Indications: HTN

MOA: Competitive inhibition of tyrosine hydroxylase - decreases levels of DA and NE

PATHWAY: Tyr-->DOPA-->dopamine-->NE-->epinephrine

Indications: HTN

MOA: inhibits VMAT uptake of monoamines - leaves monoamines susceptible to degradation by MAO

Adverse effects: not only prevents dopamine from getting into vesicles, it also prevents serotonin, NE, epi.. people were getting depressed so they took it off the market and later reintroduced it at lower doses

Indications: Ventricular arrhthymia

MOA: inhibits AP generation and calcium dependent synaptic vesicle fusion - hyperpolarizes membrane of the neuron. Bretylium has affinity for, and is taken up by reuptake transporters proteins that normally take up NE.

Indications: analgesia in surgery

MOA: blocks monoamine reuptake

Adverse effects: you might become a coke wh*re

Other: Reuptake inhibitor drugs are highly effective because reuptake is the MAIN way that adrenergic neurotransmission is ceased

Indications: opioid overdose (Naloxone) or dependence as well as alcoholism (Naltrexone)

MOA: Non-peptide blockers of opioid receptors in CNS

Indications: depression/anxiety

MOA: selective inhibition of serotonin reuptake transporter

Indications: HTN

MOA: inhibits peptide cleavage of AT I to AT II (a potent vasoconstrictor)

Adverse effects: dizziness, irregular heartbeats

Indications: depression

MOA: blockade of cytoplasmic metabolism of monoamines

Contraindications: tyramine in cheeses, chianti = hypertensive crisis, merperidine, triptan

Indications: Parkinson's Disease

MOA: Precursor of dopamine, stimulates dopamine production

Adverse effects: cardiovascular system due to enhanced NE neurotransmission in the peripheral autonomic nerves 

Indications: Parkinson's Disease

MOA: Blocks L-DOPA conversion to dopamine, does not cross BBB, so protects peripheral adrenergic neurons from producing too much dopamine and NE when taking L-DOPA

Indications: not therapeutic - ingested in diet

MOA: competes with NE for transport into synaptic vesicle

Contraindications: MAO inhibitors

Indications: depression

MOA: blocks monoamine reuptake

Adverse effects: depleting NE from use in cardiovascular system 

Indications: cosmetic purposes, diplopia, paralysis of overactive muscles

MOA: prevents calcium dependent exocytosis of NT by inhibiting SNARE docking for vesicular release

Adverse effects: muscle weakness, trouble swallowing

Other: Botulinum Toxin can only get into CHOLINERGIC neurons

Indications: anaphylaxis, shock, cardiac arrest, heart block, bronchospasm

MOA: alpha and beta agonist -- at low conc, B2 receptor causes peripheral vasodilation and decreases DIASTOLIC BP (but systolic pressure still increases)and B1 receptor has pos inotropic and chronotropic effects, increasing systolic BP. At higher doses, a1 receptor activation predominates (= peripheral vasoconstriction and elevated diastolic pressure). B2 receptor causes bronchodilation and a1 causes dec in bronchiole secretions.

Adverse effects: arrhythmias, cerebral hemorrhage, anxiety, cold extremities, pulmonary edema

Contraindications: late term pregnancy due to unpredictable effects on fetal blood flow

Other: short acing due to susceptibility to degradation; B-receptor effects predominate at low concentrations

Indications: acute hypotension due to vasodilatory shock

MOA: alpha-agonist, beta1-agonist; a1 causes peripheral vasoconstriction (inc TPR and diastolic BP), B1 causes increased systolic BP. Overall inc in MAP. Reflex baroreceptor response will cause a DECREASE in HR.

Adverse effects: arrhythmias, ischemia, HTN

Contraindications: pre-existing excessive vasoconstriction and ischemia and late term pregnancy

Other: NE has limited affinity for B2 receptors

REMEMBER NE CAUSES A REFLEX BRADYCARDIA

Indications: CARDIOGENIC SHOCK

MOA: stimulates D1 receptors at low conc (decreases TPR), stimulates B1 receptors at medium conc (increases contractility and HR), stimulates a-receptors at higher infusion rates (increases BP and TPR)

Adverse effects: low infusion rates - hypotension; high infusion rates-ischemia

Contraindications: uncorrected tachyarrhythmias or ventricular fibrillation

Other: advantageous during cardiogenic shock due to vasodilatory effect in renal and mesenteric vascular beds

Indications: BRONCHOSPASM (during anesthesia or bradycardia), transient heart block if TPR is high

MOA: non-selective B-agonist; B2 promotes peripheral vasodilation, decreased diastolic BP; B1 - positive inotropy and chronotropy = TRANSIENT increased systolic BP that is overcome by vasodilatory effect (overall small decrease in MAP). Reflex HR INCREASE. Bronchodilation.

Adverse effects: tachyarrhythmias

Contraindications: angina, particularly with arrhythmias REMEMBER ISO CAUSES A REFLEX TACHY WITH WIDENED PULSE PRESSURE

Indications: Short term Rx for low cardiac contractility in CHF, cardiogenic shock or excess B-blockade

MOA: selective B1-agonist; increased CO, positive inotropic effect > positive chronotropic effect due to lack of B2-mediated vasocilation and reflex tachycardia [BUT at higher doses, it may act as a B2 agonist and cause hypotension with reflex tachycardia]

Adverse effects: arrhythmias, hypotension (high doses), hypertension (low doses)

Contraindications: subaortic stenosis

Other: it is rapidly degraded by COMT

Indications: Prevent and reverse bronchospasm in asthma, bronchitis and emphysema

MOA: B2-agonist

Adverse effects: tachycardia, tolerance, skeletal muscle tremor (by activation of B2 receptors expressed on pre-synaptic nerve terminals of cholinergic somatomotor neurons) 

Indications: Bronchial SM relaxation

MOA: B2-agonist

Adverse effects: tachycardia, tolerance, skeletal muscle tremor (by activation of B2 receptors expressed on pre-synaptic nerve terminals of cholinergic somatomotor neurons) 

Indications: Pressor agent for anesthesia or shock, nasal decongestant, dilate pupil for eye exam (mydriatic agent), paroxysmal supraventricular tachycardia

MOA: selective a1-agonist; peripheral vasoconstriction and increased BP, activates baroreceptor reflex and decreases HR; decreases bronchial and upper airway secretions

Adverse effects: hypertension

Contraindications: hypertension

Other: Phenylephrine is not a catecholamine and therefore is not subject to rapid degradation by COMT. It has a much longer duration of action.

Indications: HTN when cause is due to excess sympathetic drive

MOA: selective a2-agonist; peripheral vasoconstriction; crosses BBB to cause reduced sympathetic outflow and REDUCES vasoconstriction and BP = OVERALL reduction in BP; reduces the tonic excitatory input to sympathetic cells which reduces sympathetic output to vascular SM

Adverse effects: dry mouth, withdrawal after chronic use can result in life-threatening hypertensive crisis

Indications: Narcolepsy, ADHD

MOA: INDIRECT SYMPATHOMIMETIC - cause release of NE from adrenergic nerve terminals via reversal of reuptake channel. No receptor binding or Ca++ influx 

Indications: ADHD

MOA: INDIRECT SYMPATHOMIMETIC - causes release of NE from adrenergic nerve terminals via reversal of reuptake channel. No receptor binding or Ca++ influx

Adverse effects: Tachycardia, palpitations, anxiety

Contraindications: HTN, atherosclerosis, history of drug abuse, Rx with MAO inhibitors within 2 weeks

Indications: pressor agent with anesthesia

MOA: INDIRECT SYMPATHOMIMETIC - cause release of NE from adrenergic nerve terminals via reversal of reuptake channel. No receptor binding or Ca++ influx

Adverse effects: Tachycardia, palpitations, anxiety

Contraindications: HTN, atherosclerosis, history of drug abuse, Rx with MAO inhibitors within 2 weeks

Indications: nasal decongestion

MOA: INDIRECT SYMPATHOMIMETIC - cause release of NE from adrenergic nerve terminals via reversal of reuptake channel. No receptor binding or Ca++ influx

Adverse effects: Tachycardia, palpitations, anxiety

Contraindications: HTN, atherosclerosis, history of drug abuse, Rx with MAO inhibitors within 2 weeks

Indications: HTN, angina due to atherosclerosis, MI

MOA: non-selective B-blocker; decrease in HR and contractility (B1), increased peripheral resistance due to unopposed a1 receptors, decreased renin release, bronchoconstriction, inhibits effects of epinephrine

Adverse effects: bronchospasm, masks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia

Contraindications: DO NOT GIVE B-BLOCKERS TO ASTHMATICS OR PTS WITH COPD, sinus bradycardia, 2nd and 3rd degree heart block, cardiogenic shock **ALSO USE WITH CAUTION IN DIABETICS -- B blockers mask anxiety caused from epi release when pts have low blood sugar

Indications: Glaucoma

MOA: non-selective B-blocker

Adverse effects: bronchospasm, masks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia

Contraindications: DO NOT GIVE B-BLOCKERS TO ASTHMATICS OR PTS WITH COPD, sinus bradycardia, 2nd and 3rd degree heart block, cardiogenic shock

**ALSO USE WITH CAUTION IN DIABETICS -- B blockers mask anxiety caused from epi release when pts have low blood sugar

Indications: long-term angina, HTN

MOA: non-selective B-blocker

Adverse effects: bronchospasm, masks symptoms of hypoglycemia, CNS effects including insomnia and depression, some can raise triglycerides, bradycardia

Contraindications: DO NOT GIVE B-BLOCKERS TO ASTHMATICS OR PTS WITH COPD, sinus bradycardia, 2nd and 3rd degree heart block, cardiogenic shock

**ALSO USE WITH CAUTION IN DIABETICS -- B blockers mask anxiety caused from epi release when pts have low blood sugar

Other: has a longer half life (24 hours) than other non-selective B-blockers (4 hours)

Indications: HTN, angina, MI

MOA: B1-antagonist -- reduced heart rate and contractility, decreased renin release, less bronchocontriction in asthmatics than non-selective B-blockers

Adverse effects: (typically mild and transient)- depression, insomnia, hypotension, bradycardia

Contraindications: sinus bradycardia, 2nd or 3rd degree heart block, cardiogenic shock

Indications: HTN, long-term angina

MOA: B1-antagonist -- reduced heart rate and contractility, decreased renin release, less bronchocontriction in asthmatics than non-selective B-blockers

Adverse effects: (typically mild and transient)- depression, insomnia, hypotension, bradycardia

Contraindications: sinus bradycardia, 2nd or 3rd degree heart block, cardiogenic shock

Indications: Supraventricular tachycardia

MOA: B1-antagonist -- reduced heart rate and contractility, decreased renin release, less bronchocontriction in asthmatics than non-selective B-blockers

Adverse effects: (typically mild and transient)- depression, insomnia, hypotension, bradycardia

Contraindications: sinus bradycardia, 2nd or 3rd degree heart block, cardiogenic shock

Other: Esmolol has a very short half-life (~9 min) so it is given i.v. in hypertensive crisis, unstable angina or arrhythmias when longer acting beta blockers may be problematic

Indications: HTN - especially when sympathetic activity is high

MOA: B-antagonist (with partial agonist activity), decreases HR and contractility but bradycardic response is limited, decreases renin release, decreases sympathetic activation

Adverse effects: (typically mild and transient)- depression, insomnia, hypotension, bradycardia

Contraindications: sinus bradycardia, 2nd or 3rd degree heart block, cardiogenic shock

*USED WHEN PTS ARE LESS TOLERANT OF BRADYCARDIC EFFECTS

Indications: Pheochromocytoma and its related HTN

MOA: IRREVERSIBLE non-selective a-blocker, can help to overcome huge outputs of catecholamines from a tumor; inhibits vasoconstriction, increases inotropy and chronotropy due to blockade of pre-synaptic a2 receptor and increased release of NE. Reflex release of NE also occurs in response to hypotension.

Adverse effects: prolonged hypotension, reflex tachycardia, nasal congestion

Contraindications: coronary artery disease

Indications: Test for pheochromocytoma, rx for pheo. before surgery, catecholamine extravasation

MOA: reversible non-selective a-blocker

Adverse effects: reflex hypotension, reflex tachycardia, nasal congestion

Contraindications: coronary artery disease

Indications: HTN

MOA: selective a1-antagonist, inhibits vasoconstriction, less cardiac stimulation than non-selective a-blockers due to preservation of a2-adrenergic function

Adverse effects: orthostatic hypotension, syncope

Indications: Prostatic hyperplasia, HTN

MOA: selective a1-antagonist, inhibits vasoconstriction, less cardiac stimulation than non-selective a-blockers due to preservation of a2-adrenergic function

Adverse effects: orthostatic hypotension, syncope

Indications: Prostatic hyperplasia, HTN

MOA: selective a1-antagonist, inhibits vasoconstriction, less cardiac stimulation than non-selective a-blockers due to preservation of a2-adrenergic function

Adverse effects: orthostatic hypotension, syncope

Indications: Withdrawal symptoms of smoking cessation

MOA: Activation of neuronal Nicotinic receptors in autonomic ganglia and CNS

Adverse effects: Irritation at site of administration and dyspepsia

Indications: Neuromuscular block for electroconvulsive shock therapy or emergency intubation because it has more rapid onset than the non-polarizing drugs

MOA: Depolarizing block of muscle nicotinic receptors;

Phase I - irreversible -- opening of the ion channel depolarizes the motor end plate. Cholinesterase inhibitors augment blockade in this phase. Phase II - after the membrane becomes repolarized, the drug can be overcome with cholinesterase inhibitors or tetanic stimulation. 

Adverse effects: muscle pain from fasciculations, hyperkalemia (from K+ release at Motor End Plate), autonomic problems due to N-ganglion stimulation, cardiac arrhythmia, can initiate malignant hyperthermia in children with undiagnosed muscle myopathies

Contraindications: familial hyperthermia, patients with skeletal muscle myopathies, or several days after multiple and wide spread skeletal muscle injury

Indications: None (it is rapidly hydrolyzed by acetyl- AND plasma cholinesterases)

MOA: Nicotinic and muscarinic agonist

Indications: Diagnosis of subclinical asthma, or test for severity of asthma

MOA: Mainly Muscarinic agonist of smooth muscle, glands and the heart

Adverse effects: bronchiolar constriction

Contraindications: Beta-blockers because the antidote to overdose is B-blockers

Notes: longer duration of action than Ach because an additional methyl group slows hydrolysis by acetylcholinesterase; Quaternary Nitrogen Analog

Indications: Applied to the Conjunctiva as a miotic agent in ocular surgery; to reduce pressure following Cataract surgery

MOA: Muscarinic AND nicotinic receptor agonist; Cannot be hydrolyzed by AchE

Adverse effects: excessive muscarinic and nicotinic receptor activation

Notes: Quaternary Nitrogen Analog

Indications: Bladder atony; urinary retention

MOA: Muscarinic agonist in GI tract and bladder; resistant to hydrolysis by Both acetyl- and plasma-cholinesterases

Adverse effects: few (because it has less activity on M2 receptors that affect the heart)

Contraindications: peptic ulcer, asthma, bradycardia

Notes: Quaternary Nitrogen Analog

Indications: Dry mouth from head and neck radiation or Sjogren's Syndrome; Narrow angle and open glaucoma

MOA: Pure muscarinic agonist, Passes BBB and has CNS effects

Adverse effects: excessive muscarinic toxicity-- slows AV conduction, bronchoconstriction

Contraindications: Beta-blockers

Notes: Naturally Occuring Tertiary Amine

Indications: Myasthenia gravis; reverses non-depolarizing neuromuscular block

MOA: reversible AchE inhibitor (long effect -- can block Ach from binding AchE for over an hour); direct stimulatory effect on nicotinic receptors at the skeletal muscle endplate (Nm receptors)

Adverse effects: excessive Ach action at peripheral muscarinic and nicotinic receptors

Contraindications: intestinal obstruction

Indications: Diagnosis of myasthenia gravis; reversal of neuromuscular block; differential diagnosis between progression of myasthenic weakness and a cholinergic crisis (If you inc Ach more in a pt whose disease is progressing, you should improve their symptoms. On the contrary, if you increase Ach more in a pt who has too much Ach (why they are having muscle weakness) you will exacerbate muscle weakness.)

MOA: reversible AchE inhibitor; stimulates nicotinic receptors at the NM jxn

Adverse effects: bradycardia, cardiac standstill

Contraindications: mechanical block of intestine and urinary tract

Indications: Antidote for muscarinic antagonist poisoning; delerium from anticholinergic drugs; topical treatment for glaucoma

MOA: reversible AchE inhibitor; Passes BBB

Adverse effects: increased Ach at muscarinic or nicotinic receptors - convulsions, respiratory and CV depression

Contraindications: asthma, cardiac insufficiency, intestinal obstruction

Indications: Alzheimer's Dx

MOA: reversible AchE inhibitor; crosses BBB

Indications: Respiratory muscle weakness in organophosphate poisoning

MOA: Peripheral AchE reactivator -- 

Pralidoxime attaches to the site where a cholinesterase inhibitor (organophosphate) has attached, then attaches to the inhibitor, removing the organophosphate from cholinesterase, allowing it to work normally again. This is known as "regenerating" or "reactivating" acetylcholinesterase allowing the breakdown of Ach at the synapse. 

Notes: Ineffective on "aged" enzyme

Indications: Open angle glaucoma

MOA: IRREVERSIBLE AchE INHIBITOR; it is an organophosphate used clinically to produce long term miosis; lasts a long time -- its effect "echoes"

Adverse effects: blurred vision (given in the Elderly, brow ache (typically both resolve)

Indications: allay freq. and urge assoc. with cystitis; hypertonic/hypermobile gut; organophosphate (cholinesterase inhibitor) poisoning; bradycardia of vagal origin; induce mydriasis and cycloplegia

MOA: Competitive Muscarinic Antagonist

Adverse effects: "blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone"

heart runs alone = tachycardia with respiratory depressions; dry mouth, difficulty swallowing, thirst, hot dry flushed skin, mydriasis, blurred vision and photophobia, tachycardia, inc BP, micturition difficulty, respiratory collapse, nervousness, confusion, hallucinations, muscular incoordination and weakness, inappropriate laughter, psychosis, 

Indications: Motion sickness, chemotherapy-induced nausea; anti-salilagogue in surgery; given as a patch

MOA: Competitive Muscarinic Antagonist

Contraindications: narrow angle glaucoma

Indications: Calms the Gut; anti-salilagogue protects against excessive muscarinic activation during reversal of neuromuscular blockade (given with Neostigmine)

MOA: Muscarinic antagonist

Adverse effects: heat stroke because pt cannot sweat

Indications: Adjuvant in surgical anesthsia, sp. abdominal wall relaxation and orthopedic procedures

MOA: Non-depolarizing blockade of muscle Nicotinic receptors -- competitive antagonist -- can be overcome by excess Ach (given in the form of AchE inhibitor) or tetanic stimulation; duration of action is shorter than plasma half-life; longest acting of the curare drugs - renal elimination

Adverse effects: Non-analgesic, apnea, muscarinic blockade

Contraindications: inhalation anesthetics (enhances effect)

Primarily renal excretion

Indications: Prototype only used in lethal injections

MOA: Non-depolarizing blockade of muscle nicotinic receptors -- competitive antagonist

Indications: Intubation, muscle relaxation during surgery or ventilation

MOA: Non-depolarizing blockade of muscle Nicotinic receptors -- competitive antagonist -- can be overcome by excess Ach (given in the form of AchE inhibitor) or tetanic stimulation; duration of action is shorter than plasma half-life; eliminated by the liver

Adverse effects: Non-analgesic, apnea, muscarinic blockade

Contraindications: inhalation anesthetics (enhances effect)

Indications: Intubation, muscle relaxation during surgery or ventilation in pts with renal failure

MOA: Non-depolarizing blockade of muscle Nicotinic receptors -- competitive antagonist -- can be overcome by excess Ach (given in the form of AchE inhibitor) or tetanic stimulation; duration of action is shorter than plasma half-life; shorting acting of the curare drugs --- metabolized by plasma cholinesterase

Adverse effects: Non-analgesic, apnea, histamine release

Contraindications: inhalation anesthetics (enhances effect)

Indications: Adjuvant in surgical anesthesia, sp. abdominal wall relaxation and orthopedic procedures

MOA: Non-depolarizing blockade of muscle Nicotinic receptors -- competitive antagonist -- can be overcome by excess Ach (given in the form of AchE inhibitor) or tetanic stimulation; duration of action is shorter than plasma half-life

Adverse effects: Non-analgesic, apnea, muscarinic blockade

Contraindications: inhalation anesthetics (enhances effect)

Indications: Spasmolytic drug -- Muscle spasticity associated with Multiple Sclerosis or spinal cord injury

MOA: Inhibits neurotransmitter release from skeletal muscle sensory afferent; GABA_B agonist = decreases calcium = reduces the release of excitatory transmitters and substance P in the spinal cord

Adverse effects: Drowsiness, mental disturbances (these side effects can be reduced if given intrathecally)

Note: Baclofen can be given orally or through an intrathecal catheter to reduce side effects

Indications: Spasmolytic drug -- Muscle spasm due to local injury (inflammation), muscle spasticity due to loss of descending inhibitory input (eg. cerebral palsy)

MOA: Facilitate GABA_A mediated pre-synaptic inhibition; increases Cl- in the cell which hyperpolarizes, inhibiting AP signal for release

Adverse effects: sedation and drowsiness 

Contraindications: glaucoma

Diazepam = Valium

Indications: Spasmolytic drug -- Muscle spasticity due to spinal cord injury or Multiple Sclerosis

MOA: Centrally acting a2-agonist - think "two"zanidine

Adverse effects: Drowsiness, hypotension

Indications: Spasmolytic drug -- Muscle spasticity (due to stroke, spinal injury, multiple sclerosis, cerebral palsy); also treats Malignant Hyperthermia (characterized by sudden and prolonged calcium release)

MOA: Blocks calcium release from SR in muscle, thus interfering with E-C coupling; fast muscle fibers are more sensitive, cardiac and smooth muscle insensitive

Adverse effects: muscle weakness, sedation, hepatitis (rare)

Indications: Strong analgesia; pain in MI, kidney stones, severe chronic pain, sickle cell (when you get a sickle cell crisis certain muscle areas get ischemic)

MOA: Strong mu opioid receptor agonist

Adverse effects: CAT = Constipation (mu-rec), Addiction, Tolerance; overdose causes asphyxia and death without getting Naloxone immediately

Contraindications:  Triprolidine (CNS depressant), Trovafloxacin (Abx), Rifampin, alcohol

Indications: Strong analgesic; antispasmotic, biliary spasm, renal colic

MOA: binds K-receptor, K+ channels, muscarinic receptor, dopamine transp. 

Adverse effects: Serotonin Syndrome, seizure, dysphoria, tremor, respiratory distress

Contraindications:  

CANNOT be countered with opioid receptor antagonist Naloxone - probably due to its anticholinergic activity

Indications: Strong analgesic; treatment of opioid dependence; cough assoc with terminal lung cancer

MOA: binds mu opioid receptor primarily but also delta opioid receptors and NMDA (glutamate receptor). Firm occupancy of opioid receptors by Methadone (sits in the receptor site for a long time); decreases desire for other opioid intake because it is producing a decrease in effect that stops withdrawal manifestations. With time, addicts can reduce craving.

Adverse effects: prolonged use may result in dependence

Contraindications:  

Indications: Moderately strong analgesic; moderate to severe pain; dry hacking/coughing assoc. with bronchitis; used in surgery to supress coughing

MOA: mu and delta receptor agonist

Adverse effects: addiction due to euphoria and mental numbness

Hydrocodone = Vicodin

Indications: Moderately strong analgesic; cough, diarrhea, IBS, narcolepsy

MOA: ?? not fully known. structurally similar to morphine

Adverse effects: physical dependence, urinary retention, depression, constipation, itching, erectile dysfunction

Indications: Analgesic to relieve mild to moderate pain; dental extraction

MOA: Agonist-antagonists -- act as an agonist at delta and kappa receptors and an antagonist at mu receptors

Adverse effects: Pentazocine weakly antagonizes the analgesic effects of morphine and meperidine; hallucinations, psychomimetic effects, CV effects; some necrosis or sepsis at the injection site

Contraindications:  

Indications: Mild to moderate anesthesia

MOA: Opioid partial agonist

Indications: prevents or reverses the effects of opioids including respiratory depression, sedation and hypotension in overdose; Depersonalization Disorder (DPD)

MOA: opioid receptor antagonist for kappa and delta receptors; high affinity for the mu-opioid receptor in the CNS 

Adverse effects: change in mood, trembling, change in heart rhythm

Indications: Generalized Anxiety Disorder, Depression (off label use with SSRIs)

MOA: 5-HT_1A Partial agonist -- activates both pre-synaptic AND post-synaptic receptors which will become desensitized in a couple of weeks and normal amts of serotonin can be released

Adverse Effects: can increase anxiety during initial treatment, drowsiness, nausea

Contraindications: 

Indications: Prophylactic for Migraine

MOA: 5-HT_1D Agonist -- inhibition of inflammatory mediator release, cerebrovasoconstriction

Adverse Effects: Coronary vasoconstriction via 5-HT1D receptor

Contraindications: Pts with coronary artery disease

Indications: Anxiety, Depression (in combination with SSRI)

MOA: Serotonin antagonist-reuptake inhibitor (SARI) that acts on 5-HT_2A/2C receptor; SSRI hypnotic, blocks side effects of SSRIs involved in insomnia and sexual dysfunction

Adverse Effects: warning of suicidality in young adults at initiation of treatment

Contraindications: MAO inhibitors

Indications: Schizophrenia with psychosis (a "positive" symptom as a result of overactivation of dopamine)

MOA: 5-HT_2A/D_2/3 Antagonist, suppresses DA release in mesolimbic pathway, but increases DA release in mesocortical pathway

Adverse Effects: weight gain, anxiety, akithesia (compulsive need to move), psychosis with abrupt discontinuation

Indications: Chemotherapy-induced emesis

MOA: 5-HT₃ Antagonist; 5-HT₃ is the receptor that is expressed on vago-sensory neurons that stimulate nausea and vomiting in the area-postrema (outside BBB in the brain)

Adverse Effects: not many

Indications: gastroparesis (delayed gastric emptying)

MOA: 5-HT₄ agonist - stimulates Ach release in myenteric plexus

Adverse Effects: Arrhythmia (long QT Syndrome)

Indications: Depression, OCD, PTSD, panic disorder, social phobia

MOA: SSRI; 5-HT transporter (reuptake) inhibitor

Adverse Effects: Sexual dysfuncion, insomnia

Contraindications: MAO inhibitor

Fluoxetine = Prozac

Indications: Depression, OCD, PTSD, panic disorder, social phobia

MOA: SSRI; 5-HT transporter (reuptake) inhibitor

Adverse Effects: Sexual dysfuncion, insomnia

Contraindications: MAO inhibitor

Sertraline = Zoloft

Indications: Parkinson's Disease

MOA: D1/2 Agonist; increases DA release in nigrostriatal pathway

Adverse Effects: Arrhythmia, nausea, anxiety, hallucinations, dyskinesia and motor fluctuations

Indications: Parkinson's Disease; concurrent with L-DOPA to reduce peripheral DA production 

MOA: inhibits AADC in peripheral tissue - AADC converts L-DOPA to dopamine but dopamine cannot cross BBB

Adverse Effects: augments SE of L-DOPA in CNS

Indications: Parkinson's Disease

MOA: ergot alkaloid with D2 agonist properties; post synaptic activation in basal ganglia, may also be neuroprotective (antioxidant, free radical scavenger, reduction of DA turnover) therefore, best used early in disease course

Adverse Effects: cardiac valvular fibrosis (long term use); impulse control disorders (relatively rare)

Indications: Parkinson's Disease (lower doses); Depression (higher doses)

MOA: Selective inhibition of MAO-B which metabolizes dopamin; can block MAO-A* at high doses

Adverse Effects: hypotension, dry mouth; at higher doses can cause hypertensive crisis or serotonin syndrome

Contraindications: concomitant use of indirect acting sympathomimetics or drugs that increase serotonin neurotransmission

MAO-A degrades tyramine in the digestive tract

Indications: Parkinson's Disease (more advanced)

MOA: inhibits COMT; prolongs and increases effect of L-DOPA, reduces "off" time, can reduce amount of L-DOPA dosing required

Adverse Effects: dyskinesia, hallucinations, nausea, hypotension

Contraindications: liver failure

Indications: Acute psychosis, long-term depot for poorly compliant schizophrenic patients

MOA: D2 antagonism

Adverse Effects: extrapyramidal motor disturbances

Indications: ADHD

MOA: DA reuptake inhibitor; increased DA release in frontal cortex

Adverse Effects: tachycardia

Contraindications: TCA, arrhythmia, HTN

Indications: Chemotherapy-induced and post-OP nausea and vomiting; gastroparesis

MOA: D2 antagonist (blocks nausea in Emetic Center and Area Postrema), also has 5-HT4 agonist properties

Adverse Effects: akathisia, focal dystonia

Contraindications: long-term rx (3 months can cause tardive dyskinesia)

Indications: local anesthetic, nerve block, subarachnoid

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; potency = 1, metabolized by plasma cholinesterase -- short duration (30-45 min); often combined with epinephrine

Adverse Effects: PABA-induced allergy

Ester Local Anesthetic

Indications: topical local anesthetic

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; potency = 2, metabolized to PABA by plasma cholinesterase; useful becuase it is the only LA that vasoconstricts; prevents reuptake of NE at adrenergic terminals

Adverse Effects: HTN, tachycardia, dependence, PABA allergy, CNS toxicity

Contraindications: HTN, alpha-agonist

Ester Local Anesthetic

Indications: spinal anesthesia (subarachnoid anesthetic)

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; potency = 16 because it is more lipophilic, metabolized to PABA by plasma cholinesterase; long lasting (2-5 hours) 

Ester Local Anesthetic

Indications: topical local anesthetic

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; it is a PABA ester that is poorly water soluble and can be applied as dusting powder or ointment to wounds or ulcerated surfaces without concern for systemic toxicity

Indications: epidural/subarachnoid, infiltration, nerve block, 

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; epinephrine is effective for inducing vasoconstriction; high hepatic extraction; not highly protein bound in the plasma

Adverse Effects: CNS toxicity before CV toxicity, Transient Neurologic Symptoms (TNS)

Contraindications: arrhythmias, hypotension

amide

Indications: infiltration, nerve block, epidural

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; epinephrine is effective for inducing vasoconstriction

Adverse Effects: seizures, CV toxicity, early transient neurobehavioral effects in neonates

amide

Indications: infiltration, nerve block, epidural - permits motor activity of abdominal muscles (B = Baby), subarachnoid; postoperative analgesia

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; epinepherine not effective because it is highly protein bound; particularly prolonged duration of action (24 hours); more potent and more toxic than mepivacaine and lidocaine

Adverse Effects: CNS toxicity, more cardiotoxic than others [Although all local anesthetics potentially shorten the myocardial refractory period, bupivacaine avidly blocks the cardiac sodium channels, thereby making it most likely to precipitate malignant arrhythmias --- treat toxicity with INTRALIPID] 

amide

Indications: epidural

MOA:  bind and blocks open or inactivated channels on the cytoplasmic side; epinepherine not effect because it is highly protein bound

Adverse Effects: CNS activation, seizures, less cardiotoxic than bupivacaine, produces less of a motor block

Contraindications: Bowel obstruction because of increased motility

amide

Indications: Gaseous anesthesia used in conjugation with other drugs in anesthesia

MOA:  NOT blood soluble, fast induction, okay for asthmatics (bronchodilator)

Adverse Effects: respiratory depressant (like all inhaled anesthetics, but metabolic O2 consumption decreases too)

Indications: Volatile anesthesic 

MOA:  very blood soluble, slow induction, HR stays the same (other VAs inc), baroreceptor reflex decreases (other VAs stay the same), CO decreases (other VAs stay the same or inc) 

Adverse Effects: almost never used today because of its sensitization to catecholamines and its potential to cause liver necrosis

Indications: Volatile anesthesic 

MOA:  less blood soluble and faster induction than Halothane; maintains CO; advantage of not raising the intracranial pressure in neurosurgery

Adverse Effects: 

Indications: Volatile anesthesic 

MOA:  less blood soluble and faster induction than Isoflurane; maintains CO; advantage of being pleasant-smelling and non-irritating to the airway; rapid induction and recovery making it especially suitable for brief outpatient procedures; minimal cardiac effects making it suitable for elderly

Adverse Effects: degraded by CO2 to Compound A which is potentially nephrotoxic

Indications: Volatile anesthesic 

MOA:  lowest blood solubity and fastest induction of the fluranes

Adverse Effects: "des" advantages = irritating to airway, increased HR, BP (due to sympathetic activation) and intracranial edema

Indications: Ultrashort-acting barbiturate; General IV anesthetic; used for rapid induction of unconsciousness

MOA:  rapid entry into the CNS is followed by a relatively quick redistribution to indifferent tissues because it is lipid soluble; "Robinhood Phenomenon"; fast recovery; useful in neurosurgical procedures because it markedly reduces intracranial pressure; stimulates inhibitory neurons = increases GABA

Adverse Effects: poor analgesic because it can increase the sensitivity to pain when administered in inadequate amounts; arterial contraction (due to baroreceptors reflex), venous hypotension, decreases respiration

Indications: Ultrashort-acting barbiturate; induces general anesthesia; anesthetic before electroconvulsive therapy for depression; epileptic cerebral mapping

MOA:  rapid entry into the CNS is followed by a relatively quick redistribution to indifferent tissues because it is lipid soluble; shows some excitatory phenomena on EEG

Adverse effects: reduces seizure threshold 

Thiopental is preferrable to use to induce anesthesia in epileptics. 

Indications: General IV Anesthetic

MOA:  NMDA antagonist (NMDA is a glutamate receptor); has more of a CENTRAL mechanism of action, depresses cortical function, stimulates limbic system including hippocampus; pts may appear awake; strong feeling of dissociation from the environment; can be administered i.m. - good for kids

Adverse Effects:  excitatory or hallucinatory phenomena as pt emerges from anesthesia; increased ICP, increased cerebral oxygen needs

Contraindications: psychiatric disorders, HTN, high ICP or head trauma

Indications: General IV Anesthetic used only for induction

MOA:  enhances GABA-ergic actions; potent hypnotic agent; good for VERY SICK pts such as those with CV disease, inc ICP, trauma, aneurysm; no hypotensive effects

Adverse Effects:  pain on injection, myoclonus, could suppress adrenocortical fxn 

Contraindications: Epileptic pts (shows stimulation on EEG), Addison's Dx (Chronic Adrenal Insufficiency)

Propofol

Indications: General IV Anesthetic (prepared in a fat solution - need to use antimicrobial with it)

MOA:  rapid -- peak effect in 60 seconds; currently favored in surgery (sense of well-being on emergence); enhances GABA-ergic actions; similar to barbiturates except it inhibits the baroreflex and induces peripheral arterial vasodilation

Adverse Effects: myoclonus, pain on injection, apnea during induction, hypotension

Contraindications: kids (could cause metabolic acidosis), asthmatics 

*killed Michael Jackson

Indications: Opioid mu agonist; strong analgesic used as a supplement in surgery

MOA:  80 times more potent than Morphine; does not cause histamine release like morphine so larger doses are tolerated without CV effects; given transdermally

Adverse Effects:  respiratory depressant, delay in wakening

Indications: 

low dose: (anti-platelet activity = permanently inhibits COX-1 through acetylation which prevents the platelets from making TXA-2) prevention of stroke and MI in pts with high rist of CVD; treatment in acute occlusive stroke; prevention of CVD after MI, stroke, angina, bypass

high dose: (anti-platelet effect of inhibiting TXA2 is offset by increasing inhibition of endothelium-derived PGI2) analgesic, anti-pyretic, anti-inflammatory

MOA:  Non-selective inhibitor of BOTH COX-1 and COX-2; UNIQUE mechanism compared to other NSAIDs -- irreversibly inhibits COX-1 by acetylating the enzyme within its active site thereby inhibiting the binding of the arachidonic substrate; also acetylates COX-2 although it is a much less potent inhibitor of this enzyme

 *can be ZERO-ORDER kinetics at high doses

Adverse Effects: delayed onset of labor, early closing of ductus arterious in fetus; salicylate intoxication = hyperthermia, hyperventilation, metabolic acidosis, hypoglycemia, confusion, tremors, seizure, coma and death

Indications: Traditional NSAID -- inflammation, pain, fever

Rapid onset of action, ideal for fever and acute pain

MOA:  inhibition of COX activity by preventing the production of prostaglandins

Adverse Effects: GI and stomach (inhibition of COX-1 that acts to inc PG --> mucous), Renal, CV system, liver, anti-platelet, hypersensitivity, CNS, skin, photosensitivity, pregnancy - D.A. does not close

Indications: Traditional NSAID -- inflammation, pain, fever

rapid onset of action  (IDEAL FOR ANTI-PYRETIC), long serum half-life of 14hours = twice-daily dosing

MOA:  inhibition of COX activity by preventing the production of prostaglandins

Adverse Effects: considered to be one of the safest NSAIDs; GI and stomach (inhibition of COX-1 that acts to inc PG --> mucous), Renal, CV system, liver, anti-platelet, hypersensitivity, CNS, skin, photosensitivity, pregnancy - D.A. does not close

Indications: Traditional NSAID -- inflammation, pain, fever; long serum half-life of 50-60 hours = once daily dosing; used in treatment of gout (increases excretion of uric acid)

MOA:  inhibition of COX activity by preventing the production of prostaglandins

Adverse Effects: GI and stomach (inhibition of COX-1 that acts to inc PG --> mucous), Renal, CV system, liver, anti-platelet, hypersensitivity, CNS, skin, photosensitivity, pregnancy - D.A. does not close

Indications: Traditional NSAID -- analgesis, potent anti-inflammatory, anti-pyretic; used to close patent ductus arteriosus 

MOA:  inhibition of COX activity by preventing the production of prostaglandins

Adverse Effects: greater toxicity than the other tNSAIDs; GI and stomach (inhibition of COX-1 that acts to inc PG --> mucous), Renal, CV system, liver, anti-platelet, hypersensitivity, CNS, skin, photosensitivity, pregnancy - D.A. does not close

Indications: Traditional NSAID -- potent analgesic, anti-inflammatory, anti-pyretic; relatively selective for COX-2

MOA:  inhibition of COX activity by preventing the production of prostaglandins

Adverse Effects: increased risk of MI or stroke; GI and stomach (inhibition of COX-1 that acts to inc PG --> mucous), Renal, CV system, liver, anti-platelet, hypersensitivity, CNS, skin, photosensitivity, pregnancy - D.A. does not close

Indications: Traditional NSAID -- mainly used as an IV analgesic for moderate/severe post-surgical pain; used as a replacement for opioid analgesics (eg. morphine)

MOA:  inhibition of COX activity by preventing the production of prostaglandins

Adverse Effects: GI and stomach (inhibition of COX-1 that acts to inc PG --> mucous), Renal, CV system, liver, anti-platelet, hypersensitivity, CNS, skin, photosensitivity, pregnancy - D.A. does not close

Indications:  NSAID - analgesic, anti-inflammatory, anti-pyretic; preferrable in pts with a prior history of GI bleeds and/or ulcers

MOA: COX-2-specific inhibitor; off-target effect (independent of COX-2 effect) that acts on Na+ ion channels in vascular smooth muscle to promote vasodilation

Adverse Effects: heart and kidney risks 

Indications:  mild to moderate pain and fever not associated with inflammation

MOA: metabolized selectively in the brain to an active metabolite (AM404) that inhibits COX-2 in the CNS and acts on the endogenous cannabinoid system in the pain and thermoregulatory centers; does not effectively inhibit either COX-1 or COX-2 expressed in the periphery

Adverse Effects: free of adverse effects a normal doses; hepatoxicity at higher doses

Indications: Salicylate -- anti-inflammatory, analgesic

MOA:  inhibits COX-1 and COX-2; does not cross the BBB = ineffective anti-pyretic; lower risk of adverse effects than aspirin because salicylates are non-acetylated and are unable to irreversibly inhibit COX2

Adverse Effects: increased risk of GI complications (e.g. gastric ulcers); increased risk of  bleeding (e.g. hemophiliacs); salicylate intoxication = hyperthermia, hyperventilation, metabolic acidosis, hypoglycemia, confusion, tremors, seizure, coma and death

Contraindications:  All salicylates are 50-90% protein bound- high potential for drug interactions e.g. warfarin, sulfonylureas