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52 Cards in this Set

  • Front
  • Back

which neurotransmitters are affected in PD?

NA, ACh, 5-HT, DA

which neurotranmitters cause nausea in PD?

5-ht

which neurotransmitters cause sleeping problems in PD?

5ht and NA

what are the stages of the hoehn and yahr scale?

1. unilateral, minimal functional disability


2. bilateral/ midline, no impaired balance


3. bilateral. mild/ moderate functional disability with impaired postural reflexes. physically independent


4. severely debilitating. can stand, walk unaided.


5. bed/ wheelchair confined

what are the hurdles to treating PD?

- dysphagia


- stomach, jejunum variable absorption


- tissue enzymes


- BBB - competition with large neutral aa's


- striatum - conversion to DA

what is chorea movement?

=irregular (not rthymic, not repetitive), quick, small to medium amplitude


- distal predilection

which diseases can cause chorea?

- HD


- levodopa side effect


- SLE

what is hemiballism/ ballism movement?

=irregular (not rthymic, not repetitive), quick, large amplitude


- proximal and arm predilection


- ONE SIDE of body



which diseases can cause ballism/ hemiballism?

- stroke/ subthalamic nucleus lesion


- levodopa side effect

what is dystonia?


give some examples.

- lasting muscle contraction = abnormal body position... improved by 'geste antagoniste'


- focal (torticollis, writer's cramp)/ generalised

which diseases can cause dystonia?

- certain activities eg. playing instrument


- levodopa side effect

what is a myoclonus?

-sudden, partly repetitive muscle contractions (at rest or in action)

which diseases cause myoclonus?

-epilepsy


-sleep


-SCI


-creutz-jacob

what are tics?

- sudden, short lasting, repetitive muscle contractions - lead to movements or noises (partially suppressible)

which diseases can cause tics?

-tourettes


-hungtintons

what forms the lentiform nucleus?

putamen, globus pallidus

what forms the basal ganglia?

caudate, putamen, globus pallidus

what is the prefrontal corticopontine output?

cortical output stopping at pons... goes through internal capsule, relays through cerebellum

what are the four major streams ordered within the internal capsule?

-optic and auditory radiations


-anterior limb


- genu


- posterior limb

what happens in damage to the posterior limb and genu of the internal capsule?

paralysis, loss of sensation, loss of vision and hearing

what happens in damage to the anterior limb of the internal capsule?

cognitive defects (personality changes)

what does damage to the cerebellum cause?

-hypotonia - pendulous reflexes


-astasia/ abasia


- ataxia (multi-joint timing/ coordination errors)


- action (intention) tremor

what happens in ataxia and intention tremor caused by cerebellar damage?

- delay initiating ipsilateral movement


- dysmetria and decomposition of complex movements


-dysdiadochokinesia

what inputs does the cerebellum recieve?

mossy fibres from:


-pontinne motor inputs


- spinal proprioceptive inputs

what are the three regions of the cerebellum, their function and their output?

1. cerebrocerebellum (neocerebellum)... motor planning, cognition... to ventrolateral thalamus


2. spinocerebellum (paleocerebellum)... posture... to red nucleus of midbrain and ventrolateral thalamus


3. vestibulocerebellum (arachicerebellum)... balance... to vestibular nuclei

what type of damage does cerebellar damage cause?

ipsilateral

which mutation is involved in parkinson's disease?

alpha-synuclein

which chromosome is hungtington's disease mutation on?

4

what change of function occurs in huntington's disease?

gain of toxic function

what is compensatory sprouting and a pathology of it?

when another motor unit takes over a dead motor neurons territory




decreases in motor neuron disease

what do non-neuronal cells do in motor neuron disease?

exacerbate disease...


microglia - release toxic factors


astrocytes - release toxic factors, can't recycle glutamate = excitoxicity

describe the mechanism of self-propagating prion proteins.

protein misfolding - protein aggregation - nucleation and propagation - release and transmission

by what molecules does increased calcium cause damage?

- proteases, endonucleases


- stress activated kinases


-phospholipases


- nitric oxide synthase (NOS)

what does current and future alzheimer's treatment involve?

-beta/gamma-secretase inhibitors for amyloid deposition


- NMDA inhibitors for excitotoxicity, inflammation


- NSAIDs for inflammation


- cholinesterase inhibitors for neurotransmitter disturbance

what is a pathological hallmark for PD (not exclusive)?

lewy bodies

what mechanisms may contribute to SNc degeneration in PD?

-oxidative stress... reduced antioxidative glutathione; increase fe2+ and impaired mitochondrial complex 1 activity, driving fenton's reaction


-excitotoxicity... low calbindin levels to mop up extra calcium


- faulty protein degradation

what does activation of the direct and indirect pathway of the basal ganglia result in?




what does dopamine do to these pathways?

direct - facilitates movement


indirect - inhibits movement




dopamine activates direct pathway and inactivates indirect and so FACILITATES movement in both

outline the drugs, with an example, used to treat Parkinson's.

-muscarinic antagonists (anticholinergics) - benzatropine


- l-dopa


- Dopa decarboxylase inhibitors - carbidopa


- COMT inhibitors - entacapone


- MAOB inhibitors - selegiline


- dopamine agonist - bromocriptine, rotigotine (patch)

what is the use of anticholingerics for parkinson's disease? what are side effects?

- mainly for tremor


- SEs: central (mood, confusion); peripheral (constipation, blurred vision, dry mouth)

what can L-dopa be administered with?

DDC inhibitors (prevents L-dopa to dopa)




COMT inhibitors

what are side effects of l-dopa?

nausea, postural hypotension, psychological (hallucinations... )

what are side effects of dopamine agonists?

as for l-dopa

what is the general first like PD treatment?

dopamine receptor agonists

what are alternative routes of drug administration to circumvent dyskinesias in PD?

-rotigotine patch


- duo-dopa

what are the surgical approaches to treating PD and their advantages/ disadvantages if applicable?

1. neuroablative surgery (irreversible, risks visual impairment, haemorrhage, speech, cognitive impairment)


2. deep brain stimulation mainly to subthalamic nucleus... reversible and graded

what are the failures of current parkinson's treatments?

- only treat some symptoms


- postural imbalance


- dyskinesias


- don't address degeneration

what are the braak stages of PD?

1+2: medulla oblongata confinement


3: upper and lower brainstem


4: also anteromedial temporal mesocortex


5+6: severe brain and neocortex involvement

what are the dopaminergic pathways of the brain?

- nigrostriatal


- mesocortical


- tuberohypophyseal

Describe the storage, release, receptors, reuptake, and degradation involving dopamine.

STORAGE - VMAT1, 2, 2H+ countertransporter


RELEASE - Ca dependent, end terminal, en passant varicosities


RECEPTORS: GPCRs, class A, rhodopsin (D1-like: D1, 5 coupled to Gs; D2-like: D2, D3, D4 coupled to Gi)


REUPTAKE: DAT, 2Na+ Cl- cotransport


DEGRADATION: COMT, MAOB... homovanillic acid

which recreational drugs involve dopamine?

cocaine, amphetamines, bromocriptine

Describe the storage, release, receptors, reuptake, and degradation involving Ach.

SYNTHESIS: ChAT, synthesised in cell bodies and transported to terminals


STORAGE: VAT, 2H+ countertransporter


RELEASE: Ca dependent, end terminals


RECEPTORS: ligand gated nicotinic; GPCR Class A, rhodopsin muscarinic (M1, 3, 5 = Gq/ll; M2,4 = Gi/o)


REUPTAKE: degraded first


DEGREDATION: Acetylcholinesterase

what recreational drugs involve Ach?

nicotine, scopalamine, henbane