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MOD 2 > Paraympathetic pharmacology > Flashcards

Paraympathetic pharmacology Flashcards

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1
Q

Pupil dilation is caused by?

A

Sympathetic

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2
Q

Bronchoconstriction is caused by?

A

Parasympathetic

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3
Q

Urination is caused by?

A

Parasympathetic

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4
Q

Dilation of blood vessels in skeletal muscle?

A

Sympathetic

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5
Q

Constipation is caused by?

A

Sympathetic

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6
Q

What brings choline into the presynaptic cleft?

A

cholinetransferase (with Na)

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7
Q

Choline acetyltransferase?

A

acetyl CoA and choline catalyzed to form acetylcholine

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8
Q

Block cholinetransferase?

A

Hemicholiniums

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9
Q

Vesamicol?

A

blocks Vesicular acetylcholine transporter, which brings Ach into vesicle

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10
Q

Acetylcholinesterase?

A

is bound and free floating, binds to Ach, breaks it down

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11
Q

Acteylcholine autoreceptor?

A

Ach binds to the receptor, stop the release

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12
Q

Heteroreceptors?

A

presynaptic receptor, different things bind to it, depending on location

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13
Q

Muscarinic receptors?

A

CNS, heart, smooth muscle, nerves, and endothelium
M1-M5 (M1-M3 functionally characterized)
Directly, Indirectly

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14
Q

Directly Muscarinic receptors?

A

binds directly to the receptor or Ach released from parasympathetic nerves
Activates muscarinic receptors on effector cells, alters organ function directly

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15
Q

Indirectly Muscarinic receptors?

A

interacts with muscarinic receptors on pre-synaptic nerve terminals to INHIBIT the release of NT
-alters organ function indirectly

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16
Q

Nicotinic receptors?

A

located on nerves and muscles
ligand gated ion channel
bind of 2 Ach molecules elicit a conformational change that allows Na to enter
-Ach initially stimulated and then blocks the receptor

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17
Q

MOA Nicotinic receptors?

A

channel opening allow Na and K ions to diffuse rapidly, cell depolarization

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18
Q

Depolarizing blockade?

A

presistent agonist occupancy at receptor, postganglionic neuron stops firing, skeletal muscle cell relaxes

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19
Q

Activate muscarinic receptors?

A

Eye, Secretory, GI, Genitourinary, respiratory, CV

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20
Q

Activated nicotinic receptors?

A

CNS, PNS, NM junction

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21
Q

Direct acting cholinomimetics?

A

Choline esters

Alkaloids

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22
Q

Choline esters?

A 
hydrophilic
hydrolyzed by actylcholinesterase in GI tract at various rates
Acetylcholine
Bethanechol
Carbachol
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23
Q

Alkaloids?

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A

well absorbed from most sites of administration
acidification of urine accelerates clearance of pilocarpine and nicotine
Pilocarpine

24
Q

Indirect acting drugs?

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A

Acetylcholinesterase (AChase)
terminate actions of ACh
act as inhibitors at the active site of the enzyme, increase endogenous ACh, (inhibit AChase, decrease breakdown of ACh)
Butyrylcholinesterase also inhibited

25
Chemistry of indirect acting cholinomimetics?
Lipid soluble, inhibitors characterized by chemical groups | -Edrophonium, Neostigmine/Physostigmine, Organophosphates, Thiophosphates
26
Absorption fo indirect acting cholinomimetics?
Poor absorption from conjunctiva, skin and lungs Physostigmine is well absorbed from all sites and sued topically in the eye organophosphate cholinesterase inhibitors are well absorbed skin, lung, gut and conjunctiva thiophosphate insecticides are lipid soluble and rapidly absorbed, must be activated in the body
27
AChases inhibitors reversible?
Edrophonium, Physostigmine, neostigmine, pyridostigmine | echothiphate (essentially irreversible)
28
Physostigmine?
forms a stable intermediate with the AChases wide range at muscarinic receptors duration 2-4 hours, can enter and stim cholinergic sites in the CNS
29
Physostigmine therapeutic use?
increase intenstinal and bladder motility miosis and spasm of accomodation and lowers intra-ocular pressure topically in the eye treat anticholinergic (atropine) drug overdoses
30
Physostigmine adverse effects?
in CNS, may lead to convulsions bradycardia and a fall in CO accumulation of ACh-- paralysis of skeletal m at the nm junction
31
Neostigmine?
not enter CNS, greater effect on skeletal m, stim contaction before paralysis 30 min- 2hr stimulate the bladder and GI tract symptomatic treatment of myasthenia gravis
32
Echothiophate?
generalized cholinergic stimulation paralysis of motor function convulsions intense miosis chronic treatment of open-angle glaucoma, may cause cataracts
33
Urinary tract and GI Cholinomimetics?
can treat decreased smooth m activity associated with (post-operative ileus, congenital megacolon, neurogenic bladder) can increase tone of lower esophageal sphincter (reflux esophogitis) most widely used drugs: - choline esters: bethanechol - AChase inhibitors: neostigmine
34
Myasthenia gravis?
Edrophonium used as a diagnositic test Pydriostigmine (AChase inhibitors, DOC) may cause excess stimulation of muscarinic receptors
35
Alzheimer disease?
AChase inhibitors (Tacrine, donepezil, rivastigmine, galantamine) delay the progression tacrine was initial drug developed, but induces severe hepatotoxicity GI distress is primary adverse effect
36
Mucarinic excess?
due to pilocarpine and choline esters - adverse reactions: DUMBBELSS - treatment: atropine
37
Acute nicotine treatment is symptomatic?
muscarinic stimulation- atropine | central stimuliation- diazepam/anticonvulsants
38
Chronic nicotine toxicity (smoking)?
replacement therapy: Gum, transdermal patch, nasal spray, inhaler Varenicline- partial nicotinic receptor agonist and antagonist, Chantix
39
Major source of toxicity is?
pesticide use in agriculture and the home - muscarinic excess-initial effects - treatment includes atropine and pralidoxime (2-PAM)
40
Anticholinesterase inhibitors (irrversible), organophosphates?
covalently binds via its phosphate group to the serine- OH group at the active site of the enzyme permanently inactivates enzyme, only way to restore is to synthesize new enzyme molecules
41
Aging?
slow release of an ethyl group makes it impossible for chemical reactivators to break the bond between drug and enzyme
42
Pralidoxime (2-PAM)?
can reactivate inhibited acetylcholinesterase displaces the phosphate group of the organophosphate and regenerates the enzyme, if given before aging, can reverse the effects of echothiophate and other agents
43
DUMBBELSS?
``` Diarrhea Urination Miosis Bronchoconstriction Bradycardia Emesis/ Excite muscles Lacrimation Salivation Sweating ```
44
Antimuscarinic drugs?
prototype: atropine
45
Antinicotinic drugs?
ganglionic blockers and NMJ blockers
46
Pharmcokinetics/dynamics of antimuscarinic?
well absorbed from gut and conjunctival membranes significant levels achieved in CNS within 30-60 min Elimination can last -15 hours (atropine) MOA: reversible blockade
47
Effects of antimuscarinic agents?
CNS, eye, CV, respiratory, GI tract, genitourinary tract, sweat glands
48
Pilocarpine on the eye?
miosis
49
Atropine on the eye?
mydriasis
50
Atropine?
binds competitively to receptor preventing ACh binding acts both centrally and peripherally duration- 4 hours
51
Clinical uses atropine?
treats bradycardia combined with opioid antidiarrheals treatment of overdoses of AChase inhibitor insecticides and some mushroom poisonings: blocks the effects of excess ACh from acetylchonesterase inhibitors
52
Scopolamine?
greater CNS action compared to atropine actions -effective anti-motion sickness, blocks short term memory, produces sedation
53
Ipratropium?
synthetic analog to atropine causes bronchodilation treating asthma and chonic obstructive pulmonary disease (COPD) Tiotrpoium similar action but longer bronchodilation effect
54
Urinary incontinence clinical pharmacology?
Oxybutynin Solifenacin Tolterodine
55
Uses for antimuscarinic?
cholinergic poisoning | atropine overdose
56
contraindications antimuscarinics?
glaucoma | BPH
57
AntiDUMBBELSS?
``` Constipation No urination Mydriasis Bronchodilation Tachycardia no emesis no tearing dry mouth no sweat ``` ``` Hot as a hare blind as a bat dry as a bone red as a beet mad as a hatter bloated as a bladder ```

MOD 2 (6 decks)

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