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Final Test: Dynamics II > Cholinergic Receptor Anatgonist3 > Flashcards

Cholinergic Receptor Anatgonist3 Flashcards

1
Q

What are the physiological effects of atropine on the cardiovascular system?

A

the effects of atropine on heart are complex;

1) low dose produce a paradoxical bradycardia which may be due to blockade of M1 autoreceptors which would result in increased ACh release
2) higher doses blockade of the M2 receptors of the heart occurs, leading to tachycardia–the rate of AV conduction is elevated
3) atropine alone has no effect on the circulation but, it will reverse the vasodilation produced by cholinergic agonist

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2
Q

What happens when doses of atropine are high enough to decrease gastric acid secreation and dilate the brochoni?

A

it will also affect all other structure under muscarinc control. as a resul atropine and most other muscarinic antagonist are not very desirable for treating peptic ulcer disease or asthma

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3
Q

What are the contraindications of atropine?

A

1) men with prostatic hypertrophy
2) closed angle glaucoma
3) cardiac disease
4) myasthenia gravis
5) GI obstruction
6) intestinal colitis and atony

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4
Q

What can happen with VERY high dose of atropine?

A

remember pharse: dry as a bone, blind as a bat, red as a beet, and mad at as hatter

@ very high doses—-> coma and death occur

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5
Q

What are the side effects of atropine comparing adult to children?

A

adults okay w/ large doeses of atropine—> treat symptoms (keep cool)

dangerous in children—> uses a little physostigmine (reverse block)

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6
Q

What are the side effects of atropine>?

A

affects organ system just described. The most obvious effects are:

The DUCT:

d-dry mouth

u-urinary retention

c-constipation

t-tachycardia—M2 blockade

in addition, pronounced sedation can occur due to CNS action

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7
Q

What are the physiological effects of atropine on the glands?

A

atropine blocks ACh—> stops sweating—> body temp goes up (bad for babies and kids)

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8
Q

What are the physiolgocial effects of atropine on the gi tract?

A

1) atropine stops ACh—-> GI tone and motility lowers (not completely stopped b/c NANC-non adrenergic non cholinergic release from enteric nervous system)
2) atropine lowers:: acid secretion, proteolytic enzymes, and mucin (H2 now replaced anti-muscarinics like atropine)

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9
Q

What are the physiolgocial effects of atropine on the respiratory system?

A

bronchodilation and reduction of secretions occur

more pronounced effects are observed in patients with asthma and chronic obstructive pulmonary disease; atropine will also prevent secretions and laryngospasm produced by inhalation anesthetics

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10
Q

What happens during an overdose with atropine?

A

overdose of atropine—-> blocks PSNS function—> 1. derilium 2. agitation 3. higher body temperature 4. flushed skin

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11
Q

Name the drug interactions of atropine?

A

1) drugs w/ anti-muscarinic effects ( tricyclic anti-depressants, antipsychotic, histamine H1 blockers)
2) CNS depressants- potentiate depression
3) MAO inhibitors- more side effects of MAOI b/c unopposed sympathetics activity

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12
Q

What are the physiological effects of atropine on the CNS?

A

at therapeutic it causes mild stimulation of the PSNS medullary centers (which may cause bradycardia) and mild sedation

at high doses excitement, agitation, hallucinations and coma may result

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13
Q

What is another name for atropine. Hint there are 5

A

1) atronet
2) atropa
3) atrosun
4) tropine
5) bellpino-atrin

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14
Q

What are the therapeutic uses of atropine? Hint 9 uses!

A

1) treat irritable bowel syndrome that fails to respond to other treatments
2) decrease gastric motility and acid secretion in conjunction w/ H2 blockers for ulcers
3) treat spastic disorders of GI and genitourinary tract
4) trat urinary incontinence and enuresis by increasing bladder capacity and reducing tone
5) decrease salivation for inhalation anesthetics
6) prevent reflex bradycardia and hypotension during surgery
7) emergency treatment of severe bradycardia
8) reverse ACh-esterase inhibitor toxicity
9) parkinsonism

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15
Q

What order does atropine impact and what happens salivary glands, sweat glands, bronchial glands, heart, eye, urinary tract, intestine, lung and stomach?

A

low to high:

salivary, sweat, and bronchial glands

heart—> eye

urinary tract—-> intestine—> lung—-> stomach

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16
Q

What does atropine do and how does it impact receptors..which receptors?

A

its a competitive antagonist at muscarinic receptors; affinity for the different muscarinic receptors are similar

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17
Q

Where does atropine come from and what is its use?

A

derived from the deadly nightshade plant–atropa belladonna; atropine has been used as poison and cosmetically dilate pupils

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18
Q

What is important to know about the structure of atropine?

A

its a tertiary amine, thus it is widely distributed and enters the CNS

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19
Q

How is atropine an important about how atropine is removed from the body?

A

its rapidly eliminated in adults but not children

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20
Q

What are the physiological effects of atropine on the eye and how long does it last ?

A

local application prevents the action of ACh on the iris sphincter muscle and ciliary muscle (effect last 7-10 days)

Physiological effects:

result in pupillary dilation (mydriasis) and paralysis of accommodation (photophobia)—-> pupillary response to light is lost

eye will focuses on far vision, near objects may appear blurred and smaller than they are due to the paralysis of accommodation

***those patients with closed angle glaucoma may have dangerous increase in intraocular pressure but with systemic atropine: little ocular effects***

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21
Q

What is the connection between atropine at different levels of doses?

A

at low doses:

salivary glands, sweat glands, bronchial glands

at intermediate doses:

heart rate increase, eyes mydriasis, blurred vision

at high doses:

urinary tract- interference w/ voiding

intestine-decreased tone and motility

lung-dilation of bronchi

at very high doses:

stomach-decreases acid secretion: note that doses of atropine that are high enough to decrease gastric acid secretion or dilate the bronchi will also affect all other structers under muscarinic control; as a result, atropine and muscarinic

as a result atropine and most other muscarinic antagonists are not very desirable for treating peptic ulcer disease or asthma

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22
Q

Describe the schematic diagram of the interaction of drugs with acetylcholine receptors on the endplate channel.

For non-depolarizing blocker.

A

for drugs such as tubocurarine–preventing the opening of the channel when it binds to the receptor

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23
Q

Describe the schematic diagram of the interactions of drugs with the acetylcholine receptor on the endplate channel.

A depolarizing blocker

A

for example a succinylcholine, both occupy the receptor and blocking the channel; normal closure of the channel gate is prevented; depolarizing blockers may “desensitive” the endplate by occupying the receptor and causing persistent depolarization

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24
Q

Where is the site of action of ganglionic blockers?

A
  • nicotinic receptors in the sympathetic & parasympathic ganglion
  • receptor on the adrenal medulla
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25
Q

Give an example of why understanding the predominant tone is important in predicting how the ganglionic blocker impacts an organ.

A

the heart has both PSNS and SNS innervation;

PSNS (slows heart) is the predominant innervation; ganglionic blocker reduce both type of innervation. PSNS will be affected the most and net effect will be SNS predominance leading to tachycardia.

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26
Q

What the predominate tone of arterioles?

A

sympathetic (adrenergic)

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27
Q

How do ganglionic blockers work?

A

they do not cuase depolarization-block transmission without intial stimulation

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28
Q

What the first ganglionic blockers?

A
  • tetraethylammonium and hexamethonium (blocked ganglionic nicotinic receptors)
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29
Q

What is trimethaphan and what is its commerical name?

A
  • ganglionic blockers
  • arfonad is the commerical name
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30
Q

Give an example of two synthetic amines and what are their properties?

A

1) mecamylamine is a synthetic amine; its a teritary amine and can be ionized or unionized depending on the pH (alkalinzation favors the unionized form); its administered orally and can cross the BBB
2) trimethaphan is another and it is a charged S+ compound; it is administered parenterally; it does not enter the CNS

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31
Q

How can AChE inhibitors help deal with non-depolarizing blockers/ competitive surmountable antagonist?

A

AChE inhibitors will surmount the block; if channel block has occured AChE inhibitors will be less effective

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32
Q

How can apena be caused other than genetic defects?

A

rapid potassium release may contribute to apnea in patients with electrolyte imbalances

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33
Q

How does long succinylcholine duration of action last?

A

very brief duration of action in blood-quickly metabolized by pseudocholinesterase–only a small fraction of drug reaches NMJ

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34
Q

How does non-depolarizing neuromuscular blockers impact the CNS?

A

positively charged-poor lipid soluble–do not enter CNS

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35
Q

How does succinylcholine impact the nicotinic receptors?

A

produce similar action as ACh but the duration of action is longer than ACh; the longer duration of action allows it to act as a blocker

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36
Q

How fast are non-depolarizing neuromuscular blockers excreted?

A

they are rapidly excreted

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37
Q

How is succinylcholine metabolized at the NMJ and how does that impact nicotinic receptors ?

A

its not metabolized by true AChE-drug has to diffuse from synapse to be metabolized; thus succinylcholine at the NMJ can interact with nicotinic receptors for a long period of time; nicotinic receptors will become desensitized because of this reason

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38
Q

How long do the actions of cyclopentolate and tropicaimide last?

A

its used more than atropine since effects are shorter in duration: 0.25 to 1 day vs. 7 days

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39
Q

Where is the site action of neuromuscular blockers?

A

the nicotinic receptors on the striated muscle—site of action of neuromuscular blockers

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39
Q

What are the uses of ipratopium bromide and tiotropium?

A

1) bronchitis
2) emphysema
3) chronic obstructive pulmonary disease (COPD)
4) with beta-2 receptor agonist for asthma

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40
Q

What is the volume of distribution for non-depolarizing neuromusular blockers?

A

the volume od distribution is about equal to the blood volume

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41
Q

what other medical procedures does neuromuscular blockers assist with?

A
  • orthopedic procedures
  • intubation
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42
Q

which patients should be cautions in taking neuromuscular blockers patients?

A
  • heart failure patients receiving digitalis or diuretics
  • soft tissue damage
  • ocular laceration
  • muscle dystrophies
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43
Q

How do non-depolarizing blockers- competitive (surmountable) antagonist impact Na+ channels?

A
  • block prejunctional Na+ channels- (top) prevent ACh release
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45
Q

What is tubocararine?

A
  • prototype agent
  • non-depolarizing neuromuscular blocker
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46
Q

What is tiotropium and what is another name for it?

A
  • Spiriva
  • quaternary amine dervative of atropine
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46
Q

How are non-depolarizing neuromuscular blockers administered?

A

not orally bioavailable; all are given IV

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48
Q

Where is the site of action of antimuscarinic drugs?

A
  • effector organs in the parasympathetic pathway
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49
Q

What is tropicamide?

A
  • antimuscarinic agent
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50
Q

Why have synthetic antimuscarinic drugs declined in usage?

A

many have been developed but their use has declined due to the discovery of more selective agents and the pronounced side effects associated with these drugs

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50
Q

What are the therapeutic uses for scopolamine? Hint there are 8.

A

1) irritable bowel disease
2) spastic biliary problems
3) renal spasm
4) enuresis
5) an anesthetic adjunct to decrease salivation
6) to reduce excitement and to promote amnesia
7) restoration of cardiac rate and arterial pressure during surgery
8) prevention of motion sickness

51
Q

What is scopolamine ?

A

a plant alkaloid; similar properties as atropine

53
Q

What is imporant to know about the structure of scopolamine and why is this significant?

A
  • scopalamine teritary amine
  • quickly absorbed after oral dose and transdermally
  • can cross BBB (blood brain barrier)—-> CNS effects
54
Q

How does the actions of scopolamine compare with atropine?

A

stronger effects than atropine—> very lipid soluble

abuse of scopolamine—-> europhoria

55
Q

What is the mechanism of action of scopolamine?

A
  • MAO (similar to atropine)
  • competitively blocks muscarinic receptors
55
Q

What are the physiological effects of scopolamine but how does it compare to atropine?

A

1) similar to atropine
2) stronger sedation and amnesia—-> CNS
3) fixes vestibular disturbance
4) scopolamine (systemic and transdermal route) —> ocular effects
5) scopolamine (opthalmic route)—-> systemic circulation

57
Q

What are anti muscarinic agents refered to as and why?

A

parasympatholytic because the selectively reduce or abolish the effects of parasympathetic stimulation

58
Q

What are anti-muscarininic agents and what do they inhibit?

A

competitive antagonist at muscarinic receptors

they inhibit both CNS and peripheral (ANS) action of ACh

59
Q

What are neuromuscular blockers used for?

A

used in surgical procedures and in the ICU to cause and maintain muscle paralysis

59
Q

What are muscles responsive to?

A

the muscle will respons to direct depolarization wit hK+ and to electrical stimulation

61
Q

What are nicotinic receptors stimulated by?

A

ACh and nicotine

61
Q

What are non-depolarizing neuromuscular blocking agents used to cause paralysis during anesthsia?

A

tubocurarine, gallamine, pancuronium, atracurium, vacuronium

62
Q

What are some benefits of neuromuscular blockers during surgery?

A

minimizes the risk of respiratory and cardiac depression-shortens recovery time after surgery

63
Q

What are some depolarizing agents?

A

decamethonium and succinylcholine

64
Q

What are the benefits of neuromuscular blockers when used with anesthesia?

A

neuromuscular blockers can be used in adjunct to anesthesia for skeletal muscle relazation that is not dependent on the depth of general anesthsia

65
Q

what are the depolarizing neuromuscular blockers?

A

succinylcholine is the only agent clinically approved in the USA they have to ACh molecules put together

66
Q

What are the effects of both non depolarizing neuromuscular-blocking agents and depolarizing neuromuscular blocking agents?

A

both classes of drugs interferes with ACh post-synaptic actions

67
Q

what are the effects of ganglionic blockade on the arterioles?

A

vasodilation and increased peripheral blood flow; hypotension

68
Q

What are the major chemical classes of non-depolarizing blockers?

A

steriodal (such as pancuronium) and isoquinolines (atracuronium)

69
Q

What are the neuromuscular blockers that block choline uptake and what is their overall function?

A

hemicholinium, triethylcholine-not used clinically anymore

inhibition of ACh synthesis

71
Q

What are the neuromuscular blockers that inhibit Ach release?

A
  • aminoglycoside antibiotics (streptomycin, neomycin)
  • botulinum toxin and beta-bungarotoxin
  • botulinum toxin- injected locally into muscles is used to treat disabling eyelid spasms (blepharospasm) as well as other types of local muscle spasms and migraines
71
Q

What are the newer agents of non-depolarizing blockers that have less side effects?

A

succinylcholine the depolarizing blocker- bradycardia, cardiac dysrhythmias due to K+ release, increase IOP, and malignant hyperthermia ( rarely)

73
Q

What are the overall physiological effects produced by a ganglionic blocker?

A

it can often be preducted by understanding the predominant innervation (PSNS and SNS) of a particular organ

74
Q

What are the side effects of tubocurarine?

A

causes ganglionic blockade, histamine release, hypotension and bronchoconstriction–has fallen out of favor

75
Q

What are two prototype agents that block ganglionic nicotinic receptors?

A

mecamylamine and trimethaphan are two agents that competitively block ganglionic nicotinic receptors

75
Q

What are the two classes of drugs used to cause paralysis during anesthesia?

A

1) non-depolarizing neuromuscular-blocking agesn
2) depolarizing neuromuscular blocking agents

77
Q

What do agents that act at neuromuscular junction and autonomic ganglia do?

A

1) inhibit nicotinic receptors-which are stimulated by both ACh and nicotine
2) ganglionic agents act by blocking actions of nicotinic agents on the postganglionic neuron
3) neuromuscular blocking agents are distinguished by whether or not they cause depolarization of motor end plate–classified as non-depolarizing blockers or depolarizing blockers

78
Q

What do competivite surmountable antagonist do to the nicotinic receptor channel?

A

reduce the frequency of nicotinic receptor channel opens but not the duration or amplitude of the opening. At higher levels the drugs can enter the channel to block ion flow (non-competitive)

79
Q

What does a therapeutic selection of neuromuscular blockers depend on?

A

achieving a pharmacokinetic profile consistent with the duration of the interventional procedure and minimizing cardiovascular complications and other side effects

80
Q

What does succinylcholine do to intracellular sites and how can this be dangerous?

A

succinylcholine can cause rapid release of K+ from intracellular sites;

succinylcholine-induced hyperkalemia is a life threatening complication of the drug

81
Q

What happened to use of mecamylamine and trimethaphan & formerly what was their use?

A

they were discontinued but before they were used for:

1) hypertensive crisis and for moderate to severe hypertension where other treatment have failed
2) acute dissecting aneurysm of the aorta
3) autonomic hyperflexia and to produced controlled hyptotenison and minimized bleeding during certain types of skin surgery

82
Q

What happens during phase 3 of succinylcholine?

A

the membrane repolarized but receptor is desensitized to effect of acetylcholine

after continual exposure, depolarization decrease at the endplate and the muscles become repolarized; ACh still cannot activate the receptor–receptors are desensitized to ACh

block still occurs because end plate is desensitized and trasmission of signal fials

83
Q

What happens during phase one of succinylcholine the depolarizing blocker?

A

in phase 1:

the membrane depolarizes, resulting in an initial discharge that produces transient fasiculations followed by flaccid paralysis

84
Q

What happens during phase two of succinylcholine depolarizing blockade?

A

phase 2:

channel opens and muscle becomes depolarized. succinylcholine is not metabolized at the synapse resulting in continous depolarization of the muscle which become unresponsive to additional stimulation;

repolarization is necessary for normal muscle tone–but since to the channel is kept open repolarization can not occur

85
Q

What happens during relaxation for non-depolaring blockers?

A

onset of relaxation:

motor weakness—–> muscle totally flaccid——–> diaphragm paralyzed.

Recovery occurin the reverse order

86
Q

What is another form of neuromuscular blockers and what do they do?

A

competitive surmountable antagonists- they combine with nicotinic receptors at the post junctional end plate of muscles to block the binding of ACh- largerly accounts for actions

87
Q

What is another name for cyclopentolate?

A

Cyclogy

88
Q

What is another name tropicamide?

A

Mydriacyl

89
Q

What is apena and how does it occur?

A

its included under the subheading of depolarizing blockers; its a result of prolonged diaphragm paralysis

apnea primarily occurs if patient has genetic defects in plasma cholinesterase

90
Q

What is curare?

A

its a mixutre of naturally occuring alkaloids found in various south american plants used as arrow poisons by South American Indans

91
Q

What is cyclopentolate?

A

an antimuscarinic agent

92
Q

What is important to note about the sturuce of non-depolarizing blockers?

A

they have one or more quaternary amine in their sturucture

93
Q

What is ipratopium bromide and what is another name for it?

A
  • Atrovent
  • quaternary amine derivative of atropine
94
Q

What is mecamylamien and what is its commericial name?

A

its a ganglionic blocker and its name is inversine

95
Q

What is the action of hexamethonium?

A

they block the channel portion of the receptor preventing the entry of Na+ into the cell

96
Q

What is the adminstration of ipratopium bromide and tiotropium and how long do the effects last?

A
  • inhalants (little systemic effect)
  • effect on target last 4-6 hours
97
Q

What is the clinical use of parasympatholytics for cardiovascular?

A

treatment of sinus bradycardia (eg after MI): IV atropine

98
Q

What is the clinical use of parasympatholytics for gastrointestinal use?

A

1) relax GI smooth muscle (antispasmodic action) and suppress gastric acid secretion
2) to faciliate endoscopy and GI radiology- scopolamine IV
3) irritable bowel syndropme, colonic diverticular disease- oral dicyclmine
4) peptic ulcer disease-pirenzepine (not in the U.S.)

99
Q

What is the clinical use of parasympatholytics for neurological use?

A

1) prevention of motion sickness- scopolamine orally or transdermally
2) parkinsonism- especially to counteract movement disorders caused by antipsychotic drugs—benztropine

100
Q

What is the clinical use of parasympatholytics for opthalmic use?

A

to dilate the pupil: tropicamide eye drops (short) and cyclopentolate eye drops (long)

101
Q

What is the clinical use of parasympatholytics for respiratory use?

A

1) asthma-ipratopium by inhalation
2) anesthetic premedication to dry secretion- atropine, scopolamine by injection; diminished use since current anesthetics are non-irritatns

102
Q

What is the depolarizing neuromuscular-blocking agents used to cause paralysis during anesthesia?

A

depolarizing neuromuscular-blocking agents: succinylcholine

103
Q

What is the difference between 3 degree and 4 degree amines for anti-muscarines?

A
  • teritary and quaternary amine- used for genitorurinary conditions
  • quaternary amine-poorly absorbed
  • teritary and quaternary- used @ does which cause side effects like atropine
104
Q

What is the effect of ganglionic blockade on salivary glands?

A

xerostomia (diminished salivary secretion)

105
Q

What is the effect of ganglionic blockade on sweat glands?

A
  • anhidrosis (absence of sweating)
106
Q

What is the effect of ganglionic blockade on the ciliary muscle?

A

cyclopegia

107
Q

What is the effect of ganglionic blockade on the heart ?

A

tachycardia

108
Q

what is the effect of ganglionic blockade on the iris?

A

mydriasis

109
Q

What is the effect of ganglionic blockage on the GI tract?

A

reduced tone and motility; constipation

110
Q

What is the effect of urinary retention on urinary bladder?

A

urinary retention

111
Q

What is the function of cholinergic receptor antagonist?

A

bind to cholinoceptors but do not trigger the usual receptor-mediated intracellular effects

112
Q

What is the function of ganglionic blockers?

A
  • inhibit nicotinic receptors on sympathetic and parasympathetic ganglia
113
Q

What is the function of ganglionic blockers?

A

major ganglion-blocking drugs all acy by inhibiting the post-synaptic and presynaptic actions of ACh

114
Q

What is the function of neuromuscular blocking agents?

A

interfere with transmission of efferent impulses to skeletal muscles

115
Q

What is the mechanism of action for ipratopium bromide and tiotropium?

A

the relaxation of bronchial smooth muscle and decrease secretion; it will not inhibit ciliary motility like other blockers so the remaining mucus can be cleared

116
Q

What is the predominant tone in the ciliary muscle?

A

parasympathetic

117
Q

What is the predominant tone in the GI tract?

A

parasympathetic

118
Q

What is the predominant tone in the iris?

A

parasympathetic

119
Q

What is the predominant tone of the heart?

A

parasympathetic (cholinergic)

120
Q

What is the predominic tone of veins?

A

sympathetic

121
Q

What is the prototypical antimuscarinic agent?

A

atropine- all other anti-muscarinic agent will exhibit the same general properties as atropine unless otherwise noted

122
Q

What is the tone of the salivary glands?

A

parasympathetic

123
Q

What is the tone of the sweat glands?

A

sympathetic

124
Q

What is the tone of the urinary bladder?

A

parasympathetic

125
Q

What is the treatment for malignant hyperthermia?

A

cool patient, give dantrolene (prevents Ca2+ release from muscles reduce heat and rigidity)

126
Q

What is the use of cyclopentolate and tropicajmide?

A

used for mydriasis and paralysis of accomadation

127
Q

What other side effects as a result of succinylcholine?

A
  • malignant hypertermia combined with halothane-muscular rigidity,
  • metabolic acidosis
  • tachycardia
  • hyperpyrexia

Final Test: Dynamics II (11 decks)

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