Neoplasia ( 5% ) Flashcards

1
Q
  1. Dysplasia
  • a. Is a feature of mesenchymal cells.
  • b. Inevitably progresses to cancer.
  • c. Is characterized by cellular pleomorphism
  • d. Is the same as carcinoma in situ.
  • e. Is not associated with architectural abnormalities.
A
  • a. Can be a feature of any cell type
  • b. may, but not necessarily, progresses to cancer.
  • c. Is characterized by cellular pleomorphism
  • d. Is a potential precurser to carcinoma in situ.
  • e. Is associated with architectural abnormalities.
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2
Q
  1. Metastasis
  • a. Unequivocally proves malignancy
  • b. Is the most common presentation of melanoma.
  • c. Is proven by lymph node enlargement adjacent to a tumour
  • d. Of breast is usually to supraclavicular nodes.
  • e. All of the above
A
  • a. Unequivocally proves malignancy
  • b. Skin lump Is the most common presentation of melanoma.
  • c. Is proven by lymph node enlargement adjacent to a tumour
    • Multiple causes including infection - does not mean it has spread past the node.
  • d. Of breast is usually to axillary nodes - hence why axillary node dissections/SNB are performed for breast cancer
  • e. All of the above
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3
Q
  1. Anaplasia is not characterized by
  • a. Pleomorphism
  • b. Abundant nuclear DNA
  • c. A nuclear-cytoplasmic ratio of 1:6.
  • d. Coarsely clumped chromatin
  • e. Lack of differentiation
A

c. A nuclear-cytoplasmic ratio of 1:6.

This is normal

Anaplasia has a ratio closer to 1:1

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4
Q
  1. To which two organs do tumours most commonly spread haematogenously?
  • a. Lungs and brain
  • b. Liver and lungs
  • c. Liver and bone
  • d. Bone and brain
  • e. Lung and bone
A

b. Liver and lungs

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5
Q
  1. With regard to characteristics of benign and malignant neoplasia
  • a. Cells of benign tumours are poorly differentiated.
  • b. Mitotic figures in benign tumours are common.
  • c. Malignant tumours can be slow growing
  • d. Malignant tumours are usually cohesive and expansile
  • e. Malignant tumours often display structures typical of originating tissue.
A
  • a. Cells of benign tumours maintain differentiation
  • b. Mitotic figures in benign tumours are uncommon, as they grow slowly
  • c. Malignant tumours can be slow growing (or fast growing. Up to the mutation)
  • d. Malignant tumours are usually cohesive and expansile
    • ?loosely bound and invasive
  • e. Malignant tumours often lose structures typical of originating tissue - poorly differentiated
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6
Q
  1. With regard to malignant disease
  • a. Arterial invasion by tumours is more frequent than venous.
  • b. Ovarian carcinoma may spread transperitoneally to the liver
  • c. The brain is a major site of lymphatic tumour spread
  • d. Basal cell carcinomas frequently metastasise to bone.
  • e. The most distinguishing feature of malignant disease is local tissue destruction.
A
  • a. Arterial invasion by tumours is less frequent than venous.
  • b. Ovarian carcinoma may spread transperitoneally to the liver
  • c. The brain is largely spared from lymphatic tumour spread, as there are few lymphatics in the brain
  • d. Basal cell carcinomas infrequently metastasise
  • e. The most distinguishing feature of malignant disease is Metastasis
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7
Q
  1. Malignant neoplasms
  • a. Are independent of hormonal influence.
  • b. Are always composed of homogenous cell lines
  • c. Arise from differentiated cells by a process of anaplasia.
  • d. Display abnormal nuclei with pale nucleoli.
  • e. Typically grow more rapidly than benign
A
  • a. Are dependent on hormonal influence
    • Different cells in the tumour may respond differently to growth factors etc. Breast cancer is under hormonal influnce, hence the use of tamoxifen etc
  • b. Often have genetic variation with each division due to a high rate of mutations
  • c. Anaplasia = loss of differentiation, not the process that gets there
  • d. Display abnormal nuclei with dark nucleoli.
  • e. Typically grow more rapidly than benign
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8
Q
  1. Regarding metastasis
  • a. All carcinomas have the ability to metastasise
  • b. Highly invasive carcinomas rarely metastasise.
  • c. Carcinomas typically spread via lymphatics compared with haematogenous spread
  • d. Tumour cells develop increased cohesiveness of their cell surface in the formation of cancer cell emboli.
  • e. Cells involved in lymphatic dissemination release degradative enzymes
A
  • a. All carcinomas have the ability to metastasise
    • Typically, the use of the word ‘all’ in medicine often precludes an answer from being right
  • b. Highly invasive carcinomas often metastasise.
  • c. Carcinomas typically spread via lymphatics compared with haematogenous spread
    • ​Carcinoma = epithelial cell derived
    • Sarcoma = mesenchymal derivation
  • d. Tumour cells develop decreased cohesiveness of their cell surface in the formation of cancer cell emboli.
    • Normal tissues dont just break off into the low pressure of lymph or veins
  • e. Cells involved in lymphatic dissemination release degradative enzymes
    • ???
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9
Q
  1. Neoplasia
  • a. Shows nuclear pleomorphism
  • b. Shows decreased nuclear-cytoplasmic ratio.
  • c. Results when protogenes are activated.
  • d. Involves proto-oncogenes in their natural form.
  • e. Is initiated by a single genetic alteration.
A
  • a. Shows nuclear pleomorphism
  • b. Shows increased nuclear-cytoplasmic ratio
    • 1:6 -> 1:1
  • c. Results when protogenes are activated.
    • Proto-oncogenes are involved, but it is not a one-step process to neoplasia
  • d. Involves proto-oncogenes in their mutated form.
  • e. Is initiated by multiple genetic alterations.
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10
Q
  1. Regarding the spread of cancers
  • a. The pleural cavity is the most commonly affected body cavity
  • b. Haematogenous spread is the most common pathway for the initial dissemination of carcinomas.
  • c. Lymphatic spread is typical of sarcoma.
  • d. Renal cell carcinoma often invades branches of the renal vein
  • e. Nodal enlargement in proximity to a cancer always means dissemination of the primary lesion
A
  • a. The pleural cavity is the most commonly affected body cavity
    • Havent looked this up, but I assume peritoneum due to the number of organs in it
  • b. Lymphatic spread is the most common pathway for the initial dissemination of carcinomas
  • c. Haematogenous spread is typical of sarcoma.
  • d. Renal cell carcinoma often invades branches of the renal vein
  • e. Nodal enlargement in proximity to a cancer always means dissemination of the primary lesion
    • Always/never = never the right fucking answer.
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11
Q
  1. Regarding benign versus malignant tumours
  • a. Benign tumours are generally less differentiated.
  • b. Large prominent nucleoli and a high nuclear-cytoplasmic ratio are characteristics of a malignant cell
  • c. Benign tumours metastasise haematogenously.
  • d. Malignant tumours always proliferate rapidly.
  • e. Malignant tumours always metastasise
A
  • a. Benign tumours are generally well differentiated.
  • b. Large prominent nucleoli and a high nuclear-cytoplasmic ratio are characteristics of a malignant cell
  • c. Benign tumours dont metastasis. Like, by definition.
  • d. Malignant tumours may proliferate rapidly.
  • e. Malignant tumours may metastasise.
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12
Q

Which of the following tumour is benign

  • Chondrosarcoma
  • Osteochondroma
  • Chondroblastoma
  • Ewing’s tumour
  • None of the above
A

Osteochondroma

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13
Q

Which of the following is malignant

  • Squamous cell papilloma
  • Hydatidiform mole
  • Chondroma
  • Mature teratoma
  • Bronchial carcinoid
A

Bronchial carcinoid

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14
Q

with regard to tumours

  • dysplasia always progresses to cancer
  • cystic teratomas are malignant
  • squamous papillomas are benign
  • the presence of mitoses indicates neoplasia
  • hypochromasia is characteristic of anaplasia
A

squamous papillomas are benign

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15
Q

Features that help differentiate benign from malignant tumours include all except

  • The degree of both morphological and functional differentiation of the cells
  • The number of mitoses
  • The presence or absence of a capsule
  • The number of cells per unit area
  • The formation of multinucleate giant cells
A

The number of cells per unit area

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16
Q

malignant neoplasms

  • are undifferentiated
  • almost always exhibit rapid growth
  • are proven by discovery of metastases
  • do not commonly exhibit mitotic figures
  • are not locally invasive
A

Nick thinks ‘are proven by discovery of metastases’, but you do not need metastases to have a malignant neoplasm (are pathgnomonic though)

I think ‘are undifferentiated’, though they can range to ‘poorly differentiated’

17
Q

The commonest cause of thyroid carcinoma is

  • Medullary
  • Follicular
  • Papillary
  • Anaplastic
  • Squamous
A

Papillary

18
Q

Regarding malignant neoplasms

  • Breast cancer is the commonest cause of death in females 55-74yo
  • There is no familial clustering of ovarian cancer
  • There is reasonable evidence available linking benzene with lung cancer
  • Rates of lung cancer have doubled in the last 40 years
  • Brain tumours are the most common cancerous cause of death in the under 15yo
A

Rates of lung cancer have doubled in the last 40 years

19
Q

Which is correct

  • Spontaneous mutation is the most common process leading to tumour formation
  • Genes that regulate apoptosis are not involved in tumour formation
  • Some organs liberate chemoattractants that tend to recruit tumour cells to the site
  • Substances which are highly mutagenic are labeled tumour promoters.
  • All cell types are equally susceptible to radiation-induced cancer formation
A

Some organs liberate chemoattractants that tend to recruit tumour cells to the site

Substances which are highly mutagenic are labeled tumour Initiators

  • tumour promoters encourage growth of a previously mutated cell*
  • Rapidly dividing/highly metabolic cells are more* susceptible to radiation-induced cancer formation
20
Q

concerning carcinogenesis

  • most benign neoplasms, given enough time, will undergo malignant transformation
  • anti-oncogenes are growth suppressed proto-oncogenes
  • non-lethal genetic damage has little to do with carcinogenesis
  • proto-oncogenes may become oncogenes by retroviral transduction (v-oncs) or by influences that alter their behaviour in situ, thereby converting them into cellular oncogenes (c-oncs)
  • chromosomal translocation usually results in underexpression of proto-oncogenes
A

proto-oncogenes may become oncogenes by retroviral transduction (v-oncs) or by influences that alter their behaviour in situ, thereby converting them into cellular oncogenes (c-oncs)

21
Q

Regarding oncogenes

  • Their products are associated with metaplasia
  • Proto-oncogenes are involved with normal cell growth and differentiation
  • Proto-oncogenes are activated by one of 4 different mechanisms
  • 40% of all human tumours carry mutated H-ras or K-ras oncogenes
  • fibroblast growth factors play a role in SCC of the lung
A

Proto-oncogenes are involved with normal cell growth and differentiation

They are a normal part of cell function, but are called proto-oncogenes because a mutation in them can lead to cancer, not that they are inherently involved in cancer

There are 4 classes of gene that can be involved in being an oncogene:

Growth promotion, growth inhibition, DNA repair, or apoptosis inducing

22
Q

The following viruses are considered to be oncogenic

  • Hepatitis B
  • Hepatitis C
  • EBV
  • HPV
  • All of the above
A

All of the above

23
Q
  1. Internal carcinoma is associated with which of the following skin disorders
    d. acanthosis nigricans
A

d. acanthosis nigricans

In gastric, lung, uterine cancers

Dermatomyositis can occur in breast and uterine cancer

24
Q
  1. All of the following are precancerous EXCEPT:
  • a. Chronic gastritis or pernicious anaemia
  • b. Solar keratosis
  • c. Crohn’s disease
  • d. Leukoplakia
  • e. Chronic ulcerative colitis
A
  • a. Chronic gastritis or pernicious anaemia - gastric cancer
  • b. Solar keratosis - early SCC
  • c. Crohn’s disease - colorectal and small intestine cancer
    • as per Nick. All seem to be able to cause cancer, but UC more carcinogenic than Crohns.
  • d. Leukoplakia - oral cancers
  • e. Chronic ulcerative colitis - colorectal cancer
25
Q
  1. Staging of cancer
  • a. T1 is insitu
  • b. M1 may be blood borne mets
  • c. N3 means goes to 3 nodes
  • d. Is a universal staging system
  • e. Grading more useful for clinical effect.
A

b. M1 may be blood borne mets

T0 = insitu cancer

N3 = multiple nodes involved, likely in different groups

Multiple staging systems used

Staging more clinically useful than grading (which is a histological diagnosis based on degree of differentiation etc)

26
Q
  1. A 50yo woman presents with back pain, Xrays suggest a malignant deposit in T10. The least likely primary would be
  • breast
  • ovary
  • thyroid
  • kidney
  • colon
A

kidney.

RCCs tend not to metastasise, but often paraneoplastic

27
Q

Malignant lymphoma include all of the following except

  • Hodgkin’s lymphoma
  • Reed-Sternberg giant cell lymphoma
  • Mycosis fungoides
  • NHL
  • Burkitt’s lymphoma
A

Reed-Sternberg giant cell lymphoma

Reed-Sternberg cells are found in Hodgkins lymphoma, they are not a seperate type

28
Q

development of metastatic potential in melanoma is heralded by

  • change in colour
  • change in size
  • nodule development
  • change in the degree of pigmentation
  • development of localized itchin
A

nodule development

29
Q

Hypercalcaemia as a paraneoplastic syndrome is most associated with

  • a. Small cell carcinoma of lung
  • b. Adult B cell leukaemia/lymphoma
  • c. Hepatocellular carcinoma
  • d. Uterine carcinoma
  • e. Renal carcinoma
A

e. Renal carcinoma

Rarely metastasise, but often cause paraneoplastic syndromes

Lung SCC -> Cushings

T-cell lymphoma/leukaemia -> hypercalcaemia (but B-cell not associated with PNPS)

Hepatocellular -> polycythaemia (as can RCC)

Uterine -> acanthrosis nigricans

30
Q
  1. All of the following characterize familial tumours EXCEPT:
  • a. Earlier age at onset
  • b. Close relatives with same tumour
  • c. Multiple or bilateral tumours
  • d. Specific marker phenotypes
  • e. Increased relative risk in siblings
A

d. Specific marker phenotypes

Familial tumours typically have a pre-mutated oncogene at birth (or something), so less mutations needed to cause cancer in life.

Thus multiple cancers more likely, and of course siblings and close-relatives more likely to be affected.

Can have earlier onset compared to others as time is not needed to cause the initial mutation.