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Pharmacology > lecture 7: Introduction to CNS medications > Flashcards

lecture 7: Introduction to CNS medications Flashcards

1
Q

The Neurotransmitter released from preganglionic parasympathetic to postganglionic parasympathetic is X and received by Y receptors

A

X: Ach
Y: Nicotinic (Nervous)

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2
Q

The adrenal gland receives the X neurotransmitter through its Y receptors

A

X: Ach
Y: Nicotinic

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3
Q

The Main neurotransmitter at a neuromuscular junction is X and received by Y receptors

A

X: Ach
Y: Nicotinic (Muscular)

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4
Q

Postganglionic sympathetic neurons release X which which is received by Y receptors

A

X: Norepinephrine
Y: Adrenergic receptors

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5
Q

the 4 types of Adrenergic receptors

A

α1 / α2 / β1 / β2

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6
Q

Muscarinic receptors are found on?

A

Effector organs Being parasympathetically innervated AND sweat glands (where Ach come from sympathetic neuronal release)

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7
Q

The Adrenal gland is sympathetically/parasympathetically innervated?

A

Sympathetically

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8
Q

The Adrenal gland is stimulated by X (category Y), received by Z receptors

A

X: Ach
Y: Sympathetic
Z: Nicotinic

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9
Q

Nicotinic and muscarinic are subtype of X innervation

A

Cholinergic

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10
Q

The 6 common types of neurotransmitters in the nervous system:

A
  1. Norepinephrine
  2. Ach
  3. Dopamine
  4. Serotonin
  5. Histamine
  6. Aminobutyric Acid
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11
Q

epinephrine is synonymous to…

A

Adrenaline

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12
Q

Nerve fibers secreting Epinephrine are called

A

Adrenergic

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13
Q

the Adenylyl cyclase pathway is activated by what type of G-protein?

A

Gs (has 3 subunits: α, β, γ)

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14
Q

The phospholipase C pathway is activated by which type of G-protein?

A

Gq (has 3 subunits: α, β, γ)

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15
Q

The 4 adrenergic receptor’s most common location?

A

α1 : Smooth muscle
α2 : GI
β1 : Cardiac tissue
β2: Smooth muscle

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16
Q

α1 receptors are X receptors, stimulated by Y and are excitatory/inhibitory in nature, acting through Gz protein pathway.

A

X: adrenergic
Y: norepinephrine
excitatory
Z: q

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17
Q

α2 receptors are X receptors which are excitatory/inhibitory in nature, acting through Gy protein pathway.

A

X: adrenergic
inhibitory (causing GI relaxation)
Y: i

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18
Q

β1 receptors are X receptors, stimulated by Y and are excitatory/inhibitory in nature, acting through Gz protein pathway.

A

X: adrenergic
Y: norepinephrine & epinephrine
excitatory
Z: s

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19
Q

β2 receptors are excitatory/inhibitory found on smooth muscles

A

inhibitory

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20
Q

Choline is taken into the neuron through what type of transport?

A

Cotransport with Na+ (energy required)

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21
Q

What blocks Choline Cotransport into the neuron?

A

hemicholinium

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22
Q

How do botulinum toxin and spider venom affect Ach vesicles?

A

Botulinum blocked vesicles releasing

Spider venom enhaces it (dramatically)

23
Q

Nicotinic Ach receptors are mostly found?

A

In Ganglia & Neuro-muscular plate (& adrenal gland)

24
Q

What category do nicotinic receptors belong to?

A

ligand-gated ion channel (requiring 2 Ach for conformational change)

25
Q

the Major draw back of cholinergic agonists, limiting their clinical usefulness is?

A

They show little specificity (enhance Ach action EVERYWHERE).

26
Q

Ach is therapeutically of no importance. why?

A

1- Multiplicity of Actions

2- Rapid inactivation by the cholinesterases

27
Q

The major innervation system of the heart is Sympathetic/parasympathetic?

A

Parasympathetic

28
Q

How does Ach lead to vasodilation?

A

Ach –> M3 receptors on smooth muscles –> production of NO –> stimulation of Protein Kinase G –> hyperpolarization & relaxation of vascular smooth muscles.

29
Q

How does Atropine counteract Ach?

A

Atropine is a muscarinic receptor blocker

30
Q

The main effects of Ach? (7)

A
  • Decreased BP
  • Vasodilation
  • Increased salivary secretions
  • Increased intestinal secretions and motility
  • Enhanced bronchiolar secretions
  • Increased tone of detrusor muscle, expulsion of urine
  • Miosis (constriction of pupil)
  • sweating (as part of glandular stimulation)
31
Q

What type of activity does Betanechol have?

A

Muscarinic activity (on GI mainly ; ineffective on muscles and ganglia). This mean Betanechol doesn’t access the CNS

32
Q

What’s the main therapeutic use of Betanechol?

A

used for non-obstructive urinary retention (she5 w 5ra).
Urination after anesthesia is the step that allows us to check the effect is over. Betanechol may be used to stimulate urination.

33
Q

What type of activity does Carbachol have?

A

Both muscarinic & nicotinic actions (it reaches the CNS (its side-effect))

34
Q

What are the main systems affected by Carbachol?

A
  • Cardiovascular
  • GI system
    Because of ganglion-stimulating activity: It first enhances the systems through nicotinic activity then represses them through muscarininc activity.
35
Q

How does Carbachol affect its systems? (long)

A

First its enhances them (GI & cardiac) through its nictotinic activity (causing postganglionic sympathetic to release Norepinephrine (also from adrenal glands)) then inhibits them (muscarinic activity acting on organs receptors (mimicing parasympathetic innervation)).

36
Q

what’s the therapeutic usage of Carbachol?

A

treatment of glaucoma & increased intraoccular pressure.

37
Q

Does Carbachol reach the CNS?

A

Yes, it has a ganglion-stimulating activity. Which is why its usage is limited to the eye (not absorbed there)

38
Q

What type of activity does Carbachol have?

A

Both Nicotinic & Muscarinic activity (starts with nicotinic and ends with muscarinic)

39
Q

What is Pilocarpine most therapeutically used for?

A

Drug of choice for emergency lowering of intraoccular pressure.

40
Q

what’s the drug of choice for emergency lowering of intraoccular pressure.

A

Pilocarpine. By opening the trabecular meshwork around schlemm’s canal, increasing drainage of aqueous fluid.

41
Q

What is Xerostomia/ how is it treated?

A

it’s intense dryness of the mouth due to lack of salivation. Pilocarpine is administered to induce salivation.

42
Q

What are the main effects of Pilocarpine?

What are the side effects?

A
  • Potent stimulator of secretions (sweat, saliva, tears)
  • Myosis
    The side effects is its ability to reach the CNS, causing disturbances (amnesia, etc..)
43
Q

How do Anticholinesterases enhance Ach activity?

A

They inhibit Ach degradation, increase its stay thus its activity (can reach CNS).

44
Q

Describe the activity of Physostigmine

A

Reversible binding to Acetylcholinesterase, causing potentiation of cholinergic activity in the body (nicotinic, muscarinic)

45
Q

The main effects of Physostigmine?

A

Mainly used for treatment of overdoses of drugs with anticholinergic activity (such as Atropine (anti-muscarinic), phenothiazines & tricyclic antidepressants)
along with..
- increased intestinal & bladder motility
- Miosis, lowering of intraoccular pressure

46
Q

Give 3 Anticholinergic drugs

A

Atropine, phenothiazines & tricyclic antidepressants

47
Q

In the case of an anti-cholinergic drug abuse, what’s you treatment of choice?

A

Physostigmine (an anticholinesterase)

48
Q

The main side effects of Physostigmine?

A
  • Hypotension

- Bradychardia

49
Q

What is Neostigmine usually used for? (2)

A
  • Antidote for tubocurarine and other neuromuscular blocking agents.
  • Treatment of Myasthemia gravis (auto-immunedegradation of nicotinic receptors at neuromuscular junction).
50
Q

What is the drug most similar to neostigmine?

A

Physostigmine. Difference is that Neostigmine doesn’t reach CNS.

51
Q

Describe the activity of Echothiophate

A

irreversible / covalent binding to the active site of acetylcholinesterase, making the enzyme permanently inactivated.

52
Q

What is Pralydoxime?

A

It’s the only know reactivator of Anticholinesterases after being bound to Echothiophate. Still has a short period of action before completly losing the enzyme.

53
Q

What kind of receptors do sweat glands have? What molecule binds it? Does this happen when sympathetically/parasympathetically innervated?

A

sweat glands have muscarinic receptors stimulated by Ach released from SYMPATHETIC neurons (called sympathetic cholinergic innervation).

Pharmacology (5 decks)

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