Loperamide is a commonly used over-the-counter (OTC) and prescription medicine that is approved to help control symptoms of diarrhea, including Travelers’ Diarrhea. The maximum approved daily dose for adults is 8 mg per day for OTC use and 16 mg per day for prescription use. It is sold under the OTC brand name Imodium A-D, as store brands, and as generics. In vitro and animal studies show that IMODIUM® (loperamide hydrochloride) acts by slowing intestinal motility and by affecting water and electrolyte movement through the bowel. Loperamide binds to the opiate receptor in the gut wall. Consequently, it inhibits the release of acetylcholine and prostaglandins, thereby reducing propulsive peristalsis, and increasing intestinal transit time. Loperamide increases the tone of the anal sphincter, thereby reducing incontinence and urgency. Loperamide is also indicated for reducing the volume of discharge from ileostomies. In man, Loperamide prolongs the transit time of the intestinal contents. It reduces the daily fecal volume, increases the viscosity and bulk density, and diminishes the loss of fluid and electrolytes. Tolerance to the antidiarrheal effect has not been observed. Loperamide is an opioid receptor agonist and acts on the mu opioid receptors in the myenteric plexus large intestines; it does not affect the central nervous system like other opioids. It works specifically by decreasing the activity of the myenteric plexus which decreases the motility of the circular and longitudinal smooth muscles of the intestinal wall. This increases the amount of time substances stay in the intestine, allowing for more water to be absorbed out of the fecal matter. Loperamide also decreases colonic mass movements and suppresses the gastrocolic reflex.

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Oxycodone is a semisynthetic opioid used for the management of acute and chronic pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Oxycodone is a highly selective full agonist of the μ-opioid receptor (MOR), with low affinity for the δ-opioid receptor (DOR) and κ-opioid receptor (KOR). After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by reducing the amount of cAMP produced, closing calcium channels, and opening potassium channels. After a dose of conventional (instant-release) oral oxycodone, the onset of action is 10–30 minutes, and peak plasma levels of the drug are attained within roughly 30–60 minutes in contrast, after a dose of OxyContin (an oral controlled-release formulation), peak plasma levels of oxycodone occur in about three hours. The duration of instant-release oxycodone is 3 to 6 hours, although this can be variable depending on the individual. Oxycodone in the blood is distributed to skeletal muscle, liver, intestinal tract, lungs, spleen, and brain. Serious side effects of oxycodone include reduced sensitivity to pain (beyond the pain the drug is taken to reduce), euphoria, anxiolysis, feelings of relaxation, and respiratory depression. Common side effects of oxycodone include constipation (23%), nausea (23%), vomiting (12%), somnolence (23%), dizziness (13%), itching (13%), dry mouth (6%), and sweating (5%).

Benzhydrocodone is a prodrug of hydrocodone. Benzhydrocodone is formed by covalently bonding hydrocodone to benzoic acid. Benzhydrocodone itself is not pharmacologically active, but must be metabolized to hydrocodone by enzymes in the intestinal tract to optimally deliver its pharmacologic effects. Hydrocodone is a full agonist of the opioid receptors with a higher affinity for the mu-opioid receptor. Upon binding, hydrocodone produces an analgesic effect with no ceiling. APADAZ a combination of benzhydrocodone and acetaminophen is FDA approved and indicated for the short-term (no more than 14 days) management of acute pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. APADAZ, even when taken as recommended, can result in addiction, abuse, and misuse, which can lead to overdose and death.

Codeine is an opiate used to manage mild to moderate pain severe enough to require an opioid. Codeine is a selective agonist for the mu opioid receptor and has an affinity to delta and kappa-opioid receptors. In some countries, this drug is regulated under various narcotic control laws, because its chronic use can cause physical dependence. In others, it is available without a medical prescription in combination with paracetamol.

Aspirin is a nonsteroidal anti-inflammatory drug. Aspirin is unique in this class of drugs because it irreversibly inhibits both COX-1 and COX-2 activity by acetylating a serine residue (Ser529 and Ser516, respectively) positioned in the arachidonic acid-binding channel, thus inhibiting the synthesis of prostaglandins and reducing the inflammatory response. The drug is used either alone or in combination with other compounds for the treatment of pain, headache, as well as for reducing the risk of stroke and heart attacks in patients with brain ischemia and cardiovascular diseases.