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Pharm Exam 1 > Autonomic Pharmacology_1 > Flashcards

Autonomic Pharmacology_1 Flashcards

1
Q

Afferent and efferent divisions of the peripheral nervous system

A

Afferent Division

Somatic sensory

visceral sensory

Special sensory

Efferent Division

Somatic motor

Autonomic motor

(sympathetic, parasympathetic, Enteric)

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2
Q

Be familiar with the basic responses of target organs in response to sympathetic and parasympathetic stimulation

A

Parasympathetic: Cranial + sacral

Sympathetic: thoracic + lumbar

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3
Q

Describe the lengths of neurons in the sympathetic vs. parasympathetic nervous system

A

Sympathetic = short preganglionic neurons, long postganglionic neurons

Parasympathetic = long preganglionic neurons, short postganglionic neuron

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4
Q

Which neurotransmitter is released at target organs by the parasympathetic nervous system

A

Acetylcholine

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5
Q

Draw the picture of the neurons with their NT and receptors

A

Sympathetic -> Adrenergic Muscarinic (sweat glands) tissue receptor

Parasympathetic -> Muscarinic tissue receptor

Somatic -> Nicotinic tissue receptor

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6
Q

What type of receptors are located at target organs of the sympathetic nervous system?

A

Alpha and beta adrenergic receptors

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7
Q

Explain the two divisions of the autonomic nervous system

A

Sympathetic

  • Fight or flight actions: energy mobilization, increased cardiac output and ventilation
  • Thoracic and lumbar nerve roots
  • Short preganglionic/long postganglionic
  • Norepinephrine (NE) and epinephrine (E) are* *main* *neurotransmitters at target organs
  • Alpha and beta-adrenergic receptors at target organs

Parasympathetic

  • Rest and digest actions: energy storage/conservation, increased digestive secretions
  • Cranial nerves and sacral roots
  • Long preganglionic/short postganglionic
  • Acetylcholine (ACh) is* *main* *neurotransmitter at target organs
  • Muscarinic ACh receptors at target organs
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8
Q

Describe the sympathetic nervous system effects on the eyes and heart

A

EYES

alpha 1 contracts the radial muscle of the iris (widens pupil)

Beta 2 relaxes ciliary muscles (flattens lenses) for far vision

HEART

Beta 1 = SA node = increase heart rate

Beta 1 and 2 = Atria = increase contractility

Beta 1 and 2 = AV node = increases conduction velocity

Beta 1 and 2 = Ventricles = increases contractility

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9
Q

Describe autonomic tone

A

one division is usually dominant

  • Ex: heart beats at ~100 beats/min with no innervation
    • parasympathetic division: decreases HR
    • Sympathetic division: increases HR
      • sympathetic effect (vagal tone) dominates, so resting HR is ~70 BPM
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10
Q

What are blood vessels primary served by?

A

sympathetic nervous system (alpha adrenergic receptors)

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11
Q

How does an increase in sympathetic activity affect blood vessels?

A

vasoconstriction

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12
Q

Acetylcholinesterase (AChE)

A

terminates signal by breaking down ACh

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13
Q

Muscarinic receptors are activated by

A

parasympathetic nervous system (ACh)

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14
Q

Explain the function of a synapse

A
  1. Neurotransmitter synthesized and packaged in vesicles
  2. Action potential arrives, carried by voltage-gated Na channels
  3. Voltage-gated Ca channels open
  4. Exocytosis of neurotransmitter
  5. Neurotransmitter binds to receptors; activation of receptors results in ion influx or second messenger formation
  6. Neurotransmitter is enzymatically degraded or pumped into presynaptic neuron
  7. Degradation of second messenger
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15
Q

Ways that a drug can increase the activity of a synapse

A
  1. Increase neurotransmitter release into the synapse
  2. Reduce reuptake of the neurotransmitter from the synapse
  3. reduce degradation of the neurotransmitter in the synapse
  4. mimic activity of a neurotransmitter at its receptor
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16
Q

Ways that a drug can decrease the activity of a synapse

A
  1. block a neurotransmitter’s receptor
  2. inhibit of synthesis of a neurotransmitter
  3. prevent the release of a neurotransmitter
  4. prevent packaging in vesicles
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17
Q

Even numbered muscarinic receptors

A

Coupled to Gi proteins

Results in decreased cAMP

typically inhibitory affect

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18
Q

Odd numbered muscarinic receptors

A

paired to Gq receptors, leads to smooth muscle contraction

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19
Q

Describe PSNS neurotransmission

A

ACh released at target organs to activate muscarinic receptors

Acetylcholinesterase (AChE) terminates signal by breaking down ACh

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20
Q

Explain Muscarinic receptors

A

Muscarine: a mushroom toxin that activates muscarinic receptors, symptoms resemble extreme PSNS activation

  • Five M receptor subtypes, M1 - M5
  • Even numbered couple to Gi
  • Odd numbered couple to Gq
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21
Q

Nicotinic cholinergic receptors

A

cause depolarization

excitatory

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22
Q

How can muscarinic receptors be indirectly activated?

A

by inhibiting AChE

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23
Q

Explain the general drug mechanisms with PSNS

A
  1. Activate M receptors directly
  2. Activate M receptors indirectly by inhibiting AChE
  3. Block M receptors
  4. Inhibit ACh release
24
Q

Drugs that enhance parasympathetic nervous system signaling

A

Parasympathomimetics or cholinomimetics

25
Q

Drugs that decrease parasympathetic nervous system signaling

A

Parasympatholytics

or

Cholinolytics

26
Q

What are the effects of cholinomimetics on the body?

A
  1. Eye: set for near vision - ciliary muscle and iris sphincter contracted
  2. Heart rate: decreased
  3. Urination: contraction of bladder detrusor and relaxation of the sphincter (leading to urination)
  4. Glandular secretions: increased (saliva, tears, etc)
  5. GI motility: increased
  6. Airways: constricted
27
Q

Bethanechol

A

Clinical use of direct-acting muscarinic agonists

Resistance to hydrolysis by AChE and very low nicotinic activity

Treatment of non-obstructive GI hypomotility (eg. postoperative ileus)

Postoperative or postpartum urinary retention

28
Q

Pilocarpine

A

aka Cevimeline

Clinical use of direct-acting muscarinic agonists

Treates Glaucoma or xerostomia

29
Q

Anticholinesterases: indirect acting cholinomimetics

A

Anticholinesterases

Reversible -> noncovalent or covalent reversible (neostigmine)

Or Covalent Irreversible (organophosphates (sarine, malathion)

30
Q

Organophosphates - sarin/malathion

A

covalent, irreversible, anticholinesterases

31
Q

Anticholinesterases

A

indirect cholinometrics

Drugs that enhance PSNS signaling

32
Q

Neostigmine

A

covalent, reversible, anticholinesterases

33
Q

Explain the difference between Normal AChE function and Covalent reversible inhibitor

A

Normal AChE function = ACh = Fast reaction (microseconds)

Covalent reversible inhibitor = Neostigmine = forms weak covalent bond = slow reaction (hours) = prevents enzyme from functioning and then inhiviting the creation

34
Q

What is the difference between a covalent reversible inhibitor (Neostigmine) and AChE?

A

AChE functions quickly, neostigmine functions very slowly

35
Q

How do organophosphates function?

A

They form a stable bond that does not spontaneously hydrolyze

  • All share in common the phosphate, phosphate forms the bond with the AChE
    • essentially this bond is permanent but there is one drug that will kick the molecule off
    • The antidote however must be given at an early stage in the reaction
36
Q

What drug can remove organophosphates if given soon after exposure?

A

Pralidoxime (2-PAM)

If not given early, aging occurs and new enzyme synthesis is only way to recover

37
Q

Clinical uses of anticholinesterases

A

Glaucoma/myasthenia gravis

38
Q

_______ Treats muscle weakness by increasing ACh at the neuromuscular junction

A

Neostigmine

Treats muscle weakness by increasing ACh at neuromuscular junction

39
Q

Insecticides that inhibit AChE preferentially within insects

A

Parathion, Malathion

  • Inhibit insect AChE preferentially due to slight differences in target receptor
  • High concentrations cause toxicity in humans
  • Exposure risk for farm workers
40
Q

What nerve agents have extremely high potency and used for possible chemical warfare?

A

Organophosphate nerve agents

Anti-cholinesterases

Engineered to disperse easily in air, lipid soluble to allow skin absorption

41
Q

What kind of symptoms appears after anticholinesterase exposure?

A

Muscarinic (SLUDGE) symptoms

Salivation

Lacrimation

Uriniation

Defication

GI upset

Emesis

42
Q

What is the antidote for nerve agent or insecticide poisoning?

A

Atropine + pralidoxime (2-PAM)

43
Q

What are the motor effects caused by anticholinesterases?

A

Nicotinic receptors on skeletal muscle = muscle weakness and respiratory failure (diaphragm)

44
Q

Cholinolytic or muscarinic antagonist examples

A

Tolterodine

Atropine

Glycopyrrolate

Scopolamine

45
Q

What are the clinical uses of atropine?

A

Atropine

  • Used to reverse bradycardia that is caused by excess vagal activity
  • Antidote for cholinergic poisoning
  • Can be used to cause mydriasis, but generally shorter-acting agents are preferred = eye dilation
  • Can be used to decrease saliva production (glycopyrrolate is another option)
  • Medicinal plant = Atropa belladonna
    • deadly nightshade
46
Q

Which drugs can be used to decrease salivation production?

A

atropine and glycopyrrolate

47
Q

What drug is used to treat an overactive bladder?

A

Tolterodine

Somewhat more selective for M3 receptors found in the bladder

48
Q

What are the anticholinergic side effects?

A

dry mouth

blurry vision

upset stomach

headache

constipation

dry eyes

dizziness

Due to the fact they all block ACh receptors…

Antihistamines and antipsychotic drugs also cause these side effects

49
Q

Sialagogue drugs

A

Pilocarpine, cevimeline

  • Used to increase salivation when problem is related to salivary gland function (sjogren’s syndrome)
  • Side effects: minor SLUDGE syndrome
  • generally should be avoided if dry mouth is due to an anticholinergic (eg. patient on tolterodine). these patients may need to use other methods to increase salivation in order to reduce risk of caries
    • would cancel the drug that they already are taking out
50
Q

Saliva reducing drugs

A

Atropine, glycopyrrolate

Reduces drooling associated with neurologic disorders (Cerebral palsy)

51
Q

Anticholinergic Toxidrome (toxidrome = collection of side-effects)

A

Antihistamines

Antidepressants (especially tricyclics)

Antipsychotics

Nightshade plants

(Atropa belladonna, Datura = jimsonweed)

52
Q

What are the anticholinergic toxidrome symptoms?

A

Mad as a hatter - CNS effects of ACh receptors/mental status

Blind as a bat - blurred vision/lens focus problem

Red as a beat - vasodilation

Hot as a hare - no sweating

Dry as a bone - no saliva

53
Q

Botulism toxin A

A

Inhibits ACh release

affects mainly skeletal muscle

54
Q

_______ is a protease produced by Clostridium botulism; results in food poisoning

A

BoNT Light Chain

Cause of botulism food poisoning - effects PNS

Mechanism is cleavage of SNARE proteins which prevents neurotransmitter vesicle fusion

Most lethal toxin known: one gram enough to kill a million people

Potential to affect neurotransmitter release from all synapses; ACh and glutamate are especially sensitive

55
Q

What is the mechanism of botulism toxin?

A

cleavage of SNARE proteins which prevents NT vesicle fusion

56
Q

What are the uses of Botulinum toxin (Botox)

A

Muscle spasms such as

  • Blepharospasm
  • Cervical dystonia (spasms of neck muscles)
  • Hyperhidrosis - sweating problems
  • Cosmetic use: flaccid paralysis of facial muscles
  • Many off-label uses

Pharm Exam 1 (5 decks)

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