Cholenergic agonist Flashcards
1
Q
What type of neurologic function is not under direct control
A
autonomic
2
Q
What does the autonomic nervous system have control over
A
Visceral functions necessary for life
-Cardiac output
-blood flow distribution
-digestion
3
Q
What causes neurologic function
A
Chemical transmission that occurs between nerve and effector cells
4
Q
What tissues are effected by the autonomic nervous system
A
Cardiac muscle
smooth muscle
vascular endothelium
exocrine glands
presynaptic nerve terminals
5
Q
How is the autonomic nervous system divided
A
Sympathetic and parasympathetic
6
Q
Which nerve fibers leave the CNS via the thoracic, lumbar, and sacral spinal nerves
A
Sympathetic preganglionic fibers
7
Q
Which nerve fibers leave the CNS via the cranial nerves
A
Parasympathetic preganglionic nerve fibers
8
Q
What is the enteric nervous system
A
The third division of the ANS
9
Q
What are the primary neurotransmitters in the body
A
norepinephrine
Acetylcholine
10
Q
What are cholinergic fibers
A
Fibers that work by releasing acetylcholine
11
Q
A large number of peripheral ANS fibers are what type of fiber classification
A
cholinergic
12
Q
What are the types of cholinergic fibers
A
all Preganglionic efferent autonomic fibers (non-autonomic)
all somatic motor fibers (skeletal muscle)
Most parasympathetic postganglionic fibers
Some sympathetic post ganglionic fibers
13
Q
What do most postganglionic sympathetic fibers release and what type of fiber are they
A
Most commonly noradernergic fibers
Release norepinephrine
14
Q
Which autonomic receptors are non-specific
A
Nicotinic
15
Q
Which autonomic receptors work almost exclusively with the parasympathetic system
A
Muscarinic
16
Q
What do adrenergic receptors respond to
A
Catecholamines (Norepinephrine)
17
Q
What do cholinoceptors respond to
A
Acetycholine
18
Q
What are the adrenoreceptors broken down into
A
alpha
beta
dopamine receptor types
19
Q
A drug that blocks action potential propagation (local anesthestic) is selective or non-selective and why
A
non-selective because it acts on a process common to all neurons
20
Q
Drugs that act on the biochemical processes involved in transmitter synthesis and storage are selective or non-selective and why
A
More selective because the biochemistry of each transmitter is different
21
Q
Which classes of drugs make up a large group that mimics acetylcholine
A
Acetylcholine-receptor stimulants
Cholinesterase inhibitor
22
Q
What are cholinomimetics
A
Drugs that mimic acetylcholine
23
Q
how are cholinomimetics classified and why
A
by MOA because some bind directly to cholinoreceptors and some act indirectly by inhibiting the hydrolysis of endogenous acetylcholine
24
Q
What do cholinesterases do
A
Allow for acetylcholine to remain activated
25
What is the MOA for direct active cholinomimetic agents
They bind directly to and activated muscarinic or nicotinic receptors
26
What is the MOA for indirect acting cholinomimetics
Inhibit acetylcholinesterase which hydrolyzes acetylcholine and acetic acid which then increases endogenous acetylcholine concentration in the synaptic cleft and neuroeffector junctions
27
What are the effects on the eye from muscarinic agonists
Miosis
accommodation
28
What are the cardiovascular effects from muscarinic agents
Decrease in slow inward Ca current
Increase in K in current cells of SA, AV, purkinje fibers
Reduction in current for diastolic depolarization
all this = Bradycardia
29
What respiratory effect happen with muscarinic agonists
Contraction of bronchial tree
Increased glandular secretion in tracheobrochial tree
30
What are the GI effects with muscarinic agonist
Increased motor and secretory activity
Stimulation of salivary and gastric glands
31
What are the effects of the GU system from muscarinic agonists
Stimulation of detrusor muscle
Relaxation of trigone and sphincter muscles
32
What are the cholinergic agonist effects on the body
Diarrhea
diaphoresis
miosis
nausea
Urinary urgency
33
What are the effects on the CNS from indirect acting cholinomimetics
Diffuse EEG activation and alert response improvement
34
What are the cardiovascular effects from indirect acting cholinomimetics
Vagal nerve activation in the heart
Negative chronotropy, dromotropy, inotropy (cardiac output falls)
35
What are the effects of the NMJ from indirect acting cholinomimetics
Increased strength of skeletal muscle contraction
36
How would acetylcholine act as a direct acting cholinergic agent
Binds to both nicotinic and muscarinic receptors which means that it would have wide spread systemic effects leaving it with limited utility
37
What would the side effects of acetylcholine be
Brief decrease in HR and Cardiac output
Vasodilation
Activation of muscarinic receptor M3 that causes endothelial release of nitric oxide
Increase salvation is intestinal motility
Increase bronchial secretion
detrusor muscle action
38
What are some direct acting cholinergic agents
Bethanechol
Pilocarpine
39
Does bethanechol act on nicotinic or muscarinic receptors
Muscarinic
40
What disease is bethanechol most commonly used on
GU diseases
41
What is the MOA of bethanechol
Stimulated the detrusor muscle of the bladder and relaxes the trigone and sphincter muscles which allow for urination
42
How is bethanechol used in postpartum and post-operative settings
to stimulate an atonic bladder
43
Is pilocarpine muscarinic or nicotinic
Muscarinic
44
What setting is pilocarpine most commonly used in
Ophthalmology
45
What is the MOA of pilocarpine
Apply topically to the eye
produces rapid mitosis and contraction of the cilliary muscles
Promotes salivation in those with xerostoma
46
What drug is very useful in glaucoma treatment and why
pilocarpine because it can lower intraoccular pressure
47
What drug is very useful in those with sjogrens syndrome or who have undergone head/neck radiation
Pilocarpine because it can help increase salivation
48
What is occurring with open angle glaucoma
there is increased resistance to aqueous humor drainage through the trabecular meshwork
49
What is occurring in closed angle glaucoma
Obstruction of drainage pathways by the iris
50
How does pilocarpine help in closed angle glaucoma
Acts of muscarninc receptor -> iris contracts
Pupil then constricts and will move the iris away from the angle
This allows opening of the trabecular meshwork around the canal of schlemm= decrease in intraoccular pressure
51
What are some indirect-acting cholinergic agents
Edrophonium
Pyridostigmine/Neostigmine
Physostigmine
Echotrophate
52
What in the MOA of edrophonium
Binds reversibly to the active center of acetylcholinesterase, preventing the hydrolysis of Ach
This will increase the concentration of Ach in the NMJ to rapidly increase muscle strength
53
What is edrophonium primarily used for
Diagnosis of M. Gravis
54
What causes M. Gravis
Autoimmune disease caused by antibodies to the nicotinic receptor in the NMJ
Antibodies then breakdown the receptors so less can interact with Ach
55
Which drugs are used in the chronic management of M. Gravis
Pyridostigmine (USA)
neostigmine (Canada)
56
What is the down side to taking pyridostigmine
works for 3-6 hours and thus needs to be taken 4-5 times a day for therapeutic effect
57
What is the MOA for physostigmine
Binds with acetylcholinesterase, making it reversibly inactivated
This stimulated the muscarinic & nicotinic sites of the ANS and nicotinic receptors of NMJ
58
What is physostigmine primarily used for
atropine overdose
59
What are the side effects of physostigmine
Miosis
hypotension
bradycardia
*high doses=convulsions
60
What is unique about echothiophate
Irreversibly binds to a phosphate group on AChE to permanently inactivate it
61
How is echothiophate used therapeutically
Treatment of ocular hypertension in chronic glaucoma
62
If echothiophate is used topically on the eye, what is the side effect
Intense miosis
63
If echothiophate is used in high doses, what can happen
Cataracts can be caused
64
What can be taken to reverse symptoms of echothiophate
High dose atropine
65
How are most organophosphate compounds used outside of echothiophate
Insecticides
chemical warfare
66
What symptoms occur with anticholinesterase toxicity
Increased urination
bradycardia
excessive secretions
pupillary constriction
67
What can be given to reverse anticholinesterase toxicity
Pralidoxime
68
How does pralidoxime work
Reactivates AChE in the periphery but it is unable to reverse the CNS effect
69
What group of cholinoceptor blocking drugs have a preference for nicotinic receptors
Ganglionic blockers
70
What group of cholinoceptor blocking drugs are useful for operative settings
Neuromuscular blocking agents (nicotinic antagonists)
71
What is the MOA for Neuromuscular blocking agents
Interfere with transmission of efferent impulses on skeletal muscle
72
What is atropine
A prototype anti-muscarinic drug
Highly selective muscarinic receptor
73
What does atropine have an effect on
Salivary, bronchial and sweat glands
*Little to no effect on skeletal NMJ
74
What type of effect does atropine have on the CNS
minimal
75
What effect does atropine have on the eye
Reduces lacrimation
Causes mydriasis, cycloplegia
76
What is mydriasis and cycloplegia
Inability to focus for near vision
77
What effect does atropine have on the respiratory system
Bronchodilation
Reduces airway secretions
78
What effect does atropine have on the cardiovascular system
Tachycardia (no BP effect)
Reduces PR interval
Blocks vasodilation of coronary arteries
79
What effect can low dose atropine have on the heart initially
bradycardia
80
What effect does atropine have on the GI system
Decrease salivary secretion
prolongs gastric emptying and intestinal transit time
81
What effect does atropine have on the GU system
Relaxes arterial / bladder wall smooth muscle
May cause urinary retention
82
What are the general side effects of cholinergic antagonists
Blurry vision, mydriasis
Decreased lacrimation, salivation, sweating
Confusion
Constipation
urinary retention
"Mad as a hatter, hot as hell, red as a beet, dry as a bone, blind as a bat"
83
How can topical atropine be used
To induce mydriasis and cycloplegia to measure refractory errors in the lens
84
How is IV atropine used therapeutically
Reversal of dangerous bradycardia
Reverse organophosphate toxicity / mushroom poisoning
blocks secretions in the upper and lower respiratory tract before surgery
85
What are some types of antimuscarinic agents
Scopolamine
ipatropium / tiotropium
86
What is scopolamine used for
Combat motion sickness
87
How is scopolamine administered
A patch
88
How is scopolamine different from atropine
Greater CNS effects
89
What is a side effect of scopolamine
Can be sedating
90
What are synthetic analogs of atropine
Ipatropium and tiotropium
91
How are ipatropium and tiotropium administered and why
Administered via aerosol route to allow for maximum targeting of bronchial tissue and reduce systemic effects
92
What are ipratropium and tiotropium used to treat
COPD either alone or with long acting beta adrenoreceptor agonist
93
What is the difference between ipratropium and tiotropium
Tiotropium is a long acting form of ipratropium
94
What are ganglionic blockers
Agents that block nicotinic receptors for both sympathetic and parasympathetic autonomic ganglia
95
What drug in the ganglionic blockers actually have therapeutic use
Nicotine
96
What is the MOA for Nicotine
Depolarizes the autonomic ganglia resulting in stimulation and then paralysis of all ganglia
causes release of dopamine and norepinephrine (pleasure and appetite suppression)
97
How can nicotine be administered and why
Gum, lozenges, MDI, transdermal patch to replicate drugs effects without smoking tobacco
98
Why are neuromuscular blockers useful during surgery
To facilitate tracheal intubation and provide complete muscle relaxation which allows for more rapid recovery of anesthesia
99
What is the MOA of neuromuscular blockers
Block cholinergic transmission between motor nerve ending and nicotinic receptors on skeletal muscle
100
How do neuromuscular blockers act on the different receptors
Antagonistic of Ach on nicotinic receptors(non-depolarizing)
agonist that causes desensitization of ACh at the NMJ endplate receptors (depolarizing)
101
What are examples or non-depolarizing neuromuscular blockers
Tubocurarine
rocuronium
vercuronion
102
What is the MOA of non-depolarizing blockers
They block ACH receptors and prevent depolarization of cell membrane which inhibits muscle contraction
103
Which muscles are paralyzed first with non-depolarizing blockers
smaller muscles (facial / ocular), then fingers, neck....
Respiratory effected last
104
What are some antidotes of non-depolarizing blockers
Neostigmine
edrophonium
105
How are non-depolarizing blockers administered and why
IV or IM
minimal bioavailability if taken orally
106
Do non-depolarizing blockers effect CNS or BBB
NO
107
What is the only depolarizing blocker in use today
succinylcholine
108
What is the MOA of succinylcholine
Causes cell membrane depolarization which produces transient fasciculations in the muscle followed by flaccid paralysis and then keeps ACh receptors desensitized to allow for continued paralysis
109
When is succinylcholine useful
Rapid ET intubation or ECT treatment
110
Complications for succinylcholine
Malignant hyperthermia
Apnea from prolonged paralysis
Hyperkalemia
