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Drugs > Musculo/Neuro/Onco > Flashcards

Musculo/Neuro/Onco Flashcards

1
Q

<p>Aspirin</p>

A

<p>1) Use: Low dose (s syndrome in children with viral infections.
4) Fun Facts</p>

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2
Q

<p class=”large” style=”text-align:center”;>NSAIDs (Ibuprofen, naproxen, indomethacin, ketorolac)</p>

A

<p class=”large” style=”text-align:center”;>1) Use: Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.

2) Class/MOA: Reversibly inhibits cycooxygenase (both COX-1 and COX-2). Block prostaglandin synthesis.
3) Side effects/ADEs: Renal damage, fluid retention, aplastic anemia, GI distress, ulcers.
4) Fun Facts</p>

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3
Q

<p>COX-2 Inhibitor (celecoxib)</p>

A

<p>1) Use: Rheumatoid and osteoarthritis; patients with gastritis or ulcers.

2) Class/MOA: Reversibly inhibits the cycooxygenase (COX) isoform 2, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain; spares COX-1, which maintains the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the GI lining.
3) Side effects/ADEs: Increased risk of thrombosis. Sulfa allergy. Less toxicity to GI mucosa (lower incidence of ulcers, bleeding than NSAIDs).
4) Fun Facts</p>

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3
Q

Timolol, betazolol, carteolol (in neurology)

A

1) Use: Glaucoma
2) Class/MOA: Beta blocker, decreases aqueous humor secretion
3) Side effects/ADEs: no pupillary or vision changes
4) Fun Facts

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3
Q

Cytarabine (arabinofuranosyl cytidine)

A

1) leukemia, lymphoma
2) pyrimidine analog –> inhibit DNA polymerase
3) leukopenia, thrombocytopenia, megaloblastic anemia
4) S-phase specific

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5
Q

<p>Bisphosphonates (Etidronate, pmidronate, alendronate, risedronate, zoledronate (IV))</p>

A

<p>1) Use: Maligancy associated hypercalcemia, Paget's diseases of the bone, postmenopausal osteoproposis.

2) Class/MOA: Inhibit osteoclastic activity; reduces both formation and resorption of hydroxyapatite.
3) Side effects/ADEs: Corrosive esophagitis (except zoledronate), nausea, diarrhea, osteonecrosis of the jaw.
4) Fun Facts</p>

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6
Q

<p>Chronic Gout Drug (Probenecid)</p>

A

<p>1) Use: Chronic Gout (urate lowering therapy)

2) Class/MOA: Inhibits resorption of uric acid in the PCT (also inhibits secretion of penicillin)
3) Side effects/ADEs:
4) Fun Facts</p>

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6
Q

<p>Chronic Gout Drug (Probenecid)</p>

A

<p>1) Use: Chronic Gout (urate lowering therapy)

2) Class/MOA: Inhibits resorption of uric acid in the PCT (also inhibits secretion of penicillin)
3) Side effects/ADEs:
4) Fun Facts</p>

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7
Q

<p class=”large” style=”text-align:center”;>Chronic Gout Drug (Allopurinol)</p>

A

<p class=”large” style=”text-align:center”;>1) Use: Chronic Gout (urate lowering therapy)

2) Class/MOA: Inhibits xanthine oxidase, decreases conversion of xanthine to uric acid. Also used in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy. Increases concentration of azathioprine and 6-MP (both normally metabolized by xanthine oxidase).
3) Side effects/ADEs: Do not dive salicylates; all but the highest dosages depress uric acid clearance. Even high doses (5-6 g/day) have only minor uricosuric activity.
4) Fun Facts</p>

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8
Q

<p>Chronic Gout Drug (Febuxostat)</p>

A

<p>1) Use: Chronic Gout (urate lowering therapy)

2) Class/MOA: Inhibits xanthine oxidase
3) Side effects/ADEs:
4) Fun Facts</p>

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8
Q

<p>Chronic Gout Drug (Febuxostat)</p>

A

<p>1) Use: Chronic Gout (urate lowering therapy)

2) Class/MOA: Inhibits xanthine oxidase
3) Side effects/ADEs:
4) Fun Facts</p>

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8
Q

Doxorubicin (Adriamycin)

A

1) solid tumors, leukemias, lymphomas
2) makes ROS; non-covalently intercalate in DNA –> breaks DNA –> decr replication
3) cardiotoxicity* (dilated cardiomyopathy; use dexrazoxane, Fe chelator, to prevent), myelosuppression, alopecia; toxic to tissues following extravasation
4) N/A

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9
Q

<p class=”large” style=”text-align:center”;>Acute Gout Drug (Colchicine)</p>

A

<p class=”large” style=”text-align:center”;>1) Use: Acute Gout (urate lowering therapy)

2) Class/MOA: Binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and deregulation.
3) Side effects/ADEs: GI side effects, especially if given orally (note: Indomethacin is less toxic, also used in acute gout).
4) Fun Facts</p>

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11
Q

<p>The alpha inhibitors (Entanercept)</p>

A

<p>1) Use: Rheumatoid arthritis, psoriasis, ankylosing spondylitis.

2) Class/MOA: Recombinant form of human TNF receptor that binds TNF.
3) Side effects/ADEs: All TNF alpha inhibitors predispose to infection including reactivation of latent TB since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbe.
4) Fun Facts: EntanerCEPT is a TNF decoy reCEPTor. </p>

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11
Q

Cyclophosphamide

A

1) solid tumors, leukemia, lymphoma, some brain CAs
2) alkylating agent: covalently X-link DNA at guanine N-7
3) myelosuppression; hemorrhagic cystitis (partly prevent w/ mesna, thiol grp of mesna binds toxic metabolite)
4) need liver bioactivation

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12
Q

<p class=”large” style=”text-align:center”;>The alpha inhibitors (Infliximab)</p>

A

<p class=”large” style=”text-align:center”;>1) Use: Chron’s disease, rheumatoid arthritis, ankylosing spondylitis.

2) Class/MOA: Anti-TNF antibody
3) Side effects/ADEs: All TNF alpha inhibitors predispose to infection including reactivation of latent TB since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbe.
4) Fun Facts INFLIimab INFLIX pain on TNF</p>

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13
Q

<p>The alpha inhibitors (Adalimumab)</p>

A

<p>1) Use: Psoriasis, rheumatoid arthritis, ankylosing spondylitis

2) Class/MOA: Anti-TNF antibody
3) Side effects/ADEs: All TNF alpha inhibitors predispose to infection including reactivation of latent TB since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbe.
4) Fun Facts</p>

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14
Q

Epinephrine (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: alpha agonist, decreases aqueous humor synthesis due to vasoconstriction
3) Side effects/ADEs: Mydriasis, stinging: do not use in closed glaucoma
4) Fun Facts

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14
Q

Epinephrine (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: alpha agonist, decreases aqueous humor synthesis due to vasoconstriction
3) Side effects/ADEs: Mydriasis, stinging: do not use in closed glaucoma
4) Fun Facts

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14
Q

Lomustine

A

1) brain tumors (incl glioblastoma multiforme)
2) alkylating agent: nitrosourea
3) CNS toxicity: dizziness, ataxia
4) needs bioactivation; X’s BBB –> CNS

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15
Q

Brimonide (in neurology)

A

1) Use: Glaucoma
2) Class/MOA: Alpha agonist, decreases aqueous humor synthesis
3) Side effects/ADEs: no pupillary of vision changes
4) Fun Facts

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15
Q

Brimonide (in neurology)

A

1) Use: Glaucoma
2) Class/MOA: Alpha agonist, decreases aqueous humor synthesis
3) Side effects/ADEs: no pupillary of vision changes
4) Fun Facts

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16
Q

Streptozocin

A

1) brain tumors (incl glioblastoma multiforme)
2) alkylating agent: nitrosourea
3) CNS toxicity: dizziness, ataxia
4) needs bioactivation; X’s BBB –> CNS

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17
Q

Acetazolamide (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: Diuretic, decreases aqueous humor secretion due to decreased HCO3- (via inhibition of carbonic anhydrase)
3) Side effects/ADEs: No pupillary or vision changes
4) Fun Facts

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17
Q

Acetazolamide (in Neurology)

A

1) Use: Glaucoma
2) Class/MOA: Diuretic, decreases aqueous humor secretion due to decreased HCO3- (via inhibition of carbonic anhydrase)
3) Side effects/ADEs: No pupillary or vision changes
4) Fun Facts

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18
Q

Direct Cholinomimetics (pilocarpine, carbachol) or Indirect Cholinomimetics (physostigmine, ecchothiophate)

A

1) Use: Glaucoma
2) Class/MOA: Cholinomimetics, increases the outflow of the aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies, very effective at opening meshwork into canal of Schlemm
3) Side effects/ADEs: Miosis, cyclospasm
4) Fun Facts

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18
Q

Direct Cholinomimetics (pilocarpine, carbachol) or Indirect Cholinomimetics (physostigmine, ecchothiophate)

A

1) Use: Glaucoma
2) Class/MOA: Cholinomimetics, increases the outflow of the aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies, very effective at opening meshwork into canal of Schlemm
3) Side effects/ADEs: Miosis, cyclospasm
4) Fun Facts

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20
Q

Opiod Analgesics (morphine, fentanyl, codeine, heroine, methandone, meperidine, dexomethophan diphenoxylate)

A

1) Use: Pain, cough suppression (dextromethophran), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance program for addicts (methadone).
2) Class/MOA: Acts as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappy = dynorphin) to modulate synaptic transmission - open K+ channels, close Ca2+ channels = decrease in synaptic transmission. Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Side effects/ADEs: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with nalazone or naltrexone (opiod receptor antagonist).
4) Fun Facts

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20
Q

Opiod Analgesics (morphine, fentanyl, codeine, heroine, methandone, meperidine, dexomethophan diphenoxylate)

A

1) Use: Pain, cough suppression (dextromethophran), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance program for addicts (methadone).
2) Class/MOA: Acts as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappy = dynorphin) to modulate synaptic transmission - open K+ channels, close Ca2+ channels = decrease in synaptic transmission. Inhibit release of ACh, NE, 5-HT, glutamate, substance P.
3) Side effects/ADEs: Addiction, respiratory depression, constipation, miosis (pinpoint pupils), addictive CNS depression with other drugs. Tolerance does not develop with miosis and constipation. Toxicity treated with nalazone or naltrexone (opiod receptor antagonist).
4) Fun Facts

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20
Q

Paclitaxel

A

1) ovarian + breast carcinomas
2) microtubule inhibitor: hyperstabilizes polymerized microtubules in M phase so mitotic spindle can’t break down (blocks anaphase)
3) myelosuppression, hypersensitivity
4) N/A

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22
Q

Tramadol

A

1) Use: Chronic pain
2) Class/MOA: Very weak opiod agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters - “tram it all” in)
3) Side effects/ADEs: Similar to opiods. Decreases seizure threshold.
4) Fun Facts

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22
Q

Tramadol

A

1) Use: Chronic pain
2) Class/MOA: Very weak opiod agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters - “tram it all” in)
3) Side effects/ADEs: Similar to opiods. Decreases seizure threshold.
4) Fun Facts

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23
Q

Etoposide

A

1) solid tumors, leukemias, lymphomas
2) topo II inhibitor –> incr DNA degradation
3) myelosuppression, GI irritation, alopecia
4) N/A

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24
Q

Carbamazepine

A

1) Use: Epilepsy drug, used in: first line in partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Increases Na+ channel inactivation
3) Side effects/ADEs: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytrochrome P-450, SIADH, Steven’s-Johnson syndrome
4) Fun Facts: fist line for trigeminal neuralgia

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24
Q

Carbamazepine

A

1) Use: Epilepsy drug, used in: first line in partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Increases Na+ channel inactivation
3) Side effects/ADEs: Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytrochrome P-450, SIADH, Steven’s-Johnson syndrome
4) Fun Facts: fist line for trigeminal neuralgia

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26
Q

Topiramate

A

1) Use: Epilepsy drug, used in: partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Blocks Na+ channels, increases GABA action
3) Side effects/ADEs: Sedation, mental dulling, kidney stones, weight loss.
4) Fun Facts

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26
Q

Topiramate

A

1) Use: Epilepsy drug, used in: partial simple, partial complex & generalized tonic clonic seizures
2) Class/MOA: Blocks Na+ channels, increases GABA action
3) Side effects/ADEs: Sedation, mental dulling, kidney stones, weight loss.
4) Fun Facts

26
Q

Prednisone

A

1) CA chemotx: CLL, non-Hodgkin’s lymphomas; immunosuppressant (autoimmune dz)
2) glucocorticoid; may trigger apoptosis; may work on non-dividing cells
3) Cushing-like sx’s; immunosuppression, cataracts, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis
4) N/A

28
Q

Valproid acid

A

1) Use: Epilepsy drug, used in: partial simple, partial complex, 1st line in tonic clonic generalized seizures and in absence generalized seizures.
2) Class/MOA: Increases Na+ channel inactivation, increases GABA concentration
3) Side effects/ADEs: GI distress, rare but fatal hepatotoxicity (measure LFT), neural tube defects in fetus (spinal bifida), tremor, weight gain. Contraindicated in pregnancy.
4) Fun Facts: Also used for myoclonic seizures

28
Q

Valproid acid

A

1) Use: Epilepsy drug, used in: partial simple, partial complex, 1st line in tonic clonic generalized seizures and in absence generalized seizures.
2) Class/MOA: Increases Na+ channel inactivation, increases GABA concentration
3) Side effects/ADEs: GI distress, rare but fatal hepatotoxicity (measure LFT), neural tube defects in fetus (spinal bifida), tremor, weight gain. Contraindicated in pregnancy.
4) Fun Facts: Also used for myoclonic seizures

30
Q

Trastuzumab (Herceptin)

A

1) HER-2 (+) breast CA
2) monoclonal ab against HER-2 (c-erbB2), a tyrosine kinase –> kill breast CA cells taht overexpress HER-2 (ab-dependent cytotoxicity)
3) cardiotoxicity
4) N/A

31
Q

Benzodiazepines for neurological problems (diazepam, lorazepam, triazolam, temazepam, oxzepam, midazolam, chlodiazepoxide, alprazolam))

A

1) Use: anxiety, spacticity, status epileptics (lorazepam and diazepam), detoxification (especially in alcohol DTs-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
2) Class/MOA: Facilitate GABAA action by increasing frequency of Cl- channel opening, decreasing REM sleep. Most have long half-lives and active metabolites. FREnzodiazepines (Increase FREquency), short acting = TOM thumb (Triazolam, Oxzepam, Midazolam … also has the highest addictive potential). Benzos, barbs, and EtOH all bind GABA(A)-R which is a ligand-gated chloride channel.
3) Side effects/ADEs: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
4) Fun Facts: treat overdose with flumazenil (competitive antagonist at GABA benxodiazepine receptor)

31
Q

Benzodiazepines for neurological problems (diazepam, lorazepam, triazolam, temazepam, oxzepam, midazolam, chlodiazepoxide, alprazolam))

A

1) Use: anxiety, spacticity, status epileptics (lorazepam and diazepam), detoxification (especially in alcohol DTs-DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)
2) Class/MOA: Facilitate GABAA action by increasing frequency of Cl- channel opening, decreasing REM sleep. Most have long half-lives and active metabolites. FREnzodiazepines (Increase FREquency), short acting = TOM thumb (Triazolam, Oxzepam, Midazolam … also has the highest addictive potential). Benzos, barbs, and EtOH all bind GABA(A)-R which is a ligand-gated chloride channel.
3) Side effects/ADEs: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates.
4) Fun Facts: treat overdose with flumazenil (competitive antagonist at GABA benxodiazepine receptor)

33
Q

Vigabatrin

A

1) Use: epilepsy drug, used in: partial simple and partial complex seizures
2) Class/MOA: Irreversibly inhibits GABA transaminase - increases GABA
3) Side effects/ADEs:
4) Fun Facts

33
Q

Vigabatrin

A

1) Use: epilepsy drug, used in: partial simple and partial complex seizures
2) Class/MOA: Irreversibly inhibits GABA transaminase - increases GABA
3) Side effects/ADEs:
4) Fun Facts

35
Q

Barbiturates (Phenobarbital, Phenobarbital, thiopental, secobarbital)

A

1) Use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
2) Class/MOA: facilitate GABAA action by increasing duration of Cl- channel opening, thus decreasing neuron firing (barbiDURATe - increase DURATion).
3) Side effects/ADEs: dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytrochrome P-450)
4) Fun Facts: treat overdose with symptom management (assist respiration, increase blood pressure). Contraindicated in porphyria.

35
Q

Barbiturates (Phenobarbital, Phenobarbital, thiopental, secobarbital)

A

1) Use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
2) Class/MOA: facilitate GABAA action by increasing duration of Cl- channel opening, thus decreasing neuron firing (barbiDURATe - increase DURATion).
3) Side effects/ADEs: dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytrochrome P-450)
4) Fun Facts: treat overdose with symptom management (assist respiration, increase blood pressure). Contraindicated in porphyria.

36
Q

Nonbenzodiazepine hypnotics (zolpidem aka ambien, zaleplon, eszopiclone)

A

1) Use: Insomnia
2) Class/MOA: act via the BZI receptor subtype and are reversed by flumazenil
3) Side effects/ADEs: Atazia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnesic effects. Lower dependence risk than benzodiazepines.
4) Fun Facts

37
Q

Selegiline

A

1) Use: Adjunctive agent to L-dopa in treatment of Parkinson’s disease.
2) Class/MOA: prevent dopamine breakdown, selective MAO type B inhibitor, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine.
3) Side effects/ADEs: may enhance adverse effects of L-dopa
4) Fun Facts

38
Q

Intravenous anesthetic: Barbiturate (thiopental)

A

1) Use & Effects: intravenous anesthetic, used for induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (I.e. skeletal muscle) and fat. Decrease in cerebral blood flow.
2) Class/MOA: high potency, high lipid solubility, rapid entry into the brain
3) Side effects/ADEs:
4) Fun Facts:

39
Q

Benztropine

A

1) Use:
2) Class/MOA: Curb excess cholinergic activity, antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia
3) Side effects/ADEs:
4) Fun Facts: Park your Mercedes-Benz

40
Q

Intravenous Anesthetic: Arylcyclohexylamines (Ketamine)

A

1) Use: intravenous anesthetic
2) Class/MOA: PCP analogs that act as dissociate anesthetics, blocks MNDA receptors.
3) Side effects/ADEs: cardiovascular stimulant, causes disorientation, hallucination and bad dreams, increases cerebral blood flow.
4) Fun Facts

41
Q

Donepezil, falantamine, rivastigmine

A

1) Use: Alzheimer’s drug
2) Class/MOA: acetylcholinesterase inhibitor
3) Side effects/ADEs: Nausea, dizziness, insomnia
4) Fun Facts

42
Q

Intravenous Anesthetics: Propofol

A

1) Use: rapid anesthesia induction and short procedures.
2) Class/MOA: Potentates GABAA receptors.
3) Side effects/ADEs: Less postoperative nausea than thiopental.
4) Fun Facts: Not recommended for home use by pop stars

44
Q

Neuromuscular Blocking Drugs, Depolarizing (Succynlcholine)

A

1) Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
2) Class/MOA:
3) Side effects/ADEs: hypercalcemia and hyperkalemia
4) Fun Facts: for reversal of blockage: Phase I) prolonged depolarization: no antidote. Block potential by cholinesterase inhibitors. Phase II) repolarized by blocked: antidote consists of cholinesterase inhibitors (e.g. neostigmine).

44
Q

Neuromuscular Blocking Drugs, Depolarizing (Succynlcholine)

A

1) Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
2) Class/MOA:
3) Side effects/ADEs: hypercalcemia and hyperkalemia
4) Fun Facts: for reversal of blockage: Phase I) prolonged depolarization: no antidote. Block potential by cholinesterase inhibitors. Phase II) repolarized by blocked: antidote consists of cholinesterase inhibitors (e.g. neostigmine).

46
Q

Dantrolene

A

1) Use: used in the treatment of malignant hypertension, which is caused by inhalation anesthetics (except N2)) and succinylcholine. Also used to treat neuropleptic malignant syndrome (a toxicity of antipsychotic drugs)
2) Class/MOA: Prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle
3) Side effects/ADEs:
4) Fun Facts

48
Q

Amatadine

A

1) Use: Parkinson’s, also used as a antiviral against influenza A and rubella; toxicity = ataxia
2) Class/MOA: Increase dopamine
3) Side effects/ADEs:
4) Fun Facts

48
Q

Amatadine

A

1) Use: Parkinson’s, also used as a antiviral against influenza A and rubella; toxicity = ataxia
2) Class/MOA: Increase dopamine
3) Side effects/ADEs:
4) Fun Facts

49
Q

L-dopa/carbidopa

A

1) Use: Parkinson’s
2) Class/MOA: increase dopamine, converted to dopamine in the CNS. Unlike dopamine, L-dopa can cross the blood brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.
3) Side effects/ADEs: Arrhythmias from peripheral conversion to dopamine. Long term use can cause dysskinesia following administration, akinesia between doses. Carbidopa, a peripheral decarboxylase inhibitor is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects.
4) Fun Facts

51
Q

Entacapone, tolcaptone

A

1) Use: Parkinson’s
2) Class/MOA: prevent dopamine breakdown, COMT inhibitor - prevent L-dopa degradation, thereby increasing dopamine availability
3) Side effects/ADEs:
4) Fun Facts

51
Q

Entacapone, tolcaptone

A

1) Use: Parkinson’s
2) Class/MOA: prevent dopamine breakdown, COMT inhibitor - prevent L-dopa degradation, thereby increasing dopamine availability
3) Side effects/ADEs:
4) Fun Facts

53
Q

Memantine

A

1) Use: Alzheimer’s drug
2) Class/MOA: NMDA receptor antagonist, helps prevent excitotocity (mediated by Ca2+)
3) Side effects/ADEs: Dizziness, confusion, hallucinations
4) Fun Facts

55
Q

Reserpine + tetrabenazine

A

1) Use: Huntington’s drug
2) Class/MOA: amine depleting
3) Side effects/ADEs:
4) Fun Facts

55
Q

Reserpine + tetrabenazine

A

1) Use: Huntington’s drug
2) Class/MOA: amine depleting
3) Side effects/ADEs:
4) Fun Facts

57
Q

Sumatriptan

A

1) Use: Acute migraine, cluster headache attacks.
2) Class/MOA: 5-HT 1B/1D agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-lifes angina), mild tingling.
4) Fun Facts: A SUMo wrestler TRIPs ANd falls on your head!

58
Q

Methotrexate (MTX)

A

1) CA: leukemia, lymphoma, choriocarcinoma, sarcoma; non-CA: abortion, ectopic preg, rheumatoid arthritis, psoriasis
2) folate analog: inhibits DHFR –> decr dTMP –> decr DNA + protein syn
3) myelosuppression (reverse w/ leucovorin); macrovesicular fatty liver change; mucositis; teratogenic
4) S-phase specific

59
Q

5-fluorouracil (5-FU)

A

1) colon CA, basal cell carcinoma (topical)
2) pyrimidine analog bioactivated to 5F-dUMP (covalently complexes folate) –> complex inhibits thymidylate synthase –> decr dTMP –> decr DNA + protein syn
3) myelosuppression (not reversible w/ leucovorin); OD rescue w/ thymidine; photosensitivity
4) S-phase specific

61
Q

Azathioprine

A

1) leukemias
2) purine (thiol) analog –> decr de novo purine syn
3) BM, GI, liver; metabolized by xanthine oxidase so incr toxicity w/ allopurinol
4) S-phase specific; activated by HGPRT

62
Q

6-mercaptopurine (6-MP)

A

1) leukemias
2) purine (thiol) analog –> decr de novo purine syn
3) BM, GI, liver; metabolized by xanthine oxidase so incr toxicity w/ allopurinol
4) S-phase specific; activated by HGPRT

63
Q

6-thioguanine (6-TG)

A

1) leukemias
2) purine (thiol) analog –> decr de novo purine syn
3) BM, GI, liver; metabolized by xanthine oxidase so incr toxicity w/ allopurinol
4) S-phase specific; activated by HGPRT

64
Q

Dactinomycin (actinomycin D)

A

1) Wilm’s tumor, Ewin’s sarcoma, rhabdomyosarcoma; peds tumors
2) intercalates in DNA
3) myelosuppression
4) N/A

66
Q

Daunorubicin

A

1) solid tumors, leukemias, lymphomas
2) makes ROS; non-covalently intercalate in DNA –> breaks DNA –> decr replication
3) cardiotoxicity* (dilated cardiomyopathy; use dexrazoxane, Fe chelator, to prevent), myelosuppression, alopecia; toxic to tissues following extravasation
4) N/A

67
Q

Bleomycin

A

1) testicular CA, Hodgkin’s lymphoma
2) ROS formation –> causes breaks in DNA strands
3) pulm fibrosis*, skin changes; minimal myelosuppression
4) N/A

69
Q

Ifosfamide

A

1) solid tumors, leukemia, lymphoma, some brain CAs
2) alkylating agent: covalently X-link DNA at guanine N-7
3) myelosuppression; hemorrhagic cystitis (partly prevent w/ mesna, thiol grp of mesna binds toxic metabolite)
4) need liver bioactivation

70
Q

Carmustine

A

1) brain tumors (incl glioblastoma multiforme)
2) alkylating agent: nitrosourea
3) CNS toxicity: dizziness, ataxia
4) needs bioactivation; X’s BBB –> CNS

72
Q

Semustine

A

1) brain tumors (incl glioblastoma multiforme)
2) alkylating agent: nitrosourea
3) CNS toxicity: dizziness, ataxia
4) needs bioactivation; X’s BBB –> CNS

74
Q

Busulfan

A

1) CML; also to ablate BM before BMT
2) alkylating agent
3) pulm fibrosis*; hyperpigmentation
4) N/A

75
Q

Vincristine

A

1) solid tumors, leukemias, lymphomas
2) microtubule inhibitor: alkaloid that binds to tubulin in M phase + blocks polymerization so mitotic spindle can’t form
3) neurotoxicity: areflexia, periph neuritis; paralytic ileus
4) N/A

76
Q

Vinblastine

A

1) solid tumors, leukemias, lymphomas
2) microtubule inhibitor: alkaloid that binds to tubulin in M phase + blocks polymerization so mitotic spindle can’t form
3) BM suppression (VinBLASTine BLASTS Bone Marrow)
4) N/A

78
Q

Cisplatin

A

1) testicular, bladder, ovary, lung carcinomas
2) X-links DNA
3) nephrotoxicity (prevent w/ amifostine, ROS scavenger), acoustic nerve damage, chloride diuresis
4) N/A

79
Q

Carboplatin

A

1) testicular, bladder, ovary, lung carcinomas
2) X-links DNA
3) nephrotoxicity (prevent w/ amifostine, ROS scavenger), acoustic nerve damage, chloride diuresis
4) N/A

81
Q

Teniposide

A

1) solid tumors, leukemias, lymphomas
2) topo II inhibitor –> incr DNA degradation
3) myelosuppression, GI irritation, alopecia
4) N/A

82
Q

Hydroxyurea

A

1) melanoma, CML, sickle cell dz (incr HbF)
2) inhibits ribonucleotide reductase –> decr DNA syn (S-phase specific)
3) BM suppression, upset GI
4) N/A

84
Q

Prednisolone

A

1) CA chemotx: CLL, non-Hodgkin’s lymphomas; immunosuppressant (autoimmune dz)
2) glucocorticoid; may trigger apoptosis; may work on non-dividing cells
3) Cushing-like sx’s; immunosuppression, cataracts, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis
4) N/A

85
Q

Tamoxifen

A

1) breast CA tx + prophylaxis; prevent osteoporosis
2) SERM: R antagonist in breast + agonist in bone; block estrogen binding to ER+ cells
3) partial agonist in endometrium –> incr endometrial CA risk; “hot falshes”
4) compare toxicity to raloxifene

86
Q

Raloxifene

A

1) breast CA tx + prophylaxis; prevent osteoporosis
2) SERM: R antagonist in breast + agonist in bone; block estrogen binding to ER+ cells
3) no incr in endometrial carcinoma b/c it’s an endometrial antagonist
4) compare toxicity to tamoxifen

88
Q

Imatinib (Gleevec)

A

1) CML, GI stromal tumors
2) Ph chr bcr-abl tyroxine kinase inhibitor
3) fluid retention
4) N/A

89
Q

Rituximab

A

1) non-Hodgkin’s lymphoma, rheumatoid arthritis (w/ MTX)
2) monoclonal ab against CD20 (found on most B-cell neoplasms)
3) N/A
4) N/A

90
Q

Vemurafenib

A

1) metastatic melanoma
2) small molec inhibitor of B-Raf kinases that have V600E mute
3) N/A
4) N/A

91
Q

Bevacizumab

A

1) solid tumors
2) monoclonal ab against VEGF –> inhibits angiogenesis
3) N/A
4) N/A

Drugs (11 decks)

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