribonucleosides Degradation

Escherichia coli
The degradation of deoxycytidine starts with deoxycytidine being introduced into the cytosol through either a nupG or nupC symporter. Once inside, it can can be degrade through water,a hydrogen ion and a deoxycytidien deaminsa resultin in the release of a ammonium and a a deoxyuridine. The deoxyuridine is then degraded through a uracil phosphorylase resulting in the release of a deoxyribose 1-phosphate and a uracil. The degradation of thymidine starts with thymidine being introduced into the cytosol through either a nupG or nupC symporter. Thymidine is then degrades through a phosphorylase resulting in the release of a thymine and a deoxyribose 1-phosphate.