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Brain and Behavior > Exam 3 (week 1) > Flashcards

Exam 3 (week 1) Flashcards

1
Q

how do endocrine glands transport secretions?

A

via capillaries, not glands

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2
Q

difference between growth and tropic hormone targets

A

growth hormones target non-endocrine tissue. tropic targets endocrine tissue

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3
Q

components of adenohypoph

A
  1. pars distalis
  2. tuberalis
  3. intermedia
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4
Q

components of neurohypoph

A
  1. pars nervosa

2. infundibulum (median eminence superiorly, infundibular process)

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5
Q

definition of pituitary stalk

A

pars tuberalis wrapped around infundibular process

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6
Q

staining of pituitary

A

pars distalis = heavily stained (secretory granules)

pars nervosa = pale (neurons)

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7
Q

embryonal origin of adenohypoph

A

ectoderm - rapthke’s pouch, groups up

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8
Q

embryonal origin of neurohypophysis

A

neuronal - infundibulum from floor of diencephalon - slides down posterior to adenohypophesis

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9
Q

embryological origin of pars intermedia

A

rathke’s pouch

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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)

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11
Q

connection between hypothalamus and neurophyophysis

A

DIRECT - via infundibulum (hypothalamoneurohypophysial tract)

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12
Q

connection between hypothalaus and adenohypophysis

A

pituitary portal vessles - arcuate makes releasing/inhibiting factors to work on adenohypophysis)

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13
Q

supra optic makes what hormone

A

vasopressin (ADH)

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14
Q

PVN makes what hormone

A

oxytocin

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15
Q

blood supply to pituitary gland (and what do they supply)

A
  1. superior hypophysial artery (supplies adenohypophysis)
  2. inferior hypophysial artery (supplies neurophypophysis)
  3. trabecular artery (connects superior and inferior)
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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

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17
Q

blood route in neurohypophysis (3)

A
  1. blood from trabecular and inferior hypophysial artery flow into
  2. capillary plexus, at which point picks up hormones from PVN and supraoptic
  3. those then leave via the hypophysial vein
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18
Q

cells under histo in pars distalis (4)

A
  1. chromophils, which include:
  2. acidophils (more numerous)
  3. basophils
  4. chromophobes (unstained cytoplasm - most likely undifferentiated cells)
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19
Q

types of acidophils (and what do they produce)

A
  1. somatotrophs (GH)

2. mammotrophs (PRL)

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20
Q

types of basophils (and what do they produce)

A
  1. thyrotrophs (TSH)
  2. gonadotrophs (FSH & LH)
  3. corticotrophs (ACTH)
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21
Q

Which are more numerous - acidophils or basohils

A

acidophils

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22
Q

on mallory stain, what color are acidophils

A

orange

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23
Q

where in pars distalis are somatotrophs located

A

on the sides of pars distalis

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24
Q

where in pars distalis are thyrotrophs and corticotrophs located

A

median portion of pars distalis

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25
Q

where are mammotrophs and gonadotrophs located in pars distalis

A

scattered

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26
Q

what percentage of cell population in adenohypophysis is somatotrophs

A

40-50%

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27
Q

when in the day are peak levels of GH released

A

before awakening

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28
Q

pathway of GH effects

A
  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 boneswhen levels of IGF-1 reach threshold, negative feedback to somatotrophs and to hypothalamus which releases somatostatin inhibit further activation of somatotrophs
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29
Q

how to inhibit somatotrophs (3)

A
  1. negative feedback due to high level sof IGF-1
  2. somatostatin from hypothalamus
  3. high levels of glucose
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30
Q

excess of GH in adults leads to

A

acromegaly (prominent jaw, big feet, big hands)

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31
Q

what percentage of cell population in adenohypophysis is mammotrophs

A

15-20% normally, higher and bigger in pregnant women

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32
Q

pathway of mammotroph activity

A
  1. (minor) prolactin-releasing factor and thyrotropin-releasing factor stimulate mammotrophs to release prolactin
  2. (major) stimulation of mammotrophs by suckling (decreases dopamine)
  3. prolactin acts of mammory gland

inhibited by dopamine release in hypothalamus

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33
Q

what is role of prolactin

A
  1. mammogenesis
  2. lactogenesis
  3. galactopoesis
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34
Q

FSH pathway

A
  1. gonadotropin releasing hormone from hypothalamus releases FSH from gonatotroph
  2. in women, FSH triggers proliferation of granuloma cells prodcuing estradiol
  3. in men, sertoli cells are triggred to make androgen binding proteins
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35
Q

what percentage of cell population in adenohypophysis is gonadotrophs

A

10%

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36
Q

LH pathway

A
  1. gonadotropin releasing hormone from hypothalamus stimulates gonadotroph to release LH
  2. in women, LH stimulates corpus luteum to make progesterone
  3. In men, Leydig cell is stimulated to make testosterone
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37
Q

what percentage of cell population in adenohypophysis is thyrotrophs

A

5%

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38
Q

TSH pathway

A
  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)
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39
Q

levels of THS, T4 and T3 in pituitary cause of hypothyroidism

A

TSH down
T4 down
T3 down

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40
Q

levels of THS, T4 and T3 in thyroid cause of hypothyroidism

A

TSH up
T4 down
T3 down

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41
Q

levels of THS, T4 and T3 in pituitary cause of hyperthyroidism

A

TSH up
T4 up
T3 up

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42
Q

levels of THS, T4 and T3 in thyroid cause of hyperthyroidism

A

TSH down
T4 up
T3 up

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43
Q

what percentage of cell population in adenohypophysis is corticotrophs

A

20%

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44
Q

ACTH pathway

A
  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
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45
Q

high levels of stress and ACTH levels

A

high levels of stress stimulate ACTH - make lots of cortisol, and then you crash because you shut down corticotrophs

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46
Q

why can’t you stop glucocorticoids quickly

A

don’t want patient to crash - taper slowly to allow corticotrophs to pick up slack and make ACTH to retain endogenous cortisol levels

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47
Q

what do you see in histo for pars intermedia

A

cysts filled with colloid

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48
Q

what cell type do you see in pars tuberalis

A

gonadotrops mostly (not physiologically significant)

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49
Q

are axons myelinated or unmyleinated in neurohypophesis

A

unmyelinated

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50
Q

cell types/structures in neurohypophysis on histo (3)

A
  1. unmyelniated axons
  2. pituicytes (glial cells) supporting axons
  3. venestrated cappilaries
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51
Q

role of oxytocin systemically (2)

A
  1. causes contraction of myometrium in uterus during labor

2. contraction of myopeithelial cells of lactating mammary alveoli (propulsion of milk)

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52
Q

role of ADH systemically (2)

A
  1. tunica media of arterioles - increase blood pressure (not significant)
  2. collecting tubule in kidney - increase water permeability
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53
Q

how to distinguish hypothalamic diabetes insipidus from nephrogenic diabetes insipidus?

A

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

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54
Q

how do hormones travel down axon in neurohypophysis and how is release regulated

A

with neurophysin transporter (1 = oxytocin, 2 = vasopressin)

pituicytes at axon ending allow connection with capillaries after neural cue

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55
Q

path between light and pineal gland (5)

A
  1. light into eye
  2. suprachiasmatic nucleus
  3. hypothalamospinal tract
  4. superior cervical ganglion
  5. pineal gland - decrease melatonin
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56
Q

embryologic origin of pineal gland

A

roof of posterior diencephalon

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57
Q

histo of pineal gland parenchyma (3)

A
  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)
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58
Q

how and when does basal ganglia suppress or promote movement (resting, purposeful, repeated)

A

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)

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59
Q

what neurotramsiter is involved in reward or punishment reinforcement of behavior

A

dopamine

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60
Q

how is OCD related to basal ganglia

A

basal ganglia are crucial for initiation, selection, “one at a time” actions

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61
Q

parkinson’s - hyper or hypokinesia

A

hypo - has trouble initiating movement

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62
Q

protein deposition related to parkinsons

A

alpha synuclein

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63
Q

4 major functions of basal ganglia

A
  1. voluntary motor activities
  2. regulatory
  3. procedural learning
  4. routine behaviors (habits)
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64
Q

tail of caudate is continuous with what

A

amygdala

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65
Q

which is more medial, globus pallidus or putamen?

A

globus pallidus - tucked under/within putamen

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66
Q

what do you also see in section where you can see subthalamic nuclei

A

mamillary bodies

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67
Q

what is corpus striatum/striatum?

A

caudate plus putamen

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68
Q

what neurotransmitter is responsible for pathways between cortex and striatum

A

glutamate (excitatory)

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69
Q

what neurotransmitter is responsible for pathways between susbtantia nigra and striatum

A

dopamine fibers onto GABA neurons (modulating)

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70
Q

projection from globus pallidus to thalamus (is it inhibitory or excitatory?)

A

inhibitory

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71
Q

what percentage of substantia nigra dopamine neurons for symptoms to begin?

A

80%

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72
Q

movement symptoms in parkinsons (3)

A
  1. resting pill rolling tremor
  2. bradykinesia
  3. hypokinesia
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73
Q

muscle symptoms of parkinsons (3)

A
  1. increased muscle tone
  2. lead-pipe rigidity
  3. cog-wheel rigidity
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74
Q

neuron type death in huntingtons

A

GABA neurons die from prefrontal to caudate

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75
Q

movement symptoms of Huntington’s

A
  1. chorea (continuous rapid movements)

2. athetosis (writhing)

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76
Q

hemiballismus cause and symptoms

A

stroke in subthalamic nucleus

periods of violent flailing movements

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77
Q

direct pathway purpose

A

to initiate movement

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78
Q

connection/interaction between VA/VL and cortex

A

VA/VL is directly/recipricolay connected to primary motor cortex, at a default is inhibited by internal globus pallidus

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79
Q

interaction between globus pallidus and thalamus for motor control

A

internal globus pallidus produces GABA inhibition of VA/VL cells to suppress all movements

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80
Q

interaction between putamen and globus pallidus for motor control

A

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

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81
Q

what makes putamen cells fire (inputs)

A

1) cerebral cortex (premotor, motor and somatosensory)
excitatory glutamatergic input

2) association cortex
3) limbic lobe

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82
Q

direct pathway purpose

A

for movement selection

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83
Q

what is VSED

A

voluntary stopping eating and drinking

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84
Q

what is the cell often targeted in neurodegenerative diseases

A

neurons (functional groups of neurons)

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85
Q

genetics of Huntingtons

A

AD, extra DNA in chromosome 4 (repeating CAG trinucleotide unit)

Huntington’s has over 36 repeats (normal is less than 34)

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86
Q

what areas of brain is affected in Huntingtons

A

both deep (caudate, putamen, thalamus) and superficial (cerebral cortex)

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87
Q

Friedreich’s ataxia genetics

A

AR extra DNA in chromosome 9 (extra repeat in GAA in frataxin gene)

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88
Q

Friedreich’s ataxia affects what part of brain

A

causes spinocerebellar degeneration

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89
Q

Peroneal muscular atrophy/charcot-marie-tooth genetics

A

AD extra DNA in chromosome 17, repeat in PMP22 gene for myelin structural protein

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90
Q

what part of CNS does peroneal muscular atrophy affect and what symptoms occur

A

myelin damage and axonal loss in peripheral nerves - distal leg weakness and muscle atrophy

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91
Q

duchenne muscular dystrophy genetics

A

X linked recessive loss of dystrophin gene in X chromosome

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92
Q

duchenne affects what cells/structures, and what symptoms occur

A

structural protein in skeletal muscle - slow progressive wasting, loss of function, respiratory paralysis

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93
Q

what protein is messed up in Shy-Drager

A

alpha synuclein

94
Q

patient with what disease might not be able to draw a cube on a piece of paper (spacial relationship disrupted)

A

Alzheimers

95
Q

ex vacuo ventricular dilation found with what (2)

A

alzheimers

huntingtons

96
Q

what lobes of brain have most atrophy in Alzheimers

A

temporal and parietal (and some frontal)

97
Q

describe Alzheimers histo (5)

A
  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
Q

connection between Down’s syndrome and alzheimers

A

amyloid APP gene is on chromosome 21 (get more Abeta peptides created)

99
Q

area of brain affected by Pick’s

A

frontal lobe and anterior 2/3 superior temporal gyrus

100
Q

histo of Pick’s

A

pick bodies - round silver-positive neuronal inclusions

101
Q

what is binswanger’s enceophalopathy

A

vascular dementia (usually caused by HTN)

102
Q

clinical triad in normal pressure hydrocephalus

A
  1. dementia
  2. gait ataxia
  3. urinary incontinence

caused by intermittent increases in CSF pressure that damages adjacent axons with ventricular enlargment

103
Q

what do you see on gross for parkinson’s

A

pallor of substantia nigra, locus ceruleus

104
Q

what do you see on histo for parkinsons

A

Lewy bodies: round pink target-like inclusions within surviving neurons in substantia nigra

105
Q

motor neuron disease areas of damage (3)

A
  1. lower motor neuron damage in spinal cord
  2. CN nuclei
  3. degen of upper motor neuron axons in corticospinal tract
106
Q

histology of motor neuron disease (2)

A
  1. neuronal loss and gliosis in ventral horns and CN motor nuclei
  2. neurogenic atrophy in denervated skeletal muscle
107
Q

types of primary motor neuron diseases (2) and what neurons are affected

A
  1. spinal muscular atrophy (SMA) - lower motor neurons

2. Amyotrophic lateral sclerosis (ALS) - upper and lower

108
Q

example of secondary motor neuron disease

109
Q

who presents with spinal msucular atrophy

A

fetus or infant

110
Q

presentation of spinal muscular atrophy

A

degeneration of lower potor neurons without corticospinal tract signs - floppy baby syndrome

111
Q

ALS on histo (2)

A
  1. loss of motor neurons in spinal cord and brain stem (degen of corticospinal tracts)
  2. loss of astrocytes
112
Q

spinal muscular atrophy on histo (2)

A
  1. loss of motor neurons in ANTERIOR spinal cord

2. atrophy of skeletal muscle

113
Q

chronic polio histo (2)

A
  1. loss of anterior horn motor neurons and

2. asymmetric muscular atrophy

114
Q

difference between dysmyelination and demyelination

A

dys = enzyme defect that produces myelin

de = destructino of normal myelin

115
Q

in leukodystrophy, what matter is most affected

A

white matter

116
Q

canavan disease

A

primary leukodystrophy - diffuse bilateral symmetric white matter degeneration

117
Q

gross thiamine deificiency in brain

A

hemorrhage and necrosis in mammillary bodies and periventricular gray matter (around 3rd ventricle)

118
Q

B12 deficiency area and type of damage

A

myelin destruction in posterior and lateral columns of spinal cord

when it’s both dorsal and lateral columns - called subacute combined degeneration

119
Q

what is subacute combined degeneration

A

in B12 deficiency - when it’s both dorsal and lateral columns that are affected with myelin loss and axonal damage

120
Q

hepatic encephalopathy on histo

A

gray matter astrocytes with swollen clear nuclei and no visible cytoplasm - aslzhimer type 2 astrocyte

121
Q

central pontine myelinolysis serum abnormality

A

abnormal sodium in serum who is too rapidly corrected (happens in alcoholics and other debilitated chornically ill patients)

122
Q

central pontine myelinolysis on gross

A

diamond-shaped area of myelin destruction in central pons

123
Q

subthalamic nucleus interaction with internal globus pallidus (2)

A 
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
Q

subthalamic nucleus interaction with external globus pallidus (indirect pathway)

A

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
Q

putamen interaction with external globus pallidus (indirect pathway)

A

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
Q

what brain pathway is involved when a batter thinks he wants to swing, and then stops at the last minute

A

cortex straight to subthalamic nucleus to abort the motion

127
Q

dopamine interaction with putamen (2) - and what receptors are used

A

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
Q

what areas of brain do you place deep brain stimulation for parkinosns

A

either STN or GPi

129
Q

definition of a tremor

A

rhythmic oscillation around a joint

130
Q

definition of rest tremor

A

tremor that occurs completely supported against gravity

131
Q

subtypes of action tremor

A
  1. postural - arms in extension

2. kinetic - goal directed (finger nose finger), task-specific (writing)

132
Q

what does accelerometry and EMG show for tremors

A

all tremors besides psychogenic tremors are not “time-locked” - R and L sides are a little bit off

133
Q

cause of enhanced physiologic tremor

A

toxic-metabolic derangement (meds, low blood sugar, cortisol)

134
Q

how does alcohol effect essential tremor

A

alcohol makes essential tremor better

135
Q

which tremor runs in families

A

essential tremor

136
Q

is essential tremor an action or resting tremor

137
Q

what is frequency of parkinsonian tremor

138
Q

what is frequency of enhanced phsiologic tremor

139
Q

what is frequency of essential tremor

140
Q

what is symmetry/asymmetry of parkinsons

141
Q

what is dystonia

A

abnormal posture

142
Q

where is problem with dysmetria

A

cerebellum

143
Q

what would make a tremor better - lighter or heavier object to hold

144
Q

what lab do you want to check when you see a tremor

A

thyroid - TSH

145
Q

what drug can give you a tremor

A

lithium SSRI

146
Q

do children get essential tremor

147
Q

what do you also see with late onset essential tremor

A

cerebellar defects

148
Q

treatments for essential tremor (3)

A
  1. propranolol, primodone (not for asthma patients)
  2. topiramate, gabapentin
  3. deep brain stim, focused U/S
149
Q

what protein is in lewy body

A

alpha synuclein

150
Q

how can you modulate the tremor in parkinsons

A

you can stress person out and make amplitude more

151
Q

what percentage of patients with parkinsons don’t presrent with tremor, and what do they present with

A

25% have atremulous, postural instability and rigidity

152
Q

what symptom does parkinsonism HAVE to have

A

bradykinesia

153
Q

what side are parkinson’s patient is slower/tremulous on

154
Q

sleep and parkinsons

A

REM issues - hypermovement during sleep

155
Q

one of the earliest symptoms of parkinsons

156
Q

what do you always give with levi dopa

A

carbidopa to avoid peripheral decarboxylation of levidopa in periphery - without vomitting (sinemet = combo)

157
Q

if someone has falls early and postural instability early, what could it be

A

progressive supranuclear palsy (tau)

158
Q

how fast (Hz) are parkinsons tremors

159
Q

L-DOPA mech of action

A

precursor of dopamine, which transports into CNS via aromatic amino acid transporter and gets decarboxylated in CNS and PNS into dopamine

160
Q

L-DOPA adverse effects (peripheral) (3)

A

L-DOPA alone will get converted to dopamine in the periphery, which causes:

  1. nausea
  2. cardiac palpitations and arrhythmias
  3. postural hypotension
161
Q

carbidopa mech of action

A

peripheral decarboxylase (L-AAD) inhibitor

162
Q

carbidopa adverse effects

A

inhibition of peripheral decarboxylase can cause shut to increase activity of COMT enzyme in the periphery

163
Q

tolcapone mech of action

A

inhibits peripheral AND central L-DOPA metabolism by COMT

164
Q

tolcapone adverse effects (2)

A

greater effects of central dopamine tox side effects (psychosis, dyskinesias, on-off phenomenon)

liver tox

165
Q

entacapone mech of action

A

inhibits ONLY peripheral L-DOPA metabolism by COMT

166
Q

entacapone adverse effects

A

greater effects of central dopamine tox side effects (psychosis, dyskinesias, on-off phenomenon)

167
Q

selegiline mech of action

A

MAO-B inhibitor within CNS

168
Q

selegiline adverse effects (2)

A

can worsen central L-DOPA side effects

oral admin causes metabolism into amphetamines

169
Q

benztropine mech of action

A

antimuscarinic - decrease inhibitory GABAergic effect using muscarining antagonists

useful if only symptom is tremor

170
Q

benztropine adverse effects (peripheral and central)

A

peripheral:
dry mouth, blurred vision, mydriasis, urinary retention and nausea

central:
drowsiness, mental slowness, confusion, inattention, restlessness

171
Q

ropinirole mech of action

A

CNS D2 agonist - alleviates on-off metabolism of dopamine

172
Q

ropinirole adverse effects (4)

A

peripheral:

  1. nausea
  2. hypotension

central:

  1. dyskinesias
  2. psychosis
173
Q

pramipexole mech of action

A

CNS D2 agonist - alleviates on-off metabolism of dopamine

174
Q

pramipexole adverse effects

A

peripheral:

  1. nausea
  2. hypotension

central:

  1. dyskinesias
  2. psychosis
175
Q

amantadine mech of action (2)

A
  1. enhance dopa release

2. inhibit dopa reuptake

176
Q

amantadine adverse effects

A

only short lived benefits

mild, if overdose can produce acute toxic psychosis

177
Q

rasagiline mech of action

A

MAO-B inhibitor within CNS

178
Q

rasagiline adverse effects

A

can worsen central L-DOPA side effects

oral admin causes metabolism into amphetamines

179
Q

MPTP story

A

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
Q

L-DOPA adverse effects (central) (3)

A
  1. psychotic sypmtoms
  2. dyskinesias
  3. on-off phenomenon
181
Q

L-DOPA contraindications (3 pre-existing conditions, 3 drugs)

A
  1. psychosis
  2. melanoma
  3. narrow angle glaucoma
  4. non-selective MAOi
  5. pyridoxine (Vit B6)
  6. anti-psychotics
182
Q

what percentage of patients is L-DOPA very, somewhat, and not effective in

A

1/3 for each

183
Q

what symptoms does L-DOPA help the most for

A
  1. bradykinesia and akinesia
184
Q

what don’t you give alongside selegeline

185
Q

who do you not give ropinirole or pramipexole

A
  1. pyschosis
  2. recent MI/vascular disease (can’t respond to orthostatic hypotension)
  3. peptic ulcers (b/c of nausea and vomitting)
186
Q

who don’‘t you give benztropine to (3)?

A

generally don’t give to elderly, but specifically contraindicated in:

  1. prostatic hypertrophy
  2. obstructive GI disease or
  3. narrow angle glaucoma
187
Q

what type of aggregate cannot be reconstituted into normal protein confirmation

188
Q

what is contained in neurofibrillary tangle

A

bunch of different proteins- tau, amyloid, synculein etc.

189
Q

unfolded protein response

A

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
Q

what makes cholesterol and apoE in brain

A

astrocytes

191
Q

pathogenesi sof neimann-Pick disease

A

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
Q

forms of apoE and disease risk

A

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
Q

forms of apoE and disease risk (4)

A

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
Q

definition of “altered brain function” (4)

A

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
Q

sections of glasgow coma scale (3) and best possible response score

A
  1. eye opening (Best = spontaneous)
  2. verbal response (best = oriented x3)
  3. motor response (Best = obeys commands)

best = 15, coma = 8 or less

196
Q

diffuse axonal injury (what’s affected and what’s the possible progression)

A

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
Q

clinical preserntation of diffuse axonal injury (motor, functioning, worst case)

A
  1. seizures/spasticity
  2. cognitive deficits/behavioral changes
  3. vegetative state/death
198
Q

molecular level, what happens with stretching of axons in diffuse axonal injury (3 outcomes)

A

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
Q

how long can metabolic disturbances last post concussion

A

up to 10 days

200
Q

what proteins are disrupted in CTE (2)

A

Abeta and tau

201
Q

what percentage of people with concussion have oculomotor problems

202
Q

what percentage of people with concussion have dizziness

A

50% (can be autonomic, vestibular, cervicogenic)

203
Q

autonomic nervous system and concussion

A

disruption causes elevated resting HR, photosensitivity, sleep problems, irritability

use treadmill exercise with target HR to restore autonomic nervous system

204
Q

cervicogenic component of TBI (What symptoms does it cause)

A

whiplash - neck injury. can cause tension type headaches, visual disturbances, dizziness and mentlal fogginess

205
Q

what part of neuro exam do you focus on with concussion (2)

A

oculomotor (EOM, tracking, vary speed, look for nystagmus or jerkiness, convergence difficulty, dizziness and nausea)

vestibular (vestibulo ocular reflex, balance, tandem gait)

206
Q

what stain do you see a loss of myelin with

A

luxol fast blue stain

207
Q

histo for MS

A

loss of myelin, perivascular plaques with lymphocytes and plasma cells, foamy macrophages, reactive astrocytes

208
Q

what is acute disseminated encephalomyelitis resemble on path

A

MS

see demyelinating lesions centered around venules with perivascular chronic inflammation and macrophages

209
Q

pathogenesis of acute diesseminated encephalomyelitis

A

acute fulminating immunologic destruction of myelin within DAYS/WEEKS of immune challenge (vacinnation or infection - rabies, smallpox, measles, rubella)

210
Q

age presentation of acute diesseminated encephalomyelitis

A

Children and adolescents

211
Q

newer definition of dementia (3)

A

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
Q

what are the domains of cognition (5)

A
  1. memory
  2. reasoning
  3. behavior
  4. perceptual/visual spatial
  5. language foil
213
Q

when someone has cognitive problems that DON’T affect function/independence

A

minor neurocognitive disorder

214
Q

rate of risk for progression from MCI to dementia annually

A

10-12% per year

215
Q

what makes you more at risk for faster progression of MCI to dementia

A

anxiety and depression

216
Q

alpha synuclein is a component of what kinds of dementia (4)

A
  1. parkinsons
  2. parkinsons with dementia
  3. dementia with lewy body
  4. multiple systems atrophy
217
Q

amyloid is component of what kinds of dementia (2)

A
  1. lewy body

2. alzheimers

218
Q

tau is a component of what kinds of dementia (5)

A
  1. alzheimers
  2. progressive supranuclear palsy
  3. frontotemporal degeneration
  4. chronic traumatic encephalopathy
  5. corticobasal degeneration
219
Q

TDP-43/ ubiquitin is a component of what kinds of depentia (3)

A
  1. frontotemporal degeneration
  2. chronic traumatic encephalopathy
  3. amylotrophic lateral sclerosis
220
Q

personality changes, poor executive function, hallucinations, REM sleep disorder associated with what disorder

A

dementia with lewy body

221
Q

when do hallucinations occur with lewy body

A

within first year, before dementia gets bad

222
Q

behavioral change, poor decisions, change in sexual drive seen in what kind of disorder

A

frontotemporal dementia

223
Q

what type of dementia has good days and bad days (3s and 8s)

224
Q

known dementia, shuffling gate, agitation, pacing, swatting and evidence of facial trauma

A

frontaltemporal dementia

maybe who was given antipsychotics - brings out motor symptoms - causes falls and worsened symptoms

225
Q

someone comes in with alzheimers and just cant talk

A

primary progressive aphasia

226
Q

MMSE parts (5)

A 
orientation
registration/recall
attention (WORLD)
language
visual spatial
227
Q

letter deficit (name L words etc.) points to what kind of dementia

A

frontotemporal

228
Q

cholinesterase inhibitors - what do they do and when are they used

A

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
Q

when must you stop using anticholinesterases

A

if there’s weight loss

230
Q

what is memantine mech of action and indication

A

NMDA receptor antagonist (neuroprotective)

moderate to severe alzheimers (late stage)

Brain and Behavior (6 decks)

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