Medications affecting the ANS

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Medications affecting the ANS
2014-06-06 20:15:55

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  1. How this system works
    skeleton ANS
    • Sympathetic
    • Adregenic
    • neuro transmission- NE
    • mydrias- diluted
    • decrease gi/gu
    • increase heart rate
    • decrease secretions

    • Parasympathetic
    • Cholingeric
    • neurotransmittor: Ach
    • miosis- constriction
    • increase gi/gu
    • decrease heart rate
    • increase secretion
  2. Parasympathetic System PNS
    House keeper/rest and digest
    • Neurotransmission: Ach
    • Cholinergic


    • Nicotinic N: neuron bodies (nerves cell/nerve transmission)
    • Nicotinic M: Skeletal muscle
    • Muscarinic: all organs of PNS (smooth muscle contraction) 90% of the time we are talking about muscarinic
  3. Sympathetic SNS

    neurotransmittor: NE

    Alpha 1: vasocontriction, increase BP, mydrias (dilute eyes)

    Alpha 2: decrease NE release; blocks sns stimulation

    Beta 1: cardiovascular: increase heart rate, contractions, and conduction, releases renin which increases your blood pressure

    Beta 2: Lungs (bronchodilator) relaxes smooth muscles, increase BS
  4. Renin
    • Angiostensin I
    • Angio II- Vasoconstriction increase BP
    • Aldosterone- reaborption of water and salt which increase BP
  5. Cholinergic Agonist
    Parasympathomimetics- mimics pns

    act directly or indirectly to promote the function of Ach

    The effects imitate the PNS
  6. Cholinergic Agonists CI
    • Stimulate the intestine and bladder
    • - atonic tone bladder/intestine, increase peristalsis, increase contractility 

    Decreases IOP (intra ocular pressure)- so if the pupils are constricted it can decrease the pressure in the eye- letting go of aqueous humor (tribecular network- separates and allows fluid to be released) glaucoma is ICP

    Promote salivation and sweating- dry mouth, not able to sweat (for pts who was on meds that create dry mouth and reduce sweating)

    terminate neuromuscular blockade- stimulant nicotinic N and M- stimulate nerve transmission

    treat Myastenia Gravis- neuromuscular disease caused by a lack of ach
  7. Direct acting Cholinergic agonist (muscurinic agonist)
    Acts directly on the cholinergic receptors in the PNS

    • Primarily works on muscarinic receptors
    • long duration of action

    Mimic the action of ach

    S/s: see PNS
  8. direct- Cholingeric agonist

    CI and SE
    CI to treat atonic bladder, bowel, and glaucoma

    • SE: mimic the PNS stimulation
    • the greater the dose the greater the effect
  9. Cholingeric agonist SE
    • GI: nausea, belching, vomiting, diarrhea
    • eye- blurred vision
    • heart rate- decrease
    • resp- bronchspasm, SOB (contracts the brochi)
    • GU: urinary frequency- increase contractility in the body
  10. Cholinergic agonist NI
    Contraindicated with GI/GU obstruction- b/c with this drug u increase perstalasis and if there is an obstruction it will get stopped and u can perforate the intestine

    Assess lung sounds and cardiac- b/c it causes bronchospasm/SOB and decrease HR

    best on an empty stomach

    drug interaction think about the side effects ie with a laxative- u would have more effects

    Antidote= if u gave too much of this drug u would have to use anticholinergic or a cholinergic blocker
  11. Benthanechol
    • direct acting muscuranic agonist
    • binds with muscarinic receptors
    • - increases smooth muscle tone/contractions primarily in the bladder

    CI- urinary retention (increases contractibility and relaxes the GU sphincter)

    • SE: oral doses, low risk SE
    • see effects PNS stimulation
  12. Pilocarpine
    • Glaucoma
    • direct acting muscarinic agent- primarily on the eye
    • eye drops local effect on the eye
    • causes miosis (constriction) and contracts cillary muscle of the eye (helps with focusing lens)
    • decrease ICP 
    • Cholingeric agonist 

    SE: blurred vision, eye irritation (local)

    NI: make sure pt knows how to give eye drop properly
  13. Indirect Acting Cholinergic agents
    Anticholineserase agents or cholinesterase inhibitor- 

    Cholineserase- an enzyme that breaks down ach- makes less ach available

    drug blocks cholineserase so ach can not be broken down

    end result u have more ach. 

    Nonselective and it effects all site of the PNS
  14. Indirect acting cholinergic agents (anticholineserase) Classification
    • short term: reversible
    • once the drug is d/c the enzyme is restored 

    • long term; irreversible
    • - a stable bond is formed with the drug and the enzyme, restoration of enzyme function is created by production of a new enzyme
    • few therapeutic uses: nerve gas, peticids
    • chemical warfare
    • u lose ach- nerve damage
  15. Indirect acting cholingeric agents  CI
    • Short term:
    • glaucoma
    • myasthenia gravis- lack of ach
    • relieve post op atony bowel and bladder- increase peristalisis
    • suppress atrial tachycardia- HR slow down
    • Alzheimers disease- b/c it is related to an imbalance of ach
    • antidote to atropine (antichol)- if u gave to much cholin u could give this
    • Long term:
    • toxic insecticides and pesticides, chemical warfare
  16. Indirect acting cholingeric agent SE
    • result of PNS stimulation
    • see PNS effect
    • blurred vision
    • diarrhea, abd cramping, urinary frequency
    • HR decrease
    • increase sweating
    • increase secretions
    • bronchocontrictions -spasm
  17. Indirect cholin NI
    same as direct acting agonist
  18. Myasthenia Gravis
    • lack of ach
    • we treat it by increasing ach
    • progressive disease that is characterized by loss of decrease of ach in the skeleton muscle
    • we dont have ach in our nicotinic M receptors (low muscle tone)- ptosis, dysphagia, disoperia (speaking), limb weakness
    • CI- cause unknown

    S/s  ptosis, dysphagia, disoperia (speaking), limb weakness, dilopia, fatigue

    • Tr: anticholinesterase drugs- to increase ach
    • block cholinerase
  19. Three drugs related to Myasthenia Gravis (anticholinesterase drugs)
    Tensilion- diagnostic (test)- IV indirect acting agent increase ach. last only a few and they will measure muscle strength

    Neostigmine/mestinon- longer acting indirect agent increasing ach. given orally- maintenance therapy
  20. Myastehnia Gravis crisis
    • Myasthenia Crisis
    • pt doesn't have enough meds
    • skipped a dose now they have muscle weakness not recplacing it so lack of ach
    • tr: neostigmine or mytelase (maintenance dose)

    • Cholinergic crisis:
    • Overdose of meds 
    • double dose
    • SE: muscle weakness too much ach
    • Tr: anticholingeric- reverse the s/s
  21. Cholinergic blocking agents
    • anticholinergics
    • cholinergics blocking agents
    • parasympatholytics- lysis the PNS
  22. Examples of cholinergic blocking agents
    • Atropine
    • decrease secretions, dilate pupils (eye exam)

    Atrovent: to bronchodilate

    Detrol: overactive bladder- slows this down
  23. Cholinergic blocking agents CI
    • treat spastic condition of GI/gu systems- decrease contractions and tone
    • preanethesia- decrease secretions- decrease risk of aspiration
    • motion sickness
    • parkinson disease ( decrease ach and incr dopamine)
    • bradycardia
    • causes mydriasis (pupil dilator)
    • poisoning of pesticides (antidote)- indirect cholin agonist
    • chronic astham- brochodilation
  24. SE cholinergic blocking agents
    • related to blocking of PNS
    • slow therapeutic window- not much wiggly room
    • increase of dosage can lead to toxicity
    • very according to age, past medical history/health)
  25. Side effects: anticholingerics
    • dry mouth
    • decrease resp/gi secretions
    • decrease gi motility
    • decrease bladder tone
    • decrease sweating- hyperthermia
    • blurred vision 
    • change in mental status
  26. Cholinergic blocking agents NI
    • contraindications- careful with pts with glaucoma
    • drug interation-  many- related to se tachycardia pt- bc increase hr
    • assess cardia status- increase HR
    • beaware that many drugs have antichol effects even OTC
    • Narrow margin safety- toxic is easy
    • overdose
    • antidote: cholinergic agent
  27. Anticholinergic overdose: s/s
    • fixed and dilated pupils
    • absent bowel sounds
    • atonic bladder 
    • seizures- cross brain blood barrier
    • dry mouth, mucous membrane, skin
    • vision
    • tachycardia
  28. Atropine
    muscarinic antagonist

    at therapeutic doses, produces selective blockade of muscarinic receptors

    at high does, blocks nicotinic receptors
  29. Atropine CI SE NI
    • increase heart rate- dose related. relaxation of smooth muscles
    • mydriasis
    • primarily using it to bronchodilate
    • effects are dose dependent
    • SE: see cholinergic
    • NI
  30. Sympathomimetics
    • adrenergic agonist
    • activation of SNS
    • mimics sns
    • selective (works on one receptor ie beta 1) and non selective (works on both beta;s)

    direct acting: most common- directly binds with the receptor

    • indirect acting:
    • - promote the release of NE
    • - inhibit NE reuptake
    • - inhibit NE inactivation

    sympathomenic- increase NE
  31. Adrenergic receptors
    • Alpha 1 stimulation
    • - neo-synephrine (protype)- alpha simulaiton
    • primarily works on vasocontriction 

    CI: nasal congestion (causes nasal contriction), hypotension, mydriasis for eye exam

    side effects: HTN, blurred vision

    NI: monitor bp, heart rate
  32. Adrenergic receptor Alpha 2
    • Alpha 2 stimulation
    • prototype (aldomet)

    effects: decreases the release of NE decreases SNS

    • CI hypertension
    • SE: hypotension, tachycardia 

    NI monitor bp
  33. Adrenergic receptor Beta 1
    prototype dobutamine

    effects increase contractility, rate, conduction and release of renin

    CI: increase BP, HR

    Sides HTN, Tachycardia, arrythmias (any time u change the rate u risk this)

    NI: monitor BP, pulse
  34. Adrenergic receptor Beta 2
    Protype Alupent

    effects: brochodilator, relaxation of smooth muscle, hyperglycemia (raise bs)

    CI: ashma, respiratory disorders

    • SE: brochospasms, SOB, BS increase
    • NI monitor lung sounds
  35. Adrenergic blocking agents
    sympatholytic agents- lysis kills sns

    causes blockade of the adrenergic receptors- selective, non selective

    reverse SNS stimulation

    inhibits/block NE synthesis, storage release and reuptake: decreas NE availablilty 

    Competive or non competive blockers of NE or adrenergic agent at the receptor sites
  36. Alpha 1 adrenergic blocking agent
    • effects: hypotension vasodilation
    • CI: htn reversal of toxicity from adrengic agonist (if u were to overdose), PVD bc it vasodilation

    • SE: related to blocking alpha 1 receptors
    • hypotension, reflex tachycardia, CNS, fatigue, syncope blurred vision, nasal stuffiness

  37. Minipress (prazosin)
    Selective alpha 1 blocker

    CI: htn

    SE: orthostatic hypotension, reflex tachycardia

    NI: assess BP, first dose effects- incidence of having syncope or vertigo bc bp drops. 1st dose tell pt not to stand up b.c of dizziness
  38. beta adrenergic blockers
    selective (beta 1) an non selective (beta 1 and 2 overtime or high dose)

    • CI
    • htn
    • angina- causes by vasocontriction
    • stage fright- u want have the symptoms of the fright
    • arrthymias
    • migraine headaches- helps to decrease vasospasm in the cerebral arteries
    • glaucoma- decrease humor production; pressure
    • anxiety
  39. Beta adrenergic blocker SE
    ARE related to blockade on the receptor

    hypotension, arrthymias, CNS disturbances (cross the brain blood barrier), fatige, gi distress, bronchspasm (blocking beta 2), hypoglycemia (blocking beta 2)
  40. Beta adrenergic blocker NI
    • Assess cardiac status
    • administer drug with BP and HR parameters- like don't give if heart rate less than 60 and bp less 100
    • drug interation- 
    • contrainic. 
    • do not abruptly withdraw the drug
    • assess respiratory status