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NERVOUS > PHYSIOLOGY > Flashcards

PHYSIOLOGY Flashcards

1
Q

3 columns of white matter?

A

posterior
lateral
anterior

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2
Q

dorsal column carries what?

type?

A

ascending

carries touch, vibration sense and proprioception

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3
Q

corticospinal tract carries what?

also called?

A

carries motor impulses fro motor cortex to skeletal muscles
DESCEDNING

pyramidal tract

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4
Q

LATERAL spinothalamic tract carries what?

A

ascending

pain and temp sensation

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5
Q

explain pathway of corticospinal tract?

A
  1. start at motor cortex AREA 4
  2. through internal capsule
  3. called cortico bulblar tract = go to contralateral cranial nuclei (doesn’t reach sc)
  4. then most fibres cross at decussation of pyramids
  5. some don’t and form anterior corticospinal tract
  6. most form lateral corticospinal tract on contralateral side into SC
  7. to skeletal muscles
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6
Q

where does this corticospinal tract run in the brainstem?

A

lateral pathway

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7
Q

where is the pyramidal decussation?

A

in medulla

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8
Q

where is the lower motor neuron?

A

when in synapses in sc

in ventral horn

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9
Q

DORSAl column - explain pathway?

A
  1. dorsal root of 1st order neuron to synapse in lower part of medulla to 2nd order neuron
  2. 2nd order neuron crosses over in medulla
  3. tract called MEDIAL LEMNISCUS
  4. travels up brainstem,
  5. 3rd order neuron starts in thalamus(VPL NUCLEUS) and then pass through IC to posterior central gyrus in parietal lobe - sensory
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10
Q

WHERE DO ALL SESNORY INFO S YNAPSE IN THALAMUS?

A

VPL NUCLEUS

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11
Q

EXPLAIN lateral spinothalamic tract?

A
  1. 1st order neuron enters and end at same level in sc
  2. 2nd order neuron crosses over into lateral column and called lateral spinothalamic tract
  3. 2nd order till thalamus and 3rd order passes through IC and radiates to post-central gyrus - sensory
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12
Q

difference with lateral spinothalaic tract?

A

decussation occurring at sc level same NOT MEDULLA

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13
Q

position of dorsal column?

A

posterior

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14
Q

stretch reflex EXPLAIN PATHWAY?

A

STIMULI
1. MUSCLE FIBRSES STIMUKATED
2. sensory neuron activated
3. monosynaptic reflex arc
-to cause muscle contraction - BY activating ALPHA MOTONEURONS IN AGONIST MUSCLE
other fibres =
polysnaptic reflex arc to inhibitory interneuron
-to cause relaxation of antagonist muscle - by deactivating alpha motoneurons in antagonist

DOES NOT GO TO BRAIN - ONLY DELT IN SC

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15
Q

reciprocal innervation/inhibition meaning?

A

innervating antagonist muscle to do opposite

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16
Q

FLEXOR/CROSSED EXTENSOR REFLEX explain pathway?

and result of it

A

pain stimuli

  1. sensory neuron activated
  2. polysnaptic reflex arc
    - some fibers - flexion and withdrawal from stimulations
    - other fibers - crossed extensor -cause response to contralateral limb - to gain balance

ipsilateral flexion
and contralateral extension

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17
Q

what mediates reflexes?

A

lower motor neurons

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18
Q

if UMN lesion what happens to reflexes?

A

exaggerated

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19
Q

UMN/LMN lesions affect on muscle tone?

A

UMN LESION - increased tone - spastic

LMN LESION - decreased tone - flaccid - no reflexes

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20
Q

if lesion - what is affected - above it or below it?

A

all stuff below it

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21
Q

if lesion is above and below decussation meaning?

A

above decussation - contralateral symptoms

below decussation - ipsilateral symptoms

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22
Q

paralysis due to what tract?

A

pyramidal - corticospinak tract

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23
Q

how many neutrons in descending and ascending tracts?

A

A - 3

D - 2

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24
Q

common site of intracranial aneurysms?

A

in branch points of circle of willis

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25
Q

what controls spinal reflexes ?

A

brainstem nuclei

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26
Q

proximal shoulder muscles go to what motoneurons?

A

medial

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27
Q

distal finger muscles go to what motoneurons?

A

lateral

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28
Q

result of stretch reflex?

A

agonist muscle stretches

antagonist muscle relaxes

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29
Q

inverse stretch reflex explain pathway?

A
  1. agonist contracted and pulls on tendon
    GTO AFFERENT firing increase
  2. inhibitory interneurons reduced firing and muscle relaxes
  3. GTO afferent to antagonist - activate excitatory interneurons - increase firing and antagonist contract
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30
Q

why is there the inverse stretch reflex?

A

protective mechanism to prevent muscle damage

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31
Q

result of flexor reflex?

A

flex on side of pain

and extend on other side

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32
Q

crossed extensor reflex compared to stretch reflex?

A

stretch reflex is faster

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33
Q

how can GTO reflexes be OVERRIDDEN?

A

voluntary input from CNS - from thalamus, cortex that synapse - some inhibit/some excite

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34
Q

descending pathways split into?

A

lateral and ventromedial

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35
Q

lateral descending pathways? 2

an what they control

A

corticospinal
rubrospinal

control distant muscles - voluntary movement

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36
Q

ventromedial descending pathways? 2

control what?

A

vestibulospinal
tectospinal

control posture and locomotion

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37
Q

area 6?

A

premotor cortex

premotor area
supplementary motor area

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38
Q

area 4?

A

precentral gyrus - primary motor cortex

motor homunculus

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39
Q

PMA and SMA cover what areas/motor units?

A

SMA - innervate distal motor units

PMA -innervate proximal motor units

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40
Q

area 6 and 4 Differences in movements? when are they active?

A

area 6: active when just thinking about movement too OR SEE SAME MOEVEMENT IN OTHERS

area 4:active when ‘doing’ the movement

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41
Q

area 5/7?

A

posterior parietal cortex

where decisions are taken - which actions/,movements to take and likely outcome

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42
Q

HOW signal goes in brain when wanting to make movement?

A

from area 6 - prep.imagined movement

to area 4 where movement is being done down to sc

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43
Q

how do feedforward and feedback ,mechanism control movement?

A

AFTER MOVEMENT - feedback messages from vestibular nuclei to sc to correct postural in stability/difficulty

BEFORE MOEVEMNT - nuclei in brainstem initiate feedforward nuclei to stabilise posture before as anticipatory adjustments

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44
Q

input into area 6 is from where?

A

ventral lateral nucleus VLo

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45
Q

Vlo recieves input from where?

A

basal ganglia

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46
Q

where does basal ganglia get info from?

A

form all over cortex - then info goes through thalamus to basal ganglia and back to SMA in cortex area 6

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47
Q

input zone of BG name and what INCLUDEs?

A

CORPUS striatum

caudate and putamen

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48
Q

putamen in BG fires before whAT movement?

A

limb/trunk movements

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49
Q

caudate fires before what movement?

A

eye movements

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50
Q

what happens to axons of putamen and caudate?

A

axons are inhibitory and project to globes pallidus

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51
Q

explain motor loop pathway? and which are inhibitory and which a

A
  1. cortex to putamen (bg) = excitatory
  2. putamen to globus pallidus - inhbitory
  3. globus pallidus to Vlo neurons - inhibitory
  4. Vlo back to SMA(area 6) - EXCITORY
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52
Q

so what is the result of activation of BG putamen?

A

excitation of SMA

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53
Q

2 DIFFERENT pathways through basal ganglia?

A

direct

indirect pathway

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54
Q

what is the role of the indirect pathway in basal ganglia?

A

to modulate direct pathway - antagonise it and suppress competing inappropriate action

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55
Q

indirect pathway in basal ganglia via what?

A

via STN - sub thalamic nuclei

where putamen inhibits external part of globus pallidus
and then internal part of GP
AND STN
BUT CORTEX EXCITES stn which excites GPi which inhibits thalamus to excite SMA

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56
Q

what role do cerebellum play in movement?

A

instructs direction, timing and force of moevemtn

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57
Q

what is motor loop through basal ganglia for?

A

for voluntary movement

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58
Q

HOW do cerebellum have their role in movement?

A

by feedback motor loop within cerebellum

  1. cortex to
  2. through pons,cerebllum
  3. through VLC ventral lateral thalamus
  4. back to cortex AREA 4
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59
Q

how cerebellum uses motor learning?

A

uses experience in past, predictions etc

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60
Q

cognition?

A

highest order of brain function - relates to behaviour that deals with thought processing - with integrating all sensory info.

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61
Q

3 structures associated with learning and memory?

A

hippocampus - form memories
cortex - store memories
thalamus - searches and accesses memories

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62
Q

limbic system made up of? 4

A

hypothalamus
hippocampus
cingulate gyrus
amygdala

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63
Q

limbic system involved with what?

A

consists of instinctive behaviour -thirst, sex and hunger and emotive behaviour etc

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64
Q

limbic system areas?

A

reward areas - feeling of well being/sexuall arousal

punishment areas - feeling of anger/pain

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65
Q

what differentiates what we remember and what we don’t?

A

experiences that neither rewarding or punishing barely remembered

only experiences deemed significant to remember - decided by frontal cortex

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66
Q

what is most key structure in forming memories?

A

hippocampus - receives all sensory info and relayys Info to other parts of limbic system

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67
Q

what function is impaired if hippocampus impaired and what is still intact?

A

unable to form new long-term memories
but
memory already formed is intact

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68
Q

immediate sensory memory means?

A

few secs -

ability to hold memory for few secs - decay fastest

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69
Q

short -term memory?

A

seconds to hrs

associated with reverberating circuits - constantly refreshing/stretnthning circuit to allow long lasting activity

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70
Q

long term memory?

explain changes 3

A

can be lifelong

associate with structural changes in synaptic connections

  • increase in nt sites to release
  • increase in number of nt vesicles
  • increase in number of presynaptic terminals
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71
Q

thalamus role in memory?

A

in searching existing memory bank

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72
Q

cerebrum role in memory?

A

store memories

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73
Q

INTERMEDIATE long term memory?

A

involves chemical changes in presynaptic neurons

increase in Ca entry/influx in terminals - more NT release

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74
Q

long term potentiation?

A

strengthening the synapse

75
Q

papez circuit?

A

where significant info - goes into circuit of limbic system

76
Q

what happens if info deemed significant?

A

reverberating activity continues between papez circuit - cortex and sensory areas until consolidation complete in long term memory

77
Q

sleep defined as a state of?

A

unconsciousness which individual can be aroused by normal stimuli

78
Q

coma defined as a state of?

A

state unconsciousness which individual cannot be aroused and does not respond to stimuli

79
Q

why do we need sleep? 4

A

it supports important physiological functions

cognition
learning and memory
immune function
conservation of body energy

80
Q

what part of brain brings about sleep state?

A

pons due to the active inhibitory processes here

reticular formation of brainstem - controls state of consciousness

-it contains arousal and sleep centres

81
Q

melatonin in connection to sleep?

and released by?
controlled by?

A

molecule that is highest level when sleeping and released by pineal gland

release is controlled by SCN in hypothalamus

melatonin corresponds to feeling of sleepiness in humans

82
Q

SCN nucleus of hypothalamus - explain its control by light?

A

inhibitory neurons in SCN are activated by light and inhibit pineal gland - no melatonin release

darkness removes inhibition aND MELAtonin is released to make you feel sleepy

83
Q

circadian rhythm?

A

seen by SCN - this rhythm controls release of melatonin

84
Q

orexin produced by hypothalamus for?

and relationship with melatonin

A

required for wakefulness

orexin is high, melatonin is low

85
Q

serotonin link to melatonin and sleep?

A

it is a precursor for melatonin and critical to fall sleep

86
Q

EEG?

A

recording patterns of brain activity

87
Q

sleep cycle? explain stages

A

1 - slow wave - non-REM - LIGHT SLEEP - theta waves

2 - freq falls - bursts of sleep spindles

3 - spindles fall - KINDA delta waves - very slow freq

4 - DELTA waves - deep sleep

the go back through 4,3,2 then REM sleep = dreams

88
Q

REM SLEEP? what occurs here

what muscles are activated and inhibited here?

A

rapid eye movements - like being awake- high freq - dreams are here

eye muscles rapidly activated

and skeletal muscles inhibited to prevent acting out dreams

89
Q

delta waves in sleep?

theta waves in sleep?

A

very low freq and high altitude - meaning deep sleep

theta - early sleep - low freq

90
Q

large amplitude of EEG means what in sleep?

A

deepest sleep

91
Q

explain how waves change in sleep EEG?

A

alpha - relaxed awake state
beta
theta
delta - deep sleep

92
Q

dysfunctional orexin release affect?

A

narcolepsy - fall asleep anytime - risk to driving etc

93
Q

what do sensory receptors do when they receive stimuli? explain physiology

A

trasnduce it into a receptor generator potential - electrical signal - which invoked action potential if reach threshold
then lead to transmission

94
Q

how do we tell intensity of stimuli to body by receptor potential?

A

size will be bigger

and action potential swill be more frequent

95
Q

receptive field of sensory receptor?

A

encodes location of stimuli

96
Q

A delta afferent fibers carry what? and type

A

cold - FAST PAIN, pressure

small myelinated

97
Q

C afferent fibers carry what? and type

A

warmth, SLOW PAIN

unmyelinated

98
Q

A beta afferent fibers carry what? and type

A

touch, pressure, vibration

large myelinated

99
Q

proprioception mediated by what primary afferent fibers? 2

A

A alpha
and
A beta

100
Q

mechanoreceptive afferent fibers? 2

A

A alpha

A beta

101
Q

thermoreceptive and nociceptive afferent fibers? 2

A

C
and
A delta

102
Q

convergence of sensory pathways meaning?

adv./disadv. of it

A

combining of different pathways

reduces acuity - can’t tell apart from stimuli

but saves neurons to travel

103
Q

lateral inhibition of sensory input?

A

activation of one sensory input causes synaptic inhibition of neighbour -
it enhances perception of stimulus and easier to see its boundaries

104
Q

referred pain?

can be due to sensory pathways doing what?

A

pain in one part of body actually due to damage to another part

due to convergence of sensory pathways etc

105
Q

nociceptors triggered by? 3

A

imaging stimuli - low pH
heat
and
local chemical mediators that indicate tissue damaged = bradykinin/histamine/prostaglandnis

106
Q

GATE CONTROL THEORY OF PAIN EXPLAIN?

A

1- alpha beta fibers IN SAME BODY REGION activate inhibtiory interneurons which inhibit NT release from ADELTA/C fibers - closing gate

2- descending ipsilateral pathways from brain also activate same inhibitory interneurons from PAG/NRM -CLOSE GATE

this inhibitory interneurons release opioid peptides that inhibit NT release

107
Q

how do NSAIDS reduce pain/analgesic?

A

they inhibit prostaglandin formation BY inhibiting enzyme cyclo-oxygenase

  • which sensitises nociceptors to bradykinin which would increase pain sensation
108
Q

how local anaesthetics analgesic?

A

block Na action potential and therefore transmission in Bbeta/Adelta/C fibers

109
Q

how TENS analgesic?

A

electric pads - use electrical stimulation to activate Abeta fibers at same body segment - which activate inhibitory internueons and close gate of nociception

110
Q

opiates how are they analgesic? 3 ways

and example

A
  • reduce sensitivity of nociceptors in periphery
  • block NT release in dorsal horn by activating Abeta fibers and activating inhibitory interneurons
  • activate descending pathway to activate inhibitory interneurons
    e. g. - morphine
111
Q

UMN LESIONS? 5

A 
weakness
increased tone 
exaggerated reflexs - brisk 
up going plantar 
pronator drift
112
Q

glasgow coma scale? explain each section

A

3-15

eye opening to - spontantaneous/ loud voice/ pain

verbal response to - orientated/ confused/inappropraites words/none

best motor response to - obeys/ localises/withdraws/none

113
Q

SCALP layers?

A 
skin 
connective tissue - dense 
aponeurotic fascia 
loose connective tissue 
pericranium
114
Q

skull fractures types 5 ?

A 
linear /hinge fracture - base of skull 
depressed - push fragments inwards 
comminuted - mosaic/fragmented skull
ring fracture - encircling foramen magnum - 
contre-coup - on opposite side of hit
115
Q

extradural haemorrhage?
caused by?
how it presents?

A

bleeding occurred between the dura and the skull - above dura

due to bleeding from middle meningeal artery - a tear

presents with lucid interval - initially seems okay but later deteriorate

116
Q

subdural haemorrhage?
caused by?
how it presents?

A

beneath dura and above arachnoid

caused by bleeding from bridging veins that go to large venous channels in dura

tear in these vein s

lucid interval seen here

accumulate slower

117
Q

subarachnoid haemorrhage?

due to?

A

bleeding beneath arachnoid membrane

rupture of cerebral artery aneurysm

118
Q

traumatic basal SAH?

A

ABRUPT rotational MOVEMENT of head leading to ruptured vertebra-basilar circulation - causing leak into subarachnoid space

119
Q

cerebral contusions?

A

bruises on brain surface

120
Q

coup contusion?

A

bruise found directly beneath the site of impact

121
Q

cerebral oedema lead to?

due to?

A

due to injury or raised ICP

may cause fatality

can lead to herniation

122
Q

CAUSES OF RAISED ICP? 4

A
  • HAEMORRAGE
  • TUMOUR
  • ABSCESS
  • OEDEMA
123
Q

SOL

space occupying lesions EXMAPLES? 3

A

TUMOUR
BLEEDING
ABCESS

124
Q

herniation through foramen magnum refered as?

A

coning

125
Q

glioma?
to do with?
met?
types? 3

A

intracranial tumour
glial cell related

do not met outside cns - but are malignant

  • atrocytoma
  • oligodendrocytes
  • ependymal
126
Q

glioblastoma type?

seen as what under microscope?

malignant?

A

type of astrocytoma - high grade type - grows quickly

necrosis seen
are malignant

127
Q

meningioma?

associated with?
met?
microscopy seen as?

A

intracranial tumour

from meninges
benign - do not met

seen as calcifications

128
Q

medullablastoma?

type?malignant/benign?

A

embryological neural cells - undifferencated cells

tumour of neuroectoderm

malignant childhood tumour

129
Q

schwannoma? other name?

WHERE?
WHAT?

A

nervous sheath tumour
around PNS
AROUND 8TH CRANIAL NERVE - acoustic neuroma

AT ANGLE BETWENN PONS AND CEREBELLUM
benign

130
Q

Pituitary oedema?

A

benign tumour of pituitary

131
Q

cns lymphoma?

common type?
met?

A

usually b -cell lymphoma

don’t really spread out of cns

132
Q

haemangioblastoma?

A

tumour of bv

may bleed

133
Q

secondary tumour in cns? 5

A 
breast 
lung 
kidney 
colon 
melanoma
134
Q

diffuse traumatic axonal injury?

due to?

what else is usually associated with this?

A

tearin og nerve fibers in white matter of brain

due to high force rotational forces applied to the brain tissue causing shearing of axons

diffuse vascular injury - bv also damaged alongside axons

135
Q

multiple sclerosis disease - what is it?

A

white matter disease
demyelination - inflamed myelin sheath

episodes/relapses of demyelination disseminated in space and time - that have occurred in different areas of CNS of days/weeks

136
Q

how does MS PRESENT?

A

as relapse-remitting course - relapse/focal upsets where symptoms worsen and followed by remission where symptom s go away

137
Q

what symptoms present in relapse of MS? 7

A

ANYWHERe IN cns

  • OPTIC NEURITIS
  • SENSORY SYMPTOMS
  • LIMB WEAKNESS
  • DIPLOPIA
  • VERTIGO
  • ATAXIA
  • internuclear opthalmoplegia
138
Q

OPTIC NEURITIS results as?

A

visual loss
optic disc swollen
seen in MS RELAPSE

139
Q

internuclear opthalmoplegia?

seen where?

A

weakness of eye muscles

seen in relapse of MS

140
Q

myelitis?

A

inflamed spinal cord

141
Q

MS on MRI seen as?

A

areas of demyelination - patchy

142
Q

CIS defined as?

A

not an MS - clinically isolated syndrome

143
Q

further relapses occur how?

A

within months/years of first relapse but varies amongst people

144
Q

progressive phase of MS means?

A

accumulation of symptoms and signs

and fewer relapses

145
Q

types of MS? 3

A

-relapsing remitting
can lead to
-secondary progressive (now no relapses now progressive)
-primary progressive (never had relapses,just progressive from onset)

146
Q

lumbar puncture in MS shows?

A

oligoclonal bands present in CSF but not serum - inflammatory bands

147
Q

MS mimics? 5

A 
auto-immune conditions 
sarcoidosis 
vasculitis 
other causes of demyelination 
ADEM
148
Q

DISEASE MODIFYING TREATMENT FOR MS?

purpose?

first line and second line of treatment?

A

reduce relapse rate

1st line =
injections - beta-interferons
oral

2nd line =
biologics

149
Q

somatosensory cortex - when there is pain only or not?

A

can be triggered without tissue damage too

150
Q

afferent fibers of pain? 2

each for wha type of pain

A

C - slow pian

A delta - fast pain

151
Q

thalamus made up of systems?2

A

medial - decide and evaluate component of pain and decide respose (cortex)
lateral - acknowledging and localising where impulse from(somatosensory cortex)

152
Q

PAG descending pathway affect on pain?

A

close gate and reduce pain signal - inhibitory system

153
Q

central sensitisation of pain?

components 3

A

a condition where
develop and maintain chronic pain
increased response to nociceptors in ons to normal or sub threshold input
increased sensitivity

  • wind up
  • long term potentiation
  • classical
154
Q

CENTRAL SENSITISATION - wind up explain?

A

amplification

activated synapses
-progressive increase in response of neurons

155
Q

central sensitisation - classical?

A

opening up new synapses - nociceptors

outlast initial stimuli duration - continue even if stimuli removed
can be maintained even if low stimuli - sub threshold

156
Q

central sensitisation - long term potentiation?

A

synaptic connections between neurons stronger with freq. activation - like when making a memory

157
Q

nociceptive pain?

A

sensory experience that occurs when specific peripheral sensory neurons/nociceptors respond to painful stimuli

158
Q

neuropathic pain?

A

pain caused by lesion or disease of somatosensory system -

159
Q

nociplastic pain?

A

no tissue damage or threatened - but pain arises from altered nociception

160
Q

acute v chronic pain?

A

acute - protective role/pain stimuli present

chronic - not purpose - presence of painful stimuli not needed

161
Q

what NT involved in pain stimuli?

A

CGRP

162
Q

SYNCOPE? due to

A

fainting/passing out due to cerebral hypoxia

163
Q

vasovagal syncope?

A

vasovagal = fall in bp - lead to fall in flow to brain -

164
Q

cardiac syncope?

examples

A

syncope caused by cardiac condition - that affects blood flow to brain -

arrhythmia
heart disease/MI

165
Q

difference between seizure/epilepsy?

A

seizure - one single event

epilepsy - condition of 2 or more unprovoked seizure attacks

166
Q

difference between syncope and seizure?

A

syncope - fainting

seizure

167
Q

epilepsy?

A

neuro condition where periods/recurrent of seizures -

168
Q

pseudo seizure?

A

seizures result from stress/metal state - psych causes

169
Q

provoked seizures causes? 5

A 
alcohol withdrawal 
drug withdrawal /abuse
trauma 
decrease sugar 
decrease NA
170
Q

when is it referred as epilepsy?

A

more than 1 unprovoked seizure

171
Q

classification of leisure?

A

focal - in one area of brain

generalised - in all areas of brain

172
Q

absence seizure?

A

generlised seizure

child
staring into space -

173
Q

tonic clonic seizure?

type

4 symptoms

A

generalised seizure

abrupt loss of consciousness,
body stiffening - jerking
shaking
loss of bladder control and biting tongue

174
Q

complex partial seizure? type?

what part of brain affected?

A

complex partial - focal seizure

with loss of consciousness/awareness

stare into space/ no response

parietal lobe

175
Q

4 anti-epileptic drugs?

and what do they all have?

A
  • sodium valproate
  • lamotrigine
  • levetiracetam
  • carbamazephine

all have side effects of their own

176
Q

status epilepticus?

A

seizure that lasts 5 mins or 2 seizures within 5 min period

177
Q

2 types of status epilepticus?

A

convulsive - jerking, drooling, grunting

non-convulsive - like daydreaming, staring

178
Q

how can glucose sugar level associate with seizure?

A

hypo can lead to seizure

179
Q

SYNAPTIC TRANSMISSION - EXPLAI BRIEFLY HOW NT RELEASED?

A

-synthesis and packing of nt into vesicles
-Na ap invades presynapse terminal
-this activates Ca voltage gated channels
-triggers Ca dependant exocytosis of vesicles
-nt travels across cleft and binds to receptors
-presynapse autoreceptors inhbit nt release
OR
-NT inactivated by extracellular breakdown

180
Q

can dopamine be given orally? and why?

SOLUTION TO THIS?

A

no

AS CANT CROSS BBB

SO GIVE DOPA
which can cross bbb and convert to dopamine once crossed

181
Q

what two enzymes used in breakdown in dopamine?

A

MAO-B

COMT

182
Q

DRUGS GIVEN FOR PARKINSONS? 5 name all ones and example if can

A
  • MAOB inhibitor
  • COMT inhibitor
  • DA PRECURSOR - LEVODOPA
  • DA AGONIST on receptors
  • DA ANTAGONIST - DOMPERIDONE
183
Q

SIDE EFFECT OF LEVODOPA?

A

DYSKINESIAS

NERVOUS (5 decks)

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