Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPT > L22 Neurological Dosorder Drugs > Flashcards

L22 Neurological Dosorder Drugs Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

Clinical motor features of Parkinsonism

A 
Pill rolling intention tremor
Lead pipe rigidity 
Bradykinesia 
Postural instability 
Fenestrating gait
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Non motor features of Parkinsonism

A 
Mood changes 
Pain 
Cognitive change 
Urinary symptoms
Sleep disorder
Sweating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diagnosis of idiopathic Parkinson’s disease

A

Exclude other causes e.g.

  • drug induced
  • vascular (affecting the basal ganglia)
  • progressive supranuclear (affects substantia nigra)
  • multiple system atrophy
  • corticobasal atrophy

Response to treatment - Levodopa
Normal structural neuroimaging
Functional neuro imaging e.g. PET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathology of IPD

A

Neurodegeneration
Lewy bodies
Loss of pigments in substantia nigra
Reduced dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathology in basal ganglia of IPD

A
  1. Loss of dopaminergic neurones in substantia nigra
  2. Therefore less inhibition in neostriatum
  3. Therefore increased production of Ach (excitatory)
  4. Chain of abnormal signalling leads to impaired mobility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Catecholamine synthesis

A
  1. L - tyrosine
  2. L - DOPA
  3. Dopamine via DOPA decarboxylase
  4. Noradrenaline
  5. Adrenaline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dopamine degradation

A

Via:
monoamine oxidases
aldehyde dehydrogenase
Catechol-o-methyl transferase COMT

To:
Homovanillic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Neurotransmitter synthesis

A

Synthesis of neurotransmitters and formation of vesicles in the cell body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DAT scan

A

Monitors the presynaptic reuptake of dopamine using a labelled tracer
Abnormal in PD but not diagnostic as abnormal in many conditions such as stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cog wheel rigidity

A

Intention tremor and lead pipe rigidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Levodopa

A

Can cross the blood brain barrier via active transport
Must be taken up by dopaminergic cells in the substantia nigra to be converted to dopamine therefore if less cells, decreased efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pharmacokinetics of L-DOPA: administration, bioavailability and half life

A

Administration- oral
Bioavailability
- 90% inactivated in intestinal wall
- 9% converted to dopamine in peripheral tissues (given DOPA decarboxylase inhibitor)
- 1% enters CNS
Half life - 2 hours with short dose interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DOPA decarboxylase inhibitor benefits

A

9% of LDOPA converted to dopamine in peripheral tissues and 90% metabolised in gut therefore an inhibitor is given to prevent Huntington’s disease and less side effects

  • reduced dose required
  • increased LDOPA reaches brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

DOPA decarboxylase inhibitor examples

A

Co-careldopa (sinemet)

Co- beneldopa (madopar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Advantages of LDOPA

A 
Highly efficacious 
Low side effects such as :
- nausea and vomiting 
- hypotension 
- Psychosis 
- tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Disadvantages of LDOPA

A 
Needs enzyme for conversion to active form 
Long term - loss of efficacy 
Involuntary movements 
Motor complications 
- dystonia 
- dyskinesia 
- freezing 
- on/ off
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Interactions of LDOPA

A

Pyridoxine (vit B6) increases peripheral breakdown of LDOPA
Monoamine oxidases risk hypertensive crisis
Antipsychotic block dopamine receptors

18
Q

Why are ergot derived dopamine receptors agonists not used

A

Cause retroperitoneal and pericardial fibrosis

19
Q

Dopamine therapy delivery

A

Patch or subcutaneous

20
Q

When are dopamine receptors agonists used

A

De novo therapy
Add on therapy
Severe motor fluctuations- apomorphine

21
Q

Dopamine advantages

A

Direct acting
Less dyskinesia/ motor complications
Possible neuroprotection

22
Q

Disadvantages of dopamine receptors agonists

A

Less efficacious
Impulse control disorder
More psychiatric side effects
Expensive

23
Q

Impulse control disorder

A 
Pathological gambling
Hypersexuality 
Compulsive shopping 
Desire to increase dosage 
Punding - collecting and rearranging random things
24
Q

Dopamine receptor agonist side effects

A 
Sedation 
Hallucinations 
Confusion 
Nausea 
Hypotension
25
Q

Monoamine oxidases B inhibitors mechanism

A

Inhibits the metabolisation of dopamine
Stand alone therapy or prolongs the action of LDOPA - add on therapy
Smooths our motor response

26
Q

Examples of MAO inhibitors

A

Selegiline

Rasagaline

27
Q

COMT inhibitors mechanism

A

Add on therapy given with LDOPA or MAOB as no therapeutic effect alone
Reduces the peripheral breakdown of LDOPA - LDOPA sparring
Reduces wear off symptoms of LDOPA

28
Q

Anticholinergic mechanisms

A

Ach May antagonise dopamine therefore reduces antagonism

Minor role in relieving tremor

29
Q

Advantages of acetylcholine

A

Treats tremor

Not acting via dopamine pathway

30
Q

Disadvantages of anticholinergics

A 
No effect on bradykinesia 
Side effects:
- confusion
- drowsiness 
- anticholinergic side effects like urinary retention
31
Q

Amantadine mechanism

A 
Enhances dopamine release 
Inhibits anticholinergic NMDA 
Low efficacy 
Few side effects 
Little effect on tremor
32
Q

Surgery

A

Done when there is:

  • significant side effects to LDOPA or unresponsive
  • no psychiatric illness
  • last line
33
Q

Myasthenia gravis

A

Antibody mediated blockade of Ach at postsynaptic Ach receptors
Type II hypersensitivity reaction

34
Q

Symptoms of myasthenia gravis

A 
Fluctuating 
Fatigue when eating 
Weakness of skeletal muscles 
- complete ptosis
- bulbar involvement - dysphagia, dysphonia, dysarthria 
- limb weakness 
- respiratory muscle involvement
35
Q

Drugs that exacerbate myasthenia gravis

A 
Aminoglycosides 
Beta blockers, CCBs 
Chloroquine 
Magnesium 
ACE inhibitors
36
Q

Myasthenia crisis

A

Acute exacerbation

37
Q

Over treatment

A

Cholinergic crisis

  • SSLUDGE
  • respiratory distress
  • dysphagia and drooling
38
Q

Management of myasthenia gravis

A

Acetylcholinesterase inhibitors

39
Q

Acetylcholinesterase inhibitor examples

A 
Pyridostigmine - oral
Neostigmine
 - oral and IV
- quicker 
- more side effects
40
Q

SSLUDGE

A 
Sweating 
Salivation
Lacrimation
Urinary incontinence 
Diarrhoea
GI upset
Emesis

CPT (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions