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Year 2 > NEURO: Primary Brain tumours, Meningitis, Encephalitis and Zoster Hepres > Flashcards

NEURO: Primary Brain tumours, Meningitis, Encephalitis and Zoster Hepres Flashcards

1
Q

What are primary tumours

A

Tumour growing at the anatomical site where tumour progression began + proceeded to form a cancerous mass

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2
Q

What is the telencephalon

A

Cerebral hemispheres

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3
Q

What is the mesencephalon

A

Midbrain

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4
Q

Role of glial cells

A

Maintain homeostasis
Support and protection for neurones
Form myelin

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5
Q

Name 4 glial cells

A
  1. Oligodendrocytes
  2. Astrocytes
  3. Ependymal cells
  4. Microglial
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6
Q

Role of astrocytes

A

Form BBB

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7
Q

Role of microglia

A

Resident macrophages of CNS

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8
Q

What are glial cell carcinomas called

A

Gliomas - malignant by the time they are diagnosed

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9
Q

Role of the pineal gland

A

Produces Melatonin which modulates sleep patterns

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10
Q

Name 4 primary tumours of the brain

A

Anaplasia
Atypic
Neoplasia
Necrosis

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11
Q

What is anaplasia

A

Loss of DIFFERENTIATED cells

Total loss of control over normal function

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12
Q

How do cells become anaplastic

A

Neoplastic tumour cells dedifferentiate to become anapaestic

Cancer stem cells over multiply (uncontrolled growth due to failure of differentiation)

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13
Q

What is Atypia

A

Cancer cells with structural abnormalities

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14
Q

What is neoplasia

A

Uncontrolled division of cells

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15
Q

How do neoplasms effect the brain

A

Grow in confined spaces increasing ICP and invading into the brain as they grow in small spaces - compression of brain structure

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16
Q

Consequences of neoplastic growth

A

ICP

Destruction of brain parenchyma

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17
Q

In what patients are primary brain tumours common

A
  1. Paediatric cancer
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18
Q

What are the main types of gliomas

A
  1. Astrocytoma (MOST COMMON PRIMARY BRAIN TUMOUR)

2. Oligodendroglioma

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19
Q

Risk factors for primary brain tumours

A
  1. Ionising radiation
  2. Vinyl Chloride
  3. Immunosuppreison
  4. Family History - Genetics
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20
Q

Name Grade I astrocytoma

A
  1. Pilocytic astrocytoma

2. Subependymoma

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21
Q

`characteristics of grade I astrocytomas

A
  1. Slow growing tumours where total remission is achieved by removal (stereotactic surgery)
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22
Q

Characteristic of grade II astrocytomas

A

Slow growing benign to malignant tumours

Invasive gliomas that penetrate into surrounding brain (CAN’T be surgically removed)

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23
Q

Name a grade II astrocytoma

A
  1. Fibrillary astrocytoma
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24
Q

Clinical presentation of grade II astrocytoma

A
  1. SEIZURES
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25
Q

Name a grade III astrocytoma

A

Anapaestic astrocytoma

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26
Q

Characteristics of grade III astrocytomas

A

Astrocytes lack vascular proliferation and necrose (These are undifferentiated gliomas)

MALIGNANT

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27
Q

How are grade III astrocytomas

A
  1. Radiotherapy
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28
Q

Name a grade IV astrocytomas

A

Glioblastoma multiform

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29
Q

Characteristics of grade IV astrocytomas

A

MALIGNANT tumours

Grow quickly and spread to other parts of the brain

So infiltrative no surgical removal of tumour impossible + RADIOTHERAPY doesn’t work

Necrosis

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30
Q

Symptoms of grade IV astrocytomas

A

BEGIN abruptly with seizures

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31
Q

What do all gliomas progress to at end-stage cancer

A

Glioblastoma Multiforme (EXCEPT pilocytic astrocytoma)

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32
Q

Clinical presentation of brain gliomas

A
  1. Headaches
  2. Vomiting
  3. Seizures
  4. Cranial nerve disorders
  5. PAPILLOEDEMA

——-INCREASED ICP symptoms——

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33
Q

Clinical presentation of spinal cord gliomas

A
  1. Pain
  2. Weakness
  3. Numbness
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34
Q

How do gliomas metastasise

A

Spread via the CSF

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35
Q

What causes malignant gliomas

A

(50-60)

  1. Initial genetic error in glucose glycolysis
  2. Mutation of ISOTRATE DEHYDROGENASE
  3. Excess build up of 2-hydroxyglutarate

This triggers instability in glial cells and oevrmitosis

OR (older)

CATASTROPHIC GENETIC MUTATION which is sporadic

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36
Q

Clinical presentation of oligodendromas

A
  1. Seizures of the frontal lobe
  2. Increased ICP symptoms
  3. Visual loss, motor weakness and cognitive decline
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37
Q

What grade cancer are oligodendromas

A

II

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38
Q

What causes oligodendromas

A

IDH-1 mutation

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39
Q

In what dura layer are meningiomas made

A

Arachnoid mater: push into brain but are usually benign

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40
Q

What are neurofibromas

A

Solid benign tumours form Shwann cells

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41
Q

Where are neurofibromas found

A

Cerebellopontine angle

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42
Q

What are craniopharyngiomas

A

Brian tumour from pituitary gland embryonic tissues

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43
Q

Where are craniopharyngiomas common

A

Children

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44
Q

Are crnaiopharyngiomas benign or malignant

A

Benign

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45
Q

If Primary brian tumours are benign how can they cause damage

A

Act as SPACE OCCUPYING LESIONS which increase ICP

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46
Q

Why is there no symptoms when tumour is small

A

Initially brain removes CSF from ventricles and spinal cord to offset increase in ICP

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47
Q

How does ICP affect brian structures

A

Midline structure shift and herniation through foramen magnum = brain damage

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48
Q

Symptoms of ICP associated headaches

A
  1. WORSE on waking in the morning (we don’t pee at night so accumulation of fluid = ICP)
  2. Pain can be so bad it can wake patient up
  3. Pain increased by coughing, straining and bending forwards (increased venous pressure in brain)
  4. Relieved by vomiting (reduces fluid levels)
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49
Q

Is papilloedema bilateral or unilateral

A

BILATERAL

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50
Q

What causes papilloedema

A

Increased ICP
Resp failure!
Guillain-Barre syndrome due to increased protein levels
Tumours of frontal lobe

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51
Q

What is papilloedema

A

Optic disc swelling

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52
Q

Clinical presentation papilloedema

A
  1. Venous engorgement
  2. Haemorrhages over optic disc
  3. Blurring of optic margins
  4. Enlarged blind spot on examination
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53
Q

Pathophysiology of papilloedema

A

Optic nerve sheath is continuous with subarachnoid space of the brain so increased ICP is transmitted through this sheath

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54
Q

how long does it take for papiloedema to present

A

DAYS

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55
Q

Clinical presentation of tumours affecting different parts of the brain

A 
Temporal - Dysphagia, amnesia
Forntal: Hemiparesis, personality change, brook's dysphagia, lack of initiative, unable to plan tasks
Parietal lobe: Hemisensory loss, reduction in 2-point discrimination, dysphagia, astereognosis (unable to recognise object from touch alone)
Occipital: Contralateral visual defects
Cerebellum: DASHING 
D - Dysdiadochokinesis
A - Ataxia
S - Slurred speech (dysarthria)
Hypotonia
Intention tremor
Nystagmus
Gait abnormality
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56
Q

What seizures are common with brian tumours

A

PARTIAL or FOCAL

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57
Q

Differential Diagnosis of primary brain tumours

A
  1. Aneurysm
  2. Abscess
  3. Cyst
  4. haemorrhage
  5. Idiopathic intracranial hypertension
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58
Q

Diagnostic of primary brain tumours

A
  1. EEG
  2. MRI and CT (looks at disruption of BBB)
  3. FBC
  4. BIOPSY
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59
Q

Why does tumour of the frontal lobe cause site loss and what kind of hemianopia is this

A

COMPRESSION of optic chiasm

Causes bilateral temporal visual field defect

60
Q

How do carry out a biopsy for primary brian tumours

A
  1. BURR-HOLES
61
Q

Why is lumbar puncture contraindicated in primary brain tumours

A
  1. Withdrawing CSF with presence of mass lesion causes CONING
62
Q

What is coning

A

Herniation of the brain through the foramen magnum resulting in BRAINSTEM COMPRESSION as it passes through foramen magnum

63
Q

Treatment for primary brain tumours

A
  1. ORAL DEXAMETHASONE
  2. ORAL CARBAMAZZEPINE (anticonvulsant)
  3. Chemotherapy
64
Q

Why is oral dexamethasone given for primary brain tumours

A
  1. Rapidly improves brain performance and reduces inflammation caused
65
Q

Why is dexamethasone not given after 2:00

A

Keep patient awake

66
Q

Chemotherapy for gliomas

A
  1. TEMOZOLOMIDE
67
Q

Where are the most common neoplasms to metastasise to CNS

A
  1. Non small cell lung
  2. Small cell lung
  3. Breast
  4. Melanoma
  5. Renal cell
  6. GI
68
Q

How is secondary brain tumours treated

A
  1. Surgery
  2. Radiotherapy
  3. Chemotherapy
  4. Palliative therapy
69
Q

What is meningitis

A

Acute inflammation of the meninges (dura, arachnoid and pia)

70
Q

What causes meningitis

A

Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenza

71
Q

Clinical presentation of meningitis

A
  1. SEVERE headache
  2. Neck stiffness due to increased muscle tone)

TRIAD:
High Fever
Altered mental health
RIGIDITY

  1. Photophobia
  2. Photophobia
    (children just look irritable and don’t suffer from 3 and 4)
  3. POSITIVE Kerning’s sign and Brudzinski’s sign
6. Signs of increased ICP:
Papilloedema
Headaches
Fevers
Malaise
  1. Patient is irritable
72
Q

How is Kerning’s sign tested on a patient

A
  1. Patient lies supine and flexes hip and kneed to 90 degrees

POSITIVE - pain limits passive extension of the knee

73
Q

How is Brudzinski’s sign tested on a patient

A
  1. Flexion of the neck causes flexion of knee and hip
74
Q

How can Neisseria meningitidis be differentiated from other forms of meningitis

A
  1. Rapidly spreading petechial rash which precedes the symptoms that is NON-BLANCHING (redness does not disappear when pressed) + purpuric skin rash
75
Q

What is a petechial rash

A
  1. Irregular purple or red spots on trunk, lower extremities, conjunctiva and palms or soles
76
Q

Clinical presentation of viral meningitis

A

1, Genital Herpes

  1. Hand
  2. Foot and Mouth disease
77
Q

How is neisseria meningitidis spread

A
  1. DROPLET SPREAD
78
Q

What causes meningitis in pregnant women

A

LISTERIA MONOCYTOGENES found in cheese (why they are told to avoid) and transmitted to baby

79
Q

Neonatal cause of meningitis

A
  1. E.coli (found in digestive system of pregnant women)
  2. Cryptococcus neoformans
  3. TB
  4. HIV
  5. Hepres simplex virus
  6. B-Haemolytic streptococcus which usually inhabit vagina
80
Q

Risk factors of meningitis

A
  1. Spinal canal drug administration
  2. Immunocompromised (FUNGAL)
  3. Elderly
  4. Pregnant
  5. Bacterial endocarditis
  6. Crowding
  7. Diabetes
  8. Malignancy
  9. IV drug abuse (FUNGAL)
81
Q

Pathophysiology of staph, pseudomonas and gram-negative bacterial meningitis

A
  1. Skull trauma allows nasal cavity bacteria to enter meningeal space (meningococcal septicaemia)
82
Q

Clinical presentation of meningococcal septicaemia

A
  1. Petechial rash (purpuric skin rash) + signs of sepsis

Pia-arachnoid is congested with polymorphs forming a layer of pus which organise to form adhesions causing cranial nerve palsy and hydrocephalus

83
Q

How does TB cause meningitis

A

Crosses BBB and forms small subpial focus

Becomes a rich focus (large sized granuloma) and ruptures = meningitis

Viscous green-grey exudate covering brain

84
Q

How is TB meningitis diagnosed

A

LUMBAR PUNCTURE

NAAT

85
Q

Viral causes of meningitis

A
  1. Herpes simplex virus
  2. Enteroviruses
  3. Mumps
86
Q

Fungal cause of meningitis

A

Cryptococcus neoformans

87
Q

Clinical presentation of viral caused meningitis

A
  1. NO pus formation with lymphocytic infiltration

NO cerebral oedema unless encephalitis develops

88
Q

Complications of meningitis

A
  1. DIC
  2. Gangrene
  3. Sepsis features
  4. Waterhouse-Friderichsen syndrome due to bleeding of adrenal glands
  5. Herniation through skull base
  6. Focal seizures
  7. Loss of consciousness
  8. Hearing loss
  9. ENCEPHALITIS
89
Q

What is Waterhouse-Friderichsen syndrome

A

Haemorrhage of adrenal glands = failure due to meningococemia

Organ failure
Low BP
Shock
DIC with widespread purport seen

90
Q

How long does viral meningitis last

A

4-10 days

91
Q

What causes chronic meningitis

A

Mycobacterium tuberculosis

92
Q

Differential diagnosis of meningitis

A
  1. Aseptic meningitis (tumour)
  2. Sub-arachnoid haemorrhage (headache more sudden)
  3. Encephalitis
93
Q

Diagnosis of meningitis

A
  1. BLOOD TEST/CULTURE FIRST
  2. Lumbar puncture (CSF PCR for viruses!!! - Culture for bacteria!!!)
  3. Throat swabs
  4. Pneumococcal serum PCR
94
Q

CSF findings in different causes of meningitis

A

Bacterial (acute): Low Glucose, High protein

Acute viral: Normal glucose, Normal protein

TB (chronic): Low Glucose, High Protein

Fungal: Low Glucose, High Protein

Malignant: Low Glucose, High Protein

95
Q

What should FBC show for meningitis

A
  1. Hyponatreamia common due to ADH over-porudction and too much IV fluid administration
96
Q

How do we test CSF for bacterial and listeria causes of meningitis

A

CULTURE it do not gram stain as it isn’t specific

97
Q

Treatment of bacterial meningitis

A
  1. Treatment using Empiric antibiotics (Cefalosporins like cefotaxime)
    Ampicillin - Listeria monocytogenes
  2. Corticosticostreoids (DEXAMETHASONE) to reduce cerebral oedema
  3. IV vancomycin in return travellers
98
Q

How long should TB meningitis be treated for

A

A year (compared to 6 months lung TB)

99
Q

Prophylaxis of meningitis

A
  1. ORAL CIPROFLOXACIN stat
100
Q

Complications of meningitis treatment

A

Hearing loss
Seizures
Developmental problems

101
Q

How is meningococcal septicaemia treated

A

IV BENZYLPENICLLIN immediately or IV CEFOTAXIME in hospitals

102
Q

When is lumbar puncture contraindicated

A
  1. Mass or abscess present
  2. ICP raised
  3. MENINGOCOCCAL SEPSIS as it causes coning of cerebellar tonsils
103
Q

What is encephalitis

A
  1. Inflammation of the brain
104
Q

Viral causes of encephalitis

A

HERPES SIMPLEX VIRUS
RABIES
POLIOVIRUS
MEASLES

105
Q

How does Herpes Simplex Virus cause encephalitis

A

1, Transmission of virus from peripheral site on face following HSV-1 reactivation along nerve axon, to the brain
2. Virus lies dormant in GANGLION of trigeminal cranial nerve

106
Q

Bacterial causes of encephalitis

A
  1. Bacterial meningitis
  2. Syphilis
  3. TB
  4. Malaria
107
Q

Risk factors of encephalitis

A

1, HIV

2. Immunocompromised

108
Q

What lobes of the brain are affected in encephalitis

A

Frontal and temporal lobes mainly but affects the whole brain

109
Q

Clinical presentation of encephalitis

A
  1. Consciousness decrease
    TRIAD: Fevre, headache and altered mental status
  2. Viral infection signs
  3. Seizures
  4. Raised ICP (papilloedema)
  5. Focal neurological deficit (hemiparesis and dysphagia)
  6. Coma

SIGNS OF MENINGITIS if caused in meaning-encephalitis

110
Q

Differential diagnosis of Encephalitis

A
  1. Meningitis
  2. Stroke
  3. Brain Tumour
111
Q

Diagnostics of Encephalitis

A
  1. MRI
  2. EEG
  3. Lumbar Puncture
  4. FBC
112
Q

Role of MRI in Encephalitis

A
  1. Shows area of inflammation and swelling of temporal lobes in HSV encephalitis
  2. May be midline shifting due to raised ICP
113
Q

Role of EEG in encephalitis

A
  1. Shows periodic sharp and slow wave complexes
114
Q

Role of lumbar puncture in Encephalitis

A
  1. CSF shows elevated lymphocyte count
  2. CSF PCR for viral detection (herpes simplex virus)
  3. FBC and CSF serology
115
Q

Treatment of encephalitis

A
  1. ANTI-VIRAL treatment - IV ACYCLOVIR before investigation
  2. Anti-seizure medication (PRIMIDONE)
  3. IM BENZYLPENICILIN if meningitis is suspected

BENXYLPENICILLIN is the emergency drug for meningitis

116
Q

What is Herpes Zoster virus

A
  1. Reactivation of varicella zoster virus - chickenpox in the dorsal root ganglia
117
Q

What is the significance of shingles developing

A
  1. Decline in cell-mediated immunity such as age
118
Q

Risk factors of shingles

A
  1. Increasing age
  2. Immunocompromised
  3. HIV, Hodgkin’s lymphoma and bone marrow transplants
119
Q

What happens when virus in dorsal root ganglia are activated

A

travels down affected nerve via sensory root in dermatomal distribution over 3-4 days

CAUSES perineurial and intramural inflammation

120
Q

In HIV patients where is site of reactivation of Herpes Zoster found

A

Thoracic nerves and trigeminal nerve

121
Q

When can a person with shingles cause chicken pox in another person

A

if they have a weeping shingles rash

122
Q

Clinical presentation of Herpes Zoster

A
  1. Pain and paresthesiae in dermatomal distribution priced rash (if thoracic then chest and abdo)
  2. Malaise, myalgia, headache and fever
  3. Rash - papules and vesicles restricted to the same dermatome
  4. Neuritic pain
  5. Crust formation and drying over next week (takes 2-3 weeks to resolve)
  6. RASH does not extend out of dermatome
123
Q

Differential diagnosis of herpes zoster

A
  1. Initial pain in chest or abdo could be cholangitis or renal stones
  2. Cluster headaches or migraines
  3. Atopic eczema, contact dermatitis or herpes simplex/impetigo
124
Q

Diagnosis of herpes zoster

A
  1. Eruption of rash is diagnostic
125
Q

Treatment of herpes zoster

A

IMMEDIATE ANTIVIRAL TEHRAPY
1. Oral ACICLOVIR X5 DAILY
Done to minimise risk of peripheral herpetic neuralgia

Topical antibiotic treatment for secondary bacterial infection

Analgesics

126
Q

Complications of herpes Zoster

A
  1. ophthalmic branch of trigeminal - SIGHT
  2. Post herpetic neuralgia (pain lasting more than 4 months after shingles, burning pain and does Not respond to analgesics)
127
Q

How is PNH treated

A
  1. Antidepressant (AMYTRYPTYLINE)
  2. GABAPENTIN - anti eplieptic)
  3. ORAL CARABMAZEPINE (anti-convulsant)
128
Q

What is the main outcome of cerebellar dysfunction

A

ATAXIA

129
Q

What ion channels are found in purkyne cells

A

Calcium ion channels

130
Q

Clinical presentation of cerebellar ataxia

A
  1. Staccato speech
  2. Choking bouts
  3. Oscillopsia
  4. Clumsiness
  5. Action Tremors
  6. Loss of fine movement
  7. Unseatdiness when walking (worse in dark)
  8. Stumbles and falls
131
Q

What is staccato speech

A

SLURRING

132
Q

What is choking bouts

A

Swallowing difficulties

133
Q

What is oscillopsia

A

Visual disturbances where objects tend to vibrate

134
Q

How do we examine cerebellar ataxia

A
  1. Gait
  2. Limb ataxia (truncal, limb and gait ataxia)
  3. Eye movements (nystagmus)
  4. Speech (dysarthria)
  5. Sensory ataxia
135
Q

What is mild ataxia

A

Only one walking aid needed for independent movement

136
Q

What is moderate ataxia

A

Mobilised and needs a walking frame

137
Q

What is severe ataxia

A

Wheelchair dependant

138
Q

What ways can cerebellar disorders be inherited

A
  1. Recessive
  2. Dominant
  3. Mitochondrial
  4. X-linked
139
Q

Example of autosomal recessive ataxia

A

Friedrich’s ataxia

Ataxia of gait and limb - absent reflexes

140
Q

Example of autosomal dominant ataxia

A
  1. Spinocerbellar ataxia 6

Slowly progressive form 40

141
Q

What toxicities can cause ataxia

A
  1. Alcohol
  2. Phenytoin
  3. Lithium
142
Q

Examples of immune-mediated cerebellar disorder

A
  1. Gluten ataxia
143
Q

Clinical presentation of neruodegerenative ataxia

A
  1. Ataxia
  2. Bulbar symptoms
  3. Resp hypoventialtion
  4. Characteristic MRI finding
144
Q

Diagnosis of cerebellar ataxia

A
  1. MRI to exclude tumours, hydrocephalus, MS etc
145
Q

What causes Friedrich’s ataxia

A

DIABETES

CARDIOMMYOPATHY

Year 2 (155 decks)

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