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660 exam 1 Flashcards

1
Q

Where does the Nigrostriatal Pathway start and end?

A

Substantia Nigra to the striatum

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2
Q

What is the issue with dopamine in the Nigrostriatal Pathway?

A

Too low → CSTC loops messed up→ we make it worse with D2 blockers → EPS

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3
Q

What causes Tardive Dyskinesia?

A

Chronic blockade of the nigrostriatal dopamine receptors.

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4
Q

How does dopamine regulate the indirect CSTC loop?

A

Dopamine inhibits the “stop” signal → produces movement

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5
Q

How long does it take for Dystonia to occur after the offending medication is given?

A

4 hours

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6
Q

How long does it take for Akinesia to occur after the offending medication is given? (Drug-induced parkinsonian symptoms)

A

4 days

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7
Q

How long does it take for Akathisia to occur after the offending medication is given?

A

4 weeks

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8
Q

How long does it take for Tardive Dyskinesia to occur after the offending medication is given?

A

months to years

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9
Q

What does dystonia look like?

A
  • eyes roll up and out
  • forced extension of neck
  • forced lateral rotation of neck
  • tongue protrudes and feels swollen but it isn’t
  • sustained facial muscle spasms
  • laryngospasms and spasticity
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10
Q

What is the treatment of Dystonia?

A

Benztropine or benadryl

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11
Q

What does drug induced Parkinsons look like? (Akinesia)

A

Rigidity, tremors, slowing of movements, loss of movements

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12
Q

What is the treatment for drug-induced Parkinsons look like? (Akinesia)

A

Benztropine, benadryl

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13
Q

Why do anticholinergics help drug induced Parkinsons? (Akinesia)

A

Dopamine typically decreases acetylcholine → if D2 inhibitor blocks, then more acetylcholine is released → Excitation of postsynaptic M1 receptors

Anticholinergics will block the acetylcholine

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14
Q

What does Akathisia look like?

A

Feelings of restlessness, jittery, dysphoria, mental unease, marching, pacing stomping

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15
Q

What is the treatment for Akathisia?

A

Betablocker and Benzos

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16
Q

What does Tardive Dyskinesia look like?

A

Constant movements – lip smacking, blinking, jaw clenching, twitchy/jerky limb movements

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17
Q

What causes TD?

A

Upregulation of dopamine receptors in the indirect pathway

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18
Q

What is the treatment for TD?

A

VMAT2 inhibitors

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19
Q

What are two VMAT2 inhibitors?

A

Deutetrabenzine and valbenzine

TAKE WITH FOOD

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20
Q

Where does the tuberoinfundibular pathway start and stop?

A

Hypothalamus to anterior pituitary

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21
Q

How does dopamine typically regulate prolactin?

A

inhibits the release

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22
Q

When should a prolactin lab be drawn?

A
  • within 2 hrs of waking
  • fasting
  • Not within 30 min of exercise
  • Stress/anxiety raises – fear of needles?
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23
Q

Which antipsychotic could you switch to if the patient is suffering from hyperprolactinemia?

A

Aripiprazole, brexpiprazole, cariprazine, or clozapine

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24
Q

Example of a dopamine agonist

A

Bromocriptine

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25
Aripiprizole indications
Schizo, Bipolar
26
Brexipiprazole indications
Schizo
27
Chlorpromazine indications
Schizo, bipolar
28
Chlorpromazine key points
- Wide range of SE - decreases seizure threshold - Photosensitivity - Very potent EPS - QT interval prolongation
29
Clozapine indications
Treatment resistant schizo
30
Clozapine key points
- Only use after two other failed antipsychotic attempts - Decreases seizure threshold - Check ANC prior and cont to monitor - ANC needs to be >1500 unless you have BEN then it needs to be >1,000
31
Clozapine SE
- Anticholinergic - Wt gain - Myocarditis - Drooling
32
What to monitor with all atypical antipsychotics
Wt, fasting glucose/ lipids, BP,
33
What labs to monitor for clozapine
ANC and ECG
34
Clozapine CYP issues
- Smoking is an inhibitor - Luvox is an inhibitor
35
Which medications have the highest risk for wt gain?
olanzapine quetiapine
36
When should be not give IM olanzapine?
When the patient is on benzos
37
Clozapines risk of EPS is
not likely
38
Haloperidol ADR
HIGH risk for EPS Prolonged QT with IV admin
39
Which first generation antipsychotics are high potency?
Haloperidol Loxapine Pimozide Thiothixene Trifluoperazine
40
Lurasidone (Latuda) key points
- Take with 350 calories - grapefruit inhibits - tegretol and st johns wort induces
41
Which antipsychotics are good to use for an overweight patient?
Lurasidone (Latuda) and Lumateperone (Caplyta) - does not cause metabolic disorder
42
Lumateperone (Caplyta) SE and keypoint
- Sedating - Take with food
43
Ziprasidone (Geodon)
- Decreased Wt gain - Take with 500 calories of food twice daily
44
Risperidone and Paliperidone key SEs
Hyper-prolactinemia and sedation
45
Olanzapine SE
- Wt gain - Rash/Photosensitivity - Sedation
46
Which antipsychotic is first choice for parkinson's?
Quetiapine
47
Which antipsychotic can cause cataracts?
Quetiapine
48
Zisprasidone (Geodone) key points
- Ask if family hx of heart issues, sudden death etc --QT PROLONGATION
49
Perphenazine SE
- catatonia - bluish gray skin - photosensitivity
50
Which medication is sublingal?
Saphris (Asenapine)
51
What are the negative s/s of Schizo?
- Anhedonia (decreased pleasure) - Asocial - Alogia (few words) - Blunted affect (decreased affect) - Avolition (decreased desire/motivation) - Apathetic (Doesn't care) - Abstract thinking is difficult
52
Which pathway is resposible for the negative s/s of schizo?
Mesolimbic
53
Which pathway is responsible for EPS and TD?
Nigrostriatal
54
Which dopamine receptor is more sensitive to dopamine, 2 or 3?
D3
55
Which area of the brain do not have DAT or D2/3 autoreceptors?
PFC
56
Which area of the brain DOES have D2/D3 autoreceptors?
Striatum
57
Dopamine (DA) receptors can be categorized as D1-like (D1 and D5 receptors) and D2-like (D2, D3, and D4 receptors). What differentiates the two groups of receptors?
D1-like receptors are excitatory and D2-like receptors are inhibitory.
58
Symptoms of schizophrenia are hypothetically attributable to malfunctioning in the:
Mesocortical and mesolimbic pathways
59
For which set of disorders is psychosis considered an associated feature rather than a defining feature for diagnosis?
Bipolar mania, Parkinson's disease, Mania
60
Where does the mesolimbic pathway start and stop?
Brainstem to Nucleus accumbens in the ventral striatum
61
Where does the mesocortical pathway start and stop?
VTA of brainstem to PFC (DL and VM)
62
Hypofunctioning NMDA receptors lead to what
excessive glutamate release in the VTA -- downstream excessive DA release in the nucleus accumbens and reduced DA release in the PFC
63
The neurodevelopmental hypothesis of schizophrenia centers heavily around the idea that aberrant competitive elimination occurs. Competitive elimination is a stage of neurodevelopment in which
Rarely used synapses are pruned, while frequently used synapses are preserved
64
How does glutamate regulate dopamine?
Glutamate in cortical brainstem regulates the mesocortical dopamine in the VTA INDIRECTLY
64
How does glutamate regulate dopamine?
Glutamate in cortical brainstem regulates the mesocortical dopamine in the VTA INDIRECTLY Too much glutamate - L2 lots of GABA -- too little dopamine
65
What three neurotransmitter systems are implicated in the neuropathology of psychosis?
Serotonin, glutamate, dopamine
66
Which receptor subtypes act as presynaptic autoreceptors to inhibit serotonin release?
5HT1A and 5HT1B/D receptors
67
Stimulation of 5HT3 receptors on GABA interneurons leads to inhibited release of:
Acetylcholine and norepinephrine
68
Psychosis in Parkinson's disease or dementia may occur due to upregulation of which postsynaptic serotonin receptor on glutamate neurons in the prefrontal cortex?
5HT2A
69
Serotonin hypothesis of psychosis
Hyperactivity of the 5HT2A receptors in the cortex causes psychosis
70
Presynaptic serotonin receptors
1A - Binding shuts down 5HT release 2B - Binding increases 5HT release 1B/D - Binding shuts down 5HT release
71
Which presynaptic serotonin receptors are inhibitory?
1A and 1B/D
72
5HT1A is always...
inhibitory
73
5HT1A / GABA /Dopamine relationship
If it inhibits a GABA neuron → you’re inhibiting the inhibitor so downstream there is a lack of inhibition → increased dopamine in the striatum and PFC
74
5HT2A receptors are always
excitatory and post synaptic
75
How does 5HT2A regulate dopamine?
Mesolimbic - directly Nigrostriatal and Mesocortical- indirectly 5HT2A receptors on cortical glutamate pyramidal neurons are stimulated and release glutamate downstream -- makes the dopamine pathway worse Blockers would help decrease the symptoms
76
How does 5HT2A regulate prolactin?
Increases it
77
5HT2C
Generally excitatory -- Located primarily on GABA interneurons → generally inhibit the downstream release of neurotransmitters
78
5HT3
Excitatory N/V --- Located in the chemoreceptor trigger zone of the brainstem --- Mediate n/v --- Located in the GI tract --- Mediate n/v/d (bowel motility) --- Blocking these may protect against serotonin-induced GI SE that often occur with 5HT release In the PFC --- Located on GABA interneurons → net inhibitory --- Inhibit NE and Ach Glutamate and 5HT regulate each other via 5HT3
79
5HT2A blockers help ...
- Decrease hallucinations - In Parkinson’s → decreased s/s bc they occupy some of the extra 5HT2A receptors that are causing too much excitatory effects - In dementia → decreased behavior SE that are caused by too much excitatory effects from decreased GABA activity L2 too much serotonin
80
Low Potency 1st gen Antipyschotic SE and Affinity
COMMON: EPS TD Sedation Orthostatic Hypotension Anticholinergic symptoms D2: moderate affinity Acetylcholine: strong H1: strong Alpha adrenergic: moderate
81
High Potency 1st gen Antipyschotic SE and Affinity
COMMON: EPS TD UNCOMMON: Sedation Orthostatic Hypotension Anticholinergic symptoms D2: Strong affinity Acetylholine, muscarinic, H1, alpha adrenergic: Weak
82
Tx for Neuroleptic Malignant Syndrome
Bromocriptine Reduce fever, correct dehydration, correct electrolytes Stop med IV benzo, IV Dantrolene (muscle relax), Bromocriptine -- dopamine agonist Amantadine - dopamine agonist with antichol effects
83
Differentiate Neuroleptic Malignant Syndrome from Serotonin Sydrome
NMS - Hyperreflexia, myoclonus, ocular clonus NMS - S/S are within 24 hrs of starting/changing therapy

Psych 660 (6 decks)

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