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Pharmacology > Other Nervous System Pharmacology > Flashcards

Other Nervous System Pharmacology Flashcards

1
Q

Nondepolarizing neuromuscluar blocking drugs

A

Used for muscle paralysis during mechanical ventilation or surgery.
Used for long term motor paralysis which may occur within 5 minutes and most agents are later excreted or metabolized by the liver

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2
Q

How do nondepolarizing neuromuscular blocking drugs work

A

Competitive antagonists with acetylcholine at the post junctional membrane nicotonic receptors of the neuromuscular junction leaving fewer bindin gsitres for ach

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3
Q

Are nondepolarizing neuromuscular blocking drugs reversible

A

Yup

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4
Q

How do you reverse nondepolarizing neuromuscular blocking drugs

A

Cholinesterase inhibitors

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5
Q

What can cholinesterase inhibitors be used to diagnose

A

Myasthenia gravis

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6
Q

Suffix of nondepolarizing neuromuscular blocking drugs

A

Rium besides tubocurarine

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7
Q

Examples of nondepolarizing neuromuscular blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronim, vecuronium, rocuronium

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8
Q

Nondepolarizing neuromuscular blocking drugs are competitive antagonists

A

With acetylcholine at the post junctional membrane nicotonic receptors of the neuromuscular junction. Leave few binding sites

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9
Q

Nondepolarizing neuromuscular blocking drugs reversal

A

Cholinesterase inhibitors

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10
Q

Nondepolarizing neuromuscular blocking drugs. What cholinesterase inhibitors may be used to reverse

A

Neostigmine and edrophonium

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11
Q

Diagnosis and treatment of myasthenia gravis

A

Diagnose with neostigmine and edrophonium

Treat with neostigmine

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12
Q

Succinylcholine

A

Paralytic agent used for surgeries or short procedures such as intubation

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13
Q

How does succinylcholine work

A

Binding at motor nicotonic acetylcholine receptors and keeping myocytes in a depolarizes state
Prevents ach from binding to receptors and muscle contraction

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14
Q

What is the first phase of succinylcholine mechanism of action

A

Phase 1-administered agent is non-reversible. Myocytes still have succinylcholine actively bound to motor nicotonic receptors and there is constantt depolarizes state.
Patients often show fasciculations and held contractions

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15
Q

What is phase 2 of succinylcholine mechanism of action

A

Receptors become sensitized and repolarize. They can only be aroused for action potential with larger amounts of acetylcholine, which is why neostigmine can be used to help reverse paralysis in phase 2

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16
Q

How can we reverse phase II of succinylcholine

A

Neostigmine (an acetylcholinesterase inhibitor )

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17
Q

Major side effect of succinylcholine

A

Malignant hyperthermia

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18
Q

Who should we not give succinylcholine to

A

Patients in a hyperkalamic state

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19
Q

Indications for succinylcholine

A

In surgery or short procedures can be used for patients in trauma care to help withintubation or those undergoing electroconvulsive therapy

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20
Q

How does succinylcholine cause neuromuscular block

A

Binds to the nicotonic acetylcholine receptor and keeps the muscular action potential stuck in a depolarizes state

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21
Q

What receptor does succinylcholine bind to

A

Motor nicotinic receptor , which normally binds ach

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22
Q

Succinylcholine is an ach receptor ___

A

Agonist

Opens sodium channels and causes membrane depolarization

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23
Q

Why does succinylcholine prevent muscular contraction

A

Cells cant repolarize and contract again

Can be observed immediately after IV. Patients fasciculate and are unable to contract again even after electrical stimulation

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24
Q

Phase 1 succinylcholine

A

Maintaining the muscle cels membrane potential above threshold.
Cells kept in a depolarizes state as succinylcholine is bound to the receptor and succinylcholine isn’t broken down quickly .
This period of paralysis cant be overcome bc no where for ach to bind

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25
Q

Phase 2 succinylcholine

A

Cells being repolarized but blocked . The myocytes become sensitive to ach; they are desensitized
This phase is reversible but needs a larger ach stimulus to cause contraction

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26
Q

How can we reverse phase 2 of succinylcholine

A

Neostigmine which prevents breakdown of ach in the plasma which leads to an increase ach concentration.

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27
Q

Why would we want to reverse phase 2 of succinylcholine

A

To overcome desensitization experience by paralyzed patients in phase 2

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28
Q

What do parkinsons drugs do

A

Counter neurotransmitter pathologies experienced by patients

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29
Q

How do parkinsons drugs work

A

Increase dopamine bioavailability or antagonizing acetylcholine

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30
Q

Describe parkinsons

A

Cell death in midbrain, with degeneration of the substantia nigra, which serves to generate dopamine. This leads to a neurotransmitter imbalance with decreased dopamine and relatively increased ach(a balance of these neurotransmitters is necessary for coordinated motor movement)

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31
Q

What are the antiparkinson drugs

A

BALSA

Bromocriptine, amantadine, levodopa, selegiline, antimuscarinics

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32
Q

Bromocriptine

A

Potent dopaminergic agonist

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33
Q

Amantadine

A

Unknown mechanism

But can also be antiviral

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34
Q

Levodopa (L-Dopa)

A

Dopamine isomer which readily crosses the BBB

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35
Q

Selegiline

A

Inhibits MAO-B , an enzyme which acts to break down dopamine.

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36
Q

Anti muscarinic drugs, like benztropine

A

Block cholinergic neuronal activity and are more successful at treating tremor and rigidity than bradykinesia

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37
Q

Parkinson

A

Neurodegeneratice disorder caused by death of dopamine generating cells in the substantia nigra. It is due to this cellular death and decreased dopamine the motor symptoms arise

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38
Q

Why do parkinsons get increase in ach

A

Bc dopamine decreases and there is an imbalance of neurotransmitters required for motor control (not a gross excess of ach, just an imbalance leading to higher ach in comparison to dopamine)

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39
Q

Bromocriptine

A

Ergot alkaloid
Dopamine agonist and increases its bioavailability
Also effects serotonergic, alpha adrenergic and glutamate receptors

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40
Q

Amantadine

A

Antiparkinsons and antiviral
Increases dopamine release by a poorly understood mechanism
Also has anticholinergic action

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41
Q

Levodopa

A

Dopamine isomer commonly administered with carbidopa
Protected from breakdown by carbidopa in the gut and periphery and readily passes through the blood brain barrier to increase central dopamine bioavailability

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42
Q

Selegiline

A

MAO-B -enzyme which metabolizes dopamine int he body

Selegiline is an MAO-B inhibitor and prevents breakdown of dopamine, increasing its bioavailability

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43
Q

Antimuscarinic drugs, like benztropine

A

Block muscarinic receptors to curb cholinergic neuron activity.
Works to alleviate tremor and rigidity associated with parkinsons but does not work well for treating bradykinesia

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44
Q

Levodopa/carbidopa

A

Levocarb
Treat parkinsons
Increases dopamine delivery in the brain.

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45
Q

Does levodopa cross the BBB

A

Yup

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46
Q

What happens to levodopa once cross BBB

A

Converted to dopamine centrally

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47
Q

Why is levodopa given with carbidopa

A

Inhibits DOPA decarboxylase, and protects L dopa from being broken into dopamine peripherally and in the gut before it crosses the BBB

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48
Q

Side effect of levocarb

A

Arrhythmia/tachyarrhythmia

Dyskinesia

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49
Q

Why does levocarb cause arrhythmia

A

Peripheral conversion of the drug into catecholamine

But usually mitigated by carbidopa

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50
Q

Why does levocarb cause dyskinesia

A

Distortion or difficulty with voluntary movement may occur with long term use

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51
Q

Carbamazepine (tegretol)

A

Anticonvulsant medication that decreases seizure activity caused by high frequency neuronal discharge

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52
Q

Indication for carbamazepine (tegretol)

A

Seizures
Trigeminal neuralgia
Symptoms associated with bipolar disorder

53
Q

Side effects of carbamazepine (tegretol)

A 
Blurred vision, vertigo, and headache are common 
Steven-johnson syndrome (SJS)
Toxic epidermal necrolysis (TEN)
Hepatotoxicity
Blood dyscrasias (aplastic anemia)
54
Q

Why not give carbamazepine (tegretol) to pregnant women

A

Teratogen

55
Q

What do when give patient carbamazepine

A

Monitor for signs of water retention

56
Q

Why not give someone on carbamazepine (tegretol) grapefruit juice

A

Increases serum carbamazepine

57
Q

How does carbamazepine work

A

Binds to sodium channels and prevents the normal action potential activity resulting in prolonged sodium channel inactivity and decreased neuronal excitability that leads to seizure activity

58
Q

Indications for carbamazepine

A

Seizures
Bipolar
Trigeminal neuralgia

59
Q

How does carbamazepine treat seizures

A

Prolongs inactivation of sodium channels and suppresses high frequency neuronal discharge that contribute to the development of partial seizures and tonic clones seizures.

This drug does not help treat absence, myoclonic, or atomic seizures

60
Q

How does carbamazepine treat bipolar

A

It is an antiepilectic drug used to suppress mania and stabilize mood.
Continued use may prevent mania and depression

61
Q

How does carbamazepine treat trigeminal neuralgia

A

Decreases neuropathic pain along the trigeminal nerve but is not indicated as an analgesic for other types of pain

62
Q

Why might carbamazepine cause nystagmus, blurred vision, and diplopia

A

Idk but tolerance with continued use

63
Q

Why does carbamazepine cause ataxia , vertigo, headache

A

In first weeks.

Minimize by starting on low dose with largest dose at bedtime

64
Q

Whay does carbamazepine cause hepatotoxicity

A

Increases the number of drug metabolizing enzymes in the liver
A dysfunctional liver may lead to liver damage and result in hepatotoxicity and hepatitis

65
Q

How manage liver concern in patient on carbamazepine

A

Do liver tests

Inform patient to contact doctor if get symptoms of liver damage

66
Q

What are symptoms of liver damage

A

Dark urine, clay colored stools, jaundice , rash

67
Q

Why does carbamazepine cause blood dyscrasias (agranulocytosis and fatal aplastic anemia)

A

May cause bone marrow suppression

68
Q

How manage blood dyscrasias in patient on carbamazepine

A

Obtain blood count before treatment
Do not give to patients with pre existing hematologist abnormalities
Notify physician if patient has symptoms of blood dyscrasias

69
Q

What are symptoms of blood dyscrasias

A

Fever, pallor, weakness, easy bruising, petechiae

70
Q

Why does carbamazepine cause water retention

A

Increases secretion of ADH and inhibits renal excretion of water. Leading to water retention and decreased blood osmolarity

71
Q

Who may water retention be determinetal to

A

Patients with heart failure

72
Q

How manage a patient on carbamazepine if concerned about water retention

A

Monitor sodium level in serum

73
Q

How does carbamazepine cause SJS, rash, toxic epidermal necrolysis

A

Genetic variation primarily found in patients of Asian descent have an increased susceptibility of developing SJS or TEN on carbamazepine

74
Q

What do if patient has rash? SJS or TEN?

A

Antihistamine

Stop the drug

75
Q

Why avoid grapefruit juice on carbamazepine

A

Grapefruit juice prevents normal drug metabolism and increases serum levels
Increases the amount of toxic carbamazepine to toxic plasma levels

76
Q

Memantine

A

NMDA receptor antagonist which helps prevent excitotoxicity in patients with Alzheimer’s disease
It is a glutamergic antagonist at NMDA receptors

77
Q

How does memantine work

A

Halting an influx of Ca preventing excitotoxicity to neurons, (neuronal excitotoxicity is mediated by Ca which activated intracellular enzymes leading to cell destruction ) this shows symptomatic improvement in patients

78
Q

Side effects of memantine

A

Confusion and hallucinations

79
Q

General purpose of memantine

A

NMDA receptor antagonist which helps prevent excitotoxicity in patients with Alzheimer’s disease

80
Q

Memantine is a glutamatergic __ at NMDA receptors

A

Antagonist (impede an influx of Ca , halting excitotoxicity to neurons) this drug is low affinity and short acting with a modest effect

81
Q

How does memantine prevent excitotoxicity

A

Antagonizing NMDA receptors

Preventing excitotoxicity

82
Q

How does excitotoxicity happen

A

Ca which activates intracellular enzymes leading to cell destruction

83
Q

Donepezil

A

Acetylcholinesterase inhibitor used to treat Alzheimer’s disease

84
Q

What other drug can be used for Alzheimer’s

A

Rivastigmine

85
Q

How does donepezil work

A

Inhibiting the actions of acetylcholinesterase which acts to break down the neurotransmitter acetylcholine
Leading to an increase in circulating ach

86
Q

Side effects of donepexzil

A

Related to excess cholinergic activity

Include dizziness, nausea, and vomiting, vivid dreams, and GI upset

87
Q

Sumatriptan

A

Triptan family

For acute migraines and cluster headaches

88
Q

Half life of sumatriptan

A

Short 2 hours

89
Q

How does sumatriptan work

A

Agonist at 5HT 1B/1D autoreceptors and acts to inhibit the firing of serotonin neurons
Causing a reduction in the synthesis and release of serotonin

90
Q

What happens when sumatriptan binds to 5HT 1B/1D receptors

A

Adenylate cyclase is inhibited via regulatory G proteins, increasing intracellular Ca and affecting other intracellular events
Eventually this results in inhibition of trigeminal nerve firing and vasoconstriction

91
Q

Side effects of sumatriptan

A

Coronary vasospasm which may lead to MI

92
Q

Who should we not give sumatriptan to

A

Prinzmetals angina or severe coronary artery disease

93
Q

How do Tristan’s inhibit trigeminal nerve activation

A

Inhibit firing of trigeminal nerve

94
Q

Why do Tristan’s cause vasoconstriction

A

Inhibit AC and intracellular Ca increases causing vasoconstriction and reduces vascular dilation

95
Q

Why does sumatripatan cause coronary vasoaspam

A

Can cause MI

96
Q

Why not give sumatriptan to people with prinzmetals angina or people with CAD

A

Due to vasospastic side effects

97
Q

Butorphanol

A

For migraine headaches and severe pain (labor pains)

98
Q

How does butorphanol work

A

Mixed actions at the receptor level and is an agonist for micro and kappa receptors while being a competitive antagonist at micro receptors

99
Q

What is the significance of butorphanol being an agonist/antagonist at micro receptors

A

It causes less respiratory depression than full opioid agonist drugs

100
Q

Side effects butorphanol

A

Withdrawal
Usually happen when patient also treated with full opioid agonist

-competing with the opioid at micro receptors competing with the adjunct opioid drug being taken leading to withdrawal

101
Q

Indications for butorphanol

A

Migraine , severe pain, labor

102
Q

How is butorphanol administered for migraine

A

Nasal spray

103
Q

Is butorphanol more effective in women or men

A

Women labor

104
Q

Micro receptors

A

Mu receptor

105
Q

Withdrawal symptoms from butorphanol . How can we treat

A

Naloxone-but cant reverse overdose really

106
Q

Gabapentin

A

To treat different seizure presentations, peripheral neuropathic pain and migraine prophylaxis
Bipolar and post herpetic neuralgia-off label though

107
Q

What was the original purpose of gabapentin

A

GABA analog but does not act on the same neuronal receptors

108
Q

How does gabapentin works

A

A lot of gaps in knowledge

Inhibitshigh coltage gated Ca channels leading to decreased levels of mono amine neurotransmitters

109
Q

Side effects of gabapentin

A

Sedation/sluggish

Ataxia

110
Q

Indication for cabapentin (primary)

A

Seizure bc has anticonvulsant actions against smile and complex partial seizures as well as tonic clonic generalized seizures (grand mal)

111
Q

Indication for gabapentin (secondary)

A

Peripheral Neuropathy (chronic neuropathic pain or fibromyalgia), postherpetic neuralgia (along dermatomic regions in response to varicella infections-but pregabalin is more commonly used), bipolar (combined with another mood stabilizer), migraine prophylaxis

112
Q

Mechanism of action gabapentin

A

Inhibits voltage gated Ca channels inhibiting their action and decreasing monoamine neurotransmitters.

113
Q

Pregabalin (Lyrica)

A

GABA analog that binds to the nerve terminals of the calcium channels and prevent calcium influx , which inhibits release of certain neurotransmitters

114
Q

Indication for pregabalin

A

Seizures, neuropathic pain and fibromyalgia

115
Q

Side effects of pregabalin

A

Dizziness, somnolence, weight gain, headache, angioedema

116
Q

Patients on pregabalin have an increased risk of developing ___ or __ __

A

Rhabdomyolysis

Drug dependence

117
Q

How does pregabalin work

A

Bind and inhibit Ca channels at nerve terminal and inhibits calcium influx.
Decreases release of glutamate, norepinephrine, and substance P

118
Q

How does decrease in neurotransmitters from pregabalin help control seizures

A

Control them and give relief to neuropathic pain

119
Q

Pregabalin is a GABA analog, does it enhance GABA inhibitory actions?

A

Nope

120
Q

How does pregabalin decrease seizure

A

Decreasing abnormal electrical activity int he brain

121
Q

How does pregabalin help with neuropathic pain

A

Alters chemicals int he brain responsible for transmitting pain signals across the nervous system and decrease neuropathic pain

122
Q

How can pregabalin help diabetics

A

Neuropathic pain associated with nerve damage

123
Q

How can pregabalin help patients with spinal cord injury caused by herpes zoster

A

Receive pain

124
Q

How can pregabalin help patients with fibromyalgia

A

They may have neuropathic pain relief

125
Q

How does pregabalin help fibromyaligai

A

Decrease pain

But decrease pain relief after a few months

126
Q

Side effects pregabalin

A

Headache, dizziness, somnolence, weight gain, angioedema (allergic type reaction), rhabdomyolysis

127
Q

What is a problem with pregabalin

A

Dependence

128
Q

Pregabalin is listed as what

A

Under schedule V of the drug enforcement agency’s controlled substances act

Pharmacology (52 decks)

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