Term
| I should also point out that the ______ antidepressants (like fluoxetine) and ______ antidepressants (like venlafaxine), which I will talk about later, are also first line treatment for most _______ disorders. |
|
Definition
|
|
Term
In major depression:
weight changes? |
|
Definition
|
|
Term
In major depression:
Sleep Changes? |
|
Definition
| Insomnia or hypersomnia occur daily. |
|
|
Term
| Major depression typically lasts for _____ to _______ and remits. |
|
Definition
|
|
Term
| If Major depression ________, pharmacotherapy may be in order. |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| SSRI’s (fluoxetine) and SNRI’s (venlaflaxine) are used to treat the affective disorders: ____________. |
|
Definition
Major (Unipolar) Depression
Dysthymia
Bipolar Affective Disorder |
|
|
Term
| Major (Unipolar) Depression is characterized by mood changes for what time extent? |
|
Definition
|
|
Term
| Major (Unipolar) Depression characterized by 2 weeks or more of: __________. |
|
Definition
-depressed mood
-anhedonia
-changes in appetite/sleep
-psychomotor agitation/retardation
-decreased concentration
-thoughts of death/suicide |
|
|
Term
|
Definition
| persistent depressed mood that lasts for 2 years or longer. |
|
|
Term
| Dysthymia symptoms: __________. |
|
Definition
|
|
Term
| The major difference between Dysthymia & Major (Unipolar) Depression is the _______ and in some cases the _______ of the symptoms. |
|
Definition
|
|
Term
| . A dysthymic patient is depressed all the time but may not be ________ as a patient who is experiencing major depression. |
|
Definition
|
|
Term
| To be diagnosed with dysthymia, the patient cannot have ___________. |
|
Definition
| an episode of major depression occurring during the 1st two years of his persistent depression. |
|
|
Term
| ____% of population affected with ___________. |
|
Definition
|
|
Term
| Some patients have a double dose of depression, that is they have a baseline of _______ with intermittent bouts of _______ called a ______ disorder. |
|
Definition
dyshymia
major depression
Mixed Disorder |
|
|
Term
| Mixed Disorder the pt. is feeling depressed everyday with ___________. |
|
Definition
| periods of 2 weeks or more where they are severely depressed |
|
|
Term
| counseling and cognitive behavioral therapy is very important for some of these patients whose depression may be ______________. |
|
Definition
| secondary to a personality disorder or other psychological disorder. |
|
|
Term
| In addition to therapy, one alternative to antidrepressant drug therapy is ____________. |
|
Definition
| electroconvulsive therapy (ECT) |
|
|
Term
| The most significant SE of electroconvulsive therapy (ECT) being that there is ______. |
|
Definition
| temporary retrograde memory loss. |
|
|
Term
| Bipolar disorder is characterized by ______________. |
|
Definition
| intermittent bouts of depression and mania or hypomania |
|
|
Term
| The manic phase of bipolar disorder is characterized by an ________ and ________. |
|
Definition
| inflated self esteem and grandiose ideas. |
|
|
Term
|
Definition
| decreased need for sleep, and the patient may sleep as little as 3 hours per night. |
|
|
Term
| Psychomotor _______ is common in bipolar. |
|
Definition
|
|
Term
| Bipolar pt may tend to have an increase in _______ activity- that is become very preoccupied with ________. |
|
Definition
goal-directed
performing tasks or doing schoolwork |
|
|
Term
| Bipolar pt become excessively preoccupied with _______ activities. |
|
Definition
|
|
Term
| The manic phase can be broken down in severity in ____ stages, with stage ___ being the worst. |
|
Definition
|
|
Term
| Stage 1 mania is milder and the patient is still _______. |
|
Definition
|
|
Term
| In stage 3 mania, the patient ___________. |
|
Definition
| is out of control and incoherent, panic stricken, desperate, and experiencing looseness of associations. |
|
|
Term
| hallucinations occur in ____ stage of mania. |
|
Definition
|
|
Term
| Some forms of bipolar disorder are characterized by a milder form of mania called _______. |
|
Definition
|
|
Term
| Of all of the affective disorders, individuals with bipolar disorder are more likely to have ____________. |
|
Definition
| co morbid psychiatric disorders |
|
|
Term
| _______ is common in bipolar. |
|
Definition
|
|
Term
| _______ were the first antidepressants marketed. |
|
Definition
|
|
Term
| MAO inhibitors act by inhibiting _____. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Blockade of monoamine oxidase (MAO) does what? |
|
Definition
| decreases the breakdown of neurotransmitter |
|
|
Term
| Blockade of monoamine oxidase (MAO) decreases the breakdown of neurotransmitter and leads to ________. |
|
Definition
| packaging of more neurotransmitter into synaptic vesicles |
|
|
Term
| MAO inhibitor's Blockade of monoamine oxidase (MAO) decreases the breakdown of neurotransmitter and leads to packaging of more neurotransmitter into synaptic vesicles and therefore increases amount of __________ in the synapse. |
|
Definition
|
|
Term
| While MAO inhibition is seen immediately, the therapeutic effects takes __________. |
|
Definition
| weeks (at least 2 weeks) to develop |
|
|
Term
| _______ & __________ are two MAO inhibitors for treatement of depression. |
|
Definition
| Tranylcypromine and Selegiline |
|
|
Term
| Tranylcypromine and Selegiline are reserved for? |
|
Definition
| patients that do not respond to SSRI |
|
|
Term
| For MAO inhibitors Drug interactions and _______ containing food interactions can lead to hypertensive crisis. |
|
Definition
|
|
Term
| MAO inhibitors inhibit metabolism of _____ such as ________. |
|
Definition
| other drugs such as meperidine. |
|
|
Term
Tranylcypromine is a irreversible/reversible
inhibitor of MAO-______ |
|
Definition
|
|
Term
| TCAs are inhibitors of _____, _____ and to a lesser extent _____ uptake. |
|
Definition
|
|
Term
|
Definition
| transporters that remove these NE, 5-HT, & DA from the synaptic cleft |
|
|
Term
| We do know that consistent with the delay in therapeutic effect for all antidepressant drugs, - we know that _______ processes are involved that lead to increase neurotransmission. |
|
Definition
|
|
Term
| Three key processes are involved in the neuroadaptive process of Antidepressants: __________. |
|
Definition
(1) At the postsynaptic membrane – there is increased adrenergic or serotonerigic receptor density or sensitivity as well as increased G-protein coupling.
(2) There is increased neurogenesis (and presumably synaptic contacts)
(3) Downregulation of the transporters for serotonin (SERT) , norepinephrine (NET) etc..and therefore increased neurotransmitter in synapse. |
|
|
Term
| So bottom line is that the intial treatment with antidepressant drug results in immediate inhibition of NT transporter with a modest increase in neurotransmission, but over time there are adaptive changes that result in a far more robust increase in the level of neurotransmission and this then has a therapeutic benefit. |
|
Definition
|
|
Term
| For TCAs there is a range of selectivity of inhibition of ____ vs _____ transporters. |
|
Definition
|
|
Term
| The tertiary amines TCAs exhibit roughly inhibtion of _______. |
|
Definition
| equal inhibition of NE and 5-HT transporters |
|
|
Term
| The Secondary amines TCAs inhibit _______. |
|
Definition
| preferentially inhibit NE over 5-HT transporters |
|
|
Term
| Given that ______ of ______ TCAs occurs metabolically, administration of a _______ TCAs will result in the patient having both parent drug and active metabolite producing antidepressant action. |
|
Definition
demethylation
tertiary amines
tertiary amines |
|
|
Term
| _______ + ____________ if tertiary amine TCA is given. |
|
Definition
| Parent Drug + Active Metabolite |
|
|
Term
Tertiary amine TCA Parent Drug + Active Metabolite:
_______--> Desipramine
________--> Nortriptylene |
|
Definition
|
|
Term
| TCAs have very degrees of _______ activity depending upon the specific drug. |
|
Definition
|
|
Term
| Anticholinergic activity of some TCAs blocks ______ receptors. |
|
Definition
|
|
Term
| Because of their Anticholinergic at muscarinic receptors, TCAs are contradicted in: ________. |
|
Definition
| glaucoma, prostatic hypertrophy, or dementia |
|
|
Term
| TCAs shouldn't be prescribed in the elderly because ________. |
|
Definition
| they are particularly sensitive to the anticholinergic effects of TCAs |
|
|
Term
| Anticholinergic side effects of TCAs? |
|
Definition
dry mouth, blurred vision
urinary retention/ileus/constipation
sexual dysfunction
delirium/confusion
precipitation of glaucoma |
|
|
Term
|
Definition
|
|
Term
| TCAs cause Orthostatic hypotension by __________. |
|
Definition
| blockade of alpha1 adrenergic receptors |
|
|
Term
| TCAs have a ______ effects on heart muscle and are concentration _______. |
|
Definition
|
|
Term
| TCA EKG changes: __________. |
|
Definition
| flattening of the T wave or T wave inversion, myocardial depression, and arrhythmias at high concentrations. |
|
|
Term
| TCAs inhibit many isoforms of ______ enzymes and thus alter the metabolism of many drugs. |
|
Definition
|
|
Term
| TCAs reduce the _______ actions of guanethidine, alpha-methyl dopa, and clonidine. |
|
Definition
|
|
Term
| TCAs _____ the _____ threshold and are not good drugs for treatment of patients with ______ disorders. |
|
Definition
|
|
Term
| TCAs are _______ and therefore have an additive effect when combined with _______. |
|
Definition
| sedating they have additive effects with other sedatives such as alcohol. |
|
|
Term
| TCAs act synergestically with ________. |
|
Definition
| other anticholinergic drugs |
|
|
Term
| TCAs should never be given with ______. |
|
Definition
|
|
Term
| TCAs should never be given with MAO inhibitors, because a ______ crisis, including ________ or _____ can result. |
|
Definition
hyperpyretic
convulsions, coma |
|
|
Term
| Tricyclic antidepressants have a _______ therapeutic window |
|
Definition
|
|
Term
| ______, ______, and ______ can occur with OD of TCAs. |
|
Definition
| Hypotension, shock, and renal failure |
|
|
Term
| With TCA OD,________ seizures and hyper________ and coma may occur |
|
Definition
Grand mal seizures
hyperpyrexia |
|
|
Term
| With TCA OD, ______ can reverse much of the anticholinergic action. |
|
Definition
|
|
Term
|
Definition
| parasympathomimetic alkaloid, specifically, a reversible cholinesterase inhibitor. |
|
|
Term
| With TCA OD, _______ and/or ________ to remove as much of the ingested dose as possible. |
|
Definition
| gastric lavage and/or activated charcoal |
|
|
Term
| TCA OD pt should be monitored in the CCU for at least 72 hours, because __________. |
|
Definition
| arrhythmias may occur after the crisis has appeared to pass. |
|
|
Term
| Tricyclic Antidepressants Other Uses: __________. |
|
Definition
Catalepsy (Narcolepsy)
OCD
Chronic Pain (Migraine) Panic Disorder
Post-traumatic Stress Disorder
Enuresis
ADHD Eating Disorders |
|
|
Term
| 3rd Generation Antidepressants Miscellaneous Drugs: _______. |
|
Definition
heterocyclics
Trazadone
Bupropion |
|
|
Term
| The heterocyclics have the _____ backbone, but also have an additional ring. |
|
Definition
|
|
Term
| The heterocyclics: __________. |
|
Definition
|
|
Term
| amoxapine is a _____ blocker. |
|
Definition
| Non-selective antidepressant (NE and 5-HT and DA) |
|
|
Term
| maprotilene is a _____ blocker. |
|
Definition
| selective at the NE transporter |
|
|
Term
| _______ pts. with _______ have been reported to respond better to maprotilene. |
|
Definition
| Depressed patients with lethargy |
|
|
Term
| Trazadone is an atypical antidepressant in a class by itself, in that it is a _________ inhibitor and has ___________. |
|
Definition
5-HT selective reuptake
no antichol effects |
|
|
Term
| Trazadone is extremely _______ and is associated with ______. |
|
Definition
| extremely sedating and is associated with sexual dysfunction in males |
|
|
Term
| Bupropion is a _______ inhibitor? |
|
Definition
| DA selective reuptake inhibitor |
|
|
Term
| Bupropion, given its effect on DA levels it is useful in controlling __________. |
|
Definition
| The craving for nicotine (smoking cessation) |
|
|
Term
| Bupropion is effective in _______ in addition to smoking cessation. |
|
Definition
|
|
Term
| Bupropion because it only targets DA has no _______ like in SSRIs. |
|
Definition
|
|
Term
| SSRIs have no effects on: ___________. |
|
Definition
Cholinergic, Histamine, or
alpha-adrenergic Receptors |
|
|
Term
| _______ prototypic SSRI (most prescribed). |
|
Definition
|
|
Term
|
Definition
| Selective Serotonin Reuptake Inhibitors |
|
|
Term
|
Definition
| Inhibition of the SERT transporter |
|
|
Term
| SSRIs don't interact with H1 receptors in CNS and therefore are __________ unlike TCAs. |
|
Definition
|
|
Term
| In addition to depression, Fluoxetine is prescribed for: ________. |
|
Definition
| OCD, bulimia, PMS, panic disorder, anxiety disorders |
|
|
Term
| SSRI side effects: __________. |
|
Definition
| Headache, Insomonia, restlessness, nausea (likely 5-HT3R mediated), anorexia, and sexual dysfunction, which includes: erectile dysfunction, delayed ejaculation in males and anorgasmia. |
|
|
Term
| Fluoxetine is a first line antidepressant approved for treatment of _____________. |
|
Definition
| major depression in children |
|
|
Term
| ________ is a ____ class of drugs that treats OCD in children. |
|
Definition
|
|
Term
|
Definition
| increased risk for suicide in children |
|
|
Term
| All SSRI’s can as a result of interactions with _________ cause the serotonin syndrome. |
|
Definition
|
|
Term
| serotonin syndrome: a rare but potentially life-threatening condition characterized by altered mental status, fever, agitation, tremor, etc. |
|
Definition
|
|
Term
| Three main SSRI: ____________. |
|
Definition
Fluoxetine (Prozac)
Sertaline (Zoloft)
Paroxetine (Paxil) |
|
|
Term
| Sertaline (Zoloft) is a _____ drug used in the treatment of _______. |
|
Definition
SSRI
Major Depression, OCD, panic disorder |
|
|
Term
| Paroxetine (Paxil) is a _____ drug used in the treatment of _______. |
|
Definition
SSRI
Major Depression, OCD, panic disorder |
|
|
Term
| In addition to Fluoxetine, Sertaline, and Paroxetine, _______ and ______ are other SSRIs. |
|
Definition
| Citalopram (Celexa) and Escitalopram (Lexapro) which is just the S-enantiomer of Citalopram. |
|
|
Term
|
Definition
| serotonin and norepinephrine selective reuptake inhibtors |
|
|
Term
|
Definition
|
|
Term
| Main side effect of SSRIs? |
|
Definition
|
|
Term
| ________ has been the treatment for bipolar disorder. |
|
Definition
|
|
Term
| At therapeutic levels, Lithium has a ________. |
|
Definition
|
|
Term
| The therapeutic window for lithium is ________. |
|
Definition
|
|
Term
|
Definition
| memory problems, weight gain, tremor, poluria, drowsiness, hypothyroidism, cardiac effects |
|
|
Term
| The therapeutic index of Lithium is _____ times for acute intoxication can cause: ___________. |
|
Definition
2-3
vomiting, profuse diarrhea, ataxia, coma, and convulsions |
|
|
Term
|
Definition
|
|
Term
| Often- in addition to lithium, a _______ is sometimes prescribed during _______ phase. |
|
Definition
antidepressant
depression |
|
|
Term
| An antidrepessant is never prescribed alone for a Bipolar pt. because it can elicit a ______ that can __________. |
|
Definition
switch
trigger a manic episode |
|
|
Term
| Because of Lithium's low TI, alternatives like: ______ have been used in the treatment of Bipolar. |
|
Definition
| anticonvulsant agents, including valproic acid, carbamezepine, lamotrignine |
|
|
Term
| Prior to starting treatment with lithium or carbamazepine for Bipolar, often an _______ like _______ will be given to stabilize the patient. |
|
Definition
|
|
Term
| Atypical antipsychotics such as ________ are sometime given as add on agents to help manage bipolar disorder and are also prescribed as add-on treatment for major depression, particularly for patients that don’t respond well to an ______. |
|
Definition
|
|
Term
|
Definition
| periodic disturbance of brain function that is recurrent and which is associated with excessive neuronal activity/discharge for which the behavioral consequence is seizure. |
|
|
Term
| The six general categories of seizures: __________. |
|
Definition
Partial Seizures:
Simple partial, Complex partial,
Partial with secondarily generalized tonic-clonic seizure
Generalized Seizures:
Absence Seizure, Myoclonic Seizure, Tonic-Clonic seizure |
|
|
Term
| Simple partial seizures key feature? |
|
Definition
| preservation of consciousness* |
|
|
Term
| Complex partial seizures are characterized by ___________. |
|
Definition
| Impaired consciousness lasting 30 seconds to two minutes |
|
|
Term
| Complex partial seizures are often associated with _______ movements such as ______ or ________. |
|
Definition
purposeless
Lip smacking or hand wringing |
|
|
Term
| Partial seizures secondarily generalized is a partial seizure that __________. |
|
Definition
|
|
Term
| Absence (_______) seizures |
|
Definition
|
|
Term
| Absence (petit mal) seizures are ____ in duration. |
|
Definition
| short (usually less than 10 seconds but not more than 45 seconds) |
|
|
Term
| Absence (petit mal) seizures are short and result in an ___________. |
|
Definition
| abrupt loss of consciousness*** |
|
|
Term
| Absence (petit mal) seizures are associated with _____-voltage, ______ synchronous, ________ spike-and-wave pattern in the EEG |
|
Definition
high
bilaterally
3-per-second |
|
|
Term
| Myoclonic is an atypical _______. |
|
Definition
| Atypical absence seizures; tonic seizures; atonic seizures; clonic and myoclonic seizures?????????? |
|
|
Term
| Myoclonic seizure description? |
|
Definition
| A brief (one second) shock like contraction of muscles that may be restricted |
|
|
Term
| Tonic-Clonic seizure is like a _______, except it is not ______. |
|
Definition
Partial with secondarily generalized tonic-clonic seizure
not proceeded by a partial seizure |
|
|
Term
| partial seizures- _____% of all epilepsies. |
|
Definition
|
|
Term
| Partial seizures are caused by ________. |
|
Definition
|
|
Term
| Partial seizures are caused by lesions resultant of: _______. |
|
Definition
| examples (tumor, malformation, or due to damage caused by trauma or stroke) |
|
|
Term
| Generalized seizures are usually _____ in etiology. |
|
Definition
|
|
Term
| Status Epilepticus is a state in which there are ___________. |
|
Definition
| recurring seizures without restoration of consciousness between seizures |
|
|
Term
| The bulk of the inhibitory synaptic activity in the CNS is mediated by the neurotransmitter, __________ and the bulk of the excitatory activity is mediated by _________. |
|
Definition
gamma amino butyric acid or GABA
glutamate |
|
|
Term
| Microinjection into the brain of antagonists of the ________ trigger seizures. |
|
Definition
|
|
Term
| Microinjection of GABAA receptor agonists or glutamate receptor subtype antagonists, ______ seizures |
|
Definition
|
|
Term
| "Epileptic" neurons show (sudden) paroxysmal depolarizing shifts of membrane potential associated with high ______ bursts, loss of ______, and synchronous discharge of _______ cells. |
|
Definition
frequency
IPSPs
surrounding |
|
|
Term
| With sufficient spread, the entire brain is involved, resulting in a ________ seizure and unconsciousness |
|
Definition
|
|
Term
| the most widely used animal model of partial epilepsy is termed “________”. |
|
Definition
|
|
Term
| Kindling refers to a process in which repeated, focal application of initially subconvulsive electrical stimulation to the ________ that result in intense partial epilepsy. |
|
Definition
|
|
Term
| Kindling refers to a process in which repeated, focal application of initially subconvulsive electrical stimulation to the amygdala that result in intense partial epilepsy. Once established, this increased hypersensitivity ____________. |
|
Definition
| persists for the life of the animal |
|
|
Term
| Another widely used model of partial epilepsy consists of spontaneous seizures occurring after repeated seizure induced by chemoconvulsants such as ________ or __________. |
|
Definition
| pilocarpine or pentylenetetrazol (ptz) |
|
|
Term
| Anticonvulsant work to elevate __________. |
|
Definition
| threshold for discharge of "epileptic" neurons |
|
|
Term
| Anticonvulsant work to prevent __________. |
|
Definition
| spread of seizure activity to normal neurons |
|
|
Term
| Anticonvulsants can result in death from ______ or _______. |
|
Definition
| aplastic anemia or hepatic failure |
|
|
Term
| Phenytoin is perscribed for ________, but not _________. |
|
Definition
1) Generalized tonic-clonic (grand mal) - adults and older children
2) Simple partial seizures - adults and older children
3) Complex partial seizures (psychomotor)
4) Status epilepticus
**** but not for absence seizures ********** |
|
|
Term
| Phenytoin has significant anticonvulsant action without ________, that is it is __________. |
|
Definition
generalized CNS depression
non-sedative |
|
|
Term
| Phenytoin acts by limiting? |
|
Definition
| maximum seizure activity & high-frequency repetitive firing of neurons |
|
|
Term
| Phenytoin acts by preventing ________ and ________ neuron membranes. |
|
Definition
|
|
Term
| Phenytoin limits the repetitive firing of action potentials in neurons evoked by __________. |
|
Definition
|
|
Term
| Phenytoin limits the repetitive firing of action potentials in neurons evoked by sustained depolarization by __________. |
|
Definition
| slowing of the rate of recovery of voltage-activated Na channels from inactivation |
|
|
Term
| Phenytoin MOA: binds to and stabilizes the __________, thereby _______ and ultimately _________. |
|
Definition
inactivated state of the Na channel
slowing the recovery from inactivation
reducing the firing rate |
|
|
Term
| A key point is that because phenytoin binds to the inactivated state, that is the sodium channels have to be ______ for phenytoin bind, and then phenytoin action is ________. |
|
Definition
activated (bc inactivated state comes after the activated state)
use-dependent |
|
|
Term
| A key point is that because phenytoin binds to the inactivated state, that is the sodium channels have to be activated for phenytoin bind, and then phenytoin action is use-dependent. This is significant because _______. |
|
Definition
| phenytoin does not affect the regular firing rates of neurons, which is why phenytoin does not lead to generalized depression of the CNS and sedation. But phenytoin does impair the high-frequency firing of neurons during seizure. |
|
|
Term
| Phenytoin is not a _______ like local anesthetics! |
|
Definition
|
|
Term
| Phenytoin will ________ sodium channels and therefore neuronal firing..BUT it will not shut it down completely like local anesthetics do. |
|
Definition
| slow the opening and closing of |
|
|
Term
| Phenytoin is administered by ______, because it will __________. |
|
Definition
IV
precipitates if given IM and remains at site |
|
|
Term
| Phenytoin protein binding? Significance? |
|
Definition
| 70-95% bound; probability of toxicity increased when albumin is low, thereby increasing free concentration; drugs that compete for binding enhance phenytoin toxicity |
|
|
Term
| Phenytoin is metabolized through _______. |
|
Definition
|
|
Term
| Phenytoin observes _____ order kinetics for metabolism. |
|
Definition
|
|
Term
| Phenytoin is _____ order kinetics at the high therapeutic dosage. |
|
Definition
|
|
Term
| Because Phenytoin observes zero order kinetics at therapeutic doses, there is potential for __________. |
|
Definition
| rapid accumulation and toxicity with small increases in dose |
|
|
Term
| Carbamzepine ______ type of drug? |
|
Definition
|
|
Term
| Carbamzepine is used to treat? |
|
Definition
1) Generalized tonic-clonic
2) Simple partial
3) Complex partial
(like Phenytoin minus Status epilepticus) |
|
|
Term
|
Definition
| Same as Phenytoin (stabilizes inactive state of Na+ channel) |
|
|
Term
| Carbamzepine slows recovery from ________ for Na+ Channels. |
|
Definition
|
|
Term
| Carbamzepine DOC for? especially for? |
|
Definition
partial seizures
complex partial |
|
|
Term
| Carbamzepine can be combined with ______ for difficult cases. |
|
Definition
|
|
Term
| Chemically carbazmebpine is related to __________. |
|
Definition
| tricyclic antidepressants |
|
|
Term
| Chemically carbazmebpine is related to tricyclic antidepressants, but in contrast to carbamazepine, TCAs enhance _________! |
|
Definition
|
|
Term
| Carbamzepine is primary agent for the treatment of _______. |
|
Definition
|
|
Term
| Phenobarbital chemical class? |
|
Definition
|
|
Term
| Phenobarbital treats: _______. |
|
Definition
1) Generalized tonic-clonic and simple partial (infants and preschool)
2) Complex partial
3) Status epilepticus (like Phenytoin, but not Carbamzepine) |
|
|
Term
| Phenobarbital and other barbiturates bind to a site in the ________ domain of the ________. |
|
Definition
transmembrane
GABAa receptor protein |
|
|
Term
| Barbiturate binding to the GABAaR allosterically modulates the receptor to ________ but not the _______ of channel openings. |
|
Definition
increase the duration
frequency |
|
|
Term
| In addition to barbiturates, what other class of drugs bind GABAaR? |
|
Definition
|
|
Term
| Barbiturates bind _____ domain of GABAaR, while Benzodiazepines binds _______. |
|
Definition
transmembrane
extracellular |
|
|
Term
Benzodiazepines affect on GABAaR?
Barbiturates affect on GABAaR? |
|
Definition
increase the frequency of channel openings but not the duration
increase the duration but not frequency |
|
|
Term
| Net result for Benzodiazepines vs Barbiturates? |
|
Definition
Same
potentiate the chloride currents mediated by the GABBA receptor channels |
|
|
Term
| The potentiating of the chloride current by Barbiturates, the neuron ________. |
|
Definition
| membrane becomes hyperpolarized |
|
|
Term
| Phenytoin advantage over Phenobarbitol? |
|
Definition
| less selective than phenytoin, that is there is more generalized depression of the CNS, hence sedation) |
|
|
Term
| Phenobarbitol is not effective in ______ seizures and may in fact ______. |
|
Definition
| Not effective in absence seizures and may exacerbate them. |
|
|
Term
| Phenobarbitol must be ______ in order to avoid seizures. |
|
Definition
|
|
Term
| Phenobarbitol protein bound? |
|
Definition
| 40-60% protein bound (vs 70-95% with Phenytoin) |
|
|
Term
|
Definition
| 25-50% excreted unchanged |
|
|
Term
| Phenobarbitol excretion, 25-50% excreted unchanged, is ______ dependent. |
|
Definition
|
|
Term
|
Definition
| 2-6 days in adults (steady state in weeks) |
|
|
Term
| Phenobarbitol has large variability in __________. |
|
Definition
| blood levels from same dose |
|
|
Term
| Phenobarbitol inhibits/induces _______ enzymes. |
|
Definition
| induces microsomal (increase metabolism of other drugs) |
|
|
Term
| Phenobarbitol main toxicity in adults? |
|
Definition
|
|
Term
| Phenobarbitol toxicity: ____________. |
|
Definition
Drowsiness in adults; interference with cognitive function; paradoxical excitement in children (may require stopping drug)
Skin rash which may rarely become severe
Nystagmus, ataxia at excessive doses
Hypoprothrombinemia in newborn, vitamin K responsive
Megaloblastic anemia due to folate deficiency
Osteomalacia (altered vitamin D metabolism) |
|
|
Term
| Phenobarbitol Contraindicated in? |
|
Definition
| acute intermittent porphyria |
|
|
Term
| Phenobarbitol drug drug interactions, increased metabolism of? |
|
Definition
| oral anticoagulants and clonazepam |
|
|
Term
| _______ can inhibit phenobarbital metabolism. |
|
Definition
|
|
Term
| Primodone is a congener of _______ and has the same spectrum of treatments, but it ___________. |
|
Definition
phenobarbitol
not a 1st DOC |
|
|
Term
| Primodone is metabolically converted to? |
|
Definition
|
|
Term
| Primodone has the same metabolism as? |
|
Definition
|
|
Term
| Why not use other barbiturates, like pentobarbital? |
|
Definition
| Phenobarbital has only 40% the efficacy of pentobarbital. Therefore Phenobarbital will suppress high-frequency firing of neurons by increasing inhibitory currents that flow-through GABAAR, but it has a much reduced effect on normal firing and hence reduced sedative properties. |
|
|
Term
|
Definition
1) Generalized tonic-clonic and simple partial (infants and preschool)
2) Complex partial
3) Status epilepticus
(same as phenobarbitol) |
|
|
Term
| Ethosuximide is DOC for _______. |
|
Definition
| uncomplicated absence (petit mal) seizures |
|
|
Term
|
Definition
uncomplicated absence (petit mal) seizures (Phenytoin, CARBAMAZEPINE, and phenobarbitol do not)
it is ineffective in all other seizures |
|
|
Term
|
Definition
| low-threshold calcium currents or T currents in neurons in the thalamus |
|
|
Term
| The thalamus plays an important role in the generation of a ________ rhythm which is typical of ______ seizures. |
|
Definition
|
|
Term
| By blocking the ______ ethosuximide inhibits absence seizures. |
|
Definition
|
|
Term
| Ethosuximide administration? |
|
Definition
|
|
Term
| Ethosuximide protein bound? |
|
Definition
| Not significantly bound to plasma proteins (unlike Phenytoin 90% and phenobarbital 50%) |
|
|
Term
|
Definition
|
|
Term
| Ethosuximide excretion _____% unchanged. |
|
Definition
| 10-20% excreted unchanged |
|
|
Term
|
Definition
Most common: GI disturbances, fatigue, lethargy, headache, dizziness.
Eosinophilia in 10%
Rare: blood dyscrasias, Stevens-Johnson syndrome |
|
|
Term
| Ethosuximide OD at toxic levels can result in __________, which is irreversible/reversible. |
|
Definition
| Psychotic behavior ; reversible |
|
|
Term
| Valproic Acid (Valproate) treats? |
|
Definition
1) Absence (like Ethosuximide)
2) Generalized tonic-clonic
3) Myoclonic and atonic (may be effective when other agents fail)
4) Mixed
5) Partial seizures
All except Status Epilepticus |
|
|
Term
| Valproate is a _______ antiepileptic agent, because it ________. |
|
Definition
broad-spectrum
has multiple actions |
|
|
Term
| Valproate actions: __________. |
|
Definition
1. Like phenytoin, valproate slows the recovery from inactivation of Na+ channels
2. Like ethosuximide, reduction in the T-currents important in absence seizures
3. inhibit enzymes responsible for degrading GABA, and therefore potentiate GABAA receptor currents (Cl-) indirectly by allowing the concentration of GABA to remain elevated. |
|
|
Term
| Valproate is frequently used ______. |
|
Definition
| in combination with other drugs |
|
|
Term
|
Definition
⋅Most common: Nausea, vomiting, anorexia (use enteric-coated formulation, Depakote, or take with
food)
⋅Serious: hepatic toxicity and pancreatitis
Neural tube defects (spina bifida) for women who took while pregnant. |
|
|
Term
| Diazepam (Valium) drug class? |
|
Definition
|
|
Term
| Diazepam (Valium) treats? |
|
Definition
| Intravenous diazepam is frequently used to terminate STATUS EPILEPTICUS |
|
|
Term
| Diazepam (Valium) used treat Status Epilepticus over ___________, because of _______. |
|
Definition
Phenobarbital and Phenytoin
more rapid |
|
|
Term
| Diazepam can cause ______ and _____ when given too rapidly, but these are less likely to occur with diazepam than with i.v. ________ or _______ for treating Status Epilepticus. |
|
Definition
respiratory and cardiovascular depression
phenobarbital or phenytoin |
|
|
Term
| Diazepam duration of action? |
|
Definition
|
|
Term
| Because Diazepam has a short duration of action it should be followed with ________. |
|
Definition
| phenytoin to avoid recurrent seizures |
|
|
Term
| in addition to Diazepam, Phenytoin, & Phenobarbital; __________ and __________ are also used in Status Epilepticus. |
|
Definition
|
|
Term
| Diazepam is an antagonist/agonist of _________. |
|
Definition
|
|
Term
| Barbiturate and benzodiazepines bind to separate sites on the GABAA receptor and act allosterically to potentiate the ______ current. |
|
Definition
|
|
Term
| Diazepam and other benzodiazepines potentiate the chloride current by __________. |
|
Definition
| increasing the frequency of channel opening without effecting the duration of the channel open time |
|
|
Term
| The principal side-effect in long-term therapy with diazepam or clonezapam is _______ and ________. |
|
Definition
|
|
Term
|
Definition
| partial seizures with or without secondary generalization in adults when used in addition to other ant seizure drugs |
|
|
Term
|
Definition
| increases the release of GABA by an unknown mechanism |
|
|
Term
| Lamotrigine for the treatment of __________. |
|
Definition
| partial seizures in adults when used in addition to other drugs |
|
|
Term
|
Definition
| slowing the rate of recovery from inactivation for sodium channels (like phenytoin and carbamazepine) |
|
|
Term
| Lamotrigine is just as efficacious as ______ but tolerated better. |
|
Definition
|
|
Term
|
Definition
| irreversible inhibitor of degradative enzyme GABA transaminase |
|
|
Term
| tau -vinyl GABA MOA leads to _______. |
|
Definition
|
|
Term
|
Definition
| partial and secondarily generalized seizures |
|
|
Term
| Felbamate was approved for the treatment of ______ seizures in 1993. An association with _______ led to its withdrawal, but has since been reintroduced. |
|
Definition
|
|
Term
|
Definition
| inhibits NMDA-evoked excitatory responses and potentiates GABA-evoked responses electro physiologically |
|
|
Term
|
Definition
| poorly controlled partial and secondarily generalized seizures |
|
|
Term
| In addition to basic types of seizures Felbamate can be used to treat? |
|
Definition
|
|
Term
| Lennox-Gastaut syndrome WIKI |
|
Definition
| difficult-to-treat form of childhood-onset epilepsy that most often appears between the second and sixth year of life, and is characterized by frequent seizures and different seizure types; it is often accompanied by developmental delay and psychological and behavioral problems. |
|
|
Term
| Hypnotic and ______ agents are frequently one and the same. |
|
Definition
|
|
Term
| Hypnosis, refers to the state of ______ and/or promotion of the onset and maintenance of ______. |
|
Definition
|
|
Term
| Hypnosis is a state from which the patient can be ________. |
|
Definition
|
|
Term
| Hypnotic agents are prescribed routinely for the treatment of ______. |
|
Definition
|
|
Term
| The _______ (like _______) and ________ (like ________) are first line treatment for most anxiety disorders. |
|
Definition
SSRI antidepressants (like fluoxetine)
SNRI antidepressants (like venlafaxine) |
|
|
Term
| Of the anti anxiety drugs marketed today, many are also used as _______. |
|
Definition
|
|
Term
| Hypnotics reduce: __________. |
|
Definition
| reduce tension, nervousness, fear, and apprehension (hence anti-anxiety use) |
|
|
Term
| Hypnotics when used for anti-anxiety are administered? |
|
Definition
| One dose is used at bedtime for hypnosis, while a reduced dose is employed during the waking hours as an anxiolytic. |
|
|
Term
| Short term insomnia: usually results from a: ____________. |
|
Definition
| stressor, such as grief, illness, or job related problems. |
|
|
Term
| The majority of Hypnotic agents that are prescribed do not produce ___________. |
|
Definition
| a completely normal state of sleep |
|
|
Term
| Hypnotics reduce the ______ that is they ____________. |
|
Definition
latency to sleep
reduce the amount of time required for the patient to fall asleep. |
|
|
Term
| Alteration of both ______ and _______ sleep are caused by hypnotics. |
|
Definition
|
|
Term
| The older Hypnotics , the _______, as well as ______, strongly depress REM sleep. |
|
Definition
|
|
Term
| Benzodiazepines depress _____ sleep to a much smaller degree than barbiturates, and strongly reduce __________ sleep. |
|
Definition
REM
stages 3 and 4 of nonREM |
|
|
Term
| Hypnotic agents tolerance issue? |
|
Definition
| lose their effectiveness in producing hypnosis in a matter of weeks. |
|
|
Term
| For Hypnotic agents; ________ lose their effectiveness within 2 weeks, whereas ________ lose their effectiveness over a matter of 4 to 6 weeks. |
|
Definition
Barbiturates
Benzodiazepines |
|
|
Term
| ______ sleep occurs after REM is suppressed for a while. |
|
Definition
|
|
Term
|
Definition
| discontinues the Hypnotic |
|
|
Term
|
Definition
| even more sleep disturbances, such as nightmares, etc. |
|
|
Term
| Rebound REM episodes and the resultant problems that they cause are a factor in ___________. |
|
Definition
| producing psychological dependence to hypnotics |
|
|
Term
| In addition to Rebound REM _________ can also occur following discontinuation of the hypnotic. |
|
Definition
|
|
Term
| Rebound insomnia results in an ___________. |
|
Definition
| the feeling of continued need for the drug |
|
|
Term
| Rebound insomnia can be minimized by? |
|
Definition
|
|
Term
| The brain has _____ levels of GABA relative to other neurotransmitters |
|
Definition
|
|
Term
| GABA acts at _ types of receptors: ______. |
|
Definition
|
|
Term
| GABAaR is inhibitory because it __________. |
|
Definition
|
|
Term
| When GABA binds to the GABAaR, the channel associated with the receptor opens, allowing ______ ions to flow through. |
|
Definition
|
|
Term
| In the presence of GABA, this theoretical neuron is hyperpolarized fro its resting membrane potential of -70 mV to _____ mV. |
|
Definition
|
|
Term
| Drug that blocks the pore of the GABAaR channel? |
|
Definition
| picrotoxin (causes seizures) |
|
|
Term
| GABAaR is made up of ____ subunits? |
|
Definition
|
|
Term
| The ligand recognition site for GABA is in the ___-terminus of the protein which rises above the ________ surface of the plasma membrane. |
|
Definition
|
|
Term
| The average GABaA receptor is probably composed of _____, _____, and _____ subunits. |
|
Definition
|
|
Term
| The site for GABA binding is located in the extracellular portion of the receptor, at the interface of the _____ & ______ subunits |
|
Definition
|
|
Term
| The site for binding of the benzodiazepines is at the interface of the ______ & ______ subunits |
|
Definition
|
|
Term
| GABA and benzodiazepines don't/do bind to the same site on the receptor? |
|
Definition
|
|
Term
| Barbiturates do not bind to either the site occupied by _____ nor the site that binds ________. |
|
Definition
|
|
Term
| Barbiturate binding site, there are two binding sites located at the interface of the _____ & _____ subunits within the ________ domain. |
|
Definition
alpha/beta
beta/gamma
transmembrane |
|
|
Term
| While barbiturates and benzodiazepines bind to separate sites, they both ________ the effects of GABA. |
|
Definition
|
|
Term
| Safer barbiturates or benzodiazepines? |
|
Definition
|
|
Term
| The binding site for _______ is located in this same region of the barbiturates binding. |
|
Definition
| general anesthetics, that is etomidate, propofol as well as Alcohol… |
|
|
Term
| Barbiturates can be conveniently divided into 3 classes based on the half-life: the long acting barbs, such as ________; short to intermediate acting (________); and ultrashort acting (_________). |
|
Definition
Long- Phenobarbital
Int- secobarbital
Short- thiopental |
|
|
Term
| Barbiturates are administered? |
|
Definition
| orally for their sedative-hypnotic effects |
|
|
Term
| Barbiturates weak bases or weak acids? |
|
Definition
|
|
Term
| _______ favors the protonated (uncharged) form of Barbiturates. |
|
Definition
| Acidosis (they are Weak acids) |
|
|
Term
| Acidosis for Barbiturates increases ______ and therefore __________. |
|
Definition
protonated (uncharged)
penetration of BBB (CNS) |
|
|
Term
| Barbiturates concern for prego? |
|
Definition
|
|
Term
| The ultrashort acting barbiturates are the most ________ and the termination of their CNS action is by ________. |
|
Definition
lipophilic
redistribution |
|
|
Term
| ultrashort acting barbiturate example? |
|
Definition
|
|
Term
| Thiopental is also metabolized, but its ______ from the brain to other tissues accounts for its short anesthetic and hypnotic/sedative action. |
|
Definition
|
|
Term
| Other than the ultrashort acting barbiturate, thiopental, barbiturates are eliminated by? |
|
Definition
|
|
Term
| Metabolism steps for barbiturates? |
|
Definition
Oxidation, desulfuration, glycosylation, and N-hydroxylation are all examples of Phase I metabolism
Next, glucuronidated and excreted by the kidney. |
|
|
Term
| Phenobarbital is ____ than other barbiturates. |
|
Definition
|
|
Term
| Between 25-50% of ______ Phenobarbital is excreted in the urine |
|
Definition
|
|
Term
| Barbiturates ________ the actions of GABA at therapeutic doses. |
|
Definition
|
|
Term
| Barbiturates ________ the actions of GABA at higher than therapeutic doses. |
|
Definition
| act as a GABA mimetic (that is at high concentrations, barbiturates directly open the GABAAR channel) |
|
|
Term
| At high concentrations, barbiturates act as ________. |
|
Definition
|
|
Term
| The CNS effects of barbiturates are concentration independent/dependent. |
|
Definition
|
|
Term
| At lower concentrations barbiturates produce: __________. |
|
Definition
| sedation, hypnosis, and cognitive impairment |
|
|
Term
| At higher concentrations barbiturates produce: ___________. |
|
Definition
|
|
Term
| At toxic doses barbiturates produce: ___________. |
|
Definition
| respiratory depression and death |
|
|
Term
| Continuum of barbiturates:_________. |
|
Definition
| sedation…..hypnosis…….anesthesia…..death |
|
|
Term
| The ______ effects are extremely modest at therapeutic doses for barbiturates. |
|
Definition
|
|
Term
| At toxic doses of barbiturates, the depression of _______ can lead to circulatory collapse. |
|
Definition
|
|
Term
| Major drawback for Barbiturates? |
|
Definition
| induce P450 enzymes. Therefore, they enhance their own metabolism, as well as that of all drugs that are metabolized by the P450 system. |
|
|
Term
| How to treat Phenobarbital poisoning? |
|
Definition
| alkalinization of the urine can promote its excretion |
|
|
Term
| A significant fraction of Phenobarbital is excreted unchanged in the urine; alkalinization will result in _______ of Phenobarbital (promoting _______ form) and enhance its excretion. |
|
Definition
deprotonation
charged form |
|
|
Term
| If less than 24 hours have elapsed since Phenobarbital ingestion, ________ should be considered, since barbiturates ________. |
|
Definition
gastric lavage
reduce GI motility |
|
|
Term
| ______ is affected early in barbiturates poisoning. |
|
Definition
|
|
Term
| In severe barbiturates poisoning, _______ are depressed and ________ falls, cardiac contractility is depressed, and depression of ______ ganglia occur. |
|
Definition
vasomotor centers
blood pressure
sympathetic |
|
|
Term
| With severe barbiturates poisoning following shock and renal failure ___________ and _______ have to be instituted. |
|
Definition
| Dopamine treatment and hemodialysis |
|
|
Term
| _______ are contraindicated in Phenobarbital intoxication. |
|
Definition
|
|
Term
| The ________ have largely replaced barbiturates as sedatives and hypnotics. |
|
Definition
|
|
Term
| With benzodiazepines compared to barbiturates, the therapeutic index is higher, tolerance and liability for abuse is lower, and less drug interactions occur. |
|
Definition
|
|
Term
| In the presence of _______, a benzodiazepine agonist, the curve is shifted to the left for GABA response. |
|
Definition
|
|
Term
| Benzodiazepines do not directly _________ at any concentration. |
|
Definition
|
|
Term
| At no concentration of diazepam alone is there any ___________, unlike with barbituates. |
|
Definition
|
|
Term
| To repeat, hypnotic benzodiazepines, enhance or potentiate the actions of GABA, but do not directly activate the channel (they are not _______) |
|
Definition
|
|
Term
| Continuum for Benzodiazepines: _______. |
|
Definition
|
|
Term
| Benzodiazepines agonists stimulate GABAA receptor function by increasing the ________. |
|
Definition
| frequency of channel openings |
|
|
Term
| Benzodiazepines agonists have a number of uses that are primarily determined by the _______. |
|
Definition
|
|
Term
| ______ acting benzodiazepines (______ or _______) are used a hypnotics, in order to ________. |
|
Definition
Shorter
Alprazolam or Flurazepam
reduce day time drowsiness |
|
|
Term
| An ingested benzodiazepine may be pharmacologically ______ , as well its ________. |
|
Definition
|
|
Term
| Ideally, benzodiazepine concentration of drug or active metabolite during the day should be so low that no _______ occur. |
|
Definition
|
|
Term
| triazolam is a ____ acting benzodiazepine? |
|
Definition
|
|
Term
| Problems with using short acting benzodiazepines in order to keep low doses in day? |
|
Definition
may not be sufficient drug present in the early morning hours, so the patient may awaken early
anxiety during the daytime
rebound insomnia upon discontinuation of the drug |
|
|
Term
| Side effects and toxicity of the benzodiazepines are mostly _______ and ________ related. |
|
Definition
| psychomotor and cognitive |
|
|
Term
| The sedative effects of benzodiazepines are worse in the ______. |
|
Definition
|
|
Term
| The therapeutic index is so _____ that it is almost impossible to ________. |
|
Definition
high
commit suicide with benzodiazepines alone |
|
|
Term
| Benzodiazepines main use is that they are good _______. |
|
Definition
|
|
Term
| In addition to be going good hypnotics benzodiazepines are excellent for ______ that occurs with or without _________. |
|
Definition
|
|
Term
| __________ is a benzodiazepine that also has antidepressant activity in addition to anti-anxiety and is commonly used when both disorders are concurrent. |
|
Definition
|
|
Term
| Benzodiazepines are very good_________ and are useful in _______ that accompanies paralysis and neurological diseases such as MS. |
|
Definition
muscle relaxants
spasticity |
|
|
Term
| ________ is an antagonist of the benzodiazepine site of the GABAA receptor. |
|
Definition
|
|
Term
| Flumazenil intrinsic activity? |
|
Definition
|
|
Term
| Flumazenil reverses the effects of ______. |
|
Definition
|
|
Term
| Flumazenil is typically given in small repeated doses so as not to precipitate __________ withdrawl- which often includes __________. |
|
Definition
|
|
Term
|
Definition
| Same site as benzodiazepines (but not chemically a benzodiazepine) |
|
|
Term
| Zolpidem unlike the benzodiazepines does not _______ and therefore has ________. |
|
Definition
| doesn’t bind to all GABAAR subunit combinations and so has a more restricted action |
|
|
Term
| Zolpidem is a good _______, but a poor _______ or _______ unlike benzodiazepines. |
|
Definition
Good hypnotic
not an effective anticonvulsant or muscle relaxant |
|
|
Term
| Zolpidem produces fewer/more effects on __________, and is far less likely to produce _______ or _______ like Benzodiazepines. |
|
Definition
fewer
REM and nonREM sleep
rebound insomnia or daytime sedation |
|
|
Term
| The FDA approved lower recommended doses for ________ for women following studies that showed that women metabolize the drug more slowly (~40%) than do men, leading to increased adverse event reporting |
|
Definition
| zolpidem (Ambien) [benzodiazepine hypnotic] |
|
|
Term
| ______ is also a non-benzodiazepine hypnotic with similar features as Zolpidem (Ambien). |
|
Definition
|
|
Term
| Zolpidem vs Zalepon on short life? |
|
Definition
| Zolpidem is shorter (1hr) |
|
|
Term
| Both Zolpidem and Zalepon are used primarily to ________, which is why with their short half life that they don't _______. |
|
Definition
reduce sleep latency
don’t affect sleep architecture significantly |
|
|
Term
| Chloral hydrate is an older hypnotic that is still sometimes used. It is metabolized by the liver to the active compound trichloroethanol. It has a short duration of action and it produces fewer hangovers than the barbiturates. Like the other hypnotics, it stimulates the function of the GABAAR. It does not induce P450 enzymes like the barbs do. It can produce tolerance and dependence. |
|
Definition
|
|
Term
| Buspirone is a unique drug in that it __________. |
|
Definition
| an anxiolytic and not a hypnotic |
|
|
Term
| Buspirone related to barbs? |
|
Definition
|
|
Term
| Buspirone related to benzodiazepines? |
|
Definition
|
|
Term
| Buspirone act on ____ receptors. |
|
Definition
Not on GABAaR (like Barbs and benzodiazepines)
5-HT1A and DA 2 receptors |
|
|
Term
|
Definition
| doesn’t produce tolerance and dependence so there are no withdraw symptoms associated with its discontinuation. |
|
|
Term
| _________ is a hypnotic drug that is neither a barb or benzodiazepine. |
|
Definition
|
|
Term
| Ramelteon is an antagonist/agonist of ________ receptor. |
|
Definition
agonist
melatonin MT1 receptor |
|
|
Term
| Activation of the melatonin receptor by Ramelteon promotes ______. |
|
Definition
|
|
Term
| Ramelteon controlled substance? |
|
Definition
|
|
Term
| Ramelteon affect on sleep patterns? |
|
Definition
|
|
Term
|
Definition
| Nope just like Buspirone (anxiolytic not a hypnotic) |
|
|
Term
| ________ like _______ are often used off-label as anxiolytics |
|
Definition
|
|
Term
| Beta- Blockers are useful as anxiolytics in treating __________. |
|
Definition
|
|
Term
| Most common beta blocker used an an anxiolytics to treat performance anxiety? |
|
Definition
|
|
Term
| ________ are good skeletal muscle relaxants that act at the GABAa receptor. |
|
Definition
|
|
Term
| _______ is a p-chlorophenyl GABA and it selectively acts at the ______ receptor for skeletal relaxation. |
|
Definition
|
|
Term
| GABAb Receptors is inhibitory of the _______. |
|
Definition
|
|
Term
| GABAb Receptors are associated with? |
|
Definition
| G-Proteins (Not Cl- channels like GABAa) |
|
|
Term
| GABAb overall effect is to reduce? |
|
Definition
|
|
Term
| GABAb reduce NT release by acting through 2nd messenger systems to ______, which in turn ________. |
|
Definition
| stimulate K channel function, which hyperpolarizes the neuronal membrane |
|
|
Term
| Baclofen inhibitory actions in the spinal cord and brain are thought to underlie their ______ actions. |
|
Definition
|
|
Term
| Baclofen is an antispasmatic useful in the treatment of _______ and ______. |
|
Definition
| multiple sclerosis or spinal injury |
|
|
Term
| Baclofen Hypnotic activity? Anti anxiety ? |
|
Definition
|
|
Term
| In addition to Baclofen, _______ is also used in the reduction of spasticity in patients with paralysis or MS. |
|
Definition
|
|
Term
|
Definition
| blocks the release of Ca from the SR in muscle cells |
|
|
Term
| Dantrolene is typically given to the nonambulatory patient because it can cause _______. |
|
Definition
|
|
Term
| Dantrolene in addition to its antispasmatic action can be used in the treatment of __________. |
|
Definition
|
|
Term
| malignant hyperthermia is a condition triggered by _______. |
|
Definition
| general anesthetics or skeletal muscle blockers |
|
|
Term
| 3) Know that barbs enhance ________ and understand the consequences. |
|
Definition
|
|
Term
| 1) Know sedative/hypnotic’s effects on stages of sleep and their interaction with the GABAAR. |
|
Definition
|
|
Term
| 2) Know advantages of benzodiazepines over barbiturates |
|
Definition
|
|
Term
| narcotic analgesics: ________. |
|
Definition
| morphine, oxycodone, heroin, etc |
|
|
Term
| narcotic analgesics act through ______ pathway. |
|
Definition
|
|
Term
| _______, an opiate receptor antagonist- the placebo effect of opiods is eliminated. |
|
Definition
|
|
Term
| Opioid compounds can be broken down into 3 main categories: __________. |
|
Definition
naturally occurring extracts of opium
synthetic opioids
endogenous peptides, or opiopeptins |
|
|
Term
| The naturally occurring extracts of opium: ____________. |
|
Definition
|
|
Term
| The naturally occurring extracts of opium: morphine and codeine are antagonists/agonists? |
|
Definition
|
|
Term
| The synthetic opioids, which may be divided into 3 subsets: _________. |
|
Definition
agonists
antagonists
mixed agonists/antagonists |
|
|
Term
| The synthetic opioids subset of agonists: are similar to ________. |
|
Definition
|
|
Term
| The synthetic opioids subset of antagonists do what? |
|
Definition
| block the actions of opiates |
|
|
Term
| The synthetic opioids subset of mixed agonists/antagonists, which simultaneously have ____________. |
|
Definition
| stimulatory actions at one or more subsets of opiate receptors and inhibitory actions at one or more subsets of opiate receptors |
|
|
Term
| The endogenous peptides, or opiopeptins: __________. |
|
Definition
| endorphins, enkephalins, and the dynorphins |
|
|
Term
| _______ is the prototypical opiate. |
|
Definition
|
|
Term
| For agonists of morphine, the substitutions are typically at the ___ or _____ positions and sometimes at the ____ position. |
|
Definition
|
|
Term
| Codeine has a _____ substituent at the ___ position, which makes it a weaker ______ that morphine |
|
Definition
methoxy
3
agonist (sub at 3) |
|
|
Term
| Hydromorphone has a _____ group at position ___ instead of a hydroxyl; this substitution makes it fairly _____ to morphine with respect to efficacy. |
|
Definition
|
|
Term
|
Definition
| acetyl group at both the 3 and 6 positions |
|
|
Term
| Because of Heroin's substitutions of acetyl group at both the 3 and 6 positions it __________. |
|
Definition
| crosses the blood/brain more quickly than morphine |
|
|
Term
| After Heroin crosses the BBB it is ________. |
|
Definition
| quickly metabolized to 6-monoacetylmorphine and morphine in nervous tissues |
|
|
Term
| Heroin itself is not _________, but its _________. |
|
Definition
pharmacologically active
metabolites are and responsible for its effects |
|
|
Term
| The mixed agonist/antagonists or pure antagonists of opiods typically have substitutions at: ___________. |
|
Definition
|
|
Term
| The ______ is modified, in mixed agonist/antagonists or pure antagonists of opiods. |
|
Definition
|
|
Term
| Receptors for opiates in CNS: ___________. |
|
Definition
| mu, kappa, delta, and sigma |
|
|
Term
| The mu receptor for opiates is responsible for: _____________. |
|
Definition
| spinal and supraspinal analgesia, respiratory depression, miosis, euphoria, reduced GI motility, and physical dependence |
|
|
Term
| Most of the _____ opiates, such as ________, that are used interact selectively with mu receptors at standard dosages. |
|
Definition
| agonists, such as morphine |
|
|
Term
| Morphine and other agonist opiates are selective for the mu receptors until? |
|
Definition
| Given at high doses (lose selectivity) |
|
|
Term
| The kappa receptor is responsible for: ___________. |
|
Definition
spinal and to a lesser extent supraspinal analgesia
respiratory depression and miosis
dysphoria |
|
|
Term
| In contrast with the mu receptor the kappa receptor produces? |
|
Definition
|
|
Term
| The delta receptor is responsible for: __________. |
|
Definition
| both spinal and supraspinal analgesia, but spinal analgesia is more robust. |
|
|
Term
| The N/OFQ /sigma receptor may or may not be a true opiate receptor. It appears to be associated with dysphoria and hallucinations and may be a site of action for PCP. |
|
Definition
|
|
Term
| Postsynaptically opiate receptors are _______ type. |
|
Definition
|
|
Term
| Postsynaptic activation of opiate receptors results in ________ of adenyl cyclase and subsequent ________ in the amount of cAMP formed |
|
Definition
|
|
Term
| Opiate receptor is pre/postsynaptically. |
|
Definition
|
|
Term
| Postsynaptically Opiate receptor activation through Gi acts to enhance ________, which leads to ______ of the neuron. |
|
Definition
| enhance K+ channel current which results in hyperpolarization of the neuron |
|
|
Term
| By hyperpolarizing the neuron through opiate receptors, there is a reduction in _______. |
|
Definition
| pain transmission…decrease pain perception |
|
|
Term
| Presynaptically: Opiate receptor activation leads to __________. |
|
Definition
| inhibition of voltage-gated Ca channels |
|
|
Term
| Presynaptically: Opiate receptor activation leads to inhibition of voltage-gated Ca channels and subsequently ________. |
|
Definition
| suppression of the release of neurotransmitters such as NE, DA, 5-HT, Ach, and Substance P is blocked. |
|
|
Term
| Overall both pre/postsynaptically opiate receptors lead to ________. |
|
Definition
| (1) inhibition of postsynaptic signaling and (2) the suppression of transmitter release |
|
|
Term
| The opiate receptors are modulated by ___________. |
|
Definition
|
|
Term
| The endogenous opiates represent 3 distinct classes of ______. |
|
Definition
|
|
Term
| The endogenous opiates represent 3 distinct classes of peptides: ___________. |
|
Definition
endorphins
enkephalins
dynorphins |
|
|
Term
| The endogenous opiate, endorphin, is derived from? |
|
Definition
|
|
Term
| The endogenous opiate, enkephalin, is derived from? |
|
Definition
|
|
Term
| The endogenous opiate, dynorphin, is derived from? |
|
Definition
|
|
Term
| Endorphins (POMC) are fairly ______ in the CNS. |
|
Definition
|
|
Term
| Endorphins (POMC) precursors are found in areas of the brain where __________ can reduce pain. |
|
Definition
|
|
Term
| Endorphins (POMC) have high levels in the _________ which projects broadly in the brainstem and limbic areas and the spinal cord. |
|
Definition
|
|
Term
| Peptides from POMC are also found in the _______ and in __________. |
|
Definition
pituitary
islet cells of the pancreas |
|
|
Term
| Precursors of enkephalins and dynorphins distribution? |
|
Definition
| Widely throughout CNS (vs restricted with endorphins) |
|
|
Term
| Proenkephalin peptides are present in the areas of the CNS that are involved in __________. |
|
Definition
|
|
Term
| Proenkephalin peptides are present in the areas of the CNS that are involved in pain perception. For instance For instance, ________ of the spinal cord, the ________ nucleus, and the ___________ area. |
|
Definition
laminae I and II of SC
spinal trigeminal nucelus
periaqueductal gray area |
|
|
Term
| enkephalins and dynorphins are found also in areas that _______ in the CNS (in addition to pain perception areas). |
|
Definition
| modulate affective behavior, motor control, and autonomic function |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Pain can be broken down into 2 basic parts: ___________. |
|
Definition
| The original painful sensation and 2) his myriad reactions to it. |
|
|
Term
| Opiate agonists can alter the ________ of pain and the _______ to pain. |
|
Definition
|
|
Term
| __________ pain is usually more responsive to opiates. |
|
Definition
|
|
Term
| nociceptive pain- ___________. |
|
Definition
| painful stimuli from injured tissue is transmitted through intact neural pathways |
|
|
Term
| _________ pain is less responsive to opiates. |
|
Definition
|
|
Term
| neuropathic pain- ___________. |
|
Definition
| result of damage to neural pathways |
|
|
Term
| Dull/Sharp pain is more effectively controlled with opiates than is Dull/Sharp pain. |
|
Definition
| Dull more effective than sharp |
|
|
Term
| . If a person is not in pain and takes an opiate agonist, he will ________. |
|
Definition
| experience more unpleasant side effects |
|
|
Term
| The existence of pain appears to alter the production or intensity of _______ with opiate administration. |
|
Definition
|
|
Term
|
Definition
| nausea and vomiting, dysphoria, apathy, and decreases in mentation |
|
|
Term
| Both _______ and ________ sites have been identified as playing a role in opiate analgesia |
|
Definition
|
|
Term
| Ascending pain pathway is carried by the ________ tract. |
|
Definition
|
|
Term
| Nociceptive reflexes are inhibited and profound analgesia is produced when opiates are administered ____________ or ___________. |
|
Definition
| intrathecally (spinal cord) or locally in the dorsal horn of the spinal cord |
|
|
Term
| In afferent fibers of the spinothalamic tract, presynaptic localization of opiate receptors __________ involved in pain transmission. |
|
Definition
| inhibits the release of neurotransmitters |
|
|
Term
| Furthermore, activation of postsynaptic opiate receptors on ______ and ______ neurons of the spinothalamaic tract that relay painful stimuli result in reduced transmission to higher brain centers. |
|
Definition
|
|
Term
| Descending pain pathway- __________. |
|
Definition
|
|
Term
| Profound analgesia can also be produced by affecting the bulbospinal tract by instillation of morphine into the _________, as well as sites in the ________ and ________. |
|
Definition
third ventricle
midbrain and medulla (periaqueductal gray matter, nucleus raphe magnus, and the locus correleus) |
|
|
Term
| Opiates effect Descending pain pathway, bulbospinal tract, by causing an _________ its activity. |
|
Definition
|
|
Term
| Opiates enhance Descending pain pathway, bulbospinal tract activity (pain modulation) by ________. |
|
Definition
| GABAaR tonic inhbibition of descending pathway is turned off |
|
|
Term
| Experimentally, there is a synergistic response to the analgesic effects of morphine when it is applied to spinal and supraspinal sites. This result suggests that administration of an opiate to a patient by oral or IV route produces analgesia through both spinal and supraspinal mechanisms. |
|
Definition
|
|
Term
| The ___________ is involved in the production of euphoria and dysphoria by opiates. |
|
Definition
|
|
Term
| Euphoria and dysphoria from opiates is caused by activation of _______ neurons in the ventral tegmentum. |
|
Definition
|
|
Term
| Euphoria and dysphoria from opiates is caused by activation of DA neurons in the ventral tegmentum. This is because opiate receptor activation ________. |
|
Definition
| turns off the inhibition of DA neurons by GABAnergic neurons |
|
|
Term
| The DA neurons of the ventral tegmentum project to the ________ and are thought to produce the ______ & _______ effects of opiates. |
|
Definition
nucleus accumbens
euphoric and reinforcing |
|
|
Term
| _____ & ______ receptors appear to be involved in the reinforcing effects of opiates. |
|
Definition
|
|
Term
| _______ opiate receptors block the firing of DA neurons and this may underlie their disphoric effects. |
|
Definition
| Kappa (contrast to Mu and delta involved in the firing of DA neurons) |
|
|
Term
| The equilibration of the hypothalamic ______ regulatory mechanism is altered, such that ___________ after opiate administration. |
|
Definition
heat
temperature usually falls slightly |
|
|
Term
| In the hypothalamus, opiates inhibit/enhance the release of ____________ & __________. |
|
Definition
| gonadotropin releasing hormone and corticotropin releasing hormone |
|
|
Term
| In the hypothalamus, opiates inhibit/enhance the release of gonadotropin releasing hormone and corticotropin releasing hormone, this results in: ________ levels falling, while: ________ levels elevating. |
|
Definition
LH, FSH, ACTH, and -endorphin levels fall
Prolaction levels are increased |
|
|
Term
| Opiates acting at the mu receptor have an _______ effect. |
|
Definition
|
|
Term
| Miosis occurs with opiates bc of activation of ________ receptors on parasympathetic/sympathetic nerves innervating the pupil. |
|
Definition
mu and kappa
parasympathetic |
|
|
Term
| Toxic doses of opiates result in _______ pupils. |
|
Definition
|
|
Term
| Convulsions with opiates are due to ________ receptors. |
|
Definition
| mu and kappa receptors (same with miosis) |
|
|
Term
| The antitussive effects of opiates are thought to be produced through suppression of the cough center in the ________. Has nothing to do with the effects of opiates on ________ |
|
Definition
|
|
Term
| Nausea and vomiting occur because opiates stimulate the _______ in the area postrema of the medulla. |
|
Definition
| chemoreceptor trigger zone (CTZ) |
|
|
Term
| Nausea and vomiting/ antitussive effects of opiates are not associated with ________. |
|
Definition
| Not mediated by mu or kappa receptors |
|
|
Term
| Respiration is _______ by opiates |
|
Definition
|
|
Term
| Therapeutic concentrations of morphine reduce: _______, ______, & _______ of respiration. |
|
Definition
| rate, minute volume, and tidal exchange (not significantly though) |
|
|
Term
| When opiates are __________ there is a greater risk for significant respiratory depression. |
|
Definition
| combined with other drugs such as general anesthetics, tranquilizers, alcohol, or hypnotics |
|
|
Term
| The ______ sensitivity of brainstem respiratory centers is reduced by opiates. |
|
Definition
|
|
Term
| With Opiates the CO2 sensitivity of brainstem respiratory centers is reduced. Suppression of brainstem centers that control ________ also occurs. |
|
Definition
|
|
Term
| With Opiates Hypoxic stimulation of chemorecptors in the aortic arch and carotid body are _______, so administration of O2 may produce ______. |
|
Definition
|
|
Term
| Death from morphine poisoning is almost always due to ________. |
|
Definition
|
|
Term
| Caution should be exercised in prescribing or administering opiates to patients having any condition that produces _______ problems. |
|
Definition
|
|
Term
| Overall opiate CNS effect on respiration? |
|
Definition
| Depresses respiratory drive and cough reflex |
|
|
Term
| Opiates cause _______ release which causes _______ (with respect to respiration). |
|
Definition
histamine release
bronchoconstriction |
|
|
Term
| Because of histamine release, opiates are problematic in ________. |
|
Definition
| asthmatic or a patient with COPD or cor pulmonale |
|
|
Term
| Morphine-like compounds at therapeutic doses have _______ effects on the CV system. |
|
Definition
| relatively modest effects |
|
|
Term
| In the _______ patient, there are relatively small effects from opiates on the bp, cardiac rate and rhythm |
|
Definition
|
|
Term
| there is some peripheral vasodilation and reduced peripheral resistance, as well as an inhibition of the baroreceptor reflex. Therefore, a patient may experience ________, when _________. This is also in part due to _______. |
|
Definition
orthostatic hypotension
moving supine to standing
histamine release |
|
|
Term
| With opiates CSF pressure may decrease/increase due to an decrease/increase in _______, which causes __________. |
|
Definition
increase
increase
pCO2
Cerebral vasodilation |
|
|
Term
| As long as ________, intracranial pressure will remain normal following opiate admin. |
|
Definition
| respiration is maintained normal |
|
|
Term
| Because of the opiate affect CSF pressure, Morphine is usually contraindicated in _______ or _______. |
|
Definition
| head injury or intracranial lesions |
|
|
Term
| The GI effects of morphine-like compounds are for the most part inhibitory/excitatory. |
|
Definition
|
|
Term
| With opiates in the stomach and small intestine, there is an increase in ______ and a decrease in ______. |
|
Definition
|
|
Term
| With opiates gastric emptying time is _________. |
|
Definition
|
|
Term
| With opiates passage of small intestine contents is _______, and ______ water is absorbed |
|
Definition
|
|
Term
| With opiates propulsive peristaltic waves in the large intestine are _______. |
|
Definition
|
|
Term
| With opiates anal sphincter tone is _______ and defecation reflex is ________. |
|
Definition
|
|
Term
| Overall GI affect from opiates? |
|
Definition
|
|
Term
| BC of its GI effects, Opiates are frequently used for control of ________. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| With Opiates, Renal function may be depressed in part due to ______ release. |
|
Definition
|
|
Term
| Urinary retention occurs with opiates because of increased ________ and suppression of __________. |
|
Definition
| of increased sphincter tone and suppression of the urinary voiding reflex. |
|
|
Term
| ________ & ________ occurs with repeated use of opiates. |
|
Definition
| Tolerance and physical dependence |
|
|
Term
| With Opiates a high degree of tolerance occurs to: ___________. |
|
Definition
| Analgesia, Euphoria, Dysphoria, Mental Clouding, Sedation |
|
|
Term
| With Opiates a moderate degree of tolerance occurs to: ___________. |
|
Definition
|
|
Term
| With Opiates no tolerance occurs to: ___________. |
|
Definition
| miosis, constipation, convulsions, and antagonistic actions |
|
|
Term
| An addict or a terminally ill individual who is taking opiates chronically typically has ______ and is _______. |
|
Definition
| miosis and is constipated |
|
|
Term
| The opioids are generally ____ absorbed from the GI tract. |
|
Definition
|
|
Term
| Some opiates are available as ______ preparations instead of oral. |
|
Definition
|
|
Term
| The more lipophilic opiates are absorbed through the _______ or ______. |
|
Definition
| nasal or (oral) buccal mucosa. |
|
|
Term
| Very lipophilic opiate compounds such as _______ may be absorbed through the skin. |
|
Definition
|
|
Term
| Morphine oral dose bioavailablity? |
|
Definition
|
|
Term
| Why does morphine have a low oral bio-availability of 25%? |
|
Definition
| High first pass metabolism when |
|
|
Term
| While morphine has a low oral bio-availability of 25%, _______ has a high oral bio-availability of 60%. |
|
Definition
|
|
Term
| Morphine can still be very effective orally; but __________. |
|
Definition
| the dose must be adjusted upward to reflect the high first pass effect. |
|
|
Term
| The more lipophilic opiates ________ more quickly than morphine. |
|
Definition
|
|
Term
| ________% of morphine reaches the brain, because of its ________. |
|
Definition
Only a small
relatively poor ability to pass the blood brain barrier |
|
|
Term
| The more lipophilic opiates are absorbed through the _______ or ______. |
|
Definition
| nasal or (oral) buccal mucosa. |
|
|
Term
| Very lipophilic opiate compounds such as _______ may be absorbed through the skin. |
|
Definition
|
|
Term
| Morphine oral dose bioavailablity? |
|
Definition
|
|
Term
| Why does morphine have a low oral bio-availability of 25%? |
|
Definition
| High first pass metabolism when |
|
|
Term
| While morphine has a low oral bio-availability of 25%, _______ has a high oral bio-availability of 60%. |
|
Definition
|
|
Term
| Morphine can still be very effective orally; but __________. |
|
Definition
| the dose must be adjusted upward to reflect the high first pass effect. |
|
|
Term
| The more lipophilic opiates ________ more quickly than morphine. |
|
Definition
|
|
Term
| ________% of morphine reaches the brain, because of its ________. |
|
Definition
Only a small
relatively poor ability to pass the blood brain barrier |
|
|
Term
| The metabolism of morphine-like compounds is through ________ of the 3 or 6 -position OH group. |
|
Definition
|
|
Term
| Both _______ and _______ are metabolized, at least in part to morphine. |
|
Definition
|
|
Term
| Neither ______ nor _______ nor ________ are pharmacologically active themselves, rather they are metabolized to morphine (the active agent). |
|
Definition
|
|
Term
| Once codeine, heroin, or oxycondone are metabolized they are metabolized how? |
|
Definition
| glucuronidation (just like morphine usually is) |
|
|
Term
| Once morphine is glucuronidated it is then __________. |
|
Definition
|
|
Term
| Morphine-glucuronide is less/more potent than morphine as an ________. |
|
Definition
|
|
Term
| Patient controlled analgesia beneficial to patients who ________ or are being treated chronically with opiates for ________. |
|
Definition
have had major surgery
a terminal illness |
|
|
Term
| Special use of opiates? is the relief of |
|
Definition
| relief of dyspnea caused by pulmonary edema with acute left ventricular failure |
|
|
Term
|
Definition
|
|
Term
| Which is more potent, morphine or heroin? |
|
Definition
|
|
Term
| Which crosses the BBB more readily, morphine or heroin? |
|
Definition
|
|
Term
| Heroin pharmalogically active? |
|
Definition
|
|
Term
| Heroin is metabolized to _______ and _________ where? |
|
Definition
| monoacetylmorphine and morphine in the brain |
|
|
Term
| heroin itself is not ______________. |
|
Definition
|
|
Term
| Strong agonist classes of opiates? |
|
Definition
phenanthrene
phenylheptylamine
phenylpiperidine |
|
|
Term
| Phenanthrene class members? |
|
Definition
|
|
Term
| Phenylheptylamine class members? |
|
Definition
|
|
Term
| Phenylpiperidine class members? |
|
Definition
Meperidine
fentanyl & sufentanyl
Diphenoxylate |
|
|
Term
| Methadone vs morphine bioavailability? |
|
Definition
|
|
Term
| Methadone is used for its _______ actions and for ______ addicts. |
|
Definition
|
|
Term
| Why is methadone used for heroin addicts? |
|
Definition
| Tolerance and dependence develop more slowly than that seen with heroin or morphine. Withdrawal from methadone is milder than that with heroin or morphine.They become dependent and tolerant on methadone and cross- tolerant to the effects of heroin. This cross tolerance prevents some of the addiction-reinforcing effects of heroin. |
|
|
Term
| Meperidine is a strong agonist of the __________ class of opiates. |
|
Definition
|
|
Term
| Meperidine more or less potent than morphine? |
|
Definition
|
|
Term
| Meperidine more or less bioavailable than morphine? |
|
Definition
|
|
Term
| In contrast with morphine, Meperidine has less action on the ______ and is not particularly _______ and also has no _________ action. |
|
Definition
bowel
constipating
no antitussive action |
|
|
Term
| Meperidine's anti______ effects can be problematic by producing ________. |
|
Definition
antimuscarinic
tachycardia |
|
|
Term
| Meperidine has a negative/positive inotropic effect. |
|
Definition
|
|
Term
| Meperidine's metabolite, normeperidine has been linked to _________. |
|
Definition
|
|
Term
| Meperidine does not hinder ______ and produces less _________ in the newborn. |
|
Definition
labor
respiratory depression |
|
|
Term
| Meperidine is used more commonly in ________ than morphine. |
|
Definition
|
|
Term
| fentanyl & sufentanyl are members of the _________ class strong agonist of opiates |
|
Definition
|
|
Term
| Unlike the other phenylpiperidine, Meperidine, fentanyl & sufentanyl are ________ when compared to morphine. |
|
Definition
|
|
Term
| Which is more potent fentanyl or sufentanyl? |
|
Definition
|
|
Term
| fentanyl & sufentanyl are ____ acting and are very useful in ______ as a part of ____________. |
|
Definition
short
surgery
balanced anesthesia |
|
|
Term
| fentanyl & sufentanyl are frequently used pre/postoperatively? |
|
Definition
|
|
Term
| Codeine is a member of the _______ class because of it’s a congener of morphine |
|
Definition
| phenathrene (along w/ Heroin) |
|
|
Term
| Codeine is a ______ agonist; it is much _______ potent than morphine. |
|
Definition
|
|
Term
| Codeine's anaglesia comes from? |
|
Definition
| 10% metabolism into mrophine |
|
|
Term
| Codeine has a direct action on the receptors in the ________ and is an excellent _________. |
|
Definition
|
|
Term
| As an antitussive, codeine is usually present in a ________ solution. |
|
Definition
|
|
Term
| Propoxyphene member of ______ class. |
|
Definition
|
|
Term
| Propoxyphene is structurally related to ________. |
|
Definition
| methadone (another phenylheptylamine) |
|
|
Term
|
Definition
|
|
Term
| Propoxyphene is frequently given with ________ (Percocet) or ________(Percodan). |
|
Definition
|
|
Term
| Propoxyphene is an ineffective? |
|
Definition
| cough suppressant (unlike Codeine) |
|
|
Term
| Diphenoxylate and Loperamide are mild agonists of the _________ class |
|
Definition
|
|
Term
| Diphenoxylate is not analgesic at standard dosages and its _________ makes it of very low _________ for parenteral administration. |
|
Definition
insolubility
abuse potential |
|
|
Term
| Loperamide does not __________. |
|
Definition
| cross the blood brain barrier |
|
|
Term
| Diphenoxylate and Loperamide are used as? |
|
Definition
|
|
Term
| The mixed agonists/antagonist opiates were developed to provide analgesia equivalent to morphine but with less ___________. |
|
Definition
|
|
Term
| The mixed agonists/antagonist opiates are ______ receptor agonists and inhibitory at ______ receptors. |
|
Definition
kappa receptor agonists
mu receptor antagonist |
|
|
Term
| Pentazocine has weak partial agonist or antagonist action at the ______ receptor. |
|
Definition
|
|
Term
| Pentazocine is a good agonist at the _______ receptor. |
|
Definition
|
|
Term
| Pentazocine is used frequently as an ________ and it is _____ potent than morphine. |
|
Definition
analgesic
less potent that morphine |
|
|
Term
| Pentazocine useful in individuals who _________ or ___________. |
|
Definition
| have chronic severe pain or those who have drug abuse problems |
|
|
Term
| _____ administered pentazocine has less addictive liability than _______ administered pentazocine |
|
Definition
|
|
Term
| Because of its mixed action at _____ receptors, pentazocine will _______ in an individual addicted to strong _____ agonist opioids. |
|
Definition
mu
Precipitates withdrawal
mu |
|
|
Term
| Repeated high doses of pentazocine can produce ________ and _______. |
|
Definition
| hallucinations and high blood pressure. |
|
|
Term
| Butorphanol is a mu receptor ________ and kappa _______. |
|
Definition
antagonist
agonist (it is a mixed agonist/antag) |
|
|
Term
| Butorphanol drug schedule? Why? |
|
Definition
| Its abuse potential is extremely low, so it is not a scheduled drug |
|
|
Term
| Butorphanol vs morphine potency? |
|
Definition
| more potent than morphine |
|
|
Term
| Butorphanol can _______ so it is not used in ________. |
|
Definition
|
|
Term
| Butorphanol Major side effects: ________. |
|
Definition
| nausea, sweating, drowsiness, and feelings of floating |
|
|
Term
| Buprenorphine is a semisynthetic opioid derived from _______, one of the compounds found in the poppy plant. |
|
Definition
|
|
Term
| Buprenorphine vs morphine potency? |
|
Definition
| It is more potent than morphine. 0.4 mg of buprenorphine is comparable to 10 mg of morphine!!!!!!!!!! (compared to 3mg with Butorphanol) |
|
|
Term
| Buprenorphine two diverging pharmacological principles: that of ______ and _______. |
|
Definition
|
|
Term
| Buprenorphine's high Potency is reflected in the _________. |
|
Definition
| lower dose that is needed relative to that of the morphine dose. |
|
|
Term
| Since Buprenorphine is only a _________, buprenorphine does not have the same _______ as larger doses of morphine. |
|
Definition
|
|
Term
| Because Buprenorphine has a lower efficacy at high doses it can __________. |
|
Definition
| ppt withdrawal in addicts if their opiate of choice is immediately replaced with buprenorphine |
|
|
Term
| Since Buprenorphine has significant activity at ________ it is still a scheduled drug. |
|
Definition
| Mu receptor (unlike Butorphanol, which is a Mu antagonist) |
|
|
Term
| The partial agonist, buprenorphine, is commonly prescribed to treat ___________. |
|
Definition
| opioid dependence or addiction |
|
|
Term
| The partial agonist, buprenorphine, unlike pure agonists has a ___________, which thereby limits its ________. |
|
Definition
| dose-ceiling effect, where the analgesic and subjective effects, such as euphoria, reach a plateau, thereby limiting abuse potential. |
|
|
Term
| Opioid antagonists have _______ physiological effects on a person who is not ___________. |
|
Definition
|
|
Term
| Opioid antagonists given to individuals to reduce the effects of _____ or _____ agonists. |
|
Definition
|
|
Term
| Opioid antagonists are used in treatment of __________. |
|
Definition
|
|
Term
| The _________ can be accomplished with opioid antagonists, but care must taken not to __________. |
|
Definition
diagnosis of an addiction to opioids
ppt a full blown withdrawal |
|
|
Term
| Small doses of opioid antagonists may also be used to reduce the SE of _______ or ______ opiates without affecting the analgesia. |
|
Definition
|
|
Term
| Opioid antagonists can be used to __________ in a neonate whose mother has received opioids is also a use. |
|
Definition
| reduce of respiratory depression |
|
|
Term
| Alcoholism has been treated with some degree of success with oral ________. |
|
Definition
|
|
Term
| Antagonists do not block the effects of alcohol, such as intoxication, nor do they block the effects of alcohol poisoning. They do seem to reduce ______. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Naloxone is used in _______? |
|
Definition
|
|
Term
| Naloxone ______ acting and therefore ______. |
|
Definition
| Very rapid and short duration and may need additional doses |
|
|
Term
| If an addict is being treated for overdose, it is possible to titrate the dose of naloxone so that ________ is reduced, without __________. |
|
Definition
respiratory depression
percipiating withdrawl |
|
|
Term
| Naloxone will not reverse the __________. |
|
Definition
| respiratory depression produced by other sedative hypnotics |
|
|
Term
| If a person has coadministered large amounts of ________ or has _________, naloxone will not reverse the resulting respiratory depression |
|
Definition
barbiturates
alcohol poisoning |
|
|
Term
| Naltrexone is a more ______ effective antagonist than Naloxone due to its __________. |
|
Definition
orally
long half-life (naxolene has a very short) |
|
|
Term
| Naltrexone is used in the treatment of _______. |
|
Definition
|
|
Term
| Naltrexone possible SE warrants? |
|
Definition
| hepatic, liver monitoring |
|
|
Term
| Acute opiate toxicity, Respiratory rate will be _______ breaths per min. |
|
Definition
| low- 2 to 4 breaths per min |
|
|
Term
| As respiratory exchanges decreases with Acute opiate toxicity, _____ will fall. |
|
Definition
|
|
Term
| Acute opiate toxicity pupils? |
|
Definition
| pinpoint and symmetrical (unless hypoxia is very severe. In that case, pupils may be dilated) |
|
|
Term
| Acute opiate toxicity triad? |
|
Definition
| coma, pinpoint pupils, and depressed respiration |
|
|
Term
| Acute opiate toxicity death from? |
|
Definition
|
|
Term
| With Acute opiate toxicity, treatment centers on ________ and reversing the effects of the opiates with _______. |
|
Definition
maintaining the patient’s airway
opiate antagonists |
|
|
Term
| Opioid addicts are very ________ to antagonists. |
|
Definition
|
|
Term
| Because opioid addicts are very sensitive to antagonists, when treating toxicity, a dose must be given that __________. |
|
Definition
| reduces the respiratory depression, but that does not ppt withdrawal |
|
|
Term
| Opiate antagonists do not block to any significant degree the sedative effects of ________. |
|
Definition
|
|
Term
| Dextromethorphan is the d isomer of levorphanol, an analog of _________, but it does not _______, but instead __________. and is found in ________. |
|
Definition
codeine
work on opiate receptors
directly on the cough receptors
over the counter cough |
|
|
Term
| Meperidine is a good _______, but is very poor as an ______ or ______ agent. |
|
Definition
analgesic
antitussive or antidiarrheal |
|
|
Term
| Diphenoxylate and loperamide are good _______ drugs, but are ineffective as ________. |
|
Definition
|
|
Term
| Cocaine is a ______ type of drug. |
|
Definition
|
|
Term
| Local anesthetics produce numbness by ________. |
|
Definition
| blocking nerve conduction |
|
|
Term
| Local anesthetics block _______ nerves. |
|
Definition
| both sensory and motor nerves |
|
|
Term
| Local anesthetics actions are completely __________. |
|
Definition
|
|
Term
| Local anesthetics MOA: ___________. |
|
Definition
| block voltage dependent Na channels |
|
|
Term
| Local anesthetics block voltage dependent Na channels and thus inhibit ___________. |
|
Definition
| action potential generation |
|
|
Term
| When ________, the local anesthetic can enter. |
|
Definition
|
|
Term
| Local anesthetics site of action? |
|
Definition
| near the intracellular end of the Na channel pore |
|
|
Term
| When When Local anesthetics bind at the site of action ___________. |
|
Definition
|
|
Term
| When Local anesthetics are ________ antagonist/agonist, and more specifically a pore blocker. |
|
Definition
|
|
Term
| the local anesthetic’s actions are _______ dependent. |
|
Definition
|
|
Term
| Local anesthetics can’t enter the pore unless _______. |
|
Definition
|
|
Term
| A nerve that is __________ will be more susceptible to local anesthetic block. |
|
Definition
|
|
Term
| Local anesthetics stabilize the ________, making it less ________. |
|
Definition
inactivated state
likely to resensitize and become available again for stimulation (can only enter when activated) |
|
|
Term
| The actions of local anesthetics are also _______ dependent because ________ is the regulator of the channel in the first place. |
|
Definition
|
|
Term
| Conditions that change the ________ alter the probability that the channel will be opened and thus the probability that the local anesthetic can reach its site of action. |
|
Definition
| resting membrane potential |
|
|
Term
| ________ conditions enhance the probability of opening and ________ conditions decrease the probability of opening of Na+ channels. |
|
Definition
depolarizing
hyperpolarizing |
|
|
Term
| Most local anesthetics are weak _______ with pka's of ________. |
|
Definition
|
|
Term
| local anesthetics are poorly water soluble as the _______, so they are typically marketed as a salt in a slightly ____ pH. |
|
Definition
|
|
Term
| local anesthetics primarily exist as the __________ form in the body. |
|
Definition
|
|
Term
| __________ and __________ are the rate limiting steps for entry into the nerve for Local anesthetics. |
|
Definition
| Lipophilicity and conversion of the charged to the uncharged form |
|
|
Term
| _____ and ______ are characteristics that make the local anesthetic bind to the Na channel more rapidly. |
|
Definition
| Small size and lipophilicity |
|
|
Term
| _______ form of LA binds to sodium channel |
|
Definition
|
|
Term
| _______ form of LA cross membrane |
|
Definition
|
|
Term
| Type _ fibers are inhibited more quickly than Type _ which are inhibited more quickly than Type _ by LA. |
|
Definition
|
|
Term
| With LA, ______ is blocked first, then ______ functions. _______ function is the last to disappear. Recovery occurs in the _______ order. |
|
Definition
pain > sensory > Motor
reverse |
|
|
Term
| The location of a nerve in a bundle can affect its sensitivity. For instance, if a motor nerve is located at the ______ of a bundle, it may be deadened before a sensory nerve that is located more ________ in the bundle. |
|
Definition
|
|
Term
| For LA: ______ linkages are more susceptible to hydrolysis than are ______ linkages. |
|
Definition
|
|
Term
| LA ability to provide blockade of nerve conduction is limited by their ________. |
|
Definition
| systemic absorption (greater the rate of removal from the injection site, the faster the offset of anesthetic action) |
|
|
Term
| Factors determine systemic absorption of an LA: __________. |
|
Definition
| 1) the intrinsic properties of the drug itself, 2) the site of administration, 3) the intrinsic degree of vasodilator activity, and 4) drug tissue binding. |
|
|
Term
As for LA drug physicochemical properties:
_______ are rapidly taken up and distributed.
_______ are so prone to ______ that their absorption is of little consequence |
|
Definition
Amides
Esters
immediate hydrolysis |
|
|
Term
| The site of injection of an LA has to factor in ______ and _______ with absorbtion (and thus limiting). |
|
Definition
| vascularity and fat content |
|
|
Term
| The more vasodilatory activity that the drug has the ______ it is likely to be absorbed. |
|
Definition
|
|
Term
| Vasoconstrictors ______ the absorption |
|
Definition
|
|
Term
| ________ are very important with regard to local anesthetic pharmacology. |
|
Definition
|
|
Term
| By ______ blood flow to and from the injection site, they can increase the duration of effect of intermediate acting LA by 50%. |
|
Definition
|
|
Term
| In addition to increasing duration, vasoconstrictors can do what for LAs? |
|
Definition
|
|
Term
| The local anesthetics are all ________ to varying degrees, except for ________, because of its activity __________. |
|
Definition
| The local anesthetics are all vasodilators to varying degrees. The only exception is cocaine, which is a vasoconstrictor because of sympathomimetic activity. |
|
|
Term
| Most commonly ________ (vasoconstrictor) is co administered with the local anesthetic. |
|
Definition
|
|
Term
| Too much vasoconstrictor can lead to local ______, so care must be taken. |
|
Definition
|
|
Term
| Avoid use of vasoconstrictors at ___________. |
|
Definition
| extremities- fingers, toes, penis,etc |
|
|
Term
| ________ rapidly metabolizes ester linked local anesthetics. |
|
Definition
|
|
Term
| Amide linked local anesthetics are metabolized by ________, so impaired __________. |
|
Definition
the hepatic microsomal system,
impaired liver function predisposes an individual to toxicity |
|
|
Term
| Ester type Local Anesthesthetics: ________. |
|
Definition
Procaine
Chlorprocaine (Cl analog of procaine)
Tetracaine
Cocaine
Benzocaine |
|
|
Term
| Procaine & Chlorprocaine duration of action? |
|
Definition
|
|
Term
| Procaine & Chlorprocaine used for? |
|
Definition
| for infiltration or nerve block or spinal anesthesia. |
|
|
Term
| Procaine & Chlorprocaine vs Tetracaine duration of action. |
|
Definition
|
|
Term
| Tetracaine administration forms? |
|
Definition
|
|
Term
|
Definition
| Bc its slow metabolism it can cause toxicity |
|
|
Term
| Tetracaine is frequently used in? |
|
Definition
| spinal anesthesia (same for Procaine & Chlorprocaine) |
|
|
Term
| Cocaine used less and less bc of ______ and _______. |
|
Definition
| abuse liability and its potential for producing toxicity |
|
|
Term
| Cocaine was once used for ophthalmic anesthetic, but it produces ________ and ________. |
|
Definition
mydriasis (excessive dilation of pupil)
corneal sloughing |
|
|
Term
| Cocaine only current use? |
|
Definition
| a respiratory tract anesthetic in a topical form |
|
|
Term
| Cocaine CNS SE: ___________. |
|
Definition
| tonic clonic seizures and pyrexia |
|
|
Term
| Cocaine CV SE: ___________. |
|
Definition
| arrythmias to cardiac failure |
|
|
Term
| Cocaine CV SEs are due to? |
|
Definition
| action on the heart and sympathetic stimulation |
|
|
Term
| The increase in ______thetic activity with cocaine is due to __________. |
|
Definition
increase sympathetic activity
blockade of catecholamine transport |
|
|
Term
|
Definition
| Topically in oinments/creams (sunscreen burn ointment) |
|
|
Term
|
Definition
|
|
Term
| Lidocaine advantages over the ester LAs: ____________. |
|
Definition
| longer lasting and does not produce hypersensitivity |
|
|
Term
| Lidocaine is efficiently absorbed through ________ and can be used in every route except __________. |
|
Definition
| efficiently absorbed from the mucous membranes, and it can be used in every route except ophthalmic |
|
|
Term
| ________ and _______ LAs are not absorbed efficiently though the mucous membranes. |
|
Definition
|
|
Term
| Bupivacaine is a _____ LA. |
|
Definition
|
|
Term
|
Definition
| very long duration of action |
|
|
Term
| Bupivacaine is useful by _______, but ineffective _______. |
|
Definition
| useful by injection, but is ineffective locally. |
|
|
Term
| Toxicity profile of local anesthetics is related to 3 main areas: __________. |
|
Definition
| Immune system, CV, and CNS |
|
|
Term
| Immune system SE of LAs only occurs with _______ and is a result of ________. |
|
Definition
some of the esters
a result of metabolic production of paraaminobenzoic acid |
|
|
Term
| CV SE of LAs occur bc of ___________. |
|
Definition
| excessive concentrations being absorbed |
|
|
Term
| Direct inhibitory actions on the heart muscle by LAs include decreased ________ and __________. |
|
Definition
conduction velocity
inotropic effect |
|
|
Term
| With LA toxicity, CV collapse and death may result from cardiac arrest due to _______ or ________. |
|
Definition
| arrhythmia or depression of pacemaker activity |
|
|
Term
| Cocaine has the added CV toxicity profile because it has _______ activity. |
|
Definition
| sympathomimetic (the other LAs do not) |
|
|
Term
| CNS toxicity of LA is usually due to the inadvertent injection of the anesthetic ___________. |
|
Definition
|
|
Term
| CNS toxicity of LAs is generalized ________. |
|
Definition
|
|
Term
| The generalized excitation by LAs inm the CNS is thought to be due to __________. |
|
Definition
| suppression of inhibitory pathways (GABAARs and GlyRs). |
|
|
Term
| CNS LA toxicity results in ________, which proceeds to convulsions, coma, and cardiorespiratory arrest |
|
Definition
|
|
Term
| Time and dose course for LA toxicity: _____________. |
|
Definition
| Excitation- Depression- Coma- Death |
|
|
Term
| __________ have been associated with overdose of chlorprocaine in ______ anesthesia. |
|
Definition
Long lasting motor and sensory deficits
spinal anesthesia |
|
|
Term
| Clinical uses for local anesthetics: __________. |
|
Definition
Surface anesthesia
Infiltration anesthesia
Nerve Block
Epidural anesthesia
Spinal anesthesia |
|
|
Term
| Surface anesthesia is provided by ________ of a number of local anesthetics, including _______ and ________. |
|
Definition
aqueous salts
benzocaine (ester) & lidocaine (amide) |
|
|
Term
| Benzocaine is particularly good for _______ and other conditions of _______, because it _______ . |
|
Definition
Burns
denuded fleshburns
isn’t absorbed |
|
|
Term
| Infiltration anesthesia is __________. |
|
Definition
| injection of the local anesthetic in a region without regard to the cutaneous route of the nerves |
|
|
Term
| Infiltration anesthesia can be used for ______ or _________. |
|
Definition
| superficial tissues or intraabdominal organs |
|
|
Term
| Nerve Block is an injection of local anesthetic ___________. |
|
Definition
| into or about peripheral nerves or nerve plexuses |
|
|
Term
| Nerve Block affects which nerves? |
|
Definition
|
|
Term
| Epidural anesthesia is commonly used for ________. |
|
Definition
|
|
Term
| The local anesthetic is injected into the epidural space which is bounded by the _______, _______, and ________. |
|
Definition
| ligamentum flavum, dura, and spinal periosteum |
|
|
Term
| The ________ are chiefly affected in Epidural anesthesia. |
|
Definition
|
|
Term
| Epidural anesthesia limitation and drawback? |
|
Definition
| A large amount is needed because diffusion is required |
|
|
Term
| However if an _______ like _______ is also onboard, the amount of LA in Epidural anesthesia can be reduced substantially |
|
Definition
|
|
Term
| Spinal anesthesia is an injection of the local anesthetic around the nerve routes where? |
|
Definition
| within the subarachnoid space in the lumbar region |
|
|
Term
| With Spinal anesthesia the entire _______ can be deadened. |
|
Definition
|
|
Term
| ________ produces the deadening of the desired region in Spinal anesthesia for LA. |
|
Definition
| Positioning of patient and use of appropriate specific gravity LA |
|
|
Term
| _______ are extremely sensitive to local anesthetics with Spinal anesthesia, so ________. |
|
Definition
Autonomic nerves
CV function is usually depressed. |
|
|
Term
| _______ and _______ from LA Spinal anesthesia must be treated aggressively to reduce the possibility of brain damage or kidney failure. |
|
Definition
| Hypotension and poor venous return |
|
|
Term
| Headache can occur with Spinal Anesthesia because ________. |
|
Definition
| presumed leak of CSF from the hole in the dura. |
|
|
Term
| distinguishing property of cocaine? |
|
Definition
| vasoconstrictor, sympathomimetic |
|
|
Term
| benzocaine- only useful ________. |
|
Definition
|
|
Term
| Antipsychotic = __________. |
|
Definition
|
|
Term
| Antipsychotic Therapeutic benefit in psychosis: Patients become less: __________. |
|
Definition
| withdrawn/ excited, agitated, hostile, irritable, anxious, and suspicous |
|
|
Term
| Antipsychotic Therapeutic benefit in psychosis: Patients become more __________ and begin to _______. |
|
Definition
| more cooperative & begin to participate in activities |
|
|
Term
| In addition to treating psychosis, the antipsychotic drugs also relieve __________. |
|
Definition
| the manic phase of bipolar affective disorder |
|
|
Term
| No proven difference in antipsychotic efficacy among ________ antipsychotic drugs |
|
Definition
|
|
Term
| However unlike conventional, ______ antipsychotic drugs may relieve symptoms in ________ patients resistant to other agents & produce a better quality of response. |
|
Definition
|
|
Term
| Conventional antipsychotic drugs are those that were _______, and which appear to act primarily by ________. |
|
Definition
approved through 1975
antagonizing dopamine receptors |
|
|
Term
| The first atypical antipsychotic agent approved in the U.S. was ________. |
|
Definition
|
|
Term
| Atypical antipsychotic agents act on: receptors __________. |
|
Definition
| 5-HT2 and D2 receptors (rather than with conventional that just antagonize DA) |
|
|
Term
| Antipsychotic uses: __________. |
|
Definition
Schizophrenia (atypicals)
Psychotic Depression
Drug-Induced Pyschosis
manic phase of bipolar |
|
|
Term
|
Definition
| prevent relapse of psychosis |
|
|
Term
| Antipsychotic general SE? |
|
Definition
| Movement (extrapyramidal) disorders |
|
|
Term
| What is newer Antipsychotic, conventional or atypical? |
|
Definition
|
|
Term
| Atypical Antipsychotic advantage? |
|
Definition
|
|
Term
| Conventional Antipsychotics: _______. |
|
Definition
Phenothiazines (e.g., Chlorpromazine)
Butyrophenones (e.g., Haloperidol)
Thioxanthenes (e.g., Thiothixene)
Miscellaneous (Loxapine, Pimozide) |
|
|
Term
| Atypical Antipsychotics: __________. |
|
Definition
Clozapine
Olanzapine
Quetiapine
Risperidone
Zaprasidone
Aripiprazole |
|
|
Term
| Although the role of conventional neuroleptics (Antipsychotics) will continue to diminish, several situations presently require their utilization, including: ___________. |
|
Definition
a. parental administration for acute agitation
b. lack of benefit or intolerance to novel agents
c. special populations (eg., pregnant patients)
d. noncompliant patients, for whom depot medication may be indicated. |
|
|
Term
| Phenothiazines Drug Class? |
|
Definition
| Conventional Antipsychotics |
|
|
Term
| Phenothiazines, the _________ structure forms the basic nucleus of this group. |
|
Definition
|
|
Term
| Phenothiazines, Substitution at position (___) imparts antipsychotic activity |
|
Definition
|
|
Term
| Phenothiazines, substitution on the ______ at position(____) alters potency and adverse effects. |
|
Definition
|
|
Term
| Phenothiazines, substitution on the nitrogen at position(10) alters potency and adverse effects. These substitutions include: __________. |
|
Definition
| aliphatic, piperidine and piperazine |
|
|
Term
| For Phenothiazines, _______ and ________ substituted compounds are called low potency antipsychotics. |
|
Definition
|
|
Term
| For Phenothiazines, _________ is an aliphatic compound & _______ is a piperidine compound. |
|
Definition
Chlorpromazine (low potency)
thioridazine (low potency) |
|
|
Term
| For Phenothiazines, ________ substituted compounds are high potency antipsychotics. |
|
Definition
|
|
Term
| For Phenothiazines, Piperazine substituted: _______. |
|
Definition
| fluphenazine and trifluoperazine (high potency) |
|
|
Term
| For Phenothiazines, Aliphatic & piperidine compounds (_______ & ______ respectively) are more likely to cause: ____________. |
|
Definition
Chlorpromazine & Thioridazine
sedation, orthostatic hypotension, hypersensitivity (jaundice, skin sensitization) |
|
|
Term
| For Phenothiazines, Aliphatic & piperidine compounds (_______ & ______ respectively) are less likely to cause: ____________. |
|
Definition
Chlorpromazine & Thioridazine
induce parkinsonism |
|
|
Term
| For Phenothiazines, Aliphatic & piperidine compounds are less likely to induce parkinsonism, i.e. Thioridazine is less likely to cause ________ than other Phenothiazines and is recommended as a second-line drug in treatment of _________. |
|
Definition
produce extrapyramidal side effects (EPS)
acute psychosis (conventional use) |
|
|
Term
| For Phenothiazines, Piperazine compounds (_______ & ________) are more likely to ________ and have ________ activity. |
|
Definition
Chlorpromazine & Thioridazine
cause EPS and have antiemetic activity |
|
|
Term
| For Phenothiazines, Piperazine compounds have less ___________ and _________. |
|
Definition
| orthstatic hypotension and sedation |
|
|
Term
| Phenothiazines are antagonists/agonists at: _______ receptors. |
|
Definition
antagonists
dopamine (D1 and D2), adrenergic & muscarinic receptors |
|
|
Term
| Phenothiazines have especially high affinity for ______ receptors which correlates with their clinical potency in treating ___________. |
|
Definition
|
|
Term
| For Phenothiazines, <____% _____ receptor occupancy in the striatum is suboptimal & >___% provides no further benefit but may increase risk of ____. |
|
Definition
<60% D2 DA receptor-> suboptimal
>80% no more benefit, increase risk for EPS |
|
|
Term
| Behavioral effects of Phenothiazines, Antipsychotic action: ________. |
|
Definition
| reduced hallucinations, delusions |
|
|
Term
| Behavioral effects of Phenothiazines, quieting of ________. |
|
Definition
|
|
Term
| Behavioral effects of Phenothiazines, ________ helps in agitated pts. |
|
Definition
|
|
Term
| Behavioral effects of Phenothiazines, Sedation, ______ develops to this effect. |
|
Definition
|
|
Term
| Phenothiazines, ______ are less sedating, but have excellent antipsychotic activity. |
|
Definition
| piperazine (more potent and also less likely to cause orthostatic hypotension) |
|
|
Term
| Behavioral effects of Phenothiazines, decreased ___________. |
|
Definition
|
|
Term
| With Phenothiazines, the effect of decreased spontaneous activity can become ________ at high doses. |
|
Definition
|
|
Term
| Phenothiazines mechanism of antipsychotic action: _________. |
|
Definition
| Dopamine receptor blockade in mesolimbic-mesocortical dopaminergic system |
|
|
Term
| The primary therapeutic action of phenothiazines and ______ appears to involve blockade of the D2-receptor, which inhibits _______. |
|
Definition
haloperidol
adenylyl cyclase |
|
|
Term
| Phenothiazines SE of lowered ________, which may require increased _________. |
|
Definition
| Lowered seizure threshold: may require increased dose of antiepileptic drug |
|
|
Term
| For Phenothiazines: __________ compounds are most likely to precipitate a seizure with first time use (all lower threshold) |
|
Definition
|
|
Term
| In addition to seizures, Phenothiazines also have can lead to a _________ state, because of their __________ effects, which is particularity troublesome in _______ pts. |
|
Definition
| Toxic confusional state: due to central anticholinergic effects; especially troublesome in older patients |
|
|
Term
| Phenothiazines causes ______ in 30-40% of patients; except for ________. |
|
Definition
EPS (Extrapyramidal side effects)
Parkinsonism??? |
|
|
Term
| Phenothiazines agents with greater propensity to induce EPS produce _______. |
|
Definition
| higher D2 receptor occupancy |
|
|
Term
| patients w/ __________ did not experience EPS. |
|
Definition
| occupancy rates below 75% |
|
|
Term
| Phenothiazines EPS: Parkinsonism, akinesia, tremor, regidity Treatment: _______. |
|
Definition
| reduce dose or change drugs (e.g., atypical or clozapine if severe); anticholinergic antiparkinson drugs or amantadine. |
|
|
Term
| Phenothiazines EPS: Parkinsonism, akinesia, tremor, regidity Treatment: Result of Antipsychotic drug antagonism of dopamine D2 receptors in ______. |
|
Definition
|
|
Term
| Phenothiazines EPS: Acute dystonia- is _______. |
|
Definition
| Spasms involving head, neck, trunk & extremities (twisting) |
|
|
Term
| Phenothiazines EPS: Acute dystonia, Treatment: ________. |
|
Definition
| benztropine or diphenhydramine |
|
|
Term
| Phenothiazines EPS: Acute dystonia, Mechanism: ________. |
|
Definition
| Dopamine receptor blockade by antipsychotic drugs |
|
|
Term
| Phenothiazines EPS: Akathisia- is _______. |
|
Definition
| State of extreme motor restlessness & drive to move |
|
|
Term
| Phenothiazines EPS: Akathisia, Treatment: ________. |
|
Definition
| reduce dose; switch to low potency or atypical; propranolol; benzodiazepines; amantadine; sometimes resistant to anticholinergic antiparkinson agents. |
|
|
Term
| Phenothiazines EPS: Tardive dyskinesia (TD)- is _______. |
|
Definition
| Stereotyped, repetitive, involuntary movements of the mouth, lips,& tongue & choreiform movements of the limbs and body. |
|
|
Term
| Phenothiazines EPS: Tardive dyskinesia (TD), Treatment: ________. |
|
Definition
gradual reduction of dose; avoid
anticholinergic drugs; switch to atypical (eg.,clozapine) |
|
|
Term
| Phenothiazines EPS: Tardive dyskinesia (TD), Mechanism: ________. |
|
Definition
| development of supersensitivity of dopamine receptors as consequence of long term blockade. |
|
|
Term
| Phenothiazines EPS: Perioral tremor- is _______. |
|
Definition
| "Rabbit Syndrome"; late appearing |
|
|
Term
| Phenothiazines EPS: Perioral tremor, Treatment: ________. |
|
Definition
| Responds to anticholinergic antiparkinson drugs or reduction in dose of antipsychotic agent. |
|
|
Term
| Out of the EPS's from Phenothiazines, __________ is a major problem that pts. may not recover from. |
|
Definition
|
|
Term
| Phenothiazines have an anti ______ side effect. |
|
Definition
|
|
Term
| The Antiemetic effect from Phenothiazines results from __________. |
|
Definition
| Blockade of chemoreceptor trigger zone or CTZ |
|
|
Term
| Phenothiazines block emesis at CTZ enduced by: ___________. |
|
Definition
|
|
Term
| Phenothiazines' Antiemetic at the CTZ is related to blockade of ______ and ______ receptors. |
|
Definition
|
|
Term
| ________ Phenothiazines are more potent Antiemetics. |
|
Definition
|
|
Term
| Despite their Antiemetic effect, Phenothiazines are not _______, except for ______ bc of its anticholinergic effects. |
|
Definition
not effective against motion sickness
promethazin |
|
|
Term
| Phenothiazines's autonomic effects stem from their blockade of ______ & ______ receptors. |
|
Definition
Alpha-adrenergic receptor blockade
Muscarinic receptor blockade |
|
|
Term
| Phenothiazines's Alpha-adrenergic receptor blockade results in _____. |
|
Definition
|
|
Term
| Phenothiazines's Alpha-adrenergic receptor blockade can result in a hypotensive response to ______. |
|
Definition
|
|
Term
Phenothiazines's Muscarinic receptor blockade anti______ side
effects are frequent & troublesome: ___________. |
|
Definition
cholinergic
dry mouth, blurred vision, urinary retention in males w/ prostatism, aggravation of glaucoma, etc. |
|
|
Term
| In addition to anti Alpha-adrenergic & anti Muscarinic, Phenothiazines also have anti ______ and ______ activity. |
|
Definition
| antihistaminic and antiserotonergic |
|
|
Term
| Phenothiazines's Cardiac effects are ___________, anti_______, and & _______ effects on the heart. |
|
Definition
| Local anesthetic, anticholinergic, & quinidine-like effects on the heart |
|
|
Term
| Phenothiazines's have an quinidine-like effect on the heart, especially _______. |
|
Definition
|
|
Term
| Phenothiazines's cardiac effects results in __________ EKG findings. |
|
Definition
| depressed T-wave & prolonged Q-T interval |
|
|
Term
| Phenothiazines's cardiac effects irreversible/reversible? |
|
Definition
|
|
Term
| Phenothiazines's Dopamine receptor blockade results in increased _________ secretion. |
|
Definition
|
|
Term
| Phenothiazines's Dopamine receptor blockade results in increased prolactin secretion, producing: ____________. |
|
Definition
| producing lactation in females, gynecomastia in males, ovulation & menstruation disturbances |
|
|
Term
| Phenothiazines's Dopamine receptor blockade results in decreased: _________ secretion. |
|
Definition
| gonadotropin, growth, and ACTH |
|
|
Term
| Phenothiazines impact temperature by causing a depression/elevation in ________ & ___________ mechanisms. |
|
Definition
| Depression of temperature regulating & vasomotor mechanisms |
|
|
Term
| Phenothiazines impact temperature by causing a depression/elevation in Depression of temperature regulating & vasomotor mechanisms, causing the pt. to ________ (________ effect). |
|
Definition
| assume the temperature of the environment (poikilothermic effect) |
|
|
Term
| Phenothiazines can cause ______ or ______ depending on the surrounding temp. |
|
Definition
| hypothermia or hyperthermia |
|
|
Term
| Phenothiazines' temperature effects are used to ____________. |
|
Definition
| preanesthetic medication to facilitate hypothermia for certain types of surgery. |
|
|
Term
| The antipsychotic drugs have a ______ therapeutic index |
|
Definition
|
|
Term
| Acute poisoning w/ antipsychotic drugs is ________. |
|
Definition
|
|
Term
| CNS adverse effects of Phenothiazines: ___________. |
|
Definition
| Drowsiness, Parkinsonism, akathisia, dystonia, lowered seizure threshold, oculogyric crisis, tardive dyskinesia, confusional state, depressive state (which can lead to suicide) |
|
|
Term
| Autonomic adverse effects of Phenothiazines: __________. |
|
Definition
| Hypotension, orthostatic hypotension, anti-cholinergic effects (dry mouth, mydriasis, cycloplegia, urinary retention, tachycardia), ECG changes, hyper- pyrexia(hypothalamic & interference w/ sweating), impaired ejaculation (alpha blockade; more common w/ aliphatic & piperidine compounds). |
|
|
Term
| Orthostatic hypotension from Phenothiazines is more common with _______. |
|
Definition
|
|
Term
| Endocrine adverse effects of Phenothiazines: __________. |
|
Definition
| Galactorrhea, gynecomastia, menstrual changes. |
|
|
Term
| Hypersensitivity adverse effects of Phenothiazines: __________. |
|
Definition
|
|
Term
| Eye adverse effects of Phenothiazines: __________. |
|
Definition
| Toxic retinopathy due to pigment deposits |
|
|
Term
| Toxic retinopathy due to pigment deposits, from Phenothiazines results from administration of: ___________ in higher than necessary doses. |
|
Definition
| thioridazine & chlorpromazine |
|
|
Term
| Neuroleptic Malignant Syndrome is characterized by: __________. |
|
Definition
| Fever, diaphoresis, marked muscular rigidity, stupor, respiratory & autonomic dysfunction, leukocytosis. |
|
|
Term
| Neuroleptic Malignant Syndrome occurs in patients who? |
|
Definition
| 0.5-1% of patients who receive high-potency neuroleptics |
|
|
Term
| Neuroleptic Malignant Syndrome death results from __________. |
|
Definition
| respiratory or renal failure, cardiovascular collapse, arrhythmias |
|
|
Term
| Neuroleptic Malignant Syndrome Mechanism: ________. |
|
Definition
| sudden decrease in dopaminergic activity |
|
|
Term
| Neuroleptic Malignant Syndrome, __________ is effective for some of symptoms, including hyperthermia, respiratory problems, stupor, autonomic changes, & rigidity. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| _________ will decrease rigidity in Neuroleptic Malignant Syndrome. |
|
Definition
|
|
Term
|
Definition
| Dantrolene sodium is a muscle relaxant that acts by abolishing excitation-contraction coupling in muscle cells, probably by action on the ryanodine receptor. |
|
|
Term
| After a Neuroleptic Malignant Syndrome, pt. should not be ________. |
|
Definition
| re-exposed to a neuroleptic drug for at least 2 weeks |
|
|
Term
| Typical Antipsychotics drug-drug interaction with CNS depressants & opioids? |
|
Definition
| Potentiation of CNS depressants & opioids |
|
|
Term
| Typical Antipsychotics synergistic __________ with _______ and inhibition of ________ leading to a __________. |
|
Definition
| Synergistic depression with ethanol & inhibition of alcohol metabolism (elevated blood alcohol) |
|
|
Term
| Typical Antipsychotics reduce therapeutic effectiveness of _______ in treating _______. |
|
Definition
|
|
Term
| Typical Antipsychotics interfere with the anti______ effect of guanethidine. |
|
Definition
|
|
Term
| Thioridazine w/ drugs that have ________ may potentiate __________. |
|
Definition
quinidine-like action
cardiotoxicity |
|
|
Term
| Typical Antipsychotics inhibit __________. |
|
Definition
|
|
Term
| Haloperidol considered a ______ potency _______ antipsychotic drug. |
|
Definition
|
|
Term
| Haloperidol is among the first-line drugs for treatment of ________. |
|
Definition
|
|
Term
| Haloperidol Basic therapeutic effects similar to the ___________. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Haloperidol, EPS more common than with __________. |
|
Definition
| aliphatic or piperidine phenothiazines (chlorpromazine or thioridazine) [Piperazine is more common to cause EPS] |
|
|
Term
| Can Haloperidol cause neuroleptic malignant syndrome? |
|
Definition
|
|
Term
| Haloperidol is a potent ______ receptor antagonist/agonist. |
|
Definition
|
|
Term
| Haloperidol has high ______ (with respect to pharomykinetics/dynamics). |
|
Definition
|
|
Term
| Haloperidol has fewer ______ effects than Phenothiazines, but still prone to cause _______. |
|
Definition
Fewer autonomic effects
orthostatic hypotension |
|
|
Term
| Haloperidol completely lacks ________ effects unlike Phenothiazines. |
|
Definition
| Lacks anticholinergic effects |
|
|
Term
| Haloperidol completely lacks anticholinergic effects unlike Phenothiazines making it useful for ________. |
|
Definition
|
|
Term
| Thiothixene is an antipsychotic resulting from minor structure changes in ___________. |
|
Definition
|
|
Term
| Thiothixene similar in pharmacology & side effects to the ________. |
|
Definition
| piperazine-substituted phenothiazines |
|
|
Term
| Thiothixene has no ________; it is simply an ________ to other agents |
|
Definition
special advantages
alternative |
|
|
Term
|
Definition
| High (just like Haloperidol and phenothiazines) |
|
|
Term
| Loxapine antipsychotic use? |
|
Definition
| alternative for patients refractory to others |
|
|
Term
| Loxapine higher likelihood of ________ & __________ than other antipsychotics. |
|
Definition
| oculogyric crisis and seizures |
|
|
Term
| Loxapine causes ________ rather than _______. |
|
Definition
| hypertension rather than hypotension |
|
|
Term
|
Definition
|
|
Term
| Molindone antipsychotic actions similar to ___________. |
|
Definition
| piperazine phenothiazines (like Thiothixene) |
|
|
Term
| Molindone advantage over other traditional antipsychotics? |
|
Definition
| unlikely to cause weight gain |
|
|
Term
|
Definition
| Low (only traditional antipysch with low) |
|
|
Term
Pimozide is a ______ antipsychotic (miscellaneous), has ____ half-life &
______ potency |
|
Definition
|
|
Term
| Pimozide is used in the suppression of __________ in patients with ___________, who have failed to respond to ________. |
|
Definition
motor & phonic tics
Tourette’s syndrome who failed to respond to haloperidol |
|
|
Term
| Pimozide is a _______ antagonist/agonist. |
|
Definition
|
|
Term
| Pimozide is a DA antagonist which also has affinity for ________. |
|
Definition
| moderately inhibits dopamine transporter (DAT) |
|
|
Term
|
Definition
| EPS (including tardive dyskinesia, akathisia & akinesia), neuroleptic malignant syndrome, stooped posture muscle tightness & speech disorder |
|
|
Term
| Pimozide can result in _______ changes as a SE. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Pimozide EKG change of QT interval prolongation can lead to __________. |
|
Definition
| ventricular tachycardia & death via ventricular fibrillation |
|
|
Term
| Pimozide contradictions: ___________. |
|
Definition
simple tics (except Tourette’s syndrome)
co-administration with methylphenidate or amphetamine for treatment of tics
congenital long QT interval syndrome
concomitant use in patients taking citalopram, escitalopram, or sertraline
clarithyromycin, erythromycin or similar antibiotics |
|
|
Term
| Atypical Antipsychotics: ___________. |
|
Definition
clozapine
olanzapine
quetiapine
risperidone
sertindole |
|
|
Term
| Atypical antipsychotics have high affinity for: ___________ receptors as antagonists/agonists. |
|
Definition
| 5-HT and DA receptors antagonists |
|
|
Term
| Atypical antipsychotics bind less strongly to ____ receptors in the _______ and hypothalamus than conventional antipsychotics and therefore ___________. |
|
Definition
bind less avidly to D2 receptors in the striatum & hypothalamus
produce less EPS & endocrine disturbance |
|
|
Term
| Atypical antipsychotics reduce positive & negative symptoms of _______ better than conventionals. |
|
Definition
|
|
Term
| Atypical antipsychotics improve ______ better than conventionals. |
|
Definition
|
|
Term
| Clozapine is a dibenzodiazepine antipsychotic drug blocks dopamine receptors in the __________ showing less dopamine D2 receptor blocking activity in the __________. |
|
Definition
mesolimbic-mesocortical system
extrapyramidal system |
|
|
Term
| Clozapine is an effective _______ agent producing minimal _______. |
|
Definition
|
|
Term
| Clozapine produces minimal EPS, with a lack of __________. |
|
Definition
|
|
Term
| tardive dyskinesia- ________ |
|
Definition
| Stereotyped, repetitive, involuntary movements of the mouth, lips,& tongue & choreiform movements of the limbs and body |
|
|
Term
| Patients w/ __________ improve while taking clozapine over the course of a few months. |
|
Definition
|
|
Term
| At appropriate doses, clozapine does not antagonize the ___________ drug. |
|
Definition
| antiparkinson effect of L-dopa |
|
|
Term
| Clozapine: characterized as an atypical antipsychotic agent since it __________. |
|
Definition
|
|
Term
| At clinically effective doses, clozapine & other atypical antipsychotics bind to _______% of striatal D2 receptors, but conventional compounds bind _____% of D2 receptors in _____, leading to EPS. |
|
Definition
only 20-60%
70-85%
basal ganglia |
|
|
Term
| Conventional antipsychotics have a much lower affinity for ______ receptors than atypical drugs. |
|
Definition
|
|
Term
| Clozapine is several times more potent in blocking _____ than ____ receptors. |
|
Definition
|
|
Term
| In addition to D2, Clozapine also has a high affinity for D_ dopamine receptors found in ______. |
|
Definition
|
|
Term
| Clozapine has potent ________ actions in caudate. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Clozapine because of its toxicity is only for patients ___________. |
|
Definition
| not responding adequately to standard anti-psychotic drugs |
|
|
Term
| Clozapine treated patients more _______ & their behavior _______ than patients treated with other anti-psychotics |
|
Definition
animated
more socially appropriate |
|
|
Term
| Adverse Effects of Clozapine: __________. |
|
Definition
Agranulocytosis
Seizures
Withdrawal
Sedation, tachycardia, dizziness, hypotension |
|
|
Term
| Most serious SE of Clozapine? |
|
Definition
|
|
Term
| Agranulocytosis SE of Clozapine occurs within ________ and is detected by an abrupt __________. |
|
Definition
first 6 months
cell count drop |
|
|
Term
| Clozapine requires ___________ monitoring. |
|
Definition
| weekly white blood cell count monitoring |
|
|
Term
| Clozapine treatment interrupted if ______ or __________. |
|
Definition
| total white cell count falls below 3000/mm3 or granulocyte count falls below 1500 |
|
|
Term
| Clozapine treatment discontinued permanently if ______ or __________. |
|
Definition
| white cell count less than 2000 or granulocytes less than 1000 |
|
|
Term
| Major Drawback of Clozapine? |
|
Definition
|
|
Term
| Clozapine Rapid withdrawal may result in ____________. |
|
Definition
| marked exacerbation of patient's psychosis |
|
|
Term
Schizophrenic patients who have
responded well to clozapine should not ____________. |
|
Definition
| be taken off w/o a valid reason |
|
|
Term
| For Clozapine to minimize ____, _____, & _______ use low doses initially. |
|
Definition
| hypotension, sedation & seizures |
|
|
Term
| Tachycardia with Clozapine can be reduced with ___________. |
|
Definition
|
|
Term
| Risperidone is a __________ antipsychotic with low EPS when ________. |
|
Definition
"quantitatively atypical"
low doses |
|
|
Term
| Risperidone effective with positive or negative symptoms of psychosis? |
|
Definition
|
|
Term
| Risperidone is a ______-line alternative to _________ antipsychotics. |
|
Definition
first
high-potency conventional |
|
|
Term
| Risperidone blocks: ________ receptors. |
|
Definition
| D2, 5HT2, & alpha1 receptors |
|
|
Term
| For Risperidone the incidence of ______ and _______ w/ low-dose therapy lower than w/ conventional drugs. |
|
Definition
|
|
Term
| With Risperidone, _______ and ______ SE occur initially especially in the elderly. |
|
Definition
| Orthostatic hypotension and reflex tachycardia |
|
|
Term
| Risperidone unlike Clozapine, does not produce: ________. |
|
Definition
| agranulocytosis, cardiac effects or seizure induction, |
|
|
Term
| Can Risperidone cause neuroleptic malignant syndrome? |
|
Definition
|
|
Term
| Olanzapine, a _______ analog, has very low ______ compared to conventionals. |
|
Definition
|
|
Term
| Olanzapine blocks: ________ receptors. |
|
Definition
| D2 & 5-HT2 & D1, D4, 5-HT3, alpha1, muscarinic1 and H1 receptors. |
|
|
Term
| Like clozapine, olanzapine exhibits selectivity for ______/________ dopamine activity, while sparing ________. |
|
Definition
limbic/frontal cortex
striatal |
|
|
Term
| Olanzapine has managed to be used in _______ patients without making EPS worse. |
|
Definition
|
|
Term
| Olanzapine weight affect? |
|
Definition
|
|
Term
| Olanzapine SE: ___________. |
|
Definition
somnolence, agitation, nervousness,
insomnia, anxiety, anticholinergic effects, orthostatic hypotension |
|
|
Term
| Quetiapine, ______ analog, with ______ potency. |
|
Definition
|
|
Term
| Quetiapine binds ____ receptors ______. |
|
Definition
| 5-HT2A, D1, D2, H1, alpha1 receptors w/ relatively low affinity |
|
|
Term
| Quetiapine exhibits only _____ prolactin elevation. |
|
Definition
|
|
Term
| Sertindole Binds to ________. |
|
Definition
| Binds to 5-HT2, D2, alpha1 receptors (same with Risperidone) |
|
|
Term
| Sertindole exhibits ______ selectivity in binding to D2 receptors vs ______ D2 receptors |
|
Definition
|
|
Term
| Sertindole hematological problems? |
|
Definition
|
|
Term
|
Definition
| schizophrenia, acute treatment of bipolar manic or mixed episodes, adjunct to lithium or valproate for maintenance treatment of bipolar disorder. Also, for acute treatment of agitation in schizophrenia |
|
|
Term
| Ziprasidone may antagonize effects of ________ and __________. |
|
Definition
| L-Dopa & dopamine agonists |
|
|
Term
| Drugs that antagonize L-Dopa |
|
Definition
ziprasidone
Typical Antipsychotics (Phenothiazines) |
|
|
Term
| Drug known for not antagonizing L-Dopa? |
|
Definition
|
|
Term
| Ziprasidone Contraindications: |
|
Definition
recent acute MI
QT prolongation |
|
|
Term
| Ziprasidone should not be coadminstered with: __________. |
|
Definition
Antipsychotics that cause QT prolongation
thioridizine, pimozide (antipsychotic used in Tourette’s syndrome), or chlorpromazine |
|
|
Term
| Sertindole has potent _____ effects in addition to its antipyschotic and is not ________, because its low _____ receptor affinity. |
|
Definition
antianxiety
Not sedative (low H1) |
|
|
Term
| Aripiprazole Drug interactions: has __ antagonism & has potential to ______________. |
|
Definition
alpha1
enhance effects of certain antihypertensive drugs |
|
|
Term
| No clear difference in ______ among the conventional antipsychotics. |
|
Definition
|
|
Term
| The atypical antipsychotics, especially _______, are viable first-line drugs |
|
Definition
|
|
Term
| Hospitalized patients may require ________ to show significant improvement with antipsychotics. |
|
Definition
|
|
Term
For treating acute manic phase of bipolar
disorder, _______ is the preferred drug |
|
Definition
|
|
Term
| haloperidol is used to gain rapid control during bipolar mania because of the _____ onset of ______. |
|
Definition
|
|
Term
| For relief of panic reactions & psychosis associated w/ drug use, _______ preferred over ____________, because of less _______ & ________ effects. |
|
Definition
haloperidol
phenothiazines
less anticholinergic & hypotensive effects |
|
|
Term
Antipyschotics can be used for relief of disturbed behavior in patients w/ _______.
disease (AD). |
|
Definition
|
|
Term
| Antipyschotics can be used for potentiation of __________ for special surgeries. |
|
Definition
|
|
Term
| ________ antipsychotics can be used for antiemetic therapy. |
|
Definition
|
|
Term
| Treatment of Tourette's disorder, __________ antipsychotic is effective. |
|
Definition
|
|
Term
| When Haloperidol doesn't work in the treatment of Tourette's, ________ antipsychotic can be used. |
|
Definition
|
|
Term
| Antipsychotics can be used to treat ________ chorea. |
|
Definition
|
|
Term
| Pts. with compliant issues with antipsychotics can be given long acting preps of ______ or ______ in IM injections as depot forms. |
|
Definition
| fluphenazine & haloperidol |
|
|
Term
| Lithium is a ________ type of drug. |
|
Definition
|
|
Term
| Lithium terminates _______ & decrease the cyclic ________. |
|
Definition
|
|
Term
| Li is effective alone or combined w/ _______ ("lithium augmen-tation") for treatment of recurrent ________. |
|
Definition
TCAs
endogenous depression |
|
|
Term
| Li takes ______ to become effective. |
|
Definition
| delayed onset due to time necessary to achieve effective brain levels (7-10 days). |
|
|
Term
| Because of the delay to achieve proper Brain Li levels, _______ is given initially to control acute mania. |
|
Definition
| antipsychotic agents (e.g.,haloperidol) |
|
|
Term
| For measurement of Li lvls, blood should be drawn ________ after the last dose. |
|
Definition
|
|
Term
| Li is distributed in _______ and eliminated by ________. |
|
Definition
| in total body water; eliminated by kidneys |
|
|
Term
| Renal excretion of Li is affected by ________. |
|
Definition
|
|
Term
| In presence of sodium _________, lithium ion selectively reabsorbed in renal tubules & may accumulate to toxic levels |
|
Definition
|
|
Term
| LOW SODIUM IN DIET -----_______ LITHIUM REABSORPTION |
|
Definition
|
|
Term
| LOW SODIUM IN DIET ---- _______ LITHIUM TOXICITY |
|
Definition
|
|
Term
| ____________ (________) markedly increase serum lithium& toxicity |
|
Definition
| Sodium-depleting diuretics (Thiazides) |
|
|
Term
| _______ drugs can reduce renal excretion of lithium. |
|
Definition
|
|
Term
| Impaired _______ function increases lithium retention & toxicity |
|
Definition
|
|
Term
| Li SE @ therapeutic serum concentrations: __________. |
|
Definition
| thirst; polyuria; fine tremor |
|
|
Term
| Fine tremor of Li SE, especially responds to _______. |
|
Definition
|
|
Term
| Li contradicted in? Because? |
|
Definition
pregnancy
Cardiac defects, renal& endocrine
disorders in infants |
|
|
Term
| Li occasional SE's at all serum concentrations: ________. |
|
Definition
| Goiter; hypothyroidism; nephrogenic diabetes insipidus; renal tubular necrosis |
|
|
Term
|
Definition
|
|
Term
| Li Renal Toxicity may result in ____________. |
|
Definition
| Nephrogenic diabetes insipidus |
|
|
Term
| _______ can be used to reduce urination in Pts. with Nephrogenic diabetes insipidus from Li Renal Toxicity. |
|
Definition
|
|
Term
| _______ drugs can interfere with Li excretion and increases chances of renal toxicity. |
|
Definition
| Thiazides (Sodium-depleting diuretics) |
|
|
Term
|
Definition
|
|
Term
| Alternatives to Li: __________. |
|
Definition
Valproic acid
Carbamazepine |
|
|
Term
| Carbamazepine also used for treatment of certain other behavior disorders & as an adjunct w/ neuroleptics in treatment of __________. |
|
Definition
|
|
Term
| Conventional Antipsychotics: ____________. |
|
Definition
chlorpromazine
thioridazine
fluphenazine
trifluoperazine
loxapine
pimozide
molindone
haloperidol
thiothixene |
|
|
Term
| Atypical Antipsychotics: ___________. |
|
Definition
clozapine
risperidone
olanzapine
quetiapine
ziprasidone
aripiprazole |
|
|
Term
| For mania and/or maintenance of bipolar disorder: __________. |
|
Definition
lithium carbonate
valproic acid
carbamazepine |
|
|
Term
| Parkinson’s Disease (PD) symptoms: __________. |
|
Definition
Resting tremor
Rigidity
Akinesia & Bradykinesia
difficulty arising from a chair & beginning to walk. |
|
|
Term
| Parkinson’s Disease (PD) Autonomic dysfunction: __________. |
|
Definition
Excessive salivation (drooling)
increased sweating |
|
|
Term
| Parkinson’s Disease (PD) CNS Symptoms: _______. |
|
Definition
Dimentia: 30% of older patient
Depression: 30-40% of patients. |
|
|
Term
| Causes of PD: ___________. |
|
Definition
Idiopathic
Iatrogenic
Other- similar clinical syndromes produced by viral or other encephalitis, arteriosclerosis, carbon monoxide poisoning & chronic manganese intoxication. |
|
|
Term
| Iatrogenic cause of PD- ___________. |
|
Definition
| induced by antipsychotic drugs |
|
|
Term
| In PD, dopaminergic mechanisms in _______ system disrupted. |
|
Definition
|
|
Term
| In PD there is degeneration of dopaminergic neurons w/ cell bodies in the _________ & terminals in __________. |
|
Definition
substantia nigra pars compacta (SNc)
striatum (caudate & putamen) |
|
|
Term
| PD Treatment goals: enhancing ________ & and reducing ________. |
|
Definition
enhancing dopaminergic activity
reducing influence of striatal cholinergic neurons |
|
|
Term
| ________ causes destruction of SNc dopaminergic neurons. |
|
Definition
|
|
Term
|
Definition
| an impurity in an illicit meperidine “designer”drug. |
|
|
Term
|
Definition
|
|
Term
| Major Drugs for Treating HD: _______. |
|
Definition
L-Dopa
Amantadine
Dopamine R Agonist
Anticholinergic
Selegiline |
|
|
Term
| MPTP (inactive/active) is transported? Where it is then _____________. |
|
Definition
| MPTP (inactive) readily crosses BBB. MAO-B converts MPTP to active, neurotoxic MPP+ |
|
|
Term
| MPP+ a ________ poison, causing ________ death. |
|
Definition
mitochondrial
dopaminergic cell |
|
|
Term
| __________ (________) fully protect against MPTP-induced neurotoxicity. |
|
Definition
| MAO-B inhibitors (selegiline) |
|
|
Term
| In addition to MAO-B inhibitors, like _______, ________'s also block MPTP-induced neurotoxicity. |
|
Definition
selegiline
Dopamine uptake blockers |
|
|
Term
| MPTP is oxidized to MPP+ where? |
|
Definition
| outside dopaminergic neurons, possibly in astrocytes or serotonergic neurons |
|
|
Term
|
Definition
|
|
Term
| Enzymatic oxidation of Dopamine by MAO produces _______ & ________. |
|
Definition
| Hydrogen peroxide & DOPAC |
|
|
Term
| In the presence of ______, hydrogen peroxide can be converted to ____________. |
|
Definition
|
|
Term
| What breaks down hydrogen peroxide safely to H2O? |
|
Definition
|
|
Term
| In treatment of PD, want to block the _______ receptor cholerngic response. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Levodopa (L-DOPA) cross BBB? |
|
Definition
|
|
Term
| Levodopa (L-DOPA) can cross the BBB via? |
|
Definition
| neutral amino acid transporter |
|
|
Term
| Once in neurons, Levodopa (L-DOPA) is __________. |
|
Definition
|
|
Term
| Essentially all effects of L-DOPA due to dopamine formed by the action of ________. |
|
Definition
|
|
Term
| 95-98% of L-DOPA converted to dopamine in the ________. |
|
Definition
|
|
Term
| Generally, L-DOPA co-administered with a _______-acting d_______ to prevent conversion in the periphery. |
|
Definition
peripherally
ecarboxylase inhibitor |
|
|
Term
| L-DOPA enhances the synthesis and ultimately the ________. |
|
Definition
|
|
Term
| ________ facilitates the release of DA. |
|
Definition
|
|
Term
| _______ inhibits the metabolism of dopamine in non-dopaminergic neurons or glial. |
|
Definition
|
|
Term
| The beneficial effects of dopamine in PD mediated via ______ receptors on _______ neurons. |
|
Definition
| dopamine D2 receptors (postsynaptically on striatal neurons). |
|
|
Term
L-DOPA Action in CNS:
Ameliorates the ______ and ______ of PD. |
|
Definition
|
|
Term
| ______ is more resistant to the effects of L-DOPA than akinesia and rigidity, but can still be reduced. |
|
Definition
|
|
Term
| ________ can be combined with L-DOPA to reduce the tremor of PD. |
|
Definition
|
|
Term
| L-DOPA major SE: _______. |
|
Definition
| dyskinesias & psychiatric disturbances |
|
|
Term
| dyskinesias- ________. WIKI |
|
Definition
| Dyskinesia is a movement disorder which consists of adverse effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea. Dyskinesia can be anything from a slight tremor of the hands to uncontrollable movement of, most commonly, the upper body but can also be seen in the lower extremities. |
|
|
Term
| L-DOPA Effect on CV: __________, but ____ develops with continual treatment. |
|
Definition
Orthostatic hypotension
Tolerance |
|
|
Term
| L-DOPA effect on CV: Arrhythmias & tachycardia incidence can be reduced by combining with _______. |
|
Definition
|
|
Term
| L-DOPA Effect on Gastrointestinal System: Nausea, vomiting &anorexia, can be reduced by __________. |
|
Definition
| combining L-DOPA & Carbidopa |
|
|
Term
| The GI effects of L-DOPA is produced by _______. |
|
Definition
| Stimulation of chemoreceptor trigger zone |
|
|
Term
| CTZ lies outside/inside the BBB? |
|
Definition
|
|
Term
| CTZ lies outside the BBB, so ______ dopamine causes the GI side effects. |
|
Definition
|
|
Term
| Use of phenothiazines as antinausea compounds would __________ of L-DOPA. |
|
Definition
| antagonize therapeutic effect (should be avoided). |
|
|
Term
| Can use _______ (has DA antagonist effects) as antiemetic in PD patients. |
|
Definition
|
|
Term
| ________ in addition to metoclopramide can be used as an anti-emetic bc of its peripheral dopamine receptor blocking activity. |
|
Definition
|
|
Term
| Endocrine Effects of L-Dopa: __________. |
|
Definition
| Inhibition of prolactin secretion |
|
|
Term
| Dopamine is the primary neuroendocrine inhibitor of the secretion of prolactin from the anterior pituitary gland. WIKI |
|
Definition
| Oh well now that makes fucking sense |
|
|
Term
| __________ can compete w/ L-DOPA for absorption from the gut, & for transport from blood to brain. |
|
Definition
| Certain amino acids (from ingested proteins) |
|
|
Term
| Therapeutic effect sometimes improved in patients with poor response to L-DOPA by careful timing of drug dose in relation to __________. |
|
Definition
|
|
Term
| L- Dopa is decarboxylated to dopamine in: ___________. |
|
Definition
| stomach, intestine, liver & other tissues so that less than 1% may enter brain |
|
|
Term
| L-DOPA causes hypo/hypertension? |
|
Definition
| Hypo (from the central effect of DA) |
|
|
Term
| _____ SE of L-DOPA limits the dosage. |
|
Definition
Dyskinesias
Mouth, face or tongue movements; bobbing or waving of head & neck; and painful dystonias |
|
|
Term
|
Definition
| (abnormal involuntary movements) |
|
|
Term
| Dyskinesias from L-DOPA reversible? |
|
Definition
|
|
Term
| With L-DOPA, drugs that enhance ________ activity can reduce dyskinesias but worsening of _______ symptoms occurs |
|
Definition
|
|
Term
| _________ well-known to increase symptoms of parkinsonism. |
|
Definition
|
|
Term
| Behavioral & personality changes from L-DOPA: ______. |
|
Definition
| Nervousness, anxiety, agitation, insomnia, depression, |
|
|
Term
| L-DOPA contraindicated in patients w/: _________. |
|
Definition
| Narrow-angle glaucoma, acute psychosis or severe psychoneurosis |
|
|
Term
|
Definition
| Neurosis is a class of functional mental disorders involving distress but neither delusions nor hallucinations, whereby behavior is not outside socially acceptable norms.[1] It is also known as psychoneurosis or neurotic disorder, and thus those suffering from it are said to be neurotic. The term essentially describes an "invisible injury" and the resulting condition. |
|
|
Term
| ________ reverses action of L-dopa due to enhancement of ___________. |
|
Definition
Pyridoxine (B6)
peripheral conversion to dopamine |
|
|
Term
| Pyridoxal phosphate (Pyridoxine (B6) a cofactor for _______, this is effected by __________. |
|
Definition
|
|
Term
| _____ combined with L-dopa result in hypertensive crisis. |
|
Definition
|
|
Term
| _________ & __________ (which are ________) counteract therapeutic effect of L-dopa. |
|
Definition
Phenothiazines & butyrophenones
dopamine blockers |
|
|
Term
| Reserpine counteracts L-DOPA by __________. |
|
Definition
|
|
Term
| Carbidopa inhibits ___________, but does not ________. |
|
Definition
| inhibits decarboxylase, but does not cross BBB |
|
|
Term
| Carbidopa generally given in fixed-dose combination with ________. |
|
Definition
|
|
Term
| Carbidopa ______ the dose of L-DOPA. |
|
Definition
|
|
Term
| Carbidopa decreases ______ side effects of L-DOPA. |
|
Definition
| Markedly diminished nausea & vomiting (from 80% to 20%) |
|
|
Term
| Carbidopa results in more quickly ________, when combined with L-DOPA |
|
Definition
| Achieve therapeutic level much more rapidly |
|
|
Term
| Unresolved effects of Peripheral Decarboxylase Inhibitors (carbidopa): __________. |
|
Definition
a) Orthostatic hypotension
b) Dyskinesias- appear earlier, more severe & persist longer
c) Adverse mental effects - may appear earlier |
|
|
Term
| After 5 years of L-DOPA therapy, some type of unpredictable ________ in clinical response occur in 50% of patients (difficult to manage). |
|
Definition
|
|
Term
| Motor Fluctuations of L-DOPA at 5 years: ___________. |
|
Definition
Freezing episodes
"Wearing-off" effect
Peak-dose dyskinesias
"On-off" phenomenon |
|
|
Term
| L-DOPA Motor Fluctuations: Freezing episodes- ________. |
|
Definition
| Periods of sudden immobility |
|
|
Term
| L-DOPA Motor Fluctuations: "Wearing-off" effect- ______. |
|
Definition
Relief of symptoms lasts only 2-3
hours rather than 4-5 hours. |
|
|
Term
| L-DOPA Motor Fluctuations: "Wearing-off" effect, ________ helps to relieve. |
|
Definition
| Small and more frequent dosage |
|
|
Term
| L-DOPA Motor Fluctuations: Peak-dose dyskinesias- ________. |
|
Definition
| dyskinesias Appear 1-2 hours after a dose. |
|
|
Term
| L-DOPA Motor Fluctuations: "Wearing-off" effect, ________ helps to relieve. |
|
Definition
decrease individual doses & give more frequently
Drug holiday |
|
|
Term
| L-DOPA Motor Fluctuations: "On-off" phenomenon- ____________. |
|
Definition
| Unpredictable motor fluctuations from a state of mobility ("on") to a state of immobility ("off") & back again |
|
|
Term
| "On-off" phenomenon happens to 15-40% on __________. |
|
Definition
| chronic treatment with L-DOPA |
|
|
Term
| Motor Fluctuations of L-DOPA can be treated successfully with ____________, ___________, or ____________. |
|
Definition
selegiline (MAO-B inhibitors) addition
"continuous" administration of L-DOPA
apomorphine (a direct dopaminergic agonist |
|
|
Term
| Anticholinergic drugs for L-DOPA would be antagonists/agonists at _______ receptors in the CNS. |
|
Definition
| antagonists Muscarinic receptor |
|
|
Term
| Anticholinergic Drugs: _______ receptor antagonists can be used in HD therapy to correct balance btwn _______ and _______ in the __________. |
|
Definition
Muscarinic receptor antagonists
correct balance between dopaminergic & cholinergic
Striatum |
|
|
Term
| Anticholinergic Drugs (Muscarinic receptor antagonists) can be used in PD to improve: ___________, but these drugs are __________. |
|
Definition
Tremor, rigidity& bradykinesia
less effective than L-Dopa |
|
|
Term
| Anticholinergic Drugs (Muscarinic receptor antagonists are often used in the control of EPS by _______ drugs. |
|
Definition
|
|
Term
| Specific Anticholinergic Agents: _______. |
|
Definition
Trihexyphenidyl
Biperiden
Diphenhydramine
Benztropine
Procyclidine
Ethopropazine |
|
|
Term
| ________ is an antiviral agent that has a beneficial effect in PD & __________. |
|
Definition
Amantadine
drug- induced EPS. |
|
|
Term
| Amantadine helps in PD and drug- induced EPS by causing _________ and decreased _______ and has ________ actions. |
|
Definition
| Releases dopamine from intraneuronal stores & decreases re-uptake & has direct DA agonist activity & anticholinergic actions. |
|
|
Term
| Specific Anticholinergic Agents: _______. |
|
Definition
Trihexyphenidyl
Biperiden
Diphenhydramine
Benztropine
Procyclidine
Ethopropazine |
|
|
Term
| ________ is an antiviral agent that has a beneficial effect in PD & __________. |
|
Definition
Amantadine
drug- induced EPS. |
|
|
Term
| Amantadine helps in PD and drug- induced EPS by causing _________ and decreased _______ and has ________ actions. |
|
Definition
| Releases dopamine from intraneuronal stores & decreases re-uptake & has direct DA agonist activity & anticholinergic actions. |
|
|
Term
| Amantadine quick drawback? |
|
Definition
| Tolerance to its action develops within a few weeks |
|
|
Term
| Amantadine is frequently with ___________ or _______. |
|
Definition
| anticholinergic agents or L-dopa |
|
|
Term
| Amantadine produces ______ effects. |
|
Definition
|
|
Term
| With Amantadine 25% of patients develop difficulty in ________. |
|
Definition
| thinking (confusion, lightheadedness, hallucinations & anxiety) |
|
|
Term
| Amantadine should be administered with caution to ______ pts. because _______. |
|
Definition
w/ renal impairment
90% of amantadine excreted in urine |
|
|
Term
| Bromocriptine is used with L-DOPA to ________. |
|
Definition
| reduce motor fluctuations (caused by L-dopa) |
|
|
Term
| Bromocriptine acts on ______ receptors as an antagonist/agonist. |
|
Definition
|
|
Term
| Bromocriptine advantage of combining with L-DOPA? |
|
Definition
| L-dopa dose reduced (also reduces motor fluctuations from L-DOPA) |
|
|
Term
| Adverse effects of Bromocriptine are all __________. |
|
Definition
| All reversible upon discontinuation |
|
|
Term
| Adverse effects of Bromocriptine are minimized by? |
|
Definition
| Minimized by slowly building up dose over 2-3 months to develop tolerance |
|
|
Term
| Need to build tolerance to the SE's of _______ and _______ of Bromocriptine. |
|
Definition
|
|
Term
| Bromocriptine SE: _______ on cold exposure |
|
Definition
|
|
Term
|
Definition
| Vasospasm refers to a condition in which a blood vessel's spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). |
|
|
Term
| Like L-DOPA, SE of Bromocriptine is ______, except less frequent. |
|
Definition
|
|
Term
|
Definition
| Erythromelalgia: red, tender, warm, edematous lower extremities |
|
|
Term
| _______ is similar to bromocriptine being Direct-acting DA agonist, but more specific. |
|
Definition
|
|
Term
| Pergolide can be used to? |
|
Definition
| reducing fluctuations on L-dopa (same as bromocriptine) |
|
|
Term
|
Definition
| Direct acting D2 receptor agonist |
|
|
Term
| Side Effects of Ropinirole: ______. |
|
Definition
| Light headedness & fainting with slowed heart beat (12% of people with early stages & 3% in late stages). |
|
|
Term
| ________ reduces excretion of ropinirole; (increasing its circulating levels). |
|
Definition
|
|
Term
|
Definition
| Treats infections. Also treats anthrax infection after possible exposure. This medicine is a fluoroquinolone antibiotic. |
|
|
Term
|
Definition
| Direct-acting DA receptor agonist |
|
|
Term
| Pramipexole is a Direct-acting DA receptor agonist with selectivity for _______. |
|
Definition
|
|
Term
| Pramipexole in addition to acting as a DA agonist, exerts a ______ effect. |
|
Definition
|
|
Term
|
Definition
| Monoamine Oxidase-B Inhibitor (MAO-B) |
|
|
Term
| MAO-B preferentially metabolizes _______ without altering metabolism of ______ & _______. |
|
Definition
dopamine
NE and serotonin |
|
|
Term
|
Definition
MPTP -> MPP+
Dopamine -> DOPAC + H2O2 |
|
|
Term
| By decreasing _______ & ________, Selegiline exerts a neuro-protective |
|
Definition
| Decreasing MAO-B -> decreases production of H2O2 & MPP+ |
|
|
Term
| A recent study of early PD cases found patients who received selegiline alone or w/ tolcapone reached a predetermined level of disability more slowly than subjects who took tolcapone alone or placebo (i.e., __________). |
|
Definition
| selegiline delays progression of early PD |
|
|
Term
| All PD patients be started on selegiline when? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| COMT Inhibitor (catechol-O-methyl transferase) |
|
|
Term
| COMT (catechol-O-methyl transferase) does what? |
|
Definition
|
|
Term
| COMT (catechol-O-methyl transferase) has central/periph activity? |
|
Definition
|
|
Term
| Tolcapone end result is ________. |
|
Definition
| more L-DOPA to remain in circulation/brain. |
|
|
Term
| Tolcapone enhances _______ of L-DOPA by ____________. |
|
Definition
effectiveness
increasing time L-DOPA effective; a longer "on" period and a shorter "off" time |
|
|
Term
| Tolcapone reduces the amount of _______ required to reduce ______. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Side Effects of Tolcapone: _________. |
|
Definition
| urine discoloration, dyskinesia |
|
|
Term
| Tolcapone precautions? requires _____ screening & ________ monitoring. |
|
Definition
Tolcapone affects liver enzymes & thus liver function should be screened.
Drug Interactions: Other drugs metabolized in liver must be monitored (e.g., warfarin). |
|
|
Term
|
Definition
| inhibits COMT (same as Tolcapone) |
|
|
Term
| Differences between Entacapone & Tolcapone? |
|
Definition
Entacapone only acts at periph
less hapatotoxicity than tolcapone |
|
|
Term
| Huntington's chorea, an inherited degenerative disease involving cortex & __________. |
|
Definition
|
|
Term
| Dopamine levels in striatum _________ in HD, meaning? |
|
Definition
normal or elevated
substantia nigra neurons intact |
|
|
Term
| In HD activities of enzymes catalyzing synthesis of ______ & _______ reduced in striatum. |
|
Definition
|
|
Term
| HD symptoms resemble some of symptoms of excessive ________ activity induced by _______. |
|
Definition
|
|
Term
| In HD, drugs enhancing _____ or ______ have done little, while drugs that antagonize ______ have been promising. |
|
Definition
enhance cholinergic or GABA activity
dopamine receptor antagonists |
|
|
Term
| In addition to DA antagonists, DA depleting drugs like: ________ & ________ are used in treating HD. |
|
Definition
| reserpine or tetrabenazine |
|
|
Term
| Drawback of DA antagonists & DA depleting drugs in the treatment of HD? |
|
Definition
| All produce iatrogenic parkinsonism |
|
|
Term
|
Definition
|
|
Term
| Tourette’s Syndrome (TS), A multiple tic disorder w/ onset in ________. |
|
Definition
| early childhood b/w ages of 5-7 years. |
|
|
Term
| Tourette’s Syndrome (TS) most common tics: _______. |
|
Definition
| excessive eye blinking, throat clearing, head shaking,& facial grimacing. |
|
|
Term
| _________- obscene or socially inappropriate speech, is an infrequent TS tic symptom. |
|
Definition
|
|
Term
| All tics of TS are aggravated by ________. |
|
Definition
| stressful environmental stimuli or settings |
|
|
Term
| TS disease associated w/ a hyperfunctioning of _______ systems since _______ drug is the first line treatment & effective in 2/3 of individuals. |
|
Definition
|
|
Term
|
Definition
Haloperidol is a dopamine inverse agonist of the typical antipsychotic class of medications. It is a butyrophenone derivative and has pharmacological effects similar to the phenothiazines.
treatment of schizophrenia and acute psychotic states |
|
|
Term
| After haloperidol, what are the secondary choices for treating TS? |
|
Definition
|
|
Term
|
Definition
levodopa
carbidopa
levodopa/carbidopa (Sinemet®)
Amantadine (antiviral, Releases dopamine from intraneuronal stores & decreases re-uptake & has direct agonist) |
|
|
Term
| Anticholinergic Agents (PD): ________. |
|
Definition
trihexyphenidyl
These were just listed.
trihexyphenidyl
diphenhydramine
biperiden
benztropine
procyclidine
ethopropazine |
|
|
Term
| COMT Inhibitor (PD): ______. |
|
Definition
tolcapone
entacapone
MPTP, MPP+(neurotoxins) |
|
|
Term
| Dopamine Agonists (PD): ____________. |
|
Definition
apomorphine
bromocriptine
pergolide
ropinirole |
|
|
Term
| MAO-B Inhibitor (PD):__________. |
|
Definition
|
|
Term
| Huntington’s Disease Drugs: ___________. |
|
Definition
Antipsychotics (phenothiazines& haloperidol DA blockers)
reserpine or tetrabenazine (Dopamine depleting agents) |
|
|
Term
| Tourette Syndrome Drugs: ___________. |
|
Definition
haloperidol (Antipsychotic)
pimozide (Antipsychotic) |
|
|
Term
| Tourette’s Syndrome (TS), A multiple tic disorder w/ onset in ________. |
|
Definition
| early childhood b/w ages of 5-7 years. |
|
|
