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MSK Final Exam > Intro To Pharm > Flashcards

Intro To Pharm Flashcards

1
Q

What is the somatic NS?

A

Includes control of skeletal muscle

Voluntary

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2
Q

What are the steps in the NMJ neurotransmission?

A
  1. Axonal conductional
  2. Junctional transmission (cholinergic neurotransmission)
  3. ACh signaling
  4. Muscle contraction
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3
Q

What events occur during junctional transmission?

A

ACh synthesis, storage, release and destruction

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4
Q

Which enzymes are used in ACh synthesis?

A

Choline transporter and choline acetyltransferase (ChAT)

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5
Q

What is the choline transporter?

A

Membrane channel that transports choline into the cell for synthesis

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6
Q

What is choline acetyltransferase (ChAT)?

A

Enzyme that combines acetyl CoA and choline to form ACh

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7
Q

Patients with Alzheimer’s disease have a reduced cerebral production of what?

A

ChAT

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8
Q

Which receptor is involved in ACh storage?

A

ACh vesicular transporter

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9
Q

What is the ACh vesicular transporter?

A

ATP dependent transporter that immediately shuttles ACh into storage vesicles after ACh synthesis

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10
Q

What structures are involved with ACh release?

A

Voltage gated Ca channels, VAMP and SNAPs

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11
Q

What is the role of voltage gated Ca channels during ACh release?

A

Open upon depolarization and allow Ca to enter the cell which then promotes vesicle membrane fusion

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12
Q

What role do VAMPs and SNAPs play during ACh release?

A

Vesicular and plasma membrane proteins that initiate vesicle plasma membrane fusion and release of ACh

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13
Q

How many vesicles rupture per AP?

A

125

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14
Q

Which enzyme is involved in ACh destruction?

A

AChE

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15
Q

What is the role of acetylcholinesterase?

A

Enzyme that cleaves ACh into choline and acetate

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16
Q

Describe what occurs during ACh destruction

A

AChE cleaves ACh into choline and acetate
Choline is recycled back into the motor neuron via the choline transporter
Endocytosis occurs at the nerve terminal to replenish the number of available vesicles

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17
Q

During ACh signaling, ACh activates two subsets of receptors known as what?

A

Nicotinic and muscarinic receptors

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18
Q

Describe nAChRs

A

Activated by ACh and nicotine
Ligand gated ion channel (Na)
Pre and post-junctional
NMJ: Na increase causes muscle AP

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19
Q

Describe mAChRs

A

Activated by ACh and muscarine
GPCR
Pre and post junctional
NOT located at skeletal NMJ

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20
Q

Almost all the steps of junctional transmission can be inhibited by what?

A

Pharmacological agents (drugs) but not all drugs are used clinically

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21
Q

What is the location and function of nAChR?

A

Skeletal muscle

Contraction

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22
Q

What is the location and function of mAChR?

A

Smooth muscle and contraction

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23
Q

What two examples of agonists for nAChR?

A

Acetylcholine and nicotine

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24
Q

Activation of mAChR leads to what?

A

A series of Intracellular events triggered by second messengers (metabotropic)
Effects measured in seconds

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25
Q

NAChRs are ligand gated ion channels that allow what?

A

Ions to pas through the channel pore when activated (ionotropic)
Fastest synaptic events in the NS (milliseconds)

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26
Q

Describe LGIC selectivity of ions

A

Ions are selected based on the charge of the amino acids lining the pore of the channel
Negatively charged amino acids line the pore of channels that pass positively charged ions and vice versa

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27
Q

Describe the structure of nAChRs

A

Aspartic acid and glutamic acid line the pore of the channel (negative charge)
Channel itself is selective to Na+, Ca2+ and K+

28
Q

What are the three subtypes of nAChRs?

A

Skeletal muscle, peripheral neuronal and central neuronal

29
Q

Where are skeletal muscle nAChRs found?

A

Skeletal NMJ (post junctional)

30
Q

What is the membrane and molecular response of skeletal nAChRs?

A

Membrane response: excitatory and contraction

Molecular: increased cation permeability (Na, K)

31
Q

What are agonists for skeletal muscle nAChRs?

A

Ach, nicotine and succinylcholine

32
Q

What are examples of antagonists for skeletal muscle nAChRs?

A

D-tubocurarine, atracurium, vecuronium and pancuronium

33
Q

List the steps of the events at the NMJ

A
  1. An AP in the motor neuron is propagated to the terminal button
  2. Presence of an AP triggers the opening of voltage gated Ca channels
  3. Ca triggers release of ACh from vesicles
  4. ACh diffuses across the synaptic cleft and activates nAChRs
  5. nAChRs open leading to a relatively large influx of Na compared to a smaller efflux of K
  6. Local current flows b/w depolarized end plate ad adjacent membrane
  7. Local flow opens voltage gated Na channels
  8. Influx of Na initiates AP which propagates throughout the muscle fiber
  9. ACh is destroyed by AChE terminating the muscle cell’s response
34
Q

Which agents affect the nerve AP?

A

Tetrodotoxin and local anesthetics

35
Q

What is tetrodotoxin?

A

Puffer fish poison (fugu, globefish, blow fish)

Not used clinically

36
Q

What is the MOA of tetrodotoxin?

A

Inhibition of voltage gated Na channels blocks axonal conduction

37
Q

What are the sx of someone affected by tetrodotoxin?

A

Weakness, dizziness, paresthesias of the face and extremities, loss of reflexes, hypotension, generalized paralysis and death can occur due to respiratory failure and hypotension

38
Q

What is the MOA for local anesthetics?

A

Inhibition of voltage gated Na channels and inhibiting axonal conduction

39
Q

What are local anesthetics utilized for?

A

Pain control during a variety of clinical procedures

Ex. Lidocaine, bupivacaine and procaine

40
Q

What agents affect vesicular ACh release?

A

Botulinum toxin and tetanus toxin

41
Q

What is botulism caused by?

A

Clostridium botulinum which is a heterogenous group of gram+ rod shaped, spore forming, obligate anaerobic bacteria that are found in vegetables, fruit and seafood
Also exists in soil and marine sediment worldwide

42
Q

What is the MOA for botulinum toxin?

A

Cleaves components of the core SNARE complex involved in exocytosis, preventing the release of ACh

43
Q

Botulism is classically described as the acute onset of what?

A

Bilateral cranial neuropathies associated with symmetric descending weakness
No sensory deficits with the exception of blurred vision

44
Q

What are symptoms of foodborne botulism?

A

Nausea, vomiting, abdominal pain, diarrhea and dry mouth

45
Q

What are some clinical uses for botulinum toxin?

A

Temporary improvement in the appearance of lines/wrinkles of the face and prophylaxis of chronic migraine HA

46
Q

What is tetanus?

A

A nervous system disorder characterized by muscle spasms that is caused by the toxin producing anaerobe clostridium tetani which is found in the soil

47
Q

What is the MOA for tetanus toxin?

A

Block fusion of synaptic vesicles by targeting synaptobrevin
After binding to the presynaptic membrane of the NMJ tetanus toxin is internalized and transported retraxonally to the spinal cord

48
Q

What is spastic paralysis caused by during tetanus?

A

The toxin’s actions on the spinal inhibitory interneurons blocking release of inhibitory neurotransmitters that normally serve to relax contracted muscle by inhibiting excitatory motor neurons

49
Q

Generalized tetanus typically presents as what?

A

Spastic paralysis with sx that include trismus (lockjaw), autonomic overactivity (restlessness, sweating tachycardia), stiff neck, board like rigid abdomen, opisthotonus and dysphagia

50
Q

Which agents affect depolarization?

A

Neuromuscular blocking drugs, curare alkaloids and succinylcholine

51
Q

Both agonists and antagonists of the nAChR can prevent what?

A

Synaptic transmission

52
Q

What is the action of agonists of nAChR?

A

Agonists activate the receptor to signal as a direct result of binding to it

53
Q

What is the action of antagonists of the nAChR?

A

Bind to receptors but do not activate generation of a signal

54
Q

What is the prototype curare alkaloid?

A

D-tubocurarine

55
Q

What is the MOA for curare alkaloids?

A

Competes with ACh for the nAChR on the motor end plate decreasing the size of the EPP (non-depolarizing competitive nAChR antagonist)
Inhibition of ACh binding to the nAChR leads to flaccid paralysis of skeletal muscle

56
Q

What are curare alkaloids used for?

A

During anesthesia to relax skeletal muscle

57
Q

What is paralysis caused by curare alkaloids reversed by?

A

Increasing ACh in the NMJ (AChE inhibitor)

58
Q

What is the MOA of succinylcholine?

A

Depolarizing neuromuscular blocker that binds to skeletal muscle nAChRs and initially causes depolarization (acts as an agonist; muscle fasciculations)
Continued depolarization leads to receptor blockade and paralysis

59
Q

What is succinylcholine used for?

A

As an induction agent for anesthesia

60
Q

How is paralysis caused by succinylcholine reversed?

A

By termination of succinylcholine’s effects (through time)

61
Q

Which agents block AChE?

A

Cholinesterase inhibitors

62
Q

What is the action of cholinesterase inhibitors?

A

Bind to AChE and block its enzymatic activity

Increase the concentration of ACh at the NMJ

63
Q

What are some clinical uses of cholinesterase inhibitors?

A

Treatment of dementia associated with Alzheimer’s or Parkinson’s disease, myasthenia gravis, nerve gas and organophosphate pesticide exposure, reversal of neuromuscular blockade during anesthesia

64
Q

Which agents affect muscle contraction?

A

Dantrolene

65
Q

What is the action of dantrolene?

A

Inhibits ryanodine receptors in the SR and blocks release of Ca

66
Q

What are the clinical uses of dantrolene?

A

Used to treat Malignant hyperthermia and spasticity associated with upper motor neuron disorders

MSK Final Exam (26 decks)

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