midterm Flashcards

1
Q

diagnosis

A

what disease is it

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2
Q

etiology

A

what caused it

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3
Q

prognosis

A

long/short term outcomes

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4
Q

incidence

A

number of new cases of a disorder in a given time period

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5
Q

Prevalence

A

Number of people within a population who exhibit a disorder during a specified time period.

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6
Q

lifetime prevalence

A

percentage of people who have been diagnosed with a specific disorder at any time in their lives.

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7
Q

Cerebral cortex

A

high order processing, bumps; gyri, grooves; sulci.

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8
Q

central sulcus

A

separates frontal and parietal lobes.

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9
Q

lateral fissure

A

separates frontal and parietal lobes from temporal lobes.

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10
Q

reflexes

A

They are independent of brain’s involvement. The pain sensation does require the brain’s processing of sensory input, the actual motor response does not involve the brain.

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11
Q

2 types brain cells

A

neurons and glia

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12
Q

glia

A

support, not background, role in development of the NS.

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13
Q

3 types neuron

A

Sensory;
interneuron; connects sensory and motor neuron in SC.
Motor Neuron: cause muscle contraction

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14
Q

pain

A

it requires sensory afferents to the brain. Motor reflex does not.

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15
Q

neurons organization

A

layered; cortex, or Nucleus, where a distinct cluster of neural cell bodies form a group.

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16
Q

organization

A

cortical networks are organized, grid-like, sub-cortical networks aren’t, irregular organization.

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17
Q

grey matter

A

cell bodies and blood vessels, subcortical nuclei, groupings of similar cell bodies.

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18
Q

structures span more than one region

A

brainstem; consists of part of the forebrain, midbrain, hindbrain…

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19
Q

lateralization

A

Left; language, math, logic

Right; emotion, orientation facial recognition, art/music…

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20
Q

Association tract

A

Connect regions within the same hemisphere.

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21
Q

Precentral gyrus

A

frontal lobe; motor cortex,

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22
Q

postcentral gyrus

A

somatosensory cortex,

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23
Q

homunculus

A

how much real estate different body regions take up.

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24
Q

basal Ganglia

A

Caudate nucleus, Putamen = striatum

Globus Pallidus, internal and external.

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25
Q

cerebrum limbic system

A

emotional control, learning and memory, Cingulate cortex: emotional processing and memory.
Amygdala; fear, agression, emotional memories, decision-making.
Hippocampus; learning and memory,

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26
Q

brainstem 3 regions,

A

diencephalon, midbrain, hindbrain

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27
Q

diencephalon

A

thalamus; sensory relay station.

Hypothalamus: homeostasis, hormone release…

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28
Q

hindbrain

A

Pons; connects cerebellum to brainstem.

Medulla: controls breathing and heart rate.

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29
Q

Midbrain

A

Tegmentum: modulates sleep, attention, reward, clusters use same chemical messanger: dopamine.

Role: link auditory and visual systems, controls orienting movements.

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30
Q

colliculi

A

superior: vision
Inferior: hearing.
For midbrain.

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31
Q

Action potential

A
  1. stimulus, move to -55
  2. threshold has to be reached.
  3. NA channels open
  4. NA positive, cell to +30
  5. at +30 Na channel closes, K channel opens.
  6. K rushes out, cell gets more negative.
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32
Q

NT

A

1, amines: dopamine, norepinephrine, epinephrine, serotonin

  1. Amino acids: glutamate, GABA (gamma-aminobutyric acid)
  2. other: acetycholine.
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33
Q

NT transmission

A

NT are synthesized and stored in the presynaptic axon.

  1. AP stimulate release of NT
  2. NT bind to receptors, post syn..
  3. receptors are coupled w ion channels that open when bound to NT. EPSP IPSP.
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34
Q

NT change

A

Fast Ionotropic: trigger ion channel to open,

Slow Metabotropic: g-protein, second messenger.

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35
Q

4 way deactivate NT**

A
  1. diffusion:
  2. Degradation: enzyme break NT down
  3. Reuptake: recycle into pre-synaptic terminal
  4. Glial cells; take up stray NT.
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36
Q

hormones 5 points

A
  1. slow, gradual
  2. Change probability or intensity of behavior (not on/off)
  3. reciprocal relationship with behaviour.
  4. have multiple effects
  5. have specific temporal pattern.
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37
Q

dif.. neural v hormonal

A

local v distant
fast v slow
voluntary v involuntary
precise v imprecise

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38
Q

norepinephrine NT and hormone

A

CNS; arousal/alertness

PNS; released by adrenal glands in response to stress/anxiety.

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39
Q

adrenal gland

A

inner–medulla: secretes epinephrine

outer–cortex; cortisol.

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40
Q

cortisol

A

steroid hormone, binds to glucocorticoid receptor, has metabolic and immune effects,

41
Q

cortisol

A

regulated by negative feedback.

42
Q

chronic stress

A

changes HPA axis, increased CRH expression, hypertrophy of adrenal cortex, Fewer GR means less negative feedback can occur.

43
Q

necrosis

A

cells rupture,

44
Q

apoptosis

A

programmed cell death. dismantle in membrane bound vesicles.

45
Q

TBI

A

two biggest risk factors are age and sex.

46
Q

TBI mechanisms

A
  1. coup: where brain skull first make contact.

2. Contre-coup: rebound damage.

47
Q

torque

A

the twisting of the brain inside the skull.

48
Q

concussion generalized damage

A

grey matter and white matter, different density, different speed on impact.

49
Q

ICP; intracranial pressure

A

swelling (edema), and bleeding (hematoma).

energy crisis: lack of oxygen (hypnoxia), lack of glucose (hypoglycemia).

50
Q

DAI, diffuse axonal injury

A

twisting and sheering forces cause axon to tear from cell body.

51
Q

Excitotoxicity

A
  1. necrosis leads to excess release of glutamate.
  2. glutamate binds and activates post-synaptic receptors, this leads to influx of Na and Ca…
  3. Too much Ca is bad. ends up mitochondria, disrupts production of ATP.
52
Q

ATP

A
  1. required to make glucose and use it.

2. ATP production requires glucose, but the energy crisis has made glucose in short supply.

53
Q

excitotoxicity

A

leads to overproduction of lactic acid, acidosis, and this damages the BBB.

54
Q

cytokines

A

hormones for immune signalling.

55
Q

Vagus Nerve

A
  1. innervate heart and digestive tract.
  2. 90% of afferent connections between bodily organs and CNS.
  3. special cells called paraganglia located along nerve that release NT when cytokines bind.
56
Q

immune **

A

because brain interacts with the immune system, it means that it is not immune privileged.

57
Q

ROS; reactive oxygen species

A

reactive, in excess under stress, leads to oxidative stress an imbalance between ROS and antiOX. need more antiOX…..

58
Q

CTE; chronic traumatic encephalopathy.

A

degenerative disease, from concussions.

59
Q

Circle of Willis

A

arteries form circle base of brain.

60
Q

ischemia

A

lack of blood flow to tissue.

61
Q

2 type stroke

A

ischemic: blockage in blood vessel. (large and small vessel thrombosis).
Hemmorhagic: rupture in….

62
Q

sham animal

A

trial condition, they are like placebo but they still have surgery just to make sure it isn’t an intervening variable.

63
Q

TIA; transient ischemic attacks

A

mini strokes, may precede a severe stroke,

but the brain can adapt if changes take place slow,

64
Q

2 damage regions after a stroke

A

Core; dead cells, fed by occluded vessel

Penumbra: outside lesion, some chance to heal.

65
Q

stroke weakened BBB

A

when blood flow reactivates, peripheral immune cells can leak through and exacerbate the immune response and….Leukocytes (white blood…) infiltrate via damaged BBB and release even more inflammatory molecules, this impedes recovery.

66
Q

why is increase Ca bad for neurons?

A
  1. triggers release of Glu, (excitotoxic cascade)
  2. Excess Ca = more ROS.
  3. ***Mitochondria can’t deal, release signals to induce apoptosis.
67
Q

mitochondria

A

release a variety of signal molecules (CASPASES) these are protease enzymes playing roles in programmed cell death and inflammation.

68
Q

Collateral circulation

A

blood flow through secondary pathways after the obstruction to the principle path occurs.

69
Q

anosognosia

A

unaware of the illness. Inability to recognize impairment. lack of self-awareness.

70
Q

genes

A

are like recipes for proteins,

71
Q

chromatin

A

DNA + histone

72
Q

alleles

A

variants of genes. cause diversity.

73
Q

** proteins

A
  1. cell structure,
  2. catalyze reactions, aid in cell metabolism
  3. hormone receptors, cytokines, membrane proteins…
74
Q

epigenetics

A

changes in gene expression related to experience.

75
Q

acetylation

A

loose, = gene expression

methylation tight = no gene expression

76
Q

huntington

A

neurodegenerative genetic disorder, autosomal-dominant pattern of inheritance.

77
Q

bradykinesia

A

rigidity, prob with voluntary movement.

78
Q

huntington MSN; medium-spiny neuron…

A

*caudate, and putamen at risk, MSN are GABA and makeup 95% STR neurons.

79
Q

basal ganglia 2 pathways…

A

direct; excitation of motor neurons, movement.

indirect; inhibition of motor neurons, …

80
Q

htt protein

A

accumulate nucleus, correlate to CAG repeats.

81
Q

huntinton

A

directionality and progression are not yet known.

82
Q

huntington excito

A

glutamate, NMDA receptors are glutamate receptor, and agonists mimic certain HD like symptoms…. thus Glu receptor stimulation may contribute to symptoms.

83
Q

ALS up low MN

A

upper motor N originate in the brain, signal to lower motor N.

LMN; info to muscles,

84
Q

Upper Motor N (cant leave CNS)

A
  1. tell LMN to carry start signals to muscles.

2. Tell LMN when to stop sending signals to contract.

85
Q

lower motor neuron

A

synapse on muscles, can pass through spinal and cranial nerves,

86
Q

spasticity

A

feature of UMN injury,

87
Q

Flaccidity

A

with LMN injury LMN is unable to tell muscle to start contracting, thus not muscle contraction and loss of muscle tone.

88
Q

UMN injury

A

hyperreflexia, increase muscle stretch reflexes,

also** extensor plantar response (Babinski sign)

89
Q

LMN injury

A

hyporeflexia; decrease in muscles stretch reflex, (limp baby),

*also hypotonia, muscle atrophy, as well as fasciculations (twitching).

90
Q

idiopathic

A

no known cause.

91
Q

ALS

A

affects only voluntary muscles,

92
Q

necroptosis

A

programmed necrosis, membrane breakdown,

93
Q

in vitro

A

petri dish…

94
Q

dementia

A

refers to a set of symptoms that are caused by disorders that affect the brain.

normal memory loss, dysfunctional neurons, not dying N.

95
Q

mild cognitive impairment

A

memory problems greater than expected for age.

96
Q

alzeymers

A

sporadic 95% cases, can only be definitively diagnosed after death.

97
Q

alzymer 2 pathological feature

A

beta-amyloid plaques: outside cell.

Neurofibrillary tangles, inside cell.

98
Q

amyloid angiopathy

A

beta-amyloid plaques can elicit an immune response by glial cells and can deposit near blood vessels

99
Q

calcium stroke

A

AP stimulates calcium and calcium is responsible for bringing vesicles to membrane thus more flutamate and more firing.