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660 exam 1 Flashcards

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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
Q

Aripiprizole indications

A

Schizo, Bipolar

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26
Q

Brexipiprazole indications

A

Schizo

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27
Q

Chlorpromazine indications

A

Schizo, bipolar

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28
Q

Chlorpromazine key points

A
  • Wide range of SE
  • decreases seizure threshold
  • Photosensitivity
  • Very potent EPS
  • QT interval prolongation
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29
Q

Clozapine indications

A

Treatment resistant schizo

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30
Q

Clozapine key points

A
  • 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
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31
Q

Clozapine SE

A
  • Anticholinergic
  • Wt gain
  • Myocarditis
  • Drooling
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32
Q

What to monitor with all atypical antipsychotics

A

Wt, fasting glucose/ lipids, BP,

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33
Q

What labs to monitor for clozapine

A

ANC and ECG

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34
Q

Clozapine CYP issues

A
  • Smoking is an inhibitor
  • Luvox is an inhibitor
35
Q

Which medications have the highest risk for wt gain?

A

olanzapine
quetiapine

36
Q

When should be not give IM olanzapine?

A

When the patient is on benzos

37
Q

Clozapines risk of EPS is

A

not likely

38
Q

Haloperidol ADR

A

HIGH risk for EPS
Prolonged QT with IV admin

39
Q

Which first generation antipsychotics are high potency?

A

Haloperidol
Loxapine
Pimozide
Thiothixene
Trifluoperazine

40
Q

Lurasidone (Latuda) key points

A
  • Take with 350 calories
  • grapefruit inhibits
  • tegretol and st johns wort induces
41
Q

Which antipsychotics are good to use for an overweight patient?

A

Lurasidone (Latuda) and Lumateperone (Caplyta) - does not cause metabolic disorder

42
Q

Lumateperone (Caplyta) SE and keypoint

A
  • Sedating
  • Take with food
43
Q

Ziprasidone (Geodon)

A
  • Decreased Wt gain
  • Take with 500 calories of food twice daily
44
Q

Risperidone and Paliperidone key SEs

A

Hyper-prolactinemia and sedation

45
Q

Olanzapine SE

A
  • Wt gain
  • Rash/Photosensitivity
  • Sedation
46
Q

Which antipsychotic is first choice for parkinson’s?

A

Quetiapine

47
Q

Which antipsychotic can cause cataracts?

A

Quetiapine

48
Q

Zisprasidone (Geodone) key points

A
  • Ask if family hx of heart issues, sudden death etc –QT PROLONGATION
49
Q

Perphenazine SE

A
  • catatonia
  • bluish gray skin
  • photosensitivity
50
Q

Which medication is sublingal?

A

Saphris (Asenapine)

51
Q

What are the negative s/s of Schizo?

A
  • Anhedonia (decreased pleasure)
  • Asocial
  • Alogia (few words)
  • Blunted affect (decreased affect)
  • Avolition (decreased desire/motivation)
  • Apathetic (Doesn’t care)
  • Abstract thinking is difficult
52
Q

Which pathway is resposible for the negative s/s of schizo?

A

Mesolimbic

53
Q

Which pathway is responsible for EPS and TD?

A

Nigrostriatal

54
Q

Which dopamine receptor is more sensitive to dopamine, 2 or 3?

A

D3

55
Q

Which area of the brain do not have DAT or D2/3 autoreceptors?

A

PFC

56
Q

Which area of the brain DOES have D2/D3 autoreceptors?

A

Striatum

57
Q

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?

A

D1-like receptors are excitatory and D2-like receptors are inhibitory.

58
Q

Symptoms of schizophrenia are hypothetically attributable to malfunctioning in the:

A

Mesocortical and mesolimbic pathways

59
Q

For which set of disorders is psychosis considered an associated feature rather than a defining feature for diagnosis?

A

Bipolar mania, Parkinson’s disease, Mania

60
Q

Where does the mesolimbic pathway start and stop?

A

Brainstem to Nucleus accumbens in the ventral striatum

61
Q

Where does the mesocortical pathway start and stop?

A

VTA of brainstem to PFC (DL and VM)

62
Q

Hypofunctioning NMDA receptors lead to what

A

excessive glutamate release in the VTA – downstream excessive DA release in the nucleus accumbens and reduced DA release in the PFC

63
Q

The neurodevelopmental hypothesis of schizophrenia centers heavily around the idea that aberrant competitive elimination occurs. Competitive elimination is a stage of neurodevelopment in which

A

Rarely used synapses are pruned, while frequently used synapses are preserved

64
Q

How does glutamate regulate dopamine?

A

Glutamate in cortical brainstem regulates the mesocortical dopamine in the VTA INDIRECTLY

64
Q

How does glutamate regulate dopamine?

A

Glutamate in cortical brainstem regulates the mesocortical dopamine in the VTA INDIRECTLY

Too much glutamate - L2 lots of GABA – too little dopamine

65
Q

What three neurotransmitter systems are implicated in the neuropathology of psychosis?

A

Serotonin, glutamate, dopamine

66
Q

Which receptor subtypes act as presynaptic autoreceptors to inhibit serotonin release?

A

5HT1A and 5HT1B/D receptors

67
Q

Stimulation of 5HT3 receptors on GABA interneurons leads to inhibited release of:

A

Acetylcholine and norepinephrine

68
Q

Psychosis in Parkinson’s disease or dementia may occur due to upregulation of which postsynaptic serotonin receptor on glutamate neurons in the prefrontal cortex?

A

5HT2A

69
Q

Serotonin hypothesis of psychosis

A

Hyperactivity of the 5HT2A receptors in the cortex causes psychosis

70
Q

Presynaptic serotonin receptors

A

1A
- Binding shuts down 5HT release

2B
- Binding increases 5HT release

1B/D
- Binding shuts down 5HT release

71
Q

Which presynaptic serotonin receptors are inhibitory?

A

1A and 1B/D

72
Q

5HT1A is always…

A

inhibitory

73
Q

5HT1A / GABA /Dopamine relationship

A

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
Q

5HT2A receptors are always

A

excitatory and post synaptic

75
Q

How does 5HT2A regulate dopamine?

A

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
Q

How does 5HT2A regulate prolactin?

A

Increases it

77
Q

5HT2C

A

Generally excitatory

– Located primarily on GABA interneurons → generally inhibit the downstream release of neurotransmitters

78
Q

5HT3

A

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
Q

5HT2A blockers help …

A
  • 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
Q

Low Potency 1st gen Antipyschotic SE and Affinity

A

COMMON:
EPS
TD
Sedation
Orthostatic Hypotension
Anticholinergic symptoms

D2: moderate affinity

Acetylcholine: strong

H1: strong

Alpha adrenergic: moderate

81
Q

High Potency 1st gen Antipyschotic SE and Affinity

A

COMMON:
EPS
TD

UNCOMMON:
Sedation
Orthostatic Hypotension
Anticholinergic symptoms

D2: Strong affinity

Acetylholine, muscarinic, H1, alpha adrenergic: Weak

82
Q

Tx for Neuroleptic Malignant Syndrome

A

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
Q

Differentiate Neuroleptic Malignant Syndrome from Serotonin Sydrome

A

NMS - Hyperreflexia, myoclonus, ocular clonus

NMS - S/S are within 24 hrs of starting/changing therapy

Psych 660 (6 decks)

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