Pathways

Hereditary coproporphyria (HCP) is a rare inborn error of metabolism (IEM) which arises from a defective gene called CPOX. This gene is responsible for mitochondrial coproporphyrinogen-III oxidase. A defect in this enzyme results in accumulation of the porphyrin precursors porphobilinogen and 5-aminolevulinic acid; increase of fecal and urinary excreation of coproporphyrins. Symptoms for this condition vary substantially, with anything from reddish-purple urine, to bouts of acute abdominal and nerve pain, to episodes of photosensitive skin eruptions so extreme that the induced scratching often leads to permanent scarring. At the present time the condition has no cure. The following are some measures which are designed to help prevent and/or regulate the above and more symptoms: a diet which is high in carbohydrates and sugars, and a balanced lifestyle which abstains from alcohol and drug use.

Heroin is a mu-opioid agonist. It acts on endogenous mu-opioid receptors that are spread in discrete packets throughout the brain, spinal cord and gut in almost all mammals. Heroin, along with other opioids, are agonists to four endogenous neurotransmitters. They are beta-endorphin, dynorphin, leu-enkephalin, and met-enkephalin. The body responds to heroin in the brain by reducing (and sometimes stopping) production of the endogenous opioids when heroin is present. Endorphins are regularly released in the brain and nerves, attenuating pain.

Heroin also known as diamorphine is a mu-opioid agonist that causes analgesia and is highly addictive. Most often, heroin is administered intravenously as a solution leading to rapid onset of its actions. Heroin is converted to morphine in the liver via liver carboxylesterase 1 and cocaine esterase. The morphine goes back into the blood where it will travel to the brain and cross the barrier to gain access to receptors on neurons. Opioids like heroin and morphine are agonists of all opioid receptors (mu, delta, and kappa), but codeine/morphine is more selective for the mu opioid receptor. Morphine will bind to mu opioid type receptors on pre-synaptic neurons. Morphine can also bind to post-synaptic neurons as well adding on to it's overall effects. On pre-synaptic mu opioid receptors, it will cause activation of them triggering inhibition of voltage gated N-type calcium channels adenylyl cyclase. Less calcium influx into the cell reduces neurotransmitter release into the synaptic cleft reducing neuronal transmission. Inhibiting adenylyl cyclase stops the conversion of ATP into cyclic AMP (cAMP) which has affects of analgesia. The mu opioid receptor activates the potassium inward rectifier channel (GIRK) moving more potassium out of the neuron hyperpolarizing the membrane potential. This makes action potentials much harder to achieve as the membrane potential is more negative. Through these effects, codeine reduces neuronal transmission of pain signals into the spinal cord and therefore less pain is perceived. Heroin has many sites of action where it can act on mu opioid receptors. It can act at the periphery to reduce neurogenic inflammation, the cingulate cortex altering the psychological response to pain, A delta and C pain fibres in the dorsal horn of the spinal chord and in the periaqueductal gray/rostral ventral medulla in the descending pain pathway that projects to the substantia gelatinosa. The inhibition of A delta and C pain fibres in the dorsal horn of the spinal cord is very important as it slows the signalling of pain into the spinal cord. Overdoses of heroin can lead to respiratory depression and eventual death.

Heroin is a mu-opioid agonist. It acts on endogenous mu-opioid receptors that are spread in discrete packets throughout the brain, spinal cord and gut in almost all mammals. Heroin, along with other opioids, are agonists to four endogenous neurotransmitters. They are beta-endorphin, dynorphin, leu-enkephalin, and met-enkephalin. The body responds to heroin in the brain by reducing (and sometimes stopping) production of the endogenous opioids when heroin is present. Endorphins are regularly released in the brain and nerves, attenuating pain.

Metabolites of Hetacillin are predicted with biotransformer.

Hexachlorophene is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Hexachlorophene passes through the liver and is then excreted from the body mainly through the kidney.