Brainscape's Knowledge GenomeTM

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


See full index

Phase 2A revision > neuro to work on COPY > Flashcards

neuro to work on COPY Flashcards

1
Q

What investigations might you do on someone with encephalitis?

A
  • MRI - shows areas of inflammation, may be midline shifting
  • EEG - periodic sharp and slow wave complexes
  • lumbar puncture
  • blood and CSF serology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the symptoms of MS?

A 
TEAM
T = tingling
E = eyes - optic neuritis
A = ataxia
M = motor - spastic paraparesis, pyramidal weakness (UL = extensors, LL = flexors)
DEMYELINATION
D = Diplopia
E = Eye movement painful
M = Motor weakness and spasticity
Y = nYstagmus
E = Elevated temperature
L = Lhermittes phenomenon
N = Neuropathic pain
A = Ataxia
T = Talking slurred
I = Impotence
O = Overactive bladder
N = Numbness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define epileptic seizure

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excess, hypersynchronous neuronal discharge in the brain

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

Give 5 causes of epilepsy

A
  1. Idiopathic (2/3)
  2. cortical scarring
  3. tumour
  4. stroke
  5. alzheimers dementia
  6. alcohol withdrawal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for focal epileptic seizures?

A 
Lamotrigine = 1st line
Carbamazepine = 2nd line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valproate = 1st line

Lamotrigine = 2nd line

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

How does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

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

Give 4 potential side effects of anti-epileptic drugs (AED’s)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give 4 differential diagnosis’s of epilepsy

A
  1. Syncope
  2. Non-epileptic seizure
  3. Migraine
  4. Hyperventilation
  5. TIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define non-epileptic seizure

A

Mental processes associated with psychological distress causes paroxysmal changes in behaviour, sensation and cognitive processes
1-20 minute duration
Closed eyes and mouth

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

Briefly describe the pathophysiology of a subarachnoid haemorrhage

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the treatment for a subarachnoid haemorrhage

A
  • NIMODIPINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
  • surgery = endovascular coiling
  • IV fluids - maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 3 risk factors of a subdural haematoma?

A
  1. Elderly - brain atrophy, dementia
  2. Frequent falls - epileptics, alcoholics
  3. Anticoagulants
  4. babies - traumatic injury (“shaking baby syndrome”)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name 3 differential diagnosis’s of a subdural haematoma

A
  1. Stroke
  2. Dementia
  3. CNS masses (tumour vs abscess)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give 3 things that modulate LMN action potential transmission to effectors

A
  1. Cerebellum
  2. Basal ganglia
  3. Sensory feedback
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 3 disease that are associated with motor neurone damage

A
  1. Motor neurone disease
  2. Spinal atrophy
  3. Poliomyelitis
  4. Spinal cord compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give 3 pathologies that are associated with ventral spinal root damage

A
  1. Prolapsed intervertebral disc
  2. Tumours
  3. Cervical or lumbar spondylosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the pyramidal pattern of weakness in the upper limbs

A

Flexors are stronger than extensors

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

Describe the pyramidal pattern of weakness in the lower limbs

A

Extensors are stronger than flexors

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

Give 3 causes of UMN weakness

A
  1. MS
  2. Brain tumour
  3. Stroke
  4. MND
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give 4 sites of UMN damage

A
  1. Motor cortex lesions
  2. Internal capsule
  3. Brainstem
  4. Spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Define motor neurone disease (MND)

A

A group of neuro degenerative disorders that selectively affect the motor neurons

Most in the anterior horn, cells of the spinal cord and the motor cranial nuclei

There are no sensory problems

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

What is the clinical presentation of MND?

A
  • results in mixed UMN and LMN presentation (LMN symptoms predominate)
  • wrist drop/foot drop
  • change in appearance of hands - wasting
  • gait disorders/tendencies to trip
  • excessive fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What investigations might you do in someone you suspect to have MND?

A 
Head/spine MRI
Blood tests = muscle enzymes, autoantibodies 
Nerve conduction studies 
EMG
Lumbar Puncture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the treatment for MND?

A
  • MDT care
  • anti-glutaminergic drugs - ORAL RILUZOLE - Na+ channel blocker, inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give 3 limb onset symptoms of MND

A
  1. Weakness
  2. Clumsiness
  3. Wasting of muscles
  4. Foot drop
  5. Tripping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 4 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP –> headache, decrease GCS, n+v, papilloedema
  2. Progressive neurological deficit –> deficit of all major functions (motor, sensory, auditory, visual) + personality change
  3. Epilepsy
  4. lethargy/tiredness - caused by pressure on brainstem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Name 2 differential diagnosis’s for a brain tumour

A
  1. Aneurysm
  2. Abscess
  3. Cyst
  4. Haemorrhage
  5. Idiopathic intracranial hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Where might secondary brain tumours arise from?

A
  1. non-small cell lung cancer
  2. small cell lung cancer
  3. breast
  4. melanoma
  5. renal cell carcinoma
  6. GI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give 3 risk factors of dementia

A
  1. Family history
  2. Age
  3. Down’s syndrome
  4. Alcohol use, obesity, HTN, hyperlipidaemia, DM
  5. Depression
  6. ? Head injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the clinical presentation of Alzheimer’s Disease

A 
● Memory - episodic and semantic
● Language - difficulty understanding or
finding words
● Attention and concentration issues
● Psychiatric changes, e.g. withdrawal,
delusions
● Disorientation, e.g. time and surroundings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does vascular dementia often present with?

A

● Characterised by stepwise progression - Periods of stable symptoms, followed by a sudden increase in severity
● Presentation varies massively but can include:
- Visual disturbances,
- UMN signs (e.g. muscle weakness, overactive reflexes, clonus),
- attention deficit,
- depression,
- incontinence,
- emotional disturbances
○ If infarct was subcortical, then expect to see dysarthria and parkinsonisms

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

what are the clinical features of Lewy body dementia

A

● Dementia is often presented initially
○ Memory loss, spatial awareness difficulties,
loss of cognitive function
● Parkinsonisms, e.g. tremor, rigidity, change in gait
● Visual hallucinations
● Sleep disorders, restless leg syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give 3 symptoms of Fronto-temporal dementia

A

● Onset tends to be insidious and progressive
● Present with 3 main symptoms:
○ Behavioural issues, e.g. loss of inhibition/empathy, compulsive behaviours, difficulty planning
○ Progressive aphasia, e.g. slow, difficult speech, grammatical errors
○ Semantic dementia, e.g. loss of vocabulary, problems understanding

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

Name the staging system that classifies the degree of pathology in AD

A

Braak staging
Stage 5/6 = high likelihood of AD
Stage 3/4 = intermediate likelihood
Stage 1/2 = low likelihood

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

what are the clinical features of myasthenia gravis?

A
  1. Muscle weakness
  2. Increasing muscular fatigue
  3. Ptosis
  4. Diplopia
  5. Myasthenic snarl
  6. Tendon reflexes normal but fatigable
● Weakness is more marked in proximal muscles
● Weakness might be seen in:
    ○ Small muscle of the hands
    ○ Deltoid and triceps muscles
    ○ Bulbar muscles
    ○ Muscles involved in chewing
● No muscle wasting, sensation is unimpaired
● Seizures can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What can weakness due to myasthenia gravis be worsened by?

A 
Pregnancy
Hypokalaemia
Infection 
Emotion
Exercise 
Drugs (opiates, BB, gentamicin, tetracycline)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Give 3 possible differential diagnosis’s for myasthenia gravis

A
  1. MS
  2. Hyperthyroidism
  3. Acute Guillain-Barre syndrome
  4. Lamert-Eaton myasthenia syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is treatment for myasthenia gravis?

A

Anti-cholinesterase = pyridostigmine
Immunosuppression = prednisolone (with alendronate - bisphosphonate)
Steroids can be combined with azathioprine or methotrexate
Thymectomy

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

Give a complication of myasthenia gravis

A

Myasthenic crisis
Weakness of respiratory muscle during relapse
Treatment = plasmapheresis and IV immunoglobulin

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

what are the clinical features of Parkinson’s disease

A

● Often an insidious onset

  • impaired dexterity,
  • fixed facial expressions,
  • foot drag

● Common associated symptoms:

  • dementia,
  • depression,
  • urinary frequency,
  • constipation,
  • sleep disturbances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What investigations might you do in someone you suspect to have PD?

A

DaTscan

Functional neuroimaging - PET

Can confirm by reaction to levodopa

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

Describe the pharmacological treatment for Parkinson’s disease

A

young onset + fit

  • Dopamine agonist (ropinirole)
  • MAO-B inhibitor (rasagiline)
  • L-DOPA (co-careldopa)

frail + co-morbidities

  • L-DOPA (co-careldopa)
  • MAO-B inhibitor (rasagiline)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How do dopamine agonists work in the treatment of PD and give an example of one?

A

Reduced risk of dyskinesia
First line in patient <60
Ropinirole, pramipexole

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

How do MAO-B inhibitors work in the treatment of PD and give an example of one?

A

Inhibit MAO-B enzymes which breakdown dopamine -> increases amount of dopamine available
Rasagiline, selegiline

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

How do COMT inhibitors work in the treatment of PD and give an example of one?

A

Inhibit COMT enzymes which breakdown dopamine

Entacapone, tolcapone

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

What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

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

Name the cardinal features of Huntington’s disease

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety

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

Name 3 signs of Huntington’s disease

A
  1. Abnormal eye movements
  2. Dysarthria
  3. Dysphagia
  4. Rigidity
  5. Ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe the treatment of Huntington’s disease

A 
poor prognosis - no treatment
- reserpine = chorea
● Benzodiazepines/valproic acid - chorea
● SSRIs = depression
● Haloperidol = psychosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the causes/risk factors of carpal tunnel syndrome

A
  1. Pregnancy
  2. Obesity
  3. RA
  4. DM
  5. Hypothyroidism
  6. Acromegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What can cause Guillain-Barre syndrome?

A

Bacteria

  • Camplylobacter jejuni
  • Mycoplasma

Viruses

  • CMV
  • EBV
  • HIV
  • Herpes zoster
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe the pathophysiology of Guillain-Barre syndrome

A

Same antigens on infectious organisms as Schwann cells (PNS) –> autoantibody mediated nerve cell damage -> via molecular mimicry
Schwann cell damage consists of demyelination, which results in a reduction in peripheral nerve conduction –> causes acute polyneuropathy

spreads from proximal to distal

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

what are the clinical features of Guillain-Barre syndrome

A 
Breathing problems
Back pain 
Sensory disturbance
Sweating
Urinary retention
  1. Ascending symmetrical muscle weakness 1-3 weeks post-infection (proximal muscles most affected - trunk, respiratory, CN) TOES TO NOSE WEAKNESS
  2. Pain in legs, back is rare
  3. sensory loss in lower extremities
  4. Reflexes lost early on (LMN sign)
  5. Autonomic features =
    • reduced sweating
    • reduced heat tolerance
    • paralytic ileus - intestinal obstruction w/o blockage
    • urinary hesitancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What investigations might you do in someone you suspect has Guillain-Barre syndrome?

A
  • Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
  • Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
  • bloods - FBC, U&E, LFT, TFT
  • Spirometry = respiratory involvement
  • ECG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the treatment for Guillain-Barre syndrome

A
  • If FVC <1.5L/80% = ventilate and ITU monitoring
  • IV immunoglobulin (IvIg) for 5 days = decrease duration and severity of paralysis
  • Plasma exchange
  • Low molecular weight heparin (LMWH) - SC ENOXAPARIN
  • Analgesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the causes of an ischaemic stroke?

A
  • small vessel occlusion by thrombus
  • atherothromboembolism (e.g. from carotid artery)
  • cardioembolism (post MI, valve disease, IE)
  • hyper viscosity
  • hypoperfusion
  • vasculitis
  • fat emboli from a long bone fracture
  • venous sinus thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the causes of an haemorrhagic stroke

A

Bleeding from the brain vasculature

  1. Hypertension - stiff and brittle vessels, prone to rupture
  2. Secondary to ischaemic stroke - bleeding after reperfusion
  3. Head trauma
  4. Arteriovenous malformations
  5. Vasculitis
  6. Vascular tumours
  7. Carotid artery dissection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what are the risk factors for ischaemic stroke?

A
  1. Age
  2. Male
  3. Hypertension
  4. Smoking
  5. Diabetes
  6. Recent/past TIA
  7. Heart disease - IHD, AF, valve disease
  8. Combined oral contraceptive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Give 3 signs of an ACA stroke

A
  1. Leg weakness - contralateral
  2. Sensory disturbance in legs
  3. Gait apraxia
  4. Incontinence
  5. Drowsiness
  6. Akinetic mutism - decrease in spontaneous speech (in a stupor)
  7. truncal ataxia - can’t sit or stand unsupported
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Give 3 signs of a MCA stroke

A
  1. Contralateral arm and leg weakness and sensory loss
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial droop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Give 3 signs of a PCA stroke

A

visual issues

  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agonisa
  4. Prosopagnoisa
  5. Dyslexia
  6. Unilateral headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Give 3 differential diagnosis’s for a stroke

A
  1. Hypoglycaemia
  2. Intracranial tumour
  3. Head injury +/- haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the treatment for an ischaemic stroke?

A

Immediate management:

  • CT/MRI to exclude haemorrhagic stroke
  • aspirin 300mg

Antiplatelet therapy

  • aspirin 300mg for 2 weeks
  • clopidogrel daily long term

Anticoagulation (e.g. warfarin) for AF

thrombolysis

  • within 4.5 hrs of onset
  • IV alteplase
  • lots of contraindications (can cause massive bleeds)

mechanical thromboectomy
- endovascular removal of thrombus

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

What is primary prevention of strokes?

A

Risk factor modifcaiton

  • Antihypertensives for HTN
  • Statins for hyperlipiaemia
  • Smoking cessation
  • Control DM
  • AF treatment = warfarin/NOAC’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is secondary prevention of strokes?

A

2 weeks of aspirin –> long term clopidogrel

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

Give 3 causes of a TIA

A
  1. Artherothromboembolism of the carotid - main cause (can hear carotid bruit)
  2. Cardioembolism - in AF, after MI, valve disease/prosthetic valve
  3. Hyperviscosity - polycythaemia, sickle cell, high WBCC
  4. hypoperfusion - postural hypotension, decreased flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what are the signs of a carotid TIA?

A
  1. Amaurosis fugax = retinal artery occlusion –> vision loss
  2. Aphasia
  3. Hemiparesis
  4. Hemisensory loss
  5. hemianopia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what are the signs of a vertebrobasilar TIA?

A
  1. Diplopia, vertigo, vomiting
  2. Choking and dysarthria
  3. Ataxia
  4. Hemisensory loss
  5. Hemianopic/bilateral visual loss
  6. tetraparesis
  7. loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are the differential diagnosis’s for a TIA

A
  1. Migraine aura
  2. Epilepsy
  3. Hypoglycaemia
  4. Hyperventilation
  5. retinal bleed
  6. syncope - due to arrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What investigations would you do in someone who you suspect to have a TIA?

A

first line = diffusion weighted MRI or CT

second line = carotid imaging (doppler ultrasound followed by angiography if stenosis is found)

Bloods

  • FBC - look for polycythaemia
  • ESR - raised in vasculitis
  • U&Es, glucose

ECG

echocardiogram

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

What is it essential to do in someone who has had a TIA?

A

Assess their risk of having stroke in the next 7 days = ABCD2 score

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

What is the ABCD2 score?

A

Assesses risk of stoke in the next 7 days for those who have had a TIA

  • age
  • BP
  • clinical features - unilateral weakness, speech disturbance
  • duration of TIA
  • presence of diabetes mellitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What classifies as a high risk stroke patient?

A
  • have ABCD2 score >4
  • have AF
  • > 1 TIA in a week
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the treatment for a TIA?

A

immediate treatment = aspirin 300mg and refer to specialist within 24hrs

control CV risk factors

  • BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN)
  • smoking cessation
  • statin - SIMVASTATIN
  • no driving for 1 month

antiplatelet therapy
- ASPIRIN 75mg daily (With Dipyridamole)
or
- CLOPIDOGREL daily

anticoagulation (e.g. WARFARIN) for patients with AF

carotid endarterectomy

  • if >70% carotid stenosis
  • reduces stroke/TIA risk by 75%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Give 3 causes of spinal cord compression

A
  • trauma,
  • tumours - most common spinal metastases are
    breast, prostate and lung cancer
  • central disc protrusion,
  • prolapsed disc (L4-5 and L5-S1 most common),
  • epidural haematoma,
  • infection,
  • cervical spondylitic myelopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Give 3 signs and symptoms of spinal cord compression

A 
Red flag signs:
- Loss of bladder or bowel function, 
- UMN signs in the lower limbs (e.g. clonus, hyperreflexia), 
- LMN signs in the upper
limbs (e.g. atrophy)

● Symptoms depend on the injury type and site

  • Can include paraplegia,
  • pain,
  • paraesthesia,
  • changes to tendon reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Give 3 causes of cauda equina syndrome

A
  1. Lumbar disc herniation at L4/5 or L5/S1
  2. Tumour
  3. Trauma
  4. Infection
  5. late-stage ankylosing spondylitis
  6. post-operative haematoma
  7. sarcoidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what are the clinical features of cauda equina syndrome

A 
● Sudden onset - hours
● Saddle paraesthesia
● bilateral sciatica
● Bladder/bowel dysfunction
● erectile dysfunction
● Motor problems
● Lower back pain
● Bilateral LMN weakness, absent ankle reflex (flaccid and areflexic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What investigations might you do to see if someone has cauda equina syndrome?

A

● Medical emergency
- immediate referral
● Rectal exam - loss of anal tone/sensation
● MRI spine
● knee flexion (L5-S1) and ankle plantar flexion (S1-S2)

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

How do you treat cauda equina syndrome?

A 
● Surgical decompression is essential
● Immobilise spine
● Anti-inflammatory agents
● Antibiotics if infection present
● Chemotherapy if indicated
  • Microdiscectomy - removal of part of the disc - may tear dura!
  • Epidural steroid injection - more effective for leg pain
  • Surgical spine fixation - if vertebra slipped
  • Spinal fusion - reduces pain from motion and nerve root inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Define spondyloisthesis

A

Slippage of vertebra over the one below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Define spondylosis

A

Degenerative disc disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what are the risk factors for Alzheimer’s disease?

A
  • Down’s syndrome,
  • ApoE E4 allele homozygosity,
  • reduced cognitive activity,
  • depression/loneliness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is the pathophysiology of frontotemporal dementia?

A

● Atrophy of the frontal and temporal lobes
● Loss of neurons, but no plaque formation
● Tau +ve or TDP-43 +ve inclusions

87
Q

what are the risk factors for frontotemporal dementia?

A

50% dominant inheritance

88
Q

what are the risk factors for vascular dementia?

A 
smoking, 
history of TIAs, 
AF,
hypertension, 
DMT1, 
hyperlipidaemia, 
obesity,
coronary heart disease
89
Q

what is the treatment for vascular dementia?

A

● Supportive therapy, e.g. carers, home changes,
routine help, cognitive simulation programmes
● No pharmacological treatment for the dementia
itself
● SSRIs or anti-psychotics to control symptoms,
e.g. lorazepam
● Prognosis is 3-5 years from diagnosis

90
Q

what are the investigations for Lewy Body dementia?

A

● MMSE or 6-item cognitive impairment test (6-CIT)
● Bloods - B12, TFTs, U&E, MRI (?other cause)
● MSU to check for urine infection

91
Q

what is the diagnostic criteria for Lewy Body dementia?

A

○ Presence of dementia with 2 of:

- fluctuating attention and concentration, 
- recurrent well-formed visual hallucinations, 
- spontaneous Parkinsonism

○ If there is only 1 of the 3 core features, diagnosis can also be made with a SPECT or PET scan showing low dopamine transporter uptake in basal ganglia

92
Q

what is the treatment for Lewy Body dementia?

A

● Refer to a specialist
● Supportive therapy - cognitive stimulation, exercise programmes, at-home care
● Cholinesterase inhibitors, e.g. rivastigmine suggested to treat cognitive decline
● Avoid use of neuroleptic drugs, e.g. haloperidol, as they can produce severe
sensitivity reactions

93
Q

what are the other causes of Parkinson’s disease?

A
  • Drug induced Parkinsonism - caused by dopamine antagonists, e.g. clozepine
  • encephalitis
  • exposure to certain toxins, e.g. manganese dust
94
Q

what is the 3 step diagnostic pathway for diagnosing Parkinson’s disease?

A

1) Diagnosis of Parkinsonian syndrome
○ Bradykinesia (required) plus one of rigidity, resting tremor, or postural instability

2) Exclusion criteria (none to be met)
○ History of stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, babinski’s sign, early severe dementia, negative response to large L-dopa dose

3) Supportive criteria (3 or more required)
○ Unilateral onset, rest tremor present, progressive, excellent response to L-dope (70-100%), visual hallucinations

95
Q

what are the causes of foot drop?

A 
injury, 
lower back damage,
tumour, 
hip replacement, 
cauda equina syndrome, 
multiple sclerosis
96
Q

what is the treatment for foot drop?

A 
● Brace or splint
● Physiotherapy
● Specialised shoes - prevent foot drop when walking
● Nerve stimulation
● Surgery if indicated
97
Q

what are the risk factors for TIA?

A
  • age
  • hypertension
  • smoking
  • diabetes
  • heart disease - AF
  • combined oral contraceptive pill
  • hyperlipidaemia
  • peripheral artery disease
  • clotting disorder
  • vasculitis
98
Q

what are the differential diagnoses for TIA?

A 
Hypoglycaemia
Migraine aura
Focal epilepsy
Vasculitis
Syncope - E.g. due to an arrythmia
Retinal bleed
99
Q

what are lacunar infarcts (ischaemic stroke)?

A
  • Small infarcts
  • From occlusion of a single small perforating artery supplying a subcortical area
  • Can happen in:
    • Internal capsule
    • Basal ganglia
    • Thalamus
    • Pons
100
Q

what is the clinical presentation of lacunar infarcts (ischaemic stroke)?

A

Depends on the area affected

One of:

  • Sensory loss
  • Weakness (unilateral)
  • Ataxic hemiparesis
  • Dysarthria
  • Motor speech problems
101
Q

which areas of the brain can be affected by lacunar infarcts (ischaemic stroke)?

A

Internal capsule
Basal ganglia
Thalamus
Pons

102
Q

what is the clinical presentation of brainstem infarcts (ischaemic stroke)?

A
  • Quadriplegia
  • Facial numbness & paralysis
  • Gaze & vision disturbances
  • Dysarthria & speech impairment
  • Vertigo, nausea, vomiting
  • Cerebellar signs
  • Palatal paralysis & diminished gag reflex
  • Altered consciousness
  • Locked-in syndrome
  • Coma
103
Q

what are the contraindications of thrombolysis (IV alteplase)?

A
  • Recent surgery last 3 months
  • Recent arterial puncture
  • History of active malignancy (highly vascular thus increased
    bleeding risk)
  • Evidence of brain aneurysm
  • Patient on anticoagulation
  • Severe liver disease (abnormal clotting)
  • Acute pancreatitis
  • Clotting disorder
104
Q

what is the treatment for haemorrhagic stroke?

A
  • frequent GCS monitoring
  • anticoagulants are contraindicated (any anticoagulants should be reversed with vitamin K)
  • control hypertension
  • decompression of raised ICP - MANNITOL
  • surgery may be required
105
Q

what is the clinical presentation of intracerebral haemorrhage?

A

similar to ischaemic stroke

pointers to haemorrhage:

  • sudden loss of consciousness
  • severe headache
  • meningism
  • coma
106
Q

what is the management for intracerebral haemorrhage?

A
  • stop anticoagulants immediately
    • effects reversed with clotting factor replacement
  • control of BP - IV drugs
  • reduce ICP
    • mechanical ventilation
    • IV mannitol
  • refer for neurosurgical intervention if:
    • hydrocephalus
    • coma
    • brainstem compression
107
Q

what are the differential diagnoses for subarachnoid haemorrhages?

A
  • headache - migraine, cluster headache
  • meningitis
  • intracerebral haemorrhage
  • cortical vein thrombosis
  • carotid/vertebral artery dissection
108
Q

what are the red flag indications for CT/MRI in migraines?

A
  • worst/severe headache i.e. “thunderclap”
  • change in pattern of migraine
  • abnormal neurological exam
  • onset > 50yrs
  • epilepsy
  • posteriorly located headache
109
Q

when are triptans contraindicated?

A

in ischaemic heart disease, coronary spasm and uncontrolled high BP

family history of CVD, stroke, DM and high cholesterol

110
Q

what are the side effects of triptans?

A
  • arrhythmias
  • angina +/- MI
  • recurrence of migraines - higher frequency
111
Q

what are the risk factors of cluster headaches?

A

Smoker
Alcohol
Male
Genetics - autosomal dominant gene has a link

112
Q

what are the preventative measures for cluster headaches?

A
  • 1st line = verapamil (CCB)
  • prednisolone
  • reduce alcohol consumption and stop smoking
113
Q

what are the triggers for tension headaches?

A
  • stress
  • sleep deprivation
  • bad posture
  • hunger
  • eyestrain
  • anxiety
  • noise
114
Q

what is the clinical presentation of wernicke’s encephalopathy?

A
  • classic triad
    • confusion
    • ataxia
    • ophthalmoplegia
  • sign
    • asterixis (liver flap) - general sign of metabolic encephalopathy
115
Q

what diseases does wernicke’s encephalopathy occur in?

A
  • chronic alcoholism
  • severe starvation
  • prolonged vomiting
116
Q

what are the investigations for wernicke’s encephalopathy?

A
  • diagnosed via clinical examination
117
Q

what are the complications of wernicke’s encephalopathy?

A

if not managed appropriately

  • fatal in 20%
  • can progress to korsakoff’s syndrome
118
Q

what is korsakoff’s syndrome?

A
  • irreversible
  • long term brain damage due to vitamin B1 deficiency
  • symptoms = decreased ability to acquire new memories, retrograde amnesia, confabulation (invented memories)
119
Q

what are the causes and risk factors of MND?

A
  • usually sporadic and unknown cause

- 5-10% are familial = SOD-1 mutation

120
Q

what are the 4 different types of MND? do they affect LMN or UMN?

A

amyotrophic lateral sclerosis (ALS) - UMN + LMN

progressive muscular atrophy (PMA) - LMN only

progressive bulbar palsy (PBP) LMN only

primary lateral sclerosis (PLS) UMN only

121
Q

what is the clinical presentation of ALS?

A

● Presents with signs of degeneration of upper and
lower motor neurons
● progressive paralysis and eventual respiratory failure
● Asymmetric onset
● Babinski sign +ve
● Fasciculations of the tongue
● Any corticobulbar signs indicate a worse prognosis:
○ Brisk jaw reflex
○ Dysarthria (difficulty speaking)
○ Dysphagia (difficulty swallowing)
○ Sialorrhoea (excess salivation)

122
Q

what are the clinical features of progressive bulbar palsy (PBP) in MND?

A

CN 9-12

  • LMN in the brain stem
  • pharyngeal muscle weakness
  • progressive loss of speech (hoarse, quiet, nasal)
  • tongue atrophy (flaccid)
123
Q

what are the clinical features of primary lateral sclerosis (PLS) in MND?

A
  • UMN of the arm, legs and face
  • movements become slow
  • progressive tetraparesis
124
Q

what are the clinical features of progressive muscular atrophy (PMA) in MND?

A
  • LMNs only
  • muscle wasting
  • clumsy hand movements
  • fasciculations
  • muscle cramps
125
Q

what are the side effects of pyridostigmine used to treat myasthenia gravis?

A
  • increased salivation
  • lacrimation
  • sweats
  • vomiting
  • miosis (excessive pupillary constriction)
  • diarrhoea
126
Q

what is the treatment for myasthenic crisis?

A
  • monitor FVC
  • plasmapheresis and IV immunoglobulin
  • identify and treat trigger of relapse e.g. infection, medications
127
Q

where are MS demyelination plaques commonly found?

A
  • optic nerves
  • around ventricles of the brain
  • brainstem and cerebellar connections
  • corpus callosum
  • cervical cord (corticospinal tract and dorsal columns)
128
Q

what are the lumbar puncture results for meningitis caused by bacteria?

A
  • cells = polymorphs
  • proteins = raised
  • glucose = low
  • CSF = turbid colour
129
Q

what are the lumbar puncture results for meningitis caused by TB?

A
  • cells = lymphocytes
  • proteins = raised
  • glucose = normal/low
130
Q

what are the lumbar puncture results for meningitis caused by viruses?

A
  • cells = lymphocytes
  • proteins = normal
  • glucose = normal
131
Q

what antibiotic is used in meningitis if S. Pneumoniae is suspected?

A

vancomycin

132
Q

what antibiotic is used in meningitis if listeria is suspected?

A

ampicillin (or amoxicillin) and gentamycin

133
Q

what are the risk factors for meningitis?

A
  • immunosuppression
  • elderly
  • pregnant
  • crowding (university)
  • diabetes
  • malignancy
  • IV drug use
  • sickle cell anaemia
  • adrenal insufficiency
134
Q

what are the risk factors for epilepsy?

A

FHx
Premature babies, especially if they are small for their gestational age
Abnormal cerebral blood vessels
Drugs eg. cocaine

135
Q

what are the characteristics of temporal lobe specific seizures?

A

Aura (80%); deja-vu, auditory hallucinations, funny smells, fear

  • Anxiety, out-of-body experiences
  • Automatisms eg. lip smacking
136
Q

what are the characteristics of frontal lobe specific seizures?

A

Motor features eg. posturing, peddling movements of leg

JACKSONIAN MARCH – seizures march up/down the motor homunculus

Post-Ictal Todd’s palsy

Starts distally in a limb & works its way upwards to the face

137
Q

what is the emergency treatment for epilepsy?

A
  • ABCDE
  • check glucose
  • RECTAL/IV DIAZEPAM or LORAZEPAM
  • IV PHENYTOIN loading
  • mechanical ventilation
138
Q

what is the treatment for generalised tonic-clonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

139
Q

what is the treatment for generalised tonic/atonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

140
Q

what is the treatment for generalised myoclonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Levetiracetam/Topiramate to females of childbearing potential

141
Q

what is the treatment for absence (petit mal) epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Ethosuximide to females of childbearing potential

142
Q

what are the side effects of sodium valproate?

A
  • weight gain
  • hair loss
  • liver failure
143
Q

what are the side effects of lamotrigine?

A

maculopapular rash
blurred vision
vomiting

144
Q

what are the side effects of carbamazepine?

A 
diplopia
rashes
leucopenia
impaired balance
drowsiness
145
Q

what are the side effects of ethosuximide?

A

rashes

night terrors

146
Q

what are the investigations for trigeminal neuralgia?

A
  • In order to diagnose needs to be at least 3 attacks with unilateral facial pain
  • Clinical diagnosis based on criteria above and based on history
  • MRI to exclude secondary causes or other pathologies
  • Not attributed to another disorder
147
Q

what are brainstem lesions caused by?

A
  • Tumour
  • MS
  • Trauma
  • Aneurysm
  • Vertebral artery dissection resulting in infarction
  • Infection - cerebellar abscess from ear
148
Q

what are the causes of CN3 palsy?

A
  • Raised ICP
  • Diabetes
  • Hypertension
  • Giant cell arteritis
149
Q

what are the causes of a CN4 palsy?

A

Trauma to the orbit - rare

150
Q

what are the causes of CN6 palsy?

A
  • MS
  • Wernicke’s encephalopathy
  • Pontine stroke - presents with fixed small pupils +/- quadriparesis
151
Q

what are the causes of CN3,4,6 palsy?

A
  • Storke
  • Tumours
  • Wernicke’s encephalopathy
152
Q

what are the signs of CN5 palsy?

A
  • Jaw deviates to side of lesion

- Loss of corneal reflex

153
Q

what are the causes of CN5 palsy?

A

trigeminal neuralgia (pain but no sensory loss),
herpes zoster,
nasopharyngeal cancer

154
Q

what are the causes of CN7 palsy?

A

• Bells palsy is the most common lesion of the facial nerve - will see
dribbling out the side of mouth
• Fractures of the petrous bones
• Middle ear infections
• Inflammation of the parotid gland - which facial nerve passes through

155
Q

what are the signs of CN9,10 palsy?

A
  • Gag reflex issues
  • Swallowing issues
  • Vocal issues
156
Q

what are the side effects of SSRIs?

A
  • GI disturbance
  • appetite and weight disturbance
  • hypersensitivity reactions
  • hyponatraemia
  • suicidal thoughts
  • seizures
  • prolonged QT interval
157
Q

what are the contraindications of SSRIs?

A
  • contraindicated with other monamine oxidase inhibitors -> may cause serotonin syndrome
  • other drugs that cause prolonged QT interval
  • increase bleeding when used with anticoagulants
158
Q

what is the mechanism of action for tricyclic antidepressants?

A
  • inhibits neuronal uptake of serotonin and noradrenaline from the synaptic cleft -> increase availability for neurotransmission
159
Q

what are the side effects of tricyclic antidepressants?

A
  • dry mouth
  • constipation
  • urinary retention
  • blurred vision
  • sedation
  • hypotension
  • arrhythmias
  • QT and QRS prolongation
  • hallucinations
  • sexual dysfunction
160
Q

when are tricyclic antidepressants contraindicated?

A
  • with other monoamine oxidase inhibitors
161
Q

what is the mechanism of action for benzodiazepines?

A
  • Benzodiazepines target the GABA-a receptor, which is a chloride channel that opens in response to binding by GABA (the main INHIBITORY NEUROTRANSMITTER)
  • opening the channel allows chloride to enter making the cell more resistant to depolarisation
  • They facilitate the enhanced binding of GABA to GABA-a receptors and have a widespread depressant effect on synaptic transmission
162
Q

when are benzodiazepines contraindicated?

A
  • in elderly
  • those with respiratory or hepatic impairment
  • neuromuscular disease
  • has sedative effects with alcohol, opioids and CYP450 inhibitors
163
Q

what are the side effects of carbamazepine?

A
  • GI disturbance
  • dizziness
  • ataxia
  • hypersensitivity rash
  • oedema
  • hyponatraemia
164
Q

when is carbamazepine contraindicated?

A
  • prior anti-epileptic hypersensitivity syndrome

- caution in hepatic, renal and cardiac disease

165
Q

what is the mechanism of action for gabapentin and pregabalin?

A

it is closely related to GABA

  • It binds voltage sensitive Ca2+ channels, where it prevents inflow of Ca2+ and thus inhibits neurotransmitter release
  • interfering with synaptic transmission and reducing neuronal excitability
166
Q

what are the side effects of gabapentin and pregabalin?

A
  • drowsiness
  • dizziness
  • ataxia
167
Q

what are the contraindications of gabapentin and pregabalin?

A
  • renal impairment

- other sedating drugs

168
Q

what are the side effects of levo-dopa?

A 
nausea
drowsiness
confusion
hallucinations
hypertension
169
Q

what are the contraindications for levo-dopa?

A
  • take care in elderly

- caution in CVS disease

170
Q

why is levo-dopa always given alongside a decarboxylase inhibitor (Co-Careldopa)?

A
  • reduce levo-dopa’s peripheral conversion before it is able to enter the brain
    this reduces nausea and lowers dose required
171
Q

give an example of a dopamine deleting drug

A

reserpine

172
Q

what is the mechanism of action for dopamine depleting drugs (reserpine)?

A
  • irreversibly blocks vescicular monoamine transporter (VMAT)
173
Q

what are the side effects of dopamine depleting drugs (reserpine)?

A
  • nasal congestion
  • GI disturbance
  • drowsiness/dizziness
  • hypotension
  • bradycardia
174
Q

what are the contraindications for dopamine depleting drugs?

A
  • asthma

- CVS disease

175
Q

give an example of MAO inhibitor?

A

selegiline

rasagiline

176
Q

what are the contraindications of MAO inhibitors?

A
  • aged cheese and alcohol -> can cause hypertensive crisis

- antidepressants and adrenaline

177
Q

give an example of ACh inhibitor

A

rivastigmine

donepezil

178
Q

what are the side effects of ACh inhibitors?

A
  • bradycardia
  • hypotension
  • hypersecretion
  • bronchoconstriction
  • GI tract hyper motility
  • prolonged muscular contraction
179
Q

what are the contraindications of ACh inhibitors?

A

urinary retention

CVS disease

180
Q

what are the causes of primary syncope?

A

Dehydration
Missed meals
Extended standing in a warm environment, such as a school assembly
A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

181
Q

what is the treatment for Bell’s palsy?

A
  • prednisolone
  • eye care
  • ?antivirals
182
Q

what are the characteristics of cushing’s triad?

A
  • bradycardia
  • irregular respirations
  • widened pulse pressure
183
Q

what is cushing’s reflex?

A
  • nervous system response to increased ICP
  • as ICP increases cerebral perfusion pressure (CPP) decreases, resulting in reduced cerebral perfusion
  • sympathetic nervous system is activated which increases BP
184
Q

what are the clinical presentation of cushing’s reflex?

A
  • cushing’s triad - bradycardia, irregular respirations and widened pulse pressure
  • hypertension
  • headache
  • vomiting
  • blurred vision
185
Q

what are the investigations for cushing’s reflex?

A
  • measure ICP - lumbar puncture or continuous monitoring via catheter in ventricle of brain
  • CT/MRI
186
Q

what is the treatment for cushing’s reflex?

A
  • mannitol
  • duiretics - furosemide
  • steroids - methylprednisolone
  • sedatives - propofol
  • hyperventilation
  • elevate head to 30 degrees (reverse trendelenburg position)
  • drain CSF
  • craniotomy
187
Q

what are the causes of 1st order horner’s syndrome?

A

stroke, tumours of hypothalamus, spinal cord lesions

188
Q

what are the causes of 2nd order horner’s syndrome?

A

tumours of upper chest cavity, trauma to the neck

189
Q

what are the causes of 3rd order horner’s syndrome?

A

lesions to carotid artery, middle ear infections, injury to base of the skull

190
Q

what are the clinical features of horner’s syndrome?

A

MAPLE

  • Miosis
  • Anhydrosis
  • Ptosis
  • Loss of ciliospinal reflex
  • Endophthalmos (sunken eyeball)
191
Q

what is the treatment for horner’s syndrome?

A

treat underlying cause

192
Q

what are the investigations for horner’s syndrome?

A

clinical examination

MRI - detect lesions

193
Q

what is the presentation of brown-sequard syndrome?

A
  • DCML = ipsilateral loss of proprioception and vibration sensation
  • spinothalamic = contralateral loss of temperature and pain sensation
  • corticospinal = ipsilateral spastic paralysis below lesion
194
Q

what are the signs of lateral medullary syndrome in ischaemic stroke?

A

Sudden vomiting and vertigo

Ipsilateral Horner’s syndrome = reduced sweating, facial numbness, dysarthria, limb ataxia, dysphagia

195
Q

what are the causes of status epilepticus?

A
  • Abruptly stopping anti epileptic treatment
  • Alcohol abuse
  • Poor compliance to therapy
196
Q

what are the secondary causes of syncope?

A 
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy
197
Q

what are the clinical features of syncope?

A 
Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache
198
Q

`what are the investigations for syncope?

A

Full history and examination

ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome

24 hour ECG if paroxysmal arrhythmias are suspected

Echocardiogram if structural heart disease is suspected

Bloods, including a FBC (anaemia), U&E (arrhythmias and seizures) and blood glucose (diabetes)

199
Q

give 3 major features of an MS plaque

A

inflammation
demyelination
axon loss

200
Q

what are muscle spindles innervated by?

A

gamma motor neurones

201
Q

what is the function of muscle spindles?

A

control muscle tone and teel you how much a muscle is stretched

202
Q

what is the fucntion of the cerebellum?

A

responsible for precise control, fine adjustment and co-ordination of motor activity based on sensory info

decides how you do somwthing

203
Q

what are the 3 layers of the cerebellum

A

molecular
purkinje
granular

204
Q

give 5 signs of cerebellar dysfunction

A 
DANISH
dysdiadochokinesis
ataxia
nystagmus
intention tremor
slurred speech
hypotonia
205
Q

how is the severity of ataxia classified?

A
  • mild = independent or requires 1 walking aid
  • moderate = requires 2 walking aids
  • severe = wheelchair dependent
206
Q

describe the physiology of muscle contraction

A
  • Ca released from sarcoplasmic reticulum to T-tubules which binds to troponin C
    troponin C moves tropomyosin to expose myosin binding site
    myosin binds to specific sites on actin (requires ATP) and there is cross bridge formation
207
Q

which protein is affected in duchenne muscular dystrophy?

A

dystrophin

208
Q

what is the inheritance pattern for duchenne musclar dystrophy?

A

x linked recessive

209
Q

what are the cardiac problems with duchenne muscular dystrophy

A

arrhythmias
conduction block
cardiomyopathy

210
Q

what would you see histologically in duchenne muscular dystrophy?

A

muscle nuclei all ove rthe place
muscle cells all different sizes
absence of dystrophin

211
Q

what is the pathophyisiology of duchenne muscular dystrophy?

A

large deletion, duplications and mutatiosn disrupt reading frame - out of frame mutations - dystrophin not produced

212
Q

what is myotonia?

A

delayed muscle relaxation

213
Q

what is the inherticance pattern of becker musclar dystrophy

A

x linked recessive

214
Q

what is the inheritance pattern of myotonic dystrophy

A

autosomal dominant

Phase 2A revision (38 decks)

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