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PMP202 > CNS week 1 + 2 +3 > Flashcards

CNS week 1 + 2 +3 Flashcards

1
Q

identify key structures in the CNS

A
  • cell body w nucleus of neurones
    -axon
    -myelin
    -dendrite
    -synapse (multiple on each neurone)
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2
Q

what are the key features of the synapse related to drug function?

A
  • pre synaptic neuron
  • post synaptic neuron
    -synaptic cleft
  • neurotransmitters diffuse across the cleft due to influx of calcium
  • binds to two type of receptors (ionotropic + GPCR)
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3
Q

what are some difficulties with drug delivery or targeting in the CNS?

A
  • The Blood brain barrier (BBB)
  • no fenestra and contain tight junctions
  • drugs used are rarely selective
  • diagnosing problems
    -synapses can change - adaptive
  • tolerance and dependence to drugs
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4
Q

features of ionotropic receptors - excitatory synapses

A

transmitter depolarizes and excites
inward positive current (e.g. influx of Na+)
excitatory postsynaptic potential - neurotransmitters are glutamate, aspartate and acetyl choline.

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5
Q

features of inhibitory ionotropic receptors

A

transmitter hyperpolarizes and inhibits
inwards current is negative e.g. influx of Cl-
inhibitory postsynaptic potential - neurotransmitters are GABA and glycine.

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6
Q

main excitatory neurotransmitter

A

Glutamate

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6
Q

key features of GCPR

A
  • coupled to G - proteins
  • can be linked to ion channels
    -linked to enzymes such as adenylyl cyclase and phospholipase C
    -many different types of neurotransmitters
  • has a second messenger
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6
Q

main inhibitory neurotransmitter

A

GABA

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6
Q

what are the key processes by which drugs alter neurotransmission

A
  • precursors (getting raw materials) and biosynthesis of making NTs
    -storage of NT in vesicles of golgi bodies
    -transport via microtubules
  • docking due to influx of calcium allows for exocytosis
    -cross synaptic gap
    -bind to postsynaptic receptors or reuptake mechanisms to recover NT
  • deactivation
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7
Q

how do neurones work and neurotransmission occurs

A
  • generation of action potential by depolarization when reaching threshold by the movement of sodium in and potassium out. (via sodium/potassium ATPase pump or ion channels)
  • starts at -70mv, threshold is -50mv.
  • action potential is then generated.
    -leads to release of neurotransmitter across synaptic cleft.
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7
Q

outline the pharmacological targets for CNS drugs

A

ionotropic receptors (voltage or ligand gated)
metabotropic receptors GPCRs
NT reuptake receptors
enzymes

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8
Q

what is use dependence?

A

targeting open-active confirmation or open-inactive confirmation

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9
Q

what is allosteric modulation?

A

non- competitive antagonism such as glutamate on a allosteric site.

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10
Q

what is the fate of the NT

A
  • bind to receptors pre or post
    -diffuse out of synaptic cleft to other cells
    -metabolise/degrade by enzymes
    -reuptake by pre-synaptic transporters
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11
Q

define epilepsy

A

when ordinary brain activity is disrupted spontaneously and recurrently

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12
Q

classify the different kinds of epileptic seizures

A

Generalised and Focal (partial)

Generalised - seizure activity involves both hemispheres of the brain

Focal - starts in one area of the brain + retains awareness but can evolve to bilateral convulsions

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13
Q

describe how a diagnosis is made for epilepsy and understand the prognosis

A
  • diagnosis is difficult and requires reliable account + use of EEG, MRI/and or CT
  • good prognosis (70-80% become seizure free, 50% withdraw from meds, 20-30% have chronic epilepsy, usually normal function between seizures, 5% will not be able to live alone)
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14
Q

describe the basis of epileptogenesis in relation to balance in neuronal networks

A

occurs when there is an imbalance of excitatory vs inhibitory neurones firing so the synaptic balance is disrupted. Can either be too much excitation and normal inhibition, too low inhibition and normal excitation or too low inhibition and too high excitation.

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15
Q

what is the MOA of anti-epileptic drugs?

A

inhibit abnormal neuronal discharge in epilepsy but don’t resolve the underlying cause

Decrease excitatory mechanisms:
(1) inhibition of Na channel function
(1) inhibition of Ca channel function
(2) directly inhibit glutamate neurotransmission

Increase inhibitory brain mechanism:
(3) enhancement of GABA action (decrease GABA inactivation, increase GABA levels or enhance postsynaptic response)

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16
Q

what is the clinical basis for the use of the most common anti-epileptic drugs?

A
  • to decrease freq or severity of seizures
  • treat symptoms not the condition
  • goal is to maximise quality of life by minimising seizures and S/E
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17
Q

what are some practical clinical aspects of epilepsy management?

A

-surgery
-antiepileptic drugs
-vagus nerve stimulation with a pacemaker
- deep brain stimulation
-ketogenic diets

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18
Q

types of generalised seizures and their characteristics

A

Tonic - clonic convulsions (most common, patient stiffens, falls + convulses, hyper-salivation, tongue biting, lasts a few mins, followed by headache)

Tonic (stiffening of body - head, typically when falling asleep)

Clonic (jerking movements, +/- impairment of consciousness, simultaneous involvement of arms and legs)

Absence attacks (petit mal) (rarer almost exclusively in childhood, goes blank, last a few seconds, child may not be aware of it)

Myoclonic seizures (brief, involuntary jerks, involve head, limbs or whole body, immediate recovery, not always epilepsy)

Atonic seizures (sudden loss of muscle tone, quick recovery, very rare)

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19
Q

Types of focal seizures

A

simple focal (abnormal discharge remains localised, consciousness not impaired, will be the same each time in each person)

Complex focal (automatic behaviours, confusion apparent drunkenness)

Secondarily generalised seizures (simple or complex focal that spreads to whole brain leads to tonic-clonic attack)

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20
Q

what is status epilepticus?

A

a serious uncontrolled seizure that lasts for 5 mins or more or one tonic-clonic seizure followed by another without the person regaining consciousness in between.

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21
Q

define mood disorders and their classifications

A

mood disorders:

Unipolar - major depression or dysthymic disorder (continuous)

bipolar - bipolar I, bipolar II or cyclothymia (mood swings)

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22
Q

examine the characteristics/symptoms and diagnosis of depression

A

mood - predominant emotion (in mood disorders there is an abnormal elevation or lowering of mood)

symptoms + characteristics:
- misery
-pessimism
-feeling of guilt
-lack of motivation
-suicidal thoughts
-indecisiveness
-slowness of action
-loss of libido
-sleep disturbance
-loss of appetite
-weight loss
-GI disturbances

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23
Q

discuss the aetiology of depression

A

unipolar:

reactive depression (75%, associated with stressful event, anxiety and temporary)

Endogenous depression (25%, familial, not related to stressor, recurrent +chronic)

Can be caused by genetic factors, neurotransmitter dysfunction and environmental factors.

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24
Q

describe the role of monoamines in depression

A

dopamine - (reward, motivation, sex)

noradrenaline - (alertness, conc, energy)

5HT - (memory, obsession, compulsion, anxiety)

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25
Q

available treatments for depression

A

-monoamine oxidase inhibitors - inhibits the degradation of neurotransmitters. MAOA (NA and 5HT) MAOB (DA) so increase in neurotransmitters. With SSRI’s can cause serotonin syndrome (fatal)

  • tricyclic antidepressants - affect the transporters by blocking the reuptake of neurotransmitters 5HT and NA transporter blockade. Elevates released amines in synaptic cleft. Can block post synaptic receptors. S/E: can cause sedation, mania, heart block, cardiac arrhythmias and respiratory depression. In vivo can be metabolised to other active compounds, very long half-lives. Metabolised by CYP enzymes so compete with other drugs –> increases TCA toxicity. Drugs can be linked to suicide

-SSRI’s - blocks 5HT SERD transporter specifically. So increases 5HT levels. Most commonly prescribed e.g. prozac, citalopram, fluvoaxamine. Long half-lives + interact with CYP enzymes which may interact with TCAs. Has withdrawal effects so reduced gradually. Safer than TCAs in overdose.

-SNRI’s - non - selective for 5HT and NA transporters.

  • Atypical antidepressants e.g. mirtazapine auto receptor antagonist. Results in NA release by blocking negative feedback. S/E leads to sedation.
  • Rapid-acting antidepressants e.g. ketamine (NMDA receptor antagonist)
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26
Q

what are the catecholamines and their pharmacore?

A

Dopamine
Noradrenaline
Adrenaline

all have catechol ring (benzene 2 hydroxyl side groups)

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27
Q

what is a indolamine and its pharmacore?

A

Serotonin - 5HT

indole ring (six-membered benzene ring fused to 5-membered nitrogen-containing ring)

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28
Q

what is the monoamine hypothesis?

A
  • dopamine and noradrenaline both derived from tyrosine and L-DOPA within neurone

-converted to dopamine

-in noradrenergic dopamine is further converted to noradrenaline

-Norepinephrine transporter and dopamine transporter help with reuptake

  • monoamine oxidase (MAO) and catechol-o-methyltransferase (COMT) enzymes help with the degradation
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29
Q

what happens at the seratonergic synapse?

A

5HT is synthesised via the hydroxylation and decarboxylation of tryptophan

It is inactivated by being taken back up via the SERT and degradation is via monoamine oxidase (MAO)

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30
Q

monoamine theory of depression

A

depression is a result of a functional deficit of 5HT or noradrenaline in the brain and mania is due to a functional excess

drug (reserpine) led to lowering of 5HT and noradrenaline leading to depressive like behaviour

Isoniazid blocked MAO - so elevated mood due to loss of degradation.

Tryptophan pre-curser increased 5HT and gave elevated mood

Inhibiting noradrenaline synthesis led to depressive mood/calm mania

tricyclic antidepressants- elevated mood by blocking amine reuptake

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31
Q

what is the cheese reaction?

A

tyramine normally metabolised by MAO. In high quantities when taking MAO inhibitors can cause severe hypertension

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32
Q

problem with monoamine theory

A

has immediate short-term pharmacological effects, but the clinical effects always take 4-8 weeks to onset.

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33
Q

how do we treat bipolar disorders?

A
  • Lithium (can cause toxicity + needs plasma monitoring)
  • Anticonvulsants
    -Atypical antipsychotics
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34
Q

explain difficulties of molecules crossing the blood brain barrier (BBB)

A
  • the presence of tight junctions.
  • absence of fenestrations
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35
Q

discuss methods of transit across the BBB

A
  • passive diffusion (no energy required, lipid-soluble molecules ,low polar SA, Low MW)
    -active efflux (ATP required, drugs+toxins, transport from endothelium to blood, some bi-directional)
    -CMT (used for polar molecules, genes/carrier proteins)
    -transcytosis (RMT-molecules that are too large to use CMT, AMT - can be positively charged)
    -cells diapedesis (most common WBC + can be manipulated)
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36
Q

what important characteristics play a role for molecules crossing the BBB

A

polar SA < 90
log P 0-3
mw <450g/mol
HBD: 5 or less
HBA: 10 or less
RB: 10 or less

37
Q

discuss chemical strategies involved in drug design and manipulation to allow for effective drug delivery into the CNS

A

lipophilic analogues - adding lipid groups to polar ends of drug molecules.

prodrugs - need to be activated in vivo

chemical delivery systems - inactive chemical derivates that are enhanced/transformed through multisteps (can be enzymatic, site specific enzyme activated, receptor based CDS)(want to add targetor and modifier

  • molecular packaging (forms part of a bulky molecule prevents recognition by peptidases) (increases lipophilicity + prevents enzyme degradation)
38
Q

lipinski’s rule of 5

A

5 or fewer H bond donors
10 or fewer H bond acceptors
molecular weight <500g/mol
Log P < 5
10 or less rotatable bonds

39
Q

describe the pathology of Parkinson’s disease

A
  • linked with aging + more predominant in males
  • <10% of normal dopamine levels in substantia nigra and corpus striatum.
  • corresponding to death of the dopaminergic nigrostriatal pathway.
    -lewy bodies present in CNS and PNS (contain alpha-synuclein)
40
Q

describe symptoms of PD + how they relate to the pathology

A

cardinal symptoms (3 or more for diagnosis) :
-tremor
-bradykinesia
-rigidity
-postural instability
classical symptoms:
-micrographia
-altered posture
-shuffling gait

symptoms though to be due to lack of dopamine in brain, now believed due to misfolding + aggregation of alphaS protein is the primary cause of dopaminergic degradation and cell death in PD. Lewy bodies cause death of neurones and deficiency in dopamine. Impacts the basal ganglia - initiation of movement. Dopamine enhances the direct pathway to the cortex, but inhibits the indirect pathway to the cortex (stimulating movement). In PD direct pathway is downregulated = less stimulation of movement.

41
Q

describe key therapies + relate these to their symptoms in PD.

A
  • replace the dopamine (L-dopa)
    -increase availability to brain AADC inhibitors
    -decrease breakdown using MAO-B inhibitors
    -dopamine agonist (post-synaptic stimulation)
    -anticholinergics for tremor
    -weak dopamine agonist for tremor
42
Q

what are the main types of dementia?

A

Alzheimers
vascular dementia
mixed dementia
dementia with lewy bodies
frontotemporal dementia

the loss of mental processing ability, communication, abstract thinking and physical abilities, such that interfere with daily living

43
Q

symptoms of AD?

A

-memory lapses
-physical abilities affected at later stage 3-20 years
- language deficit
- repetitive behaviour
-visuo-spatial deficits
-impaired judgement
-effects on social function

44
Q

pathologies of symptoms in AD

A

presence of plaques and tangles extra and intracellularly in the brain.

temporal lobe (memory + language) and frontal cortex (intelligence and behaviour) loss of neurones and causes brain to shrink

extracellular plaques (amyloid) - build up of beta amyloid oligomerises and becomes insoluble –> fibrils–> plaques (amyloid hypothesis)

intracellular neurofibrillary tangles (NFTs) contain protein called tau. Naturally occurring protein in axons, abnormally phosphorylated in AD

45
Q

main therapies used for AD

A

acetyl cholinesterase inhibitors (stops breakdown of acetylcholine)
NMDA receptor inhibitors (stops overactivation of NMDA receptors caused by too much glutamate in AD) (reduces excitotoxicity due to calcium influx) e.g. memantine

do not affect underlying disease (beta amyloid), only treats symptoms + no delay in disease progression.

46
Q

causes of AD

A

genetics
mutations in APP
mutations in presenilins
age
hearing loss
head injury
smoking
depression
obesity

47
Q

describe the natural reward and reinforcement pathways in the brain

A

reward is given by a feeling of happiness and is subjective.

reinforcement is more objective and performing a behaviour in order to obtain stimulus (reward).

Rewarding substances and behaviours can lead to addiction.

48
Q

describe the process of dopamine release and its target responses

A

Most rewarding sites in the medial forebrain bundle. Most sensitive area in VTA (ventral tegmental area) from where dopamine is released + communicates to the nucleus accumens.

dopamine is responsible for reward and reinforcement pathway.

acts on D1-D5 receptors (G protein coupled receptors) G stimulatory postsynaptic neurone.

D2 -D4 G inhibitory presynaptic neurone

Dopamine reuptake transporter retakes dopamine to presynaptic neurones.

49
Q

describe the molecular targets of drugs of abuse and how they concurrently affect dopamine release and reward system in the brain

A

increase DA levels in the nucleus accumbens.

cocaine inhibits DA uptake, blocks reuptake of DA. DA transporter target.

amphetamine increases DA release (releases the NT without electrical impulse)

opiates e.g. morphine. Inhibit GABA inhibitory neurones. Leads to more DA.

Cannabis - activation of THC receptor leads to more DA release.

Alcohol - increases excitation of VTA neurones blocking k channels –> increased firing + more stimulus for DA release.

Nicotine - acts on nicotinic ACh receptors + excites VTA neurones + increases glutamate release –> increases DA.

50
Q

describe the key processes by which prolonged/repeated dose of agonists/drugs desensitise the receptors and lead to tolerance

A

curve shifts right side, meaning higher conc of drug is required to see the same response at the receptor.

Repeated exposure means a higher conc is required for the same efficacy. Rightward shift in drug potency (EC50 values)

repeated stimulus causes receptor desensitisation. dopamine binds to receptor –> Intracellular Beta arrestin binds to the G protein –> alpha GTP can’t go back and bind to the receptor. This limits receptor availability. Can also make GPCR undergo endocytosis.

Exhaustion of NTs due to drugs such as cocaine and methaphetamine

pharmacokinetics - altered ADME increased drug metabolism.

51
Q

describe various CNS conditions e.g. Parkinson’s disease and their clinical management

A

PD - chronic neurodegenerative disorder caused by loss of dopamine-containing cells in the substantia nigra. Dystonia, freezing + postural instability (motor symptoms).

Clinical management:

  • older generation antipsychotics, antihistamines (cinnarizine, methyldopa) and antiemetics e.g. metoclopramide inhibit action of dopamine in brain.
52
Q

outline the role of pharmacists in various sectors with regards to these conditions

A

help with management of motor and non-motor symptoms by having the knowledge give medications and optimise therapy. Check with drug and food interactions.

53
Q

state the relevant doses, common s/e and counselling points for various drugs used to treat PD.

A
  • DA precursor e.g. Levodopa (co-carelopa) long term use can result in dyskinesia + missed doses contribute risks of severe complications.
  • DA agonists e.g. pramipexole and ropinirole comes as immediate release + modified release some available via patch if patient has swallowing difficulties. S/E include hypersexuality, binge eating, addictive gambling. Monitor hepatic + renal + CV function.

COMTi - inhibit the breakdown of levodopa e.g. entacapone which can be taken with levodopa

Glutamate antagonists e.g. amantadine used to reduce dyskinesia caused by levodopa

Monoamine oxidase B inhibitors e.g. Rasagline and selegiline used to increase length of time taken for DA to breakdown. Cautioned with use of antidepressants (serotonin syndrome)

54
Q

describe dementia and their clinical management

A

progressive disease that is characterised by changes in behaviour, cognition and memory which reduces the ability to carry out daily activities.

diagnosis made from history, cognitive tests and formal neuropsychological assessment.

Management of moderate dementia:
structured group cognitive stimulation programme, group reminiscence therapy

Management of AD: Donepezil (increase Ach), Galantamine, Rivastigmine

55
Q

outline the role of the pharmacist in various sectors with regards to these conditions (dementia)

A

try to manage them in their own environment (familiar setting)

56
Q

state relevant doses, S/E + counselling points for various drugs used to treat dementia.

A

Donepezil -

Galantamine -

Rivastigmine -

57
Q

What is the dose of donepezil for mild to moderate dementia in Alzheimer’s disease

A

5mg OD for 1 month, increased up to 10mg daily, taken at bedtime

58
Q

when is a prescription for donepezil for elderly inappropriate?

A

Patients with persistent bradycardia
patients with heart block

59
Q

counsel patients on the use of donepezil oral dispersible tablets

A

place on the tongue, allow to disperse, and swallowed

60
Q

when are antiemetics prescribed

A

when there is a known cause of vomiting

61
Q

what treatment can be used for motion sickness

A

a sedative e.g. hyoscine hydrobromide, cinnarizine, cyclizine, promethazine

62
Q

what can be used to treat GI and biliary disease

A

metoclopramide

63
Q

what can be used to treat vomiting in chemotherapy

A

dopamine antagonist e.g. prochlorperazine

64
Q

what can be used to treat vomiting in palliative care

A

antipsychotics e.g. haloperidol and levomepromazine

65
Q

what can be used to treat vomiting post-op

A

5HT3 - receptor antagonists e.g. ondansetron, dexamethasone and haloperidol

66
Q

what can be used to treat N+V caused by opioids

A

cyclizine

67
Q

Describe MHRA advice with metoclopramide

A
  • risk of neurological adverse effects–> restrict dose and duration of use.
    -prescribed for up to 5 days
  • 10mg TDS, max dose 500micrograms/kg
  • S/E: acute dystonic reactions involving facial and skeletal muscle spasms that stop within 24hr of stopping.
68
Q

Describe MHRA advice with the use of Domperidone

A
  • for N+V lack of efficacy in children + reminder of contraindications in adults and adolescents.
    -not for children < 12 yo or <35kg
    -use lowest effective dose for shortest duration possible
    -should not exceed 1 week
  • patients advised on signs of arrhythmia + seek medical attention if palpitation.
  • contraindicated with cardiac disease, GI obstruction + haemorrhage
69
Q

How do you treat nausea + vomiting in pregnancy

A

1- self care advice (hydration, rest and diet)
2- available support groups
3- antiemetics e.g. chlorpromazine, cyclizine and metoclopramide

69
Q

list monitoring requirements for lisdexamphetamine in ADHD

A
69
Q

List important prescribing information that you need to remember for methylphenidate in ADHD

A
69
Q

What are the monitoring requirements for methylphenidate in ADHD

A
70
Q

list the 5 classifications of controlled drugs and what they mean

A

schedule 1 (CD LIC POM) - no therapeutic use, license required for production e.g. LSD

schedule 2 (CD POM) - pharmacists can prescribe includes opiates.

schedule 3 (CD no register POM) - less likely misused, minor stimulants e.g. temazepam.

schedule 4 (CD BENZ POM or CD ANAB POM) -
BENZ: benzodiazepines
ANAB: contains most anabolic steroids + growth hormones

schedule 5 (CD INV POM OR CD INV P) - certain CD preparations that are exempt from full control at specifically low strengths.

70
Q

what drugs require safe custody

A

schedule 2 + 3 under the schedule 2 of safe custody regulations.

71
Q

prescription requirements for schedule 2 + 3 CD

A

signature
date
date when signed
only valid 28 days from appropriate date
prescribers address
name of CD (good practice)
form
strength
dose clearly defined
quantity written in numbers and letters
max quantity should not exceed 30 days.
name + address of patient
marking of prescription

72
Q

describe the symptoms and aetiology of schizophrenia?

A

delusions, hallucinations (positive) or disorganized speech(negative), and reflect an impaired ability to function (cognitive).

2 or more symptoms over 1 month to make diagnosis

  • genetic predisposition
  • environmental insult (none specific)
  • neurodevelopment defect
    -structural abnormalities
    -functional abnormalities
73
Q

describe work on biomarkers - structural and functional changes

A

MRI scans - enlarged ventricles + loss of neuronal tissue
EEG - changes in response to external stimuli

74
Q

discuss the role of dopamine in aetiology and actions of antipsychotics

A

-too much dopamine
- midbrain origin (SN and VTA)
-VTA to hippocampus (mesolimbic pathway)
-VTA to cortex (mesocortical pathway)

action of antipsychotics targets these dopamine pathways to reduce the amount of dopamine. Block the D2 receptor. Higher affinity = better efficacy (how well it blocks D2 dopamine receptor).

typical antipsychotics:

on target S/E: dystonia, sexual dysfunction, tremor, bradykinesia.

non DA off target S/E: sedation, hypotension, dry mouth.

75
Q

discuss the role of 5HT

A

atypical 2nd generation antipsychotics have higher affinity for 5HT2 receptor, less side effects than typical antipsychotics.

Increased levels of 5HT in schizophrenics

76
Q

Discuss role of glutamate

A

neurodevelopment change
disordered migration
synaptic loss
there is reduced glutamate in CSF of patients with schizophrenia

77
Q

Describe various CNS conditions (e.g. Schizophrenia) and their clinical management

A

-most common psychotic disorder which cause positive, negative and cognitive symptoms.

-antipsychotic drugs are usually used and most effective at treating positive symptoms.

-give drug + psychological therapy, start low and titrate up, optimum dose for 4-6 weeks. Only prescribe one at a time, long acting injectables can be used to promote adherence.
-if given a high-dose, only give a single dose and monitor the patient every 15 mins. Monitor vital signs every hour.

78
Q

Outline the role of the pharmacist in various sectors with regards to these conditions (schizophrenia)

A

patient monitoring and ensuring high-dose is last resort.

79
Q

State the relevant doses, common side effects and counselling points for the various drugs used to treat these conditions (schizophrenia)

A

common S/E: extrapyramidal symptoms (tremor, dystonia, akathisia, tardive dyskinesia) with first generation e.g. clozapine, olanzapine.

  • Hyperprolactinaemia. Aripiprazole is a partial agonist so side effects are less and reduces prolactin conc. Can cause sexual dysfunction.
  • first generation are most likely to give sexual dysfunction, aripiprazole is least likely to give this side effect.
    -hypotension can be caused by some second generation drugs.
    -some can give diabetes (second generation)
80
Q

what is neuroleptic malignant syndrome (NMS)

A
  • can be deadly, leads to hyperthermia and antipsychotic must be discontinued.
    -can be treated with bromocriptine and dantrolene
81
Q

Discuss the importance of the structure of Levodopa for activity and the role carbidopa plays in being co-administered

A
  • used for parkinson’s disease
    -precursor for dopamine (decarboxylation in vivo)
  • given with carbidopa to inhibit DOPA decarboxylase, they do not pass the BBB so minimise peripheral degradation.
82
Q

Discuss how the activity of Donepezil relates to its chemical structure and ability to cross the BBB and treat Alzheimer’s Disease

A

Used to treat Alzheimer’s disease
selectively and reversibly inhibits acetylcholinesterase enzyme.

competitive inhibitor of acetylchloinesterase

allows for extra Ach in the body

carrier mediated transport across the BBB

83
Q

Explain the relationship between the structure of methylphenidate to its activity and metabolism in the body

A
  • first line stimulant used to treat ADHD
    non comp inhibitor of dopamine transporter and noradrenaline transporter enters via diffusion.
    -4 active isomers
84
Q

Put into practice the theory of drugs crossing the BBB for other drug classes such as SSRIs

A
85
Q

Describe the physiology and pathophysiology of essential and pathological anxiety

A

-pathological when non-threatening situation is interpreted as threatening
-individuals with anxiety disorder have a higher activity in the limbic system.
-amygdala mainly impacted and responsible for fear perception.
-HPA maintains stress responsiveness through release of ACTH and cortisol.
- start to feel dizzy, increased breathing, increased sweating (increased sympathetic activity)
-ACh is the main neurotransmitter to maintain general arousal.
-GABA inhibits other neurotransmitter pathways.

General causes:
-medical
-drug-induced
-drug withdrawal

86
Q

Discuss the spectrum of anxiety disorders

A
  • Generalised anxiety disorder - motor tension, autonomic hyperactivity
    -Phobic anxiety - simple phobias
    -Panic disorders - acute attacks of fear
    -obsessive-compulsive behaviours - repetitive ideas and behaviours.
87
Q

Describe the pharmacotherapies to treat/manage anxiety

A
  • adrenergic beta receptor blockers (treats symptoms)

serotonergic pathways
- e.g. partial agonist at 5HT receptors Buspirone.
- antidepressants SSRIs e.g. fluoxetine and citalopram
-SNRIs e.g. venflaxine and duloxetine

  • delayed clinical response (3-4 weeks)

GABAergic pathways Glutamate –> GABA by Glutamate decarboxylase. Overdose of GABA drugs can lead to sig resp depression. e.g. benzodiazepines

88
Q

Define anaesthesia and describe the various stages and types of anaesthesia

A

-loss of sensation
-anaesthetic agents - unconsciousness
-neuromuscular blocking agents - muscle relaxation
-analgesics- pain relief

General - loss of sensation throughout the whole body
Regional - loss of sensation to a specific region of the body
Local - small area of the body loses sensation.

89
Q

Describe the types and drugs used in the induction and maintenance of surgical anaesthesia

A

-Inhalation: gasses usually halogenated ethers or hydrocarbons, controllable and rapid
-Intravenous: very rapid onset e.g. thiopental (positive allosteric modulator of GABA) CNS depression

90
Q

Describe the pharmacological mechanisms of general anaesthetic drugs

A
  • lipid theory - more potent if more lipophilic
    They act to enhance inhibitory receptors and inhibit excitatory receptors.
    -closing of Na channels not allowing depolarisation and action potential
91
Q
A

PMP202 (5 decks)

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