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Stage 3 - Case 2 (Central Nervous System) > Lecture 5 & 6: Parkinsons Disease Pathophysiology, Pharmacology And Pharmaceutical Care > Flashcards

Lecture 5 & 6: Parkinsons Disease Pathophysiology, Pharmacology And Pharmaceutical Care Flashcards

1
Q

What is Parkinson’s disease?

A
  • A lifelong, chronic & progressive neurodegenerative disorder that primarily affects movement and can involve non-motor symptoms (not movement related)
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2
Q

At what age does Parkinson’s disease mainly affect individuals?

A

Over 65

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3
Q

What happens to neurons in Parkinson’s disease?

A
  • Nerve cells in the substantia nigra become damaged or die, leading to decreased dopamine production.
  • This leads to the symptoms
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4
Q

Who is responsible for diagnosing Parkinson’s disease?

A

A hospital clinician with expertise.

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5
Q

What are the common symptom of Parkinson’s disease?

A
  • Tremor
  • Rigidity
  • Bradykinesia
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6
Q

What does rigidity in Parkinson’s disease refer to?

A
  • Stiffness and resistance to limb movement caused by increased muscle tone.
  • Excessive contraction of muscles and joint pain
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7
Q

Define bradykinesia in the context of Parkinson’s disease.

A
  • Slow movement, difficulty planning, initiating, and executing movement.
  • Problems w/ fine motor movement (writing)
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8
Q

Name some other symptoms associated with Parkinson’s disease.

A
  • Depression
  • REM sleep behavior disorder
  • Gait instability (difficulty maintaining balance when walking. Stooped posture)
  • Eye problems
  • Fatigue
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9
Q

What is postural hypotension?

A

A fall in blood pressure when rising.

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10
Q

What are the affected dopamine pathways in Parkinson’s disease?

A
  • Nigrostriatal
  • Mesocortical
  • Mesolimbic
  • Tubero-infundibular
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11
Q

What is the role of the nigrostriatal pathway?

A
  • Transmits dopamine from the substantia nigra to the striatum, crucial for voluntary movements.
  • Typical symptoms
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12
Q

What symptoms are associated with the mesolimbic pathway dysfunction and what does it control?

A
  • Depression, reduced motivation, and pleasure.
  • Links the ventral tegmental area (VTA) to the Limbic system
  • It regulates emotion, reward and motivation
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13
Q

What happens to the tuberoinfundibular pathway when dopamine levels are reduced?

A
  • This pathway connects dopamine neurons to the arcuate nucleus of the hypothalamus to the pituitary gland
  • Prolactin secretion increases, leading to hyperprolactinemia and galactorrhea (milk production not associated with/ breastfeeding)
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14
Q

What is the consequence of dopamine depletion in Parkinson’s patients?

A
  • Normal: Substantia Niagra has dopanergic neurons and signal travels to basal ganglia and striatum in which dopamine binds to D1 and D2 receptors
  • In the striatum dopamine controls/ regulates GABAergic activity (inhibitory). This system/ neurotransmitter is inhibited therefore glutamergic system (motor cortex and frontal lobe) is activated. This promotes excitatory and causes movement
  • In Parkinsons Patient: Dopamine depletion reduces activation of receptors; Inhibitory mechanism is overactive (more GABA) – difficulty moving
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15
Q

What are the different strategies to be used in treatment:

A
  • Promote more dopamine to be made
  • Activate receptors with agonist (not dopamine)
  • Reduce breakdown of dopamine (MAO)
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16
Q

How is dopamine synthesised?

A
  • Tyrosine (amino acid) -> L-DOPA (produced by enzyme Tyrosine Hydroxylase) -> dopamine (produced by DOPA decarboxylase)
17
Q

What are common long-term side effects of L-DOPA therapy?

A
  • Dyskinesia (uncontrollable/ eratic movement)
  • End of dose deterioration (effect of first dose will wear off before next dose)
  • Freezing (Walk then just stop)
  • Dopamine dysregulation (amount of dopamine is dysregulated in the brain)
18
Q

What is the role of monoamine oxidase in the context of Parkinson’s disease?

A
  • It metabolizes dopamine in the CNS, particularly MAO-B.
  • Therefore need something to inhibit this so dopamine remains (Selegiline/rasagiline)
19
Q

What does COMT do in relation to dopamine?

A
  • Breaks down catecholamines like L-DOPA and dopamine in peripheral & CNS
  • therefore inhibitors increase dopamine (Tolcapone).
  • Given in conjunction w/ L-DOPA
20
Q

Fill in the blank: The pathway that connects dopaminergic neurons in the arcuate nucleus of the hypothalamus to the pituitary gland is called the _______.

A

Tubero-infundibular

21
Q

What is the function of carbidopa when combined with L-DOPA?

A

Inhibits the enzyme (DOPA decarboxylase) that converts L-DOPA to dopamine in the periphery.

22
Q

What is the function of the mesocortical dopamine pathway?

A
  • Connects the VTA to the prefrontal cortex, regulating cognition, attention, and executive function.
  • Difficulty with planning and decision-making.
23
Q

What is first line, second line and third line symptomatic treatments of early Parkinsons Disease?

A
  • Levodopa + decarboxylase inhibitor (can use domperidone alongside to reduce N&V)
  • Oral/transdermal dopamine agonists: Bind w/ receptor + combined with levodopa. Mimics effect. Dont offer ergot derived for first line
  • Monoamine oxidase B inhibitors (Rasagiline) used alongside levodopa to reduce end of dose deterioation
24
Q

What are some complications of Parkinsons Disease?

A
  • Communication
  • Family/carers
  • Non-motor symptoms - distracted/ diminished attention
25
Q

What is the difference between early and late Parkinsons Disease?

A
  • Early Disease: Functional disability and require symptomatic therapy
  • Late Disease: People on levodopa who have developed motor complications
26
Q

What are some issues with ergot derived dopamine agonists?

A
  • Cabergoline - long half life
  • Associated w/ cardiac valvulopathy & pleural fibrosis
  • Monitoring needed: renal function tests. (usage has declined)
27
Q

What are some side effects of ergot and non-ergot derived agonists?

A
  • Impulse control disorders
  • Daytime drowsiness
  • Peripheral oedema
  • Nausea & dizziness & constipation
28
Q

Why are Anticholinergic and beta blockers not used in early Parkinsons Disease?

A
  • Anticholinergic: Less dopamine seceretion promotes activity of cholinergic in brain (dementia) & cause sedation/ glaucoma & constipation
  • Beta Blockers: Risk of falls and changes to BP
29
Q

What are symptoms of later Parkinsons Disease?

A
  • Physical symptoms no longer controlled by meds
  • Medication side effects (problematic)
  • End of dose deterioration and akinesia (loss of movement)
  • Dyskinesia
  • Freezing
  • Levodopa tolerance
30
Q

How do you treat long term treatment side effects w/ Levodopa?

A
  • Dopamine agonist can be used to reduce motor fluctuations
  • Use non-ergot. If ergot given monitoring required
31
Q

What are treatment strategies for later Parkinsons Disease?

A
  • Levodopa + dopa decarboxylase inhibitor
  • Oral/ transdermal dopamine agonists
  • Monoamine oxidase B inhibitors
  • COMT inhibitors
  • Amantadine
  • Apomorphine
  • Intestinal gels & produodopa (new subcutaneous
32
Q

What is apomorphine?

A
  • Non-ergot dopamine agonist
  • Delivered injections/ continuous infusion (avoids first pass metabolism)
  • Those who have severe off periods that arent responsive to changes in oral meds
  • Risk of confusion and hallucinations
33
Q

What is amantadine?

A
  • Weak dopamine agonist with modest effects
  • Increase dopamine release
  • Weak antagonist of the NMDA type glutamate receptor
  • Less effective than levodopa
  • Can be used alongside levodopa to improve muscle control & reduce stiffness
34
Q

What should be done/given when patient is drooling, N&V and constipation?

A
  • Drooling: SALT review/ botulinum toxin A injected into salivary gland (specialist)
  • N&V: Low dose domperidone
  • Constipation: Lifestyle/ fibre/ laxatives
35
Q

What should be done/given when patient is Pain, sleep disorder & depression?

A
  • Pain: simple analgesia/ exercise
  • Sleep disorder: sleep hygiene
  • Depression: SSRI (watch for worsening restless legs), TCA (cognitive impairment and falls risk)
36
Q

What are some prescribing points of Parkinsons Disease meds?

A
  • Shouldnt be withdrawn suddenly or allowed to fail due to poor absorption (to avoid potential akinesia - loss of voluntary movement or neuroleptic malignant syndrome - rare but life threatening w/ fever/ muscular rigidity
  • Dose timing is critical - missed/late should be avoided
  • Doses should be given as close to usual times
  • Avoid drugs that act as dopamine antagonists: metoclopramise, haloperidol
37
Q

Patient arm shakes approx 1 hour before dose and gets painful cramps at night. What alterations should be given to minimise effects?

A
  • Reduce amount given in each dose
  • Increase administration to last longer
  • More prolonged release
  • Management of pain
  • Administer MAO-B inhibitors

Stage 3 - Case 2 (Central Nervous System) (10 decks)

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