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Neorologia > Nicotinics and AChE > Flashcards

Nicotinics and AChE Flashcards

1
Q

Where does ACh bind on Muscle nicotinic receptors

A

alpha - delta interface
or
alpha - epsilon interface

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2
Q

How many molecules of ACh are required to open a nicotinic ion channel?

A

2

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3
Q

Which nicotinic receoptor is Jim’s favorite?

A

Alpha7 homopentamer

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4
Q

Where does ACh bind on neuronal AChRs?

A

Homomeric: Alpha-Alpha interface
Heteromeric: Alpha-Beta interface

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5
Q

Alpha7 AChR homopentamer Ion selectivity and location

A

Ca++&raquo_space; Na+

Brain and Ganglia

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6
Q

Alpha subunit primarily found in the brain

A

Alpha 2

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7
Q

Alpha subunit primarily found in ganglia

A

Alpha 3

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8
Q

Alpha subunit most common in CNS

A

Alpha 4

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9
Q

Alpha subunit primarily found in skeletal muscle

A

Alpha 1

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10
Q

Varenicline (Chantix)

A

Partial nicotinic agonist

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11
Q

Bupropion (Wellbutrin; Zyban)

A

DAT/NET blocker

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12
Q

Clonidine (Catapres)

A

Alpha2 agonist. Roll in smoking cessation?

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13
Q

Chantix concerning side effect

A

Major sleep disruptions, bad dreams, etc.

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14
Q

What makes a light cigarette?

A

More holes -> infuses more air -> less cough reflex -> deeper inhale

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15
Q

If you want to increase nicotine receptor density in the brain, would you give nAChR agonist or antagonist?

A

Trick question you could use either.

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16
Q

Current hypothesis for why nicotine (or agonist) can cause upregulation of receptor

A

Receptor homologously desensitized so chronic activation and desensitization leads to receptor synthesis

17
Q

Where are most neuronal nicotinic receptors located?

A

Presynaptic nerve terminals

18
Q

How doe presynaptic nerve terminal nAChRs facilitate nerotransmitter release?

A

Increased Ca++ levels; increased NT release

19
Q

Nicotine Withdrawl symptoms

A 
Negative Mood
Depressed
Anxious
Inattentive
Hungry
Cognitively Impaired
Achy
20
Q

Skeletal muscle relaxants MOA

A

Indirect: Decrease ACh release in somatic NS

Direct acting: Block muscle nAChRs

21
Q

d-tubocurare (Tubarine) MOA

A

Direct antagonist. Binds nAChR orthosteric binding site

22
Q

How to reverse Curare

A

AChE inhibitors and mAChR antagonists

23
Q

Depolarizing neuromuscular blockers

A

Succinylcholine (Anectine)

24
Q

Succinylcholine (Anectine) MOA

A

Depolarizes NMJ initially, then produces long-lasting blockade

25
Q

Succinylcholine metabolism

A

Plasma cholinesterase

26
Q

Succinylcholine ADR

A
  1. Postop muscle pain ( due to fasciculations)
  2. Hyperkalemia
  3. Malignant hyperthermia - number one cause of death during surgery
27
Q

Ganglionic Blocking Drugs

A

Mecamylamine (Inversine)

Hexamethonium

28
Q

Mecamylamine (Inversine) MOA

A

Blocks nAChRs in ganglia -> decreased postganglionic release of NE -> decreased BP

*Also blocks parasympathetic –> Anti-sludge ADR

29
Q

Mecamylamine (Inversine) Effects

A
  • Decreased BP
  • Loss of cardiovascular reflexes
  • Severe orthostatic hypotension
  • Constipation, urinary retention, drymouth
  • Partial mydriasis
30
Q

AChEIs Use

A
  • Recovery from NMJ blockers
  • Autoimmune myasthenia gravis
  • Atropine Poisoning (comp. musc. antag)
  • TCA overdose
  • Cognitive improvement in dementia
31
Q

Carbamates (AChEIs) that Cross the BBB

A
  • *Donepezil (Aricept)
  • *Galanthanmine (Reminyl)
  • Physostigmine (Antilirium)
  • Tetrahydroacridine (THA) (Tacrine)
  • Rivastigmin (Exelon)
32
Q

Donepezil (Aricept) MOA

A

CNS AChEI -> increased central ACh activity

33
Q

Galanthamine (Reminyl) MOA

A

CNS AChEI -> increased ACh concentration

Also nAChR APL

34
Q

Carbamates that don’t cross BBB

A

Pyridostigmine (Mestinon)

35
Q

Pyridostigmine (Mestinon) Use

A

Myasthenia Gravis and prophylaxis during the PGW

36
Q

ADRs of AChEIs

A

Indirect agonism of nAChRs and mAChRs

ANS+Somatic+CNS symptoms

Neorologia (12 decks)

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