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92 Cards in this Set

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  • Back
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hypokinetic movements caused by what?
reduced DA or increased ACh
hyperkinetic movements caused by what
increased DA relative to ACh
PD defined by:
50% loss of DA in substantia nigra which causes:
80% loss of DA in striatum
DA released from
axonal varicosities
end of dose wearing off effect
when disease progresses and neuron availability and recycling mechanisms are no longer relavent
What is responsible for the decrease in therapeutic window as PD progresses for Sinemet?
end of dose wearing off effect occurs in brain only and there is a increased risk of toxicity in periphery
cofactor of AAAD?
pyridoxine (thus deficiency prevetns peripheral Ldopa conversion)
on-off phenomenon
sudden onset of PD during treatment due to sensitization of Glu in striatum associated with sawtoothing levodopa levels
Early treatment of PD
indirecting acting agonists and antimuscarinics to promote normal physiological actions; also use direct acting agonists because they are neuroprotective
why is levodopa for late stage PD
most effective when you need it most but most side effects
HD neuronal unbalance
loss of GABA and increased DA tone which leads to chorea
Goal of Dystonia therapy
anti-muscarinics, antispasmodics
Tourette's neuronal imbalance?
increased movement from DA (hyperdopaminergic)
What are schizo positive symptoms? negative?
positive: hallucinations and delusions
negative: poverty of speech, socially inapropes behaviors
What is the DA theory of schizophrenia?
pharmacocentric: since DA antagonists work in schizo's, the disease must be caused by +DA
but schizo brains have no increase or decrease in DA receptor number
what is the hypofrontality hypothesis of psychosis?
failure of parahippocampal gyrus to develop; this prefrontal cortex doesn't develop (- symptoms)and can't inhibit n. accumbens; disinhibition causes + symptoms
Drugs that can control both negative and positive symptoms in schizos target whta?
D4 receptors and 5HT receptors such as clozapine
fallicy of DA theory of schizo?
DA only induces + symptoms, no change in DA receptor #, PCP causes psychosis but not full range of symptoms
EPSEs result from what?
DA receptor blockade in regions of brain not intended for antipsychotic therapy, mainly the nigro-striatal pathway
EPSEs
extrapyramidal side effects: Dystonia, then akathisia, then parkinsonian
Classes of antidepressants
TCAs
Heterocyclics
Antimanic Drugs
MAOIs
SSRIs
(THAMS)
What are the new heterocyclics?
NDRIs
SNRIs
NaSSA
Theory of depression
It is a consequence of brain biogenic amine deficiency
NTs deficient in depression?
NE (either increase or decrease) and 5HT (indoleamine)
patients with reduced 5HT think of what?
suicide ideation
What is SAD?
prolonged dark causes increased melatonin which inhibits 5HT-ergic neurons to cause depression
What explans sleepiness in depressed patients?
production of melatonin in depressed folk
What explains efficacy delay?
upregulation of NE receptors due to uprfulation of NE
net effect of NE?
it normally inhibits interneurons; massive influx inhibits noise

increased noise = depression
net effect of 5HT in brain?
increases limbic input to cortex, without this, emotion pathways r fucked
What is Quinidine?
anti-arrythmic agent.

OD: slows dromotropy and causes arrhythmias
domotropic
affecting AV conduction velocity of the heart
What is serotonin syndrome?
hyperthermia, rigidity, myoclonus, fluctuations in vital signs

(stiff, cold, twitching, unstable!)
Why is compliance higher in SSRIs?
less side effects
side effects of SSRIs?
serotonin syndrome,
insomnia
impotence
increased risk of suicide
Why does MAOI have more effect on serotonin?
because NE is also catabolized by COMT
which MAO is responsible for 5HT and NE mostly?
MAO-A; MAO-B does DA more
What indicates use of SSRIs?
reduced 5HIAA
What indicates use of desipramine or nortriptyline?
reduced VMA or MHPG
What is the amphetamine procative test?
patient improves with amphetamine which indicates use of a noradrenergic agent
dexamethasone suppresion test?
indicates use of a 5HT agent; if symptomes don't improve w dex, it means there is a problem with 5HT which regulates cortisol levels.
manic phase
bipolar phase where pts have grandiose thinking, insomnia, risk-taking, high self esteem
rapid cyclers
rapid shifts between manic and depressive
switch phenomenon
tricyclics with antimuscarinic activity can precipitate mania in a depressed patient
Action of drugs used as anxiolytics
CNS depressants, some without sedation (anxioselective)
Conscienceness continuum
CASH OSCD
Conciousness:
Alertness
Sedation
Hypnosis
Obtundation
Stupor
Coma
Death
Binding sites on GABA
1)GABA
2) Benzodiazepine
3) Barbituate
4) Beta Carbolines (inverse agonist)
Safest CNS depressant? Why?
benzodiazepine because all others can cause death
Brain stem activity/ bilateral thalamic and cortical activity is required for what?
consciousness
Parts of brain active and depressed during sleep?
brainstem depressedl forebrain activated
How is sleep atony accomplished?
activation of gigantocellular region which activates glycinergic Renshaw interneuron which depresses LMN.
How does ACh facilitate sensory traffic into cortex and thus arousal?
increase thalamus to thalamo-cortical fiber firing rate to facilitate sensory traffic
Why does sleepiness increase during the day?
adenosine accumulates and binds to receptors on cholinergic neurons to decrease ACh release
How does caffeine wake you up?
antagonizes adenosine so it disinhibits ACh release and therefore facilitates sensory traffic.
What pathologies can occur in stage IV of sleep?
night enuresis and pavor nocturnus
How do sedative hypnotics used to treat enuresis and pavor nocturnus?
alter sleep cycle architecture
pathology associated with early onset of REM
depression
what is differential rates of tolerance
some mechanisms gain tolerance faster than the other so efficacy changes over time
what is the safety factor built into barbituates?
differential rates of tolerance:
tolerance to sedation increases faster than anti-resp and anti-epileptic tolerance

TI antiseizure activity remains same while TI of sedation increases :)
mediates fear response
amygdala nucleus
NTs in amygdala
GABA, Glu, 5HT, NE
Why is fear learned?
Glu in amygdala can undergo LTP through NMDA receptors
main cause of seizure foci development
trauma that reduces capacity to buffer extracellular K or cell packing
what induces epilepsy?
loss of inhibition
PDS - an elevated sustained resting potential
What does use-dependency mean in terms of Na channel antagonism?
just like anesthetics, they work where more Na channels are open and therefore affects most active neurons the most
Symptoms of non-migraine headache
bilateral, nonthrobbing, usually stress related
Treatment for nonmigraine headaches
1) behavioral
2) NSAIDS
3) muscle relaxants
Excedrine
ASA, acetominophen, caffeine combo (excedrine)
how to avoid rebound headache
taper nsaid dose
vascular hypothesis of wolff?
5HT maintains tone and vasoconstriction. During ischemia, vessels vasodilate and this loss of tone allows CT to be manipulated by pulsing pressure which causes pain
sterile inflammatory hypothesis of migraines
unknown inflammatory process that releases histamine and peptides
biobehavioral hypothesis of migraines
wave of depolarizatoin causes activation of opthalmic branch of trigem which is where headaches are thought to originate
Why can't migraneuers absorb antimuscarinics?
they have gastric stasis as a symptom
What is MAC?
minimum alveolar concentration - gas amnt in blood needed to produce no reflex response to a knife cut ED50 at RT at SL
how does solubility affect speed of anesthesia?
the more soluable, the longer the induction of anesthesia
what is a closed system?
the idea that gas (volatile) anesthetics can only go in lungs, blood, brain, and these 3 compartments will equilibrize
only anesthetic to be biotransformed?
liver
how are most anesthetics terminated?
exit lung just like they entered, except for halothane
Overton-meyer hypothesis
The Overton-Meyer hypothesis suggests that these drugs disrupt membrane fluidity changes transmembrane protein structures and thus activity of Na channels. Potency related to oil:gas partition.
What does Enk do?
reduces release of SubP from peripheral C fibers
What do endorphins do?
released by POMC and have paracrine effects
Receptors in the enkephalin receptor system?
Mu, kappa, delta, epsilon
What do mu receptors mediate?
Analgesia-mediating in suprasegmental and segmental systems
What side effects are initiated by mu receptors?
euphoria and respiratory depression
kappa mediates what?
spinal cord and CNS but not as potent as mu
delta receptors mediate what?
limbic and spinal cord; more emotional and behavioral
How does mu cause euphoria
increased DA,NE, forebrain
how does Mu/delta/kappa cause respiratory depression?
reduces sensitivity to CO2 in medulla
how does morphine cause hypotension?
direct histamine displacement from mast cells and delta medullary depression
how is RUQ pain associated with morphine?
morphine causes spincter of oddi spasms
Why shouldn't you give oxygen to someone in a coma?
O2 will stop hypoxic drive and cause breathing
toxic triad of opiod toxicity
Respiratory depression, Coma, Miosis