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Medical Studies 2A > 2.2 Space Occupying Lesions > Flashcards

2.2 Space Occupying Lesions Flashcards

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USMLE® Step 1 flashcards
1
Q

Outline some different types/causes of space-occupying lesions

A
  • Cerebral oedema
  • Haematoma
  • Malignant tumours
  • Non-malignant lesions
  • Generalised swelling
  • Increased vascular volume
  • Increased CSF volume
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2
Q

Describe the mechanics of how CSF enters into the dural venous sinus

A

Arachnoid granulations have arachnoid villi, which are one-way valves. When pressure is ~3-5mmHg greater in CSF, they open, and resorption occurs.

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3
Q

Differentiate communicating vs non-communicating hydrocephalus

A

Comm: No blockage in ventricular system; prevention blockage elsewhere (usually a problem with resorption, sometimes production)
Non-Comm: Blockage within ventricular system

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4
Q

Triad of symptoms associated with normal pressure hydrocephalus

A
  • Gait impairment
  • Cognitive decline
  • Urinary incontinence
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5
Q

Describe the pathogenesis of acute vs slow-onset non-communicating hydrocephalus

A

Acute: Intraventricular bleed; sudden blockage
Slower: Tumour, other more incremental blockage

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6
Q

List some causes of non-communicating hydrocephalis

A
  • Aqueductal stenosis
  • Tumours/masses
  • Infection
  • Haemorrhage/haematoma
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7
Q

True or false: in most patients, the temporal horns of the lateral ventricle are invisible on brain CT.

A

This is true; in younger patients, visibility could indicate hydrocephalus

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8
Q

What is the acute treatment for hydrocephalus?

A

External Ventricular Drain

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9
Q

Describe the more long-lasting treatment for non-communicating hydrocephalus

A

Ventriculo-peritoneal shunt. CSF is reabsorbed by the peritoneal membrane.

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10
Q

True or false: neoplasm means cancer

A
  • False
  • Neoplasm = new growth = tumour
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11
Q

What are the two components of a tumour?

A

Parenchyma: neoplastic versions of previous, functioning cells

Stroma: host-derived connective tissue and blood vessels (provides structure for tumour)

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12
Q

Summarise benign vs malignant tumours

A
  • Benign slow growing, malignant fast
  • Benign no metsastatic potential, malignant metastatic potential
  • Benign well differentiated, malignant not well differentiated
  • Benign contained, malignant not contained
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13
Q

What does it mean if a neoplasm is “differentiated”?

A

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)

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14
Q

How long does it take for a benign tumour to progress into a malignant tumour.

A
  • Trick question.
  • Malignancy is an innate attribute, not a step in a pathway
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15
Q

Benign tumours can cause serious pathology, such as…

A
  • Obstruction
  • Compressing on surrounding tissues and nerves (e.g. brainstem)
  • Potential for ulceration/haemorrhage
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16
Q

True or false; benign tumours are typically surrounded by a fibrous capsule

A

True

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17
Q

Outline the pathology of malignant tumours

A
  • Actively destroy tissue (incl. vital structures)
  • Obstruction
  • Systemic cachexia
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18
Q

Describe the macroscopic appearance of a malignant tumour

A
  • Poorly defined margins
  • Can have areas of necrosis/haemorrhage
19
Q

Primary vs secondary tumour

A

1°: Original tumour
2°: Result of metastasis

20
Q

What is metastasis?

A
  • “Next placement”
  • Cells detach from 1° tumour, and move through blood, lymph or cavity to 2° area
21
Q

List some mutations that a tumour must undergo before undergoing metastasis

A
  • Detach from 1° tumour
  • Be mobile
  • Gain access to means of spreading (blood/lymph/cavity)
  • Stimulate angiogenesis
  • Adhere to new tissue
    etc.
22
Q

Metastasis vs direct invasion

A

Metastasis: Cells detach, and start growing at a site distant to origin

Direct invasion: Occurs as extension of original tumour (no detaching)

23
Q

Cancer cells ___ the basement membrane

A

Cross through

24
Q

List some common sites of metastasis

A
  • LLBB (large blood supply)
  • Liver
  • Lung
  • Bone
  • Brain
25
Q

When cells metastasise, do they take the appearance of cells of the new tissue?

A

No

(Like invasive colonisers)

26
Q

Tumour suffixes

A

Benign: -oma
Malignant: -sarcoma (mesoderm), -carcinoma (other 2 layers)

27
Q

True or false: a melanoma that metastasizes to the brain is now a brain tumor

A
  • False
  • It is still a melanoma; a secondary tumour
28
Q

List some characteristics of cancer

A
  • Self-sufficient growth signals
  • Ignore antigrowth
  • Evasion of apoptosis
  • Limitless replicative potential
  • Tissue invasion/metastasis
29
Q

How do cancer cells have unlimited replicative potential?

A

Active telomerase enzyme enables replenishing of telomeres

30
Q

What are some properties of all cancer cells that enable them to metastasise?

A
  • Lytic enzymes
  • Decreased cell adhesion
  • Increased motility
  • Expression of comp. adhesion molecules
31
Q

In what ways can cancer cells avoid detecion by tumour-specific T cells

A
  • Immuno-suppressive cytokines
  • Lack of presentation of tumour on MHC Class 1 (no MHC, or no antigen)
32
Q

Why do tumours need blood supply?

A
  • Nutrients/oxygen
  • Growth factors
  • Haematogenous spread
33
Q

What are the two prognostic indicators of cancer cells called? How do we determine them?

A

Grade: Macroscopic differentiation (G1/G2 well diff; G3/G4 poor diff)

Stage: Size, depth, degree of spread

34
Q

What are the three kinds of glial tumours?

A
  • Astrocytoma
  • Oligodendroglioma
  • Ependymoma
35
Q

What are the presenting features of a brain tumour?

A
  • Headaches associated with raised ICP
  • Seizures (especially development of epilepsy in adult)
  • Focal neurological defecit
36
Q

What are the most common primary brain tumours in adults?

A

Astrocytoma (80%)

37
Q

Describe the AMEN criteria for astrocytoma, and it’s relation to grading

A

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…)

38
Q

Primary vs secondary glioblastoma

A

Primary: always glioblastoma
Secondary: progressed from grades II or III

39
Q

Which type of glial tumour cannot be diagnosed without a loss of heterozygosity of 1p and 19q?

A

Oligodendroglioma

40
Q

What differentiates a Grade II from a Grade III oligodendroglioma

A
  • 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)

41
Q

Where do ependymomas more commonly arise in children vs adults?

A

Children: 4th ventricle
Adults: spinal canal

42
Q

Most ependymomas are ___ differentiated and are classified as WHO Grade __

A

Well-differentiated. Classified as WHO Grade II.

43
Q

Ependymomas commonly present alongisde ____

A

Hydrocephalus (blockage of CSF)

44
Q

IDH1 mutations are diagnostic criteria for oligodendroglioma, and are associated with ____ prognosis in other glial tumours

A

Better.

Medical Studies 2A (110 decks)

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