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Pharmacology > Neuropharm extras (do last) > Flashcards

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
Q

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

A

nausea
diarrhea
bleed (platelet function)

26
Q

Besides depression, what are other indications for SSRIs?

A

anxiety d/o
eating d/o
PMDD
ADHD

27
Q

“Discontinuation syndrome” is more likely to occur with a drug that has a _______(shorter/longer) half life.

A

shorter

28
Q

SNRIs have all the side effects of SSRIs plus what?

A

increase blood pressure

29
Q

Besides depression, what are other indications for duloxetine?

A

neuropathic pain
fibromyalgia
anxiety d/o

30
Q

SSRIs or SNRIs combined with ___________ (name 3) can cause serotonin syndrome.

A

MOAIs
St John’s Wort
methadone

31
Q

The efficacy of SSRIs and SNRIs is the same. However, which one is less reliant on dietary tryptophan?

A

SNRI

32
Q

Name 2 drugs that block SERT, NET plus some muscarinic, histamine, and alpha adrenergic receptors.

A

amitriptyline

desipramine

33
Q

What are side effects of anticholinergics?

A

dry mouth
constipation
vision loss
conduction block

34
Q

People taking TCAs might complain of what side effects upon starting therapy?

A

drowsiness
increased appetite and wt gain
sexual dysfunction
autonomic sx (dry mouth, constipation)

35
Q

Why are people taking TCAs at high risk of toxicity?

A 
low TI
half life >24 hours
metabolites also have long half life
metabolized by CYPs
10 day supply is enough to kill
36
Q

Besides depression, what are other indications for TCAs?

A

anxiety
enuresis
neuropathic pain
migraine

37
Q

Unique adverse effect of MAOI

A

postural hypotension

38
Q

What are the symptoms of serotonin syndrome?

A 
akathisia
tremor
altered mental status
clonus
muscle rigidity
hyperthermia
death
39
Q

Definitely avoid in pregnancy:

A

tranylcypromine (MAOI)

40
Q

“Risk cannot be ruled out” in pregnancy:

A

fluoxetine
sertraline
(SSRI)

41
Q

Possible risk of fetal limb malformation in some studies:

A

amitryptiline (TCA)

42
Q

Tolerance does not develop for which adverse effects of antidepressants?

A 
sexual dysfunction
cardiac toxicity (TCAs)
43
Q

Activation of _____________ is a key step in the inflammatory response, it catalyzes production of EPA and AA from membrane phospholipids.

A

Phospholipase A2

P.S. the type of fat in our diet influences what type of fatty acids comprise our membrane phospholipids

44
Q

Prostaglandins, thromboxanes, and leukotrienes are _______________, derivatives of AA and EPA via cyclooxygenase and lipooxygenase enzymes.

A

eicosanoids

arachidonic acid & EPA

45
Q

Eicosanoids specifically produced via cyclooxygenase are called___________.

A

prostanoids

these act uniquely on different tissue

46
Q

Inhibition of COX ______(1 or 2) leads to GI-related side effects.

A

1

COX-1 is expressed in most tissues for “housekeeping” functions.

47
Q

Expression of COX _____(1 or 2) is induced by stress, growth factors, cytokines, and inflammatory mediators.

A

2

48
Q

Inhibition of COX ______ (1 or 2) causes the antipyretic, analgesic, and anti-inflammatory actions of _______(drug class).

A

2

NSAIDS

49
Q

EPA is metabolized into omega ____ (3 or 6) eicosanoids.

A

omega 3

50
Q

Arachidonic acid is metabolized into omega _____ (3 or 6) eicosanoids.

A

omega 6

51
Q

Which eicosanoid family stimulates bronchoconstriction?

A

leukotrienes

52
Q

Which has more potent inflammatory activity? Omega 6 (AA) or omega 3 (EPA) fatty acids?

A

Omega 6 (AA)

53
Q

What enzymes do AA (omega 6) and EPA (omega 3) compete for ?

A

cyclooxygenase

lipooxygenase

54
Q

Which eicosanoid family stimulates platelet aggregation?

A

thromboxanes

55
Q

The primary biologic effect of NSAIDS is inhibition of _________ synthesis from COX-1 & 2.

A

prostaglandin

56
Q

You need ________(higher/lower) doses of NSAIDS to have anti-inflammatory benefit.

A

higher

Pharmacology (6 decks)

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