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Patho- Exam 5: Cancer Basics

Total questions: 36

Worksheet time: 20mins

Name
Class
Date
1.

A tumor is said to be ________ when its microscopic and gross characteristics are considered to be relatively innocent, implying that it will remain localized and is amendable to local surgical removal. (Encapsulated, well circumscribed, no invasion, cell proliferation is low)

a)

benign

b)

malignant

2.

________, as applied to a neoplasm, implies that the lesion can invade and destroy adjacent structures and spread to distant sites (metastasize) to cause death. (invasion, rapid growth, loss of capsule, ability of spread [metastasis], anaplasia)

a)

Benign

b)

Malignant

3.

Most epithelial carcinomas spread through _________.

a)

lymphatics

b)

blood (hematogenous)

4.

Most sarcomas (arising in the bones, connective tissue such as fat and muscle) spread through ___________.

a)

lymphatics

b)

blood (hematogenous)

5.

Directly damage DNA, leading to mutations and eventually cancer

a)

chemical carcinogens

b)

radiation carcinogenesis

c)

viral and bacterial oncogenesis

6.

causes chromosome breakage, chromosome rearrangements, and, less frequently, point mutations, any of which may affect cancer genes and thereby drive carcinogenesis

a)

chemical carcinogens

b)

radiation carcinogenesis

c)

viral and bacterial oncogenesis

7.

HPV (cervical cancer), EBV (Burkett's lymphoma), HCB (hepatocellular carcinoma), H. Pylori (MALT lymphoma)

a)

chemical carcinogens

b)

radiation carcinogenesis

c)

viral and bacterial oncogenesis

8.

Tumor markers are produced by malignant tumors exclusively.

a)

true

b)

false

9.

Where can tumor markers be found?

a)

present in or on the tumor cells

b)

blood, urine, CSF

c)

in the art supply section

10.

What do tumor markers include?

a)

hormones

b)

genes

c)

enzymes

d)

antigens

e)

antibodies

11.

What do hypercalcemia, Cushing syndrome, and nonbacterial thrombotic endocarditis are all indications of what condition?

a)

paraneoplastic syndrome

b)

lung cancer

c)

prostate cancer

d)

breast cancer

12.

What can tumor markers be used for?

a)

screening individuals at high risk for cancer

b)

diagnosis

c)

following the clinical course of a tumor

13.

__________ of tumors is determined by cytologic appearance and is based on the idea that behavior and differentiation are related, with poorly differentiated tumors having more aggressive behavior.

a)

Grading

b)

Staging

14.

___________ (extent of tumor), determined by surgical exploration or imaging, is based on size, local and regional lymph node spread, and distant metastases.

a)

Grading

b)

Staging

15.

_________ is of greater clinical value than ________.

a)

Grading, staging

b)

Staging, grading

16.

Choose the major forms of neoplasia associated with the following clinical syndrome: Cushing syndrome

a)

small cell carcinoma of lung

b)

pancreatic carcinoma

c)

neural tumors

d)

intracranial neoplasm

e)

squamous cell carcinoma of lung

17.

Choose the major forms of neoplasia associated with the following clinical syndrome: syndrome of inappropriate anti-diuretic hormone secretion

a)

small cell carcinoma of lung

b)

intracranial neoplasms

c)

squamous cell carcinoma of lung

d)

breast carcinoma

e)

renal carcinoma

18.

Choose the major forms of neoplasia associated with the following clinical syndrome: hypercalcemia

a)

squamous cell carcinoma of lung

b)

breast carcinoma

c)

renal carcinoma

d)

adult T cell leukemia/lymphoma

e)

fibrosarcoma

19.

Choose the major forms of neoplasia associated with the following clinical syndrome: hypoglycemia

a)

fibrosarcoma

b)

other mesenchymal sarcomas

c)

ovarian carcinoma

d)

small cell carcinoma of lung

e)

pancreatic carcinoma

20.

What is the causal Mechanism(s)/Agent(s) of the following clinical syndrome: Cushing syndrome

a)

ACTH or ACTH-like substance

b)

Anti-diuretic hormone or atrial natriuretic hormones

c)

Parathyroid hormone-related protein, TGF-α

d)

Insulin or insulin-like substance

21.

What is the causal Mechanism(s)/Agent(s) of the following clinical syndrome: syndrome of inappropriate anti-diuretic hormone secretion

a)

ACTH or ACTH-like substance

b)

Anti-diuretic hormone or atrial natriuretic hormones

c)

Parathyroid hormone-related protein, TGF-α

d)

Insulin or insulin-like substance

22.

What is the causal Mechanism(s)/Agent(s) of the following clinical syndrome: hypercalcemia

a)

ACTH or ACTH-like substance

b)

anti-diuretic hormone or atrial natriuretic hormones

c)

Parathyroid hormone-related protein, TGF-α

d)

Insulin or insulin-like substance

23.

What is the causal Mechanism(s)/Agent(s) of the following clinical syndrome: hypoglycemia

a)

ACTH or ACTH-like substance

b)

Anti-diuretic hormone or atrial natriuretic hormones

c)

Parathyroid hormone-related protein, TGF-α

d)

Insulin or insulin-like substance

24.

in laboratory setting, normal cells stop growth when they reach the edge of culture dish; cancer cells will continue to grow and pile on top of one another

a)

lack contact inhibition

b)

anchorage independent

c)

immortal

d)

differentiation

25.

normal cells will not grow unless they are attached to a surface; cancer cells will grow when suspended in soft agar

a)

lack contact inhibition

b)

anchorage independent

c)

immortal

d)

differentiation

26.

normal cells will divide 10-50 times in a lab; cancer cells will divide indefinitely

a)

lack contact inhibition

b)

anchorage independent

c)

immortal

d)

differentiation

27.

cancer cells show defects; anaplasia (reversion to a less mature form); may be pleomorphic (variable size and shape)

a)

lack contact inhibition

b)

anchorage independent

c)

immortal

d)

differentiation

28.

Cancer cells perform glycolysis with and without oxygen

a)

true

b)

false

29.

When the cancer cells perform glycolysis without regard to presence of oxygen, is this a dysfunction?

a)

yes

b)

no- genetic mutations promote this shift, allow for more efficient use of lactate and metabolites for production of cellular binding blocks for rapid growth

30.

Define oncogenes

a)

genes that induce a transformed phenotype when expressed in cells by promoting increased cell growth

b)

mutated or over expressed versions of normal cellular genes

31.

Define proto-oncogenes

a)

genes that induce a transformed phenotype when expressed in cells by promoting increased cell growth

b)

mutated or over expressed versions of normal cellular genes

32.

Genes that normally prevent uncontrolled growth and, when mutated or lose from a cell, allow the transformed phenotype to develop. Transformation generally only occurs when both alleles of these cells are damaged.

a)

tumor suppressor genes

b)

oncogenes

c)

proto-oncogenes

33.

There are two types of tumor suppressor genes. Which one acts as important brakes on cellular proliferation?

a)

guardian

b)

governors

34.

There are two types of tumor suppressor genes. Which one is responsible for sensing genomic damage?

a)

governors

b)

guardians

35.

Genes that regulate __________ primarily act by enhancing cell survival, rather than stimulating proliferation per se.

a)

apoptosis

b)

tumor growth

36.

Genes of this class that protect against apoptosis are often ___________ in cancer cells, whereas those that promote apoptosis tend to be _________ or functionally inactivated by mutations.

a)

over expressed, under expressed

b)

under expressed, over expressed