final review Flashcards

1
Q

What is SS?

A

-Fever, tachycardia, HTN, CLONUS(hyperflex), Shits/shivers
-a/w: SSRI, SNRI, MAOI, triptans, analegisics, St Wort, cough med, tryptophan
-TX: NO BB, NO antichol. GIVE BZD, Cyproheptadine (antihistamine), olanzapine.

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2
Q

What is NMS?

A

-Fever, Tachy, HTN, RIGIDITY!, abn labs (high CK, high WBC, rhabdo).
- seen with FGA more often
-TX: antichol (Dantrolene, bromocriptine, amantadine) Give some dopa back bc it’s too blocked.

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3
Q

EPS? Three reversible manifestations

A

-Dystonia: oculogyric crisis, sustained muscle contraction, torticollis– eyes, neck, long muscle contracts
-Akathesia: restless!
-Parkinson’s

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4
Q

How to treat 3 reversible manifestations of EPS

A

-Dystonia: antichol: benzotropine, biperden, antihist:diphenhydramine
-Akathesia: BB, mirtazapine (tetracyclic antidepressant), cyproheptadine (antihistamine), BZD
-Parkinsons: antichol–benzotropine (avoid w/ older ppl); amantadine

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5
Q

Irreversible EPS

A

TD: chronic; involn lower face, limbs, trunk movement.
TX: VMAT inhib: Valbenazine, deutetrabenzine
SGA: clozapine
Gingko biloba

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6
Q

Whate are 4 dopamine pathways ?

A

-Mesocortical: neg schz symptoms– flat affect, impaired cognition
-Mesolimbic: positive schz symptoms– SUD = attempt to correct pathway but, may activate positive symptoms
-Nigrostriatal: regulated coordination of movement. Parkinson’s has ~ 80% decrease in this area
-Tuberinfundibular: prolactin secretotion

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7
Q

6 neurotransmitters

A
  1. DA
  2. NE
  3. Serotonin
  4. Glumate
  5. GABA
  6. Acetycholine
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8
Q

Dopamine hypothesis

A

-decreasing mesocort; increasing mesolimb; neutral nigro & tuberoinfund.
-meds attempting to dec dopa activity in mesolimbic to stop psychosis
-mesocortical pathway has incr dopa causing neg symptoms

~~ D2 receptor gatekeepers; occupy = neg feedback; disease or meds that inc dopa will produce or enhance positive symptoms.

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9
Q

Defining feature of schiz?

A

psychosis
– a/w schiz, mania, depression, cognitive disorders, bipolor, dementia, PTSD, depression, BPD

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10
Q

Schiz: positive & negative symptoms

A

-Positive: most dramatic, hosp maybe, target of most meds
-Neg: few meds target this; make life hard to fxn

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11
Q

FGA

A

-D2 anatag: HIGH EPS & NMS risks
–emotional quiet, affective indiff, psychomotor slowing
MEDS:
-thorazine
-chlopromazine : se of corneal deposits
-thioridazone
-haldol: high potency: EPS risk, QTc prolong–torsades
-fluphenazine, procholorperazine, loxapine, periciazine, trifluoperazine, flupentixol, zuclopentixol, methotrimeprazine

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12
Q

SGA

A

-D2/5HT2A antagonist (less D2=less risk EPS)
–more weight gain, metobolic SE, Inc chol, DM2
MEDS::
-clozapine: agranulocytosis; REM program– last resort
-risperadone: prolactin- gynecomastia, low BP
-paliperidone: like risperadone
-quetiapine: sedating
-olanzapine: wt gain, sedating
-ziprasidone: QTc prolong
-asenapine: SL– w/o food/water
-lurasidone: good for bipolar depression

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13
Q

Third Gen antipsychotic

A

aripiprazole

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14
Q

Which antipsychotics are used with ped population?

A

Aripiprazole, risperidone= metformin maybe for wt gain

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15
Q

Which antipsychotics r/t sedation?

A

PINES: quetiapine, olanzapine, clozapine, asenapine (SL)
less pip, rip, done

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16
Q

Which antipsychotics wt gain?

A

PINES
less pip, rip, done

17
Q

Which antipsychotic causes anticholinergic SE?

18
Q

Which antipsychotic causes EPS?

A

DONES
less in pines

19
Q

Which antipsychotics can cause hypotension?

A

PINES & DONES– less in brex, cariprazine, lurasidone

20
Q

Which antipsychotics causes QTc ?

A

PINES & DONES
less with pip, rip, zole

21
Q

Significant SE of SSRI

A

hyponatremia, SS, discontinue syndrome, suicide risk, sexual dysfxn, dec seizure w/ wellbutrin

22
Q

SGA MOA

A

5HT2A (antagonist/inverse agonist)
5HT2A stimulated by serotonin & blocks DOP release (dec dopamine).

23
Q

Pimavanserin

A

5HT2A inverse agonist– parkinson’s psychosis