Pharmacology -Autonomic Nervous System

Central Nervous System

consists of brain and spinal cord

What are the primary receptors of the PNS

Cholinergic receptors: Muscarinic and Nicotinic

Muscarinic receptors

• on target tissues affected by postganglionic neurons in parasympathetic division

• ONLY on target organs/cells

• smooth muscle and heart rate

• These are the main receptors for the PNS

Nicotinic receptors

• sensitive

• dont have medications that direct towards them unless you are in a crisis

• in ganglia synapse in both para and sympathetic (ONLY in the synapse)

• skeletal muscle (somatic nervous system)

Neurotransmitter

communication, a chemical messenger that travles across the synpatic gap between neurons, allowing them to communicate with each other

Synapse

inside the ganglia, gap between neurons where communication occurs

Cholinergic crisis

• large accumulation of Ach at cholinergic synapse= intense PNS stimulation

• S: salivation

• L: lacrimation

• U: urination

• D- defecation

• G: gastric upset

• E: emesis

• muscle weakness/twitching

• antidote: atropine (anticholinergic)- turns off PNS, turns on SNS

anticholinergic =

antirespiration

Do you have control over your ANS?

No, involuntary control

Do you have control of your SNS?

yes, voluntary control

What organs/muscles does the ANS control?

intestines, heart, brain, pupils, kidneys, stomach, lungs

Basic functions of ANS

• monitor changes

• process changes

• react to changes

• ex’s: running from someone, car accident

• changes accordingly, increases or decreases PNS or SNS depnding on situation

What activates the parasympathetic nervous system and what response does it produce?

Activated under nonstressful situations, Rest & Digest, Feed & Breed

What does your body do when the PNS is activated?

• Pupils- constrict (miosis)

• Salivary Gland- increases salvation

• heart - decreases heart rate

• Lungs- constrict bronchioles (normal breathing), when running they will dilate bc you need more air flow, but here you don’t need much air so they will constrict

• Stomach- stimulate digestion

• Blood vessels- dilates- decreases BP (less pressure against vessels)

• Liver- releases bile, increases glucose storage, stored in liver/muscles to save it bc we don’t need it

• Contracts bladder- promote urination

• Gastrointestinal- increases peristalsis, most digestion going on

What cranial nerves are associated with parasympathetic nervous system?

• Oculomotor(III)- pupils

• Facial nerve (VII)- tears

• Glossopharyngeal (IX)- Saliva

• Vagus (X)- PNS

What neurotransmitter is part of the PNS

acetylcholine

what is acetylcholine released by?

cholinergic nerves

What does acetycholine affect?

• muscle movement

• memory

• breathing

• systems affected: CV, Respiratory, GI & GU

Parasympathetic pathway main things

• acteylcholine= neurotransmitter

• cholinergic receptors: nictonic and muscarinic

Parasympathomimetic vs Parasympatholytic

• Parasympathomimetics (cholinergics): stimulate the parasympathetic nervous system (rest-and-digest) by mimicking acetylcholine

• Parasympatholytics (anticholinergics): inhibit it by blocking acetylcholine receptors

Cholinergic drug

• parasympathomimetic

• muscarinic agonist

• mimics PNS

• not widely used due to potential for serious side effects

• mainly used in ophthalmology (reduces intraocular pressure in glaucoma) & bowel/urinary smooth muscle

• PROTOTYPE: Bethanecol

Anticholinergic drug

• Parasympatholytic

• muscarinic antagonist

• Blocks PNS

• GI, ophthalmic, cardiac abnormalities, anesthesia adjunct, asthma & COPD, overactive bladder, Parkinson’s

• PROTOTYPE: Atropine

agonist vs antagonist

• agonist: mimics the expected response

• antagonist: blocks the receptor, inhibiting the expected response

What are the two PNS prototypes?

Bethanecol (Cholinergic drug) and Atropine (anticholinergic drug-cholinergic blocking)

• Bethanechol vs Atropine

• Bethanechol: direct-acting cholinergic agonist, direct-acting (selective) parasympathomimetic

• Atropine: cholinergic antagonist, cholinergic blocking

cholinergic therapy

• affect parasympathetic nervous system (PNS): “rest and digest” or “feed and breed”

  • digestion, elimination, sexual arousal, helps calm down body

What makes benthanechol different?

it is a direct-acting cholinergic agonist (selective parasympathomimetic) meaning it only affects the targeted area, not the whole body

Why would a patient need to take bethanechol?

• THINK BLADDER CONTROL

• patients who had surgery and were under anesthesia for a long period of time

• taking out a Foley catheter

• Bladder retention (older population)

• Spinal cord injury that affects signals to the bladder

bethanechol (Urecholine) Prototype

• Therapeutic class: treatment of urinary retention

• Pharmacologic class: Muscarinic Cholinergic receptor, e.g. direct-acting parasympathomimetic

• Action: directly stimulates muscarinic receptors increasing the tone of the detrusor urinae muscle (smooth muscle) of the bladder, giving a contraction adequately effective to initiate micturition (peeing) as well as in digestive tracts

• Uses: post-operative (non-obstructive) urniary retention, neurogenic bladder (spinal cord injury or shock)

• Adverse effects: don’t give to someone with an obstuctive GI, active ulcer or urinary obstructio as it will aggravate the disorder, caution with COPD

• Side effects: increases salivation, sweating, abdominal cramping and hypotension (could lead to fainting)

• Nursing considerations:

  • contradictions: do not give to pts with asthma, benign prostatic hyperplasia (BPH), peptic ulcer disease, bradycardia

  • monitor: blood pressure, HR, and respirations

  • antidote: atropine

  • interactions: drug-decrease effects with atropine, epinephrine

  • herb: scopolia (scopolamine patch is an anticholinergic)

why would a patient need atropine?

• during surgery, code blue, increase respirations

Atropine Prototype

• therapeutic class: treatment for bradycardia, antidote for anticholinersterase poisoning (cholinergic crisis)

• pharmacologic class: anticholinergic, muscarinic receptor blocker

• action: inhibits the effects of the parasympathetic action of Ach, inducing fight or flights, increase in ♡ rate, bronchodilation, decreased GI and respiratory secretions

• Uses: pre-operatively to decrease GI and respiratory secretions, anticholinesterase poisoning, treatment of bradycardia, dilate pupils

• adverse effects: delirium, coma

  • monitor patient for tachycardia and palpitations

  • may cause urinary retention in elderly patients

  • may cause constipation due to slowed GI motility

• Side effects: dry mouth, constipation, urinary retention, increased heart rate

• nursing considerations:

  • contraindications: avoid in acute hemorrhage and patients with glaucoma(benign prostatic hyperplasia (BPH), disorders of GI tract, cardiac ins

  • monitor: blood pressure, HR, respirations

  • Antidote: physostigmine

  • Interactions: drug-decrease effect with antihistamines

What receptors are part of the SNS?

nicotinic (cholinergic) and alpha/beta (adrenergic)

What are the two prototypes that affect the SNS?

Adrenergic drugs and Adrenergic blocking drugs

What are the two adrenergic drugs?

phenylephrine (Neo-Synephrine) and prazosin (Minipress)

Endogenous catecholamine

hormones made by adrenal glands in response to physical or emotional stress

what is Norepinephrine?

• aka noradrenaline

• stress response

• blood pressure

• kidneys (reaches kidneys and thells them to release renin, initiates RAAS which kicks in to increase BP)

• liver (release glucose for energy)

• eyes

• cognition

what is Dopamine?

• reward chemical

• pleasure, mood, movement

what does Epinephrine do?

• aka adrenaline

• common for code events

• increase heart rate and BP

• anaphylaxis

• asthma attack

What does your body do when the SNS is activated?

• Pupils- dilate (mydriasis) (so you can run in the dark)

• Lungs- dilates bronchioles (so you can breathe)

• Heart- tachycardia (more blood to skeletal muscles)

• Blood Vessels- constricts (which increases BP)

• Liver- increased glucose production (+energy)

• Gastrointestinal- relaxes (smooth muscle)

• Bladder & Uterus- Relaxes (smooth muscle)

What is the primary neurotransmitter of the SNS?

Norepinephrine

• released by postganglionic nerve terminals

• greater affinity for alpha cells

• epinephrine greater affinity for beta cells

• works on cardiovascular, renal, respiratory, GI, reproductive, eye

What are the primary receptors of the SNS?

• adrenergic receptors (can be selective or non selective)

  • Alpha 1&2

  • Beta 1&2

What do alpha and beta receptors do?

• Alpha receptors = causes constriction

• Beta receptors = causes dilation

Alpha 1 receptors

• located: blood vessels, eyes, and smooth muscle

• action: vasoconstriction, pupil dilation (mydriasis), urinary retention, smooth muscle contraction (piloerection) —> increases BP, increases blood return to the heart, increases circulation

• used to treat: hypotension, nasal congestion (vasoconstriction) and used for eye dilation known as mydirasis (smooth muscle, arterioles)

Alpha 2 receptors

• location: presynaptic nerve terminals

• action: inhibit the release of norepinephrine (decreased norepinephrine) —> decreases HR &BP, decreases peripheral vascular resistance

• used to treat: hypertension, reduces the release of NE at axon

Beta 1 receptors

• location: heart and kidneys

• action: increases HR, increases contractility/force of contraction, increases renin

• used to treat: cardiac arrest, heart failure, shock

Beta 2 receptors

• location: all target organs except heart (lungs, uterus, skeletal muscle vessels)

• action: bronchodilation, vasodilation, uterine relaxation

• used to treat: bronchoconstriction, asthma, preterm labor contractions

Adrenergic vs adrengic blocker

• Adrenergic

  • sympathomimetic

  • treats shock, hypotension

  • Prototype: phenylephrine (Neo-senephrne)- decongestant (vasoconstriction)

• Adrenergic blocker

  • sympatholytic

  • treats hypertension

  • Prototype: prazosin (Minipress)- anti-hypertensive

Sympathomimetic vs Sympatholytic

• Sympathomimetics (e.g., epinephrine, albuterol) mimic norepinephrine/epinephrine to increase heart rate, blood pressure, and bronchodilation

• Sympatholytics (e.g., beta-blockers, clonidine) oppose this system, reducing adrenergic activity to lower blood pressure and heart rate. 

What are the actions of SNS drugs based on?

The receptor affected

side effects of sympathomimetics

too much of the intended action

sympathomimetics vs smypatholytic

• mimetics: adrenergic drugs

• lytic: adrenergic blocking

clinical applications of sympatholytic

• These drugs have WIDE therapeutic application in treatment of hypertension.

  • Alpha Blockers – relax vascular smooth muscle – used to treat hypertension (alpha 1)

  • Beta Blockers – work on cardiovascular system – also used to treat hypertension (this is reduced by decreasing HR (cardiac output) and reduction of renin in kidneys (blocks the RAAS system).

adverese effects of sympatholytic

• mostly due to beta blockade

  • make heart falure worse (blocking that increases force of contraction)

  • make asthma/COPD worse (blocking bronchodilation)

  • Note: beta blockers can cause hypoglycemia or hyperglycemia and may mask the symptoms of hypoglycemia in patients with diabetes

phenylephrine (Neo-synephrine, Sudafed) Prototype

• Therapeutic class: nasal decongestant, anti-hypotensive

• Pharmacologic class: adrenergic drug (sympathomimetic)

• Action: selective, alpha 1-adrenergic agonist. Comes in nasal, topical, parenteral and oral formulations

• Uses:

  • Intranasal: reduces nasal congestion by constricting small blood vessels in nasal mucosa (Contraindications: do not use for more than 5 days due to rebound congestion)

  • Topical: used in eye drops to cause pupil dilation (Contraindications: do not use in those with narrow angle glaucoma)

  • Parenteral: can reverse hypotension due to spinal anesthesia or vascular shock. Lack of beta selectivity means it has few cardiac side effects. (Contraindications: use in caution in those with advanced coronary artery disease, hypertension or hyperthyroidism)

• Adverse effects: burning of mucosa, rebound congestion, narrow-angle glaucoma, reflex bradycardia

• Antidote: phentolamine (alpha-blocker)- may be needed to treat hypertension

• Black box warning: severe reactions, including DEATH may occur with IV infusion- even if drug is diluted properly. Use with caution and only when other routes are not feasible

prazosin (Minipress) Prototype

• Therapeutic Class: antihypertensive

• Pharmacologic Class: adrenergic-blocking drug

• Actions & uses:

  • alpha-1 adrenergic antagonist that competes with NE at its receptor on smooth muscles in arterioles and veins

  • major action is a rapid decrease in peripheral resistance that reduces blood pressure

  • Has little effect on cardiac output or heart rate

• Adverse effects:

  • Can cause orthostatic hypotension, can cause unconsciousness about 30 minutes after 1st dose.

  • First dose effect : 1st dose should be very low and given at bedtime to avoid orthostatic hypotension

  • Dizziness, drowsiness and lightheadedness

  • Reflex tachycardia could occur due to rapid drop in BP

• Nursing Considerations:

  • caution in older patients

  • use cautiously with other antihypertensives and diuretics