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Neuropharm extras (do last) Flashcards

1
Q

glutamate originates in the __________

A

cortex

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2
Q

norepinephrine originates in the __________

A

locus coeruleus

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3
Q

serotonin originates in the ____________

A

raphe nucleus

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4
Q

dopamine originates in the ______________ and ____________

A

ventral tegmental area

substantia nigra

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5
Q

acetylcholine originates in the ___________ and ___________

A

septal nuclei

nucleus basalis

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6
Q

histamine originates in the______________

A

tuberomamillary nucleus of hypothalamus

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7
Q

the biochemical amines have _________ pathways

A

ascending

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8
Q

glutamate terminates in the __________

A

hippocampus

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9
Q

norepinephrine and serotonin both terminate in the __________, __________, and _________

A

cortex
hippocampus
cerebellum

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10
Q

____________ terminates in the ____________ which is involved in addiction

A

dopamine

nucleus accumbens

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11
Q

which NT terminates in the striatum?

A

dopamine

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12
Q

which NT are involved in epilepsy and how?

A

glutamate - overactive

GABA - underactive

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13
Q

which NT are involved in depression and how?

A

serotonin and norepinephrine - underactive

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14
Q

which NT play a role in anxiety and how?

A

GABA and serotonin – underactive

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15
Q

which NT are involved in Parkinson’s disease and how?

A

acetylcholine - overactive

dopamine - underactive

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16
Q

which NT is involved in schizophrenia and how?

A

dopamine - hyperactive

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17
Q

which NT is involved in Alzheimers and how?

A

acetylcholine - underactive

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18
Q

which NT are excitatory in the CNS?

A

glutamate

acetylcholine

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19
Q

which is the major inhibitory NT in the CNS?

A

GABA

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20
Q

which NT is involved in migraine and how?

A

serotonin - too low

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21
Q

List 4 peptide neurotransmitters: ODEE

A

Opiods
Dynorphin
Endorphin
Enkephalin

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22
Q

List 4 amino acid neurotransmitters: GGGA

A

GABA
Glutamate
Glycine
Aspartate

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23
Q

List 5 biogenic amine neurotransmitters: SADEN

A 
Serotonin
Acetylcholine
Dopamine
Epinephrine
Norepinephrine
24
Q

Increased synaptic 5-HT in the CNS causes what side effects?

A

insomnia

agitation

25
Increased synaptic 5-HT in the GI causes what side effects?
nausea diarrhea bleed (platelet function)
26
Besides depression, what are other indications for SSRIs?
anxiety d/o eating d/o PMDD ADHD
27
"Discontinuation syndrome" is more likely to occur with a drug that has a _______(shorter/longer) half life.
shorter
28
SNRIs have all the side effects of SSRIs plus what?
increase blood pressure
29
Besides depression, what are other indications for duloxetine?
neuropathic pain fibromyalgia anxiety d/o
30
SSRIs or SNRIs combined with ___________ (name 3) can cause serotonin syndrome.
MOAIs St John's Wort methadone
31
The efficacy of SSRIs and SNRIs is the same. However, which one is less reliant on dietary tryptophan?
SNRI
32
Name 2 drugs that block SERT, NET plus some muscarinic, histamine, and alpha adrenergic receptors.
amitriptyline | desipramine
33
What are side effects of anticholinergics?
dry mouth constipation vision loss conduction block
34
People taking TCAs might complain of what side effects upon starting therapy?
drowsiness increased appetite and wt gain sexual dysfunction autonomic sx (dry mouth, constipation)
35
Why are people taking TCAs at high risk of toxicity?
``` low TI half life >24 hours metabolites also have long half life metabolized by CYPs 10 day supply is enough to kill ```
36
Besides depression, what are other indications for TCAs?
anxiety enuresis neuropathic pain migraine
37
Unique adverse effect of MAOI
postural hypotension
38
What are the symptoms of serotonin syndrome?
``` akathisia tremor altered mental status clonus muscle rigidity hyperthermia death ```
39
Definitely avoid in pregnancy:
tranylcypromine (MAOI)
40
"Risk cannot be ruled out" in pregnancy:
fluoxetine sertraline (SSRI)
41
Possible risk of fetal limb malformation in some studies:
amitryptiline (TCA)
42
Tolerance does not develop for which adverse effects of antidepressants?
``` sexual dysfunction cardiac toxicity (TCAs) ```
43
Activation of _____________ is a key step in the inflammatory response, it catalyzes production of EPA and AA from membrane phospholipids.
Phospholipase A2 | P.S. the type of fat in our diet influences what type of fatty acids comprise our membrane phospholipids
44
Prostaglandins, thromboxanes, and leukotrienes are _______________, derivatives of AA and EPA via cyclooxygenase and lipooxygenase enzymes.
eicosanoids arachidonic acid & EPA
45
Eicosanoids specifically produced via cyclooxygenase are called___________.
prostanoids these act uniquely on different tissue
46
Inhibition of COX ______(1 or 2) leads to GI-related side effects.
1 COX-1 is expressed in most tissues for "housekeeping" functions.
47
Expression of COX _____(1 or 2) is induced by stress, growth factors, cytokines, and inflammatory mediators.
2
48
Inhibition of COX ______ (1 or 2) causes the antipyretic, analgesic, and anti-inflammatory actions of _______(drug class).
2 NSAIDS
49
EPA is metabolized into omega ____ (3 or 6) eicosanoids.
omega 3
50
Arachidonic acid is metabolized into omega _____ (3 or 6) eicosanoids.
omega 6
51
Which eicosanoid family stimulates bronchoconstriction?
leukotrienes
52
Which has more potent inflammatory activity? Omega 6 (AA) or omega 3 (EPA) fatty acids?
Omega 6 (AA)
53
What enzymes do AA (omega 6) and EPA (omega 3) compete for ?
cyclooxygenase lipooxygenase
54
Which eicosanoid family stimulates platelet aggregation?
thromboxanes
55
The primary biologic effect of NSAIDS is inhibition of _________ synthesis from COX-1 & 2.
prostaglandin
56
You need ________(higher/lower) doses of NSAIDS to have anti-inflammatory benefit.
higher

Pharmacology (6 decks)

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