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Mech. 2 > Exam 2.3 > Flashcards

Exam 2.3 Flashcards

1
Q

Structure CNS

A

Organ=brain and SC
Org.=overall command center
Function=process/integrate into

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2
Q

Structure PNS

A

Organs=N. and gang.
Org.=receive/send to and from CNS
Function=Mediator some reflex

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3
Q

Function-motor

A

CNS/PNS=axon transmit N. impulses from CNS–>muscle/gland
Somatic=voluntary of sk. muscle
Automatic=involun. control of sm. muscle cardiac/glands

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4
Q

Function-SENSORY

A

CNS/PNS=both(axon transmit N. impulse from peripheral strucutre–>CNS)
-Eye and ears=PNS
Somatic=transmit input from skin, fascia, joint and sk. muscle
Automatic=transmit input from stomach and intestine (viscera)

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5
Q

light traveling and reflection

A

goes from axon layer–>retinal pigmented epith. and goes back up

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6
Q

Glaucoma-Pathogenesis

A

Incre. intraocular P.
-incre. production/decre. vitreous humor
Block blood flow through intraocular vessel in uvea(compress)
Decre. BF=depriving retinal from nutrients
-atrophy of retinal layer

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7
Q

Glaucoma-tx

A

reduce fluid prod. or drain

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8
Q

Glaucoma-damage and S/S

A

Retinal damage=blurred vision, impaired dark adaptation
Corneal damage=halos around lights
Optic N. atrophy

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9
Q

Glaucoma-retinal atrophy

A 
Disrupt N. fiber layer 
-AKA axon layer 
Ganglion cell layer 
Damage to layers of rod/cons
Thinning of retina
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10
Q

Middle ear dis.

A

Otosclerosis

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11
Q

Otosclerosis-symp or not

A

Genetic is usually asymp.

Other times symp.

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12
Q

Otosclerosis-oval window involvement

A

Bony growth around oval window (stapes dnt move window)
-no reabsoprt. b/c incre. bone= decre. stapes mov.
:no vibration transmitted (even if Incus moving)

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13
Q

Otosclerosis-path.

A 
Uncoupling of resorption/deposition 
Fibrosisi and vascularization of temporal bone 
Dense new bone replace fibrotic tissue 
-anchor footplate of stapes
-no vibration=deaf
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14
Q

Inner ear dis.

A

Tinnitus

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15
Q

Tinnitus

A

Ears ringing
-also hissing, whistling, humming and roaring
Transient not assoc. w/ dis.
-excessive stim. of hair cells
Persistent is assoc. w/ hearing loss
-assoc. w/ cochlear or CN VII dysfunction

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16
Q

Neuromuscular dis. vs. myelin sheath dis.

A

Neurmusc.=myasthenia gravis

Myelin sheath.=multiple sclerosis

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17
Q

Neuromuscular junction- synapse type on terminal motor axons synapse w/ sarcolemma

A 
Chemical synapse 
-NT activate ion uptake in post. synp. memb. (dendrites/sk. muscle) 
Electrical synp. 
-ion travel through gap junction 
-common in cardiac, sm. muscle
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18
Q

NT

A

1st discovered=Ach and N.epi
Activate and inhib.
Usually amine, AA or small peptide
Degraded in synaptic clef or taken up by endocytosis
-stop prolong stim.
-post/pre syn. memb.
may act as paracrine horm. outside N. syst.

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19
Q

Myasthenia gravis-immune dis.

A 
Autoimmune dis.-->antiBD med. 
-antBD to ach Recep. 
-induce aggregation and degradation of recep. 
Reduced ach Recep. 
-post-synp. memb. 
-decre. resp. to ach=muscle wk. 
AntiBD also interact w/ thymus 
-benign thymoma 
-thymic hyperplasia 
  :B cell follicles in thymus (not just overgrow)
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20
Q

Myasthenia gravis-symp.

A

Fluctuating wk.
-incre. over the course of the day
-incre. upon exertion
-decre. muscle responsiveness upon repeated stim.
Involvement of extra-ocular muscles(unusual for myopathy)
-diplopia/ptosis

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21
Q

Myasthenia Gravis-Tx

A

Acetylcholinesterase inhib.
-ach persisits in synaptic cleft
Immunosuppressive thearpy (glucocorticoids) or plamapheresis
Thymectomy for pts. w/ thymoma

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22
Q

Myelin sheath.-chact.

A 
Layers of memb. surround an axon 
CNS=white matter macroscopic 
Import. for sig. transmission 
Salutatory Conduction
- signals jumps from node to node
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23
Q

Myelin sheath dis?

A

Multiple sclerosis

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24
Q

MS is autoimmune dis?

A

yes

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25
Q

MS-autoimmune dis.

A

Immune response to myelin sheath
Chronic immune cell (T cell/MAC) around myelin sheath plaque (lost myelin)
Complex multigene dis.
-link to MHC comp. DR2
-Also IL-2/IL-7 Recep.
Lesion w/in M. Sheath decr. N. transmission efficiency
Relapsing episode of N. Def.
-variable duration (wks or yrs)
-grad./partial recovery=each recovery (steady decline)
Freq. incre. w/ time while recovery=P. Restrict dis.

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26
Q

MS-immune response

A

T helper cell initiate immune response against
Cytokines release promote MAC and leuko. infiltration
MAC and leuko. release agents to damage invades
Agents myelin sheath instead
-since there r no invaders

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27
Q

MS-tissue damage

A

Consist w/ others immune dis. have studied
Immune response itself produce tissue damage
Lesion r firmer than surrounding tissue
-sclerosis b/c myline incre. lipid components
:usual fibrosis but ~ b/c tissue is lost

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28
Q

MS-S/S

A 
Unilateral visual impair=b/c optic N. b4 optic chiams 
Brain stem
-CN signs (no hear/taste)
-Ataxia=impaired coordinate 
-Nystagmus=involv. Rhythmic eye mov. 
-Internuc. Ophthalmogplegia 
  :eye goes one way and other drags behind it 
Spinal cord lesion
-motor/sensory N. (muscle control)
-Spascity and lost bladder control
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29
Q

CNS dis.

A 
Ethanol toxicity 
Cerebrovascular dis. 
Prion dis. 
Motor N. dis. (degenerative)
Degenerative dis. 
Dementia (degenerative)
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30
Q

Cerebrovascular dis.

A

Cerebral edema

Focal cerebral ischemia

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31
Q

Toxic CNS damage

A

ethanol toxicity

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32
Q

creutzfeldt-jakob dis.

A

prion dis.

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33
Q

ALS

A

motor n. dis.

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34
Q

Parkinson’s dis.

A

degenerative dis.

35
Q

alzheimer dis.

A

dementia

36
Q

Toxic N. Damage

A

Cellular and tissue loss due to toxicity
Unique Consideration in CNS
-isolation (BBB)=toxin in blood dnt affect and need to cross barrier
-incre. metabolic needs=ie gluc. need (more sensitivity)
-repair cap.=limited
:harder to recover from toxicity

37
Q

Acute vs. chronic ethanol induced toxicity

A

Acute=abuse is gen. reversible

Chronic=alcohol abuse assoc. w/ metabolic disturbances

38
Q

Ethanol toxicity-hepatic encephalopathy

A

Glial response w/in CNS (w/in cerebral cortex/basal gang.)
changes liver
Incre. Ammonia and pro-inflam. cytokines
Astrocyte changes=alzheimer type II cell
-enlarged nuclei
-minimal reactive cytop.

39
Q

ethanol toxicity-thamine def.

A

Malnutrient or malabsorp.
Assoc. w/ chronic ethanol abuse
Acute=wernicke encephalopathy
Chronic=Korsakoff synd.

40
Q

Wernicke Encephalopathy

A

Acute thiamine def.
Reversible (w/ thiamine supplement)
Ophthalmoplegia
Psychotic symp.

41
Q

Korsakoff synd.

A 
Chronic thiamine def. Irreversible
Assoc. w/ lesion in the thalamus 
-short term memory prob. 
-Confabulation 
Pathology 
-Early=dilated cap. w/ prominent endoth. cell
-hemorrhagic/necrotic foci in ventricular walls 
-eventual cyst formation
42
Q

Ethanol toxicity in CNS

A

Direct/2dry to malnutrition
Cerebellar dysfunction in 1% of chronic alcoholics
-ant. vermis
Atrophy and loss of granules cell (interN. –>purkinje cells)

43
Q

Atrophy/loss of granule cells

A

Excite sig. form res of N. syst.
Participate in processing visual and motor info
-learn and memory

44
Q

Ethanol toxicity CNS-clinical

A

truncal ataxia
Unsteady gate
Nystagmus

45
Q

Cerebral Edema

A

Sig.=accum excess fluid w/in brain parenchyma
-not w/in CSF but around N. cell
Cause=excess fluid leakage from BV or CNS cell damage
Caused by
-vasogenic=BBB disruption and incre. perm. allowing fluid to move from w/in vasculature to w/in parenchymal space
-cystotoxic=2ndry to cell memb. injury (N., glial, endoth.)
:generalized hypoxia/ischemia
:Metabolic disruption-ionic homeostasis

46
Q

Cerebral edema-2 pathway

A

Vasogenic=BBB disruption and incre. perm.
-allowing fluid to move from w/in vasculature to w/in parenchymal space
Cytotoxic=2ndry to cell memb. injury (N., glial, endoth.)
-generalized hypoxia/ischemia
-Metabolic disruption-ionic homeostasis

47
Q

Cerebral edema-BRAIN pathology/morphology

A

Gyri flattened/sulci narrow
Ventricles compressed
If untx=herniation

48
Q

Cerebral edema-death

A

range from subtle neurolgical deficits to death

49
Q

Focal Cerebral Ischemia

A 
Sig.=Limited to no BF to specific area of brain
Cause=Arterial occlusion/hyoperfusion 
Caused by
-embolism 
-vascular inflam. 
-In-situ thrombosis (athersclerosis MC)
50
Q

focal cerebral ischemia-response

A 
N. stress=red N. b/c eosin 
MAC/reactive gliosis to clean up damage 
Repair
-removal of tissue 
-loss of architecture 
-gliosis (incre. glial)
51
Q

Cause rapidly progressive neurodegenerative disorders

A 
Human
-creutzfeldt-jakob dis. 
-fatal familial insomnia 
-Kuru
Sheep/goat=scrapie 
Bovine spongiform encephalopathy=mad cow dis.
52
Q

Kuru

A 
Plaque w/in humans tissue 
Extracell aggregated PrPsc
Detectable w/ PAS or congo red 
W/in cerebellum 
Also varients CJD(vCJD)
53
Q

Bovine spongiform encephalopathy

A

vCJD=dnt change PrP gene
Ingest contaminated beef w/ prions or blood
Damage cerebral cortex

54
Q

Conformational change of prions

A

Abnormal forms of cellular protein
-specific protein termed prion protein (PrP)
Alpha helix containing isoform(PrPc)–>abnorma. beta shee isoform(PrPsc)
Rapid progressive N. degen. disorder
-sporadic, familial or transmitted

55
Q

spongiform changes Common pathology

A

Caused by intracellular vacuoles in N. and glia
Cerebral cortex
Progressive dis.=not rapidly noticed atrophy
-only seen in grow examine
Avg. survival is 7 mo.

56
Q

spongiform symp.

A

Changes in memory/behavior
Dementia
Start myoclonus=abnormal jump instead of jerk

57
Q

Amyotrophic lateral sclerosis(ALS) AND what does the name mean

A

Motor N. dis.
Amyotrophic
-muscle paralysisi w/ no atrophy
-hypertonia(rigid) and exaggerated deep muscle tendon reflexes
Lateral sclerosis
-corticospinal tract degen.
-produce upper/lower motor N. paralysis in extremities

58
Q

Lou Gehrig’s dis.

A

ALS-motor N. dis.

59
Q

ALS-motor N. loss

A 
Loss of lower motor N. 
-Spinal cord and brain stem 
Loss of upper motor N. 
-projection into spinal cord 
-NOT brain stem
60
Q

familial ALS

A

GOF of coper-zinc superoxide dismutase (SOD1)
-dnt eliminate ROS originally thought to kill N.
-UPR induced by misfold SOD1=new
-contribute to malfunction of glial cells
Other mutation
-dynactin(retrograd transport)
-VAMP-assoc. prot B (reg. of vesicle transport)
-Alsin=guanine exchange factor domaine
-reg. endosomal trafficking

61
Q

ALS-pathogenesis

A

SOD1 mutation
Altered axonal transport
Neurofilament abnorm.
Glutamate toxicity=excited death(overstim. cell death)
-incre. intracell. Ca2+
Develop protein aggregation
-Bunina bodies(PAS-binding inclusion in cytop.)

62
Q

ALS-S/S

A 
Motor/N. loss 
-hand weakness 
-Arm and leg spascity/cramp
Eventually
-muscle strength/bulk decre. -fasciculation
-Death=resp. muscles
63
Q

Parkinson-degenerative dis.

A

Substantia Nigra degen. in basal ganglia
S/S=tremor, rigidity, bradykinesia
L-dopa response=damage cell

64
Q

Parkinson like dis.

A

Assoc. w/ toxin or other cuase

Dopamine antagonist

65
Q

Parkinson-degen. of N. has a lack of what

A

dopamine

66
Q

Parkinson-substantia Nigra

A

Loss pigmented N.

Assoc. gliosis

67
Q

Parkinson-lewy bodies

A

Eosinophilic cytoplasmic inclusion

alpha-synuclein fiber

68
Q

Parkinson dis.- alpha synuclein

A

Lipid-binding prot. assoc. w/ synapses
Mutation assoc. incre. gene copy=gene dosage effect
Overexpression induce lewy body formation in mice
Inhib. melanin production in skin
-linked to melanoma incidence
-enzymes for dopamine’s reg. tyrosine hydroxlase
Activates melanin production in N.
-Neuromelanin linked ot incre oxidative stress susceptability in dopaminergic N.

69
Q

Parkinson-molecular genetic

A 
Familial PD not common BUT instructive 
Assoc. GOF 
-leucin rich repeat kinase 2(LRRK2)
-alpha synuclein 
-DJ1 (redox stress response)
-PINK1(kinase that regulates mitoch. function)
LOF=parkin(assoc. w/ juvenile form)
70
Q

Parkinson-Genetic Mech.

A 
Stress reposne(UPR/ROS)=alpha synunclin, DJ1
Defective proteasome function=parkin
Change mitoch. function=DJ1 and PINK1
71
Q

Parkinsonian disorder name and mitoch. toxin

A

1-methyl-4-phenyl-1,2,3,5-tetrahydrophridine
Byproduct of synthetic opioid production
Mitochondrial toxin
-generate model syst. for PD research
-selectively injure dopaminergic N.
:unkown mech. for selectivity
:dopamine eposure can incre. ROS=cells may be more sensitive

72
Q

MPTP MOA

A

MPTP–>MPP+(N-methyl-4-phenylpyridinium) in astrocyte
-takes up dopa
MPP+ inhib. complex of ETC
Decre. ATP production and oxygen metabolism
Incre. ROS generation
-oxidative damage to lipid, prot., NA

73
Q

dementia

A

inhib. memory or other cortical function w/ alert

74
Q

Alzheimer dis.

A

MC of dementia

First sign is impaired learning and recall of recent memories

75
Q

Alzheimer-presence of specific amyloid plaq.

A

Extracell
W/in cerebral cortex and BV walls (meningeal and cerebral)
AKA neurtic plaques
Central amyloid Beta core w/ halo prot.
Surrounded by netwrk of misshapen N. process/nutrients
Microglial and reactive astrocyte periphery
-immune response

76
Q

Alheimer dis. intracel. protein

A

Neurofibrillary tangels (NFT)
-not specific AD
-paired helical filaments contain hyperphos. tau
:aggregate b/c microtub. binding prot.
-Found in N. processes (neurities) surrounding plaques

77
Q

type of N. in alzheimer dis.

A

N. and synaptic loss and presence of reactive astrocytosis and microglial prolif.

78
Q

Alzhimers-reactive astrocytosis

A

Incre. size and number in response to traumatic injury
Synthesis and release cytokine
Induce migration of immune cells into CNS
Astrocytes also remove excess glutamate through specific transplates
-TX=glutamine cytoxicty

79
Q

alzheimer assoc. prot.

A

Presenilin (GOF)
Apolipoprotein E4
Amyloid Beta(AB) N. damage
N. loss consequence

80
Q

Presenilin

A

Subunit of gama-secretase(from amyloid beta)
Import for proper amyloid processing
-other substrate critical N. function

81
Q

Apolipoprotein E4

A

Mediates LDL binding to recp.
Promote Ab formation and deposition (possibly through binding)
ApoE3 bind tau

82
Q

amyloid B(AB) N. damage

A 
Directly cytotoxic 
-plaque number no correlate to dis. 
Synaptic dysfusntion 
-block long-term potnetiation 
-other memb. change 
Inflammatory response 
-mediators induce localized damage 
-affect tauP
-Cause oxidative damage
83
Q

Alzheimer’s-atrophy in cerebral cortex

A 
Frontal lobe
-planning complex behavior/multitasking 
-controling impulses, emotions, thoughts 
Temporal lobe 
-speech(cnt find the right word)
-reading/writing 
Parietal lobe
-integrates visual and auditory info.
84
Q

Alzheimers-memory issues

A 
Limbic system network 
-hippocampus thalamus, hypothalamus 
-necessary for learning and memory storage 
Posterior cortical areas
-language comprehension 
Cortical assoc. area
-storage of remote memories

Mech. 2 (8 decks)

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