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Pharmacology > ANS Pharmacology > Flashcards

ANS Pharmacology Flashcards

1
Q

Autonomic Nervous System

Main activities

A

•Three main activities
–Contraction of smooth muscle of the bronchi, blood vessels, gastrointestinal tract, eye, and genitourinary tract
–Contraction of cardiac muscle
–Secretion of salivary, sweat, and gastric glands

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2
Q

Structure and Function of the ANS
Two divisions
Organs and glands

A 
•Two divisions
–Sympathetic
–Parasympathetic
•Organs and glands
–Receive nerves from both branches
–Opposing actions
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3
Q

Fight-or-Flight Response (SNS)

What happens in the body?

A 
Brain
–Increased alertness and readiness
•Cardiovascular
–Increased heart rate and blood pressure
•Musculoskeletal
–Ready for sudden, intense physical activity
•GI
–Liver produces more glucose for energy; Decreased peristalsis
•Respiratory
–Dilation of bronchi, increased respirations
•Pupils
–Dilation, increased vision
•Integumentary
–Warm, increased perspiration
•Genitourinary
–Decreased urine formation
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4
Q

Rest-and-Digest (PNS)

What happens in the body?

A 
•GI
–Increased secretions
–Increased peristalsis
•Cardiovascular
–Decreased heart rate and blood pressure
•Respiratory
–Constriction of bronchi, decrease respirations
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5
Q

What are the ANS Neurotransmitters?

A
  • Norepinephrine (NE)

* Acetylcholine (Ach)

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6
Q

Classification of Autonomic Drugs

A 
Stimulation of SNS
–Sympathomimetics, adrenergic-agonists
•Stimulation of PNS
–Parsympathomimetics, muscarinic agonists
•Inhibition of SNS
–Adrenergic antagonists or blockers
•Inhibition of PNS
–Anticholinergics, parasympatholytics, muscarinic blockers
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7
Q

What are cholinergic receptors

A
  • Can be activated directly or indirectly
  • Found in the autonomic nervous system at the ganglia and the neuroeffector junctions
  • Found in the somatic nervous system at the neuromuscular synapses
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8
Q

Direct Cholinergic Agonists

A

•Produce rest-and-digest responses
–Activate cholinergic synapses by releasing Ach into the synaptic cleft
–Drug binds to Ach receptors, enhancing action potential
–Drug inactivated by AchE

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9
Q

Indirect Cholinergic Agonists

A

•Drug binds AchE, preventing Ach from being destroyed
–Increases amount of Ach remaining in synaptic cleft
•Results in a greater effect

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10
Q

Effects of Muscarinic Agonists

A
  • Increase degree of smooth muscle tone and contractions of the GI tract
  • Stimulate smooth muscle of the urinary tract
  • Stimulate most exocrine glands
  • Cause contraction of the iris sphincter
  • Contraction of bronchial smooth muscle
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11
Q

Precautions or muscarinic agonists

A

•Do not administer to patients with:
–Suspected obstructive disease of the gastrointestinal or genitourinary tract
–Asthma or COPD
•Monitor patients for reflex tachycardia
–Particularly hyperthyroid or cardiovascular patients

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12
Q

Indirect Acting
(Anticholinesterase Agents)
Side effects

A

•Common side effects
–Involuntary contraction or twitching of muscles, nausea/vomiting, miosis, increased salivation
•Serious adverse effects
–Bradycardia, hypotension, dyspnea, seizures, bronchospasm, cholinergic crisis, death due to paralysis of respiratory muscles

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13
Q

Potential Uses for AchE Inhibitors

A
  • Alzheimer’s disease
  • Glaucoma
  • Protect against bioterrorist attack with nerve gases
  • Myasthenia gravis
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14
Q

What are Muscarinic Antagonists?

And what are the reasons for their uses?

A
  • Primarily block receptors in the parasympathetic nervous system
  • May also be known as anticholinergics, cholinergic blockers, muscarinic antagonists, or parasympatholytics
  • Work by competing with Ach for binding at muscarinic receptors, allowing sympathetic activation to dominate
•Are used for their parasympathetic actions
–Dilation of the pupils
–Increased heart rate
–Drying of secretions
–Bronchodilation
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15
Q

Uses of Muscarinic Antagonists

A

GI disorders such as IBS
•Ophthalmic procedures
•Cardiac rhythm disorders
•Adjuncts to anesthesia to decrease secretions
•Asthma for bronchodilation effects
•Antidotes for poisoning from muscarinic drugs
•Neurogenic bladder; Urge incontinence
•Parkinson’s disease
•Antidotes for poisoning from muscarinic drugs
•Urge incontinence

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16
Q

What are adrenergic receptors?

A

•Site where adrenergic drugs (neurotransmitters) bind and produce their effects
•Catecholamine’s (neurotransmitters) Act on receptor sites throughout the body – known as adrenergic receptors.
–Two major types of receptors-alpha and beta.
–Two subtypes for each :
● alpha 1 and alpha 2
●beta 1 and beta 2

17
Q

Adrenergic receptors

How it acts on the alphas and beta

A 
Act on:
•Alpha 1- on postsynaptic effector cells
–Tissue
–Muscle
–Organ
•Alpha 2- on presynaptic nerve terminals (actually on the nerve)
–Control release of neurotransmitters
•Beta 1 – postsynaptic effector cells
–Heart
•Beta 2 – postsynaptic effector cells- smooth muscles of:
–Bronchioles
–Arterioles
–Visceral organs (e.g. uterus)
18
Q

Sympathomimetics

How to they work?

A

•Exert effects via two mechanisms
–Directly
●Binding to and activating adrenergic receptors
●Epinephrine, norepinephrine, dopamine
–Indirectly
●Increasing amount of norepinephrine available at adrenergic synapses

19
Q

Adrenergic Agonists

What do they do?

A

•Activate sympathetic receptors in sympathetic nervous system
•Induce fight-or-flight response
•Two receptor types
–Alpha
–Beta
•Include norepinephrine, epinephrine, dopamine

20
Q

Alpha1-Receptor Agonists

Why are they prescribed and what can they be used for?

A
  • Generally prescribed for nasal congestion and hypotension

* May be used to produce mydriasis during ophthalmic exams

21
Q

Beta1-Receptor Agonists

What are they for and what do they do?

A 
•Critical care drugs
–Heart attack
–Heart failure
–Shock
•Have powerful affects on heart
22
Q

Beta2-Receptor Agonists

What are they used for?

A
  • Used to treat asthma

* Reduce preterm labor contractions of uterus

23
Q

Vasoactive adrenergics
What are they used for/ what do they do?
What are some examples?

A

Used to support a failing heart or to treat shock
•Very potent, quick-acting, and their effects quickly cease when they are stopped
–epinephrine (Adrenaline), alpha & beta adrenergic, treat shock
–Dopamine- (Intropin) -beta1 adrenergic, IV only, to raise B/P,
–Norepinephrine- (Levophed) Alpha & Beta adrenergic
–dobutamine (Dobutrex)-beta 1 adrenergic, to treat cardiac decompression

24
Q

Adrenergic drugs side/adverse effects

Alpha and beta

A

Alpha:
– headaches, restlessness, excitement, insomnia, euphoria
–Cardiovascular: chest pain, vasoconstriction, HTN, tachycardia, dysrhythmias
–Anorexia, dry mouth, N/V, taste changes
•Beta:
–Mild tremors, H/A, nervousness, dizziness
–Cardiovascular: increased heart rate, palpitations, dysrhythmias, B/P fluctuations
–Sweating, N/V, muscle cramps

25
Q

Alpha1-Adrenergic Antagonists
Where are they located?
What do they do?
How do they do it?

A
  • Receptors located on smooth muscle of heart, genitourinary and gastrointestinal systems, and brain
  • Most important action of these agents is on arterial smooth muscle and cardiovascular system
  • Blockade of alpha receptors dilates blood vessels, lowering blood pressure
26
Q

Adrenergic Blocking agents
Antagonists
Alpha blockers

A

Antagonists- bind to adrenergic receptors inhibiting or blocking stimulation of the sympathetic nervous system, AKA sympatholytics
–Alpha blockers- block at the alpha adrenergic receptor. Causes vasodilation, decreased B/P, miosis (constriction of pupil), suppressed ejacuation
–Beta blockers-
–Alpha-beta blockers

27
Q

Alpha Blockers
What do they do?
What times of blockades are there?

A

Interrupt or block the stimulation of the SNS at the alpha-adrenergic receptor
–Leads to vasodilatation, decreased blood pressure, constriction of the pupil (miosis), or suppressed ejaculation
–Some alpha blockers (ergots) cause vasoconstriction
•Competitive Blockade- compete for sites with NE. Occupy the site before the neurotransmitter NE or push off the NE- reversible blockade.
•Noncompetitive Blockade- irreversible, forms a bond at the receptor.

28
Q

When do we use alpha-blockers?

A

•Migraines
–Ergot alkaloid – ergotamine tartrate
•Constricts arterioles in the brain
•Control postpartum bleeding and increases uterine contractions
–* oxytocin (Pitocin) Induces local vasoconstriction
•Hypertension
–doxazosin, prazosin, terazosin, tamsulosin
•Alpha-blocker that causes both arterial and venous dilation
•Reduces peripheral vascular resistance
•Benign Prostatic hyperplasia
–Tamsulin (Flomax)- reduces ctx of bladder neck & prostate portion of the urethra

29
Q

Side effects of alpha-blockers in the different body systems?

A

Cardiovascular: palpitations, orthostatic hypotension, tachycardia, edema, dysrhythmias, chest pain
•CNS: dizziness, headache, drowsiness, anxiety, depression, vertigo, weakness, numbness, fatigue
•GI: nausea, vomiting, diarrhea, constipation, abdominal pain
•Other: Incontinence, nose bleeding, tinnitus, dry mouth, pharyngitis, rhinitis

30
Q

Management of overdose of alpha-blockers

A
  • Acute overdose need to empty stomach (i.e. ipecac syrup, gastric lavage)
  • Activated charcoal to bind the drug and remove it from the stomach and circulation
  • Treat symptoms
  • ABC
31
Q

Beta-blockers
What do they do?
Selective vs. nonselective

A

Block SNS stimulation of the beta-adrenergic receptors by competing with the endogenous catecholamines; norepinephrine and epinephrine
•May be selective (beta 1-blocking agents)
–Cardioselective beta Blockers
–Block the beta-adrenergic receptor site on the surface of the heart
•Nonselective (beta 1 & beta 2- blocking agents), block cardiac and respiratory and smooth muscle of blood vessels
•Cardioprotective effects

32
Q

Beta-blockers

Cardioselective vs. non-selective

A

Cardioselective:
•atenolol (Tenormin)
–Used to prevent future myocardial infarctions (MI) in patients who have had an MI, hypertension, and angina
•metoprolol (Lopressor and Toprol XL)
–Used in post MI patients, increases survival in patients who had a MI
•acebutolol (Sectral)
–Used for treatment of hypertension, ventricular and supraventricular dysrhythmias, and angina
Non-selective:
•labetalol (Nomodyne and Trandate)
–Used in treatment of severe hypertension and hypertensive emergencies
–Can block both alpha- and beta- adrenergic receptors
•propanolol (Inderal)
–Used in treatment of hypertension, angina, tachydysrhythmias, pheochromocytoma, migraines
•carvedilol (Coreg)
–Used in treatment of heart failure (slows progression of heart failure), hypertension, and angina

33
Q

Beta-Adrenergic Antagonists

Selective

A

•Selective
–Block only beta1 receptors
–Cardioselective
–Fewer noncardiac side effects
–Little effect on bronchial smooth muscle
–Can be safely given to clients with asthma and COPD

34
Q

Beta-Adrenergic Antagonists

Nonselective

A

Nonselective
–Block beta1 and beta2 receptors
–Produce more side effects than selective beta1 antagonists
–Serious side effect is bronchoconstriction
–Caution in patients with COPD or asthma

35
Q

Side effects of beta blockers in different body systems?

A

Cardiovascular: AV block, bradycardia, heart failure, peripheral vascular insufficiency
•CNS: dizziness, mental depression, lethargy, hallucinations
•GI: nausea, dry mouth, vomiting, constipation, diarrhea, cramps
•Other: impotence, rash, alopecia, bronchospasms

36
Q

Management of overdose/toxicity of beta-blockers

A

Acute overdose need to empty stomach (i.e. ipecac syrup, gastric lavage)
•Treat symptoms and provide supportive care
–atropine to treat bradycardia
–Vasopressors for hypotension
–diazepam (Valium) to treat seizures

37
Q

Beta-blockers

Nursing Implications/Teach patient:

A

Nursing Implications/Teach patient:

–Wear medical alert bracelet, necklace, etc.
–Information on medications taken in purse, wallet, etc.
–Never abruptly stop medications (may lead to rebound hypertension). Don’t double up meds
–Adrenergic blocking agents- avoid caffeine & other CNS stimulants
–Avoid Alcohol- leads to vasodilatation increasing hypotension & orthostatic Hypotension
–Rise slowly
–Report weight gain, SOB, excessive fatigue, syncope, confusion, depression, hallucinations, palpitations.

38
Q

Similar Drugs

A 
Carteolol (Cartrol, Ocupress)
•Carvedilol (Coreg)
•Labetalol (Normodyne, Trandate)
•Metipranolol (OptiPranolol)
•Nadolol (Corgard)
•Penbutolol (Levatol)
•Pindolol (Visken)

Pharmacology (8 decks)

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