Nervous System Pharm 4: Cholinergic Pharmacology

Front 1

Choline + ACoA is converted to ACh by this

Back 1

Choline acetyltransferase

Front 2

Is ACh formed in the vesicle or outside the vesicle in a nerve terminal?

Back 2

outside the vesicle, thus it requires a vesicle transporter

Front 3

These channels are responsible for ACh release

Back 3

voltage gated calcium channels

Front 4

Name the 2 cholinergic receptors

Back 4

muscarinic
nicotinic

Front 5

Muscarinic or Nicotinic

1. ionophore-type receptor
2. fast response
3. initiates a response
4. chronic stimulation leads to "depolarization blockade"

Back 5

describes nicotinic receptors

Front 6

Muscarinic or Nicotinic

1. transduction-type receptor
2. slow response
3. modulation of response
4. chronic stimulation leads to continued effect

Back 6

Muscarinic receptors

Front 7

Location of muscle nicotinic receptors

Back 7

NMJ

Front 8

Location of neuronal nicotinic receptors

Back 8

ganglia
adrenal medulla
CNS

Front 9

Is metabolism or reuptake the major mechanism of ACh removal from synapse?

Back 9

metabolism by AChE

Front 10

ACh breakdown products are (blank) and (blank).

Back 10

acetic acid & choline

Front 11

Where is AChE found?

Back 11

1. cholinergic synapses
2. RBC membrane

Front 12

Does AChE hydrolyze succinylcholine?

Back 12

Nope. But BChE does.

Front 13

Where is BChE found?

Back 13

plasma

*NOT IN SYNAPSES*

Front 14

2 types of cholinergic agonists

Back 14

1. choline esters
2. alkaloids

Front 15

List 2 reasons why ACh is not a good drug?

Back 15

1. not receptor selective (stimulates muscarinic & nicotinic)
2. metabolized rapidly by ChE

Front 16

Name the muscarinic selective agonist

Back 16

Bethanechol

Front 17

3 properties of Bethanechol

Back 17

1. muscarinic selective
2. no AChE hydrolysis
3. no CNS action

Front 18

3 cholinergic alkaloids

Back 18

1. muscarine
2. pilocarpine
3. arecoline

Front 19

Where is Muscarine found?
Where is Arecoline found?

Back 19

Muscarine is in mushrooms
Arecoline is in Betel nut

Front 20

Effects of cholinergic agonists on blood vessels

Back 20

no PSNS innervation, but muscarinic receptors are stimulated to release NO.

produces vasodilation

Front 21

Effects of cholinergic agonists on heart

Back 21

decreased HR via direct action

Front 22

Effects of cholinergic agonists on eyes

Back 22

miosis
accomodation for near vision
decreased intraocular pressure

Front 23

Effects of cholinergic agonists on bronchioles.

Back 23

bronchioconstriction
bronchiosecretion

Front 24

Too much cholinergic agonists leads to (parasympathetic/sympathetic) stimulation

Back 24

parasympathetic

bradycardia, miosis, near vision, diarrhea, vomiting, urination

Front 25

Would you give a cholinergic agonist to a patient with asthma or ulcers?

Back 25

Nope. Cholinergic agonists increase bronchosecretions, bronchoconstriction and GI secretions

Front 26

4 groups of AChE inhibitors

Back 26

1. short-acting competitive inhibitor
2. noncompetitive inhibitor
3. carbamates
4. organophosphates

Front 27

Initial effects of AChE inhibitors on heart

Back 27

tachycardia due to the decrease in blood pressure (caused by ganglionic blockade)

Front 28

Upon prolonged exposure at high doses, AChE inhibitors produce this change in HR

Back 28

bradycardia, due to direct effect on heart

Front 29

Do AChE inhibitors have much effect on blood vessels?

Back 29

No. Blood vessels have very little PSNS innervation

Front 30

TRUE OR FALSE
AChE inhibitors have the same effects as direct acting cholinergic agonists.

Back 30

true

Front 31

What are the initial effects of AChE at NMJ? What happens with continued use of high AChE doses?

Back 31

initial: muscle twitching

eventually: paralysis

Front 32

Name 2 agents used to treat AChE toxicity

Back 32

1. Atropine
2. Pralidoxime

Front 33

Does Donepezil act at the active site of AChE?

Back 33

nope. it blocks channel entry of ACh to the active site but it does not work at the active site of AChE

Front 34

Which AChE inhibitors acts at only the esteratic site of AChE?

Back 34

organophosphates

Front 35

Which AChE inhibitor is very quick-acting?

Back 35

Edrophonium

Front 36

Which AChE inhibitors are suicide inhibitors?

Back 36

Carbamates

-stigmines & Carbaryl

Front 37

Which of the "---stigmine" group are quaternary derivatives?

Back 37

Neostigmine & Pyridostigmine

Front 38

They are both thiophosphates.

Back 38

Malathion
Parathion

Front 39

Describe what happens in the cardiovascular system upon initial AChE inhibitor exposure. What happens later?

Back 39

AChE inhibitors produce tachycardia due to decrease in BP...eventually bradycardia will be produced

Front 40

Describe what happens to the following in the presence of either a muscarinic agonist or AChE inhibitor

-eye
-airway
-GI
-glands

Back 40

eye: miosis, lacrimation

airway: constriction, congestion

GI: nausea, vomiting, cramps, diarrhea

glands: sweating, lacrimation, salivation

Front 41

Describe the effects of AChE inhibitors on the CNS

Back 41

confusion, convulsion, coma, respiratory depression

Front 42

Describe prouction/flow of aqueous humor.

Back 42

Production happens at ciliary process in posterior chamber.

Aqueous humor flows thru pupil into anterior chamber.

Aqueous humor exits thru trabecular meshwork into Canal of Schlem and then into the circulatory system

Front 43

Describe open-angle glaucoma.

Back 43

most common form of glaucoma

develops slowly as drainage canals become ineffective

Front 44

Describe closed-angle glaucoma.

Back 44

occurs when pupil enlarges too much or too fast and the outer edge of the iris blocks the eye's drainage canals

produces a sudden & severe rise in eye pressure

Front 45

Why would a muscarinic agonist be used to treat glaucoma?

Back 45

produce miosis to increase angle between cornea & iris

this increases outlfow

Front 46

Why would a AChE inhibitor be used to treat glaucoma?

Back 46

contracts ciliary muscle to realign trabecular meshwork

facilitates outflow

Front 47

Are adrenergic agonists good treatment for narrow-angle glaucoma?

Back 47

nope

they dilate vessels to faciliate outflow but this would exacerbate the already very-narrow angle in closed angle glaucoma

Front 48

What's decreased in myasthenia gravis?

Back 48

number of functional nicotinic cholinergic receptors due to IgG attack

Front 49

How is Edrophonium used in the diagnosis of myasthenia gravis?

Back 49

give the Edrophonium

in patient w/ normal receptors: decreased muscle strength

in patient w/ myasthenia gravis: increased muscle strength

Front 50

What 3 alkaloids are muscarinic blockers?

Back 50

Atropine
Hyoscyamine
Scopolamine

Front 51

What 2 synthetic muscarinic blockers have CNS activity?

Back 51

Benztropine
Ipratropium

Front 52

Describe the effects that muscarinic blockers would have on the following

-heart
-blood vessels
-eye
-glands
-GI
-lungs
-CNS
-

Back 52

heart: tachycardia due to blocked vagal tone

blood vessels: little direct effect but since sweat glands are blocked, get vasodilation (to counter the hyperthermia)

eye: mydriasis, photophobia, cycloplegia

glands: block secretions; no sweating means possible hyperthermia

GI: constipation

lungs: dilation

CNS: drowsiness, amnesia

Front 53

Describe the hierarchy of organs affected by increasing doses of muscarinic blockers.

Back 53

low doses: salivation & sweating are blocked

increase: eye & heart affected

more increse: GI, bladder, CNS affected

highest dose: gastric secretions

Front 54

What's the one major contraindication of muscarinic antagonists?

Back 54

don't give them to people who are predisposed to narrow angle glaucoma!!

Front 55

Are muscarinic antagonists used at OTC sleeping pills and cold tablets?

Back 55

yep

Front 56

Which muscarinic antagonist would you give to a patient with COPD?

Back 56

Ipratropium