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59 Cards in this Set
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- Back
- 3rd side (hint)
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Where does the Mesolimbic Dopaminergic pathway begin & end?
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begins = midbrain ventral Tegmental Area
Ends = limbic system and nucleus accumbens |
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What role does the dopaminergic mesolimbic system play?
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emotional behavior
- auditory hallucinations - delusions - thought disorders - pleasure sensation - euphoria of drug abuse |
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Hyperactivity of dopamine in the mesolimbic pathway causes?
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Positive symptoms of schizophrenia
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What are CHARACTERISTICS of positives symptoms of schizophrenia?
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hyper DA
hypo 5HT antipsychotic drugs block DA receptors added to clinical picture delusions/hallucinations & agitations |
mesolimbic system (frontal)
emotion & hallucinations |
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Positive symptoms of schizo is type I or type II?
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Type I
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What are positive symptoms of Schizo?
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- disturbance of thought form
- disturbances of content (delusion) - perceptual disorders (hallucinations) - Behavioral Disorders - Qualitative changes |
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Where does the dopaminergic mesocortical pathway begin & end?
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begins = midbrain VTA
ends = limbic cortex-prefrontal cortex |
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What disease is caused by deficit of DA in the mesocortical pathway?
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negative and/or cognitive symptoms of Schizo
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What are CHARACTERISTICS of negative symptoms of Schizo?
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- hyper 5HT
- inhibit DA system - antipsychotics drugs block 5HT receptors - subtracted from clinical picture - blunted affect, social w/draw, apathy, anhedonia, poverty |
prefrontal cortex (mesocortical)
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What are negative symptoms of Schizo?
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- Blunted affect
- flat affect (can't read face) - social w/draw - apathy (dulled emotional tone - alogia (restriction in thought & speech fluency) - avolition (can't act willingly) - anhedonia (does not experience pleasure) |
cognitive blunting
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Where does the DA nigrostriatal pathway begin & end?
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begins = substantia nigra
ends = basal ganglia/striatum |
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Block of which dopaminergic pathway causes extrapyramidal SE?
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block/deficiency of DA in the basal ganglia of the Nigrostriatal pathway
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What are extrapyramidal SE are experienced when DA is blocked in the basal ganglia of the Nigrostriatal pathway?
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- Parkinsonism
- Dystonia - Akathesia - tardive dyskinesia |
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What are extrapyramidal SE are experienced when there is excessive DA in the basal ganglia of the Nigrostriatal pathway?
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- chorea
- dyskinesia - tics |
associated w/ Hyperkinetic movement disorders
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What is dystonia?
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movement disorder which causes involuntary contraction resulting in TWISTING & REPETITIVE MOVEMENTS
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What is akathesia?
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excessive usually repetitive movements (pacing, foot tapping, rocking) --> feeling that you're going to come out of your skin
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What is dyskinesia?
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Jerky dance like movements of the ARM or HEAD
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What are tics?
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sudden repetitive, nonrhythmic movements
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Which TCAs are weak inhibitors of D2 receptors?
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Amoxapine (CNS) most potent D2 receptor inhibitor
Trimipramine (CNS) Clomipramine (CNS) Maproline |
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TCAs such as Amoxapine, Trimipramine, Clomipramine, & Maprotiline cause what kind of SE?
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If block at NIGROSTRIATAL pathway --> get extrapyramidal SE
If block at the MESOLIMBIC pathway --> since in CNS, also helps w/ psychotic features |
What happens when DA receptors are blocked in the Nigrostriatal pathway & the mesolimbic pathway
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Which TCAs are associated w/ seizures?
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Amoxapine
Bupropion Clomipramine Maprotiline |
similar to TCAs that are weak inhibitors of D2 receptors
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What is the MOA of TCAs that have been associated w/ Seizures?
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They lower seizure threshold therefore inducing seizures
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What types of patients are at an increased risk of developing seizures?
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- pt w/drawing from EtOH + sedatives
- pt diagnosed w/ eating disorder |
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Which TCAs are the most potent H1 & alpha 1 receptor blockers?
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Amitriptyline
Trimipramine Doxepine |
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Which TCAs are the least potent H1 receptor blockers?
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Desipramine
Amoxapine |
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Which TCAs are the least potent alpha 1 receptor blockers?
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Desipramine
Protriptyline |
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Which TCA(s) is the most potent D2 receptor inhibitor?
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Amoxapine
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Which TCA(s) is more selective at blocking 5HT receptor?
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Clomipramine
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Some TCAs block H1 receptors in addition to NE. What SE are caused by blocking H1 receptors?
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Hypotension (central & peripheral)
sedation drowsiness weight gain |
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Can TCAs that are also alpha 1 blockers be used w/ centrally acting alpha 2 agonist (clonidine)?
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No b/c TCAs w/ alpha 2 activity cause dilation + stimulation of alpha 2 in CNS also causes dilation
together = orthostatic hypotension |
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Can TCAs w/ alpha 1 blocking activity be used in patients on alpha 1 anti-hypertensive drugs? Why or why not?
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No b/c they both block alpha 1 --> TCA would potentiate anti-hypertensive effects (hypotension)
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What do you use to treat hypotention caused by patients on both TCA w/ alpha 1 blocking activity & alpha 1 antihypertensive?
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NE, phenylephrine, or Metaraminol
Do NOT use Epi b/c it will worsen |
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What are symptoms of abrupt withdraw of TCAs?
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hypersalivatioin
N/V abdominal cramps diarrhea HA sleep disturbance |
TCAs = blocking cholinergic (parasympathetic) --> dry mouth, etc
Don't block = get excessive cholinergic effects |
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What are drug interactions of TCA?
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TCAs + Neuroleptics = incr anti-cholinergic SE d/t M1 block
TCAs + Neuroleptics = incr sedation SE d/t H1 block TCAs + Neuroleptics = incr hypotension SE d/t alpha 1 block TCA + CYP inducers (barbiturates, carbamazepine) = accelerate TCA metabolism (decreasing TCAs effectiveness) TCAs + enzyme inhibitors (Valproates) = TCA toxicity |
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Which MAO(s) is found in the brain?
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MAO-B
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Which neurons is MAO-B found in the brain & what does it primarily metabolize?
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MAO-B is found in the 5HT neurons & it metabolizes DA & tyramine
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B.S.
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Which MAO(s) is found in the GI tract?
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MAO-A & MAO-B
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Which neurons is MAO-A found in the brain & what does it primarily metabolize?
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MAO-A is found in NE & DA neurons & primarily metabolizes NE & 5HT
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Do MAO-Is effects occur right away?
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No
MAO inhibition occurs 5-10 days after taking MAO-I, but antidepressant effects are NOT observed until after 3-4 wks of tx |
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Which MAO-I is most potent & why?
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Tranylcypromine b/c it has amphetamine like structure (meaning it also releases NE therefore more potent than other MAO-Is & produces quicker antidepressant effects
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Which MAO-I is also effective in treating aneric and/or treatment resistant depression?
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Tranylcypromine
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Which MAO-I is also effective in the mgmt of melancholic & atypical depression; panic disorders & social phobia?
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Phenelzine
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Which MAO-Is are irreversible
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Phenelzine
Isocarboxazide Tranylcypromine Clorgyline Selegyline |
PIT C S
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What are general indications of MAO-Is?
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Atypical Depression (anxiety, chronic pain, vegetative symp such as loss of libido, anorexia, insomnia)
Melancholic depression (persistently lower mood w/ feelings of worthlessness, helplessness, hopelessness, guilt, blame, pessimism) |
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What is the jingle for MAO-Is?
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Angelina & Brad PIT At BCM b/c of Bad Seizures
PIT drugs = block MAO A & B BCM drugs = block MAO-A only Selegyline blocks MAO-B only |
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List MAO-I drugs?
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Phenelzine
Isocarboxazide Tranylcypromine Brofaromine Clorgyline Moclobemide Selegyline |
A & B PIT A BCM b/c Bad Seizures
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What SE are seen in TCAs but not MAO-Is?
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MAO-Is do NOT have
- sedative (no H1 block) - anticholinergic (no M1 block) - cardiotoxic |
TCAs block NE receptors & also alpha 1, alpha 2, M1, H1, & DA receptors
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What are food interactions w/ MAO-Is?
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avoid food containing Tyramine (cheese, wine)
causes HTN, palpitations, N/V, sweating, mydriasis, restlessness, pyrexia/hyperpyrexia, cerebral hemorrhage/stroke |
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What are some drug interactions with MAO-Is?
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MAO-Is + sympathomimetics (amphetamine, phenylpropanolamine, pseudoephedrine) = NO b/c MAO-I = more NE therefore sympathomimetics = bad b/c too much NE
MAO-Is + narcotics = produce potentially lethal syndrome (characterized by agitation, fever, HA, seizures, coma) |
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Depression is cause by too little _______ & ________?
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NE & 5HT
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Like MAO-Is, SSRIs take ____ - _____ wks to achieve therapeutic effects
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3 - 4 wks
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Which SSRI has the longest half life & how long is it?
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t1/2 of Fluoxetine = 2-3 days
t1/2 of norfluoxetine (fluoxetine metabolite) = 7-15 days |
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Compare & contrast the CYP450 enzymes that TCAs & SSRIs are substrates for.
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TCA SSRI
1A2 1A2 2D6 2D6 3A4 3A4 2C19 |
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List some drug interactions w/ SSRIs?
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Fluvoxamine (inhibits 1A2) + theophylline = theophylline toxicity
Cigarette smoking (CYP 1A2 inducer) = increase theophylline metabolism Fluoxetine (CYP 3A4 inhibitor) + Amitriptyline (TCA, inactivated by 3A4) = amitryptyline toxicity |
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Lists some SSRIs?
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paroxetine
setraline fluoxetine fluvoxamine citalopram escitalopram venlafaxine |
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Which SSRI(s) blocks both 5HT & NE (meaning it's an SNRI --> Seritonin NE reuptake inhibitor)?
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Venlafaxine (Effexor)
Other SNRIs: Sibutramine (Meridia) for obesity Tramadol (Ultram) - CNS depressant and analgesic Milnacipran (Lxel) Duloxetine (Cymbalta) |
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What SE are seen in TCAs & MAO-Is but NOT SSRIs & why?
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SSRIs = weak antagonists of M1, H1, alpha 1, & D2 therefore less SE than TCAs & MAO-Is
anticholinergics SE of hypotension/seizures/wt gain virtually absent |
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What SE are seen in SSRIs?
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sexual dysfcn
decrease libido reduced arousal impaired orgasmic fcn GI problems tremor sweating anxiety |
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What receptors does venlafaxine block at low dose? At high dose?
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At low dose = blocks 5HT
At high dose = blocks NE |
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