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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
Q

What effects does SNS have

A
  • 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
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26
Q

Is the SNS essential for life?

A

NO

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27
Q

Is the PNS essential for life?

A

YES

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28
Q

What response does the PNS have

A

Rest and digest

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29
Q

What is the reflex response

A

Response from the efferent impulses of ANS

It does not involve consciousness

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30
Q

What is an example of the reflex response

A

Baroreceptors in the heart

That sense BP

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31
Q

T/F strong emotion can modify the activity of the ANS

A

True

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32
Q

What is dual innervation

A

Organs in the body are innervated by both divisions of the ANS

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33
Q

What organs receive ONLY sympathetic innervation?

A

Blood vessels
Adrenal medulla
Sweat glands

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34
Q

What are the sympathetic actions of the eye

A

Contraction of iris radial muscle

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35
Q

What are the parasympathetic actions of the eye

A
  • Contraction of the IRS sphincter

- contraction of ciliary muscle

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36
Q

What are the sympathetic actions of the trachea and bronchioles

A

Dilates

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37
Q

What are the parasympathetic actions of the trachea and bronchioles

A

Constricts and increases secretions

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38
Q

What are the sympathetic actions of the heart

A

Increased heart rate

Increased contractility

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39
Q

What are the parasympathetic actions of the heart

A

Decreased heart rate

Decreased contractility

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40
Q

What are the sympathetic actions of the blood vessels

A

Dilation and constriction

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41
Q

What NT are important to the ANS

A

ACh
NE
Epi

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42
Q

What are the steps of neurotransmission of Cholinergic neurons

A
  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
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43
Q

What is the rate limiting stop of ACh synthesis

A

The uptake of choline into the cell

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44
Q

What does release of ACh do to the membrane

A

Depolarizes it. Opens up Ca2+ channels allowing the vesicles to move towards the membrane

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45
Q

What step do Botox and spider venom affect?

A

The release of ACh

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46
Q

Does Botox inhibit or increase release of ACh

A

Inhibit

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47
Q

Does spider venom inhibit or increase ACh release

A

Increase

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48
Q

What are the negative feedback inhibitory receptors for epinephrine

A

a2, B2,

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49
Q

What are the negative feedback nicotinic receptors

A

M2

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50
Q

What are the negative feedback receptors for dopamine

A

D2

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51
Q

Where are M1 receptors found

A

CNS

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52
Q

Where are M2 receptors found

A

Heart

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53
Q

Where are M3 receptors found

A

All organs and some sweat glands

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54
Q

What receptors are Gq

A

M1, 3, 5

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55
Q

What are Gi receptors

A

M2, 4

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56
Q

What are muscarinic agonists (not examples)

A

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

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57
Q

What are the M agonist drugs (5)

A 
Bethanechol
Carbachol
Methacholine
Pilocarpine
Cevimeline
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58
Q

What receptor is found in the GI system

A

M3

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59
Q

What affect do M agonists have on the GI system

A

Increase tone
Increase amplitude of contractions
Increase peristaltic contractions
Increase secretions

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60
Q

What are some side effects of M agonists on the GI system

A

N/V
Belching
Cramps
Defecation

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61
Q

What receptors are in the urinary tract

A

M3

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62
Q

What affects do M agonists have on urinary tract

A 
Increase peristalsis
Contract detrusor muscle
Relax the trigone and sphincter muscles 
Increase voiding
Decrease capacity of the bladder
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63
Q

What receptors are found in the heart

A 
M2 
And M3 (no known function)
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64
Q

What receptors are found on blood vessels

A

Alpha 1
Beta 2
M 3

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65
Q

What blood vessel receptor is innervated

A

Alpha 1

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66
Q

Epineprhine activates what blood vessel receptors

A

Alpha 1 and beta 2

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67
Q

What activates M3 receptors on blood vessels

A

It cannot be physiologically activated, but it can be pharmacologically activated

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68
Q

Bethanechol is used to stimulate what system

A

GI tract and bladder

“Bowels and bladder”

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69
Q

What is methacholine used for

A

Bronchoconstriction

Is used to diagnose asthma

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70
Q

What is pilocarpine used for

A

Glaucoma

And xerostoma

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71
Q

What is xerostomia

A

Difficulty swallowing because they have low saliva, they are very dry.
Occurs with radiation treatments and Sjögren’s syndrome

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72
Q

What does glaucoma treatment involve

A

Decreasing the production of aqueous

Increase the drainage of aqueous

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73
Q

What effect do muscarinic agonists have on aqueous

A

Increase drainage

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74
Q

What are some toxicity side effects of M agonists

A 
Mitosis
Bradycardia
Bronchoconstriction 
Increase gastric acid production
Diarrhea
Increase urination
Flushing
Salivation
Lacrimation
Sweating
75
Q

Are M agonists given locally or systemically?

A

Locally/topically

76
Q

What is given to treat M angst toxicity reactions

A

Atropine sulfate (M antagonist)

Epinephrine

77
Q

What are AChase inhibitors

A

They are competitive, therapeutically useful

78
Q

What are some AChase inhibitors

A 
Physostigmine
Pyridostigmine
Neostigmine
Edrophonium 
Donepezil
79
Q

What does physostigmine do

A

It is a tertiary amine so it can enter the CNS

Used for treatment of ACh toxicity

80
Q

What is pyridostigmine and neostigmine used for

A

To treat MG
Reversal of non-depolarizing blocking agents

Quaternary amines

81
Q

What is edrophonium used for

A

Diagnosis of MG
Has a short half life
Rapid increase of muscle strength

82
Q

What receptor does MG affect

A

The antibodies attack Nm

83
Q

What is donepezil used for

A

To treat mild-moderate Alzheimer’s

Can enter the CNS

84
Q

What causes Alzheimer’s

A

Loss of neurons in the cortex

Disproportionate loss of cholinergic neurons

85
Q

What are some ACHase inhibitors

A

Sarin
And nerve agents

Parathion and malathion (organophosphates)

86
Q

What is used to treat ACH inhibitor overdose

A

A chemical reacivator

Pralidoxime (PAM)

87
Q

What are toxicity symptoms of AChase inhibitors

A 
DUMBBEELSS
Diarrhea
Urination
Mitosis
Bradycardia
Bronchoconstriction
Excitation of CNS and skeletal M
Emesis
Lacrimation
Salivation
Sweating
88
Q

What is treatment for AChase inhibitors

A

Atropine

+pralidoxime in severe exposure

89
Q

What are antimuscarinic agents

A

Selective for muscarinic recptors

But they are not selective

90
Q

What affects does atropine have

A

Belladonna
Block M receptors in CNS and PNS

Tertiary amine
Half life is 2 hours
Except in the eye (72 hours)

91
Q

What is the mechanism of action of antimuscarinic agents

A

Competitive antagonists at M receptors

Overcome with addition of M agonists or AChase inhibitors

92
Q

Look at table on page 22

A

Effects of M blockers

93
Q

What are the ocular uses of M blockers

A

Dilate pupil
Paralyze accommodation

Atropine
Homatropine
Cyclopentolate
Tropicamide

94
Q

What are the CNS uses of M blockers

A

Scopolamine for motion sickness

DOPA fro Parkinson’s

95
Q

What causes Parkinson’s

A

Loss of D neurons

Dopamine is too low ACh is too high

96
Q

What are the bronchial uses of M blockers

A

Asthmas and COPD

97
Q

What bladder uses for M blockers

A

Tolterodine
Oxybutynin

They reduce urgency

98
Q

What are the symptoms of M antagonist toxicity

A 
Dry as a bone
Red as a beet
Hot as a pistol
Mad as a hatter
Blind as a bat
99
Q

Atropine causes fever what is this lethal in

A

Infants

100
Q

When is acute angle closure glaucoma dangerous in

A

Elderly

101
Q

What are the steps of norepinephrine usage

A

Synthesis
Storage
Release
Binding/metabolized/reuptake/negative feedback

102
Q

What are the steps of Ne production

A

Tyrosine
DOPA
Dopamine
Norepinephrine

103
Q

What is the rate limiting step in the formation of Ne

A

The conversions of tyrosine to DOPA

104
Q

How is Ne stored

A

Dopamine is transported into vesicle where it is converted to Ne

It is protected from degradation in the vesicle

105
Q

What causes the release of Ne

A

AP causes membrane depolarization

Ca channels open
Ca moves into the cell
Vesicle fuses with the membrane

106
Q

What are the fates of NE

A

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
Q

What inhibits the reuptake of Ne

A

Cocaine

108
Q

A1 receptors are G_

A

Gq

109
Q

A2 receptors are G_

A

Gi

110
Q

B receptors are G_

A

Gs

111
Q

What are Epi, NE, and DOPA?

A

Catecholamines

112
Q

What metabolizes Epi, NE, and DOPA

A

COMT

MAO

113
Q

Why doe Epi, NE, and DOPA have a short half life

A

The are rapidly metabolized by COMT and MOA

114
Q

A1 affects what organs

A

BV
Radial muscle (iris)
Prostate

115
Q

What receptor is on the prostate

A

A1a

116
Q

What affect do A1 have on BV

A

Vasoconstriction
Increase TPR
Increase BP

117
Q

What affect does A1 have on pupil

A

Dilates

118
Q

What affect does A1 have on prostate

A

Decrease urine output

119
Q

What organs are affected by A2

A

Adrenergic nerve terminals

Pancreatic B cells

120
Q

What affect do A2 have on adrenergic nerve terminals

A

Inhibit transmitter release

121
Q

What affect do A2 have on pancreatic B cells

A

Inhibits insulin release

122
Q

What organs are affected by B1

A

Heart

JGA

123
Q

What affects are B1 on the heart

A

Stimulates rate and force

124
Q

What affect do B1 have on JGA

A

Stimulates renin release

Increase RAAS

125
Q

What organs does B2 affect

A

Lung/uterus/BV
Liver
Skeletal muscle

126
Q

Are B2 innervated? What activates them

A

NO

Epi activates them

127
Q

What affect does B2 have on lung/uterus/BV

A

Relaxes
Bronchodilate
Uterine contraction

128
Q

What affect do B2 have on liver

A

Glycogenolysis

129
Q

What affect does B2 have on skeletal muscle

A

Causes a tremor

130
Q

What organ does B3 affect

A

Fat cells

131
Q

What does B3 do to fat cells

A

Stimulate lipolysis

132
Q

What organ does D1 affect

A

Renal and splacnhnic BV

133
Q

What affect does D1 have on renal and splanchnic BV

A

Vasodilation

134
Q

Do catecholamines enter the CNS?

A

No

135
Q

What affect does A1 have on GU tract

A

Contraction of bladder sphincter

136
Q

What do B3 do to BU system

A

Relax detrusor

137
Q

What does A1 agonist do to BV

A

Increase vascular resistance and venous pressure

Can cause compensatory reflex bradycardia

138
Q

If you have a low BP what happens to HR

A

Increases

139
Q

If you have a high BP what does it do to HR

A

Decrease

140
Q

T/F A2 agonist accumulates in the CNS

A

True

141
Q

What do B2 agonists reduce

A

Peripheral vascular resistance

142
Q

Where do baclofen, tizanidine, and diazepam work

A

In the CNS

143
Q

Where does dantrolene work

A

At the muscle

144
Q

Where does Botox work

A

At the neuromuscular junction

145
Q

What happens when you block the endplate at NMJ

A

It causes muscle relaxation

146
Q

What is muscle relaxation important for

A

Surgical relaxation
Tracheal intubation
Control of ventilation

147
Q

What if the steps of a muscle contraction

A
  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
Q

What receptors are at the NMJ

A

Nm

149
Q

What are the nondepolarizing NM blocking Drugs

A 
TuboCURarine
AtraCURium
PanCURonium 
VeCURonium
RoCURonium
CisatraCURium
150
Q

How do Nicotinic antagonist-competitive antagonists (nondepolarizing) work?

A

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
Q

How are nonpolarization NM blockers reversed

A

AChase inhibitors

152
Q

What is the down side to non-depolarizations NM blocking drugs

A

They do not cause analgesia

They can still feel pain and hear/see they just cant move

153
Q

What does atraCURium clearance involve

A

Rapid breakdown to form laudanosine

Which can cause seizures

154
Q

What is the most common muscle relaxant in clinic

A

CistraCURium

155
Q

What is the duration of action of nondepolarizing NM blocking drugs

A

Long acting
More potent
Low concentration doses

156
Q

What drugs can be used to reverse non-depolarizing NM blockers

A

ACHase inhibitors
Neostigmine
Sugammadex

157
Q

What does sugammadex work on

A

RoCURonium

VeCURonium

158
Q

What drugs are depolarizing NM blockers

A

Succinylcholine

159
Q

How does succinylcholine work

A

It is an analogue of ACh that stimulates al cholinergic receptors
Leads to transient fasiculations after muscle paralysis
Prevents muscle contraction

160
Q

What can succinylcholine cause

A

Hyperkalemia

161
Q

What breaks down succinylcholine

A

Psuedocholinesterase

162
Q

Who do you NOT want to use succinylcholine on

A

Inherited myopathies
Burns (72 hours)
Crash, injuries (72hours)

163
Q

Why is it better to overestimate the dose of succinylcholine

A

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
Q

Who is succinylcholine ABSOLUTELY contraindicated in

A

Patients with personal or family history of malignant hyperthermia
And patients at high risk of developing severe hyperkalemia

165
Q

What can atropine be used for?

A

Rescue medication if bradycardia occurs

166
Q

What is malignant hyperthermia

A

A myopathy metabolic disorder that is characterized by sympathetic hyperactivity, muscular rigidity, acidosis, hyperthermia

167
Q

What are the 2 phases of the reversal blockade

A
  1. Depolarization, fasculation, prolong depolarization, flaccid paralysis
  2. Desensitization
168
Q

What phases is affected by ACHase inhibitors

A

Phase 1 increased

May reverse phase 2

169
Q

GABAa is ______ channel

A

Ligand gated

170
Q

GABAb is ______ channel

A

G coupled

171
Q

Benzodiazepines work through

A

GABAa receptors

172
Q

Baclofen works through

A

GABAb receptors

173
Q

What are spasmolytic drugs

A

They dont look like ACh in structure or effect

Act in CNS and sometimes skeletal muscle

174
Q

Where do baclofen, diazepam, and tizanidine work

A

Spinal cord

175
Q

What do spasmolytics reduce

A

Excess muscle tone or spasm in injury of DNS dysfunction

176
Q

What is the MOA of diazepam

A

Reduces neuronal depolarization
Decreases AP
Tightly binds GABAa, and increases the frequency of Cl channels opening

177
Q

What are the uses and side effects of diazepam

A

Uses: muscle spasms

side effects: drowsiness, confusion, fatigue

178
Q

What is the MOA of baclofen

A

Activates GABAb in Shona cord

Muscle relaxtion

179
Q

What are the uses and side effects of baclofen

A

Use muscle spasm

Side effects: drowsiness, confusion, fatigue

180
Q

What is the MOA of tizanidine

A

Alpha 2 agonist

Reduces spasticity

181
Q

What are the side effects of tizanidine

A

Drowsiness, dizziness

182
Q

What is the MOA of skeletal muscle

A

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
Q

What is the MOA of botulinum toxin A

A

Prevents the release of ACh release at the NMJ
Temporary paralysis
Reduces pain caused by severe pain

184
Q

Are baclofen, diazepam, dantrolene, and Botox used in acute or chronic spasms?

A

Chronic

Pharmacology (4 decks)

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