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Medicine year 2 semester 2 > Case 22- dementia treatment > Flashcards

Case 22- dementia treatment Flashcards

1
Q

The classes of taste receptors

A

There are two classes of taste receptors – ligand-gated ion channel and G-protein coupled receptor.
Taste cells release neurotransmitters that depolarise the primary sensory neurons

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2
Q

AD treatment- Galantamine

A

Found in bulbs of several plants, AChE inhibitor and acts on nicotinic ACh receptors as a Positive Allosteric Modulator which increases the ionic flow through the receptors. Lower affinity than other AChEI’s however, this is then combined with its effect on nicotinic receptors. Binds to allosteric site on alpha subunit of nicotinic AChR and promotes opening at physiologically relevant concentration (0.1-1µM) - recommended daily dosage 16 to 24 mg

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3
Q

Memantine- NMDA receptors open channel blocker

A
  • Binding site is inside channel, so only binds when the channel is open
  • Uncompetitive, low-affinity, open-channel blocker; it enters the receptor-associated ion channel preferentially when it is open for a long duration.
  • Off-rate is relatively fast so that it does not substantially accumulate in the channel to interfere with normal synaptic transmission
  • Acts preferentially on extra-synaptic receptors, which measure glutamate in the system
  • Thought to reduce glutamate mediated cell death
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4
Q

Memantine- clinical use

A
  • Modest effect in moderate-to-severe Alzheimer’s disease and in dementia with Lewy bodies
  • Little evidence of effect on mild Alzheimer’s disease
  • For patients who are intolerant of or have a contraindication to AChE (acetylcholinesterase) inhibitors or those with severe Alzheimer’s disease.
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5
Q

Side effects of Donepezil

A

Approved for- all stages

Side effects- nausea, vomiting, loss of appetite, muscle cramps and increased frequency of bowel movements

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6
Q

Side effects of Galantamine

A

Approved for- mild to moderate dementia

Side effects- nausea, vomiting, loss of appetite and increased frequency of bowel movements

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7
Q

Side effects of Memantine

A

Approved for- moderate to severe

Side effects- headache, constipation, confusion and dizziness

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8
Q

Side effects of Rivastigimine

A

Approved for mild to moderate dementia

Side effects- nausea, vomiting, loss of appetite and increased frequency of bowel movements

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9
Q

Side effects of Memantine and Donepezil

A

Approved for- moderate to severe

Side effects- nausea, vomiting, loss of environment

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10
Q

Principles of Parkinson’s medication

A

No medications to slow down the progression of Parkinson’s disease. Most of the motor symptoms are due to the lack of dopamine.

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11
Q

Parkinsons- Medical treatment

A
  • Dopamine replacement therapy– Levodopa, Dopamine agonists
  • Reduction of Levodopa/Dopamine Breakdown- Catechol-O-methyltransferase (COMT) inhibition, Monoamine oxidase isoenzyme type B (MAO-B) inhibition
  • Anticholinergics- stop tremor but can cause cognitive issues
  • Amantadine- doesn’t stop motor symptoms but can stop the Levodopa induced dyskinesia
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12
Q

Dopamine replacement therapy

A

Levodopa exerts in affects through conversion to dopamine by the enzyme AADC (Aromatic L-amino acid decarboxylase)

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13
Q

Levodopa preparation- Standard release preparation

A

Quick effects after intake:
• Sinemet (levodopa/carbidopa)
• Madopar (levodopa/ benserazide)
• Stalevo (levodopa/benserazide/entacapone)

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14
Q

Levodopa- slow release preparation

A

Provides a more constant level during the day but doesn’t reach high concentrations:
• Sinemet CR (levodopa/carbidopa)
• Madopar CR (levodopa/ benserazide)

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15
Q

Levodopa preparations- Intestinal gel

A

Intestinal gel for use with enteral tube- Duodopa (levodopa/carbidopa), more powerful especially in patients who don’t have good absorption of Levadopa.

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16
Q

Parkinson’s- Dopamine replacement therapy

A

Dopamine agonists= D2 like receptor agonistic activity produces the symptomatic antiparkinsonian effect. Can cross the blood brain barrier and bind directly to the Dopamine receptors. Not as effective as Dopamine, active on only some receptors. Mimic dopamine.

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17
Q

Parkinsons- Dopamine agonist preparations

A
  • Oral preparations= Pergolide, Cabergoline, Bromocriptine, Lisuride, Pramipexole, Ropinirole
  • Subcutaneous- Apomorphine
  • Transdermal- Rotigotine, used if the patient has problems with absorption
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18
Q

Parkinson’s pharmacokinetics- reduction of Levodopa/Dopamine breakdown- COMT

A

Catechol-O-methyltransferase (COMT) inhibition= COMT inhibition reduces the metabolism of levodopa, extending its plasma half life and prolonging the action of each levodopa dose. Reduces peripheral breakdown, more Levadopa can be converted into Dopamine
Oral preparation= Entacapone, Opicapone, Tolcapone
Tolcapone can cause liver toxicity

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19
Q

Parkinsons pharmokinetics- reduction of Levodopa/Dopamine breakdown (MAO-B)

A

Monoamine oxidase isoenzyme type B (MAO-B) inhibition= MAO-B inhibtion prevents the breakdown of dopamine, leading to greater dopamine availability
Oral preparation= Selegiline, Rasagiline, Safinamide

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20
Q

Surgical treatment for Parkinsons

A
  • Ablative surgery
  • Deep brain stimulation- used in advanced Parkinsons. Provides an electrical current to the Subthalmic nucleus, Internal globus pallidus and the Pedunculopontine nucleus. This resets these structures, reducing activity and improving symptoms. Reduce bradykinesia, tremor and rigidity.
  • Striatal grafts
  • Infusion of neurotrophic factors
  • Gene therapy
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21
Q

Surgical treatment for Parkinsons

A
  • Ablative surgery
  • Deep brain stimulation- used in advanced Parkinsons. Provides an electrical current to the Subthalmic nucleus, Internal globus pallidus and the Pedunculopontine nucleus. This resets these structures, reducing activity and improving symptoms. Reduce bradykinesia, tremor and rigidity.
  • Striatal grafts
  • Infusion of neurotrophic factors
  • Gene therapy
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22
Q

Parkinsons- dopamine supplementation

A
  • DA precursors= L-DOPA
  • DA agonists
  • Agents that protect L-DOPA and DA
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23
Q

L-DOPA

A
  • Readily absorbed from the GI tract
  • Poor access to the brain, only 1% enters the CNS
  • Metabolised in the liver and periphery to Dopamine (and then to NE and adrenaline) by DOPA- decarboxylase
  • Usually given with carbidopa (which inhibits DOPA-decarboxylase) and/or COMT inhibitors to improve its availability
  • Secreted in the urine
  • Primary way to manage Parkinsons symptoms
  • Fluctuations in drug levels cause On and Off symptoms. They can get relieve but not too much dopaminergic stimulation, there dopamine levels can then drop and they get the typical negative Parkinson’s symptoms.
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24
Q

L-DOPA On and Off symptoms

A
  • Initially the patient responds well to L-DOPA and dopamine agonists
  • Over time patients develop motor fluctuations, due to fluctuating medication and dopamine levels
  • Motor fluctuations oscillate between ‘off’ times and ‘on’, brief time in between where there is no symptoms. About 40% of Parkinsons patients will experience motor fluctuations within 4-6 years of onset. You get Dyskinea in the ‘On’ periods.
  • These fluctuations are not just for the motor symptoms also sensory, autonomic (i.e. urinary incontinence and profuse sweating) and psychiatric symptoms which can be more disabling then motor changes
  • Controlled release levodopa was developed to double the duration of the effect but only some patients benefit and the decrease in ‘off’ time is modest, and for some dyskinesias become more severe as the dopamine levels increased
25
Q

Dopamine agonists- Ergot class

A
  • Dopamine agonists i.e. Ropinirole become the most popular choice of therapy especially for early stage Parkinsons. Directly stimulates the Dopamine receptors
  • They stimulate dopamine receptors and have a longer lasting effect than levodopa
  • Ergot class i.e. Bromocriptine- D2 agonists also active at 5HT and adrenergic receptors, less commonly used due to side effect profile
26
Q

Dopamine agonists- Non-ergot and Apomorphine

A
  • Non-ergot i.e. Ropinirole, pramipexole- oral, 6h halflife, CYP metabolism. Most common DA agonists for PD, D2 agonist, some 5HT activity (less). Some efficacy in PD depression.
  • Apomorphine- morphine derivative with no action at opioid receptors. Injected agent. Strong emetic. Strong D2, moderate D1, 5HT and adrenergic agonist. Rapid acting, used as rescue treatment the on time is for 5-12 minutes and maintains the effect for all area- motor, sensory and psychiatric for a period of 30 to 120 minutes. Very effective at relieving symptoms, used when patients want a clear time when they will be symptom free
27
Q

Parkinson’s pharmacokinetics- Dopamine protectors locations

A
  • Entacapone, tolcapone and carbidopa protect Dopamine in the periphery- COMT
  • Selegiline (low dose) rasagiline and Tolcapone protect Dopamine in the CNS- MAO-B
28
Q

Parkinson’s pharmacokinetics- dopamine protectors, Mono amine oxidase B inhibitors

A
  • Mono amine oxidase B inhibitors- Selegiline, Rasageline
  • Mono amine oxidase B inhibitors normally break down Dopamine in the CNS (striatum)
  • The main difference is the drug metabolites, the old formation selegiline created amphetamine metabolites through first pass metabolism the newer oral dissolving tablets bypass this
  • Early promotion of rasagiline suggested neuroprotective action if given early but there is no good supportive data
29
Q

Parkinson’s pharmacokinetics- Carbidopa

A

A dopamine protector which reduces the amount of levodopa required to produce a given response by about 75%. Stops the breakdown of levodopa and reduces levodopa side effects.

30
Q

COMT inhibitors- Dopamine protectors

A
  • Entacapone- rapid oral absorption, reaches peak plasma concentration in around an hour. Elimination by metabolism- fecal
  • Tolcapone- rapidly absorbed orally with peak plasma concentration in around 2 hours. The half life is 2-3 hours. Urine and fecal elimination
31
Q

Drugs targetting dopamine in Parkinson’s disease

A
  • L-DOPA and Carbidopa- increases dopamine synthesis
  • Monoamine Oxidase inhibitors- Selegiline, Rasagiline, inhibits dopamine breakdown/metabolism
  • COMT inhibitors- Entacapone, inhibits L-DOPA and dopamine breakdown
  • Dopamine D2 receptor agonist- Pramipexole, ropinirole, rotigotine, apomorphine. Causes a direct effect on post synaptic dopamine receptors
32
Q

Parkinson’s- Anticholinergic drugs (muscarinic antagonists)

A

Benztropine, normalises the imbalance in DA/ ACh by inhibiting Ach transmission.

33
Q

Types of Dopamine agonists

A
  • Ergot derivatives i.e. bromocriptine, pergolide

* Non-ergot derivatives i.e. ropinirole, pramipexole

34
Q

Combinations of L-dopa and dopa decarboxylase

A

• + carbidopa = co-careldopa
• +benseraside = co-beneldopa
Early and excessive use of L-DOPA is associated dyskinesias especially in younger patients.

35
Q

Effects of Levodopa

A

1) More improvement in motor symptoms
2) More improvements in activities of daily living
3) More motor complications
4) Fewer specified adverse events

36
Q

Effects of dopamine agonists

A

Less improvements in motor symptoms
Less improvements in activities of daily living
Fewer motor complications
More specified adverse events

37
Q

Effects of monoamine oxidase- B (MAO-B) inhibitors

A

Less improvements in motor symptoms
Less improvements in activities in daily living
Fewer motor complication
Fewer specified adverse events

38
Q

First line treatment recommendations

A
  • Offer Levodopa to people in the early stages of Parkinson’s disease where the motor symptoms impact their quality of life
  • Consider a choice of dopamine agonists, levodopa or monoamine oxidase B (MAO-B) inhibitors for people in the early stages of Parkinsons disease whose motor symptoms do not impact their quality of life
  • Do not offer ergot-derived dopamine agonists as first line treatment for parkinsons disease
39
Q

Treatment for advanced Parkinson’s

A
  • Apomorphine (subcutaneous)- penject or continuous
  • Duodopa- tube which delivers medication to the jejunum. Invasive, the tube can get blocked. Can lead to vitamin B12 deficiency
  • Deep brain stimulation- via the thalamus, globus pallidus (interna) and subthalmic nucleus
40
Q

Problems with L-DOPA

A
  • High levels of aromatic amino acid decarboxylase/DOPA decarboxylase in the periphery
  • The majority of L-DOPA gets metabolised in the periphery so it needs to be given at very high concentrations in order to reach the brain
41
Q

Side effects of Antiparkinsonian drugs

A
  • Ergot agonist related valve disease
  • Addictive behaviour and dopamine agonists
  • Livedo reticularis associated with amantadine
42
Q

SPECT vsPET

A

SPECT is cheaper but produces imaged that are comparatively poor contrast

43
Q

Areas of the brain- function

A 
Right parietal cortex lesions- the left side of space doesn't exist
Language- frontal and temporal areas
Memory- medial part of the temporal lobe
Spatial and perceptual- parietal lobe
Executive function- frontal lobe
44
Q

What type of prion disease originated from mad cow disease

A

Variant CJD

45
Q

The hallmark of Parkinson’s disease

A

Alpha- synuclein

46
Q

The hallmark of neurodegenerative diseases

A 
Alpha- synuclein= Parkinsons disease
Beta-amyloid= Alzheimers
FET= Frontotemporal dementia
TAU= Parkinson's and Alzheimer's
TDP-43= Frontotemporal dementia and motor neurone disease
47
Q

The neuropathological feature neurodegenerative diseases

A

Beta-amyloid plaques= Alzheimer’s disease
Striatal atrophy= Huntington’s disease
Neurofibrillary tangles=Alzheimer’s disease
Spongiform changes= Prion disease

48
Q

What disease is associated with enlargement of the anterior horn of the lateral ventricles

A

Huntington’s disease

49
Q

Role of the Hippocampus

A

The hippocampus has a role in memory consolidation and early retrieval

50
Q

The role of the reticular activating system

A

Influences learning and memory

It influences motor function and planned behaviour

51
Q

What structure is found within the olfactory bulb

A

Mitral cells

The olfactory ensheathing cell is associated with the cribiform plate
In the olfactory epithelium you get olfactory receptor cell bodies and Sustentacular cell
The uncus is found in the medial temporal lobe

52
Q

Role of the Neocortex

A

Involved in declarative memory long term storage, known as the ‘slow learning cortex’

53
Q

What side effect is more common in dopamine agonists then levodopa

A

Impulse control disorders

54
Q

Role of Carbidopa

A

A dopa decarboxylase inhibitor
It increases the levodopa that reaches the brain
It may increase levodopa induced dyskinesia

55
Q

MoA of different Alzheimer drugs

A

Donepezil- a cholinesterase inhibitor
Memantine- blocks glutamate excitotoxicity
Rivastigmine- a cholinesterase inhibitor
Tacrine- a cholinesterase inhibitor

56
Q

What receptor type is associated with long term potentiation when upregulated

A

NMDA receptors along with AMPA glutamate receptors are upregulated in memory formation

57
Q

Which visual stream is referred to as the ‘what’ pathway

A

Ventral

58
Q

Nerve sensation to the anterior 2/3 of the tongue

A

General- Lingual nerve- mandibular division of the trigeminal nerve
Taste- Chorda tympani- facial

Medicine year 2 semester 2 (47 decks)

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