Pharmacology – Drug Classes

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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