-vasoconstriction of nasal passages

    ephedrine

    phenylephrine (Neo-Synephrine)

Adrenergic Agonists
Stimulates all alpha and beta receptors
MOA: 

vasoconstriction, increases BP

Cardiac stimulant

Bronchodilator

    epinephrine (Adrenalin)

     
Alpha-1 Adrenergic Blocker
binds to alpha-1 receptors and blocks them
MOA:  

relaxation of smooth muscle 

vasodilation of blood vessels, decreases BP

relaxes smooth muscle of ureters and increases urine flow

         prazosin (Minipress)

 

Beta-1 Adrenergic Agonist
MOA: 

Low dose-stimulates dopaminergic (d-1) receptors in kidneys causing vasodilation and increased renal blood flow

Moderate dose-stimulates  beta 1 receptors-heart, increases force of contraction and cardiac output 

High dose- stimulates alpha-1 receptors causing vasoconstriction  increase in blood pressure

          dobutamine 

 

Beta-2 Adrenergic Agonist
stimulates beta 2 receptors
MOA: 

relaxation of the smooth muscle of the lungs, bronchodilation 

relaxation of the smooth muscle of the uterus

         formoterol (Foradilâ)

Beta Blocker - Nonselective
block beta-1 and beta-2 receptors 

MOA: 
decreases force of contraction  (negative inotropic), decreases cardiac output

decreases HR  
(negative chronotropic) 

decreases conduction
(negative dromotropic)

decrease in cardiac output also decreases BP

can cause bronchoconstriction

     nadolol (Corgard)

                  Selective
beta-1 receptor is blocked (antagonizes beta-1 effects of NE and EPI)
MOA: 

 decreases force of contraction  (negative inotropic), decreases cardiac output

decreases HR  (negative chronotropic) 

decreases conduction (negative dromotropic)

decrease in cardiac output also decreases BP

     atenolol (Tenormin)                             metoprolol (Lopressor)

Moderate dose-stimulates  beta 1 receptors-heart, increases force of contraction and cardiac output 

High dose- stimulates alpha-1 receptors causing vasoconstriction -> increase in blood pressure

Acetylcholine (ACH)
Released at the ganglia from postganglionic nerve endings (both systems)
End Organ Response -
Arteries: not affected
Heart: Decreased heart rate, conduction, and contractility
GI: Increased digestion, increased urination and defecation
Urinary bladder: Contracts
Urinary Sphincter: Relaxes

directly stimulate/bind to the muscarinic receptors in the parasympathetic division 

mimics ACH

          acetylcholine
          MOA: pupil constriction

          pilocarpine (Pilocar)
          MOA: pupil constriction;                     decreases amount of fluid in 
         eye; decreases  intraocular     
         pressure

         bethanechol (Urecholine)
         MOA: stimulates muscarinic             receptors of bladder and GI 
         tract to prevent constipation 
         and urinary retention post-op             and in the elderly

inhibit acetylcholinesterase, the enzyme that destroys ACH in the synapse

increases ACH

       neostigmine (Prostigmin)

Anticholinergic  
MOA: 

bind to a cholinergic receptor 

acts as a blocking drug; competitive antagonism

   atropine                           
   dicyclomine (Bentyl)
   ipratropium bromide (Atrovent®)

binds to nicotinic 2/Nm receptor and induces depolarization à muscle fasciculations

alters the Nicotinic 2/Nm receptor, so it cannot respond to endogenous ACH and prevents contractions from occurring

                 succinylcholine

            Non-depolarizing Agent
MOA: occupies the nicotinic 2 / Nm receptor sites, ACH cannot bind, no contraction occurs, no depolarization can occur

                  rocuronium bromide         
                  (Zemuron)

             Direct Acting
MOA: inhibits skeletal muscle contraction, blocks Ca++ release within the muscle fiber, does NOT affect the Nicotinic 2/Nm receptor or spinal cord conduction

                   dantrolene (Dantrium)

   

     Centrally Acting
MOA: decrease number of impulses available to produce a contraction at motor neurons, block conduction within the spinal cord           cyclobenzaprine (Flexeril)

     cromolyn Sodium 
     (Intal® / Nasalcrom®)

 

Sympathomimetics “B-2 agonist”  (Short and long acting)
MOA: stimulate beta-2 adrenergic receptors

      albuterol (Proventil®/Ventolin®)

               

Xanthine Derivatives
MOA: increases cyclic AMP (formed from sympathetic activation) -> bronchodilation; mucociliary clearance

      theophylline (Theo-Dur)

 

Cysteinyl Leukotriene Receptor Antagonist
MOA: anti-inflammatory, inhibits formation of prostaglandin derivatives called leukotrienes (bronchoconstriction, mucus production, inflammation)

      montelukast    (Singulair®)

 

Anticholinergic
MOA: blocks muscarinic receptors, blocks actions of ACH -> bronchodilation

      ipratropium bromide     
      (Atrovent®)

 

Combination Bronchodilator
MOA: •Anticholinergic + beta 2 agonist

     ipratropium bromide and      
     albuterol sulfate (Combivent®)

Antihistamines
MOA: block histamine from H-1 receptors
Generation I (sedating)

 

Corticosteroid
(asthma or allergic rhinitis)
MOA: inhibit inflammatory response

     budesonide (Rhinocort® or      
     Pulmicort®)

 

Antitussives - Narcotic
MOA: prevents cough center in brain from being stimulated

 

Antitussives - non-narcotic
MOA: prevents cough center in brain from being stimulated

 

Decongestants
MOA: vasoconstrictors; stimulate alpha-1 receptors, decrease swelling of mucous membranes, alleviate nasal stuffiness, allow secretions to drain

 

Expectorants
MOA: increase respiratory secretions, lubricate and liquefy mucus

Liquefy bronchial secretions
acetylcystine

Location:
blood vessels, bronchial smooth muscles, intestinal smooth muscles, CNS

Location:
stomach, heart, uterine tissue, blood vessels

Neurons, Presynaptic areas of the brain, H-4-WBCs