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Year 2 - Control > Control - Clinical > Flashcards

Control - Clinical Flashcards

1
Q

what is consciousness vs wakefulness

A

c - awareness, alertness, appropriate responses (thinking feeling etc)

w - activity of reticular activating substance from the brainstem associated with connections between cells and areas of the cerebral cortex

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2
Q

what is coma and how it is measured

A

eyes not open, no command response, no voluntary movement
not secondary use to paralytic agents

measured using Glasgow coma scale (GCS) - come = lower than 8

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3
Q

what is locked in syndrome

A

aware awake and breathe
cannot move or speak
damage to ventral pons
can blink, feel pain, autonomic system still works

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4
Q

what is vegetative state vs persistent VS

A

no evidence of awareness of self or environment
no language
no voluntary moves or expression

PVS - after 30 days not response
50% chance improve
reflex autonomic and sponanteous behaviours yes but not awareness of self or environment

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5
Q

what causes a vegetative state

A

destruction of cortex and hemispheres but intact ascending reticular activating substance

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6
Q

what is minimal conscious state

A

severely altered consciousness

reproducible but inconsistent

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7
Q

how do you measure level of disorders of consciousness

A

SMART - sensory modality assessment and rehabilitation technique

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8
Q

what is brain stem death and how do you test for it

A

no breathe or conscious, destroy brainstem, no electrical activity

absent brain stem reflexes - persistent apnoea - requires 2 assessments on two occasions

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9
Q

what are the three types of anaesthesia

A

general - total loss
regional - region or part of body
local - topical, infiltration

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10
Q

what are the three A’s of anaesthesia

A

amnesia - unconsciousness
analgesia - pain relief
akinesia - paralysis

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11
Q

what is balanced anaesthesia and what is the triad of balanced anaethsisa

A

smaller doses of a combination of drugs - max benefit and final toxic

unconsciousness , analgesia, muscle relaxation

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12
Q

what does the process of anaesthesia involve

A

induction, maintenance and reversal of process

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13
Q

describe how you would induce loss of consciousness

and common agents

A

IV - modulate transmitters gated ion channels acting on PNS/cerebral cortex/ RAS, basal ganglia, cerebellum, motor pathways

thiopentone, ketamine, etomiidate, propofol

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14
Q

how do we maintain loss of consciousness in aneasthtsia

A

vapour - NO, soflurane, desflurane
uses minimum alveolar consciousness - minimum amount of vapour to prevent reaction to standard surgical stimuli in 50% subjects

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15
Q

what are the problems with being under general anaesthesia for too long

A

hangover effects, stored in fat cells and releases slowly

amnesia, hypnosis, vasodilation, organ perfusion and hepatotoxicity

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16
Q

what type of agents are used for analgesia in anaesthetic

A

opioids - short or long acting

fentanyl, morphine, paracetamol

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17
Q

how do you reverse muscle relaxation in anaesthesia

A

reversal with neostigmine and glycopyrrolate

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18
Q

what is the clinical diagnosis of stroke

A

sudden onset
focal neurological deficit
of presumed vascular origin
symps last more than 24 hours or leading to death
if symps last less than 24 hours classed as TIA

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19
Q

what are the two types of strokes and how common are they

A

ischemic (85%) and haemorrhage (15%)

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20
Q

what are the causes and risks of ischamic stroke

A

thrombosis of large extra cranial arteries
small arteries intracranially
embolism (in the heart or vital arteries)
(most common is large vessel atherosclerosis)

risks - hypertension, obesity, diet, cardiac, diabetes

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21
Q

what are the best treatments for secondary stroke prevention

A

aspirin, warfarin - anticoagulants and decrease risk of clotting
carotid endarterectomy
drugs to lower BP such as aspirin and clopidogrel

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22
Q

what does FAST mean in stroke

A

face
arms
speech
time

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23
Q

what is the pathophysiology of stroke

A

initial reduction in cerebral blood flow - alteration sin cellar chemistry caused by ischemia and cellular necrosis

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24
Q

what are the thresholds of cerebral ischamia

A

normal is 50 ml/100g/min which can be above 20 ml

10-20 is electrical malfunctions

7.5-10 - release K and water out intracellularly

0-7.5 - cell death

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25
Q

describe the ischeamic penumbra

A

zone of reversible ischaemia around core or irreversible infarction
overtime from 1 to 30 min the ischamia increase in the penumbra
after a couple jours the ischamia reaches the oligemia where blood flow is reduced but no damage

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26
Q

what is sentrievers used for

A

halt stroke in time

stent across occlusion to reperfuse the brain

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27
Q

what is the definition of TIA

A

neurological defect lasting less than 24 ours attributable to cerebral or retinal ischamiea - may or may not have brain damage

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28
Q

what are the causes of TIA

A

vascular risk factors - arterial disease - cardiac embolism

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29
Q

what types of diseases does TIA mimic

A 
siezures 
syncope 
hypoglycaemia 
migraine
acute confusion states
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30
Q

what are the signs of TIA

A

dysphasia
transit blindness in one eye
ataxia, diplopia, vertigo

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31
Q

what is the scoring system for TIA

A

ABCD2
age blood pressure clinical features
duration of symptoms
diabetes

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32
Q

what is the treatment of TIA

A

polypill - statin, aspirin, folic acid

carotid endarectomy
targeting unstable plaque
occluded carotid artery

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33
Q

what are the three layers of the skin

A

epidermis (top) - stratified squamous, produces keratin - no blood vessels

dermis - fibrous and adipose - blood vessels nerve supply and sensory receptors

subcutis - boots - large blood vessels and supporting fat

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34
Q

ho would you describe the epithelium of the epidermis

A

keratinised stratified squamous epithelium

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35
Q

what are the 5 layers of thick skin

A 
basal layer - stratum basale 
prickle cell layer - stratum spinosum 
granular layer - stratum granulosum 
stratum lucidum (only in skin of sole) 
keratin layer (stratum corneum)
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36
Q

what is the stratum lucidum

A

several layers of flattened dead cells

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37
Q

how do keratinocytes change as they move to the top of the skin

A

get more mature as they move up and lose nucleus and become flatter

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38
Q

what are three types of cells found in the epidermis

A

keratinocytes
melanocytes
langerhans cells

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39
Q

what is the function of langerhans cell is n the epidermis

A

APC’s of the skin
migrate to dermis then lymphatics
irregularly lobulated nuclei

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40
Q

what are the “extras” of the skin and what is their role

A

sebaceous gland - secrete sebum into hair follicle and surface of skin
hair follicle
eccrine glands - thermoregulation - sweat production
apocrine glands
erector pilli muscle - smooth muscle - contract when cold for thermoregulation

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41
Q

what are the skin differences between the scalp and the foot

A

foot = no hair, glabourous, dermis thicker, epidermis thicker,

scalp - lots of hair, thin epidermis, no basket weaved keratin

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42
Q

what are the 4 skin receptors

A

meissners corpuscles - fast adapting discriminatory touch and vibration

merkel - slow adapting discrimantory touch and pressure

pacinian - encapsulated boddie sin deep skin - fast adapting rapid vibration (deepest)

ruffini ending

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43
Q

which layers of skin do you find the sensory receptors merkel cells and meissners corpuscle

A

merkel cells - intra epidermal receptors of the basal layer

meissners corpuscle - superficial dermis

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44
Q

what are the three degrees of burn

A

1st - no damage to dermis, superficial burn affecting epidermis
no sensory receptors in epidermis so feel pain

2nd - damage to dermis and epidermis - pain

3rd - full thickness burn - damage to epidermis dermis and subcutaneous tissue - does not hurt as all receptors burnt away

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45
Q

what are the kinds of sensations we feel from the outside vs internal

A

outside - touch

inside - temperature and pain

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46
Q

what are the 4 main classes of somatosensory receptors

A

tactile (innocuous) sensations - low threshold mechanoreceptors - merkel, ruffini, meissner, pacinian

proprioception - muscle spindle and joint golgi tendon

thermal sensations - thermorecerptors localised to decree zones

nociceptive - mechanical, thermal and polymodal nociceptors

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47
Q

what are the specific locations of the sensory receptors of the skin

A

meissners and merkel beneath dermis Meissners between dermal papillae
merkel aligned with pupillage
pacinian located in subcutaneous tissue
ruffians located deep in there dermis

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48
Q

what is the morphology of the 4 skin receptors

A

meissners - looping axonal terminals that intertwine supporting cells

merkels - dome structure atop axon terminals

pacinain corpuscle - sensory axon surrounded ny fluid (onion)

ruffini - nerve terminals intertwined with collagen fibrils

noicceptors - free nerve endings penetrate epithelial cells

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49
Q

what is the adaption vs receptive field size of the 4 skins receptors

A

fast adapting - mesissners and pacinian

slow adapting - ruffini / merkels

small receptive field - messiness and merkels

large receptive field ruffians and pacianin

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50
Q

which sensory receptors are used in braille

A

merkel afferents

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51
Q

describe the 2 point discrimination in different areas of sensitivity

A

sensitivity is correlated with density of the sensory innervation
areas of high sensitivity - fingertips and face can distinguish between two points very small apart

areas of low - toros and limbs - can’t discriminate two stimuli close

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52
Q

which family of receptors are responsible for thermal

A

TRP family

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53
Q

what is capsaicin and what receptors does it affect

A

chemical in the vanilloids cause burning sensation in mouth

act on thermal VR1 receptors also activated by heat

54
Q

what are the two receptors involved in proprioception

A

the scull spindle - sensory feedback from muscle fibres on body poison and movement

golgi tendon - regulate muscle tension or force of contraction and prevent muscle eoverlaod

55
Q

describe the 4 groups of sensory axons from the skin

A

Aa - largest diameter - proprioceptors of the skin - low threshold mechanoreceptors - rapid conducting

Ab - mechanoreceptors

Ad - pain / temperature - slow conducting

C - temperature, pain, itch

56
Q

what is the relationship between axon diameter and speed of conduction

A

larger the diameter than quicker the conduction

57
Q

which virus affects dermatomes

A

herpes zoster - chicken pox - primary sensory neurons - inflammation and blistering of skin of affected dorsal root

58
Q

what is the main role of the two ascending spinal pathways

A

dorsal column - innocuous sensitivity (not harmful)

spinothalamaic - noxious and thermal sensitivity

59
Q

where is crossing of the ascending spinal tracts

A

doral column crosses midline in medulla

spinothalamic crosses midline in the spinal cord

60
Q

what is the difference in axon fibres in the ascending pathways

A

dorsal column = Aa/b/d

spinothalamic = Ad/c

61
Q

what is agnosia

A

inability to recognise objects despite normal sensory functioning

62
Q

where is the sensory integration area

A

posterior parietal cortex

63
Q

what is astereoagnosia

A

inability to identify objects on basis of touch alone

damage to posterior parietal cortex

64
Q

what is neglect syndrome

A

parietal cortical lesion - part of visual world in ignored

most common to the right hemisphere

65
Q

describe the schematic representation of somatosensory processing

A

mechanorerptors - spinal cord - dorsal column in medulla - ventrobasal complex in thalamus - posterior parietal and post central gyrus - limbic system/motor system/ association pathways

66
Q

what is brown sequared syndrome

A

hemicord lesion - inflammation of the spinal cord = myelitis

67
Q

what is wallenburgs syndrome

A

stroke by occlusion of posterior inferior cerebellar artery

68
Q

what are the red flags of a headache

A

cognitive effects, seizes, fever, visual disturbance, vomiting and weight loss

69
Q

what is raised intracranial pressure due to

A 
mass effect 
brain swelling 
increased  venous pressure 
hydrocephalus 
increased CSF
70
Q

what are the symptoms of raised intracranial pressure

A

headache - worse when lying, vomiting, seizures, papilloedema

71
Q

what is the acute treatment for increased intracranial pressure

A

broad spectrum IV antibiotics such as cefotaxmie

steroids (dexamethasone)

72
Q

what is temporal arteritis and treatment

A

inflammation of temporal arteries
transient loss of vision and tenet temporal artery
high dose steroids - prednisolone

73
Q

how does a migraine occur

A

unilateral headache
cortical spreading depression caused by sleeping deprivation, hunger stress and oestrogen - releases chemically active irritants

74
Q

what medications are used for migraine

A

naproxen
triptans
paracetamol

75
Q

what are trigeminal autonomic cephalgia

A

activation of trigeminal - parasympathetic systems

causes short lasting headaches with unilateral pain

76
Q

what are the types of headaches associated with trigeminal autonomic cephalgia

A

cluster headache
paroxysmal hemicranial
SUNCT

77
Q

what is the management of trigeminal autonomic cephalgia

A

pain relief - sumatriptan and high flow oxygen

prevention - prednisolone, verapamil

78
Q

what is a tension headache and its management

A

constricting high band
relaxation and massage
acupunture

79
Q

what arse the causes of new daily persistent headache

A

raised ICP
Low ICP
chronic meningitic
post head injury

80
Q

what is the definition of chronic daily headache and the causes

A

headache lasting more than 4 hours more than 15 days a most

de novo via new daily persistent headache
previous episodic headache

81
Q

what are the categories of epilepsy

A

generalised or focal

82
Q

what is the difference between generalised or focal epilepsy

A

g - whole brain affected with tonic clonic seizure

f - begin in certain part of the brain

83
Q

what are some causes of symptomatic epilepsy

A

birth injury, infection, trauma, cavernoma

84
Q

what disease shows grey matter around the ventricles and is a congenital malformation

A

perivenricualr nodular dysplasia

85
Q

what is a cavernoma

A

blood vessel abnormality - raspberry look, risk of bleeding and seizure

86
Q

what are the differential diagnosis of seizure

A

syncope
psychiatric illness
hypoglycaemia
cataplexy or sudden raised ICP

87
Q

when taking history of epilepsy who do you need to question

A

witness of the event mainly

88
Q

what is the difference between vasovagal and cardiac syncope

A

v - cause = illness or injury, rapid recovery prodrome of warmth light headedness and visual impairment - treat by recognise prodrome and lie down or raise legs

c - older people, vascular risk factors - pacemaker treatment

89
Q

what is the cause of dissociative seizures

A

psychiatric cause - brain reacts by shutting down

90
Q

who is affected most by dissociative seizures and what is the treatment

A

young females

psychological support

91
Q

what is used to treat patient after first generalised tonic-clonic convulsion

A

anti-epileptic drugs (AED)

92
Q

what is the treatment after first seizure

A

none

93
Q

what are some counselling topics when you have epilepsy

A 
management 
prevention 
occupational issues 
bathing
driving 
leisure
94
Q

what is the most common generalised type of epilepsy and what is it caused by

A

juvenile myoclonic epilepsy caused by sleep deprivation and stress

95
Q

give an example of effective AED’s in juvenile myoclonic epilepsy

A

levetiracetam

96
Q

what are the difference in side effects of lamotrigine vs topiramate/zonisamide

A

l - mood stabiliser

T/Z - makes moods worse

97
Q

15 year old boy has vacant attacks over 3 months with memory loss and auditory hauulicinations - what is the likely cause

A

medial temporal lobe epilepsy

98
Q

what is the most common focal epilepsy

A

medial temporal lobe epilepsy

99
Q

which AED;s are used for medial temporal lobe epilepsy

A

lamotrigine and carbamazepine

100
Q

what is the MRI difference in medial temporal lobe epilepsy vs frontal lobe epilepsy

A

temporal - high signal and atrophy in left hippocampus

frontal - small area high signal in frontal lobe

101
Q

what symptoms are frontal lobe epilepsy associated with

A

tonic-clonic movements and psychiatric presentation

102
Q

what is lennox gas taut syndrome and its treatment

A

1-7 y/o
nocturnal, atonic, myoclonic
slow wave ecg
t - sodium valproate, ketogenic diet (hunger = seizure control), vagus nerve stimulator

103
Q

what are the top 3 neurological conditions

A

headache stroke epilepsy

104
Q

what is the definition of epilepsy

A

abnormally excessive and hypersynchronous activity of neurones located predominantly in the cerebral cortex

105
Q

what is secondary generalised seizures

A

partial seizure that later spreads to involve majority of 2 cerebral cortexes

106
Q

what is status epilepticus

A

brain is in constant state of seizure - long lasting seizures

107
Q

what are the two types of partial seizure

A

simple - when consciousness not impaired

complex - impairment of awareness and responsiveness

108
Q

describe the montreal procedure

A

local anaesthetic during surgery - removal brain tissue after cortical stimulation

109
Q

what is the neuronal mechanism of generalised seizures

A

thalamocortical circuitry attack and synchronised firing of neurones brain wide - bilateral symmetry

110
Q

what is the main diagnostic tool in epilepsy

A

EEG

electroencephalogram

111
Q

what are causes of seizures

A

hypoxia, infection, trauma, tumour, congenital abnormalities

112
Q

what is the type of inheritance pattern of epilepsy

A

polygenic (not mendelian inheritance)

113
Q

what are the usual tumours of the CNS in males vs females

A

male s- glioma

f - meningioma

114
Q

what is the histological criteria for malignancy in brain tumours

A

mitotic activity
necrosis - secrete TNF to kill cells
vascular proliferation

115
Q

what are microscopical features of astrocytic tumours

A

fine fibrillary and microcystic background
inc cellular density
pleomorphism

116
Q

what is the difference between diffuse astrocytoma 2 and anapaestic astrocytoma 3

A

2 - fibrillary, low cellular density, mild atypia, no mitotic activity

3 - mitosis, moderate cellular density + pleomorphism

117
Q

what are the 3 features of glioblastoma 4

A

high cellular density and mots is

necrosis and vascular proliferation

118
Q

what are the features of pilocytic astrocytoma 1

A

children in cerebellum
pliocyetes
rosenthal fibres

119
Q

what disease would you see round uniform nucelar cytoplasm and fried egg apparence with calcification of astrocytes

A

oligodendroglioma

120
Q

what are three types of glioma

A

astrocytoma
oligodendroglioma
ependyoma

121
Q

what are the features of ependyoma

A

well define tumour of ventricles

pseudo-rosettes

122
Q

what would be present in a meningioma and who is affected more

A

women

whorls and psammoma bodies

123
Q

what is PNET 4 (medulloblastoma) and who does it affect

A

children - high cellular density

rosette formation

124
Q

what are three types of nerve sheath tumours

A

spindle cell tumour
shwannoma 1
neurofibroma 1

125
Q

what are the presentation, signs and symptoms of intracranial tumours

A

raised ICP
epilepsy
headaches (morning)
blurred vision

126
Q

give three examples of intracranial tumour markers

A

aFP, Bhcg, PSA

127
Q

what are some investigations into intracranial tumours

A

fMRI
MRS
cerebral angiography

128
Q

what are 4 surgical options for intracrhail tumours

A

stereotactic
neuro-navigation
endoscopic
free hand

129
Q

which CNS tumour is the hardest to treat

A

high grade glioma - glioblastoma

130
Q

which hemisphere is most dominant in language

A

left hemisphere

131
Q

where would the lesion likely be in someone who is withdrawn, apethtic and bad tempered vs numbness down one side of body

A

frontal lobe - personality changes

parietal - sensory loss, dyspraxia

Year 2 - Control (16 decks)

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