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PNS drugs > PNS drugs > Flashcards

PNS drugs Flashcards

1
Q

drugs that directly activate receptors

A

agonists

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2
Q

drugs that prevent receptor activation

A

antagonists

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3
Q

drugs can interfere with the termination of transmitter action by two mechanisms

A

blockage of transmitter uptake
or
inhibition of transmitter degradation

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3
Q

drugs can interfere with the termination of transmitter action by two mechanisms

A

blockage of transmitter uptake
or
inhibition of transmitter degradation

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4
Q

selectivity is one of the most desirable qualities a drug can have

A

many neuropharmacologic drugs exhibit high selectivity

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5
Q

to understand any particular PNS drug you need 3 types of information

A

1- the type or types of receptors through which the drug acts
2-the normal response to activation of those particular receptors
3-what the drug in question does to receptor function (increase or decrease)

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6
Q

What are the three effects that drugs can have on transmitter synthesis?

A

1- increase transmitter synthesis
2-decrease transmitter synthesis
3- cause the synthesis of transmitter molecules that are more effective than the natural transmitter itself

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7
Q

Functions of the parasympathetic Nervous system

A
  • slow heart rate
  • increase gastric secretion
  • emptying the bladder
  • emptying the bowel
  • focusing the ye for near vision
  • constricting the pupil
  • contracting bronchial smooth muscle
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8
Q

Therapeutic agents that alter the Parasympathetic nervous system are primarily used for their effects on

A

GI tract
bladder
eye

occasionally used for effects on : heart or lungs

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9
Q

the sympathetic nervous system has three main functions

A
  • regulating the CV system
  • regulating body temp
  • implementing the acute stress response (fight or flight)
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10
Q

The sympathetic nervous system influences the heart and blood vessels to achieve three homeostatic objectives

A
  • maintenance of blood flow to the brain
  • redistribution of blood flow during exercise
  • compensation for blood loss, primarily by causing vasoconstriction
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11
Q

The sympathetic nervous system causes

A
  • increased heart rate and BP
  • shunting blood away from the skin and viscera and into the skeletal muscles
  • dilating the bronchi to improve oxygenation
  • dilating the pupils
  • mobilize stored energy, providing glucose for the brain and fatty acids for the muscles
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12
Q

Describe feedback regulation

A

s process that allows a system to adjust itself by responding to incoming information.

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13
Q

What are the main elements of a feedback loop?

A

1 sensor : monitor the status of the physiological process
2 effector: makes appropriate adjustments in the process
3 neurons connecting the sensor to the effector:

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14
Q

What is the baroreceptor reflex?

A

feedback loop that helps regulate blood pressure

1) baroreceptors located in the carotid sinus and aortic arch monitor changes in BP and send this info to the brain
2) the brain sends impulses along nerves of ANS including heart and blood vessels to behave in a way to restore BP to normal

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15
Q

What is autonomic tone?

A

the steady day to day influence exerted by the ANS on a particular organ or organ system

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16
Q

What are the main neurotransmitters of the PNS?

A

acetylcholine (neurotransmitter employed at each of the junctions of the PNS

norepinephrine (transmitter released by practically all post-ganglionic neurons of sympathetic nervous system

epinephrine (major transmitter released by the adrenal medulla)

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17
Q

What are the two basic receptor categories associated with the PNS?

A

Cholinergic receptors (mediate responses to ACh)

Adrenergic Receptors (mediate responses to epinephrine and norepinephrine)

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18
Q

What are the three sub-types of cholinergic receptors?

A

Nicotinic - N

Nicotinic - M

Muscarinic

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19
Q

What are the four sub-types of adrenergic receptors?

A

alpha 1
alpha 2
beta 1
beta 2

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20
Q

Nicotinic N (neuronal)
name where they are found
name response to activation

A

found: all autonomic system ganglia and the adrenal medulla
response: STIMULATION of PARASYMPATHETIC and SYMPATHETIC post ganglionic nerves & release of epinephrine from the adrenal medulla

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21
Q

Nicotinic M (muscular)
name where they are found
name response to activation

A

found: neuromuscular junction
activation: contraction of skeletal muscle

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22
Q

muscarinic
name where they are found
name response to activation

A

found: all parasympathetic target organs (eye, heart, lung, bladder, GI tract, sweat glands, sex organs, blood vessels)

activation : eye (contraction of ciliary muscle/focus for near vision)
heart: decreased rate
lung: constriction of bronchi, promote secretion
bladder: contraction of detrusor muscle = increased bladder pressure/relaxion of
sphincters = urine leave bladder
GI tract: salivation, increased GI secretions, increased intestinal tone and motility
sweat glands: generalized sweating
sex organs: erection
blood vessels: vasodilation

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23
Q

alpa 1 (adrenergic receptor)
name where they are found
name response to activation

A

Location: eye, arterioles, skin, viscera, mucous membranes, veins, sex organs (males) , prostatic capsule, bladder

activation: eye (increased pupil size) arterioles (constriction) veins (constriction) sex organs (ejaculation), prostatic capsule (contraction), bladder, contraction of trifgone and sphincter

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24
Q

alpa 2(adrenergic receptor)
name where they are found
name response to activation

A

location: presynaptic nerve terminals
activation: inhibition of transmitter release

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25
Q

Receptor specificity of adrenergic receptors is

A

more complex than the receptor specificity of ACh.

ACh can activate all 3 subtypes of cholinergic receptors, not every adrenergic transmitter (epinephrine, norepinephrine, dopamine) can interact with each of the 5 subtypes of adrenerguc receptors

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26
Q

Epinephrine can activate…

A

all alpha and beta receptors but NOT dopamine receptors

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27
Q

Norepinephrine can activate…

A

alpha 1, alpha 2 and beta 1 but NOT beta 2 or Dopamine receptors

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28
Q

Dopamine can activate…

A

alpha, beta and dopamine receptors

dopamine is the only transmitter capable of activating dopamine recptors

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29
Q

the only transmitter that acts on Beta 2 receptors is…

A

epinephrine

epinephrine is released from the adrenal medulla (not from neurons)
epinephrine prepares body for fight or flight

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30
Q

Cholinergic drugs are

A

agents that act upon the cholinergic receptors

either mimic or block the actions of ACh

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31
Q

What are the 6 categories of cholinergic drugs?

A 
muscarinic agonists
muscarinic antagonists
cholinesterase inhibitors
ganglionic stimulating agents
ganglionic blocking agents
neuromuscular blocking agents
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32
Q

Responses to Muscarinic agonists closely resemble responses similar to what

A

the parasympathetic nervous system

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33
Q

Bethanechol is what type of drug?

A

a muscarinic agonist

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34
Q

What is the MOA of bethanechol?

A

direct-acting muscarinic agonist

acts selectively on muscarinic receptors

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35
Q

What are the pharmacologic effects of bethanechol?

A

act on eyes (constrict pupils and focus for near sight), heart (bradycardia), exocrine glands (increase sweating, salivation and bronchial secretions, secretions of gastric acid), bladder (emptying)

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36
Q

What are the pharmacokinetics of Bethanechol?

A

PO administration

30-60 mins onset and persist for about 1 hours

only small portion of each dose is absorbed

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37
Q

Therapeutic uses for Bethanechol?

A

urinary retention (post-op & postpartum) and to treat retention secondary to neurogenic atony of the bladder

GI uses (off label for GI reflux) also can help treat d/o with GI paralysis 
--* SHOULD NOT be given with GI obstruction
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38
Q

Adverse effects of Bethanechol?

A

CV- hypotension
GI- excessive salivation and GI secretions, involuntary defecation
Urinary-hazardous for thouse w/ urinary obstruction-increases bladder pressure
Lungs -exacerbation of asthma (bronchoconstriction)

CONTRAINDICATED for pts w/ hyperthyroidism (dysrythmmias r/t barorecptors)

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39
Q

receptor location for muscarinic

A

sweat glands, blood vessels, all organs regulated by parasympathetic nervous system

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40
Q

receptor location for nicotinic N

A

all ganglia of aurtonomic nervous system

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41
Q

receptor location for nicotinic M

A

neuromuscular junctions

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42
Q

effects of receptor activation of muscarinic

A

decreased heart rate
increased gland secretion
smooth muscle contraction

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43
Q

effects of receptor activation of nicotinic N

A

promotes ganglionic transmission

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44
Q

effects of receptor activation of nicotinic M

A

skeletal muscle contraction

45
Q

example of receptor agonist for muscarinic

A

Bethanechol

46
Q

example of receptor agonist for nicotinic N

A

Nicotine

47
Q

example of receptor agonist for nicotinic M

A

Nicotine (much higher dose)

48
Q 
Summary of key prescribing points for Bethanechol
therapeutic goal?
baseline data?
monitoring?
identifying high risk pts?
evaluating therapeutic effects?
minimizing adverse effects?
A

TG- tx of non obstructed urinary retention
BD- VS, urinary trends (I &O)
Monitoring - I&O, observe s/s of abnormal muscarinic response (over salivation, bradycardia etc)

High risk-contraindicated -obstruction (GI or urinary) asthma, hyperthyroidism, hypotension, coronary insufficienct

eval- no bladder distension

min adv effects- take on empty stomach to decrease n/v

49
Q

muscarinic (cholinergic) toxicity

A

DUMBELS

Diaphoresis/diarrhea
Urination
Miosis
Bradycardia/Bronchospasm
Emesis
Lacrimation
Salivation
50
Q

Pt education for muscarinic agonists

A

take 1 h b4 food or 2 h after meals

teach about manifestations of muscarinic excess and advise to seek med tx is occur

51
Q

What is cevemiline?

A

muscarinic agonist

used to tx dry mouth

52
Q

What is pilocarpine?

A

muscarinic agonist

therapy of glaucoma

53
Q

What are cholinesterase inhibitors?

A

drugs that prevent the degradation of ACh

increase the amount of ACh available to activate receptors= enhancing cholinergic action

do not bind directly with recptors so they are INDIRECT-acting cholinergic agonists

54
Q

what are the 2 basic categories of cholinesterase inhibitors?

A

1- reversible (produce effects of moderate duration)

2-irreversible (produce effects of long duration)

55
Q

what is Pyridostigmine?

A

a reversible cholinesterase inhibitor

tx of Myasthenia Gravis

poorly absorbed so minimal effect on brain or fetus

56
Q 
Summary of key prescribing considerations for Pyridostigimine
TX goal
Baseline Data
MonitoringHigh risk pts
Eval
min Adverse effects
A

TX goal-tx of myasthenia gravis
Baseline Data: HR, BP, ECG, ability to swallow, muscle strength ptosis
Monitoring:HR, BP, ECG, ability to swallow, muscle strength ptosis
High risk pts- obstruction (urinary or GI) pts w/ poor renal function start low dose
Eval: change in muscle strength and control
min Adverse effects

57
Q

Irreversible cholinesterase inhibitors

A

only one indication ; Tx of glaucoma

high lipid solubility
well absorbed

high affinity for toxic - poisoning

58
Q

what are muscarinic antagonists?

A

a type of anticholinergic drug
block the actions of ACh
act directly on receptors to block ACh

EX: Atropine

59
Q

anticholinergic drug in children?

A

prominent role in management of respiratory conditions

administration via inhalation decrease systemic s/e

no contraindication d/t age but d/t numerous adverse effects benefits should be weighed against risks

60
Q

anticholinergic drug in pregnant women?

A

oxybutinin relatively safe

but minimal studies _ caution recommended

61
Q

anticholinergic drug in breastfeeding women?

A

may inhibit lactation in some women = decreased breast milk production

due to lack of studies full range of risks unknown

if breastfeeding, infant should be monitored for possible anticholinergic effects

62
Q

anticholinergic drug in older adults?

A

potentially inappropriate

blurry vision, confusion, tachycardia, urinary retention and constipation

63
Q

What is atropine?

A

the best known muscarinic antagonist

from a plant - like belladona!

64
Q

MOA of atropine?

A

competitive blocking of muscarinic receptors

at low dose - decreased secretion of salivary glands, sweat glands and bronchial glands

at high dose- increased HR, urinary-lack of voiding, decreased GI motility, dilation of bronchi, decreased stomach acid secretion

65
Q

Pharmacologic effects of atropine?

A

exert influence primarily on heart (increase HR), eyes (relaxation of ciliary muscles and dilation of pupil) , exocrine glands (decreased secretion), and smooth muscles (relaxation of bronchi, decreased motility of GI, decreased tone of bladder)

66
Q

Pharmacokinetics of atropine?

A

topically to eye
+
parenterally (IM/IV/SQ)

peak - 30 mins
half-life 3 hours

10-17 hours in older pts

hepatic metabolism and renal excretion

67
Q

Therapeutic uses of Atropine?

A

except for eye uses is used short term
-prior to surgery
antidote to anticholinesterase poisoning
tx of sinus bradycardia and AV block

asthma - bronchial dilation
excessive GI motility
disorders of eyes or before eye exa

68
Q

Adverse effects of atropine?

A 
dry mouth
blurred vision
elevation of intra ocular pressure
urinary retention
constipation
lack of sweating
tachycardia
asthma
69
Q 
key prescribing considerations for atropine
Tx goal
Baseline data
Monitoring
High risk pts
Eval therapy
Min adverse effects
A

Tx goal- bradycardia or AV block, preanesthesia or antidote to anticholinerase poisoning
Baseline data - HR, BP ECG
Monitoring-HR BP recheck ECG
High risk pts- pts w/ no bradycardic dysrhythmias, MIs,
Eval therapy- restroation of normal sinus rhythm, prevention of surgical complications
Min adverse effects-tx dry mouth w/ fluids, manage photophobia w/ redused lighting or sunglasses, void prior to taking meds to avoid urinary retention

70
Q

What is scopolamine?

A

an anticholinergic drug with many actions like atropine HOWEVER
therapuetic doses of Scopolamine produces sedation
and this drug suppresses emesis

principle use: motion sickness

71
Q

Patient education for muscarinic antagonists

A
  • dry mouth relived by sipping fluids
  • avoid hazardous activities d/t potential for blurred vision
  • void before use
  • constipation reduced by increasing dietary fiber and fluids
  • avoid exercise in warm environments to prevent hyperthermia
72
Q

Antimuscarinic toxicity

A 
Hot as a hare (hyperthermia)
Dry as a bone (dry eyes, mouth, skin)
Red as a beet (flushed face)
Blind as a bat (mydriasis)
Mad as a hatter (delirium)
73
Q

What are adrenergic agonists?

A

drugs that produce their effects by activating adrenergic receptors

sympathetic nervous system acts through these same receptors

adrenergic agonists therefore produce similar effects as the stimulation of sympathetic nervous system

broad spectrum of indications: heart failure, asthma, preterm labor ….

74
Q

What are the mechanisms of adrenergic receptor activation?

A

direct receptor binding (most common mechanism) - bind to receptor and mimic actions of natural transmiters

promotion of norepinephrine release-act on the terminal ends of symapthetic nerves to cause NE release (amphetamines and ephedrine)

inhibition of norepinephrine reuptake- block NE reuptake thus causing NE to accumulate and increase receptor activation (cocaine and tricyclic antidepressants)

Inhibition of norepinephrine inactivation (drugs that inhibit MAO can increase the amount of NE available for release)

75
Q

What are the two major chemical classes of the adrenergic agonists

A

catecholamines and noncatecholamines

76
Q

What are catecholamines

A

contain a catechol group and an amine group

because of their chemistry all catecholamines have three properties in common

1) cannot be used orally (rapid inactivation by MAO and COMT (enzymes)
2) have brief duration of action
3) cannot cross the blood brain barrier

norepinephrine, epinephrine, isoproterenol, dopamine, dobutamine

77
Q

What are noncatecholemines?

A

adrenergic agonosts

no not contain a catechol
-ephendrine, albuterol, phenylephrine

less polar than catecholamines so are more able to cross the blood brain barrier
do not degrade quickly by liver metabolism (like catecholemines) so can be given PO

longer half-lives than catecholemines

78
Q

Which receptors are albuterol selective for?

A

highly selective for only Beta 2

79
Q

Which receptors are isoproterenol selective for?

A

less selective than albuterol

acts on beta 1 & beta 2

80
Q

Which receptors are epinephrine selective for?

A

less selective
acts on all four adrenergic receptors
alpha 1, alpha 2, beta 1 , beta 2

81
Q

what are the therapeutic applications of alpha 1 activation?

A

** 1) vasoconstriction (blood vessels of the skin, viscera, and mucous membranes)
(stopping bleeding-hemostasis, nasal decongestion, adjunct to local anesthesia -delay systemic absorption of anesthesia, elevation of BP–not primary use)
2)mydriasis

** alpha 1 agonists most often used for vasoconstriction

82
Q

What are adverse effects of alpha 1 activation?

A

hypertension (r/t widespread vasoconstriction)
necrosis (IV infusion seeps to surrounding tissue + vasocontriction to site)
bradycardia (vasoconstriction elevates BP -triggers baroreceptor response and BP drops)

83
Q

what are the clinical consequences of activating alpha 2 receptors?

A

alpha 2 receptors are primarily located presynaptically
their activation INHIBITS NE release
HOWEVER activating alpha 2 receptors in the periphery has little clinical significance

THOUGH activating alpha 2 receptors in CNS are of great significance

  • reduction of sympathetic outflow to heart and blood vessels
  • relief of severe pain
84
Q

What are therapeutic applications of Beta 1 activation?

A

Heart failure- improve cardiac contractibility and cardiac output

Shock- (characterized by hypotension and reduced tissue perfusion) increase heart rate and force of contraction

AV heart block (impulses from atria to ventricles impeded or blocked entirely) enhance impulse conduction through AV node

Cardiac arrest initiate contractions in asystole or pulseless ventricular rhythms. (not the preferred Tx) —epinephrine IV

85
Q

What are the adverse effects of activating Beta 1 receptors?

A

all the adverse effects are r/t activating beta 1 receptors in the heart /activating renal beta 1 receptors not associated w/ adverse outcomes

altered heart rate or rhythm (overstimulation of receptors-tachycardia)

angina pectoris (not enough perfusion and O@ to meet heart demands…beta 2 increase contractibility)

86
Q

what are clinical consequences of beta 2 activation

A

related to
lungs
&
uterus

87
Q

What are therapeutic uses for activating beta 2 receptors?

A

asthma (activation of receptors promotes vasodilation—use albuterol for its high selectivity)

delay of preterm labor (relaxes uterine smooth muscle- can delay early labor)

88
Q

What are some adverse effects of activating beta 2 receptors?

A

hyperglycemia - activation of beta 2 receptors in liver and skeletal muscles promotes breakdown of glycogen

tremor - MOST COMMON SE of beta 2 agonists - activation of beta 2 receptors in skeletal muscles enhances contraction– tremor usually fades with time and ca often be minimized by initiating therapy w/ low doses

89
Q

What are clinical consequences of activating dopamine receptors?

A

dilation of renal vasculature

for SHOCK

dilating renal blood vessels improves renal perfusion to reduce risk of renal failure

DOPAMINE is the ONLY drug that can activate dopamine receptors

when dopamine is given for shock it also enhances cardiac performance through activation of beta 1 receptors in the heart

90
Q

What is the patho of anaphylaxis?

A

manifestation of a severe allergy

hypotension (widespread vasodilation)
bronchoconstriction
edema of the glottis

histamine contributes - though other mediators (leukotrines ) contribute so antihistamines aren’t particularly useful

91
Q

What is the treatment for anaphylaxis?

A

Epinephrine
injected IM or IV

activated alpha 1, beta 1, beta 2 receptors

increases cardiac output, elevates BP, vasoconstriction and activation of b2 receptors can counteract bronchoconstriction

92
Q

What is the patient education for epinephrine auto-injectors?

A
  • fill Rx immediately and replace if expires
  • keep with you at all times
  • use immediately if needed (do not wait to see if symptoms will worsen)
  • after using call for EMS and take injector with you
93
Q

What is the receptor sensitivity and chemical classification of Epinephrine?

A

alpa 1, alpha 2, beta 1 , beta 2

catecholamine

94
Q

What is the receptor sensitivity and chemical classification of Norepinephrine?

A

alpha 1, alpha 2, beta 1

catecholamine

95
Q

What is the receptor sensitivity and chemical classification of Isoproterenol?

A

beta 1 and beta 2

catecholamine

96
Q

What is the receptor sensitivity and chemical classification of dopamine?

A

dopamine, beta 1 and at high does alpha 1

catecholamine

97
Q

What is the receptor sensitivity and chemical classification of dobutamine?

A

beta 1

catecholamine

98
Q

What is the receptor sensitivity and chemical classification of Phenylephrine?

A

alpha 1

noncatecholamine

99
Q

What is the receptor sensitivity and chemical classification of albuterol

A

beta 2

noncatecholamine

100
Q

What is the receptor sensitivity and chemical classification of Ephedrine?

A

alpha 1, alpha 2, beta 1, beta 2

noncatecholamine

101
Q

What are the therapeutic uses for Epinephrine?

A

can activate all four subtypes of adrenergic receptors therefore can produce a broad spectrum of effects

alpha 1- delay absorption of local anesthetics, elevate BP
beta 1 - overcome AV block, restore cardiac function in pt w/ certain cardiac arrest (v-fib, pulseless v tach, asystole)
beta 2- lungs - bronchodilation- asthma (not first choice for this)
alpha and beta together - choice for SHOCK

102
Q

What are the pharmacokinetics of epinephrine?

A

topically or injection
NOT PO d/t catecholamines undergo fast degstruction by enzymes (MAO and COMT)

has short half-life

103
Q

What are the adverse effects of epinephrine?

A

because of the activation of all four subtype of receptors it can have MANY adverse reactions

HTN crisis - vasoconstriction secondary to alpha 1 activation
Dysrhythmias-beta 1 receptors in heart
Angina Pectoris- beta 1 receptors in heart
Post-extravasation necrosis-
Hyperglycemia- secondary to b2 receptor actiavtion in skeletal muscles and liver

104
Q

What are some drug interactions with epinephrine

A

MOA inhibitors

tricyclic antidepressants - block the uptake of catecholamines (can prolonf effects of epinephrine)

general anesthetics

alpha adrenergic blocking agents

beta adrenergic blocking agents

105
Q

How is NE different from Epinephrine and what is NE indicated for?

A

NE doesn’t activate Beta 2 receptors - (no SE of hyperglycemia because this results from B2 activation)

limited clinical applications

indicated for: hypotensive status and cardiac arrest

106
Q

What are the therapeutic uses for Isoproterenol?

A

activates Beta 1 receptors in the heart

mange AV block
improve outcomes in cardiac arrest
increase cardiac output during shock

107
Q

What are the adverse effects from Isoproterenol?

A

fewer adverse effects than EPi or NE because doesn’t activate alpha receptors

tachydysrhythmias
heart pain
hyperglygcemia

108
Q

what are the therapeutic uses for Dopamine?

A

the major indication for dopamine is shock
benefits derive from the effects on the heart and renal blood vessels

dopamine activates B1 receptors and dopamine receptors.
At very high doses activates alpha 1 receptors as well

109
Q

What are the therapeutic uses for albuterol?

A

PNS drugs (1 decks)

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