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BECOM 2 > BECOM Exam #5 (Week 3) > Flashcards

BECOM Exam #5 (Week 3) Flashcards

1
Q

Lower motor neuron:
Alpha motor neurons
Gamma motor neurons

INNERVATE was fibers

A

Lower motor neuron:
Alpha motor fibers -> innervate extrafusal fibers
Gamma motor fibers -> innervate intrafusal fibers (polar ends)

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2
Q

Alpha motor neurons consist of two types and what they innervate (large vs small)

A

Large motor neuron = fast twitch muscles (high force/velocity)
Small motor neuron = slow twitch muscles (postural, endurance)

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3
Q

intrafusal fiber types and afferent neuron type

A

Nuclear bag fibers: Large number of nuclei packed in middle portion
-Type Ia afferent -> faster response

Nuclear chain fibers
-Type Ia and type II afferent -> slower response

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4
Q

stretch reflex pathwaw

A

intrafusal fibers stretched –> Type Ia or type II afferent fiber to spinal cord –>

Efferent response:

  1. Alpha -> all muscel fibers
  2. Gamma -> tip (polar regions of fiber)
    - contract polar part of intrafusal fibers causes stretch of fibers -> keeps sensitivity

AND

alpha efferent inhibition to antagonist muscle

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5
Q

Dynamic myotatic reflex vs. Static (tonic) myotatic reflex

  • define
  • afferent fibers
A

Dynamic myotatic reflex: strong, fast reaction causing sudden contraction of the whole muscle and opposes sudden lengthening of the muscles
-type Ia afferent fibers

Static (tonic) myotatic reflex: slower and weaker than dynamic stretch important for posture and muscle tone
-type Ia and type II afferent fibers

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6
Q

Inverse myotatic reflex (Glogi tendon reflex)

  • normal situation
  • extreme situation
A

Stretching of golgi tendon -> inhibition to same muscle that got stretched and excitation of opposite muscle
-allows find control

In extreme cases (caring something heavy) Golgi tendon will cause relaxation of entire muscle to protect the muscle from tearing

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7
Q

Flexor withdrawal reflex

A

Harmful stimulus
Ipsilateral side:
Flexion activate
extension inhibited

Contralateral side:
flexion inhibited
extension activated

-also used in walking

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8
Q

Afterdischarge

A

keep muscle contraction for a little bit longer time

-cross extension lasts longer than flexion -> keep balance

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9
Q

Central pattern generator

A

produces the alternating contractions of limb flexors and extensors even with the connection to brain cut

  • response must be located in spinal cord
  • sensory input is important for fine tuning of motion but not for gross movement
  • important in infants and paraplegic individuals
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10
Q

Supplementary motor area (SMA) use

A
  • bimanual tasks
  • skilled movements
  • responsible for planning movements
  • together with the premotor areas -> complicated movement program
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11
Q

Premotor cortex

A
  • contains MIRROR neurons

- together with the SMA -> complicated movement program

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12
Q

Motor apraxia

A
  • disorder of the execution of learned movements, not due to weakness, loss or coordination, or sensory loss.
  • can lead to inability to organize actions (example putting clothes on wrong part of body)
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13
Q

Unilateral lesions in corticobulbar tract

A

VII unilateral lesion -> opposite side lower face

XI unilateral lesion > tongue pulls towards side of lesion

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14
Q

Posterior limb of internal capsule lesion

A
  • area where corticospinal tract runs through brain

- loss of contralateral fine motor control

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15
Q

Pyramidal tract (upper motor neurons from corticospinal tract or corticobulbar) control

A
  • open and close the spinal reflex arc
  • pyramidal tract controls the flexors
  • in paraplegia, exaggerated planterflexion (foot it extended bc flexion is lost from corticospinal tract)
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16
Q

Corticorubrospinal tract

A

Serves as alternative pathway for transmitting cortical signals to the spinal cord that causes contraction of muscle groups (gross movement)

  • cortex -> red nucleus -> spinal cord
  • lacks fine control
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17
Q

Reticulospinal tract tract pontine vs medullary control

A

Posture
Pontine: PEM
-excitatory
-lateral

Medullary: MIL

  • inhibitory
  • lateral
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18
Q

Tectospinal tract (inferior and superior colliculus)

A

superior colliculus receives input from retina and the frontal eye field -> conjugate eye movements and reflex movement towards moving object

Auditory stimuli reach the superior colliculus via the inferior colliculus -> auditory reflex towards source of stimulus

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19
Q

Head angular acceleration (head rotation) is detected by

A

semicircular canals (ampula)

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20
Q

Head linear acceleration (translational motion and gravity)

  • forward/backward acceleration
  • nodding up and down
  • GRAVITY
A

saccule and utricle (macula)

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21
Q

initial movement vs. sudden stop in ampulla

A

initial movement: depolarization
sudden stop: hyperpolarization
*slightly depolarized at rest

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22
Q

Horizontal canals
LARP (left anterior right canal and right posterior canal)
RALP (right anterior canal and left posterior canal)
-corresponding muscles

A

Horizontal canals: lateral and medial recti.
LARP: left vertical recti, right obliques.
RALP: right vertical recti, left obliques.

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23
Q

Physiological nystagmus

A

rapid movement of eyes from one object to another

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24
Q

Vestibulo-ocular reflex

A

keep the eyes still in space when the head moves (extremely fast, bisynaptic).

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25
Q

Vestibulo-collic reflex

A

keeps the head still in space – or on a level plane when body is moving

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26
Q

Vestibular-spinal reflex

A

maintain posture during rapid cages in position

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27
Q

lateral vestobulospinal tract

A
  • Ipsilateral
  • Allows the legs to adjust for head movements.(EXTENSORS)
  • Provides excitatory tone to extensor muscles -> leads to rigidity when corticospinal tract is lesions (inhibition)
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28
Q

Medial Vestibulospinal Tract

A

Keeps the head still in space – mediating the vestibulo-colic reflex.

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29
Q

vestibular nucleus combines visual and vestibular signals

A
  • Initial recognition of movement is by the vestibular system but this does not give constant stimulation if movement continues
  • Retinal motion by head movement compensates
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30
Q

Benign positional vertigo

A

debris from the otoconia in the utricle float into the posterior canal, causing interference with cupula function, brought out by motion in the plane of the affected posterior cana

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31
Q

Phase I Reactions

A
  1. Oxidations
    - Flavin monooxygenase
    - Amine oxidase
  2. Reductions
  3. Hydrolysis
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32
Q

Phase II Reactions

A 
GLUCURONIDATION
AcetylatioN
GLUTATHIONE CONJUGATION
Glycine conjugation
Sulfation
Methylation
Water conjugation

cyp independent

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33
Q

cyp associated with acetaminophen break down?

A

cyp2E1

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34
Q

most drugs are metabolized by?

A

Cyp 3A4/5 or UGT

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35
Q

drugs that are enzyme inducers

A

Carbamazepine
Rifampin
Warfarin (Coumarin) not an inducer just influenced by a bunch of other inducers

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36
Q

drugs that are inhibitors

A

Cimetidine
Ethanol
Grapefruit juice

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37
Q

Enterohepatic Circulation

A

-highly lipophilic drugs

Bile in GI tract -> Hepatic Portal Vein -> Liver -> Bile -> Bile released to GI tract

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38
Q

zero order vs. first order elimination

A

Zero order: half life is changing but elimination rate is staying the same
-linear

First order: elimination rate is changing but half life is staying the same

  • exponential
  • 95% of drug is gone after 5 half lives
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39
Q

increase vs decrease Vd

A

Increase Vd: more drug in peripheral compartment (lipophilic)

  • dec clearance
  • dec elimination
  • inc half life

Decrease Vd: less drug in peripheral compartment

  • inc clearance
  • inc elimination
  • dec half life
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40
Q

Maintenance Dose Rate =

A

Desired Drug plasma con x CL (clearance) x Dose interval / F (bioavailability)

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41
Q

Loading Dose =

A

Desired Drug plasma con x Vd / F

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42
Q

half life =

A

0.7 x Vd / CL

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43
Q

clearance =

A

Vd x Ke (elimination constant)

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44
Q

pharmacodynamics

A

is the study of the relationship between drug concentration in the body and the physiological response to that concentration of drug

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45
Q

pharmacokinetics

A

d

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46
Q

Partial agonist

A

Partial agonist: bind to both inactive state and active conformation
-A partial agonist serves as an agonist in the absence of a full agonist but decreases the response of full agonist when given together

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47
Q

Potency

A

Dose of a drug necessary to produce 50% of drug’s total response, expressed as an ED50 value

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48
Q

Efficacy

A

total response produced by a drug

-clinical effectiveness of a drug depends on its maximal efficacy (Emax) and not the potency (ED50/KD)

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49
Q

Inverse Agonist

A
  • Antagonists that measurably decrease spontaneous receptor activity
  • bind to receptors that are constantly on at base level with the absence of ligand and turn them all the way off
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50
Q

Chemical Antagonism

A

Binding of one drug to another and making it unavailable for binding to its receptor

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51
Q

Physiological (Functional) Antagonism

A

Two drugs having opposite physiological effect/response through completely different mechanisms, for example, glucocorticoids increase blood glucose levels whereas insulin decreases it

52
Q

Allosteric Modulation

A

When a drug binds to a receptor at a completely different site and modifies the response of the receptor to the agonist binding

53
Q

tracts into superior cerebellar peduncle

A

Anterior spinocerebellar tract

-Information coming from ipsilateral side

54
Q

tracts into middle cerebellar peduncle

A

Pontocerebellar tract

-Information coming from ipsilateral side

55
Q

tracts into inferior cerebellar peduncle

A

Posterior spinocerebellar tract
Olivocerebellar tract

-Information coming from ipsilateral side

56
Q

tracts out of superior cerebellar peduncle

A

Dentothalamic pathway

Dentorubrothalamic pathway

57
Q

tracts out of inferior cerebellar peduncle

A

Cerebelloreticular

58
Q

Anterior lobe syndrome of cerebellum

A

staggering gate and ataxia in the legs

-Broad based, staggering gait

59
Q

Neocerebellar Syndrome of cerebellum

A

effects lateral hemisphere of the cerebellum

  • Changes in muscle tone, reflexes, and coordination of voluntary movements all ipsilateral to side of damage
  • have trouble pointing at objects
  • have trouble touching nose
60
Q

purkinje fibers

A

Successive inhibitory feed -> damping of the DCN excitatory output -> prevents overshooting/ oscillation

61
Q

Deep cerebellar nucleus control

A

Inhibitory influence arise from Purkinje cells, excitatory from afferent input to the cerebellum
-afferent: climbing fibers and mossy fibers

62
Q

Climbing fibers

A

communicate directly with 10-20 purkinje fibers as well as the deep cerebellar nucleus

  • route through the INFERIOR OLIVE nucleus then to the cerebellum
  • when learning a new task the climbing fibers are the many fibers used (complex spikes)*
63
Q

Mossy fibers

A

communicate with he granular cell which then send thousands of fiber to communicate with thousands of purkinje cell

64
Q

Basket cells
Stellate cells
Golgi cells
in cerebellum

A 
Basket cells (receives input granule cells): inhibit Purkinje fibers
Stellate cells (receives input from granule cells/paralell fibers): inhibit Purkinje cells 
Golgi cells: inhibit granule cells

*Important for lateral inhibition (sharpening of the signal) to modulate signal from purkinje fibers

65
Q

Vestibulocerebellum controls

A

Important in controlling balance between agonist and antagonist muscles of the spine, hips and shoulders during rapid changes in body position

  • keeping balance while swinging a bat
  • predictive balance before a movement occurs
  • sends DIRECT projections to vestibular nuclei
66
Q

Spinocerebellum receives and controls

A

Receives input from:

  1. Copy efferent: From cerebral motor cortex, descending tracks or interneurons (intended sequential plan)
  2. Feedback from peripheral receptors: Reafferent fibers from M spindles, GTO, and proprioceptors (actual movement input)
    * Important for feedback control of distal limb movements*
67
Q

Cerebellar functions on movements

A
  1. Prevents overshooting
  2. Prevents back and forth oscillation of movements (intention tremors)
  3. Facilitates rapidly alternating movements and bilateral coordination (supination and pronation with both hands opposite -> hard)
68
Q

Cerebrocerebellum arises from and controls

A

-Arises from the LATERAL zones of the cerebellum
-Planning of sequential movements (ability to progress smoothly from one movement to another)
Timing of sequential movements (ability to progress in timely order)
-wide wobbly gate

69
Q

Dysdiadochokinesia caused by

A

lesion of cerebellum –> can’t supinate and pronate both hands at same time

70
Q

inhibition of vestibuloocular reflex (eyes staying fix on target while moving head)

A

inhibited by vestibulocerebellar

71
Q

Potency equation

A

1 / Kd

72
Q

Spare receptors

A

arereceptorsthat exist in excess of those required to produce a full effect
-dont need to bind to all receptors to get max response

73
Q

Quantal Dose-Response Curve

A

determines the drug dose required to produce a specified magnitude of effect in a large number of individual patients or experimental animals
-At what dosage can the most people get the most effect

74
Q

Therapeutic Window

A

Therapeutic window is the range of steady-state concentrations of drug that provides therapeutic efficacy with minimal toxicity (range from minimum effective dose to minimum toxic dose)

75
Q

ED50 definition

A

the dose where half of the population tested will respond to the drug

76
Q

lethal dose (LD50) or median toxic dose (TD50) definition

A

the dose where half of the animals tested will not survive

77
Q

certain safety factor (CSF) equation

A

TD1 / ED99

78
Q

therapeutic index (TI) equation and definition

A

TD50 / ED50

-the safety of a drug

79
Q

Specificity

A

If a drug has one effect, and only one effect on all biological systems.

80
Q

Selectivity

A

Most drugs act on more than one receptor site once they reach an appropriately high concentration

81
Q

most common drugs with Narrow Therapeutic Index Drugs

A

warfarin, levothyroxine

-ED50 is high or LD50 is really low

82
Q

Cytokine receptor

A

receptor does not phosphorylate like ligand receptor but rather recruits a other protein when activated to phosphorylate

  • JAK/STAT = inc gene expression
  • long lasting compared to ligand enzyme receptors
83
Q

Pharmacodynamic Tolerance

A

A decreased responsiveness to a drug or hormone stimulation that occurs slowly over time i.e. cellular adaptation

84
Q

striatum includes

A
  1. putamen
  2. caudate nucleus
  3. nucleus accumbens
85
Q

Hemiballismus

A
  • Uncontrolled flailing of one arm and leg
  • lesion in contralateral subthalamic nuclei
  • STN usually excites the GPi which inhibits the thalamus, when it is injured, the Gpi is not excited and inhibition of the thalamus is reduced creating unwanted movements
86
Q

Huntington’s disease

A
  • Caused by neural degeneration that is severe in striatum

- C shows MRI reconstructions from 20 patients to show the pattern of degeneration of the caudate nucleus and putamen

87
Q

Parkinson’s Disease

A

Parkinson’s usually has a decrease in pigmentation of the substantia nigra
decrease in dopamine levels. Treatment was proposed to administer doses of L-dopa
-inhibition of wanted muscle movements and inc in unwanted movements (tremors)

88
Q

Association cortex primarily projects to
Sensorimotor cortex primarily projects to
Limbic area primarily projects to

A

Association cortex primarily projects to caudate nucleus
Sensorimotor cortex primarily projects to the putamen
Limbic area primarily projects to nucleus accumbens

89
Q

Basal ganglia function

A
  • Selection of the more important moves (action selection)

- Operational learning (deciding favored actions based on outcomes, based on timing)

90
Q

Default status of basal ganglia

A

suppress all movements

91
Q

Lead-pipe rigidity

Cogwheel rigidity

A

Lead-pipe rigidity (BG lesion)
-Continuous resistive tone throughout stretch
Cogwheel rigidity (PD and related disorders)
-Rigidity with superimposed tremor

92
Q

left eye right and up muscle

A

inf oblique

93
Q

(SO4LR6)

A

Sup. oblique - trochlear
Lateral rectus - abducens
Everything else - oculomotor

94
Q

loss of oculomotor nerve (III)

A

eye turned down and out
ptosis (drooping of eyelid)
mydriasis (constant dilated pupil)

95
Q

loss of trochlear nerve (IV)

A

diplopia (double vision)

distortion of eye (eye turns away from nose)

96
Q

loss of abducens (VI)

A

diplopia

medial deviation of eye

97
Q

Saccadic movements

A

conjugate eye movement rapidly from one target to another

98
Q

control of horizontal gaze and pathway

A

pons (paramedian pontine reticular formation)

  • left frontal eye field (cortex) –decussate–> paramedian pontine reticular formation -> abducens nucleus ->
    1. lateral rectus
    2. medial longitudinal fasciculus oculomotor nucleus -> oculomotor nerve -> medial rectus
99
Q

control of vertical gaze (up, down)

A

midbrain (rostral interstitial nucleus of the medial longitudinal fasciculus)

  • up - dorsal aspect
  • down - ventral aspect
100
Q

cant look up, down issues

A
  • pineal gland tumor

- dilation of cerebral aqueduct

101
Q

optokinetic movements

A

combination of saccade and smooth pursuit movement

102
Q

angular gyrus

  • role
  • lesion
A

role: makes out meaning of visually perceived words
lesion: cant understand written language but can understand spoken language

103
Q

prefrontal lobotomy effects

A
  • Inability to solve complex problems
  • Inability to string together sequential tasks to reach complex goals
  • Inability to learn to do several parallel tasks at the same time
  • Placid
  • Inappropriate social responses (loss of morals and increase sexual activity)
  • Mood swings
104
Q

prosopagnosia

A

Cant recognize faces due to lesion

  • fusiform gyrus lesion
  • superior temporal lobe
105
Q

left vs right hemisphere

A

Right:

  • Specialized for spoken and written language
  • Sequential and analytical reasoning (math and science)
  • Breaks information into fragments and analyzes it in a linear way

Left:

  • Perceives information in a more integrated holistic way
  • Seat of imagination and insight
  • Musical and artistic skill

*corpus collosum allows communication between two hemispheres

106
Q

non dominant broca area

non dominant Wernicke’s area

A

non dominant broca area: speech with variable tones

non dominant Wernicke’s area: appreciation of subliminal meanings, humor

107
Q

Tetanic stimulation vs Posttetanic potentiation

A

Tetanic stimulation: rapid arrival of repetitive signals at a synapse causes Ca2+ accumulation and postsynaptic cell more likely to fire

Posttetanic potentiation:to jog a memory

  • Ca2+ level in synaptic knob stays elevated
  • Little stimulation needed to recover memory
108
Q

what makes unified long term memories and where are they stored?

A

hippocampus and are stored in

  • superior temporal lobe: faces and vocabulary
  • prefrontal cortex: plans and social roles
  • amygdala: emotional memory
109
Q

haircell neurotransmitter

A

glutamate

aspartate

110
Q

toxins that can cause vestibular dysfunction

A

streptomycin and gentamycin

111
Q

vestibular nuclei -> ventral thalamus -> parietoinsular cortex
-lesions of parietoinsular cortex causes

A

difficulty perceiving the vertical: they think vertical lines tilt away from the side of the lesion

112
Q

general area controlling brain activity level

A

bulboreticular facilitatory area

113
Q

Lateral hypothalamus limbic control

A

↑general activity, overt rage and fighting

114
Q

Ventromedial nucleus limbic control

A

tranquility (also satiety)

115
Q

Bilateral lesions of lateral hypothalamus cause

A

extreme passivity and dramatically reduced eating and drinking

116
Q

Bilateral lesions of ventromedial nucleus

A

excessive rage upon slightest provocation (sham rage), hyperactivity, excessive drinking and eating

117
Q

PVN to secrete

A

CRH into portal veins. CRH evokes release of ACTH from the pituitary which evokes release of cortisol from adrenal cortex. Cortisol ↑ glucose levels & amino acid, fat breakdown, release of neutrophils & ↑ memory

118
Q

Reward centers

Punishment center

A

Reward centers: medial forebrain bundle (receive treat)
Punishment center: amygdala
-Storage of memories that are associated with good and bad memories

119
Q

Hippocampus and memories

A

Hippocampus is not were all memory is stored but where new memories are made
- Lesion -> cant make new memories but can remember old memories

120
Q

Amygdala

A

sex, fear

-fight or flight (freeze up)

121
Q

Kluver - Bucy Syndrome

A

-removal of temporal lobe
Pre-op: aggressive, raging
Post-op: docile, orally fixated, increased sexual and compulsive behaviors

122
Q

Cingulotomy (cutting fibers of anterior cingulate) relieves

A

persistent pain and depression

123
Q 
Locus ceruleus 
Raphe nucleus
Tuberomammilary nucleus
Periaquiductal grey matter
Periofornical area
-neurotransmitters
A

Locus ceruleus -> NE
Raphe nucleus -> serotonin (wakes you up, antiserotonin will put you to sleep)
Tuberomammilary nucleus -> histamine
Periaquiductal grey matter -> dopamine
Periofornical area -> orexin (def. can cause narcolepsy and can promote hunger)

124
Q

ventrolateral preoptic area stimulation

-what triggers

A

= sleep

  • release of adenosine (coffee binds adenosine receptors)
  • IL-1 (inflammation), prostaglandin, insulin (meal)
125
Q

narcolepsy caused by what kind of def.

A

orexin insufficiency

126
Q 
Stage 1
Stage 2
Stage 3
Stage 4
REM
waves
A 
Stage 1: alpha
Stage 2: theta, k complexes, sleep spindles
Stage 3: low freq theta and some delta
Stage 4: delta
REM: sharp theta

BECOM 2 (7 decks)

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