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Pharmacology > CNS Pharmacology > Flashcards

CNS Pharmacology Flashcards

1
Q

What are anxiolytic drugs?

A

Drugs used to treat anxiety

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2
Q

What are hypnotic drugs?

A

Drugs used to treat sleep disorders

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3
Q

What is anxiety?

A

Anticipatory fear response which is often independent of external events, general anxiety is an ongoing state of an excessive version of this

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4
Q

Panic disorders

A

Sudden attack of overwhelming fear, sweating, tachycardia, chest pains, trembling and choking
Has a genetic component

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5
Q

Phobias

A

Strong fear response to specific object or situations

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6
Q

Social anxiety

A

Fear of being with and interacting with people

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7
Q

PTSD

A

Anxiety triggered by recall of a stressful situation

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8
Q

OCD

A

Compulsive ritualistic behaviour driven by irrational anxiety

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9
Q

What is the elevated cross test?

A

Time animal spends in the safer environment and is less exposed is measured
Anxiolytic drugs reduce fear response so animals time spent in the more exposed environment will increase

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10
Q

What is the target for anxiolytics?

A

GABA receptors

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11
Q

GABA A receptors

A

Ionotropic with 5 subunits
Chloride selective
Mediate fast inhibitory transmission postsynaptically

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12
Q

What is the orthosteric site?

A

The agonist binding site responsible for switching on signalling by a receptor

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13
Q

What are allosteric sites?

A

Additional sites that don’t themselves switch on signalling, but modify the function or signalling of the agonist bound receptor

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14
Q

GABA A orthosteric agonists and antagonists

A

agonist is muscimol
antagonist is bicuculline/picrotoxin

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15
Q

Why does pharmacology involving GABA A vary in the CNS?

A

Different combinations of subunits are expressed in different parts of the brain so depending on the GABA A subunit composition, pharmacology varies

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16
Q

What are the physiological effects of benzodiazepine agonists?

A

Sedation, hypnosis, anterograde amnesia, anti-convulsant, reduction of muscle tone

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17
Q

Why are benzodiazepines often abused after chronic clinical treatment and are linked to dependence and addiciton?

A

Activation of midbrain dopamine neurons which could possibly hijack the mesolimbic system

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18
Q

What are benzodiazepines?

A

Positive allosteric site regulators of GABA A receptors
Increase activity of GABA A receptor by increased Cl- current across membrane but only when GABA is present

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19
Q

How are benzos mechanism of action different to other anxiolytics?

A

Benzos increase probability of channels opening whereas barbituates and steroids increase mean open time
Both result in more current flow and increased response

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20
Q

Beta carboline

A

Negative allosteric regulator of GABA A that decreases channel openings
Anxiogenic and a proconvulsant

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21
Q

Flumanzenil

A

Antagonist at benzodiazepine site so it binds there but doesn’t effect receptor
Can be used to reverse effects of benzodiazepine overdose

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22
Q

Positive allosteric modulators of GABA

A

Stabilise the receptor in a state with increased affinity for GABA
Causes a leftward shift in conc response curve

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23
Q

Negative allosteric modulators of GABA

A

Stabilise the receptor in a state thta has reduced affinity for GABA
Remains closed or harder to open

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24
Q

What are the adverse effects of using benzodiazepine agonists?

A

Tolerance, misuse, physical dependence characterised by withdrawal- increased anxiety, insomnia, CNS excitability and convulsions

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25
Q

Propanolol

A

Beta blocker

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26
Q

Anti-depressants / SSRIs

A

Selective serotonin reuptake inhibitors- useful for generalised anxiety, phobias, PTSD and OCD

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27
Q

Buspirone

A

A 5HT1A partial agonist used for generalised anxiety

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28
Q

What other types of drugs can also be used for generalised anxiety?

A

Atypical antipsychotics and anti-epileptic drugs

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29
Q

What drugs are used to treat insomnia?

A

Drug choice depends on underlying cause and whether it is short term or chronic
Melatonin receptor agonists, orexin receptor antagonists, over the counter sleep aids (H1 receptor antagonists)

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30
Q

What are the three types of general anaesthetics?

A

Chemical- inhalational, nitrous oxide
Physical- low pressure or hypothermia
Intravenous- halogenated hydrocarbons like isofluorane, barbituates and steroids

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31
Q

How do general anaesthetics work?

A

Regulation of activity of neuronal ion channels, most increase GABA action at GABA A receptors
Volatile GAs bind at interface of alpha and beta subunits
Intravenous GAs bind only on beta subunit

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32
Q

How do ketamine and nitrous oxide work?

A

Blocking NMDA receptors

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33
Q

How does isoflurane work?

A

In the neurohypophyseal terminal it reversibly blocks Na+ currents and APs
In the rat calyx it reversibly reduces synaptic vesicle exocytosis

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34
Q

What are the effects of general anaesthetic on neuronal transmission when in low concentrations?

A

Synaptic transmission in the CNS is decreased, reticular formation is unconscious, effects on hippocampus mean short term amnesia, effects on thalamic sensory relay nuclei parts of the cortex mean analgesia, some inhibit spinal reflexes

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35
Q

What happens when general anaesthetics are in high concentrations?

A

All brain functions are affected- loss of motor control, reflexes, respiration, autonomic regulation
So absence of artificial respiration leads to death

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36
Q

How are general anaesthetics different to local ones?

A

Effects on axonal conduction is important for local anaesthetis but not for general ones

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37
Q

What are the 4 stages of anaesthesia?

A

Analgesia
Excitation
Surgical anaesthesia
Medullary paralysis

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38
Q

What stages should be avoided?

A

Excitation
Medullary paralysis- loss of cardiovascular refelxes and respiratory paralysis which causes death

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39
Q

What is the ideal for anaesthesia for surgery?

A

Rapid induction and loss of consciousness
Analgesia
Muscle relaxation
Rapid recovery

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40
Q

What are the advantages of intravenous GAs?

A

Easy to administer, rapid induction and rapid metabolism so faster recovery and less hangover

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41
Q

What are the disadvantages of intravenous GAs?

A

Pain at site of injection, complex pharmacokinetics, high lipid solubility means rapid induction but short duration of action due to redistribution, hangover from accumulation in body fat

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42
Q

Ketamine

A

Dissociative anaesthetic used in pediatrics and veterinary practice
Sensory loss, powerful analgesia, amnesia but no complete loss of consciousness and no respiratory depression

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43
Q

What is malignant hypothermia?

A

Can be triggered by halogenated general anaesthetics
Induces a drastic and uncontrolled increase in oxidative metabolism in skeletal muscle
Often inherited and is an autosomal dominant disorder

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44
Q

What does malginant hypothermia lead to?

A

Overwhelms the bodys capacity to supply oxygen and remove carbon dioxide and regulate body temp
Eventually leads to circulatory collapse and death if not immediately treated

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45
Q

What is dantrolene and what is it used for?

A

RYR antagonist and muscle relaxant that is given before anaesthesia to people that are susecptible to malignant hypothermia

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46
Q

What general anaesthetics can cause malignant hypothermia?

A

Volatile halogenated anaesthetics
Succinylcholin- neuromuscular blocking agent

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47
Q

What is constitutive activity?

A

Occasionally channels open in the absence of an agonist

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48
Q

What is an inverse agonist?

A

When bound they reduce constitutive activity

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49
Q

What is epilepsy?

A

Unprovoked seizures from high frequency discharge by a group of neurons
Spread can be partial or generalised

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50
Q

What are generalised seizures?

A

Involve both hemispheres of the brain

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51
Q

What are complex seizures?

A

Includes loss of conscious (simple seizures don’t)

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52
Q

What can seizures be triggered by?

A

Changes in blood glucose or pH, stress, fatigue, and flashing lights

53
Q

How are seizures diagnosed?

A

EEG will show abnornal firing patterns that are associated with epilepsy
Generalised seizures show synchronous abnormal activity on all frequencies
Reflects rhythmic contraction and relaxation of muscles

54
Q

What do uncontrolled and continued seizures lead to?

A

Neuronal death

55
Q

What is a partial seizure?

A

Activity shows limited spread between the two hemispheres and not all electrode show abnormal activity

56
Q

What is an absence seizure?

A

Loss of conscious occurs but is very brief and the patient doesn’t fully collapse

57
Q

What mutations are linked to familial epilepsy?

A

Mutations in voltage gated Na+ channels meaning channel is overactive, leading to increased neuronal excitability
Or loss of function K channel mutations

58
Q

What are kindling models?

A

Repeated low level electrical stimulus is done to brain over course of weeks, causing rodent to have seizures in that specific area so drugs can be used against it

59
Q

What is status epilepticus?

A

A seizure that doesn’t stop and lasts longer than 5 minutes- can lead to permanent brain damage or death
The only time benzos and barbiturates are used for treatment

60
Q

What anti-epileptics are metabolic inhibitors? What problems do they have?

A

Vigabatrin and valproate
Depression and high protein binding, rarely hepatotoxic and teratogenic

61
Q

How is GABA made? How does this relate to finding neurons that express GABA?

A

Synthesised from glutamate to glutamic acid, which is converted to GABA by glutamic acid decarboxylase
By looking for expression of this enzyme you can find neurons that express GABA

62
Q

What are HDACs?

A

Histone de-acetylases control the structure of DNA

63
Q

What is transaminase? How is this knowledge used to treat epilepsy?

A

Transaminase breaks down GABA
So blocking this enzyme will prevent GABA’s breakdown and it will accumulate

64
Q

How are HDACs used to treat epilepsy?

A

They can be inhibited to increase transcription of glutamic acid decarboxylase in order to form more GABA

65
Q

How do anti-epileptic drugs that target excitatory neurons work?

A

They limit the release of glutamate from hyperexcitable neurons or stabilise the inactive state of voltage gated Na+ channels, so less of them are open to cause depolarisation
Good for partial seizures as they only target very specific areas

66
Q

What is the most common drug used to treat epilepsy?

A

Carbamazepine

67
Q

What other ion channel do anti-epileptic drugs target? What type of seizure do these work well for?

A

T-type Ca2+ channels which drive oscillatory behaviour
Good for absence seizures

68
Q

How do GABApentin and pregabalin work?

A

Originally developed for control of chronic pain but work for epilepsy
Bind to a subunit of Ca2+ channels and reduce trafficking to these channels

69
Q

What do new drug targets for epilepsy include?

A

Binding to a protein found on synaptic vesicles that controls glutamate to reduce the amount of it released synaptically
Medicinal cannabis

70
Q

What are the amine transmitters in the CNS?

A

Noradrenaline, dopamine, 5-hydroxytryptemine and acetylcholine

71
Q

A1 noradrenergic receptors

A

Widely distributed and involved in motor control, cognition and fear

72
Q

A2 noradrenergic receptors

A

Involved in the regulation of blood pressure, sedation and analgesia

73
Q

B1 noradrenergic receptors

A

Found in the cortex, striatum and hippocampus
Contribute to long term effects of anti-depressants

74
Q

What neurological disorders is dopamine involved in?

A

Parkinsons disease, schizophrenia, ADD, drug dependance and some endocrine disorders

75
Q

What parts of the brain is dopamine present in?

A

High in the striatum and forms part of the extrapyramidal motor system
Nigrostriatal pathway
Mesocortical and mesolimbic pathway
Tuberohypophyseal pathway

76
Q

What is the purpose of the nigrostriatal pathway?

A

Fine motor control

77
Q

What is the purpose of the mesolimbic and mesocortical pathways?

A

Stereotypical behaviour, perseverance, pleasure-euphoria-reward, motivation and compulsion

78
Q

What is the purpose of the tuberohypophyseal pathway?

A

Pituitary hormone secretion

79
Q

What happens to dopamine following release?

A

Action is terminated by enzymes COMT and MAO which are both found extracellularly and intracellularly by action of reuptake transporters

80
Q

How does reserpine work?

A

Blocks dopamine storage and eventually leads to depletion

81
Q

What is reserpine used for?

A

To positively control the positive symptoms of schizophrenia

82
Q

How do D1 and D5 receptors work?

A

Gs coupled receptors so they stimulate adenylyl cyclase, which then increases cAMP, PKA and protein phosphorylation

83
Q

How do D2, D3 and D4 receptors work?

A

Gi coupled receptors so they inhibit adenylyl cyclase which activates K+ channels, inhibiting VGCC and opposing effects of D1 activation

84
Q

What are the differences in D1 and D2 receptor activation?

A

D1 leads to increased activity in the mesolimbic system and symptoms of schizophrenia
D2 leads to decreased activity in the mesocortical system and contributes to negative symptoms, more pharmacologically important than D1

85
Q

What does the lack of selectivity of dopamine receptor agonists mean?

A

Unwanted side effects as drugs that increase dopamine release will affect all pathways

86
Q

How do amphetamines work?

A

Stimulate secretion of dopamine and noradrenaline by displacing them from vesicles, causing reuptake tranpsorters to work in reverse

87
Q

How does cocaine work?

A

Inhibition of dopamine and serotonin reuptake transporters

88
Q

What are amphetamine-like drugs used to treat? How?

A

Narcolepsy to stimulate wakefulness
ADHD to increase concentration

89
Q

What is schizophrenia?

A

One of the most common and debilitating mental illnesses
Symptoms characterised by disturbances in areas of the brain assocaiated with thought, perception, attention, motor control and emotion

90
Q

What are the positive symptoms of schizophrenia?

A

Hallucinations and voices, paranoia, thought disorders, defects in selective attention, bizarre behaviour, aggression, stereotyped movements and catatonia

91
Q

What are the negative symptoms of schizophrenia?

A

Blunting of emotions, withdrawal from social contacts, flattening of emotional responses, anhedonia, reluctancy to perform every day tasks

92
Q

What are the neurological differences between positive and negative schizophrenic symptoms?

A

Positive are prevalent in young patients and D2 receptors are implicated
Negative are prevalent in elderly patients and D1 receptors are implicated

93
Q

What is selective attention?

A

When a patient appears unable to accomodate or dismiss stimuli of a familar or inconsequential nature
Difficulty in discriminating between significant and insignificant stimuli

94
Q

What are the environmental factors of schizophrenia?

A

Consumption of cannabis in adolescence
trauma

95
Q

Is schizophrenia genetic or environmental?

A

Combination- abnormalities in early life can arise and disrupt normal development of the brain
No single gene is responsible but there is a strong hereditary tendancy

96
Q

What are the structural differences between a healthy brain and a schizophrenic brain?

A

Schizophrenic brains tend to have larger lateral ventricles and a smaller volume of tissue in the left temporal lobe

97
Q

What drugs increase and reduce positive schizophrenic symptoms?

A

Increased by drugs that enhance dopamine signalling
Reduced by D2 blocking drugs

98
Q

How does LSD relate to investigating schizophrenia?

A

LSD is known to produce hallucinations and some schizophrenia like symptoms which provided evidence of the 5HT pathways contributing to disease

99
Q

What pathways are associated with the positive and negative symptoms of schizophrenia?

A

Positive- overactivity of mesolimbic pathway and increased D2 activity
Negative- decreased activity of mesocortical pathway and D1 activity

100
Q

What are the side effects of treating parkinsons with levadopa?

A

Hallucinations

101
Q

What type of drugs are used to treat schizophrenia?

A

Dopamine D2 antagonists
80% occupancy is needed to reduce positive symptoms

102
Q

What are first generation anti-psychotics?

A

Referred to as typical, classical or conventional
Side efffects include motor disturbances form extrapyramidal effects and prolactin secretion

103
Q

What are second generation anti-psychotics?

A

Referred to as atypical and have less extrapyramidal side effects

104
Q

What are the unwanted effects of antipsychotic drugs?

A

Parkinsons disease like symptoms, acute reversible dystonias, slowly developing irreversible tardive dyskinesia, increased prolactin release, sedation, hypotension, weight gain, dry mouth and blurred vision

105
Q

What are the two types of depression?

A

Unipolar- mood always swings in the same direction and is 75% reactive, 25% endogenous
Bipolar- depression alternates with mania, often associtaed with other disorders including anxiety, eating disorders and addiction

106
Q

What is mania characterised by?

A

Excessive exuberance, enthusiasm, self confidence and may be combined with irritability, impatience and aggression

107
Q

What does reactive and endogenous mean in terms of depression?

A

Reactive is associated with stressful lifestyles and accompanied by anxiety and agitation
Endogenous is unrelated to external stresses
Both treated in the same way

108
Q

What parts of the brain are implicated in depression?

A

Prefrontal cortex, amygdala and hippocampus

109
Q

What are the typical symptoms of depression?

A

Anhedonia, negative thoughts, misery, pessimism, irritability, apathy, loss of interest in daily activities, severe loss or gain of weight/appetite, low self esteem and feelings of worthlessness and guilt, sleep disturbances (insomnia or excessive sleep), loss of libido, inability to think or concentrate

110
Q

How is depression qualititively diagnosed?

A

Patients exhibiting depressed behvaiour for more than 2 weeks and symptoms disrupt normal social and occupational function

111
Q

What causes depression?

A

Stressful life events which can include personal loss, financial or professional crises
Genetic risk of 40%
Secondary to illness or side effect of a drug

112
Q

What deep brain structures have antidepressant effects when stimulated?

A

Subgenual cingulate cortex
Nucleus accumbens

113
Q

What mediates susceptibility to social stress?

A

Increased activity dependant release of BDNF within the mesolimbic dopamine circuit

114
Q

How does stress effect the CNS?

A

Decreases the concentrations of BDNF, the extent of neurogenesis, complexity of neuronal processes in the hippocampus, decrease in CREB activity

115
Q

What is BDNF?

A

Brain derived neurotrophic factor helps regulate synaptic plasticity, so it is important for learning and memory

116
Q

What hormones also have an impact on the hippocampus and limbic regions?

A

Ghrelin and leptin- produce mood related changes
Cortisol

117
Q

Why are anti-depressants important?

A

Depression can cause changes in brain chemistry that can only be reversed by those drugs, even if the reason for depression is gone people will stay depressed due to synaptic changes

118
Q

Animal model for antidepressant efficacy

A

Rodents are placed in an inescapable container of water on two occasions
On the second occasion antidepressant drugs increase their escape behaviours

119
Q

Chronic mild stress models

A

Animals subjected to sequence of changing stressors mean they experience unpredictable chronic stress
Observed to develop a range of behavioural, neurochemical and biochemical changes that reflect symptoms of depression

120
Q

How long do antidepressants take to take effect? What does this mean?

A

Neurochemical effects occur within minutes-hours but effects take weeks to develop suggesting secondary adaptive changes in the brain are responsible
Suggests regulatory mechanisms are involved

121
Q

What neurotransmitters are involbved in depression?

A

Deficit in noradrenaline and 5HT
BDNF and TrkB reduced neurogenesis
Glutamatergic NMDA neurodegeneration

122
Q

What brain regions known to control alertness, awareness and emotion are significantly modulated by monoamine projections?

A

Dopamine from ventral tegmental area
Serotonin from dorsal raphe nuclei in periaqueductal grey
Noradrenaline from locus coeruleus

123
Q

What are the different types of antidepressants?

A

MAO inhibitors
Classical tricyclic antidepressants
Selective serotonin reuptake inhibitors
MAO receptor antagonists

124
Q

How do TCAs work?

A

Inhibition of the neuronal uptake of 5HT and noradrenaline

125
Q

How is noradrenaline related to depression?

A

Noradrenaline function includes arousal and attention and mood
Has a role in regulating sensory processing which relates it to withdrawal, increased sleep and anorexia
Inhibition of NA reuptake in the forntal cortex improves mood

126
Q

What are the functions of 5HT/serotonergic pathways in the CNS?

A

Hallucinations, sleep and wakefulness, mood and emotion, Feeding behaviours, sensory pathways and nociception, body temp and vomiting
Role in regulating limbic processing relates it to anhedonia

127
Q

GABA A allosteric agonists and antagonists

A

agonists are benzodiazepines, antagonist is flumazenil

128
Q

Phenytoin

A

Ataxia, skin rashes, vertigo
Complex pharmacokinetics so can’t be taken with other drugs

Pharmacology (5 decks)

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