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JMP Semester 1 > Week 4 "Ageing and Control" > Flashcards

Week 4 "Ageing and Control" Flashcards

1
Q

What is the soma?

A

The cell body of a neuron

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2
Q

What are dendrites and where are they located?

A

Connecting to the soma (cell body) at the presynaptic end of a neuron.

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3
Q

What is the role of the axon?

A

where a (depolarisation) signal it transferred from the cell body to the synaptic terminal.

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4
Q

What is the purpose of myelin sheaths on the axon?

A

Myelin increases the speed of depolarisation signal along the axon as does not need to wait for membrane depolarisation under myelinated areas.

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5
Q

What is the three key parts of the synaptic terminal?

A

Presynaptic axon terminal-where neurotransmitters are released
Synaptic cleft- gap
Postsynaptic dendrite- neurotransmitters bind.

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6
Q

What is the resting potential of the average nerve cell?

A

-70mV

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7
Q

What drives this resting membrane potential?

A

Efflux of K+ would set the cell at -90mV but an influx of Na+ into the cell makes the cell more positive at -70mV.

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8
Q

What keeps the balance between K+ and Na+ in a resting state nerve cell?

A

The balance of these ions is regulated by the K+/Na+ pump.

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9
Q

How is an Action potential generated in a nerve cell.

A
  1. Excitatory stimulus opens ligand gated Na+ channels (causing Na+ influx)
    1. Membrane will depolarise till hitting “threshold” approximately -55mV
    2. At threshold voltage gated Na+ channels open (causing huge depolarisation with an overshoot)
    3. Voltage gated Na+ channels are inactivated at higher potential (closed) and voltage gated K+ channels open (efflux of K+)
      Cell repolarises to -70mV
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10
Q

Specifically what order are ion channels utilised in an Action potential?

A
  1. Ligand gated Na+ channels (influx) (move potential to threshold)
  2. Voltage gated Na+ channels (influx) (responsible for large depolarisation with overshoot)
  3. Voltage gated K+ channels (efflux) repolarises cell while Voltage gated Na+ channels are inactivated after depolarisation.
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11
Q

How can an action potential be described.

A
  1. All or nothing response

2. Has a refractory period.

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12
Q

What is a neurotransmitter?

A

A chemical substance which is released at the end of a nerve fibre by the arrival of a nerve impulse.

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13
Q

Broadly what kind of effect can a neurotransmitter have on post synaptic dendrites?

A

Excitatory or Inhibitory

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14
Q

Describe what drives the release of neurotransmitters into the synaptic cleft.

A
  1. Action potential arrives at synapse.
  2. Voltage gated Ca+ channels open (Ca+ influx)
  3. internal Ca+ concentration drives vesicles containing neurotransmitter to fuse with membrane and be released into the synaptic cleft.
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15
Q

Where can released neurotransmitters bind?

A

They can bind to post synaptic receptors (mainly) but also bind to presynaptic receptors to affect the cell currently releasing neurotransmitters. (negative feedback)

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16
Q

What is another name for receptor coupling to an ion channel?

A

Ligand-gated ion channels.

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17
Q

What is the benefits of Ligand-gated ion channels?

A
  1. They are highly selective as to what can bind and activate the channel.
  2. They are very fast acting (something needed in nerve cells)
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18
Q

What is an example of a inhibitory neurotransmitter action?

A

Gaba neurotransmitters:
Will bind to ligand-gated (K+ or Cl-) channels to cause a hyperpolarisation in the post synaptic dendrite. cell has harder time hitting AP threshold

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19
Q

What is an example of an excitatory neurotransmitter action?

A

Glutamate neurotransmitters:

Activate ligand-gated Na+ channels (Na+ influx). will cause deoplarisation of the synaptic dendrite.

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20
Q

What determines the magnitude of neurotransmitter effect?

A
  1. Amount of neurotransmitter in the synaptic terminal (how much is stored in vesicles)
    1. Amount of neurotransmitter released
    2. Period of availability in the synaptic cleft (determined by reuptake/degradation)
    3. Number of receptors (presynaptic and postsynaptic)
      Sensitivity of receptors
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21
Q

Parts of the Central Nervous System

A

Brain and spinal cord

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22
Q

Parts of the Peripheral nervous system

A

Consists of all the nerves and ganglia outside the brain and spinal cord.

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23
Q

What are the subclasses of the peripheral nervous system

A

Somatic Nervous system

Autonomic Nervous system:

  1. sympathetic
  2. parasympathetic
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24
Q

What is the general role of the brain stem?

A

respiration, HR, BP

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25
Q

What is the general role of the spinal cord

A

transmission of nerve signals from and to the brain.

26
Q

What is the general role of the cerebellum?

A

balance

27
Q

What are the 4 major divisions of the cerebrum and their function?

A
  1. Occipital lobe- visual input processing
  2. Temporal lobes-auditory processing
  3. Parietal lobe- sensation and feeling
  4. Frontal lobe- complex tasks-movement etc
28
Q

What is the general role of the basal ganglia

A

motor activity

29
Q

What is the role of the somatic nervous system

A

All voluntary muscular control

30
Q

What are the two major pathwyas used by the somatic nervous system

A
  1. Somatomotor (efferent)- from brain to muscle

2. Somatosensory (afferent)- from sensory receptor to brain

31
Q

What are the major functions of the autonomic nervous system?

A
  1. gut movement
  2. heart contractions
  3. visceral sensations
32
Q

What is the best way to summarise the sympathetic system?

A

fight or flight

33
Q

What is the best way to summarise the parasympathetic system?

A

rest and digest

34
Q

What is the main mechanism which the nervous system uses to maintain homeostasis?

A

Negative feedback loops.

35
Q

What is the difference between pharmacology and clinical pharmacology?

A

Pharmacology is the fundamental science behind chemical action within biological system (cells tissue etc) whereas clinical pharmacology is focused on pharmacology and its effects on patients.

36
Q

What is pharmacodynamics?

A

Mechanism of action

37
Q

What is pharmacokinetics?

A

what happens to a drug when inside the body. metabolism and excretion ect

38
Q

What is pharmacogenomics?

A

effects on genetics and response to drugs

39
Q

What is the difference between a drug and a medicine?

A

A drug is a chemical that causes change in a biological system

A medicine is a drug that is used to treat or prevent disease within the body.

40
Q

What are the different names a drug may have?

A
  1. chemical
  2. generic
  3. trade
41
Q

What are the four phases of pharmacokinetics within the body?

A

(ADME)
Absorption- drug entering the blood stream
Distribution- movement of drug around the body
Metabolism- alterations of drug in the body (usually by liver)
Excretion- disposal of drugs out of the body (usually by the kidneys)

42
Q

What is parenteral form of drug admission?

A

Injections.

43
Q

What is the speed of Intermuscular, intravenous and subcutaneous injections absorption

A

V-fast
M-medium
S-slow

44
Q

What is bioavailability?

A

The proportion of a drug that enters the circulation system of the body where it can have an active affect.

45
Q

What is Clearance vs Half life for a drug.

A

Clearance is the rate at which a drug is removed from the circulatory system (measured in litres/hour)
Half life is the time taken for a drugs concentration to be half of its original value.

46
Q

What does it mean by a drugs in a steady state?

A

Steady state is the concentration of a drug remains within the therapeutic range between doses of a drug. (steady within a range)

47
Q

Describe the drug action in terms of speed and effect.

ligand gated channels

A

Ligand activated- very fast(milliseconds), eg nicotinic or Ach receptors.

48
Q

Describe the drug action in terms of speed and effect.

G-protein coupled receptors

A

secondary messenger generation- fast (seconds) eg muscarinic or Ach receptors

49
Q

Describe the drug action in terms of speed and effect.

Kinase linked receptors

A

Kinases phosphorylates proteins, can cause protein synthesis effect very slow (takes hours) eg insulin

50
Q

Describe the drug action in terms of speed and effect.

Nuclear receptors

A

Causes direct change in gene transcription and protein synthesis very slow (takes hours), eg steroids as they can access the nucleus eg oestrogen.

51
Q

What is an agonist?

A

A drug that binds to a receptor and activates it.

52
Q

What is an antagonist?

A

Binds to a receptor and activates it but does not produce the full effect of an agonist.

53
Q

what is a Partial agonist?

A

A drug that competitively binds to a receptor but does not cause activation -instead prevents activation.

54
Q

What is the general mechanism of a benzodiazepine?

A

Drug that binds to a Cl- channel to boost the effect of binding neurotransmitters. In this case the result is an increased suppression of neuron activity

55
Q

What is the relationship between drug dose and response.

A

More drug = higher response

Until a plateau is reached.

56
Q

What is Emax and EC50?

A

Emax = Dose in which greatest response is reached (plateau)

EC50 = Dose in which 50% response is reached

57
Q

What effect would an antagonist have on the dose-response curve of an agonist?

A

The antagonist would shit the dose-response curve to the right (higher dosing required)

While it shifts to the right there is no impact on the curve itself.

58
Q

What is the importance of receptor selectivity on the use of a drug.

A

The more specific the better. But offtarget effects are potentially dangerous and need to be monitored

59
Q

Define drug Affinity

A

how well a drug will bind to a receptor

60
Q

Define drug Efficiency

A

how well a drug will act when bound to a receptor

61
Q

Define drug Potency

A

how much drug is needed to initiate a response

JMP Semester 1 (12 decks)

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