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521-Pharmacology > Exam 2 Review > Flashcards

Exam 2 Review Flashcards

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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

Study These Flashcards
A

-Sialorrhea
-highest metabolic offender
-high risk of anticholinergic

24
Q

Olanzapine and Risperidone

Study These Flashcards
A

-SGA (D2 antagonist)
-Schizophrenia

25
Olanzapine side effect
DRESS
26
Paliperidone side effect
QT prolongation
27
Ziprasidone side effect
DRESS
28
Aripiprazole, Cariprazine, Brexpiprazole
-D2 partial agonist -Schizophrenia -insomnia
29
Caffiene MOA
1) Blockade of adenosine receptors -Block A1: prevents inhibition of wake promoting neurons -Block A2A: prevents activation of sleep promoting neurons
30
What is the primary effect of caffeine on adenosine receptors?
Antogonist
31
Which subtype of adenosine receptor is responsible for sedative effects of Adenosine?
A1 (but bot A1 and A2A have effects)
32
What is the primary mechanism by which caffeine promotes wakefulness?
-block both A1 and A2A adenosine receptors -prevents inhibition of wake promoting neurons -prevents activation of sleep promoting neurons
33
What is involved in action of caffeine?
-blockade of adenosine receptors -inhibition of PDE: increase cAMP and cGMP levels -elevate intracellular calcium
34
amphetamine MOA release of NTs
-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
Amphetamine MOA: inhibition of reutake
-clock reuptake of DA and NE -inhibit transporters
36
Amphetamine MOA: increase DA synthesis
1) increase activity of TH: synthesize tyrosine to L-DOPA 2)decrease activity of MAO: stops break down of DA
37
Name 3 MOA for amphetamines
-release of NTs -Inhibit reuptake -increase intracellular DA synthesis
38
What is true about amphetamines?
-initially increase cytoplasmic DA, which further increases DA concentrations in synaptic cleft
39
What is the primary effect of increased NT levels induced by amphetamines in the synaptic cleft?
prolonged activation of postsynaptic receptors
40
What is the primary MOA of cocaine as a CNS stimulant?
-inhibition of dopamine reuptake by DAT -increases extracellular DA concentration
41
How does phentermine act on the CNS to suppress appetite?
-Activates release of norepinephrine
42
What is the primary MOA of phentermine?
-increases release of NE and DA, activating POMC neurons to suppress appetite
43
Role of bupropion in appetite regulation?
-blocks NE and DA reuptake -activates POMC neurons -negative feedback loop
44
What is the primary MOA of Liraglutide?
Acts on GLP-1 receptors to suppress appetite
45
GLP-1 (as incretin)
enhances both insulin secretion and inhibits glucagon release
46
How does Orlistat contribute to weight loss?
-inhibits fat absorption in GI tract
47
What types of fat does Orlistat affect?
-Monoglycerides -triglycerides -free fatty acids
48
Clozapine
-agranulocytosis -seizure rist -myocarditis -Orthostasis -Sialorrhea(M4 agonism) -Affected by CYP1A2
49
Olanzapine
-Sedation -anticholinegic -Orthostasis -1A2
50
Quetiapine
-hyperlipidemia -QT prolongation
51
Risperidone and Paliperidone
-similiar clinical profiles -higher risk for EPS/TD/prolactin`
52
Ziprasidone
-lowest risk for weight gain -Greatest risk for QT prolongation
53
Lumateperone
-good side effect profile -sedation is most common
54
Lurasidone
-cariac arrthymia -no weight gain
55
Ariprazole
-no weight gain -INSOMNIA -akathisia No action at D2

521-Pharmacology (11 decks)

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