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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
MS-autoimmune dis.
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.
26
MS-immune response
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
27
MS-tissue damage
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
28
MS-S/S
``` 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 ```
29
CNS dis.
``` Ethanol toxicity Cerebrovascular dis. Prion dis. Motor N. dis. (degenerative) Degenerative dis. Dementia (degenerative) ```
30
Cerebrovascular dis.
Cerebral edema | Focal cerebral ischemia
31
Toxic CNS damage
ethanol toxicity
32
creutzfeldt-jakob dis.
prion dis.
33
ALS
motor n. dis.
34
Parkinson's dis.
degenerative dis.
35
alzheimer dis.
dementia
36
Toxic N. Damage
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
Acute vs. chronic ethanol induced toxicity
Acute=abuse is gen. reversible | Chronic=alcohol abuse assoc. w/ metabolic disturbances
38
Ethanol toxicity-hepatic encephalopathy
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
ethanol toxicity-thamine def.
Malnutrient or malabsorp. Assoc. w/ chronic ethanol abuse Acute=wernicke encephalopathy Chronic=Korsakoff synd.
40
Wernicke Encephalopathy
Acute thiamine def. Reversible (w/ thiamine supplement) Ophthalmoplegia Psychotic symp.
41
Korsakoff synd.
``` 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
Ethanol toxicity in CNS
Direct/2dry to malnutrition Cerebellar dysfunction in 1% of chronic alcoholics -ant. vermis Atrophy and loss of granules cell (interN. -->purkinje cells)
43
Atrophy/loss of granule cells
Excite sig. form res of N. syst. Participate in processing visual and motor info -learn and memory
44
Ethanol toxicity CNS-clinical
truncal ataxia Unsteady gate Nystagmus
45
Cerebral Edema
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
Cerebral edema-2 pathway
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
Cerebral edema-BRAIN pathology/morphology
Gyri flattened/sulci narrow Ventricles compressed If untx=herniation
48
Cerebral edema-death
range from subtle neurolgical deficits to death
49
Focal Cerebral Ischemia
``` 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
focal cerebral ischemia-response
``` 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
Cause rapidly progressive neurodegenerative disorders
``` Human -creutzfeldt-jakob dis. -fatal familial insomnia -Kuru Sheep/goat=scrapie Bovine spongiform encephalopathy=mad cow dis. ```
52
Kuru
``` Plaque w/in humans tissue Extracell aggregated PrPsc Detectable w/ PAS or congo red W/in cerebellum Also varients CJD(vCJD) ```
53
Bovine spongiform encephalopathy
vCJD=dnt change PrP gene Ingest contaminated beef w/ prions or blood Damage cerebral cortex
54
Conformational change of prions
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
spongiform changes Common pathology
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
spongiform symp.
Changes in memory/behavior Dementia Start myoclonus=abnormal jump instead of jerk
57
Amyotrophic lateral sclerosis(ALS) AND what does the name mean
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
Lou Gehrig's dis.
ALS-motor N. dis.
59
ALS-motor N. loss
``` Loss of lower motor N. -Spinal cord and brain stem Loss of upper motor N. -projection into spinal cord -NOT brain stem ```
60
familial ALS
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
ALS-pathogenesis
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
ALS-S/S
``` Motor/N. loss -hand weakness -Arm and leg spascity/cramp Eventually -muscle strength/bulk decre. -fasciculation -Death=resp. muscles ```
63
Parkinson-degenerative dis.
Substantia Nigra degen. in basal ganglia S/S=tremor, rigidity, bradykinesia L-dopa response=damage cell
64
Parkinson like dis.
Assoc. w/ toxin or other cuase | Dopamine antagonist
65
Parkinson-degen. of N. has a lack of what
dopamine
66
Parkinson-substantia Nigra
Loss pigmented N. | Assoc. gliosis
67
Parkinson-lewy bodies
Eosinophilic cytoplasmic inclusion | alpha-synuclein fiber
68
Parkinson dis.- alpha synuclein
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
Parkinson-molecular genetic
``` 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
Parkinson-Genetic Mech.
``` Stress reposne(UPR/ROS)=alpha synunclin, DJ1 Defective proteasome function=parkin Change mitoch. function=DJ1 and PINK1 ```
71
Parkinsonian disorder name and mitoch. toxin
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
MPTP MOA
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
dementia
inhib. memory or other cortical function w/ alert
74
Alzheimer dis.
MC of dementia | First sign is impaired learning and recall of recent memories
75
Alzheimer-presence of specific amyloid plaq.
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
Alheimer dis. intracel. protein
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
type of N. in alzheimer dis.
N. and synaptic loss and presence of reactive astrocytosis and microglial prolif.
78
Alzhimers-reactive astrocytosis
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
alzheimer assoc. prot.
Presenilin (GOF) Apolipoprotein E4 Amyloid Beta(AB) N. damage N. loss consequence
80
Presenilin
Subunit of gama-secretase(from amyloid beta) Import for proper amyloid processing -other substrate critical N. function
81
Apolipoprotein E4
Mediates LDL binding to recp. Promote Ab formation and deposition (possibly through binding) ApoE3 bind tau
82
amyloid B(AB) N. damage
``` 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
Alzheimer's-atrophy in cerebral cortex
``` 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
Alzheimers-memory issues
``` 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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