Brainscape's Knowledge GenomeTM

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


See full index

VET410 Endocrine/Reproduction > V412 EXAM I > Flashcards

V412 EXAM I Flashcards

1
Q

(L1) How is a malignant epithelial tumor named differently from a malignant mesenchymal tumor?

A

Malignant epithelial tumor = carcinoma

Malignant mesenchymal tumor = sarcoma

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

(L1) What is the value of doing a cytology on a mass?

A

Cytology can:

  1. differentiate whether something is infectious/inflammatory or neoplastic
  2. differentiate between an epithelial, mesenchymal, or round cell tumor
  3. aid in monitoring a tumor
  4. help determine prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

(L1) What is anisocytosis?

A

Irregularly shaped and sized cells

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

(L1) What is anisokaryosis?

A

Irregularly shaped and sized nuclei

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

(L1) What are cytological criteria for malignancy?

A
  1. anisokaryosis
  2. anisocytosis
  3. cytoplasmic vacuoles
  4. abnormal nucleoli
  5. pleomorphism
  6. nuclear molding
  7. high N/C ratio
  8. cytoplasmic basophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

(L1, LAB1) What are cytological signs that would support a diagnosis of a carcinoma?

A 
Highly cellular smear
Round cells with lots of cytoplasm
Cells clumped together with indistinct boundaries
\+/- keratinization 
\+/- vacuoles and granules
\+/- formation of ducts, glands, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

(L1, LAB1) What are cytological signs that would support a diagnosis of a sarcoma?

A 
Poorly cellular smear
Cells tend to be individualized or in small clusters
Spindle- or comet-shaped cells
Plump nuclei
Indistinct cellular boundaries 
\+/- ECM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

(L1-2, LAB1) What are cytological signs that would support a diagnosis of a round cell tumor?

A

Highly cellular smears
Well-defined cell borders
Cells either individualized or in aggregates
Round cells with extremely high N:C ratio and basophilic cytoplasm

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

(L2) Define hyperplasia. How is it different from neoplasia?

A

Hyperplasia is an increase in cell number in the correct location often driven by a stimulus. Unlike neoplasia, removal of the stimulus should stop the proliferation.

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

(L2) Define hamartoma. How is it different from neoplasia?

A

A hamartoma is caused by normally differentiated cells in the right location, but the cells are either arranged incorrectly or they form structures that are too large.

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

(L2) Define choristoma. How is it different from neoplasia?

A

A choristoma is histologically normal tissue in the wrong location. The latter two, though abnormal, involve normally differentiated cells whereas neoplasms do not respect normal cellular and tissue architecture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

(L2) What is dysplasia? How is this different from neoplasia?

A

Dysplasia is the loss of normal cellular architecture. It can be considered a precursor to neoplasia, but the cells still respect basement membranes and tissue margins. Dysplasia is actually similar to carcinoma in situ, with the only difference being the degree of neoplastic proliferation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

(L2) What is metaplasia?

A

Metaplasia is the replacement of one cell type for another.

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

(L2) Neoplasms can either manifest as a palpable mass or as…

A

Diffuse infiltration and/or destruction of a tissue.

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

(L2) What are some pros and cons of submitting a core biopsy of a tumor for evaluation as opposed to the whole mass?

A

A biopsy could allow for identification of a mass and can help form a treatment plan without complete surgery. However, it lacks much of the information that a complete sample could provide e.g. demarcation, interaction with adjacent tissues, etc.

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

(L2) Mitotic indices often serve as a crude assessment of how much a tumor is proliferating. What is a common IHC marker used to assess a mitotic index?

A

Ki-67 is a protein that is expressed in the nuclei of cells transitioning into S phase. Using this marker catches all cells either undergoing or about to initiate mitosis, which can often be missed in a visual examination.

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

(L2) How is the demarcation of a tumor associated with prognosis?

A

Tumors with worse and worse demarcations (“dirty margins”) are associated with poorer prognoses and increased risk of recurrence. It’s much more difficult to completely excise these tumors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

(L2) Distinguish between the preferred routes of metastasis of sarcomas and carcinomas.

A

In general, sarcomas often met through blood vessels while carcinomas more often travel via lymphatic ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

(L2) How do necrosis and apoptosis relate to prognosis?

A

The extent of necrosis is associated with rapid tumor proliferation, and thus, aggressiveness. Apoptosis occurs normally and doesn’t reflect tumor behavior. It’s often the result of the accumulation of too many mutations, which impairs normal cellular function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

(L2) What is a schirrhous response?

A

Epithelial tumors can induce marked fibrosis, referred to as a schirrhous response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

(L3) What is a DNA histogram analysis and what does it tell you?

A

A DNA histogram analysis quantifies the amount of DNA in cells and the results can be interpreted as the number of cells in each phase of the cycle. For example, cells in G0 or G1 phase are going to have less DNA than cells undergoing S phase, which are going to have less DNA than cells undergoing mitosis. The sub-G1 category denotes cells with less than 2N DNA, suggesting that they’re experiencing apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

(L3) What protein-ligand complex regulates movement through the cell cycle?

A

Cyclin dependent kinase and its substrate cyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

(L3) CDK4 is required for a cell to progress past the restriction point in the cell cycle. How does it participate in initiating S phase?

A

CDK4, when it binds to cyclin D, phosphorylates the Rb (retinoblastoma) protein. Once it does this, CDK2 bound to cyclin E, proceeds to continue phosphorylating Rb until it releases the transcription factor E2F. E2F is required for DNA replication and can upregulate the expression of more CDK2 in a feedforward loop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

(L3) Palbociclib is a CDK4 inhibitor. What does that entail about its effect on cell proliferation?

A

Without CDK4, the cell can’t progress past the restriction point in the cell cycle. Thus, palbociclib arrests cells in G1 phase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

(L3) p53 is a tumor suppressor gene - the most frequently mutated gene in cancer. How does it work?

A

When DNA damaged is sensed, p53 (the protein product) is activated and binds to the gene p21. p21 (the protein product) binds to and inhibits CDK4, preventing movement through the cell cycle and eventual apoptosis.

26
Q

(L3) Mutant p53 is oncogenic. How so? What are some possible treatment options specifically involving mutant p53?

A

Mutant p53 gains a function, becoming capable of activating growth promoting genes instead of inhibiting them. In tumors with mutant p53, we can find methods to convert the mutant into the normal wild-type or to degrade the mutant.

27
Q

(L3) What is MDM2?

A

MDM2 (the protein product) binds to and inhibits p53 (the protein product). It is removed from p53 when DNA damage is detected, activating the latter.

28
Q

(L3) What is caspase?

A

Caspase in involved in initiating the signaling cascade that ultimately leads to apoptosis. More specifically, initiator caspases activate executioner caspases, which cleave intracellular proteins and DNA.

29
Q

(L3) Describe the extrinsic pathway for apoptosis.

A

The extrinsic pathway is associated with T cell signaling. When a T cell binds a cell’s death receptors, caspases are activated, initiating apoptosis.

30
Q

(L3) Describe the intrinsic pathway for apoptosis.

A

The release of cytochrome c from mitochondria creates a protein complex, the apoptosome. The apoptosome then activates the caspase signaling cascade.

31
Q

(L3) Bcl2 is an oncogone. How does it work?

A

Bcl2 (the protein product) binds to specific mitochondrial membrane transporters and inhibits the release of cytochrome c, inhibiting the initiation of apoptosis.

32
Q

(L5, 11) Describe the initiation, promotion, progression model for carcinogenesis

A

Initiation is when a cell is exposed to a risk factor, causing it to gain a mutation. Only when stimulated by a promoter, some external influence, does the initiated cell begin acting neoplastic. Progression is when the cell continues to accumulate mutations (+/- constant external stimulus) to the point that it becomes neoplastic.

33
Q

(L5, 11) Describe insertional mutagenesis and how it can contribute to cancer.

A

Insertional mutagenesis is one mechanism through which a retrovirus can cause cancer. A virus, when it infects a cell, inserts its own DNA into the host genome. If the inserted viral DNA is near an oncogene, the oncogene can be upregulated by proxy, causing unregulated growth.

34
Q

(L5) Describe retroviral transduction and how it can contribute to cancer.

A

Retroviral transduction is one mechanism through which a retroirus can cause cancer. When a virus infects a cell, it undergoes recombination and adds a bit of the host DNA into its own genome. When the virus infects another cell, it inserts its genome again which acts like an oncogene, causing unregulated proliferation.

35
Q

(L5) What is an oncogene?

A

Oncogenes are the gas pedal of the cell cycle - they accelerate cell growth and proliferation.

36
Q

(L5) How would a mutation in an oncogene cause unregulated growth?

A

A mutation alters gene, and subsequently, protein structure. If the mutation changed the gene or protein so that it’s constitutively on, it could result in uncontrolled cell proliferation.

37
Q

(L5) How could a chromosomal rearrangement contribute to cancer?

A

There are two ways chromosomal rearrangement would cause cancer. First, if an oncogene was moved to be a gene promoter that was constitutively on, then the oncogene could also be constitutively activated. Second, if an oncogene was fused with another gene, the chimeric protein product could behave abnormally.

38
Q

(L5) How would gene amplification cause cancer?

A

If an oncogene was duplicated, it cause induce unregulated growth.

39
Q

(L5) What is a tumor suppressor gene?

A

Tumor suppressor genes are brakes to cell proliferation.

40
Q

(L5) What are the two types of tumor suppressor genes? What do they do?

A
  1. Gatekeepers - they inhibit cell signaling pathways

2. Caretakers - they maintain genomic stability and participate in DNA repair

41
Q

(L5) How does the two hit model apply to retinoblastoma?

A

According to the model, an affected individual inherits a germ line mutation (the first hit) to Rb, a tumor suppressor gatekeeper. A second hit at any point in their life the second Rb allele would cause the development of retinoblastoma.

42
Q

(L6) What is the fractional cell kill hypothesis? How does the actual rate of cell kill differ between in vivo and in vitro settings?

A

According to the fractional cell kill hypothesis, a chemotherapeutic kills a constant fraction of cells within a population independent of the absolute number of cells. With each administration of a drug, the proportion of cells killed shouldn’t change. However, in vivo, there is almost no consistent log kill effect.

43
Q

(L6) Adhering to the fractional cell kill hypothesis, what are two biggest determinants affecting the results of chemotherapy?

A

1- The dose of the drug

2- The number and frequency of drug administrations

44
Q

(L6) With chemotherapeutics like doxorubicin and drugs that behave like it, what is the biggest reason why tumors don’t exhibit an ideal cell kill rate (as suggested by the fractional cell kill hypothesis)?

A

A major determinant of chemotherapeutic efficacy is the rate of cell growth. For drugs like doxorubicin, only mitotically active cells exhibit high sensitivity, while quiescent cells don’t.

45
Q

(L6) What can we do to increase a tumor’s sensitivity to doxorubicin?

A

Debulking a tumor through radiotherapy, chemotherapy, or surgery can stimulate a quiescent tumor to become more proliferative, making it more susceptible to drugs that target mitotically active cells.

46
Q

(L6) What are some broad explanations for why our chemotherapeutic therapy could fail?

A
  1. Inadequate drug dosing
  2. Suboptimal administration schedule
  3. Sanctuary sites i.e. neoplastic cells hiding behind immunoprotective barriers
  4. Poor diffusion and distribution into tumors d/t poor vascularization or lack of appropriate membrane transporters
47
Q

(L6) What aspects of pharmacokinetics determine how effective a chemotherapeutic is?

A
  1. How well the drug is absorbed
  2. How the drug is metabolized
  3. How the drug is eliminated
  4. Drug-drug interactions
48
Q

(L7) Describe how different routes of administration would affect the bioavailability of a chemotherapeutic.

A

A drug e.g. doxorubin that is given IV has 100% bioavailability.
The bioavailability of oral chemotherapeutics e.g. cyclophosphamide depends on gut absorption and concurrent GI lesions may reduce the rate and extent of absorption.
There are also chemotherapeutics like cytosine arabinoside that are given subcutaneously and their bioavailability is affected by the perfusion rate of the administration site.

49
Q

(L7) How are most chemotherapeutics metabolized?

A

Phase 1 metabolism by cytochrome p450 enzymes in the liver. Phase 2 metabolism is only important for some chemotherapeutics.

50
Q

(L7) Cyclophosphamide is a prodrug whereas vincristine is an active parent drug. How would modulating CYP450 activity affect these two classes of drugs?

A

Increasing the activity of liver enzymes would increase the efficacy of of prodrugs like cyclophosphamide, but also increase the rate of inactivation for active parent drugs like vincristine. Inhibiting hepatic metabolism could cause the accumulation of vincristine, contributing to toxicity, or reduce of the effectiveness of prodrugs.

51
Q

(L7) What are two ways that chemotherapeutics can be eliminated? What features of a given drug affect how it’s eliminated?

A

Small, hydrophilic drugs that are not substantially metabolized are excreted in the urine. Larger, lipophilic drugs that are metabolized like cyclophosphamide are excreted in bile.

52
Q

(L7) For doxorubicin, what pharmacokinetic property is the best determinant of toxicity?

A

Area under the curve, which is a measure of total systemic exposure or how much of a drug gets into the body.

53
Q

(L7) How can we reduce the risk of acute toxicity associated with doxorubicin administration?

A

Give a longer infusion, which reduces the maximum concentration the patient is exposed to.

54
Q

(L7) For carboplatin, what pharmacokinetic property is the best determinant of toxicity?

A

Area under the curve, which is a measure of total systemic exposure or how much of a drug gets into the body.

55
Q

(L8) Describe how angiogenesis is relevant to tumor metastasis.

A

Without adequate blood flow, tumor cells cannot grow. However, the vessels that are induced to develop by neoplastic cells can be compromised and lack basement membranes, allowing tumor cells to invade and reach general circulation.

56
Q

(L8) How do adherin proteins and collagenases relate to metastasis?

A

Normal cells express adherins on their surface to participate in cell-cell adhesion. Without these proteins, a cell can detach from its neighbors and the basement membrane. Metastatic cells also over-express collagenases, which allow them to chew and migrate through tissues.

57
Q

(L8) What is metastatic inefficiency?

A

Not all malignant tumor cells posses to the ability to metastasize.

58
Q

(L8) Why aren’t all tumor cells capable of metastasis?

A

It’s thought that not all neoplastic cells are capable of surviving circulation or, even if a cell implants on distal site, they aren’t compatible with the local environment (the seed-soil model).

59
Q

(L8) What aspects about an individual cells or a group of cells might help a metastatic cell survive the journey to a distal site?

A
  1. Cells travel clumped together
  2. Neoplastic cells travel bound to platelets, leukocytes, etc.
  3. Neoplastic cells have more plastic/flexible plasma membranes
60
Q

(L8) How does a metastatic cell get from the lumen of a blood vessel into adjacent tissue?

A

Tumor cells can initiate an inflammatory response that increases the leakiness of the endothelial wall, allowing them to migrate into tissue. Similarly, tumor cells can also bind to the endothelium like leukocytes can via chemokine signaling and integrin/ selectin binding, facilitating extravasation.

61
Q

(L8) What is tumor dormancy?

A

When a metastatic cell invades a distal site, instead of proliferating, it can enter a state of quiescence.

VET410 Endocrine/Reproduction (5 decks)

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