11.2 Treating ND Conditions Flashcards Preview

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Flashcards in 11.2 Treating ND Conditions Deck (37):
1

What is Parkinsons Disease?

A slow, progressive neurodegenerative condition of the dopinergic neurones in the substantia nigra, affecting the nigrostriatal pathway

2

What can cause Parkinsons Disease?

Drug Induced - anti-psycotics
Vascular
Idiopathic
Progressive Supranuclear Palsy

3

How do you diagnose IPD?

Rule out other causes
Clinical Signs
If responds to treatment it is idiopathic
Can do a functional MRI scan - PET, DAT

4

What is a DAT scan?

A scan which highlights the presynaptic dopiminergic neurones in the SNi as they synapse on the striatum.
In PD there will be less glowing

5

What are the symptoms of Parkinsons Disease?

Bradykinesia
Pill-rolling Tremor
Postural Instability

Cog-wheel rigidity, Lead Pipe Rigidity
Pedestal Turning, Slow to Start, Fenestrating Gait
Lack of expression/monotone voice

Other:
Non-motor (mood changes, sleep disturbances and cognitive disturbances)

6

What is the pathophysiology of Parkinsons Disease?

Damage to SNi D neurones
Accumilations of misfolded alpha-synclein proteins
Form Lewy Bodies
These damage the neurones leading to cell death

7

What are the PD treatments?

Dopamine Replacement
Dopamine Receptor Agonists
MOAB-inhibitors
COMT Inhibitors

8

How does Levidopa work?
What does it improve?

It is L-DOPA, a precursor to Dopamine. It can cross the BBB and uses the dopaminergic neurones to change into Dopamine.
Need to use with a decarboxylase inhibitor to prevent breakdown in the periphery
This improves the motor symptoms.

9

What are the ADRs of Levidopa?

Hallucinations
Lack of Sleep
Hypotension
Can increase the tremor
Nausea
Tachycardia

10

Describe the PK of Levidopa?

It is Oral
Has a poor oral bioavailabilty (only 1% goes to brain)
Active transport (vs amino acids) through gut wall
90% broken down in intestinal wall
Short Half Life
Distributed in periphery ( 9% converted into dopamine )
Crosses the BBB

11

Any DDIs with Levidopa?

Vitamin B6

12

What are Dopamine Receptor Agonists?

Agonists of the D receptors in the striatum
They are either ergot or non-ergot derived

13

Examples of Dopamine Receptor Agonists?

Ropinirole

14

Why use Dopamine Receptor Agonists?

Less dyskinesia
Might be neuroprotective

15

What are the ADRs of Dopamine Receptor Agonists?

Ergot derived: Fibrosis
Impulse Control Disturbances
Sedation (daytime sleepiness)
Hypotension

16

How do you take Dopamine Receptor Agonists?

Patch
Subcutaneous

17

What drugs inhibit the breakdown of Dopamine?

Decarboxylase Inhibitors (in periphery)
COMT inhibitors (mostly act on peripheral breakdown)
MOA-B inhibitors

18

Describe the breakdown of Dopamine

Dopamine is broken down either by MOA orCOMT
into two different things (3,4 Dihydrophylacetic Acid, 4-Methoxytyramine)
They then unite at a common point - homovanillic acid

19

Describe how Dopamine is created

Created from Precursor - L-DOPA
Converted by enzyme - DOPA Decarboxylase

20

When do you use COMT inhibitors?

Alongside Levidopa
Prolongs motor effects of Levidopa

21

Why do you use MOA-B inhibitors?

Alongside Levidopa or on its own
May be neuroprotective
Reduces motor effects of IPD

22

What is Myasthenia Gravis?

Autoimmune
IgG blocks ACh receptor on post-synaptic membrane
Increases ACh breakdown by AChE

23

What are the symptoms of Myasthenia Gravis?

Fast tiring, fatiguable, weak muscles
No problems with reflexes
Cannot hold upwards gaze too long

24

How do we treat Myasthenia Gravis?

Corticosteroids or Azathroprine
AChE inhibitors

25

What drugs can worsen Myasthenia Gravis?

Aminoglycosides
Beta Blockers
Chloraquins
ACE Inhibitors
Succinylcholine
Magnesium

26

What is a Myasthenia Crisis?

A flare up of MG (acute exaccerbation)
Can weaken respiratory muscles and require ventilation

27

What is a Cholinergic Crisis?

When you overtreat a patient with MG with AChE-i
You get:
Salivation
Sweating
Lacrimation
Urinary Incontinence
Diarrhoea
GI disturbances
Emesis

28

How do AChE inhibitors work?

Block the enzyme which breaks down ACh
ACh stays in the cleft longer
Increases its action

29

Why is timing of AChE-i crucial?

Lasts for 3-6 hours
Time it well to meals as it can affect whether someone can swallow or not

30

What are the ADRs of AChE-i?

Cholinergic Side Effects
SSLUDGE

31

How do you take AChE-i?

Oral
IV
Pyridostigmine

32

What surgery can you do for PD?

DBS on STN
Lesion in the thalamus (reduce tremor)
Lesion in the GPi (lessen dyskinesia)

33

How could Anticholinergic drugs help PD?

Believed ACh antagonises dopamine
Could treat the tremor but has no effect on bradykinesia

34

How could you use Amantidine?

Weak Evidence
May enhance dopamine release and inhibit ACh
Poor but few side effects

35

What does COMT do?

Inhibits breakdown to 3-MO
So dopamine is around longer
3-MO normally inhibits the transport into the CNS as well

36

Why use MOAB-i not just a MOA-i?

As B are normally found in dopamine regions of the brain
Don't have a risk of hypertensive crisis unlike non selective ones

37

Examples of MOA-B Inhibitors

Rasagaline
Selegiline