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Year 2 Session 2 > 3301 - Clin Neuro > Flashcards

3301 - Clin Neuro Flashcards

1
Q

What is dementia

A

Umbrella term for a disease that affect memory, thinking and reasoning - a deterioration in cognitive function.

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2
Q

Cognitive changes in dementia (8)

A

Memory loss, confusion, disorientation and difficulties with communicating, visual and spatial abilities, reasoning/problem-solving, complex tasks, planning/organising, coordination/motor functions.

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3
Q

Psychological changes in dementia (5)

A

Personality changes, depression, anxiety, agitation and hallucination

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4
Q

Types of dementia (10)

A

Alzheimers, Lewy-body disease, alcohol-related (Korsakoff’s), genetic (Huntington’s), vascular, fronto-temporal (Pick’s), Parkinson’s, younger-onset, infections (AIDS), Creutzfeldt-Jakob

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5
Q

Korsakoff’s disease cause

A

Thiamine (vit B1) deficiency from alcohol

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6
Q

Pick’s disease cause

A

Buildup of tau protein accumulate as Pick’s bodies

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7
Q

Lewy body dementia cause

A

Unknown. Changes in sleep, behaviour, movement and cognitive ability

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8
Q

Creutzfeldt-Jakob cause

A

Prion protein - contracted by consumption of infected tissue

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9
Q

Laws of dementia (2)

A
  1. Law of Disturbed Encoding - new memories not formed (no short > long)
  2. Law of Rollback - memory loss starts with most recent
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10
Q

What causes the reduction in brain mass in Alzheimers disease

A

A loss of communication between neurons causes them to die and brain shrinks

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11
Q

Causes of Alzheimers disease

A

Amyloid plaques, Neurofibrillary tangles, inflammation, degeneration of cholinergic neurons

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12
Q

What are amyloid plaques

A

Aggregates of amyloid beta generated by cleavage of amyloid beta precursor protein by β- and γ-secretase.

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13
Q

Stages of amyloid beta

A

small aggregates (oligomers - most toxic 42aa) > large aggregates (protofibrils) > fibrils > plaques

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14
Q

Effect of amyloid plaques

A

plaques on nerve endings stop messages getting out of neuron

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15
Q

What are neurofibrillary tangles

A

Hyperphosphorylated tau becomes paired-helical-filament (PHF) tau which form neurofibrillary tangles (NFTs)

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16
Q

Alternative splicing of gene MAPT produces

A

6 soluble isoforms of tau protein

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17
Q

Function of tau

A

stabilises microtubules in axons

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18
Q

Cholinergic hypothesis (AD)

A

loss of cholinergic (ACh) neurotransmission contributes to deterioration of cognitive function

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19
Q

How does inflammation contribute to AD

A

Amyloid beta may cause prolonged activation of microglia leading to neuron damage/death.

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20
Q

Familial Alzheimers mutations. % of cases?

A

APP, presenilin (PS1, PS2). 3% cases

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21
Q

Sporadic Alzheimers causes. % cases?

A

Risk factors (diabetes, female, age), life style, hormones, mutation in apolipoprotein E (APOE) (E4> 50%)

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22
Q

Down syndrome link to AD

A

Down syndrome patients have 3 copies of chromosome 21, 3 APP genes > amyloid-beta overproduction

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23
Q

Drugs for AD causes (3)

A

Cholinesterase inhibitors (mild/medium): Donepezil, Rivastigmine, Galantamine
NMDA receptor antagonist (moderate/severe): Memantine
Monoclonal antibody (severe) - Aducanumab

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24
Q

Drugs for AD symptoms (4)

A

antidepressants: specific serotonin reuptake inhibitors (citalopram, sertraline)

antipsychotics
typical antipsychotics (haloperidol)
atypical antipsychotics (risperidone)

mood stabilisers:
anticonvulsants (carbemazepine)

Aromatherapy with essential oils
melissa officinalis (lemon balm)
lavendula officinalis (lavender)

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25
Q

Function of (acetyl)cholinesterase

A

Acetylcholine (ACh) > acetate + choline

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26
Q

function of Acetyl-CoA Synthetase

A

Converts acetate to acetyl CoA

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27
Q

acetyl CoA + choline >

A

acetylcholine

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28
Q

Which cholinesterase inhibitor can be applied through transdermal patches

A

Rivastigmine

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29
Q

Side effects of cholinesterase inhibitors (6)

A

nausea, vomiting, diarrhoea, slow heartbeat, lack of appetite, weight loss

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30
Q

What is a combination drug for AD

A

Namzaric

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31
Q

Role of NMDA receptors in AD

A

Amyloid beta oligmers (and glutamate) stimulate NMDA receptors. NMDA receptors cause Ca influx, AMPA receptors move to membrane causing Na influx. Excess glutamate from drugs etc + Aβ > excess Ca > cell rupture and death

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32
Q

what is Remacemide

A

NMDA antagonist for epilepsy

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33
Q

what is Riluzole

A

NMDA antagonist for ASL

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34
Q

What is produced when APP gene is cleaved by a) a-secretase b) b-/y- secretase

A

a) soluble APP
b) amyloid beta protein

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35
Q

BACE 1 inhibitor MOA (+fun fact)

A

Target β- mainly and y- secretases to prevent amyloid-beta fragements forming (failed clinical trials)

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36
Q

Aducanumab is used to

A

Help clearance of amyloid beta oligomers

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37
Q

What is Ginkgo Biloba + SE?

A

Extract from Chinese plant has anti-inflammatory and anti-oxidant properties. Helps with memory and functions. SE: bleeding

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38
Q

What is Curcumin

A

Yellow pigment in turmeric. anti-oxidant, anti-inflammatory, cholesterol lowering, reducing amyloid accumulating

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39
Q

Biomarkers (tests) for ante-mortem AD diagnosis (6)

A

Brain scans (MRI, CT, PET- FDG, PiB), CSF, blood, genetic, ocular biomarkers, and cognitive tests. Blood and ocular not yet in clinical use.

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40
Q

What does a FDG-F18 PET show (fluorodeoxyglucose)

A

Shows active parts of the brain that use glucose

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41
Q

What does a PiB-PET show (Pittsburg compound)

A

PiB binds to amyloid-beta plaques to quantify levels in brain

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42
Q

Defining and staging AD uses

A

A (+/-) amyloid beta plaques
T (+/-) tau - neurofibrillary tangles
N (+/-) neurodegeneration

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43
Q

How does CSF biomarker work?

A

CSF is taken with a needle from lumbar region. In AD CSF is higher in tau and lower in amyloid beta

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44
Q

Why are blood tests not useful to diagnose AD?

A

Molecules of interest are in brain, low concentrations in systematic circulation

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45
Q

How can AD associated inflammation be detected?

A

Using a PET scan. C11 PBR28 binds to translocator protein (TSPO) on outer mitochondrial membrane of microglia. When microglia detect amyloid beta they release IL-3.

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46
Q

Cognitive test for dementia

A

Mini mental status examination (MMSE) and Alzheimer’s Disease Assessment Scale-Cognitive (ADAS-Cog). Other tests for memory, attention, language, movement, mood

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47
Q

Limitation of cognitive tests for dementia

A

Doesn’t account for low education

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48
Q

What are ocular biomarkers? What tests are used?

A

Retina allows for viewing of nerves and blood vessels. AD can lead to a loss of retinal ganglion and macular ganglion cell complex. Viewing is done with OCT, ERG and VEP. Curcumin binds to amyloid beta aiding in imaging. Hyperspectral imaging can discriminate b/n high and low Aβ load on cerebral PET scanning.

49
Q

Can neurofibrillary tangles be extracellular?

A

No

50
Q

What can PET scans be used for?

A

To asses structural changes, metabolic differences, brain activity, correlates with progression and informs about inflammation processes

51
Q

Does memantine inhibit generation of amyloid from glial cells with anti-inflammatory function

A

No

52
Q

Which chromosome have genes a)PS1, b)PS2 and c)APP?

A

a) 14, b) 1, c) 21

53
Q

Define: a) seizures b) epilepsy c) epileptogenesis

A

a) abnormal electrical signals in brain. b) a disorder of the brain state that supports seizures. c) process of which a normal brain is altered to allow seizures.

54
Q

Seizure types (3)

A

Focal, generalised, unknown

55
Q

Epilepsy syndrome types (3)

A

Onset in neonates/infants (<2yr), onset in childhood (<17), any age onset (>18)

56
Q

Categories of epilepsy syndrome in neonates

A

Self-limited epilepsy, developmental and epileptic encephalopathies, and aetiology-specific

57
Q

Which category of epilepsy is Dravet Syndrome

A

Developmental and epileptic encephalopathies in neonates/infants

58
Q

categories of epilepsy in childhood onset

A

self-limited focal epilepsies, generalised epilepsies and developmental/epileptic encephalopathies

59
Q

Categories of epilepsy in any age onset

A

focal, generalised, combined focal and generalised

60
Q

Methods to diagnose epilepsy (4)

A

Medical history, physical examination, EEG, neuro-imaging (MRI, CT)

61
Q

Physical and neurological indicators of epilepsy

A

Lateral tongue biting, dysmorphic features (indicate genetic pre-disposition e.g. downs), poor memory, behaviour and QOL

62
Q

Treatments for epilepsy (4)

A

Anti-seizure drugs, surgery, neurostimulation (vagus n and deep brain - ant nucleus of thalamus), diet (keto - high fat, low protein, low carb / atkins)

63
Q

anti-seizure drugs MOA

A

blockage of Na/Ca/NMDA (glutamate) channels, restore GABA A activity

64
Q

Aetiology of epilepsy (6)

A

Genetic
Acquired - structural, metabolic, infections, immune
Unknown

65
Q

What channel is affected in Dravets Syndrome

A

Na channels

66
Q

Which GABA receptor is affected in epilepsy, explain

A

GABA A receptor has impaired function, loss of inhibitory signals leads to seizures

67
Q

Epigenetics changes that can cause epilepsy (5)

A

DNA methylation, histone modification, chromatin remodelling, histone-DNA cross talk and non coding RNAs

68
Q

Three phases of epileptogenesis

A

Trigger, latent phase, seizures

69
Q

mTOR pathway and epilepsy

A

mTOR pathway responds to glutamate transmission to regulate neuronal structure, synapses, expression of ion channels and receptors. Mutations in parts of the mTOR pathway lead to epilepsy

70
Q

What are the two GABAergic neurons affected in epilepsy

A

In hippocampus: Somatostatin +ve interneurons (SOM)
In cortex: parvalbumin +ve, fast spiking interneurons (PV)

71
Q

What is status epilepticus

A

one seizure longer than 5min or more than 1 in 5 min w/o returning to normal consciousness in b/n. EMERGENCY!

72
Q

Genetic cause of Dravets syndrome

A

mutation in SCN1A gene which encodes for alpha subunit of Na channel, Nav1.1. This reduces Na influx in inhibitory interneurons

73
Q

What is glaucoma and cause

A

A group of diseases of the optic nerve usually caused by high intraocular pressure, otherwise caused by poor blood supply to optic nerve or structural issues with optic nerve.

74
Q

Open angle glaucoma vs closed angle

A

Open angle is caused by fluid passing too slowly through trabecular meshwork, closed angle is obstruction of meshwork. Closed angle is fast onset and has many symptoms - redness, headache, halo, blurred vision.
Open angle is usually asymptomatic until severe.
Both have dilated pupil (mydriasis)

75
Q

Treatment for closed-angle glaucoma

A

eyedrops, oral acetazolamide and laser

76
Q

What are cataracts

A

Clouding of the lens caused by clumping of proteins

77
Q

Three main types of cataracts

A

nuclear (occur in centre of lens), cortical (periphery of lens and move towards centre) and sub-capsular (beneath or w/n capsule of lens)

78
Q

What is the difference between wet and dry macular degeneration

A

Dry: clumping of yellow drusen in retinal pigment epithelium (RPE) beneath photoreceptors. RPE cells may then die causing loss of function of the photoreceptors.
Wet/neovascular degeneration: new blood vessels grow under retina. Leaking and scarring from these vessels can damage photoreceptors.
> Leads to blurring of central vision and distortion of vision.
Dry has no treatment, wet is treated with intravitreal injections

79
Q

Proliferative vs non-proliferative diabetic retinopathy. Pain?

A

Non-proliferative: Diabetes > poor glucose control > microaneurysms (swelling of vessel), retinal haemorrhages (leak blood), hard exudates (leak lipids) > spots/floaters and swelling/oedema > decreased vision.
Microvascular occlusion > ischaemia > retinal necrosis (cotton wool spots). Proliferative: ischaemia > VEGF > abnormal blood vessel growth > scarring > retinal detachment and glaucoma. No pain

80
Q

What is retinitis pigmentosa

A

A group of genetic eye diseases that lead to damaged photoreceptors

81
Q

What is a pterygium? Cause? Pain?

A

A non-cancerous growth of the conjunctiva. Cause is unknown but people working outdoors are more likely to develop. Painless.

82
Q

Order of cells from vitreous humour to choroid plexus

A

ganglion cells, bipolar cells, photoreceptors (rods/cones), RPE (all in retina), choroid plexus

83
Q

Where is the highest concentration of photoreceptors

A

The fovea

84
Q

blood supply to eye - dual

A

internal carotid > ophthalmic > central retinal artery (retina) and ciliary arteries (choroid). Other parts of eye (cornea, photoreceptors..) supplied by diffusion

85
Q

Extraocular muscles of eye (7)

A

Rectus (4) sup, inf, lat, med. Oblique (2) sup/inf. Levator palpebrae superioris

86
Q

CN supply of extraocular eye muscles

A

3,4,6
CNIII: SR, IR, MR, IO, levator
CNIV: SO
CNVI: LR

87
Q

what is visual acuity. What does 6/12 mean?

A

a measure of the eye to distinguish shapes at a certain distance. 6/12: normal person can read at 6m, pt read at 12m - cannot drive

88
Q

Pupil size can be affected by (3)

A

Para/symp nerve pathology, horners syndrome (symp lesion - pupil constricts + ptosis), CN 3 palsy (para lesion - pupil dilated)

89
Q

what does swinging torch test do

A

Tests for afferent pupillary defect - pupil not constricting with light shining in it

90
Q

Mydriatic vs miotic pupil

A

dilated pupil vs constricted pupil

91
Q

what is light-near dissociation? Cause?

A

Pupil does not constrict with light but does accomodate for near-sight (referred to as Argyll Robertson pupil) caused by neurosyphilis

92
Q

Red reflex variants and causes

A

A darkened red reflex indicates obstruction preventing light from reflecting e.g cataracts. White reflex indicates cataract, retinoblastoma or retinal detachment

93
Q

Anterior and posterior lesions respect which meridian? why?

A

Optic nerve axons before chiasm are organised into horizontal hemifields - anterior lesion respects horizontal meridian. Axons cross over in chiasm so posterior lesions respect vertical meridian and are bilateral

94
Q

Types of refractive error (4)

A

Myopia (short sighted) - eyeball too long - corrected w concave lens
Hyperopia (long sighted) - eyeball too short - corrected w convex lens
Astigmatism (blurry) - irregular curved cornea - rays focus at different points
Presbyopia (loss of accomodation) - inflexible lens with age

95
Q

Risk factors for cataracts

A

age, ocular trauma, ocular inflammation, steroids, systemic disease

95
Q

Risk factors for macular degeneration

A

Smoking, age, poor diet

96
Q

what systematic diseases can have ocular manifestations?

A

Diabetes, hypertension, thyroid disease, CN palsies, inflammatory disease (vasculitis, autoimmune)

97
Q

What happens in hypertensive retinopathy

A

High blood pressure initially causes arteriovenous nicking and arteriosclerosis followed by retinal haemorrhages, cotton wool spots and hard exudates, followed by optic nerve swelling

98
Q

Signs and symptoms of thyroid eye disease

A

lid swelling, bulging eyes (proptosis), exposure of eye can cause ulceration of cornea and irritation, eye swelling - can cause optic n compression and vision loss

99
Q

Thyroid eye disease is mainly associated with what hyperthyroidism disease

A

Graves disease

100
Q

Cranial nerve palsies - 3,4,6. Pain?

A

Affect movement of eye as CN3, 4 and 6 control extraocular muscles. Caused by aneurysms or tumours, sometimes diabetes or hypertension. Painful

101
Q

What is iritis / uveitis

A

Inflammation inside the eye. Associated with autoimmune/inflammatory conditions (arthritis, Crohns, lupus)

102
Q

Signs and symptoms of iritis/uveitis

A

Pain, blurred vision, keratic
precipitates, hypopyon (WBC accumulation), redness

103
Q

Treatment of iritis/uveitis

A

steroids

104
Q

What is giant cell arteritis/temporal arteritis. Signs/symptoms

A

Inflammation of arteries typically ext carotid branches but also aorta and vertebral arteries causes bad headaches, jaw pain, polymyalgia, anaemia, weight loss and transient vision loss

105
Q

Treatment for giant cell arteritis

A

Steroids (IV administration), temporal artery biopsy for prescense of inflammatory cells

106
Q

What are two blood biomarkers for inflammation

A

C-reactive protein (CRP) and Erythrocyte sedimentation rate (ESR)

107
Q

Non-ocular causes of eye disorders (5)

A

Vitamin deficiencies: A-night vision, B-optic nerve
Drugs e.g corticosteroids > cataract, gluacoma
Emboli: from carotid plaques or calcification in heart
Tumours - often in choroid, melanoma in eye
Systemic infections - TB, HIV, syphilis

108
Q

How is conjunctivitis and corneal ulcers treated with

A

antibiotics, antivirals, antifungals

109
Q

How is glaucoma treated

A

intra-ocular pressure lowering drops: beta blockers, alpha agonists, carbonic anhydrase inhibitors (slow production of aqueous humour) and prostaglandins (help outflow)

110
Q

What drugs dilate pupil and why

A

Atropine and mydriatic drops to examine back of eye

111
Q

Treatment of proliferative diabetic retinopathy and wet macular degeneration

A

Anti-VEGF (-mab) injections to stop new vessel formation

112
Q

Future research areas for eye disorders (5)

A

genetics (RPE65 gene), neuroprotection, stem cell regeneration, implants - restore accomodation, bionic eyes

113
Q

What is the connection b/n AD and epilepsy

A

AD is associated caused by a buildup of tau. Tau binds to a post-synaptic complex that allows for excitotoxic signalling > seizures

114
Q

What is excitotoxic signalling

A

Neuronal damage that results from excessive levels of neurotransmitters and results in toxic receptor down stream signalling.

115
Q

What does P38-ɣ do?

A

Phosphorylates tau dissociating it from the complex and therefore blocking its excitotoxic effect. Can be used as gene therapy.

116
Q

What do vigabatrin and sodium valproate do

A

maintain high GABA at synaptic cleft

117
Q

In Dravets syndrome seizures are worsened by __ channel ___, such as carbamazepine, lamotrigine,
oxcarbazepine, and phenytoin

A

Na channel blockers

118
Q
A

Year 2 Session 2 (4 decks)

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