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Psychopharmacology > Lecture 4 Cholinergics & Adrenergics > Flashcards

Lecture 4 Cholinergics & Adrenergics Flashcards

1
Q

Cholinergic and Adrenergic Drugs

A
  • Drugs that effect the ANS are divided into 2 subgroups - Are classified based on the type of neuron involved - These drugs either stimulate or block neurons of ANS
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2
Q

Cholinergic Drugs

A
  • Act on receptors that are activated by Acetylcholine
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3
Q

Adrenergic Drugs

A
  • Act on receptors that are stimulated by norepinephrine or epinephrine
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4
Q

Sympathomimetic

A
  • Drugs that act directly on receptors
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5
Q

Adrenergic Drugs and NE (norepinephrine), EPI (Epinephrine)

A
  • Drugs that block the action ro by interrupting the release of NE or EPI
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6
Q

Adrenergic Neurons

A
  • Release NE as a Neurotransmitter and are found in the CNS also in the Sympathetic nervous system
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7
Q

Synthesis of NE (Norepinephrine):

A
  • Tyrosine is transported by NA linked into the adrenergic neuron - Hydroxylated into DOPA (dihydroxyphenylalanine) by tyrosine hydroxylase which is the rate-limiting step in the formation of NE - DOPA is decarboxylated to form dopamine - Dopamine is transported into synaptic vesicles - Dopamine is hydroxylated into NE by dopamine hydroxylase - In the adrenal medulla NE is converted into EPI
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8
Q

Adrenergic

A
  • Upon stimulation the adrenal medulla releases 85% EPI and 15% NE - Binding by receptor: NE will bind post and presynaptic - Removal of NE: catechol O methyltransferase (COMT) will metabolize NE or by reuptake which can be inhibited by TCAs or Cocaine - MAO will deactivate NE - inactive products of NE are excreted in the urine
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9
Q

Adrenergic Alpha 1

A
  • Vasoconstriction, increased peripheral resistance, increased blood pressure, mydriasis, increased closure of internal sphincter of the bladder
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10
Q

Adrenergic Alpha 2

A
  • Inhibition of NE release, inhibition of insulin release
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11
Q

Adrenergic Beta 1

A
  • Tachycardia, increased lipolysis, increased myocardial contractility
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12
Q

Adrenergic Beta 2

A
  • Vasodilation, slightly decreased peripheral resistance, bronchodilation, increased muscles and liver glycogenolysis, increased release of glucagon, relaxed uterine smooth muscles
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13
Q

Adrenergic Alpha 1 Agonist

A
  • EPI, NE, DA, Dobutamine, Phenlephrine
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14
Q

Adrenergic Alpha 1 Blocker

A
  • Phenotolamine, Prazosin
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15
Q

Adrenergic Beta 1 Agonist

A
  • EPI, NE, DA, Dobutamine, Isoproterenol
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16
Q

Adrenergic Beta 1 Blocker

A
  • Propranolol, Metoprolol, Atenolol
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17
Q

Adrenergic Beta 2 Agonist

A
  • EPI, DA, Dobutamine, Isoproterenol, Albuterol
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18
Q

Adrenergic Beta 2 Blocker

A
  • Propranolol
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19
Q

Clinical Uses - Epinephrine

A
  • Hypotension - Bronchospasm - Nasal Decongestant - Ophthalmic
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20
Q

Clinical Uses - Dopamine

A
  • Decompensated Congestive Heart Failure - Hypotension - Renal Perfusion
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21
Q

Clinical Uses - Dobutamine

A
  • Congestive Heart Failure
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22
Q

Clinical Uses - Phentolamine

A
  • Coronary Artery Disease - Peptic Ulcer
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23
Q

Clinical Uses - Phenylephrine

A
  • Nasal Decongestant
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24
Q

Clinical Uses - Prazosin

A
  • Hypertension - Benign Prostatic Hyperplasia
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25
Q

Clinical Uses - Clonodine

A
  • Antihypertensive - Opiod Withdrawal - Antidiarrheal in diabetic patients W/Autonomic Neuropathy
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26
Q

Clinical Uses - Metoprolol

A
  • Arrhythmias - Chronic CHF
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27
Q

Clinical Uses - Propranolol

A
  • Ischemic Heart Disease - Hypertension - Arrhythmias - Essential Tremors - Stage Fright - Migraine Precention
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28
Q

Clinical Uses - Alcuterol

A
  • Bronchospasm - Asthma - Bronchitis - COPD
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29
Q

Clinical Uses - Indirect Sympathomimetic - Cocaine

A
  • Potentiates NE by blocking repute of catecholamines - Clinical use – Surface anesthesia
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30
Q

Clinical Uses - Indirect Sympathomimetic - Ephidrine

A
  • Stimulates release of NE from sympathetic neurons - Clinical use – nasal decongestion, orthostatic hypotension, promotes urinary continence
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31
Q

Clinical Uses - Indirect Sympathomimetic - Amphetamine

A
  • After presynaptic uptake this agent causes the release of endogenous NE - Clinical use – ADHD, Obesity, Narcolepsy
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32
Q

Cholinergic Neuron - AcH

A
  • AcH released from the synaptic vesicles diffuses across the synaptic space and binds to either postsynaptic receptors on the target cell or to presynaptic receptors in the membrane of the neuron that released the AcH
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33
Q

Cholinergic Neuron - Degradation of Acetylcholine

A
  • Occurs in the synaptic cleft by acetylcholinesterase
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34
Q

Cholinergic Neuron - Recycling of Choline

A
  • Occurs by a uptake system that transport the molecule back into the neuron, is acetylated and stored until released by action potential
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35
Q

2 types of Cholinoceptors

A
  • Muscarinic Receptors - Nicotine Receptors
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36
Q

Cholinergic Neuron - Muscarinic Receptors

A
  • Bind AcH and muscarine (poisonous mushrooms) weak affinity for nicotine - Found on ganglia of the PNS and autonomic effector organs (heart, smooth muscles, brain) also on gastric parietal cells
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37
Q

Cholinergic Neuron - Nicotine

A
  • Depolarizes ganglia, first effects are stimulating followed by paralysis of all ganglia - First effects increase blood pressure and cardiac rate due to release of transmitter for adrenergic terminals and from the adrenal medulla - Increase peristalsis and secretions
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38
Q

Nicotine Stimulation - Release of Glutamate

A
  • A neurotransmitter involved in learning and memory - Glutamate enhances the connections between sets of neurons. These stronger connections mat be the physical basis of what we know as memory - When you use nicotine, glutamate may create a memory loop of the good feelings you get and further drive the desire to use nicotine - Nicotine also increases the level of other neurotransmitters and chemicals that modulate how your brain works. For example, your brain makes more endorphins in response to nicotine
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39
Q

Nicotine stimulation - Endorphins

A
  • Are small proteins that are often called the body’s natural pain killer - It turns out that the chemical structure of endorphins is very similar to that of heavy-duty synthetic painkillers like morphine - Can lead to feelings of euphoria - “runners high” = endorphin rush, this outpouring of chemicals gives you a mental edge to finish the race while temporarily masking the nagging pains you might otherwise feel
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40
Q

Chantix Anti-smoking Med

A
  • Binds to nicotine receptors and blocks them so that nicotine can no longer activate those receptors - This means that when someone is trying to quit and they lapse and smoke they probably won’t get much satisfaction from it and will be less likely to smoke another
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41
Q

Chantix - Secondary mechanism

A
  • It triggers some of the same effects that nicotine has (an “agonist” effect) - This includes a small release of dopamine, the reward neurotransmitter in the brain - In this way chantix dampens down nicotine withdrawal symptoms and cravings
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42
Q

Cholinergic Neuron - Inhibition of Acetylcholinesterase

A
  • Inhibition of Aceytlcholinesterase at the skeletal neuromuscular junction causes the accumulation of acetylcholine and ultimately results in paralysis of skeletal muscles
How well did you know this?
1
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2
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43
Q

Myasthenia Gravis

A
  • An autoimmune disorder caused by antibody-mediated loss of AcH receptors in the neuromuscular junction-impacting transmission between neuron and muscle - Neostigmine and Pyridostigmine are used to treat Myasthenia Gravis
44
Q

Cholinergic Neuron - Antimuscarinic

A
  • Atropine has affinity for muscarinic receptors and acts on CNS and PNS, Used to dilate pupils, GI and antispasmodic, reduce hyper-motility states in the bladder - DUCT - Ipratropium (Atrovent) is used to treat chronic obstructive pulmonary disease - Scopolamine (Scopace) use is limited to prevention of motion sickness and blocking short term memory
45
Q

DUCT

A
  • Dry Eyes and Mouth - Urinary retentions - Constipation - Tachycardia - Often caused by drugs that block Acetylcholin
46
Q

Acetylcholinesterase Inhibitors - Alzheimer’s

A
  • The most common neurodegenerative disease (2/3 of dementia) - Irreversible loss of neurons-cerebral cortex and hippocampus - The cause and progression of Alzheimer’s are not well understood - Research indicates that the disease is associated with plaques and tangles in the brain
47
Q

Alzheimer’s Disease

A
  • Has been identified as a protein misfolding disease caused by accumulation of abnormally folded A-beta and tau proteins in the brain - There is no cure, Available treatments offer small symptomatic benefit but remain palliative in nature - Current treatments can be divided into pharmaceutical, psychosocial and care-giving
48
Q

Acetylcholinesterase Inhibitors

A
  • Are employed to reduce the rate at which acetylcholine (ACh) is broken down, thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons
49
Q

Treat Alzheimer’s

A
  • Cholinesterase inhibitors such as Donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon) are approved for treatment - There is efficacy in mild to moderate ALZ’s and some evidence for their use in advanced stage
50
Q

Aricept - Alzheimer’s

A
  • Improves the function of nerve cells in the brain - Works by preventing the breakdown of acetylcholine which is important for the processes of memory, thinking, and reasoning
51
Q

Cholinergic drugs act on

A
  • receptors that are activated by acetylcholine
52
Q

Adrenergic drugs act on

A
  • receptors that are stimulated by NE or EPI
53
Q

Cholinergic or Adrenergic drugs work by

A
  • Stimulating or blocking neurons of the autonomic nervous system
54
Q

Reversed Prompt

  • Drugs that effect the ANS are divided into 2 subgroups - Are classified based on the type of neuron involved - These drugs either stimulate or block neurons of ANS
A

Cholinergic and Adrenergic Drugs

55
Q

Reversed Prompt

  • Act on receptors that are activated by Acetylcholine
A

Cholinergic Drugs

56
Q

Reversed Prompt

  • Act on receptors that are stimulated by norepinephrine or epinephrine
A

Adrenergic Drugs

57
Q

Reversed Prompt

  • Drugs that act directly on receptors
A

Sympathomimetic

58
Q

Reversed Prompt

  • Drugs that block the action ro by interrupting the release of NE or EPI
A

Adrenergic Drugs and NE (norepinephrine), EPI (Epinephrine)

59
Q

Reversed Prompt

  • Release NE as a Neurotransmitter and are found in the CNS also in the Sympathetic nervous system
A

Adrenergic Neurons

60
Q

Reversed Prompt

  • Tyrosine is transported by NA linked into the adrenergic neuron - Hydroxylated into DOPA (dihydroxyphenylalanine) by tyrosine hydroxylase which is the rate-limiting step in the formation of NE - DOPA is decarboxylated to form dopamine - Dopamine is transported into synaptic vesicles - Dopamine is hydroxylated into NE by dopamine hydroxylase - In the adrenal medulla NE is converted into EPI
A

Synthesis of NE (Norepinephrine):

61
Q

Reversed Prompt

  • Upon stimulation the adrenal medulla releases 85% EPI and 15% NE - Binding by receptor: NE will bind post and presynaptic - Removal of NE: catechol O methyltransferase (COMT) will metabolize NE or by reuptake which can be inhibited by TCAs or Cocaine - MAO will deactivate NE - inactive products of NE are excreted in the urine
A

Adrenergic

62
Q

Reversed Prompt

  • Vasoconstriction, increased peripheral resistance, increased blood pressure, mydriasis, increased closure of internal sphincter of the bladder
A

Adrenergic Alpha 1

63
Q

Reversed Prompt

  • Inhibition of NE release, inhibition of insulin release
A

Adrenergic Alpha 2

64
Q

Reversed Prompt

  • Tachycardia, increased lipolysis, increased myocardial contractility
A

Adrenergic Beta 1

65
Q

Reversed Prompt

  • Vasodilation, slightly decreased peripheral resistance, bronchodilation, increased muscles and liver glycogenolysis, increased release of glucagon, relaxed uterine smooth muscles
A

Adrenergic Beta 2

66
Q

Reversed Prompt

  • EPI, NE, DA, Dobutamine, Phenlephrine
A

Adrenergic Alpha 1 Agonist

67
Q

Reversed Prompt

  • Phenotolamine, Prazosin
A

Adrenergic Alpha 1 Blocker

68
Q

Reversed Prompt

  • EPI, NE, DA, Dobutamine, Isoproterenol
A

Adrenergic Beta 1 Agonist

69
Q

Reversed Prompt

  • Propranolol, Metoprolol, Atenolol
A

Adrenergic Beta 1 Blocker

70
Q

Reversed Prompt

  • EPI, DA, Dobutamine, Isoproterenol, Albuterol
A

Adrenergic Beta 2 Agonist

71
Q

Reversed Prompt

  • Propranolol
A

Adrenergic Beta 2 Blocker

72
Q

Reversed Prompt

  • Hypotension - Bronchospasm - Nasal Decongestant - Ophthalmic
A

Clinical Uses - Epinephrine

73
Q

Reversed Prompt

  • Decompensated Congestive Heart Failure - Hypotension - Renal Perfusion
A

Clinical Uses - Dopamine

74
Q

Reversed Prompt

  • Congestive Heart Failure
A

Clinical Uses - Dobutamine

75
Q

Reversed Prompt

  • Coronary Artery Disease - Peptic Ulcer
A

Clinical Uses - Phentolamine

76
Q

Reversed Prompt

  • Nasal Decongestant
A

Clinical Uses - Phenylephrine

77
Q

Reversed Prompt

  • Hypertension - Benign Prostatic Hyperplasia
A

Clinical Uses - Prazosin

78
Q

Reversed Prompt

  • Antihypertensive - Opiod Withdrawal - Antidiarrheal in diabetic patients W/Autonomic Neuropathy
A

Clinical Uses - Clonodine

79
Q

Reversed Prompt

  • Arrhythmias - Chronic CHF
A

Clinical Uses - Metoprolol

80
Q

Reversed Prompt

  • Ischemic Heart Disease - Hypertension - Arrhythmias - Essential Tremors - Stage Fright - Migraine Precention
A

Clinical Uses - Propranolol

81
Q

Reversed Prompt

  • Bronchospasm - Asthma - Bronchitis - COPD
A

Clinical Uses - Alcuterol

82
Q

Reversed Prompt

  • Potentiates NE by blocking repute of catecholamines - Clinical use – Surface anesthesia
A

Clinical Uses - Indirect Sympathomimetic - Cocaine

83
Q

Reversed Prompt

  • Stimulates release of NE from sympathetic neurons - Clinical use – nasal decongestion, orthostatic hypotension, promotes urinary continence
A

Clinical Uses - Indirect Sympathomimetic - Ephidrine

84
Q

Reversed Prompt

  • After presynaptic uptake this agent causes the release of endogenous NE - Clinical use – ADHD, Obesity, Narcolepsy
A

Clinical Uses - Indirect Sympathomimetic - Amphetamine

85
Q

Reversed Prompt

  • AcH released from the synaptic vesicles diffuses across the synaptic space and binds to either postsynaptic receptors on the target cell or to presynaptic receptors in the membrane of the neuron that released the AcH
A

Cholinergic Neuron - AcH

86
Q

Reversed Prompt

  • Occurs in the synaptic cleft by acetylcholinesterase
A

Cholinergic Neuron - Degradation of Acetylcholine

87
Q

Reversed Prompt

  • Occurs by a uptake system that transport the molecule back into the neuron, is acetylated and stored until released by action potential
A

Cholinergic Neuron - Recycling of Choline

88
Q

Reversed Prompt

  • Muscarinic Receptors - Nicotine Receptors
A

2 types of Cholinoceptors

89
Q

Reversed Prompt

  • Bind AcH and muscarine (poisonous mushrooms) weak affinity for nicotine - Found on ganglia of the PNS and autonomic effector organs (heart, smooth muscles, brain) also on gastric parietal cells
A

Cholinergic Neuron - Muscarinic Receptors

90
Q

Reversed Prompt

  • Depolarizes ganglia, first effects are stimulating followed by paralysis of all ganglia - First effects increase blood pressure and cardiac rate due to release of transmitter for adrenergic terminals and from the adrenal medulla - Increase peristalsis and secretions
A

Cholinergic Neuron - Nicotine

91
Q

Reversed Prompt

  • A neurotransmitter involved in learning and memory - Glutamate enhances the connections between sets of neurons. These stronger connections mat be the physical basis of what we know as memory - When you use nicotine, glutamate may create a memory loop of the good feelings you get and further drive the desire to use nicotine - Nicotine also increases the level of other neurotransmitters and chemicals that modulate how your brain works. For example, your brain makes more endorphins in response to nicotine
A

Nicotine Stimulation - Release of Glutamate

92
Q

Reversed Prompt

  • Are small proteins that are often called the body’s natural pain killer - It turns out that the chemical structure of endorphins is very similar to that of heavy-duty synthetic painkillers like morphine - Can lead to feelings of euphoria - “runners high” = endorphin rush, this outpouring of chemicals gives you a mental edge to finish the race while temporarily masking the nagging pains you might otherwise feel
A

Nicotine stimulation - Endorphins

93
Q

Reversed Prompt

  • Binds to nicotine receptors and blocks them so that nicotine can no longer activate those receptors - This means that when someone is trying to quit and they lapse and smoke they probably won’t get much satisfaction from it and will be less likely to smoke another
A

Chantix Anti-smoking Med

94
Q

Reversed Prompt

  • It triggers some of the same effects that nicotine has (an “agonist” effect) - This includes a small release of dopamine, the reward neurotransmitter in the brain - In this way chantix dampens down nicotine withdrawal symptoms and cravings
A

Chantix - Secondary mechanism

95
Q

Reversed Prompt

  • Inhibition of Aceytlcholinesterase at the skeletal neuromuscular junction causes the accumulation of acetylcholine and ultimately results in paralysis of skeletal muscles
A

Cholinergic Neuron - Inhibition of Acetylcholinesterase

96
Q

Reversed Prompt

  • An autoimmune disorder caused by antibody-mediated loss of AcH receptors in the neuromuscular junction-impacting transmission between neuron and muscle - Neostigmine and Pyridostigmine are used to treat Myasthenia Gravis
A

Myasthenia Gravis

97
Q

Reversed Prompt

  • Atropine has affinity for muscarinic receptors and acts on CNS and PNS, Used to dilate pupils, GI and antispasmodic, reduce hyper-motility states in the bladder - DUCT - Ipratropium (Atrovent) is used to treat chronic obstructive pulmonary disease - Scopolamine (Scopace) use is limited to prevention of motion sickness and blocking short term memory
A

Cholinergic Neuron - Antimuscarinic

98
Q

Reversed Prompt

  • Dry Eyes and Mouth - Urinary retentions - Constipation - Tachycardia - Often caused by drugs that block Acetylcholin
99
Q

Reversed Prompt

  • The most common neurodegenerative disease (2/3 of dementia) - Irreversible loss of neurons-cerebral cortex and hippocampus - The cause and progression of Alzheimer’s are not well understood - Research indicates that the disease is associated with plaques and tangles in the brain
A

Acetylcholinesterase Inhibitors - Alzheimer’s

100
Q

Reversed Prompt

  • Has been identified as a protein misfolding disease caused by accumulation of abnormally folded A-beta and tau proteins in the brain - There is no cure, Available treatments offer small symptomatic benefit but remain palliative in nature - Current treatments can be divided into pharmaceutical, psychosocial and care-giving
A

Alzheimer’s Disease

101
Q

Reversed Prompt

  • Are employed to reduce the rate at which acetylcholine (ACh) is broken down, thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons
A

Acetylcholinesterase Inhibitors

102
Q

Reversed Prompt

  • Cholinesterase inhibitors such as Donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon) are approved for treatment - There is efficacy in mild to moderate ALZ’s and some evidence for their use in advanced stage
A

Treat Alzheimer’s

103
Q

Reversed Prompt

  • Improves the function of nerve cells in the brain - Works by preventing the breakdown of acetylcholine which is important for the processes of memory, thinking, and reasoning
A

Aricept - Alzheimer’s

104
Q

Reversed Prompt

  • receptors that are activated by acetylcholine
A

Cholinergic drugs act on

105
Q

Reversed Prompt

  • receptors that are stimulated by NE or EPI
A

Adrenergic drugs act on

106
Q

Reversed Prompt

  • Stimulating or blocking neurons of the autonomic nervous system
A

Cholinergic or Adrenergic drugs work by

Psychopharmacology (4 decks)

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