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2b deck > NEURO IMPORTANT > Flashcards

NEURO IMPORTANT Flashcards

1
Q

What are the categories of the glasgow coma score?

How are scores used after head injury?

A
  1. Eye opening (none=1, to pain =2, to speech=3, spontaneously=4)
  2. Verbal response (none=1, incomprehensible=2, inappropriate=3, confused=4. oriented=5)
  3. Motor (none=1, extensor to painful stimulus=2, flexion to painful stimulus=3, withdraws from pain=4, localised pain to stimulus=5, obeys commands=6)

CT head immediately if <13 on initial assessment or <15 at 2 hours post op

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2
Q

cause of foot drop/weakness in ankle dorsiflexion

A

peroneal nerve palsy, localised to L4-5

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3
Q

Facial nerve palsy sparing the forehead

A

CONTRALATERAL upper motor neuron lesion e.g. stroke/tumour

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4
Q

Facial nerve palsy not sparing any of the face

A

IPSILATERAL lower motor neuron e.g. parotid tumour, Bell’s palsy

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5
Q

Horizontal diplopia cause

A

Abducens palsy

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6
Q

CHA₂DS₂-VASc Score use + criteria

A

risk of stroke in patients with Atrial Fibrillation, congestive heart failure, hypertension, age (over 75=2, 65-74=1), diabetes, prior stroke/TIA, vascular disease, sex (female)

Score of 2 or more offer anticoag, score of 1 in men=anticoag

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7
Q

ABCD2 score use

A

assess patients at risk of stroke who had a suspected TIA

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8
Q

Quada equina syndrome diagnostic test

A

urgent MRI

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9
Q

management of acute seizure

A
  1. check airway and apply oxygen if needed
  2. Recovery position
  3. Benzodiazepam (recommended rectal diazepam)
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10
Q

Past medical history of cancer and new onset back pain are features highly suggestive of

A

metastatic cord compression

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11
Q

lumbar puncture needle is inserted below

A

L3 level, past dura mater (epidural does not go past epidural space)

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12
Q

Extradural haemorrhage- presentation, appearance on scan and vessels involved

A

loss of consciousness, lucid period, loss of consciousness. On scan= letiform, convex appearance on scan. Caused by meningeal vessels

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13
Q

subdural haemorrhage normally occurs in …

vessels involved

A

patients with dementia or alcoholics (ppl with smaller brain). Caused by bridging veins which are small so bleeding stops quickly but haematoma forms in following weeks causing a rise in ICP

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14
Q

subarachnoid haemorrhage presentation and cause

A

sudden onset headache/photophobia/thunderclap headache/reduced consciousness, caused by rupture of berry aneurysm in circle of willis

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15
Q

organisms which cause meningitis

A

meningococcus, pneumococcus

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16
Q

diagnosis of meningitis

A

lumbar puncture (usually done after CT)- CSF shows increased white blood cells, increased protein and low glucose

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17
Q

Symptoms meningitis

A

headaches, fever, neck stiffness, photophobia/phonophobia, Kernig’s sign, Bruzdinski sign

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18
Q

Kernig’s sign

A

pain + resistance on passive knee extension with hip fully flexed, used to diagnose meningitis

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19
Q

Brudzinski sign

A

Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed. Indicative of meningitis

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20
Q

treatment for bacterial meningitis
(1) if organism unknown

(2) menigococcal meningitis or pneumococcal meningitis

A

(1) Intravenous cefotaxime aged up to 50, >50 then cefotaxime and amoxicillin
(2) cefotaxime, but can also give benzylpenicillin for meningococcal instead

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21
Q

Meningococcal sepsis - signs + treatment

A

non-blanching petechial rash, cold hands and feet, fall in BP
treatment= fluid restriction, inotropes/vasopressors, aim for pressure >70mmHg and urine output >30ml/h

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22
Q

presentation of encephalitis

A

fever, headache, focal neural signs, seizures, history of travel, tremors/hallucination

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23
Q

treatment of encephalitis

A

aciclovir within 30 mins of arriving, supportive therapy + phenytoin for seizures

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24
Q

tetanus cause, symptoms + treatment

A

cause- clostridium tetani
symptoms- muscle spasms that begin in the jaw and progress to rest of body
treatment- immunisation, tetanus immune globulin, muscle relaxants and
removal + cleaning of tissue around wound

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25
Q

MS- basic pathology

A

T cells are activated by Myelin, changing the blood-brain barrier cells to allow entry of more T cells. Leads to a Type IV hypersensitivity reaction (cell mediated) –> T cells release cytokines which attract B cells and macrophages which release antibodies and attack/destroy myelin. Leads to scarring

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26
Q

MS symptoms

A

dysarthria, nystagmus, intention tremor, muscle weakness, spasms, ataxia

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27
Q

MS investigations

A

(1) MRI shows plaques- lesions disseminated through time and space
(2) VEP
(3) lumbar puncture shows high level of antibodies

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28
Q

MS- pharmacology

A

1- acute relapse- short course steroids (methylprednisolone)
2- preventing relapse:
- B-interferon : must have had 2 attacks in the last 3 years followed by a reasonable recovery. This drug helps reduce the relapse rate + reduce the occurrence of plaques on MRI but doesn’t alter long term outcome. Only used in relapsing and remitting MS
- Glatiramer acetate : a synthetic polypeptide. Given IV. Reduces number of relapses but doesn’t alter long term outcome
- Mitoxantrone : a cytotoxic antibiotic. Is experimental. May improve long term outcome when given at 3 monthly intervals
- Natalizumab : a monoclonal antibody that inhibits adhesion so reduces the number of inflammatory cells that are able to cross the blood brain barrier. Reduces relapse rate
- Baclofen : often used as symptomatic treatment. Is an antagonist of GABA receptors.

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29
Q

neurotransmitters involved in epilepsy

A

In generalized epilepsy, a hypoactivity of GABA, which exerts a presynaptic inhibitory function, and a hyperactivity of glutamate, which acts mainly as an excitotoxic, postsynaptic excitatory neurotransmitter and partly as a presynaptically inhibitory neurotransmitter, have been reported

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30
Q

4 types of seizure

A

1- focal- in one hemisphere/lobe of cortex
2- generalised seizure- involves both cortexes. Can be tonic/clonic/atonic/myclonic (short muscle twitches)/absence seizures
3- focal onset bilateral tonic-clonic- begins in a focal region and then spreads to second hemisphere, causing generalised seizure
4- status epilepticus- seizure lasts over 5 mins, is ongoing or consists of multiple seizures without returning to normal between. Usually tonic clonic- LIFE THREATENING, TREAT STATUS EPILEPTICUS WITH RECTAL DIAZEPAM/LORAZEPAM (benzos which enhance inhibitory neurotransmitter GABA)

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31
Q

focal seizure- presentations

A

seizure limited to one hemisphere/lobe of cerebral cortex. Can be with impaired awareness (loss of awareness/responsiveness) or without (small area of brain affected causing strange sensations and movements. “jacksonian march” may be present where jerking movements start in one group and spread to other groups of muscles)

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32
Q

treatment- generalised tonic-clonic seizures

A

1st line: sodium valporate

2nd line: lamotrigine, carbamazepine

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33
Q

treatment- absence seizures

A

sodium valproate or ethosuximide

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34
Q

treatment myoclonic seizures

A

sodium valproate

second line: clonazepam, lamotrigine

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35
Q

focal seizures- treatment

A

1st line: carbamazepine or lamotrigine

2nd line: levetiracetam, oxcarbazepine or sodium valproate

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36
Q

Epilepsy diagnosis

A

(1) clinical diagnosis- eyewitness account/any physical evidence of seizure
(2) determine seizure type
(3) EEG used to assist in underlying cause/classification identification

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37
Q

Parkinson’s triad (+ other features!)

A 
1- resting tremor 
2- cogwheel rigidity 
3- Bradykinesia/hypokinesia 
- no weakness! 
-Parkinson gait- slow shuffling
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38
Q

microscopic presentation of parkinson’s

A

lewy bodies present in the substantia nigra neurons in the pars compacta section of substantia nigra

39
Q

treatment of parkinson’s

A
  • Levadopa (dopamine replacement) 1st line if motor symptoms affect quality of life- delivered with carbidopa to prevent breakdown at BBB
  • If motor symptoms not affecting quality of life, dopamine agonist or MAO inhibitor (e.g. selegliene)
40
Q

1- medications that can cause parkinsonism

2- other conditions that can cause parkinsonism

A

1- antipsychotics e.g. haloperidol; metoclopramide (dopamine antagonist anti-emetic)
2- wilson’s disease + lewy body dementia

41
Q

cerebellar syndrome presentation `

A

loss of coordination and nystagmus

42
Q

oculomotor nerve palsy presentation

A

ptosis, DOWN AND OUT eye, dilated + fixed pupil

43
Q

trochlear nerve palsy presentation

A

defective downward gaze (vertical diplopia)

44
Q

trigeminal nerve palsy presentation

A
  • trigeminal neuralgia
  • loss of corneal reflex (afferent)
  • loss of facial sensation
  • paralysis of mastication muscles
  • deviation of jaw to weak side
45
Q

abducens nerve palsy presentation

A

palsy results in defective abduction (horizontal diplopia)

46
Q

glossopharyngeal nerve palsy presentation

A
  • hypersensitive carotid sinus reflex

- loss of gag reflex (afferent)

47
Q

vagus nerve palsy presentation

A
  • uvula deviates away from site of lesion

- loss of gag reflex

48
Q

accessory nerve palsy presentation

A

weakness turning head to contralateral side

49
Q

hypoglossal nerve palsy presentation

A

tongue deviates towards side of lesion

50
Q

ALS (MND) effect on motor neurons + presentation

A 
UPPER AND LOWER MOTOR NEURON SIGNS 
- symmetrical weakness + wasting, fasciculations (LMN signs) 
- hyperreflexia (UMN signs) 
- progressive weakness of limbs 
- MND NEVER AFFECTS EYE MOVEMENTS 
-
51
Q

drugs for ALS

A

cannot be cured but;
rituzole- sodium channel blocker slows disease progression
baclofen- GABA agonist helps reduce spasticity
propantheline- antimuscarinic, helps improve drooling

52
Q

giant cell arteritis- arteries predominantly affected

A

an inflammatory disease of blood vessels most commonly
involving large and medium arteries of the head, predominantly
branches of the external carotid artery. Thought to be autoimmune (giant cell granulomas and fibrosis in vessel walls)

53
Q

giant cell arteritis presentation for
1-temporal branch of carotid
2- opthalmic artery

A

1- headaches
2- blindness due to occlusion of the ophthalmic artery leading to
ischaemia of the eyes

54
Q

symptoms of giant cell arteritis

A

unilateral headache, facial pain, visual disturbances, jaw

claudication, flu-like symptoms, polymyalgia rheumatica

55
Q

investigations for giant cell arteritis + treatment

A

1- ESR >100
2- Biopsy shows giant cells in elastic lumina

Treatment: corticosteroids given to weaken immune system

56
Q

myasthenia gravis pathology

A

type II hypersensitivity reaction; B cells inappropriately make antibodies against nicotinic acetylcholine receptors on the post-synaptic side of the neuromuscular junction

57
Q

Myasthenia gravis symptoms

A
  • wake up fine but PROGRESSIVELY WEAKER THROUGH THE DAY
  • weakness in extraocular muscles = ptosis/diplopia
  • problems with chewing/swallowing/speaking
58
Q

myasthenia gravis investigations

A
  • antibodies- Anti-AChR antibodies
  • single fibre electromyography
  • CT scan to eclude thymic neoplasm
59
Q

Myasthenia gravis treatment

A

1- Acetylcholinesterase inhibitor (e.g. neostigmine or pyridostigmine) = stops
the break down of acetylcholine by inhibiting acetylcholinesterase (the
enzyme that degrades ACh) which increases the concentration of ACh at the neuromuscular junction
2- immunosupressants e.g. prednisolone (used in relapses of MG)
3- surgical removal of thymus

60
Q

Guillain-Barre Syndrome- what is it?

A

acute inflammatory demyelinating polyneuropathy-

A rapid onset muscle weakness caused by the immune system damaging the peripheral nerves following an infection.

61
Q

Guillain-Barre Syndrome symptoms

A
  • muscle weakness BEGINNING IN HANDS AND FEET, SYMMETRICALLY ASCENDS over a few weeks after infection
  • Reflexes are reduced or absent
  • Pain is common in back and limbs in early stages
  • possible autonomic dysfunction- in BP, heart rate (higher pulse),
    sweating & arrhythmias
62
Q

organisms that can trigger Guillain-Barre Syndrome

A 
Camylobacter jejuni (most common)
Cytomegalovirus 
Epstein-Barr virus 
HIV 
Mycoplasma 
Zoster
63
Q

investigations for Guillan-Barre syndrome

A
  • lumbar puncture- rise in protein (>5.5 g/L) with normal white blood cell count
  • nerve conduction studies show slow nerve conduction
  • if respiratory involvement, measure FVC every 4 hours
64
Q

Guillain-Barre syndrome treatment

A
  • ventilation if respiratory involvement
  • IV immunoglobulin
  • plasmapheresis
65
Q

anterior cerebral artery stroke presentation

A

contralateral hemiparesis and sensory loss, lower extremity > upper

66
Q

Middle cerebral artery stroke presentation

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

67
Q

Posterior cerebral artery stroke presentation

A

Contralateral homonymous hemianopia with macular sparing

Visual agnosia

68
Q

Homonymous quadrantanopia causes

A

superior: lesion of temporal lobe
inferior: lesion of parietal lobe
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

69
Q

Bitemporal hemianopia causes

A

lesion of optic chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

70
Q

Homonymous hemianopia causes

A

incongruous defects: lesion of optic tract
congruous defects: lesion of optic radiation or occipital cortex
macula sparing: lesion of occipital cortex

71
Q

Basilar artery stroke presentation

A

‘Locked-in’ syndrome

72
Q

Lacunar stroke presentation

A

present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule

73
Q

ischaemic stroke management

A

1- aspirin 300mg for 2 weeks (once haemorrhagic ruled out) + statin
2- Thrombolysis with ALTEPLASE if within 4.5 hours of onset of stroke, thrombectomy within 6 hours
3- Secondary prevention: clopidogrel long term OR aspirin + dipyridamole

74
Q

stroke investigations

A
  • FAST/ROSIER scores

- non-contrast CT head

75
Q

TIA presentation + relation to stroke

A
  • resolves within 24h
  • sudden dimming/loss of vision (amaurosis fugax), aphasia, dysarthria, menrtal confusion
  • having TIA increases risk of stroke in future
76
Q

TIA diagnosis

A
  • imaging by MRI
  • ABCD2 score for stroke risk
  • carotid doppler to look for carotid atheroma/stenosis
77
Q

Huntington’s presentation + pathology

A
  • irritability, depression and incoordination
  • chorea, abnormal eye movements and poor coordination
  • Due to abnormal repeated sequence (CAG) on nucleotides of the Huntington gene on chromosome 4 –> results in decreased GABA, decreased ACh, increased dopamine
78
Q

Treatment of huntington’s

A

neuroleptics- dopamine receptor antagonists (because of increased dopamine- treat chorea)
- Tetrabenazine- depletes dopamine

79
Q

Migraine treatment

A

1- first line= oral triptan AND NSAID or paracetamol
2- if not effective, can add metoclopromide
3- propanalol for prophylaxis

80
Q

cluster headaches management

A
  • 100% oxygen for 15mins via non-rebreathable mask
  • Sumatriptan at onset of headache
  • Lithium and verapamil= secondary prevention
81
Q

trigeminal neuralgia treatment

A

pharm: CARBEMAZAPINE, lamogitrine, Phenytoin, gabapentin
surgery at peripheral nerve/trigeminal nerve root
microvascular decompression- if problem is due to abnormal intracranial blood vessels

82
Q

cauda equina- symptoms

A
  • saddle anaesthesia
  • decreased anal tone
  • faecal/urinary incontinence
  • sexual dysfunction
  • back/leg pain
83
Q

causes of cauda equina

A

normally due to herniated disc

also tumour/met

84
Q

cauda equina treatment

A

SURGERY to remove compression

if tumour, can use radiotherapy

85
Q

carpal tunnel syndrome treatment

A
  • splinting
  • local steroid injection
  • decompression surgery
86
Q

alzheimer’s pathology

A

accumulation of B-amyloid peptide results in progressive neuronal damage, neurofibrillary tangles, increasing numbers of amyloid plaques and loss of ACh

87
Q

Alzheimer’s management

A
  • Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine and galantamine)
  • NMDA antagonist
  • antipsychotics
88
Q

first line treatment for Parkinsons affecting quality of life

A

Co-cateldopa

89
Q

history of crampy exertional calf pain which improves on rest

A

intermittent claudication –> caused by atherosclerosis of arteries in the calves. (GB syndrome would present with weakness and numbness.)

90
Q

TB drug which interacts with the oral contraceptive

A

Rifampicin

91
Q

temporal cell arteritis treatment

A

prednisolone

92
Q

Ramsay hunt syndrome

A

a form of shingles affecting the facial nerve, associated with a rash on the outer ears. As the facial nerve is affected, patient presents with Bell’s palsy. Can be prevented with shingles vaccine

93
Q

Charcot triad- what is it? what is it used for?

A

RUQ pain, fever and jaundice

ASCENDING CHOLANGITIS

94
Q

optic neuritis may be a sign of

A

multiple sclerosis

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