Psychopharm

Front 1

The prefrontal cortex is a major area for ___________________

Back 1

Judgment, EF, decision making

Front 2

Primary divisions of the PFC include...

Back 2

Dosolateral Prefrontal Cortex (DLFPC)
cognitive fucntioning (EF, prob. solv., analyze)
Orbito Frontal Cortex (OF)
Impulses, compulsions, drives
Anterior Cingulate Cortex (ACC)
Top (dorsal) related to selective attention
Lower (ventral or subgenual) related to emotions such as depression and anx
Ventromedial PFC
Emotional processing

Front 3

Secondary divisions of the PFC include....

Back 3

Hippocampus - memory, neurgenesis
Amygdala - fear processing (emotion)
NT Nodes
cell bodies in brainstem etc
projections to PFC etc
Some overlap, some are unique

Front 4

What activity can help determine how well the PFC is fx'ing?

Back 4

Stroop Color Word Task

Front 5

DA projections are primarily ascending or descending?

Back 5

Ascending

Front 6

What are the two DA projections?

Back 6

Ventral tegmental area
thalamus

Front 7

What does the ventral tegmental area regulate?

Back 7

movement, pleasure and reward, cognition, psychosis (esp. positive symptoms)

Front 8

NE projections are primarily ascending or descending?

Back 8

Both

Front 9

The ascending NE pathway begins with what/where and regulated what?

Back 9

Locus Coeruleus,
mood, arousal, cogntions

Front 10

5HT projections are primarily ascending or descending?

Back 10

Both

Front 11

5HT projections are involved in....

Back 11

mood, anxiety, sleep, pain

Front 12

what are the two primary AcH pathways?

Back 12

brain stem, basal forebrain

Front 13

AcH medications are commonly a treatment for what diagnosis?

Back 13

Alzheimer's

Front 14

Describe the biological components of PTSD

Back 14

Hippocampus has stored traumatic memories that can trigger the amygdala. The amygdala releases cortisol which changes breathing

Front 15

Histamine (HA) projections begin in the________and continue to the

Back 15

Tuberomammilary nucleus (TMN) in Hy to PFC, SC

Front 16

HA is related to the control of

Back 16

Arousal, wakefulness and sleep
can make you sleep but make it difficult to stay asleep

Front 17

What is the NT and route in the pain pathway?

Back 17

Primarily NE, but also 5HT
from lateral tegmental NE cell system, descending into spinal cord, in brain stem

Front 18

"Classic neuro-transmission occurs via

Back 18

G-protein linked receptors

Front 19

Most psychotropic drugs target _________ or ______________

Back 19

transporters or G-protein linked receptors

Front 20

the purpose of transporters is to

Back 20

transport NT across membranes and/or facilitate re-storage of NT in vesicles

Front 21

Plasma membrane transporters are AKA _____________ and are classified as ____________________

Back 21

reuptake pump
SLC6 (NT's besides Glu) or SLC1 (Glu only)
SLC = solute carrier

Front 22

How are SSRI's selective?

Back 22

selective in its affinity for allosteric sites; when something binds allosterically in prevents the NT from binding and it is not taken back up into the cell

Front 23

Where does the energy for NT transport come from?

Back 23

sodium pumps (Na+) constantly pumping sodium out of the cell

Front 24

True/Fale: Transporters only have binding sites for NA

Back 24

False, they also have monoamine sites and allosteric sites

Front 25

What process and chemical(s) can cause increased concentrations of GABA in the synapse?

Back 25

GAT1 targeting SNRIs like anitconvulsant tiagabine/Gabitril; also alcohol

Front 26

What results from inhibited Glu?

Back 26

Potential for lower levels of excitation, cell damage

Front 27

Which NT does not have a transport system? How does it work?

Back 27

Histamine: it targets other actions, such as enzymatic destruction

Front 28

Why do amphetamines have a phasic burst?

Back 28

Targets DATs and NETs (presynaptic pumps) as well as VMATs (intracellular synaptic vesicle transporter) causing a reversal of reuptake pump action and a flood of DA into synapse

Front 29

True/False: Constitutive activity = no activity

Back 29

False: it = no CHANGE in activity, i.e. baseline

Front 30

What is required for an antagonist to alter effects of a chemical?

Back 30

Presence of an agonist; otherwise it is neutral (prevents change while maintaining baseline)

EX. GABA-A antagonist Flumazenil
-used for Benzo OD bc it blocks PAM
-unmedicated, non anxious ppl, show no response (silent agonist)
-unmedicated anxious ppl show increase panic/anx bec inhibition of GABA stops

Front 31

What is the opposite of an agonist?

Back 31

inverse agonist

Front 32

What are the types of ion channels, what is the difference b/w them?

Back 32

Ligaand-gated - opened by NTs
Voltage sensitive - opened by charge

Front 33

Which is faster, ligand-gated or G-protein linked channels?

Back 33

Ligand-gated; though both begin with 1st messenger NTs

Front 34

Explain net effects

Back 34

eg - partial agonist = net agonist in presence of full agonist; antagonist = net agonist in presence of inverse agonist

Front 35

Why is it ok/not ok to drink alcohol with benzos?

Back 35

Its not b/c Benzos increase GABA activity as does alcohol

Front 36

What is the difference between positive/negative allospheric modulation?

Back 36

PAM boosts NT effect, opens more and more often than a full agonist alone, but only in the presence of the NT
Ex - benzo's + alcohol
NAM blocks/reduces NT effect; closes more/more often than NT alone

Front 37

What are some of the basics for understanding tolerance, withdrawal, drug interactions, cross dependence?

Back 37

Desensitization - prolonged exposure to agonist
Inactivation - stablized closed after inverse agonist
Net effects
Speed of ion channels vs G-protein linked
Competitive binding vs allosteric

Front 38

Explain excitation-secretion coupling

Back 38

sodium channels first activation on the axon, later calcium opens which pulls in vesicles towards the membrane , all the positive NTs are pumped in; part of signal transduction

Front 39

What percent of meds target enzymes? Are they usually inhibitory/excitatory?

Back 39

10%, inhibitory

Front 40

True/false: enzyme inhibition is permanent?

Back 40

False

Front 41

Describe the rational approach to treatment outlined by Stahl. What are its shortfalls?

Back 41

Construct a diagnosis
Deconstruct the diagnosis into its component symptoms
Match each symptom to its hypothetically malfunctioning circuit
Consider the NTs that theoretically regulate each circuit
Select a tx that targets the NT regulating the circuit
Add or switch to another tx if the symptom is not relieved
Repeat for each sx until the pt is asymptomatic or in remission
Shortcomings:
knowing when to switch vs combine
how long to wait to combine
difficulty interpreting/predicting interaction effects
working from clinical experience/intuition to research questions

Front 42

What are the 5 levels of mood descriptors?

Back 42

Mania
Hypomania
Euthymic
Dysthymia
Depression

Front 43

What are the 3 temperaments?

Back 43

Hyperthymic (above normal but not psychopathic)
Depressive (bw euthymic and dysthymic, not pathological)
Cyclothymic

Front 44

Malfunctioning circuits associated with Major Depressive Episode

Back 44

PFC - concentration, interest, pleasure, psycho-motor, mental fatigue, guilt, suicidal, worthlessness, mood
Amygdala - guilt, suicidality, worthlessness, mood
Striatum - psychomotor fatigue
Hypothalamus - sleep, appetite (only sxs not caused by PFC)
Cerebellum - psychomotor
NA - concentration, interest, pleasure

Front 45

What is the difference b/w MAOI’s, tricyclic antidepressants, and SSRI’s?

Back 45

MAOI's are Dopamine-Epinepherine-Norepinephrine-Seratonin agonists
Tricylcic Anti-d's are Norephinephrine-Serotonin agonists
SSRIs are Serotonin agonists

Front 46

Name some brand name SSRI’s

Back 46

Prozac, Zoloft, Paxil

Front 47

Name some name brand SNRIs

Back 47

Effexor, Cymbalta

Front 48

Name some name brand NDRI's

Back 48

Wellbutrin, Zyban

Front 49

What is a name brand NRI

Back 49

Strattera

Front 50

most likely consequence of neuroleptic drugs

Back 50

Tardive dyskinesia

Front 51

Chlorpromzaine

Back 51

aka Thorazine
neuroleptic drug

Front 52

Tricyclic drugs

Back 52

imipramine
clomipramine
amitryptyline

Front 53

SSRI's

Back 53

fluoxetine
sertraline
paroxetine
Straterra
Lexapro
Cymbalta
Saragem
Luvox
Celexa
Paxil

Front 54

fluoxetine

Back 54

Prozac
SSRI

Front 55

sertraline

Back 55

Zoloft
SSRI

Front 56

paroxetine

Back 56

Paxil
SSRI

Front 57

MAOI's

Back 57

phenelzine
tranylcypromine

Front 58

Nardil

Back 58

phenelzine

Front 59

Parnate

Back 59

tranylcypromine

Front 60

what class of drugs are most widely prescribed for anxiety?

Back 60

Benzodiazepines

Front 61

diazepam

Back 61

Valium (benzo)

Front 62

alprazolam

Back 62

Xanax (benzo)

Front 63

clonazepam

Back 63

Klonopin (benzo)

Front 64

lorazepam

Back 64

Ativan (benzo)

Front 65

triazolam

Back 65

Halcion (benzo)

Front 66

Barbituates

Back 66

replaced by benzo's for anxiety bc they're safer

Front 67

Thiopental

Back 67

barbituate

Front 68

amabarbital

Back 68

Barbituate

Front 69

secobarbital

Back 69

Barbituate

Front 70

conventional antipsychotics are more useful in treating what symptoms of schizophrenia?

Back 70

positive

Front 71

Haloperiodal

Back 71

aka Haldol
conventional antipsychotic

Front 72

OCD medications

Back 72

Anafranil (clomipramine)
Prozac (fluoxetine)
Luvox (fluvoxamine)
Paxil (paroxetine)
Zoloft (sertraline)
Celexa (citalopram)

Front 73

serotonin hypothesis of OCD

Back 73

medications that reduce OCD sx's increase available levels of serotonin
serotonin antagonists (atypical antipsychotics) increase OCD sx's in patients, but not in controls

Front 74

Anticholinergic Effects

Back 74

block Ach
dry mouth
blurred vision
constipation
memory impairment
urinary retention
confusional states

Front 75

extrapyramidal effects

Back 75

dopamine blockade in basal ganglia
Parkinson=like effects: ridigity, shffling gaint, tremor, flat affect, lethargy
dystonias: spasms in neck and other muscle groups
akathisia: intense, uncomfortable sense of inner restlessness
tardive dyskinesia: often a persistent movement disorder (lip smacking, writhing movements, jerky movements)

Front 76

autonomic effects

Back 76

especially orthostatic hypotension, which can cause dizziness and imbalance, and in the elderly esp can cause falls and fractures

Front 77

unclassified antidepressant

Back 77

does not work selectively on serotonin levels
Wellbutrin

Front 78

Lithium is prescribed to treat

Back 78

Bopilar I

Front 79

Buspar is prescribed to treat

Back 79

anxiety disorders

Front 80

haloperidol is prescribed to treat

Back 80

Schizophrenia and Tic Disorders

Front 81

withdrawal from ____________ (type of drug) can be fatal is done abruptly

Back 81

benzodiazepine (Valium)
has a potential for addiction

Front 82

withdrawal from alcohol can include

Back 82

dangerous seizures

Front 83

tricyclic antidepressants

Back 83

block the reuptake of norep. and serotonin
cause anticholinergic side effects
more side effects than SSRIs

Front 84

MAOIs

Back 84

block the enzyme that breaks down norep. and serotonin
have to avoid foods with thyramine (red wine, cheeses, etc)