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Pharmacology > Block 10 > Flashcards

Block 10 Flashcards

1
Q

The CNS includes

A

Brain

Spinal cord

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2
Q

The PNS includes

A

Nerves that leave and enter the CNS

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3
Q

Where is the cell body located in a pre-ganglionic neuron located?

A

CNS

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4
Q

Where does the post-ganglionic neuron orginate

A

In the ganglia

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5
Q

Sympathetic originates from what region of the spinal cord

A

Thoracolumbar

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6
Q

What region of the spinal sword does the PNS originate from?

A

Craniosacral

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7
Q

Cholinergic nerves release what kind NT

A

ACh

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8
Q

Adrenergic nerves release what NT

A

NE

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9
Q

Dopaminergic nerves release what NT

A

Dopamine

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10
Q

What are cholinergic receptors?

A

Nn
Nm
M

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11
Q

What are adrenergic receptors?

A

Alphas and betas

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12
Q

What are dopaminergic receptors?

A

D1

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13
Q

Where are parasympathetic muscarinic receptors found

A

Cardiac and smooth muscle
Gland cells
Nerve terminals

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14
Q

Where are sympathetic muscarinic receptors found?

A

Sweat glands

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15
Q

Where are sympathetic alpha and beta receptors found?

A

Cardiac and smooth muscle
Gland cells
Nerve terminals

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16
Q

Where are sympathetic dopaminergic receptors found?

A

Renal vascular

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17
Q

What does the adrenal medulla act as?

A

A ganglia

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18
Q

What does the adrenal medulla release?

A

Epi and NE into the blood

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19
Q

Where are somatic nicotinic receptors found?

A

Skeletal muscle

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20
Q

Pre-ganglionic PNS neurons are ________

A

Long

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21
Q

Post-ganglionic PNS nerves are

A

Short

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22
Q

Pre-ganglionic SNS nerves are

A

Short

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23
Q

Post-ganglionic SNS nerves are

A

Long

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24
Q

SNS has what response

A

Fight or flight

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25
What effects does SNS have
- Increases HR and BP - Increase blood flow to skeletal muscles and heart - mobilizes energy stores - decreases blood flow to skin and internal organs - dilates pupils - dilates bronchioles
26
Is the SNS essential for life?
NO
27
Is the PNS essential for life?
YES
28
What response does the PNS have
Rest and digest
29
What is the reflex response
Response from the efferent impulses of ANS It does not involve consciousness
30
What is an example of the reflex response
Baroreceptors in the heart That sense BP
31
T/F strong emotion can modify the activity of the ANS
True
32
What is dual innervation
Organs in the body are innervated by both divisions of the ANS
33
What organs receive ONLY sympathetic innervation?
Blood vessels Adrenal medulla Sweat glands
34
What are the sympathetic actions of the eye
Contraction of iris radial muscle
35
What are the parasympathetic actions of the eye
- Contraction of the IRS sphincter | - contraction of ciliary muscle
36
What are the sympathetic actions of the trachea and bronchioles
Dilates
37
What are the parasympathetic actions of the trachea and bronchioles
Constricts and increases secretions
38
What are the sympathetic actions of the heart
Increased heart rate | Increased contractility
39
What are the parasympathetic actions of the heart
Decreased heart rate | Decreased contractility
40
What are the sympathetic actions of the blood vessels
Dilation and constriction
41
What NT are important to the ANS
ACh NE Epi
42
What are the steps of neurotransmission of Cholinergic neurons
1. Synthesis of ACh 2. Storage of ACh in vesicles 3. Release of ACh 4a. ACh bind to receptors on postsynaptic neuron 4b. Degradation of ACh by AChase 4c. Choline binds to receptor on pre-synaptic neuron
43
What is the rate limiting stop of ACh synthesis
The uptake of choline into the cell
44
What does release of ACh do to the membrane
Depolarizes it. Opens up Ca2+ channels allowing the vesicles to move towards the membrane
45
What step do Botox and spider venom affect?
The release of ACh
46
Does Botox inhibit or increase release of ACh
Inhibit
47
Does spider venom inhibit or increase ACh release
Increase
48
What are the negative feedback inhibitory receptors for epinephrine
a2, B2,
49
What are the negative feedback nicotinic receptors
M2
50
What are the negative feedback receptors for dopamine
D2
51
Where are M1 receptors found
CNS
52
Where are M2 receptors found
Heart
53
Where are M3 receptors found
All organs and some sweat glands
54
What receptors are Gq
M1, 3, 5
55
What are Gi receptors
M2, 4
56
What are muscarinic agonists (not examples)
They mimic the actions of ACh it have a longer half life.(because they are not metabolized by ACHase to the same extent) They have parasympathetic effects and sweating
57
What are the M agonist drugs (5)
``` Bethanechol Carbachol Methacholine Pilocarpine Cevimeline ```
58
What receptor is found in the GI system
M3
59
What affect do M agonists have on the GI system
Increase tone Increase amplitude of contractions Increase peristaltic contractions Increase secretions
60
What are some side effects of M agonists on the GI system
N/V Belching Cramps Defecation
61
What receptors are in the urinary tract
M3
62
What affects do M agonists have on urinary tract
``` Increase peristalsis Contract detrusor muscle Relax the trigone and sphincter muscles Increase voiding Decrease capacity of the bladder ```
63
What receptors are found in the heart
``` M2 And M3 (no known function) ```
64
What receptors are found on blood vessels
Alpha 1 Beta 2 M 3
65
What blood vessel receptor is innervated
Alpha 1
66
Epineprhine activates what blood vessel receptors
Alpha 1 and beta 2
67
What activates M3 receptors on blood vessels
It cannot be physiologically activated, but it can be pharmacologically activated
68
Bethanechol is used to stimulate what system
GI tract and bladder "Bowels and bladder"
69
What is methacholine used for
Bronchoconstriction Is used to diagnose asthma
70
What is pilocarpine used for
Glaucoma | And xerostoma
71
What is xerostomia
Difficulty swallowing because they have low saliva, they are very dry. Occurs with radiation treatments and Sjögren's syndrome
72
What does glaucoma treatment involve
Decreasing the production of aqueous | Increase the drainage of aqueous
73
What effect do muscarinic agonists have on aqueous
Increase drainage
74
What are some toxicity side effects of M agonists
``` Mitosis Bradycardia Bronchoconstriction Increase gastric acid production Diarrhea Increase urination Flushing Salivation Lacrimation Sweating ```
75
Are M agonists given locally or systemically?
Locally/topically
76
What is given to treat M angst toxicity reactions
Atropine sulfate (M antagonist) Epinephrine
77
What are AChase inhibitors
They are competitive, therapeutically useful
78
What are some AChase inhibitors
``` Physostigmine Pyridostigmine Neostigmine Edrophonium Donepezil ```
79
What does physostigmine do
It is a tertiary amine so it can enter the CNS Used for treatment of ACh toxicity
80
What is pyridostigmine and neostigmine used for
To treat MG Reversal of non-depolarizing blocking agents Quaternary amines
81
What is edrophonium used for
Diagnosis of MG Has a short half life Rapid increase of muscle strength
82
What receptor does MG affect
The antibodies attack Nm
83
What is donepezil used for
To treat mild-moderate Alzheimer's | Can enter the CNS
84
What causes Alzheimer's
Loss of neurons in the cortex | Disproportionate loss of cholinergic neurons
85
What are some ACHase inhibitors
Sarin And nerve agents Parathion and malathion (organophosphates)
86
What is used to treat ACH inhibitor overdose
A chemical reacivator | Pralidoxime (PAM)
87
What are toxicity symptoms of AChase inhibitors
``` DUMBBEELSS Diarrhea Urination Mitosis Bradycardia Bronchoconstriction Excitation of CNS and skeletal M Emesis Lacrimation Salivation Sweating ```
88
What is treatment for AChase inhibitors
Atropine | +pralidoxime in severe exposure
89
What are antimuscarinic agents
Selective for muscarinic recptors | But they are not selective
90
What affects does atropine have
Belladonna Block M receptors in CNS and PNS Tertiary amine Half life is 2 hours Except in the eye (72 hours)
91
What is the mechanism of action of antimuscarinic agents
Competitive antagonists at M receptors Overcome with addition of M agonists or AChase inhibitors
92
Look at table on page 22
Effects of M blockers
93
What are the ocular uses of M blockers
Dilate pupil Paralyze accommodation Atropine Homatropine Cyclopentolate Tropicamide
94
What are the CNS uses of M blockers
Scopolamine for motion sickness | DOPA fro Parkinson's
95
What causes Parkinson's
Loss of D neurons | Dopamine is too low ACh is too high
96
What are the bronchial uses of M blockers
Asthmas and COPD
97
What bladder uses for M blockers
Tolterodine Oxybutynin They reduce urgency
98
What are the symptoms of M antagonist toxicity
``` Dry as a bone Red as a beet Hot as a pistol Mad as a hatter Blind as a bat ```
99
Atropine causes fever what is this lethal in
Infants
100
When is acute angle closure glaucoma dangerous in
Elderly
101
What are the steps of norepinephrine usage
Synthesis Storage Release Binding/metabolized/reuptake/negative feedback
102
What are the steps of Ne production
Tyrosine DOPA Dopamine Norepinephrine
103
What is the rate limiting step in the formation of Ne
The conversions of tyrosine to DOPA
104
How is Ne stored
Dopamine is transported into vesicle where it is converted to Ne It is protected from degradation in the vesicle
105
What causes the release of Ne
AP causes membrane depolarization Ca channels open Ca moves into the cell Vesicle fuses with the membrane
106
What are the fates of NE
It can bind to the receptor on organ It can be metabolized into an inactive form Reuptake in the neuron Can bind to the neuron for negative feedback
107
What inhibits the reuptake of Ne
Cocaine
108
A1 receptors are G_
Gq
109
A2 receptors are G_
Gi
110
B receptors are G_
Gs
111
What are Epi, NE, and DOPA?
Catecholamines
112
What metabolizes Epi, NE, and DOPA
COMT | MAO
113
Why doe Epi, NE, and DOPA have a short half life
The are rapidly metabolized by COMT and MOA
114
A1 affects what organs
BV Radial muscle (iris) Prostate
115
What receptor is on the prostate
A1a
116
What affect do A1 have on BV
Vasoconstriction Increase TPR Increase BP
117
What affect does A1 have on pupil
Dilates
118
What affect does A1 have on prostate
Decrease urine output
119
What organs are affected by A2
Adrenergic nerve terminals | Pancreatic B cells
120
What affect do A2 have on adrenergic nerve terminals
Inhibit transmitter release
121
What affect do A2 have on pancreatic B cells
Inhibits insulin release
122
What organs are affected by B1
Heart | JGA
123
What affects are B1 on the heart
Stimulates rate and force
124
What affect do B1 have on JGA
Stimulates renin release | Increase RAAS
125
What organs does B2 affect
Lung/uterus/BV Liver Skeletal muscle
126
Are B2 innervated? What activates them
NO Epi activates them
127
What affect does B2 have on lung/uterus/BV
Relaxes Bronchodilate Uterine contraction
128
What affect do B2 have on liver
Glycogenolysis
129
What affect does B2 have on skeletal muscle
Causes a tremor
130
What organ does B3 affect
Fat cells
131
What does B3 do to fat cells
Stimulate lipolysis
132
What organ does D1 affect
Renal and splacnhnic BV
133
What affect does D1 have on renal and splanchnic BV
Vasodilation
134
Do catecholamines enter the CNS?
No
135
What affect does A1 have on GU tract
Contraction of bladder sphincter
136
What do B3 do to BU system
Relax detrusor
137
What does A1 agonist do to BV
Increase vascular resistance and venous pressure Can cause compensatory reflex bradycardia
138
If you have a low BP what happens to HR
Increases
139
If you have a high BP what does it do to HR
Decrease
140
T/F A2 agonist accumulates in the CNS
True
141
What do B2 agonists reduce
Peripheral vascular resistance
142
Where do baclofen, tizanidine, and diazepam work
In the CNS
143
Where does dantrolene work
At the muscle
144
Where does Botox work
At the neuromuscular junction
145
What happens when you block the endplate at NMJ
It causes muscle relaxation
146
What is muscle relaxation important for
Surgical relaxation Tracheal intubation Control of ventilation
147
What if the steps of a muscle contraction
1. AP is sent, inside becomes more positive and opens Ca channels 2. Ca comes in, activates vesicles, ACh released 3. ACh is released in gap 4. ACh binds to muscle, and Na channels open 5. Na moves into the muscle fiber 6. Na causes an AP, can muscle contracts
148
What receptors are at the NMJ
Nm
149
What are the nondepolarizing NM blocking Drugs
``` TuboCURarine AtraCURium PanCURonium VeCURonium RoCURonium CisatraCURium ```
150
How do Nicotinic antagonist-competitive antagonists (nondepolarizing) work?
They compete with ACh for receptors, they prevent ACh from working at the NMJ Can be overcome by increasing the amount of agonist in synaptic cleft
151
How are nonpolarization NM blockers reversed
AChase inhibitors
152
What is the down side to non-depolarizations NM blocking drugs
They do not cause analgesia | They can still feel pain and hear/see they just cant move
153
What does atraCURium clearance involve
Rapid breakdown to form laudanosine | Which can cause seizures
154
What is the most common muscle relaxant in clinic
CistraCURium
155
What is the duration of action of nondepolarizing NM blocking drugs
Long acting More potent Low concentration doses
156
What drugs can be used to reverse non-depolarizing NM blockers
ACHase inhibitors Neostigmine Sugammadex
157
What does sugammadex work on
RoCURonium | VeCURonium
158
What drugs are depolarizing NM blockers
Succinylcholine
159
How does succinylcholine work
It is an analogue of ACh that stimulates al cholinergic receptors Leads to transient fasiculations after muscle paralysis Prevents muscle contraction
160
What can succinylcholine cause
Hyperkalemia
161
What breaks down succinylcholine
Psuedocholinesterase
162
Who do you NOT want to use succinylcholine on
Inherited myopathies Burns (72 hours) Crash, injuries (72hours)
163
Why is it better to overestimate the dose of succinylcholine
Larger doses result in the same level of paralysis and do not increase the risk to the patient Inadequate doses can leave the patient inadequately paralyzed and difficult to incubate
164
Who is succinylcholine ABSOLUTELY contraindicated in
Patients with personal or family history of malignant hyperthermia And patients at high risk of developing severe hyperkalemia
165
What can atropine be used for?
Rescue medication if bradycardia occurs
166
What is malignant hyperthermia
A myopathy metabolic disorder that is characterized by sympathetic hyperactivity, muscular rigidity, acidosis, hyperthermia
167
What are the 2 phases of the reversal blockade
1. Depolarization, fasculation, prolong depolarization, flaccid paralysis 2. Desensitization
168
What phases is affected by ACHase inhibitors
Phase 1 increased May reverse phase 2
169
GABAa is ______ channel
Ligand gated
170
GABAb is ______ channel
G coupled
171
Benzodiazepines work through
GABAa receptors
172
Baclofen works through
GABAb receptors
173
What are spasmolytic drugs
They dont look like ACh in structure or effect Act in CNS and sometimes skeletal muscle
174
Where do baclofen, diazepam, and tizanidine work
Spinal cord
175
What do spasmolytics reduce
Excess muscle tone or spasm in injury of DNS dysfunction
176
What is the MOA of diazepam
Reduces neuronal depolarization Decreases AP Tightly binds GABAa, and increases the frequency of Cl channels opening
177
What are the uses and side effects of diazepam
Uses: muscle spasms side effects: drowsiness, confusion, fatigue
178
What is the MOA of baclofen
Activates GABAb in Shona cord | Muscle relaxtion
179
What are the uses and side effects of baclofen
Use muscle spasm Side effects: drowsiness, confusion, fatigue
180
What is the MOA of tizanidine
Alpha 2 agonist Reduces spasticity
181
What are the side effects of tizanidine
Drowsiness, dizziness
182
What is the MOA of skeletal muscle
Induces muscle relaxation by directly affecting the contractile response Prevents the release of Ca from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor
183
What is the MOA of botulinum toxin A
Prevents the release of ACh release at the NMJ Temporary paralysis Reduces pain caused by severe pain
184
Are baclofen, diazepam, dantrolene, and Botox used in acute or chronic spasms?
Chronic

Pharmacology (4 decks)

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