Exam 2 Review Flashcards

1
Q

Treatments for bipolar

A

1-lithium
2-Antiepileptics
3-antipsychotics

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2
Q

Lithium MOA

A

-not understood
-possibly stimulates inhibitory neurotransmission and dampens excitatory neurotransmission
-may uncouple G proteins from receptors
may inhibit enzymes
-may modulate NTs
-May reduce arachidonic acid turnover in brain

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3
Q

Lithium effects on INOSITOL

A

-depletes free inositol and membrane PIP2 in CNS
-impact PKC activity affecting neurolasticity

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4
Q

Lithium effects on GSK-3

A

-inhibitory effects on GSK-3
-modulate metabolism
-promote neuroprotection
-increase neuroplasticity

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5
Q

Lithium characteristics

A

-slow onset
-use has declined
-Narrow therapeutic index

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6
Q

Lithium clearence

A

-reduced during pregnancy
-reverts immediately after delivery

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7
Q

Lithium side effects

A

-tremor
-nausea
-diarrhea
-Leukocytosis
-cognitive impairment
-sexual dysfunction
-exaberate psoriasis

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8
Q

Lithium toxicity

A

-N/V, diarrhea, neurologic symptoms
-Dehydration, sodium depletion, kidney impairments, medications that decrease clearance can also contribute

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9
Q

Lithium considerations in pregnancy

A

-crosses placenta
-teratogenic
-excreted in breast milk

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10
Q

Antiepileptic drugs in Bipolar disorder

A

-Valproic acid
-carbamazepine
-lamotrigine

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11
Q

Valproic acid

A

-inositol depletion
-indirectly reduce GSK-3 activity
-inhibits histone deacetylase

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12
Q

Carbamazepine

A

-inositol depletion
-may be a CYP3A4 inducer
-blood dyscrasias less of an issue

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13
Q

Lamotrigine

A

-not effective in acute mania
-maintenance med and can be used in bipolar depression
-may have GSK-3 inhibitory effects

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14
Q

Antipsychotics in bipolar

A

-mostly second gen./atypical used
-D2 agonists
-can be used in combination with lithium or valproate

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15
Q

Second gen antipsychotics MOA

A

-5-HT2A blockade
-higher affinity for 5HT than D2
-lower risk of side effects

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16
Q

Effects of D2 antagonism

A

-positive symptoms become normal
-negative symptoms become worse

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17
Q

D2 blockade effects

A

-acute dystonia
-parkinsonism
-perioral tremor
-akathisia
-tardive dyskinesia
-hyperprolactinemia

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18
Q

Deutetrabenazine

A

-VMAT2 inhibitor: depletes vesicular monoamines
TD prevention/management

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19
Q

Deutetrabenazine side effects

A

-prolong QT interval
-fatigue
-somnolence
-HA

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20
Q

Clozapine

A

-M4 Agonist
-D2 antagonist
-Schizophrenia

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21
Q

Haloperidol

A

-FGA: high potency
-Schizophrenia

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22
Q

Chlorpromazine

A

-FGA: low potency
-Schizophrenia

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23
Q

Clozapine side effects

A

-Sialorrhea
-highest metabolic offender
-high risk of anticholinergic

24
Q

Olanzapine and Risperidone

A

-SGA (D2 antagonist)
-Schizophrenia

25
Q

Olanzapine side effect

A

DRESS

26
Q

Paliperidone side effect

A

QT prolongation

27
Q

Ziprasidone side effect

A

DRESS

28
Q

Aripiprazole, Cariprazine,
Brexpiprazole

A

-D2 partial agonist
-Schizophrenia
-insomnia

29
Q

Caffiene MOA

A

1) Blockade of adenosine receptors
-Block A1: prevents inhibition of wake promoting neurons
-Block A2A: prevents activation of sleep promoting neurons

30
Q

What is the primary effect of caffeine on adenosine receptors?

A

Antogonist

31
Q

Which subtype of adenosine receptor is responsible for sedative effects of Adenosine?

A

A1 (but bot A1 and A2A have effects)

32
Q

What is the primary mechanism by which caffeine promotes wakefulness?

A

-block both A1 and A2A adenosine receptors
-prevents inhibition of wake promoting neurons
-prevents activation of sleep promoting neurons

33
Q

What is involved in action of caffeine?

A

-blockade of adenosine receptors
-inhibition of PDE: increase cAMP and cGMP levels
-elevate intracellular calcium

34
Q

amphetamine MOA release of NTs

A

-increase release of NTs (DA and NE)
-reverse transport of vesicles: interferes with VMAT
-inhibits DA transport: increases concentration
-further increases extracellular DA concentrations

35
Q

Amphetamine MOA: inhibition of reutake

A

-clock reuptake of DA and NE
-inhibit transporters

36
Q

Amphetamine MOA: increase DA synthesis

A

1) increase activity of TH: synthesize tyrosine to L-DOPA
2)decrease activity of MAO: stops break down of DA

37
Q

Name 3 MOA for amphetamines

A

-release of NTs
-Inhibit reuptake
-increase intracellular DA synthesis

38
Q

What is true about amphetamines?

A

-initially increase cytoplasmic DA, which further increases DA concentrations in synaptic cleft

39
Q

What is the primary effect of increased NT levels induced by amphetamines in the synaptic cleft?

A

prolonged activation of postsynaptic receptors

40
Q

What is the primary MOA of cocaine as a CNS stimulant?

A

-inhibition of dopamine reuptake by DAT
-increases extracellular DA concentration

41
Q

How does phentermine act on the CNS to suppress appetite?

A

-Activates release of norepinephrine

42
Q

What is the primary MOA of phentermine?

A

-increases release of NE and DA, activating POMC neurons to suppress appetite

43
Q

Role of bupropion in appetite regulation?

A

-blocks NE and DA reuptake
-activates POMC neurons
-negative feedback loop

44
Q

What is the primary MOA of Liraglutide?

A

Acts on GLP-1 receptors to suppress appetite

45
Q

GLP-1 (as incretin)

A

enhances both insulin secretion and inhibits glucagon release

46
Q

How does Orlistat contribute to weight loss?

A

-inhibits fat absorption in GI tract

47
Q

What types of fat does Orlistat affect?

A

-Monoglycerides
-triglycerides
-free fatty acids

48
Q

Clozapine

A

-agranulocytosis
-seizure rist
-myocarditis
-Orthostasis
-Sialorrhea(M4 agonism)
-Affected by CYP1A2

49
Q

Olanzapine

A

-Sedation
-anticholinegic
-Orthostasis
-1A2

50
Q

Quetiapine

A

-hyperlipidemia
-QT prolongation

51
Q

Risperidone and Paliperidone

A

-similiar clinical profiles
-higher risk for EPS/TD/prolactin`

52
Q

Ziprasidone

A

-lowest risk for weight gain
-Greatest risk for QT prolongation

53
Q

Lumateperone

A

-good side effect profile
-sedation is most common

54
Q

Lurasidone

A

-cariac arrthymia
-no weight gain

55
Q

Ariprazole

A

-no weight gain
-INSOMNIA
-akathisia
No action at D2