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MSK Final > Pharmacology > Flashcards

Pharmacology Flashcards

Pharm (92 cards)

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1
Q

Agents that affect the Nerve action potential

A

Tetrodotoxin and Local Anesthetics

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2
Q

Agents that affect vesicular acetylcholine release

A

Botulinum toxin and Tetanus toxin

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3
Q

Agents that affect depolarization

A

Nueromuscular blocking drugs: Curare alkaloids and Succinylcholine

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4
Q

Agents that inhibit acetylcholinesterase

A

Acetylcholinesterase inhibitors

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5
Q

Agents that affect the nerve action potential

A

Tetrodotoxin

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6
Q

Agents that affect muscle contraction

A

Dantrolene

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7
Q

What is the primary neurotransmitter of the somatic nervous system?

A

Acetylcholine (ACh)

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8
Q

What are nAChRs?

A

Nicotinic acetylcholine receptors

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9
Q

Where are nAChRs found?

A

Membranes of POST-synaptic muscle cells, but can be found prejunctional

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10
Q

What is the motor end plate (NMJ)?

A

The site of innervation on the muscle cell surface - AKA Myoneural junction

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11
Q

The sodium potassium pump pumps what where and how many of each?

A

3 Na+ ions are pumped out for every 2 K+ ions pumped into the cell

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12
Q

Na+ and Cl- ions are present in higher concentrations inside or outside the cell?

A

Na+ and Cl- ions are present in higher concentrations outside the cell.

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13
Q

List the three stages of an action potential

A

Resting stage, Depolarization stage and Repolarization stage

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14
Q

During the Resting Stage of an AP, what is the polaization of a cell membrane?

A

The membrane is considered “polarized” at around -70 to -80 mV

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15
Q

What does the depolarization stage do to the membrane potential?

A

The membrane becomes less negative, and swings toward a zero value and can become a positive value in large nerve and muscle fibers.

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16
Q

During depolarization, the cell membrane becomes permeable to what ion?

A

Sodium (Na+) - rapidly - (Na+ ions defuse into cell)

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17
Q

During repolarization stage, which channels close and which channels open?

A

Na+ channels close (Na+ stops entering the cell)K+ channels open and K+ rapidly diffuses down its concentration gradient into the extracellular space.

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18
Q

What is axonal conduction?

A

Passage of an impulse (AP) along an axon or muscle fiber

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19
Q

What initiates an AP?

A

Depolarization above the threshold level

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20
Q

What is junctional transmission?

A

The passage of an AP across a synaptic junction

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21
Q

Outline the series of events following the arrival of an action potential at a muscle nerve

A

1: release of ACh from axon2: Diffusion of ACh across the synaptic cleft3: Activation of th skeletal muscle nAChRs4: Induction of an action potential in the muscle and subsequent contraction5: Destruction of ACh

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22
Q

What is choline acetyltransferase (ChAT)?

A

An enzyme that combines the acetyle moiety of acetyl coenzyme A with choline in the cytoplasm of the neuron (the final step in synthesis of ACh)

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23
Q

What is the first step in ACh synthesis?

A

A high affinity choline trasporter transport choline from the plasma into the neurons

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24
Q

The choline transport system is dependent on what extracellular molecules?

A

Na+ and choline

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25
Where is ACh sequestered upon synthesis?
Synaptic vesicles
26
Where is Acetyl CoA synthesized?
mitochondria
27
Is inhibiting ChAT via pharmaceutcal agents worthwhile?
No, because the uptake of choline is the rate-limiting step in ACh synthesis.
28
Where is ACh stored?
ACh is stored in synaptic vesicle located at the nerve terminals by the ACh vesicular transporter
29
When an AP reaches the axonal terminal, depolarization causes voltage gated channels of what ion to open?
Ca2+ (flows into the neuron)
30
What do elevated Ca2+ levels promote?
Elevated Ca2+ levels promote fusion of the vesicular membrane with the cell membrane and exocytosis of ACh into the synaptic cleft
31
What superfamily of proteins mediate fusion between vesicle and presynaptic membranes?
SNARE proteins (vesicle SNARES and target SNARES)
32
Synaptobrevin (VAMP), syntaxin and SNAP-25 do what?
These SNARE proteins for the core SNARE complex that brings the vesicle and presynaptic membranes into close contact.
33
What is synaptotagmin and what does it trigger?
Synaptotagmin is a calcium sensor protein located on the ACh vesicle membrane which triggers vesicle fusion and exocytosis.
34
What ion must be present for Synaptotagmin to trigger ACh vesicle fusion and exocytosis?
Calcium 2+
35
After release of ACh into the synaptic cleft, what two proteins bind to the SNARE complex?
alpha-SNARE and the ATPase NSF
36
What do alpha-SNARE and ATPase NSF do?
They bind to the SNARE complex and disassemble the SNARES and recycle the ACh vesicle.
37
When ACh binds to its receptor nAChRs on the skeletal muscle fibers, what receptor channls open?
Binding of ACh to nAChRs on skeletal muscle causes the receptor channel to open and allow Na+ to enter the muscle. K+ exits the muscle.
38
Influx of Na+ inside a muscle fiber membrane causes what?
A local depolarization (swing towards positive) which initiates a propagated muscle action potential in the muscle fiber.
39
Why must ACh be immediately removed from the neuromuscular junction?
To prevent lateral diffusion and sequential activation of adjacent receptors.
40
What is acetylcholinesterase (AChE)?
An enzyme that cleaves ACh into acetate and choline, thus eliminating ACh from the synapse.
41
Following ACh cleaving, where does acetate and choline go?
Acetate diffuses out of the cleft. Most choline is recycled into the nerve terminal through the choline transporter.
42
What is clathrin?
A contractile protein that coats the pits and is involved in endocytosis. Involved in ACh vesicle reformation following an AP.
43
What are muscarinic acetylcholine receptors (mAChRs)
G-protein coupled receptor alternative for ACh. Is also activated by muscarine.
44
What are nicotinic acetylcholine receptors?
Ligand-gated ion channel receptor for ACh. Is also activated by nicotine
45
Where are nAChRs found?
Generally, skeletal muscle
46
Where are mAChRs found?
Both smooth and cardiac muscle
47
What is an ionotropic receptor?
Receptors that when activated allow ions to pass through the ion channel pore
48
What is a metabotropic receptor?
Receptors that lead to a series of intracellular events triggered by second messengers. They do not have a channel pore.
49
nAChRs is a metabotropic or an ionotropic receptor?
nAChRs is an ionotropic receptor (allows Na+ to pass through the ion channel pore)
50
mAChR is a metabotropic or an ionotropic receptor?
mAChR is a metabotropic receptor
51
nAChRs can be found on which side of a junction?
Both prejunctional and postjunctional sites
52
List the three types of nAChRs receptors
Skeletal muscle, Peripheral neuronal, Central neuronal
53
Skeletal muscle nAChRs are located where and have what type of membrane response?
Skeletal neuromuscular junction (postjunctional) and they are both excitatory and promote muscle contraction
54
Peripheral neuronal nAChRs are located where and have what type of membrane response?
Autonomic ganglia; adrenal medulla and they are both excitatory and depolarizing
55
Central neuronal nAChRs are located where and have what type of membrane response?
CNS and excitatory/prejunctional control of ACh release
56
Describe the skeletal arrangment of nAChR pore receptor structure
nAChR structure is a pentamer composed of four distinct subunits and is the prototype for all pentameric ligand - gated ion channels (GABA, glycine receptors)
57
How many subunits surround the central pore?
5 subunits are arranged around the central pore
58
Name the four distinct subunits of nAChR and how many of each there are
alpha, beta, delta, epsilon::2, 1, 1, 1
59
Where are the ACh-binding sites on nAChR?
The interface of two of the five subunits (between one alpha subunit and an adjacent subunit)
60
How many molecules of ACh are required to open a nAChR?
Two ACh's
61
When closed, ACh is bound or unbound to nAChr?
When ACh is not bound to nAChR, the pore is closed and no ions can pass through it
62
What happens when ACh binds to nAChR?
A rapid conformational change occurs in the receptor, allowing it to open.
63
What ions are permitted to pass through the nAChR?
Positive ions (mostly Na+, but also K+ and Ca2+). All ions pass down concentration gradient
64
What cannot pass through nAChR and why?
Negatively charged ions are unable to pass through the pore due to strong negative charges placed at the mouth of the nAChR channel.
65
What is the result of an influx of positive ions through the nAChR channel?
The creation of a localized positively charged potential change inside the muscle fiber membrane due to influx of Na+ ions (mostly). This ultimately generates an action potential along the muscle membrane.
66
What is the method of action of tetrodotoxin?
Selectively blocks axonal conduction by blocking voltage gated Na+ channels.
67
What fish is tetrodotoxin found in?
Puffer fish/blow fish
68
List symptoms of tetrodotoxin pufferfish poisoning
Weakness, dizziness, paresthesias of the face and extremities, nausea and loss of reflexes. High doses can cause paralysis with consciousness. Death due to respiratory failure and hypotension
69
What is MOA of local anesthetics?
Block neuronal conduction by inhibiting voltage-gated Na+ channels.
70
List three examples of local anesthetics
Lidocaine, bupivacaine, procaine
71
What is MOA of hemicholinium?
Inhibits choline trasporter, blocks reuptake of choline into presynaptic terminal and depletes ACh stores
72
Botulism is a rare but life threatening neuroparalytic syndrome resulting from the action of a neurotoxin from what bacterium?
Clostridium botulinum
73
C botulinum is gram positive or negative?
Gram positive
74
Where is C botulinum found?
Veggies, fruits, seafood, soil...ubiquitous
75
What is the MOA for botulinum?
Cleaves components of the core SNARE complex involved in exocytosis of ACh, thereby prohibiting ACh release.
76
Uses of botulinum clinically:
Treatment of strabismus and blepharospasm associated with dystonia, temporary improvement in the appearance of lines/wrinkles of the face, prophylaxis of chronic migraine headache
77
Tetanus is caused by what anaerobe
Clostridium tetani
78
MOA of tetanus toxin
block fusion of synaptic vesicles by targeting synaptobrevin (SNARE complex)Can be internalized via the presynaptic membrane and trasported to the spinal cord, causing spastic paralysis on the spinal inhibitory interneurons. Blocks inhibitory neurotransmitters that serve to relax contracted muscle
79
Symptoms of tetanus toxin
Spastic paralysis with trismus (lockjaw), restlessness, sweating, tachycardia, stiff neck, rigid abdomen
80
Agonists activate...
The receptor to signal as a direct result of binding it
81
Antagonists bind...
receptors but do not activate generation of a signal
82
Curare alkaloids MOA
competes with ACh for the nAChR on the motor end plate, decreases the size of the EPP
83
Inhibition of ACh binding to nAChR due to curare alkaloids leads to
flaccid paralysis of skeletal muscleUsed during anesthesia to relax skeletal muscleParalysis can be reversed with the use of an acetylcholine esterase inhibitor
84
Succinylcholine MOA
depolarizes neuromuscular blocker that binds to skeletal muscle nAChRs and initially causes depolarization (agonist); continued depolarization leads to receptor blockade and paralysis
85
Succinylcholine is used as an induction agent for...
anesthesia
86
Succinylcholine causes muscle twitch due to...
agonist activity
87
Succinylcholine's paralysis effects are reversed
by time and termination of its effects...
88
Acetylcholinesterase MOA
inhibits acetylcholinesterase and the hydrolysis of ACh, thereby increasing ACh concentration in the synaptic cleft. Results in increased activation of AChRs
89
Uses of acetylcholinesterase inhibitors
Treatment of dementia associated with Alzheimer or Parkinson disease, myasthenia gravis, urinary retention
90
Dantrolene MOA
inhibits ryanodine receptors in the sarcoplasmic reticulum and blocks the release of Ca2+
91
Dantrolene is used to treat:
malignant hyperthermia and spasticity associated with upper motor neuron disorders (spinal cord injury, stroke, cerebral palsy MS)
92
Metabolic poisons
Anything that prevents the synthesis and formation of ATP will ultimately impair muscle contraction

MSK Final (7 decks)

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