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Drugs MSK Module 2 > ANS drugs > Flashcards

ANS drugs Flashcards

1
Q

Malathion

A

Irreversible Anticholinesterase inhibitor

Organophosphate groups irreversibly bind to active portions of AChE to form an extremely stable complex, which prevents ACh breakdown.

•This drug is toxic!

  • Increased ACh stimulates receptors causing muscle paralysis and death
  • Effects overcome with synthesis of new AChE — which may take up to 6 weeks.
  • Toxic; used in Pesticides
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2
Q

Botulinum Toxin

A

Prevents release of ACh

Inhibits release of ACh by degrading synaptobrevin (SNARE), which prevents vesicle fusion / exocytosis

• Used clinically to treat focal dystonias (paralyze select muscle groups in which there is excessive tone).
• Unmasking subclinical Eaton-Lambert syndrome.
• Also used to clinically treat hyperhydrosis.
• Patients with botulism suffer respiratory paralysis / death.
• Systemic administration of
Botox can result in muscle weakness or paralysis (depending on dose) and can be fatal.

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3
Q

Neostigmine

A

(Less lipid soluble than physostigmine; does not cross blood brain barrier)

Reversible Anticholinesterases inhibitor

Anticholinesterase drugs bind to the cholinesterase (both acetylChE and pseudoChE) and prevent the enzyme from
degra ding.

Contractions will get weaker until flaccid paralysis occurs; occurs due to VG Na inability to return to
“resting state” [depolarization block ade]

Only affects nicotinic receptors

• Increase parasympathetic tone
(parasympathomimetric)

• Decrease intraocular
pressure (from glaucoma) by increasing outflow of aqueous humor.

• Increase smooth muscle motility of GI tract.
• Reversal of anticholinergic poisoning (ex: atropine).
• Increase central cholinergic neurotransmission in dementia
• Reversal of paralysis from non-depolarizing neuromuscular blockers
• Excessive muscarinic (parasympathetic) stimulation
• Salivation, lacrimation, miosis, diarrhea, bradycardia.
• Excessive nicotinic stimulation
• Muscle weakness and paralysis
• Chemical warfare
• Used as nerve gas.
• Symptoms include muscle
weakness and paralysis. Can be fatal if there is paralysis of respiratory muscle.
• Note: Nerve gas is treated with atropine and pralidoxime; can also give artificial ventilation and O2.

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4
Q

Physostigmine

A

(Highly lipid soluble and crosses the blood brain barrier.)

Reversible Anticholinesterases inhibitor

Anticholinesterase drugs bind to the cholinesterase (both acetylChE and pseudoChE) and prevent the enzyme from
degra ding.

Contractions will get weaker until flaccid paralysis occurs; occurs due to VG Na inability to return to
“resting state” [depolarization block ade]

Only affects nicotinic receptors

• Increase parasympathetic tone
(parasympathomimetric)

• Decrease intraocular
pressure (from glaucoma) by increasing outflow of aqueous humor.

• Increase smooth muscle motility of GI tract.
• Reversal of anticholinergic poisoning (ex: atropine).
• Increase central cholinergic neurotransmission in dementia
• Reversal of paralysis from non-depolarizing neuromuscular blockers
• Excessive muscarinic (parasympathetic) stimulation
• Salivation, lacrimation, miosis, diarrhea, bradycardia.
• Excessive nicotinic stimulation
• Muscle weakness and paralysis
• Chemical warfare
• Used as nerve gas.
• Symptoms include muscle
weakness and paralysis. Can be fatal if there is paralysis of respiratory muscle.
• Note: Nerve gas is treated with atropine and pralidoxime; can also give artificial ventilation and O2.

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5
Q

Pyridostigmine

A

(Similar to Neostigmine but has longer half life)

Reversible Anticholinesterases Inhibitor

Anticholinesterase drugs bind to the cholinesterase (both acetylChE and pseudoChE) and prevent the enzyme from
degra ding.

Contractions will get weaker until flaccid paralysis occurs; occurs due to VG Na inability to return to
“resting state” [depolarization block ade]

Only affects nicotinic receptors

• Increase parasympathetic tone
(parasympathomimetric)

• Decrease intraocular
pressure (from glaucoma) by increasing outflow of aqueous humor.

• Increase smooth muscle motility of GI tract.
• Reversal of anticholinergic poisoning (ex: atropine).
• Increase central cholinergic neurotransmission in dementia
• Reversal of paralysis from non-depolarizing neuromuscular blockers
• Excessive muscarinic (parasympathetic) stimulation
• Salivation, lacrimation, miosis, diarrhea, bradycardia.
• Excessive nicotinic stimulation
• Muscle weakness and paralysis
• Chemical warfare
• Used as nerve gas.
• Symptoms include muscle
weakness and paralysis. Can be fatal if there is paralysis of respiratory muscle.
• Note: Nerve gas is treated with atropine and pralidoxime; can also give artificial ventilation and O2.

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6
Q

Edrophonium

A

(Very short half-life compared to others)

Reversible Anticholinesterases Inhibitor

Anticholinesterase drugs bind to the cholinesterase (both acetylChE and pseudoChE) and prevent the enzyme from
degra ding.

Contractions will get weaker until flaccid paralysis occurs; occurs due to VG Na inability to return to
“resting state” [depolarization block ade]

Only affects nicotinic receptors

• Increase parasympathetic tone
(parasympathomimetric)

• Decrease intraocular
pressure (from glaucoma) by increasing outflow of aqueous humor.

• Increase smooth muscle motility of GI tract.
• Reversal of anticholinergic poisoning (ex: atropine).
• Increase central cholinergic neurotransmission in dementia
• Reversal of paralysis from non-depolarizing neuromuscular blockers
• Excessive muscarinic (parasympathetic) stimulation
• Salivation, lacrimation, miosis, diarrhea, bradycardia.
• Excessive nicotinic stimulation
• Muscle weakness and paralysis
• Chemical warfare
• Used as nerve gas.
• Symptoms include muscle
weakness and paralysis. Can be fatal if there is paralysis of respiratory muscle.
• Note: Nerve gas is treated with atropine and pralidoxime; can also give artificial ventilation and O2.

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7
Q

Succinylcholine

A

Neuromuscular Nicotinic Agonist

  • Depolarizing neuromuscular blocker! that prevents muscle contraction by activating nAChR
  • Only drug that activates the neuromuscular receptor but has little effect on the ganglionic receptor.• To produce muscle paralysis
    during a short duration surgery/
    procedure.

• Extremely short half life (a few
min), so paralyzing effects quickly wear off.

Drug is metabolized by pseudocholinesterase. Some individuals have a genetic defect of this enzyme, resulting in lengthy time of metabolism.

• These patients must be artificially ventilated until effects completely wear off.

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8
Q

Pancuronium

A

Neuromuscular Nicotinic Antagonist

  • A competitive antagonist of ACh at the nAChR on skeletal muscles.
  • Binds to and occupies the nAChR at the NMJ.
  • Has NO action of its own but prevents ACh from binding and exerting its contractile effect.
  • Causes muscle paralysis.
  • Induction of flaccid muscle paralysis in surgery.
  • Hypertension, apnea, bronchospasm, salivation, flushing, and respiratory failure
  • Paralyzing effects overcome by increasing ACh levels: neostigmine.
  • Increasing level of ACh would overcome effects of Pancuronium, but ACh would exacerbate depolarization blockade; its half-life is too short as well to be effective. For this reason, anticholinesterase is given, not acetylcholine
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9
Q

Pilocarpine

A

Muscarinic Agonists (parasympathomimetric)

These drugs activate the activity of muscarinic acetylcholine receptors.

Treat glaucoma
• Activates mAChR on
circular muscles of eye, causing miosis. This enhances drainage of aqueous humor of eye, thus decreases intraocular pressure

  • Treat dry mouth in Sjogrens Syndrome
  • Negligible since it is localized
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10
Q

Bethanechol

A

(Almost completely selective for muscarinic receptors)

Muscarinic Agonists (parasympathomimetric)

These drugs activate the activity of muscarinic acetylcholine receptors.

Stimulates gastrointestinal and urinary tract motility; assists in bladder emptying (particularly post-operative, post-partum, and drug-related urinary retention).

• Miosis, bradycardia, salivation, bronchoconstriction

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11
Q

Methacholine

A

(3x resistant to hydrolysis by AChE and possesses little affinity for nicotinic receptors.)

Muscarinic Agonists (parasympathomimetric)

These drugs activate the activity of muscarinic acetylcholine receptors.

Inhalation of methacholine results in bronchoconstriction. This is used in diagnosis of asthma.

  • Asthmatics are more sensitive to the bronchial secreting actions of methacholine.
  • Asthmatics will respond at a lower dose than non- asthmatic patients.
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12
Q

Atropine

A

(Atropine poisoningof Atropa Belladonna)

Muscarinic Antagonist

Atropine binds to muscarinic receptors and prevent ACh from exerting its effects (competitive antagonists). This allows sympathetic responses to predominate.

  1. To produce mydriasis for ophthalmological examination.
  2. To reverse sinus bradycardia caused by excessive vagal tone.
  3. To inhibit excessive salivation and mucous secretion during anesthesia and surgery.
  4. To counteract the effects of muscarine poisoning and poisoning with anticholinesterases.
  5. Reduces GIT motility and tone, bladder motility, and sweating.
  6. Reduces salivation, lacrimation, urination, diaphoresis (sweating) GIT motility, and emesis.

• Due to blockade of muscarinic receptors: cardiac arrhythmias, raised intraocular pressure, tachycardia, constipation, xerostomia (dry mouth), and blurred vision.

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13
Q

Amphetamine

A

Inhibitors of Catecholamine storage

• Several actions on sympathetic nerve terminals:
• Release NE and DA from nerve terminals
• Block reuptake of NE by blocking NET.
• Weak inhibitor of MAO • Overall increase of NE
levels in synaptic cleft in sympathetic NS and in CNS.
• Previously used Treatment of narcolepsy

• Drug causes increased
alertness, reduced fatigue,
insomnia.

  • Treatment of ADHD
  • Improves attention span and alleviates many behavioral problems associated with ADHD, in addition to reducing hyperkinesia.
  • Drug abuse: Causes both dependence and tolerance. • Increased DA levels in brain can cause paranoid hallucinations and schizophrenic-like behavior.
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14
Q

Pseudoephedrine

A

Inhibitors of Catecholamine storage

  • Releases stored NE from nerve terminals.
  • ⍺ and ß agonist activity
  • Treatment of nasal and sinus congestion
  • CNS stimulation
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15
Q

Cocaine

A

Inhibitors of Catecholamine reuptake

Inhibits NE transporter (NET)

• Previous use = Local anesthetic

High potential for drug abuse. Chronic intake of cocaine leads to depletion of DA from dopaminergic nerve terminals in the CNS, which triggers vicious cycles of craving.

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16
Q

Imipramine

A

Inhibitors of Catecholamine reuptake

Blocks NET
• Used for treating mild depression
• Postural hypotension and tachycardia

17
Q

Ipronizaid

A

Inhibitor of Catecholamine metabolism

•
•Blocks metabolism of NE in the nerve terminals. MAOIs increase NE levelswhich provide more NE available for release into synaptic cleft.

• Treat depression. Effects are on central adrenergic systems rather than peripheral sympathetic system.

•Individuals taking MAOIs
must not eat food containing tyramine since it causes real ease of NE from nerve terminals. Can cause massive vasoconstriction leading to “hypertensive crisis”, which can result in stroke

18
Q

Epinephrine

A

⍺ and ß agonist

  • Released from the adrenal medulla during sympathetic activation.
  • In low concentrations, acts predominantly on ß receptors.

• In high concentration it also acts on ⍺1 receptors.
• EPI, via its ß2 activity causing bronchodilation, acts as a powerful antagonist to histamine/leukotriene bronchoconstricting effect.
• Ineffective orally.
• Short half life.
• [Can use albuterol for
asthma treatment]
• Restore cardiac rhythm in
patients with cardiac arrest. • Treat anaphylactic shock;
Injected EPI causes vasoconstriction via ⍺1 receptor activation, helping to return blood pressure to normal.
• Combined w/ local anesthetic to prevent drug from being washed away into systemic circulation.
• Poor penetration of CNS.

19
Q

Norepinephrine

Levartenerol

A

⍺ and ß agonist

Has affinity for ⍺1 and ß1 receptors.

Relatively little effect on ß2 receptors
• Shock due to circulatory collapse.
• Causes a profound vasoconstriction via ⍺1 receptors
• Increases both systolic (increased CO
diastolic blood pressure (peripheral vasoconstrictio

20
Q

Oxymetazoline

A

⍺1 and ⍺2 agonists

• Cause vasoconstriction that
increases total peripheral resistance and increases BP.

• No effect on heart but due to causing an increased BP
will cause reflex bradycardia (baroreceptor reflex).

  • Nasal decongestant (relief due to nasal vasoconstriction).
  • “Nasal Spray”

• Ophthalmic hyperemia
(vasoconstriction of the conjunctiva)
• Eye drops to relieve redness and itchy eyes

21
Q

Phenylephrine

A

⍺1 agonist

  • Cause vasoconstriction that increases total peripheral resistance and increases BP.
  • No effect on heart but due to causing an increased BP will cause reflex bradycardia (baroreceptor reflex).
  • Emergency treatment of shock.
  • Nasal decongestant (relief due to its vasoconstrictor effect on nasal mucosa)
22
Q

Clonidine

A

⍺2 agonist

  • Cause vasoconstriction that increases total peripheral resistance and increases BP.
  • No effect on heart but due to causing an increased BP will cause reflex bradycardia (baroreceptor reflex).
  • Treatment of hypertension.
  • Use in treatment of symptoms associated with drug withdrawal.
23
Q

Propranolol

A

(Non-selective ß-blocker)

All beta blockers are competitive antagonists.
• There are no clinically useful ß2 antagonists.
• Decrease HR and CO (attenuate response to exercise)
• Decrease cardiac O consumption
• Decrease SA and AV nodal activity

Note to side effects:
Non-competitive, thus more severe sedation, bronchodilation, and dyspnea.
• Treatment for hypertension and angina.
• Bronchoconstriction
• Contraindicated in patients patients with
asthma or COPD.
• Metabolic disturbances due to decreased glycogenolysis and glucagon secretion. (fasting hypoglycemia).
• Contraindicated in patients with diabetes mellitus.

24
Q

Atenolol

A

(Selective ß-blocker)

All beta blockers are competitive antagonists.
• There are no clinically useful ß2 antagonists.
• Decrease HR and CO (attenuate response to exercise)
• Decrease cardiac O consumption
• Decrease SA and AV nodal activity

Note to side effects:
Sedation and dyspnea
• Treatment for hypertension and angina, reduces blood volume via decreased renin production

  • Bronchoconstriction
  • Contraindicated in patients patients with asthma or COPD.
  • Metabolic disturbances due to decreased glycogenolysis and glucagon secretion. (fasting hypoglycemia).
  • Contraindicated in patients with diabetes mellitus.
25
Q

Pindolol

A

(Partial B1 antagonist)

  • Partial agonists are weak “antagonists,” thus weak stimulatory effects on both ß1 and ß2 receptors.
  • Treatment for hypertension in patients with bradycardia or low cardiac reserve.
26
Q

Phenoxybenzamine

A

(irreversible and non- competitive)

⍺1 and ⍺2 antagonists

These agents prevent sympathetically mediated vasoconstriction and hence cause vasodilation and
profound fall in BP. (Effects are more profound in an upright individual)

  • Given prior to removal of tumor surgically as to avoid hypertensive crisis (manual manipulation of tumor can cause massive release of epinephrine)
  • Given for long-term management of pheochromocytoma where surgery not an obvious option.

side effects
• Postural hypotension • Nasal congestion
• Failure of ejaculation

27
Q

Phentolamine

A

(reversible and competitive antagonist of NE/EPI)
⍺1 and ⍺2 antagonists

These agents prevent sympathetically mediated vasoconstriction and hence cause vasodilation and
profound fall in BP. (Effects are more profound in an upright individual)

  • Treatment of Pheochromocytoma.
  • This drug is preferable to phenoxybenzamine since it is reversible.

• Although it will not affect vascular resistance because ⍺1 receptors are blocked, but may observe increased
heart rate due to NE effect on cardiac ß receptors.

28
Q

Prazosin

A

⍺1 antagonists

These agents prevent sympathetically mediated vasoconstriction and hence cause vasodilation and
profound fall in BP. (Effects are more profound in an upright individual)

Used to reduce blood pressure.

side effects
• Marked postural hypotension (particularly after first dose)

29
Q

Tamsulosin

A

⍺1 antagonists

These agents prevent sympathetically mediated vasoconstriction and hence cause vasodilation and
profound fall in BP. (Effects are more profound in an upright individual)

Used to treat Benign prostatic hyperplasia.

Relaxes internal sphincter of bladder and relaxes smooth muscle associated with prostate gland, which relieves urinary hesitancy characteristic of condition in older men.

• ⍺1A subtype of the ⍺ receptor preferentially expressed in genitourinary SM.

side effects
• Postural hypotension • Nasal congestion
• Less reflex tachycardia

30
Q

Dobutamine

A

ß1 agonist

  • Increase HR and force of contraction, thus increase cardiac output.
  • Used in acute management of heart failure.
  • (Not usually used for treatment of chronic heart failure since they also increase HR, which makes the heart work harder)

• Not usually used for
treatment of chronic heart failure since they also increase HR, which makes the heart work harder

31
Q

Albuterol

A

ß2 agonist

• Powerful bronchodilator
effect due to relaxation of bronchial smooth muscle.

  • Used for treatment of Asthma; selectively avoids cardiac (ß1) and skeletal (ß2) side effects.
  • Restlessness, apprehension, anxiety.

side effects
• Tachycardia with high doses due to stimulation of cardiac ß1 receptors.

Drugs MSK Module 2 (1 decks)

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