Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 |