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Pharm > Test 2 Lecture 1 > Flashcards

Test 2 Lecture 1 Flashcards

1
Q

Describe the 5 steps involved in neurotransmission.

A
  1. NT synthesis
  2. Vesicular storage
  3. Synaptic release
  4. Binding to receptor
  5. Termination of transmission
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2
Q

How does botulism toxin (botox) work? (give detail)

A
  1. Endocytosed into cholinergic neurons
  2. Degrades SNAREs
  3. Prevents calcium-dependent exocytosis of ACh
  4. Leads to temporary calming of m. contractions
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3
Q

Metyrosine:

  • Indication
  • Mechanism of action
A

Indication - HTN
MoA - Competitive inhibitor of tyrosine hydroxylase

(Decreased NE production cuz it comes after dopamine is made)

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4
Q

Reserpine

  • Indication
  • Mechanism of action

Adverse effects?

A

Indication: HTN
MoA: Inhibits VMAT (vesicular monoamine transporter) of monoamines into vesicles (can’t be released)

Can cross the BBB and block monoamine vesicular uptake in CNS neurons which can contribute to depression

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5
Q

Bretylium

  • Indication
  • Mechanism of action
A
  • Ventricular arrhythmia
  • Inhibit AP generation and Ca2+-dependent synaptic vesicle fusion, thus reducing NE release

(specifically binds adrenergic receptors that nlly take up NE)
(wiki: inhibits release of NE)

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6
Q

Cocaine

  • Indication
  • Mechanism of action
A
  • Analgesia in surgery

- Blocks monoamine reuptake

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7
Q

Amphetamine or ephedrine

  • Indication
  • Mechanism of action
A
  • Narcolepsy, ADHD

- Reverse monoamine reuptake transporters (*calcium-independent NT release)

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8
Q

Naloxone, naltrexone

  • Indication
  • Mechanism of action
A
  • Opiate OD or dependence
  • Non-peptide blockers of opioid receptors in CNS (acts on neuropeptide receptor)

Naloxone is a small lipophilic molecule widely used to reverse opioid OD. Naltrexone has a longer duration of action and is used in the tx of opiate addiction and alcoholism.

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9
Q

SSRIs

  • Indication
  • Mechanism of action
A
  • Depression/Anxiety

- Selective inhibition of serotonin reuptake transporters

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10
Q

ACE inhibitors (e.g. lisinopril)

  • Indication
  • Mechanism of action
A
  • HTN

- Inhibits peptide cleavage of Ang I to Ang II

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11
Q

Phenylephrine

  • Indication
  • Mechanism of action
A
  • Hypotension during surgery
  • Direct agonist of adrenergic receptors

Resistant to degradation by the enzyme and so have a longer half-life.

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12
Q

MAO inhibitors

  • Indication
  • Mechanism of action
A
  • Depression
  • Blockade of cytoplasmic metabolism of monoamines

As NE accumulates in the cytoplasm, the xporter protein reverses direction
leading to expulsion of NE
into the synapse.

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13
Q

L-DOPA

  • Indication
  • Mechanism of action

Adverse effects?

A
  • PD
  • Precursor of dopamine, stimulates dopamine production

Since DOPA and dopamine are also precursors of NE, DOPA loading can have adverse effects on the CV system due to enhanced NE neurotransmission in the
peripheral autonomic nerves.

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14
Q

Carbidopa

  • Indication
  • Mechanism of action

What drug is it typically given with and why?

A
  • PD
  • Blocks L-DOPA conversion to dopamine

Doesn’t cross the BBB, so it can be used to reduce the CV side effects of L-DOPA in peripheral adrenergic nerves, and preserve the beneficial effects of L-DOPA treatment for Parkinson’s disease within
the CNS.

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15
Q

Tyramine

  • Indication
  • Mechanism of action
A
  • Ingested in diet, not therapeutic

- Competes w/NE for transport into synaptic vesicles

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16
Q

Regarding metabolism mechanism, monoamines 5-HT, NE and DA, are terminated by _________________________, while
ACh is metabolized via _______________________.

A
  • re-uptake into the pre-synaptic cell

- degradation in the synaptic cleft

17
Q

What is the original starting precursor of DA, Epi, and NE that is transported into cells?

A

Tyrosine

DA is precursor to NE and epi

18
Q

*What is the rate-limiting enzyme/step in the production of catecholamines?

A

Hydroxylation of tyrosine to DOPA by tyrosine hydroxylase

19
Q

Alpha-adrenergic
receptors can ______, while
beta-adrenergic receptors can _______
neurotransmitter release.

A
  • inhibit

- facilitate

20
Q
  • Termination of exogenously administered NE is mediated, in large part, by metabolism in plasma by __________________.
  • A second metabolic enzyme,
    _____________________, is present within the cell cytoplasm and rapidly oxidizes any NE and DA within the cytoplasm that is not transported into
    synaptic vesicles w/in time.
A
  • Catecholamine-O-methyltransferase (COMT), which is outside the cell
  • Monoamine oxidase (MAO), which digests catecholamines inside the cell (eg backed up)
21
Q

What are neuropeptides stored in, prior to their release?

A

Dense core vesicles (vs. typical small synaptic vesicles)

This packaging occurs at the ER and so is difficult to target selectively

22
Q

Dense core vesicles reside farther away from the pre-synaptic membrane than do small synaptic vesicles. How does this affect the stimulus needed for release?

A
  • Need longer duration stimulus

(Neuropeptides are often produced within other neuronal types and are co-released
when the nerve terminal is activated)

23
Q

The major mechanism of neuropeptide inactivation is ____________________.

A

cleavage via peptidases

Neuropeptides are not taken up into the nerve terminal

24
Q

What happens if someone on MAO inhibitors ingests excess tyramine?

A

Nlly subject to first-pass metab by MAOs in the liver. W/tx w/ MAOIs, the cytoplasmic accumulation of NE can reverse the concentration gradient across the PM and cause the reversal of the reuptake xporter. The resulting excessive release of NE can lead to a hypertensive crisis due to excessive vasoconstriction by NE in the periphery

Pharm (32 decks)

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