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Nursing Pharmacology > Module 14a > Flashcards

Module 14a Flashcards

1
Q

Stud of how drugs affect the function of the CNS.

A

Neuropharmacology

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2
Q

There are many disorders in the CNS, and most of them have a component that is mediated by a ________ imbalance. We treat this imbalance with _____.
Unfortunately, these only treat the ________ of disease, not the ______.

A

biochemical
drugs
symptoms
cause

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3
Q

Cells in the brain that act to process and transmit signals and information.

A

Neurons

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4
Q

The start of information transfer in the neuron begins at the ________, which receives a signal from another neuron.

A

dendrite

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5
Q

The resting membrane potential of cells is approximately ____. This means that the inside of the cell is _______ with respect to the outside.

A

-70mV

negative

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6
Q

During depolarization of a neuron, positively charged ____ ions enter the cell through these.

A

Na+

voltage-gated Na+ channels

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7
Q

During repolarization of a neuron, these ions leave the neuron.

A

potassium

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8
Q

Only a few potassium channels are open. Potassium can freely move in and out of cells. The membrane potential does not change.

A

Resting potential.

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9
Q

IF a depolarizing stimulus is received, it opens a few sodium channels. This allows sodium to enter the cell, until this point is reached.

A

Threshold

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10
Q

If threshold is achieved, other sodium channels open and sodium rushes in. the membrane potential increases further.

A

rising phase

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11
Q

Sodium channels close and potassium channels open. Potassium rushes out of the cell and the membrane potential decreases. As the membrane potential approaches resting potential even more potassium channels open.

A

Falling phase

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12
Q

The membrane potential undershoots the RMP due to excess potassium leaving the cell

A

Hyperpolarization

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13
Q

Describe the transmission of the chemical signal from one neuron, to another.

A

The action potential reaches the pre-synaptic nerve terminal.
This induces calcium influx into the neuron.
Calcium causes vesicles to fuse with the pre-synaptic membrane, and release NTs into the synpatic cleft.
NTs travel through the synaptic cleft and bind to receptors on the post-synaptic membrane, inducing an action potential in the post-synaptic neuron

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14
Q

What are the major NT classes?

A

Monoamines (Epinephrine, NE, Dopamine, Serotonin)
Amino acids (Glutamate, GABA, aspartate, glycine)
Other (ACh)

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15
Q

What NTs fall in the monoamine class?

A

Serotonin, Epinephrine, NE, Dopamine

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16
Q

What NTs fall in the amino acid class?

A

Glutamate, GABA, aspartate, glycine

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17
Q

What NT falls in the other class?

A

ACh (acetylcholine)

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18
Q

Excitatory amino acid NTs.

A

Glutamate, aspartate

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19
Q

Inhibitory amino acid NTs

A

GABA, glycine

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20
Q

5 ways in which drugs that treat CNS disorders may act.

A 
Replacement
Agonists/Antagonists
Inhibiting NT breakdown
Blocking reuptake
Nerve stimulation
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21
Q

The drug acts to replace NTs that are low in diseases

A

Replacement

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22
Q

A drug that directly binds to receptors on the post-synaptic membrane

A

Agonists/Antagonists

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23
Q

NT metabolism is inhibited

A

Inhibiting NT breakdown

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24
Q

NT reuptake into the pre-synaptic membrane is blocked

A

Blocking reuptake

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25
Q

The drug directly stimulates the nerve causing it to release more NT

A

Nerve stimulation

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26
Q

Parkinson’s was first described in 1817 by ______ Parkinson.

A

James

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27
Q

PD is caused by a progressive loss of _________ neurons in the ________ _______ of the brain.

A

dopaminergic

substantia nigra

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28
Q

Is progressive loss of dopaminergic neurons a normal process of aging?

A

yes, however in PD, this number is very elevated

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29
Q

There are distinct symptoms of Parkinsons, these are? (6)

A 
Tremor
Rigidity
Bradykinesis
Masklike face
Postural instability
Dementia
30
Q

Slowness of movement, especially slow to initiate movements

A

Bradykinesia

31
Q

Patient’s cannot show facial expression and have difficulty blinking and swallowing

A

Masklike face

32
Q

Balance is impaired; patients have difficulty balancing while walking

A

Postural instability

33
Q

Pd is a chronic movement disorder that is caused by an imbalance between ____ and _______ in the brain.

A

ACh, dopamine

34
Q

In healthy patients (i.e. without PD, there is a normal balance of ACh and dopamine which results in normal ________ release.

A

GABA

35
Q

Describe the NT imbalance, the result of this imbalance and the overall manifestation as a result of the imbalance, in PD.

A

Decreased dopamine release, thus Ach release exceeds it greatly
GABA release is not inhibited by dopamine, but stimulated by ACh.
Excess GABA release causes the movement disorders of PD

36
Q

________ inhibits GABA release; _______ stimulates GABA release.

A

Dopamine

ACh

37
Q

The etiology of PD is largely _______.

A

idiopathic

38
Q

Describe how drugs may play a role in development of PD.

A

A by-product of illlicit street drug synthesis is MPTP - which causes irreversible death of dopaminergic neurons

39
Q

Genetics plays a role in predisposing patients to PD, mutations in these 4 genes have been implicated.

A

Alpha synuclein, parkin, UCHL1, DJ-1

40
Q

Certain environmental toxins, ________, have been associated with PD

A

Pesticides

41
Q

Trauma to the brain predisposes patients for PD.
_____ are known to cause degeneration to dopaminergic neurons. There is a link between _______ induced ______ damage. and Parkinson’s.

A

ROS
diabetes
oxidative

42
Q

The main treatment modality in Parkinson’s is what?

A

Improve the balance between ACh and Dopamine

43
Q

There are 5 different major classes of drugs that act by increasing dopamine neurotransmission, what are they?

A 
Dopamine replacement - L-DOPA
Dopamine agonist
Dopamine release
Catecholamine-O-Methyltransferase inhibitor
Monoamine oxidase-B inhibitor
44
Q

the most effective drug for PD treatment.

A

Levodopa

45
Q

Unfortunately, the beneficial effects of _______ decrease over time as PD progresses.

A

levodopa

46
Q

L-DOPA crosses the blood brain barrier by an _______ transport protein.
L-DOPA is ________, but is converted to dopamine in dopaminergic nerve terminals.
Conversion of L-DOPA is mediated by ____________ enzymes in the brain.
The cofactor ________ (vitamin ___) speeds up this reaction

A 
active
inactive
decarboxylase
pyridoxine
vitamin B6
47
Q

What are the reasons why dopamine is not given to treat PD?

A

Dopamine cannot cross the BBB

Dopamine has a very short half-life in blood

48
Q

L-DOPA may cause nausea and vomitting due to dopamine mediated activation of the _________ trigger zone in the _______.

A

chemoreceptor

medulla

49
Q

Cardiac dysrhythmias may occur when taking L-DOPA, because its conversion to dopamine in the periphery can result in activation of these receptors.

A

cardiac beta 1 receptors

50
Q

What are the adverse effects of L-DOPA?

A

Nausea/vomitting (chemoreceptor trigger zone in the medulla)
Dyskinesias
Cardiac dysrhythmias (dopamine in periphery - cardiac beta 1 receptors)
Orthostatic hypotension
Psychosis

51
Q

Only approximately _% of the total L-DOPA dose reaches the brain.
The remaining is metabolzied int he peripheral tissues (mostly the _______), before reaching the brain.
Thus, L-DOPA is almost always given with ________, a ________ inhibitor that inhibits the peripheral metabolism of L-DOPA.
In this case, approximately __% of L-DOPA now reaches the brain.

A 
1%
intestine
carbidopa
carboxylase inhibitor
10%
52
Q

Carbidopa allows a _______ dose of L-DOPA to be administered and _______ the incidence of cardiac dysrhythmias and nausea and vomiting. Explain.

A

lower
decreases
Lower amount of peripheral metabolism, means there is less dopamine to interact with cardiac beta 1 receptors, and (to a lesser degree), with the chemoreceptor trigger zone int he medulla

53
Q

There are two types of loss of effects that L-DOPA taking patients may expreince, what are they?

A

Wearing off - gradual loss of effect

On-off - abrupt loss of effect

54
Q

Usually occurs at the end of the dosing interval of L-DOPA and indicates that drug levels might be low.

A

Wearing off

55
Q

Wearing off of L-DOPA may be minimized by these three methods.

A

Shortening the dosing interval
Administer with a COMT inhibitor (inhibits L-DOPA metabolism)
Add a dopamine agonist to the therapy

56
Q

Can occur even when L-DOPA levels are high and is difficult to treat this loss of effect.

A

On-off

57
Q

What are the three ways in which on-off may be minimized in L-DOPA treatment?

A

Divide the medication into 3-6 doses per day
Use a controlled release formulation
Move protein containing meals to the evening

58
Q

Acts to stimulate release of dopamine from dopaminergic neurons and also blocks dopamine reuptake; also blocks the NMDA receptor.

A

Dopamine releasers

59
Q

Dopamine releasers
- Response is ______, usually within - days
Usually used in combination with _______, or alone in the case of ______ PD.

A

fast, 2-3 days
L-DOPA
mild

60
Q

The blockade of NMDA receptors by dopamine releasers is thought to decrease this side effect.

A

Dyskinesia

61
Q

Side effects of dopamine releasers.

A

dizziness, nausea, vomiting, lethargy, and anticholinergic side effects

62
Q

Enzyme that adds a methyl group to dopamine and L-DOPA, making them inactive

A

COMT

63
Q

Adverse effects of COMT inhibitors are similar to those of L-DOPA, what are they?

A

Nausea/vomitting
orthostatic hypotension
vivid dreams and hallucinations

64
Q

Enzyme that oxidatively metabolizes dopamine and L-DOPA, inactivating them.
Located in these two areas.

A

Monoamine oxidase-B

Brain and periphery

65
Q

Inhibiting oxidative metabolism of L-DOPA allows more conversion to dopamine in the brain, and also allows more dopamine to remain in _______ ______ and be released following an action potential.

A

nerve terminals

66
Q

Adverse effects of MAO-B inhibitors.

A

insomnia, orthostatic hypotension, dizziness

67
Q

Can patients taking MAO-B inhibitors have tyramine containing foods?

A

Yes, as at therapeutic levels, these drugs do not inhibit MAO-A in the liver. Thus no hypertensive crisis

68
Q

Excess acetylcholine causes what types of symptoms in PD patients?

A

Urinary incontinence, salivation, diaphoresis

69
Q

Block the binding of ACh to its receptor.

A

Anticholinergic drugs

70
Q

Anticholinergic drugs may increase the effectiveness of _____. In doing so, these drugs may decrease the incidence of these ACh related symptoms.

A

L-DOPA

urinary incontinence, diaphoresis, salivation

Nursing Pharmacology (30 decks)

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