PhrmDyn- 20C Flashcards

1
Q

Definition of pharmacodynamics

A

effects of drugs on body

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2
Q

Define inhibitor

A

drug that interferes with the normal function of the NT transporter

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3
Q

Define antagonist

A
  • molecule that has no intrinsic NT effects that blocks any ligand from acting
  • it is LITERALLY A BLOCKER, ALL BODY NO BRAIN!!
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4
Q

Define inverse agonist

A
  • causes receptor activity to drop below basal levels

- eg. Nuplazid- Primavansarin- antipsychotic for the treatment of psychosis in Parkinson’s disease

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5
Q

Name the 2 types of antagonists

A
  • competitive

- non-competitive antagonist

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6
Q

Define partial agonist

A

-molecule with reduced intrinsic activity that mimics that that of NT but at reduced intensity

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7
Q

How do pre-synaptic agonists work

A

-they increase negative feedback therefore decreasing the release of NT from the terminal

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8
Q

Types of pre-synaptic agonists

A
  • autoreceptors

- hetero-receptors (decrease release of a different terminal NT)

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9
Q

Examples of partial agonists

A
  • buprenorphine
  • aripiprazole
  • buspirone
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10
Q

Examples of pre-synaptic agonists

A
  • clonidine/guanfacine

- alpha 2 agonism leads to inhibition of release of monoamines

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11
Q

Two types of NT receptor types

A
  • ligand-gated ion channels

- G protein-coupled receptors coupled to second messenger cascade

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12
Q

How do the tryptans work?

A
  • 5HT1D direct receptor agonists

- cause constriction of cranial arteries

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13
Q

How do the SSRIs work?

A

-block activity of the serotonin transporter

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14
Q

How do SNRI’s work?

A

-block activity of the serotonin and norepinepherine transporters

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15
Q

How does buproprion work?

A

-DNRI

blocks activity of the DA and NE transporters

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16
Q

How does mirtazapine work?

A
  • pre-synaptic alpha 2 antagonism (antidepressant)
  • post-synaptic alpha 1 antagonism (orthostasis)
  • histamine receptor antagonism (weight gain and sedation)
17
Q

How do the SGAs work?

A
  • D2 receptor blockade

- 5HT2 receptor blockade

18
Q

How does ziprasidone work?

A
  • D2 receptor blockade
  • 5HT2 receptor blockade
  • serotonin transporter blockade
19
Q

How does amphetamine work?

A
  • increased release of NE and DA
  • blocks MAOI
  • block NE and DA transporters
20
Q

How do clonidine and guanfacine work?

A

-decrease monoamine release through increasing alpha-2 negative feedback

21
Q

How does rivastigmine work?

A

-blocks AChE and BChE (present on glial cells in CNS)

22
Q

What are the groups of monoamines?

A
  • Catecholamines
  • Tryptamines
  • Histamines
23
Q

Name the cardiac effects of monoamines

A

-supraventricular tachycardias
(prolonged PR interval)
-ventricular tachycardias
(prolonged QT interval)

24
Q

Rules of thumb regarding the QTc

A
  • QTc >= 500 mg : 2-3 times increased risk of TdP

- or if increase in QTc of more than 60 ms stop the medication

25
Q

Normal QTc?

A

<420 ms

26
Q

Medications that prolong QTc Interval

A
  • TCAs
  • SSRI
  • SNRI
  • FGA: pimozide (Rx resistant Tourette’s)
  • SGA
  • Lithium
  • Opioids: methadone
27
Q

Describe Mirtazapine’s anticholinergic effects

A

-mirtazapine has VERY LOW anticholinergic effects

28
Q

Which antidepressants have high anticholinergic effects?

A
  • TCA’s
  • Paroxetine
  • Duloxetine
29
Q

Precipitating factors for closed angle glaucoma

A
  • sympathomimetics
  • anticholinergics (un-opposed sympathetic tone)
  • occurs at the angle of Schlemm
30
Q

What is SIADH?

A
  • too much water retained leading to hyponatremia (Na < 130)
  • death rate with hyponatremia increased 60 fold
31
Q

Some drugs that cause SIADH

A
  • Nicotine
  • Carbamazepine
  • TCA’s
  • SSRI’s
32
Q

Symptoms of central pontine myelinolysis

A
  • spastic quadraparesis
  • pseudobulbar palsy
  • delirium
  • coma
33
Q

Hypotension causing medications

A
  • Clonidine and guanfacine
  • prazosin
  • mirtazapine
  • MAOIs
  • FGAs and SGAs (Chlorpormazine, Clozapine, Quetiapine