Brainscape's Knowledge GenomeTM

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


See full index

Neurology Y2 > L5 - Neoplastic Diseases in the Nervous System > Flashcards

L5 - Neoplastic Diseases in the Nervous System Flashcards

1. Understand the forms of neoplasia that may arise from cells. 2. Understand the distinction between neoplasia and dysplasia. 3. Concepts of staging and grading. 4. Revise the different cell types of the nervous system and associated tissues. 5. Learn that tumours may metastasise to the nervous system or affect the nervous system remotely (paraneoplastic effects) 6. Learn about the pathological complications of brain tumours.

1
Q

What is Wnt signalling in cancer?

A
  • Signalling of Wnt family of secreted glycolipoproteins
  • via transcription co-activator Beta-cantenin
  • Beta-cantenin: cell proliferation, polarity and determination.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are proto-oncogenes?

A
  • Normal gene
  • however, when altered by mutation
  • becomes a oncogene that contributes to cancer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

State examples of tumour supressor genes?

A

p53 and pRB

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

Briefly describe the role of p53?

A

Activity stops formation of tumours.

  • p53 protein will bind DNA, stimulating another gene to produce p21 that interacts with cdk2 (cell division-stimulating protein)
  • when p21 complexed with cdk2 cell cannot pass through to next stage of cell division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How may mutant p53 cause cancer?

A
  • Can no longer bind DNA effectively.
  • p21 protein not made available to act as the stop signal for cell division.
  • Hence cells divide uncontrollably.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is pRB?

A
  • Retinoblastoma protein.

- Rb, Prevents excessive cell growth by inhibiting cell cycle progression until cell is ready to divide.

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

What role does Rb play when a cell is ready to divide?

A

Rb phosphorylated to pRb.

  • inactivation of activity of RB
  • cells allowed to enter cell cycle state.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the greek name given to a new formation?

A

neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define pre-malignant?

A

Tissue that is not yet malignant (cancerous) but has potential to be.
Malignant: located in tissue of origin

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

Define metastatic?

A

Secondary: spread of cancer to new areas of body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

State different ways cancer might spread?

A
  • Direct
  • Haemotogenous (blood)
  • Lymphatic
  • Transcoelomic (across peritoneal cavity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a harmartoma?

A
  • Excessive cells
  • disorganised
  • resembles neoplasm in tissue of its origin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is heterotopia?

What is periventricular heterotopia?

A
  • Normal number of cells at the wrong site.

Periventricular heterotopia: nerve cells do not migrate properly during early development of the foetal brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hyperplasia

A

Excessive number of normal cells at the correct site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hypertrophy

A

normal number, increased size of normal cells at correct site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Metaplasia

A

Terminally differentiated cells replaced by another terminally differentiated cell

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

Dysplasia

A

Expansion of immature cells

18
Q

Anaplasia

A
  • cells with poor cellular differentiation

- lose morphological characteristics of mature cells.

19
Q

State four major pathological microscopic changes that characterise dysplasia

A

Anisocytosis: cells of unequal size

Poikilocytosis: abnormally shaped cells including nuclear atypia

Hyperchromatism: excessive pigmentation

Presence of mitotic figures: abnormal number of cells currently dividing

20
Q

Abnormal appearance of cell nuclei?

A

Nuclear atypia

21
Q

Briefly state the progression model of cancer development?

A

Normal - Hyperplasia - dysplasia - cancer

22
Q

Describe Grade I of neoplasia

A

Slow growing, non-malignant, associated with long term survival

23
Q

Grade II neoplasia

A

One criterion: cytological atypia

  • tumour slow growing but recur as high-grade tumours.
24
Q

Grade III neoplasia

A

2 criteria: anaplasia and mitotic tumours.

tumours are malignant and often recur as high grade tumours.

25
Q

Grade IV neoplasia

A

3/4 criteria: anaplasia, mitotic activity with microvascular proliferation and/or necrosis.
- tumour reproduce rapidly
- very aggressive malignant tumours
THE WORST

26
Q

Briefly describe isocritrate dehydrogenase mutations in cancer?

A
  • IDH : enzyme in Krebs

- If enzyme malfunctions can cause products of the kreb cycle to accumulate.

27
Q

What is staging?

A
  • Microscopic anatomical location of disease
  • Special dye called contrast can enhance lesions.
  • New BV abnormal so will leak out the contrast which then lights up.
28
Q

What is the most common brain tumour?

A

Glioma
Classified grade IV.
- develop’s from lineage of astrocytes (star shaped glial cells) that support nerve cells.

29
Q

Describe brain infiltration by cancer cells?

A
  • Metastatic cells detach from primary tumour
  • survive in blood, cross blood brain barrier
  • colonise vascular place by adhering to endothelial cells.
30
Q

What is a meningioma?

A

tumour that forms on membranes that cover the brain and spinal cord.

31
Q

Paraneoplastic

A

When cancer-fighting antibodies (T-cell) mistakenly attack normal cells.

32
Q

What is a common paraneoplastic syndrome associated with lung cancer?

A

SIADH (syndrome of inappropriate ADH hormone) secretion.

  • water retention
  • low level of Na+ (hyponatremia) because increased water, increases pressure
33
Q

Describe glioblastoma’s?

A
  • Malignant Grade IV.
  • Large portion of tumor cells are reproducing and dividing at any given time
  • Made up of abnormal astrocytic cells and areas of dead cells.
34
Q

How may glioblastoma’s infiltrate and invade other regions of brain?

A

Through brain connection fibers, known as corpus callosum.

35
Q

What are microglia?

A
  • Resident macrophage in brain and spinal cord.

- First and main form of active immune defence in the CNS.

36
Q

What cells contribute to the blood brain barrier?

A

Astrocytes.

37
Q

How may primary tumors present? (4)

A
  1. Pressure symptoms.
  2. Haemorrhage.
  3. Seizures.
  4. Personality change.
38
Q

What is a meningioma?

A

Overgrowth of arachnoid cap cells.

  • often asymptomatic
  • present with vague neurological deficit
39
Q

Give examples of loss of function?

A

Amenorrhoea - absence of menstruation

Hypothyroid - when thyroid doesnt produce enough of certain hormones.

40
Q

Give examples of gain of function?

A

Acromegaly - pituitary produces too much growth hormone. Bones increase in size.
Cushing’s - caused by pituitary tumor, leads to excessive ACTH production, stimulates adrenal cortex to produce high levels of cortisol.

41
Q

Examples of treatments available

A
  • Cytoreduction - surgery
  • Cytological disruption - radiotherapy, chemo
  • Genomic disruption - radiotherapy and chemotherapy

Neurology Y2 (24 decks)

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