Brainscape's Knowledge GenomeTM

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


See full index

Medical School Finals > Core: Neurology > Flashcards

Core: Neurology Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

MND Aetiology

A
  1. Often unknown
  2. Mutations in SOD-1, TDP43, FUS
  3. Familial - C9orf72 w/ hexanucleotide repeat GGGGCC on chromosome 9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MND pathophysiology

A
  • Oxidative damage to neurones
  • Damaged motor neurones then die.
  • Progressive weakness UMN and LMN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MND Fasciculation causes

A
  • Abnormally large motor units due to MN death, fewer nerve fibres to innervate large units.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MND classic presentation

A
  • Weakness + wasting + fasciculation

- UMN and LMN signs = wasted muscle + brisk reflexes.

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

MND other presentations

A
  1. Progressive muscular atrophy - purely LMN. Starting in one limb and progressively involving others.
  2. Progressive bulbar and pseudobulbar palsy - lower CN nuclei involvement. Dysarthria, dysphagia, nasal regurgitation and choking. Tongue fasciculations and emotional incontinence.
  3. Primary lateral sclerosis - Slow progressive tetraparesis and pseudobulbar palsy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Patient - Over 40, stumbling spastic gait, foot drop, proximal myopathy, weak grip, fasciculations

A

MND

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

MND Ix

A
  1. Often clinical

2. EMG

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

MND Rx

A
  1. Riluzole - antiglutaminergic
  2. Symptom management; Drooling = propantheine, amitriptyline
    Dysphagia = blend foods
    Pain = analgesic ladder
    Respiratory distress = NIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Patient - Any age, acute onset headache, neck stiffness and fever. ?purpuric rash

A

Meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Meningitis Aetiology

A
  1. Bacteria - Meningococcus, S.pneumoniae, S.aureus, GBS, TB, listeria, E.coli
  2. Viral - Enterovirus, mumps, HSV, HIV, EBV
  3. Fungal - Crytococcus (HIV), candida.
  4. IT drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Meningitis Pathology

A
  • Inflammation of the meninges
  • Transmission often via direct extension from ear, nose, throat, blood or direct trauma.
  • Pia-arachnoid space becomes congested w/ neutrophils and a layer of pus forms.
  • Adhesions can be formed which can cause CN palsies.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Meningitis Presentation

A
  • Headache
  • Neck stiffness
  • Fever
  • Photophobia
  • N&V
  • Rash
  • SHOCK
  • Kernig’s sign.
  • Bulging fontanelle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Meningitis Ix

A
  1. Clinically suggested
  2. Sepsis 6
  3. FBC
  4. LP if not contraindicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Meningitis Rx

A
  1. In the community = 1.2g benpen stat or 1g cefotaxime IM
  2. Sepsis 6
  3. Cefotaxime IV 2g/6hr + amoxicillin (if listeria suspected)
  4. Rx empirically according to MC&S
  5. Notify PHE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Meningitis Contact prophylaxis

A
  1. Rifampicin 600mg/12hr 2 days or ciprofloxacin 500mg PO 1 dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Patient - Any age, meningism, no rash, behavioural changes, seizures and focal neurology

A

Encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Encephalitis Aetiology

A
  1. Viral - HSV, VZV, Enterovirus, adenovirus. SSPE following measles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Encephalitis Pathology

A
  • Virus replicates in the bloodstream.

- Enters neural cells and causes congestion and disruption of function within the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Encephalitis Presentation

A
  • Meningism (often less severe than meningitis)
  • Personality and behavioural change
  • Viral prodrome
  • lethargy
  • Seizure
  • CN issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Encephalitis Ix

A
  1. MRI brain - parenchymal inflammation and swelling.
  2. EEG - Periodic sharp and slow wave complexes
  3. CSF - raised lymphocytes
  4. Viral PCR.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Encephalitis Rx

A
  1. Immediate IV acyclovir (10mg/kg 3xdaily for 14-21 days)

2. Symptom control –> Seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Patient - Headaches (worse on coughing, leaning forward), vomiting, new onset seizure, progressive defect.

A

Mass lesion in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mass lesion aetiology

A
  • Commonly metastasis from the bronchus, breast, stomach, prostate, thyroid and kidney.
  • Primary = astrocytoma, oligodendroglioma, cerebral lymphoma
  • Benign = meningioma, neurofibroma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Mass lesion pathology

A
  • Mass effect.
  • As the lesion grows, its shifts structures within the brain creating pressure against the cranium.
  • Direct infiltration of brain tissue.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Mass lesion presentation

A
  • Raised ICP
  • New onset seizure
  • Focal neurology curtailing to a certain part of the brain
  • Personality changes etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Mass lesion Ix

A

1) CT/MRI
2) Biopsy
3) XR and PET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Mass lesion Rx

A

1) Surgical resection if possible
2) Cerebral oedema - dexamethasone
3) Chemo/radio (gamma knife)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Patient - Old, alcoholic, post traumatic head injury … reducing GCS ?

A

Subdural haematoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Subdural haematoma Aetiology

A
  • Head trauma
  • Spontaneous
  • Coagulopathy or blood thinners
  • Intracranial HTN
  • Child abuse … shaken baby y’all
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Subdural haematoma pathology

A
  • Venous bleed.
  • Atrophic brains - greater stretch of a bridging vein which connects the brain to a dural sinus.
  • Low pressure bleed dissects the arachnoid from the dura and blood pools in the cranium.
  • Herniation can occur.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Subdural haematoma Presentation

A
  • Elderly
  • Alcoholic
  • Headache
  • Reducing GCS or drowsiness, confusion
  • Focal neurology; paresis or sensory losses
  • Seizure
  • Coma
  • Coning !!!!! Arghhhhh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Subdural haematoma Ix

A

1) CT - hyperdense white crescent moon shaped mass at skull edge. midline shift.
2) Bloods - coag screen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Subdural haematoma Rx

A

1) ABCDE
2) Neurosurgery
3) Reduce cerebral pressure and oedema w/ mannitol if present risk of herniation

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

Patient - 40, sudden onset occipital headache, ‘worst i’ve ever had darling’, neck stiffness.

A

Fuckkkkkk - SAH

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

SAH Aetiology

A
  • Idiopathic
  • Berry aneurysm
  • AVM
  • Association w/ PKD, meningitis, coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

SAH pathology

A
  • Spontaneous arterial bleed
  • Circle of willis berry aneurysm
  • Downstream ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SAH presentation

A
  • Sudden onset occipital headache
  • Worst ever doc
  • Or presents with low GCS at ED oops.
  • Vomiting
  • Coma
  • Raised ICP signs
  • Hx of other smaller similar headaches (sentinel bleeds)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

SAH Ix

A

1) CT ASAP - Subarachnoid blood, intraventricular blood, star sign.
2) LP - xanthochromia
3) CT angiography to find aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

SAH Rx

A

1) ABCDE
2) bed rest with best supportive care
3) Manage BP - nimodipine (CCB) for 3 weeks
4) Decompressive craniotomy
5) Coil/clip the aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Patient - Young rugby player, been to the pub, punched in the side of the head. Brief LOC at the time and has felt fine since.

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

Extradural haemorrhage aetiology

A
  • Traumatic injury to the temporal bone

- Following LP

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

Extradural haemorrhage Pathology

A
  • Temporal bone fracture
  • Torn middle meningeal artery whose foramen passes through the bone.
  • Pooling of blood between the bone and brain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Extradural haemorrhage presentation

A
  • Brief LOC at time of injury followed by lucid injury.
  • Developing stupor, ipsilateral dilated pupil and contralateral hemiparesis.
  • Coning
  • Raised ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Extradural haemorrhage Ix

A

1) CT head - hyper dense lenticular mass
2) Skull XR for fracture
3) bloods - FBC and coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Extradural haemorrhage Rx

A

1) ABCDE

2) Neurosurgery - decompressive craniotomy

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

Patient - Old man, pill rolling tremor, narrow suffering gait and slow like a tortoise. Keeps kicking his wife in bed and can’t smell how bad his feet smell.

A

Parkinson’s disease

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

PD Aetiology

A
  • Unknown
  • Mixed genetics and environmental
  • Oxidation hypotheses
  • PARK gene
48
Q

PD pathology

A
  • loss of pigmented dopaminergic neurones in the substantia nigra and the presence of lewy bodies.
  • Loss of dopaminergic neurones lead to decreased movement .
49
Q

PD Presentation

A
  • Tremor
  • Bradykinesia
  • Rigidity
  • Anosmia
  • Depression
  • Lack of expression
  • Autonomic issues; urinary urgency and hypotension
  • Micrographia
50
Q

Parkinson Plus

A

1) Progressive supranuclear palsy = parkinsonism + postural instability + falls + pseudo bulbar palsy + dementia
2) Multiple system atrophy = Autonomic Sx + ataxia + Parkinsonism

51
Q

PD Ix

A

1) Clinical

2) DAT scan

52
Q

PD Rx

A

1) Urgent neurology referral
2) Education
3) Dopamine replacement w/ levodopa combined w/ a dopa decarboxylase inhibitor (co-beneldopa or co-careldopa)
4) Deep brain stimulation

53
Q

Epilepsy Aetiology

A
  • Idiopathic
  • Mass lesions
  • Vascular changes
  • Neurodegeneration
  • Drugs and alcohol
54
Q

Epilepsy Pathology

A
  • Sudden synchronous discharge of cerebral neurones causing signs or symptoms apparent to the patient or/and observer
  • Abnormalities in ion channels which influence neurotransmitters and cause aberrant firing.
  • Triggers = sleep deprivation, alcohol, drugs, strobe lights
55
Q

Epilepsy presentation

A
  • Prodrome
  • Aura
  • Seizure (focal, simple, complex, absence, GTCS, myoclonic, atonic)
  • Post-ictal periods of confusion
56
Q

Partial seizure - simple

A
  • Patient is conscious

- One limb jerking (jacksonian)

57
Q

Partial seizure - complex

A
  • Loss of patient consciousness

- one limb jerking

58
Q

Generalised absence seizure

A
  • often start in childhood
  • LOC and vacant expression
  • Patient doesn’t realise that any time has passed.
59
Q

Generalised tonic clonic seizure

A
  • Tonic phase (stiffness)
  • Clonic phase (limbs jerking)
  • Often w/ tongue biting and incontinence
60
Q

Generalised Myoclonic

A
  • Loss of consciousness

- Jerking or twitching only

61
Q

Generalised Atonic seizure

A
  • Drops to the ground w/ a complete loss of tone.
62
Q

Epilepsy Ix

A

1) Bloods - including calcium
2) ECG
3) MRI brain for mass lesion
4) EEG
5) Drug screen and hx

63
Q

Epilepsy Rx

A

1) ABCDE
2) Anti-epileptic drugs;
GTCS = Valproate, lamotrigine, carbamazepine, topiramate Focal = carbamazepine, lamotrigine.
Myoclonic = Valproate. Absence = Valproate

64
Q

Status epilepticus

A

Early <30min - O2 + ECG/BP + Bloods + Lorazepam IV 4mg and repeat if needed.
Established status 30-90min - phenytoin 15mg/kg IV
Persisting status - Phenobarbital 10mg/kg IV or valproate 25mg/kg
Still persisting - RSI and intubation.

65
Q

Patient - Sudden loss of neurological function (dropping face + arm weakness) only lasts a few mins and fully resolves

A

TIA

66
Q

Patient - sudden loss of neurological function (drooping face, weak arm and slurred speech) persisting over 24hrs

A

Stroke

67
Q

CVA aetiology

A
  • Atherosclerotic disease
  • AF
  • RF’s = HTN, smoking, alcohol, high cholesterol, AF, obesity
68
Q

CVA Pathology

A
  • Either brief or persistent downstream ischemia following embolus or haemorrhage.
  • Neuronal death and loss of function.
  • Transient (TIA) or persistent (stroke)
69
Q

CVA Presentation

A
  • SUDDEN loss of function.
  • Carotid system = amaurosis fugax, aphasia, hemiparesis, sensory loss and hemianopic visual loss.
  • Vertebrobasilar system = Diplopia, vertigo, chocking, ataxia.
70
Q

CVA Ix;

A

1) Clinical judgement
2) CT or MRI to assess damage
3) ECG
4) Bloods including; FBC, COAG, culture
5) Carotid artery Doppler

71
Q

CVA Rx

A

1) ABCDE
2) Thrombolysis (window 4.5hrs) - alteplase
3) 300mg aspirin if not apt for thrombolysis.
4) Haemorrhage - control BP and refer to neurosurgery.
5) stroke rehab
6) TIA = Clopidegrel and statins for life.

72
Q

Patient - Middle aged woman, increasing tiredness throughout the day, evening double vision and slurring of the speech. This is worse w/ repeated movements.

A

Myasthenia Gravis

73
Q

Patient - receiving therapy for small cell bronchial carcinoma, foot weakness which improves w/ exercise and use.

A

Labert eaton

74
Q

MG Aetiology

A
  • Acquired
  • Causes unknown
  • Associated w/ thymoma or thymic hyperplasia
  • Associated w/ other autoimmune disease.
75
Q

MG pathology

A
  • Antibodies to ACH receptor proteins are found.

- Immune complexes on the post-synaptic membrane prevent ACH binding at the NMJ.

76
Q

MG presentation

A
  • Fatigability of actions and reflexes.
  • Proximal limbs, extraocular muscles, facial muscles.
  • Fluctuating and fatiguable weakness.
  • Can effect resp muscles.
77
Q

MG Ix

A

1) Serum anti-ACHr antibodies and anti-MUSK
2) Repetitive nerve stimulation leading to weakness.
3) Tensilon test - immediate improvement in weakness.
4) CXR for thymoma

78
Q

MG Rx

A

1) Pyridostigmine 60mg. 3-4hr duration. Inhibits ACH breakdown
2) Immunosuppression - AZA, MM
3) Thymectomy
4) Plasmapheresis + IVIG for exacerbations.

79
Q

Patient - Middle life, fidgety progressing to uncontrollable limb movements, family history, depression

A

Huntingtons disease

80
Q

HD Aetiology

A
  • CAG nucleotide repeat expansion - huntingtin
  • Toxic gain of function.
  • Anticipation phenomenon
  • AD inherited
81
Q

HD Pathology

A
  • selective neuronal loss in the neostratum, caudate nucleus and putamen.
82
Q

HD Presentation

A
  • middle life
  • Fidgetiness progressing to chorea
  • Psychiatric issues such as depression and mania.
  • Chorea is eventually replaced by parkinsonism.
  • Dysarthria and dysphagia
  • Tics and myoclonus.
83
Q

HD Ix

A

1) Clinical
2) Genetic testing for CAG
3) FHx
4) Genetic counselling

84
Q

HD Rx

A

1) Benzo, valproate etc for chorea
2) Rx depression and psych empirically
3) Nil

85
Q

Patient - Elderly, impaired memory function over a number of months/years, autobiographical memory, language, word finding w/ lack of self insight

A

AD dementia

86
Q

Patient - Elderly, visual hallucinations often small animals and people, fluctuating cognition, parkinsonism

A

LB dementia

87
Q

Patient - Step-wise cognitive decline following overt or covert CV events. Apraxic gait, pyramidal signs.

A

Vascular dementia

88
Q

Patient - Middle aged, personality change, affect blunting, inappropriate behaviour, impaired language and fluent speech. Sx of ALS

A

FTD

89
Q

Dementia Aetiology

A
  • Degenerative = AD, LBD, FTD, HD, PD, CJD
  • Vascular
  • Metabolic = Uraemia, Thiamine
  • Toxins = alcohol, drugs
90
Q

Dementia Pathology

A
  • AD = UK, amyloid plaques, neurofibrillary tangles.
  • LBD = presence of lewy bodies, associated with PD.
  • FTD = familial, TAU mutations or MND associated.
91
Q

Dementia Presentation

A
  • Memory loss
  • Cognition loss
  • Permanent not transient
  • See patient summaries for more in detail explanation of diseases.
92
Q

Dementia Ix

A

1) MMSE, MOCA, AMT
2) Bloods; FBC, TFT, B12 etc. rule out organics.
3) Psych evaluation - depression can cause pseudo-dementia
4) Brain imaging - mass lesion or brain atrophy, evidence of vascular insults.
5) Memory clinic evaluation

93
Q

Dementia Rx

A

1) General = lifestyle and continued cognitive work
2) Cholinesterase inhibitors - rivastigmine, donepezil, galantamine
2) NMDA receptor antagonist = memantine

94
Q

Patient - Young female, presents with eye pain and blurred vision, few weeks later w/ limb weakness. other Sx on questioning = vertigo, and dysphagia

A

MS

95
Q

MS aetiology

A
  • Genetics - multi-gene and complex
  • Environment - vitamin D association due to increased prevalence further from equator
  • Autoimmune
  • Viral trigger - EBV etc
96
Q

MS Pathology

A
  • Demyelination of the CNS
  • Often white matter
  • Common in optic nerves, corpus callosum, brainstem.
97
Q

MS Presentation

A
  • Varied and vague signs and symptoms
  • Visual changes (optic neuritis)
  • Sensory symptoms
  • Clumsiness
  • Urinary symptoms
  • Can be relapse and remitting, secondary progressive or primary progressive.
98
Q

MS Ix

A

1) 2 episodes disseminated in space and time
2) MRI w/ gadolinium enhancement
3) LP - CSF show oligoclonal bands IgG

99
Q

MS Rx

A

1) No cure
2) General; education, MDT
3) Rx Sx
4) Relapses - IV pred 1g daily for 3 days
5) DMD’s - Beta-interferon
6) Aggressive = Natalizumab or fingolimod (oral)

100
Q

Patient - Episodic headache. Aura (lights, sounds, feelings). Photophobia. N&V.

A

Migraine

101
Q

Migraine Aetiology

A
  • Genetics - multiple. Neuronal excitability
  • Environmental triggers;
    C - Chocolate
    H - hangovers
    O - orgasm
    C - cheese
    O - OCP
    L - lie-ins
    A - alcohol
    T - tumult
    E - exercise
102
Q

Migraine pathology

A
  • Neurogenic spreading cortical depolarisation.
  • wave of neuronal activity followed by a period of depression
  • Activation of CN5 nerves leads to headache.
103
Q

Migraine Presentation

A
  • starts around puberty w/ increasing prevalence to the 4th decade of life.
  • Headache + photophobia + N&V + aura (zig zag lines, image fragmentation, shimmering)
  • Dx criteria =
    Headache lasting 4hrs 3x monthly.
    + 2 of the following
    1) unilateral pain
    2) Throbbing pain
    3) mod to severe in intensity
    4) motion sensitivity.
    + 1 of the following
    1) N&V
    2) photophobia
104
Q

Migraine Ix

A

1) Clinical

2) Rule out other causes if suspicious

105
Q

Migraine Rx

A

1) Explain
2) Educate around triggers
3) Acute attacks = analgesia, metoclopramide (N&V), triptans
4) Suppression = propanolol, amitryptaline, valproate, topiramate

106
Q

Patient - Progressing weakness in the distal limb muscles and/or distal numbness. Following viral infection or food poisoning. Absent reflexes and the weakness in progressing proximally.

A

GBS

107
Q

GBS aetiology

A
  • Molecular mimicry post infection - CMV or
    campylobacter.
  • Monophasic - doesn’t reoccur.
108
Q

GBS Pathology

A
  • Molecular mimicry - immune system attacks the myelin as the pathogen mimics these.
  • Demyelinating.
109
Q

GBS Presentation

A
  • 1-3 weeks post infection
  • Progressive weakness and numbness in the distal muscles of a limb spreading proximally.
  • autonomic nerves involvement.
  • Resp muscles may be involved.
110
Q

GBS Ix

A

1) clinical
2) Confirmed w/ nerve conduction studies.
3) Raised CSF protein

111
Q

GBS Rx

A

1) Monitor vital capacity for rest difficulties
2) LMWH and teds
3) IVIG in the first 2 weeks can reduce severity
4) Self limiting

112
Q

Stroke thrombolysis time window

A

4.5hrs

113
Q

PPS - Progressive supra nuclear palsy

  1. Features
  2. Management
A
  • Impairment of vertical gaze (going down stairs - CN exam of ocular muscles)
  • Parkinsonism
  • Falls
  • Slurred speech
  • Cognitive impairment
  1. Poor response to L-dopa
    - Sx control
114
Q

Degenerating cervical myelopathy

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. RF = smoking due to its effects on the iV discs and high axial loading.
  2. Pain
    - Loss of motor function (dexterity, stiffness and odd gait)
    - Loss of sensory function
    - Loss of autonomic function
    - Hoffman’s sign
  3. Gold standard = MRI c spine - disc degeneration and ligament hypertrophy and cord signal change.
  4. Urgent spinal surgery assessment.
    - Damage can be permanent if not sorted ASAP.
    - Decompressive surgery is definitive.
115
Q

Valproate

  1. MOA
  2. SE
A
  1. Increases GABA activity
  2. P450 Inhibitor
    - Nausea
    - Weight gain
    - Ataxia
    - Tremor
    - Hepatotoxic
    - TTP
    - Teratogenic
116
Q

Syringomyelia

  1. Causes
  2. Features
A
  1. Dilatation of the CSF space in the spinal cord.
    - Occurs in thoracic segments and causes compression of spinothalamic tracts decussating in the anterior white commissure.
    - Arnold chiari malformation (herniation of cerebellar tonsils through the foramen magnum, congenital or acquired.)
  2. Loss of sensation of pain. temp and crude touch.
    - Cape like.
117
Q

Intracranial venous thrombosis

  1. Causes
  2. Presentation
  3. Ix
  4. Rx
A
  1. Cerebral infarction due to tissue congestion and obstruction.
    - Infections
    - Trauma
    - Pregnancy
    - COCP
    - Hypercoaguable states.
    - SLE
  2. Lateral sinus (headache)
    - Cavernous sinus (compressive Sx and nerve palsies)
    - Stroke type syndrome.
    - Headache, severe, similar to SAH.
    - Seizure
    - Impaired consciousness
    - Focal neurology.
  3. MR venogram
    - CT
    - Bloods for clotting.
  4. Similar to stroke pts.
    - Anticoagulation or thrombolysis.

Medical School Finals (24 decks)

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