Pharmacology Exam 2 - Drugs Only

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  1. Mechloroethamine
    • Highly reactive anti-tumor bifunctional alkylator
    • Meaning, it causes crosslinking of guanine residues in DNA
    • Aka: Nitrogen mustard
  2. Cyclophosphamide
    • Less highly-reactive derivative of mechlorethamine
    • Anti-tumor bifunctional alkylator
    • Meaning, it causes crosslinking of guanine residues in DNA
    • Requires activation in liver or tumor tissues
    • Inactivation also uses liver enzymes
  3. Ifosfamide, chlorambucil
    Anti-tumor bifunctional alkylator
  4. Nitrosoureas
    • A class of anti-tumor DNA alkylating agents
    • Is great when used with other alkylating agents because of a synergistic effect and little cross-resistance
    • Cross BBB, so are useful against brain tumors
  5. Procarbazine
    • Anti-tumor DNA alkylating agent
    • Requires metabolism to become an alkylating agent
    • Used for Hodgkin's disease with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP regimen)
    • Is leukemogenic: Mutagenic, carcinogenic; large chance of developing cancer from treatment
  6. Carmustine, lomustine, busulfan, dacarbazine
    • Anti-tumor DNA alkylators
    • Dacarbazine is used in the ABVD regimen against Hodgkin and other lymphomas
  7. Methotrexate
    • Anti-tumor antimetabolite
    • Folic acid analog that accumulates in cells as a polyglutamate derivative, enhancing cytotoxicity
    • Blocks synthesis of DNA, RNA, and protein precursors by preventing dihydrofolatereductase (DHFR) from recycling FH2 to FH4
    • S-phase specific
    • Resistance: Amplification of DHFR gene, DHFR gene mutation
  8. Folinic acid
    • AKA: Leucovorin
    • Used to "rescue" immune system from effects of Methotrexate to stop side effects
  9. 6-mercaptopurine
    • Anti-tumor antimetabolite
    • Replaces the DNA/RNA base intermediate, hypoxanthine
    • Is inactivated by xanthine oxidase, so don't take with milk! Allopurinol inhibits XO, so if administered together, greatly decrease dose of 6-mercaptopurine
    • Resistance: Often by downregulating HGPRT, the enzyme that is responsible for converting the drug into a NMP/NTP by attaching a sugar-phosphate
  10. 6-thioguanine
    • Anti-tumor antimetabolite
    • Replaces guanine
    • Resistance: Often by downregulating HGPRT, the enzyme that is responsible for
    • converting the drug into a NMP/NTP by attaching a sugar-phosphate
  11. 5-fluorouracil
    • AKA: 5-FU
    • The metabolite of this, fluorodeoxyuridine monophosphte (FdUMP), inhibits thymidylate synthetase, resulting in thymineless death
    • S-phase specific
  12. Capecitabine
    • Oral prodrug of fluorouracil
    • May be preferentially activated in tumor tissues
    • Approved for colon cancer and refractory breast cancer
  13. Cytarabine
    • AKA: Cytosine arabinoside
    • This is converted into araCMP, then araCTP, which is an inhibitor of DNA synthesis
    • AraCTP is also incorporated into DNA leading to mutations and DNA strand breaks (chain terminating nucleotide)
    • The activation of cytarabine is performed by deoxycytidine kinase
    • Resistance: Mutational loss of deoxycitidine kinase
  14. Daunorubicin, doxorubicin, dactinomycin D
    • Anti-tumor antibiotics: Anthracyclines
    • Intercalate in DNA and stop DNA pol II, causing scission of DNA
    • Also are topoisomerase "inhibitors" because they form a complex with topoisomerase II and DNA, interfering with religation of the double-strand break
    • Toxicity: Irreversible cardiac toxicity at high doses
    • Liver: Site of extretion/metabolism/inactivation
  15. Bleomycin
    • Anti-tumor antibiotic
    • Cause DNA scission/strand breaks
    • Broad spectrum of tumor specificity
    • Toxicity: Pulmonary fibroses at high doses
    • Anaphylactic reactions do occur against this drug, since it is a natural product
    • No significant myelosuppression: It is great used in combination regimens
  16. Vinblastine
    • Mitotic spindle poison: Vinca alkyloid
    • M-phase specific
    • Inhibits microtubule polymerization, causing mitotic arrest
    • Side effects: Acute nausea, vomiting, and dose-limiting bone marrow depression
    • Effective against Hodgkin and other lymphomas, especially when combined with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD regimen)
    • Resistance: Tubulin gene mutations
  17. Vincristine
    • Mitotic spindle poison: Vinca alkyloid
    • M-phase specific
    • Inhibits microtubule polymerization, causing mitotic arrest
    • Side effects: No acute side effects and milder, non-dose-limiting bone marrow depression; significant neurotoxicity/muscle weakness occurs
    • Effective in treating acute childhood leukemia or Hodgkin's disease in the MOPP regimen
    • Resistance: Tubulin gene mutations
    • Liver: Site of extretion/metabolism/inactivation
  18. Paclitaxel
    • Mitotic spindle poison: Paclitaxel
    • Enhances tubulin polymerization, and blocks microtubule disassembly
    • Used for ovarian and advanced breast cancers
  19. Docetaxel
    Mitotic spindle poison
  20. Topotecan, irinotecan, camptothecin
    • Topoisomerase I "inhibitors"
    • Bind to the "cleavable complex" of DNA topoisomerase I and DNA; block religation of single-strand break
    • Double-strand breaks then occur with DNA replication, making this S-phase specific
  21. Etoposide, teniposide
    • Topoisomerase II "inhibitors"
    • Form complexes with DNA topoisomerase II and DNA, blocking religation of double-strand break, causing DNA scission
    • The anthracycline antibiotics (daunorubicin and doxorubicin) also do this
  22. Cisplatin, carboplatin
    • Platinum coordination complexes
    • Cross-link DNA at any part of the cell cycle
    • Great for use in various combination regimens, but especially for ovarian and testicular cancer
    • Toxicity: Nephrotoxicity (due to hydration?), and acoustc nerve dysfunction causing tinnitis, or ringing in the ears
    • Resistance: DNA repair still occurs
    • Kidney: Site of extretion/metabolism/inactivation
  23. Tamoxifen
    • Anti-tumor hormone partial agonist
    • Acts as a competitive inhibitor of estrogen by binding to the estrogen receptor
    • This is called a selective estrogen response modulator (SERM)
    • Toxicity: Little; manageable, such as hot flashes
    • Used in cancers of estrogen-responsive tissues: female and male breast (40% are ER+) and uterine endometrium
    • Also used as a prophylactic treatment to prevent breast cancer for high-risk women, but it hasn't been shown to significantly increase lifespan; it has been shown to reduce risks of bone fractures in postmenopausal women (just like postmenopausal estrogen replacement therapy)
    • Remember, a partial agonist is an effective antagonist because it causes a decreased effect of the original hormone binding the receptor
  24. Raloxifene
    • Anti-tumor hormone targeting agent
    • SERM: Selective estrogen response modulator
    • Used for prevention of breast cancer in patients with osteoporosis
    • Has lower risks of endometrial cancer and thrombotic events than tamoxifen by the Study of Tamoxifen And Raloxifene (STAR) study
  25. Letrozole, anastrozole, and exemestane
    • Aromatase inhibitors
    • Block conversion of androgens to estrogen in postmenopausal women
    • Not used in premenopausal women because of compensatory gonadotropin and ovarian estrogen production (feedback causes increased estrogen production from these sites)
    • More effective than tamoxifen for ER+ breast cancers in postmenopausal women
    • Exemestane: Also used as prophylaxis in high-risk postmenopausal women
    • Toxicity: No enhanced incidence of thrombosis or uterine cancer (contrasted to SERMs); joint pain and loss of bone density occur
  26. Leuprolide
    • Anti-androgen therapy for cancer
    • Synthetic peptide analog of GnRH that is a GnRH receptor agonist (this doesn't make sense to me)
    • If we give pulsatile infusions, then we end up getting elevated levels of androgens in men and estrogens in women
    • Continuous, high-dose treatment instead greatly lowers androgen levels in men and estrogen levels in premenopausal women
    • Chemical castration, androgen ablation
    • This is as effective as estrogen therapy or orchiectomy in treatment of prostate cancer with fewer side effects
  27. Flutamide
    • Anti-androgen therapy for cancer
    • Androgen reeptor antagonist
    • Resistance: Gained rapidly in prostate cancer if this agent is used alone
    • But if used in conjunction with leuprolide, the effects of teh initial pulse of androgen levels and associated flare of prostate cancer at the start of leuprolide therapy is blocked
  28. GnRH receptor antagonists
    • Anti-androgen therapy for cancer
    • These work by preventing release of LH from the pituitary gland in response to GnRH
    • Good for treatment of prostate cancer
  29. Prednisone
    • Adrenocorticosteroid
    • Induces apoptosis in leukemia cells
    • Used in multirug regimens for leukemia, lymphoma, and myeloma
    • Is not curative, but helps induce remission in leukemias of childhood; palliative agent in other cancers
  30. EGF receptor protein tyrosine kinase inhibitors
    • Targeted agents
    • This tyrosine kinase is overexpressed in various lung, brain, head, and neck cancers
    • Erlotinib: Small molecule inhibitors that are improved for non-small cell lung cancers
    • Cetuximab: Chimerc EGF receptor antibody approved for use in colon cancer and head and neck cancer
  31. HER2 protein tyrosine kinase inhibitors
    • Targeted agents
    • This tyrosine kinase is overexpressed in various cancers
    • Lapatinib: Small molecule EGFR and HER2 kinase inhibitor used for breast cancer
    • Trastuzumab: "Humanized" HER2 antibody used in HER2+ breast cancers (30%), especially for refractory metastatic breast cancer; recognizes HER2/Neu on the cell surface
  32. Imatinib
    • Targeted agent
    • An inhibitor of the activated bcr/abl protein tyrosine kinase that arises from gene rearrangement/fusion in chronic myelogenous leukemia (Philadelphia chromosome)
  33. Brentuximab vedotin
    • Targeted agent
    • A chimeric IgG for CD30 surface antigen, that is attached to a highly toxic mitotic spindle poison vedotin with a cleavable linker
    • Upon binding to CD30+ tumor cells (found in Hodgkin lymphomas and anaplastic large cell lymphoma), the antibody-conjugated vedotin is internalized and proteolytically cleaved to release toxin
  34. Tyrosine Kinase inhibitors
    • All end in -ib
    • Imatinib, gefitinib, erlotinib, sorafenib, sunitinib, dasatinib, lapatinib, nilotinib
    • Antibodies end in -ab
  35. Naloxone
    • Opioid antagonist
    • Given through IV, it provides respiratory and cardiovascular support following actue opioid intoxication/overdose
  36. Morphine
    • Mu opioid receptor agonist
    • Onset of action: 10-15 minutes
    • Peak effects: 30 minutes
    • Clinical duration: 4 hours
    • This is because only 20% of morphine is in uncharged form, which crosses BBB better than charged; results in slow onset of action
    • Metabolism: Glucuronidation in the kidney; this results in a little active metabolite (M-6-glucuronide), that is 10x more potent than morphine; and a lot of an inactive metabolite (M-3-glucuronide)
    • Liver disease can change the pharmacokinetics little, but renal disease/failure can greatly influence the effects of morphine
    • MS Contin or Morphine SR: Extended release forms
    • Dosage is 3-5 times higher by PO because of poor oral bioavailability than IV
    • Other ways of administering: Intrathecal (subarachnoid) or epidural for chronic or acute pain, respectively to target the spinal mu receptors in the dorsal horn
  37. Hydromorphone
    • Mu opioid agonist
    • Given IV or PO
    • 5 times more potent than morphine! This is becaues it is more lipid soluble than morphine with a faster onset
    • Metabolism in the kidney results in an inactive metabolite and a less efficacious active metabolite
  38. Hydrocodone
    • Mu opioid agonist
    • Metabolized to hydromorphone
    • This is the number one prescribed drug
  39. Oxycodone
    • Mu opioid agonist
    • Metabolized to oxymorphone
  40. Oxymorphone
    • Given PO
    • Available in Oxymorphone ER
    • Ethanol consumption increases absorption, causing toxicity
  41. What is commonly combined with opioid therapy?
    • Acetaminophen
    • This is to produce pain relief at lower levels to avoid severe side effects
  42. Codeine
    • Mu opioid agonist
    • Converted to morphine by demethylation
    • Some people do not get relief because they are poor metabolizers of codeine
    • DO NOT use in pregnant mothers, because the child could be a fast metabolizer
    • These fast metabolizers are the CYP 2D6 polymorphism, lacking the enzyme (up to 10% of people)
  43. Heroin
    • Mu opioid agonist
    • Prodrug converted to monoacetyl morphine, and then morphine
    • Rapid onset due to an acetyl structure that helps heroin get to the brain faster than morphine
  44. Methadone
    • Mu opioid analgesic
    • Oral, ultra-long-acting half life of 15-60 hours
    • Used for maintenance for opioid drug addiction
    • Structure is nothing like morphine
  45. Meperidine
    • Mu opioid analgesic
    • Less potent than morphine, but faster onset due to more lipid soluble
    • Converted by liver to nor-meperidine, which is a proconvulsive metabolite
    • Patients with renal failure are more likely to experience bad side effects because the action of the drug is prolonged, but excretion is decreased
    • Risk of serotonin syndrome
  46. Fentanyl and other similar drugs
    • Mu opioid analgesics
    • Oral, IV, epidural, intrathecal, or transdermal application
    • Sufentanil, alfentanil, remifentanil are similar
    • Fentanyl is highly lipid-soluble, so has a high potency and fast onset, but a shorter duration of action
    • It's effects are terminated by redistribution
    • Antagonized by naloxone
    • Also used in premedication of anesthesia
    • It reduces the MAC of volatile anesthetics
    • Does produce marked respiratory depression, but with little effects on blood pressure
  47. Sulfentanil, alfentanil
    • Mu opioid analgesics
    • Potent, fast-onset, short-acting opioids
  48. Remifentanil
    • Mu opioid analgesic
    • Metabolized by plasmaa esterase, so can be used as an infusion continuously
  49. Tramadol and tapentadol
    • Mu opioid partial agonists
    • Have weak analgesic activity, and are used for mild to moderate acute and chronic pain
    • They also have monoamine reuptake inhibitor activity, which also contributes to analgesic activity
  50. Pentazocine, butorphanol, nalbuphine
    • Opioid agnoists and partial agonists/antagonists at varying receptors
    • Used for management of acute, short-term pain; not for chronic
    • Also used to manage side effects, such as itching that accompanies morphine
  51. Buprenorphine
    • Opioid agonist at multiple receptors
    • Partial mu receptor agonist and kappa agonist
    • Difficult to provide analgesia because of high mu receptor affinity
  52. Diphenoxylate, loperamide
    • Opioid agonists
    • Used as antidiarrheals
  53. Naltrexone
    • Opioid antagonist
    • Given orally
    • Prevents effects of opioids
    • Naloxone is given IV
  54. Alvimopan
    • Opioid antagonist
    • Poorly absorbed orally, but given that way to antagonize the GI side effects of opioids
  55. Methylnaltrexone
    • Opioid antagonist
    • Positively charged; given through IV for constipation
  56. Abuse-resistant opioids
    • Extened relief morphine combined with sequestered naloxone
    • Provides pain relief while preventing opioid abuse
  57. Isoflurane
    • Volatile anesthetic
    • Irritating to the airways
    • Higher blood-gas partition coefficient
    • Myocardial depression is minimal
  58. Desflurane
    • Volatile anesthetic
    • Irritating to the airways
    • Produces prompt recovery because it has the lowest blood-gas partition coefficient
    • Myocardial depression is minimal
  59. Sevoflurane
    • Volatile anesthetic
    • Is non-irritating to the airways, so can be used for induction
    • Produces prompt recovery
    • Myocardial depression is minimal
  60. Nitrous oxide
    • Volatile anesthetic
    • Adjunct to the potent volatile anesthetic agents
    • Reduces MAC requirements
    • Very insoluble
    • Has little side effects
  61. Propofol
    • Anesthetic induction agent
    • Can also be used for maintenance
    • Dissolved in intralipid
    • Produces cardiovascular and respiratory depression
    • Cannot be antagonized
    • Least "hangover" effect
  62. Etomidate
    • IV anesthetic induction agent
    • Produces respiratory depression without cardiovascular depression (good for trauma patients)
    • Cannot be antagonized
  63. Ketamine
    • Anesthetic induction agent
    • Glutamate receptor antagonist
    • "Dissociative" anesthetic, meaning it causes a different pattern on EEG
    • Does not produce respiratory or cardiovascular depression
    • Cannot be antagonized
    • Emergence delirium caused by too much
  64. Methohexital
    • IV anesthetic induction agent
    • It's an oxybarbiturate
  65. Thiopental
    Anesthetic induction agent
  66. Barbiturates
    • Used for IV induction of general anesthesia, but it is very expensive and causes lots of "hangover effects"
    • Highly lipid soluble, so has a rapid, profound effect causing unconsciousness; recovery occurs in 5-8 minutes
    • Produces marked respiratory depression and decreases sympathetic outflow from the brain
    • No antagonists exist
  67. Midazolam, diazepam, lorazepam
    • Anesthetic premedication agents
    • Benzodiazapenes
    • Highly lipid-soluble
    • IV administration can produce respiratory depression
    • Antagonized by flumazenil
    • Diazepam and lorazepam: Also used to treat status epilepticus via IV, but tolerance develops after 1-6 months
  68. Flumazenil
    • Antagonizes benzodiazepenes, to reverse the preanesthetic state; also can precipitate withdrawal in benzodiazepene- or barbiturate-dependent persons
    • Does this by blocking the GABAa receptor
  69. Amitriptyline, nortriptyline, imipramine, amoxapine
    • Tricyclic antidepressants: Nonspecific blockers of monoamine reuptake
    • All have similar efficacy
    • Takes greater than 2 weeks to see effects
    • High binding to plasma proteins
    • Slew of side effects
  70. Fluoxetine, citalopram, escitalopram, sertraline
    • SSRIs
    • All have similar efficacy with different side effect profiles
    • Fewer side effects than TCAs because SSRIs cause fewer anticholinergic effects
    • Cause neurogenesis after 2 weeks because they raise levels of BDNF (brain-derived neurotrophic factor)
    • Mood improves after 2 weeks
  71. Venlafaxine, duloxetine
    • SNRIs
    • Venlafaxine is only bound to plasma proteins 1/3rd
    • Duloxetine is highly bound to plasma proteins
    • Metabolized by liver
    • Eliminated by kidneys
    • Fewer side effects than TCAs
  72. Buproprion
    • Atypical antidepressant
    • Inhibits dopamine reuptake; useful for treating rapid-cycling bipolar disorder
  73. Nefazodone
    • Atypical antidepressant
    • Blocks reuptake of serotonin and blocks 5-HT2 receptors
  74. Mirtazapine
    • Atypical antidepressant
    • Increases NE and serotonin release by blocking alpha2 receptors
  75. Phenelzine, tranylcypromine, selegiline
    • MAOIs
    • Block MAO irreversibly
    • Therapeutic effect requires 2-4 weeks
    • Eliminated via kidneys
    • Cheese effect: Elevated tyramine levels cause elevated catecholamine levels, resulting in hypertension, cardiac arrhythmias, stroke, headache, nausea
    • Must be on restricted diet!
  76. Lithium salts
    • Treatment for bipolar disorder
    • Onset takes 3-4 weeks
    • Substitutes for sodium and produces undesirable effects
    • Very toxic; extremely low therapeutic index
    • Enhances glutamate reuptake by blocking formation of phosphatidylinositol inside the cell
    • No binding to plasma proteins because is a soluble ion
    • Eliminated by kidneys
    • Side effects: Low therapeutic index! Tremors, mental confusion, convulsions, coma, arrhythmias, teratogenic effects
  77. Dextroamphetamine
    • Stimulant: amphetamine
    • Prevents narcolepsy and treats ADHD
    • Oral administration
    • Metabolized by liver
    • Excreted by kidneys
  78. Methylphenidate
    • Stimulant: Amphetamine
    • Narcolepsy and ADHD
    • Oral administration
    • Excreted by kidneys
  79. Methamphetamine
    • Stimulant: Amphetamine
    • No clinical uses
  80. Atomoxetine
    • NE reuptake inhibitor
    • Not a psychostimulant, not habit forming, not a controlled substance
    • Used to treat ADHD
  81. Modafinil
    • Used to treat narcolepsy
    • Mechanism is unclear
  82. Bicuculline
    • GABA antagonist
    • Competitive block of GABA
    • Reduces inhibition of neuronal activity and produces convusions
  83. Picrotoxin
    • GABA Antagonist
    • Non-competitive block of GABA
    • Blocks the chloride channel
    • Reduces inhibition of neuronal activity and produces convulsions
  84. Diazepam
    • Benzodiazepine
    • Used for anxiety, withdrawal, and for muscle relaxant
    • 1 hour peak concentration; long elimination half life
  85. Lorazepam
    • Benzodiazepine
    • Used for insomnia, anxiety, muscle relaxant
    • 1 hour peak concentration; intermediate half-life
  86. Alprazolam
    • Benzodiazepine
    • Used for insomnia and anxiety
    • 1 hour peak concentration; short elimination half-life
  87. Midazolam
    • Benzodiazepene
    • Used as pre-anesthetic medication
    • 0.2 hour peak concentration; super-short elimination half-life
  88. Zolpidem, zaleplon
    • Non-benzodiazepines that work on BZ-receptors
    • Increase frequency of GABA-mediated Cl channel opening, to hyperpolarize neuron, inhibiting it
    • Induce sleep
    • Metabolized by liver to make inactive metabolites
  89. Phenobarbital
    • Barbiturate
    • Used as an anticonvulsant and antianxiety
    • Long half-life and long onset of duration [see other card]
  90. Pentobarbital
    • Barbiturate
    • Used as preoperative sedation
    • Short to intermediate onset; intermediate half-life
  91. Amobarbital, thiopental
    • Barbiturates
    • Used as preoperative sedation or anesthesia induction
    • Ultra-short onset; short half-life
  92. Propranolol, buspirone
    • Miscellaneous antianxiety drugs
    • Propranolol: Blocks beta-adrenergic receptors
    • Used for disabling situational anxiety
    • Buspirone: Partial agonist for serotonin receptor; produces only anxiolytic effects without CNS depression
    • No additive depression with ethanol
    • Onset of action is 1-3 weeks
  93. Phenytoin
    • Antiepileptic
    • Blocks voltage-gated Na channels
    • Drug of choice for initial therapy of epilepsy in adults
    • Good for partial seizures (simple and complex) and tonic-clonic; give orally
    • Also used for emergency treatment of status-epilepticus via IV
    • Can make absence seizures worse!
    • High plasma protein binding
    • Most is metabolized by liver; can become saturated and mess with other drug metabolism
    • Less than 5% is excreted by the kidneys
    • Specific side effects: Gingival hyperplasia, megaloblastic anemia, teratogenic effects
  94. Carbamazepine
    • Antiepileptic
    • Blocks voltage-gated Na channels
    • Good for partial (both simple and complex), and tonic-clonic seizures
    • Also used for trigeminal neuralgia or bipolar disorder
    • Oral administration
    • Slowly absorbed, but crosses BBB readily
    • Metabolizes the P450 enzymes in liver, but also induces them; it therefore induces self tolerance, making us increase dose after pt takes it for months
    • Drug interactions: Increases P450 system so increases metabolism of other antiepileptics (phenytoin)
    • Specific side effects: Hepatotoxicity, teratogenic effects
  95. Valproic acid
    • Antiepileptic
    • Blocks voltage-gated Na and Ca channels and facilitates GABAergic synaptic transmission
    • Good for myoclonic seizures
    • Second-line drug for tonic-clonic and absence seizures due to hepatotoxicity
    • Orally effective
    • High level of plasma protein binding
    • Metabolized by liver P450 enzymes
    • Specific side effects: Hepatotoxicity, thrombocytopenia, teratogenic effects
  96. Ethosuximide
    • Antiepileptic
    • Blocks voltage-gated T-type Ca channels in thalamic neurons to suppress rhythmic activity
    • Used to treat absence seizures
    • Well absorbed orally
    • Not bound to plasma proteins
    • Long half-life
    • Most is metabolized by liver, but some is excreted unchanged in urine
  97. Phenobarbital and primidone in epilepsy
    • Barbiturates
    • Facilitate activation of GABA receptors to increase inhibitory tone
    • Used for simple partial and recurrent tonic-clonic seizures, and febrile seizures in children
    • Specific side effects: Teratogenic effects (phenobarbital); megaloblastic anemia (primidone)
    • Primidone: Prodrug of phenobarbital
    • Well absorbed orally
    • Freely penetrates brain
    • 75% is inactivated by liver
  98. Lamotrigine
    • Antiepileptic
    • Inhibits release of glutamate (suppresses excitatory tone)
    • New class; used for treatment of simple or complex partial seizures and generalized tonic-clonic seizures
    • Metabolized by liver
    • Half-life is increased by valproic acid and decreased by carbamazepine and phenytoin
  99. Gabapentin
    • Antiepileptic
    • Blocks Ca channels and release of glutamate; enhances GABAergic synaptic transmission
    • Used to treat simple or complex partial seizures and generalized tonic-clonic seizures
    • Is not metabolized and does not induce hepatic enzymes
    • Not bound to plasmaa proteins
    • Short half-life
    • Eliminated by kidneys
    • Negligible drug interactions
  100. Pregabalin
    • Antiepileptic
    • Blocks Ca channels and release of glutamate
    • Used for simple and complex partial seizures
    • Specific side effects: Thrombocytopenia
  101. Topiramate
    • Antiepileptic
    • Blocks Na channels, increases activity of postsynaptic GABAa receptors
    • Used for simple and complex partial seizures and generalized tonic-clonic seizures
  102. Levetiracetam
    • Antiepileptic
    • Modifies glutamate and GABA release via binding to the synaptic protein SV2A
    • Used for adjuncive treatment of simple and complex partial seizures and generalized tonic-clonic seizures
  103. Chlorpromazine
    • Typical antipsychotic
    • Blocks activation of D2 receptors
    • Least potent
    • Side effects: Hyperthermia, tachycardia, urinary retention, memory impairment, blurred vision, constipation, and confusion all happen due to additional cholinergic muscarinic receptor block
    • Side effects: Vasodilation, orthostatic hypotension and light-headedness, reflex tachycardia, and sexual dysfunction all happen due to alpha-adrenergic block
    • Side effects: Sedation and weight gain; happen due to H1 histamine receptor block
    • However, this H1 block results in antiemetic effects
  104. Haloperidol, fluphenazine, thiothixene
    • Typical antipsychotics
    • Blocks activation of D2 receptors
    • Haloperidol and fluphenazine are most potent
  105. Olanzapine, risperidone, clozapine
    • Atypical antipsychotics
    • Block activation of D2 receptors and block activation of 5-HT2a receptor
  106. Apiprazole
    • Atypical antipsychotic
    • Partial D2 agonist; blocks activation of 5-HT
    • Discontinuation must be done gradually to avoid marked withdrawal or relapse
  107. L-DOPA
    • Increases dopamine synthesis
    • Parkinson's treatment
    • Has a "wearing off" effect after 3-5 years
    • Side effects: Nausea, vomiting, anorexia, cardiac arrhythmias, orthostatic hypotension; dyskinesia (abnormal involuntary movements), visual and auditory hallucinations, mood changes
  108. Carbidopa
    • Increases dopamine synthesis
    • Parkinson's treatment
    • Blocks peripheral metabolism of L-DOPA and thereby increases L-DOPA available to brain
    • Allows to reduce the dose of L-DOPA greatly
  109. Entacapone
    • Increases dopamine synthesis
    • Parkinson's treatment
    • Further decreases peripheral metabolism of L-DOPA, so is also great in combination with L-DOPA and carbidopa
  110. Selegiline
    • Decreases dopamine catabolism
    • Parkinson's treatment
    • Inhibits monoamine oxidase type B
    • Good adjunctive treatment
    • Orally active
    • Metabolized to methamphetamine and amphetamine, so causes insomnia
  111. Rasagiline
    • Decreases dopamine catabolism
    • Parkinson's treatment
    • Selective inhibitor of brain MAO type B
    • Is not metabolized to an amphetamine-like substance
  112. Bromocriptine, ropinirole, pramipexole
    • Dopamine receptor agonists
    • Parkinson's treatment
    • Are effective as monotherapy early in the disease or as an adjunct to L-DOPA later on
    • Side effects: Cardiovascular effects (arrhythmias), postural hypotension, depression, confusion, hallucinations, sleepiness, impulsivity, nausea, vomiting
    • Contraindicated in patients with heart or mental problems
  113. Apomorphine
    • Dopamine receptor agonist
    • Parkinson's treatment
    • Acute treatment of patients with advanced disease for "off" periods
    • Subcutaneous injection (NOT IV; may lead to thrombus formation and PE)
    • Side effects: Nausea, vomiting, arrhythmias, postural hypotension, hallucinations, sleepiness
  114. Benztropine, trihexyphenidyl
    • Muscarinic antagonists
    • Parkinson's treatment
    • Used to alleviate tremor and rigidity
    • In Parkinson's disease, the loss of the nigrostriatal dopamine neurons results in increased firing of striatal cholinergic interneurons and overstimulation of muscarinic receptors; these drugs block that firing
    • Side effects: Antimuscarinic effects, such as blurred vision, dry mouth, urinary retention, constipation, aggravation of glaucoma; may also produce delirium, psychosis, memory impairment
  115. Amantadine
    • Enhances dopamine release, blocks cholinergic muscarinic receptors and glutamatergic NMDA receptors
    • Parkinson's treatment
    • Alleviates bradykinesia and rigidity before initiation of L-DOPA
    • Side effects: Hallucinations and confusion, nausea, dizziness, rash of the low extremeties; special caution taken with CHD or glaucoma patients
    • It's also an antiviral drug for the treatment and prophylaxid of influenza
  116. Donepezil, galantamine, rivastigmine, tacrine
    • Acetylcholinesterase inhibitors
    • Alzheimer's treatment
    • Produce modest improvements in some patients
    • Good oral bioavailability
    • Metabolized by liver except for rivastigmine, which is metabolized by plasma cholinesterase
    • Side effects: Tremors, bradycardia, nausea/vomiting, diarrhea, anorexia
    • Tacrine can produce hepatotoxicity
  117. Memantine
    • NMDA receptor antagonist
    • Alzheimer's treatment
    • Similar to amantadine (for Parkinson's)
    • By blocking NMDA receptors, memantine protects neurons from Ca2+ overload that can lead to nuronal death (excitotoxicity)
    • Benefits are additive when given with donezepil
    • Side effects: Dizziness, headache, confusion, agitation, constipation
  118. Acetazolamide
    • Carbonic anhydrase inhibitor
    • Works in proximal tubule, stopping bicarbonate from being reabsorbed
    • Results in increased Na, K, HCO3-, and H2PO4 excretion and decreased H+
    • Potassium waster
    • Good for counteracting diuretic-induced metabolic alkalosis (since getting rid of bicarbonate)
    • It is a self-limiting diuretic (not very effective) because of TGF
    • Adverse reactions: Metabolic acidosis; allergic reactions; kidney stones; bone marrow depression
  119. Glycerin, mannitol
    • Osmotic diuretics
    • Act on the loop on Henle to wash out the medullary salt gradient by increasing renal blood flow
    • Also increase water going into blood by raising the osmolarity
    • Water efflux is also decreased in the proximal convoluted tubule due to osmotic gradient
    • Used pre- and post-op for neurosurgery to reduce brain swelling, glaucoma, acute renal failure
    • Potassium wasters
    • Adverse reactions: Hyponatremia, converting pulmonary congestion to pulmonary edema, dehydration with hyponatremia, hyperglycemia from glycerin
  120. Furosemide, bumetanide, ethacrynic acid, torsemide
    • Loop diuretics
    • - Inhibit Na/K/2Cl symporter in thick ascending limb of loop of Henle
    • - Furosemide is also a weak carbonic anhydrase inhibitor; it also acutely increases systemic venous capacitance; is glucuronidated in the kidney, not the liver
    • - All have short half-lives and have high ceilings for diuresis since they are not limited by TGF because distal segments cannot rescue Na absorption
    • - Potassium wasters
    • - Used for acute pulmonary edema and congestive heart failure; good for HTN, nephrotic syndrome, edema, and chronic renal failure
    • - Adverse reactions: Hypo-ions; arrhythmias due to potassium loss; volume depletion; metabolic alkalosis; ototoxicity
    • NSAIDs reduce diuretic response by constriction of afferent arterioles to glomerulus
  121. Hydrochlorothiazide, chlorothiazide, metolazone
    • Thiazide or thiazide-like diuretics
    • Block the Na/Cl symporter from importing in the distal convoluted tubule
    • Potassium waster
    • Medullary salt gradient is not disturbed, so water retention during dehydration is preserved
    • Used for edema, hypertension, diabetes insipidus (reduces urine volume by half! unknown reasons)
    • Adverse effects: Hypotension, hypokalemia/natremia, metabolic acidosis, hypercalcemia, hyperuricemia
    • Contraindicated with sulfonamide sensitivity
    • NSAIDs reduce diuretic response
    • Probenecid may increase effective dose
    • May decrease glucose tolerance
  122. Amiloride, triamterene
    • Inhibitors of renal Na+ channels
    • Potassium sparing
    • Result in increased excretion of sodium and chloride only
    • Strongly increases potassium reabsorption while only slightly increasing sodium excretion
    • African Americans can have a polymorphism that make these drugs really good at decreasing HTN
    • Also used as an aerosol in cystic fibrosis to clear mucous
    • Adverse reactions: Hyperkalemia resulting in cardiac arrhythmia and death, AIDS patients getting hyperkalemia, NSAIDs may decrease diuretic efficiency
    • Amiloride can be an antidiuretic too!
    • Used for lithium-induced nephrogenic diabetes insipidus by blocking uptake of lithium by Na channels in the collecting duct
  123. Spironolactone, eplerenone
    • Mineralocorticoid antagonists
    • Antagonize effects of ADH in distal convoluted tubule/collecting tubule, which results in increased secretion of sodium and chloride only
    • Efficacy depends upon how much water retention is due to ADH
    • These are the only diuretics that exert their influence from the "blood side"
    • Potassium sparing
    • Used for potassium sparing action, treatment of hyperaldosteronism, and treatment of ascites and edema with cirrhosis
    • Adverse effects: Hyperkalemia; there is some cross-reactivity with other steroid receptors, and can cause feminization or menstrual irregularities; diarrhea, gastritis, gastric bleeding, rash, CNS symptoms
    • NSAIDs may decrease diuretic efficiency
  124. Vasopressin
    • Antidiuretic drug
    • Used for diabetes insipidus
    • Adverse effects: Coronary artery constriction, water intoxication
  125. Chlorpropamide
    • Antidiuretic drug
    • Used to be used for Type II diabetes, but increases ADH secretion
  126. Allopurinol
    • Inhibits xanthine oxidase
    • Gout treatment
  127. Colchicine
    • Reduces neutrophil activity
    • Reduces gout inflammation
  128. Probenecid
    • Uricosuric agent
    • Decreases excretion of uric acid, posibly by blocking organic acid transport into the tubular lumen
    • Once in the lumen, urate reabsorption is inhibited resulting in increased urate excretion
    • I think that uric acid goes into the tubule in the glomerulus, then probenecid stops it from moving in/out, causing more to be excreted
    • Adverse effects: Risk for renal stones; interferes with renal excretion of MANY drugs; interferes with diuretics by preventing transport into the tubular lumen
  129. Benzocaine
    • Topical anesthetic
    • Ester
    • Causes methemaglobinemia, which reduces hemaglobin oxygen-carrying capacity
  130. Lidocaine
    • Local anesthetic
    • Amide
    • Used for infiltration anesthesia
    • Good for starting IVs and for minor surgery
  131. Cocaine
    • Topical anesthetic
    • Ester
    • Vasoconstrictor
    • Toxicity: Myocardial ischemia, myocardial infarction, arrhythmias, seizures, hypertension, death
  132. Ropivacaine
    • Less toxic with similar potency to bupivacaine
    • (Very potent)
Card Set:
Pharmacology Exam 2 - Drugs Only
2013-10-17 06:23:28
Pharmacology Carver College Medicine Medical School

Pharm drugs at CCOM for second exam
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