# data[].attributes.body
Mast Cell Stabilizers
MOA: inhibits mast cell release of histamine-decreases histamine, prophylaxis

cromolyn Sodium
(Intal® / Nasalcrom®)

Bronchodilators

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

albuterol (Proventil®/Ventolin®)

formoterol    (Foradil®)                        terbutaline (Brethine®)                        salmeterol (Serevent )

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

theophylline (Theo-Dur)

aminophylline (Paladron)

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)

brompheniramine (Dimetapp®)

chlorpheniramine (Chlor-Trimeton®)

clemastine (Tavist®)

diphenhydramine (Benadryl®)

hydroxyzine (Atarax®)

promethazine (Phenergan®)

azelastine (Astelin® or Astepro®)

Generation II (non-sedating)

loratidine (Claritin®)

fexofenadine (Allegra®)

cetirizine (Zyrtec®)

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

budesonide (Rhinocort® or
Pulmicort®)

mometasone (Nasonex® or
Asmanex®)

fluticasone
(Flonase® /Flovent®)

flunisolide (Nasalide®)

triamcinolone
(Nasacort®/Azmacort®)

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

hydrocodone (Hycodan®)

codeine/guaifenesin
(Robitussin AC®)

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

dextromethorphan/guaifenesin (Robitussin DM®)

benzonatate  (Tessalon Perles®)

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

oxymetazoline (Afrin®)

pheniramine (Dristan®)

phenylephrine (Neo-Synephrine®)

pseudoephedrine (Sudafed®)

Expectorants
MOA: increase respiratory secretions, lubricate and liquefy mucus

guaifenesin (Robitussin®, Mucinex®, Organidin®)

Mucolytics
MOA:

Liquefy bronchial secretions
acetylcystine

# data[].attributes.body
Skeletal Muscle Relaxants

Peripherally Acting

Depolarizing Agent:
MOA:  two step process

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)

carisoprodol (Soma)

methocarbamol (Robaxin)

orphenadrine citrate (Norflex)

chlorzoxazone  (Parafon Forte)         metaxalone (Skelaxin)

# data[].attributes.body
Direct Acting Cholinergic Agonist
MOA:

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

Indirect Acting Cholinergic Agent
MOA:

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®)

# data[].attributes.body
Alpha-1
location:
glands, smooth muscle, eyes, most arteries and veins

Alpha-2
location:
adrenergic nerve ending

Beta-1
location: Heart

Beta-2
location:
Lungs,  smooth muscle, uterus, skeletal and coronary arteries

# data[].attributes.body
Muscarinic
location:
cardiac, smooth muscle and glands

Nicotinic 1 (Nn)
location:
at ganglia of both sympathetic and parasympathetic nerves

Nicotinic 2
location:
neuromuscular junction

# data[].attributes.body
Cholinergenic
Rest and Digest

# data[].attributes.body
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

# data[].attributes.body
Adrenergenic
Fight, Flight, Freeze

# data[].attributes.body
Neurotransmitters
Epinepherine (EPI)-
Produced and released by adrenal medulla
End Organ Response - stimulates whole body
Arteries:
vasoconstriction (exceptions are cardiac and skeletal arteries)
Heart: Increase Rate, Contractility and AV conduction
GI: Decreased activity and secretions
Postganglionic NT: norephinepherine released
Pupil: Mydriasis
Urinary bladder: Relaxes
Urinary Sphincter: Contricts

Norepinepherine -
Synthesized from Dopamine
Released: at post ganglionic nerve endings and adrenal medulla
End Organ Response -
Arteries: Vaso-Constriction
Heart: Increase Rate, Contractility and AV conduction
Pupil: Mydriasis
no beta -2 receptors are stimulated

Dopamine
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

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

# data[].attributes.body
classifications:

Alpha-1 Adrenergic Agonists
-alpha-1 receptor is stimulated
MOA:
-contraction of smooth muscle, blood vessels constrict, ^ BP

-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)

terazosin (Hytrin)

doxazosin (Cardura)

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)

albuterol (Proventil/Ventolin)

terbutaline (Brethine)

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)

propranolol (Inderol)

timolol (Blocadren)

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)

# data[].attributes.body
H-1 Receptors (associated with allergies)

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

H-2 Receptors: (GI issues)

Location:
stomach, heart, uterine tissue, blood vessels

H-3 and H-4 receptors (pain and inflammation)

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