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Pathology 1 > New Material for Final > Flashcards

New Material for Final Flashcards

1
Q

Which countries have the highest incidence of HIV?

A

African countries (South Africa and Nigeria, Kenya and Mozambique) as well as India

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2
Q

Be able to describe the replication cycle of HIV

A

HIV infects CD4 cells and macrophages by gp120, gp41, CCR5, and CXCR4; replication in metabolically active cells with reverse transcriptase, using our cell membrane for the envelope.

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3
Q

Why do 10% of hemophiliacs not progress to AIDS?

A

Possibility of no CCR5 receptors

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4
Q

What are the phases of HIV infection that lead to AIDS?

A

Acute Phase: infection, reduced VD4 with viremia, seroconversion, mono-like symptoms

Latent Phase: lymphadenopathy, viral replication, low viremia, opportunistic infections, average length of 10 years

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5
Q

What 2 neoplasms are most often seen in AIDS?

A

Hairy leukoplakia and Kaposi Sarcoma (also non-Hodgkin lymphoma)

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6
Q

What is the diagnostic criteria of AIDS, and what lab tests are used to test for HIV?

A

CD4 count <200 cells/microliter, viremia re-emergence, AIDS-defining diseases
HIV Testing: ELISA and Western blot

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7
Q

What lab tests are used to monitor HIV infection?

A

CD4 count and HIV1 RNA viral load (PCR)

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8
Q

What are mitotic bodies/figures, and what do they tell you about a cancer?

A

Cells (and the chromosomes specifically) undergoing mitosis - one can visualize the mitotic division on a histology slide of the cancer.
It indicates that the cancer is growing.

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9
Q

In what types of tissues do sarcomas arise, and how do they prefer to spread?

A

Muscles and connective tissue

spread in blood stream

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10
Q

What are adenocarcinomas?

A

Glandular cancers

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11
Q

Which tissues are most sensitive to ionizing radiation, and why?

A

Cells in mitosis or the G2 phase

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12
Q

Does the ending “-oma” always mean the cancer is benign?

A

NO! –OMA means tumor.

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13
Q

How does the Ames test work, and for what reasons might it be misleading?

A

The Ames Test works by detecting mutagenic effects of potential carcinogens (potential drugs to weed out possible carcinogens) via inducing frameshift mutations.

Example: Mutated Salmonella cannot produce its own histadine. The bacteria will die without histidine. You place these bacteria in a low-histidine medium (plate) with a potentially mutagenic chemical. If they are mutagenic then the Salmonella can revert back. This will not show epigenetic changes.

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14
Q

Worldwide, which cancer kills the most females, and which kills the most men?

A

MEN: hepatocellular carcinoma
WOMEN: cevical cancer

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15
Q

In the “first world”, at what age range does cancer incidence peak?

A

Peak range: 80-84 years old

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16
Q

What are the MEN syndromes?

A

MEN I: PPP – pituitary adenoma, parathyroid hyperplasia, pancreatic tumors

MEN IIA: PPM – parathyroid hyperplasia, pheochromocytoma, medullary thyroid carcinoma

MEN IIB: PMMM – mucosal neuromas, marfanoid body habitus, medullary thyroid carcinoma, pheochromocytoma

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17
Q

What is the difference between a preneoplastic disorder, and a paraneoplastic syndrome?

A

Paraneoplastic syndromes: occur when neoplasms elaborates a substance that results in an effect that is not directly related to growth, invasion, or metastasis of the tumor itself (hormone-like substances, etc). The syndrome may precede the neoplastic diagnosis and may serve as a signal.

Preneoplastic disorders: may be acquired; issues that increase the likelihood of reaching a cancerous stage and are correlated directly with the cancer (ie HepB and liver cancer).

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18
Q

What is the difference between direct-acting and indirect-acting chemical carcinogens?
What is an initiator?
What are procarcinogens?

A
  • Direct-acting chemical carcinogens (Initiator) modify DNA to cause cancer
  • Indirect-acting chemical carcinogens (procarcinogens) get altered metabolically within us to form active carcinogens
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19
Q

What is the difference between a genotoxic and non-genotoxic mechanism?

A

Genotoxic mechanisms employ DNA damage, chromosomal misentegration, etc
Non-genotoxic mechanisms employ chronic irritation/cell death, ROS, epigenetic silencing, immunosuppression, etc

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20
Q

What do geneticists look for when they are trying to find promoter regions on genes, and why do you increase the risk of malignancy as you increase the number of methylations at these sites?

A

Promoter region alterations are looked at because the mutations are found in all cancers ever studied. Methylation at the CpG island ends with complete silencing of a gene.

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21
Q

What type of solar radiation is the most carcinogenic?

A

UVB

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22
Q

How does UVB cause cancer?

A

It produces pyrimidine dimers in DNA leading to transcriptional errors and mutations of proto-oncogenes and tumor suppressor genes

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23
Q

What type of radiation is the hospitals friend?

aka “The radiation oncologists friend” or “The friend of sterilization”

A

Ionizing radiation (higher-energy radiation)

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24
Q

Why is neutron radiation not used?

A

Neutron radiation doesn’t interact as well and penetrates deeper into the body, only ionizing indirectly

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25
Q

What 3 essential activities are proto-oncogenes involved in?

A

Growth, cellular differentiation, and gene regulation (?)

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26
Q

Know what is meant by gain-of-function and loss-of-function mutations and how many “hits” to the alleles are needed to produce each.

A

Gain-of-Function: oncogenes; one-hit process; creation of a more active protein and stimulation of the cell cycle

Loss-of-Function: tumor suppressors; two-hit process; creates no active proteins and inhibits the cell cycle

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27
Q

Why was Mrs. Rous upset with Dr. Rous? – In his garage, what did he find out that would eventually lead to the understanding that 20% of human cancers come from?

A

Mad b/c he used her blender to blend up chicken tumors
Dr. Peyton Rous found Rous Sarcoma virus.
Discovered that cancer can be transmitted by virus.

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28
Q

How do viruses cause cancer? What is an acutely transforming retrovirus and how does the process work?

A

Viruses can cause cancer/tumors by either carrying in oncogenes or inserting their genome into our genome (possibly into a tumor suppressor, etc).

From microbiology, an acutely transforming retrovirus doesn’t have the proofreading mechanisms that would disallow mutations from occurring.

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29
Q

Fred and Freda both have grade II Stage IIa adenocarcinoma of the distal esophagus. What is it about the same type of tumor at the same stage, that still may make the prognosis in these two individuals different? (hint: think about how clonal expansion of surviving cell variants work)

A

Hormone receptivity/sensitivity.

Estrogen-sensitive cancers may grow more rapidly, but also show a greater sensitivity to radiation therapies.

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30
Q

What are the 7 fundamental changes in cell physiology that are needed for the tumor to behave in a malignant fashion?

A 
Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals
Evasion of apoptosis
Limitless replicative potential
Sustained angiogenesis
Ability to invade and metastasize
Defects in DNA repair
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31
Q

What is the guardian of the genome, and what phase does it normally stop the cell from entering if the cell has damaged DNA?

A

P53 prevents a cell with damaged DNA from entering the S ph

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32
Q

What is Li-Fraumeni syndrome, and what does it cause? What year was it described first in?

A

Li-Fraumeni syndrome: first described in 1969; germ-line rotation of p53; high rate of many types of tumors; childhood sarcomas, breast cancer, brain tumors, leukemia

33
Q

Apoptosis is regulated by which two genes?

A

BCL-2 (inhibits) and p52 (promotes)

34
Q

What is FNA (fine needle aspiration), and what does it not give the pathologist?

A

Basically, the syringe is coated in cells that allows the pathologist to determine metastatic qualities of the cells, but not the morphologic qualities

35
Q

How, on an angiogram, can you tell if vessel growth is normal, or has been caused by angiogenesis resulting from a neoplasm?

A

Normal angiogenesis will show more of a “tree-branching”(fractal) pattern with an appropriate diminishment in size of the blood vessels. A non-fractal pattern with vessels that are tortuous, irregularly-shaped, leaky, with no decreased size or rate of growth would indicate tumor-derived vessels.

36
Q

Why are mice, and not horses or rabbits, sometimes chosen to produce monoclonal antibodies to human cancers in?

A

Cost-effectiveness and increased amount of offspring/litter/year allows you to see epigentic changes more quickly.

37
Q

What do monoclonal antibodies specifically target in human cancers? (hint: CA-125, CA-19-9 {what are these})

A 
Shown on the NCCN website.
CA 19-9: pancreatic CA
CA 125: ovarian CA
Others:
CEA: colon CA, stomach CA, some breast and ovarian CAs
AFP: liver CA
Β-HCG: testicular CA
PSA: prostate CA
BRCA 1, 2: breast CA
CA 15-3: some breast CAs
AFP, HCG: testicular CA
HER2: TISSUE CA ONLY
38
Q

What is the difference between tumor grading and staging?

A

Tumor Grading: specific for each type of tissue and cancer within it; doesn’t indicate prognosis well; more about histology
Tumor Staging: T (size of primary tumor), N (extent of lymph node spread), M (presence of metastatic disease – standard for all cancers); better predictor of prognosis once TNM is placed

39
Q

What is Grade 4 cancer, and what is Stage 4 cancer?

A

Grade 4 Cancer: glands are fused; no intervening stroma

Stage 4 Cancer: METASTASIS

40
Q

What would a grade 4, stage 4 cancer indicate? (in terms of prognosis)

A

Metastatic and not a good prognosis.

41
Q

In tumor progression, what does genetic instability mean? What does this translate to, for people that have a cancer recurrence, and need chemotherapy again? Is this analogous to antibiotic resistance in bacteria?

A

Genetic instability: malignant cells are more prone to mutate and accumulate additional defects (and survive!).

For those who have cancer recurrence, this would mean that the selective growth advantage of the continued cell lines would give way to malignancy. This would – in part – be analogous to antibiotic resistance in bacteria.

42
Q

What is the difference between seeding and transplantation as it relates to metastasis?

A

Seeding is when a cancer in a certain body cavity breaks off and travels and implants within the body cavity.

Transplantation happens during surgery; if the surgeon cuts into the cancer and then it gets transplanted somewhere else this is transplantation- pretty rare.

43
Q

Who was Sister Mary Joseph, and what principle of metastasis did she discover?

A

Sister Mary Joseph was a nurse who discovered periumbilical nodes which correlate to pancreatic cancers

44
Q

What 3 cancers like to metastasize to the brain, and what 3 to the bone?

A

Brain: skin, breast, lung
Bone: breast, lung, prostate (kidney, thyroid)

45
Q

On x-ray, what cancers produce osteoblastic vs. osteolytic lesions?

A

Osteoblastic lesions: prostate cancer

Osteolytic lesions: renal and breast cancers

46
Q

What test can you use on physical exam to test for possible bony metastasis to the spine?

A

(according to Max) spinous process percussion

BUT possibly tuning fork too

47
Q

What is an induction treatment?

A

Induction: sole treatment; used for advanced diseases or when no other treatment exists

48
Q

What is a neoadjuvant treatment?

A

Neoadjuvant: chemotherapy is given first, followed by a secondary treatment

49
Q

What is an adjuvant treatment?

A

Adjuvant: combination with another modality; given after other treatments are used

50
Q

What is a salvage treatment?

A

Salvage: for tumors that fail to respond to initial chemotherapy

51
Q

Which two types of tumors are very radiosensitive to XRT? – WHY?

A

Seminomas and lymphomas because their cells are always replicating and turning over quickly (M-phase)

52
Q

Which two types of tumors are very radioresistant? – why?

A

Epithelial and sarcomas

53
Q

What is the NCCN? – Why might you want to sign up for an account? How do you use it?

A

National Comprehensive Cancer Network
Dr. Chamberlin loves it, so you should sign up for an account. Also, because the site shows you staging and allows you to look up possible therapies or beneficial stories.

54
Q

What are the odors that suggest a diagnosis?

What do arsenic and cyanide smell like?

A

Bitter almonds: cyanide
Fruity: diabetic ketoacidosis; isopropanol
Garlic: organophosphates, arsenic, DMSO, Se
Mothballs: Naphthalene, camphor

55
Q

How often do patients with carbon monoxide poisoning turn cherry red?

A

Rarely

56
Q

What poisoning often accompanies carbon monoxide poisoning in residential fires, yet was not even know of until very recently? How are each treated?

A

Cyanide poisoning is clinically indistinguishable from carbon monoxide poisoning in the field. Carbon monoxide poisoning can be determined through a pulse oximeter.
Tx for carbon monoxide poisoning is first remove them from the area and then put them in a hyperbaric oxygen chamber w/100% oxygen.
Tx for cyanide poisoning is a cyanide antidote package which includes amyl nitrite, sodium nitrite and sodium thiosulfate.

57
Q

What is generally meant by heavy metals, and what 2 ways are their exposures described in?

A

Heavy metals are metals or metalloids of environmental concern; can be Pb, Hg, Cd (all denser than Fe) or thallium, antimony, Ag, Se, Zn, Cu, Ni, Co, Cr, As.
Acute and chronic exposures are seen.

58
Q

Do radioisotopes bioconcentrate? How do they get into the air? (hint: no water… fuel rods get hot… they melt together…. they start a fire…. Smoke is released into the air containing _________?

A

Biomagnification/bioconcentration is the process of the concentration of toxic substances in living organisms as they move up each step of the food chain. ???

59
Q

Does a bottle of wine made in 1924 contain Cesium?

A

No, bottles of wine up until the 1942 won’t have cesium in them.

60
Q

How can you increase the toxicity of Hg? (hint: it involves a well-known chemical process that you hear about in school every day and can’t seem to get away from unless you stay home)

A

Methylation of mercury is more water-soluble and can cross the BBB and placental barrier; consumption of carnivorous fish can cause bioaccumulation. ???

61
Q

Hg causes 2 main toxicities…. What are they?

A

Neurotoxicity and nephrotoxicity.

62
Q

Why is arsenic poison? Is it poison to everything on earth?

A

Acute poisoning from arsenic causes CAN toxicity and hemorrhagic gastroenteritis. Chronic poisoning causes malaise, abdominal pain, skin changes, and Mees lines. Complications of squamous cell carcinoma of the skin/lung and angiosarcoma of the liver also occur.
Arsenic can/has serve/d as a backbone for certain species’ genomes, so no it is not always poisonous.

63
Q

What is the difference between Mees lines and lead lines?

A

Mees lines are transverse bands on the fingernails seen in arsenic poisoning.
Lead lines are lead depositions at the gingivodental line.

64
Q

Why is lead poisoning so much more destructive in children?

A

There are additional complications for children, mainly having to do with CNS toxicity (lethargy, somnolence, cognitive impairment, developmental delay, cerebral edema, and peripheral neuropathy).

65
Q

What is Pica? What is basophilic stippling?

A

Pica is the desire to eat dirt (as well as ice, etc). It is a genetic condition seen in children.

Basophilic stippling is seen in conjunction with microcytic anemia in lead poisoning. The ribosomes of the cells are spread throughout the cell, showing small dots at the periphery.

66
Q

Why do people that start smoking at age 30 or 40 usually not get COPD?

A

People usually have a lesser chance of getting COPD because epithelial transition ends beginning around age 20- lung tissue is basically set down by 20.

67
Q

Why is 20 pack years a notable number in lung cancer?

A

It will show significant enough tissue damage/change to cause a larger effect on the body- basically you are on the road to getting cancer.

68
Q

What are the 3 main illness in children that second hand smoke seems to increase the risk of ​getting?

A

SIDS, otitis media, asthma/URIs

69
Q

Know what photochemical smog is, and how it differs from smog when it was first described in ​1905

A

Photochemical smog is the chemical reaction of sunlight, NOs, and VOCs in the atmosphere, leading airborne particles and ground-level ozones. It is a mixture of aldehydes, NOs, trophospheric ozone, and VOCs. Smog in 1905 was “pea soup fog” caused by burning large amounts of coal in a city; it contained soot particles, sulfur dioxide, etc.

70
Q

What are VOC’s and how are they made? Through what chemical reaction are we making ​Ozone? Where does the ozone go if there is an air inversion?

A

VOCs are volatile organic compounds.
How are they made???
Ozone is formed in the atmosphere; NO is a byproduct of combustion and will break up upon contact with sunlight; three of the “freed” oxygen molecules will combine to form ozone.
Ozone gets trapped very close to the earth within the smog during an air inversion.

71
Q

Why is silicosis the most common pneumoconiosis?

A

Pneumoconiosis is most commonly caused by inhalation of dust or pollutants in smog and these are around every day sooooo= pneumoconiosis.

72
Q

What is silicosiderosis?

A

Silicosiderosis is the disease caused by the inhalation of mixed dust particles containing silica and iron.

73
Q

What is Caplans syndrome?

A

Caplan’s syndrome is pneumoconiosis in combination with multiple pulmonary rheumatoid nodules found in RA patien

74
Q

What is the difference between silicates, silicon, and silicone?

A

Silicates: addition of other atoms onto silica to make minerals.
Silicon: chemical element, but almost always in combination with oxygen.
Silicone: synthetic polymer of silicone with carbon and oxygen; found as solid, liquid, or gel.

75
Q

What are the two meanings of “pathognomonic”? In what disease are eggshell calcifications ​seen on CXR? Are they pathognomonic in both definitions for this disease?

A

Pathognomonic: 1) a symptom/sign that is characteristic of a disease, 2) this will – without a doubt – tell you that it is one disease and not another.
Eggshell calcifications indicate silicosis. YES it is pathognomonic in both definitions.

76
Q

How do inhaled particles of silicates, asbestosis, and many other things cause fibrosis in the ​lungs?

A

Macrophage ingestion of the asbestos fibers triggers a fibrogenic response via the release of growth factors, promoting collagen deposition by fibroblasts.

77
Q

Where in the lungs do the fibers of asbestosis localize? What are these fibers called, and what ​type of lung cancer do they cause? Where is this lung cancer localized? Why?

A 
The fibrosis will appear as brown nodules in the septum of the alveolus and in the distal lung and may have a rod/dumbbell shape with multiple segmentations.
Causes mesothelioma (1000-fold more common with asbestos exposure) that involves the lower lobes and pleura. The issues can begin as fibrotic plaques. ???
78
Q

How many fold does a person’s risk of getting lung cancer increase if they are exposed to ​asbestosis?
How about if they are exposed to asbestosis and smoke?
What does this ​relationship tell us about the nature of environmental toxins, or for toxins in general?

A

A person’s risk of getting lung cancer increases 5-fold when exposed to asbestos
If they smoke and are exposed to asbestos, then their chances increase 55-fold
This is a demonstration of the additive effect (“the whole is greater than the sum of its parts”) because it exponentially increases your risk of developing the cancer.

Pathology 1 (6 decks)

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