2.2 Space Occupying Lesions Flashcards
Outline some different types/causes of space-occupying lesions
- Cerebral oedema
- Haematoma
- Malignant tumours
- Non-malignant lesions
- Generalised swelling
- Increased vascular volume
- Increased CSF volume
Describe the mechanics of how CSF enters into the dural venous sinus
Arachnoid granulations have arachnoid villi, which are one-way valves. When pressure is ~3-5mmHg greater in CSF, they open, and resorption occurs.
Differentiate communicating vs non-communicating hydrocephalus
Comm: No blockage in ventricular system; prevention blockage elsewhere (usually a problem with resorption, sometimes production)
Non-Comm: Blockage within ventricular system
Triad of symptoms associated with normal pressure hydrocephalus
- Gait impairment
- Cognitive decline
- Urinary incontinence
Describe the pathogenesis of acute vs slow-onset non-communicating hydrocephalus
Acute: Intraventricular bleed; sudden blockage
Slower: Tumour, other more incremental blockage
List some causes of non-communicating hydrocephalis
- Aqueductal stenosis
- Tumours/masses
- Infection
- Haemorrhage/haematoma
True or false: in most patients, the temporal horns of the lateral ventricle are invisible on brain CT.
This is true; in younger patients, visibility could indicate hydrocephalus
What is the acute treatment for hydrocephalus?
External Ventricular Drain
Describe the more long-lasting treatment for non-communicating hydrocephalus
Ventriculo-peritoneal shunt. CSF is reabsorbed by the peritoneal membrane.
True or false: neoplasm means cancer
- False
- Neoplasm = new growth = tumour
What are the two components of a tumour?
Parenchyma: neoplastic versions of previous, functioning cells
Stroma: host-derived connective tissue and blood vessels (provides structure for tumour)
Summarise benign vs malignant tumours
- Benign slow growing, malignant fast
- Benign no metsastatic potential, malignant metastatic potential
- Benign well differentiated, malignant not well differentiated
- Benign contained, malignant not contained
What does it mean if a neoplasm is “differentiated”?
Well differentiated resemble mature, original cells. Maintain some function, have little mitotic activity.
Poorly differentiated have less resemblance to mature cells. More mitotic activity (may grow out of control)
How long does it take for a benign tumour to progress into a malignant tumour.
- Trick question.
- Malignancy is an innate attribute, not a step in a pathway
Benign tumours can cause serious pathology, such as…
- Obstruction
- Compressing on surrounding tissues and nerves (e.g. brainstem)
- Potential for ulceration/haemorrhage
True or false; benign tumours are typically surrounded by a fibrous capsule
True
Outline the pathology of malignant tumours
- Actively destroy tissue (incl. vital structures)
- Obstruction
- Systemic cachexia
Describe the macroscopic appearance of a malignant tumour
- Poorly defined margins
- Can have areas of necrosis/haemorrhage
Primary vs secondary tumour
1°: Original tumour
2°: Result of metastasis
What is metastasis?
- “Next placement”
- Cells detach from 1° tumour, and move through blood, lymph or cavity to 2° area
List some mutations that a tumour must undergo before undergoing metastasis
- Detach from 1° tumour
- Be mobile
- Gain access to means of spreading (blood/lymph/cavity)
- Stimulate angiogenesis
- Adhere to new tissue
etc.
Metastasis vs direct invasion
Metastasis: Cells detach, and start growing at a site distant to origin
Direct invasion: Occurs as extension of original tumour (no detaching)
Cancer cells ___ the basement membrane
Cross through
List some common sites of metastasis
- LLBB (large blood supply)
- Liver
- Lung
- Bone
- Brain
When cells metastasise, do they take the appearance of cells of the new tissue?
No
(Like invasive colonisers)
Tumour suffixes
Benign: -oma
Malignant: -sarcoma (mesoderm), -carcinoma (other 2 layers)
True or false: a melanoma that metastasizes to the brain is now a brain tumor
- False
- It is still a melanoma; a secondary tumour
List some characteristics of cancer
- Self-sufficient growth signals
- Ignore antigrowth
- Evasion of apoptosis
- Limitless replicative potential
- Tissue invasion/metastasis
How do cancer cells have unlimited replicative potential?
Active telomerase enzyme enables replenishing of telomeres
What are some properties of all cancer cells that enable them to metastasise?
- Lytic enzymes
- Decreased cell adhesion
- Increased motility
- Expression of comp. adhesion molecules
In what ways can cancer cells avoid detecion by tumour-specific T cells
- Immuno-suppressive cytokines
- Lack of presentation of tumour on MHC Class 1 (no MHC, or no antigen)
Why do tumours need blood supply?
- Nutrients/oxygen
- Growth factors
- Haematogenous spread
What are the two prognostic indicators of cancer cells called? How do we determine them?
Grade: Macroscopic differentiation (G1/G2 well diff; G3/G4 poor diff)
Stage: Size, depth, degree of spread
What are the three kinds of glial tumours?
- Astrocytoma
- Oligodendroglioma
- Ependymoma
What are the presenting features of a brain tumour?
- Headaches associated with raised ICP
- Seizures (especially development of epilepsy in adult)
- Focal neurological defecit
What are the most common primary brain tumours in adults?
Astrocytoma (80%)
Describe the AMEN criteria for astrocytoma, and it’s relation to grading
AMEN = Atypia, Mitoses, Endothelial proliferation, necrosis
Atypia alone = Grade II
+ Mitoses = Grade III
+ Necrosis +/- endothelial proliferation = Grade IV
(Technically, AMNE; the pope isn’t as smart as we thought…)
Primary vs secondary glioblastoma
Primary: always glioblastoma
Secondary: progressed from grades II or III
Which type of glial tumour cannot be diagnosed without a loss of heterozygosity of 1p and 19q?
Oligodendroglioma
What differentiates a Grade II from a Grade III oligodendroglioma
- Increased atypia and mitotic activity
- Necrosis and endothelial proliferation are still possible (unlike astrocytomas, where this would be Grade IV)
(Remember: these are the only two grades of oligodendroglioma, whereas astrocytoma have 2, 3, and 4)
Where do ependymomas more commonly arise in children vs adults?
Children: 4th ventricle
Adults: spinal canal
Most ependymomas are ___ differentiated and are classified as WHO Grade __
Well-differentiated. Classified as WHO Grade II.
Ependymomas commonly present alongisde ____
Hydrocephalus (blockage of CSF)
IDH1 mutations are diagnostic criteria for oligodendroglioma, and are associated with ____ prognosis in other glial tumours
Better.
