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Pharmacology: Exam 1 > Module 2: Peripheral Nervous System Drugs (Adrenergic/Cholinergic Drugs) > Flashcards

Module 2: Peripheral Nervous System Drugs (Adrenergic/Cholinergic Drugs) Flashcards

1
Q

Nervous System Divisions

A

Central Nervous System (CNS):

  1. Brain: receives and processes sensory information, initiates responses, stores memories, and generates thoughts and emotions
  2. Spinal cord: conducts signals to and from the brain, and controls reflex activities

Peripheral Nervous System (PNS):

  1. Sensory neurons (sensory organs to CNS)
  2. Motor neurons (CNS to muscles and glands); it is further divided into the (1) Somatic Nervous System (controls voluntary movements) and (2) Autonomic Nervous System (controls involuntary responses)

Autonomic Nervous System (ANS) divisions:
1. Parasympathetic Nervous System (PSNS) — “rest or digest” (cholinergic system)

  1. Sympathetic Nervous System (SNS) — “fight or flight” (adrenergic system)
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2
Q

ANS Functions

A

Functions of the ANS:
1. Regulation of the heart

  1. Regulation of the secretory glands
  2. Regulation of smooth muscle of the bronchi, blood vessels, urogenital tract, and GI
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3
Q

Mechanism of Action Potential (AP) and Neurotransmitter (NT)

A

Mechanism of NT release:
1. NTs are synthesized from precursor molecules

  1. NTs are packaged into a vesicle
  2. NTs are released in response to an AP
  3. NTs travel across the synaptic cleft, bind to receptors on the post-synaptic cell, and produce a response; at some point NTs dissociate from the receptors, terminating the action and response
  4. After dissociation, a NT can undergo (1) re-uptake into the pre-synaptic nerve terminal, (2) enzymatic degradation, or (3) diffuse away from the nerve terminal
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4
Q

PNS Anatomy

A

Pre-ganglionic neurons originate in the CNS, innervate at a ganglion (synapse), and release acetylcholine (ACh) at the nicotinic receptor on the post-ganglionic neuron (which leads to the end organ)

**If drugs targeted the pre-ganglionic neuron and NT, they would NOT be specific; instead, drugs target post-ganglionic neurons, NTs, and end organ receptors

**In the somatic system, there is just one neuron that originates in the CNS, and extends to the skeletal muscles where it releases ACh on nicotinic receptors in the neuromuscular junction

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5
Q

Parasympathetic Nervous System (PSNS)

A

a.k.a. Cholinergic system

Receptor = Muscarinic (M)
NT = ACh

Location of M receptors (in the PSNS):

  1. Cardiac and smooth muscle
  2. Gland cells
  3. Nerve terminals

**Sweat glands (in the SNS) also use M receptors and ACh

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6
Q

Acetylcholine (ACh)

A

Drugs that interfere with ACh function:
1. Agonist drugs — mimic ACh by binding at M or N receptors

  1. Antagonist drugs — block the effect of ACh, by binding at M or N receptors
  2. Influence enzymatic breakdown of ACh via acetylcholinesterase (AChE)
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7
Q

Parasympathetic Stimulation

A

Effects (“rest and digest”):
1. Slowing HR

  1. Increased gastric secretion
  2. Empty bowel and bladder
  3. Focusing the eye for near vision
  4. Constricting the pupil
  5. Contracting bronchial smooth muscle
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8
Q

Parasympathetic Blockade

A

Causes the opposite effects of parasympathetic stimulation

Excess blockade results in:
1. “Mad as a hatter” — psychosis and seizures

  1. “Dry as a bone” — decreased secretions
  2. “DrySLUDS” — Decreased: salivation, lacrimation, urination, defecation, sweating
  3. “Blind as a bat” — eyes cannot accommodate (cannot see up close), pupils cannot constrict, and photophobia
  4. “Red as a beet” — dilation of cutaneous blood vessels
  5. “Hot as a hare” — skin feels warm
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9
Q

Sympathetic Nervous System (SNS)

A

a.k.a Adrenergic system

Adrenergic receptors:
1. Alpha-1: BVs, bladder, liver, pupils — NT: EPI, NE, DA, and phenylephrine

  1. Alpha-2: CNS — NT: EPI and NE
  2. Beta-1: Heart — NT: EPI, NE, DA, and dobutamine
  3. Beta-2: Lungs, BVs, bladder, liver, uterus — NT: EPI and albuterol
  4. DA: Kidneys — NT: DA

**Non-adrenergic: M: Sweat glands — NT: ACh

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10
Q

Norepinephrine (NE) & Epinephrine (EPI)

A

The “fight or flight” response is mediated by the release of NE or EPI by the adrenal medulla (there is no post-ganglionic neuron) upon ACh binding on N receptors

NE is synthesized from precursors like dopamine, and is then stored in vesicles; when an AP travels down the axon, it is released and binds to either alpha-1 or beta-2 post-synaptic receptors

After NE dissociates from the receptor, it can either (1) undergo re-uptake into the pre-ganglionic cell, or (2) bind to alpha-2 receptors on the pre-receptor neuron (acting as a shut-off valve)

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11
Q

Sympathetic Stimulation

A

Effects (“Fight or flight”):
1. Regulating CV system

  1. Regulating body temp.
  2. Increase HR and BP
  3. Shunt blood away from skin and viscera and into skeletal muscles
  4. Dilate bronchi
  5. Dilate pupils
  6. Mobilize stored energy

**Sympathetic blockade: cause opposite effects of sympathetic stimulation

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12
Q

Baroreceptor Reflex and Feedback Loop of the ANS

A

The baroreceptor reflex helps regulate BP; thus, it opposes pharmacologic interventions that alter BP (and often requires multiple drug therapies)

Baroreceptors are specific receptors located in the carotid sinus and the aortic arch in the heart that monitor changes in BP, and send information to the brain

If a drug that lowers BP is admin., the baroreceptors in the heart detect that information, and in response, the brain sends impulses along nerves to the ANS, instructing the heart and blood vessels to vasoconstrict in attempt to increase CO, and bring the BP back to previous basal range

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13
Q

Somatic Nervous System

A 
Receptor = Nicotinic (N)
NT = ACh

N receptors in skeletal muscle

Musculoskeletal blockade: opposite effects of somatic stimulation (skeletal muscle paralysis)

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14
Q

Cholinergic Drugs

A

Types of cholinergic drugs:
1. Muscarinic agonists

  1. Muscarinic antagonists (Anticholinergics)
  2. Cholinesterase inhibitors
  3. Neuromuscular blocking agents (NMBAs)
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15
Q

Cholinergic Drug Type #1: Muscarinic Agonists

A

Prototype: Bethanechol

MOA: Direct muscarinic agonist (GI tract and bladder selective)

Therapeutic use:

  1. Non-obstructive urinary retention (promotes urination)
  2. GI paralysis (promotes digestion and absorption)

AEs:

  1. Hypotension
  2. Bradycardia
  3. Excessive GI secretions
  4. Asthma exacerbation (due to bronchoconstriction)

RN implications:

  1. Admin. on empty stomach
  2. Have bedpan readily available
  3. Monitor I&Os and cholinergic excess

Muscarinic agonist overdose:

  1. S/S: Profuse salivation, lacrimation, visual disturbances, bronchospasm, diarrhea, bradycardia, hypotension
  2. Tx: Atropine — blocks muscarinic receptors, preventing activation
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16
Q

Cholinergic Drug Type #2: Muscarinic Antagonist (Anticholinergics)

A

Prototype: Atropine

MOA: Blocks muscarinic receptors (prevents ACh from binding)

Therapeutic uses:

  1. Dilate pupil for eye exam
  2. Treat bradycardia
  3. Muscarinic agonist overdose/poisoning
  4. Preanesthetic agent — decrease salivations and bronchial secretions

AEs:

  1. Dry eyes and mouth
  2. Blurred vision
  3. Photophobia
  4. Constipation
  5. Urinary retention
  6. Tachycardia

RN implications: Pt education on minimizing anticholinergic AEs

Anticholinergic overdose:

  1. S/S: PSNS blockade mnemonics
  2. Tx: Activated charcoal (absorbs drug in GI tract), and Physostigmine (increases amount of ACh at receptors)
  3. Warning: Differentiate between overdose and actual psychotic episode

**Anticholinergics are on “Beers List”

17
Q

Cholinergic Drug Type #3: Cholinesterase Inhibitors

A

Prototype: Neostigmine

MOA: Blocks the action of AChE, increasing the amount of ACh that is available at receptor sites

Therapeutic uses:

  1. Myasthenia gravis
  2. Reversal of non-depolarizing NMBAs

AEs:

  1. Muscarinic effects: N/D/, increased salivation and bronchial secretions, bronchoconstriction
  2. Nicotinic effects: muscle cramps

DDIs:

  1. Anticholinergic (opposing effects)
  2. Competitive depolarizing NMBAs — increase the activity of NMBA

RN implications: Pt education on recognizing extreme AEs (specifically for those with Myasthenia gravis)

Cholinesterase inhibitor overdose:

  1. S/S: Excessive muscarinic stimulation and respiratory depression; DrySLUDS, and killer Bs (bradycardia, bronchospasm, and bronchorrhea)
  2. Tx: Atropine, suction (due to increased secretions), and mechanical ventilation (reverses respiratory depression, and counteracts muscle weakness or paralysis)
18
Q

Myasthenia Gravis

A

Autoimmune disorder in which antibodies attack N receptors on the motor end plate, causing fluctuating muscle weakness and rapid fatigue

Cholinesterase inhibitor drug therapy (used for symptomatic relief) increases the amount of ACh at receptor sites, allowing for a more prolonged effect of ACh; thus, there is increased muscle strength

19
Q

Cholinergic Drug Type #4: Non-depolarizing Neuromuscular Blocking Agents (NMBAs)

A

Prototype: Pancuronium (-ronium & -curium)

MOA: Blocks the action of ACh at neuromuscular junction (mainly on nicotinic receptors)

Therapeutic use:

  1. Adjunct to general anesthesia
  2. Mechanically ventilated pts
  3. Intubation

AEs:

  1. Respiratory arrest — must provide mechanical ventilation
  2. Electrolyte disturbances

DDIs:

  1. General anesthetics
  2. Some antibiotics

Med. safety concerns:

  1. Caution in pts with renal and hepatic dysfunction, and Myasthenia gravis
  2. Tx: Cholinesterase inhibitors for reversal
  3. Sedate prior to admin.
  4. High alert med.: use is restricted to ICU/OR/ED or with code team (due to risk for respiratory arrest and death)
20
Q

Cholinergic Drug Type #4: Depolarizing Neuromuscular Blocking Agents (NMBAs)

A

Prototype: Succinylcholine

MOA: Depolarizes muscle fiber, preventing the action of ACh at neuromuscular junction (mainly on nicotinic receptors)

Therapeutic use: Muscle relaxation during endotracheal intubation (short-acting)

AEs:

  1. Respiratory arrest
  2. Hyperkalemia (due to depolarization)
  3. Muscle pain
  4. Malignant hyperthermia — Antidote: Dantrolene inhibits heat generation by reducing the metabolic activity of skeletal muscle; Tx: Discontinuation, ice packs, IV infusion

Med. safety concerns:

  1. Caution in pts with Myasthenia gravis
  2. Cholinesterase inhibitors do NOT reverse AEs — they increase the activity of succinylcholine
  3. High alert meds.: use restricted to ICU/OR/ED or with code team (due to risk for respiratory arrest and death)
21
Q

Adrenergic Drugs

A

Types of adrenergic drugs:
1. Adrenergic agonists

  1. Adrenergic antagonists
22
Q

Adrenergic Agonists

A

a.k.a. Sympathomimetics, catecholamines (not all)

4 receptor types: alpha-1, alpha-2, beta-1, and beta-2

23
Q

Adrenergic Agonists #1: Alpha-1, Beta-1 Agonists

A

Prototype: NE, EPI, and DA

Therapeutic uses:

  1. Support cardiac function
  2. Vasoconstriction and/or increased force of contraction
  3. EPI (IM) used for anaphylaxis
  4. Phenylephrine (topically) used for nasal congestion

Route: Continuous IV infusion, IM (EPI), and topical (Phenylephrine)

AEs:

  1. Cardiac complications (i.e. dysrhythmias)
  2. Necrosis after extravasation
  3. Hyperglycemia
  4. Tremors

RN implications:

  1. Identify high risk pts (i.e. heart disease)
  2. Monitor IV site for extravasation (necrosis), EKG, BP
  3. IV admin. via continuous infusion pump in critical care setting

Med. safety concerns:

  1. High alert meds.
  2. Continuous infusions should be administered via library in smart pump
  3. EPI autoinjecter devices — pen design has led to incorrect use and accidental self-admin.
24
Q

Adrenergic Agonist #2: Beta-2 Agonist

A

Prototype: Albuterol

MOA: Activation of beta-2 receptors

Therapeutic use: Bronchodilator

AEs:

  1. Tremors
  2. Tachycardia
  3. Palpitations
25
Q

Adrenergic Agonist #3: Alpha-2 Agonist

A

Prototype: Clonidine

MOA: Alpha-2 agonist (central effect) — large amounts of NE or EPI bind to alpha-2 receptors on pre-synaptic neuron (acting as a shut-off valve)

Therapeutic use:

  1. HTN
  2. Narcotic withdrawal
  3. Pain
  4. ADHD
  5. Analgesia

AEs:

  1. Drowsiness & dry mouth
  2. Rebound HTN — when discontinued abruptly
  3. Orthostatic hypotension
  4. CNS effects

Forms: Oral, transdermal patch, epidural

RN implications:

  1. Abuse potential
  2. Beers criteria
  3. Patch admin. issues

Issues associated with transdermal patch admin.:

  1. Remove old patch
  2. Rotate site of application — prevents local irritation
  3. Partial patches — can be cut (for children or small adults)
  4. Anonymous patches
  5. Unintentional overdose from heat — increases absorption rate
  6. Disposal
  7. Adhesion failure
  8. Electronic ordering/eMAR issues
26
Q

Adrenergic Antagonist #1: Non-selective Alpha Blocker

A

Prototype: Phentolamine

MOA: Blocks alpha-1 and alpha-2 receptors

Therapeutic use: Reverses local vasoconstriction effect of extravasated alpha-1 agonists (NE, EPI, and DA)

Admin.: Region should be infiltrated per institutional extravasation management guidelines

27
Q

Adrenergic Antagonist #2: Selective Alpha Blocker

A

Prototype: Prazosin (-osin)

MOA: Blocks alpha-1 receptors

Therapeutic use:

  1. BPH (primary use) — relaxes smooth muscle
  2. HTN

AEs:

  1. Orthostatic hypotension
  2. Reflex tachycardia — if discontinued abruptly
  3. Nasal congestion — due to vasodilation

RN implications:

  1. Orthostatic hypotension
  2. First-dose effect — 1% lose conscious (rare) within first 30-60 min. of admin. (use small first dose)
28
Q

Adrenergic Antagonist #3: Non-selective Beta Blocker

A

Prototype: Propranolol (-olol, -alol, -ilol)

MOA: Blocks beta-1 and beta-2 receptors

Therapeutic use:

  1. HTN
  2. Angina
  3. Dysrhythmias
  4. HF
  5. Migraine prophylaxis — can cross BBB and elicit CNS effects (vasodilation improves migraine symptoms)

AEs:

  1. Bradycardia (most common) that can lead to AV block and reflex tachycardia
  2. Bronchospasm — avoid in pts with asthma and COPD
  3. CNS effects
  4. Can mask hypoglycemia (especially tachycardia)

Individual variation:

  1. HF — improves mortality, but can also worsen heart function (use low dose)
  2. Asthma

DDIs: Calcium channel blockers (used to treat angina and HTN) — jointly cause bradycardia

RN implications: Warn pts of abrupt discontinuation — reflexive issues (i.e. rebound HTN, tachycardia, or worsening HF)

Med. safety concerns:

  1. High alert meds. (especially IV)
  2. Dose conversion from PO to IV (first pass effect)
  3. Mix ups with ER dosage forms
  4. Sotalol on Beers list
29
Q

Adrenergic Antagonist #4: Selective Beta Blocker

A

Prototype: Metoprolol (-olol, -alol, -ilol)

MOA: Blocks beta-1 receptors — less likely to cause bronchospasm (high doses may become nonselective)

Therapeutic use:

  1. HTN
  2. Angina
  3. HF
  4. Dysrhythmias
  5. Post-MI care

AEs:

  1. Bradycardia which can lead to AV block and reflex tachycardia
  2. HF
  3. Can mask hypoglycemia

Individual variation:

  1. HF
  2. Asthma (high doses)

DDIs: Calcium channel blockers

RN implications: Warn pts of abrupt discontinuation

Med. safety concerns:

  1. High alert meds. (especially IV)
  2. Dose conversion from PO to IV (first pass effect)
  3. Mix ups with ER dosage forms

Pharmacology: Exam 1 (9 decks)

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