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Principles > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is the process by which a drug enters the body from its site of administration?

A

absorption

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2
Q

what is the process by which a drug leaves the circulation and enters tissues perfused by blood?

A

distribution

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3
Q

what is the process by which tissue enzymes (principally in the liver) catalyze the chemical conversion of a drug to a more polar form that is more readily excreted from the body?

A

metabolism

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4
Q

what is the process that removes the drug from the body (principally the kidneys)?

A

excretion

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5
Q

metabolism + excretion =

A

elimination

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6
Q

what are the 4 physicochemical factors that control drug absorption?

A
  1. solubility
  2. chemical stability (ie will it be destroyed by stomach acid or enzymes?)
  3. lipid to water partition coefficient
  4. degree of ionisation
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7
Q

what does the lipid to water partition coefficient mean?

A

the relative solubility of the drug in lipid compared to water.
as the partition coefficiant increases (ie the lipid solubility increases), the rate of diffusion across a membrane will increase

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8
Q

why does the degree of ionisation affect the drug absorption?

A

because most drugs exist in equilibrium between ionised and unionised forms, but only unionised forms readily diffuse across the lipid bilayer

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9
Q

what is pKa?

A

the pH at which 50% of drug is ionised and 50% unionised

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10
Q

What is the henderson-hasselbalch equation to work out the ionisation ratio for a base?

A

pH - pKa = log(B/BH+)

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11
Q

What is the henderson-hasselbalch equation to work out the ionisation ratio for an acid?

A

pH - pKA = log(A-/AH)

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12
Q

in an acid environment, what happens to the ionisation ratio of an acidic drug?

A

less ionised

and so more readily absorbed

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13
Q

in an acid environment, what happens to the ionisation ratio of a basic drug?

A

more ionised

and so less readily absorbed

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14
Q

in a basic environment, what happens to the ionisation of an acidic drug?

A

more ionised

and so less readily absorbed

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15
Q

in a basic environment, what happens to the ionisation of a basic drug?

A

less ionised

and so more easily absorbes

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16
Q

ionisation ratio depends on what 2 factors?

A

pKa of the drugs

pH of the loval environment

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17
Q

compare absorption of strong and weak acids/bases.

A

weak acids and weak bases are well absorbed

strong acids and strong bases are poorly absorbed

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18
Q

what are the 5 factors for drug absorption in the gut?

A
  1. gastrointersinal motility
  2. pH at absorptive site
  3. blood flow to the stomach and intestines
  4. the way in which the drug is manufactured ie is it slow release
  5. physiochemical interations (eg the rate of absorption might be affected by some foods)
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19
Q

what is oral availability?

A

the fraction of drug that reaches systemic circulation after oral ingestion

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20
Q

what is systemic availability?

A

the fraction of drug that reaches the systemic circulation after absorption

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21
Q

what route of administration provides 100% systemic availability?

A

IV

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22
Q

what are the 8 routes of drug administration?

A
  1. inhalation (INH)
  2. oral (PO)
  3. Sublingual (SL)
  4. Subcutaneous (subcut)
  5. Intravenous (IV)
  6. Rectal (PR)
  7. Intramuscular (IM)
  8. topical (top.)
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23
Q

what are 3 the advantages of the oral route of administration?

A

convenient
non-sterile
good absorption generally

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24
Q

what are the 4 disadvantages of the oral route of administration?

A

inactivation of some drugs by acid/enzymes
variable absorption
first pass metabolism
GI irritation

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25
Q

what are the 2 advantages of the sublingual and rectal route of administration?

A

by-passes portal system and so avoids first pass metabolism

avoids gastric acid

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26
Q

what is the main disadvantage of the sublingual route of administration?

A

few preparations are actually available

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27
Q

what are the 2 disadvantages of the rectal route of administration?

A

variable absorption

aesthetically unacceptable in UK

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28
Q

what are 4 advantages of the IV route of administration?

A

rapid onset
continuous infusion
complete systemic availablity
can be used for drugs that cause local tissue damage

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29
Q

what are the 3 disadvantages of the IV route of administration?

A

sterile preparation required
risk of sepsis or embolism
high drug levels at the heart

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30
Q

what are the 2 advantages for intramuscular and subcutaneous routes of administration?

A

rapid onset of lipid soluble drugs

slow prolonged release possible

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31
Q

what are the 3 disadvantages of intramuscular and subcutaneous routes of administration?

A

painful
tissue damage with some drugs
absorption variable

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32
Q

What are the 3 advantages of the inhalational route of administration?

A

lungs have high surface area
good for volatile agents (such as anaesthetic gases)
ideal fo local effect

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33
Q

what is the main advantage of the topical route of administration?

A

ideal for local effect

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34
Q

what type of drug (free or bound) is allowed to move between body fluid compartments)?

A

free drug

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35
Q

what is the volume of distribution? (Vd)

A

the apparent volume in which a drug is dissolved in

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36
Q

for a drug administered intravenously what is Vd?

A

dose/ plasma concentration

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37
Q

what does a Vd >15L imply?

A

distribution throughout total body of water OR concentrated in certain tissues
reason: highly lipid soluble drug

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38
Q

what does pharmacodynamics mean?

A

what a drug does to the body

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39
Q

what does pharmacokinetics mean?

A

what the body does to a drug

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40
Q

what is an agonist?

A

a drug that binds to a receptor to produce a cellular response

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41
Q

what is an antagonist?

A

a drug that blocks that actions of an agonist

inhibits receptor

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42
Q

what is affinity?

A

the strength of association between ligand and receptor

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43
Q

as affinity increases, what happens to dissociation rate?

A

decreases

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44
Q

what is efficacy?

A

the ability of an agonist to evoke a cellular response

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45
Q

as the efficacy increases, what happens to the response rate?

A

response rate increases

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46
Q

compare antagonists and agonists in terms of affinity and efficacy.

A

agonists have affinity and efficacy

antagonists have affinity but lack efficacy

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47
Q

what type of relationship exists between the agonist concentration and the response?

A

hyperbolic relationship
as the concentration of agonist increases, the percentage of receptors occupied increases (and therefore response increases) until it levels our and all receptors are occupied

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48
Q

what is EC(50)?

A

effective concentration at 50%

the concentration of agonist that elicits a half maximal response

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49
Q

what type of graph expands the lower range of the x axis and so gives a more acurate reading?

A

logarithmic graph

relationship becomes sigmoidal

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50
Q

what does equipotent mean?

A

the drugs have the same EC(50)
ie the drugs have the same concentration for which they elicit half a maximal response (it doesnt matter if one has a better percentage response than the other- efficacy)

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51
Q

what is competitive antagonism?

A

binding of agonist and antagonist occur at the same orthosteric site, so they are in competition with each otehr

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52
Q

what is non competitive antagonism?

A

agonist binds to orthosteric site but antagonist binds to separate allosteric site.
both may occupy the receptor simutaneously but activation cannot occur when the antagonist is bound.

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53
Q

what does a competitive antagonist do to potency of the agonist?

A

reduces potency

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54
Q

what does a non competitive antagonist do to potency of the agonist?

A

nothing

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55
Q

what does a competitive antagonist do to efficacy of the agonist?

A

nothing

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56
Q

what does a non competitive antagonist do to efficacy of the agonist?

A

decreases efficacy

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57
Q

compare the efficacy of partial agonists and full agonists.

A

partial agonists have a lower efficacy than full agonists

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58
Q

how many glycoprotein subunits are there in a Nicotinic Acetylcholine (ACh) receptor?

A

5

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59
Q

what type of channel is a nicotinic acetylcholine (Ach) receptor?

A

cation conducting channel

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60
Q

what are the 9 steps of cholinergic transmission at a synapse?

A
  1. uptake of choline
  2. synthesis of ACh
  3. Storage of ACh
  4. Depolarisation by action potential
  5. Ca2+ influx
  6. Ca2+ induced release ACh
  7. Activation of ACh receptors (either nicotinic or muscularis)
  8. Degradation of Ach to choline and acetate
  9. Reuptake and use of choline
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61
Q

within the nerve terminal of the pre-synaptic neurone, how is choline uptake achieved?

A

via transporter

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62
Q

within the nerve terminal of the pre-synaptic neurone, how it ACh synthesised?

A

Choline + AcCoA

via choline acetyltransferase (CAT)

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63
Q

Within the nerve terminal of the pre-synaptic neurone, what happens to ACh as it is stored in transporters?

A

becomes more concentrated

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64
Q

Within the nerve terminal of the pre-synaptic neurone, how does the Ca2+ influx come about?

A

Ca2+ influx through voltage-activated Ca2+ channels

remember the cell has just become depolarised

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65
Q

what does depolarisation mean?

A

the membrane potential becomes positive

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66
Q

for volatage-activated Ca2+ channels to become open, what must the membrane potential be?

A

positive

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67
Q

how does the Ca2+ induced release of ACh occur from the pre-synaptic neurone?

A

exocytosis

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68
Q

what does activation of the nicotinic ACh receptors on the post-synaptic cell cause?

A

Na+ influx into post-synaptic cell, causing depolarisation

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69
Q

What enzyme degrades ACh to choline and acetate?

A

acetylcholinesterase (AChE)

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70
Q

what 2 types of ACh receptors are there?

A

nicotinic

muscarinic

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71
Q

what kind of action potential is formed from the post-synaptic depolarisation?

A

all-or-none action potential

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72
Q

along the post-synaptic neurone how is the AP (depolarisation wave) sent?

A

voltage-activated Na+ channels

a wave of Na+ influx

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73
Q

what type of molecular mechanism dows hexamethonium use?

A

open channel block

a form of non-competitive antagonism

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74
Q

in parasympathetic neuroeffector junction, what particular receptors are stimulated by ACh?

A

g-coupled muscarinic ACh receptors

subtypes M1-M3

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75
Q

what G protein does M1 receptor have coupled to it?

A

Gq

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76
Q

What does activation of Gq protein cause?

A

stimulation of phospholipase C

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77
Q

What type of muscarinic receptor is involved in the stimulation of increased stomach acid secretion?

A

M1

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78
Q

what G protein does M2 receptor have coupled to it?

A

Gi

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79
Q

what does activation of Gi protein cause?

A

inhibition of adenylyl cyclase

opening of K channels

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80
Q

what type of muscarinic receptor is involved in decreasing heart rate?

A

M2

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81
Q

what G protein does M3 receptor have coupled to it?

A

Gq

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82
Q

what type of muscarinic recptor is involved in the contraction of the bronchiole smooth mucle?

A

M3

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83
Q

describe the 8 steps of Noradrenerigc (NA) transmission?

A
  1. synthesis of NA
  2. storage of NA
  3. depolarisation by action potential
  4. Ca2+ influx
  5. Ca2+ induced release of NA
  6. Activation of adrenoceptor subtypes on effector cell
    7, reuptake of NA by transporters
  7. metabolism of NA
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84
Q

in the nerve terminal of the pre-synaptic neurone, what does storage of NA in transporters do?

A

concentrate NA

85
Q

How is the Ca-induced release of NA achieved?

A

exocytosis

86
Q

what are the 2 forms of NA reuptake?

A 
Uptake 1 (U1)- on presynaptic neurone
Uptake 2 (U2)- on effector cell
87
Q

for U1 of NA at the presynaptic neurone, what enzyme metabolises NA?

A

Monoamine oxidase (MAO)

88
Q

for U2 of NA at the effector cell, what enzyme metabolises NA?

A

catechol-O-methyltransferase

COMT

89
Q

what G protein is coupled to B1 adrenoceptor?

A

Gs

90
Q

What does activation of Gs protein cause?

A

stimulation of adenylyl cyclase

91
Q

what adrenoceptor is involved in increasing heart rate and increasing stroked volume?

A

B1 adrenoceptor

92
Q

what G protein is coupled to B2 adrenoceptor?

A

Gs

93
Q

what adrenoceptor is involved in causing the relaxation of bronchial and vascular smooth muscle?

A

B2 adrenoceptor

94
Q

What G protein is coupled to A1 (alpha 1) adrenoceptor?

A

Gq

95
Q

what adrenoceptor is involved in causing the contraction of vascular smooth muscle?

A

A1 adrenoceptor

96
Q

what G protein is coupled to A2 adrenoceptor?

A

Gi

97
Q

what adrenoceptor is involved in the inhibition of NA release?

A

A2 adrenoceptor

98
Q

what do presynaptic autoreceptors (either muscurinic or adrenoceptors) do?

A

mediate negative feedback inhibition of transmitter release

99
Q

what do agonists do when stimulating the autoreceptor of a presynaptic neurone?

A

decrease neurotransmitter release

100
Q

what do antagonists do when inhibiting the autoreceptor of a presynaptic neurone?

A

increase neurotransmitter release

101
Q

how does cocaine work?

A

U1 antagonist,

increases NArelease

102
Q

what do peripheral actions of cocaine cause?

A 
vasoconstriction (due to increased A1 adrenoceptor stimulation by NA)
cardiac arrhythmias (due to increased B1 adrenoceptor stimulation by NA)
103
Q

how does amphetamine work?

A

U1 agonist
MAO antagonist
pushes NA out of transporters and into cytoplasm causing it to be released by U1 (‘runs backwards’)
so decreases NA metabolism and increases NA release

104
Q

what do peripheral actions of amphetamine cause?

A 
vasoconstriction (due to increased A1 adrenoceptor simultation by NA)
cardia arrhythmias (due to increased B1 adrenoceptor stimulation by NA)
105
Q

what is prazosin?

A

an anti-hypertensive

106
Q

how does prazosin work?

A

selective, competitive antagoinist of A1 (reduces constraction of vascular smooth muscle)

107
Q

what is atenolol?

A

a beta blocker:

used as anti-anginal and anti-hypertensive

108
Q

how does atenolol work?

A

selective, competitive antagonist of B1 (reduces heart rate and force)

109
Q

how does salbutamol work?

A

selective, agonist of B2

relaxes the smooth muscle in the bronchioles

110
Q

how does atropine work?

A

competitive antagonist of muscurinic ACh receptors (blocks M1, M2, M3), widespread effects by blockade of parasympathetic division of ANS

111
Q

what is atropine used for?

A

to reverse bradycardia following MI

112
Q

what signals move from CNS to PNS?

A

efferent

113
Q

what signals move from PNS to CNS

A

afferent

114
Q

what part of the ANS coordinates the body’s basic homeostatic function?

A

parasympathetic

115
Q

what part of the ANS coordinates the bodys response to stress, associated with fight, flight and fright reactions?

A

sympathetic

116
Q

what transmitter does the parasympathetic neurones use?

A

ACh

117
Q

what transmitter does the sympathetic preganglionic neurone use?

A

ACh

118
Q

what transmitter does the sympathetic postganglionic neurone usually use?

A

NA

119
Q

as the adrenal gland only has preganglionic innervation, what transmitter is used?

A

ACh

120
Q

what type of vertebral ganglia make up the sympathetic chain?

A

paravertebral ganglia

121
Q

where are parasympathetic ganglia usually found?

A

in the target organs themselvers

122
Q

what part of the ANS increases heart rate and stroke volume?

A

sympathetic

123
Q

what part of the ANS decreases heart rate?

A

parasympathetic

124
Q

what part of the ANS relaxes bronchi (via the release of adrenaline)?

A

sympathetic

125
Q

what part of the ANS decreases mucus production to reduce airway resistance?

A

sympathetic

126
Q

what part of the ANS constricts bronchi?

A

parasympathetic

127
Q

what part of the ANS stimulated mucus production to increase airway resistance?

A

parasympathetic

128
Q

what part of the ANS reduces motility and constricts sphincters in the GI tract?

A

sympathetic

129
Q

what part of the ANS increases motility and relaxes sphincters in the GI tract?

A

parasympathetic

130
Q

what part of the ANS constricts vasculature (but also relaxes vasculature in skeletal muscle)?

A

sympathetic

131
Q

what part of the ANS releases adrenaline from the adrenal gland?

A

sympathetic

132
Q

what part of the ANS is reponsible for ejaculation?

A

sympathetic

133
Q

what part of the ANS is responsible for erection?

A

parasympathetic

134
Q

where are nicotinic ACh receptors found?

A

in the synapse between the pre-ganglion neurone and post ganglion neurone

135
Q

where are adrenoceptors found?

A

in the synapse between the post-ganglion neurone and the effector cell (sympathetic)

136
Q

where are muscurinic receptors found?

A

in the synapse between the post-ganglion neurone and the effector cell (parasympathetic)

137
Q

what are the 3 conformations of ligand-gated ion channels? (eg nicotinic)

A

unoccupied and closed
occupied and closed
occupied and open

138
Q

what do ligand-gated ion channels such as nicotinic channels allow?

A

rapid altering of the membrane potential

139
Q

how do muscarinic receptors signal to effector protein?

A

through G proteins

relatively slow compared to transmitter-gated ion channels

140
Q

what is the basic structure of a muscarinic receptor?

A

integral membrane protein
single polypeptide with extracellular NH2 and intracellular COOH terminals
contains 7 transmembrane spans connected by 3 extracellular and 3 intracellular connecting loops

141
Q

how many polypeptide units does a G-protein have?

A

3 (alpha, beta, gamma)

142
Q

what does G-protein stand for?

A

guanine nucleotide binding protein

143
Q

what does a G-protein contain in the alpha subunit?

A

guanine nucleotide binding site that can hold GTP or GDP

144
Q

when the muscarinic receptor is activated what 4 steps occur involving the G protein?

A
  1. G protein couples with receptor
  2. GDP dissociates
  3. GTP binds to alpha subunit
  4. G protein alpha unit dissociates and combines with effector
145
Q

what type of enzyme does the alpha subunit of the G protein act as?

A

GTPase

hydrolyses GTP to GDP and Pi (then signal is turned off)

146
Q

what is the critical concentration a drug must reach in the plasma to achieve an effect?

A

MEC: minimum effective concentration

147
Q

what is the critical concentration of a drug in the plasma, which above would cause significant unwanted effects?

A

MTC: maximum tolerated concentration

148
Q

The therapeutic window is between what 2 values?

A

MEC and MTC

minimum effective concentation and maximum tolerated concnetraion

149
Q

the therapeutic ratio (TR) =

A

MTC/MEC

150
Q

if a drug has a high therapeutic ratio it is classed as what kind of drug?

A

‘safe drug’

151
Q

if a drug has a low therapeutic ratio it is classed as what kind of drug?

A

‘unsafe drug’

152
Q

what is K(abs)?

A

the rate of absorption of drug to the body fluid compartment

153
Q

what is K(el)?

A

the rate the drug is removed from the body fluid comparment

154
Q

what route of administration by-passes absorption?

A

IV

155
Q

for an IV drug how do you calculate the initial concentration?
C(0) =

A

Dose /V(d)
ie mass/volume

(this will only be true for time = 0)

156
Q

what is the half life of the drug?

A

the time taken for C(t) to fall by 50%

157
Q

for first order kinetics, where K(el) is directly proportional to drug concentration, how do you calculate the concentration at a particular time?
C(t) =

A

C(0)e^[-K(el).t]

concentration at time 0 times e to the power of [-rate of elimiation x time]

158
Q

half life of a drug can be found by t(1/2) =

A

0.69/K(el)

159
Q

for drugs that exhibit first order kinetics, what happens to the K(el) or t(1/2) when dose administered changes?

A

nothing

elimination rate and half life remains the same for the same drug at a different initial dose

160
Q

what is clearance?

A

the volume of plasma cleared of drug in unit time

a constant that relates rate of elimination to plasma concentration

161
Q

what does clearance determine?

A

the maintenance dose rate

ie the dose per unit time required to maintain a given plasma concentration

162
Q

K(el) =

A

Cl x Cp

clearance (constant) x plasma concentration

163
Q

what two values must be the same at steady state?

A

K(abs) = K(el)

rate of absorption equals rate of elimination

164
Q

when is Css reached?

concentration at steady state

A

5 half lives approx

165
Q

why does metabolism of drugs convert them into more polar metabolites?

A

polar molecules are not readily reabsorbed in the renal tubules thus facilitating excretion

166
Q

what are the 4 ways metabolism can change a drug?

A
  1. make drug less active
  2. make drug more active
  3. unchanged
  4. possess a different type of activity
167
Q

what are the 2 sequential phases of metabolism?

A

phase 1: oxidation, reduction ,hydrolysis
phase 2: conjugation
[although remember some drugs are unchanged]

168
Q

what does phase 1 of metabolism achieve?

A

makes drugs more polar, adds a chemically reactive group permitting conjugation

169
Q

what does phase 2 of metabolism achieve?

A

adds an endogenous compound further increasing polarity

170
Q

what plasma components are not filtered through the glomerlus?

A

plasma proteins

therefore only unbound drug molecules can filtrate via glomerular filtration

171
Q

CL(fil) =

[clearance by filtration]

A

GFR x F(up)

glomerulur filtration rate x fraction of drug unbound in plasma

172
Q

what is the normal glomerulus filtration rate?

A

120 ml/min

173
Q

what do epithelial cells of the proximal tubule contain that help with the tubular secretion of drugs?

A

2 transporter systems that actively secrete drugs into the lumen of the nephron

174
Q

what are the 2 transporter systems in the epithelium cells of the proximal tubule?

A

organic anion transporter: handles acidic drugs, endogenous acids and the marker for renal plasma flow (PAH)
organic cation transporter: handles basic drugs

175
Q

what are the 2 factors about tubular secretion of drugs that make it so efficient?

A
  1. can concentrate drugs in the tubular fluid against an electrochemical gradient
  2. can secrete highly protein-bound drugs
176
Q

what is Tm (transport maximum)?

A

the maximum amount of drug the carrier can transport

tubular secretion is a saturable process

177
Q

what are the factors influencing tubular reabsorption?

A
  1. lipid solubility
  2. polarity
  3. urinary flow rate
  4. urinary pH
178
Q

how does lipid solubility affect tubular reabsorption?

A

drugs with highly lipid solubility will be extensively reabsorbed

179
Q

how does polarity affect tubular reabsorption?

A

highly polar drugs will be excreted without reabsorption

180
Q

how does urinary flow rate affect tubular reabsorption?

A

diuresis (increased urine outpue) will decrease reabsorption

181
Q

how does urinary pH affect tubular reabsorption?

A

the degree of ionisation of weak acids and bases strongly influences how readily absorbed the drug is

182
Q

what does an alkaline urinary pH cause?

A

makes acidic drugs more ionised and so less easily reabsorbed:
increases excretion of acids

183
Q

what does an acidic urinary pH cause?

A

maked alkaline drugs more ionised and so less easily reabsorbed:
increases excretion of bases

184
Q

what does depolarisation mean?

A

membrane potential becomes less negative (postitive)

185
Q

what does hyperpolarisation mean?

A

the membrane potential becomes more negative

186
Q

what is passive movement of an ion through an ion channel driven by?

A

an electrochemical gradient for that ion

187
Q

what is the normal resting membrane potential for neurones?

A

-80mV

188
Q

what is the equilibrium potential for Na+?

A

E(Na) = +60mV

189
Q

what determines the direction of ion movement?

A

Vm - E(ion)
(membrane potential - equilibrium potential for a specific ione)
if the answer is negative- INFLUX
if the answer is positive- EFFLUX

190
Q

explain why sodium influx occurs in response to opening of cell membrane sodium selective channels?

A

Vm -E(Na)
-80 - 60 = -140 mV
negative value = INFLUX

191
Q

what is the equilibrium potential for K+?

A

-90mV

192
Q

explain why potassium influx occurs in response to opening of cell membrane potassium-selective channels?

A

Vm -E(K)
-80 - -90= +10
positive value = EFFLUX

193
Q

what happens when Na channels open?

A

Na influx causing the membrane potential to be driven towards E(Na) [+60mV]

194
Q

what happens when K channels open?

A

K efflux causing the membrane potential to be driven towards E(K)
[-90mV]]

195
Q

what are the 3 forms of ion-gate?

A
  1. voltage gated ion channels- dependent on membrane voltage
  2. ligand-gated ion channels- dependent on chemical substances
  3. mechanical, thermal etc- dependent on physcial stimuli
196
Q

what are action potneitals?

A

brief electrical signals in which the polarity of the nerve cell membrane is momentarily reversed

197
Q

why do you need a threshold depolarising stimulus to start an action potential?

A

because there ‘all or none’

198
Q

in an AP, when the threshold for depolarisation is reached what happens to cause the huge sudden depolarisation?

A

voltage gated sodium channels opening causing sodium influx and depolarisation

199
Q

in an AP, when the membrane potential nears the equilibrium potential for sodium what happens to cause the repolaristion?

A

voltage gated potassium channels open (slight delay) causing potssium efflux and repolarisation

200
Q

what type of feedback is the activation of Na channels?

A

positive feedback- the opening of a few channels causes further channels to open and thus causes further depolarisation etc

201
Q

what type of feedback is the activation of K channels?

A

negative feeback- efflux of K causes repolarisation which turns off the stimulus for opening K channels

202
Q

what 3 states do voltage activated Na channels have?

A

closed state- non conducting
open state- conducting
inactivated state- non conducting

203
Q

when do Na channels enter a inactivated state?

A

during maintained depolarisation

204
Q

what does the inactivated state of the Na channels contribute to?

A

the repolarising phase of action and is responsible for refractory period

205
Q

what is an absolute refractory period?

A

no stimulus, however strong, can elicit a second action potential
(because all Na channels are inactivated
-occurs during the repolarisation phase of the AP

206
Q

what is a relative refractory period?

A

a stronger stimulus may elicit a second action potential
(because there is a mixed population of closed channels and inactivated channels and the membrane potential is below resting potential)
-occurs after the repolarisation phase of the AP

207
Q

what helps to increase passive current spread of an AP?

A

myelination of the axons

208
Q

what are the areas on the axons that arent insulated with myelin?

A

nodes of Ranvier, the only place where ions can exchange and therefore an AP can come about and so the AP is regenerated at each node of Ranvier

209
Q

what is the name of propragation of APs along myelinated axons from one node of ranvier to the next?

A

saltatory conduction

Principles (8 decks)

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