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Pharmacology > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

What is the NS divided into?

A

Central NS + Peripheral NS

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2
Q

What is the CNS divided into?

A

Spinal cord - nerves between the brain + periphery NS

Brain stem - connects brain to spinal cord

Brain - divided into hindbrain, midbrain + forebrain

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3
Q

What is the PNS divided into?

A

Autonomic NS - sympathetic NS (fight + flight) + parasympathetic NS (fest + digest)

Somatic NS (voluntary)

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4
Q

Where does the PNS + SNS have OPPOSING factors?

A

Heart, GI + bladder

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5
Q

Where does the PNS + SNS have the SAME factors?

A

Salivary glands

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6
Q

In what tissues does only 1 system represent?

A

Sweat glands + blood vessels (mainly sympathetic)

Ciliary muscle (mainly parasympathetic)

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7
Q

Adrenoceptors are what type of receptors?

A

G-protein coupled receptors

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8
Q

What are the key + ancillary symptoms of depression?

A

Key features

  • low mood
  • Anhedonia (lack of pleasure)
  • lack of energy

Ancillary symptoms (may be there)

  • sleep (hypersomnia (too much) or asomnia (too little)
  • weight
  • appetite change
  • low self esteem
  • guilt
  • suicidal thoughts
  • difficulty in concentration
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9
Q

What are the 2 types of depression?

A
  • unipolar (mood always low with thoughts of suicide)

- bipolar (mood swings: low (depression), high (mania)

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10
Q

What is necessary for a diagnosis of depression?

A

Min 2 weeks, min 2 key symptoms + 3 ancillary

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11
Q

What are the 3 main NT involved in depression?

A

There is a functional deficiency in CNS monoamine transmission

NA
-attention 
-motivation
-pleasure
-reward
(When stressed, you release more NA = pay more attention

Dopamine (DA)

  • pleasure/reward
  • energy
  • alertness

Serotonin

  • mood
  • development of obsessions + compulsions
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12
Q

What are the main causes of depression?

A
  • family history
  • stress
  • +/- events
  • certain medication
  • chronic alcohol use
  • imbalance of chemicals in brain
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13
Q

How can we modify transmission?

A
  • block re-uptake (antagonist) = increase NT in synapse
  • activate receptor (agonist)
  • increase released NT
  • block calcium channels = NT can’t be released
  • act on synthesis + storage of NT
  • use drugs which act on enzymes which breakdown NT
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14
Q

What is synaptic plasticity?

A

Long term adaption (e.g. gene regulation)

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15
Q

What is neurogenesis?

A

Generation of new neurones, mostly responsible for synaptic plasticity

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16
Q

What is neuromodulator?

A

Mediator that cats by modulating e.g. facilitating action of NT

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17
Q

What is neurotrophic factor?

A

Regulate the growth + development of neurones

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18
Q

What do tricyclic antidepressants do?

A
  • NA + serotonin reuptake inhibitors e.g. imipramine + amitriptyline
  • block alpha 1 = alpha 1 expressed in blood vessels = postural hypotension
  • predominantly NA reuptake inhibitors e.g. desipramine
  • block receptors for ACh
    • block peristalsis = constipation
    • block salivary production = dry mouth
    • block H1 = sleepiness
  • give active metabolites (breakdown molecules but keep them active)
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19
Q

What are the 3 types of TCAs?

A

NA-selective e.g. desipramine

Non-selective (close to 1) e.g. amitriptyline (blocks serotonin + NA equally)

Serotonin-selective (SSRIs) e.g. citalopram

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20
Q

What phase 1 enzyme is responsible for metabolising 1/4 of all clinical drugs? What does this mean?

A

CYP2D6

Higher risk of drug interactions, as lots of different drugs uterlise same enzyme

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21
Q

What does polymorphic mean?

A

You can have lots of variants of the gene

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22
Q

What is pharmacogemomics?

A

Area of pharmacology that studies the genetic variance of enzymes involved in drug metabolism

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23
Q

What are the 4 types of genertic variance?

A

Non-functional

  • e.g. CYP2D6*4
  • will express an enzyme that is either slow/non functioning
  • the phenotype, the pt would be called POOR METABOLISER
  • there is a high concentration of drug in blood = more side effects + toxicity

Reduced function

  • e.g. CYP2D6*10
  • phenotype would be an INTERMEDIATE METABOLISER
  • rate of functioning slower

Fully functional

  • e.g. CYP2D6*1
  • phenotype would be an extensive metaboliser

Multiplied gene

  • e.g. CYP2D6*2xN (gene multipled)
  • phenotype would be an ultra-rapid metaboliser
  • rapidly broken down into metabolites = little therapeutic effect
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24
Q

What is the effect of SSRIs being active metabolites?

A

The effect stays for longer because the metabolism of the antidepressant leads to another antidepressant

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25
Q

Where is serotonin produced?

A

1% produced in brain, rest in periphery = has an important role in platelet aggregation

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26
Q

What are the effects of serotonin syndrome?

A
  • diaphoresis (pallor)
  • agitation
  • tachycardia
  • clonus movement (mixture of contracting + relaxing of libs esp lower limbs
  • tremor
  • hyperthermia
  • hyperreflexia
  • increased bowel sounds (may have diarrhoea)
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27
Q

What drugs or combo of drugs cause serotonin syndrome?

A
  • Opioids e.g. tramadol taken alongside MAOi
  • MAOi + SSRIs
  • Ecstacy overdose
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28
Q

What are SNRIs? And what is there side effects?

A

Serotonin/NA re-uptake inhibitors e.g. duloxetine

  • lower doses inhibit serotonin re-uptake
  • larger doses inhibit serotonin + NA

SE

  • N
  • anxiety
  • insomnia
  • sexual dysfunction
  • gastric upset
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29
Q

What is tyramine and what is it’s effect on cardiovascular system?

A

Tyramine is produced in GI tract
It can combine with NA re-uptake molecule and be transported inside presynpatic termination of norageneric neurone to be metabolised = increased release NA

The more tyramine accumulated the more NA released = tachycardia, increased HR

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30
Q

What do MAOi do? And what are the side effects?

A

Inhibit enzyme MAO (breaks down main monoamines + tyramine) = more monoamines + tyramine (restriction on food that contains tyramine e.g. cheese) = hypertension

SE

  • N
  • headache
  • stiff neck
  • dry mouth
  • drug/food interaction
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31
Q

What is the 1st choice for antidepressants?

A

SSRIs e.g. fluoxetine = less side effects

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32
Q

What are the side effects of SSRIs?

A
  • N
  • anxiety
  • insomnia
  • sexual dysfunction
  • gastric upset
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33
Q

What is lithium used for?

A

Treatment of mania, bipolar or unipolar recurrent disorder.
Has narrow therapeutic range =dangerous drug

SE

  • N+V
  • diarrhoea
  • polyuria
  • hair loss
  • weight gain
  • enlarged thyroid
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34
Q

What other drugs are used to treat bipolar depression?

A

Antiepileptics

  • e.g. carbamazepine
  • blocks Na+ channels
  • better tolerance than lithium
  • SE; diarrhoea, N, hair loss, weight gain

Antipsychotics

  • e.g. risperidone
  • SE; agitation, blurred vision, Parkinsonian symptoms, drowsiness, dizziness, hypertension, GI disturbances, hyperglycaemia + hypercholesterolemia
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35
Q

What is anxiety?

A

An unpleasant state on tension, apprehension or uneasiness that seems to arise from an unknown source

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36
Q

What is an anxiety disorder?

A

An abnormal response that it umpires daily activity

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37
Q

What are the different classifications of anxiety?

A
  • generalised anxiety disorder
  • panic disorder
  • social phobia
  • OCD
  • PTSD
  • phobias - specific to particular que e.g. acrophobia (fear of open spaces)
38
Q

What NTs are involved in anxiety?

A

NA, serotonin + GABA

39
Q

What happens when GABA binds to a GABA receptor on chloride ion?

A
  • causes shape modification = opens chloride channel
  • chloride enters cell = makes potential inside more negative (more hyperpolarised state makes it harder to induce an AP).
40
Q

Why are benzodiazepines used to treat anxiety?

A

They are neuromodulators, that don’t act directly, but modify GABA transmission. Only facilitate action of GABA.
Positive allosteric modulation of GABA A receptor.

Only alpha 1,2,3,5 are BZ sensitive. If GABA A has alpha 4 or 6 BZs won’t bind (means BZs won’t act on certain tissues).

BZs bind to GABA on another site (allosteric modulation). = Makes GABA more effective as it binds to receptors for longer

Causes;

  • Reduction of anxiety, aggression
  • induction of sleep (hypnotic)
  • reduction of muscle tone (acting on spinal cord)
  • anticonvulsant effect

Overdose - only certain amount of GABA, so cause side effects e.g. sleepiness, resp depression

41
Q

Barbiturates are also prescribed for anxiety, depression. Why is overdose of barbiturates much worse then BZs?

A

High doses of barbiturates can open chloride channels, when BZs can’t

42
Q

BZs are classified on duration of effect, what are the 3 classifications?

A 
Short acting (3-5h)
-e.g. triazolam

Intermediate (6-24h)
-e.g. lorazepam

Long acting (24-72h)
-e.g. diazepam
43
Q

What are the side effects of BZs?

A
  • drowsiness, confusion, amnesia
  • minimal CV/resp depression
  • tolerance + dependence
  • withdrawal symptoms (rebound insomnia)
  • prolonged sleep (overdose - flumazenil antidote)
44
Q

What are the interactions of BZs?

A
  • CNS depressants e.g. alcohol, barbiturates, antihistamines (increase effect of BZs)
  • cytochrome P450 inhibitors e.g. cimetidine (increase side effects)
  • CYT P450 inducers e.g. rifampicin (reduce therapeutic effect)
45
Q

When are BZs contraindicated?

A
  • acute pulmonary insufficiency
  • sleep apnea
  • neuromuscular respiratory weakness
  • unstable myasthenia gravis
46
Q

What other drugs are used to treat anxiety?

A

SSRIs e.g. fluoxetine

  • uses; depression, anxiety disorders, OCD, phobia
  • they are selective serotonin reuptake inhibitors

TCAs

  • uses; depression, anxiety with depression, panic attacks
  • they are serotonin + NA reuptake inhibitors

Buspirone

  • uses; mild anxiety, NOT for panic attacks
  • 5-HT1A partial agonist (increase action of serotonin in brain)

beta blockers e.g. propranolol

  • uses; phobias
  • work by blocking beta receptors of sympathetic system

Zolpidem + zaleplon

  • uses; sleep disorders
  • action similar to BZs
47
Q

What is psychosis, and what are the important types?

A

It’s an abnormal condition of the mind, causing chronic disordered thinking + disturbed behaviour.

Most important types;

  • Schizophrenia
  • affective disorders (mania)
  • organic psychosis e.g. alcoholism
48
Q

What are the positive + negative symptoms of schizophrenia?

A

Positive symptoms (caused by hyperaction of doperminergic receptors e.g. in some neurones of mesolimbic pathyway)

  • delusions
  • hallucinations
  • combativeness
  • insomnia

Negative symptoms (caused by deficiency of dopamine in the mesocortical pathway)

  • poor speech
  • Social withdrawal
49
Q

What are the 4 main types of DA pathway?

A

Mesolimbic
-regulates emotions, behaviour, role in pleasure

Mesocortical
-regulation of behaviour

Nigrostriatal
-regulation of movements

Tubero-infundibular
-regulation of certain hormones

50
Q

Antipsychotics are used to treat SCZ, how do they work?

A

Act on CNS by;
- block D2 receptors on;
- mesolimbic system = sedation + antipsychotic impaired performance
- nigrostriatal System = gives extra-pyramidal side effects (EPSs) =
effects motor coordination in extra-pyramidal system). Gives effects
similar to Parkinson’s (Parkinsonism)
- tubers-infundibular System = effects pituitary gland; causes
endocrine effects e.g. impotence, weight gain + gynaescomastia
-blocks musclarinic receptors = dry mouth, constipation
-blocks alpha receptors = hypotension
-blocks histamine + serotonin = sedation

51
Q

What are antipsychotics classified into?

A

Typical (1st gen e.g. haloperidol)

  • has extra-pyramidal effects
  • less effective on negative symptoms

Atypical e.g. clozapine, risperidone

  • has LESS extra-pyramidal effects
  • more effect on negative symptoms
52
Q

What are psychostimulants classified into?

A

-respiratory stimulants e.g. doxapram (used for post anaesthetic
resp depression
-convulsants
-psychomotor stimulants e.g. amphetamine, modafinil (increase DA + NA release)
-hallucinogens or psychotomimetic drugs

53
Q

What are the clinical uses of psychostimulants?

A
  • ADHD e.g. detamphetamine
  • apnoea of premature
  • narcolepsy e.g. modafinil

Side effects;

  • euphoria, insomnia, anorexia + psychosis
  • tolerance + dependence
  • hypertension, inhibition of GI motility
54
Q

What are methylxanthines?

A

They are a psychomotor stimulant. Antagonism of A2 receptors
E.g. caffeine, theophylline

Uses;

  • caffeine + aspirin for pain
  • caffeine + ergotamine for migraine
  • caffeine + apnoea for prematurity
  • theophylline as bronchodilator
55
Q

How do cognition enhancers work and what are there uses?

A

E.g. piracetam
Increases motivation, concentration, memory + cognitive. Reduces fatigue.

MOA

  • increases blood flow
  • supports neural metabolism
  • enhancement of neurotransmission

Uses;

  • AD
  • dementia
  • mild cognitive impairment
  • brain surgery
56
Q

What are chronic neurodegenerative diseases caused by?

A

Protein misfolding + consequent aggregation. This is because misfolding causes hydrophobic residues that are normally buried in the core of the protein to be exposed on its surface = gives strong tendency of molecule to stick to cell membrane + aggregate.

In NS aggregates often form structures known as amyloid deposits.

If the result is a large insoluble aggregate the neurones die. Dead neurones in the CNS are NOT replaced, nor can there terminals regenerate when there axons are disturbed.

E.g. AD (beta-amyloid misfolding), Huntington’s Disease (Huntingtin misfolding)

57
Q

What protective mechanisms does the brain have that limits the accumulation of protein aggregates?

A
  • chaperone proteins - bind to newly synthesised or misfolded proteins + encourage them to fold correctly.
  • uniquitination reaction - prepares the protein for destruction within cell

Accumulation of protein deposits occurs when the protective mechanisms are unable to cope.

58
Q

How are misfolded proteins usually removed?

A

Intracellular degradation pathways

59
Q

What are the 2 main systems in CNS involved in motor coordination + postural tone?

A
  • pyramidal

- extraparamadal. Causes; rigidity, tremor, hypokinesia, postural instability

60
Q

What are some features of PD?

A
  • onset usually >50
  • slowly progressive
  • stooped posture
  • bradykinesia
  • reduced blinking + inability to show emotions
  • tremors
  • mental deterioration
  • muscle rigidity
  • depression
  • shuffling gait
  • rarely occurs in black population
61
Q

What’s the pathophysiology of PD?

A

-Progressive degeneration of DA neurones in nigrostriatal
pathway = means you lose doperminergic inhibition + also get
excess stimulation of cholinergic neurones = causes imbalance of DA/
ACh = loss of muscle tone + coordination of movements
If pt loses >80% of neurones in this pathway = Parkinsonism symptoms
-2 NT involved in regulation of motion;
- DA = inhibits cholinergic neurones , regulate voluntary + involuntary
movement, inhibits ACh neurones
-ACh = excitatory

62
Q

What are the 2 types of PD?

A

Primary
-maybe genetic

Secondary

  • infection
  • trauma
  • drugs
63
Q

What is PD treatment aimed at?

A
  • increasing DA
  • decreasing ACh

To restore balance to DA/ACh

64
Q

What drugs are used in neurodegenerative diseases?

A
  • dopaminergic drugs e.g. levodopa
  • anti musclarinic drugs = reduces ACh effect
  • MAOb e.g. selegiline
65
Q

How can you increase doperminergic transmission?

A
  • Give levodopa in doperminergic neurones = transformed to dopamine
  • block enzymes that break down dopamine
  • activate dopamine receptors
66
Q

How is levodopa broken down?

A
  • 70% metabolised in GI tract
  • 30% absorbed
    • 27-29% metabolised in peripheral tissue
    • only 1-3% crosses BBB + reached brain
67
Q

What are the adverse effects of levodopa?

A

Initial

  • postural hypotension
  • N+V
  • cardiac arrhythmias - dopamine is precursor of NA = more dopamine = more NA
  • exacerbation of asthma

Prolonged

  • abnormal movements
  • cognitive effects
  • anxiety, psychosis, confusion
  • inappropriate sexual behaviour
68
Q

Why do you give levodopa nor dopamine?

A

Dopamine can’t cross BBB but levodopa can, so if you gave dopamine, you would only get peripheral effects

69
Q

What are the drug interactions with levodopa?

A
  • antipsychotics esp 1st gen, block action of levodopa by blocking D2 receptors
  • anticholinergics -reduce absorbed of levodopa from stomach
  • non-specific MAOi - prevents degradation of peripherally synthesised DA = hypertension
70
Q

Why is levodopa effective at start of PD but not near the end?

A

Levodopa needs neurones to convert to dopamine. However, as PD progresses, fewer neurones survive.

71
Q

What are the 2 proteins involved in AD?

A

Beta amyloid and neurofibrillary tangles

72
Q

What changes occur in brain of someone with AD?

A
  • shrinking of hippocampus
  • shrinking of cerebral cortex (impaired cortex)
  • enlarged vesicles
73
Q

What are the treatments of AD?

A
  • NMDA antagonist e.g. memantine. It mimics the action of glutamate which normally works on that receptor. It excites cells
  • cholinersterase inhibitors e.g. donepezil. acetylcholinesterase breaks down ACh = increase ACh (important for memory + cognitive processes)
74
Q

Epilepsy is categorised into what 2 categories?

A
  • convulsive (violent, involuntary muscle contraction)

- non-convulsive

75
Q

When are seizures classified as epilepsy?

A

When seizures are chronic + recurrent

76
Q

How to seizures come about?

A

When a set of neurones depolarise at high rates with sincronised acitivity. If it starts at particular part of brain = foci. It can spread + propagate to rest of body.

  • focal onset
    • motor
    • non-motor (absence)
    • focal to bilateral tonic clonic
  • generalised onset (start everywhere and at same time)
    • motor = tonic clonic or other motor
  • unknown onset
    • motor

If it starts on a particular part + spreads to rest of brain = called secondary generalised (secondary to focal onset).

77
Q

How are seizures diagnosed?

A

Using electroencephalography, it detects electrical activity of cortex

78
Q

What are the 2 classifications of epilepsy?

A

Generalised - both hemispheres, convulsive or not

  • tonic-clonic (grand mal)
    • tonic phase = sustained powerful muscle contraction
    • clonic phase = alternating contraction + relaxation of muscles
  • absence (petit mal)

Partial (localised)

  • only one side of brain
  • if there’s motor disturbance, generally affects opposite side of body
    • simple
    • complex
79
Q

What are the 4 glutamate receptors?

A
  • NMDA - slow excitatory
  • AMPA - fast excitatory
  • kainate - fast excitatory
  • mGlu - regulate synaptic transmission
80
Q

What are the antiepileptic drugs?

A

Na+ channel blocker e.g. carbamazepine, phenytoin

  • uses; partial, generalised seizures
  • 🙁 affects immune system cells, N + visual disturbances
  • Ca2+ channel blocker e.g. valproic acid
  • increase GABA neurotransmission e.g. BZs
  • NMDA blockade e.g. felbamate
  • glutamate blockade e.g. lamotrigine
81
Q

What are the 2 main types of drug abuse?

A
  • hard - lead to physical addiction, more dangerous e.g. alcohol, nicotine
  • soft - no physical addition, still at risk of psychological dependence e.g. cannabis, LSD
82
Q

What causes the rewarding effect of drugs?

A

Increase in DA in the mesolimbic system

83
Q

What is the replacement from for opioids?

A

Methadone

84
Q

What is the drug interaction between Amiodarone + amitriptyline?

A

Both prolong QT

85
Q

What enzyme breaks down GABA?

A

GABA transaminase.

This is inhibited by vigabatrin (used in epilepsy)

86
Q

What does binding of GABA to GABAA do?

A

Increases Cl- permeability = hyperpolarises the cell =reduces its excitability

87
Q

What does binding of GABA to GABAB do?

A

Inhibits calcium channels + opens potassium channels = reducing excitability

Baclofen is a selective inhibitor at GABAB receptor + is muscle relactant

88
Q

What does Gabapentin do?

A

Can increase GABA release or decrease removal

89
Q

To reduce unwanted conversion of levodopa, what can it be combined with?

A

Carbidopa

90
Q

What are the side effects of levodopa?

A
  • conversion to dopamine in peripheries causes N+V due to stimulation of the CTZ
  • postural hypotension due to peripheral vasodilation
  • dyskinesia
  • GI bleeding
  • SCZ like syndrome
91
Q

What do catechol-O-methyltransferase inhibitors do in treatment of SCZ?

A

Inhibit enzyme that breaks down about 30% of levodopa

Pharmacology (11 decks)

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