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Pharm Test 2 > 9/16 > Flashcards

9/16 Flashcards

1
Q

What are heteroreceptors?

A

A receptor on the neuron that responds to something that neuron is not releasing

i.e. a neuron releases norepinephrine, but has a receptor on it that acetylcholine binds to. ACh might slow down or speed up the release of norepinephrine

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2
Q

What are autoreceptors?

A

a receptor on a neuron that binds with the same neurotransmitter typically excreted by that neuron.
i.e. neuron normally releases norepinephrine, has a receptor that also binds with norepinephrine and increases or decreases the amount of norepinephrine released.

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3
Q

Positive feedback

A

Increases the effect already being produced

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4
Q

Negative feedback

A

Decreases the effect already being produced

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5
Q

What is the primary pacing node in the heart?

A

SA node

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6
Q

What is the sympathetic activity on the heart at beta 1 and 2 receptors?

A

It accelerates the SA node and increases contractility

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7
Q

What is the parasympathetic activity on the heart at the muscarinic 2 receptors?

A

decelerates the SA node and decreases contractility

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8
Q

What is the sympathetic activity on the blood vessels at beta 2 and alpha1 receptors?

A

Increases blood flow by relaxing skeletal vessels allowing more blood flow, and contracts smooth muscle blood vessels increasing blood pressure

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9
Q

What is the parasympathetic activity on the blood vessels on the M3 receptors?

A

relaxes the smooth muscle blood vessels

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10
Q

What is the sympathetic activity on the bronchiolar smooth muscle beta2 receptors?

A

Relaxing

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11
Q

What is the parasympathetic activity on the bronchiolar smooth muscle M3 receptors?

A

Contracts

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12
Q

Skeletal muscles at rest take up about what percent of circulating blood flow?

A

20% (can go up to 80% during physical activity or during sympathetic nervous system stimulation)

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13
Q

What is another term for cholinomimetics?

A

parasympathomimetics

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14
Q

what do cholinomimetics do?

A

they mimic the activity of the parasympathetic nervous system by mimicking endogenous acetylcholine

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15
Q

what is another term for parasympatholytics?

A

antimuscarinics

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16
Q

What do antimuscurinics do?

A

they block the effect of the parasympathetic nervous system

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17
Q

what are sympathomimetics?

A

they mimic the Sympathetic nervous system

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18
Q

what are sympatholytics?

A

alpha and beta blockers, they block the sympathetic nervous system

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19
Q

all neurons coming off of the central nervous system release

A

acetylcholine

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20
Q

all neurons coming off of the central nervous system in the autonomic nervous system encounter

A

a ganglia which is the next neuron in the chain. this neuron will then release norepinephrine, acetylcholine, or even dopamine depending on the target organ

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21
Q

What is the space between the neuron and effector organ cell, muscle, or other neurons called?

A

synapse. very thin space

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22
Q

What is another name for the telodendria?

A

synaptic bouton

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23
Q

Inputs on a neuron is called a

A

dendtrite

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24
Q

the axon hillock generates what?

A

an action potential

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25
Q

What is saltatory conduction?

A

jumping of action potential over the myelin

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26
Q

Where is a neurotransmitter stored?

A

in the synaptic boutons or telodendria

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27
Q

Describe information going from the dendrites to the next synapse.

A

Information comes in through the dendrites
it is sent to the nucleus as a go or no-go
if it’s go nucleus becomes active
This activates the axon hillock
Axon hillock generates an action potential
AP goes down the axon
Reaches the telodentria which are capped with synaptic boutons
boutons release neurotransmitter into the synapse

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28
Q

Where is saltatory conduction very common?

A

in the somatic nervous system. If someone throws a ball at your head you want to be able to life your mitt up to catch it

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29
Q

Where are neurotransmitters largely made?

A

in the neuron itself

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30
Q

Can one axon have many telodendria?

A

Yes

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31
Q

Where do Telodendria get energy?

A

from a mitochondria found in the telodendria

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32
Q

What are the 2 types of synapses?

A

chemical and electrical?

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33
Q

Where are gap junctions found?

A

in the heart, this allows the atria and ventricles to contract together

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34
Q

What do we do with neurotransmitters after they are released into the synapse?

A

They will keep signaling if we don’t get rid of them.
A lot of synapses have enzymes in them to degrade neurotransmitters

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35
Q

What breaks down acetylcholine?

A

acetylcholine esterase

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36
Q

what does acetylcholine esterase break acetylcholine down to?

A

acetate
choline

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37
Q

What happens to acetic acid and choline after acetylcholine esterase breaks down acetylcholine?

A

They can be reabsorbed into the presynaptic cell to be reassembled into acetylcholine

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38
Q

In the CNS we have En Passant synapses, what is this?

A

swellings in the axons where neurotransmitters can be released into a synapse

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39
Q

What are the main stages of synaptic transmission?

A

AP in synaptic bouton
opening of VG Ca++ channels
Calcium influxes
secretion of neurotransmitter then inactivation of neurotransmitter
activation of receptor 2 options:
1. opening of ion channels
-increased Na+= depolarization (EPSP) and excitation
-increased Cl-= hyperpolarization(IPSP) and inhibition
2. Dissociation of G-protein
-activation of second messenger system
-modulation of ion channel activity
-slow modulation of neural excitability

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40
Q

What is EPSP?

A

excitatory post synaptic potential

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41
Q

What is IPSP?

A

Inhibitory post synaptic potential

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42
Q

What are the fates of used neurotransmitters?

A

It is decreased in the synapse
1. diffuses away
2.degraded by enzymes
3. uptake into pre-synaptic cell
4. uptake into surrounding cell(blood stream, muscle cells etc.)

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43
Q

What is an ester?

A

something that has an r group, carbon, double bond group to oxygen, another bond to oxygen, and another r group

acetylcholine

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44
Q

What is a monoamine?

A

a single amine
norepinephrine
serotinin
dopamine

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45
Q

What is an amino acid neurotransmitter?

A

Glutamate GABA

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46
Q

What is a purine neurotransmitter?

A

adenosine
ATP

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47
Q

How is nitric oxide different from the other neurotransmitters?

A

It can’t be stored so it is made as needed

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48
Q

What are the 6 classes of neurotransmitters?

A
  1. esters
  2. monoamines
  3. amino acids
  4. purines
  5. peptides
  6. inorganic gases
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49
Q

What is an example of peptide neurotransmitters?

A

substance P, endorphins

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50
Q

What are cholinergic fibers?

A

specific fibers that release acetylcholine

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51
Q

Nicotinic are what kind of channels?

A

ion channels
fast

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52
Q

Muscarinic are what kind of channels?

A

g protein
slow

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53
Q

Where is acetylcholine found?

A
  • almost all preganglionic fibers
  • all somatic fibers (skeletal)
  • postganglionic
    -all parasympathetic
    a few sympathetic

nearly all efferent fibers leaving the CNS

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54
Q

Monoamines are

A

derivatives of amino acids

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55
Q

What are norepinephrine and epinephrine made from?

A

the amino acid tyrosine

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56
Q

What releases norepinephrine and epinephrine

A

adrenergic or noradrenergic fibers

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57
Q

What gives a rewarding or pleasurable sensation?

A

dopamine

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58
Q

Which monoamine is associated with addiction?

A

dopamine

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59
Q

What is associated with depression?

A

serotonin

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60
Q

What is the Lovheim cube?

A

if you are deficient on any of these 3 neurotransmitters (noradrenaline, dopamine, serotonin) in the CNS, then you can’t feel a full range of emotion

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61
Q

How does an SSRI work?

A

It selectively inhibits the reuptake of serotonin, leaving serotonin in the synapse for a longer period of time

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62
Q

What are the 3 main amino acid neurotransmitters?

A

Glutamate
Glycine
Gaba

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63
Q

What is the most important excitatory neurotransmitter amino acid in the brain?

A

Glutamate

mating is exciting

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64
Q

Glycine and GABA are both

A

Inhibitory

produce postsynaptic inhibition

65
Q

What does the poison strychnine do?

A

blocks the glycine receptor resulting in fatal convulsions d/t not having control over the inhibition

66
Q

What do neuropeptides do?

A

mediate pain and analgesia

67
Q

Key targets for pharmaceutical intervention features of neurotransmitters at synaptic terminal are

A

-synthesis
-storage
-release
-activation of receptors
-termination of action

68
Q

One round of acetylcholine at a cholinergic synapse

A
  1. action potential ends in the terminal bouton
    2.Terminal bouton becomes depolarized
  2. This lets Ca++ in
  3. Ca++ binds to vesicles
  4. vesicles bind to surface of the cell
  5. exocytosis of ACh into the synapse
  6. ACh binds to the ACh receptor
  7. this opens Na+ channels
  8. this depolarizes the postsynaptic cell
  9. this influxes Ca++
  10. postsynaptic cell depolarizes= muscle contraction.

ACh is now targeted by acetylcholinesterase
ACh is broken down

69
Q

Where is ACh synthesized?

A

in the cytoplasm of the cell that releases it

70
Q

What is Acetyl-CoA?

A

a carrier molecule that attaches an acetyl group to choline

71
Q

Where do we get choline?

A

in our diet
eggs

72
Q

what enzyme combines acetyl-CoA and choline?

A

choline acetyltransferase ChAT

73
Q

Where is ChAT found?

A

inside the neuron

74
Q

Where is AChE (Acetylcholine esterase) found?

A

in the synapse

75
Q

Once ACh is made, where is it stored?

A

in a vesicle

76
Q

How much ACh is found in a vesicle?

A

1,000-50,000

77
Q

What is release of ACh dependent on?

A

extracellular Ca++ coming in and destabilizing the storage vesicles

78
Q

What is CHT?

A

a choline transporter that takes choline down it’s concentration gradient through facilitated diffusion co-transporting Na+ and choline into the cell

79
Q

Once ACh is made it is transported into a vesicle by

A

Vessicular Acetylcholine Transporter

80
Q

What is a docking molecule?

A

a protein that anchors a vesicle near the synapse so we can have rapid release of the vesicle

81
Q

what is a collective name of docking molecules?

A

SNARE complex

like a net

82
Q

Which SNARE proteins are associated with the vesicle?

A

Syntaxin
SNAP -25

83
Q

Which SNARE protein is a part of the membrane?

A

Vesicular Associated Membrane Protein

84
Q

What is Synaptotagmin?

A

A very important SNARE protein that senses the calcium influx and facilitates the rapid exocytosis of the vesicles filled with ACh

85
Q

What is priming?

A

it comes after docking of the ACh vesicles.
It is like the cocking of a gun, it is ATP dependent that prepares the vesicle for rapid exocytosis

86
Q

What are the 3 steps of ACh transmission?

A

docking
priming
fusion

87
Q

What is a choline transporter inhibitor?

A

hemicholiniums- a molecule used in research

88
Q

How does a calcium channel blocker effect nerve transmission?

A

It blocks the voltage gated calcium channel meaning Ca++ can’t get into the cell. No Ca++ = no activation of synaptotagmin = no exocytosis of ACh = no reaction in the effector cell

89
Q

Cholinergic inhibitors can inhibit other than being a receptor antagonist by

A

inhibiting some other part of the docking, priming, or fusion process

90
Q

Examples of cholinergic inhibitors that are not direct antagonists?

A

Hemicholiniums- CHT
Vesamicol- VAT
Caclium channel blocker- vg Ca++ channels
botulinum toxin- vesicle release fusion proteins
sarin (nerve gas)- AChE inhibitor

91
Q

How does Botox cause something to be paralyze?

A

it blocks the fusion proteins from releasing ACh which means the effector cell never gets activated

92
Q

Sarin (nerve gas) overdoses us on

A

ACh

93
Q

What is the treatment for Sarin nerve gas?

A

Atropine

94
Q

In what case would you want to block the AChE?

A

Myasthenia Gravis- body makes antibodies against acetylcholine receptors causing less and less muscle control

inhibiting AChE therefore increases the amount of ACh in the synapse

95
Q

Tyrosine is a precursor for

A

DOPA
norepinephrine
epinephrine

96
Q

What happens to Norepinephrine after it is used in the synapse?

A

It is reuptaken into the neuron by NorEpinephrine Transporter
or is diffused away from the site

97
Q

After used NE is brought back into the neuron by NET, what happens to it?

A

can either be redocked into vesicles
or
can be broken down by MonoAmine Oxidase

98
Q

What are MAOI’s used for clinically?

A

The treatment for severe depression. The inhibit the breakdown of dopamine, serotonin, NE

99
Q

Why are MAOI’s very dangerous?

A

They can lead to overdose of neurotransmitters and have a lot of drug interactions

100
Q

What is a VMAT?

A

Vesicular Mono Amine Transporter

101
Q

Delete

A

Me

102
Q

What are the targets for drug actions for adrenergic transmission?

A
  1. Synthesis of neurotransmitter -inhibition of tyrosine
  2. storage of neurotransmitter-no current therapeutics
  3. vesicle secretion-botox
  4. vesicle cycling and endocytosis- no current therapeutics
  5. Reuptake of neurotransmitter- SSRI, Cocaine, molly, tricyclic antidepressants
  6. biotransformation of neurotransmitter-MAOI
  7. Neurotransmitter receptor-agonists, antagonists
103
Q

cholinergic agonist and antagonists bind to which receptors?

A

nicotinic and muscarinic receptors

104
Q

Why can’t you give ACh exogenously?

A

There are so many AChE in the blood that it is broken down within seconds

105
Q

What are direct acting drugs?

A

They are agonists

106
Q

What are indirect acting drugs?

A

antagonists (they block AChE)

107
Q

What are irreversible indirect acting drugs that can affect cholinoreceptors?

A

Nerve gas and toxins

108
Q

How did muscarinic receptors get their name? (pharm)

A

from the fungi muscarine

109
Q

What are the symptoms of parasympathetic

A

Salivation
Lacrimation
Urination
Defecation
Gi motility
Emesis
Myosis -constriction of the pupil

110
Q

What is mycetism?

A

mushroom poisoning

111
Q

Why is atropine the treatment for mycetism?

A

It blocks muscarinic receptors

112
Q

Acetocholine is both ___________ But Nicotine only binds to _________ receptors

A

nicotinic and muscarinic
nicotinic

113
Q

ganglion cells are labeled as

A

nicotinic

114
Q

The odd number muscarinic receptors (M1,M,3M5) increase _______ which leads to calcium release within the cell

A

IP3

115
Q

The even number muscarinic receptors (m2&M4) inhibit adenylyl cyclase which

A

decreases CAMP

116
Q

Drugs that bind to muscarinic receptors are:

A

esters of choline
alkaloids

117
Q

What are alkaloids?

A

plant based compounds that are bitter (high pH)

118
Q

If you have a drug that excites or inhibits a muscarinic receptor, they’re not going to JUST excite or inhibit M1, or M2, they will target

A

either all of the odd or all of the even

119
Q

Esters of choline are charged and lipid insoluble molecules and so they

A

don’t cross barriers easily. (can’t be given transdermally)

120
Q

Methacholine is used for

A

diagnosis of asthma
short lived and causes people to have an asthma attack

121
Q

ACh drugs can be used for

A

pupillary constriction

122
Q

carbachol is used for

A

decreasing intraocular pressure (constricting the pupil)

123
Q

Bethanechol is used for

A

bladder dysfunction and reflux disease

stimulates the parasympathetic response

124
Q

What is pilocarpine?

A

a plant based alkaloid that’s chiefly muscarinic

125
Q

What is Arecoline?

A

nicknamed the betel nut
an alkaloid found in other countries that is used as a stimulant

126
Q

Because we have nicotinic receptors in both the sympathetic and parasympathetic, we can activate

A

both of them simultaneously, although sympathetic response usually predominates

127
Q

muscarinic effects in the eye?

A

pupil contraction

128
Q

muscarinic effects in the cardiovascular system

A

Reduction in PVR and vasodilation
reduces bp

129
Q

What is glaucoma?

A

Increase in intraocular fluid called aqueous humor which is formed by the ciliary bodies in the ciliary muscle.

130
Q

What does the ciliary muscle do?

A

it holds the lens in the eye and changes it’s shape to focus on something either far away or up close

131
Q

Where does aqueous drainage drain?

A

Through the canal of schlem

132
Q

Drainage is possible through the canal of schlem because

A

the iris is fairly flat compared to the cornea, which juts up out from the eye

133
Q

With open angle glaucoma, pts. can ______ drain their aqueous humor into the canal of schlem

A

easily

134
Q

If a patient with open angle glaucoma has a build up of too much aqueous humor, what can we do to help?

A

give something that will constrict the pupil and open the angle even more

like bethenicol or methicoline

135
Q

If a patient has closed angle glaucoma the iris is ________ causing a high degree of interocularpressure

A

bulged forward

136
Q

if we constrict the iris in a patient with closed angle glaucoma,

A

it may not be enough because the angle is already so closed

137
Q

Closed angle glaucoma can be a medical emergency if we give

A

atropine
atropine dilates the iris, compressing on the canal of schlem even more and can cause blindness quickly

138
Q

airway tone is important because

A

we need our airway to have a consistent tone because we don’t want smog and smoke particulates to get down deep in the lungs so it is important to decrease the flow and surface area where mucous membranes can bind to that particulate matter

139
Q

what is the parasympathetic response in our lungs?

A

increased muscle tone
increased mucous secretion

140
Q

what are the parasympathetic responses in the GI tract?

A

increased gastric secretions and motor activity, sphincters relax

141
Q

what are the parasympathetic responses in the CNS?

A

brain- mainly muscarinic sites but muscarine doesn’t cross very easily, so nicotine has a greater effect.
it’s mildly alerting, releases dopamine

142
Q

in large enough doses, nicotine can cause

A

tremors, emesis, stimulates the respiritaroty center, convulsions, fatal coma

143
Q

If we have something that is going to bind to a nicotinic receptor and keeps it open for a while, we end up with

A

a depolarization blockage (flaccid paralysis)
this is what succs does.

we’ve depolarized and can’t repolarize because the substance is still there

144
Q

Indirect acting cholinomimetics have what effect on the body?

A

the same as direct acting cholinomimetics, they just happen a different way by blocking AChE

145
Q

Neostigmine is used to treat

A

post-op ileus

146
Q

What are the classes of indirect cholinomimetics?

A

simple alcohols
carbamic acid esters of alcohols
organic derivatives of phosphoric acid

147
Q

alcohols work how long as a cholinomimetics? What is an example of this type of drug?

A

5-15mins short lived
edrophonium

148
Q

carbamates work how long as a cholinomimetics? What is an example of this type of drug?

A

neostigmine 0.5-2 hrs
pyridostigmine 3-6 hrs

149
Q

organophosphates work how long as a cholinomimetics? What is an example of this type of drug?

A

Echothiophate 100 hours
this forms a covalent bond

150
Q

How does an organophosphate work as an indirect cholinomimetic?

A

It forms a covalent bond with the AChE and hydrolyses it.
Thought of as irreversible
Can be broken if you give pralidoxime within the first few hours
after that the aging makes the covalent bond stronger

151
Q

How is myasthenia gravis diagnosed?

A

baseline muscle test
2mg iv watch for negative reaction
8mg iv improvement in muscle action= myasthenia gravis
Now we can give longer lasting AChE inhibitors for treatment

152
Q

AChE inhibitors can reverse the effects of paralysis by

A

increasing the amount of ACh in the synapse

153
Q

Bella donna gives us

A

atropine intoxication

154
Q

Direct acting muscarinic stimulants act like

A

muscarine.
Same effect of parasympathetic actions but stronger

155
Q

If you see SLUDGEM give

A

atropine

156
Q

What does night cap do? A. Phalloides mushroom

A

inhibits mRNA synthesis and kills in 4-7 days

157
Q

if a person is working out in the field and a plane comes by dumping bug poison, we would look for _____ symptoms and give ______

A

SLUDGEM
atropine

158
Q

Pralidoxime is useful for

A

organophosphates

159
Q

atropine is used to combat

A

extremely high parasympathetic overdose

Pharm Test 2 (9 decks)

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