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Pathology 2220 > Week 8: Neoplasia 1 > Flashcards

Week 8: Neoplasia 1 Flashcards

1
Q

What is the traditional definition of neoplasia?

A

An abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissues and persists in the same excessive manner after the apparent cessation of the stimuli that evoked the change

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2
Q

What is the modern definition of neoplasia?

A

A disorder of cell growth that is triggered by a series of acquired mutations affecting a single cell and its clonal progeny. These mutations give the cells a survival and growth advantage resulting in excessive proliferation that is independent of physiologic growth signals

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3
Q

What are the 2 components of a neoplasm?

A

Parenchyma and Stroma

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4
Q

What is the parenchyma of tumour?

A
  • Neoplastic cells that make up the tumour
  • Classification is based on these cells
  • Biological behaviour of tumour is largely determined by these cells
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5
Q

What is the stroma of a tumour?

A
  • Connective tissue, vessels and inflammatory cells
  • Influence growth and spread
  • Lots of collagen
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6
Q

How do we name mesenchymal benign tumours?

A

cell type of origin + oma

i.e. Chondroma, Fibroma, Lipoma

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7
Q

What is an Adenoma?

A

A benign epithelial neoplasm that is derived from glandular tissue

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8
Q

What is a Papilloma?

A

A benign epithelial neoplasm comprised of finger-like projections

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9
Q

What is a Cystadenoma?

A

A lesion that forms cystic masses

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10
Q

What is a Polyp?

A

A macroscopically visible projection above a mucosal surface

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11
Q

How do we name a malignant tumour arising from epithelial cells?

A

Region of origin + carcinoma

i.e. Adenocarcinoma, Squamous cell carcinoma

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12
Q

How do we name a malignant tumour arising from mesenchymal cells?

A

Region of origin + sarcoma

i.e. Chondrosarcoma, Osteosarcoma

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13
Q

How do we name malignant tumours arising from the blood forming cells?

A

Leukaemia or Lymphoma

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14
Q

What is a mixed tumour?

A

A tumour whose parenchymal cells show different differentiation, they are pleomorphic

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15
Q

What is a teratoma?

A

A tumour containing mature cells from more than one germ layer, they contain a multitude of tissues

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16
Q

What are the macroscopic features of benign tumours?

A
  • Well circumscribed
  • Even cut surface
  • No necrosis or haemorrhage
  • May have a capsule
  • May compress surrounding tissue
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17
Q

What are the microscopic features of a benign tumour?

A
  • Well organised
  • Similar appearance to normal tissue
  • No cytological features of malignancy
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18
Q

What are the macroscopic features of malignant tumours?

A
  • Irregular, infiltrative outline
  • Necrosis and haemorrhage
  • May invade adjacent structures
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19
Q

What are the microscopic features of a malignant tumour?

A
  • Diosrganised architecture
  • Nuclear pleomorphism (variation in size and shape)
  • Increased Nucleus:Cytoplasm ratio
  • Hyperchromasia
  • Mitotic cells
  • Disorder, loss of polarity
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20
Q

Define dysplasia:

A

Disordered growth of tissue

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21
Q

What are the characteristics of dysplasia:

A
  • Typically in epithelia
  • Loss of uniformity
  • Disorganisation
  • Loss of differentiation
  • Nuclear enlargement
  • Hyperchromasia
  • Pleomorphism
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22
Q

What is carcinoma in situ?

A

A neoplasm whose dysplastic changes are marked and involve the full thickness of the epithelium (without penetrating the basement membrane).

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23
Q

What is metastasis?

A

The spread of a tumour to sites that are physically discontinuous with the primary tumour

They mark tumours as malignant

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24
Q

What are the pathways for initial metastasis?

A 
Lymphatic system (Most common)
Vascular system
25
Q

What is the normal histology of the cervix?

A

Ectocervix: lined by non-keratinising squamous epithelium

Endocervix: lined by mucinous columnar epithelium

26
Q

What is the most important factor in developing cervical cancer?

A

HPV

27
Q

What is the transition zone?

A

The portion where columnar epithelium is ultimately replaced by squamous epithelium

28
Q

HPV infects the ______ cells present in the ___________.. Most infections are _________, _________ and __________________________..

A

Basal cells
Transition zone
Transient, asymptomatic and eliminated by the host

29
Q

What are the risk factors for HPV infection?

A

Multiple partners
Impaired immune response
Coexisting infection
Poor nutrition and other health risks (i.e. smoking and obesity)

30
Q

What are the most important high risk HPV subtypes?

A

HPV 16 (Accounts for 60% of cases) and HPV 18

31
Q

What are the most important low risk HPV subtypes?

A

HPV 6 and HPV 11

They cause genital warts

32
Q

How does cervical cancer present?

A
  • Most are asymptomatic
  • Abnormal bleeding or discharge
  • Pain
  • Abnormal pap smear
  • Late symptoms: bladder symptoms, weight loss, metastases
33
Q

What are the 2 main cervical cancer subtypes and their precursors?

A

Squamous Cell Carcinoma (80%):
- precursor is high grade squamous intraepithelial lesion (HSIL) or cervical intraepithelial neoplasia (CIN)

Adenocarcinoma (15%):
- precursor is adenocarcinoma in situ

34
Q

What is the histological features of of Squamous Cell Carcinoma?

A
  • Malignant squamous epithelium invading through the basement membrane into the stroma
  • Graded as well, moderate or poorly differentiated depending on how easily the “squamous” nature of the cells can be detected
35
Q

What are the histological features of Squamous Cell Carcinoma?

A
  • Proliferation of malignant cells showing glandular differentiation
  • Usually moderately or well differentiated
  • Multiple variants
36
Q

Where do invasive carcinomas spread?

A
  • Directly to the bladder, uterus, rectum and vagina
  • Local pelvic and distant lymphnodes
  • Distant metastases can be found in the liver, lungs and bone marrow
37
Q

How do most cervical cancer patients die?

A

Most often the local extension into the bladder and uterus which leads to ureteric obstruction, pyelonephritis and uremia

38
Q

How do we treat cervical cancer?

A
  • Early treatment by cone biopsy
  • Most invasive lesion treated by hysterectomy and lymph node removal
  • Advanced lesions treated with surgery and radiotherapy and chemotherapy
39
Q

How do we grade premalignant squamous cervical lesion?

A

Low-grade Squamous Intraepithelial lesion (SIL) [CIN I]:
- dysplastic cells in lower third of the epithelium

High-grade SIL [CIN II]:
- expansion of dysplastic cells into the middle third of the epithelium

High-grade SIL [CIN III]:
- loss of maturation, and expansion of dysplastic cells to epithelial surface

40
Q

__% of LSIL regress spontaneously, __% persist and __% progress to HSIL

A

60
30
10

41
Q

__% of High Grade Squamous Intraepithelial lesions (HSIL) regress, __% persist and __ progress to carcinoma.

A

30
60
10

42
Q

How do we identify cervical cancer?

A

Pap Smears - ID abnormality and grade
Colposcopy - ID exact site and extent
Cervical Punch Biopsy - Exact histological diagnosis
Cone Biopsy - Surgically Removes abnormal area

43
Q

How is a Pap smear performed?

A
  • Cells are obtained from the transition zone with a spatula/brush
  • Cells are put on a slide and stained using the papanicolaou method and washed into a liquid based medium
44
Q

What is HPV DNA testing and what is it used for?

A
  • Used as a adjunct to cytology or liquid based preparations

- Tests women with a high grade abnormality to ensure the virus has been cleared

45
Q

What are the 2 vaccines for HPV in Australia?

A

Gardasil - Quadvalent for HPV 6, 11, 16 and 18
Cervarix - Bivalent for HPV 16 and 18

They protect for up to 5 years

46
Q

What is a Hysterectomy?

A

Removal of the uterus, cervix, bilateral fallopian tubes and pelvic lymph nodes

47
Q

Colorectal Cancer is also called:

A

Bowel Cancer
Large Intestinal Cancer
Colorectal Carcinoma

48
Q

What is the pattern of Colorectal Carcinogenesis?

A
  • Most is sporadic

- Only 1-3% are familial and associated with predisposing conditions like Inflammatory Bowel Disease

49
Q

What are the 2 major pathways of colorectal carcinogenesis?

A 
Chromosomal Instability (APC)
Microsattelite Instability (MSI)
50
Q

Give a brief summary of the APC pathway of colorectal carcinogenesis:

A
  1. Accumulation of genetic changes causes the growth of an adenoma (polyp)
  2. Adenoma then progresses to Carcinoma via more changes
51
Q

Give a brief summary of the MSI pathway of colorectal carcinogenesis:

A
  1. Genetic changes destabilise the DNA and result in the formation of a Sessile Serrated Adenoma (SSA)
  2. SSA then progresses to Carcinoma via more changes
52
Q

What are the risk factors of Colorectal cancer?

A
  • Age (Over 50)
  • Other colonic inflammatory diseases
  • Family History
  • Alcohol, Smoking, Inactivity
  • High Calorie, Low fibre
  • Genectic syndromes like Familial Adenomatous Polyposis coli (FAP) and Lynch Syndrome
53
Q

What is the clinical presentation of Colorectal cancer?

A
  • Fatigue
  • Anaemia
  • Weakness
  • Blood in stool
  • Altered bowel habits
  • Metastatic disease
  • May be assymptomatic
54
Q

How do we diagnose colorectal cancer?

A

Endoscopy
Radiology
Biopsy

55
Q

What is the morphology of a Colorectal cancer?

A 
Macro:
-Polypoid
- Exophytic
- Ulceration
- Stricture
Micro:
- Features of an adenocarcinoma
56
Q

How is colorectal cancer staged?

A

With respect to the extent of dysplasia and the invasion of the mucosa and before

57
Q

All colorectal adenomas are ________ with ___________________.

A

Dysplastic

No invasion

58
Q

What are the treatments for colorectal cancer?

A

Surgery
Radiation therapy
Chemotherapy
Targeted therapy

Pathology 2220 (10 decks)

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