Iowa Med Pharm2

Front 1

naloxone

Back 1

opioid antagonist (Narcan)
- used to reverse acute opioid overdose
- parenteral
- respiratory and cardiovascular support may also be required

Front 2

morphine

Back 2

opioid agonist, at mu receptor
- 3:1, charged:uncharged
- slow onset, 4hr duration (t1/2=2)
- glucuronidation in liver
- excretion of glucuronides by kidneys
- x3-5 IV to PO conversion

Front 3

hydromorphone

Back 3

opioid agonist, at mu receptor (Dilaudid)
- more lipid soluble than morphine, therefore faster onset.
- 5x more potent than morphine
- hydromorphone-6-glucuronide is less agonist activity than morphine-6-glucuronide

Front 4

hydrocodone

Back 4

opioid agonist, at mu receptor (Vicodin)
- metabolized to hydromorphone by CYP2D6, causing patient variability in effectiveness.
- can be combined with acetaminophen (Lortab)

Front 5

oxycodone

Back 5

opioid agonist, at mu receptor (Oxycodone, Oxycontin)
- metabolized to oxymorphone by CYP2D6
- can be combined w/acetaminophen (Percocet)

Front 6

oxymorphone

Back 6

opioid agonist, at mu receptor (Opana)
- available in extended release PO

Front 7

codeine

Back 7

opioid agonist, at mu receptor
- metabolized to morphine by CYP2D6
- combined w/acetaminophen (Tylenol 3)

Front 8

propoxyphene

Back 8

opioid agonist, at mu receptor (Darvon)
- metabolized to morphine
- weak analgesic efficacy
- combined w/acetaminophen (Darvocet)
- can be toxic, causing organ failure
- Do Not Use.

Front 9

heroin

Back 9

opioid agonist, at mu receptor (diacetyl morphine)
- converted to monoacetyl morphine and morphine in brain
- rapid onset, highly addictive
-

Front 10

methadone

Back 10

opioid agonist, at mu receptor
- long duration, t1/2 = 15-60hrs PO
- not a morphine analog
- maintenance for opioid addiction and pain management

Front 11

meperidine

Back 11

opioid agonist, at mu receptor (Demerol)
- not a morphine analog
- more lipid soluble, faster onset
- IV, PO
- 1/10th potency of morphine
- metabolized to nor-meperidine in liver, excreted by kidney
- nor-meperidine causes CNS stimulation, convulsions.
- can cause serotonin syndrome when combined w/MAOI

Front 12

fentanyl

Back 12

opioid agonist, at mu receptor
- not a morphine analog
- more lipid soluble, faster onset
- patch, oral, epidural, intrathecal
- patch for severe chronic pain
- epidural/intrathecal for labor
- also sufentanil, alfentanil, remifentanil

Front 13

tramadol

Back 13

partial mu opioid agonist and MAOI (Ultram)
- used for mild to moderate acute and chronic pain
- combined w/acetaminophen (Ultracet)

Front 14

pentazocine

Back 14

opioid, mixed agonist/antagonist
- kappa receptor agonist
- mu receptor partial agonist/antagonist
- Used for management of acute pain.
- Not for management of chronic pain.
- Used to manage side effects

Front 15

nalbuphine

Back 15

opioid, mixed agonist/antagonist
- kappa receptor agonist
- mu receptor partial agonist/antagonist
- Used for management of acute pain.
- Not for management of chronic pain.
- Used to manage side effects

Front 16

buprenorphine

Back 16

opioid, mixed agonist/antagonist
- kappa receptor agonist
- mu receptor partial agonist/antagonist
- high mu affinity, therefore difficult to reverse
- complicates anesthesia use for surgery
- used for drug abuse/addiction therapy

Front 17

diphenoxylate

Back 17

opioid agonist, antidiarrheal (Lomotil)
- poorly absorbed PO
- reduces GI motility

Front 18

loperamide

Back 18

opioid agonist, antidiarrheal (Imodium)
- poorly absorbed PO
- reduces GI motility

Front 19

naltrexone

Back 19

opioid antagonist
- used to reverse side effects of opioids and manage opioid/alcohol addiction
- PO

Front 20

nalmefene

Back 20

opioid antagonist
- used to reverse side effects of opioids and manage opioid dependence
- parenteral

Front 21

alvimopan

Back 21

opioid antagonist
- poorly absorbed orally
- active opioid antagonist that antagonizes the GI side effects of opioids.

Front 22

BCG

Back 22

Adjuvant immunomodulator
– Live attenuated bacillus calmette‐guerin.
– Surface antigens interact directly with pattern recognition receptors on antigen presenting cells and increase their APC activity.
– Useful in some cancer therapies (bladder cancer).
– Direct activation of leukocytes (principally macrophages) can produce a systemic inflammatory response and septic shock.

Front 23

azathioprine

Back 23

general growth inhibitor
- metabolized to a mercaptopurine (6‐thioguanine) which inhibits purine synthesis and becomes incorporated into DNA as a thioguanine nucleotide. Inactivated by xanthine oxidase (decreased when combined with allopuranol).
- uses: renal and other tissue transplantation, some autoimmune diseases (e.g., lupus, rheumatoid arthritis)
- toxicity: myelosuppression, nausea, vomiting

Front 24

cyclophosphamide

Back 24

general growth inhibitor
- very effective immunosuppression by crosslinking DNA and killing proliferating cells, thus preventing expansion of antigenspecific lymphocytes.
- uses: many auto‐immune diseases, bone marrow transplant.
- toxicity: myelosuppression, nausea, vomiting, infertility

Front 25

leflunomide

Back 25

general growth inhibitor
- metabolized to A77‐1726 (its active form). Inhibits dihydroorotate dehydrogenase, leading to decreased pyrimidine synthesis. A77-1726 is subject to enterohepatic recirculation and has a half‐life of 19 days
- uses: similar to methotrexate.
- toxicity: diarrhea, modest hepatotoxicity, myelosuppression less pronounced than other anti‐metabolites.

Front 26

methotrexate

Back 26

general growth inhibitor
- inhibits aminoimidazolecarboxamide (AICAR) tranformylase and thymidylate synthetase; inhibiting inosine and thymidine synthesis.
- uses: drug of choice in rheumatoid arthritis, some autoimmune diseases.
- toxicity: nausea, mucosal ulcers, modest hepatotoxicity, myelosuppression less pronounced than other anti‐metabolites.

Front 27

mycophenolate mofetil

Back 27

general growth inhibitor
- hydrolyzed to mycophenolic acid (its active form). Inhibits inosine monophosphate dehydrogenase.
- uses: solid organ transplant as an alternative to cyclosporine,
some auto‐immune diseases.
- toxicity: similar to azathioprine.

Front 28

prednisone

Back 28

glucocorticoid
- First-line immunosuppressant for solid organ and hematopoietic stem cell transplantation.
- Combined anti-inflammatory/ immunosuppressant activity is useful in management of various immune-based disorders (e.g., certain autoimmune diseases, asthma, allergic reactions, systemic inflammation, etc.).
- Toxicity: (generally only with greater than 2 weeks daily systemic administration): Cushing’s Syndrome, Osteoporosis, Glucose intolerance, Hypertension, Susceptibility to infection
– NO serious marrow toxicity

Front 29

sirolimus

Back 29

mTOR inhibitor
- prevents cytokine-induced growth by inhibiting mTOR
- Can be used alone or in combination therapies to preserve solid organ transplants.
- May be useful in steroid-resistant graft v. host disease in hematopoietic stem cell transplants.
- Antagonizes tacrolimus effects, but synergizes with cyclosporine (consistent with selective dependence on immunophilins)
- Toxicity: profound myelosuppression, hepatotoxicity

Front 30

cyclosporine

Back 30

calcineurin inhibitor
- prevent TCR-induced cytokine expression by inhibiting calcineurin activity.
- Can be effective without use of other immuno‐suppressants in some patients, though it is often combined with other agents.
- Commonly useful in kidney, liver, and cardiac transplants.
- Can by useful in a variety of autoimmune disorders, and may have applications in some inflammatory diseases (e.g., asthma).
- Toxicity: nephrotoxicity, hypertension, hyperglycemia, liver dysfunction.
- Increased cancer incidence documented, although perhaps no greater than other immunosuppressants.

Front 31

tacrolimus

Back 31

calcineurin inhibitor
- prevent TCR-induced cytokine expression by inhibiting calcineurin activity.
- 10-100x more potent than cyclosporine
- Can be effective without use of other immuno‐suppressants in some patients, though it is often combined with other agents.
- Commonly useful in kidney, liver, and cardiac transplants.
- Can by useful in a variety of autoimmune disorders, and may have applications in some inflammatory diseases (e.g., asthma).
- Toxicity: nephrotoxicity, hypertension, hyperglycemia, liver dysfunction.
- Increased cancer incidence documented, although perhaps no greater than other immunosuppressants.

Front 32

Anti-lymphocyte globulin (ALG)

Back 32

antibody immunomodulator
- product of repeated injection of human cells into horse, rabbit, sheep, or goats. Purified serum IgG.
• Mechanism: blocks T cell surface receptors and opsonizes T cells.
• Toxicity: cytokine release syndrome, serum sickness on repeat usage.
• Effect: Produces prolonged T cell depletion (more than one year). Potential for late rejection as lymphoid system recovers.

Front 33

muromonab-CD3 (OKT3)

Back 33

antibody immunomodulator
- mouse monoclonal antibody
• Mechanism: blocks and opsonizes T cell receptor (TCR).
• Toxicity: Massive cytokine release syndrome resulting from
transient activation of T cells before they become inactive and are depleted (more severe than with ATG).
• Effect: Produces prolonged T cell depletion.
• Reuse is limited by the production of neutralizing antibodies against the mouse antibody.

Front 34

basiliximab

Back 34

antibody immunomodulator
- anti-IL2 receptor (anti-CD25) humanized antibodies
• Mechanism: Blocks and opsonizes the alpha‐chain of IL‐2 receptor (CD25) that is present on ACTIVATED T cells.
• Toxicity: Well tolerated.
• Effect: Depletes only antigen‐activated T cells. Moderate effect compared to ATG. Appropriate for patients with low‐to‐moderate risk of rejection.

Front 35

daclizumab

Back 35

antibody immunomodulator
- anti-IL2 receptor (anti-CD25) humanized antibodies
• Mechanism: Blocks and opsonizes the alpha‐chain of IL‐2 receptor (CD25) that is present on ACTIVATED T cells.
• Toxicity: Well tolerated.
• Effect: Depletes only antigen‐activated T cells. Moderate effect compared to ATG. Appropriate for patients with low‐to‐moderate risk of rejection.

Front 36

Rh(D) immune globulin

Back 36

antibody immunomodulator
• Rh-negative mothers can be sensitized to the “foreign” D antigen of an Rh‐positive fetus. In subsequent pregnancies, maternal antibodies against Rh-positive cells can transfer to the fetus leading to hemolytic disease.
• Rh(D) immune globulin is a concentrated solution of human IgG with a high titer of Rh(D)antibodies. Maternal administration of Rh(D) immune globulin prevents initiation of a maternal immune response to the fetal Rh(D) antigen.
• The mechanism of immune suppression by Rh(D) antibodies is mediated through inhibition of naïve Rh(D) reactive B cells. T
cell responses are not effected, but are not harmful to the fetus.

Front 37

interleukin-2

Back 37

cytokine
– Increased proliferation of activated T cells, production of IFN-gamma, and cytotoxic killer cell activity.
– Applications in treatment of metastatic melanoma and renal cell carcinoma.
– Associated with serious capillary leak syndrome, hypotension, and reduced organ perfusion. Can be fatal.

Front 38

interferons

Back 38

cytokines
– IFN-gamma (Actimmune®) stimulate cell mediated cytotoxic immune response. Applications in treating severe recurrent infections.
– IFN-alpha (Intron A®), IFN-beta (Avonex®, Rebif®): produced by most cells in response to a variety of stimuli including viral infection.
• Useful in treating chronic viral infection (e.g., hepatitis).
• Anti-proliferative activities are useful in treating several cancers. (e.g., hairy cell leukemia, melanoma, some lymphomas)
• Reduces frequency of exacerbating episodes in multiple sclerosis patients (probable immunomodulatory activity).

Front 39

cetirizine

Back 39

2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects.

Front 40

dimenhydrinate

Back 40

1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types.
- marked sedation
- used for motion sickness
- salt of diphenhydramine

Front 41

diphenhydramine

Back 41

1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types.
- marked sedation
- used for motion sickness

Front 42

fexofenadine

Back 42

2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects.

Front 43

loratadine

Back 43

2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects.

Front 44

meclizine

Back 44

1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types.
- slight sedation
- used for motion sickness

Front 45

promethazine

Back 45

1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types.
- marked sedation
- used for motion sickness
- used as antiemetic

Front 46

terfenadine

Back 46

2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects.
- converted to fexofenadine by CYP3A4.
- blocks potassium channels in heart causing lethal ventricular arrhythmias in unconverted form
- Antifungal imidazoles & erythromycin antibiotics inhibit CYP3A4

Front 47

adalimimab

Back 47

Anti TNF-alpha agent
- human antibody
– Binds to TNFalpha
• Prevents interaction with its receptor.
• Reduces circulating and localized levels of TNFalpha
– Applications: inflammatory disease involving TNFalpha.
• Rheumatoid arthritis (usually in combination with methotrexate).
– Elevated TNFalpha in joints.
• Crohn’s disease
– Elevated TNFalpha in stool
– Complications: increased frequency of infections (upper respiratory, urinary).

Front 48

infliximab

Back 48

Anti TNF-alpha agent
- humanized antibody
– Binds to TNFalpha
• Prevents interaction with its receptor.
• Reduces circulating and localized levels of TNFalpha
– Applications: inflammatory disease involving TNFalpha.
• Rheumatoid arthritis (usually in combination with methotrexate).
– Elevated TNFalpha in joints.
• Crohn’s disease
– Elevated TNFalpha in stool
– Complications: increased frequency of infections (upper respiratory, urinary).

Front 49

etanercept

Back 49

Anti TNF-alpha agent
– Fusion protein containing the ligand binding domain of the TNFalpha receptor and the Fc domain of human IgG.
– Binds to TNFalpha
• Prevents interaction with its receptor.
• Reduces circulating and localized levels of TNFalpha
– Applications: inflammatory disease involving TNFalpha.
• Rheumatoid arthritis (usually in combination with methotrexate).
– Elevated TNFalpha in joints.
• Crohn’s disease
– Elevated TNFalpha in stool
– Complications: increased frequency of infections (upper respiratory, urinary).

Front 50

aspirin (acetylsalicylic acid, ASA)

Back 50

Nonselective COX inhibitor
- OTC analgesic, antipyretic
- irreversibly inhibits COX1 on platelets

Front 51

diclofenac

Back 51

Nonselective COX inhibitor
- Rx arthritis, anti-inflammatory
- 0.3 COX1/COX2
- combined w/ misoprostol to prevent COX1 inhibition

Front 52

ibuprofen

Back 52

Nonselective COX inhibitor
- OTC analgesic, antipyretic
- 2.6 COX1/COX2

Front 53

indomethacin

Back 53

Nonselective COX inhibitor
- Rx arthritis, anti-inflammatory
- 10 COX1/COX2
- high frequency of intolerance

Front 54

ketorolac

Back 54

Nonselective COX inhibitor
- Post-surgical analgesic
- 395 COX1/COX2

Front 55

naproxen

Back 55

Nonselective COX inhibitor
- Rx, OTC anti-inflammatory
- 3.8 COX1/COX2

Front 56

acetaminophen

Back 56

Nonselective COX inhibitor
- activity is substantially reduced in the presence of peroxides (often elevated at sites of inflammation).
- lacks significant effects on platelets, cardiovascular, and gastrointestinal systems.
- analgesic and antipyretic effects equivalent to aspirin.
- Usage: analgesic and antipyretic only; negligible anti-inflammatory activity.
- Generally well tolerated.
- Hepatotoxicity with overdose.

Front 57

celecoxib

Back 57

COX-2 selective inhibitor
- 10-20 times more selective for Cox-2 than for Cox-1
- evidence of increased cardiovascular risk

Front 58

rofecoxib

Back 58

COX-2 selective inhibitor
- 200 times more selective for Cox-2 than for Cox-1
- evidence of increased cardiovascular risk
- removed from market

Front 59

albuterol

Back 59

B2 adrenergic agonist
• Stimulate adenyl cyclase and cAMP induced relaxation of bronchial smooth muscle.
• Used for short term relief during acute asthmatic episodes.
 Inhaled forms preferred over systemic administrations for faster onset (30 min., lasting 3 – 4 hours) and fewer side effects (tachycardia, muscle tremors, headache).
• Increased usage may indicate lack of effective control by maintenance therapy.

Front 60

salmeterol

Back 60

B2 adrenergic agonist
• Long-acting (12 hrs. or more) beta2 agonists must be combined with corticosteroids when used as part of maintenance therapy.
 NOT for use as a short term reliever during acute attacks.
- combined with fluticasone (Advair®)

Front 61

beclomethasone

Back 61

corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma.

Front 62

budesonide

Back 62

corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma.

Front 63

fluticasone

Back 63

corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma.

Front 64

prednisone

Back 64

corticosteroid
- Oral or intravenous administration useful where symptoms are not adequately controlled by maintenance therapy and treatment with bronchodilators.
• Provide a “burst” of anti inflammatory and immunosuppressive activity, giving intermediate term relief.
• Reduction in airway inflammation can perpetuate a reduction in airway hyper‐responsiveness sufficient to gain control of the disease.

Front 65

triamcinolone

Back 65

corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma.

Front 66

montelukast

Back 66

Leukotriene receptor antagonist
▬ Generally well tolerated as part of a long-term maintenance therapy for asthma (PO).
▬ Can allow reduction in corticosteroid dosage.
▬ LTD4 receptor antagonists reduced bronchoconstriction and edema associated with inflammatory responses.

Front 67

zafirlukast

Back 67

Leukotriene receptor antagonist
▬ Generally well tolerated as part of a long-term maintenance therapy for asthma (PO).
▬ Can allow reduction in corticosteroid dosage.
▬ LTD4 receptor antagonists reduced bronchoconstriction and edema associated with inflammatory responses.

Front 68

zileuton

Back 68

Leukotriene synthesis inhibitor
- asthma therapy
▬ Inhibition of 5‐lipoxygenase inhibits synthesis of LTB4, and LTD4 in mast cells and eosinophils.
▬ Effectiveness varies among individuals, but can be an effective component of long-term maintenance therapy (Oral administration).
▬ Can be associated with liver toxicity, and inhibited activity of cytochrome P450 1A2, 2C9, and 3A4 can decrease metabolism of other drugs.

Front 69

cromolyn

Back 69

degranulation inhibitor
- asthma therapy
- Inhibits degranulation of Mast cells, possibly associated with the inhibition of Ca+2 channels.
- Inhibition of Cl- channels may also contribute to reduced nerve
activity and inhibition of cough.
- Poorly soluble salts: must be topically absorbed (e.g., inhaled powder aerosol)
- Only effective prophylactically as part of a long-term maintenance therapy.
-Generally well tolerated.

Front 70

nedocromil

Back 70

degranulation inhibitor
- asthma therapy
- Inhibits degranulation of Mast cells, possibly associated with the inhibition of Ca+2 channels.
- Inhibition of Cl- channels may also contribute to reduced nerve
activity and inhibition of cough.
- Poorly soluble salts: must be topically absorbed (e.g., inhaled powder aerosol)
- Only effective prophylactically as part of a long-term maintenance therapy.
-Generally well tolerated.

Front 71

ipratropium

Back 71

muscarinic antagonist
- asthma therapy
• quaternary ammonium derivative of atropine - does not readily enter CNS.
• Administer by inhalation.
• Slower acting and less effective as compared to B2-agonists.
• only inhibit responses associated with parasympathetic
responses, which vary among individuals.
• May be most useful with patients intolerant of B2‐agonists.

Front 72

omalizumab

Back 72

Anti-IgE monoclonal antibody
- asthma therapy
- Humanized mouse antibody to the Fc domain of human IgE. This antibody blockades interaction between IgE and FcR, and also reduces circulating levels of IgE.

Front 73

theophylline

Back 73

bronchodilator (methylxanthine)
- asthma therapy
– Inhibit phosphodiesterase degradation of cAMP, thereby increasing cAMP levels and relaxation of bronchial smooth muscle. Also may block adenosine receptors.
– Can be used as part of long term maintenance therapy (oral administration).
– Significant variability in individual metabolic clearance rates.

Front 74

desflurane

Back 74

volatile general anesthetic
- MAC 7.25%
- blood-gas partition 0.42
- Is metabolized at only 0.02%
- Irritating to the airways
- Myocardial depression is minimal
- Desflurane produces prompt recovery

Front 75

isoflurane

Back 75

volatile general anesthetic
- MAC 1.15%
- blood-gas partition 1.4
- Is metabolized at only 0.2%
- Irritating to the airways
- Myocardial depression is minimal

Front 76

enflurane

Back 76

volatile general anesthetic
- MAC 1.68%
- blood-gas partition 1.9
- Is metabolized at only 2.0%

Front 77

sevoflurane

Back 77

volatile general anesthetic
- MAC 2.05%
- blood-gas partition 0.68
- Is metabolized at 2-5%
- Non-irritating to the airways
- Myocardial depression is minimal
- prompt recovery

Front 78

nitrous oxide

Back 78

general anesthetic gas
- MAC 105-110% (round to 100%)
- blood-gas partition 0.46
- adjunct to the potent volatile anesthetic agents
- reduces MAC requirements
- very insoluble
- has little side effects

Front 79

dantrolene

Back 79

treats malignant hyperthermia

Front 80

succinylcholine

Back 80

can trigger malignant hyperthermia

Front 81

thiopental

Back 81

anesthesia induction agent
- Thiobarbiturate
• Used for intravenous induction of general anesthesia
• Highly lipid soluble
• Produce rapid, profound unconsciousness due to rapid uptake into the brain
• Produce marked respiratory depression
• Recovery occurs in 5-8 min
• Prompt recovery is due to redistribution from the brain to other tissues
• No drugs are available to reverse barbiturates
• Decrease sympathetic outflow from the brain

Front 82

methohexital

Back 82

anesthesia induction agent
- Oxybarbiturate
• Used for intravenous induction of gneral anesthesia
• Highly lipid soluble
• Produce rapid, profound unconsciousness due to rapid uptake into the brain
• Produce marked respiratory depression
• Recovery occurs in 5-8 min
• Prompt recovery is due to redistribution from the brain to other tissues
• No drugs are available to reverse barbiturates
• Decrease sympathetic outflow from the brain

Front 83

ketamine

Back 83

anesthesia induction agent
- A phencyclidine derivative
- NMDA receptor antagonist
- “Dissociative” anesthetic
• Used in induction for general anesthesia
• Produces sedation, amnesia and analgesia
• Does not produce respiratory depression or cardiovascular depression
• Can not be antagonized
• Emergence delirium

Front 84

etomidate

Back 84

• Used in induction for general
anesthesia (IV)
• Produces respiratory depression
• Does not produce cardiovascular depression
• Can not be antagonized

Front 85

propofol

Back 85

newest anesthesia induction agent
• Can also be used for maintenance
• Produces cardiovascular and
respiratory depression
• Can not be antagonized
• Least ‘hangover effect’

Front 86

alfentanil

Back 86

- Like fentanyl, a potent, fast onset, short acting opioid

Front 87

sufentanil

Back 87

- Like fentanyl, a potent, fast onset, short acting opioid

Front 88

fentanyl

Back 88

opioid agonist
• Useful for premedication for general anesthesia
• Reduce the MAC of volatile
anesthetics
• Produces marked respiratory
depression
• Usually not much effects on
blood pressure
• Fast onset
• Highly lipid soluble
• Like induction agents, fentanyl’s effects are terminated by redistribution
• Can be antagonized by naloxone

Front 89

remifentanil

Back 89

- Like fentanyl, a potent, fast onset, short acting opioid
- metabolized by plasma esterase; it can be used as an infusion.

Front 90

flumazenil

Back 90

used to antagonize midazolam and other benzodiazepines

Front 91

midazolam

Back 91

anxiolytic agent
- may be used w/opioids as premedication prior to induction of general anesthesia.
• Highly lipid soluble
• Produce sedation and amnesia
• Intravenous benzodiazepines can produce respiratory depression
• Can be antagonized by flumazenil

Front 92

cocaine

Back 92

topical local anesthetic
- ester
– also a vasoconstrictor
• Toxicity - Myocardial ischemia, Myocardial infarction, Arrhythmias, Seizures, Hypertension
- degraded by plasma esterase

Front 93

procaine

Back 93

local anesthetic (Novocaine)
- ester
- low potency, low hydrophobicity
- degraded by plasma esterase

Front 94

tetracaine

Back 94

local anesthetic
- ester
- high potency, high hydrophobicity
- degraded by plasma esterase

Front 95

lidocaine

Back 95

local anesthetic
- amide
- intermediate potency, hydrophobicity
- shorter duration of action
- 1% lidocaine used for infiltration
- metabolized in liver

Front 96

mepivacaine

Back 96

local anesthetic
- amide
- intermediate potency, hydrophobicity
- metabolized in liver

Front 97

bupivacaine

Back 97

local anesthetic
- amide
- hight potency, hydrophobicity
- longer duration of action
- metabolized in liver

Front 98

prilocaine

Back 98

local anesthetic
- amide
- shorter duration of action
- metabolized in liver

Front 99

ropivacaine

Back 99

local anesthetic
- amide
- newer, s-entantiomer only
- metabolized in liver

Front 100

amitriptyline

Back 100

tricyclic antidepressant
- nonspecific blocker of monoamine reuptake
- used to treat severe major depression
- also blocks muscarinic, adrenergic and histamine receptors
- Numerous side effects: cardiovascular (tachycardia, blockade of the A-V conductance), antimuscarinic effects, orthostatic hypotension, sedation, weight gain, sexual dysfunction, seizures, psychosis, mania
- metabolized by liver, eliminated via kidneys

Front 101

amoxapine

Back 101

tricyclic antidepressant
- nonspecific blocker of monoamine reuptake
- used to treat severe major depression
- also blocks muscarinic, adrenergic and histamine receptors
- Numerous side effects: cardiovascular (tachycardia, blockade of the A-V conductance), antimuscarinic effects, orthostatic hypotension, sedation, weight gain, sexual dysfunction, seizures, psychosis, mania
- metabolized by liver, eliminated via kidneys

Front 102

imipramine

Back 102

tricyclic antidepressant
- nonspecific blocker of monoamine reuptake
- used to treat severe major depression
- also blocks muscarinic, adrenergic and histamine receptors
- Numerous side effects: cardiovascular (tachycardia, blockade of the A-V conductance), antimuscarinic effects, orthostatic hypotension, sedation, weight gain, sexual dysfunction, seizures, psychosis, mania
- metabolized by liver, eliminated via kidneys

Front 103

nortriptyline

Back 103

tricyclic antidepressant
- nonspecific blocker of monoamine reuptake
- used to treat severe major depression
- also blocks muscarinic, adrenergic and histamine receptors
- Numerous side effects: cardiovascular (tachycardia, blockade of the A-V conductance), antimuscarinic effects, orthostatic hypotension, sedation, weight gain, sexual dysfunction, seizures, psychosis, mania
- metabolized by liver, eliminated via kidneys

Front 104

citalopram

Back 104

serotonin-specific reuptake inhibitor (Celexa)
- First-line drug to treat depression
- may promote neurogenesis via BDNF
- Fewer side-effects than TCAs
- Side effects: anorexia, sexual dysfunction, tremors, drug interactions
- block liver P450 enzymes (drug
interaction)
- eliminated via kidneys

Front 105

escitalopram

Back 105

serotonin-specific reuptake inhibitor (Lexapro)
- First-line drug to treat depression
- may promote neurogenesis via BDNF
- Fewer side-effects than TCAs
- Side effects: anorexia, sexual dysfunction, tremors, drug interactions
- block liver P450 enzymes (drug
interaction)
- eliminated via kidneys

Front 106

fluoxetine

Back 106

serotonin-specific reuptake inhibitor (Prozac)
- First-line drug to treat depression
- may promote neurogenesis via BDNF
- combined with olanzapine to treat bipolar disorder
- demethylated to the active
metabolite norfluoxetine (half-life time up to 30 days)
- Fewer side-effects than TCAs
- Side effects: anorexia, sexual dysfunction, tremors, drug interactions
- block liver P450 enzymes (drug
interaction)
- eliminated via kidneys

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sertraline

Back 107

serotonin-specific reuptake inhibitor (Zoloft)
- First-line drug to treat depression
- may promote neurogenesis via BDNF
- Fewer side-effects than TCAs
- Side effects: anorexia, sexual dysfunction, tremors, drug interactions
- block liver P450 enzymes (drug
interaction)
- eliminated via kidneys

Front 108

bupropion

Back 108

atypical antidepressant (Wellbutrin)
- inhibits dopamine reuptake
- also useful for treating rapid-cycling bipolar disorder
- has fewer side-effects than TCAs (fewer anticholinergic effects and no significant cardiotoxic effects)
- common side-effects: headache, nausea, tinnitus, insomnia and nervousness

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mirtazapine

Back 109

atypical antidepressant
- Increases NE (5-HT) release by blocking alpha2 receptors
- has fewer side-effects than TCAs (fewer anticholinergic effects and no significant cardiotoxic effects)
- common side-effects: headache, nausea, tinnitus, insomnia and nervousness

Front 110

nefazodone

Back 110

atypical antidepressant
- inhibits the reuptake of serotonin and blocks the 5-HT2 receptors
- has fewer side-effects than TCAs (fewer anticholinergic effects and no significant cardiotoxic effects)
- common side-effects: headache, nausea, tinnitus, insomnia and nervousness

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venlafaxine

Back 111

atypical antidepressant
- inhibits the reuptake of serotonin and norepinephrine
- has fewer side-effects than TCAs (fewer anticholinergic effects and no significant cardiotoxic effects)
- common side-effects: headache, nausea, tinnitus, insomnia and nervousness

Front 112

phenelzine

Back 112

monoamine oxidase inhibitor
- Third-line drugs (after SSRIs and TCAs) for depression in patients resistant to other antidepressants
- inhibits MAO type A and B
• Numerous severe side effects: CNS (hallucinations, agitation, convulsions), hypotension, weight gain
• When combined with SSRIs may lead to the serotonin syndrome
• Restrictions in diet: tyramine-free food (cheese effect)

Front 113

selegiline

Back 113

monoamine oxidase inhibitor
- transdermal
- Third-line drugs (after SSRIs and TCAs) for depression in patients resistant to other antidepressants
- inhibits MAO type B
- reversible
• Numerous severe side effects: CNS (hallucinations, agitation, convulsions), hypotension, weight gain
• When combined with SSRIs may lead to the serotonin syndrome
• Restrictions in diet: tyramine-free food (cheese effect)

Front 114

tranylcypromine

Back 114

monoamine oxidase inhibitor
- Third-line drugs (after SSRIs and TCAs) for depression in patients resistant to other antidepressants
- inhibits MAO type A and B
• Numerous severe side effects: CNS (hallucinations, agitation, convulsions), hypotension, weight gain
• When combined with SSRIs may lead to the serotonin syndrome
• Restrictions in diet: tyramine-free food (cheese effect)

Front 115

lithium

Back 115

• Drug of choice for maintenance treatment of bipolar disorder
- salts of carbonate and citrate
• Alone or in combination with antidepressant drugs, neuroleptics and antiepileptics
• Orally active, no binding to plasma proteins, half-life is 20-24 hrs, therapeutic effects require 3-4 weeks, eliminated via the kidneys
• Very toxic - extremely low therapeutic index
• Numerous side effects: CNS (tremors, mental confusion, convulsions and even coma), arrhythmias, decreased thyroid function, teratogenic effects,
drug interactions (thiazide diuretics, NSAIDs)

Front 116

carbamazepine

Back 116

anticonvulsant used in the treatment of bipolar disorder

Front 117

valproic acid

Back 117

anticonvulsant used in the treatment of bipolar disorder

Front 118

amphetamine

Back 118

stimulant
• Treatment of ADHD and narcolepsy
• Act by increasing release of DA and NE in the brain
• Numerous side effects affecting CNS, CV and GI systems; the most concerning are: paranoia, psychoses, suicidal/homicidal impulses, arrhythmias, hypertension, potential for addiction

Front 119

atomoxetine

Back 119

used in the treatment of ADHD
• NE reuptake inhibitor
– It is not a psychostimulant
– Not habit forming and is not a controlled substance

Front 120

dextroamphetamine

Back 120

stimulant
• Treatment of ADHD and narcolepsy
• Act by increasing release of DA and NE in the brain
- short term weight loss
• Numerous side effects affecting CNS, CV and GI systems; the most concerning are: paranoia, psychoses, suicidal/homicidal impulses, arrhythmias, hypertension, potential for addiction

Front 121

methylphenidate

Back 121

stimulant
• Treatment of ADHD and narcolepsy
• Act by increasing release of DA and NE in the brain
• Numerous side effects affecting CNS, CV and GI systems; the most concerning are: paranoia, psychoses, suicidal/homicidal impulses, arrhythmias, hypertension, potential for addiction

Front 122

modafinil

Back 122

used to treat narcolepsy
- The mechanism of action is unclear; likely involves NE and DA systems
- New drug with fewer psychoactive and euphoric effects, as well as effects on the mood and thinking

Front 123

diazepam

Back 123

benzodiazepine (Valium)
- long half live (>24hr)
- Anxiety, withdrawal, muscle relaxant

Front 124

chlordiazepoxide

Back 124

benzodiazepine (Librium)
- long half live (>24hr)
- Anxiety, withdrawal, muscle relaxant

Front 125

alprazolam

Back 125

benzodiazepine (Xanax)
- short half-life (2-6hr)
- Insomnia, anxiety

Front 126

oxazepam

Back 126

benzodiazepine
- short to int half-life

Front 127

triazolam

Back 127

benzodiazepine
- ultra short half-life

Front 128

lorazepam

Back 128

benzodiazepine (Ativan)
- intermediate half-life (6-24hr)
- Insomnia, anxiety, muscle relaxant

Front 129

temazepam

Back 129

benzodiazepine

Front 130

midazolam

Back 130

benzodiazepine (Versed)
- ultra short half-life (<2hr)
- pre-anesthetic medication

Front 131

flumazenil

Back 131

antagonist of bz site on GABA receptor
- Blocks the effects of both agonists and inverse agonists
- Have no biological effects themselves
- Can precipitate withdrawal in dependent persons
- Short acting (2hr)

Front 132

pentobarbital

Back 132

barbiturate
- intermediate half-life (15-50hr)
- preoperative sedative

Front 133

phenobarbital

Back 133

barbiturate
- long half-life (60-80hrs)
- anticonvulsant

Front 134

amobarbital

Back 134

barbiturate
- short half-life (10hr)
- preoperative sedative

Front 135

thiopental

Back 135

barbiturate
- ultra short half-life (3-10hr)
- anesthesia induction

Front 136

meprobamate

Back 136

non-benzodiazepine
- anxiolytic and sedative-hypnotic drug

Front 137

chloral hydrate

Back 137

non-benzodiazepine
- anxiolytic and sedative-hypnotic drug

Front 138

buspirone

Back 138

non-benzodiazepine
- anxiolytic
- partial agonist of serotonin receptor
- Produces only anxiolytic effects, no CNS depression
- No physical dependence
- No additive depression with ethanol
- Onset of action is 1 to 3 weeks - limits its usefulness in acute anxiety states

Front 139

zolpidem

Back 139

non-benzodiazepine (interact with BZ receptors) (Ambien)
- hypnotic
- Agonist at BZ receptor to produce pharmacological actions
- Increases the frequency of GABA-mediated Cl- channel opening
- rapid onset (peak plasma level at 1-2hr) induces sleep

Front 140

zaleplon

Back 140

non-benzodiazepine (interact with BZ receptors) (Sonata)
- hypnotic
- Agonist at BZ receptor to produce pharmacological actions
- Increases the frequency of GABA-mediated Cl- channel opening
- rapid onset (peak plasma level at 1-2hr) induces sleep

Front 141

carbamazepine

Back 141

anti-epileptic drug
• Drug of choice for partial simple, partial complex and tonic-clonic seizures
• Other use: trigeminal neuralgia, bipolar disorder
• Blocks voltage-activated Na+ channels
• Suppresses firing of action potentials and propagation of abnormal electrical waves throughout the brain
• Oral administration (tablets or oral suspension)
• Slowly absorbed
• Highly lipid soluble - rapid penetration into the brain
• Metabolized by the hepatic P-450 enzymes (CYP1A2, CYP2C8, CYP2C9, CYP3A4)
• Induces the P-450 enzymes, which increases its own metabolism during chronic administration (10-15 hrs half-life) and metabolism of other antiepileptics

Front 142

ethosuximide

Back 142

anti-epileptic drug
• Drug of choice to treat absence seizures
• Blocks voltage-activated T-type Ca2+ channels in thalamic neurons
• As a result, suppresses rhythmic activity
• Well absorbed orally
• Not bound to plasma proteins
• Long half-life time (30-60 hrs)
• ~75% is metabolized by the hepatic P-450 enzymes (CYP3A4)
• ~25% excreted unchanged in the urine

Front 143

gabapentin

Back 143

anti-epileptic drug
• Treatment of simple or complex partial seizures and generalized tonic-clonic seizures
• Enhances GABAergic synaptic transmission
• Is not metabolized and does not induce hepatic enzymes
• Not bound to plasma proteins
• Short half-life (5-8 hrs)
• Elimination by the kidneys
• Negligible drug interactions
• Side effects: dizziness, sedation, ataxia, fatigue, headache, tremor

Front 144

Lamotrigine

Back 144

antiepileptic drug
• Treatment of simple or complex partial seizures and generalized tonic-clonic seizures
• Inhibits release of glutamate (suppresses excitatory tone)
• Blocks voltage-activated Na+ channels (prevents repetitive firing)
• Metabolized by the liver
• Drug interactions: half-life time of lamotrigine is decreased by enzyme-inducing drugs (carbamazepine, phenytoin) and is increased by valproic acid
• Side effects: dizziness, headache, nausea and skin rash

Front 145

phenobarbital

Back 145

barbiturate used as antiepileptic drug
• Simple partial and recurrent tonic-clonic seizures, and febrile seizures in children
• In combination with carbamazepine and phenytoin allowing to use smaller doses
• Other use: to treat anxiety
• Facilitate activation of GABA receptors to increase inhibitory tone

Front 146

phenytoin

Back 146

antiepileptic drug
• Drug of choice for initial therapy of epilepsy in adults
• Is effective in suppressing partial simple, partial complex
and tonic-clonic seizures
• Emergency treatment of status-epilepticus via I-V (intravenous administration)
• Other use: treating arrhythmias, similar to lidocaine (class 1B)
• NOT used for absence seizures
• Blocks voltage-activated Na+ channels
• Suppresses repetitive action potential firing
• Also blocks voltage-activated Ca2+ channel
• Oral administration for chronic treatment and I-V for emergency
• Oral absorption is slow, but once it occurs, distribution is rapid and brain concentrations are high
• High plasma protein binding (~90%)
• ~95% is metabolized by the hepatic hydroxylation system (CYP2C9 and CYP2C19) that can become
saturated at high dosage (400-600 mg/day)
• <5% unchanged excreted via the kidneys)
• Fosphenytoin is a prodrug and is rapidly (min) converted to phenytoin. Used via IM and IV.

Front 147

valproic acid

Back 147

antiepileptic drug
• Drug of choice for myoclonic seizures
• Second-line drug (due to hepatotoxicity) for treating tonic-clonic and absence seizures
• Blocks voltage-activated Na+ and Ca2+ channels
• Facilitates GABAergic synaptic transmission
• Overall effect, reduces propagation of abnormal electrical discharge in the brain
• Orally effective and is rapidly absorbed
• High level of plasma protein binding (~90%)
• Metabolized by the liver P-450 enzymes (CYP2C9, CYP2C19)
• Divalproex is a combination of sodium valproate and valproic acid; improves GI tolerance

Front 148

pregabalin

Back 148

antiepileptic drug
• Blocks Ca2+ channels (via binding to alpha2-delta subunit) and release of glutamate
• Simple and complex partial seizures
• Drowsiness, dizziness, poor concentration, weight gain, skin rashes

Front 149

topiramate

Back 149

antiepileptic drug
• Blocks Na+ channels, increases activity of postsynaptic GABA receptors
• Simple and complex partial seizures and generalized tonic-clonic seizures
• Drowsiness, dizziness, ataxia, irritability, nausea, weight loss, hyperthermia

Front 150

zonisamide

Back 150

antiepileptic drug
• Blocks Na+ channels, blocks T-type Ca2+ channels
• Simple and complex partial seizures and generalized tonic-clonic seizures
• Drowsiness, ataxia, nausea, vomiting, confusion, skin rash

Front 151

clonazepam

Back 151

benzodiazepine used to treat myoclonic and absence seizures

Front 152

diazepam

Back 152

benzodiazepine (Valium) used to rapidly treat status epilepticus

Front 153

lorazepam

Back 153

benzodiazepine (Ativan) used to rapidly treat status epilepticus

Front 154

chlorpromazine

Back 154

antipsychotic
- D2 receptor antagonist
- phenothiazine derivative
- lower potency, D2 affinity

Front 155

fluphenazine

Back 155

antipsychotic
- D2 receptor antagonist
- phenothiazine derivative
- "typical" (older) drug
- Not highly selective for D2 receptors
- High potential for extrapyramidal effects (Parkinsonism or tardive dyskinesia)

Front 156

thioridazine

Back 156

antipsychotic
- D2 receptor antagonist
- phenothiazine derivative
- "typical" (older) drug
- Not highly selective for D2 receptors
- High potential for extrapyramidal effects (Parkinsonism or tardive dyskinesia)

Front 157

haloperidol

Back 157

antipsychotic
- D2 receptor antagonist
- butyrophenone derivative
- "typical" (older) drug
- Not highly selective for D2 receptors
- High potential for extrapyramidal effects (Parkinsonism or tardive dyskinesia)

Front 158

clozapine

Back 158

antipsychotic
- D2 receptor antagonist
- "atypical" (newer) drug
- More selective for D2 receptors
- Low incidences of extrapyramidal effects
- No prolactin elevation
- Induces weight gain

Front 159

olanzapine

Back 159

antipsychotic
- D2 receptor antagonist
- "atypical" (newer) drug
- More selective for D2 receptors
- Low incidences of extrapyramidal effects
- No prolactin elevation
- Induces weight gain

Front 160

risperidone

Back 160

antipsychotic
- D2 receptor antagonist
- "atypical" (newer) drug
- More selective for D2 receptors
- Low incidences of extrapyramidal effects
- No prolactin elevation
- Induces weight gain

Front 161

thiothixene

Back 161

antipsychotic
- D2 receptor antagonist
- thioxanthene derivative
- moderate potency, D2 selectivity

Front 162

levodopa

Back 162

enhancer of DA synthesis (L-DOPA)
• The precursor of dopamine that crosses blood brain barrier
• Decreases the rigidity, tremors and other symptoms of parkinsonism
• After 3-5 years, patients experience decline in response to the medication
• Orally available; rapidly absorbed from the small intestine
• Only 1-3% of L-DOPA reaches the brain; the rest is metabolized peripherally by aromatic l-amino acid decarboxylase
• Extremely short half-life time (1-2 hrs)

Front 163

carbidopa

Back 163

enhancer of DA concentration
• Levodopa/Carbidopa (Sinemet®) is a medication of choice for symptomatic treatment of Parkinson’s disease, especially at advanced stage
• Carbidopa (aromatic l-amino acid decarboxylase inhibitor) blocks peripheral metabolism of L-DOPA and therefore increases L-DOPA availability in the brain
• Allows to reduce the dose of L-DOPA by 4-5 fold and, consequently, significantly reduces the side effects of peripheral DA

Front 164

entacapone

Back 164

enhancer of DA concentration
- adjuvant Parkinsons therapy
- Combination of levodopa/carbidopa with entacapone (inhibitor of catechol-O-methyltransferase) further decreases peripheral metabolism of levodopa at the periphery and increases levodopa availability in the brain

Front 165

amantadine

Back 165

• Used to alleviate bradykinesia and rigidity (not very helpful for tremor) in patients with mild to moderate disease prior to initiation of L-DOPA
• Mechanisms: moderately increases DA release, blocks cholinergic muscarinic receptors and glutamatergic NMDA receptors
• Side-effects: hallucinations and confusion, nausea, dizziness, dry mouth, rash of the low extremeties; special caution should be taken when prescribing to patients with congestive heart disease and with glaucoma
• Other comments: has been developed as an antiviral drug for the treatment and prophylaxis of influenza

Front 166

apomorphine

Back 166

dopamine receptor agonist
• Acute treatment of patients with advanced Parkinson's disease for “off” periods (marked bradykinesia, immobility)
• Administered via subcutaneous injection (NOT for I-V - may lead to thrombus formation and pulmonary embolism)
• Side-effects: nausea, vomiting,
arrhythmias, postural hypotension, hallucinations, pronounced sleepiness

Front 167

bromocriptine

Back 167

dopamine receptor agonist
- D2 agonist and D1 partial agonist
• Are effective as monotherapy early in the disease or as an adjunct to L-DOPA in later stages of Parkinson’s disease
• Orally active
• Begin with low doses

Front 168

pramipexole

Back 168

dopamine receptor agonist
- D2 and D3 agonist
• Are effective as monotherapy early in the disease or as an adjunct to L-DOPA in later stages of Parkinson’s disease
• Orally active
• Begin with low doses

Front 169

ropinirole

Back 169

dopamine receptor agonist
- D2 and D3 agonist
• Are effective as monotherapy early in the disease or as an adjunct to L-DOPA in later stages of Parkinson’s disease
• Orally active
• Begin with low doses

Front 170

benztropine

Back 170

muscarinic antagonist
- Used to alleviate tremor and rigidity (not very helpful for bradykinesia) as monotherapy or along with other drugs
• Mechanism: Normally, nigrostriatal DA neurons inhibit acetylcholine release from striatal interneurons. The loss of nigrostriatal neurons in Parkinson’s patients leads to increased firing of striatal cholinergic interneurons and overstimulation of muscarinic receptors. Muscarinic cholinergic antagonists will block this effect
• Side-effects: typical antimuscarinic effects

Front 171

trihexyphenidyl

Back 171

muscarinic antagonist
- Used to alleviate tremor and rigidity (not very helpful for bradykinesia) as monotherapy or along with other drugs
• Mechanism: Normally, nigrostriatal DA neurons inhibit acetylcholine release from striatal interneurons. The loss of nigrostriatal neurons in Parkinson’s patients leads to increased firing of striatal cholinergic interneurons and overstimulation of muscarinic receptors. Muscarinic cholinergic antagonists will block this effect
• Side-effects: typical antimuscarinic effects

Front 172

rasagiline

Back 172

Selective inhibitor of brain MAO-B
- decreases DA metabolism
• Also decreases production of the byproduct hydrogen peroxide, therefore limiting formation of neurotoxic free radicals
• Is approved as adjunctive treatment in Parkinson’s patients receiving levodopa
• Show little benefit when taken alone
• Orally active, half-life time is 7-9 hrs, renal excretion
• Is not metabolized an amphetamine-like substance

Front 173

selegiline

Back 173

Selective inhibitor of brain MAO-B
- decreases DA metabolism
• Also decreases production of the byproduct hydrogen peroxide, therefore limiting formation of neurotoxic free radicals
• Is approved as adjunctive treatment in Parkinson’s patients receiving levodopa
• Show little benefit when taken alone
• Orally active, half-life time is 7-9 hrs, renal excretion
• Is metabolized to methamphetamine and
amphetamine (insomnia)

Front 174

donepezil

Back 174

acetylcholinesterase inhibitor (Aricept)
- Alzheimer's therapy
• Block catabolism of acetylcholine (ACh) and therefore increase the amount of ACh in presynaptic terminals available for the release
• Produce modest (although statistically significant) improvement in some patients. These benefits may retain for several years
• Good oral bioavailability
• half-life time: 70hrs
• metabolized by P450 liver enzymes

Front 175

galantamine

Back 175

acetylcholinesterase inhibitor
- Alzheimer's therapy
• Block catabolism of acetylcholine (ACh) and therefore increase the amount of ACh in presynaptic terminals available for the release
• Produce modest (although statistically significant) improvement in some patients. These benefits may retain for several years
• Good oral bioavailability
• half-life time: 7hrs
• metabolized by P450 liver enzymes

Front 176

rivastigmine

Back 176

acetylcholinesterase inhibitor
- Alzheimer's therapy
• Block catabolism of acetylcholine (ACh) and therefore increase the amount of ACh in presynaptic terminals available for the release
• Produce modest (although statistically significant) improvement in some patients. These benefits may retain for several years
• Good oral bioavailability
• half-life time: 1.5 hrs
• metabolized by plasma cholinesterase

Front 177

tacrine

Back 177

acetylcholinesterase inhibitor
- Alzheimer's therapy
• Block catabolism of acetylcholine (ACh) and therefore increase the amount of ACh in presynaptic terminals available for the release
• Produce modest (although statistically significant) improvement in some patients. These benefits may retain for several years
• Good oral bioavailability
• half-life time: 3 hrs
• metabolized by P450 liver enzymes
- Hepatotoxicity

Front 178

memantine

Back 178

NMDA receptor antagonist (low affinity) (Namenda)
- Alzheimer's therapy
- derivative of amantadine
• By blocking NMDA receptors, memantine protects neurons from Ca2+ overload that can lead to neuronal death (excitotoxicity)
• Improved daily activities and cognitive functions
• Benefits are additive when given with donezepil

Front 179

acetazolamide

Back 179

carbonic anhydrase inhibitor
- acts in lumen and cells of proximal tubule
- leaves NaHCO3 in urine
- also excretes K+ and H2PO4-
• based on the Sulfanilimide chemotherapeutic drugs
• Potassium wasting due to high Na delivery to distal nephron
- not for patients with sulfa allergies

Front 180

methazolamide

Back 180

carbonic anhydrase inhibitor
- acts in lumen and cells of proximal tubule
- leaves NaHCO3 in urine
- also excretes K+ and H2PO4-
• based on the Sulfanilimide chemotherapeutic drugs
• Potassium wasting due to high Na delivery to distal nephron
- not for patients with sulfa allergies

Front 181

dichlorphenamide

Back 181

carbonic anhydrase inhibitor
- acts in lumen and cells of proximal tubule
- leaves NaHCO3 in urine
- also excretes K+ and H2PO4-
• based on the Sulfanilimide chemotherapeutic drugs
• Potassium wasting due to high Na delivery to distal nephron
- not for patients with sulfa allergies

Front 182

glycerin

Back 182

osmotic diuretic
- leads to the excretion of Na, K, Ca, Mg, Cl, HCO3, H2PO4, uric acid
- indicated for acute edema and cerebral swelling, renal failure, tubular necrosis, and glaucoma
- acts primarily at the loop of Henle
- increases renal blood flow
- potassium wasting
- may be metabolized and cause hyperglycemia
- IV or PO as stool softener

Front 183

mannitol

Back 183

osmotic diuretic
- leads to the excretion of Na, K, Ca, Mg, Cl, HCO3, H2PO4, uric acid
- indicated for acute edema and cerebral swelling, renal failure, tubular necrosis, and glaucoma
- acts primarily at the loop of Henle
- increases renal blood flow
- potassium wasting
- IV administration only

Front 184

bumetanide

Back 184

loop diuretic
• Inhibit the Na+, K+, 2Cl- Symporter in the ascending thick loop of Henle
• Enter the urine via organic ion
transporters in proximal tubules
- leads to the excretion of Na, K, H, Ca, Mg, Cl, HCO3, H2PO4, uric acid
• Potassium wasting diuretic
- short half-life
- high ceiling

Front 185

ethacrynic acid

Back 185

loop diuretic
• Inhibit the Na+, K+, 2Cl- Symporter in the ascending thick loop of Henle
• Enter the urine via organic ion
transporters in proximal tubules
- leads to the excretion of Na, K, H, Ca, Mg, Cl, HCO3, H2PO4, uric acid
• Potassium wasting diuretic
- short half-life
- high ceiling
- may cause ototoxicity

Front 186

furosemide

Back 186

loop diuretic (Lasix)
• Inhibit the Na+, K+, 2Cl- Symporter in the ascending thick loop of Henle
- also a weak carbonic anhydrase inhibitor
- a sulfonamide moiety
• Enter the urine via organic ion
transporters in proximal tubules
- leads to the excretion of Na, K, H, Ca, Mg, Cl, HCO3, H2PO4, uric acid
• Potassium wasting diuretic
- short half-life
- high ceiling
- acutely increases systemic venous capacitance (useful in heart failure)
- uniquely glucuronidated in the KIDNEY not the liver

Front 187

torsemide

Back 187

loop diuretic
• Inhibit the Na+, K+, 2Cl- Symporter in the ascending thick loop of Henle
• Enter the urine via organic ion
transporters in proximal tubules
- leads to the excretion of Na, K, H, Ca, Mg, Cl, HCO3, H2PO4, uric acid
• Potassium wasting diuretic
- short half-life
- high ceiling

Front 188

chlorothiazide

Back 188

thiazide diuretic
• Block Na+Cl- symport but not K+
• Act on the distal collecting tubule
- leads to increased excretion of Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid
- Ca2+ excretion is reduced, resulting in increased Ca plasma levels
• Sulfonamide analogs but not usually carbonic anhydrase inhibitors
• Very commonly used; does not lead to dehydration
• Potassium Wasting
- t1/2 = 1.5 hrs

Front 189

hydrochlorothiazide

Back 189

thiazide diuretic
• Block Na+Cl- symport but not K+
• Act on the distal collecting tubule
- leads to increased excretion of Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid
- Ca2+ excretion is reduced, resulting in increased Ca plasma levels
• Sulfonamide analogs but not usually carbonic anhydrase inhibitors
• Very commonly used; does not lead to dehydration
• Potassium Wasting
- t1/2 = 2.5 hrs
- used for acute diuresis

Front 190

hydroflumethiazide

Back 190

thiazide diuretic
• Block Na+Cl- symport but not K+
• Act on the distal collecting tubule
- leads to increased excretion of Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid
- Ca2+ excretion is reduced, resulting in increased Ca plasma levels
• Sulfonamide analogs but not usually carbonic anhydrase inhibitors
• Very commonly used; does not lead to dehydration
• Potassium Wasting
- t1/2 = 17 hrs

Front 191

trichlormethiazide

Back 191

thiazide diuretic
• Block Na+Cl- symport but not K+
• Act on the distal collecting tubule
- leads to increased excretion of Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid
- Ca2+ excretion is reduced, resulting in increased Ca plasma levels
• Sulfonamide analogs but not usually carbonic anhydrase inhibitors
• Very commonly used; does not lead to dehydration
• Potassium Wasting
- t1/2 = 2-7 hrs

Front 192

metolazone

Back 192

thiazide-like diuretic
- does not decrease renal blood flow.
- used in cases of renal disease.

Front 193

amiloride

Back 193

renal Na+ channel inhibitor
• Cause small increases in NaCl excretion but are generally used for their ability to block K+ excretion in combination with other diuretics.
• Acts on distal convoluted tubule and collecting duct
- enhanced excretion of Na and Cl
- reduced excretion of K, H, Ca, Mg
• Potassium SPARING
- removed by kidney

Front 194

triamterene

Back 194

renal Na+ channel inhibitor
• Cause small increases in NaCl excretion but are generally used for their ability to block K+ excretion in combination with other diuretics.
• Acts on distal convoluted tubule and collecting duct
- enhanced excretion of Na and Cl
- reduced excretion of K, H, Ca, Mg
• Potassium SPARING
- removed by liver
• Triamterene is a folate antagonist and may lead to megaloblastic anemia in cirrhosis
• Triamterene side effects include reduced glucosetolerance, photosensitization, interstitial nephritis and renal stones.

Front 195

eplerenone

Back 195

mineralocorticoid antagonist
- inhibit aldosterone binding in cells of the DCT and Collecting Ducts
- enhanced Na, Cl excretion
- reduced K, H, Mg excretion
- Potassium SPARING
- Typically coadministered with thiazides and loop diuretics for potassium sparing actions

Front 196

spironolactone

Back 196

mineralocorticoid antagonist
- inhibit aldosterone binding in cells of the DCT and Collecting Ducts
- enhanced Na, Cl excretion
- reduced K, H, Mg excretion
- Potassium SPARING
- Typically coadministered with thiazides and loop diuretics for potassium sparing actions
• used for treatment of primary hyperaldosteronism in adrenal adenomas and adrenal hyperplasia.
• used for secondary hyperaldosteronism resulting from cardiac failure, cirrhosis, nephrotic syndrome, severe ascites.
- treatment of choice for ascites and edema associated with cirrhosis

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chlorpropamide

Back 197

antidiuretic drug
• A sulfonylurea previously used
for Type II diabetes.
-Also increases ADH secretion

Front 198

desmopressin

Back 198

antidiuretic drug
- synthetic analog of arginine
vasopressin with little V1 activity
• Stimulate water resorption in distal tubule and collecting duct by stimulating the production of aquaporins in the epithelium.

Front 199

lypressin

Back 199

antidiuretic drug (lysine vasopressin)
• Synthetic lysine vasopressin is based on pig sequence
• Stimulate water resorption in distal tubule and collecting duct by stimulating the production of aquaporins in the epithelium.

Front 200

vasopressin

Back 200

antidiuretic drug (ADH)
- binds V1 receptors
• Stimulate water resorption in distal tubule and collecting duct by stimulating the production of aquaporins in the epithelium.

Front 201

probenecid

Back 201

uricosuric agent
- gout therapy
• Probenecid is an organic acid transporter competitive antagonist in the proximal tubule (initial effect) and in the DISTAL TUBULE (long term effect) promotes excretion

Front 202

sulfinpyrazone

Back 202

uricosuric agent
- gout therapy
• an organic acid transporter competitive antagonist in the proximal tubule (initial effect) and in the DISTAL TUBULE (long term effect) promotes excretion

Front 203

allopurinol

Back 203

uricosuric agent
- inhibits xanthine oxidase, thereby stopping the formation of uric acid
- not related to nephron function

Front 204

colchicine

Back 204

used as uricosuric agent
- impairs the ability of neutrophils to carry uric acid crystals into joints.