Week 6 Flashcards

1
Q

MS is due to degenration of ___

A

myelin in the nerves of the CNS

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2
Q

what basal ganglia control

A

unwanted movements

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3
Q

where is the synapse begween upper and lower motor neurons

A

anterior horn

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4
Q

what are 2 skelteal muscle disroders of the motor unit

A

disuse atrophy

msular dystophy
- gentic
prgressive deeneraotion - necrosis
muscle fibers replaced by adipose and connective tissue

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5
Q

what is mysathenia gravis

A

autoimmune - attack on the nictoninic acetylcholine erceptors

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6
Q

myasthenins is due to a defct in upper and lower MN. True or false .

A

false - due to muscle fibres (nicotninc acetylcholine receptors)

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7
Q

what is amyotophic lateral sclerosis ?

A

rapidly prgresing degenrative diases of motor neurons
- protein misfolding -> neuronal death + degernation

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8
Q

what part of the nueromuscular system does amyotophic alteal sclerosis affect?

A
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9
Q

what are some symptoms involved with amyotophic lateral sclerosis

brainstem specific?

end stage:

A

msucle weakness, spcity ,imparied fine mtoor control, hyporeflexia

brainstem: dysphagia (swallowing dificulty), dysarthia (speech articularion)

end stage: paralysis, respiratory failure

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10
Q

what is MS

A

inflammatory immune - affects conudciton of neural imnpulses

degenration of nerusons in the CNS by loss of myelin + inflammmation

  • diffuse patches of demyeliantion –> scar tissue formation
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11
Q

whatcells does MS affect that myeliante nerves in the CNS

A

oligodendrocytes

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12
Q

what is the cause of MS

A

unkown - link to gentics, environmental, virus

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13
Q

what do symtpoms of MS?

A

lcoation -severity demyelination, type of neurons

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14
Q

in MS can myelin be reapired? what a bt repeasted attacks?

A

it can but after repeatd attacks the repari become less effective

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15
Q

what is sclerosis mean?

A

scar tisue formation

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16
Q

what determines the symptom tyoe of MS

A

wherver tge demyeliantion occurs + extent determines severity

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17
Q

MS pathophy

A
  1. unknown tirgger
  2. actiavted T cells cross blood brain barrier
  3. cytokines secreted
  4. more immune cells recuied

5.a ttack oligodendrocytes

  1. myeline damaged and breaks down
  2. scar tissue formation + axonal dwestructipn
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18
Q

what is the end result of MS afte rmueline breask down

A

scar tissue formation + axon desruction

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19
Q

what is the single tratment of MS

A

there is none - it is multideicplinary

incldues immosuppresants, pahrmaetuicals, physio + exercise,

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20
Q

what are some treatments for MS

A

disease mod drugs - immunosuppresnats min frequency of exacerbations - slower progression

pharmecuitcals can help w symptoms like fatigue, spactiicty ,dpression, bladder dysfunction

physio + exercise to maintain strngth and mobility

ocupation support ADL

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21
Q

what are 3 considerataion for those with MS?

A

prescroiibe within phsycical limiations

consider use of supportative equipment

strength varies from week to week

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22
Q

what is the impact od exrcise on brain volueme and clinical disability in those with MS

A

brean voluem remains higher for those engaing in lifelong exercise, still higher for those engaging after diagnosis

clincial disability less in lifeslong + exrise after MS

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23
Q

wher does cerbreal palsy arise form? what type of condition?

A

arises form something that happens during declopment (pre or pst natl). neurodevelopmental condition

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24
Q

what does the affect of cerebreal pasly depend on?

A

the muscles affected depdns on th part of braiin affected

it can be spastic - if upper motor neurons damaged

dyskinetic - (involunatry movement - basl ganglia damged) or ataxic -damage to cerebllume

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25
what 3 parts of the brain can cerbreal palsy affect and what is the effect of each?
upper motor neurons - spastic basal ganglia - dyskinetic (ivoluntary movemnts) cereblluiem - ataxic (lack of coorindation/balcnce)
26
what happens if upper motor neurons ar damged in cerbreal palsey
spastic movements
27
what happens if basal ganglia is affecte din cerebal palsy?
dykinetic - uncocontrolle involuntary moevemtns
28
what happens if cerebblum is affected in cerbreal palsey
ataxic - lack of control/coordination
29
what is parkinsons diseae?
synaptic transmission - dopamine release is reduced - nigiostriatal pathways (neruons from susbatntia nigra v ot the striatum in the basal gangllia)
30
parkisons disease is destruction of the neurons in the ____
nigrostraital pathways - neurons from the substantia nigra
31
what is the progression of parkinsons ?
cardinal symtpoms - then demntia - thend eath
32
what is etiology of parkinsons?
unknown - environment + gentic (environmental toxins may icnrase risk) sevral genes to icnreased risk
33
wher are dompaine neruons located in the basl ganglia>
nigro-striatal pathway in substantia nigra
33
what are the normal responsibiit of dapminergic neurons of substantia nigra ?
1) allow signal to cerebral cortex for movemnt intiaition 2) fine uning signals to preven unwatned moivemt
34
what can be seen in the affected neruons of people with aprkisons diseas bfore theyd ie?
lewy bodys (protein deposits)
35
what is the trigger of aprkinsons disease?
unknown
36
explain pathophys of parkisons disease?
unnkown trigger - degen of neruons of substantia nigra that release dopmaine less dopamine onto neurons of striatum imbalnce of excit + inhib nt released in striatum result of too much incoluntary and not enough voluntary
37
what does dopmaine do?
produce inhibitory/excitatory stimulus on postsynaptic neurons
38
what part of brain is involved of dopamine sytemin the basal ganglia -these neurons affected in parkisnons
striatum
39
what are the 4 cardinal symptoms of parkinsons?
bradykinesia (slow mvement) muscle rigidity (spastic movemnt) resiting tremor postural instability
40
what is common treatment for those with parkinsons?
dopamine replacement therapy - dopamine cant cross blood-brain barrier, give L - Dopa - converted to dpamione in brain drugs taht inhibt dopamine breakdowm - dopamine produce dlast longer exerices physio occuaptional therapy - maintain moboltiy +stability, maintain strenghth balance fflex safe use of asaptive devicec, faciliate ADL, optimize QOL
41
degenration of neruons of the ____ stop dopamine form being released onto neurons of the _____
substantia nigra - striatum
42
When travelling to certain areas, it’s important to take malaria medication in order to prevent onset of disease. This is an example of
prophylaxis
43
Karen had been feeling fatigued and generally unwell for quite some time before eventually experiencing joint pain and in-the- end she was diagnosed with Rheumatoid Arthritis. The initial nonspecific symptoms could be classified as
prodromal
44
John is experiencing extreme nausea as a result of his chemotherapy treatment. The cause of the nausea is thus considered
) Iatrogenic
45
compare pahrmacokinetics and pharmacodynamics
46
comapre pharmacokinetics and pharmacodynamics?
pharmacokinetics is the effect of the body on the drug - inolves abosrpotion, distubtion, metbaolism and elimination of the drug - drug conc vs time pharmaco dynamic is the effect of the drug on the body and involces potency and efficacy - therapeui effect potency is strength of drug at particular dose efficacy is the max effect achieved by the drug
47
a complication of congestive heart failure is pulmonary edem becaue of ___
increased hyrosttic pressure in pulm cap.
48
when u sprain ur ankle the sweeling taht occurs is a result of
increased local capillary permeability
49
Excess sweating while running on a hot day followed by water intake to compensate could lead to: a) Hypokalemia b) Hyperkalemia c) Hyponatremia d) Hypernatremia
hyponatremia
50
Compare Respiratory vs Metabolic Acidosis in terms of their general cause and how the body compensates.
respiratory cause: incrase CO2 in. blood comp - increase ventialtion - blow off Co2 increase HCO3, decrease H+ by kidneys metabolic incrase H+ in blood (decrsase HCo3-) comp: incrase ventilation ncrease (reabsorbs) HCO3, decrease (excrete) H+ by kidneys
51
Decreased number of dopamine releasing neurons make this disease, bradykinesia, msucle rigidity (spastic movement). resting tremor, postural instability
parkinsons
52
Dendritic cells are considered the ‘bridge’ between innate and adaptive immune response because they ‘present’ an antigen to
T cells
53
Which of the following neurotransmitters is released by the primary afferent neuron in response to a nociceptive (pain) stimulus? a) Substance P b) Serotonin c) Enkephalin d) Acetylcholine
substance P
54
In an acute inflammatory response, chemical mediators are released. List 3 local actions of these chemical mediators.
Pain response: bind to nocireceptores vascular respone: vasodiation + increased cap perm cellular response: chemoatxis 9attract immune cells) increased capillary permability, vasodilation, chemotaxis
55
Why would an immunosuppressant medication be prescribed for an autoimmune condition such as Rheumatoid Arthritis
rheumatoid arthritis is an autoimmuen condition where immune syten is promtoing a reaction whe it shoudlnte and sttacks healthy tisssue with antibodies. Prescribing immunosuppresant would decrease activitu of immunesystem and decrease the autoimmune response.
56
Sanjit is 7 years old and fell off the monkey bars and broke his radius. The break is considered a greenstick fracture because the bone is not fully severed. This would be classified as a(n) ______ fracture
incomplete
57
Place the steps of bone healing process in the correct order 3. Clot formation (hematoma), fibrin meshwork & Inflammatory Response 1. Granulation Tissue Growth 4. Chondroblasts produce cartilage, forming a procallus 2. Osteoblasts deposit bone (callus) 5. Bone remodeling
1. clot fomation hematoma, fibring meshwotk + inflammatory 2. granulation tissue growth 3. chonroplast prod cartillag, forming procallus 4. osteoblas depost bone - callus 5. bone remodelling
58
Place the following steps of Osteoarthritis pathophysiology in order: 1 - Inflammation of the synovium 2 - Chondrocytes release degradative enzymes 3 - Cracks form in the cartilage 4 - Exposed bone leads to development of osteophytes 5 - Synovial cells remove debris
1. chondroytes release degradtive enymees - breakdown of catilage 2. synovial cells remove debris 3. inflammation of synovium 4. crack in cartillage 5. exposed bone leads to deelopment of osteophytes
59
When RANK ligand is released, it binds to and activates osteoclasts. In females post-menopause, estrogen levels drop. This results in
increase expression and release of rank likand, icnrease =, decrease opg
60
Progressive demyelination of neurons of the central nervous system leads to impaired nerve function. The impairment can be sensory or motor depending on the nerve affected. what disease?
MS
61
autoimmune condition that results in an attack on the nicotinic Acetylcholine receptors located on muscle fibers. Leads to skeletal muscle weakness, paralysis
myasthenia gravis
62
An individual has experienced a spinal cord injury resulting in an incomplete loss of sensory function with complete loss of motor function. Based on this information, what is their ASIA score?
Incomplete B
63
hwo is thymus gland involve in immune system
makes T cells
64
what is spleens role in immuen sytem
filter blood - fight infeciton +dteect (antibodies_
65
what is tonsils role in immune system
pruce immune cells -trape and filter pathogens
66