Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

JMP Y2S1 > Week 39- Focal Brain Dysfunction: Seizure > Flashcards

Week 39- Focal Brain Dysfunction: Seizure Flashcards

1
Q

What is consciousness?

A

A state of awareness of one’s self, place and environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the general functions of the cerebrum? (3)

A
  1. Conscious thought processes –> intellectual functions
    1. Memory storage and processing
    2. Conscious and subconscious regulation of skeletal muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the general functions of the cerebellum?

A

Posture, balance, coordination

Complex somatic motor patterns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is the diencephalon located?

A

Top of the brain stem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the key components of the diencephalon?

A

Thalamus

Hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the general role of the thalamus?

A

Relay and processing centres for sensory information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the general role of the hypothalamus?

A

Centres controlling emotion
autonomic functions
hormone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is the mesencephalon located?

A

Between the pons and the diencephalon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the general role of the mesencephalon?

A

Processing of visual and auditory data
Generation of reflex
Maintenance of consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where is the pons located?

A

Bulge in the brainstem –> above the medula oblonggata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the general role of the pons?

A

Relays sensory information to the cerebellum and thalamus

Subconscious somatic and visceral motor centres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is the medula oblongata located?

A

Bottom of the brain stem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the general role of the medula?

A

Relays sensory information to rest of brain stem

Autonomic centres for regulation of visceral function (cardiovascular, resp, GIT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are Reticular formation in the brain?

A

Embedded in the brainstem –> major nuclear groups for noradrenergic, adrenergic, dopaminergic and serotonergic neurons of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the two divisions of the Reticular formations in the brain?

A

Lateral reticular formation (parvocellular)

Medial reticular formations (magnocellular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the main functions of the Lateral reticular formation (parvocellular)?

A

Reflex connections to local cranial nerve motor nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the main functions of the Medial reticular formation (parvocellular)?

A

Long ascending and descending axons involved in control of movement, posture, pain, autonomic function and arousal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why do seizures occur?

A

Too much excitatory effects

And/or impaired inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the roles of the Noradrenergic locus coeruleus?

A

Within the spinal cord –> modulation of autonomic reflexes and pain

Within the cerebrum –> vigilance and responsiveness to unexpected environmental stimuli –> mood regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What route does the Noradrenergic locus coeruleus take through the brain?

A

Originates in coeruleus locus –> On the superior posterior side of the brain stem to the pons:
Down –> brainstem to spin and cerebellum
Up –> loops to thalamus and hypothalamus and travels around a loop around the corpus callosum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the roles of the Dopaminergic cell groups?

A

Influence motor responses by projections to BG (nigrostriatal pathway)
Influence emotion, thought and memory (mesocortical, mesolimbic pathway)
Influence sympathetic preganglionic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the routes of the Dopaminergic cell groups in the brain?

A

Origin –> ventral tegmental region –> central to triatum under corpus callosum
Origin –> ventral tegmental region –> anterior along frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is another name for the serotonergic cell groups?

A

Raphe Nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are Raphe nuclei (serotonergic cell groups) located?

A

Medial line up the brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the roles of the serotonergic cell groups?

A
  1. Motor and autonomic system of spinal cord
  2. Modulate pain
  3. Hypothalamic cardiovascular and thermoregulatory control
  4. Forebrain responsiveness of cortical neurons and regulation of sleep-wake cycles and mood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the route of the serotonergic neuronal circuits in the brain?

A

Loops everywhere:
Stem –> cerebellum
Stem –> basal ganglia and corpus callosum
Stem –> loop anterior via frontal all the way to occipital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the roles of the neuronal circuits with Cholinergic Cell groups?

A

PMT (pontomesencephalo-tegmental complex) and basal nuclei –>influences cortical arousal during waking states and dreaming (REM)
Medial septal nuclei –> hippocampus, memory and learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the route of the Collinergic Cell groups?

A

Brain stem nears pons loops around frontal to occipital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the role of the Histaminergic cell group?

A

Help maintain arousal in forebrain (explains drowsiness caused by antihistamines crossing the BBB)
Arousal response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are some examples of the monoaminergic cell groups?

A

Noradrenaline, serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the effects of the noradrenaline and serotonin cell groups within the cerebral cortex and thalamus?

A

Wakefulness and responsiveness of cortical and thalamic neurons to sensory stimuli = arousal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the two major cholinergic pathways?

A

Inputs from pedunculopontine and laterodorsal tegmental nuclei:

  1. To intralaminar nuclei of thalamus –> projecting widely upon the cortex
  2. Lateral hypothalamic area to join with hypothalamic and basal forebrain cholinergic projections to cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where is the central sulcus located and what direction does it run?

A

Midbrain –> coronal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What two areas does the central sulcus separate?

A 
Primary Motor cortex (front)
Somatosensory cortex (back
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the role of the primary motor complex?

A

Voluntary movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the role of the somatosensory cortex?

A

Somaesthetic sensation and proprioception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What lies anterior to the primary motor complex?

A

Premotor complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the role of the premotor complex?

A

Coordination of complex movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is anterior to the premotor complex?

A

Frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the role of the frontal lobe?

A

Planning of voluntary activities
Decision making
Personality traits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the small area within the inner brain posterior to the frontal lobe?

A

Broca’s area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the role of Broca’s area?

A

Speech formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the two main lobes on the lateral sides of the brain?

A

Temporal lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the role of the temporal lobes?

A

Integration of sensory inputs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where is the primary auditory complex located?

A

Middle superior edge of the temporal lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where is the limbic association cortex located?

A

Mostly inner and bottom surface of temporal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the role of the limbic association cortex?

A

Motivation
Emotion
Memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Where is the occipital lobe located?

A

Posterior side of brain (above cerebellum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where is the primary visual cortex?

A

Posterior edge of occipital lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the lobe behind the somatosensory cortex?

A

Parietal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the roll and location of the posterior parietal cortex?

A

Integration of somatosensory and visual input –> important for complex movements
Located –> immediately posterior to somatosensory cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Where is Wernicke’s area located?

A

Inner of the parietal lobe (posterior brain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the role of Wernicke’s area?

A

Speech understanding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Where is the PFC orbitofrontal?

A

Inferior side of the frontal cortex (as it wraps back under the brain and tucks in near the temporal lobes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are deficits in the PFC orbitofrontal linked with?

A 
Disinhibition
Altered personality 
Lack of empathy
Socially inappropriate behaviour
Reactive aggression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Where is the dl-PFC (dorsolateral)?

A

Lateral side of the prefrontal cortex both sides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are some affects of deficits in the dl-PFC?

A

Reduced attentional control
Preseveration
Impaired exacutive functions (working memory, sequencing, planning, creativity, reasoning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Where is the medial prefrontal cortex (m-PFC)?

A

Medial inner wrap around of the frontal lobe (sits under the corpus callosum frontal protrusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are deficiets in the m-PFC linked to?

A

Decreased motivation
Apathy
Akinesia
Impaired detection of mismatches or errors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does arousal and wakefulness depend on?

A

Functioning of the cerebral hemispheres and the reticular activating system of the brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does content and cognition; emotions (affect) depend on?

A

Functioning cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is unconsciousness?

A

Lack of such awareness/responsiveness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the general states which are regarded as conscious?

A 
Being awake from low levels to high levels of alertness:
Drowsiness
Indifference
Normal quiet state
Vigilance
Hyper-arousal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are some levels low to high in terms of unconsciousness?

A

Sleep
General anaesthesia
Coma
Vegetative state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the clinical aspects of confusion?

A

Issues with self, space and time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is clinical delirium?

A

Reduced awareness of the environment
Reduced attention
Changes in cognition (false beliefs)
Changes in perception (hallucinations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is clinical obtundation?

A

Mental blunting with mild to moderate reduction in alertness
Reduced pain sensation
Can happen in trauma, mistreatment or psychological stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is clinical Stupor?

A

A state of lethargy and immobility with diminished responsiveness to stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the 5 wave types seen on an ECG?

A 
Delta
Theta 
Alpha
Beta
Gamma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the Hz and situation were you would see Delta EEG activity?

A

< 4 Hz –> slow-wave sleep/ coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the Hz and situation were you would see Theta EEG activity?

A

4-7Hz –> drowsiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the Hz and situation were you would see Alpha EEG activity?

A

8-15 Hz –> relaxed wakefulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the Hz and situation were you would see Beta EEG activity?

A

16-30 Hz –> active wakefulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the Hz and situation were you would see Gamma EEG activity?

A

30-100 Hz –> mainly a artifact introduced by muscular activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the origins of EEG readings?

A

Synchronous contribution from a very large number of neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What potentials contribute to EEG waves?

A

Post synaptic potentials (excitatory and inhibitory)

Aps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What picks up the EEG reading?

A

EEG electrode on the outside of the skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is resting membrane mainly determined by?

A

Mainly by the concentration gradient of K+ –> loss of K+ results in the negative charge seen in neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Where is K+ and Na+ in higher concentration in regards to cells?

A

K+ higher inside cells

Na+ higher outside the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What allows for the generation of transmembrane potentials and ion concentration gradients across cell membranes?

A

Na+/K+ ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is an Action potential?

A

Nerve impulse –> electrical spike which can propagate along the axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What triggers neurotransmitter release at the presynaptic region?

A

Opening of voltage gated Ca+ channels triggers vesicle mobilisation and release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is depolarisation?

A

Change in voltage driving the resting potential towards 0 from the resting negative voltage

84
Q

What is hyperpolarisation?

A

Increase in the negative potential –> further polarised

85
Q

What is the three main phases of action potentials?

A

Depolarisation
Repolarisation
Undershoot (hyperpolarisation) –> relative refractory period

86
Q

How do ions flow in voltage gated ion channels?

A

According to pre-existing electrochemical gradients (after required voltage is achieved)

87
Q

What is some typical domains of Na voltage gated channels?

A

S4

S5-S6

88
Q

What is the mechanism of S4 domain voltage channel gates?

A

S4 –> voltage sensor –> sensor is positively charged –> when voltage changes it undergoes a conformational change –> gating

89
Q

What is the mechanism of S5-S6 domain voltage channel gates?

A

S5-S6 –> pore loop domains

90
Q

What is the two subunits within voltage gated sodium channels?

A

Single Na alpha subunit forms complex with auxillary Na Beta subunits

91
Q

What is the activation gate for voltage gates channels?

A

Gate that opens inside the cell membrane to open the channel

92
Q

What is an inactivation gate?

A

Time dependant gate present in Na channels

93
Q

What is a way apart from voltage is voltage gated Na channels regulated?

A

Phosphorylation

94
Q

What is the impact of phosphorylation on voltage gated sodium channels?

A

Can slow its inactivation

95
Q

What gate is responsible for the rising phase in action potential?

A

Voltage gated sodium channels opening

96
Q

What makes the voltage gated sodium channels to stop functioning and allow for repolarisation during an action potential?

A

Time dependant inactivation gates

97
Q

How does tetrodotoxin have its affect?

A

Prevent Na+ flow by binding to the outside of the pore

98
Q

What is the structure of a voltage dependant calcium channel?

A

Single alpha subunit forms complex with axillary subunits (similar to Na+)

99
Q

How are Ca+ voltage dependant calcium channels subtyped?

A

According to their alpha subunit and their threshold of activation (low or high voltage activated)

100
Q

What do calcium voltage channels normally respond to?

A

Membrane depolarisation

101
Q

What is the structure of the voltage dependant potassium channel?

A

Four alpha subunits each containing 6 subunits (S1-S6) and a membrane re-entering P-loop

102
Q

What phase are K+ voltage channels involved in?

A

Repolarisation phase (efflux of K+ repolarises cell)

103
Q

What is the structure of a voltage gated chloride?

A

Subunits contain multiple transmembrane domains and channels arranged as dimers (each subunit contains a pore)

104
Q

What determines the speed of a voltage gated chlorine channel?

A

The opening and closing of the dimer pores.

Fast gating –> when pores are individually opened and chlorine can pass with just 1 open

Slow gating –> when both pores need to be open before chlorine can pass

105
Q

What makes ligand gated ion channels open?

A

Typically requires binding of one or more neurotransmitter molecule

106
Q

What are some examples of excitatory ligand gated ion channels?

A

Nicotinic
NMDA
AMPA

107
Q

What is an example of a inhibitory ligand gated ion channel?

A

GABA

108
Q

What type of proteins are the nicotinic acetylcholine receptors?

A

Ligand gated Na+ enters/K+ exits channel

109
Q

What is the effect of the Nicotinic acetylcholine receptors?

A

Movement of cations –> excitatory response in post synaptic cell

110
Q

What activates the NMDA receptor?

A

Glutamate

111
Q

What movement does NMDA receptor allow?

A

Influx –> Sodium and calcium

Efflux –> Potassium ions

112
Q

What activates the AMPA receptor?

A

Glutamate

113
Q

What ions are moved through the channel activated by the AMPA receptor?

A

Influx –> Na+

Efflux –> Potassium

114
Q

Are NMDA and AMPA excitatory or inhibitory?

A

Excitatory

115
Q

Is GABA-A receptor excitatory or inhibitory?

A

Inhibitory

116
Q

What channels do GABA A receptors activate?

A

Chloride ion channels

117
Q

What types of receptors control depolarisation?

A

Sodium
Calcium
AMPA and NMDA

118
Q

What types of receptors control polarisation/hyperpolarisation?

A

Potassium

GABA-A

119
Q

What is the most common ion channel type at the presynaptic side?

A

Voltage gated

120
Q

What is the most common ion channel type at the post-synaptic side?

A

Ligand gated

121
Q

What happens to cortical neurons during seizure?

A

Abnormal, hypersynchronous discharge of a population of neurons

122
Q

What is Epilepsy?

A

Group of neurological disorders which exhibit recurrent seizures unprovoked by acute systemic or neurologic insult

123
Q

What happens during seizure initiation?

A

Sudden membrane depolarisation for a few seconds
Burst of action potentials
Abnormal and excessive synchronisation of neighbouring populations of cortical cells
Triggered by –> missed meds, drugs/alcohol, lack of sleep, hormones, stress, lights, noise

124
Q

What is the accompanied burst of action potentials in seizures known as?

A

Paroxysmal depolarising shift

125
Q

What happens during seizure propagation?

A

Partial seizure spreads within the brain

126
Q

What are the steps of seizure propagation?

A

Activation of nearby neurons (abnormally activated) –> prolonged action of excitatory transmitter
Loss of surrounding inhibition –> loss of brakes

127
Q

How can hyperexcitable states arise?

A

Too much excitation –> sustained overt depolarisation

Too little inhibition –> defects in hyperpolarisation –> low GABA etc

128
Q

What does repetitive discharge lead to?

A

Accumulation of Ca2+ in presynaptic terminals –> enhances neurotransmitter release
Depolarisation induced NMDA activation –> enhances neurotransmitter release
Increase in extracellular K+

129
Q

What kind of mutations have been identified in epilepsy?

A

Ion channel mutations of both:
Excitatory channels –> that switches it on
Inhibitory channels –> that switches it off

130
Q

What do many epileptic drugs target?

A

Voltage gated and ligand gated ion channels

131
Q

What is the paroxysmal depolarisation shift?

A

Prolonged depolarisation with rapid spikes in a synchronous way

132
Q

What is surround inhibition within neuronal activity?

A

The areas surrounding a central signal are inhibited to sharpen the contrast between the signal

133
Q

What does surround inhibition normally prevent?

A

Synchronisation of adjacent neurons

134
Q

What is the goals of treatment with anti-epileptic drugs?

A

Suppress existing seizures and also decrease probability of future seizures

135
Q

What are the three activation states of voltage-gated sodium channels?

A 
Resting state (closed)
Activated state (open)
Inactivated state (closed)
136
Q

Do phenytoin, carbamazepine and Lamotrigine all bind to the same spot on the voltage gated sodium channel?

A

No –> different areas

137
Q

What is the mechanism of Phenytoin and Carbamazepine and Lamotrigine?

A

Decreases rate of recovery of voltage-gated Na+
channels –> prevents rapid firing of neurons

Phenytoin –> does not affect GABA or Glu transmission

Lamotrigine –> impedes Glu release to prevent excitatory transmission

138
Q

When is Phenytoin indicated for use?

A

Most seizure types
NOT absence seizures
NOT good for temporal lobe epilepsy

139
Q

What is carbamazepine indicated for?

A

Used for most seizure types –> unlike phenytoin it is the drug of choice for temporal lobe epilepsy
NOT good for absence seizures

140
Q

When is Lamotrigine indicated for use?

A

Used for many seizure types INCLUDING absence seizures

141
Q

What is the function of Barbiturates like phenobarbitone?

A

Augments neuronal inhibition via GABA-A receptors:
Prolongs duration but not the frequency of GABA currents
Limits sustained repetitive firing at higher concentrations

142
Q

What is the mechanism behind barbiturates function?

A

They are channel modulators –> they act like a chemical “stent” to keep the channel open longer
They are NOT agonists
They just make the channel stay open longer when it does open they do not open the channel

143
Q

What other affects do Barbiturates have apart from their action on GABA channels?

A

Can inhibit voltage gated Ca2+ channels –> mediates decreased Glu release and thus decrease excitotoxicity neurotransmission
Can have some sedative activity –> tolerance develops rapidly

144
Q

What seizures are Barbiturates indicated?

A

Tonic-closure, partial seizures, absence seizures

145
Q

What do Benzodiazepines do?

A

Augment neuronal inhibition via GABA-A receptors –> they increase the frequency in which the Cl- ion channels are open (not the duration)
Drives influx of Cl- –> inhibits activity and stabilises membranes of target neurons

146
Q

Are Benzodiazepines agonists?

A

Yes

147
Q

What paediatric seizures are benzodiazepines indicated for?

A

Myoclonic and absence seizures

148
Q

What is an example of a Benzodiazepine?

A

Clobazam

149
Q

What does clonazepam get used for?

A

Standing treatment
Status epilepticus
Also inhibits T-type calcium channels which makes it useful for absence seizures

150
Q

What does gabapentin do?

A

Changes GABA release from neurons

Inhibits high voltage activated calcium channels –> less neurotransmitter release

151
Q

What seizures is gabapentin used for?

A

Partial seizures with or without secondary generalisations

–> often in conjunction with other drugs

152
Q

What neurons does ethosuximide target?

A

Thalamic neurons only

153
Q

What is the affect of ethosuximide?

A

Blocks low-threshold Ca2+ channels
Reduces current –> prevent electrical activity spread (hallmark of absence seizures)
No affect on inactivation state, recovery time or voltage dependence of currents
No affect on GABA, Glu or repetitive firing

154
Q

What seizures are ethosuximide (thalamic calcium channel blocker used for)?

A

Absence seizures

Cant be used for other seizures –> can trigger tonic-clonic seizures

155
Q

What is valproate indicated for?

A

All types of seizures including absence seizures

NOT used for temporal lobe epilepsy

156
Q

How many mechanisms does Valproate have?

A

3

157
Q

What are the 3 mechanisms of Valproate?

A
  1. Prolongs recovery rate of Na+ channels –> similar to phenytoin and carbamazepine
  2. Inhibits T type Ca2+ channels –> in thalamic neurons to treat absence seizures
  3. Augments GABA production and impedes metabolic breakdown which changes resting potentials –> reduces chance of AP
158
Q

What is topiramate indicated for?

A

Partial and generalised tonic-clonic seizures

159
Q

What is the mechanism of topiramate?

A

Blocks voltage gated Na+ channels
Activates K+ hyperpolarising currents
Enhances post-synaptic GABA-A activity
Limits activation of AMPA and glutamate receptors

160
Q

What is the issue of anti-convulsant and pregnancy?

A

They are associated with birth defects

161
Q

What is the term for a drug that disturbs development of an embryo/foetus?

A

Teratogenic

162
Q

How has incidence and types of defects been monitored for anti-convulsant association?

A

Voluntary registries to track

163
Q

What is the malformation rate during pregnancy with use of anticonvulsants?

A

6% on average

But no good data on actual risk

164
Q

What are some types of birth defects associated with anticonvulsants?

A

Spina bifida
Cleft palate
Congenital heart defects
Microcephaly

165
Q

What is a seizure?

A

A seizure is a sudden, uncontrolled electrical disturbance in the brain. –> usually of abnormal and excessive synchronisation of a population of cortical neurons

166
Q

What is the mechanism behind seizures?

A

An increase in excitation or a decrease in inhibition –> affects of ion channel disturbances leads to the synchronisation of groups of neurons with large depolarisations happening at once.

167
Q

What are some common causes of seizures?

A 
Abnormal levels of glucose
Abnormal electrolytes (Na+, K+ and Ca2+)
Traumatic brain injury
Stroke
TIA
Fever
Drug abuse 
Epilepsy 
High blood pressure 
Intracranial mass
168
Q

What is epilepsy?

A

Epilepsyis a chronic disorder that causes unprovoked, recurrent seizures.

169
Q

How does epilepsy differ from seizure?

A

Epilepsy is the increased chance for chronic or reoccurring cases of seizure

Seizure can be termed when it is a chance occurrence and not an ongoing predisposition

170
Q

What are the two main seizure types?

A
  1. Focal /partial seizures

2. Generalised seizures

171
Q

What are focal seizures?

A

Focal seizures are seizures which originate in one area or side of the brain.

172
Q

What are generalised seizures?

A

Wide spread seizure activity in the left and right hemispheres of the brain

173
Q

What are the two main types of focal seizure?

A

Focal seizure with retained awareness (simple partial seizure)
Focal seizure with loss of awareness (complex partial seizure)

174
Q

What are the different types of generalised seizures that may occur?

A 
Absence seizures
Tonic-clonic
Atonic seizures 
Clonic seizures 
Tonic seizures 
Myoclonic seizures
175
Q

What might a focal seizure look like?

A

Frontal lobe –> motor –> kicking, pedaling, twitching, head or eyes turn
Occipital –> lights, colours, visual change, eyelid fluttering
Parietal lobe –> numb, odd sensation in affected area, struggle reading, writing
Temporal lobe –> auditory halucinations/changes, odd taste/smell
Etc –> normally one sided affects as starts on one side of the brain

176
Q

What are some features of an absence seizure?

A

Lapses of awareness –> staring for a few seconds
Person is unaware during the seizure normally
Immediate recover after the seizure

177
Q

What does tonic/clonic refer to?

A 
Tonic = normal muscle tone
Clinic = rhythmical jerking
178
Q

What happens during myoclonic seizures?

A

Quick uncontrolled muscle jerks

179
Q

How can an EEG change in response to a seizure?

A

There will be a large increase in activity
Focal –> in focal seizures only a few leads will be impacted
Generalised –> lots more leads will show an affect

180
Q

What can be some psychosocial impacts of seizure disorders?

A

People may be scared, treat you differently
Impacts ability to drive
Requires sustained treatments

181
Q

What are some other space occupying intracranial lesions other than tumours?

A

Cysts
Parasites
Haematoma
Inflammatory

182
Q

Common causes of headache?

A 
Stress
Lack of sleep
Fatigue
Hunger
Withdrawal (caffeine etc)
Alcohol 
Some food and drink
183
Q

What is myasthenia gravis?

A

Disorder of neuromuscular junction –> Ach receptor issue –> leads to muscle weakness

184
Q

What is the difference between benign vs malignant?

A

Benign –> does not invade surrounding tissue

Malignant –> invades surrounding tissue

185
Q

What is a primary brain mass?

A

Tumours from cells in the brain

186
Q

How common is primary masses in the brain?

A

1.2% of all new cancers

187
Q

What is a secondary mass?

A

Tumours from the cells from outside the brain

188
Q

How common are secondary masses in the brain?

A

10 times more common than primary brain masses

189
Q

What can be some of the effects of tumours on the brain?

A

Local brain invasion
Compression
Raised intracranial pressure

190
Q

How are brain metastasis diagnosed?

A 
Symptoms of cancer
Evidence of cancer elsewhere 
Focal neurological deficits
CT
MRI brain
Biopsy --> hard to get biopsy --> not needed normally
191
Q

How do paediatric brain masses differ to adult brain masses?

A

Paediatric –> primary are second most common cancer –> leading cause of death (20% of childhood malignancies)
Adults –> most in cerebral cortex –> Gliomas, meningiomas, pituitary tumours

192
Q

What are some risk factors for brain tumours?

A 
Majority are sporadic but:
Ionising radiation
Hereditary syndromes:
Neurofibromatosis 
Von Hippel Lindau
Tuberous sclerosis
193
Q

How common are benign vs malignant brain masses in adults?

A

2/3 benign, 1/3 malignant

194
Q

What is the most common benign tumours in adults?

A

Meningiomas

195
Q

What cancers is radiation primary treatment?

A

Prostate, head and neck, cervix, lung, oesophagus, skin bladder, brain, lymphoma

196
Q

Can radiation be used palliatively?

A

Yes

197
Q

What are the sources of radiation for therapy?

A

External beam –> linear accelerator, non invasive –> targeted to area
Brachytherapy –> radioactive source (eg Iridium 192) placed next to point of interest

198
Q

What kind of radiation is used for therapy?

A

X rays

199
Q

Why is the multiple treatments normally for radiation therapy?

A

Total dose needed to maximise chance of cure –> if does in one go there ill be bad side effects
Normal tissue gets to recover
Make sure the treatment targets cancer cells in the right cell cycle phase

200
Q

What is the standard dose unit for radiation therapy?

A

Gray (Gy)

1 Gy is Joule absorption per Kg

201
Q

How does radiation therapy cause cancer cell death?

A

DNA damage and induced cell apoptosis/death

202
Q

Where do the side affects of radiation occur?

A

Locally to the treatment site

203
Q

What does adjuvant mean?

A

Radiation is an addon treatment

204
Q

What is palliative treatment?

A

Helps with pain and other symptoms on a short term

205
Q

What are some side affects of radiation therapy?

A 
fatigue (tiredness)
dry, red or itchy skin.
loss of appetite.
nausea (feeling sick)
digestive problems.
hair loss.
dry or sore throat or mouth.
cough or shortness of breath.

JMP Y2S1 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions