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Health.2 > CNS Drugs 🧠 > Flashcards

CNS Drugs 🧠 Flashcards

1
Q

L: intro to CNS

what can input to CNS be described as (2 words)

A

afferent

sensory

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2
Q

what can output to CNS be described as (2 words)

A

efferent

motor

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3
Q

2 functions of the brain

A

sensory: reception vs perception
motor: decision based activity

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4
Q

What is reception?

A

stimulation of a receptor such as light, touch, or sound

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5
Q

What is perception?

A

process of organizing and interpreting sensory information, enabling us to recognize meaningful objects and events

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6
Q

What is memory?

A
  • storage and retrieval of information

- info can be relied on and used to compare future experiences

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7
Q

What is the independent motor function?

A
  • ability for motor function to occur without the use of sensory info
  • useful in decision-based activity
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8
Q

How does information get in to (and out of) the brain?

A
  • different tracts that carry axons and sensory info to the brain and feedback to the muscles
  • sensory neurons send information from the eyes, ears, nose, tongue, and skin -> brain
  • motor neurons carry messages away from the brain -> rest of body
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9
Q

What is Brodmann’s map?

A

The Brodmann areas are a way of mapping the cortex and its distinguished functions
.. where the info goes to

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10
Q

How may areas are found on the Brodmann map?

A
  • 52 areas
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11
Q

2 cell types on brain and what are their funcitons?

A

neurones: info processing
glia: other functions

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12
Q

What is the consequence of damage to different areas of the Broadmann map

A

changes in an individual’s behaviour or personality

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13
Q

examples of areas of Brodmann mapping and function (vision, speech and language perception)?

A
  • vison (area 17)
  • speech (45)
  • language reception (32)
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14
Q

What is a homonculus?

A

topographical-organized map of the proportional representation of the contralateral somatosensory or motor neurons on the cortex or passing through a part of the brain.

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15
Q

What are the primary sensory or motor cortices?

A
  • areas of the cortex that are able to receive simple sensory/motor information
  • the same info can be passed to other areas of the cortex that can deal with this info in a more complex way
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16
Q

What are the secondary sensory or motor cortices?

A
  • info from the primary corticies are passed here
  • The neurons in this secondary area are still able to process the information
    unimodal association
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17
Q

Why are secondary cortices unimodal?

A

still processing 1 source of info (auditory) in a more complicated way

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18
Q

What are the tertiary sensory or motor cortices?

A
  • multimodal areas
  • bring info together from different sensory modalities and compare it to what is stored as info within the brain
  • gives 3D representation, pain (combines detection of painful stimuli with memories of painful emotions in the past) and create a mental image
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19
Q

What is a connectome?

A
  • a neural map of the connections within the brain
  • shows the interactions between >1000 neurons to form circuits?
  • circuits, synapses
  • vast connectivity
  • neuropharmacology
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20
Q

3 examples of drugs affecting neurotransmission

A

LDopa: mimics NT (Parkinsons)
SSRI: impact reuptake into synaptic terminal : depression
Opioid: act as NT receptor: pain

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21
Q

what drugs affect ion channels?

A

anti-epileptics- have unusual elect activity

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22
Q

brain= complex but to simplify, what 2 tyoes of signals?

A

electrical: APs
chemical: NT released @ synapses

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23
Q

L: drug abuse and addiction

What is drug misuse and an example?

A
  • Using meds in ways other than intended use
  • like taking 4 tablets when you were supposed to take 2

prescribed

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24
Q

what is drug abuse?

A
  • Excessive use of a drug inconsistent with medical practice
  • can lead to to psychoactive effects
  • drug doesn’t have to be illegal

not prescribed

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25
Q

What is hedonism?

A
  • pursuit of pleasure

- likely cause as to why people go back and repeat the same actions (taking drugs)

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26
Q

What is the mesolimbocortical system?

A
  • comprised of 2 dopaminergic pathways: the mesolimbic and a mesocortical system
  • also called the reward system
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27
Q

Where do the mesolimbic and a mesocortical pathways originate?

A

in the midbrain

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28
Q

How does the mesolimbic system cause pleasure?

A
  • Neurones leave the ventral tegmental area (VTA) and run to other parts of the brain
  • these neurons travel to the nucleus accumbens
  • dopamine is the primary neurotransmitter
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29
Q

How does the mesocortical system cause pleasure?

A
  • sends neurons from the VTA to the frontal lobe of the brain

– this area does all the high-level activity (abstract/rational thinking, problem solving)

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30
Q

What is the consequence of blocking the mesocortical system?

A
  • issues with abstract/rational thinking, problem solving
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31
Q

What events can stimulate the dopaminergic pathways?

A
  • natural rewards

- eating, drinking, sex, and extreme sports

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32
Q

How does heroin work?

A
  • Binds to opiate receptors
  • blocks inhibitory neurotransmitters (GABA) form binding to receptors
  • there is an increased dopamine release at synapse and act on the nucleus accumbens
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33
Q

What factors are reached with chronic use of addictive substances?

A

o Tolerance

o Physical dependence

o Psychological dependence

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34
Q

What does increased tolerance to something mean?

A

with continued use there is a decrease in effect of the substance

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35
Q

How does drug tolerance affect behavioural adaptation?

A

Body gets used to drug in the system and may affect behaviour

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36
Q

How does drug tolerance effect metabolic processes?

A

increased exposure of liver cells to a drug may ⬆ production of metabolic enzymes and drug is metabolized quicker (person must take more drug)

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37
Q

How does drug tolerance effect neurobiological factors?

A

There are adaptive processes in the Mesolimbocortical pathway which decrease the level of dopamine transmission for exposure to any drug at a dose

  • To get the same effect more drug must be taken
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38
Q

What would happen if someone taking drugs was to stop for a week and start again?

A
  • body adjusts during the break

- on second exposure body may not be able to handle these amounts (overdose – may be fatal)

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39
Q

What is the physical dependence in drug addiction?

A
  • refers to withdrawal symptoms

- body functions differently in absence of drug

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40
Q

What are the withdrawal symptoms in drug addiction?

A

o Caffeine-withdrawal headache

o Pain hypersensitivity with opioids

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41
Q

What are the neurological effects in drug addiction?

A
  • Adaptive processes

- NS is used to presence of drug – in absence there is a degree of overcompensation -> symptoms

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42
Q

What is the psychological dependence in drug addiction?

A
  • can be long term
  • patient expresses a compulsion/urge to take the drug
  • compulsion or need for the drug can override the person’s thinking and lead to impaired decision making (criminal behaviour)
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43
Q

What are the neurobiological effects in drug addiction?

A

o These can change the physical structure of the brain, new synapses and connections between neurons and different pathways

o When the drug is absent the physical changes can remain – leading to craving for long periods after stopping

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44
Q

What is the difference in the initial stage of drug taking compared to the addiction phase?

A
  • initially taking this drug was used for pleasure

- in addiction the motivation for taking the drug is to avoid withdrawal symptoms or craving as opposed to for pleasure

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45
Q

What may affect ease of addiction for certain drugs?

A
  • level/ speed of dopamine release

- severity/ length of withdrawal symptoms

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46
Q

why are some drugs more addictive than others?

Why is crack more addictive than cocaine which is more addictive than coca leaves?

A
  • The extent of addiction depends on the PK of substance

- crack is inhaled which has a faster onset than snorting or chewing (cocaine/ coca leaves)

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47
Q

What can effect ability to become addicted to certain things?

A

o Genetics

o Quality of life

o Economical status

o What is available - If people don’t have the means to obtain these addictive substances there would be no way for them get addicted

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48
Q

How can addiction be treated (non-drug)?

A
  • Motivational Interviewing
  • Social Skills Training
  • Combined behavioural and substance replacement
  • Structured family and couple therapy
  • Family training
  • Detoxification
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49
Q

How can addiction be treated (drug)?

A
  • reducing the dose gradually allows the body enough time to readjust to a lower dose and readapt to a non-drug state
  • use substances with different PK properties (Heroin vs methadone) - Liquid has a slower onset than injection of heroin while still stimulation opioid receptors
  • nicotine patches

BUT inc chance of relapse… timing of intervention critical

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50
Q

L: drugs affecting synaptic transmission in CNS

What is a must for centrally (brain) acting drugs?

A

must be able to cross the BBB – has to be lipophilic at blood pH

lipid soluble (unionised) at blood pH!

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51
Q

What are some centrally acting drugs?

A

· Drugs treating psychiatric and neurological disorders

· General anesthetics and analgesics must cross the BBB as well

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52
Q

What is synaptic transmission?

A

the process of information transfer at a synapse

transmitter through vesicle out of pre synatpic-> post synaptic thorugh cleft… to receptor

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53
Q

Where are neurotransmitters stored?

A

in vesicles within neuron endings

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54
Q

Where are neurotransmitters made?

A
  • cell body of a neuron

- produced by enzymes

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55
Q

What is the process in order to fire an action potential?

A
  • sodium influx @ axon hillock via voltage gated channels
  • sodium depolarized the cell until the threshold is reached

– now an AP can be fired

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56
Q

What is the process in order to release an neurotransmitter?

A
  • Depolarisation of the neuron stimulates calcium influx via the voltage gated Ca2+ channels
  • calcium influx triggers exocytosis of NTs
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57
Q

What is the process neurotransmitter-receptor coupling and post synaptic effect?

A
  • NT is released into the synaptic cleft
  • NT diffuses to receptors on postsynaptic membrane
  • NT-receptor binding allows for the firing of an AP from the post synaptic neuron
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58
Q

What are the 2 mechanisms of termination of synaptic transmission?

A
  1. Re-uptake of NTs

2. Enzymatic Breakdown of NT

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59
Q

What is the re-uptake termination mechanism?

A
  • reuptake of the NT into the presynaptic terminal

- After reuptake, the NT can be metabolized

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60
Q

What is the enzymatic breakdown mechanism?

A

enzyme is present in synapse and can degrade the NT once it has been released from the Presynaptic terminal

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61
Q

process of synapse?

A
  1. biosynthesis: synthetic enzymes loaded into vesicles
  2. AP propagation: Na+ jumps
  3. NT release… Ca2+ triggers vesicles to release into cleft
  4. Receptor coupling: enz in vesicles then go to receptor of post synaptic neuron
  5. post synaptic effect
  6. signal termination: reuptake (presyn. takes enz back up)
    OR
    enzymatic breakdown by mitochondria in syn cleft
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62
Q

Which drugs can target neurotransmitter biosynthesis?

A
  • L-DOPA - used in dopamine replacement therapy

- this used to treat parkinson’s disease

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63
Q

Which drugs can target Action potential propagation?

A
  • Sodium channel blockers - used to treat epilepsy (phenytoin + carbamazepine)- anticonvulsant
  • this decreases the high frequency firing of APs
  • These drugs selectively block the inactivated state of the channel
  • allow regular firing but only target high frequency firing channels
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64
Q

Which drugs can target Neurotransmitter release?

A
  • calcium channel blockers
  • reduce NT release due to inhibition for calcium influx
  • Phenytoin = used in epileptic fit treatment
  • Ethosuximide = used to treat absence epilepsy
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65
Q

Why are Post-synaptic receptor antagonists used?

A

o prevent the NT from binding to the postsynaptic receptors and generating a potential in the postsynaptic neuron

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66
Q

What are examples of Post-synaptic receptor antagonists?

A
  • D2 receptor antagonist (neuroleptics - haloperidol)
  • Ach muscarinic Antagonist (antiparkinsonian - benztropine)
  • Serotonin antagonists (antiemetics - ondansetron)
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67
Q

Why are Post-synaptic receptor agonists used?

A

bind to receptors and stimulate a signal in the post synaptic neuron

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68
Q

What are examples of Post-synaptic receptor agonists?

A
  • D1 receptor agonist (antiparkinsonian - Bromocriptine)
  • µ-receptor agonists (analgesic - morphine)
  • Serotonin (5-HT1A) agonists (Anxiolytic - buspirone)
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69
Q

What are allosteric modulators?

A
  • group of substances that bind to a receptor to change that receptor’s response to stimulus.
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70
Q

What are some positive modulators of GABA-A receptors? and uses?

A

o Benzodiazepines (diazepam) or barbiturates (phenobarbitone)

o These enhance inhibitory transmission

o Can be used as a sedative/ hypnotic/anxiolytic

o Also used as a anticonvulsant or a general anesthetic

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71
Q

What drugs inhibit the uptake of Noradrenaline?

A
  • Tricyclic antidepressants -Amitriptyline

- Unselective between noradrenaline and serotonin reuptake

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72
Q

What drugs inhibit the uptake of Serotonin?

A
  • Selective serotonin re-uptake inhibitors/ SSRIs (fluoxetine/ Prozac)
  • used as an antidepressant
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73
Q

What drugs inhibit the uptake of GABA?

A
  • GABA uptake (GAT-1) blocker (tiagabine)

- Used as an anticonvulsant

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74
Q

What drugs inhibit the uptake of Dopamine?

A
  • Dopamine uptake inhibitor (nomifensine)

- Used as an antiparkinsonian (antidepressant)

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75
Q

Which drugs can inhibit the enzymatic degradation of neurotransmitters?

A
  • Monoamine oxidase inhibitors (MAOIs) - antidepressants (phenelzine)
  • Selective MAO-B inhibitor - antiparkinsonian (selegiline)
  • GABA transaminase inhibitor - anticonvulsant (vigabatrin)
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76
Q

Which drugs can inhibit the negative feedback on the release of neurotransmitters?

A
  • Mianserin - α2 antagonist properties

- Also used as an antidepressant

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77
Q

DRUGS by clinical indication

What can be targeted to treat depression?

A

o The reuptake of inhibitory NTs

o The enzymatic degradation of inhibitory NTs

o The auto-receptors in negative feedback (antagonism)

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78
Q

What is the monoamine hypothesis?

A
  • Depression is associated with low levels of serotonin and norepinephrine in the brain
  • Low activity of monoaminergic receptors
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79
Q

How can Parkinson’s be treated?

A

o Replacement therapy via precursor (L-DOPA)

o Direct agonism

o Re-uptake inhibition

o Degradative enzyme inhibition

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80
Q

How can epilepsy be treated?

A

o Na+ channel blockers – decreases AP propagation (reduce over firing)

o Ca2+ channel blocker – decreases NT release (reduce over firing)

o GABAA receptor (positive) allosteric modulation

o GABA re-uptake inhibition

o GABA degradative enzyme inhibition

81
Q

What is Alzheimer’s disease?

A

degenerative type of dementia that affects memory, thinking and behavior.

loss of acetylcholine ACh

82
Q

What was attempted to treat Alzheimer’s?

A
  • admin of ACh precursor and agonists of ACh receptor

- these had NO success

83
Q

How is Alzheimer’s treated?

A
  • inhibition of ACh metabolism via acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine)
84
Q

L: general anaesthesia

What is the definition of anaesthesia?

A

the abolition of sensation

85
Q

What needs compose the triad of general anaesthesia?

A
  • need for unconsciousness
  • need for analgesia
  • need for muscle relaxation (primarily loss of reflexes)
86
Q

What does general anaesthesia do to CNS activity?

A

it depresses it

87
Q

What 2 theories attempt to explain the mechanism of action behind anaesthesia?

A
  • the lipid theory

- the protein theory

88
Q

What is the general chemical structure of inhalation anaesthetic compounds?

A
  • simple
  • unreactive
  • short-chain
  • different chemical classes
89
Q

What did Meyer do in 1899 to test the ‘lipid theory’ of anaesthetics?
and conclusion made?

A
  • added diff anaesthetics to water in a jar for tadpoles
  • plotted a graph of MIC (for tadpoles to stop moving) against olive oil: partition coefficient to see relationship LogP
  • concentration of agent = inversely proportional to lipid:water coefficient
  • i.e. lipid solubility is important for anaesthetics to work - cell membrane, axon of myelin sheath?
90
Q

According to the lipid theory, how do anaesthetics work?

A

anaes volume expansion or increasing the fluidity of the membrane

91
Q

According to the lipid theory, what two parameters at what values are defined as anaesthesia?

A
  • anaesthetic concentration in the cell membrane has reached 0.05mM
  • the volume has expanded by 0.4%
92
Q

According to the lipid theory, what can be done to reverse anaesthesia?

A

increasing the pressure

93
Q

According to the protein theory, how do anaesthetics work?

A
  • proteins = target
  • lipid solubility required to bypass cell membrane and access proteins
  • also required to bind to hydrophobic pockets in proteins
94
Q

What are the two evidence points to support the protein theory?

A
  • the ‘cut-off’ phenomenon

- stereoselectivity

95
Q

Explain how the ‘cut-off’ phenomenon supports the protein theory.

A

⬆ C chain length of short-chain compounds ⬆ lipid solubility, ⬆ anaesthetic potency (lipid theory) but up to a certain point (protein theory)

  • therefore if the molecule is too big, it can no longer ‘fit’ - indicates it needs to fit something, like a protein
96
Q

Explain how stereoselectivity supports the protein theory.

A
  • compounds can have isomers with identical lipid solubility but different potencies
  • e.g. isoflurane’s +ve isomer > -ve isomer
  • therefore due to affinity and binding of protein, not just lipid solubility
  • stereo selectivity of anaesthetic potency is preserved w protein binding
97
Q

What are the excitatory molecular targets of anaesthetics?

A

anaesthetics bind to and block the channels of:

  • ACh
  • NMDA glutamate receptor
  • 5-HT
98
Q

What are the inhibitory molecular targets of anaesthetics?

A

anaesthetics bind to and enhance the channels of:

  • GABA-a
  • glycine
  • K*
99
Q

What is the effect when anaesthetics bind to K+ channels?

A

inhibitory
will enhance the channel, allowing more K+ out-> hyperpolarisation of cell membrane …less excitable

CNS will be depressed

100
Q

The majority of effects of anaesthesia are achieved through inhibition of s_ t_.

A

The majority of effects of anaesthesia are achieved through inhibition of s_ t_.

101
Q

How does anaesthesia inhibit synaptic transmission?

A
  • decreases NT release

- decreases post-synaptic responsiveness (axonal conduction has little importance here)

102
Q

Of the general anaesthesia triad, action at where in the brain mediates unconsciousness?

A

depression at the reticular formation in the midbrain

103
Q

Of the general anaesthesia triad, action at where in the brain mediates analgesia?

A

depression at the thalamus

104
Q

After increasing the anaesthetic concentration to a certain level, what effects do you see on a %responders against [anaesthetic] graph? order of inc conc?

A
  1. loss of ability to form memory
  2. loss of consciousness
  3. loss of movement (+ motor reflexes)- surgical procedure anaesthesia
  4. CVS and resp system depression -fatal OD-> death
105
Q

What are the 4 stages of classic anaesthesia?

A
  • analgesia
  • delirium (induction)
  • surgical procedure
  • medullary paralysis
106
Q

Describe the first stage of anaesthesia

A

analgesia:

  • reflexes still intact
  • patient still conscious
  • still feel pain
  • drowsiness
107
Q

Describe the second stage of anaesthesia

A

delirium (induction)… when most px die, v dangerous

  • excitement
  • delirium
  • incoherent speech
  • loss of consciousness !!
  • unresponsive to non-painful stimuli
  • muscle rigidity
  • spasmodic movements
  • vomiting
  • choking
  • cardiac arrhythmias
108
Q

Describe the third stage of anaesthesia

A

surgical anaesthesia:

  • regular breathing
  • abolition of reflexes
  • synchronised ElectroEncephaloGraph (brain activity)
  • unresponsive to painful stimuli
  • muscle relaxation
109
Q

Describe the fourth stage of anaesthesia

A

medullary paralysis:

  • medulla in charge in respiratory/cardiovascular centres
  • respiration and circulation ceases
  • death
  • pupillary dilation
  • EEG wanes
110
Q

A good anaesthetic agent must be p_ and f_ _

A

potent and fast-acting

111
Q

What parameter is used to measure anaesthetic potency?

A

minimum alveolar concentration (MAC)

  • minimum conc required to produce immobility in 50% of patients in response to noxious stimuli
  • i.e. there’s a 1 in 2 chance that at the patient will be anaesthetised at this concentration
112
Q

Why does MAC vary between patients?

what are units?

A

Patients have different sexes, heights and weights

% in % of inspired air (v/v)

113
Q

How does MAC relate to lipid solubility?

A
  • MAC is inversely proportional to lipid solubility
  • i.e. the more lipid soluble an agent is, the lower the conc required in patient’s inspired air ( %v/v) to produce anaesthesia
114
Q

What assumption is made based on MAC at equilibrium about the anaesthetic concentrations?

A

inspired concentration = alveolar concentration = brain concentration

115
Q

Based on the relationship between MAC and lipid solubility, what is the determinant of anaesthetic potency?

A

lipid solubility

potent =/=> fast acting

116
Q

Why is it important to control the depth of anaesthesia?

A
  • allows for prevention of OD

- allows for rapid induction and recovery of anaesthesia

117
Q

What are the are the main factors determining the PK aspects of inhalation anaesthetics? 2

A
  • properties of anaesthetic itself

- physiological factors

118
Q

What are the different compartments in equilibrium that inhaled anaesthetics move between?

A
  • gas
  • blood
  • brain
119
Q

What partition coefficients exist and between what compartments for inhaled anaesthetics?

A
  • between gas and blood: blood:gas partition coefficient

- between blood and brain: tissue:blood partition coefficient

120
Q

What factors speed up the transfer of inhaled anaesthetic from gas to alveoli (lungs)?

A
  • increasing the concentration of anaesthetic
  • increasing the rate and depth of breathing

all -> increase in the speed of induction

121
Q

What factor speeds up the transfer of inhaled anaesthetic from alveoli to blood?

A
  • the gas’ solubility in blood
  • the rate of pulmonary flow
  • the partial pressure in mixed venous return
122
Q

If the anaesthetic is in highly soluble gas, what is the nature of its transfer to the blood?

A
  • blood has large capacity of anaesthetic to dissolve in

- therefore need higher conc to saturated blood before anaesthetic will want to leave blood and enter tissue

123
Q

If the anaesthetic is in insoluble gas, what is the nature of its transfer to the blood?

A
  • relatively (still need some solubility to enter blood) blood insoluble gas transfers to the brain faster
  • this is due to the lower blood:gas coefficient (λ)
  • leads to increased speed of induction
124
Q

What is the relationship between the speed of induction the blood:gas coefficient?

A
  • they’re inversely proportional
  • lower the blood:gas coefficient (λ)= higher the speed of induction

= main factor driving the speed of induction

125
Q

How does the rate of pulmonary blood flow impact the transfer of anaesthetic to the blood?

A

Inc CO to pulmonary circulation => faster transfer

  • this is because more blood is supplying the lung

PP in mixed venous return:

  • increases w time
  • hence speed of transfer will slow down
126
Q

What factors affect the rate of anaesthetic transfer from blood to tissue (and hence the speed of induction)?

A
  • anaesthetic solubility in lean tissue
  • anaesthetic solubility in adipose tissue
  • tissue blood flow
  • anaesthetic concentration in blood vs in tissue
127
Q

What is lean tissue?

A

brain grey matter, muscle, essentially anything that’s not adipose tissue

128
Q

How does anaesthetic solubility in lean tissue affect the rate of transfer from blood to tissue?

A
  • tissue:blood partition coefficient for anaesthetics in lean tissue is 1
    = will readily leave the blood and enter tissue
  • hence anaesthetic conc in the brain increases quickly
129
Q

How does anaesthetic solubility in adipose tissue affect the rate of transfer from blood to tissue?

A
  • tissue:blood partition coefficient is&raquo_space;>1 in adipose tissue
  • patient’s carrying a lot of fat will have a slower speed of induction
  • slows down the rate of transfer and speed of induction - also potential for accumulation
130
Q

How does tissue blood flow affect the rate of transfer from blood to tissue?

A
  • high in lean tissue
  • low in adipose tissue
  • increases rate of transfer to lean tissue

p737!!

131
Q

How does anaesthetic concentration in blood vs tissue affect the rate of transfer from blood to tissue?

A

as anaesthetic concentration in tissue increases, the rate of transfer decreases

132
Q

How are inhalation anaesthetics metabolised?

A
  • via lung
  • excreted mainly unchanged
  • e.g. only 0.2% of isoflurane and only 0.04% of N2O is changed
133
Q

What inhalation anaesthetics have different metabolic profiles? How are they different?

A
  • methoxyflurane (~50%)

- halothane (~30%) (toxicity possibility)

134
Q

halothane

  • ads
  • disads
A
  • potent, fairly fast

- possible liver tox

135
Q

enflurane

  • ads
  • disads
A
  • less liver damage

- possible seizures

136
Q

isoflurane

  • ads
  • disads
A
  • rapid acting, muscle relaxation

- bad smell

137
Q

sevoflurane

  • ads
  • disads
A
  • pleasant odour, rapid recovery

- metabolites could cause renal damage?

138
Q

nitrous oxide 1:1 O2 (Entonox)

  • ads
  • disads
A
  • rapid, good analgesic

- low potency: normally has to be combined with other agents

139
Q

What is the definition of balanced anaesthesia?

A

using combinations of different drugs to increase the safety

140
Q

Apart from inhalation anaesthetics, what other anaesthetics are used? when?

A

IV anaes

for short procedures and alone

141
Q

How does the mechanism of intravenous anaesthetics differ to that of inhalation anaesthetics?

A
  • interacts w specific single ligand-gated channels instead of multiple
  • or NMDA receptor antagonist (ketamine)
142
Q

How does ketamine work?

A
  • NMDA receptor antagonist
  • prevents glutamate (excitatory) action

rapid onset

143
Q

What are the effects of ketamine?

A
  • sensory loss
  • analgesia
  • no loss of consciousness
  • paralysis
  • surgical anaesthesia
144
Q

What ligand-gated receptors do intravenous anaesthetics interact with? and what affect: enhance/depress

A

enhance GABA-A receptor action

145
Q

What are 3 categories of adjuncts to general anaesthetics?

A
  • pre-medication
  • muscle relaxants
  • anti-emetics
146
Q

What are drug classes used in pre-medication?

A
  • benzodiazepines (sedation, anxiolysis)
    • diazepam
    • lorazepam
  • opioids (pain relief)
  • anti-muscarinics (aid w intubation and dry up secretions in lungs allowing anaesthetic access)
147
Q

What are examples of opioids used in pre-medication?

A
  • fentanyl
  • pethidine
  • morphine
148
Q

What are examples of anti-muscarinics used in pre-medication?

A
  • atropine
  • hyoscine
  • glycopyronium
149
Q

What is the purpose of pre-medication as an adjunct?

A

anxiolysis, sedation, amnesia

150
Q

What is the purpose of muscle relaxants as an adjunct?

A

relax abdominal, tracheal, respiratory muscles

151
Q

What is the purpose of anti-emetic as an adjunct?

A

reduce peri-operative nausea e.g. metoclopramide

152
Q

What are examples of neuromuscular blockers as muscle relaxants?

A

atropine, hyoscine, glycopyronium

same as anti-muscarinics used in pre-medication

153
Q

What drug classes are used as muscle relaxants?

A
  • benzodiazepines

- neuromuscular blockers

154
Q

L:Schizophrenia and anti pyschotic drugs

What are the clincial features of schizophrenia?

A
  • onset: adolescence or early adulthood
  • males, females equal
  • after first diagnosis of pyschotic break symptoms can be controlled and go away woth meds but episodes can occur
  • In chronic state you get a progressive decline in function
155
Q

What does DSM stand for?

A

Diagnostic and Statistical Manual of Mental Disorders

156
Q

Outline some of the positive type I symptoms?

A

delusions, hallucinations, disorganised speech, grossly disorganised or catatonic behaviour

157
Q

Outline the negative type II symptoms?

A

reduced expression of emotion, social withdrawal, absence of normal responses and behaviours

158
Q

schizophrenia is mainly

A

heridetary

159
Q

describe what the Dopamine hypothesis is?

A

dopaminergic hyperactivity underlies schizophrenia and hyperactvity signalling is related to symptoms

160
Q

Where does the evidence base come from to support the dopamine hypothesis?

A

the effects of dopaminergic agents

161
Q

Outline how amphetamine abuse be used as evidence to support the dopamine hypothesis?

A
  • dopamine releasing drug
  • can -> toxic pyschosis (delirium)
  • this manifests as paranoid delusions, visual or auditory delusions or compulsive behaviours
  • If given to patient type I symptoms worsen so perhaps type I symptoms are due to dopamine
162
Q

What other drugs behave in the same way as amphetamines i.e. symptoms manifest as type I symptoms thus provide evidence to support the dopamine theory?

A

Dopamine D2 recetpor agonists and L-DOPA

163
Q
  1. too much LDOPA (dopamine precursor)–>?
A

Type I like symptoms

disappear when dose reduced

164
Q

Which treatment drug was originally an antihistamine, does not cause excessive sedation, attentuates positive symptoms and became part of the first gen of neuroleptics?

A

Chlorpromazine

165
Q

What are the 3 main classes of first gen neuroleptics?

A

Phenothiazines,
butyrophenones
thioxanthines

165
Q

What are the 3 main classes of first gen neuroleptics?

A

Phenothiazines,
butyrophenones
thioxanthines

166
Q

Which class of drug do chlorpromazine and fluphenazine belong to?

A

Phenothiazines

167
Q

Which class of drug do haloperidol and doperidol belong to?

A

Butyrophenones

168
Q

Which class do flupenthixol and clopenthixol belong to?

A

thioxanthines

169
Q

First gen neuroleptics are receptor antagonists. Which receptors do they block to cause anti pyschotic activity?

A

dopamine receptors

170
Q

Why are first gen neuroleptics esp phenothiazines termed as dirty drugs?

A 
they lack specificity and bind to a number of different receptors including:
dopamine: D1, D2,
muscarinic, 
histamine, 
noradrenaline
5HT
171
Q

Which gen of neurolepics are termed as atypical?

A

second gen

172
Q

How do atypical neuroleptics differ from typical neuroleptics?

A
  • different pharmacological profile e.g higher dopamine selectivity
  • fewer motor extrapyrimadal side effects
  • more effective against negative symptoms
  • more effective in treatment of resistant schizophrenia
173
Q

Which second gen neuroleptic is especially good at inducing fewer motor effects and are more effective negative symptoms?

A

clozapine

174
Q

Why is clozapine not able to be licensed for first line use?

A

risk of serious side effects: agranulocytosis and myocarditis

175
Q

What are the four classes of atypical neuroleptics?

A

selective dopamine receptor antagonists (D2/D3), multi acting receptor targeted agents (MARTAS), serotonin-dopamine antagonists
novel types

176
Q

Sulpiride and amisulpride belong to which class of atypical neuroleptics?

A

selective dopamine receptor antagonists

177
Q

clozapine and olanzapine belong to which class of atypical neuroleptics?

A

MARTAS

178
Q

risperidone, zotepine and sertindole belong to which class of atypical neuroleptics?

A

serotonin-dopamine antagonists

179
Q

quetiapine and aripiprazole belong to which class of atypical neuroleptics?

A

novel types

180
Q

2 areas in the brain with dopaminergic cell bodies?

A

ventral tegmental area and substantia nigra

181
Q

There are 3 major dopaminergic pathways. Where do these originate?

A

2 from VTA and 1 from substantia nigra

182
Q

The mesocortical pathway is released in the frontal cortex. What is this area of the brain responsible for?

A

thinking, cognition and memory

183
Q

The mesolimbic pathway ends in the nucleus accumbens, the part of the brain which is responsible for?

A

rewards and pleasure

184
Q

What do neuroleptic drugs block in the limbic area and what is the effect of this?

A
  • block dopamine receptors (D2) post synaptically
  • decrease transmission of mesolimbic signalling
  • stopping type I symptoms as that region may be responsible for dopamine hyperactivity

antipsychotic

185
Q

What is the cause of motor side effects and how can these be avoided by ‘cleaner’ drugs?

A

receptors are blocked at the end of the nigrostriatal pathway which is crucial to normal movements
cleaner drugs are more selective therefore fewer side effects

186
Q

List some of the dopaminergic side effects as a result of treatment?

A
  • antiemesis
  • increased prolactin release
  • extra pyramidal symptoms
  • acute motor disturbances such as dystonias
  • chronic motor symptoms such as tardive dyskinesia
187
Q

How might neuroleptic drugs cause antiemesis?

A

due to D2 receptor blocking in chemoreceptor trigger zone of the brain. When activating vomiting is stimulated

188
Q

How might treatment lead to increased prolactin release?

A

released by pit gland. usually inhibited by dopamine but as dopamine is inhibited more is released

189
Q

What side effects might men and women experience if they have increased prolactin release as a result of neuroleptic treatment?

A

breast swelling, pain and lactation

190
Q

Dystonias go away if the drug dose is reduced. What is this and why does it occur in the first place?

A
  • involuntary parkinsonian movements of face, tongue and neck
  • due to blockade of D2 receptor in striatum
191
Q

SE: motor disturbances of neuroleptic drugs

  • acute
  • chronic
A
  • dystonias

- tardive dyskinesia

192
Q

Tardive diskinesia is a chronic symptom involving involunatary movements of the face, tongue, limbs or trunk after taking the drug for a long time. Which drug has this never been seen in?

A

Clozapine

193
Q

Non dopaminergic side effects are related to the blockage of other receptor sites. Outline these?

A
  • antimuscarinic such as dry mouth and constipation
  • postural hypotension due to adrenoceptor block
  • sedation due to histamine h1 receptor block
194
Q

Why do atypical neuroleptics have an increased liklihood of compliance?

A

better side effect profiles due to greater selectivity

lower incidence of motor disturbances

195
Q

Which neuroleptics are the least likely to cause motor disturbances?

A

aripiprazole, MARTAs and quetiapine

196
Q

non compliance can be reduced by changing the route of admin from oral to?

A

long acting depot injection

197
Q

When are long acting depot injections used?

A

maintainence therapy when compliance is unrelated

198
Q

long acting depot injections are deep IM injections of sustained release. How long are the intervals of treatment and how long do side effects last?

A
  • intervals are 1-4 weeks

- side effects may persist for weeks despite the dose

Health.2 (19 decks)

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