Pharmacology

α1 agonists

Phenylephrine

Phenylephrine

agonist of α1 and promotes vasoconstriction; useful for decreasing nasal congestion

α1 antagonists

Prazosin

Prazosin

α1 antagonist; promotes vasodilation; can be used to treat high blood pressure

α2 agonist

Clonidine

Clonidine

α2 agonist; reduces the activity of the sympathetic nervous system by inhibiting the release of NE; reduces heart rate & promotes vasodilation; useful for the management of hypertension

β1 agonists

Dobutamine

Dobutamine

β1 agonist; increases heart rate & force of contraction; used during the treatment of heart failure

β1 antagonist

Atenolol

Atenolol

β1 antagonist; decreases heart rate & force of contraction; can be used to treat high blood pressure

β2 agonists

Albuterol

Albuterol

β2 agonist; causes bronchodilation; administered by inhalation; used to treat asthma & chronic obstructive pulmonary disease (COPD)

β3 agonist

Mirabegron

Mirabegron

β3 agonist; causes relaxation of the detrusor muscle in the bladder; increases bladder capacity; used to treat urinary incontinence

Adrenergic Receptors

Receptors that are targets for catecholamines like epinephrine and norepinephrine.

α1 Receptors

Coupled to 'Gq' alpha subunit; activate phospholipase C, leading to vasoconstriction.

α2 Receptors

Coupled to 'Gi' alpha subunit; inhibit adenylyl cyclase, reducing norepinephrine release.

β1 Receptors

Located in the heart; increase heart rate and force of contraction.

β2 Receptors

Located in smooth muscles; cause bronchodilation and urinary retention.

β3 Receptors

Located in detrusor muscles of the bladder; promote relaxation of bladder muscle.

Sympathomimetic Drugs

Drugs that activate α1, β1, β2, & β3 adrenergic receptors.

Sympatholytic Drugs

Drugs that activate α2 adrenergic receptors.

Potency

The amount of drug required for a response.

Efficacy

How good a drug is at getting a desired response.

Therapeutic Index

Margin of safety measured in a ratio of toxic dose-effect to therapeutic dose effect.

Nociception

The sensory process that conveys pain signals to the brain in response to noxious stimuli.

General Anesthesia

A state of controlled unconsciousness that includes loss of awareness and sensation, important for surgical procedures.

Primary Afferents

Neurons that relay information about pain from nociceptors to the brain.

Nociceptors

Sensory receptors that detect noxious stimuli and send pain signals to the central nervous system.

Aδ Fibers

Myelinated afferent nerve fibers responsible for fast pain transmission.

C Fibers

Unmyelinated afferent nerve fibers that transmit slower pain signals.

Stages of General Anesthesia

The phases include induction/sedation, excitement, surgical anesthesia, and overdose.

Inhalation Anesthetics

Gases administered to produce general anesthesia, such as sevoflurane and nitrous oxide.

Intravenous Anesthetics

Anesthetics administered via injection, acting on receptors like GABA to induce unconsciousness.

Local Anesthesia

Numbs a specific area of the body without causing loss of consciousness.

Mechanism of General Anesthetics

Involves suppression of neuronal activity to produce unconsciousness and prevent pain responses.

Halogenated ethers

Sevoflurane, Isoflurane, & Desflurane; inhalation; cause a loss of consciousness, analgesia, & muscle relaxation; used during induction & maintenance of general anesthesia

Inorganic gases

N2O (laughing gas) & Xenon; inhalation; only good at blocking pain; typically used during maintenance phase in general anesthesia

GABAa allosteric modulators

Propofol, Etomidate, Barbituric acid, & generic structure of Benzodiazepines; intravenous; suppress neuronal activity to produce unconsciousness (what its best at); commonly used during induction in general anesthesia

Ketamine

intravenous; sleep-producing, pain-relieving, & short-term memory loss effects; used in induction & maintenance in general anesthesia

Dexmedetomidine

intravenous; useful for rapid onset but not unconsciousness; used during maintenance for general anesthesia

Local Anesthetics

Drugs that act on voltage-gated sodium channels (VGSC) to produce transient loss of sensory perception without causing unconsciousness.

Mechanism of action

Local anesthetics bind to the intracellular side of VGSCs to block Na+ ion conductance, preventing action potentials.

Binding form

Local anesthetics cross the plasma membrane in an unprotonated (uncharged) form but bind in a protonated (charged) form.

Frequency of activity

Local anesthetics preferentially bind to open or inactivated VGSCs, affecting neurons with more frequent activity first.

Cocaine

Where many local anesthetics are derivatived

Opioid

Any drug that interacts with an opioid receptor.

μ (MOP) receptor

One of the three main opioid receptors involved in pain relief.

Endogenous agonists

Neuropeptides known as Enkephalins, Dynorphins, & Endorphins that bind to opioid receptors.

Opiate

A natural opioid derived from the poppy plant, such as Morphine and Codeine.

Semi-synthetic opioids

Opioids synthesized from poppy compounds; examples include Oxycodone and Hydrocodone.

Synthetic opioids

Manufactured opioids like Fentanyl, which are significantly more potent than natural opiates.

Naloxone

Opioid receptor antagonist used to treat opioid overdose.

Buprenorphine

A partial agonist opioid that can be used to treat opioid use disorder.

Fentanyl

A synthetic opioid that is 100x more potent than morphine.

Methadone

A long-acting opioid agonist used for treating opioid withdrawal symptoms.

Respiratory depression

A serious risk associated with opioid overdose, leading to decreased breathing.

NSAIDs

Non-steroidal anti-inflammatory drugs; not opioids, but an alternative for pain relief.

Acetaminophen

Not an NSAID; it reduces pain and fever without anti-inflammatory effects.

NSAIDs

Non-Steroidal Anti-Inflammatory Drugs that reduce inflammation, pain, and fever by inhibiting COX enzymes.

COX-1

Cyclooxygenase-1, an enzyme that is consistently active and is involved in the production of protective prostaglandins.

COX-2

Cyclooxygenase-2, an enzyme that is upregulated in response to inflammation and injury, producing prostaglandins that promote inflammation, pain, and fever.

Aspirin

A non-selective NSAID that irreversibly inhibits both COX-1 and COX-2, affecting platelet aggregation.

Ibuprofen

A non-selective NSAID that acts on both COX-1 and COX-2, useful for reducing inflammation and pain.

Naproxen

A non-selective NSAID useful for the reduction of inflammation, pain, and fever.

Acetaminophen

Not an NSAID; acts to reduce pain and fever by reducing prostaglandin synthesis in the CNS, lacking the GI side effects associated with COX-1 inhibition.

Arachidonic acid

A fatty acid that is hydrolyzed by Phospholipase A2 to act on COX-1 and COX-2 during the inflammation pathway.

Prostaglandins

Lipid compounds that are derived from arachidonic acid and involved in the processes of inflammation, pain, and fever.

Thromboxane

A type of prostaglandin produced by COX-1 that promotes platelet aggregation.

δ (DOP)

One of the three main opioid receptors involved in pain relief.

κ (KOP)

One of the three main opioid receptors involved in pain relief.