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z F1: Pharmacology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Parasympathetic Nervous System (ANS subset)

A

rest and digest
conserve energy

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2
Q

Sympathetic Nervous System (ANS subset)

A

fight or flight
(continuously active)

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3
Q

ANS has a two neuron system what are the neurons called

A

preganglionic and postganglionic
(synapse combines them together)

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4
Q

What molecule has to be produced within a neuron, released when stimulated (ca2+ dependent), inactivated after release, and produce physiological responses

A

neurotransmitters

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5
Q

What system has a NT that is ACh -> cholinergic transmission

A

parasympathetic system (rest and digest)

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6
Q

In the parasympathetic system what is released at the first synapse and what is released at the second synapse

A

preganglionic: ACh (binds to soma receptors)
postganglionic: ACh (activates receptors in tissue to produce effect)

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7
Q

Synapses in pre and postganglionic axons in parasympathetic ganglia are terminal ganglia and intramural ganglia what do they do

A

terminal ganglia: close to target tissue
intramural ganglia: in target tissue

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8
Q

What are the two systems in the parasympathetic system (cholinergic system)

A

Parasympathetic system: Contains ganglia
Somatic Nervous System: NOOO ganglia

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9
Q

What is the somatic nervous system, what does it activate, how is it activated

A

one neuron pathway
CNS to skeletal muscle (NO ganglia)
Motor neurons are myelinated
NT is ACh
Activates muscle contraction

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10
Q

ACh is synthesized in the ________ by acetylation of choline

A

cytoplasm

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11
Q

Where is Choline acetyltransferase (ChAT) synthesizes and transported

A

synthesized in soma and transported down axon to nerve terminal (it marks cholinergic neurons)

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12
Q

What two things are needed for ACh synthesis

A

AcetylCoA from pyruvate
Choline

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13
Q

What are the two places you can get choline

A

diet
liver
(choline is formed from ACh metabolism)

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14
Q

Choline is recycled to be resued for ACh synthesis, it is transported inside neurons with what and by what transporter

A

Transported with Na+ by choline transporter (CHT1)
(Rate limiting step in ACh synthesis, high affinity)

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15
Q

High choline demand -> _____ affinity choline uptake (LACU) system assists in transporting additional choline into ________

A

low affinity
choline into neurons

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16
Q

CHT1 is a symporter, what does it symport

A

Choline and Na+ into cell
(needs Na+ /K+ ATPase antiport)

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17
Q

What does hemicholinium (hemicholine) do

A

blocks the transporter of CHT1
-indirect acetylcholine antagonist decreases ACh synthesis

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18
Q

ACh is stored in small synaptic vesicles which protect them from what

A

degregation

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19
Q

What is vesicular acetylcholine transporter (VAChT)

A

(Used for storage of ACh)
Located in the membrane of vesicles and relies on the H+ pump

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20
Q

What is the mechanism of the VAChT (vesicular acetylcholine transporter)

A

Antiporter
transports ACh inside the vesicles in exchange for protons
H+ are provided by the proton pump

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21
Q

What do vesamicols do to VAChT

A

They decrease ACh release
Depletion of ACh at synpase
(noncompetitive and reversible inhibitor)

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22
Q

How is ACh released from the synaptic vesicles

A
  1. Axon potential throughout the anion
  2. Activation of voltage-gated Ca2+ channels
  3. Exocytosis
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23
Q

ACh release is blocked by botulinum and tetanus toxins from __________

A

Clostridium

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24
Q

Transient vesicle fusion requires _________ proteins and Ca2+

A

SNARE
(SNARE proteins = soluble NSF attachment protein receptor, NSF = N-ethylmaleimide sensitive fusion proteins)

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25
Q

Inhibition of Exocytosis:
Botulinum and tetanus toxins induce what

A

muscle paralysis
(proteases that hydrolyze some SNARE proteins)

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26
Q

Inhibition of Exocytosis:
Toxins are polypeptides that contain two chains what are they

A

Heavy chain - binding
Light chain - Zn2+ dependent protease

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27
Q

What is botulism

A

-Neurotoxins are absorbed in intestine, pass into bloodstream, travel to synapse in the nervous system
-Flaccid paralysis, preventing release of ACh at NT junctions

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28
Q

What is infant boutlism caused by

A

honey

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29
Q

What is tetanus

A

-Hyperactivity of motor neurons increase muscle activity
-muscle contractions starts in jaw and neck muscles progresses to the rest of the body

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30
Q

ACh mechanism

A
  1. ACh is made from choline and acetyl coA
  2. In synaptic cleft ACh is rapidly broken down by enzyme acetylcholinesterase
  3. Choline is transpored back into the axon terminal and is used to make more ACh
    (butytylcholinesterace is a secondary mechanism)
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31
Q

AChE (acetylcholinesterase)

A

localized to postsynaptic membranes in synaptic cleft
inactivation time of ACh -> very fast mechanism
Specific inhibitors for AChE -> used in clinic

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32
Q

What are the two catalytic sites in AChE

A

anionic site that binds ACh
Esteratic site includes a Ser, His, Glu, site for ACh hydrolysis and AChE acetylation

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33
Q

AChE mechanism

A

-binding of ACh to the enzyme
-hydrolysis of ester bond forming acetyl enzyme
-hydrolysis of acetyl enzyme resulting in elimination of acetate originating free enzyme, reactivation of AChE

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34
Q

What are the two classes of cholinergic receptors

A

Muscarinic Receptors: stimulated by muscarine (agonist)
Nicotonic Receptors: stimulated by nicotine (agonist)

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35
Q

What are the three cholinergic transmission sites effectors

A

smooth muscle
cardiac tissue
glands

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36
Q

What are the two types of Nicotinic Receptors

A

Muscle-type (N1) and neuronal-type (N2) receptors
-receptor converts ligand binding (2ACh) into electrical depolarization

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37
Q

Nicotinic receptors have ___ subunits arranged around a central pore

A

5
the alpha and beta subunits are present in many different combinations

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38
Q

In nicotinic receptors, the number of ACh binding sites depends on the composition of the ________

A

receptor (interfaces of alpha-subunits)

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39
Q

Nicotinic receptor subtypes are selective primary to _____ and secondary to _____

A

Na+
Ca2+

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40
Q

Muscarinic receptors are ______ onset and _______ duration responses

A

slow onset long duration

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41
Q

M1, M3, M5 receptors

A

couple to Gq family
phosphotidyl inoaitol -> IP3, DAG -> Excitation

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42
Q

M2 and M4 receptors

A

couple to Gi/o family
adenylyl cylase -> cAMP -> Inhibition

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43
Q

ACh activates the postganglionic neuron by binding to receptors in the _____ of the postganglionic neuron releasing ACh at the synapse

A

soma

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44
Q

Postsynaptic membrane in postganglionic nurons effect what

A

tissues or organs

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45
Q

presnaptic receptors regulate the release of what

A

NTs

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46
Q

Nicotinic receptors enhance NT release mainly in the

A

CNS

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47
Q

Muscarinic receptors inhibit _____ release

A

NT

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48
Q

M2 and M4 receptors ______ the effect of ACh

A

decrease

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49
Q

M1 and M3 receptors ________ an effect or response

A

activate

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50
Q

Muscarinic Autoreceptors

A

presynaptic muscarinic receptors that regulate ACh release -> regulate its own NT
Autoreceptors inhibit NT release -> mechanism or negative feedback

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51
Q

Muscarinic Heteroreceptors

A

-Presynaptic muscarinic receptors that regulate other NTs release
-ACh released from a cholinergic neuron activates M5R present in a dopaminergic neuron
-Activation of M5R increases dopamine release in nucleus accumbens

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52
Q

Are blood vessels innervated by the parasympathetic system, but they have muscarinic receptors

A

No

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53
Q

What are the three effect of ACh in the heart (cardiac system): SA, AV node and cardiomyocyte

A

Pacemaker cells (SA node): Decrease heart rate (negative chronotropic effect)
Pacemaker cells (SA and AV node): Decrease rate of conduction (negative domotropic effect)
Cardiomyocyte cells: Decrease force of cardiac contraction (negatice inotropic effect)

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54
Q

Phase 4 of pacemaker cells

A

Slow depolarization
-slow Na+ channels open (-60)
–I(f) open -> efflux of K+
-T-type (transient) Ca2+ channels open (-55 to -50)
-L-type (long lasting) Ca2+ channels open (-40)

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55
Q

Phase 0: Depolarization

A

Leads to action potential
-Slow inward of Ca2+
-L-type voltage gated Ca2+ channels open
-At threshold = action potential

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56
Q

Phase 3: Repolarization

A

Open of delayed recifier K+ channels (voltage-gated channels)
K+ efflux -> outward current
Inactivation and closing of L-type Ca2+ channels
Membrane potential becomes negative

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57
Q

A decrease in phase 4 slope causes what

A

Increase time to reach threshold increasing heart rate

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58
Q

How does ACh effect the SA node

A

decreases activity of L-type Ca2+ channels (4 and 0)
decrease depolarization of SA node cells decreasing heart rate
Large stimulus can produce bradycardia and SA block

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59
Q

ACh effect on potassium channels

A

-Decrease rate of spontaneous depolarization in SA node
-Activation of ACh-sensitive K+ channels by beta-gamma subunits causing an increase of K+ efflux
-Increase in repolarizing K+ current leading to hyper polarization, decreasing heart rate

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60
Q

ACh effects in AV node conduction

A

Decreases L-type Ca2+ channels
decrease depolarization of AV node cells
decrease rate of conduction increasing refractory period
Large stimulus can produce bradycardia and AV block

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61
Q

ACh effect in myocardial cells

A

parasympathetic innervation is higher in atria than ventricles
Modest reduction in atrial and ventricular contractility
-parasympathetic innervation is lower than sympathetic

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62
Q

Cholineric system and blood vessels in parasympathetic

A

Parasympathetic system does not innervate blood vessels
Postganglionic. neurons do not synapse with blood vessels

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63
Q

Blood vessels contains M3 receptors

A

M3 receptors are present on Endothelium Cells and release nitric oxide

64
Q

Activation of M3 receptors cause vasodilation, how does this occur

A

If there is high concentration of ACh found in circulation

65
Q

M3 production of cGMP and PKG activation

A

decreases ca2+ by inhibition of the channel
activation of MLC phosphatase -> MLC dephosphorylation
Relaxation of smooth muscle

66
Q

Constrictor or pupillary muscle

A

Muscle in the iris
encircles the pupil of the iris
M3R
Miosis

67
Q

Cillary muscle

A

muscle in the ciliary body that attaches to the ligament that gold the lens
Changes the shape of the lens (round)
M3R
Near vision

68
Q

ACh effects in the respitatory tract

A

Bronconstriction (M3R in smooth muscle)
increase secretion
M2R in presynaptic causing ACh level decrease

69
Q

ACh effects in the urinary tract

A

Increase detrusor muscle contraction
relaxation of the sphincter
promotes bladder emptying urination

70
Q

GI tract by ACh

A

M3R > M2R (more ACh produced)
Increase secretion
Increase muscle contraction
Increase peristalsis and bowel movements

71
Q

What is different about Sweat Glands in the sympathetic system

A

Postganglioni fiber releases ACh instead of NE
Cholinergic stimulation of muscarinic receptors induces sweating

72
Q

What is the eccrine and apocrine glands

A

Eccrine: open onto skin surface
Apocrine: open into hair follicle

73
Q

Muscarinic Agonists: ACh related esters

A

Methacholine (provocholine)
Carbamylcholine (carbahol)
Bethanechol (urecholine)

74
Q

Muscarinic Agonists: natural products

A

Muscarine
Pilocarpine (salagen, pilocar)
Arecoline

75
Q

Selectivity of muscarinic vs nicotinic receptors in Methacholine, Carbamylcholine, Bethanechol

A

Methacholine: more specificty for muscarinic receptors
Carbamylcholine: equal activity for muscarinic activity and nicotinic activity
Bethanechol: Muscarinic activity but no nicotinic activity

76
Q

Selectivity of muscarinic vs nicotinic receptors in source of arecoline, muscarine, pilocarpine

A

Arecoline: nuts, equal muscarinic and nicotinic activity
Muscarine: mushroom, muscarinic activity
Pilocarpine: leaves, muscarinic activity

77
Q

Structure, absorption oral administration, BBB crossing in Methcholine, carbachol, bethanechol, muscarine

A

Quaternary amine
Poorly absorbed
Limited BBB crossing

78
Q

Structure, absorption oral administration, BBB crossing in Arecoline, Pilocarpine

A

Tertiary amine
Readily absorbed
can cross BBB

79
Q

Bathanechol gastrointestinal disorders

A

Bethanechol (urecholine) useful in stimulating GI motility
Largely replaced by compounds with combined cholinergic agonist and dopamine antagonist properties -> GI motility and antimetic effect

80
Q

Bathanechol urinary bladder disorders

A

Useful in treating urinary retention and inasequate bladder emptying
-postoperative or postpartum urinary retention
-enhances contraction of the bladder detrusor muscle -> avoids catheterizations

81
Q

Xerostomia

A

Sjogren’s syndrome
-Autoimmune disorder
-decrease seretions from salivary and lacrimal glands
-Head and neck chemotherapy and radiation therapy, trauma, and drugs

82
Q

Treatment to promote salivation pilocarpine (salagen) and cavimeline (evoxac)

A

pilocarpine (salagen): adverse effects include profuse sweating
cavimeline (evoxac): newer with fewer side effects, preferentially activate M1R and M3R

83
Q

Opthalmolgical use of pilocarpine

A

-In glaucoma (increased intraocular pressure)
-Pilocrine a mitotic agent decreases intraocular pressure by increasing the drainage of intraocular fluid
-Ocular insert allows for release of 20mg of pilocarpine per hour over 7 days

84
Q

Clinical uses of carbachol

A

eye drops (miostat)
treats open-angle glaucoma by increasing fluid outflow

85
Q

Bronchial challenger test- bronchial hyperreactivity

A

use of methacholine (by inhalation) to assist in diagnosis of asthma
-provokes broncoconstriction or narrowing of the airways
-asthmatics will react to lower doses of drug -> spirometry to check degree of narrowing

86
Q

Agonists common adverse effects

A

Sweating
Diarrhea
Bladder tightness
Hypotension
Limited administration

87
Q

ACh has virtually no therapeutic application because it has ______ inactivation

A

rapid inactivation (causing no pills to be able to be administered)

88
Q

Drugs that inhibit AChE are referred to as what two things

A

Cholinesterase inhibitors
Anticholinesterase

89
Q

Acetylcholinesterase inhibitors cause what at the synapse and increase of what receptors

A

Increase of ACh levels at the synapse
Increase activation of muscarinic and nicotinic receptors

90
Q

What are the three types of acetylcholinesterase inhibitors

A

Noncolvalent inhibitors
Reversible carbamate inhibitors
Organophosphorus inhibitors

91
Q

acetylcholinesterase inhibitors: Noncolvalent inhibitors

A

Reversible binding and inhibition
Edrophonium and donepezil

92
Q

acetylcholinesterase inhibitors: reversible inhibitors

A

Physostigmine and neostigmite

93
Q

acetylcholinesterase inhibitors: Organophosphorus inhibitors

A

Hemisubstrates
Diisopropyl fluorophosphate (DFP)

94
Q

Edrophonium (tensilon): structure, administration, bioavailability, CNS penetration, half life, elimination, therapeutic use

A

structure: Quaternary Amine
administration: IV, IM, SubQ
bioavailability: N/A
CNS penetration: PNS
half life: short
elimination: Urine
therapeutic use: Diagnosis of myastenia gravis

95
Q

Donepezil (Aricept): structure, administration, bioavailability, CNS penetration, half life, elimination, therapeutic use

A

structure: Tertiary Amine
administration: Oral
bioavailability: 100%
CNS penetration: Yes
half life: long
elimination: Urine & Feces
therapeutic use: Alzheimer’s

96
Q

Reversible inhibitors mechanism

A

Rapid onset of action and shortest duration of any AChE inhibors
No covalent attachments to AChE
No enzyme intermediate

97
Q

Carbamate Inhibitors

A

Neostigmine (prostigmin)
Physostigmine
Pyridostigmine (mestinon)
Rivastigmine (exelon)

98
Q

Neostigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use

A

structure: Quaternary Amine
administration: IV, IM, oral
absorption: Poor
onset action: very short
CNS penetration: No
metabolism: Plasma and liver esterases
half life: shorter
elimination: Urine
therapeutic use: Myasthenia Gravis

99
Q

Pyridostigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use

A

structure: Quaternary Amine
administration: IV, IM, oral
absorption: Poor
onset action: very short
CNS penetration: Yes
metabolism: plasma and liver esterases
half life: shorter
elimination: Urine
therapeutic use: Myasthenia Gravis

100
Q

Physostigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use

A

structure: Tertiary Amine
administration: IV, IM
absorption: Readily
onset action: 5 minutes
CNS penetration: Yes
metabolism: plasma and liver esterases
half life: shortest
elimination: Urine
therapeutic use: Reverse toxic anticholinergic effects

101
Q

Rivastigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use

A

structure: Tertiary Amine
administration: Oral, patch
absorption: Readily
onset action: n/a
CNS penetration: Yes
metabolism: plasma and liver esterases
half life: short
elimination: Urine, feces
therapeutic use: Alzehimer’s, Parkinson’s

102
Q

Carbamate Inhibitors: mechanism

A

Inhibitors are substrates of AChE
Hydrolyzed by AChE but slowly
Form Carbamoylated AChE intermediate
-prolonged inhibition of AChE

103
Q

Organophosphorus Inhibitors

A

Therapeutics: Echothiophate (phospholine), treat glaucoma
Toxic nerve gas: Sarin, Soman, Tabun
Pesticides: Parathion, Diazinon, Chlorpyrifos, Malathion

104
Q

Absorption properties of organophosphorus inhibitors

A

Rapid onset of action
Highly lipid soluble liquids
Dispersed as aerosols or particles
(excreted in urine)

105
Q

Organophosphorus Inhibitors mechanism

A

Formation of phosphorylated AChE intermediate
Enzyme regeneration is very slow

106
Q

Aging process of phosphorylated enzyme intermediate

A

Stability of the phosphorylated enzyme is enhanced through aging
Conformational change of AChE-organophosphorus complex
Again results from lost of alkyl group with time
AChE after aging is virtually impossible to regenerate

107
Q

Regeneration of AChE by Pralidoxine

A

Regenerated by hydrolysis of the phosphorylated ester
Pralidoxmine exerts a nucleophile attack and can’t cross BBB
High dose inhibit AChE

108
Q

Reactivation of AChE

A

Reactivating action of oximes in vivo is most marketed at the skeletal neuromusculat junction
Less effect at autonomic effect site -> quaternary ammonium group restricts entry into CNS

109
Q

What are the effect of AChE inhibitors (DUMBBELLS)

A

D: diarrhea
U: urination
M: miosis
B: bronchospasm
B: bradycardia
E: emesis
L: lacrimation
L: sweating
S: salivation

110
Q

Neuromuscular Junction

A

Released ACh binds to nicotinic receptors
Depolarization of the muscle cells
Activation of muscle contraction

111
Q

Actions of AChE inhibitors at neuromuscular junction

A

Increase ACh levels, producing excitation and muscle fasciculation
-High concentrations of ACh, depolarization predominated following by blockage due to extended depolarization
Paralysis of muscles specially respiratory muscles

112
Q

CNS effects from Action of AChE inhibitors at Neuromuscular junction

A

Confusion, ataxia, slurred speech, loss of reflexes, altered respiration, convulsions, coma, respiratory paralysis

113
Q

Toxic effects mechanism

A

-Excessive stimulation of the cholinergic system
-Accidental intoxication
-AChE inhibitors also used for suicidal and homicidal purposes
-Duration of toxicity depends on properties of compound

114
Q

Toxic effects: Inhalation

A

ocular and respitory effects appear first
-miosis, blurred vision, rhinorrhea, difficulty breathing

115
Q

Toxic effects: Ingestion

A

GI symptoms occur earlier
-nausea and vomiting, abdominal cramps and diarrhea

116
Q

Toxic effects: Percutaneous absorption

A

Sweating and muscle fasciculation

117
Q

Toxic nicotinic effects

A

Include muscle fatigue and weakness involuntary twitching or fasciculations, and paralysis
-Paralysis of the respiratory muscles is most serious consequence

118
Q

Toxic CNS effects

A

Confusion, ataxia, slurred speech, loss of reflexes, altered respiration, convulsions, coma and respiratory paralysis
-Time of death may range from 5 to 24 hr depending on the dose, route, agent (respiratory failure is the main cause)

119
Q

Myasthenia Gravis: What does it do and how does AChE impact it

A

Autoimmune disease -> antibodies against nicotinic receptor
AChE inhibitors increase ACh which increases channel opening and muscle stimulation

120
Q

How to diagnose and treat Myasthenia Gravis

A

Diagnose: Edrophonium (tensilon)
Treatment: Pyridostigmine, neostigmine, ambenonium (mytelase)

121
Q

Common adverse effects of AChE inhibitors

A

GI track problems, dizziness, headache, bradycardia, AV block

122
Q

AChE inhibitors drug interactions

A

Drugs affecting AChE inhibitors:
Cholinergic agents -> additive effects
Anticholinergic agents -> decrease effects

AChE inhibitors affect other drugs
Beta-blocker increase bradycardia
Nondepolarizing neuromuscular blocking agents exaggerated muscle relaxation

123
Q

Muscarinic Receptor effector organs

A

Eye
Heart
Lungs
Stomach
Kidneys
Bladder

124
Q

Muscarinic Antagonists compounds derived from natural sources

A

Solanaceae family
Alkaloids
Atropine
Scopolamine

125
Q

Muscarinic Antagonists synthetic analogs

A

Quaternary amines used by inhalation -> effects on respiratory tract

126
Q

Analog of Atropine and analog of atropine’s analog

A

Ipratropium (tiotropium): analog of atropine, 4-6 hrs
Tiotropium (Spiriva): analog of ipratropium, last 24 hrs

127
Q

Mydriasis and cycloplegia

A

mydriasis: pupil dilation
cycloplegia: paralysis of accommodation and ciliary muscle

128
Q

Antagonist drugs used in the eye

A

Homatropine (Isopto homatropine)
Ophthalmic drops (tertiary amines)
-Cyclopentolate hydrochloride (cyclogyl)
-Tropicamide (mydriacyl)

129
Q

Antagonist effects in the respiratory tract

A

Brocodilation
Decrease mucus secretion

130
Q

Muscarinic antagonist Ipratropium (atrovent): Route, onset, duration, metabolism

A

route: inhalation
onset: quick
duration: short
metabolism: non-enzymatic ester cleavage to tropic acid and tropane

131
Q

Muscarinic antagonist Tiotropium (Spiriva): Route, onset, duration, metabolism

A

route: inhalation
onset: quick
duration: day
metabolism: non-enzymatic ester cleavage to tropic acid and tropane

132
Q

Muscarinic antagonist Aclidinium Bromide (Tudorza Pressair) and Glycopyrrolate (Seebri Neohaler): Route, onset, duration, metabolism

A

Route: inhalation and oral
Onset: fast
Duration: day
Metabolism: Hydrolysis by esterases for aclidinium, Hepatic for glycopyrrolate

133
Q

Muscarinic antagonist Umeclidinium Bromide (Incruse Ellipta): Route, onset, duration, metabolism

A

route: inhalation
onset: quick
duration: day
metabolism: Hepatic via CYP2D6

134
Q

Muscarinic Antagonist effects in respiratory disorders

A

Bronchodilators -> dry mouth side effect
Treatment: Asthma, COPD

135
Q

Side effects of muscarinic antagonists

A

Dry mouth (M3R, M1R)
blurred vision (M3R)
Urinary Retention (M3R)

136
Q

Antagonist effects in heart

A

Block M2 Receptors: increase heart rate and AV conduction causing tachycardia

137
Q

Antagonist effects in urinary tract

A

Decrease detrusor muscle contraction, decrease normal tone, promoting urinary retention

138
Q

Drugs used in urinary disorders

A

Solifenacin (Vesicare)
Tolterodine (Detrol)
Trospium (Sanctura)
Fesoterodine (Toviaz)

139
Q

Adverse effects in the urinary system

A

Dry mouth and dry eyes: affinity for M3R
CNS drowsiness, dizziness, confusion

140
Q

Effects of antagonists on GI

A

Decrease movement of GI tract
Use dicyclomine

141
Q

Antagonist effects in exocrine gland

A

Use glycopyrrolate
Reduces secretions (treats hyperhidrosis)
Side effect is dry mouth

142
Q

Scopolamine

A

CNS: Drowsiness, fatigue
Toxic: Hallucinations, coma
Help with motion sickness or vomiting

143
Q

Skeletal muscle is inner aged by motor neurons that release ____

A

ACh

144
Q

Neuromuscular transmission

A

Ligand gated ion channel activated by ACh influx of sodium
Have multiple subunits

145
Q

Two classes of antagonists based on the selectivity for nicotinic receptors what are they

A

Neuromuscular blocking drugs
Ganglionic blocking drugs

146
Q

Neuromuscular blocking drugs

A

Inhibit ACh action
Do not have CNS effect
Administration by IV
Muscle relaxing drugs

147
Q

Isoquinoline derivatives

A

Tubicurarine
Metocurine
Atracurium
Cistracurium
Doxacurium
Mivacurium

148
Q

Ammonia steroid derivatives

A

Pancuronium
Pipecuronium
Rocuronium
Vecuronium

149
Q

Non depolarizing blockers

A

Competitive antagonists
Compete with ACh for receptors
Block ACh, block neuromuscular transmission
Prevent opening of channel

150
Q

Effects of nondepolarizing blockers

A

Motor weakness and then flaccid muscle paralysis
Hypotension and bronospasm

151
Q

Reversal of nondepolarizing blockage

A

Increase in ACh displaces drug from receptors
AChE inhibitors: neostigmine, phridostigmine, edrophonium

152
Q

Succinylcholine is a depolarizing drug what does it do in phase 1 block

A

Drug binds a long time
Long lasting depolarization and prolong activation of receptor
Repetitive excitation
Muscle twitching

153
Q

Phase 2 block of succinylcholine

A

Channels remain blocked and in a close state
Flaccid paralysis

154
Q

Succinylcholine is metabolized by what

A

Butyrylcholinesterase

155
Q

Clinical uses of neuromuscular blocking drugs

A

Short term muscle relaxation in anesthesia and intensive care
Rapid on set drugs (used in surgery with intubation)

z F1: Pharmacology (4 decks)

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