Brainscape's Knowledge GenomeTM

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


See full index

Semester 3: Mind and Movement > Last Minute Shit I dont know > Flashcards

Last Minute Shit I dont know Flashcards

1
Q

Which protein initiates expression of primitive steak?

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

Which protein initiates expression of primitive node??

A
  • HNF-3B
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain how laterality of the primitive streak occurs

A
  • Serotonin upregulates FGF in left side of streak
  • Serotonin is inhibited in right side of steak by MAO
  • FGF and LEFTY-2 upregulated PITX2 which establishes left sidedness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes ventralising of mesoderm?

A
  • BMP4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes dorsalising of mesoderm?

A
  • Antagonism of BMP4

- By expression of Brachyury (T) gene

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

Outline molecular regulation of invagination

A
  • FGF downregulates E-cadherin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline molecular regulation of neurulation

A
  • FGF upregulates chordin and noggin

- Which inhibits BMP

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

Outline molecular regulation of neural crest cells

A
  • Intermediate levels of BMP
  • Upregulates PAX3, SNAIL, FOXD3 which causes neural crest specification
  • SLUG promotes neural crest migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outline molecular regulation of ventrolateral patterning of nervous system

A
  • Dorsal region: Ectoderm secretes BMP4 which expresses TGF proteins which activates PAX3 and PAX7
  • Ventral region: Notochord secretes SHH which activates NKX2.2 and NKX6.1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline anteroposterior patterning of nervous system

A
  • Hindbrain: Retinoic acid shifts HOX gene expression anteriorly causing cranial rhombomeres to differentiate into caudal types
  • Forebrain/Midbrain: Anterior neural ridge and rhombencephalic isthmus induce LIM1 (prechordal plate) and OTX2 (neural plate) which resulting in expression of FOXG1 (forebrain) and engrailed genes (midbrain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain how the threshold for activation of nociceptors is lowered

A
  • Injured C fibres liberate substance P
  • Substance P binds to mast cells and causes histamine release
  • Histamine receptors develop on nerve terminals
  • Histamine binds to histamine receptors and causes release of arachidonic acid
  • The enzyme COX converts arachidonic acid to prostaglandins
  • Prostaglandin causes sensitisation of nociceptors
  • Manifested as allodynia and hyperalgesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline the lateral pain pathway

A
  • Spinothalamic pathway
  • First order neurons from dorsal root ganglion to laminae 1,2 and 4
  • Second order neurons from spinal lamina decussate and pass in anterior and lateral fasciculus, which converge as spinal lemniscus, and terminate on VPN
  • Third order neurons from VPN to relevant part of somatosensory cortex in postcentral gyrus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline the medial pain pathway

A
  • Spinoreticulothalamic pathway
  • First order neurons from dorsal root ganglion to laminae 5-7
  • Second order neurons from spinal lamina terminate on intralaminar nucleus of thalamus
  • Third order neurons from intralaminar nucleus of thalamus to anterior cingulate gyrus
  • Which is responsible for affective component of pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the axon reflex

A
  • Noxious stimulus is transduced
  • Axons send impulses in antidromic direction to nociceptive nerve endings
  • Which releases substance P which binds to mast cells and causes release of histamine
  • Which causes vasodilation (flare) and oedema (wheal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline supraspinal nociception

A
  • Raphespinal tract descends from magnus raphe nucleus
  • It terminates on posterior tract of lissauer and terminates on inhibitory internuncials resulting in synaptic inhibition
  • MRN is stimulated by periaqueductal grey, which is disinhibited during pain by beta-endorphins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline wind-up phenomenon

A
  • Sustained activation of neurones in spinothalamic and spinoreticular tracts by glutamate activating NMDA receptors.
  • Repetitive activation of NMDA glutamate receptors
  • Gene transcription resulting in additional NMDA receptors on dendrites
  • Non-serotonergic neurons acting on magnus raphe nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Outline process of X-rays

A
  • X-ray beams are collimated to appropriate areas
  • X-ray beams are attenuated to different degrees by different tissues
  • Bone attenuates X-ray beams most, it is exposed to few rays so remains white
  • Air attenuates X-ray beams least, it is exposed to most rays so appears black
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Outline process of MRI

A
  • Protons in water act as magnet
  • Patient placed in magnetic field which aligns magnets
  • Radio waves are passed through patient which deflect and emit small radio waves
  • Which produce a signal which is passed to a computer to create an image
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outline process of withdrawal syndrome

A
  • Super activation of adenylyl cyclase
  • Increase in cAMP and protein kinase A
  • Causing phosphorylation of neurotransmitter transporters, which increases neurotransmitter release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Outline the process of drug tolerance

A
  • Activation of intracellular kinases e.g. mitogen-activated protein kinase
  • Which phosphorylates and desensitises opioid receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Identify 3 drugs that effect pupillary diameter and their mechanism of action

A
  • Phenylephrine: Mydriasis due to a1 agonism
  • Tropicamide: Mydriasis due to M3 antagonism
  • Pilocarpine: Miosis due to M3 agonism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Identify 3 refractive errors, and the type of lens used to correct each

A
  • Hyperopia, farsightedness due to too short an eyeball, corrected using convex lenses which converge light rays
  • Myopia, shortsightedness due to too long an eyeball, corrected using concave lenses which diverge light rays
  • Astigmatism, curvature of cornea is different in two different planes so light rays do not come to a focal point, corrected using both a spherical (converges light rays to a focal point) and cylindrical lens (converges light to a focal line)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is strabismus, what is its cause and how is it treated?

A
  • Misalignment of the two eyes in one or more co-ordinates
  • Caused by an abnormal set of the fusion mechanism, one eye focuses satisfactorily while the other does not
  • Vision therapy, including eye exercises, or surgert
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is amblyopia and how is it treated?

A
  • Reduction in visual acuity cause which can lead to blindness
  • Caused by failure of the two overlapping images from each eye to be sent to the brain, resulting in the visual image being suppressed in one eye
  • Patching the non-amblyopic eye with an eye patch, vision therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Outline the 9 layers of the retina and the cell type associated with each

A
  • Pigmented layer: Vitamin A and melatonin
  • Layers of rods and cones
  • Outer nuclear layer: cell body of rods and cones
  • Outer plexiform layer: horizontal cells
  • Inner nuclear layer: bipolar cells
  • Inner plexiform layer: amacrine cells
  • Ganglionic layer
  • Layer of optic nerve fibres
  • Inner limiting membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline the process of phototransduction

A
  • Light focuses on retina
  • Conformational change in 11-cis retinal to all-trans retinal, causing it to move away from opsin, which activates rhodopsin
  • Activated rhodopsin activates transducin which activates cGMP phosphodiesterase
  • Which degrades cGMP, resulting in closure of cationic channels in rod cell membrane
  • Causing hyperpolarisation of cell, which results in glutamate release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the difference between felt stigma and enacted stigma?

A
  • Felt stigma: change in self-identify categorised by shame, guilt and withdrawal
  • Enacted stigma results from societal reactions and may be caused by direct mistreatment (direct enacted) or by rules, systems or procedures (indirect enacted)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is perception? Identify two types of processing

A
  • Knowledge based and partly learned
  • Inferential so we receive the whole person not half
  • Categorical meaning we categorise what we mean
  • Relational meaning size depends on context
  • Adaptive meaning significant things are perceived better than insignificant
  • Bottom up processing: comparing features of a stimuli with sets of features existing in the brain
  • Top-down processing: people see what they expect to see
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Identify which layers of the LGN receive signals from the temporal side of the retina and which receive signals from the nasal side

A
  • Temporal: 2, 3 and 5

- Nasal: 1, 4 and 6

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

Identify which layers of the LGN receive signals are called magnocellular layers (and why) and which layers are called parvocellular (and why)

A
  • Magnocellular: 1 and 2, large Y cells which are rapidly conducting and conduct black and white
  • Parvocellular: 3, 4, 5 and 6 medium sized X cells which transmit colour and accurate spatial information
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe how different regions of the basilar membrane differ in response to different frequency of sound

A
  • Near round window, basilar fibres are short and stiff and vibrate better at high frequency
  • Near helicotrema, basilar fibres are long and loose and vibrate better at low frequency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe Webber’s test including the tuning fork used, the procedure and the results

A
  • 512 Hz tuning fork is placed on centre of forehead
  • Ask the patient if they can hear it, and if it sounds the same on both sides
  • Conductive hearing loss: Sound hear loudest in affected side
  • Sensorineural hearing loss: Sound heart loudest in unaffected side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe Rinne’s test including the tuning fork used, the procedure and the results

A
  • 512 Hz tuning fork is placed on mastoid process
  • Ask the patient if they can hear it and ask them to tell you when they no longer hear it
  • When they no longer hear it place the tuning fork near the ear
  • Conductive hearing loss: Bone conduction is greater than air conduction (cannot hear tuning fork over ear) Rinne’s negative
  • Sensorineural hearing loss: Air conduction is greater than bone conduction, Rinne’s positive, this is a normal finding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the pathways from the two cochlear nuclei. What is the role of the superior olivary nucleus?

A
  • Dorsal cochlear nuclei: Via dorsal acoustic stria to contralateral lateral lemniscus which terminates in contralateral inferior colliculus
  • Ventral cochlear nuclei: Via trapezoid body to superior olivary nucleus, and from here via ipsilateral and contralateral lemniscus to contralateral inferior colliculus
  • Superior olivary nucleus detects which direction sound is coming from by comparing intensities (lateral SON) and time lag (medial SON)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe the structure of the static labyrinth, what it detects and what its function is

A
  • Composed of utricle and saccule and their maculae
  • Maculae are horizontal in utricle and vertical and saccule
  • Macula composed of supporting cell invested by hair cells which invest into a gelatinous matrix which contains otoconia
  • Movement of otoconia causes hair cells to bend in direction of kinocilium with opening of cation channels allowing influx of potassium-rich endolymph
  • Threshold is exceeded and an action potential is generated in the vestibular nerve
  • Detects linear acceleration in horizontal and vertical planes
  • Activates extensor antigravity muscles via the lateral vestibulospinal tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the structure of the kinetic labyrinth, what it detects and what its function is

A
  • Composed of three semicircular canals and their cristae
  • Cristae composed of supporting cells invested by hair cells which invest into a gelatinous matrix called the cupula
  • Movement of the head pushes the cupula against the stationary endolymph
  • This causes hair cells to bend in direction of kinocilium with opening of cation channels allowing influx of potassium-rich endolymph
  • Threshold is exceeded and an action potential is generated in the vestibular nerve
  • Detects angular acceleration of the head
  • Activates the vestibulo-ocular reflex, activation of the ipsilateral oculomotor and contralateral abducens nuclei
  • To cause eye movements that are equal and opposite the movement of the head to keep the gazed fixed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the symptoms of BPPV, how it is diagnosed and how it is treated

A
  • Vertigo lasting seconds to minutes which is precipitated by head movement
  • Diagnosed using Hallpike manoeuvre
  • Treated using Epley manoeuvre
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the symptoms of Meniere’s disease, how it is diagnosed and how it is treated

A
  • Vertigo last minutes to hours
  • Classically associated with low frequency sensorineural hearing loss, feeling of fullness in affected ear, loss of balance, tinnitus and vomiting
  • Treated using a low-salt diet, betahistine, cinnarizine (H1 agonist, an antiemetic drug) and chemical labyrinthectomy using gentamicin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the process of language development including developmental milestones

A
  • Children discriminate sounds that correspond to phonemes (the sound produced by each letter)
  • At 1 children begin to speak
  • At 1-2 children speak about people, animals and body parts
  • At 1.5-2.5 they begin acquiring phrases and using sentences
  • Critical period for language development is between 4 and 12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Outline Piaget’s theory of cognitive development

A
  • Sensorimotor, 0-2, trial and error, experimentation
  • Preoperational, 2-7, imagination and memory
  • Concrete operational, 7-12, logical thought
  • Formal operation, 12-18, abstract thought
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe the innervation of the hypoglossal and facial nerves and the lesions associated with them

A
  • Hypoglossal nerve is contralaterally innervated resulting in deviation of tongue to affected side (unilateral lesion) or global wasting (bilateral lesion)
  • Upper part of facial nerve is bilaterally innervated and lower part is contralaterally innervated. Unilateral upper motor neuron lesion causes sparing of muscles above eyes, but lower motor neuron does not (Bell’s palsy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Outline the pathology of ischaemic stroke and reperfusion injury

A
  • Reduced blood flow results in anaerobic respiration
  • Which causes results in acidosis due to accumulation of lactate
  • Failure of energy-dependent pumps results in calcium influx via glutamate channels resulting in activation of destructive enzymes and destruction of organelles
  • When blood flow returns there is activation of oxygen-free radical systems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Outline the pathology of a TIA, and three clinical features of a TIA in the anterior and posterior circulation

A
  • Ischaemia without infarction
  • Anterior: Amaurosis fugax, hemiparesis, aphasia
  • Posterior: Diplopia, vertigo, vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Outline the pathology, investigations, clinical features and treatment of a cerebral infarction

A
  • Typically caused by infarction in internal capsule
  • MRI shows ischaemic penumbra around site of lesion
  • Features include contralateral hemiparesis, and aphasia lasting over 24 hours or to death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Identify four signs of a brainstem infarction

A
  • Lateral medullary syndrome (Wallenberg’s syndrome) presenting with acute vertigo and cerebellar signs
  • Coma
  • Locked in syndrome
  • Pseudobulbar palsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is lacunar infarction?

A
  • Symptomless infarction associated with hypertension

- Small infarcts seen on MRI

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

What is hypertensive encephalopathy?

A
  • Cerebral oedema causing headaches, nausea and vomiting

- MRI shows oedematous white matter

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

What is Anton’s syndrome?

A
  • Caused by visual cortex infarction due to posterior cerebral artery infarction
  • Person is blind but is unaware of this
49
Q

What is Weber’s syndrome?

A
  • Ipsilateral oculomotor nerve palsy due to unilateral infarct
  • With contralateral hemiplegia and paralysis of upward gaze
50
Q

What is a watershed infarction?

A
  • Infarction of areas around the regions supplied by anterior, middle and posterior cerebral artery
  • With visual loss, memory loss and intellectual impairment
51
Q

What are the neurological deficits associated with an ischaemic stroke affecting the left middle cerebral artery?

A
  • Right sided weakness involving face and arm then leg
52
Q

What are the neurological deficits associated with an ischaemic stroke affecting the right middle cerebral artery?

A
  • Left sided weakness involving face and arm then leg
53
Q

What are the neurological deficits associated with an ischaemic stroke affecting the posterior cerebral artery?

A
  • Homonymous hemianopia

- Homonymous quadrantanopia in upper quadrant (temporal lobe lesion) or lower quadrant (parietal lobe lesion)

54
Q

What are the neurological deficits associated with an ischaemic stroke affecting the carotid artery dissection?

A
  • Ipsilateral Horner’s syndrome due to compression of sympathetic plexus
55
Q

Outline the pathology, investigations, clinical features and treatment of an intracerebral haemorrhage? Which genotype is associated with tendency to re-bleed

A
  • Caused by rupture of deep penetrating vessels (Charcot-Bouchard aneurysm) at basal ganglia, pons or cerebellum
  • Resulting in severe headache
  • Apolipoprotein E
56
Q

Outline the pathology, investigations, clinical features and treatment of a cerebellar haemorrhage?

A
  • Aneurysm in one of cerebral arteries
  • Causing skew deviation / gaze deviation
  • Stupor coma
  • Nystagmus
57
Q

Outline the clinical picture of an extradural haematoma? What is the usual cause?

A
  • Unconsciousness followed by stupor

- With ipsilateral dilated pupil and contralateral hemiparesis

58
Q

Outline the clinical picture of a cortical venous thrombosis

A
  • Headache, epilepsy, fever
59
Q

Outline the clinical picture of a dural venous sinus thrombosis

A
  • Ocular pain, proptosis, chemosis
60
Q

Outline working memory theory

A
  • Retrieval of items from long term memory for a task at hand, includes:
  • Central executive: cognitive tasks
  • Phonological loop: auditory information
  • Visuospatial sketchpad: visual and spatial information
  • Episodic buffer: Linking information between domains and chronological ordering
61
Q

What is the role of VMAT? Name a drug that blocks VMAT

A
  • Vesicular monoamine transporter
  • Transports free cytoplasmic NA, 5-HT and DA into vesicles for subsequent release
  • Reserpine
62
Q

Identify 5 drugs that are used to treat MS and their MoA

A
  • Beta interferon: prevents T-cell activation, proliferation and transport
  • Glatiramer acetate: competitive inhibitor of MHC-2, similar structure to MBP
  • Oral fingolimod: Sphingosine-1-phosphate receptor modulator that prevents T-cells from leaving lymph nodes
  • Natalizumab: Alpha-4-integrin adhesion molecule, prevents T-cells entering CNS
  • Alemtuzumab: Anti CD52 molecule responsible for lymphocyte depletion
63
Q

Outline the interaction between serotonin and noradrenaline

A
  • NA acting on alpha-1 receptors on 5-HT neurons increases 5-HT release
  • Blockage of alpha-2 autoreceptors on NA neurons increases NA release
64
Q

Identify two SSRIs, their mechanism of action, side effects and dose

A
  • Fluoxetine, sertraline
  • Inhibitor of SERT transporter
  • Nausea, anorexia, insomnia, anorgasmia
  • 50 mg daily
65
Q

Identify two TCAs, their mechanism of action, and side effects

A
  • Nortriptyline, clomipramine
  • Inhibitor of NET, SERT and DAT
  • Dry mouth, dry eyes, blurred vision, constipation and urinary retention, hypotension, QT prolongation, sedation
66
Q

Identify an SNRI, its mechanism of action, side effects and dose

A
  • Venlafaxine
  • Inhibitor of NET and SERT
  • Nausea, hypertension
  • 75 mg daily
67
Q

Identify the mechanism of action of mirtazapine

A
  • Blocks alpha-2 autoreceptors enhancing NA and 5-HT release
  • Blocks 5-HT2C receptors preventing 5-HT reuptake
68
Q

Identify the mechanism of action of trazodone

A
  • Blocks 5-HT2A and 5-HT2C receptors

- Preventing 5-HT reuptake

69
Q

Identify the mechanism of action of mainserin and a side effect

A
  • Blocks 5-HT2A preventing 5-HT reuptake
  • Blocks alpha-2 autoreceptors enhancing NA and 5-HT release
  • Also blocks H1 and alpha-1 receptors
  • Causes bone marrow depression
70
Q

Identify two non-selective monoamine oxidase inhibitors, their mechanism of action and side effects

A
  • Phenelzine and tranylcypromine
  • Irreversibly inhibit MAO-A and MOA-B resulting in increased levels of 5-HT, NA
  • Cheese reaction, due to less inactivation of tyramine and other endogenous amines resulting in hypertension
71
Q

Identify a monoamine oxidase A inhibitor, its mechanism of action and side effects

A
  • Moclobemide
  • Reversibly inhibits MOA-B resulting in increased levels of 5-HT, NA
  • Fewer side effects
72
Q

Outline the role of chronic stress in depression

A
  • Increased stress results in increased CRF release from hippocampus, ACTH release from pituitary and increased cortisol release from adrenal glands
  • Increased sympathetic tone for flight or flight response, with increase MAO and decrease BDNF
  • Decreased BDNF causes reduced neurogenesis and a reduced hippocampal volume
  • Which maintains abnormal release of CRF from hippocampus resulting in a vicious cycle
73
Q

Outline the NICE guidelines for depression

A
  • Mild to moderate depression: CBT or psychotherapy
  • Severe depression: Stepwise treatment
  • 1: SSRI (fluoxetine)
  • 2: SNRI (venlafaxine) or MRA (mirtazapine)
  • 3: Antipsychotic (quetiapine) or lithium
  • 4: TCA (nortriptyline)
  • 5: MAO-I (phenelzine)
74
Q

How is each of these neurotransmitters removed from the synaptic cleft?

NA, 5-HT, DA, Glutamate, GABA, ACh

A
  • NA, 5-HT, and DA by uptake into pre-synaptic membrane by NET and SERT and DAT
  • Glutamate uptake into presynaptic membrane and astrocytes by excitatory amino acid transporters (EAAT)
  • GABA uptake into presynaptic membrane and astrocytes GABA transporters
  • ACh: Acetylcholinesterase (membrane bound) butyrylcholinesterase (free in plasma)
75
Q

What are the different types of receptor for each of the following neurotransmitters?

NA, 5-HT, DA, Glutamate, GABA, ACh

A
  • NA: Alpha-1 and alpha-2 both of which are G-protein coupled
  • 5-HT: 5-HT1-7, all of which are G-protein coupled aside from 5-HT3
  • DA: All G-protein coupled D1 (D1,D5) which are excitatory via activation of adenylyl cyclase, D2 (D3,D4,D5) which are inhibitory via inhibition of adenylyl cyclase
  • Glutamate: Ionotropic: AMPA, kainate (fast postsynaptic), NMDA (slow postsynaptic), metabotropic : mGlu1 (postsynaptic excitatory) mGlu2-3 (presynaptic excitatory)
  • GABA: GABAA (ligand gated, inhibitory) GABAB (G-protein coupled, inhibitory)
  • AChRs: Nicotinic (G-protein coupled) muscarinic (ligand-gated M1,M3,M5 are excitatory activating inositol phosphate, M2,M4 are inhibitory inhibiting adenylyl cyclase)
76
Q

What are the actions of each of the following neurotransmitters

NA, 5-HT, DA, Glutamate, GABA

A
  • NA: Motor control conditioning fear, analgesia, sedation, blood pressure control, antidepressant effects
  • 5-HT: Hallucinations, sleep, wakefulness and mood, feeding behaviour and pain
  • DA: Motor control (nigrostriatal) endocrine control (tuberohypophyseal), behavioural effects (mesolimbic and mesocortical)
  • ACh: Arousal (from nucleus basalis to cortex), memory (septohippocampal pathway), motor control (cholinergic interneurons)
77
Q

Why are 5-HT2a receptor antagonists important in the control of extrapyramidal side effects of antipsychotics?

A
  • 5-HT2a receptors cause inhibition of dopaminergic nigrostriatal neurons
  • Antagonism of these receptors enhances dopamine release into dorsal striatum
  • So blocks unwanted motor affects of D2 blockage
78
Q

Identify an adverse effect of an antipsychotic that means that white cell count should be monitored. Which drug is this associated with and what percentage of patients experience this side effect?

A
  • Agranulocytosis
  • Leukopenia
  • Clozapine in 1-2% of patients
79
Q

Explain the importance of muscarinic antagonism of antipsychotics

A
  • Dopamine causes inhibition of cholinergic neurons by binding to D2 receptors in dorsal striatum
  • D2 antagonism causes disinhibition of cholinergic neurons resulting in extra-pyramidal motor effects

Dopamine binds to D2 receptors to inhibit choline

  • Block of
80
Q

What type of receptors are CB1 receptors? Where are they receptors located on what is their effect?

A
  • G-protein coupled
  • Presynaptic nerve terminals
  • Opening of inward rectifying potassium channels and closure of voltage gated calcium channel causing hyperpolarisation
81
Q

What are endocannabinoids? Identify two of them and identify two properties

A
  • Endogenous ligands for CB receptors
  • Anandamide and 2-AG
  • Analgesic and anxiolytic properties
82
Q

What is depolarisation induced suppression of inhibition? (DSI)

A
  • Activation of CB receptors in hippocampal pyramidal cells suppresses GABA mediated inhibition
83
Q

Identify a drug that blocks DSI and what it is used for

A
  • Rimonabant
  • A CB1 antagonist
  • Used to treat obesity, drug and alcohol dependence
84
Q

Antipsychotic drugs block H1 receptors producing..

A
  • Sedation
  • Drowsiness
  • Weight gain
85
Q

Antipsychotic drugs block muscarinic receptors producing..

A
  • Blurred vision
  • Increased intraocular pressure
  • Dry mouth
  • Dry eyes
  • Urinary retention
  • Constipation
86
Q

Antipsychotic drugs block alpha adrenoreceptors producing..

A
  • Transient hypotension
87
Q

Antipsychotic drugs block 5-HT receptors producing..

A
  • Weight gain

- Increased risk of cardiovascular disease

88
Q

Which anti-psychotic produces jaundice?

A
  • Chlorpromazine
89
Q

Identify a fatal adverse effect of antipsychotics

A
  • Antipsychotic malignant syndrome

- Muscle rigidity and hyperthermia

90
Q

Identify the pathology, clinical features and treatment of Huntington’s

A
  • Trinucleotide repeats of CAG
  • Resulting in more than 40 glutamine residues on huntingtin protein
  • Reduction in glutamic acid decarboxylase resulting in reduced GABA
  • Producing hyperactivity of dopaminergic synapses
  • Chorea (flicking movements of distal limbs)
  • Treated with GABA agonists (baclofen), dopamine antagonists (chlorpromazine) and tetrabenazine
91
Q

What are athetosis, hemiballismus and chorea? What causes them?

A
  • Athetosis: writhing of arms face and neck, globus pallidus, levodopa
  • Ballismus, flailing of entire limb, subthalamic nucleus
  • Chorea: flicking movements, putamen
92
Q

What is apraxic gait and what causes it?

A
  • Small shuffling steps (marche a petit pas)

- Caused by frontal lobe damage e.g. hydrocephalus

93
Q

What is hemiplegic gait and what causes it?

A
  • Flexed upper limb, extended lower limb, circumduction of leg
  • Unilateral UMN lesion
94
Q

What is diplegic gait and what cause it?

A
  • Patient walks stiffly on the toes and has problems turning

- Bilateral UMN lesion causing bilateral spasticity

95
Q

What is neuropathic gait and what causes it?

A
  • High stepping, slaps foot down

- Common fibular nerve palsy

96
Q

What is ataxic gait and what causes it?

A
  • Broad based gait, side-swinging, poor tandem gait

- Cerebellar lesion

97
Q

What is myopathic gait and what causes it?

A
  • Pelvis bent forward and walk with waddle

- Muscle or hip disease

98
Q

Outline the three effects of anaesthetics on ion channels

A
  • Both intravenous and inhalation anaesthetics are GABA agonists (intravenous bind to beta subunit, inhalation bind to alpha and beta subunit)
  • Inhalation anaesthetics bind to TREK and TASK subunits of potassium channels and cause hyperpolarisation
  • Xenon inhibits NMDA receptors by competing with glycine for its regulatory site
99
Q

Discuss propofol

A
  • Intravenous anaesthetic used to induce (and maintain due to continuous infusion) replaced thiopental
  • Rapid initiation and metabolism so good for day time surgeries (little nausea)
  • Caused respiratory and cardiovascular depression, painful injection
  • Dose = 1.5 - 2.5 mg/ Kg
100
Q

Discuss isoflurane

A
  • Inhalation anaesthetic used to maintain anaesthesia
  • High blood:gas partition so slow onset and recovery (produces hangover effect)
  • Produces coronary steal
  • Dose: 1-2.5%
101
Q

Discuss atracurium

A
  • Non-depolarising neuromuscular blocking drug
  • Competitive inhibitor of ACh for nAChR
  • Onset between 2-3 minutes, recovery in less than 30
  • Stable at acidic pH, unstable at alkaline pH (respiratory alkalosis due to hyperventilation)
  • Spontaneous hydrolysis in plasma
  • Produces hypotension (histamine release from mast cells)
  • Dose: 300-600 mg / Kg increased by 100-200 mg / Kg as needed
102
Q

Discuss suxamethonium

A
  • Depolarising neuromuscular blocking drug
  • Onset 2-3 minutes lasting 10 minutes
  • Slower hydrolysis by AChE so desensitises nAChR
  • Action longer if deficiency of plasma cholinesterase (dibucaine number to test) anticholinesterase drugs or liver disease
  • Can cause bradycardia, hyperkaleamia, post-op muscle pain (related to fasciculation) and malignant hyperthermia (mutation of ryanodine receptor)
  • Dose is 1-1.5 mg / Kg
103
Q

Discuss neostigmine

A
  • Reverse effects of atracurium
  • Anticholinesterase so increases likelihood that ACh will bin to nAChR
  • Also used to treat myasthenia gravis
  • Side effects include mydriasis, bronchoconstriction, bradycardia (all treated with atropine, a muscarinic antagonist) and increased salivary secretions (treated with glycopyrrolate, a muscarinic antagonist)
  • Dose is 2.5 mg
104
Q

What are the different responses in eye opening and what scores are attributed to them?

A
  • Nil: 1
  • Response to pain: 2
  • Response to speech: 3
  • Spontaneous: 4
105
Q

What are the different motor responses and what scores are attributed to them?

A
  • Nil: 1
  • Extensor plantar response: 2
  • Abnormal flexion: 3
  • Withdraws: 4
  • Localises: 5
  • Obeys: 6
106
Q

What are the different verbal responses and what scores are attributed to them?

A
  • Nil: 1
  • Sounds: 2
  • Words: 3
  • Conversation: 4
  • Oriented: 5
107
Q

Difference between partial and generalised seizure? Types of each? Treatment of seizures (mechanism)

A
  • Generalised: General e.g. absence, grand mal, myotonic, hypertonic, atonic
  • Partial: Focal e.g. simple partial, complex partial, partial with secondary generalisation
  • Antiepileptics: GABA inhibition (benzodiazepines) Na+ blockage hyperpolarisation (carbamazepine ,valproate), Ca2+ blockage reduced transmitter release (lamotrigine)
108
Q

What is carried by the posterior spinocerebellar tract? Where does this tract terminate?

A
  • Unconscious proprioception from lower limbs

- Ipsilateral inferior cerebellar cortex

109
Q

What is carried by the rostral spinocerebellar tract? Where does this tract terminate?

A
  • Unconscious proprioception from upper limbs

- Ipsilateral inferior cerebellar cortex

110
Q

What is carried by the anterior spinocerebellar tract? Where does this tract terminate?

A
  • State of play around the internuncial neurons of the spinal cord (lower limbs)
  • Ipsilateral superior cerebellar cortex (fibres decussate once)
111
Q

What is carried by the rostral spinocerebellar tract? Where does this tract terminate?

A
  • State of play around the internuncial neurons of the spinal cord (upper limbs)
  • Ipsilateral superior cerebellar cortex
112
Q

Where is the ‘What?’ Pathway located and what is it concerned with?

A
  • Medially in association area
  • Colour medially
  • Faces in the middle region
  • Form laterally
113
Q

Where is the ‘Where?’ Pathway located and what is it concerned with?

A
  • Laterally in association area

- Movement in contralateral visual hemifield

114
Q

Which gyrus is associated with alexia and agraphia?

A
  • Left angular gyrus
115
Q

Which gyri are Broca’s and Wernicke’s area located?

A
  • Broca: Inferior frontal gyrus

- Wernicke’s: Superior temporal gyrus

116
Q

Outline the part of the basal ganglia involved in control of gaze

A
  • Pathway from striatum to superior colliculus via pars reticulata
117
Q

What is the fornix?

A
  • Pathway from hippocampus to neocortex
118
Q

What are the mamillary bodies and the mamillothalamic tract?

A
  • Contained within posterior surface of hypothalamus

- Mamillothalamic tract connects mamillary bodies to thalamus

119
Q

Outline PARK loci and protein coded

A
  • PARK-1: Alpha Synuclein (Lewy bodies)
  • PARK-2: Parkin (early onset)
  • PARL-6: Pink01 (mitochondrial function)
  • PARK-8: LRRK (sporadic PD)

Semester 3: Mind and Movement (21 decks)

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