Drug Classes

Front 1

Aminoglycosides
(Mechanism of Action)

Back 1

Mechanism of Action: Inhibits protein synthesis by blocking the translocation of a ribosome along the RNA codon

Front 2

Aminoglycosides
(Therapeutic Effects)

Back 2

Used to treat systemic, aerobic, gram negative infections such as meningitis, endocarditis, and multi-drug resistant tuberculosis

Front 3

Aminoglycosides
(Pharmacokinetics)

Back 3

Plasma binding: 10% bound
Poorly metabolized by the liver and are excreted unchanged by the kidneys
Some do not pass the BBB

Front 4

Sulfonamides
(Mechanism of Action)

Back 4

Inhibits folic acid and nucleotide biosynthesis in bacteria, so cell is unable to for purine/pyrimides needed for DNA

Front 5

Sulfonamides
(Therapeutic Effects)

Back 5

Used to treat UTIs
Broad spectrum antibiotic

Front 6

Penicillins
(Mechanism of action)

Back 6

Inhibit cell wall synthesis
Cause increased osmosis (increased O2 influx resulting in cell lysis)

Front 7

Penicillins
(Therapeutic Effects)

Back 7

More effective against gram positive, rather than gram negative bacteria
Used to treat respiratory infections, gastrointestinal infections, and genitourinary tract infections

Front 8

Penicillins
(Pharmacotoxicology)

Back 8

People can develop penicillin resistance via the production of beta-lactamases (penicillinases)

Front 9

How is the sensitivity to penicillinases different between natural and synthetic penicillins?

Back 9

Decreased sensitivity to penicillinase as penicillin gets more synthetic.

Front 10

Vancomycin
(Mechanism of action)

Back 10

Inhibit cell wall synthesis
Cause increased osmosis (increased O2 influx resulting in cell lysis)

Front 11

Vancomycin
(Therapeutic effects)

Back 11

Active only against gram positive microorganisms
Used to treat severe infections such as endocarditis and MRSA

Front 12

Vancomycin
(Drug/Drug Interactions)

Back 12

Vancomycins combined with furosemide or aspirin increase ototoxicity

Front 13

Vancomycin Resistant Enterococci (VRE)

Back 13

Bacteria found in intravascular catheters that is becoming more common

Front 14

Microlides
(Mechanism of Action)

Back 14

Inhibits protein synthesis by inhibiting protein chain elongation during transcription

Front 15

Microlides
(Therapeutic Uses)

Back 15

Used to treat respiratory tract infections, syphilis, and is used as a substitute for patients with penicillin allergies

Front 16

Lincomycins
(Mechanism of Action)

Back 16

Inhibits protein synthesis by inhibiting peptide chain elongation during transcription

Front 17

Lincomycins
(Therapeutic Uses)

Back 17

Used to treat gram-positive respiratory tract and skin infections (Group A streptococci infections). Also used as a substitute treatment for patients allergic to penicillin.

Front 18

Tetracycline
(Mechanism of Action)

Back 18

Inhibits tRNA, so transcription cannot be done.

Front 19

Tetracycline
(Administration)

Back 19

Must administer around the clock, since tetracylines do not kill bacteria

Front 20

Tetracycline
(Therapeutic effects)

Back 20

Used as a broad specturm antibiotic against gram positive and negative bacteria. Used to treat UTIs and gastrointestinal infections

Front 21

Tetracyclines
(Pharmacotoxicology)

Back 21

Reduce effectiveness of oral contraceptives, increase sensitivity to light, and cause nausea, vomiting, diarrhea, skin rash, and perineal itching

Front 22

Quinolones
(Mechanism of Action)

Back 22

Topoisomerase inhibitors that block the unwinding of DNA and DNA repair that is essential for DNA replication and cell division.

Front 23

Quinolones
(Therapeutic effects)

Back 23

Used to treat STIs (ex: gonorrhea) and respiratory infections

Front 24

Example of a Quinolone:

Back 24

Ciprofloxicin

Front 25

What is Cephalosporin metabolized by?

Back 25

Metabolized by hepatic microsomal enzymes

Front 26

Cephalosporin
(Mechanism of Action)

Back 26

Inhibit cell wall synthesis and increases osmosis (increased H20 influx causes cell lysis)

Front 27

Cephalosporin
(Therapetic Effects)

Back 27

Used as surgical prophylaxis
Used to treat skin, bone, urinary tract, brain, and spinal cord infections
Not effective against MRSA

Front 28

Cepahlosporin
(Drug/drug interactions)

Back 28

Interferes with ETOH metabolism

Front 29

Benzodiazepines
(Mechanism of action)

Back 29

Binds to the GABA-A receptor, which is composed of 5 protein subunits (that includes two alpha and two beta subunits, and a gamma protein that together form a chloride channel). As a GABA receptor agonist, it hyperpolarizes neuron membranes (via chloride influx) and supresses their activity.

Front 30

Non-Benzodiazepines
(Mechanism of action)

Back 30

Same as Benzodiazepines:
Binds to the GABA-A receptor, which is composed of 5 protein subunits (that includes two alpha and two beta subunits, and a gamma protein that together form a chloride channel). As a GABA receptor agonist, it hyperpolarizes neuron membranes (via chloride influx) and supresses their activity.

Front 31

Barbituates
(Mechanism of action)

Back 31

Same as Benzodiazepines
Binds to the GABA-A receptor, which is composed of 5 protein subunits (that includes two alpha and two beta subunits, and a gamma protein that together form a chloride channel). As a GABA receptor agonist, it hyperpolarizes neuron membranes (via chloride influx) and supresses their activity.

Front 32

Benzodiazepines
(Therapeutic Effects)

Back 32

Used to treat anxiety disorders (including ETOH withdrawal symptoms), induce sedation and skeletal muscle relaxation (motor control centors in CNS), and treat some seizures

Front 33

Benzodiazepines
(Pharmacotoxicology)

Back 33

Can cause withdrawal symptoms induced by abrupt discontinuation of short actin benzodiazepines. When combined with other depressants (ETOH, antihistamines, narcotics, etc.) it can lead to respiratory depression/coma. CNS effects can be extended by CYP enzyme inhibitors that include cimetidine and oral contaceptives. They can cause prolonged sedation ("hang-over"), anterograde memory disturbances, and sleep disorders (alterations in REM sleep)

Front 34

What is the ending for Benzodiazepines?

Back 34

-am

Front 35

What is the ending for non-benzodiazepines?

Back 35

-em

Front 36

Non-benzodiazepines
(Therapeutic effects)

Back 36

Induces sedation and hypnosis. Non-Benzodiazepines have a rapid onset of action and have fewer prolonged psychomotor depressant effects as seen with BDZs and Barbituates.

Front 37

Barbituates
(Therapeutic effects)

Back 37

Sedation, hypnosis, surgical anesthesia (thiopental), anticonvulsant medication (Phenobarbital)

Front 38

What is the ending for Barbituates?

Back 38

-tal

Front 39

Barbituates
(Pharmicotoxicology)

Back 39

Can cause prolonged sedation, anterograde memory disturbances, sleep disorders (alterations in REM sleep), Euphoria, and addiction.
Barbituates are Microsomal enzyme CYP inducer, which alters the metabolism of other drugs.

Front 40

Selective Serotonin Reuptake Inhibitors (SSRIs)
(Mechanism of action)

Back 40

Inhibits the reuptake of serotonin into the presynaptic cell. This increases serotonin levels in the synapse.

Front 41

Selective Serotonin Reuptake Inhibitors (SSRIs)
(Therapeutic Effects)

Back 41

Anoxiolytic effect
SSRIs have little effect on memory and motor activity. They have a low potential for abuse and dependence when compared to benzodiazepines.

Front 42

Selective Serotonin Reuptake Inhibitors (SSRIs)
(Pharmacotoxicology)

Back 42

They can provide mild CNS stimulation and anticholinergic effect.

Front 43

What ending do SSRIs have?

Back 43

-tine

Front 44

Buspirone
(Mechanism of Action)

Back 44

Partial agonist for serotonin 5-HT 1A receptors in the CNS

Front 45

Buspirone
(Therapeutic effects)

Back 45

Reduces anxiety states without sedation (asseen with benzodiazepines)

Front 46

Which medications fit into the "First Generation Antipsychotics" category?

Back 46

Phenothiazides and haloperidol

Front 47

First generation antipsychotics
(Mechanism of Action)

Back 47

D2 dopamine receptor antagonists in many areas of the CNS that possess dopamine (DA) pathways.
They act as antihistamine, antimuscarinic, and alpha1 adrenergic receptor antagonists that mediate many of the side effects.

Front 48

What is the ending for first generation antipsychotics (except Haloperidol)?

Back 48

-azine

Front 49

Second Generation Antipsychotics
(Mechanism of Action)

Back 49

Act as low affinity D2 dopamine receptor antagonists in the mesolimbic (behavioral) pathways while at the same time not significantly suppressing dopamine actions in the nigrostraital (motor system) and hypothalamo-hypophyseal (endocrine) dopamine pathways.

Front 50

Second Generation Antipsychotics
(Therapeutic Effects)

Back 50

Effective in treating both positive and negative symptoms. They act as mood stabilizers, and can treat the manic phase of bipolar disorders.

Front 51

First and Second Generation Antipsychotics
(Therapeutic Effects)

Back 51

Treatment of tourette's syndrome, severe behavioral problems in children with attention deficit disorders, intractable hiccups, and can be used as antiemetics.

Front 52

First and Second generation antipsychotics
(Pharmacotoxicology)

Back 52

Can cause sever sedation, mediated at least in part by antihistamin effects. They can also cause anticholinergic effects (Can't see, can't pee, can't spit, can't shit). They can cause hypotension because they block alpha1 adrenergic receptors. They can also cause movement disorders with Parkinsonism-like tremors, Tardive dyskinesis, and suppression of the motor control systems in the CNS.

Front 53

Monoamine Oxidase Inhiitors (MAIOs)
(Mechanism of Action)

Back 53

Inhibit the activity of monoamine oxidase, which prevents the breakdown of monoamine neurotransmitters and therby increases their availability.

Front 54

Monoamine Oxidase Inhiitors (MAIOs)
(Pharmacotoxicology)

Back 54

MAIOs can induce CNS stimulation. They can effect blood pressure if person has a diet high in tyramine (found in aged cheeses, beer, and red wine). MAIOs can have some anticholinergic and antihistamine effects.

Front 55

Tricyclics
(Pharmacotoxicology)

Back 55

Tricyclics can induce CNS sedation, hypotension, and strong anticholinergic effects.

Front 56

NSAIDS
(Mechanism of Action)

Back 56

NSAIDS are Cyclooxygenase (COX) inhibitors. When the COX isoenzyme is blocked, prostaglandins can not be formed. When the COX-I enzyme is blocked, it effects a broad number of tissues. When the COX-II enzyme is blocked, it targets inflammatory responses, while avoiding or reducing GI/GU side-effects

Front 57

NSAIDs
(Therapeutic effects)

Back 57

Treatment of inflammatory diseases, antipyretics, mild analgesics, antithrombics, and treatment of menstrual cramping.

Front 58

NSAIDs
(Pharmacotoxicology)

Back 58

NSAIDs can cause gastric distress by increasing HCl secretion in parietal cells. They can also cause spontaneous hemorrhage due to their antithrombic properties. NSAIDs are ototoxic and are in pregnancy categories C and D.

Front 59

Glucocorticoids
(Mechanism of Action)

Back 59

Cortisol receptor agonists. Glucocorticoids mimic the natural hormone cortisol, produced in the adrenal cortex. They suppress genes that regulate inflammatory responses and decrease cell-mediated and humoral immunity. Glucocorticoids can induce leukocyte apoptosis.

Front 60

Glucocorticoids
(Therapeutic Effects)

Back 60

Can treat chronic asthma, rheumatoid arthritis, inflmatory bowel disease, adrenal insufficiency (Addison's disease), Leukemia (provide apoptosis), and can prevent organ and tissue transplant rejection.

Front 61

Glucocorticoids
(Pharmacotoxicology)

Back 61

Can cause gastric and intestinal irritation, clotting disorders, induction of hyperglycemia, induce redistribution of body fat, mimic the effects of aldosterone in the kidneys (induction of hypernatremia and hypokalcemia, electorlyte disorders)

Front 62

Expectorants
(Mechanism of action)

Back 62

Stimulate secretion of water that dilutes mucus and makes it easier to dislodge form the airways.

Front 63

Expectorants
(Therapeutic Uses)

Back 63

Treatment of airway congestion associated with respiratory infections and allergies

Front 64

Mucolytics
(Mechanism of Action)

Back 64

Breaks disulfide bondes within mucoproteins that are secreted by mucous cells that line the respiratory tract. Mucolytics reduce viscosity of mucus, making it easier to dislodge from the airways.

Front 65

Mucolytics
(Therapeutic uses)

Back 65

Treatment of cystic fibrosis by reducing mucus accumulation.

Front 66

Cromolyn Preparations
(Mechanism of Action)

Back 66

Cromolyn is a mast cell "stabilizer", which reduces mast cell release of histamine in response to an allergen. This reduces mucus secretion and congestion.

Front 67

Cromlyn Preparations
(Therapeutic Uses)

Back 67

Used for the prophylactic treatment of asthmatic attacks and allergies.

Front 68

Antihistamines
(Mechanism of Action )

Back 68

H1 histamine receptor agonist that reduces histamine-induced mucous secretion and congestion.

Front 69

Antihistamines
(Therapeutic effects)

Back 69

Used to treat acute allergic reactions, rhinitis, urticaria (hives), conjunctivits, and motion sickness.

Front 70

Anticholinergics
(Mechanism of action )

Back 70

Muscarinic Cholinergic Receptor Antagonist located on the target tissue. Produces a PNS response.

Front 71

Anticholinergics
(Therapeutic effects)

Back 71

Reduces cholinergic receptor mediated bronchioconstriction asssociated with repiratory disorders.

Front 72

Leukotriene "system" Inhibitors
(Therapeutic uses)

Back 72

Treatment of leukotriene mediated bronchioconstriction associated with asthma and allergic responses.

Front 73

Leukotriene "system" Inhibitors
(Mechanism of Action)

Back 73

Can either be a lipooxxygenase inhibitor or a leukotriene receptor antagonist.

Front 74

Antiussives
(Therapeutic Uses)

Back 74

Supress cough reflexes assciated with mucus accumulation along respiratory airways.

Front 75

Fibrolytic Drugs
(Mechanism of Action )

Back 75

Enzymes catalyze plasmin formation within a clot that leads to fibrolysis (depolymerization of the fibrin network)

Front 76

Cardiac Glycosides
(Therapeutic effects)

Back 76

Increases PNS activity by inducing positve inotropic effects on the myocardium: Increased cardiac output that helps to maintain tissue perfusion

Front 77

Thrombolytic Drugs
(Therapeutic Effects)

Back 77

Prevent platelet plug formation and prevent reoccurrence of blood clot formation

Front 78

Antacids
(Mechanism of Action)

Back 78

Bufferes neutralize gastric acids and decrease pH dependent conversion of pepsinogen to pepsin (Needs HCl)

Front 79

Antacids
(Therapeutic Effects)

Back 79

Reduces gastritis and peptic ulcer disease

Front 80

Antimicroials/Antibiotics
(Mechanism of Action)

Back 80

Bismuth increases mucus secretion and disrupts bacterial cell wasll adhesion to gastric mucosa and reduces bacterial damage. Antibiotics inhibit bacterial cell growth and eliminate infection by Heliobacter pylori.

Front 81

Histamine Receptor Antagonists
(Mechanism of Action)

Back 81

They block parietal cell H2 receptors, which are responsible for activating the proton pump for gastric secetions.

Front 82

Histamine Receptor Antagonists
(Therapeutic Effects)

Back 82

Used to treat peptic ulcer disease, gastritis, and GERD

Front 83

What is the ending for Histamine Receptor Antagonists?

Back 83

-tidine

Front 84

Proton Pump Inhibitors
(Mechanism of Action)

Back 84

PPIs directly inhibit proton pumps on parietal cells. They have a generally slow onset of action.

Front 85

Synthetic Prostagandins
(Mechanism of Action )

Back 85

Prostaglandin receptor agonists that mimic the inhibitory effects of prostaglandins on parietal cells.

Front 86

Synthetic Prostaglandins
(Therapeutic Effects)

Back 86

Used to treat gastritis and peptic ulcer disease caused by NSAIDs.