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Pharm 1 Undergrad > Autonomic Drugs Part 2 > Flashcards

Autonomic Drugs Part 2 Flashcards

1
Q

What class of drugs are Parasympathetic effects mimicked by?

A
  • Muscarinic Receptor Agonists (promote parasympathetic effects)
  • AChE Inhibitors (relax muscle instead of stimulate)
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2
Q

Parasympathetic activity can be blocked by?

A
  • Muscarinic receptor antagonists

- Skeletal NMJ Blockers

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3
Q

What are some typical therapeutic uses of Parasympathetic drugs?

A
  1. Reduce intraocular pressure in the eyes
    Eg) Pilocarpine opens the trabecular meshwork and allows the aqueous humour to drain.
  2. Increase the motility of GI tract
    - Bethanecol
  3. Increase Motility of the Urinary Tract:
    - Bethanecol
    - Causes the constriction of the detrusor muscle, relaxation of the sphincter and allows urine to exit the bladder.
  4. Increases Salivary Secretions
    - ->Pilocaprine used to treat xerostomia
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4
Q

What is the role of Cholinesterase Inhibitors? (ChE)

A
  • Allows for an increased time ACh is available in the synapse
  • ->Drugs can cause paralysis.
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5
Q

What are the 2 types of Cholinesterase Inhibitors?

A
  • AChE (Acetylcholineasterase)
  • Breaks down ACh
  • BuChE (Butyrlcholinesterase)
  • Breaks down Succinylcholine
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6
Q

What is an Aceylation Drug Interaction?

A
  • Drug causes Acetylation of the enzyme (caused by ACh)

- Quick recovery/ reversible binding

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7
Q

What is a Carbomylation Drug Interaction?

A
  • Reversible Inhibition (Carbamylation of enzyme takes 3-4 hours to overcome)
  • Enzyme is still available to ACh but there is competition due to drug.
  • Can be overcome by more ACh present at the synapse.
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8
Q

What is a Phosphorylation Drug Interaction?

A
  • Irreversible binding due to Covalent Bonds
  • ->ACh is unable to unbind from the synapse (can easily cause poisoning.

–>After some time, phosphorylated drugs undergo Aging (phosphorylated enzyme loses chemical group and new chemical created has no enzymatic activity)

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9
Q

What type of drug is Neostigmine?

A
  • Reversible AChE inhibitor
  • Carbamylation (3-4 hours)
  • Can be overcome by adding more ACh
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10
Q

What type of drug is DFP?

A
  • Irreversible AChE inhibitor

- Takes VERY long for enzyme to dephosphorylate.

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11
Q

What can overcome Aging in a Phosphorylation drug reaction?

A
  • Oxime, such as 2-PAM

- Binds enzyme before aging- donates phosphate moiety cause enzyme inhibition to be reversed.

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12
Q

What is the result of reversible cholinesterase inhibition?

A

-Increased cholinergic activity where it is lacking (decreased Acetylcholinesterase activity= more frequent contractions, increased GI motility, ect.)

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13
Q

Cholinesterase Inhibition results in:

Inhibiting AChE/ BuChE release

A
  • Increase motility of GI tract
  • Increased activity of the Urinary bladder
  • To treat symptoms of Alzheimer’s disease
  • Can be used to diagnose/ treat Myasthenia gravis
  • To improve skeletal muscle contraction
  • Can topically be used to treat conjunctiva causing miosis.
  • Cause aqueous humour outflow/ a decrease in intraocular pressure
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14
Q

What is the downside of using a ChE inhibitor on the eyes?

A
  • ->Allow ChE inhibitor can be used to treat glaucoma, it can cause cataracts with long-term use
  • ->Only used in aphakic patients
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15
Q

What is the effect of ChE Inhibitors on competitive neuromuscular blockers, as a tubocurarine?

A

Reverses their antagonism (lessens their blocking effects?)

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16
Q

Clostridium botulism mechanism of action?

A

Blocks ACh release from the synapse

  • Acts as a depolarizing neuromuscular blocker
  • Causes muscle paralysis in muscles with involuntary muscle tone
Clinical Uses of BOTOX include: 
-Removes wrinkles
-Strabismus (corrects unaligned lines of visions of the eyes)  
-Blepharospasm (Contracted eyelids)
Hemifacial Spasms (relaxes spasms)
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17
Q

Muscarinic Receptor Blockers:

A

Two different Types:
Belladonna Alkaloids- Scopolamine and Atropine
Semisynthetic/ Synthetic: Oxybutynin

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18
Q

What kind of drug is Atropine?

A

Muscarinic Antagonist

-Acts to prevent ACh from binding at the synapse (anti-spasmic drug)

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19
Q

What effects do Muscarinic Antagonists have on the body?

A
  • Mydriasis (Pupil Dilation)
  • Relaxation of smooth muscle in the GI tract, bronchi and urinary bladder.
  • Inhibit secretions of various exocrine glands.
  • In high doses, muscarinic antagonists act to completely block parasympathetic effects of ACh (for example, atropine- a muscarinic antagonist, can bind all available enzymes and actually cause an increase in heart rate.
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20
Q

What drug can be used to treat motion sickness?

A

Scopolamine (Muscarinic Antagonist Effects)

-Blocks the M1 receptor of the vestibular apparatus.

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21
Q

What is the difference between Atropine and Scopolamine?

A
  • ->(Scopolamine is 10x more potent for producing CNS effects than atropine)
  • More scopolamine is unionized at physiological pH than atropine, allowing it to easily pass through the skin.
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22
Q

Would a muscarinic antagonist promote Miosis or Mydriasis?

A
  • ->Would indirectly promote sympathetic activity by inhibiting parasympathetic activity
  • -> Mydriasis (pupil dilation)
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23
Q

Would a muscarinic antagonist cause an increase or decrease in GI motility/ secretion?

A

Decrease in parasympathetic GI activity
–>Decreased secretions/ GI motility
(Treat IBS)

24
Q

What types of Urinary Incontinence would a muscarinic antagonist treat?

A

Overactive bladder problems

  1. Daytime urinary frequency
  2. Nigh time urinary frequency (Nocturia)
  3. Urgency
  4. Incontinence (unable to control bladder)
25
Q

Oxybutyrin is used to treat which condition?

A
  • -> Semi-synthetic/ synthetic muscarinic antagonists
  • ->Anti spasmic drug
  • Can be used to treat an overactive bladder.
  • ->Binds M2 and M3 (uroselective)
26
Q

Which muscarinic antagonists are used to treat COPD? (Emphysema, asthma and chronic bronchitis?)

A
  • ->Ipratropium and Tiotropium - derivatives of atropine
  • Decrease bronchial secretions and cause bronchodilation
  • Not absorbed into systemic circulation
27
Q

What is the main cause of COPD physiologically?

A

-Increased bronchial secretions

28
Q

What are 2 drugs used to treat Parkinson’s disease?

A

Trihexyphenidyl and Benztropine
–>Muscarinic antagonists which reduce ACh binding in the synapse- less frequent contractions which cause tremors in patients.

29
Q

What are the side effects caused by Muscarinic Antagonists?

A
  • Urinary retention (due to supressed Urinary Bladder)
  • Constipation (due to supressed GI tract)
  • Tachycardia (When all ACh receptors are bound)
  • Dry Mouth (supressed secretions)
  • Mydriasis (Supressed miosis)
  • Blurred Vision (inadequate AH drainage?)
  • Inhibition of sweating (reduced secretions)
  • Toxic Psychosis
30
Q

Neuromuscular Junction Blockers?

A

Block ACh from binding Nicotinic receptors.

31
Q

What is the mechanism of ACh binding nicotinic receptors?

A

-ACh binding the nicotinic receptors leads to an influx of Na+ ions, membrane depolarization which causes the release of Ca2+ from the sarcoplasmic reticulum, leading to muscle contraction.

32
Q

What is the mechanism of a Competitive Neuromuscular Blocker?

A
  • Competitively antagonizing the actions of the agonist (ACh) at the nicotinic receptor.
  • Produce flaccid paralysis
  • Chemical structure is different than ACh.
  • Block can be overcome by increasing ACh in synapse.
  • ->Main example is Curare (tubocurarine)
33
Q

What is the mechanism of a Depolarizing Neuromuscular Blocker?

A
  • Irreversibly binds nicotinic receptor
  • Prevents repolarization and makes the muscle fibre’s refractory period during further nerve impulses (this is called depolarizing block)
  • Chemical structure resembles ACh
  • Main drug used is Succinylcholine
34
Q

Contraction is partially impaired when what fraction of receptors are bound to a competitive drug?

A

75-80%

35
Q

Contraction is fully impaired when what fraction of receptors are bound to a competitive drug?

A

90-95%

36
Q

Which drugs are commonly used to reverse competitive neuromuscular blockers?

A
  • ->ChE inhibitors
  • Neostigmine
  • Edrophonium
  • Pyridostigmine
  • Reduces acetylcholinesterase in the synapse and allows for more ACh to overcome drug competition.
37
Q

What is the sequence of Competitive Neuromuscular Blockers?

A

-Small, rapidly moving muscles are paralysed first.
Then moves to the Limbs, Trunk, Intercostal Muscles, the Diaphragm which would lead to respiratory failure.

–>Recovery occurs in the reverse order.

38
Q

What are the main side effects of Competitive Neuromuscular Blockers?

A
  • Ganglionic Blockade
  • (Fall in BP and tachycardia)
  • Block of the vagal response
  • Histamine release
39
Q

Which is the only Depolarizing neuromuscular junction blockers used clinically?

A

Succinylcholine

  • Binds nicotinic receptors
  • IS NOT metabolized by AChE
  • ->Metabolized by Butyrylcholinesterase (BuChE)
40
Q

What is a common problem with succinylcholine breakdown?

A

-Several patients display isoforms of BuCHE, which can lead to prolonged synaptic transmission/ more extensive neuromuscular block.

41
Q

What are common side effects of depolarizing NMJ blockers?

A
  • Can release excess K+ from intracellular sites.

- Can lead to hyperkalemia (elevated blood K+ levels, rhamdomyolysis and cardiac arrest.

42
Q

Why is Hyperkalemia dangerous in patients on digoxin or diuretics?

A

-Digoxin is a cardiac contraction stimulant drug which is supposed to increase contractions of the heart. Increasing K+ concentrations could lead to heart failure/ blocking this drugs effects.

43
Q

What is Malignant Hyperthermia a common symptom of?

A
  • Depolarizing NMJ blocker side effect
  • Due to genetic abnormality of the ryanodine receptor
    (1: 3000)
  • Causes Ca2+ release from SR into the skeletal muscle which can lead to contracture, rigidity, heat production from muscles, hyperthermia, accelerated muscle metabolism, metabolic acidosis and tachycardia.
44
Q

Which drug is Malignant Hyperthermia treated by?

A

Dantrolene (Blocks Ca2+ release)

45
Q

What are some of the main uses of Neuromuscular blockers?

A
  • Surgical anesthesia
  • Orthopedic procedures to realign bone fractures and dislocations.
  • To facilitate tracheal intubation*
  • To prevent trauma during electroshock therapy
46
Q

Sympathetic effects can be mimicked by which classes of drugs?

A
  • Adrenergic receptor agonists (Epi, albuterol)
  • Norepinephrine Uptake Blockers (Cocaine, imipramine)
  • Monoamine Oxidase and COMT inhibitors
  • NE releasing agents
47
Q

What is the mechanism of Monoamine Oxidases and COMT inhibitors ?

A

-Delay the breakdown of NE and prolong it’s action

48
Q

Which drugs can block sympathetic effects?

A

Adrenergic Receptor Antagonists

Examples include: Prazosin and Propranolol

49
Q

How is NE removed from the synapse?

A

Uptake of NE occurs in the presynaptic terminal of the synapse.
-Re-uptake can be blocked by several drugs, including cocaine.

50
Q

What is the effect of increasing Re-uptake blockers?

A

Sympathetic activity at the synapse

NE can’t be removed

51
Q

What is the role of Baroreceptors?

A
  • Sense changes in arterial pressure & cause activation of the sympathetic/ parasympathetic systems.
  • Increase in blood pressure causes vasodilation (Parasympathetic Activity)
  • Decrease in blood pressure causes vasoconstriction (Sympathetic Activity)
52
Q

What are examples of Adrenergic Receptor Agonists?

A
  1. Epinephrine (binds Alpha and Beta receptors)
  2. NE- Can bind Alpha1 and Beta 2- has little effect binding Beta2
  3. Isoproterol- Most POTENT sympathomimetic amine
    - Acts on BETA receptors
  4. Dopamine (Activates BETA1 receptors)
53
Q

What is the result of Epinephrine binding B2 receptor?

A

Vasodilation

54
Q

Epinephrine brining properties?

A
  • ->Binds Beta1 to cause an increase in HR
  • ->Binds Beta2 to cause vasodilation
  • ->Binds Alpha 1 and causes vasoconstriction
55
Q

Norepinephrine brining properties?

A
  • ->Binds Beta 1 and causes an increase in HR

- ->Binds Alpha 1 and causes vasoconstriction

56
Q

Clinical uses of Adrenergic Agonists?

A
  • Allergic reactions–> Epinephrine (EPIPEN)
  • Bronchodilators (asthma)
  • As presser agents (Hypotension- increase CO and HR)

Pharm 1 Undergrad (9 decks)

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