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241 Cards in this Set
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what classification is: - Amobarbital - Aprobarbital - Butabarbital - Pentobarbital - Phenobarbital - Secobarbital |
Barbituates |
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What classification is: - Estazolam - Flurazepam - Quazepam - Temazepam - Triazolam - Diazopam (valium) |
Benzodiazepines |
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Characteristics of Barbituates |
- strong sedatives - Low TI - addictive - Used for anxiety in the past |
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Characteristics of Benzodiazepines |
- Less addictive than Barbituates, but still habit forming - lipid-like, can pass BBB - easily absorbed in intestines - can be long lasting, short lasting and in between |
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effects of long lasting benzodiazepines? |
- protects against seizures, anxiety - metabolized by liver into active intermediate chemical |
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effects of short lasting benzodiazepines |
sedative |
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Barbituate effect on GABA |
GABA Agonist |
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Benzodiazepines effect on GABA |
GABA Potentiator |
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What does a GABA potentiator need |
- needs existing GABA |
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Classification of: - Zolpidem - Zaleplon - Chloral hydrate - Ethchlorvynol - Glutethimide |
Sedative - Hypnotic drugs - GABA receptor Agonists |
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Classification of: - Alprazolam - Chlordiazepoxide - Clonazepam - Clorazepate - Diazepam - Lorazepam |
Benzodizepine anti anxiety drugs |
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what is Buspirone (BuSpar) |
- anti anxiety - Serotonin (5-HT1A) receptor agonist - no sedation - no tolerance or dependence potential |
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What is Propanolol? |
- Beta Blocker - reduces situational anxiety by preventing increased HR and BP |
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What is Paroxetine and Venlafaxine? |
- SSRI anti depressent
- effective against anxiety w/out sedation or dependence |
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characteristics of Zolpidem (ambien) and Zaleplon (Sonata) |
- sedative hypontic (new) - NOT A BZP, but bind to GABA receptors - less problems with rebound insomnia |
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what is rebound insomnia |
when brain tries to activate itself in presence of sedative - increased anxiety |
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Eszopiclone (Lunesta) |
- Sedative Hypnotic - Non BZP - binds to GABA receptors at/near BZP sites |
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Ramelteon (Rozeram) |
Sedative-hypnotic Melatonin receptor agonist |
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drawbacks of BuSpar? |
slow onset, moderate efficacy |
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what secondary use do antidepressants have? |
axiolytic bc pt. often have anxiety with depression - fewer side effects and less addictive |
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adverse effects of sedative hypnotics and anti-anxiety drugs? |
- residual hangover effects - anterograde amnesia - rebound effect - tolerance and dependence (barbituates) |
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Rehab concerns of sed-hyp. |
- they treat symptoms, not cause
- trade off |
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what happens in a synapse when it is overstimulated |
immediate - receptors inactivate (proteins uncouple) long term - receptors are internalized |
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what is depression? |
incapacitating sadness - most common mental illness |
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what is the current theory on cause of depression? |
caused by defect in CNS biogenic Amines (NE/Dopamine/Serotonin) |
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what is the drug strategy of treating depression? |
increase/prolong effects of amine transmitters |
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what are the types of antidepressants? |
- tricyclics - MAO (Monoamine oxidase) inhibitors - 2nd Generation drugs |
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What are the mechanisms in which Antidepressants prolong amine NT effects? |
- inhibiting NT reuptake (tricyclics, 2G) - decreasing NT breakdown (MAO inhibitors) |
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classification of: - Amitriptyline - Amozapine - Clomipramine - Desipramine - Doxepin - Imipramine - Nortriptyline - Protriptyline |
Tricyclics |
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Classification of: - isocarboxazid - Phenelzine - Tranylcypromie - Selegiline |
MAO inhibitors |
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Classification of: - Escitalopram - Sertraline - Mirtazapine - Venlafaxine - Bupropion - Citalopram - Trazodone - Flucoxamine |
2G agents |
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classification of: - Citlopram (Celexa) - Excitalopram (Lexapro) - Fluoxetine (Prozac) - Fluvoxamine (Luvox) - Paroxetine (Paxil) - Sertraline (Zoloft) |
Selective Serotonin Reuptake inhibitors |
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Classification of: -Amitriptyline (Elavil) - Amoxipin (Asendin) - Desipramine (Norapramin) - Doxepin (Sinequan) - Nortriptyline (Pamelor) |
Tricyclics |
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Classification of: - Isocarboxazid (Marplan) - PHenelizine (nardil) - Tanylcypromine (Parnate) |
MAO Inhibitors |
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What are some MAO inhibitors being used for now? |
parkinson's |
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what is one of the effects of SSRI's |
overstim effects because serotonin stays in synapse |
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what are tricyclics used for? |
neurogenic pain |
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What are the types of 2G agents? |
- nonselective - SSRI - Serotonin-NE selective |
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Adverse effects of Tricyclics and MAO inhibitors? |
- anticholinergic effects - orthostatic hypotension - Sedation |
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what are adverse effects of 2G SSRI's |
- better tolerated, but some GI problems (nausea) |
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Rehab concerns of antidepressants? |
- Time lag before beneficial effects - Chance of increased depression during initial treatment - Need to recognize/acknowledge mood changes |
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Classic treatment of bipolar syndrome? |
lithium |
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Antidepressant effects on depression severity? |
work better than placebo in severe depression but about the same in mild depression |
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what is the issue with treating bipolar disorder with lithium? |
becomes toxic as it accumulates |
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effects of mild lithium toxicity |
- metallic taste - fine tremor - nausea - weakness |
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effects of moderate lithium toxicity |
- vomiting - diarrhea - increased tremor - dizziness - incoordination - blurred vision |
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effects of severe lithium toxicity |
- confusion/hallucinations - nystagmus - dysarthria - fasciculations |
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Other drugs besides lithium helpful for bipolar? |
- antipsychotic (DA receptor antagonists) - Antiseizure drugs |
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Cause of psychosis |
increased dopamine activity in specific CNS Pathways |
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what do antipsychotics do? |
block CNS dopamine receptors |
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what are the types of antipsychotics? |
- traditional - atypical |
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why are atypical antipsychotics generally preferred? |
fewer/milder side effects |
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classification of: - chlorpomazine (Thorazine) - Haloperidol (Haldol) - Fluphenazine |
Tradtional antipsychotics
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classification of: Clozapine (clozaril) Risperidone (risperdal) Olanzapine (Zyprexa) Quetiapine (Seroquel) Aripiprazole (abilify) |
Atypical antipsychotics |
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MOA for atypical antipsychotics? |
partial dopamine agonists |
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MOA for typical antipsychotics |
dopamine agonists |
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adverse effects of traditional antipsychotics |
- orthostatic hypotension - sedation - anticholinergic effects |
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adverse effects of atypical agents |
- weight gain - disturbed lipid/glucose metabolism |
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what is the primary adverse effect of ALL antipsychotics? |
-extrapyramidal side effects |
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what are extrapyramidal side effects? |
- shuffling gait - stiffness - tongue protruding from mouth - tardive dyskensthia - akathisia |
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Antipsychotics rehab concerns |
- benefits vs. sedation - orthostatic hypotension - extrapyramidal side effects |
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what is dopamine activity like during psychosis? |
increased cognitive activity, normal motor activity |
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what causes side effects of antipsychotics
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the slow down dopamine activity so it is normal in cognition but below normal for motor activity |
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why are antipsychotic side effects like parkinson's |
because parkinsons is a decreased amount of dopamine activity in motor cortex |
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what are seizure disorders? |
recurrent, uncontrolled cerebral excitation |
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what causes parkinson's in adults |
normally secondary to an event - unknown in children |
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how are seizure disorders classified? |
- according to extent of cerebral involvement, EEG activity, Symptoms |
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what are the classes of seizures? |
- partial - generalized seizures - unclassified |
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what are partial seizures? |
simple complex |
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what are generalized seizures |
- absence (annoying french accent) - tonic clonic - petit mal |
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Goal of antiseizure medication |
selective effect on hyperexcitable neurons |
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what are the different classifications of antiseizure drugs?
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- barbituates - benzodiazepines - carboxylic acid - 2G |
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what are the MOA of carboxylic acids? |
- inhibition of Na+ channels - inhibition of GABA reuptake transporter - inhibition of GABA transaminase |
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classification of: Phenytoin (delantin) carbamazepine (Tegretol) Ethozuximide (Zarontin) Valproic Acid (Depakene) |
Primary antiseizure agents |
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classification of: Gabapentin (neurontin) Lamotrigine (lamictal) Levetiracetam (keppra) pregabalin (lyrica) Tiagabine (Gabitrill) Topiramate(Topamax) |
2G antiseizure drugs |
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what are the characteristics of 2G antiseizure drugs? |
- not necessarily more effective than traditional - Tend to have milder side effects - more predictable - allow more combinations - some used for neuropathic pain |
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what are the primary MOA for antiseizure medications |
- increase Na+ entry into rapidly firing neurons - Decreased Ca++ entry to thalamic neurons - increased GABA inhibition - decreased release of effects of excitatory amino acids |
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minor side effects of antiseizure meds |
- sedation - headache - dizziness - incoordination - GI problems |
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serious side effects of antiseizure meds |
- liver toxicity - blood dyscrasias (aplastic anemia, agranulocytosis) - increased risk of birth defects |
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Chemical classifications of antiepileptic meds |
Hydantoins Iminostilebenes Succinimides |
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classification of: Phenytoin (Dilantin) Mephenytoin (Mesantoin) |
Hydantoins |
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what is MOA of Hydantoins? |
inhibition of Na+ channels |
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classification of: - Carbamazepine (Tegretol) - Ozcarbazepine (Trileptal) |
Iminostilbenes |
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what is the MOA of Iminostilbenes |
inhibition of Na+ channels, similar to phenytoin |
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classification of: - Ethosuximide (Zarontin) - Methsuximide (Celontin) |
Succinimides |
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what is the MOA of Succinimides? |
inhibition of Ca2+ channels, more effective for absence seizures |
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Rehab concerns of antiseizure meds |
- Be aware if pt. is on them - document any seizure activity - be alert to common adverse effects |
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what to do in case of seizure? |
- put pt in sidelying - keep airway clear - clear area if pt. convulsive - lower pt. slowly if gait training |
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what is Parkinson's disorder? |
Neurodegenerative disorder |
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what are the classic symptoms of Parkinson's? |
- rigidity - resting tremor - bradykinesia - postural instability |
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what is the primary cause of parkinsonism? |
- degeneration of dopaminergic neurons in substantia nigra - decreased dopamine release causes unchecked ACh influence |
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what is the rationale for L-Dopa therapy for parkinson's? |
- attempt to increase dopamine content in basal ganglia - direct admin of dopamine ineffective because of BBB - must provide precursor to dopamine (L-Dopa) |
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What is the goal of Parkinson's drug treatment? |
try to activate dopamine receptors |
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what is the first symptom of parkinson's to show up? |
depression |
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Why is carbidopa used? |
L-Dopa will be converted to dopamine before reaching brain |
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what does carbidopa do? |
- inhibits dopa decarboxylase - prevents premature conversion |
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what is Sinemet
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L-dopa and carbidopa contained in same pill - Most used parkinson's treatment |
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what are the side effects of the L-dopa treatment? |
- GI irritation - hypotension - psychotropic effects - dyskinesias |
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what are dyskinesias? |
SLOW movements |
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what happens at end of dose? |
akinesia - decreased response twd end of dose cycle |
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what is the on-off phenomenon |
- response fluctuates within dose cycle of L-Dopa |
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what happens with long-term use of L-Dopa |
benefits may be lost after 4-5 years |
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why does L-Dopa decrease in efficacy after long term use? |
- tolerance to drug - disease progression |
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what are other antiparkinson medications? |
- COMT inhibitors - anticholinergic agents - dopamine agonists - Amantadine - Selegiline |
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Classifications of: Tolcapone (Tasmar) Entacapone (Comtan) |
COMT Inhibitors
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what do COMT inhibitors do? |
- inhibit the COMT enzyme that breaks down L-dopa in peripheral tissues - allow more L-Dopa to reach brain |
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What are side effects of COMT inhibitors? |
- GI distress (diarrhea) - orthostatic hypotension - increased dyskinesia |
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Classifications of: - Benztopine mestylate - biperiden - orphenadrine - diphenhydramine |
ACh |
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MOA of anticholinergic agents? |
- decrease ACh infleunce - may decrease regidity and tremor |
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Why are anticholinergic agents rarely used?
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anticholinergic package of unpleasant side effects |
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Classification of: Bromocriptine (Parlodel) Pergolide (Permax) |
Dopamine agonists |
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what are characteristics of Dopamine agonists? |
- Cross BBB to directly stimulate dopamine receptors - May be combined with L-dopa for best effects |
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problems with dopamine agonists? |
- nausea/vomiting - confusion, hallucinations - postural hypotension |
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Classification of: Amantadine (symmetrel) |
Antiviral agent - antiparkinsons effects discovered by chance |
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MOA of Amantadine? |
antagonist for NMDA receptor in brain, decreases influence of excitatory amino acids |
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what is Primary use of Amantadine? |
adjunct therapy with L-Dopa |
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What are the problems of Amantadine? |
- orthostatic hypotension - psychotropic effects - dizziness - blurred vision |
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MOA of Selegiline (Eldepryl) |
- inhibits MOA-B
- prolongs dopamine effect at synapses - Combined with L-dopa to increase/prolong effects |
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what are problems Selegiline? |
no major concerns |
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Rehab concerns of antiparkinson drugs? |
- coordinate rehab sessions with drug therapy - ideally 30-60 minutes after meds - Recognize synergistic effects of physical rehab and drug therapy |
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what do General Anesthesia drugs normally consist of?
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- sedative/hypnotic - gaseous anesthetic - NM blockade - Opiate pain reliever |
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Classifications of: - Desflurane - Enflurane - Halothane - Isoflurane - Sevoflurane - Nitrous Oxide |
Inhaled anesthetics |
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Precautions to take when a person comes to from general anesthesia |
- Post op weakness (NM Blockade recovery) - Post op nausea - Post op pain - Post op loss mobility |
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Classification of: - articane - benzocaine - bupivacaine - lidocaine - mepivacaine - procaine - tetracaine |
Common local anesthetics |
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Characteristics of Local anesthesia? |
- injected sensory nerve blockade - goal is to keep at site of injection - causes numbness and possible motor neuron blockade - well known -Caine drugs |
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Primary goal of muscle relaxants |
selective decrease skeletal muscle excitability |
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primary use of muscle relaxants |
- muscle spasms - spasicity |
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what are the types of drugs used to treat muscle spasms? |
- polysynaptic inhibitors - diazepam (Valium) |
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Classification of: - Carisoprodol - Chlorphenesin - Chlorzoxazone - Cyclobenzaprine - Metaxalone - Methocarbamol - Orphenadrine Citrate |
Polysynaptic inhibitors |
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characteristics of Diazepam |
- Benzodiazepine agent (originally an antianxiety drug) - Works in CNS, increases inhibitory effects of GABA |
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MOA of Valium |
- increases GABA-mediated inhibition of alpha motor neuron - less excitation leads to muscle relaxation |
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What is valium used for?
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- spasms/ spasticity - causes sedation |
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what causes spasticity? |
CNS malfunction, loss of inhibition of reflex contractions due to: - CVA - Cerebral Palsy - MS - Traumatic injury to brain or cord |
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These are used to treat what? Diazepam Baclofen alpha-2 agonists gabapentin dantrolene botunlinum toxin |
spasticity |
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long-term effects of diazepam? |
tolerance and dependence |
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characteristics of Baclofen |
- synthetic GABA - stims GABA receptors in cord - GABA B AGONIST - decreases excitation of alpha motor neuron |
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how is Baclofen administered? |
intrethecally |
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How does local anesthetic stay local? |
creates vasoconstriction - slowly goes into the bloodstream (concentration stays low) |
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when is intrathecal baclofen used? |
severe Spasticity |
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how is intrathecal baclofen delivered? |
- catheter and pump deliver drug to subarachnoid space |
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what is the advantage of intrathecal baclofen? |
decrease spasticity with less drug, fewer side effects |
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what is Tizanidine classified as? |
alpha-2 agonist |
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how do alpha-2 agonists work? |
- stim alpha-2 receptors located on spinal interneurons - cause inhibition of interneurons - decreases excitatory input on alpha motor neuron |
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alpha-2 agonist vs. baclofen |
similar efficacy to oral baclofen but less generalizeed muscle weakness |
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Gabapentin characteristics |
- Originally an antiseizure druge - Enhances GABA effect in SC |
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What is Gabapentin used for now? |
- MS - Spinal Cord infection |
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side effects of Gabapentin? |
- sedation - dizziness - ataxia |
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why is Gabapentin not used more often? |
- not the highest efficacy |
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What is Dantrolene sodium |
- only direct acting muscle relaxant |
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Dantrolene sodium MOA |
inhibits release of calcium from skeletal muscle SR |
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Dantrolene Sodium side effects |
muscle weakness |
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what is Botulinum Toxin |
- muscle paralytic, works locally for severe spasms like torticollis, laryngospasms |
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MOA for botulinum toxin |
inhibits ACh release at skeletal NMJ |
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what is Type A botulinum characteristics(Botox) |
- longer duration of action
- longer half life - higher potency |
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what is Type B Botulinum used for? |
myobloc |
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what are the antispasticity effects of botulinum toxin? |
- injected into muscle - relaxation/paralysis occurs in 3-7 days and lasts 2-3 mos. - reduces spastic dominance |
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what happens as a result of the reduced spastic dominance from Botulinum toxin?? |
- increased residual function - improved ADL, Bracing |
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what are some problems of Botulinum toxin? |
- Local irritation at injection site - Large enough molecule that immune system may develop antibodies - limits the dosage that can be given |
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what are the dose limits of Botulinum toxin? |
- 300-400 units (Type A) - 2500-5000 unites (Type B) |
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what are the rehab concerns with muscle relaxants |
- generalized weakness - sedation - possible drastic change in muscle tone over short time period |
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Drugs to treat what: - Carisoprodol - Chlorphenesin carbamate - Chlorzoxazone - Cyclobenzaprine - Diazepam - Mataxalone - Methocarbamol - Orphenadrine Citrate |
Skeletal muscle spasms |
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Classification of: - Baclofen - Dantrolene Sodium - Diazepam - Gabapentin - Tizanidine - Botulinum Toxin |
Antispasticity Drugs |
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divisions of analgesics |
- opioids - nonopioids |
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divisions of anti-inflammatory agents |
- NSAIDs - Glucocorticoids |
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Characteristics of Opioid analgesics |
- alter pain perception - inhibit pain pathways - used in moderate-severe pain |
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what are opioids indicated in? |
- acute pain (surgery, trauma) - Chronic pain (cancer) |
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difference between opioids and opiates |
- opioids are morphine-like (Synthetic) - opiates are morphine and opium poppy extracts |
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which type of opioids are best at suppressing pain? |
- exogenous |
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what are the different types of opioids? |
- strong agonists - moderate agonists - antagonists - mixed agonist/antagonist |
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Classification of: - codeine - oxycodone? |
- moderate agonist opioids |
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classification of: - butorphanol - nalbuphine - pentazocine |
mixed agonists/antagonist opioids |
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classification of: - Naloxone - Naltrexone |
opioids antagonists |
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classification of: - morphine - meperidine - fentanyl |
opioid strong agonists
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which opioid calssifications are addictive |
strong and moderate agonists |
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what is the purpose of the opioid mixed agonist/antagonists |
provide pain relief without euphoria |
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where do opioids primarily act on? |
- SC (Dorsal Gray matter) - Brain (Medial thalamus, hypothalamus) |
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which receptors do opioids bind to? |
- presynaptic nerve terminals - postsynaptic neurons |
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adverse effects and rehab concerns of opioids? |
- sedation - mood changes - confusion - Respiratory depression - Postural hypotension - nausea - constipation - tolerance/dependence |
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what is cause of death in opioid OD? |
respiratory depression |
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what is drug tolerance and why does it happen? |
need more of the drug to achieve same effect, happens bc receptors are inactivated and internalized |
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what is physical dependence |
onset of abstinence syndrome if drug is suddenly stopped |
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Besides pain relief, what are opioids good at? |
cough suppression
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what is the main eurphoria receptor that creates the addictive potential of opioids? |
mu receptor |
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issue with nonopiod analgesics? |
- less efficacious |
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primary effects of NSAIDs |
- analgesic - anti-inflammatory - antipyretic - anticoagulant (@ low doses) |
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Classification of: - ibuprofen - naproxen - ketoprofen |
OTC NSAIDs |
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Classification of: - etodolac - fenoprofen - ketorolac - Melclofenamate - Piroxicam |
prescription NSAIDs |
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what are the side effects of NSAIDs |
gastric irritation |
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what are the therapeutic differences in OTC to Rx NSAIDs |
maybe more efficacious w/ more side effects |
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MOA of NSAIDs |
inhibit synthesis of prostaglandins by inhibiting CYCLOOXYGENASE (no C fiber pain) |
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what are prostaglandins
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- lipid compounds produced in cells, mediating various effects (pain, fever, inflammation, platelet aggregation) |
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Leukotryenes are responsible for what? |
- mediator of asthma response |
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What precautions need to be taken with NSAIDs because of Leukotryenes? |
can causes asthma attack in ppl with light asthma |
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2 primary subtypes of cyclooxygenase (COX) enzyme |
COX-1 COX2 |
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COX-1 enzyme characteristics |
- normal constituent - synthesizes PG's to protect cells, maintain function (Stomach, kidneys, platelets) |
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COX-2 enzyme characteristics |
- induced when cell is injured - synthesizes PG's for pain mediation and inflammation (RA) |
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what are COX-2 selective drugs good for? |
- inhibit synthesis of PGs in pain, inflammation - don't block producation of beneficial PGs in stomach, kidneys, platelets - decrease pain/inflammation with less toxicity |
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why have some COX-2 inhibitors (Vioxx and Bextra) been recalled? |
- increased risk of heart attack and stroke - because vessels are stickier inside but platelet aggregation is not effected |
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Characteristics of acetaminophen |
- analgesic and antipyretic effects - no gastric irritaiton - no anti-inflammatory or anti coagulant effects |
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what can be caused by high doses of acetaminophen? |
- liver toxicity |
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how are acetaminophen and opioid combos identified? |
brand name indicates the mixture |
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why are acetaminophen and opioids combined? |
- there is a synergistic effect because the MOA is different in each drug |
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adverse effects and rehab concerns of nonopioids? |
- Gastric irritation (ulcers) - Hepatic, renal toxicity |
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symptoms of aspirin intoxication? |
- tinnitus (1st sign) - hearing loss - confusion - headache |
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Vedaclidine characteristics |
- new analgesic - mixed agonist-antagonist at musarinic receptors - side effects - salivation and tremor in OD |
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Flupirtine characteristics |
- new analgesic/ muscle relaxer - K channel opener - weak NMDA antagonist/ GABA modulator - Side effects - liver toxicity |
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These antiseizure drugs are also good for what: - carbamazepine - pregabalin - gabapentin - tricyclic |
neuropathic pain |
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how do NSAIDs work as anti inflammatory? |
- inhibit PG biosynthesis - this dose is higher than analgesic dose - needs to be used continuously until inflammation is resolved |
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what are glucocorticoids (steroids) used for?
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- powerful anti-inflammatory - immunosuppression |
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MOA of glucocorticoids? |
act on inflammatory cells - binds to glucocorticoid receptor in cytoplasm - travels to nucleus to DECREASE expression of inflammatory proteins and INCREASE expression of antiinflammatory proteins |
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Classification of: - betamethasone - cortisone - dexamethasone - hydrocortisone - paramethasone - prednisolone - prednisone |
glucocorticoids (CATABOLIC Steroids) |
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primary problem with glucocorticoids? |
- catabolic(breakdown) effect on bone, muscle, ligament, tendon, skin |
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what are other side effects of glucocorticoids? |
- salt/water retention - increased infectino - gastric ulcers - glucose intolerance - glaucoma - adrenal suppression |
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how can the side effects of glucocorticoids be avoided? |
take holidays from the drug and slowly ween off of it |
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how do glucocorticoids cause adrenocoritical shock? |
- vascular collapse from severe hypotension and organ damage - occurs when they are suddenly discontinued |
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What is OA |
- defects in joint cartilage/subchondral bone - failure to repair normal wear of joint cartilage - excess growth of subchondral bone - NOT an immune attack |
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what causes OA? |
- injury - genetic variation - excessive wear/tear - joint weakness |
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what is synovitis? |
occurs secondarily to joint damage |
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what is appropriate to treat synovitis? |
- NSAIDs for both pain and inflammation relief - acetaminophen for pain |
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what non-drug therapies are effective for OA? |
- PT - Wt. loss - joint replacement - viscosupplementation - dietary supplements |
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what is viscosupplementation |
injections into joint of hyaluronic acid that restores viscosity and lubricating property of synovial fluid |
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why is hyaluronic acid used for viscosupplementation? |
- high molecular weight which slows loss of HA from joint - has osmotic effect which draws more H20 into the joint |
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why is the viscosupplementation treatment used? |
delay need for surgical repair |
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Classification of: Glucosamine Chondroitin Sulfate? |
OA dietary Supplements - precursors for components of cartilage and synovial fluid |
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What is the argument against OA dietary supplements? |
precursors are easily synthesized by cells from readily available glucose and Amino acids - Clinical evidence mostly negative |
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What is Rheumatoid Arthritis? |
- autoimmune disease - immune system attacks the joints |
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What is the goal of RA drug therapy? |
- suppressing immune attack of joints - suppressing inflammatory component |
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what are DMARDs (disease-modifying antirheumatic drugs)? |
- interfere with disease process of auto immune attack on connective tissue
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what are the MOAs of DMARDs? |
- immune suppressive agents (General or specific) |
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Classification of: Chloroquine Hydroxychloroquine |
Anti-Malarials |
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MOA of anti-malarials |
- inhibit several functions of immune cells - reduce immune attack |
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what precautions must be taken with anti-malarials |
closely monitored by ocular exam to ensure there is no renal toxicity (less so in hydrochloroquine) |
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General Classification of: - Cyclophosphamide - Chlorambucil - Azathioprine - Leflunomide - Methotrexate |
Cytotoxic agents for RA |
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MOA for cyctotoxic agentS? |
- interfere with nucleic acid synthesis |
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what are cytotoxic agents also used for? |
anticancer chemo |
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adverse effects of cytotoxic agents? |
- hair loss - nausea - blood disorders - infecctions (especially cyclophosphamide) |
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Specific Classification of: - cyclophosphamide - Chlorambucil |
DNA damaging agent
(cytotoxic) |
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Specific classification of: - azathioprine - leflunomide - methotrexate |
Nucleic acid synthesis inhibitors - Antimetabolites |
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which class of cytotoxic drugs have more serious adverse effects? |
DNA damaging agents |
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administration of: - Etanercept - Adalimumab - Certolizumab Pegol - Golimumab |
Prefilled Syringe |
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administration of: Infliximab abatacept rituximab Tocilizumab |
IV Infusion |
