Adrenergic Agents
stimulate the sympathetic nervous system and induce symptoms characteristic of the fight-or-flight response
Sympathomimetics
Adrenergic Agents
Alpha-1 receptor
treatment of nasal congestion or hypotension; caused mydriasis during ophthalmic examinations
Alpha-2 receptor
treatment of HTN , reduces the release of norepinephrine
Beta-1 receptor
treatment of cardiac arrest, HF, shock
Beta-2 receptors
treatment of asthma, premature labor contractions
Adrenergic Antagonists
act by directly blocking adrenergic receptors, specific to either alpha or beta blockade
Cholinergic Agents
mimic the action of the parasympathetic nervous system, induce the rest-and-digest response
Parasympathomimetics
Cholinergic Agents
Cholinergic-Blocking Agents
inhibit parasympathetic impulses, suppress flight-or-flight response
Anticholinergics
Cholinergic-Blocking Agents
Benzodiazepines
act by binding to the gama-aminobutyric acid (GABA) receptor-chloride channel molecule
Barbiturates
act by binding to GABA receptor-chloride channel molecules, intensifying the effect of GABA throughout the brain
Anxiety and Insomnia
mechanism unclear, but appears to be related to D2 Dopamine receptors in the brain, agonist effects on presynaptic dopamine receptors and a high affinity for serotonin receptors
Anti-seizure Pharmacology
goal is to suppress neuronal activity just enough to prevent abnormal or repetitive firing
GABA
primary inhibitory neurotransmitter in the brain
Phenobarbital
able to suppress abnormal neuronal discharges without causing sedation
Hydantoin and Phenytoin-Like Drugs
desensitize sodium channels resulting in delayed depolarization of the neuron
Succinmides
suppress seizures by delaying calcium influx into neurons
Tricyclic Antidepressants
act by inhibiting the presynaptic reuptake of both norepinephrine and serotonin
Selective Serotonin Reuptake Inhibitors (SSRIs)
slow the reuptake of serotonin into presynaptic nerve terminals
Serotonin-norepinephrine Reuptake Inhibitors (SNRIs)
inhibit the reabsorption of serotonin and norepinephrine and elevate mood by increasing the levels of these agents in the CNS
Monoamine Oxidase Inhibitors (MAOIs)
inhibit monoamine oxidase, the enzyme that terminates the actions of neurotransmitters such as dopamine, norepinephrine, epinephrine, and serotonin
Glutamate Inhibitor / Serotonin Receptor Antagonist
thought to alter ionic activity and the activities of neurons containing dopamine norepinephrine, epinephrine, and serotonin by influencing their release, synthesis and reuptake
CNS stimulant
drugs stimulate specific areas of the CNS to heighten alertness and increase focus
Phenothiazines
act by preventing dopamine and serotonin from occupying critical neurologic receptor sites
NonPhenothiazines
blocking postsynaptic D2 dopamine receptors
Atypical Antipsychotics
block D2 receptors and block serotonin (5-HT) and alpha-adrenergic receptors
Opioid Agonists
bind to opioid receptors and produce multiple responses
Opioid Antagonists
compete with opioids for access to opioid sites, blocking opioid activity
NSAIDs
inhibit cyclooxygenase, an enzyme responsible for the formation of prostaglandins
Triptans / Ergot Alkaloids
serotonin (5-HT) agonists, thought to act by constricting certain intracranial vessels
Esters / Amides
act by blocking neuronal pain impulses
Inhalation Gaseous Agent
produce analgesia caused by suppression of pain mechanisms in the CNS
Depolarizing blocker
works by binding to acetylcholine receptors at neuromuscular junctions to cause total skeletal muscle relaxation
Non-depolarizing blocker
cause muscle paralysis by competing with acetylcholine for cholinergic receptors at neuromuscular junctions
Dopaminergics
block the effects of acetylcholine within the corpus striatum
Anticholinergics / Cholinergic Blockers
inhibit the action of acetylcholine in the brain
Acetylcholinesterase Inhibitors
(Parasympathomimetics) – act by intensifying the effects of acetylcholine at the cholinergic receptor
Glatiramer Acetate (Copaxone)
a synthetic protein that stimulates myeline basic protein, an essential part of the nerve’s myelin coating
Centrally Acting Skeletal Muscle Relaxants
act at various levels of the CNS, generate their effects by inhibiting upper motor neuron activity, causing CNS depressant effects, or altering simple spinal reflexes
Catecholamine Reuptake Inhibitor
acts by depressing motor activity primarily in the brainstem, limited effects also occur in spinal cord
Nicotinic Blocking Agents
interfere with the binding of acetylcholine, thereby preventing voluntary muscle contraction
Ganglionic Blocking Agents
dampen parasympathetic tone and produce effects like increased HR, dry mouth, urinary retention and reduced GI activity / dampen sympathetic tone resulting in reduced sweating, dec. epinephrine release
HMG-CoA Reductase Inhibitors / Statins
interfere with the HMG-CoA Reductase in the process of synthesizing cholesterol
Bile Acid Resins (Sequestrants)
bind bile acids, increasing the excretion of cholesterol in the stool
Nicotinic Acid (Niacin)
used in combo with a statin or bile acid-binding agent to lower LDLs
Fibric Acid Agents
mechanism unknown; 50% reduction in VLDLs with an increase in HDLs
Cholesterol Absorption Inhibitors
blocks the absorption of cholesterol from the intestinal lumen by cell sin the jejunum of the small intestine
Potassium-Sparing Diuretics
block the action of aldosterone (sodium and water retention), which results in potassium retention and the secretion of sodium and water
Thiazide Diuretics
work in the early distal convoluted tubule, block the reabsorption of sodium and chloride, and prevent the reabsorption of water at this site
Loop/High-Ceiling Diuretics
work in the ascending limb of loop of Henle, block reabsorption of sodium and chloride and to prevent reabsorption of water
Osmotic Diuretics
reduce intracranial pressure and intraocular pressure by raising serum osmolality and drawing fluid back into the vascular and extravascular space
Calcium Channel Blockers (nifedipine)
blocking of calcium channels in blood vessels
Calcium Channel Blockers (verapamil, diltiazem)
blocking of calcium channels in the myocardium, the SA node, and the AV node
ACE Inhibitors
produce their effects by blocking the production of angiotensin II
Angiotension II Receptor Blockers
medications block the action of angiotensin II
Alpha Adrenergic Blockers / Sympatholytics
Selective alpha1 blockade resulting in dilation and smooth muscle relaxation of the prostatic capsule and bladder neck
Centrally Acting Alpha2 Agonists
act within the CNS to decrease sympathetic outflow resulting in decreased stimulation of the adrenergic receptors
Beta Adrenergic Blockers / Sympatholytics
a result of beta1-adrenergic blockade in the myocardium and in the electrical conduction system of the heart
Hypertensive Crisis
direct vasodilation of arteries and veins resulting in rapid reduction of blood pressure
Alpha-1 Adrenergic Antagonists
lower blood pressure directly by blocking sympathetic receptors in arterioles, causing the vessels to dilate
Alpha-2 Adrenergic Antagonists
decrease the outflow of sympathetic nerve impulses from the CNS to the heart and arterioles
Adrenergic Neuron Blockers
non-selective agents that block nerve transmission at the ganglia or at both alpha and beta-adrenergic receptors (reserpine – only drug on the market)
Direct-acting Vasodilator
acts through a direct vasodilation of arterial smooth muscle; has no effect on the veins
Cardiac Glycosides
acts to cause the heart to beat more forcefully (positive inotropic effect) /(digoxin – only drug on the market in US)
Phosphodiesterase Inhibitors
block phosphodiesterase in cardiac and smooth muscle, increase amount of calcium available for myocardial contraction
Organic Nitrates
have the ability to relax both arterial and venous smooth muscles, and dilate coronary arteries
Thrombolytics
dissolve clots that have already formed by conversion of plasminogen to plasmin, which destroys fibrinogen and other clotting factors
Anticoagulants/parenteral
prevent bleeding by inactivation of thrombin formation and factor Xa, resulting in inhibition of the formation of fibrin
Anticoagulant/oral
antagonize vitamin K, thereby preventing the synthesis of four coagulation factors: factor VII, IX, X, and prothrombin
Antiplatelets
prevent platelets from clumping together by inhibiting enzymes and factors that normally lead to arterial clotting
Antidysrhythmic – Sodium Channel Blockers
stabilize cardiac membranes
Antidysrhythmic – Beta-adrenergic Blockers
prevent sympathetic nervous system stimulation of the heart
Antidysrhythmic – Potassium channel Blockers
prolong the action potential and refractory period of the cardiac cycle
Antidysrhythmic – Calcium Channel Blockers
depress depolarization and decrease oxygen demand of the heart
Erythropoietic Growth Factors
act on the bone marrow to increase production of red blood cells
Leukopoietic Growth Factors
stimulates the bone marrow to increase production of neutrophils
Granulocyte Macrophage Colony Stimulating Factor
acts on the one marrow to increase production of WBCs
Thrombopoietic Growth Factors
increase the production of platelets
Antianemic Agent – Iron Salts (Preparations)
provide iron needed for RBC development and oxygen transport to cells
Antianemic Agent – Vit. B12 – Cyanocobalamin
necessary to convert folic acid from its inactive form to its active form
Antianemic Agent – Folic Acid
essential in the production of DNA and erythropoiesis
Vaccinations
causes production of antibodies that prevent illness from a specific microbe
Active natural immunity
develops when the body produces antibodies in response to exposure to a live pathogen
Active artificial immunity
develops when an immunization is given and the body produces antibodies in response to exposure to a killed or attenuated virus
Passive natural immunity
occurs when antibodies are passed from the mother to the newborn/ infant through the placenta and then breast feeding
Passive artificial immunity
is temporary, and occurs after antibodies in the form of immune globulins are administered to an individual who requires immediate protection against a disease after exposure has occurred
Biologic Response Modifiers
Increases immune response and decreases pro-duction of cancer cells
Calcineurin Inhibitor
bind to intracellular messenger calcineurin to disrupt T-cell function
Glucocorticoid
inhibit the biosynthesis of prostaglandins, with ability to suppress histamine release and inhibit certain functions of phagocytes and lymphocytes
Centrally Acting COX Inhibitor / Acetaminophen
slows the production of prostaglandins in the central nervous system
Penicillins
destroy bacteria by weakening the bacterial cell wall
Cephalosporins
beta-lactam antibiotics, similar to penicillins that destroy bacterial cell walls causing destruction of micro-organisms
Carbapenems
beta-lactam antibiotics, that destroy bacterial cell walls causing destruction of micro-organisms (used for pneumonia, UTIs, peritonitis)
Monobactams
beta-lactam antibiotics, that destroy bacterial cell walls causing destruction of micro-organisms, (used for MRSA, C. difficile)
Tetracyclines
broad-spectrum antibiotics that inhibit micro-organism growth by preventing protein synthesis (bacteriostatic)
Macrolides
inhibit protein synthesis (bacteriostatic) but can be bactericidal if given for susceptible bacteria at high enough doses
Aminoglycosides
bactericidal antibiotics that destroy micro-organisms by disrupting protein synthesis
Fluoroquinolones
bacteriocidial and affect DNA synthesis by inhibiting DNA gyrase and topiosomerase IV
Sulfonamides / Trimethoprim
inhibit bacterial growth by preventing the synthesis of folic acid, essential for DNA, RNA and proteins
Antituberculosis / Antimycobacterial
inhibits growth of mycobacteria by preventing synthesis of mycolic acid in the cell wall
Histamine2 Receptor Antagonist
suppress secretion of gastric acid by
blocking H2 receptors in the stomach
Proton Pump Inhibitor
reduce gastric acid secretion by irreversibly inhibiting the enzyme that produces gastric acid
Mucosal Protectant
sulcrafate binds to ulcer, protecting it from further injury caused by acid or pepsin
Antacids
neutralize gastric acid and inactivate pepsin
Prostaglandin E Analog
decrease acid secretion, increase secretion bicarbonate and protective mucus, and
promote vasodilation to maintain submucosal blood flow
Bulk-forming laxatives
soften fecal mass and increase bulk,
which is identical to dietary fiber
Surfactant laxatives
lower surface tension of the stool to
allow penetration of water
Stimulant laxatives
result in stimulation of intestinal peristalsis
Osmotic laxatives
draw water into the intestine to increase
the mass of stool, stretching musculature
Antidiarrheals
activate opioid receptors in the GI tract to decrease intestinal motility and to increase the absorption of fluid and sodium in the intestine
Prokinetic Agents
controls nausea and vomiting by blocking dopamine and serotonin receptors in the CTZ
IBS – Diarrhea
selective blockade of 5-HT3 receptors, which innervate the viscera
IBS – Constipation
Increases fluid secretion in the intestine to promote intestinal motility
5-Aminosalcylates
decrease inflammation by inhibiting prostaglandin synthesis
Calcium Supplements
maintenance of normal musculoskeletal, neurological, and cardiovascular function.
Estrogen Receptor Modulators
works as endogenous estrogen in bone, lipid metabolism, and blood coagulation
Bisphosphonates
decrease the number and action of osteoclasts, which thereby inhibits bone resorption
Calcitonin
decreases bone resorption by inhibiting the activity of osteoclasts in osteoporosis

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