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Z MD1 neurology > pharmacology > Flashcards

pharmacology Flashcards

1
Q

4 ways you can inactivate NA once released from pre synaptic terminal

A
  • neuronal uptake (major)
  • metabolism by the pre synaptic terminal by monoamine oxidase
  • extraneuronal uptake
  • post synaptic metabolism by monoamine oxidase and COMT
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2
Q

action of cocaine at synapses

A

prevents neuronal reuptake of NA at the pre-synaptic terminal –> and therefore there is increased activation of the receptors –> increased response when nerves being activated

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3
Q

action of amphetamine/ephedrine at synapses

A

indirectly acting sympathomimetics –> displace NA from the vesicles even with no activation by an AP –> non-exocytotic release of NA and activation of response

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4
Q

pathway for making NA

A

tyrosine –> L-DOPA –> dopamine –> NA –> adrenaline

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5
Q

pathways that dopamine is involved in…

A
  • movement
  • behaviour
  • dependence
  • pituitary function –> prolactin secretion
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6
Q

how does cocaine become addictive

A

linked to its dopaminergic action

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7
Q

which NT does cocaine act on

A
  • blocks dopamine, NA, and serotonin uptake
  • blocks Na channels
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8
Q

which areas of the brain are involved in the extrapyradmidal motor system

A

corpus striatum

substantia nigra

globis pallidum

Subthalamic nucleus

thalamus

motor cortex

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9
Q

which NTs are involved in the extrapyramidal motor system

A

dopamine

glutamate

GABA

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10
Q

what causes parkinson’s disease (in general - NTs)

A

degeneration of dopaminergic pathways

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11
Q

treatment for parkinson’s disease

A

L-DOPA (precusor for dopamine that can piggy back on an amino acid carrier) and peripheral dopamine decarboxylase inhibitor (so that the L-DOPA is only used in the CNS and not wasted in the PNS)

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12
Q

what causes Huntington’s disease (in general - NTs)

A

GABA deficiency

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13
Q

treatment for huntington’s

A

GABA agonist

dopamine antagonists

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14
Q

how can a NT be both excitatory and inhibitory at different places

A

depends on which receptors are present

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15
Q

what is the difference between local and general anaesthetic

A

local - regionalised inhibition of pain/sensory pathways with no loss of consciousness

general - depresses cortical processing of pain/sensory signal with a loss of consciousness

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16
Q

what is analgesia

A

stops sensitization of the sensory nerve endings by prostaglandins

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17
Q

how do local anaesthetic agents work?

A

they reversibly block conduction of nerve impulses at the axonal membrane

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18
Q

what are the 3 broad types of local anaesthetics?

A

aminoesters (procaine)

aminoamides (lignocaine)

benzocaine

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19
Q

difference in duration and metabolism between aminoesters and aminoamides

A

aminoesters - shorter acting, and are hydrolysed by esterases

aminoamides - longer acting and are metabolised through hepatic metabolism

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20
Q

what is the proportion of the blockade of sensory and motor functions in a nerve with local anaesthetics

A

when sensory 100% blocked, motor only ~25% blocked

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21
Q

where do local anaesthetics bind to

A

the transmembrane domain (IC) of the Na channel

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22
Q

What are the two mechanisms of the local anaesthetics getting to the I/C transmembrane domain of the Na channel

A

1) hydrophobic (benzocaine)
2) hydrophillic (aminoesters and aminoamides)

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23
Q

what is the hydrophobic mechanism of local anaesthetics blocking the Na channel

A

crosses the lipid membrane (no matter whether the channel is activated or not) as it is mostly in the non-ionized form. It then binds to and blocks the channel, preventing Na influx and therefore preventing threshold and AP

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24
Q

what is the hydrophilic mechanism of local anaesthetics blocking the Na channel

A

crosses through the membrane predominantly in the uncharged form. Once IC it promotes the formation of the charged from. The charged form binds to the Na channel only when the Na channel is open (needs activated channels) –> prevents Na influx and therefore prevents threshold and AP

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25
Q

which mechanism of the way local anaesthetics work is faster

A

the hydrophobic way - eg. benzocaine

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26
Q

do local anaesthetics change the resting membrane potential of the axon?

A

no

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27
Q

which nerves are the most sensitive to local anaesthetics? Motor, sensory or Autonomic?

A

sensory (smallest)

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28
Q

methods of administration of general anaesthetics

A

inhalation

intravenous

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29
Q

respiratory side effects of general anaesthetics

A
  • impaired ventilation
  • depression of respiratory centre
  • obstruction of airways
  • retention of secretions
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30
Q

cardiovascualr side effects of GA

A
  • decreased vasomotor centre function
  • depress contractility
  • peripheral vasodilation
  • cardiac arrythmias
  • inadequate response to fall in BPor CO
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31
Q

2 theories of how GA works

A

1) Lipid theory - accumulation of GA in the lipid space causes expansion –> squashes the proteins –> cant work very well
2) inhibition of excitatory receptors or enhancement of inhibitory receptors

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32
Q

what is thought to cause epilepsy

A

too little inhibitory input to motor nerve or too much excitatory input to motor nerve

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33
Q

treatment of epilepsy

A
  • benzodiazepines (enhance inhibitory (GABA) receptor activity)
  • phenytoin (limits excitatory nerve activation

others

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34
Q

what are benzodiazepines used for

A

epilepsy

anxiety

sleep disorders - insomnia

premedication

acute alcohol withdrawal

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35
Q

which drugs can be used to treat anxiety

A

benzodiazepines

non-benzodiazepines (B-adrenoceptor antagonists, Buspirone, zopiclone, zolpidem)

barbiturates

36
Q

why are barbituates bad?

A
  • very toxic
  • low therapeutic index
  • induction of liver enzymes
  • abrupt withdrawal can cause death
  • highly addictive
37
Q

why are benzodiazepines better than barbituates

A

less depression of respiratory and cardiovascular centres less dependence considered safe in overdose only increase the frequency of Cl ion channel opening not increase the duration of the opening

38
Q

how do benzodiazepines work

A

they act on the GABA A receptor by binding to the allosteric site modulating: increasing the affinity of the R for GABA –> increased Cl- influx into the cell

(increasing the number of times the channel opens)

39
Q

what are the effects of allosteric modulators

A
  • ceiling effect of inhibitors –> increased therapeutic window
  • positive modulation of endogenous agonist rather than continuous effect of exogenous agonist
  • great receptor subtype selectivity possible
40
Q

what are the unwanted side effects of benzodiazepines

A

drowsiness

confusion

impaired coordination

tolerance - increased dose needed over time

dependence

41
Q

what does benzodiazepines interact with

A

alcohol, antihistamines and barbituates

42
Q

what is potency

A

the relative position of the dose-effect curve along the dose axis

43
Q

how do barbituates work

A

bind the orthostatic site of the GABA A receptor causing increased Cl- ion influx

44
Q

what is drug efficacy

A

the ability of a drug to do the right thing

45
Q

what is pharmacological efficacy

A

the strength of the receptor activation

46
Q

what is clinical efficacy

A

the strength of the beneficial effect

47
Q

what are 2 non benzodiazepines that act as hypnotics

A

zolpidem and zopiclone

48
Q

what is a non benzodiazepine that acts as an anxiolytic

A

buspirone

49
Q

explain the NTs in the extrapyramidal motor system

A
  • inhibitory dopamine released from substantia nigra to corpus striatum
  • corpus striatum release stimulatory ACh onto GABA neuron which stimulates substantia nigra
50
Q

what causes Parkinson’s disease

A

degeneration of the dopaminergic neurons of the substantia nigra to corpus striatum leading to reduced dopamine levels

51
Q

what are the motor symptoms of Parkinson’s disease

A

tremor

rigidity of limbs

bradykinesia

impairment of postural reflexes

facial muscles impassive and no blinking

monotonous, hypophonic speech

parkinson’s gait (shuffling and fasiculations)

decreased manual dextretiy

52
Q

what are some of the non-motor signs of Parkinson’s disease

A

olfactory deficiencies

bowel and bladder problems

cognitive deficiencies

depression

raised anxiety levels

sleep disturbances

fatigue

pain

sexual dysfuncion

53
Q

what are the “first signs” of Parkinson’s disease

A

loss of smell and bowel and bladder problems

54
Q

how much of the dopaminergic neurons need to be degenerated for you to show symptoms of Parkinson’s disease

A

~80%

55
Q

what are ways in which we can replace the dopamine in the substantia nigra

A
  • increase dopamine synthesis
  • increase dopamine release
  • give dopamine receptor agonists
  • reduce dopamine metabolism
56
Q

why do we give cholinergic antagonists with dopamine replacement

A

to try and restore the dopaminergic/cholinergic balance in the striatum

57
Q

why do we give L-DOPA and not straight dopamine to Parkinson’s patients

A

because dopamine doesnt cross the BBB causes you to vomit violently

58
Q

what is in levodopa

A

amino acid isomer of L-DOPA and a peripheral dopamine decarboxylase inhibitor

59
Q

why do we give a peripheral dopamine decarboxylase inhibitor with L-DOPA administration

A

to prevent dopamine conversion in the periphery, so the majority can get into the brain

60
Q

what does peripheral conversion of L-DOPA cause

A

nausea, vomiting, orthostatic hypotension, cardiac dysrhythmias, pupil dilation (avoid giving to patients with glaucoma)

61
Q

why is their a debate on when to start treatment of Parkinson’s with Levodopa

A
  • requires some functional dopaminergic neurnos (so cant start too late)
  • effectiveness declines with time (cant start too early)
62
Q

what are the central side effects of levodopa

A

visual and auditory hallucinations

abnormal motor movements

mood changes

depression and anxiety

63
Q

what are the drug interactions of levodopa

A

vitamin B6

MAO inhibitors

inhalational anaesthetic

anticonvulsants and neuroleptics

64
Q

other than Levodopa, what are the other drugs available for Parkinsons patients

A
  • dopamine agonists (may be preferred in younger patients)
  • DDC inhibitor (in gut and periphery)
  • MAO(B) inhibitor (reduce metabolism of dopamine)
  • COMT inhibitor (reduction metabolism of L-DOPA)
  • Amantadine (anti-viral - enhances release of dopamine)
65
Q

which treatment option for Parkinson’s may delay disease progression? and how?

A

MAO(B) inhibitors - may reduce formation of free radicals that degenerate the dopaminergic neurons

66
Q
A
67
Q

What is drug dependence

A

state where drug use becomes compulsive taking precedance over other needs

68
Q

what is drug abuse

A

use of illicit substances characterised by recurrent and clinically significant adverse consequences

69
Q

why do people become dependent on drugs

A
  • rewarding effect (positive reinforcement, craving)
  • habituation or adaptation (rely on drug to feel well desire to avoid negative symptoms)
70
Q

Which part of the brain is involved in “dependence”?

A

nucleus accumbens and ventral pallidum

71
Q

what are the key NTs involved in modulating dopaminergic transmission

A

ACh

Serotonin

NA

GABA, glutamate

opoids

72
Q

what causes you to die with an overdose of amphetamine

A

peripheral consequences - hyperthermia, tachycardia, increased BP, vascular collapse

73
Q

what causes the suppression of appetite when taking amphetamines

A

linked to its effect on serotonin

74
Q

what is the action of MDMA

A

releases dopamine and serotonin

75
Q

how does LSD work

A

it is an agonist of 5HT2 receptors

  • activates autoreceptors on 5-HT neurons in raphe
76
Q

action of caffeine

A

adenosine antagonist

phsophodiesterase inhibitor

77
Q

how does ethanol cause depression of the CNS

A
  • inhibits Ca channel opening
  • enhances GABA action
  • inhibits glutamate receptors
78
Q

why do you get marked tolerance of ethanol

A

heavy drinking causes the activation of liver enzymes and therefore it is eliminated quicker

79
Q

what is the effect of cannibis

A

inhibits adenylate cyclase –> therefore inhibition of transmission

80
Q

what are the first, second and third generation drugs for treating depression

A

1st - tricyclic antidepressants and MAO inhibitors

2nd - SSRIs and SSNRI

3rd - novel monoaminergic drugs, and non-monoaminergic drugs

81
Q

what is the pharmacological action of tricyclic antidepressants

A
  • inhibit neuronal uptake of NA and serotonin
  • antagonise alpha adrenoceptors, muscurinic receptors, histamine receptors and serotonin receptors
  • membrane stabilising activity at high concentrations
82
Q

why are tricyclic antidepressants considered “not as good” as newer antidepressants

A
  • poor selectivity
  • narrow therapeutic window
  • longish half lives (gradual accumulation)
83
Q

what is the pharmacological action of MAO inhibitors

A

increase the levels of serotonin, NA and DA

84
Q

which antidepressant has a “cheese reaction”

A

irreversible MAO inhibitor

85
Q

what are the advantages of SSRIs

A
  • selective for serotonin uptake
  • few adrenergic, histaminergic and cholinergic actions
  • high therapeutic index
86
Q

what are the 2 precautions when prescribing SSRIs

A
  • can cause suicidal tendencies in young adolescents
  • can cause serotonin syndrome if combined with MAOIs and TCAs
87
Q
A

Z MD1 neurology (17 decks)

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