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Pathology-Exam 3 > Final > Flashcards

Final Flashcards

1
Q

which countries have the highest incidence of HIV?

A

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

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2
Q

replication cycle of HIV

A

HIV infects CD4 cells & 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 CD4 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/mL, viremia re-emergence, AIDS-defining disease
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

mitotic bodies are one of the possible signs of possible malignancy that stain differently histologically. If you see mitotic bodies it is indicative of dividing cells–> what you would expect to see of cancerous cells

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9
Q

in what types of tissue 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

in what types of tissues do carcinomas arise, and how do they prefer to spread?

A

epithelium spread through lymphatic system

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11
Q

what are adenocarcinomas?

A

glandular cancers

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12
Q

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

A

cells in mitosis or the G2 phase

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13
Q

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

A

No! -OMA means swelling/tumor. Have to memorize cancers on a case by case basis.

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14
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. Mutated Salmonella cannot produce its own histidine. 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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15
Q

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

A

MEN: hepatocellular carcinoma
WOMEN: cervical cancer

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16
Q

in the first world, at what age range does cancer incidence peak?

A

80-84 y/o

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17
Q

Know you MEN syndromes!!!

A

MENI: PPP- pituitary, parathyroid hyperplasia, pancreatic tumors
MENIIA: PPM- parathyroid hyperplasia, pheochromocytoma, medullary thyroid carcinoma
MENIIB: PMMM- mucosal neuromas, marfanoid body habitus, medullary thyroid carcinoma, pheochromocytoma

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18
Q

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

A

Paraneoplastic syndromes occur when a neoplasms elaborates a substance that results in an effect that is not directly related to growth, invasion, or metastasis of the tumor itself (hormone, etc). The syndrome may precede the neoplastic diagnosis and may serve as a signal.
Preneoplastic disorders may be acquired and are issue that increase the likelihood of reaching a cancerous stage and are correlated directly with the cancer (Hep B and liver cancer)

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19
Q

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

A

initiator: direct-acting chemical carcinogens modify DNA to cause cancer; indirect-acting chemical carcinogens (procarcinogens) get altered metabolically within us to form active carcinogens

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20
Q

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

A

genotoxic mechanisms employ DNA damage, choromosomal misentegration, etc.
non-genotoxic mechanisms employ chronic irritation/cell death, ROS, epigenetic silencing, immunosuppression, etc

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21
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 mutations here are found in all types of cancers. Methylation at the CpG islands ends with complete silencing of a gene

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22
Q

what type of solar radiation is the most carcinogenic

A

UVB

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23
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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24
Q

what type of radiation is the hospitals/oncologists/sterilization friend?

A

Ionizing radiation (higher-energy radiation)

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25
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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26
Q

what 3 essential activities are proto-oncogenes involved in?

A

growth, cellular differentiation, and gene regulation

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27
Q

what is meant by gain-of-function and loss-of-function mutations? 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
loos-of-function: tumor suppressors; two-hit process; creates no active proteins and inhibits the cell cycle

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28
Q

how do viruses do this? 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 microbio, 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?

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 phase

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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

BLC-2 (inhibits) and p53 (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 (confirms presence of cancer but not type of cancer)

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 torturous, 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

37
Q

what do monoclonal antibodies specifically target in human cancers? (hint: CA-125, CA19-9)

A

CA 125: ovarian cancer

CA 19-9: pancreatic cancer

38
Q

what is the difference between tumor grading and staging?

A

tumor grading: is specific for each type of tissue and cancer within it; doesn’t indicate prognosis well; more about histologic estimate of the malignancy of tumor (degree of differentiation)
tumor staging: clinical estimate of the extent of tumor spread; TNM staging system: T (size of primary tumor), N (extent of lymph node spread), M (presence of metastatic disease- standard for all cancers); better predictor of prognosis than tumor grading

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 prognoss

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 something is growing on the surface of a cavity and will metastasize to another site/area within the same cavity/tissue.
transplantation occurs when “clean margins” are not maintained and, for instance, a surgical incision may take the cancerous cells to another site in the body.

43
Q

who was Sister May Joseph, and what principle of metastasis did she discover?

A

Sister Mary Joseph was a nurse who discovered periumbilical nodes correlated to pancreatic cancer

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

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 a physical exam to test for possible bony metastasis to the spine?

A

spinous percussion using a tuning fork

47
Q

induction

A

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

48
Q

neoadjuvant

A

chemotherapy is given first, followed by a secondary treatment

49
Q

adjuvant

A

combination with another modality; given after other treatments are used

50
Q

salvage

A

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 becase they are not replicating as quickly

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. it will show you staging and allow you to look up possible therapies or beneficial stories.

54
Q

what are odors that suggest a diagnosis?

A

fruity- diabetic ketoacidosis, ispropanol

garlic breath- arsenic poisoning

55
Q

what do arsenic and cyanide smell like?

A

arsenic- garlic

cyanide- bitter almonds

56
Q

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

A

rarely

57
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 and if pt is treated for CO and doesn’t clear, treat for cyanide poisoning using cyanide antidote package.

58
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 any other similarly toxic metal, or metalloid like arsenic, regardless of its density. Each described in terms of acute and chronic exposure.

59
Q

do radioisotopes bioconcentrate? how do they get into the air?

A

fuel rods get hot, they melt together, they start a fire, smoke is released into the air containing radioisotope or its fallout.

60
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

61
Q

how can you increase the toxicity of Hg?

A

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

62
Q

Hg causes 2 main toxicities…what are they?

A

neurotoxicity and nephrotoxicity

63
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 served as a backbone for certain species’ genomes, so no it is not always poisonous.

64
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.

65
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).

66
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.

67
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. When you start smoking later, the cumulative effects take later to appear.

68
Q

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

A

It was the old belief that if you had not had 20 pack years of smoking, then you would not get cancer. It will show significant enough tissue damage/change to cause a larger effect on the body.

69
Q

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

A

sudden infant death (SIDS), otitis media OM), asthma/upper respiratory infections (URIs)

70
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.

71
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.
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.

72
Q

Why is silicosis the most common pneumoconiosis?

A

Pneumoconiosis is occupational lung disease caused by inhalation of dust. SILICONE MORE HAZARDOUS THAN COAL BECAUSE IT EXISTS IN SO MANY FORMS (solid, liquid, gel)- WILL BE EXPOSED IF WORKING WITH IT

73
Q

What is silicosiderosis?

A

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

74
Q

What is Caplans syndrome?

A

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

75
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

76
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.

77
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.

78
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. Asbestos tends to like the outer linings of the lungs.
Causes mesothelioma (1000-fold more common with asbestos exposure) that involves the lower lobes and pleura. The issues can begin as fibrotic plaques.
79
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-Exam 3 (1 decks)

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