Mechanism:Blocks voltage gated Na channels

Structure: Ester

Potency: Low

Duration of action: Medium

Uses:Topical-laryngeal, nasal, urogenital

Adverse effects: CNS-restless, dizziness, confusion, paraesthesias, tinnitus, tremors, hypotension, heart block , cardiac arrest. Peripheral neurotoxicity; Hypersensitivity, constact dermitis

Lidocaine

Mechanism:Blocks voltage gated Na channels

Structure:Amide

Potency:Intermediate

Duration:Short

Uses:Paenteral uses-Epidural, infiltration, nerve block, spinal; Topical uses-dermal, laryngeal, oral.

Adverse effects: Same as cocaine but more likely to cause cardiac toxicity bc ischemic myocardium is more sensitive to lidocaine.

Mechanism:Block voltage gated Na channels

Structure:Amide

Potency:High

Duration:Medium

Uses:Parenteral uses-Epidural, infiltration, nerve block, spinal

Adverse effects:Same as cocaine

Mechanism:Blocks voltage gated Na channels

Structure: Amide

Potency: Intermediate

Duration:Short

Uses:parenteral uses-epidural, infiltration, nerve block, spinal

Adverse effects: Same as cocaine

Mechanism:Block voltage gated Na channels

Structure:Ester

Potency:Low

Duration:Short

Uses:Parenteral uses-Infiltration, nerve block, spinal anesth.

Adverse effects: Same as cocaine.

Mechanism:Blocks voltage gated Na channels.

Structure:Ester

Potency:

Duration:

Uses:

Adverse effects:Same as cocaine

Mechanism:Block voltage gated Na channels

Structure:Ester

Potency:Low

Duration:Medium

Uses:Topical uses-Dermal, laryngeal, oral

Adverse effects:Same as cocaine.

Type: Non-halogenated

MAC: >100

Blood:Gas Partition Coef: 0.47

Rate of Induction: Fast

Metabolism:None

Skeletal mm relaxation: None

Other:Can never be used alone bc MAC too high

Type:Halogenated

MAC:6

Blood:Gas Partition Coef: 0.42

Rate of Induction: Fast

Metabolism: <2%

Skeletal mm relaxation: Medium

Other: Decrease vascular resistance but NOT cardiac output.

Type:Halogenated

MAC:1.7

Blood:Gas Partition Coef: 1.9

Rate of Induction:medium

Metabolism: 5% flouride (nephrotoxic)

Skeletal mm relaxation:Medium

Other: Decreaes CO; causes bronchodialation

Type:Halogenated

MAC:0.75

Blood:Gas Partition Coef: 2.3

Rate of Induction: Slow

Metabolism: 20% (can cause hepatitis)

Skeletal mm relaxation: low

Other: Decrease CO; causes bronchodilation

Type:Halogenated

MAC: 1.2

Blood:Gas Partition Coef: 1.4

Rate of Induction: Medium

Metabolism: <2% fluroide

Skeletal mm relaxation: Medium

Other: Decrease vascular resistance but NOT cardiac output; causes bronchodilation

Type: Halogenated

MAC: 1.9

Blood:Gas Partition Coef: 0.63

Rate of Induction:Fast

Metabolism: <2%

Skeletal mm relaxation: Medium

Other:

Mechanism: Facilitates GABA at GABA-Cl-ionophore

Side Effects: decrease BP, respiration, Cerebral blood flow, ICP

Pros: Antimetic, good for traumatic

Cons: NOT analgesic/ amnestic if conscious

Emergence: Rapid, less confusion (compared to thiopental)

Uses: Orthopedics, bone marrow transplant in kids

Other: Prepared as interlipid; Avoid bacterial contamination, unconciousness as fast as thiopental

Mechanism: Facilitates GABA

Side Effects:Amnesia

Pros: Little effect on CV system, less respiratory depression than thiopental or propofol; doesn't irritate veins.

Cons:Slower unconciousness but longer duration than thiopental

Emergence:

Uses:Colonoscopy, cardiac cath, induce anesthesia

Other: Water soluble, benzodiazepine.

Mechanism: Blocks NMDA receptors

Side Effects: Increase HR, BP, ICP, sympathetic tone.

Pros:Dissociative anesthesia (dreamlike but not loss of conciousness), analgesia, decrease sensory preception, immobility, amnesia.

Cons:Delirium and hallucinations

Emergence: Rapid onset and recovery

Uses: Trauma, sedation of children-radition therapy and burns

Other: Related to PCP, coadminister with benzodiazepine to prevent delirium and hallucinations.

Mechanism:Barbituate

Side Effects: Decrease CNS, respiratory depression, decrease CV function

Pros: Unconcious in 5-10 secs, last about 10 minutes

Cons: Short duration of action but stays in body for 12 hours. Redistribution.

Emergence: ~10 minutes

Uses: Induction of anesthesia

Other: Goes to ares of high  blood flow first ( brain, kidney, heart) then redistributes to fat and muscle.

Opiod Peptide

Precursor: POMC

Major Products: Beta endorphin (major endorphin in CNS), Beta MSH, ACTH

Where it is made: Arcuate Nucleus-hypothalamus, corticotrophs of anterior pituitary (with ACTH)

Receptors: Mu and delta

Other: The peptide made in the hypothalamus may contribute to analgesia, reinforcement and respiratory depression.

Opiod Peptide

Precursor: Proenkephalin

Major Products: leu enkephalin, Met enkephalin

Where it is made: Periaqueductal grey, lamina 1 and 2 of spinal cord and spinal trigeminal nucleus (areas of pain perception)

Receptors: Mu and delta

Other:Made in small interneurons.

Opiod Peptide

Precursor: Prodynorphin

Major Products: Dynorphin A, Dynorphin B, alpha-neoendorphin

Where it is made: Widely distributed, often w enkephalins

Receptors: Kappa>Mu and Delta

Other:

Opiod

Mechanism: Agonist at mu, kappa, and delta receptors; inhibit adenyl cyclase; activate K+ currents-> hyperpolarization; suppression of Ca+2 currents.

Effects: CNS: Analgesia, euphoria/dysphoria, inhibition of cough reflex, miosis, physical dependence, respiratory depression, sedation; CV :decrease myocardial O2 demand, vasodilation d/t histamine, hypotension GI:constipation, increase biliary shincter tone and pressure, nausea, vomiting, increase bladder sphincter tone, prolongation of labor, urinary retention.

Other Effects: Inhibition of LH release, stimulation of ADH and prolactin release, suppression of NK cell function, flushing of skin, prutitis.

Site of Action: Inhibit ascending signal from dorsal horn; activate pain control circuits that descend from midbrain via medulla, to dorsal horn, stimulate periqueductal grey

Signs of Withdrawal:diarrhea, vomiting, chills, fever, lacrimation, rhinorrhea, tremors, abdominal cramps, irritability, insomnia, drug craving and seeking behavior.

Other: Perception of pain is altered but pain may still be present. High first pass affect.

Uses: periph, peripherally at sights of inflammation, pain postop, associated with acute MI, renal, or biliary colic, chronic, non malignant pain.

Opiod

Mechanism:

Effects:

Potency:  3x more potent than morphine

Onset/duration:Faster onset than morphine

Uses:diacetylmorphine.

Mechanism:

Effects/Side Effects: couch suppressant for mid-moderate pain.

Site of Action:

Potency:1/10th morphine

Onset/duration:

Other:Used an antitussive in alcohol based liquid

Uses: Mild/moderate pain, lower addiction liability, less constipation, less sedation, less respiratory, usually in combo w. acet. or aspirin; for 3rd molar removal. the best is to use Codeine w/ ibuprofen bc of antiinflammatory properties.

Mechanism:

Effects/Side Effects: Metabolized to normeperidine which can accumulate in renal insufficiency, risk of seizures

Site of Action:

Potency:1/10th that of morphine

Onset/duration: short duration, 2-4 hours

Other: poor oral absorption; normal doses: miosis, high doses: mydriasis

Uses: post surgical pain, colonoscopy.

Mechanism:

Effects/Side Effects: less sedative and spasmgenic than morphine.

Site of Action:

Potency:slightly more potent.

Onset/duration: Slow onset, long duration

Other: Tolerance develops slowly

Uses:Metadone detox, Methadone maintenance.

Percocet: Acetametaphin + oxycodone

Percodan: Aspirin+oxycodone

Oxycontin: Sustained release

Mechanism:

Effects/Side Effects: Possible muscle rigidity (limited use)

Site of Action:

Potency: 100x more potent than morphine

Onset/duration: 3 days for transdermal patch

Other:

Uses:Anesthesia, transdermal patch for chronic pain.

Mechanism: NMDA receptor anatagonist at high doses

Effects/Side Effects: Cough suppressant (not as good as codeine)

Site of Action:

Potency:

Onset/duration:

Other: Not analgesic or sedative in usual doses

Uses:OTC antitussive.

Mechanism:

Effects/Side Effects:

Site of Action:

Potency:

Onset/duration:

Other: VICODIN- acetaminophan w/ hydrocodone

VICOPROFEN- ibuprofen w/hydrocodone.

Uses:

Mechanism:

Effects/Side Effects: overdose can cause seizure and toxic psychosis

Site of Action:

Potency: less potent and less efficacious than codeine.

Onset/duration:

Other:Darvocet=Acetominophen+prorpoxyphene

Uses:

Mechanism: Synthetic codeine analog, weak mu receptor and agonist and also inhibits uptake of NE and 5HT

Effects/Side Effects: Nausea, vomiting, dizziness, dry mouth, sedation, headache, seizure

Site of Action:

Potency:

Onset/duration:

Other:

Uses:Used for mild to moderate pain.

Mechanism: partial mu agonist and kappa agonist

Effects/Side Effects:

Site of Action:

Potency:

Onset/duration:

Other: Not really used anymore

Uses:

-Antagonist at mu and agonist at kappa.

-Respiratory depression reaches maximum at low doses, fewer dysphoric effect than pentazocine.

-partial mu agonist

-analgesia, sedation, nausea with dizziness but with a max.

-in physically dependant patients on morphine or heroin it prevents symptoms of withdrawal but at high doses it acts as an antagonist and can precipitate withdrawal, sometimes combined with naloxone.

-Used for treatment of opiod dependance, may be safer tahn methadone; 10x more expensive than methadone.

Mechanism: Opiod receptor antagonist

Duration of action: 2 hours

Administration: IV

Uses: Precipitates abstinence in all types of opiod physical dependance.

Mechanism: Opiod receptor antagonist

Duration: longer duration than naloxone.

Administration: Oral

Uses: Prevent relapse in chronic alcoholics

Mechanism: Camphorated tincture of opium

Uses:Treatment of diarrhea

Mechanism: Analog of meperidine; insoluble in aqueous media.

Uses: Treament of diarrhea

Mechanism: Meperidine derivative; excluded from the brain by a P-glycoprotein transporter in the BBB

Uses: Treatment of diarrhea.