Week 2 Flashcards
(48 cards)
Describe potential infectious diseases of the CNS.
Meningitis: inflammation of the leptomeninges (most commonly arachnoid and Pia mater) 4 agents: bacterial, viral, parasitic and fungal. streptococcus pneumoniae and neisseria meningitidis being the most common bacteria. Herpes simplex or HIV being the most common viruses
Encephalitis: inflammation of brain parenchyma. Can be caused by bacterial, viral, parasitic and fungal agents. Most common agent - herpes simplex virus.
Cerebral abscess: collection of pus in the brain often caused by bacterial or fungal infection. Can develop from infections elsewhere or direct spread from nearby areas such as sinuses or ears.
Clinical features of meningitis (and key triad)
Key triad:
Fever
Nuchal rigidity - stiffness in neck muscles
Altered mental - confusion/decreased conciousness
Other symptoms:
Nausea - due to increased ICP
Vomiting - due to nausea and raised ICP
Photophobia - dislike of bright lights
Clinical features of encephalitis
Headache - brain inflammation and raised ICP
Nausea/vomiting - irritation of brain + raised ICP
Seizures - abnormal electrical activity
Focal deficits - neurological impairments.
Investigations for meningitis and encephalitis
LP - abnormalities in CSF such as glucose (bacterial meningitis), proteins (viral meningitis)
CBE - markers indicative of infection. High WBC, CRP
Serology - identify a bacterial, viral and/or fungal infective agents.
CT - brain abnormalities (non-infective) such as abscesses, haemorrhage, or mass lesions
MRI - identify inflammation, lesions etc. detailed.
EEG - detect abnormal electrical activity in brain. May be present in encephalitis, can differentiate from other conditions.
Pathophysiology of bacterial meningitis
Most often caused by streptococcus pneumoniae bacteria. Pathophysiology can change depending on bacterium. CLIN features most severe in bacterial.
Bacteria enter subarachnoid space —> bacterial replication/bacterial lysis?
—> Release of inflmmatory mediators + neutrophils recruited to site of bacterial infection = increased in BBB permeability —> albumin enters the brain —> cerebral oedema
Complications of meningitis
Cerebral oedema - abnormal accumulation of fluid within brain. Raises ICP. Can be life threatening.
Hydrocephalus - abnormal build up of CSF in the ventricles. Raised ICP and enlarged ventricles.
List different space occupying lesions
Non-neoplastic lesion: haemorrhage, abscess, swollen infarct, benign meningeal tumour.
Malignant tumour: primary or secondary.
Generalised swelling: vasogenic oedema, cytoxic oedema.
Increased vascular volume: high partial pressure of CO2 (pCO2)
Increased CSF volume: obstructive hydrocephalus
Clinical features of space occupying lesions
Headache - non-neoplastic lesion, malignant tumour, generalised swelling, increased CSF volume.
Focal neurological deficits - malignant tumour, swelling, increased vascular volume
Seizures - malignant tumour, swelling, increased CSF
Impaired cognition - malignant tumour, swelling
Nausea/vomiting - non-neoplastic lesion, malignant tumour, swelling, increased CSF volume
Papilloedema (optic disc swelling) - malignant tumour, swelling, increased CSF volume
Motor weakness - generalised swelling, increased CSF volume.
Investigations for space occupying lesions
MRI - non invasive, magnetic fields, detailed cross sectional images of brain anatomy
CT - x ray based imaging provided cross sectional views of the brains structure.
Cerebral angiography - injection of contrast dye into blood vessels to visualise and assess vascular abnormalities
Positron emission tomography (PET) - detects metabolic activity aiding in distinguishing between benign and malignant brain lesions
Pathogenesis of hydrocephalus
Abnormal accumulation of CSF within brains ventricles due to imbalance between production and absorption of CSF. Can occur as result of various factors including CSF flow, impaired absorption in arachnoid villi or overproduction of CSF.
Classification of hydrocephalus
Communicating:
Impaired CSF absorption or circulation within subarachnoid space, often caused by conditions such as meningitis, subarachnoid haemorrhage or arachnoid scarring.
Non-communicating:
Obstruction within ventricular system hindering CSF flow, typically caused by conditions such as congenital aqueduct stenosis, tumours, or cysts obstructing.
Idiopathic:
Hydrocephalus of unknown cause. Possibly related to abnormalities with CSF production or absorption mechs. Occurs without identifiable underlying cause.
Treatment of hydrocephalus
External ventricular drain - catheter inserted through skull into lateral ventricle to drain CSF.
Remove obstruction - surgical means to clear blockages in pathway of CSF
Ventriculo-peritoneal shunt - implantation of device to redirect excess CSF from brains ventricles to the peritoneal cavity
Endoscopic third ventriculostomy - surgical creation of new pathway for CSF to bypass obstructions
Pharmacological treatment - acetazolamide, diuretics, corticosteroids
Differentiate between benign and malignant tumours
Benign: tumour that is contained, non invasive, well-differentiated and slowly grows
Malignant: tumour that is not contained, invasive, poorly differentiated, faster growing
In situ: tumour confined to site of origin without invading surrounding tissues
What is a neoplasm (tumour)?
Caused by alterations in cellular genome; they do not respond to normal signals that control growth.
Cells proliferate excessively in a poorly regulated manner, forming a lump or tissue mass.
These changes are permanent and non reversible.
Differentiate between primary and secondary tumours
Primary tumour:
An initial abnormal growth originating from the tissue in which it develops.
Secondary tumour:
Abnormal growth formed from the spread of cancer cells from a primary tumour to distant sites within the body (metastasis)
Understand and explain tumour nomenclenture
Prefix = line of differentiation
Suffix = malignant or benign
Prefixes
Adeno- Glandular
Leiomyo- Smooth muscle
Osteo- Bone
Suffixes
-oma Benign; any origin
-carcinoma malignant; epithelial
-sarcoma. malignant; bone, cartilage, muscle
Example: adenoma - benign tumour of glandular origin, osteosarcoma - malignant tumour of bone
Describe stage vs grade of brain tumours
Grade = histological and microscopic prognostic criterion
Stage = macroscopic criterion
Describe the 4 cancer grades
Grades reflect extent to which tumour cells resemble normal cells histologically. Ranked on level of:
- resemblance to normal cells
- cytologic atypia
- mitotic activity
Well differentiated tumours closely resemble mature cells with minimal cytologic atypia, low mitotic activity and are often chategorised as G1 or G2.
Poorly differentiated tumours exhibit less resemblance to normal cells, increased cytologic atypia, higher mitotic activity, usually classed as G3 or G4. Suggests increased aggressiveness, invasiveness and metastatic potential.
Describe the 4 cancer stages
Represent progression of malignancy in terms of local spread and metastasis. Determined by:
- tumour size
- depth of invasion of primary tumour
- location of metastasis
Stages typically asses through radiological (involve scans to detect tumour hotspots seperate from primary tumour) and pathological evaluations (removal of humph nodes to determine extent of spread).
Grouped into stages I, II, III, IV indicating severity and extent of disease.
List and outline common types of brain tumours
Diffuse astrocytoma (grade 2 astrocytoma) - slow growing, originates from astrocytes.
Anaplastic astrocytoma (grade 3 astrocytoma) - more aggressive characterised by rapid growth, cellular atypia, arises from astrocytic cells.
Glioblastoma (grade 4 astrocytoma) - most common and aggressive of primary brain tumour, rapid growth, highly invasive behaviour of astrocytes
Oligodendroglioma - arises from oligodendrocytes, distinct appearance under microscope and slow growth.
Ependymomas - arises from Ependymal cells lining ventricles of brain or central canal of spinal cord. Often found in children and young adults
Describe common types of cerebral oedema, their pathogenesis and potential complications.
Accumulation of fluid in either the intracellular or extracellular spaces (or both).
2 types typically not in isolation but a continuum:
Vasogenic - increase in extracellular fluid that surrounds brain cells due to breakdown of the BBB
Cytoxic - swelling of brain cells due to an increase in the fluid in the intracellular space, generally due to failure of the ion pumps.
Describe components that drive and regulate ICP
The monro-kellie doctrine
- total volume inside the ridgid skull remains constant
“non expandable, non contractile, freely communicating space, pressure of fluid contents and the brain itself must be directly proportional to each other in order to maintain a constant pressure. If one increases, another must decrease in order to compensate”
Compensation mechanisms for ICP:
- removal of CSF: increase CSF absorption, decrease production
- venous vasoconstriction: decrease volume of blood within the venous system
- arterial vasoconstriction: decrease volume of blood within the arterial system; can result in low perfusion to the brain (BAD)
Describe potential complications of raised ICP.
- compression of vital brain structures can result in neurological deficits such as altered conciousness, focal neurological signs or even coma.
- increased ICP can impeded cerebral blood flow by compressing blood vessels, leading to ischaemia and subsequent neuronal injury.
- herniation syndromes, brain tissue is displaced into areas of the skull where it should not normally be. Further damage and compromising brain function.
- untreated ICP can do irreversible brain damage and even death.
Others: hypercapnia (high CO2 levels due to decreased perfusion), hypoxia (due to increased build up of waste), death (ICP = systolic arterial pressure, perfusion to brain ceases)
Outline common brain herniations
Subfalcine/cingulate herniation:
When the cingulate gyrus is pushed under the falx cerebri often due to unilateral hemispheric swelling.
- may compress the anterior cerebral artery leading to ischaemia of frontal lobes
Transentorial/uncal:
medial temporal lobe displaced downward through tectorial notch, compressing midbrain and leads to symptoms like ipsilateral pupil dilation (CN III compression) and contralateral hemiparesis.
Tonsillar: downward displacement of cerebellar tonsils through foramen magnum. Can compress medulla, leads to life threatening cardio resp failure
