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117 Cards in this Set
- Front
- Back
in terms of fatally...what is the difference between BENZODIAZEPINES and BARBITURATES
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BARBITUATES
1. produce a dose dependent CNS depression 2. FATAL depression of the cardio and respiratory sys. BENZODIAZEPINES 1. DO NOT produce surgical anesthesia nor FATAL respiratory depression 2. FATAL if used with ETHANOL |
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BENZODIAZEPINES used for general anesthesia
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Midazolam (Versed)
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what is the main mechanism for BENZODIAZEPINES, NON-BDZ and BARBITURATES
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1. potentiate the actions of GABA
2. GABA is the primary inhibitory CNS neurotransmitter 3. potentiate through variety of different mechanisms resulting in increased inhibition 4. potentiate on GABA-A receptors |
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what are the three classes of BENZODIAZEPINES?
general mechanism |
1. agonist: increase Cl- current
2. inverse agonist: decrease Cl- current 3. antagonist: blocks receptors, used to reverse BENZODIAZEPINES overdose |
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BENZODIAZEPINES antagonist
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Flumazenil:
1. Antagonizes the effects of any agent that binds to BDZ receptor binding sites. 2. DOES NOT block action of Barbiturates |
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what BENZODIAZEPINES are used for anxiety
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DC. COLA
1. Diazepam (L) 2. Chlordiazepoxide (L) 3. Clorazepate (L) 4. Alprazolam (M) 5. Lorazepam (M) 6. Oxazepam (S) |
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what BENZODIAZEPINES are used for insomnia
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FET
1. Flurazepam (L) 2. Estazolam (M) 3. Triazolam (S) |
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what BENZODIAZEPINES is used for SEIZURES and PANIC DISORDERS
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CLONAZEPAM
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in terms of duration how should BENZODIAZEPINES be prescribed
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1. BDZs should ONLY be prescribed for SHORT periods
2. tolerance and dependence with prolonged use |
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what are two importants things to note about BENZODIAZEPINES
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1. low doses of BDZs can be FATAL if taken with other depressants like alcohol and barbiturates
2. all BDZs can be abused |
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what are the THREE NON BENZODIAZEPINES
what are they mainly used for |
1. Eszopiclone (Lunesta)
2. Zolpidem (Ambien) 3. Zaleplon (Sonata) *relieve sleep onset insomnia |
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what does barbiturates do to benzodiazepines binding
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barbiturates can ENHANCE the binding of benzodiazepines to the BDZ1 and BDZ2 binding sites
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what barbiturates have selective anticonvulsant properties?
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1. phenobarbital (DOC)
2. mephobarbital |
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abrupt withdrawal of ____ can cause status epilepticus
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phenobarbital
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what are major side effects of barbiturates
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1. TOLERANCE develops
2. strong physiological DEPENDANCE 3. ABSOLUTE CONTRAINDICATED in patients with PORPHYRIA 4. rapid IV injection can cause CARDIO COLLAPSE!! |
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barbiturates in relation to OVERDOSE
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1. NO DRUGS to treat OVERDOSE
2. renal excretion can be increased be diuresis or alkalinization of the urine (phenobarbital can be execreted UNCHANGED) |
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what are barbiturates mainly used for
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1. induction/maintenance of anesthesia
2. anticonvulsants |
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Buspirone:
mechanism? what is it mainly used for |
1. partial agonism of 5HT1A serotonin receptors
2. 1 week for the anxiolytic effects to be observed so it is not useful for acute anxiety 3. used for GENERAL ANXIETY |
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Parkinson's Disease symptoms are caused by...
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1. a loss of dopaminergic neurons in one structure within the Basal Ganglia the substantia nigra pars compacta
2. causing increase in the activity of the INDIRECT (inhibitory) pathway and a decrease in the DIRECT (activation) pathway |
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what medications are used in dopaminergic replacement therapy?
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1. CARBIDOPA (peripheral decarboxylase inhibitor, DOES NOT enter CNS)
2. L-DOPA *Sinemet and Atamet are also decarboxylase inhibitors |
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what are some complications of L-DOPA combo therapy
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1. Dose related (acidic breakdown in stomach and must take on empty stomach)
2. Dyskinesia 3. Treatment related 4. FLUCTUATIONS IN RESPONSE (wearing off or end of dose AKINESIA) |
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what pathway is most beneficial in dopamine receptor agonist treatment
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D2 (indirect pathway) activation is more beneficial
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what are the dopamine receptor agonist
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BRAP
1. Bromocriptine (D2) 2. Ropinirole (D2) 3. Apomorphine (Mixed) 4. Pramipexole (Mixed) |
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what are the MAO-B inhibitors
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1. Selegiline
2. Rasagiline both are IRREVERSIBLE |
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what are the COMT (catechol-o-methyltransferase) inhibitors
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1. Tolcapone (peripheral and central action)
2. Entacapone (peripheral action) |
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what is Amantadine
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ANTICHOLINERGIC
1. useful early in disease for treating TREMORS 2. also antiviral for influenza A |
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what is Huntington's Disease
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degeneration of medium spiny neurons in the striatum
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what is the DOPAMINE HYPOTHESIS
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states that excessive dopaminergic activity cause schizophrenia and this is the basis for treatment rationale
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what are the three classes of antipsychotics
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1. phenothiazines*
2. thioxanthenes* 3. butyrophenone derivatives* 4. atypical antipsychotics *conventional antipsychotics |
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general mechanism of antipsychotics
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ability to block D2 receptors in the mesolimbic mesocortical pathway (controls behavior) in the brain
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what are the FOUR different pathways that can be affected by dopamine blockade?
what are the effects |
1. mesolimbic-mesocortical
-antipsychotic effectiveness 2. nigro-striatal -can cause parkinsonism, TARDIVE DYSKINESIA, akathisia, and dystonia 3. tuberinfundibular system -increased prolactin secretion from the pituitary -infertility and impotence 4. chemoreceptor trigger zones -antiemetics |
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what is the most important unwanted side effect of antipsychotics
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Tardive Dyskinesia
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what is approved for monotherapy for mania
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Olanzapine (Zyprexa)
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what atypical antipsychotic can cause fatal agranulocytosis in 1% in patients
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Clozapine
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what ATYPICAL antipsychotic is the first line agent for psychoses
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RISPERIDONE
-high affinity for 5-HT2 serotonin receptors -high potency -low toxicity |
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what is the amine hypothesis?
flaws? |
1. depression is a result of decreased amine mediated neurotransmission in the brain
2. too simplistic, action of drugs is immediate but clinical efficacy takes weeks to develop 3. properties of post synaptic cell and auto regulatory mechanisms are likely to be involved |
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what is the general mechanism of TCAs, SSRIs, NRIs...
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all block the reuptake of either serotonin and/or norepinephrine into the presynaptic nerve terminal
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what is the mechanism for MAO inhibitors
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blocks the major metabolic pathway for the monoamine neurotransmitters
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what the dangerous drug interactions of antidepressants
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1. MAOI can cause dangerous levels of catecholamines if given with sympathomimetics
2. Serotonin Syndrome can result from combining SSRIs with MAOI |
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what TCA is Non FDA approved for use in NEUROPATHIC PAIN
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AMITRIPTYLINE
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what TCA agent is the most selective for inhibition of SEROTONIN reuptake
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CLOMIPRAMINE
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what TCA is less sedating and may be used as a STIMULANT
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PROTRIPTYLINE
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what TCA is the most selecitve and potent inhibitor of NOREPINEPHRINE reuptake
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DESIPRAMINE
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which TCA has a unique mechanism from the others in the class
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TRIMIPRAMINE
-does not alter the reuptake of either serotonin or norepinephrine and yet maintain efficacy for depression -highly sedating |
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Atomoxetine:
what is it? what is it used for? |
1. Norepinephrine selective reuptake inhibitor
2. blockade NE transporter without affecting serotonin transporters 3. FDA approved for ADHD 4. off label for DEPRESSION |
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what is the first line agents for the treatment of depression
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serotonin selective reuptake inhibitors (SSRIs)
-immediate and irreversible |
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what are the SSRIs
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1. Fluoxetine (PROZAC)
2. Citalopram 3. Fluvoxamine 4. Paroxetine 5. Sertraline |
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what are heterocyclics (atypical antidepressants) used for
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reserved for patients refractive to other antidepressants
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what are the THREE MAOI?
what are their specific mechanisms? |
1. Phenelzine: irreversible inhibition of MAO A+B
2. Tranylcypromine: reversiblu inhibit MAO A+B 3. Moclobemide: Reversibly Inhibit MAO A (RIMA) |
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what type of patients can MAOI be used in?
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MAOI are only used for patients refractive to SSRIs and TCAs
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contraindications of MAOI?
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contraindications:
1. hypertensive crisis with sympathomimetics 2. treat with 5mg IV phentolamine |
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what is the mechanism for mania in Bipolar Disorder
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manic phase is related to EXCESS CATECHOLAMINERGIC activity in the brain and drugs that increase catecholamines like anti-depressants can exacerbate mania
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what are the primary headaches
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1. tension
2. migraine 3. cluster |
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what is the mechanism for classical antihistamines
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block the H1 receptor selectively
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what is the classic presentation of intradermal injection of histamine
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Wheal Flare Response
1. reddening of the area (vascular smooth muscle dilation) 2. edematous wheal (endothelium) 3. red irregular flare around wheal (axon reflex) |
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____ is a physiological antagonist of histamine
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epinephrine (EpiPen)
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what are the 2nd generation antihistamine?
what are the topicals? |
Second Generation
1. Loratadine (Claritin) 2. Cetirizine (Zyrtec) *DO NOT CROSS BBB Topical (ophthalmic): 1. Bepotastine (Bepreve) 2. Levocabastine (Livostin) |
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what are the first generation antihistamines?
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Enthanolamine: (MS and sedation)
1. Dramamine 2. Benadryl Piperazine (MS and sedation) 1. Cyclizine 2. Meclizine Alkylamines (cold med.) 1. Bromopheniramine 2. Chloropheniramine Phenothiazine (MS and sedation) 1. Promethazine |
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what is the difference between First and Second Generation Antihistamines
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First:
1. More Sedating 2. More Autonomic receptor blockade Second: 1. Less sedation 2. does not cross BBB easily if at all |
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what the are medications used to treat EPISODIC TENSION headaches
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NSAIDs:
1. OTC NSAIDs 2. Diclofenac (Cataflam) OPIOIDS: 3. Tylenol w/ Codeine 4. Percocet (tyl + oxy) 5. Meperidine (Demerol) |
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what the are medications used to treat CHRONIC TENSION headaches
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TCAs:
1. Amitriptyline (Elavil) 2. Nortriptyline (Pamelor) Muscle Relaxants: 3. Skelaxin (Metaxalone) 4. Cyclobenzaprine (Flexeril) 5. BOTOX |
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what is the relationship of serotonin in migraines
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1. vasodilation of carotid arteriovenous anastomoses causes shunting of blood flow causing HYPOXIA and ISCHEMIA
2. serotonin agonists have a high affinity for the 5HT1B and 5HT1D serotonin receptors 3. stimulation of serotonin causes vasoconstriction |
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what are the types of NSAIDs/COMBOS that can be used to treat MIGRAINES
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1. Execedrin (Aspirin+Acetaminophen+Caff)
2. Fiorinal (Aspirin+Butalbital+Caff) 3. Fiorinal C (above + Codeine) 4. Fioricet (Acetaminophen+Butalbital+Caff) |
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what are the types of Serotonin Agonists that are used for Migraines
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1.Ergotamine/Dihydroergotamine
*Cafegot *Wigraine 2. Triptans *Sumatriptan (NO IV, prototype) *Rizatriptan (fast onset) *Almotriptan (fast onset) |
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what is the 1st line agents to abort acute mild to moderate migraines?
contraindications? |
TRIPTANS
1. sumatriptan is the prototype, but should not be given IV 2. rizatriptan and almotriptan have the fastest onset and most efficacious 3. CONTRAINDICATED IN VASCULAR DISEASE |
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what type of serotonin agonist have a higher occurrence of recurring or rebound headaches
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TRIPTANS:
recurring or rebound headaches may be more common than with ergotamines |
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what is the general mechanism for opioids
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1. analgesic efficacy is mediated primarily through μ receptors
2. alleviate psychological responses to pain 3. inhibit ASCENDING PAIN TRANSMISSION through activation of opioid receptors in the DORSAL HORN (and thalamus) 4. |
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what TWO types of pain?
which one responds well to opiates? |
1. Nociceptive: stimulation along INTACT neural pathway
2. Neuropathic: DAMAGED neuronal structures *Nociceptive pain responds well to OPIATES *Neuropathic pain responds poorly to opiates, may respond to higher dose |
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what is the mechanism for HYPERALGESIA
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K receptors are also present in the descending pathway and when activated can cause HYPERALGESIA
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what are considered STONG OPIOIDS AGONISTS
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Phenanthrenes:
1. Morphine 2. Hydromorphone (Dilaudid) 3. Oxymorphone 4. Diacetylmorphine (heroin) Phenylheptylamines: 5. Methadone Phenylpiperidines: 6. Meperidine 7. Fentanyl |
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what are considered WEAK OPIOIDS AGONISTS
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CHOP DL
Phenanthrenes: 1. Codeine 2. Oxycodone 3. Hydrocodone Phenylheptylamines: 4. Propoxyphene Phenylpiperidines: 5. Diphenoxylate 6. Loperamide |
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what are the CNS physiological effects of opioids
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1. analgesia
2. euphoria 3. respiratory depression (most likely cause of death) 4. cough suppression 5. MIOSIS 6. CONVULSIONS 7. CONSTIPATION 8. muscle rigidity 9. nausea and vomitting 10. hypothalamic heat and hormone dysfunction |
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NO TOLERANCE DEVELOPS TO MIOSIS, CONSTIPATION AND CONVULSANTS ACTIONS
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NO TOLERANCE DEVELOPS TO MIOSIS, CONSTIPATION AND CONVULSANTS ACTIONS
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what is OPIOID ROTATION
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since cross tolerance is often incomplete, as the analgesic effect wanes it is possible to switch the patient to another agonist and regain some analgesic benefits
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opioids in relation to oral and parental administration
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1. some agents have a high FIRST PASS metabolism resulting in poor oral bioavailability
2. MORPHINE better IV than ORAL 3. Codeine better ORAL than IV |
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____ has a very long elimination time making it an ideal opioid to treat withdrawal effects (detox)
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Methadone
NALOXONE ALSO WORKS |
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what is special about NALBUPHINE...in terms of respiratory depression
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1. respiratory depression effects reaches a ceiling where further depression does not occur with increasing doses
2. agonist at K and an antagonist at μ receptors |
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what agent with mixed receptor agent can be used for DETOX of opioid abuse and cocaine withdrawal
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BUPRENORPHINE
1. detoxification of opioid abuse 2. combined with antagonist NALOXONE for cocaine withdrawal |
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what are the drugs interactions that opioids can have
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1. SEDATIVE HYPNOTICS: increased CNS/respiratory depression
2. ANTIPSYCHOTICS: increased sedation, respiratory/cardio effects 3. MAOI: CONTRAINDICATED!! (COMA) 4. AMPHETAMINES dramatically increase analgesia and euphoria |
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what is the general mechanism for NSAIDs
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1. blocks COX 1, 2, and 3
2. inhibit formation of prostaglandins 3. STEROIDS block phospholipases inhibiting arachidonic acids |
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what type of NSAIDs is useful in patients with ulcers
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COX 2 selective agents
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what is special about ASPIRIN in terms of half life and duration
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1. aspirin is IRREVERSIBLE its effects are longer than that predicted by its half life
2. COX enzymes must be resynthesized to return to normal function *all other NSAIDs are reversible |
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aceteminophen has NO _____ action but acts in the brain as antipyretic and analgesic
what else?? |
1. aceteminophen has NO ANTIINFLAMMATORY action but acts in the brain as antipyretic and analgesic
2. does not inhibit peripheral COX enzymes 3. does not inhibit platelet aggregation 4. does not cause severe GI problems |
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platelet function disturbances in NSAIDs use
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1. PGI2 in platelets normally acts to suppress platelet activation
2. inhibiting the formation of prostacyclins can lead to over activation of platelets and cause potential THROMBOTIC events |
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Acetaminophen Toxicity?
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1. fatal hepatic necrosis
2. acute renal failure treat with MUCOSIL |
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Aspirin Toxicity?
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1. irreversible acetylation in platelets can last a long time
2. FATAL at high doses (10-30g) 3. Reye's syndrome is linked to aspirin in kids with viral infections and fever |
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what are the non selective cylcooxygenase inhibitors
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1. asprin
2. acetaminophen 3. indomethacin 4. ibuprofen 5. naproxen 6. ketoprofen 7. tolmetin 8. ketorolac |
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what is the benefit if COX2 selective inhibitor
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antiinflammatory and analgesic effects without the GI and platelet dysfunction due to COX1 inhibition
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what are the THREE main COX2 selective inhibitors
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1. Celecoxib (Celebrex)
2. Diclofenac 3. Meloxicam |
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what is gout?
what are the THREE main approaches for treatment? |
uric acid crystals in joints and cartilage
1. reduce inflammation 2. increase the elimination of uric acid 3. decrease the production of uric acid |
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what is Colchicine used for?
mechanism? |
1. relieves the pain and inflammation
2. binds to and blocks tubulin |
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what NSAID is beneficial in gout
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INDOMETHACIN
1. inhibit prostaglandins 2. inhibit phagocytosis of urate crystals |
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what NSAIDs should NOT be used in gout
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ASPIRIN
1. increase retention of uric acid in kidneys |
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what is Xanthine Oxidase inhibitors used for?
what are the TWO DRUGS? |
prevent uric acid biosynthesis
1. allopurinol 2. febuxostat (Uloric) |
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what are the Uricosuric Agents?
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Probenecid
Sulfinpyrazone 1. decrease the body pool of urate by INCREASING EXCRETION |
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what is the general mechanism of lithium in treating bipolar disorder
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1. reduction of catecholaminergic transmission through a combination of mechanism.
2. specific mechanism unknown |
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what is dangerous about lithium
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1. renal elimination is markedly affected by SODIUM intake
2. low sodium levels lead to an accumulation of lithium due to excessive reabsorption in the tubules 3. due to small therapeutic window there is toxicities 4. plasma concentration must be monitored!! 5. toxicities can happen in therapeutic window |
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if the patient is become refractive to lithium treatment, what is the next medication that should be given?
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VALPROATE (Depakene)
1. less toxicity than lithium 2. therapeutic dose rapidly obtained |
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besides lithium, what are other agents used for bipolar disorder
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1. Valproate (1st line drug)
2. Carbamazepine 3. Olanzapine |
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what is the general mechanism of lithium in treating bipolar disorder
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1. reduction of catecholaminergic transmission through a combination of mechanism.
2. specific mechanism unknown |
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what is dangerous about lithium
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1. renal elimination is markedly affected by SODIUM intake
2. low sodium levels lead to an accumulation of lithium due to excessive reabsorption in the tubules 3. due to small therapeutic window there is toxicities 4. plasma concentration must be monitored!! 5. toxicities can happen in therapeutic window |
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if the patient is become refractive to lithium treatment, what is the next medication that should be given?
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VALPROATE (Depakene)
1. less toxicity than lithium 2. therapeutic dose rapidly obtained |
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besides lithium, what are other agents used for bipolar disorder
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1. Valproate (1st line drug)
2. Carbamazepine 3. Olanzapine |
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what are the three mechanism of antiepileptics
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1. prolonging the inactivation of voltage gated Na+ channels
2. enhancement of synaptic inhibition by increasing GABA 3. treating a less common form of epilepsy, generalized absence seizures, is accomplished through the inhibition of T-type voltage gated calcium channels |
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what is the mechanism of Phenytoin
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1. locks voltage gated Na+ channels in the inactivated state
2. both voltage and use dependent |
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primary use of Phenytoin
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1. partial and generalized tonic-clonic seizures
2. NOT ABSENCE SEIZURES |
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what is significant about elimination of Phenytoin
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1. elimination is dose dependent
2. very low blood levels follows FIRST ORDER 3. as blood level rise within the therapeutic range, the maximum capacity of the live to metabolize phenytoin is approached causing the elimination to follow ZERO ORDER |
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what is the mechanism of Carbamazepine
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locks Na+ channels in inactivated state
anticonvulsant treats bipolar depression |
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what is Carbamazepine used for
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1. drug of choice for PARTIAL SEIZURES
2. frequently the first choice for generalized tonic-clonic seizures |
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what is the first agent used for controlling seizures?
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Phenobarbital
-stimulation of GABA -reduction in excitatory neurotransmission |
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what drug is metabolized into phenobarbital, and used to control partial and tonic clonic seizures?
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Primidone
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what is the mechanism of Vigabatrin
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1. irreversibly inhibits GABA aminotransferase
2. promotes the accumulation of GABA at the synapse 3. thus increasing GABA activity and thus inhibiting high freq neuronal firing |
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what is the first choice medication for ABSENCE SEIZURES
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1. Ethosuximide
2. Methsuximide 3. Phensuximide |
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what is Valproic Acid used for
|
preferred choice for ABSENCE seizures concomitant with TONIC-CLONIC seizures
CONTRAINDICATION: 1. Liver Disease 2. Urea Cycle Disorders |
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what are the two factors that limit the usefulness of BDZs in long term treatment of epilepsy
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1. pronounced sedative effects
2. tolerance; seizures may respond initially but recur within a few months |
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what is the general mechanism for drugs that treat absence or myotonic seizures
|
blocking T-type calcium channels
1. Ethosuximide 2. Valproic Acid |
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what is particularly harmful about Lamotrigine in treating seizures
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1. inactivates sodium channels
2. SEVERE LIFE THREATENING RASH (stop drug) |