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Neurology - Sem 3 > Case 7 - Parkinson's disease > Flashcards

Case 7 - Parkinson's disease Flashcards

1
Q

Define:

  • mortality rate
  • Morbidity rate
  • Incidence rate
  • Prevalence rate
A
  • Number of deaths in 1 year compared with previous or subsequent years
  • The incidence rate or prevalence rate
  • Measure of morbidity based on the number of new episodes of illness in a population over time. e.g. affected persons per 1000 individuals at risk
  • Measure of morbidity based on current levels of disease in population either at a time (Point prevalence) or stated period (Period prevalence)
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2
Q
  1. What are the 3 methods of assessing Quality of Life?
  2. What are unidimensional measures?
  3. What are multidimensional measures?
  4. What are individual QoL measures?
A
  1. Unidimensional measures, multidimensional measures, and individual QoL measures
  2. Focus on 1 particular aspect of health e.g. pain
  3. Assess health in the broadest sense
  4. Ask the individual to rate their own health
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3
Q

Define:

  • Quality Adjusted life years (QALY)
  • Disability adjusted life years (DALY)
A
  • How long a successfully treated patient can expect to live. Each expected year = 1 point, Each year with degree of illness or disability – <1. Death = 0
  • Seeks to minimise the buren of the disease
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4
Q
  1. What is emotion?
  2. What part of the brain is most important for fear?
  3. What happens when a person has a bilateral amygdala lesion?
A
  1. Mental state that arises spontaneously rather than through conscious effor and is accompanied by physiological changes
  2. Amygdala
  3. Fear conditioning is abolished, impaired ability to recognise emotion, and fear.
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5
Q

Identify the following:

  • Cerebral cortex
  • Corpus callosum
  • Hypothalamus
  • Amygdala
  • Pituitary gland
  • Thalamus
  • Hippocampus
A
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6
Q
  1. What are the 2 components of long term memory?
  2. What are the 2 components of Declarative memory?
  3. What are the 3 components of Implicit memory?
  4. What are the 2 components of short term memory?
  5. What is retrograde amnesia?
  6. What is anterograde amnesia?
A
  1. Declarative (Explicit) & Implicit memory
  2. Episodic (Events) & Sematic (Facts)
  3. Procedural (skills) & Priming & Conditioning
  4. Sensory & Working memory
  5. Cannot remember events prior to the brain damage
  6. Cannot later remember events that occur after the brain damage
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7
Q
  1. What is long term potentiation?
  2. What happens to the receptors?
  3. Where does it happen?
A
  1. How we learn/memorise - Strenghtening of the synapses and causing long term increase in signal transmission b/w neurons.
  2. There is an increase in the number of receptors
  3. Happens in the Hippocampus
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8
Q
  1. What cells in the brain produce the metabolites for neurons?
  2. What does the brain use for energy? (2)
  3. What is the danger of anaerobic respiration?
  4. Why is energy important in the brain?
A
  1. Astrocytes
  2. Glucose to produce ATP
  3. Produces lactic acid which is damaging to neurons
  4. To maintan the ionic gradients
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9
Q
  1. What other metabolite does the brain use during starvation?
  2. What do neurons use for metabolism?
  3. What is the short term energy reserve astrocytes have?
A
  1. Ketone bodies
  2. Lactate and Pyruvate
  3. Glycogen
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10
Q
  1. What are the 3 major classes of NT?
  2. What is a NT?
  3. What is a neuron that releases more than 1 NT called?
A
  1. Amines, Amino acids, & Peptides
  2. Molecule produced and stored in presynaptic neuron, released on stimulation and produces response in postsynaptic cell
  3. Co-transmitter
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11
Q
  1. What NT do cholinergic neurons release?
  2. What enzyme is required to synthesise acetylcholine?
  3. Where is ACh synthesised?
  4. Where does the Acetyl come from?
  5. How is choline transported into the cell?
  6. What is exchanged in order for the ACh to enter the vesicle?
A
  1. Acetylcholine (ACh)
  2. Choline Acetyltransferase
  3. Cytosol of the neuron
  4. From Acetyl CoA
  5. Via choline transporter which is transported along with Na+
  6. H+ ion
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12
Q
  1. What 2 receptors does ACh act on? What types of receptors are they?
  2. What enzyme is used to degrade ACh?
  3. What does ACh get broken down into?
  4. What happens if you inhibit the enzyme AChE?
A
  1. Muscarinic (G protein) receptors & Nicotonic receptors (Ionotropic)
  2. Acetylcholinesterase (AChE)
  3. Choline + Acetic acid
  4. ACh is not broken down and there is constant stimulation of the receptors e.g. in skeletal muscle and cardiac muscle
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13
Q

1. What are the 3 catecholaminergic NTs?

  1. What are they all originally derived from?
  2. Fill in the following order of production:
  • Tyrosine – ______ – ______ – _______
    4. Where is noradrenaline produced?
A
  1. Dopamine (DA) & Noradrenaline & Adrenaline
  2. Tyrosine
  3. Tyrosine – Dopamine – Noradrenaline – Adrenaline
  4. Locus Ceruleus
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14
Q
  1. Which enzyme catalyses NE from DA?
  2. Which enzyme converts NE to E?
  3. What does E also act as in the body? Where is it released?
  4. Which enzyme is used to degrade NE & E?
  5. What are the 2 reuptake transporters for NE?
A
  1. DBH
  2. PNMT
  3. Hormone, Adrenal glands
  4. MAO
  5. NET & NAT
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15
Q
  1. What is seratonin also called? Where is it made?
  2. Which amino acid is it derived from?
  3. What is its role?
  4. Complete this: Tryptophan – ____ – ____
  5. Where do we get tryptophan from?
  6. How is 5-HT removed from the synaptic cleft? (2)
  7. What is used to degrade it?
  8. What type are its receptors except for 1?
  9. What type of receptor is the 5-HT3 receptor?
A
  1. 5-HT, Raphe Nuclei
  2. Tryptophan
  3. Regulation of mood, emotional behaviour, apetite, and sleep
  4. Tryptophan – 5-HTP – 5-HT
  5. Diet
  6. by the Serotonin Reuptake receptor & 5HTT
  7. MAO
  8. G-protein coupled
  9. Ligand gated cation channel
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16
Q
  1. Which serotonin receptors are positive coupling?
  2. Why type of receptors are they?
  3. What does NA do to 5HT neurons?
  4. What do the a2 receptors do?
A
  1. All except for 5HT1 and 5HT5
  2. G protein except for 5HT3
  3. Activates a1 receptor, Increases firing of the 5HT cell
  4. Decrease firing, so switches off 5-HT release
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17
Q
  1. What are the 3 amino acids used as NT?
  2. What are glutamate and glycine synthesised from?
  3. What are the 3 types of glutatame receptors?
  4. What is GABA synthesised from?
  5. Which enzyme converts it?
A
  1. Glutamate & Glycine & GABA
  2. Glucose
  3. AMPA, NMDA, Kainate receptors
  4. Glutamate
  5. Glutamic acid decarboxylase (GAD)
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18
Q
  1. What molecules which is used for cellular metabolism is also used as a NT?
  2. What are cannabinoids?
  3. What is their mechanism of action?
A
  1. ATP
  2. Lipid molecules
  3. Reduce the opening of presynaptic Ca+ channels so reduce the ability of presynaptic terminal to release its NT
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19
Q
  1. What are AMPA cahnnels permeable to?
  2. What does the opening of these channels lead to?
  3. What do NMDA receptors do?
  4. What molecule blocks the channel ordinarily?
  5. What opens the channel?
  6. What do GABA receptors do?
  7. Which sub-unit binds the NT?
A
  1. Na+ and K+ ions
  2. excess of cations into the cell, so there is a rapid depolarisation – Excitatory
  3. Excitation of the cell, they allow Na+ into the cell
  4. Mg+
  5. Glutamate
  6. Allows Cl- ions into the cell, so hyperpolarises it
  7. A sub-unit
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20
Q
  1. What are the 3 sub-units of G proteins?
  2. In the resting state what is the a subunit bound to?
  3. When a ligand binds to the receptor what happens?
  4. What does the activated GTP bound G protein split into? (2)
  5. What does the G a sub-unit act as?
  6. At rest what is the combination of the sub-units?
  7. What do Gs and Gi mean?
A
  1. a, b, and gamma
  2. GDP
  3. The G protein releases its GDP and exchanges it for GTP from cytosol
  4. alpha sub-unit + GTP & G beta/Gamma sub-unit complex
  5. An enzyme that can break down GTP – GDP
  6. They are all joined together
  7. G stimulatory protein, and G inhibitory protein
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21
Q
  1. What are the 2 types of effectors for G proteins?
  2. What happens when a G protein receptor is activated?
  3. What does Adenylyl cyclase do?
  4. What downstream enzyme is subsequently activated?
  5. What happens when an inhibitory G protein is activated?
A
  1. G protein gated ion channels & G protein activated enzymes (2nd messengers)
  2. G protein is activated, and this stimulates Adenylyl cyclase (membrane bound enzyme)
  3. Converts ATP to cAMP (Increase)
  4. PKA (Protein Kinase A)
  5. Suppresses the activity of adenylyl cyclase
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22
Q
  1. What is Phospholipase C?
  2. What does it act on?
  3. What does it split it into? (2)
  4. What does DAG activate?
  5. What does IP3 do?
  6. What do protein kinases do?
  7. What are used to inhibit protein kinases?
A
  1. Enzyme floating in the membrane
  2. PIP2
  3. IP3 and DAG
  4. Activates PKC
  5. Binds to receptors and cause organelles to release Ca+ stores
  6. Phosphrylate proteins (Transfer phosphate) to change their activity e.g. open channels etc.
  7. Protein phosphatases
23
Q
  1. Where is DA most abundant?
  2. What enzyme do DA neurons lack so they cant convert it further to NA?
  3. What is tyrosine converted to in the first step?
  4. Which enzyme does this?
  5. What is Dopa then converted to?
  6. Which enzyme does this?
  7. What types of receptors are DA receptors?
A
  1. Corpus Striatum
  2. B hydroxylase
  3. Dopa
  4. Tyrosine Hydroxylase
  5. Dopamine
  6. Dopa decarboxylase
  7. Metabotropic (G protein coupled)
24
Q
  1. What transporter recaptures DA once released?
  2. What 2 enzymes metabolise DA?
  3. What is it metabolised into? (2)
  4. How is it excreted?
  5. What are the 4 DA pathways in the CNS?
A
  1. Monoamine transporter
  2. MAO and COMT
  3. DOPAX & HVA
  4. In the urine
  5. Mesocortical pathway & Tuberoinfundibular pathways & Nigrostriatal pathway & Mesolimbic pathway
25
Q
  1. Where are the cell bodies of the Nigrostriatal pathway?
  2. Where do the axons terminate?
  3. Where are the cell bodies of the mesolimbic pathway?
  4. Where do the axons project to?
  5. Where are the cell bodies of the mesocortical pathway?
  6. Where do the axons project to?
  7. Where are the cell bodies of the tuberoinfundibular pathway?
  8. Where do the axons project to?
A
  1. Substantia nigra
  2. Corpus striatum
  3. Ventral tegmental area
  4. Limbic system (Nucleus accumbens & Amygdaloid nucleus)
  5. VTA
  6. DLPFC
  7. Ventral hypothalamus
  8. Pituitary gland
26
Q
  1. What are the descending spinal tracts?
  2. What are the 2 groups of pathways making up the descending spinal tracts?
  3. What 2 pathways make up the lateral tracts?
  4. What 4 pathways make up the ventromedial pathways?
A
  1. Pathways through which the brain communicated with the motor neurons of the spinal cord
  2. Lateral column of the spinal cord & Ventromedial pathways
  3. Corticospinal tract & Rubrospinal tract
  4. Vestibulospinal tract & Tectospinal tract & Pontine + Medullary Reticulospinal tract
27
Q

Identify the following descending tracts:

  • Corticospinal tract
  • Rubrospinal tract
  • Medullary reticulospinal tract
  • Pontine reticulospinal tract
  • Vestibulospinal tracts
  • Tectospinal tracts
28
Q
  1. Where are the cell bodies of the corticospinal tract?
  2. Where do the axons pass through in the brain?
  3. What do they form in the medulla?
  4. Where does the tract decussate?
  5. Where do the fibers collect?
  6. Where do the axons terminates in the spinal cord?
  7. Which part of the brain controls the R side?
A
  1. Motor cortex of the frontal lobe
  2. Internal capsule
  3. Medullary pyramid (Tract)
  4. Pyramidal decussation
  5. Lateral column of the spinal cord
  6. Dorsolateral region of the ventral horn
  7. L cerebral hemisphere
29
Q
  1. Where is the origin of the rubrospinal tract?
  2. Where do its fibers decussate?
  3. Where do its axons terminate?
A
  1. Red nucleus of the midbrain
  2. Pons, at same level as corticospinal tract
  3. Ventral horn of the spinal cord
30
Q
  1. Where does the vestibulospinal tract originate?
  2. Where does it receive sensory information from?
  3. Where does component 1 of the tract terminate?
  4. Does it decussate?
  5. Where does component 2 of the tract terminate?
  6. Does it decussate?
A
  1. Vestibular nuclei of the medulla
  2. Vestibular larbynth of the inner ear
  3. Lateral horn of the cervical spinal circuits
  4. No, descends bilaterally
  5. Lateral horn of the lumbar spinal circuits
  6. No, descends ipsilaterally
31
Q
  1. Where does the tectospinal tract originate?
  2. Where does it receive input from?
  3. Does it decussate?
  4. Where does it terminate?
A
  1. Superior colliculus of the midbrain
  2. Retina & visual cortex
  3. Yes, after leaving the superior colliculus
  4. Lateral horn of the spinal cord
32
Q
  1. Where does the Pontine reticulospinal tract originate?
  2. Is it medial or lateral?
  3. Where does the medullary reticulospinal tract originate?
  4. Is it medial or lateral?
  5. Where do they terminate?
A
  1. Reticular formation of the pons
  2. Medial
  3. Reticular formation of the medulla
  4. Lateral
  5. Lateral horns of the spinal cord
33
Q

Identify the following components of the basal ganglia:

  • Caudate nucleus
  • Putamen
  • Globus pallidus (GPi & GPe)
  • Subthalamic nucleus (STN)
  • Substantia nigra
  • Thalamus
34
Q

Identify the following components of the basal ganglia:

  • Caudate nucleus
  • Putamen
  • Globus pallidus internal segment
  • Globus pallidus external segment
  • Subthalamic nucleus (STN)
  • Substantia nigra
35
Q
  1. What makes up the striatum? (2)
  2. What are the 2 parts of the substantia nigra?
  3. What is found in the striatum? (2)
A
  1. Caudate nucleus + Putamen
  2. Substantia nigra pars compacta + Substantia nigra pars reticulata
  3. D1 & D2 receptors
36
Q
  1. Which receptors are used in the direct pathway?
  2. What is the neuropeptide associated with it? (2)
  3. What is the function of DA in this pathway?
  4. What does the receptor do when DA is bound?
  5. What is the final result?
A
  1. D1 receptors
  2. PPE-B & Dynorphin
  3. Stimulatory (Gs)
  4. Increase production of Adenylyl cyclase
  5. Increase in cAMP in the cell, so promotes desired movement
37
Q
  1. What receptor is used in the indirect pathway?
  2. What is the neuropeptide involved? (2)
  3. What is the action of DA on this pathway?
  4. What does the receptor do when DA is bound?
  5. What is the overall result?
A
  1. D2 receptor
  2. PPE-A, and Enkephalin
  3. Inhibitory (Gi)
  4. Decrease amount of Adenylyl cyclase
  5. Decreased cAMP, therefore inhibition of unwanted movements
38
Q

What is the Direct pathway? Remember what releases DA

Is it inhibitory?

  1. — 2. — 3. — 4. — 5. — 6.
A
  1. SNpc releases DA to the D1 receptors
  2. D1 receptor then releases more GABA
  3. GPm/SNpr is inhibited by the D1 receptor, so releases less GABA
  4. Less inhibition of VL thalamus & brainstem = More movement
  5. Less inhibition of VL thalamus, then means more release of Glutamate (Excitation) to the Cerebral cortex
  6. Cerebral cortex releases more glutamate to the D1 receptors
39
Q

What is the indirect pathway? Remember what releases DA

  1. — 2. — 3. — 4. — 5. — 6.
A
  1. SNpc releases DA
  2. D2 receptors are inhibitory so releases LESS GABA
  3. GABA inhibits the GPi which releases less GABA
  4. Less inhibition of the STN (Which is excitatory) and Gpm/SNpr which is inhibitory
  5. Overall effect is more inhibition of VL thalamus & brainstem
  6. More inhibition = less glutamate to Cortex and back to Striatum
40
Q

Define the following:

  • Hyperkinesia
  • Akinesia
  • Bradykinesia
  • Hypokinesia
A
  • Execess movement
  • Difficulty initiating movement
  • Slow movement or lack
  • Little to no movement
41
Q
  1. What are the symptoms of parkinsons?
  2. What is the effect on the DA pathways?
  3. Which neuropeptides are increased?
  4. What is the overall result?
A
  1. Bradykinesia, Akinesia, Rigidity, Micrographia, Tremor (Resting)
  2. Reduced D1 activity, increased D2 activity
  3. PPE-A and Enkephalin
  4. Less activation of wanted movements, more inhibition of movement
42
Q

Define:

  • Chorea
  • Dementia
  • Dyskinesia
A
  • Spontaneous uncontrollable movements
  • Impaired cognitive abilities
  • Abnormal movements
43
Q
  1. What are the symptoms of Huntingdons disease?
  2. What causes it?
  3. Which receptor is affected?
  4. What is the effect on the pathways?
  5. What is the overall effect?
  6. Which neuropeptide is increased?
A
  1. Hyperkinesia, Chorea, Dyskinesia
  2. Expanded CAG repeats in Huntingtin gene (Chromosome 4)
  3. D2 receptor
  4. Direct pathway is more active, and indirect pathway is less active
  5. More initiation of movement, less inhibition of unwanted movement
  6. PPE-B and Dynorphin
44
Q
  1. What is Ballism?
  2. What is Hemiballism?
  3. What causes it?
  4. What is tourette syndrome?
  5. What is it caused by?
A
  1. Violent, flinging movements of the extremeties
  2. Symptoms on 1 side of the body only
  3. Damage to STN - so less inhibition of unwanted movements
  4. Repetitive stereotyped movements of head or limbs or vocalisations
  5. Loss of GABAergic neurons, and reduced BG inhibition
45
Q
  1. Which 4 genes are thought to be responsible for parkinson’s?
  2. Which toxin causes parkinsonian symptoms?
  3. What are Lewy bodies? What do they contain?
A
  1. Parkin & Alpha synuclein & SNCA & LRRK2
  2. MPTP
  3. Dense cored bodies which damage DA neurons, contain alpha synuclein
46
Q
  1. What is a PET scan? What do the scanners detect?
  2. What is 18 FDG?
  3. What cells take it up?
  4. What does it show?
  5. What is 18 F Flouradopa?
  6. What does it assess?
A
  1. Scanner used to look at soft tissues, camera detects gamma radiation
  2. Radionucleide derivative of glucose
  3. Astrocytes
  4. Metabolic activity in the area
  5. Radionucleide of L-DOPA
  6. To assess nigrostriatal pathway
47
Q
  1. What is SPECT?
  2. What is detected?
  3. Is it cheaper or more expensive than PET?
  4. Why is it not as good?
A
  1. Imaging of radionucleide put into the patient, via injection
  2. Gamma radiation
  3. Cheaper
  4. Less quality image
48
Q
  1. What is Levadopa?
  2. What does carbidopa do?
  3. What does Entacopone do?
  4. What are the side effects?
  5. What are the more serious side effects?
A
  1. Combination of Carbidopa & Entacopone
  2. Metabolised to DA in the brain
  3. Prevents DA being produced in the periphery, by breaking it down
  4. Dyskinesia & On off effect (Hypokinesia worsen for patient, due to fluctuating plasma concentration)
  5. Nausea, and postural hypotension
49
Q
  1. What do Dopamine agonists do?
  2. Give some examples
  3. Why are they not used?
A
  1. Potentiate the DA receptors
  2. Pramipexole, Ropinirole
  3. Side effects, and compulsive behaviours
50
Q
  1. What are MAO-B inhibitors?
  2. Give examples?
  3. What are the side effects?
A
  1. Selective MAO-B inhibitors which prevent DA breakdown
  2. Selegiline & Rasagiline
  3. Can cause anxiety, and insomnia
51
Q
  1. What is Amantadine?
  2. Why is it not used?
A
  1. Antiviral drug that Releases DA
  2. Less effect than Levadopa
52
Q
  1. What is Benztropine?
  2. What is its effect?
  3. What are the side effects?
A
  1. Muscarinic ACh receptor antagonist
  2. Supression of muscarinic receptors stops inhibition of DA neurons
  3. Dry mouth, constipation, urinary retention
53
Q
  1. What is deep brain stimulation?
  2. What is lesional stimulation?
  3. What is a Pallidotomy?
A
  1. Electrical Stimulation of the subthalamic nuclei with implanted electrodes
  2. Formation of lesions to suppress overactivity of subcortical areas
  3. Destruction of the GP by surgery, to control dyskinesia

Neurology - Sem 3 (15 decks)

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