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MD1 Neuroscience > Regulating Neuronal Excitability > Flashcards

Regulating Neuronal Excitability Flashcards

1
Q

What is an example of a neurotransmitter not stored in a vesicle?

A

NO

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2
Q

What kind of inputs do motor nerves receive?

A

Excitatory

Inhibitory

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3
Q

What happens in epilepsy?

A

Excessive discharge
Too little inhibition - get spasms
Too much excitation - excessive motor stimulatio

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4
Q

What are the two neurotransmitters relevant to epilepsy?

A

GABA

Glutamate

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5
Q

What is the best target for modulating inhibitory activity in epilepsy?

A

Enhance GABA receptor activity

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6
Q

How do benzodiazepines work?

A

Used to treat epilepsy
Enhance GABA receptor activity
Allosteric modulators
Increase GABA binding

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7
Q

How do you reduce excitatory input in epilepsy?

A 
Limit excitatory nerve activation
Inhibit T-type Ca channels
- Specific to some neurons
- More readily expressed on excitatory nerves
Inhibit NMDA receptor
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8
Q

Describe phenytoin

A

Used in treating epilepsy

Stops nerve action by inhibiting Na channels

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9
Q

Describe ethosuximide

A

Inhibits T-type Ca channels

Stops vesicle release

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10
Q

Describe felbemate

A

Inhibits NMDA receptor

Enhances GABA receptor

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11
Q

What else do many epileptic drugs cause?

A

Sedation; eg:
- Benzodiazepines
- Some others
Analgesia

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12
Q

What are some examples of analgesics?

A

NSAIDs
Anti-pyuretics
Opioids

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13
Q

What is an analgesic?

A

Targets pain/sensory pathways
Sets threshold to determine what degree of excitation is sent to brain
Increases pain threshold

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14
Q

What is a local anaesthetic?

A

Targets pain/sensory nerves as well as others in the region

No loss of consciousness

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15
Q

What is a general anaesthetic?

A

Depresses cortical processing of pain/sensory signal
Causes loss of consciousness
Not regionalised

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16
Q

Which drug category has the highest degree of selectivity?

a) Analgesics
b) Local anaesthetics
c) General anaesthetics

A

b) Local anaesthetics

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17
Q

What was the first local anaesthetic?

A

Cocaine

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18
Q

Describe local anaesthetic agents

A

Drugs that reversibly block conduction of nerve impulses at axonal membrane - influence action potential

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19
Q

What are the weak base local anaesthetics?

A 
Aminoesters
- Eg: procaine
- Shorter acting
- Hydrolysis by choliesterases
Aminoamides
- Eg: lignocaine, bupivicaine, ropivicaine
- Longer acting = 1-1.5 hrs
- Hepatic metabolism
Benzocaine
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20
Q

What are examples of lethal toxins that share a target with local anaesthetics?

A

Tetrodotoxin in puffer fish

Saxitoxin in dinoflagellates

21
Q

Describe the clinical use of local anaesthetics

A

Safe
- Very specific binding to Na channel
- Reversible binding with no nerve damage
- Will affect all nerves/excitable tissues because Na channel fundamental to all excitable tissues
Local application to limit systemic distribution - makes them safe

22
Q

What are the effects if local anaesthetics act on non-sensory nerves?

A 
Peripheral motor nerves
- Paralysis
Autonomic nerves
- Hypotension
- CNS convulsions
- Coma
Heart
- Anti-dysrhythmic
- Cardiac arrest
23
Q

What happens to the nerves with increasing concentrations of local anaesthetic?

A

More sensory block
More motor block because drug reaches these fibres
More autonomic block

24
Q

What is the relative sensitivity of nerve types to local anaesthetics?

A

Sensory > autonomic > motor

25
Q

What is the site of interaction of local anaesthetics?

A

Intracellular transmembrane domain on Na channel

26
Q

What is the difference in binding between local anaesthetics and toxins that share the same receptor target?

A

Local anaesthetics bind intracellularly and toxins bind extracellularly

27
Q

What are the two mechanisms of action of local anaesthetics?

A 
Hydrophobic
- Faster
- Non-use dependent
- Eg: benzocaine
Hydrophilic
- Slower
- Use dependent
Eg: aminoesters, aminoamides
- Mainly ionised at physiological pH
28
Q

What determines the rate of onset/offset of local anaesthetics?

A

Rate of diffusion across membrane

29
Q

Describe how hydrophobic local anaesthetics block the Na channel

A

Enter cell by diffusing across lipid membrane

Block gate like plug

30
Q

Describe how hydrophilic local anaesthetics block the Na channel

A

Non-ionised form diffuses across membrane into cell
Re-ionises
Blocks channel in ionised form

31
Q

What are the general properties of local anaesthetics?

A

Prevemt propagation of nerve action potential
Small fibres more sensitive
Stabilise axon membrane
- No change in resting membrane potential
Effect more pronounced in basic medium
- Allows more drug to cross membrane
Greater effect at high frequency

32
Q

What happens when local anaesthetics are used during an infection?

A

Infection creates more acidic environment

Decreases effect of drug, therefore need higher concentration to get same effect as normal

33
Q

What is the toxicity of local anaesthetics?

A

Generally safe
Toxicity proportional to blood level - if they enter bloodstream
Cardiovascular effects
- Direct myocardial depression
- Depression of vasomotor centre
- Hypotension - except cocaine > causes hypertension instead
Can cross BBB > CNS effects
- Inhibitory fibres more sensitive > excitation
- Tremor
- Convulsion
- Respiratory arrest

34
Q

Are hypersensitivity reactions proportional to blood level?

A

No

35
Q

Who can get hypersensitivity reactions to local anaesthetics?

A

Both patient and practitioner, as even handling drugs can cause development

36
Q

Describe the topical application of local anaesthetics

A

Over the counter
- Lozenge: throat drops containing benzocaine
- Gels: generally poorly absorbed across skin and over inflamed areas because even though fibres exposed, at low pH
- Contain very low concentrations of lignocaine
- Menthol doing most of the work
Professional use only
- Eye drops: ocular procedures, often including a dye
- Injection: specific procedural use; eg: IV lignocaine for dysrhythmia

37
Q

What are the types of ways local anaesthetics are used when injected?

A

Infiltration: combination with vasoconstrictor prolongs action
Nerve block: injection close to major nerves
Epidural and intrathecal

38
Q

What are the stages of anaesthesia?

A 
Stage 1
- Amnesia
- Euphoria
Stage 2
- Excitement
- Delirium
- Resistance to handling
Stage 3
- Unconsciousness
- Regular respiration
- Decreasing eye movement
Stage 4
- Medullary depression
- Respiratory arrest
- Cardiac depression and arrest
39
Q

How can general anesthetics be formulated?

A

Inhalation

IV

40
Q

What does formulation of general anaesthetics influence?

A

Slight differences in pharmacokinetics

41
Q

What are some inhaled general anaesthetics?

A

Desflurane
Sevoflurane
Isoflurane

42
Q

What are some IV general anaesthetics?

A

Propofol

Thiopentone

43
Q

What are the relevant pharmacokinetics for general anaesthetics?

A 
Dose and duration of action
Absorption - when inhaled
Distribution
- Vd
- t1/2
- Get into compartments other than brain
Metabolism
Elimination
- Kidneys
- Liver
- Lungs
Drug interactions
44
Q

What are the side effects of general anaesthetics?

A 
Happen at final endpoint depression = stage 4
Respiratory
- Impaired ventilation
- Depression of respiratory centre
- Obstruction of airways
- Retention of secretions
Cardiovascular
- Decreased vasomotor centre function
- Depress contractility
- Peripheral vasodilation
- Cardia arrythmias
- Inadequate response to fall in BP or CO
45
Q

What is given to counteract the retention of secretions that happens when a patient is given general anaesthetics?

A

Anti-muscarinics administered

46
Q

What are the two theories on mechanism of action of general anaesthetics?

A

Lipid theory

Receptor interaction

47
Q

What is the lipid theory in relation to mechanism of action of general anaesthetics?

A

Close correlation between anaesthetic potency and lipid solubility
Anaesthesia caused by volume expansion of membrane lipids
Effect can be reversed by pressure - pushed out of membranes

48
Q

What is the receptor interaction in relation to mechanism of action of general anaesthetics?

A

Many anaesthetic agents inhibit excitatory receptors
- Glutamate
- NMDA
Many anaesthetic agents enhance effects on inhibitory receptors
- GABA
- Glycine

49
Q

What is an NMDA receptor agonist?

A

Ketamine

MD1 Neuroscience (55 decks)

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