Exam 3 (week 1) Flashcards
(230 cards)
1
Q
how do endocrine glands transport secretions?
A
via capillaries, not glands
2
Q
difference between growth and tropic hormone targets
A
growth hormones target non-endocrine tissue. tropic targets endocrine tissue
3
Q
components of adenohypoph
A
- pars distalis
- tuberalis
- intermedia
4
Q
components of neurohypoph
A
- pars nervosa
2. infundibulum (median eminence superiorly, infundibular process)
5
Q
definition of pituitary stalk
A
pars tuberalis wrapped around infundibular process
6
Q
staining of pituitary
A
pars distalis = heavily stained (secretory granules)
pars nervosa = pale (neurons)
7
Q
embryonal origin of adenohypoph
A
ectoderm - rapthke’s pouch, groups up
8
Q
embryonal origin of neurohypophysis
A
neuronal - infundibulum from floor of diencephalon - slides down posterior to adenohypophesis
9
Q
embryological origin of pars intermedia
A
rathke’s pouch
10
Q
embryological cell developmental issue with pituitary development
A
some remnants of rathke’s pouch of ectoderm origin of adenohypoph can remain and divide, becoming CRANIOPHARYNGOMA (benign tumor that compresses pituitary gland causing compression of optic chiasma)
11
Q
connection between hypothalamus and neurophyophysis
A
DIRECT - via infundibulum (hypothalamoneurohypophysial tract)
12
Q
connection between hypothalaus and adenohypophysis
A
pituitary portal vessles - arcuate makes releasing/inhibiting factors to work on adenohypophysis)
13
Q
supra optic makes what hormone
A
vasopressin (ADH)
14
Q
PVN makes what hormone
A
oxytocin
15
Q
blood supply to pituitary gland (and what do they supply)
A
- superior hypophysial artery (supplies adenohypophysis)
- inferior hypophysial artery (supplies neurophypophysis)
- trabecular artery (connects superior and inferior)
16
Q
blood route in adenohypophysis (5)
A
1) superior hypophysial to
2) primary capillary plexus (collects tropic hormones from hypothalamus)
3) portal veins carry hormones down to
4) secondary capillary plexus to stimulate endocrine cells is pars distalis
5) those hormones leave via phypophysial vein to system
17
Q
blood route in neurohypophysis (3)
A
- blood from trabecular and inferior hypophysial artery flow into
- capillary plexus, at which point picks up hormones from PVN and supraoptic
- those then leave via the hypophysial vein
18
Q
cells under histo in pars distalis (4)
A
- chromophils, which include:
- acidophils (more numerous)
- basophils
- chromophobes (unstained cytoplasm - most likely undifferentiated cells)
19
Q
types of acidophils (and what do they produce)
A
- somatotrophs (GH)
2. mammotrophs (PRL)
20
Q
types of basophils (and what do they produce)
A
- thyrotrophs (TSH)
- gonadotrophs (FSH & LH)
- corticotrophs (ACTH)
21
Q
Which are more numerous - acidophils or basohils
A
acidophils
22
Q
on mallory stain, what color are acidophils
A
orange
23
Q
where in pars distalis are somatotrophs located
A
on the sides of pars distalis
24
Q
where in pars distalis are thyrotrophs and corticotrophs located
A
median portion of pars distalis
25
where are mammotrophs and gonadotrophs located in pars distalis
scattered
26
what percentage of cell population in adenohypophysis is somatotrophs
40-50%
27
when in the day are peak levels of GH released
before awakening
28
pathway of GH effects
1. GHRH released by hypothalamus triggers release of GH.
2. GH in liver stimulates release of IGF-1
3. IGF-1 binds to receptors on chondrocytes on long bones
-------
when levels of IGF-1 reach threshold, negative feedback to somatotrophs and to hypothalamus which releases somatostatin inhibit further activation of somatotrophs
29
how to inhibit somatotrophs (3)
1. negative feedback due to high level sof IGF-1
2. somatostatin from hypothalamus
3. high levels of glucose
30
excess of GH in adults leads to
acromegaly (prominent jaw, big feet, big hands)
31
what percentage of cell population in adenohypophysis is mammotrophs
15-20% normally, higher and bigger in pregnant women
32
pathway of mammotroph activity
1. (minor) prolactin-releasing factor and thyrotropin-releasing factor stimulate mammotrophs to release prolactin
1. (major) stimulation of mammotrophs by suckling (decreases dopamine)
2. prolactin acts of mammory gland
-----
inhibited by dopamine release in hypothalamus
33
what is role of prolactin
1. mammogenesis
2. lactogenesis
3. galactopoesis
34
FSH pathway
1. gonadotropin releasing hormone from hypothalamus releases FSH from gonatotroph
2. in women, FSH triggers proliferation of granuloma cells prodcuing estradiol
2. in men, sertoli cells are triggred to make androgen binding proteins
35
what percentage of cell population in adenohypophysis is gonadotrophs
10%
36
LH pathway
1. gonadotropin releasing hormone from hypothalamus stimulates gonadotroph to release LH
2. in women, LH stimulates corpus luteum to make progesterone
2. In men, Leydig cell is stimulated to make testosterone
37
what percentage of cell population in adenohypophysis is thyrotrophs
5%
38
TSH pathway
1. thyrotrophic releasing hormone released from hypothalamus to trigger thyrotrop to release TSH
2. TSH travels to thryroid gland to make T4 and T3 (only active component)
----
Levels of T3 feedback inhibition to hypothalamus ONLY (not pituitary)
39
levels of THS, T4 and T3 in pituitary cause of hypothyroidism
TSH down
T4 down
T3 down
40
levels of THS, T4 and T3 in thyroid cause of hypothyroidism
TSH up
T4 down
T3 down
41
levels of THS, T4 and T3 in pituitary cause of hyperthyroidism
TSH up
T4 up
T3 up
42
levels of THS, T4 and T3 in thyroid cause of hyperthyroidism
TSH down
T4 up
T3 up
43
what percentage of cell population in adenohypophysis is corticotrophs
20%
44
ACTH pathway
1. corticotropin releasing hormone from hypothalamus activates corticotrophs to release ACTH from pituitary
2. ACTH travels to adrenal gland to release cortisol (mostly)
3. cortisol travels to liver to be processed
4. when cortisol levels are too high feedback to hypothalamus and pituitary
45
high levels of stress and ACTH levels
high levels of stress stimulate ACTH - make lots of cortisol, and then you crash because you shut down corticotrophs
46
why can't you stop glucocorticoids quickly
don't want patient to crash - taper slowly to allow corticotrophs to pick up slack and make ACTH to retain endogenous cortisol levels
47
what do you see in histo for pars intermedia
cysts filled with colloid
48
what cell type do you see in pars tuberalis
gonadotrops mostly (not physiologically significant)
49
are axons myelinated or unmyleinated in neurohypophesis
unmyelinated
50
cell types/structures in neurohypophysis on histo (3)
1. unmyelniated axons
2. pituicytes (glial cells) supporting axons
3. venestrated cappilaries
51
role of oxytocin systemically (2)
1. causes contraction of myometrium in uterus during labor
| 2. contraction of myopeithelial cells of lactating mammary alveoli (propulsion of milk)
52
role of ADH systemically (2)
1. tunica media of arterioles - increase blood pressure (not significant)
2. collecting tubule in kidney - increase water permeability
53
how to distinguish hypothalamic diabetes insipidus from nephrogenic diabetes insipidus?
in HDI, ADH levels are down (inability to reuptake water) - can treat with exogenous ADH
in NDI - see loss of function of ADH V2 or AQP-2 genes (inability to reuptake water) - refractive to exogenous ADH
54
how do hormones travel down axon in neurohypophysis and how is release regulated
with neurophysin transporter (1 = oxytocin, 2 = vasopressin)
pituicytes at axon ending allow connection with capillaries after neural cue
55
path between light and pineal gland (5)
1. light into eye
2. suprachiasmatic nucleus
3. hypothalamospinal tract
4. superior cervical ganglion
5. pineal gland - decrease melatonin
56
embryologic origin of pineal gland
roof of posterior diencephalon
57
histo of pineal gland parenchyma (3)
1. pinealocytes (95%) - oval poorly stained loose chromatin
2. glial interstitial cells (5%) dense chromatin, elongated nuclei
3. BRAND SAND - black calcified concretions (increases with age)
58
how and when does basal ganglia suppress or promote movement (resting, purposeful, repeated)
in resting state, basal ganglia suppress all movements
when we choose to move a certain way, basal ganglia select appropriate movements and suppress all others
repeated and sequential movements become habits (freeing up cerebral cortex to think about other things)
59
what neurotramsiter is involved in reward or punishment reinforcement of behavior
dopamine
60
how is OCD related to basal ganglia
basal ganglia are crucial for initiation, selection, "one at a time" actions
61
parkinson's - hyper or hypokinesia
hypo - has trouble initiating movement
62
protein deposition related to parkinsons
alpha synuclein
63
4 major functions of basal ganglia
1. voluntary motor activities
2. regulatory
3. procedural learning
4. routine behaviors (habits)
64
tail of caudate is continuous with what
amygdala
65
which is more medial, globus pallidus or putamen?
globus pallidus - tucked under/within putamen
66
what do you also see in section where you can see subthalamic nuclei
mamillary bodies
67
what is corpus striatum/striatum?
caudate plus putamen
68
what neurotransmitter is responsible for pathways between cortex and striatum
glutamate (excitatory)
69
what neurotransmitter is responsible for pathways between susbtantia nigra and striatum
dopamine fibers onto GABA neurons (modulating)
70
projection from globus pallidus to thalamus (is it inhibitory or excitatory?)
inhibitory
71
what percentage of substantia nigra dopamine neurons for symptoms to begin?
80%
72
movement symptoms in parkinsons (3)
1. resting pill rolling tremor
2. bradykinesia
3. hypokinesia
73
muscle symptoms of parkinsons (3)
1. increased muscle tone
2. lead-pipe rigidity
3. cog-wheel rigidity
74
neuron type death in huntingtons
GABA neurons die from prefrontal to caudate
75
movement symptoms of Huntington's
1. chorea (continuous rapid movements)
| 2. athetosis (writhing)
76
hemiballismus cause and symptoms
stroke in subthalamic nucleus
periods of violent flailing movements
77
direct pathway purpose
to initiate movement
78
connection/interaction between VA/VL and cortex
VA/VL is directly/recipricolay connected to primary motor cortex, at a default is inhibited by internal globus pallidus
79
interaction between globus pallidus and thalamus for motor control
internal globus pallidus produces GABA inhibition of VA/VL cells to suppress all movements
80
interaction between putamen and globus pallidus for motor control
putamen usually is quiet, but when action is initiated, putamen fires GABA-ergic potential to the interal globu pallidus to allow VA/VL to send info to primary motor cortex
81
what makes putamen cells fire (inputs)
1) cerebral cortex (premotor, motor and somatosensory)
excitatory glutamatergic input
2) association cortex
3) limbic lobe
82
direct pathway purpose
for movement selection
83
what is VSED
voluntary stopping eating and drinking
84
what is the cell often targeted in neurodegenerative diseases
neurons (functional groups of neurons)
85
genetics of Huntingtons
AD, extra DNA in chromosome 4 (repeating CAG trinucleotide unit)
Huntington's has over 36 repeats (normal is less than 34)
86
what areas of brain is affected in Huntingtons
both deep (caudate, putamen, thalamus) and superficial (cerebral cortex)
87
Friedreich's ataxia genetics
AR extra DNA in chromosome 9 (extra repeat in GAA in frataxin gene)
88
Friedreich's ataxia affects what part of brain
causes spinocerebellar degeneration
89
Peroneal muscular atrophy/charcot-marie-tooth genetics
AD extra DNA in chromosome 17, repeat in PMP22 gene for myelin structural protein
90
what part of CNS does peroneal muscular atrophy affect and what symptoms occur
myelin damage and axonal loss in peripheral nerves - distal leg weakness and muscle atrophy
91
duchenne muscular dystrophy genetics
X linked recessive loss of dystrophin gene in X chromosome
92
duchenne affects what cells/structures, and what symptoms occur
structural protein in skeletal muscle - slow progressive wasting, loss of function, respiratory paralysis
93
what protein is messed up in Shy-Drager
alpha synuclein
94
patient with what disease might not be able to draw a cube on a piece of paper (spacial relationship disrupted)
Alzheimers
95
ex vacuo ventricular dilation found with what (2)
alzheimers
| huntingtons
96
what lobes of brain have most atrophy in Alzheimers
temporal and parietal (and some frontal)
97
describe Alzheimers histo (5)
1. neuritic plaques: center of aggregates of AMYLOID core, with neurites with Tau positive filament
2. neurofibrillary tangles (TAU) pyramidal silver stained
3. lysosomes with altered cytoskeletal proteins (granulovacuolar degen)
4. hirano bodies (abnormal actin and neurons) - look like pink cylinders
5. amyloid angiopathy
98
connection between Down's syndrome and alzheimers
amyloid APP gene is on chromosome 21 (get more Abeta peptides created)
99
area of brain affected by Pick's
frontal lobe and anterior 2/3 superior temporal gyrus
100
histo of Pick's
pick bodies - round silver-positive neuronal inclusions
101
what is binswanger's enceophalopathy
vascular dementia (usually caused by HTN)
102
clinical triad in normal pressure hydrocephalus
1. dementia
2. gait ataxia
3. urinary incontinence
caused by intermittent increases in CSF pressure that damages adjacent axons with ventricular enlargment
103
what do you see on gross for parkinson's
pallor of substantia nigra, locus ceruleus
104
what do you see on histo for parkinsons
Lewy bodies: round pink target-like inclusions within surviving neurons in substantia nigra
105
motor neuron disease areas of damage (3)
1. lower motor neuron damage in spinal cord
2. CN nuclei
3. degen of upper motor neuron axons in corticospinal tract
106
histology of motor neuron disease (2)
1. neuronal loss and gliosis in ventral horns and CN motor nuclei
2. neurogenic atrophy in denervated skeletal muscle
107
types of primary motor neuron diseases (2) and what neurons are affected
1. spinal muscular atrophy (SMA) - lower motor neurons
| 2. Amyotrophic lateral sclerosis (ALS) - upper and lower
108
example of secondary motor neuron disease
polio
109
who presents with spinal msucular atrophy
fetus or infant
110
presentation of spinal muscular atrophy
degeneration of lower potor neurons without corticospinal tract signs - floppy baby syndrome
111
ALS on histo (2)
1. loss of motor neurons in spinal cord and brain stem (degen of corticospinal tracts)
2. loss of astrocytes
112
spinal muscular atrophy on histo (2)
1. loss of motor neurons in ANTERIOR spinal cord
| 2. atrophy of skeletal muscle
113
chronic polio histo (2)
1. loss of anterior horn motor neurons and
| 2. asymmetric muscular atrophy
114
difference between dysmyelination and demyelination
dys = enzyme defect that produces myelin
de = destructino of normal myelin
115
in leukodystrophy, what matter is most affected
white matter
116
canavan disease
primary leukodystrophy - diffuse bilateral symmetric white matter degeneration
117
gross thiamine deificiency in brain
hemorrhage and necrosis in mammillary bodies and periventricular gray matter (around 3rd ventricle)
118
B12 deficiency area and type of damage
myelin destruction in posterior and lateral columns of spinal cord
when it's both dorsal and lateral columns - called subacute combined degeneration
119
what is subacute combined degeneration
in B12 deficiency - when it's both dorsal and lateral columns that are affected with myelin loss and axonal damage
120
hepatic encephalopathy on histo
gray matter astrocytes with swollen clear nuclei and no visible cytoplasm - aslzhimer type 2 astrocyte
121
central pontine myelinolysis serum abnormality
abnormal sodium in serum who is too rapidly corrected (happens in alcoholics and other debilitated chornically ill patients)
122
central pontine myelinolysis on gross
diamond-shaped area of myelin destruction in central pons
123
subthalamic nucleus interaction with internal globus pallidus (2)
```
RESTING:
subthalamic nucleus (glutamatergic) tonically fires, enhancing firing of internal segment of globus pallidus - inhibiting VA/VL and suppressing movement
```
MOVEMENT:
subthalamic nucleus increasing glutamatergic firing when movement is initiated
124
subthalamic nucleus interaction with external globus pallidus (indirect pathway)
REST:
external globus palidus (GABA) tonically fires low levels to subthalamic nucleus
MOVEMENT:
during initiation of movement, external globus pallidus pauses firing, thus allowing increased firing of subthalamic nucleus to internal globus pallidus and increased movement inhibition
125
putamen interaction with external globus pallidus (indirect pathway)
during initiation of movement, cortical input causes putamen to fire GABA signals to external globus palidus to cause pause of firing to subthalamic nucleus, cauign increased glutamatergic firing to internal globus pallidus, which inhibits VA/VL
126
what brain pathway is involved when a batter thinks he wants to swing, and then stops at the last minute
cortex straight to subthalamic nucleus to abort the motion
127
dopamine interaction with putamen (2) - and what receptors are used
via D1: dopamine decreases output from GPi, allowing VA/VL to fire more - allows initiation of movement (direct pathway) - smoothness of movement
via D2: decreases putamen input to GPe, which increases firing of GPe, which inhibit subthalamic nucleus more, which decreases GPi, inhibiting VA/VL less - allowing more movement
128
what areas of brain do you place deep brain stimulation for parkinosns
either STN or GPi
129
definition of a tremor
rhythmic oscillation around a joint
130
definition of rest tremor
tremor that occurs completely supported against gravity
131
subtypes of action tremor
1. postural - arms in extension
| 2. kinetic - goal directed (finger nose finger), task-specific (writing)
132
what does accelerometry and EMG show for tremors
all tremors besides psychogenic tremors are not "time-locked" - R and L sides are a little bit off
133
cause of enhanced physiologic tremor
toxic-metabolic derangement (meds, low blood sugar, cortisol)
134
how does alcohol effect essential tremor
alcohol makes essential tremor better
135
which tremor runs in families
essential tremor
136
is essential tremor an action or resting tremor
action
137
what is frequency of parkinsonian tremor
slow
138
what is frequency of enhanced phsiologic tremor
fast
139
what is frequency of essential tremor
fast
140
what is symmetry/asymmetry of parkinsons
asymmetry
141
what is dystonia
abnormal posture
142
where is problem with dysmetria
cerebellum
143
what would make a tremor better - lighter or heavier object to hold
heavier
144
what lab do you want to check when you see a tremor
thyroid - TSH
145
what drug can give you a tremor
lithium SSRI
146
do children get essential tremor
no
147
what do you also see with late onset essential tremor
cerebellar defects
148
treatments for essential tremor (3)
1. propranolol, primodone (not for asthma patients)
2. topiramate, gabapentin
3. deep brain stim, focused U/S
149
what protein is in lewy body
alpha synuclein
150
how can you modulate the tremor in parkinsons
you can stress person out and make amplitude more
151
what percentage of patients with parkinsons don't presrent with tremor, and what do they present with
25% have atremulous, postural instability and rigidity
152
what symptom does parkinsonism HAVE to have
bradykinesia
153
what side are parkinson's patient is slower/tremulous on
L side
154
sleep and parkinsons
REM issues - hypermovement during sleep
155
one of the earliest symptoms of parkinsons
hyposmia
156
what do you always give with levi dopa
carbidopa to avoid peripheral decarboxylation of levidopa in periphery - without vomitting (sinemet = combo)
157
if someone has falls early and postural instability early, what could it be
progressive supranuclear palsy (tau)
158
how fast (Hz) are parkinsons tremors
4-6Hz
159
L-DOPA mech of action
precursor of dopamine, which transports into CNS via aromatic amino acid transporter and gets decarboxylated in CNS and PNS into dopamine
160
L-DOPA adverse effects (peripheral) (3)
L-DOPA alone will get converted to dopamine in the periphery, which causes:
1. nausea
2. cardiac palpitations and arrhythmias
3. postural hypotension
161
carbidopa mech of action
peripheral decarboxylase (L-AAD) inhibitor
162
carbidopa adverse effects
inhibition of peripheral decarboxylase can cause shut to increase activity of COMT enzyme in the periphery
163
tolcapone mech of action
inhibits peripheral AND central L-DOPA metabolism by COMT
164
tolcapone adverse effects (2)
greater effects of central dopamine tox side effects (psychosis, dyskinesias, on-off phenomenon)
liver tox
165
entacapone mech of action
inhibits ONLY peripheral L-DOPA metabolism by COMT
166
entacapone adverse effects
greater effects of central dopamine tox side effects (psychosis, dyskinesias, on-off phenomenon)
167
selegiline mech of action
MAO-B inhibitor within CNS
168
selegiline adverse effects (2)
can worsen central L-DOPA side effects
oral admin causes metabolism into amphetamines
169
benztropine mech of action
antimuscarinic - decrease inhibitory GABAergic effect using muscarining antagonists
useful if only symptom is tremor
170
benztropine adverse effects (peripheral and central)
peripheral:
dry mouth, blurred vision, mydriasis, urinary retention and nausea
central:
drowsiness, mental slowness, confusion, inattention, restlessness
171
ropinirole mech of action
CNS D2 agonist - alleviates on-off metabolism of dopamine
172
ropinirole adverse effects (4)
peripheral:
1. nausea
2. hypotension
central:
1. dyskinesias
2. psychosis
173
pramipexole mech of action
CNS D2 agonist - alleviates on-off metabolism of dopamine
174
pramipexole adverse effects
peripheral:
1. nausea
2. hypotension
central:
1. dyskinesias
2. psychosis
175
amantadine mech of action (2)
1. enhance dopa release
| 2. inhibit dopa reuptake
176
amantadine adverse effects
only short lived benefits
mild, if overdose can produce acute toxic psychosis
177
rasagiline mech of action
MAO-B inhibitor within CNS
178
rasagiline adverse effects
can worsen central L-DOPA side effects
oral admin causes metabolism into amphetamines
179
MPTP story
MPTP gets converted to MPP+ by MOA-B, creating a model of parkinsonism by being taken up by dopaminergic cells and killing them off
180
L-DOPA adverse effects (central) (3)
1. psychotic sypmtoms
2. dyskinesias
3. on-off phenomenon
181
L-DOPA contraindications (3 pre-existing conditions, 3 drugs)
1. psychosis
2. melanoma
3. narrow angle glaucoma
1. non-selective MAOi
2. pyridoxine (Vit B6)
3. anti-psychotics
182
what percentage of patients is L-DOPA very, somewhat, and not effective in
1/3 for each
183
what symptoms does L-DOPA help the most for
1. bradykinesia and akinesia
184
what don't you give alongside selegeline
an MAOi
185
who do you not give ropinirole or pramipexole
1. pyschosis
2. recent MI/vascular disease (can't respond to orthostatic hypotension)
3. peptic ulcers (b/c of nausea and vomitting)
186
who don''t you give benztropine to (3)?
generally don't give to elderly, but specifically contraindicated in:
1. prostatic hypertrophy
2. obstructive GI disease or
3. narrow angle glaucoma
187
what type of aggregate cannot be reconstituted into normal protein confirmation
fibrillar
188
what is contained in neurofibrillary tangle
bunch of different proteins- tau, amyloid, synculein etc.
189
unfolded protein response
stressed ER - slows down protein synth by phosphorylating things. chaperon and heat shock expression increases to help folding to catch up. if it's too damaged, will undergo cell death
190
what makes cholesterol and apoE in brain
astrocytes
191
pathogenesi sof neimann-Pick disease
deficiency of NPC1 protein, so not able to transport out cholesterol esters when you need them, they build up, and you get a lot of cholesterol ester deposits --> chidlhood alzhemiers
192
forms of apoE and disease risk
apoE4 is usually not that common. has arginine and arginine - which repel each other and destabilize. apoE4 alelles increases risk of alzeheimers
because of increased deposition of Abeta plaques (not able to clear the fragments well enough)
193
forms of apoE and disease risk (4)
apoE4 is usually not that common. has arginine and arginine - which repel each other and destabilize the protein
apoE4 is not as efficient at picking up and clearing large (40-42) Abeta fragments created by beta enzyme. increased deposition of Abeta plaques
apoE4 binds to solubule Abeta, creating new plaques as well
truncation of apoE4 causes neurofibrillary tangles
194
definition of "altered brain function" (4)
any of the following:
1. loss/decreased consciousness
2. retrograde amnesia
3. neurologic deficits
4. alteration in mental status (confusion/disorientation)
or other (visual, labs, imaging)
195
sections of glasgow coma scale (3) and best possible response score
1. eye opening (Best = spontaneous)
2. verbal response (best = oriented x3)
3. motor response (Best = obeys commands)
best = 15, coma = 8 or less
196
diffuse axonal injury (what's affected and what's the possible progression)
messing up white matter tracks esp corticothalamic circuitry - seen in traumatic brain injury
some can recover, some can degenerate and cause premanent deficet (WALLERIAN DEGENERATION)
197
clinical preserntation of diffuse axonal injury (motor, functioning, worst case)
1. seizures/spasticity
2. cognitive deficits/behavioral changes
3. vegetative state/death
198
molecular level, what happens with stretching of axons in diffuse axonal injury (3 outcomes)
triggers unregulated ion flux - increased intra-axonal calckum which releases excess glutamate which can be NEUROTOXIC
overworked membrane pumps trying to correct this imbalance can cause depletion of energy stores, calcium influx into mitochondria, leading to ACIDOSIS and EDEMA
199
how long can metabolic disturbances last post concussion
up to 10 days
200
what proteins are disrupted in CTE (2)
Abeta and tau
201
what percentage of people with concussion have oculomotor problems
30-65%
202
what percentage of people with concussion have dizziness
50% (can be autonomic, vestibular, cervicogenic)
203
autonomic nervous system and concussion
disruption causes elevated resting HR, photosensitivity, sleep problems, irritability
use treadmill exercise with target HR to restore autonomic nervous system
204
cervicogenic component of TBI (What symptoms does it cause)
whiplash - neck injury. can cause tension type headaches, visual disturbances, dizziness and mentlal fogginess
205
what part of neuro exam do you focus on with concussion (2)
oculomotor (EOM, tracking, vary speed, look for nystagmus or jerkiness, convergence difficulty, dizziness and nausea)
vestibular (vestibulo ocular reflex, balance, tandem gait)
206
what stain do you see a loss of myelin with
luxol fast blue stain
207
histo for MS
loss of myelin, perivascular plaques with lymphocytes and plasma cells, foamy macrophages, reactive astrocytes
208
what is acute disseminated encephalomyelitis resemble on path
MS
see demyelinating lesions centered around venules with perivascular chronic inflammation and macrophages
209
pathogenesis of acute diesseminated encephalomyelitis
acute fulminating immunologic destruction of myelin within DAYS/WEEKS of immune challenge (vacinnation or infection - rabies, smallpox, measles, rubella)
210
age presentation of acute diesseminated encephalomyelitis
Children and adolescents
211
newer definition of dementia (3)
intereferes with independence
significant decline from baseline activity - physician who can't see patients anymore etc.
2 domains of cognition need to be affected (memory, reasoning, behavior, language, perception)
212
what are the domains of cognition (5)
1. memory
2. reasoning
3. behavior
4. perceptual/visual spatial
5. language foil
213
when someone has cognitive problems that DON'T affect function/independence
minor neurocognitive disorder
214
rate of risk for progression from MCI to dementia annually
10-12% per year
215
what makes you more at risk for faster progression of MCI to dementia
anxiety and depression
216
alpha synuclein is a component of what kinds of dementia (4)
1. parkinsons
2. parkinsons with dementia
3. dementia with lewy body
4. multiple systems atrophy
217
amyloid is component of what kinds of dementia (2)
1. lewy body
| 2. alzheimers
218
tau is a component of what kinds of dementia (5)
1. alzheimers
2. progressive supranuclear palsy
3. frontotemporal degeneration
4. chronic traumatic encephalopathy
5. corticobasal degeneration
219
TDP-43/ ubiquitin is a component of what kinds of depentia (3)
1. frontotemporal degeneration
2. chronic traumatic encephalopathy
3. amylotrophic lateral sclerosis
220
personality changes, poor executive function, hallucinations, REM sleep disorder associated with what disorder
dementia with lewy body
221
when do hallucinations occur with lewy body
within first year, before dementia gets bad
222
behavioral change, poor decisions, change in sexual drive seen in what kind of disorder
frontotemporal dementia
223
what type of dementia has good days and bad days (3s and 8s)
lewy body
224
known dementia, shuffling gate, agitation, pacing, swatting and evidence of facial trauma
frontaltemporal dementia
maybe who was given antipsychotics - brings out motor symptoms - causes falls and worsened symptoms
225
someone comes in with alzheimers and just cant talk
primary progressive aphasia
226
MMSE parts (5)
```
orientation
registration/recall
attention (WORLD)
language
visual spatial
```
227
letter deficit (name L words etc.) points to what kind of dementia
frontotemporal
228
cholinesterase inhibitors - what do they do and when are they used
help cells to remain active and live longer before dying
used for early to moderate disease. used in lewy body to level out disease
229
when must you stop using anticholinesterases
if there's weight loss
230
what is memantine mech of action and indication
NMDA receptor antagonist (neuroprotective)
moderate to severe alzheimers (late stage)
