PHYSIOLOGY Flashcards
(183 cards)
1
Q
3 columns of white matter?
A
posterior
lateral
anterior
2
Q
dorsal column carries what?
type?
A
ascending
carries touch, vibration sense and proprioception
3
Q
corticospinal tract carries what?
also called?
A
carries motor impulses fro motor cortex to skeletal muscles
DESCEDNING
pyramidal tract
4
Q
LATERAL spinothalamic tract carries what?
A
ascending
pain and temp sensation
5
Q
explain pathway of corticospinal tract?
A
- start at motor cortex AREA 4
- through internal capsule
- called cortico bulblar tract = go to contralateral cranial nuclei (doesn’t reach sc)
- then most fibres cross at decussation of pyramids
- some don’t and form anterior corticospinal tract
- most form lateral corticospinal tract on contralateral side into SC
- to skeletal muscles
6
Q
where does this corticospinal tract run in the brainstem?
A
lateral pathway
7
Q
where is the pyramidal decussation?
A
in medulla
8
Q
where is the lower motor neuron?
A
when in synapses in sc
in ventral horn
9
Q
DORSAl column - explain pathway?
A
- dorsal root of 1st order neuron to synapse in lower part of medulla to 2nd order neuron
- 2nd order neuron crosses over in medulla
- tract called MEDIAL LEMNISCUS
- travels up brainstem,
- 3rd order neuron starts in thalamus(VPL NUCLEUS) and then pass through IC to posterior central gyrus in parietal lobe - sensory
10
Q
WHERE DO ALL SESNORY INFO S YNAPSE IN THALAMUS?
A
VPL NUCLEUS
11
Q
EXPLAIN lateral spinothalamic tract?
A
- 1st order neuron enters and end at same level in sc
- 2nd order neuron crosses over into lateral column and called lateral spinothalamic tract
- 2nd order till thalamus and 3rd order passes through IC and radiates to post-central gyrus - sensory
12
Q
difference with lateral spinothalaic tract?
A
decussation occurring at sc level same NOT MEDULLA
13
Q
position of dorsal column?
A
posterior
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
15
Q
reciprocal innervation/inhibition meaning?
A
innervating antagonist muscle to do opposite
16
Q
FLEXOR/CROSSED EXTENSOR REFLEX explain pathway?
and result of it
A
pain stimuli
- sensory neuron activated
- 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
17
Q
what mediates reflexes?
A
lower motor neurons
18
Q
if UMN lesion what happens to reflexes?
A
exaggerated
19
Q
UMN/LMN lesions affect on muscle tone?
A
UMN LESION - increased tone - spastic
LMN LESION - decreased tone - flaccid - no reflexes
20
Q
if lesion - what is affected - above it or below it?
A
all stuff below it
21
Q
if lesion is above and below decussation meaning?
A
above decussation - contralateral symptoms
below decussation - ipsilateral symptoms
22
Q
paralysis due to what tract?
A
pyramidal - corticospinak tract
23
Q
how many neutrons in descending and ascending tracts?
A
A - 3
D - 2
24
Q
common site of intracranial aneurysms?
A
in branch points of circle of willis
25
what controls spinal reflexes ?
brainstem nuclei
26
proximal shoulder muscles go to what motoneurons?
medial
27
distal finger muscles go to what motoneurons?
lateral
28
result of stretch reflex?
agonist muscle stretches
| antagonist muscle relaxes
29
inverse stretch reflex explain pathway?
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
30
why is there the inverse stretch reflex?
protective mechanism to prevent muscle damage
31
result of flexor reflex?
flex on side of pain
| and extend on other side
32
crossed extensor reflex compared to stretch reflex?
stretch reflex is faster
33
how can GTO reflexes be OVERRIDDEN?
voluntary input from CNS - from thalamus, cortex that synapse - some inhibit/some excite
34
descending pathways split into?
lateral and ventromedial
35
lateral descending pathways? 2
| an what they control
corticospinal
rubrospinal
control distant muscles - voluntary movement
36
ventromedial descending pathways? 2
| control what?
vestibulospinal
tectospinal
control posture and locomotion
37
area 6?
premotor cortex
premotor area
supplementary motor area
38
area 4?
precentral gyrus - primary motor cortex
motor homunculus
39
PMA and SMA cover what areas/motor units?
SMA - innervate distal motor units
| PMA -innervate proximal motor units
40
area 6 and 4 Differences in movements? when are they active?
area 6: active when just thinking about movement too OR SEE SAME MOEVEMENT IN OTHERS
area 4:active when 'doing' the movement
41
area 5/7?
posterior parietal cortex
where decisions are taken - which actions/,movements to take and likely outcome
42
HOW signal goes in brain when wanting to make movement?
from area 6 - prep.imagined movement
| to area 4 where movement is being done down to sc
43
how do feedforward and feedback ,mechanism control movement?
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
44
input into area 6 is from where?
ventral lateral nucleus VLo
45
Vlo recieves input from where?
basal ganglia
46
where does basal ganglia get info from?
form all over cortex - then info goes through thalamus to basal ganglia and back to SMA in cortex area 6
47
input zone of BG name and what INCLUDEs?
CORPUS striatum
| caudate and putamen
48
putamen in BG fires before whAT movement?
limb/trunk movements
49
caudate fires before what movement?
eye movements
50
what happens to axons of putamen and caudate?
axons are inhibitory and project to globes pallidus
51
explain motor loop pathway? and which are inhibitory and which 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
52
so what is the result of activation of BG putamen?
excitation of SMA
53
2 DIFFERENT pathways through basal ganglia?
direct
| indirect pathway
54
what is the role of the indirect pathway in basal ganglia?
to modulate direct pathway - antagonise it and suppress competing inappropriate action
55
indirect pathway in basal ganglia via what?
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
56
what role do cerebellum play in movement?
instructs direction, timing and force of moevemtn
57
what is motor loop through basal ganglia for?
for voluntary movement
58
HOW do cerebellum have their role in movement?
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
59
how cerebellum uses motor learning?
uses experience in past, predictions etc
60
cognition?
highest order of brain function - relates to behaviour that deals with thought processing - with integrating all sensory info.
61
3 structures associated with learning and memory?
hippocampus - form memories
cortex - store memories
thalamus - searches and accesses memories
62
limbic system made up of? 4
hypothalamus
hippocampus
cingulate gyrus
amygdala
63
limbic system involved with what?
consists of instinctive behaviour -thirst, sex and hunger and emotive behaviour etc
64
limbic system areas?
reward areas - feeling of well being/sexuall arousal
punishment areas - feeling of anger/pain
65
what differentiates what we remember and what we don't?
experiences that neither rewarding or punishing barely remembered
only experiences deemed significant to remember - decided by frontal cortex
66
what is most key structure in forming memories?
hippocampus - receives all sensory info and relayys Info to other parts of limbic system
67
what function is impaired if hippocampus impaired and what is still intact?
unable to form new long-term memories
but
memory already formed is intact
68
immediate sensory memory means?
few secs -
ability to hold memory for few secs - decay fastest
69
short -term memory?
seconds to hrs
associated with reverberating circuits - constantly refreshing/stretnthning circuit to allow long lasting activity
70
long term memory?
explain changes 3
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
71
thalamus role in memory?
in searching existing memory bank
72
cerebrum role in memory?
store memories
73
INTERMEDIATE long term memory?
involves chemical changes in presynaptic neurons
increase in Ca entry/influx in terminals - more NT release
74
long term potentiation?
strengthening the synapse
75
papez circuit?
where significant info - goes into circuit of limbic system
76
what happens if info deemed significant?
reverberating activity continues between papez circuit - cortex and sensory areas until consolidation complete in long term memory
77
sleep defined as a state of?
unconsciousness which individual can be aroused by normal stimuli
78
coma defined as a state of?
state unconsciousness which individual cannot be aroused and does not respond to stimuli
79
why do we need sleep? 4
it supports important physiological functions
cognition
learning and memory
immune function
conservation of body energy
80
what part of brain brings about sleep state?
pons due to the active inhibitory processes here
reticular formation of brainstem - controls state of consciousness
-it contains arousal and sleep centres
81
melatonin in connection to sleep?
and released by?
controlled by?
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
SCN nucleus of hypothalamus - explain its control by light?
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
circadian rhythm?
seen by SCN - this rhythm controls release of melatonin
84
orexin produced by hypothalamus for?
and relationship with melatonin
required for wakefulness
orexin is high, melatonin is low
85
serotonin link to melatonin and sleep?
it is a precursor for melatonin and critical to fall sleep
86
EEG?
recording patterns of brain activity
87
sleep cycle? explain stages
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
REM SLEEP? what occurs here
what muscles are activated and inhibited here?
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
delta waves in sleep?
theta waves in sleep?
very low freq and high altitude - meaning deep sleep
theta - early sleep - low freq
90
large amplitude of EEG means what in sleep?
deepest sleep
91
explain how waves change in sleep EEG?
alpha - relaxed awake state
beta
theta
delta - deep sleep
92
dysfunctional orexin release affect?
narcolepsy - fall asleep anytime - risk to driving etc
93
what do sensory receptors do when they receive stimuli? explain physiology
trasnduce it into a receptor generator potential - electrical signal - which invoked action potential if reach threshold
then lead to transmission
94
how do we tell intensity of stimuli to body by receptor potential?
size will be bigger
| and action potential swill be more frequent
95
receptive field of sensory receptor?
encodes location of stimuli
96
A delta afferent fibers carry what? and type
cold - FAST PAIN, pressure
small myelinated
97
C afferent fibers carry what? and type
warmth, SLOW PAIN
unmyelinated
98
A beta afferent fibers carry what? and type
touch, pressure, vibration
large myelinated
99
proprioception mediated by what primary afferent fibers? 2
A alpha
and
A beta
100
mechanoreceptive afferent fibers? 2
A alpha
| A beta
101
thermoreceptive and nociceptive afferent fibers? 2
C
and
A delta
102
convergence of sensory pathways meaning?
adv./disadv. of it
combining of different pathways
reduces acuity - can't tell apart from stimuli
but saves neurons to travel
103
lateral inhibition of sensory input?
activation of one sensory input causes synaptic inhibition of neighbour -
it enhances perception of stimulus and easier to see its boundaries
104
referred pain?
| can be due to sensory pathways doing what?
pain in one part of body actually due to damage to another part
due to convergence of sensory pathways etc
105
nociceptors triggered by? 3
imaging stimuli - low pH
heat
and
local chemical mediators that indicate tissue damaged = bradykinin/histamine/prostaglandnis
106
GATE CONTROL THEORY OF PAIN EXPLAIN?
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
how do NSAIDS reduce pain/analgesic?
they inhibit prostaglandin formation BY inhibiting enzyme cyclo-oxygenase
- which sensitises nociceptors to bradykinin which would increase pain sensation
108
how local anaesthetics analgesic?
block Na action potential and therefore transmission in Bbeta/Adelta/C fibers
109
how TENS analgesic?
electric pads - use electrical stimulation to activate Abeta fibers at same body segment - which activate inhibitory internueons and close gate of nociception
110
opiates how are they analgesic? 3 ways
and example
- 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
UMN LESIONS? 5
```
weakness
increased tone
exaggerated reflexs - brisk
up going plantar
pronator drift
```
112
glasgow coma scale? explain each section
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
SCALP layers?
```
skin
connective tissue - dense
aponeurotic fascia
loose connective tissue
pericranium
```
114
skull fractures types 5 ?
```
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
extradural haemorrhage?
caused by?
how it presents?
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
subdural haemorrhage?
caused by?
how it presents?
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
subarachnoid haemorrhage?
| due to?
bleeding beneath arachnoid membrane
rupture of cerebral artery aneurysm
118
traumatic basal SAH?
ABRUPT rotational MOVEMENT of head leading to ruptured vertebra-basilar circulation - causing leak into subarachnoid space
119
cerebral contusions?
bruises on brain surface
120
coup contusion?
bruise found directly beneath the site of impact
121
cerebral oedema lead to?
due to?
due to injury or raised ICP
may cause fatality
can lead to herniation
122
CAUSES OF RAISED ICP? 4
- HAEMORRAGE
- TUMOUR
- ABSCESS
- OEDEMA
123
SOL
| space occupying lesions EXMAPLES? 3
TUMOUR
BLEEDING
ABCESS
124
herniation through foramen magnum refered as?
coning
125
glioma?
to do with?
met?
types? 3
intracranial tumour
glial cell related
do not met outside cns - but are malignant
- atrocytoma
- oligodendrocytes
- ependymal
126
glioblastoma type?
seen as what under microscope?
malignant?
type of astrocytoma - high grade type - grows quickly
necrosis seen
are malignant
127
meningioma?
associated with?
met?
microscopy seen as?
intracranial tumour
from meninges
benign - do not met
seen as calcifications
128
medullablastoma?
type?malignant/benign?
embryological neural cells - undifferencated cells
tumour of neuroectoderm
malignant childhood tumour
129
schwannoma? other name?
WHERE?
WHAT?
nervous sheath tumour
around PNS
AROUND 8TH CRANIAL NERVE - acoustic neuroma
AT ANGLE BETWENN PONS AND CEREBELLUM
benign
130
Pituitary oedema?
benign tumour of pituitary
131
cns lymphoma?
common type?
met?
usually b -cell lymphoma
| don't really spread out of cns
132
haemangioblastoma?
tumour of bv
| may bleed
133
secondary tumour in cns? 5
```
breast
lung
kidney
colon
melanoma
```
134
diffuse traumatic axonal injury?
due to?
what else is usually associated with this?
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
multiple sclerosis disease - what is it?
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
how does MS PRESENT?
as relapse-remitting course - relapse/focal upsets where symptoms worsen and followed by remission where symptom s go away
137
what symptoms present in relapse of MS? 7
ANYWHERe IN cns
- OPTIC NEURITIS
- SENSORY SYMPTOMS
- LIMB WEAKNESS
- DIPLOPIA
- VERTIGO
- ATAXIA
- internuclear opthalmoplegia
138
OPTIC NEURITIS results as?
visual loss
optic disc swollen
seen in MS RELAPSE
139
internuclear opthalmoplegia?
seen where?
weakness of eye muscles
seen in relapse of MS
140
myelitis?
inflamed spinal cord
141
MS on MRI seen as?
areas of demyelination - patchy
142
CIS defined as?
not an MS - clinically isolated syndrome
143
further relapses occur how?
within months/years of first relapse but varies amongst people
144
progressive phase of MS means?
accumulation of symptoms and signs
| and fewer relapses
145
types of MS? 3
-relapsing remitting
can lead to
-secondary progressive (now no relapses now progressive)
-primary progressive (never had relapses,just progressive from onset)
146
lumbar puncture in MS shows?
oligoclonal bands present in CSF but not serum - inflammatory bands
147
MS mimics? 5
```
auto-immune conditions
sarcoidosis
vasculitis
other causes of demyelination
ADEM
```
148
DISEASE MODIFYING TREATMENT FOR MS?
purpose?
first line and second line of treatment?
reduce relapse rate
1st line =
injections - beta-interferons
oral
2nd line =
biologics
149
somatosensory cortex - when there is pain only or not?
can be triggered without tissue damage too
150
afferent fibers of pain? 2
| each for wha type of pain
C - slow pian
| A delta - fast pain
151
thalamus made up of systems?2
medial - decide and evaluate component of pain and decide respose (cortex)
lateral - acknowledging and localising where impulse from(somatosensory cortex)
152
PAG descending pathway affect on pain?
close gate and reduce pain signal - inhibitory system
153
central sensitisation of pain?
components 3
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
CENTRAL SENSITISATION - wind up explain?
amplification
activated synapses
-progressive increase in response of neurons
155
central sensitisation - classical?
opening up new synapses - nociceptors
outlast initial stimuli duration - continue even if stimuli removed
can be maintained even if low stimuli - sub threshold
156
central sensitisation - long term potentiation?
synaptic connections between neurons stronger with freq. activation - like when making a memory
157
nociceptive pain?
sensory experience that occurs when specific peripheral sensory neurons/nociceptors respond to painful stimuli
158
neuropathic pain?
pain caused by lesion or disease of somatosensory system -
159
nociplastic pain?
no tissue damage or threatened - but pain arises from altered nociception
160
acute v chronic pain?
acute - protective role/pain stimuli present
chronic - not purpose - presence of painful stimuli not needed
161
what NT involved in pain stimuli?
CGRP
162
SYNCOPE? due to
fainting/passing out due to cerebral hypoxia
163
vasovagal syncope?
vasovagal = fall in bp - lead to fall in flow to brain -
164
cardiac syncope?
| examples
syncope caused by cardiac condition - that affects blood flow to brain -
arrhythmia
heart disease/MI
165
difference between seizure/epilepsy?
seizure - one single event
| epilepsy - condition of 2 or more unprovoked seizure attacks
166
difference between syncope and seizure?
syncope - fainting
seizure
167
epilepsy?
neuro condition where periods/recurrent of seizures -
168
pseudo seizure?
seizures result from stress/metal state - psych causes
169
provoked seizures causes? 5
```
alcohol withdrawal
drug withdrawal /abuse
trauma
decrease sugar
decrease NA
```
170
when is it referred as epilepsy?
more than 1 unprovoked seizure
171
classification of leisure?
focal - in one area of brain
| generalised - in all areas of brain
172
absence seizure?
generlised seizure
child
staring into space -
173
tonic clonic seizure?
type
4 symptoms
generalised seizure
abrupt loss of consciousness,
body stiffening - jerking
shaking
loss of bladder control and biting tongue
174
complex partial seizure? type?
what part of brain affected?
complex partial - focal seizure
with loss of consciousness/awareness
stare into space/ no response
parietal lobe
175
4 anti-epileptic drugs?
and what do they all have?
- sodium valproate
- lamotrigine
- levetiracetam
- carbamazephine
all have side effects of their own
176
status epilepticus?
seizure that lasts 5 mins or 2 seizures within 5 min period
177
2 types of status epilepticus?
convulsive - jerking, drooling, grunting
non-convulsive - like daydreaming, staring
178
how can glucose sugar level associate with seizure?
hypo can lead to seizure
179
SYNAPTIC TRANSMISSION - EXPLAI BRIEFLY HOW NT RELEASED?
-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
can dopamine be given orally? and why?
SOLUTION TO THIS?
no
AS CANT CROSS BBB
SO GIVE DOPA
which can cross bbb and convert to dopamine once crossed
181
what two enzymes used in breakdown in dopamine?
MAO-B
| COMT
182
DRUGS GIVEN FOR PARKINSONS? 5 name all ones and example if can
- MAOB inhibitor
- COMT inhibitor
- DA PRECURSOR - LEVODOPA
- DA AGONIST on receptors
- DA ANTAGONIST - DOMPERIDONE
183
SIDE EFFECT OF LEVODOPA?
DYSKINESIAS
