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204 Cards in this Set
- Front
- Back
naloxone
|
opioid antagonist (Narcan)
- used to reverse acute opioid overdose - parenteral - respiratory and cardiovascular support may also be required |
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morphine
|
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 |
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hydromorphone
|
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 |
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hydrocodone
|
opioid agonist, at mu receptor (Vicodin)
- metabolized to hydromorphone by CYP2D6, causing patient variability in effectiveness. - can be combined with acetaminophen (Lortab) |
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oxycodone
|
opioid agonist, at mu receptor (Oxycodone, Oxycontin)
- metabolized to oxymorphone by CYP2D6 - can be combined w/acetaminophen (Percocet) |
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oxymorphone
|
opioid agonist, at mu receptor (Opana)
- available in extended release PO |
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codeine
|
opioid agonist, at mu receptor
- metabolized to morphine by CYP2D6 - combined w/acetaminophen (Tylenol 3) |
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propoxyphene
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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. |
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heroin
|
opioid agonist, at mu receptor (diacetyl morphine)
- converted to monoacetyl morphine and morphine in brain - rapid onset, highly addictive - |
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methadone
|
opioid agonist, at mu receptor
- long duration, t1/2 = 15-60hrs PO - not a morphine analog - maintenance for opioid addiction and pain management |
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meperidine
|
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 |
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fentanyl
|
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 |
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tramadol
|
partial mu opioid agonist and MAOI (Ultram)
- used for mild to moderate acute and chronic pain - combined w/acetaminophen (Ultracet) |
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pentazocine
|
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 |
|
nalbuphine
|
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 |
|
buprenorphine
|
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 |
|
diphenoxylate
|
opioid agonist, antidiarrheal (Lomotil)
- poorly absorbed PO - reduces GI motility |
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loperamide
|
opioid agonist, antidiarrheal (Imodium)
- poorly absorbed PO - reduces GI motility |
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naltrexone
|
opioid antagonist
- used to reverse side effects of opioids and manage opioid/alcohol addiction - PO |
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nalmefene
|
opioid antagonist
- used to reverse side effects of opioids and manage opioid dependence - parenteral |
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alvimopan
|
opioid antagonist
- poorly absorbed orally - active opioid antagonist that antagonizes the GI side effects of opioids. |
|
BCG
|
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. |
|
azathioprine
|
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 |
|
cyclophosphamide
|
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 |
|
leflunomide
|
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. |
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methotrexate
|
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. |
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mycophenolate mofetil
|
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. |
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prednisone
|
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 |
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sirolimus
|
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 |
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cyclosporine
|
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. |
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tacrolimus
|
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. |
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Anti-lymphocyte globulin (ALG)
|
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. |
|
muromonab-CD3 (OKT3)
|
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. |
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basiliximab
|
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. |
|
daclizumab
|
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. |
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Rh(D) immune globulin
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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. |
|
interleukin-2
|
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. |
|
interferons
|
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). |
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cetirizine
|
2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects. |
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dimenhydrinate
|
1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types. - marked sedation - used for motion sickness - salt of diphenhydramine |
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diphenhydramine
|
1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types. - marked sedation - used for motion sickness |
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fexofenadine
|
2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects. |
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loratadine
|
2nd generation antihistimine
-High selectivity for H1 sites and have few anti-cholinergic side effects. Penetrate poorly into CNS, reducing sedative effects. |
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meclizine
|
1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types. - slight sedation - used for motion sickness |
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promethazine
|
1st generation antihistimine
- H1 receptor antagonist, but also blocks other receptor types. - marked sedation - used for motion sickness - used as antiemetic |
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terfenadine
|
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 |
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adalimimab
|
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). |
|
infliximab
|
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). |
|
etanercept
|
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). |
|
aspirin (acetylsalicylic acid, ASA)
|
Nonselective COX inhibitor
- OTC analgesic, antipyretic - irreversibly inhibits COX1 on platelets |
|
diclofenac
|
Nonselective COX inhibitor
- Rx arthritis, anti-inflammatory - 0.3 COX1/COX2 - combined w/ misoprostol to prevent COX1 inhibition |
|
ibuprofen
|
Nonselective COX inhibitor
- OTC analgesic, antipyretic - 2.6 COX1/COX2 |
|
indomethacin
|
Nonselective COX inhibitor
- Rx arthritis, anti-inflammatory - 10 COX1/COX2 - high frequency of intolerance |
|
ketorolac
|
Nonselective COX inhibitor
- Post-surgical analgesic - 395 COX1/COX2 |
|
naproxen
|
Nonselective COX inhibitor
- Rx, OTC anti-inflammatory - 3.8 COX1/COX2 |
|
acetaminophen
|
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. |
|
celecoxib
|
COX-2 selective inhibitor
- 10-20 times more selective for Cox-2 than for Cox-1 - evidence of increased cardiovascular risk |
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rofecoxib
|
COX-2 selective inhibitor
- 200 times more selective for Cox-2 than for Cox-1 - evidence of increased cardiovascular risk - removed from market |
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albuterol
|
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. |
|
salmeterol
|
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®) |
|
beclomethasone
|
corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma. |
|
budesonide
|
corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma. |
|
fluticasone
|
corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma. |
|
prednisone
|
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. |
|
triamcinolone
|
corticosteroid
- Administered topically to the airway by aerosol inhalation for longterm reduction in symptoms of asthma. |
|
montelukast
|
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. |
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zafirlukast
|
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. |
|
zileuton
|
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. |
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cromolyn
|
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. |
|
nedocromil
|
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. |
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ipratropium
|
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. |
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omalizumab
|
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. |
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theophylline
|
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. |
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desflurane
|
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 |
|
isoflurane
|
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 |
|
enflurane
|
volatile general anesthetic
- MAC 1.68% - blood-gas partition 1.9 - Is metabolized at only 2.0% |
|
sevoflurane
|
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 |
|
nitrous oxide
|
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 |
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dantrolene
|
treats malignant hyperthermia
|
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succinylcholine
|
can trigger malignant hyperthermia
|
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thiopental
|
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 |
|
methohexital
|
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 |
|
ketamine
|
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 |
|
etomidate
|
• Used in induction for general
anesthesia (IV) • Produces respiratory depression • Does not produce cardiovascular depression • Can not be antagonized |
|
propofol
|
newest anesthesia induction agent
• Can also be used for maintenance • Produces cardiovascular and respiratory depression • Can not be antagonized • Least ‘hangover effect’ |
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alfentanil
|
- Like fentanyl, a potent, fast onset, short acting opioid
|
|
sufentanil
|
- Like fentanyl, a potent, fast onset, short acting opioid
|
|
fentanyl
|
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 |
|
remifentanil
|
- Like fentanyl, a potent, fast onset, short acting opioid
- metabolized by plasma esterase; it can be used as an infusion. |
|
flumazenil
|
used to antagonize midazolam and other benzodiazepines
|
|
midazolam
|
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 |
|
cocaine
|
topical local anesthetic
- ester – also a vasoconstrictor • Toxicity - Myocardial ischemia, Myocardial infarction, Arrhythmias, Seizures, Hypertension - degraded by plasma esterase |
|
procaine
|
local anesthetic (Novocaine)
- ester - low potency, low hydrophobicity - degraded by plasma esterase |
|
tetracaine
|
local anesthetic
- ester - high potency, high hydrophobicity - degraded by plasma esterase |
|
lidocaine
|
local anesthetic
- amide - intermediate potency, hydrophobicity - shorter duration of action - 1% lidocaine used for infiltration - metabolized in liver |
|
mepivacaine
|
local anesthetic
- amide - intermediate potency, hydrophobicity - metabolized in liver |
|
bupivacaine
|
local anesthetic
- amide - hight potency, hydrophobicity - longer duration of action - metabolized in liver |
|
prilocaine
|
local anesthetic
- amide - shorter duration of action - metabolized in liver |
|
ropivacaine
|
local anesthetic
- amide - newer, s-entantiomer only - metabolized in liver |
|
amitriptyline
|
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 |
|
amoxapine
|
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 |
|
imipramine
|
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 |
|
nortriptyline
|
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 |
|
citalopram
|
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 |
|
escitalopram
|
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 |
|
fluoxetine
|
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 |
|
sertraline
|
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 |
|
bupropion
|
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 |
|
mirtazapine
|
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 |
|
nefazodone
|
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 |
|
venlafaxine
|
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 |
|
phenelzine
|
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) |
|
selegiline
|
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) |
|
tranylcypromine
|
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) |
|
lithium
|
• 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) |
|
carbamazepine
|
anticonvulsant used in the treatment of bipolar disorder
|
|
valproic acid
|
anticonvulsant used in the treatment of bipolar disorder
|
|
amphetamine
|
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 |
|
atomoxetine
|
used in the treatment of ADHD
• NE reuptake inhibitor – It is not a psychostimulant – Not habit forming and is not a controlled substance |
|
dextroamphetamine
|
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 |
|
methylphenidate
|
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 |
|
modafinil
|
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 |
|
diazepam
|
benzodiazepine (Valium)
- long half live (>24hr) - Anxiety, withdrawal, muscle relaxant |
|
chlordiazepoxide
|
benzodiazepine (Librium)
- long half live (>24hr) - Anxiety, withdrawal, muscle relaxant |
|
alprazolam
|
benzodiazepine (Xanax)
- short half-life (2-6hr) - Insomnia, anxiety |
|
oxazepam
|
benzodiazepine
- short to int half-life |
|
triazolam
|
benzodiazepine
- ultra short half-life |
|
lorazepam
|
benzodiazepine (Ativan)
- intermediate half-life (6-24hr) - Insomnia, anxiety, muscle relaxant |
|
temazepam
|
benzodiazepine
|
|
midazolam
|
benzodiazepine (Versed)
- ultra short half-life (<2hr) - pre-anesthetic medication |
|
flumazenil
|
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) |
|
pentobarbital
|
barbiturate
- intermediate half-life (15-50hr) - preoperative sedative |
|
phenobarbital
|
barbiturate
- long half-life (60-80hrs) - anticonvulsant |
|
amobarbital
|
barbiturate
- short half-life (10hr) - preoperative sedative |
|
thiopental
|
barbiturate
- ultra short half-life (3-10hr) - anesthesia induction |
|
meprobamate
|
non-benzodiazepine
- anxiolytic and sedative-hypnotic drug |
|
chloral hydrate
|
non-benzodiazepine
- anxiolytic and sedative-hypnotic drug |
|
buspirone
|
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 |
|
zolpidem
|
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 |
|
zaleplon
|
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 |
|
carbamazepine
|
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 |
|
ethosuximide
|
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 |
|
gabapentin
|
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 |
|
Lamotrigine
|
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 |
|
phenobarbital
|
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 |
|
phenytoin
|
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. |
|
valproic acid
|
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 |
|
pregabalin
|
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 |
|
topiramate
|
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 |
|
zonisamide
|
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 |
|
clonazepam
|
benzodiazepine used to treat myoclonic and absence seizures
|
|
diazepam
|
benzodiazepine (Valium) used to rapidly treat status epilepticus
|
|
lorazepam
|
benzodiazepine (Ativan) used to rapidly treat status epilepticus
|
|
chlorpromazine
|
antipsychotic
- D2 receptor antagonist - phenothiazine derivative - lower potency, D2 affinity |
|
fluphenazine
|
antipsychotic
- D2 receptor antagonist - phenothiazine derivative - "typical" (older) drug - Not highly selective for D2 receptors - High potential for extrapyramidal effects (Parkinsonism or tardive dyskinesia) |
|
thioridazine
|
antipsychotic
- D2 receptor antagonist - phenothiazine derivative - "typical" (older) drug - Not highly selective for D2 receptors - High potential for extrapyramidal effects (Parkinsonism or tardive dyskinesia) |
|
haloperidol
|
antipsychotic
- D2 receptor antagonist - butyrophenone derivative - "typical" (older) drug - Not highly selective for D2 receptors - High potential for extrapyramidal effects (Parkinsonism or tardive dyskinesia) |
|
clozapine
|
antipsychotic
- D2 receptor antagonist - "atypical" (newer) drug - More selective for D2 receptors - Low incidences of extrapyramidal effects - No prolactin elevation - Induces weight gain |
|
olanzapine
|
antipsychotic
- D2 receptor antagonist - "atypical" (newer) drug - More selective for D2 receptors - Low incidences of extrapyramidal effects - No prolactin elevation - Induces weight gain |
|
risperidone
|
antipsychotic
- D2 receptor antagonist - "atypical" (newer) drug - More selective for D2 receptors - Low incidences of extrapyramidal effects - No prolactin elevation - Induces weight gain |
|
thiothixene
|
antipsychotic
- D2 receptor antagonist - thioxanthene derivative - moderate potency, D2 selectivity |
|
levodopa
|
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) |
|
carbidopa
|
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 |
|
entacapone
|
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 |
|
amantadine
|
• 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 |
|
apomorphine
|
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 |
|
bromocriptine
|
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 |
|
pramipexole
|
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 |
|
ropinirole
|
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 |
|
benztropine
|
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 |
|
trihexyphenidyl
|
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 |
|
rasagiline
|
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 |
|
selegiline
|
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) |
|
donepezil
|
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 |
|
galantamine
|
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 |
|
rivastigmine
|
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 |
|
tacrine
|
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 |
|
memantine
|
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 |
|
acetazolamide
|
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 |
|
methazolamide
|
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 |
|
dichlorphenamide
|
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 |
|
glycerin
|
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 |
|
mannitol
|
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 |
|
bumetanide
|
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 |
|
ethacrynic acid
|
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 |
|
furosemide
|
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 |
|
torsemide
|
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 |
|
chlorothiazide
|
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 |
|
hydrochlorothiazide
|
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 |
|
hydroflumethiazide
|
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 |
|
trichlormethiazide
|
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 |
|
metolazone
|
thiazide-like diuretic
- does not decrease renal blood flow. - used in cases of renal disease. |
|
amiloride
|
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 |
|
triamterene
|
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. |
|
eplerenone
|
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 |
|
spironolactone
|
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 |
|
chlorpropamide
|
antidiuretic drug
• A sulfonylurea previously used for Type II diabetes. -Also increases ADH secretion |
|
desmopressin
|
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. |
|
lypressin
|
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. |
|
vasopressin
|
antidiuretic drug (ADH)
- binds V1 receptors • Stimulate water resorption in distal tubule and collecting duct by stimulating the production of aquaporins in the epithelium. |
|
probenecid
|
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 |
|
sulfinpyrazone
|
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 |
|
allopurinol
|
uricosuric agent
- inhibits xanthine oxidase, thereby stopping the formation of uric acid - not related to nephron function |
|
colchicine
|
used as uricosuric agent
- impairs the ability of neutrophils to carry uric acid crystals into joints. |