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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
Drugs that decrease parasympathetic nervous system signaling
Parasympatholytics or Cholinolytics
26
What are the effects of cholinomimetics on the body?
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
Bethanechol
**_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
Pilocarpine
aka Cevimeline Clinical use of direct-acting muscarinic agonists Treates Glaucoma or xerostomia
29
Anticholinesterases: indirect acting cholinomimetics
Anticholinesterases Reversible -\> noncovalent or covalent reversible (neostigmine) Or Covalent Irreversible (organophosphates (sarine, malathion)
30
Organophosphates - sarin/malathion
covalent, irreversible, anticholinesterases
31
Anticholinesterases
indirect cholinometrics Drugs that enhance PSNS signaling
32
Neostigmine
covalent, reversible, anticholinesterases
33
Explain the difference between Normal AChE function and Covalent reversible inhibitor
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
What is the difference between a covalent reversible inhibitor (Neostigmine) and AChE?
AChE functions quickly, neostigmine functions very slowly
35
How do organophosphates function?
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
What drug can remove organophosphates if given soon after exposure?
Pralidoxime (2-PAM) If not given early, aging occurs and new enzyme synthesis is only way to recover
37
Clinical uses of anticholinesterases
Glaucoma/myasthenia gravis
38
\_\_\_\_\_\_\_ Treats muscle weakness by increasing ACh at the neuromuscular junction
Neostigmine Treats muscle weakness by increasing ACh at neuromuscular junction
39
Insecticides that inhibit AChE preferentially within insects
**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
What nerve agents have extremely high potency and used for possible chemical warfare?
**Organophosphate** nerve agents Anti-cholinesterases Engineered to disperse easily in air, lipid soluble to allow skin absorption
41
What kind of symptoms appears after anticholinesterase exposure?
Muscarinic (SLUDGE) symptoms Salivation Lacrimation Uriniation Defication GI upset Emesis
42
What is the antidote for nerve agent or insecticide poisoning?
Atropine + pralidoxime (2-PAM)
43
What are the motor effects caused by anticholinesterases?
Nicotinic receptors on skeletal muscle = muscle weakness and respiratory failure (diaphragm)
44
Cholinolytic or muscarinic antagonist examples
Tolterodine Atropine Glycopyrrolate Scopolamine
45
What are the clinical uses of atropine?
***_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
Which drugs can be used to decrease salivation production?
atropine and glycopyrrolate
47
What drug is used to treat an overactive bladder?
***_Tolterodine_*** Somewhat more selective for **M3 receptors** found in the bladder
48
What are the anticholinergic side effects?
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
Sialagogue drugs
**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
Saliva reducing drugs
**Atropine, glycopyrrolate** Reduces drooling associated with neurologic disorders (Cerebral palsy)
51
Anticholinergic Toxidrome (toxidrome = collection of side-effects)
Antihistamines Antidepressants (especially tricyclics) Antipsychotics Nightshade plants (Atropa belladonna, Datura = jimsonweed)
52
What are the anticholinergic toxidrome symptoms?
**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
Botulism toxin A
Inhibits ACh release affects mainly skeletal muscle
54
\_\_\_\_\_\_\_ is a protease produced by Clostridium botulism; results in food poisoning
**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
What is the mechanism of botulism toxin?
cleavage of SNARE proteins which prevents NT vesicle fusion
56
What are the uses of Botulinum toxin (Botox)
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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